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Incidence of cystic changes in impacted lower third molar. To assess the incidence of cystic changes in the impacted lower third molar (ILTM) in which the pericoronal (follicular) space is less than 2.5 mm as measured from the radiograph. The relationship between the cystic changes and patient's age, sex, and angular position and contact of ILTM with adjacent tooth was also evaluated. Follicular space less than 2.5 mm as measured from the panoramic radiograph was included in the study. A total of 73 tissue samples collected during the extraction ILTM were examined histopathologically. Then the data were analyzed for associations with age, sex, angular position, and contact of the ILTM with an adjacent tooth. There were 37 male and 36 female patients, age ranging from 17 to 35 years (mean 23.95 years). Out of 73 specimens, 17 (23.3%) showed cystic changes; among them 16 (22.1%) showed dentigerous cysts and 1 (1.2%) showed odontogenic keratocysts. Most of the cystic changes occurred in the 26-30 year age range. The cystic changes showed male predominance but could not gain statistical significance. The relationship between cystic changes and angular position was statistically significant (P < 0.05). Higher probability was found in distoangular positioned ILTM. The relationship between cystic changes and communication of ILTM with the second molar was not statistically significant. Incidence of cystic changes in ILTM justifies extraction of the impacted tooth associated with symptoms. The decision to extract or not to extract impacted third molar should be individualized, rather than generalized.

A crisis in the analyst's life: self-containment, symbolization, and the holding space. Most analysts will experience some degree of crisis in the course of their working life. This paper explores the complex interplay between the analyst's affect during a crisis in her lifeü and the affective dynamics of the patient. The central question is "who or what holds the analyst"--especially in times of crisis. Symbolization of affect, facilitated by the analyst's self-created holding environment, is seen as a vital process in order for containment to take place. In the clinical case presented, the analyst's dog was an integral part of the analyst's self-righting through this difficult period; the dog functioned as an "analytic object" within the analysis.

SHARE THIS POST: I had the pleasure of spending some quality time with the amazingly talented indie dev community at the Monthly Seattle VR Meetup last night. As a co founder of this Meetup group, I am excited each month to gather with so many passionate individuals with an evening intended to push VR to its highest potential, and to welcome newcomers to the community with open arms. This month’s meetup focused on art and VR creation tools such as Tilt Brush and Oculus Medium. We had multiple workstations set up and lines of people eagerly waiting to show off their artistic skills on a digital canvas. While the focus last night was on art, it didn’t stop some of us from having some great conversations about other VR related content. As I have grown to expect, I met an indie dev who was anxious to put a GearVR on my head to show off his latest creation. I enjoy this sort of interaction because it gives me a chance to help build up a good indie dev by being honest and delivering constructive feedback. The experience was great. It had simple control, basic mechanics, and an arcade feel that made me want to keep playing. I took the GearVR off my head and immediately said, ‘Three months of fine tuning, and this could be a million dollar game.’ The reaction was not what I expected. What he showed me was just a small part of a much larger vision that he had for this game. The dev described to me a much more elaborate experience, with high end graphics, a back story, controllable weapons, touch interface, etc. My analysis of what I felt was a 90% completed game was not in line with his final plans. I encouraged him to continue with his grand plan, but he could also put out this separate smaller version in the interim. Then he said, ‘I wouldn’t want to release it in this state. I don’t want to put out Shovelware.’ Later in the evening, I was approached by yet another energetic indie dev who showed be various videos of projects he had built over the last few months. After seeing his portfolio, I suggested that he should publish a few of them and get them into Steam or an app store. His reply? ‘I don’t really think any of it is ready.’ As a developer myself, I understand the pressure we put on ourselves to protect our creations until they are perfect. Even the thought of someone playing an incomplete version of my game sends chills down my spine. I don’t want any form of opinion or criticism on my unfinished product because I’m not done with it yet. What indie devs truly need to realize is that maybe we are living inside a bubble that doesn’t allow us to see the value in what we’ve already created. Maybe our goal of absolute perfection is blinding us from seeing a much closer finish line. We have a relatively young VR market, with a sparse selection of titles. I think every indie dev should reevaluate their goals, and possibly crop their scope a bit to ge their title out sooner rather than later. It’s not Shovelware. It would be different if we had hundreds of thousands of titles in the VR space. Then, I could see wanting to wait a bit, expanding your scope, and tweaking the game enough to rise to the top of a massive market. We don’t have a big enough selection for that to be necessary for success. It’s not Shovelware if your filling a hole. You can’t flood a market that isn’t even full yet. Indie devs, this is a call to arms. Grab that fun little arcade title that you built at the last hackathon, polish it for a few months, and get it in the store ASAP. Keep working on your ambitious MMO or your super realistic Bop-It simulator, but also share your fun little pet projects with the world. Make a name for yourself. Don’t worry. When it starts to become Shovelware, I’ll let you know. SHARE THIS POST:

Review by peter verified purchaser Rating 100 Great, powerful, little processor PCB. I'm using these as remote camera platforms and it's fun and easy. Can do so much with so little, and Core's price can't be beat! (Posted on 16/09/2020) Review by Bruce verified purchaser Rating 100 Excellent product with excellent service. (Posted on 16/09/2020) Review by Melissa verified purchaser Rating 100 Very impressive SBC for it's size. Works great on 18650 batteries only consuming ~110mA at idle (Posted on 15/09/2020) Review by Steven verified purchaser Rating 100 Fun to get all the bits to work on a minimum spec pc... and works well as can be expected... the rip 0 just falls below min spec. As just cannot work without built in Wi-Fi n blue tooth. This rpi0 W trumps it at a bit higher price tag (Posted on 15/09/2020) Review by Steven verified purchaser Rating 100 Fun to get all the bits to work on a minimum spec pc... and works well as can be expected... the rip 0 just falls below min spec. As just cannot work without built in Wi-Fi n blue tooth. This rpi0 W trumps it at a bit higher price tag (Posted on 15/09/2020) Review by Joel verified purchaser Rating 60 Good board but I wish they kept a normal size hdmi and I wish they made a official microusb Ethernet adapter. The wifi performance is appalling. I should have bought the non wifi model. (Posted on 14/09/2020) Review by Richard verified purchaser Rating 100 Great little device. Good instructions on how to setup are on the site, although how to do a headless setup need a little updating due to some changes to raspbian. Anyhow, is now up and running and working well! (Posted on 13/09/2020) Review by Conrad verified purchaser Rating 100 Awesome value for the price. It’s a fully functional computer in a tiny size which is great for bespoke needs including IOT. (Posted on 11/09/2020) Review by Gaurav verified purchaser Rating 100 This board is powerful. I bought this for setting up Pi-hole and it works flawlessly. (Posted on 11/09/2020) Review by Bob verified purchaser Rating 100 Product as advertised and prompt service, thanks people. (Posted on 10/09/2020) Review by Henry verified purchaser Rating 100 $20 for a network wide adbloker with Pi-Hole that also improves network performance? Can't get better than that! (Posted on 10/09/2020) Review by Daryl verified purchaser Rating 100 Works great , being used as part of our home automation system. Easy to setup and use. (Posted on 9/09/2020) Review by James verified purchaser Rating 100 Arrived promptly, thank you (Posted on 9/09/2020) Review by Steven verified purchaser Rating 100 3rd pi product and 1st zero For the price and size perfect for new comers to the raspberry world (Posted on 8/09/2020) Review by Samuel verified purchaser Rating 100 Fantastic little product, cheap and fast shipping was a bonus. (Posted on 8/09/2020) Review by Ben verified purchaser Rating 100 Perfect little Pi. Thanks for the headless setup tutorial - hides out of view and taps into the Wi-Fi. (Posted on 14/08/2020) Review by Martin verified purchaser Rating 100 Nice little SPC. Will do perfectly for the BOINC Cluster I wanted to try out (Posted on 2/06/2020) Review by Gabriel verified purchaser Rating 100 Great product, delivery was spot on. Thanks guys. (Posted on 2/06/2020) Review by Jeffery verified purchaser Rating 100 Smallest device I have ever used as a computer. Next they will be the size of an SD card. Works great (Posted on 29/05/2020) Review by Chris verified purchaser Rating 100 Awesome :)! Love these things. (Posted on 25/05/2020) Review by Adrian verified purchaser Rating 60 Seems to work fine, but the GPi case it's used with is a problem. (Posted on 25/05/2020) Review by Adrian verified purchaser Rating 100 Seems to work fine, but the GPi case it's used with is a problem. (Posted on 25/05/2020) Review by Mark verified purchaser Rating 100 The Raspberry Pi has to be one of the greatest personal computers in history. This Zero edition is amazing value. A fantastic headless, tiny, low power computer for the price of lunch! You can't go wrong. (Posted on 22/05/2020) Review by Paul verified purchaser Rating 100 Worked great first time. Best price and only stock in Sydney. Delivery was reasonably priced too. Very very happy. (Posted on 22/05/2020) Review by James verified purchaser Rating 100 Love this thing - note no headers are connected so you need to sort that out yourself! (Posted on 19/05/2020) Review by Bill verified purchaser Rating 100 I love the small form factor on the PI Zero which is ideal for my Magic Mirror project. I've used a PI 3 for a while now so was (wrongly) expecting a similar performance. Of course the Zero is not designed to compete on performance however it is adequate run Chromium Browser, albeit a bit slower to start up. (Posted on 18/05/2020) Review by Lucas verified purchaser Rating 80 Neat little unit, only annoying in that I didn't have an OTG adapter handy. (Posted on 15/05/2020) Review by Daniel verified purchaser Rating 100 This thing is amazing! Despite its tiny size, I've managed to get selenium running in python on it and using a headless browser it'll do fun little automated web scraping tasks! Also makes a handy little Spotify streamer when coupled with a https://core-electronics.com.au/adafruit-i2s-audio-bonnet-for-raspberry-pi-uda1334a.html (Posted on 15/05/2020) Review by Stephen verified purchaser Rating 100 An excellent device, perfect as a Plex Client ! (Posted on 14/05/2020) Review by Greg verified purchaser Rating 100 Great as it is so easy to setup and immediately start and do projects (Posted on 14/05/2020) Review by Carl verified purchaser Rating 100 Great. Works as expected. (Posted on 13/05/2020) Review by Chris verified purchaser Rating 100 Great little device, and prompt service from the Core Electronics team. (Posted on 13/05/2020) Review by Ian verified purchaser Rating 100 I dont understand this order. I clicked on the link to find out what it is about and it seems I have to fill a review first. Well many months ago I purchased a Pi Zero and it wouldnt work. 11 days ago this order appeared in my emails for no reason. Nothing has arrived in the mail. I thought you may have been kind enough to replace the failed one but I dont know what is going on. (Posted on 11/05/2020) Review by Steve verified purchaser Rating 100 Excellent (Posted on 11/05/2020) Review by Colin verified purchaser Rating 100 Great little product. Have about 4 of them now. Installed one with the camera in a clear perspex case and mounted on the back of my caravan. Had an old wireless router so I streamed the video to that and can now see who is behind me by logging on with an old ipad. (Posted on 11/05/2020) Review by Stuart verified purchaser Rating 100 Great, working well, running it off my Makita 18V, 5Ah battery. (Posted on 7/05/2020) Review by Lou verified purchaser Rating 100 Great piece of tech (Posted on 6/05/2020) Review by Bradley verified purchaser Rating 100 Working great for my Octoprint server!! (Posted on 5/05/2020) Review by Peter verified purchaser Rating 100 It's tiny! (Posted on 5/05/2020) Review by Nikolas verified purchaser Rating 100 Make sure you have a mini-HDMI adapter if you want to plug this into a monitor! (Posted on 3/05/2020) Review by Max verified purchaser Rating 100 I'm having a great time with this little beast. these guys sent me this because they sent me the older version when i ordered this. They let me keep the other Pi! these core electronics sure know how to satisfy a dodgy order. These are legit boards. thank you so much my dudes (Posted on 30/04/2020) Review by Kancelot verified purchaser Rating 100 A great tiny device that runs Linux with plenty of grunt for IoT and sensor applications. I have mine tracking presence with Bluetooth LE and a whole bunch of sensors connected measuring temperature, humidity and air quality. (Posted on 30/04/2020) Review by gareth verified purchaser Rating 100 Great little machine. Works really well. Very happy with my purchase and great service too :) (Posted on 29/04/2020) Review by Paul verified purchaser Rating 100 Product is as described and shipped in a the next day. (Posted on 29/04/2020) Review by Adrian verified purchaser Rating 100 Amazing value. So much fun to play with. Love it, and love these guys. Great follow up support and always quick to respond. (Posted on 28/04/2020) Review by Ryan verified purchaser Rating 100 Perfect, exactly what I needed with zippy shipping (Posted on 28/04/2020) Review by Christopher verified purchaser Rating 100 Definitely the best new computer $20 can buy. I bought this to use in the GPI Case and it has run well. I was surprised at how small it was. (Posted on 28/04/2020) Review by Andrew verified purchaser Rating 100 awesome device, quick shipping, definitely buying from Graham and the team again. (Posted on 27/04/2020) Review by Jesse verified purchaser Rating 100 Awesome little project board! (Posted on 26/04/2020) Review by Gary verified purchaser Rating 100 Great product, GUI was slow to load with the NOOBS card that came with it. WiFi transfer rate was very slow. Resolved this by running headless, no gui. (Posted on 23/04/2020) Review by Andrew verified purchaser Rating 100 Great product! There were supply issues which meant I couldn't get this delivered immediately but Core Electronics made estimates very clear throughout the process and it arrived even sooner than I expected. Very helpful recommendations for additional items to purchase, too. (Posted on 21/04/2020) Review by Jeff verified purchaser Rating 100 Got this to setup Pi-Hole on home wifi network and works a treat (Posted on 21/04/2020) Review by Geoffrey verified purchaser Rating 100 Great price and service. Happy to deal with and will buy again. Thank you! (Posted on 20/04/2020) Review by Shannon verified purchaser Rating 80 Took forever to come probably due to the chaos but it came in a nice box :) (Posted on 20/04/2020) Review by Luke verified purchaser Rating 100 Fantastic iteration of a well known and loved platform. Extremely easy to set up and get going right away (provided you have the right adaptors!) Received it within 2 weeks of ordering, despite the site indicating that it would be a couple of months wait. Highly recommended! (Posted on 20/04/2020) Review by David verified purchaser Rating 100 It's a Pi - and it's tiny. I think the Zero is the most fun Pi because it's so small. (Posted on 18/04/2020) Review by Cathy verified purchaser Rating 100 Really good - functioned as I expected. As always, service was brilliant. (Posted on 17/04/2020) Review by Jason verified purchaser Rating 100 Perfect for my first project building a pi-hole, soon to me a VPN :) (Posted on 9/04/2020) Review by Scott verified purchaser Rating 100 great little computer. Simple to setup and takes up barely any space. The possibilities just keep growing! (Posted on 11/03/2020) Review by Cameron verified purchaser Rating 100 Pi Zero + pihole. No ads in your household ever again for under $20. (Posted on 2/03/2020) Review by Malcolm verified purchaser Rating 100 Great little unit, very happy. (Posted on 26/02/2020) Review by Matthew verified purchaser Rating 100 Awesome product, very easy and quick to setup and start using. Found the Core Electronics headless article/video a great starting point. (Posted on 30/01/2020) Review by Kevin verified purchaser Rating 100 What an amazing little device - a full blown computer barely larger than a credit card. But don't expect super-computer performance - but it will probably outdo a quad-core Intel running Windoze. ;) Get one and have a play. The "down" side: you'll have to learn Linux. (Don't even think about putting Win10 on a Pi.) Oh, and don't connect 5V to a GPIO pin. ;) :( (Posted on 27/01/2020) Review by Rick verified purchaser Rating 100 Great product at a great price, (Posted on 27/01/2020) Review by David verified purchaser Rating 100 Fast delivery. Great for home projects - like a watering system with integrated web server! (Posted on 24/01/2020) Review by Jarrod verified purchaser Rating 100 It's exactly as described - nothing more, nothing less. Mine is settling in quite nicely as an integral part of my home automation. (Posted on 23/01/2020) Review by Lucas verified purchaser Rating 100 Very handy particularly when combined with the new 8MP Pi camera board. Makes a cheap IP camera and 2nd camera for a 3D printer. (Posted on 23/01/2020) Review by Chris verified purchaser Rating 100 Great product tuned it into a network wide ad tracker blocker using Pi-Hole (Posted on 23/01/2020) Review by Max verified purchaser Rating 100 Tiny isn't it? My Pi is now doing a fine job of UPS management (NUT), remote access (OpenVPN) and web site host (Python3, Flask, Apache). Webmin is a little slow but also works well. All the hardware plugged in and worked, no problems at all. (Posted on 16/01/2020) Review by Leigh verified purchaser Rating 100 Raspberry Pi Zero W is a damn game changer. I've deployed a few of these at home and work, they're such a great and cost effective way to prototype up a quick device. (Posted on 14/01/2020) Review by Leigh verified purchaser Rating 100 Raspberry Pi Zero W is a damn game changer. I've deployed a few of these at home and work, they're such a great and cost effective way to prototype up a quick device. (Posted on 14/01/2020) Review by Aaron verified purchaser Rating 100 These little things are amazing! Run your own PiHole to remove ads on your home network or grab a RetroFlag GPi case for some retro gaming fun. (Posted on 13/01/2020) Review by Patrick verified purchaser Rating 100 Does exactly what it says on the tin. (Posted on 6/01/2020) Review by Matt verified purchaser Rating 100 What can I say, it's an amazing little device! Shipping was fast. (Posted on 6/01/2020) Review by Daniel verified purchaser Rating 100 Did not realise just how small the pi zero is, pretty amazing! The first raspberry pi device I have bought and excited to experiment (Posted on 5/01/2020) Review by Nick verified purchaser Rating 100 Fantastic product does exactly what I need it to. The price is outstanding I will be buying more Raspberry Pi Zero to expand my projects. (Posted on 4/01/2020) Review by Benjamin verified purchaser Rating 100 Amazing value for people just getting started, absolutely astounded with the RPi Zero but definitely vying for a fully fledged RPi on my next project! (Posted on 3/01/2020) Review by Subhajit verified purchaser Rating 100 Full fledged Linux machine, very small footprint, sufficient power. (Posted on 3/01/2020) Review by Paul verified purchaser Rating 100 This little SBC is more powerful than I first believed! I'm using it to run a digital photo frame with Raspbian Lite and a stripped down version XFCE it works very well. The wireless is strong. (Posted on 31/12/2019) Review by Joel verified purchaser Rating 100 The popularity of the Pi0w is completely justified. I’ve used one as an RTL-SDR server, another as a Hoobs (Homebridge) server and still another as a portable network diagnostics tool. The only potential issue for beginners is the soldering of the headers for use with hat, etc, but it’s not too difficult with a bit of practice. It’s a remarkable device, particularly for the price. I’ve used them with a Wombat prototyping breadboard with great results. For passive displays the Waveshare ePaper 2.13 hat fits perfectly with no fuss. (Posted on 25/12/2019) Review by Stephen verified purchaser Rating 100 Perfect and well packed all up and running with no trouble at all. Thanks guys (Posted on 23/12/2019) Review by Josh verified purchaser Rating 100 Great performer for such a low price! (Posted on 20/12/2019) Review by John verified purchaser Rating 100 A neat compact product. Interfaced back to my linux desktop easily by wireless and ssh. Need a good tutorial about ssh over usb but got it working, by setting fixed mac addresses at the rpi end. Now working on the rest of my project ... (Posted on 19/12/2019) Review by Mal verified purchaser Rating 60 Worked well until I moved it on the bench. Not a particularly hard move but the hdmi cable caught and broke off the hdmi connector. The solder providing the physical strain relief on said connector were dry joints. (Posted on 17/12/2019) Review by Anthony verified purchaser Rating 100 I used to buy the pi zero from the UK. Now I buy them from C. E. Very helpful people and very quick delivery. Highly recommended. (Posted on 16/12/2019) Review by bong fong verified purchaser Rating 100 Very happy with the service, prompt delivery and responsive and friendly support from the team. I will surely come back to this website to get more products when needed. (Posted on 16/12/2019) Review by Evgueni verified purchaser Rating 100 great little computer (Posted on 5/12/2019) Review by M.J.Lees verified purchaser Rating 100 Works fine -- using it with an MMDVM hat for DMR. (Posted on 4/12/2019) Review by Peter verified purchaser Rating 80 Hard to beat for the price but I found somewhat underpowered for my requirements, i.e. electronic signage, especially if other than simple graphics are to be displayed. Will purchase a PI 4 when I am ready but I am sure I will find a use for the Zero. (Posted on 2/12/2019) Review by Aaron verified purchaser Rating 100 Great little board, (Posted on 30/11/2019) Review by Tamas verified purchaser Rating 100 Great, working nice as i expected for my project (Posted on 23/11/2019) Review by Carl verified purchaser Rating 100 Works great! (Posted on 16/11/2019) Review by Jason verified purchaser Rating 100 A great little unit for logging fermentation progress. Good customer support from Core Electronics (Posted on 16/11/2019) Review by russel verified purchaser Rating 100 The fastest delivery yet I wish all other delivery could be as fast as this was ..Raspberry Pi Zero, and W work as expected nice and small and Its pitty you can only buy one per order .thanks CORE ELECRTONICS (Posted on 15/11/2019) Review by Jono verified purchaser Rating 100 Great product to add to my collection of gadgets. Can't wait to get some more :) (Posted on 15/11/2019) Review by Peter verified purchaser Rating 100 Well, what can you say? It's a Raspberry-Pi Zero W and works as expected! It's replacing an old Pi 2 and works perfectly in that role. If you're setting one up headless from scratch, pay careful attention to the instructions on defining the WiFi SSID before your first boot... (Posted on 15/11/2019) Review by Daniel verified purchaser Rating 100 Bought for a project that I haven't started yet. It arrived well packaged and I expect it will perform well. (Posted on 15/11/2019) Review by Tim verified purchaser Rating 100 Good customer support. (Posted on 31/10/2019) Review by Rob verified purchaser Rating 100 Great service from Graham and the team at Core. Stock of the model I ordered was delayed so they offered me a free upgrade, which was brilliant. Fast shipment on all items. I have the Pi successfully setup as a data logger in my brewery and it was probably the easiest thing I have done brewing-wise (google TiltPi For details). (Posted on 23/10/2019) Review by John verified purchaser Rating 100 All of my previous Pi Zero W units were with headers. This is the first I've used without headers as I only needed 4 connections for an I2C device and it required less work and a smaller profile using the headerless unit. As with the other Zero W units, it is great for simple jobs. (Posted on 8/10/2019) Review by Greg verified purchaser Rating 100 Great product, good postage rate and fast service. (Posted on 7/10/2019) Review by Daniel verified purchaser Rating 100 What else needs to be said, it's the pi zero w. The only place in Australia I purchase mine from. Great bit of gear and a great service. (Posted on 4/10/2019) Review by Phil verified purchaser Rating 100 For the purpose I needed this for, it works extremely well, as does all the other Pi devices I have purchased. Never struck a problem yet. (Posted on 3/10/2019) Review by Hans verified purchaser Rating 100 Meet my new pi-hole! Happy to get one locally, no fuss, from core. Not much more to say - just don’t get me started on Australia Post, they s p e e d (Posted on 30/09/2019) Review by Steve verified purchaser Rating 100 For hobby enthusiasts the Raspberry Pi Zero W is a solid entry level micro computer which has the added benefit of wireless and bluetooth technology onboard making dialogue and transfers a breeze. Performs very well as an emulation system up to and including the Playstation era. Highly recommended. (Posted on 26/09/2019) Review by William verified purchaser Rating 100 A fantastic little device. (Posted on 24/09/2019) Review by Andrew verified purchaser Rating 100 Very happy with the Pi kit. Fast delivery and no complaints whatsoever. (Posted on 23/09/2019) Review by Harley verified purchaser Rating 100 very good (Posted on 23/09/2019) Review by Ryan verified purchaser Rating 100 This was my first Raspberry Pi and it was so easy to get running. If you're going to connect it to a hidden SSID, I'd recommend you look at this https://blog.sebastian-martens.de/development/raspberry-pi-hidden-ssid/ as most guides assume your SSID is broadcasting. I'm using mine to run Pi Hole and OpenVPN at this stage. (Posted on 17/09/2019) Review by carl verified purchaser Rating 100 thanks happy with my purchase (Posted on 16/09/2019) Review by Daniel verified purchaser Rating 100 Used it to run a Node.JS server for HomeBridge, setup of the Pi was easy, and was done completely headless, such a small and cheap yet powerful device. Delivery was a slight issue due to Fastway, but other than that, A+ (Posted on 10/09/2019) Review by Darrin verified purchaser Rating 100 I already want another one. (Posted on 21/08/2019) Review by Ryan verified purchaser Rating 100 brilliant, arrived very quickly and works great. perfect for my robotics projects. (Posted on 19/08/2019) Review by Travis verified purchaser Rating 100 A great little board for doing simple bash scripting. Easily reusable in a dozen more future projects. Don't forget to get a mini HDMI adapter for simpler and quicker configuration! (Posted on 12/08/2019) Review by Jonathan verified purchaser Rating 100 Quick delivery, good price, pi works well. Very happy. (Posted on 12/08/2019) Review by Iain verified purchaser Rating 100 Great little IoT device. I have it polling my solar inverter and uploading every 5 minutes to PVOutput. Shipping from Core Electronics was quick and painless, and their follow up communication outstanding. Will be ordering a Pi 4 very soon. (Posted on 10/08/2019) Review by Sven verified purchaser Rating 100 Perhaps the greatest invention since the wheel, this tiny device is so cool. It isn't the fastest, but if you plan your projects well, and tailor them for the zero W, it will certainly impress your friends. (Posted on 6/08/2019) Review by Matthew verified purchaser Rating 100 Works great, very happy with the wireless addition. (Posted on 6/08/2019) Review by Martin verified purchaser Rating 100 Great little Pi that suited my project well. Had it up and running in no time! (Posted on 6/08/2019) Review by Zac verified purchaser Rating 100 Perfect (Posted on 2/08/2019) Review by Martin verified purchaser Rating 100 Case works perfectly. And as a bonus my CPU now runs ~ 1 degree cooler averaging about 15.9 degrees above ambient compared to the official raspberry pi case where CPU temps averaged 16.9 degrees above ambient. (Posted on 30/07/2019) Review by David verified purchaser Rating 100 Can’t wait to get this installed into my project (Posted on 27/07/2019) Review by Dane verified purchaser Rating 100 Great litte Pi for smaller/lower power devices. Great for when you need small & headless without wired ethernet/USB hub. Dongles are an option but other Pis provide these things onboard. (Posted on 24/07/2019) Review by Michael verified purchaser Rating 100 All good (Posted on 19/07/2019) Review by sean verified purchaser Rating 100 Great product, use it as an IP cam (Posted on 18/07/2019) Review by Duane verified purchaser Rating 100 Awesome little package, using it as a homebridge to Apple HomeKit for my hacked together bits. No problems at all, it just works! (Posted on 16/07/2019) Review by Stephen verified purchaser Rating 100 Great value, excellent delivery time. Product worked as expected. (Posted on 15/07/2019) Review by Owen verified purchaser Rating 100 Using one to manage my UPS via Network UPS Tools. Perfect size and wireless means no more network cables for my ups connected devices. (Posted on 10/07/2019) Review by Jin verified purchaser Rating 100 Beautiful board. (Posted on 3/07/2019) Review by Rodney verified purchaser Rating 100 I was pleasantly surprised by just how much power this little thing has. Set up as a Pi camera server it maintains a 720p mjpeg stream @ 30fps, which for the price is great. Onboard WiFi is such a great bonus & makes it much more compact & you know it'll work with Raspbian unlike some USB WiFi dongles. I'll be getting more for extra cameras around the place. (Posted on 27/06/2019) Review by Anton verified purchaser Rating 100 The Raspberry Zero if great value for a cut-down Pi. (Posted on 20/06/2019) Review by Feng verified purchaser Rating 100 not as much power as the b+ but gets the job done for low complexity jobs (Posted on 12/06/2019) Review by Greg verified purchaser Rating 100 Worked fine. Not exactly a Cray but does the job. (Posted on 12/06/2019) Review by Ben verified purchaser Rating 100 You are not going to get better customer service or products anywhere else other than from the team at Core Electronics. Excellent communications and email updates on order progress, even on weekends :-) Postage is also very reasonable. Yes, you can purchase some clone products cheaper from China but please consider what you are paying for. With a Core Electronics purchase you are creating local jobs, local taxes and supporting small, local businesses here in Australia. Small businesses are the most important private sector employers in Australia. Cheers, Ben (Posted on 10/06/2019) Review by Dave verified purchaser Rating 100 Dinky! Bit underpowered to run the GUI - Don't try browser the internet :) WiFi is only 2.4Ghz which was a bit disappointing. Runs well as my Pi-hole (Posted on 28/05/2019) Review by Benny verified purchaser Rating 100 Used this little gem to control when to switch on the electric water heater when the solar panel inverter produces enough watts. (Posted on 20/05/2019) Review by Robert verified purchaser Rating 100 Small and handy with a low power draw. Currently running it as a pihole and a custom webhook server using docker / docker-compose / flask and more at the same time and it handles it without breaking a sweat. A little over achiever. (Posted on 17/05/2019) Review by Robert verified purchaser Rating 100 Ripping little computer, smaller and much faster than expected! (Posted on 16/05/2019) Review by Paul verified purchaser Rating 100 Great little device (Posted on 7/05/2019) Review by Matthias verified purchaser Rating 100 Great product, running my pihole without braking a sweat. Top tip - use a power supply with lan connector (like for a Chromecast Ultra) and you won't need wifi, of course you could buy the Pi Zero to do that. (Posted on 7/05/2019) Review by Rodney verified purchaser Rating 100 My hinting lady friend wanted love the day this turned up. I told her she'd have to get her own Zero. Been a few days now, and Pi and I getting along well. Not sure where my woman friend is though. (Posted on 1/05/2019) Review by Mark verified purchaser Rating 100 This is cool! Amazing how much hardware you can get for this cheap. Very powerful. (Posted on 1/05/2019) Review by Jan verified purchaser Rating 100 Tiny, yet powerful device is a pleasure to use and achieve a lot (Posted on 11/04/2019) Review by Max verified purchaser Rating 100 Excellent little Single Board Computer. I use it to run pi-hole (network wide ad blocking) and it works a treat. Powered from the USB port on my router and connected over wifi. (Posted on 10/04/2019) Review by Michael verified purchaser Rating 100 Performance seems OK for the low cost. Fine for undemanding applications. Wifi easy to setup as if it is not already connected it creates an access point one can connect to. (Posted on 1/04/2019) Review by Ray verified purchaser Rating 100 works out of the box, easily booted with my choice of Raspbian OS (Full), about to attach the Bad-USB for a quick USB plug and test out my Bitcoin mining. (Posted on 22/03/2019) Review by Roy verified purchaser Rating 100 Being used in challenging wifi environment (2 brick walls) and is performing well. Performs better than mk802 it replaces (Posted on 8/03/2019) Review by Ian verified purchaser Rating 100 Very nice device (Posted on 8/03/2019) Review by Charles verified purchaser Rating 100 RasPi Zero W has almost everything, looking forward to using it. (Posted on 3/03/2019) Review by Mark verified purchaser Rating 100 Crazy small, works like a dream. Easy to install the OS. Completes my collection of Pi's. (Posted on 14/02/2019) Review by Bruce verified purchaser Rating 100 Ultra light and small, just what I need for an aerial platform running Python3. I'm taking care not to destroy this one by overloading the USB port. I highly recommend using the wireless keyboard and mouse - works effortlessly. (Posted on 7/02/2019) Review by Anthony verified purchaser Rating 100 This is my 3rd Pi Zero W. I have been using these for small home automation projects. This one will be my controller for an automatic garage door opener, using Apple HomeKit via Homebridge. (Posted on 21/01/2019) Review by Luke verified purchaser Rating 100 Top little board! Perfect for simple projects with a great range of accessories and support. A great choice for the beginning enthusiast all the way to the seasoned solderer. Core Electronics is fantastic resource for this and all of your tinkering needs. =) (Posted on 11/01/2019) Review by David verified purchaser Rating 100 Love the Raspberry Pi Zero W building a wireless mesh network and its going great and got the case as well fantastic. (Posted on 11/01/2019) Review by Jayden verified purchaser Rating 100 Very happy with this product. It looks in great condition and works very well. Would recommend. (Posted on 10/01/2019) Review by Richard verified purchaser Rating 100 What can I say? Raspberry Pi products are great and Core is a pleasure to do business with. (Posted on 4/01/2019) Review by Alexei verified purchaser Rating 100 nothing special, expect nice price - all good. Thx (Posted on 4/01/2019) Review by Heinz verified purchaser Rating 100 good little pi! such a shame I can't buy more than one, as I need the header on the bottom! (Posted on 2/01/2019) Review by Daniel verified purchaser Rating 100 Working great with audio streaming over WiFi (Posted on 29/12/2018) Review by Andrew verified purchaser Rating 100 Plays HD video all day with Kodi like a champ (Posted on 20/12/2018) Review by HAMISH verified purchaser Rating 100 Incredible value for the price. Great pi for a simple application needing wifi and/or Bluetooth. (Posted on 18/12/2018) Review by Deborah verified purchaser Rating 100 Great product & fast efficient delivery (Posted on 17/12/2018) Review by Darren verified purchaser Rating 100 Fast delivery, great items (Posted on 17/12/2018) Review by Harshil verified purchaser Rating 100 This is my first Raspberry Pi product and I loved it! The versatility of such a small unit still amazes me. Postage quick and after a few youtube videos I was up and running. Just a word of advice, if this is your first pi it’s best to use a micro sd less than 64gb for installing NOOBs and Raspbian, as I experienced unknown problems with high capacity micro sd cards :/ (Posted on 12/12/2018) Review by Fraser verified purchaser Rating 100 great as described (Posted on 7/12/2018) Review by Budi verified purchaser Rating 100 All good (Posted on 27/11/2018) Review by Colin verified purchaser Rating 100 Delivered on time, good service (Posted on 26/11/2018) Review by Colin verified purchaser Rating 100 Delivered on time, good service (Posted on 26/11/2018) Review by Alan verified purchaser Rating 100 Have not put to use as yet, however product is well made and all software provided functions seemlesly (Posted on 19/11/2018) Review by Fiham verified purchaser Rating 100 Loving it will definitely order more (Posted on 19/11/2018) Review by Jon verified purchaser Rating 100 Packaged well, works great. (Posted on 15/11/2018) Review by Geoffrey verified purchaser Rating 100 Great product as described. Fast service (Posted on 15/11/2018) Review by Paul verified purchaser Rating 100 Great little unit in a discrete package, perfect for set-and-forget ADS-B monitoring (Posted on 13/11/2018) Review by Alan verified purchaser Rating 100 This is a great product - amazing capability for the price with heaps of support and info online - good quick start guide on the Adafruit web site for example. Highly recommended. (Posted on 8/11/2018) Review by Keith verified purchaser Rating 100 great little device, great price, great delivery time. core electronics have great tutorials on how to set up and use the device also. (Posted on 8/11/2018) Review by Michael verified purchaser Rating 100 Great SBC - totally covert and mobile, it may be underpowered compared to the B+ but that's kinda the point, and you'll learn a lot from seeing how others are using the Zero W. Pretty sure you'll have fun with it like most are. Highly recommended. (Posted on 5/11/2018) Review by Snowy verified purchaser Rating 100 15AUD for a wireless low-end internet capable device that you can use as the base for all sorts of projects? Pretty hard to beat. (Posted on 31/10/2018) Review by Patrick verified purchaser Rating 100 Great product and so many possibilities! This one will be used to block ads, what a great idea! (Posted on 30/10/2018) Review by Pietro verified purchaser Rating 100 Good Packaging, all OK. I've used and works OK .Happy with it (Posted on 25/10/2018) Review by Dane verified purchaser Rating 100 One of many great products offered by Core Electrinics - easily ordered through the website and arrived quickly. (Posted on 25/10/2018) Review by Josh verified purchaser Rating 100 The Pi Zero has almost all the connectivity of the bigger Pi 3 but with a much smaller footprint. It runs a slower processor, has mini HDMI (which is a very strange connector), and two micro USB 'OTG' ports. But more importantly it has the same 40 pin header as the Pi 3/2, so many hats are cross-compatible (if they physically fit) My particular use-case was to connect a hat that was designed for the Pi Zero to turn it into a USB flash drive, and it worked with no issues at all. I'll probably buy a few more for other various projects. (Posted on 23/10/2018) Review by Greig verified purchaser Rating 100 LOVE the Pi Zero W. I seem to be raising a fresh order for another one each week... One tiny trap I've not found documented anywhere: the Wireless won't connect to 5GHz, only 2.4G networks. (Posted on 21/10/2018) Review by Michael verified purchaser Rating 100 Everything they said it is :D (Posted on 19/10/2018) Review by Matt verified purchaser Rating 100 Great item :) works great for many applications and arrived quickly as always! (Posted on 14/10/2018) Review by Mark verified purchaser Rating 100 A tenny tiny wireless Pi. What's not to like. Don't bother trying to run X on this, but as a small, low power computer/controller, this is great. (Posted on 8/10/2018) Review by Jake verified purchaser Rating 100 Arrived perfectly and undamaged. My only problems came from not reading the product description properly. First, It didn't come with headers to solder to the board (it wasn't an issue I had some laying around). Secondly, it has no direct audio pins, but with the help of a few online tutorials this can also be overcome. Aside from that it is a great product and functions perfectly out of the box (or bag in this case). (Posted on 29/09/2018) Review by Stuart verified purchaser Rating 100 Seriously Impressive product and at a price that lets you use it in your projects without a thought. Core service is high and the delivery costs are low, just the way we want it (Posted on 24/09/2018) Review by Nikki verified purchaser Rating 100 Fantastic little multipurpose computer, with good gpio capabilities, in an amazingly small form factor. (Posted on 21/09/2018) Review by Jie sheng verified purchaser Rating 100 The product arrived quickly and carefully packed in bubble wrap. It is just as I expected it to be. The only problem now is... too little time for all the things I want to make with it! Thanks. (Posted on 18/09/2018) Review by Leon verified purchaser Rating 100 Fast delivery, good prices, why go anywhere else? (Posted on 11/09/2018) Review by phil verified purchaser Rating 100 great value for money - I use Pi Ws in lot of places. (Posted on 10/09/2018) Review by William verified purchaser Rating 100 Very cool board! Will more than likely be getting more in the future. To anyone who is considering to purchase a RBP Zero W - Do not cheap out on the SD card, get a decent 32GB card (I learnt this the hard way...) (Posted on 10/09/2018) Review by Greg verified purchaser Rating 100 Great little devices. Core are excellent on the speed of delivery and the team are great on after sales service so I heartily recommend them. Sham ewe don't get them for less though (like some of the $5 deals in the USA) (Posted on 10/09/2018) Review by Mark verified purchaser Rating 100 Great piece of kit. The Zero W does everything I need. Good service and postal speed, excellent price point too. Cheers! (Posted on 6/09/2018) Review by M. Sana Ullah verified purchaser Rating 100 This product is awesome. It is a little computer in itself. I am using it headless and have set up a web server on it and hey ... it is running as smooth as silk with no interruptions. Beside it, I am running nodeJS and lengthy Python scripts on it without any problem. Core Electronics community is a great place to take a good start and seek help. I definitely recommend this raspberry pi 0 W with full confidence. (Posted on 3/09/2018) Review by Will verified purchaser Rating 100 Love this little board, can be a little slow if you put too many tasks on it. (Posted on 30/08/2018) Review by David verified purchaser Rating 100 I got this Pi as I was looking for a lite weight computer to run a complex model railroad since. The Pi Zero gives lots of power and WiFi. This runs a number of locomotives and controls servo driven point, road signals and even mobile phone and tablet apps. (Posted on 28/08/2018) Review by Richard verified purchaser Rating 100 The RPi Zero W is the perfect SoC based computer for IoT-style uses. I have used RPi's since the very first release, and have found the Zero W model to be the best for my home IoT applications. (Posted on 27/08/2018) Review by Greg verified purchaser Rating 100 Absolutely awesome price! Thanks guys! (Posted on 23/08/2018) Review by Nicholas verified purchaser Rating 100 Don't forget to get the switched usb hub like I did, the guys at Core have them for less than 4 bucks great value. (Posted on 21/08/2018) Review by Dave verified purchaser Rating 100 Hi all, what an awesome little guy the Raspberry Pi ZERO. How to have fun playing games, creating projects all for a ridiculous price under $20, how can you go wrong. Ability to connect to the internet on-board WIFI. This midget SBC is a must to have in your collection or even if it is the base for your entire setup. DON'T LET IT'S SIZE FOOL YOU. I enjoy mine, with a variety of hats and displays, ZERO 4 U board that gives you 4 extra USB 2 ports and also a 2 pin LIPO battery connector allowing the benefit of not needing mains power. Check them out, you wont be disappointed. (Posted on 20/08/2018) Review by Brenton verified purchaser Rating 100 Fast shipping. Great price. Very nice! (Posted on 20/08/2018) Review by Arthur verified purchaser Rating 100 Great! Tiny board looks promising (Posted on 19/08/2018) Review by Denver verified purchaser Rating 100 Amazing product, great for any pocket-sized project! Cheap, fast shipping, definitely 5 stars from me. (Posted on 18/08/2018) Review by Ian verified purchaser Rating 100 Prompt delivery, great product - absolutely no complaints. (Posted on 17/08/2018) Review by Mark verified purchaser Rating 100 Excellent service, speed of delivery at a great price. (Posted on 14/08/2018) Review by David verified purchaser Rating 100 Excellent service and great product. (Posted on 13/08/2018) Review by Rob verified purchaser Rating 100 Needed a Pi Zero W for a Prusa i3 MK3 and got it pretty quick. Excellent response, good price and friendly service. Tnanks! (Posted on 7/08/2018) Review by Peter verified purchaser Rating 100 Needed to replace one that I managed to mangle. Good fun product (Posted on 6/08/2018) Review by James verified purchaser Rating 100 Exactly as described, fast shipping. (Posted on 2/08/2018) Review by Kim verified purchaser Rating 100 Love it! great fun (Posted on 31/07/2018) Review by Russell verified purchaser Rating 100 These boards are a lot of fun and so easy to reconfigure for whatever takes your interest (Posted on 31/07/2018) Review by Jared verified purchaser Rating 100 Great device and price, works perfectly as part of my night-time camera project. (Posted on 31/07/2018) Review by Peter verified purchaser Rating 100 Used it on my 3d printer to run Octoprint. Works a treat and now I can run my printer over wifi. (Posted on 31/07/2018) Review by Ryan verified purchaser Rating 100 Great little board for my security camera work. (Posted on 26/07/2018) Review by Mark verified purchaser Rating 100 Arrived exactly as ordered! (Posted on 25/07/2018) Review by Ross verified purchaser Rating 100 Great size. Very handy for my small projects. :-) (Posted on 19/07/2018) Review by Jose verified purchaser Rating 100 Excellent mini version of the Raspberry pi . I found this little single core computer was able to handle the computational requirements for an ALL SKY camera that take 180 deg images of the night sky. Excellent value ! (Posted on 17/07/2018) Review by Alan verified purchaser Rating 100 Did not quite finish last time. I think attempting a headless setup using Windows is NOT to be recommended as per your notes. (Posted on 6/07/2018) Review by Hamish verified purchaser Rating 100 A great little Raspberry Pi, great instructions on the core electronics website to get started. (Posted on 3/07/2018) Review by Hamish verified purchaser Rating 100 A great little Raspberry Pi, great instructions on the core electronics website to get started. (Posted on 3/07/2018) Review by Chris verified purchaser Rating 100 I've set this baby up as a cheap BLE beacon for an IoT project I'm working on. It was super easy to do and very happy with it. (Posted on 26/06/2018) Review by Arvind verified purchaser Rating 100 Great for a small system. (Posted on 22/06/2018) Review by Sebastian verified purchaser Rating 100 The raspberry pi zero w arrived earlier than expected and works great! A great price for such an amazing peice of hardware. Have had no problems so far. (Posted on 18/06/2018) Review by Paul verified purchaser Rating 100 OMG, so small but what it can achieve. Have built what is called a Jumbo Hotspot which allows me to connect my two-way radio and talk to other operators around the world via internet access. When using Pi devices, recommend a quality micro SD card was cheaper ones may fail. (Posted on 18/06/2018) Review by Namal verified purchaser Rating 100 Nice little computer for my home lab. Core Electronics was the best place I found to buy. Quality service and fast delivery. (Posted on 11/06/2018) Review by Alan verified purchaser Rating 100 This is a great board. I have used it along with a rf board to make an rf hot spot for amateur radio. I have been able to build an rf hotspot for a fraction of the price of a commercially made unit. The board works extremely well, load your software and configuration and away you go. This board can be used for virtually anything. You are only limited by your imagination. (Posted on 5/06/2018) Review by Daniel verified purchaser Rating 100 quick service, fast delivery. I would buy from Core Electronics again (Posted on 31/05/2018) Review by Dean verified purchaser Rating 100 What a bargain and what a powerhouse! I'm building a network analyser that is powered off the USB port on a router. Small, powerful and secure tools readily accessible on the network. Love it! (Posted on 29/05/2018) Review by Matthew verified purchaser Rating 100 Such a great price for such a neat little unit. I'm still amazed by the rPi Zero W. (Posted on 25/05/2018) Review by Lasantha verified purchaser Rating 100 Nice little board to run Kodi and make a movie player. (Posted on 22/05/2018) Review by Frank verified purchaser Rating 100 great device cheap and useful. top price (Posted on 18/05/2018) Review by Jay verified purchaser Rating 100 remember this does not come with a header (Posted on 14/05/2018) Review by Mick verified purchaser Rating 100 Great little computer, tiny footprint but has wireless and bluetooth. I’m using this inside a controller as a retro arcade machine. (Posted on 14/05/2018) Review by Damien verified purchaser Rating 100 The Pi zero W unit is a great testbed for learning a new programming language. It is small enough to there for you when you workout coding solution. The added benefits cone from seeing how fast you can get the code to run on such a small unit. I was able to test my R code to the point where I was happy it was yhe most efficient. (Posted on 14/05/2018) Review by David verified purchaser Rating 100 Perfect hardware to connect any device to wifi. In my case my old printer. (Posted on 9/05/2018) Review by Anand verified purchaser Rating 80 I really like my new raspberrypi (Posted on 9/05/2018) Review by Matt verified purchaser Rating 100 Compact, powerful and cheap. (Posted on 7/05/2018) Review by Barry verified purchaser Rating 100 Excellent product complimented with outstanding service.. (Posted on 7/05/2018) Review by Chris verified purchaser Rating 100 The Pi Zero W makes an excellent DNS filter to block ads on websites. Search for "Pi hole". I attach them with double-sided tape to a small usb charger, and plug in somewhere within wifi range of the router. They are also great for any IOT project. A small MQTT server will run on them. They are a great development system for controlling just about anything. (Posted on 5/05/2018) Review by Brendon verified purchaser Rating 100 Best priced Pi in Aus. Great compact decive for use as a ADSB receiver. (Posted on 29/04/2018) Review by Steven verified purchaser Rating 100 The Pi Zero W is great value for money at $15 and runs surprisingly fast! (Posted on 28/04/2018) Review by Nick verified purchaser Rating 100 Arrived quickly, item working as described. (Posted on 28/04/2018) Review by Amos verified purchaser Rating 100 The Pi Zero is an awesome piece of kit! It is a full computer that is smaller than a credit card. I have so many ideas for how I can use it, but for now I have set up a Gitea server for my software development work. As soon as I find my box of electronics components in the back shed I can't wait to begin tinkering with the GPIO pins. Only two real complaints here: 1) There is no power on indicator (there is a disk activity light though); 2) You need to solder on some GPIO headers if you want to start tinkering. (Posted on 28/04/2018) Review by Todd verified purchaser Rating 100 Tiny, flexible and with built-in wifi whats not to like (Posted on 19/04/2018) Review by travis verified purchaser Rating 100 As described and well packaged (Posted on 18/04/2018) Review by David verified purchaser Rating 100 Works perfectly out of the box after adding an SD card with my OS on it. The product was dispatched very quickly after I ordered, and the customer support since then has been nothing short of incredible! (Posted on 17/04/2018) Review by Charlie verified purchaser Rating 100 Great little board. Purchased to run as a server for my 3D printer. (Posted on 17/04/2018) Review by tim verified purchaser Rating 100 lover it all good (Posted on 17/04/2018) Review by Matthew verified purchaser Rating 100 I have used the Raspberry Pi Zero W with switches and LEDs after soldering on headers, to do some experiments with Node Red programming. I'm hoping to make a remote controlled robot, using my phone as the controller. The Raspberry Pi is excellent. Very easy to use. The web browser is very slow so it is hard to use YouTube but apart from that it works really well. (Posted on 15/04/2018) Review by Robert verified purchaser Rating 100 Perfect small computer for DIY projects around the house and for network tinkering, love it. shipped quickly and safely and had the product in stock, unlike many other sources, definitely saving core electronics in my bookmarks bar for future purchases. reliable and affordable (Posted on 10/04/2018) Review by Chris verified purchaser Rating 100 Super fast delivery (Posted on 9/04/2018) Review by Ollencio verified purchaser Rating 100 Easy access to top, in demand, product almost the same week! Incredible! At a very reasonable price too! No discordant deliveries - excellent! (Posted on 4/04/2018) Review by Matt verified purchaser Rating 100 Even though this thing is slow as hell if you attempt to use it for web browsing, YouTube, whatever, I'm still giving it five stars. If you have a computer and an spare micro SD card laying around, this is all you need to wet your feet. I'd recommend a case and the GPIO header, but neither are essential. (Posted on 2/04/2018) Review by Dean verified purchaser Rating 100 Fast shipping. Product works but note it won't run Windows 10 IoT. (Posted on 2/04/2018) Review by Harry verified purchaser Rating 100 perfect, as advertised (Posted on 30/03/2018) Review by Brett verified purchaser Rating 100 Great little SBC. The onboard wifi is surprisingly good and makes it very easy to get started. Whilst it's not that powerful, for simple uses and to run off battery it's fantastic. (Posted on 30/03/2018) Review by Brian verified purchaser Rating 100 Cheap and delivered quickly, was packaged well to (Posted on 29/03/2018) Review by James verified purchaser Rating 100 Nice little device. There are too many reasons for having one of these little devices around home, or the office - must resist temptation to buy more... (Posted on 26/03/2018) Review by Jim verified purchaser Rating 100 Great learning tool for those who want to experiment with low cost entry into Linux or use as an experimental platform. I soldered a 40 pin header so that I could easily access the IO options. Fast turnaround on the order. (Posted on 22/03/2018) Review by Joel verified purchaser Rating 100 This product works as expected - sits in my drawer next to my raspberry Pi 1, 2 and 2x3's! Does it really work? I bet it sure does and I'll get around to using it one day. (Posted on 21/03/2018) Review by Barney verified purchaser Rating 100 It's tiny! Works very well and is easy to setup out-of-the-box. (Posted on 20/03/2018) Review by Paul verified purchaser Rating 100 Amazing functionality for such a small package. Cloned an SD card from a larger Raspberry Pi and and once triggering Recovery Mode on boot, everything set itself up as expected. Hard to believe that a board like this costing less than $20 can run a full Linux instance. (Posted on 19/03/2018) Review by ian verified purchaser Rating 100 I am very pleased with their performance (Posted on 16/03/2018) Review by Nguyen Le verified purchaser Rating 100 cheap, small, and lightweight. Perfect for a portable build (Posted on 12/03/2018) Review by Nigel verified purchaser Rating 100 Great product and really fast delivery time! The Pi W Zero is just a brilliant device and "Core Electronics" was able to provide great pre-sales support and give a really good recommendation on my purchase based on my requirements. Built in Bluetooth and WiFi functionality is a great part of what gives this little IOT computer an edge. (Posted on 10/03/2018) Review by Eric or Robyn verified purchaser Rating 100 Amazing piece of tech! Works perfectly, I'd recommend this to anyone. (Posted on 7/03/2018) Review by Andrew verified purchaser Rating 100 this raspberry pi is the best raspberry pi in my raspberry pi collection. would buy again (Posted on 7/03/2018) Review by Daryl verified purchaser Rating 100 Very nice, remarkably painless to get running. You could make it easier to find the headless setup though, and fix the country code required for WIFI to work correctly. I don't have full time internet and had to download the video which while good was inaccurate, and had to go looking for answers next time. (Posted on 5/03/2018) Review by John verified purchaser Rating 100 Purchased this to replace old Pi v2 without wireless (wireless USB device had failed). Just copied old SD card to micro SD card, plugged it in. Added 26 header pins to match old Pi. plugged old 26 pin plug in and applied power. Irrigation system now working and it is back on my Wi-Fi network. Much easier than getting used to a new laptop :-). (Posted on 2/03/2018) Review by Bernard verified purchaser Rating 80 It's a pi zero with wifi... and does what a wifi pi zero would do! Tiny computer. A little limited in power, but good for basic tasks (just manages octoprint minus video at the moment) (Posted on 1/03/2018) Review by Paul verified purchaser Rating 100 This pi is a great little computer which I have turn into a music player with the pimoroni Phat DAC. It is not as quick as my pi 2 but for the small form factor it is perfect for smaller pi projects. (Posted on 28/02/2018) Review by luke verified purchaser Rating 100 Great! Always on time. Great product. (Posted on 27/02/2018) Review by Brennan verified purchaser Rating 100 The wireless was really easy to setup once I found the right tutorial, and has worked beautiful. (Posted on 27/02/2018) Review by Richard verified purchaser Rating 100 Current project is a DMR radio hotspot using a pi-hat device. Project originally setup on a pi 3 and migrated seamlessly to the pi zero w. Having a matching GPIO bus meant just plugging together and transferring the SD card. Great little device. Looking forward to the next pi zero w project.. - Richard VK4RY (Posted on 27/02/2018) Review by Jed verified purchaser Rating 100 Great product, I will definitely be buying this product again. (Posted on 27/02/2018) Review by Nicholas verified purchaser Rating 100 Very please with the delivery time. pretty good service when you consider the delays from other sources. (Posted on 26/02/2018) Review by Ross verified purchaser Rating 100 It is great to get this a such a good price without going offshore. It was delivered promptly freight free. Happy! (Posted on 26/02/2018) Review by Peter verified purchaser Rating 100 Using all the items provided in the KIt made life very easy. Once everything was plugged in, I selected the OS I wanted and installation started. Once complete, I had a completely working Pi Zero W. Haven't tried the Bluetooth yet, but am amazed at how much you get in such a small package. (Posted on 25/02/2018) Review by Malcolm verified purchaser Rating 100 Arrived quickly via standard post in excellent condition and worked first time without any hassels. (Posted on 25/02/2018) Review by Alexey verified purchaser Rating 100 Amazingly small and yet useful for projects (Posted on 24/02/2018) Review by Stefan verified purchaser Rating 100 Before buying it a new the product was great. But the service and fast shipment of Core Electronics surprised me. Really good. Will buy more from these guys. (Posted on 22/02/2018) Review by Sean verified purchaser Rating 100 I configured the Pi Zero W to run Octoprint hooked up the Prusa MK3 3d printer. Runs like a charm AAA+ (Posted on 21/02/2018) Review by Sam verified purchaser Rating 100 Excellent service and arrived promptly, got to work on some of my hobby projects pretty promptly! (Posted on 21/02/2018) Review by Mark verified purchaser Rating 100 Excellent price very competitive and the delivery was very quick this is the second one I have bought and will be buying more as I have an ongoing project for a security camera setup even the staff were very helpful with the questions I had for online help one very happy customer. (Posted on 19/02/2018) Review by Jeremiah verified purchaser Rating 100 Excellent value and compact perfection. (Posted on 19/02/2018) Review by Ali verified purchaser Rating 100 Great product to fit small IoT projects (Posted on 19/02/2018) Review by Stephen verified purchaser Rating 100 These are fantastic for small Iot projects around the home. (Posted on 16/02/2018) Review by Michael verified purchaser Rating 100 What a great little board! I was actually surprised at how small it was when it arrived. (Posted on 15/02/2018) Review by Det verified purchaser Rating 100 A great product at a very reasonable price and tiny package. I am using four of these, one running RasPlex as my MediaStation, connected to a Plex server by WiFi and controlled through my Samsung TV remote via HDMI. The other three run MMDVM digital voice modems for DMR, D-Star, Yaesu Fusion and P25 digital amateur radio. They connect to the Internet via WiFi and my home broadband or via Bluetooth and my phone as a hotspot. I love this product and especially the prompt shipping and friendly service from Core-Electronics - keep up the good work. (Posted on 14/02/2018) Review by Trevor verified purchaser Rating 100 small! but I like it... One problem.... It has a single usb port and wont easily accept a USB Hub... either unpowered OR powered... This is an issue if you want to attach multiple usb drives or peripherals... Lots of ppl on line have same issue and resolution seems hard to come by :( (ps.. I use a bluetooth keyboard and mouse to drive it normally) Also not good for video playback (eg youtube) I have a rasperry pi 3B as well and it has 4 usb(2) ports standard and quad core chip. It also has no problem with internet and video... I'm sure the Raspberry Pi Zero W (Wireless) has a multitude of uses for teaching/projects and you can find lots of stuff on line to use it with.. Cheers.. (Posted on 13/02/2018) Review by John verified purchaser Rating 100 Excellent and super compact. Tried to set it up headless with RASPBIAN STRETCH LITE, but wifi didn't work. I put full raspbian on (and selected 2.4g) and all worked fine! (Posted on 6/02/2018) Review by Jesse verified purchaser Rating 100 It's a great product. It works great with MotionEyeOS. (Posted on 5/02/2018) Review by John verified purchaser Rating 100 Great product, compact and easy to connect to wifi. You can get away without adapters for mini HDMI and usb but it's easier to get started with them. The processor is not as powerful as Pi3 but these issues are offset by the size and price. (Posted on 2/02/2018) Review by Simon verified purchaser Rating 100 Excellent product. Delivery was very prompt. (Posted on 2/02/2018) Review by Jack verified purchaser Rating 100 Perfect, lots of fun to be had (Posted on 1/02/2018) Review by Rajkumar verified purchaser Rating 100 It's a piece of cake. The packaging was good. I received the board in good condition. I tested the board and it booted like charm. I am still buying the same product, because one can buy only one piece in one order. (Posted on 1/02/2018) Review by Jeremy verified purchaser Rating 100 Loved it, using it for a Pi Hole! (Posted on 31/01/2018) Review by Jeremy verified purchaser Rating 100 Loved it, using it for a Pi Hole! (Posted on 31/01/2018) Review by Jeremy verified purchaser Rating 100 Loved it, using it for a Pi Hole! (Posted on 31/01/2018) Review by Trevor verified purchaser Rating 100 Great product. Handles what I needed it to do easily, and small footprint made it easy to incorporate into my project. (Posted on 30/01/2018) Review by Daniel verified purchaser Rating 100 Great little unit (Posted on 28/01/2018) Review by Max verified purchaser Rating 100 Works well, awesome for basic emulation + wifi projects (Posted on 28/01/2018) Review by David verified purchaser Rating 100 Works ok running retropie not as well as a pi3 but still not bad. Core was fast in post even at the cheapest option. Wireless model does use more battery if your using for a portable project but if not its certainly the way to go if you like to connect bluetooth devices and send files over network. (Posted on 26/01/2018) Review by Iain verified purchaser Rating 100 Fantastic little piece of kit, would benefit from a bit more room between micro-usb ports but otherwise spot on. (Posted on 25/01/2018) Review by Peter verified purchaser Rating 100 I've given this little rocket a hard time since I got it and it has survived. There are so many applications for a small, capable system on a card that the mind boggles. It works as a web-server. File sharing has a latency issue but it's amazing at the price. Video streaming is a no-go, not even a slideshow. Throw in WiFi and Bluetooth and that's quite a package. I'll be getting more of these. (Posted on 25/01/2018) Review by Nathan verified purchaser Rating 100 Used the Pi zero as an octoprint server. The size and built in wireless made it perfect for my setup. (Posted on 24/01/2018) Review by Peter verified purchaser Rating 100 Awesome little machine! Only pain was soldering the gpio up for use. (Posted on 22/01/2018) Review by Craig verified purchaser Rating 100 Fantastic little computer (Posted on 20/01/2018) Review by Craig verified purchaser Rating 100 Fantastic little computer (Posted on 20/01/2018) Review by Eric verified purchaser Rating 100 Works precisely as advertised. I'm very pleased with the pi zero w. It's not as powerful as pi 3 so don't expect to browse the internet with a graphical user interface. (Posted on 18/01/2018) Review by Eric verified purchaser Rating 100 Works precisely as advertised. I'm very pleased with the pi zero w. It's not as powerful as pi 3 so don't expect to browse the internet with a graphical user interface. (Posted on 18/01/2018) Review by Patrick verified purchaser Rating 100 Great little device. For $15 you cannot go wrong. The Core Electonics guides were great to get it up and running in Zero (pun intended) time. (Posted on 17/01/2018) Review by Samuel verified purchaser Rating 100 Very cool little device, easy to setup and the Core Electronics guides actually can in handy more than once. Very happy with my now Pi-Hole DNS server. (Posted on 16/01/2018) Review by Paul verified purchaser Rating 100 This is my second Pi Zero W and it won't be the last. They are a great little computer. Not as powerful as a Pi3 but so small, so cheap and so capable. (Posted on 13/01/2018) Review by Ian verified purchaser Rating 100 This is a great board, I have used it in place of a Model 3 to keep it compact. It runs perfectly with the Radio project I am working on. This Pi Zero W just works as it should. (Posted on 11/01/2018) Review by Troy verified purchaser Rating 100 Amazing piece of technology! I quickly swapped out the SD card from my Raspberry Pi 3B running my 3D printer (OctoPrint), put it in this Pi Zero W, plugged in the power and OTG cable. It did take a little longer to boot than the Pi3, but it has had no problems with the last 3 print jobs I have sent it. I did notice that the ribbon cable socket, no longer fits my camera I had on the PI3B, so I'll be ordering that tomorrow. Great speedy delivery from Core Electronics too. I'm a first time orderer here, but won't be my last! (Posted on 4/01/2018) Review by Mike verified purchaser Rating 100 Great little board. Perfect for home automation, by adding Relay Board and I2C Temperature Sensor. Fast dispatch. Cheers, Mike. (Posted on 3/01/2018) Review by Guy verified purchaser Rating 100 Brilliant and cheap. Buy one today! (Posted on 2/01/2018) Review by Phil verified purchaser Rating 100 A very handy product to relieve my Pi3 once a project has been committed to. The WiFi connectability is great. Just watch the micro sockets for HDMI and USB. (Posted on 1/01/2018) Review by Nicholas verified purchaser Rating 100 very fast delivery and very reasonably priced. will shop through you again. (Posted on 29/12/2017) Review by rod verified purchaser Rating 100 expected rpi zero, recieved rpi zero. (Posted on 19/12/2017) Review by William verified purchaser Rating 100 You won't believe how small this is. A lightweight, powerful addition to your electronic toolbox. (Posted on 11/12/2017) Review by Asher verified purchaser Rating 100 Small and very capable. (Posted on 6/12/2017) Review by Mike verified purchaser Rating 100 Delivered faster than expected, well packaged, and great value. A lot of fun for such a small outlay. (Posted on 4/12/2017) Review by David verified purchaser Rating 100 What a terrific piece of gear. Its got enough horsepower to run a homebuilt multimode digital voice radio modem interfacing via wifi to the internet. The pi.zeroW simplifies the hardware setup greatly compared to a rpi3 and its associated add-ons. It arrived out here in the bush quickly and well packed. Very happy, thanks to the staff at Core. (Posted on 30/11/2017) Review by Patrick verified purchaser Rating 100 Managed to get this up and running in about 20 minutes. Great little product to tinker with. (Posted on 30/11/2017) Review by Maxx verified purchaser Rating 100 Love this product. Super easy to get started from the tutorials here. The hardest bit is deciding on the first project to do. (Posted on 28/11/2017) Review by Christopher verified purchaser Rating 100 All it promised for a very small outlay. I develop on the larger RPi but use this unit for as the embedded unit for the project. This pne is running my irrigation system which includes a flow measurement device. Very easy to plug into a motherboard and apache and/or SSH make for very easy remote control. (Posted on 27/11/2017) Review by Josh verified purchaser Rating 100 Great product, set it up running Node-RED for a home automation project and works like a charm. (Posted on 25/11/2017) Review by daniel verified purchaser Rating 100 Great product. Not really worth getting the PiZero, just get the PiZeroW as its less of a ballache having the wifi built in. The core-electronics headless guide was very useful. https://core-electronics.com.au/tutorials/raspberry-pi-zerow-headless-wifi-setup.html (Posted on 24/11/2017) Review by Benjamin verified purchaser Rating 100 Had the Pi Zero before, but now with the WiFi. I dont need to mess around with USB WiFi dongles to communicate. Still just as small and perfect for my small robot projects. (Posted on 23/11/2017) Review by Joseph verified purchaser Rating 100 Works well, product came as expected. The product itself is amazing. such a small processor with wifi connectivity means you can accomplish very interesting projects. For me, I used it to create a wireless print server to make my old corded printer wireless. (Posted on 22/11/2017) Review by Nigel verified purchaser Rating 100 Simply awesome... I'm ordering some more today! One, small caveat.. I popped an SD card in from a RaspberryPi B+, hoping it would boot but it didn't. A fresh install did the trick though and the wireless came up with no fuss at all. I haven't needed to put a monitor on it at all. (Posted on 20/11/2017) Review by Phil verified purchaser Rating 80 great quick delivery to Perth. (Posted on 19/11/2017) Review by John verified purchaser Rating 100 Great product. Quick delivery. (Posted on 17/11/2017) Review by Alfie verified purchaser Rating 100 Pi Zero W There comes a time in a man’s life when he need to man up and stand up for what he believes in, a time to overcome fears and place courage above all other priorities. This is not one of those moments… But it is a moment to enjoy to fruits of the Raspberry Pi foundations labour and cramp this tiny SBC into your future projects. Boasting 1 GHZ processor and 512mb of RAM this little board can handle all the basic commands and instructions your finger and type at it. Whether you’re running a small home camera system, triggering relays remotely or running a retro gaming setup this little gem and do it all & now with the added bonus of WiFi and Bluetooth it’s a no brainer to have a few of this in your modernized home, diy projects & prototyping or retro gaming nostalgic experience. one of the best features of this SBC is that it does not require much power consumption so you can use most USB power supplies you have lying around, a USB charging power pack or a space USB port on your computer, Monitor or Television. The possibilities are only limited to your imagination and for this price! How can you not!!!! (Posted on 16/11/2017) Review by Justin verified purchaser Rating 100 Incredible value. Shipping was also very affordable and took 3 days to Sydney. Fantastic after-sales support with helpful tutorials (Posted on 13/11/2017) Review by Tom verified purchaser Rating 100 GREAT wee board I am using it to write this and have watched a couple of movies on my tv . (Posted on 11/11/2017) Review by sagar verified purchaser Rating 100 The product is very good. (Posted on 10/11/2017) Review by Neil verified purchaser Rating 100 great little board easy to work with (Posted on 8/11/2017) Review by Andrew verified purchaser Rating 100 The Raspberry Pi Zero W is slightly smaller in the flesh than I expected and I got out the ruler before ordering! As someone comfortable with UNIX the platform is a simple way to dip a toe into the embedded world while retaining familiar comforts. (Posted on 7/11/2017) Review by Jacob verified purchaser Rating 100 Its so tiny! Works really running retropie (NES/SNES/SMS/SMD), kids are entertained playing games I grew up with. (Posted on 30/10/2017) Review by Ian verified purchaser Rating 100 Great little computer. Cheap and good fun to play around with. (Posted on 30/10/2017) Review by Steven verified purchaser Rating 100 Much smaller than I imagined but works great. Check the actual size and get hdmi and usb adapters at the same time. (Posted on 26/10/2017) Review by David verified purchaser Rating 100 Excellent. Amazing that such a device is so small! (Posted on 26/10/2017) Review by Rob verified purchaser Rating 80 Small form factor, integrated Wi-Fi and low price -- the Pi Zero W is the perfect computer for low-power projects. (As long as you get the special cable adapters!) (Posted on 25/10/2017) Review by Naveenu verified purchaser Rating 100 Good Product / Support. Received all the products on time. (Posted on 24/10/2017) Review by David verified purchaser Rating 100 Purchased as part of the essentials kit. Together with your setting up headless Pi Zero tutorial have it up and running my FlightAware app in a couple of hours. (Posted on 19/10/2017) Review by warren verified purchaser Rating 100 Awesome board, definitely my favorite board out of many other boards I have including beaglebone black, arduino (nano, leo, mega, mini) NodeMCU, OrangePi H3, Orange Pi Zero, esp8266, Banana Pi M2, Rpi3, Rpi2. I love this board, powerful enough to run servers and use hardly no electricity, I run them as headless stand-alone wireless servers powered from anything with a spare usb (tv, router, eg) they are not power hungry like the full sized Raspberry Pi and only draw a max 170mA. (Posted on 18/10/2017) Review by Christopher verified purchaser Rating 100 This product meet all my expectations Small compact design with built in Wi-Fi made it a perfect fit in controling my garage door using MQTT (Posted on 17/10/2017) Review by Jay verified purchaser Rating 100 Great response time and quick to ship. Will definitely deal again! (Posted on 13/10/2017) Review by Adam verified purchaser Rating 100 Genuine Official Raspberry Pi Zero W, works exactly as intended. GR8 M8 R8 8/8! (Posted on 13/10/2017) Review by Aldrin verified purchaser Rating 100 The delivery was fast and the board was perfectly fine. One happy customer here! (Posted on 12/10/2017) Review by Albert verified purchaser Rating 100 Powerful little computer. (Posted on 10/10/2017) Review by paul verified purchaser Rating 100 Excellent fast delivery and great product (Posted on 6/10/2017) Review by Mark verified purchaser Rating 100 Received my board in very quick time and now coming to grips with setting it up, but thanks to there great Tutorials it was made easy. Thanks you Core Electronics for the great service. (Posted on 29/09/2017) Review by Rodney verified purchaser Rating 100 Your products are fantastic. Original manufactures and the pricing is amazing. But the big plus for me is you are an Australian electronics dealer. Thank you. (Posted on 26/09/2017) Review by Jon verified purchaser Rating 100 Amazeballs:) (Posted on 19/09/2017) Review by Haidar verified purchaser Rating 100 So slow compared to normal pizero (Posted on 19/09/2017) Review by John verified purchaser Rating 100 Worked a treat when combined with Tilt Hydrometer for home brew (Posted on 18/09/2017) Review by Tom verified purchaser Rating 80 Amazing for it's price and size, and great build quality. Just watch that you have enough processing power for your project. (Posted on 18/09/2017) Review by Craig verified purchaser Rating 100 Great little device, haven't powered it up yet as didn't get the correct camera connector or the other kits. You can set these up without the mini hdmi by burning the micro sd then editing the wireless info on config.txt file directly. (Posted on 14/09/2017) Review by Aaron verified purchaser Rating 100 Awesome little board that will do just about anything! I only wish there was more stock from the Raspberry Pi guys, so we could order a heap of them :) (Posted on 11/09/2017) Review by Mat verified purchaser Rating 100 My Pi Zero W PCB is of good quality and the board is well made. Mine has been running Raspbian Lite Jessie for a couple weeks without a reboot now and I've had no problems at all. Thanks Guys. (Posted on 11/09/2017) Review by Peter verified purchaser Rating 100 Great service. Will use again. I bought the raspberry pi as I know Core can support me if need them. Thx Core...... :) (Posted on 10/09/2017) Review by Andrew verified purchaser Rating 100 Excellent product (Posted on 10/09/2017) Review by Robert verified purchaser Rating 100 https://hackaday.io/project/16568-cosmic-array (Posted on 8/09/2017) Review by Mark verified purchaser Rating 100 The speedy delivery was really appreciated! (Posted on 8/09/2017) Review by Ron verified purchaser Rating 100 Love this little piece of Pi! Whilst slower than its big brother, it's great for integrating into projects that just don't have the space for the larger board. And it's CHEAP!! (Posted on 7/09/2017) Review by Austen verified purchaser Rating 100 Excellent product. Great price. Fast Delivery. Would highly recommend. A+ (Posted on 6/09/2017) Review by colin verified purchaser Rating 100 Fantastic product (Posted on 5/09/2017) Review by John verified purchaser Rating 100 Its 15 bucks and WiFi and Bluetooth enabled. Why haven't you got one yet? (Posted on 4/09/2017) Review by Corey verified purchaser Rating 100 These are amazing for the price and form factor, running linux on a $15 device with wifi and bluetooth still blows me away. (Posted on 4/09/2017) Review by evan verified purchaser Rating 100 Nice functional Pi, bought this for a RetroPie that could fit in a small custom case. Built in Bluetooth and wireless work flawlessly. (Posted on 31/08/2017) Review by Rick verified purchaser Rating 100 Fantastic little computer. It makes a very good WiFi controlled camera with the Pi camera board and Pi Zero case. (Posted on 31/08/2017) Review by Daniel verified purchaser Rating 100 The Pi zero W is very good quality. I had no issues from the start. (Posted on 30/08/2017) Review by John verified purchaser Rating 100 Very easy to get up and running, great for retrieving sensor information or pictures/video remotely through WiFi. Only difficulty I encountered was only having a OTG cable with a right-angled plug. (Posted on 28/08/2017) Review by Darren verified purchaser Rating 100 Great build quality as you would expect from Raspberry Pi and fast postage form Core electronics, looking forward to many future purchases. (Posted on 25/08/2017) Review by Tom verified purchaser Rating 100 Inexpensive and flexible. Powered from a USB port on our modem, our PiZero is running an AirPrint server for the iPad users in our home. (Posted on 25/08/2017) Review by Hari verified purchaser Rating 100 Smooth process and quick delivery. (Posted on 23/08/2017) Review by Vince verified purchaser Rating 100 Great little SBC. The addition of Wifi and Bluetooth has made the Pi Zero so much more usable. I look forward to tinkering with this little gadget. (Posted on 23/08/2017) Review by Beau verified purchaser Rating 100 Cheap, powerful and fit anywhere! Just built a dashcam with one of these, and it worked out great :) (Posted on 22/08/2017) Review by Simon verified purchaser Rating 100 Works really well, set for static IP address and trying all sorts of stuff. Have just upgraded to Raspian Stretch to give it a shot. WIFi and Bluetooth are a real bonus on the ZeroW. (Posted on 22/08/2017) Review by Greg verified purchaser Rating 100 Running this with FlightAware software and radio dongle to track aircraft. Going really well. Even with the (international) freight costing as much as the unit it was still more economical than using a full Pi3b. Can’t wait for the one per customer limit to be over. (Posted on 21/08/2017) Review by Shane verified purchaser Rating 100 An excellent little computer great for budding enthusiasts, people wanting to experiment with different operating systems or for embedded projects. It's compact size, low cost and low power draw as well as robust online experience make this an excellent learning tool. (Posted on 18/08/2017) Review by Stephanie verified purchaser Rating 100 this is a very good product small in size, with wifi and bluetooth (Posted on 18/08/2017) Review by Eugenij verified purchaser Rating 100 Great value and hard to find elsewhere! It's low in power consumption and has been perfect for my daily use IoT MQTT server (Posted on 17/08/2017) Review by Greg verified purchaser Rating 100 Amazing little computer. The wifi and camera additions make this ideal for low power IOT. (Posted on 17/08/2017) Review by daniel verified purchaser Rating 100 runs games very nicely i love it (Posted on 15/08/2017) Review by Kirin verified purchaser Rating 100 Good product, timely delivery. (Posted on 14/08/2017) Review by Daniel verified purchaser Rating 100 Great little device. Only thing to remember is that it uses a mini HDMI port so I had to get an adapter. It works very well though (Posted on 14/08/2017) Review by Finley verified purchaser Rating 100 Amazing device! I absolutely love the direction of the Raspberry Pi company, and equally love their products. The Zero is no different, and is even better with a wireless antenna. Will definitely be making some great projects with this. Buy One Now! (Posted on 14/08/2017) Review by George verified purchaser Rating 100 Very fast shipping, well packaged. (Posted on 14/08/2017) Review by gary verified purchaser Rating 100 Very quick service and the item works well. Thank you (Posted on 11/08/2017) Review by Rob verified purchaser Rating 100 Soo many kinds of amazing! this really stands up to its name, very happy with my purchase. will be grabbing another few soon Thanks Rob. (Posted on 9/08/2017) Review by ankit verified purchaser Rating 100 Great product at great price. (Posted on 8/08/2017) Review by Jimmy verified purchaser Rating 100 Works really well, great power. (Posted on 8/08/2017) Review by Gary verified purchaser Rating 100 Cant believe how small it is in real life !! Good little performer (Posted on 7/08/2017) Review by Liam verified purchaser Rating 100 Awesome. I use these in all my projects from Game Boy Zeros to mintyPis :D - The new WiFi and Bluetooth functionality really makes things easier. (Posted on 7/08/2017) Review by Alex verified purchaser Rating 100 Great bit of kit. Possibilities are almost endless with this one. Fast delivery and well packed from Core. (Posted on 7/08/2017) Review by Daniel verified purchaser Rating 100 Easily one of the top mini devices available. Highly recommended to all. Plus easy ordering and fast delivery from Core. (Posted on 7/08/2017) Review by Dominique verified purchaser Rating 100 Nice and small item. Enough powerful for many projects, specially what I want to make with it : a timelapse camera with a light power bank battery charger. It needs a case, easy to buy. Very satisfied with it. Has bought a second one for travelling. (Posted on 2/08/2017) Review by Brett verified purchaser Rating 100 Very nice product. Works as my 3d Printer server. Just what I needed with its built in WIFI. (Posted on 1/08/2017) Review by Justin verified purchaser Rating 100 Can't go wrong with a $15 SBC with WiFi and Bluetooth. Just be aware that the microHDMI port is set back a few mm so you either need a case that accommodates the setback (doesn't exist yet) or an adapter with a long connector (if you don't want to cut an adapter to fit). (Posted on 1/08/2017) Review by Martin verified purchaser Rating 100 Great device. Received quickly. Fantastic service and product. (Posted on 31/07/2017) Review by Andrew verified purchaser Rating 100 Raspberry Pi W is literally the greatest thing of all time. It will make you more attractive, richer, and healthier. (Posted on 31/07/2017) Review by Dominic verified purchaser Rating 100 Absolutely brilliant! Didn't realise how small this was until it came in; works like a charm. (Posted on 31/07/2017) Review by Jaron verified purchaser Rating 100 Great little device, easy to set up and get going, very please with it. (Posted on 30/07/2017) Review by mouhsen verified purchaser Rating 100 Really good condition when came it's very handy for me (Posted on 28/07/2017) Review by Mike verified purchaser Rating 100 Great little 'mini computer'. particularly now that it comes with WiFi and Bluetooth. I installed Raspbian and Kodi headless and all went smoothly. Have now added a Bluetooth Keyboard/Mouse combo and monitor and am building the software library for a Media Centre. The Raspberry pi Zero W is ideal for this purpose! Thanks Core. (Posted on 28/07/2017) Review by Kim verified purchaser Rating 100 Excellent device and booted up without any issues first time. If you are new to Raspberry Pi and are wanting to learn all about them the Raspberry Pi 3 b is a better option. With the zero you only have one USB for keyboard, mouse and anything else and you have to solder on a header if you want to use GIO. (Posted on 28/07/2017) Review by Dave verified purchaser Rating 100 Fantastic little board. So many possibilities, currently using it to run octopi on my 3d printer. (Posted on 26/07/2017) Review by Garth verified purchaser Rating 100 Brilliant! (Posted on 26/07/2017) Review by Dan verified purchaser Rating 100 What a great little board. More and more keeps getting packed onto the RPi series and the Zero is just perfect for IoT tinkering. (Posted on 26/07/2017) Review by Geoff verified purchaser Rating 100 An excellent version of the Raspberry Pi family SBCs. It's small form factor makes it ideal for projects where small and unobtrusive is required. The wireless / Bluetooth range and signal quality are exceptional given that there are no external aerials. The USB OTG port is compatible with an Ethernet to USB converter and a powered USB hub via the adapter, cable so there are plenty of opportunities for expansion if needed including Bluetooth for peripherals. Overall I am very impress with the Pi Zero W. Now I just need to think up more projects to use it in! (Posted on 26/07/2017) Review by d verified purchaser Rating 100 Quickly delivered. Really happy with the service and the product. Using this as a wifi print server and it's doing the job really well. (Posted on 26/07/2017) Review by Christopher verified purchaser Rating 100 Excellent product and service. Can't wait to use it and will definitely buy from Core again. (Posted on 25/07/2017) Review by Andrew verified purchaser Rating 100 Perfect for every project (Posted on 22/07/2017) Review by Marlin verified purchaser Rating 80 Fantastic board... great value for money. Limited wifi range though (Posted on 17/07/2017) Review by Daryl verified purchaser Rating 100 Great device for those low powered projects. For those of you familiar with the Pi 1 and above - there are 2 essentials when setting up one of these: 1 a powered USB hub and 2 a mini HDMI adapter. If you are like me tou have all the other bits in your parts bin. (Posted on 12/07/2017) Review by Simon verified purchaser Rating 100 Excellent item that works exactly perfectly. Very fast shipping too. (Posted on 11/07/2017) Review by Tim verified purchaser Rating 100 This is a wonderful little device. I had no idea how small it was! I have installed PiMusicbox on it and it works a treat. (Posted on 11/07/2017) Review by Stefan verified purchaser Rating 100 Works great out of the box. (Posted on 10/07/2017) Review by Rebecca - The Pi Zero is so small! verified purchaser Rating 100 The Pi Zero is so small, cheap, and worked just like a standard Raspberry Pi out of the package. The only downside is the need for additional USB and HDMI adapters. However, it's possible to set it up on wireless and completely headless from the get go following this tutorial https://core-electronics.com.au/tutorials/raspberry-pi-zerow-headless-wifi-setup.html Great product and great price. Cheers. (Posted on 7/07/2017) Review by Anthony verified purchaser Rating 100 Great little system and very stable. Followed the tutorial for headless setup and it worked a treat! (Posted on 6/07/2017) Review by Tom verified purchaser Rating 100 Great little machine for the price of a toy. Great for cheap little projects (Posted on 5/07/2017) Review by Samuel verified purchaser Rating 100 Perfect for running my 3D printer on octoprint! (Posted on 5/07/2017) Review by Jason verified purchaser Rating 100 Whilst not as fast as it's older Brother, this little guy still packs a punch. Its a $15 Computer, how awesome can you get? (Posted on 4/07/2017) Review by David verified purchaser Rating 100 Good board for dedicated light processing applications. I'm using to build Homebridge HomeKit devices. Pros Wifi and Bluetooth interfaces. Same GPIO as 3B Small size. Less power. Cons No wired Ethernet Only single core processor. (Posted on 3/07/2017) Review by Timothy verified purchaser Rating 100 Great little machine. Runs web servers well. (Posted on 3/07/2017) Review by Alex verified purchaser Rating 100 Capable little single-board computer for an excellent price. Great for embedded projects because of the form factor. Shipping was lightning fast as well. Can't recommend Core Electronics enough. (Posted on 3/07/2017) Review by James verified purchaser Rating 100 product works fine and packaging was reasonable. Shipping to New Zealand took about 2 weeks. (Posted on 2/07/2017) Review by Robert verified purchaser Rating 100 Great product for small projects. I have purchased many for small low power Linux servers and they perform as can be expected. (Posted on 30/06/2017) Review by Michael verified purchaser Rating 100 The PiZero-W is perfect for those retro computing projects. Not only can you use it to interface your 80s computer with the modern world, you can slip it inside your Apple][, C64, Tandy, or any classic computer and compute like it's 1980 while connected to 2017. (Posted on 29/06/2017) Review by Douglas verified purchaser Rating 100 Good value and shipped fast (Posted on 28/06/2017) Review by Thinh verified purchaser Rating 100 Learning Linux, how to build your own electronics, need a home or office solution? this is where you start. Amazing board. (Posted on 27/06/2017) Review by Ryan verified purchaser Rating 100 Awesome little single board PC with multiple uses. (Posted on 27/06/2017) Review by Bruce verified purchaser Rating 100 Brilliant, easy to set up. Runs tightvncserver nicely. Runs current Raspbian system (4.9.28+) with 32Gb microSD card. Runs test driver we are developing on RPi3 Runs off a iPhone battery pack. Easy to connect to local WiFi. All in all amazing machine. (Posted on 26/06/2017) Review by Michael verified purchaser Rating 80 Essentially a header-less and ethernet-less form factor of the original Raspberry Pi. This version includes WiFi and Bluetooth. Great for low power applications, although soldering on a header can be a pain. (Posted on 26/06/2017) Review by Steve verified purchaser Rating 100 This is tiny! Seeing it online doesn't do it justice. I couldn't believe how tiny it was when it arrived. Runs linux smoothly, along with Postfix, Dovecot, and Unbound. (Posted on 25/06/2017) Review by Brett verified purchaser Rating 100 What a great little unit. I have set this up as a Photo Booth controller, with the case an camera. (Posted on 24/06/2017) Review by Jun verified purchaser Rating 100 Small yet powerful with everything I need. I will recommend Wireless version over the non-wireless version just because it can save you a lot of efforts when you are developing something. (Posted on 23/06/2017) Review by Geoff verified purchaser Rating 100 Excellent product, very fast delivery. (Posted on 22/06/2017) Review by Rob verified purchaser Rating 100 Hopefully it will arrive soon. (Posted on 20/06/2017) Review by Ken verified purchaser Rating 100 Core-electronics a pleasure to shop with. Would recommend to a friend. Support local Australian online businesses where possible. /Ken (Posted on 19/06/2017) Review by Samuel verified purchaser Rating 100 Quick delivery, great for headless pi projects (Posted on 18/06/2017) Review by Jadon verified purchaser Rating 100 Awesome gadget. Here's what I did with it!: https://core-electronics.com.au/projects/p0wer-control-mains-outlets-over-wifi (Posted on 18/06/2017) Review by Cedric verified purchaser Rating 100 Super powerful little processor with just enough I/O to do some useful things without needing specialized connectors. Great tutorials available here to get up and running with this too! (Posted on 18/06/2017) Review by Damian verified purchaser Rating 100 Perfect device for the IOT doorbell implementation with wireless connectivity. I just need to work out a way of getting it powered remotely too. (Posted on 16/06/2017) Review by Paul verified purchaser Rating 100 I recently purchased a Pi Zero from Core Electronics. Found the price to be excellent along with the service. Remember to check out the really comprehensive tutorials, they will get you up and running in no time. (Posted on 15/06/2017) Review by Ian verified purchaser Rating 100 Great little computer - used for developing a weather station. It is powered by a 4 port usb hub via the USB OTG cable into the Mini USB port on the zero. Saving on using power supply. Will be linked with a Pi SenseHat for the temp, humidity and barometric pressure. (Posted on 14/06/2017) Review by Zane verified purchaser Rating 100 A great product with many applications to personal electronic projects. Efficient and satisfactory shipping of the device to. Nothing to complain about. (Posted on 12/06/2017) Review by Com verified purchaser Rating 100 I owned a Pi zero and this one even better because it had wireless and bluetooth on board. (Posted on 12/06/2017) Review by Kip verified purchaser Rating 100 The best place to get a Raspberry Pi Zero at a decent price. Postage was pretty quick. Perfect for miniaturising projects that require a fully capable operating system. Love it! (Posted on 12/06/2017) Review by paul verified purchaser Rating 100 Absolutely amazing and kudos to Core Electronics for passing on the cheap pricing, best store ever! (Posted on 10/06/2017) Review by Kurt verified purchaser Rating 80 This is a great unit considering is small size. Compact, low power, enough processing power for what I needed. (Posted on 9/06/2017) Review by Kai Feng verified purchaser Rating 100 Received in good condition and works great! (Posted on 7/06/2017) Review by Stephen verified purchaser Rating 100 I love this Pi great for iot running Linux you can modify programs without access to the hardware unlike the Arduino and it has more memory. Can do complex computation. Love it Steve (Posted on 6/06/2017) Review by Micheal verified purchaser Rating 100 Fast safe delivery, great value. Having a Raspberry Pi Zero W is amazing, perfect for Kodi or Raspberry desktop Os , there is so many alternative uses like iot , and more, perfect solution for children to design projects. (Posted on 6/06/2017) Review by Andreas verified purchaser Rating 100 Fast shipping, product looks of high quality. Have not tested yet though. (Posted on 6/06/2017) Review by Anthony verified purchaser Rating 100 It is amazing that a computer has twice the memory and 42% more processing speed with less than half the footprint space than the original Model A could be purchased at more than 2/3 off Model A's the original price! Though it does not have composite video output (analogue video), sound and an ethernet it is compensated for with builtin WiFi and Bluetooth. One can connect a 40 pin header and perform all the operations like the latest 40 pin models, Come to think about it, the power in the RPiWZ is comparable to a laptop that could be purchased 10 years ago for $1000 and is 30 times more powerful than a 486 machine (of yesteryear). (Posted on 6/06/2017) Review by Andrew verified purchaser Rating 100 Easy start and use (Posted on 6/06/2017) Review by Daniel verified purchaser Rating 100 I couldn't give more praise to the speed and ease of purchase with core electronics. I'm currently using my pi as a media server and have loved setting it up and am looking forward to my next project because tinkering is half the fun! (Posted on 5/06/2017) Review by Fraser verified purchaser Rating 100 As described. Fast delivery. Good condition. Works well (Posted on 5/06/2017) Review by Bob verified purchaser Rating 100 Great product at an excellent price. (Posted on 5/06/2017) Review by Shaun verified purchaser Rating 100 I thought the original Pi was small, but this is tiny. Its amazing (Posted on 2/06/2017) Review by Shaun verified purchaser Rating 100 I thought the original Pi was small, but this is tiny. Its amazing (Posted on 2/06/2017) Review by Vicus verified purchaser Rating 100 Great little device, worked for me straight away in my application. Excellent wifi coverage with onboard antenna. Superfast shipping by Core Electronics as well. (Posted on 2/06/2017) Review by Joo Aun verified purchaser Rating 100 Small form factor SBC, powerful CPU at a low cost. Good value for money. (Posted on 1/06/2017) Review by Ju-Wei verified purchaser Rating 100 Nice compact small portable computer. (Posted on 1/06/2017) Review by Nigel verified purchaser Rating 100 A great piece of gear at a very good price - worth the wait :-) (Posted on 31/05/2017) Review by Tamar verified purchaser Rating 100 Amazingly compact, a great companion to a full size Pi especially for headless use (Posted on 31/05/2017) Review by Gerardo verified purchaser Rating 100 The product was delivered promptly and without faults. I highly recommend the store and would not hesitate to use it again myself. Also, couldn't find many other suppliers of pi zero. They get two thumbs up from me and five stars for sure. (Posted on 31/05/2017) Review by Kent verified purchaser Rating 100 The Pi Zero W is now my IoT platform of choice. You can get the equivalent of a Pi A/B with WiFi and Bluetooth dongles for less than the price of the dongles. And all in a smaller and lower power package. If you don't need the grunt of a Pi2 or Pi3 then a ZeroW is the way to go. If only you could order more than one at a time! (Posted on 30/05/2017) Review by Javad verified purchaser Rating 100 Absolutely amazing product. Dispatched and delivered in no time, and arrived in perfect condition. Worked like a charm and even exceeded my expectations, more powerful than I had anticipated. 5 stars! (Posted on 30/05/2017) Review by Marc verified purchaser Rating 100 Works great especially in gadget mode (Posted on 30/05/2017) Review by marco verified purchaser Rating 100 Excellent board! Was the first time using a raspberry pi and I already start to create more prototypes around my house! First with retro pie and now using for another project with plant watering. (Posted on 29/05/2017) Review by Terrence verified purchaser Rating 100 Raspberry Pi needs no introduction and this version is simply fantastic, the wifi set up perfectly first time and performed as expected. 10/10 from me. (Posted on 29/05/2017) Review by Glen verified purchaser Rating 100 Fantastic service from Core with fast shipping. Great little genuine Pi product, and with the tutorials available on the Core site, I was able to get it up and running in no time! (Posted on 29/05/2017) Review by Callum verified purchaser Rating 100 Works great running my octopi 3D printer server (Posted on 29/05/2017) Review by James verified purchaser Rating 40 Super slow, probably should've saved for the rpi3 kinda deal. Sitting in my office wondering what to do with it as all my Kodi / Retropie installations are too intensive for this thing. (Posted on 27/05/2017) Review by Evan verified purchaser Rating 100 Great product great price. Make sure you are running the latest version of Raspbian or Noobs or make sure that with the version you are running you have done a Pi firmware update with 'sudo apt-get update' and 'sudo rpi-update' or the WiFi device will not be found. (Posted on 27/05/2017) Review by Christopher verified purchaser Rating 100 This feels like a huge leap forward for RPis. Most projects and media centres don't need the kind of power the RPi3. WiFi and Bluetooth and a $15 price tag makes a whole range of projects much easier. Lower power consumption helps too when running off a battery pack. The device is solid, easy to use as expected and lots of support and documentation available. Just don't forget the HDMI port is mini and you'll need an OTG cable for a keyboard for setup. (Posted on 27/05/2017) Review by Marco verified purchaser Rating 100 Very happy with this kit. Shipped fast. (Posted on 27/05/2017) Review by Asanga verified purchaser Rating 100 Love it! Fast shipping and a really good deal! (Posted on 27/05/2017) Review by Adrian verified purchaser Rating 100 Zero = over 9000! (Posted on 27/05/2017) Review

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Diastereomeric stilbene glucoside dimers from the bark of Norway spruce (Picea abies). As part of a long-term study of the chemical defenses of Norway spruce (Picea abies) against herbivores and pathogens, a phytochemical survey of the phenolics in the bark was carried out. Eight stilbene glucoside dimers, designated as piceasides A-H (1a-4b), were isolated as four 1:1 mixtures of inseparable diastereomers. Their structures were determined by extensive spectroscopic means including 1D (1H and 13C) and 2D NMR (1H-1H COSY, HSQC, HMBC, ROESY) spectra, and were supported by enzymatic hydrolysis and computational analysis.

Meet The Newest Member Of The Brangelina Bunch! Three-year-old Pax Thien Jolie (little boy on far left) is such a cutie! Pax Thien Jolie was born Pham Quang Sang, but Angelina changed his name to Pax Thien Jolie which means Peaceful Sky – Pax is peace in Latin and Thien is sky in Vietnamese. He was born in November 2003. Angelina and big brother Maddox picked up the little boy Thursday in Vietnam. “They tried to make friends with the Vietnamese boy, who cried when he saw them because for him, they are strangers,” said Nguyen Van Trung, the director of the Tam Binh centre for orphans and abandoned children. “Jolie was very moved. Both of them tried to comfort the little boy.” Angelina tried some Vietnamese to comfort him, repeating the phrase “khong sao dau,” or “no problem,” to the boy. The children and female staff at the orphanage “said farewell to Jolie and the two boys” and gave the actress flowers. The little boy, abandoned in a local hospital when he was a month old, had to be soothed by orphanage staff who promised him a “fun excursion.” Angelina’s rep confirmed that Angelina arrived in Vietnam yesterday and that the adoption became official today. Angelina, Maddox and Pax Thien will stay in Vietnam for another week until the boy’s passport is ready. Brad was unable to go to Vietnam due to his filming commitments in LA. Below Angelina and five-year-old Maddox are pictured in Vietnam yesterday. I think Angelina Jolie should no be someone whome we admire and celebrate as she stole Jennifers hisband and broke up a woderful couple. When ever I hear the name Angelina Jolie I am disgusted in what she has done and even more so having a baby with Brad who should have been the father of Jennifers baby instead. Jolie is a cheat and husband stealer. She gets involved with any man, married or not she doesnt care about anyone but herself. she doesnt deserve to be a mother or a role model for anyone #26 ROCKS! I AGREE. YOU SAID IT ALL THE ONLY THING I WISH TO ADD IS THAT BRAND AND ANGIE ARE REACHING OUT AND NOT BEING SELF ABSORBED LIKE MOST OF HOLLYWOOD. THEY ARE REMARKABLE HUMAN BEINGS AND HAVE A HEART FOR CHILDREN OF ALL RACES. MOST PEOPLE ONLY “TALK” BUT SHE IS NO HYPOCRITE AND PRACTICES WHAT SHE PREACHES. This message is for the two who were discussing about “celeb gossip and minding their own business,” I just want to say that people are going to voice their opinion whether other people like it or not. The reason I even bothered to post my comment on this topic in the first place because I like what Angelina is doing, it is a good cause (saving innocent lives that deserves a better chance in ife)! The other reason is because I truly was pleased with her open-mindedness to go as far as doing the unheard of or the unusual, which is adopting a child from Cambodia. I was like Whoa! That’s my people, ah right, so mad props to Angelina. She isn’t just adopting needy children from other countries, but I’m sure she also did her research and wanted to express her appreciation towards diversity that probably drove her to want to do something out of the ordinary. Instead of adopting kids from the well-known countries such as China, Japan, or Africa, she took a different route, the one less traveled or less likely to be known for it’s existence such as Ethiopia and Cambodia, and made her decision to adopt accordingly within these two countries. As a Cambodian, I get really excited whenever I hear about my people being mentioned about, or spoken about by people because it seldom happens. So thank you Angelina, not only are you contributing to such a needy cause and help by adopting, but you are also helping to bring the Khmer society into the spotlight. This can be an educational learning tool, which could help teach those people who may be a litthe ignorant and may not know much about diversity, a thing or two about how diverse the Southeast Asian community are and that there are alot more different ethnicities besides the Chinese, Japanese, and Phillipines. Thanks to Jolie, now you can add Cambodia to your tiny list of knowledge, which I hope the knowledge will expand within time. But seriously, I’m not trying to imply anything bad towards anyone in particular. Those who are reading this right now please take what you will be reading next seriously and really try to help me to solve this issue (which isn’t much of an issue, but to me I am still bothered by it so here goes). I just want to express my feelings and let it be heard that sometimes it does hurt when the people I meet know so little about my ethnic background, and then try to sound smart or well-rounded by asking me this,” What nationality are you; Chinese, Korean, Philiippines?” Hello! Those aren’t the only 3 nationalities that exist on earth. If you paid any attention in your history class, you would know that there is also a Southeast Asian portion of Asia which consists of ethnic backgrounds such as Cambodia, Laos, Thailand, Vietnam, Indonesia, Malaysia, etc. It is best for people to just ask the question,” What is your nationality?” and leave the answer options alone, because it will make you look a lot better, giving that you know very little about what you you are talking about. It is better to not make assumptions. You don’t often hear someone ask a Caucasian person, “What is your nationality? Is it French, English, or Scottish? If it was me, I would just ask the question and allow the person that I am asking to do he honor and educate me of my ignorance. Well all said and done have a terrific day at school or work and I hope you work on finding ways to help you to become more educated about diversity. It is inevitable and a need for somewhat a survival tool in school and work because we live in such a diverse country, it is more to our advantage that we learn to be more educated about differences within us all and to hopefully one day in the future, we will all be competent in diversity and be able to understand each other a whole lot more. Man how the hell did I go from Angelina Jolie and her babies to discussing about diversity. Man I guess this is a touchy subject for me. Lastly, anyone reading this and may be offended, I apologize I am not writing about this to piss off anyone, it is only simply my opinion on the issue, and there is no pain or harm intended towards anyone. So please do not take any of my message the wrong way and if you have a concern and would like to dicuss feel free to ask and I shall respond accordingly to whatever the question may be. If not, God bless. And peace out! Learn to embrace diversity, for it is a part of the world that we live in today. P.S. Do a stranger a favor today and take the initiative to be the one to make the approach and take a moment to find out who this beautiful stranger is. The reason being is it can be rewarding in a sense that today the stranger may be just a stranger whom you barely met, but down the line, you never know what the outcome of this newly established relationship may end up in. The possibilities of what this stranger can become are endless: the person can definitely be the friend you can wave at across the campus, which can help make you look cool instead of a loner as you are making your way passing on by the frats and sorior. handout spot all by yourself, they can be someone you can say “hey how’s it going?”, they could end up being potential bf or gf, a study buddy who you could copy their notes from (since you’ve missed all two weeks worth of work and in need of those notes from class that you missed), which can save you from failing the couse, or perhaps you were the one that made an impact on the stranger’s life. What if it was you who made them feel special, like they mattered, or needed that little something whatever it is: notes, buddy, someone to say hi to, whatever, and needed you to inspire them to want to continue on and not give up, what if you help take away that feeling of being so lonely. So think about this, the next time you see that someone might be a loner, be the brave soul and go up to introduce yourself to them, just in case that person might be shy! Seriously, nothing can beat this feeling you get from knowing that you just made someone’s day or were the one who made this person smiled for once in his or her life, or even worst, what if it was you who kept them alive and the one to help chase away that thought of sucide, of giving up life. As difficult and demanding our life may be, we are the easiest creatures to please because all we ever needed to keep us alive is food, friends, and a sense of belonging. So go out there and start being heros and save lives, you’ll never who’s life you will save next, for the person who was saved may never want to tell! I just wanted to voice my opinion on the subject concerning 3 year old Pax from Vietnam in regards to the issue people seem to have with his name change. I can almost guarantee that the name change won’t effect Pax because a child at such a young age as pax’s, he won’t have much of a memory or won’t be able to remember much anyway. My own childhood experience of growing up as well as migrating to the USA at such a young age, I’m not sure how old I was when I first flew on a plane to come live here, but I am guessing I was probably between 2-3 years of age. Seriously, the furthest of my childhood memories that I can recall back were from my preschool memories, which honestly still seems real fuzzy and quite unclear. I can remember the songs we sang in class, however I cannot remember who my teachers were or my classmates besides my friends who were real close to me, other than that I can only remember the small glimpse and bits of pieces of memories in grade school from K-1 (which still seemed fuzzy as well). So Pax will be perfectly fine and he’s in great shape because he won’t be too old that his childhood memories will corrupt him since he probably won’t be able to remember much from his orphange days in Vietnam, but rather only know of the life he had with his happy family, not to mention have parents who are Hollywood Stars, rich, famous, and good looking. Best wishes to the Brangelina Family and I hope these kids don’t drive the parents up the wall, because there are more than 1 child living in the home, not to mention that they are all very young in age, so I can’t wait to read about their teenage life stories. Good Luck Angelina and Brad, you guys rock by the way! We need more people like you guys out there! Well “jaja”, then you shouldn’t care about other people caring about Angelina Jolie, right? You say it’s a waste of energy, sure, but aren’t the rules the same for you? Didn’t you waste your time now? I’m pretty sure you wanted to know what people wrote, didn’t you? You shouldn’t care about what other people chose to do with their time, cause we’re pretty many people in this world, trying to live our lives in a good way! I am in here looking into famous people lives, read about their joy and happiness, why is it so wrong? Maybe you want to get away from you’re own life a couple of seconds and just do what you want to do. WHY do all of you care to gossip about these people you don’t even know?! I just happened to come upon this site, blog, and can’t believe all of you take so much time to gossip about these people, whom the press feeds their egos (good or bad) like all of you are doing. Who cares what Angelina and Brad do, why do all of you care so much about their private lives? It seems all of you have too much time on your hands and need to get a life of your own, and not worry about people you don’t even know. Stop reading this stuff and watching the news and gossip mags, and all of you will have happier lives. Happily live your own life and don’t wonder what others are doing, it’s a waste of energy ! He’s such a cutie. 🙂 I hope he’ll be OK, but with his older brother I think it’s perfect. Maddox seems to be a very caring little person. And the name is great. First, I thought just like some of you, does she HAVE to take away the only name he’s ever known, just because it doesn’t fit with the other names? But then I started to realize, what if he would feel like an outsider in his own family, just because of his name? Pax is easy to say, he doesn’t have to tell his friends how they’re gonna pronounce it. And it starts with a P, which means he’ll listen to it even when he’s not used to it. The name he has know will probably help him to better adjust to america. Pax is an easier name to adjust to in america than Pham Quang Sang. i had to copy and paste because i could not remeber it. Pax is easier to pronounce. It wil also make it easier for his new parents, family, and school. Imagine if your parents kept on mispronouncing your name because they didn’t know how to say it? I like Pax. It’s nice that Jolie learned some Vietnamese to help soothe him. She will be a great mother to him. Chichi, you may be right. Brad and Jen’s marriage was childless and loveless. Hay, if Brad wants to go back to that 38 years old woman. It’s his choice. That would be interesting to watch. I’m totally fan of Angelina. With or without Brad, Angelina is Angelina. With Angelina, Brad is Brad the father. Without Angelina, Brad was the half of so called Golden Couple. Hmmm…… who knows? Brad may be more interested in the latter. How do you say? I found this website while looking for pictures of Angelina’s new son. I follow the life of the Angelina, Brad and their children, not because I hero worship them, but because I admire the fact that they are doing something about what’s wrong in the world. People are so quick to critizize the efforts of others while not putting foward any effort of their own. I was so surprised to see so many petty comments about such mundane things (like the little boy’s name change). I guess Angelina should have just left him in the orphange with no future and then he could have kept his name. People please look at the big picture. This little boy has a future now (whereas he didn’t have one before). Maybe with the future Brad and Angelina are providing for him he can one day become someone who can go back and help the people of his country. I believe God was looking down on that poor little soul and decided that his time had come to shine. I just want to end by saying God bless to Angelina, Brad and the kids. I hope everything turns out well. One more thing – I’ve been reading about how miserable people think the family looks. Well, your kids would probably be crying and crabby after travelling and having peolpe in your face all the time when you are out. Maddox has obviously learned to behave on these outings in an apropriate way for snapping cameras and nosey journalists. The media would just love to catch the Jolie kids spazzing out. I’m sure they’re happy enough in the private setting of their home. As a young mother of three I have constantly had friends kids over, making the numbers 4, 5 , 6 etc. It is so fun being a Mom. It isn’t fun being the maid, cook, etc. Angelina is lucky that she is able to leave all the mundane “chores” behind that have to do with child raising. She can focus on educating and having fun with the kids. It would be no problem managing and giving attention to the bunch she has, with the resources available to her. As for getting used to more siblings, every child wishes they could have tons of sisters and brothers. These kids are lucky. It would be nice if Pitt/Jolie would get married and teach the kids something about old fashioned values that go hand in hand with family life. The adoption agency that Angelina used issued the following response to clear up rumors regarding Pax’s adoption: “In applying to adopt 3-yr-old Pax Thien, Ms. Jolie followed the same course as all prospective adoptive parents who apply to our Vietnam program. Throughout her adoption process, which began in the summer of 2006, she has received no preferential treatment from the Vietnamese government or Adoptions From The Heart, and contrary to earlier reports, her application was not fast tracked. Despite rumors that she chose her child, Ms. Jolie received a referral, just like any other parent adopting from Vietnam. In late 2006, she was referred a child who had been legally determined to be available for adoption and who fit within the parameters for which she had been approved to adopt. She accepted the first and only referral given to her. In addition, we can confirm the statement given by Nguyen Van Trung, Director of Tam Binh Orphanage, that Ms. Jolie has neither made, nor promised to make, any financial contributions to his orphanage. Adoptions From The Heart celebrates the miracle of adoption with the Jolie-Pitt family, as we do with all of our clients, and wish them much joy.” I’m the complete opposite. I rarely give money that goes to those in the U.S. Almost all of my charitable givings go overseas. My reason is quite simple. I feel that those in the U.S. (even the poor) are quite a bit better off than the poor in the third world. In the U.S., the government at least makes sure that you don’t starve to death. You can get welfare, food stamps, and government funded housing. Education in this country is free, so every poor child here has the opportunity to pull themselves out of despair and make a better life for themselves. Here in the U.S., there is hope. In the third world, the government does not help because they literally cannot afford to. Education is not free in the third world. If you can’t pay the tuition, you don’t go. How can a child hope for a better life when they can’t even read? In certain countries in Africa, people starve to death, not because they can’t afford food, but because there isn’t any. There is no industry and thus no job opportunities. In the third world, there is little hope. As for adoption, many do not like to adopt within the U.S. because of our country’s horrible adoption laws. In many states, the birth mother has up to a year after the adoption is final to change her mind. Most adoptive parents are not willing to take that kind of a chance. The laws are way to biased in favor of the biological parent. I for one applaud the efforts of Bono, Bill Gates, Warren Buffet, Brad Pitt, and Angelina Jolie. This world is bigger than just the U.S. Everyone on this planet deserves help regardless of religion, gender, race, or country. We’re all human beings. The money should go to where the greatest need lies. And right now, that is Africa and Asia. Iam glad after the hoopla of this one, her advisors will tell her that adopting another is not winning her any more favours. Word around in L.A is that Brad is on the phone to Jen 24/7. Thought I thought their relationship sucked, this will be intersting. I can’t wait for Jolie to come back and some ass kicking starts. The pussy whipped bro should know his place. Bare-foot and pregnant in the kichen. LOL #63-I think Oprah defended herself really well when someone brought up this very point to her: She said the reason she does not donate nearly as much money to kids in the US as opposed to overseas is that the kids in the US actually have opportunities available to them. There are resources available there for them to someday, somehow take advantage of and make themselves a better life. The children she tends to help the most are the ones with no hope of ever overcoming the life they were born into. There is no one advocating on their behalf, whereas in the States, there are always people like yourself, who are kind enough to donate anything they can to help the less fortunate. There is no one able to do that in 3rd world countries. while I think it is wonderful that Brad and Angelina adopt needy children, I think it is unnecessary for them to always go to other countries to do so when we have so many children that are needy here in our own country. I also get sick of all these moneymakers ( Bono is at the forefront) who have multiple houses, cars, vacations, paychecks etc. most of which is made by the people in the USA or located here, and yet they champion the causes of everywhere except here. What about the poor and needy here in the US? I do not send any of my donated dollars out of the US anymore.Its bad enough our jobs are leaving the country, leave our $$’s here. Sorry to ramble on…this has been a thorn in my side for awhile….. Miapooca, I didn’t mean to insult you, lol. It is just that I went to that scientology place because I remembered you dissing scientology a lot and like many people I wanted to know what was the catch! I mean what is the deal that it means so much to you to diss it on all blogs all the time? By the way, I discovered that xenu is not a god but an evil creature. And it was not real but just an imaginary Illustration by Hubbard. Also I noticed that all the celebs who are scientologists are the most sane people in hollywood. They are not addicts like Britney. Infact Britney should just become a scientologist for a while. organise her life and leave later otherwise she is gonna die from an overdose. I have no heart for religions but they have some pretty sensible advice. Look at me spreading a cult! LOL Miapocca, remember you got me interested in the first place! And every one on this site usually insults you and calls you crazy!!!!! I mean read what you write from an objective point and you will see why. You sound pretty strange! I agree with whoever said that the Jolie Pitt family looks very miserable. Something is amiss since Brad joined them. My worry is especially for Maddox. He looks so sad all the time. Different from the boy we knew. i like likethatmatter. small detail: so let those ppl make it to the forbes – their money is usually denoted by terms such accumulation, surplus, and is pretty much linked to exploitation – and then ask them to redistribute a bit of it, after they’ve gone around the world and exploited ppl of all various shapes. likathatmatter has a point though: it’s better than nothing. and in that pic, jolie-pitts don’t account for much. but jolie hasn’t been able to articulate this yet. let’s see how far she’ll go Why can’t people say anything about Tori Spelling? I think she is more evil–she stole somebody else’s husband–while the ex-wife was pregnant. And has she done any humanitarian works? I don’t think so… Please don’t judge, and please respect, appreciate anybody who’s just trying to help out through adoptions, donations, counseling, personal visitations, community outreach programs, or any other supports–even a hug and a smile make a difference. ~ Maddox Chivan, 5: Jolie changed her first child’s name from Rath Vibol to Maddox Chivan. Maddox is a Celtic word meaning “beneficent” and Chivan has no identifiable origin. The family uses his nickname Mad. ~ Zahara Marley, 2: Zahara was born with the name Tena Adam. Zahara means “flower” in Swahili and “to shine” in Hebrew. Marley is a reference to the reggae singer Bob Marley. ~ Shiloh Nouvel, 10 months: Jolie gave birth to the Shiloh last year in the African country of Namibia. Shiloh means “peaceful one,” in Hebrew. Nouvel is a reference to Jean Nouvel, a famous French architect Check out the Forbes list of the world’s most rich 849 person, add their wealth together, and match the amount to the resources necessary to eliminate basic survival problems: the right to have food, the right to survive, the right to be secure. Assume that all names on that list donate 1/3 of only their “yearly income”. Also check the nationalities of these people and inequality and poverty inherent in their own countries. You will see according to that list, JPs are not “rich” or even “wealthy”. If my calculations are correct, with their current wealth level, Jolie and Pitt need to work 30 more years without spending a nickel to be placed in that list, assuming all else equal. Here is another question on amassing real estate wealth: Do you know the number of North Americans buying homes in Central Europe and Latin America as summer vacation homes for investment purposes? Your problem should not be JPs efforts, whatever they do, still their effort is not more than a drop. Your problem should be the redistributive justice in the world, and it starts from the Forbes list asking what these names give back to the deprived in the societies they live in. And for this reason, your outrage is misplaced and backfiring. 1. Pax was abandoned as a nameless new-born and registered as Pham Quang Sang by the whim of some bureaucrat in the Vietnamese legal system. The name was not the meaningful bequest of loving parents. If the kid was American, an identical bureaucrat would have called him John Smith. Or even John Doe. 2. No American parents would keep this exact original name. In Vietnam family name come first, then a middle name chosen from a very short list of possibilities and at last the given name. So if AJ and BP had decided to keep Pax’s Vietnamese name he would in effect be called Smith Doe John. 3. So I suppose all the onomastics experts (cof) who have been criticising AJ will graciously concede that she would at least have to change the order of the kid’s names – which gives us Sang Quang Pham. 4. And the same onomastics and adoption experts (cof cof) will also kindly concede that she would have to change Pax’s meaningless surnames to those of his parents – which gives us Sang Jolie or, in the near future, Sang Jolie-Pitt (gosh, they will go cuckoo again next week when Brad and Angie petition the American courts to change the surname to Jolie-Pitt due to Brad adopting the kid). 5. Those onomastics, adoption and child psychology experts (cof cof cof) will moreover benevolently concede that a toddler is not particularly attached to a middle name, which is usually more symbolic, frequently used to remember an ancestor, a patron saint, some cultural heritage. Thus accepting that AJ is not endangering Pax’s well-being by choosing a symbolic middle name, such as Thien – which gives us Sang Thien Jolie-Pitt. 6. Now, dear beloved onomastics, adoption, child psychology and pedagogy experts (cof cof cof cof), we may surely agree that little Pax is going to grow in a western society, as a member of a western family, with at least (gosh they will go absolutely bananas when the next pregnancy is announced) three siblings who all have meaningful given names lovingly chosen by their parents? 7. So, darling multi-experts, would you want little Pax to be the only Jolie-Pitt without a western sounding given name? The only Jolie-Pitt without a given name chosen by his loving parents? Tss, tss… and the trauma? The identity crisis? The horror! Therefore… I give you Pax Thien Jolie-Pitt! 8. Finally, you multi-idiots, rest assured that the transition from Sang to Pax is going to be smooth. Little Pax’s mother took the trouble (as the most babbling orphanage director in the world informed us) to learn some Vietnamese, in order to ease communication with her new son. Do you think she is going to start shouting Pax! Pax! Pax! to the toddler until he identifies with the name? To induce recognition and identity in a 3-year-old (in every 3-year-old) is a daily task. And a very basic and straightforward one too. By the time the fifth Jolie-Pitt kid arrives, Pax will be Pax will be Pax – and won’t even remember he was once a Sang Doe in some orphanage. THE WORLD needs someone like Angelina.Shes true to herself and commited to help the orphans all over the world. I HOPE THAT AMERICA WILL SEE WHAT SHES DOING AND FOCUS ON HELPING HER FOR THE BETTER .TO THE WORLD AND HUMANITY.And I hope that some hollywood stars will follow her not for their publication but to help the problem of the present situation of the world. Angie would take all the kids but Shiloh with her probably, since those will be the main ones she will feel responsible for. Brad will be visiting and keeping them for her when she travels around the country as she does now if he is able to do so. And Brad’s mom will help him raise Shiloh, and Brad will happily be helping support them forever! I just hope they don’t give Pax the same haircut as Maddox. The whole mohawk phase is is a little 80’ish to me. Let them look like normal children. Anyways, I wouldn’t be surprised if Shiloh has pink hair by the time she’s 2. I don’t know if its just me, but this family never looks happy in pictures. The kids, and the parents are never smiling. And what would happen with these kids if Brad & Angelina ever separated?? Jolie is hard to understand..she is not mormal, that said if you are looking for a playmate for your kids you send them to a diverse school and set up play dates..;.oops.oh forgot ,they dont really have nay friends to set up play dates with… If all couple want company for each and every child based on thier ethnicity , then it defeats the purpose of getting along in a diverse environment. That siad, ..I know a lot of Asians who have different names for each country they visit..Xiaopin is known as Grace in the USA and Marie in France..However is some African cultures , a name signifies a long line of ancestors.. Changing a name at 3yrs old is a bit tough, but as most say children adjust pretty fast, and I really do wish this child well and hope he can cope with the family….However in any event this child wants to track down his biological parents , he will have lots of press clippings to tell him his orphanage name as well as previous name… I have come to understand that the rich and fmaous have certain previledge, in these developign countries money talks big time and corruption is quite normal..so hey she can have her way..however the adopting as a single mom and wihtout Brad being involved in this whole pick smells a bit fishy….hhhahahah but hey they are both wierd, do it may b enormal for thier family What ever the psycho mama’s reason for adoption ..the children will be living in a lap of luxury, better than an orphange fo rsure, but is it really emotionally beneficial to be living with a mentally challenged mama or a host of other children in an orphanage….hmmm ,..I dont know..only the future MAY tell………. Here comes jackie..who is craxy about some scientology family and hero worships cruiseology but is taking issues with a name change …yikes you got you head majorly screwed up…and by the way thanks for the many insults on the tomkat blog……… Is it me or Maddox looks so sad these days. Gone is the boy who shot at the paps and was so cute and smiley. Now he looks like a sad little man and getting a new bro to steal away his lime light is not going to make him any happier. Every one has not considered all the changes he has had in the last two years. From being the centre of his mother’s world to having to share her with 4 new people. I remember being jelous of my husband and my daughter. I know it was strange but true. Even men get jealous when attention shifts from them to a new baby. Poor Maddox. He is going to be a troubled little tyke! On changing pax’s name, I think that was a wrong move. For such an ‘old’ child whose life is changing too drastically. I wouldn’t worry too much about Pax. I’m sure Angie and Maddox have learned the basic words they need to know to comunicate with him. My cousins were born and raised in Central America, whole different language. But when they visited every couple of years, (and there were 7 of them) even the youngest would get thier point across with only knowing a few English words. Young children learn quickly. Maddox knows English and French and some Khmer. I’m sure they have someone helping with comunication between all three. Lots of people adopt children, even older, from other countries, they adapt and learn quickly. No need to worry. Angie and Brad have the resources to do whats best. How could they be sure he was okay with the name change when he just cried when he met them and left with them? He doesn’t know them, they are strangers to him, a three year old doesn’t understand these things! Does he even speak English? How do you know he even understands what they say to him? I honestly do not know why so many people are criticizing them for adopting yet another child. They are GREAT hands on parents, they love their kids, & they can provide for them. Why would you criticize wealthy people for adopting when the childs living conditions were crappy in the orphanage? Every child deserves a parent. As for changing his name..I say good for them! Its a new start for this little guy, he is three afterall, I bet you they made sure he was OK with the name change. It should be a joyous day, but sadly there is something that is disturbing with this woman . If i did not know her past maybe i would feel different. # 35 i too feel she needs to be stopped. In a few years we will hear about this family and it is not going to be pretty. Nonsence!!!!!!!!!! Is she going to adopt 20 kids and learn their language and culture. Give me a break lady, you cant save the world. Adopt a child in your own country and save them, there are tons, I have one of ours and he’s amazing!! I don’t believe the birth order is that big a deal. If it was then single parents probably shouldn’t remarry because the combined children would have their birth order altered. And every first or previous child loses his baby of the family status when his sibling arrives. Adoption is also another way for saying chosen. In the days of the ancient Romans you could disown a birth child but not an adopted child because adoption was serious. Adoption is another way of saying special too. And as for the name I am not certain that it is that big a deal. Look how many people go by a nickname ,a deriviative of their name such as Bob for Robert , change their name upon marriage, keep their name upon marriage, or use a different name altogether for their carreers such as actors and authors. If it is a big deal to the child he probably just will insist on the use of the first names in daily life. And kids can certainly mean business! Cute kid, cute name, I think this child will flourish and be just fine with them. Very lucky little boy! As usual she has on her black outfit, she really has a fascination for the color black still after all these years. Shouldn’t Maddox be in a regular school program before too long? Of course she can hire tutors for all of them and learning different languages is wonderful for them to be bilingual, I think that is really a nice thing for them. I think it was a very smart move on her part to take Maddox with her to pick up this little boy, good for both the kids, I would like to see them in a stable settled home though instead of being uprooted all the time from city to city, country to country. I think this transition period will go by quickly and the boys will be very happy together, will be interesting to see how jealous Zahara gets over the new addition. Funny, Gina, that the way you describe Angelina “messing up” the birth order in her family could be generalized to include a huge population of people who adopt older children and have kids at home. It’s not quite that I am defending Angelina, as much as I am defending anybody who does the same thing she’s done everyday!! You are simply trying to find something wrong with this whole process, and unfortunately by flapping your gums too quickly you managed to insult a great number of people, not just my “hero”, Angelina. Good God, Gina. According to you, no one should ever adopt if they already have kids at home unless it’s a baby?? Give me a break, you are hyper-critical and it’s so annoying. I think kids also identify with their parents bringing another human being into their family unit!! You are ridiculous. ————————————————- Simmer down, there “honey.” The way some of you over-emotional women take these things so personally is frightening. Take a step back from the computer and give your hormonal head a shake. Good God. You are NOT Angelina Jolie, no matter how much you hero worship her, so my opinions should not ignite you with this much venom. The fact that they do says a lot about you and has nothing to do with me or your hero Ange. minnie, good point – not craddle, rather the end of history, the peak of civilization and quite the contrary thus to the dark, demised africa. as for the craddle, of the enlighted, therefore western world, that is greece. at least it is considered to be so. as for the rest of the naming business, it happened to other powerless ones too, such as places and places in india, africa, etc. angie should read some history of colonization together with international law that she has been doing. vietnam by the way, is one of those places that the superpowerful america has not resisted in meddling with, along with other places such as latin america etc. maybe their poverty and deprivation has to do with that bit of history too. again, angie should be more sensible in not flamming the old patterns of power of who does business where. such symbolisms are just too powerful, and exceed the mother-scale of angie’s love People! Have your own opinions about Angelina Jolie, but can we at least acknowledge that she is doing something good! As far as the name thing goes, parents get to choose names for their kids when they give birth biologically, why not with adoption? The kid is only 3 years old, he will adjust fine. Children are very adaptable. Everyone seems to be making a big deal out of the fact that only Angelina and Maddox went to pick up the new child. When that entire family travels though, the paps. go psychotic for pics. It may be easier for the child to adjust to the cameras if there aren’t as many around. For all we know, maybe brad couldn’t be present at the adoption due to Vietnamese law. Congratulations to the family-he is a cute kid. He’s really a cute little boy. He’ll need time to adjust, so I hope that Angelina has set aside plenty of time for that. I think it was a great move to bring Maddox with her because he looks similar to Pax, which is probably comforting for him. Maddox can also be a big help just in the way he intereacts with Angelina. Sort of showing Pax the ropes. I think Maddox and Angelina are the closest in that family, so Pax will really be able to see the love they have for each other, and hopefully he’ll join in. I hope for great things for this family. Congratulations!!! once upon a time, people grabbed other people and brought them over to america the craddle of civilization and in the name of showing them the face of civilization. they were called slaves. the owner were powerful. the owned were not. even to object to their names being changed – mainly because the owners couldn’t pronounce the original ones. despite her honorable intentions Angelina should shy away from certain gestures – even for the simple fact that they simply resonate with unfortunate and ugly ones. Lisa – I wouldn’t try logic like that! I completely agree with you but how does a well balanced argument help the terminally egotistical?! He looks sweet, I’m touched that she (allegedly) approached him slowly on her knees over 20 minutes and learnt enough of his language to comfort him. The fact that maddox was (apparently) so accepting suggests that someone has taken the time and love to introduce him to this new sibling with care and sensitivity. But the rules mean that people will pick a celebrity and bash them to fit their world view and not accept new ideas. What’s with the name thing? When my parents adopted my sisters and brother, they changed their names and they were 6, 4, and 2. They got along just fine. Kids adjust very fast. Birth order is not really an obstacle either. When the kids came into our family, my bio sister was the youngest and the 6 year old was the oldest in her sibling set. Both had to adjust to their new position in the line up. Both handled the change just fine. It’s an adjustment anytime a new child enters a family. Mad and Zee managed to adjust to Shi. I don’t see any major problems with Pax. This poor boy has only existed in some god forsaken vietnamese orphanage, under a name assigned to him by the government and you are nit-picking about the name change. My father came to this country at age 11 from hungary and he chose to later in life legally change his name. So, this BS about how terrible it is that “poor” boy got adopted and about his name change is rubbish. My daughter has no memories of the apartment we lived in until she was three, never mind the beautiful life that awaits this poor orphan. Face it guys, Brad was not happy with Jennifer Aniston, their marriage ended and no matter how nasty your posts get about Brangelina it will not bring back your “golden” couple… He is abosultely gorgeous. He does remind me of Maddox when he was that age. I am so happy for that little boy (any child that is adopted to a happy family) and I’m also very happy for AJ and BP along with the other kids. I wish them all the happiness in the world. as for those critizing her for changing his name…enough is enough…why can’t you people be happy for this little boy! He has A HOME!!! A LOVING FAMILY!!! you people are rediculous! I’m not a fan of AJ but I’m still happy for her and her family and most of all for this little boy. He’s 3 YEARS OLD for God sakes! He is going to adjust wonderfully. and in no time, he and Maddox will be great friends and even better brothers. Just be happy for them is that so much to ask for????? Good God, Gina. According to you, no one should ever adopt if they already have kids at home unless it’s a baby?? Give me a break, you are hyper-critical and it’s so annoying. I think kids also identify with their parents bringing another human being into their family unit!! You are ridiculous. He looks a lot like big brother maddox maybe thats what made him stand out for Brad & Angelina! Hes Going to Have a Wonderful Life He Will Adjust Hes Only 3 So I Don’t think That will Be Much Of a Problem.congrats to them all! gina–She upset the birth order? How?? Mad is still the oldest, Zahara is the oldest girl and Shiloh is still the baby. Maddox is still the big brother, now Pax is the younger brother. Zahara and Shiloh are still the little sisters. Best wishes to thie family. she’s also upset the birth order of her family. children very much identify with their birth order, it is a huge part of the family heirarchy and it isn’t smart to mess with it. kids identify themselves as little sister, big brother, younger brother … she’s upset that. Maybe by changing his name she wants to signify that his life from here on will be a new, better life. I see nothing wrong with it. I like the new name now that I know what Pax means. Thien is a good name. A peaceful sky is bright and essentially that’s what his Vietnamese name ‘Quang Sa’ng’ alludes to. After the rain, the dark clouds are gone and the sun is out, the Vietnameses say ‘tro+`i quang’ (the sky is clear / bright). And when darkness is gone we say ’sa’ng ro^`i’ (there’s light). All in all, there is nothing to make of the changing of the name. His was not truly his any way since he was abandoned. A child can adapt quickly, especially when there are kids his age, even more so when there is one his gender. By next month I’m sure he’ll know enough English to let his new family know he’s hungry, thirsty, needs to go pee, and so on. A child born into a harsh world isn’t like one born into a country with massive welfare and social programs such as America. He or she will be just fine in the new environment. Angie did make an effort to learn some Vietnamese phrases so she can comfort the boy. That is commendable. I am just happy that she decided to adopt a Vietnamese boy. He is now saved from a life without education, on the hard streets of Saigon where he could be tricked into prostituting himself to survive. He will have education, dreams and very possibly have at least one of his dream fulfilled. He’s 3 yrs old, he knows his name and has lived with it his whole life…I to think she could’ve at least kept it the same or the first name at least and changed the Middle…. Now he has to get used to being called a new name… I don’t think that’s right. At one year old or younger it would be an easier transition to learn a new name.. I think 3 years old is too old to be changing it.IMO Meg Ryan changed her little girls name she was a year old. She had a new family, new language and a new name. She seems to be doing fine. A name assigned to you by staff mambers or one picked with love from your new family. I like his name. Maddox knows English, French and some Khmer. They will all learn a new language together. Why would she change his name? Wasn’t it cool enough for her? New family new language new faces and a new name? Is this for his benefit or hers? Her adoptions are becomming disturbing to me. If she actually cared about his well being she wouldn’t change his name. How confusing is that for the poor little guy>? The Oscar-winning actress collected the boy from a Ho Chi Minh City orphanage after a short and tearful farewell. … Nguyen Van Trung, the director of the orphanage, said it was an emotional moment when she left with her new three-year-old son. “They tried to make friends with the Vietnamese boy, who cried when he saw them because for him, they are strangers,” he told reporters. “Jolie was very moved. Both of them tried to comfort the little boy,” he added. This is going to be quite an adjustment for this little boy, with all the attention his parents get. I hope it’s an easy transition for everyone. It’s really too bad Brad couldn’t be there too, I can’t believe his contract wouldn’t allow for him to greet his new son! Babyrazzi.com is a website that focuses on the entertainment and lifestyle needs of today's family.Babyrazzi offers work-safe and family-friendly insight into the latest celebrity gossip, paparazzi photos, and up-to-the minute pop culture news with a targeted focus on celebrity babies, pregnancies, and all things family and relationships. We also offer product review and important product recall information. The INO blog family includes Babyrazzi.com, ImNotObsessed.com, and LadyandtheBlog.com. BabyRazzi LLC publishes rumors and conjecture in addition to accurately reported facts. Information on this site may or may not be true and BabyRazzi LLC makes no warranty as to the validity of any claims.

### **Praise for** **_Diet for a New America by_** **John Robbins** _"Diet for a New America_...is the most important book of our generation." —Dan Millman, author of _Way of the Peaceful Warrior_ "A most extraordinary [and] compelling book, one bound to shake our innermost core. _Diet for a New America_ is a must for anyone concerned about ecology, health, and life." _—The Las Vegas Sun_ _"Diet for a New America_ is a powerful tool on the journey towards consciousness and compassion. I recommend it without reservation, and hope that many, many people will read it." —Gary Zukav, author of _The Seat of the Soul_ _"Diet for a New America_ will vitalize the awakening of America. This easy-to-read yet mind-boggling book has its place in the kitchen and in the doctor's office, in every classroom, from preschool to university. For those involved in ecological and political issues, this book is a must; so it is for all of us who long for a practical economical way to foster a more sane, ethical, and loving world." —Laura Huxley, author of _This Timeless Moment_ _"Diet for a New America_ is a powerful indictment of our dietary practices that should be read by everyone interested in healthy living. It is a well-researched, well-documented, and eye-opening account of the myths and truths about meat, milk, fat, and protein. I will recommend this book to patients, friends, and relatives." —Andrew Weil, MD, author of _Spontaneous Healing_ "From the outset of reading this volume I was enthralled. The book is a pleasure to read, as engrossing as the most exciting novel. Yet this is no novel—it deals directly with the most important personal issues and decisions of our lives. When I finished reading _Diet for a New America,_ I knew that in my hands lay one of the most profound studies ever written of how our eating habits affect our lives, and indeed all of life on our planet...If you read only one book this year, let it be this one." _—Vegetarian Times_ "In a tender, not strident, voice, Robbins shows us why a humane society cannot be built upon an inhumane system of food production. Robbins does not play on our guilt, but shows us how our own well-being is linked to the development of radically new sensibilities to nonhuman life. I promise you what you perceive behind the supermarket meat counter will never be the same after reading _Diet for a New America."_ —Frances Moore Lappé, author of _Diet for a Small Planet_ _"Diet for a New America_ is excellent! I can't speak highly enough of it. This book is a breakthrough in the science of health and a joy to read. No one who suffers (or whose loved ones suffer) from the diseases of our time can afford to ignore this potent message. In his captivating style, John Robbins shows us how to create health for ourselves, our children, and the world we live in." —Dr. John McDougall, author of _The McDougall Plan_ "Every so often a book comes along which has the capacity to awaken the conscience of a nation. _Silent Spring_ was one such book. I believe John Robbins's volume is destined to be another. With consummate intelligence, thoroughness, and skill, Robbins takes us on a multifaceted journey which should cause all sensitive people to question their eating habits most searchingly. I couldn't put it down." —Cleveland Amory, president of the Fund for Animals and author of _The Cat Who Came for Christmas_ # **DIET FOR A NEW AMERICA** ### **Also by John Robbins** _No Happy Cows: Dispatches from the Frontlines of the Food Revolution_ _The New Good Life: Living Better Than Ever in an Age of Less_ _Healthy at 100: The Scientifically Proven Secrets of the World's Healthiest and Longest-Lived Peoples_ _The Food Revolution: How Your Diet Can Help Save Your Life and Our World_ _May All Be Fed: A Diet for a New World_ (including recipes by Jia Patton and friends) _Reclaiming Our Health: Exploding the Medical Myth and Embracing the Sources of True Healing_ _The Awakened Heart: Meditations on Finding Harmony in a Changing World_ H J Kramer _published in a joint venture with_ New World Library Editorial office: | Administrative office: ---|--- H J Kramer | New World Library P.O. Box 1082 | 14 Pamaron Way Tiburon, California 94920 | Novato, California 94949 Copyright © 1987 by John Robbins Epilogue copyright © 2012 by John Robbins Publisher's preface copyright © 2012 by H J Kramer Originally published in 1987 by Stillpoint Publishing All rights reserved. This book may not be reproduced in whole or in part, stored in a retrieval system, or transmitted in any form or by any means—electronic, mechanical, or other—without written permission from the publisher, except by a reviewer, who may quote brief passages in a review. Graphics by Deo Robbins Text design by Tona Pearce Myers Library of Congress Cataloging-in-Publication Data is available. First printing of 25th anniversary edition, November 2012 ISBN 978-1-932073-54-6 Printed in Canada on 100% postconsumer-waste recycled paper New World Library is proud to be a Gold Certified Environmentally Responsible Publisher. Publisher certification awarded by Green Press Initiative. www.greenpressinitiative.org 10 9 8 7 6 5 4 3 2 1 ## **CONTENTS** Acknowledgments Publisher's Prologue to the 25th Anniversary Edition Foreword by Joanna Macy Introduction **Part One** 1. All God's Critters Have a Place in the Choir 2. Brave New Chicken 3. The Most Unjustly Maligned of All Animals 4. Holy Cow 5. Any Way You Slice It, It's Still Bologna **Part Two** 6. Different Strokes for Different Folks 7. The Rise and Fall of the Protein Empire 8. Food for the Caring Heart 9. Losing a War We Could Prevent 10. An Ounce of Prevention **Part Three** 11. America the Poisoned 12. All Things Are Connected Epilogue to the 25th Anniversary Edition Endnotes Index About the Author ## **ACKNOWLEDGMENTS** My gratitude and thanks to: Deo Robbins, who nursed the book and me through thick and thin, her utterly unique wit providing me a continual source of renewal. Her example is a living demonstration that health comes through love. Don Rosenthal, whose keen eye and high editorial standards helped sharpen the focus of my thoughts. Ocean Robbins, whose love for all of life is a continuous inspiration to all who know him. Salima Cobb and Martha Rosenthal, who believed in my ability to write this book, even when my faith flickered. Kali Rae, for her support in the original inspiration for the book. All the animals I've been fortunate enough to know. Simply by being themselves, they have encouraged me to be a voice for the voiceless. My thanks also to the numerous physicians, nutritionists, environmentalists, researchers, and other concerned people who read and criticized the book as it took shape. And to all those yet to be inspired by the vision of _Diet for a New America._ _May All Be Fed, May All Be Healed, May All Be Loved._ ## **PUBLISHER'S PROLOGUE TO THE 25TH ANNIVERSARY EDITION** D _iet for a New America_ was first published in 1987. In the following seven years, beef consumption in the United States decreased by 20 percent, from 75 pounds per person annually in 1987 to 60 pounds per person in 1994. That year, during a National Public Radio debate, a representative of the National Cattlemen's Beef Association accused the book's author, John Robbins, of being single-handedly responsible for this decline. Of course, many other reasons were responsible as well, but _Diet for a New America_ has played a leading role in changing the way Americans view the food they eat and the industrial food system that produces it. Since the book's publication, Robbins has received over 60,000 letters from people who have read the book or heard him speak, describing how the book's message has changed their lives. Most of them reported either giving up meat or significantly reducing how much they consume. The book's message has prevented heart attacks and cancer, protected tropical rain forests from destruction, saved species from extinction, and spared millions of animals the cruelty of feedlot and factory farm existences. A few years after the book was published, the Los Angeles PBS affiliate KCET produced a documentary based on the book, titled _Diet for a New America,_ which became one of PBS's all-time most successful fund-raising programs. Stations around the country aired it during their pledge drives, receiving an extraordinary response from viewers. In 2000, largely due to the ongoing impact of _Diet for a New America,_ readers of TheVegetarianSite.com voted John Robbins the most influential individual of all time to the vegan movement. Indeed, when the book was first published, most mainstream Americans viewed the vegetarian lifestyle as the province of "crunchy" granola-eaters. But in the ensuing years, eating a plant-strong diet has moved from the outermost margins of our culture to widespread acceptance. Today, President Bill Clinton, actors Alicia Silverstone and Woody Harrelson, and comedian Ellen DeGeneres and her wife, actor Portia de Rossi, are vegans, along with countless other celebrities. The list of prominent athletes who have become vegetarian or vegan is long and growing, including nine-time Olympic gold medal winner Carl Lewis, former world heavyweight champion boxer Mike Tyson, baseball slugger Prince Fielder, and Atlanta Falcon tight end Tony Gonzalez, who holds numerous NFL records. Veganism is also becoming more popular among business leaders: Twitter cofounder Biz Stone, Ford Motor Company executive chairman Bill Ford, billionaire publisher Mort Zuckerman, and music label mogul Russell Simmons have embraced a vegan lifestyle. Steve Wynn, the Las Vegas casino magnate, not only is a vegan but has put vegan options in all his resort restaurants. Thanks to the ongoing work of medical doctors like Dean Ornish and Caldwell Esselstyn, researchers like T. Colin Campbell, filmmakers like Robert Kenner and Morgan Spurlock, and authors like Jonathan Safran Foer, Kathy Freston, Eric Schlosser, and Michael Pollan, the message of _Diet for a New America_ continues to grow stronger. Americans are growing increasingly aware that what we do to the earth, we do to ourselves; that how we treat animals says something important about who we are as people; and that confining animals in factory farms is wrong and produces food that is damaging to the health of our bodies, our world, and our spirits. While corporations continue to have great influence, the movement toward food that is organic, sustainable, locally grown, and produced with respect for human and animal rights will continue to grow ever more powerful. We hope this 25th anniversary edition, with a new epilogue from the author bringing the book up-to-date, will introduce a new group of readers to these essential issues. —Linda Kramer August 2012 ## **FOREWORD** After reading this book for the second time, I took a walk on the beach below the oil refineries on San Francisco Bay. Seagulls careened in the afternoon sun. A tanker hooked up a half mile out on the jetty. As I watched idly, my thoughts still occupied with the book, a strange fantasy arose in my mind. It was a scenario of what would happen if Americans no longer found animal products attractive. Say they simply woke up one day and found meat and poultry and dairy products unappealing. Given U.S. eating habits, that speculation borders on the absurd, I know. But suppose some magical transformation took place that would diminish our attraction to animal-based foods and at the same time increase our appetite and enjoyment for other foods that really nourish and are far better for us. What would happen? What would it mean for our lives and our world? Would that tanker, for example, still be making its deliveries of imported oil? Would those refineries stretch back for as many miles as they do now? Would there be as much DDT in the gulls overhead or in my own body? Would they and I be likely to live longer and healthier lives? The research that John Robbins has done for us in this book, gathering and distilling an extraordinary amount of little-known but vital information, allows us to deduce what would happen in such a scenario. From the evidence accrued in hundreds of recent medical, agricultural, economic, and environmental studies, which he presents in terms easy for the layperson to grasp, we can indeed estimate the results if Americans were to change their eating habits and kick the habit of overconsuming animal proteins and animal fats. I imagine then the scenario, as I walk along the water's edge: The effects on our physical health are immediate. The incidence of cancer and heart attack, the nation's biggest killers, drops precipitously. So does the incidence of many other diseases now demonstrably and causally linked to consumption of animal proteins and fats, such as osteoporosis, a major affliction among older women. My mother suffers from it; I fear it. The hormonal imbalances causing miscarriages and increasing aberrations of sexual development similarly drop away, as we cease ingesting with our meat, poultry, and milk the drugs pumped into our livestock. So do the neurological disorders and birth defects due to pesticides and other chemicals, as we begin to eat lower on the food chain where these poisons are far less concentrated. Mother's milk, where they concentrate in greatest intensity, becomes safe again; we can nurse our babies without fear. Since these toxins attack the gene pool itself, causing irreversible damage, the change in diet improves the health of my children's children's children and generations to come. The social, ecological, and economic consequences as we Americans turn away from animal food products are equally remarkable. We find that the grain we previously used to fatten livestock can now feed five times the U.S. population; so we have become able to alleviate malnutrition and hunger on a worldwide scale. We discover what it is like for us to sit down to eat without feeling guilt. Once relieved of it, we realize how great was that burden, that unspoken sense of being watched and judged by those who were hungry. We find ourselves also relieved of fear. For on a semiconscious level we knew all along that the old disparities in consumption were turning our planet into a tinderbox, breeding resentments and desperations that could only eventuate in war. We breathe easier, letting ourselves be emotionally in touch again with _all_ our brothers and sisters. The great forests of the world that we had been decimating for grazing purposes (that was, we discover, the major cause of deforestation) begin to grow again. Oxygen-producing trees are no longer sacrificed for cholesterol-producing steaks. The water crisis eases. As we stop raising and grinding up cattle for hamburgers, we discover that ranching and farm factories had been the major drain on our water resources. The amount now available for irrigation and hydroelectric power doubles. Meanwhile, the change in diet frees over 90 percent of the fossil fuels previously used to produce food. With this liberation of water energy and fossil fuel energy, our reliance on oil imports declines, as does the rationale for building nuclear power plants. As expenditures for food and medical care drop, personal savings rise—and with them the supply of lendable funds. This lowers the interest rates, as does the drop in oil imports, which eases the pressure on the national debt. A less obvious effect of our meat-free diet, but perhaps more telling on the deep psychological level, is the release that it brings from the burden and guilt of cruelty inflicted on other species. Only a few of us had been able to face directly the obscene conditions we inflicted on animals in our farm factories and modern slaughterhouses; but most of us knew on some level that they entailed a suffering that was too much to "stomach." We can appreciate now what it did to us to eat animals kept long in pain and terror. Because the mass methods employed to raise and kill animals for our tables were relatively new, we did not fully realize the deprivation and torture they entailed. Only a few of us guessed that the glandular responses of the cattle and pigs and chickens pumped adrenalin into their bodies and that we ate with their flesh the rage of the chickens, the terror of the pigs and cattle. It is good for our bodies, our relationships, and our politics to have stopped ingesting fear and anger. Acting now with more respect for other beings, we find we have more respect for ourselves. As I picked my way over the shale and driftwood, I thought to myself, "This scenario is wildly, absurdly Utopian. It is also clearly the way we are meant to live, built to live." And I wondered what the means could be that could alter our taste for animal food products and increase our appetite and appreciation for the foods that really are good for us. Then I stopped short, realizing with a laugh that the means is here at hand. I had just read it. It is this very book! One might argue that information alone is insufficient to alter patterns of behavior. But information of this kind weds itself with both compassion and self-interest. Fifteen years ago such considerations were enough to prompt our whole family to stop eating red meat. Our concerns then were world hunger concerns: a pound of beef costs 10 pounds of grain. That change did not strike us as any kind of sacrifice; as a matter of fact, we felt better physically and found our food costs dropping substantially. Now I see how reading John Robbins's book has changed our eating habits again for the better. Like many of our friends, we who had once relished barbecues and roast beef, bacon and eggs, and a chicken-every-Sunday lifestyle, are changing our eating habits without any trauma or fanfare. Still, I did not know how much was at stake until I read _Diet for a New America._ For this book reveals the causal links between our animal food habits and the current epidemics of cancer, heart disease, and many other modern health disorders. It reveals as well the role these habits play in the present ecological crisis—in the depletion of our water, topsoil, and forests. It shows how the production of animal foods puts toxins into our environment and how our consumption of these foods increases in turn our susceptibility to these toxins. Eating high on the food chain can be seen now as a kind of vicious circle, in which the chemicals we inflict on the environment and other life-forms mount exponentially, and in which we ourselves as consumers become progressively more vulnerable to them. It was clearly not an easy book to write, as John Robbins acknowledges. For he uncovers not only a massive horror in what we as a society are doing to other beings and to ourselves; he uncovers massive deception as well. The information he gives us about what he calls the Great American Food Machine amounts to a powerful indictment of the meat and dairy industries, both in regard to their cruel and dangerous methods of food production and in regard to the falsehoods they purvey. Through their advertising and especially through the "educational" materials that they distribute and that get taught through our public schools, these industries persuade us of dietary requirements that are inaccurate and promote dietary habits that shorten our lives. In his exposé of their corrupt and corrupting practices, John Robbins stands in the fine American tradition of courageous whistle-blowers, like Ralph Nader and Rachel Carson. In this case, it is both ironic and strangely fitting that the message comes from—or through—the scion of America's largest ice cream company. A major contribution of _Diet for a New America_ is the welcome news it brings that we need far less protein than we thought we did. Many of us who turned from meat protein in an effort to live more lightly on the earth believed we should compensate by eating an equal amount of dairy and vegetable protein and by combining grains and legumes to produce it. Frances Moore Lappé, in the first edition of her milestone book _Diet for a Small Planet,_ showed us how to do that. Robbins's book marks an equally significant milestone, for it shows convincingly that our actual protein requirements are far lower than previously assumed. Using a plethora of recent medical studies, including research and revisions by Lappé herself, _Diet for a New America_ debunks what it calls the protein myth, showing that if we eat less protein we can not only survive but live healthier lives. The incidence of osteoporosis, to take an example, declines with lowered protein consumption. I am grateful that this book is not a sermon. It is too important for that—too important for our health as individuals, as families, as a society, and as a planet. John Robbins does not scold or moralize; he takes us on a journey with him, sharing his love for life and his reverence for all life-forms, ours included. While he shares as well his surprise and pain at what he discovers in the Great American Food Machine, he wisely lets us draw our own conclusions about how we want to live. The title is appropriate. There _is_ a new America taking birth in our time. I encounter it everywhere I go in this land, in cities and small towns, in churches and schools, where folks are fed up with violence and disease and alienation, where they are creating new forms, new lifestyles, determined to live in ways that lend meaning and sanity to their lives. This new America takes seriously the values of individual dignity, freedom, and justice that were heralded at the birth of our nation. It wants to share these values with all beings—knows it _must_ share them in order to survive. It is fed up with consuming over half the world's resources; it is sick of being sick. That is why, I suspect, the fantasy that occurred to me on the beach may not be so unrealistic. —Joanna Macy Author of _Active Hope_ ## INTRODUCTION Iwas born in the heart of the Great American Food Machine. From childhood on it was expected that I would someday take over and run what has become the world's largest ice cream company—Baskin-Robbins. Year after year I was groomed and prepared for the task, given an opportunity to live the Great American Dream on a scale very few people can ever hope to attain. The ice cream cone–shaped swimming pool in the backyard of the house in which I lived was a symbol of the success awaiting me. But when the time came to decide, I said, "Thank you very much, I appreciate the kind offer, but no!" I had to say no, because something else was calling me, and no matter how hard I tried, I could not ignore it. There is a sweeter and deeper American dream than the one I turned down. It is the dream of a success in which all beings share, because it is founded on a reverence for life. A dream of a society at peace with its conscience because it respects and lives in harmony with all life-forms. A dream of a people living in accord with the laws of Creation, cherishing and caring for the natural environment, conserving nature instead of destroying it. A dream of a society that is truly healthy, practicing a wise and compassionate stewardship of a balanced ecosystem. This is not my dream alone. It is really the dream of all human beings who feel the plight of the earth as their own and sense our obligation to respect and protect the world in which we live. To some degree, all of us share in this dream. Yet few of us are satisfied that we are doing all that is needed to make it happen. Almost none of us is aware of just how powerfully our eating habits affect the possibility of this dream becoming a reality. We do not realize that one way or another, how we eat has a tremendous impact. _Diet for a New America_ is the first book to show in full detail the nature of this impact, not only on our own health but in addition on the vigor of our society, the health of our world, and the well-being of its creatures. As it turns out, we have cause to be grateful, for _what's best for us personally is also best for the other life-forms and for the life-support systems on which we all depend._ The more I have uncovered about the dark side of the Great American Food Machine, the more appropriate it has felt to have declined the opportunity to be part of it. And the more urgent it has seemed that people be made aware of the profound and far-reaching consequences of their eating habits. _Diet for a New America_ exposes the explosive truths behind the food on America's plates. These are truths the purveyors of the Great American Food Machine don't want you to know, for in many cases they are not pretty truths. But if exposing them makes America healthier, and the world a kinder and more life-sustaining place, then so be it. In the past few decades, the animals raised for meat, dairy products, and eggs in the United States have been subjected to ever more deplorable conditions. Merely to keep the poor creatures alive under these circumstances, even more chemicals have had to be used, and, increasingly, hormones, pesticides, antibiotics, and countless other chemicals and drugs end up in foods derived from animals. The more unnaturally today's livestock are raised, the more chemical residues end up in our food. But that's just the half of it. The suffering these animals undergo has become so extreme that to partake of food from these creatures is to partake unknowingly of the abject misery that has been their lives. Millions upon millions of Americans are merrily eating away, unaware of the pain and disease they are taking into their bodies with every bite. We are ingesting nightmares for breakfast, lunch, and dinner. _Diet for a New America_ reveals the effects on your health, on your consciousness, and on the quality of life on earth that come from eating the products of an obscenely inhumane system of food production. You don't have to forgo animal products to derive great benefit from this book. You don't have to be a vegetarian to be concerned about your health, and to want your life to be a statement of compassion. _It's not the killing of the animals that is the chief issue here, but rather the unspeakable quality of the lives they are forced to live._ The purveyors of the Great American Food Machine don't want you to know how the animals have lived whose flesh, milk, and eggs end up in your body. They also don't want you to know the health consequences of consuming the products of such a system, nor do they want you to know its environmental impact. Because they know only too well that if word got out, the resultant public outcry would shake the foundations of their industry. But I want you to know. I'm letting the cat out of the bag. I don't care about their profits. I care about your health, your well-being, and the welfare of our planet and all its creatures. Eating should be a pleasure. It should be a celebration and a communion with life. The information in this book will provide you access to a whole new sense of pleasure in eating—a pleasure all the deeper for being at no one's expense, a pleasure all the more wonderful for being productive of radiant health. Exciting things have been learned in the past few decades regarding health and food choices. There have at last been enormous breakthroughs in the science of human nutrition, and for the first time we are now receiving irrefutable scientific evidence of how different eating patterns affect health. We've always known that it was best to eat a "balanced diet," but now we are finding out just what a balanced diet really is, and it's not at all what we had thought. Thousands of impeccably conducted modern research studies now reveal that the traditional assumptions regarding our need for meats, dairy products, and eggs have been in error. _In fact, it is an excess of these very foods, which were once thought to be the foundations of good eating habits, that is responsible for the epidemics of heart disease, cancer, osteoporosis, and many other diseases of our time._ _Diet for a New America_ is the first book to reveal the latest findings of nutritional research in a language anyone can understand and at the same time document these findings so you can rest assured of their legitimacy. It takes into account the marvelous and undeniable fact that you are a unique person, with your own special tastes, needs, and biochemical individuality. It does not sell you short by presenting rigid rules you have to follow obsessively. On the contrary, the goal is for you to be truly healthy and happy in every dimension of your being, and to be free from any kind of compulsion. _Diet for a New America_ contains no dogmatic list of _shoulds_ and _shouldn'ts_ but instead gives you information that will help you select and enjoy foods that day by day will make you healthier and happier. It shows you how to protect yourself against heart attacks, cancer, osteoporosis, diabetes, strokes, and the other scourges of our time. It shows you how to keep your body free from cholesterol, saturated fat, artificial hormones, antibiotic-resistant bacteria, pesticides, and the countless other disease-producing agents found all too often in many of today's foods. It shows you how you can enjoy eating food that leaves your mind and heart clear and unpolluted. As Americans we are indeed privileged to have the option of selecting the optimum diet. But for most of the world, the struggle is a far different one; it is for survival itself. _Diet for a New America_ shows you how your food choices can be of tremendous benefit, not only to your own life, but to the less fortunate of the world as well. It calls for no self-deprivation but simply the understanding that the healthiest, tastiest, and most nourishing way to eat is also the most economical, most compassionate, and least polluting. Heeding this message is without doubt one of the most practical, economical, and potent things you can do today to heal not only your own life but also the ecosystem on which all life depends. You benefit, the rest of humankind benefits, the animals benefit, and so do the forests and the rivers and the soil and the air and the oceans. There is enormous suffering today that stems from people's feeling isolated and alienated from nature. _Diet for a New America_ is a statement of our interexistence with all forms of life and provides a means to experience the profound healing powers of our interconnectedness. _You'll learn how to care for your health and to improve the quality of your life. You'll see that the very eating habits that can do so much to give you strength and health are exactly the same ones that can significantly reduce the needless suffering in the world and do much to preserve our ecosystem._ And you'll discover the profound liberation that comes from bringing your eating habits into harmony with life's deepest ecological basis. You will become increasingly sensitive and increasingly able to live and act as an agent of world spiritual awakening. Few of us are aware that the act of eating can be a powerful statement of commitment to our own well-being and at the very same time to the creation of a healthier habitat. In _Diet for a New America_ you will learn how your spoon and fork can be tools with which to enjoy life to the fullest, while making it possible that life itself might continue. In fact, you will discover that your health, your happiness, and the future of life on earth are rarely so much in your own hands as when you sit down to eat. When I declined to be a top cog in the Great American Food Machine and turned down the opportunity to live the American Dream, it was because I knew there was a deeper dream. I did it because I knew that with all the reasons that each of us has to despair and become cynical, there still beats in our common heart our deepest prayer for a better life and a more loving world. The book you hold in your hands is a key that will enable you to be an instrument of this prayer. —John Robbins Summer 1987 _The lives of the animals raised for food in the United States today stand in glaring contradiction to our hopes for a better way of life. In order to understand the full significance of what is being done to these animals, it will be helpful to understand what kind of creatures animals really are. This, then, is where our story begins—with a look at the nature of the creatures we call animals, and at our attitudes toward them. The astounding truth may surprise you as much as it has surprised me..._ ## 1. **ALL GOD'S CRITTERS HAVE A PLACE IN THE CHOIR** _I care not much for a man's religion whose dog or cat are not the better for it._ —ABRAHAM LINCOLN You will not find very many monuments to dogs in this world. But in Edinburgh, Scotland, in a public area known as Greyfriar Square, there stands a statue, erected by the local citizens, in honor of a little terrier named Bobby. Why did the townspeople erect this statue? Because this little dog taught them a lesson in the years he lived with them—a most important lesson. Bobby the Scottish terrier had no owner. And as often happens to small-town dogs with no master, he was kicked around by just about everybody and had to scrounge through garbage to get anything to eat. Not what you would call an ideal life, even for a dog. But it happened that there was in the village a dying old man named Jock. In his last days, the old man noticed the plight of the sorry little dog. There wasn't much he could do, but he did buy the little fellow a meal one evening at the local restaurant. Nothing fancy, just some scraps. But it would be hard for anyone to overestimate the extent of little Bobby's gratitude. Shortly thereafter, Jock died. When the mourners carried his body to the grave, the terrier followed them. The gravediggers ordered him away, and when he refused to leave they kicked him and threw rocks at him. But still the dog stood his ground and would not leave, no matter what they did. From then on, for no less than 14 years, little Bobby honored the memory of the man who had been kind to him. Day and night, through harsh winter storms and hot summer days, he stood by the grave. The only time he ever left the gravesite was for a brief trip each afternoon back to the restaurant in which he had met Jock, in hopes of scavenging something to eat. Whatever he got he would solemnly carry back to the grave and eat there. The first winter Bobby had almost no shelter, huddling underneath tombstones when the snow was deep. By the next winter, the townspeople were so touched by his brave and lonely vigil that they erected a small shelter for him. And 14 years later, when little Bobby died, they buried him where he lay—alongside the man whose last gesture of kindness he had honored with such devotion. ### **The Most Selfless Animal in the World** If the little Scottish terrier whose monument still stands in Edinburgh is not the most selfless animal who ever lived, a dolphin named Pelorus Jack might well be. For many years, this dolphin guided ships through French Pass, a channel through the D'Urville Islands off New Zealand. This dangerous channel is so full of rocks, and has such extremely strong currents, that it has been the site of literally hundreds of shipwrecks. But none occurred when Pelorus Jack was at work. There is no telling how many lives he saved. He was first seen by human beings when he appeared in front of a schooner from Boston named _Brindle,_ just as the ship was approaching French Pass. When the members of the crew saw the dolphin bobbing up and down in front of the ship, they wanted to kill him—but, fortunately, the captain's wife was able to talk them out of it. To their amazement, the dolphin then proceeded to guide the ship through the narrow channel. And for years thereafter, he safely guided almost every ship that came by. So regular and reliable was the dolphin that when ships reached the entrance to French Pass they would look for him, and if he was not visible, they would wait for him to appear to guide them safely through the treacherous rocks and currents. On one sad occasion, a drunken passenger aboard a ship named the _Penguin_ took out a gun and shot at Pelorus Jack. The crew was furious, and when they saw Jack swim away with blood pouring from his body they came very close to lynching the passenger. The _Penguin_ had to negotiate the channel without Pelorus Jack's help, as did the other ships that came through in the next few weeks. But one day the dolphin reappeared, apparently recovered from his wound. He had evidently forgiven the human species, because he once again proceeded to guide ship after ship through the channel. When the _Penguin_ showed up again, however, the dolphin immediately disappeared. For a number of years thereafter, Pelorus Jack continued to escort ships through French Pass—but never the _Penguin,_ and the crew of that ship never saw the dolphin again. Ironically, the _Penguin_ was later wrecked, and a large number of passengers and crew were drowned, as it sailed—unguided—through French Pass. ### **Who Is the Animal?** A San Francisco science fair recently awarded a prize to a junior high school student whose science project consisted of cutting the head off a live frog with a pair of scissors, to find out whether frogs swim better with or without their brains. Of course, this is not the only case of frogs being treated cruelly in our schools. They are often dissected by children ostensibly learning "how life works." But what did this youngster learn through his experiment? I think he learned that it is all right to treat other living things as if they have no feelings, as if they are nothing but machines. I think he learned disrespect for life. And I wouldn't call that a good thing. The science fair judges, however, obviously disagree with me, for they commended the boy on his contributions to the forward march of science, predicted great things for his future, and rewarded him for scientifically proving that: "Frogs will not swim with brain missing unless harassed. A frog swims better with head on." The attitude we develop toward animals when we are children tends to stay with us through the rest of our lives. And it continues to influence our experience not only of animals but of other people, ourselves, and life itself. There is a great deal of evidence from all over the world indicating that people who have learned as children to care for animals grow up more capable of caring for themselves and for other people. By the same token, people who later become criminals have very often abused animals as children. We find high statistical correlations in every country and culture where research has been done. The way we treat animals is indicative of the way we treat our fellow humans. One Soviet study, published in _Ogonyok,_ found that over 87 percent of a group of violent criminals had, as children, burned, hanged, or stabbed domestic animals. In our own country, a major study by Dr. Stephen Kellert of Yale University found that children who abuse animals have a much higher likelihood of becoming violent criminals. Studies of inmates in a number of U.S. prisons reveal that almost none of the convicts had a pet as a child. None of them had this opportunity to learn to respect and care for another creature's life, and to feel valuable in so doing. But these attitudes can be reversed, even in criminals. Heartwarming research has been done in which convicts nearing their release dates were allowed to have pet cats in their cells with them. The result? "Of the men who loved and cared for their cats, not a single one later failed as a free man to adjust to society." This in a penal system where over 70 percent of released convicts are expected to return to jail. The attitudes toward animals shown by the youngster at the science fair, and by the Soviet criminals when they were youths, are not at all unusual. We've all grown up in a system that condones such cruelty. Our public stance is basically that animals are ours to treat any way we wish, and that kindness to animals and sensitivity to them as fellow beings is an option some may choose if they want to, but it is no more incumbent upon us than being nice to plastic dolls. This attitude toward animals has been given voice even by modern religious leaders, one of whom said the following of animals being slaughtered: _Their cries should not arouse unreasonable compassion any more than to red-hot metals undergoing the blows of a hammer, seeds spoiling underground, branches crackling when they are pruned, grain that is surrendered to the harvester, wheat being ground by the milling machine._ For this religious leader, animals are not creatures who merit any sort of empathy. They are merely machines, bundles of reflexes and instincts, mechanical things with no feelings to speak of, objects that we can treat without qualm in any way whatever. This is a far cry from the attitude of Albert Schweitzer, who believed the following: _Any religion which is not based on a respect for life is not a true religion... Until he extends his circle of compassion to all living things, man will not himself find peace._ Toward the end of his long life, Schweitzer was awarded the Nobel Peace Prize for dedicating his whole life to teaching that: _We must never permit the voice of humanity within us to be silenced. It is man's sympathy with all creatures that first makes him truly a man._ ### **Dolphins to the Rescue** The official position of the Catholic Church has long been that animals don't have souls. During a Church council in the Middle Ages a vote was taken on whether women and animals have souls. Women squeaked by. Animals lost. One thing is sure. Yvonne Vladislavich would give you quite an argument if you tried to tell her animals don't have souls. In June 1971, Yvonne was aboard a yacht that exploded and sank in the Indian Ocean. Utterly terrified, she was thrown into shark-infested waters. Then she saw three dolphins approach her. One of them proceeded to buoy her up, while the other two swam in circles around her and guarded her from the sharks. The dolphins continued to take care of Yvonne and protect her, until she finally drifted to a marker in the sea and climbed up onto it. When she was rescued from this marker, it was determined that the dolphins had stayed with her, kept her afloat, and protected her across more than 200 miles of open sea. And there's more. On May 28, 1978, four fishermen became lost in a fog off the coast of Dassen Island, South Africa. They knew there were dangerous rocks in the vicinity, and they feared running into them because the fog had become so thick they couldn't see where they were going. Then they became aware of a group of dolphins nudging and pushing the boat, forcing them to change course. Suddenly, through the fog, they saw sharp rocks protruding through the water. The rocks only became visible as they floated by them, and the fishermen realized at once that the dolphins had saved their lives. Meanwhile, the dolphins continued to push the boat along a course known only to them, until it reached calm waters. Then they swam away, evidently feeling their job was done. When the fog lifted, the men were flabbergasted to find themselves in the very bay from which they had originally set out early that morning. ### **Man's Best Friend at His Best** Human contact with dolphins is limited. In recent years, the animal with whom most of us have had the greatest contact is the dog. One doesn't have to be a dog lover to recognize that these beings have provided enormous amounts of companionship, devotion, and loyalty to people over the years. Television shows like _Lassie_ and _The Adventures of Rin Tin Tin_ were not wholly contrived fantasies. They were dramatic representations of the loyalty, devotion, and intelligence of dogs. There are actually thousands of fully documented and independently verified incidents that make the adventures of Lassie and Rin Tin Tin pale by comparison. One day in Coeur d'Alene, Idaho, in 1955, a man named Ken Wilson was trying to teach a horse to accept a saddle in his corral. Ken wasn't at all concerned about his three-year-old son, Stevie, who he thought was playing at a neighbor's. But what he didn't know was that little Stevie had wandered off alone, fallen into a pond, and sunk to the bottom. The boy's dog, Taffy, however, saw the disaster and immediately raced to the corral, barking uproariously and demanding Mr. Wilson's attention. When the man ignored him, Taffy made a big show of charging into the pond, all the while continuing to bark at the top of his lungs. Then he raced back and nipped at the horse's legs. Finally Mr. Wilson realized the dog was trying to tell him something and dismounted. Immediately, Taffy bolted to the pond, barking for the bewildered man to follow him. When Wilson got to the pond, he saw his little son's red jacket floating on the surface of the water. Finally realizing what had happened, he dove headlong into the four-foot-deep water, found his unconscious son, and lifted him from the bottom. It was six hours before Stevie regained consciousness. But when he did, the first thing he saw was his little dog Taffy, sitting prayerfully beside his bed. Stevie is not the only child whose life has been saved by a dog. There are thousands of such cases, fully documented and verified. One such child was two-year-old Randy Saleh, of Euless, Texas. Little Randy wandered away from home one day. When his parents noticed his absence and couldn't find him anywhere, they called the police. But even a two-hour police search did not locate young Randy. The parents were becoming extremely alarmed, and when they noticed that the boy's dog, a St. Bernard named Ringo, was also missing, they found themselves praying that the big dog was with their little son and was somehow protecting him. Meanwhile, a man named Harley Jones had to stop his car for a traffic jam on a highway about three-quarters of a mile from Randy's home. Getting out of his car, he asked other stopped motorists if they knew what the problem was. They told him the trouble was "caused by a mad dog in the road ahead." Curious, Jones walked toward the head of the line of stopped cars to see for himself what was going on. What he saw was a St. Bernard, stationed resolutely in the center of the highway, barking wildly and letting no car move by in either direction. Jones saw the dog was protecting a little boy who was merrily playing in the center of the heavily traveled thoroughfare. The dog would stop any car that dared attempt to drive through the area and then would immediately rush back to the little boy and nudge him toward the side of the road. But the little fellow, thinking the whole thing was just a game, would return to the center of the highway. Jones spoke soothingly to the St. Bernard and managed to calm him down. But the dog would not let a single car move by until little Randy was safely off the road. I think you'd have a hard time convincing little Randy's parents that animals are just mechanical contraptions. Now, if you are like me, you may get a little choked up when you learn of these incidents. These are not just cases of dogs waking up their masters because they are panicking in the midst of a fire and then later getting credit. This is not the work of machines without feeling, driven only by instincts and reflexes. They are demonstrations of courage and devotion and selfless love. They are intelligent and brave responses to emergencies. ### **Unlikely Heroes** It is not only dogs and dolphins who have shown their reverence and devotion to human life by going to enormous lengths to save it. The animal kingdom, it turns out, is full of remarkable samaritans. In 1975, a desperate shipwreck victim off the coast of Manila was stupefied to see a giant sea turtle swimming toward her, seemingly offering its aid. The floundering woman climbed aboard the turtle, which then did something turtles supposedly never do. Sea turtles spend most of their time underwater, but this one must have somehow known that the poor woman needed constant support to survive, and must also have wanted very much to take care of her. It proceeded to stay at the surface for two full days, going without food itself, so it could continue to carry her and keep her alive. When human rescuers finally appeared, "eyewitnesses thought the woman was floating on an oil drum until she was safely on board—whereupon the 'oil drum' circled the area twice and disappeared." To be taken for an oil drum might not have surprised the turtle all that much. You see, for many years, turtles were not legally recognized as animals in the United States. One of the earliest crusaders for animal protection, Henry Bergh, found this out when he tried to stop the torments visited upon green turtles. These great animals, which have been known to live for hundreds of years and grow to 600 pounds or more, are sought after as a status source of soup and steak for the wealthy, with the young turtles being eaten when they weigh only about 50 pounds. Bergh found that the turtles were transported by ships from the tropics to the Fulton Fish Market in New York. En route, the turtles did not exactly travel first-class. For several weeks they lay on their backs out of the water, with nothing to eat or drink, like so much upside-down luggage. They were held in place by ropes strung through holes punched in their flippers. Bergh did everything he could to halt this activity, but when he brought the perpetrators to court, the judge acquitted them on the grounds that a turtle was "not an animal within the meaning of the law." Accordingly, ruled the judge, even the barest minimum of protection against cruelty that was afforded animals by the law at that time could not be applied to turtles. Most of us, like that judge, are conditioned by a culture that thinks of animals as mere machinery and could never imagine that a sea turtle would be capable of saving a human life. Nor would that same type of thinking allow us to believe that a canary, however sweet its song and pretty its feathers, could be much more than a decorative and bright adornment to a house. But the residents of Hermitage, Tennessee, know better. In 1950 in Hermitage there lived an elderly woman who was known to everyone around simply as Aunt Tess. The old lady lived alone with only her cat and a canary named Bibs. Aunt Tess's niece and her husband lived a few hundred yards away from her house, and they were concerned lest something happen to the aging woman without anyone knowing. One night they were awakened by what seemed like a tapping on the window. It wasn't loud, and they tried to ignore it, but the tapping continued. Finally, the niece got out of bed and went to the window to investigate. She drew back the curtains, and there, to her amazement, beating frantically against the windowpane, was Aunt Tess's canary, Bibs. The little bird had never before been outside the aunt's house, but she had somehow managed not only to get out but then to find her way several hundred yards to the niece's window. The task took all the little bird had, however. Before the niece's eyes, Bibs literally dropped dead from exhaustion on the windowsill. The niece and her husband immediately rushed over to Aunt Tess's house and there found the old lady lying unconscious and bleeding on the floor. She had suffered a bad fall and may well have died had not help arrived when it did. The canary had given its own life to save that of Aunt Tess. The more I have learned about animals, the more I have realized how conditioned I have been in my attitudes toward them. I never would have imagined a bird capable of this kind of thing. Nor would I have thought a pig likely to be a lifesaver. But I would have been wrong. A couple of years ago United Press International carried a photograph and story that were picked up and printed in many of the country's major newspapers. The photo was of Carol Burk; her 11-year-old son, Anthony Melton; and a pig. What made the story newsworthy was that mother and son had gone swimming in a Houston lake. The boy had inadvertently strayed too far from shore, panicked, and begun to sink. The boy's pet pig, Priscilla, had evidently felt his distress because she rushed into the water and began to swim toward him. While Anthony's anguished mother watched helplessly, the boy managed to stay afloat until the pig reached him. Then he caught hold of her leash. Anthony's mother watched awestruck as Priscilla the pig proceeded to tow her son safely to shore. ### **The Value of Life Itself** Human-centered animal that I am, I find it easiest to appreciate the heroism of animals who save human lives, who rescue people. But I've come to be impressed, too, by the numerous accounts of animals inexplicably going out of their way to save the lives of other animals. Now, the official government-run Soviet News Agency TASS does not ordinarily carry human-interest stories. But in September 1977, TASS reported a remarkable incident that occurred in the Black Sea. A Russian fishing boat found itself being circled by a small group of dolphins. The animals seemed to want something and kept circling until the sailors decided to raise anchor. Immediately, the dolphins sped off, as if they had been waiting for the anchor to be lifted and wanted to be followed. The puzzled sailors decided to follow along to see what would happen and were led to a buoy near which they saw a young dolphin trapped in a fishing net. Understanding now why the dolphins had come to them, the men released the trapped dolphin. The dolphins then proceeded to guide the boat back to the exact spot where it had been originally anchored. In this case, dolphins teamed up with human beings to save the life of one of their own kind. But there are many cases, perhaps even more remarkable, in which dolphins and human beings have collaborated to save the lives of other species, such as whales. On September 30, 1978, about 50 pilot whales became beached just north of Auckland, New Zealand. Government officials tried in every way to lure the great whales out to sea, because if they remained where they were they would all certainly die. Nothing worked. Then the officials got the idea of guiding a passing group of dolphins into the harbor. This they did, and when the dolphins saw the whales they seemed instantly to understand the whole situation. Wasting no time, the dolphins immediately took charge and literally herded the whales back to the open sea, thereby saving their lives. Of all the accounts I have on record of dolphin heroism, perhaps the most amazing comes, once again, from TASS. Their report tells of sailors on board the fishing vessel _Neverskoil,_ which was sailing off the coast of Kamchatka on August 14, 1978. The sailors heard a sea lion bellowing for help and saw that the creature was surrounded by a number of killer whales. But before the whales could devour the sea lion, a group of dolphins appeared, and the whales backed off. The sailors watched as the dolphins then swam away, and they thought this high drama of the seas was over. But the whales made another run at the beleaguered sea lion, who again began bellowing in fear. I can't help but think that what the sailors saw next must have astounded even these hardened veterans of the sea. The dolphins, hearing the distressed cries of the sea lion, realized that the killer whales were again homing in on the creature. They rushed back to the scene, leapt over the heads of the whales, and formed a ring around the sea lion, protecting it. They did not leave until the killer whales were well out of sight. There are reports of dolphins coming to the aid of whales giving birth. When sharks are menacingly near, the dolphins take up positions around a mother whale and her female "attendants," forming a ring around the helpless mother during her labor and delivery. Should the sharks attack, the dolphins bump them away with their bottle-nosed beaks. There are so many cases of dolphins saving lives—both human and non-human—that we should really think of them as the "lifeguards of the seas." We should. But we don't. Instead, we often treat them with utter contempt. One type of dolphin, called the Dall's porpoise, often swims in the water above salmon and tuna schools. Current salmon- and tuna-fishing methods use huge nets that trap the salmon and tuna—and the dolphins. In the past 10 years, according to official figures, 1,649,189 were killed in the course of tuna fishing. The Marine Mammal Protection Act of 1972 required fishermen to gradually reduce their porpoise kill to zero. However, in September 1981, President Reagan's administration convinced Congress to exempt the U.S. commercial tuna fleet, resulting in the continued use of purse seine, which trap and kill thousands of dolphins along with the tuna. Thus 50 dolphins will be killed in the time it takes you to read this chapter. Two have been killed while you've been reading this page, and this rate of massacre goes on 24 hours a day, 365 days a year. The huge corporations that own the fishing fleets tell the public they have modified the nets to permit the porpoises to escape. But they don't tell the public that many of the animals are netted and released, netted and released, until they are mangled and dead. The Reagan administration has also allowed the Japanese to kill porpoises while fishing for salmon in the U.S. waters of the North Pacific. Over a million dolphins have died in their huge nets, which also trap and kill seals and birds. As a result, organizations like Friends of Animals Inc. have called for a boycott of all tuna and salmon products. The more I've learned, the harder it has become to avoid the conclusion that animals are capable of a respect and reverence for life that cuts across species boundaries. One veterinarian reports: _I have six cases on record of pet dogs and cats becoming depressed and calling mournfully when a companion animal in the same house has been taken away to be put to sleep because of some incurable disease. In all cases, at about the same time that the companion pet was being destroyed, the surviving animal showed a sudden and obvious change in behavior. In one case, the owner did not know that the vet had put the other pet to sleep until he called an hour later, and for an hour before, her cat had been calling frantically and showing distress._ I find it difficult to dismiss these cases by attributing them merely to instinct. They speak to me rather of a thread binding all creatures in the great web of life. ### **A Guide Duck for the Blind** One of the most marvelous examples of animals caring for each other is recalled by Cleveland Amory in his lovely little book _Animail._ He tells of a scientist named Dr. Arthur Peterson, who lives in DeBary, Florida. A few years ago, Dr. Peterson noticed some odd activity by ducks on a lake on his property. Becoming extremely fascinated with what he saw, Dr. Peterson began to study the ducks and soon realized that a male duck (whom he called, for the sake of clarity, John-Duck) was uncannily and persistently attentive to a certain female duck (whom Dr. Peterson called Mary-Duck). It was not mating season, so there was no apparent explanation for this behavior, but he was terribly curious and kept observing the ducks, looking for clues. One day he noticed that John-Duck had left Mary-Duck alone for a minute, and he quickly approached her, slipped a net over her, and examined her. To his astonishment, Dr. Peterson found that Mary-Duck was completely blind. Touched by the implications of his discovery, Dr. Peterson released the unseeing Mary-Duck. Moments later, John-Duck reappeared and went immediately over to her. Then this "seeing-eye duck" gave a loud series of reassuring quacks and guided her off. ### **The Trapper and the Beaver Cubs** Animals with whom humans have little contact also have the potential for kindness and friendship. One man who came to understand something of the spirit of such animals was the Englishman Archie Belanie, who later became known as Grey Owl when he turned his back on his past and totally adopted American Indian ways. A prodigiously successful trapper, he fell in love with an Iroquois woman named Anahareo. One day the two of them came upon a female beaver who had been killed in one of Grey Owl's traps. They were about to leave with the fur when two small heads appeared above the water. At Anahareo's urging, Grey Owl rescued the little beavers, whose mother had been killed in his trap, and took them home. Getting to know these two little beaver kittens was such a powerful experience for the great trapper that he never trapped animals again. He wrote movingly of _their almost childlike intimacies and murmurings of affection, their rollicking good fellowship with not only each other but ourselves, their keen awareness, their air of knowing what it was all about. They seemed like little folk from some other planet, whose language we could not quite understand. To kill such creatures seemed monstrous. I would do no more of it._ ### **You Reap What You Sow** All animals—including those we have been taught to fear—can respond to love and give it. Nowhere has this been proven more profoundly than by Ralph Helfer and his wife, Toni, two of Hollywood's foremost wild-animal trainers. Helfer operates an animal park and training center in Buena Vista, California, where he handles and trains the fiercest of animals. Conventional wisdom has it that training these wild animals for show business requires instilling fear in the creatures and breaking their will. But Helfer is successful with a radically different approach. He says the idea first came to him in a hospital bed: _Violence begets violence, I mused, as I lay in my hospital bed 25 years ago after being mauled by a 500-pound lion. The big cat had been "fear-trained," with whips, chairs, and screams, as animals in captivity traditionally are; and though he performed his tricks well enough, he had no love for humans. Just as a battered child grows up to be a child abuser, a battered animal awaits its chance to do unto others as has been done unto him. I had been done unto royally by that lion, and I had plenty of time during a long convalescence to figure out why. That lion had attacked me, as so many other animals have attacked humans over the centuries, not because he was "wild," but because he was unloved. Your dog or cat is no different, nor is your horse or fish or pig or bird._ _The idea of affection-training was born in that hospital bed. Animals respond to their lives emotionally, I reasoned. If an animal could be trained by addressing its negative emotions (with threats and punishment), he could probably also be trained by appealing to his positive emotions. Surely the results would be even better with love than with pain, for the animal would be motivated to cooperate. Where pain might get the horse to water, love could induce him to drink._ _Since that time, I've proved my theory with almost every animal known to man. I've traveled from the jungles of Africa to the forests of India, working with everything from hippopotami to tarantulas._ When I first heard of training wild animals through affection, I was skeptical. But Helfer's success record, "with everything from hippopotami to tarantulas," is hard to discount. His animals have been used in many television shows, movies, and commercials. There is one thing, however, that affection-training cannot accomplish. There are some circus tricks that animals can be forced to perform through threats and fear but that they cannot be coaxed to perform through positive means. The reason for this is simple: the tricks we see in circus rings are often in violation of the anatomical structure and deepest instincts of the animals. Horses dancing on their hind feet, bears roller-skating, dogs walking on their back legs and pushing prams, cats firing off cannons, tigers jumping through burning hoops. These are displays, not of the magnificent natural capacities of the animals, but of their degrading obedience to the dominance of their trainers, a dominance achieved in the ugliest of ways. The quickest and least expensive method of breaking the spirits of the animals held prisoner by the circus trainers is by using whips, electric shocks, sharp hooks, loud noises, and starvation. The training is done in seclusion, and if local SPCAs get too nosey about what is being done to the animals to force their compliance, the animals are moved to foreign countries where there are no restrictions on animal treatment. One elephant, trained to dance and to play "Yes, Sir, That's My Baby" on the harmonica, was described recently as being probably the meanest elephant in the United States. I wouldn't be at all surprised if he had good reason. ### **The Easiest Way to Be Wrong Again** The conventional assumption of our culture is still that animals do not have any of the higher feelings of which we are capable, such as compassion and love and reverence for life. It can be difficult for us to see how tainted we might be by the culturally sanctioned misunderstanding that animals are only mechanical bundles of instincts and reflexes, with no hearts or souls. Few of us have had the opportunity to learn to respect them for what they are—creatures of marvelous complexity, beauty, and mystery. The idea of animals as machines without feeling has held sway in the collective psyche for so long that it has acquired a momentum of its own. We have gotten stuck in a very deep mental rut, a habit from which it is not easy to uproot ourselves. And habit, as Laurence Peter put it, is often "simply the easiest way to be wrong again." We have seen this mental habit given credence by the church and philosophical expression through thinkers such as Descartes. To him, the body and soul were completely separate; thinking and feeling were attributes of the soul, not the body, and the body itself was simply a machine. Since animals could not speak, it followed for Descartes that they had no soul and so could not feel. According to Descartes's point of view, which still permeates the psychic atmosphere of our times, all the nonhuman animals, from the ants up to what he called the "ape-machines," have no capacity for ideas, freedom of action, choice, knowledge of any kind, or feeling. They are merely robots, driven by instincts. He likened animals to watches and clocks, with wheels, springs, gears, and weights. Marvelously contrived though they might be, they are, said Descartes, "mere automatons." Descartes would sometimes kick his dog, just to "hear the machine creak." ### **Do Animals Suffer?** I'm sorry to say that the point of view that animals are only machines, and thus incapable of suffering, is still very much with us today. It is part of our cultural heritage, and I am still frequently amazed as I discover how conditioned I am by it. In the culture at large, it is so taken for granted that it is rarely questioned. I don't know if the gentlemen of Kewaskum, Wisconsin, are still enjoying their annual Kiwanis turkey shoots. But I know that as of 1971 they had not felt any compunction about their annual "fun and games." What, you may wonder, could be amiss in the "sport" from which the Kiwanis Club members derived so much amusement? Well, turkeys, those great birds who so astounded the Pilgrims when they first arrived in this land, may not be the smartest of God's creatures, but with a dignity all their own they have long been a symbol of the New World for many Europeans seeking freedom. Dignity notwithstanding, at the annual Kiwanis festival they were tied into stalls by the legs in such a way that their heads were exposed as a target for the participants in the "gala" event. The birds couldn't do anything to free themselves and they were shot at again and again by the drunken celebrants. In fact, they were tied in such a way as to guarantee that if they broke their wings or legs in their struggle to save their lives, as they often did, their heads would nevertheless be kept jiggling and exposed to the aim and merriment of the "brave" hunters. Champions of the idea that other animals don't feel pain as we do say that animals operate entirely from instinct. Thus the Kiwanis marksmen felt no more pangs of conscience than they would if the turkeys whose heads they gaily shot off were made of cardboard. They probably honestly believed turkeys don't suffer. But a reliance on instincts is very different from a lack of ability to feel pain. The capacity to feel pain has an obvious survival value to any species, enabling it to avoid sources of injury. It is with our senses and nervous systems that we feel pain, not with our capacity for abstract thought. The nervous systems of nonhuman animals are finely tuned to their environments. Their senses, in many cases, are vastly more sensitive and refined than our own. Physiologically, there is no basis at all for saying that animals don't feel pain. In fact, in _The Spectrum of Pain,_ Richard Serjeant writes: _Every particle of factual evidence supports the contention that the higher mammalian vertebrates experience pain sensations at least as acute as our own. Apart from the complexity of the cerebral cortex (which does not directly feel pain) their nervous systems are almost identical to ours and their reactions to pain remarkably similar..._ The senses of animals often make ours look pathetic in comparison. For example, the cells essential for smelling are ethmoidal cells. We have about five million of these in our noses. A German shepherd, by way of contrast, has about 200 million. And when it comes to hearing, once again we pale in comparison. The German shepherd can hear sounds clearly at 200 yards that we cannot detect at a mere 20. Even the much maligned shark has enormously sensitive hearing. An Australian named Theo Brown has taken advantage of this fact to develop a musical shark repellent. He conceived the idea when he discovered that if he played fox trots or waltzes the sharks were attracted from great distances, but if he played rock music they left at once. ### **We All Need Love** Proponents of the attitude that animals are ours to use, while sometimes acknowledging that animals may experience pain at a physical level, assert that they are not capable of suffering as we know it because their pain has no meaning to them. It is, say these "experts," just sensation. Accordingly, animals can't suffer as we can because their sensations of pain have no emotional meaning for them. I don't agree. There are many kinds of emotional suffering that we human beings have the ability to experience and all are connected, in one way or another, to our capacity to feel with other beings. And animals have that capacity. There is a relationship between the capacity of a being to love and its capacity to suffer, regardless of its species. If a being, of whatever species, has the capacity to give and receive love, then certainly it will suffer if that capacity is thwarted. This is one of the reasons all the wisdom traditions of the world teach us that a sure way to make yourself miserable is not to express your love. We need both to receive and to give love. Love is food for our souls, and without it we suffer greatly, just as we suffer physically if we starve. Have you ever watched an infant carefully, while it is being stroked and petted? We all know babies love and thrive on this kind of attention, but have you ever looked closely at the physiological changes they undergo? There is a distinct and well-defined pattern in their young nervous systems. The heart rate slows down, muscles relax, peristaltic waves increase, and digestive juices flow. Among other things, these changes allow for the formation of the crucial mother-child bonding. And so if the little one is not petted and stroked, and thus does not undergo these physiological changes, the bonding will not occur. One of the results of this is that the little human baby will have a hard time establishing social bonds in its later life. Another result when an infant is deprived of touching is that it literally shrivels. Because its digestive juices are not fully activated, it fails to receive proper nourishment and so its physical growth is retarded. The little one will do the best it can to survive under the circumstances, and this may mean developing what we call neurotic or, in extreme cases, psychotic symptoms, in the attempt somehow to compensate for the missing mother love. If the deprivation is sufficiently severe, the infant will habitually repeat the gestures of its compensation for the rest of its life. Now, it may surprise people who think animals are objects, but every single word you have just read about human infants, about their physiological and emotional responses to stroking and petting, and about the consequences if they are deprived of this attention, is true not only for human babies. It is also true, in every detail, for puppies, kittens, baby monkeys, and a large number of other mammals. Dr. Harry Harlow, at the University of Wisconsin, has done extensive studies on the influence of love and affection in the lives of subhuman primates. In one appalling experiment, monkeys were deprived of their mothers. The result? _They have shown many signs of extreme neuroticism and even psychosis. Most of them spend their time sitting passively staring out into space, not interested in other monkeys or anything else._ _Some of them tensely wind themselves into tortured positions, and others tear at their flesh with their teeth...These are all symptoms found in human adults confined in institutions for the insane._ Mother dolphins nurse their young for 18 months, and the mother-child bond is deep and enduring. Dolphins four to six years old have been known to seek out their mothers from a group when they become sleepy or frightened. So devoted are these animals to the welfare of one another that they will not abandon or desert a fellow dolphin who seems to be injured or distressed even if it costs them their life. When infant dolphins are caught in tuna nets, their mothers will go to extraordinary lengths to join their doomed young. Once in the nets, they will huddle together with their offspring, singing to them. The tuna industry takes note of this only to acknowledge that the majority of dolphins killed in their nets are females and infants. It's not only with dolphins, and it is not only in the parent-child relationship that animal love is evident. Even hard-nosed scientists who have studied wolves have been consistently amazed at the exceptional degree of what can only be called love and affection they show for one another. Gordon Haber, who has studied wolves for decades and is recognized as one of the world's leading wolf experts, notes that one of the outstanding features of these animals is their profound devotion and caring for one another. For example, he saw a wounded wolf in Alaska, its shoulder shattered and bleeding from being kicked by a caribou, limp into an abandoned cabin and lie down, seemingly to die alone as animals often do. But each night another wolf crept into the cabin and fed its crippled friend by bringing it chunks of meat. He continued to care for the wounded wolf until it recovered. Many animals, including beavers, geese, eagles, wolves, hawks, penguins, lynxes, and mountain lions, mate monogamously for life and are utterly devoted to their mates in a way that most married humans—who have pledged to care for each other "until death do us part"—could never imagine. Animals can suffer precisely because they have the ability to give and receive love, and a need to do so. ### **Intelligence** Still the blindness continues. Those who say that animals can't suffer in any meaningful way often claim that any pain sensations the animals might feel have no meaning because they are too stupid to know that they hurt. However, it seems to me remarkably limited for us to assume that because an animal does not display intelligence as we know it, it is therefore stupid. _It is just like man's vanity and impertinence to call an animal dumb because it is dumb to his dull perceptions._ —MARK TWAIN Even among our own species, we often don't recognize forms of intelligence that are perhaps a little different from the norm. Albert Einstein's parents were sure he was retarded because he spoke haltingly until the age of nine and even after that would respond to questions only after a long period of deliberation. He performed so badly in his high school courses, except mathematics, that a teacher told him to drop out, saying, "You will never amount to anything, Einstein." Charles Darwin did so poorly in school that his father told him, "You will be a disgrace to yourself and all your family." Thomas Edison was called "dunce" by his father and "addled" by his high school teacher and was told by his headmaster that he "would never make a success of anything." Henry Ford barely made it through school with the minimum grasp of reading and writing. Sir Isaac Newton was so poor in school that he was allowed to continue only because he was a complete flop at running the family farm. Pablo Picasso was pulled out of school at the age of 10 because he was doing so badly. His father hired a tutor to prepare him to go back to school, but the tutor gave up on the hopeless pupil. Giacomo Puccini, the Italian opera composer, was so poor at everything as a child, including music, that his first music teacher gave up in despair, concluding the boy had no talent. If we can be so far amiss in recognizing types of intelligence that are a bit different from the norm and yet belong to members of our own species who are destined to make great contributions, it seems likely we might fail to recognize some forms of intelligence that belong to beings of other species. Researchers have done exhaustive studies of animal and human brains. Most of these studies have been motivated by a desire to find a biological basis for the belief that there is a profound difference between human and animal forms of intelligence. No cut-and-dried dividing line has emerged. Comparing the "structure and function of the human brain with the brains of other animals," scientists have found that humans and other animals differ less than is commonly thought. _Surprisingly, the similarities are greater than the differences...A striking similarity between the human and non-human mammalian brain is seen in the electrical activity patterns of electroencephalograph (EEG) readings. A dog, for example, has the same states of activity as man, its EEG patterns being almost identical in wakefulness, quiet sleep, dreaming, and daydreaming. As for the chemistry of the central nervous and endocrine systems, we know that there is no difference in kind between human and other animals. The biochemistry of physiological and emotional states (of stress and anxiety, for example) differ little between mice and men._ ### **Incredible Journeys** There are so many instances in which animals have demonstrated profound intelligence that, frankly, I wonder sometimes about the intelligence of the people who insist that animals are dumb. Everyone has heard tales of dogs traveling great distances across unknown terrain to rejoin their people. What you might not know, however, is that many of these stories are documented, verified, and, incredible as they seem, literally true. For example, Mr. and Mrs. Robert Martin moved from Des Moines to Denver. But their German shepherd, Max, evidently preferred Des Moines, because he went back on his own, a distance of 750 snow-covered miles. Another German shepherd, living in Italy, missed his human companion, who had recently moved from Brindisi to Milan and left the animal behind. It took the dog four months to cover the 745 miles, but he managed to do it and found his person to boot. Even more remarkable is a shorter journey of "only" 200 miles, described by Sheila Burnford in her book _The Incredible Journey._ Three animals—an old English bull terrier, a young Labrador retriever, and, believe it or not, a Siamese cat—stayed together, took care of each other, and found their way across 200 miles of rugged Canadian wilderness in northwestern Ontario. I would never have thought a cat capable of such a feat. But I was wrong. There are actually many documented and verified accounts of cats traveling great distances to be with their people. The longest I know of is also one of the best authenticated. It concerns a New York veterinarian who moved to a new job and house in California and had to leave his cat behind, expecting to send for him later. But the cat disappeared prematurely, so the doctor understandably assumed he had seen the last of his cat. Five months later, however, the cat "calmly walked into the (new) house, and jumped onto its favorite armchair." As you might imagine, the vet was startled. For a moment, he was so shocked he just stood there, gaping. Was this his cat? Then he remembered that his cat had once been in a bad fight, in which its tail had been bitten. The injury had left a distinct growth on the fourth vertebra of the cat's tail. Remembering this, the vet walked over to the cat and felt its tail. Sure enough, there, on the fourth vertebra, was the telltale growth We may surely be justified in considering the possibility that animals have access to a kind of intelligence beyond our comprehension. It is hard to attribute such accomplishments to mere instinct. _Animals are interesting creatures..._ _with their own unique kinds of intelligence and beauty..._ _When treated well, most kinds of animals are friendly to people..._ _Pigs are as capable of friendship with us as dogs and cats..._ _But the animals raised for meat, eggs, and dairy products in the United States today..._ _are treated terribly..._ _Chickens are crammed into cages so tightly they can barely move and are driven insane..._ _From below, the view is nothing to put on a picture postcard._ _When treated well, pigs are remarkably happy..._ and friendly creatures... _But today they are crammed together so tightly that they go crazy..._ _and often bite one another's tails and rears, even killing one another..._ _When you realize what friendly and intelligent animals pigs are by nature_... _it's terribly sad to see the desolate lives they are forced to live today, treated like cars in a parking lot..._ _From childhood on they are treated like merchandise..._ _with no respect for the fact that they are living beings..._ _Yesterday's cows spent their whole lives grazing happily in pastures..._ _but today this is no longer the case..._ _The love and bonding between mother cows and their calves..._ _is strong and deep..._ _But today's veal calves are taken away from their mothers as soon as they are born..._ _and forced to live their entire lives in unspeakably miserable conditions..._ _These are little babies, separated from their mothers, and they desperately seek anything to suck on..._ _But they are never allowed to suck, and instead are fed a diet deliberately designed to make them anemic. Anyone who treated a dog or cat the way millions of baby veal calves are treated today would be arrested..._ _We prefer to numb ourselves psychically to the fact of the slaughterhouse. We don't like to remember that a hamburger is a ground-up cow..._ _In fact, some people evidently think chickens are vegetables. When someone says, "I'm a vegetarian," these people say, "Yes, but you do eat chicken, don't you?"_ _The author of_ Diet for a New _America, John Robbins shows us how our health, our happiness, and the future of life on earth depend on our shifting to a compassionate way of eating._ ### **An Elephant with a Sweet Tooth** If the only time you've seen an elephant is in a zoo, you've only seen the most devastated and abused specimens of this grand species. But even captive elephants are capable of sophisticated reasoning. One five-ton lady elephant, known as Bertha, was kept for years in the Nugget Casino in Las Vegas. She used to wake up her handler, Jenda Smaha, when it was time for a show by brushing her eyelashes against his cheek! Also, she had a clever way of getting at the sweets Jenda used in the show but kept stored between times in a cabinet in Bertha's house. Of course, Bertha was an enormously powerful animal and could easily have smashed the cabinet to smithereens and nabbed the goodies. But that, evidently, would have been too gross a strategy for a being of her subtlety. Instead, when a stranger would wander into the elephant house, Bertha would grab his arm with her trunk. You can imagine how this would startle just about anybody, so Bertha, sensitive as she was to others' feelings, was just as gentle about it as she could be. But if her captive tried to pull away, she'd tighten her grip enough to let him know who was boss. Thus ensnared, the stranger would be guided to the cabinet where the sweets were stored. Then Bertha would place the person's hand on the handle and hope the human had enough intelligence to deduce what was wanted of him. On one occasion, however, the cabinet was unexpectedly locked, and the poor woman in Bertha's grasp didn't know what to do. When Bertha let go of her, she made a beeline for the door, trying to get out of there as fast as possible but trying at the same time not to move so quickly as to panic the "dumb beast." Just before she could reach the door, however, there came a tap on her shoulder. Astonished, she turned around and found herself staring at the great elephant. In her trunk the elephant held the key to the cabinet, which she now dropped carefully into the woman's hand. Almost always, what is taken for rank stupidity on the part of animals turns out to be, instead, a lack of understanding on our human part. Ostriches, for example, are famed for stupidly sticking their heads in the sand when they want not to be seen. The truth of the matter, though, is that ostriches do not put their heads in the sand at all. When they sit on their massive eggs, their long necks and prominent heads make them a conspicuous and vulnerable target, visible to their enemies for miles. And so they have developed an ingenious and effective method of camouflaging themselves when they sense danger but must remain on their eggs. By stretching their necks down and along the sand, they not only become less conspicuous but also, from a distance, look very much like a small hill of sand. The more I learn about animals, the more they astound me. There are birds who fly halfway around the globe and yet return precisely to the same spot year after year. There are dolphin midwives who usher the newborn dolphins up for their first breath of air while other dolphin midwives stay with the new mother and care for her. There are whales who communicate with one another through sound patterns of such wondrous beauty that some feel they have more intricacy than even a Beethoven symphony. But sometimes it seems as if we humans will recognize their forms of intelligence as worthy of our respect only if they discuss matters with us in English and over tea. ### **Fresh from the Lap of God** There is always something adorable to me about a newborn fawn or a freshly hatched duckling or a newborn calf or, in fact, a newborn animal of any kind, including human newborns. They shine; there is a luster about them, a shimmering statement of the freshness they bring to life. To me, the fact that newborn human infants and newborn animal babies of all kinds glow with this ineffable sweetness testifies to our common source. They are born as we are—fresh from the lap of God, wanting to express their qualities in the service of the divine spark within them. They are born, as we are, thirsting for life. They are born, as we are, wanting to be all they are and to become all they can become. They want to play their part in the universe, live the lives they were born to live. In many ways they remain like babies as they age, even if they grow as big as an elephant, for their lives are always intense with immediacy, rich with emotional and sensory experience. Animals are part of our world, part of our existence. They give us reasons to celebrate life. They are part of us. Sometimes they bring us challenges, sometimes they bring us the opportunity to help them, sometimes they bring us companionship. Often, they bring us play, beauty, and laughter as they go about their business of being themselves. What we would miss if they were not here! "If the stars should appear one night in a thousand, how men would believe and adore!" So said Ralph Waldo Emerson. Can you imagine how we would feel if such were the fate of animals? ### **What the Children Know** Sometimes children understand these things better than adults do. A young Girl Scout named Karyl Carter wrote a simple report that says it all so well. _A beaver who swam, dove and somersaulted among canoeing Girl Scouts—that's what you would have seen at Camp Sacajawea Girl Scout Camp in Newfield, New Jersey, this summer._ _It was a late morning discovery. Girls from Holly Shores Girl Scout Council were taking canoeing lessons in Sacy's Lake when a large stump started to move and perform numerous swimming feats. Hearing laughter, squeals and screams, the waterfront director canoed out to the girls, identified the stump as a real beaver, and yelled to those on the beach, "Go get the rest of the camp...they've never seen anything like this before." In no time flat, the entire camp lined the lakefront, playing audience to a most talented but different kind of swimmer._ _The waterfront director, who was wary but excited, told the canoers, "Just keep canoeing, don't pet the beaver, but enjoy the experience." Meanwhile, a beach bystander ran to the camp office and called Hope Buyukmihci, naturalist and author, at Unexpected Wildlife Refuge, three miles away. "Are you missing a beaver...a very friendly one?" The answer was yes. The beaver was Chopper, an orphan Ms. Buyukmihci had raised from infancy, and he was now over a year old and beginning to make it on his own in the wild._ _Minutes later, Hope drove in to Camp Sacy to con Chopper back home. But the next day Chopper was back in Sacy's lake, entertainingcampers with his swimabatics. "Maybe he's building a dam. Maybe he's going to raise a family," said some of his young admirers._ _All of us were excited over these prospects. We told Hope about Chopper's whereabouts. She said he could stay and was happy that Chopper was on his own._ _Every day the staff members kept Hope informed of Chopper's activities. "He may try to climb into your boats," she said, "but he's just playing. He'll dive off immediately. And he might just swim along or wrestle with you if you're in the water!"_ _For the next three days, campers, leaders and staff members observed, petted, fed and just plain enjoyed Chopper. The Girl Scouts also learned about the looks, diet, habits and temperament of a beaver who is accustomed to the world of people._ _During these beaver days, the atmosphere in the camp drastically changed. There was a profound awareness that there really was something alive and friendly out there in the woods and waters._ _One afternoon the camp director decided to take some pictures of Chopper. He found him swimming in a swampy area near the Comanche campsite. An animal enthusiast, the director walked right into the swamp, click-clicked the camera, and was then promptly but playfully grabbed around the leg by Chopper. The following day was hectic, with camp closing and campers leaving. It wasn't until late Saturday afternoon that a few remaining staff members decided to walk down to the lake to say goodbye to Chopper._ _As we approached the lakefront, there were other last-minute beaver admirers standing on the dock. They screamed—"Come quickly!!!" We ran, only to find Chopper lying on the edge of the dock, dead._ _These people, many of whom were young campers, had just witnessed an unidentified fisherman maliciously beat Chopper to death._ _It seemed Chopper was disturbing this trespassing man's sport. The fisherman, who was rowing away, shouted to us, "That thing tried to climb into my boat, so I hit it with my fishing pole. Then it started to hiss at me. I had to hit it with my oar."_ _We wrapped Chopper up in a beach towel._ _We cried..._ ### **My Dream** I have a dream. I see humankind understanding that the spirit that sings in our hearts sings as well in the hearts of the other animals. I see us realizing that there are many kinds of intelligence, many kinds of souls, many kinds of suffering and striving. I see us knowing that all creatures are endowed with the same will to live that we possess. I see us respecting theirs, as we would like our own to be respected were we in the less powerful position and they dominant upon the earth. I see us grateful for these extraordinary companions. I see our lives rich with animals. I see us with many animal friends. I see our cities sprinkled with wild places, shorelines, parks, ravines, and creek-canyons, where wild creatures can live. I see all life-forms working together in harmony, cultivating the full potential of the planet. I see us appreciating the different needs, different kinds of intelligence, and different responsibilities of the various animals. I see us sensing the unique ways in which they feel, they think, they suffer, and they love. I see us learning to treat with respect those who are, in the greater scheme of things, but our younger brothers and sisters. I see us realizing they, too, are expressions, in their individual ways, of the universal life force. I see us acting from the knowledge that it is the same GodForce that gives us all breath. I see us realizing that all God's critters have a place in the choir. 2. **BRAVE NEW CHICKEN** _Teaching a child not to step on a caterpillar is as valuable to the child as it is to the caterpillar._ —BRADLEY MILLER _The greatness of a nation can be judged by the way its animals are treated._ —GANDHI Like most people, I would like to minimize the unnecessary suffering in the world. I want to eliminate needless violence and pain, and I give my support, wherever I can, to a positive approach to this goal. But like most people I never gave much of a thought to the impact my way of eating had on the world. Sure, I knew animals were killed for meat, but isn't that the way of nature? Isn't that the way of life's food chains? But I've learned that the animals used for food in the United States today are not just killed; something else happens to them. And finding out about it has changed me forever. The more I've learned, the more I've felt that if people knew what really goes on they would make major changes in their food choices. Major changes that would go a very long way, not only toward improving their own health, but toward reducing the suffering in the world as well. Let's start with chickens. In order to understand what happens to these animals, it helps to have a feeling for what kinds of beings they are. Unfortunately, most of us have rather stereotyped visions of them. The word "chicken" is often used as a synonym for "coward." But that is a human moniker. Chickens, while high-strung and quick to startle, are anything but gutless, timid creatures. Roosters are renowned for their pride and ferocity and the adamant assertion of their power. Many cultures have exploited this fact in the so-called sport of cock fighting. And throughout the world a wide variety of cultures have acknowledged the potent spirit of the cock by using his name as a synonym for the male penis. In languages all over the world the word for the male chicken is also used to signify human male sexual potency. Female hens are likewise not the craven creatures we've been conditioned to think they are. They can be absolutely fierce in defending their little ones, even against terrible odds and much larger predatory birds. A scientist who studied chickens for years, E. L. Watson, watched a mother hen defend her little chicks against the awesome attack of the dreaded raven. _I have known one little old hen who reared chicks on the far western coast of Scotland near cliffs where ravens built their nests. On ordinary occasions, ravens are the terror of domesticated fowls, that fly to shelter at the first sight of the black wings. They dare not face beaks so much stronger than their own. (But) this little mother of a brood of ten would stand her ground with her hackles up, eyes glaring defiance. Such was her courage that she lost but one of her brood when two ravens came against her._ Chickens are not the fearful creatures we have been conditioned to think. And the generally agreed-upon idea that they are stupid is equally ungrounded in fact. Now, I'm not saying that chickens are the most brilliant of animals. But I do know that our understanding of what constitutes intelligence is utterly relative. If an aborigine drafted an I.Q. test, for example, all of Western civilization would probably flunk. We have a very convenient and self-serving way of defining intelligence. If an animal does something, we call it instinct. If we do the same thing for the same reason, we call it intelligence. Personally, I wouldn't be too quick to try to define the intelligence of chickens. I'd be afraid of judging them by standards that are irrelevant to them. For the more I've learned about the kinds of creatures they are and what they have been known to do, the more I've been impressed by their unique kind of intelligence. One naturalist gave a chicken hen 21 guinea fowl eggs he had found, just to see what would happen. These small, hard-shelled eggs are a far cry from a chicken's eggs. But the hen took the task to heart and somehow managed to tend to all 21 of the eggs without a sign of protest. As a product of our conditioned conventional notions about chickens, I originally thought she did this simply because she was too stupid to notice they weren't her own eggs. When the chicks hatched, she didn't seem at all perturbed by the fact that they weren't chickens. Their small partridge-like appearance and unfamiliar ways evidently presented no problem to her. Again, I thought she was simply too stupid to notice they were not chickens. But I was wrong. She was far more tuned in to reality than I knew. After a few days of brooding the little guinea fowl, she took them away out into the cover of some bushes. Instead of asking them to feed on the ordinary mash that was given the chickens, she scratched in some ants' nests for the white pupae. Chickens don't eat such food, but guinea fowl do! The little ones took to it with instinctive relish. How could she have known? What form of intelligence was she displaying? Was she perhaps sufficiently tuned in to have received some sort of message from their collective psyche? That's more than man can do! On another occasion, a naturalist gave a chicken hen some duck eggs. She tended them and hatched them as if they were her own, yet wasn't fazed at all when ducklings emerged from her labors instead of chicks. Utterly undaunted by the situation, she proceeded to do something neither she nor any other chicken in the area had ever done before. She walked up on a plank bridging a stream. Then, clucking, she invited the little ducklings into the water. It is a mystery to me how these mother hens knew what to do for the babies they hatched who were of another species. But somehow they did. It appears that when we speak of being taken under someone's wing we are correctly referring to a remarkably caring and sensitive kind of nurturing. Living as divorced from nature as most of us unfortunately do, we may not have much personal experience with chickens anymore and so may not know what wonderful mothers they are. But throughout recorded history the hen has been a supreme symbol of the best kind of mothering. In fact, the Romans thought so much of the maternal qualities of the hen that they frequently used the phrase "son-of-a-hen" to mean a fortunate and well-cared-for man. **Naked amid the Ruins** Although the experiences and memories most of us have of chickens are colored by ill-founded biases, it is hard to forget the feeling of seeing freshly hatched baby chicks, their little yellow heads pushing out from under their mother hen's feathers, their tiny yellow beaks just beginning to peck about. To many of us, freshly hatched baby chicks are the very picture of innocence and adorability. Yet perhaps they also speak of something deeper, something inspirational. In pecking their way out of the egg, they can seem as well to symbolize our ongoing need to outgrow old limitations, our deep need to push against and expand beyond boundaries that have served a needed purpose but that now must be left behind. In this, the little ones stand for the very opposite of the gutlessness we have been conditioned to think of as "chicken." They stand for courage. They peck their way out, not knowing what will await them. And when they emerge, they stand naked and new amidst the ruins of a past to which they can never return, having undertaken an irreversible journey into the unknown, simply because it is their destiny to do so. Somehow these little chicks remind me of the bravery of the human spirit and, as well, of our situation as a species. Are we not also driven by an evolutionary imperative, by the call of our own growth and potential for expansion? Are we not, as a race, standing now amidst the slime and eggshells of our primeval past, not knowing what will become of us yet already dreaming of the stars? One thing's for sure. Chickens are far more sensitive than most of us give them credit for. A study at Virginia Polytechnic Institute found that chickens flourished when treated with affection. Researchers there spoke and sang gently to a group of baby chicks. As a result the chickens were friendlier and put on more weight for the amount of feed consumed than did chickens who were ignored. The well-treated birds were also more resistant to infection than the other chickens. **Welcome to Chicken Heaven** The raising of chickens in the United States today is not, however, a process that overflows with compassion for these animals. Nor is it anything like the barnyard operation that comes to most of our minds when we imagine the lives of chickens. Fundamental changes have taken place in the past 30 years. Formerly, chickens were free-range birds, scratching and rooting around in the soil for grubs, earthworms, grass, and larvae. They knew the sun and the wind and the stars, and the rooster crowing at the break of day was only one of many signs that showed they were deeply attuned to the natural cycles of light and dark. But today this has all changed. The raising of chickens in the United States has become completely industrialized. We no longer live in the day of the barnyard chicken. We live now, I'm sorry to say, in the day of the assembly-line chicken. There is a story behind today's poultry and eggs that we would never know from the clean little packages for sale in brightly lit modern supermarkets. It all looks so neat, comfortable, and dependable, so carefully wrapped and labeled. As I stand in a tastefully decorated supermarket, serenaded by piped-in music, looking at egg cartons and poultry packages with happy drawings of smiling chickens, I find it hard indeed to imagine anything could be amiss. Every attempt is made to assure us that the chickens of today couldn't be happier or better cared for, and that no expense is spared in bringing us quality eggs and produce. Advertisements for Perdue, Inc., one of the nation's largest producers of chickens for meat, are typical. In them, the company president, Frank Perdue, tells us that his chickens live in "a house that's just chicken heaven." But it turns out there's not a great deal of truth in describing contemporary chicken accommodations as "chicken heaven." To begin with, today's chicken farms are not really farms anymore, but should more accurately be called chicken factories. Factories, because the chickens live their whole lives inside buildings entirely devoid of natural light. The day of the barnyard is long gone. There are no barns and no yards in today's mechanized world of poultry production, only assembly lines, conveyor belts, and fluorescent lights. Factories, because these proud and sensitive creatures are treated strictly as merchandise, with utter contempt for their spirits, with not a trace of feeling or compassion for the fact that they are living, breathing animals. Factories, because the chickens are systematically deprived of every conceivable expression of their natural urges. Today's chicken factories are not farming as most of us conceive it. They are living expressions of the attitude that animals are things, raw materials to be consumed however we might wish. I wish I were exaggerating. I wish I were describing isolated cases of negligent management. But I'm not. I'm describing the standard operating procedures of the egg and poultry industries today. I'm describing the operations that produce 98 percent of our eggs and poultry. I'm describing techniques and practices that are outlined and discussed every day of the week in trade journals such as _Poultry World, Poultry Tribune, Poultry Digest_ , _Farmer and Stockbreeder,_ and _Farm Journal._ In the assembly-line world of today's chicken factories, chickens aren't called chickens anymore. If they have been bred for their flesh, they are called broilers. If they have been bred for their eggs, they are called layers. Now, not calling animals by their animal names, but giving them new names according to their food value to humans, may not seem like a big deal in itself, but it is part of a process that deeply conditions us all into forgetting the spirit of the animals as living beings with their own dignity. In fact, the industry makes a deliberate point of not seeing the animals as animals. _The modern layer is, after all, only a very efficient converting machine, changing the raw material—feedstuffs—into the finished product—the egg—less, of course, maintenance requirements._ _—F ARMER AND STOCKBREEDER_ **Happy Birthday Factory Style** Male chicks, of course, have little use in the manufacture of eggs. So what do you think happens to the males? How are the little fellows greeted when, having pecked their way out of their shells, expecting to be met by the warmth of a waiting mother hen, they look around and seek to begin their lives on earth? _They are, literally, thrown away. We watched at one hatchery as "chickenpullers" weeded males from each tray and dropped them into heavy-duty plastic bags. Our guide explained: "We put them in a bag and let them suffocate."_ It's not a picture to bring joy to a mother's heart, but over half a million little baby chicks are "disposed of" in this fashion every day of the year in the United States. In the seconds it takes you to read this paragraph, over 2,000 newborn male chicks will be thrown by human hands into garbage bags to smother among their brothers, without the slightest acknowledgment that they are alive. And they are, perhaps, the lucky ones. Because for those chicks allowed to live, the "life" that follows is truly a nightmare. In today's modern factories, chickens, exquisitely sensitive to the earth's natural rhythms of light and dark, never see or feel the light of the sun. Broiler chicks arrive at the producers via conveyor belt, in batches of tens of thousands. Fresh from the incubators and mechanized hatcheries, only a few hours old, the fluffy yellow babies peep constantly in frail little voices for their missing mothers. But they will never know the sound of their mother's voice, nor the warmth of her body, nor the comfort of her protection. There will be no scratching in the dust for tasty bugs, no strutting and preening, no crowing to announce the dawn. These little chicks come equipped with a God-given life expectancy of 15 to 20 years. But under the conditions of modern factory farming, modern broilers might make it to the ripe old age of two months. In comparison, the layers are veritable Methuselahs—the longest lived among them might possibly live as long as two years. The more I've learned about these factories, the more ironic it has seemed to call them chicken heavens. Consisting of windowless warehouses, with tiers of cages stacked on top of one another from floor to ceiling, like shipping crates, the environment has been systematically designed to maximize the profits of the agribusiness corporations that own the sheds and the birds. It has not been designed with any concern whatever for the chickens' natural urges, minimum comfort, or even health. Inside the windowless warehouse, every aspect of the birds' environment is totally controlled, in order to make them grow as fast as possible or produce as many eggs as possible, at the least possible cost to the company that owns the operation. Incidentally, the companies that own our nation's chicken factories are not generally agricultural enterprises, as you might have imagined. As Peter Singer has shown in his excellent _Animal Liberation,_ they are companies like Textron Inc., a manufacturer of pencils and helicopters. These companies go into the business simply because it looks like a profitable venture. Accordingly, they apply to chickens the business practices that work with pencils and helicopters, thus treating these breathing, passionate animals with the same consideration they use for pencils. **The Social Life of Hens** The renowned English ethologist Desmond Morris, author of _The Naked Ape,_ has written about today's methods of raising hens in cages (also called batteries). _Anyone who has studied the social life of birds carefully will know that theirs is a subtle and complex world, where food and water are only a small part of their behavioral needs. The brain of each bird is programmed with a complicated set of drives and responses which set it on the path to a life full of special territorial, nesting, roosting, grooming, parental, aggressive and sexual activities, in addition to the feeding behavior. All of these activities are totally denied the battery hens._ Chickens are by nature highly social animals. In any kind of natural setting, be it a farmyard or the wild, they develop a social hierarchy, often known as a pecking order. Every bird yields, at the food trough and elsewhere, to those above it in rank and takes precedence over those below. The social order is extremely important to these birds. According to studies published in _The New Scientist,_ chickens can maintain a stable pecking order, with each bird knowing all the others individually and aware of its place among them, in flocks with up to 90 chickens. Beyond 90 birds, however, things can get out of hand. Of course, in any kind of natural setting, flocks would never get nearly that large. But in today's "chicken heavens," flocks tend to be larger than the 90-bird limit. How much larger? _Poultry Digest_ reports that the flock size in a typical egg factory is 80,000 birds per warehouse **Just Like a Mother Hen** In such a situation the birds are completely unable to satisfy one of the most basic and intense priorities of their nature, which is to develop a sense of social order and their place within it. The results aren't very pretty. Unable to establish any kind of social identity for themselves, the cooped-up animals fight constantly with one another. They are driven berserk by the lack of space and the complete frustration of their primal need for a social order. In their frustration they peck viciously at one another's feathers, frequently try to kill one another, and even try to eat one another alive. The industry takes note of these developments, but only in terms of their effect on profits. _Feather-pecking and cannibalism easily become serious vices among birds kept under intensive conditions. They mean lower productivity and lost profits._ _—T HE FARMING EXPRESS_ Any behavior among chickens that threatens profits is known in the trade as a vice, a term that truly gives me pause. Where is the virtue in keeping birds in these conditions? Since the animals insist on behaving like the proud and sensitive creatures they are, and trying even under these bizarre conditions to express their natural urges, the experts who manage today's factory farms have to respond. They have to do something, because if very many of the birds kill one another, money is lost, and that is the one thing they can't let happen. They know that the birds' berserk behavior arises out of the unnatural ways in which the birds are kept. So what do the factory managers do? Make the conditions even more unnatural, of course. The preferred method in the industry today is to cut off part of the chickens' beaks, a process known as de-beaking. This does nothing to reduce the conditions that drive the chickens so mad that they attack one another viciously. But it renders them incapable of doing much harm to company profits. The people who run today's poultry factories are not concerned that the process of cutting off part of the chickens' beaks requires cutting through highly sensitive soft tissue, similar to the tender sensitive flesh under human fingernails, and causes the animals severe pain. Nor do they mind the fact that they are crippling the animals and cutting off the animals' most important member. Today's poultry producers are highly satisfied with de-beaking. Employed almost universally in the industry today, this practice helps the producers to keep the chickens alive under the stressful, inhumane, and overcrowded conditions that are the cause of the animals' unnatural aggression and cannibalism in the first place. Even from a strictly dollars-and-cents viewpoint, however, there are a few drawbacks to the procedure. As one farm publication noted: _Sometimes the irregular growth of beaks on a de-beaked bird makes it difficult or impossible to drink where a normal bird would have no trouble._ The factory experts are not pleased with the tendency of ungrateful young de-beaked birds either to die of thirst because they are unable to drink from nipple-type watering devices or else to starve to death within inches of their food supply because they can't manage to eat. Nor are they happy with the birds who survive but can't gain weight according to schedule because they have trouble eating. This is not something they want to see, because chicken flesh is sold by the pound. Not ones to be defeated by the deaths and disabilities of de-beaked birds, however, today's producers have sought to counter such losses and increase profits through advertising. They simply tell the public that their chickens couldn't be happier. One huge broiler producer, Paramount Chickens, has aired TV commercials in which a smiling Pearl Bailey (who probably doesn't know the truth any more than most of us) reassures us that Paramount looks after their chickens "just like a mother hen." This is a remarkable statement. How many mother hens have been known to cut the beaks off their babies and force them to live under conditions in which they cannot establish a social identity and so are driven berserk? **Enlightened?** You have probably heard the magnificent trumpeting of roosters at daybreak, the passionate, full-throated announcement that dawn has come. The sound with which they welcome the day testifies, not only to their proud and passionate spirits, but also to how sensitive chickens are to light. This is a fact that modern poultry men know and do not hesitate to exploit. In the windowless warehouses we are asked to believe are chicken heavens, the artificial lighting is manipulated in the most unnatural ways to maximize profits and minimize costs. Broilers are often subjected to bright light 24 hours a day for the first two weeks. Then the lights may be dimmed slightly and go off and on every two hours. At about six weeks of age, the animals have gone so completely crazy from all this that the lights must be turned off completely in an attempt to calm them down. But even then the absence of any outlet whatsoever for the birds' natural energies and drives leads to a great deal of fighting, with the de-beaked birds pecking painfully at one another in the dark, often managing despite the mutilation of their beaks to kill one another. It's at times like this that farm managers will sometimes reveal the depth of their compassion for the animals in their care. _It's a damn shame when they kill each other. It means we wasted all the feed that went into the damn thing._ —HERBERT REED, POULTRY PRODUCER The lighting conditions for young layer hens (called pullets) are a little different from those provided for broilers, though not exactly what you'd call natural. These youngsters are kept in "grow-out" buildings that are usually kept completely dark except at feeding times. Then, when the young hens reach the age at which they can begin to lay eggs, everything suddenly changes. Having lived their entire lives in complete darkness, except at feeding times, the hens now find themselves subjected to harsh and continuous light. _At one farm, a period of 23 hours lighting a day has been tested._ **Agribusiness Lays an Egg** The folks who design what the industry tells us are chicken heavens are real virtuosos when it comes to manipulating the environment of the animals for maximum profit. When a layer hen's production begins to slacken, the producers do not just sit back and let her output wane. Not when they have found it possible to bolster her egg production by a procedure known in the trade as force-moulting. The already panicked and exhausted hen will suddenly find herself plunged into complete darkness. The artificial lighting, which heretofore had been on for upward of 17 hours a day, is now completely cut off, and at the same time her food and water are removed. After two days of starving without even water in the dark, the bird, still without food or light, is allowed water. Eventually lighting and food will be returned to what passes for normal. Those hens who survive this ingenious procedure will have been shocked into physiological processes associated, under natural conditions, with the seasonal loss of plumage and growth of fresh feathers. After the forced moulting, those hens who survive the ordeal may be sufficiently productive to be kept around for another two months. Then they join those who did not survive the procedure in the first place in our chicken soup. Hopefully, the hen will have learned something from the days without food or water, because the farm managers certainly have. During her last 30 hours before slaughter she will again receive no food. A headline in _Poultry Tribune_ reminded poultry producers: "Take Feed Away from Spent Hens." The trade journal brilliantly calculated that food given to hens during the last 30 hours of their lives doesn't have time to turn into flesh. It stays in the digestive system and so, counsel the experts, is nothing but a waste of feed. **The Panic Button** Despite being treated consistently as machinery in today's chicken factories, the chickens still stubbornly refuse to settle down and devote themselves single-mindedly to producing as many eggs as possible and growing as fat as they can, in the shortest possible length of time. Instead, they insist on thinking of themselves as animals, with drives and needs. But today's chickens are allowed no expression of their natural urges. They cannot walk around, scratch the ground, build a nest, or even stretch their wings. Every instinct is frustrated. The bizarre lighting manipulations allow these light-sensitive creatures no vestige of a natural sleep cycle. They cannot establish a pecking order, or any sense of social identity. They cannot keep out of one another's way, and weaker birds have no escape from the stronger ones, already maddened by the grotesque conditions in which they live. The result is that these passionate creatures live in a state of perpetual panic. They fly into an uproar at the slightest disturbance and show every sign of having been driven completely out of their minds. One naturalist noted: _The battery chickens I have observed seem to lose their minds about the time they would normally be weaned by their mothers and off in the weeds chasing grasshoppers on their own account. Yes, literally, the battery becomes a gallinaceous madhouse._ Another reporter states: _The birds in the laying house are hysterical... Birds squawk, cackle and cluck as they scramble over one another for a peck at the automatically controlled grain trough or a drink of water. This is how the hens spend their short life of ceaseless production._ Another account, this one from a scientist who has spent his whole life observing animal behavior, tells us that today's chickens are prone to stampedes. _With no apparent cause, a wave of hysteria sweeps over the whole battery; wild, unnatural chirps, jumbled screams, and a fluttering as if every feather on every chicken had become possessed and frantic._ In their panic, the birds will sometimes pile on top of one another and some will smother to death. Poultry producers are not by and large what you would call sentimental types, but since smothered birds represent a waste of feed, this is the type of thing that will definitely spur them into action. Not to be outsmarted, they have found the piling problem can be decreased by crowding the chickens so tightly into wire cages they can hardly move. This way, when they panic, they can't pile on top of one another as readily. The cages produce a few problems of their own, however, that make the calling of them chicken heavens even more deceitful: the caged hens still try to behave as if they were designed by Nature to live on the earth, instead of in wire cages. For instance, their toenails continue to grow. With no solid ground to wear the nails down, they become very long and can get permanently entangled in the wire. The ex-president of a national poultry organization wrote in the _Poultry Tribune_ about the many times when, on removing a batch of hens from a cage, _we have discovered chickens literally grown fast to the cage. It seems the chickens' toes got caught in the wire mesh in some manner and would not loosen. So, in time, the flesh of the toes grew completely around the wire._ Needless to say, those birds who get stuck in the back of the cage, where they cannot reach food or water, starve to death. Once again, however, the minds that created this whole situation have come up with an ingenious solution to prevent such a distressing waste of feed. The idea is simply to cut off the toes of the little chicks when they are a day or two of age. In most cages, there is at least one poor bird who has undergone these grotesque conditions and has entirely lost the will to live. These sad creatures no longer resist being shoved aside, pushed underfoot, and trampled by the other birds. They are probably the birds who, in a natural flock, would be low on the pecking order. Although they would defer to the others and not have much status, they would nevertheless play a needed part in the life of the flock. They would mate, have chicks to care for, and live out their lives. In the cages, however, life is not very kind to the little guy. The results are pathetic. _These birds can do nothing but huddle in a corner of the cage, usually near the bottom of the sloping floor, where their fellow inmates trample over them as they try to get to the food or water trough._ **Space for Rent** I have met quite a few people who seem to think that chickens are vegetables. When someone says he or she is a vegetarian, these people reply with something like, "Yes, but you do eat chicken, don't you?" I feel reasonably confident that most of today's poultry producers know their stock well enough to realize that chickens aren't vegetables. But they seem unable to grasp the fact that they are animals, and as such have profound territorial needs. At the Hainsworth Farm in Mt. Morris, New York, naturalist Roy Bedichek found four and even five hens squeezed into cages 12 inches by 12 inches. Under these conditions, the birds are unable to lift a single wing. In fact, they are squeezed together so tightly that they have a great deal of difficulty even turning around in place. This is not seen by the factory managers as a bad thing, though. With their bodies in forced contact at all times on all sides with other chickens, they absorb heat from their fellow inmates, so this cuts down on heating costs. The Hainsworth farm is an extreme example. But the industry norm isn't much better. A surprisingly large percentage of the eggs eaten in Los Angeles come from the 345-acre "Egg City" in Moorpark, California. Here, some 2,200,000 eggs are laid daily by three million hens. The hens are housed five to each 16-by-18 cage. To get a chicken's-eye view of these conditions, picture yourself standing in a crowded elevator. The elevator is so crowded, in fact, that your body is in contact on all sides with other bodies. Even to turn around in place is difficult. And one more thing to keep in mind—this is your life. It is not just a temporary bother, until you get to your floor. This is permanent. Your only release will be at the hands of the executioner. By the way, in your picture of the elevator, you may have imagined the other people trapped with you as doing the very best they can to hold still and not make things difficult for you. But what if all the others do not have the ability to understand what is happening? What if they react to the terror of it all with raw instinct, without even a trace of a civilized veneer? What if, like you, they have powerful territorial needs, and the utter frustration of the situation has driven them literally insane, prone to erupt into violence with or without provocation? Now imagine further that the floor of the elevator is slanted sharply, so gravity tends to push you all in one direction. The ceiling is so short that you and the others can only stand upright toward one side, and the floor is made of a wire mesh that is terribly uncomfortable to everyone's feet. And to complete this approximation of the living conditions in today's factory farms, what if some of the others trapped with you in the elevator have, in their madness, become cannibalistic? These are the conditions that the industry tells us are a chicken heaven. This is the actual living situation of the chickens whose flesh and eggs Americans eat. **Breeding a "Better" Chicken** Chicken breeders have been hard at work developing a "better" chicken, which to their way of thinking is the heaviest possible one. (Remember, profit is per pound.) The result is a bird whose skeleton becomes, every year, less able to support his increasingly massive weight. The fleshy bodies of broilers today grow so fast that their bones and joints can't keep pace. The trade journal _Broiler Industry_ reports that the chickens raised for meat today can hardly stand under their weight, so they spend most of their time huddling "down on their haunches." _Skeletal disorders are common. Many of these animals crouch or hobble about in pain on flawed feet and legs._ Problems like these are not considered particularly noteworthy by the industry that tells us they take care of their chickens "just like a mother hen," because lameness affects only the living animal, not the price to be had for his flesh. Animals can be sold for meat whether or not they are crippled. The same breeders who brought us these grossly top-heavy birds are hard at work to accomplish other grotesque feats of genetic engineering. You may have thought, as I did, that God pretty much knew what He was doing when He designed animals. But the folks at the Animal Research Institute of Agriculture, Canada, have a better idea. The director of the institute, R. S. Gowe, enlightened me on the subject when he spoke at a conference in Ottawa in December 1978 on "Livestock Intensive Methods of Production." Said Gowe, proudly: _At the Animal Research Institute, we are trying to breed animals without legs, and chickens without feathers._ I must admit it took me a while to comprehend why anyone would want to breed a chicken without feathers. But I finally came to understand why at least six universities in the United States and Canada are presently trying to do so. If only chickens didn't have feathers, then the folks who care for them "just like a mother hen" would be spared the bother of plucking them out. **Flipped Out** There are many other ways, besides having feathers, that chickens make themselves difficult to their caretakers. _Poultry Digest_ describes the growing problem of "flip-over syndrome." This condition _is characterized by birds jumping into the air, sometimes emitting a loud squawk, and then falling over dead._ Postmortem exams show the birds' hearts are full of blood clots, but it is not known whether this is a result or a cause of their deaths. The problem of "flip-over syndrome" has the experts stymied. They don't have any idea what makes the birds suddenly jump into the air and die. I don't know, either, but I think it is probably safe to say that the birds are not jumping into the air because they cannot restrain a spontaneous upsurge of joy and delight. **The Fine Cuisine of Chicken Heaven** What do you think the lucky residents of today's chicken heavens dine on before we dine on them? Researchers who wrote an article titled "Poultry Production" in _Scientific American_ investigated contemporary chicken cuisine, and they were seriously concerned with its quality: _The modern fowl thrives on a diet almost totally foreign to any food it ever found in nature. Its feed is a product of the laboratory._ A poultry man summarized the matter this way: _Virtually all chickens raised in the United States today are fed a diet laced with antibiotics from their first day to their last. Without antibiotics, the industry could not maintain the intensive farming practices. An awful lot of them die anyway, before we can get our profit out of them. Without antibiotics, why, we'd be back to the backward practices of yesteryear._ Heaven forbid! Why, back then the chickens were deprived of a steady supply of sulfa drugs, hormones, antibiotics, and nitrofurans. And what on earth did the poor birds ever do without the arsenicals? Over 90 percent of today's chickens are fed arsenic compounds. I had assumed that the diet fed to chickens would be one chosen for its ability to keep the animals healthy. But such, I have found, is not the case. Broilers fetch a price according to their weight, not according to their health, so their diet is selected purely for its ability to maximize their weight as cheaply as possible. Similarly, the diet fed to layers is selected strictly for its ability to stimulate egg production at the lowest possible cost. As a result, these are not the healthiest animals you could find. According to _Poultry Digest_ , an increasing number of today's chickens suffer from "caged layer fatigue." These birds undergo the withdrawal of minerals from their bones and muscles and eventually are unable to stand. Caged layer fatigue is actually only one of many health problems that flourish among modern chickens, whose diet is not designed with their health in mind. In the classic work on contemporary animal agriculture _Animal Factories,_ Peter Singer and Jim Mason report: _Vitamin deficiencies common in poultry factories... result in a variety of conditions, including retarded growth, eye damage, blindness, lethargy, kidney damage, disturbed sexual development, bone and muscle weakness, brain damage, paralysis, internal bleeding, anemia, and deformed beaks and joints. Dietary deficiencies and other factory conditions can cause a variety of bodily deformities. In poultry, fragile bones, slipped tendons, twisted lower legs, and swollen joints are among the symptoms of mineral deficient diets... Some poultry diseases can leave birds with malformed backbones, twisted necks, and inflamed joints._ These poor animals are riddled with disease. In fact, due to the danger of humans' contracting diseases from chickens, the Bureau of Labor has listed the poultry-processing industry as one of the most hazardous of all occupations. Many of the health problems that occur regularly to these sad creatures were unknown only a few years ago. It is common today for caged birds to lose their feathers. It isn't known whether this is from rubbing constantly against the wire, from feather-pecking by other birds, or because of the totally unnatural diet and lack of sunlight. But whatever the cause, the result is that without their feathers the chickens' skin begins to rub directly against the wire. When I first saw these birds I was startled by the sight and didn't even recognize they were chickens. Their skin is raw and sore and bright red. They look more like a walking wound than a bird. It is hard to underestimate the health of today's chickens. Driven to a state of hysteria, their raw skin rubbing constantly against the wire cages in which they are packed like living sardines, a staggering percentage of these animals contract cancer. A government report found that over 90 percent of the chickens from most of the flocks in the country are infected with chicken cancer (leukosis) You and I may wonder at the level of health in food produced by a system that so totally disregards the health and well-being of its animals. But today's poultry producers are rarely hampered by such considerations. They are a dedicated group, with a steadfast single-mindedness of purpose. Only their purpose is not, as you might have thought, to produce healthy food. As Fred C. Haley, president of a 225,000-hen Georgia poultry firm put it: _The object of producing eggs is to make money. When we forget this objective, we have forgotten what it is all about._ The money Mr. Haley is talking about is not made by the farmer who spends his day with the animals. It is made by agribusiness oligopolies. The actual chicken farmer amounts to a mere hired hand who virtually works for the huge "integrated chicken processors" and "amalgamated poultry producers." He is the one in daily contact with the birds; he is the one who sees and lives with the animals; and he may very well have feelings about what is being done to them. But if he protests, well, he can always be replaced by someone better suited to the job. He is not the one who has devised the production strategies that prevail in the industry today, and though he may have to implement them, he is not the one who profits by them. A study by the director of the Agribusiness Accountability Project, Jim Hightower, showed that in 1974, when chicken prices were running 80 to 90 cents a pound in the supermarket, the chicken farmers themselves were getting just two cents a pound. Of course, the corporate managers who are making the money love to portray themselves in the public eye as old-fashioned farmers. In one case, a number of the top executives of one of the international cartels that control the nation's poultry production testified before Congress dressed in overalls. **An Assembly-Line Chicken in Every Pot** We are a nation with an assembly-line chicken in every pot. We do not know that we eat the bodies and eggs of tortured creatures. We do not know they have been inoculated, dosed with hormones and antibiotics, and injected with dyes so that their meat and yolks will appear to be a "healthy-looking" yellow. How far out of touch we have become, not only with animals but with our own taste buds, to be susceptible to being so deceived. Some people are beginning to suspect, however, that today's poultry products aren't what they should be. The comedian George Burns spoke of the first time he ate scrambled eggs without ketchup. _I never knew they tasted like that. They tasted like the chicken wasn't getting paid._ Needless to say, with money at stake, the industry isn't taking the matter of tasteless chicken lying down. The trade journal _Broiler Industry_ has come up with an idea they think will remedy the situation. It is an idea that exemplifies their whole approach to food production. _We've been accused of selling a chicken with less flavor than the "old-time" chicken... Attempts are being made at overcoming the flavor problem by injection._ That should take care of everything! In another issue, _Broiler Industry_ saliently proposes: _It should be possible to uncover a material, or materials, that could impart that "old-fashioned flavor" to chickens._ And if that doesn't do the trick, don't think for a moment that the agribusiness experts are going to admit defeat. In spite of the universal use of ever more chemicals and drugs in egg production today, one industry leader tersely advises a marketing strategy designed to take care of the problem once and for all. His suggestion? _Slant egg carton copy along this line: "Eggs are a health food. A natural human food. No additives, no preservatives."_ I find the latest developments in poultry production truly disturbing. The huge multinational conglomerates, and those who must compete with them or be forced out of business, in their utter disregard for the suffering of innocent animals, have lost touch with something very basic. Today's egg and poultry consumers know nothing of this. We have been deliberately kept in the dark about what modern poultry production has become and have no idea of the relentless and systematic misery in which the chickens live. Every day people eat the flesh and eggs of these poor creatures, utterly unaware of what they have suffered. What are the consequences of eating the products of such a system? Could it be that when we consume the flesh and eggs of these poor animals, something of the sickness, misery, and terror of their lives enters us? Could it be that when we take their flesh or eggs into our bodies, we take in as well something of the kind of life they have been forced to endure? Instinctively, I can't help but believe this is so. **In Search of the Natural Bird** You may wonder whether you'd be better off eating turkey. Sorry, but the methods applied to the factory production of poultry and eggs are also applied today to other birds, such as turkeys, geese, and ducks. These birds are treated with equal disdain for their natural urges and needs, and equal fixation on using them for profit. Turkeys are de-beaked, stuffed into wire cages, and fed the same sort of unnatural diet as chickens, complete with chemicals, drugs, and antibiotics. There are, however, alternatives. One is to consume only free-range, organic, or natural poultry products. Natural food stores often carry items so labeled, but you have to be awfully careful. Words like "organic" and "natural" and "free range" mean different things to different people, and much money has been made by people lying about such terms. The USDA has regulations governing the use of the word "natural," but these regulations are so loose that virtually anything can be so labeled. There are no restrictions at all on the use of antibiotics or on the housing conditions the animals must endure. Some health food store owners are more scrupulous than others, but even the best of them may not know all the facts. Many in California carry "Happy Hen Ranch Fresh Eggs," which come in a carton with a picture of a cheerful hen in the midst of luxurious fields. However, I've seen the socalled happy hens of the Happy Hen Ranch (near San Jose, California), and they do not look very happy to me. They do not live in the spacious fields depicted on the egg carton. They are kept in cages. In 1986, _East-West_ published a conscientious report titled "In Search of the Natural Chicken." Their research found that almost all the poultry products currently sold in the United States as "natural" or "organic" come, unfortunately, from chickens whose living conditions are hardly better than the industry norm. Summarizing the investigation, the author noted, none too encouragingly: _Some eggs sold as "fertile, laid by free-range hens" are produced by hens that actually are kept in barns in a space no greater than those kept in cages...(With only two exceptions) no sellers of natural poultry products that we contacted suggested that their chickens enjoyed anything resembling a free-range existence._ The best bet, if you really want to eat poultry products, is to raise them yourself or buy them from someone you know personally. A distant second would be to buy them from a natural food store, but you had better be willing to make a nuisance of yourself with lots of uncomfortable questions. The people who run the store should know the details of how the chickens whose eggs and flesh they sell have been raised and fed. If they don't know, or if their answers are vague or evasive, then, unfortunately, the truth is likely not what you would wish it to be. The Farm Animals Concern Trust (FACT) has established humane standards for keeping layer hens without cages. Farms complying with these standards are given use of the FACT trademark—NEST EGGS®. Though this is not yet widely available, if you buy eggs bearing this trademark, you can be sure you are not partaking of, or contributing to, the conditions described in this chapter. An alternative many informed people are taking is to stop eating poultry products altogether. If you wonder whether you could satisfy your protein and other nutritional needs if you did not partake of the products of chicken factories, the answer, as chapters 6 through will show, is an emphatic yes. The most rigorous scientific research has determined that these foods are far from the ultimate nutritional cornerstones the industry would like us to believe. In fact, they contribute mightily to the ravages of heart disease, cancer, strokes, and many other serious diseases. I have too much respect for the human journey to take it upon myself to decide for you what you should or shouldn't eat, and where you should draw the line. We are each unique. We have different needs, different emotional associations to different foods, and different biochemistry. We have our individual life situations to deal with, and our individual paths to forge. We are each of us responsible for our own choices and for the consequences of our choices. However, the better informed we are, the more intelligently we are able to make food choices that serve our true needs. **Now What?** The poultry producers consider themselves innocent of any wrongdoing. They say they do what they do to bring down the price we pay for our eggs and poultry. To that end, they claim they are simply people committed to a well-defined sense of purpose, which is to raise broilers for the slaughterhouse and layer hens for eggs by the most cost-effective means possible. That this should happen to involve the brutalization of billions of innocent animals is, as far as they are concerned, irrelevant. The agribusiness companies have their eyes firmly set on the bottom line. But they cannot see there is yet a deeper bottom line. Although they cannot see the more far-reaching consequences of their actions, these consequences nonetheless exist. None of us is immune from the repercussions of our actions and choices. As we sow, so shall we reap. _There is a destiny that makes us brothers,_ _None goes his way alone–_ _All that we send into the lives of others_ _Comes back into our own._ —AUTHOR UNKNOWN I don't know what shall be the destinies of those responsible for the animal factories of today. But regardless of the future, it is already sadly true that they live in a heartless world. Treating animals like machines, they are profoundly separated from nature, deeply alienated from kinship with life. They are already in a kind of hell. If we buy and eat the products of this system of food production, are we not colluding with them in creating this hell? _Is that how we want to vote with our lives?_ 3. **THE MOST UNJUSTLY MALIGNED OF ALL ANIMALS** _Whenever people say "we mustn't be sentimental," you can take it they are about to do something cruel. And if they add, "we must be realistic," they mean they are going to make money out of it._ —BRIGID BROPHY _There is a single magic, a single power, a single salvation, and a single happiness, and that is called loving._ —HERMANN HESSE In our human blindness concerning the feelings, intelligence, and sensitivity of animals, there is one in particular about whom we've been most wrong. If it were possible to measure our misunderstanding about our fellow creatures on some giant scale, our ignorance of this particular animal might well be the greatest of all. This is an animal who has been abused and ridiculed by people for centuries but who is actually a friendly, forgiving, intelligent, and good-natured animal when he isn't mistreated. I am talking, you may be surprised to find out, about the pig. **The Hidden Truth about Pigs** To call a man a pig, or a woman a sow, is one of the worst insults in our common speech. This fact testifies not to the nature of pigs but to our beliefs about them and only shows how far out of touch we are with these animals. The commonly held image of pigs as greedy, fat, and filthy creatures, gross beasts who eat anything that isn't fastened down, and who selfishly indulge their basest instincts without a trace of sensitivity, could hardly be further from the truth. Pigs actually have one of the highest measured I.Q.s of all animals, surpassing even the dog's. They are friendly, sociable, fun-loving beings as well. One person very familiar with pigs was naturalist W. H. Hudson. He wrote in his acclaimed _Book of a Naturalist_ : _I have a friendly feeling toward pigs generally, and consider them the most intelligent of beasts, not excepting the elephant and the anthropoid ape... I also like his attitude toward all other creatures, especially man. He is not suspicious, or shrinkingly submissive, like horses, cattle and sheep; not an impudent devil-may-care like the goat; nor hostile like the goose; nor condescending like the cat; nor a flattering parasite like the dog. He views us from a totally different, a sort of democratic standpoint as fellow-citizens and brothers, and takes it for granted, or grunted, that we understand his language, and without servility or insolence he has a natural, pleasant, camerados-all or hail-fellow-well-met air with us._ In the common mind, pigs are disgusting creatures, but in fact the only thing disgusting about pigs is our attitude toward them. They are playful, sensitive, friendly animals who like to roll around and rub on things and consider the earth their home and not something with which to avoid contact. In a state of nature, pigs love to wallow in the mud, just as stags and buffaloes and many other animals do. But pigs don't love mud for its own sake. They use it to cool themselves off and to gain relief from the flies. They enjoy themselves exuberantly because it is their way to enjoy what they do with robust good nature. People who have seen them in mud have accused them of being filthy animals, not understanding their simple love of the earth. However, when living in anything even remotely resembling their natural conditions, pigs are as naturally clean as any other forest creature. If at all possible, they will never soil their own bedding, eating, or living areas. But for many years it was the belief in Europe that the filthier the state in which a pig was kept, the better tasting the pork would be. Hence it became commonplace for pigs to be kept in a fashion that made it impossible for them to stay clean. Even then, though, they would often go to great lengths to maintain as clean a living situation as they could manage. **Hudson's Pig** Did you know that pigs recognize people, remember individuals clearly, and appreciate human contact when it is not hostile? The naturalist W. H. Hudson wrote a beautiful account of a pig: _Not knowing my sentiments, [the pig] looked askance at me and moved away when I first began to visit him. But when he made the discovery that I generally had apples and lumps of sugar in my coat pockets he all at once became excessively friendly and followed me about, and would put his head in my way to be scratched, and licked my hands with his rough tongue to show that he liked me. Every time I visited the cows and horses I had to pause beside the pigpen to open the gate into the field; and invariably the pig would get up and coming toward me salute me with a friendly grunt. And I would pretend not to hear or see, for it made me sick to look at his pen in which he stood belly-deep in the fetid mire; and it made me ashamed to think that so intelligent and good-tempered an animal should be kept in such abominable conditions..._ _One morning as I passed the pen he grunted—spoke, I may say—in such a pleasant friendly way that I had to stop and return his greeting; then, taking an apple from my pocket I placed it in his trough. He turned it over with his snout, then looked up and said something like "Thank you" in a series of gentle grunts. Then he bit off and ate a small piece, then another small bite, and eventually taking what was left in his mouth he finished eating it. After that, he always expected me to stay a minute and speak to him when I went to the field; I knew it from his way of greeting me, and on such occasions I gave him an apple. But he never ate it greedily; he appeared more inclined to talk than to eat, until by degrees I came to understand what he was saying. What he said was that he appreciated my kind intentions in giving him apples. But, he went on, to tell the real truth, it is not a fruit I am particularly fond of. I am familiar with its taste as they sometimes give me apples, usually the small unripeor bad ones that fall from the trees. However, I don't actually dislike them. I get skim milk and am rather fond of it; then a bucket of mash, which is good enough for hunger; but what I enjoy most is a cabbage, only I don't get one very often now. I sometimes think that if they would let me out of this muddy pen to ramble like the sheep and other beasts in the field, or on the downs, I should be able to pick up a number of morsels which would taste better than anything they give me. Apart from the subject of food, I hope you won't mind me telling you that I'm rather fond of being scratched on the back._ _So I scratched him vigorously with my stick and made him wriggle his body and wink and blink and smile delightedly all over his face. Then I said to myself: "Now what the juice can I do more to please him?" For though under sentence of death, he had done no wrong, but was a good, honest-hearted fellow mortal, so that I felt bound to do something to make the miry remnant of his existence a little less miserable._ _I think it was the word "juice" I had used—for that was how I pronounced it to make it less like a swear-word—that gave me an inspiration. In the garden, a few yards back from the pen, there was a large clump of old eldertrees, now overloaded with ripening fruit—the biggest clusters I had ever seen. Going to the trees, I selected and cut the finest bunch I could find, as big round as my cap, and weighing over a pound. This I deposited in his trough and invited him to try it. He sniffed at it a little doubtfully, and looked at me and made a remark or two, then nibbled at the edge of the cluster, taking a few berries into his mouth, and holding them some time before he ventured to crush them. At length he did venture, then looked at me and made more remarks, "Queer fruit this! Never tasted anything like it before, but I really can't say yet whether I like it or not."_ _Then he took another bite, then more bites, looking up at me and saying something between the bites, 'til, little by little, he had consumed the whole bunch; then, turning round, he went back to his bed with a little grunt to say that I was now at liberty to go on to the cows and horses._ _However, the following morning he hailed my approach in such a lively manner, with such a note of expectancy in his voice, that I concluded he had been thinking a great deal about elderberries, and was anxious tohave another go at them. Accordingly, I cut him another bunch, which he quickly consumed, making little exclamations the while—"Thank you, thank you, very good, very good indeed!" It was a new sensation in his life, and made him very happy, and was almost as good as a day of liberty in the fields and meadows and on the open green downs._ _From that time on I visited him two or three times a day to give him huge clusters of elderberries. There were plenty for the starlings as well; the clusters on those trees would have filled a cart._ _Then one morning I heard an indignant scream from the garden, and peeping out saw my friend, the pig, bound hand and foot, being lifted by a dealer into his cart with the assistance of the farmer._ It made Hudson happy to feel he could bring cheer to the last days of this sociable and sensitive animal, destined though he was for the butcher. Of course, it is not to be expected that the average person should be quite as sensitive in translating the grunts and growls as a trained naturalist. Nevertheless, I want to stress the good-naturedness of pigs because we have done them such a terrible injustice in the way we think of them, even to using their name as a vile insult. But why have we given such a bad name to an animal who is full of intelligence and honest-hearted zest for life; why have we so demeaned a creature capable of endearing and lasting friendships with human beings? It would perhaps be easier to understand if we did this to the crocodile, for example, who historically has been a real threat to our lives and seems to have something about him of the darkness. But the pig? The loyal, friendly, likable pig? Part of the answer, at least, is rather simple. The pig is guilty of having flesh that human beings find tasty. _Man has an infinite capacity to rationalize his rapacity, especially when it comes to something he wants to eat._ —CLEVELAND AMORY Since few of us have any direct experience with pigs anymore, we can think and speak of them as foul and unwholesome beasts without being disturbed by the facts of the matter. But down through the ages, people who have kept pigs have sensed their undeniable intelligence and friendliness. Only by looking the other way could human beings manage to justify what they have done in order to have bacon and ham, just as black humans were dehumanized in the minds of whites in order to justify their oppression and slavery. **Schweitzer's Pig** When Albert Schweitzer was in Africa running a volunteer hospital, he had a standing offer out to the natives that if they brought him an animal that they would otherwise have killed, he'd pay them for it. In such manner did he save numerous animal lives, create an entourage of assorted critters around him, and show the natives new possibilities of interacting with the local animals. He wrote a remarkable account of meeting a pig. _One day a Negro woman brought me a tame wild boar about two months old. "It is called Josephine, and it will follow you around like a dog," she said. We agreed upon five francs as the price. My wife was just then away for a few days. With the help of Joseph and n'Kendju, my hospital assistants, I immediately drove some stakes into the ground and made a pen, with the wire netting rather deep in the earth. Both of my black helpers smiled._ _"A wild boar will not remain in the pen; it digs his way out from under it," said Joseph. "Well, I should like to see this little wild boar get under this wire netting sunk deep in the earth," I answered. "You will see," said Joseph._ _The next morning the animal had already gotten out. I felt almost relieved about it, for I had promised my wife that I would make no new acquisition to our zoo without her consent, and I had a foreboding that a wild boar would not, perhaps, be to her liking._ _When I came up from the hospital for the midday meal, however, there was Josephine waiting for me in front of the house, and looking at me as if she wanted to say: "I will remain ever so faithful to you, but you must not repeat the trick with the pen." And so it was._ _When my wife arrived she shrugged her shoulders. She never enjoyed Josephine's confidence and never sought it. Josephine had a very delicate sensibility about such things. In time, when she had come to understand that she was not permitted to go up on the veranda, things becamebearable. On a Saturday some weeks later, however, Josephine disappeared. In the evening the missionary met me in front of my house and shared my sorrow, since Josephine had also shown some attachment to him._ _"I feel sure she has met her end in some Negro's pot," he said._ _"It was inevitable."_ _With the blacks a wild boar, even when tamed, does not fall within the category of a domestic animal but remains a wild animal that belongs to him who kills it. While he was still speaking, however, Josephine appeared, behind her a Negro with a gun._ _"I was standing," he said, "in the clearing, where the ruins of the former American missionary's house are still to be seen, when I saw this wild boar. I was just taking aim, but it came running up to me and rubbed against my legs! An extraordinary wild boar! But imagine what it did then. It trotted away with me after it, and now here we are. So it's your wild boar? How fortunate that this did not happen to a hunter who is not so quick-witted as I."_ _I understood his hint, complimented him generously, and gave him a nice present._ Later, writing of the same boar, Schweitzer spoke of her coming to church and causing an uproar by behaving like a wild pig, but then gradually learning to "behave more properly in church." Struck again and again by the spirit of this animal, Schweitzer wrote: _How shall I sufficiently praise your wisdom, Josephine! To avoid being bothered by gnats at night, you adopted the custom of wandering into the boys' dormitory, and of lying down there under the first good mosquito net. How many times because of this have I had to compensate, with tobacco leaves, those upon whom you forced yourself as a sleeping companion. And when the sand fleas had so grown in your feet that you could no longer walk, you hobbled down to the hospital, let yourself be turned over on your back, endured the knife that the tormentors stuck into your feet, put up with the burning of the tincture of iodine, with which the wounds were daubed, and grunted your sincere thanks when the matter was once and for all done with._ **The Fragrance of the Farm** Since I have found that pigs are such endearing and friendly chaps, I don't look at pork chops the way I once did. And there's something else I've learned that has forever changed the way I feel about such things as bacon and ham. What I have learned is that the pork farmers have by and large followed the lead of the poultry industry in recent years. Instead of pig farms, today we have more and more pig factories. The result is not a happy one for today's pigs. Some of today's pig factories are huge industrial complexes, with over 100,000 pigs. You might think that would require an awful lot of pigpens. But the pigpen, like the chicken yard, is rapidly becoming a thing of the past. Every day, more and more of these robust creatures are placed in stalls so cramped that they can hardly move. If you were to peek inside one of the buildings in which these stalls are kept, you'd see row upon row upon row upon row of pigs, each standing alone in his narrow steel stall, each facing in exactly the same direction, like cars in a parking lot. But you would hardly notice what you saw, because you'd be so overwhelmed by the stench. The overpowering ammonia-saturated air of a modern pig factory is something no one ever forgets. You see, many modern pig stalls are built on slatted floors over large pits, into which the urine and feces of the animals fall automatically. Thousands of this type of confinement system are in operation, in spite of the fact that many serious diseases are caused by the toxic gases (ammonia, methane, and hydrogen sulfide) that the excreta produce and that rise from the pits and become trapped inside the building. Pigs have a highly developed sense of smell and their noses are, in a natural setting, capable of detecting the scents of many kinds of edible roots, even when those roots are still underground. In today's pig factories, however, they breathe night and day the stench of the excrement of the hundreds of pigs whose stalls are in the same building. No matter how much they might want to get away, no matter how hard they might try, there is no escape. The pig factory I am describing is unfortunately not an isolated bad example. It's par for the course today. Just a couple of years ago, the owner of Lehman Farms of Strawn, Illinois, was chosen Illinois Pork All-American by the National Pork Producers Council and the Illinois Pork Producers Association. The Lehman farm is considered an industry model, and it is, in fact, one of the more enlightened swine management programs around today. But it seems to leave a little bit to be desired from the point of view of the pigs who call it home. When a "herdsman" at Lehman Farms, Bob Frase, was asked about the effect the ammonia-saturated air had on the pigs, he replied: _The ammonia really chews up the animals' lungs. They get listless and don't want to eat. They start losing weight, and the next thing you know you've got a real respiratory problem—pneumonia or something. Then you'll see them huddled down real low against one another trying to get warm, and you'll hear them coughing and gasping. The bad air's a problem. After I've been working in here awhile, I can feel it in my own lungs. But at least I get out of here at night. The pigs don't so we have to keep them on tetracycline._ **"Forget the Pig Is an Animal"** In my visits to modern pig factories, I keep thinking about pigs I have met, social critters much like Albert Schweitzer's Josephine, very capable of warm relationships with people. I remember their friendly grunts and their enjoyment of human contact. This is why I have such a hard time accepting the advice of contemporary pork producers: _Forget the pig is an animal. Treat him just like a machine in a factory. Schedule treatments like you would lubrication. Breeding season like the first step in an assembly line. And marketing like the delivery of finished goods._ _—H OG FARM MANAGEMENT_, SEPTEMBER 1976 Modern pig farmers, who like to be called pork production engineers, pride themselves on having a clear purpose. The trade journal _Hog Farm Management_ put it concisely: _What we are really trying to do is modify the animal's environment for maximum profit._ Even if an individual pig raiser feels an empathy with the animals in his charge and has a desire to do things in a more natural way, he is today practically forced to go along with the agribusiness momentum. The trend is set. Trade journals like _Hog Farm Management, National Hog Farmer, Successful Farming,_ and _Farm Journal_ are constantly telling farmers: "Raise Pork the Modern Way." The trade journals tend to be downright hostile to anything but the most mechanized agribusiness ways of producing pork. Recently, _National Hog Farmer_ became irate at the USDA and editorialized, "Why don't we just turn the Department of Agriculture over to the do-gooders?" What on earth had the USDA done to provoke such a terrifying thought? It had proposed spending two hundredths of 1 percent of its budget for two small projects that would have encouraged small-scale, local production of food, such as roadside markets and community gardens in urban areas. The trade magazines, it must be remembered, derive their income from advertisers, and these are just the people who profit from the swing to total-confinement systems of pork production—the huge commercial interests who sell equipment and drugs to the farmers. They're the ones who take out full-page ads and pay for space in the journals to tell the farmers: "How to Make $12,000 Sitting Down!" That's quite a way to catch the attention of an exhausted farmer, who is only too glad to sit down at all after laboring on his feet all day. So he reads on. And what does he find? The way to success in today's pork production world is through buying a "Bacon Bin." This wonderful new doorway to success, he is told, "is not just a confinement house... It is a profit producing pork production system." Actually, the Bacon Bin is a completely automated system whose designers clearly have overcome any vestiges of the anachronistic idea that pigs are sentient beings. In a typical Bacon Bin setup, 500 pigs are crammed into individual cages, each getting seven square feet of living space. It's difficult for us to conceive how confined this is. Every pig spends his entire life cramped into a space less than one-third the size of a twin bed. The Bacon Bin system comes complete with slatted floors and automated feeding systems, so that it takes only one person to run the whole show. Another advantage of the system is that, with no room to move about, the pigs can't burn up calories doing "useless" things like walking, and that means faster and cheaper weight gain, and so more profit. A typical example of Bacon Bin farming was happily described in the _Farm Journal_ beneath the title: "Pork Factory Swings into Production." The article begins proudly: _Hogs never see daylight in this half-million dollar farrowing-to-finish complex near Worthington, Minnesota._ This is something to brag about? **Pig's Feet Modern Style** Pigs' feet and legs were designed to scratch for food, to kick or claw if needed for defense, and to stand and move on different kinds of natural terrain. But in today's pig factories, the floors are either metal slats or concrete. Peter Singer and Jim Mason, authors of _Animal Factories,_ the classic book on contemporary food-animal raising, have described what happens to pigs' feet under these conditions. _Pigs are cloven-hoofed animals, and, in most, the outer half of the hoof ("claw") is longer than the inner half. Outdoors, the extra length is absorbed by the natural softness of the soil. On the concrete or metal floors of the factory pen, however, only the tissue in the foot can "give." As a result, many confined pigs develop painful lesions in their feet which can open and become infected. Pigs with these foot sores usually develop... abnormal posture in an attempt to relieve the pain. Eventually, the crippling may worsen when this abnormal movement and weight distribution overworks joints and muscles in the legs, back, and other parts of the pig._ One Nebraska study showed that nearly 100 percent of all pigs raised on concrete or metal slats had damaged feet and legs. Providing bedding can reduce the problem, but bedding is rarely provided in the modern homes of the pigs destined to become America's pork chops, because straw costs money, and the pain and suffering the pigs endure from damaged feet and legs is not figured into the financial equations that determine policy. Of course, the pork producers are aware that the animals are crippled by the flooring, but they are not disturbed. As the editors of _Farmer and Stockbreeder_ explain: _The slatted floor seems to have more merit than disadvantage. The animal will usually be slaughtered before serious deformity sets in._ In other words, the pigs are usually slaughtered before their deformities become so extreme as to affect the price their flesh will fetch. One producer summarized industry thinking rather colorfully. _We don't get paid for producing animals with good posture around here. We get paid by the pound _ As I look at the situation, I doubt whether the pigs who spend their painful lives on these devastating floors, hobbling about on distorted skeletons, are able fully to appreciate this kind of logic. **Improving on Mother Nature** It may not be wise to tamper with nature. It may even be disastrous. But you can be sure that if it's profitable, someone is certain to give it a try. The leading edge in pork production these days is in getting more pigs per sow per year. The idea is to turn sows into living reproductive machines. _The breeding sow should be thought of, treated as, a valuable piece of machinery, whose function is to pump out baby pigs like a sausage machine._ _—N ATIONAL HOG FARMER_, MARCH 1978 In a barnyard setting, a sow will produce about six piglets a year. But modern interventions have cranked her up to over 20 a year now, and researchers predict the number to reach 45 within a short time. Producers rave about the prospect of being able to force sows to give birth to over seven times the number of children nature designed them for. They've got it down to a science. First of all, piglets are taken away from their mothers much earlier than would ever occur in any natural situation. Without her babies to suck the milk from her breast, the sow will soon stop lactating, and then, with the help of hormone injections, she can be made fertile much sooner. Thus, more piglets can be extracted from her per year. Unfortunately, the poor sow is not up-to-date enough in her thinking to appreciate the wonders of a system in which she will spend her whole life producing litter after litter, only to have her babies taken away from her as soon as possible after each birth. The sow calls and cries for them, though her distressed sounds always go unheeded. Not having gotten the hang of modern factory life, she only knows that her whole being is filled with an inexorable instinct to find her lost babies and care for them. Most pork producers have found that they have to let the piglets suckle from their mother for a couple of weeks before taking them away, or else they die, which, of course, defeats the whole purpose. But at least one large manufacturer of farm equipment sees the waste in such an operation and is now strongly promoting a device it calls Pig Mama. This is a mechanical teat that replaces the normal one altogether and allows the factory manager to take the piglet away from his mother immediately and get her back to the business of being pregnant, just a couple of hours after birth. Noting this development, _Farm Journal_ said it was looking forward to "an end to the nursing phase of pig production." The result, they predicted gleefully, would be a _tremendous jump in the number of pigs a sow could produce in a year._ For years now, pork breeders have also been hard at work developing fatter and fatter pigs. Unfortunately, the resulting products of contemporary pork breeding are so top-heavy that their bones and joints are literally crumbling beneath them. However, factory experts see nothing amiss in this because there is additional profit to be made from the extra weight. There are, however, a few problems with the new model pig rolling across the assembly line in today's pork factories that do concern the factory experts. Singer and Mason point out a few of these problems in _Animal Factories._ _The pig breeders' emphasis on large litters and heavier bodies, coupled with a lack of attention to reproductive traits, has produced... high birth mortality in these pigs. These new, improved females produce such large litters that they can't take care of each piglet. To cure this problem, producers began to select sows with a greater number of nipples—only to discover that the extra nipples don't work because there's not enough mammary tissue to go around._ Not to be dismayed, however, the genetic manipulators are continuing their efforts to "improve" the pig and convert this good-natured and robust creature into a more efficient piece of factory equipment. _Breeding experts are trying to create pigs that have flat rumps, level backs, even toes, and other features that hold up better under factory conditions._ **Hormone City** What they can't accomplish with genetics, today's pork producers shoot for with hormones. Hormones, as you may know, are incredibly potent substances that are naturally secreted, in minute amounts, by the glands of all animals, pigs and humans included. It takes minuscule amounts of these substances to control our entire endocrine and reproductive systems. If our taste buds were as sensitive to flavor as our target cells are to hormones, we could detect a single grain of sugar in a swimming pool of water. Given the immensely powerful effects that hormones have on animals' reproductive systems, even in concentrations so low they are discernible only by the most sophisticated laboratory technology, many scientists are extremely concerned about their use in animal farming, acknowledging that we know very little about many of the potentially dangerous effects of these substances. The factory experts, however, look through very different eyes. When they first realized the new drugs gave them the power to control a sow's estrus, and thus to induce or delay her fertility, they were overjoyed. _Estrus control will open the doors to factory hog production. Control of female cycles is the missing link to the assembly line approach._ _—F ARM JOURNAL_ One pork producer was so taken with this new development that he called it the _greatest advance in hog production since the development of antibiotics._ Another new innovation that has the industry astir is called embryo transfer. Here a specially chosen sow is dosed with hormones to cause her to produce huge numbers of eggs, rather than the usual one or two. These eggs are fertilized by artificial insemination, then surgically removed from the sow and implanted in other females. It is not uncommon for a breeder sow to go repeatedly through this unnatural violation until the stress kills her. At the University of Missouri, work is being done in test tubes to combine sperm and eggs that have been taken from specially selected breeding animals. The newly fertilized eggs are then implanted surgically in ordinary females. Once a sow in today's pork factories is pregnant, she is injected with progestins or steroids to increase the number of piglets in her litter. She will also be given products like the new feed additive from Shell Oil Company. Called XLP-30, it is designed to "boost pigs per litter," though it has a name that makes it sound like it should be added to motor oil instead of animal food. Incredibly, a Shell official acknowledges—"we don't know why it works." Undeterred by such ignorance, however, the industry is not at all reluctant to tamper with the reproductive systems of the animals whose flesh is designed for human consumption. Anything that can speed up the assembly line and improve profits is considered fair practice. **A Life of Suffering** It is difficult for us to fathom the suffering of today's pigs. They are crammed for a lifetime into cages in which they can hardly move, and forced against their natures to stand in their own waste. Their sensitive noses are continuously assaulted by the stench from the excrement of thousands of other pigs. Their skeletons are deformed and their legs buckle under the unnatural weight for which they have been bred. Their feet are full of painful lesions from the concrete and slatted metal floors on which they must stand. I have looked into their eyes and I can tell you it's a terrifying sight. These sensitive, tortured creatures have been literally driven mad. In this respect, they are similar to the chickens who live in today's "chicken heavens." Chickens, you may remember, when forced into unbearably crowded conditions, go crazy and develop "vices" such as feather-pecking and cannibalism. Forced into equally bizarre conditions, pigs are likewise driven completely out of their minds. One reporter noted: _Some animals may become so fearful that they dare not move, even to eat or drink. They become runts and die. Others remain in constant, panicked motion, neurotic perversions of their instinct to escape. Cannibalism is common in swine... operations._ One of the most common problems in modern pork factories is known in the trade as "tail-biting." The trade journals are full of discussions about tail-biting and what to do about it. When I first heard the phrase "tail-biting," I rather naively pictured some kind of playful nipping at little, curly, pink tails. But I have since learned how very far from the mark I was. "Tail-biting" is the industry's term for the deranged and desperate actions of powerful animals driven berserk by the frustration of every single one of their natural urges. _Acute tail-biting... frequently results in crippling, mutilation, and death...Many times the tail is bitten first, and then the attacking pig or pigs continue to eat further into the back. If the situation is not attended to, the pig will die and be eaten._ Tail-biting, naturally, disturbs the managers of the pork factories, who can't sell a pig that's been eaten by another pig. Not being the types to sit back and let a disaster like that occur, they've come up with a number of bizarre solutions. One strategy is to keep the pigs in total darkness. A March 1976 edition of _Farm Journal_ carried an article titled "Cut Light and Clamp Down on Tail Biting." This report reassured pork producers: _They can still eat—total darkness has no effect on their appetites._ The preferred method of preventing tail-biting in today's pork factories, however, is a trick the pork producers picked up from the poultry men. They can't, of course, de-beak pigs, because pigs don't have beaks. But they have found another way of preventing tail-biting that, like chicken de-beaking, does absolutely nothing to correct the grotesque conditions that give rise to the behavior in the first place. They cut off the pigs' tails. This practice, known in the trade as "tail-docking," is now standard operating procedure in United States pork production. Its application is nearly universal today, despite the fact that it causes severe pain to the animals and drives them even crazier. I asked one pork farmer about tail-docking, and he replied, somewhat angrily: _They hate it! The pigs just hate it! And I suppose we could probably do without tail-docking if we gave them more room, because they don't get so crazy and mean when they have more space. With enough room, they're actually quite nice animals. But we can't afford it. These buildings cost a lot._ This farmer's remarks don't reflect his thoughts alone. They are typical of the rationale behind virtually all of the steps being taken today toward even more mechanized pork production. Having invested great sums of money in confinement buildings and automated feeding systems, today's producers feel they must use every trick in the book to get the maximum number of piglets per sow and cram as many pigs as possible into the buildings. In fact, the trade journal _Hog Farm Management_ has an even better idea than the parking lot–like stalls. How about stacking the pigs in cages, one on top of another, like shipping crates? Just think how many more animals you could get in a building this way. Explaining the brilliance of having not only wall-to-wall pigs but floor-to-ceiling pigs as well, the journal reasoned: _There's too much wasted space in a typical controlled-environment single-deck nursery. The cost of the building is just too big a cost factor. Stacking the decks spreads the building cost out over more pigs._ A number of today's largest pig factories have been so impressed with this idea that they've wasted no time in employing it. You might not think that it would make that much difference to a pig who is already crammed into a cage so small he can hardly move, whether there are other pigs above him in the same plight. But it does. The excrement from the pigs in the upper tiers falls steadily on the pigs in the lower tiers. **Anger and Tears from a Pork Producer** It's actually gotten to the point that many of today's pig farmers are being forced to do things even they find abhorrent. I'm not talking now about people who are particularly empathetic toward animals. I'm referring to people who long ago came to accept bashing an animal's brains out or slitting its throat as all in a day's work. These are hardened veterans of the everyday brutalities of animal farming, but even they are increasingly disgusted by what is happening today. In a 1976 issue of _Farmer and Stockbreeder,_ a letter appeared that expressed the concern of such an old-timer. He was writing in response to a report on a new cage system for pigs. _May I dissociate myself completely from any implication that this is a tolerable form of husbandry? I hope many of my colleagues will join me in saying that we are already tolerating systems of husbandry which, to say the least of it, are downright cruel... Cost effectiveness and conversion ratios are all very well in a robot state; but if this is the future, then the sooner I give up both farming and farm veterinary work the better._ The same year, a retired farm veterinarian sent a thoughtful letter to the factory farming journal _Confinement._ _More and more I find myself developing an aversion to the snow-balling trend toward total confinement of livestock... If we regard this unnatural environment as acceptable, what does it portend for mankind itself?... How can a truly human being impose conditions on lower animals that he would not be willing to impose on himself? Freedom of movement and expression should not be the exclusive domain of man...What (then) of human behavior (in the future)? Will it sink to the nadir of contempt for all that is naturally bright and beautiful? Will all of us become tailbiters without recognizing what we have become?_ These two letters were written in 1976, just as total-confinement systems for pork production were gathering steam. Since then, despite the pleas of these and other warning voices, the trend has continued: more total confinement, more frustration of all the animals' natural urges, more farming by automation and technology, more drugs, and more assembly-line pork. And what happens to those farmers who just can't stand to do this to animals whom they know are intelligent and capable of lasting friendships with people? Most have quit the whole affair in disgust and failure. Others have continued on, often with an aching sense of frustration and defeat as they capitulate time and time again out of financial necessity to the harsh economic reality of modern farming. One such pig farmer told me, angrily: _Sometimes I wish you animal lovers would just drop dead! Just go and fall off a cliff or something. It's hard enough to make a living these days without having to be concerned about all this stuff!_ Later that night, after dinner and a long talk in which he opened up to his true feelings, this same farmer told me, with tears in his eyes: _I'm sorry I got so mad at you before. It's not your fault. You are just showing me what I already know, but try not to think about. It just tears me up, some of the things we are doing to these animals. These pigs never hurt anybody, but we treat them like, like, like I don't know what. Nothing in the world deserves this kind of treatment. It's a shame. It's a crying shame. I just don't know what else to do._ **The American Pork Queen Speaks** The National Pork Council and related organizations spend millions of dollars a year to convince the public that today's pigs are as happy as can be with the way they are raised. In May 1987, the Council officially and unabashedly proclaimed that pork producers "have historically treated their farm animals with the utmost care and respect." Each year, the Pork Council sends an official American Pork Queen out across the country to enlighten schools and community groups about the joys of modern pork production. Speaking about her work, one year's American Pork Queen, Pam Carney, explained: _Well, I kind of told about myself from the perspective of being a pig...You see, we are getting a lot of questions from people now who are for animal rights and who are worried about pigs being put into small pens and farrowing crates. So, I talked about how much we pigs like the new confinement barns as opposed to living outside in the natural environment, because a herdsman can keep a close eye on us, watch for disease, give us warmth, good feed, and clean water._ The American Pork Queen reassures us today's pigs receive good feed and clean water. But the truth, as you might guess, is a little different. In nature, pigs live with gusto and passion, foraging in the earth for their food. Even in a barnyard setting they root around as much as they can, and their diet consists of table scraps along with the foods they can root from the earth. But today, they are fed a completely unnatural diet designed with one thing alone in mind—to make them as fat as possible, as cheaply as possible. Their feed is routinely laced with antibiotics, sulfa drugs, and countless other products of the laboratory. It is a menu that often features recycled waste. One modern pig farmer proudly announced in _Hog Farm Management_ that in his system pregnant sows don't need to be fed for 90 days. Presenting his ingenuity as a model for the forward-thinking pig man, he boasted that he simply allows them only what they can find in the manure waste pits beneath the slatted floor cages where young pigs are being fattened for slaughter. His excitement about how much money he saves was not dampened by the fact that during pregnancy the nutritional needs of pigs, like those of any mammal, are especially critical. The industry norm isn't much better. Today's pigs are routinely fed recycled waste, even though this waste consistently contains drug residues and high levels of toxic heavy metals, such as arsenic, lead, and copper. Often the helpless creatures are simply given raw poultry or pig manure. I don't know about you, but eating their own excrement doesn't strike me as an ideal diet. But if what today's pigs are fed leaves a little to be desired, it's almost a picnic compared to the water they receive to drink. Sometimes the only water they get comes from an _oxidation ditch, which channels the liquid wastes from factory manure pits back to the animals; they have to drink it because it's the only "water" offered to them._ Interestingly enough, the industry's public stance is that the health and well-being of today's pigs is better than ever. But over 80 percent of today's pigs have pneumonia at the time of slaughter. One Minnesota plant found pneumonia in the lungs of 95 percent of the pigs inspected. In 1970, 53 percent of all U.S. pigs had stomach ulcers. The Livestock Conservation Institute reports that pig producers lose more than $187 million each year from dysentery, cholera, abscesses, trichinosis, and other swine diseases. A disease known as pseudorabies has been wiping out whole herds of factory pigs in the Midwest since 1973. The National Pork Council wants the government to pay for a five-year program to eradicate pseudorabies. _Hog Farm Management_ thinks this would cost taxpayers $90 million. Of course, that's not a lot of money compared to the bill for another disease, African swine fever, which is beginning to infect pigs raised the modern way in this country. _National Hog Farmer_ expects the cost of coping with this disease to be in the neighborhood of $290 million. The pork industry says these diseases amount to only minor technical problems in the assembly-line production of pork. With the help of taxpayers' money and the application of more drugs, they say, the problems can be solved in no time. As to the possibility that today's pigs are not really all that healthy, the industry points to the impressive weights the animals attain as proof that they are as robust as can be. This is a remarkable argument, in that it attempts to equate systematically induced obesity with good health. That's certainly not true for humans; why should it be true for pigs? **And Then** The pigs I've known have been friendly and sensitive critters, like Albert Schweitzer's Josephine. They can be good friends, playful, loyal, and affectionate. Watching what happens to these good-hearted creatures in today's pig factories has not been at all easy for me. At each stage of the assembly line they are treated with complete disdain for the fact that they are our fellow creatures. But they are sentient beings, and they remain so to the end. _Before they reach their end, the pigs get a shower, a real one. Water sprays from every angle to wash the farm off them. Then they begin to feel crowded. The pen narrows like a funnel; the drivers behind urge the pigs forward, until one at a time they climb unto a moving ramp... Now they scream, never having been on such a ramp, smelling the smells they smell. I do not want to overdramatize because you have read all this before. But it was a frightening experience, seeing their fear, seeing so many of them go by. It had to remind me of things no one wants to be reminded of anymore, all mobs, all death marches, all mass murders and extinctions._ **The New Question** Seeing what happens to today's pigs is especially difficult for me because I know what friendly animals they can be by nature. We have come to know pigs as fat only because we have bred and fed them that way. We have come to know pigs as mean only because we have tortured them and deprived them of any conceivable expression of their energies. We have made them what they are. Could it be, then, that when we eat the flesh of animals who have been treated with such complete contempt, we assimilate something of their experience and carry it forward into our own lives? Could it be that eating the products of such an insane system may contribute significantly to the feeling pervading mankind today that this earth sometimes resembles the lunatic asylum of the universe? People of the stature of Plato, Tolstoy, and Gandhi have also refused to eat meat. But today the question of meat-eating has taken on a far more urgent significance than ever before. There is something uniquely painful happening in the way contemporary animals are being raised for meat. Animals have been treated cruelly before, and in some cases sadistically—but the process has never before been institutionalized on such an overwhelming scale. And never before has the cold expertise of modern technology and pharmacology been employed to this end. Throughout history, there have been people who sensed that eating the flesh of animals killed unnecessarily was not the best thing we could do toward the goal of bringing peace to ourselves and to the world. The more I've learned of modern meat production, the more I've felt that their message is even more vital today. _While we ourselves are the living graves of murdered beasts, how can we expect any ideal conditions on this earth?_ —GEORGE BERNARD SHAW _I have no doubt that it is part of the destiny of the human race in its gradual development to leave off the eating of animals, as surely as the savage tribes have left off eating each other when they came into contact with the more civilized._ —HENRY DAVID THOREAU _The time will come when men such as I will look on the murder of animals as they now look on the murder of men._ —LEONARDO DA VINCI **4. HOLY COW** _I tremble for my species when I reflect that God is just._ —THOMAS JEFFERSON _Each man is haunted until his humanity awakens._ —WILLIAM BLAKE As I've learned what is being done to today's farm animals I've become increasingly distressed. If our society is to reflect any kind of compassion and respect for life, how can we allow such extreme abuses of sentient beings to continue? The problem is that the behemoths of modern agribusiness seek profit without reference to any ethical sensitivity to the animals in their keeping. And at present we have virtually no laws restraining cruelty to animals being raised for food. I look forward to the day when this has been corrected, when our society is at peace with its conscience because it respects and lives in harmony with all forms of life. I look forward eagerly to the enactment of laws against such cruelty to animals, laws that will guide humankind to actions consistent with an ethic of appreciation for Creation and respect for the lives of our fellow creatures. Though I have felt anger at the outrages inflicted on innocent animals, I know that many of today's farmers are basically decent human beings who have become caught in a vicious circle of economic necessity, seeing no choice but to follow the lead of the multinational agrichemical conglomerates. The laws that are needed to restrain those who would in their insensitivity abuse animals will not arise out of ill will toward those who have become instruments of such cruelty. True justice never punishes for the sake of punishment but instead seeks to provide the experiences that will educate and reform. Since insensitivity to nature is the real problem, our intent should be not to blame but to guide these unfortunate people to an awareness of the lives and needs of other living creatures, and thus to their own potential for living in an ethical relationship with the rest of life. Those who are so alienated from other beings that they would mistreat them are in need of a deeper respect for life, for themselves, and for a more meaningful sense of their own value and integrity. We need laws against cruelty to animals, not just for the animals' sake. Interestingly, legend has it that there was once a time when such a form of justice actually prevailed. This was a time, it is said, when an ancient people sought to live in accord with the laws of Creation. As a result, when disputes and conflicts arose, the remedy was often remarkable. Here is such a case, chronicled from ancient Egypt. The times are different, but the message is the same. A 15-year-old boy has gotten himself in trouble time after time for his cruelty to animals. In spite of repeated punishments from his father, however, his actions have persisted. Neighbors have finally appealed to the judge for help, and he has decreed that the boy be watched without his knowledge. This is done, and the boy is seen burying a cat alive. When confronted with his action, the boy shows no sense of shame or remorse and says defiantly, "You can beat me, but I won't mind. I'm used to being beaten, but you can never make me scream!" He pulls off his shirt and displays a back that is deeply scarred from the previous beatings his father has administered. To the counselor who comes in to see him he brags about the number of animals he has tortured, and the amount of pain that has been inflicted upon him in return. It is not an easy case for the judge to handle. But fortunately, there is a seer who can look into the boy's psyche and see what has occurred that has made him this way. The seer understands the pattern the boy is locked into. He understands that in the boy's clouded mind, his cruelty to animals is actually part of an effort to expiate the guilt he feels for his mother having died during his birth, something his father never lets him forget. It is plain to the seer that it would be pointless to punish the boy, for to do so would simply reinforce the guilt that motivated the whole behavior in the first place. The seer decides to take drastic steps. The next day, in the boy's food there is mixed a violent cathartic. As soon as the boy's bowels start cramping he is told that he has a rare and dangerous disease and is warned that unless he is both brave and obedient he will likely die. Over the next few days he is given other concoctions, which keep him intermittently in pain and also make him sufficiently weak to prevent him from having any desire to exert his independence and reconstruct his accustomed self-image. Exactly as though he is suffering from a very serious disease, he is cared for by one who is in training to become a true healer, a girl of 20 who is both beautiful and compassionate. She holds his hand to help him bear the pain and smooths his forehead until he falls asleep. She washes and feeds him as though he is a baby, and when he grows a little stronger, she tells him stories of the ways of peace and love. As he convalesces, he conceives a deep devotion and gratitude to his nurse and asks that he might be allowed to serve her in however humble a capacity. She tells him that one of her duties is to look after the geese, that the geese are very special to her, and that it would be a great help if he would do this for her. Her words cause him to remember his many cruelties, and he begins to cry bitterly and says that he dare not do what she asks, for sometimes almost against his will he has been cruel to animals, and so he is very afraid that he might attack her geese, an act that, to him now, would be like causing her personal injury. She says to him: "You were so ill that you might have died. I asked the gods that you might be born again; they listened, and you recovered. The cruelty that you once inflicted and the pain you suffered are as though they had never been. They are dead, but you are alive. Because of the link between us, you will never forget again the link between you and your younger brothers and sisters." The boy is filled with hope but even so does not entirely believe her. She brings him a kitten, but he protests, saying he can't be trusted with the kitten. She smiles and teaches him how to scratch the kitten's throat and ears and points out how loudly it purrs when he does so. "It likes you," she says. "It knows you can be trusted, and I know you can be trusted, too, so I will leave you alone with the kitten now." The boy doesn't know what to think and protests, but she just smiles and kisses his forehead. When she returns, several hours later, she finds the boy asleep, with the kitten curled up beside him, purring. The boy grows to become one of the kindest veterinarians in all the land, and his manner with animals is so gentle and clear that even the most terrified and injured of them instinctively know they can trust him. It looks to me as if many of the people who mistreat the animals raised for today's meats and eggs are not that different from this boy, likewise crying out for wise and compassionate help. The lack of caring they display for the animals in their keeping stems from an alienation from themselves and from life, not from innate cruelty. Merely blaming and hating them does nothing to heal the separation and isolation out of which their cruelties spring. Our goal should be to help them learn to act according to an authentic respect for other creatures, for in so doing they can come to feel a kinship with life and their own value as part of Creation. We urgently need laws that would guide them in this direction. Of course, in some instances it may take a serious remedy to be effective. Sometimes only a severe corrective is able to produce the needed empathy in someone who otherwise remains indifferent to the suffering of his fellow creatures. Here is another such case from ancient times. A man is accused of mistreating his oxen. The judge inspects the animals and sees that they are indeed in bad condition and have deep sores on their shoulders from an ill-fitting yoke. He tells the owner that this is not good, thinking that perhaps the man is ignorant, or stupid, and has not seen the hurt done to the animals. But the man protests defensively that his oxen are thin because they are too lazy to eat, that the work they do in the fields is light enough for a child, and that he envies the oxen their contentment. And the judge says: "There shall be no longer any need for you to have to envy them. For now you will have the opportunity to share their contentment, by doing yourself this work you say is 'child's play.' Tomorrow you shall be yoked to the plow, and you will draw it back and forth under the hot sun until the field is furrowed." The judge gives the man's oxen to a neighbor whose animals are well cared for and says that the man may regain his oxen when he has finished furrowing the field. Furthermore, his oxen will be inspected thereafter, and if it is found that he has mistreated them, he will receive unto himself whatever treatment he has given unto them. But if it is found that he now treats them well, then it will be known that he can be trusted with oxen, and so his herd will be expanded. If a person refuses time and again to imagine how he would feel in another creature's shoes, sometimes the only remedy that will bring about the needed empathy is to physically place him there. In some cases the conditions suffered by today's food animals arise simply because greed has clouded the eyes of those responsible, and they can no longer see the pain of their fellow creatures. In such cases, the best justice may be that which serves not only to right the wrong that has been done but also to clear the vision that has become so clouded. Here is one more case of ancient wisdom, uniquely pertinent to the issue of greed. In one village there are two men who dispute ownership of a wild ass. Both claim ownership by right of having seen the animal first. One of the men is more prosperous than the other, yet he keeps bemoaning his poverty, the number of his children, and the poorness of his fields and he protests that the ass should be given to him because his is by far the greater need. A wise judge says to him: "You tell me that your need is the greater because you are poor and this other man is far wealthier than you; and when he says he is the poorer you say he is lying. Therefore I shall give a judgment that will adjust the wrong that he does to you. You, who are the poorer man, shall have the wild ass. And to show you how much you are favored, you and this other man shall exchange all your possessions." Now the man cries out in self-pity and says he has been robbed. At this, the judge pretends to be surprised. "Robbed? When I have given to you the greater possessions of your neighbor? Surely you don't believe his claim that his possessions are meager, when you yourself have just assured me that he lies and his holdings are great. As an honest man, you must admit the exchange has indeed favored you." **A Cow Testifies in Court** In our own times, courtroom justice is not always so poetic or profound. But our judges sometimes manage to come up with creative ways of getting to the truth of a dispute. On July 6, 1953, a California man named Mike Perkins was formally accused of stealing a calf from his neighbor's ranch and then branding it with his own ranch's insignia to conceal the theft. Mike stood before the judge and vehemently denied the charges, saying his neighbor had made the whole thing up out of jealousy. The judge was going to find Perkins innocent, because the only evidence against him was the other farmer's word. But then he had an idea: he sent the sheriff out to Perkins's ranch and had him bring to a yard adjacent to the courthouse all of Perkins's calves who were about the age the allegedly stolen calf was reputed to be. Then he sent the sheriff out to the accusing neighbor's ranch and had him bring to the yard the cow who was alleged to be the mother of the stolen calf. When the mother cow arrived, she began calling loudly and seemed to be trying to move toward the roped-in calves. The judge decreed that she be allowed freedom of movement. When she was let go, the cow gave her testimony to the court in no uncertain terms. She went directly over to the calves, nudged her way to one in particular, and began to lick it over and over, right on the hip, where Perkins's brand "P" was located. I probably don't have to tell you Mike Perkins was found guilty. **What They're Really Like** When I first heard what happened in this California court, I was surprised. There was an image in my mind of what cows could and couldn't do, and I wouldn't have thought this kind of thing possible. I was still, more than I knew, a prisoner of the common notion that animals are automata, with perhaps a dash of intelligence. But everything I have learned since then has shown me how wrong I was. The truth is that cows have a special kind of intelligence and sensitivity. But because they are such patient and gentle souls who rarely hurry or make a fuss about things, we tend to think they are dumb and don't recognize their unique presence. Rooted deeply in the rhythms of the earth, they move through life with a peacefulness that is not easy to disturb. They are not troubled by much of what bothers us, and when they are alarmed—usually by things we cannot see—they are still slow to panic and rarely overreact. Aldous Huxley once said that in this century we have added onto the seven original deadly sins an eighth that is just as deadly—the sin of hurry. In terms of this sin, at least, cattle are saints. Few of us today have much opportunity to experience for ourselves what kind of creature cattle are, and so we are easy prey to the common prejudices about them, which are born and thrive in ignorance. But a naturalist who knew cows well, W. H. Hudson, spoke movingly of _the gentle, large-brained, social cow, that caresses our hands and faces with her rough blue tongue, and is more like man's sister than any other non-human being—the majestic, beautiful creature with the Juno eyes._ People of less sophisticated times, living in closer contact with the earth, had great respect for these patient and gentle souls. 2,000 years ago, the poet Ovid wrote: _Oh ox, how great are thy desserts! A being without guile, harmless, simple, willing for work._ **How Now, Brown Cow?** For centuries, these animals have pulled our plows, sweetened our soils, and given their milk to our children. Today, however, these peaceful and patient creatures have been rewarded for their centuries of service by being treated in much the same way as today's chickens and pigs. You might think there are laws requiring them to be treated humanely. But harkening back to darker times, the Animal Welfare Act specifically excludes creatures intended for use as food from its regulations governing the "humane" treatment of animals. And though this law places some restrictions on how cruelly animals can be treated, cows, pigs, and chickens are evidently not considered animals within the meaning of the act. The current philosophy is that you can be as cruel as you like, as long as the animal is later going to be eaten. The result isn't very pretty. You may wonder, as I have, how the people who actually handle the animals rationalize what they do. I asked a livestock auction worker named George Kennedy if he was ever uncomfortable with the way the animals were handled. He replied: _Look, if you want beef, this is the only way you can have it. There's no room in this business for a "be nice to animals" attitude. There's work to be done, and that's all there is to it._ Later, I talked with the owner of the auction, a man named Henry F. Pace. I asked him how he felt about the charges from animal rights groups that the auctions were cruel to the cattle. He sized me up for a moment, then answered: _It doesn't bother me. We're no different from any other business. These animal rights people like to accuse us of mistreating our stock, but we believe we can be most efficient by not being emotional. We are a business, not a humane society, and our job is to sell merchandise at a profit. It's no different from selling paper clips or refrigerators._ In the eyes of the law, Henry Pace is right. There are almost no legal limits on what can be done to the animals destined for our dinner tables. A federal law, passed in 1906, does put certain basic restraints on the way cattle can be shipped by railroad. This law was passed to curb the cruelty that most of us would like to think belonged to a less enlightened time. But this law puts no restraints on the way animals can be shipped by truck, because trucks did not yet exist at the time this act was passed, and apparently the cattle industry has managed through the years to block the passage of any legislation that might extend the cow's protection to include more modern transportation. With a sharp eye for this kind of loophole, the meat industry today almost always ships cattle by truck. The journey, as you can probably guess by now, is a horror from start to finish. If you were to step inside one of these trucks you'd be immediately struck by the smell. It wouldn't take you very long to know that the ventilation is terrible. And you'd soon find out that the temperatures are scorching hot in the summer and bitterly cold in the winter. You'd see that these animals—ruminants whose stomachs function properly only with a more or less continuous supply of food—may spend as long as three days and nights without being fed or watered. One authority wrote: _It is difficult for us to imagine what this combination of fear, travel sickness, thirst, near-starvation, exhaustion, and (in winter)... severe chill feels like to the cattle. In the case of young calves, which may have gone through the stress of weaning and castration only a few days earlier, the effect is still worse._ Today's cattlemen regard it as a normal part of the business that some of the animals will die in transit. It's a calculated loss. They find it more profitable to absorb the loss due to deaths and injuries than to handle the animals differently. They fully expect to find some of the animals dead on arrival, and they calculate the loss simply as one of the costs of transporting the animals, along with the price of gasoline. Most of the deaths are caused by a form of pneumonia known quite appropriately as shipping fever. More than one animal dies of this disease for every 100 cattle that reach market. The Livestock Conservation Institute has called it the most costly animal disease in the United States today. Accordingly, livestock producers today routinely use a dangerous antibiotic called chloramphenicol to treat shipping fever. It helps keep shipping fever deaths down and profits up. The Food and Drug Administration, however, is not very happy about the use of chloramphenicol in the beef industry, and frankly, I don't blame them. _The Book of Lists #2_ has a remarkable listing titled "Nine Travesties of Modern Medical Science," which ranks chloramphenicol right along with the thalidomide tragedies and other horrors. The reason is that in a small but significant percentage of people even minute quantities of chloramphenicol cause a fatal blood disorder called aplastic anemia. Chloramphenicol has legitimate medical uses in extreme cases where human lives are at stake and no other antibiotic will work. But it is an extremely dangerous drug. Even infinitesimal amounts will kill susceptible human beings by preventing their blood marrow from producing red blood cells. And there is no way to know who is susceptible! Dr. Joseph A. Settepani, a veterinarian who works for the FDA in the area of human food safety, says amounts as low as 32 milligrams of chloramphenicol have killed human beings. This is an amount you would ingest from consuming a quarter pound of meat with a residue count of eight parts per million. Commercial beef from animals treated with chloramphenicol for shipping fever has been found to have residue counts 100 times that high. If you were to watch today's cattle being shipped, you'd see that shipping fever is only one cause of death for cattle in transit. There are other causes, too, and none of them leads to a particularly easy death for these gentle animals. You'd see cattle freeze to death in the winter. You'd see them collapse and die from heat prostration and severe dehydration in summer. You'd see them suffocate when other animals pile on top of them as the overcrowded trucks go around curves. If you were on hand when the animals arrive at their destination you'd see that those who survive the journey are not in the best of shape, either. Not only may they have contracted shipping fever, but they have suffered a great deal of bruising and may be crippled from the pounding they have taken. Incidentally, the trade definition of a "cripple" is _an animal that must be carried or dragged from the vehicle._ In other words, an animal that can manage to limp along even though its legs are mangled and broken is not a cripple. By the same token, an animal is not considered officially bruised unless its injuries are so bad its flesh must be condemned as unsuitable for human consumption. Apparently bruising counts only when it affects the pocketbook. **Home Sweet Home?** For the animals who survive the journey, arrival does not immediately signify it's time to relax and enjoy life again. Exhausted, depleted, and ill, bewildered by the harsh handling they have received, these peace-loving creatures may be welcomed to their new home by being dipped in a trough full of insecticides. Then they may be castrated, de-horned, branded, and injected with various chemicals. All in all, it's a little less than the ideal homecoming. Castration is the removal of the testicles of a bull in order to produce a steer and is an extremely painful process for the animals to undergo. I had thought it was done to produce more docile, easier-to-handle animals, and this is, in fact, one of the reasons for the operation. But the main reason is that steers have a higher percentage of body fat than bulls, and the industry grades meats according to fat content, with the most expensive grades being those with the most fat marbled through the flesh, where it cannot be trimmed off. To a meat producer, that's sufficient reason to inflict any degree of pain. Castrated animals have more fat and so fetch a higher price. Removing the testicles of a bull substantially reduces its natural hormone production. But this presents no problem to today's cattlemen. The steers are simply implanted with synthetic hormones to offset the natural hormone deficiencies caused by castration. The fact that these synthetic hormones may produce carcinogenic residues in the meat from these animals is rarely seen by the industry as anything other than a public relations issue. "Castration is a beastly business, even to the hardened pig man," wrote the British trade journal _Pig Farming_. I can't help but wonder, if it's so difficult for the hardened pig men, how bad it must be on the pig or bull itself. And if it's so beastly in Britain, where anesthetics by law must be used, how much worse is it in the United States, where there is no such legislation and painkillers are rarely used. The farmers who actually do the work know what is involved. A California cattleman, Herb Silverman, told me: _I hate castrating them. It's really horrible. After you put the ring on its scrotum the calf will lie down and kick and wring its tail for half an hour or more, before the scrotum finally goes numb. It's obviously in agony. Then it takes about a month before its balls fall off. You can do it faster with a special kind of pliers, but I can't bear to use those because I can't take how they carry on._ By nature the most mellow and easygoing of animals, cattle do not usually become riled unless a great deal of pain has been systematically applied to get them upset. If you have been to a modern rodeo, with events like bull riding and steer wrestling, you've seen what appear to be vicious, mean, and ornery animals. You've heard them described by the rodeo announcers as "rampaging brute fury" or some other term designed to make you tremble in your seat. And though you may have felt the carnival atmosphere of the proceedings, and sensed that their meanness was in some way hyped-up, you probably didn't know to what extreme measures rodeo personnel have to resort to make these animals—placid by nature—into a living picture of fury and agitation. To this end, they fit an animal with a flanking strap, which causes him immense pain and from which he does everything in his power to gain release. He bucks not because he is a wild and furious beast but because an excruciatingly painful strap has been cinched, tightly, in the areas of his genitals and intestines. Sometimes a nail, tack, piece of barbed wire, or other sharp metal object has been placed under the strap, to further infuriate him. And just before the animal is let out of the chute, an electric prod known in the trade as the "hot shot," is applied to his rectum, all to provoke this gentle animal into dashing madly into the arena, to put on an "exciting" exhibition that is really nothing but the poor fellow's pain and panic. Cattlemen acknowledge that except in extremely crowded conditions there is no need to de-horn cattle, because these peaceful animals will not hurt one another unless they are crammed so tightly together that they cannot help it. And cattlemen also know the process is extremely painful to the animals, often resulting in hemorrhage, maggot infestations, and infections. But today's cattle are routinely de-horned because today's cattle feedlots, where the great majority of today's cattle spend the last half of their lives, are unbelievably overcrowded. And they are not likely to become less crowded in the foreseeable future. The trend is toward ever-increasing crowding, known in the jargon of the trade as "stock density." Studies at the University of Minnesota suggest maximum profits can be obtained by allowing each of these large animals 14 square feet of living space. To realize what this means, consider that a typical 12-by-15-foot bedroom is 180 square feet. Imagine 13 half-ton steers in your bedroom and you've got the picture. **The Pharmaceutical Farm** Most of us, with images in our minds of the cows of yesteryear, can hardly believe the extent to which the meat industry today relies on chemicals, hormones, antibiotics, and a plethora of other drugs. It is a business, and a very competitive one. Even the small cattlemen are eager to use anything the drug companies can convince them will make their work easier, make their animals gain weight faster, or enable them to mask the signs of disease and gross stress in their animals so they can be sold to the slaughterhouse—anything to give them an edge in the marketplace. I asked cattleman Herb Silverman how he felt about the high levels of drugs fed to today's cattle. He replied: _It's not good. Instead of improving husbandry practices, which would make the animals healthier, we just shoot 'em up with drugs. It's cheaper that way, and because this is a competitive business I've got to do it, too. But in the meantime the general public is catching on and getting afraid of residues in the meat. And I'll tell you something. I don't blame them._ The avalanche of drug usage has occurred in the past 20 to 30 years, coincidental with the shift in production methods from range grazing to feedlots. Before 1950, almost all the nation's cattle spent their lives grazing and foraging for their food in something like the wide-open spaces most of us picture as cattle country. But no more. By the early 1970s, three-quarters of U.S. cattle were trucked off to spend half their lives in feedlots. Some of the larger feedlots have as many as 100,000 "units." Here the animals are fed a diet designed for one purpose only—to fatten them up as cheaply as possible. This may include such delicacies as sawdust laced with ammonia and feathers, shredded newspaper (complete with all the colors of toxic ink from the Sunday comics and advertising circulars), "plastic hay," processed sewage, inedible tallow and grease, poultry litter, cement dust, and cardboard scraps, not to mention the insecticides, antibiotics, and hormones. Artificial flavors and aromas are added to trick the poor animals into eating the stuff. Meanwhile, scientists at the University of Arizona are studying the biological processes that curb a cow's appetite. Their reason? _Obviously, if the thing that turns a beef animal away from the feed bunk were found, and could be overcome, it would mean a lot._ It sure would, because the whole idea is to make them as fat as possible as cheaply as possible. The massive agribusiness conglomerates that own the feedlots are very excited about the prospect of having chemicals that would give these placid animals insatiable appetites. The industry recognizes that major health problems ensue from the way today's cattle are fed. But it doesn't matter to them if the animal is ill, even if the illness is so severe it is dying, so long as it can be kept alive with drugs long enough to be slaughtered and sold to the consumer. **Milk from Contented Cows?** If life in today's feedlots isn't the greatest thing that could ever happen to a cow, neither is life in a modern milk factory. The trouble seems to stem from the modern cow's insistence in asserting her fundamental nature. She still wants to do what cows have always done: devotedly care for her young, quietly forage and ruminate, and patiently live with the rhythms of the earth. Such outdated ideas, of course, put her at cross-purposes with an industry that looks upon her as a four-legged milk pump, a machine whose purpose is to provide milk for profit. She is bred, fed, medicated, inseminated, and manipulated to a single purpose—maximum milk production at minimum cost. The industry points today with considerable pride to the fact that the average commercial cow now gives three or more times as much milk in a year as her bucolic ancestors. They don't mention that her udder is so large that her calves would have a hard time suckling from it and might easily damage it if they were allowed to try. Nor do they mention that under natural conditions Old Bessie would live 20 to 25 years. In the unbelievably stressful world of today's dairy factories, however, she is so severely exploited that she will be lucky if she sees her fourth birthday. Old Bessie may spend her whole life in a concrete stall or, worse yet for her legs and feet, on a slatted metal floor. She is pregnant all the time, and her nervous system has been made so ragged by breeding practices devoted exclusively to milk production and a lifestyle that affords her no exercise that this most mellow and patient of animals has become something else. She is today so tense, nervous, and hyperactive that she often has to be given tranquilizers. If Old Bessie lives in a factory that brings portable milking machines to the cows, she may remain for months in her cramped, narrow stall, chained at the neck. On the other hand, she may call home the type of dairy factory that wishes her to come to the milking apparatus. One method for transporting Old Bessie to the equipment has been designed by Alfa-Laval, a Swedish agricultural company. _Each cow is placed in a contraption called "Unicar" which is a kind of cage on wheels that moves along a railway line. The cages, with cows in them, spend most of their time filed in rows in a storage barn. Two or three times a day, the farmer pushes a button in the milking parlor. Rows of cows then move automatically up to the milking parlor like a long train. As they go, their car wheels trip switches which feed, water, and clean the cars. After milking, the cows, still in the cages, roll back to the storage area. The cows live in the cages for ten months of the year, during which time they are unable to walk or turn around._ Today's dairy cows are commonly implanted with hormones to promote milk production, but after a while, under these conditions, their output inevitably drops. Then it is time for Old Bessie, exhausted and depleted, to climb into the truck for one last journey. **Her Babies** Old Bessie never knows what becomes of the babies who are taken from her at birth. And it is probably a good thing she doesn't. For the most part, her daughters are raised to follow in her hoof-steps. But her sons, the little boy calves, cannot be converted into four-legged milk pumps. So another fate lies in store for them. These little fellows are sent to auctions when they are all of a day old. There, bewildered and terrified, barely able to stand, their umbilical cords still attached, they are purchased to be "made" into veal, a process that takes about four months. It is a process which to my eyes may be the most obscene of all the cruelties I've seen in modern animal factories. Anyone who has struggled with young calves, perhaps striving to teach them to drink milk from a bucket, knows how strong, wayward, and vital these creatures can be. They suck at a finger pushed into their mouth, gulp the milk, toss their head, tug at whatever they can. Young calves are playful and exuberant, with a powerful desire to frolic. Newborn, they are utterly vulnerable, and their eyes are beautiful with a special kind of innocence and awe. But in today's dairy factories these little fellows are placed onto a veal production assembly-line within hours of their births. Most meat eaters think the pale, tender flesh they eat comes from a particular type of calf, bred for veal. But this is not so. It comes from the male calves born to dairy cows. **The Latest Thing in Veal** In a hotel room I stayed in recently there was a menu for the hotel restaurant. In the tradition of fine dining to which this hotel aspired there were three specialties of the house featured. These were all veal dishes—veal scallopini, veal Oscar, and veal piccata. Veal dishes are expensive and sound very high-class. With an Italian name, they bring to mind the haute cuisine of continental Europe. Few people know that in the past few decades there has been a revolution in the world of veal. Chef James Beard wrote in _American Cookery_ : _Good veal has always been difficult to find. But recently a Dutch process has come to our shores and is giving us a limited quantity of much finer veal than was generally available before...The calves...have delicate whitish-pink flesh and clear fat and are deliciously tender._ —JAMES BEARD, _A MERICAN COOKERY_ There is a secret to how this new Dutch process manages to provide veal that is so "delicate whitish-pink" and so "deliciously tender." Learning about this secret has changed me, forever. The veal that has traditionally been prized by gourmets is whitish, and its tender texture comes from muscles that have never been used. This veal has come from the flesh of a baby calf that has consumed only its mother's milk. Since calves normally start nibbling grass and other solid food within a few days of their birth, it doesn't take very long before their flesh, whitish when they are born, begins to turn pink. Veal was prized in Europe because of the very fact that it was a rare and expensive commodity. But then came the revolutionary thinking that originated in Holland after World War II and was brought to America by Provimi, Inc. of Watertown, Wisconsin. Provimi proudly takes credit for developing this "new and complete concept of veal raising," which totally dominates the industry today. But as we shall soon see, it's not something I'd be all that proud about. Traditionally, the veal calf had to be slaughtered shortly after his birth, before his flesh acquired color, which meant before he exercised and developed muscles, and before he ate anything besides his mother's milk. Traditionally, veal calves were slaughtered at about 150 pounds, which isn't much more than their birth weight. But the Provimi method enables much more profit to be obtained from each calf by keeping the calves' flesh white and tender up to a weight of 350 pounds. Fattening baby calves while keeping their flesh white and their muscles undeveloped is the heart of the Provimi method. First of all, the calf is taken away from his mother immediately after birth. Veal producers are aware that this deprives the infant calf of the colostrum in its mother's milk and so renders the little one very susceptible to disease. But they separate mother and child at birth anyway, because the large udder of today's dairy cow can be damaged by suckling, and the cow will produce more milk if attached to a machine. Additionally, according to Dr. Jack Albright, professor of animal science at Purdue University and consultant to the veal industry, it is important that the calf not bond with his mother, as he would if she nursed him. If the calves are taken away from their mothers after this bond develops, the cows will cause a great deal of trouble and even try to break down fences to be with their calves. The newborn calves are taken to veal sheds and placed in what are euphemistically called stalls. These stalls will be their homes until they are slaughtered at the age of four months, unless, of course, they die first. A high percentage are not able to survive even four months, so horrid are the conditions. The stalls have been designed to keep the calves' flesh "tender enough to be used for baby food." If the calves were let outside, or even kept in a pen, their frisky nature would lead them to romp around and they would soon develop muscles. This, of course, must not happen. So the infant calves are shut tightly in their stalls and allowed no exercise whatsoever, right from the start. Every year, one million newborn calves are shut up in such stalls in the United States, to be raised for veal. These youngsters not only never have a chance to romp or play; they never even walk! Remember these are babies, only a day or so old, cut off from their mothers and imprisoned in this way. The newborns are isolated in stalls all of 22 inches wide and 54 inches long—far less than the space that can be found in the trunk of the smallest cars. The stalls are so tiny the animals can hardly move. They are so narrow that in order to lie down the calves must hunch into a position no cow ever normally assumes. They cannot stretch out into their natural sleeping posture. They cannot turn around. Chained around the neck, the baby calves cannot even twist their heads to lick and groom themselves with their tongues, though this is one of their most basic and innate desires. They can move only a few inches back and forth and side to side. Their stall is as cramped as a shipping crate. As the days pass, and the calves grow, they become even more cramped, so that any movement at all becomes nearly impossible. **The Real Meaning of "Special-Fed"** Keeping infant calves confined to stalls so small they cannot take a single step is Provimi's ingenious method of preventing any muscular development in the calves, and so keeping their flesh "tender enough for baby food." In order to keep the flesh the whitish-pink color traditionally associated with prize veal, Provimi has come up with another macabre idea, creating the diet that accounts for the names "special-fed veal" and "milk-fed veal." Provimi is proud of developing this "special" diet, which can bring the calves to a weight of 350 pounds yet retain the whiteness of flesh of the newborn infant. When I first heard the phrase "special-fed veal," I got an image of something fancy. Knowing that veal is an expensive "delicacy" supposedly associated with "fine Continental cuisine," I surmised that "special-fed" veal calves must receive a diet that is better in some way, and probably more expensive, than that of normal calves. I supposed that "special-fed" calves were probably extremely healthy. I had the idea they were in some way the cream of the crop. I was wrong. The special diet fed these calves achieves its objective, which is to keep the calves' flesh white, by systematically inducing anemia in the young animals. It is a diet that is deliberately and profoundly iron deficient. Calves are born with stores of iron in their bodies, primarily in the form of extra hemoglobin in the blood, with lesser amounts stored in the liver, spleen, and bone marrow. During the four months the veal calf is confined and "special fed," these reserves decline steadily. The veal producers are pleased to have achieved their objective: the calves' flesh remains white while they put on weight. Producers would like to take the calves to even heavier weights, but by the time four months have passed and they have reached about 350 pounds, the calves have become so seriously anemic that those still alive would soon die in their stalls. Deliberately deprived of iron, the little calves develop an insatiable craving for the mineral. They lick any iron fittings in their stalls in a desperate effort to obtain some iron, but today's vealers are not ones to be outsmarted by such maneuvers. Provimi tells its producers: _The main reason for using hardwood instead of metal boxstalls is that metal may affect the light veal color...Keep all iron out of reach of your calves._ Vealers are also cautioned to make sure the calves have no access to rusty nails or any other kind of metal they might lick. No straw or other bedding material is provided, because in the calf's craving for iron, he would eat it. Producers are told to test the iron level in the water used to mix the animals' feed, and not to hesitate to use an iron filter. All possible sources of iron must be kept from the young calves. This is one of the reasons why the stalls are so narrow and the calves are chained around the neck. The results of this treatment are not pleasant. For example, calves, like pigs, will normally not go near their own manure or urine. But because their urine does contain tiny amounts of iron, the calves, in their desperate natural craving for this nutrient, would, if they could, lick the floor where their urine fell. Veal producers, however, are not about to let the baby calves get away with something like that. Accordingly, they have arranged it so the calves cannot turn around and get even the little bit of iron they might obtain in this pitiful way. With their mothers, baby calves would suckle an average of 16 times a day. Sucking is perhaps their strongest and most essential instinct and need. Deprived not only of their mothers but of any conceivable source of stimulation and interest, the little baby calves crave something to suck on. Their urge is strong to begin with and becomes absolutely ravenous when they are deprived of any opportunity to do so. The result is that they frantically try to suck some part of their stall. But once again the superior intelligence of the veal producers has the upper hand. They have carefully planned the stalls so there is nothing at all for the calves to suck on. If you move close to a veal calf's head, he will try frantically to suck on your hand or your elbow or your shirt or your purse or your umbrella or anything at all he can reach. It is hard to avoid feeling that these calves in bondage are not veal machines but ill little babies, desperately craving what might heal their disease. **Aces up Their Sleeves** It is difficult to imagine how conditions could be made any worse for the wretched animals. Yet today's veal producers have a few other aces up their sleeves that increase the profits they can make from their "units." One of these is to give the calves no water. This way the calves must try to quench their thirst by consuming the only source of liquid they have, the government-surplus-skim-milk-and-fat mixture they are fed. This clever tactic forces them to consume far more of the stuff than they otherwise would and so put on weight out of their desire to avoid dying of thirst. Many of today's veal calves are also exposed to a final insult: they are forced to live in complete darkness except for their two daily feedings. The producers are delighted with this maneuver, seeing it as an effective way to put more fat on the animals. They are not at all disturbed that, under these conditions, many of the calves go blind. There is some indication, however, that the calves themselves are not all that pleased with the situation, as they quite frequently express their displeasure by dying shortly after losing their sight. **A Picture of Health?** Though the special diet the little calves are fed is supposed to keep them alive, the steadily worsening anemia makes the animals extremely susceptible to pneumonia and enteric diseases. Even dosed with a massive and constant supply of antibiotics and other drugs, many of the animals don't survive the four months. Authorities on contemporary veal production say the calves _get sick despite the precautions and must be treated frequently with drugs by mouth and injection. Two of the four most common drugs used are nitrofurazone and chloramphenicol._ Nitrofurazone is a recognized carcinogen. And chloramphenicol, as you may remember from the discussion of shipping fever, causes a fatal blood disorder in a significant percentage of humans, even in infinitesimal concentrations. Such dangerous drugs must be used to keep the little calves alive because the animals are so extremely unwell, and safer medications are not strong enough. The Farm Animals Concern Trust (FACT) is an organization trying to improve the lot of today's veal calves. In one of their mailers, they made the following charges against the industry. _Veal calves are:_ • _denied sufficient mother's milk_ • _trucked to auctions when only a day or two old_ • _commingled with sick and dying animals_ • _sold to veal factories where they are chained for life in individual crates only 22 inches wide_ • _fed government surplus skim milk_ • _denied solid food to chew on_ • _made anemic_ • _kept in the dark to reduce their restlessness_ • _plagued by respiratory and intestinal disease_ • _unable to lie down normally_ • _deprived of any bedding_ • _unable to walk at all, let alone romp and play._ A veal producer got hold of the mailer but didn't know how to counter the statements it made. So he sent the mailer to the editor of the industry's journal requesting an effective rebuttal from the industry experts. The editor of _The Vealer USA,_ a man named Charles A. Hirschy, looked over the charges made by the FACT mailer and then answered as follows. _Thank you for the information about FACT. We've read the information and regret that we are unable to counter their statements._ FACT has developed a new husbandry method for raising nonanemic veal calves outdoors on pasture. As yet this far more humane method of raising veal calves is followed by only a few farms. But if you see veal marked RAMBLING ROSE BRAND™, you can trust it was not raised by the Provimi method. **A Wolf in Sheep's Clothing** The Humane Society of the United States does not normally concern itself with animals being raised for food. But it has sponsored a "No Veal This Meal" campaign in an effort to educate the public to the darker side of this white "gourmet" meat. It also printed "No Veal" cards and is asking people to leave them in restaurants. The cards read: "Dear Restaurateur, I enjoyed my meal here, but I did not choose a veal entree because I believe milk-fed veal is inhumanely raised. I would prefer it if you did not offer this veal on your menu." The Humane Society is not alone in expressing its opposition to contemporary veal-raising practices. The American Society for the Prevention of Cruelty to Animals chose the veal calf as its 1987 Animal of the Year, to bring attention to the cruelties inflicted upon animals raised for food. At the same time, the Humane Farming Association, which is spearheading a campaign against the abuses of factory farming, is coordinating nationwide veal boycott demonstrations in front of restaurants and other establishments that continue to sell anemic veal. These actions have generated nationwide media coverage and informed the public about the real story behind today's veal. As a result, a number of restaurants have stopped selling the product. Furthermore, the Humane Farming Association has introduced legislation to outlaw the practice of raising veal calves in crates. This is the first legislation that would protect farm animals from intense confinement and immobilization. Provimi Inc., whose name is practically synonymous with the veal industry in the United States today, has not been unaffected by the pleas that veal calves be treated humanely. Their response has been to call upon the "farm" community to boycott the Humane Society. And they have pledged $200,000 to fight the "No Veal" campaign. Meanwhile, the American Veal Association, alarmed at the rising tide of public opposition to veal production practices, has taken a step to quell the objections, though it does not seem likely to improve the fate of today's veal calves. They have hired a public relations firm to improve their public image—Jackson, Jackson, and Wagner. For a number of years, the industry has had an organization called the Coalition for Animal Agriculture, whose specific duty it has been to defend factory farming and present it to the public in a positive light. Losing a bit of ground as of late due to the Humane Society campaign and the work of many other dedicated individuals and groups concerned for the welfare of animals, the Coalition for Animal Agriculture has come up with a brilliant move. It has changed its name to the Farm Animal Welfare Council and now presents itself to the public as an organization devoted solely to the welfare of the animals. The treasurer of the Farm Animal Welfare Council is a vice president of Provimi Inc. In another ploy, John Mahlman, sales manager for Provimi, defended the veal industry by saying: "What we are talking about here is world hunger." Unfortunately, he did not exactly explain the relationship between anemic veal, at $9 to $14 a pound, and world hunger. Despite such maneuvers to whitewash the veal industry, major TV news shows are beginning to get wind of what's going on and investigate. KARE-TV in Minneapolis and KRON-TV in San Francisco both recently did programs presenting the results of their inquiries. The programs did not please the veal industry apologists, bearing titles such as "Misery on the Menu," and "Unpalatable Treatment." The reports naturally included interviews with the vealers themselves, and these, to my mind at least, proved the old adage in favor of free speech: "The best thing to do in the case of a fool is to encourage him to advertise that fact by speaking." One vealer, a man named Marv Pratt, said to the television audience of his veal calves: "Hey, they live like kings!" **Never Before** Today's veal producers are not alone in their crimes. They are only a particularly blatant and grotesque example of an industry run amok. All of today's food animals—the proud and passionate chickens, the friendly and steadfast pigs, the gentle-hearted cows—are treated in a manner that would, I believe, sicken any open-hearted person who had eyes to see what was actually happening. Throughout history there have been people who have chosen to be vegetarians because they did not feel it was right to kill animals for food when this was not necessary, when there was other nourishing food available. But today, because of the way animals are raised for market, the question of whether or not to eat meat has a whole new meaning, and a whole new urgency. Never before have animals been treated like this. Never before has such deep, unrelenting, and systematic cruelty been mass-produced. Never before has the decision of each individual been so important. 5. **ANY WAY YOU SLICE IT, IT'S STILL BOLOGNA** _A missionary was walking in Africa when he heard the ominous padding of a lion behind him. "Oh Lord," prayed the missionary, "grant in Thy goodness that the lion walking behind me is a good Christian lion." And then, in the silence that followed, the missionary heard the lion praying too: "Oh Lord," he prayed, "we thank Thee for the food which we are about to receive."_ —CLEVELAND AMORY _Custom will reconcile people to any atrocity._ —GEORGE BERNARD SHAW It has often been pointed out that there were many good-thinking and decent Germans who listened to Adolf Hitler as he rose to power, knew him for what he was, and yet did nothing. They sensed that his campaign rhetoric masked an insatiable drive for power that would stop at nothing to achieve its ends. But they stood silently by and watched the Nazis take over, because they were afraid to open their mouths. One man who did open his mouth was Edgar Kupfer, and he paid dearly for trying to awaken a sense of conscience in his countrymen. Kupfer was imprisoned in the concentration camp at Dachau during World War II. His crime? He was a pacifist. In this hell of hells, Edgar Kupfer managed to steal scraps of paper and bits of pencils. Stealthily, he kept a diary. Between the few precious moments when he was able to write in his diary, Kupfer kept his secret work buried underground. He knew what would happen if the Nazis found it. On April 29, 1945, Dachau was liberated. Edgar Kupfer was free. And so were his buried diaries. The _Dachau Diaries_ of Edgar Kupfer are now preserved in a Special Collection of the Library of the University of Chicago. In one of his essays, called "Animals, My Brethren," Kupfer wrote: _The following pages were written in the Concentration Camp in Dachau, in the midst of all kinds of cruelties. They were furtively scrawled in a hospital barrack where I stayed during my illness, in a time when Death grasped day by day after us, when we lost twelve thousand within four and a half months..._ _You asked me why I do not eat meat and you are wondering at the reasons of my behavior... I refuse to eat animals because I cannot nourish myself by the sufferings and by the death of other creatures. I refuse to do so, because I suffered so painfully myself that I can feel the pains of others by recalling my own sufferings..._ _I am not preaching... I am writing this letter to you, to an already awakened individual who rationally controls his impulses, who feels responsible, internally and externally, for his acts, who knows that our supreme court is sitting in our conscience..._ _I have not the intention to point out with my finger... I think it is much more my duty to stir up my own conscience..._ _That is the point: I want to grow up into a better world where a higher law grants more happiness, in a new world where God's commandment reigns: You shall love each other._ Edgar Kupfer had seen enough of the opposite to want to live in a world where love would reign. May his prayers be granted. After the war, Kupfer moved to Chicago. There is a sad irony here, because for years Chicago was the central slaughterhouse of the United States, and it is still the location for the killing of millions of animals every year. But what was once the hub of Chicago's animal slaughter industry, the notorious Union Stockyards, is now closed. All that is left of it is the entrance gate, designated a historic landmark by Mayor Daley. Poignantly, this gate is said to "very closely resemble" the gate marking the entrance to the concentration camp in Dachau. During the war, millions of Germans knew vaguely that Jews, Gypsies, and pacifists like Edgar Kupfer were being sent to places like Auschwitz and Dachau. But they didn't know the immensity of the horror that was done in these places. And most of them, it must be admitted, preferred not to know. In fact, when a few brave souls like Edgar Kupfer tried to tell them, these valiant voices were often silenced for their efforts, for trying to awaken some vestige of dormant humanity in the German psyche. A web of repression permeated the time, a collective determination to avoid the immense pain that would have come from really seeing what was happening. In conquered countries as well, the psychic numbing took place. While there were always some people who resisted, who did what they could to save the lives of those hunted by the Nazis, often risking their own lives in so doing, most others tried to ignore the horrors, tried to keep a stiff upper lip and pretend nothing amiss was happening. Though it was hard to avoid knowing at least part of the horrid truth, they found ways of blocking the impact. They busied themselves with other matters, conjured up rationalizations, narrowed their awareness, and looked the other way. Today, the process of denial is once again rampant. We all know at some level today that our world is in great peril. We all sense the ever-present threat of nuclear war, the increasingly rapid destruction of our life-support system, and the growing misery of half the planet's people. We are continuously bombarded by signals of profound planetary anguish, some of which, whether we know it or not, come from the factory farms and slaughterhouses. Often it seems too painful to even think about, so we block it out. We tend to deny the pain we feel because it hurts so deeply, and because it can be so frightening. Yet the more we succeed in numbing ourselves to our deepest human responses, the more powerless, futile, and isolated we feel. The more we avoid our pain for the world, the more disconnected we become, and we repress our own painful feelings by filtering out the information that provokes them. Yet this is the very information, painful though it may be, that cries out for our response. Only by facing the enormity of what is happening can we discover in ourselves the response that will free us from creating such needless horrors and at the same time free the animals from such needless pain. _Each act of denial, conscious or unconscious, is an abdication of our power to respond._ —JOANNA MACY The healing that is called for asks us to move beyond denial, to acknowledge and express our feelings about these catastrophes without apology or timidity. In the heart of our grief we can find our connection with one another, and the power to act. As I've learned what is done to animals today, again and again I have had to face my own tendencies to withdraw and go numb. There have been times I felt so overcome with grief and rage that I doubted whether there was any point in continuing to unearth the seemingly endless parade of cruelties. There have been times I seemed to want, with every cell of my body, to forget I had ever heard of a factory farm. But in my willingness to face the immensity of what is actually happening, something just as immense has welled up from the depths of my humanity. A power has arisen in response to the horrors; a power that has transformed isolation, indifference, and passivity into a commitment to exposing this madness for what it is. **Phony Bologna** There are powerful interests today who are profiting from the web of repression about modern farming. It is to their advantage that we not know too much about or be too interested in what goes on in factory farms and slaughterhouses. They don't want us to know what actually happens to the animals whose flesh they sell. These people are particularly interested in "protecting" young children from the truth. Children aren't as quick to rationalize and numb themselves as adults are. The least repressed among us, they are also the most impressionable. So those who profit from our collective denial go out of their way to make sure our children receive heavily sugar-coated pictures of animal farming. The seeds of denial are thus planted early and deep. The National Livestock and Meat Board makes it a point to "reach the children of the land at an early age" and "prepare them for a lifetime of meateating." As they put it in their 1974–1975 report: _The 37 million elementary and 15 million high school students in the United States constitute a special Meat Board audience._ By calling our country's children a "special Meat Board audience" they are not expressing a particularly noble interest in the education of our youngsters. Consider the pictures on page 108, taken from what are called "educational coloring books" for children. These coloring books reassure us that they are "factual stories," approved in one case by the American Egg Board and in the other by the National Dairy Council and Milk Industry Foundation. Such nice pictures, aren't they? So sweet and wholesome and appealing. I just wish they were true. Pictures like these of the lives of chickens and cows are perhaps similar to the ones you carried in your mind before finding out otherwise. Such was certainly the case for me. Similarly, the American Meat Institute also distributes "educational materials" to thousands of schools. One such title is _The Story of Beef_ (see page 109). You might notice something missing from this fairy tale, however: there is no trace of the animal suffering in any way at any time. At first the calf is shown romping innocently alongside his happy mother; next we see him looking like the very picture of sunshine and cheer in a feedlot; then we see him being happily shipped to the stockyards; and finally we see him evidently delighted as can be as different companies bid for the right to kill him. The lucky creature, it would seem, is tickled pink at every step of the path to the meat counter. Other "educational materials" paint equally contrived versions of the animal's experience. In _The Story of Pork,_ children are shown a pig smiling delightedly all the way until he is "made into eating meat." The manager of the California Beef Council says that about 800 junior and senior high schools in California, about half of the public schools in the state, receive the Beef Council's consumer information program. In a given year, he says, about half a million pieces of literature are distributed in California high schools alone. Over 1,000 teachers are sent "beef teaching manuals, lesson plans, charts, and other such material." At last the special day has come, She is so very proud, As she looks down at her very first egg She clucks and clucks so loud. _It is usually only a few days after she is in the laying house that she lays her first egg. Chickens do actually "cluck" or "sing" after laying an egg... it really seems to make them happy. Incidentally, there are no roosters (male birds) in these laying houses. The hen just lays eggs naturally. The rooster is required for a fertile or hatching egg._ The cow now goes with many others To the pasture to drink water and eat grass. Some may stop at the salt box To take a lick of salt as they pass. _In the summer the cows are turned out to pasture to eat grass. The dairy farmer keeps a salt box in the pasture because cows need salt. Cows also need a lot of water. It is important in helping them to digest food and to make milk. Water also helps to keep the cow cool in the summer. She may drink as much as twenty gallons of water a day._ "Educational" coloring books for children, described as "factual story approved by The American Egg Board" and "factual story reviewed by The National Dairy Council and Milk Industry Foundation." Copyright 1975 and copyright 1976, Know-About Publications Inc., Harrisburg, PA. Before you have a steak (whether it's porterhouse or chopped), a cow has to have a calf. This is the story of one particular calf. **1.** This calf was born on a Texas ranch. Several acres of grazing land are required to support each cow and calf. **2.** As a yearling, the calf was sold to an Iowa farmer for "finishing" in feed lot. Proper feeding of corn and protein supplements adds many extra pounds and a lot of extra eating quality to our beef. **3.** After several months in the feed lot, our calf, now a full-grown steer, was sent by rail or truck to the stockyards and consigned to a marketing firm for sale. **4.** Buyers for several local and out-of-town meat packing companies put in bids based on the going consumer price of beef. This steer was one of a carload bought by an Ohio meat packing company. **5.** At the packing plant, the "beef crew" turned beef on the hoof into meat for the store. Beef was inspected, chilled and graded, prepared for shipment. **6.** Under refrigeration, the quarters of beef were shipped to New York's wholesale meat district — 1500 miles from Texas, where the calf was born. **7.** Owner of a Brooklyn meat market, after comparing prices and quality, selected a quarter of our steer. **8.** In the store, a quarter of beef was turned into steaks, roasts, stew, and hamburger; was displayed for customer's selection competing with other meats. **9.** Yesterday, a housewife looked over everything in the counter, compared values, decided on steak, porterhouse or chopped, depending on what she wanted to spend. Source: From _The Story of Beef,_ The American Meat Institute (Chicago). Proudly, the manager of the Beef Council of California announces: _We have established ourselves as a responsible and unbiased source of information on beef and the beef industry._ It is amazing to me that the California Beef Council wants us to believe it is unbiased, given that it is an organization whose sole purpose is to promote the sale of beef. I'd be very surprised, for example, if the Beef Council ever arranged for schoolchildren to take a field trip to a factory farm or a slaughterhouse. None of these educational materials allow a child to ever guess anything resembling the truth about how animals are kept today in the factory farms. Nor would they guess that chickens, pigs, and cows are killed by human hands to provide meat. That meat is actually the flesh of an animal is a fact that is systematically overlooked. Words like "killed" and "slaughtered" are not used—words that, while hardly doing justice to the gruesomeness of the actual process, are at least accurate labels for what is done. Instead there appear euphemisms like "dispatched," "processed," "turned beef on the hoof into meat for the store," and "turn the pig into eating meat." Children are taught to overlook the fact that hamburger meat is ground-up cow. McDonald's, the multinational hamburger chain, has spent many millions of dollars on an advertising campaign targeted at youngsters that presents a rather unique version of reality. Obviously feeling that little things like the truth are unimportant when talking to children, they have produced a series of commercials in which a lovable clown named Ronald McDonald tells his impressionable young audience that hamburgers grow in hamburger patches. (Incidentally, the man who played the part of Ronald McDonald, Jeff Juliano, has evidently discovered that hamburgers do not actually grow in hamburger patches. He is now a vegetarian.) Most children love animals, and those who happen to learn the truth about meat are often abhorred. But they are usually "protected" from such a moment of truth. How can children see through the veil when their teacher passes out a booklet like _Hooray for the Hot Dog,_ distributed free to schools, as "nutritional education," by Oscar Mayer? The picture children receive about meat is a sugar-coated lie, only it's not that innocent. The Oscar Mayer meat company is very proud of its efforts to reach young schoolchildren. I remember the fun I had as a child when the Oscar Mayer Wienermobile came around. We had a great time and were given bits of sausage and bacon to eat after being entertained. With all the festivities, however, we had no idea we were being indoctrinated. I remember singing the company jingle which I had heard so many times on TV: _Oh I wish I were an Oscar Mayer wiener, For that is what I'd really like to be. For if I were an Oscar Mayer wiener, Everyone would be in love with me._ This theme song was for many years the heart of a campaign of national network television advertising aimed at America's youth. It was sung in the ads by a happy choir of children, and as a child hearing and singing along with the ditty, I, too, felt happy. Of course, I didn't have anything approaching the sophistication to question what was happening, so how could I have known this happy little song had within it an obscene lie? You see, the song produces in its young audience the belief that by eating Oscar Mayer wieners they are actually "loving" the animals who seem to be singing with eagerness to become wieners. _If we believe absurdities, we shall commit atrocities._ —VOLTAIRE Today, Oscar Mayer distributes what they call "nutritional education" materials to schools throughout the country. These include an elaborate presentation of the "I Wish I Were an Oscar Mayer Wiener" song, complete with lyrics, musical notation, and chords. Their suggestion is that school children sing the song at a march tempo. In their more recent ads aimed at children, a band of happy youngsters are shown eating bologna and gaily singing, "My Bologna Has a First Name." Again the effect is produced of delighted animals offering themselves to children as friendly things to eat. The National Dairy Council distributes a 16 mm sound and color film to schools titled _Uncle Jim's Dairy Farm: A Summer Visit with Aunt Helen and Uncle Jim._ It all sounds so sweet and wholesome. The picture children get of a modern dairy farm, however, is far indeed from the reality. It reminds me of a major advertising campaign for a dairy in which a human voice pretending to be a cow says "Us cows do our best for Jerseymaid." As if the cows were so touched by the loving way they are treated that their milk is a natural expression of their gratitude. In another ad, a deep male voice tells us that a particular company's milk comes from contented cows. Maybe they are referring to the tranquilizers these most placid of all animals must sometimes be given. **Any Way You Slice It, It's Still Bologna** From our earliest years in this culture we've been taught a cotton candy version of what happens to food animals. We have been taught to repress the bloody truth. We've worn our blinders for so long that it is hard to see them for what they are, particularly when our parents most likely wore them as well, and the culture as a whole takes such repression completely for granted. I have seen egg cartons with pictures of smiling hens. The message is that these birds are pleased as punch with the whole situation and lend their blessings and radiant happiness to our consumption of their eggs. Frankly, I have to wonder how the chickens would feel about this—the real-life birds who are crammed into wire cages, their beaks cut off so they won't kill each other in their panic at being unable to express any of their natural urges. In front of me right now is an advertisement from a local market that was dropped into my mailbox this morning. It shows a cartoon drawing of a bull, winking at me with a big smile on his friendly face. Apparently he is an expert on beef, because he is shown playfully pointing with his tail to certain items of meat, happily beckoning me to try them. This and millions of other such advertisements hammer home the message over and over that bulls are delighted for us to eat bull flesh. I can't help but think that the correct term for this type of thing is "bullshit!" I've seen ads and I'm sure you have, too, in which animals are shown offering themselves to be eaten, virtually begging us to dine on them. In one television commercial, cartoon hens, looking as happy and playful as the Rockettes, dance the can-can in a chorus line. What, you may wonder, are they so jubilant about? They're singing joyfully about how much we will enjoy their legs. And how about those ads in which Charlie the Tuna is heartbroken because he has not been killed and made into canned tuna fish? It's common in cookbooks to find "cute" little pictures next to the recipes. In one book, accompanying a Mexican chicken dish, there is a picture of a happy chicken lazing about in the sun with a big sombrero on his head. For a chicken-on-toast recipe, we see an enthusiastic chicken surfing on a piece of toast. In each case, the message is that animals simply love being eaten by us and are delighted to participate in the whole process. People will pat their bellies after eating, and say, "Yummy, that was a good chicken." But somehow I'm afraid the compliment is lost on the poor bird. You won't often hear someone say what they actually mean: "Yummy, I sure liked the taste of that dead chicken's body." Only yesterday I was in a market that proudly proclaimed their chickens were "fresh." And here all along I had thought they were selling "dead" chickens. I suggested to the manager that he might be able to clear up any confusion on the matter in the minds of his clientele by changing the sign to read "freshly killed chickens," but he didn't seem overly grateful for my suggestion. **Piercing the Veil** What, then, is it like for someone if, for a moment, he somehow manages to pierce through this veil of repression? Well, it can be downright shocking and can stir up a great deal of confusion and disturbance. Henry S. Salt gives us an account of his experience in his book _Seventy Years among Savages:_ _And then I found myself realizing, with an amazement which time has not diminished, that the "meat" which formed the staple of our diet, and which I was accustomed to regard like bread or fruit, or vegetables—as a mere commodity of the table, was in truth dead flesh—the actualflesh and blood—of oxen, sheep, and swine, and other animals that were slaughtered in vast numbers._ Another person recounts: _I was shocked speechless. I just sat there staring at my plate. It was a_ God Damned Turkey _I was eating! I couldn't believe it! Those were its legs, right there in front of me, disguised by all the cranberries and sauce! What did it have to be thankful for on this great Thanksgiving Day?_ The meat business depends on our repressing the unpleasant awareness that we are devouring dead bodies. Thus we have refined names like "sweetbreads" for what really are the innards of baby lambs and calves. We have names like "Rocky Mountain oysters" for something we might not find quite so appealing if we knew what they really were—pig's testicles. Our very language becomes an instrument of denial. When we look at the body of a dead cow, we call it a side of beef. When we look at the body of a dead pig, we call it ham or pork. We have been systematically trained not to see anything from the point of view of the animal, or even from a point of view that includes the animal's existence. In Alexandra Tolstoy's book, _Tolstoy: A Life of My Father,_ she tells of a time her aunt came to dinner, and her father chose to burst the bubble of repression by which she kept herself isolated from the truth about her diet: _Auntie was fond of food and when she was offered only a vegetarian diet she was indignant, said she could not eat any old filth and demanded that they give her meat, chicken. The next time she came to dinner she was astonished to find a live chicken tied to her chair and a large knife at her plate._ _"What's this?" asked Auntie._ _"You wanted chicken," Tolstoy replied, scarcely restraining his laughter. "No one of us is willing to kill it. Therefore we prepared everything so that you could do it yourself."_ Apparently, Auntie was appalled at the thought of killing the animal she wished to eat. Like most of us, she did not enjoy being reminded of where meat actually comes from. Most of us are willing to eat the flesh of animals but dislike the sight of their blood and prefer to think of ourselves, not as killers, but as consumers. It is all very simple. 1. The whole show is a charade. It is a game based on repression and untruth. 2. Awareness is bad for the meat business. 3. Conscience is bad for the meat business. 4. Sensitivity to life is bad for the meat business. 5. _Denial, however, the meat business finds indispensable._ **The Great American Steak Religion** As the sun dawns across North America every morning, the wave of slaughter begins. Each day in the United States nine million chickens, turkeys, pigs, calves, and cows meet their deaths at human hands. In the time it takes you to have your lunch, the number of animals killed is equal to the entire population of San Francisco. In our "civilized" society, the slaughter of innocent animals is not only an accepted practice but an established ritual. We do not usually see ourselves as members of a flesh-eating cult. But all the signs of a cult are there. Many of us are afraid to even consider other dietstyle choices, afraid to leave the safety of the group, afraid when there is any evidence that might reveal that the god of animal protein isn't quite all it's cracked up to be. Members of the Great American Steak Religion frequently become worried if their family or friends show any signs of disenchantment. A mother may be more worried if her son or daughter becomes a vegetarian than if the child takes up smoking. We are deeply conditioned in our attitudes toward meat. We have been taught to believe that our very health depends on our eating it. Many of us believe our social status depends on the quality of our meat and the frequency with which we eat it; and we take it for granted that only someone who can't afford meat would do without it. Males have been conditioned to associate meat with their masculinity, and quite a few men believe their sexual potency and virility depend on eating meat. Many women have been taught that a good woman feeds her man meat. Our cultural conditioning tells us we must eat meat and at the same time systematically overlooks the basic realities of meat production. We've been indoctrinated so thoroughly that it has become the ocean in which we swim. Our language is so disempowered by euphemisms and clichés, our shared experience so weakened by repression, our common sense so distorted by ignorance, that we can easily be held prisoner by a point of view beneath the threshold of our awareness. **The Truth** It has often been said that if we had to kill the animals we eat, the number of vegetarians would rise astronomically. To keep us from thinking along such lines, the meat industry does everything it can to help us blank the matter out of our minds. As a result, most of us know very little about slaughterhouses. If we think about them at all, we probably assume and hope that the animals enjoy a quick and painless death. But such, regrettably, is not the case. The reality of the slaughterhouse, unfortunately, is as different from the images we tend to have of it as the reality of the factory farms is from the barnyard images most of us still carry. But the men who actually do the killing for us know what it's like. They finish their shifts, punch the time clock, change out of their blood-spattered clothes, and go home. And something of the slaughterhouse goes home with them: _Barely three months had passed since Yoineh Meir had become a slaughterer, but the time seemed to stretch endlessly. He felt as though he were immersed in blood and lymph. His ears were beset by the squawking of hens, the crowing of roosters, the gobbling of geese, the lowing of oxen, the mooing and bleating of calves and goats; wings fluttered, claws tapped on the floor. The bodies refused to know any justification or excuse—every body resisted in its own fashion, tried to escape, and seemed to argue with the Creator to its last breath._ Meatpacking plants, as slaughterhouses are euphemistically called, are not exactly the most pleasant of working environments. Just being surrounded by death and killing takes an incredible toll on a human being. The turnover rate among slaughterhouse workers is the highest of any occupation in the country. The Excel Corporation plant in Dodge City, Kansas, for example, had a turnover rate of 43 percent per month in 1980—the equivalent of a complete turnover of its entire 500-person work force every two and a half months. Slaughterhouses are particularly difficult to describe because we have been systematically taught not to think about them at all. You probably don't know where a single one is located, so whitewashed have been our minds to their existence. But I can tell you they are not places Walt Disney would want to make a movie about. One writer called them _infernos of nauseous smells, pools of blood, and screams of terrified animals._ Just about everybody finds the atmosphere of the slaughterhouse uncomfortable. Even the meat producers themselves don't exactly want to spend their vacations there. One meat producer described a typical meatpacking plant atmosphere: _Earphone-type sound mufflers help mute the deadening cacophony of high-pressure steam used for cleaning, the clanging of steel on steel as carcasses move down the slaughter line, the whine of the hide and tallow removers and the snarling of a chain saw used to split carcasses into sides of beef here on the killing-room floor._ _The killing room... is filled with animals, minus their hooves, heads, tails and skins, which dangle down from an overhead track and slowly snake their way past the various stations of the various slaughterhouse workers like macabre piñatas..._ _The animals (have) their throats... slit, and then—with tongues hanging limply out of their mouths—their bodies are unceremoniously hooked behind the tendons of their rear legs and are swung up into the air onto the overhead track, which moves them through the killing room like bags of clothes on a dry cleaner's motorized rack. Once bled, their hoovesare clipped off with a gigantic pair of hydraulic pincers. They are then beheaded, skinned... and finally eviscerated._ Amid this carnage, workers in blood-spattered white coats and helmets are in constant motion, removing cattle legs with electric shears, skinning hides with whirring air knives, disemboweling animals with razor-bladed straight knives. The floors are slick with animal grease, and the air is thick with stench. It is a terribly difficult atmosphere in which to work. According to U.S. Labor Department statistics, the rate of injury in meatpacking houses is the highest of any occupation in the nation. Every year, over 30 percent of packinghouse workers suffer on-the-job injuries requiring medical attention. It's a few steps removed from anything you'd see at Disneyland. **We Do It All for You** But if the slaughterhouse environment is less than ideal for the workers, it falls even shorter of the mark for the billions of terrified veal calves, pigs, chickens, and cows who find themselves there. When they arrive at the slaughterhouse, they are most likely exhausted, sick, and starving. Most likely they were given little food, water, or any other care for their needs on the journey. And now they may not be fed upon arrival, because any food that would be given them would not have time to turn into marketable flesh. I'm sure most of the workers do their best to be humane, under the circumstances. But these people are under great pressure, in a hurry, and stressed beyond their capacity by the nature of the environment in which they work. It's a tremendous drain on their inner resources to take continually for granted the constant agonized cries of the animals being killed. As a result, they often vent their frustrations the only place they can, on the animals. The men whose job it is to move the animals along are called floggers, a term that accurately suggests that their dealings with the animals are not always considerate. One industry spokesman pointed his finger at the animals themselves for the unpleasantries that often occur: _Hogs... are slow-moving and considered obstinate. These characteristics often provoke a handler to the point of undue violence vented through the toe of a boot, closest club, or even a rock or piece of concrete._ The hogs are accused of provoking the violence by refusing to do what is asked of them. But there is a reason the animals resist moving along; they are, as are all animals, more closely tuned in to their environment than man, and they profoundly sense the danger awaiting them. The industry calls the animals obstinate, but the truth is they are terrified for their lives. **Empty Words** You may have assumed an effort is made in this day and age to spare the animals unnecessary pain in the killing. That's what I assumed. Unfortunately, I was wrong. The Federal Humane Slaughter Act says, in part: _It is therefore declared to be the policy of the United States that the slaughtering of livestock and the handling of livestock in connection with slaughter shall be carried out only by humane methods._ This sounds lovely, but in practice the act falls tragically short of accomplishing its admirable aims. Technically, we now have the means to render the animals unconscious before they are killed, which would greatly reduce the pain they must undergo. But often this is not done. Calves are frequently still butchered in full sight of their mothers. Chickens are piled in crates on the floor with a bird's-eye view of their brethren being butchered. The whole thing is handled with monstrous callousness and total disregard for the animals' feelings. The Federal Humane Slaughter Art sounds good, but in practice it is so riddled with loopholes as to be virtually meaningless. Less than 10 percent of the country's slaughterhouses are inspected for compliance with the act, and only a very small percentage of even these few plants are under any legal obligation to observe its guidelines anyway. Furthermore, chickens, turkeys, ducks, and geese are not considered animals by the act and so receive no protection, even in the few cases where the act does apply. The vast majority of slaughterhouses today may legally use any method they choose and are under no obligation whatsoever to take the slightest concern for the animals. With profits being the sole motivation, the result, as you might expect, is not a happy one for these poor creatures. The same attitudes that determine policies in factory farms govern decisions in slaughterhouses, and these are not attitudes of compassion for the animals. A leading poultry producer discussed the philosophy underlying his endeavors in the trade journal _Poultry World_ : _I am in this business for what I can make out of it. If it pays me to do this or that, I do it and so far as I am concerned that is all there is to say about it._ The industry chooses the cheapest possible methods of killing. They do not purposefully choose to be brutal and sadistic. It just works out that way. The captive-bolt pistol is one of the most effective methods of stunning cow, pigs, and other animals unconscious prior to killing them. Unfortunately, however, the cost of the charges used to fire the thing is enough to deter many slaughterhouses from using it. You may wonder how much money is saved thus, at the cost of forcing the animal to be fully conscious when killed. I've become somewhat accustomed to the industry's callousness, but I was still stunned to learn that the savings amount to approximately a single penny an animal. **When Kosher Isn't Kosher** Now you may think, when you hear a phrase like "ritual slaughter" or "kosher slaughter," that this refers to a better kind of killing. You may think, as I did, that the act is done with respect for the dignity of the animal and concern that it suffer as little as possible. You may think, as I did, that kosher ways of slaughter are more compassionate than "ordinary" slaughterhouse deaths. This was doubtless the original purpose at the time when this code of slaughter was conceived, and its standards probably produced the most humane and hygienic form of killing then available. But today, to kill the animals this way produces something far removed from the original intent of these laws. Orthodox Jewish and Moslem dietary laws forbid consumption of meat from animals that are not "healthy and moving" when killed. Religious orthodoxy today interprets this to mean that kosher meat must come from animals who have not been stunned before being killed. They must be fully conscious when it's done. Further, in order to qualify for the kosher stamp of approval, the animal must have its throat slit in a particular way. The consequences of this interpretation of kosher slaughtering are a travesty for the poor creatures involved. You see, the Pure Food and Drug Act of 1906 requires, for sanitary reasons, that no slaughtered animal fall in the blood of a previously slaughtered animal. What this means, in practice, is that animals must be killed while suspended from a conveyor belt, rather than while lying on the floor. Stringing up an animal before delivering the final blow doesn't cause it any pain if it has already been rendered unconscious. But when an animal must be conscious when killed, as kosher regulations stipulate, and also must have its throat cut in the particular way kosher law requires, the animal is forced to undergo an enormous amount of extra pain: _Animals being ritually slaughtered in the United States are shackled around a rear leg, hoisted into the air, and then hang, fully conscious, upside down on the conveyer belt for between two and five minutes—and occasionally much longer if something goes wrong on the "killing line"—before the slaughterer makes his cut._ It is difficult for us to imagine what these poor animals must suffer. The cows are exhausted and terrified to begin with. A heavy iron chain is clamped around one of their rear legs, then they are jerked off their feet and hung upside down by a single leg. Now cows are by nature as peaceful a creature as you could ever hope to find, but this situation is too much for even these most mellow of animals. They are provoked into hysteria. _The animal, upside down, with ruptured joints and often a broken leg, twists frantically in pain and terror, so that it must be gripped by the neckor have a clamp inserted in its nostrils to enable the slaughterer to kill the animal with a single stroke, as religious law prescribes._ In actual practice, kosher deaths have become a hideous perversion of the original intent of the dietary laws; the procedure adds incalculably to the agony they must suffer. You may think that today, because relatively few people "eat kosher," only a very small percentage of animals would be "killed kosher." You may also think that even including the nonreligious people who seek out kosher meat, mistakenly believing it to be better, this still wouldn't amount to a significant percentage. And finally you are probably quite sure that if you buy meat that isn't labeled kosher, you are certainly not consuming meat from animals killed in this fashion. But, I'm sorry to say, you'd be wrong on each account. You see, for meat to be passed as kosher by Orthodox rabbis, it is not enough for the animal merely to have been conscious when killed and to have its throat slit in the required way. A kosher Jew is also forbidden to consume the blood of an animal, so the veins and arteries must be cut out of kosher meat. In many parts of a cow, however, removing the blood vessels is very costly, and so the meat packers have resolved this difficulty by removing the blood vessels only from those parts of the animal from which they can be cut out inexpensively. Thus, even though the whole animal was killed kosher, only these parts are then sold as kosher meat. In other words, there 's a lot of meat left over. This means that a great deal of the meat in our supermarkets and restaurants, while not labeled kosher, is in fact from animals hoisted and slaughtered according to kosher regulations. One authority states: _It has been estimated that over 90 percent of the animals slaughtered in New Jersey—whose slaughterhouses supply New York City as well as their own state—are slaughtered by the ritual method._ Another report states: _Although less than 5 percent of the flesh in the United States is bought kosher, as much as 50 percent of the animals are slaughtered as such._ There is a debate going on now among Orthodox Jews as to whether to allow animals killed by more humane methods to be considered as kosher. In Sweden, at least, the Orthodox rabbis have come to allow animals to be stunned before slaughter. I like to think there is some possibility that the American rabbis will follow suit. **No Picnic** Though kosher procedures take the cake when it comes to cruelty, even under the best of conditions slaughtering is no day at the beach. In the past, much of the killing of animals was done at the farms where the animals lived. The creatures were not starved, exhausted, and disoriented from days of travel as they are today. They didn't have to smell or listen to thousands of their fellow creatures being killed as they waited their turn. And the people who did the job usually tried to minimize the animals' pain. But, still, it was a disturbing thing to do. _I never saw our farm manager more upset than the day we were getting ready to butcher five pigs. He shot one through the nose rather than through the brain. It ran screaming around the pen and he almost cried. It took two more bullets to finish the animal off, and this good man was shaking when he finished. "I hate that," he said to me. "I hate to have them in pain. Pigs are so damned hard to kill clean."_ The more I've seen of animals being killed, the more I've understood why McDonald's tells little children that hamburgers grow in little hamburger patches. And why the web of repression is so thick that otherwise intelligent people will say: "Don't tell me what happens to the animals. It will spoil my dinner." The more I've learned about what goes on in slaughterhouses, the more I've understood why these places are deliberately kept from our sight, and why the workers are under strict instructions not to talk to the press. I can see why the meat industry spends so much money feeding our children a cotton candy story of meat. Animals do not "give" their lives to us, as the sugar-coated lie would have it. No, we take their lives. They struggle and fight to the last breath, just as we would do if we were in their place. The friendly and intelligent pig whose life we take does not simply accept his death as a necessary step in the production of bacon. And he does not line up for his turn at the slaughterhouse singing about how happy he is to be on the way to becoming an Oscar Mayer wiener. Chickens do not approach the knife that will kill them wanting to dance and sing about how much we will enjoy eating their legs. The gentle and patient cow does not surrender docilely to the knife. She twists and bellows for all she's worth, even as she hangs upside down by a leg broken from the strain. The poet Dylan Thomas once admonished us, "Do not go gentle into that dark night." The animals whose lives we methodically take by the millions day in and day out would have understood his meaning. They do not go gently. They go kicking and screaming, bellowing their protest, fighting for their lives, and calling, to the last, to be saved. Calling for somebody, somewhere, to please hear them. **Hearing Them** The people responsible for today's slaughterhouses do not find any of this disturbing. They are professionals. To them, the whole business is almost ordinary. They have become so locked into denial that they simply go about their work, which just happens to involve coldly butchering millions of innocent animals. Interviewing them, I've seen what Hannah Arendt saw when she probed the minds of the Nazis. She called it the "banality of evil"—human beings matter-of-factly carrying out unspeakable cruelty, then going home and playing with their children. I asked one manager if the killing ever bothered him. "No," he said. "Some of the new guys have problems, but I tell them this is the way it's done. It's natural." I did not particularly want to get into an argument with this man, but neither could I let his remark slide by. So I gestured with my hand toward the machinery and conveyor belts in the main room and shook my head sadly, as if to say, "God help us if this is natural." "Do you have some kind of problem?" he asked none too kindly, insinuating that if such were the case I was suffering from a significant defect in character. My heart felt heavy as I looked into the face of so much denial. What could I say? Later, I went out to my car and cried. My tears were not only for the animals; they were for this poor man who had become such a stranger to mercy. **Beyond Denial** It is painful to break the shell of repression. It takes courage to see what these poor animals endure. It is painful to see how calloused human beings can become. It can be shattering to see that in our ignorance we have eaten the products of such a system. It takes courage to keep our eyes open to such tragedy, and our hearts open to our deepest human responses. The feelings that arise when we learn what is being done to today's animals are not signs of weakness. They are proof that there is still hope for us, that we have not totally succumbed to psychic numbing. In a culture that takes indifference and denial for granted, we may fear that our distress at these developments indicates weakness, a signal that we can't cope, evidence that we have a problem. But the distress we feel at what is being done is real, valid, and healthy. It speaks of our commitment to stopping this madness. It is a measure of our humanity. The pain we feel is not ours alone. Many of us, conditioned to take seriously only those feelings that pertain to our individual needs and wants, may not realize that we can suffer on behalf of others. But we can, and we do. We suffer on behalf of the animals when we learn of their plight. We suffer on behalf of the people who in their blindness are the instruments of such cruelty. We suffer on behalf of a society that perpetuates such tragedy. And we suffer on behalf of life itself. Our pain arises from our kinship with life. We hurt because we are not separate from animals, nor from the people who are the agents of such suffering. We hurt because these animals are our fellow mortals; and because the people administering such cruelty are our fellow human beings. We hurt because we are part, as they are, of the great web of life. Our pain is not something to fear, for in the heart of our grief we can find our connection to one another, and our power to act. Our power lies in our connection to all life. Our power lies in our deepest human responses. Our power does not lie in looking the other way. 6. **DIFFERENT STROKES FOR DIFFERENT FOLKS** _Sit down before fact like a little child, and be prepared to give up every preconceived notion, follow humbly wherever and to whatever abyss Nature leads, or you shall learn nothing._ —T. H. HUXLEY The whole justification for the factory farms and slaughterhouses, of course, is that we need their products for our health and happiness. But do we really? In the past few decades, there has been a revolution in medicine, a revolution that throws an extremely important light on the significance of our eating habits. As a result of the most exhaustive investigations in medical history of the health consequences of different diet-styles, scientists have now begun to understand for the first time the correlation between human food choices and human health. Very clear guidelines have finally emerged about the relative advantages and disadvantages of eating animal products. Conventional wisdom has it that animal products constitute two of the four basic food groups and are essential for human health. But the most rigorous, solid, and careful nutritional research on the effects of diet-styles on human health points in a decidedly different direction. Because the question of what might be the optimum diet is an emotionally charged one for many people, and because many of us have quite a significant emotional investment in believing our opinions and habits to be correct, I want to emphasize that what follows is not merely my own or anyone else's unfounded opinion. It is the result of the most conscientious research, as reported in established and reputable publications such as the _New England Journal of Medicine,_ the _British Medical Journal,_ the _Journal of the National Cancer Institute_ , the _American Journal of Clinical Nutrition,_ the _Journal of the American Medical Association,_ the _Journal of Pediatrics,_ the _Canadian Medical Association Journal,_ the _Journal of Immunology_ , the _American Journal of Digestive Diseases_ , the British medical publication _Lancet_ , and other sources of equal stature. Of course there are many other factors influencing your health besides the food choices you make. Exercise and laughter are health giving. Smoking and excessive drinking are not. Expressing your feelings is health giving. Stifling and repressing them is not. And a positive attitude toward life might well be the most important health-giving factor of all. To paraphrase Mark Braunstein: The person who eats beer and franks with cheer and thanks will probably be healthier than the person who eats sprouts and bread with doubts and dread. This does not mean, however, that there are not sound nutritional guidelines to assist us in living full and joyful lives. Indeed, the findings of modern nutritional scientific research point ever more strongly to the critical role nutrition plays in human welfare and happiness. **Is There a Doctor in the House?** You might think that your doctor would be a reliable guide to your optimum diet and would convey to you any emerging truths of sound nutritional research that significantly affect your health. But actually, most doctors don't know very much about nutrition. You'd think they would, but they don't. That's not their department. They have been trained to treat disease with drugs and surgery. They have not been trained to prevent disease through healthy life- and diet-styles. Nutritional education is not just inadequate in contemporary medical schools; in most cases it's nonexistent. At the 69th annual meeting of the American Medical Women's Association, one doctor drew knowing laughs when she told the audience about her lack of nutritional training. Said Dr. Michelle Harrison: _They had one lecture—on a Saturday morning—and it wasn't compulsory. I don't remember what was in the lecture, because I didn't go._ Only 30 of the nation's 125 medical schools have a single required course in nutrition. A recent Senate investigation revealed that the average physician in the United States received less than _three hours of training in nutrition during four years of medical school_. And few doctors have time for personal research: _The job of the practicing physician is far from easy. He is constantly being faced with situations in which he must make immediate decisions on the basis of too little evidence. He has neither the leisure nor the facilities to base his diagnoses and prescriptions on his own research. To be effective at all, he must rely on those standards, precepts and procedures that he has been so carefully taught._ Since what today's doctors have been taught makes virtually no mention of the role of nutrition in building health and preventing disease, they can hardly be blamed for not relaying the emerging truths of nutritional research to their waiting patients. Instead, says Roger Williams, doctors are trained to _wait until deformed and mentally retarded babies are born, then give them loving attention; wait until heart attacks come, then, if the patient is still alive, give him or her the best care possible; wait until mental disease strikes, and give considerate treatment; wait until alcoholism strikes, then turn to the task of rehabilitation; wait until cancer growth becomes apparent, then try to cut it out or burn it out with suitable radiation._ Thirty years ago, when many doctors smoked cigarettes themselves, it would have been pretty hard to elicit sound advice from them on the health consequences of smoking. Many doctors, in fact, recommended smoking to nonsmokers, as a way of dealing with social nervousness. It wasn't that these doctors were evil people, or lackeys for the tobacco industry. It was, rather, that they hadn't been told anything in medical school about the relationship between smoking and major health problems. They lived in the same culture as everyone else, in which smoking was seen as totally legitimate. They saw the same advertisements as everyone else, which sold people on the pleasures and social advantages of smoking. In fact, a famous Camel cigarette commercial loudly trumpeted: "More doctors smoke Camels than any other cigarette," and made a point of linking good health care with smoking their brand of cigarette. Today, a similar situation exists with respect to the health consequences of a meat habit. Today's physician is exposed to the same propaganda promoting meat and dairy product consumption as the rest of us, and he hasn't the nutritional training that would enable him to evaluate these messages any more intelligently than we can. Furthermore, the meat, egg, and dairy industries are particularly keen on "educating" doctors with their biased views of nutrition. The Meat Board, for example, has published a series of extremely expensive full-page color ads in the _Journal of the American Medical Association_ , presenting a nutritional slant that one nutritional authority, Dr. Kenneth Buckley, did not find at all impressive. He called it _slick and deceitful propaganda, coloring and twisting the facts in the most manipulative way._ The very presence of these expensive ads in medical journals shows that the meat industry knows it must now fight for the loyalty of a medical profession whose allegiance it once took for granted. Not so very long ago ads like this would have been unnecessary. Everybody "knew" meat was a healthy food to eat. But 25 years ago everybody "knew" cigarette smoking was harmless. **Three Million Human Guinea Pigs** The first suspicion by the larger scientific community that traditional assumptions about meat were open to serious doubt came after World War I. During the war, the Allied blockade cut Denmark off from all imports. The Danish government, dreading the possibility of severe food shortages, appointed Dr. Mikkel Hindhede to develop and coordinate a rationing program for the country. Dr. Hindhede's response, which he later reported in the _Journal of the American Medical Association,_ was to stop feeding the nation's grain to livestock in order to provide meat and instead to feed the grain directly to the people. It was a mass experiment in vegetarianism, with over three million subjects. Scientists were flabbergasted at the results. When they calculated the death rate in Copenhagen from October 1917 to October 1918, the period when food restrictions were the most severe, they found that the overall mortality rate from disease was by far the lowest in recorded history. It was, in fact, a drop of over 34 percent from the average for the preceding 18 years It was hard to avoid considering the possibility that there might be a connection between the nation's vegetarian diet and the greatly lowered death rate. Scientists thinking along these lines received more food for thought from World War II. At that time, Norway was occupied by the Germans, and the Norwegian government was forced to reduce sharply, and in many cases completely eliminate, the availability of meat to its citizens. Once again, scientists were amazed by the results. The death rate from circulatory diseases dropped dramatically. After the war the Norwegians returned to their former diet, and, sure enough, their death rate rose accordingly. Throughout these changing times the correlation between animal fat consumption and deaths from circulatory diseases bordered on true mathematical precision (see figure on page 134). Researchers who stumbled across this correlation wondered if it was a coincidence. So they looked at other countries. They knew that the consumption of meat and other animal products had also been cut significantly in Britain and Switzerland during World War II. Now they found that in these countries there had also been significant improvements in health. In Britain, infant and postnatal deaths dropped to their lowest rate ever, and instances of anemia dropped markedly. Children's growth rates and dental health were demonstrably better than ever before, and there were many other signs of greatly improved general health. The possibility that a vegetarian diet might have something to recommend it was becoming increasingly difficult to dismiss. **The Lowest and Highest Life Expectancies in the World** Of course, medical researchers knew these wartime experiments in vegetarianism didn't constitute scientific proof of anything. But the results were indeed suggestive, and many researchers were moved to study comprehensively the effects of different diet-styles on human health. **IT IS HARD TO MISS THE PATTERN BETWEEN ANIMAL FAT CONSUMPTION AND CIRCULATORY DISEASE DEATHS** **(Norway, 1938-1948)** **Scarcity of animal fats during World War II years in Norway resulted in a strikingly lower death rate from circulatory diseases.** Source: Data derived from H. Malmros, "The Relation of Nutrition to Health," _Acta Medica Scandinavia,_ Supplement No. 246 (1950). This had never really been done before on anything like the scale that occurred after World War II. For 99.999 percent of history, mankind has eaten whatever it could find or grow or kill or raise. Issues of what might be the optimum diet, and what the health consequences might be of various diets, were never studied in any depth. Such thoughts were a luxury we had not yet attained. But after World War II, scientists began for the first time to compile comprehensive statistics correlating the diet-styles and health of all the populations in the world. One fact that emerged consistently was the strong correlation between heavy flesh eating and short life expectancy. The Eskimos, the Laplanders, the Greenlanders, and the Russian Kurgi tribes stood out as the populations with the highest animal flesh consumption in the world—and also as among the populations with the lowest life expectancies, often only about 30 years. It was found, further, that this was not due to the severity of their climates alone. Other peoples living in harsh conditions but subsisting with little or no animal flesh had some of the highest life expectancies in the world. World health statistics found, for example, that an unusually large number of the Russian Caucasians, the Yucatan Indians, the East Indian Todas and the Pakistan Hunzakuts have life expectancies of 90 to 100 years. The United States has the most sophisticated medical technology in the world, and one of the most temperate climates. One of the highest consumers of meat and animal products in the world, it also has one of the lowest life expectancies of industrialized nations. The cultures with the very longest life spans in the world are the Vilcambas, who reside in the Andes of Ecuador, the Abkhasians, who live on the Black Sea in the USSR, and the Hunzas, who live in the Himalayas of northern Pakistan. Researchers discovered a "striking similarity" in the diets of these groups, scattered though they are in different parts of the planet. All three are either totally vegetarian or close to it. The Hunzas, who are the largest of the three groups, eat almost no animal products. Meat and dairy products combined account for only _1½ percent_ of their total calories. Particularly striking to researchers who have visited these cultures is that the people not only live so long but enjoy full, active lives throughout their many years and show no signs of the many degenerative diseases that afflict the elderly in our culture. _They work and play at 80 and beyond; most of those who reach their 100th birthday continue to be active, and retirement is unheard of. The absence of (excess protein) in their diets engenders slower growth and slim, compact body frames. With age, wisdom accumulates, but physical degeneration is limited so the senior citizens of these remote societies have something unique to contribute to the lives of others. They are revered._ **One of the World's Greatest Labor-Saving Devices** Ignoring the growing weight of worldwide evidence to the contrary, the Beef Council tells us in massive multimillion-dollar advertising campaigns that "beef gives strength." But since I have seen the results of rigorous scientific research on the subject, I can't help but be reminded of Laurence Peter's wonderful remark: _Prejudice is one of the world's greatest labor-saving devices; it enables you to form an opinion without having to dig up the facts._ It is not, of course, a coincidence that the Beef Council and other meat promoters have fostered the common prejudice that meat-eating brings strength. The meat industry profits in direct proportion to the degree this idea flourishes. As a result, it has conscientiously spent millions of dollars to get us to believe that if we are so foolhardy as to "risk" not eating meat, then we are well on our way to ending up looking like the starving masses of India. So widely held is the prejudice that meat-eaters as a group are stronger and more fit than vegetarians, that this proposition is not generally recognized for what it is. But then again, prejudices have a way of seeming like truth when enough people agree on them. The belief that vegetarians are risking their health by not eating meat is deeply ingrained in our collective psyche. It's as if each would-be vegetarian, as he or she considers or begins to embark upon the adventure, must listen to an incessant droning in the back of the mind—"meat gives strength, you are weakening yourself, meat gives strength, you are weakening yourself..." Even long-standing and well-informed vegetarians are not immune from the force of this collective thought-form and can become prickly, snobby, and defensive in the face of the prevailing cultural assumptions. They may feel they are in a constant battle to justify their diet-style against the assumptions of this collective agreement even when they are not spoken aloud. It can be like a nagging and constant undertow, pulling in a different direction from which they are going, and against which they feel they must defend themselves. But what happens if we consult the scientific studies that have not relied on the labor-saving device of prejudice but have actually worked to dig up the facts of the matter? Numerous studies, published in the most reputable scientific and medical journals, have compared the strength and stamina of people adhering to different diet-styles. According to these studies, all of them rigorous, the common prejudice that meat gives strength and endurance, though plastered on thousands of billboards and drummed into us since childhood, has absolutely no foundation in fact. **The Lab Results Speak** At Yale, Professor Irving Fisher designed a series of tests to compare the stamina and strength of meat-eaters against those of vegetarians. He selected men from three groups: meat-eating athletes, vegetarian athletes, and vegetarian sedentary subjects. Fisher reported the results of his study in the _Yale Medical Journal._ His findings do not seem to lend a great deal of credibility to the popular prejudices that hold meat to be a builder of strength. _Of the three groups compared, the... flesh-eaters showed far less endurance than the abstainers (vegetarians), even when the latter were leading a sedentary life._ Overall, the average score of the vegetarians was over double the average score of the meat-eaters, even though half of the vegetarians were sedentary people, while all of the meat-eaters tested were athletes. After analyzing all the factors that might have been involved in the results, Fisher concluded: _The difference in endurance between the flesh-eaters and the abstainers (was due) entirely to the difference in their diet... There is strong evidence that a... non-flesh... diet is conducive to endurance._ A comparable study was done by Dr. J. Ioteyko of the Academie de Medicine of Paris. Dr. Ioteyko compared the endurance of vegetarians and meat-eaters from all walks of life in a variety of tests. The vegetarians averaged two to three times more stamina than the meat-eaters. Even more remarkably, they took only one-fifth the time to recover from exhaustion compared to their meat-eating rivals. In 1968, a Danish team of researchers tested a group of men on a variety of diets, using a stationary bicycle to measure their strength and endurance. The men were fed a mixed diet of meat and vegetables for a period of time, and then tested on the bicycle. The average time they could pedal before muscle failure was 114 minutes. These same men at a later date were fed a diet high in meat, milk, and eggs for a similar period and then retested on the bicycles. On the high-meat diet, their pedaling time before muscle failure dropped dramatically—to an average of only 57 minutes. Later, these same men were switched to a strictly vegetarian diet, composed of grains, vegetables, and fruits, and then tested on the bicycles. The lack of animal products didn't seem to hurt their performance—they peddled an average of 167 minutes. Wherever and whenever tests of this nature have been done, the results have been similar. This does not lend a lot of support to the supposed association of meat with strength and stamina. Doctors in Belgium systematically compared the number of times vegetarians and meat-eaters could squeeze a grip-meter. The vegetarians won handily with an average of 69, while the meat-eaters averaged only 38. As in all other studies that have measured muscle recovery time, here, too, the vegetarians bounced back from fatigue far more rapidly than did the meateaters. I know of many other studies in the medical literature that report similar findings. But I know of not a single one that has arrived at different results. As a result, I confess, it has gotten rather difficult for me to listen seriously to the meat industry proudly proclaiming "meat gives strength" in the face of overwhelming evidence to the contrary. **World Records** On the athletic field, as in the laboratory, the endurance and accomplishments of vegetarians make me question whether we need animal products for fitness. The achievements of vegetarian athletes are particularly noteworthy considering the relatively small percentage of vegetarian entrants. Athletes, after all, are not immune from the cultural conditioning that meat alone gives the required strength and stamina. Yet some have adopted vegetarian diets and the results invite scrutiny. Dave Scott, of Davis, California, is a scholar-athlete who is well acquainted with the scientific literature on diet and health. He is also universally recognized as the greatest triathlete in the world. He has won Hawaii's legendary Ironman Triathlon a record four times, including three years in a row, while no one else has ever won it more than once. In three successive years, Dave has broken his own world's record for the event, which consists, in succession, of a 2.4-mile ocean swim, a 112-mile cycle, and then a 26.2-mile run. Dave's college major was exercise physiology, and he says he keeps up on the latest developments in the field by reading "an incredible amount" of books and journals. He calls the idea that people, and especially athletes, need animal protein a "ridiculous fallacy." There are many people who consider Dave Scott the fittest man who ever lived. Dave Scott is a vegetarian. I don't know how you might determine the world's fittest man. But if it isn't Dave Scott it might well be Sixto Linares. This remarkable fellow became a vegetarian in high school. _My parents were very very upset that I wouldn't eat meat... After 14 years, they are finally accepting that it's good for me. They know it's not going to kill me._ During the 14 years that Sixto's parents begrudgingly came to accept that his diet wasn't killing him, they watched their son set the world's record for the longest single-day triathlon and display his astounding endurance, speed, and strength in benefits for the American Heart Association, United Way, the Special Children's Charity, the Leukemia Society of America, and the Muscular Dystrophy Association. So deeply ingrained, however, is the prejudice against vegetarianism that even as their son was showing himself possibly to be the fittest human being alive, his parents only reluctantly came to accept his diet. Sixto says he experimented for a while with a lacto-ovo vegetarian diet (no meat, but some dairy products and eggs) but now eats no eggs or dairy products and feels better for it. It doesn't seem to be weakening him too much. In June 1985, at a benefit for the Muscular Dystrophy Association, Sixto broke the world record for the one-day triathlon by swimming 4.8 miles, cycling 185 miles, and then running 52.4 miles. Robert Sweetgall, of Newark, Delaware, is another fellow who doesn't just sit around all day. He is the world's premier ultra–distance walker. In the past three years, Robert has walked a distance greater than the 24,900-mile equatorial circumference of the earth. He says he is a vegetarian for moral reasons. _There's enough food on earth for us not to have to kill animals to eat._ Though not chosen for its health value alone, Sweetgall's vegetarian diet doesn't seem to put him at too much of a disadvantage. After walking a 10,600-mile perimeter around the United States, he set out on a loop that would take him, via about 20 million footsteps, through parts of all 50 states within the next year. Then there is Edwin Moses. No man in sports history has ever dominated an event as Edwin Moses has dominated the 400-meter hurdles. The Olympic gold medalist went eight years without losing a race, and when _Sports Illustrated_ gave him their 1984 Sportsman of the Year award, the magazine said: _No athlete in any sport is so respected by his peers as Moses is in track and field._ Edwin Moses is a vegetarian. Paavo Nurmi, the "Flying Finn," set 20 world records in distance running and won nine Olympic medals. He was a vegetarian. Bill Pickering of Great Britain set the world record for swimming the English Channel, but that performance of his pales beside the fact that at the age of 48 he set a new world record for swimming the Bristol Channel. Bill Pickering is a vegetarian. Murray Rose was only 17 when he won three gold medals in the 1956 Olympic games in Melbourne, Australia. Four years later, at the 1960 Olympiad, he became the first man in history to retain his 400-meter freestyle title, and he later broke both his 400-meter and 1,500-meter freestyle world records. Considered by many to be the greatest swimmer of all time, Rose has been a vegetarian since he was two. You might not expect to find a vegetarian in world championship bodybuilding competitions. But Andreas Cahling, the Swedish bodybuilder who won the 1980 Mr. International title, is a vegetarian, and has been for over 10 years of highest-level international competition. One magazine reported that Cahling's _showings at the "Mr. Universe" competitions, and at the professional body-building world championships, give insiders the feeling he may be the next Arnold Schwarzenegger._ Another fellow who is not exactly a weakling is Stan Price. He holds the world record for the bench press in his weight class. Stan Price is a vegetarian. Roy Hilligan is another gentleman in whose face you probably wouldn't want to kick sand. Among his many titles is the coveted Mr. America crown. Roy Hilligan is a vegetarian. Pierreo Verot holds the world's record for downhill endurance skiing. He is a vegetarian. Estelle Gray and Cheryl Marek hold the world's record for cross-country tandem cycling. They are complete vegetarians, not even consuming eggs or dairy products. The world's record for distance butterfly-stroke swimming is held jointly by James and Jonathan deDonato. They are both vegetarians. If you wanted to be an evangelist for the "meat gives strength" cult and were looking for a 97-pound vegetarian weakling to pick on, you'd probably be better off staying away from Ridgely Abele. He recently won the United States Karate Association World Championship, taking both the Master Division title for fifth-degree black belt and the overall grand championship. Abele, who has won eight national championships, is a complete vegetarian who eats no meat, eggs, or dairy products. The list goes on and on. Toronto, Canada, is the home of a national fitness institute that tests all the top athletes in that country. For a number of years tennis pro Peter Burwash consistently ranked between 50th and 60th. Then, as an experiment, he switched to a vegetarian diet, though he thought at the time that vegetarians were emaciated, unhealthy creatures. Now, however, he knows better. One year after making the switch, Peter Burwash was tested at the institute and found to have the highest fitness index of any athlete in any sport in the entire country of Canada. Another man you might have a hard time convincing that a meat dietstyle yields superior physical performance is Marine captain Alan Jones of Quantico, Virginia. I would never have believed that one could be a vegetarian Marine, but Jones is managing to do it, and his health doesn't seem to be suffering too much for his efforts. Although crippled by polio when he was five years old, Jones is another candidate for world's fittest man and has amassed a record of physical accomplishments unmatched by any other human being that ever lived. Not only does he hold the world record for continuous sit-ups (17,003), but in one particular 15-month period he accomplished possibly the most remarkable array of physical achievements ever attained by a human being: _September 1974: Lifted a 75-pound barbell over his head 1,600 times in 19 hours_ _February 1975: Made 3,802 basketball free throws in 12 hours, including 96 out of 100_ _June 1975: Swam 500 miles in 11 days through the Snake and Columbia Rivers, from Lewiston, Idaho, to the Pacific Ocean_ _September 1975: Skipped rope 43,000 times in five hours_ _October 1975: Skipped rope 100,000 times in 23 hours_ _November 1975: Swam over 68 miles in the University of Oregon swimming pool without a sleeping break_ _December 1975: Swam ½ mile in 32°F (0°C) water without a wet suit in the Missouri River near Sioux City, Iowa_ _January 1976: Performed 51,000 sit-ups in 76 hours_ Meanwhile, across the Pacific Ocean, the Japanese are every bit as serious and fanatic about baseball as are Americans. So, in October 1981, when Tatsuro Hirooka took over as manager of a professional team that had finished in last place the previous season, he knew some changes had to be made. But the changes he made were not the ones most of us would expect. He told the players on the Siebu Lions that meat and other animal foods increase athletes' susceptibility to injury and decrease their ability to perform. Therefore, said the new manager, like it or not, they were all going on a vegetarian diet. The Lions took quite a ribbing during the 1982 season. One rival manager sneered that they were "only eating weeds" and made some rather derogatory remarks about their masculinity. But the sneerer had to eat his words when the Lions beat his team for the Pacific League championship and then went on to defeat the Chunichi Dragons in the equivalent of our World Series. Lest anyone think this was a fluke, the vegetarian Lions came back the next year and once again trounced the opposition, winning again both the league and national championships. Please note that I have not provided this listing of athletic accomplishments of some vegetarians because I think this in itself proves the vegetarian diet superior. It doesn't. It proves only that for these given individuals, with their specific biochemical individualities, a vegetarian diet worked superbly at a particular time. But when we couple the experiences of Dave Scott, Edwin Moses, Murray Rose, Alan Jones, and all the rest with the data from systematic laboratory research published in reputable scientific journals, then, perhaps, we might have serious grounds to doubt the widely held prejudice that assumes greater weakness as an inevitable consequence of a vegetarian diet. **A Self-Fulfilling Prophecy** Although studies show that a vast majority (over 95 percent) of former meat-eaters report that a switch to a vegetarian diet increases their energy, vitality, and overall feeling of well-being, there are a few exceptions. Some don't. How are we to account for people who report experiencing greater strength when eating meat? Might these cases show there is something to the "meat gives strength" view after all? First off, assessing the health consequences of any diet, we must not forget the principle of biochemical individuality. We have different concentrations of gastric juices; our stomachs are shaped and function differently; we metabolize our food according to patterns that are unique to us; our digestive processes are as individualized as snowflakes. So, when someone tells me he or she feels better as a meat-eater, I take that seriously. One possible explanation is that they have made the switch away from meat too abruptly for their particular systems and not allowed enough time for the adjustment. Different people require different transition times. Some can go cold turkey and get along fine. Others have to gradually shed red meat, then chicken, and work their way along slowly. Another possibility is that the people who report they feel better with meat in their diet have been eating a nutritionally inadequate vegetarian diet. There are many kinds of vegetarian diets. Some are excellent, but others leave plenty to be desired. Just because a diet is vegetarian doesn't guarantee that it's healthier. Vegetarian diets that include too many empty calories (calories that supply no nutrients) can be nutritionally deficient. Such foods as white flour products, sugar, refined and processed foods, alcohol, and foods high in fat fill us up and may give us something to burn temporarily, but give us little nurturance. Fruit Loops, Twinkies, and Coca-Cola are all vegetarian foods, but they don't provide anyone, no matter what his biochemical individuality, with what he needs to be healthy. Some people will show the deficiency sooner than others, but empty calories will eventually take their toll on anyone. There is yet another little-known but significant way for a vegetarian diet to fall short nutritionally, producing a craving for meat and a sense of strength when it is eaten. Surprisingly, if you consume too many dairy products, be they in the form of milk, cheese, yogurt, butter, ice cream, or whatever, there is a real possibility of iron deficiency. The best sources of iron are most vegetables. Calorie for calorie, kale has 14 times as much iron as a typical sirloin steak. Furthermore, vitamin C in fresh fruits and vegetables greatly increases the body's ability to absorb and utilize iron. But if you consume a lot of dairy products when you give up meat (perhaps haunted by the nagging cultural fear—"are you getting enough protein?"), then the dairy products tend to crowd out some of the needed grains, vegetables, and fruits from your diet. Cow's milk is so low in iron that you'd have to drink 50 gallons to get the iron available from a single bowl of spinach (see figure below.) There is another important reason why you can become iron deficient if you overdo milk products. They not only provide no iron but also block its absorption. Breast-fed babies, for example, have a much higher rate of iron absorption than those fed cow's formulas, even if the formulas are especially fortified with extra iron. **IRON CONTENT OF COMMON FOODS** **(milligrams per 100 calories)** Although they do not provide as much iron as many vegetables, most meats do provide some. And meats are the iron sources most of us depended on as we grew up. Consequently, iron-deficient vegetarians may well feel an attraction to meat—the well-remembered source of iron—and feel better when they eat it. Such people are not very likely to consider that the source of the problem might be the overconsumption of dairy products. They don't know the "nutritional education" materials used in the school systems of the United States—the ones telling us to drink three glasses of milk a day, urging us to drink lots of milk for our health's sake, and humbly calling milk nature's most perfect food—were provided to the schools by the National Dairy Council. Vegetarians who have therefore become convinced that only animal products provide strength sometimes consume more dairy products than their particular biochemical individualities can handle. As a result they do in fact end up weakened and desirous of meat. Should they then replace some of the dairy with meat they may well feel stronger, since they will be adding more iron to their potentially deficient system. Ironically, their belief in the strength-giving attribute of meat has now become a self-fulfilling prophecy. For many people, almost any dairy products can be too much. At about the age of four, a surprisingly large percentage of people begin to lose the ability to digest lactose, the carbohydrate found in milk, because they no longer synthesize the digestive enzyme lactase. This condition, known as lactose intolerance, results in symptoms of diarrhea, gas, and stomach cramps. Different people have different degrees of lactose intolerance, but it is especially high in adult Blacks and Asians, occurring in as many as 90 percent of these genetic populations. If lactose-intolerant individuals switch to a vegetarian diet and try to substitute dairy products for meat, they may not understand that it is the added dairy products, not the lack of meat, causing the problems. **The Power of Belief** Alexander Pope once said, "All looks yellow to the jaundiced eye." He was referring, of course, to the power of prejudice to color our perceptions of reality. _In Rhodesia, a white truck driver passed a group of idle natives and muttered, "They're lazy brutes!" A few hours later he saw natives heaving 200-pound sacks of grain onto a truck, singing in rhythm to their work. "Savages!" he grumbled. "What do you expect?"_ —GORDON ALLPORT Recent medical history provides a particularly striking example of how potently an erroneous belief can color people's experience. Surgeons tend to look for surgical answers to disease; it's how they make their living. And sometimes, in their zeal to provide new surgical procedures, they may employ new techniques a bit prematurely, before determining through appropriate experimentation just exactly what value or lack of value the new techniques may have. In the early 1950s, physicians were hard-pressed to come up with an effective treatment for the pains of angina pectoris. But then surgeons hit on a surgical procedure that they thought might solve the problem. The surgery consisted of opening the chest and tying off the internal mammary artery, which supplies blood to the muscles of the inner chest wall. A branch of this vessel brings blood to the pericardium, the sac enclosing the heart. Theoretically, it was supposed that tying off the artery below the branch might increase the blood flow to the heart. (The chest walls, it was known, could find alternative supplies.) And, in fact, a large number of patients who underwent this surgery reported a decrease of angina pain after recovering from the severe trauma of the operation. The surgeons thought they had come up with a dandy of an operation, and it became the fashionable treatment for angina. However, in 1960, there appeared in the _American Journal of Cardiology_ a remarkable report that shed a completely different light on the reasons why angina sufferers who underwent the surgery experienced decreased pain. It seems that a number of surgeons, aware that this particular procedure had never been adequately tested and also aware that angina is notoriously responsive to placebo treatment, had begun to consider the possibility that the patients experienced a decrease in pain only because they believed in the surgery—in other words, that this major operation was, in fact, totally worthless. Doctors have known for centuries of the placebo effect. You can give patients pills specifically designed to be devoid of any conceivable medical efficacy, and some of these patients, because they believe they are receiving substances with genuine medical value, will report improvement. Now doctors were beginning to consider the staggering possibility that the reported benefits from the angina surgery were the result of a placebo effect. How were they to find out? It's relatively easy to test pills for a placebo effect. You simply do a double-blind study, giving some patients the real thing, others placebos, and see what happens. But it's not so easy to put surgery to the test. The ethics of performing sham surgical operations are sticky, to say the least. In this case, however, the doctors were sure enough of their hunch that they did, in fact, eventually perform a number of sham, or placebo, operations. They then reported the results in the _American Journal of Cardiology._ Amazingly, the patients who underwent the sham surgery reported the same degree of angina relief as those undergoing the real surgery! The verdict was unavoidable. The fashionable operation had derived its efficacy entirely from the placebo effect. Surgeons now realized that this operation was no longer ethically justifiable. But they were not so easily to be deprived of a chance to operate on angina sufferers. They conceived an even more intrusive procedure—internal mammary artery implant. This involved poking a hole in the heart muscle, cutting the artery, and then inserting the cut end of the artery into the heart, hoping it would sprout new branches, thus supplementing the coronary arteries and bringing more blood to the heart. Again, patients who underwent the surgery reported decreases in angina pain after recovering from the surgical trauma, and again the surgeons trumpeted their success. No one ever put this procedure to the test of comparison with sham surgery. However, autopsies later done on patients who received this surgery showed that the implanted arteries had not sprouted new branches or provided any new blood supplies to the heart, as had been hoped. In short, any success this massive intervention had was due, again, to the placebo effect. So great had been the faith of the patients in surgery as a healing modality, that even though they underwent traumatic surgery that was, in fact, physically worthless, many of them reported symptomatic relief. It seems we haven't even begun to scratch the surface of understanding how profound and powerful a thing faith is. Is it any wonder, then, given the faith we have all been continuously programmed to have in meat, that some people report they feel better when meat is part of their diet? To me, given the extent of our meat habit programming, the amazing thing is that such a great majority of meat-eaters who switch to a vegetarian diet-style actually report more energy, greater vitality, new feelings of lightness and ease in their bodies, and increased well-being. When I see the very high percentage of former meat-eaters who are delighted with the switch in diet-style, in spite of massive cultural conditioning to the contrary, I have to wonder whether those who report they feel stronger eating meat might possibly be a bit more under the influence of the prevailing cultural assumptions than they realize. That would be understandable. Prejudices are hard to uproot when they are not recognized as such, and even more so when they are still being repeatedly reinforced within the culture at large. But what would happen if we were simply to _consider the possibility_ that our long-standing belief in meat as the best dietary source of health and fitness might not be the whole story? Perhaps then it would be time for a new journey to begin. 7. **THE RISE AND FALL OF THE PROTEIN EMPIRE** _Think of the fierce energy concentrated in an acorn! You bury it in the ground, and it explodes into a giant oak! Bury a sheep, and nothing happens but decay!_ —GEORGE BERNARD SHAW _You put a baby in a crib with an apple and a rabbit. If it eats the rabbit and plays with the apple, I'll buy you a new car._ —HARVEY DIAMON I am sitting in elementary school. The teacher is bringing out a nice colored chart and telling all us kids how important it is to eat meat and drink our milk and get lots of protein. I'm listening to her and looking at the chart, which makes it all seem so simple. I believe my teacher, because I sense that she, herself, believes what she is saying. She is sincere. She is a grown-up. Besides, the chart is decorated and fun to look at. It must be true. Protein, I hear, that's what's important. Protein. Lots of it. And you can only get good-quality protein from meat and eggs and dairy products. That's why they make up two of the four basic food groups on the chart. That day at lunch I feel like doing something good for myself and the world, so I spend the 10 cents I have left of my weekly allowance for another carton of milk. Now I am an adult and, looking back, I know my teacher had all she could handle to keep control of the classroom and teach a few basics. When teaching aids were given to her that helped get the class's attention and helped ease her burden, she was grateful. Not for a moment did it occur to her to wonder about the political dynamics that led to the development of those aids. Neither she nor any of us little kids could have imagined that the pretty chart was actually the outcome of extensive political lobbying by the huge meat and dairy conglomerates. Nor could we have imagined the many millions of dollars that had been poured into the campaigns that produced those pretty charts. My teacher believed what she taught us and never for a moment suspected she was being used to relay industrial propaganda. Our innocent and captive little minds soaked it all up like sponges. And most of us, as planned, have been willing and unquestioning consumers of vast amounts of meat and dairy products ever since. Even those few of us who have come to experiment with vegetarian diet-styles are often still haunted by the voices of our teachers and the lessons of those charts. When things aren't going well, a voice in the back of our minds whispers: "Maybe you aren't getting enough protein..." **Step Right Up, Step Right Up** Of course, just because the concept of the basic four food groups was promoted by the National Egg Board, the National Dairy Council, and the National Livestock and Meat Board, doesn't mean it is necessarily false. Just because there were hucksters in our classrooms doesn't mean the hucksters lied. But it does mean their motives were a little less pure than we thought, and their "concern" for our education a little more self-interested than we knew. It might cast a shadow on the wisdom of unquestioningly accepting the "truths" we were taught. It might mean, for example, that we should consult sources of information less biased than the Egg Board or the Meat Board or the others who applied so much political and economic pressure to get those nice pretty charts to say what they wanted them to say. Since I've discovered that the National Dairy Council is the foremost supplier of "nutritional education" materials to classrooms in the United States, and seen in a thousand other ways how heavily organizations specifically trying to promote the sale of animal products influence our nutritional education, I've had to wonder whether we might have been misled about our protein needs. Feeling a little unsure, I've turned to the light of recent unbiased scientific research to get a better understanding of what our protein needs might actually be. These are studies produced by groups without a product to sell. I've found that not all authorities agree on a precise figure for our daily needs of protein, but their calculations do fall within a specific range. (See figure on page 154.) It is a range that runs from a low estimate of _2½ percent_ of our total daily calories up to a high estimate of over _8 percent_. The figures at the high end include built-in safety margins and are not minimum allowances but rather recommended allowances. Interestingly, I have found that there is a great deal of controversy in the scientific community about the wisdom of including such safety margins. Not everyone thinks it's necessary. One passionate nutritional commentator, Dr. David Reuben, spoke for many informed scientists when he was asked who it is who needs the extra 30 percent allowance of protein. He answered: _The people who sell meat, fish, cheese, eggs, chicken, and all the other high prestige and expensive sources of protein. Raising the amount of protein you eat by 30 percent raises their income by 30 percent. It also increases the amount of protein in the sewers and septic tanks of your neighborhood 30 percent as you merrily urinate away everything that you can't use that very day. It also deprives the starving children of the world the protein that would save their lives. Incidentally, it makes you pay 30 percent of your already bloated food bill for protein that you will never use. If you are an average American family, it will cost you about $40 a month to unnecessarily pump up your protein intake. That puts another $36 billion a year into the pockets of the protein producers._ Other authorities hold the view that the 30 percent safety margin is important to protect those few individuals whose protein needs are unusually high. But there needn't be any conflict if we bear biochemical individuality in mind. Clearly, some people, owing to their biochemical individualities, will need the extra 30 percent. But just as clearly, others will need 30 percent less than the norm. Fortunately, we do not have to arrive at a single figure that would ostensibly be best for everyone. Roger Williams, the biochemist and nutrient researcher who has probably contributed more to our understanding of biochemical individuality than any other scientist alive, suggests that the range of protein needs among people may vary as much as fourfold. Interestingly, a fourfold range is just the span covered by the extremes of current scientific thinking. For if we top off the highest figures to make room for the extra protein needs of the most extreme cases, we have a spectrum ranging from _2½ percent_ at the low end up to _10 percent_ at the top. Science tells us that the protein needs of the vast majority of people would be easily met within that range. **WHAT ARE OUR PROTEIN NEEDS ACCORDING TO IMPARTIAL EXPERTS? The answer is a spectrum.** 2½% | At the low end of the curve are estimates of human protein needs reported in the _American Journal of Clinical Nutrition_ that say we need 2½% of our daily calories from protein. Many populations have, in fact, lived in excellent health on this amount. ---|--- 4½% | The World Health Organization has established a minimum daily requirement of 32 grams of protein for a 150-pound man. Since there are four calories in a gram of protein, this means WHO stipulates such a man should get 128 calories of protein a day. This amounts, according to WHO statistics, to 4½% of caloric intake. Official WHO figures for women are similar. | The Food and Nutrition Board recommends in their official report that we get .213 gram of protein per pound of body weight per day. This translates to 4½% of our daily calories from protein. 6% | The Food and Nutrition Board takes it a step further. After giving what amounts of a 4½% figure for a minimum daily requirement, they add a 30% safety margin, designed to "meet the needs of 98% of the United States population." This gives them a figure of just under 6%, which they call a recommended daily requirement. 8% | The National Research Council also figures in a substantial safety margin and comes up with a figure of just over 8% of our calories needing to be from protein. This figure is not a minimum daily requirement but rather is issued as a recommended daily requirement and is presented as more than adequate for 98% of the population. Nature, it seems, would agree totally. Human mother's milk provides 5 percent of its calories from protein. Nature seems to be telling us that little babies, whose bodies are growing the fastest they will ever grow, and whose protein needs are therefore at a maximum, are best served by the very modest level of 5 percent protein. **What If We Need a Whole Lot?** But what if we happen to be one of those people whose biochemical individualities are such that we need a whole lot of protein? What if we are at the high end of the spectrum? Don't we need to eat meat in order to get enough? And if not meat, don't we then need eggs or dairy products? The answers to those questions are shown quite graphically in the chart on page 156, which shows the percentage of calories from protein in various nonmeat, nondairy foods. Even, in fact, were we at the very top end of the spectrum in terms of our protein needs, needing to derive a full 10 percent of our calories from protein, unless we were trying to live only on fruits and sweet potatoes, vegetarian foodstuffs easily provide for our protein needs. If we ate only brown rice, and if our biochemical individualities required the maximum amount of protein, then, of course, we would fall a little short. But if we do nothing more than include beans or fresh vegetables to complement the rice, then our protein needs are easily and well satisfied without recourse to any animal products. This is true even in the most extreme case, where our protein needs are at the very highest end of the spectrum. If we ate nothing but wheat (which is 17 percent protein) or oatmeal (15 percent) or pumpkin (15 percent), we would easily have more than enough protein. If we ate nothing but cabbage (22 percent), we'd have over double the maximum we might need. **PERCENTAGE OF CALORIES FROM PROTEIN** LEGUMES --- Soybean sprouts | 54% Mung bean sprouts | 43% Soybean curd (tofu) | 43% Soy flour | 35% Soybeans | 35% Soy sauce | 33% Broad beans | 32% Lentils | 29% Split peas | 28% Kidney beans | 26% Navy beans | 26% Lima beans | 26% Garbanzo beans | 23% VEGETABLES --- Spinach | 49% New Zealand spinach | 47% Watercress | 46% Kale | 45% Broccoli | 45% Brussels sprouts | 44% Turnip greens | 43% Collards | 43% Cauliflower | 40% Mustard greens | 39% Mushrooms | 38% Chinese cabbage | 34% Parsley | 34% Lettuce | 34% Green peas | 30% Zucchini | 28% Green beans | 26% Cucumbers | 24% Dandelion greens | 24% Green pepper | 22% Artichokes | 22% Cabbage | 22% Celery | 21% Eggplant | 21% Tomatoes | 18% Onions | 16% Beets | 15% Pumpkin | 12% Potatoes | 11% Yams | 8% Sweet potatoes | 6% GRAINS --- Wheat germ | 31% Rye | 20% Wheat, hard red | 17% Wild rice | 16% Buckwheat | 15% Oatmeal | 15% Millet | 12% Barley | 11% Brown rice | 8% FRUITS --- Lemons | 16% Honeydew melons | 10% Cantaloupe | 9% Strawberries | 8% Oranges | 8% Blackberries | 8% Cherries | 8% Apricots | 8% Grapes | 8% Watermelons | 8% Tangerines | 7% Papayas | 6% Peaches | 6% Pears | 5% Bananas | 5% Grapefruit | 5% Pineapple | 3% Apples | 1% NUTS AND SEEDS --- Pumpkin seeds | 21% Peanuts | 18% Sunflower seeds | 17% Walnuts, black | 13% Sesame seeds | 13% Almonds | 12% Cashews | 12% Filberts | 8% Source: Data obtained from _Nutritive Value of American Foods in Common Units,_ USDA Agriculture Handbook No. 456. **COMPARISON OF THE MILKS OF DIFFERENT SPECIES** ** Species** | **Percent of Calories as Protein** | **Time Required to Double Birth Weight (days)** ---|---|--- **Human** | **5%** | **180 days** **Mare** | **11%** | **60 days** **Cow** | **15%** | **47 days** **Goat** | **17%** | **19 days** **Dog** | **30%** | **8 days** **Cat** | **40%** | **7 days** **Rat** | **49%** | **4 days** Source: Data derived from G. Bell, _Textbook of Physiology and Biochemistry,_ 4th ed. (Williams and Wilkins, Baltimore, 1954), 167–70. Adapted in J. McDougall, _The McDougall Plan_ (New Century Publishers, 1983), 101. In fact, if we ate nothing but the lowly potato (11 percent protein) we would still be getting enough protein. This fact does not mean potatoes are a particularly high protein source. They are not. Almost all plant foods provide more. What it does show, however, is just how low our protein needs really are. There have been occasions in which people have been forced to satisfy their entire nutritional needs with potatoes and water alone. I wouldn't recommend the idea to anyone, but under deprived circumstances it has been done. Individuals who have lived for lengthy periods of time under those conditions showed no signs whatsoever of protein deficiency, though vitamin deficiencies have occurred. **Learning to Shout Hooray for Meat and Milk** I am back in my elementary school again. The teacher is telling us kids that animal protein is superior to vegetable protein. It's the only complete protein. That sounds good. I have learned to root for the good guys on television shows, and now I learn that "good" protein comes only from meat and dairy products. Inside I shout "Hooray!" for meat and milk. At lunch I wish my mother had put more bologna on my sandwich, so I could be stronger and better at football. Since then I have learned that the belief in animal protein as superior to vegetable protein goes back to 1914, when Osborn and Mendel did some of the earliest laboratory research on protein requirements. They were studying rats and (in studies I do not ethically condone) found the rats grew faster on animal protein than they did when the source of protein in their diet was plants. It wasn't long before investigators began to classify meat, eggs, and dairy foods as class A proteins, and to classify plant origin proteins as class B. Studies in the 1940s clarified the matter further when researchers found the 10 particular amino acids that are essential to the growth of rats. If any of these particular substances were removed from the rats' diet, they found the rats' growth was impaired. By laborious experiments, the optimum proportion of amino acids that produced the fastest growth was determined and the amino acid pattern that emerged was similar to that found in animal protein, particularly to that found in eggs. There was no way to duplicate these experiments on human subjects. So while we now knew the optimum amino acid pattern for rat growth, we had no equivalent information for human beings. Based on what we knew for rats, however, it was assumed by some investigators that the proportion of essential amino acids that promoted the most rapid growth in rats would be the best for human beings as well. No serious investigator took this to be more than a working hypothesis, but it did at least give us something to go on. Meanwhile, with less than uncompromising respect for the truth, the National Egg Board took the opportunity to begin actively promoting the idea that eggs were the ideal protein food. It wasn't only the Egg Board that saw a chance to jump on the bandwagon. The Dairy Council, the Livestock and Meat Board, and virtually all the other organizations whose purpose it was to promote the sale of animal products joined the campaign, and none of them seemed overly concerned with minor details, such as the fact that the data were known only for rats. Through their well-funded efforts, the idea that animal protein was superior to vegetable protein became virtually the official nutrition doctrine of the United States. Anyone who thought otherwise came to be seen as some kind of crank, zealot, or nut. **_Diet for a Small Planet_** Then, in the late 1960s, a woman named Frances Moore Lappé wrote an influential book titled _Diet for a Small Planet._ She accepted the hypothesis that the pattern of amino acids found in animal protein was superior for human nutrition to that found in vegetable protein. And she accepted the pattern of amino acids found in eggs as the ultimate standard against which to measure all other proteins. But then she showed that when plant foods are mixed in certain ways, the result is that the amino acids in the "inferior" vegetable proteins combine to produce proteins that more closely approximate the ideal egg standard. In fact, she showed that in many cases, thanks to the synergistic effect of protein complementarity, mixed vegetable proteins actually outrank meat in their value to the body. Lappé was delighted to discover that almost all the traditional societies had independently evolved diets that combined vegetable proteins in a way that brought their combined amino acid patterns closer to that of the egg. And since she accepted the egg as the ideal pattern, she saw the workings of a deep inherent wisdom in these traditional diet-styles. In Latin America, it was corn tortillas with beans, or rice with beans. In the Middle East, it was bulgur wheat with garbanzo beans (chickpeas), or pita bread with hummus (made from garbanzo beans and sesame seeds). In India, it was rice or wheat chapatis with dahl (lentils). In southern China, Japan, and much of Indonesia, it was soy products with rice. In northern China, it was soy products with wheat or millet. In Korea it was soy foods with barley. Lappé's enthusiasm for protein combining was contagious. Her book was beautifully written and contained charts and tables that gave the details of how complementary vegetable proteins increased each other's nutritional value by bringing each other up toward the egg standard. Furthermore, Lappé tapped a deep and powerful spring in the psyche of the times when she showed the terrible waste of a meat-centered diet and how it is part of a pattern of consumption that deprives millions of people the essentials of life. Her book sold over three million copies. Many people whose nutritional education had hitherto been overseen by the National Dairy Council and the Meat Board now saw, for the first time, scientific evidence that they did not have to eat meat in order to get the "best-quality" protein. Numerous individuals were freed from thinking only animal proteins could meet their dietary needs. Lappé did not, however, really question the position of the egg at the top of the protein ladder. She was evidently not aware that its placement there derived only from experiments with rats, not human beings. However, Nathan Pritikin, whose Longevity Centers featured diet-style counseling as the basis for dramatic success in treating and preventing heart disease, was one of the many nutritionists who spotted this flaw in Lappé's work. He could not agree that eggs were the ideal, having seen far too much clinical evidence to the contrary. Although applauding the spirit in which Lappé had written _Diet for a Small Planet,_ many experts felt, with Pritikin, that because she had proceeded from a wrong premise her conclusions were misleading. In her enthusiasm for protein complementarity, they felt she had unintentionally cast regular old "uncomplemented" vegetable protein in a less favorable light than the truth warranted. Pritikin said: _Unfortunately, the book is one of the most misleading documents in the last few years because everybody now thinks food balancing is essential. [The book] gives the impression that vegetable proteins don't have sufficient percentages of amino acids._ Actually, Lappé never really said it was necessary to combine vegetable proteins to get enough. She only said that if you did they came much closer to the level of eggs and usually surpassed meats. It is clear she never meant to cast a shadow over uncombined vegetable proteins. She wrote _Diet for a Small Planet_ specifically to show how wasteful meat habits are, and to show that animal protein isn't necessary. But ironically, the very popularity of her work served to reinforce the idea that animal protein was superior, though it was now understood by many that with careful combining, vegetable proteins could be made quite competitive. Many of her readers inferred that if you don't eat animal protein, then you need a doctorate in chemistry and had better keep a slide rule in your kitchen. Many felt obligated to check amino acid tables and food-combining charts before preparing a meal. Meanwhile, Lappé herself was learning more and revising her judgments about the value of uncomplemented vegetable protein. She became convinced that her emphasis in _Diet for a Small Planet_ on protein complementarity had been misplaced. So she rewrote _Diet for a Small Planet,_ and in 1981 reissued an almost completely new 10th anniversary edition. Now she said: _In 1971 I stressed protein complementarity because I assumed that the only way to get enough protein... was to create a protein as usable by the body as animal protein. In combating the myth that meat is the only way to get high-quality protein, I reinforced another myth. I gave the impression that in order to get enough protein without meat, considerable care was needed in choosing foods. Actually, it is much easier than I thought... [I] helped create a new myth—that to get the protein you need without meat you have to conscientiously combine nonmeat sources... With a healthy, varied diet, concern about protein complementarity is not necessary for most of us._ It is very rare that well-known figures are willing to reverse themselves publicly, especially when the issue is the very one that made them famous. I can't help but admire this kind of integrity. And obviously, Frances Moore Lappé is convinced that her earlier emphasis on protein combining was unwarranted. In the original 1971 edition of _Diet for a Small Planet,_ over 200 of the 280 pages dealt specifically with the ins and outs of protein combining. In the 1981 edition, only about 60 of the 455 pages deal with the matter, and much of this is an explanation of how her thinking has changed. The details of protein complementarity, which made up the bulk of the original book, are relegated in her revised edition to a short appendix at the back of the book. **CAN YOU EASILY GET ENOUGH PROTEIN WITHOUT EGGS OR DAIRY PRODUCTS? YES! WITHOUT EVEN TRYING Hypothetical All-Plant Food Diet** **Meal** | **Calories** | **Total Protein (grams)** ---|---|--- **BREAKFAST** 1 cup orange juice 1 cup cooked oatmeal ½ oz. sunflower seeds 1 T. brown sugar 3 T. raisins | 111 148 80 52 87 | 1.7 5.4 3.5 0.9 **LUNCH** 2 T. peanut butter 2 slices whole wheat bread 1 T. honey 1 apple 2 carrots, small | 172 112 64 87 42 | 7.8 4.8 0.1 0.3 1.1 **DINNER** 1 cup cooked beans 1 cup cooked brown rice 2 stalks broccoli (1½ c.) 4 mushrooms 2 T. oil 1 cup apple juice ½ banana | 236 178 52 28 248 109 64 | 15.6 3.8 6.2 2.7 0 0.3 0.8 **SNACK** 1½ cups popcorn, with oil | 123 | 2.7 **TOTAL** | **1,993** | **57.7** National Academy of Sciences recommended allowance for a 128-pound woman | **2,000** | **44.0** Source: From Frances Moore Lappé, _Diet for a Small Planet,_ rev. ed. (New York: Ballantine Books, 1982). In the new _Diet for a Small Planet,_ the woman who brought the concept of complementing vegetable proteins to the world goes out of her way to show it isn't necessary. She writes: _If people are getting enough calories, they are virtually certain of getting enough protein... The simplest way to prove the overall point is to propose a diet which most people would consider protein-deprived, and ask, does its protein content add up to the allowance recommended by the National Academy of Sciences?_ She then puts together a day's menu with no meat, no dairy products, no eggs, and no protein supplements and comments: _Even without accounting for improved protein usability due to combining complementary proteins, this diet has adequate protein without exceeding calorie limits._ Lappé's hypothetical menu on page 162 is for a 128-pound woman. It contains 57.7 grams of protein, far more than the 44 grams recommended by the National Academy of Sciences for a woman that size. She points out that even if we were to assume the superiority of animal protein and completely ignore any conceivable benefits that might be gained from vegetable protein combining, her hypothetical menu would still exceed the allowance with ease. Men might wonder whether they would get enough protein in this fashion. They would indeed, since caloric needs and protein needs rise hand in hand. What matters is the _percentage_ of the total caloric intake derived from protein. Men, eating proportionately more calories than Lappé's 128-pound woman, would get proportionately more protein and be covered. We saw earlier that a spectrum of 2½ percent to 10 percent would be adequate for just about everybody. Without meat, eggs, or dairy products, Lappé's hypothetical menu still derives over _11½ percent_ of its calories from protein. **The Incredible Oversold Egg** It is not only Frances Moore Lappé whose mind is changing as new evidence comes in from protein research; the most rigorous scientific journals are likewise convinced. An editorial in the medical journal _Lancet_ reports: _Formerly, vegetable proteins were classified as second-class, and regarded as inferior to first-class proteins of animal origin, but this distinction has now been generally discarded._ What are we to make of this turnaround? Is it possible that even if we accept the dubious hypothesis that the egg is the ultimate protein standard for humans, we still do not need meat, eggs or dairy products in order to get adequate protein? Could it be that the whole issue of getting enough protein is actually just a figment of our collective imaginations, with nothing behind it except for the propaganda of the meat, dairy, and egg industries? That, remarkably, seems to be the case. The Food and Nutrition Board of the National Academy of Sciences, hardly a bastion of nutritional radicalism, spoke of people who consume no dairy products, meat, or eggs: _Pure vegetarians from many populations of the world have maintained... excellent health._ A team of Harvard researchers, investigating the effects of a strictly plant food diet, found: _It is difficult to obtain a mixed vegetable diet which will produce an appreciable loss of body protein without resorting to high levels of sugar, jams and jellies, and other essentially protein-free foods._ A clinical study reported in the _Journal of the American Dietetic Association_ compared the intake of the essential amino acids for meat-eaters, lacto-ovo vegetarians (those consuming dairy products and eggs), and pure vegetarians (no eggs or dairy products). This study raised the protein requirements for each amino acid to a height that would cover even the needs of pregnant women and growing adolescents. They found that not only were all three diet-styles sufficient, but they were all _well above sufficient:_ _Each group exceeded twice its requirement for every essential amino acid and surpassed this amount by large amounts for most of them._ At an annual meeting of the American Association for the Advancement of Science, the eminent nutritionist Dr. John Scharffenberg gave a major presentation that was later made into a book. He did not seem to feel that getting enough protein was a major worry: _Let me emphasize, it is difficult to design a reasonable experimental diet that provides an active adult with adequate calories that is deficient in protein._ Many consider Nathan Pritikin the foremost expert on nutrition in modern times. Thousands of people came to his Longevity Centers. Some came in wheelchairs or preparing for coronary bypass operations. Many went jogging home a month later. Most improved tremendously. The heart of Pritikin's program was his diet. He said: _Vegetarians always ask about getting enough protein. But I don't know any nutrition expert that can plan a diet of natural foods resulting in a protein deficiency, so long as you're not deficient in calories. You need only six percent of total calories in protein... and it's practically impossible to get below nine percent in ordinary diets._ It seems Nature must have wanted us to have enough protein, for simply following the instinct of hunger and eating enough natural food of whatever kind, we find it almost impossible to be deficient in this vital nutrient. And it doesn't matter very much whether or not we hold one form of protein to be superior. Either way, and whatever the demands of our biological individuality, the evidence forces us to conclude that we will get enough protein, even without meat, dairy products, eggs, or protein complementarity. I admit that I have sometimes had a hard time accepting these truths. I have been powerfully programmed and have become emotionally attached to the old ideas about protein. But dispassionate appraisal of the evidence virtually forces me to conclude that the "problem" of where vegetarians will get their protein is in actuality a nonproblem, even for those who forgo dairy products and eggs. In fact, researchers who purposely want to design diets deficient in protein often have a devil of a time. It is possible, but it's far from easy. By the same token, it is possible for a vegetarian to be deficient in protein, but it takes some doing. Here's how it can be done: **The Nonprotein Diet** 1. By eating excessive junk food. Such "food"—which includes fatty, highly refined, and processed foods, most sweets, and excess alcohol—gives us only empty calories. These are calories that provide momentary fuel but do not nourish our cells or organs. They provide little in the way of vitamins, minerals, protein, or fiber. A diet with a lot of fat, candy, soda pop, white bread, pastries, and/or fried foods will probably lead to protein deficiency, as well as a deficiency in every other nutrient we need. 2. By trying to live on fruit alone. Of course, most of us wouldn't consider fruit as a staple for any length of time and so needn't worry about this. But there are some who try to be "fruitarians." Usually, their reasons are more spiritual than nutritional, and it is a good thing, because from a nutritional point of view, a fruitarian diet may lack adequate protein. 3. By eating only those few crops whose protein content is unusually low. This would be nearly impossible in the United States. But there are parts of West Africa where the staple food is the cassava root, which provides only about two percent of its calories as protein. Sadly, people there sometimes have little else to eat. Some of them, as a result, encounter protein deficiency. 4. If an infant were to be fed just grains and vegetables, it might have difficulty absorbing enough protein due to the immaturity of its digestive system. Studies have shown potatoes can supply 100 percent of an infant's protein needs, but grains may fall short. Of course, if an infant is breast-fed, then there is nothing to worry about. 5. The only other way vegetarians could fail to fulfill their protein needs would be by starving. If you don't get enough food, then you aren't going to get enough protein. Of course, you aren't going to get enough carbohydrates or vitamins or fiber or minerals or anything else, either. This condition, which tragically occurs among the very poorest of the world, is known as kwashiorkor. But we hardly need a fancy name for someone who is starving to death. **Growing Up Big and Strong** I'm back in the classroom again. My teacher is telling us kids that if we want to be big and strong we had better eat lots of protein. And when we work hard and play hard, we need even more protein. I'm thinking of my Superman comic books and remembering the pictures of Charles Atlas on the back, with his huge muscles and rippling vitality. Squinting my eyes a little, I resolve to bite the bullet and ignore my intense dislike for meatloaf. Some things are more important than whether they taste good or not. Most of us, naturally, still believe what our teachers taught us. But one man who doesn't quite go along with all this, and who would appear to know what he's talking about, is a man who might be capable of kicking sand in even Charles Atlas's face. I'm speaking of Arnold Schwarzenegger, the virtual symbol of male muscular development. In his book, _Arnold's Bodybuilding for Men,_ Schwarzenegger writes: _Kids nowadays... tend to go overboard when they discover body building and eat diets consisting of 50 to 70 percent protein—something I believe to be totally unnecessary...[In] my formula for basic good eating: eat about one gram of protein for every two pounds of body weight._ This formula is in keeping with the range we have already discovered. To meet Arnold Schwarzenegger's suggested protein quota, you'd do fine without meat, eggs, or dairy products. If you ate only broccoli, I'd probably wonder whether you had lost your marbles, but you'd get more than four times Schwarzenegger's suggested requirement. When it comes to the relationship between protein and physical work, it turns out that once again my teacher, bless her heart, didn't quite hit the nail on the head. True, we need protein to replace enzymes, rebuild blood cells, grow hair, produce antibodies, and fulfill certain other specific tasks. But there is virtually no greater demand for any of these functions to perform hard physical work. If we are working or playing hard, it is not more protein we need; rather, we require more carbohydrates to burn, because it is carbohydrates that provide our fuel. Study after study has found that protein combustion is no higher during heavy exercise than under resting conditions. This is why Dave Scott can set world records for the triathlon without consuming lots of protein. And why Sixto Linares can swim 4.8 miles, cycle 185 miles, and run 52.4 miles in a single day without meat, dairy products, eggs, or any kind of protein supplement in his diet. The popular idea that we need extra protein if we are working hard turns out to be simply another part of the whole mythology of protein, the "beef gives strength" conditioning foisted upon us by those who profit from our meat habit. Such thoughts have been planted in our minds since we were little children and have, for many of us, become so much a part of our psychic landscape that we simply "know" they are true. We have come to take them for granted as given facts, much as people once took for granted that the world was flat. But today, even the conservative National Academy of Sciences, an organization hardly renowned for going out on a limb and taking controversial positions, says: _There is little evidence that muscular activity increases the need for protein._ Modern nutritional science tells us clearly that our protein needs are easily met without any fuss. And yet many of us are haunted, somewhere in the back of our minds, by the fear that if we do not eat enough protein we may end up looking like one of the people on a CARE poster. Because we absorbed this fear when we were very young, it has become part of the very foundations of our psyche. We have become living examples of the old German proverb _An old error is always more popular than a new truth._ We have become protein obsessed, and we pay an incalculable price for it. We feed an enormous amount of grain to livestock that could otherwise be fed to the world's hungry. We cause a great deal of needless suffering to animals. And finally, we seriously compromise our health. Though we know that almost anything in excess can be harmful, be it aspirin or alcohol, sex, food, or sunshine, we rarely apply this understanding to our protein consumption. We have for the most part been so afraid of not getting enough protein that we have ignored the growing body of scientific research that points to the serious health consequences of ingesting too much. **Osteoporosis and the Protein Connection** By now, if my grade school teacher is still alive, she is probably gray haired and in her sixties. If she is like most women that age in the United States, her "old bones" are probably not quite what they used to be. She may be a little stooped over with age, and she may well have lost significant height from the days when she towered over a classroom of youngsters. Actually, if she is like most women that age in the United States, her old bones are far indeed from what they once were. They have lost significant amounts of minerals, especially calcium, and as a result are springy, fragile, and weak. It is not at all uncommon for the bone mineral losses in postmenopausal women to cause them chronic back pain while at the same time making them susceptible to frequent fractures. Often they lose height and find themselves increasingly stooped over, for the weakened vertebrae just cannot support the body load. Unfortunately, this crumpling of the body posture is not just an aesthetic misfortune. Increased pressure is put on the inner organs, and they are unable to function as they should. I remember my teacher fondly and wouldn't wish this on her for all the world. But in fully 25 percent of 65-year-old women in the United States, bone mineral losses (called bone resorption) are so severe that the condition is given the clinical name "osteoporosis." For a person technically to qualify for this label, it means she has lost 50 to 75 percent of the original bone material from her skeleton. Fully one out of every four women 65 years old in our culture has lost over half her bone density. Today, more deaths are caused by osteoporosis than by cancer of the breast and cervix combined. Unfortunately, the loss of calcium and other minerals from the bones is a gradual process that goes on steadily for a long time before it becomes evident. There is no flashing red light to warn us that our bodies are losing calcium. And it is usually not apparent until loose teeth, receding gums, or a fractured hip show how brittle and chalky the bones have become. The end result of the skeletal structure's gradual erosion is calcium-deficient bones that may break with the slightest provocation. Even a mere sneeze may crack a rib. **THE RAVAGES OF OSTEOPOROSIS** **On the standard American diet, almost all females suffer significant loss of bone density as they age.** Source: Derived from Morris Notelovitz and Marsha Ware, _Stand Tall_ (Gainesville, FL: Triad Publishing Company, 1982), 32. One of the reasons the decreasing bone density is hard to detect until it reaches such an unfortunate stage is that even in extreme cases of osteoporosis, the calcium level of the blood is usually normal. In the body's ranking of needs, the blood level of calcium takes definite priority over the bone level of calcium. The body needs calcium in the blood for vital operations, such as controlling muscular contractions, including the heart's, blood clotting, and the transmission of nerve impulses. When the body needs to supply calcium to the blood for any reason, it acts as if the bones are a bank of stored calcium, and through a series of biochemical reactions a check is drawn on the calcium bank. Your body draws calcium from your bones to supply calcium to your blood. I used to believe that bones lost calcium only if there was not enough calcium in our diets. The National Dairy Council is the foremost spokesman for this point of view, and the solution they propose, not all that surprisingly, is for us all to drink more milk and eat more dairy products. In fact, the dairy industry has of late spent a great deal of money promoting this point of view. And it does seem logical. But modern nutritional research clearly indicates a major flaw in this perspective. Osteoporosis is, in fact, a disease caused by a number of things, the most important of which is excess dietary protein The correspondence between excess protein intake and bone resorption is direct and consistent. Even with very high calcium intakes, the more excess protein in the diet, the greater the incidence of negative calcium balance, and the greater the loss of calcium from the bones. The figure on page 172 shows the results of the independent work of five different research teams studying the effect of low- and high-protein diets on calcium balance. On the chart, a positive calcium balance means the bones are not losing calcium, while a negative calcium balance means they are, and osteoporosis is developing. One long-term study found that with as little as 75 grams of daily protein (less than three-quarters of what the average meat-eating American consumes) more calcium is lost in the urine than is absorbed by the body from the diet—a negative calcium balance. In every study the same correspondence was found: the more protein that is taken in, the more calcium that is lost. This is true even if the dietary calcium intake is as high as 1,400 milligrams per day, far higher than in the standard American diet. In other words, the more protein in our diet, the more calcium we lose, regardless of how much calcium we take in. The result is that high-protein diets in general, and meat-based diets in particular, lead to a gradual but inexorable decrease in bone density and produce the ongoing development of osteoporosis. **IS OSTEOPOROSIS DUE TO CALCIUM DEFICIENCY OR EXCESS PROTEIN?** **Study No.** | **Calcium Intake (milligrams)** | **Change in Calcium Balance with a Low-Protein Diet** | **Change in Calcium Balance with a High-Protein Diet** ---|---|---|--- **1** 2 3 4 5 **Average** | 500 500 800 1,400 1,400 920 | +31 +24 +12 +10 +20 +19 | -120 -116 -85 -84 -65 -94 Study no. 1 | C. Anad, "Effect of Protein Intake on Calcium Balance of Young Men Given 500 Mg Calcium Daily," _Journal of Nutrition_ 104 (1974): 695. ---|--- Study no. 2 | M. Hegsted, "Urinary Calcium and Calcium Balance in Young Men as Affected by Level of Protein and Phosphorous Intake," _Journal of Nutrition_ 111 (1981): 53. Study no. 3 | R. Walker, "Calcium Retention in the Adult Human Male as Affected by Protein Intake," _Journal of Nutrition_ 102 (1972): 1297. Study no. 4 | N. Johnson, "Effect of Level of Protein Intake on Urinary and Fecal Calcium and Calcium Retention of Young Adult Males," _Journal of Nutrition_ 100 (1970): 1425. Study no. 5 | H. Linkswiler, "Calcium Retention of Young Adult Males as Affected by Level of Protein and of Calcium Intake," _Transactions of the New York Academy of Science_ 36 (1974): 333. | Source: Data as per Dr. John McDougall, _McDougall's Medicine_ (New York: New Century Publishers, 1985). Summarizing the medical research on osteoporosis, one of the nation's leading medical authorities on dietary associations with disease, Dr. John McDougall, says: _I would like to emphasize that the calcium-losing effect of protein on the human body is not an area of controversy in scientific circles. The many studies performed during the past 55 years consistently show that the most important dietary change that we can make if we want to create a positive calcium balance that will keep our bones solid is to decrease the amount of proteins we eat each day. The important change is not to increase the amount of calcium we take in._ The National Dairy Council has spent tens of millions of dollars to make us think that osteoporosis can be prevented by drinking more milk and eating more dairy products. But the only research that even begins to suggest that the consumption of dairy products might be helpful has been paid for by the National Dairy Council itself. **Osteoporosis around the World** Throughout the world, the incidence of osteoporosis correlates directly with protein intake. In any given population, the greater the intake of protein, the more common and more severe will be the osteoporosis. In fact, world health statistics show that osteoporosis is most common in exactly those countries where dairy products are consumed in the largest quantities—the United States, Finland, Sweden, and the United Kingdom. Nathan Pritikin studied the medical research on osteoporosis and found no basis at all for the Dairy Council viewpoint: _African Bantu women take in only 350 mg. of calcium per day. They bear nine children during their lifetime and breast feed them for two years. They never have calcium deficiency, seldom break a bone, rarely lose a tooth. Their children grow up nice and strong. How can they do that on 350 mg. of calcium a day when the (National Dairy Council) recommendation is 1200 mg.? It's very simple. They're on a low-protein diet that doesn't kick the calcium out of the body... In our country, those whocan afford it are eating 20 percent of their total calories in protein, which guarantees negative mineral balance, not only of calcium, but of magnesium, zinc, and iron. It's all directly related to the amount of protein you eat._ The Bantus consume much less calcium than do Americans. Yet even their oldest women are essentially free of osteoporosis, while the disease is epidemic in older American women. The dairy industry has said that the Bantus' far higher bone densities on much lower calcium intakes may be due to genetic factors. But genetic relatives of the Bantus living in the United States and eating the standard American diet-style have levels of osteoporosis that equal those of their white neighbors. Therefore, the only sensible conclusion, in light of all the research, is that the Bantus' far lower protein consumption has kept their bones healthier. At the other end of the scale from the Bantus are the native Eskimos. If osteoporosis were a calcium deficiency disease it would be unheard-of among these people. They have the highest dietary calcium intake of any people in the world—more than 2,000 milligrams a day from fish bones. If, however, osteoporosis is caused by excess protein in the diet, they will suffer greatly from the disease, because their diet is also the very highest in the world in protein—250 to 400 grams a day from fish, walrus, and whale. As it happens, unfortunately, the native Eskimo people have one of the very highest rates of osteoporosis in the world. Studies comparing the bone densities of people with different diet-styles show a pattern completely opposed to the dairy industry's declarations. The research invariably reveals greater bone resorption and development of osteoporosis with a greater intake of meat and dairy products, not the other way around. On August 22, 1984, the _Medical Tribune_ reported a major study of bone densities in the United States. The conclusion was typical of the many such studies: vegetarians were found to have "significantly stronger bones." In March 1983, the _American Journal of Clinical Nutrition_ reported the results of the largest study of this kind ever undertaken. Researchers at Michigan State and other major universities found that, by the age of 65 in the United States: • _Male vegetarians had an average measurable bone loss of 3 percent._ • _Male meat-eaters had an average measurable bone loss of 7 percent._ • _Female vegetarians had an average measurable bone loss of 18 percent._ • _Female meat-eaters had an average measurable bone loss of 35 percent._ By the time she reaches the age of 65, the average meat-eating woman in the United States has lost over a third of her skeletal structure. In contrast, older vegetarian women tend to remain active, maintain erect postures, and are less likely to fracture or break bones even with their increased physical activity. If their bones do break or fracture, they heal faster and more completely. **Why Are Vegetarians Protected?** You may wonder, since osteoporosis seems to be caused by excessive dietary protein, why vegetarians seem so protected from its ravages. Isn't it possible to overdose on vegetarian proteins? A United States Department of Agriculture survey found that American vegetarians consume, on the average, 150 percent of their actual protein requirements. The biggest overdose is found among children aged three to eight. These youngsters, many of whom are told to drink three glasses of milk a day, consume, on the average, 209 percent of their actual protein needs. I suspect that many of the parents of these vegetarian children, who are no doubt vegetarians themselves, are afraid their children won't get enough protein. Attempting to appease the protein tyrant in their own minds, they make doubly sure their kids eat lots of milk and cheese and yogurt and eggs, thinking they are doing them a good turn. The kids end up eating far more protein than they actually need, even with all their growing requirements taken into account. Even haunted by the protein myth, however, vegetarians tend not to overconsume protein to the extent that meat-eaters do, and this is one reason they do not suffer nearly as much osteoporosis. But even if a vegetarian were to consume as much excess protein as a meat-eater, he or she would still have stronger bones because meat, eggs, dairy products, and fish contribute to osteoporosis in yet other ways. **Keeping pHit** Keeping our blood at an essentially neutral pH is a top priority for the body. If our blood were to become too acidic we would die. Accordingly, if the diet contains a lot of acid-forming foods, then the body, in its wisdom, withdraws calcium from the bones and uses this alkaline mineral to balance the pH of the blood. As we can see from the figure on page 177, meat, eggs, and fish are the most acid-forming foods, and hence the ones that cause calcium to be drawn from the bones to restore the pH balance. Most fruits and vegetables, on the other hand, generally yield an alkaline ash and so require no depletion of calcium stores from the bones to maintain the neutrality of the blood. There is yet another reason why vegetarians are relatively immune to osteoporosis, even though the Dairy Council keeps telling us that calcium intake is the answer to this disease. What they neglect to mention is that the body's ability to absorb and utilize calcium depends directly on the amount of phosphorus in the diet. In one study, young women maintained a positive calcium balance when their diets provided 1,500 milligrams of calcium and 800 milligrams of phosphorus per day. But when phosphorus intake was raised to 1,400 milligrams a day, the women went into negative calcium balance, even though their calcium intake had not been reduced. More important, apparently, than the amount of calcium taken in is the calcium:phosphorus ratio. The lower this ratio, the greater the loss of bone density, and the greater the development of osteoporosis. The higher the calcium:phosphorus ratio, the less bone loss and the stronger the skeleton, assuming the intake of protein is not excessive. The foods whose calcium is least available, because their calcium: phosphorus ratio is low, are liver, chicken, beef, pork, and fish, in that order. The calcium in vegetables and fruits, in sharp contrast, is much more available, due to their higher calcium:phosphorus ratios. Lettuce, for example, is not particularly high in calcium, but its calcium is readily utilized by the body because its ratio of calcium to phosphorus is comparatively high—70 times higher than that of liver, and 23 times higher than that of beef or pork. The foods whose calcium is best utilized are those with the highest calcium:phosphorus ratios, such as the green leafy vegetables. The calcium in these foods is dramatically more available than that found in animal products. If the calcium:phosphorus ratio for mustard greens, for example, were to be represented by a towering skyscraper, the equivalent ratio for chicken would barely amount to a small doghouse. **ACID- AND BASE-FORMING CAPACITIES OF SELECTED FOODS** Source: R. A. McCance and E. M. Widdowson, _The Composition of Foods_ (London: Her Majesty's stationery office, 1960), 22, 124. **Fudging the Truth** The claims of the dairy industry are based on the idea that bone loss is due solely to a diminished intake of dietary calcium. So drink your milk. But the only studies in the medical literature to support this contention were sponsored by the National Dairy Council itself. Remarkably, even those studies funded by the National Dairy Council for the express purpose of showing the benefits of milk for women susceptible to osteoporosis have, in fact, ended up showing something quite different. In one Dairy Council–sponsored study, women who drank an extra three eight-ounce glasses of low-fat milk every day for a year showed no significant increase in calcium balance. Even with all the extra mild-derived calcium, they were still in negative calcium balance after a full year of the regime. The scientists who conducted the test knew why. They said the women continued to have a negative calcium balance, and continued to develop osteoporosis, due to _the average thirty percent increase in protein intake during milk supplementation._ The additional protein load from the milk tended to wash calcium and other minerals out of the subjects' bodies and thus throw them into negative calcium balance. Not surprisingly, the Dairy Council is not keen to have the public know the results of this and the many similar studies. In 1984, the _British Medical Journal_ published a report indicating that calcium intake is, in fact, completely irrelevant to bone loss. The researchers enlisted postmenopausal women, who agreed to take 500 milligrams of supplemental calcium every day for two years. They were divided into three groups: 1) those whose diets contained less than 550 milligrams of calcium, 2) those who consumed between 550 mg and 1,100 milligrams of calcium daily, and 3) those whose diet provided more than 1,100 milligrams. At the end of two years, there was no difference in bone demineralization among the three groups. In fact, their bone losses were virtually the same as those found in women taking no calcium supplements at all, and whose diets contained less than the recommended daily allowance of calcium. This was true even though some of the women in the test were taking huge amounts of calcium from food and supplemental sources—in some cases, over 2,000 milligrams a day. Even the most conservative medical investigators no longer deny the connection between excess protein and osteoporosis. In a report published in _Lancet_ , Drs. Aaron Watchman and Daniel Bernstein commented on work sponsored by the United States Department of Health and Harvard University. They called the association of meat-based diets with the increasing incidence of osteoporosis "inescapable." There are, of course, other factors besides getting lots of protein that contribute to osteoporosis. Small, light-skinned Caucasian women are more susceptible, as are women who bear no children and those who've had their ovaries removed. Lack of exercise is a factor, as is the consumption of soft drinks (they are very high in phosphorus), junk food, excess salt, and acidforming foods. Smoking increases the risk, as do certain anticonvulsant medications. Yet though there are a number of factors that can contribute to osteoporosis, excess protein consumption clearly towers above them all as the chief causative influence. Quite frankly, the more I've studied the conclusions of the hundreds of studies in the medical literature, the harder it has gotten for me to abide the National Dairy Council's promotion of milk for strong bones. In spite of its high calcium content, milk, due to its high protein content, appears actually to _contribute_ to the accelerating development of osteoporosis. The occurrence of this disease in the United States has reached truly epidemic proportions, and the promotion of dairy products as an answer to the suffering of millions seems not only self-serving but absolutely immoral and downright dishonest. **Enough Is Enough** As if osteoporosis weren't enough, it turns out there are other problems derived from too much protein, particularly too much animal protein. One such problem is kidney stones. The calcium lost from our bones due to excess protein has to go somewhere after it has served its purpose in our bloodstream. And so does the calcium we have ingested but have not been able to absorb due to low calcium: phosphorus ratios. It all ends up in our urine, producing very high levels of calcium in the kidney system and all too often crystallizing into kidney stones. This is why kidney stones, the most painful of all medical emergencies, occur far more frequently in meat-eaters than in vegetarians. Additionally, there is a great deal of evidence implicating excessive protein consumption in the destruction of kidney tissue and the progressive deterioration of kidney function. Extra protein doesn't just trickle out of the body. It takes hard work on the part of the kidneys to get rid of the excess. Many animal studies have shown that the higher the protein in the diet, the greater the incidence and the more severe the cases of kidney hypertrophy and inflammation. The same things happen to human kidneys if we overconsume protein. People who have suffered kidney damage or loss are usually able to preserve their remaining kidney function only if they are put on a protein-restricted diet. Those kidney patients whose protein intake is not restricted, and particularly those who continue to eat meat, show rapid deterioration of their kidneys, to the point that many become dependent on kidney dialysis machines. It is important to stress that the link between kidney disease and excess protein consumption, like the link between osteoporosis and excess protein consumption, is no longer considered merely probable within the informed medical community. Too many tests by too many researchers under too wide a variety of conditions have been too consistent in their implications. It is now considered certain. As the evidence against too much protein mounts, you may shake your head and wonder just how our protein obsession ever got started in the first place. Almost all the early nutritional research was done on livestock, at the behest of people raising animals for meat and milk. Their objective was to produce the biggest animals in the shortest length of time. The idea that rapid growth and large size are inherently desirable was implicit in the undertaking. Nutritional research was therefore geared to finding what diets would accomplish this aim. Early experiments which found that rats grew faster when fed animal protein led to the hypothesis that animal protein was superior. Further research has validated that rats so fed do indeed grow faster. But the "bigger is better" mentality has been dealt quite a blow by other discoveries. It has been found that rats fed animal protein also die sooner, plus they suffer from a multitude of diseases vegetarian rats do not. A report aptly titled "Rapid Growth, Short Life" appeared in the _Journal of the American Medical Association._ It showed that high-animal-protein diets measurably shortened the life spans of a number of different animals. These findings corroborate the world health statistics that show human meat-eating populations do not, as a rule, live as long as vegetarian populations. It has also been discovered that meat-eaters have higher rates of cancer than do vegetarians. Just how excess protein may be linked to cancer is not yet understood, but there is growing evidence that they are indeed linked. The meat and dairy industries like to question the credentials of anyone who suggests their products might not promote optimum health. But it would be hard to doubt the credentials of T. Colin Campbell, a professor in the division of Nutritional Sciences at Cornell University and the senior science adviser to the American Institute for Cancer Research. He said recently that there is _a strong correlation between dietary protein intake and cancer of the breast, prostate, pancreas, and colon._ Other authorities with equally impeccable credentials agree. Myron Winick, director of Columbia University's Institute of Human Nutrition, says the data indicate _a relationship between high-protein diets and cancer of the colon._ It just goes on and on... **Now What?** I'm back in my grade school classroom. The teacher is telling all us little kids about the importance of eating lots of meat and drinking lots of milk. She is pointing to a colorfully decorated chart, which makes it all seem so simple. She is telling us about the importance of getting enough protein and making it clear that animal protein is the only complete protein. Her voice rings with authority, because she believes every word she is saying. I'm listening, but not completely. I'm thinking about my pet kitten, about how furry and cuddly and playful he is, and about a neighbor's dog who recently had puppies. My teacher's voice drifts over me and slides away. I look outside the window and see a bird who seems to feel my attention, because as I look she begins to sing. That day at lunch I feel like doing something good for myself and the world. I decide to save my milk money and give it to people who do not have enough to eat. 8. **FOOD FOR THE CARING HEART** _People often say that humans have always eaten animals, as if this is a justification for continuing the practice. According to this logic, we should not try to prevent people from murdering other people, since this has also been done since the earliest of times._ —ISAAC SINGER The human heart doesn't actually look very much like a valentine, but it is nevertheless a wondrous and beautiful muscle. About the size of a clenched fist, it begins to beat only a few weeks after conception and thereafter pumps forth the rhythm of our lives through every moment of our uterine and earthly existence. Only at the moment of our death does it cease. This beating has a definite purpose: to pump blood to all parts of the body. The life of our very cells depends on the oxygen and nutrition brought to them by the flow of our blood. If for some reason any muscle did not receive a fresh flow of blood, it would quickly die. Since the heart is also a muscle, it, too, must continuously receive a fresh flow of blood, and you might think that receiving a blood supply would never be a problem for the heart, since its chambers are always full of blood. But the heart is not able to directly use any of the blood contained within its pumping chambers, any more than a stereo amplifier can plug into itself. Instead, the heart muscle feeds from the blood supplied to it through two specific vessels, called the coronary arteries. In a healthy person, the blood flows freely and easily through the coronary arteries, and the well-fed heart keeps pumping away as it should. But if one of the coronary arteries, or one of its branches, should become blocked off and so be unable to supply the heart with blood, then even though the heart's chambers are full of blood, that part of the heart dependent on the blocked-off artery will die. In medical terminology, this is called a myocardial infarction. Most of us know it by another name—a heart attack. Heart attacks are by far the largest cause of death in the United States today. Every 25 seconds another person is stricken. Every 45 seconds another person dies. If a heart attack victim is fortunate, and the part of the heart that dies is small, he or she will survive, and the dead tissue will come gradually to be replaced by scar tissue. But if a larger part of the heart is deprived of blood, there really isn't very much that can be done to save the person's life. Many heart attack victims die within minutes of the unexpected seizure. Heart attack victims often never have the slightest warning anything is wrong. There are no bodily symptoms to signal the oncoming disaster. They may have only that morning heard their physician pronounce them fit as a fiddle. But, then, suddenly, the victims feel a sudden, severe, crushing pain in their chests. Often the pain shoots down the arm, and sometimes it flares up the neck, particularly on the left side. There may be cold sweating, nausea, vomiting, and shortness of breath. The symptoms are accompanied by a feeling of being overwhelmed by enormous terror and dread. Though heart attacks strike suddenly, and often without forewarning, they do not just happen. A heart attack is the inexorable final step of a slow and lengthy process. You can put cold water in a pot, put the pot on the stove, and turn on the heat. For a while nothing much will seem to change as you watch. But if the heat is high enough, at a certain point bubbles will appear on the surface of the water. You will see very little change all the while the water heats from 32° toward 212°. But then, suddenly, just as it approaches the threshold of 212°, there are dramatic visible changes, and the water boils. Similarly, the apparent suddenness of a coronary artery closing off and the consequent heart attack is actually quite misleading. In reality, for this final step to occur, our arteries must have been approaching "the boiling point" for some time. The slow and steady process that takes place in our arteries and inexorably increases our heart attack susceptibility has a name. This process, which is, in fact, the deeper cause of almost all heart attacks, is called atherosclerosis. Atherosclerosis is often referred to in common speech as hardening of the arteries, and although this is not an entirely inaccurate way of describing what happens, "narrowing of the arteries" would be a better catchphrase, though this, too, would be less than exact. Atherosclerosis is the process by which arteries gradually accumulate fatty and waxy deposits on their inner walls—thus reducing the size of the openings through which the blood can flow. The foreign deposits that adhere to the inner walls of the arteries are called atheromas or plaques. When these plaques become advanced enough, the fatty contents of the deposits will rupture into the artery and form a clot. These clots may clog up the already reduced arterial opening and thus entirely prevent the flow of blood through the artery. If a clot forms in one of the two coronary arteries that supply the heart with its only source of life-giving blood, and the coronary artery becomes blocked by the clot, the heart is deprived of its supply of life-giving blood, and the result is a heart attack. There could be no heart attack unless the coronary arteries had already become partially closed and irritated by atherosclerotic deposits. Atherosclerosis, the real culprit, is what must be eliminated to prevent heart attacks. There is another part of the body particularly vulnerable to having its blood supply cut off by an obstructed artery. It is the part of the body whose functioning, or lack of it, has often been the source of wit: _The brain is a wonderful organ; it starts working the moment you get up in the morning and does not stop until you get into the office._ In truth, however, the physical failure of the brain to function is far from a laughing matter. Strokes, like heart attacks, often occur with no prior warning, and, like heart attacks, they often kill. Strokes account for more deaths in the United States today than any other cause except heart attacks and cancer. In fact, strokes are very similar to heart attacks, except that the two events take place in different body locations. For just as atherosclerotic deposits in the arteries feeding the heart set the stage for heart attacks, atherosclerotic deposits in the arteries feeding the brain set the stage for strokes. And just as the affected part of the heart dies when its blood supply becomes blocked off, so the affected part of the brain dies when its blood supply is compromised by arterial blockage. As with the heart, this can only occur when the arteries have become hardened, narrowed, and encrusted with atherosclerosis. **THE 10 LEADING CAUSES OF DEATH IN THE UNITED STATES, 1970** Source: Roy Walford, MD, _Maximum Life Span_ (New York: W. W. Norton & Co., 1983), 8. If we add up the deaths caused by heart attacks, strokes, and other consequences of atherosclerosis, we get a figure larger than all other causes of death in the United States combined. Statistically, you and I each have better than a 50-50 chance of dying from a disease directly caused by the clogging up of our arteries. **Hope** For years it was thought that heart disease and strokes were simply misfortunes we had to somehow learn to accept. But over the past 30 years, this has changed. The most comprehensive research in medical history has discovered something of marvelous and far-reaching consequence: we are not helpless victims of atherosclerosis. It is a disease that, knowingly or unknowingly, we bring upon ourselves and, by the same token, can prevent. I am reminded of one of Aesop's fables: _The Eagle and the Arrow_ _An eagle sat on a lofty rock, watching the movements of a hare whom he sought to make his prey. An archer, who saw the eagle from a place of concealment, took accurate aim and wounded him mortally. The eagle gave one look at the arrow that had entered his heart and saw in that single glance that its feathers had been furnished by himself._ _"It is a double grief to me," he exclaimed woefully, "that I should perish by an arrow feathered from my own wings."_ The most advanced medical knowledge in history is telling us that heart attack and stroke victims—50 percent of us—perish from a disease nurtured by our own hands. The growth in the medical understanding of heart disease that has taken place in the past 30 years is one of the great stories in medical history. With each passing year, more and more of the most respected medical organizations in the world have come to the same conclusion: Diets high in saturated fat and cholesterol raise the level of cholesterol in the blood, produce atherosclerosis, and lead directly to heart disease and strokes. Diets low in saturated fat and cholesterol lower the level of cholesterol in the blood, decrease atherosclerosis, and lower the likelihood of heart disease and strokes. The medical statistics are clear. We can virtually stab ourselves in the heart with our forks by eating a diet that promotes atherosclerosis. Or we can overwhelmingly reduce our potential for heart disease by eating a diet that supports the health of our cardiovascular system. Many a deeply inspiring story has emerged from the dedicated medical researchers working day in and day out year after year to discover what has been learned. At the same time, however, there are other stories that are anything but inspiring. There are powerful interests who profit from the sale of foods high in saturated fat and cholesterol who recognize that the advances in medical understanding are not to their financial advantage. And though they have not been able to impede the growth of medical knowledge, they have been remarkably successful in preventing the public from having the full benefit of what has been learned, employing ruse after ruse in their efforts to keep our nation hooked on foods high in saturated fat and cholesterol. What the tobacco industry is for lung cancer, these industries have become for the heart attack. **The First Evidence** Some of the first evidence indicating that atherosclerosis was not simply a consequence of growing old but was rooted in our dietary intake of saturated fat and cholesterol came inadvertently from the Korean War. Soldiers who had been killed were autopsied, and medical researchers were stunned by what they found. More than 77 percent of the American soldiers had blood vessels that were already narrowed by atherosclerotic deposits, while the arteries of the equally young soldiers of the opposing forces showed no similar damage. At the time, it was thought that the pronounced differences in the conditions of the soldiers' arteries might be more a consequence of genetic predisposition than of their differing diet-styles. But this idea became quickly untenable when a large group of Korean soldiers were put on the U.S. Army diet. They rapidly developed significant increases in their blood cholesterol levels, an unmistakable sign of developing atherosclerosis. Traditional nutritionists had thought highly of meat, dairy products, and eggs ever since the early animal experiments that showed rats grew faster on animal protein. As well, the first vitamin ever discovered, vitamin A, had originally been isolated from butterfat, which also added to the aura of supremacy these foods enjoyed. But as a result of the autopsies, the possibility that dairy products, meat, and eggs might be seriously involved in heart disease now had to be taken seriously for the first time. Meat, dairy products, and eggs are the chief source of dietary saturated fat. Along with fish, they are the _only_ sources of dietary cholesterol. Stirred by the results of the Korean War autopsies, medical researchers undertook a major effort to learn more. From 1963 to 1965, a worldwide study of heart disease and stroke patterns was done, called the International Atherosclerotic Project. This truly mammoth undertaking involved examining the arteries of over 20,000 autopsied bodies throughout the world. The findings revealed an unmistakable pattern: people who lived in areas where consumption of saturated fat and cholesterol was high had markedly more atherosclerosis, more heart attacks, and more strokes. It took a while for medical researchers to grasp the full implications of what was being learned, because the emerging truth required them to do a complete about-face from their well-entrenched assumptions. The meat, dairy, and egg industries, meanwhile, were not exactly eager to support the researchers' new findings. They financed numerous studies that attempted to vindicate their products and discredit what they called the saturated fat and cholesterol "theory" of atherosclerosis. Some pointed out that animal foods were not the only products high in saturated fat and attempted to point an accusing finger at plant sources. Directing attention to coconuts, palm kernel oil, and chocolate, which are all high in saturated fat, they loudly proclaimed that meat, dairy products, and eggs should not be singled out and found guilty as the sole suppliers of saturated fats in our diets. But scientists who were not on the payroll of these industries, and who were perhaps a bit more impartial in their motivation, pointed out that coconuts, palm kernel oil, and chocolate are the _only_ plant foods significantly high in saturated fat. They also suggested that meat, eggs, and dairy products probably make up a larger percentage of most people's diets than do coconuts, palm kernel oil, and chocolate. Further, they pointed out that cholesterol cannot be found in any plant food. As the figure on page 191 shows, our entire intake of cholesterol is necessarily derived from meat, fish, dairy products, and eggs. **The Mounting Consensus** With each new study the evidence was becoming harder and harder to brush aside. The industries that foresaw their profits seriously threatened by the advancing knowledge, however, managed to overlook much that was being learned, and to insist that hereditary influences were more important than one's intake of saturated fat and cholesterol. To find out if there could be any truth to this, Dr. M. G. Marmot and his coworkers at the University of California, Berkeley, undertook a major study of the heart disease rates of men of Japanese descent who lived in different parts of the world and ate according to the various local diet-styles. The results stunned a medical world still finding it hard to believe meat, dairy products, and eggs were suspect. The study found an almost exact statistical correlation for all groups between consumption of saturated fat and cholesterol and deaths due to coronary heart disease. With each passing year the evidence mounted. In 1970, Dr. Ancel Keys of the University of Minnesota School of Public Health published the results of a massive seven-country study analyzing the role of diet in heart disease. The study involved over 12,000 men in Finland, Greece, Italy, Japan, the Netherlands, the United States, and Yugoslavia. It found telling correlations between the amount of saturated fat and cholesterol in a people's diet, the levels of cholesterol in their blood, and their death rate from heart disease. Of these nations, the United States and Finland had the highest consumption of animal products, the highest consumption of saturated fat, the highest consumption of cholesterol—and the highest death rate from heart disease. **CHOLESTEROL CONTENT OF COMMON FOODS** **ANIMAL FOOD** Cholesterol Content (in milligrams per 100-gram portion) | **PLANT FOOD** Cholesterol Content (in milligrams per 100-gram portion) ---|--- Egg, whole Kidney, beef Liver, beef Butter Oysters Cream cheese Lard Beefsteak Lamb Pork Chicken Ice cream | 550 375 300 250 200 120 95 70 70 70 60 45 | All grains All vegetables All nuts All seeds All fruits All legumes All vegetable oils | 0 0 0 0 0 0 0 Source: J. Pennington, _Food Values of Portions Commonly Used,_ 14th ed. (New York: Harper & Row, 1985). It was becoming increasingly difficult to deny the evidence implicating saturated fat and cholesterol, though the industries whose products were being incriminated were trying diligently. Unable to counter the accumulating evidence, they ignored it, continuing to insist that hereditary factors were primary. Dr. Keys's massive study and others like it, however, indicated otherwise. It was common knowledge that different groups of the men under study, such as clerks, miners, mechanics, farmers, and doctors, tend to have their own diet-styles, with their corresponding levels of saturated fat intake. And it was also common knowledge that Japanese who lived in the West had diet-styles different from those in Japan. But when the levels of saturated fat in the diets of each of these various groups were compared to their blood cholesterol counts, the results were spectacular. As the figure on page 193 shows, the correlation between saturated fat consumption and blood cholesterol levels could hardly have been more exact. Even those researchers most attached to traditional ideas were coming to conclude that the more saturated fat and cholesterol there was in a person's diet, the more cholesterol would be in his blood, the worse shape his arteries would be in, and the more likely a candidate he would be for a heart attack or a stroke. The meat, dairy, and egg industries were far from pleased with the way things were going. **Increasing Clarity** The evidence implicating the traditional mainstays of the Western diet was not accepted overnight. Because firmly established beliefs were being so seriously threatened, it was subjected to the most rigorous testing in medical history. Though I do not ethically condone most laboratory experiments on animals, the results of such tests were another nail in the coffin for conventional dietary wisdom. At the University of Chicago, Dr. Robert Wissler and his coworkers fed a standard American diet to rhesus monkeys. To a second group of monkeys they fed a diet different only in that it was lower in saturated fat, cholesterol, and calories. After a time, they killed the monkeys and examined their arteries. The monkeys fed the standard American diet had six times as much atherosclerosis as the other monkeys. Scientists were not only finding that they could produce atherosclerosis in animals by feeding them diets with saturated fat and cholesterol but also finding that they could then unclog the arteries of the animals by reducing their intake of these particular substances. At the University of Iowa, Dr. Mark Armstrong and his colleagues fed a group of monkeys a diet rich in egg yolk, one of the leading suppliers of saturated fat and cholesterol in the American diet. The coronary arteries of these monkeys rapidly became encrusted with atherosclerosis. After the arteries of the monkeys had become over half closed, the researchers markedly reduced the amount of saturated fat and cholesterol that the monkeys consumed. A year and a half later, the atherosclerosis in the monkeys' arteries was less than one-third what it had become on the diet high in saturated fat and cholesterol. Spokesmen for the meat, dairy, and egg industries tried to discount the experiments, but researchers were increasingly impressed because these and similar experiments were repeated with a variety of different animals and the findings were consistent. The only animals able to handle saturated fat and cholesterol without developing substantial atherosclerosis were the natural carnivores. Dr. William S. Collens wrote of these studies in _Medical Counterpoint:_ **THE MORE SATURATED FAT YOU EAT, THE HIGHER YOUR BLOOD CHOLESTEROL WILL BE** Percentage of calories derived from fat in the diets of 284 Japanese men, and the resulting blood cholesterol levels. Diet-styles are largely determined by income and lifestyle in the given locations. Source: Data adopted from Ancel Keys, PhD, "Diet and the Epidemiology of Coronary Heart Disease," _Journal_ of th _e American Medical Association_ 164 (1957): 1916. _Recent studies, many of them in my laboratory at the Maiominides Medical Center, appear to indicate that the carnivorous animal has almost unlimited capacity to handle saturated fats and cholesterol, whereas the vegetarian and herbivorous animals have a very restricted capacity to handle these food components. It is virtually impossible to produce atherosclerosis in the dog, for example, even when 120 grams (½ pound) of butter fat are added to his meat ration...On the other hand, adding only two grams of cholesterol daily to a rabbit's chow for two months produces striking fatty changes in its arterial wall._ With each passing year and new set of studies, it was becoming increasingly clear that, like the primates who are closest to us biologically, human beings are among the animals unable to handle saturated fat and cholesterol. The more of these we eat, the more we develop atherosclerosis, and the more likely we are to die of heart disease. **More Evidence** In 1964, the heart specialist Dr. Paul Dudley White, renowned for his treatment of President Eisenhower's heart attack, went to visit the Hunzas of Kashmir, to see for himself whether the claims were true that these people lived to exceedingly old ages without any heart disease. He did blood pressure, blood cholesterol, and electrocardiogram studies, yet found not a trace of coronary heart disease, even in the 25 men he studied who were over the age of 90. In his report, published in the _American Heart Journal_ , Dr. White suggested a causative correlation between the Hunzas' diet-style, which was almost pure vegetarian, and their astounding lack of heart disease. Scientists began to reason that if meat, eggs, and dairy products were, in fact, the culprits they were becoming to appear, then it would be expected that lacto-ovo vegetarians, who do not eat meat, would have lower heart attack rates and lower heart disease mortality than meat-eaters. If this theory were correct, pure vegetarians, who consume no eggs, dairy products, or meat, would have even lower rates. Numerous studies were undertaken to find out if this might be the case. One of the largest studies of this kind was conducted at Loma Linda University in California and involved no less than 24,000 people. Reported in the _American Journal of Clinical Nutrition,_ this study found the heart disease mortality rates for lacto-ovo vegetarians to be only one-third that of meat-eaters. Pure vegetarians had truly impressive figures—only one-tenth the heart disease death rate of meat-eaters. Other studies verified these findings. Lacto-ovo vegetarians suffer much less heart disease than do meat-eaters. And pure vegetarians suffer much less than do lacto-ovo vegetarians. The meat, dairy, and egg industries were beginning to panic now and, grasping for straws, suggested that other lifestyle factors, such as smoking, were to blame. The staff of the Medical Research Center in Cardiff, Wales, took this possibility seriously and decided to check it out. Their major study statistically eliminated other lifestyle factors, including smoking, as variables. The mortality rate from heart disease was still found to be far less for vegetarians than for nonvegetarians. Even _Time_ magazine got into the act. Never particularly known for taking controversial stands on dietary issues, _Time_ did a cover story on the latest medical findings regarding cholesterol and heart disease and noted: _In regions where...meat is scarce, cardiovascular disease is unknown._ The medical consensus linking meat, dairy products, and eggs to heart disease was becoming virtually unanimous. An article by cardiologist Dr. Kaare Norum, published in the _Journal of the Norwegian Medical Association,_ left no doubt about the universality of the growing consensus. Dr. Norum polled a large international cross section of scientists who were "actively engaged in arteriosclerosis problems." Ninety-nine percent of the heart disease researchers affirmed the link between diet and heart disease. The dietary culprits they cited were too many calories, too much saturated fat, and too much cholesterol. It was getting to the point that a medical researcher would just about have to bury his head in the sand to avoid seeing the pattern. **Smoke Screen** The growing certainty that saturated fat and cholesterol promote heart disease and strokes was a foreboding omen for the meat, dairy, and egg industries. They found themselves increasingly on the defensive, in a position as embarrassing as the one occupied in recent years by the tobacco industry. The medical evidence regarding the tragic health consequences of smoking is utterly overwhelming. But the tobacco industry does what it can to confuse the issue. One writer caricatured the tobacco industry's stance toward the latest medical research: _The Tobacco Industry..._ 1. _...still insists that the three main causes of lung cancer are flat feet, backgammon, and gargling with Top Job._ 2. _...considers a scientific test to be inconclusive unless it kills everyone who takes it._ 3. _...hopes that enough kids will start smoking to make up for all the older smokers who are dropping dead._ 4. _...has warned the Surgeon General that telling everything he knows may be hazardous to his health._ 5. _...won't even concede that inhaling water causes drowning._ In order to say that the final word isn't yet in on the "alleged" link between smoking and lung cancer, the tobacco industry funds studies specifically designed to confuse the issues. It then uses these contrived studies in its attempt to convince the public that the question of whether smoking causes cancer is still unanswered. A recent Federal Trade Commission survey discovered that the industry's advertising campaign calling for an open debate on the "unsubstantiated perils of smoking" is apparently working. Half of all smokers still actually doubt that smoking is dangerous to their health. **THE MOUNTING CONSENSUS With each passing year more and more expert organizations publicly affirmed the role of saturated fat and cholesterol in heart disease.** source: Patricia Hausman, _Jack Sprat's Legacy_ (New York: Richard Marek Publishers, 1981). In giving the impression that there are legitimate arguments on both sides and that the issues have not yet been resolved, the tobacco industry has succeeded in creating what we might call a smoke screen. Placed in an increasingly parallel position to that of the tobacco industry by the latest medical research, the saturated fat industries have responded in like fashion. They have actively promoted the illusion that there is still confusion concerning the issues of saturated fat, cholesterol, and heart disease. They have done whatever they could to keep the public from knowing that the evidence incriminating saturated fat and cholesterol is now overwhelming. The executive director of the Center for Science in the Public Interest, Michael Jacobson, is aware of the tactics of these industries. Says Jacobson: _Despite the massive amount of scientific evidence linking fat to heart disease, a relative handful of researchers has created in many minds the illusion that great controversy surrounds the "theory"... For instance, in June 1980, a committee of the National Academy of Sciences issued a report defending the current fatty diet. The main authors of the report were professors who had for many years received grants from or were paid consultants to the National Dairy Council, the National Livestock and Meat Board, the American Egg Board... and other industries whose profits depend on Americans' pathogenic diet. One such professor was quoted in the press as being surprised that people thought the $250,000.00 he received as a consultant to the egg and other industries would cloud his objectivity regarding the nutritional value of eggs..._ _Dietary fat and cholesterol...speed the development of some of the most dreaded diseases and contribute to hundreds of thousands of deaths a year. These diseases include coronary heart disease, peripheral arteriosclerosis, gangrene, hearing loss, cancers of the breast and colon, and cerebral hemorrhage..._ _While doctors have developed methods to prevent or cure most infectious diseases, they have found the chronic diseases much tougher to eradicate. The bacteria and other microbes that cause infectious diseases haveno friends or allies to defend their interests, and can be treated mercilessly as the health menaces they are. However... some of the agents that cause degenerative diseases have powerful allies in the industrial world..._ _Over the years, the "fat lobby"—the meat, dairy and egg industries, and their academic and political allies—has not only influenced our nation's food and nutrition policies, it has determined those policies._ **The Battlefield** You might think that with the growing wave of evidence indicating saturated fat and cholesterol as killers of more Americans than all the wars in our nation's history combined, the meat, dairy, and egg industries would be hard-pressed to maintain control over our food and nutrition policies. But the cards are stacked. They may not have interests of public health on their side, but their lobbying groups and political action committees are well financed, battle-hardened veterans of political in-fighting. Opposing them are scientists and medical researchers whose skills don't lie in the political sphere and who have little financial backing compared to what the industries provide their representatives. The fight is far from fair. _As a rule, scientists and medical researchers make poor players in the complex game of special-interest politics, although they often think otherwise. They are not well endowed with the stamina, patience, and shrewdness that this game requires, and deep down they view it as an anti-intellectual activity beneath their scholarly dignity. Even when organized into illustrious professional groups they shrink from combat and bloodletting. This is more a reflection of the unsuitedness of their training and temperament to the political arena than it is a mark of weakness of conviction._ On one side of the battlefield stands a formidable and experienced alliance of meat, egg, and dairy producers, with their purchased political and scientific allies. On the other side stands a relatively unorganized collection of independent medical researchers, underfinanced public interest and consumer groups, and the handful of political leaders who are willing to endure the sizable risk of an unpopular stance. In this battle, the industries who sell us foods high in saturated fat and cholesterol have produced multimillion-dollar public relations campaigns, telling us brightly of the "incredible, edible egg," repeating that beef is "nutrition you can sink your teeth into," and reassuring us that "milk does a body good." They do not mention that these foods clog our arteries and promote heart disease and strokes. Of course, no advertising mentions the disadvantages of the products it promotes. But time and time again these industries have drawn the ire of consumer groups, the courts, and medical researchers for their flagrant disregard of fact. In 1985, the Beef Council had the dubious distinction of being a repeat winner of the Harlan Page Hubbard Memorial Award for the year's most deceptive and misleading advertising. The award, named for a famous charlatan who glowingly advertised a worthless patent medicine, is given by a collection of consumer groups who are used to the distortions and exaggerations that typify Madison Avenue. But even to their weathered eyes the "beef gives strength" campaign took the cake for implying that beef is low in fat. The servings shown in the ads were only three ounces, when, according to USDA data, the average beefsteak serving is double that. By not explaining that the serving shown in the ad is only half the size of the portion most people eat, the industry conveyed the impression that servings of beef are much lower in fat than they actually are. In announcing the award, Bonnie Liebman of the Center for Science in the Public Interest also pointed out that the technicians who did the laboratory analysis that produced the calorie and fat counts referred to in the ads used scalpels to remove every possible bit of fat from the meat samples. Thus the fat and calorie levels reported were not only for a serving size much smaller than viewers understood it to be but also for a serving that had been trimmed of fat with a meticulousness no homemaker could possibly match. The industry ads also did not mention that cholesterol is found mostly in lean tissues, not in fat, and so no matter how meticulously you trim away the fat you cannot significantly reduce the level of cholesterol. The industry ads have to go to such great lengths to give the impression their products are healthy because the truth is so incriminating. Meanwhile, the California Milk Producers presented a series of expensive television ads in which celebrities such as columnist Abigail Van Buren ("Dear Abby"), swimmer Mark Spitz, baseball player Vida Blue, and dancer Ray Bolger proclaimed: "Everybody needs milk." The Federal Trade Commission, however, didn't agree. It took legal steps toward prosecuting the milk producers and their advertising agency, calling the advertising "false, misleading and deceptive." The dairymen quickly changed their tune and came up with a new slogan—"Milk has something for everybody." One medical researcher familiar with the matter laughed when he saw their latest deception. Said Dr. Kevin McGrady, "Milk has something for everybody, all right—higher blood cholesterol and increased risk of heart disease and strokes." **Egg on Their Face** The meat and dairy industries are not alone in their misleading presentations to the public. The egg industry has also produced advertising campaigns designed to deny the saturated fat and cholesterol problems arising from consumption of their product. Of all foods, eggs are the highest in cholesterol, but the egg industry has not been one to stand by and let a fact like that take a bite out of its profits. In 1971, after the American Heart Association took its stand on dietary cholesterol and heart disease, the egg producers countered by forming the National Commission on Egg Nutrition for the specific purpose of fighting the American Heart Association viewpoint. To accomplish this goal, the newly formed commission presented a series of expensive ads in the _Wall Street Journal_ and elsewhere. These ads attacked what they called the theory that saturated fat and cholesterol promote heart disease. A typical ad stated: _There is absolutely no scientific evidence that eating eggs, even in quantity, will increase the risk of a heart attack._ On seeing these ads, the American Heart Association immediately asked the Federal Trade Commission to prohibit this "false, deceptive and misleading advertising." The Federal Trade Commission considered both sides of the matter and then filed a formal complaint against the National Commission on Egg Nutrition and its advertising agency, Richard Weiner, Inc. Understandably dismayed by this turn of events, the egg industry hired the best legal counsel it could find. The attorneys studied the matter in depth, then turned around and told the egg industry that its "chances of beating the lawsuit on scientific grounds are almost nil." There followed a lengthy court battle, in which the egg producers tried, among other rationalizations, to defend their ad campaign under the First Amendment guarantee of free speech. But the judge wasn't convinced; in his 101-page decision, he called the statements made by the National Commission on Egg Nutrition _false, misleading, deceptive and unfair._ Ruled Judge Ernest G. Barnes: _There exists a substantial body of competent and reliable scientific evidence that eating eggs increases the risk of heart attacks or heart disease... This evidence is systematic, consistent, strong and congruent._ The ruling also chastised the egg industry for deceptively camouflaging their intentions by naming their organization the National Commission on Egg Nutrition: _[The name] National Commission on Egg Nutrition implies an impartial, independent, quasi-governmental health commission, when in fact it is an association of persons engaged in the egg industry._ The National Commission on Egg Nutrition was unable to convince the Federal Trade Commission, the court, and even its own attorneys that eggs do not raise blood cholesterol and promote heart disease. But this did not prevent the egg industry from trying to make the American public believe eggs were not a danger. In its efforts to scramble the public mind, the egg industry designed and paid for numerous studies they hoped would give the appearance that the cholesterol in eggs is harmless. An authority on clinical nutrition research, Dr. John McDougall, studied the medical literature and noticed something interesting: _Of the six studies in the medical literature that fail to demonstrate a significant rise in blood cholesterol level with the consumption of whole eggs, three were paid for by the American Egg Board, one by the Missouri Egg Merchandising Council, and one by the Egg Program of the California Department of Agriculture. Support for the sixth paper was not identified..._ _The trick is in knowing how to design your experiment so you will get the results you are looking for. To get little or no increase in cholesterol results, you first saturate your subjects with cholesterol from other sources, because studies show that once people consume more than 400 to 800 milligrams of cholesterol per day, additional cholesterol has only a minor effect on blood cholesterol levels... Well designed studies by investigators, independent of the food industry, clearly demonstrate the detrimental effects of eggs on blood cholesterol levels._ The studies financed by the egg industry seemed to exonerate eggs. But independent investigators consistently got very different results. At the University of Minnesota, scientists found that a diet with 380 milligrams of egg yolk cholesterol per day caused an average blood cholesterol level 16 milligrams higher than a diet with only 50 milligrams cholesterol. At the Harvard School of Public Health, Dr. Mark Hegstead achieved similar results, finding that each 100 milligrams of egg yolk cholesterol raised blood cholesterol levels in adult men an average of four to five milligrams. Still, the egg industry continued to insist that egg consumption did not raise blood cholesterol, and to claim their studies were valid. In 1984, yet another impartial study was undertaken to resolve the issue. This study, published in the British medical journal _Lancet,_ sought to test the effects of egg consumption on blood cholesterol with as much objectivity as humanly possible. The experiment was imaginative. A group of subjects was fed an egg daily, disguised in a dessert. Another group of subjects was fed an identical dessert, without the egg. Otherwise their diets were identical and contained no eggs or other high-cholesterol foods. In order to insure the test's objectivity, the whole thing was done double-blind: neither the researchers nor the subjects knew who had eaten the eggs until the test was completed. The results were convincing and the egg industry's position was dealt quite a blow when, after only three weeks, the subjects whose desserts contained the egg showed a 12 percent rise in their blood cholesterol levels; the other group showed no such rise. It is hard to overestimate the significance of this information. A 12 percent rise in blood cholesterol levels amounts to a 24 percent rise in heart attack risk. The egg industry, however, was not dismayed. They realized that in any struggle there are bound to be obstacles that must be surmounted. They resolutely continued to deny the link between eggs and heart disease. When the Senate Select Committee on Nutrition and Human Needs, under the chairmanship of Senator George McGovern, met to establish guidelines for the nation's food choices, the egg industry presented five different research studies that they claimed exonerated eggs. These reports, however, were so confusing that McGovern asked the National Heart, Lung and Blood Institute for an expert opinion on their validity. The institute carefully examined each of the five studies, then reported to Congress that the studies seemed deliberately designed to distort the facts. The institute's impartial appraisal was that the studies were "seriously flawed,... meaningless and should be discarded." Undaunted, the egg industry did the only thing it could. It hired an advertising agency and began a massive publicity campaign based on the very studies that had been so thoroughly discredited. Fliers were inserted into many millions of egg cartons reassuring egg consumers that "eggs don't raise cholesterol." Through it all the egg industry has remained as dedicated as they could be. They evidently figure that if two wrongs don't make a right, perhaps three or four might do the trick. **More Shenanigans** The shenanigans continue to this day. The industries profiting from our consumption of saturated fat and cholesterol have had to search desperately for a means to defend their products, but they have been willing to do so. You may have heard that cholesterol is necessary for bodily functioning. This was one of the key features of the National Commission on Egg Nutrition's advertising campaign that was ruled false, misleading, deceptive, and unfair. The ads headlined the fact that cholesterol plays an essential role in the body's biochemistry. Featuring "facts about cholesterol," the ads proclaimed the many bodily functions that are dependent on cholesterol for their operation. The courts put a stop to this false advertising. But to this day "educational materials" supplied to our nation's schools by the meat, dairy, and egg industries continue to assert that cholesterol is indispensable to human life processes. At one level, the claims are correct. Cholesterol does play an essential role in the body's biochemistry. However, the implication is strongly made that there is therefore a value in consuming cholesterol in our diets—an implication with absolutely no basis in fact. In reviewing the egg industry's defense of dietary cholesterol on these grounds, the court heard testimony from many of the nation's top medical researchers. The egg industry, of course, brought in its own experts. After considering all the presentations and arguments, the court found that there is not a single case on record of anyone ever suffering from a deficiency of dietary cholesterol. _As far as we can determine, all of us would do just as well if we had no cholesterol in our diet. Cholesterol can be made by all of the cells in the body so we don't need to take in any._ —DR. ROBERT LEVY, DIRECTOR OF THE NATIONAL HEART, LUNG AND BLOOD INSTITUTE _There is no known evidence that low-cholesterol diets are harmful, or that dietary cholesterol is an essential nutrient in any human condition._ —TASK FORCE TO THE AMERICAN SOCIETY OF CLINICAL NUTRITION Under court order, the egg industry finally had to stop running ads that represented cholesterol as an essential dietary nutrient. And the court told them once again to stop denying the link between cholesterol and heart disease. Undaunted, however, the egg industry simply reversed its field and carried on its campaign to muddle the issues. It began now to join the meat and dairy industries in their protestations that the body tends to produce less cholesterol as more is consumed in the diet. They implied, therefore, that dietary cholesterol is harmless. We can eat as much as we want, they said, because our bodies will compensate. To support this, the meat, dairy, and egg industries have repeatedly referred to some of the earliest cholesterol experiments, undismayed by the fact that the results have been retracted by the very people who performed them. These early studies were done before it was discovered that the body can absorb cholesterol only if it is accompanied by fat. Not knowing this, the researchers used pure cholesterol crystals. We know now that it was only because the cholesterol was given in crystalline form that blood cholesterol levels didn't rise in these early experiments. The industries that profit from our cholesterol consumption still refer to these early studies, using them as "proof" our bodies compensate for cholesterol intake by producing proportionately less. They have chosen to disregard the public statements made by the researchers themselves that these early experiments have no bearing whatsoever on the health consequences of cholesterol consumption, because, unlike cholesterol crystals, cholesterol in food is always accompanied by sufficient fat to be absorbed by the body. The industries wanting to keep us hooked on cholesterol have to resort to such shenanigans because current medical research gives them no other place to stand. It is true that as we eat more cholesterol, we produce a bit less. But the decrease in body production is nowhere near equal to the amount consumed. Until we reach dangerous saturation points, every milligram of dietary cholesterol tends to elevate the amount of cholesterol in our blood, cause atherosclerosis, and open the door to heart attacks and strokes. The _American Journal of Clinical Nutrition_ reported an impartial study designed to measure the effect of different amounts of dietary cholesterol on blood cholesterol levels. A number of men were put on cholesterol-free diets for 21 days, and their blood cholesterol levels carefully monitored. Then the men were divided into four groups. For the next 42 days, each group was fed a diet with a specific cholesterol level. Then their blood was measured to see how they had fared. The results, shown in the figure on page 207, lived up to the egg industry's worst fears. The more cholesterol the subjects consumed, the more rapidly and the higher their blood cholesterol counts rose. **YOUR BLOOD CHOLESTEROL LEVEL IS DIRECTLY AFFECTED BY YOUR CHOLESTEROL INTAKE** A study was done to measure the effect of dietary cholesterol on blood cholesterol. 56 men were put on a cholesterol-free diet for 21 days. They were then divided into four groups. Each group was given a diet with a fixed cholesterol intake for the next 42 days. Then their blood cholesterol levels were measured. The results: **Number of Men** | **Dietary Cholesterol Intake (mg/1,000 cal.)** | **Blood Cholesterol Levels (mg%)** | **Net Changes** ---|---|---|--- 18 | 0 | 164.7 | 3.4 11 | 106 | 174.7 | 13.0 13 | 212 | 181.4 | 23.8 14 | 317 | 198.4 | 40.5 Source: F. Mattson, "Effect of Dietary Cholesterol on Serum Cholesterol in Man," _American Journal of Clinical Nutrition_ 25 (1972): 589. Literally dozens of independent studies have shown the same thing. But the meat, egg, and dairy industries, in their efforts to make the whole thing appear controversial, have managed to ignore them all. They have not always been able to avoid stumbling over the truth, but they seem always to manage to pick themselves up and carry on as if nothing had happened. **Hucksters in the Classroom** Perhaps the most insidious weapon of the saturated fat industries is the deep credibility and legitimacy they have in the public mind. They can count on our loyalty because for decades they have provided schools with much of the materials used for nutritional education. Dr. Pascal Imperato, former commissioner of health for New York City and chairman of the Department of Medicine at New York's Downstate Medical Center, notes: _The National Dairy Council, with the government's permission, [is still] the largest and most important provider of nutrition education in the country... That the Dairy Council can still convincingly promote saturated fat and cholesterol-rich diets reflects...the credibility it built in the days before the link between these elements and atherosclerosis was known._ Most of us grew up thinking of the National Dairy Council as a benign organization whose purpose was wholesome and pure. Just as the National Commission on Egg Nutrition sounds like an independent health organization concerned with our well-being, the name National Dairy Council seems to imply an impartial group of elders who have come together to provide us their wisdom and counsel. When they told us milk was nature's most perfect food, we believed them. When they told us to drink a glass of milk with every meal, we did as we were told. Little did we know this was an organization especially organized to sell the American public as much milk, and particularly as much milk fat, as possible. The trade magazine _Dairyman_ understands that the Dairy Council's job is to promote the sale of milk. As they explained: _It's important to understand the unique role the Dairy Council plays in promoting milk. The Dairy Council does no paid consumer advertising. That noncommercial status is important. As a highly respected education entity its programs give the dairy industry entry into areas difficult to penetrate with straight product promotion, especially the schools and medical-dental professions._ The Dairy Council "penetrates" the school with a nutritional message that is far from unbiased, though they present it as if it were. They do not mention that the research they use to support their position is usually research they have themselves funded. But in a self-profile titled "Milk Still Makes a Difference," the Dairy Council says of such research: _Research supported through the National Dairy Council's grant-in-aid program seeks to set the record straight about the influence of diet on heart disease. We cannot rest until our product is completely vindicated and put into proper perspective._ Frankly, I wonder what sort of objectivity can be found in research sponsored by a National Dairy Council grant given specifically to vindicate their product. The Center for Science in the Public Interest is not overly taken with the scientific rigor behind the Dairy Council's message. Says the center's executive director, Michael Jacobson: _In virtually every school district in the country, the minds of two generations of children have been fed the self-serving pap served up in generous portions by the National Dairy Council._ With active chapters in 128 U.S. cities, the National Dairy Council has over $14 million to invest each year for the sole purpose of getting the public to spend its money on dairy products. And because milk products are priced by federal law according to a pricing structure that provides the dairymen more profit on higher-fat products, the Dairy Council particularly pushes those dairy products with the highest percentage of fat. It apparently does not concern itself with the fact that these are precisely the dairy products that make the greatest contribution to heart disease and strokes. A child may be only three or four years old when he or she first gets a taste of National Dairy Council materials, such as "Little Ideas," a set of food pictures ostensibly designed to help preschoolers identify foods. It starts out with butter and continues on with 16 other milk products, most of which are high in saturated fat. As the child progresses, he or she unknowingly continues to receive the Dairy Council message. The Dairy Council provides a sequence of curriculum packages to nursery, elementary, junior high, and senior high schools, called, ironically, "Food: Your Choice." These materials, which are specifically designed to help youngsters choose dairy products, have been the chief source of nutritional information for countless American children. The package designed for three-to-five-year-old children, called "Food: Early Choices," cheerfully provides hand puppets, playing cards, posters, puzzles, and records—along with a message that makes high-saturated-fat milk products sound enticingly attractive. The package designed for first graders, called "Food: Your Choice, Level One," is a large box filled with colorful materials, including bright posters about making milk shakes and pancakes. The recipes call for ice cream and butter. When yogurt and milk are indicated, it is never the low-fat versions that are mentioned. The kit also includes mimeograph supplies to enable the teacher to give handouts to the children. Of the many handouts available, none features low-fat dairy products. Instead, cream cheese, ice cream, whole milk, and butter are pictured and happily recommended. These are, of all dairy products, the very highest in saturated fat. You may never have thought of ice cream as a health food, but in "Ice Cream for You and Me," the Dairy Council advises its captive subjects that: _Ice cream is a healthful food made from milk and cream along with other good foods._ Included in the National Dairy Council's idea of the "healthful milk group," along with ice cream, is another food you might not have realized is a health food—chocolate pudding. The National Dairy Council demonstrates its devotion to milk fat and its unique version of a balanced diet by telling the children: _Drink milk at every meal and have some in foods like these: cheese, ice cream, baked custard, bowl of cream of tomato soup, with a pat of butter on top._ The Dairy Council likes to reach children when they are youngest and most impressionable, and then to reinforce their ideas of "basic four" nutrition at every age level. All the way up through elementary, junior high, and senior high schools, youngsters are bombarded with the Dairy Council message. Teenagers are the target for the Dairy Council's helpful little publications _A Boy and His Physique_ and _A Girl and Her Figure._ What do you imagine overweight teenagers receive as their first suggestion from the Dairy Council? _[Drink] whole milk most of the time, skim milk part of the time, if you need to lose weight._ Also highly recommended are "stay-slim sundaes," comprising ice cream with fruit instead of chocolate sauce for a topping. Perhaps the most remarkable suggestions offered by the Dairy Council to overweight teenagers are the items listed in the "lower-calorie section." One bright idea for youngsters with a weight problem is cream cheese, softened with cream, molded into balls, rolled in peanuts, and served with fruit Honest! I'm not making this up! Another helpful "low-calorie" item is angel food cake and ice cream. Given these outrageous recommendations, it is hard to avoid the conclusion that the Dairy Council is more concerned with getting youngsters hooked on a lifetime pattern of high-fat dairy product consumption than with providing sound nutritional education. **How to Lie with Statistics** Quantifying the amount of fat in a given food is another sensitive area, since there are several ways the fat content of food can be measured. The method generally recognized as the most accurate and reliable is to measure the percentage of calories in a given food that are provided as fat. A second method, useful in certain specific cases, is to measure the grams of fat in a serving of a given food. By both these methods, meat, eggs, and almost all dairy products are seen as what they are—high-fat foods. **PERCENTAGE OF CALORIES AS FAT** MEATS --- Sirloin steak, hipbone, lean w/fat | 83% Pork sausage | 83% T-bone steak, lean w/fat | 82% Porterhouse steak, lean w/fat | 82% Bacon, lean | 82% Rib roast, lean w/fat | 81% Bologna | 81% Country-style sausage | 81% Spareribs | 80% Frankfurters | 80% Lamb rib chops, lean w/fat | 79% Duck meat, w/skin | 76% Salami | 76% Liverwurst | 75% Rump roast, lean w/fat | 71% Ham, lean w/fat | 69% Stewing beef, lean w/fat | 66% Goose meat, w/skin | 65% Ground beef, fairly lean | 64% Veal breast, lean w/fat | 64% Leg of lamb, lean w/fat | 61% Chicken, dark meat w/skin, roasted 56% Round steak, lean w/fat | 53% Chuck rib roast, lean only | 50% Chuck steak, lean only | 50% Turkey, dark meat w/skin | 47% Sirloin steak, hipbone, lean only | 47% Lamb rib chops, lean only | 45% Chicken, light meat w/skin, roasted 44% FISH --- Tuna, chunk, oil-packed | 63% Herring, Pacific | 59% Anchovies | 54% Bass, black sea | 53% Perch, ocean | 53% Caviar, sturgeon | 52% Mackerel, Pacific | 50% Sardines, Atlantic, in oil, drained | 49% Salmon, sockeye (red) | 49% VEGETABLES --- Mustard greens | 13% Kale | 13% Beet greens | 12% Lettuce | 12% Turnip greens | 11% Mushrooms | 8% Cabbage | 7% Cauliflower | 7% Eggplant | 7% Asparagus | 6% Green beans | 6% Celery | 6% Cucumbers | 6% Turnips | 6% Zucchini | 6% Carrots | 4% Green peas | 4% Artichokes | 3% Onions | 3% Beets | 2% Chives | 1% Potatoes | 1% LEGUMES --- Tofu | 49% | Soybeans | 37% | Soybean sprouts | 28% | Garbanzo beans | 11% | Kidney beans | 4% | Lima beans | 4% | Mung bean sprouts | 4% | Lentils | 3% | Broad beans | 3% | Mung beans | 3% | | | Source: _Nutritive Value of American Foods in Common Units_ , USDA Handbook No. 456. **PERCENTAGE OF CALORIES AS FAT** DAIRY PRODUCTS --- Butter | 100% Cream, light whipping | 92% Cream cheese | 90% Cream, light or coffee | 85% Egg yolks | 80% Half-and-half | 79% Blue cheese | 73% Brick cheese | 72% Cheddar cheese | 71% Swiss cheese | 66% Ricotta cheese, whole-milk type | 66% Eggs, whole | 65% Ice cream, 16% | 64% Mozzarella cheese, part-skim type 55% Goat's milk | 54% Cow's milk | 49% Yogurt, plain | 49% Ice cream, regular | 48% Cottage cheese | 35% Low-fat milk (2%) | 31% Low-fat yogurt (2%) | 31% Ice milk | 29% Nonfat cottage cheese (1%) | 22% MEAT AND FISH PRODUCTS --- Hormel Spam luncheon meat | 77% Mrs. Paul's Buttered Fish Filets | 75% Del Monte Bonito | 67% Morton Beef Tenderloin | 64% Mrs. Paul's Fried Shrimp | 58% Mrs. Paul's Clam Crepes | 55% Hormel Dinty Moore Corned Beef 53% Swanson Salisbury Steak | 52% Nabisco Chicken in a Biskit | 51% Morton House Beef Stew | 49% Mrs. Paul's Flounder | 48% Swanson Veal Parmigiana | 48% Swanson Fried Chicken | 46% Hormel Dinty Moore Beef Stew | 45% Morton Beef Pot Pie | 45% Mrs. Paul's Fish Au Gratin | 43% Morton Chicken Croquettes | 40% | FRUITS --- Olives | 91% Avocados | 82% Grapes | 11% Strawberries | 11% Apples | 8% Blueberries | 7% Lemons | 7% Pears | 5% Apricots | 4% Oranges | 4% Cherries | 4% Bananas | 4% Cantaloupe | 3% Pineapple | 3% Grapefruit | 2% Papayas | 2% Peaches | 2% Prunes | 1% GRAINS --- Oatmeal | 16% Buckwheat, dark | 7% Rye, dark | 7% Whole wheat | 5% Brown rice | 5% Corn flour | 5% Bulgar | 4% Barley | 3% Buckwheat, light | 3% Rye, light | 2% Wild rice | 2% NUTS AND SEEDS --- Coconut | 85% Walnuts | 79% Sesame seeds | 76% Almonds | 76% Sunflower seeds | 71% Pumpkin seeds | 71% Cashews | 70% Peanuts | 69% Chestnuts | 7% Source: _Nutritive Value of American Foods in Common Units_ , USDA Handbook No. 456. The industries who profit from our consumption of saturated fat, however, realize that widespread understanding of this fact would erode their profits. In a classic example of the art of lying with statistics, they have come up with a method of measuring fat that disguises the high-fat levels of meats, dairy products, and eggs: they measure fat as a percentage of weight. Patricia Hausman of the Center for Science in the Public Interest notes: _The method of measuring... the percentage of fat by weight... has been abused as a clever way of deceiving consumers about the fat content of food. When expressed as a percentage of a food's weight, the fat content of most foods will sound deceptively low. Whole milk, for example, contains only 3 to 3.7 percent fat by weight, simply because milk, like most foods, contains large amounts of water. By weight, whole milk is 87 percent water. Fat supplies half the calories in milk._ The National Livestock and Meat Board has produced extremely expensive advertising campaigns announcing that hot dogs are "calorie conscious," and contain only "30 percent fat." Nowhere in the ads does it mention that this "30 percent" figure is calculated by a method specially chosen for its ability to create a misleadingly low number. Similarly, Oscar Mayer uses the "30 percent" figure in the "nutritional education" materials it supplies free of charge to schools, telling its young audience it is a myth that _sausage products, including wieners and cold cuts, are fatty._ Oscar Mayer then proceeds to make its products seem like a veritable dream come true when it comes to fat, by comparing them with foods that are the very highest in fat to be found anywhere—margarine, mayonnaise, salad dressing, and cream cheese. Similarly, they have found a way for their meats to come out looking absolutely fabulous on their cholesterol charts—they simply compare them to eggs, the highest of all foods in cholesterol. In another instance they proudly compare the nutritional value of their wieners to a food item that doesn't exactly provide the stiffest competition—a 12-ounce can of Coke. In fact, the Oscar Mayer company has made an art of making their fatty, unhealthy products look nutritionally attractive to children by comparing them to a competition that couldn't have been better chosen for the task. The degree to which meat and dairy products are actually health giving was recently clarified when the Center for Science in the Public Interest officially renamed Wendy's Triple Cheeseburger "The Coronary Bypass Special." Tongue in cheek, perhaps, but definitely right on target. **Safe and Sensible** One Dairy Council publication is called _The Basic Four Ways to Safe and Sensible Weight Control._ Words like "safe" and "sensible" and "basic" portray the feeling most of us grew up having about the Dairy Council, its message, and its products. But this publication turns out, like other Dairy Council materials, to represent something far removed from an objective understanding of weight control. It prescribes a glass of whole milk and a pat of butter at every meal to the dieter. Heading its list of lower-calorie snacks is a product you probably never realized was such a boon to the overweight—ice cream. It is hard for us to imagine how immense a role the National Dairy Council has played in making us feel we are well fed only when we consume the foods its industry produces. We have been made to feel that to do without these foods would be a severe deprivation, and in the back of most of our minds there lives the belief, planted there unbeknownst to us by the Dairy Council, that milk is nature's most perfect food. In fact, milk is nature's most perfect food for a baby calf, an animal who, with its four stomachs, will double its weight in 47 days. Even vegetarians continue to be heavily influenced by the hidden persuasions of the Dairy Council. In fact, vegetarians are often especially vulnerable to the pull of its message. Having to some extent defied the prevailing cultural norms by giving up meat, they can easily feel attracted to dairy products as a way of paying their dues to the "basic four" concepts. They may not follow the Dairy Council's specific commandment to drink three glasses of milk a day, but there lingers in their minds a residue that makes cheese, yogurt, and sometimes even ice cream seem desirable, safe, and even necessary for a wholesome diet. This is not an accident. The Dairy Council has spent enormous amounts of money to create these feelings in you and me and the rest of the American public. Their staff provides workshops in most major cities to train teachers in the Dairy Council's brand of nutrition. In 1977, Congress began the National Nutritional Education Training Program, designed to educate children, teachers, and school cafeteria personnel about good nutrition. So accustomed have most states become to the National Dairy Council as the source of their nutritional education materials, that over half the states simply used the additional federal money to buy more Dairy Council supplies. As I have uncovered the grip that the Dairy Council holds over our schools, I have had to wonder how they ever got such a position within an educational system that is supposed to be noncommercial. The answer is that they have been getting away with it for so long that hardly anyone thinks to question the matter. It was back in 1915 that the dairy farmers founded the National Dairy Council, for the expressed purpose of "educating the public about the importance of drinking milk and consuming dairy products." At that time, nutritionists and teachers knew the Dairy Council had a vested interest in getting children to drink their milk, but they didn't mind. Nothing was known back then, in the early infancy of nutritional science, to contraindicate the use of dairy products, and the teachers were glad to have the materials. The result was that the Dairy Council became the nation's de facto nutrition educator. Over the years, the Dairy Council has been able continually to strengthen its foothold in our school systems because it would be impossible at this point for any private company to compete with them in supplying educational materials. Their prices are extremely low because they receive many millions of dollars a year in subsidies from the milk producers who profit from our continued consumption of dairy products, particularly those high in fat. The dairy industry is also one of the nation's largest advertisers, producing TV commercials and putting up billboards across the country promoting milk, cheese, and butter consumption. Using catchy slogans like "Milk, the fresher refresher" and "Every body needs milk," it spends many millions of dollars every year on an advertising budget whose purpose is the same as any other advertising budget's—to get us to buy their products. The only difference is that when we see an ad for Marlboro cigarettes, we know the Marlboro company paid a lot of money for the chance to grab our attention and sway our habits. But because we were educated by National Dairy Council materials, and because their programming has gone so deeply into our psyches as to seem like the given truth, when we see ads for milk and dairy products we tend to think we are seeing a public service message. The dairy industry is not terribly unhappy about this and in fact has been known to end their messages with an announcement, in a sincere and sober voice, that the "preceding announcement has been brought to you as a public service by the National Dairy Council." **Keeping Us Hooked** In its battle to keep Americans consuming high levels of saturated fat and cholesterol, the dairy industry has many friends. McDonald's donates a "Nutrition Action Pack" to classrooms across the country. The material comes complete with the Golden Arches trademark at the bottom of each page and is something less than the unbiased nutritional presentation it pretends to be. The coverage of the four basic food groups represents the Bread and Cereal group with hamburger buns. On September 21, 1983, McDonald's ran a 16-page color insert in the _Chicago Tribune_ that extolled the virtues of what it called a "properly balanced diet." It was an interesting version of a properly balanced diet, in that it basically amounted to Big Macs, fries, and shakes. Extra copies of the insert were then distributed in the schools through the Chicago Board of Education. It was, in the words of the Aaron Cushman Public Relations Agency, "a combination textbook and advertisement." Another organization devoted to keeping us hooked on saturated fat and cholesterol is the National Livestock and Meat Board. After the American Heart Association came on record publicly indicting saturated fat and cholesterol as agents of heart disease, the Meat Board promptly began an extensive advertising campaign designed to discredit the American Heart Association. They actually tried to make it seem as if the vast majority of reputable scientists had never even heard of this "supposed" connection between saturated fat, cholesterol, and heart disease. As Patricia Hausman of the Center for Science in the Public Interest noted: _To anyone who relied on the Meat Board for information, it looked like the American Heart Association had a few maniacs running its show,while the vast majority of scientists thought the diet-heart connection was hopelessly off base._ In its ongoing effort to discredit the "theory" that saturated fat and cholesterol promote heart disease, the Meat Board has come up with one argument that has been particularly effective because it actually sounds eminently reasonable. You are supposed to believe that there is no reason to be concerned about your intake of saturated fat and cholesterol as long as your blood cholesterol count is normal. But what is a normal blood cholesterol level? And furthermore, what is the advantage of being normal if that means an average that is already too high? You see, if you go to a physician to have your blood cholesterol level tested, he or she will send a sample of your blood to a lab. The lab will then send the results back to your doctor. Your blood cholesterol level, usually called serum cholesterol or plasma cholesterol, will be expressed in units of milligrams per 100 milliliters (mg/ml), which is commonly called "milligram percent" (mg%). Usually, along with the actual figures, the lab will mark in the right-hand column whether each specific blood parameter for which they tested was found to be normal or abnormal. Most busy doctors simply run down the right-hand column looking for abnormalities. Many labs consider values up to 330 mg% to be normal, while other labs may set the cutoff point as low as 290 mg%. The problem, however, is that though a man with a blood cholesterol count of 290 mg% will often be considered normal, he has more than 10 times the likelihood of dying from a heart attack as a man of similar age with a count of 190 mg% Even smaller differences are of tremendous importance. A person with a blood cholesterol level of 260 mg% is at least five times more likely to die from a heart attack than a person with a level of 200 mg%. The problem with being normal is that the normal population of our country is suffering from severe atherosclerosis that is getting worse with every passing meal. As one authority put it: _The average male in [our] society has a greater than 50 percent chance of dying from a heart attack. Under these circumstances, no consolation should be gained from being average._ Nathan Pritikin, who probably knew as much about preventing heart disease as any man who ever lived, dismissed the myth of normal blood cholesterol levels: _If your blood cholesterol level is more than 100 plus your age, up to a maximum of 160, you have closed arteries. [But] anyone with cholesterol below 160 is considered "abnormal" or "subnormal" in our country. "Normal" cholesterol levels are 160–330..._ _Every so-called "normal" level in our country is guaranteed to close arteries. "Normal" in our country simply means that you can walk from one room to another. Our cholesterol levels are not normal. They are averages for asymptomatic people, but the next day those people could drop dead from a heart attack._ The meat, dairy, and egg industries tell us not to worry unless our blood cholesterol levels are abnormal. But people with normal levels are dying, literally by the millions, from the high levels of saturated fat and cholesterol in the meat, dairy products, and eggs they eat. **The Battle Continues** In its ongoing struggle to convince us that normal cholesterol counts are fine and dandy, the industry has resorted to all sorts of chicanery. When the _British Journal of Nutrition_ reported a study that measured the blood cholesterol levels of a group of men known for high consumption of saturated fat, the Meat Board triumphantly announced to the public that these men's _serum cholesterol levels were within reasonable limits._ It depends on what you call reasonable. The blood cholesterol counts of the studied group were high enough to give them 10 times the probability of suffering a fatal heart attack compared to what would otherwise be expected. Recently, in an effort to confuse you even more, the saturated fat sellers have begun to talk a great deal about high-density lipoproteins and low- density lipoproteins. They are eager to point out that in cases where most of the cholesterol in the blood is carried by high-density lipoproteins, the risk of heart disease is much less than when it is carried by low-density lipoproteins. This, they imply, is the key factor, not blood cholesterol levels. They are not so eager to point out that less than 10 percent of people with high blood cholesterol fall into the fortunate high-density lipoprotein category. Nor do they seem all that enthusiastic about informing the public that low- fiber diets lower high-density lipoprotein levels, thereby raising the risk of heart attacks. Perhaps their lack of enthusiasm has something to do with the fact that meat, dairy products, and eggs provide no fiber, and so the more of these we eat, the less likely we are to be one of the lucky few protected by high-density lipoproteins. In their ongoing campaign to make their products look good no matter what, the meat, dairy, and egg industries have often pointed out that people sometimes die of heart attacks even after they have lowered their blood cholesterol counts. It is true that lowering your blood cholesterol after a lifetime of high levels cannot guarantee freedom from a heart attack. But studies have shown that atherosclerosis can definitely be reversed, and a great many heart attacks and strokes prevented, when a lowered blood cholesterol level is maintained over a period of time. Researchers at the University of California studied subjects ranging in age from 29 to 65. Those who dropped their blood cholesterol levels by an average of 65 mg% and maintained the lower figures through reduced intake of saturated fat and cholesterol showed marked decreases in atherosclerotic deposits. Even in the most advanced cases of atherosclerosis, diet-style changes can be of enormous benefit. In a major study in Montclair, New Jersey, 100 patients with confirmed coronary artery disease who had suffered previous heart attacks were put on a diet low in saturated fat and cholesterol. Over a 10-year period, 16 of them suffered fatal heart attacks. In a control group of 100 other men in similar conditions whose diet was not reduced in saturated fat and cholesterol, 28 men died from heart attacks. Other studies have gotten similar results. Patricia Hausman reports: _Dr. Thomas Lyon and his colleagues reported that recurrence of heart attack and death was four times as common in patients who admitted they were not adhering to the very low-fat diet prescribed by the doctors..._ _Dr. A. Koranyi reported a study of 125 patients asked to follow a diet very low in fat. The death rate in the low-fat group was 9 percent, compared to 19 percent among patients not asked to restrict their fat intake._ Such studies raise the interesting moral dilemma of whether, with our present state of knowledge, it is even ethical for doctors not to ask heart patients to restrict their fat consumption. Remarkably, diet-style changes have sometimes produced spectacular results in even the most advanced cases. Writing in _Lancet_ and the _American Heart Journal,_ two British doctors reported treating cases of severe angina pectoris with a pure vegetarian diet. All the patients had suffered severe chest pain due to a restriction of blood supply to the heart, were unable to exercise, and were considered most likely candidates for fatal heart attacks. After six months on a pure vegetarian diet, they were all free of angina pain and "able to engage in strenuous activities." Five years later, the patients were all still alive, still adhering to the pure vegetarian diet, and still free of angina symptoms. **The Fight Gets Rough** Though the meat, egg, and dairy industries have not been successful in their attempts to impede the growing medical understanding regarding diet and heart disease, they have been remarkably successful in maintaining control of our nation's food policies. In 1982, the Department of Agriculture was about to publish an article in its magazine _Food/2_ that was mildly critical of diets high in saturated fat and cholesterol. The meat, dairy, and egg lobbies, however, got wind of this and brought the matter to the attention of Deputy Secretary of Agriculture Richard Lyng. A former president of the American Meat Institute, Lyng dutifully vowed the article would be "published over my dead body." The article was deleted, and Mr. Lyng is not only still with us but has now become the secretary of agriculture, placing him in an even better position to oversee what the government tells the public, and what it does not. The political power of the saturated fat industries is remarkable. In 1961, when the American Heart Association first publicly and officially urged Americans to substitute polyunsaturated fat for some of the saturated fat in their diets, the dairy industry did not find this turn of events to their liking and quickly got the FDA to prohibit margarine and vegetable oil companies from calling attention to the fact that their products were polyunsaturated. So successful was the immense pressure exerted by the dairy industry that the word "polyunsaturated" was virtually made taboo. By law, no product could be labeled polyunsaturated, even if it was 100 percent polyunsaturated. For many years, the American Heart Association and many other public health groups have asked that foods containing saturated fat be so labeled. But the saturated fat lobby has thwarted every effort in that direction, thereby keeping the vast majority of Americans unaware of which of their food choices expose them to this danger. The lengths to which the saturated fat industries are willing to go to defend their profits speaks of how shaky they know the ground to be on which they stand. When the American Heart Association publicly announced its massively documented position condemning saturated fat and cholesterol as agents of heart disease, the dairy industry countered by threatening them with multimillion-dollar lawsuits unless they stopped giving "misleading" advice to the public. Though not particularly delighted by the prospect of a drawn-out and costly court battle, the American Heart Association bravely stood its ground and would not retract its position. The dairy industry then went to work on the various state chapters of the Heart Association, seeking to undermine its foundations. In Wisconsin, the state known as America's Dairyland, dairy farmers exerted tremendous pressure on the local chapter, threatening they would never raise another cent if the state chapter went along with the diet recommendations of the national Heart Association. When the state chapter protested that it was not in their legal power to differ from the national guidelines and set their own course, the dairy interests were less than sympathetic. They promised a multimillion-dollar lawsuit unless the state chapter repudiated the national policy. Frightened by the prospect of a costly legal battle that would break them financially, intimidated by the prospect of dwindling donations, and aware that the dairymen had the money to carry out their threats, the Wisconsin chapter of the American Heart Association capitulated. They formed a Task Force on Nutrition and Cardiovascular Disease to review the matter and make recommendations. Membership on the task force included such legendary champions of science in the public interest as the executive director of the Dairy Council of Wisconsin. The task force recommended a policy that came as no surprise to anyone who knew its membership. It recommended that the Wisconsin chapter of the American Heart Association repudiate the official position of the national organization. The dairy industry was ecstatic, and the Dairy Council's national office sent a letter of congratulations. The Wisconsin Dairy Council passed a formal resolution commending the Wisconsin chapter of the American Heart Association for its "wisdom" in recognizing that _diets to lower blood cholesterol... are not warranted by the general public._ The American Heart Association was appalled. But there was little they could do, because by now the Wisconsin chapter had been virtually taken over by the dairy interests. The public health messages of the Wisconsin Heart Association, instead of drawing attention to the role of saturated fat and cholesterol in producing heart disease, acted as if there were no connection. In fact, if people requested this information, what they received was a copy of the task force's statement, written under the watchful eye of the executive director of the Dairy Council. In case that wasn't enough to discredit the saturated fat and cholesterol "theory," they also received a statement from the Dairy Council, reassuring the inquirers they could put their full faith in dairy products. You might wonder how on earth the Wisconsin chapter of the American Heart Association could justify not informing the public that diets high in saturated fat and cholesterol lead to heart disease. One high-ranking official of the state chapter explained: _We don't aggressively promote it [the message that saturated fat and cholesterol promote heart disease] any more than a tobacco state would promote the tobacco [link with cancer] message._ But on closer inspection, that statement is telling, for every day, the meat, dairy, and egg industries are finding themselves more and more in a posture as medically untenable as that held by the tobacco industry. Every year the research incriminating these foods becomes more incontrovertible. **The Clincher** In 1984, the United States federal government announced the results of the broadest and most expensive research project in medical history. It took over 10 years of systematic research and cost over $150,000,000. The project director of the study, Basil Rifkind, concluded that the mammoth undertaking _strongly indicates that the more you lower cholesterol and fat in your diet, the more you reduce your risk of heart disease._ George Lundberg, editor of the _Journal of the American Medical Association,_ which first published the results of this gargantuan study, said that 25 years from now this study would be looked upon as the one _that secured the cholesterol theory in heart disease._ The study not only demonstrated that our blood cholesterol levels directly determine our risk of heart disease but also proved that even very small changes in our blood cholesterol levels produce considerable changes in heart disease rates. Dr. Charles Glueck, director of the University of Cincinnati Lipid Research Center, one of the 12 major centers participating in the project, noted: _For every one percent reduction in total cholesterol level, there is a two percent reduction of heart disease risk._ Columbia University cardiologist Robert Levy, who directed the entire project, agreed: _If we can get everyone to lower his cholesterol by ten to fifteen percent by cutting down on fat and cholesterol in the diet, heart attack deaths in this country will decrease by twenty to thirty percent._ Even that small reduction would save more lives in a year than are lost to motor vehicle accidents in a decade! **Finally** The meat, dairy, and egg industries to this day maintain that we shouldn't jump to any conclusions, because all the facts aren't in. When asked what kind of study would be adequate, their demands have been so prohibitive as to be utterly absurd, in one case demanding a study involving at least 50,000 people, lasting a minimum of 30 years, and costing over a billion dollars. As time has gone along, however, and study after study after study has pointed an ever more accusatory finger at saturated fat and cholesterol, some industry spokespeople have finally been forced to admit that their products promote atherosclerosis. Even then, however, they declare: _Consumers have an inalienable right to clog up their arteries if they want to._ But in the past 30 years scientists have learned for the first time how we can stop clogging up our arteries. And we are now certain that of all the factors involved in heart disease—including obesity, lack of exercise, sugar consumption, total fat consumption, caffeine consumption, smoking, high blood pressure, lack of fiber in the diet, and chlorinated drinking and cooking water—there is one culprit that towers mightily above the rest. We now know that culprit is saturated fat and cholesterol. **Now** We know today how to prevent heart attacks and strokes. We know how to prevent the killers that account for more than half of the deaths in the United States every year. But most of us, thanks to the dedicated endeavors of the meat, dairy, and egg industries, have not gotten the good news. We still think we must eat animal products in order to be healthy. We still think heart attacks and strokes are a regrettable but more or less inevitable byproduct that comes with living well and growing old. The heart attack has become so much a part of American life as to virtually be an institution. We take it for granted. Few of us know that our passive attitude is perpetuated by the deliberate efforts of those who profit from our staying hooked on the foods that cause heart disease. As long as we remain passive we cannot make the real choices that empower us. Although there are people who do not want us to make such choices and are willing to do almost anything to confuse us, we now have for the first time in history sufficient knowledge to take control over our bodies and our lives. Now we can make food choices that we know will dramatically improve the health of our cardiovascular system, prevent heart disease and strokes, and at the same time reduce the suffering in the world. A well-known publication editorialized: _A vegetarian diet can prevent 97 percent of our coronary occlusions._ This publication was not the _Vegetarian Times_ , nor was it the _New Age Journal._ It was the _Journal of the American Medical Association._ ## 9. **LOSING A WAR WE COULD PREVENT** _When Health is absent Wisdom cannot reveal itself, Art cannot become manifest, Strength cannot be exerted, Wealth is useless and Reason is powerless._ —HEROPHILES, 300 B.C. In 1971, President Nixon signed the Conquest of Cancer Act, thereby officially inaugurating what has become known as the war on cancer. Today, the war continues. Every day the National Cancer Institute spends over three million dollars. They are joined in the fray by organizations such as the American Cancer Society, which spend another million dollars a day. You might think that with so much money being spent, we'd be making progress. But the war on cancer isn't going very well. We aren't massacring the enemy; it's massacring us. _Everyone should know the war on cancer is largely a fraud._ —DR. LINUS PAULING, TWO-TIME NOBEL PRIZE WINNER The most common cancers—cancers of the lung, colon, breast, prostate, pancreas, and ovary—together account for most cancer deaths. The death rate from these cancers has either stayed the same or increased during the past 50 years. And the statistics for the less common cancers are equally bleak. The three cancer treatments most fashionable today are surgery, radiation, and chemotherapy. Each is invasive; each has devastating side effects; each treats only symptoms. And their rate of success is thoroughly underwhelming. ### **Halfway Where?** Organizations like the National Cancer Institute and the American Cancer Society appeal for funds by pleading: "Don't quit on us now, we're halfway there." But they have had a hard time documenting their progress. One man who knows to what lengths these organizations are sometimes forced to go in their effort to retain public confidence is John Bailar, former editor of the _Journal of the National Cancer Institute._ Bailar, who worked for the institute for 25 years, told the 1985 annual meeting of the American Association for the Advancement of Science that today more people with benign or mild diseases are being included in the statistics, in order to make it seem like more cancer victims are being cured. Another tactic, which makes it appear things are getting better than they are, is to define a cancer patient as cured if he or she has survived for five years after being diagnosed and is free of obvious symptoms. With early enough detection, many cancer victims will indeed fit this criteria of "cured." However, in many cases, this early detection does not change the date of death, but only the length of time the person is aware he or she has cancer. One prominent physician who has seen more than enough of modern cancer treatment has grown very cynical: _The real beneficiaries of early detection are the providers of health care, who now have a longer time in which to treat the victims before they die. This means they can charge more for doctor's visits, more procedures, more tests, and longer hospital stays. The American Cancer Society...has put hope up for sale. Unfortunately to date, it has been selling mostly false hope._ Today, treating cancer is a huge business. Every 30 seconds another American is diagnosed as having the disease. Typical cancer patients spend over $25,000 to try to treat their condition, often exhausting savings that took a lifetime to accumulate. Sadly, they don't get very much today for their money. Every 55 seconds, another American dies of cancer. ### **Two Searches** There is a tragedy here. Billions upon billions of dollars are being poured into the search for the magic bullet that will cure cancer, a search that has thus far been utterly unsuccessful. And yet, at the same time, another search that has borne great fruit has been under way. Unbeknownst to the public, we have been learning more and more about how to prevent the disease in the first place. The tragedy is that the American people have been continually cajoled into putting their trust and their money into the thus-far-futile search for a cure and have not been told what has been learned about prevention. Without this information, Americans every day unknowingly choose to eat foods that contribute heavily to their risk of cancer. In 1976, the United States Senate Select Committee on Nutrition and Human Needs, under the chairmanship of Senator George McGovern, convened public hearings on the health effects of the modern American diet. After listening to the testimony of the nation's leading cancer experts, McGovern was not particularly delighted with the war on cancer, calling it a "multi-billion dollar medical failure." At one point in the proceedings, McGovern pointedly asked National Cancer Institute director Arthur Upton how many cancers are caused by diet. The head of the largest cancer organization in the world replied "up to 50 percent." McGovern was dumbfounded. "How can you assert the vital relationship between diet and cancer," he demanded, "and then submit a preliminary budget that only allocates a little more than one percent [of National Cancer Institute funds] to this problem?" Dr. Upton responded sheepishly: "That question is one which I am indeed concerned about myself." The problem is that diet is not a magic bullet. It is a way of preventing cancer, but only in rare cases a way of cure. Organizations like the National Cancer Institute are not encouraged to focus much attention on prevention because there is vastly more money to be made in treatment, and far more glamour in the possibility, however remote, of a cure. Attention is further drawn away from prevention by food industries whose products are known to be involved. They apply immense pressure on government and public health organizations to keep them from informing the public as to what is known about dietary prevention. The result is that you and I are continually being told to put our faith and our money into cancer treatment, and into the hope for an eventual cure. We are not told how to keep cancer from happening in the first place. The tragic result is that we are losing a war we could prevent. ### **Prevention** Meanwhile, with 1,400 Americans dying of cancer every day, cancer researchers have investigated just which lifestyle factors produce high rates of cancer. In the prestigious _Advances in Cancer Research,_ they conclude: _At present, we have overwhelming evidence...[that] none of the risk factors for cancer is...more significant than diet and nutrition._ Conducting hearings on the health effects of the modern American diet, the Senate Select Committee wanted an expert opinion on what medical science now understands about diet and cancer. They summoned Dr. Gio B. Gori, the deputy director of the National Cancer Institute's Division of Cancer Cause and Prevention. Dr. Gori's credentials are indeed impressive: he is also the director of the National Cancer Institute's Diet, Nutrition and Cancer Program. He testified: _Nutritional science is coming of age...No other field of research seems to hold better promise for the prevention and control of cancer and other illnesses, and for securing and maintaining human health._ Of course, the Senate wanted to know just what the dietary influences are that promote cancer. Most of us think of chemical additives, such as preservatives and artificial colors and flavors. But bad as these are, it turns out they are not the chief culprits. Dr. Gori told Congress: _Until recently, many eyebrows would have been raised by suggesting that an imbalance of normal dietary components could lead to cancer and cardiovascular disease...Today, the accumulation of...evidence...makes this notion not only possible but certain....[The] dietary factors responsible [are] principally meat and fat intake._ You will recall that the meat, dairy, and egg industries didn't open their arms wide to welcome the news that saturated fat and cholesterol cause heart disease. Nor have they been all that pleased about what has been learned about the causes of cancer, for once again, meat and fat intake have been increasingly implicated. The Federal Trade Commission wanted an impartial expert witness to assist their efforts in determining whether the same diets that cause heart disease could also cause cancer. They called in a nutritional scientist from Harvard University, Dr. Mark Hegstead. He testified: _I think it is clear that the American diet is indicted as a cause of coronary heart disease. And it is pertinent, I think, to point out the same diet is now found [guilty] in terms of many forms of cancer: breast cancer, cancer of the colon, and others._ In light of this, the meat, dairy, and egg industries have done the only thing they could. They have joined hands with the tobacco industry to do whatever they can to confuse the issue and make the public think "anything can cause cancer." The more people feel anything can cause cancer, the less they will focus attention on those specific things that, in fact, are known to cause cancer. The more confused and powerless people feel, the less likely they are to make the choices that would actually decrease their risk of cancer. It's not that these industries want people to get cancer; it's just that they want us to continue buying their products. The fact that their products do, in fact, cause cancer is, to their minds, a deeply unfortunate public relations issue. ### **Colon Cancer** Most of the medical researchers who have done the work investigating dietary causes of cancer are people who were, along with the rest of us, unknowingly schooled in the National Dairy Council brand of nutritional education. Accordingly, most of them became members in good standing of the Great American Steak Religion. But then, in the 1970s, a number of studies were published in the _Journal of the National Cancer Institute_ that reported what was then startling news. Researchers were finding that the incidence of colon cancer was high in precisely those regions where meat consumption was high, and low where meat consumption was low. It was found, in fact, that _there is not a single population in the world with a high meat intake that does not have a high rate of colon cancer._ The meat industry, true to form, did what it could to deny the emerging truths, but the more studies that were done, the clearer the correlation became. With each succeeding year, it became harder for even the meat industry's paid scientific consultants to avoid the conclusion that meat-eating is involved in the production of a killer that affects over 20 percent of the families in the United States. Even the conservative journal of the Association for the Advancement of Science concluded: _Populations on a high-meat, high-fat diet are more likely to develop colon cancer than individuals on vegetarian or similar low-meat diets._ The meat industry countered by saying that genetic factors were responsible. They couldn't deny that those populations who eat the most meat get the most cancer; the evidence was too strong. But they said it was only a coincidence, and the real reason was that such populations were hereditarily disposed toward the disease. Dr. John Berg and his associates at the National Cancer Institute decided to find out. It was known that the Japanese had lower rates of colon cancer than Americans, and that they ate less meat. Dr. Berg and his coworkers undertook a major study to see what happened to Japanese who immigrated to the United States and adopted the standard American diet-style. If the industry point of view were correct, these people would maintain their lower colon cancer rates, even though they now ate more meat. One more sacred cow toppled with the results of this rigorous study. The colon cancer rates of the Japanese immigrants had, in fact, risen to match the colon cancer rates of their American neighbors. The meat industry now found itself decidedly on the defensive but countered by protesting that it could be anything in the American diet-style that was responsible. To single out meat as the culprit, they avowed, was unscientific. In an effort to isolate precisely which dietary factors were responsible, Dr. Berg and his colleagues at the National Cancer Institute now undertook a major study that correlated colon cancer rates with intake patterns for no less than 119 specific foods. Dr. Berg then reported the results in the _Journal of the National Cancer Institute._ Meat didn't fare very well. In fact, of all foods studied, it was by far the most strongly associated with colon cancer. Wrote Dr. Berg: _Risks of beef, pork and chicken all rose with frequency of use, and the composite picture suggests an underlying dose-response relationship._ Faced with rigorous data that told us what we could do to prevent colon cancer, spokesmen for the meat industry now parried by saying more studies needed to be done. They were confident, they said, that meat would be vindicated. As more research was indeed done over the following years, things didn't work out the way the industry hoped. Further research discovered that another dietary factor involved in colon cancer is fat consumption. It became increasingly apparent that the more fat people consume, the greater their risk of colon cancer. Then another factor was isolated—fiber consumption. Researchers discovered that the less fiber in a person's diet, the more likely he or she is to get colon cancer. These were not the results the meat industry had hoped for, either, because meats, like eggs and most dairy products, are high in fat and provide absolutely no fiber whatsoever. Until very recently of course, most of us didn't know that a lack of fiber in our diets was a problem. In fact, most of us didn't even know what fiber was, and for years National Dairy Council nutritional education materials ignored fiber altogether. But medical research is increasingly finding fiber to be a most important dietary component. Fiber acts like a broom in your intestines, sweeping things along. Without it, waste gets blocked up, and the length of time your food takes to pass through your colon is greatly increased. This is particularly true if your diet contains animal fat, because animal fats are solid at body temperature. They clog up your intestines just as grease clogs up drains. **THE MORE FAT YOU CONSUME THE GREATER YOUR RISK OF COLON CANCER** Source: Data adapted from K. Carroll, "Experimental Evidence of Dietary Factors and Hormone-Dependent Cancers," _Cancer Research_ 35 (1975): 3374. One of the functions of the bowel walls is to absorb moisture from the bowel contents. If, for some reason such as bacterial or amoebic contamination, the body discharges the bowel contents in a rush, without allowing time for the bowel walls to absorb moisture, what comes out will be watery. Victims of dysentery often become extremely dehydrated and can, in extreme cases, die from the dehydration that results from diarrhea. But without enough fiber the problem is the opposite. The waste material remains in the colon longer, and more moisture is absorbed by the colon walls. The longer it takes for the contents of the colon to complete their transit, the drier and harder will be the stools that finally emerge. Researchers have found that the stools of people whose diets are low in fiber tend to be harder, drier, and smaller than the stools of people whose diets are higher in fiber. On a low-fiber diet, people typically have to strain to evacuate. People whose diets are high in natural fiber, in contrast, have been found to produce large, soft, moist, and plentiful stools—and these are the same people who show low rates of colon cancer. There seem to be a number of reasons why high-fiber diets protect against colon cancer, and fiber-deficient diets promote the disease. The longer transit times produced by low-fiber diets provide more opportunity for the bowel walls to reabsorb the toxins the body is trying to eliminate. In other words, the material hangs around longer, the toxicity in the colon increases, and the colon walls absorb more toxins. In addition, fiber helps to dilute, bind, and deactivate many carcinogens. **FIBER CONTENT OF COMMON FOODS** **FOOD ITEM** | **FIBER (g/kg)** ---|--- Blueberries | 15.2 Brussels sprouts | 13.5 Oat flakes | 13.5 Pumpkin | 12.0 Cooked carrots | 9.6 Brown rice | 8.1 Swiss chard | 6.8 Lettuce | 6.3 Cucumbers | 5.7 Applesauce | 5.3 Ground beef | 0 Sirloin steak | 0 Lamb chops | 0 Pork chops | 0 Chicken | 0 Ocean perch | 0 Salmon | 0 Cheddar cheese | 0 Whole milk | 0 Eggs | 0 Source: John D. Kirshman, _Nutritional Almanac_ (Revised), Nutritional Research, Inc. (New York: McGraw Hill Book Co., 1979). With the growing awareness of the importance of dietary fiber, many meat-eaters are beginning to add bran or other fibers to their diets. This, in fact, is now the belated recommendation of the National Dairy Council, which manages to get in a plug for dairy products as it recommends _bran flakes with milk, or cream, if you are concerned with fiber._ Adding fiber to your diet will speed up transit time, which is good. And the extra fiber will help to absorb some of the toxins in the colon, which is also good. But just adding fiber to a meat-based diet may not help all that much in reducing the risk of colon cancer. You see, the digestion of meat itself produces strong carcinogenic substances in the colon, and meat-eaters must produce extensive bile acids in their intestines to deal with the meat they eat, particularly deoxycholic acid. This is extremely significant, because deoxycholic acid is converted by clostridia bacteria in our intestines into powerful carcinogens. The fact that meat-eaters invariably have far more deoxycholic acid in their intestines than do vegetarians is one of the reasons they have so much higher rates of colon cancer. Researchers who analyze and test human feces can distinguish the feces of meat-eaters from those of vegetarians by their smell. They report that the eliminations of meat-eaters smell far stronger and more noxious than those of non-meat-eaters. There is a serious reason. Putrefying animal products are far more toxic than rotting plant products, and meat-eaters' colons are continually subjected to these toxins. The human intestine has a very hard time handling the putrefying bacteria, high levels of fat, and lack of fiber that characterize meat, dairy products, and eggs. There are other animals, though, whose intestines seem designed for the task. The human intestine is anatomically very different from that of the natural carnivores, such as dogs and cats. Because of the design of their intestines, these animals are virtually guaranteed short transit times. **THE BOWELS OF HUMANS AND CARNIVORES ARE STRIKINGLY DIFFERENT** PORTION OF A TYPICAL CARNIVORE BOWEL (Note the smooth, stovepipe shape) PORTION OF A TYPICAL HUMAN BOWEL (Note the puckering and pouching) **The human bowel twines back and forth along a convoluted pathway, with many twists and hairpin turns. Carnivores' bowels, in contrast, take a relatively direct and straightforward route. As a result, their transition times are much shorter than ours. They can handle cholesterol and fat and have much less need for fiber to move things along.** Our bowel walls are deeply puckered; theirs are smooth. Ours are full of pouches; theirs have none. Our colons are long, complex pathways, like a winding mountain road full of hairpin turns; theirs are short, straight chutes, like wide-open freeways. The toxins from putrefying flesh are not the problem for them that they are for us because everything passes through them so much more quickly. Dogs, cats, and the other natural carnivores do not get colon cancer from high-fat, low-fiber, flesh-based diets. But we do. Statistics show clearly that the more fat we eat, the more likely we are to die of colon cancer. The more meat we eat, the more likely we are to die of colon cancer. The less fiber we eat, the more likely we are to die of colon cancer. It's as simple as that. Faced with an ever-increasing preponderance of medical evidence indicting their products as agents of colon cancer, the meat, dairy, and egg industries have found it difficult to defend their products. But they have time and again shown remarkable ingenuity and dedication in attempting to rise to the challenge. With their backs to the wall, these industries have made much of several studies that seem to associate low blood cholesterol levels with colon cancer. They have claimed these studies prove that low blood cholesterol promotes colon cancer. If this were true, it would make meat, dairy products, and eggs look pretty good, because they are well known for raising blood cholesterol levels. Spokesmen for the saturated fat lobby have even tried to persuade the public, governmental agencies, and even cancer researchers that if your blood cholesterol is high you might tend to get heart disease, but if your blood cholesterol is low you may very well get colon cancer. The more likely you are to get one, the less likely you are to get the other. So it balances out in the long run, and there's no point worrying. But as the figure on page 239 shows, the mortality pattern for these two diseases is far indeed from opposite. In fact, they often run quite parallel, and both correlate explicitly with meat consumption. The real reason why some people with low blood cholesterol levels have higher rates of colon cancer is actually quite simple. While most people carry diet-derived cholesterol in their blood and deposit it in their arteries, thus causing heart disease, there are some people who instead send the excess cholesterol to their bowels. Accordingly, these people show low levels of blood cholesterol, even if their diets are high in saturated fat and cholesterol. But they have very high levels of cholesterol in their stools and in their intestines—and very high rates of colon cancer. On the other hand, people whose blood cholesterol is low because their intake of saturated fats and cholesterol is low do not show high levels of cholesterol in their stools and intestines, and their rates for colon cancer are, in fact, very low. **THE PATTERN IS REMARKABLY PARALLEL** Source: Data adapted from Journal of the National Cancer Institute 51 (Dec. 1973); and Foreign Agricultural Circular—Livestock and Meat (Washington, DC: USDA, 1976). But the saturated fat lobby has a point in all this, even if it is not the one they wish to make. When it was first found that high blood cholesterol causes heart disease, there was a rush to find ways to lower it. When it was discovered that the intake of polyunsaturated fats could accomplish this purpose to some extent, many felt an answer was to replace saturated fats in the diet with polyunsaturated fats. It wasn't known yet that polyunsaturated fats lower the levels of cholesterol in the blood by driving it out of the blood and into the colon. The answer isn't simply to replace saturated fats in the diet with polyunsaturated fats, as was once thought. The answer is to lower the intake of fats, per se, in order to be protected across the board. Replacing saturated fats with polyunsaturated fats will help some, because saturated fats are far and away the worst offenders, guilty of producing heart disease, strokes, cancer, and just about every other degenerative disease known to man. But too much fat of any kind is not good. Vegetarians need to be aware that not only meat, eggs, and dairy fats are harmful to health. Vegetable fats such as salad oils and margarines need to be used in moderation. And much the same is true for nuts, seeds, olives, and avocados. We know today with remarkable accuracy which diet-styles promote colon cancer. But you wouldn't know it from the statements of the meat, dairy, and egg industries. On May 7, 1976, John Morgan, president of Riverside Meat Packers, announced: _We shouldn't jump to any conclusions and do something foolish just because some study seems to say something that we know from common sense isn't true. Beef is the backbone of the American diet and it always has been. To think that meat of all things causes cancer is ridiculous._ On March 13, 1982, John Morgan died of cancer of the colon. ### **Breast Cancer** In the time it takes you to read this chapter, 100 women in the United States will be told by their doctors that they have breast cancer. Very few of them will ever have been told that the higher the percentage of fat in a woman's diet, particularly animal fat, the greater the risk she runs of getting the disease. Nor will any of them likely have been told that the prognosis for a woman with breast cancer varies statistically according to her fat intake. The less fat she has eaten in her lifetime, the greater hope she has, statistically, of beating the disease, and the longer time she will, on the average, survive. **SEE THE PATTERN?** Source: Data adapted from K. Carroll, "Experimental Evidence of Dietary Factors and Hormone-Dependent Cancers," _Cancer Research_ 35 (1975): 3374. Sadly, one out of every 10 women in the United States will eventually develop breast cancer, while billions of dollars continue to be poured into surgical techniques, sophisticated methods of radiotherapy, and the widespread use of chemotherapy. Yet the death rate for breast cancer has hardly changed since the days before the automobile was invented. It is a classic and truly tragic case of losing a war we could prevent. The largest cancer studies in medical history have been headed by Dr. Takeshi Hirayama, at the National Cancer Research Institute in Tokyo, where as many as 122,000 people have been monitored for decades. In one study, Dr. Hirayama and his coworkers investigated the risk of breast cancer for women according to their intake of meat, eggs, butter, and cheese. The findings were not easy for the meat, dairy, and egg industries to swallow. Those who consume meat daily face an almost four times greater risk of getting breast cancer than those who eat little or no meat. Similarly, the more eggs consumed, the greater the risk of breast cancer. The more butter and cheese consumed, the greater the risk of breast cancer. (See figure on page 243.) Interestingly, an examination of Dr. Hirayama's report makes it appear initially that the incidence of breast cancer rises with a rising intake of butter and cheese up to a certain point but then drops off. The explanation for this seeming deviation in the pattern is that many lacto-ovo vegetarians consume butter and cheese daily, and yet, because they do not eat meat, their breast cancer rates are lower than those for meat-eating women who eat less cheese and butter. This and other studies reveal the same pattern for breast cancer as has been found true for heart disease, strokes, and colon cancer: _Breast Cancer Mortality_ _(highest incidence ranked first)_ 1. _Meat-eating women_ 2. _Lacto-ovo vegetarians_ 3. _Pure vegetarians_ A number of studies have found that vegetarian girls have later menarche (onset of menses) than meat-eating girls. In Japan, as diets have become less traditional and more Western, with increasing amounts of animal fat, one result for Japanese girls has been earlier and earlier menarches. Dr. Hirayama and his colleagues at the National Cancer Research Institute have found that women who have an earlier menarche (under 13 years of age) have over four times the incidence of breast cancer as women who have a later menarche (over 17 years of age). **A WOMAN'S RISK OF BREAST CANCER RISES DRAMATICALLY WITH HER INTAKE OF MEAT, EGGS, CHEESE, AND BUTTER** Source: Data derived from paper presented by Takeshi Hirayama at the Conference on Breast Cancer and Diet, U.S.–Japan Cooperative Cancer Research Program, Fred Hutchinson Cancer Center, Seattle, WA, March 14–15, 1977. Studies from other parts of the world corroborate the Japanese findings. The more fat in a young girl's diet, the earlier her menses will begin, and the higher will be her risk of breast cancer. Studies have also shown that as animal fat consumption rises, menstrual periods become heavier, further apart, longer, and more painful, with greater premenstrual difficulties. Diets high in meats, dairy products, and eggs not only force an early menarche but also delay menopause. A report published in the _British Medical Journal_ found that women whose diets are high in fat and protein reach menopause at an average age of 50. They stand in marked contrast to women whose diets are low in or void of animal fat, who reach menopause at an average age of 46. Sadly for meat-eating women, there is a distinct correlation between later menopause and breast cancer. ### **Cervical Cancer** Cervical cancer is frequently linked to injuries sustained by the cervix during childbirth; however, like breast cancer, it is highest among women who consume diets high in fat, particularly animal fat. Studies show the incidence of cervical cancer in women in developed countries who began intercourse before age 17 is two to three times higher than for those who began later. Poignantly, those girls who have the earliest sexual encounters in these countries are typically the same ones who have the earliest menarches. They are thus more susceptible to both breast and cervical cancer. Both their difficulties have repeatedly been correlated to diets high in protein and fat, most notably animal protein and animal fat. ### **Cancer of the Endometrium (Uterus)** Many women today take estrogen pills to prevent osteoporosis. They don't know they could accomplish the same purpose by simply not eating concentrated animal proteins. Nor do they know they are greatly increasing their risk of developing uterine cancer. The relationship between fat consumption and uterine cancer is the same as it is for the other female cancers: the more fat eaten, the more cancers. In fact, almost every single one of the factors currently acknowledged as a risk indicator for uterine cancer—obesity, early puberty, late menopause, estrogen pills, high blood pressure, and diabetic tendencies—occur disproportionately in women whose diets are high in fat. **THE MORE ANIMAL FAT EATEN, THE EARLIER THE ONSET OF PUBERTY (AND THE MORE CANCER)** **Japanese girls are reaching puberty four years earlier than their ancestors did, due to dietary changes. Since World War II their traditional rice and vegetable fare has been replaced by a diet much higher in animal fat.** Source: Data adapted from Y. Kagawa, "Impact of Westernization on the Nutrition of Japan: Changes in Physique, Cancer..." _Preventative Medicine_ 7 (1978): 205. Those countries with the lowest consumption of fat, such as Japan and Nigeria, have the lowest rates of uterine cancer. Those countries with the highest consumption of fat, such as the United States and other meat-eating countries, have the highest rates of uterine cancer. **WHICH ARE REALLY THE HIGH-FAT FOODS? Percentage of Calories as Fat** VIRTUALLY ALL FAT (80–100%) --- Butter | 100% Salad oils | 100% Cream, light | 92% Coconut | 85% Pork sausage | 83% Sirloin steak | 83% Avocados | 82% Bologna | 81% Frankfurters | 80% VERY HIGH FAT (60–79%) --- Half-and-half | 79% Brick cheese | 72% Cheddar cheese | 71% Sunflower seeds | 71% Peanuts | 69% Swiss cheese | 66% Eggs | 65% Ground beef, lean | 64% Tuna, oil packed | 63% HIGH FAT (40–59%) --- Chicken, dark w/skin, roasted | 56% Mozzarella, part skim | 55% Bass, black sea | 53% Salmon, sockeye | 49% Yogurt | 49% Milk | 49% Ice cream | 48% Sirloin steak, lean | 47% Chicken, light w/skin, roasted | 44% MEDIUM FAT (20–39%) --- Soybeans | 37% Cottage cheese | 35% Low-fat milk | 31% Low-fat yogurt | 31% Nonfat cottage cheese | 22% LOW FAT (0–19%) --- Oatmeal | 16% Garbanzo beans | 11% Cabbage | 7% Green beans | 6% Macaroni | 5% Whole wheat | 5% Spaghetti | 5% Brown rice | 5% Apricots | 4% Artichokes | 3% Peaches | 2% Potatoes | 1% Source: _Nutritive Value of American Foods in Common Units,_ USDA Handbook No. 456. ### **Ovarian Cancer** The July 19, 1985, issue of the _Journal of the American Medical Association_ contained a report by Dr. John Snowden, an epidemiologist at the University of Minnesota's School of Public Health, summarizing a 20-year study of diet and ovarian cancer. The results were a tremendous blow to an already-reeling egg industry: _Women who ate eggs...three or more days each week had a three times greater risk of fatal ovarian cancer than did women who ate eggs less than one day per week._ As with the other female cancers, the incidence of ovarian cancer rises not only with egg consumption but with the consumption of any form of animal fat. Dr. Ronald Phillips concluded a report in _Cancer Research_ by saying the evidence is now overwhelming: vegetarian diets strongly reduce the incidence of breast, uterine, ovarian, colon, and many other cancers. ### **Prostate Cancer** Prostate cancer is one of the most virulent forms of a virulent disease. It has usually spread before it is detected and is usually fatal. Prostate cancer is highly correlated to fat consumption. The figure on page 248 shows why the meat, dairy, and egg industries do not particularly want to publicize the worldwide pattern. Nor are they encouraged by studies such as the one done at California's Loma Linda University. This 20-year undertaking involved over 6,500 men and found that those who consumed large amounts of meat, cheese, eggs, and milk had 3.6 times the incidence of prostate cancer as men who ate those foods sparingly or not at all. Even for men who do not develop prostate cancer, the effects of different diet-styles on the health of their prostates can be considerable. By the age of 60, 40 percent of U.S. males have enlarged prostates. While most of these are not malignant, they can be forerunners of cancer and are often quite uncomfortable. Worldwide, autopsies reveal that wherever the diet-style is similar to the American fare—with high animal fat consumption—close to 25 percent of all men develop latent cancer of the prostate by their old age. The hormonal changes that high-fat diets cause in men are not as easily observable as those produced in women, because men do not have such obvious milestones in their sexual evolution as menarche and menopause. But there are strong indications that high-fat (and particularly high-animal-fat) diet-styles stimulate the early development of sexuality in boys as much as they do in girls. And just as girls with early menarche run into the most trouble later on with breast cancer, boys with early onset of puberty later find themselves the most susceptible to prostate enlargement and prostate cancer—particularly if they continue this diet-style throughout their lives, as they usually do. **AGAIN AND AGAIN, THE SAME PATTERN** Source: Data adapted from B. S. Reddy, et al., "Nutrition and Its Relationship to Cancer," _Advances in Cancer Research_ 32 (1980): 237. Diets high in saturated fat and cholesterol tend to clog up our arteries, thereby reducing the blood flow to our hearts and brains and sometimes, tragically, obstructing them altogether. Atherosclerosis also tends to reduce the flow of blood to our other organs, including our reproductive ones, thus producing impotence in men. Painfully, the same diet that induces atherosclerosis also tends to produce high levels of androgens, the male sex hormones, which may lead to a greater need for sexual release. Thus some authorities feel these diets produce in older men, not only heart attacks and strokes, but the unfortunate situation of chronic sexual pressure that cannot be expressed in a satisfying manner. The resulting frustration may lead to enlarged prostates, and often to prostate cancer. ### **Lung Cancer** The Marlboro Man may not know this, but vegetarians have much lower rates of lung cancer than the general population. The meat industry would like us to believe this is only because vegetarians smoke less than meat-eaters. But many studies have consistently shown that the higher the blood cholesterol count of a smoker, the greater his or her risk of lung cancer. Vegetarian smokers have distinctly lower rates of lung cancer than do meat-eating smokers. The tobacco industry capitalizes on the link between smoking and meat, particularly in their ads aimed at men. The Marlboro Man is a cowboy, and a veritable embodiment of the Great American Steak Religion. I sometimes wonder which will get him first, a heart attack or lung cancer. ### **Whatever Happened to the War on Cancer?** The war on cancer is a tragedy. Billions upon billions of dollars are being spent to develop and apply treatments that are invasive, expensive, painful, often mutilating, and in many cases of little benefit. Meanwhile, most of us are unknowingly increasing the probability of cancer with our every meal. The more I've learned about diet and cancer, the more stunned I've been at our ignorance of their close relationship. We do not have to quake helplessly in the face of cancer, hoping to escape its clutches. We do not have to sit by passively, watching our loved ones succumb to this disease. We do not have to spend our life savings, undergoing painful and devastating treatments that do little or no good. We are blessed now with the knowledge that enables us to make clear, life-giving choices. We need only make them in time. ## 10. **AN OUNCE OF PREVENTION** _Loyalty to a petrified opinion never yet broke a chain or freed a human soul._ —MARK TWAIN Over the past 25 years, there have been unprecedented breakthroughs in our understanding of food choices and health. However, there is an enormous gap between what has been discovered and what the public has learned of it. As a result, tens of millions of American men, women, and children are suffering needlessly. We have been given an extraordinary opportunity. We now hold an infinitely precious gift in our hands—our health, the health of our children, the possibility of a truly healthy world. These are no longer mere dreams; they could be our destiny. The time is at hand when heart disease, atherosclerosis, strokes, and cancer could be things of the past. And I can see a future when people will hardly be able to believe the ancient legend that once, before they knew better, human beings sickened themselves by eating the corpses of animals whose lives had been hell. With a diet-style that is compassionate and healthy, we can become something far healthier and greater than we have yet been. Compared to what is possible, our present physical bodies are like lightbulbs without current, waiting to be lit. The more I've learned about the diet-health connection, the more amazed I've been by how much is already known. Not only heart disease and cancer but many other diseases have been traced directly to today's dietary blindness. Scientific studies have shown not only that these diseases and the immense suffering they entail can often be prevented by intelligent food choices but that in many cases they can be treated by diet-style changes with direct, consistent, and powerful benefits. ### **Diabetes** Diabetes is a good example. Millions of Americans suffering enormously from this disease do not know their agony could be greatly relieved by different food choices. One of the reasons diabetes is the eighth-leading cause of death in the United States is that diabetics are extremely vulnerable to atherosclerosis. Highly prone to heart attacks and strokes, their life expectancies are much shorter than normal. But it is not just that their lives are shortened; the damage atherosclerosis does to their cardiovascular system has profound consequences to the quality of their lives. Degeneration in the arteries bringing blood to their eyes is so severe that 80 percent of diabetics suffer serious eye damage, and diabetes is the leading cause of new cases of blindness in the country. The blood supply to their kidneys is often compromised, and as a result diabetics have 18 times the average rate of serious kidney failure. Many spend the last years of their lives tied to the ordeal of a kidney machine. Circulation to their extremities is cut down to such an extent that an infection in a toe which for most of us would be minor can, for a diabetic, easily lead to gangrene, may require amputation of a foot or a leg, and can even be life threatening. As if this weren't enough, since atherosclerosis decreases circulation to the reproductive organs, diabetic males have a much higher rate of impotence than the general population. Yet, with all the terrible damage atherosclerosis does to diabetics, most of them do not know which diets promote atherosclerosis and which diets reduce it. Most eat the standard American diet. As a result, within 17 years of the onset of their illness, most diabetics today suffer a major health catastrophe, such as heart attack, kidney failure, stroke, or blindness. This is especially tragic because it is so needless. Different diet-styles produce very different results. In _Lancet,_ Dr. Inder Singh reported a remarkable study in which 80 diabetic patients were restricted to very-low-fat diets—20 to 30 grams a day—and forbidden any sugar consumption. Within six weeks, over 60 percent of the patients no longer required insulin. In the weeks that followed, the figure rose to over 70 percent, and those who still needed insulin therapy needed only a small fraction of what they had required before the diet change. All 80 cases were monitored for periods ranging from six months to five years, and the success of the dietary changes was confirmed over time. There's a reason why the low-fat diet helped so much. The pancreas operates according to a kind of thermostat. Just as a heater governed by a thermostat will switch on and off as the temperature changes in the room, the pancreas secretes insulin in response to sugar in the blood in order to keep blood sugar levels within a certain range. Many diabetics need to give themselves insulin shots, but this is not, as commonly thought, because the pancreas is not secreting enough insulin. In fact, many diabetics produce more insulin than a normal person, yet still need these injections. The reason is that their insulin is not able to do its job, and their blood sugar levels skyrocket out of control unless medication is given. It turns out that a common cause for the malfunction of the diabetic's own insulin is the high level of fat in their blood. Thus the reduction of dietary fat, particularly saturated fat, can be of greatest significance to diabetics, for it lowers the concentration of fat in the blood and thus allows their own insulin to do its job. The _American Journal of Clinical Nutrition_ reported a study in which 20 diabetics, all of whom needed insulin, were put on a high-fiber, very-low-fat diet. After only 16 days, 45 percent of these patients were able to discontinue the insulin injections. Other studies have produced similar results. Approximately 75 percent of diabetics who have needed insulin therapy and 90 percent of diabetics who have needed diabetic pills (sulphonylureas) can be freed from their need for medication in a matter of weeks on a low-fat, high-fiber diet. For a diabetic to be freed from his or her need for medication is a great blessing, for compared to the pancreas's function, medications are a vastly inferior means of controlling blood sugar levels. Furthermore, they have serious side effects. The pills more than double the risk of heart attack and sometimes cause jaundice, skin rashes, and anemia. Overdoses of medication are common because the body's needs change all the time and are impossible for patients to monitor with anything remotely resembling the accuracy of the pancreas. Insufficient food intake can easily precipitate disorienting bouts of hypoglycemia (low blood sugar). The insulin pump is a recent, sophisticated improvement, but it is expensive, must be worn at all times, produces infections at the injection site a third of the time, and markedly worsens the eye diseases so common to diabetics. Additionally, the pumps are machines; machines can malfunction, and a malfunctioning insulin pump can be fatal. Low-fat diets, particularly those without any saturated fat, have demonstrated a remarkable success rate in allowing diabetics to dispense with their pills, shots, and pumps. Happily, these are the very same diets that protect against the ravages of atherosclerosis to which diabetics are otherwise so terribly prone. There is a rare and very serious form of diabetes called childhoodonset diabetes that is in many ways a different disease. It is not the result of the body's own insulin being rendered ineffective but is rather a situation in which the pancreas has been seriously injured and either cannot secrete insulin at all or does not secrete enough. Even for victims of this singularly destructive form of diabetes, however, wise food choices are of enormous value. Those who omit meat and other high-fat, low-fiber foods need 30 percent less insulin, have more stable blood sugar levels, are (in medical terms) less "brittle," and are significantly protected from the complications of atherosclerosis that otherwise would cause them such immense suffering. The scientific breakthroughs of the past 25 years have found that the same diet-styles that can do so very much to help diabetics are the very ones that prevent the disease in the first place. Worldwide, the disease is rare or nonexistent among peoples whose diets are primarily grains, vegetables, and fruits. If these same people switch to rich meat-based diets, however, their incidence of diabetes balloons. In Micronesia there is a small island called Nauru, near the equator, just west of the Gilbert Islands. Before World War II, the native Polynesians lived here in isolation and were such a healthy and happy people that the island used to be known as Pleasant Island. On this island there are enormous deposits of bird dung that have accumulated over the centuries. After the war, the phosphates from this bird dung were coveted by the industrialized nations. As a result, the Nauruans became very wealthy and began to emulate the West—gorging themselves on rich foods, canned and frozen meats, fish, oils, white rice, soft drinks. Their consumption of fiber plummeted and their consumption of fat skyrocketed. Now the island is not so pleasant. Tragically, over one-third of these people have developed diabetes. An enormous scientific project, which studied more than 25,000 people for 21 years, found that vegetarians have a much lower risk of diabetes than meat-eaters. One of the authors of the study, University of Minnesota epidemiologist Dr. David Snowden, summarized the findings: _We suspect it is the absence of meat that may explain our findings. In this study we looked at various levels of meat consumption, and as those levels got lower and lower, the risk of diabetes also decreased._ In a more personal vein, Dr. Snowden confided: _My meat consumption has dropped significantly...since completing the diabetes study._ ### **Hypoglycemia** The disorientation caused by mild cases of hypoglycemia is so common in the United States today that most people think it's normal. They do not realize the sense of weakness, dizziness, or confusion they sometimes experience is the result of a drop in their blood sugar level. And they also do not realize this is a product of their food choices. Hypoglycemia is found wherever people consume significant amounts of meat, sugar, and fats. In its mildest form, hypoglycemia causes feelings of confusion, uncertainty, and a lack of confidence in oneself. In more difficult cases, victims may temporarily not know who or where they are. The result in extreme cases can be coma and death. You may assume that moderating your sugar consumption is the chief factor in preventing hypoglycemia; but decreasing fat consumption is also greatly involved. Dr. J. Shirley Sweeney fed young healthy medical students a very-high-fat diet for two days. Then he gave them a glucose tolerance test. All of the subjects showed signs that their blood sugar metabolism had been driven completely out of whack by the excess fat. On another occasion, Dr. Sweeney fed the same students a diet consisting of sugar, candy, pastry, white bread, baked potatoes, syrup, bananas, rice, and oatmeal. After two days of this high-sugar, high-starch fare, he administered another glucose tolerance test. The blood sugar metabolism of the subjects was not nearly as off balance as it had been from the high-fat diet. If you want to get hypoglycemia, or if you already have it and want to make it worse, eat lots of fat, sugar, animal protein, dairy products, and processed foods. Stay away from fresh vegetables and whole grains. Don't believe all that stuff you hear about smoking and meat being dangerous to your health. And don't worry about getting your vitamins and minerals from your food—you can always pop a vitamin pill anytime you want. There is no need for regular meals, as long as you really load up when you have the chance. Remember that coffee is the key to mental alertness, and alcohol is the path to relaxation and freedom from your fears. And, God forbid, don't exercise. Such a regime is guaranteed to make your pancreas forget it ever knew health and alter your consciousness in a decidedly unpleasant direction. ### **Multiple Sclerosis** Today's doctors have been taught in medical school that nothing can be done to prevent multiple sclerosis, and that nothing can be done to treat it. They tell their patients that this terrible disease is incurable. This represents one of the most profound examples of needless suffering perpetuated by an ignorance of what has been learned about diet and health. If you know anyone who suffers from multiple sclerosis, please share this information with him or her. The onset of MS usually occurs in the mid-30s. Women have a slightly higher incidence than men. It is the most common disease of the central nervous system in Americans aged 20 to 50 years. Over 250,000 Americans are afflicted with this devastating disease, and the numbers are rising daily. Multiple sclerosis is a disease that attacks the brain, spinal cord, and nervous system over a period of years. According to conventional medical doctrine, the attacks just keep coming, and the patient can only look forward to getting ever worse. There is no way to predict when the next attack might occur, or what might set it off. Today's doctors tell their MS patients nothing can be done to prevent the attacks from seriously injuring their nervous system, causing weakness, dizziness, numbness, and/or blindness. Modern orthodox medical opinion says that within 10 years of most MS victims' first attack they will be permanently and seriously disabled. The pessimism of conventional medicine is indeed warranted—for MS victims who consume the standard American diet. For those on a different diet, however, another outcome is possible. During World War II, when the diets of people in occupied western European countries were dramatically reduced in animal fat consumption, researchers noticed that MS victims in these areas suddenly had fewer attacks, less frequent hospitalizations, and fewer deaths. This observation gave rise to studies which revealed that there is a great variation in the worldwide incidence of the disease. It is most common where consumption of animal fats is high, and least common where such consumption is low or nonexistent. Per capita fat intake in the nine nations with the greatest prevalence of MS ranges from 105 to 151 grams per day; per capita fat intake in the nine nations with the least incidence of MS ranges from 24 to 60 grams per day. Investigators also did brain tissue analysis of persons with MS and found a higher saturated fat content than in people without the disease. The next piece of the puzzle fell into place when it was discovered that children who are fed cow's-milk formulas grow up into adults with a higher susceptibility to MS than children who are breast-fed. Cow's milk contains only one-fifth the linoleic acid of human milk, and skim cow's milk is utterly void of this important nutrient. Linoleic acid is an essential nutrient for human nervous systems, which is just where MS strikes. Researchers suspect that the nervous system of children raised on a diet that derived its fat from animal sources such as cow's milk might be deprived of sufficient linoleic acid at a critical juncture in the development of their nervous systems and so become more susceptible to MS in later life. Ironically, one of the arguments put forth by the meat, dairy, and egg industries to justify consumption of saturated fats is that fats contain essential nutrients. In fact, the only nutrient we must get from fat is linoleic acid, and animal fats are very poor sources. One tablespoon of safflower oil, for example, provides as much linoleic acid as a cup and a half of butter, and more than two whole cups of beef fat. The standard American diet—beginning with the substitution of cow's milk for breast milk and continuing on with high levels of animal fat—is thus a breeding ground for multiple sclerosis. Different diet-styles, however, not only serve to prevent MS, but have actually been shown to be of great benefit in treating it. In fact, most people would be astounded if they became familiar with the nutritional research on this supposedly incurable disease. Dr. Roy Swank, head of the Department of Neurology at the University of Oregon, began treating "incurable" MS patients with a very-low-fat diet. In one instance he put 146 MS patients on a diet that was very low in fat (30–40 grams a day), low in protein, and supplemented with moderate doses of vitamins A, C, D, and B complex. Then he carefully monitored their progress over a period of 20 years. The results Dr. Swank obtained in this experiment and those of many other studies border on the miraculous. About 90 percent of the MS patients who began the low-fat diet during the early stages of the disease not only arrested the disease process but actually improved over the next 20 years. Of those MS victims who began the diet when their disease had already reached an intermediate stage, over 65 percent were able to prevent further damage and even after seven years on the diet had suffered no further deterioration. Perhaps most amazing were the results for those MS victims who entered Dr. Swank's care and began the low-fat diet when their disease had already progressed to an advanced stage of severe disability. Over 30 percent were able to arrest the inexorable devastation of the disease and showed no further decline. In this and many other studies, a very-low-fat diet for multiple sclerosis produced a profound reduction in the frequency of attacks, the severity of attacks, the damage done by the attacks, and the death rate. Dr. Swank has now treated several thousand MS patients with a low-fat diet over a period of 35 years. His results have met every challenge presented by the medical community and are enormously superior to those achieved by any other known form of treatment for this otherwise crippling and usually fatal disease. Dr. Swank has found that if MS is caught early enough, then MS victims stand a 95 percent chance of arresting the disease and not getting any worse. For many, there is the very real possibility of a cure. Other physicians have followed up on Dr. Swank's work and achieved results comparable to his. One clinic found that a pure vegetarian diet, very low in fat, has been of significant benefit even to the most advanced cases of multiple sclerosis. ### **Ulcers** Peptic (digestive) ulcers occur as a result of the mucous membranes of the stomach and/or duodenum being literally eaten away by gastric secretions. This happens when the gastric secretions become extremely acidic. With stomach ulcers as common and as painful as they have become today, a great deal of work has naturally been done to determine the effect of different diet-styles on ulcers. But the public, by and large, has not learned the results of these studies. There are powerful economic interests who'd prefer we not know that ulcers occur most frequently, and most seriously, in people whose diets are acid forming, low in fiber, and high in fat. Meats, fish, and eggs are the most acid forming of all foods. Meats, fish, dairy products, and eggs contain no fiber. With few exceptions, these foods are all high in fat. Orthodox Western medicine traditionally prescribed dairy products and antacids to treat digestive ulcers—a treatment approach called the "Sippy diet." This treatment originated when doctors noticed that ulcer patients obtained immediate pain relief by drinking milk and taking antacids. However, investigators who sought to find out whether this treatment actually does any good, beyond the temporary relief of pain, found that dairy products produce no improvement in ulcer disease and, in fact, often make things worse. Milk does contain calcium, which tends to neutralize stomach acids, providing temporary relief. But they found that milk actually increases natural acid production, which further erodes the linings of the duodenum and stomach. Researchers also found another excellent reason for staying away from milk. Ulcer disease patients treated with dairy products were found to have two to six times the number of heart attacks as ulcer patients treated without dairy products. Fortunately for ulcer sufferers, there are foods that tend to neutralize excess stomach acids that do not stimulate the body to produce more of them and do not increase the risk of heart attacks. Members of the cabbage family—cabbage, broccoli, cauliflower, and, even more potently, mustard greens, turnip greens, kale, and collards—contain a substance so effective in treating ulcers it has sometimes been called vitamin U. This substance is not stored in the body, however, so ulcer patients would be advised to eat these foods regularly. Chewing one's food well is also quite important in the treatment and prevention of ulcers because human saliva is highly alkaline. It acts as a buffering agent in the duodenum and stomach, protecting the linings of the digestive organs from becoming too acidic. People who don't chew their food well, who wolf it down, are unknowingly courting ulcers. Wolves and other natural carnivores, by the way, can wolf down their food without getting ulcers because their digestive systems (unlike ours) are anatomically designed to be highly acidic environments. Their saliva is highly acidic, while ours is highly alkaline. Their digestive secretions are far more highly acidic than ours, so highly acidic, in fact, that they can dissolve the bones of their prey. The natural carnivores are designed to wolf down their food. Their teeth are long and pointed, suited for seizing prey and ripping off chunks of flesh. Our teeth, in contrast, are designed for the grinding of grains, vegetables, and fruits. Without the aid of steak knives and cooking, we'd be hard-pressed indeed to handle flesh. That we tend to get ulcers if we wolf down our food is an example of how eating habits that are anatomically unnatural to our species create disease. Heart attacks and strokes are other examples, because, as we have seen, the natural carnivores can tolerate any amount of cholesterol without their arteries suffering. Fortunately, the suffering caused by ulcers, like that caused by atherosclerosis, is entirely preventable and in many cases can be cured by a natural vegetarian, low-fat diet. ### **Constipation and Other Intestinal Problems** _A good reliable set of bowels is worth more to a man than any quantity of brains._ —HENRY WHEELER SHAW _We aren't what we eat. We are what we don't shit._ —HUGH ROMNEY With diets that are low in fiber, there is little in the intestines to form a stool, except bacteria. It is not uncommon for the feces that ensue from low-fiber, meat-based diets to be as high as 75 percent bacteria. On the average American diet, the average American turd is actually half bacteria! This creates problems. With little roughage to stimulate peristaltic action, the material takes a long time to transit through the colon. The longer it takes, the drier it gets, and old dry feces do not gently plop from the body but have to be pushed out by force. Laxatives are often employed to move the bowels when the stools have become stuck, but in the long run these only make things worse because they irritate the bowel walls. The real answer is a diet low in fat and high in fiber. People who choose foods such as sprouts, whole grains, vegetables, and fruits tend to have large, soft, moist, well-formed stools that glide along easily through the intestines. Hemorrhoids, commonly known as piles, also result from diets that are low in fiber and high in fat. South African whites consume one of the highest-fat and lowest-fiber diets in the world and have one of the highest hemorrhoid rates in the world. The diet of South African blacks, in contrast, is much lower in fat and higher in fiber, and these people suffer virtually no hemorrhoids. Researchers once thought that this striking contrast might be due to heredity. But those blacks in South Africa who do eat meat have higher hemorrhoid rates than the other blacks; and American blacks have the same incidence of hemorrhoids as American Caucasians. In the United States, millions of people buy over-the-counter preparations that they are told will shrink their hemorrhoids. Sadly, these people are rarely told the real causes of their suffering and the road to its healing. Straining to eliminate hard, dry stools increases the pressure of blood in the veins of the rectum and legs. Over a period of time this leads to the formation of hemorrhoids, which are actually varicose veins of the rectum. Varicose veins of the legs also commonly result from the same mechanism. Diets high in fiber and low in fat yield soft, moist, plentiful stools, eliminate the need for straining, and are of great help in preventing and treating not only constipation but hemorrhoids and varicose veins. There are additional problems that arise from straining to push hard, compact stools out of the colon. Such effort forces the stomach up against the diaphragm. Eventually, this repeated pressure enlarges the diaphragm opening, and part of the stomach may be pushed through the opening. This is called a hiatal hernia and results in chest pains, indigestion, and belching. This discomfort can be extremely intense and is entirely preventable with low-fat, high-fiber diets. A very high percentage of elderly people in the United States experience intractable constipation, bleeding, and abdominal pain. What has happened is that the continual presence of old, dry material in their intestines has pushed the colon out of shape, forcing the formation of little pockets called diverticula. Though this condition, called diverticulosis, is very rare in countries where fiber intake is high and fat intake is low, it is so common as to be considered almost inevitable in countries where the consumption of meats, dairy products, and other high-fat foods is the norm. In the United States, over 75 percent of those over the age of 75 suffer from diverticulosis. These people experience repeated attacks, during which the intestines become inflamed and bleeding increases. Not knowing what's really going on, many turn to laxatives, which unfortunately further irritate the intestinal linings. Eventually, in many cases, relief can only be obtained by undergoing major surgery in which segments of the colon are removed. The good news is that none of this is necessary. Not only can diverticulosis be prevented by a diet that is high in fiber and low in fat, but it can often be successfully treated with such a diet as well. A report in the _American Journal of Digestive Disorders_ tells of 62 diverticulosis patients who were put on a high-fiber diet. Fully 85 percent of the patients reported complete disappearance of their symptoms. In another study, 70 diverticulosis patients were put on a high-fiber diet. In this case, 88 percent of their symptoms were relieved or eliminated. And the number of patients requiring laxatives was reduced from 49 to seven. If you wish to add fiber to your diet in a supplementary form, psyllium husks are a better choice than wheat bran. They are milder, smoother, and less abrasive in their intestinal action. Take them with plenty of water, an hour or more before a meal. However, a health-supporting, high-fiber diet is not achieved by merely adding fiber to a low-fiber diet. Studies in which such shortcuts have been employed do not show nearly as much success as when fiber-deficient and high-fat foods are eliminated, particularly those high in saturated fat. The most common gastrointestinal disease seen by physicians in general practice in the United States today is known as irritable colon syndrome, or spastic colon. The chief symptoms are usually pain in the lower abdomen, alternating constipation and diarrhea, and mucus appearing in small-caliber stools. Today's doctors have been taught that this condition is caused by emotional disturbances, but doctors who have switched their patients to a high-fiber, low-fat diet have consistently seen this "psychological" problem cured. Appendectomies are the most frequent emergency operation in the United States today. They are needed when the opening of the appendix becomes blocked. In such an occurrence the appendix cannot drain properly, bacteria multiply, and the appendix swells painfully. The appendicitis victim experiences acute pain, usually in the right lower quadrant of the abdomen. The culprit that blocks the appendix and creates all these problems is very often a small piece of hard, dry feces. The underlying reason behind most appendicitis is a diet-style that produces slow moving, fiber-deficient stools. This results in the small, dry concretions of fecal matter called fecaliths, which lodge in and block the opening to the appendix. The incidence of constipation, hemorrhoids, hiatal hernias, diverticulosis, spastic colons, and appendicitis corresponds very closely to the amount of fiber and fat in people's food choices. Unfortunately, many people who do not understand the enormous impact our food choices have on the health of our intestines end up requiring surgery and undergoing constant pain. This is particularly sad because it is so unnecessary. It is hard to exaggerate the amount of suffering from these diseases that could be prevented by highfiber, low-fat diets. ### **Obesity** Yankee Stadium was originally built in the 1920s to accommodate the great crowds who wanted to see Babe Ruth play baseball. When it was renovated in the 1970s, the seating capacity had to be reduced by 9,000 seats. The seating reduction was necessary because, in the 50 years since the Babe swung his bat, the average American fanny had increased in width by four inches. And so the ballpark seats had to be widened from 15 to 19 inches. Television ads tell us why beef is great if you're watching your weight. In other ads, we are shown feasts of beef fit for the bulging banquet tables of a king. The decorations are lavish, the music elegant, the furnishings posh, and the people gorgeous, and the costumes speak of great wealth. All of this, we are told, for only 300 calories. We are never told it is actually an undersized, surgically defatted sliver of beef that has only 300 calories. The meat and dairy industries have spent many millions of dollars to promote the belief that carbohydrates, such as potatoes, bread, and pasta, are the real culprits that cause excess weight gain. But literally thousands of impartial studies have shown this to have no basis in fact. Due to their high fat content, meats are far indeed from calorie conscious. The renowned Harvard nutritionist Dr. Jean Mayer explained the matter this way: _In becoming a vegetarian, you will eat a greater percentage of your calories from cereal grains, dried beans and peas, potatoes and pasta—the very foods most dieters avoid with zeal. And you will lose weight._ Because people eating the standard American diet eat such a very high percentage of their calories as fat, most of them fight a never-ending "battle of the bulge." But obesity is not merely an aesthetic issue. It has been found to be a significant cofactor in all the degenerative diseases that kill and cripple modern man. The obese, and to a lesser but still significant extent the overweight, have higher rates of heart disease, diabetes, liver disorders, gallbladder disease, cancer, arthritis, and virtually every other degenerative disease. Infant mortality rates are far higher for babies born to obese mothers. Obese teenagers have a life expectancy that is 15 years shorter than normal. **WHICH ARE REALY THE FATTENING FOODS? Calorie Concentration (calories per gram)** Source: _Nutritive Value of American Foods in Common Units,_ USDA Handbook No. 456. Clinically, the term "obesity" refers to excessive levels of body fat. It is, quite literally, a case of being fat. From a clinical standpoint, the body weight most of us think of as normal is anything but healthy. As one authority wrote: _A teenager who remains 20 percent under the normal weight enjoys a 15 year increase over and above normal life expectancy. Lower than normal weight is also associated with marked reductions in the incidence of cancer, cardiovascular diseases, diabetes, and other degenerative diseases. In a very real sense, then, U.S. and European weight standards are excessive, and the overwhelming majority of Americans and Europeans are detrimentally overweight..._ _The U.S. Public Health Service estimates 60 million Americans are overweight. In reality, the number of Americans who are above optimal weight may be three times the government estimate._ When we realize that so-called normal weights are actually too high for optimum health, and a very high percentage of Americans are above even these weights, a picture emerges that is neither flattering nor healthy. What is considered normal in our culture is actually a moderate form of obesity. Major studies published in the _American Journal of Clinical Nutrition,_ the _New England Journal of Medicine,_ and elsewhere have found that vegetarians suffer far less from being overweight than do meat-eaters. And pure vegetarians tip the scales in an even healthier fashion. Almost everyone has observed that the more body fat people have, the less they are likely to exercise. We all know people whose only exercise seems to be moving the food from their plate to their palate. Usually, we tend to think their weight problem is caused by a lack of exercise. But research is showing that it works the other way around, too. The higher a person's percentage of body fat, the less he or she typically _wants_ to exercise. Obese individuals tend to spend more time in bed and remain otherwise sluggish. Studies of people playing tennis showed that the higher their percentage of body fat, the fewer calories they burned per minute, even though with their additional weight to move around they burned more calories per movement. Their movements were less frequent, smaller, and slower. Thus the overweight person tends to be caught in a classical dilemma, where lack of exercise increases the weight problem, which in turn lowers the willingness to exercise—an unfortunate vicious circle, which can't help but contribute significantly to a speeding up of the system's degeneration. ### **Arthritis** Many of the elderly in the United States—and quite a few of the not so elderly—experience terrible pain in their joints. Their fingers may become twisted and swollen, and they may be unable even to button a coat without large doses of anti-inflammatory drugs such as aspirin. Many come to feel crippled and useless. By the age of 35, 35 percent of Americans have diagnosable arthritis in their knees. At least 85 percent of those over the age of 70 have it, and many have it severely. There are 180,000 people in the country today who are bedridden or confined to a wheelchair because of this disease. The official position of the Arthritis Foundation is that diet and arthritis are not related. But, astoundingly, there has been very little research done to justify this assertion. Up until now, virtually all arthritis research money has gone to test drugs. At Wayne State University Medical School, however, there were a few medical researchers willing to investigate the heresy that diet might have something to do with arthritis. They put six rheumatoid arthritis patients on a fat-free diet. The results were startling. In seven weeks, all of the subjects showed total disappearance of their symptoms. When fats were reintroduced into their diets, it took only three days for the symptoms to reappear. In 1981, the _British Medical Journal_ reported another instance that suggests the Arthritis Foundation's conclusions might be premature. It involved a 38-year-old woman who for 11 years had been suffering from steadily worsening rheumatoid arthritis. Three weeks after doctors removed all dairy products from her diet she showed signs of improvement. In four months, her arthritic symptoms had completely disappeared. She remained free of symptoms until, in the interests of scientific curiosity, she once again ate some cheese and milk. The next day her joints were swollen, stiff, and painful. Fortunately, her symptoms again disappeared as she resumed her abstinence from dairy products. In parts of the world where the diets are low in fats and cholesterol and moderate in protein, and where the consumption of processed and junk foods is minimal, even old people who have done hard physical work their whole lives are essentially free of arthritis. This presents quite a contrast to the United States, where so many are crippled by the disease that it is rare to find an older person who is not affected. One study found not a single case of rheumatoid arthritis in a rural black South African community of over 800 people who ate no meats or dairy products. Another study found that black South Africans who ate significant amounts of meat and other high-fat foods had almost four times the incidence of arthritis as those whose diet was very low in meat and fat. Arthritis patients characteristically suffer severely from atherosclerosis, and their blood cholesterol levels tend to be higher than normal. There is evidence that the fat and cholesterol that accumulates on the linings of the blood vessels in atherosclerosis prevent the normal transfer of oxygen to the joint tissues. Joint tissues that are thus deprived of oxygen become inflamed and arthritic. As well, nodes or knots made up primarily of cholesterol are frequently found near arthritic joints. And arthritis patients often have severe atherosclerosis in the body's main artery, the aorta. Gouty arthritis is acknowledged even by the Arthritis Foundation as being diet related. In fact, gout is one of the most easily controlled of all diseases when proper dietary guidelines are followed. Gout occurs when uric acid in the body forms needle-like crystals that become deposited in a joint. When that happens, there is severe pain and swelling in a joint, often the big toe. Avoiding foods that are high in either purines or protein has been shown to be of enormous benefit to gouty arthritis sufferers. Shellfish, fish, poultry, beef, pork and legumes are all high in purines. Some people, particularly Filipinos, are especially susceptible to gout. But on a low-purine, low-protein diet, gout is almost nonexistent, even among those people most genetically disposed toward it. During World War II, when gout sufferers in occupied European countries were suddenly forced to consume fewer meats and dairy products, the incidence of gouty arthritis plummeted. There are many kinds of arthritis, including osteoarthritis, rheumatoid arthritis, gout, lupus erythematosus, and ankylosing spondylitis. The connection with diet and gout is crystal clear, but far more work needs to be done for the other forms of arthritis. The evidence strongly suggests that diets very low in saturated fat, low in protein, high in fiber, and without any cholesterol would be best for the prevention of arthritis and as an important element in treatment. ### **Kidney Stones** Kidney stones cause indescribable pain and have been referred to as one of the most painful ordeals known to medicine. The severe pain they cause is completely unnecessary and preventable. Over 99 percent of all kidney stones can be prevented by low-protein, high-fiber, low-fat diets that contain no cholesterol, saturated fat, or empty calories. Kidney stones vary according to their chemical composition. Some are made up chiefly of calcium oxalate, others of calcium phosphate, and others of uric acid. The formation of all of these types of kidney stones is directly attributable to diets high in animal protein. The more animal protein we eat, the more calcium our kidneys have to excrete. When our urine is high in calcium, it tends to precipitate out little crystals of calcium in the urinary system. It is around these crystals that kidney stones grow. So sensitive are our urine calcium levels to protein intake that the concentrations of calcium in our urine can be lowered in a matter of hours by decreased protein consumption. Vegetarians in the United States have fewer than half the kidney stones of the general population. Pure vegetarians have almost none. ### **Gallstones** The main ingredient in almost all gallstones is cholesterol. The more cholesterol there is in the diet, the more will be present in the gallbladder fluids, and the more readily gallstones will form. Dietary fiber also influences gallstone incidence, but in the other direction. Fiber tends to bind cholesterol and carry it out in the stool. Diets high in fiber produce lower rates of cholesterol gallstones. Worldwide, the greatest incidence of gallbladder disease, gallstones, and gallbladder cancer is found in people whose food choices are low in fiber, high in cholesterol, and high in fat, such as the average American. Gallstone sufferers usually turn to surgery to relieve the intense pain. But low-fat, high-fiber diets not only prevent gallstones; they have been clinically shown to often relieve the pain of gallstones so significantly as to make surgery unnecessary. ### **Hypertension (High Blood Pressure)** Each year Americans make 275 million visits to their doctors. The most common of all reasons, accounting for one out of every 11 visits, is high blood pressure. Nine times out of 10, patients leave with a prescription for a drug. More prescriptions are written in this country for hypertension than for any other disease. Hypertension is so common in America today that, like heart attacks, we tend to think of it as an inevitable price we must pay for growing old. Doctors prescribe so many drugs for hypertension because they know how dangerous the disease can be. If your blood pressure is high, compared to that of a person your age whose blood pressure is normal, you have • _Double the risk of dying in the next year_ • _Triple the risk of dying from a heart attack_ • _QuadrupIe the risk of heart failure_ • _Seven times the risk of a stroke_ Studies of people whose blood pressure remains low as they age, however, have revealed that these people share certain characteristics. Their diets are low in fats, cholesterol, and salt and high in fiber. They eat whole grains, fresh vegetables, and fruits, and their intake of processed and refined foods is minimal. Their body fat levels are low, and they get plenty of exercise. In countries where the intake of salt, fats, and cholesterol is low, hypertension is unknown. In many cases, people in their 80s have the same blood pressure as teenagers. These are the same countries where strokes and heart attacks are few and far between. This is not because these people are genetically favored. When people from these lands move to other countries and take on diets high in saturated fat, cholesterol, and salt, their blood pressure levels shoot right up alongside ours. Salt increases blood pressure by drawing water into the blood, increasing the pressure on the arterial walls. But salt is not the only cause of high blood pressure. If you partially block the end of a hose with your thumb, thereby increasing the resistance against which the water flows, it will shoot out under greater pressure. This is akin to what happens in our bloodstreams if we suffer from atherosclerosis. The deposits clogging our arteries narrow the channels, thereby increasing the resistance against which our blood flows, raising our blood pressure. Hypertension is an announcement that the circulatory system is not well. When the blood pressure is very high, this announcement should be construed as a veritable fire alarm, calling for immediate attention to serious trouble in the cardiovascular system. Sadly, the conventional medical response is all too often simply to prescribe drugs to silence the alarm, while doing nothing about the problem the alarm is trying to draw to our attention. Lowering blood pressure without doing something to improve the health of the cardiovascular system is like turning off the fire alarm and going back to sleep without fixing what set it off in the first place. In addition, these drugs have disturbing side effects. The beta blockers (propanolol, metoprolol, nadolol, atenolol, etc.) often make patients feel fatigued and listless. The diuretics (hydrochlorothiazide, other thiazides, chlorthalidone, furosemide, spironolactone, etc.) raise blood cholesterol levels, and double the risk of fatal heart attacks. And the blood vessel dilators (apresoline, hydralizine, etc.) have a wide range of common and unpleasant side effects, most commonly producing impotence in males. The blood vessels are expanded to the point that the blood supply simply cannot engorge the penis and produce an erection. Females experience a decrease or total loss of sexual interest with blood vessel dilators. These drugs do have a part to play in hypertension treatment, since they do bring down the blood pressure, which can be lifesaving. But would it not be a far greater service to show patients that by changing their diets they can accomplish the same results without all the disturbing side effects? Then these drugs could be used with discretion in the transition period, as a temporary bridge to a healthier life. And it's not hard to know what the proper diet should be, for the same food choices that raise blood cholesterol levels also raise blood pressure levels. In fact, high blood pressure is almost invariably accompanied by high blood cholesterol. You may recall that the dairy industry greeted the news that saturated fat and cholesterol promote heart disease with something less than humble respect for the truth. They have responded similarly with regard to high blood pressure, for the same reason: their products are deeply implicated, this time on two counts. Cheese is among the foods highest in salt content, and the dairy industry is America's second-leading seller of saturated fat, tipping its hat only to the meat industry. But as you know by now, the dairy industry has not felt shy about taking profound liberties with the truth in order to defend its products. True to form, the National Dairy Council has issued reports saying drinking milk and eating cheese lower blood pressure, and that eating salt does not raise it. Impartial scientists have been amazed at such audacity. The association between foods high in saturated fat and cholesterol, such as dairy products, and high blood pressure has been established and documented in literally hundreds of rigorous studies. The Dairy Council claims that the increased calcium from dairy products will lower blood pressure, but the truth is that such a decrease is minimal at best, and if obtained via dairy products, any such temporary benefits are more than outweighed by the increased development of atherosclerosis. Their claim that eating salt does not raise blood pressure testifies profoundly to a lack of respect both for the truth and for the health of the American public. Hypertension patients can get almost immediate relief from some of the problems of high blood pressure when they cease to consume saturated fats and cholesterol. Saturated fats cause blood-clotting elements in the blood, called platelets, to stick together, forming clumps that slow down the flow of blood. These dumpings cause the blood pressure to rise sharply within hours of a meal rich in saturated fat and account for the many heart attacks that occur within hours of rich meals. Many studies have compared the blood pressure levels of people who have different diet-styles. Even when the data have been adjusted to eliminate salt as a variable, the following pattern is consistent: _Blood Pressure Levels_ _(highest ranked first)_ 1. _Meat-eaters_ 2. _Lacto-ovo vegetarians_ 3. _Pure vegetarians_ One study, reported in the _American Journal of Epidemiology,_ found the blood pressure levels of vegetarians to be significantly less than the levels found in meat-eaters, even when the data had been adjusted to compensate for any conceivable advantage the vegetarians might have had from their generally lesser intake of salt, alcohol, tobacco, tea, and coffee. The study's author attributed the difference in blood pressure readings to "intake of animal protein and animal fat." This information is not having an easy time finding its way into the public awareness. The meat and dairy industries do not like what has been learned and are up to their usual shenanigans to prevent people from knowing. But it is not only the meat and dairy industries. The incentive for those who would educate the public is small. In a drug-oriented culture fond of instant results with a minimum of effort, it's an uphill battle all the way. If you come up with a drug that lowers blood pressure, you can make millions of dollars. But if you want to show people how to eat so their blood pressure won't become elevated in the first place, enthusiasm dwindles. There are millions of Americans at this very moment suffering profoundly from the consequences of high blood pressure. This is especially tragic because it is so thoroughly needless. ### **Anemia** The belief that vegetarians tend to be anemic is common among people who have been unknowingly schooled according to the "basic four" nutritional propaganda. This is a classic example of how ignorance can cause needless suffering. Such people may very well sense that dropping meat is a good idea, yet still find themselves reluctant to do so because they have been so deeply conditioned to believe that they will become iron deficient. **IRON CONTENT OF FOODS (milligrams per 100 calories)** VEGETABLES --- Spinach | 11.3 Beet greens | 11.2 Mustard greens | 8.3 Turnip greens | 6.5 Cucumbers | 6.0 Cauliflower | 4.2 Kale | 4.0 Chinese cabbage | 4.0 Iceberg lettuce | 3.8 Collards | 3.4 Bell peppers | 3.3 Broccoli | 3.1 Mushrooms | 3.0 Zucchini | 2.7 Peas | 2.7 Green beans | 2.7 Tomatoes | 2.4 Red cabbage | 2.4 Celery | 2.4 Green cabbage | 2.4 Carrots | 1.8 Beets | 1.6 Onions | 1.4 Sweet potatoes | 0.6 MEATS AND FISH --- Sirloin steak, lean only | 1.9 Pot roast, lean only | 1.2 Ground beef, lean only | 1.1 Tuna, canned and drained | 0.9 Ham roast | 0.9 Pork chop | 0.9 Salami | 0.9 Sirloin steak | 0.8 Chicken breast | 0.8 Turkey, light meat | 0.7 Ocean perch | 0.6 Salmon | 0.6 Bacon | 0.6 Rib roast | 0.6 Leg of lamb | 0.6 Bologna | 0.6 Frankfurter | 0.5 Lamb chop | 0.3 DAIRY PRODUCTS --- Cheddar cheese | < 0.1 Bleu cheese | < 0.1 Cottage cheese | < 0.1 Mozzarella cheese | < 0.1 Low-fat (2%) milk | < 0.1 Ice milk | < 0.1 Low-fat yogurt | < 0.1 Whole milk | < 0.1 Ice cream | < 0.1 Whipping cream | 0.0 Butter | 0.0 FRUITS --- Strawberries | 2.7 Dried apricots | 2.3 Lemons | 2.0 Blueberries | 1.7 Raspberries | 1.6 Blackberries | 1.5 Peaches | 1.3 Cantaloupe | 1.3 Grapefruit | 1.1 Plums | 1.0 Pineapple | 1.0 Bananas | 0.8 Oranges | 0.8 GRAINS, SEEDS, LEGUMES --- Lima beans | 2.3 Navy beans | 2.3 Lentils | 2.0 Pumpkin seeds | 2.0 Sunflower seeds | 1.4 Split peas | 1.4 Oats | 1.1 Rye | 1.1 Wheat | 1.0 Walnuts | 0.9 Almonds | 0.8 Source: Consumer and Food Economics Institute, USDA, _Nutritive Value of Foods_ (Washington, DC: U.S. Government Printing Office, 1977). It turns out, however, that hardly anything could be further from the truth. Impartial and rigorous studies have consistently shown that vegetarians suffer less anemia than do meat-eaters. The figure on page 274 shows the iron content of various foods, according to official U.S. government figures. Popeye wasn't far off the mark. Calorie per calorie, spinach has 14 times the iron of a typical sirloin steak. Although meat is a decent source of iron, vegetables are actually better. The only iron-deficient foods are dairy products, sugar, fats, and processed foods. So iron deficient are dairy products that you'd have to eat a hunk of butter as big as your refrigerator to get as much iron as you would get from a bowl of broccoli. For years our schools have been provided nutritional education materials by the Dairy Council and meat industry which compare the iron levels of different foods according to their weight. Intentionally or not, this has served to make meat appear unfairly advantageous when compared to vegetables and fruits, because the latter are high in water content, and the weight of the water in the plant foods dilutes their figures when so calculated. Iron absorption is greatly assisted by the presence of vitamin C. In fact, a lack of this vitamin can prevent the body from effectively using the iron it is given. Fresh vegetables, sprouts, and fruits are the best sources of vitamin C, whereas meats, dairy products, eggs, fats, and sugar provide none. At least 20 percent of all women of child-bearing age in the United States are iron deficient. This is primarily due to the monthly loss of iron in their menstrual flow, coupled with their intake of sugar, dairy products, and fats, none of which provide any iron to replace that which is lost. And meat-eaters consistently have a heavier buildup of tissue on the inside lining of the uterus. The bleeding from these thickened tissues is heavier and longer, so more iron is lost per period than would be the case with a lighter diet. Vegetarian women, as a rule, have less estrogen in their bodies, lighter, shorter, and easier periods, and so less iron loss. Vegetarian women who do become anemic have frequently been so cowed by National Dairy Council propaganda that they fear something dreadful will surely happen if they don't get enough protein. Not wishing to eat meat, they overconsume dairy products just to be sure. Because dairy products are woefully iron deficient, these well-meaning women may unknowingly be eating their way into anemia. Young children sometimes become anemic due to significant iron loss from intestinal bleeding. This problem has been the subject of very thorough study. The results of exceedingly conscientious and painstaking studies show that over half the intestinal bleeding in children is a reaction to dairy products. The misguided belief that vegetarians tend to be anemic is sadly ironic in light of the many studies that have measured the hemoglobin levels (which reflect the amount of iron in the blood) of people with different diet-styles. Vegetarians consistently fare better in these tests than do meat-eaters. Long-term studies show no iron deficiencies arising from lacto-ovo or pure vegetarian diets. The only people who run into trouble are the ones who eat a lot of dairy products, fatty foods, sugar, and junk foods. A deficiency of vitamin B12 can result in a serious disease called pernicious anemia. Since only animal products reliantly contain appreciable amounts of this vitamin, it is possible that abstaining from all eggs and dairy products, as well as meat, may produce this serious condition. Accordingly, I advise all strict vegetarians to take supplementary B12. Such supplements are readily available from plant sources and are very inexpensive. The sublingual form is far better absorbed by the body than the swallowed tablet form. It is especially important for nursing mothers on a pure vegetarian diet to take supplementary B12. This is necessary because the vitamin B12 stored in the mother's body will not go into her breast milk, thus exposing the infant to possible danger unless the mother takes B12 through a supplement. ### **Asthma** Researchers at the University Hospital in Linkoping, Sweden, put bronchial asthma patients whose condition was so severe that they required cortisone or other medication on a pure vegetarian diet, without any eggs or dairy products. The results were extremely promising. After one year of the diet, _more than 90 percent_ of the patients who completed the project reported a major improvement in the severity and frequency of asthma attacks. Also, levels of medication dosages dropped an average of 50 to 90 percent. A number of the patients were so improved that they were able to discontinue medication altogether with the pure vegetarian diet. ### **Salmonellosis** Salmonellosis is a bacterial infection derived from contaminated animal products. The disease is, at best, a miserable nuisance; people experience nausea, diarrhea, abdominal cramps, fever, and sometimes vomiting and chills. For the aged, the ill, and infants, however, and for those whose immune systems are compromised, it's another story: the disease can be fatal. Over four million cases of salmonellosis poisoning are known to occur annually in the United States. Many more than that are taken to be bad cases of the flu. But salmonellosis is far more than a flu. The National Research Council of the National Academy of Sciences evaluated the salmonellosis problem and stated: _Salmonellosis is one of the most important communicable disease problems in the United States today._ You may assume the meat you buy has been inspected for salmonellosis. But inspection for this disease is not required by USDA regulations, and the meatpacking plants are hardly eager to provide this or any other extra service when not required to by law. There is, in fact, not a single meatpacking plant in the entire country today that inspects its products for salmonellosis. Knowing this, the American Public Health Association (composed of federal, state, and local public health officials) feels the public is woefully misled by meat inspection seals that seem to imply safety and wholesomeness. So upset was the American Public Health Association by this flagrant deceit that they filed a suit demanding a court order requiring meat labels to read: _Caution—Improper handling and inadequate cooking of this product may be hazardous to your health._ A frowning meat industry responded that it would be "unfair" to "stigmatize" meat by "warning consumers of the hazards associated with flesh eating." One meat industry spokesman pointed out that life is full of risks, as if that somehow justified keeping the public in the dark. He declared: _Sure, you can get food poisoning from contaminated meat, but you can get it from unclean vegetables, too._ Ironically, the man had a point, though I'm not entirely sure it was the one he wanted to make. Utensils, cutting boards, and human hands that come into contact with salmonellosis-infected meat can spread the disease. In a kitchen where meat is prepared, it can easily spread to salad vegetables. Since these foods are not cooked, the salad eater may get salmonellosis. And even cooked foods are placed in bowls and on plates and eaten with cutlery that have been touched by hands that may have touched the contaminated meat. Thus the disease is liable to be spread in any kitchen that it enters, be it in a home, a restaurant, or a public service institution. Congress wanted to know just how commonly meat in the United States today is infected with salmonellosis. They summoned Dr. Richard Novick, of the Public Health Research Institute, and asked for his expert testimony. The authority didn't mince his words: _The meat we buy is grossly contaminated with both coliform bacteria and salmonella._ One of the reasons our meat supply is so heavily contaminated with these disease agents is the way the animals are handled today. To begin with, they are sick creatures, due to how they are kept, and thus susceptible to just about any disease that comes down the pike. Then they are fed contaminated byproducts from the slaughterhouse and crowded into cages, feedlots, trucks, and holding pens that are perfect environments for diseases to spread. And as if that weren't enough, the slaughterhouses themselves could hardly be better designed for the spread of disease. It is not just food reformers and vegetarians who are concerned. The _Journal of the American Veterinary Medical Association_ surveyed a cattle slaughterhouse and found a very high percentage of the carcasses were contaminated with salmonellosis. When _60 Minutes_ asked the head of the USDA Inspection Service, Dr. Donald Houston, about salmonella contamination, he answered (in March 1987) that if you go into a supermarket anywhere in the United States and buy a chicken, the odds are better than one in three that it will be contaminated. Alarmed, _60 Minutes_ conducted its own test, and the results brought no peace of mind. Over half the birds they purchased were found to be contaminated with salmonellosis. Amazed, they interviewed a number of meat inspectors who publicly acknowledged, on national television, that the inspection system provides no protection to the consumer. Even the industry acknowledges this is the case. _Poultry Science,_ a journal of the poultry trade, reported that 90 percent of the dressed product from a poultry processing plant was contaminated with salmonellosis. The National Research Council, evidently not believing things could be this bad, conducted its own survey and found out things were worse. No less than 90 percent of the poultry from a federally inspected plant they examined was contaminated with salmonellosis. ### **Good-Bye Antibiotics** At the same time, salmonella poisoning is becoming harder and harder to treat. The continuous feeding of antibiotics to livestock could hardly have been better designed to breed strains of bacteria, including salmonella, that are resistant to the drugs. Antibiotic-resistant bacteria flourish inside the animals as organisms vulnerable to antibiotics are killed off. As a result, diseases (including salmonellosis) that used to be treatable with antibiotics are becoming increasingly dangerous, and much more often fatal. Tragically, salmonella bacteria are only one of many disease-producing organisms that are becoming increasingly resistant to antibiotics, due to the continuous feeding of these drugs to livestock. For example, only a few years ago, less than 10 percent of staphylococci bacteria (notorious for causing skin, bone, and wound infections as well as pneumonia and food poisoning) were resistant to penicillin. But today over 90 percent of staphylococci are resistant to penicillin. Ominously, a major 1987 study by the Federal Center for Disease Control reported in the _New England Journal of Medicine_ that the extremely hardy salmonella bacteria thriving in today's factory farms are not only increasingly resistant to antibiotics but also not all killed by most forms of cooking. As a result, scientists predict that we will be seeing more and more cases of salmonella poisoning in the days to come, and that the cases will be increasingly serious. The chronic use of antibiotics in factory farms has created the likelihood (some say inevitability) of an epidemic of untreatable salmonella food poisoning. It is no exaggeration to say that the indiscriminate use of antibiotics in factory farms is systematically producing disease-causing agents that are invulnerable to the modern wonder drugs. To keep the animals alive under such horrid conditions, antibiotics are, as a matter of course, placed in their feed. This use of the substances that are responsible for so many medical miracles is creating an "anti-miracle." It is a situation that could hardly have been better designed to breed and develop bacteria that are resistant to the medicines that have saved countless millions of lives from the epidemic scourges of the past. Unless we restrict the habitual use of antibiotics in livestock feed, these lifesavers are well on their way to becoming utterly ineffective, and physicians will find themselves as helpless in the treatment of many infectious diseases as they were in the pre-antibiotic Middle Ages. Already, many of us who have eaten the products of factory farms have resistant organisms residing as members of our intestinal flora. We remain reasonably healthy, however, because their numbers are held in check by the many kinds of normal bacteria residing in our intestines. But as Dr. Kenneth Stoller, vice president and public health affairs director for the American Association for Science and Public Policy, has explained, if we should require antibiotic treatment for any reason, "all hell can break loose." The normal organisms, which have not developed immunity to the medicines, are killed, and the resistant bugs can now multiply unchecked. The consequences can be severe. A recent review in _Science_ revealed that over 4 percent of infections caused by strains of salmonella that have become resistant to antibiotics are now fatal. For other infectious diseases also, our wonder drugs are rapidly losing their wonder. This is why, in the 1970s, Great Britain and the European Economic Community (EEC) forbade the chronic use of antibiotics in livestock feed. But the pharmaceutical and livestock industries have to this day demonstrated something less than the utmost commitment to public welfare by successfully defeating every single attempt to follow suit in the United States. ### **And Now** We live in a crazy time, when people who make food choices that are healthy and compassionate are often considered weird, while people are considered normal whose eating habits promote disease and are dependent on enormous suffering. Yet we are also living in a time of great discoveries, when every day we learn more about the consequences of our food choices and so gradually grow more able to make our choices wisely. The more I've studied the findings of the past few decades of medical research, the more I've realized that it is now really in our hands. Something is possible now that's never been possible before. We are learning how to create a truly healthy world. I believe that each of us, at heart, wants to use our brief time in these bodies and on this planet to contribute something of value. I believe that each of us, at heart, wants to help make the world a better, safer place, a more loving and beautiful place. The healthier we are, the more able we will be to make whatever contribution we can. We all know our world needs healing. Each of us experiences the planetary anguish of our time in our own way, but all of us know that not only our own lives but the very existence of life on earth is hanging in the balance. I have discovered that our eating habits affect the world we share far more profoundly than I had ever dreamed. They have an impact that extends far beyond issues of our own health. I have found that there are repercussions to our eating habits that are so immense and far-reaching as to make the matters of human health, as profound as they are, seem relatively trivial. In the next two chapters, we will turn to how our food choices affect, not only our health, but our children, the gene pool, and the very possibility of life continuing to exist on earth. And we will explore the recent developments that speak in one voice, saying that never before in the history of mankind has a new direction in diet-style been needed with such aching urgency. ## 11. **AMERICA THE POISONED** _There are those who want to set fire to our world; We are in danger; There is only time to work slowly; There is no time not to love._ —DEENA METZGER There is a major problem with the medical research we have been discussing. It takes time for degenerative diseases to develop, and so the medical research that has correlated cancer, heart disease, and virtually every other degenerative disease of our time with conventional diet-styles is actually out-of-date. The cases of these diseases that modern medical research has studied actually developed, for the most part, on the meats, dairy products, and eggs of the early and middle part of this century. But today's meats, dairy products, and eggs are vastly different commodities from those of even 30 years ago. For one thing, they are no longer the products of traditional farming methods. They are instead the products of assembly-line, mass-production factory farming. Factory farm animals are much higher in fat than pasture-raised animals, because they get little or no exercise and their feeds are intentionally designed to fatten them as rapidly and cheaply as possible. Further, their fat is far more highly saturated than that of free-range livestock. The 1975 World Conference on Animal Production issued a report titled "A Re-evaluation of the Nutrient Role in Animal Products," which revealed the remarkable fact that factory-farmed animals have as much as 30 times more saturated fat than yesterday's pasture-raised creatures While touted as suppliers of protein for the American public, today's factory farms are actually suppliers of saturated fat. But as startling as this increase in saturated fat is, it is actually small potatoes compared to far more ominous changes that have occurred in today's meats, dairy products, and eggs. Today's factory farm livestock are subject to vast quantities of toxic chemicals and artificial hormones. Residues are then transmitted to the people who eat their flesh and partake of their milk. Hardly any of these chemicals even existed before World War II, and so we have yet to witness the longer-term health consequences of eating the products of factory farms, which invariably contain residues from pesticides, hormones, growth stimulants, insecticides, tranquilizers, radioactive isotopes, herbicides, antibiotics, appetite stimulants, and larvicides. We have some important knowledge, though, about the long-range consequences of ingesting these substances, and I am not exaggerating when I say they are profoundly terrifying. ### **The Sexual Nightmare** The author of _Modern Meat,_ Orville Schell, interviewed Dr. Carmen A. Saenz: _"For years I have been encountering periodic cases of precocious puberty," Dr. Saenz tells me when she is finished seeing the last of that morning's young patients. "But in 1980, when I started finding one or two children like this in my waiting room every day, I knew that something quite serious was wrong. From the symptoms they were exhibiting, I was sure that they are being contaminated with some kind of estrogen."_ _I ask Dr. Saenz to describe the symptoms. Without replying, she picks up a handful of Polaroid photos from the top of her desk and hands them to me. Each shows the small body of a naked young girl. As I slowly thumb through them, Dr. Saenz gives me a case-by-case commentary in a tone of voice that matches the expression on her face—a mixture of outrage, sadness, and determination._ _In the first photo, a four-and-a-half-year-old girl with delicate coffee-colored skin, doelike brown eyes and almost fully developed breasts lies on an examining table. She smiles with a sweet innocence at thecamera, seemingly unaware of the dramatic changes that have gone on in her body._ _"She had an ovarian cyst," says Dr. Saenz tersely._ _A twelve-year-old boy stands against a white wall looking with blank bewilderment into the camera. He wears a silver crucifix around his neck, which dangles down between two grossly swollen breasts._ _"We've had to schedule him for surgery," says Dr. Saenz matter-of-factly. "The emotional stress on him is incredible."_ _A one-year-old girl, whose teeth have not even completely come in, lies on the examining table with a ruler stretched across her chest to measure the diameter of her enlarged breasts. She has a pacifier in one of her hands. Dr. Saenz says nothing. She just shakes her head._ _A five-year-old girl, looking wild-eyed into the camera as if a weapon were being aimed at her, lies on the examining table. Her breasts are as large and well-developed as a fourteen-year-old's. Her mons veneris is covered with a scraggly tangle of pubic hair._ _"This one had a well-developed uterus and had begun to have some vaginal bleeding," says Dr. Saenz. "These are developments that we would not usually expect until eight or nine years of age at the very earliest...I have seen hundreds of children like this, and I am certain that there are thousands more going undiagnosed because this problem has become so widespread that even many doctors are no longer getting alarmed about it."_ Dr. Saenz explained the cause of this epidemic of premature sexual development in the February 1982 _Journal of the Puerto Rico Medical Association:_ _The detailed analysis of histories on all of our patients discards their use of medications or creams containing estrogens [as a cause], and none had neurological or other adrenal disorders...It was clearly observed in 97 percent of the cases that the appearance of abnormal breast tissue was...related to local whole milk in the infant group. At a later age [the culprit was]...consumption of local whole milk, poultry and beef._ When Dr. Saenz was asked how she could be sure the children were contaminated with hormones from meat and milk rather than from some other source, she replied simply: _When we take our patients off meat and fresh milk, their symptoms usually regress._ Regulations regarding hormone use in livestock are not enforced as well in Puerto Rico as they are in the United States, and this partially explains the epidemic there of premature sexual development. But U.S. regulations are often laughed at in the rough-and-tumble world of the American "cowboy," who tends to figure that if a little is good, more is probably better. As a result, doctors in the United States are seeing earlier and earlier puberties in both boys and girls, more and more frequent cases of small children developing sexual characteristics, and an ever-expanding assortment of sexual aberrations. Other countries are also experiencing the same trend. An English medical journal reported that hormone traces in the meat of chemically fattened livestock are causing British schoolgirls to mature sexually at least three years earlier than in the past. There is no telling how many such cases occur. Meanwhile, both adults and children in our society are experiencing a plethora of behavior disorders connected to uncertain and confused sexual identities. The evidence that these arise at least in part from hormonal imbalances is mounting steadily. We are also seeing a startling increase in sexual abuse of children and other tragic indications that human hormonal systems have gone haywire. When hormones were first introduced into livestock production, after World War II, the meat industry was virtually ecstatic. The manufacturer of diethylstilbestrol, known as DES, humbly hailed the event as the most important moment in the history of food production. Because it produced more fat and more weight on the animals, and thus more profit for the meat industry, DES came to be used on more than 90 percent of America's cattle. It was called a miracle. Meanwhile, farmers who accidentally absorbed, inhaled, or ingested even minute amounts of this "miracle" were not always fully able to appreciate its wonders. _They exhibited symptoms of impotence, infertility, gynecomastia [elevated and tender breasts], or changes in voice register._ Both adults and children were affected. The breast enlargement of a number of young children was directly traced to their having accidentally absorbed DES. Nevertheless, literally tons of this hormone continued to be administered routinely to animals whose flesh and milk were destined for human consumption. Then it was discovered that DES causes cancer even in the smallest doses imaginable. Lab animals developed cancer from daily doses of the hormone of as little as one-quarter of a hundred-millionth of an ounce. FDA biochemist Jacqueline Verret reported: _Researchers from the National Cancer Institute assured Congressmen that it might be possible for only one molecule of DES in the 340,000,000,000,000 present in a quarter pound of beef liver to trigger human cancer._ After a fiercely fought political battle, it was finally made illegal to administer DES to livestock. But the meat industry simply shrugged its shoulders and carried on as usual. Several years after the ban went into effect, the FDA discovered how much respect the industry had for the law of the land. No less than half a million cattle were found to have been illegally implanted with DES. Today, many factory farms in the country continue to use DES illegally. Others have simply switched to the other sex hormones on the market, which have the same effects and contain many of the same substances as DES. These hormones, such as Steer-oid, Ralgro, Compudose, and Synovex, are used in virtually every feedlot in the country. ### **_Silent Spring_** The loose-handed use of hormones in today's factory farms is sufficiently disturbing. But there is actually a far more ominous kind of contamination that people eating today's meats, dairy products, and eggs unknowingly consume. In 1962, Rachel Carson issued an epic warning to humanity in her prophetic book, _Silent Spring_. She showed how pesticides were killing off birds, fish, and other wildlife at an alarming rate, in some cases to the point of extinction after only a few years' use. The book drew its title from the fact that DDT and other pesticides were drastically reducing the populations of many bird species. Carson cautioned that the day was fast arriving when spring would come but no bird songs would be heard: _Over increasingly large areas of the United States, spring now comes unheralded by the return of birds, and the early mornings are strangely silent where once they were filled with the beauty of bird song. This sudden silencing of the song of birds, this obliteration of the color and beauty and interest they lend to our world have come about swiftly, insidiously, and unnoticed by those whose communities are as yet unaffected._ This is not what most of us would wish for our planet. But we have not heeded her warning about these lethal poisons. We produce pesticides today at a rate more than 13,000 times faster than we did only 35 years ago. Our environment and food chains are being inundated by a virtual avalanche of pesticides. What three decades ago took us six years to produce, we now produce every couple of hours. It is hard for us to imagine how destructive these substances are. Pesticides are extraordinarily concentrated and powerful chemicals that have been intentionally developed to kill living creatures. In fact, some of them were originally developed to kill human beings. Phosgene, used today to produce chemical herbicides and insecticides, was originally developed for use in chemical warfare and was, in fact, the agent of almost all deaths due to poison gas in World War I. Zyklon-B, another modern pesticide, is the substance that the Nazis used to produce deadly hydrogen cyanide gas, used to kill millions upon millions at Auschwitz, Dachau, and other concentration camps. Many of today's most widely used pesticides—including malathion and parathion—are members of the nerve gas family. So lethal is parathion that a chemist who swallowed an infinitesimal dose, amounting to 0.00424 of an ounce, was instantaneously paralyzed and died before he could take an antidote he had prepared in advance and had at hand. Pesticides are not the kind of substances you'd want to have hanging around in your environment. But hang around many of them do. In fact, the chlorinated hydrocarbon pesticides—DDT, aldrin, kepone, dieldrin, chlordane, heptachlor, endrin, mirex, PCBs, toxaphene, lindane, etc.—are extremely stable compounds. Ominously, they do not break down for decades or in some cases, centuries. ### **The Food Chain** Rachel Carson titled her book _Silent Spring_ in memory of the songbirds who have begun to disappear from our world. The reason it is birds, of all animals, who are the first to go, is that many of them are predators at the top of long food chains and thus receive extremely concentrated doses of these chemicals. You see, pesticides don't just affect the creature who ingests them first. They accumulate in the tissues of animals, and then, as one organism is eaten by another, they build up in ever higher concentrations at each successively higher rung on the food chain. A worm living in the soil will store in its tissues all the pesticides it ever accumulates both from what it eats and what it absorbs through its skin. A bird that eats worms will thus ingest all the pesticides ever eaten or contacted by all the tens of thousands of worms it eats. At each successive stage up the food chain, the concentration of toxic chemicals is greatly increased. Thus, a fish will accumulate in its body the total amount of poisons accumulated by all the thousands of smaller fish it eats. And each of these smaller fish will have collected in their flesh the total amount of toxic chemicals ever ingested by all the thousands of still smaller fish they have eaten. It's an exponential progression. Predator birds who eat fish often ingest extremely high concentrations of these deadly substances. By the same token, a cow or chicken or pig will retain in its flesh all the pesticides it has ever consumed or absorbed, and factory farm animals build up especially high concentrations of chemical toxins for several reasons. 1) They are fed great quantities of fish meal. 2) Their other feeds are often grown on land heavily sprayed with the most dangerous pesticides. 3) They are dipped in, sprayed with, and intentionally fed many toxic compounds never encountered by animals raised in a more natural way. These poisons are retained in the fat of the animals. With each inevitable step up the food chain, animals become ever more concentrated carriers of the most deadly chemicals ever known. Man, of course, sits at the very top of the chain whenever he eats fish, meats, eggs, or dairy products. The _Pesticides Monitoring Journal,_ published by the EPA, chronicles scientific studies and research findings regarding these toxins. The journal confirmed what numerous studies have discovered: _Foods of animal origin [are] the major source of...pesticide residues in the diet._ Recent studies indicate that of all the toxic chemical residues in the American diet, almost all, 95 percent to 99 percent, come from meat, fish, dairy products, and eggs. If you want to include pesticides in your diet, these are the foods to eat. Fortunately, you can overwhelmingly reduce your intake of these poisons by eating lower on the food chain and not choosing foods of animal origin. ### **What's Good for Dow Chemical Company** Because the chlorinated hydrocarbon pesticides have such an extremely poisonous and persistent nature, environmentally aware people have urged and pleaded and demanded and begged that this entire chemical family be outlawed. But the very poisonous and persistent qualities of these toxic chemicals have made them big moneymakers for the chemical companies who market them aggressively. These corporations have applied enormous political and economic pressure to keep their products in use. The tragic result is that millions of pounds of these lethal agents continue to be used every year. In the 1970s, mounting public concern overrode pressures from the chemical companies and forced the passage of the Toxic Substances Control Act. But this act has not in practice turned out to be the boon to environmental health it was intended to be. More than three years after the act became law, the agency responsible for its administration had not yet ordered testing for a single one of the more than 50,000 toxic chemicals on the market. The Reagan administration was particularly instrumental in preventing the Toxic Substances Control Act from being enforced. Evidently believing what's good for Dow Chemical Company is good for America, the Reagan administration abolished or crippled many of the country's most important health and environmental laws, including those regulations designed to protect the public from the misuse of pesticides. The current philosophy of toxic chemical management is to let the chemical companies regulate themselves. The chemical companies think this is a grand idea, though they know they must remain ever watchful lest the public become too concerned and require toxic pesticides to be legitimately assessed for their environmental impact. To prevent such a potentially embarrassing occurrence, they have come up with an ingenious and effective strategy: they have promoted the idea that dangerous chemicals have all been banned, and the government can be trusted to protect us, so there's nothing to worry about. By and large the public has bought their story. President Reagan did. In fact, he publicly complained: _The world is experiencing a resurgence of deadly diseases spread by insects because pesticides like DDT have been prematurely outlawed._ But Reagan couldn't be more wrong. ### **The Truth** One reporter who uncovered the shocking truth regarding chemicals and our environment is the outstanding environmentalist Lewis Regenstein. In _How to Survive in America the Poisoned,_ his superbly documented report on the use and effect of deadly chemicals, he writes that although the chemical industry wants us to believe that the really dangerous pesticides have been banned, this is not at all what has actually occurred: _Despite the overwhelming evidence that pesticides cause cancer and are extremely dangerous to humans and the environment, almost none of these chemicals has ever been "banned" by the government in the true sense of that word. In the very few cases where pesticides have been the subject of suspensions, cancellation proceedings, and/or court actions, the results have usually been restrictions or bans placed on some or most uses, while other applications have been allowed to continue._ **PESTICIDE RESIDUES IN THE U.S. DIET 1964–68 Levels of DDT, DDE, and TDE** Source: Data derived from P. E. Cornellussen, Pesticide Residues in Total Diet," _Pesticides Monitoring Journal_ 2 (1969): 140–52. Even in the few cases in which the use of a pesticide has been restricted, the poison does not simply disappear from the environment. Quite the contrary; toxic chemicals like DDT take decades or even centuries to degrade. Even if by some miracle we stopped all pesticide use today, these chemicals would remain with us, contaminating our environment and our food chains for the foreseeable future. DDT, one of the earliest pesticides, is one of a mere handful of these poisons that has actually been banned. Yet four years after the moratorium on DDT had been declared, the government tested soils in Arizona that had once been treated with DDT and found no measurable decrease in the amount in the soil. Twelve years after the chemical was banned in the United States, researchers checked 27 bottle-nosed dolphins found dead off the coast of California. They found "extremely high" concentrations of DDT in every one. So persistent is DDT in the environment that even now it continues to be found in the bodies of penguins and seals in Antarctica, seals in the Arctic Ocean, and frogs living at very high altitudes in remote regions of the Sierra Nevada mountains. ### **The Tip of the Iceberg** While DDT has gotten most of the publicity, there are unfortunately many other toxic chemicals that are equally widespread in the environment and actually more poisonous. The pesticide dieldrin, for example, is five times more poisonous than DDT when swallowed, and 40 times more so when absorbed by the skin. Yet, by the time dieldrin was finally banned in 1974, the FDA found it in 96 percent of all the meat, fish, and poultry in the country, in 85 percent of all dairy products, and in the flesh of 99.5 percent of the American people Sadly, dieldrin will remain with us for a long time; it is one of the most biologically stable of all pesticides, taking many decades to break down. Dieldrin is also one of the most potent carcinogens ever known. It causes cancer in lab animals at every dosage tested, down to the most infinitesimal concentrations measurable by modern, sophisticated equipment. In humans, low levels of exposure cause convulsions, severe liver damage, and rapid destruction of the central nervous system. After a World Health Organization antimalarial program used dieldrin, workers foamed at the mouth, went into convulsions, and died. Others, who had only the most minimal exposure to the substance, suffered convulsions for months after-ward. This doesn't sound like a substance you'd particularly want in your food. But for many years, dieldrin was applied to virtually all the acreage in the United States still used to grow corn, oats, barley, soybeans, and alfalfa for livestock feed. In March 1974, the USDA discovered that almost 10 million chickens in Mississippi were heavily contaminated with dieldrin, from feed grown on land to which the pesticide had been applied. The chickens were destroyed, but the Agriculture Department admits it has no way of knowing how often this kind of incident occurs and acknowledges that we are fortunate if we become aware of even the tiniest fraction of such occurrences. On June 26, 1980, the USDA revealed that turkey products from Banquet Foods Corporation contained intolerable levels of dieldrin. Eventually two million packages of frozen turkey dinners, turkey pies, and other turkey products were recalled. While dieldrin is no longer being applied to our soils as it once was, it remains in the soils to which it was once applied. These are the soils that grow the grains that are fed to the animals whose flesh, milk, and eggs Americans consume. For the foreseeable future, dieldrin will continue to work its poisonous way up the food chain, collecting in the fatty tissues of the animals. The only bright side to this is that you can do a great deal to avoid consuming dieldrin by eating low on the food chain. ### **Dioxin** During the Vietnam War, Agent Orange was sprayed by U.S. air forces over Vietnamese jungles and farmlands. The pilots who flew these missions were assured of the safety of the substance and had a motto that expressed their flippant attitude toward their missions: "Only we can prevent forests." On some occasions they would engage in playful spray fights with Agent Orange, their cavalier attitude unfortunately exemplifying our national point of view toward toxic chemicals. Many Vietnam veterans no longer have a casual attitude toward these poisons. They have suffered grievously for their exposure to Agent Orange and watched in dismay as their children were born with extremely high rates of birth defects. One veteran, Michael Ryan of Long Island, testified before congressional hearings on Agent Orange and brought with him his daughter Kerrie, who was born with severe deformities, although neither of her parents had any family history of birth defects. A _Washington Post_ reporter, Margot Hornblower, described the scene: _During the emotion-laden hearing, Kerrie, a frail child with short brown hair, sat in her wheelchair gazing wide-eyed at the television cameras, the Congressmen high on the wood-paneled dais and the roomful of lobbyists and reporters._ _"She's a dynamite little kid," said her mother to the committee._ _Kerrie was born eight years ago with 18 birth defects: missing bones, twisted limbs, a hole in her heart, deformed intestines, a partial spine, shrunken fingers, no rectum. During surgery, a blood clot developed and she suffered brain damage. Doctors say she will never walk._ It may seem to you and me that Agent Orange is a horrible weapon of war, and certainly not something to spray on land used to grow food. But its two active ingredients—2,4-D and 2,4,5-T—are, in fact, sprayed today on land used to grow food for livestock. Millions of pounds continue to be used, even though 2,4,5-T contains a particular substance that is so toxic it makes DDT look like a glass of champagne. 2,4,5-T contains dioxin. The head of the Toxic Effects Branch of the EPA's National Environmental Research Center, Dr. Diane Courtney, called dioxin _by far the most toxic chemical known to mankind._ She also testified that dioxin is present in beef and dairy products from cattle that have grazed on land treated with 2,4,5-T. The EPA has officially recognized the fact that cattle that graze on land sprayed with 2,4,5-T accumulate dioxin in their fat. But Dow Chemical Company, which profits greatly from the sale of 2,4,5-T, would rather the public not be concerned. According to them: _2,4,5-T is about as toxic as aspirin._ It would be a good thing if it were, because millions of pounds of this lethal chemical have been sprayed on land in the United States. And since dioxin is stored and concentrated as it moves up the food chain, cows, pigs, and chickens contain in their flesh the dioxin residues from all the plants they have ever eaten. Pesticide authority Lewis Regenstein warns: _Humans who eat beef...can get a concentrated dose of dioxin that has built up over several years._ Dioxin causes cancer, birth defects, miscarriages and death in lab animals at the lowest levels possible to test—in some cases as low as one part per trillion. In fact, dioxin's toxicity makes it difficult to use in conducting cancer research; it tends to kill the test animals before they have a chance to produce tumors, even when given in the lowest possible doses, such as a few parts per trillion. A single drop of dioxin can kill 1,000 people. To kill a million people would take only an ounce. Yet it could be in the meat, dairy products, and eggs sold in your supermarket. ### **Heptachlor** When Rachel Carson first alerted the nation to the enormous dangers of the toxic chemicals we were flooding into the environment, and to the fact that these poisons tended to collect and concentrate in the food chain, the chemical companies were disturbed. Their response, however, did not demonstrate the most enlightened regard for the public welfare. Before _Silent Spring_ was published in book form, segments were serialized in the _New Yorker._ The secretary and general counsel of Velsicol Chemical Corporation, Louis A. McLean, responded by sending a threatening and intimidating letter to Carson's publisher, Houghton Mifflin Inc., attempting to prevent the book from being published. The letter charged that Carson had made "inaccurate and disparaging" statements about one of Velsicol's biggest moneymakers, a pesticide named heptachlor. To their credit, Houghton Mifflin decided to print the book anyway, knowing the truth of Rachel Carson's dire warning that heptachlor accumulates in the food chain and has disastrous effects on living tissue. Velsicol Chemical did not give up its efforts to keep the substance in widespread use, however, and heptachlor continued to be sprayed on millions of acres of land used to grow corn for animal feed. Finally, in October 1974, the Environmental Defense Fund (EDF) petitioned the EPA to ban heptachlor (and the associated compound chlordane), on the grounds that it posed "an imminent health hazard to man." The EDF pointed out: _The incidence of heptachlor in human food is currently very high in the United States, especially in meat, poultry, fish and dairy products...Heptachlor is carcinogenic at the lowest levels tested (one-half part per million) in laboratory experiments._ In November 1974, the EPA finally began hearings and appeals to determine if the chemical should be banned. But heptachlor was such a huge moneymaker for Velsicol Chemical Corporation that the company spent literally tens of millions of dollars on legal maneuvers to fight a possible ban at every step of the way. The company's tactics included withholding lab reports from the EPA that showed malignant tumors had been produced in animals exposed to heptachlor. When this "accidental oversight" was discovered, several company officials were indicted by a federal grand jury. In the meantime, Velsicol continued to manufacture and sell millions of pounds of heptachlor, and the poison is still used today for many applications. As a result, it will continue to accumulate in the food chain for years to come, slowly poisoning unknowing consumers of the foods highest on the food chain—meats, dairy products, and eggs. ### **Poisoned Pork** Several years after heptachlor was finally restricted, the Department of Agriculture discovered that, as part of its school lunch program, it had sent 40,000 pounds of heptachlor-contaminated ground pork to school systems in Louisiana and Arkansas. By the time they realized what had been done, over 14,000 pounds of poisoned pork had been consumed by the children. When we hear a phrase like "poisoned pork," most of us think of someone immediately getting sick, perhaps with stomach cramps, diarrhea, fever, and so on, because these are the usual symptoms for bacterial poisons that are carried in pork and other meats. But with pesticides, there is considerable lag time between the ingestion of these compounds and the eventual manifestation of cancer, birth defects, and other devastation. Of course, if the dosage is high enough, there are immediate repercussions, including death. But for most of us, the problem is the gradual accumulation of these substances over a period of time. And it is a problem whose occurrence we have no way of recognizing until a deformed baby is born, a miscarriage or stillbirth happens, or a tumor appears. By that time we have virtually no way of tracing the mental and emotional disorders we experience to the toxic chemicals we have ingested. In instances like the contaminated ground pork being sent to the children in the South, we were very fortunate indeed to discover the high concentrations of heptachlor in these foods. But there is no way we can be aware of more than the tiniest percentage of such incidents. The tests to determine the existence of these chemicals in foods are expensive and time-consuming and require sophisticated equipment. As a result, they are rarely performed. Heptachlor disasters will be with us for some time. In December 1986, Banquet Foods admitted that 200,000 chickens in Arkansas had to be destroyed because they were found to be contaminated with a variety of heptachlor known as chlordane. In April 1986, milk contaminated with dangerously high levels of heptachlor had to be recalled in Arkansas, Texas, Louisiana, Kansas, Missouri, and Oklahoma. At the same time, beef supplied by the USDA Donated Food Program to California elementary and high schools had to be recalled due to heptachlor contamination. Most frightening of all, Arkansas authorities found heptachlor contamination in the breast milk of 70 percent of nursing mothers. Nevertheless, we are told not to be alarmed, even though a Hawaii study of 120 infants whose supply of breast milk was discovered to be contaminated with heptachlor found the development of the infants' brains to be significantly retarded. It is hard to avoid the feeling that we have seen only the barest glimmer of the top of the toxic chemical iceberg. ### **There Goes Michigan** One of the saddest features of the pesticide story is that there are people who have been consistently successful in knowingly covering up the dangers. As a result, the public is still, for the most part, unaware of the gravity of what is happening. It is not only the chemical companies who would like to keep us ignorant of the hazards of pesticides. Some government officials have also come to think we would be better off not knowing. A particularly dramatic instance of such a misguided attitude occurred in Michigan in 1973 and 1974 and involved one of the worst cases of pesticide poisoning yet to come to light. Here, the poison involved was PBBs (polybrominated biphenyls). When the U.S. Congress finally investigated the fiasco six years later, they asked expert witnesses about PBBs. The answers were not reassuring. Impartial experts testified: _PBB's are persistent and can be passed on for generations. PBB's are stored in the body fat, where they can remain indefinitely. During pregnancy, they can cross the placenta to the developing fetus...PBB is...capable of producing physical defects in offspring in utero._ Not substances you'd particularly want in your hamburgers. Yet in 1976 alone, several years after the PBB contamination occurred, Michigan residents ate over five million pounds of hamburger contaminated with PBBs. What had happened was that this toxic chemical had somehow gotten mixed into livestock feed that was dispersed throughout the state. When the PBBs were first discovered in virtually all of Michigan's meat and dairy products, state officials tried in every way to cover up the incident. Had the public been notified of the extreme urgency of the situation, a great deal of tragedy could have been avoided. But as it is, according to testimony before Michigan's Senate Commerce Subcommittee on March 29, 1977, nearly all of Michigan's residents now have unacceptable levels of PBBs in their bodies. It is quite likely that every single person who consumed meats, dairy products, or eggs in the state of Michigan during 1976 or 1977 now has significant amounts of these carcinogens in his or her organs. Tests in 1976 found that 96 percent of nursing mothers in Michigan had PBBs in their milk. It is very difficult for us to grasp the magnitude of today's toxic chemical pollution, and the degree to which our food choices can expose us to such dangers. And especially tragic is the fact that there are people who don't want the public to know, people who perceive it to be in their own interests to keep the public ignorant. There are industries that are profiting from our use of these chemicals, and from our continuing to make our food choices high on the food chain. They tell us all the bad pesticides have been banned, and the government is on top of things. They tell us there's nothing to worry about. But they lie! Even in the few cases, such as with DDT, in which a pesticide has actually been banned, we are far indeed from off the hook. The Library of Congress estimates that over 2.2 million tons of DDT have been used worldwide, more than a pound for every human being on earth. The Environmental Defense Fund estimates that the American people today have, collectively, some 20 tons of DDT in their bodies—which works out to one and a half grams per person. In the face of such mind-boggling statistics there is a tremendous temptation to go blank, to feel powerless and numb. We may want to erect a wall of denial, to retreat back into ignorance. But one thing is certain: in this case, ignorance is not bliss, though the companies that profit from our ignorance would like us to believe it is. They see no problem at all in the continuing use of these poisons, nor in you and me unknowingly making food choices that daily expose us to residues from the most toxic substances ever known to mankind. ### **Our Immune Systems Aren't Immune** We are presently seeing an enormous outbreak of immune system diseases that weren't a problem years ago—diseases like cancer, AIDS, and herpes. Some immune system diseases, such as chlamydia trachomatis are so new that most people have never heard of them. Chlamydia struck close to four million Americans in 1985, and the numbers are mounting rapidly. In the early stages, women usually don't know they have chlamydia. Untreated, however, it moves into the uterus and fallopian tubes, causing pelvic inflammatory disease, chronic pain, fever, and in many cases sterility. In 1900, cancer was the 10th-leading cause of death in the United States and was responsible for only 3 percent of all deaths. Today, it ranks second and causes about 20 percent of all deaths. More Americans will die of cancer _this year_ than died in World War II, the Korean War, and the Vietnamese War combined. Many scientists now feel that the presence of toxic chemicals in our bodies is largely responsible for these epidemics. A case in point is a substance that was once considered among the safest of germ-killing compounds—hexachlorophene. Routinely used as an antiseptic in hospitals, clinics, and doctor's offices, hexachlorophene was never imagined to be a menace. Newborn infants were bathed in it, and to this day hospital personnel sometimes wash their hands in it. The compound was widely used in baby creams, oil, and powders. It was routinely incorporated into many common household products, including mouthwashes, antiperspirant deodorants, shaving cream, first-aid kits, and over-the-counter medications for acne and psoriasis. In fact, hexachlorophene became practically a household word when Dial soap commercials brightly announced the good news that Dial soap now contained this wonderfully effective germ killer. But it turns out that hexachlorophene is not the boon its manufacturers would like the public to believe. In 1972, 35 healthy newborn infants in Paris, France, died after being dusted with talcum powder high in hexachlorophene. In 1978, a Swedish study showed that nurses in Swedish hospitals who had regularly washed their hands in a hexachlorophene solution had given birth to an extraordinarily large number of deformed children. Hexachlorophene, it was discovered, contains trace amounts of dioxin. The manufacturers of hexachlorophene still maintain the substance is safe. But there is growing evidence that the dioxin it contains severely damages the human immune system. The April 18, 1986, issue of the _Journal of the American Medical Association_ contained a major report by joint researchers from the Center for Disease Control in Atlanta, the Missouri State Health Department, and St. Louis Medical School. To keep down dust in a Missouri mobile home park, sludge mixed with oil had once been sprayed on a dirt road. This is a fairly common occurrence, but in this case the sludge had come from a plant that made hexachlorophene. Researchers painstakingly studied the people who lived in the mobile home park over the years and compared them to a control group of men, women, and children living in another mobile home park where the sludge had not been used. The text was exhaustively scrupulous. The two groups were virtually identical in race, employment, history of illness, use of pesticides, and use of tobacco and alcohol. The results suggest why so many scientists today associate toxic chemicals with the current epidemic of immune system diseases. The researchers found _significant damage to the immune systems of the exposed people._ ### **AIDS and More** There is evidence that dioxin and other toxic chemicals damage the thymus gland, which plays a vital role in the body's immune system. Thus, people suffering from toxic chemical poisoning may be more susceptible to bacterial and viral infections of all kinds. They may experience the symptoms of common ailments and have no way of tracking their impaired health to the pesticides they have slowly accumulated. And worst of all, with impaired immune systems, they may also become more susceptible to the frightening prospect of diseases such as AIDS and cancer. Current estimates are that 25 to 75 percent of the people who are exposed to the AIDS virus (human T-cell lymphotropic virus-III, also known as HTVL-III) are eventually stricken by this deadly disease of the immune system. There is much we don't know yet about AIDS. And while it is homosexuals and intravenous drug users who are especially at risk, the disease is unfortunately spreading rapidly into other segments of the populations. The presence of this disease, which could produce the most devastating epidemic in human history, makes the strength and health of your immune system particularly significant today. We know that the accumulation of toxic chemicals in the body compromises the immune system. And we know that among people who are exposed to the AIDS virus it is those with weakened immune systems who are most likely to contract the disease. Many scientists see the spreading of the AIDS epidemic as a consequence, therefore, at least in part, of the toxic chemical pollution of our environment, food chains, and bodies. In today's world, anything we can do to strengthen our immune systems is especially important. In this light it is particularly sad how often people are ignorant of the role their food choices play. Not knowing the consequences of eating high on the food chain, they may expose themselves unnecessarily to the worst enemies our immune systems have ever known. Given the immense quantity of these poisons we have spewed into the environment, you may wonder why there are not more glaring birth defects, and why there is not an even greater epidemic of cancers. Part of the answer lies in the lag time necessary before the most conspicuous problems arise. A lab animal with a life span measured in months will develop cancer within months when exposed to these substances, whereas humans are on a much slower timetable, so it often takes decades for the damage to show up. It is only comparatively recently that the deluge of pesticides has occurred, though already the lamentable consequences are beginning to appear in our children. Forty years ago, cancer in children was a medical rarity. Today, more children die of cancer than from any other cause. In lab tests, the offspring of animals exposed to pesticides can be killed and autopsied for evidence of internal birth defects. As a result of such tests, we know these substances cause birth defects in animals in even the most infinitesimal concentrations. It is not so easy, however, to determine the number of human children being born with birth defects, since most birth defects are not glaring external deformities of the kind suffered by thalidomide babies. Most are internal and not immediately apparent at birth. Children with learning disabilities, hyperactivity, lowered I.Q.s, lessened resistance to disease, weakened immune systems, damaged livers or kidneys, chronic ailments that resist diagnosis, and/or emotional problems are rarely studied to see if contamination by toxic chemicals in utero may have done the damage. I'm sure that if they were, the results would be very interesting. There is no telling how many of us suffer from dullness of spirit, frazzled nervous systems, confusion, irritability, emotional instability, or some other form of unease due to toxic chemical pollution. And there is no way of measuring or tracing most of the damage that has been done. As a result, most people are unaware of the ominous dangers these poisons represent, and of the correspondingly crucial importance of our food choices. This problem is particularly distressing because it is so needless and avoidable. A new direction for America's agriculture and diet-style might yet mean that our immune systems could be strengthened and our children grow up to live healthy lives and bear healthy children in a world increasingly safe from pollution. ### **PCBs** Time and again I've been amazed to learn how widespread in the environment are the toxic chemicals that collect and concentrate in the food chains. Probably the most widespread of all are the notorious PCBs. In the United States alone, nearly a _million tons_ of PCBs have been produced—over five pounds for every man, woman, and child. Because of its biological longevity, almost all of this poison still persists in the environment. PCBs have been found in significant concentrations in wild polar bears and in fish from the deepest and most remote parts of the world's oceans. It is now likely that there is not a single human being anywhere on this planet who does not carry PCBs in his or her flesh. This does not bode particularly well for the health of our species or our world, for if there were a competition for the world's most toxic substance, PCBs would be right in there along with DDT, dieldrin, dioxin, and the others. A few parts per billion can cause birth defects and cancer in lab animals. Primates have developed fatal cancers and given birth to deformed children after ingesting doses as low as one part per million. Ominously, a recent government study found PCBs present in 100 percent of the human sperm samples tested. They also found a correlation between high PCB levels and low sperm count. PCBs are considered one of the chief reasons for the staggering fact that the average sperm count of the American male is today _only 70 percent of what it was only 30 years ago._ Tests done at several major universities have found that nearly 25 percent of today's college students are sterile. This is a terrifying trend. Only 35 years ago, the sterility rate was less than one-half of 1 percent. Perhaps the leading researcher in the country in this field is Dr. Ralph Dougherty of Florida State University. He blames the drastic increase in sterility on the chlorinated hydrocarbons, such as PCBs, that have collected in the food chain. PCBs were first introduced by Monsanto, a company whose motto, "Without chemicals, life itself would be impossible," seems ludicrous in view of what PCBs are doing to human fertility. It wasn't long after Monsanto began producing PCBs that it became apparent that these chemicals posed major problems for human beings. Three years after production began, the faces and bodies of 23 out of 24 workers in the Monsanto plant had become disfigured. But that didn't stop Monsanto. Since then, more than 750,000 tons of these deadly poisons have been produced. They can be found today in every river in America, in the snows of the Arctic and Antarctic, and probably in the tissues of every single fish in the waters of this planet. ### **Something Smells Fishy** Toxic chemical authorities agree that human contamination with PCBs comes mainly from eating fish from waters in which PCB levels are high. Fish have a remarkable ability to absorb and concentrate toxic chemicals from their watery environments. For one thing, their food chains are extremely long, with phytoplankton being eaten by zooplankton, who are in turn eaten by tiny fish, who are then eaten by larger fish, and so on. More significantly, fish literally breathe the water they swim in, so they are also continually accumulating more and more contaminants in this manner. The net effect is almost as if they were underwater magnets for toxic chemicals. The EPA estimates fish can accumulate up to nine million times the level of PCBs in the waters in which they live By the food chain effect, fish may thus become loaded with enormous concentrations of these toxic chemicals. Shellfish that filter water, such as oysters, clams, mussels, scallops, and other mollusks, are especially vulnerable to pesticide saturation. An oyster will filter up to 10 gallons of water every hour. In only a month, an oyster will accumulate toxic chemicals at concentrations 70,000 times the amount in the water. While it is our lakes, rivers, and other inland waterways that are the most polluted with toxic chemicals, the oceans, regrettably, have not been spared. Over 110 million pounds of DDT alone have ended up in the oceans of North America. Tragically, there is substantial evidence that DDT levels in the oceans have damaged a major source of the world's oxygen supply—the microscopic phytoplankton. Livestock in today's factory farms are fed huge quantities of fish meal. Half of the world's fish catch is fed to livestock. In fact, more fish are consumed by U.S. livestock than by the entire human populations of all the countries of western Europe combined. But don't bet too heavily on the meat or dairy industries voluntarily spending the amount of money it would require to test the fish meal they feed their animals for toxic chemicals. When they do test, the results can be hard to stomach. Ritewood Farms in Idaho is one of the world's largest chicken factories. In 1979, the concentrations of PCBs in their chickens were found to be so high that one poultry sample could not even be measured. Almost three million dollars worth of egg and poultry products had to be destroyed. It remains anyone's guess how many Americans will never have children or will give birth to deformed children, or will get cancer as a result of eating products from the eggs and chickens that were not tracked down and destroyed. We have yet to see the impact of what has already been done. And the future is rapidly approaching. Whenever cases like this are discovered, the chemical, meat, and dairy industries often become extremely concerned about the public's response. One poultry executive justified his company's commitment to covering up the matter by saying: _There's no point in scaring people. We have a duty to protect the public's peace of mind._ These industries had a hard time doing their self-appointed duty in 1970, when 146,000 chickens in New York had to be destroyed because high levels of PCBs were found by the Campbell Soup Company. And again in 1971, when 88,000 chickens and 123,000 pounds of egg products from North Carolina met a similar fate. The chickens had eaten fish meal disastrously high in PCBs. In 1978, Ralston Purina had to recall 2,500,000 pounds of animal feed they had sold that was made from fish meal which they discovered, belatedly, to be heavily contaminated with PCBs. Millions of eggs and almost half a million chickens were destroyed because the birds had already eaten the feed. It must have been hard for the companies involved to maintain the public's peace of mind when the FDA admitted it had no idea how many contaminated chickens and eggs were consumed. Pesticide authority Lewis Regenstein writes of such occurrences: _It can be assumed that such examples represent a tiny fraction of the number of actual incidents, and that most cases of PCB contamination go undetected and/or unreported. Thus, most of the PCBs that contaminate our food end up being consumed by the public._ ### **Keep It Down...Someone Might Be Listening** It is remarkable how indifferent the companies that profit from these substances can be, not only to public health, but to the welfare of their own employees. In 1974, a Virginia plant began manufacturing the pesticide kepone. Within three weeks, workers became sick with tremors, dizziness, and nervousness. When they sought medical help, what they received left a little bit to be desired. Many were given tranquilizers. One was referred to a psychiatrist. A year later, Virginia state officials found out that over 70 workers, plus 10 spouses and children, had been seriously poisoned by kepone. Many had become sterile. This did not stop Life Sciences Inc., a subsidiary of Allied Chemical Corporation, from dumping great quantities of kepone into the James River in Virginia in the 1970s. They did this despite knowing that this deadly chemical causes cancer, birth defects, and neurological disorders; and despite knowing that the James River is the seedbed for one-quarter of the country's oysters. Predictably, the kepone spread into Chesapeake Bay, which produces 90 percent of America's soft-shell crabs, 40 percent of all commercial oysters, and 15 percent of all soft-shell clams, besides a significant percentage of the nation's commercial fishing catch. Eventually the pollution was discovered and traced to Allied Chemical. Their crimes discovered, Allied Chemical stubbornly refused to repent. According to Senator Patrick Leahy, who chaired a Senate committee investigating the matter: _Allied Chemical took a position that makes Pontius Pilate look like Mother Theresa of Calcutta. That is giving them the benefit of the doubt._ As a result of the contamination, the entire area had to be closed to commercial fishing. Within a few years, however, pressures from the fishing industry caused the area to be reopened, even though kepone levels remained dangerously high. Today, many of us eat fish from the James River and Chesapeake Bay, even though experts say these waters will remain seriously contaminated with kepone for another two centuries The least likely of all places in the world to find an uncontaminated fish is in the United States. We have the dubious distinction of being the world's largest producer of pesticides. We use 1.1 billion pounds of pesticides a year—about five pounds for every member of the population. This amounts to 30 percent of the entire world's use. You may be wondering if any fish are safe. Unfortunately, even for research purposes, it is almost impossible now for scientists to find fish anywhere in U.S. waters that do not carry toxic chemicals in their flesh. Lewis Regenstein writes: _From a health standpoint, the least dangerous fish to eat are smaller, deep-ocean fish that do not live or spawn near the coast, such as cod, halibut, and pollack, or freshwater fish from high-altitude streams that are not contaminated from industrial or agricultural runoffs or dumping. But even these fish will carry some pollutants. Unfortunately, uncontaminated fish and other animal products may simply no longer exist._ A major study reported in Tufts University's _Diet and Nutrition Letter_ compared the offspring of 242 women who ate varying amounts of fish from Lake Michigan. The study found that the more fish the mothers had eaten, the more their babies showed abnormal reflexes, general weaknesses, slower response to stimuli, and various signs of depression. Even mothers eating the fish _only two or three times a month_ produced babies weighing seven to nine ounces less at birth, with smaller heads. A 1986 follow-up study cast an even less favorable light on Lake Michigan fish. A definite correlation was found between the amount of fish the mothers had eaten, _even if it was only once a month,_ and the children's subsequent brain development. The youngsters were given the "fixation to novelty" test, which is recognized as an accurate indicator of future verbal I.Q. Their scores were inversely proportional to the amount of fish their mothers had eaten. The more fish their mothers had eaten, the poorer they did. We are again and again told not to be alarmed. This is ridiculous because it is not too late to begin to reverse the damage. Our grandchildren might yet live in a healthy world, where people gather joyfully at night around crackling campfires, laughing about times in the distant past when human beings were so foolish as to spread such poisons into the environment. "It's a good thing," they might yet say happily, "that we learned better in time." ### **The Pharmaceutical Farm** We won't arrive at such a happy future eating the products of today's factory farms. These animals are not only fed huge quantities of often-contaminated fish but are subject to a distressing array of toxic chemicals. Cattle, pigs, sheep, and other livestock are often routinely doused with a chemical called toxaphene to kill the parasites that breed in the crowded and grossly unsanitary conditions of modern factory farms. This substance is a chlorinated hydrocarbon, a member of the deadly family that includes DDT, kepone, dieldrin, heptachlor and PCBs. Like other members of its chemical family, toxaphene is biologically stable, fat soluble, and a deadly poison. In the most microscopic doses it produces cancer and birth defects and causes bones to dissolve in lab animals. Even a few parts per trillion disturb the reproduction of fish, and a few parts per billion turn their backbones to chalk. Yet every day in the United States this chemical is routinely administered by untrained factory farm workers to the animals whose flesh and milk the public eats. If there were a competition for the world's most deadly substance, toxaphene would definitely have its supporters, including, perhaps, Dr. Adrian Goss, the chief scientist for the EPA's Hazards Evaluation Division. A world-renowned expert on toxic chemicals, he was formerly associate director of the FDA's scientific investigations office. His opinion of toxaphene is unequivocal: _[It is] abundantly clear that toxaphene is an extremely potent carcinogen...I have never encountered an agent purposefully introduced into the environment...which had a carcinogenic propensity as clearly marked and as pervasive._ Yet each year in the United States over a million cattle are dipped in or sprayed with several million gallons of toxaphene solution to kill parasites that thrive in factory farm environments. This is done despite the fact that toxaphene, like the other chlorinated hydrocarbons, can be absorbed through the skin of animals and is retained in their flesh. In December 1978, veterinarians for the California Department of Food and Agriculture were concerned about mange in the 850-head herd of Chico, California, farmer George Neary. Neary pleaded with them not to use toxaphene, but they assured him they knew what they were doing, and insisted. Within a few weeks, nearly 100 cows had died. Five hundred others either aborted their fetuses or gave birth to calves that died soon after birth. A dog that ate some flesh from one of the dead cows evidently did not find it to his liking. He dropped dead seconds later. The administrators of the toxaphene program concluded they had used too concentrated a solution. Sorry, George! As if that's not enough, modern factory farms often swarm so thickly with flies that farmhands have to turn on their windshield wipers in order to be able to make it home from work. The flies can just about drive the men crazy, and workers will go to great lengths to kill them. Many of the sprays commonly used to kill flies around livestock (including Fly-Die, Duo-Kill, Vapona, and others) have as their primary ingredient a substance that would also have some supporters in a competition for the world's worst poison—a chemical called dichlorvos. So toxic is dichlorvos that the World Health Organization has set its acceptable daily intake at only 0.004 mg/kg, an amount exceeded by someone who merely stays in the same room with a small No-Pest strip containing the chemical for nine hours. But this doesn't prevent the decision makers in the meat industry from giving the cows, chickens, pigs, and steers in today's animal factories a continuing stream of dichlorvos products. In their never-ending battle against flies, factory farm workers will often mix toxic larvicides into the animals' feed. The poisons go in the animals' mouths, through their stomachs and intestines, and out the other end—in so doing rendering the manure chemically toxic to the flies that will breed there. One farmer told me these larvicides are a nifty idea. He laughed when I told him that the most popular of the larvicides, Rabon, has as its principal ingredient a substance that can cause extreme damage to the human nervous system and send people into convulsions, even in minute doses. He quickly pulled out an advertisement in which Rabon's manufacturer, Diamond Shamrock, says there is no need to worry about residues showing up in the meats and milk from animals fed Rabon. Indeed, they recommend feeding the poison to dairy cows while they are being milked, and to beef cattle right up to slaughter. How trustworthy are the reassurances of such companies? When the manager of technical services and development at Diamond Shamrock was asked about problems with Rabon, he replied that the only problem was "getting the compound approved by the EPA." ### **The Government as Protector** Twenty years ago, the amount of toxic substances used in animal farming was only a trickle compared to the torrent it has become today. Yet even then, when the USDA tested 2,600 poultry samples from every federally inspected plant in the nation, they could not find a single sample that was not contaminated with toxic pesticides. In 1966, it was admitted in congressional hearings that: _No milk available on the market, today, in any part of the United States, is free of pesticide residues._ Unfortunately, the situation has grown steadily worse since then. Most of us are deeply conditioned to believe that the government's meat inspection system takes good care of us and would never allow unhealthy animals to reach the public. But in reality that is hardly the case. The animals often whiz by the inspectors faster than one per second, giving them only the briefest possible glimpse for the most glaring of problems. Detection of toxic chemicals requires complex laboratory equipment and a great deal of time and expense. In fact, the USDA _tests only one out of every quarter million_ slaughtered animals for toxic chemical residues. And even then, it tests for less than 10 percent of the toxic chemicals known to be present in the country's meat supply. In 1976, less than 150 animals in the United States were condemned for drug residues, 57 for pesticidal residues, and 29 for miscellaneous residues. That's a grand total of less than 300 animals out of 119 million—not counting poultry. So low are our meat inspection standards that inspectors from the European Economic Community (EEC) in 1984 declared 11 of America's largest meat packers ineligible to export their products through the Common Market. The chemical companies would like us to believe that we are protected from harmful chemical residues and that the problem is under control. But impartial scientists don't see it that way. Lewis Regenstein writes: _A review of the government's policy in setting and enforcing tolerance levels for toxic pesticides leads to the inescapable conclusion that the program exists primarily to reassure the public that it is being protected from harmful chemical residues. In fact, the program, as currently administered, does little to minimize or even monitor the amount of poisons in our food, and serves the interests of the users and producers of pesticides rather than those of the public..._ _The prime source of toxic pesticides and other chemicals for most Americans is in the consumption of food high in fat content, such as meat and dairy products. A vegetarian diet, or one that minimizes animal products, can substantially reduce one's exposure to most of these cancer-causing chemicals._ The relationship between toxic chemicals and meat was ironically dramatized on April 5, 1973. On that day, the FDA finally banned the artificial coloring agent Violet No. 1 as a carcinogen. Up until then, the Department of Agriculture had been using the dye to stamp meats with the grades of "Choice," "Prime," and "U.S. No. 1 USDA." For over 20 years, the USDA had been reassuring customers their meat was healthy by stamping the meat with a cancer-causing dye. ### **The Good News** Fortunately, there are alternatives to pesticides. Agricultural techniques such as organic farming and integrated pest management (IPM) are decidedly on the upswing today. These utilize natural insect controls, such as predatory insects, weather, crop rotation, pest-resistant varieties, soil tillage, insect traps, and other environmentally sound practices. IPM systems use chemicals when necessary but recognize that tolerable quantities of pest insects may actually be desirable, because they provide food for beneficial insects. Organic and IPM systems realize that "controlling" insects by poisoning them is not the best strategy. Even speaking strictly in terms of short-term output and crop losses due to pests, pesticides are not the blessing the companies who sell them would like us to believe. Of the 25 most serious agricultural pests in 1970, 24 were either pesticide-aggravated or pesticide-induced pests. Despite staggering increases in pesticide use, the percentage of U.S. crops lost to insects doubled between 1950 and 1974—mostly because the ecological balance has been so severely disturbed by the chemicals. The chemical companies would like us to believe that the chemicals increase food production. But in their penetrating study of the causes of world hunger, _Food First,_ Frances Moore Lappé and Joseph Collins found quite otherwise: _In country after country, there is a regular progression of events. For the first few years [after pesticides are introduced] insects are controlled at reasonable cost and yields are higher than before. The growers, seeing the bugs literally drop from the plants, feel the pesticides give them power over forces that have always been beyond their control. Gradually, however, the pest species develop resistant strains through a survival-of-the-fittest selection._ _It is not true that the only good bug is a dead bug. Some bugs are parasites or flesh-eating predators that live off the insect species doing the plant damage. Some eat only very specific parts of the crop plant. Studies show that the vast majority of insect species never cause sufficient damage to justify the cost of insecticide treatment. Their numbers are restricted below injury levels by the action of these parasites and predators. But, when an insecticide kills some of these parasites and predators, many ordinarily insignificant pests are able to multiply faster._ A case in point is the spider mite: _Only 25 years ago, the spider mite was a minor pest. Repeated use of pesticides supposedly aimed at other pests has decimated the natural enemies and competitors of the mite. Today, the mite is the pest most seriously threatening agriculture worldwide..._ _The irony...is that the more effective an insecticide is in killing susceptible individuals of a pest population, the faster resistant individuals evolve._ Fortunately, pesticides are not necessary. Organic and IPM techniques not only work but often work even in cases where the most powerful pesticides won't. One of the worst pests corn growers face is the corn rootworm, and chemicals have not been much help in this battle. The worm has developed almost total resistance to the major pesticides. Integrated pest management systems solved the problem by simply rotating crops. The corn rootworm cannot eat the soybean plant. So, when soybeans are planted alternately with corn, the rootworm has nothing to eat and cannot survive. The soybean plants have the added benefit of supplying nitrogen to the soil and so reducing the need for fertilizer for the ensuing corn crop. Unfortunately for pesticide-addicted agriculture, however, simply switching to crop rotation after years of pesticide use can run into a few difficulties. Some of the weed killers used today on corn crops persist in the soil and kill noncorn plants. Soybean plants die if planted in soil to which these chemicals have been applied. Farmers who have been led to rely on pesticides can find themselves in a vicious circle. They may have created soil in which nothing will grow except corn. So they must plant corn year after year, thereby virtually inviting insects, disease, and weed problems. Earl Butz, secretary of agriculture under Nixon, used to say that before the United States could consider organic farming, it would have to decide which 50 or 60 million Americans were going to be allowed to starve. His attitude exemplified the stance that government and agribusiness have taken in the past: that organic farming is a luxury we can ill afford, and we need these chemicals to feed ourselves. The chemical companies, as you might imagine, have spent millions to reinforce this way of thinking. But it could hardly be less true. Up until World War II, American farmers grew huge harvests without relying on pesticides. And happily we could now do even better, thanks to our greatly increased understanding of IPM techniques. For example, it is now possible to rear large numbers of sterilized male insects and then release them into an area in which this particular insect has become a problem. They mate with the females in the wild, and soon there is a drastic reduction in the population of the problem insect. It is also now possible to rear large numbers of beneficial insects and release them to prey on the insect pests in an infested area. We could now do even better than ever without pesticides because our understanding of environmental systems is so much more sophisticated than it was before World War II, and because we can learn from the mistakes we have made. We know enough now to appreciate that while insects often become resistant to pesticides, no insect ever becomes resistant to a bird. And birds handle themselves pretty well around insects. A brown thrasher can eat 6,180 insects in a day. A swallow will devour 1,000 leafhoppers in 12 hours. A house wren will feed 500 spiders and caterpillars to its young during one summer afternoon. A pair of flickers consider 5,000 ants a mere snack. A Baltimore oriole eats 17 caterpillars a minute. In fact, government studies on the feasibility of organic types of farming have been extremely encouraging. A 1979 Agriculture Department task force of scientists and economists formed to study the matter came to _positive conclusions on the importance of organic farming and its potential contributions to agriculture and society._ The USDA task force found that some farmers actually experienced no reduction at all in yields when they gave up the use of chemicals. And those who did lose some production still made more money because they didn't have to pay for expensive chemicals. Probably the most complete research project ever undertaken to assess the feasibility of organic agriculture was conducted by the Center for the Study of Biological Systems at Washington University in St. Louis. This study matched a group of farms with similar soil conditions, crops, and acreage, half of which used chemicals, half of which did not. At the end of the study, the center director concluded: _A five-year average shows that the organic farms yielded, in dollars per acre, exactly the same returns. In terms of yield, the organic farms were down about 10 percent. The reason why the economics came out is that the savings in chemicals made up for the difference._ You might think that a 10 percent reduction in yield would mean food shortages. But it is important to realize that the vast majority of American agriculture does not grow food for people. It grows food for animals, whose flesh, milk, and eggs we then consume. Most of it, actually, gets turned into manure, which cannot be recycled because it does not fall onto the land itself but instead is concentrated in unbelievable quantities at feedlots and confinement sheds and ends up in our already amply polluted water. If we were simply to grow food for people, we would need less than 30 percent of the yield we now require from our agricultural acreage. We could cut our yield in half and still have far more than enough food to feed ourselves. And since the switch to IPM and other organic-type methods does not actually entail much loss of production, we could, in fact, feed the entire world if we grew food directly for people instead of supplying what are really manure and saturated fat factories. In doing so, we would also stop flooding the environment with lethal poisons. Our children might yet live in an increasingly safe and clean world. ### **Reducing Your Intake of Pesticides** The most effective way to reduce your intake of toxic chemicals is to minimize or eliminate your intake of meats, fish, dairy products, and eggs. Choosing organic or unsprayed produce would be the next step. It also helps to reduce your intake of imported foods such as coffee, sugar, tea, and bananas, because farmers in countries such as Ecuador, Mexico, Guatemala, and Costa Rica use much greater concentrations of pesticides than even American agriculture is allowed to use. Pesticides, incidentally, which they often buy from U.S. chemical companies, and which are usually manufactured in this country. It is likewise a good idea to beware of imported fruits and vegetables. You're safest if you stick with in-season, locally grown fruits and vegetables. U.S. regulations for pesticide use make many exceptions for Hawaii, with the result that fruit from Hawaii can be as heavily contaminated as that from Latin America. Among the worst of all foods are fast-food hamburgers, because they are often made from beef imported from Central America. Some people feel that eating "organically raised" beef and poultry is a good way to limit their intake of pesticides. It is important to realize, though, that while meat products labeled "natural" or "organic" may be better than the typical factory farm commercial products, they still will include the concentrated toxins from all the foods the livestock ate. These lethal chemicals accumulate in the fatty tissues of animals in much greater concentrations than are found in fruits and vegetables. Pesticide authority Lewis Regenstein writes: _Meat contains approximately 14 times more pesticides than do plant foods; dairy products 5 1/2 times more. Thus, by eating foods of animal origin, one ingests greatly concentrated amounts of hazardous chemicals. Analysis of various foods by the FDA shows that meat, poultry, fish, cheese and other dairy products contain levels of these pesticides more often and in greater amount than other foods._ In 1975, the Council on Environmental Quality concluded a lengthy analysis of the problem of pesticide residues in food by stating that dairy and meat products account for over 95 percent of the population's intake of DDT. The same percentage holds true for the other pesticides. Sadly, people who have not been told this fact continue to eat high on the food chain, thus unknowingly exposing themselves day after day to large amounts of some of the most virulent poisons known to man. The bright side is that, knowing this, we can do something about it. A new direction for America's agriculture and diet-styles would mean that our children and their children might yet have healthy bodies and a healthy environment in which to live. ### **Contaminated Mother's Milk** You might think that any way toxic chemicals could possibly be eliminated from the human body would be a good thing. But, disturbingly, the most common way these stored-up poisons are released is in the breast milk of nursing mothers. Just as dairy cows tend to excrete into their milk the stores of lethal chemicals they have absorbed, so, too, does human milk become contaminated from the stores of these poisons in the mother's body fat. The tragic results have been portrayed by the Ecology Action Center in a poster that shows a nude pregnant woman. On her effulgent breasts there is a label: "Caution—Keep Out of Reach of Children." Unfortunately, this poster is not intended as a joke. A nursing woman's body draws on its body fat reservoirs to make milk. Stored in her body fat reservoirs are virtually all the toxic chemicals she has ever ingested, inhaled, or absorbed through her skin. These poisons are thus incorporated into her milk. Breast-fed babies thereby may consume extraordinarily large amounts of the most toxic substances ever known to man. So high is most mother's milk in DDT, PCBs, dieldrin, heptachlor, dioxin, and so on that it would be subject to confiscation and destruction by the FDA were it to be sold across state lines. In 1976, the EPA found significant concentrations of DDT and PCBs in over 99 percent of mother's milk from every part of the country. Other studies have confirmed these levels of saturation. In 1975, the President's Council on Environmental Quality found DDT in 100 percent of the breast milk it sampled. The other poisons that work their way up the food chain were similarly ubiquitous. The EPA has concluded that the average American breast-fed infant ingests nine times the permissible level of dieldrin, one of the most potent of all cancer-causing agents known to modern science. As if that weren't enough, the EPA concludes that the average American breast-fed infant also consumes 10 times the FDA's maximum allowable daily intake level of PCBs. In 1981, the breast milk of over 1,000 Michigan mothers was tested for PCBs. Every single case showed residues of a chemical so toxic it causes birth defects and cancer in lab animals in doses as low as a few parts per billion. Some women are so alarmed by these terrifying facts that they decide not to breast-feed their young. But this is not usually the best decision for a number of important reasons: 1) Human breast milk is nutritionally vastly superior for a human infant to any cow's-milk formula. 2) The formulas are also likely to be contaminated with toxic chemicals. 3) Human breast milk contains antibodies that are crucial for the newborn. 4) Breast-feeding provides the bonding and emotional nurturance that are tremendously important to the well-being of both mother and baby. Fortunately, there are ways a woman of childbearing age can minimize the risk to her young. Many studies have shown direct correlations between the amount of animal fat in a woman's diet and the amount of residues in her milk. The less meat, butter, eggs, cheese, milk, poultry, and fish in a woman's diet, the fewer toxic chemicals will be found in the milk that flows from her breast to her young. In 1976, the EPA analyzed the breast milk of vegetarian women and discovered the levels of pesticides in their milk to be far less than the average. A study published in the _New England Journal of Medicine_ made a similar comparison and found: _The highest levels of contamination in the breast milk of the vegetarians was lower than the lowest level of contamination...[in] non-vegetarian women...The mean vegetarian levels were only one or two percent as high as the average levels in the United States._ This is a tremendously important statistic. The breast milk of the average vegetarian nursing mother in the United States contains only _1 or 2 percent_ of the pesticide contamination experienced in the national average. If the national average for breast milk contamination were to be represented by the weight of a compact automobile (1,600 pounds), the comparable vegetarian average would be equivalent to the weight of only a very small suitcase (16 to 32 pounds). No studies to my knowledge have been done on the breast milk of pure vegetarian women, but there is every indication their milk would be again many times safer. Women, and even little girls, who think they may wish to have and breast-feed a baby in the future would do well to realize that the diet they eat today will greatly affect the health of their young. Any chemicals they ingest now will be stored in their tissues until released in their milk. And because mother's milk is often an infant's only source of food, the concentrations of pesticides in its milk are crucial indeed. The Environmental Defense Fund has shown that the average American nursing infant receives 100 times more PCBs, on a body-weight basis, than the average adult. Further, the effective dose is yet more toxic, since the infant's immature liver is completely incapable of detoxifying these chemicals. It is extremely important that young women know that by eating wisely today, they will be creating better breast milk for their babies tomorrow. We know enough now to take the right path. The mothers of the future might yet nurse their babies, grateful in the knowledge that their milk is safe and pure. They might yet feed their young, with only a distant memory of the time when breast milk was a danger. Men who think they may someday wish to father a child would do well to realize that the toxic chemicals they ingest today, including those especially damaging to sperm cells, tend to collect and concentrate in the male reproductive tract. The result is that a very high number of birth defects stem from the male's absorption of these chemicals. This is why the offspring of Vietnam veterans who were involved with Agent Orange have such a high rate of birth defects, and why a University of Southern California Medical School study found distinct correlations between brain tumors in children and their fathers' exposure to toxic chemicals. Even if a man does not father a child, he should be concerned. His sperm will still collect these chemicals. And, during intercourse, they will be transmitted to the female. She will absorb them through her vaginal mucosa and then store them in her womb, like the worst kind of biological time bomb, waiting to cause birth defects and cancer. Fortunately, wise food choices today can do a great deal to protect the health of the as-yet unborn. ### **The Gene Pool** It is almost impossible to exaggerate the profound threat toxic chemicals present to the human species. They can damage the very blueprint of life itself—the DNA molecule. Hence the epidemic of the runaway cellular growth process we know as cancer; hence the epidemic of sterility; hence the epidemic of birth defects. What is happening is that the human gene pool itself is in danger of being irreparably harmed. This gene pool is the culmination of at least three billion years of evolution and is the primary resource of the human species. Defects in the DNA blueprint cause diseases that henceforth become hereditary. These tragedies will then persist for untold generations in the future. Scientists tell us: _Changes in the chromosomes of sperm or our precursor cells may be transmitted to all future generations of humans. The heredity of man, his greatest treasure, is thereby at stake. Once irreversibly injured, the chromosomes cannot be repaired by any process known to man._ The mutagenic effect of these chemicals takes at least a generation to manifest. It is only in this generation that the biosphere and the food chains have been inundated with toxic chemicals that represent the highest summation of technological expertise at killing living creatures. We have not yet seen the impact of what has already been done. But as Red Skelton used to say, "If we don't change the direction in which we are going, we will end up where we are headed." ### **Now What?** Facing this ominous future, I've been filled with many emotions. I've felt overwhelmed by the sheer quantity of these substances that have been produced; overwhelmed by such great damage that can be done by such infinitesimal amounts; and overwhelmed with rage at those who lie and profit from such abominations. It is not easy to see a man like Paul Oreffice, the president of Dow Chemical Company, appear on NBC's _Today_ show and tell us that "there's absolutely no evidence of dioxin doing any damage to humans." He said this despite knowing that the amount of dioxin sufficient to kill 10 million people could fit in a space smaller than a human hand. I don't think anyone could become aware of the immensity of what is involved and not feel pain for our world and our collective future. This pain goes beyond the personal, beyond any of our individual lives. It is the human journey itself that is now at stake. Sometimes I've wished I could cover my eyes and it would all go away; I've wanted to believe that when the chips are down "they" would never allow our whole world to be poisoned. Other times, when my attempts to psychically numb myself have failed and the reality of the situation has sunk in, I've felt other forms of grief. I've felt angry that we must see our lives and the lives of our children darkened by such avoidable tragedy. I've felt guilty, because as part of this society I can't help but feel implicated in this great misfortune. I've felt scared for what may yet lie in store. Mostly, though, there has been sorrow. Confronting what is happening can bring a sadness beyond telling. This sorrow belongs to us all, and I have learned it is not something to fear. For in the depths of our shared pain, we also experience our shared caring, our mutual prayers, and our common capacity to act. The pain we feel is the cracking of the shell that encloses our power to respond. Something precious can be born in times like these. In our shared pain we labor together to bring it to birth. The pain we feel is not ours alone. It is rooted in caring, not just for ourselves and our children, but for all of humanity and all of life. Our distress is a statement of our interconnectedness with all beings. Something much larger than our individual selves and destinies is at work here. Our distress is an urgent statement from the depths of our being that this horrible pollution must not be allowed to continue. It is the awakening within our individual and collective conscience of the most profoundly transforming human responses. It is the source of the courage to redirect our lives. Obviously the work of healing our world and ourselves is not a separate or passing chapter in our lives. The changes that are necessary won't come about simply because we stop eating meat, or simply because, on occasion, we meet or march or donate or lobby. It will take everything we are, and it will take all of us, and in forms we cannot yet even begin to imagine. We will meet this challenge that asks so much because there is something inside us that is sacred, our conscience, that says this is what we are here to do. I look out into the world and I see a deep night of unthinkable cruelty and blindness. Undaunted, however, I look within the human heart and find something of love there, something that cares and shines out into the dark universe like a bright beacon. And in the shining of that light within, I feel the dreams and prayers of all beings. In the shining of that beacon I feel all of our hopes for a better future. In the shining of the human heartlight there is the strength to do what must be done. ## 12. **ALL THINGS ARE CONNECTED** _Destiny, or karma, depends upon what the soul has done about what it has become aware of._ —EDGAR CAYCE _Each of us is the last frontier._ —MERLE SHAIN There is an old story that tells of a man who lived a long and worthy life. When he died, the Lord said to him, "Come, I will show you hell." He was taken to a room where a group of people sat around a huge pot of stew. Each held a spoon that reached the pot, but had a handle so long it couldn't be used to reach their mouths. Everyone was famished and desperate; the suffering was terrible. After a while, the Lord said, "Come, now I will show you heaven." They came to another room. To the man's surprise, it was identical to the first room—a group of people sat around a huge pot of stew, and each held the same long-handled spoon. But here everyone was nourished and happy and the room was full of joy and laughter. "I don't understand," said the man. "Everything is the same, yet they are so happy here, and they were so miserable in the other place. What's going on?" The Lord smiled. "Ah, but don't you see—here they have learned to feed each other." ### **Wasting the Food We Have** The livestock population of the United States today consumes enough grain and soybeans to feed over five times the entire human population of the country. We feed these animals over 80 percent of the corn we grow, and over 95 percent of the oats. It is hard to grasp how immensely wasteful is a meat-oriented diet-style. By cycling our grain through livestock, we end up with only 10 percent as many calories available to feed human mouths as would be available if we ate the grain directly. Less than half the harvested agricultural acreage in the United States is used to grow food for people. Most of it is used to grow livestock feed. This is a drastically inefficient use of our acreage. For every 16 pounds of grain and soybeans fed to beef cattle, we get back only one pound as meat on our plates. The other 15 are inaccessible to us. Most of it is turned into manure. The developing nations are copying us. They associate meat-eating with the economic status of the developed nations and strive to emulate it. The tiny minority who can afford meat in those countries eat it even while many of their people go to bed hungry at night, and mothers watch their children starve. _Love is feeding everybody._ —JOHN DENVER To understand the return on the food investment we get through cattle feeding, imagine you took $1,000 of your money and put it into a bank. A year later, you go to withdraw your money, expecting as well to collect the interest it has earned over the 12 months. But instead the bank teller hands you only $100 and says that is all you get. All the rest is gone. Not only do you not get any interest on your investment, but you have lost 90 percent of it. That is better than the protein efficiency of a meat-based diet. We lose over 90 percent of the protein we invest as feed in our livestock. Beef is the least efficient—we lose 94 percent of the protein we feed beef cattle. Dairy cattle are the most efficient—but here, too, we still lose 78 percent of our protein investment. With pigs and chickens our losses are in between. We lose 88 percent of the protein we feed pigs and 83 percent of our protein investment in poultry. _Forty thousand children starve to death on this planet every day._ —INSTITUTE FOR FOOD AND DEVELOPMENT POLICY To supply one person with a meat habit food for a year requires three and a quarter acres. To supply one lacto-ovo vegetarian with food for a year requires one-half acre. To supply one pure vegetarian requires only one-sixth of an acre. In other words, a given acreage can feed 20 times as many people eating a pure vegetarian diet-style as it could people eating the standard American diet-style. Lester Brown of the Overseas Development Council has estimated that if Americans were to reduce their meat consumption by only 10 percent, it would free over 12 million tons of grain annually for human consumption. That, all by itself, would be enough to adequately feed every one of the 60 million human beings who will starve to death on the planet this year. _I've known what it is to be hungry, but I always went right to a restaurant._ —RING LARDNER By cycling our grain through livestock, we not only waste 90 percent of its protein; in addition, we sadly waste 96 percent of its calories, 100 percent of its fiber, and 100 percent of its carbohydrates. Meanwhile, malnutrition is the principal cause of infant and child mortality in developing nations. In many of them, over 25 percent of the population die before reaching the age of four. In Guatemala, 75 percent of the children under five years of age are undernourished. Yet every year Guatemala exports 40 million pounds of meat to the United States. It borders on the criminal! Many of us believe that hunger exists because there's not enough food to go around. But as Frances Moore Lappé and the antihunger organization Food First have shown, the real cause of hunger is a scarcity of justice, not a scarcity of food. Enough grain is squandered every day in raising American livestock for meat to provide every human being on earth with two loaves of bread. Hunger is really a social disease caused by the unjust, inefficient, and wasteful control of food. In Costa Rica, beef production quadrupled between 1960 and 1980. But almost all this beef is exported to the United States, and what does stay in the country is eaten by a tiny minority. Though more and more Costa Rican land is being turned over to meat production, the population is not eating more meat for the change. The average family in Costa Rica eats less meat than the average American housecat. _The law, in its majestic equality, forbids the rich as well as the poor to sleep under bridges, to beg in the streets, and to steal bread._ —ANATOLE FRANCE The world's cattle alone, not to mention pigs and chickens, consume a quantity of food equal to the caloric needs of 8.7 billion people—nearly double the entire human population of the planet. _He would daily throw out crumbs for the sparrows in the neighborhood. He noticed that one sparrow was injured, so that it had difficulty getting about. But he was interested to discover that the other sparrows, apparently by mutual agreement, would leave the crumbs which lay nearest their crippled comrade, so that he could get his share, undisturbed._ —ALBERT SCHWEITZER According to Department of Agriculture statistics, one acre of land can grow 20,000 pounds of potatoes. That same acre of land, if used to grow cattle feed, can produce less than 165 pounds of beef. In a world in which a child dies of starvation every two seconds, an agricultural system designed to feed our meat habit is a blasphemy. Yet it continues, because we continue to support it. Those who profit from this system do not need us to condone what they are doing. The only support they need from us is our money. As long as enough people continue to purchase their products they will have the resources to fight reforms, pump millions of dollars of "educational" propaganda into our schools, and defend themselves against medical and ethical truths. A rapidly growing number of Americans are withdrawing support from this insane system by refusing to consume meat. For them, this new direction in diet-style is a way of joining hands with others and saying we will not support a system that wastes such vast amounts of food while people in this world do not have enough to eat. _The day that hunger is eradicated from the earth there will be the greatest spiritual explosion the world has ever known. Humanity cannot imagine the joy that will burst into the world on the day of that great revolution._ —FEDERICO LORCA ### **War Is Hell** Because the raising of livestock requires a much greater use of resources, it puts us in a situation in which there is not enough to go around. In this kind of a dilemma there lurks a fear in us all that we will be the one who won't get enough. Thus, as long as there are people on this planet who are starving, we must all live in fear. It is out of such fears that war arises. Conflicts stemming from territorial disputes become more frequent and more intense. Basic human needs become less important than property rights. We are set off against each other. Fear is the real disease. The nuclear bombs are only symptoms. Is it not fear that makes us build and stockpile such terrible weapons? Whatever we can do to reduce fear reduces the possibility of war. We've already begun when we realize that our daily lives have a genuine impact on the level of fear in the world. The understanding that meat-eating makes food scarce and puts us at odds with each other, so promoting war, is not new. The Bible is full of examples of conflicts arising from the competing needs of livestock raisers. World history is full of battles that were fought because meat-eating societies needed more land to feed their stock. In our century, we have had Gandhi urging us to "live simply so others might simply live." But his message was not new. Over 2,000 years ago, another wise man—Socrates—said much the same thing. In Plato's _Republic,_ he extols the peace and happiness that come to people eating a vegetarian diet. Speaking to Glaucon, Socrates says: _And with such a [vegetarian] diet they may be expected to live in peace and health to a good old age, and bequeath a similar life to their children after them._ But Glaucon is skeptical. He tells Socrates that he doesn't think people will be satisfied with so simple a life; they will want to eat "pig's flesh." Socrates answers that this would not be good, for people should avoid things "not required by any natural want." In fact, in describing the woes that will befall mankind if it eats animal flesh, Socrates seems uncannily prophetic—predicting both the medical consequences of meat-eating, which we are only now discovering, and the wars that throughout history it has brought in its wake: _Socrates:_ | _And there will be animals of many other kinds, if people eat them?_ ---|--- _Glaucon:_ | _Certainly._ _Socrates:_ | _And living in this way we shall have much greater need of physicians than before?_ _Glaucon:_ | _Much greater._ _Socrates:_ | _And the country which was enough to support the original inhabitants will be too small now, and not enough?_ _Glaucon:_ | _Quite true._ _Socrates:_ | _Then a slice of our neighbors' land will be wanted by us for pasture and tillage, and they will want a slice of ours, if, like ourselves, they exceed the limit of necessity, and give themselves up to the unlimited accumulation of wealth?_ _Glaucon:_ | _That, Socrates, will be inevitable._ _Socrates:_ | _And so we shall go to war, Glaucon, shall we not?_ Socrates spoke in a time when wars were ugly and vicious, but when the weapons of destruction were as nothing compared to today's nuclear stockpiles. Never before has it been so important as it is now to distinguish between basic human needs and excessive cravings. Never has it been more important to understand and defuse the fears that drive men to war. If any human being on the planet is starving, we all feel it. Meat-eating contributes to the fear in the world by putting us in a position in which there is not enough to go around. But that's not all. Meat-eaters ingest residues of the animals' biochemical response to the horror of the slaughterhouse. Programmed by millions of years of evolution to fight or flee when in danger for their lives, the animals react to the slaughterhouse in sheer terror. Powerful biochemical agents are secreted that pump through their bloodstreams and into their flesh, energizing them to fight or flee for their lives. Like screaming air raid sirens, these chemical agents produce instinctual panic. Today's slaughterhouses virtually guarantee that the animals will die in terror. Certain Indian tribes would not eat the flesh of an animal who died in fear, because they did not want to take into themselves the terror of such an animal. When we eat animals who have died violent deaths we literally eat their fear. We take in biochemical agents designed by nature to tell an animal that its life is in the gravest danger, and it must either fight or flee for its life. And then, in our wars and daily lives, we give expression to the panic in which the animals we have eaten died. A new direction for America's diet-style would be a significant step toward a nonviolent world. It is a way of saying: "Let there be peace on earth, and let it begin with me." A nonviolent world has roots in a nonviolent diet. ### **The Ground beneath Our Feet** From dust we came and to dust we return. Archaeologists tell us that soil erosion played a determining role in the decline and demise of many great civilizations, including those of ancient Egypt, Greece, and the Mayans. In _Topsoil and Civilization,_ Vernon Carter and Tom Dale point out that wherever soil erosion has destroyed the fertility base on which civilizations have been built, these civilizations have perished. Topsoil is the dark, nutrient-rich soil that holds moisture and feeds us by feeding our plants. It is the most basic foundation of our sustenance upon this earth. Two hundred years ago, most of America's croplands had at least 21 inches of topsoil. Today, most of it is down to around six inches of topsoil, and the rate of topsoil loss is accelerating. We have already lost 75 percent of what may well be our most precious natural resource. As a result, the U.S. Department of Agriculture says that the productivity of the nation's cropland is down 70 percent, with much of it on the brink of becoming barren wasteland. The USDA admits this is an unparalleled disaster but claims that _halting soil erosion and degradation would be prohibitively expensive._ As long as we require our agriculture to feed our meat habit, this is no doubt true. But with a change in diet-style, we would need far less from our land. We would not have to force it artificially to supply the hyped-up demands we require to feed huge numbers of livestock. With a change in diet-style, halting soil erosion would cost us nothing. It would occur naturally, as part of sound soil management practices. Up until now we have resembled a sick man taking more and more pills to disguise his symptoms, even though the medications make him sicker. We have managed to mask the decline in our soil's fertility by saturating it with ever-increasing amounts of chemical fertilizers and pesticides. American farmers now apply more than 20 million tons of chemical fertilizers to our farmlands every year, more than the combined weight of the entire human population of the country. Although we have been virtually mainlining chemical fertilizers, our chemical "fixes" have done nothing to stop the erosion of our topsoil. In fact, they have made it far worse. It takes nature 500 years to build an inch of topsoil. Currently, we lose an inch of topsoil every 16 years. It takes nature a century to create 50 tons of topsoil on an acre of cropland. Today, thanks to the agricultural techniques we employ to produce massive amounts of livestock feed, one hard rainfall or one strong wind can erode that much topsoil from an acre of land in a couple of hours. _Food shortages will be to the 1990s what energy shortages have been to the 1970s and 1980s._ —ARMAND HAMMER, CHAIRMAN, OCCIDENTAL PETROLEUM The U.S. Soil Conservation Service reports that over four million acres of cropland are being lost to erosion in this country every year. That's an area the size of Connecticut. Our annual topsoil loss amounts to 7,000,000,000 tons. That is 60,000 pounds for each member of the population. Of this staggering topsoil loss, 85 percent is directly associated with livestock raising. _I never give them hell. I just tell the truth and they think it's hell._ —HARRY S. TRUMAN Without a diet-style change, we are well on our way to losing what many scientists feel has always been the basis of our strength as a nation. If the present pace of soil erosion continues, it is just a matter of time until the people of the United States, the inheritors of the world's richest farmlands, will be forced to depend on foreign imports for food. That is, if there's any available. Already, our agricultural practices are utterly dependent on foreign imports for the massive injections of chemical fertilizers on which our meat habit depends. We now import 85 percent of our potash and significantly increasing amounts of nitrogen and phosphorus. A new direction for America's diet-style would reverse this pattern, making us far less dependent on foreign fertilizers and thus less likely to be forced into intervening militarily in the affairs of other nations. It would allow us to feed ourselves, and help others, without destroying our land in the process. It would give us a chance to halt the erosion of our topsoil and regain our footing in a sound and renewable agriculture. _We don't inherit the land from our ancestors, we borrow it from our children._ —PENNSYLVANIA DUTCH SAYING It is really quite astounding how much is to be gained from a shift in diet-style. Pure vegetarian food choices make less than 5 percent of the demand on the soil of meat-oriented choices. By drastically reducing the demands on our soil, a new direction for America's diet-style would enable us to break our addiction to chemical fertilizers and pesticides. It would mean we could halt the horrendous overuse of nitrogenous fertilizers that are contributing to the destruction of the earth's ozone layer. It would mean we could stop raping the earth that sustains us. It would mean our children might yet have good rich soil in which to grow their food. ### **Mother Earth** Over 100 years ago, the great Indian chief Seattle was faced with the loss of his tribe's land. He responded out of his love and respect for the land, with utter honesty and heartbreaking eloquence: _We are part of the earth and it is part of us._ _The perfumed flowers are our sisters; the deer, the horse, the great eagle, these are our brothers. The rocky crests, the juices of the meadows, the body heat of the pony, and man— all belong to the same family._ _So, when the Great Chief in Washington sends word_ _that he wishes to buy our land, he asks much of us..._ _If we decide to accept, I will make one condition: The white man must_ _treat the beasts of this land as his brothers. I am a savage and do not understand any other way._ _I have seen a thousand rotting buffalos on the prairie, left by the white_ _man who shot them from a passing train. I am a savage and I do not understand how the smoking iron horse can be more important than the buffalo that we kill only to stay alive._ _Where is man without the beasts? If the beasts were gone, men would die from a great loneliness of spirit. For whatever happens to the beasts soon happens to man. All things are connected. This we know. The earth does not belong to man; man belongs to the earth. This we know._ _All things are connected_ _like the blood which unites one family._ _All things are connected._ _Whatever befalls the earth befalls the sons of the earth. Man did not weave the web of life, he is merely a strand in it. Whatever he does to the web, he does to himself._ ### **Timber!** The current agricultural system, designed to supply America's meat habit, wastes almost all the food it grows by feeding it to livestock rather than people. This creates a constant pressure to get the highest possible immediate yields out of the land, at whatever ecological cost. As a result, we have lost hundreds of millions of acres to soil erosion. In trying to replace it, we have spawned another major ecological catastrophe: we are destroying our forests. In fact, the United States has converted approximately 260 million acres of forest into land that is now needed to produce the wasteful diet-style most Americans take for granted. Since 1967, the rate of deforestation in this country has been one acre every five seconds. _They took all the trees,_ _and put them in a tree museum._ _Then they charged all the people_ _a dollar and a half just to see them._ _They paved paradise, and put up a parking lot._ —FROM A SONG BY JONI MITCHELL Although Joni Mitchell rightly sensed the rapid deforestation of our land, she was wrong in attributing the destruction of our trees to urban development. For each acre of American forest that is cleared to make room for parking lots, roads, houses, shopping centers, and so on, _seven acres_ of forest are converted into land for grazing livestock and/or growing livestock feed. Deforestation is occurring to make land for meat production. In fact, researchers who have studied the uses to which deforested land are put concluded: _More than three times as much meat is derived from formerly-forested...land as is derived from range land. That ratio is climbing each year as erosion and soil degradation claim more and more of the nation's range land and ever more forest land is converted to...land [for meat production]._ It doesn't help matters that the Forest Service and the Bureau of Land Management do whatever they can to assist the meat industry. Enormous amounts of federal forest lands are leased each year to cattle ranchers at a tenth the price they would have to pay to graze their cattle on private land. And the cattlemen are allowed to clear-cut the forests on federal land to boot. Forests, by the way, are one of the few places in the country where topsoil erosion isn't occurring. But after being cleared for use in livestock production, ex-forestland begins to lose topsoil rapidly. Builders and people wishing to buy firewood have seen the price of wood skyrocket in the past few decades. But we have seen only the beginning if present trends continue. America's most important wood product is softwood lumber, yet our national resources of this essential natural resource fell 41 percent from 1952 to 1977. We have been importing more and more softwood from Canada, with the result that even Canada, with its seemingly limitless forests, is feeling the pinch. According to United Nations and Canadian Forest Service statistics, Canada's softwood reservoir could be exhausted in 40 years. The editor of _World Wood Review,_ Herbert Lambert, tells us that we "will be unable to look northward beyond the year 2000" for our lumber. The fact is that if present trends continue, we are fast approaching the time when there will be nowhere at all to look for lumber or any other wood products. _I think that I shall never see a poem lovely as a tree._ —JOYCE KILMER At the present rate of deforestation in the United States, it won't be long before we never see a tree, period. I was stunned to learn that at the rate we are going, the United States will be stripped completely bare of _all_ its forests in 50 years ### **Our Oxygen Partners** We need our forests. They are vital sources of oxygen. They moderate our climates, prevent floods, and are our best defense against soil erosion. Forests recycle and purify our water. They are homes for millions of plants and animals. They are a source of beauty, inspiration, and solace to millions of people. The Bureau of Land Management and the Forest Service say there is nothing we can do to stem the tragic destruction of our forests. "People have to eat," said one agency official, shaking his head. And he's right—assuming the present meat habit, there is nothing we can do to save our forests. But diet-style changes could not only halt the process of deforestation but actually reverse it. Of the 260 million acres of American forest that have been converted into land now used to produce the standard American high-fat, low-fiber diet-style, well over 200 million acres could be returned to forest if Americans were to stop raising food to feed livestock and instead raise food directly for people. Indeed, so direct is the relationship between meat production and deforestation that Cornell economist David Fields and his associate Robin Hur estimate that for every person who switches to a pure vegetarian diet, an acre of trees is spared every year. A lacto-ovo vegetarian diet-style is also helpful, particularly if dairy and egg product consumption is low. A new direction for Americans' diet-style would go a long way beyond just saving our forests and rebuilding the ones we have destroyed. It would mean that our children could yet have wood with which to build and could yet live in a world rich with trees. It is probably the most potent single act most individuals can take at the present time in the effort to halt the destruction of our environment and preserve our precious natural resources. ### **Half of All Species on Earth** It is not only American forests that are being cut down to support our meat habit. An ever-increasing amount of beef eaten in the United States is imported from Central and South America. To provide pasture for cattle, these countries have been clearing their priceless tropical rain forests. It stretches the imagination to conceive how fast the timeless rain forests of Central America are being destroyed so Americans can have seemingly cheap hamburgers. In 1960, when the United States first began to import beef, Central America was blessed with 130,000 square miles of virgin rain forest. But now, only 25 years later, less than 80,000 square miles remain. At this rate, all of the tropical rain forests of Central America will be gone in another 40 years. These tropical rain forests are among the world's most precious natural resources. Amounting to only 30 percent of the world's forests, the rain forests contain 80 percent of the earth's land vegetation and account for a substantial percentage of the earth's oxygen supplies. These forests are the oldest ecosystems on earth and have developed extreme ecological richness. Half of all species on earth live in the moist tropical rain forests. But these jewels of nature are being rapidly destroyed to provide land on which cattle can be grazed for the American fast-food market. According to the Meat Importers Council of America, we now import 10 percent of our beef consumption, and over 90 percent of that is from Central and Latin America. In 1985, we imported over 100,000 tons of meat from Costa Rica, El Salvador, Guatemala, Honduras, Nicaragua, and Panama. The Meat Importers Council reports that almost all of this meat ends up as fast-food restaurant hamburgers. Interestingly, the rapidly growing trees and plants of the ageless Central and Latin American rain forests have consumed virtually all the minerals from the soil. Far more than in northern forests, tropical rain forests store their nutrients in their trees and plants, and not in the soil. As a result, when these forests are cleared, the grazing land that is produced is not the same as, say, Texas grazing land. It is so poor in minerals that vegetation has a hard time growing back at all. Further, without a plant cover the heavy rains cause extremely rapid soil erosion. Immediately after clearing, two and a half acres of ex–rain forest land can support a steer. But within a few years the land becomes so eroded that a single steer needs 12 acres. In 10 years, so barren has the land become that a steer may now require 20 acres. America's meat habit is turning the lush tropical rain forests into deserts useless even for cattle grazing. Meanwhile, the native people suffer increasingly. As valuable farmland is used to grow food for cattle, the price and availability of native foods is pushed beyond the reach of many of the local people. The result is that many of them are starving to death. In addition, there is increased flooding and firewood scarcity. And, tragically, native rain forest tribes are being wiped out completely by the destruction of their environment. What is left of the rain forests still contains much of the world's greatest treasures. Though a third of Costa Rica is today given over to cattle raising, the remainder of this tiny country still houses more bird species than all of the United States combined. But the continuing destruction of the rain forests jeopardizes the very existence of the animals, plants, and peoples whose natural habitats are being rapidly hacked out of existence. With the decimation of the Central American rain forests, many of our migratory birds are losing their winter homes. As a result, they are dying. This is tragic not merely because these birds provide so much beauty to our lives. They also play a major role in keeping down the populations of insect pests in the United States. The destruction of the rain forests in Central America is thus producing a substantial increase in pesticide use in this country. This destruction is occurring just as integrated pest management programs that entail selected breeding of adapted species of insects are showing great promise to supplant pesticides as a method of controlling insect pests. "Ironically, many of the most promising biological control programs involve importing beneficial insects from the tropical rainforests." At the present pace of our meat habit, however, many of the potentially beneficial insect species will be destroyed, along with their habitats, before we get a chance to use them to replace pesticides. It is truly frightening to note that the current rate of species extinction in the world is 1,000 species a year, and most of that is due to the destruction of rain forests and related habitats in the tropics. And as these environments continue to be destroyed, the rate of extinction is rising rapidly. If present trends continue, in the 1990s the figure will reach 10,000 a year (that's over one species every hour). In the next 30 years, over a million species will become extinct. We still know very little about the natural treasures of the tropical rain forests, although it is clear that their preservation is essential to the ecology, not only of our hemisphere, but of the world. One-quarter of our medicines derive from raw materials found in these forests. Indeed, a child suffering from leukemia now has an 80 percent chance of survival instead of only a 20 percent chance, thanks to the alkaloidal drugs vincristine and vinblastine, which are derived from a rain forest plant called the rosy periwinkle. Since less than 1 percent of the plant species of the tropical rain forests have been tested for medicinal benefits, researchers feel that here lie what could be the medicines of the future. So damning is the evidence against U.S. hamburger chains in the destruction of the rain forests that the Rainforest Action Network has called for a national campaign to boycott Burger King. Calling the company "a driving force behind this environmental disaster," the Rainforest Action Network has purchased a series of ads in major newsmagazines to inform the public of the hidden price we pay for such meat: _Before the rainforest was bulldozed and burned, it was home to thousands of rare and exotic species. After the cattle have come and gone, it's an eroded wasteland, practically empty of life...Activists in more than a dozen nations are fighting back—for the jaguars, orchids and howler monkeys. And for the millions of human beings who directly depend on the living rainforests for physical and cultural survival._ A new direction for America's eating habits would go a long way toward saving the remaining tropical rain forests and the countless species that will otherwise become extinct. The rain forests also produce extremely significant amounts of the world's oxygen supply. A new direction for America's diet-style would mean our children could yet have plentiful oxygen to breathe. ### **The Fountain of Life** Life on earth began in water and has always depended for its very existence on water. With water, life can thrive and bloom, and deserts can be transformed into gardens, lush forests, or thriving metropolises like Tel Aviv or Los Angeles. Without water, we die. Yet most of us are so used to having this precious resource at our fingertips that we have come to take it for granted. Sadly, we are fast approaching the time when we will be forced to learn the inestimable value of this natural treasure the hard way. Our supply of good water is disappearing at a terrifying rate. The source of this ominous trend can be traced directly to our meat habit. Over half the total amount of water consumed in the United States goes to irrigate land growing feed and fodder for livestock. Enormous additional quantities of water must also be used to wash away the animals' excrement. It would be hard to design a less water-efficient diet-style than the one we have come to think of as normal. To produce a single pound of meat takes an average of 2,500 gallons of water—as much as a typical family uses for all its combined household purposes in a month. To produce a day's food for one meat-eater takes over 4,000 gallons; for a lacto-ovo vegetarian, only 1,200 gallons; for a pure vegetarian, only 300 gallons. It takes less water to produce a _year's_ food for a pure vegetarian than to produce a _month's_ food for a meat-eater. The amount of water consumed by America's meat habit is staggering. It takes up to 100 times more water to produce a pound of meat than it does to produce a pound of wheat. Rice takes more water than any other grain, but even rice requires only a tenth as much water per pound of production as meat. It's not easy to conceive how huge are the quantities of water consumed in the production of meat. _Newsweek_ magazine, with an eye to the picturesque phrase, portrayed the situation this way: _The water that goes into a 1,000 pound steer would float a destroyer._ Consumption of so much water has serious economic, as well as ecological, consequences. The economic costs are hidden from us, though, because our federal and state governments subsidize the meat industry's water consumption at every stage of the process. If these costs were not borne unknowingly by the taxpayer, but instead showed up at the supermarket cash register, the industry would long ago have gone bankrupt. If the cost of water needed to produce a pound of meat were not subsidized, the cheapest hamburger meat would cost more than $35 a pound! Cornell economist David Fields and his associate Robin Hur have studied the fiscal consequences of water subsidies to the meat industry: _Reports by the General Accounting Office, the Rand Corporation, and the Water Resources Council have made it clear that irrigation water subsidies to livestock producers are economically counterproductive. Every dollar that state governments dole out to livestock producers, in the form of irrigation subsidies, actually costs tax payers over seven dollars in lost wages, higher living costs, and reduced business income..._ _The 17 Western states receive limited precipitation, yet their water supplies could support an economy and population twice the size of their present ones. But most of the water goes to produce livestock, either directly or indirectly. Thus, current water use practices now threaten to undermine the economies of every state in the region._ When I first heard statements like these, I was flabbergasted. I could not understand how water subsidies to livestock producers could be undermining the economies of every western state. I thought these economists must be exaggerating, to make a point. But the more I've learned, the more I've seen how severe indeed are the fiscal ramifications of pouring away such prodigious quantities of water to support our meat habit. For example, in the Pacific Northwest (Oregon, Washington, and Idaho), meat production accounts for over half the water consumed in the entire region. And yet, even though the meat producers of the Pacific Northwest use such a disproportionate share of the area's water, they aren't all that productive. These states have to import most of their meat. You may think the Pacific Northwest is amply supplied with rain and rivers. But the people of this area are paying an onerous price for spending so much water to produce so little meat, a price concealed in the region's soaring electrical costs. These states get over 80 percent of their electricity from hydropower plants, many of which are located along the Snake River in Idaho and the Columbia River in Washington. The water flowing in these rivers is the source of much of the state's electrical power. But the water used for livestock production in the Pacific Northwest also comes mainly from these same rivers, and it is taken from the rivers at points upstream from the power plants. The quantity of water taken from these rivers to grow livestock feed and otherwise produce meat is so huge that the amount of water left in the rivers to generate electricity is substantially reduced. Thus, electricity becomes more expensive to produce, the price rises, and the government must look elsewhere for sources of electricity. Hence the need for nuclear power plants in the area. Not only do livestock producers deplete the state's electrical power capacities through siphoning off water that would otherwise generate power, but they also use enormous amounts of electricity to pump the water from the rivers to the point of use. All in all, economists calculate that the three-state area loses 17 billion kilowatt hours of electricity a year to the gluttonous water use of livestock production. That's enough to light every house in the entire nation for a month and a half. The enormous loss of electrical power to the meat industry in the Pacific Northwest is one of the main reasons the region has had to continue the construction of the two nuclear power plants near Hanover, Washington, despite the fact that the cost overruns on these plants have been ludicrous, and hardly anyone is convinced they are safe. Area residents have already had to pay $4,000 per household for the privilege of living in the shadow of these nuclear plants, and current estimates are that by the time the nuclear plants are in operation, each household will have to pay another $3,000. Those who cannot pay will have to go into debt. Many already have. Due to their outrageous water consumption, the livestock industries of the Pacific Northwest account for more energy loss than will be gained by the nuclear plants. Farther south, we have the sunny state of California. California is known for its great grape vineyards, its lush fields of strawberries and artichokes, its vast acreages of lettuce and broccoli, its immense orange, lemon, and avocado orchards. Yet livestock producers are California's biggest water consumer. You might think that all this water consumption would at least create jobs. But no other industry in the country even comes close to the meat industry when it comes to the paucity of jobs created per gallon of water consumed. For every job created by livestock production in California, it uses 30 million gallons of water a year, far more than any other industry. Economist Douglas McDonald estimates that if water subsidies were withdrawn from California livestock producers, the income of the state's other businesses and workers would rise over $10 billion annually. Other economists have exposed the cost of water subsidies to the meat industry that are hidden in the state's rising prices for water rights and thus housing. Economists Fields and Hur calculate the overall price of subsidizing the California meat industry's water to be $24 billion. That's $1,000 for every man, woman, and child in the nation's most populous state—a state that imports most of its meat. Though the economic consequences of water subsidies to livestock producers are not always apparent to the uninformed public, they are felt by every citizen in every part of the country. Fields and Hur have concluded that while the meat industry likes to portray itself as the backbone of the American economy, in truth it is more of a back-breaking burden. Half of the nation's grain-fed beef is produced in the High Plains regions of Kansas, Nebraska, Oklahoma, Colorado, and New Mexico. The enormous amount of water needed for what amounts to the lion's share of the nation's meat production comes from a single source—the Ogallala Aquifer. Fifty years ago, the great Ogallala Aquifer remained virtually inviolate, hardly touched by the amount of water being pumped out of her enormous reservoirs. But with the advent of factory farming and feedlot beef, the amount of water drawn from the Ogallala has risen dramatically. At the present time, over 13 trillion gallons of water are being taken from this enormous aquifer every year, and the vast majority of that is used to produce meat. More water is withdrawn from the Ogallala Aquifer every year than is used to grow all the fruits and vegetables in the entire country. It took nature millions of years to form the great Ogallala Aquifer. And she still contains as much water as any of the Great Lakes. But the American meat habit is taking its toll on this priceless wonder of nature. Water tables are dropping precipitously. Wells are going dry. And water resource experts are estimating that at the current rate of water consumption, the Ogallala Aquifer may be exhausted in 35 years. If this happens, the High Plains of the United States will be completely uninhabitable to human beings. _The frog does not drink up the pond in which he lives._ —BUDDHIST PROVERB All over the country, the utterly disproportionate share of our water resources being used by the meat industry is creating shortages requiring deeper wells, which are more expensive to drill and more expensive to pump. In many areas, people and industries are being forced to settle for water of poorer and poorer quality, at higher and higher costs. Just in the past 20 years alone, Texas has used up one-quarter of its entire supply of groundwater. Most of that water was used to grow sorghum to feed cattle. A new direction for America's diet-style would plug the drain through which our nation's water is being lost. It would enable us to conserve this most precious of natural resources. It would mean that our children could yet have ample water to drink. ### **Quite a Pile** The standard American diet of today not only wastes prodigious amounts of water; it pollutes much of what is left. Fifty years ago, most of the manure from livestock returned to enrich the soil. But today, with huge numbers of animals concentrated in feedlots, confinement buildings, and other factory farm locations, there is no economically feasible way to return their wastes to the soil. As a result there is a continuing decline in soil humus and soil fertility, an increasing dependence on chemical fertilizers and pesticides, and an accelerating loss of topsoil. It is far removed indeed from the natural ecological cycle, in which animal wastes return to the soil and provide the nutrients for next year's crops. Sadly, instead of being returned to the soil, the wastes from today's animals often end up in our water. This is extremely significant, because the quantity of waste is so immense. It is a real challenge to our imaginations to conceive how much manure is produced by the animals in this country being raised for meats, dairy products, and eggs. Every 24 hours, the animals destined for America's dinner tables produce 20 billion pounds of waste. That is 250,000 pounds of excrement a second. The livestock of the United States produce _20 times as much excrement as the entire human population of the country_ Over half this staggering production—over a billion tons a year—comes from confinement operations from which it cannot be recycled. A typical egg factory, with 60,000 hens, produces 165,000 pounds of excrement every week. But that's chicken feed, so to speak, compared to a relatively small pork operation, with, say, 2,000 pigs. Here an average day's production includes four tons of manure and five tons of urine. When you start talking about cows, however, you really get into the big time. _One cow produces as much waste as 16 humans. With 20,000 animals in our pens, we have a problem equal to a city of 320,000 people._ —HARRY J. WEBB, PRESIDENT, BLAIR CATTLE COMPANY, BLAIR, NEBRASKA The largest feedlots, with 100,000 cattle, have a problem equal to that of the most populous American cities. Unlike the residents of New York, Los Angeles, or Chicago, however, the residents of feedlots do not pay taxes out of which sewage systems can be constructed. The result is that their waste tends to end up in our water. Animal waste is high in nitrogen, which is one of the chief reasons it makes such good fertilizer if it's returned to the soil. But unreturned, much of the nitrogen converts to ammonia and nitrates. The dumping of livestock wastes into our water is one of the reasons more and more rural wells are encountering dangerously high nitrate levels. Even city water supplies are increasingly high in nitrates. This is an ominous trend, because levels of nitrates in water that do no harm to adults cause serious brain damage, and even death, to infants. It may not seem to you or me that dumping vast amounts of livestock wastes into our nation's streams, rivers, and lakes makes ecological sense. But the U.S. Department of Agriculture used to encourage beef producers to locate their feedlots on hillsides near streams to make it easier to channel the wastes into the water. Feedlots are no longer encouraged simply to dump their wastes into our waterways, but a lot of it still ends up there. The result is algae overgrowth and oxygen depletion. As a consequence, many of our rivers, streams, and lakes can now barely support fish or any other animal life. When _Newsweek_ asked Dr. Harold Bernard about the runoffs from U.S. feedlots, the EPA agricultural expert did not mince words. He said feedlot wastes are _ten to several hundred times more concentrated than raw domestic sewage...When the highly concentrated wastes in a runoff flow into a stream or river, the results can be, and frequently are, catastrophic. The amount of dissolved oxygen in the waterway will be sharply reduced, while levels of ammonia, nitrates, phosphates and bacteria soar._ I must admit that I have had a hard time comprehending the overwhelming quantity of water pollution in the United States that ensues directly from livestock production. But animal wastes account for more than 10 times as much water pollution as the total amount attributable to the entire human population Astoundingly, the meat industry single-handedly accounts for more than three times as much harmful organic waste water pollution as the rest of the nation's industries combined A new direction for America's diet-style would do more to conserve and clean up our nation's water than any other single action. Indeed, each family that stops eating meat spares our waterways ever more pollution. A new direction for America's diet-style would mean that the water in our children's lives might yet be clean. ### **The Energy Crisis and Nuclear Power** When most of us think of the energy crisis, we think of lowering thermostats, weather-stripping doors and windows, and remembering to turn off the lights. We think of driving compact instead of luxury cars. We think of OPEC and the volatile price of oil. Some of us remember long gas lines and the very real threat of oil shortages that could cripple the economy and devastate our lives. Some of us fear that our dependence on foreign oil may force us to become militarily involved in the Persian Gulf. Very few of us realize how much our food choices have to do with all this. Growing any kind of food, and getting it to our homes and restaurants, takes energy. But some foods take considerably more than others. Turning an amber field of wheat into Twinkies uses up a lot more energy than turning it into whole-wheat bread. Refining and processing foods uses up more energy than consuming these foods in their more natural states. A regular-size box of Wheaties costs $1.65 at my local market; yet it contains only $0.06 worth of wheat. The box itself costs more than that. When it comes to resource and energy wastage, however, meat products are in a class by themselves. Scientists compute the energy costs of foods by the value of the raw materials consumed in the production of that food. Frances Moore Lappé reports: _A detailed 1978 study sponsored by the Departments of Interior and Commerce produced startling figures showing that the value of raw materials consumed to produce food from livestock is greater than the value of all oil, gas, and coal consumed in this country._ The same study revealed the equally startling fact that the production of meats, dairy products, and eggs accounts for _one-third of the total amount of all raw materials used for all purposes in the United States._ In contrast, growing grains, vegetables, and fruits is a model of efficiency, using less than 5 percent of the raw material consumption of the production of meat. A new direction for America's diet-style would mean a savings of over 30 percent of all the raw materials presently consumed in the country for all purposes. Another way scientists compute the energy costs of various foods is to assess the amount of fossil fuel needed to produce them. An American scientist, David Pimentel, calculates that if the whole world were to eat according to U.S. agricultural practices, the planet's entire petroleum reserves would be exhausted in 13 years. It is actually quite astounding how much energy is wasted by the standard American diet-style. Even driving many gas-guzzling luxury cars can conserve energy over walking—that is, when the calories you burn walking come from the standard American diet This is because the energy needed to produce the food you would burn in walking a given distance is greater than the energy needed to fuel your car to travel the same distance, assuming that the car gets 24 miles per gallon or better. This remarkable fact does not arise because our cars deserve a gold medal for energy efficiency. They don't. They burn up enough energy to blow up a bridge every four miles. But today's meat production systems are an energy conservationist's worst nightmare come true. On a traditional farm, pigs and chickens kept warm in the winter by nestling in bedding. And in the summer they would cool off in shady, damp soil. In today's factory farms, however, there is no bedding and no shady, damp soil. In order to maximize the animals' weight gain under these conditions, temperatures must be artificially controlled, and that takes energy. Further heat is needed because the young animals are separated from the warmth of their mothers' bodies. Baby animals by nature are vulnerable to chills, and their situation is more precarious when they are taken from their mothers and put on cold concrete or drafty metal-slat floors. More energy is needed to bring feed to the animals. And more is needed to move their wastes away. In fact, the whole assembly-line factory farming system is explicitly designed at every step to minimize human labor and instead use machines that consume energy. As a result, these factories provide hardly any jobs, considering the size of the operations. And they tend to use up our limited stores of fossil fuels as if there were no tomorrow. At the rate they're going, there won't be. Agricultural engineers at Ohio State University compared the energy costs of producing poultry, pork, and other meats with the energy costs of producing soybeans, corn, and other plant foods. They found that even the _least_ energy-efficient plant food is _nearly 10 times_ as efficient as the _most_ energy-efficient animal food: _Even the best of the animal enterprises examined returns only 34.5 percent of the investment of fossil energy to us in food energy, whereas the poorest of five crop enterprises examined returns 328 percent._ Other studies show the same pattern. Corn and wheat provide 22 times more protein per calorie of fossil fuel expended than does feedlot beef. Soybeans are even better—40 times more efficient than feedlot beef We can see why a feature article in _Scientific American_ devoted to the energy crisis warned: _The trends in meat consumption and energy consumption are on a collision course._ A new direction to America's diet-style would save an immense amount of energy. If we kicked the meat habit there would be no need for nuclear power plants. Our electric bills would be far lower than they are now. Our dependence on foreign oil would be greatly reduced. We would have the time and resources to develop solar and other environmentally sound energy sources. Our children might yet live in a world abundant with energy resources. ### **Hard-Nosed Businessmen** Over and over again, as I've envisioned the possibilities ensuing from a new direction for America's diet-style, I've been struck by what might be gained by such a move. I've seen how helpful it could be toward reducing world hunger, toward reducing the fear in the world that leads to wars, toward preserving our precious topsoil and forests, toward saving thousands of species in the tropical rain forests from extinction, toward cleaning up and preserving our water. And I've been moved by how much animal suffering would be alleviated, how our health would improve, and how greatly we could diminish our use and intake of toxic chemicals that threaten so seriously the future of our species. But there is yet another factor pointing in the same direction, one that might turn the heads of even the most hard-nosed American businessmen: it is actually quite astounding how good a new American diet would be for the economy. Economists Fields and Hur report: _A nationwide switch to a diet emphasizing whole grains, fresh fruits and vegetables—plus limits on export of nonessential fatty foods—would save enough money to cut our imported oil requirements by over60 percent. And, the supply of renewable energy, such as wood and hydroelectric, would increase 120 to 150 percent._ Extrapolating from these energy savings, these economists have analyzed the impact such a diet-style switch would have on the economy. The impact they see is formidable. They see substantial increases in personal savings accruing from reduced expenditures for food, prescription drugs, medical care, and insurance. And within a short time, they see even more personal savings accruing from savings on housing, energy, transportation, and clothing. As a result, they say: _A typical household of three could expect to save $4,000 a year in the short run. And, if they put aside 30 percent of those savings—and it is quite possible they could put aside up to half—the supply of lendable funds from personal savings would rise 50 percent._ Such a rise in lendable funds from personal savings would be extremely important to the economy. Personal savings are the economy's main source of funds for expansion. As the supply of such funds rose, the price of these funds—otherwise known as interest rates—would come down. Interest rates would be brought down from another angle as well. Savings on energy imports would ease the pressure on the national debt. This, in turn, would substantially reduce government borrowing needs. Currently, to finance the ungodly growth of the national debt, the government has to siphon off half the reservoir of funds, mainly personal savings that are the fuel for the nation's economic growth. But the combination of increased personal savings and lowered government borrowing, say economists Fields and Hur, would be a _double-barreled blast at high interest rates._ As interest rates dropped, the snowball of economic benefits to the country would really get rolling. And meanwhile, a meatless diet-style would be saving enormous amounts of money presently spent on medical care and person-hours lost to sickness. Say these economists: _Savings on health care alone could be expected to reach $100 billion within five years._ As the economy began to really hum with the decreased energy expenditures, savings would come from every direction, including reduced interest on the national debt as the government's borrowing needs continued to diminish. The savings on water subsidies to meat producers alone would be worth billions of dollars a year. Within five years, calculate Fields and Hur, total savings would reach $80 billion a year. In 20 years, according to their estimates, savings would reach $200 billion a year. At present, the hideous growth of the federal deficit amounts to the mortgaging of our children's future. The legacy we are now leaving them is a debt so large many economists foresee no way they could ever hope to repay it. But if the economic scenario of Fields and Hur is correct, the savings deriving from a new direction in America's diet-style would enable the United States government to eliminate the federal deficit. Perhaps our children might yet live in a sane and prosperous world. ### **The Unforgettable Dream** At the present time, when most of us sit down to eat, we aren't very aware of how our food choices affect the world. We don't realize that in every Big Mac there is a piece of the tropical rain forests, and with every billion burgers sold another 100 species become extinct. We don't realize that in the sizzle of our steaks there is the suffering of animals, the mining of our topsoil, the slashing of our forests, the harming of our economy, and the eroding of our health. We don't hear in the sizzle the cry of the hungry millions who might otherwise be fed. We don't see the toxic poisons accumulating in the food chains, poisoning our children and our earth for generations to come. But once we become aware of the impact of our food choices, we can never really forget. Of course we can push it all to the back of our minds, and we may need to do this, at times, to endure the enormity of what is involved. But the earth itself will remind us, as will our children, and the animals and the forests and the sky and the rivers, that we are part of this earth, and it is part of us. All things are deeply connected, and so the choices we make in our daily lives have enormous influence, not only on our own health and vitality, but also on the lives of other beings, and indeed on the destiny of life on earth. Thankfully, we have cause to be grateful—what's best for us personally is also best for other forms of life, and for the life-support systems on which we all depend. The Indians who dwelt for countless centuries in what we now call the United States lived in harmony with the land and with nature. Their societies were each unique, yet all were founded on a reverence for life that conserved nature rather than destroying it, and that lived in balance with what we today call the ecosystem. To them, it was all the work of God. Every shining pine needle, every sandy shore, every mist in the dark woods, every humming insect was holy. When the white man forced them to make the ultimate sacrifice and sell their land, the great Chief Seattle spoke for his people and asked one thing in return. He did not ask something for himself, or for his tribe, or even for the Indian people. There were, of course, many things of immense importance he must have wanted at such a time. He could have asked for more blankets, horses, or food. He could have asked that the ancestral burial grounds be respected. He could have asked many things for himself or for his people. But what stood above all else in importance had to do with the relationship between humans and other animals. His one request was as prophetic as it was plain: _I will make one condition._ _The white man must treat the beasts of this land_ _as his brothers...._ _For whatever happens to the beasts_ _soon happens to man._ _All things are connected._ Chief Seattle spoke for a people whose bond with the natural world was unimaginably profound. Yet the white man called them savages and utterly disregarded his plea. The factory farms that produce today's meats, dairy products, and eggs are living testimony to how totally we have disdained the one condition he made. The white man thought Chief Seattle an ignorant savage. But he was a prophet whose wisdom and eloquence arose from living contact with Creation. And his words are astoundingly similar to those of a book written long, long ago. The Bible, too, tells us that the fates of humans and animals are intimately intertwined. _For that which befalleth the sons of men befalleth the beasts._ _Even one thing befalleth them:_ _as the one dieth, so dieth the other;_ _yea, they have all one breath,_ _so that a man hath no pre-eminence above a beast._ —ECCLESIASTES 3:19 Chief Seattle did not know that centuries before a book called the Bible had spoken in words almost identical to his own. But he spoke on behalf of life itself, and the wisdom of the ages poured through him. Today, when we have strayed so very far from an ethical relationship to other creatures and to the welfare of the world we share, his message remains with us as a light of immeasurable brilliance. Never before has the truth of his words been so apparent: _One thing we know: Our God is the same. This earth is precious to Him... This we know:_ _The earth does not belong to man:_ _Man belongs to the earth._ _This we know:_ _All things are connected_ _Like the blood which unites one family._ _All things are connected._ _Whatever befalls the earth_ _Befalls the sons of the earth._ _Man did not weave the web of life._ _He is merely a strand in it._ _Whatever he does to the web,_ _He does to himself._ ## **EPILOGUE TO THE 25TH ANNIVERSARY EDITION** There have been a tremendous number of important developments since _Diet for a New America_ was first published in 1987. Some of what has happened and continues to happen is bright and promising. But it is in the nature of our times that some of what is taking place, unfortunately, is much darker and more foreboding. ### **Animals** On the bright side on the animal front, we've seen an emerging recognition that all beings are related, and that how we treat animals says something important about who we are as people. There has also been a growing understanding that the confinement of animals in factory farms is a crime against nature, a violation of the ancient bond between humans and animals, and produces food that is damaging to the health of our bodies, our world, and our spirits. As the awareness of the intense cruelty involved in factory farms and feedlots has increased, a market has emerged for grass-fed beef, free-range eggs, and organic dairy products. But with no actual certification by third parties, agribusiness corporations have taken advantage of the situation to promote their products as humanely produced when in fact their practices are often barely, if at all, better than the industry norm. A case in point is the multimillion-dollar "Great cheese comes from happy cows—happy cows come from California" ad campaign. Featuring talking cows and extolling California cheese, the ads (which feature lush green pastures but were actually filmed in New Zealand) make a mockery of genuine consumer concerns for animal welfare. In fact, conditions in large California dairies are among the worst in the nation, which is why I have joined PETA in suing the California Milk Producers Association, which is responsible for the ads, for false advertising. When Oprah Winfrey learned about the unnatural feeds given to U.S. beef cattle, including the ground-up remains of dead cows, she declared on her popular TV show that she would never eat another hamburger. The cattlemen responded in 1996 by suing her for $20 million, claiming her actions unfairly stigmatized their business and, worst of all, reduced consumer demand for their products. They said they would drop the suit if she would, on air, eat a hamburger. She wouldn't, they didn't, and a landmark trial was held in Amarillo, Texas. It was a long and drawn-out battle, but Oprah ended up winning. Immediately after the verdict was rendered, she declared, "Free speech not only lives; it rocks." Then she added, "I'm still off hamburgers." The cattlemen weren't able to silence Oprah, but their efforts to stifle criticism continued. In 2006, the industry managed to get passed the Animal Enterprise Terrorism Act. Under this federal legislation, according to Congressman Robert Scott of Virginia, people "who conscientiously believe that it is their duty to peacefully protest" through civil disobedience could be labeled terrorists. Penalties for convictions can include "terrorism enhancements," which may add decades to sentences. What is the real purpose of such legislation if not to silence dissent? Nonviolent civil disobedience has a long and proud place in our nation's history, from early economic resistance to British rule, to Martin Luther King Jr. and the civil rights movement, and even the recent Occupy Wall Street protests. Laws that treat civil disobedience as terrorism threaten the rights of everyone. I've often thought that if people really knew how animals were treated in today's factory farms and slaughterhouses there would be a tremendous outcry. The livestock industry's need to keep the public blind to what actually takes place has led to bills being proposed in many states, including Florida, Iowa, Minnesota, and New York, that would specifically outlaw photographing and videotaping animal enterprises. Even taking a photograph of a factory farm from a public road would be punishable by jail time. A bill in Utah would treat videotaping a factory farm the same as assaulting a police officer. These ag-gag bills, as they are called, would turn factory farms into safe havens not only for animal abuse but also for environmental and food safety violations, dangerous working conditions, and other illegal behavior. On the one hand, recent decades have seen a growing public awareness of the intense abuse of animals that takes place every day in the meat, dairy, and egg industries. On the other hand, the livestock industry has been making a concerted effort to deflect public scrutiny from its practices. It remains to be seen which will prevail—the public's right to know or the industry's desire to conceal and deceive. ### **Health** On the health front, there has been a lot of bright news since the initial publication of _Diet for a New America._ The brilliant work of doctors like T. Colin Campbell, Caldwell Esselstyn, Dean Ornish, and Joel Fuhrman, along with many other dedicated health professionals, has made it increasingly clear that for the vast majority of people, a plant-strong diet is indeed a path to health and vitality. Dr. Campbell and his son Thomas wrote the bestseller _The China Study,_ describing the groundbreaking research that led them to conclude that the more nutrients we get from plants and the fewer from animal products, the healthier we are likely to be. The _New York Times_ called Dr. Campbell's original work "the most comprehensive large study ever undertaken of the relationship between diet and the risk of developing disease." Meanwhile, Dean Ornish, MD, president of the Preventive Medicine Research Institute, promotes a program focused on a low-fat, whole foods, near-vegan diet. Dr. Ornish has published a long series of peer-reviewed studies in the most prestigious medical journals, demonstrating that three-quarters of the patients who follow his program are able to not just arrest but actually reverse heart disease without surgery. Medicare has joined many insurance companies that now pay for patients to adopt the Ornish program. Nearly 80 percent of patients with severely clogged arteries are able to avoid bypass or angioplasty through the program. Caldwell B. Esselstyn, MD, director of the cardiovascular prevention and reversal program at the Cleveland Clinic Wellness Institute, reported in the _American Journal of Cardiology_ that in his study, "Patients became virtually heart-attack proof." Dr. Esselstyn's results were phenomenal. All the patients in his study had severe heart disease at the outset, and most were expected to live less than a year. Yet after 12 years on the program, 95 percent of them were alive and well. At the core of his program is a diet nearly identical to that advocated by Drs. Campbell and Ornish—a nutrient-dense, whole foods, low-fat, near-vegan diet. Even Bill Clinton was impressed. When he became president, his appetite was legendary and his waistline showed it. He loved hamburgers and doughnuts and was never known to turn down food on health grounds. But unbeknownst to Clinton, and undetected by White House doctors, plaque was building up in the arteries leading to his heart. In 2004, less than four years after leaving office, the 58-year-old Clinton underwent quadruple bypass surgery to restore blood flow to his heart. "I was lucky I did not die of a heart attack," he told CNN's Dr. Sanjay Gupta. In 2010, Clinton underwent another heart procedure. Two stents were placed inside one of his coronary arteries that had once again become clogged. Then Clinton made a decision that transformed his life and made him the world's most famous vegan. He lost more than 25 pounds and felt healthier than ever. He proudly told the press that he was now following the guidance of Drs. Campbell, Ornish, and Esselstyn. Some say that this kind of a diet is too radical, but Bill Clinton obviously doesn't think so. And neither does Dr. Esselstyn. He writes: _Some criticize this exclusively plant-based diet as extreme or draconian. Webster's dictionary defines draconian as "inhumanly cruel." A closerlook reveals that "extreme" or "inhumanly cruel" describes not plant-based nutrition, but the consequences of our present Western diet. Having a sternum divided for bypass surgery or a stroke that renders one an aphasic invalid can be construed as extreme; and having a breast, prostate, colon, or rectum removed to treat cancer may seem inhumanly cruel. These diseases are rarely seen in populations consuming a plant-based diet._ Dr. Ornish speaks similarly: _I don't understand why asking people to eat a well-balanced vegetarian diet is considered drastic, while it's medically conservative to cut people open or put them on powerful cholesterol-lowering drugs for the rest of their lives...Animal products are the main culprit in what is killing us. We can absolutely live better lives without them._ The growing awareness of the health value of a plant-strong diet is inspiring. So, too, is the movement toward food that is organic, sustainable, locally grown, minimally processed, and produced with respect for human rights. On the darker side, though, recent years have seen the widespread application of genetically engineered foods (also known as genetically modified organisms, or GMOs). As the agricultural biotechnology corporation Monsanto and its allies have sought to control the world's food supplies, they have ferociously fought every attempt to require labeling of foods made from their genetically modified seeds. They recognize, correctly, that if people knew, many wouldn't buy these "Frankenfood" products. Monsanto says there is no reason to be concerned, but I think there is. Genetically modified foods have been linked to toxic and allergic reactions in humans; sickness, sterility, and fatalities in livestock; and damage to virtually every organ studied in lab animals. Although it is difficult to be certain to what extent there is a causal connection, the spread of GMOs has exactly coincided with a substantial increase in food allergy rates, particularly in children. Genetically modified crops such as Bt corn and Bt cotton produce pesticides in every cell of the plant. This kills or deters insects, but the plants themselves are living pesticide factories. They are toxic, and not just to insects. Farmers in India who let their sheep graze on Bt cotton plants after the harvest saw thousands of sheep inexplicably die. Currently, the primary genetically engineered crops in the United States are soy, cotton, canola, corn, sugar beets, and Hawaiian papayas. Products derived from these crops are widely found in processed foods that include corn, soy, canola or cottonseed oil; soy protein; soy lecithin; cornstarch; corn syrup; high fructose corn syrup; and many other ingredients made from these plants. If you want to avoid GMOs, a great resource is www.nongmoshoppingguide.com. And if you want more information about GMOs and the effort to get them labeled, a terrific source is www.responsibletechnology.org. ### **The Environment** For the past few decades, there has been a growing awareness that what we do to the earth, we do to ourselves, and that we can't continue to inflict harm on the planet without endangering all that we love. In 1989, two years after the original _Diet for a New America_ was published, Bill McKibben wrote _The End of Nature,_ the first book for a general audience about something then called the greenhouse effect. It's now called global warming, and many scientists say it is becoming the most dangerous threat ever experienced by human civilization. Ed Ayres, the former editorial director of the Worldwatch Institute, called it "the most world-changing event in the history of our species—more world-changing than World War II, or the advent of the nuclear age, or the computer revolution." Summarizing our current predicament, the Worldwatch Institute says that if we do not radically change course, _Children born today will find their lives preoccupied with a host of hardships created by an inexorably warming world. Food supplies will be diminished and many of the world's forests will be destroyed._ It's taken us a while to grasp the significance of global warming, and I'm not sure we have even now. The idea that a species could irreversibly alter the planetary climate system is extremely new. Many of us have found it difficult to believe that the way we go about our daily lives could have such a tremendous impact. Events with enormous consequences are happening so rapidly that even the most well informed of us are having trouble keeping up. As recently as 1989, when NASA scientist James Hansen first told Congress that global warming had, in fact, begun, it was news even to most climatologists. Three years later, the United Nations held a landmark world summit on the environment in Rio de Janeiro. Nearly every government on earth participated, and more than 100 sent their heads of state. It was the largest gathering in world history devoted to the state of the earth. But the declaration issued at its conclusion made no mention of climate change. It still wasn't on the radar even of most environmentalists. Even today, many news-watching and otherwise educated people have only the haziest awareness of the significance of what is taking place. But the fact is, we have unbalanced the composition of gases in our atmosphere so dramatically that we are already seeing the consequences. In 2009, Bill McKibben, the author who first alerted the public to the treacherous waters ahead if we did nothing to avert global warming, spoke of how we have already altered, among many other things, the planet's hydrological cycles: _One of the key facts of the twenty-first century turns out to be that warm air holds more water vapor than cold: in arid areas this means increased evaporation and hence drought. And once that water is in the atmosphere, it will come down, which in most areas...means increased deluge and flood. Total rainfall across our continent is up 7 percent, and that huge change is accelerating. Worse, more and more of it comes in downpours...across the planet, flood damage is increasing by 5 percent a year._ That same year, Oxfam released an epic report titled "Suffering the Science." Even if we were now to put into practice all "the strictest possible curbs" on carbon emissions, the report concluded, "the prospects are very bleak for hundreds of millions of people, most of them among the world's poorest." Things are changing so fast it's hard to stay oriented. Even most oceanographers have been shocked at the speed with which the world's seas are acidifying. The oceans have been absorbing some of the excessive carbon dioxide we've been spewing into the atmosphere, and they've already become more acidic than at any time in the past 800,000 years. At current rates, by 2050 they will be more corrosive than at any time in the past 20 million years. Since most life in the oceans is extremely sensitive to even small changes in acidity, what may this bode for the future of our oceans? Certain species play such critical roles in the healthy functioning of natural systems that it's no exaggeration to say we depend on them for our very survival. Microscopic phytoplankton in the oceans, for example, produce half of the earth's oxygen. Rising ocean acidity has already led to a dramatic decline in the global population of these one-celled plants. If we reach a point where there is a sudden phytoplankton die-off, the consequences for all oxygen-dependent species could be catastrophic. The truth is that our actions are causing changes that are of enormous import to life on this planet. They are happening now. And they are happening fast. At this moment, every major glacier on earth is shrinking. In 20 years, those in Montana's Glacier National Park will be gone entirely. By the end of this century, it is virtually certain that the earth will be the hottest it has been in more than two million years. Within a decade or two, at the North Pole in the summer there will be no ice—just open ocean. There will still be ice on Greenland but much less than there is now. In just the past five years, more than a trillion tons of the island's ice has melted. The Greenland ice sheet is still vast, containing 8 percent of the freshwater on earth. But it is melting at an ever-accelerating rate, and if someday it melts entirely, low-lying coastal areas including New York, Miami, Tokyo, Shanghai, Venice, Mumbai, Dhaka, and Singapore would be flooded. And not only would many of the world's coastal cities be completely underwater, but so would the rice-growing river deltas of Asia, upon which a large portion of the human race depends for food. Climate refugees would number in the billions. The fossil fuel industries and others profiting from business as usual are not overly fond of the data about global warming. They have responded by doing everything they can to deflect responsibility and to confuse both the public and our elected officials. Their goal has been to "reposition global warming as theory rather than fact," according to an internal strategy memo unearthed by journalist Ross Gelbspan. Their motives are transparent. ExxonMobil made more money in 2006, 2007, and 2008 than any other company in the history of the world. Chevron was close behind. To some extent, this disinformation campaign has been successful. Many of us believe that considerable controversy about global warming still exists. Are scientists sure it is a reality? And even if the planet is warming, is the trend being caused by human activities or by natural events? But the consensus seems quite clear. In 2010, a study published in the _Proceedings of the National Academy of Sciences_ found that 97 percent of scientific experts agree that it is "very likely that anthropogenic [human-caused] greenhouse gases have been responsible for most of the unequivocal warming of the Earth's average global temperature in the second half of the twentieth century." What about the 3 percent who remain unconvinced? The study found their average expertise to be far below that of their colleagues, as measured by publication and citation rates. Every day, we hear politicians speak of global warming in the future tense, as something that we should heed, if at all, out of concern for our grandchildren. As Senator Joe Lieberman recently said: _Shame on us if 100 or 200 years from now our grandchildren and greatgrandchildren are living on a planet that has been irreparably damaged by global warming, and they ask, "How could those who came before us, who saw this coming, have let this happen?"_ But the truth we are struggling to face is that the problem is not something that will need to be reckoned with in 100 or 200 years. The more disturbing reality is that, during the past 20 years, while U.S. politicians have achieved a perfect bipartisan record of doing nothing about the threat, both the scale and the pace of the peril have been increasing exponentially. One of the most alarming aspects of climate change is that the warming caused by greenhouse gas emissions generates self-reinforcing feedback loops. For example, ice is white and reflects the sun's warmth. Land and ocean surfaces, in contrast, absorb more of the sun's warmth. Warming temperatures melt ice, which leads to more heat absorption, which leads to warmer temperatures, which melts more ice. It's a vicious circle. Enormous amounts of methane, to give another example, have been locked in Arctic permafrost for countless centuries. As the planet warms and the permafrost thaws, methane begins to escape into the atmosphere, where it causes more warming, which leads to more melting permafrost, which leads to more warming. There are so many such feedback mechanisms, in which the consequences of warming cause more warming, that a new and disconcerting phrase has entered the vocabulary of climatologists—"runaway climate change." It's tempting, when faced with such catastrophic scenarios, to want to close our eyes, to retreat behind a wall of denial, to escape, deflect, and distract. Our capacity for denial is part of our humanity and at times helps us to cope with overwhelming pressures. But in this case it also makes us receptive to the efforts of ExxonMobil and its allies, who would have us believe that there is a great deal of controversy in scientific circles, and that many scientists think man-made global warming is a myth. In 2012, the Union of Concerned Scientists declared: _There is no longer any doubt in the expert scientific community...The Earth is warming and human activity is the primary cause. Climate disruptions put our food and water supply at risk, endanger our health, jeopardize our national security, and threaten other basic human needs. Some impacts—such as record high temperatures, melting glaciers, and severe flooding and droughts—are already becoming increasingly common._ Many of us, of course, fervently hope the scientists are wrong. Would that they were, for it would be a source of tremendous relief if it turned out that the overwhelming consensus of the world's scientific community was completely mistaken. But for hope to be meaningful it must embrace reality and be grounded in the world as it is, not merely the world as we would like it to be. Real hope, mature hope, is predicated on understanding one of the defining realities of our time: The climate of our planet, the climate on which life as we know it utterly depends, is being dramatically altered by the way we live our lives. Under such circumstances, it is clear that if there is anything we can do to change course and help avert catastrophe, it is imperative that we know what this change is, and make it. Thankfully, there is. ### **A Step We Can Take** In late 2006, the Food and Agriculture Organization (FAO) of the United Nations released a seminal report, titled "Livestock's Long Shadow." Stunningly, the report found that "livestock are responsible for 18 percent of greenhouse gas emissions, a bigger share than that of transport." That is, the production of meat and other animal food products accounts for a far greater share of global warming gases than all the cars, trucks, ships, and airplanes in the world. The study found compelling evidence that "livestock are one of the most significant contributors to today's most serious environmental problems." Industrial livestock production, researchers found, is shrinking the earth's forests, eroding its soils, depleting its aquifers, collapsing its fisheries, elevating its temperatures, and melting its ice sheets. Strikingly, every single one of the serious ecological problems threatening to undercut human civilization would be made dramatically and rapidly better by a shift to a plant-strong diet. This is true, most centrally, of global warming. The costs of truly addressing the implications of what we are doing to the climate have been seen as insurmountable. But a follow-up study was published in the journal _Earth and Environmental Science,_ titled "Climate Benefits of a Changing Diet." Researchers came to the spectacular conclusion that a "global transition to a low-meat diet" would by itself reduce by 50 percent the anticipated costs of stabilizing the climate. They found that cutting back on industrial meat from feedlots and factory farms could save a staggering amount of money, wiping "$20 trillion off the cost of fighting climate change." The research has kept coming. Scientists at the University of Chicago calculated that switching from a standard American diet to a vegan one would have a greater impact than trading in a gas guzzler for a Toyota Prius. A study out of Carnegie Mellon University found that going meatless one day a week would do more for the climate than eating a totally locally grown diet. A 2009 study in _Scientific American_ found that beef contributes 13 times the greenhouse gas impact of chicken and 57 times that of potatoes. The meat industry, of course, would like us to believe that the issue is far from settled and so it would be rash to take action. But if you wanted to make such a case, you probably wouldn't want to debate the issue with Rajendra Pachauri, who is probably as knowledgeable about climate change as anyone on earth. He is the head of Yale University's Climate and Energy Institute and is the twice-elected chairperson of the Intergovernmental Panel on Climate Change, which was awarded the Nobel Peace Prize during his tenure. He stresses repeatedly that the production of modern meat is causing a stunningly high percentage of the problem, so much so that the best way to combat global warming is to eat less meat. "In terms of...the feasibility of bringing about reductions [in greenhouse gas emissions] in a short period of time, it clearly is the most attractive opportunity," he says. "Give up meat for one day [a week] at least initially, and decrease it from there." If people gave up meat for one day a week, would it really do any good? The Centre for Agriculture and Environment in the Netherlands found that if the people of the U.S. were to make one day a week meatless for a year, it would save the greenhouse gas emissions equivalent to 90 million passenger airplane flights between New York and Los Angeles. A 2007 study by the National Institute of Livestock and Grassland Science in Japan found that a single kilogram of beef is responsible for the equivalent amount of carbon dioxide emitted by the average European car every 155 miles and burns enough energy to light a 100-watt lightbulb for nearly 20 days. The take-home message? It's far more important to change your diet than to change your lightbulbs. Not too many people read the reports of the National Institute of Livestock and Grassland Science, but many do read the mainstream press. A feature article in _Time_ magazine asked the provocative question, "Which is responsible for more global warming: your BMW or your Big Mac?" The answer: "Believe it or not, it's the burger." In such articles the mainstream press has echoed the ever-increasing chorus of scientific studies that say that if you want to do something about global warming, if you want see our society lower its greenhouse gas emissions, one of the most important things you can do is to eat a plant-strong diet. This means getting more of your nutrients from plant foods and less from meat, dairy products, and eggs. It means eating mostly, if not exclusively, plants. These studies show us where our power lies and how we can really be effective. Of course, reversing global warming will require far more than a change in our diets. We need to replace fossil fuels with solar, wind, geothermal, and other renewable and nonpolluting sources of energy. We need to create economic policies that take into account the ecosystem on which all economic life depends. We need to invest our genius and our resources less in making war and more in reforestation, soil conservation, education, and family planning. We need to halt the liquidation of the planet's natural assets. We need to develop food systems with a lower carbon footprint that are more local and more organic. And while we're doing these things, we need to heed the avalanche of studies telling us that shifting to a plant-strong diet is clearly one of the most effective things we can do if we want to protect the climate. Not surprisingly, the U.S. meat industry has tried to counter these studies and has protested that livestock production isn't to blame for global warming. In particular, livestock interests have tried to persuade the public, opinion leaders, and government officials that the FAO indictment of meat titled "Livestock's Long Shadow" is overstated. But in 2009, the prestigious Worldwatch Institute published a landmark report that made the FAO report seem understated in comparison. This meticulously thorough study, written by World Bank agricultural scientists Robert Goodland, who spent 23 years as the World Bank's lead environmental adviser, and Jeff Anhang, an environmental specialist for the World Bank, came to a staggering conclusion: Animals raised for food actually account for more than half of all human-caused greenhouse gases. Eating plants instead of animals, the authors conclude, would be by far the most effective strategy to reverse climate change, because it "would have far more rapid effects on greenhouse gas emissions and their atmospheric concentrations—and thus on the rate the climate is warming—than actions to replace fossil fuels with renewable energy." Whether the percentage of greenhouse gas emissions attributable to livestock is 18 percent, as the FAO found, or more than 50 percent, as the World Bank scientists' research indicates, or perhaps somewhere in between, it is without question a staggering amount. And because changing our diets is something we all can do today, it is almost certainly the single most important key any individual holds to stabilizing our climate before it is too late. Writing in the _Washington Post,_ Ezra Klein spoke of why eating less meat is so clearly the best option: _Eating pasta...doesn't require a long commute on the bus or the disposable income to trade up to a Prius. It doesn't mean you have to scrounge for change to buy a carbon offset. In fact, it saves money. It's healthful. And it can be done immediately. A Montanan who drives 40 miles to work might not have the option to take public transportation. But he or she can probably pull off a veggie stew. A cash-strapped family might not be able to buy a [more efficient] new dishwasher. But it might be able to replace meatballs with mac-and-cheese...That is the whole point behind the cheery [peanut-butter-and-jelly sandwich] campaign, which reminds that "you can fight global warming by having a PB &J for lunch." Given that a PB&J is delicious, it's not the world's most onerous commitment._ _It's also worth saying that this is not a call for asceticism. It's not a value judgment on anyone's choices. Going vegetarian might not be as effective as going vegan, but it's better than eating meat, and eating meat less is better than eating meat more. It would be a whole lot better for the planet if everyone eliminated one meat meal a week than if a small core of die-hards developed perfectly virtuous diets...If we're going to take global warming seriously...there's no reason to ignore the impact of what we put on our plates._ Unlike shifting to hydrogen-powered vehicles or setting up electrical grids whose energy source is wind power, eating a plant-strong diet takes no new expensive infrastructure. Unlike putting solar panels on your roof, it requires no up-front investment of money. Shifting to a plant-strong diet actually saves you money (while also improving your health and sparing animals needless suffering). I often see very well-intentioned people spending significant amounts of money and going to all sorts of lengths to live a greener lifestyle. It's sadly ironic that they sometimes ignore what would be the most effective thing they could be doing. If we are really committed to saving the environment, we need to know where our leverage is. We need to know which of the actions we can take will be the most effective, and we need to focus where we can get the most benefit. Eating a plant-strong diet is a potent and profound point of leverage for everyone who longs to make a positive difference in this world. It is probably the single most immediately effective thing you can do to take a stand for life on earth. ### **Taking a Stand** In the past half century, the human relationship with the earth has fundamentally transformed. We have become a defining planetary force, massively impacting the soil, air, water, and climate of the entire world. In the nearly 4 billion years that life has existed on earth, no other species has ever attained anything resembling this kind of power. We have assumed this capacity at a mind-boggling speed. In a microsecond of geological time, we are now reshaping the biological and physical features on the planet. We are genetically engineering entirely new life-forms and releasing them, fundamentally untested, into the world and into our food supply on a vast scale. We are making choices that determine which species will survive and which will go extinct. And we are altering the chemistry of the atmosphere with potentially catastrophic effects. It is not easy to accept the notion that if we continue with business as usual we will bring about our own demise. But it isn't just the earth, or the animals with whom we share this planet, whose fate now hangs in the balance. It is also our own. Humanity, some might say, is facing its final test. Will we retreat into ever-narrower and more destructive forms of selfindulgence? Or will we finally learn to cooperate with our highest possibilities and fashion an effective response? I do not know the outcome. But I do know that every single effort that each of us makes is needed and important. I thank you for everything you have done, and everything you yet will do, to live with respect for yourself, for others, and for the web of life on our precious and endangered planet. May we find a way of life that enriches rather than depletes our world. _May All Be Fed, May All Be Healed, May All Be Loved._ ## **ENDNOTES** ##### **Chapter One. All God's Critters Have a Place in the Choir** . Account adapted from various sources, including Michael Fox, _Returning to Eden_ (New York: Viking Press, 1980), 3, and Cleveland Amory, _Animail_ (New York: Windmill Books, 1976), 34–35. . Account adapted from various sources, including B. Henkin, "Eight Unusual Dolphin Incidents," in Irving Wallace et al., _The Book of Lists #2_ (New York: Bantam Books, 1980), 107–8, and Amory, _Animail,_ 14–15. . Amory, _Animail,_ 193. . Soviet study in _Ogonyok_ cited in Jon Wynne-Tyson, ed., _The Extended Circle_ (Fontwell, UK: Centaur Press, 1985), 230, and Amory, _Animail,_ 188. . Stephen R. Kellert and Alan R. Felthous, "Childhood Cruelty toward Animals among Criminals and Noncriminals," _Human Relations_ 38, no. 12 (December 1985): 1113–20. . Rosanne Amberson, _Raising Your Cat_ (New York: Crown Publishers, 1969). . Gerald Carson, _Men, Beasts, and Gods: A History of Cruelty and Kindness to Animals_ (New York: Charles Scribner's Sons, 1972), 65; Dix Harwood, _Love for Animals and How It Developed in Great Britain_ (Lewiston, NY: Edwin Mellen Press, 1928/2002), 13–14n; Desmond Morris, _The Human Zoo_ (New York: McGraw-Hill, 1969), 76; Pope Pius XII, quoted in J. Quinn, "A Proper Respect for Men and Animals," _U.S. Catholic_ (June 1965). . Albert Schweitzer, letter to Japanese Animal Welfare Society, 1961. . Albert Schweitzer, quoted in Wynne-Tyson, _Extended Circle._ . Albert Schweitzer, _The Animal World of Albert Schweitzer_ (Boston: Beacon Press, 1950). . Henkin, "Eight Unusual Dolphin Incidents." . Ibid. . Account adapted from Quaker Oats Co. Ken-L-Ration "Dog Hero of the Year Award," in Amy Wallace, David Wallechinsky, and Irving Wallace, _The Book of Lists #3_ (New York: Bantam Books, 1983), 124–28. . Ibid. . Amory, _Animail,_ 18. . Carson, _Men, Beasts, and Gods,_ 65. . Account adapted from "Henry Bergh's Story," _Philadelphia Press,_ September 22, 1884, and ASPCA First Annual Report (New York, 1867) in Sydney Coleman, _Humane Society Leaders in America_ (Albany, NY: American Humane Association, 1924), 42–43. . Ibid. . Amory, _Animail,_ 31–32. . Henkin, "Eight Unusual Dolphin Incidents." . Ibid. . Ibid. . Fox, _Returning to Eden,_ 4. . Amory, _Animail,_ 185. . Lovat Dickson, _Wilderness Man_ (New York: Atheneum Press, 1973). . Cleveland Amory, _Man Kind?: Our Incredible War on Wildlife_ (New York: Harper & Row, 1974). . Ralph Helfer, quoted in Amory, _Animail,_ 92–93. . René Descartes, _Discourse on the Method of Rightly Conducting the Reason, and Seeking Truth in the Sciences,_ trans. John Veitch (Chicago: Open Court Publishing, 1920), iv. . Ibid., 5. . Carson, _Men, Beasts, and Gods,_ 64. . Richard Serjeant, _The Spectrum of Pain_ (London: Hart-Davis, 1969), 72. . Amory, _Animail,_ 59–60. . Ashley Montagu, _Touching_ (New York: Columbia University Press, 1971). . Lewis Regenstein, _The Politics of Extinction_ (New York: Macmillan Publishing Co., 1975), 52–59. . Ibid., 163–85. . R. K. Rasmussen, in Wallace, _Book of Lists #2,_ 270. . Ibid. . Ibid. . Ibid. . Ibid., 271. . Ibid. . Ibid. . Fox, _Returning to Eden,_ 10–11. . Amory, _Animail,_ 12. . Ibid. . Sheila Burnford, _The Incredible Journey_ (Boston: Little, Brown & Co., 1961). . Michael Fox, _Understanding Your Cat_ (New York: Coward, McCann & Geoghegan, 1974), 78. . Amory, _Animail,_ 28–29. . Karyl Carter, quoted in Amory, _Animail,_ 190–92. ##### **Chapter Two. Brave New Chicken** . Page Smith and Charles Daniel, _The Chicken Book_ (Boston: Little, Brown & Co., 1975), 51–124. . Ibid. . E. L. G. Watson, _Animals in Splendour_ (Camp Hill, PA: Horizon Press, 1967), 88. . Watson, _Animals in Splendour,_ 89. . Ibid. . Juvenal, cited in Smith and Daniel, _The Chicken Book,_ 160. . Study described in _Vegetarian Times_ (January 1984): 64. . Peter Singer, _Animal Liberation_ (New York: Avon Books, 1975), 102. . _Farmer and Stockbreeder,_ January 30, 1962. . Jim Mason and Peter Singer, _Animal Factories_ (New York: Crown Publishers, 1980), 5. . Textron from _Wall Street Journal,_ August 9, 1967. . Desmond Morris, "The Clockwork Egg," Food Animals Concern Trust (Chicago), FACT sheet no. 28 (February 1983). . Ian Duncan, "Can the Psychologist Measure Stress?" _New Scientist_ (October 18, 1973). . "How Egg Industry Changed during the Last 20 Years," _Poultry Digest_ (July 1978): 232. . _Farming Express,_ February 1, 1962. . Singer, _Animal Liberation,_ 99. . Ibid. . C. I. Angstrom, "Mechanical Failures Plague Cage-Layers," _Onondaga County Farm News_ (December 1970): 13. . Singer, _Animal Liberation,_ 103. . Ibid., 97. . Herbert Reed, personal communication with author. . Mason and Singer, _Animal Factories,_ 5. . Ruth Harrison, _Animal Machines_ (London: Vincent Stuart, 1964), 147. . Singer, _Animal Liberation,_ 112. . _Poultry Tribune,_ March 1974. . Roy Bedichek, _Adventures with a Texas Naturalist_ (Austin: University of Texas Press, 1961). . _Upstate,_ August 5, 1973. . Bedichek, _Texas Naturalist._ . _Poultry Tribune,_ February 1974. . Singer, _Animal Liberation,_ 111. . _Upstate,_ August 5, 1973. . Norris McWhirter, _Guinness Book of World Records_ (New York: Bantam Books, 1982), 377. . _National Geographic,_ February 1970. . J. North, "Catching Up on Smaller Profit Leaks," _Broiler Industry_ (June 1976): 41. . Mason and Singer, _Animal Factories,_ 42. . R. S. Gowe, director of the Animal Research Institute of Agriculture, Canada, at conference on "Livestock Intensive Methods of Production," Ottawa, December 6–7, 1978. . "Naked Chick Gets Serious Attention," _Broiler Industry_ (January 1979): 98; ABC News Closeup, "Food: Green Grow the Profits," December 21, 1973. . M. Dendy, "Broiler 'Flip-Over' Syndrome Still a Mystery," _Poultry Digest_ (September 1976): 380. . W. Wilson, "Poultry Production," _Scientific American_ (July 1976): 58. . Herbert Reed, personal communication with author. . Mason and Singer, _Animal Factories,_ 56–58. . Ibid. . Richard Wall, "Caged Layer Fatigue," _Poultry Digest_ (January 1976): 23. . Mason and Singer, _Animal Factories,_ 29. . Ibid. . Singer, _Animal Liberation,_ 110. . D. Shurter and E. Walter, "The Meat You Eat," _The Plain Truth_ (October-November 1970). . Fred Haley, quoted in _Poultry Tribune,_ January 1974. . Jim Hightower, _Eat Your Heart Out_ (New York: Crown Publishers, 1975). . William Stadelman, "Old-Time Flavor: New Injectables Possible," _Broiler Industry_ (April 1975): 79. . G. Leonardos, "Brand Life May Depend on Unique Flavors," _Broiler Industry_ (October 1976): 33. . Monroe Babcock, "Shrinking Egg Market Is Our Own Fault," _Egg Industry_ (January 1976): 29–30. . Mason and Singer, _Animal Factories,_ 8. . Richard Battaglia and Vernon Mayrose, _Handbook of Livestock Management Techniques_ (Minneapolis, MN: Burgess Publishing Co., 1981). . Bill Thompson, "In Search of the Natural Chicken," _East-West_ (April 1986): 38–45. ##### **Chapter Three. The Most Unjustly Maligned of All Animals** . W. H. Hudson, _The Book of a Naturalist_ (New York: George Doran Publishers, 1919), 295–302. . E. L. G. Watson, _Animals in Splendour_ (Camp Hill, PA: Horizon Press, 1967), 43–47. . Hudson, _Book of a Naturalist._ . Charles Joy, ed., _The Animal World of Albert Schweitzer_ (Boston: Beacon Press, 1950), 114–15. . Ibid., 116–17. . Orville Schell, _Modern Meat_ (New York: Random House, 1984), 59. . Ibid., 61–62. . J. Byrnes, "Raising Pigs by the Calendar at Maplewood Farm," _Hog Farm Management_ (September 1976): 30. . M. Hall, "Heating Systems for Swine Buildings," _Hog Farm Management_ (December 1975): 16. . N. Black, "Let's Give USDA to Do-Gooders, Gardeners," _National Hog Farmer_ (August 1976): 26. . _Farm Journal,_ August 1966. . Ibid. . Ibid. . _Farm Journal,_ November 1968. . Ibid. . Jim Mason and Peter Singer, _Animal Factories_ (New York: Crown Publishers, 1980), 30. . Peter Singer, _Animal Liberation_ (New York: Avon Books, 1975), 117. . _Farm Journal,_ May 1973. . _Farmer and Stockbreeder,_ July 11, 1961. . J. Messersmith, personal communication with author. . L. Taylor, _National Hog Farmer_ (March 1978): 27. . _Farm Journal,_ April 1970. . Singer, _Animal Liberation,_ 118. . Ibid. . Ibid. . Mason and Singer, _Animal Factories,_ 30–31, 42. . Ibid., 42. . Ibid., 43–44. . Schell, _Modern Meat,_ 186. . E. Ainsworth, "Revolution in Livestock Breeding on the Way," _Farm Journal_ (January 1976): 36. . J. Messersmith, personal communication with author. . Mason and Singer, _Animal Factories,_ 45. . "Scientist Studies 'Test Tube Pig,'" _Hog Farm Management_ (April 1975): 61. . "New Treatment Boosts Pigs per Litter," _Farm Journal_ (March 1976): 2. . Ibid. . Mason and Singer, _Animal Factories,_ 23–24. . "Tail-Biting Is Really Anticomfort Syndrome," _Hog Farm Management_ (March 1976): 94. . H. Sterkel, "Cut Light and Clamp Down on Tail-Biting," _Farm Journal_ (March 1976): 6. . Singer, _Animal Liberation,_ 114. . F. Butler, personal communication with author. . Mason and Singer, _Animal Factories,_ 45. . J. Byrnes, "Stacking 3 Decks of Pigs," _Hog Farm Management_ (January 1978): 16. . _An Enquiry into the Effects of Modern Livestock Production on the Total Environment_ (London: The Farm and Food Society, 1972), 12. . A. Koltveit, _Confinement_ (November-December 1976): 3. . Schell, _Modern Meat,_ 95. . Mason and Singer, _Animal Factories,_ 63. . Ibid., 49. . Ibid. . "Pig Health Losses Total $187 Million," _Farm Journal_ (September 1978): 2. . "Pseudorabies Eradication Plan Drafted," _National Hog Farmer_ (March 1977): 136. . J. Byrnes, "Demand Grows for PRV Vaccine," _Hog Farm Management_ (May 1977): 18–20. . "Area Depopulation Plan Suggested for Dominican," _National Hog Farmer_ (December 1978): 34. . R. Rhodes, "Watching the Animals," _Harper's_ (March 1970). ##### **Chapter Four. Holy Cow** . Story adapted from Joan Grant, _Lord of the Horizon_ (New York: Avon Books, 1969), 73–75. . Ibid., 79. . Story adapted from Joan Grant, _Winged Pharoah_ (Columbus, OH: Ariel Press, 1985), 78. . W. H. Hudson, _Afoot in England,_ cited in _The Extended Circle,_ ed. Jon Wynne-Tyson (Fontwell, UK: Centaur Press, 1985), 130. . Ovid, _Metamorphoses,_ cited in Wynne-Tyson, _Extended Circle,_ 232. . "Livestock Auction—An Arena of Animal Abuse," _Mainstream_ (Spring 1985): 16. . Peter Singer, _Animal Liberation_ (New York: Avon Books, 1975), 148. . Official Proceedings of the 58th Annual Meeting, Livestock Conservation, Omaha, Nebraska, May 1974, 44, 93. . Ibid. . Irving Wallace et al., _The Book of Lists #2_ (New York: Bantam Books, 1980), 240. . "Chloramphenicol Use by Cattlemen Said to Be Dangerous," _Vegetarian Times_ (September 1984): 6. . Singer, _Animal Liberation,_ 150. . Richard Battaglia and Vernon Mayrose, _Handbook of Livestock Management Techniques_ (Minneapolis, MN: Burgess Publishing Co., 1981). . _Pig Farming,_ September 1973. . Battaglia and Mayrose, _Livestock Management._ . Ibid. . R. Smith, quoted in _Farm Journal,_ December 1973. . Orville Schell, _Modern Meat_ (New York: Random House, 1984). . Singer, _Animal Liberation,_ 129. . Details in this paragraph from Dudley Giehl, _Vegetarianism_ (New York: Harper & Row, 1979), 119–20; Jim Hightower, _Eat Your Heart Out_ (New York: Crown Publishers, 1975), 99; Beatrice Hunter, _Consumer Beware_ (New York: Simon & Schuster, 1971), 113–14; Frances Moore Lappé, _Diet for a Small Planet_ (New York: Ballantine, 1982), 67–68; Schell, _Modern Meat,_ 125–26, 137, 143, 148–49, 167, 179–80; Singer, _Animal Liberation,_ 129; Jim Mason and Peter Singer, _Animal Factories_ (New York: Crown Publishers, 1980), 29–30, 48–49, 72; Vic Sussman, _The Vegetarian Alternative_ (Emmaus, PA: Rodale Press, 1978), 173–74. . "What Tells Cattle to Stop Eating?" _Beef_ (November 1976): 33. . _Farm Journal,_ December 1971. . James Beard, _American Cookery_ (New York: Little, Brown & Co., 1972), 331–32. . Quoted in Singer, _Animal Liberation,_ 126. . Food Animals Concern Trust (Chicago) newsletter. . "Sentenced for Life to a Factory Farm," Food Animals Concern Trust (Chicago) newsletter. . Food Animals Concern Trust (Chicago), FACT sheet no. 55 (June 1984). . Ibid. . Ibid. . Food Animals Concern Trust (Chicago), FACT sheet no. 23 (August 15, 1982). ##### **Chapter Five. Any Way You Slice It, It's Still Bologna** . Edgar Kupfer, "Animals, My Brethren," in Mark Braunstein, _Radical Vegetarianism_ (Los Angeles: Panjandrum Books, 1981), 133–35. . Braunstein, _Radical Vegetarianism,_ 113. . "Meat Board Report 1974–1975," National Livestock and Meat Board, 23. . Henry Salt, _Seventy Years among Savages_ (London: George Allen & Unwin, 1921), 9. . Isaac Bashevis Singer, "The Slaughterer," in _The Seance_ (New York: Avon Books, 1969), 24. . K. Gullo, "An Inside Look at the American Meat-Packing Industry," _Vegetarian Times_ (September 1983): 46–47, adapted from a five-part series by L. Ackland, _Chicago Tribune,_ June 5–9, 1983. . Ibid. . Orville Schell, _Modern Meat_ (New York: Random House, 1984), 308–9. . Gullo, "American Meat-Packing Industry." . Official Proceedings of the 58th Annual Meeting, Livestock Conservation, Omaha, Nebraska, May 1974, 49–50. . _Poultry World,_ June 14, 1962. . Peter Singer, _Animal Liberation_ (New York: Avon Books, 1975), 153. . Ibid., 155. . Ibid. . Ibid., 156. . Braunstein, _Radical Vegetarianism,_ 92. . R. Rhodes, "Watching the Animals," _Harper's_ (March 1970): 91. ##### **Chapter Six. Different Strokes for Different Folks** . Philip Kapleau, _To Cherish All Life_ (San Francisco: Harper & Row, 1981), 59. . John McDougall and Mary Ann McDougall, _The McDougall Plan_ (Piscataway, NJ: New Century Publishers, 1983), 7. . Roger J. Williams, _Nutrition against Disease_ (New York: Bantam Books, 1973), 12. . Ibid., 189. . For one example among many, see the _Journal of the American Medical Association_ (June 29, 1979): 2833. . Kenneth Buckley, personal communication with author. . Mikkel Hindhede, "The Effect of Food Restrictions during War on Mortality in Copenhagen," _Journal of the American Medical Association_ 74, no. 6 (1920): 381. . Ibid. . A. Strom and R. A. Jensen, "Mortality from Circulatory Diseases in Norway, 1940–1945," _Lancet_ 260 (1951): 126–29. . Vic Sussman, _The Vegetarian Alternative_ (Emmaus, PA: Rodale Press, 1978), 55. . Strom and Jensen, "Mortality from Circulatory Diseases," 67. . Ibid. . Robin Hur, _Food Reform: Our Desperate Need_ (Austin, TX: Heidelberg Publishers, 1975), 95. . Ibid., 2, 95–96. . A. Leaf, _National Geographic_ 143 (1973): 93. . Strom and Jensen, "Circulatory Diseases," 95. . Irving Fisher, "The Influence of Flesh Eating on Endurance," _Yale Medical Journal_ 13, no. 5 (1907): 205–21. . Ibid. . Ibid. . J. Ioteyko et al., _Enquete scientifique sur les vegetariens de Bruxelles_ (Brussels: Henri Lamertin), 50. . Per-Olaf Astrand, _Nutrition Today_ 3, no. 2 (1968): 9–11. . A. Schouteden, _Ann de Soc. des Sciences Med. et Nat. de Bruxelles_ (Belgium) I. . P. Dallman, _American Journal of Clinical Nutrition_ 33, no. 86 (1980); M. Murray, _American Journal of Clinical Nutrition_ 33, no. 697 (1980); and M. Abdulla, _American Journal of Clinical Nutrition_ 34, no. 2464 (1981). . D. Narins, in Anatoly Bezkorovainy, _Biochemistry of Nonheme Iron_ (New York: Plenum Press, 1980), 47–126. . Andrew Weil, _Health and Healing_ (Boston: Houghton Mifflin, 1983), 87–88. . E. G. Diamond et al., "Comparison of Internal Mammary Artery Ligation and Sham Operation for Angina Pectoris," _American Journal of Cardiology_ 5 (1960): 483. . Ibid. ##### **Chapter Seven. The Rise and Fall of the Protein Empire** . Patricia Hausman, _Jack Sprat's Legacy_ (New York: Richard Marek Publishers, 1981), 16–17, 25–39. . N. Scrimshaw, "An Analysis of Past and Present Recommended Dietary Allowances for Protein in Health and Disease," _New England Journal of Medicine_ (January 22, 1976): 200; M. Irwin, "A Conspectus of Research on Protein Requirements of Man," _Journal of Nutrition_ 101 (1975): 385. . David Reuben, _Everything You Always Wanted to Know about Nutrition_ (New York: Avon Books, 1978), 154–55. . D. Hegsted, "Minimum Protein Requirements of Adults," _American Journal of Clinical Nutrition_ 21 (1968): 3520; W. Rose, "The Amino Acid Requirements of Adult Man, XVI..." _Journal of Biological Chemistry_ 217 (1955): 997. . E. Stare, "Nutrition," _Annual Review of Biochemistry_ 14 (1945): 431. . World Health Organization, _Protein Requirements: Report of a Joint FAO/WHO Expert Group,_ WHO Technical Report Series No. 301 (Geneva: World Health Organization, 1965). . C. Pfeiffer, _Mental and Elemental Nutrients_ (New Canaan, CT: Keats Publishing, 1975). . Food and Nutrition Board, _Recommended Daily Allowances_ (Washington, DC: National Academy of Sciences). . National Research Council, _Recommended Dietary Allowances,_ 9th ed. (Washington, DC: National Academy of Sciences, 1980), 46. . Roger J. Williams, "We Abnormal Normals," _Nutrition Today_ 2 (1967): 19–28. . Data from _Nutritive Value of American Foods in Common Units,_ Agriculture Handbook No. 456; see also _Ford Heritage, Composition and Facts about Foods_ (Mokelumne Hill, CA: Health Heritage, 1971). . P. Markakis, "The Nutritive Quality of Potato Protein," in _Protein Nutritional Quality of Foods and Feeds,_ pt. 2, ed. M. Friedman (New York: M. Dekker, 1975); E. Kofranyi et al., "The Minimum Protein Requirement of Humans...," in Keith Akers, _A Vegetarian Sourcebook_ (New York: G. P. Putnam's Sons, 1983), 205; S. Kon, "The Value of Potatoes in Human Nutrition," _Journal of Biological Chemistry_ 22 (1928): 258. . T. Osborn, "Amino Acids in Nutrition and Growth," _Journal of Biological Chemistry_ 17 (1914): 325. . W. Rose, "Comparative Growth of Diets...," _Journal of Biological Chemistry_ 176 (1948): 753. . A. Sanchez et al., "Nutritive Value of Selected Proteins and Protein Combinations," _American Journal of Clinical Nutrition_ 13, no. 4 (October 1963): 247; John McDougall and Mary Ann McDougall, _The McDougall Plan_ (Piscataway, NJ: New Century Publishers, 1983), 96. . S. B. Vaghefi et al., "Lysine Supplementation of Wheat Proteins," _American Journal of Clinical Nutrition_ 27 (1974): 1231. . Frances Moore Lappé, _Diet for a Small Planet_ (New York: Ballantine Books, 1982). . Nathan Pritikin, quoted in V _egetarian Times_ 43 (1981): 22. . Lappé, _Diet for a Small Planet._ . Ibid., 162, 172. . Ibid., 162. . Ibid. . Editorial, _The Lancet_ 2 (1959): 956. . Mervyn Hardinge et al., "Nutritional Studies of Vegetarians: Part V, Proteins...," _Journal of the American Dietetic Association_ 48, no. 1 (January 1966): 27; Mervyn Hardinge et al., "Nutritional Studies of Vegetarians: Part I...," _Journal of Clinical Nutrition_ 2, no. 2 (March–April 1984): 81; P. Hausman, "Protein: Enough Is Enough," _Nutrition Action_ (October 1977): 4. . Food and Nutrition Board, _Vegetarian Diets_ (Washington, DC: National Academy of Sciences, 1974), 2. . D. Hegsted, cited in U. D. Register et al., "The Vegetarian Diet," _Journal of the American Dietetic Association_ 62, no. 3 (1973): 255. . Hardinge, "Nutritional Studies." . Ibid. . John Scharffenberg, _Problems with Meat_ (Santa Barbara, CA: Woodbridge Press, 1982), 90. . Nathan Pritikin, quoted in _Vegetarian Times_ 43 (1981): 21. . Hardinge, "Nutritional Studies"; D. McLaren, "The Great Protein Fiasco," _Lancet_ 2 (1974): 93. . B. Nicol et al., "The Utilization of Proteins and Amino Acids in Diets Based on Cassava...," _British Journal of Nutrition_ 39, no. 2 (1978): 271. . C. Gopalan, "Effect of Calorie Supplementation on Growth of Undernourished Children," _American Journal of Clinical Nutrition_ 26 (1973): 563; Michael Golden, "Protein Deficiency, Energy Deficiency, and the Oedema of Malnutrition," _Lancet_ 2 (1974): 93; Guillermo Lopez de Romana, "Prolonged Consumption of Potato-Based Diets by Infants and Small Children," _Journal of Nutrition_ 111 (1981): 1430; Guillermo Lopez de Romana, "Utilization of the Protein and Energy of the White Potato by Human Infants," _Journal of Nutrition_ 110 (1980): 1849. . McLaren, "Great Protein Fiasco," 95; Gopalan, "Calorie Supplementation"; Emmett Holt, _Protein and Amino Acid Requirements in Early Life_ (New York: New York University Press, 1960), 12; D. McLaren, "A Fresh Look at Protein-Calorie Malnutrition," _Lancet_ 2 (1966): 485. . Arnold Schwarzenegger, _Arnold's Bodybuilding for Men_ (New York: Simon & Schuster, 1981). . National Academy of Sciences, _Recommended Dietary Allowances,_ 8th ed. (Washington, DC, 1974), 43. . O. Bodansky, _Biochemistry of Disease,_ 2nd ed. (New York: Macmillan, 1952), 784. . V. Barzel, _Osteoporosis_ (New York: Grune & Stratton, 1970). . Ibid. . R. Heaney, "Calcium Nutrition and Bone Health in the Elderly," _American Journal of Clinical Nutrition_ 36 (1982): 986; C. Paterson, "Calcium Requirements in Man: A Critical Review," _Postgrad Medical Journal_ 54 (1978): 244; Alexander Walker, "The Human Requirement of Calcium: Should Low Intakes Be Supplemented?," _American Journal of Clinical Nutrition_ 25 (1972): 518; "Symposium on Human Calcium Requirements: Council on Foods and Nutrition," _Journal of the American Medical Association_ 185 (1963): 588. . Nancy Johnson et al., "Effect of Level of Protein Intake on Urinary and Fecal Calcium and Calcium Retention...," _Journal of Nutrition_ 100 (1970): 1425; L. Allen et al., "Protein-Induced Hypercalcuria: A Longer-Term Study," _American Journal of Clinical Nutrition_ 32 (1979): 741. . L. Solomon, "Osteoporosis and Fracture of the Femoral Neck in the South African Bantu," _Journal of Bone and Joint Surgery_ 50B (1968): 2; John McDougall, _McDougall's Medicine_ (Piscataway, NJ: New Century Publishing, 1985), 61–96. . Allen, "Protein-Induced Hypercalcuria"; Steven Altchuler, "Dietary Protein and Calcium Loss: A Review," _Nutritional Research_ 2 (1982): 193; McDougall and McDougall, _McDougall Plan,_ 101. . Solomon, "South African Bantu"; M. Hegsted, "Urinary Calcium and Calcium Balance in Young Men as Affected by Level of Protein and Phosphorus Intake," _Journal of Nutrition_ 111 (1981): 553; C. Anand, "Effect of Protein Intake on Calcium Balance in Young Men Given 500 mg Calcium Daily," _Journal of Nutrition_ 104 (1974): 695; R. Walker, "Calcium Retention in the Adult Human Male as Affected by Protein Intake," _Journal of Nutrition_ 102 (1972): 1297; Johnson, "Fecal Calcium and Calcium Retention," 1425; H. Linkswiler, "Calcium Retention of Young Adult Males as Affected by Level of Protein and Calcium Intake," _Transactions of the New York Academy of Science_ 36 (1974): 333; Altchuler, "Dietary Protein." . McDougall, _McDougall's Medicine,_ 75. . J. Chalmers, "Geographic Variations of Senile Osteoporosis," _Journal of Bone and Joint Surgery_ 52B (1970): 667. . Walker, "Human Requirement of Calcium"; McDougall, _McDougall's Medicine,_ 67. . Nathan Pritikin, quoted in _Vegetarian Times_ 43 (1981): 22. . Alexander Walker, "Osteoporosis and Calcium Deficiency," _American Journal of Clinical Nutrition_ 16 (1965): 327. . R. Smith, "Epidemiologic Studies of Osteoporosis in Women of Puerto Rico and Southeastern Michigan...," _Clinical Orthopaedics and Related Research_ 45 (1966): 32. . Solomon, "South African Bantu"; Walker, "Human Requirement of Calcium"; Alexander Walker, "The Influence of Numerous Pregnancies and Lactations on Bone Dimensions in South African Bantu and Caucasian Mothers," _Clinical Science_ 42 (1972): 189; Walker, "Osteoporosis and Calcium Deficiency." . Richard Mazess and Warren Mather, "Bone Mineral Content of North Alaskan Eskimos, _Journal of Clinical Nutrition_ 27 (1974): 916. . Ibid. . Ibid. . Frey Ellis et al., "Incidence of Osteoporosis in Vegetarians and Omnivores," _American Journal of Clinical Nutrition_ 25 (1972): 555. . _American Journal of Clinical Nutrition,_ March 1983. . Ellis, "Incidence of Osteoporosis"; Aaron Watchman et al., "Diet and Osteoporosis," _Lancet_ (May 4, 1968): 958. . _Vegetarian Times_ (April 1984): 32. . R. A. McCance and E. M. Widdowson, _The Composition of Foods_ (London: Her Majesty's Stationery Office, 1960). . Robin Hur, _Food Reform: Our Desperate Need_ (Austin, TX: Heidelberg Publishers, 1975), 98–107; B. G. Shah et al., _Journal of Nutrition_ 92, no. 1 (1967): 30. . Hur, _Food Reform,_ 102. . Hur, _Food Reform,_ 103; and from USDA Handbook No. 8 (1963). . R. Recker, "The Effect of Milk Supplements on Calcium Metabolism, Bone Metabolism, and Calcium Balance," _American Journal of Clinical Nutrition_ 41 (1985): 254. . L. Nilas, "Calcium Supplementation and Postmenopausal Bone Loss," _British Medical Journal_ 289 (1984): 1103. . Watchman, "Diet and Osteoporosis." . W. Robertson, "Should Recurrent Calcium Oxalate Stone Formers Become Vegetarians?" _British Journal of Urology_ 51 (1979): 427; E. Coe, "Eating Too Much Meat Called Major Cause of Renal Stones," _Internal Medicine News_ 12 (1979): 1; "Urinary Calcium and Dietary Protein," _Nutritional Review_ 38 (1980): 9; "Diet and Urinary Calculi," _Nutritional Review_ 38 (1980): 74; P. Shah, "Dietary Calcium and Idiopathic Hypercalcuria," _Lancet_ 1 (1981): 786. . B. Brenner, "Dietary Protein Intake and the Progressive Nature of Kidney Disease...," _New England Journal of Medicine_ 307 (1982): 652; M. Walser, "Nutritional Support in Renal Failure: Future Directions," _Lancet_ 1 (1983): 340. . E. Shilling, _Nutrition Abstracts and Reviews_ 33 (1963): 114. . Brenner, "Dietary Protein Intake"; Walser, "Nutritional Support in Renal Failure"; M. Walser, "Does Dietary Therapy Have a Role in the Predialysis Patient?," _American Journal of Clinical Nutrition_ 33 (1980): 1629. . McDougall and McDougall, _McDougall Plan,_ 103–4. . M. H. Ross, "Protein, Calories, and Life Expectancy," _Fed Proc_ 18 (1959): 1190–1207; A. Exton-Smith, "Physiological Aspects of Aging: Relationship to Nutrition," _American Journal of Clinical Nutrition_ 25 (1972): 853–59; P. Krohn, "Rapid Growth, Short Life," _Journal of the American Medical Association_ 171 (1959): 461; Henry Sherman, _Chemistry of Food and Nutrition_ (New York: Macmillan, 1952), 208; Henry Sherman, _The Science of Nutrition_ (New York: Columbia University Press, 1943), 177–98. . Krohn, "Rapid Growth, Short Life." . T. Colin Campbell, quoted in S. Lang, "Diet and Disease," _Food Monitor_ (May/June 1983): 24. . Myron Winick, quoted in D. Goodman, "Breaking the Protein Myth," _Whole Life Times_ (July/August 1984): 26. ##### **Chapter Eight. Food for the Caring Heart** . For further details on these dietary correlations, see the following: T. Gordon, "Premature Mortality from Coronary Heart Disease: The Framingham Study," _Journal of the American Medical Association_ 215 (1971): 1617; Cedric Bainton, "Deaths from Coronary Heart Disease...," _New England Journal of Medicine_ 268 (1963): 569; William Kannel, "Incidence and Prognosis of Unrecognized Myocardial Infarction—An Update on the Framingham Study," _New England Journal of Medicine_ 311 (1984): 1144; Dean Ornish, "Effects of Stress Management Training and Dietary Changes in Treating Isochemic Heart Disease," _Journal of the American Medical Association_ 249 (1983): 54; L. Thuesen, "Beneficial Effect of a Lowfat Low-Calorie Diet on...Angina Pectoris," _Lancet_ 2 (1984): 59; Frey Ellis, "Angina and Vegan Diet," _American Heart Journal_ 93 (1977): 803; Nathan Pritikin, "Diet and Exercise as a Total Therapeutic Regimen for...Severe Peripheral Vascular Disease," 52nd Annual Session of the American Congress of Rehabilitation Medicine, Atlanta, 1975; J. Ribeiro, "The Effectiveness of a Low Lipid Diet...Coronary Artery Disease," _American Heart Journal_ 108 (1984): 1183; L. Goldman, "The Decline in Ischemic Heart Disease Mortality Rates...," _Annals of Internal Medicine_ 101 (1984): 825; "Trials of Coronary Heart Disease Prevention," _Lancet_ 2 (1982): 803; Tavia Gordon, "Diet and Its Relation to Coronary Heart Disease...," _Circulation_ 63 (1981): 500; V. Kallio, "Reduction in Sudden Deaths...after Acute Myocardial Infarction," _Lancet_ 2 (1979): 1091; Lipid Research Clinics Program, The Lipid Research Clinics Coronary Primary Prevention Trial Results, "I. Reduction in Incidence of Coronary Heart Disease," _Journal of the American Medical Association_ 251 (1984): 351; Lipid Research Clinics Program, The Lipid Research Clinics Coronary Primary Prevention Trial Results, "II. The Relationship of Reduction in Incidence of Coronary Heart Disease to Cholesterol Lowering," _Journal of the American Medical Association_ 251 (1984): 365; W. Connor, "The Key Role of Nutritional Factors in the Prevention of Coronary Heart Disease," _Preventive Medicine_ 1 (1972): 49; C. Taylor, "Spontaneously Occurring...of Cholesterol," _American Journal of Clinical Nutrition_ 32 (1979): 40; Charles Welch, "Cinecoronary Arteriography...," _Circulation_ 42 (1970): 647; Irvine Page, "Prediction of Coronary Heart Disease...," _Circulation_ 42 (1970): 625; A. Zampogna, "Relationship between Lipids and Occlusive Coronary Artery Disease," _Archives of Internal Medicine_ 140 (1980): 1067; P. Cohn, "Serum Lipid Levels...Coronary Artery Disease," _Annals of Internal Medicine_ 84 (1976): 241; P. Jenkins, "Severity of Coronary Artherosclerosis...," _British Medical Journal_ 2 (1978): 388; William Kannel, "Cholesterol in the Prediction of Atherosclerotic Disease: New Perspectives Based on the Framingham Study," _Annals of Internal Medicine_ 90 (1979): 85; J. Anderson, "The Dependence of the Effects of Cholesterol...," _American Journal of Clinical Nutrition_ 29 (1976): 1784; R. Jackson, "Influence of Polyunsaturated and Saturated Fats...," _American Journal of Clinical Nutrition_ 39 (1984): 589; M. Flynn, "Serum Lipids in Humans Fed Diets Containing Beef or Fish and Poultry," _American Journal of Clinical Nutrition_ 34 (1981): 2734; M. Flynn, "Dietary 'Meats' and Serum Lipids," _American Journal of Clinical Nutrition_ 35 (1982): 935; B. O'Brien, "Human Plasma Lipid Responses to Red Meat, Poultry, Fish, and Eggs," _American Journal of Clinical Nutrition_ 33 (1980): 2573; R. Acheson, "Does Consumption of Fruit and Vegetables Protect against Stroke?" _Lancet_ 1 (1983): 1191; R. Shekelle, "Diet, Serum Cholesterol, and Death from Coronary Heart Disease," _New England Journal of Medicine_ 304 (1981): 65; Denis Burkitt, "Some Diseases Characteristic of Modern Western Civilization," _British Medical Journal_ 1 (1973): 274; F. Mattson, "Effect of Dietary Cholesterol on Serum Cholesterol in Man," _American Journal of Clinical Nutrition_ 25 (1972): 589; Ancel Keys, "Serum Cholesterol Response to Changes in Dietary Lipids," _American Journal of Clinical Nutrition_ 19 (1966): 175; K. Carroll, "Hypocholesterolemic Effect of...," _American Journal of Clinical Nutrition_ 31 (1978): 1312; D. Kritchevsky, "Dietary Fiber and Other Dietary Factors in Hypercholesteremia," _American Journal of Clinical Nutrition_ 30 (1977): 979; Kyu Taik Lee, "Geographic Studies of Atherosclerosis: The Effect of a Strict Vegetarian Diet...," _Archives of Environmental Health_ 4 (1962): 14; R. Walden, "Effect of...among Seventh Day Adventists," _American Journal of Medicine_ 36 (1964): 271; Mervyn Hardinge, "Nutritional Studies of Vegetarians: IV Dietary Fatty Acids and Serum Cholesterol Levels," _American Journal of Clinical Nutrition_ 10 (1962): 522; J. Barrow, "Studies in Atherosclerosis...," _Annals of Internal Medicine_ 52 (1960): 372; Ancel Keys, "Serum Cholesterol...The Effect of Cholesterol in the Diet," _Metabolism_ 14 (1965): 759; Ancel Keys, "Serum Cholesterol...Particular Saturated Fatty Acids," _Metabolism_ 14 (1965): 776; D. Hegsted, "Quantitative Effects of Dietary Fat on Serum Cholesterol in Man," _American Journal of Clinical Nutrition_ 17 (1965): 281; R. Mahley, "Alterations in...Plasma Cholesterol, Induced by Diets High in Cholesterol," _Lancet_ 2 (1978): 807; William Kannel, "Serum Cholesterol, Lipoproteins, and the Risk of Coronary Heart Disease," _Annals of Internal Medicine_ 74 (1971): 1; W. Castelli, "HDL-Cholesterol...in Coronary Heart Disease," _Circulation_ 55 (1977): 767; Thomas Robertson, "Epidemiologic Studies of Coronary Heart Disease and Stroke...," _American Journal of Cardiology_ 39 (1977): 244; M. Miettinen, "Effect of Cholesterol-Lowering Diet on Mortality from Coronary Heart Disease...," _Lancet_ 2 (1972): 835. . William Enos, "Pathogenesis of Coronary Disease in American Soldiers Killed in Korea," _Journal of the American Medical Association_ 158 (1955): 912; William Collens, "Atherosclerotic Disease: An Anthropologic Theory," _Medical Counterpoint_ (December 1969): 54. . Kyu Taik Lee, "Chemicopathologic Studies...," _Archives of Internal Medicine_ 109 (1962): 426; Patricia Hausman, _Jack Sprat's Legacy_ (New York: Richard Marek Publishers, 1981), 28, 196. . Hausman, _Jack Sprat's Legacy,_ 53. . Ibid., 53–61, 68, 85–86. . M. Marmot, "Epidemiologic Studies of Coronary Heart Disease and Stroke in Japanese Men...," _American Journal of Epidemiology_ 102 (1975): 511. . Ancel Keys, ed., _Coronary Heart Disease in Seven Countries,_ American Heart Association monograph no. 29, Circulation 41, Supplement 1 (1970): 211; Ancel Keys, ed., _Seven Countries—A Multivariate Analysis of Death and Coronary Heart Disease in Ten Years_ (Cambridge, MA: Harvard University Press, 1980). . Ibid. . Robert Wissler, "Studies of Regression of Advanced Atherosclerosis in Experimental Animals and Man," _Annals of the New York Academy of Science_ 275 (1976): 363. . Mark Armstrong, "Regression of Coronary Atheromatosis in Rhesus Monkeys," _Circulation Research_ 27 (1970): 59. . Collens, "Atherosclerotic Disease." . R. Phillips, "Coronary Heart Disease Mortality among Seventh Day Adventists with Differing Dietary Habits," Abstract, American Public Health Association Meeting, Chicago, November 16–20, 1975. . J. Ruys, "Serum Cholesterol...in Australian Adolescent Vegetarians," _British Medical Journal_ 6027 (1976): 87; Frank Sacks, "Plasma Lipids and Lipoproteins in Vegetarians and Controls," _New England Journal of Medicine_ 292 (1975): 1148; Frank Sacks, "Blood...in Vegetarians," _American Journal of Epidemiology_ 100 (1974): 390; B. Armstrong, "Blood...," _American Journal of Epidemiology_ 105 (1977): 444; C. Sirtori, "Soybean Protein Diet...," _Lancet_ 8006 (1977): 275; Barrow, "Studies in Atherosclerosis"; Phillips, "Coronary Heart Disease Mortality"; R. Phillips, "Coronary Heart Disease...Differing Dietary Habits: A Preliminary Report," _American Journal of Clinical Nutrition_ 31 (1978): 181. . C. Walles, "Hold the Eggs and Butter: Cholesterol Is Proved Deadly and Our Diet May Never Be the Same," _Time,_ March 26, 1984, 62. . Kaare Norum, "What Is the Expert's Opinion on Diet and Coronary Heart Diseases?" _Journal of the Norwegian Medical Association_ (February 12, 1977), cited by Senator Edward Kennedy in testimony to Senate Select Committee on Nutrition and Human Needs, March 24, 1977. . Pascal Imperato and Greg Mitchell, _Acceptable Risks_ (New York: Viking, 1985), 9–24; Michael Coleman, "The Research Smokescreen: Moving from Academic Debate to Action on Smoking," _New York State Journal of Medicine_ 13 (1983): 1280; Ken Cummins, "The Cigarette Makers: How They Get Away with Murder, with the Press as an Accessory," _Washington Monthly_ 3 (1984): 14; Alan Blum, ed., "The Cigarette Pandemic," _New York State Journal of Medicine_ 83 (1983): 13; A. Hartz, "Smoking, Coronary Artery Occlusion...," _Journal of the American Medical Association_ 246 (1981): 851; William Kannel, "Cigarettes, Coronary Occlusions and Myocardial Infarction," _Journal of the American Medical Association_ 246 (1981): 871. . Tom Koch, "The Mad Nasty Book," _Mad_ (Winter 1985): 56. . Michael Jacobson, preface to Hausman, _Jack Sprat's Legacy,_ 13–19. . Imperato and Mitchell, _Acceptable Risks,_ 69. . "Hubbards Awarded for Worst Ads of the Year," Associated Press, _Santa Cruz Sentinel,_ June 14, 1985, A-6. . B. Liebman, Center for Science in the Public Interest, in _Nutrition Action,_ cited in _Vegetarian Times_ (July 1985). . Frank Oski, _Don't Drink Your Milk_ (Chicago: Wyden Books, 1977), 6. . Cited in Dudley Giehl, _Vegetarianism_ (New York: Harper & Row, 1977), 3. . J. Mayer, "Egg vs. Cholesterol Battle," _New York Daily News,_ October 9, 1974, 48. . Hausman, _Jack Sprat's Legacy,_ 218. . Ibid. . Ibid., 219. . "Orders a Stop on Egg Claims," _New York Daily News,_ December 12, 1975, 62. . Ibid. . Cited in Hausman, _Jack Sprat's Legacy,_ 219. . M. Flynn, "Effect of Dietary Egg on Human Serum Cholesterol and Triglycerides," _American Journal of Clinical Nutrition_ 32 (1979): 1051; G. Slater, "Plasma Cholesterol and Triglycerides in Men with Added Eggs in the Diet," _Nutrition Reports International_ 14 (1976): 249; T. Dawber, "Eggs, Serum Cholesterol, and Coronary Heart Disease," _American Journal of Clinical Nutrition_ 36 (1982): 617; M. Porter, "Effect of Dietary Egg on Serum Cholesterol and Triglyceride of Human Males," _American Journal of Clinical Nutrition_ 30 (1977): 490; E. Flaim, "Plasma Lipid...," _American Journal of Clinical Nutrition_ 34 (1981): 1103. . John McDougall and Mary Ann McDougall, _The McDougall Plan_ (Piscataway, NJ: New Century Publishers, 1983), 56. . O'Brien, "Human Plasma Lipid Responses"; S. Roberts, "Does Egg Feeding (i.e. Dietary Cholesterol) Affect Plasma Cholesterol Levels in Humans? The Results of a Double Blind Study," _American Journal of Clinical Nutrition_ 34 (1981): 2092; M. McMurry, "Dietary Cholesterol and the Plasma Lipids...," _American Journal of Clinical Nutrition_ 37 (1982): 741; Mattson, "Effect of Dietary Cholesterol." . Hausman, _Jack Sprat's Legacy,_ 214. . Ibid. . Frank Sacks, "Ingestion of Egg Raises Plasma Low Density Lipoproteins in Free-Living Subjects," _Lancet_ 1 (1984): 647. . U.S. Senate Select Committee on Nutrition and Human Needs, "Diet Related to Killer Diseases, Volume 6, Response Regarding Eggs," hearing July 26, 1977. . Hausman, _Jack Sprat's Legacy,_ 221. . Robert Levy, quoted in Hausman, _Jack Sprat's Legacy,_ 215. . Task Force to the American Society of Clinical Nutrition, quoted in Hausman, _Jack Sprat's Legacy,_ 93–94. . Ibid., 216. . Ibid., 214–16. . Roberts, "Does Egg Feeding"; O'Brien, "Human Plasma Lipid Responses"; Mattson, "Effect of Dietary Cholesterol"; William Connor, "The Interrelated Effects of Dietary Cholesterol and Fat upon Human Serum Lipid Levels," _Journal of Clinical Investigation_ 43 (1964): 1691. . Mattson, "Effect of Dietary Cholesterol." . Imperato and Mitchell, _Acceptable Risks,_ 65–66. . Quoted in Hausman, _Jack Sprat's Legacy,_ 205. . "Milk Still Makes a Difference," National Dairy Council, quoted in Hausman, _Jack Sprat's Legacy,_ 206. . Jacobson, preface to Hausman, _Jack Sprat's Legacy,_ 17. . Sheila Harty, _Hucksters in the Classroom_ (Washington, DC: Center for Study of Responsive Law, 1979), 23. . National Dairy Council, Nutrition Education Materials catalog 1985–1986, pp. 16–22. . Ibid., 16, reference no. 0920N. . Ibid., 17, reference no. 092IN. . Quoted in Hausman, _Jack Sprat's Legacy,_ 207. . Harty, _Hucksters in the Classroom,_ 24. . Quoted in Hausman, _Jack Sprat's Legacy,_ 207. . Ibid. . Ibid. . Ibid. . Harty, _Hucksters in the Classroom,_ 24. . Ibid. . Hausman, _Jack Sprat's Legacy,_ 40–49. . Ibid., 44–45. . "Myths and Facts about Meat Products," Oscar Mayer, Inc. . "Dietary Fitness—A Meat Lover's Guide," Oscar Mayer, Inc. . Ibid. . Ibid. . Imperato and Mitchell, _Acceptable Risks,_ 75. . Hausman, _Jack Sprat's Legacy,_ 194. . Ibid., 82. . McDougall and McDougall, _McDougall Plan,_ 65. . Connor, "Coronary Heart Disease"; Kannel, "Atherosclerotic Disease." . Ibid. . McDougall and McDougall, _McDougall Plan,_ 117. . Nathan Pritikin, quoted in _Vegetarian Times_ 43 (1981). . J. Elliot, "An 'Ideal' Serum Cholesterol Level?" _Journal of the American Medical Association_ 241 (1979): 1979. . Quoted in Hausman, _Jack Sprat's Legacy,_ 180. . Ibid., 180–81. . A. Tall, "Current Concepts; Plasma High-Density Lipoproteins," _New England Journal of Medicine_ 299 (1978): 1232; Mary Flanagan, "The Effects of Diet on High Density Lipoprotein Cholesterol," _Journal of Human Nutrition_ 34 (1980): 43; G. Bradby, "Serum High-Density Lipoproteins in Peripheral Vascular Disease," _Lancet_ 2 (1978): 1271. . Robert Barndt, "Regression and Progression...," _Annals of Internal Medicine_ 86 (1977): 139; L. Basta, "Regression of Atherosclerotic...," _American Journal of Medicine_ 61 (1976): 420; J. Hubbard, "Nathan Pritikin's Heart," _New England Journal of Medicine_ 313 (1985): 52; Ornish, "Treating Isochemic Heart Disease." . Barndt, "Regression and Progression." . Alton Blakesless and Jeremiah Stamler, _Your Heart Has Nine Lives_ (Englewood Cliffs, NJ: Prentice-Hall, 1963), 67–69. . Hausman, _Jack Sprat's Legacy,_ 90. . F. Ellis and T. Sanders, "Angina and Vegetarian Diet," letter to the editor, _Lancet_ (May 29, 1976); F. Ellis and T. Sanders, "Angina and Vegan Diet," _American Heart Journal_ 93 (June 1977): 803. . Quoted in Imperato and Mitchell, _Acceptable Risks,_ 78. . "Eating the Moderate Fat and Cholesterol Way," deleted chapter in _Food 2_ (Washington, DC: USDA, 1982). . Hausman, _Jack Sprat's Legacy,_ 151. . Imperato and Mitchell, _Acceptable Risks,_ 70–71; Hausman, _Jack Sprat's Legacy,_ 202–4. . Ibid. . Quoted in Hausman, _Jack Sprat's Legacy,_ 203. . Imperato and Mitchell, _Acceptable Risks,_ 70–71; Hausman, _Jack Sprat's Legacy,_ 202–4. . Quoted in Hausman, _Jack Sprat's Legacy,_ 204. . Lipid Research Clinics Program, "I. Reduction in Incidence" and "II. The Relationship of Reduction." . C. Walles, "Hold the Eggs and Butter," 56. . Lipid Research Clinics Program, "I. Reduction in Incidence" and "II. The Relationship of Reduction." . Ibid. . Walles, "Hold the Eggs and Butter," 58. . Ibid. . Hausman, _Jack Sprat's Legacy,_ 90–91. . Quoted in Imperato and Mitchell, _Acceptable Risks,_ 79. . Tavia Gordon, "Diabetes, Blood Lipids, and the Role of Obesity in Coronary Heart Disease Risk...," _Annals of Internal Medicine_ 87 (1977): 393; Peter Wood, "Plasma Lipoprotein Distributions in Male and Female Runners," _Annals of the New York Academy of Science_ 301 (1977): 748; Joseph Price, _Coronaries, Cholesterol, Chlorine_ (New York: Jove Books, 1981); O. Forde, "The Tromso Heart Study: Coffee Consumption and...," _British Medical Journal_ 290 (1985): 893; J. Little, "Coffee and Serum-Lipids in Coronary Heart Disease," _Lancet_ 1 (1966): 732; Hartz, "Smoking, Coronary Artery Occlusion"; Kannel, "Cigarettes, Coronary Occlusions." . "Diet and Stress in Vascular Disease," _Journal of the American Medical Association_ 176, no. 9 (June 3, 1961): 806. ##### **Chapter Nine. Losing a War We Could Prevent** . "85 Million for Research on Cancer," _San Francisco Chronicle,_ March 26, 1986. . Linus Pauling, quoted in P. Chowka, "Cancer Research—The $20 Billion Failure," _Vegetarian Times_ (December 1981): 32. . For further details on cancer rates, see the following: I. Henderson, "Cancer of the Breast—The Past Decade," parts 1 and 2, _New England Journal of Medicine_ 302 (1980): 17–78; Michael Baum, "The Curability of Breast Cancer," _British Medical Journal_ 1 (1976): 439; M. Costanza, "Adjuvant Chemotherapy: Eight Years Later," _Journal of the American Medical Association_ 252 (1984): 2611; R. Kerbel, "Facilitation of Tumour Progression by Cancer Therapy," _Lancet_ 2 (1982): 977; D. Greenberg, " 'Progress' in Cancer Research—Don't Say It Isn't So," _New England Journal of Medicine_ 292 (1975): 707; C. Mueller, "Bilateral Carcinoma of the Breast—Frequency and Mortality," _Journal of Surgery_ 21 (1978): 459; J. Stehlin, "Treatment of Carcinoma of the Breast," _Surgery Gynecology and Obstetrics_ 149 (1979): 911; Allan Langlands, "Long Term Survival of Patients with Breast Cancer: A Study of the Curability of the Disease," _British Medical Journal_ 2 (1979): 1247; John McDougall, _McDougall's Medicine_ (Piscataway, NJ: New Century Publishing, 1985), 6; H. Vorherr, "Adjuvant Chemotherapy of Breast Cancer: Reality, Hope, Hazard?" _Lancet_ 2 (1981): 1413; Cancer Surveillance, Epidemiology, and End Results (SEER) Program, _Cancer Patient Survival—Report No. 5,_ Department of Health, Education, and Welfare publication no. (NIH) 77-992, 1976; H. Vorherr, "Adjuvant Chemotherapy of Breast Cancer: Tumour Kinetics and Survival," _Lancet_ 2 (1981): 690. . "War on Cancer a Failure, Says Former Scientist," _Animals' Agenda_ (September 1985): 14. . Ibid.; Petr Skrabanek, "False Premises and False Promises of Breast Cancer Screening," _Lancet_ 2 (1985): 316; C. Mueller, "Breast Cancer in 3,558 Women...," _Surgery_ 83 (1978): 123. . McDougall, _McDougall's Medicine,_ 7. . Chowka, "The $20 Billion Failure." . Statement by Arthur Upton, director of the National Cancer Institute, "Status of the Diet, Nutrition, and Cancer Program," hearing before the Subcommittee on Nutrition, October 2, 1972. . Committee on Diet, Nutrition, and Cancer: Assembly of Life Sciences, National Research Council, _Diet, Nutrition, and Cancer_ (Washington, DC: National Academy Press, 1982); _American Cancer Society,_ "Nutrition and Cancer: Cause and Prevention," special report, CA 34 (1984): 121; U.S. Senate Report, _Dietary Goals for the United States_ (Washington, DC: Government Printing Office, 1977); B. Reddy, "Nutrition and Its Relationship to Cancer," _Advances in Cancer Research_ 32 (1980): 237; A. Tannenbaum, "The Genesis and Growth of Tumours, III: Effects of a High-Fat Diet," _Cancer Research_ 2 (1942): 468; "Nutrition in the Causation of Cancer," _Cancer Research_ 35 (1975): 3231; K. Carroll, "Dietary Fat in Relation to Tumour Genesis," _Progress in Biochemical Pharmacology_ 10 (1975): 308; Bruce Armstrong and Richard Doll, "Environmental Factors and Cancer Incidence and Mortality in Different Countries," _International Journal of Cancer_ 15 (1975): 617. . Reddy, "Relationship to Cancer." . Gio Gori, quoted in Chowka, "The $20 Billion Failure," 34. . Gio Gori, quoted in Vic Sussman, _The Vegetarian Alternative_ (Emmaus, PA: Rodale Press, 1978). . Patricia Hausman, _Jack Sprat's Legacy_ (New York: Richard Marek Publishers, 1981), 103–19. . Ibid., 116. . Takeshi Hirayama, "Epidemiology of Breast Cancer with Special Reference to the Role of Diet," _Preventive Medicine_ 7 (1978): 173; Ernst Wynder, "Dietary Fat and Colon Cancer," _Journal of the National Cancer Institute_ 54 (1975): 7; John Berg, "Can Nutrition Explain the Pattern of International...Cancers?" _Cancer Research_ 35 (1975): 3345; Ernst Wynder, "The Dietary Environment and Cancer," _Journal of the American Dieticians Association_ 71 (1977): 385; J. Weisburger, "Nutrition and Cancer—On the Mechanisms Bearing on Causes of Cancer of the Colon, Breast, Prostate, and Stomach," _Bulletin of the New York Academy of Medicine_ 56 (1980): 673; G. Mann, "Food Intake and Resistance to Disease," _Lancet_ 1 (1980): 1238; Committee on Diet, Nutrition, and Cancer, "Diet, Nutrition, and Cancer"; American Cancer Society, "Nutrition and Cancer"; U.S. Senate Report, _Dietary Goals;_ B. Reddy, and Ernst Wynder, "Large Bowel Carcinogenesis: Fecal Constituents of Populations with Diverse Incidence of Colon Cancer," _Journal of the National Cancer Institute_ 50 (1973): 1437; M. Hill, "Bacteria and the Aetiology of Cancer of the Large Bowel," _Lancet_ 1 (1971): 95; Reddy, "Relationship to Cancer"; B. Reddy, "Metabolic Epidemiology of Large Bowel Cancer," _Cancer_ 42 (1978): 2832; M. Hill, "Colon Cancer: A Disease of Fiber Depletion or of Dietary Excess," _Digestion_ 11 (1974): 289; A. Walker, "Colon Cancer and Diet with Special References to Intakes of Fat and Fiber," _American Journal of Clinical Nutrition_ 34 (1981): 2054; J. Cummings, "Progress Report: Dietary Fiber," _Gut_ 14 (1983): 69; Ronald Phillips, "Role of Lifestyle and Dietary Habits in Risk of Cancer...," _Cancer Research_ 35 (1975): 3513; Mervyn Hardinge, "Nutritional Studies of Vegetarians: III. Dietary Levels of Fiber," _American Journal of Clinical Nutrition_ 6 (1958): 523; J. Weisburger, "Colon Cancer—Its Epidemiology...," _Cancer_ 40 (1977): 2414. . _Science,_ February 1974, p. 416. . Reddy, "Relationship to Cancer"; _New York Times,_ September 29, 1972, p. 24; William Haenszel, "Studies of Japanese Migrants, I. Mortality from Cancer...," _Journal of the National Cancer Institute_ 40 (1968): 43. . _Journal of the National Cancer Institute_ (December 1973): 1771. . In addition to citations by Walker, Wynder, Berg, and Weisburger in note 15, see also B. Reddy, "Metabolic Epidemiology of Large Bowel Cancer," _Cancer_ 42 (1978): 2832. . In addition to the citations in note 15, see also K. Liu, "Dietary Cholesterol, Fat, and Fiber and Colon-Cancer Mortality," _Lancet_ 2 (1979): 782; J. Cruse, "Dietary Fiber...and Experimental Colon Cancer," _Gut_ 19 (1978): A983; Denis Burkitt, "Epidemiology of Cancer of the Colon and Rectum," _Cancer_ 28 (1971): 3–13; Denis Burkitt, "Some Diseases Characteristic of Modern Western Civilization," _British Medical Journal_ 1 (1973): 274; Hugh Trowell, "Ischemic Heart Disease and Dietary Fiber," _American Journal of Clinical Nutrition_ 25 (1972): 926. . John McDougall and Mary Ann McDougall, _The McDougall Plan_ (Piscataway, NJ: New Century Publishers, 1983), 120. . In addition to citations by Reddy and Wynder in note 15, see also G. Hepner, "Altered Bile Acid Metabolism in Vegetarians," _American Journal of Digestive Diseases_ 20 (1975): 935; M. Hill, "The Effect of Some Factors on the Fecal Concentration of...," _Journal of Pathology_ 104 (1971): 239. . Dr. Martin Hoye, personal communication with author. . See citations in note 15. . M. Pearce, "Incidence of Cancer in Men on a Diet High in Polyunsaturated Fat," cited in Hausman, _Jack Sprat's Legacy,_ 173. . L. Bennion, "Risk Factors for the Development of Cholelithiasis in Man," _New England Journal of Medicine_ 299 (1978): 1221; S. Broitman, "Polyunsaturated Fats, Cholesterol, and Large Bowel Tumorigenesis," _Cancer_ 40 (1977): 2455; K. Carroll, "Dietary Polyunsaturated Fat Versus Saturated Fat in Relation to Mammary Carcinogenesis," _Lipids_ 14 (1979): 155. . P. Nestel, "Lowering of Plasma Cholesterol...with Consumption of Polyunsaturated Ruminant Fats," _New England Journal of Medicine_ 288 (1973): 379. . "Meat-Packer Defends Beef," _Riverside Herald,_ May 8, 1976, A-1. . Obituary column, _Riverside Herald,_ March 14, 1982, C-1. . A. Lea, "Dietary Factors Associated with...," _Lancet_ 2 (1966): 332; Hirayama, "Epidemiology of Breast Cancer"; McDougall, _McDougall's Medicine,_ 18–50; A. Morrison, "Some International Differences in Treatment and Survival in Breast Cancer," _International Journal of Cancer_ 18 (1976): 269; T. Nemoto, "Differences in Breast Cancer between Japan and the United States," _Journal of the National Cancer Institute_ 58 (1977): 193; Bruce Armstrong and Richard Doll, "Environmental Factors and Cancer Incidence and Mortality in Different Countries," _International Journal of Cancer_ 15 (1975): 617. . Takeshi Hirayama, paper presented at Conference on Breast Cancer and Diet, U.S.–Japan Cooperative Cancer Research Program, Fred Hutchinson Cancer Center, Seattle, Washington, March 14–15, 1977. . Ibid. . Y. Kagawa, "Impact of Westernization on the Nutrition of Japanese: Changes in Physique, Cancer...," _Preventive Medicine_ 7 (1978): 205; P. Hill, "Diet, Life-Style, and Menstrual Activity," _American Journal of Clinical Nutrition_ 33 (1980): 1192; Jerzy Staszewski, "Age at Menarche and Breast Cancer," _Journal of the National Cancer Institute_ 47 (1971): 935. . D. Frommer, "Changing Age of the Menopause," _British Medical Journal_ 2 (1964): 349; Bruce Armstrong, "Diet and Reproductive Hormones, A Study of Vegetarian and Non-vegetarian Postmenopausal Women," _Journal of the National Cancer Institute_ 67 (1981): 761; P. Hill, "Environmental Factors of Breast and Prostatic Cancer," _Cancer Research_ 41 (1981): 3817; Dimitrios Trichopoulos, "Menopause and Breast Cancer Risk," _Journal of the National Cancer Institute_ 48 (1972): 605. . See citations in note 34. . See citations in note 9. . Robin Hur, _Food Reform: Our Desperate Need_ (Austin, TX: Heidelberg Publishers, 1975), 24. . McDougall, _McDougall's Medicine,_ 60–89. . Harry Zeil, "Increased Risk of Endometrial Carcinoma...," _New England Journal of Medicine_ 293 (1975): 1167; Donald Smith, "Association of Exogenous Estrogen and Endometrial Carcinoma," _New England Journal of Medicine_ 294 (1976): 1262; T. Mack, "Estrogens and Endometrial Cancer...," _New England Journal of Medicine_ 294 (1976): 1262. . Berg, "Can Nutrition Explain"; Wynder, "Dietary Environment and Cancer." . Phillips, "Role of Lifestyle"; Hardinge, "Nutritional Studies of Vegetarians"; "Nutrition in the Causation of Cancer," _Cancer Research_ 35 (1975): 3231; Bennion, "Cholelithiasis in Man"; S. Malhotra, "A Comparison of...Diet in the Management of Duodenal Ulcer," _Postgrad Medical Journal_ 54 (1978): 6; W. MacDonald, "Histological Effect...," _Canadian Medical Association Journal_ 96 (1967): 1521; Ernst Wynder, "Epidemiology of Adenocarcinoma of the Kidney," _Journal of the National Cancer Institute_ 53 (1974): 1619; R. Stuverdant, "Increased Prevalence of Cholethiasis in Men Ingesting a Serum Cholesterol Lowering Diet," _New England Journal of Medicine_ 288 (1973): 24. . Hill, "Breast and Prostatic Cancer." . N. Breslow, "Latent Carcinoma of Prostate at Autopsy in Seven Areas," _International Journal of Cancer_ 20 (1977): 680. . R. Virag, "Is Impotence an Arterial Disorder?" _Lancet_ 1 (1985): 181. . McDougall, _McDougall's Medicine,_ 96–126. . F. Lemon, "Death from Respiratory Disease," _Journal of the American Medical Association_ 198 (1966): 117. . J. Stamler, "Elevated Cholesterol May Increase Lung Cancer Risk in Smokers," _Heart Research Letter_ 14 (1969): 2. . Lemon, "Death from Respiratory Disease." ##### **Chapter Ten. An Ounce of Prevention** . Roy Walford, _Maximum Life Span_ (New York: W. W. Norton & Co., 1983), 11; G. Tokuhata, "Diabetes Mellitus: An Underestimated Public Health Problem," _Journal of Chronic Diseases_ 28 (1975): 23; S. Kaplan, "Diabetes Mellitus," _Annals of Internal Medicine_ 96 (1982): 635; William Kannel, "Diabetes and Cardiovascular Risk Factors: The Framingham Study," _Circulation_ 59 (1975): 8. . In addition to citations in note 1, see also A. Cohen, "Myocardial Infarction and Carbohydrate Metabolism," _Geriatrics_ 23 (1968): 158; "The Complications of Diabetes Mellitus," _New England Journal of Medicine_ 298 (1978): 1250. . Robin Hur, _Food Reform: Our Desperate Need_ (Austin, TX: Heidelberg Publishers, 1975), 67–73; John McDougall, _McDougall's Medicine_ (Piscataway, NJ: New Century Publishing, 1985), 203–30. . Report of the National Commission on Diabetes to Congress, vol. III, part 2, Department of Health, Education, and Welfare Publication no. (NIH) 76-1022, 1975. . Inder Singh, "Low-Fat Diet and Therapeutic Doses of Insulin in Diabetes Mellitus," _Lancet_ 263 (1955): 422. . D. Kipnis, "Insulin Secretion in Normal and Diabetic Individuals," _Advances in Internal Medicine_ 16 (1970): 103. . H. Himsworth, "The Physiological Activation of Insulin," _Clinical Science_ 1 (1933): 1; J. Shirley Sweeney, "Dietary Factors That Influence the Dextrose Tolerance Test...," _Archives of Internal Medicine_ 40 (1927): 818; J. Olefsky, "Reappraisal of the Role of Insulin in Hypertriglyceridemia," _American Journal of Medicine_ 57 (1974): 551; P. Davidson, "Insulin Resistance in Hyperglyceridemia," _Metabolism_ 14 (1965): 1059. . James Anderson, "High Carbohydrate, High-Fiber Diets for Insulin Treated Men with Diabetes Mellitus," _American Journal of Clinical Nutrition_ 32 (1979): 2312. . A. Asmal, "Oral Hypoglycaemic Agents...," _Drugs_ 28 (1984): 62; Tae Kiehm, "Beneficial Effects of a High Carbohydrate, High Fiber Diet on Hyperglycemic Diabetic Men," _American Journal of Clinical Nutrition_ 29 (1976): 895; H. Simpson, "A High Carbohydrate Leguminous Fiber Diet Improves All Aspects of Diabetes Control," _Lancet_ 1 (1981): 1; Anderson, "High Carbohydrate, High-Fiber Diets"; R. Simpson, "Improved Glucose Control in Maturity-Onset Diabetes Treated with High-Carbohydrate Modified-Fat Diet," _British Medical Journal_ 1 (1979): 1753; Singh, "Insulin in Diabetes Mellitus,"; J. Brunzell, "Improved Glucose Tolerance with High Carbohydrate Feeding in Mild Diabetes," _New England Journal of Medicine_ 284, no. 10 (1971): 521. . McDougall, _McDougall's Medicine,_ 210. . "Acute Mishaps during Insulin Pump Treatment," _Lancet_ 1 (1985): 911; J. Rosenstock, "Insulin Pump Therapy: A Realistic Appraisal," _Clinical Diabetes_ 3 (1985): 25; K. Dahl-Jorgensen, "Rapid Tightening of Blood Glucose Control Leads to Transient Deterioration of Retinopathy in Insulin Dependent Diabetes Mellitus," _British Medical Journal_ 290 (1985): 811. . James Anderson, "Hypolipidemic Effects of High-Carbohydrate, High-Fiber Diets," _Metabolism_ 29 (1980): 551; Marc Blanc, "Improvement of Lipid Status in Diabetic Boys...," _Diabetes Care_ 6 (1983): 64; W. Van Eck, "The Effect of a Lowfat Diet on the Serum Lipids in Diabetes," _American Journal of Medicine_ 27 (1959): 196. . McDougall, _McDougall's Medicine._ . Ryoso Kawate, "Diabetes Mellitus and Its Vascular Complications in Japanese Migrants on the Island of Hawaii," _Diabetes Care_ 2 (1979): 161; H. Trowell, "Dietary Fiber Hypothesis of the Etiology of Diabetes Mellitus," _Diabetes_ 24 (1975): 762; H. Ringrose, "Nutrient Intakes in an Urbanized Micronesian Population with a High Diabetes Prevalence," _American Journal of Clinical Nutrition_ 32 (1979): 1334. . See citations in note 14. . David Snowden, quoted in _Vegetarian Times_ (August 1985). . Ibid. . John McDougall, "Healthy by Choice," _Vegetarian Times_ (December 1985). . Sweeney, "Dietary Factors That Influence." . C. Hollenbeck, "The Effects of Variations...," _Diabetes_ 34 (1985): 151; Olefsky, "Insulin in Hypertriglyceridemia"; G. Haber, "Depletion and Disruption of Dietary Fiber, Effects on Satiety, Plasma-Glucose, and Serum-Insulin," _Lancet_ 2 (1977): 679; Anderson, "High-Carbohydrate, High-Fiber Diets"; Perla Miranda, "High-Fiber Diets in the Treatment of Diabetes Mellitus," _Annals of Internal Medicine_ 88 (1978): 482. . R. Baker, _Lancet_ 1 (1963): 26. . B. Agranoff, "Diet and the Geographical Distribution of Multiple Sclerosis," _Lancet_ 2 (1974): 1061; M. Alter, "Multiple Sclerosis and Nutrition," _Archives of Neurology_ 23 (1970): 460. . Department of Health and Social Security, "Present-Day Infant Feeding Practice Report," no. 9 (1974); M. Crawford, "Essential Fatty Acids Requirements in Infancy," _American Journal of Clinical Nutrition_ 31 (1978): 2181; Agranoff, "Distribution of Multiple Sclerosis"; USDA Home Economics Report No. 7, "Fatty Acids in Food Fats." . Roy Swank, _Low-Fat Diet: Reasons, Rules, and Recipes_ (Eugene: University of Oregon Books, 1959); Roy Swank, "Multiple Sclerosis: Twenty Years on a Low-Fat Diet," _Archives of Neurology_ 23 (1970): 460; Roy Swank, _A Biochemical Basis of Multiple Sclerosis_ (Springfield, IL: Charles C. Thomas, 1961), 3, 44–45. . Emanuel Cheraskin and W. M. Ringsdorf, _New Hope for Incurable Diseases_ (New York: Arco, 1971), 32. . See citations in notes 22, 23, 24, and 25. . Ibid. . McDougall, "Healthy by Choice." . A. Malhotra, "A Comparison of Unrefined Wheat and Rice Diet in the Management of Duodenal Ulcer," _Postgraduate Medical Journal_ 54 (1978): 6; A. Rydning, "Prophylactic Effect of Dietary Fiber in Duodenal Ulcer Disease," _Lancet_ 2 (1982): 736; P. Childs, "Peptic Ulcer, Pylorplasty, and Dietary Fat...," _Annals of the Royal College of Surgeons_ 59 (1977): 143; H. Trowell, "Definition of Dietary Fiber," _American Journal of Clinical Nutrition_ 29 (1976): 417; Denis Burkitt, "Dietary Fiber and Disease," _Journal of the American Medical Association_ 229 (1974): 1068. . A. Ippoliti, "The Effect of Various Forms of Milk on Gastric-Acid Secretions, Studies in Patients with Duodenal Ulcers...," _Annals of Internal Medicine_ 84 (1976): 286; Hur, _Food Reform,_ 118. . W. Hartroft, "The Incidence of Coronary Heart Disease in Patients Treated with the Sippy Diet," _American Journal of Clinical Nutrition_ 15 (1964): 205; R. Briggs, "Myocardial Infarction in Patients Treated with Sippy and Other High Milk Diets," _Circulation_ 21 (1960): 538. . Hur, _Food Reform,_ 118. . Robert Gray, _The Colon Health Handbook_ (Oakland, CA: Rockridge Publishing Co., 1983). . Denis Burkitt, _Lancet_ 2 (1972): 1408. . Denis Burkitt, "Varicose Veins, Deep Vein Thrombosis, and Haemorrhoids: Epidemiology and Suggested Aetiology," _British Medical Journal_ 2 (1972): 556. . Robert Holt, _Hemorrhoids_ (Laguna Beach, CA: California Health Publications, 1977); W. Thompson, "The Nature of Hemorrhoids," _British Journal of Surgery_ 62 (1975): 542. . Denis Burkitt, "Dietary Fiber and Disease," _Journal of the American Medical Association_ 229 (1974): 1068; G. Prasad, "Studies on Etipathogenesis of Hemorrhoids," _American Journal of Proctology_ (June 1976); Burkitt, "Varicose Veins, Deep Vein Thrombosis"; John McDougall and Mary Ann McDougall, _The McDougall Plan_ (Piscataway, NJ: New Century Publishers, 1983), 117. . Denis Burkitt, "Hiatus Hernia: Is it Preventable?" _American Journal of Clinical Nutrition_ 34 (1981): 428. . Denis Burkitt, "Some Diseases Characteristic of Modern Western Civilization," _British Medical Journal_ 1 (1973): 274. . "Keep Taking Your Bran," _Lancet_ 1 (1979): 1,175; Corinne Robinson and Fairfax Proudfit, _Normal and Therapeutic Nutrition,_ 13th ed. (New York: Macmillan, 1967), 386; N. Painter, "The High Fiber Diet in the Treatment of Diverticular Disease of the Colon," _Postgraduate Medical Journal_ 50 (1974): 629; McDougall and McDougall, _McDougall Plan,_ 117–19. . P. Berman, _American Journal of Digestive Disorders_ 17 (1972): 741. . N. Painter, "Fiber Deficiency and Diverticular Disease of the Colon," in _Fiber Deficiency and Colonic Disorders,_ ed. Richard Reilly and Joseph Kirsner (New York: Plenum Medical Book Co., 1975). . J. Piepmeyer, "Use of Unprocessed Bran in Treatment of Irritable Bowel Syndrome," _American Journal of Clinical Nutrition_ 27 (1974): 106; A. Manning, "Wheat Fiber and Irritable Bowel Syndrome," _Lancet_ 2 (1977): 417; "Management of the Irritable Bowel," _Lancet_ 2 (1978): 557; McDougall and McDougall, _McDougall Plan,_ 119. . Denis Burkitt, "Appendicitis," in _Refined Carbohydrate Foods and Disease,_ ed. Denis Burkitt and H. Trowell (New York: Academic Press, 1978); C. Westlake, "Appendectomy and Dietary Fiber," _Journal of Human Nutrition_ 34 (1980): 267; A. Walker, "Appendicitis, Fiber Intake, and Bowel Behavior in Ethnic Groups in South Africa," _Postgraduate Medical Journal_ 49 (1973): 243. . Sandra Friday and Heidi Hurwitz, _The Food Sleuth Handbook_ (New York: Atheneum Publishers, 1982). . Jean Mayer and Jeanne Goldberg, "Nutrition," _Washington Post,_ July 6, 1981. . P. Tamer, "Cholesterol and Obesity as Prognostic Factors and...," _Cancer_ 47 (1981): 2222; W. Donegan, "The Association of Body Weight with Recurrent Cancer...," _Cancer_ 41 (1978): 1590; "Obesity—The Cancer Connection," _Lancet_ 1 (1982): 1223. . Hur, _Food Reform,_ 74. . Frey Ellis, "Veganism, Clinical Findings, and Investigations," _American Journal of Clinical Nutrition_ 23, no. 3 (1970): 249; Frank Sacks, "Plasma Lipids and Lipoproteins in Vegetarians and Controls," _New England Journal of Medicine_ 292, no. 22 (May 1975): 1148; Frey Ellis, "Angina and Vegan Diet," _American Heart Journal_ 93, no. 6 (June 1977): 803; Mervyn Hardinge, "Nutritional Studies of Vegetarians...," _American Journal of Clinical Nutrition_ 2 (1974): 73. . Hur, _Food Reform,_ 76–77. . S. Blaw and D. Schultz, _Arthritis_ (New York: Doubleday, 1974); J. Kellgren, "Osteo-arthrosis...," _Annals of Rheumatic Diseases_ 17 (1958): 388; McDougall, _McDougall's Medicine,_ 237. . McDougall, _McDougall's Medicine,_ 231–50. . P. Lucas, "Dietary Fat Aggravates Active Rheumatoid Arthritis," _Clinical Research_ 29 (1981): 754A. . A. Parke, "Rheumatoid Arthritis and Food...," _British Medical Journal_ 282 (1981): 2027. . H. Valkenburg, "Osteoarthritis in Some Developing Countries," _Journal of Rheumatology_ 10 (1983): 20; L. Solomon, "Rheumatic Disorders in the South African Negro," parts I and II, _South African Medical Journal_ 49 (1975): 1292, 1737; R. Beasley, "Low Prevalence of Rheumatoid Arthritis in Chinese...," _Journal of Rheumatology_ 10 (1983): 11. . P. Beighton, "Rheumatoid Arthritis in a Rural South African Negro Population," _Annals of Rheumatic Diseases_ 34 (1975): 136. . Solomon, "Rheumatic Disorders." . Roger Williams, _Nutrition against Disease,_ 10th ed. (New York: Bantam Books, 1981), 134. . N. Zollner, "Diet and Gout," _Proceedings of the Ninth International Congress on Nutrition_ 1 (1975): 267. . A. Hall, "Epidemiology of Gout and Hyperuricemia," _American Journal of Medicine_ 42 (1967): 27; Donald Berkowitz, "Blood Lipid and Uric Acid...," _Journal of the American Medical Association_ 190 (1964): 856. . L. Healey, "Hyperuricemia in Filipinos...," _American Journal of Human Genetics_ 19 (1967): 81. . F. Derrick, "Kidney Stone Disease: Evaluation and Medical Management," _Postgraduate Medical Journal_ 66 (1979): 115. . W. Robertson, "Dietary Changes and the Incidence of Urinary Calculi...," _Journal of Chronic Diseases_ 32 (1979): 469. . K. Heaton, "Gallstones and Cholecystitis," in _Refined Carbohydrate Foods and Diseases,_ ed. Denis Burkitt and H. Trowell (New York: Academic Press, 1978); H. Sarles, "Diet and Cholesterol Gallstones," _Digestion_ 17 (1978): 121. . A. Walker, "Colon Cancer and Diet with Special Reference to Intakes of Fat and Fiber," _American Journal of Clinical Nutrition_ 29 (1976): 1417. . Boston Collaborative Drug Surveillance Program, "Surgically Confirmed Gallbladder Disease... _," New England Journal of Medicine_ 290 (1974): 15; W. Grache, "The Natural History of Silent Gallstones," _New England Journal of Medicine_ 307 (1982): 798. . Carlene Baum, "Drug Use in the United States in 1981," _Journal of the American Medical Association_ 251 (1984): 1293. . William Kannel, "Should All Mild Hypertension Be Treated? Yes," in _Controversies inTherapeutics_ , ed. L. Lasagna (Philadelphia: W. B. Saunders Co., 1980), 299; McDougall, _McDougall's Medicine;_ P. Evans, "Relation of Longstanding Blood Pressure Levels to Atherosclerosis," _Lancet_ 1 (1965): 516. . Edward Freis, "Salt, Volume, and the Prevention of Hypertension," _Circulation_ 53 (1976): 589; "Why Does Blood Pressure Rise with Age?" _Lancet_ 2 (1981): 289; Lewis Kuller, "An Explanation for Variations in Distribution of Stroke and Arteriosclerotic Heart Disease among Populations and Racial Groups," _American Journal of Epidemiology_ 93 (1971): 1. . Freis, "Prevention of Hypertension." . Edward Freis, "Hemodynamics of Hypertension," _Physiol Review_ 40 (1960): 27; P. Parfrey, "Relation between Arterial Pressure, Dietary Sodium Intake...," _British Medical Journal_ 283 (1981): 94. . Norman Kaplan, "Mild Hypertension: When and How to Treat," _Archives of Internal Medicine_ 143 (1985): 255; Neil McAlister, "Should We Treat 'Mild' Hypertension?" _Journal of the American Medical Association_ 249 (1983): 379; G. Boyd, "The Pressure to Treat," _Lancet_ 2 (1980): 1134; Norman Kaplan, "Therapy for Mild Hypertension—Toward a More Balanced View," _Journal of the American Medical Association_ 249 (1983): 365. . "Fatigue as an Unwanted Effect of Drugs," _Lancet_ 1 (1985): 123; R. Stone, "Proximal Myopathy during Beta-Blockade," _British Medical Journal_ 2 (1979): 1583. . Ingar Holme, "Treatment of Mild Hypertension with Diuretics...," _Journal of the American Medical Association_ 25 (1984): 1298. . J. David Curb, "Long-Term Surveillance for Adverse Effects of Antihypertensive Drugs," _Journal of the American Medical Association_ 253 (1985): 3263. . Jeremiah Stamler, "Hypertension Screening...," _Journal of the American Medical Association_ 235 (1976): 2299; H. McGill, "Persistent Problems in the Pathogenesis of Atherosclerosis," _Atherosclerosis_ 4 (1984): 443. . W. Hartroft, "The Incidence of Coronary Heart Disease in Patients Treated with the Sippy Diet," _American Journal of Clinical Nutrition_ 15 (1964): 205; Frank Oski, "Is Bovine Milk a Health Hazard?" _Pediatrics_ 75 (suppl.) (1985): 182; J. Belizan, "Reduction of Blood Pressure with Calcium Supplementation in Young Adults," _Journal of the American Medical Association_ 249 (1983): 1161; Nancy Johnson, "Effects on Blood Pressure of Calcium Supplementation of Women," _American Journal of Clinical Nutrition_ 42 (1985): 12; M. Sowers, "The Association of...Calcium with Blood Pressures among Women," _American Journal of Clinical Nutrition_ 42 (1985): 135. . M. Friedman, "Serum Lipids and Conjunctival Circulation after Fat Ingestion...," _Circulation_ 29 (1984): 874; M. Friedman, "Effect of Unsaturated Fats upon Lipemia and Conjunctival Circulation," _Journal of the American Medical Association_ 198 (1976): 882; J. O'Brien, "Acute Platelet Changes after Large Meals of Saturated and Unsaturated Fats," _Lancet_ 1 (1976): 878. . M. Burr, "Plasma Cholesterol and Blood Pressure in Vegetarians," _Journal of Human Nutrition_ 35 (1981): 437; Frank Sacks, "Blood Pressure in Vegetarians," _American Journal of Epidemiology_ 100 (1974): 390; B. Armstrong, "...Blood Pressure in Vegetarians," _American Journal of Clinical Nutrition_ 32 (1979): 2472; O. Ophir, "Low Blood Pressure in Vegetarians," _American Journal of Clinical Nutrition_ 37 (1983): 755; Norman Kaplan, "Non-drug Treatment of Hypertension," _Annals of Internal Medicine_ 102 (1985): 359; "Lowering Blood Pressure without Drugs," _Lancet_ 2 (1980): 459; Ian Rouse, "Blood Pressure Lowering Effect of a Vegetarian Diet...," _Lancet_ 1 (1983): 5. . B. Armstrong, "Blood Pressure in Seventh Day Adventists," _American Journal of Epidemiology_ 105 (1977): 444. . P. Dallman, _American Journal of Clinical Nutrition_ 33 (1980): 86; M. Murray, _American Journal of Clinical Nutrition_ 33 (1980): 697; M. Abdulla, _American Journal of Clinical Nutrition_ 34 (1981): 2464. . J. Wilson, _Journal of Pediatrics_ 84 (1974): 335. . Olov Lindahl, "Vegan Regimen with Reduced Medication in the Treatment of Bronchial Asthma," _Journal of Asthma_ 22 (1985): 44. . National Academy of Sciences, _An Evaluation of the Salmonella Problem,_ report to the U.S. Department of Agriculture and Federal Drug Administration, prepared by the Committee on Salmonella, National Research Council, 1969. . Dudley Giehl, _Vegetarianism_ (New York: Harper & Row, 1979). . National Academy of Sciences, _Evaluation of the Salmonella Problem,_ 125. . Statement by Richard Novick, hearings before the Subcommittee on Agricultural Research and General Legislation of the Committee on Agriculture, Nutrition and Forestry, September 21, 1977. . "Salmonellae in Slaughter Cattle," _Journal of the American Veterinary Medical Association_ 160, no. 6 (1972): 884. . "Salmonella Contamination in a Commercial Poultry Processing Operation," _Poultry Science_ 53 (1974): 814–21. . Harrison Wellford, _Sowing the Wind_ (New York: Bantam Books, 1973), 133–34. . Irvin Molotsky, "Antibiotics in Animal Feed Linked to Human Ills," _New York Times,_ February 22, 1987. . New Jersey State Health Department, Division of Environmental Health, cited in J. Scharffenberg, _Problems with Meat_ (Santa Barbara, CA: Woodbridge Press, 1982), 60; Kenneth Stoller, "Feeding an Epidemic," _Animals' Agenda_ (May 1987): 32–33. ##### **Chapter Eleven. America the Poisoned** . Roger Williams, "The Trophic Value of Foods," _Proceedings of the National Academy of Sciences_ 70, no. 3 (March 1973): 710–13; A. Tolan, "The Chemical Composition of Eggs Produced under Battery, Deep Litter, and Free Range Conditions," _British Journal of Nutrition_ 30 (1974): 181, 185. . M. A. Crawford, "A Re-evaluation of the Nutrient Role of Animal Products," in _Proceedings of the Third World Conference on Animal Production,_ ed. R. L. Reid (Sydney: Sydney University Press, 1975), 24. . Orville Schell, _Modern Meat_ (New York: Random House, 1984), 283–84. . Carmen A. Saenz de Rodriguez, _Journal of the Puerto Rico Medical Association,_ February 1982, cited in Schell, _Modern Meat,_ 286–87. . Schell, _Modern Meat,_ 287. . Quoted in "Drugs in Animals Affect Human Growth," _Health Bulletin_ (November 6, 1965): 6, cited in Beatrice Hunter, _Consumer Beware_ (New York: Simon & Schuster, 1971), 116. . Schell, _Modern Meat,_ 197. . Ibid., 198. . W. Hadlow, "Stilbestrol-Contaminated Feed and Reproductive Disturbances in Mice," _Science_ 122 (1955): 643–44. . Jacqueline Verrett and Jean Carper, _Eating May Be Hazardous to Your Health_ (New York: Simon & Schuster, 1974), 170. . Schell, _Modern Meat,_ 254. . Ibid., 257–68. . Rachel Carson, _Silent Spring_ (New York: Fawcett Crest Books, 1962). . Ibid., 97. . "Pesticide Safety: Myths and Facts," _National Coalition against the Misuse of Pesticides._ . Lewis Regenstein, _How to Survive in America the Poisoned_ (Herndon, VA: Acropolis Books, 1982), 103. . Carson, _Silent Spring,_ 35–37. . Rachel Carson, cited in Regenstein, _America the Poisoned,_ 106. . R. Duggan, "Dietary Intake of Pesticide Chemicals in the United States (11), June 1966–April 1968," _Pesticides Monitoring Journal_ 2 (1969): 140–52. . S. Harris, "Organochlorine Contamination of Breast Milk," Environmental Defense Fund, Washington, DC, November 7, 1979; J. Balbien, S. Harris, and T. Page, "Diet as a Factor Affecting Organochlorine Contamination of Breast Milk," Environmental Defense Fund, Washington, DC . R. Severo, _New York Times,_ May 6, 1980. . F. Barringer, "Thirty More Regulations Targeted for Review," _Washington Post,_ August 13, 1981, A-27; Merrill Brown, "Reagan Wants to Ax Product Safety Agency," _Washington Post,_ May 10, 1981; "Stockman Moves to Kill Consumer Safety Panel," _New York Times,_ May 9, 1981. . "True or False," League of Conservation Voters, Washington, DC, 1980. . Regenstein, _America the Poisoned,_ 348. . Council on Environmental Quality, _Environmental Quality_ — _1975,_ The Sixth Annual Report of the Council on Environmental Quality, Washington, DC (December 1975), 369. . "DDT and the Dolphin," _Animals'Agenda_ (September 1985). . William Longgood, _The Darkening Land_ (New York: Simon & Schuster, 1972), 143. . Carson, _Silent Spring;_ J. Highland, "Corporate Cancer," Environmental Defense Fund, Washington, DC. . Council on Environmental Quality, _Environmental Quality—1975; A Brief Review of Selected Environmental Contamination Incidents with a Potential for Health Effects,_ prepared by the Library of Congress for the Committee on Environment and Public Works, U.S. Senate (August 1980), 173–74; _Aldrin/Dieldrin,_ criteria document, U.S. Environmental Protection Agency, Washington, DC (1976). . Highland, "Corporate Cancer." . Regenstein, _America the Poisoned,_ 355. . Carson, _Silent Spring,_ 33–34, 88. . Regenstein, _America the Poisoned,_ 352–353. . Robert Boyle and Environmental Defense Fund, _Malignant Neglect_ (New York: Alfred Knopf, 1979), 128; Council on Environmental Quality, _Environmental Quality_ — _1974,_ The Fifth Annual Report of the Council on Environmental Quality, Washington, DC (December 1974), 161. . Associated Press, "Banquet Foods Recall Turkey," _Washington Post,_ June 27, 1980, A-8. . M. Cimons, "Veterans Gaining Ground in Agent Orange Struggle," _Los Angeles Times,_ December 27, 1979. . Regenstein, _America the Poisoned,_ 58; Margot Hornblower, "A Sinister Drama of Agent Orange Opens in Congress," _Washington Post,_ June 27, 1979; _Effects of 2,4,5-T on Man and the Environment,_ hearings before the Subcommittee on Energy, Natural Resources, and the Environment, U.S. Senate, April 1970, 1. . Hornblower, "A Sinister Drama." . Regenstein, _America the Poisoned,_ 19. . Diane Courtney, testimony before Senate Commerce Committee Subcommittee on the Environment, August 9, 1974. . Federal Register, December 13, 1979, pp. 72, 325. . _A Plague on Our Children_ , NOVA (Boston: WGBH Educational Foundation, 1979), DVD. . Regenstein, _America the Poisoned,_ 48. . Council on Environmental Quality, _Environmental Quality_ — _1979,_ The Tenth Annual Report of the Council on Environmental Quality, Washington, DC (December 1979); _A Plague on Our Children,_ NOVA; R. Severo, "Two Studies for National Institue Link Herbicide to Cancer in Animals," _New York Times,_ June 27, 1980. . R. Nordland and J. Friedman, "Poison at Our Doorstep," _Philadelphia Inquirer,_ reprint of September 23–28, 1979. . Frank Graham, _Since Silent Spring_ (New York: Fawcett Crest Books, 1970), 59–66. . H. Denton, "Contaminated Pork Shipped to Schools," _Washington Post,_ May 24, 1980, A-1. . Environmental Protection Agency, "Train Suspends Major Uses of Chlordane/Heptachlor...," _Environmental News_ (Washington, DC, December 24, 1979). . W. Butler and J. Warren, "Petition for Suspension and Cancellation of Chlordane/Heptachlor," Environmental Defense Fund, Washington, DC (October 1974). . Regenstein, _America the Poisoned,_ 368; Environmental Protection Agency, _Vesichol Chemical Co. et al., Consolidated Heptachlor/Chlordane Hearing,_ Federal Register (February 19, 1976), 7556. . _The EPA and the Regulation of Pesticides,_ staff report to the Subcommittee on Administrative Practice and Procedure, U.S. Senate (December 1976), 24. . Environmental Protection Agency, _Pesticide Products Containing Heptachlor or Chlordane,_ Federal Register (November 26, 1974), 41,300; Committee on Government Operations, _Report on Export ofProducts Banned by U.S. Regulatory Agencies,_ U.S. House of Representatives (October 4, 1978), 8; Denton, "Contaminated Pork Shipped." . Denton, "Contaminated Pork Shipped," A-1, 8. . "New Danger in Mother's Milk," _Time,_ April 7, 1986, 31. . "Schools Ground Beef Blocked over Pesticides," _San Francisco Chronicle,_ April 7, 1986, 31. . "New Danger in Mother's Milk," _Time._ . "Breast Milk Contamination," _Birth Defect Prevention News_ (January-March 1986). . Jim Mason and Peter Singer, _Animal Factories_ (New York: Crown Publishers, 1980), 59–60. . Subcommittee on Crime, _Corporate Crime,_ U.S. House of Representatives (May 1980), 25–28. . E. Grzech and K. Warbelow, "Distribution Hid Facts of PBB Peril," _Detroit Free Press,_ March 13, 1977; E. Grzech and K. Warbelow, "State Knew But Did Not Warn Farmers of PBB-Tainted Feed," _Detroit Free Press,_ March 14, 1977; E. Grzech and K. Warbelow, "How State Leaders Ducked PBB Issue," _Detroit Free Press,_ March 15, 1977. . In addition to citations in notes 59 and 60, see J. Brody, "Farmers Exposed to a Pollutant Face Medical Study...," _New York Times,_ August 12, 1976, C-20; "PBB Michigan Contamination Continues," _Guardian,_ May 4, 1977, 2; Associated Press, "Michigan Study Indicates 97% Have Traces of PBB," _Washington Post,_ December 31, 1981. . Ibid. . Cited in Regenstein, _America the Poisoned,_ 341. . Longgood, _The Darkening Land,_ 132–34. . _Whole Earth Review_ 48, Fall 1985, p. 51. . National Cancer Institute, _Surveillance, Epidemiology, and End Results: Incidence and Mortality Data, 1973–1977,_ monograph 57, U.S. Department of Health and Human Services (Bethesda, MD: National Institute of Health, June 1981), 4. . Regenstein, _America the Poisoned,_ 74. . Thomas Whiteside, _The Pendulum and the Toxic Cloud_ (New Haven, CT: Yale University Press, 1979), 134. . R. Hoffman, K. Webb, and W. Schramm, "Health Effects of Long-Term Exposure to 2,3,7,8-Tetrachlorodibenzo-P-Dioxin," _Journal of the American Medical Association_ 255 (April 18, 1986): 2031. . D. Perlman, "New Evidence Reported on Dioxin as Health Hazard," _San Francisco Chronicl_ e, April 18, 1986, A-1, 4. . _British Medical Journal_ 290 (1985): 808; Lewis Regenstein, personal correspondence with author. . Boyle, _Malignant Neglect,_ 59, 62; _Plague on Our Children,_ NOVA; J. Culhane, "PCBs: The Poisons That Won't Go Away," _Reader's Digest,_ December 1980, 113, 115; Council on Environmental Quality, _Toxic Chemicals and Public Protection,_ report to the president by the Toxic Substances Strategy Committee, Washington, DC (1980), 3; Ralph Nader et al., _Who's Poisoning America_ (San Francisco: Sierra Club Books, 1981), 177; "Pesticides Found in Wild Polar Bears," _Animals' Agenda_ (September 1985). . Culhane, "PCBs: The Poisons." . Regenstein, _America the Poisoned,_ 293. . _Plague on Our Children,_ NOVA. . Ibid. . B. Richards, "Drop in Sperm Count Is Attributed to Toxic Environment," _Washington Post,_ September 12, 1979; J. Brody, "Sperm Found Especially Vulnerable to Environment," _New York Times,_ March 10, 1981; "Unplugging the Gene Pool," _Outside,_ September 1980; E. Jansson, "The Impact of Hazardous Substances upon Infertility among Men in the U.S., and Birth Defects," Friends of the Earth (Washington, DC: November 17, 1980). . Ibid. . Ibid. . Ibid. . Regenstein, _America the Poisoned,_ 295. . Council on Environmental Quality, _Environmental Quality_ — _1979,_ 11, 99–100, 448–49. . Regenstein, _America the Poisoned,_ 298. . Longgood, _The Darkening Land,_ 132, 134. . Council on Environmental Quality, _Environmental Quality—1975,_ 368, 375, 387; _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 223. . Graham, _Since Silent Spring,_ 113; C. Wurster, "DDT Reduces Photosynthesis by Marine Phytoplankton," _Science_ (1968): 1474–75; Longgood, _The Darkening Land,_ 137. . S. Holt, "The Food Resources of the Ocean," _Scientific American_ 221 (1969): 178–94. . Georg Borgstrom, _The Hungry Planet_ (New York: Collier Books, 1967), 311. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 284; B. Nelson, "PCB Pollution Grave Question, US Says," _Los Angeles Times,_ October 7, 1979; _Congressional Quarterly,_ September 6, 1980, 2643; Associated Press, "PCBs Discovered in Foods in West," _Washington Star,_ September 15, 1979. . G. Frederickson, personal communication with author, January 13, 1986. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 284–87; Longgood, _The Darkening Land,_ 495; Boyle, _Malignant Neglect,_ 77. . Ibid. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works. . Regenstein, _America the Poisoned,_ 304. . Council on Environmental Quality, _Toxic Chemicals and Public Protection,_ 2; "Chemical First Strike," _Washington Post,_ May 17, 1980, A-18. . Ibid. . Council on Environmental Quality, _The Global Environment and Basic Human Needs,_ a report to the Council on Environmental Quality by the Worldwatch Institute, Washington, DC (1978), 20; Council on Environmental Quality, _Toxic Chemicals and Public Protection,_ xiv; _EPA Is Slow to Carry Out Its Responsibility to Control Harmful Chemicals_ (Washington, DC: General Accounting Office, October 28, 1980), 1. . Boyle, _Malignant Neglect,_ 7; Council on Environmental Quality, _Environmental Quality—1979,_ 198. . See articles by Grzech and Warbelow in note 60. . L. Cavalieri, "Carcinogens and the Value of Life," _New York Times,_ July 20, 1980; Regenstein, _America the Poisoned,_ 232. . Boyle, _Malignant Neglect,_ 196–98. . David Pimentel, "Pesticides...," _BioScience_ 27 (March 1977); James Turner, _A Chemical Feast: The Ralph Nader Study Group Report on Food Protection and the Food and Drug Administration_ (New York: Grossman, 1970); David Pimentel, "Realities of a Pesticide Ban," _Environment_ (March 1973). . Regenstein, _America the Poisoned,_ 275. . "Infant Abnormalities Linked to PCB Contaminated Fish," _Vegetarian Times_ (November 1984): 8. . Sandra Jacobson, "The Effect of Intrauterine PCB Exposure on Visual Recognition Memory," _Child Development_ 56 (1985). . Regenstein, _America the Poisoned,_ 233. . Environmental Protection Agency, _Toxaphene: Position Document_ 1, Toxaphene Working Group, Washington, DC (April 19, 1977), 19–20. . Ibid. . R. Taylor, "Cattle Deaths Stir Pesticide Debate," _Los Angeles Times,_ November 5, 1979. . Regenstein, _America the Poisoned,_ 336. . Taylor, "Cattle Deaths Stir Pesticide"; Ed Bradley, _60 Minutes,_ CBS News, November 22, 1981. . Schell, _Modern Meat,_ 155. . Ibid. . Ibid., 164–65. . _USDA Food Processing/Marketing Report_ (1965), cited in Hunter, _Consumer Beware,_ 155. . Department of Agricultural Appropriations, _Effects, Uses, Control, and Research of Agricultural Pesticides,_ a report by the Surveys and Investigations Staff, USDA, presented at hearings before a subcommittee on appropriations, 89th Cong., House of Representatives, part 1, 174. . _Mainstream,_ Summer 1983, 17. . Ibid. . _USDA Statistical Summary: Federal Meat and Poultry Inspection for 1976,_ January 1977, 3. . "U.S. Meat Banned for Export through the Common Market," _Vegetarian Times_ (October 1984): 17. . Regenstein, _America the Poisoned,_ 86, 272. . United Press, "Food and Drug Administration: Meat Dye May Cause Cancer," _Washington Post,_ April 6, 1973. . Robert Luck, "Chemical Insect Control," _BioScience_ (September 1977). . Frances Moore Lappé and Joseph Collins, _Food First—Beyond the Myth of Scarcity_ (Boston: Houghton Mifflin, 1977), 63. . Ibid., 64. . Ibid., 71. . D. Bottrell, _Integrated Pest Management,_ Council on Environmental Quality, Washington, D.C. (1980), iv–viii, 39, 99. . "What One Bird Can Do," Garden Club of America, cited in Regenstein, _America the Poisoned,_ 127. . J. Fillip, "American Farmers and USDA Start to Take Organic Seriously," _Not Man Apart,_ September 1980. . Ibid. . David Weir and Mark Schapiro, _Circle of Poison_ (San Francisco: Food First/Institute for Food and Development Policy, 1981); David Weir and Mark Schapiro, "The Corporate Crime of the Century," _Mother Jones,_ November 1979; David Weir, "The Boomerang Crime," _Mother Jones,_ November 1979; R. J. Smith, "US Beginning to Act on Banned Pesticides," _Science,_ June 29, 1979. . Regenstein, _America the Poisoned,_ 273. . Council on Environmental Quality, _Environmental Quality—1975,_ 375. . Cited in Regenstein, _America the Poisoned,_ 250. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 289. . Boyle, _Malignant Neglect,_ 206–7; Stephanie Harris and Joseph Highland, _Birthright Denied_ (Washington, DC: Environmental Defense Fund, 1977), 11; Regenstein, _America the Poisoned,_ 297. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 289. . Harris, "Organochlorine Contamination," 2. . Council on Environmental Quality, _Environmental Quality—1975,_ 375; Harris and Highland, _Birthright Denied,_ 2. . Boyle, _Malignant Neglect,_ 206–7. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 289. . D. Katz, "PCBs Found in Milk in All Michigan Mothers Tested," _Detroit Free Press,_ February 1, 1981. . Council on Environmental Quality, _Environmental Quality_ — _1975,_ 375. . Harris, "Organochlorine Contamination." . _New England Journal of Medicine,_ March 26, 1981. . _Selected Environmental Contamination Incidents,_ Committee on Environment and Public Works, 289. . Regenstein, _America the Poisoned,_ 255–56. . P. Hilts, "Chemicals at Parents' Job May Cause Child's Tumor," _Washington Post,_ July 3, 1981. . _Council on Environmental Quality, Chemical Hazards to Human Reproduction,_ Washington, DC (January 1981), II-3, 12. . "Politics of Poison," KRON-TV, San Francisco, 1979. . J. Gofmann and A. Tamplin, quoted in Stewart Brand, "Human Harm to Human DNA," _CoEvolution Quarterl_ y (Spring 1979): 11. ##### **Chapter Twelve. All Things Are Connected** . Mary Bralove, "The Food Crisis: The Shortages May Pit the 'Have Nots' against the 'Haves,'" _Wall Street Journal,_ October 3, 1974, 20. . H. J. Maidenburg, "The Livestock Population Explosion," _New York Times,_ July 1, 1973, Finance section; Jane E. Brody, "The Quest for Protein," from _Give Us This Day_ (New York: Arno Press, 1975), 222. . Frances Moore Lappé, _Diet for a Small Planet,_ 10th ed. (New York: Ballantine Books, 1982), 69; Aaron Altschul, _Proteins: Their Chemistry and Politics_ (New York: Basic Books, 1965), 264; Folke Doyring, "Soybeans," _Scientific American,_ February 1974. . _The World Food Problem,_ a report by the President's Science Advisory Committee, vol. 2, May 1967; Food Animals Concern Trust (Chicago), FACT sheet no. 26 (November 1982). . See citations in note 3. . Boyce Rensberger, "Curb on U.S. Waste Urged to Help World's Hungry," _New York Times,_ October 25, 1974. . _Acres, U.S.A._ (Kansas City, Missouri) 15, no. 6 (June 1985): 2. . Boyce Rensberger, "World Food Crisis: Basic Ways of Life Face Upheaval from Chronic Shortages," _New York Times,_ November 5, 1974, 14. . See citation in note 3. . Alastair MacKay, _Farming and Gardening in the Bible_ (Old Tappan, NJ: Spire Books, 1970), 224; Genesis 13:5–7; Numbers 31:32–33; Deuteronomy 12:20. . Plato, _The Republic,_ Book II, trans. Benjamin Jowett (London: Oxford University Press, 1892), 233. . Ibid. . Vernon Gill Carter and Tom Dale, _Topsoil and Civilization,_ rev. ed. (Norman: University of Oklahoma Press, 1974). . William Brune, State Conservationist, Soil Conservation Service, Des Moines, Iowa, testimony before Senate Committee on Agriculture and Forestry, July 6, 1976; Seth King, "Iowa Rain and Wind Deplete Farmlands," _New York Times,_ December 5, 1976, 61; Curtis Harnack, "In Plymouth County, Iowa, the Rich Topsoil's Going Fast, Alas," _New York Times,_ July 11, 1980. . Robin Hur, "Six Inches from Starvation: How and Why America's Topsoil Is Disappearing," _Vegetarian Times_ (March 1985): 45–47. . Ibid. . Ibid. . Harnack, "In Plymouth County, Iowa." . Hur, "Six Inches from Starvation"; David Pimentel et al., "Land Degradation: Effects on Food and Energy Resources," _Science_ 194 (October 1976); National Association of Conservation Districts, _Soil Degradation: Effects on Agricultural Productivity,_ Interim Report No. 4, National Agricultural Lands Study, Washington, DC (1980), 20; Seth King, "Farms Go Down the River," _New York Times,_ December 10, 1978, for citing Soil Conservation Service; as per estimates cited in Lappé, _Diet for a Small Planet,_ calculated from estimates by Medard Gabel, the Cornucopia Project (Emmaus, PA: Rodale Press). . Harnack, "In Plymouth County, Iowa." . Hur, "Six Inches from Starvation." . Robin Hur, quoted in Lappé, _Diet for a Small Planet,_ 80; Soil and Water Resources Conservation Act—Summary of Appraisal, USDA Review Draft, 1980, 18; Pimentel, "Land Degradation"; National Association of Conservation Districts, _Soil Degradation;_ USDA, Economics and Statistics Service, _Natural Resource Capital in U.S. Agriculture: Irrigation, Drainage, and Conservation Investments since 1900,_ ESCS Staff Paper (March 1979). . Medard Gabel, the Cornucopia Project, preliminary report (Emmaus, PA: Rodale, Inc.); C. A. Wolfbauer, "Mineral Resources for Agricultural Use," in _Agriculture and Energy,_ ed. William Lockeretz (New York: Academic Press, 1977), 301–14; U.S. Bureau of Mines, _Facts and Problems,_ 1975, 758–868; General Accounting Office, _Phosphates: A Case Study of a Valuable Depleting Mineral in America,_ report to the Congress by the Comptroller General of the United States, EMD-80-21 (November 30, 1979). . See citations in note 3. . Chief Seattle's testimony, an 1854 oration cited in _The Extended Circle,_ ed. Jon Wynne-Tyson (Fontwell, UK: Centaur Press, 1985). . Robin Hur and David Fields, "Are High-Fat Diets Killing Our Forests?" _Vegetarian Times_ (February 1984). . Ibid. . Ibid. . Ibid. . Ibid. . Ibid. . Ibid. . Ibid. . James Parsons, "Forest to Pasture: Development or Destruction?" _Revista de Biologia Tropical_ 24, supplement 1 (1976); Norman Myers, "Cheap Meat vs. Priceless Rainforests," _Vegetarian Times_ (May 1982); Billie DeWalt, "The Cattle Are Eating the Forest," _Bulletin of the Atomic Scientists_ (January 1983); "The World Conservation Strategy in Brief," World Wildlife Fund, 1980. . _Acres, U.S.A._ (Kansas City, Missouri) 15, no. 6 (June 1985): 2. . Ibid. . Ibid. . Ibid. . Lappé, _Diet for a Small Planet._ . Georg Borgstrom, presentation to the Annual Meeting of the American Association for the Advancement of Science, 1981. . Altschul, _Proteins: Their Chemistry._ . Paul Erlich and Anne Erlich, _Population, Resources, Environment_ (San Francisco: W. H. Freeman, 1972), 75–76. . "The Browning of America," _Newsweek,_ February 22, 1981, p. 26. . David Fields and Robin Hur, "America's Appetite for Meat Is Ruining Our Water," _Vegetarian Times_ (January 1985). . Ibid. . Ibid. . Ibid. . Ibid. . Ibid. . Ibid. . Philip Raup, "Competition for Land and the Future of American Agriculture," in _The Future of American Agriculture as a Strategic Resource,_ ed. Sandra Batie and Robert Healy (Washington, DC: Conservation Foundation, 1980); William Lagrone, "The Great Plains," in _Another Revolution in US Farming?,_ Lyle Schertz et al., USDA, ESCS, Agricultural Economic Report No. 441 (December 1979); Joe Harris, resource economist, part of four-year government-sponsored study, "The Six State High Plains Ogallala Aquifer Agricultural Regional Resource Study," cited in Lappé, _Diet for a Small Planet,_ 466; Fields and Hur, "America's Appetite for Meat." . Lagrone, "The Great Plains"; "Report: Nebraska's Water Wealth Is Deceptive," _Omaha World-Herald,_ May 28, 1981. . David Pimentel, "Energy and Land Constraints in Food Protein Production," _Science,_ November 21, 1975; H. A. Jasiorowski, "Intensive Systems of Animal Production," _Proceedings of the III World Conference on Animal Production,_ ed. R. L. Reid (Sydney: Sydney University Press, 1975), 384; Jackie Robbins, _Environmental Impact Resulting from Unconfined Animal Production,_ Environmental Protection Technology Series (Cincinnati: USEPA, Office of Research and Development, Environmental Research Information Center, February 1978), 9; _Environmental Science and Technology_ 4, no. 12 (1970): 1098, cited in Lappé, _Diet for a Small Planet._ . Jim Mason and Peter Singer, _Animal Factories_ (New York: Crown Publishers, 1980), 84. . Raymond Loehr, _Pollution Implications of Animal Wastes—A Forward Oriented Review,_ Water Pollution Control Research Series (Washington, DC: USEPA, Office of Research and Monitoring, 1968), 26, table 7, cited in Mason and Singer, _Animal Factories._ . Bruce Myles, "U.S. Antipollution Laws May Boost Cattle-Feeders' Cost—and Meat Prices," _Christian Science Monitor,_ March 11, 1974, 3-A. . _Newsweek,_ November 8, 1971, p. 85. . Georg Borgstrom, cited in Lappé, _Diet for a Small Planet,_ 1975 edition, 22. . Ibid. . Vivian Spencer, _Raw Materials in the United States Economy 1900–1977,_ technical paper 47, U.S. Department of Commerce, U.S. Department of Interior, Bureau of Mines, p. 3, cited in Lappé, _Diet for a Small Planet,_ 66. . J. T. Reid, "Comparative Efficiency of Animals in the Conversion of Feedstuffs to Human Foods," _Confinement_ (April 1976): 23. . Robin Hur and David Fields, "How Meat Robs America of Its Energy," _Vegetarian Times_ (April 1985). . Ibid. . W. L. Roller et al., "Energy Costs of Intensive Livestock Production," paper no. 75-4042 (St. Joseph, MI: American Society of Agricultural Engineers, June 1975): 14, table 7, cited in Mason and Singer, _Animal Factorie_ s. . Pimentel, "Energy and Land Constraints." . _Scientific American,_ February 1974, 19–20. . Hur and Fields, "How Meat Robs America." . Ibid. . Ibid. . Ibid. ##### **Epilogue to the 25th Anniversary Edition** . M. J. Stephey, "Top 10 Oprah Controversies," _Time,_ May 25, 2011, <http://www.time.com/time/specials/packages/article/0,28804,1939460_1939452_1939475,00.html> (accessed May 14, 2012). . Congressman Robert Scott, U.S. House of Representatives session on Animal Enterprise Terrorism Act, November 13, 2006, C-SPAN Video Library, <http://www.c-spanvideo.org/appearance/595633183> (accessed May 18, 2012). . Jane E. Brody, "Huge Study of Diet Indicts Fat and Meat," _New York Times,_ May 8, 1990, http://www.nytimes.com/1990/05/08/science/huge-study-of-diet-indicts-fat-and-meat.html?pagewanted=all&src=pm (accessed May 14, 2012). . Bridget Murray, "Getting to the Essential 'We' in Wellness," _Monitor on Psychology,_ American Psychological Association (November 2002), <http://www.apa.org/monitor/nov02/wellness.aspx> (accessed May 14, 2012). . "Best Results: Cleveland Clinic Study Stops Progress of Heart Disease with Diet and Cholesterol Drugs," Heartattackproof.com, <http://www.heartattackproof.com/news_info.htm> (accessed May 14, 2012). . David S. Martin, "From Omnivore to Vegan: The Dietary Education of Bill Clinton," CNN.com, August 18, 2011, <http://www.cnn.com/2011/HEALTH/08/18/bill.clinton.diet.vegan/index.html> (accessed May 14, 2012). . Caldwell B. Esselstyn, "Making the Change," Heartattackproof.com, <http://www.heartattackproof.com/morethan04_change.htm> (accessed May 14, 2012). . Dean Ornish, quoted in Roberto Suro, "Hearts and Minds," _New York Times Magazine,_ December 29, 1991, 28. . Ed Ayres, "Why Are We Not Astonished?" _World Watch,_ May/June 1999, <http://www.worldwatch.org/system/files/EP123B.pdf> (accessed May 14, 2012). . Christopher Flavin and Robert Engelman, "The Perfect Storm," _State of the World 2009: Into a Warming World,_ Worldwatch Institute, 5, <http://www.worldwatch.org/files/pdf/SOW09_chap1.pdf> (accessed March 27, 2012). . Bill McKibben, _Eaarth: Making a Life on a Tough New Planet_ (New York: Holt, 2010), xii. . "Suffering the Science: Climate Change, People, and Poverty," Oxfam briefing paper 130, July 6, 2009, <http://www.oxfam.org/sites/www.oxfam.org/files/bp130-suffering-the-science.pdf> (accessed May 14, 2012). . "What Is Ocean Acidification?" Oceana.org, <http://oceana.org/en/our-work/climate-energy/ocean-acidification/learn-act/what-is-ocean-acidification> (accessed May 14, 2012). . Jessica Ellis, "Montana's Melting Glaciers: The Poster-Child for Climate Change," CNN, October 6, 2010, <http://articles.cnn.com/2010-10-06/world/montana.glaciers.climate_1_glaciers-mountain-ecosystems-climate-change?_s=PM:WORLD> (accessed May 16, 2012). . Greenpeace International, "Climate Science," <http://www.greenpeace.org/international/en/campaigns/climate-change/science/> (accessed May 16, 2012). . "Greenland Melt Seems to Be Picking Up Speed," _New York Times,_ December 17, 2008, <http://www.nytimes.com/2008/12/17/world/americas/17iht-climate.1.18749442.html?_r=2> (accessed May 16, 2012). . Ross Gelbspan, _The Heat Is On_ (New York: Basic Books, 1998), 34. . Doyle Rice, "Report: 97 Percent of Scientists Say Manmade Climate Change Is Real," _USA Today,_ June 22, 2010, <http://content.usatoday.com/communities/sciencefair/post/2010/06/scientists-overwhelmingly-believe-in-man-made-climate-change/1#.T3JSr5j_6ao> (accessed March 27, 2012). . "Committee Approves Lieberman-Coauthored Clean Power Bill," website of Senator Joe Lieberman, June 27, 2002, <http://lieberman.senate.gov/index.cfm/news-events/news/2002/6/committee-approves-liebermancoauthored-clean-power-bill> (accessed May 15, 2012). . Union of Concerned Scientists, "Global Warming Science," <http://www.ucsusa.org/global_warming/science_and_impacts/science>, and "Global Warming," <http://www.ucsusa.org/global_warming/> (accessed May 15, 2012). . Food and Agriculture Organization of the United Nations, "Spotlight 2006: Livestock Impacts on the Environment," <http://www.fao.org/ag/magazine/0612sp1.htm> (accessed May 16, 2012). . Food and Agriculture Organization of the United Nations, "Livestock a Major Threat to Environment: Remedies Urgently Needed," FAO Newsroom, November 29, 2006, <http://www.fao.org/newsroom/en/news/2006/1000448/index.html> (accessed May 16, 2012). . Elke Stehfest et al., "Climate Benefits of a Changing Diet," _Earth and Environmental Science_ 95, no. 1 (2009). . Jim Giles, "Eating Less Meat Could Cut Climate Costs," _New Scientist,_ February 10, 2009, <http://www.newscientist.com/article/dn16573-eating-less-meat-could-cut-climate-costs.html> (accessed May 16, 2012). . Tracy Fernandez Rysavy, "Eat Less Meat, Cool the Planet," _Green American,_ September/October 2007, <http://www.greenamerica.org/livinggreen/lessmeat.cfm> (accessed May 16, 2012). . Ezra Klein, "Gut Check: Here's the Meat of the Problem," _Washington Post,_ July 29, 2009, <http://www.washingtonpost.com/wp-dyn/content/article/2009/07/28/AR2009072800390.html> (accessed May 16, 2012). . Nathan Fiala, "How Meat Contributes to Global Warming," _Scientific American,_ February 2009, <http://www.scientificamerican.com/article.cfm?id=the-greenhouse-hamburger> (accessed May 16, 2012). . Bryan Walsh, "Meat: Making Global Warming Worse," _Time,_ September 10, 2008, <http://www.time.com/time/health/article/0,8599,1839995,00.html> (accessed May 16, 2012). . "Meat the Truth: CO2 Effect of Eating No Meat for 1 Day a Week," YouTube video, 0:30, from the documentary _Meat the Truth_ by the Nicholas G. Pierson Foundation, posted by meatthetruth, October 21, 2008, http://www.youtube.com/watch?v=bwtgEs1h6Ws&list=UUelxb3dT6PEb-ZEYIviBjKg&index=9&feature=plcp (accessed May 18, 2012). . Daniele Fanelli, "Meat Is Murder on the Environment," _New Scientist,_ July 18, 2007. . Bryan Walsh, "The Global Warming Survival Guide: Skip the Steak," _Time,_ April 9, 2007, <http://www.time.com/time/specials/2007/environment/article/0,28804,1602354_1603074_1603171,00.html> (accessed May 16, 2012). . Robert Goodland and Jeff Anhang, "Livestock and Climate Change: What If the Key Actors in Climate Change Are...Cows, Pigs, and Chickens?" _World Watch,_ November/December 2009, <http://www.worldwatch.org/files/pdf/Livestock%20and%20Climate%20Change.pdf> (accessed May 16, 2012). . Klein, "Gut Check." ## **INDEX** Page numbers given in _italics_ indicate illustrations or material contained in their captions. Tables and graphs are indicated by _t._ following the page number. **A** Aaron Cushman Public Relations Agency, Abele, Ridgely, 141–42 Abkhasian people, Academie de Medicine (Paris), Aesop's fables, affection training, 15–17, African swine fever, Agent Orange, 296–97, ag-gag bills, agribusiness advertising by, 355–56 criticism stifled by, 356–57 disconnection from nature, , 53–54 farmers and, 49–50, organic farming downplayed by, profits of, , , public relations efforts of, 101–2, 106–13, _108–9,_ , _See also_ chicken factories; dairy industry; egg industry; meat industry; pig factories Agribusiness Accountability Project, AIDS, , 304–5 Albright, Jack, 95–96 alcohol, , , aldrin, 290–91 Alfa-Laval, algae, alkaloidal drugs, allergic reactions, Allied Chemical Corporation, Allport, Gordon, American Association for Science and Public Policy, American Association for the Advancement of Science, 164–65, , American Cancer Society, , _American Cookery_ (Beard), American Egg Board, , _,_ , 158–59, , American Heart Association, , , 216–17, 222–23 _American Heart Journal,_ , American Institute for Cancer Research, _American Journal of Cardiology,_ 147–48, _American Journal of Clinical Nutrition,_ , _,_ , , , , _American Journal of Digestive Diseases,_ _American Journal of Digestive Disorders,_ _American Journal of Epidemiology_ , American Meat Institute, American Medical Women's Association, 130–31 American Pork Queens, 72–73 American Public Health Association, American Society for the Prevention of Cruelty to Animals, American Society of Clinical Nutrition, American Veal Association, Amory, Cleveland, , , amputations, Anahareo, anemia, , , 273–76 angina pectoris, 147–49 _Animail_ (Peterson), 14–15 animal cruelty, 5–7 animal cruelty laws in ancient times, 80–84 food animals excluded from, , , 85–86 need for, , Animal Enterprise Terrorism Act (2006), _Animal Factories_ (Singer and Mason), , , 67–68 animal fats, 234 _t._, , 247–49, 291–92 _Animal Liberation_ (Singer), animal protein, Animal Research Institute of Agriculture (Canada), 46–47 animals affection of, 15–17 emotional capacities of, 20–22 human connection with, 26–29, human misunderstandings about, intelligence of, 22–26 long journeys of, as machines, 6–7, , 17–18, 53–54 as meat, objectification of, selfless behavior of, 3–5, 7–13, 14–15 senses of, suffering capacities of, 18–19 "Animals, My Brethren" (Kupfer), animal slaughterhouses American cultural conditioning about, 115–16 animals' perspective at, 118–19, 123–24 diseased animals in, field trips to, industry PR about, 106–13, _108–9_ , injury rates at, inspections at, killing methods at, 119–20 kosher/ritual slaughter at, 120–23 panic state in, public awareness about, 113–15, 125–26 public denial about, 105–6, , , 124–25 work environment at, 116–18 worker turnover rate at, Animal Welfare Act, 85–86 ankylosing spondylitis, antibiotics, , , , 87–88, 91–92, in livestock feed, 280–81 salmonella-resistant, 279–81 appendectomies, appendicitis, aquifer depletion, 344–45 Arendt, Hannah, Arkansas, , Armstrong, Mark, 192–94 _Arnold's Bodybuilding for Men_ (Schwarzenegger), arthritis, , 267–69 Arthritis Foundation, Asia, complementary vegetable proteins in, Asians, lactose intolerance in, asthma, 276–77 atherosclerosis arthritis patients vulnerable to, blood pressure and, defined, diabetics vulnerable to, health consequences of, 185–87 prevention of, , , saturated fat/cholesterol as cause of, 188–96, 218–19 athletes, vegetarian, 139–43 attitude, Ayres, Ed, **B** Bacon Bins, 64–65 Bailar, John, Bailey, Pearl, Banquet Foods Corporation, , Bantu people, 173–74 Barnes, Ernest G., Beard, James, beavers, human contact with, , 27–28 beef antibiotics in, environmental impact of, grass-fed, imports, , industry PR about, , _,_ , , "organically raised," pesticide residues in, use of term, wastefulness of, , Beef Council, beef fat, Belanie, Archie, Berg, John, 232–33 Bergh, Henry, Bernard, Harold, Bernstein, Daniel, Bertha (elephant), beta blockers, Bible, Bibs (canary), biochemical individuality, , 153–55 bird migrations, , birth defects, , , Blacks, lactose intolerance in, blindness, blood pressure, high, , 270–73 blood sugar, 253–54, 255–56 blood vessel dilators, Blue, Vida, Bobby (dog), 3–4 body fat, , , body weight, 265–66 Bolger, Ray, bone resorption, _Book of a Naturalist_ (Hudson), _Book of Lists #2, The,_ bran, branding, Braunstein, Mark, breast cancer, , 240–44, 241 _t._, breast-feeding, 319–21 _Brindle_ (ship), _British Journal of Nutrition,_ _British Medical Journal,_ , , , _Broiler Industry_ (journal), , 50–51 Brophy, Brigid, Brown, Lester, Brown, Theo, Bt crops, 359–60 Buckley, Kenneth, Burger King, Burk, Carol, 11–12 Burnford, Sheila, Burns, George, Burwash, Peter, butter, , 243 _t._, Butz, Earl, **C** cabbage, caffeine, cage crowding, 43–46 caged layer fatigue, cage stacking, 71–72 Cahling, Andreas, calcium, 178–79, , California, 343–44 California Agriculture Department, California Beef Council, 107–10 California Food and Agriculture Department, 311–12 California Milk Producers Association, , calories concentrations of, in foods, 265 _t._ empty, fat as percentage of, 246 _t._ meat diet and waste of, from protein, 156 _t._ calves, , _See also_ veal calves Campbell, T. Colin, , , Campbell, Thomas, Campbell Soup Company, Canadian Forest Service, _Canadian Medical Association Journal,_ cancer, , breast, , 240–44, 241 _t._, cervical, in children, colon, 181–82, 232–40 common types, death rates from, , , gallbladder, hormones as cause of, lung, meat diet as cause of, 181–82 obesity and, ovarian, pancreatic, pesticides as cause of, , , , , preventability of, 230–31, , prostate, , 247–49, 248 _t._ treatment for, 228–30, uterine, 244–45, vegetarianism and, , war on, 227–28, , 249–50 _Cancer Research_ (journal), cannibalism, , captive-bolt pistols, carbohydrates, , carbon dioxide, 361–62 Carnegie Mellon University, 365–66 Carney, Pam, 72–73 Carson, Rachel, 289–91, Carter, Karyl, 27–28 Carter, Vernon, cassava root, castration, Catholic Church, cattle dairy cows, 92–93 feedlot experience of, 88–92 feeds given to, hormone use with, intelligence/sensitivity of, , pesticide residues in, pesticides used on, shipping of, 86–88 slaughtering of, stereotypes of, 84–85 _See also_ veal calves cattle prods, Cayce, Edgar, Center for Disease Control (Atlanta, GA), Center for Science in the Public Interest, 198–99, , , , 216–17 Centre for Agriculture and Environment (Netherlands), cervical cancer, cheese, , , _t.,_ , chemical fertilizers, , 333–34, chemical industry, 308–10, , , Chevron, chewing, Chicago (IL), animal slaughter industry in, Chicago Board of Education, _Chicago Tribune_ , chicken cancer (leukosis), chicken factories aggression/cannibalism in, , as assembly lines, 35–38, cage crowding in, 43–46, "chicken pullers" at, 36–37 chicken's-eye view of, 45–46 de-beaking in, 39–41 diseased birds in, 48–49 excremental waste from, feed diet in, 47–49 flip-over syndrome in, flock sizes in, force-moulting in, human consumption of products of, 50–51, , industry view of, as "chicken heavens," , , 40–41, lighting conditions in, natural-food alternatives to, 51–53 ownership of, panic state in, 42–45, slaughtering at, , stampedes in, 43–44 weight maximization in, , chicken farmers, 49–50 chickens "better," breeding of, 46–47 broilers, , 46–47, contaminated, environmental impact of, intelligence of, 32–33 layers, , 41–42, light sensitivity of, maternal qualities of, 33–34 pesticide residues in, , , , 307–8 sensitivity of, social order of, 38–39 stereotypes of, 31–32, symbolic meanings of, as vegetables, children cancer in, deformed, , , industry "educational materials" aimed toward, 107–13, _108–9_ starvation of, undernourished, _China Study, The_ (Campbell and Campbell), chlamydia trachomatis, chloramphenicol, 87–88, chlordane, , , cholesterol, , , , animal foods vs. plant foods, 191 _t._ atherosclerosis caused by, 188–96 cancer and, controversy over, 199–201, 219–24 heart disease caused by, 190–96, 197 _t._, , meat/dairy industry obfuscations, 201–6, 216–17 medical understanding of, 206–8, 207 _t._, 220–21, 224–26 plant sources of, saturated fat consumption and, 193 _t._ circus animals, training of, 15–17 civil disobedience, 356–57 civil rights movement, Cleveland Clinic Wellness Institute, climate change, 360–65 climate refugees, Clinton, Bill, Coalition for Animal Agriculture, cock fighting, Collens, William S., Collins, Joseph, colon cancer, 232–40 blood cholesterol and, fat consumption and, 234 _t._ fiber consumption and, 233–36, 235 _t._ meat diet as cause of, 181–82, 232–33, 236–40, , 239 _t._ vegetarianism and, colons, human vs. animal, 236–37, __ colons, spastic, Colorado, Columbia River, 342–43 Columbia University, , Common Market, community gardens, _Confinement_ (farming journal), Conquest of Cancer Act (1971), 227–28 constipation, , cookbooks, corn, , 349–50, 359–60 Cornell University, , corn rootworms, 315–16 Costa Rica, , , , cotton, 359–60 council. _See_ National Livestock and Meat Board Council on Environmental Quality, Courtney, Diane, crop rotation, **D** Dachau concentration camp, 103–4 _Dachau Diaries_ (Kupfer), Dairy Council of Wisconsin, dairy cows, 92–93, _,_ dairy industry advertising by, 257–58, atherosclerosis "theory" and, 189–90 cancer and,231 lawsuits against, lobbying efforts of, "nutritional education" materials of, 151–52, obfuscations by, , 196–99, 205–6, political power of, 221–24 PR campaigns of, scientific studies sponsored by, _See also_ National Dairy Council _Dairyman_ (trade magazine), dairy products acidity formed by, 177 _t._ advertising by, cancer risk and, , 243 _t._ health consequences of, iron deficiencies from, 144–46, __ , 275–76 as iron sources, 274 _t._ organic, osteoporosis and, , , 175–76, 179–80 overconsumption of, 275–76 pesticide residues in, 291–92, 298–99 as protein source, 151–52, 158–59 Dale, Tom, Darwin, Charles, DDT, 290–91, 294–95, , , , , , de-beaking, 39–41 deDonato, James, deDonato, Jonathan, deforestation, 335–37, 338–40 de-horning, , Denmark, WWI vegetarian experiment in, 132–33 Denver, John, deoxycholic acid, DES (diethylstilbestrol), 288–89 Descartes, René, diabetes, , 252–55, dialysis, Diamon, Harvey, Diamond Shamrock, 312–13 dichlorvos, dieldrin, 290–91, 295–96, , , _Diet and Nutrition Letter_ (Tufts University), _Diet for a New America_ (Robbins), , , _Diet for a Small Planet_ (Lappé), 159–63, 162 _t._ diet-style, health consequences of, 129–30, 133–36, anemia, 273–76 arthritis, 267–69 asthma, 276–77 cancer, 229–31, diabetes, 252–55 heart disease, 251–52 hypertension, 270–73 hypoglycemia, 255–56 intestinal problems, 261–64 kidney stones, medical research supporting, , 357–60 MS, 256–59 obesity, 264–66 salmonellosis, 277–81 ulcers, 259–60 diet-styles changes in, long-term consequences of, pesticides and, 294 _t._ _See also_ diet-style, health consequences of dioxin, 296–98, , , , , , disease resistance, diuretics, diverticulosis, 262–63 DNA, dogs, human contact with, 3–4, 8–9 dolphins birthing behavior of, emotional capacities of, massacre of, in fishing nets, 13–14, selfless behavior of, 4–5, 7–8, 12–13 Dougherty, Ralph, Dow Chemical Company, 292–93, , Downstate Medical Center (NY), ducks, 14–15, , Dunsany, Lord, **E** "Eagle and the Arrow, The" (Aesop), _Earth and Environmental Science_ (journal), _East-West_ (journal), Ecclesiastes, Book of, Ecology Action Center, Ecuador, Edison, Thomas, 22–23 Egg City (Moorpark, CA), egg factories, , , , , , _,_ egg industry advertising by, , 201–2, , 257–58 atherosclerosis "theory" and, 189–90 cancer and, , "nutritional education" materials of, obfuscations by, 205–6 political power of, 221–24 scientific studies sponsored by, 202–3, _See also_ American Egg Board eggs acidity formed by, 176–78, 177 _t._, cancer risk and, 243 _t._, free-range, health consequences of, 175–76 industry PR about, pesticide residues in, 291–92, 298–99 as protein source, 151–52, 158–59 eggs, naturally produced, Einstein, Albert, electricity, meat diet and cost of, 342–43 elephants, intelligence of, El Salvador, embryo transfer, Emerson, Ralph Waldo, endrin, energy crisis, 347–50 Environmental Defense Fund (EDF), 298–99, , Eskimos, , Esselstyn, Caldwell B., , 358–59 estrogen pills, European Economic Community (EEC), 280–81, Excel Corporation (Dodge City, KS), excremental wastes, from factory farms, 345–47 exercise, , 167–69, , , ExxonMobil, , eye damage, **F** factory farms American cultural conditioning about, 115–16 animal cruelty in, antibiotics use in, 279–80 diseased animals in, energy consumption to support, field trips to, flies in,312 hormone use in, 286–89 industry PR about, 106–13, _108–9_ public awareness about, , public denial about, 105–6 as saturated fat suppliers, 285–86 toxic chemical use in, 310–13 water pollution resulting from, 345–47 _See also_ chicken factories; pig factories Farm Animals Concern Trust (FACT), , 99–100 Farm Animal Welfare Council, 101–2 _Farmer and Stockbreeder_ (journal), , , farmers, _Farming Express, The_ (journal), _Farm Journal_ , , , , , fast-food industry, fat, dietary, , 246 _t._ _See also_ saturated fats feather-pecking, fecaliths, feces, human, Federal Center for Disease Control, 279–80 Federal Humane Slaughter Act, Federal Trade Commission, 196–97, 201–2, feedback loops, 363–64 feedlots, 88–92, 346–47 feelings, expression of, fertilizers, , 333–34, fiber, 233–36, 235 _t._, , , , 268–69, Fields, David, , , 350–52 Finland, fish acidity formed by, , 177 _t._, as iron source, 274 _t._ pesticide residues in, 298–99, 307–10 Fisher, Irving, 137–38 fishing nets, 13–14 fish meal, , , 310–11 flanking straps, flies, flip-over syndrome, floggers, 118–19 flooding, Florida, Florida State University, Food and Agriculture Organization (FAO), , Food and Nutrition Board, __ , food chain, , , 291–92, , 298–99, Food First, _Food First_ (Lappé and Collins), food groups, basic, , , , food imports, _Food/2_ (magazine), force-moulting, Ford, Henry, forests, as oxygen sources, fossil fuel industries, 362–63 fossil fuels, France, Anatole, Frase, Bob, "free range," use of term, Friends of Animals Inc., frogs, dissections of, fruit diet, , , , as iron sources, 274 _t._ Fuhrman, Joel, **G** gallbladder disease, , gallstones, 269–70 Gandhi, Mohandas, , , geese, , Gelbspan, Ross, General Accounting Office, genetically modified organisms (GMOs), 359–60 Glacier National Park, glaciers, melting of, global warming, 360–65, 366–67 glucose tolerance, 255–56 Glueck, Charles, Goodland, Robert, Gori, Gio B., 230–31 Goss, Adrian, gout, Gowe, R. S., 46–47 grains, , , , , 274 _t._, Gray, Estelle, grazing land, deforestation to create, 335–37, 338–40 Great Britain, 280–81 Great Britain, WWII meat consumption diminished in, greenhouse effect, _See also_ global warming greenhouse gas emissions, 363–64, Greenlanders, Greenland ice sheet, melting of, Grey Owl, groundwater depletion, 344–45 Guatemala, , , Gupta, Sanjay, gynecomastia, **H** Haber, Gordon, 21–22 Hainsworth Farm (Mt. Morris, NY), Haley, Fred C., Hammer, Armand, Hansen, James, Harlow, Harry, Harrison, Michelle, 130–31 Harvard University, , , , Hausman, Patricia, , 216–17, 220–21 Hawaii, health food stores, heart, arteries in, 183–84 heart attacks atherosclerosis as cause of, , 218–19 defined, diabetics vulnerable to, , 253–54 hypertension drugs and risk of, prevention of, 225–26 ulcer disease patients vulnerable to, heart disease, blood cholesterol and, controversy over, 199–201, 219–24 diet as cause of, , 239 _t._, 251–52 factors involved in, meat/dairy industry obfuscations, , 196–99, 201–6, 216–17 medical understanding of, 187–88, 190–96, 197 _t._, 206–8, 220–21, 224–26 obesity and, pattern studies, preventability of, saturated fat/cholesterol as cause of, 190–96, 197 _t._, vegan diets and reversal of, Hegstead, Mark, , Helfer, Ralph, Helfer, Toni, hemorrhaging, hemorrhoids, 261–62, hens, maternal qualities of, 33–34 heptachlor, , 298–300, , hernias, hiatal, , Herophiles, herpes, Hesse, Hermann, hexachlorophene, 302–3 Hightower, Jim, Hilligan, Roy, Hindhede, Mikkel, Hirayama, Takeshi, Hirooka, Tatsuro, Hirschy, Charles A., _Hog Farm Management_ (journal), 63–64, , Honduras, _Hooray for the Hot Dog_ (meat industry educational material), hormones, , , 68–69, , 91–92, , 286–89 Hornblower, Margot, 296–97 Houghton Mifflin Inc., Houston, Donald, _How to Survive in America the Poisoned_ (Regenstein), Hudson, W. H., , 57–59, Humane Farming Association, Humane Society of the United States, 100–101 Hunzakut people, , Hur, Robin, , , 350–52 Huxley, Aldous, Huxley, T. H., hyperactivity, hypertension, 270–73 hypoglycemia, , 255–56 **I** ice cream, as health food, , Idaho, 342–43 immune system diseases, 302–5 Imperato, Pascal, impotence, _Incredible Journey, The_ (Burnford), infant mortality, infections, infertility, , insecticides, 88–89, 91–92 insect pests, Institute for Food and Development Policy, insulin pumps, insulin therapy, integrated pest management (IPM), , 315–17, , interconnectedness, 26–29, , , 328–29, 334–35, 352–54, interest rates, 351–52 International Atherosclerotic Project, intestinal problems, 261–64 intestines, human vs. animal, 236–37, __ Ioteyko, J., Iowa, IQs, iron content, _,_ 274 _t._ iron deficiencies, 144–46, 273–76 Ironman Triathlon, irritable colon syndrome, Islam, ritual slaughter, 120–23 **J** Jackson, Jackson, and Wagner, Jacobson, Michael, 198–99 James River, Japan, 191–92, 232–33, , , 245 _t._ Jerseymaid, job creation, 343–44, John-Duck, 14–15 Jones, Alan, , Jones, Harley, Josephine (wild boar), 60–61, _Journal of Immunology_ , _Journal of Pediatrics,_ _Journal of the American Dietetic Association,_ _Journal of the American Medical Association,_ , , , , , _Journal of the American Veterinary Medical Association,_ _Journal of the National Cancer Institute,_ , , , _Journal of the Norwegian Medical Association,_ 195–96 _Journal of the Puerto Rico Medical Association,_ 287–88 Judaism, kosher slaughter, 120–23 Juliano, Jeff, junk food, , , **K** Kansas, , KARE-TV (Minneapolis, MN), Kellert, Stephen, Kennedy, George, kepone, 290–91, , Kewaskum (WI), 18–19 Keys, Ancel, 190–91 kidney disorders, 180–81, kidney failure, kidney stones, , Kilmer, Joyce, King, Martin Luther, Jr., Klein, Ezra, Koranyi, A., Korean War, 188–89 kosher slaughter, 120–23 KRON-TV (San Francisco, CA), Kupfer, Edgar, 103–5 Kurgi people, kwashiorkor, **L** lacto-ovo vegetarian diet, , , , , lactose intolerance, Lambert, Herbert, lambs, _Lancet_ (journal), , 163–64, , , Laplanders, Lappé, Frances Moore, 159–63, 162 _t._, , , Lardner, Ring, larvicides, 312–13 Latin America, complementary vegetable proteins in, laughter, laxatives, Leahy, Patrick, learning disabilities, Lehman Farms (Strawn, IL), Leonardo da Vinci, Leukemia Society of America, leukosis, Levy, Robert, , Library of Congress, 301–2 Lieberman, Joe, Liebman, Bonnie, life expectancy, diet-style choice and, 135–36 Life Sciences Inc., Linares, Sixto, 139–40, Lincoln, Abraham, lindane, linoleic acid, 257–58 lipoproteins, liver disorders, , Livestock Conservation Institute, , livestock feed, 280–81, , , , , 310–11, , , , "Livestock's Long Shadow" (report), , local foods, , , Loma Linda University, , Longevity Centers, , Lorca, Federico, Louisiana, , low-fat diets, 220–21, 258–59, 262–63, 268–69, Lundberg, George, lung cancer, lupus erythematosus, Lyng, Richard, 221–22 Lyon, Thomas, **M** Macy, Joanna, maggot infestations, Mahlman, John, male reproductive tract, pesticide residues in, 321–22 Marek, Cheryl, Marine Mammal Protection Act (1972), Marmot, M. G., Martin, Robert, Mary-Duck, 14–15 Mason, Jim, , , 67–68 Mayer, Jean, McDonald, Douglas, McDonald's, , McDougall, John, , McGovern, George, , McGrady, Kevin, McKibben, Bill, , McLean, Louis A., Meat Board. _See_ National Livestock and Meat Board meat diet acidity formed by, 176–78, 177 _t._, American cultural conditioning about, 115–16, , 147–49 deforestation as result of, 335–37, 338–40 energy consumption to support, 347–50 environmental effects of, , fear consumed in, health consequences of, , 171–73, 175–76, 232–33, 236–40, 239 _t._, 247–49, as iron source, , 274 _t._ new questions about, 76–77, , 328–29 obesity and, pesticide residues in, 291–92, 298–99, 318–19 as protein source, 151–52, 158–59, 326–27 smoking and, , suffering caused by, switching away from, 365–69 territorial disputes as result of, 329–31 vegetarian stamina/strength compared to, 137–39 wastefulness of, , , , 326–29, 340–45 water consumption to support, 340–45 WWI reductions in, , Meat Importers Council of America, meat imports, , meat industry advertising by, , , 257–58, atherosclerosis "theory" and, 189–90 cancer and,231 criticism stifled by, 356–57 government collusion with, , 341–42, , lobbying efforts of, "nutritional education" materials of, 151–52, , , , obfuscations by, , 196–99, 205–6, 216–17, , 280–81, 356–57 political power of, 221–24 scientific studies sponsored by, _See also_ National Livestock and Meat Board meat inspections, 277–79, 313–14 meat labels, , meatpacking plants. _See_ animal slaughterhouses _Medical Counterpoint_ (Collens), medical research, as out-of-date, _Medical Tribune,_ medicines of the future, Melton, Anthony, 11–12 menarche, 242–44, menopause, , , methane, Metzger, Deena, Mexico, Michigan, 300–301 Michigan, Lake, Michigan Senate Commerce Subcommittee, Michigan State University, 174–75 Micronesia, 254–55 Middle East, complementary vegetable proteins in, milk arthritis and, cancer risk and, industry PR about, , , 210–11 linoleic acid in, MS risk and, osteoporosis and, 179–80 pesticide residues in, production of, 92–93 as protein source, , 157 _t._ Milk Industry Foundation, , __ Miller, Bradley, Minnesota, mirex, miscarriages, Missouri, Missouri Egg Merchandising Council, Missouri State Health Department, Mitchell, Joni, _Modern Meat_ (Schell), 286–88 Moffett, Thomas, Monsanto, , Montclair (NJ), Morgan, John, Morris, Desmond, Moses, Edwin, , multiple sclerosis, 256–59 Muscular Dystrophy Association, **N** _Naked Ape, The_ (Morris), National Academy of Sciences, , , , , National Cancer Institute, , , 229–30, 232–33, National Cancer Research Institute (Tokyo, Japan), National Commission on Egg Nutrition, 201–2, , National Dairy Council, , _,_ , advertising by, , 216–17 financial resources of, founding of, "nutritional education" materials of, , 208–11, , , obfuscations by, , 215–17 osteoporosis and, , 173–74, , protein diet promoted by, 158–59 research studies sponsored by, , , National Egg Board. _See_ American Egg Board National Environmental Research Center, National Heart, Lung and Blood Institute, _National Hog Farmer_ (journal), , National Institute of Livestock and Grassland Science (Japan), National Livestock and Meat Board, , , , 158–59, , , 216–17, National Nutritional Education Training Program, National Pork Council, 72–73, National Research Council, _,_ Native Americans, natural foods poultry, 51–53 use of term, natural food stores, Nauru (Micronesia), 254–55 Neary, George, 311–12 Nebraska, NEST EGGS trademark, _Neverskoil_ (fishing vessel), _New England Journal of Medicine,_ , , 279–80 New Mexico, _New Scientist, The_ (journal), _Newsweek_ , , New York, _New Yorker_ , _New York Times_ , Nicaragua, Nigeria, nitrofurazone, Nixon, Richard M., , North Carolina, Norum, Kaare, 195–96 Norway, WWII meat consumption diminished in, , __ Norwegian Medical Association, 195–96 "No Veal This Meal" campaign, 100–101 Novick, Richard, nuclear power plants, Nurmi, Paavo, nutrition "basic four" propaganda about, cancer and, 229–31 health consequences of, 129–30, 133–36 medical community ignorance about, 130–32 nutritional science, **O** oats, obesity, , , 264–66 Occupy Wall Street protests, ocean acidification, 361–62 Ogallala Aquifer, _Ogonyok_ (Soviet journal), Ohio State University, Oklahoma, , Oreffice, Paul, Oregon, 342–43 "organic," use of term, organic farming, , 315–18 organic produce, Ornish, Dean, 357–58 Oscar Mayer meat company, 110–11, osteoarthritis, osteoporosis dairy industry obfuscations and, 178–79 health consequences of, 169–70, __ protein excess as cause of, 169–73, 172 _t._, 178–80 research on, 173–75 treatment for, in U.S., 179–80 vegetarianism and, 175–76 ostriches, 25–26 ovarian cancer, ovarian cysts, Overseas Development Council, oxygen, ozone depletion, **P** Pace, Henry F., Pachauri, Rajendra, Panama, pancreas, , , pancreatic cancer, Paramount Chickens, Pauling, Linus, PBBs (polybrominated biphenyls), PCBs, , 305–8, , , Pelorus Jack (dolphin), 4–5 _Penguin_ (ship), 4–5 Perdue, Frank, Perdue, Inc., Perkins, Mike, permafrost, methane emissions from, pesticides alternatives to, 314–18 "banning" of, 293–95, 301–2 in breast milk, 319–21 chemical stability of, 290–91, chlorinated hydrocarbon, 290–91, corporate obfuscations, 308–10 environmental effects of, 289–90 in food chain, 291–92, , 298–99 future threat posed by, 322–23 in GMOs, 359–60 human consumption of products containing, in livestock feed, 307–8, 310–11 management/regulation of, 292–93 marketing of, mass poisonings from, 299–301 meat inspections and, 313–14 mutagenic effect of, 322–23 production rates, public unawareness of, , reducing intake of, 318–19 resistance to, 315–17 time lag between ingestion and effects, 299–300, 304–5 in U.S. diet, 294 _t._ use of, and crop losses, 314–15 use of, in factory farms, 310–13 _See also specific pesticide_ _Pesticides Monitoring Journal,_ PETA, Peter, Laurence, , Peterson, Arthur, 14–15 pH, 176–78, 177 _t._, pharmaceutical industry, , 280–81 Phillips, Ronald, phosgene, phytoplankton, , Picasso, Pablo, Pickering, Bill, pig factories as assembly lines, 63–65, , 75–76, breeding procedures in, 66–69 confinement areas in, 64–66, 71–73 diseased animals in, , , excremental waste from, feed diet in, , 73–74 foot/leg crippling in, 65–66, hormone use in, 68–69 human consumption of products of, industry PR about, 72–73, lighting conditions in, number of pigs in, slaughtering at, , , , smell of, 62–63, tail-biting in, 70–71 weight maximization in, , pig farmers, 72–73 _Pig Farming_ (journal), Pig Mama, pigs cleanliness of, 56–57 friendliness of, 57–61, , 74–75 intelligence of, olfactory sense of, pesticide residues in, pesticides used on, selfless behavior of, 11–12 stereotypes of, 55–57, Pimentel, David, placebo effect, plant-strong diet, switching to, 365–69 Plato, , 329–30 pneumonia, , , Polynesians, 254–55 Pope, Alexander, pork industry PR about, pesticide residues in, 299–300 use of term, _Poultry Digest_ (journal), , , , _Poultry Science_ (journal), _Poultry Tribune_ (journal), , , _Poultry World_ (journal), , Pratt, Marv, President's Council on Environmental Quality, Preventive Medicine Research Institute, Price, Stan, Priscilla (pig), 11–12 Pritikin, Nathan, , , 173–74, _Proceedings of the National Academy of Sciences,_ processed foods, , , prostate cancer, , 247–49, 248 _t._ prostates, enlarged, protein animal vs. vegetable, calories from, 156 _t._ complementary vegetable, 159–66, 162 _t._ daily needs, 153–57, deficiencies, , 165–66 diets moderate in, excess of, as osteoporosis cause, 169–73, 172 _t._, 178–80 excess of, health consequences of, 180–82 exercise and, 167–69 gout and,268 meat/dairy industry promotion of, 151–52, 158–59 poultry and, research on, , 163–65 protein efficiency, 326–27 Provimi, Inc., 95–98, , , psyllium husks, puberty, early onset of, , 245 _t._, , 286–88 Public Health Research Institute, public schools animal protein promoted in, , 158–59, dairy industry "educational materials" at, , , frog dissections in, meat industry "educational materials" at, 107–13, _108–9,_ Puccini, Giacomo, Puerto Rico, 287–88 Pure Food and Drug Act (1906), purines, purse seines, 13–14, **R** Rabon, 312–13 railroads, cattle shipping regulations of, Rainforest Action Network, rain forest destruction, 338–40 RAMBLING ROSE BRAND, Rand Corporation, Reagan, Ronald, 13–14, 292–93 Reed, Herbert, "Re-evaluation of the Nutrient Role in Animal Products, A" (report), Regenstein, Lewis, , , , , 313–14, 318–19 renewable energy, , _Republic_ (Plato), 329–30 Reuben, David, rheumatoid arthritis, , Rifkind, Basil, Ringo (dog), Rio de Janeiro (Brazil), environmental summit in, Ritewood Farms (Idaho), 307–8 ritual slaughter, 120–23 Riverside Meat Packers, "Rocky Mountain oysters," rodeos, Romney, Hugh, roosters, , Rose, Murray, , Ryan, Kerrie, 296–97 Ryan, Michael, **S** Saenz, Carmen A., 286–88 safflower oil, Saleh, Randy, salmonellosis, 277–81 salmon fishing, 13–14 salt, , 270–71 Salt, Henry S., 113–14 saturated fats atherosclerosis caused by, 188–96 blood cholesterol and, 193 _t._ controversy over, 199–201, 219–24 in factory farm animals, 285–86 heart disease caused by, 190–96, 197 _t._, measurement of, 211–15, 212–13 _t._ meat/dairy industry obfuscations, 201–6, 216–17 medical understanding of, 220–21, 224–26 nutrients contained in, 257–58 plant sources of, Scharffenberg, John, 164–65 Schell, Orville, 286–88 school lunches, poisoned pork in, 299–300 Schwarzenegger, Arnold, Schweitzer, Albert, , 60–61, , _Science_ (magazine), _Scientific American_ (journal), , , Scott, Dave, , , Scott, Robert, Seattle (Native American chief), 334–35, 353–54 Serjeant, Richard, serving sizes, Settepani, Joseph A., _Seventy Years among Savages_ (Salt), 113–14 sexual abuse, sexuality, early development of, , 286–89 Shain, Merle, Shaw, George Bernard, , , Shaw, Henry Wheeler, sheep, shellfish, , Shell Oil Company, shipping fever, 87–88 Siebu Lions (Japanese baseball team), _Silent Spring_ (Carson), 289–91, Silverman, Herb, , Singer, Isaac, Singer, Peter, , , , 67–68 Singh, Inder, "Sippy diet," _60 Minutes_ (TV news program), 278–79 Smaha, Jenda, smoking, , , , , , , Snake River, 342–43 Snowden, David, Snowden, John, Socrates, 329–30 soil erosion, 331–34, , , 338–39, solar power, soybeans, , 349–50 spastic colons, Special Children's Charity, species extinction, 339–40 _Spectrum of Pain, The_ (Serjeant), sperm counts, spider mites, Spitz, Mark, _Sports Illustrated,_ stamina, of vegetarians vs. meat eaters, 137–39 staphylococci bacteria, starvation, , sterility, , , St. Louis Medical School, stock density, Stoller, Kenneth, stomach ulcers, , 259–60 _Story of Beef, The_ (meat industry educational material), , __ _Story of Pork, The_ (meat industry educational material), strength, of vegetarians vs. meat eaters, 137–39 strokes, , 185–87, , , , , , _Successful Farming_ (journal), suffering meat diet as cause of, minimization of, sugar consumption, , sulphonylureas, 253–54 Swank, Roy, 258–59 Sweeney, J. Shirley, 255–56 sweetbreads, Sweetgall, Robert, Switzerland, WWII meat consumption diminished in, **T** Taffy (dog), 8–9 tail-biting, 70–71 tail-docking, TASS (Soviet news agency), , terrorism, civil disobedience as, 356–57 Texas, , Textron Inc., Thomas, Dylan, Thoreau, Henry David, _Time_ magazine, , tobacco industry, , , Toda people, _Today_ (TV morning show), Tolstoy, Alexandra, 114–15 Tolstoy, Leo, _Topsoil and Civilization_ (Carter and Dale), Toronto (Canada), toxaphene, , 311–12 toxic chemical pollution hormones, 286–89 immune system diseases caused by, 302–5 _See also_ pesticides Toxic Substances Control Act, truck, cattle shipping by, 86–88 Truman, Harry S., Tufts University, tuna fishing, 13–14, turkeys, , , turkey shoots, 18–19 turtles, human contact with, Twain, Mark, , 2,4-D, 2,4,5-D, **U** ulcers, , 259–60 _Uncle Jim's Dairy Farm_ (dairy industry educational material), Unicars, Union of Concerned Scientists, Union Stockyards (Chicago, IL), United Nations, , , United States arthritis rates in, cancer rates in, 232–33, 240–41, 241 _t._, chicken factories in, death causes in, , 186 _t._, , deforestation rates in, heart disease in, hemorrhoid medications in, life expectancy and diet-style in, osteoporosis in, 179–80 pesticide production in, 305–6, stool quality in, topsoil loss in, 331–34 vegetarian bone density in, 174–75 United States Bureau of Land Management, , United States Department of Agriculture (USDA), , , , , 278–79, , , , , , , , United States Department of Commerce, United States Department of Health, United States Department of Interior, United States Environmental Protection Agency (EPA), , , , , United States Food and Drug Administration, , , , , , United States Forest Service, , United States Karate Association World Championship, 141–42 United States Labor Department, United States Public Health Service, United States Senate Committee on Nutrition and Human Needs, , , 230–31 United States Soil Conservation Service, United Way, University Hospital (Linkoping, Sweden), 276–77 University of Arizona, University of California, , University of Chicago, , University of Cincinnati, University of Iowa, 192–94 University of Minnesota, , 190–91, , , University of Missouri, University of Oregon, 258–59 University of Southern California Medical School, Upton, Arthur, uterine cancer, 244–45, **V** Van Buren, Abigail, varicose veins, veal boycotts, 100–101 veal calves auctioning of, 93–94 diet of, 96–99 FACT husbandry method, lighting conditions for, opposition to raising methods, 99–102 Provimi raising method, 95–98 slaughtering of, , stall size for, , veal cuisine, _Vealer USA, The_ (journal), vegan diets, 357–59, vegetable oils, , vegetables, cabbage family, and ulcer treatment, calcium/phosphorus ratios in, 176–78, 177 _t._ diet of, and hypertension, diet of, and stool quality, as iron sources, 144–45, , 274 _t._, salmonella bacteria spread to, vegetarianism American cultural conditioning about, 115–16, 136–37, 147–49 anemia myth about, 273–76 athletes as, 139–43 breast-feeding women and, 320–21 chicken and, dairy industry PR and, diet types, economic benefits of, 350–52 health benefits of, 132–36, , 174–75, , , , 276–77 hypothetical diet, 162 _t._, kidney stones and, lacto-ovo, , , , , meat-eater stamina/strength compared to, 137–39 meat industry personalities as, meat production methods and, 76–77, , menarche and, obesity and, osteoporosis and, 175–76 protein needs met in, 155–57, 159–66, 162 _t._ switching to, 365–69 unsuccessful switches to, 143–46, __ water consumption and, WWI mass experiment in, 132–33 Velsicol Chemical Corporation, 298–99 Verot, Pierreo, Verret, Jacqueline, Vietnam veterans, Vilcamba people, Violet No. , Virginia, Virginia Polytechnic Institute, vitamin A, vitamin B12, vitamin B-complex, vitamin C, , , vitamin D, vitamin deficiencies, Vladislavich, Yvonne, voice register, changes in, Voltaire, **W** _Wall Street Journal,_ war, and meat diet, 329–30 _Washington Post,_ 296–97, Washington State, 342–43 Washington University (St. Louis, MO), Watchman, Aaron, water pollution, 345–47 Water Resources Council, water subsidies, 341–42, water supply, 340–45 Watson, E. L., Wayne State University Medical School, Webb, Harry J., whales, White, Paul Dudley, Williams, Roger, , 153–55 Wilson, Ken, 8–9 Winfrey, Oprah, Winick, Myron, Wisconsin Heart Association, Wissler, Robert, wolves, 21–22, World Bank, 367–68 World Conference on Animal Production (1975), World Health Organization, _,_ , world hunger, World War I, 132–33 World War II German concentration camps during, 103–4 meat consumption diminished during, , _,_ , pesticide use following, Worldwatch Institute, _World Wood Review_ (journal), **X** XLP-30 (feed additive), **Y** _Yale Medical Journal,_ 137–38 Yale University, , Yankee Stadium (New York, NY), yogurt, Yucatan Indians, **Z** Zyklon-B, ## ABOUT THE AUTHOR John Robbins is the author of nine bestsellers that have been translated into twenty-six languages. As an advocate for a compassionate and healthy way of life, he is the recipient of the Rachel Carson Award, the Albert Schweitzer Humanitarian Award, the Peace Abbey's Courage of Conscience Award, Green America's Lifetime Achievement Award, and many other accolades. John is the founder and board chair emeritus of EarthSave International, and has served on the boards of many nonprofit organizations working for a sustainable, just, and spiritually fulfilling human presence on this planet. His life and work have been featured in an award-winning hour-long PBS special titled _Diet for a New America._ John lives with his wife of 45 years, Deo; their son, Ocean, and his wife, Michele; and their grandsons, River and Bodhi, outside Santa Cruz, California. Their home is powered entirely by solar electricity. For further information, visit www.johnrobbins.info. 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1. Field of the Invention The present invention relates to a wireless communication system, and a wireless communication method in the wireless communication system. 2. Description of the Related Art Awareness of crime prevention has improved year by year. In recent years, a demand for the realization of entrance monitors or the like through simple installation at a low cost even in single occupant households such as detached houses as well as studio apartments is increasing. According to such a demand for the simple installation at a low cost, an entrance monitor in which a slave device of the entrance monitor or a master device of the entrance monitor is driven by a battery, and both of the devices are caused to perform wireless communication, making wiring work unnecessary, has begun to spread. In this case, since work for battery replacement occurs when the battery lifetime of the battery mounted on the slave device or the monitor master device expires, there is a need for a wireless communication system for reducing power consumption. As a method of implementing reduction of power consumption of such a wireless communication system, a wireless communication technology in which a called station repeats regular reception, and a calling station continuously transmits a capture signal longer than an interval of the regular reception of the called station to transition to a constant operation, disclosed in, for example, Japanese Patent Unexamined Publication No. 2003-087180, is known. Further, technology of a wireless master device (calling device) for suppressing useless continuous transmission when a call signal is continuously transmitted to an intermittently receiving wireless slave device (locator) so as to establish synchronization of transmission and reception, disclosed in, for example, Japanese Patent Unexamined Publication No 2014-082615, is known. However, although the technology disclosed in Japanese Patent Unexamined Publication No. JP 2003-087180 can achieve a certain object of reducing power consumption of the called station (slave device), reduction of power consumption on the master side has not been considered. Further, the technology disclosed in Japanese Patent Unexamined Publication No. 2014-082615 is intended to reduce the power consumption for a transmission operation on the master side, in addition to reduction of the power consumption of the wireless slave device (locator), but reduction of power consumption of operations, including a reception operation, has not been considered.

--- abstract: 'The nonlinear problem of steady free-surface flow past a submerged source is considered as a case study for three-dimensional ship wave problems. Of particular interest is the distinctive wedge-shaped wave pattern that forms on the surface of the fluid. By reformulating the governing equations with a standard boundary-integral method, we derive a system of nonlinear algebraic equations that enforce a singular integro-differential equation at each midpoint on a two-dimensional mesh. Our contribution is to solve the system of equations with a Jacobian-free Newton-Krylov method together with a banded preconditioner that is carefully constructed with entries taken from the Jacobian of the linearised problem. Further, we are able to utilise graphics processing unit acceleration to significantly increase the grid refinement and decrease the run-time of our solutions in comparison to schemes that are presently employed in the literature. Our approach provides opportunities to explore the nonlinear features of three-dimensional ship wave patterns, such as the shape of steep waves close to their limiting configuration, in a manner that has been possible in the two-dimensional analogue for some time.' address: 'School of Mathematical Sciences, Queensland University of Technology, QLD 4101, Australia' author: - Ravindra Pethiyagoda - 'Scott W. McCue' - 'Timothy J. Moroney' - 'Julian M. Back' title: | Jacobian-free Newton-Krylov methods with GPU acceleration\ for computing nonlinear ship wave patterns --- three–dimensional free–surface flows ,nonlinear gravity waves ,Kelvin ship wave patterns ,boundary–integral method ,preconditioned Jacobian-free Newton-Krylov method ,GPU acceleration Introduction {#sec:intro} ============ This study is concerned with steady three-dimensional free-surface profiles that are caused by a disturbance to a free stream. These profiles are characterised by the distinctive Kelvin ship wave patterns that are observed at the stern of a vessel or even behind a duck swimming in an otherwise still body of water. While free-surface flows of this type have ongoing practical applications to ship hull design, as we mention below, the structure of these patterns has sparked renewed interest in the physics literature, with observations that ships moving sufficiently fast may give rise to wake angles that decrease with ship speed [@darmon14; @ellingsen14; @rabaud13], in apparent contradiction to the well-known Kelvin angle of $\arcsin (1/3)\approx 19.47^\circ$ [@lighthill], which is derived from linear theory. In contrast to these approaches, our purpose here is to treat the fully [*nonlinear*]{} equations, and present algorithms for the accurate computation of nonlinear ship wave profiles. The mathematical analysis of ship wave patterns has a very long history, the overwhelming majority of which concerns linear theories. For example, for the classic problem of flow past a pressure distribution applied to the surface of the fluid $z=\zeta(x,y)$, if the pressure is small enough then the kinematic and Bernoulli boundary conditions on $z=\zeta(x,y)$ can be linearised onto the undisturbed plane $z=0$ [@havelock19; @noblesse09b; @scullen11]. This framework is used to model the wave pattern caused by an air-cushioned vehicle such as a hovercraft or a high-speed “flat ship” with a small draft. Another approach is to consider the ship wave pattern due to a thin ship. In this case the no-flux conditions on the ship hull are linearised onto the centreplane $y=0$, while the thinness of the ship is assumed to produce small-amplitude waves, so the free surface conditions are again linearised onto the plane $z=0$ [@michell98; @noblesse09a; @tuck01]. This set-up has obvious applications to ship hull design, especially for vessels with narrow hulls. Another geometry of interest involves flow past a submerged object, such as a spheroid, or, in a fluid of finite-depth, a bottom topography. If the magnitude of the disturbance is again small, then the usual linearisation of the surface conditions applies [@havelock31]. Furthermore, one can apply the thin ship approximation to submerged bodies as well [@tuck02]. Flows past submerged bodies have applications to submarine design and detection [@reed02], for example. In all of the linear formulations cited above, the linear problem of Laplace’s equation in a known domain can be solved in principle with Fourier transforms [@lighthill]. The velocity potential $\phi(x,y,z)$ and free surface $z=\zeta(x,y)$ are then given as quadruple integrals that involve the Havelock potential (the Green’s function or fundamental solution). In practice, the challenge of evaluating the resulting singular integrals with rapidly oscillating integrands has lead to analytical approximations such as the method of stationary phase [@crapper64; @tuck71; @ursell60], although accurate numerical computations have been conducted more recently [@noblesse09a; @noblesse09b; @scullen11]. Of particular interest here, we note that the Havelock potential is the velocity potential for the linearised flow past a single submerged point source singularity [@havelock32; @lustrichapman13; @noblesse78; @noblesse81; @peters49]. Thus we see that the problem of computing the wave pattern caused by turning on a submerged source in a uniform stream acts as a building block for all the other flows mentioned (as an example, the thin-ship theory effectively states that the flow past a thin ship hull is equivalent to the flow past a distribution of point sources on the centreplane $y=0$ whose strength is proportional to the hull slope $\partial y/\partial x$ [@tuck01]). Our focus in this study is to compute nonlinear flows, for which the full nonlinear boundary conditions on the actual displaced free surface $z=\zeta(x,y)$ apply. Nonlinear versions of the above problems have been considered by a number of authors (see [@higgins12; @parau02; @tuck02], for example). In particular, following the framework of Forbes [@forbes89], the approach we are most interested in is to apply a boundary-integral technique that relies on Green’s second formula. The result is a singular integro-differential equation which holds on the unknown free surface $z=\zeta(x,y)$. That is, the free-surface problem in three dimensions is reduced to a two-dimensional problem for the free surface $z=\zeta(x,y)$ and the velocity potential $\phi(x,y,\zeta(x,y))$. To proceed numerically, the rough approach is to place a mesh of $N\times M$ grid points over the truncated $(x,y)$-plane, so that the integro-differential equation and Bernoulli’s equation can both be applied at each of the $(N-1)M$ half-mesh points. A radiation-type condition for the four unknown functions is applied at each of the $M$ grid points upstream. Newton’s method is then used to solve the resulting nonlinear system of $2(N+1)M$ equations for the $2(N+1)M$ unknowns (which are slopes $\partial\zeta/\partial x$, $\partial\phi/\partial x$ and the values of $\zeta$, $\phi$ on the upstream grid points). As discussed by Forbes [@forbes89], moderate efficiencies can be gained by exploiting the symmetry of the problem and using an inexact Newton’s method which re-uses the Jacobian a number of times if possible. In more recent times, over a series of papers, Părău, Vanden-Broeck and Cooker have applied Forbes’ formulation to solve fully three-dimensional nonlinear ship wave problems and have typically used meshes of between $60\times 20$ and $80\times 40$ grid points [@parau02; @parau11; @parau07b; @parau07c; @parau07a; @parau10]. The same authors applied the same formulation to study three-dimensional solitary waves with typical meshes of $50\times 40$ grid points [@parau05a; @parau05b; @parau11], while Forbes & Hocking [@forbes05] used a mesh of $101\times 101$ points when applying the method to a three-dimensional withdrawal problem. To put the method into context, other approaches for three-dimensional ship wave problems use a similar grid size; for example, Tuck & Scullen [@tuck02] apply a mesh of $91\times 25$ grid points with their Rankine source method, while similar resolution is provided for a Rankine source method in [@Janson03]. The level of grid refinement demonstrated for the three-dimensional problems just mentioned is to be contrasted with the vast literature on two-dimensional flows. For example, by applying a boundary-integral method in two dimensions combined with a straight-forward Newton approach, authors can easily use in excess of 1000 grid points over the two-dimensional surface [@mccue02; @ogilat11; @wade14] or, in more recent times, even 2000 points [@lustri12; @trinh14; @trinh11]. Although most authors end up using fewer than 1000 points for their two-dimensional calculations, generally an accepted procedure is to continue to refine the mesh until the results are grid-independent, at least visually. Turning our attention back to three-dimensional flows, with less than 100 points used along the $x$-direction, the resolution over each wavelength is simply not of a sufficient standard for any claims about grid-independence to be made. Indeed, this is one of the key reasons why there has been little to no detailed study of the effect of high nonlinearity for three-dimensional ship wave problems. In the present paper, we use a variation of the numerical scheme developed by Forbes [@forbes89] for the problem of flow past a submerged source singularity, and apply Jacobian-free Newton-Krylov methods and exploit graphics processing unit (GPU) acceleration to drastically increase the grid refinement and decrease the run-time when compared with schemes published in the literature. We choose this particular geometric configuration since, as mentioned above, it can be thought of as the most fundamental flow type within the class that produces three-dimensional ship wave patterns. Further, this is precisely the geometry that Forbes [@forbes89] used when presenting the boundary-integral technique described above. Thus we have a direct correspondence and a bigger picture view of how far the community has progressed since that time. Finally, all of our ideas should generalise for other configurations (such as flows past pressure distributions), provided there is a linear problem that arises in the small disturbance regime. In the following section we formulate the problem of interest and provide a summary of the boundary-integral technique developed by Forbes [@forbes89] and Părău and Vanden-Broeck [@parau02]. The numerical scheme is described in Section \[sec:numerical\], which leads to a nonlinear system of equations $${\bf E}({\bf u})={\bf 0}, \label{eq:nonlinearsys}$$ where ${\bf u}$ is the vector of unknowns of length $2(N+1)M$. The damped Newton’s method approach leads to the iteration $$\textbf{u}_{k+1} = \textbf{u}_{k} + \lambda_k \delta\textbf{u}_k, \label{eq:newtonstep0}$$ where $\textbf{u}_{k}$ is the $k$th iterate in the sequence $\{ {\bf u}_k \}_{k=0}^{\infty}\rightarrow {\bf u}$ and the damping parameter $\lambda_k\in(0,1]$ is chosen such that $||\textbf{E}(\textbf{u}_{k+1})||<||\textbf{E}(\textbf{u}_{k})||$ at every iterate. The Newton step $\delta\textbf{u}_k$ satisfies $$\textbf{J}(\textbf{u}_k) \delta\textbf{u}_k = -\textbf{E}(\textbf{u}_k), \label{eq:newtonstep}$$ where ${\bf J}=\partial {\bf E}/\partial {\bf u}$ is the Jacobian matrix. The integral nature of our governing equations results in all of the entries in ${\bf u}$ contributing to the evaluation of each component of $\bf E$ that corresponds to enforcing the integral equation, which means that the lower-half of the Jacobian ${\bf J}$ is fully dense. This density has been a significant factor in limiting the number of grid points used in previously published numerical simulations. A key aspect of our approach is the use of a Jacobian-free Newton-Krylov method to solve the system (\[eq:nonlinearsys\]). A Jacobian-free Newton-Krylov method requires the action of the Jacobian only in the form of Jacobian-vector products, which can be approximated using difference quotients without ever forming the Jacobian itself [@knoll04]. In practice, the underlying Krylov subspace iterative solver requires preconditioning in order to achieve a satisfactory rate of convergence, meaning the overall method is not typically fully matrix-free; however, for preconditioning purposes, an approximation of the Jacobian is all that is required, and this is where significant savings can be made. While Jacobian-free Newton-Krylov methods are most commonly associated with problems for which the Jacobian matrices are sparse, they have been used successfully in a number of applications that give rise to dense Jacobian matrices [@chacon00; @khatiwala08; @moroney13]. In each of these applications, a sparse approximation of the Jacobian was used in constructing the preconditioner. We take the same approach in this work. The type of approximation we find to be the most effective involves a banded structure, with its nonzero entries coming from the linearised problem for a Havelock source mentioned above. We emphasise that this approximation is used only for preconditioning purposes; the action of the dense Jacobian is still felt throughout the Newton solver, which distinguishes our approach from the inexact method of Forbes [@forbes89] and others. In Section \[sec:results\] we present our results. We choose to present most of our results for a particular set of parameter values, which includes the same Froude number as used by Forbes [@forbes89], and a moderately large value of the dimensionless strength of the submerged source. While Forbes showed results computed with a mesh of $45\times 13$ grid points in 1989, we are able to easily use a $361\times 121$ mesh on a modern desktop PC, computed in under 75 minutes. By utilising graphics processing unit (GPU) acceleration on a more powerful workstation, the same solution was computed in roughly 3.5 minutes. Furthermore, with this technology we are able to significantly improve upon the resolution, and generate results for a $721\times 241$ mesh (in under 2 hours). This sort of resolution is important for three-dimensional ship wave problems, as it provides opportunities to explore the effect that nonlinearity has on the flow field in the same way as has been done in numerous instances for two-dimensional flows. Finally, we close the paper in Section \[sec:discussion\] with our discussion, including directions as to where our work can be applied. Mathematical formulation {#sec:formulation} ======================== Governing equations ------------------- We consider the irrotational flow of an inviscid, incompressible fluid of infinite depth, bounded above by a free surface, upon which gravity is acting. The effects of surface tension are ignored. Suppose that initially there is a free stream of fluid travelling with uniform speed $U$ in the positive $x$-direction, and that a source singularity of strength $m$ is introduced at a distance $H$ below the surface. The disturbance caused by the source will lead to transient waves being generated on the free-surface. We are interested in the steady-state problem that arises in the long-time limit of this flow. The problem is nondimensionalised by scaling all lengths with respect to $H$ and all speeds with respect to $U$. By labelling the free-surface $z=\zeta(x,y)$, the dimensionless problem is to solve Laplace’s equation for the velocity potential $\Phi(x,y,z)$: $$\begin{aligned} \nabla^2\Phi=\frac{\partial^2 \Phi}{\partial x^2}+\frac{\partial^2 \Phi}{\partial y^2}+\frac{\partial^2 \Phi}{\partial z^2}=0 \quad \text{for} \quad z<\zeta(x,y),\label{eqn:NondimLap}\end{aligned}$$ except at the source singularity itself, whose dimensionless location is at $(x,y,z)=(0,0,-1)$. The appropriate limiting behaviour is $$\begin{aligned} \Phi\sim-\frac{\epsilon}{4\pi\sqrt{x^2+y^2+\left(z+1\right)^2}} \quad \text{as} \quad (x,y,z)\rightarrow(0,0,-1),\label{eqn:NondimSource}\end{aligned}$$ where $$\epsilon=\frac{m}{UH^2}\label{eqn:epsilon}$$ is the dimensionless source strength. On the free surface there are the kinematic and dynamic boundary conditions $$\begin{aligned} \Phi_x\zeta_x+\Phi_y\zeta_y&=\Phi_z \quad \text{on} \quad z=\zeta(x,y),\label{eqn:NondimKin}\\ \frac{1}{2}(\Phi^2_x+\Phi^2_y+\Phi^2_z)+\frac{\zeta}{F^2}&=\frac{1}{2} \quad\;\: \text{on} \quad z=\zeta(x,y),\label{eqn:NondimDyn}\end{aligned}$$ being satisfied, where the second of two dimensionless parameters in the problem is the depth-based Froude number $$F=\frac{U}{\sqrt{gH}}.\label{eqn:Froude}$$ Finally, the flow will approach the free stream both far upstream (the radiation condition) and infinitely far below the free surface, providing the final two conditions $$\begin{aligned} (\Phi_x,\Phi_y,\Phi_z)\rightarrow(1,0,0),&\quad \zeta \rightarrow 0\quad\text{as} \quad x\rightarrow-\infty,\label{eqn:NondimUp} \\ (\Phi_x,\Phi_y,\Phi_z)\rightarrow(1,0,0),&\qquad\qquad\;\;\text{as}\quad z\rightarrow-\infty.\label{eqn:NondimFar}\end{aligned}$$ The governing equation (\[eqn:NondimLap\]) subject to (\[eqn:NondimSource\])-(\[eqn:NondimFar\]) make up a nonlinear free-surface problem with no known analytical solution. Boundary-integral method ------------------------ In order to solve (\[eqn:NondimLap\])-(\[eqn:NondimFar\]) numerically, we first reformulate the problem in terms of an integral equation using Green’s second formula. The full derivation is provided in Forbes [@forbes89], while very similar approaches are outlined in a variety of other papers [@forbes05; @parau02; @parau11; @parau05a; @parau05b; @parau07b; @parau07c; @parau07a; @parau10]. By setting $\phi(x,y)=\Phi(x,y,\zeta(x,y))$, the final boundary-integral equation is $$\begin{aligned} 2\pi(\phi(x^*,y^*)-x^*)=&-\frac{\epsilon}{\left({x^*}^2+{y^*}^2+(\zeta(x^*,y^*)+1)^2 \right)^\frac{1}{2}}\notag\\ &+\int\limits_{0}^{\infty}\int\limits_{-\infty}^{\infty}(\phi(x,y)-\phi(x^*,y^*)-x+x^*)K_1(x,y;x^*,y^*)\,\, \text{d}x\,\text{d}y\notag\\ &+\int\limits_{0}^{\infty}\int\limits_{-\infty}^{\infty}\zeta_x(x,y)K_2(x,y;x^*,y^*)\,\, \text{d}x\,\text{d}y,\label{eqn:IntegroEqn}\end{aligned}$$ which holds for any point $(x^*,y^*)$ in the $(x,y)$-plane. Here $K_1$ and $K_2$ are the kernel functions $$\begin{aligned} K_1(x,y;x^*,y^*)=&\frac{\zeta(x,y)-\zeta(x^*,y^*)-(x-x^*)\zeta_x-(y-y^*)\zeta_y}{\Bigl((x-x^*)^2+(y-y^*)^2+\bigl(\zeta(x,y)-\zeta(x^*,y^*)\bigr)^2\Bigr)^\frac{3}{2}}\\ &+\frac{\zeta(x,y)-\zeta(x^*,y^*)-(x-x^*)\zeta_x-(y+y^*)\zeta_y}{\Bigl((x-x^*)^2+(y-y^*)^2+\bigl(\zeta(x,y)-\zeta(x^*,y^*)\bigr)^2\Bigr)^\frac{3}{2}},\\ K_2(x,y;x^*,y^*)=&\frac{1}{\sqrt{(x-x^*)^2+(y-y^*)^2+\bigl(\zeta(x,y)-\zeta(x^*,y^*)\bigr)^2}}\\ &+\frac{1}{\sqrt{(x-x^*)^2+(y+y^*)^2+\bigl(\zeta(x,y)-\zeta(x^*,y^*)\bigr)^2}}.\end{aligned}$$ The integral equation (\[eqn:IntegroEqn\]) identically satisfies Laplace’s equation (\[eqn:NondimLap\]) and the kinematic condition (\[eqn:NondimKin\]), as well as the limiting condition (\[eqn:NondimSource\]) and the far-field conditions (\[eqn:NondimUp\])-(\[eqn:NondimFar\]). Thus we are left to solve (\[eqn:IntegroEqn\]) and the dynamic condition (\[eqn:NondimDyn\]). It proves convenient to rewrite (\[eqn:NondimDyn\]) with the help of (\[eqn:NondimKin\]) to be $$\begin{aligned} \frac{1}{2}\frac{(1+\zeta_x^2)\phi_y^2+(1+\zeta_y^2)\phi_x^2-2\zeta_x\zeta_y\phi_x\phi_y}{1+\zeta_x^2+\zeta_y^2}+\frac{\zeta}{F^2}=\frac{1}{2}, \quad &\text{on} \quad z=\zeta(x,y). \label{eqn:freeSurfCond}\end{aligned}$$ Linearised problem {#sec:linearproblem} ------------------ While our focus is on generating numerical solutions to (\[eqn:NondimLap\])-(\[eqn:NondimFar\]), it will prove instructive to note the linearised problem which arises in the weak source strength limit $\epsilon\ll 1$. The problem is formulated by writing $\Phi=x+\epsilon \Phi_1(x,y,z)+\mathcal{O}(\epsilon^2)$, $\zeta=\epsilon\zeta_1(x,y)+\mathcal{O}(\epsilon^2)$, and considering the formal limit $\epsilon\rightarrow 0$. As a result, the linear problem becomes $$\begin{aligned} \nabla^2\Phi=\frac{\partial^2 \Phi}{\partial x^2}+\frac{\partial^2 \Phi}{\partial y^2}+\frac{\partial^2 \Phi}{\partial z^2}=0 \quad \text{for} \quad z<0,\label{eqn:NondimLaplinear}\end{aligned}$$ subject to the linearised kinematic and dynamic conditions $$\begin{aligned} \zeta_x&=\Phi_z \quad \text{on} \quad z=0,\label{eqn:NondimKinlinear}\\ \Phi_x-1+\frac{\zeta}{F^2}&=0 \quad\;\: \text{on} \quad z=0.\label{eqn:NondimDynlinear}\end{aligned}$$ The near-source behaviour (\[eqn:NondimSource\]) and the far-field conditions (\[eqn:NondimUp\])-(\[eqn:NondimFar\]) remain the same. As discussed in the Introduction, the solution to this linear problem can be found using Fourier transforms [@noblesse81]; however, for our purposes we shall pursue the equivalent boundary-integral approach as that used for the nonlinear problem. This time if we set $\phi(x,y)=\Phi(x,y,0)$, the application of Green’s second formula gives $$2\pi(\phi(x^*,y^*)-x^*)= -\frac{\epsilon}{\left({x^*}^2+{y^*}^2+1\right)^\frac{1}{2}} +\int\limits_{0}^{\infty}\int\limits_{-\infty}^{\infty}\zeta_x(x,y)K_3(x,y;x^*,y^*)\,\, \text{d}x\,\text{d}y,\label{eqn:IntegroEqnlinear}$$ where $$K_3(x,y;x^*,y^*)=\frac{1}{\sqrt{(x-x^*)^2+(y-y^*)^2}} +\frac{1}{\sqrt{(x-x^*)^2+(y+y^*)^2}}.$$ Again, the integral equation (\[eqn:IntegroEqnlinear\]) identically satisfies Laplace’s equation (\[eqn:NondimLaplinear\]), the kinematic condition (\[eqn:NondimKinlinear\]), the far-field conditions (\[eqn:NondimUp\])-(\[eqn:NondimFar\]) and the near-source condition (\[eqn:NondimSource\]). Numerical discretisation {#sec:numerical} ======================== For the discretisation of the nonlinear boundary-integral equation (\[eqn:IntegroEqn\]), we use a slight variant of the method outlined in Părău and Vanden-Broeck [@parau02], which is based on the original approach of Forbes [@forbes89]. This involves laying a regular mesh of nodes $(x_1, y_1), \ldots, (x_N, y_M)$ on the free surface with spacings of $\Delta x$ and $\Delta y$ in the $x$ and $y$ directions, respectively. For a given $N$ and $M$, we shall refer to the mesh as being an $N\times M$ mesh. The free-surface position $\zeta(x,y)$ and the velocity potential $\phi(x,y)$ are represented by discrete values $\zeta_{k,\ell}$ and $\phi_{k,\ell}$ at the points $(x_k,y_\ell),\, k=1,\dots,N,\, \ell=1,\dots,M$. We define the vector of $2(N+1)M$ unknowns $\textbf{u}$ to be $$\begin{aligned} \textbf{u}=&[\phi_{1,1},(\phi_x)_{1,1},\dots,(\phi_x)_{N,1},\phi_{1,2},(\phi_x)_{1,2},\dots,(\phi_x)_{N,2},\ldots,\phi_{1,M}, (\phi_x)_{1,M},\dots,(\phi_x)_{N,M}, \nonumber \\ &\zeta_{1,1},(\zeta_x)_{1,1},\dots,(\zeta_x)_{N,1},\zeta_{1,2},(\zeta_x)_{1,2},\dots,(\zeta_x)_{N,2},\ldots, \zeta_{1,M},(\zeta_x)_{1,M},\dots,(\zeta_x)_{N,M}]^T, \label{eq:unknowns}\end{aligned}$$ comprising the $x$-derivatives of the functions $\phi$ and $\zeta$ at the free-surface mesh points, together with the values of $\phi$ and $\zeta$ at the upstream boundary of the truncated domain. The values of these unknowns are related via $2(N+1)M$ nonlinear equations, of the form (\[eq:nonlinearsys\]), which we now derive. Given the elements of the vector of unknowns (\[eq:unknowns\]), the remaining values of $\zeta$ are obtained by trapezoidal-rule integration using the values of $\zeta_x$: $$\begin{aligned} \zeta_{k+1,\ell}&=\zeta_{k,\ell}+\frac{1}{2}\Delta x\bigl((\zeta_x)_{k,\ell}+(\zeta_x)_{k+1,\ell} \bigr),\\ \ell&=1,\dots,M,\quad k=1,\dots,N-1. \end{aligned}\label{eqn:zetaapprox}$$ The values of $\zeta_y$ are then computed by fitting a cubic spline through the points $\zeta_{k,1},\dots,\zeta_{k,M}$ for $k=1,\dots,N$. Values of $\phi$ and $\phi_y$ at each grid point are similarly computed using $\phi_x$. We must now enforce the integro-differential equation (\[eqn:IntegroEqn\]), which will be evaluated on the half-mesh points $(x_{k+\frac{1}{2}},y_\ell),\, k=1,\dots,N-1,\, \ell=1,\dots,M$ using two-point interpolation. The domain is truncated to the rectangle $x_1\leq x\leq x_N,\ y_1\leq y\leq y_M$. The singularity in the second integral of (\[eqn:IntegroEqn\]) is removed by the addition and subtraction of the term $$\zeta_x(x^*,y^*)\int\limits_{y_1}^{y_M}\int\limits_{x_1}^{x_N}S_2(x,y;x^*,y^*)\,\, \text{d}x\,\text{d}y, \label{eqn:I2DashDash}$$ where $$\begin{aligned} S_2(x,y;x^*,y^*)=&\frac{1}{\sqrt{A(x-x^*)^2+B(x-x^*)(y-y^*)+C(y-y^*)^2}}\\ &+\frac{1}{\sqrt{A(x-x^*)^2-B(x-x^*)(y+y^*)+C(y+y^*)^2}},\label{eqn:S2}\end{aligned}$$ with $$A=1+\zeta_x^2(x^*,y^*),\quad B=2\zeta_x(x^*,y^*)\zeta_y(x^*,y^*),\quad C=1+\zeta_y^2(x^*,y^*).$$ The second integral of the equation (\[eqn:IntegroEqn\]) becomes $$\int\limits_{y_1}^{y_M}\int\limits_{x_1}^{x_N}\zeta_x(x,y) K_2(x,y;x^*,y^*)-\zeta_x(x^*,y^*)S_2(x,y;x^*,y^*)\,\, \text{d}x\,\text{d}y +\zeta_x(x^*,y^*)I,$$ where $$I=\int\limits_{y_1}^{y_M}\int\limits_{x_1}^{x_N}S_2\,\, \text{d}x\,\text{d}y.\label{eqn:IS2}$$ The integral $I$ now contains the singularity; it can be evaluated exactly in terms of logarithms [@forbes89; @parau02]. The integrals in the approximation to equation (\[eqn:IntegroEqn\]) are discretised using the trapezoidal rule and then evaluated for all half-mesh points $(x_{k+\frac{1}{2}},y_\ell),\, k=1,\dots,N-1,\, \ell=1,\dots,M$. This results in $(N-1)M$ nonlinear algebraic equations for the unknowns in the vector $\textbf{u}$. An additional $(N-1)M$ equations are given by evaluating the free surface condition (\[eqn:freeSurfCond\]) at the half mesh points. The final $4M$ equations are provided to enforce the far-field condition (\[eqn:NondimUp\]) on the relevant boundary of the truncated domain by applying the upstream radiation condition using the approach outlined by Scullen [@scullen98]. The idea here is to enforce an equation of the form $xf_x+n f=0$ along the boundary $x=x_1$ for the four functions $\zeta$, $\zeta_x$, $\phi-x$ and $\phi_x-1$. The value of $n>0$ represents how fast the functions decay to zero upstream, and in our calculation was taken to be $n=0.05$ (larger values of $n$ were found to amplify the small spurious upstream waves mentioned below). This method for applying the radiation condition gives us the $4M$ equations $$\begin{aligned} x_1((\phi_x)_{1,\ell}-1)+n(\phi_{1,\ell}-x_1)&=0,\\ x_1(\phi_{xx})_{1,\ell}+n((\phi_x)_{1,\ell}-1)&=0,\\ x_1(\zeta_x)_{1,\ell}+n\zeta_{1,\ell}&=0,\\ x_1(\zeta_{xx})_{1,\ell}+n(\zeta_x)_{1,\ell}&=0, \end{aligned}\label{eqn:numUpRadiation}$$ for $\ell=1,\dots,M$, where second derivatives are computed by a forward difference approximation on the first derivative. We now have $2(N+1)M$ equations for our vector of unknowns (\[eq:unknowns\]). In order to optimise our scheme we have ordered these equations very carefully. This ordering is explained in \[appendixA\]. This numerical scheme has two main sources of error. The first is truncation error introduced when approximating the infinite domain of integration with a finite domain. This truncation has the potential to lead to errors if the chosen upstream truncation point ($x_1$) is too close to the source, as the upstream radiation condition (\[eqn:numUpRadiation\]) may no longer be accurately enforced. Indeed, truncating the domain upstream appears to generate very small nonphysical waves on the surface, as discussed later. Truncating the domain downstream (at $x_N$) may also introduce significant errors as the amplitude of the wavetrain decays slowly with space, and contribution to the integrals from the truncated waves is nonzero. The second main source of error is from the discretisation of the integrals. Both the mesh spacing and the chosen integration weighting scheme will have an effect on the accuracy of the final result. Jacobian-free Newton-Krylov method ================================== Overview -------- The system (\[eq:nonlinearsys\]) is solved with a Jacobian-free Newton-Krylov method. At the outer, nonlinear level, this is simply the damped Newton iteration (\[eq:newtonstep0\]), with $\lambda_k$ chosen via a simple linesearch to ensure a sufficient decrease in the nonlinear residual is obtained with each iteration. At the inner, linear level, the system (\[eq:newtonstep\]) is solved using the iterative Generalised Minimum Residual algorithm [@saad86] with right preconditioning. After $m$ iterations of this algorithm, the approximate solution for the Newton correction $\delta \mathbf{u}_k$ is found by projecting obliquely onto the preconditioned Krylov subspace $$\mathcal{K}_m(\textbf{J}_k\mathbf{P}^{-1},\textbf{E}_k)=\mathrm{span}\{\textbf{E}_k,\textbf{J}_k\mathbf{P}^{-1}\textbf{E}_k,\dots,(\textbf{J}_k\mathbf{P}^{-1})^{m-1}\textbf{E}_k\},$$ where we are now using the notation $\textbf{J}_k=\textbf{J}(\textbf{u}_k)$, $\textbf{E}_k=\textbf{E}(\textbf{u}_k)$. The matrix $\mathbf{P} \approx \mathbf{J}_k$ is the preconditioner matrix – a sparse approximation to $\textbf{J}_k$ which is discussed in more detail in the next subsection. Its function is to reduce the dimension $m$ of the Krylov subspace required to obtain a sufficiently accurate solution for $\delta \mathbf{u}_k$. Krylov subspace methods are very attractive as linear solvers in the context of nonlinear Newton iteration, because they do not require explicit formation of the Jacobian matrix. Indeed, only the action of the Jacobian matrix in the form of Jacobian-vector products is required to assemble a basis for the preconditioned Krylov subspace $\mathcal{K}_m$. These Jacobian-vector products can be approximated without needing to form $\textbf{J}_k$ by using first order difference quotients: $$\textbf{J}_k\mathbf{P}^{-1}\textbf{v} \approx \frac{\textbf{E}(\textbf{u}_k+h\,\mathbf{P}^{-1}\textbf{v})-\textbf{E}(\textbf{u}_k)}{h},\label{eqn:JvApprox}$$ where $\textbf{v}$ represents an arbitrary vector used in building the Krylov subspace, and $h$ is a suitably-chosen shift [@brown90]. Since the Newton correction is solved for only approximately, and the action of the Jacobian in computing this solution is itself only approximated, we are left with an inexact Newton method, which exhibits superlinear, rather than quadratic, convergence [@knoll04]. The reduction in the convergence rate is of little practical consequence, given the enormous performance gains realised by removing the burden of forming the (dense) Jacobian matrix. Furthermore, only solving for the Newton correction approximately can actually improve performance in the early stages of the nonlinear iteration, by not wasting operations computing an extremely accurate value of the Newton correction which, even if it were computed exactly, would only reduce the nonlinear residual by so much [@knoll04]. For most values of the parameters $F$ and $\epsilon$, it proves sufficient to use a flat surface as the initial guess ${\bf u}_0$ in the Newton iteration, which corresponds to: $$\phi_{1,\ell}=x_0, \quad (\phi_x)_{k,\ell}=1, \quad \zeta_{1,\ell}=0, \quad (\zeta_x)_{k,\ell}=0,$$ for $k=1,\dots, N$ and $\ell=1,\dots, M$. Another approach is to use the exact solution to the linear problem outlined in Section \[sec:linearproblem\] (given in [@noblesse81], for example). However, for highly nonlinear solutions with large values of $\epsilon$, a further alternative approach is to apply a bootstrapping process in which a solution is computed using ${\bf u}_0$ for a moderate value of $\epsilon$, and then this solution is used as an initial guess for a slightly larger $\epsilon$, and so on. Preconditioning {#sec:preconditioning} --------------- In forming the preconditioner matrix $\mathbf{P}$, the goal is to construct an approximation to the Jacobian $\mathbf{J}_k$ that is cheap to form and to factorise, such that the spectrum of the preconditioned Jacobian $\mathbf{J}_k\mathbf{P}^{-1}$ exhibits a clustering of eigenvalues [@knoll04]. A common starting point in building such a preconditioner is to consider a matrix constructed from the same problem under simplified physics [@knoll04]. In the present context, this is achieved by applying our numerical scheme to the linearised governing equations which apply formally in the limit $\epsilon\rightarrow 0$. These equations make up the well-studied linear problem of computing the Havelock potential for flow past a submerged point source [@havelock32; @lustrichapman13; @noblesse78; @noblesse81; @peters49], as discussed in the Introduction and Section \[sec:linearproblem\]. The numerical discretisation of the integrals in (\[eqn:IntegroEqnlinear\]) allows for easy differentiation by hand, so that all elements of the linear Jacobian can be calculated exactly, requiring considerably less computational time. The details are included in \[appendixB\]. \ In Figure \[fig:TwoJacVis\], the Jacobian matrix for the full nonlinear problem ((a) “nonlinear Jacobian”) for $\textbf{u}_k={\bf u}_0$ with parameters $\epsilon=1$ and $F=0.7$ is compared to its counterpart for the linear problem ((b) “linear Jacobian”) by means of the magnitude of their entries. The comparison confirms that, although there are slight differences in the magnitude of these entries (in particular, the grey triangular regions near the diagonal in the upper-left submatrix in Figure \[fig:TwoJacVis\](a) do not appear in Figure \[fig:TwoJacVis\](b)), the general structure of the two matrices is the same. The eigenvalue spectra of the nonlinear Jacobian before and after preconditioning with the linear Jacobian are exhibited in Figure \[fig:TwoJacEig\]. The figure reveals that the application of the preconditioner has resulted in a tight clustering of the eigenvalues around unity, confirming its effectiveness. While the linear Jacobian is significantly cheaper to compute than its nonlinear counterpart, its lower-right submatrix is nonetheless fully dense, which would ultimately limit the number of mesh nodes that could be used in the discretisation due to storage and factorisation considerations. Therefore, we focus attention on the lower-right submatrix of the two Jacobians (Figure \[fig:TwoJacVis\] (c), (d)), which reveals that the magnitudes of the entries decay with distance from the main block diagonal. This observation suggests using a block-banded approximation to this portion of the matrix for our preconditioner, whereby we keep only the nonzero entries of the lower-right submatrix of the linear Jacobian within a stated block bandwidth $b$, with block sizes $(N+1)\times(N+1)$. By varying this bandwidth, the sparsity of the preconditioner can be controlled such that the storage and factorisation costs are manageable. The method of storing, factorising and applying the preconditioner is outlined in \[appendixC\]. In Figure \[fig:ThreeBBandEigenPlots\] we illustrate that even with block bandwidth $b = 1$ (that is, a block diagonal approximation), the linear Jacobian still functions effectively as a preconditioner, providing the required eigenvalue clustering. The tightness of this clustering can be further improved by increasing the bandwidth, as the results for $b = 3$ and $b = 5$ confirm. \ \ Results {#sec:results} ======= We have computed solutions using both a standard desktop computer[^1] with all code written in MATLAB, and using a more powerful workstation with GPU accelerator[^2] using a mixture of MATLAB and CUDA (Compute Unified Device Architecture) code. In all cases the KINSOL [@hindmarsh05] implementation of the Jacobian-Free Newton-Krylov method was used. In the following, recall that an $N\times M$ mesh involves $N$ grid points in the $x$ direction and $M$ grid points in the $y$ direction. Desktop Computer ---------------- We present results obtained by solving our system of nonlinear equations on a typical desktop computer for a contemporary mesh ($91\times 31$, $\Delta x=\Delta y=0.3$, $x_0=-9$) as well as for a significantly finer mesh ($361\times 121$, $\Delta x=\Delta y=0.15$, $x_0=-14$). The parameter values we focus on are $F=0.7$ and $\epsilon=1$, which are representative of a moderately small Froude number and a moderately nonlinear flow regime. For the contemporary mesh, the resulting problem size is sufficiently small that the full preconditioner (without taking the banded approximation) can be formed and factorised without difficulty on today’s desktop machines. Using the Jacobian-free Newton-Krylov method with this dense preconditioner, the solution was obtained in under 26 seconds. Calculating numerical solutions like this one in such a small time is useful for exploring the effect of different parameter values on the free surface; however, as can be seen in Figure \[fig:4\], the resulting surface is rather coarse, and does not reveal much detail of the wave pattern. By using the block-banded preconditioner with our Jacobian-free Newton-Krylov method, we are able to compute the solution on the much finer mesh ($361\times 121$) in under 75 minutes on the desktop computer. A block bandwidth of $b = 31$ is used for the Jacobian, which means it essentially fills all of the available system memory. This level of mesh refinement represents a comfortable size of problem for the given machine, and produces a free surface profile that is significantly smoother than the one computed with a $91\times 31$ mesh (again, see Figure \[fig:4\]). With a modest degree of further refinement, the problem may still be solved on the desktop computer, however the effectiveness of the preconditioner is reduced owing to the limited number of bands that can be accommodated in memory. Workstation with GPU Accelerator -------------------------------- By coding the nonlinear discretisation in CUDA and executing each evaluation (hereafter a “function evaluation”) on the GPU, we were able to significantly accelerate the computations as demonstrated in Table \[tab:FuncEvalTimes\]. Here we are experiencing an approximately 25 times speed up in function evaluation times over the multicore MATLAB code for the larger meshes. This leads to a reduced overall runtime, for example, calculating the solution on the same $361\times 121$ mesh with GPU acceleration took only 3.5 minutes. This dramatic reduction in computational time coupled with the extra system memory available on the workstation allowed us to produce solutions on much finer meshes in a practical amount of time. Our most detailed solution using a $721\times 241$ mesh with $\Delta x=\Delta y=0.075$ and $x_0=-14$, was computed in 1.5 hours. The corresponding free surface profile is illustrated in Figure \[fig:5\]. ----------------- ------------------ ------------------ -------------------- Mesh Multicore MATLAB Multicore MATLAB MATLAB with on desktop on workstation GPU on workstation $91\times 31$ 1.43 0.87 0.02 $181\times 61$ 11.26 4.38 0.18 $271\times 91$ 54.47 20.40 0.83 $361\times 121$ 169.46 64.35 2.52 $451\times 151$ 410.34 153.91 6.04 ----------------- ------------------ ------------------ -------------------- : A comparison of the function evaluation times using multicore MATLAB on the desktop PC and the workstation with and without GPU acceleration for different meshes with parameters $\epsilon=1$ and $F=0.7$. Time is in seconds.[]{data-label="tab:FuncEvalTimes"} \ Towards grid independence ------------------------- As mentioned in the Introduction, a common procedure in the free-surface literature is to explore grid independence by computing solutions on a given truncated domain with more grid points (twice as many, say) and visually comparing the free surface profiles to test whether the grid refinement has not significantly altered the solution. Similarly, authors often keep the spatial increment the same and increase the size of the truncated domain (make it twice as long, say), again to test whether the solution changes. For steady two-dimensional flows, this exercise is reasonably straight forward (in principle), as the free surface profile is a curve. Examples of these tests for two-dimensional problems that involve a downstream wavetrain can be found in [@mccue99; @mekias91; @zhang96], all of which were published at a time when demonstrating grid independence was still a difficult issue. More recently, equivalent tests of grid independence have been attempted for three-dimensional flows past disturbances [@parau02; @parau07b; @parau07c]. In this case, as the wave pattern is a two-dimensional surface, the domain was divided in half, with one part showing a solution computed with a particular grid, and the other part with a solution computed with a more refined or extended grid. Such a comparison is also given in Figure \[fig:4\]. What we can see from Figure \[fig:4\] is that the solution computed on the $91\times 31$ mesh is clearly not grid independent, as the more refined surface corresponding to a $361\times 121$ mesh appears to be different, even on this larger scale. We have conducted the same comparison exercise for a variety of parameter sets and meshes for our problem, and conclude that the number of grid points used presently in the literature (for a range of very similar problems) is not nearly enough for authors to claim their solutions are grid independent. Similarly, noting that Părău and coauthors [@parau02; @parau07c] call these visual comparisons ‘accuracy checks’, we would not say that solutions computed with contemporary meshes are accurate. Of course it is understandable that these coarse meshes have been used in published studies, given the dense nature of the nonlinear Jacobian, the lack of a Jacobian-free approach such as we are using here, and computational power. We hope that the algorithms presented here will allow much more accurate computations in the future. Another obvious approach for observing the degree of grid independence is to plot the centreline of the free surface ($z=\zeta(x,0)$) for a number of difference meshes, as shown in Figure \[fig:CentrelineEp1Fr7All\]. In addition to the $91\times 31$ and $361\times 121$ meshes used in Figure \[fig:4\], we have also included the centreline plot for the $721\times 241$ mesh used in Figure \[fig:5\]. Recall that this latter mesh was implemented a workstation with GPU acceleration. We see there is quite good agreement between the solutions for the $361\times 121$ and $721\times 241$ meshes, at least over the first four or five wavelengths. Further downstream the amplitudes of the waves appear to agree well, but the actual wavelength is slightly out. This comparison suggests that while we can not yet claim our solutions will not be affected by further grid refinement, we argue that meshes of the order of $361\times 121$ and $721\times 241$ are required for solutions to begin to appear independent of the mesh spacing and truncation. ![A comparison of the centreline profiles for $F=0.7$ and $\epsilon=1$ computed on three different grids. The dashed curve has 91 nodes in the $x$-direction with $\Delta x=0.3$. The surface made up by solid circles has 361 nodes with $\Delta x=0.15$. Note that each circle here represents an actual grid point (the illusion of uneven grid spacing is due to the vastly different scales in the $x$ and $z$ directions). The solid curve has 721 nodes with $\Delta x=0.075$. The inset shows a close up of this comparison near $x=0$.[]{data-label="fig:CentrelineEp1Fr7All"}](Fig6.pdf){width="0.85\linewidth"} It is worth making some comments about the truncation errors we discussed at the end of Section \[sec:numerical\]. First, we note that truncating the domain upstream at $x=x_1$ has the effect of introducing very small spurious (almost two-dimensional) waves throughout the domain. These may be seen in Figures \[fig:4\] and \[fig:5\], both ahead of the source and also outside of the Kelvin wedge. This numerical artefact has been an issue for two-dimensional flows for many years, and the associated spurious waves have been eliminated by employing a variety of upstream boundary conditions [@parau02; @zhang96]. A detailed discussion for two-dimensional flows is given by Grandison & Vanden-Broeck [@grandison06]. In our scheme, the enforcement of the radiation condition via (\[eqn:numUpRadiation\]) has the effect of dramatically reducing the size of these spurious waves (the coefficient $n$ is chosen based on these observations). This issue deserves further attention. Further, we note any truncation of the domain at $x=x_N$ will introduce errors in the system, as the contribution from the wavetrain to the integrals for $x>x_N$ will be ignored. Visually, we can see in Figure \[fig:CentrelineEp1Fr7All\] that the final wavelength of the free surface seems affected by this truncation. Again, strategies have been developed to deal with these errors in much simpler two-dimensional problems [@grandison06], and similar work is needed for the types of three-dimensional flows considered here. Details of wave patterns ------------------------ The free-surface profiles presented in Figures \[fig:4\]-\[fig:5\] are computed for the moderately small value of the Froude number, $F=0.7$. In this regime, the transverse waves, which run perpendicular to the flow direction, are prominent. These are the waves we observe in the centreline plot in Figure \[fig:CentrelineEp1Fr7All\]. The other type of waves are the divergent waves, whose crests appear to form ridges pointing diagonally away from the source. The amplitude of the transverse waves decays as $x$ increases, leaving the divergent waves to dominate at larger distances away from the source. It is the divergent wave pattern that characterises the well-known V-shaped Kelvin wake. A free-surface profile computed for $F=1.4$ and $\epsilon=1$ is presented in Figure \[fig:7\]. For this moderately large Froude number, we see that the divergent waves dominate closer to the source, making it more difficult to view the transverse waves. Note that the wavelength of the transverse waves increases with Froude number, which means we need to truncate further downstream for larger Froude numbers in order to capture the same amount of detail. The solution in this figure was computed using a mesh of $721\times 241$ on a workstation with GPU acceleration. With this resolution, we can see fine details of the surface in part (a) of the Figure. \ Discussion {#sec:discussion} ========== We have considered the fully nonlinear problem of the free-surface flow past a submerged point source. Following Forbes [@forbes89], we apply a boundary-integral technique based on Green’s second formula to derive a singular integro-differential equation for the velocity potential $\Phi(x,y,z)$ and the shape of the surface $z=\zeta(x,y)$. This equation, together with Bernoulli’s equation, is discretised and satisfied at midpoints on a two-dimensional mesh. The resulting system of nonlinear algebraic equations is solved using Newton’s method. In the past, numerical approaches of this sort were hindered by the fact that the Jacobian matrix in Newton’s method is dense. Our contribution is to apply a Jacobian-free Newton-Krylov method to solve the nonlinear system, thus avoiding the need to ever form or factorise the Jacobian. As such, we are able to use much finer meshes than used in the past by other authors. Further, in order to ensure efficiency, we use a banded matrix preconditioner whose nonzero entries come from the linearised problem. Finally, we code the function to run efficiently on a GPU, to greatly speed up function evaluation times. The resolution of the mesh we use is now essentially up to the standard of many two-dimensional schemes published in the literature. As discussed in the Introduction, the problem of flow past a source singularity can be thought of as a building block for more complicated configurations such as flow due to a steadily moving applied pressure distribution (like a hovercraft), a thin ship hull, or a submerged body (like a submarine). The next stage in this research is to adapt the present techniques for these more complicated flows. We expect that the key ideas developed in this paper will generalise in a straightforward manner, provided there is a natural linearised version of the problem at hand. With the accuracy and efficiency of our approach, one may be able to devise appropriate optimisation schemes for designing ship hulls with minimal resistance, and so on. Our approach should also translate to time-dependent problems, such as the study by Părău et al. [@parau10], who apply a similar boundary integral approach, discretised with $60\times 40$ meshes, to solve for time-dependent flows past a pressure distribution (see [@dias06; @fochesato06; @grilli01] for a thorough discussion of further issues that arise in time-dependent problems). We leave all this work for further study. With the degree of accuracy our numerical schemes allow, we are now in a position to explore the effect of strong nonlinearity on the wave pattern, as has been done extensively in the two-dimensional analogue. For example, as the nonlinearity in a steady ship wave problem increases (for our problem this tendency comes from increasing $\epsilon$), the waves will become more nonlinear in shape, perhaps with sharper crests. Given the flow is steady, we expect that the waves will ultimately “break” when the most nonlinear wave reaches a limiting configuration (this occurs when the highest wave crest reaches the dimensionless height $F^2/2$). While this general behaviour is well understood for two-dimensional waves, with studies of highly nonlinear waves producing highly accurate calculations of near-breaking waves [@cokelet77; @dallaston10; @Lukomsky02; @schwartz74; @williams81] (the breaking point corresponding to the Stokes limiting configuration with a $120^\circ$ angle at the wave crest), the highly nonlinear regime for fully three-dimensional problems is relatively unexplored. Indeed, the extra dimension makes the pattern structure much more complicated, and so it is not always obvious what part of the domain will break first. As such, the challenge of generalising the two-dimensional results to three dimensions remains. Acknowledgement {#acknowledgement .unnumbered} =============== SWM acknowledges the support of the Australian Research Council via the Discovery Project DP140100933. The authors thank Prof. Kevin Burrage for the use of high performance computing facilities and acknowledge further computational resources and support provided by the High Performance Computing and Research Support (HPC) group at Queensland University of Technology. References {#references .unnumbered} ========== [99]{} P. N. Brown and Y. Saad. Hybrid Krylov methods for nonlinear systems of equations. *SIAM J. Sci. Stat. Comp.*, 11:450–481, 1990. L. Chacón, D. C. Barnes, D. A. Knoll, and G. H. Miley. An implicit energy-conservative 2D Fokker-Planck algorithm: II. Jacobian-free Newton-Krylov solver. *J. Comp. Phys.*, 157:654–682, 2000. E. D. Cokelet. Steep gravity waves in water of arbitrary uniform depth. *Phil. Trans. Roy. Soc. Lond. A*, 286:183–230, 1977. G. D. Crapper. Surface waves generated by a travelling pressure point. *Proc. Roy. Soc. Lond. A*, 282:547–558, 1964. M. C. Dallaston and S. W. McCue. Accurate series solutions for gravity-driven Stokes waves. *Phys. Fluids*, 22:082104, 2010. A. Darmon, M. Benzaquen, and E. Raphaël. Kelvin wake pattern at large Froude numbers. *J. Fluid Mech.*, 738:R3–8, 2014. F. Dias and T. J. Bridges. The numerical computation of freely propagating time-dependent irrotational water waves. *Fluid Dyn. Res.*, 38:803–830, 2006. S. . Ellingsen. Ship waves in the presence of uniform vorticity. *J. Fluid Mech.*, 742:R2–11, 2014 C. Fochesato and F. Dias. A fast method for nonlinear three-dimensional free-surface waves. *Proc. Roy. Soc. A*, 462:2715–2735, 2006. L. K. Forbes. An algorithm for 3-dimensional free-surface problems in hydrodynamics. *J. Comp. Phys.*, 82:330–347, 1989. L. K. Forbes and G. C. Hocking. Flow due to a sink near a vertical wall, in infinitely deep fluid. Comp. Fluids, 34:684–704,2005. S. Grandison and J.-M. Vanden-Broeck. Truncation approximations for gravity-capillary free-surface flows. *J. Eng. Math.*,54:89–97, 2006. S. T. Grilli, P. Guyenne, and F. Dias. A fully non-linear model for three-dimensional overturning waves over an arbitrary bottom. *Int. J. Numer. Meth. Fluids*, 35:829–867, 2001. T. H. Havelock. Wave resistance: Some cases of three-dimensional fluid flow. *Proc. Roy. Soc. Lond. A*, 95:354–365, 1919. T. H. Havelock. The wave resistance of a spheroid. *Proc. Roy. Soc. Lond. A*, 131:275–285, 1931. T. H. Havelock. The theory of wave resistance. *Proc. Roy. Soc. Lond. A*, 138:339–348, 1932. P. J. Higgins, W. W. Read, and S. R. Belward. Analytical series solutions for three-dimensional supercritical flow over topography. *J. Eng. Math.*, 77:39–49, 2012. A. C. Hindmarsh, P. N. Brown, K. E. Grant, S. L. Lee, R. Serban, D. E. Shumaker, and C. S. Woodward. SUNDIALS: Suite of nonlinear and differential/algebraic equation solvers. *ACM Trans. Math. Soft.*, 31:363–396, 2005. C.-E. Janson, M. Leer-Andersen, and L. Larsson. Calculation of deep-water wash waves using a combined Rankine/Kelvin source method. *J. Ship Res.*, 47:313–326, 2003. S. Khatiwala. Fast spin up of ocean biogeochemical models using matrix-free Newton-Krylov. *Ocean Modell.*, 23:121–129, 2008. D. A. Knoll and D. E. Keyes. Jacobian-free Newton-Krylov methods: a survey of approaches and applications. *J. Comp. Phys.*, 193:357–397, 2004. J. Lighthill. *Waves in Fluids*. Cambridge University Press, Cambridge, 1978. V. Lukomsky, I. Gandzha, and D. Lukomsky. Steep sharp-crested gravity waves in deep water. *Phys. Rev. Lett.*, 89:164502, 2002. C. J. Lustri and S.J. Chapman. Steady gravity waves due to a submerged source. *J. Fluid Mech.*, 732:660–686, 2013. C. J. Lustri, S. W. McCue, and B. J. Binder. Free surface flow past topography: A beyond-all-orders approach. *Euro. J. Appl. Math.*, 23:441–467, 2012. S. W. McCue and L. K. Forbes. Bow and stern flows with constant vorticity. *J. Fluid Mech.*, 399:277–300, 1999. S. W. McCue and L. K. Forbes. Free-surface flows emerging from beneath a semi-infinite plate with constant vorticity. *J. Fluid Mech.*, 461:387–407, 2002. H. Mekias and J.-M. Vanden-Broeck. Subcritical flow with a stagnation point due to a source beneath a free surface. *Phys. Fluids A*, 3:2652–2658, 1991. J. H. Michell. The wave resistance of a ship. *Phil. Mag.*, 45:106–123, 1898. T. J. Moroney and Q. Yang. A banded preconditioner for the two-sided, nonlinear space-fractional diffusion equation. *Comp. & Math. App.*, 66:659–667, 2013. F. Noblesse. The steady wave potential of a unit source, at the centerplane. *J. Ship Res.*, 22:80–88, 1978. F. Noblesse. Alternative integral representations for the Green function of the theory of ship wave resistance. *J. Eng. Math.*, 15:241–265, 1981. F. Noblesse, G. Delhommeau, H. Y. Kim, and C. Yang. Thin-ship theory and influence of rake and flare. *J. Eng. Math.*, 64:49–80, 2009. F. Noblesse, G. Delhommeau, and C. Yang. Practical evaluation of steady flow resulting from a free-surface pressure patch. *J. Ship Res.*, 53:137–150, 2009. O. Ogilat, S. W. McCue, I. W. Turner, J. A. Belward, and B. J. Binder. Minimising wave drag for free surface flow past a two-dimensional stern. *Phys. Fluids*, 23:072101, 2011. A. S. Peters. A new treatment of the ship wave problem. *Comm. Pure Appl. Math.*, 2:123–148, 1949. E. Părău and J.-M. Vanden-Broeck. Nonlinear two- and three-dimensional free surface flows due to moving disturbances. *Euro. J. Mech. B/Fluids*, 21:643–656, 2002. E. Părău and J.-M. Vanden-Broeck. Three-dimensional waves beneath an ice sheet due to a steadily moving pressure. *Phil. Trans. R. Soc. A*, 369:2973–2988, 2011. E. Părău, J.-M. Vanden-Broeck, and M. J. Cooker. Nonlinear three-dimensional gravitycapillary solitary waves. *J. Fluid Mech.*, 536:99–105, 2005. E. Părău, J.-M. Vanden-Broeck, and M. J. Cooker. Three-dimensional gravity-capillary solitary waves in water of finite depth and related problems. *Phys. Fluids*, 17:122101, 2005. E. Părău, J.-M. Vanden-Broeck, and M. J. Cooker. Nonlinear three-dimensional interfacial flows with a free surface. *J. Fluid Mech.*, 591:481–494, 2007. E. Părău, J.-M. Vanden-Broeck, and M. J. Cooker. Three-dimensional capillary-gravity waves generated by a moving disturbance. *Phys. Fluids*, 19:082102, 2007. E. Părău, J.-M. Vanden-Broeck, and M. J. Cooker. Three-dimensional gravity and gravity-capillary interfacial flows. *Math. Comp. Sim.*, 74:105–112, 2007. E. Părău, J.-M. Vanden-Broeck, and M. J. Cooker. Time evolution of three-dimensional nonlinear gravity-capillary free-surface flows. *J. Eng. Math.*, 68:291–300, 2010. M. Rabaud and F. Moisy. Ship wakes: Kelvin or Mach angle? *Phys. Rev. Lett.*, 110:214503, 2013. A. M. Reed and J. H. Milgram. Ship wakes and their radar images. *Ann. Rev. Fluid Mech.*, 34:469–502, 2002. Y. Saad and M. H. Schultz. GMRES: A generalised minimum residual algorithm for solving nonsymmetric linear systems. *SIAM J. Sci. Stat. Comp.*, 7:856–869, 1986. L. W. Schwartz. Computer extension and analytic continuation of Stokes expansion for gravity waves. *J. Fluid Mech.*, 62:553–578, 1974. D. C. Scullen. *Accurate computation of steady nonlinear free-surface flows.* PhD thesis, The University of Adelaide, 1998. D. C. Scullen and E. O. Tuck. Free-surface elevation due to moving pressure distributions in three dimensions. *J. Eng. Math.*, 70:29–42, 2011. P. H. Trinh and S. J. Chapman. The wake of a two-dimensional ship in the low-speed limit: results for multi-cornered hulls. *J. Fluid Mech.*, 741:492–513, 2014. P. H. Trinh, S. J. Chapman, and J.-M. Vanden-Broeck. Do waveless ships exist? Results for single-cornered hulls. *J. Fluid Mech.*, 685:413–439, 2011. E. O. Tuck, J. I. Collins, and W. H. Wells. On ship wave patterns and their spectra. *J. Ship Res.*, 15:11–21, 1971. E. O. Tuck and D. C. Scullen. A comparison of linear and nonlinear computations of waves made by slender submerged bodies. *J. Eng. Math.*, 42:255–264, 2002. E. O. Tuck, D. C. Scullen, and L. Lazauskas. Ship-wave patterns in the spirit of Michell. In *IUTAM Symposium on Free Surface Flows*, pages 311–318. Springer. F. Ursell. On Kelvin’s ship-wave pattern. *J. Fluid Mech.*, 8:418–431, 1960. S. L. Wade, B. J. Binder, T. W. Mattner, and J. P. Denier. On the free-surface flow of very steep forced solitary waves. *J. Fluid Mech.*, 739:1–21, 2014. J. M. Williams. Limiting gravity waves in water of finite depth. *Phil. Trans. Roy. Soc. Lond. A*, 302:139–188, 1981. Y. Zhang and S. Zhu. Open channel flow past a bottom obstruction. *J. Eng. Math.*, 30:487–499, 1996. Ordering the equations {#appendixA} ====================== The left-hand side of $\textbf{E}(\textbf{u})=0$ is a vector valued function made up of six different functions taken from the numerical scheme. The free surface condition (\[eqn:freeSurfCond\]) and boundary integral equation (\[eqn:IntegroEqn\]) evaluated at the half mesh points $(x_{k+\frac{1}{2}},y_\ell)$ are denoted $\textbf{E}_{1_{k,\ell}}$ and $\textbf{E}_{2_{k,\ell}}$, respectively, for $k=1,\dots,N-1$ and $\ell=1,\dots,M$. We also have the radiation conditions (\[eqn:numUpRadiation\]) denoted: $$\begin{aligned} \textbf{E}_{3_{\ell}}&=x_1((\phi_x)_{1,\ell}-1)+n(\phi_{1,\ell}-x_1),\\ \textbf{E}_{4_{\ell}}&=x_1(\phi_{xx})_{1,\ell}+n((\phi_x)_{1,\ell}-1),\\ \textbf{E}_{5_{\ell}}&=x_1(\zeta_x)_{1,\ell}+n\zeta_{1,\ell},\\ \textbf{E}_{6_{\ell}}&=x_1(\zeta_{xx})_{1,\ell}+n(\zeta_x)_{1,\ell}, \end{aligned}$$ for $\ell=1,\dots,M$. We order these equations as $$\begin{aligned} \textbf{E}=&[\textbf{E}_{3_{1}},\textbf{E}_{4_{1}},\textbf{E}_{1_{1,1}},\dots,\textbf{E}_{1_{N-1,1}},\textbf{E}_{3_{2}},\textbf{E}_{4_{2}},\textbf{E}_{1_{1,2}},\dots,\textbf{E}_{1_{N-1,2}},\ldots,\textbf{E}_{3_{M}},\textbf{E}_{4_{M}},\textbf{E}_{1_{1,M}},\dots,\textbf{E}_{1_{N-1,M}}, \nonumber \\ &\textbf{E}_{5_{1}},\textbf{E}_{6_{1}},\textbf{E}_{2_{1,1}},\dots,\textbf{E}_{2_{N-1,1}},\textbf{E}_{5_{2}},\textbf{E}_{6_{2}},\textbf{E}_{2_{1,2}},\dots,\textbf{E}_{2_{N-1,2}},\ldots,\textbf{E}_{5_{M}},\textbf{E}_{6_{M}},\textbf{E}_{2_{1,M}},\dots,\textbf{E}_{2_{N-1,M}}]^T,\end{aligned}$$ which results in the Jacobian structure illustrated in Figure \[fig:TwoJacVis\]. The linear Jacobian {#appendixB} =================== To construct the linear Jacobian, we need to apply the same numerical discretisation outlined in Section \[sec:numerical\] to the linear problem derived in Section \[sec:linearproblem\]. The singularity in (\[eqn:IntegroEqnlinear\]) is dealt with in the same way as with the nonlinear problem, by adding and subtracting the term (\[eqn:I2DashDash\]), except that now $S_2(x_i,y_j;x^*_k,y^*_\ell)=K_3(x_i,y_j;x^*_k,y^*_\ell)$, which simplifies the details. The linear system then becomes $$\begin{aligned} \textbf{E}_{1_{k,\ell}}&=\phi^*_{x_{k,\ell}}+\frac{\zeta^*_{k,\ell}}{F^2}-1,\\ \textbf{E}_{2_{k,\ell}}&=2\pi(\phi^*_{k,\ell}-x^*_k)+\frac{\epsilon}{\left({x^*_k}^2+{y^*_\ell}^2+1 \right)^\frac{1}{2}} -\sum\limits_{i=1}^{N}\sum\limits_{j=1}^{M} w(i,j)\left[\zeta_{x_{i,j}}-\zeta^*_{x_{k,\ell}}\right]K_{3_{i,j,k,\ell}} -\zeta^*_{x_{i,j}}I,\\ \textbf{E}_{3_{\ell}}&=x_1\phi_{x_{1,\ell}}+n\phi_{1,\ell}-x_1(n+1),\\ \textbf{E}_{4_{\ell}}&=\frac{x_1}{\Delta x}\phi_{x_{2,\ell}}+(n-\frac{x_1}{\Delta x})\phi_{x_{1,\ell}}-n,\\ \textbf{E}_{5_{\ell}}&=x_1\zeta_{x_{1,\ell}}+n\zeta_{1,\ell},\\ \textbf{E}_{6_{\ell}}&=\frac{x_1}{\Delta x}\zeta_{x_{2,\ell}}+(n-\frac{x_1}{\Delta x})\zeta_{x_{1,\ell}}, \end{aligned}\label{eqn:SystemEquation}$$ for $k=1\dots(N-1)$, $\ell=1\dots M$ where **E** is constructed from these equations and $$\begin{aligned} K_{3_{i,j,k,\ell}}&=K_3(x_i,y_j;x^*_k,y^*_\ell),\end{aligned}$$ $I$ is given by $$I=\int\limits_{y_1}^{y_M}\int\limits_{x_1}^{x_N} K_3\, \text{d}x\,\text{d}y,\label{eqn:IS2linear}$$ and $w(i,j)$ is the weighting function for numerical integration. As before, $I$ can be evaluated exactly in terms of logarithms. The next step is to determine how $\phi$, $\phi^*$, $\zeta$ and $\zeta^*$ depend on the unknowns in (\[eq:unknowns\]). We first expand the trapezoidal-rule integration of $\zeta$ in (\[eqn:zetaapprox\]) which gives $$\zeta_{k,\ell}=\zeta_{1,\ell}+\frac{\Delta x}{2}\zeta_{x_{1,\ell}}+\Delta x\sum\limits_{i=2}^{k-1}\zeta_{x_{i,\ell}}+\frac{\Delta x}{2}\zeta_{x_{k,\ell}},\quad \text{for }k=2,\dots,N\text{, }\ell=1,\dots,M.\label{eqn:zetaApproxExpand}$$ Similarly, we expand $\phi$ as $$\phi_{k,\ell}=\phi_{1,\ell}+\frac{\Delta x}{2}\phi_{x_{1,\ell}}+\Delta x\sum\limits_{i=2}^{k-1}\phi_{x_{i,\ell}}+\frac{\Delta x}{2}\phi_{x_{k,\ell}},\quad \text{for }k=2,\dots,N\text{, }\ell=1,\dots,M.$$ This result immediately provides the values for $\phi^*$ using two point interpolation $$\phi^*_{k,\ell}=\frac{1}{2}(\phi_{k,\ell}+\phi_{k+1,\ell}).$$ Substituting this expression and its equivalent in $\zeta^*_x$ and $\zeta^*$ into (\[eqn:SystemEquation\]) gives the resulting linear system in terms of the unknowns, $$\begin{aligned} \textbf{E}_{1_{k,\ell}}&=\frac{1}{2}(\phi_{x_{k,\ell}}+\phi_{x_{k+1,\ell}})+\frac{1}{F^2}\left(\zeta_{1,\ell}+\frac{\Delta x}{2}\zeta_{x_{1,\ell}}+ \Delta x\sum\limits_{i=2}^{k-1}\zeta_{x_{i,\ell}}+\frac{3\Delta x}{4}\zeta_{x_{k,\ell}}+\frac{\Delta x}{4}\zeta_{x_{k+1,\ell}}\right)-1,\notag\\ \textbf{E}_{2_{k,\ell}}&=2\pi \left[\phi_{1,\ell}+\frac{\Delta x}{2}\phi_{x_{1,\ell}}+\Delta x\sum\limits_{i=2}^{k-1}\phi_{x_{i,\ell}}+\frac{3\Delta x}{4}\phi_{x_{k,\ell}}+\frac{\Delta x}{4}\phi_{x_{k+1,\ell}}-x^*_k\right]+\frac{\epsilon}{\left({x^*_k}^2+{y^*_\ell}^2+1 \right)^\frac{1}{2}}\notag\\ &-\sum\limits_{i=1}^{N}\sum\limits_{j=1}^{M} w(i,j)\left[\zeta_{x_{i,j}} -\frac{1}{2}(\zeta_{x_{k,\ell}}+\zeta_{x_{k+1,\ell}})\right]K_{3_{i,j,k,\ell}}-\frac{1}{2}(\zeta_{x_{k,\ell}}+\zeta_{x_{k+1,\ell}})I,\notag\\ \textbf{E}_{3_{\ell}}&=x_1\phi_{x_{1,\ell}}+n\phi_{1,\ell}-x_1(n+1),\label{eqn:SystemEquationsInZetaX}\\ \textbf{E}_{4_{\ell}}&=\frac{x_1}{\Delta x}\phi_{x_{2,\ell}}+(n-\frac{x_1}{\Delta x})\phi_{x_{1,\ell}}-n,\notag\\ \textbf{E}_{5_{\ell}}&=x_1\zeta_{x_{1,\ell}}+n\zeta_{1,\ell},\notag\\ \textbf{E}_{6_{\ell}}&=\frac{x_1}{\Delta x}\zeta_{x_{2,\ell}}+(n-\frac{x_1}{\Delta x})\zeta_{x_{1,\ell}},\notag\end{aligned}$$ for $k=1\dots(N-1)$, $\ell=1\dots M$. Finally, to calculate the linear Jacobian, the equations in (\[eqn:SystemEquationsInZetaX\]) can be differentiated with respect to $\phi_{1,m}$, $\phi_{x_{n,m}}$, $\zeta_{1,m}$ and $\zeta_{x_{n,m}}$ to give: $$\begin{aligned} \frac{\partial \textbf{E}_{1_{k,\ell}}}{\partial \phi_{1,m}}&= 0,\notag\\ \frac{\partial \textbf{E}_{1_{k,\ell}}}{\partial \phi_{x_{n,m}}}&= \begin{cases} \frac{1}{2} & \text{for }n=k,k+1\text{ and }m=\ell\\ 0 & \text{otherwise}\\ \end{cases},\label{eq:PreA}\\ \frac{\partial \textbf{E}_{1_{k,\ell}}}{\partial \zeta_{1,m}}&= \begin{cases} \frac{1}{F^2} & \text{for }m=\ell\\ 0 & \text{otherwise}\\ \end{cases},\notag\\ \frac{\partial \textbf{E}_{1_{k,\ell}}}{\partial \zeta_{x_{n,m}}}&= \begin{cases} \frac{\Delta x}{4F^2} & \text{for }n=1\text{, }k=1\text{ and }m=\ell\\ \frac{\Delta x}{2F^2}& \text{for }n=1\text{, }k>1\text{ and }m=\ell\\ \frac{\Delta x}{F^2} & \text{for }n<k\text{ and }m=\ell\\ \frac{3\Delta x}{4F^2}& \text{for }n=k\text{ and }m=\ell\\ \frac{\Delta x}{4F^2} & \text{for }n=k+1\text{ and }m=\ell\\ 0 & \text{otherwise}\\ \end{cases},\label{eq:PreB}\\ \frac{\partial \textbf{E}_{2_{k,\ell}}}{\partial \phi_{1,m}}&= \begin{cases} 2\pi & \text{for }m=\ell\\ 0 & \text{otherwise}\\ \end{cases},\notag\\ \frac{\partial \textbf{E}_{2_{k,\ell}}}{\partial \phi_{x_{n,m}}}&= \begin{cases} \frac{\pi\Delta x}{2} & \text{for }n=1\text{, }k=1\text{ and }m=\ell\\ \pi\Delta x & \text{for }n=1\text{, }k>1\text{ and }m=\ell\\ 2\pi\Delta x & \text{for }n<k\text{ and }m=\ell\\ \frac{3\pi\Delta x}{2}& \text{for }n=k\text{ and }m=\ell\\ \frac{\pi\Delta x}{2} & \text{for }n=k+1\text{ and }m=\ell\\ 0 & \text{otherwise}\\ \end{cases},\label{eq:PreC}\end{aligned}$$ $$\begin{aligned} \frac{\partial \textbf{E}_{2_{k,\ell}}}{\partial \zeta_{1,m}}&= 0\notag\\ \frac{\partial \textbf{E}_{2_{k,\ell}}}{\partial \zeta_{x_{n,m}}}&= \begin{cases} \frac{1}{2}\sum\limits_{i=1}^{N}\sum\limits_{j=1}^{M}w(i,j)K_{3_{i,j,k,\ell}}-\frac{1}{2}I-w(n,m)K_{3_{n,m,k,\ell}} & \text{for }n=k,k+1\text{ and }m=\ell\\ -w(n,m)K_{3_{n,m,k,\ell}} & \text{otherwise}\\ \end{cases}\label{eq:PreD},\end{aligned}$$ for $k=1\dots(N-1)$, $\ell=1\dots M$ and $n=1\dots N$, $m=1\dots M$. The derivatives for $\textbf{E}_{3_{\ell}},\textbf{E}_{4_{\ell}},\textbf{E}_{5_{\ell}},\textbf{E}_{6_{\ell}}$ can be easily calculated and will not be explicitly written here. Our preconditioner is formed by ordering these Jacobian entries in the manner described in \[appendixA\]. Preconditioner storage and factorisation {#appendixC} ======================================== \[sec:InvPre\] As shown in Figure \[fig:TwoJacVis\], the preconditioner can be divided up into four equal submatrices of size $(N+1)M\times(N+1)M$. This preconditioner can then be factorised using the block decomposition, $$\textbf{P}=\left[ \begin{matrix} A & B\\ C & D\\ \end{matrix}\right]= \left[\begin{matrix} I & 0\\ CA^{-1} & I\\ \end{matrix}\right] \left[\begin{matrix} A & 0\\ 0 & D-CA^{-1}B\\ \end{matrix}\right] \left[\begin{matrix} I & A^{-1}B\\ 0 & I\\ \end{matrix}\right],$$ where $A$, $B$, $C$, and $D$ are primarily given by equations (\[eq:PreA\]), (\[eq:PreB\]), (\[eq:PreC\]) and (\[eq:PreD\]), respectively. Thus we can solve the system $\textbf{P}\textbf{r}=\textbf{b}$ by performing the following operations, $$\left[\begin{matrix} \textbf{t}_1\\ \textbf{t}_2 \end{matrix}\right] = \left[\begin{matrix} \textbf{b}_1\\ \textbf{b}_2-CA^{-1}\textbf{b}_1 \end{matrix}\right],\quad \left[\begin{matrix} \textbf{s}_1\\ \textbf{s}_2 \end{matrix}\right] = \left[\begin{matrix} A^{-1}\textbf{t}_1\\ (D-CA^{-1}B)^{-1}\textbf{t}_2 \end{matrix}\right],\quad \left[\begin{matrix} \textbf{r}_1\\ \textbf{r}_2 \end{matrix}\right] = \left[\begin{matrix} \textbf{s}_1-A^{-1}B\textbf{s}_2\\ \textbf{s}_2 \end{matrix}\right].$$ This method provides several advantages. First, $A$ is tridiagonal, allowing for easy storage and fast factorisation and inversion when needed. Second, $B$ and $C$ are only used in matrix vector multiplication operations and thus can be implemented as functions that perform these operations rather than stored as matrices. Furthermore, $A$, $B$ and $C$ are block diagonal, and each diagonal block is identical within a given matrix, meaning $CA^{-1}B$ need only be computed for one block. Finally, $D$ appears only in the Schur complement $(D-CA^{-1}B)$, which we store and factorise in the preconditioner set-up phase. These advantages mean we only store a $3\times(N+1)M$ matrix for $A$ and a block-banded matrix for the Schur complement $(D-CA^{-1}B)$ when constructing and factorising the preconditioner. [^1]: Intel Core i7-2600 CPU with 3.40 GHz processor and 8 GB of system memory [^2]: 2x Intel Xeon E5-2670 CPUs with 2.66 GHz processor, M2090 Nvidia Tesla GPU and 124 GB of system memory

Weightlifting at the 2013 Mediterranean Games – Men's 62 kg The men's 62 kg competition of the weightlifting events at the 2013 Mediterranean Games in Mersin, Turkey, was held on June 21 at the Erdemli Sports Hall. Each lifter performed in both the snatch and clean and jerk lifts, with the final score being the sum of the lifter's best result in each. The athlete received three attempts in each of the two lifts; the score for the lift was the heaviest weight successfully lifted. This weightlifting event was the lightest men's event at the weightlifting competition, limiting competitors to a maximum of 62 kilograms of body mass. Schedule All times are Eastern European Summer Time (UTC+3). Results 7 athletes from seven countries will take part. Snatch Clean & Jerk References External links Category:Weightlifting at the 2013 Mediterranean Games

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Edit: This deck in the following article was a theory craft and untested. I just played a few runs and it’s a little weaker against fliers than I’d like. Geomar with combat tricks could pick off fliers and gain life. So we need some more removal. Probably something like -1 Healers Cloak +1 Vanquish and a Scorpion Wasp or another Desert Marshal in the Market -1 Hourglass. The two main deck hourglass should suffice. Inspired by CVH’s fantastic “Budget-ify” Series from Elder Scrolls Legends, and a few people asking for budget lists, I wanted to take one of my top performing gauntlet lists and budgetize it. This is the deck I called “Enduring Combrei” (yes, I’m awful at naming things). For those interested in CVH’s series here’s the link: https://www.youtube.com/watch?reload=9&v=hGMkB1ZHF9w First, I have an exciting announcement! I am always thinking about how to better engage with the community. As such, I would like to announce that I have started a new subreddit https://www.reddit.com/r/AIEternal/ This is meant to merely compliment https://www.reddit.com/r/EternalCardGame/ and I created it after realizing that Gauntlet and Forge players account for a much smaller percentage of the playerbase than Ranked and Draft. I feel that having a smaller separate space with focused community discussion will be beneficial. My site is linked in the sidebar, and I encourage other producers of content to DM me if they would like their site added to the sidebar as well. This will be a community space, and as such I will not be posting any of my articles or decklists in the AIEternal Forums. Again, my site will be in the sidebar for those who wish to read it. I will still be a very active member in EternalCardGame, and I encourage all of you to stay active as well. Just to reiterate, AIEternal is meant to compliment EternalCardGame with focused discussion of AI related modes, in much the same way as CustomEternal is for focused Custom Cards discussion and compliments the Custom card thread on EternalCardGame. I will continue to post some of the major strategy articles to EternalCardGame, but everything else you can check my blog or my EternalWarcry lists which link here. Lets get to the deck discussion! Another name for my deck could easily be something like Flying Shiftstone Pile or Flying Wallet Combrei. The point is that this deck is not cheap, costing 51,700 Shiftstone or 200,000 in Premium(!). And after all, (Image and paraphrased quote from The Matrix – The Wachowski Brothers and Warner Bros. Entertainment Inc.) So, here’s the fully powered legendary filled list: 4 Finest Hour (Set1 #130) 2 Infinite Hourglass (Set1 #67) 4 Lingering Influence (Set4 #100) 2 Sharpened Reflex (Set4 #102) 4 Amaran Armadillo (Set4 #60) 4 Awakened Student (Set1 #331) 2 Desert Marshal (Set1 #332) 2 Vanquish (Set1 #143) 4 Auralian Merchant (Set4 #70) 2 Stand Together (Set1 #334) 4 Unseen Commando (Set3 #122) 4 Valkyrie Enforcer (Set1 #151) 4 Geomar, the Steel Tempest (Set4 #128) 2 Sword of Unity (Set4 #249) 4 Amilli, Cloudmarshal (Set3 #136) 6 Justice Sigil (Set1 #126) 7 Time Sigil (Set1 #63) 4 Combrei Banner (Set1 #424) 4 Crest of Progress (Set4 #247) 2 Crownwatch Standard (Set4 #97) 4 Seat of Progress (Set0 #58) ————–MARKET————— 1 Lumen Defender (Set1 #115) 1 Xenan Obelisk (Set1 #103) 1 Sword of Unity (Set4 #249) 1 Stand Together (Set1 #334) 1 Infinite Hourglass (Set1 #67) Lets start with a general example. The first thing we want to do when we make a budget deck is be honest with ourselves. Take Elysian Midrange in Ranked. Do we really want to play Beckoning Lumen, Sandspitter, or Snapping Brushstalker to have a four drop that gets back Dawnwalker? Absolutely not. Sandstorm Titan does so many more things for that deck. There is no budget substitute. “But wait, that’s not helpful, I want to play Elysian!” Good news, you still can, but you would approach the deck differently. Maybe play a tempo build with Whispering Wind and Praxis Displacer for example. Now we’ll take a look at my list in this mindset. Commons and Uncommons are no problem. The rares I use are extremely core from Ranked so you should craft them as soon as you can or already have them, with the exception being Amaran Armadillo. However, it does so much work in the deck that we can’t cut it. Cutting the powerful legendaries is where we will save the vast majority of our shiftstone. However, remember back to my Titan example that this isn’t just something you sub out for a budget card at that same cost. First off, I absolutely love this card in gauntlet! It is an extremely powerful lifegain and damage dealer. That said, I have my doubts as to this card in Ranked so I usually don’t recommend crafting unless you have extra shiftstone in the Auric Bank. However, we have a Market! But, not for Justice cards unfortunately. So we need a substitute for four cards. An extreme budget option would be Karmic Guardian, but it’s not going to perform well unless we run it alongside more weapons, which would change the way the deck plays a lot. There are better options at Rare. I think the best option is a 2/2 split of Marisen’s Disciple which can stump the AI with a deadly 1/1 or 2/2 Flier and plays well with Obelisk and 2x Peacekeeper’s Prod. We usually dont want the 3/3 overwhelm with this deck for Disciple. With Prod, we have the Justice influence to hit that on curve, and the stun helps us race and make up for missing lifesteal from Geomar. There is no substitute at all for the lategame power of Amilli with Obelisk and Stand Together. The good news is that this deck often doesn’t even need Amilli to win, it just adds a few percentage points against some of the grindier decks. This is an open slot for us. This weapon has overperformed to the extent that I ended up adding one to the market in addition to 2x in the main. In the interest of staying budget, you can craft one just for the market or run 2x Healer’s cloak main, and probably another in the Market or maybe a Devoted Theurge Market if you have the Horus Traver campaign (not in the main because TT is hard to hit on curve in this deck. Sword is an exception because it is often a turn six play.) Combrei Healer is another option as this would gain you life with six power Merchant + Healer if you really need to stabilize that turn, and make a bigger blocker or pop Aegis to set up Vanquish. The new decks have really strong aggro AI so we really need lots of lifegain. Here is what a list might look like. Keep in mind this is untested and is a theory craft based on the principles of this article. I hope this will guide your thought processes on how to budgetize a deck. If you try it out and find we don’t need that much lifegain, cut the Cloaks for Hammer of Might: 4 Finest Hour (Set1 #130) 2 Infinite Hourglass (Set1 #67) 4 Lingering Influence (Set4 #100) 2 Sharpened Reflex (Set4 #102) 4 Amaran Armadillo (Set4 #60) 4 Awakened Student (Set1 #331) 2 Desert Marshal (Set1 #332) 2 Vanquish (Set1 #143) 4 Auralian Merchant (Set4 #70) 2 Stand Together (Set1 #334) 4 Unseen Commando (Set3 #122) 4 Valkyrie Enforcer (Set1 #151) 2 Copperhall Elite (Set1 #340) 2 Healer’s Cloak (Set1 #98) 2 Marisen’s Disciple (Set1 #104) 2 Peacekeeper’s Prod (Set2 #86) 2 Throne Warden (Set1 #514) 7 Time Sigil (Set1 #63) 6 Justice Sigil (Set1 #126) 2 Crownwatch Standard (Set4 #97) 4 Combrei Banner (Set1 #424) 4 Crest of Progress (Set4 #247) 4 Seat of Progress (Set0 #58) ————–MARKET————— 1 Infinite Hourglass (Set1 #67) 1 Combrei Healer (Set1 #333) 1 Stand Together (Set1 #334) 1 Xenan Obelisk (Set1 #103) 1 Lumen Defender (Set1 #115) One thing you might notice is there are now a lot of two-ofs. This is because we need to fill the shoes of strong four-of legendaries with more situational cards. The deck will work well, but not as consistently as with four-ofs. I hope you enjoyed this article. Be sure to check out the reddit thread. Let me know if you liked this format, and if you want to see this done for other decks. One last card that I don’t think was necessary with all my fliers in the original list was Randori (we are rarely getting blocked in the air). It’s a cool and potentially powerful combat trick that is a lot more relevant with on the ground attacking units, so in this budget version it might be worth testing out. The name also brings back memories of my couple months of Judo classes. Randori is sparring in the Japanese art of Judo. I’ll not soon forget the pain of being thrown to the thin mat repeatedly, and the Sensei saying how HE trained on hard wooden floors, and I need to more or less “git gud” at break-falls. Good times. One more thing, I wanted to share something from my personal life. My Chameleon recently passed away. I don’t want to get into too many details but suffice it to say, the pet store recommended dirt or whatever for the floors of cages is a choking hazard. We believe she was also pregnant so it sucks even more. As such, I am changing my name on Discord and EternalWarcry to FallenChameleon (hopefully in-game as well) to remember her. This is something my girlfriend encouraged me to do. Since Reddit doesn’t allow name changes I’ll stay as MagicTurtle_TCG as it’s not that big of a deal, and I really don’t want to start with a new account anyway even if I could as I have so much content there and it’s just too confusing in my opinion. You can call me by either name, or just Chameleon or Turtle for short. On a positive note, if you see FallenChamelon on ladder you’ll know it’s me, and not one of the at least two other MagicTurtles from ingame. Also, if anyone was wondering how I came up with my MagicTurtle name originally, it was from back in my Heartstone days. I was thinking up names, most of them lame mtg related things like “BoltSnapBolt” so I just used the random name generator and it came up with that on the first try. I had just bought a pet Turtle a few days prior so I figured, why not? Next week, I’ll have a special article for you regarding Game Theory Optimal Play, Exploitative Play, understanding Variance and handling Tilt. It’s something I’ve been meaning to write for over a year now and finally have the time to write it! I will draw on my experience as a Poker player and coach at the low-mid stakes live no limit holdem games. I’ll format it as an example from poker immediately followed by Eternal play. It will apply to all the formats in the game, including Gauntlet. Speaking of tilt, I’ll leave you with this gem. Yep, the AI tilts too! Thanks for reading, FallenChameleon (MagicTurtle)

"Previously on eureka..." "You may get to him but you won't get to me." "There's only one thing I want from you, Jojo." " What is that?" " It's a modified version of the memory neutralizer that I designed years ago." "Can I borrow this?" "Sure." "We've been searching for a... unifying theory of everything." "You're talking about the akashic field." "Just wish I could see what was going on inside of his head." "Why this is happening to him." "His brain is wired like no one else's." "He's created a connection to the field." "Albert Einstein said science without religion is lame, and religion without science is blind." "But is there still a place for faith in a world of science?" "Has our ability to unravel the mysteries of rainbows made them any less miraculous?" "Science may be the method by which we give name to God's miracles." "But faith is the question that arises every time an old mystery is solved." "The elegant explanations discovered every day in Eureka are the very reason to believe in something greater." "Something beyond mathematics." "Something divine." "Dad!" "Hey!" "What are you doing here?" "I was just cleaning out my closet for donations, as requested." "And..." "I brought you breakfast." "Thank you." "Now..." "What is it?" "Scrambled egg whites with spinach and tofu." "SARAH said your cholesterol's been running high from too much pizza." "That's crazy talk." "Almost forgot." "I got you your sunday paper." "Here you go." " What do you want?" " Who said I want anything?" "It's sunday morning." "You're up before noon." "You{\'re} do chores." "You{\'re} bring me the morning paper." "What do you want?" "I wanna get a tattoo." "No!" "Okay, I'm being serious." "Oh, okay." "No." " Can we talk about this?" " Sure, yeah." "We can talk about it." "And the answer is..." "No." "Are you amused with yourself?" "I'm pretty amusing." "Gotta drop this off." "I am so telling SARAH." "Thought-provoking sermon, Reverend." "I mean, the most beautiful emotion we can experience is the mysterious." "I couldn't agree more." "Unfortunately, I'm literally preaching to the choir." "{\Well, }You knew you were gonna have a small crowd when you took the job." "It's not the size of the congregation that counts." "It's..." "The commitment." "Still, a little more size could be nice." "Mom?" "And a little more time." "Excuse me, Reverend and Henry." "Diane, another lovely musical arrangement." "Thank you very much, Reverend." "How are you?" "Hanging in there." " You know, working helps." " Tell me about it." "Anytime you need to talk, drop by." "I will." "Thanks." " Bye, Henry." " Bye-bye." "How many people could understand the pain of losing a spouse?" "Well, we all deal in our own way." "{\Still, }I'm glad you've been there for her." "Yeah, me too." "Thanks." " See you next sunday?" " Absolutely." "Sheriff Carter." "Hi." "You're early..." "For next sunday." "Yeah..." "It..." "It's Jo's day off, and I drew the short straw." "So... what have we got there?" "Donations..." "Spring cleaning." "We'll make sure we get these to those in need." "A lot of need." "It's not even mine." "I blame you for her death." "I can't look at you without thinking that you{\'re the one who} did this." "That you're the one who took her away from me." "You okay, Sheriff?" "Yeah, I just... remembered who I borrowed this from." "Well, if you ever want to borrow my book..." " Yeah." " See you next sunday, maybe?" "I'll work on it." "I'll put these up front..." "For you." "I kind of wish I hadn't even told him." "I don't understand the appeal of painting oneself permanently." "Maybe because, in your case, it would be considered graffiti." "I thought every kid from LA had a tattoo." "Oh, yeah, and preschoolers have body piercings." "Haven't you guys ever been to, like, a big city?" "Nope." "Oh!" "We did have that one wild weekend in Vegas." "We did." " Really?" " Okay, so it was a virtual Vegas," " but it was like we were{\ really} there." " You{\ guys} really need to get out{\ more}." "I'll tell you what." "This weekend, we'll take my car and we..." "Well, what?" "Don't leave us in suspense." "Spit it out." " Zoe, what's wrong?" " I can't talk." "Should I alert sheriff Carter?" "Zoe?" "Pilar?" "What's happening?" " What's happening to me?" "" "{\pos(192,168)}The Projet-SG Team" "{\pos(192,188)}presents:" "{\pos(90,260)}Timing:" "Golgi, Linwelin," "{\pos(150,280)}Moochie, Ricana." "{\pos(240,35)}Edition:" "Golgi, Linwelin," "{\pos(300,55)}Moochie, Ricana." "{\pos(270,100)}Proofreading:" "Golgi, Linwelin." " Season 2 |" "Episode 10 - God is in the Details (v. 1.03)" "{\pos(192,230)}What exactly are you doing?" "{\pos(192,230)}It's a portable MRI." "{\pos(192,230)}Allows me to see inside her throat." " You're making her nervous." " Just tell me what's wrong with her." "{\pos(192,210)}I don't know, it's not laryngitis." "{\pos(192,210)}They're{\ all} suffering from some sort sort of" "{\pos(192,210)}vocal cord paralysis." "From what?" "I'm not sure yet." "Okay, I'll..." "Hang out while you tinker with her voice box." "I don't tinker." "Carter, just..." "Give him some time." "Yeah." "I know." "I know." "Me too." "Everything's gonna be all right." "He's pretty good at what he does." "{\pos(192,210)}We're gonna keep Zoe and the other girls here for observation at GD." "{\pos(192,210)}Until we have an answer." "{\pos(192,210)}I'm gonna check out the house." "{\pos(192,210)}Just..." "See if I can find anything." "{\pos(192,210)}I already sent a science team." "{\pos(192,210)}They can handle it." "{\pos(192,210)}Yeah, I'd prefer to do my own digging." "{\pos(192,210)}It's... {\pos(192,210)}I'll see you soon." "Okay?" "What is that?" "What..." "What?" "!" "You..." "God!" "So you weren't asking for permission to get a tattoo." "You were just covering your ass, right?" "Is..." "{\pos(192,210)}You know, I'm just gonna do everything I can to get you healthy." "{\pos(192,210)}And then we're gonna talk about that." "So... sunday special is fallout flapjacks." "That's pumpkin pancakes with{\ a} radioactive swirl of cream cheese and nutmeg." "That sounds great, Vince, but I'm waiting for somebody." "Really?" "Who's the lucky lady?" "No!" "Yes." "I'm impressed." "Yeah, so am I." "And just a teeny bit scared." "Yeah." "If all church girls look like you, I might consider converting." "You should join me sometime and find out." "Oh, I would, but I'm allergic." "I'd have to... get a new inhaler." "It'd be a whole..." "Thing." " After you." " Chivalry." "Not something I was expecting from a felon." "Hey, never convicted, but the day is still young." "Try anything, and I'll deviate your septum." "That is so hot." "I'm sorry, Sheriff." "It was my responsibility to keep an eye on them, and I failed." " Bad house." " It's all right, SARAH." "One minute, they were talking about tattoos, the next, they couldn't speak." "I was against her getting one, by the way." "Well, not that it helped, but thanks." "Did you run tests on the air?" "Did you check the filters?" "If anything unusual had been detected," "I would have sealed off the affected areas." "Where were they?" "In the living room." "What is that?" "I don't know." "It wasn't there before." "Neither was that." "This is truly a mystery." "This shouldn't happen." "Crystalline glass is made{\ up} of atoms that bond with more density than ordinary{\ glass}, making windows stronger, more light resistant." " More thermally efficient." " What could do it?" "It'd take an incredible heat source." "{\Well, }SARAH checked. {\She }Said there was no trace of heat in the house." "Like I said, it's a mystery." "I need help." "Zoe can't talk." " You checked..." "GD's entire..." " Active project roster." "Of course." "But {\there is}nothing would cause a problem like this." " Well, something caused it." " Jack, we're doing all we can, as fast as we can." "So why does a special forces bad-ass quit a life of excitement to become the deputy of Sleepy Hollow?" "Well, same reason an anti-establishment anarchist agrees to a cushy consulting job at Global Dynamics." "The money... {\'Cause}You wouldn't believe what they're paying me." "Well, the opportunity." "You know, this isn't just anywhere, it's Eureka." "True..." "If I'd come here sooner, things may have turned out differently{\ for me}." "Like you wouldn't have gone to MIT when you were 15?" "Actually, MIT was great." "I could spend weeks at a time focused on a single variable in a lattice gauge equation." "It was heaven." "I had the same feeling assembling a chromium flash suppression barrel for my grenade launcher." "Yeah, but that's simple mechanics." "Particle and theoretical physics, that's the real mind, Candy." "Well, some of us like practical application." "Oh, yeah, no." "That's all good." "But, I mean, let's be honest." "The particle accelerator only gets built after someone comes up with the idea." "Right?" "So how about a Vinspresso to top things off?" "That's an excellent idea." "No, thanks." " Should be getting back to the office." " I thought you had sundays off." "Yeah, just remembered, I have some paperwork I forgot to finish." "Thanks for brunch." " Hello?" " Still can't find the cause, but the good news is, it's not getting any worse." "Well, I guess that's something." "Are you doing okay?" "Yeah, just..." "Seeing Carter so worried about Zoe just got to me." " I know how he feels." " Well, try and relax." "You been under a lot of stress lately." "I'll keep at it 'till I figure something out." "I know you will." " Good night." " Good night." "What in the world?" "{\pos(192,250)}Hey, there." "Welcome back." "{\pos(192,250)}" " What's happening to me?" " Apparently" "{\pos(192,250)}your inner glow is becoming your outer glow." "Please don't joke." "What were you doing before this happened?" "I helped Kevin with his homework." "Then I took a shower and..." "So Kevin was home." " Yeah." "Why?" " I wonder if he was responsible." " Why would he..." " I don't know." "But we've seen what kind of power he has." "If I'm right, and he's tapping into the akashic field, then he's... tapping into a very powerful energy collective." "Holy crap!" "What did you do?" "I took a shower." "You look radiant." "We tested the water.{\ There's} Nothing in it{\ that} could cause bioluminescence." "How does it happen?" "Enzymes in the skin pigment become oxidized, and then they emit light." "But that's with insects and marine life." "Not anymore." "It may be a kind of bacterial reaction." "Okay, you know what?" "Glowing or not, I'm still the head of GD." " And unless this is contagious..." " No, no, no!" " I gotcha." " The human body is not built for this." "Whatever is causing your bioluminescence is also attacking your nervous system." "Allison, does GD have any projects in bioluminescence in development?" "Not at GD, but maybe off-site." "And you're not gonna like who the project manager is." "Why do you automatically assume I'm responsible?" "Are you really surprised?" "I work in bioluminescence now, Sheriff." "Ever since you torched my necrosomnium violacea," "I needed a change of scenery." "I'm a busy man." "Do you mind getting to the point?" "The point is that Allison Blake is shining like the northern lights." " Fascinating." " Seth, what's the new project?" "Botanical marine cross-hibernization to create bioluminescent specimens." "I mate plants and fish to make them glow." "Why would you do that?" "That's classified." "The head of Global Dynamics is a human glow stick, so unclassify it." "I've only just isolated the mitochondrial strains responsible for bioluminescence." "Phase one includes simple organisms." "Let me guess..." "Phase two is human trials." "Well, yeah." "But I'm years away from that." "Still gonna need a sample." " Waste of time." " Ah, we'll see." "Until then, don't leave the aquarium." "At least you can't light it on fire!" "Sorry I couldn't be here sooner." "You okay?" "We're still going over the smart house, and Fargo is running a full diagnostic on SARAH." "Okay, so don't worry..." "We'll find something soon." "How'd it go with Zane?" "We can talk about that later." "Or now." "Or now." "Bottom line:" "he's... brilliant." "I'm not." "It's the story of my life trying to get a date in this town." "He likes you." "But how long before he realizes" "I can't keep up with him?" "Anyway, I'm more concerned about you." "I'll live." "I'm worried about Allison." "I know." "Me too." "What the..." "Why is it every time you show up, my work gets ruined?" "I'm not the one who turned your aquarium into a theme park for the Shining." "I didn't do this." "This just... happened." "This doesn't just happen." "Water doesn't turn into..." "Blood?" "That's what you're thinking, right?" " Yeah." " Great." "Then you can deal with this." "I don't do blood." "I'm a plant guy." "What's that?" "It's a filtration system." "Or it was." "There was a hole like that at the smart house." "What does that have to do with this?" "Exactly." "Hey, who's gonna fix my tank?" "No one." "This just became a crime scene." " Well, we didn't notice any before." " Yeah, we weren't really looking." " Bingo." " {\So }Everything that's happened is related?" "Yeah." "But I'm not sure to what." "What'd you find out?" "That the smart house had a circle of melted glass, as did Allison's house, and Seth's aquarium." "What happened at the aquarium?" "The water in the marine tanks turned to blood." " Or a blood-like substance." " You test the water?" "Yeah, it didn't match when we compared it to her chem panel." " How bad is she?" " Whatever's triggering Allison's bioluminescence is working as a neurotoxin." "It's shutting down her bodily systems." "Now, the reason I brought her here is I've been working on a nerve agent antidote for the military." "Can you give it to her?" "He can't." "It doesn't exist yet." "But you're close." "How much time does she have?" " Now, Carter..." " How long?" "12 hours." "Maybe less." "{\pos(192,250)}Hey..." "You okay?" "{\pos(192,250)}What's happening?" "{\pos(192,250)}Well, we..." "We've got a few more incidents, so..." " A few?" "!" " Yeah." "We're gonna figure this out." "You're gonna be fine." "Okay?" "But..." "About your tattoo." "I overreacted." "I didn't hear you out." "And... that's just..." "I'm sorry." "I mean, I do think what you did was wrong." "But..." "It's a tattoo." "That's just... not important anymore." "I... think you should just focus on getting better." "Okay?" "Am I going to die?" "No!" "I was trying to..." "I just..." "No, you're not gonna die." "We got it all under control." "Just hang on one second." "Okay?" " Hope you have some good news." " {\Yeah, well, }You were right." "All the glass melted the same way from the inside out." "And all the locations affected were using crystalline glass." "Guess that's why every window in Eureka didn't go all Salvador Dali." "Exactly, so I'm gonna run this data with Nathan." " Maybe {\this is }the break we were looking for." " Great." "Hey..." " Thanks." " Keep the faith." "Believe me, I'm trying." "Well, Henry just figured something out that might help us, so..." "You just hang in there." "Okay?" "Hey, Larry." "What, studying to be pope?" "No." "But with what's happening around town," "I thought I should cover my bases..." "Religion-wise." "What's religion have to do with anything?" "Well, call it what you like." "But girls losing their voices..." "That's like the Tower of Babel." "God smote those workers so they couldn't communicate." "And Dr. Blake..." "Glowing, like saints rising to heaven." "That's what the Bible calls trans..." "Transfiguration." "What if GD was built over a Hell mouth?" " A Hell mouth?" " Say what you want, but when water turns to blood, I say it's time to pray." "You might wanna run that{\ one} by the reverend." "{\I'm s}Sure she'll get a laugh out of it." "Considering she's the one I borrowed these books from," "I think I'll stick to my game plan." " Harper gave you these?" " She's giving them to everyone." "Things are happening all over town..." "In case you haven't noticed," "God's come to Eureka." " Thanks." " For what?" "You may have pointed me down the path of righteousness." " Hallelujah, my brother!" " Shut up, Larry." "Excuse me." "Do you know where I can find the reverend?" "She just stepped out, but she'll be back for evening service." "And..." "All these people?" "They just come here to pray on their own." " Sure." " People seek comfort in time of crisis." "And reverend Harper's door is always open." " How long've you known her?" " I have been the church's musical director since day one." "So..." "A while." "Don't take this the wrong way, but I hear the... sunday sermons aren't quite..." "selling out." " Please." " Sure, sure." "Eureka's built on science." "So it's hard for people here to just open up to something as uncertain as faith." "Reverend Harper was a theoretical physicist, so she has a way of bridging that divide." "And, as a churchgoing scientist, I appreciate that." "Do you believe in miracles?" " I have to." " And, what if they're just being used to get people in the pews?" "Reverend's only concern is helping others." " Sure about that?" " She helped me." "When my husband Daniel passed away, I wanted to..." "Join him." "And the reverend showed me that where there is faith, there's hope." "She saved my life." "Okay." "It must be pretty bad." "I am running through every variation of the neurotoxin antiserum." "I will find the solution." "Except I probably won't be around for it." " Let's discuss worst-case scenarios." " Not yet." "I have to." "For Kevin's sake." "Nathan, if something happens to me," "I need you to take care of him." "You know I would." "And I want you to tell the DOD what's happening." "No." "No, not yet." "One more hour, I'll know if this last trial worked." "What if I don't make it through this?" "You will." "You have to." "I love you." "I won't let you die." "I won't allow it." "We're getting reports all over town." "I promise he'll get to you as soon as he can." "You should really wear your hair down more often." "Really not a good time." "No, I got that impression when you took off." "Look..." "Forget it." "It's nothing." "I think it is." "{\So either }Tell me why you're pissed{\ at me}, or I'll hold my breath until you do." " What are you, three?" " Hey, I black out, it's on you." "Okay..." "You didn't do anything." "It's me." "It's this whole town." "Is this about the whole miracles thing?" "'Cause, seriously, there's no such thing." "Right, because only dumb people believe in something beyond tachyons and particle accelerators." "Maybe you should think this through before you start making accusations." "Accusations against who?" "I tried to call you, but my radio's out." "I think{\ that} reverend Harper might be responsible for what's happening." " You're both going to hell." " No!" "Look, look." "We got an empty church and a series of alleged miracles." "So I don't think it's crazy to ask who stands to benefit." "God." " Carter, you're way off base this time." " I hope so." "But before reverend Harper took up theology, she used to be a physicist." " You still think I'm going to hell?" " Probably." " I think you're jumping to conclusions." " Okay, bottom line:" "if she's responsible, we're in for a lot more." "Yeah, like, a plague of locusts, or fiery hail, or total darkness." "You had to say it." "{\pos(192,250)}Welcome to the end of the world, Sheriff." "Not if I can help it." "Thanks..." "Hi, Reverend." "Sheriff..." "Welcome." " We need to talk to you for a sec." " Actually, he wants to talk to you." " Thanks for the support." " You're welcome." " What is it?" " Well..." "Obviously, a lot of strange things have been happening." "One might say..." "Religious things." " Some might..." "Not me." " Or me." "I'm trying to work here, guys." "What's your point, Sheriff?" "I was wondering... and forgive this..." "Who would stand to gain the most by... the sudden appearance of apocalyptic-type signs?" "All of us, I would think." "Or maybe someone who's been preaching to an empty church every sunday." "You do have a point." " Really?" " Sure." "But whatever's happening, divine or not," "I had nothing to do with it." "And as much as I would love to believe that, you had the motive and the knowledge to pull it off." "We know about your background in physics." "Theoretical physics, yes." "But there's a reason why I left research for the clergy, Sheriff." "I... wasn't much of a scientist." "But I am a very good preacher." "Well, we're still gonna have to ask you in for questioning." "Just relax." "What's that?" "How do you have music during a blackout?" "It's a crystal radio system, powered by piezoelectricity." "Crystal..." "Radios..." "Henry, could radios be responsible for what's been happening?" "Radio waves, at the exact right frequency..." "Yes." " They might{\ have} caused the interference." " Can we test for that?" "Reverend, we're gonna have to borrow that receiver." "If this is happening all over town, how come we haven't heard it sooner?" "Well, let's see." "Sound waves can carry infrasonic frequencies that occur outside the range of human hearing." "And this crystalline glass is the same as we found in all three places." "And..." "Seth's aquarium is made of the same stuff?" "Yes..." "Microorganisms in the water were sonically agitated," " creating a red tide effect." " Okay, what about Zoe?" "Human tissues have the capacity to transduce pressure from sound waves." "Infrasonic frequencies may be putting pressure on her vocal cords." "So Allison is" "Sonoluminescence." "Sound waves reacting with water... causing objects to glow." "So who could pull this off?" "Anyone with a background in acoustics and infrasonic research." " I'm gonna make a list." " Diane Lancaster is the head of acoustic engineering here at GD." "I just spoke to her." "She's... the music director at the church." "Here's the latest test results on Allison Blake, Doctor." "I'm sorry, Dr. Stark." "All right, what do I do?" "You've done all you can." "No." "Alright, is that fireflies?" "Bioluminescent fireflies." "This must be the place." "Her husband died a few months ago." "She's... been working at home ever since." "Working on what?" " And that would be?" " A temporal rift." "Or a portal to heaven." "No!" "Don't you come any closer!" " She wants to cross over." " Into what?" "Eternity." "What you're thinking about seems pretty permanent." "You wanna talk about it{\ for a second}?" "There's nothing to talk about." "You don't understand." "I have found where everything meets." "The place where different points in dimensional space-time converge." "Where Daniel is waiting for me." "Okay, let's..." "Stick a pin in that." " Okay, that can't be heaven?" " Why not?" "I mean, if she's really discovered a... a gateway to the multiverse." " Not helping." " I have faith that it is." "Revelations, chapter four, verse one:" ""After this, I looked, and behold a door was opened in Heaven."" "You understand, don't you, Henry?" "Mom?" "Mom's sick, Kev." "And I can't help her." "But you're special, Kevin." "Maybe you can." "Do you realize what you're about to do?" "I'm going to see my husband again." "He's gone, Diane." "And we need you here." "There's a lot of people suffering out there because of your machine." "And your knowledge might be able to save them." "You gonna..." "Walk away from that?" " You just gonna let 'em die?" " No!" "Is that what Daniel would want?" "I didn't mean to cause all these problems." "I just..." "Wanna be with him again." "And you will." "You just have to have a little faith." "Jack, what if..." "What if this really is what she thinks it is?" "I mean, Kim could be..." "You gotta turn it off." "I'm turning it off." "Dad?" "Oh, thank God." "Are you really gonna make me beg?" " You're here." " Yeah, well..." "I had to see if you were lying about all the babes who go to church." "And you definitely were not." "So..." "How are you?" "I'm miserable." "But I'm here." "Have faith." "We'll see them again." "I promise." "I know we will, Henry." "It means a lot to me that you came, Nathan." "Anything for you." "You saved my life." "It wasn't me." "And it wasn't shutting down Diane's machine, either." "What do you mean?" "He controls the field now, Allie." "He's evolving." "Reverend..." "For the record," "I'm really glad that I was wrong." "So we'll see you next sunday, then?" "It's a tough one." "The Dodgers are playing the Mets." "So..." "Have a slice of pepperoni for me." "That I can do." "Thanks." "See ya." "Hang on for a second." "'Scuse me." " Sheriff." " Hey, Henry." "I borrowed this book from you." "I just wanted to return it." "I don't remember that, but, I hope you enjoyed it." "Yeah." "I mean, it really opened my eyes." "As all good books should do." " Yeah, Henry..." " Yeah?" "You're my best friend, you know." "Yeah." "Yeah, I know." "Is it a sin that my favorite part was the music?" "Well..." "You stayed awake, right?" "You hear the guy snoring behind us?" " Like a chainsaw." " Yeah." "So, Dad..." "You know my rose tattoo?" "It's fake." " It's fake?" " Yes." "But since you seemed okay with it," "I can get a real one now, right?" " Yeah." " Really?" " Absolutely." " Really?" "When Hell freezes over, yeah."

1. Carbohydrate Esterases and the CE4 Family {#sec1-ijms-19-00412} ============================================ Carbohydrate esterases (CEs) are enzymes that catalyze the de-*O*- or de-*N*-acetylation of glycans and substituted saccharides. To date (December 2017), there are 15 different CE families classified in the CAZY data base (Carbohydrate Active Enzymes, [www.cazy.org](www.cazy.org)) \[[@B1-ijms-19-00412]\]. The substrates used by CE enzymes are very diverse, and the enzyme classes are named according to substrate preference: chitin deacetylases, peptidoglycan deacetylases, acetylxylan esterases, polysaccharide deacetylases, acetyl esterases, feruloyl esterases, pectin acetyl esterases, pectin methylesterases, glucuronoyl esterases, and enzymes catalyzing the de-*N*-acetylation of low molecular mass aminosugar derivatives \[[@B2-ijms-19-00412],[@B3-ijms-19-00412],[@B4-ijms-19-00412],[@B5-ijms-19-00412]\]. The CE4 family is composed mainly of chitin deacetylases (CDAs) (EC 3.5.1.41) and chitooligosaccharide deacetylases (EC 3.5.1.-), peptidoglycan *N*-acetylglucosamine deacetylases (EC 3.5.1.104), peptidoglycan *N*-acetylmuramic acid deacetylases (EC 3.5.1.-), and poly-β-1,6-*N*-acetylglucosamine deacetylase (EC 3.5.1.-), though it also contains some acetylxylan esterases (EC 3.1.1.72) \[[@B6-ijms-19-00412]\]. These enzymes share a conserved region known as the NodB homologous domain, due to its similarity to the NodB oligosaccharide deacetylase, one of the first deacetylases of this family to be characterized \[[@B7-ijms-19-00412]\]. Deacetylases have been found in bacteria, fungi, and insects \[[@B3-ijms-19-00412],[@B8-ijms-19-00412]\]. The first active CDA was identified and partially purified from extracts of the fungus *Mucor rouxii* \[[@B9-ijms-19-00412]\]. Later, some active CDAs were identified and purified from very diverse organisms, such as archaea, marine bacteria, fungi, and insects, which in many cases, are not even capable of producing chitosans \[[@B10-ijms-19-00412]\]. These enzymes, like their sources, are very diverse in their characteristics and optimal working conditions. Their molecular masses vary from 12.7 to 150 kDa, their isoelectric points (pIs) vary from 2.7 to 4.8, the optimum pH ranges from 4.5 to 12, and they show significant thermal stability, as their optimum temperatures for activity range from 30 to 60 °C. Most CDAs are highly inactive on crystalline chitin and have a preference for soluble chitins, such as glycol-chitin or chitin oligomers, as well as partially deacetylated chitin (chitosans). The inactivity on insoluble chitin is most likely due to the inaccessibility of the acetyl groups in the tightly packed chitin structure. Some CDAs contain carbohydrate binding modules (CBM) fused to the catalytic domain that seem to increase the accessibility of the chitin chains to the catalytic domain, resulting in a (slightly) enhanced deacetylase activity \[[@B11-ijms-19-00412]\]. Recently, it has been shown that the addition of a lytic polysaccharide monooxygenase (LPMO), which oxidatively cleaves the chitin chains on the surface of the fibrils, greatly increased the activity of a CDA on β-chitin \[[@B12-ijms-19-00412]\]. In terms of their cellular localization, CDAs are found extracellularly, in the periplasm or in the cytosol. In fungi, periplasmic CDAs are generally tightly coupled to a chitin synthase to rapidly deacetylate newly synthesized chitins before their maturation and crystallization. Extracellular CDAs are secreted to alter the physicochemical properties of the cell wall to either protect the cell wall from exogenous chitinases or to initiate autolysis. In bacteria, CDAs are either intracellular, as in *Rhizobium* species where they are involved in Nod factor biosynthesis, or extracellular, involved in the catabolism of chitin, as in marine bacteria \[[@B8-ijms-19-00412],[@B10-ijms-19-00412],[@B13-ijms-19-00412]\]. 2. Substrates of CE4 Family Enzymes {#sec2-ijms-19-00412} =================================== 2.1. Chitin, Chitosan, and Their Oligomers {#sec2dot1-ijms-19-00412} ------------------------------------------ Chitin was first isolated from fungi by Braconnot in 1811 \[[@B14-ijms-19-00412]\], and its structure was determined in 1929 by Hofmann \[[@B15-ijms-19-00412]\]. Chitin is a linear polysaccharide of β(1→4)-linked *N*-acetylglucosamine monomers ([Figure 1](#ijms-19-00412-f001){ref-type="fig"}A). It is the most abundant natural amino polysaccharide, and it is also regarded as one of the most abundant molecules in nature after cellulose. Chitin is widely distributed, as a major structural component of the exoskeletons of arthropods (including insects and crustaceans), in the endoskeletons of mollusks (such as squid), and in the cell walls of fungi and diatoms \[[@B14-ijms-19-00412],[@B16-ijms-19-00412],[@B17-ijms-19-00412]\]. Chitin is present as ordered macrofibrils, mainly in two allomorphs, α-chitin (the most abundant, usually isolated from the exoskeleton of crustaceans, particularly from shrimps and crabs) and β-chitin (extracted from squid pens), and additionally as γ-chitin, which appears to be a combination of the α and β structures (found in fungi and yeast) \[[@B18-ijms-19-00412]\]. The processing of the chitin polymer in the form of depolymerization and de-*N*-acetylation reactions produces a series of new compounds, including chitosan and chitooligosaccharides. Chitosan is the result of de-*N*-acetylation of chitin. In nature, this reaction is almost never complete, meaning that chitosan is a generic name for heteropolymers composed of *N*-acetylglucosamine (GlcNAc) and glucosamine (GlcNH~2~). Only some fungi of the *Zygomycota*, *Basidiomycota*, and *Ascomycota* phyla have been reported to be capable of naturally producing chitosans \[[@B19-ijms-19-00412]\]. The deacetylated units have free amino groups that, at slightly acidic conditions, convey positive charges to the polymers, making them the only known natural polycationic polysaccharides \[[@B14-ijms-19-00412],[@B16-ijms-19-00412],[@B19-ijms-19-00412]\]. They interact with polyanionic biomolecules, such as proteins, nucleic acids, polyanionic phospholipidic membranes, and sulfated polysaccharides, like the human glycosaminoglycans at cell surfaces. Depolymerization of both chitin and chitosan yields their respective oligosaccharides \[[@B20-ijms-19-00412]\]. Chitin and chitosans mainly act as structural polymers, while their oligomers are involved in molecular recognition events, such as cell signaling and morphogenesis, and act as immune response elicitors and host--pathogen mediators \[[@B21-ijms-19-00412],[@B22-ijms-19-00412],[@B23-ijms-19-00412],[@B24-ijms-19-00412],[@B25-ijms-19-00412]\]. Hence, CDAs are candidates for the design of antifungals and antibacterials \[[@B8-ijms-19-00412],[@B10-ijms-19-00412]\], and chitin derivatives have uses in medical, pharmaceutical, and cosmetic applications \[[@B26-ijms-19-00412],[@B27-ijms-19-00412]\]. Chitosan polysaccharides and oligosaccharides are characterized by their degree of polymerization (DP), degree of acetylation (DA), and pattern of acetylation (PA). 2.2. Peptidoglycan {#sec2dot2-ijms-19-00412} ------------------ Peptidoglycan (PG) is a net-like molecule found in the cell wall surrounding the cytoplasmic membrane of almost all bacteria. It is a fundamental and specific structural element that helps preserve cell shape and protect cells against the internal osmotic pressure. As a result, any inhibition of its biosynthesis or its degradation during cell growth leads to cell lysis. However, it also serves as a scaffold for the attachment of specific proteins and other cell wall components \[[@B28-ijms-19-00412],[@B29-ijms-19-00412],[@B30-ijms-19-00412],[@B31-ijms-19-00412]\]. Its chemical composition comprises long glycan chains crosslinked by short peptides, creating a large macromolecule. The glycan structure is a heteropolymer consisting of long chains of *N*-acetylglucosamine (GlcNAc) and *N*-acetylmuramic acid (MurNAc) residues linked β-1→4 in an alternating fashion ([Figure 1](#ijms-19-00412-f001){ref-type="fig"}B). The crosslinking peptide show some interesting characteristics, such as the presence of non-proteogenic aminoacids (e.g., diaminopimelic acid, lanthionine), alternating [d]{.smallcaps}- and [l]{.smallcaps}-isomers, and a γ-bonded [d]{.smallcaps}-glutamic acid. Peptidoglycan hydrolases have critical functions in peptidoglucan maturation, turnover, elongation, septation, and recycling, as well as in cell autolysis \[[@B32-ijms-19-00412]\]. Post-synthetic modification of PG represents an important strategy for pathogenic bacteria to evade innate immunity and control autolysins. Modifications of the glycan backbone are generally restricted to the C-6 hydroxyl and C-2 amino moieties, with the most common being acetylation and deacetylation \[[@B33-ijms-19-00412]\]. In particular, peptidoglycan *N*-deacetylases hydrolyze the amide linkage of the 2-*N*-acetyl groups of GlcNAc or MurNAc residues, some being active on complex peptidoglycan structures, but others having a preference for the saccharide chain after peptide release \[[@B33-ijms-19-00412],[@B34-ijms-19-00412],[@B35-ijms-19-00412],[@B36-ijms-19-00412]\]. 2.3. Acetylxylan {#sec2dot3-ijms-19-00412} ---------------- Acetylxylan is a plant polysaccharide that is a major component of the hemicellulose fraction of plant cell walls \[[@B37-ijms-19-00412]\]. Like cellulose, most hemicelluloses function as supporting material in the cell wall \[[@B38-ijms-19-00412]\]. Cellulose is entrapped in a hemicellulose matrix that includes several heteropolysaccharides formed by hexoses and pentoses. In hardwood trees, and some other annual plants, the main hemicellulose element is acetyl-[d]{.smallcaps}-glucurono-[d]{.smallcaps}-xylan ([Figure 1](#ijms-19-00412-f001){ref-type="fig"}C). Its backbone is formed by β-1,4-linked [d]{.smallcaps}-xylopyranosyl residues. Some of the xylose residues are α-1,2-substituted with 4-*O*-methyl-α-[d]{.smallcaps}-glucuronic acid, and almost every xylose residue is acetylated at positions 2 or 3, or both \[[@B38-ijms-19-00412],[@B39-ijms-19-00412],[@B40-ijms-19-00412]\]. Acetyl xylan esterases de-*O*-acetylate the substituted xylosyl units with different specificities \[[@B4-ijms-19-00412],[@B40-ijms-19-00412],[@B41-ijms-19-00412]\]. 2.4. β-1,6-Glucan {#sec2dot4-ijms-19-00412} ----------------- Poly-β-1,6-*N*-acetyl-[d]{.smallcaps}-glucosamine (PNAG) ([Figure 1](#ijms-19-00412-f001){ref-type="fig"}D), also referred to as polysaccharide intercellular adhesin, is an exopolysaccharide that makes up the extracellular matrix of some bacterial biofilms \[[@B42-ijms-19-00412]\]. Biofilm formation increases the survival of a colony during microbial infections by limiting the diffusion of antimicrobials and preventing phagocytosis \[[@B43-ijms-19-00412]\]. Partial enzymatic deacetylation of PNAG is important for the maintenance of biofilms, since fully acetylated PNAG impedes biofilm formation \[[@B44-ijms-19-00412]\]. Therefore, understanding the structure--activity relationships of PNAG deacetylases is relevant for the design of biofilm formation inhibitors \[[@B45-ijms-19-00412],[@B46-ijms-19-00412]\]. 3. CE4 Enzymes Active on Chitooligosaccharides and Their Substrate Specificities {#sec3-ijms-19-00412} ================================================================================ Here, we focus on CE4 enzymes with characterized activity on chitooligosaccharides (COS) and/or a solved 3D structure by X-ray crystallography. These include CDAs (EC 3.5.1.41), as well as some peptidoglycan deacetylases and acetylxylan esterases for which activity on COS has been reported. Additionally, some poly-β-1,6-GlcNAc deacetylases, although with no reported activity on COS, are included because their substrate specificities and 3D structures are closely related to those of CDAs. The deacetylation pattern exhibited by chitin deacetylases and related CE4 enzymes active on COS is diverse, reflecting different substrate specificities and pattern recognition on their linear substrates. Enzymatic action patterns for enzymes that modify in-chain units on a linear polysaccharide may be divided into three main types, designated multiple-attack, multiple-chain, and single-chain mechanisms ([Figure 2](#ijms-19-00412-f002){ref-type="fig"}) \[[@B3-ijms-19-00412]\]. In the multiple-attack mechanism, binding of the enzyme to the polysaccharide chain is followed by a number of sequential deacetylations, after which the enzyme binds to another chain. (i.e., *M. rouxii* \[[@B47-ijms-19-00412],[@B48-ijms-19-00412]\]). In the multiple-chain mechanism, the enzyme forms an active enzyme--polymer complex, and catalyzes the hydrolysis of only one acetyl group before it dissociates and forms a new active complex (i.e., *C. lindemuthianum* CDA \[[@B49-ijms-19-00412],[@B50-ijms-19-00412]\]). Finally, a single-chain mechanism refers to processive enzymes in which a number of catalytic events occur on a single substrate molecule, leading to sequential deacetylation. This last group also includes the few CDAs with specificity for deacetylating a single position in chitooligosaccharide substrates (i.e., *Rhizobium* NodB or *Vibrio* CDA or COD, see below). While the multiple-chain mechanism with no preferred attack will result in a binary hetero-polysaccharide with a random distribution of the units, the multiple-attack and the single-chain mechanisms will generate block-copolymer structures. A major challenge is understanding how these enzymes define the distribution of GlcNAc and GlcNH~2~ moieties in the oligomeric chain. Analysis of their substrate specificity in conjunction with their 3D structures and multiple sequence alignments provides the background of a structural model on the determinants of substrate specificity that dictates the deacetylation patterns. [Table 1](#ijms-19-00412-t001){ref-type="table"} summarizes the CE4 enzymes considered in this study. It includes chitin deacetylases that have been biochemically characterized with regard to their specificity on COS, and other CE4 family members with solved 3D structures (released on the PDB up to December 2017), such as peptidoglycan GlcNAc and MurNAc deacetylases, and acetylxylan esterases (some of them also active on COS), poly-β-1,6-GlcNAc de-*N*-acetylases (not active on COS), and putative polysaccharide deacetylases with reported 3D structures that either have unknown substrates or are inactive enzymes. The relevant information that has been reported on the substrate specificity of each enzyme listed in [Table 1](#ijms-19-00412-t001){ref-type="table"} is summarized below. 3.1. Chitin Deacetylases (CDAs) {#sec3dot1-ijms-19-00412} ------------------------------- ### 3.1.1. Fungal Chitin Deacetylases {#sec3dot1dot1-ijms-19-00412} Fungal CDAs are involved in fungal nutrition, morphogenesis, and development \[[@B3-ijms-19-00412],[@B8-ijms-19-00412]\], participating in cell wall formation and integrity \[[@B51-ijms-19-00412]\], in spore formation \[[@B52-ijms-19-00412]\], germling adhesion \[[@B53-ijms-19-00412]\], and fungal autolysis \[[@B54-ijms-19-00412]\]. Pathogenic fungi must evade host immune responses to successfully penetrate and gain access to host tissues. Plants protect themselves by secreting chitinases that break the fungal cell wall chitin down to chitooligosaccharides (COS), which are recognized by plant chitin-specific receptors triggering resistance responses \[[@B55-ijms-19-00412]\]. Plant fungal pathogens secrete CDAs during infection and the early growth phase in the host \[[@B8-ijms-19-00412]\]. It has been hypothesized that fungi evade plant defense mechanisms by partially deacetylating either their exposed cell wall chitin or the chitooligosaccharides produced by the plant chitinases, hence, the resulting partially deacetylated oligomers are not further recognized by the specific receptors \[[@B55-ijms-19-00412],[@B56-ijms-19-00412],[@B57-ijms-19-00412],[@B58-ijms-19-00412]\]. *Mucor rouxii CDA* (*Mr*CDA). The *Mucor rouxii* CDA was one of the first enzymes to be identified as a deacetylase. *M. rouxii* is a dimorphic fungus with a cell wall mainly composed of chitin, chitosan, and mucoric acid. *Mr*CDA is a specific enzyme for β-1,4-GlcNAc polymers, such as glycol-chitin, colloidal chitin, chitosan, and chitin; it also deacetylates acetylxylan, but it is inactive on peptidoglycan or acetyl heparin polymers \[[@B6-ijms-19-00412],[@B9-ijms-19-00412]\]. It is active on chitooligosaccharides, and its activity increases with the degree of polymerization (DP) \[[@B9-ijms-19-00412],[@B59-ijms-19-00412],[@B60-ijms-19-00412]\], with triacetylchitotriose being the smallest substrate it acts on \[[@B48-ijms-19-00412]\]. It has been reported that the enzyme deacetylates its substrates following a multiple-attack mechanism \[[@B47-ijms-19-00412]\], but the resulting pattern depends on the DP of the substrate: DP3, DP6, and DP7 substrates are not fully deacetylated, leaving the reducing GlcNAc unmodified \[D~n−1~A\], whereas DP4 and DP5 substrates are fully deacetylated. In all cases, deacetylation starts at the non-reducing end residue, and then proceeds to the neighboring monomer towards the reducing end \[[@B48-ijms-19-00412]\]. *Colletotrichum lindemuthianum CDA* (*Cl*CDA). The plant pathogen deuteromycete fungus *C. lindemuthianum* is the causative agent of the anthracnose, which affects economically important crop species \[[@B78-ijms-19-00412]\]. It secretes a CDA that is active on both chitin polymers (glycol-chitin) and chitin oligomers. It is able to fully deacetylate chitooligosaccharides with a DP equal to or greater than 3, while it only deacetylates the non-reducing GlcNAc of *N*,*N*′-diacetylchitobiose \[[@B49-ijms-19-00412],[@B79-ijms-19-00412]\]. For substrates longer than DP3, it performs a multiple-chain mechanism, following a pathway in which the first residue to be deacetylated is the second from the reducing end \[[@B49-ijms-19-00412],[@B50-ijms-19-00412]\]. The initial mono-deacetylation reaction shows no dependency of *k*~cat~ on DP, but *K*~M~ decreases with increasing DP \[[@B50-ijms-19-00412],[@B61-ijms-19-00412]\]. However, when analyzing the full deacetylation kinetics, an increase in *k*~cat~ and reduction in *K~M~* correlates with an increase in substrate DP \[[@B80-ijms-19-00412]\]. It has been reported that this enzyme is reversible, as it is also able to catalyze the acetylation of chitosan oligomers \[[@B81-ijms-19-00412],[@B82-ijms-19-00412],[@B83-ijms-19-00412]\]. *Aspergillus nidulans CDA* (*An*CDA). *An*CDA is secreted into the extracellular medium to deacetylate the chitin oligomers produced by chitinases during cell autolysis \[[@B54-ijms-19-00412],[@B84-ijms-19-00412],[@B85-ijms-19-00412],[@B86-ijms-19-00412]\]. The enzyme is active on soluble chitins (CM-chitin, glycol-chitin), colloidal chitin, chitosan, acetylxylan, and acetylated glucuronoxylan, but not on peptidoglycan \[[@B12-ijms-19-00412],[@B87-ijms-19-00412]\]. *An*CDA is active towards chitooligosaccharides with a DP of 2 to 6 \[[@B12-ijms-19-00412]\]. Long incubations with high enzyme concentration showed that the enzyme is inactive towards GlcNAc, and catalyzes the mono-deacetylation of (GlcNAc)~2~. For longer substrates, fully deacetylated products were produced. The deacetylation rate exhibits a counter-intuitive relationship with the length of the chitooligosaccharide substrates: odd-numbered chitooligosaccharides (DP5, DP3) have higher apparent rate constants than even-numbered oligomers (DP4, DP2). Monitoring of products formation with the DP6 substrate showed that the first deacetylation event occurs at random positions, except for the reducing end, which reacts much more slowly to yield the fully deacetylated product. With the DP5 substrate at short reaction times, the kinetic constants are *k~cat~* = 1.4 s^−1^ and *K~M~* = 72 μM, similar to those reported for *Cl*CDA. *Puccinia graminis f.* sp. *Tritici CDA* (*Pgt*CDA). *Puccinia graminis f.* sp. *Tritici* is a biotrophic basidiomycete that is the causative agent of the stem rust \[[@B88-ijms-19-00412]\]. *Pgt*CDA is active on polymers such as colloidal chitin and glycol-chitin, as well as on chitosans, where activity increases with the degree of acetylation. It is not active on insoluble polymers such as α- or β-chitin. With chitooligosaccharides, it was found that the minimal substrate is tetraacetylchitotetraose, as the enzyme is not able to act on shorter substrates. The sequence of the products obtained by enzymatic deacetylation of tetramers to hexamers reveals that the enzyme specifically deacetylates all but the last two GlcNAc units on the non-reducing end \[AA(D)~n−2~\] via a multiple-chain mechanism \[[@B89-ijms-19-00412]\]. *Pestalotiopsis* sp. *CDA* (*Pes*CDA). *Pestalotiopsis* sp. is an endophytic fungus found in tropical areas that lives inside the tissues of its plant hosts \[[@B90-ijms-19-00412]\]. PesCDA acts better on colloidal chitin as substrate, but it is also active on chitosans with a DA of 10--60% (higher activity with a higher DA), as well as on chitooligosaccharides \[[@B58-ijms-19-00412]\]. It is not able to deacetylate crystalline chitin, neither α- or β-allomorphs. When analyzing the activity on oligomers, tetraacetylchitotetraose is the minimal substrate, but no substrate preferences or kinetic parameters have been reported for longer oligomers \[[@B48-ijms-19-00412]\]. The enzyme follows a multiple-chain mechanism in which all residues are deacetylated, except the reducing end, and the last two GlcNAc residues from the non-reducing end, with a pattern of deacetylation \[AA(D)~n−3~A\] \[[@B58-ijms-19-00412]\]. *Podospora anserina CDA* (*Pa*CDA). *Podospora anserina* is a filamentous ascomycete living as a saprophyte on herbivore dung \[[@B91-ijms-19-00412]\]. *Pa*CDA has been recombinantly expressed in *Hansenula polymorpha* as a full length protein composed of the CE4 domain flanked by two CBM18 domains \[[@B11-ijms-19-00412]\]. The enzyme is active on soluble glycol-chitin, chitosan polymers with a high DA, and chitooligosaccharides, and shows low activity on insoluble α- and β-chitin, which is reduced further by deletion of the CBM domains. On chitooligosaccharides, it is active against oligomers with a DP ≥ 2, leading to fully deacetylated products \[D~n~\]. The mode of action on DP3 and DP4 substrates revealed that it follows a multiple-chain mechanism. With the trimer, all possible isomers are found for both mono- and di-deacetylated intermediate products, although the first deacetylation event has a clear preference for the reducing end. This is not the case for the tetramer and pentamer substrates, where the residue next to the reducing end is preferentially deacetylated first, with the second deacetylation occurring mainly next to the existing GlcNH~2~ unit on either side. Overall, larger oligomers are deacetylated faster, with deacetylation of the reducing end occurring as a late event \[[@B11-ijms-19-00412]\]. *Pochonia chlamydiosporia CDA (Pc*CDA). *Pochonia chlamydosporia* is a fungus belonging to the *Ascomycota* family that infects females and eggs of cyst or root-knot nematodes. It is used as a biocontrol agent against a number of plant parasitic nematodes in food-security crops \[[@B92-ijms-19-00412],[@B93-ijms-19-00412],[@B94-ijms-19-00412]\]. *Pc*CDA deacetylates chitooligosaccharides, requiring at least four GlcNAc units in order to be active, but it prefers longer substrates. For DP4 and DP5 substrates, it first deacetylates the penultimate residue from the non-reducing end, and continues to the next residue towards the reducing end, with a pattern of acetylation \[ADDA~n−3~\] \[[@B95-ijms-19-00412]\]. ### 3.1.2. Bacterial Chitin Deacetylases {#sec3dot1dot2-ijms-19-00412} *Sinorhizobium meliloti NodB* (NodB). Rhizobial NodB deacetylases were the first enzymes of the CE4 family to be described in detail \[[@B7-ijms-19-00412],[@B96-ijms-19-00412],[@B97-ijms-19-00412]\]. NodB deacetylases are involved in the biosynthesis of Nod factors, the morphogenic signal molecules produced by rhizobia, which initiate the development of root nodules in leguminous plants \[[@B98-ijms-19-00412]\]. NodB is active on chitooligosaccharides from DP2 to DP5 with no differences in *k~cat~*, but *K~M~* decreases with increasing DP. Specifically, *k~cat~*/*K~M~* is 5-fold higher for DP5 than for DP2 substrates \[[@B7-ijms-19-00412],[@B99-ijms-19-00412]\]. DP4 or DP5 substrates are the natural substrates depending on the rhizobial strain. NodB only deacetylates the non-reducing end residue \[DA~n−1~\] \[[@B7-ijms-19-00412],[@B100-ijms-19-00412],[@B101-ijms-19-00412]\], but traces of a second deacetylation event were seen upon long incubations \[[@B100-ijms-19-00412]\]. *Vibrio cholera CDA* (*Vc*CDA or COD). Chitin oligosaccharide deacetylases (COD) from the *Vibrionaceae* family are involved in the chitin degradation cascades occurring in sea water \[[@B102-ijms-19-00412],[@B103-ijms-19-00412],[@B104-ijms-19-00412],[@B105-ijms-19-00412]\]. They have been identified in many *Vibrio* species, such as *V. algynolyticus* \[[@B106-ijms-19-00412],[@B107-ijms-19-00412]\], *V. parahaemolyticus* \[[@B108-ijms-19-00412],[@B109-ijms-19-00412]\], *V. cholera* \[[@B110-ijms-19-00412]\], and others. Whereas *V. parahaemolyticus* or the *Vibrio* sp. SN184 only deacetylate DP2 and DP3 substrates, the *Vibrio cholera* chitin deacetylase (*Vc*CDA) has a broader specificity, being active on DP2 to DP6 substrates \[[@B62-ijms-19-00412],[@B110-ijms-19-00412]\]. *Vc*CDA is 10-fold more active on DP2 than DP4 substrates \[[@B62-ijms-19-00412]\], and it is highly specific for deacetylation of the penultimate residue from the non-reducing end, generating monodeacetylated products with the pattern \[ADA~n−2~\] \[[@B62-ijms-19-00412],[@B100-ijms-19-00412],[@B110-ijms-19-00412]\]. *Arthrobacter* sp. *CDA* (*Ar*CE4). Arthrobacter species are Gram-positive bacteria known to grow on chitin and secrete chitinases \[[@B111-ijms-19-00412],[@B112-ijms-19-00412],[@B113-ijms-19-00412]\]. ArCE4 was identified from a search of monodomain and extracellular deacetylases in annotated genomes and metagenomes \[[@B64-ijms-19-00412]\]. *Ar*CE4 is active on α- and β-chitin, chitosan (DA 64%), and acetylxylan. On COS substrates, activity increases with increasing DP, with higher activity against DP5 compared to DP6, and no activity on GlcNAc. The enzyme acts by a multiple-chain mechanism, as shown with the DP5 substrate, where different mono- and di-deacetylated products were obtained. The first deacelylation happens at all three internal positions, whereas di-deacetylation mainly occurs at the GlcNAc unit next to the reducing end, and at either of the two other internal units (ADDAA and ADADA). Although other minor products are formed, it seems that the reducing end unit is not deacetylated \[[@B64-ijms-19-00412]\]. 3.2. Peptidoglycan Deacetylases {#sec3dot2-ijms-19-00412} ------------------------------- ### 3.2.1. GlcNAc Peptidoglycan Deacetylases {#sec3dot2dot1-ijms-19-00412} *Streptococcus pneumoniae Sp*PgdA. *S. pneumoniae* is a Gram-positive bacteria, and one of the most important human pathogens, responsible for pneumonia, otitis media, and meningitis \[[@B114-ijms-19-00412]\]. Deacetylation of the peptidoglycan is used as a defense mechanism, reducing the likelihood of being hydrolyzed by lysozyme \[[@B26-ijms-19-00412]\]. On peptidoglycan, *Sp*PgdA deacetylates up 84% of the GlcNAc residues, but also deacetylates MurNAc residues to a lesser extent (10% of the total) \[[@B35-ijms-19-00412]\]. It can also deacetylate chitin oligomers, having been tested so far on triacetylchitotriose and pentaacetylchitopentaose, and being inactive on GlcNAc \[[@B65-ijms-19-00412],[@B115-ijms-19-00412]\]. Only the central residue of the DP3 substrate is deacetylated \[ADA\] \[[@B65-ijms-19-00412]\]. With the DP5 substrate, mono-, di-, and tri-deacetylated chitosan oligomers are obtained, but the deacetylation pattern has not been reported \[[@B115-ijms-19-00412]\]. Interestingly, it is not capable of using soluble low molecular weight oligomers of its own peptidoglycan or peptidoglycan from other species. *Streptococcus mutans Sm*PgdA. *SmPgdA* is involved in protecting this pathogenic bacteria from the innate immune system \[[@B66-ijms-19-00412]\]. *SmP*gdA seems to have no activity on peptidoglycan, and its natural substrate is yet unidentified \[[@B66-ijms-19-00412]\]. However, it exhibits de-*N*-acetylase activity towards hexaacetylchitohexaose. No activity was observed with shorter chitooligosaccharides or a synthetic peptidoglycan tetrasaccharide. *Bacillus cereus Pgd BC1960* (*Bc*Pgd). *Bacillus cereus* is a Gram-positive bacteria found in soil and food that can cause diarrhea in humans \[[@B116-ijms-19-00412]\]. The genome of *B. cereus* contains eleven ORFs for putative polysaccharide deacetylases, five of which have been identified as peptidoglycan GlcNAc deacetylases. BC1960 (*Bc*Pgd) is active on peptidoglycan, but partially hydrolyzed peptidoglycan is a better substrate than the native form. It has been found that up to 85% of the GlcNAc residues are modified by the enzyme \[[@B117-ijms-19-00412]\]. Small peptidoglycan fragments are not substrates. It is also able to deacetylate peptidoglycans from other species, and it is not active on xylan or acetyl-heparin. *Bc*Pgd deacetylates soluble chitin and chitooligosaccharides. In terms of *k~cat~*, the order of preference for chitooligosaccharides is DP4 \> DP3 \> DP2 \> DP5 \> DP6, whereas *K~M~* decreases with DP \[[@B118-ijms-19-00412]\]. The pattern of acetylation of the products \[D~n−1~A\] indicates that the enzyme deacetylates all the residues but the reducing end, although fully deacetylated products are observed with DP3 and DP4 substrates upon long incubation times. Other *B. cereus* peptidoglycan deacetylases have also shown promiscuous substrate specificity, being active on peptidoglycan, glycol-chitin, and chitooligosaccharides. BC3618 has a kinetic behavior similar to *Bc*Pgd (BC1960) on chitooligosaccharides, and it does not deacetylate the reducing end GlcNAc, with final products having the pattern \[D~n−1~A\] \[[@B118-ijms-19-00412]\]. Likewise, BC1974, BC2929, and BC5204 deacetylate hexaacetylchitohexaose with different deacetylation patterns, but do not deacetylate the reducing and non-reducing terminal GlcNAc residues of the oligosaccharide \[[@B119-ijms-19-00412]\]. *Eubacterium rectale Pgd (Er*Pgd). *Eubacterium rectale* is part of the adult human distal gut microbial community, and belongs to Clostridium Cluster XIVa, one of the most common gut *Firmicutes* clades \[[@B120-ijms-19-00412]\]. The 3D structure of a predicted peptidoglycan GlcNAc deacetylase has been solved, but its biochemical characterization has not yet been reported. Although it should be included in the "unknown" subclass in [Table 1](#ijms-19-00412-t001){ref-type="table"}, it is placed in the group of characterized peptidoglycan GlcNAc deacetylases, due to its high similarity and active site motif conservation with other subclass members, as discussed below. ### 3.2.2. MurNAc Peptidoglycan Deacetylases {#sec3dot2dot2-ijms-19-00412} *Bacillus subtilis PdaA (Bs*PdaA). *Bacillus subtilis* is a Gram-positive bacteria found in soil and the gastrointestinal tract of some animals, and has the ability to form spores to survive harsh environmental conditions \[[@B121-ijms-19-00412]\]. *Bs*PdaA is involved in autolysis during spore germination \[[@B122-ijms-19-00412]\]. It deacetylates MurNAc residues of the glycan chain after peptide removal from the peptidoglycan by Cwld (an [l]{.smallcaps}-alanine amidase) \[[@B123-ijms-19-00412]\]. The deacetylated MurNH~2~ is a precursor for muramic δ-lactam synthesis, which involves transpeptidase activity. Introduction of the *pdaA* and *cwlD* genes into *E. coli* cells led to lactam formation in peptidoglycan, which suggests that PdaA participates in both steps, the de-*N*-acetylation of muramic acid residues, and the transpeptidase reaction for lactam cyclization \[[@B124-ijms-19-00412]\]. However, no transpeptidase activity was detected in vitro, where PdaA only deacetylates *N*-acetylmuramic acid residues without peptide side chains. It does not recognize native peptidoglycan, soluble chitin, chitin oligomers, or GlcNAc as substrates \[[@B123-ijms-19-00412]\]. *Bacillus anthracis Pda* (*Ba*Pda). *B. anthacis* is a Gram-positive spore forming bacteria that is the causative agent of anthrax \[[@B125-ijms-19-00412]\]. Like its close relative *B. cereus*, its genome contains ten ORFs for putative CE4 deacetylases, with more than 90% identity to the corresponding orthologues in *B. cereus*, including GlcNAc and MurNAc deacetylases \[[@B118-ijms-19-00412]\]. In particular, *Ba*Pda (BA0424) has been crystallized \[[@B69-ijms-19-00412]\], and it is closely related to *B. subtilis* PdaA, thus suggesting a similar substrate specificity on MurNAc residues of the peptidoglycan polymer. 3.3. Putative Polysaccharide Deacetylases (PPda) {#sec3dot3-ijms-19-00412} ------------------------------------------------ Four enzymes in [Table 1](#ijms-19-00412-t001){ref-type="table"} with solved 3D structure have unknown substrates or are inactive enzymes. *Bacillus cereus BC0361*. Of the eleven ORFs encoding for putative polysaccharide deacetylases, five have been experimentally proven to be active on peptidoglycan, as discussed above. BC0361 has been crystallized, and its 3D structure has been solved \[[@B70-ijms-19-00412]\]; it is predicted to be a peptidoglycan GlcNAc deacetylase for which the substrate remains unknown. *Bacillus anthracis BA0330.* BA0330 and BA0331 are the only lipoproteins among the eleven known or putative polysaccharide deacetylases of *B. anthracis*. The 3D structure of BA0330 has been solved. The enzyme is not active against glycol-chitin, chitooligosaccharides, synthetic muropeptide, or *p*-nitrophenyl acetate \[[@B71-ijms-19-00412]\]. It maintains the conserved metal-coordination motif and catalytic residues, but with some arrangements and alterations that will be discussed later. *Bacillus anthracis BA0150*. Another putative Pda from *B. anthracis* (*Ba*PdaB, BA0150) has been crystallized \[[@B72-ijms-19-00412]\]. However, the crystal structure does not contain a catalytic metal ion, and the protein does not contain the conserved Asp--His--His metal-binding triad that is found in most of the CE4 enzymes, indicating that it is not a functional polysaccharide deacetylase. However, since it contains the conserved Asp and His catalytic residues, BA0150 may have some other hydrolytic activity \[[@B72-ijms-19-00412]\]. *Encephalitozoon cuniculi ECU11_0510*. The microsporidian *E. cuniculi* is an intracellular eukaryotic parasite \[[@B126-ijms-19-00412],[@B127-ijms-19-00412]\]. ECU11_0510 was annotated as a putative polysaccharide deacetylase but was found to be unable to deacetylate chitooligosaccharides or crystalline β-chitin. It lacks the conserved aspartic residue, acting as catalytic base in all CE4 family members. It has been speculated that it is an inactive enzyme that evolved from a former chitin deacetylase, since the organism has developed an infectious mechanism that may require rigidity of the infectious spore which is enhanced by the presence of chitin and that would be disrupted by chitosan production \[[@B73-ijms-19-00412]\]. 3.4. Acetylxylan Esterases {#sec3dot4-ijms-19-00412} -------------------------- *Streptomyces lividans AXE* (*Sl*AxeA). *Streptomyces lividans* is a Gram-positive bacteria known to secrete large quantities of proteins involved in the catabolism of plant cell walls \[[@B128-ijms-19-00412]\]. Acetylxylan esterases are an important part of the xylanolytic enzyme system \[[@B129-ijms-19-00412],[@B130-ijms-19-00412],[@B131-ijms-19-00412]\], since they deacetylate acetylglucuronoxylans and acetylglucuronoarabinoxylans, making them accessible to endo-xylanases. *Sl*AxeA can deacetylate both 2 and 3 *O*-acetylated positions of xylose, but shows a preference for the 2 position. Its activity on double substituted xyloses is very slow, due to the requirement of a free OH in the 2 or 3 position. After the first deacetylation event, the second one occurs orders of magnitude faster \[[@B132-ijms-19-00412],[@B133-ijms-19-00412],[@B134-ijms-19-00412]\]. The enzyme also catalyzes the hydrolysis of *N*-acetyl groups in chitinous materials of variable degrees of polymerization and acetylation, such as glycol-chitin, chitosans with low DAs, and chitooligosaccharides \[[@B135-ijms-19-00412]\]. The activities of wild type *Sl*AxeA and mutants (obtained by random mutagenesis) on hexaacetylchitohexaose reveals a multiple-chain mechanism, generating a mixture of mono- to pentadeacetylated products. Full deacetylation was not observed but, interestingly, some partially deacetylated products are deacetylated at the reducing end \[[@B136-ijms-19-00412]\]. Additionally, it seems to be more active on chitin oligomers than on long polysaccharides \[[@B6-ijms-19-00412]\]. The addition of Co^2+^ has a larger activating effect on chitinous substrates than on xylan substrates, with a 7-fold increase in activity on *N*,*N*′-diacetylchitobiose \[[@B6-ijms-19-00412],[@B137-ijms-19-00412]\]. *Clostridium thermocellum AXE* (*Ct*AxeA). *C. thermocellum* is a Gram-positive bacteria known for its efficient plant cell wall degradation capabilities through a cell-bound multi-enzyme complex known as cellulosome \[[@B138-ijms-19-00412],[@B139-ijms-19-00412]\]. One of these enzymes is the Xyn11A, which comprises a complex multi-domain structure, including a GH11 endoxylanase domain followed by a family 6 CBM, a dockerin domain, and the typical CE4 deacetylase domain (*Ct*AxeA) \[[@B140-ijms-19-00412]\]. The *Ct*Axe module \[[@B74-ijms-19-00412]\] is active on acetylxylans with Co^2+^ as the preferred cation \[[@B140-ijms-19-00412],[@B141-ijms-19-00412]\]. No activity has been reported on chitinous substrates. 3.5. Poly-β-1,6-GlcNAc de-N-acetylase {#sec3dot5-ijms-19-00412} ------------------------------------- Bacterial poly-β-1,6-GlcNAc de-*N*-acetylases are involved in biofilm formation, and are targets for the design of inhibitors \[[@B46-ijms-19-00412],[@B142-ijms-19-00412],[@B143-ijms-19-00412],[@B144-ijms-19-00412],[@B145-ijms-19-00412],[@B146-ijms-19-00412]\]. The X-ray structure of four poly-β-1,6-GlcNAc de-*N*-acetylases have been reported ([Table 1](#ijms-19-00412-t001){ref-type="table"}). Although not active on β-1,4-linked GlcNAc substrates, their structures and active site topology provide additional insights into the substrate specificities of the CE4 enzyme family. *Escherichia coli* PgaB (*Ec*PgaB) deacetylates 3--20% of the GlcNAc residues of the PNAG, and facilitates its transport through the periplasmic space to the extracellular matrix. *Ec*PgaB specifically deacetylates GlcNAc polymers linked through β-1,6-linkages, and it is not able to use β-1,4-chitinous substrates \[[@B46-ijms-19-00412]\]. Its activity increases with the DP of the substrate up to the hexamer. On the tetramer, deacetylation occurs at the second or third position from the non-reducing end, whereas on the pentamer, it first deacetylates the central GlcNAc residue, followed by the next residue on the reducing end side to generate a di-deacetylated product \[[@B75-ijms-19-00412],[@B76-ijms-19-00412]\]. As will be discussed later, *Ec*PgaB has some variation in the positioning of the conserved CE4 catalytic residues, which explains the low efficiency of the enzyme, having a *k~cat~*/*K~M~* of 0.25 M^−1^s^−1^ for the β-1,6-pentasaccharide substrate \[[@B46-ijms-19-00412]\]. Other poly-β-1,6-GlcNAc de-*N*-acetylases with solved X-ray structures, so far, are *Ad*IcaB from *Ammoniex degensii* \[[@B77-ijms-19-00412]\], *Bb*BpsB from *Bordetella bronchiseptica* \[[@B45-ijms-19-00412]\], and *Aa*PgaB from *Aggregatibacter actinomycetemcomitans* \[[@B147-ijms-19-00412]\]. All of these enzymes show low activity on β-1,6-glucan, a common property of this enzyme subclass within family CE4. 4. Structural and Sequence Features of CE4 Enzymes Active on Chitooligosaccharides {#sec4-ijms-19-00412} ================================================================================== 4.1. Domain Organization {#sec4dot1-ijms-19-00412} ------------------------ Some CE4 enzymes are monodomain proteins, but some others have a multidomain architecture composed of the CE4 catalytic domain (referred as the NodB homology domain) and several other domains, including carbohydrate binding modules (CBMs) and domains with unknown function. The function of CBMs is to facilitate the solubilization of substrates and enzyme--substrate recognition, but they are also involved in protein localization by concentrating the appended enzyme on to the polysaccharide substrate \[[@B148-ijms-19-00412]\]. [Table 2](#ijms-19-00412-t002){ref-type="table"} summarizes the domain organization of the CE4 enzymes listed in [Table 1](#ijms-19-00412-t001){ref-type="table"} as predicted by Interpro, with the Uniprot accession codes. 4.2. X-ray Structures {#sec4dot2-ijms-19-00412} --------------------- The CE4 enzyme members with solved 3D structure by X-ray crystallography are listed in [Table 1](#ijms-19-00412-t001){ref-type="table"}, and their 3D structures are presented in [Figure 3](#ijms-19-00412-f003){ref-type="fig"}. The first structure of the CE4 family was that of *Bacillus subtilis* peptidoglycan deacetylase (*Bs*PdaA) in 2004 (PDB 1W17) \[[@B68-ijms-19-00412]\]. After that, the structure of *Streptococcus pneumoniae* peptidoglycan GlcNAc deacetylase (*Sp*PgdA) was solved at 1.75 Å resolution (PDB 2C1G) and unraveled that the enzyme, and by extension other CE4 members, are metalloenzymes using a His--His--Asp zinc-binding triad \[[@B65-ijms-19-00412]\]. The first structure of a CDA was that of *Choletotrichum lindemuthianum* in 2006 \[[@B61-ijms-19-00412]\], which also showed that the enzyme employs a conserved His--His--Asp zinc-binding triad, closely associated with the conserved catalytic base (aspartic acid) and acid (histidine), to carry out acid/base catalysis. The *Aspergillus nidulans* CDA structure also reinforced the structural conservation of active site residues in chitin deacetylases \[[@B12-ijms-19-00412]\]. The structure of the CE4 domain is characterized by an (β/α)~8~ barrel fold, which is frequently distorted, and may even appear as an (β/α)~7~ barrel that lacks one of the αβ repeats of regular TIM barrels, which creates a groove into which the extended polymer substrate binds \[[@B2-ijms-19-00412],[@B65-ijms-19-00412],[@B76-ijms-19-00412]\]. The central core comprises seven or eight parallel β-strands that form a greatly distorted β-barrel surrounded by α-helices. A series of loops decorate the β-barrel and make up the majority of the carbohydrate binding pocket. There are significant topological differences among CE4 enzymes, with some having the N/C-termini on the same side of the barrel (as in *Cl*CDA), whereas in others, the N/C-termini are located on opposite ends (as in *Sp*PgdA and *Bs*PdaA). So far, all the structurally defined members of the CE4 family adopt a degree of "secondary structure swapping" from the canonical (β/α)~8~ fold \[[@B61-ijms-19-00412]\]. A few other CE4 enzyme members were subsequently crystallized in their unliganded forms ([Table 1](#ijms-19-00412-t001){ref-type="table"}, [Figure 3](#ijms-19-00412-f003){ref-type="fig"}). Acetylxylan esterases from *S. lividans* and *C. thermocelum* \[[@B74-ijms-19-00412]\] show the canonical active topology and metal coordination in this enzyme family, as well as other peptidoglycan deacetylases (*S. mutants* \[[@B74-ijms-19-00412]\], *B. anthracis* \[[@B69-ijms-19-00412]\], and *B. cereus* \[[@B150-ijms-19-00412]\]). The case of poly-β-1,6-GlcNAc deacetylases is different \[[@B75-ijms-19-00412],[@B76-ijms-19-00412],[@B77-ijms-19-00412],[@B147-ijms-19-00412]\], as they have a circularly permutated CE4 domain and some variations in the positioning of active site residues, as discussed below. It was not until 2014 that the first crystal structure of a CE4 enzyme in complex with substrates was solved, that of the *Vibrio cholera* CDA \[[@B62-ijms-19-00412]\], providing new information on loop organization and insights into the structural determinants of substrate binding, specificity, and catalysis. 4.3. Multiple Sequence Alignment of the CE4 Domain {#sec4dot3-ijms-19-00412} -------------------------------------------------- The multiple sequence alignment of the CE4 domain of the enzymes reported in [Table 1](#ijms-19-00412-t001){ref-type="table"} is presented in [Figure 4](#ijms-19-00412-f004){ref-type="fig"}. Since standard multiple sequence alignment algorithms (based on sequence composition only) fail to reproduce the structural conservation of CE4 enzymes, the alignment was guided by the structural superposition of the available X-ray structures of these enzymes. This ensures that the alignment reproduces the conserved spatial distribution of amino acids, which is important for deciphering the structure--function relationships detailed in the following sections. Sequences of enzymes without structural data were incorporated into the alignment by means of Hidden Markov Model (HMM) comparisons. The 3D structures of *Vc*CDA and *Ec*PgaB were key to obtaining a complete multiple sequence alignment that spanned the whole CE4 domain. On one hand, the *Vc*CDA sequence exhibits substantially longer insertions than most of the other CE4 members do. On the other hand, the *Ec*PgaB sequence is shuffled around the C-terminus, which is a specific feature of the poly-β-1,6-GlcNAc deacetylase subfamily within the CE4 family (a circularly permuted CE4 domain). The shuffling point of *Ec*PgaB and related enzymes is indicated with an arrow in [Figure 4](#ijms-19-00412-f004){ref-type="fig"}. The multiple sequence alignment reveals an even distribution of conserved motifs and non-conserved insertions along the sequences of CE4 enzymes. Conserved motifs related to enzymatic activity are numbered from Motif 1 to Motif 5 (detailed in the next section). These are typically located at the center of the active site structure. Insertions are of variable length and variable sequence composition throughout the family. This variability decreases when considering only CE4 subfamilies with concrete enzymatic specificity. These insertions correspond to both unstructured and structured loops of variable geometry that surround the active site. These loops are numbered from Loop 1 to Loop 6 ([Figure 4](#ijms-19-00412-f004){ref-type="fig"}), and their influence in determining the substrate specificity of CE4 enzymes is discussed in the last section of this review. 4.4. NodB Domain and Active Site Conserved Motifs {#sec4dot4-ijms-19-00412} ------------------------------------------------- CE4 family members share the NodB homology domain, which is approximately 150 aa long. This region is generally defined by five conserved motifs, named Motif 1 to Motif 5 according to the order they appear in the sequence. These consensus motifs were first proposed after the 3D structure of *Sp*PgdA was solved in 2005, in combination with a multiple sequence alignment of representative members of the CE4 family \[[@B65-ijms-19-00412]\]. These motifs form the active site, and are required for enzymatic activity. As new 3D structures have been reported, the description of the conserved motifs can be refined based on more extensive sequence and structural alignments. Active site conserved motifs are highlighted in [Figure 4](#ijms-19-00412-f004){ref-type="fig"} and shown in [Figure 5](#ijms-19-00412-f005){ref-type="fig"}. Motif 1 (TFDD) includes the general base aspartate (first D) and the metal-binding aspartate (second D). Motif 2 contains the consensus sequence H(S/T)xxH, which is regarded as a zinc-binding motif, where the two His residues bind the metal cation and the Ser or Thr residue forms a hydrogen bond with the second His, stabilizing the local conformation of the loop-shaped motif. The metal-binding Asp from Motif 1, plus the two His residues in Motif 2, are often designated the His--His--Asp metal-binding triad of CE4 enzymes. Motif 3 (RxPY) forms one of the sides of the active site groove, and establishes stabilizing interactions with other active site residues. Motif 4 (DxxD(W/Y)) forms the other side of the active site groove, including a hydrophobic residue exposed to the solvent and a buried Asp. Motif 5 is defined by I(V/I)LxHD, which contains a Leu as part of the hydrophobic pocket that accommodates the acetate methyl group of the substrate and the general acid His residue for catalysis. 5. Substrate Recognition and Catalysis {#sec5-ijms-19-00412} ====================================== 5.1. Catalytic Mechanism {#sec5dot1-ijms-19-00412} ------------------------ CDAs and related CE4 enzymes operate by metal-assisted acid/base catalysis, analogous to other metal-dependent hydrolases \[[@B151-ijms-19-00412]\]. The first CE4 structure solved (*Bs*PdaA \[[@B68-ijms-19-00412]\]) was not conclusive regarding metal binding, but the subsequent structures of *Sp*PgdA \[[@B65-ijms-19-00412]\] and xylan esterases \[[@B74-ijms-19-00412]\] supported the proposed mechanism of metal-dependent CE4 enzymes. *Cl*CDA was also shown to contain a zinc cation in the active site, even though the enzyme was not inhibited by the metal chelator EDTA, indicating that the metal cation is tightly bound to the enzyme active site \[[@B61-ijms-19-00412]\]. Further support arrived with the 3D structure of *Vc*CDA in complex with substrates \[[@B62-ijms-19-00412]\]. The structure of complexes of an inactive mutant (at the general base Asp residue) with *N,N′*-diacetylchitobiose (DP2) and *N*,*N*′,*N*′′-triacetylchitotriose (DP3) in productive binding for catalysis showed that a sugar hydroxyl group of the substrate also participates in metal coordination. Specifically ([Figure 6](#ijms-19-00412-f006){ref-type="fig"}A), the carboxylate group of Asp40 and the imidazole rings of His97 and His101 are involved in Zn^2+^ coordination, which is also coordinated to the O7 atom of the *N*-acetyl group and O3 hydroxyl of the GlcNAc ring. A water molecule completes the distorted octahedral coordination to the divalent metal cation. Upon activation, this water molecule is proposed to be the nucleophile responsible for removal of the *N*-acetyl group \[[@B62-ijms-19-00412]\]. The consensus mechanism of CDAs and related CE4 deacetylases is shown in [Figure 6](#ijms-19-00412-f006){ref-type="fig"}B. The carbonyl amide of the substrate is coordinated with the metal cation, and catalysis proceeds by nucleophilic attach of a water molecule activated by the general base (Asp) leading to a tetrahedral oxyanion intermediate. This oxyanion is stabilized by the metal and other active site residues. Protonation of the nitrogen group of the intermediate by the general acid (His) then facilitates C--N bond breaking with the generation of a free amine in the de-*N*-acetylated product, and release of acetate. Hammett linear free energy correlations using α-haloacetamido substrate analogues performed on the *Cl*CDA enzyme provided further kinetic evidence of the presence of an oxyanion tetrahedral intermediate, and significant negative charge development at the transition state \[[@B61-ijms-19-00412]\]. This charge would be stabilized by the oxyanion hole generated by the Tyr backbone nitrogen (Y145 in *Cl*CDA, Y169 in *Vc*CDA, shown in [Figure 6](#ijms-19-00412-f006){ref-type="fig"}) and the zinc cation. The general acid and base residues are part of two conserved "charge relay" side chain pairs consisting of the catalytic base (Asp) tethered by a conserved Arg (in MT3, **R**xxPY), and the catalytic acid (His) tethered by a conserved Asp (in MT4, Dxx**D**(W/Y)), which may contribute to tuning the p*K*~a~ of the catalytic residues \[[@B61-ijms-19-00412],[@B65-ijms-19-00412]\]. Although the conserved motifs MT1--5 are a signature for the family, close inspection of the positioning of active site residues within the five conserved motifs in the sequence alignment or in the 3D structures reveals different special arrangements that seem (tentatively, given the reduced number of proteins with experimentally proven specificity ([Table 1](#ijms-19-00412-t001){ref-type="table"})) to be characteristic of each enzyme subfamily ([Figure 5](#ijms-19-00412-f005){ref-type="fig"}). Motif 1 (TFDD, with Y substituted for F in a few cases) is highly conserved within all CE4 members, except for peptidoglycan MurNAc deacetylases. They lack the Asp residue involved in metal coordination, and have an Asn insertion that points away from the metal ion into the core of the protein (*Bs*PdaA \[[@B68-ijms-19-00412]\], *Ba*Pda \[[@B69-ijms-19-00412]\]). The *E. coli* protein ECU11_0510 lacks the general acid Asp, and consequently, it is an inactive protein with unknown function \[[@B73-ijms-19-00412]\]. In MT2 (H(S/T)xxH), poly-β-1,6-GlcNAc deacetylases have four residues separating the two metal binding His residues, as opposed to three in the other subfamilies. Significantly, inactive proteins classified as "unknown" in [Table 1](#ijms-19-00412-t001){ref-type="table"} lack these conserved His residues. The MT3 motif is well conserved, except for poly-β-1,6-GlcNAc deacetylases, where the Arg residue interacting with the general base in the other CE4 members (**R**xPY) occurs further in the sequence just before MT4 \[[@B75-ijms-19-00412]\]. Poly-β-1,6-GlcNAc deacetylases also differ in MT4; they have a water molecule in place of the conserved Asp that interacts with (and presumably activates) the catalytic acid His in the other CE4 members. It has been hypothesized that this water molecule would not be able to activate the catalytic acid in the same manner that an aspartic acid residue would, which is consistent with the lower specific activity of these enzymes relative to the other CE4 subfamilies \[[@B75-ijms-19-00412]\]. Finally, the general acid His in MT5 is strictly conserved. These motifs also play important roles in substrate recognition, and these will be described below. 5.2. Substrate Recognition and Specificity {#sec5dot2-ijms-19-00412} ------------------------------------------ ### 5.2.1. The Case of *Vc*CDA: Enzyme·Substrate Complexes Show an Induced Fit Mechanism {#sec5dot2dot1-ijms-19-00412} The series of crystal structures of *Vibrio cholera*e chitin oligosaccharide deacetylase reported in 2014 \[[@B62-ijms-19-00412]\] were the first 3D structures of a CE4 enzyme in complex with substrates. These new data paved the way for deciphering detailed structure--function relationships for this family of enzymes. Currently available structures of *Vc*CDA include the unliganded form of the enzyme, and the binary complexes with *N*-acetyl-glucosamine (DP1), *N*,*N*′-diacetylchitobiose (DP2), and *N,N*′*,N*′′-triacetylchitotriose (DP3), ([Figure 7](#ijms-19-00412-f007){ref-type="fig"}A). Both the DP2 and DP3 complexes revealed the exact location of the substrate in the active site of the enzyme in a competent binding mode for catalysis. These structures provided further evidence for the proposed metal-assisted acid/base catalytic mechanism, and revealed key enzyme--substrate interactions, along the catalytic itinerary (discussed in the previous section, [Figure 6](#ijms-19-00412-f006){ref-type="fig"}). Remarkably, the binding cavity at the catalytic center is dynamically assembled upon substrates binding (DP ≥ 2): important conformational changes in a loop in the structure (namely, Loop 4, see later) take place induced by the binding of different substrates. The structure of this loop alternates between an open conformation in the unliganded *Vc*CDA and *Vc*CDA·DP1 complex, and a completely closed conformation in the *Vc*CDA·DP2 complex, or a semi-closed conformation in the *Vc*CDA·DP3 complex ([Figure 7](#ijms-19-00412-f007){ref-type="fig"}B). Such induced-fit conformational changes upon substrate binding are triggered by the CH--π stacking interaction \[[@B152-ijms-19-00412],[@B153-ijms-19-00412]\] established between Trp238 (located in Loop4, MT4 motif DxxD(**W**/Y)), and the *N*-acetylglucosamine unit at the catalytic center. Since either a tryptophan or tyrosine residue is predominantly observed in the equivalent position in other CE4 structures ([Figure 5](#ijms-19-00412-f005){ref-type="fig"}), it is reasonable to think that similar induced-fit conformational changes may occur in other CE4 enzymes as well. ### 5.2.2. Determinants of Substrate Specificity: The Subsite Capping Model {#sec5dot2dot2-ijms-19-00412} The diversity of deacetylation patterns exhibited by chitin deacetylases and related CE4 enzymes active on COS ([Table 1](#ijms-19-00412-t001){ref-type="table"}) can be attributed to the differential accessibility of the linear chitin oligosaccharide to the separate subsites along the substrate binding cleft of their structures. The ability of the substrate to slide along the binding cleft or to bind in different modes will determine which *N*-acetylglucosamine units can be exposed to the catalytic site, where the actual deacetylation reaction occurs, thus dictating the deacetylation pattern. The structural superposition of all available structures of CE4 enzymes active on COS revealed the significance of loop topology as a determinant of such substrate binding specificities ([Figure 8](#ijms-19-00412-f008){ref-type="fig"}), leading to the formulation of the "Subsite Capping Model" \[[@B62-ijms-19-00412]\]. The distinctive α/β barrel of the NodB homology domain is highly conserved. The substrate binding cleft is located on one side of the barrel, where structural variability is notably higher. This variability is provided by a series of loops surrounding the active site that connect the α/β elements of the barrel. There are six loops (Loop 1 to Loop 6) of different length, structure, and sequence composition that modulate the shape of the binding cleft exposed to the substrate in each particular enzyme ([Figure 8](#ijms-19-00412-f008){ref-type="fig"}). Taking as reference the 3D structure of *Vc*CDA in complex with *N,N*′*,N*′′-triacetylchitotriose, these loops define three different substrate binding subsites along the binding cleft of the enzyme ([Figure 7](#ijms-19-00412-f007){ref-type="fig"}). Analogously to the numbering of subsites in glycosyl hydrolases, these are numbered as −n, 0 and +n, from the non-reducing end to the reducing end of the substrate, with subsite 0 being the site of deacetylation (catalytic center) \[[@B49-ijms-19-00412]\]. In *Vc*CDA, the non-reducing *N*-acetylglucosamine unit is placed at subsite −1 (defined by Loops 1, 2, and 6), whereas the reducing *N*-acetyl glucosamine unit is placed at subsite +1 (defined by Loops 3, 4, and 5). No additional binding subsites can be identified in the structure of *Vc*CDA, towards neither the reducing nor the non-reducing ends, that would allow binding of longer substrates. The binding cavity is so tight that substrates cannot slide along the cleft, such as a multiple-attack mechanism would require ([Figure 2](#ijms-19-00412-f002){ref-type="fig"}). Indeed, subsite 0 is exclusively occupied by the *N*-acetylglucosamine unit located at the second position after the non-reducing end. These facts are in agreement with the preferential activity of *Vc*CDA towards short chitin oligosaccharides, and with strict specificity for a single deacetylation event and a unique pattern of deacetylation. An equivalent distribution of subsites along the substrate binding cleft can be observed in all the structures of CE4 enzymes active on COS ([Figure 8](#ijms-19-00412-f008){ref-type="fig"}). The catalytic site defined by the metal coordination triad is located exactly at the center of this loops bundle (subsite 0), and the accessibility to additional substrate binding subsites is differentially blocked by these loops. On one hand, Loop 1, Loop 2, and Loop 6 contribute to define the negative subsites, where the non-reducing end of the substrate is placed. For instance, Loop 1 and Loop 6 are notably longer in *Vc*CDA and NodB compared to the rest of CDAs. As a consequence, negative subsites are partially hindered, and deacetylation takes place specifically at the non-reducing-end edge of the substrates. On the other hand, Loop 3, Loop 4, and Loop 5 contribute to define the positive subsites, where the reducing end of the substrate is placed. Except in *Vc*CDA, these loops are relatively short in all CDAs, and positive subsites are highly exposed to the solvent and substrates. The scarce existence of CDAs that efficiently deacetylate the reducing end of COS may indicate that binding of a GlcNAc unit at subsite +1 is essential for the enzymatic activity. *Vc*CDA is the only known CE4 enzyme able to exclusively deacetylate the reducing end unit of *N,N*′-diacetylchitobiose. In this enzyme, positive subsites are completely blocked by Loop 4 and the longest Loop 5 in the family, which dynamically assemble the substrate binding pocket (see above). Finally, it is interesting to note that the shuffling point along the sequence of poly-β-1,6-GlcNAc deacetylases takes place within Loop 5. A second X-ray structure of a CDA in complex with substrate has been recently reported (November 2017), that of *Ar*CE4 from a marine *Arthobacter* species \[[@B64-ijms-19-00412]\]. Even though the enzyme was co-crystallized with a DP4 substrate, only the electron density for a GlcNAc dimer occupying subsite 0 and +1 could be solved. Apparently, the other two rings are not stabilized by any protein--ligand interactions, and they may adopt multiple orientations. *Ar*CE4 has short loops 1 to 6, resulting in an open cleft with only two defined subsites (0 and +1) and allowing binding of longer substrates on a shallow binding cleft. Binding of the sugar in the +1 subsite seems to be dominated by a stacking interaction with a Trp residue. Similarly to *Vc*CDA, the GlcNAc unit bound in subsite 0 is properly oriented for catalysis, and has multiple interactions with the enzyme. *Vc*CDA and *Ar*CE4 deacetylases represent opposite cases with regard to the size of the loops surrounding the active site cleft. *Vc*CDA, with long loops shaping the binding cleft, prefers a short DP2 substrate, and the activity decreases with increasing chain length of the oligosaccharide substrate; Loops 1 and 6 block the accessibility of additional subsites on the non-reducing end site of the deep binding cleft and they dictate the specificity for deacetylation at the penultimate residue from the non-reducing end, whereas Loops 4 and 5 limit productive binding of longer substrates. In contrast, *Ar*CE4, with short loops (the shortest among characterized CE4 enzyme, [Figure 4](#ijms-19-00412-f004){ref-type="fig"}) and an open and shallow binding cleft, shows increasing activity with longer substrates, and follows a multiple-chain mechanism. Not only do the size and shape of the loops contribute to define the specificity and pattern of acetylation, but their dynamics also participate in this process. Evidence was provided by the *Vc*CDA enzyme, where docking simulations of longer substrates than those co-crystallized with the enzyme (DP2 and DP3, [Figure 7](#ijms-19-00412-f007){ref-type="fig"}) were unable to accommodate the ligands in productive binding modes, because Loop 5 was blocking access to additional positive subsites beyond the already exposed subsite +1 (as seen in the *Vc*CDA·DP3 complex). However, longer oligosaccharides, such as DP4 and DP5 COS, are substrates of the enzyme, although with a 10-fold reduced efficiency \[[@B62-ijms-19-00412]\]. Both molecular dynamic simulations and loops engineering, where mutations are introduced to impact their dynamics, are supportive of the model \[[@B154-ijms-19-00412]\], providing exciting new opportunities to modify and tune deacetylation patterns. The topology and dynamics of these loops also mediate specific enzyme--substrate interactions that seem to be related to the different substrate specificities of CE4 enzyme subfamilies. Tyr169 (hereafter *Vc*CDA numbering is used as a reference) located in Loop 3 (MT3 motif RxP**Y**) establishes a hydrophobic interaction with the substrate ring located at subsite 0. An aromatic amino acid residue is always present in the reported CE4 enzymes active on COS, but not in MurNAc peptidoglycan deacetylases, which have an arginine at this position. Trp229 and Leu293 (located at subsite 1, L293 being part of the MT5 motif **L**xHD) define a hydrophobic pocket that accommodates the methyl group of the reactive *N*-acetylglucosamine unit at subsite 0, and the methylene unit of the hydroxymethyl group of the substrate GlcNAc located at subsite +1. Trp229 and Leu293 are highly conserved in the family, except for some fungal enzymes and poly-β-1,6-GlcNAc deacetylases. Asp232 (located at subsite +1, the first D of the MT4 motif **D**xxD) establishes a hydrogen bond with the hydroxyl of the hydroxymethyl group of the GlcNAc unit located at subsite +1, as well as a water-mediated hydrogen bond with the catalytic histidine (His295). The polarity of this amino acid is conserved within the family, except for MurNAc peptidoglycan deacetylases, which carry a non-polar alanine amino acid instead, and poly-β-1,6-GlcNAc deacetylases, which have a leucine at that position. Trp238 (located in Loop 4, MT4 motif DxxD(**W**/Y)) establishes a CH--π interaction with the substrate ring located at subsite 0. An aromatic side chain is predominant in this position within the family, with very few exceptions. Phe297 (located in Loop 6) establishes hydrophobic interactions with the substrate ring located at subsite −1. This is a well conserved hydrophobic position in the family, except for poly-β-1,6-GlcNAc deacetylases, which have a polar substituent. Finally, although not strictly conserved, Asn65, Trp67, and His68 (located at the beginning of Loop 1) coordinate a water molecule that is hydrogen-bonded to the hydroxyl group of the hydroxymethyl substituent of the substrate ring located at subsite −1. The reducing end of the substrate is not deacetylated, or it is the least reactive GlcNAc unit for most CDAs and related CE4 enzymes active on COS. In the 3D structure of the *Ar*CE4·DP2 complex \[[@B64-ijms-19-00412]\], binding of the GlcNAc unit of the substrate in the +1 subsite seems to be dominated by the stacking interaction with a Trp in Motif 4. This aromatic residue is highly conserved (MT4, DxxD(**W**/**Y**), with few exceptions. CE4 enzymes having this aromatic residue seem to prefer a sugar bound in the +1 subsite, and do not deacetylate the reducing end of their substrates, as shown for the *Ar*CE4 enzyme, as well as for *Pes*CDA \[[@B89-ijms-19-00412]\] and *Pc*CDA \[[@B95-ijms-19-00412]\], or the reducing end is the slowest position to be deacetylated, as shown for *Cl*CDA \[[@B49-ijms-19-00412]\] and *An*CDA \[[@B12-ijms-19-00412]\]. On the contrary, *Vc*CDA has the equivalent aromatic residue in a slightly different position after a two-amino acid insertion in the MT4 motif, and it is part of the Loop 4 that moves from an open to a closed conformation upon substrate binding. As a consequence of the induced fit, the Trp residue establishes a stacking interaction with the GlcNAc unit in subsite 0. DP2 is the preferred substrate of *Vc*CDA, and it is deacetylated at the reducing end \[[@B62-ijms-19-00412]\]. Likewise, *Pgt*CDA lacks the +1 aromatic residue, and it deacetylates the reducing end GlcNAc unit of all substrates from DP4 to DP6 \[[@B89-ijms-19-00412]\]. Although these observations seem a general trend, there is still limited information to gain insights into the structural determinants that dictates specificity and deacetylation patterns, and more structural data on enzyme·substrate complexes is required for better understanding the functionality of CE4 enzymes. 6. Conclusions {#sec6-ijms-19-00412} ============== The CE4 family is composed of deacetylases that act on structural polysaccharides, such as chitin and chitosans, peptidoglycans, acetylxylans, and β-1,6-GlcNAc polysaccharides. Here, we have reviewed the characterized enzymes in the family that deacetylate chitin and chitooligosaccharide (COS) substrates. The CE4 family members share an (β/α)~8~ three-dimensional fold, and are metal-depended hydrolases, with Zn^2+^ and Co^2+^ as the most common metal cations. A signature of the family is the conservation of five active site motifs that include the His--His--Asp metal binding triad, and the catalytic Asp and His residues as general base and general acid, respectively. The structural determinants of substrate specificity and deacetylation pattern exhibited by CDAs and related CE4 enzymes active on COS remain poorly understood. The recently solved crystallographic structures of few family members, particularly those of the *Vibrio cholerae* CDA in complex with substrates, have provided some insights into structure-specificity relationships. The substrate binding cleft, located on one side of the distinctive β/α barrel of the NodB homology domain, is shaped by a series of loops that surround the active site. These loops, which differ in length, sequence composition, structure and dynamics, modulate the exposure of the different subsites along the binding cleft to the substrate in each particular enzyme. Long loops at the edges of the binding cleft are found in chitin oligosaccharide deacetylases, such as *Vc*CDA and rhizobial NodB deacetylases, which are specific for a single site deacetylation. Short loops make up a more open binding cleft able to bind chito-oligomers in different manners, as found in CDAs that can catalyze multiple deacetylations on COS substrates, and are active on polymeric substrates. The surface charge distribution along the binding cleft and other structural features may also participate in defining the mode of action and deacetylation pattern exhibited by each particular enzyme. The discovery of novel CDAs with different specificities and the resolution of new enzyme--substrate complex structures will provide further insights into structure-specificity relationships. This knowledge is relevant for the biotechnological applications of CDAs and other CE4 enzymes to design inhibitors targeting CDAs as antimicrobial agents, and to engineer these enzymes as biocatalysts for the production of well-defined partially deacetylated COS with biological activities. Work supported by Grant BFU2016-77427-C2-1-R from MINECO, Spain. Hugo Aragunde acknowledges a predoctoral fellowship from Generalitat de Catalunya. Antoni Planas and Xevi Biarnés conceived and designed the review; Hugo Aragunde, Xevi Biarnés and Antoni Planas wrote the paper. The authors declare no conflict of interest. The founding sponsors had no role in the design of the study, in the writing of the manuscript, and in the decision to publish the results. AXE Acetylxylan estarase A n (GlcNAc) n CDA Chitin deacetylase COS Chitooligosaccharides D n (GlcNH 2 ) n DA Degree of acetylation DP Degree of polymerization GlcNAc N -acetylglucosamine GlcNH 2 Glucosamine MurNAc N -acetylmuramic acid PA Pattern of acetylation PDB Protein data bank PG Peptidoglycan PNAG Poly-β-1,6- N -acetyl- d -glucosamine PPda Putative polysaccharide deacetylase ![Structures of the substrates of CE4 enzymes and representative deacetylated products. (**A**) Chitin oligosaccharide substrate of chitin deacetylases; (**B**) Peptidoglycan fragment substrate of peptidoglycan MurNAc deacetylases (a) or peptidoglycan GlcNAc deacetylases (b); (**C**) Acetyl-[d]{.smallcaps}-glucurono-[d]{.smallcaps}-xylan substrate of acetylxylan esterases; (**D**) β-1,6-Glucan substrate of poly-β-1,6-*N*-acetylglucosamine deacetylases.](ijms-19-00412-g001){#ijms-19-00412-f001} {#ijms-19-00412-f002} {ref-type="table"}. The *Vp*CDA structure (3WX7) is essentially identical to that of *Vc*CDA. Loops are colored as in [Figure 4](#ijms-19-00412-f004){ref-type="fig"}.](ijms-19-00412-g003){#ijms-19-00412-f003} {ref-type="table"}. Loops are highlighted with colored boxes according to \[[@B62-ijms-19-00412]\]. Conserved catalytic motifs are labelled MT1--5. The "His--His--Asp" metal binding triad (▼), catalytic base (\*), and catalytic acid (◊) are labelled. The mark inside Loop 5 for poly-β-1,6-GlcNAc deacetylases (four last sequences) indicates the shuffling point of the circularly permuted CE4 domain.](ijms-19-00412-g004){#ijms-19-00412-f004} {ref-type="table"}. Subfamilies separated by a line: CDAs, peptidoglycan GlcNAc deacetylases, peptidoglycan MurNAc deacetylases, unknown, acetylxylan esterases, and poly-β-1,6-GlcNAc deacetylases.](ijms-19-00412-g005){#ijms-19-00412-f005} ![(**A**) Active site residues in the X-ray structure of the *Vc*CDA·DP2 complex, showing Zn^2+^ coordination and substrate binding; (**B**) Metal-assisted general acid/base mechanism proposed for CE4 deacetylases. Scheme based on the 3D structure of the enzyme--substrate complex *Vc*CDA~D39S~·DP2 \[[@B62-ijms-19-00412]\]. D39 is the general base and His295 is the general acid.](ijms-19-00412-g006){#ijms-19-00412-f006} {#ijms-19-00412-f007} {ref-type="table"}). The core of the proteins (in grey) is highly conserved, and main differences are on the loops surrounding the binding site cleft. Loops colored as in A; (**C**) Comparison of topology of Loops 1 to 6 for the enzymes overlaid in B.](ijms-19-00412-g008){#ijms-19-00412-f008} ijms-19-00412-t001_Table 1 ###### CE4 enzymes active on chitooligosaccharide and GlcNAc-containing polysaccharides. Subfamil ^(1)^ Enzyme Organism PDB (Year) Ref ^(2)^ Polymer Substrates COS Substrates ^(3)^ Metal PA ^(4)^ (on A~n~) --------------------- ----------------------------------------- ---------------------------- -------------------------- ------------------------------------------------------------------------- --------------------------------------------- ------------------------ ---------------------- -------------------- **Chitin DA** *Mr*CDA *Mucor rouxii* \-- Chitin, chitosan ≥DP3 Zn^2+^ D~n,~ D~n−1~A *Cl*CDA *Colletotrichum lindemuthianum* **2IW0** (2006) \[[@B61-ijms-19-00412]\] Glycol-chitin DP6\>DP5\>DP4\>DP3\>DP2 Co^2+^ Zn^2+^ D~n~ *An*CDA *Aspergillus nidulans* **2Y8U** (2012) \[[@B12-ijms-19-00412]\] Glycol-chitin, chitin, CM-chitin, acetylxylan DP2\>DP3\>DP4\>DP5 Co^2+^ D~n~ *Pgt*CDA *Puccinia graminis* \-- Glycol-chitin, colloidal chitin, chitosans DP6\>DP5\>DP4 n.r. ^(5)^ AAD~n−2~ *Pes*CDA *Pestolotiopsis* sp. \-- Colloidal chitin, chitosan DA10-60% DP6-DP5-DP4 n.r. AAD~n−3~A *Pa*CDA *Podospora anserina* \-- Glycol-chitin ≥DP2 Zn^2+^ D~n~ *Pc*CDA *Pochonia chlamydosporia* \-- n.r. DP5\>DP4 n.r. ADDA~n−3~ NodB *Sinorhizobium meliloti* \-- COS DP5\>DP2 (DP4, DP3) Mn^2+^ Mg^2+^ DA~n−1~ *Vc*CDA (COD) *Vibrio cholera* **4NY2** (2014) \[[@B62-ijms-19-00412]\] COS DP2\>DP3\>DP4\>DP5\>DP6 Zn^2+^ ADA~n−2~ *Vp*CDA (COD) *Vibrio parahaemolyticus* **3WX7** (2014) \[[@B63-ijms-19-00412]\] COS DP2, DP3 Zn^2+^ n.r. *Ar*CE4 *Arthrobacter* sp. **5LFZ** (2017) \[[@B64-ijms-19-00412]\] Chitin, chitosan, acetylxylan DP5\>DP6=DP4\>DP3\>\>DP2 Ni^2+\ (6)^ A3D2 **GlcNAc DA** *Sp*PgdA *Streptococcus pneumoniae* **2C1G** (2005) \[[@B65-ijms-19-00412]\] GlcNAc DA on peptido-glycan (GlcNAc)~3~ Zn^2+^ ADA *Sm*PgdA *Streptococcus mutants* **2W3Z** (2008) \[[@B66-ijms-19-00412]\] GlcNAc DA on peptidoglycan DP6 Zn^2+^ n.r. *Bc*Pgd (BC1960) *Bacillus cereus* **4L1G** (2014) \[[@B67-ijms-19-00412]\] GlcNAc DA on peptido-glycan, glycol-chitin DP6-DP5-DP4\>\>DP3\>DP2 Co^2+^ D~n−1~A *Er*Pgd *Eubacterium rectale* **5JMU** (2016) GlcNAc deacetylase (annotated) Zn^2+^ **MurNAc DA** *Bs*PdaA *Bacillus subtilis* **1W17** (2005) \[[@B68-ijms-19-00412]\] MurNAc DA on peptido-glycan (Cwld digested) No active on COS Cd^2+\ (6)^ *Ba*Pda (BA0424) *Bacillus anthracis* **2J13** (2006) \[[@B69-ijms-19-00412]\] MurNAc DA on peptido-glycan n.r. Zn^2+^ **PPda (unk)** BC0361 *Bacillus cereus* **4HD5** (2012) \[[@B70-ijms-19-00412]\] Substrate unknown Putative GlcNAc DA Zn^2+^ BA0330 *Bacillus anthracis* **4V33** (2015) \[[@B71-ijms-19-00412]\] Unknown. Not active on glycol-chitin, COS, pNPAc, synthetic muropeptide Zn^2+^ BA0150 *Bacillus anthracis* **4M1B** (2014) \[[@B72-ijms-19-00412]\] Presumably inactive (no metal coordination) No metal ECU11_0510 *Encephalitozoon cuniculi* **2VYO** (2009) \[[@B73-ijms-19-00412]\] Inactive (lack of Asp general base and His metal-binding) No metal **AXE** *Sl*AxeA *Streptomyces lividans* **2CC0** (2006) \[[@B74-ijms-19-00412]\] Acetylxylan, glycol-chitin, chitosan DP2-DP4-DP6 Co^2+^ DDD (A1D2) *Ct*AxeA *Clostridium thermocellum* **2C71** (2006) \[[@B74-ijms-19-00412]\] 2-*O*-acetylxylan No active on COS Co^2+^ **β-1,6-GlcNAc DA** *Ec*PgaB *Escherichia coli* **3VUS** (2012) \[[@B75-ijms-19-00412],[@B76-ijms-19-00412]\] Poly-β-1,6-GlcNAc de-*N*-acetylase β-1,6-GlcNAc oligomers Co^2+^ Ni^2+^ Zn^2+^ *Ad*IcaB *Ammonifex degensii* **4WCJ** (2014) \[[@B77-ijms-19-00412]\] Poly-β-1,6-GlcNAc de-*N*-acetylase β-1,6-GlcNAc oligomers Ni^2+^ Co^2+^ Zn^2+^ *Bb*BpsB *Bordetella bronchiseptica* **5BU6** (2015) \[[@B45-ijms-19-00412]\] Poly-β-1,6-GlcNAc de-*N*-acetylase β-1,6-GlcNAc oligomers Ni^2+^ Co^2+^ *Aa*PgaB *Aggregatibacter actinomycetemcomitans* **4U10** (2015) Poly-β-1,6-GlcNAc de-*N*-acetylase β-1,6-GlcNAc oligomers Zn^2+^ ^(1)^ Chitin DA: chitin deacetylase; GlcNAc DA: peptidoglycan *N*-acetylglucosamine deacetylase; MurNAc DA: peptidoglycan *N*-acetylmuramic deacetylase; PPda (unk): putative polysaccharide deacetylase (unknown); AXE: acetylxylan esterase; β-1,6-GlcNAc DA: poly-β-1,6-*N*-acetylglucosamine deacetylase. ^(2)^ 3D structure publication. ^(3)^ Activity on chitooligo-saccharides (β-1,4-linked GlcNAc oligomers) as a function of the degree of polymerization (DP). ^(4)^ Pattern of acetylation (PA). Structure of the main final deacetylated product. A: GlcNAc, D: GlcNH~2~. Other patterns of acetylation with specific substrates are given in the text. ^(5)^ n.r.: not reported. ^(6)^ No evidence for native metal, but indicated the metal from purification/crystallization experiments. ijms-19-00412-t002_Table 2 ###### Modular organization of domains in CE4 enzymes. Modular structures were defined using the Interpro database tools \[[@B149-ijms-19-00412]\]. Enzyme Uniprot AC \# aa FL ^1^ CE4 (aa) ^2^ Modular Structure ------------------ ------------------ -------------- -------------- ----------------------------- *Mr*CDA CDA_AMYRO 421 151--349  *Cl*CDA Q6DWK3_COLLN 248 30--246  *An*CDA B3VD85_EMEND 249 44--245  *Pgt*CDA E3K3D7_PUCGT 269 38--236  *Pes*CDA A0A1L3THR9_9PEZI 298 27--236  *Pa*CDA B2AAQ0_PODAN 396 120--307  *Pc*CDA \-- 455 107--303  NodB NODB_RHIME 217 15--213  *Vc*CDA Q9KSH6_VIBCH 431 26--338  *Vp*CDA A6P4T5_VIBPH 427 28--326  *Ar*CE4 A0A2C8C1T7_9MICC 246 42--227  *Sp*PgdA Q8DP63_STRR6 463 264--454  *Sm*PgdA Q8DV82_STRMU 311 103--308  *Bc*Pgd BC1960 B9J460_BACCQ 275 68--266  *Er*Pgd C4ZEZ9_AGARV 496 290--482  *Bs*PdaA PDAA_BACSU 266 68--253  *Ba*Pda Q81Z49_BACAN 260 45--255  BC0361 Q81IM3_BACCR 360 195--360  BA0330 Q81ZD9_BACAN 360 195--360  BA0150 Q81VP2_BACAN 254 52--237  ECU11\_ YB51_ENCCU 254 26--210  *Sl*AxeA Q54413_STRLI 335 44--221  *Ct*Axe (*XynA*) O87119_CLOTM 683 477--655  *Ec*PgaB PGAB_ECOLI 672 65--349  *Ad*IcaB C9RCK9_AMMDK 280 67--280  *Bb*BpsB A0A058YIS5_BORBO 701 66--355  *Aa*PgaB A5HJW8_AGGAC 638 48--334  ^1^ Total number of amino acid residues in the full length protein. ^2^ Amino acid numbering for the CE4 catalytic domain.

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All relevant data are within the paper and its Supporting Information file. We have now included 4 supplementary databases in our revised manuscript. File S1 is a general database with demographic and clinical data. Files S2, S3, and S4 show the processed OCT-A data for the macular SCP, macular DCP, and peripapillary RCP. Introduction {#sec005} ============ Optical coherence tomography angiography (OCT-A) is a recent imaging modality that allows non-invasive, rapid, depth-resolved visualization of all the chorioretinal vascular layers. \[[@pone.0205773.ref001], [@pone.0205773.ref002]\] OCT-A devices use different algorithms, all of which are based on the assumption that erythrocytes in the blood vessels are the only moving structures within sequentially acquired B-scans and that they act as a natural motion contrast. Since its recent introduction, OCT-A has gained increased popularity and has been applied to a broad spectrum of disease. \[[@pone.0205773.ref003]\] En face OCT angiograms can be subjectively evaluated for presence of abnormalities, or can be further post-processed to obtain quantitative, objective metrics. Vessel density, defined as the percentage of the angiocube occupied by retinal vessels, has gained increasing popularity, and represents a promising imaging endpoint for future clinical trials. Its reliability, however, needs to be fully validated. \[[@pone.0205773.ref004]\] Previous studies demonstrated good intra- and inter-operator repeatability of vessel density for images acquired in the same location, with the same angiocube size, machine, and quantification algorithm. \[[@pone.0205773.ref005], [@pone.0205773.ref006]\] Vessel density results, however, can significantly differ among various devices and depend on angiocube size, scan location, signal strength. \[[@pone.0205773.ref005], [@pone.0205773.ref007]--[@pone.0205773.ref009]\] The reported thresholding algorithms employed to binarize OCT-A angiograms and calculate vessel density, are highly heterogeneous. Some instruments use their own proprietary software, these include Cirrus (AngioPlex software, Carl Zeiss Meditec, Inc., Dublin, CA, USA), \[[@pone.0205773.ref005], [@pone.0205773.ref010]\] AngioVue software (Optovue, Inc., Fremont, CA, USA), \[[@pone.0205773.ref011], [@pone.0205773.ref012]\] and RS -3000 Advance (Nidek, Gamagori, Japan). \[[@pone.0205773.ref006]\] In the majority of the studies, however, images are exported and post-processed with a variety of different thresholding methods, including fixed cutoffs, \[[@pone.0205773.ref013]--[@pone.0205773.ref015]\] dynamic cutoff (e.g., mean, \[[@pone.0205773.ref009], [@pone.0205773.ref016], [@pone.0205773.ref017]\] ImageJ \[National Institutes of Health, Bethesda, MD\] default algorithm, \[[@pone.0205773.ref018]\] Otsu's algorithm), \[[@pone.0205773.ref019], [@pone.0205773.ref020]\] prototype software, \[[@pone.0205773.ref021], [@pone.0205773.ref022]\] and more complex methods combining preprocessing filters and multilevel thresholds strategies. \[[@pone.0205773.ref023]--[@pone.0205773.ref026]\] It is still uncertain whether different algorithms lead to the same or, at least, similar results and findings from many studies could have been influenced by the algorithm utilized. The aims of this study were to compare macular and peripapillary vessel density values calculated with seven different binarization strategies, to calculate conversion formulas between the algorithms, and to compare their diagnostic performance in differentiating healthy subjects from patients affected by diabetic retinopathy (DR) and glaucoma. Material and methods {#sec006} ==================== Study design and patients {#sec007} ------------------------- One hundred thirty-two eyes of 84 subjects that had OCTA at the Glaucoma Unit, and Medical Retina and Imaging Unit of the Department of Ophthalmology, University Vita-Salute, San Raffaele Hospital, Milan, Italy, were retrospectively evaluated. The study was approved by the San Raffaele Hospital scientific committee, and it adheres to the recommendations of the Declaration of Helsinki. Informed written consent was obtained from all the subjects included. Electronic clinical records, SD-OCT (Cirrus HD-OCT 5000; Carl Zeiss Meditec, Inc.), and swept source (SS)-OCT-A (PLEX Elite 9000, Carl Zeiss Meditec, Inc., Dublin, CA, USA) images from healthy subjects, patients with DR, and patients with glaucoma were reviewed. General inclusion criteria were age ≥18 years old, refractive error between -6 and +3 diopters, and availability of structural OCT and 6x6 mm OCT-A scans with a signal strength ≥ 7. General exclusion criteria included previous ocular surgery other than uncomplicated cataract extraction and intraocular lens implantation performed \>6 months before enrollment, and artifacts on OCT-A images. Inclusion criteria specific to the DR group were: type 1 or 2 diabetes, and presence of diabetic retinopathy. Inclusion criteria specific to the glaucoma group were: (i) history of primary open-angle glaucoma; (ii) documented glaucoma damage at the optic disc; (iii) repeatable glaucomatous perimetric damage, defined as a glaucoma hemifield test (GHT) result outside normal limits, and a pattern standard deviation (PSD) with p value \<5% normal limits; or (iv) presence of a cluster of ≥3 adjacent points on the pattern deviation plot with a probability of \<5%, including at least 1 point having a probability \<1% on at least two consecutive standard achromatic visual fields; (v) peripapillary retinal nerve fiber layer (pRNFL) thickness with p \<5% in at least one quadrant. Presence of diseases other than DR and glaucoma, respectively, in the DR and glaucoma groups was also an exclusion criterion. Healthy subjects met the following inclusion criteria: (i) no history or evidence of any posterior segment disease; (ii) normal-appearing optic disc and retina on dilated fundus examination; (iii) normal foveal profile on the structural macular SD-OCT scan; (iv) average and quadrant pRNFL thickness within 99% confidence limits; and (v) at least one reliable normal visual field, defined as PSD within 95% confidence limits of the normative database, and a GHT results within normal limits. Structural SD-OCT measurements {#sec008} ------------------------------ The structural SD-OCT images consisted of the Optic Disc Cube 200x200, and Macular Cube 512x128 patterns. Control subjects and glaucoma patients had both scans, whereas diabetic patients had only the macular scan. The manufacturer's software was used to calculate the average pRNFL thickness and central macular thickness (CMT) values on the peripapillary and macular scans, respectively. SS-OCTA device and scanning protocol {#sec009} ------------------------------------ The SS-OCTA device (PLEX Elite 9000, Carl Zeiss Meditec, Inc., Dublin, CA, USA) uses a swept laser source with a central wavelength of 1040--1060 nm (980--1120 nm full bandwidth) and operates at 100,000 A-scans per second. The axial and transverse resolutions of the system are ∼6 μm and ∼20 μm in tissue, respectively. The OMAG algorithm, which is based on variations in both the intensity and phase information between sequential, co-registered B-scans, was used to generate an OCT-A image. \[[@pone.0205773.ref027], [@pone.0205773.ref028]\] The 6x6 mm angiocube consisted of 500x500 A-scans. En face images consist of a 1024x1024-pixel array with 5.9 μm spacing between pixels. For DR eyes, all scans were centered on the fovea and automated segmentation of the layers carried out to define superficial (SCP) and deep (DCP) capillary plexuses were reviewed. The device's projections removal algorithm was applied to DCP images. For the glaucoma group, scans were centered on the optic nerve; the segmentation algorithm defined the area between the inner limiting membrane and the outer boundary of the RNFL to isolate the peripapillary radial capillary plexus (RCP). Healthy subjects had both macular and peripapillary OCT-A angiograms. Anonymized raw files were downloaded from the Zeiss PLEX Elite 9000 instruments and uploaded in the Advanced Retina Imaging (ARI) network portal. En face angiograms were then exported in PNG (Portable Network Graphics) format. Quantitative analysis of OCT-A images {#sec010} ------------------------------------- Seven different threshold strategies were used to binarize en face angiograms and calculate vessel density. The algorithms included the Macular Density algorithm v 0.6.1 developed by Zeiss, a manual thresholding technique, three ImageJ autothresholding algorithm (i.e., mean, default, Otsu), a semiautomatic method using a fixed threshold, and a method combining preprocessing filters with multilevel threshold strategies. Besides the analysis performed with the Zeiss macular density algorithm, all the other ones were carried out using the ImageJ software v 1.51 (National Institutes of Health, Bethesda, MD). At the end of the binarization process, the ratio between the number of white pixels (i.e., vessels) and the number of total pixels was calculated to obtain the vessel density. [Fig 1](#pone.0205773.g001){ref-type="fig"} illustrates an example of binarization outcomes with the employed methods. {#pone.0205773.g001} ### ARI Zeiss macular density algorithm v 0.6.1 {#sec011} This is a prototype, proprietary algorithm that allows quantification of vascular density both at the SCP and DCP in the macular area. Two indices are generated: perfusion density and vessel density. The former is generated through image binarization, while the latter relies on a skeletonization process. In this manuscript, we included only the first index in our analysis since it is the one based on thresholding, as the other algorithms tested. Since the algorithm was developed for quantification of macular perfusion parameters, it was not used for measuring the peripapillary vasculature. Macular density algorithm was run directly in the ARI portal. ### Manual thresholding {#sec012} Three independent operators (AR, RS, FG) independently binarized all the images using a manual, semiautomatic method. Each image was opened twice in the ImageJ software: one was not processed and used as reference, the other was binarized using a manual threshold. Each operator arbitrary chose a cutoff for each image to obtain the best correspondence with the one used as reference. ### Mean, default, Otsu autothreshold algorithms {#sec013} Each image was loaded in the ImageJ software and processed using three different autothreshold algorithms: mean, default, and Otsu. Specification of these algorithms can be found online (<https://imagej.net/Auto_Threshold>). Briefly, the mean algorithm sets the mean level of grey in the image as cutoff. The default is a special method used by ImageJ software, which is a modification of the IsoData algorithm. The Otsu algorithm performs a two cluster-based binarization applying a threshold, which minimizes and maximizes the intra-class and inter-class variances, respectively. ### Fixed threshold {#sec014} In this scenario, the same cutoff was utilized for every image of the same plexus. The median level of gray of macular SCP, macular DCP, and peripapillary RCP of the control group was chosen as threshold value. For the macula centered images, we used "59" and "32" for the SCP and DCP, respectively. For the optic nerve centered images, a value of "74" was used as cutoff. ### Preprocessing filtering with multilevel thresholds strategies {#sec015} The method used was previously described. \[[@pone.0205773.ref023]\] Briefly, images were pre-processed using a top-white filter with a window size of 12 pixels. Then, the image was duplicated. One copy underwent binarization through the median auto local threshold; the other one was processed with a Hessian filter and binarized using a Huang autothreshold. The two binarized images were compared and only pixels positive with both methods were counted as vessels. Statistical analysis {#sec016} -------------------- Data were tested for normality with the Pearson-D'Agostino test. Differences for demographic and main clinical data across groups were evaluated with analysis of variance (ANOVA) and Kruskal-Wallis test, respectively for parametric and non-parametric variables, and Dunnet and Dunn tests were used as post-hoc tests to compare patients with glaucoma and DR groups to healthy subjects for parametric and non-parametric variables, respectively. Differences for categorical variables were assessed with the chi-square test. Differences between glaucoma patients and healthy subjects for VCDR and pRNFL were evaluated with the t-test and the Mann-Whitney test, respectively. Differences among the algorithms for vessel density values were evaluated with the repeated measures ANOVA or Friedman test for parametric and nonparametric variables, respectively. Pairwise comparisons were investigated with the Tukey test or Dunn's multiple comparisons as post-hoc tests for parametric and nonparametric data, respectively. Differences in vessel density between healthy and affected eyes at each plexus and with each method were investigated with a linear mixed effect model with presence of disease and age as fixed factors, and fellow eye as random factor. Inter-algorithm reliability and inter-operator reliability for manual threshold selection were evaluated with the intraclass correlation coefficient (ICC) and the 95% confidence interval (CI) based on a single rating, concordance, 2-way mixed effect model. Values of ICC between 0 and 0.5 indicate poor reliability, moderate reliability between 0.5 and 0.75, good reliability between 0.75 and 0.9, and excellent reliability above 0.9. \[[@pone.0205773.ref029]\] We used Bland-Altman analysis to evaluate inter-algorithm agreement and limits of agreement (LOA) were set at 1.96 standard deviations (SDs) as this gives the 95% CI. A structural equation model was used to generate calibration equations to quantify systemic bias between each pair of algorithms, and to elaborate conversion formulas from one method to another. Ability to discriminate affected eyes from healthy eyes at each plexus was evaluated with receiver operating characteristic (ROC) curves. ROC curves were estimated on a generalized linear model in order to adjust for age, and eyes of the same patients were considered as clustered to account for correlations between eyes. \[[@pone.0205773.ref030]\] Area under the curve (AUROC) values and 95% confidence intervals were calculated. AUROCs of 0.5 and 1 represent lack of and perfect discrimination, respectively. Pairs of ROC curves were compared with the DeLong's test. All statistical analyses were performed with R software (R Foundation for Statistical Computing, Vienna, Austria, <https://www.r-project.org>), GraphPad Prism software 6.0 (GraphPad Software, Inc., San Diego, CA, USA), and SPSS software 21 (SPSS Inc., Chicago, IL, USA). A p-value \<0.05, after adjustments with the Benjamini-Hochberg test, was considered significant. Results {#sec017} ======= [Table 1](#pone.0205773.t001){ref-type="table"} summarizes the demographic and main clinical data of the cohort of patients. Patients in the glaucoma groups were significantly older than those in control group (p = 0.008), and they had increased VCDR (p \<0.0001) and reduced pRNFL thickness (\<0.0001). Patients with DR had significantly greater CMT compared with controls (p = 0.001), and 18 eyes (40.9%) featured diabetic macular edema. In the DR group, 28 and 3 patients suffered from type 1 and 2 diabetes, respectively, with a mean hemoglobin A1c of 6.9 ± 1.1%. Severity of DR was mild in 1 eye, moderate in 6 eyes, severe in 8 eyes, proliferative in 28 eyes, and unknown in 1 eye. 10.1371/journal.pone.0205773.t001 ###### Demographic and main clinical data of study population. {#pone.0205773.t001g} Parameters Overall Controls DR p-value Glaucoma p-value ---------------------- -------------------------------------------------- -------------- -------------- ------------ -------------- --------------- No. Patients / Eyes 132 / 84 27 / 44 31 / 44 n/a 26 / 44 n/a Age years, mean ± SD 54.2 ± 16.2 47.7 ± 17.9 54.6 ± 15.4 0.17 60.5 ± 13.1 **0.008** Race, caucasian 84 27 31 n/a 26 n/a Sex, male / female 37/ 47 15 / 12 11 / 20 0.79 11 / 15 0.63 Eye, right / left 63 / 69 22 / 22 20 / 24 0.91 21 / 23 0.98 CMT, μm, mean ± SD 282.9 ± 57.8 265.8 ± 21.8 310.0 ± 82.9 **0.0014** 268.2 ± 29.0 0.99 VCDR, mean ± SD 0.61 ± 0.17[\*](#t001fn001){ref-type="table-fn"} 0.52 ± 0.17 n/a n/a 0.70 ± 0.13 **\< 0.0001** pRNFL, μm, mean ± SD 81.6 ± 13.8[\*](#t001fn001){ref-type="table-fn"} 88.8 ± 10.9 n/a n/a 74.5 ± 12.6 **\< 0.0001** \*This value does not include eyes belonging to DR group. BCVA: best corrected visual acuity; CMT: central macular thickness; DR: diabetic retinopathy; SD: standard deviation; CMT: central macular thickness; VCDR: vertical cup-to-disc ratio; pRNFL: peripapillary retinal nerve fiber layer. [Fig 2](#pone.0205773.g002){ref-type="fig"} and [Table 2](#pone.0205773.t002){ref-type="table"} show the macular SCP, DCP and peripapillary RCP vessel density values estimated with the different methods. Healthy eyes exhibited higher vessel density values at all plexuses compared with eyes with disease regardless the algorithm used (p \< 0.01). No significant difference between diabetic eyes with and without DME estimated with every method at both SCP and DCP was found (p-value \> 0.31). Vessel density values were significantly different among the different methods at all the plexuses (p \< 0.0001). All the pairwise comparisons for the macular SCP ([Table 3](#pone.0205773.t003){ref-type="table"}) were significant (p \< 0.05), except for the pairs ARI and mean (p = 0.99), ARI and fixed (p = 0.70), mean and fixed (p = 0.10), and Otsu and multilevel (p = 0.20). At the macular DCP level ([Table 4](#pone.0205773.t004){ref-type="table"}), all the pairwise comparisons were significant (p\< 0.01), except for the pairs ARI and multilevel (p = 0.99), manual and default (0.99), manual and Otsu (p = 0.13), manual and fixed (p = 0.49), Otsu and fixed (0.99). At the peripapillary RCP level ([Table 5](#pone.0205773.t005){ref-type="table"}), all pairs had significantly different vessel density values (p \< 0.001), except for manual and mean (p = 0.08), mean and default (p = 0.99), and Otsu and multilevel (p = 0.99). {#pone.0205773.g002} 10.1371/journal.pone.0205773.t002 ###### Vessel density values estimated with the different methods. {#pone.0205773.t002g} Macula---superficial capillary plexus Macula---deep capillary plexus ONH---radial peripapillary capillary plexus ---------------- --------------------------------------- -------------------------------- --------------------------------------------- ------------- ------------ ------------- ------------ ------------ ------------ **ARI** 43.9 ± 4.1 41.6 ± 3.7 46.2 ± 3.0 26.2 ± 7.6 20.8 ± 6.0 31.7 ± 4.5 n/a n/a n/a **Manual** 48.6 ± 4.4 45.5 ± 4.1 51.6 ± 1.9 37.1 ± 9.0 29.4 ± 5.2 44.9 ± 3.7 49.6 ± 3.7 47.3 ± 3.5 51.8 ± 2.2 **Mean** 44.9 ± 1.7 43.9 ± 1.9 45.9 ± 0.8 44.3 ± 2.7 42.2 ± 2.0 46.4 ± 1.2 48.0 ± 2.1 46.7 ± 2.2 49.3 ± 0.9 **Default** 39.1 ± 3.6 37.1 ± 3.6 41.1 ± 2.2 38.6 ± 6.6 33.0 ± 4.3 44.2 ± 2.5 46.4 ± 5.2 43.4 ± 5.4 49.5 ± 2.5 **Otsu** 37.3 ± 3.3 35.8 ± 3.5 38.8 ± 2.2 35.5 ± 6.2 30.3 ± 4.3 40.7 ± 2.0 45.0 ± 5.1 41.9 ± 5.2 48.1 ± 2.5 **Fixed** 42.5 ± 8.3 37.5 ± 8.0 47.5 ± 4.9 33.3 ± 10.9 30.3 ± 8.1 36.3 ± 12.6 43.4 ± 9.2 37.1 ± 7.2 49.7 ± 6.1 **Multilevel** 34.5 ± 1.3 33.9 ± 1.5 35.1 ± 0.7 27.4 ± 9.6 22.9 ± 0.7 31.9 ± 12.1 40.0 ± 1.5 39.3 ± 1.5 40.8 ± 1.0 Data are presented as mean ± standard deviation. DR: diabetic retinopathy; ONH: optic nerve head. 10.1371/journal.pone.0205773.t003 ###### Inter-algorithm agreement, reliability, and pairwise comparison in the superficial capillary plexus for the entire cohort of patients. {#pone.0205773.t003g} -------------------------------------------------------------------------------------------------------------------------------------- Algorithm comparison Agreement\ Reliability Pairwise comparison (Bland Altman Analysis) ---------------------- ------------------------- ------------- --------------------- ------ -------------------------- --------------- ARI Manual -4.6 -11.4/2.1 13.5 0.674 (0.542--0.774) **\< 0.0001** ARI Mean -1.0 -6.8/4.8 11.6 0.556 (0.393--0.685) 0.99 ARI Default 4.8 0.1/9.6 9.5 **0.800 (0.710--0.864)** **\< 0.0001** ARI Otsu 6.7 1.7/11.6 9.9 **0.768 (0.667--0.842)** **\< 0.0001** ARI Fixed 1.4 -9.6/12.5 22.1 0.625 (0.479--0.378) 0.70 ARI Multilevel 9.4 3.1/15.8 12.7 0.428 (0.241--0.584) **\< 0.0001** Manual Mean 3.7 -2.6/9.9 12.5 0.552 (0.389--0.682) **0.0012** Manual Default 9.5 4.0/15.0 11.0 **0.756 (0.650--0.833)** **\< 0.0001** Manual Otsu 11.3 5.0/17.6 12.6 0.654 (0.516--0.759) **\< 0.0001** Manual Fixed 6.1 -5.3/17.4 22.7 0.620 (0.472--0.733) **\< 0.0001** Manual Multilevel 14.1 7.0/21.1 14.1 0.393 (0.201--0.556) **\< 0.0001** Mean Default 5.8 2.0/9.7 7.9 **0.760 (0.655--0.836)** **\< 0.0001** Mean Otsu 7.6 4.2/11.1 6.9 **0.775 (0.676--0.847)** **\< 0.0001** Mean Fixed 2.4 -10.9/15.8 26.7 0.351 (0.154--0.521) 0.10 Mean Multilevel 10.4 8.6/12.2 3.6 **0.830 (0.751--0.885)** **\< 0.0001** Default Otsu 1.8 0.3/3.3 3.0 **0.976 (0.963--0.984)** **0.0109** Default Fixed -3.4 -13.7/6.9 20.6 0.663 (0.527--0.765) **0.0220** Default Multilevel 4.6 -0.4/9.6 10.0 0.562 (0.400--0.690) **\< 0.0001** Otsu Fixed -5.2 -16.2/5.8 22.0 0.602 (0.449--0.720) **\< 0.0001** Otsu Multilevel 2.8 -1.7/7.2 8.9 0.585 (0.429--0.708) 0.20 Fixed Multilevel 8.0 -6.1/22.2 28.3 0.257 (0.051--0.441) **\< 0.0001** -------------------------------------------------------------------------------------------------------------------------------------- MD: mean difference; LoA: limits of agreement; ICC: intraclass correlation coefficient; CI: confidence interval 10.1371/journal.pone.0205773.t004 ###### Inter-algorithm agreement, reliability, and pairwise comparison in the deep capillary plexus for the entire cohort of patients. {#pone.0205773.t004g} -------------------------------------------------------------------------------------------------------------------------------------- Algorithm comparison Agreement\ Reliability Pairwise comparison (Bland Altman Analysis) ---------------------- ------------------------- ------------- --------------------- ------ -------------------------- --------------- ARI Manual -10.9 -23.8/1.9 25.7 0.689 (0.561--0.784) **\< 0.0001** ARI Mean -18.0 -29.1/-6.9 22.2 0.502 (0.328--0.643) **\< 0.0001** ARI Default -12.4 -21.1/-3.6 17.5 **0.804 (0.715--0.867)** **\< 0.0001** ARI Otsu -9.3 -17.9/-0.7 17.2 **0.799 (0.709--0.864)** **\< 0.0001** ARI Fixed -7.1 -24.7/10.6 35.3 0.540 (0.373--0.673) **\< 0.0001** ARI Multilevel -1.2 -19.8/17.5 37.3 0.397 (0.205--0.559) 0.99 Manual Mean -7.1 -20.8/6.5 27.3 0.445 (0.260--0.598) **\< 0.0001** Manual Default -1.4 -10.2/7.2 17.4 **0.842 (0.768--0.894)** 0.99 Manual Otsu 1.6 -7.3/10.5 17.8 **0.827 (0.748--0.883)** 0.13 Manual Fixed 3.8 -19.8/27.5 47.3 0.274 (0.069--0.456) 0.49 Manual Multilevel 9.8 -8.0/27.5 35.5 0.525 (0.356--0.611) **\< 0.0001** Mean Default 5.7 -2.5/13.8 16.3 0.662 (0.527--0.765) **0.0021** Mean Otsu 8.7 1.4/16.0 14.6 0.693 (0.566--0.788) **\< 0.0001** Mean Fixed 11.0 -8.7/30.6 39.3 0.205 (-0.003--0.397) **\< 0.0001** Mean Multilevel 16.9 -0.3/34.1 34.4 0.225 (0.017--0.414) **\< 0.0001** Default Otsu 3.1 0.4/5.7 5.3 **0.978 (0.966--0.985)** **\< 0.0001** Default Fixed 5.3 -14.3/24.9 39.2 0.388 (0.195--0.552) **0.0008** Default Multilevel 11.2 -6.1/28.5 34.6 0.430 (0.243--0.586) **\< 0.0001** Otsu Fixed 2.3 -16.9/21.3 38.2 0.398 (0.206--0.560) 0.99 Otsu Multilevel 8.2 -9.1/25.4 34.5 0.408 (0.219--0.568) **0.0002** Fixed Multilevel 5.9 -27.9/39.8 67.7 -0.409 (-0.569 ---0.219) **\< 0.0001** -------------------------------------------------------------------------------------------------------------------------------------- MD: mean difference; LoA: limits of agreement; ICC: intraclass correlation coefficient; CI: confidence interval 10.1371/journal.pone.0205773.t005 ###### Inter-algorithm agreement, reliability, and pairwise comparison in the peripapillary radial capillary plexus for the entire cohort of patients. {#pone.0205773.t005g} -------------------------------------------------------------------------------------------------------------------------------------- Algorithm comparison Agreement\ Reliability Pairwise comparison (Bland Altman Analysis) ---------------------- ------------------------- ------------- --------------------- ------ -------------------------- --------------- Manual Mean 1.6 -3.2/6.3 9.5 0.672 (0.539--0.772) 0.08 Manual Default 3.2 -3.6/9.9 13.5 0.709 (0.588--0.800) **0.0005** Manual Otsu 4.6 -2.0/11.1 13.1 0.718 (0.599--0.806) **\< 0.0001** Manual Fixed 6.2 -7.3/19.7 27.0 0.518 (0.347--0.656) **\< 0.0001** Manual Multilevel 9.6 3.7/15.4 11.7 0.439 (0.254--0.593) **\< 0.0001** Mean Default 1.6 -4.5/7.7 12.2 0.690 (0.563--0.786) 0.99 Mean Otsu 3.0 -3.0/9.0 12.0 0.693 (0.567--0.788) **\< 0.0001** Mean Fixed 4.6 -9.8/19.0 28.8 0.390 (0.198--0.554) **\< 0.0001** Mean Multilevel 8.0 5.7/10.3 4.6 **0.789 (0.694--0.856)** **\< 0.0001** Default Otsu 1.4 0.3/2.5 2.2 **0.994 (0.991--0.996)** **\< 0.0001** Default Fixed 3.0 -7.0/13.1 20.1 **0.765 (0.662--0.840)** **\< 0.0001** Default Multilevel 6.4 -1.5/14.3 15.8 0.442 (0.257--0.596) **\< 0.0001** Otsu Fixed 1.6 -8.4/11.6 20.0 **0.764 (0.661--0.839)** 0.99 Otsu Multilevel 5.0 -2.7/12.7 15.4 0.452 (0.269--0.603) **0.0006** Fixed Multilevel 3.4 -12.5/19.2 31.7 0.246 (0.039--0.432) **\< 0.0001** -------------------------------------------------------------------------------------------------------------------------------------- MD: mean difference; LoA: limits of agreement; ICC: intraclass correlation coefficient; CI: confidence interval Inter-algorithm ICC values of the SCP, DCP, and RCP are illustrated in Tables [3](#pone.0205773.t003){ref-type="table"}, [4](#pone.0205773.t004){ref-type="table"} and [5](#pone.0205773.t005){ref-type="table"}, respectively. Default and Otsu algorithms had an excellent reliability at every plexus. Reliability of ARI algorithm was good when compared with default and Otsu methods. At the SCP, a good reliability was observed also for the pairs mean and default, mean and Otsu, and mean and multilevel. At the DCP, the manual algorithm had a good reliability in comparison with both default and Otsu methods. The pairs mean and multilevel, default and fixed, and Otsu and fixed had a good reliability at the peripapillary RCP. All the other pairs exhibited a moderate to poor reliability. Notably, fixed and multilevel had a negative ICC at the DCP since their vessel density values were negatively correlated. Results of Bland-Altman analysis for the inter-method agreement of the SCP, DCP, and RCP are also displayed in Tables [3](#pone.0205773.t003){ref-type="table"}, [4](#pone.0205773.t004){ref-type="table"} and [5](#pone.0205773.t005){ref-type="table"}, respectively. Limits of agreement and mean differences were wider in the DCP, indicating a lower level of agreement between methods for this plexus. Otsu and default algorithms exhibited an excellent agreement. On the contrary, the fixed algorithm had a poor agreement with all the other methods. As shown in [Fig 3](#pone.0205773.g003){ref-type="fig"}, the inter-operator reliability for the manual method was moderate for the DCP overall and in the subset of patients with DR, and poor for all the other groups. Vessel density values were significantly different between each pair of operator, except the comparison between operator 1 and 2 at the DCP for the cohort of all patients, and between operator 3 and both operators 1 and 2 for the DCP of the patients with DR. {#pone.0205773.g003} [Table 6](#pone.0205773.t006){ref-type="table"} displays the calibration equations for the methods. The conversion formula from one instrument to another was available for all the tested algorithms, except for the conversion from multilevel to fixed (and vice versa) at the DCP since observed values measured by these two algorithms were negatively correlated. Notably, the default and Otsu algorithms at the peripapillary RCP had almost no bias, and a small bias at the other plexuses, meaning that the systematic error between these two algorithms is extremely low. A substantial bias was evident between many algorithms. The comparative plots for the SCP, DCP, and peripapillary RCP are graphically shown in Figs [4](#pone.0205773.g004){ref-type="fig"}, [5](#pone.0205773.g005){ref-type="fig"} and [6](#pone.0205773.g006){ref-type="fig"}, respectively. {#pone.0205773.g004} {#pone.0205773.g005} {#pone.0205773.g006} 10.1371/journal.pone.0205773.t006 ###### Calibration equations to convert vessel density value from one algorithm into the equivalent from another algorithm. {#pone.0205773.t006g} Algorithm Calibration equation ------------ ----------------------------------------------------------------- ---------------------------------------------------------------- ----------------------------------------------------------------- ARI -2.86 + 0.96 [\*](#t006fn001){ref-type="table-fn"} Manual -9.68 + 0.97 [\*](#t006fn001){ref-type="table-fn"} Manual n/a -45.51 + 1.99 [\*](#t006fn001){ref-type="table-fn"} Mean -93.05 + 2.70 [\*](#t006fn001){ref-type="table-fn"} Mean n/a 6.76 + 0.95 [\*](#t006fn001){ref-type="table-fn"} Default -14.45 + 1.05 [\*](#t006fn001){ref-type="table-fn"} Default n/a 3.02 + 1.10 [\*](#t006fn001){ref-type="table-fn"} Otsu -13.34 + 1.11 [\*](#t006fn001){ref-type="table-fn"} Otsu n/a 25.11 + 0.44 [\*](#t006fn001){ref-type="table-fn"} Fixed -19.04 + 1.36 [\*](#t006fn001){ref-type="table-fn"} Fixed n/a -53.29 + 2.88 [\*](#t006fn001){ref-type="table-fn"} Multilevel -10.49 + 1.34 [\*](#t006fn001){ref-type="table-fn"} Multilevel n/a Manual 2.97 + 1.04 [\*](#t006fn001){ref-type="table-fn"} ARI 10.01 + 1.03 [\*](#t006fn001){ref-type="table-fn"} ARI n/a -44.27 + 2.07 [\*](#t006fn001){ref-type="table-fn"} Mean -86.21 + 2.79 [\*](#t006fn001){ref-type="table-fn"} Mean -15.83 + 1.36 [\*](#t006fn001){ref-type="table-fn"} Mean 9.99 + 0.99 [\*](#t006fn001){ref-type="table-fn"} Default -4.93 + 1.09 [\*](#t006fn001){ref-type="table-fn"} Default 23.58 + 0.56 [\*](#t006fn001){ref-type="table-fn"} Default 6.11 + 1.14 [\*](#t006fn001){ref-type="table-fn"} Otsu -3.78 + 1.15 [\*](#t006fn001){ref-type="table-fn"} Otsu 24.13 + 0.57 [\*](#t006fn001){ref-type="table-fn"} Otsu 35.46 + 0.22 [\*](#t006fn001){ref-type="table-fn"} Fixed -9.68 + 1.41 [\*](#t006fn001){ref-type="table-fn"}Fixed 34.94 + 0.34 [\*](#t006fn001){ref-type="table-fn"} Fixed -54.42 + 2.99 [\*](#t006fn001){ref-type="table-fn"} Multilevel -11.66 + 1.77 [\*](#t006fn001){ref-type="table-fn"} Multilevel -41.82 + 2.28 [\*](#t006fn001){ref-type="table-fn"} Multilevel Mean 21.42 + 0.48 [\*](#t006fn001){ref-type="table-fn"} ARI 34.53 + 0.37 [\*](#t006fn001){ref-type="table-fn"} ARI n/a 21.16 + 0.49 [\*](#t006fn001){ref-type="table-fn"} Manual 31.11 + 0.36 [\*](#t006fn001){ref-type="table-fn"} Manual 11.62 + 0.73 [\*](#t006fn001){ref-type="table-fn"} Manual 26.25 + 0.48 [\*](#t006fn001){ref-type="table-fn"} Default 29.17 + 0.39 [\*](#t006fn001){ref-type="table-fn"} Default 28.93 + 0.41 [\*](#t006fn001){ref-type="table-fn"} Default 24.37 + 0.55 [\*](#t006fn001){ref-type="table-fn"} Otsu 29.58 + 0.41 [\*](#t006fn001){ref-type="table-fn"} Otsu 29.3 + 0.42 [\*](#t006fn001){ref-type="table-fn"} Otsu 35.21 + 0.23 [\*](#t006fn001){ref-type="table-fn"} Fixed 27.46 + 0.51 [\*](#t006fn001){ref-type="table-fn"} Fixed 32.27 + 0.25 [\*](#t006fn001){ref-type="table-fn"} Fixed -4.91 + 1.45 [\*](#t006fn001){ref-type="table-fn"} Multilevel 29.44 + 0.54 [\*](#t006fn001){ref-type="table-fn"} Multilevel -19.08 + 1.68 [\*](#t006fn001){ref-type="table-fn"} Multilevel Default -7.10 + 1.05 [\*](#t006fn001){ref-type="table-fn"} ARI 13.71 + 0.95 [\*](#t006fn001){ref-type="table-fn"} ARI n/a -10.12 + 1.01 [\*](#t006fn001){ref-type="table-fn"} Manual 4.52 + 0.92 [\*](#t006fn001){ref-type="table-fn"} Manual -42.10 + 1.79 [\*](#t006fn001){ref-type="table-fn"} Manual -54.97 + 2.09 [\*](#t006fn001){ref-type="table-fn"} Mean -74.55 + 2.56 [\*](#t006fn001){ref-type="table-fn"} Mean -70.36 + 2.43 [\*](#t006fn001){ref-type="table-fn"} Mean -3.93 + 1.15 [\*](#t006fn001){ref-type="table-fn"} Otsu 1.05 + 1.06 [\*](#t006fn001){ref-type="table-fn"} Otsu 0.98 + 1.01 [\*](#t006fn001){ref-type="table-fn"} Otsu 19.30 + 0.47 [\*](#t006fn001){ref-type="table-fn"} Fixed -4.36 + 1.29 [\*](#t006fn001){ref-type="table-fn"} Fixed 20.29 + 0.60 [\*](#t006fn001){ref-type="table-fn"} Fixed -65.25 + 3.03 [\*](#t006fn001){ref-type="table-fn"}Multilevel 0.06 + 1.40 [\*](#t006fn001){ref-type="table-fn"} Multilevel -116.76 + 4.08 [\*](#t006fn001){ref-type="table-fn"}Multilevel Otsu -2.75 + 0.91 [\*](#t006fn001){ref-type="table-fn"} ARI 11.98 + 0.90 [\*](#t006fn001){ref-type="table-fn"} ARI n/a -5.36 + 0.88 [\*](#t006fn001){ref-type="table-fn"} Manual 3.29 + 0.87 [\*](#t006fn001){ref-type="table-fn"} Manual -42.65 + 1.77 [\*](#t006fn001){ref-type="table-fn"} Manual -44.23 + 1.82 [\*](#t006fn001){ref-type="table-fn"} Mean -71.59 + 2.42 [\*](#t006fn001){ref-type="table-fn"} Mean -70.62 + 2.41 [\*](#t006fn001){ref-type="table-fn"} Mean 3.41 + 0.87 [\*](#t006fn001){ref-type="table-fn"} Default -1.00 + 0.95 [\*](#t006fn001){ref-type="table-fn"} Default -0.97 + 0.99 [\*](#t006fn001){ref-type="table-fn"} Default 20.13 + 0.40 [\*](#t006fn001){ref-type="table-fn"} Fixed -5.12 + 1.22 [\*](#t006fn001){ref-type="table-fn"} Fixed 19.12 + 0.60 [\*](#t006fn001){ref-type="table-fn"} Fixed -53.14 + 2.62 [\*](#t006fn001){ref-type="table-fn"} Multilevel -0.22 + 1.30 [\*](#t006fn001){ref-type="table-fn"} Multilevel -116.57 + 4.04 [\*](#t006fn001){ref-type="table-fn"} Multilevel Fixed -56.71 + 2.26 [\*](#t006fn001){ref-type="table-fn"} ARI 14.00 + 0.74 [\*](#t006fn001){ref-type="table-fn"} ARI n/a -63.18 + 2.18 [\*](#t006fn001){ref-type="table-fn"} Manual 6.88 + 0.71 [\*](#t006fn001){ref-type="table-fn"}Manual -130.58 + 2.96 [\*](#t006fn001){ref-type="table-fn"} Manual -159.50 + 4.50 [\*](#t006fn001){ref-type="table-fn"} Mean -54.42 + 1.98 [\*](#t006fn001){ref-type="table-fn"} Mean -150.49 + 4.04 [\*](#t006fn001){ref-type="table-fn"} Mean -41.45 + 2.15 [\*](#t006fn001){ref-type="table-fn"} Default 3.38 + 0.78 [\*](#t006fn001){ref-type="table-fn"} Default -33.69 + 1.66 [\*](#t006fn001){ref-type="table-fn"} Default -49.89 + 2.48 Otsu 4.19 + 0.82 [\*](#t006fn001){ref-type="table-fn"} Otsu -32.06 + 1.68 [\*](#t006fn001){ref-type="table-fn"} Otsu -181.59 + 6.50 [\*](#t006fn001){ref-type="table-fn"} Multilevel n/a[\*](#t006fn001){ref-type="table-fn"} -227.53 + 6.77 [\*](#t006fn001){ref-type="table-fn"} Multilevel Multilevel 19.22 + 0.35 [\*](#t006fn001){ref-type="table-fn"} ARI -7.86 + 0.75 [\*](#t006fn001){ref-type="table-fn"} ARI n/a 18.22 + 0.34 [\*](#t006fn001){ref-type="table-fn"} Manual 6.58 + 0.56 [\*](#t006fn001){ref-type="table-fn"} Manual 18.31 + 0.44 [\*](#t006fn001){ref-type="table-fn"} Manual 3.40 + 0.69 [\*](#t006fn001){ref-type="table-fn"} Mean -54.65 + 1.86 [\*](#t006fn001){ref-type="table-fn"} Mean 11.38 + 0.60 [\*](#t006fn001){ref-type="table-fn"} Mean 21.57 + 0.33 [\*](#t006fn001){ref-type="table-fn"} Default -0.04 + 0.71 [\*](#t006fn001){ref-type="table-fn"} Default 28.64 + 0.25 [\*](#t006fn001){ref-type="table-fn"} Default 20.27 + 0.38 [\*](#t006fn001){ref-type="table-fn"} Otsu 0.17 + 0.77 [\*](#t006fn001){ref-type="table-fn"} Otsu 28.88 + 0.25 [\*](#t006fn001){ref-type="table-fn"} Otsu 27.95 + 0.15 [\*](#t006fn001){ref-type="table-fn"} Fixed n/a[\*](#t006fn001){ref-type="table-fn"} 33.61 + 0.15 [\*](#t006fn001){ref-type="table-fn"} Fixed \* Calibration equation not available since fixed and multilevel algorithms were negative correlated at the DCP. SCP: superficial capillary plexus; DCP: deep capillary plexus; RPC: radial peripapillary capillaries. ROC curves for the identification of patients with DR (macular SCP, DCP) and glaucoma (peripapillary RCP) are illustrated in [Fig 7](#pone.0205773.g007){ref-type="fig"}. At the SCP level, ARI and manual algorithms performed better (p \< 0.05) than all the other methods, but they did not significantly differ each other (p = 0.6). At the DCP level, the manual, Otsu, mean, and default algorithms had higher AUROCs than other methods, and the difference was significant (p \<0.05) except for the pair mean and ARI (p = 0.1). At the ONH level, the fixed algorithm had the best performance to distinguish glaucomatous patients from healthy subjects, although the difference was significant only in comparison with multilevel (p = 0.029). {#pone.0205773.g007} Discussion {#sec018} ========== In the present study, we compared seven different methods to calculate vessel density on OCT-A angiograms in the macular and peripapillary areas in healthy subjects, and in patients with either DR or glaucoma. Methods tested included the ARI Zeiss proprietary algorithm v 0.6.1, a manual method, a static algorithm using the same fixed threshold for all eyes, three dynamic autothresholds (i.e., mean, default, Otsu) adapting their values in relationship to image properties, and a more complex algorithm employing a preprocessing filter followed by a multilevel thresholding strategy. We evaluated the inter-algorithm differences, reliability, and agreement. Moreover, we provided a calibration between algorithms to generate conversion formulas from one method to another. Finally, we investigated the ability of the algorithms to identify differences in vessel densities between healthy subject and patients with DR or glaucoma, and we compared their diagnostic performance. Since its commercialization, OCT-A has gained increasing popularity in the ophthalmic community. The capability to image the retinal and choroidal vasculatures in non-invasive, fast, three-dimensional, depth-resolved fashion represents a considerable advantage of this technique over the traditional, dye-based diagnostic tests. Inspection of OCT-A angiograms may be of great help for the clinician in the diagnostic process. Identification of choroidal neovascularization in an asymptomatic patient with "dry" AMD or in a patient suffering from central serous chorioretinopathy are two examples where this new technology has a significant, clinical impact. OCT-A angiograms can be post-processed to obtain quantitative, objective measurements. Two established indices are the vessel density and, specific to the macular region, the fovea avascular zone (FAZ) area. The latter is a capillary-free zone corresponding to the foveola, while the former is the percentage of angiocube occupied by retinal vessels. A number of studies investigated changes in such indices in various ocular pathologies and their relationship with disease severity, activity, and response to treatments in several chorioretinal diseases, including diabetic retinopathy, \[[@pone.0205773.ref031], [@pone.0205773.ref032]\] retinal vein occlusion, \[[@pone.0205773.ref033]\] age-related macular degeneration, \[[@pone.0205773.ref011], [@pone.0205773.ref034]\] and retinal dystrophies. \[[@pone.0205773.ref013]--[@pone.0205773.ref015], [@pone.0205773.ref017]\] Vessel density applications are not limited to the retinal field, and are also useful in optic nerve diseases such as glaucoma \[[@pone.0205773.ref010], [@pone.0205773.ref022]\] and anterior ischemic optic neuropathy. \[[@pone.0205773.ref012]\] According to Cole et al., \[[@pone.0205773.ref004]\] vessel density could become a future surrogate endpoint for clinical trials. In a recent commentary, however, Garrity and Sarraf \[[@pone.0205773.ref035]\] claimed the need of additional technical and clinical research to fully elucidate properties and reliability of quantitative indices before their application in research trials and clinical practice. There is substantial evidence that the intra- and inter-operator repeatability of vessel density is good for images acquired in the same location, with the same angiocube size, machine, and quantification algorithm. \[[@pone.0205773.ref005], [@pone.0205773.ref006], [@pone.0205773.ref036]\] Nevertheless, some other factors both in the acquisition and in the post-processing phase can negatively affect its reliability. Some retinal diseases, such as cystoid macular edema, can profoundly disorganize the retinal architecture leading to inaccurate and unreliable results. \[[@pone.0205773.ref035]\] Low signal strength is correlated with lower vessel density, and this should be considered in patients with cataract or ocular surface disease. \[[@pone.0205773.ref005]\] Corvi et al \[[@pone.0205773.ref007]\] evaluated the reliability of quantitative indices, including vessel density, measured with seven different instruments in a cohort of healthy patients, and they found a poor reliability among the tested devices. These results are not surprisingly since different instruments have varying properties, including wavelength of laser beam, number of A-scans, algorithm used to detect flow, segmentation boundaries, and image resolution. In a previous study, we demonstrated that vessel density significantly differs across different angiocubes sizes since wider images are characterized by lower resolution compared to smaller, denser, scans. \[[@pone.0205773.ref009]\] Uji and colleagues \[[@pone.0205773.ref023], [@pone.0205773.ref037]\] evaluated the impact of multiple *en face* angiograms averaging, and found that it increases the image quality and impacts on the quantitative measurements reducing the variability. Only one study has provided some information about the impact of different post-processing imaging. Pedinielli et al \[[@pone.0205773.ref038]\] observed that the same image may lead to different macular vessel density values if quantified by means of skeletonization, mean thresholding, or proprietary AngioVue software (Optovue, Inc., Fremont, CA, USA). Differences between vessel density obtained by means of skeletonization and thresholding were predictable since they measure different units. Skeletonization does not take into account the vessel dimension and treats all the vessels in the same way irrespective to their size, so it minimizes the impact of large retinal vessels over the capillary network. On the contrary, image thresholding reveals the real percentage of retinal vasculature. Our results partially corroborate and expand the previous findings. Differences among methods were highly significant, and reliability and agreement values were mostly poor to moderate, with few exceptions. Differences were highest at the macular DCP with Manual, Default, Otsu, and fixed showing less differences, while ARI and Mean appear to report notably lower and higher values, respectively. The calibration equations revealed that systematic differences between algorithms were pretty consistent, and most of them exhibited a non-constant bias. A conversion formula was present for all the algorithms except for multilevel and fixed thresholds at the DCP. These two algorithms displayed very poor reliability and agreement, and, in the DCP, they surprisingly exhibited a negative correlation meaning that studies based on these algorithms may potentially lead to opposite results. On the other hand, we appreciated an excellent reliability and agreement between Otsu and default algorithms. These two methods demonstrated a small systemic bias for the macular area and, notably, no bias in the peripapillary area, suggesting that values derived from these algorithms are almost interchangeable. Conversion formulas provide a method to convert values from one algorithm to another, and, theoretically, longitudinal monitoring could be performed with images processed with different algorithms. However, most of the most methods exhibited a substantial, non-costant bias. Performance of these formulas should be validated in a different larger dataset before one may confidently switch from one algorithm to another during the follow-up. In the light of these considerations, we suggest to use the same algorithm in the longitudinal follow-up since processing methods are not directly interchangeable. Several authors have conducted studies on large cohorts of healthy subjects to build normative databases for quantitative metrics, including vessel density. Coscas et al \[[@pone.0205773.ref039]\] were the first group to provide macular vessel density values in a Caucasian population. Iafe et al \[[@pone.0205773.ref040]\] also reported vessel density values in 70 healthy subjects, and Garrity et al \[[@pone.0205773.ref041]\] reported results of repeated analyses on the same cohort of patients updating the previous results based on more sophisticated software enabling projection removal and improvement of the segmentation algorithm with isolation of the intermediate capillary plexus. Bazvand et al \[[@pone.0205773.ref042]\] published a normative quantitative database for the papillary and peripapillary area. Other studies provided macular vessel density values in different populations (i.e., in Asia, Middle-East), and in pediatric subjects. \[[@pone.0205773.ref043]--[@pone.0205773.ref045]\] The results of these studies should be interpreted with extreme caution, and are not generalizable since vessel density values are dependent on the device, angiocube size, image averaging, and, as shown here, post-processing algorithm employed. Although not formally demonstrated in the present study, the updates of the proprietary software released by manufacturers could also cause changes in vessel density affecting longitudinal follow-up of patients. Several studies unequivocally demonstrated that patients with DR and glaucoma have lower macular and peripapillary vessel density values, respectively. \[[@pone.0205773.ref002], [@pone.0205773.ref003], [@pone.0205773.ref021], [@pone.0205773.ref022], [@pone.0205773.ref024], [@pone.0205773.ref026], [@pone.0205773.ref031]\] In this study, we tried to replicate these well-established findings analyzing the same pool of images with seven different methods. All algorithms found a significant reduction in vessel density in the patients with glaucoma and DR compared to healthy subjects. We believe this is an important finding since it indicates that previous studies were not biased by the algorithm used at least for those tested in this study. We investigated which algorithm had the best diagnostic performance to discriminate patients from healthy subjects. No method outperformed the others in all the retinal plexuses, but the performance depended on the selected plexus. In the macular area, manual and ARI methods had the best AUROCs with regard to the SCP. At the DCP level, manual and autothresholds (i.e., mean, default, Otsu) algorithms had the best discriminating ability. As to the peripapillary RCP, all algorithms had a similar performance except for the multilevel, which had the smallest AUROC. These differences may be related to differences in the levels of grey in images segmented at different plexuses. Manual algorithms had a good discrimination ability in all the three analyzed plexuses, and this could indicate the flexibility of this method that allows the rater to manually adjust the threshold value based on a visual feedback. Unfortunately, manual algorithm is highly subjective and has a poor inter-rater reliability. Moreover, it is highly time-consuming and it requires trained raters. Limitations of this study should be kept in mind. The retrospective nature dictated the fact that some variables (e.g., axial length) potentially affecting vessel density were not available. \[[@pone.0205773.ref046]\] Many methods to quantify vessel density have been published, and their relationship with those assessed in the present study remain unknown. Nevertheless, we tested a large number of methods using different strategies (including manual method, semiautomatic method with fixed threshold, semiautomatic methods with dynamic thresholds, and multilevel methods preceded by image filtering). All the images were acquired with the same device, and results might not be generalizable to other instruments. The calibration equations have not been tested on an external dataset, so they need to be fully validated. Also, they were based on the vessel density values of the study sample, and the relationship between two methods can differ for observations outside the range. Finally, our study was limited at the retinal vascular plexuses, and does not provide information about choroidal circulation. In conclusion, we provide an extensive comparison of methods to quantify vessel density on OCT-A angiograms. Absolute values calculated with different algorithms are not directly interchangeable since methods have systemic differences, poor reliability, and poor agreement. Nevertheless, all the tested algorithms revealed significant differences between healthy and affected eyes, although they had different discriminatory abilities, which varied according to the plexus analyzed. This study indicates that longitudinal monitoring of the vessel density should be carried out with the same instrument, same scan pattern and location, and same algorithm. Studies adopting vessel density as an outcome should not rely on external normative database but include their own control groups. Knowledge of the properties for each algorithm could help researchers to select the best algorithm according to the plexus studied. Supporting information {#sec019} ====================== ###### General dataset for demographic and clinical data. Readable table containing general data of the study population, including age, sex, eye laterality, presence of glaucoma, presence and stage of diabetic retinopathy, presence and type of diabetes, levels of hemoglobin A1c, presence of diabetic macular edema (DME), vertical cup-to-disc ratio (VCDR), retinal nerve fiber layer thickness (RNFL), and macular thickness. Missing or not applicable data are indicated as "NA". (CSV) ###### Click here for additional data file. ###### Dataset for superficial capillary plexus. Optical coherence tomography angiography processed data for the macular superficial capillary plexus. DME: diabetic macular; OP1: operator 1; OP2: operator 2; OP3: operator 3. Missing or not applicable data are indicated as "NA". (CSV) ###### Click here for additional data file. ###### Dataset for deep capillary plexus. Optical coherence tomography angiography processed data for the macular deep capillary plexus. DME: diabetic macular; OP1: operator 1; OP2: operator 2; OP3: operator 3. Missing or not applicable data are indicated as "NA". (CSV) ###### Click here for additional data file. ###### Dataset for peripapillary radial capillary plexus. Optical coherence tomography angiography processed data for the peripapillary radial capillary plexus. DME: diabetic macular; OP1: operator 1; OP2: operator 2; OP3: operator 3. Missing or not applicable data are indicated as "NA". (CSV) ###### Click here for additional data file. [^1]: **Competing Interests:**Kouros Nouri-Mahdavi: Heidelberg Engineering (F,R). Giuseppe Querques is consultant for: Alimera Sciences, Allergan Inc, Bayer Shering-Pharma, Fidia-Sooft, Heidelberg, KHB, Lumithera, Novartis, Roche, Sandoz (Berlin, Germany), Topcon, Zeiss. Francesco Bandello has the following disclosures: Allergan (S), Alimera (S), Bayer (S), Farmila-Thea (S), Schering Pharma (S), Sanofi-Aventis (S), Novagali (S), Pharma (S), Hoffmann-La Roche (S), Genentech (S), Novartis (S). This does not alter our adherence to PLOS ONE policies on sharing data and material.

/* * linux/fs/jbd2/journal.c * * Written by Stephen C. Tweedie <sct@redhat.com>, 1998 * * Copyright 1998 Red Hat corp --- All Rights Reserved * * This file is part of the Linux kernel and is made available under * the terms of the GNU General Public License, version 2, or at your * option, any later version, incorporated herein by reference. * * Generic filesystem journal-writing code; part of the ext2fs * journaling system. * * This file manages journals: areas of disk reserved for logging * transactional updates. This includes the kernel journaling thread * which is responsible for scheduling updates to the log. * * We do not actually manage the physical storage of the journal in this * file: that is left to a per-journal policy function, which allows us * to store the journal within a filesystem-specified area for ext2 * journaling (ext2 can use a reserved inode for storing the log). */ #include <linux/module.h> #include <linux/time.h> #include <linux/fs.h> #include <linux/jbd2.h> #include <linux/errno.h> #include <linux/slab.h> #include <linux/init.h> #include <linux/mm.h> #include <linux/freezer.h> #include <linux/pagemap.h> #include <linux/kthread.h> #include <linux/poison.h> #include <linux/proc_fs.h> #include <linux/seq_file.h> #include <linux/math64.h> #include <linux/hash.h> #include <linux/log2.h> #include <linux/vmalloc.h> #include <linux/backing-dev.h> #include <linux/bitops.h> #include <linux/ratelimit.h> #define CREATE_TRACE_POINTS #include <trace/events/jbd2.h> #include <asm/uaccess.h> #include <asm/page.h> #ifdef CONFIG_JBD2_DEBUG ushort jbd2_journal_enable_debug __read_mostly; EXPORT_SYMBOL(jbd2_journal_enable_debug); module_param_named(jbd2_debug, jbd2_journal_enable_debug, ushort, 0644); MODULE_PARM_DESC(jbd2_debug, "Debugging level for jbd2"); #endif EXPORT_SYMBOL(jbd2_journal_extend); EXPORT_SYMBOL(jbd2_journal_stop); EXPORT_SYMBOL(jbd2_journal_lock_updates); EXPORT_SYMBOL(jbd2_journal_unlock_updates); EXPORT_SYMBOL(jbd2_journal_get_write_access); EXPORT_SYMBOL(jbd2_journal_get_create_access); EXPORT_SYMBOL(jbd2_journal_get_undo_access); EXPORT_SYMBOL(jbd2_journal_set_triggers); EXPORT_SYMBOL(jbd2_journal_dirty_metadata); EXPORT_SYMBOL(jbd2_journal_forget); #if 0 EXPORT_SYMBOL(journal_sync_buffer); #endif EXPORT_SYMBOL(jbd2_journal_flush); EXPORT_SYMBOL(jbd2_journal_revoke); EXPORT_SYMBOL(jbd2_journal_init_dev); EXPORT_SYMBOL(jbd2_journal_init_inode); EXPORT_SYMBOL(jbd2_journal_check_used_features); EXPORT_SYMBOL(jbd2_journal_check_available_features); EXPORT_SYMBOL(jbd2_journal_set_features); EXPORT_SYMBOL(jbd2_journal_load); EXPORT_SYMBOL(jbd2_journal_destroy); EXPORT_SYMBOL(jbd2_journal_abort); EXPORT_SYMBOL(jbd2_journal_errno); EXPORT_SYMBOL(jbd2_journal_ack_err); EXPORT_SYMBOL(jbd2_journal_clear_err); EXPORT_SYMBOL(jbd2_log_wait_commit); EXPORT_SYMBOL(jbd2_log_start_commit); EXPORT_SYMBOL(jbd2_journal_start_commit); EXPORT_SYMBOL(jbd2_journal_force_commit_nested); EXPORT_SYMBOL(jbd2_journal_wipe); EXPORT_SYMBOL(jbd2_journal_blocks_per_page); EXPORT_SYMBOL(jbd2_journal_invalidatepage); EXPORT_SYMBOL(jbd2_journal_try_to_free_buffers); EXPORT_SYMBOL(jbd2_journal_force_commit); EXPORT_SYMBOL(jbd2_journal_inode_add_write); EXPORT_SYMBOL(jbd2_journal_inode_add_wait); EXPORT_SYMBOL(jbd2_journal_init_jbd_inode); EXPORT_SYMBOL(jbd2_journal_release_jbd_inode); EXPORT_SYMBOL(jbd2_journal_begin_ordered_truncate); EXPORT_SYMBOL(jbd2_inode_cache); static void __journal_abort_soft (journal_t *journal, int errno); static int jbd2_journal_create_slab(size_t slab_size); #ifdef CONFIG_JBD2_DEBUG void __jbd2_debug(int level, const char *file, const char *func, unsigned int line, const char *fmt, ...) { struct va_format vaf; va_list args; if (level > jbd2_journal_enable_debug) return; va_start(args, fmt); vaf.fmt = fmt; vaf.va = &args; printk(KERN_DEBUG "%s: (%s, %u): %pV\n", file, func, line, &vaf); va_end(args); } EXPORT_SYMBOL(__jbd2_debug); #endif /* Checksumming functions */ static int jbd2_verify_csum_type(journal_t *j, journal_superblock_t *sb) { if (!jbd2_journal_has_csum_v2or3_feature(j)) return 1; return sb->s_checksum_type == JBD2_CRC32C_CHKSUM; } static __be32 jbd2_superblock_csum(journal_t *j, journal_superblock_t *sb) { __u32 csum; __be32 old_csum; old_csum = sb->s_checksum; sb->s_checksum = 0; csum = jbd2_chksum(j, ~0, (char *)sb, sizeof(journal_superblock_t)); sb->s_checksum = old_csum; return cpu_to_be32(csum); } static int jbd2_superblock_csum_verify(journal_t *j, journal_superblock_t *sb) { if (!jbd2_journal_has_csum_v2or3(j)) return 1; return sb->s_checksum == jbd2_superblock_csum(j, sb); } static void jbd2_superblock_csum_set(journal_t *j, journal_superblock_t *sb) { if (!jbd2_journal_has_csum_v2or3(j)) return; sb->s_checksum = jbd2_superblock_csum(j, sb); } /* * Helper function used to manage commit timeouts */ static void commit_timeout(unsigned long __data) { struct task_struct * p = (struct task_struct *) __data; wake_up_process(p); } /* * kjournald2: The main thread function used to manage a logging device * journal. * * This kernel thread is responsible for two things: * * 1) COMMIT: Every so often we need to commit the current state of the * filesystem to disk. The journal thread is responsible for writing * all of the metadata buffers to disk. * * 2) CHECKPOINT: We cannot reuse a used section of the log file until all * of the data in that part of the log has been rewritten elsewhere on * the disk. Flushing these old buffers to reclaim space in the log is * known as checkpointing, and this thread is responsible for that job. */ static int kjournald2(void *arg) { journal_t *journal = arg; transaction_t *transaction; /* * Set up an interval timer which can be used to trigger a commit wakeup * after the commit interval expires */ setup_timer(&journal->j_commit_timer, commit_timeout, (unsigned long)current); set_freezable(); /* Record that the journal thread is running */ journal->j_task = current; wake_up(&journal->j_wait_done_commit); /* * And now, wait forever for commit wakeup events. */ write_lock(&journal->j_state_lock); loop: if (journal->j_flags & JBD2_UNMOUNT) goto end_loop; jbd_debug(1, "commit_sequence=%d, commit_request=%d\n", journal->j_commit_sequence, journal->j_commit_request); if (journal->j_commit_sequence != journal->j_commit_request) { jbd_debug(1, "OK, requests differ\n"); write_unlock(&journal->j_state_lock); del_timer_sync(&journal->j_commit_timer); jbd2_journal_commit_transaction(journal); write_lock(&journal->j_state_lock); goto loop; } wake_up(&journal->j_wait_done_commit); if (freezing(current)) { /* * The simpler the better. Flushing journal isn't a * good idea, because that depends on threads that may * be already stopped. */ jbd_debug(1, "Now suspending kjournald2\n"); write_unlock(&journal->j_state_lock); try_to_freeze(); write_lock(&journal->j_state_lock); } else { /* * We assume on resume that commits are already there, * so we don't sleep */ DEFINE_WAIT(wait); int should_sleep = 1; prepare_to_wait(&journal->j_wait_commit, &wait, TASK_INTERRUPTIBLE); if (journal->j_commit_sequence != journal->j_commit_request) should_sleep = 0; transaction = journal->j_running_transaction; if (transaction && time_after_eq(jiffies, transaction->t_expires)) should_sleep = 0; if (journal->j_flags & JBD2_UNMOUNT) should_sleep = 0; if (should_sleep) { write_unlock(&journal->j_state_lock); schedule(); write_lock(&journal->j_state_lock); } finish_wait(&journal->j_wait_commit, &wait); } jbd_debug(1, "kjournald2 wakes\n"); /* * Were we woken up by a commit wakeup event? */ transaction = journal->j_running_transaction; if (transaction && time_after_eq(jiffies, transaction->t_expires)) { journal->j_commit_request = transaction->t_tid; jbd_debug(1, "woke because of timeout\n"); } goto loop; end_loop: write_unlock(&journal->j_state_lock); del_timer_sync(&journal->j_commit_timer); journal->j_task = NULL; wake_up(&journal->j_wait_done_commit); jbd_debug(1, "Journal thread exiting.\n"); return 0; } static int jbd2_journal_start_thread(journal_t *journal) { struct task_struct *t; t = kthread_run(kjournald2, journal, "jbd2/%s", journal->j_devname); if (IS_ERR(t)) return PTR_ERR(t); wait_event(journal->j_wait_done_commit, journal->j_task != NULL); return 0; } static void journal_kill_thread(journal_t *journal) { write_lock(&journal->j_state_lock); journal->j_flags |= JBD2_UNMOUNT; while (journal->j_task) { write_unlock(&journal->j_state_lock); wake_up(&journal->j_wait_commit); wait_event(journal->j_wait_done_commit, journal->j_task == NULL); write_lock(&journal->j_state_lock); } write_unlock(&journal->j_state_lock); } /* * jbd2_journal_write_metadata_buffer: write a metadata buffer to the journal. * * Writes a metadata buffer to a given disk block. The actual IO is not * performed but a new buffer_head is constructed which labels the data * to be written with the correct destination disk block. * * Any magic-number escaping which needs to be done will cause a * copy-out here. If the buffer happens to start with the * JBD2_MAGIC_NUMBER, then we can't write it to the log directly: the * magic number is only written to the log for descripter blocks. In * this case, we copy the data and replace the first word with 0, and we * return a result code which indicates that this buffer needs to be * marked as an escaped buffer in the corresponding log descriptor * block. The missing word can then be restored when the block is read * during recovery. * * If the source buffer has already been modified by a new transaction * since we took the last commit snapshot, we use the frozen copy of * that data for IO. If we end up using the existing buffer_head's data * for the write, then we have to make sure nobody modifies it while the * IO is in progress. do_get_write_access() handles this. * * The function returns a pointer to the buffer_head to be used for IO. * * * Return value: * <0: Error * >=0: Finished OK * * On success: * Bit 0 set == escape performed on the data * Bit 1 set == buffer copy-out performed (kfree the data after IO) */ int jbd2_journal_write_metadata_buffer(transaction_t *transaction, struct journal_head *jh_in, struct buffer_head **bh_out, sector_t blocknr) { int need_copy_out = 0; int done_copy_out = 0; int do_escape = 0; char *mapped_data; struct buffer_head *new_bh; struct page *new_page; unsigned int new_offset; struct buffer_head *bh_in = jh2bh(jh_in); journal_t *journal = transaction->t_journal; /* * The buffer really shouldn't be locked: only the current committing * transaction is allowed to write it, so nobody else is allowed * to do any IO. * * akpm: except if we're journalling data, and write() output is * also part of a shared mapping, and another thread has * decided to launch a writepage() against this buffer. */ J_ASSERT_BH(bh_in, buffer_jbddirty(bh_in)); new_bh = alloc_buffer_head(GFP_NOFS|__GFP_NOFAIL); /* keep subsequent assertions sane */ atomic_set(&new_bh->b_count, 1); jbd_lock_bh_state(bh_in); repeat: /* * If a new transaction has already done a buffer copy-out, then * we use that version of the data for the commit. */ if (jh_in->b_frozen_data) { done_copy_out = 1; new_page = virt_to_page(jh_in->b_frozen_data); new_offset = offset_in_page(jh_in->b_frozen_data); } else { new_page = jh2bh(jh_in)->b_page; new_offset = offset_in_page(jh2bh(jh_in)->b_data); } mapped_data = kmap_atomic(new_page); /* * Fire data frozen trigger if data already wasn't frozen. Do this * before checking for escaping, as the trigger may modify the magic * offset. If a copy-out happens afterwards, it will have the correct * data in the buffer. */ if (!done_copy_out) jbd2_buffer_frozen_trigger(jh_in, mapped_data + new_offset, jh_in->b_triggers); /* * Check for escaping */ if (*((__be32 *)(mapped_data + new_offset)) == cpu_to_be32(JBD2_MAGIC_NUMBER)) { need_copy_out = 1; do_escape = 1; } kunmap_atomic(mapped_data); /* * Do we need to do a data copy? */ if (need_copy_out && !done_copy_out) { char *tmp; jbd_unlock_bh_state(bh_in); tmp = jbd2_alloc(bh_in->b_size, GFP_NOFS); if (!tmp) { brelse(new_bh); return -ENOMEM; } jbd_lock_bh_state(bh_in); if (jh_in->b_frozen_data) { jbd2_free(tmp, bh_in->b_size); goto repeat; } jh_in->b_frozen_data = tmp; mapped_data = kmap_atomic(new_page); memcpy(tmp, mapped_data + new_offset, bh_in->b_size); kunmap_atomic(mapped_data); new_page = virt_to_page(tmp); new_offset = offset_in_page(tmp); done_copy_out = 1; /* * This isn't strictly necessary, as we're using frozen * data for the escaping, but it keeps consistency with * b_frozen_data usage. */ jh_in->b_frozen_triggers = jh_in->b_triggers; } /* * Did we need to do an escaping? Now we've done all the * copying, we can finally do so. */ if (do_escape) { mapped_data = kmap_atomic(new_page); *((unsigned int *)(mapped_data + new_offset)) = 0; kunmap_atomic(mapped_data); } set_bh_page(new_bh, new_page, new_offset); new_bh->b_size = bh_in->b_size; new_bh->b_bdev = journal->j_dev; new_bh->b_blocknr = blocknr; new_bh->b_private = bh_in; set_buffer_mapped(new_bh); set_buffer_dirty(new_bh); *bh_out = new_bh; /* * The to-be-written buffer needs to get moved to the io queue, * and the original buffer whose contents we are shadowing or * copying is moved to the transaction's shadow queue. */ JBUFFER_TRACE(jh_in, "file as BJ_Shadow"); spin_lock(&journal->j_list_lock); __jbd2_journal_file_buffer(jh_in, transaction, BJ_Shadow); spin_unlock(&journal->j_list_lock); set_buffer_shadow(bh_in); jbd_unlock_bh_state(bh_in); return do_escape | (done_copy_out << 1); } /* * Allocation code for the journal file. Manage the space left in the * journal, so that we can begin checkpointing when appropriate. */ /* * Called with j_state_lock locked for writing. * Returns true if a transaction commit was started. */ int __jbd2_log_start_commit(journal_t *journal, tid_t target) { /* Return if the txn has already requested to be committed */ if (journal->j_commit_request == target) return 0; /* * The only transaction we can possibly wait upon is the * currently running transaction (if it exists). Otherwise, * the target tid must be an old one. */ if (journal->j_running_transaction && journal->j_running_transaction->t_tid == target) { /* * We want a new commit: OK, mark the request and wakeup the * commit thread. We do _not_ do the commit ourselves. */ journal->j_commit_request = target; jbd_debug(1, "JBD2: requesting commit %d/%d\n", journal->j_commit_request, journal->j_commit_sequence); journal->j_running_transaction->t_requested = jiffies; wake_up(&journal->j_wait_commit); return 1; } else if (!tid_geq(journal->j_commit_request, target)) /* This should never happen, but if it does, preserve the evidence before kjournald goes into a loop and increments j_commit_sequence beyond all recognition. */ WARN_ONCE(1, "JBD2: bad log_start_commit: %u %u %u %u\n", journal->j_commit_request, journal->j_commit_sequence, target, journal->j_running_transaction ? journal->j_running_transaction->t_tid : 0); return 0; } int jbd2_log_start_commit(journal_t *journal, tid_t tid) { int ret; write_lock(&journal->j_state_lock); ret = __jbd2_log_start_commit(journal, tid); write_unlock(&journal->j_state_lock); return ret; } /* * Force and wait any uncommitted transactions. We can only force the running * transaction if we don't have an active handle, otherwise, we will deadlock. * Returns: <0 in case of error, * 0 if nothing to commit, * 1 if transaction was successfully committed. */ static int __jbd2_journal_force_commit(journal_t *journal) { transaction_t *transaction = NULL; tid_t tid; int need_to_start = 0, ret = 0; read_lock(&journal->j_state_lock); if (journal->j_running_transaction && !current->journal_info) { transaction = journal->j_running_transaction; if (!tid_geq(journal->j_commit_request, transaction->t_tid)) need_to_start = 1; } else if (journal->j_committing_transaction) transaction = journal->j_committing_transaction; if (!transaction) { /* Nothing to commit */ read_unlock(&journal->j_state_lock); return 0; } tid = transaction->t_tid; read_unlock(&journal->j_state_lock); if (need_to_start) jbd2_log_start_commit(journal, tid); ret = jbd2_log_wait_commit(journal, tid); if (!ret) ret = 1; return ret; } /** * Force and wait upon a commit if the calling process is not within * transaction. This is used for forcing out undo-protected data which contains * bitmaps, when the fs is running out of space. * * @journal: journal to force * Returns true if progress was made. */ int jbd2_journal_force_commit_nested(journal_t *journal) { int ret; ret = __jbd2_journal_force_commit(journal); return ret > 0; } /** * int journal_force_commit() - force any uncommitted transactions * @journal: journal to force * * Caller want unconditional commit. We can only force the running transaction * if we don't have an active handle, otherwise, we will deadlock. */ int jbd2_journal_force_commit(journal_t *journal) { int ret; J_ASSERT(!current->journal_info); ret = __jbd2_journal_force_commit(journal); if (ret > 0) ret = 0; return ret; } /* * Start a commit of the current running transaction (if any). Returns true * if a transaction is going to be committed (or is currently already * committing), and fills its tid in at *ptid */ int jbd2_journal_start_commit(journal_t *journal, tid_t *ptid) { int ret = 0; write_lock(&journal->j_state_lock); if (journal->j_running_transaction) { tid_t tid = journal->j_running_transaction->t_tid; __jbd2_log_start_commit(journal, tid); /* There's a running transaction and we've just made sure * it's commit has been scheduled. */ if (ptid) *ptid = tid; ret = 1; } else if (journal->j_committing_transaction) { /* * If commit has been started, then we have to wait for * completion of that transaction. */ if (ptid) *ptid = journal->j_committing_transaction->t_tid; ret = 1; } write_unlock(&journal->j_state_lock); return ret; } /* * Return 1 if a given transaction has not yet sent barrier request * connected with a transaction commit. If 0 is returned, transaction * may or may not have sent the barrier. Used to avoid sending barrier * twice in common cases. */ int jbd2_trans_will_send_data_barrier(journal_t *journal, tid_t tid) { int ret = 0; transaction_t *commit_trans; if (!(journal->j_flags & JBD2_BARRIER)) return 0; read_lock(&journal->j_state_lock); /* Transaction already committed? */ if (tid_geq(journal->j_commit_sequence, tid)) goto out; commit_trans = journal->j_committing_transaction; if (!commit_trans || commit_trans->t_tid != tid) { ret = 1; goto out; } /* * Transaction is being committed and we already proceeded to * submitting a flush to fs partition? */ if (journal->j_fs_dev != journal->j_dev) { if (!commit_trans->t_need_data_flush || commit_trans->t_state >= T_COMMIT_DFLUSH) goto out; } else { if (commit_trans->t_state >= T_COMMIT_JFLUSH) goto out; } ret = 1; out: read_unlock(&journal->j_state_lock); return ret; } EXPORT_SYMBOL(jbd2_trans_will_send_data_barrier); /* * Wait for a specified commit to complete. * The caller may not hold the journal lock. */ int jbd2_log_wait_commit(journal_t *journal, tid_t tid) { int err = 0; jbd2_might_wait_for_commit(journal); read_lock(&journal->j_state_lock); #ifdef CONFIG_JBD2_DEBUG if (!tid_geq(journal->j_commit_request, tid)) { printk(KERN_ERR "%s: error: j_commit_request=%d, tid=%d\n", __func__, journal->j_commit_request, tid); } #endif while (tid_gt(tid, journal->j_commit_sequence)) { jbd_debug(1, "JBD2: want %d, j_commit_sequence=%d\n", tid, journal->j_commit_sequence); read_unlock(&journal->j_state_lock); wake_up(&journal->j_wait_commit); wait_event(journal->j_wait_done_commit, !tid_gt(tid, journal->j_commit_sequence)); read_lock(&journal->j_state_lock); } read_unlock(&journal->j_state_lock); if (unlikely(is_journal_aborted(journal))) err = -EIO; return err; } /* * When this function returns the transaction corresponding to tid * will be completed. If the transaction has currently running, start * committing that transaction before waiting for it to complete. If * the transaction id is stale, it is by definition already completed, * so just return SUCCESS. */ int jbd2_complete_transaction(journal_t *journal, tid_t tid) { int need_to_wait = 1; read_lock(&journal->j_state_lock); if (journal->j_running_transaction && journal->j_running_transaction->t_tid == tid) { if (journal->j_commit_request != tid) { /* transaction not yet started, so request it */ read_unlock(&journal->j_state_lock); jbd2_log_start_commit(journal, tid); goto wait_commit; } } else if (!(journal->j_committing_transaction && journal->j_committing_transaction->t_tid == tid)) need_to_wait = 0; read_unlock(&journal->j_state_lock); if (!need_to_wait) return 0; wait_commit: return jbd2_log_wait_commit(journal, tid); } EXPORT_SYMBOL(jbd2_complete_transaction); /* * Log buffer allocation routines: */ int jbd2_journal_next_log_block(journal_t *journal, unsigned long long *retp) { unsigned long blocknr; write_lock(&journal->j_state_lock); J_ASSERT(journal->j_free > 1); blocknr = journal->j_head; journal->j_head++; journal->j_free--; if (journal->j_head == journal->j_last) journal->j_head = journal->j_first; write_unlock(&journal->j_state_lock); return jbd2_journal_bmap(journal, blocknr, retp); } /* * Conversion of logical to physical block numbers for the journal * * On external journals the journal blocks are identity-mapped, so * this is a no-op. If needed, we can use j_blk_offset - everything is * ready. */ int jbd2_journal_bmap(journal_t *journal, unsigned long blocknr, unsigned long long *retp) { int err = 0; unsigned long long ret; if (journal->j_inode) { ret = bmap(journal->j_inode, blocknr); if (ret) *retp = ret; else { printk(KERN_ALERT "%s: journal block not found " "at offset %lu on %s\n", __func__, blocknr, journal->j_devname); err = -EIO; __journal_abort_soft(journal, err); } } else { *retp = blocknr; /* +journal->j_blk_offset */ } return err; } /* * We play buffer_head aliasing tricks to write data/metadata blocks to * the journal without copying their contents, but for journal * descriptor blocks we do need to generate bona fide buffers. * * After the caller of jbd2_journal_get_descriptor_buffer() has finished modifying * the buffer's contents they really should run flush_dcache_page(bh->b_page). * But we don't bother doing that, so there will be coherency problems with * mmaps of blockdevs which hold live JBD-controlled filesystems. */ struct buffer_head * jbd2_journal_get_descriptor_buffer(transaction_t *transaction, int type) { journal_t *journal = transaction->t_journal; struct buffer_head *bh; unsigned long long blocknr; journal_header_t *header; int err; err = jbd2_journal_next_log_block(journal, &blocknr); if (err) return NULL; bh = __getblk(journal->j_dev, blocknr, journal->j_blocksize); if (!bh) return NULL; lock_buffer(bh); memset(bh->b_data, 0, journal->j_blocksize); header = (journal_header_t *)bh->b_data; header->h_magic = cpu_to_be32(JBD2_MAGIC_NUMBER); header->h_blocktype = cpu_to_be32(type); header->h_sequence = cpu_to_be32(transaction->t_tid); set_buffer_uptodate(bh); unlock_buffer(bh); BUFFER_TRACE(bh, "return this buffer"); return bh; } void jbd2_descriptor_block_csum_set(journal_t *j, struct buffer_head *bh) { struct jbd2_journal_block_tail *tail; __u32 csum; if (!jbd2_journal_has_csum_v2or3(j)) return; tail = (struct jbd2_journal_block_tail *)(bh->b_data + j->j_blocksize - sizeof(struct jbd2_journal_block_tail)); tail->t_checksum = 0; csum = jbd2_chksum(j, j->j_csum_seed, bh->b_data, j->j_blocksize); tail->t_checksum = cpu_to_be32(csum); } /* * Return tid of the oldest transaction in the journal and block in the journal * where the transaction starts. * * If the journal is now empty, return which will be the next transaction ID * we will write and where will that transaction start. * * The return value is 0 if journal tail cannot be pushed any further, 1 if * it can. */ int jbd2_journal_get_log_tail(journal_t *journal, tid_t *tid, unsigned long *block) { transaction_t *transaction; int ret; read_lock(&journal->j_state_lock); spin_lock(&journal->j_list_lock); transaction = journal->j_checkpoint_transactions; if (transaction) { *tid = transaction->t_tid; *block = transaction->t_log_start; } else if ((transaction = journal->j_committing_transaction) != NULL) { *tid = transaction->t_tid; *block = transaction->t_log_start; } else if ((transaction = journal->j_running_transaction) != NULL) { *tid = transaction->t_tid; *block = journal->j_head; } else { *tid = journal->j_transaction_sequence; *block = journal->j_head; } ret = tid_gt(*tid, journal->j_tail_sequence); spin_unlock(&journal->j_list_lock); read_unlock(&journal->j_state_lock); return ret; } /* * Update information in journal structure and in on disk journal superblock * about log tail. This function does not check whether information passed in * really pushes log tail further. It's responsibility of the caller to make * sure provided log tail information is valid (e.g. by holding * j_checkpoint_mutex all the time between computing log tail and calling this * function as is the case with jbd2_cleanup_journal_tail()). * * Requires j_checkpoint_mutex */ int __jbd2_update_log_tail(journal_t *journal, tid_t tid, unsigned long block) { unsigned long freed; int ret; BUG_ON(!mutex_is_locked(&journal->j_checkpoint_mutex)); /* * We cannot afford for write to remain in drive's caches since as * soon as we update j_tail, next transaction can start reusing journal * space and if we lose sb update during power failure we'd replay * old transaction with possibly newly overwritten data. */ ret = jbd2_journal_update_sb_log_tail(journal, tid, block, WRITE_FUA); if (ret) goto out; write_lock(&journal->j_state_lock); freed = block - journal->j_tail; if (block < journal->j_tail) freed += journal->j_last - journal->j_first; trace_jbd2_update_log_tail(journal, tid, block, freed); jbd_debug(1, "Cleaning journal tail from %d to %d (offset %lu), " "freeing %lu\n", journal->j_tail_sequence, tid, block, freed); journal->j_free += freed; journal->j_tail_sequence = tid; journal->j_tail = block; write_unlock(&journal->j_state_lock); out: return ret; } /* * This is a variaon of __jbd2_update_log_tail which checks for validity of * provided log tail and locks j_checkpoint_mutex. So it is safe against races * with other threads updating log tail. */ void jbd2_update_log_tail(journal_t *journal, tid_t tid, unsigned long block) { mutex_lock(&journal->j_checkpoint_mutex); if (tid_gt(tid, journal->j_tail_sequence)) __jbd2_update_log_tail(journal, tid, block); mutex_unlock(&journal->j_checkpoint_mutex); } struct jbd2_stats_proc_session { journal_t *journal; struct transaction_stats_s *stats; int start; int max; }; static void *jbd2_seq_info_start(struct seq_file *seq, loff_t *pos) { return *pos ? NULL : SEQ_START_TOKEN; } static void *jbd2_seq_info_next(struct seq_file *seq, void *v, loff_t *pos) { return NULL; } static int jbd2_seq_info_show(struct seq_file *seq, void *v) { struct jbd2_stats_proc_session *s = seq->private; if (v != SEQ_START_TOKEN) return 0; seq_printf(seq, "%lu transactions (%lu requested), " "each up to %u blocks\n", s->stats->ts_tid, s->stats->ts_requested, s->journal->j_max_transaction_buffers); if (s->stats->ts_tid == 0) return 0; seq_printf(seq, "average: \n %ums waiting for transaction\n", jiffies_to_msecs(s->stats->run.rs_wait / s->stats->ts_tid)); seq_printf(seq, " %ums request delay\n", (s->stats->ts_requested == 0) ? 0 : jiffies_to_msecs(s->stats->run.rs_request_delay / s->stats->ts_requested)); seq_printf(seq, " %ums running transaction\n", jiffies_to_msecs(s->stats->run.rs_running / s->stats->ts_tid)); seq_printf(seq, " %ums transaction was being locked\n", jiffies_to_msecs(s->stats->run.rs_locked / s->stats->ts_tid)); seq_printf(seq, " %ums flushing data (in ordered mode)\n", jiffies_to_msecs(s->stats->run.rs_flushing / s->stats->ts_tid)); seq_printf(seq, " %ums logging transaction\n", jiffies_to_msecs(s->stats->run.rs_logging / s->stats->ts_tid)); seq_printf(seq, " %lluus average transaction commit time\n", div_u64(s->journal->j_average_commit_time, 1000)); seq_printf(seq, " %lu handles per transaction\n", s->stats->run.rs_handle_count / s->stats->ts_tid); seq_printf(seq, " %lu blocks per transaction\n", s->stats->run.rs_blocks / s->stats->ts_tid); seq_printf(seq, " %lu logged blocks per transaction\n", s->stats->run.rs_blocks_logged / s->stats->ts_tid); return 0; } static void jbd2_seq_info_stop(struct seq_file *seq, void *v) { } static const struct seq_operations jbd2_seq_info_ops = { .start = jbd2_seq_info_start, .next = jbd2_seq_info_next, .stop = jbd2_seq_info_stop, .show = jbd2_seq_info_show, }; static int jbd2_seq_info_open(struct inode *inode, struct file *file) { journal_t *journal = PDE_DATA(inode); struct jbd2_stats_proc_session *s; int rc, size; s = kmalloc(sizeof(*s), GFP_KERNEL); if (s == NULL) return -ENOMEM; size = sizeof(struct transaction_stats_s); s->stats = kmalloc(size, GFP_KERNEL); if (s->stats == NULL) { kfree(s); return -ENOMEM; } spin_lock(&journal->j_history_lock); memcpy(s->stats, &journal->j_stats, size); s->journal = journal; spin_unlock(&journal->j_history_lock); rc = seq_open(file, &jbd2_seq_info_ops); if (rc == 0) { struct seq_file *m = file->private_data; m->private = s; } else { kfree(s->stats); kfree(s); } return rc; } static int jbd2_seq_info_release(struct inode *inode, struct file *file) { struct seq_file *seq = file->private_data; struct jbd2_stats_proc_session *s = seq->private; kfree(s->stats); kfree(s); return seq_release(inode, file); } static const struct file_operations jbd2_seq_info_fops = { .owner = THIS_MODULE, .open = jbd2_seq_info_open, .read = seq_read, .llseek = seq_lseek, .release = jbd2_seq_info_release, }; static struct proc_dir_entry *proc_jbd2_stats; static void jbd2_stats_proc_init(journal_t *journal) { journal->j_proc_entry = proc_mkdir(journal->j_devname, proc_jbd2_stats); if (journal->j_proc_entry) { proc_create_data("info", S_IRUGO, journal->j_proc_entry, &jbd2_seq_info_fops, journal); } } static void jbd2_stats_proc_exit(journal_t *journal) { remove_proc_entry("info", journal->j_proc_entry); remove_proc_entry(journal->j_devname, proc_jbd2_stats); } /* * Management for journal control blocks: functions to create and * destroy journal_t structures, and to initialise and read existing * journal blocks from disk. */ /* First: create and setup a journal_t object in memory. We initialise * very few fields yet: that has to wait until we have created the * journal structures from from scratch, or loaded them from disk. */ static journal_t *journal_init_common(struct block_device *bdev, struct block_device *fs_dev, unsigned long long start, int len, int blocksize) { static struct lock_class_key jbd2_trans_commit_key; journal_t *journal; int err; struct buffer_head *bh; int n; journal = kzalloc(sizeof(*journal), GFP_KERNEL); if (!journal) return NULL; init_waitqueue_head(&journal->j_wait_transaction_locked); init_waitqueue_head(&journal->j_wait_done_commit); init_waitqueue_head(&journal->j_wait_commit); init_waitqueue_head(&journal->j_wait_updates); init_waitqueue_head(&journal->j_wait_reserved); mutex_init(&journal->j_barrier); mutex_init(&journal->j_checkpoint_mutex); spin_lock_init(&journal->j_revoke_lock); spin_lock_init(&journal->j_list_lock); rwlock_init(&journal->j_state_lock); journal->j_commit_interval = (HZ * JBD2_DEFAULT_MAX_COMMIT_AGE); journal->j_min_batch_time = 0; journal->j_max_batch_time = 15000; /* 15ms */ atomic_set(&journal->j_reserved_credits, 0); /* The journal is marked for error until we succeed with recovery! */ journal->j_flags = JBD2_ABORT; /* Set up a default-sized revoke table for the new mount. */ err = jbd2_journal_init_revoke(journal, JOURNAL_REVOKE_DEFAULT_HASH); if (err) { kfree(journal); return NULL; } spin_lock_init(&journal->j_history_lock); lockdep_init_map(&journal->j_trans_commit_map, "jbd2_handle", &jbd2_trans_commit_key, 0); /* journal descriptor can store up to n blocks -bzzz */ journal->j_blocksize = blocksize; journal->j_dev = bdev; journal->j_fs_dev = fs_dev; journal->j_blk_offset = start; journal->j_maxlen = len; n = journal->j_blocksize / sizeof(journal_block_tag_t); journal->j_wbufsize = n; journal->j_wbuf = kmalloc_array(n, sizeof(struct buffer_head *), GFP_KERNEL); if (!journal->j_wbuf) { kfree(journal); return NULL; } bh = getblk_unmovable(journal->j_dev, start, journal->j_blocksize); if (!bh) { pr_err("%s: Cannot get buffer for journal superblock\n", __func__); kfree(journal->j_wbuf); kfree(journal); return NULL; } journal->j_sb_buffer = bh; journal->j_superblock = (journal_superblock_t *)bh->b_data; return journal; } /* jbd2_journal_init_dev and jbd2_journal_init_inode: * * Create a journal structure assigned some fixed set of disk blocks to * the journal. We don't actually touch those disk blocks yet, but we * need to set up all of the mapping information to tell the journaling * system where the journal blocks are. * */ /** * journal_t * jbd2_journal_init_dev() - creates and initialises a journal structure * @bdev: Block device on which to create the journal * @fs_dev: Device which hold journalled filesystem for this journal. * @start: Block nr Start of journal. * @len: Length of the journal in blocks. * @blocksize: blocksize of journalling device * * Returns: a newly created journal_t * * * jbd2_journal_init_dev creates a journal which maps a fixed contiguous * range of blocks on an arbitrary block device. * */ journal_t *jbd2_journal_init_dev(struct block_device *bdev, struct block_device *fs_dev, unsigned long long start, int len, int blocksize) { journal_t *journal; journal = journal_init_common(bdev, fs_dev, start, len, blocksize); if (!journal) return NULL; bdevname(journal->j_dev, journal->j_devname); strreplace(journal->j_devname, '/', '!'); jbd2_stats_proc_init(journal); return journal; } /** * journal_t * jbd2_journal_init_inode () - creates a journal which maps to a inode. * @inode: An inode to create the journal in * * jbd2_journal_init_inode creates a journal which maps an on-disk inode as * the journal. The inode must exist already, must support bmap() and * must have all data blocks preallocated. */ journal_t *jbd2_journal_init_inode(struct inode *inode) { journal_t *journal; char *p; unsigned long long blocknr; blocknr = bmap(inode, 0); if (!blocknr) { pr_err("%s: Cannot locate journal superblock\n", __func__); return NULL; } jbd_debug(1, "JBD2: inode %s/%ld, size %lld, bits %d, blksize %ld\n", inode->i_sb->s_id, inode->i_ino, (long long) inode->i_size, inode->i_sb->s_blocksize_bits, inode->i_sb->s_blocksize); journal = journal_init_common(inode->i_sb->s_bdev, inode->i_sb->s_bdev, blocknr, inode->i_size >> inode->i_sb->s_blocksize_bits, inode->i_sb->s_blocksize); if (!journal) return NULL; journal->j_inode = inode; bdevname(journal->j_dev, journal->j_devname); p = strreplace(journal->j_devname, '/', '!'); sprintf(p, "-%lu", journal->j_inode->i_ino); jbd2_stats_proc_init(journal); return journal; } /* * If the journal init or create aborts, we need to mark the journal * superblock as being NULL to prevent the journal destroy from writing * back a bogus superblock. */ static void journal_fail_superblock (journal_t *journal) { struct buffer_head *bh = journal->j_sb_buffer; brelse(bh); journal->j_sb_buffer = NULL; } /* * Given a journal_t structure, initialise the various fields for * startup of a new journaling session. We use this both when creating * a journal, and after recovering an old journal to reset it for * subsequent use. */ static int journal_reset(journal_t *journal) { journal_superblock_t *sb = journal->j_superblock; unsigned long long first, last; first = be32_to_cpu(sb->s_first); last = be32_to_cpu(sb->s_maxlen); if (first + JBD2_MIN_JOURNAL_BLOCKS > last + 1) { printk(KERN_ERR "JBD2: Journal too short (blocks %llu-%llu).\n", first, last); journal_fail_superblock(journal); return -EINVAL; } journal->j_first = first; journal->j_last = last; journal->j_head = first; journal->j_tail = first; journal->j_free = last - first; journal->j_tail_sequence = journal->j_transaction_sequence; journal->j_commit_sequence = journal->j_transaction_sequence - 1; journal->j_commit_request = journal->j_commit_sequence; journal->j_max_transaction_buffers = journal->j_maxlen / 4; /* * As a special case, if the on-disk copy is already marked as needing * no recovery (s_start == 0), then we can safely defer the superblock * update until the next commit by setting JBD2_FLUSHED. This avoids * attempting a write to a potential-readonly device. */ if (sb->s_start == 0) { jbd_debug(1, "JBD2: Skipping superblock update on recovered sb " "(start %ld, seq %d, errno %d)\n", journal->j_tail, journal->j_tail_sequence, journal->j_errno); journal->j_flags |= JBD2_FLUSHED; } else { /* Lock here to make assertions happy... */ mutex_lock(&journal->j_checkpoint_mutex); /* * Update log tail information. We use WRITE_FUA since new * transaction will start reusing journal space and so we * must make sure information about current log tail is on * disk before that. */ jbd2_journal_update_sb_log_tail(journal, journal->j_tail_sequence, journal->j_tail, WRITE_FUA); mutex_unlock(&journal->j_checkpoint_mutex); } return jbd2_journal_start_thread(journal); } static int jbd2_write_superblock(journal_t *journal, int write_flags) { struct buffer_head *bh = journal->j_sb_buffer; journal_superblock_t *sb = journal->j_superblock; int ret; trace_jbd2_write_superblock(journal, write_flags); if (!(journal->j_flags & JBD2_BARRIER)) write_flags &= ~(REQ_FUA | REQ_PREFLUSH); lock_buffer(bh); if (buffer_write_io_error(bh)) { /* * Oh, dear. A previous attempt to write the journal * superblock failed. This could happen because the * USB device was yanked out. Or it could happen to * be a transient write error and maybe the block will * be remapped. Nothing we can do but to retry the * write and hope for the best. */ printk(KERN_ERR "JBD2: previous I/O error detected " "for journal superblock update for %s.\n", journal->j_devname); clear_buffer_write_io_error(bh); set_buffer_uptodate(bh); } jbd2_superblock_csum_set(journal, sb); get_bh(bh); bh->b_end_io = end_buffer_write_sync; ret = submit_bh(REQ_OP_WRITE, write_flags, bh); wait_on_buffer(bh); if (buffer_write_io_error(bh)) { clear_buffer_write_io_error(bh); set_buffer_uptodate(bh); ret = -EIO; } if (ret) { printk(KERN_ERR "JBD2: Error %d detected when updating " "journal superblock for %s.\n", ret, journal->j_devname); jbd2_journal_abort(journal, ret); } return ret; } /** * jbd2_journal_update_sb_log_tail() - Update log tail in journal sb on disk. * @journal: The journal to update. * @tail_tid: TID of the new transaction at the tail of the log * @tail_block: The first block of the transaction at the tail of the log * @write_op: With which operation should we write the journal sb * * Update a journal's superblock information about log tail and write it to * disk, waiting for the IO to complete. */ int jbd2_journal_update_sb_log_tail(journal_t *journal, tid_t tail_tid, unsigned long tail_block, int write_op) { journal_superblock_t *sb = journal->j_superblock; int ret; BUG_ON(!mutex_is_locked(&journal->j_checkpoint_mutex)); jbd_debug(1, "JBD2: updating superblock (start %lu, seq %u)\n", tail_block, tail_tid); sb->s_sequence = cpu_to_be32(tail_tid); sb->s_start = cpu_to_be32(tail_block); ret = jbd2_write_superblock(journal, write_op); if (ret) goto out; /* Log is no longer empty */ write_lock(&journal->j_state_lock); WARN_ON(!sb->s_sequence); journal->j_flags &= ~JBD2_FLUSHED; write_unlock(&journal->j_state_lock); out: return ret; } /** * jbd2_mark_journal_empty() - Mark on disk journal as empty. * @journal: The journal to update. * @write_op: With which operation should we write the journal sb * * Update a journal's dynamic superblock fields to show that journal is empty. * Write updated superblock to disk waiting for IO to complete. */ static void jbd2_mark_journal_empty(journal_t *journal, int write_op) { journal_superblock_t *sb = journal->j_superblock; BUG_ON(!mutex_is_locked(&journal->j_checkpoint_mutex)); read_lock(&journal->j_state_lock); /* Is it already empty? */ if (sb->s_start == 0) { read_unlock(&journal->j_state_lock); return; } jbd_debug(1, "JBD2: Marking journal as empty (seq %d)\n", journal->j_tail_sequence); sb->s_sequence = cpu_to_be32(journal->j_tail_sequence); sb->s_start = cpu_to_be32(0); read_unlock(&journal->j_state_lock); jbd2_write_superblock(journal, write_op); /* Log is no longer empty */ write_lock(&journal->j_state_lock); journal->j_flags |= JBD2_FLUSHED; write_unlock(&journal->j_state_lock); } /** * jbd2_journal_update_sb_errno() - Update error in the journal. * @journal: The journal to update. * * Update a journal's errno. Write updated superblock to disk waiting for IO * to complete. */ void jbd2_journal_update_sb_errno(journal_t *journal) { journal_superblock_t *sb = journal->j_superblock; read_lock(&journal->j_state_lock); jbd_debug(1, "JBD2: updating superblock error (errno %d)\n", journal->j_errno); sb->s_errno = cpu_to_be32(journal->j_errno); read_unlock(&journal->j_state_lock); jbd2_write_superblock(journal, WRITE_FUA); } EXPORT_SYMBOL(jbd2_journal_update_sb_errno); /* * Read the superblock for a given journal, performing initial * validation of the format. */ static int journal_get_superblock(journal_t *journal) { struct buffer_head *bh; journal_superblock_t *sb; int err = -EIO; bh = journal->j_sb_buffer; J_ASSERT(bh != NULL); if (!buffer_uptodate(bh)) { ll_rw_block(REQ_OP_READ, 0, 1, &bh); wait_on_buffer(bh); if (!buffer_uptodate(bh)) { printk(KERN_ERR "JBD2: IO error reading journal superblock\n"); goto out; } } if (buffer_verified(bh)) return 0; sb = journal->j_superblock; err = -EINVAL; if (sb->s_header.h_magic != cpu_to_be32(JBD2_MAGIC_NUMBER) || sb->s_blocksize != cpu_to_be32(journal->j_blocksize)) { printk(KERN_WARNING "JBD2: no valid journal superblock found\n"); goto out; } switch(be32_to_cpu(sb->s_header.h_blocktype)) { case JBD2_SUPERBLOCK_V1: journal->j_format_version = 1; break; case JBD2_SUPERBLOCK_V2: journal->j_format_version = 2; break; default: printk(KERN_WARNING "JBD2: unrecognised superblock format ID\n"); goto out; } if (be32_to_cpu(sb->s_maxlen) < journal->j_maxlen) journal->j_maxlen = be32_to_cpu(sb->s_maxlen); else if (be32_to_cpu(sb->s_maxlen) > journal->j_maxlen) { printk(KERN_WARNING "JBD2: journal file too short\n"); goto out; } if (be32_to_cpu(sb->s_first) == 0 || be32_to_cpu(sb->s_first) >= journal->j_maxlen) { printk(KERN_WARNING "JBD2: Invalid start block of journal: %u\n", be32_to_cpu(sb->s_first)); goto out; } if (jbd2_has_feature_csum2(journal) && jbd2_has_feature_csum3(journal)) { /* Can't have checksum v2 and v3 at the same time! */ printk(KERN_ERR "JBD2: Can't enable checksumming v2 and v3 " "at the same time!\n"); goto out; } if (jbd2_journal_has_csum_v2or3_feature(journal) && jbd2_has_feature_checksum(journal)) { /* Can't have checksum v1 and v2 on at the same time! */ printk(KERN_ERR "JBD2: Can't enable checksumming v1 and v2/3 " "at the same time!\n"); goto out; } if (!jbd2_verify_csum_type(journal, sb)) { printk(KERN_ERR "JBD2: Unknown checksum type\n"); goto out; } /* Load the checksum driver */ if (jbd2_journal_has_csum_v2or3_feature(journal)) { journal->j_chksum_driver = crypto_alloc_shash("crc32c", 0, 0); if (IS_ERR(journal->j_chksum_driver)) { printk(KERN_ERR "JBD2: Cannot load crc32c driver.\n"); err = PTR_ERR(journal->j_chksum_driver); journal->j_chksum_driver = NULL; goto out; } } /* Check superblock checksum */ if (!jbd2_superblock_csum_verify(journal, sb)) { printk(KERN_ERR "JBD2: journal checksum error\n"); err = -EFSBADCRC; goto out; } /* Precompute checksum seed for all metadata */ if (jbd2_journal_has_csum_v2or3(journal)) journal->j_csum_seed = jbd2_chksum(journal, ~0, sb->s_uuid, sizeof(sb->s_uuid)); set_buffer_verified(bh); return 0; out: journal_fail_superblock(journal); return err; } /* * Load the on-disk journal superblock and read the key fields into the * journal_t. */ static int load_superblock(journal_t *journal) { int err; journal_superblock_t *sb; err = journal_get_superblock(journal); if (err) return err; sb = journal->j_superblock; journal->j_tail_sequence = be32_to_cpu(sb->s_sequence); journal->j_tail = be32_to_cpu(sb->s_start); journal->j_first = be32_to_cpu(sb->s_first); journal->j_last = be32_to_cpu(sb->s_maxlen); journal->j_errno = be32_to_cpu(sb->s_errno); return 0; } /** * int jbd2_journal_load() - Read journal from disk. * @journal: Journal to act on. * * Given a journal_t structure which tells us which disk blocks contain * a journal, read the journal from disk to initialise the in-memory * structures. */ int jbd2_journal_load(journal_t *journal) { int err; journal_superblock_t *sb; err = load_superblock(journal); if (err) return err; sb = journal->j_superblock; /* If this is a V2 superblock, then we have to check the * features flags on it. */ if (journal->j_format_version >= 2) { if ((sb->s_feature_ro_compat & ~cpu_to_be32(JBD2_KNOWN_ROCOMPAT_FEATURES)) || (sb->s_feature_incompat & ~cpu_to_be32(JBD2_KNOWN_INCOMPAT_FEATURES))) { printk(KERN_WARNING "JBD2: Unrecognised features on journal\n"); return -EINVAL; } } /* * Create a slab for this blocksize */ err = jbd2_journal_create_slab(be32_to_cpu(sb->s_blocksize)); if (err) return err; /* Let the recovery code check whether it needs to recover any * data from the journal. */ if (jbd2_journal_recover(journal)) goto recovery_error; if (journal->j_failed_commit) { printk(KERN_ERR "JBD2: journal transaction %u on %s " "is corrupt.\n", journal->j_failed_commit, journal->j_devname); return -EFSCORRUPTED; } /* OK, we've finished with the dynamic journal bits: * reinitialise the dynamic contents of the superblock in memory * and reset them on disk. */ if (journal_reset(journal)) goto recovery_error; journal->j_flags &= ~JBD2_ABORT; journal->j_flags |= JBD2_LOADED; return 0; recovery_error: printk(KERN_WARNING "JBD2: recovery failed\n"); return -EIO; } /** * void jbd2_journal_destroy() - Release a journal_t structure. * @journal: Journal to act on. * * Release a journal_t structure once it is no longer in use by the * journaled object. * Return <0 if we couldn't clean up the journal. */ int jbd2_journal_destroy(journal_t *journal) { int err = 0; /* Wait for the commit thread to wake up and die. */ journal_kill_thread(journal); /* Force a final log commit */ if (journal->j_running_transaction) jbd2_journal_commit_transaction(journal); /* Force any old transactions to disk */ /* Totally anal locking here... */ spin_lock(&journal->j_list_lock); while (journal->j_checkpoint_transactions != NULL) { spin_unlock(&journal->j_list_lock); mutex_lock(&journal->j_checkpoint_mutex); err = jbd2_log_do_checkpoint(journal); mutex_unlock(&journal->j_checkpoint_mutex); /* * If checkpointing failed, just free the buffers to avoid * looping forever */ if (err) { jbd2_journal_destroy_checkpoint(journal); spin_lock(&journal->j_list_lock); break; } spin_lock(&journal->j_list_lock); } J_ASSERT(journal->j_running_transaction == NULL); J_ASSERT(journal->j_committing_transaction == NULL); J_ASSERT(journal->j_checkpoint_transactions == NULL); spin_unlock(&journal->j_list_lock); if (journal->j_sb_buffer) { if (!is_journal_aborted(journal)) { mutex_lock(&journal->j_checkpoint_mutex); write_lock(&journal->j_state_lock); journal->j_tail_sequence = ++journal->j_transaction_sequence; write_unlock(&journal->j_state_lock); jbd2_mark_journal_empty(journal, WRITE_FLUSH_FUA); mutex_unlock(&journal->j_checkpoint_mutex); } else err = -EIO; brelse(journal->j_sb_buffer); } if (journal->j_proc_entry) jbd2_stats_proc_exit(journal); iput(journal->j_inode); if (journal->j_revoke) jbd2_journal_destroy_revoke(journal); if (journal->j_chksum_driver) crypto_free_shash(journal->j_chksum_driver); kfree(journal->j_wbuf); kfree(journal); return err; } /** *int jbd2_journal_check_used_features () - Check if features specified are used. * @journal: Journal to check. * @compat: bitmask of compatible features * @ro: bitmask of features that force read-only mount * @incompat: bitmask of incompatible features * * Check whether the journal uses all of a given set of * features. Return true (non-zero) if it does. **/ int jbd2_journal_check_used_features (journal_t *journal, unsigned long compat, unsigned long ro, unsigned long incompat) { journal_superblock_t *sb; if (!compat && !ro && !incompat) return 1; /* Load journal superblock if it is not loaded yet. */ if (journal->j_format_version == 0 && journal_get_superblock(journal) != 0) return 0; if (journal->j_format_version == 1) return 0; sb = journal->j_superblock; if (((be32_to_cpu(sb->s_feature_compat) & compat) == compat) && ((be32_to_cpu(sb->s_feature_ro_compat) & ro) == ro) && ((be32_to_cpu(sb->s_feature_incompat) & incompat) == incompat)) return 1; return 0; } /** * int jbd2_journal_check_available_features() - Check feature set in journalling layer * @journal: Journal to check. * @compat: bitmask of compatible features * @ro: bitmask of features that force read-only mount * @incompat: bitmask of incompatible features * * Check whether the journaling code supports the use of * all of a given set of features on this journal. Return true * (non-zero) if it can. */ int jbd2_journal_check_available_features (journal_t *journal, unsigned long compat, unsigned long ro, unsigned long incompat) { if (!compat && !ro && !incompat) return 1; /* We can support any known requested features iff the * superblock is in version 2. Otherwise we fail to support any * extended sb features. */ if (journal->j_format_version != 2) return 0; if ((compat & JBD2_KNOWN_COMPAT_FEATURES) == compat && (ro & JBD2_KNOWN_ROCOMPAT_FEATURES) == ro && (incompat & JBD2_KNOWN_INCOMPAT_FEATURES) == incompat) return 1; return 0; } /** * int jbd2_journal_set_features () - Mark a given journal feature in the superblock * @journal: Journal to act on. * @compat: bitmask of compatible features * @ro: bitmask of features that force read-only mount * @incompat: bitmask of incompatible features * * Mark a given journal feature as present on the * superblock. Returns true if the requested features could be set. * */ int jbd2_journal_set_features (journal_t *journal, unsigned long compat, unsigned long ro, unsigned long incompat) { #define INCOMPAT_FEATURE_ON(f) \ ((incompat & (f)) && !(sb->s_feature_incompat & cpu_to_be32(f))) #define COMPAT_FEATURE_ON(f) \ ((compat & (f)) && !(sb->s_feature_compat & cpu_to_be32(f))) journal_superblock_t *sb; if (jbd2_journal_check_used_features(journal, compat, ro, incompat)) return 1; if (!jbd2_journal_check_available_features(journal, compat, ro, incompat)) return 0; /* If enabling v2 checksums, turn on v3 instead */ if (incompat & JBD2_FEATURE_INCOMPAT_CSUM_V2) { incompat &= ~JBD2_FEATURE_INCOMPAT_CSUM_V2; incompat |= JBD2_FEATURE_INCOMPAT_CSUM_V3; } /* Asking for checksumming v3 and v1? Only give them v3. */ if (incompat & JBD2_FEATURE_INCOMPAT_CSUM_V3 && compat & JBD2_FEATURE_COMPAT_CHECKSUM) compat &= ~JBD2_FEATURE_COMPAT_CHECKSUM; jbd_debug(1, "Setting new features 0x%lx/0x%lx/0x%lx\n", compat, ro, incompat); sb = journal->j_superblock; /* If enabling v3 checksums, update superblock */ if (INCOMPAT_FEATURE_ON(JBD2_FEATURE_INCOMPAT_CSUM_V3)) { sb->s_checksum_type = JBD2_CRC32C_CHKSUM; sb->s_feature_compat &= ~cpu_to_be32(JBD2_FEATURE_COMPAT_CHECKSUM); /* Load the checksum driver */ if (journal->j_chksum_driver == NULL) { journal->j_chksum_driver = crypto_alloc_shash("crc32c", 0, 0); if (IS_ERR(journal->j_chksum_driver)) { printk(KERN_ERR "JBD2: Cannot load crc32c " "driver.\n"); journal->j_chksum_driver = NULL; return 0; } /* Precompute checksum seed for all metadata */ journal->j_csum_seed = jbd2_chksum(journal, ~0, sb->s_uuid, sizeof(sb->s_uuid)); } } /* If enabling v1 checksums, downgrade superblock */ if (COMPAT_FEATURE_ON(JBD2_FEATURE_COMPAT_CHECKSUM)) sb->s_feature_incompat &= ~cpu_to_be32(JBD2_FEATURE_INCOMPAT_CSUM_V2 | JBD2_FEATURE_INCOMPAT_CSUM_V3); sb->s_feature_compat |= cpu_to_be32(compat); sb->s_feature_ro_compat |= cpu_to_be32(ro); sb->s_feature_incompat |= cpu_to_be32(incompat); return 1; #undef COMPAT_FEATURE_ON #undef INCOMPAT_FEATURE_ON } /* * jbd2_journal_clear_features () - Clear a given journal feature in the * superblock * @journal: Journal to act on. * @compat: bitmask of compatible features * @ro: bitmask of features that force read-only mount * @incompat: bitmask of incompatible features * * Clear a given journal feature as present on the * superblock. */ void jbd2_journal_clear_features(journal_t *journal, unsigned long compat, unsigned long ro, unsigned long incompat) { journal_superblock_t *sb; jbd_debug(1, "Clear features 0x%lx/0x%lx/0x%lx\n", compat, ro, incompat); sb = journal->j_superblock; sb->s_feature_compat &= ~cpu_to_be32(compat); sb->s_feature_ro_compat &= ~cpu_to_be32(ro); sb->s_feature_incompat &= ~cpu_to_be32(incompat); } EXPORT_SYMBOL(jbd2_journal_clear_features); /** * int jbd2_journal_flush () - Flush journal * @journal: Journal to act on. * * Flush all data for a given journal to disk and empty the journal. * Filesystems can use this when remounting readonly to ensure that * recovery does not need to happen on remount. */ int jbd2_journal_flush(journal_t *journal) { int err = 0; transaction_t *transaction = NULL; write_lock(&journal->j_state_lock); /* Force everything buffered to the log... */ if (journal->j_running_transaction) { transaction = journal->j_running_transaction; __jbd2_log_start_commit(journal, transaction->t_tid); } else if (journal->j_committing_transaction) transaction = journal->j_committing_transaction; /* Wait for the log commit to complete... */ if (transaction) { tid_t tid = transaction->t_tid; write_unlock(&journal->j_state_lock); jbd2_log_wait_commit(journal, tid); } else { write_unlock(&journal->j_state_lock); } /* ...and flush everything in the log out to disk. */ spin_lock(&journal->j_list_lock); while (!err && journal->j_checkpoint_transactions != NULL) { spin_unlock(&journal->j_list_lock); mutex_lock(&journal->j_checkpoint_mutex); err = jbd2_log_do_checkpoint(journal); mutex_unlock(&journal->j_checkpoint_mutex); spin_lock(&journal->j_list_lock); } spin_unlock(&journal->j_list_lock); if (is_journal_aborted(journal)) return -EIO; mutex_lock(&journal->j_checkpoint_mutex); if (!err) { err = jbd2_cleanup_journal_tail(journal); if (err < 0) { mutex_unlock(&journal->j_checkpoint_mutex); goto out; } err = 0; } /* Finally, mark the journal as really needing no recovery. * This sets s_start==0 in the underlying superblock, which is * the magic code for a fully-recovered superblock. Any future * commits of data to the journal will restore the current * s_start value. */ jbd2_mark_journal_empty(journal, WRITE_FUA); mutex_unlock(&journal->j_checkpoint_mutex); write_lock(&journal->j_state_lock); J_ASSERT(!journal->j_running_transaction); J_ASSERT(!journal->j_committing_transaction); J_ASSERT(!journal->j_checkpoint_transactions); J_ASSERT(journal->j_head == journal->j_tail); J_ASSERT(journal->j_tail_sequence == journal->j_transaction_sequence); write_unlock(&journal->j_state_lock); out: return err; } /** * int jbd2_journal_wipe() - Wipe journal contents * @journal: Journal to act on. * @write: flag (see below) * * Wipe out all of the contents of a journal, safely. This will produce * a warning if the journal contains any valid recovery information. * Must be called between journal_init_*() and jbd2_journal_load(). * * If 'write' is non-zero, then we wipe out the journal on disk; otherwise * we merely suppress recovery. */ int jbd2_journal_wipe(journal_t *journal, int write) { int err = 0; J_ASSERT (!(journal->j_flags & JBD2_LOADED)); err = load_superblock(journal); if (err) return err; if (!journal->j_tail) goto no_recovery; printk(KERN_WARNING "JBD2: %s recovery information on journal\n", write ? "Clearing" : "Ignoring"); err = jbd2_journal_skip_recovery(journal); if (write) { /* Lock to make assertions happy... */ mutex_lock(&journal->j_checkpoint_mutex); jbd2_mark_journal_empty(journal, WRITE_FUA); mutex_unlock(&journal->j_checkpoint_mutex); } no_recovery: return err; } /* * Journal abort has very specific semantics, which we describe * for journal abort. * * Two internal functions, which provide abort to the jbd layer * itself are here. */ /* * Quick version for internal journal use (doesn't lock the journal). * Aborts hard --- we mark the abort as occurred, but do _nothing_ else, * and don't attempt to make any other journal updates. */ void __jbd2_journal_abort_hard(journal_t *journal) { transaction_t *transaction; if (journal->j_flags & JBD2_ABORT) return; printk(KERN_ERR "Aborting journal on device %s.\n", journal->j_devname); write_lock(&journal->j_state_lock); journal->j_flags |= JBD2_ABORT; transaction = journal->j_running_transaction; if (transaction) __jbd2_log_start_commit(journal, transaction->t_tid); write_unlock(&journal->j_state_lock); } /* Soft abort: record the abort error status in the journal superblock, * but don't do any other IO. */ static void __journal_abort_soft (journal_t *journal, int errno) { if (journal->j_flags & JBD2_ABORT) return; if (!journal->j_errno) journal->j_errno = errno; __jbd2_journal_abort_hard(journal); if (errno) { jbd2_journal_update_sb_errno(journal); write_lock(&journal->j_state_lock); journal->j_flags |= JBD2_REC_ERR; write_unlock(&journal->j_state_lock); } } /** * void jbd2_journal_abort () - Shutdown the journal immediately. * @journal: the journal to shutdown. * @errno: an error number to record in the journal indicating * the reason for the shutdown. * * Perform a complete, immediate shutdown of the ENTIRE * journal (not of a single transaction). This operation cannot be * undone without closing and reopening the journal. * * The jbd2_journal_abort function is intended to support higher level error * recovery mechanisms such as the ext2/ext3 remount-readonly error * mode. * * Journal abort has very specific semantics. Any existing dirty, * unjournaled buffers in the main filesystem will still be written to * disk by bdflush, but the journaling mechanism will be suspended * immediately and no further transaction commits will be honoured. * * Any dirty, journaled buffers will be written back to disk without * hitting the journal. Atomicity cannot be guaranteed on an aborted * filesystem, but we _do_ attempt to leave as much data as possible * behind for fsck to use for cleanup. * * Any attempt to get a new transaction handle on a journal which is in * ABORT state will just result in an -EROFS error return. A * jbd2_journal_stop on an existing handle will return -EIO if we have * entered abort state during the update. * * Recursive transactions are not disturbed by journal abort until the * final jbd2_journal_stop, which will receive the -EIO error. * * Finally, the jbd2_journal_abort call allows the caller to supply an errno * which will be recorded (if possible) in the journal superblock. This * allows a client to record failure conditions in the middle of a * transaction without having to complete the transaction to record the * failure to disk. ext3_error, for example, now uses this * functionality. * * Errors which originate from within the journaling layer will NOT * supply an errno; a null errno implies that absolutely no further * writes are done to the journal (unless there are any already in * progress). * */ void jbd2_journal_abort(journal_t *journal, int errno) { __journal_abort_soft(journal, errno); } /** * int jbd2_journal_errno () - returns the journal's error state. * @journal: journal to examine. * * This is the errno number set with jbd2_journal_abort(), the last * time the journal was mounted - if the journal was stopped * without calling abort this will be 0. * * If the journal has been aborted on this mount time -EROFS will * be returned. */ int jbd2_journal_errno(journal_t *journal) { int err; read_lock(&journal->j_state_lock); if (journal->j_flags & JBD2_ABORT) err = -EROFS; else err = journal->j_errno; read_unlock(&journal->j_state_lock); return err; } /** * int jbd2_journal_clear_err () - clears the journal's error state * @journal: journal to act on. * * An error must be cleared or acked to take a FS out of readonly * mode. */ int jbd2_journal_clear_err(journal_t *journal) { int err = 0; write_lock(&journal->j_state_lock); if (journal->j_flags & JBD2_ABORT) err = -EROFS; else journal->j_errno = 0; write_unlock(&journal->j_state_lock); return err; } /** * void jbd2_journal_ack_err() - Ack journal err. * @journal: journal to act on. * * An error must be cleared or acked to take a FS out of readonly * mode. */ void jbd2_journal_ack_err(journal_t *journal) { write_lock(&journal->j_state_lock); if (journal->j_errno) journal->j_flags |= JBD2_ACK_ERR; write_unlock(&journal->j_state_lock); } int jbd2_journal_blocks_per_page(struct inode *inode) { return 1 << (PAGE_SHIFT - inode->i_sb->s_blocksize_bits); } /* * helper functions to deal with 32 or 64bit block numbers. */ size_t journal_tag_bytes(journal_t *journal) { size_t sz; if (jbd2_has_feature_csum3(journal)) return sizeof(journal_block_tag3_t); sz = sizeof(journal_block_tag_t); if (jbd2_has_feature_csum2(journal)) sz += sizeof(__u16); if (jbd2_has_feature_64bit(journal)) return sz; else return sz - sizeof(__u32); } /* * JBD memory management * * These functions are used to allocate block-sized chunks of memory * used for making copies of buffer_head data. Very often it will be * page-sized chunks of data, but sometimes it will be in * sub-page-size chunks. (For example, 16k pages on Power systems * with a 4k block file system.) For blocks smaller than a page, we * use a SLAB allocator. There are slab caches for each block size, * which are allocated at mount time, if necessary, and we only free * (all of) the slab caches when/if the jbd2 module is unloaded. For * this reason we don't need to a mutex to protect access to * jbd2_slab[] allocating or releasing memory; only in * jbd2_journal_create_slab(). */ #define JBD2_MAX_SLABS 8 static struct kmem_cache *jbd2_slab[JBD2_MAX_SLABS]; static const char *jbd2_slab_names[JBD2_MAX_SLABS] = { "jbd2_1k", "jbd2_2k", "jbd2_4k", "jbd2_8k", "jbd2_16k", "jbd2_32k", "jbd2_64k", "jbd2_128k" }; static void jbd2_journal_destroy_slabs(void) { int i; for (i = 0; i < JBD2_MAX_SLABS; i++) { if (jbd2_slab[i]) kmem_cache_destroy(jbd2_slab[i]); jbd2_slab[i] = NULL; } } static int jbd2_journal_create_slab(size_t size) { static DEFINE_MUTEX(jbd2_slab_create_mutex); int i = order_base_2(size) - 10; size_t slab_size; if (size == PAGE_SIZE) return 0; if (i >= JBD2_MAX_SLABS) return -EINVAL; if (unlikely(i < 0)) i = 0; mutex_lock(&jbd2_slab_create_mutex); if (jbd2_slab[i]) { mutex_unlock(&jbd2_slab_create_mutex); return 0; /* Already created */ } slab_size = 1 << (i+10); jbd2_slab[i] = kmem_cache_create(jbd2_slab_names[i], slab_size, slab_size, 0, NULL); mutex_unlock(&jbd2_slab_create_mutex); if (!jbd2_slab[i]) { printk(KERN_EMERG "JBD2: no memory for jbd2_slab cache\n"); return -ENOMEM; } return 0; } static struct kmem_cache *get_slab(size_t size) { int i = order_base_2(size) - 10; BUG_ON(i >= JBD2_MAX_SLABS); if (unlikely(i < 0)) i = 0; BUG_ON(jbd2_slab[i] == NULL); return jbd2_slab[i]; } void *jbd2_alloc(size_t size, gfp_t flags) { void *ptr; BUG_ON(size & (size-1)); /* Must be a power of 2 */ if (size < PAGE_SIZE) ptr = kmem_cache_alloc(get_slab(size), flags); else ptr = (void *)__get_free_pages(flags, get_order(size)); /* Check alignment; SLUB has gotten this wrong in the past, * and this can lead to user data corruption! */ BUG_ON(((unsigned long) ptr) & (size-1)); return ptr; } void jbd2_free(void *ptr, size_t size) { if (size < PAGE_SIZE) kmem_cache_free(get_slab(size), ptr); else free_pages((unsigned long)ptr, get_order(size)); }; /* * Journal_head storage management */ static struct kmem_cache *jbd2_journal_head_cache; #ifdef CONFIG_JBD2_DEBUG static atomic_t nr_journal_heads = ATOMIC_INIT(0); #endif static int jbd2_journal_init_journal_head_cache(void) { int retval; J_ASSERT(jbd2_journal_head_cache == NULL); jbd2_journal_head_cache = kmem_cache_create("jbd2_journal_head", sizeof(struct journal_head), 0, /* offset */ SLAB_TEMPORARY | SLAB_DESTROY_BY_RCU, NULL); /* ctor */ retval = 0; if (!jbd2_journal_head_cache) { retval = -ENOMEM; printk(KERN_EMERG "JBD2: no memory for journal_head cache\n"); } return retval; } static void jbd2_journal_destroy_journal_head_cache(void) { if (jbd2_journal_head_cache) { kmem_cache_destroy(jbd2_journal_head_cache); jbd2_journal_head_cache = NULL; } } /* * journal_head splicing and dicing */ static struct journal_head *journal_alloc_journal_head(void) { struct journal_head *ret; #ifdef CONFIG_JBD2_DEBUG atomic_inc(&nr_journal_heads); #endif ret = kmem_cache_zalloc(jbd2_journal_head_cache, GFP_NOFS); if (!ret) { jbd_debug(1, "out of memory for journal_head\n"); pr_notice_ratelimited("ENOMEM in %s, retrying.\n", __func__); ret = kmem_cache_zalloc(jbd2_journal_head_cache, GFP_NOFS | __GFP_NOFAIL); } return ret; } static void journal_free_journal_head(struct journal_head *jh) { #ifdef CONFIG_JBD2_DEBUG atomic_dec(&nr_journal_heads); memset(jh, JBD2_POISON_FREE, sizeof(*jh)); #endif kmem_cache_free(jbd2_journal_head_cache, jh); } /* * A journal_head is attached to a buffer_head whenever JBD has an * interest in the buffer. * * Whenever a buffer has an attached journal_head, its ->b_state:BH_JBD bit * is set. This bit is tested in core kernel code where we need to take * JBD-specific actions. Testing the zeroness of ->b_private is not reliable * there. * * When a buffer has its BH_JBD bit set, its ->b_count is elevated by one. * * When a buffer has its BH_JBD bit set it is immune from being released by * core kernel code, mainly via ->b_count. * * A journal_head is detached from its buffer_head when the journal_head's * b_jcount reaches zero. Running transaction (b_transaction) and checkpoint * transaction (b_cp_transaction) hold their references to b_jcount. * * Various places in the kernel want to attach a journal_head to a buffer_head * _before_ attaching the journal_head to a transaction. To protect the * journal_head in this situation, jbd2_journal_add_journal_head elevates the * journal_head's b_jcount refcount by one. The caller must call * jbd2_journal_put_journal_head() to undo this. * * So the typical usage would be: * * (Attach a journal_head if needed. Increments b_jcount) * struct journal_head *jh = jbd2_journal_add_journal_head(bh); * ... * (Get another reference for transaction) * jbd2_journal_grab_journal_head(bh); * jh->b_transaction = xxx; * (Put original reference) * jbd2_journal_put_journal_head(jh); */ /* * Give a buffer_head a journal_head. * * May sleep. */ struct journal_head *jbd2_journal_add_journal_head(struct buffer_head *bh) { struct journal_head *jh; struct journal_head *new_jh = NULL; repeat: if (!buffer_jbd(bh)) new_jh = journal_alloc_journal_head(); jbd_lock_bh_journal_head(bh); if (buffer_jbd(bh)) { jh = bh2jh(bh); } else { J_ASSERT_BH(bh, (atomic_read(&bh->b_count) > 0) || (bh->b_page && bh->b_page->mapping)); if (!new_jh) { jbd_unlock_bh_journal_head(bh); goto repeat; } jh = new_jh; new_jh = NULL; /* We consumed it */ set_buffer_jbd(bh); bh->b_private = jh; jh->b_bh = bh; get_bh(bh); BUFFER_TRACE(bh, "added journal_head"); } jh->b_jcount++; jbd_unlock_bh_journal_head(bh); if (new_jh) journal_free_journal_head(new_jh); return bh->b_private; } /* * Grab a ref against this buffer_head's journal_head. If it ended up not * having a journal_head, return NULL */ struct journal_head *jbd2_journal_grab_journal_head(struct buffer_head *bh) { struct journal_head *jh = NULL; jbd_lock_bh_journal_head(bh); if (buffer_jbd(bh)) { jh = bh2jh(bh); jh->b_jcount++; } jbd_unlock_bh_journal_head(bh); return jh; } static void __journal_remove_journal_head(struct buffer_head *bh) { struct journal_head *jh = bh2jh(bh); J_ASSERT_JH(jh, jh->b_jcount >= 0); J_ASSERT_JH(jh, jh->b_transaction == NULL); J_ASSERT_JH(jh, jh->b_next_transaction == NULL); J_ASSERT_JH(jh, jh->b_cp_transaction == NULL); J_ASSERT_JH(jh, jh->b_jlist == BJ_None); J_ASSERT_BH(bh, buffer_jbd(bh)); J_ASSERT_BH(bh, jh2bh(jh) == bh); BUFFER_TRACE(bh, "remove journal_head"); if (jh->b_frozen_data) { printk(KERN_WARNING "%s: freeing b_frozen_data\n", __func__); jbd2_free(jh->b_frozen_data, bh->b_size); } if (jh->b_committed_data) { printk(KERN_WARNING "%s: freeing b_committed_data\n", __func__); jbd2_free(jh->b_committed_data, bh->b_size); } bh->b_private = NULL; jh->b_bh = NULL; /* debug, really */ clear_buffer_jbd(bh); journal_free_journal_head(jh); } /* * Drop a reference on the passed journal_head. If it fell to zero then * release the journal_head from the buffer_head. */ void jbd2_journal_put_journal_head(struct journal_head *jh) { struct buffer_head *bh = jh2bh(jh); jbd_lock_bh_journal_head(bh); J_ASSERT_JH(jh, jh->b_jcount > 0); --jh->b_jcount; if (!jh->b_jcount) { __journal_remove_journal_head(bh); jbd_unlock_bh_journal_head(bh); __brelse(bh); } else jbd_unlock_bh_journal_head(bh); } /* * Initialize jbd inode head */ void jbd2_journal_init_jbd_inode(struct jbd2_inode *jinode, struct inode *inode) { jinode->i_transaction = NULL; jinode->i_next_transaction = NULL; jinode->i_vfs_inode = inode; jinode->i_flags = 0; INIT_LIST_HEAD(&jinode->i_list); } /* * Function to be called before we start removing inode from memory (i.e., * clear_inode() is a fine place to be called from). It removes inode from * transaction's lists. */ void jbd2_journal_release_jbd_inode(journal_t *journal, struct jbd2_inode *jinode) { if (!journal) return; restart: spin_lock(&journal->j_list_lock); /* Is commit writing out inode - we have to wait */ if (jinode->i_flags & JI_COMMIT_RUNNING) { wait_queue_head_t *wq; DEFINE_WAIT_BIT(wait, &jinode->i_flags, __JI_COMMIT_RUNNING); wq = bit_waitqueue(&jinode->i_flags, __JI_COMMIT_RUNNING); prepare_to_wait(wq, &wait.wait, TASK_UNINTERRUPTIBLE); spin_unlock(&journal->j_list_lock); schedule(); finish_wait(wq, &wait.wait); goto restart; } if (jinode->i_transaction) { list_del(&jinode->i_list); jinode->i_transaction = NULL; } spin_unlock(&journal->j_list_lock); } #ifdef CONFIG_PROC_FS #define JBD2_STATS_PROC_NAME "fs/jbd2" static void __init jbd2_create_jbd_stats_proc_entry(void) { proc_jbd2_stats = proc_mkdir(JBD2_STATS_PROC_NAME, NULL); } static void __exit jbd2_remove_jbd_stats_proc_entry(void) { if (proc_jbd2_stats) remove_proc_entry(JBD2_STATS_PROC_NAME, NULL); } #else #define jbd2_create_jbd_stats_proc_entry() do {} while (0) #define jbd2_remove_jbd_stats_proc_entry() do {} while (0) #endif struct kmem_cache *jbd2_handle_cache, *jbd2_inode_cache; static int __init jbd2_journal_init_handle_cache(void) { jbd2_handle_cache = KMEM_CACHE(jbd2_journal_handle, SLAB_TEMPORARY); if (jbd2_handle_cache == NULL) { printk(KERN_EMERG "JBD2: failed to create handle cache\n"); return -ENOMEM; } jbd2_inode_cache = KMEM_CACHE(jbd2_inode, 0); if (jbd2_inode_cache == NULL) { printk(KERN_EMERG "JBD2: failed to create inode cache\n"); kmem_cache_destroy(jbd2_handle_cache); return -ENOMEM; } return 0; } static void jbd2_journal_destroy_handle_cache(void) { if (jbd2_handle_cache) kmem_cache_destroy(jbd2_handle_cache); if (jbd2_inode_cache) kmem_cache_destroy(jbd2_inode_cache); } /* * Module startup and shutdown */ static int __init journal_init_caches(void) { int ret; ret = jbd2_journal_init_revoke_caches(); if (ret == 0) ret = jbd2_journal_init_journal_head_cache(); if (ret == 0) ret = jbd2_journal_init_handle_cache(); if (ret == 0) ret = jbd2_journal_init_transaction_cache(); return ret; } static void jbd2_journal_destroy_caches(void) { jbd2_journal_destroy_revoke_caches(); jbd2_journal_destroy_journal_head_cache(); jbd2_journal_destroy_handle_cache(); jbd2_journal_destroy_transaction_cache(); jbd2_journal_destroy_slabs(); } static int __init journal_init(void) { int ret; BUILD_BUG_ON(sizeof(struct journal_superblock_s) != 1024); ret = journal_init_caches(); if (ret == 0) { jbd2_create_jbd_stats_proc_entry(); } else { jbd2_journal_destroy_caches(); } return ret; } static void __exit journal_exit(void) { #ifdef CONFIG_JBD2_DEBUG int n = atomic_read(&nr_journal_heads); if (n) printk(KERN_ERR "JBD2: leaked %d journal_heads!\n", n); #endif jbd2_remove_jbd_stats_proc_entry(); jbd2_journal_destroy_caches(); } MODULE_LICENSE("GPL"); module_init(journal_init); module_exit(journal_exit);

Xiangyang Subdistrict, Weinan Xiangyang Subdistrict () is a subdistrict in Linwei District, Weinan, Shaanxi, China. , it has 26 residential communities under its administration. See also List of township-level divisions of Shaanxi References Category:Township-level divisions of Shaanxi Category:Weinan

Welcome to my home in the blogosphere. I'll be exploring my favorite books, movies, and the writing world in general, along with discovering my new home, California. I'll also be sharing my old home, New Hampshire with you. Thanks for popping in and I hope you enjoy some romance under the moonlight. I'm a member of EPIC, Writing.com, and Military Writers of America A Gentleman and a Rogue Saturday, April 30, 2011 Victoria Holt was born Eleanor Alice Burford on 1 September 1906 near London. Eleanor left her readers and fans an amazing legacy of written material. She's best know for her pens names "Victoria Holt" and "Jean Plaidy." Today, I though I'd take a look at the reminder of her writing career, and how her writing has resonated with authors today. Before Eleanor picked up her pen, she went to business college and studied shorthand, typewriting, and languages. She even worked in a jewelry store. In her early twenties, she married George Percival Hibbert and discovered that married life gave her the freedom to writer. Eleanor's literary heroes included the Bröntes, Charles Dickens, and Victor Hugo. Her earliest work stems from the 1930. She wrote nine novels which focused on a serious psychological study of contemporary life. The novels were not published and she was told to write something that was "saleable" – romantic fiction. Eleanor's first novel was published in 1941 under her maiden name. She generally wrote contemporaries under this name. Her many pen names include: Elbur Ford, Katthleen Kallow, Ellalice Tate, and Phillipa Carr. Her least known pen name is Anna Percival which used for just one novel. She took pleasure in collecting dusty old books, reading them, and then interpreting the narratives. Despite her wealth, writing consumed Eleanor. She had a modern flat overlooking Hyde Park where she did the majority of her writing. She had a place she rented in Sandwich and furnished gothic style, but this was too distracting to her writing so she went back to her apartment in London. Gothic literature, including romantic gothic that she wrote under her pen name, "Victoria Holt," has events that on the surface appear supernatural origins, but upon investigation they have very natural causes. Eleanor once experienced a premonition that deeply affected her. At 1:20 am on 17 DEC 1983, she dreamed of a violent explosion nearby. Exactly 12 hours later, it occurred next to Harrods and was set off by the IRA. Eleanor wrote 183 books in all. Her stories have influenced a new generations of authors. I'd like to thank the following authors for sharing their thoughts on how Victoria Holt made an impact with them. I hope you've enjoyed this 3 part series on Eleanor's Burford Hibbet's life. Victoria Holt was one of the first “grown-up” authors I discovered. After my parents separated, my mom moved us 40 miles away to a coastal island. That first summer was incredibly lonely, but it was just a short walk to the library. There were two librarians and they say that I’d read all the young adult books (though it wasn’t called that then). Since I had read many of the Nancy Drew and Hardy Boys books multiple times, one librarian went over and pulled a Victoria Holt from the adult section as a suggestion. I walked back on the beach to our rented cottage and spent the rest of the day reading that book. The next day I was back for more. VH wrote beautiful scenery, and I ended up armchair traveling to places like Greece and Italy. Her genre, I believe, was called suspense. There was usually two men, one good, one out for his own personal gain, and one bewildered but intrepid heroine. I so identified with her lead characters. Here I am years later and those are still the types of story I love best, ones with an element of mystery and danger, along with a smidge of romance. I went on to read other writers like VH, but she really stood out like a sentinel beacon in my early teen years, guiding me past the emotional turbulence of my life into her safe harbor where a happy ending was guaranteed. From Maggi AndersenAuthor of The Reluctant MarquessWebsite: http://www.maggiandersenauthor.com I discovered Victoria Holt through my mother who loved her books. I came to love them too and read them voraciously along with Mary Stewart, Daphne Du Maurier and Georgette Heyer. As well as wonderful characters, these authors were superb at world creation. Du Maurier and Holt both had a great love of Cornwall. That part of the English coast with all its history fascinated me and I had to visit it although it was years before I did. The inspiration for my Victorian romance, Night Garden -- set in an ancient abbey in Cornwall with touches of the Gothic, came from those author's books: Holt's Mistress of Mellyn, Bride of Pendorric, Menfreya and Du Maurier's Rebecca. Night Garden was also influenced by a mysterious night scene painted by my mother, who was an award-winning artist. A woman in a red dress stands at the lighted doorway of a cottage looking out at the moonlit garden. I have to mention Rosamunde Pilcher another English writer who set her books in Cornwall, like the famous Nancherrow. As I'm sure you are aware, Holt published under other pseudonyms in other genres, but her writings as Victoria Holt were my favorite. A quote from Holt: Never regret. It it's good it's wonderful. If it's bad it's experience. I was a teenager when I plucked my first Victoria Holt novel from the library shelf. Even then—then being 1966—I was a voracious reader. After the first couple pages of Mistress of Mellyn, I was drawn in for the emotional ride of Holt’s novel. Classic themes: young headstrong nanny, ignored willful child, handsome aloof father and Lord of the manor, a dead wife—and a secret. All these threads were woven intricately into a lovely English tapestry. So much so, that I became interested in all things English. Over the next ten years I read every Victoria Holt novel I could get my hands on. She taught me romance. She taught me the thrill of gleaning emotions from the printed page. Thank you, Victoria. Lisa LickelAuthor, website:http://www.lisalickel.com OH my goodness – I found Victoria and some of her incarnations when I was in junior high, and still pick up a book of hers now and again. It was taking a vacation to exotic lands, Cornwall and England and Australia. Bride of Pendorric and the Shivering Sands were particular favorites. She introduced me to delicious and passionate romance with such delicacy, always with a bit of mystery and danger. I loved her stories. Of course her own life was so mysterious too, like Agatha Christie. I think those early books influenced the way I like to write, always a little twist, a little of the exotic and, of course, romance. I discovered Victoria Holt after I graduated from Nancy Drew. I knew nothing about genre and thought she was pure mystery. I loved her books and read each one I could find, and continued reading those and books by her other pen names. She had a great style. Stephanie BurkhartAuthor of "The Count's Lair"http://www.stephanieburkhart.com I discovered Victoria Holt as a teenager. I loved her novels. I loved the heroine, the dark hero, the dark settings and secrets! What was the secret? Reading Victoria Holt stimulated me. I loved to close my eyes and imagine. That's was Victoria Holt did for me. She made me imagine. In my paranormal writing today I weave in exotic settings and secrets. What's a good paranormal without secrets? Shay I fell in love with Victoria Holt and Mary Stewart (the author, not the queen) in the 1960's. I never read any Jean Plaidy books, but I love Victoria Holt's gothic romances. I think that's why I write paranormal romance (ghost stories, not vampires, werewolves etc.) In all but one Victoria Holt/Mary Stewart novel, none of the ghosts were real. When I began writing, I decided, if I'm going to write paranormal (formally known as gothic) romance, my ghosts would be real. Friday, April 29, 2011 I’m Felicity Heaton and I’m here today as part of my year-long Paranormal Pandemonium 2011 Blog Tour. Steph kindly invited me to come and share an excerpt of Hunter’s Moon, a werewolf/vampire romance novel in my Vampires Realm series with you all. Thanks for having me here today and if any readers have any comments or questions, please feel free to voice them and I’ll answer them as soon as possible. Hunter’s MoonF E Heaton The horror of the night he failed to save his werewolf pack from the cruelty of their vampire masters has haunted Nicolae for one hundred years, driving him deep into the Canadian wilderness in search of peace. That peace is threatened when unfamiliar hunters and the scent of blood lead him to a beautiful woman and a hard decision—face his past and help her or risk losing everyone he cares about again. Bearing a heart filled with grief and with vengeance on her mind, Tatyana is intent on killing the hunters she’s tracking and returning to her vampire bloodline, but her plan didn’t include being shot with poisoned arrows or rescued by a glowering alpha werewolf who stirs forbidden hunger in her. When the hunters make their move, will Nicolae be able to stop them before it’s too late? Will he be able to overcome the darkness in his heart and embrace his desire for a vampire? And can Tatyana face her fears and risk her life for the sake of forbidden love? Read the official excerpt or find out where to buy: http://www.felicityheaton.co.uk/ EXCERPTTatyana winced as she attempted to sit up on the bed in the corner of the cramped room. Her stomach ached and growled at the enticing scent of blood. She tried to move towards the smell but pain burned in waves radiating from her side, stealing what little strength she had, and she collapsed back onto the bed. Her insides twisted with hunger, mouth watering at the thought of feeding, and her fangs itched to descend. She could taste it on her tongue. The man stared at her. Werewolf. She had bitten him. Her memories were hazy, but she couldn’t forget the way he tasted. Her gaze flickered to the right side of his chest. She had scratched him too. The scent of fresh blood lingered on him. Not his blood. Nothing as strong as that. It was a strange smell—subtle and buttery. “Animal blood, I’m afraid.” He held his left hand up and she went to look at it but her gaze caught on the rifle over his right shoulder. She hadn’t noticed it before. The black strap melted into his thick shirt. His fingers grasped it tightly. Her gaze shifted to his face. Black messy strands of hair caressed his forehead, brushing his jetty eyebrows and making him look like some sort of wild animal when combined with his bright honey brown eyes. There was hunger in them that she had seen before in the eyes of the werewolves at her bloodline’s mansion. It was as though he was looking at her with his wolf eyes, not his human ones. A predator. That made her the prey. She didn’t like that one bit. There was an unmistakable Eastern European note to his accent. Not a local werewolf. Where had he come from? Was she in danger with him? What had made her wonder such a thing? The thought had bubbled up from nowhere, driven by instinct and the way her senses reacted to him, speaking of him as a threat. She tried to convince herself that it was only her injuries and current vulnerable state that was making her feel he was a danger to her but it plagued her, telling her to protect herself before it was too late. The man before her was strong, vicious by nature, and could easily overpower her. She had witnessed the savage brutality a male werewolf was capable of and she didn’t want to be on the receiving end of an attack by him. Tatyana berated herself for thinking in such a backward way, presuming he would hurt her just because he was a werewolf. She knew better than to label him as a killer, one only interested in eradicating her kind. She knew werewolves. They were as violent as her kind, but they didn’t kill without cause and he had no reason to hurt her. Besides, he had given her a valid reason to trust him. He had saved her and had bound her wounds. Although, she had bitten him. Was that reason enough? Was that why he was looking at her with hard eyes and his lips compressed into a thin line? The dark feelings between vampires and werewolves were mutual. The two species had never been close, often warring with each other in a fight for dominance that had ended with the enslavement of hundreds of his kind by hers. But he had saved her. And as payment for his kindness, she had bitten and clawed him. If she told him that she hadn’t been in control of herself, that the need for blood and to survive had been so strong that it had forced her to react in order to save herself, would it soften the anger in his eyes? The muscles in his jaw tensed. “I made a deal with the timber wolf pack. A deer in exchange for you.” A flicker of disgust crossed his face and his tone hardened, any trace of warmth gone from it. “I thought you were human. I made a mistake. I think they got the better deal.” That cut her, but she refused to let it show. He wasn’t like the werewolves at her bloodline’s home after all. They had been civil to her, and she had even built a tentative friendship with the ones she had known for most of her life. Or as close to a friendship as the law allowed. Tatyana looked away when he placed the rifle down on the couch and toed his heavy boots off, leaving them on the rug. He crouched in front of the fire and her gaze crept back to him against her will. It was difficult to see him when she was lying down. She tried to move and pain blazed up her right side. She drew in a sharp wheezing breath and closed her eyes. “I would keep still, if I were you,” he said, voice dead and cold. “I’m surprised you’re already awake.” Why, because of the wounds and the poison? Tatyana looked down at the bandages wrapped tightly around her waist and left shoulder. As he stoked the fire, the room brightened and she realised that the dark marks on the white material weren’t blood. They were black. She knew only one liquid that colour. He had drugged her. She sat up sharply, hissed as pain tore through her, and clutched her side. Panic pushed her on. She had to get away. He was going to kill her. He had come with a rifle and hadn’t expected her to be awake. He had intended to shoot her while she had been unconscious. The werewolf sighed and came over to her. Tatyana stared up the full height of him as he towered over her, broad and imposing, his face half in shadow. She growled and her fangs sharpened, her claws extending. Her senses locked on him. He was stronger than she was but she wasn’t going to give up easily. Deep aching waves of pain pulsed along her bones and nerves, stripping away the strength that had flooded her at the thought of being under threat, and she struggled to retain her true form. They were overwhelming, crushing what little energy she had and dulling her senses. Her vision wavered and fangs receded, and she barely clung to consciousness. Her eyes met his and she silently accepted her defeat. She wasn’t strong enough to fight him. His light brown irises turned golden in the firelight. Had she been mistaken earlier and this was his wolf side showing through? His eyes were beautiful but they looked like death to her. She glanced at his neck where she had bitten him and her eyes widened when she saw the faint lines of scarring around his throat. A compound werewolf? Out here? A thousand tiny needles pricked down her spine. He really was going to kill her. Tatyana tried to back away, grimacing as every part of her burned, but there was no escape. He grabbed her ankle, yanked it so she landed flat on her back on the bed and pressed his bloodstained left hand down on her shoulder, pinning her to the mattress. The force of it kept her still but only because she could sense how strong he was now that he was touching her skin on skin. She was no match for him. She wouldn’t be even at full strength. He could butcher her if he wanted to. She closed her eyes, not wanting to see her end when it came. Read the official excerpt or find out where to buy: http://www.felicityheaton.co.uk/ Biography: Felicity Heaton is a romance author writing as both Felicity Heaton and F E Heaton. She is passionate about penning paranormal tales full of vampires, witches, werewolves, angels and shape-shifters, and has been interested in all things preternatural and fantastical since she was just a child. Her other passion is science-fiction and she likes nothing more than to immerse herself in a whole new universe and the amazing species therein. She used to while away days at school and college dreaming of vampires, werewolves and witches, or being lost in space, and used to while away evenings watching movies about them or reading gothic horror stories, science-fiction and romances. Having tried her hand at various romance genres, it was only natural for her to turn her focus back to the paranormal, fantasy and science-fiction worlds she enjoys so much. She loves to write seductive, sexy and strong vampires, werewolves, witches, angels and alien species. The worlds she often dreams up for them are vicious, dark and dangerous, reflecting aspects of the heroines and heroes, but her characters also love deeply, laugh, cry and feel every emotion as keenly as anyone does. She makes no excuses for the darkness surrounding them, especially the paranormal creatures, and says that this is their world. She’s just honoured to write down their adventures. If you want to know more about me, or want to get in touch, you can find me at the following places:My website: http://www.felicityheaton.co.ukVampires Realm series website: http://www.vampiresrealm.com My blog: http://www.indieparanormalromancebooks.com Facebook: http://www.facebook.com/feheatonTwitter: http://twitter.com/felicityheatonGoodreads: http://www.goodreads.com/felicityheaton Monday, April 25, 2011 Welcome to the Desert Breeze Birthday Blog Tour. Enjoy a slice of rich German chocolate cake and a tasty excerpt with my post.*smiles* First, I just want to say "Happy 2 year Anniversary!!" to Desert Breeze. It's been a heck of a ride for me with some amazing coincidences. In August 2009, I started shopping around for publishers for my paranormal romance. The one I wanted to go with never got back to me. I waited about three weeks and then queried Desert Breeze. Gail said she liked the premise, but she wanted it in the 3rd person. I agreed and a contract was born. Then, about a week after I signed the contract, the other publisher I queried replied to me. They apologized profusely saying there was a glitch with Yahoo and they didn't get their emails over a two-week period. They were interested and said send the manuscript. Too late, I'd signed with Desert Breeze. (This other company has a great reputation and we all know Yahoo can be YaHell at times so I totally believed them when they said there was a glitch with the email.) Coincidence #1. Coincidence #2 – Gail lived in the same town I did – Castaic, CA! Castaic is a small little town just north of LA and Santa Clarita. The population is small. How uncanny was that? Once I got to talking with Gail coincidence #3 popped up: She had lived most of her life in New Hampshire! I grew up in NH! Meeting Gail was like meeting a kindred spirit. She understands my New England sensibilities, my work ethic, and "New England heartiness." She understands my sarcasm and sense of humor. It was then and there I felt as if God wanted us to meet and wanted me at Desert Breeze. And yes, while Desert Breeze embraces "sweet" romance, I'm a sucker for a good old-fashioned romantic love scene which most of my stories includes. And I don't apologize for that. –wink-- Meeting Jenifer Ranieri was like finding the cherry on top. I absolutely love Jen's laughter and her sense of humor warms my heart. Her intuition is amazing and her graphic eye is "spot on." I've worked with her in November 2009 & 2010 during National Novel Writing Month and she made the challenge worth the effort. Leave a comment on my blog today and I'll pick a winner to receive a PDF of Moonlight Sonata, the prequel to the Count's Lair along with the ARC of The Count's Lair. Enjoy this excerpt: Amelia surveyed the compact room. A double bed rested against the side wall, next to a small door. On the opposite side of the bed was a nightstand. Across from it, next to the fireplace, was a dresser, along with a mirror and another small door. Anton walked toward the door on the other side of the bed. "This is the washroom, and a small closet is over there." Amelia nodded. Anton placed her vase of flowers on the dresser. She went to the window and looked out. It faced the Danube and the parliament building. "What a nice view," she whispered. He walked up behind her and wrapped his arms around her, pressing his chest against her back. "That's why I chose it for you. The view is magnificent." His seductive voice and intimate touch made her insides grow warm. She loved to feel the full length of his hard body against hers. They didn't say anything for several minutes. Then he slowly turned her in his arms and kissed her. She molded her body to his, threading her fingers through his hair, pulling him toward her. She needed to feel him. His sweet tongue pierced the warm barrier of her mouth, and she gladly allowed him to explore. Uncomfortable warmth pooled inside her and slowly radiated out to her arms and legs. "I've missed this," he whispered between deep kisses. "So have I." He trailed his honey wet lips down her neck. "I've dreamed of you, Amelia. I've dreamed of you running your hands over my body--" She placed her hands against his cheeks and broke contact with his mouth to look into his eyes, recalling her earlier thoughts about turning him into a mess. "You want me to touch you? More intimately?" He said nothing, only his eyes, now a deep sapphire blue, expressed his desire. She placed her hands on his white shirt and slid them under his dinner jacket. He wiggled his shoulders, and the garment dropped to the floor. Then she wrapped her hands around his neck, undid his tie, and placed it on the dresser. He put his hands on her waist, drawing her closer. She started at the top button on his shirt and unfastened them. Her fingers fumbled on the third or fourth one, and he placed his hands over hers, helping to guide her. When she finished, his white shirt hung loosely over his shoulders. Friday, April 22, 2011 STEPH: I'd like to welcome Author Rhonda Lee Carver to the blog today. Rhonda, How long have you been writing? RHONDA: Through the years I’ve played around with writing. I’d write something by hand and put it away. Two years ago I decided it was time to take the big plunge and dedicate myself full-time. I haven’t regretted it once. STEPH: What genres do you write? Do you prefer a certain genre? RHONDA: I am a romantic at heart. I write western, suspense, erotica and paranormal—all with a love story. STEPH: What attracts you to writing romance? RHONDA: When I was 13 I picked up my first romance novel, a Harlequin, and read it from cover to end in one sitting. I was hooked. I knew what my calling was; it just took me a few years to find the path. STEPH: Where do you find the inspiration for your stories? RHONDA: A movie, a song, a vacation…you name it. There’s something about my mind and one sentence can trigger a while storyline. If I meet someone and they’re wearing a certain style of clothing, have a specific job or an accent, I can conjure up a character with that one trait. But what really motivates me? Laying in bed and my thoughts travel and I think up scenarios and situations. There are times when I will toss and turn, fighting sleep, until I get up and write the idea into words. That’s when I am most creative. STEPH: Do you have any marketing tips to share with other writers? RHONDA: Eer…uhh…let me see. I’m probably the worse marketer you’ll ever come across. Seriously. But if I had to give any advice I would say research how other writers are marketing. Take what works and put your own twist on it. For instance—blogging is huge. In this market, though, everyone is blogging. You’ve got to be creative and make it original. And you must be committed. STEPH: Do you have any advice for aspiring writers? RHONDA: Join a critique group…not just any…but one that trades projects frequently, has a good balance of published and non-published writers and has a group of people who don’t mind being honest—even when it hurts. STEPH: Do you own an ebook reader? If so, which one. RHONDA: Yikes, I don’t know if I should admit this or not since I’m an eBook writer, but I don’t. It is on my list of “purchases.” When it comes time I will love to ask for advice on which to buy. STEPH: Tell us a little about the place where you live in. RHONDA: Ohio. Heard of it? We’re know as “The Heart of it All.” Or, Farmland Central. Miles and miles of hills, cows, barns, and…hmm…just plain country. I live close enough to the city so if I want a taste of glamour it’s only an hour away, but at heart, I’m a small-town girl. STEPH: Are you a plotter or a panster? RHONDA: Panster. Plotting?!?! What is that? STEPH; How important is setting to a story? RHONDA: If you do your job at setting a scene readers are going to want to jump on the first plane just to check it out. For me, although I love to travel, it’s just not practical. And if you’re writing about a real place, readers want it to be accurate. Although I have written about real locations, it’s only when I’ve had the pleasure of visiting that I’ll use it as a setting. Otherwise, I love being creative and create my own town—I take a little of what I know and mix it with a lot of imagination. Second Chance Cowboy excerpt: Carly squeezed her hands into fists. “My poor husband. How difficult it is for him to manage his inflated ego and keep his zipper closed.” “We’re divorced, remember?” His voice reeked of sarcasm. She groaned in irritation. Her pulse pounded in her ears like the beating of a drum. Her claws were showing. Chance didn’t blink an eye as he gazed at her across the room. “Honey, I can keep my pants zipped just fine. Problem is, you can’t keep your fingers off my zipper.” Carly’s palm itched to slap him. “We live in a small town, Chance. How do you think it’s possible we haven’t run into each other more than three times in the last two years?” She cocked her chin. “Let me fill you in. I’ve done everything in my power to keep from bumping into you. Do you realize how difficult it is to plan my schedule weeks in advance so I don’t have to see you? Is that a description of a woman who can’t keep her fingers off your zipper?” “No, more like a woman who’s afraid she’ll forget what screwed up our marriage in the first place, realize she’s made a huge mistake and get her ass back home.” “Humph, fat chance that’ll ever happen.” She fumbled with the sheet in irritation and gave her hair a toss over one shoulder.Damn, he did have a point, although she’d never admit it to him. “Yeah, right, Carly, because you can’t ever forgive and forget, can you? You think you’re the only one who has lost, don’t you?” His eyes became steely pools of green. His voice turned low and controlled. “I lost Devon, too. He was my son--our son. How long are you going to keep blaming me for his death?” “We do?” His bitter laugh split the air with its razor-sharp intensity. “I know you want to hold on to the belief that I am the bad guy who drove you away, but isn’t it time you took half the responsibility for the failure of our marriage?” A trace of compassion softened his expression. He tugged on his shirt and finger-combed his hair. “It wasn’t my fault you cheated.” Once she said it, she wanted to yank the words back. Too late, just like their relationship.“You’re a broken record, sweetheart. It’s not worth denying the accusation any longer. Maybe eventually you’ll believe your words and feel justified in leaving. Devon died, Carly. He’s gone and we can’t change the truth. One of us needed to make the decision to let him go and I made it. I held out hope you’d eventually find a sliver of forgiveness in your cold heart. I guess I was wrong.” The old wound broke open and her lungs emptied of oxygen. She wanted to lash out at him, tell him to go to hell, but the words didn’t come. Instead, she whispered, “I’m going to the bathroom. When I get back I want you gone.” “Carly, you’ve become an expert at sucking all the joy out of your life and pushing away anyone who reaches out to you. You’re living in a self-made prison, founded on guilt and pain, and there is no key to unlock the cell door.” I hope everyone will check out my new blog. Each week I do Sex-Recipe Monday, Tuesday Author Interviews, and Friday Author Blog Specials. In between I throw in my blogs. Delaney’s Sunrise will be released June 20th, 2011 with www.lyricalpress.com Blurb for Delaney’s Dee met Jacob’s brother, Abe Delaney, and knew she’d made a mistake by agreeing to marry Jacob. Sometimes an attraction is too hard to deny, but Dee and Abe resist temptation. Jacob has a secret and when he tells Dee that he is having an affair with a man. He pleads with Dee to keep his secret. Jacob is killed in a car accident soon after. Dee wants to tell Abe the truth about Jacob, but she is bound by a promise even after Jacob’s death. Abe was overwhelmed in guilt that he’d loved his brother’s girl and withdraws within himself. Jacob’s will is read and Abe is floored. Jacob had left his half of the family farm to Dee. This was all the excuse he needed to sink further into his anger and bitterness toward Dee. Hurt, Dee leaves the farm, but now, years later, she returns. Can Dee and Abe work out their conflict regarding the farm? How will they handle the attraction that is still lingering between them, now stronger than ever? Jacob’s past lover views Dee as a threat and he will go to any means necessary to protect his reputable place in society—including murder. My BIO: Rhonda is a full-time romance author and a freelance editor. She enjoys writing contemporary, paranormal, suspense, and erotica. Her specialty is bad-ass heroes (charcoal hair, copper eyes, and heart of gold) and smart and sassy heroines. And her favorite subject is…men in military uniform. They make the perfect hero. Reading her first romance novel at age thirteen, Rhonda was hooked. Her talent of bringing interesting characters to print and shaping happy endings are not only a passion of hers, but a dream career. She thinks the love between hero and heroine should be so steamy that it melts the ink off the pages. If she’s not at her computer crafting a story, Rhonda enjoys reading romance, hanging out with her loved ones, or watching a movie that either pushes her to tears or has her rolling with laughter…and preferably both. She lives in Ohio where she is a mother by day and a sensual writer by night. She has too many pets to name but has a place in her heart for each of them. She believes everyone deserves romance in their life—one page at a time. The Queen of Gothic Romance was Victoria Holt. Her stories were populated with secrets, spooky castles/manors, heroines in distress, and 19th Century locales. Through the 1960-1980's she revitalized the gothic romance. Victoria Holt, however was a pen name for Eleanor Hibbert, and while it was her most famous pen name which earned her the most money, I believe Eleanor found the most enjoyment and fulfillment with the Jean Plaidy pen name. My Own Personal Experience with Jean Plaidy I had read Victoria Holt in high school, (1982-86) and at the time, I got my fix at the local library. I loved the Manchester, NH library with its open rooms. Then I joined the Army in 1986 and went to Germany for my first assignment. In July 1988, I discovered my first Jean Plaidy book. I was sent a "care package" and Queen in Waiting was in it. It's the story of George II and Caroline of Ansbach. I took the book to Berlin with me, devouring it on the duty train. I LOVED this book. To this day, it is one of my favorites. George and Caroline's romantic love story touched a chord in me. Fairytales do come true and while George II was not perfect, what I loved about Plaidy was that she made George II deliciously human and sympathetic, and I, as a reader, appreciated that. When I got back to the states, I went on a hunt for Jean Plaidy books. I simply could not get enough of her wonderful historicals that wove fiction and truth so effortlessly. Author Jean Plaidy During World War II, Eleanor Hibbets and her husband lived in Cornwall near a secluded yet picturesque beach called – Plaidy. The beach inspired Eleanor's new pen name: Jean Plaidy. Her first Jean Plaidy novel was "Together They Ride" in 1945! It was set in the 18th century about Cornish smugglers. It was well written, but not very successful. Plaidy's next novel was "Beyond the Blue Mountains" and established the relationship between her and her publisher, Robert Hale which would last until her passing in 1993. "Beyond the Blue Mountains" was over 500 pages and was rejected by several publishers before it was published in 1958. It spanned 3 generations of women and began in the mid-18th century. Over the course of the next 15 years, Plaidy turned her attention to bringing history to life. Her earlier stories involved Jane Shore (Edward IV's mistress, I believe), Katherine Parr, (Henry VIII's 6th wife) and Henry VIII's sisters, Mary and Margaret. Plaidy's career reached its height between 1960-70's, and she became one of Britain's most popular and accomplished authors. While fictionalized history, her novels were methodically and carefully researched. She loved reading dusty old history books and putting scenes into her words, making them vivid and exciting. Eleanor described her writing as "pure entertainment," but she believed it was nicer to be read than to receive reviews. One article in the Sunday Times summed up her success as such: "Jean Plaidy, by skillful blending of superb storytelling and meticulous attention to authenticity of detail and depth of characterization, has become one of the county's most widely read novelists." For me, looking back, this is exactly why I enjoy Plaidy's novels. The bulk of Plaidy's historical works is extensive. From 1967-1971 she wrote the Georgian Saga (which I've read) and in the 1970's she wrote the Plantagenet Saga (15 books! I've read most) and in the 1980's she wrote the Queens of England, which I've enjoyed. So how historically correct was Plaidy? Very. She researched her writing well and if she mentioned a little known fact in her novels, then there was a historical basis for it. One of the most fascinating little tidbits I read? In "The Queen's Secret" about Henry V and Katherine of Valois, Plaidy mentions that a fortune teller told Henry V if his son was born at Windsor Castle then his son would live long, but lose everything Henry V won. If his son was NOT born at Windsor Castle, he would not live long, but would hold onto what Henry had won. Henry V believed this down to his bones and when Katherine was pregnant, sought out her reassurances often that she would not have their children at Windsor Castle. Katherine's favorite castle however, was Windsor Castle. She firmly intended to honor her husband's request not to have the child at Windsor, but stayed too long. A winter storm struck, and she had the child at Windsor. When Henry V was told, he fell to his knees and wept. He died 8 months later. His son, Henry VI, was haunted by what we now know was schizophrenia. He lived long, but lost everything Henry V had won in battle. You rarely find this depth of research in other historical novels. Starting in 1952, Plaidy published 2 novels a year, but in 1981, raised her output to 3 novels a year. In 1983, Eleanor was in her late 70's. Her last Plaidy novel was "William's Wife" about Queen Mary II, which was released in 1992. Do you have a favorite Jean Plaidy book? What drew you to Eleanor's Jean Plaidy pen name? Friday, April 15, 2011 Theresa is a fellow author with me at Desert Breeze and has a release out this month, "Saving Pale Moon." She's here today to talk about her story. Welcome, Theresa. STEPH: How long have you been writing? THERESA: I started way back in my teens. I remember I started writing a historical set in the West. I wrote it long hand and never finished it. All I remember about it was the beginning. She was on a train, thinking about why she was on the train. I didn't write 'the end' on a book until the mid1980s. STEPH: What attracts you to romance writing? THERESA: I've always read them. Romances are empowering. The main characters go through so many things, but they always manage to resolve them and get their happy ever after. Real life isn't always that way. STEPH: Where do you find inspiration for your stories? THERESA: I find my inspiration everywhere I look. I can sit in a restaurant and watch people and come up with characters, or a possible plot. LIstening to people, watching tv, and reading have given me ideals. Once I even dreamed a major scene and I built a story around it. But I think my inspiration comes mostly from the secondary characters of my finished books. Just about everyone of them has at least one person screaming at me to write their story. STEPH: Tell us a little about Saving Pale Moon. THERESA: Jessica Callaway isn’t happy. Maybe meeting her birth mother now would be a good thing. And it would be if only for her brother. Blake Hunter doesn’t trust her. Why is she here now, after finding out about Abby twenty years ago? She does look like his adopted mother, but he plans on keeping a cool head until the verifying blood tests are done. Jessie senses his distrust, but she is still way too aware of him. The mere sound of his voice sets her on edge. When her birth mother tells her Blake is adopted, she relaxes her guard and decides to enjoy her time in Texas . With all the horses surrounding her, especially Pale Moon, she’s in heaven. Unfortunately Blake isn’t as accepting as the other Hunters. Has she done the right thing coming to Texas ? Or has Jessie made the biggest mistake of her life? STEPH: How long did it take to write? THERESA: I had the ideal for this book for a long while before I actually started writing it. I've lived with these sisters for about fifteen years. I let them go when I couldn't sell the original first book to the series. Jessie stayed in my head all those years so I finally sat down and started writing her story. I don't remember the actually date, but I finished it way back in 2007. It went through a lot of changes since then. STEPH: Did you have to do a lot of research for the story? THERESA: No, not really. I did do some research on dude ranches and horses. STEPH: What's the theme of Saving Pale Moon? THERESA: I think it letting go and learning how to trust. STEPH: Cast the characters? Who are the leads for Saving Pale Moon? THERESA: Jessie Callaway is the heroine. She needs to find answers to question her adopted parents can't help her with so she decides to meet her birth mother. Life hasn't been treating her well lately. More than just possible health problems have convinced her to come to the ranch. Blake Hunter is her birth mother's adopted son. He doesn't believe her reasoning for coming to the ranch now, when things are looking up for the Hunters. He doesn't want to get involved with her because he thinks he's like his abusive birth father. This is the main reason he doesn't want to trust her. STEPH: Tell us a little about the state you live in. THERESA: Right now I live in Georgia. My husband and I just moved here half a year or so ago, but I love the area. We live in an RV, in a campground in Savannah. The city is beautiful with a lot of history. We haven't really had a chance to see much of it yet but we plan on taking one of the bus tours of the city. And I'd love to do a ghost tour. STEPH: Do you have an ebook reader? If so, which one? THERESA: No, not yet. My birthday is coming up in May so I'm hoping my husband will get me a Kindle. I do so want one. It'll be so much easier curling up with an ebook reader. Right now I have to read all my books on the laptop. STEPH: What's your writing space like? THERESA: The kitchen table. We live in an RV so we have very limited space. BIO Theresa Stillwagon has been writing most of her life. Since one of her teachers praised a poem she wrote for a class assignment, she's been putting words together in the hopes of seeing them in print. Not caring if anyone other than herself ever read them. Her dream came to reality in 2008 when she signed her first writing contract. She's now just signed her fourth one, the first story in a series of five called The Sisters Callaway. A former resident of the state of Ohio, Theresa now lives in her RV in the sunny city of Savannah, Georgia, with her husband of twenty-eight years and her two cats, Fred and Barney. She's currently searching for a job while hard at work working on the next installment of The Sisters Callaway series. You can find more out about her by visiting her website at http://TheresaStillwagon.webs.com. Thursday, April 14, 2011 San Luis Obispo is on the central coast of California. It's very nice country, rural, picturesque, and San Simeon, where the Hearst castle is, isn't that far away. It's been 9 years since I've been out that way and for me it's about a 4 hour drive north of Castaic on U.S. Rte 101. In 1867 President Andrew Johnson issued an executive order to have the lighthouse built. At the time, the land was called Port Harford. It would take 10 years before a bill was introduced into the House of Representatives for the construction of the lighthouse. Meanwhile, a pier had been constructed on the land in 1864. This was a 540 foot pier. In 1878, a tidal wave struck the area and washed this pier out to sea. During low tide, you can still see the pilings of the old pier from the Availa Pier that is now there. As I research these lighthouses for my series, I discover there's always a story behind the house. It was 1888 and still no lighthouse had been built at Port Harford. A passenger and cargo steam ship called "The Queen of the Pacific" was traveling the harbor around 2 am. It was dark and the captain misjudged his clearance. The ship was 500 feet away from the pier when it sunk in 22 feet of water. Thankfully, most of the ship was still above water and no lives were lost. The ship eventually refloated but it was argued that had there been a light, the ship would have safely made it to the pier. Construction on the lighthouse began in 1889. The lighthouse was finished in 1890. Amazing what a shipwreck can do, isn't it? In 1893, the kerosene lamp was replaced with an electric one. During World War II, a radio listening station was built in front of the lighthouse. In 1961, the Coast Guard pushed the original double building over the cliff using a bulldozer and replaced the structure with a more modern one. In 1969, the Fresnel lens was retired. An automated electric light was installed. Note: A Fresnel lens design allows the construction of lenses of large aperture and short focal length without the mass and volume of material that would be required by a lens of conventional design. Compared to conventional bulky lenses, the Fresnel lens is much thinner, larger, and flatter, and captures more oblique light from a light source, thus allowing lighthouses to be visible over much greater distances. In 1974, the lighthouse was closed and in 1976, the Fresnel lens went to stay in the San Luis Obispo Country Historical Society. The station has since been restored and opened to the public. The Fresnel lens was returned to the lighthouse for the public to see. Wednesday, April 13, 2011 I'd like to welcome author Sarah Grimm to the blog today. Sarah is the author of "Not Without Risk," a romantic suspense set in San Diego. I just recently read her book and LOVED it!SmilesSteph **** STEPH: Sarah, thank you for visiting Romance Under the Moonlight. Can you tell us a little about yourself? SARAH: Thanks for having me here today, Steph. Let’s see, I live in West Michigan with my husband, two teenaged sons, three miniature schnauzers, and a guinea pig named Lilly. Recently I went from being a stay-at-home mom who kept the books for my husband’s business, to working full time as an Office Manager/Bookkeeper. STEPH: How long have you been writing? SARAH I’ve been writing for as long as I can remember. I have notebooks filled with poems, story ideas, and partial chapters from as far back as age five. Yes, thanks to my older sister, I could read and write by age five. And I did. I read everything I could get my hands on, usually re-writing the story in my head as I went. STEPH: What attracts you to romance writing? SARAH: I’m a romantic—a die hard romantic. I believe in love, not just as a fundamental part of human relationships, but as a force that really can heal emotional scars. I truly believe there is someone for everyone—the person they are meant to find. Their other half. Their soul mate. So it makes sense that I chose to write about two people finding each other, falling in love, foiling the villain and living happily-ever-after. STEPH: What genres of romance do you prefer to write? SARAH: I write romantic suspense—stories where the romance and the suspense play an equal part—and also contemporary romance, with a bit of suspense woven in. I’ve tried to write without any danger or suspense, but can’t seem to do it. No matter my plans when I begin a story, before I know it, one of my characters is facing an enemy that wants them dead. STEPH: Where do you find the inspiration for your stories? SARAH: From everyday life: The stories I read, the music I listen to. Even conversations I overhear while grocery shopping or sitting at the DMV. STEPH: Not Without Risk is a Nominee for Book of the Year with LASR! Congrats. Can you tell us a little about it? SARAH: Thanks. Not Without Risk was the first time I saw down and wrote a book from the beginning to the end, so it will always have a special place in my heart. As you can imagine, I’m absolutely thrilled by the great reviews it’s received, even more so when I learned of the nomination from LASR. I didn’t win, but came in third behind Toni Blake and Jill Shalvis respectively. Pretty good for a debut author, I thought. Not Without Risk is a romantic suspense with a wounded hero—the story of Sergeant Justin Harrison, who returns to his job as a San Diego homicide detective after six months of medical leave. Determined to prove he’s fit for active duty, he doesn’t need the self-doubt that plagues him, or his growing feelings for the leggy brunette who is at the center of his homicide investigation. STEPH: How long did it take to write Not Without Risk? SARAH: I have at least four different, completed versions of the book, a couple from when I called it by a completely different name. I wrote it, set it aside, went back and rewrote it from the beginning, then set it aside…well, you get the idea. I have no idea how long it took before I was satisfied with it. A long time. ☺ STEPH: How important was setting? Have you been to San Diego? SARAH: The setting isn’t really important beyond the fact that it’s so far away from Boston, where Paige grew up. Any city in California would have worked. I chose San Diego because of its beauty and history. Have I been there? Unfortunately, no, but the next time I’m in LA visiting my brother, I plan to go. STEPH: Did you do a lot of research for Not Without Risk? SARAH: I didn’t do any research for Not Without Risk specifically. It was all things I’ve learned over the years of reading both fiction and non-fiction. Wait, I guess I did quiz a security system installer to make certain what I wanted to do with Paige’s system was feasible. STEPH: Cast the movie! Who plays the leads Justin &Paige? SARAH: Paige is easy, from the first draft of the story, I've always pictured Angie Harmon as Paige. I changed her hair and eye color, but the height, build and smile...all Paige. Justin, hmm…that’s a tough one. I guess I’d have to pick Joe Manganiello. STEPH: Do you own an ebook reader? If so, which one? SARAH: I have a first generation Amazon Kindle that I love. Until a few weeks ago I had no plans to upgrade to a newer e-reader, then I saw a special on e-readers and discovered that Barnes and Noble has plans to add Apps to their Nook color. I want one! STEPH: Do you have an advice for aspiring authors? SARAH: Don’t let anything keep you from achieving your dream. Anything is possible when you want it badly enough. STEPH: For fun: Monet, Picasso, or Renoir? BUY LINK: KINDLE LINK FOR NOT WITHOUT RISK: http://www.amazon.com/Not-Without-Risk-ebook/dp/B00365FI5I/ref=sr_1_1?ie=UTF8&m=AG56TWVU5XWC2&s=digital-text&qid=1302012249&sr=1-1SARAH: Monet. Tuesday, April 12, 2011 I thought I'd share my recent book review for "Not Without Risk," by Sarah Grimm. I LOVED this book. It had everything - romance, heat, sexual tension, a compelling plot, and a twist you wouldn't expect. Tomorrow, Sarah will be with us for a guest interview. Grimm crafts an edge-of-your seat romantic suspense with "Not Without Risk." Photographer Paige Conroy finds an old friend, Leroy St. John, dead in a hotel room. Unknown to her, she's opened up a can of worms. Can Detective Justin Harrison keep her safe? Set in present day San Diego, CA, Grimm puts the reader right into the action when detective Justin Harrison and his partner are called out to the scene of a murder. As he investigates, he learns the victim, St. John, is a cop from back East. A local photographer, Paige Conroy, found the body. When Justin meets Paige, the sparks fly. Justin and Paige acknowledge their physical attraction, but each have emotional hang-ups. The danger increases when Paige is sent an email with pictures of her apartment – taken at night when she was sleeping. Spooked, Paige goes to the police – and Justin. Justin is determined to put the clues together, but remains stymied. When Paige's classic car is blown up, Justin throws professional caution to the wind and insists Paige stay with him for her safety. Justin's partner, Allan, is concerned Justin is blurring the lines between his job and his heart. Paige holds the key to cracking the case, but can Justin solve it before he loses his heart – and his objectivity? Grimm's writing is sharp. The plot is tight with several twists and turns that will keep the reader on their toes. Grimm engages the reader immediately, placing them in the scene with Justin. The dialogue is crisp. The descriptions are spot on, never lingering, and there's the perfect blend to set the scenes. Both Justin and Paige are compelling characters. Paige has been hurt before. She was once engaged to a police officer who put the job before her. Her fiancé died performing his job, and Paige is reluctant to commit to Justin emotionally. She's uncertain if Justin is worth the risk. Justin is deeply committed to his job. Unfortunately, he received a bullet wound while off duty and the effects of the injury are still lingering. Justin's never really let a woman into his life. The danger Paige faces easily brings out all his protective instincts, yet letting Paige into his heart is not without risk. The novel is sophisticated for romance readers. Grimm's love scenes are sensual, full of heat, and capture the intense connection between Paige and Justin. "Not Without Risk" is a heart pounding suspense that does not disappoint. Monday, April 11, 2011 Note: This is an excerpt from my upcoming novel, "The Wolf's Torment" which will be released by Desert Breeze 1 MAY. It may vary upon publication. The set up: In this scene, Theresa's father, wants to give Mihai "the son-in-law" talk - witch style. ********** Theresa stood and grinned at hearing her father's voice. He walked over, arms extended, and she ran into his burly embrace. He parted from her, gripping his hands on her upper arms. There was no mistaking thepride in his eyes. "You look wonderful." "Papa! That must have been the fifth time you said that." "Oh, let me be proud of my little girl. Now, when is your honeymoon?" "We leave tomorrow morning." "So soon?" "Yes." Theresa's father looked up from her and then at Mihai. "I must talk with your husband. You don't mind if I take him aside, do you?" "You're not going to scold him, are you?" A playful spark danced in her father's eyes. "No, I'm just going to threaten him. If he doesn't treat you right--" "Oh, Papa! No threats." Her father chuckled. Mihai gestured toward the door. "We can talk in the study." "Papa--" "It will be fine, Theresa. I had the same talk with Victoria's husband." Theresa sighed. "I'll keep you company," said Sonia. "I'm sure my father had the same talk with Viktor." "Thank you." Mihai squeezed Theresa's hand and escorted her father outside of the ballroom. Edward and Victoria joined them. Theresa's father looked at him. "I asked them to join us." When he opened the door to his study, Mihai found Beatrice sitting in a chair, waiting for them. He didn't know if he should be worried, insulted or flattered. Why did Theresa's whole family have to be here? "Would you like a drink?" Mihai asked. "No, I want to get right to business."Mihai gestured for him to take the couch. Theresa's father sat down. Edward and Victoria sat next to him. Beatrice stayed in her chair. Mihai grabbed a spare chair from a corner and joined the circle. Theresa's father steepled his fingers. "I often wondered what happened to Esmeralda. She had such promise and her father was reckless with her future." "You knew my mother?" "Yes, I knew Esmeralda Vacay." Mihai's heart leapt. What luck! His bride's father had known his mother, but of course, he would -- he was a witch. "What do you mean, her father was reckless?" "He wanted revenge for a minor insult and promised Esmeralda into service to Hecuba and her coven. Esmeralda refused to go and disappeared. I learned years later through Count Brancoveanu that she married into Moldavia's royal house." "Hecuba?" questioned Mihai. The witch who killed his mother! Theresa's father looked at him, his expression serious. "Hecuba isn't your problem. The wolf in your house is." "Viktor." Mihai drew in a breath. Viktor wasn't the same man he knew in London. Mihai's heart went out to his friend as he struggled with to hold onto his caring and kind nature. "Beatrice told me what occurred and that you and your sister received lessons from her." "She has been a good teacher." "Good. You'll need to keep learning and practicing on your own. Beatrice must accompany us back to Austria. When I can, I'll spare her for a visit or two, but you must be diligent or the wolf will ruin your house." "Viktor would do no such thing." "Yes, he will. He is a wolf. He wants two things -- blood and sex. This feral need will consume his human body, and when it does, he will plot against you, purposely hurt you, and eventually try to kill you." "Nonsense." Theresa's father snapped to his feet. "You indignant boy! Do not presume to dictate to me how Viktor will behave. I know the wolf mentality and every man succumbs to the feral nature." Mihai stood as well, unsure of how to react, but convinced the elder witch was very serious and he needed to be serious as well. "Tell me what to do." "I sense reluctant acceptance coming from you, but you must not be reluctant to act when the time comes. Not only that, but the situation is complicated by Theresa's ignorance." "Why did you raise her not to know her talents?" asked Mihai. "I foresaw her future at birth and it dictated she must be ignorant of her heritage. If she ever practices witchcraft, she faces death." "Death?" A wave of apprehension threaded through him. He'd wanted to explore witchcraft with her. What did her father mean? Saturday, April 9, 2011 I very rarely have a chance to hang out with my son on Cub Scouts events. Usually, with my schedule, I'm working during the times of the meeting or I have to watch our younger guy, Joe. This time around, the Santa Barbara Zoo Snooze was being held during vacation week and Gramme was able to watch Joe, so I had a chance to accompany Andrew (who is a Bear Scout) and my husband on the Santa Barbara Zoo Snooze. The Zoo Snooze was held 2-3 APR 2011 at the Santa Barbara zoo. What is it? From the website: Our adventure starts in the evening when you set up camp on a lawn next to the lion exhibit or in our heated, indoor classroom. Then our instructors lead your group through a series of exciting, hands-on educational activities including up-close animal encounters and behind-the-scenes explorations. An evening snack is also provided. In the morning, your group will enjoy a delicious pancake breakfast, another up-close animal encounter with one of our zookeepers, a train ride, and creating a special breakfast treat for one of our Zoo animals. At the conclusion of our program, you are welcome to explore the Zoo with your group on your own to see all of your favorite animals in the light of day! Link:http://www.santabarbarazoo.org/sleepovers.asp Feeding the giraffes I can't say enough wonderful things about the Snooze! Our day started at Longboards in Santa Barbara. We met up with a couple of families from Andrew's den and had dinner at the restaurant on the wharf there in Santa Barbara. For me, what I LOVE about Santa Barbara is that it's about an hour's travel north of where we live, but it's quiet, low key, and there's plenty to do and see. It makes a great day trip if you just want to get out. I really enjoyed getting out and just visiting with the other cub scout adults in Andrew's den. The day was a bit overcast and misty, but it wasn't anything that we couldn't adjust to. I loved the view of the ocean and the seacoast from the wharf. After we ate, we headed off to the zoo. We got there a little early and waited in the parking lot for the majority of the pack to show up. Andrew belongs to Cub Scout Pack 40 out of Santa Clarita, CA. At 6:30 pm we were let into the zoo and led to the little knoll near the lions. There we set up our tents. Our tent was a little small, but we did fit a queen size air mattress in it. While my husband put most of the tent up, Andrew and I helped a little. After our gear was in the tent we were broken down into 4 groups. If anything, my only unhappiness with the zoo snooze was that it was a bit of a hike to the bathrooms. LOL!! Stephanie, our guide, with "Rosy Boa." We had a great instructor/guide. Her name was Stephanie and she was very knowledgeable. Our first stop: Feeding the giraffes. The zoo has 3 giraffes. Selma is about 20 years old (human years). Then there's Audrey, 3 years, and when they got Audrey last year, she had a surprise for them - she was pregnant. Baby Daniel is now 6 months old and he's a cutie. Giraffes have really funky tongues - purple and slimy, the better to eat vegetation with. The sun was setting and there was a light mist when the giraffe feeding was done. Stephanie took us for a behind the scenes look at the zoo. Our first stop: The animal hospital. At the animal hospital, we learned the animals get their yearly checkups there. Only two animals in the zoo don't – the elephants and the giraffes. We had to wipe our feet on antibacterial stuff before we went in. After that we went to the animal kitchen. After our tour of the kitchen we went to the BE room. I can't quite remember what BE stood for "Behavioral Environment?" possibly, but every animal needs to be stimulated intellectually, and the BE room had a lot of things in it including scents, old tennis shoes, and cardboard. In essence, the BE room had a lot of toys in it. After the BE, Stephanie took us to the "Ewww" exhibits were we saw a lot of creepy, crawly things. She even brought out a rosy boa, a type of snake, for us to pet and check out. When we finished visiting with "Rosy" we had a popcorn snack near the elephants. The ambience was cool, but we were downwind of bird poop. ☹ Stanley, the bird. Stephanie was a great guide. She interacted well with the kids and was able to answer all our questions. The evening finished, we retired to our tents. It was around 10:00 pm. Our tent was a little cozy and it did mist while we were sleeping. At 4 am, the lions gave us a wake up call with a couple of roars, but I was so tired I went right back to sleep. 7 am we got our zoo snooze official wake up call. It was still overcast, but no mist. We packed up, brought our gear to the truck and it was time for breakfast. Breakfast was fab – pancakes, coffee, bacon, sausage, oj. I enjoyed it. And I was hungry. Being 40 something and all, I just don't have the same energy I had when I was 20 something and the breakfast hit the spot. After breakfast I got a couple of zoo snooze t-shirts for the boys in the gift shop, and then we went to the elephant pen to come up with a BE for the elephants. We hid food in boxes and all around their pen. It was really cool. If anything, though, I thought it was a small space for them. There were two elephants, Suzie and Little Mac. I think the bigger of the one weighed in at about 8,900 pounds! We also visited with Stanley, the bird. I can't remember what type of bird he was, but he wasn't an owl. Stanley was very friendly, but he trainer said he was a little lazy. It was a amazing just how well he blended in with a tree. BE for the Elephants We had a train ride around the zoo. The best part was chugging past the lions. The male lion was on his back – paw on his stomach – sleeping. The bum! LOL!! After the elephants we were released from the snooze and checked out the gorilla. When we left we hit up Rusty's Pizza near the wharf before heading home. I had a great time. Andrew & my husband did, too. If you ever get a chance to check out a similar-like program with your zoo or get a chance to do it in Santa Barbara, I highly recommend it. It's a great learning experience outside of the classroom. Kids and adults will both have a great time. Thursday, April 7, 2011 Just a couple of weeks ago, I took my 8-year-old son, Andrew, to the Reagan Presidential library. I have to admit it was a real treat – not only to have presidential library in my backyard, but the Reagan library. He was president when I was coming of age. He inspired America to believe in itself again. He was president when I joined the Army and I was proud to serve for him. Reagan's library is located in Simi Valley, CA. Construction began in 1998 and it was dedicated on 4 NOV 1991. (I was married on 14 NOV!) Interesting historical note: Presidents Nixon, Ford, Carter, Reagan, and George H.W. Bush were present when the library was dedicated. The Reagan library has some cool exhibits including Reagan's early years in Dixon, IL, his career in film, and his time as California's governor in the 1960's. What struck me, especially with the governor's exhibit, was that Reagan faced the same challenges that California faces now. California was in debt and facing an energy crisis. By the time he left office, California had made some hard decisions and was on the road to recovery. What resonated with me, however, was the Cold War displays. There is a piece of the Berlin Wall on the grounds. I had been to Berlin and even have pieces of the wall myself. I saw the wall before it fell. I had a front row seat to the end of the Cold War in Nov 1989 as I was stationed in Germany when East Germans stormed the wall. I can still hear Reagan's voice. "Mr. Gorbachev, tear down this wall."The most impressive exhibit is Air Force One, the Boeing 707 aircraft which carried Reagan and many other presidents around the world. It was retired in 2011 and transported to the library in pieces. The exhibit began showing in 2005. Currently, Air Force One rests on pedestals 25 feet above the ground and you can walk through the plane, acquiring a feel for presidential travel. The Reagan library is still an active place. In 2008, it hosted the GOP presidential debates. President Reagan was laid to rest on the grounds against a view that embodies the love and affinity he felt for California and the west. Does anyone want to share their thoughts and impression of the Reagan years? Monday, April 4, 2011 Blurb: When Darrin falls for his beautiful Polish interpreter, will Sophia's faith give him his heart back?The Set up: Darrin and Sophia are finishing dinner at a local restaurant. The waiter came and Darrin gave him his credit card. "I'd invite you shopping with us, but I'm afraid you have a lot of work to do." Darrin frowned. He did, but he hated to miss the opportunity to learn about the Easter basket and go shopping for it. "Why don't you join us for mass on Palm Sunday?" "Really? A mass? I haven't been in months. I'd need a confession." "Do you want me to ask Father William if it would be permissible for me to translate for him? He takes confessions on Saturday afternoons." "All right." "You can work in the morning. I'll call you in the afternoon. Do you mind taking the metro again?" "That's fine." "What if he can't take your confession?" asked Sofia. "I'll still go to mass with you, but I'd like to be able to receive the Eucharist." Her smile widened, warming his heart. "I would like that. I'll do my best to help get you a confession." The waiter returned and Darrin signed the bill. They left. Sofia's car was parked in front of her house. The car ride back to his hotel was silent. She'd given him a lot to think about. How did he want to live his life? Falsely, trying to meet his parents' expectations? Or did he want to let his heart breathe? He was twenty-nine. Wasn't he entitled to let himself follow his own course? He had a good job, a nice apartment – he just had to live the way he wanted. And he had to guard his heart, turn away dishonesty and keep his eyes firmly on the path ahead, as the rest of the verse advised. Sofia pulled up to the front of the hotel and put the car in park. Darrin turned to face her. The fringes of her lashes cast shadows on her cheeks, softening her expression. He reached out and gently took her hand in his. Her touch sent warm tendrils of desire through him. With the other hand, he cupped her cheek. She closed her eyes, and drew in a sharp breath before opening them again. Lightly, he rubbed his thumb against her jaw. "May I kiss you?" His voice was low and husky. "Yes." He leaned forward, his lips feather light, touching hers with tantalizing persuasion until she opened up to him. He kept the kiss slow, thoughtful, enjoying the hints of berries and currants that lingered from the malbec. He pulled away gently. "That was nice," she whispered."Call me tomorrow.""I will."Darrin opened the door and stepped out. He waved to Sofia and she waved back as she drove away. Darrin went to his room and revisited his luggage, removing his travel Bible from an inner pocket. He always took it with him, just in case. Opening it up, he went to the book of Proverbs, sat up against the headboard of the bed, and began to read. Friday, April 1, 2011 One of the first authors I read as a teenager that left a resonating impression with me was Victoria Holt. And while I sheepishly admit that I can't remember my first Victoria Holt novel, I recall that I loved the ambience of her novels, the gothic settings, the spooky mansions, and the clever heroine. These elements of storytelling echo in my own paranormal romances. So who was Victoria Holt? Enjoy this first part of a three part series. Victoria Holt was a pen name for Eleanor Alice Burford. She was born on 1 September 1906 near London. Young Eleanor claimed to have inherited her love of reading from her father, Joseph Burford. Eleanor loved London and considered herself lucky to have lived there. As a young woman, she went to business college and studied shorthand, typewriting, and languages. She also worked for a jeweler. In her early 20's, Eleanor married George Hibbert. Married life gave her the freedom to follow her writing. In 1961, Eleanor created the Victoria Holt pen name. Her first novel as Holt was "Mistress of Mellyn." Her intention was to revive the once popular genre of gothic romance. Very deliberately, she set her stories in gloomy old manors and usually in the 19th century. Most of Holt's gothic romances are told in the first person by the heroine who is usually a governess or a ladies companion. What made Eleanor stand out is that she carefully researched these novels to capture a certain degree of authenticity. The Victoria Holt pen name was her biggest money earner. Despite her wealth, Eleanor lived a simple life. Her only hobby was generally to take a 2-3 month cruise in the winter. Typically, she wrote 5 hours a day, 7 days a week, beginning at 7:30 am. She usually had finished 5,00 words by noon. In the afternoon, she personally replied to fan letters. It's amazing to believe that Eleanor never had a chance to use a word processing computer program and that she typed her novels on typewriters! Eleanor loved her writing, even taking her typewriter on her cruises. She died 18 JAN 1993 while on a cruise ship during her winter vacation. Next: Eleanor's early novels and Jean Plaidy. Question: Do you remember the first Victoria Holt novel you read? Do you have a favorite? 2012 Romance of the Year Journey of the Heart AMAZON BEST SELLER! It's 1946 - can James help Rachel save her winery after the ravages of war? Visit me on Twitter at: StephBurkhart My Official Online Newsletter I release my official online newsletter once a month, around the middle of the month. The newsletter includes: a genre writing article, self-editing tips, news from the publishing world, a look at a small press, a receipe, reviews, and announcements. The newsletter is free. Just fill out the form and send it in. To comply with new FTC regulations, please assume all books reviewed on this site have been provided free of charge by the publisher or the author. Please note links to buy books are provided as a convenience, and do not serve as an endorsement by this blog. *********** Quotes on writing: "Transitions are critically important. I want the reader to turn the page without thinking she's turning the page. It must flow seamlessly." - Janet Evanovich "You can stroke people with words."~ F. Scott Fitzgerald "Words are... the most powerful drug used by mankind."~ Rudyard Kipling Write drunk; edit sober.- Ernest Hemingway "A word is deadWhen it is said, Some say.I say it just Begins to liveThat day."~ Emily Dickenson "Never Regret. If it's good, it's wonderful. If it's bad, it's experience." - Victoria Holt By Heart and Compass Recommended Read: Danielle Thorne's released, July 2010 Recommended Read: "Drew realizes the true meaning behind her need for touch, when a tiger shark shifter walks out of her dreams and takes her to his underwater world." About Me A member of Generation X, Stephanie was born in Manchester, New Hampshire. After graduating from Central High, she joined the U.S. Army. She spent 11 years in the military, 7 stationed in Germany. While in the military she earned her B.S. in Political Science from California Baptist University in Riverside, CA in 1995. She left the Army in 1997 and settled in California. She now works for LAPD as a 911 Dispatcher. The New England Patriots are still her favorite football team. Stephanie has been married for over 19 years. She has two boys, Andrew, 8, and Joseph, 4.

Q: How could I remove the last character from a string if it is a punctuation, in ruby? Gah, regex is slightly confusing. I'm trying to remove all possible punctuation characters at the end of a string: if str[str.length-1] == '?' || str[str.length-1] == '.' || str[str.length-1] == '!' or str[str.length-1] == ',' || str[str.length-1] == ';' str.chomp! end I'm sure there's a better way to do this. Any pointers? A: str.sub!(/[?.!,;]?$/, '') [?.!,;] - Character class. Matches any of those 5 characters (note, . is not special in a character class) ? - Previous character or group is optional $ - End of string. This basically replaces an optional punctuation character at the end of the string with the empty string. If the character there isn't punctuation, it's a no-op.

Donald Trump's Twitter followers have earned an oft-deserved bad rap for their unsavory online antics. They've purportedly doxed student activists, launched a series of anti-Semitic attacks against Jewish authors and journalists, and were just this week implicated in a campaign of harassment against the actress Leslie Jones. But even as repugnant as Trump Twitter can get, Trump Reddit looks far worse. That's according to an investigation we carried out over the past few days, which found that the moderators of some of Trump's Reddit fan clubs rub elbows with neo-Nazis and white supremacists, among others. "The overwhelming majority of Trump supporters do not sympathize with Neo-Nazis or virulent racism," said r/teh_donald, who moderates r/the_donald, Reddit's second-largest and most active pro-Trump subreddit. Still, he admits, that element does exist: Earlier this month, r/the_donald dismissed one of its own moderators for plotting a pro-Trump white supremacist subreddit. Among social networks, Reddit is unique for a variety of reasons. For one thing, it has historically been a free-for-all: The "government of a new type of community," per former CEO Yishan Wong, where "every man is responsible for his own soul" and where even the most vile or hateful communities could flourish without fear of removal. (The Southern Poverty Law Center once ruled it a "black hole" and the home of the "most violently racist Internet content.") For another thing, users don't belong to one massive pool, a la Twitter. Instead, they self-organize into smaller affinity communities, called subreddits, which are controlled by user volunteers. By mapping these affinity groups according to the people who run them, it's possible to nail down which groups share moderators in common. It also suggests the degree to which certain affinities or interests overlap: For instance, the group r/thedangerousfa**ot, a fan club for gay Breitbart tech reporter Milo Yiannopoulos, shares two mods in common with r/rightwingLGBT. So there is a clear overlap there, at least to a certain degree. When it comes to the Trump universe — which we began mapping from the largest groups, and spiralled out from there — many of those overlaps are precisely what you'd expect. Several moderators of r/the_donald are also involved in groups aligned with the "alt-right," an insurgent and uniquely Internet-y strain of conservatism. And several mods who are big on Trump Reddit also oversee pages like r/the_farage, r/Danish and r/European, which are devoted to Europe's nationalist movement. But there are more unsettling affinities, as well. The largest Trump group on Reddit, with 276,000 subscribers, is r/DonaldTrump2016. One of the moderators of that group also oversees r/Quranimals, which self-identifies as an anti-Muslim "hate sub," and r/Rapefugees, which is virulently anti-migration. Other mods of the group are involved with r/eugenics and r/betauprising (which advocates a society in which women cannot "choose with whom they want to have sex.") Another mod, r/RamblinRambo3 — who also works with r/PURE_TRUMP — also moderates groups devoted to decrying Islam as a "violent and oppressive ideology," as well as a group devoted to "far right, possibly illegal memes." As Trump subreddits go, r/PURE_TRUMP, with its 600 subscribers, isn't particularly large. But all of its mods have unsavory affiliations. For starters, there is enormous overlap between the moderators of r/PURE_TRUMP and those who oversee a cluster of "public watch" clubs, which basically exist to slur liberals, Black Lives Matter activists and members of the LGBT community in extravagantly offensive terms. On top of that, three of r/PURE_TRUMP moderators are also involved with r/ArbeitMachtFrei, whose politics should be fairly obvious from its name. ("Arbeit Macht Frei" is the German phrase that appeared on Auschwitz's gates.) Three oversee r/ShoahThoughts, a forum for "Antisemitic/Anti-Zionist jokes." Two are involved in r/f*gworldproblems, which has been quarantined by Reddit for its "highly offensive" attacks on gay people. One r/PURE_TRUMP moderator, u/Haizenberg, is involved in five separate groups that mock Jews or invoke Hitler or the Holocaust. To be clear, the Trump campaign has no official presence on Reddit, and it's impossible for any candidate to control the online behaviour of its fans. Trump isn't even the only candidate to face these sorts of problems: Earlier this year, the Bernie Sanders campaign scrambled to deal with overt sexism and gender-based harassment by some of its online followers. But while staffers from that campaign locked down the Sanders subreddit, apologized to victims and denounced the behaviour, the Trump campaign has taken a different approach. "They have not done a good job distancing themselves from this," said Patrick Ruffini, a digital strategist for Republican campaigns. "Whenever one of these issues bubbles up, (the Trump campaign) sends the signal that they're OK with this activity happening on their behalf, as long as it happens on their behalf. They haven't come out strongly and denounced it." "There's kind of this wink-wink, nod-nod to white supremacists," Ruffini added. "And so they keep doing it." Ruffini is hopeful the campaign will change tack as more attention is drawn to it. Already, he said, the national outrage over Trump's posting of a "Star of David" meme from 4chan suggests that the public has become more sensitive to the far-right proclivities of some in Trump's audience. Tuesday night, Twitter also permanently banned the account of the aforementioned Yiannaopolous, an outspoken Trump supporter, reportedly in connection with harassment of Jones. And r/the_donald continues to crackdown on bad behaviour. "This is about doing what is best for Donald Trump," teh_donald wrote in his June 21 post disavowing white nationalist activity in the sub. " ... They are people that Trump would want nothing to do with. Just as Trump would, we disavow them."

Kara Tointon has spoken about the "nerve-wracking' scene she had to do for upcoming ITV drama The Halcyon. Speaking to the RadioTimes about the series, which the actress claims will be a "sexier Downton [Abbey]", Tointon talked about a scene where her character, hotel bar singer Betsey Day, is discovered in The Halcyon Hotel owner Lord Hamilton's bathtub. "That was interesting because it's not such a sexy scene; it's just her standing up with nothing on. It made it more nerve-wracking, actually," Tointon said. "I didn't argue against that scene. It is a funny scene, that's why I didn't. Sometimes when those things come up you question whether it's needed , but I absolutely thought it was great because it introduces you to someone in one swoop: that she doesn't care, and that's what she's about. She's fun." Lord Hamilton is played by Alex Jennings (King Leopold in Victoria), while Olivia Williams plays his wife Lady Hamilton. Hermione Cornfield performs the role of Emma Garland, who works in the family business, while Matt Ryan - best known for his role in Constantine - performs the American journalist Joe O'Hara. (ITV (ITV) The new series will alternate between the life of the aristocratic Hamilton family and the staff who work downstairs. It will include storylines about inter-racial and homesexual relationships, and is set in London during the run-up to the Blitz.

Possible control of paternal imprinting of polymorphisms of the ADAM33 gene by epigenetic mechanisms and association with level of airway hyperresponsiveness in asthmatic children. ADAM33 is the candidate gene most commonly associated with asthma and airway hyperreactivity (AHR). The aim of this study was to determine whether level of AHR is associated with certain alleles or haplotypes of the ADAM33 gene in asthmatic children. One hundred and nine asthmatic children and 46 controls from the general population were examined with spirometry before and after histamine and methacholine inhalation. All subjects were genotyped for single-nucleotide polymorphisms (SNPs) of the ADAM33 gene. Haplotypes were determined according to genotypes of the patient's parents. We found the three most frequent ADAM33 haplotypes (a1-3) were associated with the highest level of AHR to methacholine and histamine in 66% of asthmatic children. The paternally transmitted GGGCTTTCGCA haplotype was seen in 73.3% asthmatic children with serious AHR to methacholine challenge (paternal and maternal origin of haplotype 73.3% to 37.5, P=0.046) Significant differences in the relative frequency of paternal haplotypes with high levels of AHR to histamine were found (P=0.013). ADAM33 haplotypes (a1, a2, a3) are associated with severity of AHR and are significantly more often transmitted in the paternal line.

"I've been brought in from the Metropolitan Police to lead a review into the investigation of the murder of Alice Monroe." "He had things entirely under his control, which leads me to think that this was not his first murder." "Go back to your review, Stella." "I don't want the two murders linked." "Failure to see that crimes are linked is the thing that will allow the killer to strike again." "Do you think her hairs been clipped?" " Where?" " There." "This is the third murder in three months, Jim." "If we don't stop him, he will kill again." "Excuse me, is this your purse?" "Thank you so much." "There's been a shooting." "The detective we saw near the Falls Road on Sunday night." "James Olson is a married man, Stella." "You were a married man when you spent a night in my bed." "He clearly has a victim type." "They are not victims of chance, they are victims of choice." "It's possible that he's out there stalking his next victim now." "There's someone to see you, ma'am." "Rose Stagg, a friend of Professor Reed Smith." "I've spent years interviewing the victims of rape." "I don't think anyone ever felt worse after talking to me about their experiences." "I have something terrible to confess." "I've been having an affair." "I called you to say it's over." "It won't be over until I stop you." "You had your chance." "Now it's too late." "We have an E-FIT from Rose Stagg." "Could he really look like that?" "Ma'am, Annie Brawley has regained consciousness." "All right, let's try something different." "If you were on the other side of your bedroom... .. standing by the window..." ".. what would you have seen?" "Me on the bed." "Him behind me." "I was on my side at first." "Tied up." "What else?" "Can you see him clearly?" " No." " That's OK." "Let's..." "take a step back." "Earlier that night you had dinner with your brother." "Do you remember what Joe had to eat?" "Do you remember what you ordered?" "What are you doing?" "Once upon a time..." "this worked for me." "You snap the band on your wrist... .. when your thoughts and feelings overwhelm you." "The Fall Season 2" " Episode 01" "Subtitles by Red Bee Media Ltd Sync:" "Marocas62" " Is that mine?" " Yes." "It's been brushed for prints." "They only found yours." "You'll see... some of the pages are dusty." "Some people find writing useful." "Putting down thoughts - whatever they may be." "Reading the entries you made might help." "I'm sorry." "I want to remember, I really do." "I know." "My diary was in a drawer in my bedroom." "Yes." "He was waiting for me in my bedroom." "If he was wearing gloves, he could have read it and not left any prints." "Yes." "Do you think that he read it?" "Yes." "You know, it's hard for everyone." "Because..." "I look the same." "The same as I did before." "But I'm not the same." "Hello?" "Hang on." "Hang on, I've got a bad signal." " Hello?" " Daddy?" "Livvy?" " Daddy." " Can you hear me?" "Yes." " Are you OK?" " Yes." "It's the middle of the night." "Why aren't you asleep?" "I can't sleep." " Why, darlin'?" " I'm really worried, Daddy." " What about?" " My dollies." "I left them behind." "All of them." "When Mummy, me and Liam left for Scotland." " What did you leave behind?" " All of my dollies." "Where did you leave them?" "In the bath, I think." " Haven't you seen them?" " No." "Haven't you had a bath in all that time?" " It hasn't been that long." " Nearly a whole week." "We have a shower downstairs." "The thing is I really need them." "Can you bring them when you come home?" "I'm not sure when that's going to be, darlin'." "Why?" "It was Mummy decided to go home... not me." "I need them, Daddy, I really do." "Please, Daddy, please." "Jesus!" "Don't you announce yourself?" "I thought that I was expected." "I wasn't sure you'd come." "Nice shoes." "Is that why I'm here - to amuse you?" "I always thought of him as stalking victims, calculating the risks, planning it all out." "Very controlled, calm, cold-blooded." "The killing of Joe was different." "It was impulsive, bloody." "Hot-blooded." "If we didn't know it then, we certainly know it now that he's... driven by huge amounts of rage." "So, we have a eyewitness who can't quite bring herself to recall the face, masked or unmasked, of the man who did all this?" "It's a question of unlocking her." "She's traumatised, grief-stricken." "She just needs more time." " And more professional help." " It's been ten days, Stella." "We're running out of time." "And money." "I... had this drawn up for the policing executive tomorrow." "Emergency funding, to support the investigation." "1.8 million?" "Well, perhaps you can... .. take a look at the figures on the way home?" "We need to make some kind of announcement soon." "Indicate some kind of progress, allay fears." "Some good news." " I know." " Where's your car?" " I'll walk you." " In those shoes?" "I'm fine." "Is this your car?" "It is, and I'd like him to get off it." "What are you doing here?" "I want all of you to move away from my car." "What's the difference between James Olson and a black cab?" "Black cab can take five in the back." "What's your name?" "What's that got to do with you, Little Bo Peep, who's lost her sheep?" "Don't come back here again." "You hear me?" "You're not welcome." "Mummy?" "Mummy?" "I've made you a cup of tea." "You know you're not supposed to boil the kettle." "I haven't." "It's lovely." "When Daddy's back, I'll make him one too, but with sugar." "Superintendent Gibson?" "Detective Superintendent Gibson, would you like to comment on the piece in today's Belfast Chronicle?" "Are the reports that the surviving victim is helping police true?" " They are." " Are you prepared to meet Mrs. Olson face-to-face to discuss your alleged affair with her husband?" " I almost didn't recognise you." " Really?" "Why are you wearing that?" "The same reason you're wearing that." " Yours is a Met uniform." " I'm a Met officer." "At least I was the last time I checked." "I thought I should look as unfeminine as possible, given this morning's Chronicle." "It hasn't worked." "Just to warn you, Monroe's spoiling for a fight." "There's a strong possibility he'll push for a 28-day review into the progress of the taskforce." " You're joking!" " What?" "!" "You think you're above such procedures?" "Well, who would do it?" "Well, we'd find someone." " What do you want?" " Cappuccino." "Two regular cappuccinos, please." "Sally." "Sally!" "Sally, did you not hear me calling you?" "I'm late for work." " What's wrong?" " What's wrong?" "I don't understand." " Don't you?" " No." " I know everything." " What are you talking about?" "Paul confessed, Katie." "There's no need to cover for him." " Confessed to what?" " Your affair." "Your three-month, underage affair." " What?" " And in my house." "Under my roof, in my bed for all I know, while my children were sleeping." "This is bullshit." " What did he say about us?" " Us?" "Jesus." "Whatever he's told you, he's lying." "Why would he lie about something like that?" " I don't know." " Just leave my family alone." "There's been no affair." "What happened is he attacked me." "What?" "That night you left us alone in the study." "I'd come over to listen to music." "He took the opportunity to attack me - pin me to the floor, climb on top of me..." "Enough!" "You have no idea who he is or what he's like." "Ask him about the lock of hair." "What's going on?" "Bitch!" "You have one new message." "I just bumped into your girlfriend." "You need to get your stories straight." "According to her there's been no affair, just some kind of sexual assault." "Jesus, Paul, what did you do to her?" "Did you rape her..." "in your study, while the kids were sleeping?" "She seems to think she knows you better than I do." "I don't know, maybe she does." "This is... this is all so humiliating." "I want you to just stay away, Paul, OK?" "From me, from the kids." "I just..." "I want..." "BELFAST STRANGLER SURVIVOR HELPS POLICE" "AND WHAT HAVE THE POLICE BEEN UP TO?" "Morning, ma'am." "Yep." "Marion Kay's in the conference room, ma'am." "Thanks." "I was thinking, ma'am, that I should go back into uniform." " Really?" " If you can spare me." "I can't." " Thank you, ma'am." " Tell me why." "I've often wondered why you took me off the street in the first place." "What do you think?" "Because I was... struggling to deal with what had happened." "Because I couldn't stop myself from shaking." "I don't go around rescuing patrol cops who are disturbed by what they've seen." "I don't think so." "It was totally selfish." "I was new." "I wanted someone by my side, someone I felt I could trust." "I was impressed by your honesty at the scene." "I think I've learned a lot." "I think I could put it to good use on the street." "Cheating death?" "Fighting for truth and justice?" "Something like that, yeah." " I'll think about it." " Thank you, ma'am." "Sorry, I have nothing new to tell you." "How is your father bearing up?" "That's what everyone always asks me first." ""How's Daddy?"" "It really pisses me off." "All the cards, all the letters of condolence - they were all addressed to Dad." "Yes, of course." "I'm sorry." "How are you?" "It's the right first question." "I know it is." "Fathers aren't supposed to bury their daughters." "But..." "But I can't remember a time in my life when Sarah wasn't there." "There are so many "if onlys"." "If only she hadn't turned the police away." "If only the locksmith had changed the back door straightaway." "If only I had just made her come and stay with us." "I just wish I could think about something else." "For five minutes even." "But there is so much stuff all the time, in the papers, on the television..." "And it is always Alice's picture." "It's never Sarah." "Today's paper even got her age wrong." "It's just to do with Alice's name, I think." "The Monroe connection, the fund that's been set up." "I worry because there's a number of victims... .. Sarah's lost her identity a bit." "Not for me." " Yeah?" " Rose Stagg has cried off - pressure of work." "All right." "The train on platform two is the Larne Harbour, Belfast Central service, calling at Larne Town, Glynn," "Magheramorne, Ballycarry, Whitehead..." "Rose, I really need to see you today." "I'm sorry, I have so much work on." "The interview you gave was informal." "I took notes, but..." "I really need to get every last bit of information from you, if I can." "Recorded, videoed, transcribed." "I know." "As I told you, when I met Peter, I already had a boyfriend." "Yes." "The boyfriend was Tom, who became my husband." "I presumed that." "And you never told him what happened?" "No." "I had bruises all over my neck, really bad headaches, my voice was hoarse." "So I simply stopped seeing him." "Rose, I understand it will be a difficult conversation... .. but there are bigger issues." "I know." " Hello?" " I'm here." "Talk to him tonight." "Come and see me tomorrow." "I can come in at noon?" "I'll see you then." "He's written and he's phoned." "He derives pleasure, it seems, from involving himself in the investigation." "And for that reason, I'd like to maintain the 24/7 monitoring of my old private phone, in the hope that maybe he will call that number again." "What kind of response to the composite likeness?" "The Rose Stagg E-FIT?" "Good." "The fact it's from eight or nine years ago has caused some confusion." "Could he now be fat?" "Could he now be bald?" "He's definitely not fat." "Do you think that looks like me?" "A wee bit, maybe." "May I?" "Go ahead." "What about now?" "A bit more now." "You think it's safe for me to go back to Belfast?" "I don't think you've got anything to worry about." "Do you live in the city?" "I do." "In South Belfast." "Two streets away from one of the girls that died." "Do you live alone?" "Yeah." " How about you?" " No." "No, I'm... travelling back to my wife and two kids." "The only possible excuse for a grown man to be travelling with four dollies in his bag." "You're blonde." "All the other girls have been dark, haven't they?" "Actually, I'm not." " Not what?" " Blonde." "What do you mean?" "It was dark, until all this started happening." "You're kidding." "There." "Proof." "I never would have guessed." "As we know, offenders tend to commit crimes in areas that they're familiar with." "The first kill usually takes place closest to that anchor point." "Near a residence or a place of work." "If we look at the spatial relationships between the crime scenes, it suggests the offender lives in the University Quarter, or Ravenhill, travelling to and from the crime scenes on foot." "And that would make the attack on Annie in the Shankhill an aberration of sorts." "Presumably, he somehow identified her as a potential victim - young, dark, attractive, educated - and disregarded the fact that she lived outside his natural territory." "And then he got into difficulties as a result." "We know that he fled on foot." "But he didn't run back towards the University Quarter, he ran out east towards the city airport." "That's a distance of three miles." "Why?" "Perhaps he has a place out there somewhere." "A lockup or a storage unit or somewhere he changes or keeps a vehicle." "A trawl of CCTV cameras along his route from the Shankhill out towards the airport has offered up these images." "No clear view of his face." "The possibility he has a beard." "I'm getting some video stills produced." "He anticipated that we would use human scent dogs and he crossed a stretch of water." "I believe he took the murder weapon with him." "The search for that weapon is still ongoing." "Truth is we're pretty much running out of time on the search for the weapon." "We've searched miles of the roadway on the route that we think he took, right up to the water's edge, where the scent dogs lost him." "We've run a line across from that point to where we think he emerged." "We're searching both sides of that line." "But the water visibility is nil." "Weeds, refuse." "My divers can only work by touch." "There's deep mud too." "Basically, we've run out of time and money." "It's been ten days now and there's been some speculation that the killer has stayed true to his word." "That he's gone away." "That he's stopped." "I don't believe that it works that way." "Remember that there is a cycle that he goes through." "After an attack, there's a cooling-off period." "But then the deviant fantasies start to kick in, and the pressure starts to build." "Remember, it's an addiction." "He takes his... fantasies and he turns them into reality." "That makes him feel superior to the rest of us mere mortals." "And, as such... .. in his own mind..." ".. he feels he has the right to decide who lives and who dies." "In order to do the terrible things that he does, the killer dehumanises his victims." "Let's do the opposite." "Let's keep them alive." "For us, for their families, friends, work colleagues, for the public." "Let's keep them alive until... this man is caught." "Jesus!" "God, you frightened me." "How did you get in?" "Your side door was unlocked." "What are you doing here?" "Why'd you say those things to Sally Ann?" "What things?" "Things about me." "You and me." " What things?" " You know what things." "I told you to stay away." "I have." "How was I supposed to know she'd be there?" "Why are you trying to make trouble for me?" "Sally Ann now thinks that I attacked you" " that night in the study." " You did." "She thinks I raped you." "She thinks we've been having an affair for months." "Where did she get that idea?" " I don't know." " Yes, you do." "You told her!" " Why would I do that?" " I've been asking myself the same thing." "And?" "Katie?" "Are you OK?" "Yeah." "This is Paul." "I'll be up in a minute." " You sure?" " Yes, I'm sure." "Why are you staring at her?" "I'm not." " She's not your type." " I don't have a type." " Liar!" " I'm not lying." "Dark-haired, beautiful." "Katie..." "Why would you lie to your wife?" "What are you covering up?" "You're playing a dangerous game." "I came here to tell you to stay away from my wife and my children." "The police officer on the television said said the killer clipped a lock of hair from each of the victims." "You had a lock of hair in your study." "I explained that." "It was my mother's hair." "I saw the footage of you at the park, in the Botanic Gardens." "We go there all the time." "It's Olivia's favourite place." "It's also where Sarah Kay went to meet her sister every Saturday lunchtime." "What are you saying?" "You said it, not me." "There's a strangler on the prowl." "And you think it's me?" "Sally Ann called me that night to babysit because she couldn't get a hold of you at work." "But then you came home in the middle of the night with a cut on your face." "You were all weird." "If you think I'm the killer, why aren't you scared?" " I am scared." " Are you?" "Yes." " You think I'm going to strangle you?" " Yes." "And your little friend upstairs?" "Do you really think the killer would identify himself so easily?" "Grow up, Katie." "I'm just a husband, a father, a man with a profession to protect." "Keep your crazy theories to yourself and stay away from my family." " Round the side there." " Yeah." "You have reached the offices of the Alice Monroe Fund." "Your office recommended your services as bereavement consellor." "I'm Paul Spector." "All right, haul her up." "We're finished here, ma'am." "Can you give me a couple more hours?" "I don't know, ma'am." "We'll find the money." " I'm hungry." " Well, you ate at Grandma's." "That was ages ago." "I'll make you some warm milk, OK?" "Livvy, ten minutes till bedtime." "Brush your teeth." ""Dear Olivia," ""I'm sending this letter to you all the way from Scotland via Pixie Post." ""I looked all day and all night" ""but I couldn't find your dollies anywhere." ""It makes me think you took them with you when you left." ""Are you sure you checked your suitcase carefully?" ""Have another look." "Check the front pocket." ""I will see you very soon." ""I love you best in the whole wide world." ""Daddy." ""P.S. The pixies prefer letters they deliver" ""to be kept a secret."" "Is this true?" "Well, it's in the paper." "It must be." "Why do you want to know?" "I did the autopsy on James Olson." "I know." "You showed me the pictures." "I had no idea that you had a personal relationship with him when I did that." "There were scratches on his back, consistent with marks left by fingernails." "Fresh marks." "The most obvious explanation was sex." "And that suggestion was put to his wife and she said she was not responsible." "I see." "And at no point did DCI Eastwood suggest that visiting you in your hotel room was part of Olson's time line." "So the marks went unaccounted for in my report." "I'm surprised by that." "By what?" "By Eastwood withholding that." "You didn't ask him to?" "No." "So, was it you..." "who made those marks?" "They don't feel sharp." "No." "Not any more." "How did you come to meet him?" "I saw him." "On the street." "At a crime scene." "I thought I would be in Belfast for a... a week, maybe two." "I didn't think he'd be shot the next night." "I'm sorry he's dead." "I really am." "But it was one night." "It didn't mean anything." "Excuse me, ma'am." "The divers might have found something." "Mummy?" "Mummy?" "I need the bathroom." "What?" "I need to do a wee." " Ask Daddy." " Where is he?" "I'm so tired, sweetheart." "Who are you?" "Don't wake Mummy." "Are you a friend of Mummy's or Daddy's?" "Your mummy." "What's your name?" "Peter." "Peter Piper." "Peter Piper picked a peck of pickled peppers." "A peck of pickled peppers Peter Piper picked." "If Peter Piper picked a peck of pickled peppers, where's the peck of pickled peppers Peter Piper picked?" "That's called a tongue twister." "You try it." " Peter Piper picked..." " .. a peck of pickled peppers." "Where's the pickled peppers that Peter Piper picked?" "Do it again but do it faster." "Peter Piper picked a pep of... .. peppers." "Where's the peck of peppers that Peter Piper picked?" "That's really good." "Just not too loud." "We don't want to wake Mummy." "Where are you sleeping?" "I'll find somewhere." "Where's your room?" "I'll show you." " Where's Mummy sleeping?" " In there." "That's nice." "I'm sorry." "Me too." "I want you to come with me now." "I want to talk to you." "I don't want to have to hurt you, Rose." "I don't want to have to hurt your beautiful family." "But I will." "I will if you scream or cry out when I release you." "Do you understand?" "OK." "One, two, three." "Peter?" "Subtitles by Red Bee Media Ltd Sync:" "Marocas62"

--- abstract: | A classical theorem due to Mattila (see [@Mat84]; see also [@M95], Chapter 13) says that if $A,B \subset {\Bbb R}^d$ of Hausdorff dimension $s_A, s_B$, respectively, with $s_A+s_B \ge d$, $s_B>\frac{d+1}{2}$ and $dim_{{\mathcal H}}(A \times B)=s_A+s_B\ge d$, then $$dim_{{\mathcal H}}(A \cap (z+B)) \leq s_A+s_B-d$$ for almost every $z \in {\Bbb R}^d$, in the sense of Lebesgue measure. In this paper, we replace the Hausdorff dimension on the left hand side of the first inequality above by the upper Minkowski dimension, replace the Lebesgue measure of the set of translates by a Hausdorff measure on a set of sufficiently large dimension and replace the translation and rotation group by a more general variable coefficient family of transformations. Interesting arithmetic issues arise in the consideration of sharpness examples. These results are partly motivated by those in [@EIT11] and [@IJL10] where in the former the classical regular value theorem from differential geometry was investigated in a fractal setting and in the latter discrete incidence theory is explored from an analytic standpoint. Fourier Integral Operator bounds and other techniques of harmonic analysis play a crucial role in our investigation. We also consider, in the spirit of the Furstenberg conjecture, inverse problems for intersections by asking how small a dimension of a set can be given that the dimension of its intersections with a suitably well-curved family of manifolds is bounded from below by a given threshold. Finally, we shall discuss applications of our estimates to the problem of estimating the number of solutions of systems of diophantine equations over integers. address: 'Department of Mathematics, University of Rochester, Rochester, NY' author: - 'Suresh Eswarathasan, Alex Iosevich, and Krystal Taylor' date: today --- [^1] Introduction ============ .125in A series of results due to Mattila (see [@Mat84], [@Mat85], [@Mat87]; see also [@M95], Chapter 13) give lower and upper bounds on the Hausdorff dimension of the intersection of subsets of the Euclidean space of a given Hausdorff dimension. \[mattilalower\] Suppose that $A,B \subset {\Bbb R}^d$ of Hausdorff dimension $s_A, s_B$, respectively, with $s_A+s_B > d$, $s_B>\frac{d+1}{2}$, then for almost every $g \in O(d)$, the group of orthogonal $d$ by $d$ matrices, $${\mathcal L}^d (\{(z \in {\Bbb R}^d: dim_{{\mathcal H}}(A \cap (gB+z)) \ge s_A+s_B-d \})>0.$$ This means that for a set of $z$s of positive Lebesgue measure and almost every rotation $g$, the Hausdorff dimension of $A \cap (gB+z)$ is at least $s_A+s_B-d$. The converse does not in general hold, but the following result gives a partial description. \[mattilaupper\] With the notation of Theorem \[mattilalower\], suppose in addition that $$\label{fair} dim_{{\mathcal H}}(A \times B)=s_A+s_B\ge d.$$ Then ([@M95]) $$\label{upper} dim_{{\mathcal H}}(A \cap (z+B)) \leq s_A+s_B-d$$ for almost every $z \in {\Bbb R}^d$, in the sense of Lebesgue measure. This tells us that if $s_A+s_B \ge d$, $s_B>\frac{d+1}{2}$, and (\[fair\]) holds, then the Hausdorff dimension of $A \cap (gB+z)$ is at most $s_A+s_B-d$ for almost every $g \in O(d)$ and almost every $z \in {\Bbb R}^d$. .125in A more general question, described in [@M95] and the references contained therein is the following. \[theproblem\] To understand the Hausdorff dimension of $A \cap T(B)$, where $A,B$ are subsets of ${\Bbb R}^d$ of suitable Hausdorff dimension and $T$ ranges contained a suitable set of transformations of ${\Bbb R}^d$. Before we give a detailed description of the goals of this papers, we wish to illustrate a simple motivating point by considering $(x-A) \cap B$, where $A,B \subset {\Bbb R}^d$. In order for the intersection to be non-empty, $x$ must be an element of the sum set $A+B$. If $A$ and $B$ are both sets of a given Hausdorff dimension $<d$, the Hausdorff dimension of $A+B$ is also quite often $<d$ and this naturally leads us to consider translates $x$ in $(x-A) \cap B$ belonging to a set of a given Hausdorff dimension and exploring thresholds on the size of this set for the natural inequalities involving the dimension of $(x-A) \cap B$ to hold. This simple point of view also indicates that arithmetic properties of $A$ and $B$ play an important role and we explore this idea below, particularly in the construction of sharpness examples in Section \[examples\] and the investigation of number theoretic implications of our results in Section \[numbertheory\]. .125in We now describe in some detail the goals of this paper: .125in - Under structural assumptions on the set $B$, with $T_zB=B+z$, prove that the set of translates $z$ for which the upper Minkowski dimension of $A \cap T_zB$ is larger than $dim_{{\mathcal H}}(A)+\dim_{{\mathcal H}}(B)-d$ does not only have Lebesgue measure $0$ but also a small Hausdorff dimension. This would be an analog of Theorem \[mattilaupper\] above where finer information on the exceptional set of translates and replacing the Hausdorff dimension on the left hand side with upper Minkowski dimension is obtained at the expense of additional assumptions on the set $B$. .125in - Without any additional assumptions on $B$, beyond Ahlfors-David regularity, to replace the Hausdorff dimension by the upper Minkowski dimension in Theorem \[mattilaupper\]. .125in - To obtain the same type of results for arbitrary sets $A,B$ with $TB=gB+z$, where $g \in O(d)$ and $z \in {\Bbb R}^d$. We shall see that for almost every $g \in O(d)$, the set of translates $z$ for which upper Minkowski dimension of the set $A \cap TB$ is greater than $dim_{{\mathcal H}}(A)+dim_{{\mathcal H}}(B)-d$ has small Hausdorff dimension. Here the regularity afforded by averaging in $\theta \in O(d)$ compensates for the lack of regularity of $B$. .125in - To use Fourier Integral Operator regularity to obtain variable coefficient variants of the previous two items under a variety of assumptions. In particular, we shall estimate the upper Minkowski dimension of the set $$\label{paradigm} \left\{y \in A: \vec{\Phi}(x^1, \dots, x^k, y)=\vec{t}, \ x^j \in E_j \subset {\Bbb R}^{n_j}, \ y \in A \subset {\Bbb R}^d, \ t \in {\Bbb R}^m \right\},$$ where $A, E_1, \dots, E_k$ are sets of given Hausdorff dimension and $\vec{\Phi}$ is a suitably regular mapping. A suitable conversion mechanism will then be employed to study the corresponding system of diophantine equations over integers. .125in - To use maximal operators to study an inverse problem of the following type. Suppose that a lower bound on the the upper Minkowski dimension of the intersection of an Ahlfors-David regular set and each member of a suitably well-curved family of smooth manifolds is given. How small can the Hausdorff dimension of the original set be? .125in The main results of this paper are described in Section \[mainresults\] below. The remainder of the paper is dedicated to proofs and remarks. Notation -------- The following notions shall be used throughout this paper: .125in - $X \lesssim Y$ means that there exists $C>0$ such that $X \leq CY$. .125in - $X \lessapprox Y$ with the controlling parameter $R$ means that given $\epsilon>0$ there exists $C_{\epsilon}>0$ such that $X \leq C_{\epsilon}R^{\epsilon}Y$. .125in - Given a Borel measure $\mu$, $\mu^{\epsilon}(x)=\mu*\rho_{\epsilon}(x)$, where $\rho$ is a smooth cut-off function, supported in the ball of radius two, identically equal to one in the ball of radius one, $\int \rho(x)dx=1$ and $\rho_{\epsilon}(x)=\epsilon^{-d} \rho \left( \frac{x}{\epsilon} \right)$. .125in - Given $A \subset {\Bbb R}^d$, $A^{\epsilon}$ denotes the $\epsilon$-neighborhood of $A$. .125in - Given $A \subset {\Bbb R}^d$, $s_A$ shall denote the Hausdorff dimension of $A$ and $\mu_A$ shall denote a probability measure on $A$. When $A$ is assumed to be Ahlfors-David regular, $\mu_A$ shall denote the restriction of the $s$-dimensional Hausdorff measure to $A$. .125in - Given a compactly supported measure $\mu$ on ${\Bbb R}^d$, $I_s(\mu)$ is the energy integral given by $\int \int {|x-y|}^{-s} d\mu(x) d\mu(y)$. By elementary properties of the Fourier transform, this expression is equivalent to $\int |\widehat{\mu}(\xi)|^2 |\xi|^{s-d}d\xi$. .125in - Given $A\subset \mathbb{R}^d$, let $M(A)$ denote the set of Radon measures $\mu$ with compact support such that the support of $\mu$ is contained in $A$ and $0< \mu(A) < \infty$. .125in Main results of this paper {#mainresults} ========================== .125in The results of this paper fall into three rough categories. First, in the subsection \[generalstuff\] we present results about intersections of general translated, dilated and rotated sets. In the subsection \[equationsoverfractals\] we study equations over fractals, which amounts to the intersection of sets of given Hausdorff dimension with families of smooth surfaces satisfying appropriate curvature assumptions. In the subsection \[inverseproblems\] we obtain a lower bound on the dimension of the set given information about the dimension of its intersection with certain families of surfaces. Various examples illuminating the results and establishing their degree of sharpness are presented in Section \[examples\]. Number theoretic implications of our investigations are explored in Section \[numbertheory\]. .125in We shall primarily work with Ahlfors-David regular sets defined as follows. \[ADreg\] We say that $E \subset {\Bbb R}^d$ is Ahlfors-David regular if for any $x \in E$ there exists $C>0$ such that $$C^{-1} \delta^{s_E} \leq \mu(B(x, \delta)) \leq C \delta^{s_E},$$ where $s_E$ is the Hausdorff dimension of $E$, $\mu$ is the Hausdorff measure restricted to $E$ and $B(x,\delta)$ is the ball of radius $\delta$ centered at $x$. Intersections of translated, rotated and dilated sets {#generalstuff} ----------------------------------------------------- .125in We begin with the following variant of Theorem \[mattilaupper\], where translation by $x \in {\Bbb R}^d$ is replaced by translation by $\vec{s}(x)$, a local diffeomorphism and the Hausdorff dimension on the left hand side is replaced by the upper Minkowski dimension at the expense of assuming that the sets being intersected are Ahlfors-David regular. \[eitmattilaupper\] Let $A,B \subset {\Bbb R}^d$, $d \ge 1$, be compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A, s_B$ respectively. Suppose that $s_A+s_B>d$. Let $\gamma(x)$ denote the upper Minkowski dimension of $A \cap (\vec{s}(x)-B)$, where $\vec{s}$ is a local ($C^{\infty}$) diffeomorphism. Let $\mu_A, \mu_B$ denote restrictions of the Hausdorff measure to $A,B$, normalized so that $\int d\mu_A=\int d\mu_B=1$. Let $N(x,\epsilon)$ denote the minimal number of $\epsilon$-balls needed to cover $A \cap (\vec{s}(x)-B)$. Then for any smooth compactly supported smooth function $\psi$, with $\int \psi=1$, and every $\epsilon>0$, there exists a universal constant $C$ such that $$\label{eitmattilaupperestquantitative} \int N(x,\epsilon) \psi(x)dx \leq C {(\epsilon^{-1})}^{s_A+s_B-d},$$ and, consequently, $$\label{eitmattilaupperest} \int \gamma(x) \psi(x) dx \leq s_A+s_B-d,$$ from which it follows that $\gamma(x) \leq s_A+s_B-d$ for almost every $x \in {\Bbb R}^d$ in the sense of Lebesgue. .125in In the case when $\vec{s}(x) \equiv x$, Theorem \[eitmattilaupper\] can be deduced from results in [@Falc94]. We include the result because our proof sets up the arguments in the remainder of the paper and due to its somewhat greater applicability. Combining Theorem \[eitmattilaupper\] with Theorem \[mattilalower\], we deduce that the upper Minkowski dimension and the Hausdorff dimension of the intersection of an Ahlfors-David regular set with a rotated copy of a Borel set quite frequently coincide. \[adregular\] Suppose that $A,B \subset {\Bbb R}^d$ compact, Borel, Ahlfors-David regular of Hausdorff dimension $s_A, s_B$, respectively, positive $s_A, s_B$-dimensional Hausdorff measure, $s_A+s_B \ge d$, $s_B>\frac{d+1}{2}$ and $s_A>1$. Then for almost every $g \in O(d)$, $$\label{adregularconclusion} {\mathcal L}^d \{z \in {\Bbb R}^d: dim_{{\mathcal H}}(A \cap (z-gB))=\overline{dim}_{{\mathcal M}}(A \cap (z-gB)) \}>0.$$ .125in It is reasonable to conjecture that under the assumptions of Corollary \[adregular\], $A \cap (z-gB)$ is Ahlfors-David regular, but this does not follow from the equality of the Hausdorff and upper Minkowski dimensions. This can be seen by taking a Cantor construction and changing the dissection ratio at each stage. The second listed author is grateful to Pertti Mattila for pointing this construction in the context of Ahlfors-David regularity. .125in If we are willing to rotate $B$ before translating it, we discover that the exceptional set, which was found to have Lebesgue measure zero in Theorem \[eitmattilaupper\] above, has a small Hausdorff dimension. \[rotated\] Suppose that $A,B \subset {\Bbb R}^d$, $d \ge 2$, are compact, Borel, with Hausdorff dimension $s_A$, $s_B$, respectively and assume, in addition, that $A$ and $B$ are Ahlfors-David regular and that $s_A + s_B >d$. Let $\mu$ be a compactly supported probability measure such that $I_{\alpha}(\mu)<\infty$, where $$\alpha+s_A>d+1.$$ Let $\gamma_{g}(x)$ denote the upper Minkowski dimension of $A \cap (x-gB)$, where $g \in O(d)$, the orthogonal group of $d$ by $d$ matrices. Let $N(x,g,\epsilon)$ denote the minimal number of $\epsilon$-balls needed to cover $A \cap (x-gB)$. Then there exists $C>0$ such that for every $\epsilon>0$ $$\label{rotatedconclusionquantitative} \int \int N(x,g, \epsilon) d\theta(g) d\mu(x) \leq C \sqrt{I_a(\mu)I_b(\mu_A)} \cdot {(\epsilon^{-1})}^{s_A+s_B-d},$$ where $a,b>0, a+b=d+1$, and, consequently, $$\label{rotatedconclusion} \int \int \gamma_g (x) d\theta(g) d\mu(x) \leq s_A+s_B-d,$$ where $d\theta(g)$ denotes the Haar measure on $O(d)$. It follows that for almost every $g \in O(d)$, $$\label{rotatedsizzle} dim_{{\mathcal H}}(\{x: \gamma_g(x)>s_A+s_B-d \})\le d+1-s_A.$$ .125in We are also able to obtain a good upper bound on the Hausdorff dimension of the exceptional set if we put additional structural assumptions on one of the sets being intersected. We say that $E \subset {\Bbb R}^d$ has Fourier dimension $\beta>0$ (see e.g. [@W04]) if $\beta$ is supremum of the set of numbers $\alpha$ such there exists a Borel measure $\mu$ supported in $E$ such that $$|\widehat{\mu}_E(\xi)| \leq C{|\xi|}^{-\frac{\alpha}{2}}.$$ \[curvedconstantcoefficient\] Suppose that $A \subset {\Bbb R}^d$, $d \ge 2$, is compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A$. Suppose that $B \subset {\Bbb R}^d$ is compact, Borel, Ahlfors-David regular and has Fourier dimension $\beta>0$. Let $\mu_A,\mu_B$ denote the probability measures on $A,B$ as before. Suppose that $\mu$ is a compactly supported probability measure with $I_{\alpha}(\mu)<\infty$ such that $$\frac{\alpha+s_A}{2}>d-\frac{\beta}{2}.$$ Let $\gamma_{A,B}(x)$ denote the upper Minkowski dimension of $A \cap (x-B)$. Let $N(x,\epsilon)$ denote the minimal number of $\epsilon$-balls needed to cover $A \cap (x-B)$. Then there exists $C>0$ such that for every $\epsilon>0$ $$\label{cccconclusionquantitative} \int N(x,\epsilon) d\mu(x) \leq C \sqrt{I_a(\mu) I_b(\mu_A)} \cdot{(\epsilon^{-1})}^{s_A+s_B-d},$$ where $a,b>0, a+b=2d-\beta$. It follows that $$\label{cccconclusion} \int \gamma_{A,B}(x) d\mu(x) \leq s_A+s_B-d.$$ It follows that $$\label{cccsizzle} dim_{{\mathcal H}}(\{x: \gamma_{A,B}(x)>s_A+s_B-d \})\le 2d-\beta-s_A.$$ .125in The extent to which this result is sharp is discussed in Example \[paraboloid\] and Example \[cccishot\] below. Observe that Theorem \[curvedconstantcoefficient\] cannot be used to obtain the conclusion of Corollary \[twospheres\] because the Fourier transform of the Lebesgue measure on the intersection of two spheres does not decay in the direction orthogonal to the lower dimension sphere where the two original spheres intersect. Observe that if $B$ is a convex body with a smooth boundary and non-vanishing Gaussian curvature, then Theorem \[curvedconstantcoefficient\] follows from Theorem \[variablecoefficient1\] by taking $\phi(x,y)=\phi_0(x-y)$, where $\phi_0$ is the Minkowski functional of $B$. .125in We say that a compact set $B \subset {\Bbb R}^d$ of Hausdorff dimension $s_B$ satisfies the hyperplane size condition of order $h$ for some $h>0$ if there exists a Borel mesure $\mu_B$ supported in $B$ such that $$\mu_B\left(H^{\delta}_{\omega}\right) \leq C{\delta}^{s_B-h},$$ where $H_{\omega}=\{x \in {\Bbb R}^d: x \cdot \omega=0\}$. Note that if $\mu_B$ is a Frostman measure, then the hyperplane size condition with $h=d-1$ always holds. This is because the intersection of $B$ with a hyperplane can be decomposed into $\approx \delta^{-(d-1)}$ $\delta$-cells, and the measure of each cell is $\leq C\delta^{s_B}$ by the Frostman property. One should think of $h$ as an upper bound on the dimension of the intersection of $B$ with a $(d-1)$-dimensional hyperplane. \[dilation\] Suppose that $A,B \subset {\Bbb R}^d$, $d \ge 2$, are compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A$ and $s_B$ respectively, with $s_A+s_B>d$. Let $\mu$ be a compactly supported probability measure with $I_{\alpha}(\mu)<\infty$. Suppose that $B$ satisfies the hyperplane size condition of order $\beta$ and $$\frac{\alpha+s_A}{2}>d-(s_B-h).$$ Let $\gamma_t(x)$ denote the upper Minkowski dimension of $A \cap (x-tB)$. Let $N(x,t,\epsilon)$ denote the minimal number of $\epsilon$-balls needed to cover $A \cap (x-tB)$. Then $$\label{dilationconclusionquantitative} \int \int_1^2 N(x,t, \epsilon) dt d\mu(x) \leq C {(\epsilon^{-1})}^{s_A+s_B-d}.$$ It follows that $$\label{dilationconclusion} \int \int_1^2 \gamma_t(x) dt d\mu(x) \leq s_A+s_B-d.$$ It follows that for almost every $t$, $$\label{dilationsizzle} dim_{{\mathcal H}}(\{x: \gamma_t(x)>s_A+s_B-d \})\le 2(d-(s_B-h))-s_A.$$ .25in Equations over fractals {#equationsoverfractals} ----------------------- In this subsection we present a series of results pertaining to the general setup described in (\[paradigm\]) in the introduction. We need a few preliminaries on generalized Radon transforms. Given $f: {\Bbb R}^d \to {\Bbb R}$, define $$\label{keyoperator} T_{\vec{\phi}_t}f(x)=\int_{\{\phi_l(x,y)=t_l; 1 \leq l \leq m\}} f(y)\psi(x,y) d\sigma_{x,t}(y),$$ where $d\sigma_{x,t}$ is the Lebesgue measure on the set $\{y: \phi_l(x,y)=t_l; 1 \leq l \leq m\}$ and $\psi$ is a smooth cut-off function. Here $\vec{\phi}=(\phi_1, \dots, \phi_m)$ and $t=(t_1, \dots, t_m)$. We shall assume throughout that $$\label{fibration} \{(\nabla_x \phi_l(x,y))\}_{l=1}^m \text{ and } \{\nabla_y \phi_l(x,y))\}_{l=1}^m$$ form two linearly independent sets of vectors in $\mathbb{R}^{d}$ in a neighborhood of the sets $$\{x: \phi_l(x,y)=t_l; 1 \leq l \leq m\}, \{y: \phi_l(x,y)=t_l; 1 \leq l \leq m\},$$ respectively. This can be justified by details in [@PhSt91] and is meant to provided an underlying manifold structure. We call $T_{\vec{\phi}_t}$ the Radon transform associated to $\vec{\phi}$. Technically, $$T_{\phi_t}: C^{\infty}(\mathbb{R}_y^n) \rightarrow C^{\infty}(\mathbb{R}_x^n \times \mathbb{R}^m_t).$$ Our first result is closely related to the main result in [@EIT11] where the classical regular value theorem was studied in a fractal setting. \[operator\] Let $A \subset {\Bbb R}^d$, $d \ge 2$, be compact, Borel and Ahlfors-David regular, of Hausdorff dimension $s_A$. Let $\mu$ be a compactly supported probability measure with $I_{\alpha}(\mu)<\infty$. Let $\vec{\phi}$ be a smooth function and let $T_{\vec{\phi}_t}$ be as in (\[keyoperator\]) above. Suppose that $$\label{sobolev} T_{\vec{\phi}_t}: L^2({\Bbb R}^d) \to L^2_s({\Bbb R}^d)$$ with constants uniform in $t \in T=T_1 \times T_2 \times \dots \times T_m$, $T_j$ an interval in ${\Bbb R}$, for some $s>0$ and assume that $$\frac{\alpha+s_A}{2}>d-s; \ s_A>m.$$ Let $\gamma_{\vec{t}}(x)$ denote the upper Minkowski dimension of $$\left\{y \in A: \vec{\phi}(x,y)=\vec{t} \right\}.$$ Then for $t \in T$, $$\label{operatorconclusion} \int \gamma_{\vec{t}}(x) d\mu(x) \leq s_A-m.$$ It follows that for $t\in T$, $$dim_{{\mathcal H}}(\{x: \gamma_{\vec{t}}(x)>s_A-m \})\le 2d-2s-s_A.$$ \[PScurvature\] (See [@PhSt91]) We say that $\phi: {\Bbb R}^d \times {\Bbb R}^d \to {\Bbb R}$ satisfies the Phong-Stein rotational curvature condition if $\phi$ is smooth away from the origin and $$det \begin{pmatrix} 0 & \nabla_{x}\phi \\ -{(\nabla_{y}\phi)}^{T} & \frac{\partial^2 \phi}{dx_i dy_j} \end{pmatrix} \neq 0$$ on the set $\{(x,y): \phi(x,y)=t \}$. It is known that if $\phi: {\Bbb R}^d \times {\Bbb R}^d \to {\Bbb R}$ satisfies the Phong-Stein rotational curvature condition, then $$\label{sobolevkt} T_{\phi,t}: L^2({\Bbb R}^d) \to L^2_k({\Bbb R}^d)$$ with constants uniform in $t$ and $k=\frac{d-1}{2}.$ \[variablecoefficient1\] Suppose that $A \subset {\Bbb R}^d$, $d \ge 2$, is compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A$. Suppose that $\mu$ is a compactly supported measure such that $I_{\alpha}(\mu)<\infty$ such that $$\alpha+s_A>d+1.$$ Let $\gamma_t(x)$ denote the upper Minkowski dimension of $$\{y \in A: \phi(x,y)=t \},$$ where $\phi$ satisfies the Phong-Stein rotational curvature assumption. Then $$\label{vc1conclusion} \int \gamma_t(x) d\mu(x) \leq s_A-1.$$ It follows that, $$dim_{{\mathcal H}}(\left\{x: \gamma_{t}(x)>s_A-1 \right\})\le d+1-s_A.$$ .125in \[maximal\] Suppose that $A \subset {\Bbb R}^d$, $d \ge 2$, is compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A$. Suppose that $\mu$ is a compactly supported probability measure with $I_{\alpha}(\mu)<\infty$ such that $$\alpha+s_A>d+2.$$ Let $\gamma(x)=\sup_{t \in [1,2]} \gamma_t(x),$ where $\gamma_t(x)$ is as in Corollary \[variablecoefficient1\] above. Then $$\label{maximalconclusion} \int \gamma(x) d\mu(x) \leq s_A-1,$$ and thus $$\label{maximalsizzle} dim_{{\mathcal H}}(\{x: \gamma(x)>s_A-1 \})\le d+2-s_A.$$ Our next result deals with the system of two equations over a fractal set and does not fall in the realm of the classical generalized Radon transform theory of Theorem \[operator\] and Corollary \[variablecoefficient1\]. \[variablecoefficient2kt\] Suppose that $A \subset {\Bbb R}^d$, $d \ge 2$, is compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A>2$. Suppose that $\mu_j$, $j=1,2$, are compactly supported probability measures with $I_{\alpha_j}(\mu)<\infty$, such that both $$\alpha_1+s_A> d+1$$ and $$\alpha_2+s_A> d+1.$$ Let $\gamma_{\vec{t}}(x^1,x^2)$ denote the upper Minkowski dimension of $$\{y \in A: \phi_1(x^1,y)=t_1, \phi_2(x^2,y)=t_2 \},$$ where $\phi_j$ satisfies the Phong-Stein rotational curvature condition. Then $$\label{vc2conclusion} \int \int \gamma_{\vec{t}}(x^1,x^2) d\mu_{1}(x^1) d\mu_{2}(x^2) \leq s_A-2.$$ \[twospheres\] Suppose that $A \subset {\Bbb R}^d$, $d \ge 2$, is compact, Borel and Ahlfors-David regular, with Hausdorff dimension $s_A>2$. Suppose that $\mu_j$, $j=1,2$, are compactly supported probability measures with $I_{\alpha_j}(\mu)<\infty$, such that both $$\alpha_1+s_A> d+1$$ and $$\alpha_2+s_A> d+1.$$ Let $\gamma_{\vec{t}}(x^1,x^2)$ denote the upper Minkowski dimension of $$A \cap \{y: |x^1-y|=t_1, |x^2-y|=t_2 \}.$$ Then $$\label{twosphereconclusion} \int \int \gamma_{\vec{t}}(x^1,x^2) d\mu_1(x^1) d\mu_2(x^2) \leq s_A-2.$$ .125in Inverse problems {#inverseproblems} ---------------- In this subsection we discuss to what extent it is possible to obtain a lower bound on the dimension of a set from a lower bound on the dimension of the intersection of this set with a suitably large collection of manifolds. This is strongly related to the generalization of the Besicovitch-Kakeya conjecture knowns as the Falconer conjecture. See, for example, [@W99] and the references contained therein. In this paper we only discuss the case of intersection of a set with families of $(d-1)$-dimensional manifolds satisfying suitably non-degeneracy assumptions. These results can be viewed as “inverse” problems with the respect to the theorems presented above. .125in \[inverse\] Let $\phi$ be as in the Definition \[PScurvature\] above and let $E$ be a compact, Borel subset of ${\Bbb R}^d$. Suppose that there exists $U \subset {\Bbb R}^d$ such that the Lebesgue measure of $U$ is positive and for each $x \in U$ there exists $t(x) \not=0$ such that $$\overline{dim}_{{\mathcal M}}\left(E \cap \{y: \phi(x,y)=t(x) \} \right) \ge \gamma>0.$$ Then $$\overline{dim}_{{\mathcal M}}(E) \ge \frac{d \gamma}{d-1}.$$ We show in the Example \[furstenberg\] below that we cannot in general expect $\overline{dim}_{{\mathcal M}}(E) \ge \gamma+1$ under the assumptions of Theorem \[inverse\] There are a couple of special cases worth noting. If $\phi(x,y)=|x-y|$, the Euclidean distance, the result says that if the intersection of $E$ with at least one dilate of many translates of $S^{d-1}$ is large, then the dimension of $E$ is also suitably large. Another interesting special case is when $\phi(x,y)=x \cdot y$. In this case, we ask for $E$ to have a large intersection with at least one hyper-plane with a given unit normal. An interesting additional feature of this case is that it suffices to take $U \subset S^{d-1}$ of positive Lebesgue measure since if the intersection condition is satisfied for a given $x$, it is also satisfied for any multiple of $x$. .125in Examples and sharpness {#examples} ====================== .125in In this section we construct a series of examples indicating the extent to which the results stated above are best possible. An example of two sets $A$ and $B$, of Hausdorff dimension $s_A$ and $s_B$, respectively, such that the Hausdorff dimension of $A \cap (x-B)$ is “generically” $s_A+s_B-d$ is easily constructed by taking $A$ and $B$ to be smooth surfaces in ${\Bbb R}^d$. A simple example in the non-integer case is obtained by considering $$A=\{r \omega: \omega \in S^{d-1}; \ r \in U \},$$ where $U$ is an Ahlfors-David regular set of Hausdorff dimension $s_U$. It is not difficult to check that the Hausdorff dimension of $A$ is $d-1+s_U$. It is also straightforward to verify that the Hausdorff dimension of $A$ and every line that intersects $A$ is at most $s_U=d-1+s_U+1-d$. Modifying this construction yields examples of this type for arbitrary $s_A, s_B>\frac{d+1}{2}$, $s_A+s_B>d$. A more complicated matter is to construct examples showing that our results proving that the upper bound on the intersection dimensions can only fail on a set of relatively small Hausdorff dimension, i.e estimates (\[rotatedsizzle\]), (\[cccsizzle\]), (\[maximalsizzle\]), (\[dilationconclusion\]) and (\[dilationsizzle\]). We are only able to do that with respect to the first two listed estimates. Our main tool is a paraboloid construction, previously employed in [@EIT11] and [@IT11] in a related context. See also [@BBCRV07], [@V05] and [@IS10] where the paraboloid example arises in an analogous context. \[paraboloid\] Let $A_{q,s}$ denote the $q^{-\frac{d}{s}}$-neighborhood of $$q^{-1} \left\{ {\Bbb Z}^d \cap \otimes_{j=1}^{d} [0,q^{\frac{d}{d+1}}] \times [0,q^{\frac{2d}{d+1}}] \right\},$$ $s \in \left[\frac{d}{2},d \right]$, where $q$ is an asymptotically large positive integer. Let $\mu_{q,s}$ denote the Lebesgue measure restricted to $A_{q,s}$, normalized to make $\in d\mu_{q,s}=1$. It is not difficult to check (see e.g. [@IT11]) that $$I_s(\mu_{q,s})=\int \int {|x-y|}^{-s} d\mu_{q,s}(x) d\mu_{q,s}(y) \approx 1.$$ If one takes $q_1=2$, $q_{i+1}>q_i^i$, then the set $A=\cap_i A_{q_i,s}$ is Ahlfors-David regular and has Hausdorff dimension $s$. See, for example, [@Falc86], Chapter 8. .125in Let $B=\{x \in {[0,1]}^d: x_d=x_1^2+\dots+x_{d-1}^2 \}$. By the classical method of stationary phase (see e.g. [@So93]), the natural surface measure $\sigma_B$ on $B$ satisfies $$\label{standarddecay} |\widehat{\sigma}_B(\xi)| \leq C{|\xi|}^{-\frac{d-1}{2}},$$ which implies that $\beta=d-1$ in Theorem \[curvedconstantcoefficient\] above. It follows that the left hand side of (\[cccconclusion\]) is $\leq s_A-1$, from which we conclude that the Hausdorff dimension of the set of $x$ such that the upper Minkowski dimension of $A \cap (x-B)$ exceeds $s_A-1$ is less than or equal to $d+1-s_A$. This establishes the sharpness of Theorem \[rotated\] and Theorem \[curvedconstantcoefficient\] up to the endpoint in the situation when $\beta=d-1$. It also establishes the sharpness of Corollary \[variablecoefficient1\]. The construction in the case of other $\beta$s is different in nature and is handled in Example \[cccishot\] below. .125in \[cccishot\] We now address the degree of sharpness of $\beta$s other than $\beta=d-1$ in Theorem \[curvedconstantcoefficient\]. Let $\mathcal{C}_\alpha$, a Cantor type set of Hausdorff dimension $0<\alpha_0<1$. Let $F_{\alpha}=\mathcal{C}_\alpha \cup \left(\mathcal{C}_\alpha+1 \right)$. Let $A={[0,1]}^{d-1} \times F_{\alpha_0}$. Then $A$ is an Ahlfors-David regular set with $dim_{{\mathcal H}}(A)=d-1+\alpha_0$. The construction and the Ahlfors-David property also guarantee that $$\label{weird} \mu_A \{ {(A \cap (x-S_m))}^{\epsilon} \} \approx \mu_A \{y: 1 \leq {||x-y||}_{l^m} \leq 1+\epsilon \},$$ where $$S_m=\{x \in {\Bbb R}^d: {|x_1|}^m+{|x_2|}^m+\dots+{|x_d|}^m=1 \},$$ with $m$ an even integer and $${||x||}_{l^m}={({|x_1|}^m+{|x_2|}^m+\dots+{|x_d|}^m)}^{\frac{1}{m}}.$$ Let $\sigma_{S_m}$ denote the surface measure on $S_m$. It is not difficult to check (see e.g. [@IoSa97]) that $$|\widehat{\sigma}_{S_m}(\xi)| \leq C{|\xi|}^{-\frac{d-1}{m}}.$$ The right hand side of (\[weird\]) is bounded from below by $$\mu_A \{y \in R: 1 \leq {||x-y||}_{l^m} \leq 1+\epsilon \},$$ where $R$ is an $\epsilon^{\frac{1}{m}} \times \dots \times \epsilon^{\frac{1}{m}} \times \epsilon$ box centered at $x+(0,0, \dots, 0,1)$. By construction and the Ahlfors-David property we see that if $x \in A$, this quantity is bounded from below by $$C\epsilon^{\frac{d-1}{m}} \cdot \epsilon^{\alpha}.$$ On the other hand, the left hand side in (\[weird\]) is bounded from above by $$C \epsilon^{s_A} \cdot N(x,\epsilon),$$ where $s_A$ is, as usual, the Hausdorff dimension of $A$ and $N(x,\epsilon)$ is the minimal number of balls needed to cover $A \cap (x-S_m)$. Plugging in $s_A=d-1+\alpha$, we see that $$N(x, \epsilon) \gtrsim {(\epsilon^{-1})}^{(d-1)(1-\frac{1}{m})},$$ which implies that the lower Minkowski dimension of $A \cap (x-S_m)$ is bounded from below by $(d-1) \left(1-\frac{1}{m} \right)$ for any $x \in A$. Thus we have shown that with $s_A=d-1+\alpha_0$ and $\beta=\frac{d-1}{m}$, $A \cap (x-S_m)$ has lower Minkowski dimension at least $(d-1) \left(1-\frac{1}{m} \right)$ for $x \in A$. Observe that $$(d-1) \left(1-\frac{1}{m} \right)>dim_{{\mathcal H}}(A)+dim_{{\mathcal H}}(S_m)-d=d-1+\alpha_0+d-1-d=d-2+ \alpha_0$$ precisely when $1-\alpha_0 \ge \frac{d-1}{m}$. This means that the expected threshold is exceeded on the set of dimension $d-1+\alpha_0$ and this quantity matches (\[cccsizzle\]) if $1-\alpha_0=\frac{d-1}{m}$. This gives us sharpness for this range of exponents. A more flexible example can be built by taking $A=F_{\alpha_1} \times F_{\alpha} \times \dots \times F_{\alpha_d}$. .125in Our next examples pertains to Theorem \[inverse\]. \[furstenberg\] It is important to note that under the assumptions of Theorem \[inverse\] we cannot in general conclude that the upper Minkowski dimension of $E$ is greater than or equal to $\gamma-1$. To see this we simply modify Wolff’s example ([@W96]) for Furstenberg sets in the plane. Indeed, let $F \subset {\Bbb R}^2$ be a set constructed in the paper which has Hausdorff dimension $\frac{1}{2}+\frac{3}{2}\alpha_0$ such that its intersection with at least one line in every direction has Hausdorff dimension at least $\alpha_0$, $\alpha_0 \in (0,1)$. Let $E=F \times {\Bbb R}^{d-2}$. Then $E$ has Hausdorff dimension $d-\frac{3}{2}+\frac{3}{2}\alpha_0$ and its intersection with at least one $(d-1)$-dimensional plane corresponding to every unit normal on $S^{d-1}$ is at least $\alpha_0+d-2$. Observe that $$d-\frac{3}{2}+\frac{3}{2}\alpha_0<\alpha_0+d-2+1$$ since $\alpha_0 \in (0,1)$. .25in Some connections with number theory {#numbertheory} =================================== .125in The sharpness examples above already suggests a strategy, developed and exploited in ([@IL05]), ([@HI05]), ([@I08]), ([@GI12]), ([@GGIP11]). The idea is that a fractal can be built via appropriate scaling and thickening of the integer lattice. If one has arithmetic information, this mechanism can be used to establish sharpness of analytic estimates as is done using the paraboloid example in Section \[examples\] above. Conversely, if one is able to estimate the size of the solution set of an equation of fractals of a given Hausdorff dimension, this information can be recycled into an estimate on the number of solutions of a diophantine equation over the integers. See, for example, [@BMP00] for a background on the discrete analogs of the problems under consideration here. The basic strategy can be described as follows. Suppose that we have an estimate on the size of the solution set of an equation, or a system of equations over a set of a given Hausdorff dimensions, as in Theorem \[variablecoefficient2kt\] for instance. We then construct a sequence of positive integers $q_i$ such that $q_1=2$ and $q_{i+1}=q_i^i$. Define $E_i$ to be the $q_i^{-\frac{d}{s}}$-neighborhood of ${[0,q_i]}^d \cap {\Bbb Z}^d$, where $s \in (0,d)$. It is known (see [@Falc86]) that the Hausdorff and Minkowski dimensions of $E=\cap_i E_i$ is equal to $s$. We note that ${\Bbb Z}^d$ can be easily replaced by $T{\Bbb Z}^d$, where $T$ is an element of $SL_d({\Bbb R})$. This construction allows us to transfer results proved over fractal to arithmetic results over the integer lattice. Moreover, it is typically sufficient to work with the iterates $E_i$ instead of taking the infinite intersection. This is because if one takes the normalized Lebesgue measure on $E_i$, denoted by $\mu_i$, the energy integral $I_s(\mu_i) \approx 1$ and it is this, rather than the dimensionality per se, is what we actually use in the estimates above. We shall focus on applications of Theorem \[variablecoefficient2kt\] to solving systems of diophantine equations. More precisely, let $\phi_j: {\Bbb R}^d \times {\Bbb R}^d \to {\Bbb R}$ denote smooth functions, homogeneous of degree one in both ($d$-dimensional) variables. Suppose that we wish to solve the system of equations $$\label{hotsystem} \begin{cases} \left| \phi_1(n^1,n)-\lambda_1 \right| \leq q^{-\frac{d}{s}+1} \\ \left| \phi_2(n^2,n)-\lambda_2 \right| \leq q^{-\frac{d}{s}+1} \end{cases}$$ for $n$, where $n^j=(n^j_1, \dots, n^j_d), n=(n_1, \dots, n_d)$; $n, n^j \in {\Bbb Z}^d \cap {[0,q]}^d$, $q$ is a large positive integer and $\lambda_j \approx q$, $j=1,2$ are real numbers. We have the following result. \[numbertheory\] Let $\nu_q(n^1,n^2)$ denote the number of solutions of the system of equations in (\[hotsystem\]). Then $$\label{latticecount} q^{-2d} \sum_{0 \leq |n^j_i| \leq q; 1 \leq i \leq d} \nu_q(n^1,n^2) \leq Cq^{d-\frac{2d}{s}}$$ for any $s>\frac{d+1}{2}$. To put it simply, this says that the typical size of $\nu_q$ is $\lesssim q^{d-\frac{2d}{s}}$, with $s>\frac{d+1}{2}$, i.e $$\nu_q \lessapprox q^{d-\frac{4d}{d+1}}=q^{d-4+\frac{4}{d+1}}.$$ To get a clearer idea of what this means, consider the case when $\phi_j(x,y)={||x-y||}_B$, where ${|| \cdot ||}_B$ is the norm induced by a symmetric convex body $B$ with a smooth boundary and everywhere non-vanishing curvature. In this case, the result is about the number of lattice points that lie close to the intersection of two dilates of $\partial B$, of diameter $\approx q$, centered at integer lattice points in the grid ${[0,q]}^d$. If $\partial B$ is the unit sphere in ${\Bbb R}^d$, then the intersection is a sphere of one dimension lower. The number of lattice points on that sphere cannot exceed $Cq^{d-3}$ by classical number theory. See, for example, [@G86]. Our result shows that even in the case when this sphere arises as an intersection of spheres centered at integer lattice points, the actual number of lattice points in the $q^{-\frac{d-1}{d+1}}$-neighborhood is considerably less. Since the intersections of two spheres is a sphere contained in a “skew" plane, it is not very surprising that its intersection with ${\Bbb Z}^d$ is smaller than the worst case. Our result makes this heuristic quantitative, not only in the case of the sphere, but also in a more general setup where standard analytic number theoretic techniques may be difficult to employ. .25in Proof of Theorem \[eitmattilaupper\] ==================================== .125in Let $\mu_A$ and $\mu_B$ be the measures supported on $A$ and $B$ respectively defined as in definition . Observe the following which holds by the Ahlfors-David regularity of the set $A$ and by the definition of upper Minkowski dimension: $$\label{obs1kt}\left( \frac{1}{\epsilon} \right)^{\gamma(x)}\epsilon^{s_A} \lesssim \mu_A({\{A\cap \vec{s}(x)-B\}^{\epsilon}}),$$ where $X^{\epsilon}$ denotes the $\epsilon-$neighborhood of the set $X$. Since ${(A \cap (\vec{s}(x)-B))}^{\epsilon} \subset \{y \in A^{\epsilon}: \vec{s}(x)-y \in B^{\epsilon} \}$, it follows that $$\label{obs22kt}\left(\frac{1}{\epsilon}\right)^{\gamma(x)}\epsilon^{s_A} \lesssim \mu_A(\{y \in A^{\epsilon}: \vec{s}(x)-y \in B^{\epsilon} \}).$$ .125in Let $\psi$ be a smooth cut-off function with $\int \psi=1$, and consider $$\label{main2}\int \mu_A(\{y \in A^{\epsilon}: \vec{s}(x)-y \in B^{\epsilon} \})\psi(x)dx.$$ By , this expression is bounded below by a constant times $$\int \left(\frac{1}{\epsilon}\right)^{\gamma(x)}\epsilon^{s_A} \psi(x) dx.$$ We now obtain an upper bound on the expression in . Let $J_s$ denote the Jacobian of the change of variables $x \to \vec{s}(x)$. We have $$\int \mu_A \{y \in A^{\epsilon}: \vec{s}(x)-y \in B^{\epsilon} \} \psi(x) dx$$ $$\lesssim \epsilon^{d-s_B} \int \int \mu^{\epsilon}_B(\vec{s}(x)-y) d\mu_A(y) \psi(x) dx$$ $$\lesssim \epsilon^{d-s_B} \int |\widehat{\mu}_A(\xi)| \cdot |\widehat{J_s \cdot \psi \circ s^{-1}}(\xi)| \cdot |\widehat{\mu}^{\epsilon}_B(\xi)| d\xi$$ $$\leq C_N \epsilon^{d-s_B} \int |\widehat{\mu}_A(\xi)| \cdot |\widehat{\mu}^{\epsilon}_B(\xi)| \cdot {(1+|\xi|)}^{-N}d\xi$$ for any $N>1$. This quantity is easily $\lesssim \epsilon^{d-s_B}$. .125in Comparing the upper and lower bounds, it follows that $$\epsilon^{s_A} \int {(\epsilon^{-1})}^{\gamma(x)} \psi(x) dx \lesssim \epsilon^{d-s_B},$$ which implies that $$\int {(\epsilon^{-1})}^{\gamma(x)} \psi(x) dx \lesssim {(\epsilon^{-1})}^{s_A+s_B-d}.$$ It follows by convexity that $${(\epsilon^{-1})}^{\int \gamma(x) \psi(x) dx} \lesssim {(\epsilon^{-1})}^{s_A+s_B-d},$$ which implies that $$\int \gamma(x) \psi(x) dx \leq s_A+s_B-d.$$ .125in Since this holds for every smooth $\psi$ with $\int \psi=1$ it follows that $$\gamma(x) \leq s_A+s_B-d$$ for almost every $x \in {\Bbb R}^d$, as desired. .25in Proof of Theorem \[rotated\] ============================ .125in Let $\mu_A$ and $\mu_B$ be the measures supported on $A$ and $B$ respectively defined as in definition . Observe the following which holds by the Ahlfors-David regularity of the set $A$ and by the definition of upper Minkowski dimension: $$\left( \frac{1}{\epsilon} \right)^{\gamma_g(x)}\epsilon^{s_A} \lesssim \mu_A({\{A\cap x-gB\}^{\epsilon}}),$$ where $X^{\epsilon}$ denotes the $\epsilon-$neighborhood of the set $X$. Since $\{A\cap x-gB\}^{\epsilon} \subset \{y \in A^{\epsilon}: x-y \in gB^{\epsilon} \}$, it follows that $$\label{obs26kt}\left(\frac{1}{\epsilon}\right)^{\gamma_g(x)}\epsilon^{s_A} \lesssim \mu_A(\{y \in A^{\epsilon}: x-y \in gB^{\epsilon} \}).$$ Consider $$\label{main6} \int \int \mu_A \{y \in A^{\epsilon}: x-y \in gB^{\epsilon} \} d\mu(x) d\theta(g).$$ By , this expression is bounded below by a constant times $$\int \int \left(\frac{1}{\epsilon}\right)^{\gamma_g(x)}\epsilon^{s_A} d\mu(x) d\theta(g).$$ We now obtain an upper bound on the expresion in . First observe, by the Ahlfors-David regularity of $B$, that this quantity is comparable to $$\label{grh+} \epsilon^{d-s_B} \int \int \int \mu^{\epsilon}_B(g(x-y)) d\mu(x) d\mu_A(y) d\theta(g)$$ $$=\epsilon^{d-s_B} \int \left( \int \widehat{\mu}^{\epsilon}_B(g\xi) d\theta(g) \right) \widehat{\mu}_E(\xi) \overline{\widehat{\mu}_A(\xi)} d\xi,$$ where, as before, $\mu_B^{\epsilon}(x)=\mu_B*\rho_{\epsilon}(x)$, where $\rho_{\epsilon}(x)=\epsilon^{-d} \rho(x/\epsilon)$, $\rho \ge 0$, smooth, supported in the ball of radius $2$ and $\int \rho=1$. \[propeller\] With the notation above, $$\left| \int \widehat{\mu}^{\epsilon}_B(g\xi) d\theta(g) \right| \leq C{|\xi|}^{-\frac{d-1}{2}}.$$ With Lemma \[propeller\] in tow, we see that the expression in (\[grh+\]) is $$\leq C \epsilon^{d-s_B} \int {|\xi|}^{-\frac{d-1}{2}} |\widehat{\mu}_E(\xi)| \cdot |\widehat{\mu}_A(\xi)| d\xi$$ $$\leq C \epsilon^{d-s_B} \sqrt{I_a(\mu)I_b(\mu_A)}$$ with $a+b=d+1$ by the Cauchy-Scwartz inequality. If $a<s_E$ and $b<s_A$, this quantity is bounded. Thus we may conclude that this quantity is bounded by a constant times $\epsilon^{d-s_B}$ if $s_E+s_A>d+1$. Combining the upper and lower bounds, we conclude that $$\int \int {(\epsilon^{-1})}^{\gamma_g(x)} \epsilon^{s_A} d\theta(g) d\mu(x) \leq C \epsilon^{d-s_B},$$ which implies that $$\int \int {(\epsilon^{-1})}^{\gamma_g(x)} d\theta(g) d\mu(x) \leq C {(\epsilon^{-1})}^{s_A+s_B-d}.$$ Applying convexity, as in the proof of Theorem \[mattilaupper\] implies that $$\int \int \gamma_g(x) d\theta(g) d\mu(x) \leq s_A+s_B-d$$ and the conclusion of Theorem \[rotated\] follows. .125in We are left to prove Lemma \[propeller\]. We have $$\int \widehat{\mu}^{\epsilon}_B(g\xi) d\theta(g)$$ $$=\int \int e^{-2 \pi i g^{-1}x \cdot \xi} d\theta(g) d\mu^{\epsilon}_B(x)$$ $$=\int \widehat{\sigma}(|x| \xi) c(x) d\mu^{\epsilon}_B(x),$$ where $\sigma$ is the Lebesgue measure on $S^{d-1}$. The modulus of this quantity is $\leq C{|\xi|}^{-\frac{d-1}{2}}$, so the proof of Lemma \[propeller\] and thus of Theorem \[rotated\] is complete. .125in Proof of Theorem \[curvedconstantcoefficient\] ============================================== .125in Let $\mu_A$ and $\mu_B$ be the measures supported on $A$ and $B$ respectively defined as in definition . Observe the following which holds by the Ahlfors-David regularity of the set $A$ and by the definition of upper Minkowski dimension: $$\left( \frac{1}{\epsilon} \right)^{\gamma_{A,B}(x)}\epsilon^{s_A} \lesssim \mu_A({\{A\cap x-B\}^{\epsilon}}),$$ where $X^{\epsilon}$ denotes the $\epsilon-$neighborhood of the set $X$. Since $\{A\cap (x-B)\}^{\epsilon}$ is contained in the set $$\{y \in A^{\epsilon}: x-y \in B^{\epsilon} \},$$ it follows that $$\label{obs28kt}\left(\frac{1}{\epsilon}\right)^{\gamma_{A,B}(x)}\epsilon^{s_A} \lesssim \mu_A(\{y \in A^{\epsilon}: x-y \in B^{\epsilon} \}).$$ Consider $$\label{main8}\int \mu_A \{y \in A^{\epsilon}: x-y \in B^{\epsilon} \} d\mu(x).$$ By , this quantity is bounded below by a constant times $$\label{lower8kt} \int \left(\frac{1}{\epsilon}\right)^{\gamma_{A,B}(x)}\epsilon^{s_A} d\mu(x).$$ We now obtain an upper bound on . Observe that this expression is comparable to $$\label{grh} \epsilon^{d-s_B} \int \int \mu^{\epsilon}_B(x-y) d\mu(x) d\mu_A(y),$$ where $ \mu^{\epsilon}_B(x)=\mu_B*\rho_{\epsilon}(x), \rho_{\epsilon}(x)=\epsilon^{-d} \rho(x/\epsilon)$, $\rho \in C_0^{\infty}({\Bbb R}^d)$, with $\int \rho(x) dx=1$. .125in The right hand side of (\[grh\]) equals $$\epsilon^{d-s_B} \int \widehat{\mu}_B(\xi) \widehat{\rho}(\epsilon \xi) \widehat{\mu}_E(\xi) \overline{\widehat{\mu}_A}(\xi) d\xi$$ $$\leq C \epsilon^{d-s_B} \int {|\xi|}^{-\frac{\beta}{2}} |\widehat{\mu}_E(\xi)| |\widehat{\mu}_A(\xi)| d\xi$$ $$\label{umm} \leq C \epsilon^{d-s_B} {\left( \int {|\widehat{\mu}_E(\xi)|}^2 {|\xi|}^{-d+a} d\xi \right)}^{\frac{1}{2}} \cdot {\left( \int {|\widehat{\mu}_A(\xi)|}^2 {|\xi|}^{-d+b} d\xi \right)}^{\frac{1}{2}}$$ $$=C \epsilon^{d-s_B} \sqrt{I_a(\mu) I_b(\mu_A)},$$ where $$\frac{a+b}{2}=d-\frac{\beta}{2}$$ and $I_a(\mu)$ is the standard enegery integral given by $$\int \int {|x-y|}^{-a} d\mu(x)d\mu(y)=c \int {|\widehat{\mu}_E(\xi)|}^2 {|\xi|}^{-d+a} d\xi.$$ It follows that that the quantity in (\[umm\]) is bounded by $C \epsilon^{d-s_B}$ due to our assumption that $\frac{\alpha+s_A}{2}>d-\frac{\beta}{2}$ and elementary properties of energy integrals. See, for example, [@M95]. Comparing the upper and lower bounds, we see that $$\int {(\epsilon^{-1})}^{\gamma_{A,B}(x)} d\mu(x) \leq C {(\epsilon^{-1})}^{s_A+s_B-d}.$$ By convexity, this implies that $${(\epsilon^{-1})}^{\int \gamma_{A,B}(x) d\mu(x)} \leq C{(\epsilon^{-1})}^{s_B+s_A-d},$$ from which we conclude that $$\int \gamma_{A,B}(x) d\mu(x) \leq s_B+s_A-d,$$ as claimed. .125in Proof of Theorem \[dilation\] ============================= Let $\mu_A$ and $\mu_B$ be the measures supported on $A$ and $B$ respectively defined as in definition . Observe the following which holds by the Ahlfors-David regularity of the set $A$ and by the definition of upper Minkowski dimension: $$\label{obs1kt}\left( \frac{1}{\epsilon} \right)^{\gamma_t(x)}\epsilon^{s_A} \lesssim \mu_A({\{A\cap x-tB\}^{\epsilon}}),$$ where $X^{\epsilon}$ denotes the $\epsilon-$neighborhood of the set $X$. Since $\{A\cap x-tB\}^{\epsilon} \subset A^{\epsilon}\cap (x-tB^{\epsilon})$, it follows that $$\label{obs2kt}\left(\frac{1}{\epsilon}\right)^{\gamma_t(x)}\epsilon^{s_A} \lesssim \mu_A({A^{\epsilon}\cap(x-tB^{\epsilon})}).$$ Consider $$\label{main13}\int \int_1^2 \mu_A({A^{\epsilon}\cap(x-tB^{\epsilon})})dt d\mu(x) .$$ By , this expression is bounded below by a constant times $$\int \int_1^2 \left(\frac{1}{\epsilon}\right)^{\gamma_t(x)}\epsilon^{s_A} dt d\mu(x).$$ We now obtain an upper bound on the expression in . Let $\rho: \mathbb{R}^d \rightarrow \mathbb{R}$ be a non-negative and smooth function which is greater or equal to one on the ball of radius two centered at the origin. Assume that $\rho$ has the additional property that its Fourier transform is a positive function which is greater or equal to one on the unit ball and has compact support. Let $\rho_{\epsilon}(x) = \frac{1}{\epsilon^d}\rho(\frac{x}{\epsilon})$. Re-write the integrand in as $$\label{obs4}\mu_A({A^{\epsilon}\cap(x-tB^{\epsilon}))}\sim (\epsilon)^{d-s_B}\int\mu_B * \rho_{\epsilon}\left(\frac{x-y}{t}\right)d\mu_A(y).$$ Integrating in $x$ with respect to the measure $\mu$ and in $t\in[1,2]$ we bound the expression in by a constant times $$\label{compareEkt}\left(\frac{1}{\epsilon}\right)^{s_B-d}\int \int \int \mu_B * \rho_{\epsilon}\left(\frac{x-y}{t}\right) \psi(t) d\mu_A(y)dt d\mu(x),$$ where $\psi$ is a translated smooth bump function equal to one on $[1,2]$. \[bosslemmakt\] With the notation above, $$\label{bosskt}\iint \int \mu_B * \rho_{\epsilon}\left(\frac{x-y}{t}\right) \psi(t) d\mu_A(y)dt d\mu(x)\lesssim 1,$$ whenever $\frac{s_A+\alpha}{2}> d-(s_B-h)$. Assuming Lemma \[bosslemmakt\] for the moment, it follows that is bounded above by a constant times $$\label{compareTkt} \left(\frac{1}{\epsilon}\right)^{s_B-d},$$ whenever $\frac{s_A+s_E}{2}>d-(s_B-h)$. Combining the upper and lower bounds for , we conclude that $$\int \int_1^2 \left(\frac{1}{\epsilon}\right)^{\gamma_t(x)}\epsilon^{s_A} dt d\mu(x) \lesssim \left(\frac{1}{\epsilon}\right)^{s_B-d}.$$ Now follows by convexity (use Jensen’s inequality). To demonstrate , we observe that implies that $$\mu(\{ x : \gamma_t(x) > s_A +s_B -d \}) =0,$$ for a.e. $t\in[1,2]$, and we conclude that holds whenever $\frac{s_A+s_E}{2}>d-(s_B-h)$.\ .125in To finish the proof of the theorem, it remains to prove Lemma \[bosslemmakt\]. Using elementary properties of the Fourier transform, we bound the right-hand-side of by $$\label{ftkt}\int\int \widehat{\mu_B}(t\xi)\widehat{\rho_{2\epsilon}}(t\xi)\widehat{\mu_A}(\xi)\overline{\widehat{\mu}(\xi)} t^d\psi(t)dt d\xi.$$ The presence of the smooth cut-off fucntion, $\widehat{\rho_{\epsilon}}$, implies that we need only consider $|\xi|< 1/\epsilon$. Additionally, the left-hand-side of restricted to $|\xi|< 1$ is bounded since the integrand is finite. It remains to see that the left-hand-side of restricted to the region where $1< |\xi|< 1/\epsilon$ is bounded. Fix $1< |\xi|< 1/\epsilon$, and consider $$\label{tintkt}\int\widehat{\mu_B}(t\xi)\widehat{\rho_{2\epsilon}}(t\xi) t^d\psi(t)dt.$$ Let $\tilde{\psi} =t^d \psi$, let $\mu_B^{\epsilon}= \mu_B* \rho_{\epsilon}$, and use the definition of the Fourier transform to re-write as $$\label{changekt} \int\widehat{\mu_B}(t\xi)\widehat{\rho_{2\epsilon}}(t\xi) \tilde{\psi}(t)dt =\int \widehat{\tilde{\psi}}(x\cdot \xi) \mu_B^{\epsilon}(x)dx.$$ We break this integral into dyadic pieces: $$\label{breakkt}=\int_{\{x: |x\cdot \xi | \le 1\}} \widehat{\tilde{\psi}}(x\cdot \xi) \mu_B^{\epsilon}(x)dx + \sum_{m=0}^{\infty} \int_{\{x: 2^m\le |x\cdot \xi | <2^{m+1}\}} \widehat{\tilde{\psi}}(x\cdot \xi) \mu_B^{\epsilon}(x)dx.$$ Since for all integers $N>1$, there exists $c_N$ so that $\widehat{\tilde{\psi}} \lesssim \min\{ 1, |\cdot | ^{-N}\}$, we may bound the first piece as follows: $$\begin{aligned} &\left|\int_{\{x: |x\cdot \xi | \le 1\}} \widehat{\tilde{\psi}}(x\cdot \xi) \mu_B^{\epsilon}(x)dx \right| \\ &\lesssim \int_{\{x: |x\cdot \xi | \le 1\}} \mu_B^{\epsilon}(x)dx\\ &= \frac{1}{\epsilon^d} \int \int_{\{x: |x\cdot \xi | \le 1\}} \rho\left( \frac{x-y}{\epsilon}\right)dx d\mu_B(y) \\\end{aligned}$$ Recall that $\rho$ is smooth, non-negative, and equal to one on the unit ball. We fix $y$ and break the integral in $x$ to consider $\{x: |x-y| < \epsilon\}$ and $\{ x: |x-y| > \epsilon\}$. Observe that $$\begin{aligned} & \frac{1}{\epsilon^d} \int \int_{\{x: |x\cdot \xi | \le 1\}\cap \{ x: |x-y| < \epsilon\}} \rho\left( \frac{x-y}{\epsilon}\right)dx d\mu_B(y) \\ &\lesssim \frac{1}{\epsilon^d} \int \int_{\{x: |x\cdot \xi | \le 1\}\cap \{ x: |x-y| < \epsilon\}} dx d\mu_B(y) \\ &\lesssim \mu_B( \{y : |y\cdot \xi| \le 1 + \epsilon |\xi|\} ). \\ &\lesssim \mu_B\left( \left\{y : \left|y\cdot \frac{\xi}{|\xi|}\right| \le \frac{1}{|\xi|}\right \}\right),\\\end{aligned}$$ where the last line follows because we have fixed $|\xi| < \frac{1}{\epsilon}$.\ Applying the hyperplane size condition of order $h$ on the set $B$, we may bound this quantity by: $$\lesssim |\xi|^{-(s_B -h)}.$$ Observe that $$\begin{aligned} &= \frac{1}{\epsilon^d} \int \int_{\{x: |x\cdot \xi | \le 1\}\cap \{ x: |x-y| > \epsilon\}} \rho\left( \frac{x-y}{\epsilon}\right)dx d\mu_B(y) \\ &\lesssim \frac{1}{\epsilon^d} \int \int_{\{x: |x\cdot \xi | \le 1\}\cap \{ x: |x-y| > \epsilon\}}\left|\frac{x-y}{\epsilon} \right|^{-N} dx d\mu_B(y) \\ &\sim \epsilon^{N-d} \sum_{j=0}^{\infty}\int \int_{\{x: |x\cdot \xi | \le 1\}\cap \{ x: \left|\frac{x-y}{\epsilon}\right| \sim 2^j\}} 2^{-jN} dx d\mu_B(y) \\ &\lesssim \epsilon^{N} \sum_{j=0}^{\infty}2^{jd} 2^{-jN}\mu_B( \{y : |y\cdot \xi| \le 1 + 2^j\epsilon |\xi|\} ). \\ &= \epsilon^{N} \sum_{j=0}^{\infty} 2^{jd}2^{-jN}\mu_B\left( \left\{y : \left|y\cdot \frac{\xi}{|\xi|}\right| \le \frac{1}{|\xi|} + 2^j\epsilon \right \}\right), \\\end{aligned}$$ where we may choose $N$ arbitrarily large. Applying the hyperplane size condition of order $h$ on the set $B$, we may bound this quantity by: $$\lesssim \epsilon^{N} \sum_{j=0}^{\infty} 2^{jd}2^{-jN} \max\left\{ |\xi|^{-(s_B-h)},(2^j\epsilon)^{s_B-h}\right\}.$$ Recalling that we have restricted our attention to the region where $1<|\xi| < \frac{1}{\epsilon}$ and recalling that we may choose $N$ arbitrarily large, we conclude that this quanity is bounded by: $$\lesssim |\xi|^{-(N + s_B-h)}.$$ In conclusion, $$\label{bound1kt}\left|\int_{\{x: |x\cdot \xi | \le 1\}} \widehat{\tilde{\psi}}(t) d\mu_B(x) \right| \lesssim |\xi|^{-s_B+h}.$$ We bound the second part of the sum in with similar estimates. Observe $$\begin{aligned} &\sum_{m=0}^{\infty}\left|\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}} \widehat{\tilde{\psi}}(x\cdot \xi) \mu_B^{\epsilon}(x)dx \right| \\ &\lesssim \sum_{m=0}^{\infty}\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}} |x\cdot \xi|^{-N}\mu_B^{\epsilon}(x)dx\\ &\lesssim \epsilon^{-d}\sum_{m=0}^{\infty}2^{-mN}\int\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}} \rho\left(\frac{x-y}{\epsilon}\right) dx d\mu_B(y).\\\end{aligned}$$ Recall that $\rho$ is smooth, non-negative, and equal to one on the unit ball. We fix $y$ and break the integral in $x$ to consider $\{x: |x-y| < \epsilon\}$ and $\{ x: |x-y| > \epsilon\}$. Observe that $$\begin{aligned} &\lesssim \epsilon^{-d}\sum_{m=0}^{\infty}2^{-mN}\int\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}\cap \{x: |x-y| < \epsilon\}} \rho\left(\frac{x-y}{\epsilon}\right) dx d\mu_B(y).\\ &\lesssim \epsilon^{-d}\sum_{m=0}^{\infty}2^{-mN}\int\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}\cap \{x: |x-y| < \epsilon\}} dx d\mu_B(y).\\ &\lesssim \sum_{m=0}^{\infty}2^{-mN}\mu_B\left( \left\{y : 2^m|\xi|^{-1}-\epsilon \le \left|y\cdot \frac{\xi}{|\xi|}\right| \le 2^{m+1}|\xi|^{-1} + \epsilon \right\} \right) \\ &\lesssim \sum_{m=0}^{\infty} 2^{-mN} 2^{m(s_B-h)} |\xi|^{-(s_B-h)} ,\\ &\lesssim |\xi|^{-(s_B-h)},\\\end{aligned}$$ for $N$ chosen sufficiently large. Observe that $$\begin{aligned} &\lesssim \epsilon^{-d}\sum_{m=0}^{\infty}2^{-mN}\int\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}\cap \{x: |x-y| > \epsilon\}} \rho\left(\frac{x-y}{\epsilon}\right) dx d\mu_B(y).\\ &\lesssim \epsilon^{-d}\sum_{m=0}^{\infty}2^{-mN}\int\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}\cap \{x: |x-y| > \epsilon\}} \left| \frac{x-y}{\epsilon} \right|^{-N}dx d\mu_B(y).\\ &\lesssim \epsilon^{N-d}\sum_{m=0}^{\infty}\sum_{j=0}^{\infty}2^{-mN}2^{-jN}\int\int_{\{x: 2^m\le|x\cdot \xi | \le 2^{m+1}\}\cap \{x: \left| \frac{x-y}{\epsilon} \right|\sim 2^j\}} dx d\mu_B(y).\\ &\lesssim \epsilon^{N}\sum_{m=0}^{\infty}\sum_{j=0}^{\infty}2^{jd}2^{-mN}2^{-jN} \mu_B\left( \left\{y : 2^m|\xi|^{-1}-2^j\epsilon \le \left|y\cdot \frac{\xi}{|\xi|}\right| \le 2^{m+1}|\xi|^{-1} + 2^j\epsilon \right\} \right) \\ &\lesssim \epsilon^{N}\sum_{m=0}^{\infty}\sum_{j=0}^{\infty}2^{jd}2^{-mN}2^{-jN} \max\left\{(2^m|\xi|^{-1})^{(s_B-h)}, (\epsilon 2^j)^{(s_B-h)} \right\}. \\\end{aligned}$$ Since $N$ may be taken arbitrarily large and since $|\xi| < (\epsilon)^{-1}$, we may bound this quantity by: $$\lesssim |\xi|^{-(s_B-h)}.$$ These observations demonstrate that the left-hand-side of is bounded by a constant times $|\xi|^{-(s_B-h)}$. It follows that the left-hand-side of is bounded by a constant times the following: $$\label{integral1kt} \left| \int |\widehat{\mu_A}(\xi)|\cdot |\widehat{\mu}(\xi)| \cdot |\xi|^{-s_B+h} d\xi \right|$$ To handle the integral in , use the Cauchy-Schwartz inequality to bound the right-hand-side of by $$\label{energykt}\left(\int|\widehat{\mu_A(\xi)}|^2 |\xi|^{(-2(s_B-h)+\gamma)/2} \right)^{1/2} \left(\int|\widehat{\mu}(\xi)|^2 |\xi|^{(-2(s_B-h)-\gamma)/2} \right)^{1/2},$$ where $\gamma$ will be choosen momentarily. Observe that (see [@Fal86], pg. 208 and [@Falc86], section 6.2) $$\label{energyAkt}\int|\widehat{\mu_A(\xi)}|^2 |\xi|^{(-2(s_B-h)+\gamma)/2}\lesssim 1,$$ whenever $(-2(s_B-h) + \gamma)/2 < s_A-d.$ Similarly $$\label{energyEkt}\int|\widehat{\mu}(\xi)|^2 |\xi|^{(-2(s_B-h)-\gamma)/2} \lesssim1,$$ whenever $(-2(s_B-h) -\gamma)/2 <\alpha -d$. Both of these conditions are satisfied when $\gamma$ is chosen such that $$-(s_B-h) -(\alpha-d) < \frac{\gamma}{2}< (s_A-d) + (s_B-h).$$ Such a choice of $\gamma$ is possible whenever $\frac{s_A+\alpha}{2}> d-(s_B-h)$. We conclude that is bounded by a positive constant which does not depend on $\epsilon$ whenever $\frac{s_A+\alpha}{2}> d-(s_B-h)$. This completes the proof of Lemma \[bosslemmakt\]. .125in Proof of Theorem \[operator\] {#opsection} ============================== .125in First notice that the $\epsilon$-neighborhood of $ A \cap \{ y: \vec{\phi}(x,y) = \vec{t} \}$ is contained in the set $\{y \in A^{\epsilon} : |\vec{\phi}(x,y) - \vec{t} | \leq \epsilon \}$. A reduction ----------- Assume that we have, after rewriting our quantities by using the above containment, $$\label{mainopint} \int \mu_A \{ y \in A^{\epsilon} : \ |\vec{\phi}(x,y) - \vec{t} | \leq \epsilon \} \ d\mu(x) \lesssim \epsilon^m.$$ The Ahlfors-David regularity of the sets $A$ and $E$ then shows that (\[mainopint\]) is bounded below by $$C \int {(\epsilon^{-1})}^{\gamma_{\vec{t}}(x)} \epsilon^{s_A} d\mu(x),$$ where $\gamma_{\vec{t}}(x)$ denotes the upper Minkowski dimension of $A \cap \{ y: \vec{\phi}(x,y) = \vec{t} \}$ and $C>0$ is a universal constant. Comparing the upper and lower bounds, we see that $$\int {(\epsilon^{-1})}^{\gamma_{\vec{t}}(x)} d\mu(x) \leq C {(\epsilon^{-1})}^{s_A-m}.$$ Convexity implies $${(\epsilon^{-1})}^{\int \gamma_{\vec{t}}(x)d\mu(x)} \leq C{(\epsilon^{-1})}^{s_A-m},$$ from which we conclude that $$\int \gamma_{\vec{t}}(x) d\mu(x) \leq s_A-m,$$ hence completing the proof of Theorem \[operator\]. Now, we continue with a slight modification of Proposition 2.2 in [@EIT11] to prove estimate (\[mainopint\]). The actual proof is almost identical to that of the referenced proposition, but we provide it below, with the necessary changes, for the sake of completeness. Decomposition of integral in (\[mainopint\]) -------------------------------------------- We start by taking Schwartz the class functions $\eta_0(\xi)$ supported in the ball $\{ |\xi| \leq 4 \}$ and $\eta(\xi)$ supported in the annulus $$\{ 1 < |\xi| < 4\} \ \text{with} \ \eta_j(\xi)=\eta(2^{-j}\xi) \text{ for } j \geq 1$$ with $$\eta_0(\xi) + \sum_{j=1}^{\infty} \eta_j(\xi) =1.$$ Define the Littlewood-Paley piece of $\mu_j$ by the relation $$\label{piece} \widehat{\mu}_j(\xi)=\widehat{\mu}(\xi) \eta_j(\xi).$$ Consider the integral in (\[mainopint\]). Using the Littlewood-Paley decomposition, this integral is bounded above by a constant times $$\label{2.3} \sum_{j,k} \int \int_{\{t_l \leq \phi_l(x,y) \leq t_l + \varepsilon: 1 \leq l \leq m \}} \psi(x,y) d\mu_{A,j}(y) \hskip.1cm d\mu_{k}(x)= \sum_{j,k} \langle \mu_{A,j},T^{\varepsilon} \mu_{k} \rangle$$ where $<\cdot,\cdot>$ denotes the $L^2(\mathbb{R}^d)$ inner product and $$\begin{aligned} \label{expanded} \nonumber T^{\varepsilon}\mu_{k}(y)&=&\int_{\{t_l \leq \phi_l(x,y) \leq t_l + \varepsilon: 1 \leq l \leq m \}}\psi(x,y) d\mu_{k}(x) \\ &=& \int_{t_1}^{t_1 + \varepsilon} ... \int_{t_m}^{t_m + \varepsilon} \int_{\vec{\phi}(x,y)=r}\psi(x,y) \mu_{k}(x) d\sigma_{y,r}(x) dr_1 ... dr_m, \end{aligned}$$ where $d\sigma_{y,r}$ is the Lebesgue measure on the set $\{x: \vec{\phi}(x,y)=r\}$ and $r = (r_1,...,r_m)$. It should be noted that the innermost integral on the right side of (\[expanded\]) is just $T_{\vec{\phi}_r}$ applied to $\mu_{k}$. It follows that the right hand side of (\[2.3\]) becomes $$\sum_{j,k} \int_{t_1}^{t_1+\epsilon} \cdots \int_{t_m}^{t_m+\epsilon}\langle \mu_{A,j}, T_{\vec{\phi_r}}(\mu_{k})\rangle dr_1 \cdots dr_m.$$ We will now use the mapping properties of $T_{\vec{\phi_r}}$ to prove $\langle \mu_A,T_{\vec{\phi_r}} \mu \rangle$ is uniformly bounded in $r$ over the the domain of integration. This, in turn, will prove our desired upper bound. We have $$\label{2.5} \hskip.1cm \langle \mu_A, T_{\vec{\phi_r}}(\mu)\rangle \hskip.1cm = \sum_{j,k} \langle \mu_{A,j}, T_{\vec{\phi_r}}(\mu_{k})\rangle$$ $$\label{2.6} = \hskip.1cm \sum_{|j-k| \leq K} \langle \mu_{A,j}, T_{\vec{\phi_r}}(\mu_{k})\rangle + \sum_{|j-k| > K} \langle \mu_{A,j}, T_{\vec{\phi_r}}(\mu_{k})\rangle$$ for $K$ large enough; the choice of $K$ will be justified later. Proof of estimate (\[mainopint\]) --------------------------------- We will estimate each of the above sums separately. ### Near-diagonal terms For the first sum, $$\label{mickey} \sum_{|j-k| \leq K}\langle \mu_{A,j}, T_{\vec{\phi_r}}(\mu_{k})\rangle \hskip.1cm \lesssim \sum_{|j-k| \leq K}2^{j\frac{d-s_A}{2}}2^{k\frac{d-s_E}{2}}2^{-ks}\lesssim 1$$ provided that $\frac{s_E+s_A}{2}>d-s$. Indeed, as $\eta_j \sim \eta_j^2$, $$\begin{aligned} \nonumber \sum_{|j-k| \leq K}\langle \mu_{A,j}, T_{\vec{\phi_r}}(\mu_{k})\rangle &=& \sum_{|j-k| \leq K}\langle \widehat{\mu_{A,j}}, \widehat{T_{\vec{\phi_r}}(\mu_{k})}\rangle\\ \nonumber &\sim& \sum_{|j-k| \leq K}\langle \widehat{\mu_{A,j}}, \widehat{T_{\vec{\phi_r}}(\mu_{k})}\eta_j\rangle\\ \nonumber &\lesssim& \sum_{|j-k| \leq K}\|\mu_{j}\|_2 \hskip.1cm \|\widehat{T_{\vec{\phi_r}}(\mu_{k})}\eta_j\|_2\\\end{aligned}$$ where we use the Cauchy-Schwartz inequality. Since $\mu$ is an Ahlfors-David regular measure on a set of Hausdorff dimension $\alpha$, we have that $$\label{wolffnotes} \| \mu_{A,j} \|_2 \lesssim 2^{\frac{j(d-s_A)}{2}}.$$ Indeed, $${||\mu_{A,j}||}_2^2=\int {|\widehat{\mu}(\xi)|}^2 \eta(2^{-j} \xi) d\xi$$ $$=\int \int \int e^{2 \pi i (x-y) \cdot \xi} \eta(2^{-j} \xi) d\xi d\mu(x) d\mu(y)$$ $$=2^{dj} \int \int \widehat{\eta}(2^j(x-y)) d\mu(x) d\mu(y).$$ The absolute value of this quantity is bounded, for every $N>0$, by $$C_N 2^{dj} \int \int {(1+2^j|x-y|)}^{-N} d\mu(x) d\mu(y)$$ $$=C_N 2^{dj} \int \int_{|x-y| \leq 2^{-j}} {(1+2^j|x-y|)}^{-N} d\mu(x) d\mu(y)$$ $$+C_N 2^{dj} \sum_{l=0}^{\infty} \int \int_{2^l \leq 2^j|x-y| \leq 2^{l+1}} {(1+2^j|x-y|)}^{-N} d\mu(x) d\mu(y)$$ $$=I+II.$$ By the Ahlfors-David property, $$I \lesssim C_N 2^{dj} 2^{-j s_A}.$$ Since $\mu$ is compactly supported, there exists $M>0$ such that $$II=C_N 2^{dj} \sum_{l=0}^{j+M} \int \int_{2^l \leq 2^j|x-y| \leq 2^{l+1}} {(1+2^j|x-y|)}^{-N} d\mu(x) d\mu(y).$$ This expression is $$\lesssim C_N 2^{dj} \sum_{l=0}^{j+M} 2^{-j s_A} 2^{l s_A} 2^{-lN} \lesssim C_N 2^{j(d-s_A)}.$$ It follows that $I+II \lesssim 2^{j(d-s_A)}$ and (\[wolffnotes\]) is established. .125in We also have that $$\label{microlocal} \|\widehat{T_{\vec{\phi_r}}(\mu_{k})}\eta_j\|_2 \lesssim 2^{-ks} 2^{\frac{k(d-s_E)}{2}}$$ by the mapping properties of the operator $T_{\vec{\phi_r}}$ in the regime of $|j-k|<K$. ### Off-diagonal terms We use the following lemma to get a bound on the second sum. \[fardiag\] For any $M>2d + m + 1$ there exists a constant $C_M>0$ such that for all indices $j,k$ with $|j-k|>K$ with $K$ large enough, $$\langle \mu_{A,j}, T_{\vec{\phi_r}}\mu_{k}\rangle \leq C_M 2^{-M \max \{j,k\}}.$$ To prove the lemma, for simplicity, we replace $T_{\vec{\phi_r}}$ by $T$ and write $$T\mu_{k}(y)= \int_{\{x: \vec{\phi}(x,y)=r\}} \psi(x,y) \mu_{k}(x)d\sigma_{y,r}(x),$$ where $d\sigma_{y,r}$ is the Lebesgue measure on the set $\{x: \vec{\phi}(x,y)=r\}$. It follows from our upcoming arguments that as long as $t_l \leq r_l \leq t_l + \varepsilon$ , the estimates hold uniformly in $r$. As $\phi_l$ satisfies the property that $\{\nabla_x \phi_l(x,y)\}_{l=1}^m$ are linearly independent on a relatively open, bounded subset of $\{x: \phi_l(x,y)=t\}$ from (\[fibration\]), we can assume that $|\sum_l \nabla_y \phi_l(x,y)| \approx 1$ on this set by making the support of $\psi$ small enough. Next, we use an approximation argument on $T$ by letting $$\label{approx} T_n\mu_{k}(y)=n^m \int_{\mathbb{R}^d} \psi(x,y) \Pi_l \chi_l(n(\phi_l(x,y)-r_l)) \mu_{k}(x)dx$$ where $\{\chi_l\}_{l=1}^m$ is a family of smooth cutoffs supported near $0$ and equal to 1 near 0. It is shown in [@GelShi66] that $$n^m\Pi_l \chi_l(n(\phi_l(x,y)-r_l)) \ dx$$ converges to the measure that appears in $T_{\vec{\phi}_r}$ as $n \rightarrow \infty$. Therefore, proving the estimate in the case where $T_{\vec{\phi}_r}$ is replaced by $T_n$ is sufficient by convergence theorems found in [@Fol84] which in turn shows the uniformity in $r$. We will drop the domains of integration in the upcoming calculations for brevity. By Fourier inversion, we have $$T_n\mu(y)= \int e^{i x \cdot \xi} e^{is \cdot (\vec{\phi}(x,y)-r)} \psi(x,y) \Pi_l\widehat{\chi_l}(n^{-1}s_l) \widehat{\mu}(\xi) d\xi ds dx$$ and therefore $$\label{FourierTransT}\widehat{T_n \mu}(\eta)= \int e^{-i x \cdot \eta} e^{i y \cdot \xi} e^{is \cdot (\vec{\phi}(x,y)-r)} \psi(x,y) \Pi_l\widehat{\chi_l}(n^{-1}s_l) \widehat{\mu}(\xi) dx dy ds d\xi.$$ Invoking the properties of the Fourier transform on $L^2$, we see that $$\begin{aligned} \langle T_n\mu_{A,j},\mu_{k} \rangle &=& \langle \widehat{T_n \mu_{A,j}}, \widehat{\mu_{k}}\rangle \\ \nonumber &=& \int e^{-i x \cdot \eta} e^{i y \cdot \xi} e^{is \cdot (\vec{\phi}(x,y)-r)} \psi(x,y) \Pi_l\widehat{\chi_l}(n^{-1}s_l) \widehat{\mu_{A,j}}(\xi) \widehat{\mu_{k}}(\eta) dx dy ds d\xi d\eta \\ \label{negativedecay} &=& \int \widehat{\mu_{A,j}}(\xi) \widehat{\mu_{k}}(\eta) \Pi_l\widehat{\chi_l}(n^{-1}s_l) I_{jk}(\xi, \eta, s) d \eta d \xi ds \end{aligned}$$ where $$\label{oscillatory} I_{jk}(\xi, \eta, s) = \psi_0(2^{-j}|\xi|)\psi_0(2^{-k}|\eta|) \int e^{is \cdot (\vec{\phi}(x,y)-r)} e^{i y \cdot \xi} e^{-i x \cdot \eta} \psi(x,y) dx dy$$ and $\psi_0$ is smooth cutoff equal to 1 on $\{1 \leq |z| \leq 10 \}$ and vanishing in the ball of radius 1/2. The justification of such cutoffs comes from the support of $\widehat{\mu_{A,j}}(\xi)$ and $\widehat{\mu_{k}}(\eta)$ and again that $\eta_j \approx \eta_j^2$. We will show that $$\label{ibpdecay}|I_{jk}(\xi, \eta, s)| \leq C_M 2^{-M max(j,k)}$$ when $|j-k|>K$ for a large enough $K$. Computing the critical points of the phase function in (\[oscillatory\]), we see that $$\sum_l |s|\tilde{s}_l \nabla_x\phi_l(x,y)=\eta \text{ and } \sum_l |s|\tilde{s}_l \nabla_y \phi_l(x,y)=-\xi,$$ where $s=|s|(\tilde{s}_1,...,\tilde{s}_m)$ and $(\tilde{s}_1,...,\tilde{s}_m) \in S^{m-1}$, the unit sphere. The compactness of the support of $\psi$ and the domain of the variable $(\tilde{s}_1,...,\tilde{s}_m)$ along with the linear independence condition from (\[fibration\]) implies that $$\left|\sum_l \tilde{s}_l \nabla_x\phi_l(x,y)\right| \approx \left|\sum_l \tilde{s}_l \nabla_y\phi_l(x,y)\right| \approx 1.$$ More precisely, the upper bound follows from smoothness and compact support. The lower bound follows from the fact that a continuous non-negative function achieves its minimum on a compact set. This minimum is not zero because of the linear independence condition (\[fibration\]). It follows that $$\label{climax} |\xi| \approx |\eta|$$ when we are near the critical points in $(x,y)$. The support of the cutoffs $\psi_0$, when $|j-k|>K$, tell us that we are supported away from critical points in $(x,y)$ since (\[climax\]) no longer holds. This condition implies that for some $h$ or $h'$ in $\{1,2,...,d\}$, $$\left(\sum_l s_l \frac{\partial \phi_l}{\partial x_h} - \eta_h \right) \neq 0 \ \text{or} \ \left(\sum_l s_l \frac{\partial \phi_l}{\partial y_{h'}} + \xi_{h'}\right) \neq 0.$$ Without loss of generality, assume the former holds and that $k> j$. It is immediate that $e^{-i x \cdot \eta} e^{is \cdot(\vec{\phi}(x,y)-r)}$ is an eigenfunction of the differential operator $$L = \frac{1}{i(\sum_l s_l \frac{\partial \phi_l}{\partial x_h} - \eta_h)} \frac{\partial}{\partial x_h};$$ We integrate by parts in (\[oscillatory\]) using this operator. The expression that we get after performing this procedure $M > 2d + m + 1$ times is $$I(\xi, \eta, s) \lesssim \sup_{x,y} \left| \sum_l s_l \frac{\partial \phi_l}{\partial x_h} - \eta_h \right|^{-M}.$$ Now, suppose that we are in the region $\{|s| << |\eta|\}$ (i.e $|s| \leq c|\eta|$ with a sufficiently large constant $c>0$). Since $| \sum_l s_l \nabla_x \phi_l| \approx |s|$ it follows, after possibly changing our initial choice of $h$, that $$\left|\sum_l s_l \frac{\partial \phi_l}{\partial x_h} - \eta_h \right| \gtrsim \left| \hskip.1cm \left|\sum_l s_l \frac{\partial \phi_l}{\partial x_h}\right| - |\eta| \hskip.1cm \right| \approx |\eta|.$$ Similarly, if $\{|s| >> |\eta|\}$ then, again after possibly changing our initial choice of $h$, $$\left|\sum_l s_l \frac{\partial \phi_l}{\partial x_h} - \eta_h \right| \gtrsim \left| \hskip.1cm \left|\sum_l s_l \frac{\partial \phi_l}{\partial x_h}\right| - |\eta| \hskip.1cm \right| \approx |s|.$$ In either region, $$|I_{jk}(\xi, \eta, s)| \lesssim \sup(|s|, |\eta|)^{-M} \lesssim 2^{-Mk} .$$ Considering (\[negativedecay\]), the integrand $(\Pi_l\widehat{\chi_l}(n^{-1}s_l)) I_{jk}(\xi, \eta, s)$ is integrable in $s$ as the first term is at most $1$ and $I_{jk}$ is bounded about by $|s|^{-M}$. Performing the remaining integrations and keeping in mind the support properties of $\widehat{\mu_{A,j}}$ and $\widehat{\mu_{k}}$, it follows that $$\label{2.9} \sum_{|j-k| > K} \langle \mu_{A,j}, T_{\vec{\phi}_r}(\mu_{k})\rangle \lesssim \sum_{|j-k| > K} C_M 2^{-(M-2d) max(j,k)} \lesssim 1.$$ This completes the proof of Lemma \[fardiag\]. Since both sums in (\[2.6\]) are bounded by 1, this implies that the left hand side of (\[2.3\]) is bounded above by $\varepsilon^m$ after completing the integrations in (\[expanded\]). Proof of Theorem \[maximal\] ============================ The following proof is a slight modification of that of Theorem \[operator\]. For the remaining details, please see Section \[opsection\]. In a similar vein as the other proofs of this article, we first notice that the $\epsilon$-neighborhood of $ A \cap \{ y: \phi(x,y) = t \}$ is contained in the set $\{y \in A^{\epsilon} : |\phi(x,y) - t | \leq \epsilon \}$. A reduction ----------- Now, the estimate we would like to prove, as a result of the above containment, is $$\label{mainmaxint} \sup_{t \in [1,2]} \int \mu_A \{ y \in A^{\epsilon} : \ |\phi(x,y) - t | \leq \epsilon \} \ d\mu(x) \lesssim \epsilon.$$ Notice that, as we are dealing only with finite-measures over compact sets with $t \in [1,2]$, there exists $t(x) \in L^1(\mathbb{R}^d)$ such that $\sup_{t \in [1,2]} \int \mu_A \{ y \in A^{\epsilon} : \ |\phi(x,y) - t | \leq \epsilon \} \ d\mu(x) = \int \mu_A \{ y \in A^{\epsilon} : \ |\phi(x,y) - t(x) | \leq \epsilon \} \ d\mu(x)$. We can rewrite the integral in the lefthand side of (\[mainmaxint\]) as $$\int (\rho^{\epsilon} * \mu_A)_{t(x)} (x) \ d \mu(x),$$ where $(\rho^{\epsilon} * \mu_A)_{t(x)} (x) = \epsilon^{-d} \int_{\{ y \in A^{\epsilon} : \ |\phi(x,y) - t(x) | \leq \epsilon \} } \rho(\frac{x-z}{\epsilon}) \ d \mu_A(z)$ and $\rho \in C_0^{\infty}(\mathbb{R}^d)$. Assuming that we have the estimate $$\int (\rho^{\epsilon} * \mu_A)_{t(x)} (x) \ d \mu(x) \lesssim \epsilon,$$ the rest of the proof follows identically to that of Theorem \[operator\], except in two places for the proof analogue of the estimate (\[mainopint\]). We briefly digress in order to give some background. Maximal functions ----------------- Unlike in Theorem \[operator\], the main operator of interest is now the maximal averaging operator $$(Mf)(x) = \sup_{t \in [1,2]} \left| \int_{\{y \ : \ \phi(x,y) = t\}} f(y) \psi(x,y) \ d \sigma_{x,t}(y) \right |,$$ where $\psi$ is a smooth cut-off. Clearly, the Schwarz kernel of this operator is same as the generalized Radon transforms described in (\[keyoperator\]), except we take the additional step of taking a supremum in $t$. Under the same non-degeneracy conditions as those for generalized Radon transforms, for all $t \in [1,2]$, we have the following Sobolev mapping property: $$\| M(f) \|_{L^2_{\frac{d-2}{2}}} \leq \| f \|_{L^2}.$$ For some standard $L^p$ estimates for maximal functions of this kind, please see [@So93]. A key example of a maximal function of this type is the spherical maximal operator, $$\sup_{t \in (0, \infty)} \left | \int_{S^{d-1}} f(x - t y) \ d \sigma(y) \right |,$$ which was introduced in the 1970s by Elias Stein. In particular, Stein was able to establish the optimal range of exponents $p$, for the mapping properties of $M$ on $L^p$, in dimensions $d \geq 3$; see [@St93]. The $d=2$ was, however, settled by Bourgain [@B86]. It is this operator, and more particularly the example of the sphere, which provides many of the intuitions in this article. Proof of estimate (\[mainmaxint\]) ---------------------------------- Returning to the proof, we make notice of the two places where the proof is different. Again, we start by taking Schwartz the class functions $\eta_0(\xi)$ supported in the ball $\{ |\xi| \leq 4 \}$ and $\eta(\xi)$ supported in the annulus $$\{ 1 < |\xi| < 4\} \ \text{with} \ \eta_j(\xi)=\eta(2^{-j}\xi) \text{ for } j \geq 1$$ with $$\eta_0(\xi) + \sum_{j=1}^{\infty} \eta_j(\xi) =1.$$ Define the Littlewood-Paley piece of $\mu_j$ by the relation $$\label{piece} \widehat{\mu}_j(\xi)=\widehat{\mu}(\xi) \eta_j(\xi).$$ Consider the integral in (\[mainmaxint\]). Using the Littlewood-Paley decomposition, this integral is comparable to $$\sup_{t \in [1,2]} \sum_{j,k} \int \int_{\{t \leq \phi(x,y) \leq t + \varepsilon \} } \psi(x,y) d\mu_{k}(y) \hskip.1cm d\mu_{A,j}(x)= \sup_{t \in [1,2]} \sum_{j,k} \langle \mu_{A,j},M_t^{\varepsilon} \mu_{k} \rangle,$$ where $$M_t^{\varepsilon}(\mu_{k})(y) = \int_{\{t \leq \phi(x,y) \leq t + \varepsilon\}} \psi(x,y) d\mu_{k}(x).$$ Using the corresponding Littlewood-Paley decomposition, we get that $$\hskip.1cm \sup_{t \in [1,2]} \langle \mu_A, M_t^{\varepsilon} (\mu)\rangle \hskip.1cm = \sup_{t \in [1,2]} \sum_{j,k} \langle \mu_{A,j}, M_t^{\varepsilon} (\mu_{k})\rangle$$ $$\leq \hskip.1cm \sum_{|j-k| \leq K} \langle \mu_{A,j}, M^{\varepsilon} (\mu_{k})\rangle + \sup_{t \in [1,2]} \sum_{|j-k| > K} \langle \mu_{A,j}, M_t^{\varepsilon} (\mu_{k})\rangle,$$ where $$M^{\epsilon}(\mu_{k})(y) = \sup_{t \in [1,2]} M_t^{\varepsilon}(\mu_{k})(y).$$ ### Near-diagonal terms Similar to the case of near-diagonal terms in the proof of Theorem \[operator\], we arrive at the estimate $$\label{mickey2} \sum_{|j-k| \leq K}\langle \mu_{A,j}, M_{\vec{\phi_r}}(\mu_{k})\rangle \hskip.1cm \lesssim \sum_{|j-k| \leq K}2^{j\frac{d-s_A}{2}}2^{k\frac{d-s_E}{2}}2^{-k(d-2)/2}\lesssim 1$$ provided that $s_E+s_A>d+2$. ### Off-diagonal terms The estimate $$\sup_{t \in [1,2]} \sum_{|j-k| > K} \langle \mu_{A,j}, M_t^{\varepsilon} (\mu_{k})\rangle \lesssim 2^{-\max(j,k) M},$$ follows immediately from Lemma \[fardiag\] for $m=1$ and its independence of the value $t$, for any $M > 2d + 2$. The main estimate (\[mainmaxint\]) is completed after performing the final integration in $r$. .125in Proof of Theorem \[variablecoefficient2kt\] =========================================== Let $\gamma_{\vec{t}}(x^1,x^2)$ denote the upper Minkowski dimension of $$A \cap \{ y: \phi_1(x^1,y) = t_1 \} \cap \{ y: \phi_2(x^2,y) = t_2 \}.$$ Let $\mu_A$ denote the measure inherit from the Ahlfors-David regularity of the set $A$, and let $\mu_{1}$ and $\mu_{2}$ be as in the statement of the theorem.\ A reduction ----------- .125in As in the proof of Theorem \[operator\], we reduce the proof of the Theorem \[variablecoefficient2kt\] to the following estimate: $$\label{mainpointkt} \iint \mu_A \{ y \in A^{\epsilon} : \ |{\phi_i}(x^i,y) - t_i | \leq \epsilon, \hspace{.1in} i=1,2 \} \ d\mu_{1}(x^1)d\mu_{2}(x^2) \lesssim \epsilon^2.$$ To see why this estimate implies the statement of the theorem, first observe that the $\epsilon$-neighborhood of $ A \cap \{ y: \phi_1(x^1,y) = t_1 \} \cap \{ y: {\phi_2}(x^2,y) = t_2 \}$ is contained in the set $\{y \in A^{\epsilon} : |{\phi_i}(x^i,y) - t_i | \leq \epsilon, \hspace{.1in} i=1,2 \}$. Here, $A^{\epsilon}$ denotes the $\epsilon$-neighborhood of the set $A$.\ Now, using the Ahlfors-David regularity of the set $A$, the left-hand-side of (\[mainpointkt\]) is bounded below by $$C \iint {(\epsilon^{-1})}^{\gamma_{\vec{t}}(x^1,x^2)} \epsilon^{s_A} d\mu_{1}(x^1)d\mu_{2}(x^2),$$ where $C>0$ is a universal constant. Comparing the upper and lower bounds, we see that $$\iint {(\epsilon^{-1})}^{\gamma_{\vec{t}}(x^1,x^2)} d\mu_{1}(x^1)d\mu_{2}(x^2) \leq C {(\epsilon^{-1})}^{s_A-2}.$$ Convexity implies $${(\epsilon^{-1})}^{\iint \gamma_{\vec{t}}(x^1,x^2) d\mu_{1}(x^1)d\mu_{2}(x^2)} \leq C{(\epsilon^{-1})}^{s_A-2},$$ from which we conclude that $$\int \gamma_{\vec{t}}(x^1,x^2)d\mu_{1}(x^1)d\mu_{2}(x^2) \leq s_A-2,$$ hence completing the proof of Theorem \[variablecoefficient2kt\]. The rest of this section is dedicated to proving estimate . Approximation operators ----------------------- Begin by re-writing equation as $$\label{rewritemainpointkt} \frac{1}{\epsilon^2}\iiint_{\{ (x^1,x^2)\in E_1 \times E_2 : \ |{\phi_i}(x^i,y) - t_i | \leq \epsilon, \hspace{.1in} i=1,2 \}} d\mu_{1}(x^1)d\mu_{2}(x^2)d\mu_A(y) \lesssim 1.$$ Rather than working directly with operators $T_{\phi, t}$, introduced in , define $$\label{mainopkt}T^{\epsilon}_{\phi,t}f(x) = \frac{1}{\epsilon}\int_{\{y: t-\epsilon\le \phi(x,y) \le t + \epsilon\}} \psi(x,y) f(y) dy,$$ where $\psi: \mathbb{R}^d \times \mathbb{R}^d \rightarrow \mathbb{R}$ denotes a positive, smooth, and compactly supported function. Now, write the left-hand-side of equation as: $$\int T^{\epsilon}_{\phi_1,t_1}\mu_{1}(y) T^{\epsilon}_{\phi_2,t_2}\mu_{2}(y) d\mu_A(y).$$ Therefore, in order to prove Theorem \[variablecoefficient2kt\], it suffices to show that $$\label{reduction1kt}\int T^{\epsilon}_{\phi_1,t_1}\mu_{1}(y) T^{\epsilon}_{\phi_2,t_2}\mu_{2}(y) d\mu_A(y)\lesssim 1.$$ Disection of range of the operators ----------------------------------- For $i=1,2$, we consider the pre-image of $T^{\epsilon}_{\phi_{i},t_i}\mu_{i}$ on a dyadic shell. Let $a$ be a non-negative integer. For $a\geq1$, set $$S^i_a=\{y: 2^{a}\le T^{\epsilon}_{\phi_{i},t_i}\mu_{i}(y) < 2^{a+1}\}.$$ For $a=0$, set $$S^i_a= \{y: T^{\epsilon}_{\phi_{i},t_i}\mu_{i}(y) < 2\}.$$ For $a,b$ fixed, set $$I_{a,b}= S_a^1 \cap S_b^2.$$ The left-hand-side of can now be re-written as $$\label{reducekt} \sum_{a=0}^{\infty}\sum_{b=0}^{\infty} \int T^{\epsilon}_{\phi_{1},t_1}\mu_{1}(y)T^{\epsilon}_{\phi_{2},t_2}\mu_{2}(y)\chi_{I_{a,b}}(y) d\mu_A(y).$$ Notice that if $a=b=0$, then the summand in is trivally bounded since $\mu_A$ is a finite measure. Therefore we may assume that $$\label{tildekt}\max\{a,b\}\neq0.$$ For simplicity of notation, we consider the case when $a\geq b$. The other case is handled by re-writing the proof with roles of $a$ and $b$ reversed. This implies that the proof of Theorem \[variablecoefficient2kt\] is reduced to showing that: $$\label{reduction2kt} \sum_{a=1}^{\infty} \sum_{b=0}^{a} \int T^{\epsilon}_{\phi_{1},t_1}\mu_{1}(y)T^{\epsilon}_{\phi_{2},t_2}\mu_{2}(y)\chi_{I_{a,b}}(y) d\mu_A(y) \lesssim 1.$$ The plan now is to bound the summand on the left-hand-side of by $ 2^{2a}\mu_A(I_{a,b})$ and to show that $\mu_A(I_{a,b})$ is sufficiently small. The following Lemma gives an upper bound on $\mu_A(I_{a,b})$. \[awesomekt\] Fix $a\geq b$ non-negative integers with $a\neq 0$. Then for any real number $\gamma$ satisfying $$\label{gamma}d-s_A < \gamma < \alpha_1 -1,$$ the following estimate holds: $$\mu_A(I_{a,b})\lesssim 2^{-2a} 2^{-\frac{2a}{s_A}(d-\gamma-s_A)}.$$ Notice that such a $\gamma$ exists whenever $\alpha_1 + s_A > d+1$. We use Lemma \[awesomekt\] to bound the summand on the left-hand-side of by a quantity which decays in $a$, and hence to finish the proof. In particular, $$\begin{aligned} \int T^{\epsilon}_{\phi_{1},t_1}\mu_{1}(y)T^{\epsilon}_{\phi_{2},t_2}\mu_{2}(y)\chi_{I_{a,b}}(y) d\mu_A(y) &\lesssim 2^{2a}\mu_A( I_{a,b})\\ &\lesssim 2^{\frac{2a}{s_A}(d-\gamma-s_A)}.\\\end{aligned}$$ Since $\gamma>d-s_A$ and since we assume that $a\geq b$, this quantity is summable in both $a$ and $b$. This completes the proof of the theorem. It remains to show that Lemma \[awesomekt\] holds. Proof of Lemma \[awesomekt\] ---------------------------- We now demonstrate that: $$\label{WTSkt}\mu_A(I_{a,b})\lesssim 2^{-2a}2^{\frac{2a}{s_A}(d-\gamma-s_A)},$$ where $a>b\geq 0$ and $\gamma \in (d-s_A, \alpha_1 -1)$. Recall that $S_{a}^1=\{y: 2^{a}\le T^{\epsilon}_{\phi_1,t_1}\mu_{1}(y) < 2^{a+1} \}.$ By elementary properties of the Fourier transform and the Cauchy-Schwarz inequality: $$\begin{aligned} \label{stuffkt} 2^{a} \mu_A(S_{a}^1) &\le \int T^{\epsilon}_{\phi_{1},t_1}\mu_{1}(y) \chi_{S_{a}^1}(y) d\mu_A(y)\\ &\label{meow}\le \left( \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{1}}(\xi)|^2 (1+|\xi|^2)^{\gamma/2}d\xi\right)^{\frac{1}{2}} \left(\int |\widehat{\mu_A\chi_{S_{a}^1}}(\xi)|^2 (1+|\xi|^2)^{-\gamma/2}d\xi\right)^{\frac{1}{2}}.\end{aligned}$$ We use the following estimates to bound the equation in from above: \[boundQkt\] If $d-s_A< \gamma < \alpha_1-1$, then $$\int |\widehat{\mu_A\chi_{S_{a}^1}}(\xi)|^2 |\xi|^{-\gamma}d\xi\lesssim \mu_A(S_{a}^1) 2^{\frac{2a}{s_A}(d-\gamma-s_A)}.$$ \[boundPkt\] If $\gamma < \alpha_1-1$, then $$\int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{1}}(\xi)|^2 (1+|\xi|^2)^{\gamma/2}d\xi\lesssim 1.$$ Now $$\label{keystepkt}2^{a} \mu_A(S_{a}^1) \le \left(\mu_A(S_{a}^1) 2^{\frac{2a}{s_A}(d-\gamma-s_A)}\right)^{1/2},$$ whenever $\gamma>d-s_A$ and $\gamma < \alpha_1-1$, and so $$\mu_A(S_{a}^1)\lesssim 2^{-2a}2^{\frac{2a}{s_A}(d-\gamma-s_A)}.$$ It remains to prove Lemmas \[boundQkt\] and \[boundPkt\]. Proof of Lemma \[boundQkt\] --------------------------- The following proof relies on Lemma \[boundPkt\] which is proved next. Set $$Q=\int |\widehat{\mu_A\chi_{S_{a}^1}}(\xi)|^2 |\xi|^{-\gamma}d\xi.$$ Before going into the details, we outline the proof of this lemma in two steps.\ **Step 1** First, we show that $Q \lesssim \mu(S_{a}^1)$ whenever $d-s<\gamma < \alpha-1$. Plugging this observations into and assuming for now that Lemma \[boundPkt\] holds, we conclude that $$\mu(S_{a}^1) \le 2^{-2a}.$$\ **Step 2** Next, we use this information to show that $$Q\lesssim \mu(S_{a}^1) 2^{\frac{2a}{s_A}(d-\gamma-s_A)},$$ whenever $\gamma>d-s_A$ and $\gamma < \alpha_1-1$. The details follow.\ **Proof of Step 1** By elementary properties of the Fourier transform, $$\begin{aligned} Q &\sim\iint |x-y|^{\gamma-d} \chi_{S_{a}^1}(x)\chi_{S^1_{a}}(y) d\mu_A(y)d\mu_A(x).\\\end{aligned}$$ Recall that $A$ is a compact subset of $\mathbb{R}^d$, and so $x,y \in A$ implies that $|x-y|\lesssim 1$. Therefore $$\begin{aligned} Q &\sim \sum_{\eta=0}^{\infty}\int \int_{\{y: 2^{-(\eta+1)}\le |x-y|< 2^{-\eta}\}}|x-y|^{\gamma-d} \chi_{S^1_{a}}(x)\chi_{S^1_{a}}(y) d\mu_A(y)d\mu_A(x).\\ &\lesssim \mu_A(S^1_{a})\sum_{\eta=0}^{\infty}2^{(d-\gamma)\eta} 2^{-\eta s_A}\\ &\lesssim \mu_A(S^1_{a}),\\\end{aligned}$$ when $\gamma> d-s_A .$ In the second line, we used the Ahlfors-David regularity of the set $A$, introduced in definition \[ADreg\], to assume that $\mu_A(\{y: |x-y|\le 2^{-\eta}\})\le 2^{-\eta s_A}$. In conclusion, when $\gamma> d-s_A$, we have that $Q\lesssim \mu_A(S^1_{a})$. Plugging this observations into and assuming for now that Lemma \[boundPkt\] holds, we conclude that $$\label{step1kt}\mu_A(S^1_{a})\lesssim 2^{-2a}.$$\ **Proof of Step 2** Next, we use to improve the estimate on $Q$. In step 1, we demonstrated that $$Q \sim \sum_{\eta=0}^{\infty}\int \int_{\{y: 2^{-(\eta+1)}\le |x-y|< 2^{-\eta}\}}|x-y|^{\gamma-d} \chi_{S^1_{a}}(x)\chi_{S^1_{a}}(y) d\mu_A(y)d\mu_A(x).$$ It follows by the Ahlfors-David regularity of the set $A$ that: $$Q \lesssim \mu_A(S^1_{a})\sum_{\eta=0}^{\infty}2^{\eta(d-\gamma)} \min\{2^{-\eta s_A}, \mu_A(S^1_{a}))\}.$$ By , it follows that: $$\begin{aligned} Q &\lesssim \mu_A(S^1_{a})\sum_{\eta=0}^{\infty}2^{\eta(d-\gamma)} \min\{2^{-\eta s_A}, 2^{-2a})\}\\ &= \mu_A(S^1_{a})\left( \sum_{\eta>2a/s_A}2^{\eta(d-\gamma)}2^{-\eta s_A} + \sum_{\eta\le 2a/s_A}2^{\eta(d-\gamma)} 2^{-2a}\right)\\ &\sim \mu_A(S^1_{a}) 2^{\frac{2a}{s_A}(d-\gamma-s_A)}.\end{aligned}$$ .125in Proof of equation ------------------ We now show that if $\gamma < \alpha_1-1$, then $$\int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{1}}(\xi)|^2 (1+|\xi|^2)^{\gamma/2}d\xi\lesssim 1.$$ The proof of the lemma relies on Lemma \[fardiag\] combined with the following observations. If $\phi$ satisfies the Phong-Stein rotational curvature condition at $t$, then the operator $T^{\epsilon}_{\phi, t}$ also satisfies . That is $$\label{sobolevepsilonkt} T^{\epsilon}_{{\phi,t}}: L^2({\Bbb R}^d) \to L^2_k({\Bbb R}^d)$$ with constants uniform in $t$ and $k=\frac{d-1}{2}.$ To prove , first notice that $$T^{\epsilon}_{\phi,t}f(x) = \frac{1}{\epsilon}\int_{t-\epsilon}^{t+\epsilon}T_{\phi,r}f(x) dr,$$ and so by Fubini’s Theorem we have $$\widehat{T^{\epsilon}_{\phi,t}f}(\xi) = \frac{1}{\epsilon}\int_{t-\epsilon}^{t+\epsilon}\widehat{T_{\phi,r}f}(\xi) dr.$$ Now $$\begin{aligned} &\int |\widehat{T^{\epsilon}_{\phi,t}f}(\xi)|^2(1+ |\xi|^2)^{k}d\xi \\ &= \int \widehat{T^{\epsilon}_{\phi,t}f}(\xi) \overline{\widehat{T^{\epsilon}_{\phi,t}f}(\xi)} (1+ |\xi|^2)^{k}d\xi \\ &= \frac{1}{\epsilon^2}\int\int_{t-\epsilon}^{t+\epsilon} \int_{t-\epsilon}^{t+\epsilon}\widehat{T_{\phi,r}f}(\xi)\overline{\widehat{T_{\phi,s}f}(\xi)}(1+ |\xi|^2)^{k}drdsd\xi \\ &= \frac{1}{\epsilon^2}\int_{t-\epsilon}^{t+\epsilon} \int_{t-\epsilon}^{t+\epsilon} \int |\widehat{T_{\phi,r}f}(\xi)|^2(1+ |\xi|^2)^{k}d\xi drds \\\end{aligned}$$ By : $$\begin{aligned} &\lesssim \frac{1}{\epsilon^2}\int_{t-\epsilon}^{t+\epsilon} \int_{t-\epsilon}^{t+\epsilon} \int | \widehat{f}(\xi)|^2d\xi drds \\ &\lesssim \int |f(x)|^2 dx.\\\end{aligned}$$ We now decompose the measure $\mu_1$ as follows: Take positive Schwartz class functions $\eta_0(\xi)$ supported in the ball $\{ |\xi| \leq 4 \}$ and $\eta(\xi)$ supported in the annulus $$\label{etakt} \{ 1 < |\xi| < 4\} \ \text{with} \ \eta_j(\xi)=\eta(2^{-j}\xi) \text{ for } j \geq 1$$ with $$\eta_0(\xi) + \sum_{t=1}^{\infty} \eta_j(\xi) =1.$$ Define the Littlewood-Paley piece, $\mu_j$, of the measure $\mu_1$ by the relation $$\widehat{\mu}_j(\xi)=\widehat{\mu_1}(\xi) \eta_j(\xi).$$ Let $\eta_m$ be as in \[etakt\] and write $\mu_1 =\sum_{j=0}^{\infty}\mu_j$, then the right-hand-side of \[boundPkt\] can be written as: $$\begin{aligned} \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{1}}(\xi)|^2 (1+|\xi|^2)^{\gamma/2}d\xi &= \sum_{j=0}^{\infty} \sum_{l=0}^{\infty} \int \widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{j}(\xi)}\overline{ \widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{l}(\xi)}} (1+|\xi|^2)^{\gamma/2}d\xi\\ &= \sum_{j=0}^{\infty} \sum_{l=0}^{\infty}\sum_{m=0}^{\infty} \int \widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{j}(\xi)}\overline{ \widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{l}(\xi)}} (1+|\xi|^2)^{\gamma/2}\eta_m(\xi)d\xi.\\\end{aligned}$$ By Cauchy-Schwartz inequality, this expression is bounded by $$\label{buster} \sum_{j=0}^{\infty} \sum_{l=0}^{\infty}\sum_{m=0}^{\infty} \left( \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{j}(\xi)}|^2 (1+|\xi|^2)^{\gamma/2}\eta_m(\xi)d\xi\right)^{1/2} \left( \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{l}(\xi)}|^2 (1+|\xi|^2)^{\gamma/2}\eta_m(\xi)d\xi\right)^{1/2}.$$ Consider $$\label{keypiecekt} \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{j}(\xi)}|^2 (1+|\xi|^2)^{\gamma/2}\eta_m(\xi)d\xi.$$ Let $K$ be as in Lemma \[fardiag\] If $|j-m|>K$, then the proof of Lemma \[fardiag\] can be used to show that for any $M$ sufficiently large, the expression in is bounded by $2^{-K\max{\{j,m\}}}$ times a constant dependent on $M$.\ When $|j-m|<K$, we use the mapping properties of the operator $T^{\epsilon}_{\phi_{1},t_1}$ along with the hypothesis of the theorem that $I_{\alpha_1}(\mu_1)$ is finite to demonstrate that the expression in is bounded by $2^{-j(\alpha_1 -1-\gamma)}$ which is summable in $j$ when $\gamma < \alpha_1 -1$. In more detail, if $|j-m|>K$ then $$\begin{aligned} \left( \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{j}(\xi)}|^2 (1+|\xi|^2)^{\gamma/2}\eta_m(\xi)d\xi\right)^{1/2} &\sim 2^{m\gamma}2^{-m(d-1)} \int |\widehat{T^{\epsilon}_{\phi_{1},t_1}\mu_{j}(\xi)}|^2 (1+|\xi|^2)^{(d-1)/2}\eta_m(\xi)d\xi\\ &\lesssim 2^{m\gamma}2^{-m(d-1)} \int |\widehat{\mu_{j}(\xi)}|^2 d\xi\\ &\sim 2^{m\gamma}2^{-m(d-1)}2^{m(d-\alpha_1)} \int |\widehat{\mu_{j}(\xi)}|^2 |\xi|^{\alpha_1-d}d\xi\\ &\sim 2^{m\gamma}2^{-m(d-1)}2^{m(d-\alpha_1)} I_{\alpha_1}(\mu_1) \\ &\sim 2^{-j(\alpha_1 - 1 -\gamma)}, \\\end{aligned}$$ which is summable in $j$ when $\gamma < \alpha_1 -1$. The second part of the summand in is handled in the same way. Since the given bounds are summable in $j$, $m$, and $l$, the expression in is bounded. .25in Proof of Theorem \[inverse\] ============================ .125in We shall need the following result that follows from the Fourier Integral Operator regularity results due to Seeger, Sogge and Stein ([@SSS91]). See also [@So93]. \[sssmaximal\] With $\phi$ as in Theorem \[inverse\], define $${\mathcal M}f(x)=\sup_{t>0} \left| \int_{\phi(x,y)=t} f(y) d\sigma_{x,t}(y) \right|,$$ where $d\sigma_{x,t}$ denotes the Lebesgue measure on $\{y: \phi(x,y)=t \}$ multiplied by a smooth cut-off function. Then if $d \ge 3$, $$\label{sssmaximal} {|| {\mathcal M}f ||}_{L^p({\Bbb R}^d)} \leq C_p {||f||}_{L^p({\Bbb R}^d)} \ \text{for} \ p>\frac{d}{d-1}.$$ Observe that Theorem \[sssmaximal\] still holds if we take a supremum over $t>t_0>0$ in the definition of the maximal function. We also linearize the operator by replacing the supremum over $t>t_0$ by $t(x)$, an arbitrary measurable function of $x$ taking on values in $(t_0, \infty)$. Denote the resulting linearized operator by $T$. Applying Theorem \[sssmaximal\] in this form to $\chi_{A^{\delta}}$, we see that $${|A^{\delta}|}^{\frac{1}{p}} \ge C_p^{-1} {|| T\chi_{A^{\delta}} ||}_{L^p({\Bbb R}^d)}$$ $$\gtrsim \delta^{d-1} \cdot {\left( \int_{support(T\chi_{A^{\delta}})} {|N(x, \delta)|}^p \right)}^{\frac{1}{p}},$$ where $N(x, \delta)$ is minimal number of $\delta$ balls needed to cover $E \cap \{y: \phi(x,y)=t(x) \}$. By definition of upper Minkowski dimension, this is quantity is $$\gtrapprox \delta^{d-1} \delta^{-\gamma}.$$ It follows that $${|A^{\delta}|}^{\frac{1}{p}} \gtrapprox \delta^{d-1} \delta^{-\gamma}.$$ On the other hand, $$|A^{\delta}| \lesssim \delta^{d-s_A},$$ where $s_A$, by Ahlfors-David regularity, is the Hausdorff dimension of $A$. It follows that $$\frac{d-s_A}{p} \leq d-1-\gamma,$$ which implies that $$s_A \ge p(\gamma+1)-d(p-1)$$ for $p>\frac{d}{d-1}$. The conclusion follows. [8]{} J. Barcelo, J. Bennett, A. Carbery, A. Ruiz, A and M. Vilela, [*Some special solutions of the Schrodinger equation*]{}, Indiana Univ. Math. J. **56** (2007), no. 4, 1581-1593. P. Brass, W. Moser and J Pach, [*Research Problems in Discrete Geometry*]{}, Springer (2000). J. Bourgain, [*Averages in the plane over convex curves and maximal operators*]{}, J. Analyse Math. **47** (1986), 69-85. S. Eswarathasan, A. Iosevich and K. Taylor, [*Fourier integral operators, fractal sets and the regular value theorem*]{}, Advances in Mathematics, 228, (2011). B. Erdogan [*A bilinear Fourier extension theorem and applications to the distance set problem*]{} IMRN (2006). K. J. Falconer, [*On the Hausdorff dimensions of distance sets*]{} Mathematika **32** (1986) 206-212. K. J. Falconer, [*The geometry of fractal sets*]{}, Cambridge Tracts in Mathematics, **85** Cambridge University Press, Cambridge, (1986). K. J. Falconer, [*Sets with large intersections*]{}, JLMS **49** (1994), 267-280. G. Folland, [*Real analysis. Modern techniques and their applications*]{} Pure and Applied Mathematics (New York). A Wiley-Interscience Publication. John Wiley & Sons, Inc., New York, (1984). I. Gel’fand and G. Shilov, [*Generalized functions*]{}, Vol. 1, Academic Press, (1966). L. Grafakos, A. Greenleaf, A. Iosevich and E. Palsson, [*Multilinear generalized Radon transforms and point configurations*]{}, (submitted for publication), (http://arxiv.org/pdf/1204.4429.pdf), (2011). A. Greenleaf and A. Iosevich, [*On triangles determined by subsets of the Euclidean plane, the associated bilinear operators and applications to discrete geometry*]{} Anal. PDE **5** (2012), no. 2, 397-409. E. Grosswald, [*Representations of integers as sums of squares*]{}, Springer Verlag, New York, Berlin (1985). L. Hormander, [*Fourier integral operators. I*]{} Acta Math. **127** (1971), no. 1-2, 79-183. S. Hofmann and A. Iosevich, [*Circular averages and Falconer/Erd�s distance conjecture in the plane for random metrics*]{}, Proc. Amer. Math. Soc. **133** (2005), no. 1, 133�1�73. A. Iosevich, [*Fourier analysis and geometric combinatorics*]{} Topics in mathematical analysis, 321�1�75, Ser. Anal. Appl. Comput., **3**, World Sci. Publ., Hackensack, NJ, (2008). A. Iosevich, H. Jorati and I. Laba, [*Geometric incidence theorems via Fourier analysis*]{}, Trans. Amer. Math. Soc. **361** (2009), no. 12, 6595-�1�711. A. Iosevich and I. Laba, [*K-distance sets, Falconer conjecture, and discrete analogs*]{}, Integers **5** (2005). A. Iosevich and E. Sawyer, [*Maximal averages over surfaces*]{}, Adv. Math. **132** (1997), no. 1, 46�1�79. A. Iosevich and S. Senger, [*Sharpness of Falconer’s estimate in continuous and arithmetic settings, geometric incidence theorems and distribution of lattice points in convex domains*]{}, (submitted for publication) (2010). A. Iosevich and K. Taylor, [*Lattice points close to families of surfaces, non-isotropic dilations and regularity of generalized Radon transforms*]{}, New York J. Math. **17** (2011), 811�1�78. J.P. Kahane, [*Sur la dimension des intersections. (French) \[On the dimension of intersections\]*]{} Aspects of mathematics and its applications, 419�1�70, North-Holland Math. Library, **34**, North-Holland, Amsterdam, (1986). P. Mattila, [*Hausdorff dimension and capacities of intersections of sets in $n$-space*]{}, Acta Math. **152** (1984), no. 1-2, 77-105. P. Mattila, [*On the Hausdorff dimension and capacities of intersections*]{}, Mathematika **32** (1985) 213-217. P. Mattila [*Spherical averages of Fourier transforms of measures with finite energy: dimensions of intersections and distance sets*]{} Mathematika, **34** (1987), 207-228. P. Mattila, [*Geometry of sets and measures in Euclidean spaces*]{}, Cambridge University Press, 44, (1995). D. Phong and E. Stein, [*Radon transforms and torsion*]{}, Inter. Math. Res. Not., **4**, (1991). A. Seeger, C. D. Sogge and E. M. Stein, [*Regularity properties of Fourier integral operators*]{}, Ann. of Math. (2) **134** (1991), no. 2, 231�1�71. C. Sogge, [*Fourier integrals in classical analysis*]{}, Cambridge University Press, (1993). E. M. Stein, [*Harmonic Analysis*]{}, Princeton University Press, (1993). P. Valtr, [*Strictly convex norms allowing many unit distances and related touching questions*]{}, manuscript 2005. T. Wolff, [*Recent work connected with the Kakeya problem. Prospects in mathematics*]{} (Princeton, NJ, 1996), 129-162, Amer. Math. Soc., Providence, RI, (1999). T. Wolff, [*Decay of circular means of Fourier transforms of measures*]{}, International Mathematics Research Notices **10** (1999) 547-567. T. Wolff, [*Lectures on harmonic analysis*]{} Edited by Laba and Carol Shubin. University Lecture Series, **29**. American Mathematical Society, Providence, RI, (2003). [^1]: The work of the second listed author was partially supported by the NSF Grant DMS10-45404

983 A.2d 1164 (2009) 411 N.J. Super. 15 MING YU HE and Jinfang He, Plaintiffs-Appellants, v. Enilma MILLER, Defendant-Respondent, and Randy Miller, Defendant. DOCKET NO. A-5685-07T3. Superior Court of New Jersey, Appellate Division. Argued December 1, 2008. Decided March 27, 2009. Remanded by Supreme Court June 5, 2009. Re-argued November 12, 2009. Decided December 15, 2009. *1166 August R. Soltis, argued the cause for appellant. Michael J. Marotte, Morristown, argued the cause for respondent (Schenck, Price, Smith & King, attorneys; Mr. Marotte, of counsel; Sandra Calvert Nathans, on the brief). Before Judges FISHER, SAPP-PETERSON and ESPINOSA. The opinion of the court was delivered by FISHER, J.A.D. We again review an order granting remittitur or, upon its rejection, a new trial on damages. We previously reversed, but the Supreme Court summarily reversed in part and remanded for the trial judge's complete and searching analysis, including an assessment of comparable jury verdicts, to be followed by our reconsideration. Having reexamined the matter, we again reverse and reinstate the jury's verdict. I The complaint filed by plaintiff Ming Yu He, and her husband, Jinfang He, against defendant Enilma Miller,[1] was tried to a jury over four days in February 2008. The jury found defendant to have been negligent and awarded plaintiff $1,000,000 for pain and suffering, $110,000 for past lost wages, and $500,000 for future lost wages; the jury also awarded plaintiff's husband $100,000 on his loss of consortium claim. Defendant filed a post-verdict motion seeking a new trial or, in the alternative, a remittitur. The trial judge granted the motion in part. He found the pain and suffering award, as well as the per quod award, to be excessive and shocking to the conscience. He granted a remittitur of the pain and suffering award to $200,000 and the per quod claim to $10,000. The judge also ordered a new trial on damages if plaintiffs rejected the remittitur. Plaintiffs rejected the remittitur and moved for leave to appeal. We granted leave to appeal and subsequently reversed by way of an unpublished opinion. He v. Miller, No. A-5685-07T3, 2009 WL 790940 at *8 (App.Div. March 27, 2009). The Supreme Court granted defendant's petition for certification, summarily reversed our judgment in part and remanded the matter to the trial judge "for a complete and searching analysis under [Johnson v. Scaccetti, 192 N.J. 256, 927 A.2d 1269 (2007)], including a `factual analysis of how the award is different or similar to others to which it is compared,' id. at 281, 927 A.2d 1269." He v. Miller, 199 N.J. 538, 539, 973 A.2d 943 (2009). The Court also directed that we reconsider our judgment "in light of the findings developed on remand." Ibid. On August 12, 2009, the trial judge rendered a decision further explaining and adhering to his finding of excessiveness. The parties have since filed briefs relating to the trial judge's most recent decision, *1167 and we have again heard the oral argument of counsel. II In our earlier unpublished opinion, we canvassed the evidence adduced at trial. To summarize, plaintiff Ming Yu He was injured when, on October 28, 2003, her motor vehicle was struck head-on by defendant's vehicle. Plaintiff was rendered unconscious by the impact and transported by ambulance to a nearby hospital. X-rays revealed no fractures and she was discharged. However, due to continuing pain, she visited a chiropractor on three occasions, but received no relief. On November 6, 2003, plaintiff was examined by Dr. Robert Kramberg, who found a limited range of motion in plaintiff's cervical spine and lower back, back spasms, bruising and abnormal nerve sensation. Dr. Kramberg prescribed various medications, including painkillers. He also started a program of physical therapy. A few weeks later, in light of plaintiff's continued complaints of pain in her neck, lower back and left knee, Dr. Kramberg ordered magnetic resonance imaging (MRI) of plaintiff's cervical and lumbar spine. The MRI revealed that plaintiff had four herniated or ruptured discs, located at C4-C5, C5-C6, L4-L5 and L5-S1. An electromyography determined that the herniated discs were causing compression of the nerves, which affected plaintiff's arms, legs and back. Dr. Kramberg concluded that plaintiff was suffering from radiculitis or radiculopathy from the herniated discs in both the cervical and lumbosacral spine. The physical therapy program failed to produce satisfactory results. As a result, Dr. Kramberg referred plaintiff to Dr. Jay Lee, who performed over thirty acupuncture treatments on plaintiff's hands, neck, waist and back. These treatments only provided temporary relief. Epidural injections of cortisone brought about no significant improvement. Indeed, plaintiff experienced a bad reaction from the cervical epidurals, and the lumbar epidural injections caused plaintiff's leg to become swollen. Consequently, plaintiff received no further injections. Dr. Kramberg referred plaintiff to a neurosurgeon. MRIs taken at that time were consistent with the earlier findings. The neurosurgeon did not recommend surgery, explaining that "whether or not a spinal patient is referred to surgery depends on the particular patient and particular injury." Dr. Kramberg also observed that not all patients do well with surgery. And once you have a failed surgery, there's nothing else you can do for the patient. They wind up on lifetime narcotic pain medication. Dr. Kramberg testified at trial that after five years of unavailing treatment, plaintiff's pain was "chronic [and] permanent." As we explained in our earlier opinion, Dr. Kramberg opined that plaintiff continued to have limited range of motion, and he believed she was medically incapable of performing her job as a housekeeper at a hotel. He continued to prescribe pain medication (Vicodin) to plaintiff and she last saw him in January 2008. In Dr. Kramberg's opinion, based upon the MRI and EMG results, the physical examination, plaintiff's complaints, and the fact that plaintiff had been completely asymptomatic prior to the accident, her injuries were causally related to the October 28, 2003 accident. [2009 WL 790940 at *2.] Dr. Kramberg also acknowledged that testing revealed plaintiff had "a little bit of arthritic degeneration on the vertebrae," *1168 which he determined was part of the "normal aging process" and "pretty much consistent with her age, being in her [forties]." Defendant's expert, an orthopedic surgeon, opined that "there's a good suspicion that a lot" of the MRI and EMG findings "are degenerative and preexisting," but acknowledged "there's really no way of ascertaining, based on these films, whether or not the disc herniations are a result of the degenerative changes or not." Plaintiff, her husband and their daughter also testified about the injury and its sequelae, which we summarized in our earlier opinion in the following way: Plaintiff testified as to how the accident and her resulting injuries impacted upon her activities of daily living. She indicated that she experienced neck and back pain "on a daily basis[,]" which often spread and caused headaches and pain in the legs and hands, and sometimes caused her to lose her grip and drop things. She was no longer able to work at the job she held for thirteen years and could not perform most normal household duties such as grocery shopping, cooking a full meal, gardening, vacuuming, cleaning, or participating in activities with her children. She also testified she was no longer able to swim or ride a bicycle. Plaintiff's husband and daughter provided similar testimony as to plaintiff's home life. Both plaintiff and her husband testified that they brought their parents to the United States from China so that they would not have to work in their old age and their daughter could take care of them, in accordance with the Chinese custom of filial piety. Now, according to plaintiffs, the situation had been reversed, with the grandparents taking care of plaintiff by helping out with the chores she could no longer perform. They both also testified that they have been completely unable to have sexual relations since the accident because their attempts to do so were continually foiled by the onset of back and neck pain for plaintiff. Plaintiff told the jury that since the accident, she felt "useless." [2009 WL 790940 at *3.] III Defendant moved for a new trial or, in the alternative, for a remittitur. Among other things, defendant argued that the $1,000,000 pain and suffering award was shockingly high because of verdicts rendered in other purportedly similar cases. Based on references in defendant's moving papers to the verdicts in thirteen other cases, defendant contended that a proper award should have fallen within a range between $50,000 and $100,000. The judge denied the motion insofar as it related to liability, the past lost wage award of $110,000, and the future lost wage award of $500,000. He did, however, conclude that the pain and suffering award of $1,000,000 and the per quod award of $100,000 were shocking to the conscience and warranted relief, explaining: Based upon the fact that surgery was never recommended for [plaintiff], that she has degenerative dis[c] disease, that she is able to care for herself, drive a motor vehicle and perform light housekeeping, as well as the fact that she did not appear to be experiencing pain and suffering during the course of the trial and was able to sit for long periods of time during the trial, I find that the jury award of $1M to [plaintiff] for her injuries constitutes a manifest injustice that shocks the judicial conscience. In so ruling, the judge made no mention of verdicts in other cases of a similar nature. *1169 Plaintiff rejected the remittitur and moved for leave to appeal. At the same time, the judge issued a written amplification of his oral decision, pursuant to Rule 2:5-1(b), which mainly explained why, if remittitur was rejected, a new trial on all elements of damages, and not just the remitted components, was required. The judge found that "in the case at bar, there is an interrelationship" between the awards he found excessive and those he found were not excessive. As noted earlier, we granted leave to appeal. Following the perfection of the appeal, we reversed by way of an unpublished opinion. The Supreme Court granted certification, reversed in part and remanded to the trial court "for a complete and searching analysis under Johnson, supra, including `a factual analysis of how the award is different or similar to others to which it is compared.'" 199 N.J. at 539, 973 A.2d 943 (quoting Johnson, supra, 192 N.J. at 281, 927 A.2d 1269). Although the trial judge's initial decision and subsequent amplification made no reference to comparable jury verdicts in finding parts of this verdict to be shockingly high, following the Supreme Court's mandate the judge rendered a written decision in which he identified certain verdicts he thought were relevant. Specifically, the judge referred to two cases over which he presided. The first, Morales v. Keith, was an action brought by a thirty-four-year old male plaintiff who, as a result of an auto accident, was diagnosed with one herniated disc and one disc bulge. The plaintiff in Morales was also diagnosed with bilateral carpal tunnel syndrome, which required surgery. The jury awarded $2500, which was increased by stipulation of the parties to nearly $50,000. The second, Ziza v. Romanelli, was an action commenced by a fifty-five-year old female plaintiff who suffered a hairline fracture of an ankle, and torn ligaments, as a result of a fall-down accident. A disputed issue at trial related to plaintiff's claim of reflex sympathetic dystrophy (RSD); she was treated for the alleged RSD through surgical implantation of a spinal cord stimulator. According to the trial judge, despite some degree of relief from the stimulator, plaintiff still experienced pain. In addition, the facts revealed that plaintiff's lifestyle and her relationship with her husband were affected by the injuries. Further, plaintiff was unable to continue working in the family bakery business where she had worked for many years. The jury awarded the plaintiff in Ziza $200,000; her husband received $25,000. The trial judge summed up the significance of these verdicts in the following way: Although the injuries sustained in the above-noted cases were not identical to those sustained by [p]laintiff in this case, the cases provided a basis for comparison to the matter involved herein, as they involved spinal and/or other serious injuries which had a significant impact on the lives of the plaintiffs. The [c]ourt found it particularly noteworthy that even in a case which required the permanent implantation of a spinal stimulator and ligament reconstruction surgery, the jury award did not exceed $200,000.00. Not only, as the judge recognized, were the injuries sustained in these two cases different from those sustained by plaintiff here, but the cases involved persons of different ages who led different lives. The judge went on to mention verdicts in other cases, but only briefly. His commentary concerning those verdicts consists only of the following: *1170 In addition to the cases over which the [c]ourt presided [i.e., Morales and Ziza], the [c]ourt reviewed and took into account cases cited by [d]efendant in support of the motion for remittitur in order to establish a frame of reference by which to evaluate the jury's award. It should be noted that the [p]laintiff did not cite any contrary cases. The [c]ourt specifically notes the following cases cited by [d]efendant: Astarita v. Tilcon Industries; Regan v. Eddy; Shamosh v. Hall; Fernandez v. Carvalho; Hossain v. Reid; and Boghdady v. Antala. As in this matter, both the Astarita and Regan cases were venued in Morris County. In Astarita, plaintiff was injured when he was struck by a motor vehicle in a parking lot. Plaintiff was diagnosed with disc herniations at L3-L4 and L4-L5 and underwent a laminotomy, a surgical procedure in which a portion of his vertebral lamina was removed. The jury returned a verdict in favor of plaintiff for $200,000.00. In Regan, plaintiff's vehicle was struck head-on by defendant's vehicle. Plaintiff was diagnosed with disc herniations at C5-C6 and C6-C7 and received conservative treatment. The jury awarded plaintiff $150,000.00. Cases venued in other counties also revealed substantially lower verdicts than the one rendered in this case. In Shamosh, plaintiff was diagnosed with disc herniations at L4-L5 and L5-S1 and lumbar radiculopathy following an accident. Plaintiff subsequently underwent decompression surgery. The jury rendered an award of $50,000.00. In Fernandez, following an accident, plaintiff was diagnosed with multiple herniations at C4-C5, C5-C6, and L5-S1, as well as a central disc protrusion at L4-L5. In that matter, the jury awarded plaintiff $100,000.00. Similarly, in Hossain, following a motor vehicle accident, plaintiff sustained a disc herniation at L4-L5 with radiculopathy. Plaintiff's treatment included, as in this matter, five epidural injections. Further, plaintiff was unable to work for an extended time period and ultimately gave up his job as a taxi driver. The jury awarded plaintiff $50,000.00. In Boghdady, as in the instant case, plaintiff was diagnosed with multiple disc herniations, specifically herniations at C3-C4, C4-C5, and C6-C7, as well as a disc bulge at C5-C6. Plaintiff underwent orthopedic treatment which included epidural injections. The jury awarded plaintiff $40,000.00. In taking into account the above-cited cases, it should be noted that the [c]ourt was only provided with limited factual details. However, the [c]ourt regards the cases cited by [d]efendant as a valid basis for comparison in light of Dr. Kramberg's findings that [p]laintiff's injuries and complaints were "pretty much a textbook case." Further, although not identical, the cited cases contain similarities to the instant case. Specifically, in each case plaintiff suffered spinal injuries following an accident. In addition, the course of treatment which the plaintiffs underwent, to varying degrees, is akin to that which [p]laintiff received in this matter. The cases establish a spectrum of jury awards which range between $40,000.00 and $200,000.00. Notably, even in those cases where major invasive surgery was indicated and/or performed, the jury award did not exceed $200,000.00. In making its comparative analysis, the [c]ourt could not help but recognize the great disparity between the award in this matter and those rendered in the cited cases where the plaintiffs sustained similarly serious injuries and, in several cases, required surgery. [Docket numbers of cited cases deleted.] *1171 Lastly, the judge referred to the twenty-two years he practiced law in Morris County, during which he concentrated "largely on plaintiffs' personal injury matters venued in Morris County." The judge explained that in his law practice he worked on a myriad of matters involving spinal injuries which had a serious impact on the client's lifestyle. In addition, the [c]ourt was aware of countless other arbitration awards and jury verdicts involving injuries similar to those sustained by [p]laintiff. Despite the [c]ourt's experience and in light of [p]laintiff's injuries in this matter, the [c]ourt could not recall an award which was equal to the amount of the jury award in this case. [Footnote deleted.] Based on this information and his own "feel of the case," the judge again concluded that the pain and suffering and per quod awards were excessive. IV The Supreme Court's mandate in this case requires that we reconsider our earlier decision "in light of the findings developed on remand." 199 N.J. at 539, 973 A.2d 943. Having carefully examined the trial judge's remand decision, we find no cause to alter our earlier judgment. In reaching that conclusion, we consider (a) the applicable principles for determining the excessiveness of a damages award, (b) the judge's examination of what he found were other comparable verdicts, and (c) the judge's description of the relevant facts and his "feel of the case." A A trial court's role in assessing a verdict is to ensure that damages awarded "encompass no more than the amount that will make the plaintiff whole, that is, the actual loss." Caldwell v. Haynes, 136 N.J. 422, 433, 643 A.2d 564 (1994). "Although `[t]he judicial role in reviewing jury verdicts... is essential to a rational system of justice,' the authority to set aside damages awards on grounds of excessiveness is `limited,'" Jastram v. Kruse, 197 N.J. 216, 228, 962 A.2d 503 (2008) (quoting Carey v. Lovett, 132 N.J. 44, 66, 622 A.2d 1279 (1993)), and should only occur "in clear cases," Fritsche v. Westinghouse Elec. Corp., 55 N.J. 322, 330, 261 A.2d 657 (1970). To put these principles in perspective, we must recognize that juries are routinely instructed that to reach a reasonable measure of damages "[t]he law does not provide you with any table, schedule or formula by which a person's pain and suffering[,] disability, loss of enjoyment of life may be measured in terms of money." Johnson, supra, 192 N.J. at 280, 927 A.2d 1269. Jurors are told that the proper measure of damages is "left to [their] sound discretion," based on their common experiences regarding "the nature of pain and suffering, disability, impairment and loss of enjoyment of life" and the "function of money," and that [t]he task of equating the two so as to arrive at a fair and reasonable award of damages requires a high order of human judgment. For this reason, the law can provide no better yardstick for your guidance than your own impartial judgment and experience. [Ibid. (quoting Model Jury Charge (Civil), 6.11F, "Damages—Personal Injuries: Disability, Impairment, Loss of Enjoyment of Life, Pain and Suffering" (1996)).] As a result, following its recognition of the broad discretion that is "uniquely reposed in the jury's good judgment," our Supreme Court has directed that "to justify judicial interference [t]he verdict must be wide of *1172 the mark and pervaded by a sense of wrongness." Jastram, supra, 197 N.J. at 229, 962 A.2d 503 (quoting Johnson, supra, 192 N.J. at 281, 927 A.2d 1269). In assessing excessiveness, the Supreme Court has determined that the trial judge's review "must be grounded substantially in the `totality of the evidence' in the record." Jastram, supra, 197 N.J. at 229, 962 A.2d 503 (quoting Baxter v. Fairmont Food Co., 74 N.J. 588, 598, 379 A.2d 225 (1977)). That evidence must be "viewed in a light most favorable to the plaintiff." Ibid. See also Johnson, supra, 192 N.J. at 281, 927 A.2d 1269; Taweel v. Starn's Shoprite Supermarket, 58 N.J. 227, 236, 276 A.2d 861 (1971), overruled on other grounds, Fertile v. St. Michael's Med. Ctr., 169 N.J. 481, 779 A.2d 1078 (2001). This evaluation must encompass the nature and extent of the injury, the medical treatment that the plaintiff underwent and may be required to undergo in the future, the impact of the injury on the plaintiff's life from the date of injury through the date of trial, and the projected impact of the injury on the plaintiff in the future. [Jastram, supra, 197 N.J. at 229, 962 A.2d 503.] The Supreme Court has also held that the trial judge "may look beyond the record to judicial `experience with other injury verdicts.'" Ibid. (quoting Fertile, supra, 169 N.J. at 501, 779 A.2d 1078). The Court cautioned, however, that if a judge goes outside the record to consider other verdicts, "it must give a factual analysis of how the award is different or similar to others to which it is compared." Id. at 229-30, 962 A.2d 503 (quoting Johnson, supra, 192 N.J. at 281, 927 A.2d 1269). Ultimately, a verdict "should not be overthrown except upon the basis of a carefully reasoned and factually supported (and articulated) determination, after canvassing the record and weighing the evidence, that the continued viability of the judgment would constitute a manifest denial of justice." Baxter, supra, 74 N.J. at 597-98, 379 A.2d 225. As a result, even if "generous," a jury verdict having "reasonable support in the record" must "be regarded as final." Jastram, supra, 197 N.J. at 230, 962 A.2d 503 (quoting Taweel, supra, 58 N.J. at 236, 276 A.2d 861). The appellate standard of review employs the same principles utilized in the trial court with the exception that the appellate court must afford "due deference" to the trial judge's "feel of the case" with regard "to the assessment of intangibles, such as witness credibility." Jastram, supra, 197 N.J. at 230, 962 A.2d 503. See also Feldman v. Lederle Labs., 97 N.J. 429, 463, 479 A.2d 374 (1984). B As we have observed, the Supreme Court mandated our reconsideration following the trial judge's further examination "including `a factual analysis of how the award is different or similar to others to which it is compared.'" 199 N.J. at 539, 973 A.2d 943 (quoting Johnson, supra, 192 N.J. at 281, 927 A.2d 1269). We, thus, turn to the judge's discussion of comparable verdicts in his remand decision.[2] As recounted earlier, the judge relied on the verdicts in two cases over which he presided. These comparables possess little similarity to the case at hand. In the first, Morales v. Keith, plaintiff suffered a disc herniation, as well as a disc bulge, but it was the carpal tunnel syndrome that required surgery. Even at that, the jury *1173 only awarded $2500, which—from the information provided in the judge's opinion—might be more likely to suggest the verdict was shockingly low, as revealed by the parties' stipulation that increased the award to nearly $50,000. The second, Ziza v. Romanelli, involved a plaintiff who sustained a hairline ankle fracture and torn ligaments; it also included a dispute between the parties regarding a diagnosis of RSD. The plaintiff in Ziza underwent surgery for the implantation of a spinal cord stimulator. She received a $200,000 award. There apparently was a lost wage claim in that case as well, but we assume from the judge's remand decision that the jury was only asked to provide a single verdict for all the components of that plaintiff's injuries. Ziza's husband received a per quod award of $25,000. From what the trial judge has said about these cases there are obvious significant differences. Only Morales dealt with a herniated disc (and not, as here, four herniated discs) and that case generated a verdict less than two percent of the amount to which the trial judge remitted the pain-and-suffering verdict in the case at hand. The Ziza case involved injuries that required spinal surgery, but it also involved an injured ankle and the verdict apparently lumped all the elements of damages together. The plaintiff in Ziza was fifty-five years old; plaintiff here was forty-six years old at the time of trial. The judge also referred to verdicts in other cases where the plaintiffs sustained spinal injuries: in Astarita, plaintiff sustained two herniated discs, underwent a laminotomy, and was awarded $200,000; in Regan, plaintiff sustained two herniated discs, was treated conservatively, and awarded $150,000; in Shamosh, plaintiff sustained two disc herniations, underwent decompression surgery and was awarded $50,000; in Fernandez, plaintiff sustained three herniated discs and one disc bulge, and was awarded $100,000; in Hossain, plaintiff sustained one herniated disc and was awarded $50,000; in Boghdady, the plaintiff sustained three herniated discs and one disc bulge, and was awarded $40,000. These cases provide some superficial support for the judge's conclusion, but what the judge has said about these cases reveals little about those particular plaintiffs and their own unique lives. The judge's discussion of those cases does not inform us of the plaintiffs' ages or how their particular injuries—undoubtedly similar to plaintiff's injuries here—impacted upon their lives. In other words, it may be fair to compare the injuries sustained by plaintiff with the injuries sustained by these other plaintiffs but we question how can it be said without more that the pain and suffering of those others, as well as the way in which their enjoyment of life was lost or impaired, is sufficiently similar to warrant comparison. Comparing the injuries sustained by individuals is not the same as comparing damages to automobiles. If a jury was asked to determine the value of a 2004 Ford Focus, which was totaled in an accident, it could safely consider the value of any other 2004 Ford Focus with similar mileage. But we are not dealing with the damage done to mechanical things—we are dealing with human beings, all of whom are in many ways similar but in many ways different from all other human beings. We can generally predict, based on past experiences in similar cases, what a reasonable jury might award for a particular type of injury, but we should not expect that all juries ought to produce the same or similar verdict. The task of a jury in such a matter is to resolve complex issues regarding the monetary value of a particular person's pain and suffering and *1174 loss of the enjoyment of life. In examining such verdicts for excessiveness, courts should not expect or require the type of exactitude that seems to form the basis for the judge's decision in this case. Given very limited information from the trial judge as to the facts and circumstances of these purported comparable verdicts,[3] we reject the notion that they provide adequate support for the judge's finding of excessiveness.[4] C In his decision following the Supreme Court's summary order in this matter, the trial judge also referred to his "feel of the case" in concluding that the pain and suffering and per quod awards were excessive. In this respect, the judge relied upon his observations of plaintiff during the course of the four-day trial, noting that she was able to sit for long periods of time without any visible signs of pain or discomfort. She was able to enter and exit the courtroom without assistance or any apparent difficulty. Plaintiff's gait and appearance did not appear to be in any way affected by her injuries. Overall, there were no outward signs of pain or discomfort observable during the course of the trial. The judge also sought to minimize plaintiff's injuries by referring to the facts that: plaintiff's treating doctors did not recommend surgery; "there was undisputed evidence of degenerative disc disease which preexisted the accident"; and, although she claimed a significant limitation in her daily activities, plaintiff "is able to care for herself, continues to perform light cleaning work, and is able to drive a motor vehicle." We emphasize that the trial judge is not "a thirteenth and decisive juror," and "may not substitute his judgment for that of the jury." Johnson, supra, 192 N.J. at 281, 927 A.2d 1269 (quoting Baxter, supra, 74 N.J. at 598, 379 A.2d 225). We pay deference to the trial judge's "feel of the case" mainly because a judge's observations are helpful in understanding a jury's findings. Those observations are not, however, to supplant the jury's findings when the evidence—viewed in the light most favorable to plaintiff— indicates the jury possessed a different view of the case. Ibid.; Taweel, supra, 58 N.J. at 236, 276 A.2d 861. Indeed, as the Court held in Baxter, a trial judge's "feel of the case" is entitled to "minimal" weight when based on things observed by the jury. Baxter, supra, 74 N.J. at 600, 379 A.2d 225. Here, it is interesting to observe that the trial judge found nothing excessive or shocking about the jury's award of future lost wages of $500,000. We gather from the jury's verdict on that aspect of damages, and the judge's finding that it was not excessive, that the jury found—as was its right—that plaintiff would remain permanently unable to return to work. The judge also determined, in amplifying his *1175 initial decision prior to our earlier opinion, that "there is an interrelationship between the pain and suffering and per quod damage awards and the lost wage awards." That being the case, we find incongruous the judge's determination that the pain and suffering award—although, as the judge held, not "fairly separable" from the lost wage award—was excessive whereas the lost wage award was not. In our earlier opinion, we provided the following comments, which remain applicable: [W]hile the factors upon which the court focused led it to conclude the pain and suffering and per quod awards were excessive, those same factors apparently did not lead the court to conclude that the jury's verdict relative to past and future lost wages was excessive. At their core, past and future loss of wages requires proof that plaintiff's injuries are causally related to plaintiff's inability to engage in her pre-accident employment responsibilities. Thus, plaintiff's inability to work is inextricably linked to the nature of injuries and the effect those injuries have upon continued employment. Consequently, we find it difficult to understand that the court could accept the jury's award for past and future lost earnings but not its award for pain and suffering and the per quod verdict. [2009 WL 790940 at *8.] In carefully examining the record on appeal, we conclude that the judge mistakenly failed to appreciate that the jury's view of the case—that is, the jury's findings regarding plaintiff's injuries, the duration and intensity of her pain and suffering, and the impact those injuries and the consequent pain had on her enjoyment of life—differed substantially from his own. While the judge determined from his own observations of plaintiff in the courtroom that she did not appear to be as limited as claimed, the jury had the same opportunity to observe plaintiff and clearly found otherwise. And the judge, in his initial oral decision, concluded from his view of the evidence that plaintiff "has degenerative disk [sic] disease." Although plaintiff's expert indicated that the MRI studies revealed "degenerative problems" in places along her spine, that expert rejected the assertion that the herniated discs were causally related to any degenerative problems due to age. Again, in light of the jury's entire verdict, including those aspects the judge found were not excessive, we must assume the jury found plaintiff's expert credible. In exalting these "degenerative problems," as a means for minimizing the extent of plaintiff's pain and suffering, the judge failed to view the evidence "in a light most favorable to the plaintiff." Jastram, supra, 197 N.J. at 229, 962 A.2d 503. In concluding as we must that the jury found persuasive all aspects of plaintiff's claim, including the intensity and chronicity of her pain, the permanency of her injuries, and the severe blow these injuries dealt to her enjoyment of life, we reject the judge's own personal view of the evidence as an appropriate yardstick by which to measure defendant's claim of excessiveness.[5] V To summarize, we have reconsidered the matter in light of the judge's *1176 written decision following the Supreme Court's remand. We conclude that the judge's additional findings regarding comparable verdicts and his "feel of the case" are inconsistent with the principles set forth in Johnson, supra, 192 N.J. at 281, 927 A.2d 1269. Moreover, the findings are plainly insufficient to establish that the verdict constituted the manifest denial of justice required to overthrow the jury's determination. See Baxter, supra, 74 N.J. at 597-98, 379 A.2d 225. In the final analysis, we find the trial judge's decision to be erroneous because he viewed as excessive a verdict that did not meet his vision of what lawyers or insurance adjusters might expect a jury to award to a plaintiff who has suffered certain injuries. In reversing, we can assume—although we think he was more conservative than warranted—that the judge was correct when he estimated the likely range of pain-and-suffering verdicts to be $40,000 to $200,000 in cases involving these types of injuries, treated in a similar way and with similar results. Finding such a range and ascertaining whether the verdict fell outside its borders, however, is not determinative of whether an award is excessive. It would indeed be strange if the law required that we instruct juries that there is no yardstick against which to measure a proper award of damages and then permit trial judges to use such a yardstick to determine excessiveness. Instead, determining what might be a predictable award in a particular case is only a starting point in such an analysis. That is, verdicts that fall outside a predictable range are not per se excessive. For example, in Jastram, supra, 197 N.J. at 235, 962 A.2d 503, the Court reinstated a jury verdict, stating: "To be sure ... this was a high verdict, but that does not mean it was excessive." Likewise, in Johnson, supra, 192 N.J. at 283, 927 A.2d 1269, the Court found a jury's award to be "undoubtedly high, perhaps overly generous," but concluded it was not "so grossly excessive that it shocks the conscience." In short, it is a mistake to conclude that a verdict is excessive and shocking because it was greater than what an experienced practitioner or judge might expect in similar circumstances. The question is not whether the verdict "missed the mark" but whether it was "wide of the mark." When the predictable range for the damages in a case has been exceeded—even when "high" or "overly generous"—the verdict must still be sustained unless it can be held and adequately articulated that the award was "so grossly excessive" as to permit a conclusion—clearly and convincingly reached—that permitting the award to stand would constitute a manifest miscarriage of justice. Id. at 281, 927 A.2d 1269. Having reexamined the matter in light of the trial judge's additional findings, we again recognize that this is a close case. It is not unreasonable to conclude that the pain and suffering award missed the mark. It may even lie around the edges of what might constitute a grossly excessive award. But, as our Supreme Court has said, a "tie must go to the jury," id. at 283, 927 A.2d 1269, because "[i]n the American system of justice the presumption of correctness of a verdict by a jury has behind it the wisdom of centuries of common law merged into our constitutional framework," ibid. (quoting Baxter, supra, 74 N.J. at 598, 379 A.2d 225). The order under review is reversed and the matter remanded for reinstatement of the jury's verdict. We do not retain jurisdiction. NOTES [1] Defendant Randy Miller was the owner of the vehicle driven by defendant. The claims against him were dismissed with prejudice prior to trial. [2] The trial judge never considered comparable verdicts in the original decision or the amplification he provided at the time we granted leave to appeal. [3] The trial judge recognized this, commenting in his written opinion that he was "only provided with limited factual details" concerning these purported comparables. [4] We also have concerns about what might constitute a fair procedure when a trial judge relies upon other jury verdicts and experiences that lie outside the record. We do not suggest any formal or lengthy procedures, but certainly—no matter how informal—a party should be given notice and a fair opportunity to be heard when a trial judge intends to rely upon comparable jury verdicts. We do not suggest that occurred here and, in light of our disposition of this appeal, we need not attempt to outline the procedures necessary to satisfy the requirements of due process in such a setting. [5] We discern from the trial judge's reasoning that in invoking his "feel of the case" the judge relied exclusively on his visceral reaction to the amount of the verdict. The judge did not refer to any deficiency in the record that would reach the level of "wrongness" required. See State v. Johnson, 42 N.J. 146, 162, 199 A.2d 809 (1964). So long as there is reasonable support in the record, as here, a verdict may not be disturbed because of the trial judge's own personal analysis of the weight of the evidence.

--- address: | International School for Advanced Studies[^1]\ via Beirut 2-4, 34014 Trieste, ITALY\ E-mail: rosati@he.sissa.it author: - Francesca Rosati title: 'Can the inflaton and the quintessence scalar be the same field?' --- Introduction ============ The very last years have witnessed growing interest in cosmological models with $\Omega_m \sim 1/3$ and $\Omega_\Lambda \sim 2/3$, following the most recent observational data (see for example the discussion in the paper by Bahcall [*et al.*]{} [@data] and references therein). A very promising candidate for a dynamical cosmological constant is a rolling scalar field, named “quintessence”. [@quint] The main motivation for constructing such dynamical schemes resides in the hope of weakening the fine tuning issue implied by the smallness of $\Lambda$. In this respect, a very suitable class of models is provided by inverse power scalar potentials which admit attractor solutions characterized by a negative equation of state. [@scalcosmo; @track] Consider the cosmological evolution of a scalar field $Q$, with potential $V(Q)=M^{4+\alpha }Q^{-\alpha }$, $\alpha >0$, in a regime in which the scalar energy density is subdominant with respect to the background. Then it can be shown [@scalcosmo; @track] that the solution $Q\sim t^{1-n/m}$, with $n=3(w_{Q}+1)$ and $m=3(w_{B}+1)$, is an attractor in phase space. We have defined $w_Q$ to be the equation of state of the scalar field $Q$, and $w_B$ that of the background ($=1/3$ for radiation and $=0$ for matter). The equation of state of the scalar field on the attractor is found to be $w_{Q}= (\alpha \, w_B -2)/(\alpha+2)$, which is always negative during matter domination. As a consequence, the ratio of the scalar to background energy density is not constant but scales as $\rho _{Q}/\rho_{B}\sim a^{m-n}$, thus growing during the cosmological evolution, since $n$ $<m$. The behaviour of these solutions is determined by the cosmological background and for this reason they have been named “trackers” in the literature. [@track] A good feature of these models is that for a very wide range of the initial conditions the scalar field will reach the tracking attractor before the present epoch. Depending on the initial time, you can have several tens of orders of magnitude of allowed initial values for the scalar energy density. This fact, together with the negative equation of state, makes the trackers feasible candidates for explaining the cosmological observation of a presently accelerating universe. The point at which the scalar and matter energy densities are of the same order depends on the mass scale in the potential. This is fixed by requiring that $\Omega_Q = {\cal O} (1)$ today. An interesting question, then, is whether the ‘quintessence’ scalar and the inflaton field, which dominate the expansion of the universe at very different times, could indeed be the same field. If this is the case, it should also be possible to uniquely fix the initial conditions for the ‘quintessential’ rolling from the end of inflation. Models in which one single scalar field drives both inflation and the late time cosmological accelerated expansion are named “quintessential inflation” models. [@pv; @noi2] A particle physics model: Supersymmetric QCD ============================================ As first noted by Binètruy [@bin], supersymmetric QCD theories with $N_{c}$ colors and $N_{f}<N_{c}$ flavors may give an explicit realization of a quintessence model with an inverse power law scalar potential. The matter content of the theory is given by the chiral superfields $Q_{i}$ and $\overline{Q}_{i}$ ($i=1\ldots N_{f}$) transforming according to the $ N_{c}$ and $\overline{N}_{c}$ representations of $SU(N_c)$, respectively. In the following, the same symbols will be used for the superfields $Q_{i}$, $\overline{Q}_{i}$, and their scalar components. Supersymmetry and anomaly-free global symmetries constrain the superpotential to the unique [*exact*]{} form $$W=(N_{c}-N_{f})\left[ \Lambda ^{(3N_{c}-N_{f})} / \, {\rm det}\, T \right] ^{ \frac{1}{N_{c}-N_{f}}} \label{superpot}$$ where the gauge-invariant matrix superfield $T_{ij}=Q_{i}\cdot \overline{Q}_{j}$ appears. $\Lambda $ is the only mass scale of the theory. We consider [@noi] the general case in which different initial conditions are assigned to the different scalar VEV’s $\langle Q_{i}\rangle = \langle \overline{Q}_{i}^{\dagger}\rangle \equiv q_i$, and the system is described by $N_{f}$ coupled differential equations. In analogy with the one-scalar case, we look for power-law solutions of the form $$q_{tr,i}=C_{i}\cdot t^{\, p_{i}}\ , \ \ i=1,\cdots ,\ N_{f}\ . \label{scaling}$$ It is straightforward [@noi] to verify that for fixed $N_f$ (and when $\rho _{Q}\ll \rho _{B}$), a solution exists with $p_i \equiv p = p(N_c)$ and $C_i \equiv C =C(N_c,\Lambda)$ and that it is the same for all the $N_f$ flavors. The equation of state of the tracker is given by $$w_{Q}=\frac{1+r}{2}w_{B}-\frac{1-r}{2}\ , \label{eosfree}$$ where we have defined $r \equiv N_{f}/N_c$. Then, even if the $q_{i}$’s start with different initial conditions, there is a region in field configuration space such that the system evolves towards the equal fields solutions (\[scaling\]), and the late-time behavior is indistinguishable from the case considered by Binetrúy [@bin] where equal initial conditions for the $N_f$ flavors were chosen. In spite of this, the multi-field dynamics introduces some new interesting features. For example, we have found that (in the two–field case) for any given initial energy density such that, for $q^{in}_1/q^{in}_2 =1$, the tracker is joined before today, there exists always a limiting value for the fields’ difference above which the attractor is not reached in time. A more detailed discussion and numerical results about the two-field dynamics can be found in Masiero [*et al*]{}. [@noi] Quintessential inflation ======================== As already discussed, the range of initial conditions which allows $\rho_Q$ to join the tracker before the present epoch is very wide. Nevertheless, it should be noted that in principle we do not have any mechanism to prevent $\rho_Q^{in}$ from being outside the desired interval. In this respect, an early universe mechanism which could naturally set $\rho_Q^{in}$ in the allowed range for a late time tracking, would be highly welcome. Moreover, if we require the quintessence scalar to be identified with the inflaton, we would at the same time obtain a tool for handling the initial conditions and a simple unified picture of the early and late time universe dynamics, which we call “quintessential inflation”. [@pv; @noi2] The basic idea is to consider inflaton potentials which, as it is typical in quintessence, go to zero at infinity like inverse powers. In this way it is possible to obtain a late time quintessential behaviour from the same scalar that in the early universe drives inflation. The key point resides in finding a potential which satisfies the condition that inflation and late time tracking both occur, and that they occur at the right times (see Peloso [*et al.*]{} [@noi2]). Two models have been shown to fulfill these two requirements. One example [@noi2] is a first-order inflation model with potential going to zero at infinity like $\phi^{-\alpha}$. A bump at $\phi \ll M_p$ allows for an early stage of inflation while the scalar field gets “hung up” in the metastable vacuum of the theory. Nucleation of bubbles of true vacuum through the potential barrier sets the end of the accelerated expansion and starts the reheating phase. After the reheating process is completed, the quintessential rolling of the scalar $\phi$ starts and its initial conditions (uniquely fixed by the end of inflation) can be shown to naturally be within the range which leads to a present day tracking. As an alternative, we considered [@noi2] the model of hybrid inflation proposed by Kinney [*et al*]{}. [@riotto] This is shown to naturally include a late–time quintessential behavior. As typical of hybrid schemes, the potential at early times (that is until the inflaton field is smaller than a critical value $\phi_c\,$) is dominated by a constant term and inflation takes place. Eventually the inflaton rolls above $\phi_c\,$, rendering unstable the second scalar of the model, $\chi$. This auxiliary field starts oscillating about its minimum and in this stage the universe is reheated. After $\chi$ has settled down, the inflaton continues its slow roll down the residual potential, which goes to zero at infinity like $\phi^{-2}$, thus allowing for a quintessential tracking solution. Also in this case the initial conditions for the quintessential part of the model are not set by hand, but depend uniquely on the value of the inflaton field at the end of reheating. Acknowledgments {#acknowledgments .unnumbered} =============== I would like to thank Antonio Masiero, Massimo Pietroni and Marco Peloso with whom I obtained the results presented in this talk. [99]{} N.A. Bahcall [*et al*]{}, . J.A. Frieman and I. Waga, ; R.R. Caldwell, R. Dave, and P.J. Steinhardt, ; M.S. Turner and M. White, . P.J.E. Peebles and B. Ratra, ; . A.R. Liddle and R.J. Scherrer, . I. Zlatev, L. Wang, and P.J. Steinhardt, ; P.J. Steinhardt, L. Wang, and I. Zlatev, . L.H. Ford, ; B. Spokoiny, ; M. Joyce and T. Prokopec, ; P.J.E. Peebles and A. Vilenkin, ; G. Felder, L. Kofman and A. Linde, . M. Peloso and F. Rosati, . P. Binétruy, . A. Masiero, M. Pietroni and F. Rosati, . W.H. Kinney and A. Riotto, ; . [^1]: Address from January 1st 2000: Centre for Theoretical Physics, University of Sussex, Falmer, Brighton BN1 9QJ, UK. E-mail: rosati@pcss.maps.susx.ac.uk.

World News Quick Take Agencies AUSTRALIA Lightning kills tourist A German tourist who was struck by lightning last week has died from her injuries, officials said yesterday. Stefanie Wiedenroth, 22, died on Monday after her parents had traveled from Germany to be at her side, the Royal Perth Hospital said. Wiedenroth was on a working holiday at a remote sheep station in Western Australia when lightning hit her on Friday morning as she was walking in a paddock. Four other people standing nearby were reportedly thrown to the ground, but not seriously injured. Her employer Darren Major said he was standing about 25m away from Wiedenroth when she was struck. “Right above us it was basically blue skies, but just off to the west of us there were clouds brewing, but nothing to be concerned about — it was basically just a normal day,” he told the West Australian newspaper. “It was just a freak lightning strike, that’s the only way I can describe it,” he added. AUSTRALIA Hitler remark causes upset The head of Vienna’s Jewish community is urging that a far-right politician running for EU parliament withdraw his candidacy over his suggestion that Adolf Hitler’s rule was more liberal than the EU. Oskar Deutsch demanded that Andreas Moelzer drop out for saying that the EU is a dictatorship that makes the Third Reich look “possibly ... liberal.” Moelzer spoke last month, but his comments were reported only recently. Deutsch said on Monday that “such people cannot represent Austria” in the EU parliament. Moelzer said he only meant to point to EU overregulation. Moelzer is on the far-right fringe of his FPO party, which has made huge gains over recent years with a strongly Euroskeptic, anti-corruption and anti-foreigner message. It now regularly polls as the most popular of all Austrian parties. THAILAND Bus crash kills at least 30 A double-decker bus carrying municipal workers on a field trip plunged off a steep road and into a ravine, killing at least 30 people and injuring 22, officials said yesterday. The accident on Monday night was the latest fatal crash on a mountain road in Tak Province known for its treacherous dips and turns where 300 accidents occurred last year, provincial governor Suriya Prasatbunditya said. The driver was trying to pass cars on a winding downhill road when it skidded off the edge and flipped several times as it tumbled about 30m into a valley before crashing into a tree, Suriya said. ISRAEL Minister accused of assault Energy Minister Silvan Shalom, tipped as a possible presidential candidate, has been accused of sexual assault against a female former employee, media reported on Monday. The alleged victim, who worked for the now 55-year-old member of Prime Minister Benjamin Netanyahu’s Likud party, has filed a complaint, the reports said. Police said they were “investigating accusations against a minister,” without giving any further details. Speaking anonymously to army radio, the former employee said Shalom had on one occasion in 1999 called her to deliver documents to a Jerusalem hotel room where he was staying, and she found him naked. Shalom, who was serving as science minister at the time, then forced her to perform oral sex on him, she said. Shalom was expected to run in a June 14 presidential election as a possible successor to Shimon Peres, and he was about to announce his candidature, according to local media.

[Recording of multiple sclerosis in Swiss cause of death statistics. A 10-year mortality follow-up of the Bern prevalence study]. Based on data from a multiple sclerosis (MS) prevalence study which had been carried out in 1986 in the canton of Berne, Switzerland, a follow-up was performed 10 years later to gather information on mortality in the original study population. The authors used information on residency and death as gathered from municipal offices and, additionally, by record-linkage with the Swiss cause of death statistics. Slightly more than 80% of the cases were identified unequivocally as of January 1996. Among them, 21% of the cases died during the ten-year period; 70% of them have an MS entry in the cause of death statistics, mostly as the main cause of death. A large proportion of the non-identifiable cases appear to be related to mortality; thus, the findings here do not provide a promising basis for certain further analyses. In conclusion, continuous updating of personal data is the only way to avoid loss to follow-up in the carefully assembled prevalence database.

The families of five men killed in the fake encounter of 2000 are not convinced that a court martial will deliver justice, reports Baba Umar Awaiting justice Abdul Rashid Khan lost his father in the Pathribal encounter Photos: Abid Bhat JUSTICE IN the Pathribal fake encounter case, in which five villagers were gunned down by the army on 25 March 2000, is being seen as a key to unlock the mystery surrounding the Chattisinghpora massacre of 35 Sikhs by “unidentified gunmen” and the legality of the Armed Forces Special Powers Act (AFSPA) in Jammu & Kashmir. However, the 12-year-old case has run into a roadblock. The case has passed through the chambers of the Anantnag District Court, the Jammu & Kashmir High Court, and the Supreme Court. Now, the army’s 16 Corps, based in Nagrota cantonment in Jammu, is conducting court martial proceedings against the five accused armymen. The victims’ families want proceedings shifted back to Kashmir and conducted in full media glare. Otherwise, they want security cover and counsels of their own choice. However, the army has refused to accept the conditions. “If the army is honest in trying its soldiers for the murders, why is it reluctant to shift the case to Kashmir, instead of making us travel 300 km to Jammu?” asks Ghulam Nabi Malik, whose brother Muhammad Yousuf Malik of Kapran village was one of the five innocent civilians gunned down by the army five days after the Chattisinghpora massacre took place on 20 March 2000. The victims were dubbed Pakistan-based Lashkar-e-Toiba militants responsible for the massacre and were buried in five unmarked graves at two different villages. Malik, whose DNA matched with the sample taken from the charred body of his brother, says, “What we can or have said in civil courts can’t be said in an army court. Those who staged the encounter and fudged DNA tests can also use our testimonials against us. Let them allow our counsels to talk on our behalf. They can make better arguments than most of our illiterate family members.” So far, the case has encountered several twists. A CBI inquiry concluded that the victims were indeed civilians. Later, the DNA samples taken from the victims’ male relatives were fudged. The samples turned out to be those of unknown females. Another lot of samples of the male relatives later proved the CBI’S findings. The CBI also nailed the roles of Brigadier Ajay Saxena, Major Bijendra Pratap Singh, Major Sourabh Sharma, Major Amit Saxena and Subedar Idrees Khan in the fake encounter. The five men killed in the Pathribal encounter were two farmers from Brari Angan, both named Jumma Khan, goatherds Bashir Ahmed Butt and Mohammad Yusuf Malik from Halan, and Zahoor Dalal, a cloth merchant from Islamabad town in Kashmir. In subsequent trials, the army opposed the chargesheet claiming immunity under AFSPA. Earlier this year, the Supreme Court directed the army to either try the accused in a court martial or allow a civil trial. In June, the army opted for the former. On 20 September and 3 October, the army sent summons to the victims’ relatives. “They wanted my grandfather Fakirullah Khan to depose before the army. But he has been dead for 30 years,” says Abdul Rashid Khan, 35, whose father Jumma Khan was killed in the Pathribal fake encounter. “We have already given DNA samples. The whole world knows why my father was killed. I’m sure the army will try to put pressure on us. That’s why we are asking them to allow the trial before the media,” he says. Rashid also lost his 20-year-old brother Mohammad Rafiq, who was leading a protest against the Pathribal killings on 3 April 2000. Eight other civilians were killed in the incident. “I lost my father and a brother. They have our DNA tests. The CBI has handed over all the evidence. What more evidence am I going to give?” he asks. Shakoor Khan, 32, whose father Jumma Khan was another victim, has also refused to attend the court martial. “First, they blocked all efforts for a civil trial by invoking AFSPA. Now they are promising us a fair trial. The CBI has already said my father’s death was cold-blooded murder. Why is the army probing it again? They are going to put pressure on us,” he says. But Shakoor feels that not going to the army’s court could also mean delay or denial of justice. “Tomorrow, the army can say, ‘We called them for evidence, but they didn’t appear in the court.’ So we are in a dilemma. My mind says the army will pressurise us into a compromise, but the heart says rejecting the summons will deny us justice,” he says. The army’s key reason against shifting the venue stems from the argument that holding the court martial in Srinagar-based 15 Chinar Corps would be unethical as “it had involved itself with the defence of the accused during the past few years”. Brigadier Sanjay Chawla of the Northern Command says the hearings are going on and the families can come with their counsels “if they wish so”. “The trial won’t be shifted to Kashmir. If the families want security, the army is ready to provide it when they reach Nagrota,” he adds. Meanwhile, human rights activist Khurram Parvez says the SC directive was “unfortunate” because “ethically and according to international laws, the army isn’t supposed to probe and pronounce judgment against itself”. “Its one branch (15 Corps) defended the culprits, while the other in Jammu (16 Corps) is claiming to offer a fair trial. Look at the ranks of the accused. They won’t hurt their own men. By asking the families to travel such a long distance, the army is making sure that justice is inaccessible. It wants to exhaust the families and wear them out,” he says.

The year 2017 will go down as the year sexual harassment claims erupted — from Hollywood to D.C., from Harvey Weinstein to Kevin Spacey, from senate candidate Roy Moore to Sen. Al Franken. Lest we forget, this year Nevada had its own sex scandal, but, unlike the others, this one was buried in secrecy and the accused allowed to resign and slink away. State Sen. Mark Manendo, a Las Vegas Democrat, resigned in July after the taxpayers shelled out $67,125.12[…] Thank goodness for the veto pen. Gov. Brian Sandoval used that veto pen this past week to block an attempt by Democratic lawmakers to rollback a modest cost-saving measure passed by the Republican-controlled 2015 Legislature. Assembly Bill 154 would have raised the cost of construction of university and public school buildings by reimposing the so-called prevailing wage on more projects. Prevailing wage laws require that workers on public construction jobs be paid no less than the “prevailing” wage in the[…] More News When Gov. Brian Sandoval declared there would be no special session to wrap up unfinished legislative business, I knew he had thrown in the towel and education savings accounts were toast. There were ways the ESAs could’ve been saved, as one newspaper columnist pointed out Sunday. Sandoval could’ve used his veto and Republican state senators could’ve held their ground. But no. They folded, surrendered, slunk away with their tails between their legs. The 8,000 to 10,000 students hoping their parents[…] Gov. Brian Sandoval signed into law this past week a legislatively passed bill that makes it illegal for any psychotherapist in Nevada to provide conversion therapy to anyone under the age of 18. Senate Bill 201 defines conversion therapy as “any practice or treatment that seeks to change the sexual orientation or gender identity of a person.” It states this therapy is barred “regardless of the willingness of the person or his or her parent[…] We now know the pecking order in Nevada. In his State of the State speech this past week Gov. Brian Sandoval boasted that the Tesla gigafactory near Sparks, in addition to making batteries for electric cars, would also be making electric motors and gearboxes, adding 550 workers. Left unsaid was who would pay for the police and fire, schools and other government services those workers would need, since Tesla was given $1.3 billion in tax breaks and credits, as well as[…] Nevada has every reason to feel like a slighted wallflower. We keep getting invited to the big sage grouse dance, but never get asked to dance. Gov. Brian Sandoval and Attorney Adam Laxalt and others have complained bitterly that state and local input on how to protect the sage grouse population and still conduct economically productive endeavors on the land the birds occupy have been roundly and almost universally ignored by the federal land agencies. A lawsuit filed by Laxalt on behalf[…] After eight years of Obama appointees trying to grab dominion over every square foot of rural land in Nevada and the West, laying claim to every mud puddle, dictating how clean the air must be and generally trampling states’ rights under a stampede of bureaucrats, President-elect Donald Trump’s pick to head the Environmental Protection Agency promises to be an abrupt about-face and double-time march toward sanity. Trump’s pick to head the EPA, Oklahoma Attorney General Scott Pruitt, has locked horns with the[…]

Posts tagged “Commander Shepard” Wasn’t quite happy with the layout of my last Civil War Video Game Avengers crossover so decided to redo the whole thing. I also updated it with a few characters that would be a better fit. Also made a youtube video with more images and showing the combinations process. Have fun and if you get a chance and like the video please give the video a like and subscribe. Thanks again everyone! I think I got a lil ambitious for my first foray into cosplay, decided to do my own custom Mass Effect Shepard N7/DeadSpace 3 Issac Clarke N7 Armor, improvised a lot but I think I got the helmet done, just one final plasti-dip coating and detail paint and it’s good to go now to construct the rest of the armor eva foam, also incorporated plans for a matching lil obi-rus compartment, but spare time is in short supply so I probably won’t be done until WonderCon 2015, but what a fun and creative way to blow off steam from the day job. Wizard World Sacramento Comic-Con was so much fun, hope it continues to grow! Taking the place of WonderCon that is usually in SF for us Northern Californians. I am glad to have a high caliber local con back in the area. Lil Obi-Rus and Big Obi-Rus got to connect with some old friends and have a geektastic time! As usual lil Obi-Rus had a great adventure with some awesome cosplayers. Major props and thanks to the cosplayers and their great costumes who took the time to take a pic with lil obi-rus they were a very busy group today thanks again! lil obi-rus also got his first rejection for a photo op (waited patiently and asked politely), won’t name names but it kind of weirded me out as most people usually get the lil obi-rus “stand in” and are cool with the concept. Well anywhoo had a great time and look forward to tomorrow! Thanks again!

Operation Plastic surgeon Dr. Josef Kulhánek, M.D. Charlotte, UK (Breast Augmentation) “I am just over 2 weeks post op and I’m in love with my new boobs! My surgeon was Dr Josef Kulhánek who was brilliant! I went from an A cup to a big C cup with 415 cc implants. The whole experience was amazing and I would reccomend Beauty In Prague to anyone. x.”

Information about Entyvio or Vedolizumab (New Medication) Happy 4th of July to all the American based or celebrating UC’ers of the world. There have been some questions over the past few weeks with regards to a relatively new medication call “Entyvio” or sometimes Vedolizumab (and I’m sure there are several other regional/country specific names that this medication has been branded as. So, in a list of links to some reliable source, I hope this info will help to answer any questions you may have/someday have regarding this new med. As a general history, the FDA (Food and Drug Administration) who is the local authority on regulations within the US approved Entyvio for treating Ulcerative Colitis on May 20th, 2014. So it has been just over one year since that date. Search Side Effects Below: Pneumonia 3 times within the 8 months I took Entyvio. Even though I had 2 pneumonia vaccines, and never previously ever had pneumonia or been sick from the flu or even colds much, I got pneumonia within a week after my first dose and two more times within the 8 months of taking Entyvio. When having a colonoscopy 9 months after starting Entyvio, my colon showed no positive effects from the drug so it was discontinued. My doctor insisted Entyvio did not cause the pneumonia, however the Dept of Health indicates that women over 60 were much more prone to pneumonia from taking Entyvio. It makes sense, since the drug cuts down one’s immune system and we are more suseptble to any infection. The effects of having pneumonia 3 times in such a short time has given me asthma and constant cough as a result. Only sulphasalazine 8 tablets a day for UC which I’ve been taking for over 30 years and had no adverse effects. April 1, 2019 Entyvio (Vedolizumab) 22 Joint and bone pain couldn’t walk. This was after 2 doses of Entyvio. Was hospitalized and put on prednisone, had an MRI. They discovered the Entyvio has this side effect in some people. No meds Ostomy since 2017Best thing got my life back March 27, 2019 Entyvio (Vedolizumab) 68 Brain fog, constipation, fatigue. December 18, 2018 Entyvio (Vedolizumab) 59 Arthritis pain muscle pain yes November 26, 2018 Entyvio (Vedolizumab) 55 joint pain runny nose Azathorprine, Apriso September 7, 2018 Entyvio (Vedolizumab) 67 rash on left side of my waist June 7, 2018 Entyvio (Vedolizumab) 18 Very tired. Headache March 7, 2018 Entyvio (Vedolizumab) 65 dry mouth March 1, 2018 Entyvio (Vedolizumab) 43 sex drive none January 18, 2018 Entyvio (Vedolizumab) 34 Tight chest shortness of breath October 5, 2017 Entyvio (Vedolizumab) 57 No sex drive September 4, 2017 Entyvio (Vedolizumab) 49 sun burn July 6, 2017 Entyvio (Vedolizumab) 18 Dry skin No June 26, 2017 Entyvio (Vedolizumab) 49 Heart flutters, pressure ImuranLialda March 28, 2017 Entyvio (Vedolizumab) 64 Fatigue February 19, 2017 Entyvio (Vedolizumab) 64 Fatigue February 19, 2017 Entyvio (Vedolizumab) 43 Joint pain in hands, wrist, ankle and elbow. Delzicol January 22, 2017 Entyvio (Vedolizumab) 50 joint pain, swelling, stiffness, weakness (hands, wrists, shoulders, knees, ankles). Pain is worse at night / through the night / first thing in the morning. The pain moves around, day to day. Started Entyvio November 2014. Had more than usual upper respiratory infections and other infections during first 1.5 years. I was in full remission after one year, and have been doing great ever since. I do best when preparing my own whole food small meals -- fruits, mostly cooked/few raw vegetables, and fish and chicken (red meat is rough on me). It is a miracle drug. Have had 11 doses over the last 1 1/2 years. Began working well between the 4th and 5th doses. Fatigue, joint and muscle pain, hot flashes and night sweats. Can live with all these side effects because it works very well. Been off Prednisone for a year, that's such a blessing. Lialda 4 pills a day July 28, 2016 Entyvio (Vedolizumab) 69 It's effective but creates fatigue. I also become nauseous after eating. I'm not sure if entyvio causes it or if it's because I'm now off the prednisone. July 28, 2016 Entyvio (Vedolizumab) 54 Tiredness at first, but gotten used to it. No effects now. This stuff is magic. Bystolic July 28, 2016 Entyvio (Vedolizumab) 42 Fatigue!!!!!! Joint pain, headaches. Had 3 doses(loading dose) and have not really seen any change. Still having alot of abdominal cramping/pain, still loose, watery stool. I have just had my 2nd infusion and can already see a very slight improvement. There is a great Facebook group called Entyvio warriors with well over 1000 people sharing experiences on this drug. It really helped me be prepared for the few minor side effects I have had. I highly suggest it if you are considering this med. We have a 5 year old with UC. We live in the US and our insurance company has denied Entyvio (our last option at this point). Does anyone know if it is available for less money in Europe or Canada or has anyone had success with the compassionate appeal process with the drug companies (we’ve already been denied through the peer to peer process). Any help, advice, etc is greatly appreciated.

hhhhsnsnnhnnhhhsnhn. 63/5168 What is prob of sequence mrrr when four letters picked without replacement from mmrrrmmmmrrmmm? 45/2002 Calculate prob of sequence eeee when four letters picked without replacement from eeeeeee. 1 Four letters picked without replacement from ppvpdpsdppppdppppvp. Give prob of sequence pvsv. 13/46512 Calculate prob of sequence anan when four letters picked without replacement from {a: 10, n: 2, y: 3}. 1/182 Two letters picked without replacement from iokokkkkkk. Give prob of sequence ok. 7/45 Two letters picked without replacement from qaaqaaapaiaasakpaa. Give prob of sequence pk. 1/153 Calculate prob of sequence ztt when three letters picked without replacement from {z: 4, w: 4, c: 4, t: 8}. 28/855 What is prob of sequence ss when two letters picked without replacement from {s: 3, r: 1, i: 1}? 3/10 Three letters picked without replacement from {y: 4, c: 3, z: 6, k: 1}. Give prob of sequence kcc. 1/364 Three letters picked without replacement from {b: 3, r: 2, w: 3}. Give prob of sequence bwb. 3/56 Two letters picked without replacement from uuuafffuuuuuuuuua. What is prob of sequence aa? 1/136 Calculate prob of sequence ay when two letters picked without replacement from yauybabbrca. 3/55 Calculate prob of sequence fccf when four letters picked without replacement from {f: 3, c: 4}. 3/35 What is prob of sequence nn when two letters picked without replacement from nnnunuuuuuun? 5/33 Four letters picked without replacement from wuuiggwuwwuwfdwwu. Give prob of sequence dwif. 1/8160 Calculate prob of sequence xzj when three letters picked without replacement from czcgxcgxjxjzcxgcce. 1/306 What is prob of sequence mx when two letters picked without replacement from {x: 3, b: 2, m: 1, o: 5, i: 6}? 3/272 Two letters picked without replacement from bbbcbpoecepebb. Give prob of sequence pp. 1/91 Calculate prob of sequence bbf when three letters picked without replacement from lllblllbblbfllbblb. 7/816 What is prob of sequence yi when two letters picked without replacement from {i: 9, y: 3}? 9/44 Three letters picked without replacement from {f: 14, y: 5}. Give prob of sequence yff. 455/2907 What is prob of sequence ff when two letters picked without replacement from cccwcmfmmfcr? 1/66 What is prob of sequence zz when two letters picked without replacement from jrzrzjwzjwzj? 1/11 Calculate prob of sequence add when three letters picked without replacement from adad. 1/6 Four letters picked without replacement from {b: 1, o: 2, v: 1, y: 2, w: 6}. Give prob of sequence wvwy. 1/198 What is prob of sequence jow when three letters picked without replacement from {w: 1, e: 1, o: 2, p: 2, k: 2, j: 1}? 1/252 Three letters picked without replacement from eeccecxccbxc. What is prob of sequence ebx? 1/220 Four letters picked without replacement from {x: 1, c: 2, b: 1, k: 1, z: 1, l: 2}. Give prob of sequence klcz. 1/420 Four letters picked without replacement from {t: 12, y: 1}. Give prob of sequence tytt. 1/13 What is prob of sequence yaya when four letters picked without replacement from {y: 8, o: 1, a: 4}? 28/715 What is prob of sequence mxmm when four letters picked without replacement from qxmqmmmmmqmmxqxx? 2/65 Calculate prob of sequence arri when four letters picked without replacement from {a: 1, c: 7, i: 1, t: 1, r: 7}. 1/1360 What is prob of sequence xd when two letters picked without replacement from {d: 1, x: 1, f: 1}? 1/6 Two letters picked without replacement from {f: 15, u: 4}. Give prob of sequence uf. 10/57 Calculate prob of sequence ki when two letters picked without replacement from {e: 3, v: 1, k: 1, z: 2, i: 1, g: 4}. 1/132 Calculate prob of sequence tzi when three letters picked without replacement from xnxqiqqxzxtqnzx. 1/1365 What is prob of sequence luul when four letters picked without replacement from lulluuuulluullluuulu? 22/323 Four letters picked without replacement from {b: 1, m: 2, a: 4, k: 2, d: 1}. Give prob of sequence abmd. 1/630 Calculate prob of sequence fv when two letters picked without replacement from vnvnnnnnnf. 1/45 Calculate prob of sequence eoye when four letters picked without replacement from {o: 1, y: 2, e: 7}. 1/60 Calculate prob of sequence kike when four letters picked without replacement from kikkkekekikkk. 12/715 Calculate prob of sequence td when two letters picked without replacement from hhnldnnltdnlll. 1/91 Two letters picked without replacement from ebbbbbbbbeebbb. Give prob of sequence bb. 55/91 What is prob of sequence zrz when three letters picked without replacement from {r: 9, z: 9}? 9/68 Two letters picked without replacement from {v: 1, d: 12}. What is prob of sequence dv? 1/13 Three letters picked without replacement from xnwuu. What is prob of sequence unx? 1/30 Four letters picked without replacement from {a: 5, r: 1, x: 1, u: 3}. What is prob of sequence axrx? 0 Calculate prob of sequence dksd when four letters picked without replacement from sskddgtksk. 1/280 Two letters picked without replacement from {a: 2, n: 8, d: 2, e: 2}. Give prob of sequence dd. 1/91 Four letters picked without replacement from qqgqqyjyjyjyjjdyjqq. Give prob of sequence jyyj. 25/3876 Two letters picked without replacement from chhgcggceeheeccec. What is prob of sequence he? 15/272 Four letters picked without replacement from {j: 5, c: 4, n: 3, t: 7}. Give prob of sequence jccj. 5/1938 Calculate prob of sequence odu when three letters picked without replacement from {o: 3, u: 12, d: 2}. 3/170 Two letters picked without replacement from mjjutbpu. What is prob of sequence pb? 1/56 Calculate prob of sequence thh when three letters picked without replacement from {b: 5, h: 3, l: 2, t: 7}. 7/680 Four letters picked without replacement from vmmvmuumvuvv. Give prob of sequence vuum. 1/99 What is prob of sequence le when two letters picked without replacement from eheezlhehhhzzhhhzhlh? 2/95 Two letters picked without replacement from udlllzzud. Give prob of sequence du. 1/18 Two letters picked without replacement from {n: 1, g: 1, t: 7}. Give prob of sequence gt. 7/72 Three letters picked without replacement from {s: 4, g: 3, l: 1, h: 2}. What is prob of sequence gsg? 1/30 What is prob of sequence eire when four letters picked without replacement from eeeeeereeieri? 12/715 Three letters picked without replacement from kguneunungp. What is prob of sequence unp? 1/110 Calculate prob of sequence uj when two letters picked without replacement from humujuemeumueye. 1/42 Two letters picked without replacement from ddddjdducducddjjc. What is prob of sequence dd? 9/34 What is prob of sequence ggg when three letters picked without replacement from {g: 6, j: 2, s: 1, c: 3, u: 2}? 5/91 Four letters picked without replacement from {d: 2, y: 4}. Give prob of sequence yydd. 1/15 Calculate prob of sequence zx when two letters picked without replacement from oizxxvez. 1/14 Two letters picked without replacement from {z: 5, k: 7, c: 2}. What is prob of sequence cc? 1/91 Three letters picked without replacement from rrrdrdrddrrrrrrd. Give prob of sequence rrd. 55/336 Three letters picked without replacement from {v: 3, m: 2, w: 3}. What is prob of sequence mvw? 3/56 Two letters picked without replacement from dxdoxdddodxxoxo. What is prob of sequence do? 4/35 Three letters picked without replacement from {r: 2, a: 2, e: 1, h: 1, g: 1}. Give prob of sequence rer. 1/105 Three letters picked without replacement from jjjejej. What is prob of sequence eej? 1/21 What is prob of sequence wiiy when four letters picked without replacement from wwiwyiwwpipw? 1/330 Calculate prob of sequence fm when two letters picked without replacement from nofwohhmhom. 1/55 Three letters picked without replacement from mlcklkcfgfkgmkl. Give prob of sequence clm. 2/455 What is prob of sequence sxo when three letters picked without replacement from {z: 1, s: 1, y: 1, x: 1, o: 4}? 1/84 Two letters picked without replacement from tniessiisndss. Give prob of sequence ie. 1/52 Calculate prob of sequence zg when two letters picked without replacement from mqmzmzquqggmgmmz. 3/80 What is prob of sequence oe when two letters picked without replacement from eebeeovxaoeeeoeooe? 5/34 Calculate prob of sequence ei when two letters picked without replace

<?php /* * Copyright 2014 Google Inc. * * Licensed under the Apache License, Version 2.0 (the "License"); you may not * use this file except in compliance with the License. You may obtain a copy of * the License at * * http://www.apache.org/licenses/LICENSE-2.0 * * Unless required by applicable law or agreed to in writing, software * distributed under the License is distributed on an "AS IS" BASIS, WITHOUT * WARRANTIES OR CONDITIONS OF ANY KIND, either express or implied. See the * License for the specific language governing permissions and limitations under * the License. */ class Google_Service_ServiceUser_Enum extends Google_Collection { protected $collection_key = 'options'; protected $enumvalueType = 'Google_Service_ServiceUser_EnumValue'; protected $enumvalueDataType = 'array'; public $name; protected $optionsType = 'Google_Service_ServiceUser_Option'; protected $optionsDataType = 'array'; protected $sourceContextType = 'Google_Service_ServiceUser_SourceContext'; protected $sourceContextDataType = ''; public $syntax; /** * @param Google_Service_ServiceUser_EnumValue */ public function setEnumvalue($enumvalue) { $this->enumvalue = $enumvalue; } /** * @return Google_Service_ServiceUser_EnumValue */ public function getEnumvalue() { return $this->enumvalue; } public function setName($name) { $this->name = $name; } public function getName() { return $this->name; } /** * @param Google_Service_ServiceUser_Option */ public function setOptions($options) { $this->options = $options; } /** * @return Google_Service_ServiceUser_Option */ public function getOptions() { return $this->options; } /** * @param Google_Service_ServiceUser_SourceContext */ public function setSourceContext(Google_Service_ServiceUser_SourceContext $sourceContext) { $this->sourceContext = $sourceContext; } /** * @return Google_Service_ServiceUser_SourceContext */ public function getSourceContext() { return $this->sourceContext; } public function setSyntax($syntax) { $this->syntax = $syntax; } public function getSyntax() { return $this->syntax; } }

sp carbon chains surrounded by sp(3) carbon double helices: directed syntheses of wirelike Pt(CC)(n)Pt moieties that are spanned by two P(CH(2))(m)P linkages via alkene metathesis. Reactions of trans-(C6F5)(Ph2P(CH2)m'CH=CH2)2PtCl (1; m' = a, 6; b, 7; c, 8; d, 9; e, 10) and H(CC)2H (HNEt2, cat. CuI) give trans-(C6F5)(Ph2P(CH2)m'CH=CH2)2Pt(CC)2H (3a-e, 80-95%). Oxidative homocouplings of 3a-d under Hay conditions (O2, cat. CuCl/TMEDA, acetone) yield trans,trans-(C6F5)(Ph2P(CH2)m'CH=CH2)2Pt(CC)4Pt(Ph2P(CH2)m'CH=CH2)2(C6F5) (4a-d, 64-84%). Treatment of 3c-e with excess HCCSiEt3 under Hay conditions gives trans-(C6F5)(Ph2P(CH2)m'CH=CH2)2Pt(CC)3SiEt3 (56-73%). Homocouplings (n-Bu4N+ F-, Me3SiCl, Hay conditions) afford trans,trans-(C6F5)(Ph2P(CH2)m'CH=CH2)2Pt(CC)6Pt(Ph2P(CH2)m'CH=CH2)2(C6F5) (13c-e, 59-64%). Reactions of 4a-d and 13c-e with Grubbs' catalyst, followed by hydrogenation, give mixtures of trans,trans-(C6F5)(Ph2P(CH2)mPPh2)Pt(CC)nPt(Ph2P(CH2)mPPh2)(C6F5) with termini-spanning diphosphines and trans,trans-(C6F5)(Ph2P(CH2)mPPh2)Pt(CC)nPt(Ph2P(CH2)mPPh2)(C6F5) with trans-spanning diphosphines (m = 2m' + 2; n = 4, 6). The latter (n = 4) are independently synthesized by similar metatheses/hydrogenations of 1a-d to give trans-(C6F5)(Ph2P(CH2)mPPh2)PtCl (49-59%), followed by analogous introductions of (CC)4 chains (66-77%). Crystal structures of complexes with termini-spanning diphosphines show sp3 chains with both double-helical (m/n = 20/4) and nonhelical (m/n = 20/6) conformations, and highly shielded sp chains. The sp3 chains of complexes with trans-spanning diphosphines exhibit double half-clamshell conformations. The dynamic properties of both classes of molecules are analyzed in detail.

God’s Goodness and Israel’s Waywardness. 1aSing° for joy° to God° our bstrength°; Shout°cjoyfully° to the dGod° of Jacob°. 2 Raise° a song°, strike°athe timbrel°, The sweet° sounding°blyre° with the charp°. 3 Blow° the trumpet° at the anew° moon°, At the full° moon°, on our bfeast° day°. 4 For it is a statute° for Israel°, An ordinance° of the God° of Jacob°. 5 He established° it for a testimony° in Joseph° When he Iawent° throughout° the land° of Egypt°. I heard° a blanguage° that I did not know°: 6 ¶ “I Iarelieved° his shoulder° of the burden°, His hands° were freed° from the IIbasket°. 7 “You acalled° in trouble° and I rescued° you; I banswered° you in the hiding° place° of thunder°; I proved° you at the cwaters° of Meribah°.ISelah°. 8 “aHear°, O My people°, and I will Iadmonish° you; O Israel°, if° you bwould listen° to Me! 9 “Let there be no°astrange° god° among you; Nor° shall you worship° any foreign° god°. 10 “aI, the LORD°, am your God°, Who brought° you up from the land° of Egypt°;bOpen° your mouth° wide° and I will cfill° it. 11 ¶ “But My people°adid not listen° to My voice°, And Israel° did not Iobey° Me. 12 “So I agave°Ithem over° to the stubbornness° of their heart°, To walk° in their own devices°. 13 “Oh° that My people°awould listen° to Me, That Israel° would bwalk° in My ways°! 14 “I would quickly°asubdue° their enemies° And bturn° My hand° against° their adversaries°. 15 “aThose who hate° the LORD° would bpretend° obedience° to Him, And their time° [of punishment] would be forever°. 16 “IBut I would feed° you with the IIafinest° of the wheat°, And with bhoney° from the rock° I would satisfy° you.” An exhortation to a solemn praising of God. 1 ¶ [[To the chief Musicianºª upon² Gittith,º [A Psalm] of Asaph.]]º Sing aloudºª unto Godº our strength:º make a joyful noiseºª unto the Godº of Jacob.º2 Takeºª a psalm,º and bringºª hither the timbrel,º the pleasantº harpº with² the psaltery.º3 Blow upºª the trumpetº in the new moon,º in the time appointed,º on our solemn feastº day.º God challengeth that duty by reason of his benefits. 4 For² this² [was] a statuteº for Israel,º [and] a lawº of the Godº of Jacob.º5 This he ordainedºª in Josephº [for] a testimony,º when he went outºª through² the landº of Egypt:º [where] I heardºª a languageº [that] I understoodºª not.²6 I removedºª his shoulderº from the burden:º² his handsº were deliveredºª from the pots.º²7 Thou calledstºª in trouble,º and I deliveredºª thee; I answeredºª thee in the secret placeº of thunder:º I provedºª thee at² the watersº of Meribah.º Selah.º God, exhorting to obedience, complaineth of their disobedience, which proveth their own hurt. 8 Hear,ºª O my people,º and I will testifyºª unto thee: O Israel,º if² thou wilt hearkenºª unto me; 9 There shall no² strangeºª godº be² in thee; neither² shalt thou worshipºª any strangeº god.º10 I² [am] the LORDº thy God,º which broughtºª thee out of the landº² of Egypt:º open thy mouthº wide,ºª and I will fillºª it. 11 But my peopleº would not² hearkenºª to my voice;º and Israelº wouldºª none² of me. 12 So I gave them upºª unto their own hearts'º lust:º [and] they walked¹ª² in their own counsels.º13 Oh¹ that² my peopleº had hearkenedºª unto me, [and] Israelº had walkedºª in my ways!º14 I should soonº have subduedºª their enemies,ºª and turnedºª my handº against² their adversaries.º15 The hatersºª of the LORDº should have submittedºª themselves unto him: but their timeº should have endured² for ever.º16 He should have fedºª them also with the finestº² of the wheat:º and with honeyº out of the rockº² should I have satisfiedºª thee.

Details:Dont miss out on these Ethereal Ghost Props! Perfect for all around your Halloween party. The props measure from 35-37 inches and can be attached by pin or tape. Comes six cutouts per package. Size: 35 inches -37 inches . You get 1 Dozen For this price!. Go above and beyond traditional Halloween Decorations with these eye catching Halloween Props!

A blind man suffering déjà vu. It sounds like a contradiction in terms - but the first case study of its kind has turned the whole theory of déjà vu on its head. Traditionally it was thought images from one eye were delayed, arriving in the brain microseconds after images from the other eye - causing a sensation that something was being seen for the second time. But University of Leeds researchers report for the first time the case of a blind person experiencing déjà vu through smell, hearing and touch. The University is a world-leader in déjà vu research. The ground-breaking work of the University's Institute of Psychological Sciences has been widely published in both the scientific and the news media. Their work is particularly aimed at understanding chronic déjà vu, where patients are constantly plagued by the feeling of having "been here before". In a new paper published in the journal Brain and Cognition*, researchers Akira O'Connor and Chris Moulin relate how mundane experiences - undoing a jacket zip while hearing a particular piece of music; hearing a snatch of conversation while holding a plate in the school dining hall - were examples of how deja experiences were triggered in the blind subject. "It is the first time this has been reported in scientific literature," said O'Connor. "It's useful because it provides a concrete case study which contradicts the theory of optical pathway delay. Eventually we would like to talk to more blind people, though there's no reason to believe this man's experiences are abnormal or different to those of others. "Optical pathway delay is a quite antiquated theory, but still widely believed - and was the basis for the déjà vu sequences in Joseph Heller's novel Catch-22. But this provides strong evidence that optical pathway delay is not the explanation for déjà vu. The findings are so obvious, so intuitive, that it's remarkable this research has never been done before." O'Connor admits that to the person experiencing déjà vu, it feels almost inexplicable. "And because it feels so subjective, psychology, in striving for objectivity, has tended to shy away from it. But psychologists have gone some way to illuminating things like the 'tip of my tongue' sensation when you can't think of a particular word. We just wanted to get to the same sort of understanding for déjà vu." O'Connor's thesis, due to be completed next year, examines the experimental induction of déjà vu through hypnosis. "We now believe that deja experiences are caused when an area of the brain that deals with familiarity gets disrupted," he said. In one experiment, students are asked to remember words, then hypnotised to make them forget - and then shown the same word again to induce a feeling that they have seen it before. Around half said this brought on a sensation similar to déjà vu - half of whom said it was definitely déjà vu. O'Connor would like to take the research further: "It would be really neat to do some neuro-imaging on people during genuine spontaneous déjà vu experiences - but it's very difficult to get them to have them on demand..." ### Akira R O'Connor, Christopher J A Moulin, 'Normal patterns of deja experience in a healthy, blind male: Challenging optical pathway delay theory'; Brain and Cognition, December 2006.

Say Goodbye to the Same Old Steakhouse That most hidebound of dining institutions is long overdue for an update ENLARGE PROGRESSIVE PROTEINS | The menu at M. Wells Steakhouse in New York extends to everything from blood sausage and foie gras gnocchi to a 'Bone-In Burger.' William Mebane for The Wall Street Journal By Joshua Ozersky Dec. 27, 2013 2:35 p.m. ET I ASSUME YOU remember the Steakhouse 1.0. You don't need to think back far, because it's always been the same and it never changes. Everything else in American culture retools every few years without fail, but somehow, against all odds, the steakhouse rolls along, its ancient engine purring, lubricated by money, gluttony and force of habit. It doesn't look much different than it did during the first Grover Cleveland administration, and how many things can you say that about? But the world around the steakhouse is changing, and the old-school version, with its windowless rooms, blackened slabs of aged beef and phoned-in side dishes, no longer has the luxury-carnivore market to itself. The Steakhouse 2.0 has arrived. These "modern meateries," as I think of them, sate the same primal appetites as their gruff and clubby predecessors, but in a more contemporary way. The classic steakhouse is a temple of beef, with a lobster or lamb chop thrown in for the lady. The modern meatery serves a whole bestiary, devoting its energies in equal parts to beef, pork, lamb, veal, various birds and even some game animals. The beef at the old steakhouse was commodity meat, bought at the lowest bid, and the product of distant and anonymous feedlots. The meat you eat at Laurelhurst Market in Portland, Ore., or Underbelly in Houston comes from a handpicked rancher and is hormone-, cruelty- and antibiotic-free as a matter of course. More significant, the typical steakhouse focuses on three choices: strip steak, ribeye and tenderloin. The modern meatery uses every part of the animal, from snout to tail, frequently including parts from the inside, too. And then there's this: The steakhouse has a guy who throws steaks under a broiler; the meatery has a chef. This isn't to say that the best of the old-school steakhouses aren't still great. New York's Peter Luger will always be the archetype; Bern's, in Tampa, is still probably the best classical steakhouse in the world; and I wouldn't want to live in a world without Gorat's in Omaha, or Musso & Frank in L.A., or Gene & Georgetti in Chicago. But a new kind of diner has emerged over the last decade or two, one who follows chefs the way some people follow bands and expects to be not merely satisfied but edified, provoked or at least entertained. This type flocks to places like M. Wells Steakhouse in New York City, a labor of love by a hyper-carnivorous young Montreal exile, chef Hugue Dufour, and his wife and co-owner, Sarah Obraitis, a former heritage-meat purveyor. At M. Wells, you can order a teetering stack of pork chops or a burger with a long bone protruding theatrically and not a little surreally from its center. At King + Duke in Atlanta, the adventurous eater is as likely to find a Mississippi rabbit as a grass-fed Wagyu steak sizzling over the live hardwood embers on the 24-foot hearth that is the restaurant's centerpiece. To veteran Dallas chef John Tesar, that's the future. "We have a saturation of steakhouses that are owned by chains and totally focused on the bottom line," he said. "Now young chefs are driving the food scene, creating independent restaurants with creativity and entrepreneurship." Mr. Tesar is currently at work on a steakhouse concept for a major restaurant group and plans to stress game, untethered veal (meaning the calves roamed free with their mothers) and other underappreciated meats. The range of prices will be just as important, Mr. Tesar added: "I want it to be approachable, affordable and casual—not some cavernous man-cave where you have to spend $1,000 for four people." ENLARGE Diners at Ox in Portland, Ore.. Leah Nash Beef prices have rocketed over the last few years, the result of catastrophic droughts in cattle country and the rising cost of feed, especially corn. A steakhouse can afford to charge $65 for a steak, but steakhouses exist in a bubble, like any luxury product. "Our customers are CEOs, vice presidents, executives," said Antonio Mora, the executive chef of Maloney & Porcelli, one of Manhattan's most successful steakhouses. "It's almost like a clubhouse for them." Corporate high-rollers with '90s-era expense accounts may not care about prices, but many others do—especially the younger, more gastronomically aware customers that drive the restaurant business. They don't mind eating cheek, or skirt, or flatiron steak at half the cost of ribeye. Pat LaFrieda, the country's best-known independent meat purveyor, has seen demand for these once-obscure cuts soar. "With beef prices where they are, it's out of necessity. Over the last few years, my customers have been looking for economy cuts in every category." What's more, many chefs are appalled by the kind of waste that some traditional places take for granted. "I worked in a steakhouse, and they went through 10 cases of tenderloin in a night," Underbelly's chef Chris Shepherd told me, incredulously. "And the tenderloin is a tiny part of the carcass! It makes you wonder what happens to the rest of the animal." I, for one, will take the intense, fire-seared Painted Hills short rib at Ox in Portland, Ore.—an explosion of beef flavor at its most primal and vivid—over any steakhouse ribeye I can think of. Greg Denton, Ox's chef and co-owner, feels the same way. "To me, short rib is the most flavorful piece of beef. You have to work a little harder [to prepare it], sure. But every bite is worth it." ‘'I want it to be approachable, affordable, casual—not some man-cave where you have to spend $1,000 for four people.'’ There's more to the modern meatery than the food on the plate, though. For a lot of diners, the problem with the old-time steakhouses isn't merely that they are uninspired, or expensive. It is that they all look and feel exactly the same. Like the German beer-hall and British chophouse from which it descends, the steakhouse has always been looked at by its proprietors more or less as a feeding pen, and its customers as bags for putting meat and liquor into. It's an overwhelmingly masculine place, a guyland where beleaguered husbands go to high-five each other over their temporary liberation from the tyranny of women. There is no such template for the meatery, at least not yet. It can have the funky faux-opulence of M. Wells, or the sunny, open simplicity of the Butcher Shop in Boston. It has no gender to speak of, and it has no conventions to obey. It might even contain, as in Laurelhurst Market, a working retail butcher counter. The modern meatery is a work in progress, looking to the future, whereas the steakhouse is a product of the past, a time capsule. Does that mean that the one will replace the other? Probably not. But ask me again in 10 years. A Contemporary Carnivore's Glossary* Asado: Argentine-style grilling, typically over live wood or coal fires. Bacon: Technically, cured pork belly, but nowadays any body part from any animal that is prepared in this style is called bacon, often with quotation marks. Berkshire/Red Wattle/Ossabaw/Kurobuta/Duroc/Mangalitsa Pork: Different breeds of pig, each held to be superior in flavor to standard cross-breeds. Kurobuta and Berkshire are actually the same breed by different names. The tastiest, in my opinion, are Mangalitsa and Ossabaw—the latter is so rare it hardly ever appears on menus. ENLARGE Illustration by Sarah Vanbelle for The Wall Street Journal Five Things to Look For 1. Live fire. Nothing is more inconvenient in a kitchen than the use of real hardwood as a cooking fuel, whether on an open grill or in an open oven. Some restaurants use "wood burning" grills that are actually mostly heated by gas flames—bluish sideways jets are the giveaway. 2. Changing meat specials. The small-farm producers favored by the best meateries don't churn out thousands of carcasses per week. And the small numbers they do harvest shift with the seasons. A constantly rotating menu of meats says they aren't coming down a factory pipeline. 3. Snout-to-tail cooking. Any self-respecting modern meatery should be bringing in whole animals and using up every bit of them. If the menu consists entirely of steaks, chops and short ribs, you may be looking at a steakhouse in meatery clothing. 4. Plainspoken menu language. While there may be many unfamiliar terms on a meatery menu, the basic language should be simple, clear and concise. The modern meatery has nothing to hide. 5. On-menu farm or ranch information. Saying something is "farm-raised" or "local" doesn't mean anything. There's no reason to believe that something is good simply because it is raised close by. Look for the name of a real farm in a real area: That way, you can find out about it if you want to. Boar: An adult male pig, especially one caught in the wild. Boar is redder, tougher and has a stronger, porkier taste than the young pigs you generally find. Boudin Noir/Blood Sausage: Exactly what it sounds like: sausage made from cooked blood. Cheeks/Jowls: An animal's jaw muscles, which are typically very chewy, but also very dense and rich and delicious. They require a lot of special treatment and low, slow cooking. Confit: Meat that has been cooked a long time in its own fat, making it obscenely tender and rich. Dry-Aged: Meat that has been left in a cool, dry room, typically for two weeks, sometimes far longer. In that time it loses water and undergoes subtle chemical and physical changes that improve both its flavor and its texture. Grass-Fed: Implies, though doesn't guarantee, that the animal has never been fed grain, corn or any food other than grass. In fact, all cattle eat grass at some point during their lives. Pastured Veal: The meat from calves that got to spend some time outdoors, as opposed to being penned in the dark for their entire brief lives. Better still is "untethered" veal, which means that the animal got to walk around with its mother, at least for a while. Piemontese Beef: An heirloom Italian breed notable for not being as good as Black Angus. At least in my opinion. Rillettes: Confit that gets cooled down, cut up and mashed into a spread. The incomparable Golden Steer in Vegas, and closer to home Marin Joe's where it is still 1962. Also found it a little hard to believe the food mecca of the west didn't garner a single mention? There are perhaps higher end joints in SF but for my money the place with with no sign has never let me down, go see Eddie at the The Brazenhead. King of ALL steakhouses, one that brought class, terrific wine and a true dining experience to the typical steakhouse experience is none other than SPARKS STEAK HOUSE in New York City, midtown east. None other like it. Period. The freshest food all around - steak, fish, salads...just love this top of the line restaurant. I'll just address Chicago, my town, Love Publican. Take ALL visitors there. Current menu has a sirloin steak on it. That's it for steaks. Girl And The Goat has a grilled skirt steak. That's it for steaks. Josh, NOBODY knows steakhouses better than you but these are note even close to steakhouses by ANY measure. Next time in town, let's go to Primehouse. My treat. "Modern meatery?" What a load of tripe (pun intended). First it was "nouvelle cuisine," next it will be "nouvelle bouef" -- dressing up cheap cuts with a fancy name. That's not to say that people can't eat anything anywhere they want - it's just not my style.Give me a nice grilled filet mignon steak anytime (medium rare). "With a median home price of $125K, it doesn't have a population that can support anything better than an olive garden." What doesn't have a population to support anything, you idiot? And what does median home price have to do with population magnitude? NOTHING you idiot! "You don't have the 5 bucks a week for a WSJ subscription so decent restaurants are off your menu." Sure I do. I just choose to spend my money on more important things, since WSJ is provided for me free with my job. Your subscription bigotry is a logical fallacy to avoid the truth of my comments, and has been reported, you idiot. The best beef by far is found in Alberta Canada. Grass-fed, antibiotic and hormone free. Cows wander around for a couple of years on open range. They are then finished for a month or two on Barley feed. The fat is pure white. It is first wet aged for 3 to 4 weeks, and then dry aged for 2 to 4 weeks. The result is Heaven. When in Calgary I go to Master Meats, a short cab ride from downtown. I call ahead and have them prepare a prime-rib for me to age it the way I like it as described above. They then trim, cut rib-eyes, and bones and cryovac the whole deal. For about C$170.00 you get 6 - 8 two inch thick steaks with absurd marbling, and a great fat cap and fat plug. They are perfect on a grill. I salt them well about 3 hours before cooking and then just grind some pepper on them. It is a sin to eat this beef cooked more than rare to very light medium rare. The result is as perfect a piece of steak as can be had anywhere on earth. I've been everywhere and there is no better beef at any price than can be had with these perfect prime steaks. The traditional old fashioned dark wood paneled white table clothed prime beef - did I say old fashioned? - steak house is just the ticket for me. A cigar bar is a plus. New-fashioned meat restaurants, as substitutes for the traditional old fashioned steak house, are not for me. We could argue about which of the old line steak houses are the best, but any one of them in many cities across this country is preferable to the 2.0-type discussed in this article. Just ate at Luger's on Christmas Eve. The one and only. There is no place anywhere else that can match it. Used to be a regular customer at Ben Bensons on 52nd St. There is no other place like that, and sadly, it is gone. There are some things that can not be improved upon. Keep your aioli and chipotle and Pho...that's peasant food and always will be. The best beef is available only in New York, at places like Keene's, Luger, perhaps Sparks, Smith and Wollensky and Palm as well. But that's it. Been all over the country, eaten at many if not most of the steakhouses, and I say, without question, the old-line NY steakhouse was the best possible. As they go away, so too does the ability--and taste--to appreciate them. So take your skirt steak, wrap it in balsamic goat cheese and flambeed hen of the woods, and do what you wish with it. I'll stick with an on-premis, dry-aged prime steak, which requires no chef or improvement. Some things are as they are and are better than anything else. throw the meat under a broiler? I know some places do that, i.e. ruths chris is one. I prefer cooked over a grill using fire. nothing better than that. as for the steakhouse 2.0? not for me. you can not improve upon a medium rare aged steak (bone-in ribeye one of my favorites) cooked over fire with a side of garlic sautéed spinach and a salad with italian or french bread with real plain butter without the herbs. keep the sour dough bread. please stop serving sour dough bread. As a steak-lover, I love the ambiance, I love the fact that I eat those cuts, specifically Chateaubriand and Porterhouse, occasionally. As the article said, I am not part of the "man's club" culture in Keen's, my favorite steakhouse, for few reasons: 1. I am a woman, 2. It is too expensive for me to eat there on a weekly basis and 3. I can't afford it, calorically. I don't want to look like a Porterhouse. A new reason added to my list, recently. After watching a documentary about the cruelty in those farms, I want a steak that comes from a Humane Certified farm. I am willing to pay the extra. I even wrote a letter to Keens, asking for that.However, as someone who considers herself a foodie and one who knows a good steak when I eat one, the Modern steakhouse doesn't appeal to me. A steak on the bone in a bun?! You are ruining my steak, my experience and ritual of cutting it to the bone. Yet, I agree, I would love to see less waste, more respect to the animal I am carving.So, given the growing generation of green-foodies, myself included, I don't see Keen's or BLT Steak go out of business. I welcome the new modern steakhouse, maybe they will push the Steakhouse 1.0 to become green, but I see the Steakhouse 2.0 more as a trend and not so much as the new establishment. In 10 years, I believe, they will be incorporated into the 1.0, where you will be offered the same cuts as today, from humane farms, and the "new" cuts like cheeks, which are most tender and moist. Most importunely, I believe we will have a new rating for humane certified restaurants. I don't see our favorite steak place morphing into a gourmet, girly-man, restaurant with a chef. It's the best steak place in town and most of the clientele go there for the steaks that they've been cooking for the last 60 years..in the same manner, with a side of baked potato, pasta, or green beans. Desserts are simple...chocolate cake, key lime pie or banana cream.The dishes are not expensive, the place is not fancy(though it is well done), the hostess is not a maitre de and the place is packed on weekends. Reservations are required.The formula works.Contrary to the philosophy or the "modern diner" who follows a chef around town, some things don't need "updating". spot on John. A $1 thousand dinner tab for four is ridiculous. Must be factoring very expensive booze. I'm richer than ever form the Texas oil boom, but I'm also cheaper than ever. Home on the grill is the way to go. I don't have time for business lunches, I can usually accomplish what I need in a short phone conversation... It's a special treat, a splurge at times........ a treat for me. Even if I am on an "expense account" as the guy that owns the joint I still pay. And yes, without expense accounts the steak houses would be up "s-hit creek" This copy is for your personal, non-commercial use only. Distribution and use of this material are governed by our Subscriber Agreement and by copyright law. For non-personal use or to order multiple copies, please contact Dow Jones Reprints at 1-800-843-0008 or visit www.djreprints.com.

IRS Agrees with House Republicans to Investigate Clinton Foundation First auditing Donald Trump, now investigating Hillary Clinton, it seems the IRS can’t help but get involved in this year’s presidential election. Although, this time the IRS had some assistance from the GOP. On July 15, 64 House Republicans, led by Rep. Marsha Blackburn, TN, sent a letter to the IRS, FBI, and Federal Trade Commission accusing the Clinton Foundation of corruption and abusing its 501(c)(3) tax-exempt status as a charity.[1] Specifically, the Clinton Foundation—and therefore Bill and Hillary Clinton as well—is accused of engineering a “‘pay to play’ sham charity” in which the Clintons traded political favors or government contracts for large donations from the world’s wealthiest individuals.[2] Besides ethically and morally repugnant, such actions also violate the strict requirements to maintain 501(c)(3) status. In other words, the Clintons could have been claiming the Clinton Foundation as a charity all of these years just to avoid paying taxes, all the while personally profiting from the business. Only one week later, on July 22, IRS Commissioner John Koskinen replied to Blackburn to inform her that the IRS forwarded the accusation to the Exempt Organizations program, part of the Tax Exempt and Government Entities Division of the IRS.[3] It is worth noting, however, that while this letter did seemingly get the personal attention of the Chief of the IRS, it is not an acknowledgment by the IRS that it will take any action against the Clintons.[4] Instead, it has been widely noted that the IRS letter is nothing more than a standard form response,[5] and the IRS has confirmed that it is standard procedure.[6] Indeed, some doubt whether the anything will result from this complaint.[7] IRS Commissioner Koskinen is already under scrutiny for playing favorites with applications for 501(c)(3) status and faces impeachment over the issue,[8] so there is a distinct disincentive to discover further problems with 501(c)(3) organizations under current IRS leadership. Perhaps the investigation into the Clintons’ business activities is meant to appear nonpartisan by evening out the scales; perhaps not. Either way, this investigation comes at a poor time for Hillary Clinton. The opinions expressed are those of the author and do not necessarily reflect the views of the firm, its clients, or any of its or their respective affiliates. This article is for general information purposes and is not intended to be and should not be taken as legal advice.

The present invention relates to a control apparatus and method of a vehicle. As a vehicle provided a gear type transmission mechanism, this type of vehicle has been conventionally known which utilizes a friction clutch as the smallest gear ratio of the gear type transmission, controls the input shaft speed of the transmission to be in synchronous to the output shaft speed by slipping this friction clutch when shifting the gear, and corrects the torque lowered in shifting the gear by means of the torque transmitted by the friction torque for the purpose of realizing smoother gear shifting. The representative one of this type of vehicle is disclosed in JP-A-61-45163. In shifting the gear, however, if the revolution speed is controlled only through the use of the friction clutch, the output shaft torque corrected by the friction clutch is made so variable that a passenger in a vehicle may disadvantageously feel uncomfortable with the vehicle. Further, when terminating the gear shifting, if the correction for the lowered torque in gear shifting, corrected by the friction clutch, is not matched to the input shaft torque transmitted to the output shaft through a mesh type clutch, disadvantageously again, the torque may be abruptly changed.

The singer-songwriter market is as crowded as a grocery store on the eve of a hurricane. Even so, artists such as Shannon LaBrie continue to make really good records. LaBrie's intimate, soulful vocals recall a less self-aware Fiona Apple. With vocal chops to spare, LaBrie is able to elevate good songs (“Lion's Cage,” “Just Be Honest”) into great ones. The musical backing on “Just Be Honest” has an old-school R&B flavor without feeling forced. The direct, Daniel Lanois-esque tones sprinkled throughout “I Remember A Boy” and “Slow Dance” hit the goose bump target with guitar straight out of the Edge's playbook. “Just Be Honest” isn't all dreamy and ethereal, as the mid-temp funk of “How Does It Feel” and “Getting Tired” effortlessly demonstrate. The album as a whole may have played better if these peppier tracks had been shuffled to an earlier slot on the album, but aside from music critics and music nerds, who listens to whole albums anymore anyway? The only problem Shannon LaBrie has is that she doesn't fit easily into a mold. The unholy Americana tag might be thrown at her, although she doesn't dress like she just tripped over Tom Joad. Mainstream rock is as dead as a hammer, so she should probably avoid that. Maybe there's room for her in the Norah Jones wing of the adult alternative market. Wherever LaBrie lands, she has a great album to stand on with “Just Be Honest.” Hopefully she'll be allowed to make another. Classic album: Mickie Most Years Artist: The Animals Label: Real Gone Rating: 4.5 out of 5 stars Everybody knows The Animals had a massive world-wide hit with “House Of The Rising Sun” in the 1960s, but they also created several albums-worth of the best blues/r&b-influenced rock ever recorded. Based around the howling vocals of Eric Burdon and fluid organ work of Alan Price, the Animals original 1963-66 run with producer Mickie Most is revelatory. Looking back on it now, it wouldn't be too much of a stretch to say the Burdon/Price model wasn't an early prototype of what Jim Morrison and Ray Manzarek would later cook up for The Doors. Aside from a few rarities and bonus tracks, the bulk of “The Mickie Most Years” focuses on the albums “The Animals,” “The Animals On Tour,” “Animal Tracks” and “Animalization” — all of which are four to five star releases in their own right. There's a bit of hoodoo regarding which songs were originally on the British releases vs. their American counterparts, but it's inconsequential. These albums contain “House Of The Rising Sun,” “Baby Let Me Take You Home,” “We Gotta Get Outta This Place,” “Don't Let Me Be Misunderstood,” and the group's masterpiece “Inside Looking Out.” Mixed in with the aforementioned hits, The Animals tear into covers of John Lee Hooker, Sam Cooke and Chuck Berry material that doesn't mimic the originals but are awe inspiring in their own right. To put it bluntly, Eric Burdon could scare the white off rice when he wanted to. With rare exception, Animals compilations throughout the years have been either ill-conceived or hampered by legal red tape. Even “The Mickie Most Years” has one flaw that keeps it from getting a full five-star rating: The absence of The Animals 1966 album “Animalism.” True, “Animalism” was produced by Tom Wilson and not Most, but it's inclusion is essential to paint a true portrait of the original Animals run. Until somebody figures out how to pull “Animalism” into the mix, “The Mickie Most Years” is without a doubt the best Animals compilation on the market. Those $10 single-disc “best of” collections at Target and Walmart look enticing, but it would be the equivalent of only looking at the Mona Lisa's forehead. Work through a few lunches and get the real thing. Jon Dawson's album reviews appear every Thursday in The Free Press. Contact Jon at 252-559-1092 or jon.dawson.@kinston.com. Jon's new book “Counterfeit Sauerkraut & The Weekend Teeth” is now available at the Free Press office and jondawson.com.

Slayed? Slayed? is the third studio album by the British rock group Slade. It was released on 1 November 1972 and reached No. 1 in the UK. It remained on the chart for 34 weeks and was certified Silver in early 1973. The album was also the band's most successful of the 1970s in the US, peaking at No. 69 and remaining in the charts for 26 weeks. In Australia, the album reached No. 1 and went Gold, knocking the band's live album Slade Alive! to No. 2. Slayed? was produced by Chas Chandler. Background After achieving their breakthrough hit with "Get Down and Get With It" in 1971, Slade would continue to achieve further success with their follow-up singles "Coz I Luv You", "Look Wot You Dun" and "Take Me Bak 'Ome". The 1972 live album Slade Alive! also gave the band their first success on the albums chart, reaching No. 2. Having achieved their second UK number one with "Take Me Bak 'Ome", the band soon finished recording their next studio album Slayed?. In August 1972, the lead single "Mama Weer All Crazee Now" was released and was another UK chart topper. Slayed? followed in November and reached No. 1. A second single, "Gudbuy T'Jane", was also released that month and reached No. 2 in the UK. In October, "The Whole World's Goin' Crazee" was released as a free 7" Flexi disc with the Music Scene magazine. The B-Side was "Bonnie Charlie" by Mike Hugg. In August 1973, "Let The Good Times Roll" was released as a single in America where it reached No. 114. In November, "Move Over" was released as a single in Japan. Song information "How D'You Ride" had originally been considered as a potential single, with Chandler particularly keen on seeing it released as one. In a 2006 interview, drummer Don Powell revealed of "I Won't Let It 'appen Agen": "If you listen to the start of that one you can hear somebody shout, 'Yeah!' That's me shouting, because it felt so good when we started, that I just couldn't help saying it. And it was kept." The idea for "Gudbuy T'Jane" came to Lea while the band was in San Diego. He completed the song on the flight home to the UK. Holder's lyrics were inspired by a woman called Jane who demonstrated a sex machine on a TV show on which the band appeared. The idea for the lyrics of "Mama Weer All Crazee Now" came from the band's show at the Boston Gliderdrome in Lincolnshire, where a bouncer had told them about another act who'd appeared there drunk – "crazy with whiskey". Critical reception Upon release, Record Mirror described the album as "all pretty stomping, insistent and bawled out stuff", adding "they deliver the goods here, alright". In the Record Mirror poll results of 1974, Slayed? was listed at No. 4 on the Top 10 list of best British albums. New Musical Express said the album was "one of the greatest rock 'n' roll releases ever". Robert Hilburn of the Los Angeles Times felt that aside from some "effective moments" on side one, side two best displayed Slade's "power and direction". He concluded: "If you've been missing the solid, raunchy rock sound in recent months, get slayed and play it loud." Tom Von Malder of The Wheeling Herald (Illinois) felt the album recalled the "kind of raw music that the Rolling Stones used to play when they did "Street Fighting Man"." Malder concluded: "Slade is punk, street rock at its best and loudest." American rock critic Robert Christgau felt the album showcased "boot-boy anthems that are every bit as overpowering as has been reported, and also more fun. Noddy Holder can wake up the crazee in my neighborhood any time he wants." Henry McNulty of the Hartford Courant described the album as a "fierce, unrelenting type of rock", as well as a "total body assault, leaving the mind free to wander in the void where the meaning ought to be." In 2010, Classic Rock considered the album an "essential classic", adding that it featured "party-hard tracks, and even something approaching a ballad with "Look at Last Nite", ensuring that Slayed? inarguably ticks all the right boxes." The Guardian noted the album's singles and other tracks as being "deservedly party riff monsters", but added: "Slayed?s majesty lies in the melancholy ballads. "Look at Last Nite's" haunting refrain fingers both empty celebrity and fame's creeping downside." The album was included in the book 1001 Albums You Must Hear Before You Die. Track listing Personnel Slade Noddy Holder – lead vocals, rhythm guitar Dave Hill – lead guitar, backing vocals Jim Lea – bass, piano, backing vocals Don Powell – drums Additional personnel Chas Chandler – producer Gered Mankowitz – cover photography Chris Charlesworth – liner notes Chart performance Certifications References Category:Slade albums Category:1972 albums Category:Polydor Records albums Category:Albums produced by Chas Chandler

523 F.Supp.2d 684 (2007) Hobert Freel TACKETT, et al., Plaintiffs, v. M & G POLYMERS USA, LLC, et al., Defendants. No. 2:07-cv-126. United States District Court, S.D. Ohio, Eastern Division. November 21, 2007. *685 *686 David Marvin Cook, Robert E. Rickey, Cook, Portune & Logothetis, Cincinnati, OH, Renate Klass, Stuart M. Israel, Martens, Ice, Klass, Legghio & Israel, P.C., Royal Oak, MI, for Plaintiffs. Nelson D. Cary, Thomas Howard Fusonie, Vorys Sater Seymour & Pease, Columbus, OH, Christopher A. Weals, Morgan, Lewis & Bockius LLP, Washington, DC, Deborah S. Davidson, Philip A. Miscimarra, Morgan, Lewis & Bockius LLP, Chicago, IL, for Defendants. OPINION AND ORDER GREGORY L. FROST, District Judge. This matter is before the Court for consideration of Defendant's motion to dismiss (Doc. # 19), Plaintiffs' memoranda in opposition (Docs.# 34, 35), Defendant's reply memorandum (Doc. # 36), and Plaintiffs' sur-replies (Docs.# 61, 62). For the reasons that follow, the Court finds the motion to dismiss well taken. I. Background This is a class action case in which the putative class — retirees, their spouses, and surviving spouses or other dependents of individuals who worked for the named defendant company-assert that although they have a right to lifetime retiree health care benefits, the company is requiring them to pay for those benefits in violation of various collective bargaining agreement ("CBA") provisions. Plaintiffs Hobert Freel Tackett, Woodrow K. Pyles, and Harland B. Conley are all Ohio residents *687 and retirees from the Point Pleasant Polyester Plant in Apple Grove, West Virginia. They and similarly situated retirees belong to a labor union, Plaintiff United Steel, Paper and Forestry, Rubber, Manufacturing, Energy, Allied Industrial and Service Workers International Union, AFL-CIO-CLC ("USW"), which represented (or at least one of its predecessor unions represented) them as employees of Defendant M & G Polymers USA, LLC ("M & G") (which bought the plant in 2000), or one of its predecessor companies, such as the Shell Chemical Company (which owned the plant from 1992 to 2000) and The Good-year Tire & Rubber Company (which owned the plant until 1992). Plaintiffs assert that various CBA provisions provide lifetime retiree health care benefits. Plaintiffs allege that on or about January 1, 2007, however, Defendant M & G unilaterally modified the health care benefits by shifting a large part of the health care costs onto the putative class members. The other named defendants are M & G-sponsored health plans through which the putative class members receive health care benefits: the M & G Comprehensive Medical Benefits Program for Employees and Their Dependents, the M & G Catastrophic Medical Plan, the M & G Medical Necessity Benefits Program of Hospital, Surgical, Medical, and Prescription Drug Benefits for Employees and Their Dependents, and the M & G Major Medical Benefits Plan. Plaintiffs filed the instant action on behalf of the named retirees and their surviving spouses or dependents, as well as other similarly situated retirees and their surviving spouses or dependents, on February 9, 2007. (Doc. # 1.) Via their amended complaint, Plaintiffs assert three counts: violation of labor agreements, actionable under Section 301 of the Labor Management Relations Act ("LMRA"), 29 U.S.C. § 185(a) (Count I); violation of employee welfare benefit plan, actionable under Sections 502(a)(1)(B) and (a)(3) of the Employee Retirement Income Security Act of 1974 ("ERISA"), 29 U.S.C. §§ 1132(a)(1)(B) and (a)(3) (Count II); and breach of fiduciary duty under Section 502(a)(3) of ERISA, 29 U.S.C. § 1132(a)(3) (Count III). (Doc. # 14 ¶¶ 26-31.) On May 15, 2007, Defendants filed a motion to dismiss the amended class action complaint. (Doc. # 19.) In connection with that briefing, Plaintiffs filed a joint motion for leave to file two sur-reply memoranda (Doc. # 42), which the Court granted (Doc. # 60). The parties have therefore completed briefing on the motion to dismiss, which is now ripe for disposition. II. Discussion A. Standard Involved Defendants move for dismissal under Federal Rules of Civil Procedure 12(b)(1) and 12(b)(6). Rule 12(b)(1) provides that an action may be dismissed for lack of subject matter jurisdiction. Under the Federal Rules of Civil Procedure, "[p]laintiffs have the burden of proving jurisdiction in order to survive a Rule 12(b)(1) motion. . . ." Weaver v. Univ. of Cincinnati, 758 F.Supp. 446, 448 (S.D.Ohio 1991) (citing Moir v. Greater Cleveland Reg'l. Transit Auth., 895 F.2d 266, 269 (6th Cir.1990)). See also Rapier v. Union City Non-Ferrous, Inc., 197 F.Supp.2d 1008, 1012 (S.D.Ohio 2002) (citing McNutt v. General Motors Acceptance Corporation of Indiana, Inc., 298 U.S. 178, 189, 56 S.Ct. 780, 80 L.Ed. 1135 (1936); Rogers v. Stratton Indus., Inc., 798 F.2d 913, 915 (6th Cir.1986)) ("The plaintiff bears the burden of establishing, by a preponderance of the evidence, the existence of federal subject matter jurisdiction"). Moreover, this Court may resolve any factual disputes when adjudicating a defendant's jurisdictional *688 challenge. See Moir, 895 F.2d at 269. In contrast to Rule 12(b)(1), Rule 12(b)(6) requires an assessment of whether Plaintiffs have set forth claims upon which this Court may grant relief. For the purpose of the analysis under Rule 12(b)(6), this Court must construe the amended complaint in favor of Plaintiffs, accept the factual allegations contained in the amended complaint as true, and determine whether Plaintiffs' allegations plausibly suggest viable claims. See NicSand, Inc. v. 3M Co., 507 F.3d 442, 448 (6th Cir.2007); Assoc. of Cleveland Fire Fighters v. City of Cleveland, Ohio, 502 F.3d 545, 548 (6th Cir.2007); cf Goad v. Mitchell 297 F.3d 497, 500 (6th Cir.2002). In other words, "a complaint will be dismissed pursuant to Rule 12(b)(6) only if there is no law to support the claims made, or if the facts alleged are insufficient to state a claim, or if on the face of the complaint there is an insurmountable bar to relief." The Limited, Inc. v. PDQ Transit, Inc., 160 F.Supp.2d 842, 843 (S.D.Ohio 2001) (citing Rauch v. Day & Night Mfg. Corp., 576 F.2d 697, 702 (6th Cir.1978)). B. Analysis Relying on Rule 12(b)(1), Defendants first argue that the Court should dismiss Plaintiffs' § 301 claim constituting Count I because the claim fails to present a breach of the CBA. Rather, Defendants assert, they have simply complied with the CBA and ancillary agreement provisions that permit the implementation of above-cap contributions. Defendants then argue that dismissal is also warranted under Rule 12(b)(1) because the National Labor Relations Board ("NLRB") has primary jurisdiction over the claim, with the caps constituting an agreed-upon mandatory subject of bargaining. Finally, Defendants posit that dismissal is warranted under Rule 12(b)(6) because the limitations on the health benefits, including caps on employer contributions, were the result of collective bargaining and disclosed in the 1991 summary plan description. The nature of Defendants' initial challenge to this Court's jurisdiction over Count I means that the Court can look outside the factual allegations of the pleadings. Were this a facial attack on the amended complaint under Rule 12(b)(1), the Court would necessarily accept the factual allegations of the amended complaint as true. See U.S. v. A.D. Roe Co., Inc., 186 F.3d 717, 721-22 (6th Cir.1999) (explaining that in "a facial attack on subject matter jurisdiction, [a court] would take the allegations in the complaint as true and construe them in the light most favorable to the non-moving party"); see also RMI Titanium Co. v. Westinghouse Electric Corp., 78 F.3d 1125, 1134 (6th Cir.1996). In the absence of a facial attack on the amended complaint, however, this Court need not accept that pleading's factual allegations as true. See RMI Titanium Co., 78 F.3d at 1134 (explaining that when a Rule 12(b)(1) motion attacks the existence of subject matter jurisdiction, apart from the pleadings, a court does not accept the pleadings as true but weighs the evidence as needed to determine jurisdiction); Wright v. United States, 82 F.3d 419, 1996 WL 172119, at *4 (6th Cir.1996) (unpublished table decision) ("Regardless of what the complaint says, the court has no subject matter jurisdiction if the factual predicates of subject matter jurisdiction do not exist."). Thus, the Court can consider evidence extrinsic to the pleadings without converting the matter into a summary judgment proceeding. See Fed.R.Civ.P. 10(c) ("A copy of any written instrument which is an exhibit to a pleading is a part thereof for all purposes."); Nichols, 318 F.3d at 677; Rogers v. Stratton Industries, *689 Inc., 798 F.2d 913, 915-16 (6th Cir.1986) (supplementation of record in Rule 12(b)(1) challenge does not convert motion to dismiss into a summary judgment motion). Consideration of such evidence — which has been properly authenticated — defeats Plaintiffs' position.[1] Defendants argue that Letter of Understanding 2003-6, dated August 9, 2005, and made part of the current CBA (which controls the period from August 9, 2005 through November 6, 2008), permits implementation of above-cap contributions. (Doc. # 19-9, Ex. 8, at 6-7.) This letter indeed contemplates caps on employer contributions to retiree health benefits and provides that "premium cost sharing charged to retirees will be based in the amount by which total cost for all retiree insurances (medical, life, etc.) exceed the caps set forth in Letter H dated January 1, 2001." (Doc. # 19-9, Ex. 8, at 6.) The letter continues to state that retirees would not be required to contribute to their premiums until January 1, 2006, and that the retiree premium contribution rates would become effective on that date. (Doc. # 19-9, Ex. 8, at 6.) Defendants additionally direct this Court to a May 15, 1991 letter ("Letter G") incorporated into the CBA effective May 15, 1991. Letter G provides both that a specific age-based cap limitation exists on the employer contributions for each employee who retires on or after May 1, 1991, and that "[i]f the average annual cost of health care benefits for [each group of retirees outlined in the letter] exceeds the specified amount, the cost in excess of that amount shall be allocated evenly to all retired employees (including surviving spouses) in such group." (Doc. # 19-3, Ex. 2, at 8.) The letter, signed by a representative of each side, then provides that "no retired employee or surviving spouse shall be obligated to contribute for such excess health care cost until July 1, 1997." (Doc. # 19-3, Ex. 2, at 8.) Plaintiffs attack Defendants' reliance on this authenticated letter and similar documents — cap letters dated July 20, 1994, May 9, 1997, and January 1, 2001 (Docs.# 19-3, 19-4, 19-5) — on the grounds that they all relate to Goodyear retirees and that Defendants have failed to show that the Goodyear documents apply to Shell and M & G employees who retired from the Apple Grove plant after it was sold by Goodyear to Shell in 1992, and then sold by Shell to M & G in 2000. In fact, in its sur-reply, Plaintiff USW even states that "M & G argues that Shell's assumption of the Goodyear CBA and P & I agreement necessarily included the 1991 Goodyear `cap' letter, but presents no evidence in support of that argument." (Doc. # 61, at 4 n. 2.) The Court has struggled with Plaintiffs' premise because it is so curious that the Court has been concerned that it is not reading Plaintiffs' briefing correctly. There is ultimately no doubt, however, that Plaintiffs are attempting in this specific context to evade the very agreements into which they voluntarily entered. There is also no doubt that, in contrast to Plaintiffs' contention, Defendants have presented ample evidence supporting application of the cap letters. The first cap letter originated in 1991. The declaration of James Kruse, the retired Goodyear employee responsible for human resources and labor relations (including collective bargaining over retiree *690 benefits), indicates that the May 15, 1991 Letter G was part of the agreement incorporated into the Master P & I Agreement and that it applied to the Apple Grove plant. The declaration also explains that Shell assumed the agreement obligations as a successor as part of its 1992 purchase of the plant. (Doc. #.37, Ex. 12.) The declaration of Dale Wunder, Shell's Vice President of Human Resources who was assigned to the Apple Grove plant, also indicates that Shell assumed the existing agreement obligations as a successor. Wunder additionally indicates that although the parties agreed not to change the agreements from using "Goodyear" to using "Shell," the parties agreed that the 1994 and 1997 Goodyear agreements were applicable to the Apple Grove plant. Notably, Wunder also indicates that Shell and the union specifically agreed that the July 20, 1994 Letter G to the 1994 P & Agreement and the May 9, 1997 Letter H to the 1997 P & I Agreement applied to retirees from the Apple Grove plant. (Doc. # 37, Ex. 13.) Thus, the caps remained applicable. In 2000, Shell sold the Apple Grove plant to M & G. The declaration of Kimm Korber, M & G's Human Resources Director, indicates that M & G assumed the preexisting CBA and its obligations as a successor to Shell, that the union asserted in negotiations that the January 1, 2001 Letter H applied, and that the eventual 2005-08 CBA included the Letter of Understanding 2003-6 that tracks and reaffirms the caps applicable to all preexisting retirees back to the original May 15, 1991 Letter G. Moreover, the declaration specifically states that the union never disputed that the retiree contributions could be collected in the form of monthly contributions. (Doe. # 37, Ex. 14.) These declarations and their attachments thus present an unbroken chain of cap letter applicability. Plaintiffs, overlooking the union's assertion during negotiations with M & G that the 2001 cap-supporting Letter H applied, argue that M & G admitted the caps did not apply. The declaration of David Dick, an attorney who represented M & G in the 2000 negotiations, clarifies that M & G's October 17, 2000 communication denying applicability of the 1994 and 1997 letters was the result of a lack of understanding on his part of the history of cap incorporation and that the denial did not modify the existing agreements and party obligations. (Doc. # 37, Ex, 15.) The text of Letter of Understanding 2003-6 unambiguously supports the unbroken application of caps to retirees (including preexisting retirees). That document explicitly references the prior 2001 cap letter and provides that "[r]etiree benefits" means "benefits for the Company's preexisting retirees." (Doc. # 19-9, at 6.) In contrast to this evidence of continued application of the caps, Plaintiffs present an argument based on inferences, selectively pointing to documents such as M & G's October 17, 2000 negotiation memorandum, while sidestepping the evidence, that placed that document in context and evidence that the caps have long and continuously applied. Four additional points warrant fuller discussion. First, Plaintiffs have unsuccessfully attempted to change the context of the argument. As previously noted, Defendants' Rule 12(b)(1) motion to dismiss is a factual, not facial, challenge to jurisdiction. Defendants in fact sought to emphasize this point, stating in the memorandum in support of their motion the applicable standard and scope of review for "[w]here, as here, a party factually challenges a court's jurisdiction to hear a claim . . ." (Doc. # 19, at 10 n. 5.) But in an effort to defeat judicial consideration of the substance of Defendants' declarations, Plaintiffs *691 attempt to recast the nature of the Rule 12(b)(1) attack as a facial attack on the amended complaint. See Doc. # 61, at 5 (Plaintiff USW argues that "alleged conversations cannot support a Rule 12(b)(1) or (6) motion, which is based on the assertion that the complaint fails to state a claim and that the Court lacks jurisdiction."); Doc. # 62, at 1 ("Plaintiff Retirees adopt the arguments set forth in Plaintiff USW's surreply regarding Plaintiffs' LMRA Section 301 claims."). Because Defendants assert a factual, not facial, attack, the Court can consider and even weigh the substance of the declarations in the Rule 12(b)(1) context, without proceeding to Rule 12(b)(6) and a subsequent conversion to a Rule 56 proceeding. See DLX, Inc. v. Kentucky, 381 F.3d 511, 516 (6th Cir.2004) ("A Rule 12(b)(1) motion . . . can attack the factual basis for jurisdiction, in which case the trial court must weigh the evidence and the plaintiff bears the burden of proving that jurisdiction exists."). Second, the October 17, 2000 M & G memorandum (itself extrinsic evidence) cannot trump the parties' agreement reached after that (ill-informed) negotiating position; the subsequent agreement reached by the parties reaffirmed the applicability of the caps. Thus, there is no modification as Plaintiffs assert, but only a validation of the preexisting cap agreements and obligations. Third, the M & G purchase agreement for the Apple Grove plant fails to defeat the applicability of the cap letters. Even if the purchase agreement excluded the cap letter obligations, this does not speak to the pre-purchase obligations of the pre-2000 retirees or the pre-purchase application of caps. And even if the purchase agreement did not include the cap provisions, the parties' subsequent dealings as outlined in the negotiations reaffirmed the application of the caps to preexisting and subsequent retirees. In other words, there might have been an argument that M & G meant to exclude these benefit obligations via the purchase agreement, but the union and the company then reaffirmed the cap and benefit obligations so as to defeat the, continued vitality of that argument. Fourth, the premise of Plaintiffs' claim, that termination of benefits for retirees who fail to contribute, similarly fails because termination does not present a breach. For the period of time at issue, there are no guaranteed benefits absent retiree contributions. This means the asserted terminations do not breach the CBAs. The end result is that Plaintiffs have failed to meet their burden of proving that jurisdiction exists. Count I of the amended complaint targets "specified lifetime health care benefits," and the specified benefits include sharing costs. The retirees are entitled to an employer contribution toward health benefits, but they must pay premium contributions; there is simply no contractual right to contribution-free health benefits, even if agreements have long deferred the eventual collection of the retirees' shares. The company's right to terminate benefits for retirees' failure to contribute is implicit. Therefore, the evidence before this Court indicates that because the caps scheme has continued to apply, Defendants are correct in asserting that there is no breach of the CBA. Absent a breach by Defendants, this Court lacks jurisdiction over the § 301 claim constituting Count I of the amended complaint. See United Gov't Sec. Officers of Am. v. Akal Sec., Inc., 475 F.Supp.2d 732, (S.D.Ohio 2006) (holding that there is no viable § 301 claim where there is no breach of a CBA); cf. Bauer v. RBX Indus., Inc., 368 F.3d 569, 578 (6th Cir.2004) ("Jurisdiction in a § 301 claim is premised upon the existence of a *692 contract, which an employer subsequently breaches. Section 301 opens the federal courthouse only to `[s]uits for violation of contracts.'" (quoting 29 U.S.C. § 185(a))). But even assuming that the Court should indeed presume jurisdiction and proceed under Rule 12(b)(6) as Plaintiffs suggest, dismissal is still warranted. Because much of this analysis in regard to the Rule 12(b)(6) attack on the Count I § 301 claim involves the same analysis related to Plaintiffs' ERISA claims in Counts II and III, the Court shall proceed to discuss the Rule 12(b)(6) inquiry together. Defendants move for dismissal of these counts pursuant to Rule 12(b)(6), for failure to state a claim upon which this Court can grant relief. Defendants argue that the Court cannot grant relief on Count I because there is no breach, given that retirees have no right to lifetime health benefits without mandated retiree contributions. Defendants then posit that dismissal of the ERISA Section 502(a)(1)(B) component of Count II is warranted because the incorporated letters referenced above provide that the issue of retiree health benefits is a mandatory subject of bargaining, which indicates that the retirees' health benefits were and are not vested as lifetime benefits as Plaintiffs contend. Defendants' rationale here is that because 29 U.S.C. § 1132(a)(1)(B) only permits a plan participant "to recover benefits due to him under the terms of his plan," the retirees cannot proceed under this ERISA provision because the parties' agreed only to retiree medical benefits contingent on retiree contributions. Thus, Defendants reason, in the absence of a retiree contribution, there is no right to an employer contribution. The analysis is that no retiree contribution equals no benefit due, which means there is no due benefit to recover under § 1132(a)(1)(B). Defendants also seek a Rule 12(b)(6) dismissal of the ERISA Section 502(a)(3) component of Count II and the entirety of Count III essentially on the grounds that the section is unavailable because ERISA Section 502(a)(1)(B) already provides a remedy. Plaintiffs argue that this is an incorrect construction of both ERISA and their amended complaint and that there have been actionable fiduciary misrepresentations. A medical benefit plan is a type of welfare benefit plan, which means that it is not subject to automatic or mandatory vesting under ERISA, but can be vested by agreement of the parties. Bauer, 368 F.3d at 584. What proves unusual in this case is that the context of this Rule 12(b)(6) aspect of the motion to dismiss precludes this Court from considering the letter agreements of the parties here, even if the Court could and did consider this material in regard to the dismissal of Count I. In addressing above the motion to dismiss Count I, this Court conducted a Rule 12(b)(1) factual inquiry that permitted and necessitated review of extrinsic evidence (i.e., Defendants' declarations, which presented the cap letters as applicable to the dispute). As Plaintiffs correctly note in their briefing, however, a Rule 12(b)(6) inquiry mandates a different approach. Under Rule 12(b)(6), the Court cannot engage in such a factual inquiry, but must accept the factual allegations contained in Plaintiffs' amended complaint as true and then decide whether these facts present a plausible claim to relief. Plaintiffs assert that the Rule 12(b)(6) inquiry means that the Court must necessarily accept that the plan documents and CBAs confer lifetime health care benefits on the retirees and that the plans and CBAs preclude termination by Defendants. Thus, Plaintiffs conclude, the pleading presents a potentially viable claim under Counts I and II. *693 Defendants indeed attack Counts I and II by relying on the letter agreements, which as discussed above rely on the declarations for validation. Although the Court can consider documents referenced in the amended complaint, the pleading generally makes vague references to the parties' agreements, without specifying what constitutes the bulk of the agreements; it is only through the "extrinsic evidence that the Court was persuaded above that the letters mattered. Defendants also rely on summary plan descriptions, which do not grow out of the pleading but are extrinsic to the amended complaint. To consider this material, the Court would have to convert the Rule 12(b)(6) motion to dismiss into a Rule 56 motion for summary judgment. Rule 12 permits such conversion, stating: If, on a motion asserting the defense numbered (6) to dismiss for failure of the pleading to state a claim upon which relief can be granted, matters outside the pleading are presented to and not excluded by the court, the motion shall be treated as one for summary judgment and disposed of as provided in Rule 56, and all parties shall be given reasonable opportunity to present all material made pertinent to such a motion by Rule 56. Fed.R.Civ.P. 12(b). What this means is that generally a court must provide the parties notice of its intent to convert, although under various circumstances notice is not always required. See Cunningham v. Osram Sylvania, Inc., 221 Fed.Appx. 420 (6th Cir.2007) (concession of both parties in Rule 12(b)(6) briefing that conversion is appropriate negates need for notice of intent to convert). Weighing against conversion and consequent consideration of Defendants' extrinsic materials is the fact that Plaintiffs have raised a demand to conduct discovery on the alleged fiduciary misrepresentations. (Doe. # 62, at 3 ("Plaintiffs are entitled, at a minimum, to conduct discovery on this claim.").) The Court in its discretion therefore declines to consider material extrinsic to the pleadings in regard to the motion to dismiss Counts I through III, which means that conversion is not necessary. Proceeding to address the motion within the confines of a Rule 12(b)(6) inquiry, then, the Court nonetheless concludes that dismissal is warranted. The aforementioned Cunningham v. Osram Sylvania, Inc. notably informs this conclusion. In Cunningham the Sixth Circuit described the relevant facts of that similar § 301 case as follows: The plaintiffs are former Sylvania employees who retired in 1998 and 2002. They brought this action on the theory that Sylvania's announcement in 2003 that its contribution to their medical insurance premiums would henceforth be "capped" at scheduled amounts constituted a unilateral modification of non-modifiable lifetime benefits granted to retirees under union contracts between their union, UAW Local 1608, and Sylvania. The company's action came in the wake of provisions in collective bargaining agreements dating back to 1993, the year that Sylvania purchased the Kentucky facility where the plaintiffs were employed. After Sylvania took over the plant, the health insurance benefits for retirees fell into two categories, based on age and length of service. The first category covered those employees who were under the age of 45 on the date of purchase and who were eligible to receive a percentage of the premium at company expense, based on their years of employment and capped at a certain amount set out in a separate schedule. Those over the age of 45 on the purchase date were subject to the same eligibility formulas, but the amounts to *694 which they were entitled were not capped. As medical insurance costs began to rise precipitously in the decade following Sylvania's takeover of the plant, however, the company negotiated minor changes in the collective bargaining agreements with the UAW and, outside the contract, made certain other changes in the retirees' health insurance coverage. Finally, in 2003, after failing to secure a change in the most recent contract, the company notified retirees that the distinction between the capped and uncapped premiums had been removed from the plan and that, henceforth, all health insurance premiums would be subject to a cap on amounts paid by the company. In response, the plaintiffs brought suit, alleging that this unilateral change in benefits was in violation of the LMRA. 221 Fed.Appx. at 421-22. This description of retirement benefit scheme based on age and length of service roughly tracks the scheme in the instant case. The Cunningham scheme provided that retirees over 45 with sufficient years of employment were entitled to receive uncapped company contributions to their health benefit premiums. This echoes the amended pleading's assertion in the instant case that retirees with "95 or more points `will receive a full Company contribution towards the cost of benefits described in Exhibit B-1.'" (Doc. # 14 ¶ 14.) To support this assertion, Plaintiffs' amended complaint cites an excerpted copy of the 2000 Pension, Insurance and Service Award Agreement "attached here as `Exhibit A.'" (Doc. # 14 ¶ 14.) But no such exhibit is attached to the amended complaint. The original complaint (Doc. # 1) did, however, include the exhibit. Assuming arguendo that this Court can consider the original complaint's attachment when construing the assertions of the amended complaint, the Court must conclude that dismissal is warranted. The Sixth Circuit explained in Cunningham that the complaint in that case omitted any facts to support the bald conclusions that "[t]he insurance benefits conferred on all retirees by the Agreements are lifetime benefits to which plaintiffs and other retirees from the Winchester, Kentucky plant are entitled for the remainder of their lives" and that those benefits "cannot be unilaterally modified or terminated by the defendant without the consent of the retirees." 221 Fed.Appx. at 422. The court of appeals therefore concluded that "[b]ecause this proposition was pleaded without factual support of any kind, in our judgment the district court could have entered an order of dismissal for failure to state a claim under Rule 12(b)(6)."[2]Id. The amended complaint sub judice similarly asserts that. "[u]nder the terms of the applicable collective bargaining agreements, [each named retiree (and in some instances his spouse)] are entitled to lifetime health care benefits, which defendants are obligated to provide." (Doc. # 14 ¶¶ 9, 10, 11.) The amended pleading similarly asserts that class members became vested in retiree health care benefits and became entitled to receive lifetime health care benefits, and their spouses and surviving spouses became vested and entitled to receive health care benefits for life or until remarriage, as were the surviving spouses of certain *695 employees who died while employed at the Plant. (Doc. # 14 ¶ 15.) Finally, echoing the language in Cunningham, the amended complaint concludes that "defendants violated these rights by shifting a large part of the costs of those benefits from defendants to Class Members, and have terminated or planned to terminate the benefits of those Class Members unable to pay or who otherwise do not pay the added costs imposed by defendants." (Doc. # 14 ¶ 16.) This Court concludes that, as in Cunningham, because Plaintiffs have plead propositions without factual support of any kind, dismissal under Rule 12(b)(6) is warranted. Plaintiffs amended complaint quotes paragraph 11 of the agreement constituting Exhibit A. Review of that agreement indicates that it does indeed state that qualifying retirees "will receive a full Company contribution towards the cost of the benefits described in this Exhibit B-1. . . ." (Doc. # 1-2, at 3 ¶ 11.) But many of the conclusions Plaintiffs draw from that statement exceed factual allegations that this Court must accept as true in the Rule 12(b)(6) context. Instead, Plaintiffs assert unsupported contentions including legal conclusions. The relevant agreement paragraph does not present vesting or preclude monthly retiree premiums and the termination of benefits for failure to pay those premiums. To reach that conclusion would be to ignore both the language employed in the quoted sentence and other sentences in that paragraph that Plaintiffs have elected not to quote in their pleading. Applying simple principles of contract construction to the key sentence upon which Plaintiffs rely — "Employees will receive a full Company contribution towards the cost of the benefits described in this Exhibit B-1. . . ." (Doc. # 1-2, at 3 ¶ 11) — the Court must recognize that "full" modifies "Company contribution" in the quoted sentence, not "cost." What the sentence therefore says is that qualifying retirees will receive the total amount of the company's potential contribution toward the cost of health benefits, not that the company will cover the full cost of the benefits if the benefits exceed the total potential (i.e., capped) contribution. "[A] full Company contribution" is consistent with caps. This construction distinguishes the agreement language at issue here from those cases to which Plaintiffs direct this Court as containing "virtually identical CBA language [that] has been held to constitute a lifetime promise of retiree medical benefits" (Doc. # 61 at 3 n, 1) For example, the language creating vested lifetime benefits in International Union, United Automobile, Aerospace and Agricultural Implement Workers of America, UAW v. Loral Corp., read as follows: "Employees who retire and who are eligible under the Loral Systems Group Retirement Plan for Bargaining Unit Employees for a pension (other than a deferred vested pension), shall receive the benefits described in this Section B. . . ." 873 F.Supp. 57, 63 (N.D.Ohio 1994), aff'd, 107 F.3d 11, 1997 WL 49077, at *2 (6th Cir.1997) (unpublished table decision). The distinction is obvious: that case's "shall receive the benefits" contrasts significantly with the instant case's "will receive a full Company contribution towards the costs of the benefits." The former promises benefits, while the latter promises a contribution that context places within a contingent retiree-contribution scheme; there is no guarantee here that the employer contribution is either unqualified or sufficient to cover the cost of benefits.[3] The agreement in the *696 case sub judice distinguishes this case from those in which a presumption of lifetime benefits — which the Sixth Circuit has described as the "Yard-Man inference" — proves correct. See Loral Corp., 1997 WL 49077, at *2. Additionally, Plaintiffs neglect that the referenced agreement paragraph also states that "[e]mployees will be required to pay the balance of the health care contribution, as estimated by the Company annually in advance, for the benefits described in this Exhibit B-1. Failure to pay the required medical contribution will result in cancellation of coverage." (Doc. # 1-2, at 3 ¶ 11.) The language of the paragraph in no way restricts the reference to "Employees" to mean only those retirees with less than the 95 qualifying points, which means that the agreement paragraph contradicts the amended pleading's assertions of vesting of lifetime noncontingent benefits and that Defendants cannot require retiree contributions and terminate benefits for a failure to make such contributions. It is beyond question that the agreement also permits termination for retirees with less than 95 points who fail to make their contributions. The apparent inferences Plaintiffs (explicitly or implicitly) ask this Court to draw are unreasonable and unwarranted in light of the foregoing language. There is thus no support for Plaintiffs' allegations behind the Count I § 301 claim or the Count II claim to enforce rights and enjoin plan violations.[4] There is also no support for lifetime benefits that cannot be terminated. The attachment exhibit in fact contravenes Plaintiffs' pleading in this regard, undercutting the plausibility of their claim to relief. This leaves Count HI. That count asserts a breach of fiduciary duty under ERISA, alleging according to Plaintiffs' own characterization that Defendants "breached their fiduciary duties by not administering the plans in a prudent manner, by failing to act for the exclusive purpose of providing benefits, and by wrongfully burdening participants and beneficiaries of the plans with monthly `premiums,' causing hardship to the retirees and, in many instance, termination of health benefits." (Doc. # 62, at 3 (tracking Amended Complaint, Doc. # 14 ¶ 34).) Even assuming arguendo that this is a viable cause of action under ERISA, Plaintiffs have failed to plead facts supporting imprudent conduct and a failure to act for the plan purpose. Moreover, as described above, Plaintiffs have failed to plead facts supporting the wrongful imposition of retiree contributions. The Court notes that the briefing includes Plaintiffs' assertion that Count III also targets the specific allegation that Defendants misled prospective retirees with promises that they would receive "no cost" health benefits during their retirement. See, e.g., Doc. # 62, at 3. It is important to note, however, that nowhere in the amended complaint do Plaintiffs plead this allegation or how or what Defendants purportedly did in this regard, beyond a reference in Count I that the CBAs promised retirees health benefits. It is a wholly unsupported factual contention derived from the briefing, and this Court is restricted under Rule 12(b)(6) to crediting the amended *697 pleading, not briefing. Accordingly, Plaintiffs' belated contention is not sufficient to present a viable Count III upon which this Court could grant relief. In summary, in addition to the 12(b)(1) attack on Count I, Plaintiffs' amended complaint also does not include "enough factual matter (taken as true) to suggest that" there is a foundation for Counts I, II, and III plausibly suggesting a right to relief. Bell Atlantic Corp. v. Twombly, ___ U.S. ___, ___, 127 S.Ct. 1955, 1965, 167 L.Ed.2d 929 (2007). Because the pleading's factual allegations are not "enough to raise a right to relief above the speculative level," see id., the Court must dismiss the complaint under Rule 12(b)(6).[5] III. Conclusion For the foregoing reasons, the Court GRANTS Defendant's motion to dismiss. (Doc. # 19.) The Court therefore need not address Plaintiffs' moot motion for a preliminary injunction (Doc. # 40) and Defendants' moot motion to strike the jury demand (Doc. # 20). The Clerk shall enter judgment accordingly and terminate this case upon the docket records of the United States District Court for the Southern District of Ohio, Eastern Division, at Columbus. IT IS SO ORDERED. NOTES [1] The Court assumes for the sake of argument that a Rule 12(b)(1) inquiry is appropriate here. See Gentek Bldg. Prods., Inc. v. Steel Peel Litigation Trust, 491 F.3d 320, 330 (6th Cir.2007) (reasoning that when a factual attack on jurisdiction implicates an element of the cause of action, a district court should conclude that jurisdiction exists and proceed to address a direct attack on the merits of the plaintiff's claim.). [2] Because the district court under review in Cunningham had instead elected to consider extrinsic evidence, the court of appeals proceeded to treat the district court's disposition of the motion to dismiss under a Rule 56 inquiry. 221 Fed.Appx. at 422-24. This Court has declined to consider extrinsic material in regard to the Rule 12(b)(6) aspect of Defendants' motion to dismiss. [3] This same rationale distinguishes the lifetime-benefits case of United Rubber, Cork, Linoleum & Plastic Workers of America, AFL-CIO, CLC v. Pirelli Armstrong Tire Corp., in which the documentation at issue provided that medical benefits "will be provided" without a termination provision, as opposed to a simple employer contribution scheme. 873 F.Supp. 1093, 1098 (M.D.Tenn.1994). [4] The lack of a foundation for an ERISA violation renders Defendants' arguments as to redundant sources of relief under the various ERISA provisions moot. [5] The Court therefore need not and does not address Defendants' moot alternative "pre-emption" ground for dismissal of Count I under Rule 12(b)(1).

G.O. shares stories about these so-called “chart manipulators”. Amid much controversy over Limez Entertainment and rumors of their chart manipulation, G.O.’s explanation that the K-Pop industry does manipulate charts has been receiving even more attention. According to G.O., starting around the year 2010, there were some singers who immediately ranked no. 1 on the charts every time they released a song. Your browser does not support video. “In order for them to hit no. 1, there has to be that many people who are waiting for that singer and the song, but statistically speaking, it just wasn’t possible for those certain singers to have that many people waiting for them.” ㅡ G.O. On the other hand, there were some groups who were extremely popular but when the made a comeback they weren’t able to reach no. 1 in the charts let alone the top 50. Your browser does not support video. “These are the singers who people actually waited for and who had endless comments on each article written about them…but they weren’t able to reach the charts.” ㅡ G.O. Because of the strange phenomena, people began to get suspicious and rumors of chart manipulation began spreading. It was during this time when these so-called “chart manipulators” visited G.O.’s agency. Your browser does not support video. “If you pay us $375,000 USD, we’ll rank your singer no.1 on the charts for one month.” ㅡ Chart manipulators G.O.’s agency rejected the offer but what he heard from one of the 2PM members was even more surprising. Your browser does not support video. “At the time, we were sharing a waiting room with 2PM and one of the members told me, ‘Hey G.O. guess what? A person came to our company and said he would manipulate charts for us for a month if we spend $500,000~$600,000 USD.'” ㅡ G.O. Eventually, these “rumors” were confirmed among the entertainment companies to be true. Your browser does not support video. “Honestly, who listens to loud dance music during the middle of the night, right?” ㅡG.O. These chart manipulating businesses apparently block domestic traffic servers and control them from abroad making it difficult to track. Your browser does not support video. In addition, there were apparently very famous artists who were rumored to have used these types of services to gain advertisements, fans, events, drama castings, etc. Your browser does not support video. G.O. emphasized that people generally don’t even get a chance to listen to great artists because many businesses such as shopping malls or cafes usually just play the top 100 songs on the chart. He added that he feels it’s unfortunate that such systems exist in the world of entertainment. Your browser does not support video. “I’m sharing this with you guys simply because I feel that it’s too bad.” ㅡ G.O. Watch G.O.’s full explanation in the clip below:

--- abstract: | We linearize the inverse branches of the iterates of holomorphic endomorphisms of ${\mathbb {P}}^k$ and thus overcome the lack of Koebe distortion theorem in this setting when $k\ge 2$. We review several applications of this result in holomorphic dynamics.\ MSC 2010: 37F10, 37G05 , 32H50.\ Key Words: Linearization, Lyapunov exponents author: - François Berteloot and Christophe Dupont date: title: 'A distortion theorem for the iterated inverse branches of a holomorphic endomorphism of ${\mathbb {P}}^k$' --- Introduction ============ Let $f : {\mathbb {P}}^k \to {\mathbb {P}}^k$ be a holomorphic endomorphism of algebraic degree $d \geq 2$. This is a ramified covering of ${\mathbb {P}}^k$ of degree $d^k$. The equilibrium measure $\mu$ of $f$ is a mixing $f$-invariant measure, see [@DS Section 1.3]. The Lyapunov exponents of $(f,\mu)$ are larger than or equal to $\log \sqrt d$, see [@BD] or [@DS Section 1.7]. Setting $J:=\textrm{Supp}\;\mu$, we thus have a non-uniform hyperbolic dynamical system $(J,f,\mu)$. The aim of the present article is to provide a substitute to the Koebe distortion theorem, which is only valid for $k=1$, to control the geometry of the iterated inverse branches of $f$ on ${\mathbb {P}}^k$. Our proof is based on a normalization of $f$ along $\mu$-typical backward orbits. Although it should face a major difficulty due to resonances on the Lyapunov spectrum, we use a simple trick to get rid of all possible resonances and stay in the setting of linear normalizations. Our Distortion Theorem allows to skip the use of delicate results on the Lie group structure of resonant maps, see [@GK; @JV; @KS; @BDM]. This is a typical feature of our approach. At the end of the article we review various applications which illustrate how it can be used.\ Let us now introduce our framework. To deal with inverse branches, we introduce the natural extension of $f$. Let $${\textsf {O}}:= \{ \hat x = (x_n)_{n \in {\mathbb {Z}}} \, \colon \, x_{n+1} = f (x_n) \}$$ be the set of orbits of $f$ and let $\tau : {\textsf {O}}\to {\textsf {O}}$ be the right shift sending $(\cdots,x_{-1},x_0,x_1,\cdots)$ to $(\cdots,x_{-2},x_{-1},x_0,\cdots)$. We say that a function $\phi_{\epsilon}: {\textsf {O}}\to ]0,1]$ (resp. ${\textsf {O}}\to [1,+\infty[$) is *${\epsilon}$-slow* (resp. *${\epsilon}$-fast*) if $$\forall \hat x \in {\textsf {O}}\ , \ e^{- \epsilon} \phi_{\epsilon}(\hat x) \leq \phi_{\epsilon}(\tau(\hat x)) \leq e^{ \epsilon} \phi_{\epsilon}(\hat x) .$$ Similarly, a sequence $(\delta_n)_{n \in {\mathbb {Z}}}$ in $]0,1]$ is *$\epsilon$-slow* if $e^{-\epsilon} \delta_n \leq \delta_{n+1} \leq e^{\epsilon} \delta_n$ for every $n \in {\mathbb {Z}}$. Let $\hat \mu$ be the unique $\tau$-invariant measure on ${\textsf {O}}$ satisfying $\pi_*\hat \mu = \mu$, where $\pi(\hat x) := x_0$, see [@CFS Chapter 10]. The measure $\hat \mu$ is mixing as $\mu$. Since the equilibrium measure $\mu$ is a Monge-Ampère mass with bounded local potentials, it does not give mass to the critical set $\CC$ of $f$. In particular, the $\tau$-invariant subset $$X := \{ \hat x = (x_n)_{n \in {\mathbb {Z}}} \, \colon \, x_n \notin \CC \ , \ \forall n \in {\mathbb {Z}}\}$$ satisfies $\hat \mu(X)=1$. For every $\hat x \in X$, we denote $f^{-n}_{\hat x}$ the inverse branch of $f^n$ which sends $x_0$ to $x_{-n}$, it is defined in a neighbourhood of $x_0$. We denote $dist$ the distance on ${\mathbb {P}}^k$ induced by the Fubini-Study metric and $B_x(r)$ the ball centered at $x$ of radius $r$. [A :]{}\[thmA\] Let $f$ be a holomorphic endomorphism of ${\mathbb {P}}^k$ and let $\mu$ be its equilibrium measure. Let $\Lambda_l < \cdots < \Lambda_1$ be the distinct Lyapunov exponents of $(f,\mu)$ and let $ k_j \ge 1$ be their multiplicities. Then for every $\epsilon < \gamma \ll \Lambda_l $ and for $\hat \mu$-almost every $\hat x \in X$, there exist - an integer $n_{\hat x} \geq 1$ and real numbers $h_{\hat x}\ge 1$ and $0 < r_{\hat x} , \rho_{\hat x} \le 1$, - a sequence $(\varphi_{\hat x,n})_{n \geq 0}$ of injective holomorphic maps $$\varphi_{\hat x,n} : B_{x_{-n}} (r_{\hat x} e^{-n(\gamma + 2\epsilon)}) \to {\mathbb {D}}^k(\rho_{\hat x} e^{n {\epsilon}})$$ sending $x_{-n}$ to $0$ and satisfying $$e^{n( \gamma - 2{\epsilon})} dist(u,v) \leq \vert \varphi_{\hat x,n} (u) - \varphi_{\hat x,n} (v) \vert \leq e^{n (\gamma + 3 {\epsilon})} \, h_{\hat x} \, dist(u,v) ,$$ - a sequence of linear maps $(D_{\hat x,n})_{n \geq 0}$ which stabilize each $$L_j := \{ 0 \} \times \cdots \times {\mathbb {C}}^{k_j} \times \cdots \times \{0 \} ,$$ satisfying $$\forall v \in L_j \ \ ,Ê\ \ e^{- n\Lambda_j + n (\gamma - \epsilon) } \abs{v} \leq \abs{D_{\hat x,n}(v)} \leq e^{- n \Lambda_j + n (\gamma + \epsilon) } \abs{v} ,$$ for which the following diagram commutes for every $n \geq n_{\hat x}$: $$\xymatrix{ B_{x_0}(r_{\hat x}) \ar[rrr]^{ f^{-n}_{\hat x} } \ar[d]_{\varphi_{\hat x , 0}}& & & B_{x_{-n}}(r_{\hat x} e^{-n(\gamma + 2 \epsilon)}) \ar[d]^{\varphi_{\hat x , n}} \\ {\mathbb {D}}^k(\rho_{\hat x}) \ar[rrr]^{ D_{\hat x,n} } & & & {\mathbb {D}}^k (\rho_{\hat x} e^{n{\epsilon}}) . }$$ Moreover, the fonctions $\hat x \mapsto h^{-1}_{\hat x}, r_{\hat x}, \rho_{\hat x}$ are measurable and $\epsilon$-slow on $X$.\ The following corollary shows how Theorem A can be used to estimate the convexity defect of the inverse branches $f_{\hat x}^{-n}\left(B_{x_0}(r_{\hat x})\right)$. A special case of such a property was recently put forward in [@BB]. [(Convexity defect)]{}\[Cor\] Let $f$ be a holomorphic endomorphism of ${\mathbb {P}}^k$ and let $\mu$ be its equilibrium measure. We keep the notations of Theorem A. Let $r'_{\hat x}:= r_{\hat x} / h_{\hat x}$ and, for every $0<t\le 1$, let $$E_{\hat x}^{-n}(t):=f_{\hat x}^{-n}\left(B_{x_0}(t r'_{\hat x})\right) \subset {\widetilde E}_{\hat x}^{-n}(t):=f_{\hat x}^{-n}\left(B_{x_0}(t r_{\hat x})\right) .$$ Then for every pair of points $p,q\in E_{\hat x}^{-n}(t)$ there exists a smooth path connecting $p$ and $q$ in ${\widetilde E}_{\hat x}^{-n}(t)$ and whose length is smaller than $e^{5n\epsilon} h_{\hat x} d(p,q)$. Let us finally mention that Theorem A and its Corollary remain valid for every invariant ergodic measure $\nu$ with positive Lyapunov exponents $\Lambda_l' < \cdots < \Lambda_1'$ and, in particular, when $\nu$ has metric entropy $h(\nu) > \log d^{k-1}$, see [@dT; @D2]. Proof of Theorem A ================== In this Section, we explain how to deduce Theorem A from a linearization statement for chains of holomorphic contractions (Theorem B in Subsection \[contrholo\]). The bundle map over $X$ generated by the inverse branches of $f$ {#affchart} ---------------------------------------------------------------- We recall in Section \[app\] basic definitions and facts concerning bundle maps. Let $(\psi_x)_{x \in {\mathbb {P}}^k}$ be a collection of affine charts $\psi_x :{\mathbb {C}}^k \to {\mathbb {P}}^k$ with uniform bounded distortion and satisfying $\psi_x(0)=x$ (for instance fix an affine chart and rotate it thanks to unitary automorphisms of ${\mathbb {P}}^k$). To simplify the exposition, we shall ignore the distortions induced by these charts. For every $\hat x \in X$, let $E_{\hat x} := \{ \hat x \} \times {\mathbb {C}}^k$ and let $\psi_{\hat x} : E_{\hat x} \to {\mathbb {P}}^k$ defined by $$\psi_{\hat x} (\hat x, v) = \psi_{x_0} (v) .$$ Let $\hat f := \tau^{-1}$ be the left shift $(\cdots,x_{-1},x_0,x_1,\cdots) \mapsto (\cdots,x_{0},x_{1},x_2,\cdots)$ on $X$, and let $$F_{\hat x} := \psi^{-1}_{{\hat f(\hat x)}} \circ f \circ \psi_{{\hat x}} .$$ Since $f$ is continuous on ${\mathbb {P}}^k$ there exist constants $M_1 \leq M_0$ such that the bundle map $$\FF : \begin{array}{rccc} & E(M_1) & \longrightarrow & E(M_0) \\ & (\hat x , v ) & \longmapsto & \left(\hat f(\hat x), F_{\hat x}(v) \right) \end{array}$$ is well defined. Note that $F_{\tau(\hat x)}$ is invertible near $0$ since $\hat x \in X$ implies $x_{-1} \notin \CC$. Let $$F^{-1}_{\hat x}:= ( F_{\tau(\hat x)})^{-1} = \left( \psi^{-1}_{\hat x} \circ f \circ \psi_{\tau(\hat x)} \right)^{-1} .$$ The following lemma specifies the domains of definition of these mappings. \[abd\] For every $\epsilon >0$, there exists a $\epsilon$-slow function $\rho_\epsilon : X \to ]0,1]$ such that the bundle map $$\FF^{-1} : \begin{array}{rccc} & E(\rho_\epsilon) & \longrightarrow & E(M_1) \\ & (\hat x , v ) & \longmapsto & \left( \tau(\hat x), F^{-1}_{\hat x}(v) \right) \end{array}$$ is well defined. [ [<span style="font-variant:small-caps;">Proof :</span> ]{}]{}Let $t(\hat x) := \vert ( d_{x_{-1}} f )^{-1} \vert^{-2}$. There exists $c >0$ depending on the first and second derivatives of $f$ on ${\mathbb {P}}^k$ such that $F^{-1}_{\hat x}$ exists on $E_{\hat x}(c \, t(\hat x))$ (see [@BD Lemma 2]). We let $\rho := \min \{ c\, t, 1 \}$. Since $\log \rho$ is $\hat \mu$-integrable (see [@DS Theorem A.31]), there exists a ${\epsilon}$-slow function $\rho_{\epsilon}: X \to ]0,1]$ such that $\rho_{\epsilon}\leq \rho$ (see [@BDM Lemme 2.1]). Oseledec-Pesin $\epsilon$-reduction {#OR} ----------------------------------- We recall that $\Lambda_l < \cdots < \Lambda_1$ denote the distinct Lyapunov exponents of $(f,\mu)$ and that $k_j \geq 1$ denote their multiplicities. For every $j \in \{ 1,\cdots, l \}$ we set $$\hat L_j := \cup_{\hat x \in X} \{ \hat x \} \times \left[ \{ 0 \} \times \dots \times {\mathbb {C}}^{k_j} \times \cdots \times \{0 \} \right] = \cup_{\hat x \in X} \{ \hat x \} \times L_j ,$$ so that $\cup_{\hat x \in X} \{ \hat x \} \times {\mathbb {C}}^k$ is equal to $\hat L_1 \oplus \cdots \oplus \hat L_l$. The Oseledec-Pesin’s theorem may be stated as follows, see [@KH Theorem S.2.10, page 666]. \[OPR\] Let $d_0 \FF^{-1}$ be the linear part of $\FF^{-1}$. For every $\epsilon > 0$ there exist an invertible linear bundle map $\CC_{\epsilon}$ over ${{\rm Id}}_X$ and a ${\epsilon}$-fast function $h_{\epsilon}: X \to [1,+\infty[$ such that 1. the linear bundle map $\AA := \CC_{\epsilon}\circ d_0 \FF^{-1} \circ \CC_{\epsilon}^{-1}$ satisfies for every $1\leq j \leq l$ : $$\ \AA(\hat L_j) = \hat L_j \ \ \textrm{and} \ \ \forall (\hat x,v) \in \hat L_j \ , \ e^{- \Lambda_j - \epsilon} \abs{v} \leq \abs{A_{\hat x}(v)} \leq e^{-\Lambda_j + \epsilon} \abs{v} .$$ 2. $\forall \hat x \in X$, $\forall v \in {\mathbb {C}}^k$, $\abs{v} \leq \abs {C_{{\epsilon}, \hat x} (v)} \leq h_{\epsilon}(\hat x) \abs{v}$. We conjugate the bundle map $\FF^{-1}$ as follows: $$\WW := \CC_{\epsilon}\circ \FF^{-1} \circ \CC_{\epsilon}^{-1} ,$$ its expansion is of the form $\WW(\hat x , v) := (\tau(\hat x) , W_{\hat x}(v) )$, where $W_{\hat x} = C_{{\epsilon},\tau(\hat x)} \circ F^{-1}_{\hat x} \circ C_{{\epsilon}, \hat x}^{-1}$. Since $\FF^{-1} : E(\rho_{\epsilon}) \to E(M_1)$ by Lemma \[abd\], Item 2 of Theorem \[OPR\] implies that $$\WW : E(\rho_\epsilon) \to E(M_1 h_\epsilon) .$$ By using $d_0 \WW = \AA$ and applying Lemma \[NN\] on tame bundle maps with ${\epsilon}' = {\epsilon}$, we obtain a $\epsilon$-slow function, still denoted $\rho_\epsilon$, such that $$\label{doublev} \WW : E(\rho_\epsilon) \to E(\rho_\epsilon) \ \ \textrm{ and } \ \ {{\rm Lip \, }}\WW \leq e^{-\Lambda_l + 2\epsilon} .$$ Resonances and constraints on $\gamma, \epsilon$ {#RC} ------------------------------------------------ As before, $\Lambda_l < \cdots < \Lambda_1$ denote the distinct Lyapunov exponents of $(f,\mu)$ and $k_j \geq 1$ denote their multiplicities. One defines the $k$-tuple $$(\lambda_i)_{1\leq i \leq k} := (\Lambda_1, \cdots , \Lambda_1 , \cdots , \Lambda_l , \cdots , \Lambda_l)$$ by repeating $k_j$ times $\Lambda_j$. For $j \in \{ 1, \cdots , l \}$, one defines the set of $j$-resonant indices by: $$\RRR_j := \{ {\alpha}\in {\mathbb {N}}^k\;\colon\; \abs{{\alpha}} \geq 2 \ \textrm{ and } \ {\alpha}_1\lambda_1 +\cdots +{\alpha}_k \lambda_k = \Lambda_j \} .$$ Since $\Lambda_l < \cdots < \Lambda_1$, one immediately sees that one has $2 \leq \abs{{\alpha}} \leq [\Lambda_j / \Lambda_l] \leq [\Lambda_1 / \Lambda_l]$ and ${\alpha}_1 = \cdots = {\alpha}_{k_1 + \cdots + k_j} = 0$ for every ${\alpha}\in \RRR_j$, where $[\cdot]$ stands for the entire part.\ For each $\gamma > 0$ one defines a shifted Lyapunov spectrum by setting: $$\Lambda_j^\gamma := \Lambda_j - \gamma .$$ Likewise, one defines the $k$-tuple $(\lambda^\gamma_i)_{1\leq i \leq k}$ by repeating $k_j$ times the $\Lambda^\gamma_j$: $$(\lambda^\gamma_i)_{1\leq i \leq k} = (\Lambda^\gamma_1, \cdots , \Lambda^\gamma_1 , \cdots , \Lambda^\gamma_l , \cdots , \Lambda^\gamma_l)$$ and one denotes $$\RRR^\gamma_j := \{ {\alpha}\in {\mathbb {N}}^k\;\colon\; \abs{{\alpha}} \geq 2 \ \textrm{ and} \ {\alpha}_1\lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k = \Lambda^\gamma_j \} .$$ We now fix a constant $0 < a < \ln 4$ such that $$\label {rol} {\alpha}_1\lambda_1 +\cdots +{\alpha}_k \lambda_k - \Lambda_j \notin [-a,a]$$ for every $j \in \{ 1 , \cdots , l \}$ and for every ${\alpha}\in {\mathbb {N}}^k\setminus \RRR_j$ satisfying $2 \leq \abs{{\alpha}} \leq [2 \Lambda_1 / \Lambda_l]$.\ One easily checks that $\cup_{j=1}^l \RRR^\gamma_j =\emptyset$ if $\gamma$ is small enough, hence there is no resonance relation for the shifted Lyapunov spectrum. More precisely, setting $$b:= {1 \over 2} \min \{ \gamma , a \} ,$$ one has ${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j \notin [-b , b]$ for $j \in \{ 1 , \cdots , l \}$ and $2 \leq \abs{{\alpha}} \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l]$ (see Lemma \[marge\] in the Appendix). We actually impose the following precise Constraints on $\gamma$ and $\epsilon$, they will play an important role in our future estimates. We stress that these constraints only depend on the Lyapunov exponents $(\Lambda_j)_j$. \[nota\] We shall assume that $\gamma,\epsilon$ satisfy the following properties. - The number $\gamma >0$ is fixed and sufficently small so that: $\gamma < \Lambda_l / 2 \ \ , \ \ \gamma ( [ \Lambda^\gamma_1 / \Lambda^\gamma_l ] -1)< a/2 \ \ \textrm{ and } \ Ê\ 4 \gamma (\Lambda^\gamma_1 / \Lambda^\gamma_l +1) \leq \Lambda_l^\gamma .$ - Any choice of $\epsilon >0$ is supposed to be small enough so that: $2 \epsilon < \gamma \ \ , \ \ 4\epsilon + 2\gamma < \Lambda_l \ \ \textrm{ and } \ Ê\ {\epsilon}( [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 3 ) < b . $ Preparatory diagram along a negative orbit {#tiro} ------------------------------------------ Let $\gamma , \epsilon >0$ satisfying Constraints \[nota\]. Let $\rho_{\epsilon}$ be the ${\epsilon}$-slow function provided by (\[doublev\]) in Section \[OR\]. Let $\hat x \in X$. For every $n \in {\mathbb {Z}}$ one sets: $$\rho_n := \rho_\epsilon (\tau^n(\hat x)) \ \ , \ \ W_n := W_{\tau^n(\hat x)} .$$ The sequence $(\rho_n)_n$ is ${\epsilon}$-slow and according to (\[doublev\]) we have: $$W_n : {\mathbb {D}}^k ( \rho_n) \to {\mathbb {D}}^k(\rho_{n+1}) \ \ , \ \ {{\rm Lip \, }}W_n \leq \theta := e^{-\Lambda_l + 2\epsilon} .$$ Let $(r_n)_n$ be any ${\epsilon}$-slow sequence such that $(r_n)_n \leq (\rho_n)_n$. We set $$r_{\hat x} := r_0 / h_{{\epsilon}} (\hat x) \ \ , \ \ r_n^\gamma := r_n e^{-n \gamma} \ \ , \ \ n_{\hat x} := \min \{ n \geq 0 \ , \ e^{n(-\Lambda_l + 4{\epsilon}+ \gamma)} h_{\epsilon}({\hat x}) \leq 1 \} .$$ The integer $n_{\hat x}$ is well defined since $4{\epsilon}+ \gamma < \Lambda_l$ by our Constraints \[nota\]. We have defined the charts $\psi_{\hat x} : E_{\hat x} \to {\mathbb {P}}^k$ in Section \[affchart\]. \[tiroir\] The following diagram commutes for every $n \geq n_{\hat x}$: $$\xymatrix{ B_{x_0}(r_{\hat x}) \ar[rrr]^{ f^{-n}_{\hat x} } \ar[d]_{C_{{\epsilon}, \hat x } \circ \psi_{\hat x}^{-1}}& & & B_{x_{-n}}(r_{\hat x} e^{-n(2{\epsilon}+ \gamma)} ) \ar[d]^{C_{{\epsilon}, \tau^n(\hat x)} \circ \psi_{\tau^n(\hat x)}^{-1} } \\ {\mathbb {D}}^k(r_0) \ar[rrr]^{ W_{n-1} \circ \cdots \circ W_0} & & & {\mathbb {D}}^k (r_n^\gamma ) . }$$ The commutation follows from our previous definitions so we only have to check that each arrow is well defined. We recall that, to simplify, we do not take into account the distortion induced by the charts $\psi_{\hat x}$. The left vertical arrow is well defined since $r_{\hat x} = r_0 / h_{{\epsilon}} (\hat x)$ and ${{\rm Lip \, }}C_{{\epsilon}, \hat x} \leq h_{\epsilon}(\hat x)$. Similarly, to see that the right vertical arrow is well defined too, we observe that $$r_{\hat x} e^{-n(2{\epsilon}+ \gamma)} h_{\epsilon}(\tau^n(\hat x)) = r_0 e^{-n(2{\epsilon}+ \gamma)} h_{\epsilon}(\tau^n(\hat x)) / h_{\epsilon}(\hat x) \leq r_0 e^{-n({\epsilon}+ \gamma)} \leq r_n e^{-n \gamma} = r_n^\gamma .$$ Now, by Constraints \[nota\] one has : $$r_0 \theta^n =r_0 e^{n(-\Lambda_l + 2{\epsilon})} \leq r_0 e^{-n ({\epsilon}+ \gamma)} \leq r_n e^{-n\gamma} = r_n^\gamma$$ which, since ${{\rm Lip \, }}W_{n-1}\circ \cdots\circ W_0 \leq \theta^n$, shows that the bottom horizontal arrow is well defined. Finally, one sees that the top horizontal arrow is well defined since, according to the definition of $n_{\hat x}$, the map $\Phi_n := (C_{{\epsilon}, \tau^n(\hat x)} \circ \psi^{-1}_{\tau^n(\hat x)}) ^{-1} \circ W_{n-1} \circ \cdots \circ W_0 \circ (C_{{\epsilon}, \hat x} \circ \psi_{\hat x}^{-1} ) $ satisfies $${{\rm Lip \, }}( \Phi_n ) \leq e^{n(-\Lambda_l + 2{\epsilon})} h_{\epsilon}(\hat x) \leq e^{-n(2{\epsilon}+ \gamma)}$$ on the ball $B_{x_0}(r_{\hat x})$ for every $n \geq n_{\hat x}$. Theorem A from the linearization of chains {#contrholo} ------------------------------------------ Theorem A follows from Theorem B below, whose proof will be given in Section \[proofTHMB\]. [B]{} \[linn\] Let $\Lambda_l < \cdots < \Lambda_1$ be positive real numbers. Let $\gamma , \epsilon > 0$ satisfying Constraints \[nota\]. Let $(\rho_n)_{n \in {\mathbb {Z}}}$ be a $\epsilon$-slow sequence and let $$W_n : {\mathbb {D}}^k ( \rho_n) \to {\mathbb {D}}^k(\rho_{n+1})$$ be a sequence of holomorphic contractions fixing the origin in ${\mathbb {C}}^k$ and such that $$\forall n \in {\mathbb {Z}}\ , \ {{\rm Lip \, }}W_n \leq \theta := e^{-\Lambda_l + 2 {\epsilon}} .$$ We assume the existence of a decomposition ${\mathbb {C}}^k = \oplus_{j=1}^l L_j$, where $L_j = \{ 0 \} \times \cdots \times {\mathbb {C}}^{k_j} \times \cdots \times \{0 \}$ such that, for every $n \in {\mathbb {Z}}$, the linear map $A_n := d_0 W_n$ satisfies $$A_n(L_j) = L_j \ , \ e^{-\Lambda_j - \epsilon} \abs{v} \leq \abs{A_n(v)} \leq e^{-\Lambda_j + \epsilon} \abs{v} \ \ \textrm{for every} \ v \in L_j .$$ Then there exists a ${\epsilon}$-slow sequence $(r_n)_n \leq (\rho_n)_n$ and a sequence of holomorphic maps $$\varphi_n : {\mathbb {D}}^k ( r^\gamma_n) \to {\mathbb {D}}^k(r_n) \ \ \textrm{where } \ \ r_n^\gamma := r_n e^{-n\gamma}$$ such that 1. $ e^{n(\gamma - 2{\epsilon})} \vert u - v \vert \leq \vert \varphi_n(u) - \varphi_n(v) \vert \leq e^{n (\gamma + 2{\epsilon})} \vert u - v \vert$, 2. the following diagram commutes: $$\xymatrix{ \cdots \ar[rr]^{ W_{n-1} } & & {\mathbb {D}}^k ( r^\gamma_n ) \ar[rr]^{ W_n } \ar[d]_{\varphi_n} & & {\mathbb {D}}^k(r^\gamma_{n+1}) \ar[rr]^{ W_{n+1} } \ar[d]_{\varphi_{n+1}} & &\cdots \\ \cdots \ar[rr]^{ A^\gamma_{n-1} } & & {\mathbb {D}}^k( 4 r_n) \ar[rr]^{ A^\gamma_n } & & {\mathbb {D}}^k( 4 r_{n+1}) \ar[rr] ^{ A^\gamma_{n+1} } & &\cdots }$$ where the maps $A_n^\gamma$ are given by $A_n^\gamma:=e^\gamma A_n$. Theorem A is simply obtained by combining Lemma \[tiroir\] with Theorem B and setting : $$\rho_{\hat x} = 4 r_0 \ , \ \varphi_{\hat x , n} = \varphi_n \circ C_{{\epsilon}, \tau^n(\hat x)} \circ \psi_{\tau^n(\hat x)}^{-1} \ , \ D_{\hat x , n} = A_{n-1}^\gamma \circ \cdots \circ A_0^\gamma.$$ Let us stress that the perturbation $A_n^\gamma = e^\gamma A_n$ precisely aims to shift the Lyapunov spectrum of $(A_n)_n$ and cancel the resonances. The statement of Theorem A only takes into account the right hand side part of the commutative diagram of Theorem B, which corresponds to the negative coordinates (the past) of $\hat x$. The fact that Theorem B concerns sequences of mappings $(W_n)_n$ indexed by ${\mathbb {Z}}$ is crucial. Indeed, we shall see in the proof of Lemma \[iter\] that the construction of the change of coordinates $\varphi_{\hat x,n}$ actually requires the positive and negative coordinates of $\hat x$. Proof of Corollary ------------------ Let $y$ be either $p$ or $q$. One sees on the commuting diagram in Theorem A that $f^n(y) \in B_{x_0}(tr'_{\hat x})$ and that $D_{\hat x,n}\circ \varphi_{\hat x,0} \left(f^n(y)\right) =\varphi_{\hat x,n}(y)$. Taking into account the Lipschitz estimates on $\varphi_{\hat x,0}$ it follows that $$\begin{aligned} \label{C1} \varphi_{\hat x,n}(p) \, , \, \varphi_{\hat x,n}(q) \in D_{\hat x,n} ( {\mathbb {D}}^k(tr_{\hat x})).\end{aligned}$$ Let us also check that $$\begin{aligned} \label{C2} D_{\hat x,n} ( {\mathbb {D}}^k(tr_{\hat x}))\subset \varphi_{\hat x,n} \left( B_{x_{-n}}(tr_{\hat x} e^{-n(\gamma+2\epsilon)})\right).\end{aligned}$$ To see this we simply observe that $$\begin{aligned} D_{\hat x,n}\left( {\mathbb {D}}^k(tr_{\hat x})\right)\subset {\mathbb {D}}^k\left(tr_{\hat x} e^{-n(\Lambda_l -\gamma -\epsilon)}\right) \subset {\mathbb {D}}^k\left(tr_{\hat x} e^{-4n\epsilon}\right) \subset \varphi_{\hat x,n} \left( B_{x_{-n}}(tr_{\hat x} e^{-n(\gamma+2\epsilon)}) \right)\end{aligned}$$ where the second inclusion comes from $\Lambda_l > 2\gamma + 4\epsilon>\gamma +5\epsilon$ (see the Constraints \[nota\]) and the last one from the Lipschitz estimate on $\varphi_{\hat x,n}$. Now, by (\[C1\]) there exists a segment $\Gamma$ connecting the two points $\varphi_{\hat x,n}(p), \varphi_{\hat x,n}(q)$ within the *convex set* $D_{\hat x,n}\left( {\mathbb {D}}^k(tr_{\hat x})\right)$. By the Lipschitz estimate on $\varphi_{\hat x,n}$, this segment $\Gamma$ satisfies $$\textrm{length}(\Gamma)\le e^{n(\gamma+3\epsilon)}h_{\hat x} d(p,q) .$$ By (\[C2\]), the image $\widetilde{\Gamma}$ of $\Gamma$ by the map $\left(\varphi_{\hat x,n}\right)^{-1}$ is a well defined smooth path connecting $p$ and $q$ and contained in $\varphi_{\hat x,n}^{-1}\circ D_{\hat x,n} ({\mathbb {D}}^k(tr_{\hat x}))$. Again by the Lipschitz estimate on $\varphi_{\hat x,n}$ we get $$\textrm{length}(\widetilde{\Gamma}) \le e^{n(-\gamma+2\epsilon)} \textrm{length}(\Gamma)\le e^{5n\epsilon}h_{\hat x} d(p,q) .$$ Finally, $\widetilde{\Gamma} \subset \varphi_{\hat x,n}^{-1}\circ D_{\hat x,n} \circ \varphi_{\hat x ,0} \left(B_{x_0}(tr_{\hat x})\right)={\widetilde E}_{\hat x}^{-n}(t)$ by the Lipschitz estimate on $\varphi_{\hat x,0}$. Linearization of chains of holomorphic contractions {#proofTHMB} =================================================== This Section is devoted to the proof of Theorem B. Step 1 : Shifting the spectrum {#step-1-shifting-the-spectrum .unnumbered} ------------------------------ \[decal\] Let $W_n : {\mathbb {D}}^k (\rho_n) \to {\mathbb {D}}^k(\rho_{n+1})$ be a sequence of holomorphic contractions satisfying the assumptions of Theorem B. Let $$\rho^\gamma_n := \rho_n e^{-n \gamma} \ \ , \ \ \Delta_n := e^{n\gamma} {{\rm Id}}_{{\mathbb {C}}^k} \ \ , \ \ W^\gamma_n := \Delta_{n+1} \circ W_n \circ \Delta_n^{-1} .$$ Then - the following diagram commutes $$\xymatrix{ \cdots \ar[rr]^{ W_{n-1} } & & {\mathbb {D}}^k ( \rho^\gamma_n) \ar[rr]^{ W_n } \ar[d]_{\Delta_n} & & {\mathbb {D}}^k(\rho^\gamma_{n+1}) \ar[rr]^{ W_{n+1} } \ar[d]_{\Delta_{n+1}} & &\cdots \\ \cdots \ar[rr]^{ W^\gamma_{n-1} } & & {\mathbb {D}}^k(\rho_n) \ar[rr]^{ W^\gamma_n } & & {\mathbb {D}}^k(\rho_{n+1}) \ar[rr] ^{ W^\gamma_{n+1} } & &\cdots }$$ - ${{\rm Lip \, }}W_n^\gamma = \theta e^\gamma <1$ and the linear part $A_n^\gamma := e^\gamma A_n$ of $W_n^\gamma$ satisfies $$e^{-\Lambda_1 - \epsilon + \gamma} \abs{v} \leq \abs{A^\gamma_n(v)} \leq e^{-\Lambda_l + \epsilon + \gamma} \abs{v} \ \ \textrm{for every} \ v \in {\mathbb {C}}^k .$$ Recall that according to Constraints \[nota\] we have $\theta e^{2 \gamma} = e^{-\Lambda_l +2\epsilon +2 \gamma} < 1$ and $(\rho_n^\gamma)_{n\in {\mathbb {Z}}}$ is $2\gamma$-slow since $\epsilon < \gamma$. In particular ${{\rm Lip \, }}W_n^\gamma = e^\gamma {{\rm Lip \, }}W_n = e^\gamma \theta<1$. It remains to check that $W_n : {\mathbb {D}}^k(\rho^\gamma_n) \to {\mathbb {D}}^k(\rho^\gamma_{n+1})$, which is clear since $\rho^\gamma_n \cdot {{\rm Lip \, }}W_n \le \rho^\gamma_n \theta \leq \rho^\gamma_{n+1} \theta e^{2\gamma} <\rho^\gamma_{n+1}$.[\ ]{} Step 2 : Improving the order of contact with the linear part {#step-2-improving-the-order-of-contact-with-the-linear-part .unnumbered} ------------------------------------------------------------ \[thm1\] Let $W_n : {\mathbb {D}}^k (\rho_n) \to {\mathbb {D}}^k(\rho_{n+1})$ be a sequence of holomorphic contractions satisfying the assumptions of Theorem B. Let $W^\gamma_n : {\mathbb {D}}^k ( \rho_n) \to {\mathbb {D}}^k(\rho_{n+1})$ be the sequence of holomorphic contractions given by Lemma \[decal\]. There exist a ${\epsilon}$-slow sequence $(r_n)_n \leq (\rho_n)_n$ and a sequence of holomorphic maps $$T^1_n : {\mathbb {D}}^k (r_n) \to {\mathbb {D}}^k (2r_n)$$ such that $d_0 T_n^1 = {{\rm Id}}_{{\mathbb {C}}^k}$ and 1. $\forall n \in {\mathbb {Z}}$, $\forall (u,v) \in {\mathbb {D}}^k(r_n) \times {\mathbb {D}}^k(r_n)$, $e^{-{\epsilon}} \abs{u-v} \leq \abs{T_n^1 (u) - T_n^1 (v)} \leq e^{\epsilon}\abs{u-v}$ , 2. the following diagram commutes $$\xymatrix{ \cdots \ar[rr]^{ W^\gamma_{n-1} } & & {\mathbb {D}}^k (r_n) \ar[rr]^{ W^\gamma_n } \ar[d]_{T^1_n} & & {\mathbb {D}}^k( r_{n+1}) \ar[rr]^{ W^\gamma_{n+1} } \ar[d]_{T^1_{n+1}} & &\cdots \\ \cdots \ar[rr]^{ X_{n-1} } & & {\mathbb {D}}^k(2 r_n) \ar[rr]^{ X_n } & & {\mathbb {D}}^k(2 r_{n+1}) \ar[rr] ^{ X_{n+1} } & &\cdots }$$ where $X_n = A^\gamma_n + O([\Lambda^\gamma_1 / \Lambda^\gamma_l] +2)$ for every $n \in {\mathbb {Z}}$. The proof consists in applying a finite number of times Lemma \[iter\] below. Let us say for convenience that a sequence $(G_n)_{n \in {\mathbb {Z}}}$ of holomorphic mappings $G_n : {\mathbb {D}}^k(a_n) \to {\mathbb {D}}^k(a_{n+1})$ is ${\epsilon}$-*slow* if $(a_n)_{n \in {\mathbb {Z}}}$ is a $\epsilon$-slow sequence. Assume that the linear part of such a sequence $(G_n)_{n \in {\mathbb {Z}}}$ is equal to $(A^\gamma_n)_{n \in {\mathbb {Z}}}$. Then, according to our discussion in Subsection \[RC\], the $\Lambda_j^\gamma$’s do not satisfy any resonance relation and thus, given any integer $p \geq 2$, Lemma \[iter\] allows to conjugate $(G_n)_{n \in {\mathbb {Z}}}$ to some new ${\epsilon}$-*slow* sequence whose linear part is still equal to $(A^\gamma_n)_{n \in {\mathbb {Z}}}$ but with no homogeneous part of degree $p$ in its Taylor expansion. The cancellation of the $p$-homogeneous part of $(G_n)_{n \in {\mathbb {Z}}}$ relies on the resolution of some so-called homological equations. We shall only sketch the proofs, the details are in [@BDM Subsection 3.2] or [@JV]. \[iter\] Let $\left(G_n \right)_{n\in {\mathbb {Z}}}$ be a ${\epsilon}$-slow sequence of holomorphic contractions fixing the origin and whose linear part is equal to $(A^\gamma_n)_{n \in {\mathbb {Z}}}$. Let $p \geq 2$ and let $G_n^{(p)}$ be the $p$-homogeneous part of the Taylor expansion of $G_n$. Then: 1. there exists a sequence of $p$-homogeneous polynomial maps $(H_n)_{n \in {\mathbb {Z}}}$ such that $$\forall n \in {\mathbb {Z}}\ \ , \ \ G_n^{(p)} + H_{n+1} \circ A^\gamma_n - A^\gamma_n \circ H_n = 0 ,$$ 2. for $S^{(p)}_n := {{\rm Id}}+ H_n$ and ${\epsilon}' > 0$ there exists a ${\epsilon}$-slow sequence $(\tau_n)_{n \in {\mathbb {Z}}}$ such that $$\forall n \in {\mathbb {Z}}\ \ , \ \ \forall (u,v) \in {\mathbb {D}}^k(\tau_n) \times {\mathbb {D}}^k(\tau_n) \ \ , \ \ e^{-{\epsilon}'} \abs{u-v} \leq \abs{S^{(p)}_n (u) - S^{(p)}_n (v)} \leq e^{{\epsilon}'} \abs{u-v}$$ and for which the following diagram commutes $$\xymatrix{ \cdots \ar[rr]^{ G_{n-1} } & & {\mathbb {D}}^k (\tau_n) \ar[rr]^{ G_n } \ar[d]_{S^{(p)}_n} & & {\mathbb {D}}^k(\tau_{n+1}) \ar[rr]^{ G_{n+1} } \ar[d]_{S^{(p)}_{n+1}} & &\cdots \\ \cdots \ar[rr]^{ G^{\widehat p}_{n-1} } & & {\mathbb {D}}^k(e^{\epsilon}\tau_n) \ar[rr]^{ G^{\widehat p}_n } & & {\mathbb {D}}^k(e^{\epsilon}\tau_{n+1}) \ar[rr] ^{ G^{\widehat p}_{n+1} } & &\cdots }$$ where $G^{\widehat p}_n = A_n^\gamma + G_n^{(2)} + \cdots + G_n^{(p-1)} + 0 + O(p+1)$. Proof of Proposition \[thm1\] {#proof-of-proposition-thm1 .unnumbered} ----------------------------- Let $p^* := [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 1$ and $\epsilon ' := \epsilon / p^*$. We successively apply Lemma \[iter\] with $$p = 2 \ , \ G_n = W_n^\gamma \ ,$$ and then with $$p=3 \ , \ G_n = (W_n^{\gamma})^{\widehat 2} \ ,$$ and so on, up to $$p = p^* \ , \ G_n = (\cdots ((((W^\gamma_n)^{\widehat {2}})^{\widehat 3})^{\widehat 4}) \cdots ) ^{\widehat{p^*-1}} \ .$$ This yieds a ${\epsilon}$-slow sequence $(r_n)_n \leq (\rho_n)_n$ such that the following diagram commutes $$\xymatrix{ \cdots \ar[rr]^{ W^\gamma_{n-1} } & & {\mathbb {D}}^k (r_n) \ar[rr]^{ W^\gamma_n } \ar[d]_{T^1_n} & & {\mathbb {D}}^k( r_{n+1}) \ar[rr]^{ W^\gamma_{n+1} } \ar[d]_{T^1_{n+1}} & &\cdots \\ \cdots \ar[rr]^{ X_{n-1} } & & {\mathbb {D}}^k(e^{p^* {\epsilon}} r_n) \ar[rr]^{ X_n } & & {\mathbb {D}}^k(e^{p^* {\epsilon}} r_{n+1}) \ar[rr] ^{ X_{n+1} } & &\cdots }$$ where $$X_n := (\cdots ((((W^\gamma_n)^{\widehat {2}})^{\widehat 3})^{\widehat 4}) \cdots ) ^{\widehat{p^*}} = A^\gamma_n + O([\Lambda^\gamma_1 / \Lambda^\gamma_l] +2)$$ and $$T^1_n := S^{(p^*)}_n \circ \cdots \circ S^{(2)}_n .$$ Since $p^* {\epsilon}< \frac{1}{2} \ln 4$ by Constraints \[nota\], we have $T^1_n : {\mathbb {D}}^k(r_n) \to {\mathbb {D}}^k(2 r_n)$. Since $p^* {\epsilon}' = \epsilon$, we also have $e^{-{\epsilon}} \abs{u-v} \leq \abs{T_n^1 (u) - T_n^1 (v)} \leq e^{\epsilon}\abs{u-v}$ on ${\mathbb {D}}^k(r_n)$. Proof of Lemma \[iter\] {#proof-of-lemma-iter .unnumbered} ----------------------- To prove Item 1 amounts to show that the following linear operator $\Gamma$, defined on the space of slow sequences of $p$-homogeneous mappings, is surjective: $$\Gamma : (H_n)_{n \in {\mathbb {Z}}} \mapsto (H_{n+1} \circ A^\gamma_n - A^\gamma_n \circ H_n)_{n \in {\mathbb {Z}}} .$$ To simplify we suppose that every exponent $\Lambda_j$ has multiplicity $k_j = 1$ (therefore $l=k$ and $\lambda_j = \Lambda_j$ for $1\le j\le k$). Let us fix $${\alpha}\in {\mathbb {N}}^k \textrm{ such that } 2 \leq \vert \alpha \vert \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 1.$$ We are going to exhibit a preimage for $\Gamma$ to the sequence $$G_n^{(p)} = (0,\cdots, a_n z^{\alpha}, \cdots , 0) ,$$ where $a_n z^{\alpha}$ is at the $j$-th place. For this purpose, we shall use the control ${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j \notin [-b , b] $ (see Subsection \[RC\]) and treat separately the cases ${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j>b$ and ${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j< -b$. In the first case, we shall solve the equation $\Gamma ( (H_n)_{n \in {\mathbb {Z}}} ) = ( G_n ^{(p)})_{n \in {\mathbb {Z}}}$ by averaging on $n\geq 0$ (which correspond to the past of $\hat x$) and by averaging on $n\leq 0$ (which correspond to the future of $\hat x$) in the second case.\ $\bullet$ If ${\alpha}_1\lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j > b$, we set $$\label{plp} \forall n \in {\mathbb {Z}}\ \ , \ \ H_n := (A_n^{\gamma}) ^{-1} G_n^{(p)} + \sum_{r \geq 1} (A^\gamma_n) ^{-1} \cdots (A^\gamma_{n+r})^{-1} \ G_{n+r}^{(p)} \ A^\gamma_{n+r-1} \cdots A^\gamma_n .$$ A formal computation shows that $\Gamma ( (- H_n)_{n \in {\mathbb {Z}}} ) = ( G_n ^{(p)} )_{n \in {\mathbb {Z}}}$, which means: $$\forall n \in {\mathbb {Z}}\ \ , \ \ G_n^{(p)} + H_{n+1} \circ A^\gamma_n - A^\gamma_n \circ H_n = 0 .$$ The convergence of the series (\[plp\]) relies on the block diagonal property of $(A^\gamma_n)_{n \in {\mathbb {Z}}}$. To simplify, let us assume that the $(A^\gamma_n)$ are truly diagonal. Writing $H_n$ as $H_n = P_{n,0} + \sum_{r \geq 1} P_{n,r}$, we obtain $$\begin{array}{rcl} \abs{P_{n,r}(z)} & \leq & \abs{ (A^\gamma_n) ^{-1} \, \cdots \, (A^\gamma_{n+r}) ^{-1} \ G_{n+r}^{(p)} \, \left( \, e^{ - r \lambda^\gamma_1 + r {\epsilon}} \, z_1 \, , \, \cdots \, , \, e^{- r \lambda^\gamma_k + r {\epsilon}} \, z_k \, \right) } \\ & \leq & \abs{ (A^\gamma_n) ^{-1} \, \cdots \, (A^\gamma_{n+r}) ^{-1} \ \left( 0 \, , \, \cdots \, , \, a_{n+r} \, e^{ - r (\, {\alpha}_1 \lambda^\gamma_1 \, + \, \cdots \, + \, {\alpha}_k \lambda^\gamma_k \, ) + \abs{{\alpha}} r {\epsilon}} \, z^{\alpha}\, , \, \cdots \, , \, 0 \, \right) } \\ & \leq & e^{r \Lambda^\gamma_j + r {\epsilon}} \, e^{ - r ( \, {\alpha}_1 \lambda^\gamma_1 \, + \, \cdots \, + \, {\alpha}_k \lambda^\gamma_k \, ) + \abs{{\alpha}} r {\epsilon}} \, \abs{a_{n+r}} \, \abs{z^{\alpha}} \\ & \leq & e^{ - r b} e^{ r ( \abs{{\alpha}} + 1 ) {\epsilon}} \, \abs{a_{n+r}} \, \abs{z^{\alpha}} \\ & \leq & e^{ - r b } e^{ r ( [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 3 ) {\epsilon}} \, \abs{a_n} \, \abs{z^{\alpha}}. \end{array}$$ where the last inequality uses $\vert \alpha \vert \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 1$ and the fact, easily checked by using Cauchy’s estimates, that $(a_n)_{n \in {\mathbb {Z}}}$ is a ${\epsilon}$-slow sequence. By Constraints \[nota\], $b - ( [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 3 ) {\epsilon}> 0$ and thus the series (\[plp\]) converge.\ $\bullet$ If ${\alpha}_1\lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_i < -b$, we proceed as before by setting $$\forall n \in {\mathbb {Z}}\ \ , \ \ H_n := - G_{n-1}^{(p)} (A^\gamma_n)^{-1} - \sum_{r \geq 1} A^\gamma_{n-1} \cdots A^\gamma_{n-r} \ G_{n-(r+1)}^{(p)} \ (A^\gamma_{n-r}) ^{-1} \cdots (A^\gamma_n)^{-1} .$$ Let us now deal with Item 2 of Lemma \[iter\]. We first set $S^{(p)}_n := {{\rm Id}}+ H_n$ and observe that $(S^{(p)}_n)^{-1} = {{\rm Id}}- H_n + O(p+1)$ and $$(S^{(p)}_{n+1})^{-1} \circ G_n \circ S^{(p)}_n = \left( A^\gamma_n + G_n^{(2)} + \cdots + G_n^{(p-1)} \right) + \left( G_n^{(p)} + H_{n+1} \circ A^\gamma_n - A^\gamma_n \circ H_n \right) + O(p+1).$$ The second term in the right hand side vanishes by construction of $(H_n)_n$. Finally, Lemma \[NNbis\] on bundle maps ensures the existence of a ${\epsilon}$-slow sequence $(\tau_n)_n$ satisfying the required properties.\ In order to prove the general case where $G_n^{(p)}$ is a $p$-homogeneous map but not a monomial map, we proceed by linearity in Item 1 to obtain: $$G_n^{(p)} + \sum H^{j,\alpha}_{n+1} \circ A^\gamma_n - A^\gamma_n \circ \sum H^{j,\alpha}_n = 0 ,$$ where the sum ranges over $j \in \{ 1 , \cdots , l \}$ et $\vert \alpha \vert = p$. Item 2 then follows by performing the change of coordinates $S^{(p)}_n := {{\rm Id}}+ \sum H^{j,\alpha}_n$. [\ ]{} Step 3: Conjugation to a linear mapping and conclusion {#step-3-conjugation-to-a-linear-mapping-and-conclusion .unnumbered} ------------------------------------------------------ Proposition \[iter2\] below is a special case of Theorem 1.1 in [@BDM], it shows that a slow sequence of holomorphic mappings $(X_n)_{n \in {\mathbb {Z}}}$ is conjugated to the sequence of its linear part $(A^\gamma_n)_{n \in {\mathbb {Z}}}$ once these two sequences have a sufficiently large contact order. Let us stress that this step does not require the fact that $(A_n^\gamma)_{n \in {\mathbb {Z}}}$ is block diagonal. \[iter2\] Let $(X_n)_{n \in {\mathbb {Z}}}$ be a ${\epsilon}$-slow sequence of holomorphic mappings with linear parts $(A^\gamma_n)_{n \in {\mathbb {Z}}}$. Assume that there exist $0 < m \leq M <1$ such that $$\forall n \in {\mathbb {Z}}\ \ , \ \ \forall v \in {\mathbb {C}}^k \ \ , \ \ m \abs v \leq \abs{A^\gamma_n (v)} \leq M \abs v$$ and that $$X_n = A^\gamma_n + O(q+1) \ \ \textrm{ where $q \geq 1$ satisfies } \ \ ( M e^{2{\epsilon}} ) ^{q+1} < m e^{-\epsilon} .$$ Then there exist a ${\epsilon}$-slow sequence $(r_n)_{n\in {\mathbb {Z}}}$ and a sequence $\left(T_n^2\right)_{n\in Z}$ of holomorphic mappings $T_n^2 : {\mathbb {D}}^k (r_n) \to {\mathbb {D}}^k (2r_n)$ such that $d_0 T_n^2 = {{\rm Id}}$ and 1. $\forall n \in {\mathbb {Z}}$, $\forall (u,v) \in {\mathbb {D}}^k(r_n) \times {\mathbb {D}}^k(r_n)$, $e^{-{\epsilon}} \abs{u-v} \leq \abs{T_n^2 (u) - T_n^2 (v)} \leq e^{\epsilon}\abs{u-v}$ , 2. the following diagram commutes: $$\xymatrix{ \cdots \ar[rr]^{ X_{n-1} } & & {\mathbb {D}}^k (r_n) \ar[rr]^{ X_n } \ar[d]_{T^2_n} & & {\mathbb {D}}^k(r_{n+1}) \ar[rr]^{ X_{n+1} } \ar[d]_{T^2_{n+1}} & &\cdots \\ \cdots \ar[rr]^{ A^\gamma_{n-1} } & & {\mathbb {D}}^k(2r_n) \ar[rr]^{ A^\gamma_n } & & {\mathbb {D}}^k(2r_{n+1}) \ar[rr] ^{ A^\gamma_{n+1} } & &\cdots }$$ Proof of Proposition \[iter2\] {#proof-of-proposition-iter2 .unnumbered} ------------------------------ To deduce the Proposition from Theorem 1.1 of [@BDM] we observe that the proof of this theorem starts by fixing a number $\theta$ such that $M^{q+1}/m<\theta<1$ and then chosing $\epsilon >0$ small enough so that $Me^{2\epsilon} \le 1$ and $e^{(q+3)\epsilon} M^{q+1}/m \le \theta$. Our assumption $(M e^{2{\epsilon}} ) ^{q+1} < me^{-\epsilon}$ implies both of these conditions, with $\theta=e^{-q\epsilon}$ for the second one. For the reader’s convenience we now sketch the proof of Proposition \[iter2\], details can be found in [@BDM Subsection 3.1]. Let $n \in {\mathbb {Z}}$ and let $$\forall p \geq 0 \ , \ A^\gamma_{p,n} := A^\gamma_{n+p} \circ \cdots \circ A^\gamma_n \ \ , \ \ X_{p,n} := X_{n+p} \circ \cdots \circ X_n$$ with the convention $A^\gamma_{-1,n} = X_{-1,n} = {{\rm Id}}$. The germs of formal limits $$T^2_n := \lim_{p \to + \infty} (A^\gamma_{p,n}) ^{-1} \circ X_{p,n}$$ satisfy $d_0 T_n^2 = Id$ and give the commutative diagram of Proposition \[iter2\]. Let us show the convergence by induction. Let $\beta := (Me^{2{\epsilon}}) ^{q+1} / m < 1$ and consider the assertion $$\PP(p) \ : \ \forall n \in {\mathbb {Z}}\ , \ \abs{ ((A^\gamma_{p,n}) ^{-1} \circ X_{p,n} - (A^\gamma_{p-1,n}) ^{-1} \circ X_{p-1,n}) (v) } \leq ( \beta^{p} / m r_n^{q+1} ) \, \abs{v}^{q+1} .$$ Then $\PP(0)$ is satisfied: the property $X_n = A^\gamma_n + O(q+1)$ indeed shows that $$\forall n \in {\mathbb {Z}}\ , \ \abs{ ( (A^\gamma_n)^{-1} \circ X_n - {{\rm Id}}) (v) } = \abs{ (A^\gamma_n)^{-1} \circ ( X_n - A^\gamma_n) (v) } \leq ( 1 / m r_n^{q+1} ) \abs{v}^{q+1} .$$ The real numbers $m$ and $r_n^{q+1}$ respectively come from the lower bound $m \abs v \leq \abs{A^\gamma_n (v)}$ and from an estimate of $(X_n - A^\gamma_n) (v)$ using Cauchy’s estimates. Now we show that $\PP(p)$ implies $\PP(p+1)$. Let us perform a right composition of $\PP(p)$ by $X_n$ (we have also replaced $n$ by $n+1$): $$\forall n \in {\mathbb {Z}}\ , \ \abs{ ((A^\gamma_{p,n+1})^{-1} \circ X_{p,n+1} - (A^\gamma_{p-1,n+1}) ^{-1} \circ X_{p-1,n+1} ) (X_n(v)) } \leq ( \beta^{p} / m r_{n+1}^{q+1} ) \abs{X_n(v)}^{q+1} .$$ Then, by using the identity $X_{p,n+1} \circ X_n = X_{p+1,n}$ and the comparison of $X_n$ to its linear part $A_n^\gamma$ given by Lemma \[NN\]: $$\forall n \in {\mathbb {Z}}\ , \ \abs{ ((A^\gamma_{p,n+1})^{-1} \circ X_{p+1,n } - (A^\gamma_{p-1,n+1})^{-1} \circ X_{p,n} ) (v) } \leq ( \beta^{p} / m r_{n+1}^{q+1} ) (M e^{\epsilon})^{q+1} \abs{v}^{q+1} .$$ A left composition by $(A^\gamma_n)^{-1}$ gives by using the fact that $(r_n)_n$ is slow: $$\forall n \in {\mathbb {Z}}\ , \ \abs{ ((A^\gamma_{p+1,n})^{-1} \circ X_{p+1,n } - (A^\gamma_{p,n})^{-1} \circ X_{p,n} ) (v) } \leq ( \beta^{p} / m r_n^{q+1} ) \, {(M e^{2{\epsilon}}) ^{q+1} \over m } \abs{v}^{q+1} .$$ This last quantity is equal to $( \beta^{p+1} / m r_n^{q+1} ) \abs{v}^{q+1}$, which shows $\PP(p+1)$. Finally, it suffices to apply Lemma \[NNbis\] to end the proof of Proposition \[iter2\].[\ ]{}\ To complete the proof of Theorem B, we successively apply Lemma \[decal\], Proposition \[iter\] and Proposition \[iter2\] with $$q = [\Lambda^\gamma_1 / \Lambda^\gamma_l] +1 \ \ , \ \ m = e^{-\Lambda^\gamma_1 - \epsilon + \gamma} \ \ , \ \ M = e^{-\Lambda^\gamma_l + \epsilon + \gamma} .$$ We have $m \abs v \leq \abs{A^\gamma_n (v)} \leq M \abs v$ from Lemma \[decal\] and $(M e^{2{\epsilon}})^{q+1} < m e^{-\epsilon}$ from Lemma \[donne\] (a consequence of Constraints \[nota\]). Theorem B follows by setting $$\varphi_n := T^2_n \circ T^1_n \circ \Delta_n .$$ This completes the proof of Proposition \[iter2\]. Applications ============ We review here some results whose proofs crucially rely on our Distortion Theorem. Proving similar results in the one-dimensional setting requires the classical Koebe distortion Theorem. Multipliers of repelling cycles {#mult} ------------------------------- The following result, first proved in [@BDM], plays an important role in the study of bifurcations within holomorphic families of endomorphisms (see [@Be] and [@BBD]). \[replyap\] Let $f : {\mathbb {P}}^k \to {\mathbb {P}}^k$ be a holomorphic endomorphism of degree $d \geq 2$. Let $\lambda_k \leq \cdots \leq \lambda_1$ be the Lyapunov exponents of its equilibrium measure. Then $$\lim_{n \to + \infty} {1 \over d^{kn}} \sum_{p \in \RR_n} \log {{\rm Jac \, }}f(p) = (\lambda_1 + \cdots + \lambda_k)$$ where $\RR_n$ is the set of $n$-periodic repelling points of $f$. <span style="font-variant:small-caps;">Sketch of proof:</span> To start with, we reprove that the equilibrium measure $\mu$ of $f$ equidistributes the repelling cycles of $f$ (this is a theorem due to Lyubich [@L] for $k=1$ and Briend-Duval [@BD] for $k\ge 1$) we follow here Briend-Duval approach. Let $B : = B_x(r)$ be a small ball around a $\mu$-generic point $x$. Since $\mu$ is mixing, we have $\mu(f^{-n}B \cap B) \simeq \mu(B)^2$ for $n$ large enough. Now let $\FF_n(B)$ be the set of inverse branches $g_n$ of $f^n$ defined on $B$ and with image in $B$. By using $f^*\mu = d^k \mu$ and the fact that the inverse branches are pairwise disjoint, the mixing property gives ${\textsf {Card }}\FF_n(B) \cdot\mu(B) / d^{kn} \simeq \mu (B)^2 $, therefore: $${1 \over d^{kn}} {\textsf {Card }}\FF_n(B) \simeq \mu (B) .$$ Since the Lyapunov exponents of $\mu$ are positive, every element $g_n$ of $\FF_n(B)$ is a contracting map from $B$ to $B$, hence produces a repelling point $p$ for the iterate $f^n$. This implies $${1 \over d^{kn}} {\textsf {Card }}\RR_n \cap B \geq \mu(B) .$$ Thus every cluster measure $\mu'$ of ${1 \over d^{kn}} \sum_{p \in \RR_n} \delta_p$ satisfies $\mu' \geq \mu$. This implies $\mu' = \mu$ since the number of $n$-periodic point of $f$ is bounded above by $d^{kn}$, see [@DS Proposition 1.3].\ To obtain Theorem \[replyap\], we combine the Distortion Theorem with the above arguments to get: $$\label{gqd} \forall g_n \in \FF_n(B) \ , \ \forall p \in g_n(B) \ , \ d_p f^n \simeq d_{g_n(x)} f^n .$$ Since $x$ is $\mu$-generic, we deduce from (\[gqd\]) and from the definition of the Lyapunov exponents: $$\label{estsi} \ {1 \over n} \log \vert {{\rm Jac \, }}f^n(p)\vert \ \simeq \ (\lambda_1 + \cdots + \lambda_k).$$ Let us specify that to make the approximations $\simeq$ precise, one has to work with the natural extension of $f$ and use the estimate concerning the change of coordinates $\varphi_{\hat x , n}$. Dimension of measures {#minor} --------------------- Let $f : {\mathbb {P}}^k \to {\mathbb {P}}^k$ be a holomorphic endomorphism and $\nu$ be an invariant measure. One defines the pointwise dimensions $\underline{d}_{\nu}$ and $\bar{d_{\nu}}$ by $$\forall x \in {\mathbb {P}}^k \ , \ \underline{d}_{\nu}(x) := \liminf_{r \to 0} \, { \log \nu (B_x(r)) \over \log r } \ \ , \ \ \bar{d_{\nu}}(x) := \limsup_{r \to 0} \, { \log \nu (B_x(r)) \over \log r } .$$ When $\nu$ is ergodic, these functions are $\nu$-almost everywhere constant and their generic values are denoted $\underline{d}_{\nu}$ and $\bar{d_{\nu}}$. Young ([@Y]) proved that if $ a \leq \underline{d}_{\nu} \leq \bar{d_{\nu}} \leq b$, then $$a \leq \dim_H(\nu) \leq b,$$ where $\dim_H(\nu) := \inf \{\dim_H(A), A \textrm{ Borel set } , \nu(A) = 1 \}$ is the Hausdorff dimension of $\nu$.\ For the equilibrium measure $\mu$ of any degree $d\ge 2$ holomorphic endomorphism on ${\mathbb {P}}^k$, it has been conjectured by Binder and DeMarco [@BDeM] that $$\dim_H (\mu) = { \log d \over \lambda_1 } + \cdots + { \log d \over \lambda_k }$$ where $\lambda_k \leq \cdots \leq \lambda_1$ are the Lyapunov exponents of $\mu$. When $k=1$, this conjecture corresponds to a result of Mañé [@M] who actually proved that $\underline d_{\mu} = \bar d_\mu = \log d / \lambda$. Our Distortion Theorem allows to obtain the following lower bounds in any dimension. \[mino\] Let $f : {\mathbb {P}}^k \to {\mathbb {P}}^k$ be a holomorphic endomorphism of degree $d \geq 2$. Let $\nu$ be an ergodic measure with positive Lyapunov exponents $\lambda_k \leq \cdots \leq \lambda_1$ and entropy $h_\nu$. Then $$\underline{d}_{\nu} \geq {\log d^{k-1} \over \lambda_1} + { h_\nu - \log d^{k-1} \over \lambda_k } .$$ The following corollary yields the lower bound of the above Conjecture in dimension $k=2$. Let $f : {\mathbb {P}}^2 \to {\mathbb {P}}^2$ be a holomorphic endomorphism of degree $d \geq 2$. Let $\mu$ be its equilibrium measure and let $\lambda_1 \geq \lambda_2$ be the Lyapunov exponents of $\mu$. Then $$\underline d_\mu \geq { \log d \over \lambda_1 } + { \log d \over \lambda_2 }.$$ The proof consists in studying the distribution of inverse branches of $f^n$ in ${\mathbb {P}}^k$ and, in particular, uses an area growth argument which requires a precise description of the geometry of these branches. This is where the Distortion Theorem enters into the picture.\ <span style="font-variant:small-caps;">Sketch of proof:</span> We first establish an upper bound for the cardinality of inverse branches of $f^n$ in generic balls of radius $e^{-n \lambda_k}$. Let $q_n$ be the entire part of $n \lambda_k / \lambda_1$ and let $B_x^{A}(r) := B_x(r) \cap A$.\ [**Fact** ]{}[ *For every ${\epsilon}>0$, there exist $\Omega_{\epsilon}\subset {\mathbb {P}}^k$ and $r > 0$ satisfying $\nu(\Omega_{\epsilon}) > 1 - {\epsilon}$ and the following property. Let $\EE_{r} \subset {\mathbb {P}}^k$ be a maximal $r$-separated subset. Then for every $x \in \Omega_{\epsilon}$ and $n$ large enough, the collection of inverse branches $$\PP_n(x) := \left \{ \, f^{-n}_{\hat y_n} B_p (r) \ , \ y \in B_x^{\Omega_{\epsilon}} (r e^{-n \lambda_k } ) \ , \ p \in \EE_r \ , \ d(p,y_n) < r \, \right \}$$ is well defined and satisfies ${\textsf {Card }}\PP_n(x) \leq d^{(k-1)(n - q_n)} e^{n{\epsilon}}$.* ]{}\ We outline the proof of this Fact in three steps. It relies on Area estimates and on our Distortion Theorem. Let ${\omega}$ denotes the Fubini-Study form on ${\mathbb {P}}^k$ and $\eta : {\mathbb {D}}^{k-1} (2) \to {\mathbb {P}}^k$ be a holomorphic polydisc. The first step is to show that $$\begin{aligned} \label{a} \forall m \geq 1 \ , \ {Area \,}\, f^{m} \circ \eta_{\vert {\mathbb {D}}^{k-1}} := \int_{{\mathbb {D}}^{k-1}} (f^m \circ \eta)^* {\omega}^{k-1} \leq d^{(k-1) m} .\end{aligned}$$ This is obtained by replacing ${\omega}$ by the Green current $T$ of $f$ (using cohomologous arguments and integration by parts) and then using $f^* T = d T$, see [@Di; @D1] for more details. For the second step, let $x \in \Omega_{\epsilon}$ and denote by $\LL_n$ the set of polydiscs $L_n : {\mathbb {D}}^{k-1} \to B_x (e^{-n \lambda_k})$. Applying (\[a\]) to $m = n - q_n$ and $\eta = f^{q_n} \circ L_n$ yields $$\begin{aligned} \label{b} {Area \,}\, f^n \circ L_n = {Area \,}f^{n-q_n} ( f^{q_n} \circ L_n ) \leq d^{(k-1)(n-q_n)} \;\textrm{for every}\; L_n \in \LL_n.\end{aligned}$$ Note that $q_n$ is chosen to produce polydiscs of uniformly bounded sizes. Indeed, since $\lambda_1$ is the largest exponent and since $q_n \lambda_1 \simeq n \lambda_k$, we have $$f^{q_n} (L_n ) \subset f^{q_n} ( B_x (e^{-n \lambda_k}) ) \subset B_{f^{q_n}(x)} (e^{-n \lambda_k} \cdot e^{q_n \lambda_1}) \simeq B_{f^{q_n}(x)}(1) .$$ The third step is to prove the existence of $\FF_n \subset \LL_n$ whose cardinality is at most $e^{n{\epsilon}}$ and such that for every $P_n \in \PP_n(x)$ there exists a $(k-1)$-polydisc $L_n \in \FF_n$ satisfying $$\begin{aligned} \label{c} {Area \,}\, f^n \circ {L_n}_{\vert L_n^{-1}(P_n)} \geq 1 . \end{aligned}$$ This relies on the geometric description of inverse branches given by our Distortion Theorem: every $P_n \in \PP_n(x)$ is indeed a parallelepiped with dimensions $e^{-n \lambda_1} \leq \cdots \leq e^{-n \lambda_k}$. Precisely, the polydisc $L_n$ is transverse to the $e^{-n\lambda_k}$-direction of $P_n$ and $\FF_n$ is a collection of hyperplanes parallel to the coordinates axis. The Fact finally comes from (\[b\]) and (\[c\]) since the inverse branches are pairwise disjoint: this gives ${\textsf {Card }}\PP_n(x) \leq d^{(k-1)(n - q_n)} e^{n{\epsilon}}$ as desired.\ Let us now explain how the Fact implies Theorem \[mino\]. We shall ignore the $e^{\pm n \epsilon}$ error terms due to the non-uniform hyperbolic setting. Let $x \in \Omega_{\epsilon}$ and $\rho_n := e^{-n \lambda_k }$. Since $\PP_n(x)$ covers the generic ball $B_x^{\Omega_{\epsilon}}(\rho_n)$ (Fact) and since $\nu ( P ) \simeq e^{-n h_\nu}$ for every $P \in \PP_n(x)$ (Brin-Katok Theorem), we get $$\nu (B_x^{\Omega_{\epsilon}}(\rho_n) ) \leq \sum_{P \in \PP_n(x)} \nu( P ) \leq \, {\textsf {Card }}\PP_n (x) \cdot e^{-n h_\nu }.$$ The Density Theorem then implies for $\nu$ almost every $x \in \Omega_{\epsilon}$ and for $n$ large enough: $$\nu \left( B_x(\rho_n) \right) \leq 2 \, {\textsf {Card }}\PP_n (x) \cdot e^{-n h_\nu }.$$ The upper bound on ${\textsf {Card }}\PP_n(x)$ given by the Fact yields: $$\label{dff} \liminf_{r \to 0} \, { \log \nu (B_x(r)) \over \log r } \, \geq \, { \log d^{k-1} \over \lambda_1 } + {h_\nu - \log d^{k-1} \over \lambda_k} .$$ This estimate occurs $\nu$-almost everywhere since $\Omega :=\limsup \Omega_{1/q}$ has full $\nu$-measure. Dimension of currents {#currents} --------------------- In this Subsection we study the thickness of currents $S$ supporting dilating ergodic measures. Precisely, we focus on a lower bound on their local upper pointwise dimension. Let $S$ be a positive closed current of bidegree $(1,1)$ on ${\mathbb {P}}^2$ and let $$\forall x \in {\mathbb {P}}^2 \ , \ \bar{d_S}(x) := \limsup_{r \to 0} \frac{\log S \wedge \omega (B_x(r))}{\log r} .$$ We have $\bar{d_S}(x) \geq 2$, see [@D Chapitre 3, §5]. For every $\Lambda \subset {\mathbb {P}}^2$, we set $$\bar{d_S}(\Lambda) := \sup_{x \in \Lambda} \bar{d_S}(x) .$$ \[dTV\] Let $f : {\mathbb {P}}^2 \to {\mathbb {P}}^2$ be a holomorphic endomorphism of degree $d \geq 2$. Let $S$ be a positive closed current on ${\mathbb {P}}^2$ of bidegree $(1,1)$ and mass $1$. Let $\nu$ be an ergodic measure with positive Lyapunov exponents $\lambda_1 \geq \lambda_2$. Assume that ${{\rm supp \, }}(\nu) \subset {{\rm supp \, }}(S)$. Let $\Lambda \subset {{\rm supp \, }}(\nu)$ be a Borel set such that $\nu(\Lambda) > 0$. Then $$\bar{d_S}(\Lambda) \geq 2 {\lambda_2 \over \lambda_1} + {h_\nu - \log d \over \lambda_1} .$$ The proof in [@dTV] uses delicate slicing arguments to analyse the pullback action of $f^n$ on $\omega$, our Distortion theorem allows to replace these arguments. As before we shall ignore the $e^{\pm n \epsilon}$ error terms due to the non-uniform hyperbolic setting.\ [Sketch of the proof:]{} Since $(f^n)^* \omega$ is cohomologous to $d^n \omega$ on ${\mathbb {P}}^2$ we have $$\label{dt1} d^n = \int_{{\mathbb {P}}^2} S \wedge (f^n)^* \omega = \int_{{\mathbb {P}}^2} (f^n)_* S \wedge \omega .$$ Let $\{ x_i \, , \, 1 \leq i \leq N_n \}$ be a $(n,2\eta)$-separated subset of $\Lambda$. Brin-Katok Theorem implies that $N_n \simeq e^{n h_\nu}$. Since the dynamical balls $(B_n(x_i, \eta))_i$ are pairwise disjoint, we get $$\label{dt2} \int_{{\mathbb {P}}^2} (f^n)_* S \wedge \omega \geq \sum_{i=1}^{N_n} \int_{{\mathbb {P}}^2} (f^n)_* \left( 1_{B_n(x_i, \eta)} S \right) \wedge \omega = \sum_{i=1}^{N_n} \int_{B_n(x_i, \eta)} S \wedge (f^n)^* \omega .$$ Now we use $B_{x_i} (\eta e^{-n \lambda_1 }) \subset f^{-n}_{{\hat f}^n(\hat x_i)} (B_{f^n(x_i)}(\eta)) \subset B_n(x_i, \eta)$ and $(f^n)^* \omega \geq e^{2n \lambda_2 } \omega$, which can be proved by using the Distortion Theorem. Combining this with (\[dt1\]) and (\[dt2\]) we obtain $$d^n \geq e^{2n \lambda_2 } \sum_{i=1}^{N_n}( S\wedge \omega ) ( B_{x_i} (\eta e^{-n \lambda_1}) ) .$$ From the definition of $\bar{d_S}(x_i)$, and then from the definition of $\bar{d_S}(\Lambda)$ and $N_n \simeq e^{n h_\nu}$ we get $$d^n \geq e^{2n \lambda_2 } \sum_{i=1}^{N_n} (\eta e^{-n \lambda_1}) ^{\bar{d_S}(x_i)} \geq e^{2n \lambda_2 } e^{n h_\nu} (\eta e^{-n \lambda_1}) ^{\bar{d_S}(\Lambda)} .$$ The comparison of the exponential growth rates gives the desired lower bound on ${\bar{d_S}(\Lambda)}$. Appendix {#app} ======== Bundle maps {#bundle} ----------- Let us recall that $\CC$ is the critical set of $f$, that $$X = \{ \hat x = (x_n)_{n \in {\mathbb {Z}}} \, \colon \, x_{n+1}=f(x_n) \ , \ x_n \notin \CC \ , \ \forall n \in {\mathbb {Z}}\}$$ and that $\tau : X \to X$ is the right shift sending $(\cdots,x_{-1},x_0,x_1,\cdots)$ to $(\cdots,x_{-2},x_{-1},x_0,\cdots)$. We denote $$E := \cup_{\hat x \in X} \{ \hat x \} \times {\mathbb {C}}^k$$ and $E_{\hat x} := \{ \hat x \} \times {\mathbb {C}}^k$. For every positive real number $a >0$ we denote $E_{\hat x}(a) := \{ \hat x \} \times {\mathbb {D}}^k(a)$. More generally, for every positive function $a : X \to {\mathbb {R}}^+_*$, we let $E_{\hat x}(a) := E_{\hat x}(a(\hat x))$ and $$E(a) := \cup_{\hat x \in X} E_{\hat x}(a) = \cup_{\hat x \in X} \{ \hat x \} \times {\mathbb {D}}^k(a (\hat x)) .$$ Let ${\sigma}\in \{ {{\rm Id}}_X , \tau \}$ and $a, b : X \to {\mathbb {R}}^+_*$ be two positive functions. A *bundle map $\KK : E(a) \to E(b)$ over ${\sigma}$* is a map of the form $$\KK(\hat x,v) = ({\sigma}(\hat x) , K_{\hat x}(v)),$$ where $$\ K_{\hat x} : E_{\hat x}(a(\hat x)) \to E_{{\sigma}(\hat x)}(b ({\sigma}(\hat x)))$$ is holomorphic and satisfies $K_{\hat x}(0)=0$ for every $ \hat x \in X$. The *linear tangent* bundle map $d_0\KK : E \to E$ is defined by $$d_0\KK (\hat x,v) = (\sigma(\hat x) , d_0 K_{\hat x} (v)).$$ We say that $\KK$ is *tame* if there exist a ${\epsilon}$-slow function $r_{\epsilon}$ and a ${\epsilon}$-fast function $s_{\epsilon}$ satisfying $$\KK : E(r_{\epsilon}) \to E(s_{\epsilon}) .$$ Results on tame bundle maps {#tamebundle} --------------------------- The following lemma simply relies on Cauchy’s estimates, see [@BDM Lemma 2.3]. It implies in particular that if $\KK$ is tame with a contracting linear part, then $\KK : E(a_{\epsilon}) \to E(a_{\epsilon})$ for some $\epsilon$-slow function $a_{\epsilon}$ and thus $\KK$ can be iterated. \[NN\] Let ${\sigma}\in \{ {{\rm Id}}_X, \tau \}$, let $\epsilon >0$ and let $\KK$ be a tame bundle map over ${\sigma}$. Assume that there exist $0< \alpha \leq \beta$ such that $$\forall {\hat x} \in X \ \ , \ \ \forall v \in {\mathbb {C}}^k \ \ , \ \ \alpha \abs{v} \leq \abs{d_0 K_{\hat x}(v)} \leq \beta \abs{v} .$$ Then the following estimates occur. 1. For every $\kappa > 0$, there exists a ${\epsilon}$-slow function $\phi_{\epsilon}: X \to ]0,1]$ such that $$\forall \hat x \in X \ , \ {{\rm Lip \, }}(K_{\hat x} - d_0 K_{\hat x}) \leq \kappa \textrm{ on } E_{\hat x}(\phi_{\epsilon}) .$$ 2. For every ${\epsilon}' >0$, there exists a ${\epsilon}$-slow function $\phi_{\epsilon}: X \to ]0,1]$ such that $$\forall \hat x \in X \ , \ \forall (u,v) \in E_{\hat x}(\phi_{\epsilon}) \times E_{\hat x}(\phi_{\epsilon}) \ , \ \alpha e^{-{\epsilon}'} \abs{u-v} \leq \abs{K_{\hat x}(u) - K_{\hat x}(v)} \leq \beta e^{{\epsilon}'} \abs{u-v} .$$ In particular, if $\beta < 1$ (contracting case) and if $\beta e^{{\epsilon}'} \leq e^{-{\epsilon}}$, then $$\KK : E(\psi_{\epsilon}) \to E(\psi_{\epsilon})$$ for every $\epsilon$-slow function $\psi_{\epsilon}$ satisfying $\psi_{\epsilon}\leq \phi_{\epsilon}$. Let $\epsilon, \epsilon' , \kappa >0$. Since $\KK$ is tame, there exist a ${\epsilon}/3$-slow (resp. fast) function $r_{{\epsilon}/3}$ (resp. $s_{{\epsilon}/3})$ such that $\KK : E(r_{{\epsilon}/3}) \to E(s_{{\epsilon}/3})$. Let $\hat x \in X$. Cauchy’s estimates on $E_{\hat x}({1 \over 2} r_{{\epsilon}/3})$ bound the second derivatives of $K_{\hat x}$ by $c s_{{\epsilon}/3}({\sigma}(\hat x)) /r_{{\epsilon}/3}(\hat x)^2$ where the constant $c$ only depends on the dimension $k$. We deduce that for every $\rho \leq {1 \over 2} r_{{\epsilon}/3}(\hat x)$: $$\label{aze} \forall t \in E_{\hat x}(\rho) \ , \ \abs{d_t (d_0 K_{\hat x} - K_{\hat x})} = \abs{d_0 K_{\hat x} - d_t K_{\hat x}} \leq { c s_{{\epsilon}/3}({\sigma}(\hat x)) \over r_{{\epsilon}/3}(\hat x)^2} \rho.$$ Let us define $$\phi_{\epsilon}:= {r_{{\epsilon}/3}^2 \over c s_{{\epsilon}/3}\circ {\sigma}} \min \{ (e^{{\epsilon}'} - 1) \beta \, , \, (1-e^{-{\epsilon}'}) \alpha \, , \, \kappa \} ,$$ which is a ${\epsilon}$-slow function. Item 1 is then a consequence of (\[aze\]). To verify Item 2 we put $\rho = \phi_{\epsilon}$ in (\[aze\]) to obtain the following estimates on $E_{\hat x}(\phi_{\epsilon})$: $$\begin{array}{rcl} \abs{K_{\hat x}(u) - K_{\hat x}(v)} & \leq & \abs{ d_0 K_{\hat x} (u) - d_0 K_{\hat x} (v) } + \abs {(d_0 K_{\hat x} - K_{\hat x})(u) - (d_0 K_{\hat x} - K_{\hat x})(v)} \\ & \leq & \beta \abs{u-v} + {c s_{{\epsilon}/3}({\sigma}(\hat x)) \over r_{{\epsilon}/3}(\hat x)^2} \phi_{\epsilon}(\hat x) \abs{u-v} \\ & \leq & \beta e^{{\epsilon}'} \abs{u-v}. \end{array}$$ We obtain similarly $\abs {K_{\hat x}(u) - K_{\hat x}(v)} \geq \alpha e^{-{\epsilon}'} \abs{u-v}$. If $\beta e^{{\epsilon}'} \leq e^{-{\epsilon}}$ and if $\psi_{\epsilon}$ is a $\epsilon$-slow function satisfying $\psi_{\epsilon}\leq \phi_{\epsilon}$ then $\abs {K_{\hat x}(u)} \leq \beta e^{{\epsilon}'} \psi_{\epsilon}(\hat x) \leq e^{-{\epsilon}} \psi_{\epsilon}(\hat x) \leq \psi_{\epsilon}({\sigma}(\hat x))$ on $E(\psi_{\epsilon})$. [\ ]{} The next lemma is useful for conjugating bundle maps, it is a corollary of Lemma \[NN\]. \[NNbis\] Let $\MM$ be a tame bundle map over ${{\rm Id}}_X$ and let $\LL$ be a tame bundle map over $\tau$. We assume that $d_0 \MM = ({{\rm Id}}_X , {{\rm Id}}_{{\mathbb {C}}^k})$ and that there exist $0< \alpha \leq \beta < 1$ such that $$\forall {\hat x} \in X \ \ , \ \ \forall v \in {\mathbb {C}}^k \ \ , \ \ \alpha \abs{v} \leq \abs{d_0 L_{\hat x}(v)} \leq \beta \abs{v} .$$ Let $0 < {\epsilon}' < {\epsilon}$ such that $\beta e^{{\epsilon}'} < e^{-{\epsilon}}$. Then there exists a $\epsilon$-slow function $\phi_{\epsilon}$ such that for every $\epsilon$-slow function $\psi_{\epsilon}\leq \phi_{\epsilon}$, 1. the bundle map $\tilde \LL := \MM \circ \LL \circ \MM^{-1}$ is well defined on $E(e^{\epsilon}\psi_{\epsilon})$. 2. the following diagram commutes: $$\xymatrix{ E(\psi_{\epsilon}) \ar[rrr]^{ \LL } \ar[d]_{\MM}& & & E(\psi_{\epsilon}) \ar[d]_{\MM} \\ E(e^{\epsilon}\psi_{\epsilon}) \ar[rrr]^{ \tilde \LL } & & & E(e^{\epsilon}\psi_{\epsilon}) . }$$ 3. $\forall \hat x \in X$, $\forall (u,v) \in E_{\hat x}(\psi_{\epsilon}) \times E_{\hat x}(\psi_{\epsilon})$, $e^{-{\epsilon}'} \abs{u-v} \leq \abs{M_{\hat x}(u) - M_{\hat x}(v)} \leq e^{{\epsilon}'} \abs{u-v}$ . Let $0 < {\epsilon}' < {\epsilon}$ such that $\beta e^{{\epsilon}'} < e^{-{\epsilon}}$. Let $\phi^1_{\epsilon}$ be a ${\epsilon}/3$-slow function provided by Item 2 of Lemma \[NN\] such that $$\forall (u,v) \in E_{\hat x}(\phi^1_{\epsilon}) \times E_{\hat x}(\phi^1_{\epsilon}) \ , \ \abs{L_{\hat x}(u) - L_{\hat x}(v)} \leq \beta e^{{\epsilon}'} \abs{u-v} \leq e^{- {\epsilon}} \abs{u-v} .$$ In particular we have $\LL : E(\phi^1_{\epsilon}) \to E(\phi^1_{\epsilon})$. Let $\phi^2_{\epsilon}$ be a ${\epsilon}/3$-slow function provided by the same lemma such that $$\forall (u,v) \in E_{\hat x}(\phi^2_{\epsilon}) \times \in E_{\hat x}(\phi^2_{\epsilon}) \ , \ e^{-{\epsilon}'} \abs{u-v} \leq \abs{M_{\hat x}(u) - M_{\hat x}(v)} \leq e^{{\epsilon}'} \abs{u-v} ,$$ hence we have $\MM : E(\phi^2_{\epsilon}) \to E(e^{\epsilon}\phi^2_{\epsilon})$. We set $\phi_{\epsilon}:= \min \{ \phi^1_{\epsilon}, \phi^2_{\epsilon}\}$, which is a ${\epsilon}$-slow function. Then $\tilde \LL := \MM \circ \LL \circ \MM^{-1}$ is well defined on $E(e^{-{\epsilon}}\phi_{\epsilon})$ and takes its values in $E(e^{{\epsilon}}\phi_{\epsilon})$. Since $d_0 \tilde \LL = d_0 \LL$ is contracting, we can replace $\phi_{\epsilon}$ by a smaller ${\epsilon}$-slow function to have $\tilde \LL : E(e^{{\epsilon}}\phi_{\epsilon}) \to E(e^{{\epsilon}}\phi_{\epsilon})$. All these properties obviously hold for every $\epsilon$-slow function $\psi_{\epsilon}\leq \phi_{\epsilon}$. Constraints on $\gamma$, $\epsilon$ and cancellation of resonances {#gamma} ------------------------------------------------------------------ We use here the notations introduced in Subsection \[RC\]. Let us recall that $0 < a < \ln 4$ is fixed such that $$\label{rol2} {\alpha}_1\lambda_1 +\cdots +{\alpha}_k \lambda_k - \Lambda_j \notin [-a,a]$$ holds for every $j \in \{ 1 , \cdots , l \}$ and for every ${\alpha}\in {\mathbb {N}}^k\setminus \RRR_j$ satisfying $2 \leq \abs{{\alpha}} \leq [2 \Lambda_1 / \Lambda_l]$. Let us also recall the Constraints \[nota\]. - The number $\gamma >0$ is fixed and sufficently small so that: $\gamma < \Lambda_l / 2 \ \ , \ \ \gamma ( [ \Lambda^\gamma_1 / \Lambda^\gamma_l ] -1)< a/2 \ \ \textrm{ and } \ Ê\ 4 \gamma (\Lambda^\gamma_1 / \Lambda^\gamma_l +1) \leq \Lambda_l^\gamma .$ - Any choice of $\epsilon >0$ is supposed to be small enough so that: $2\epsilon < \gamma \ \ , \ \ 4\epsilon + 2\gamma < \Lambda_l \ \ \textrm{ and } \ Ê\ {\epsilon}( [\Lambda^\gamma_1 / \Lambda^\gamma_l] + 3 ) < {1 \over 2 } \min \{ \gamma , a \} =: b . $ We now prove two elementary results. \[donne\] $ $ 1. For every $j \in \{ 1 , \cdots , l \}$ and every ${\alpha}\in {\mathbb {N}}^k \setminus\RRR_j$ such that $2 \leq \abs{{\alpha}} \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l]$, we have $${\alpha}_1\lambda_1 +\cdots +{\alpha}_k \lambda_k - \Lambda_j \notin [-a,a] .$$ 2. If $q := [\Lambda^\gamma_1 / \Lambda^\gamma_l] +1$, $m := e^{-\Lambda^\gamma_1 - \epsilon + \gamma}$ et $M := e^{-\Lambda^\gamma_l + \epsilon + \gamma}$, then $(M e^{2{\epsilon}})^{q+1} < m e^{-\epsilon}$. The first statement immediately follows from (\[rol2\]) after observing that $\gamma < \Lambda_l / 2$ yields $[ \Lambda^\gamma_1 / \Lambda^\gamma_l ] \leq [2 \Lambda_1 / \Lambda_l]$. For the second statement, one has $$( - \Lambda^\gamma_l + 3\epsilon + \gamma ) ( [\Lambda^\gamma_1 / \Lambda^\gamma_l] +2) \leq ( - \Lambda^\gamma_l + 3 \epsilon + \gamma) (\Lambda^\gamma_1 / \Lambda^\gamma_l +1) = - \Lambda_1^\gamma - \big\{ \Lambda_l^\gamma - (3{\epsilon}+ \gamma) (\Lambda^\gamma_1 / \Lambda^\gamma_l +1) \big\}$$ and $\big\{\;\;\big\}\geq \Lambda_l^\gamma - 4\gamma (\Lambda^\gamma_1 / \Lambda^\gamma_l +1) \geq 0 > 2\epsilon - \gamma$. [\ ]{} \[marge\] For every $j \in \{ 1 , \cdots , l \}$ and every $2 \leq \abs{{\alpha}} \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l]$, one has $${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j \notin [-b , b] .$$ In particular, the $\lambda_i^\gamma$’s do not satisfy any resonant relation: $\cup_{j=1}^l \RRR_j^\gamma = \emptyset$. Let us fix $j \in \{ 1 , \cdots , l \}$ et $\alpha \in {\mathbb {N}}^k$ such that $2 \leq \abs{{\alpha}} \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l]$. We have $${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j = \alpha \cdot \lambda - \gamma \vert \alpha \vert - (\Lambda_j - \gamma) = \alpha \cdot \lambda - \Lambda_j - \gamma (\vert \alpha \vert -1) .$$ Assume first that ${\alpha}\in \RRR_j$. Since $\alpha \cdot \lambda - \Lambda_j = 0$ and $\vert \alpha \vert \geq 2$, one has $${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j = - \gamma (\vert \alpha \vert -1) \leq - \gamma < - b.$$ Let us now assume that ${\alpha}\notin \RRR_j$. We use here the first assertion of Lemma \[donne\].\ If $\alpha \cdot \lambda - \Lambda_j > a$ then, as $\abs{{\alpha}} \leq [\Lambda^\gamma_1 / \Lambda^\gamma_l]$, one gets $${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j > a - \gamma ([\Lambda^\gamma_1 / \Lambda^\gamma_l] - 1) > a/2 \geq b .$$ If $\alpha \cdot \lambda - \Lambda_j < -a$ then, as $\abs{{\alpha}} \geq 2$, one gets $${\alpha}_1 \lambda^\gamma_1 +\cdots +{\alpha}_k \lambda^\gamma_k - \Lambda^\gamma_j < - a -\gamma (\vert \alpha \vert -1) \leq -a < - b .$$ This completes the proof of the lemma. [&lt;100&gt;]{} F. Berteloot, *[Bifurcation currents in holomorphic families of rational maps]{}, Lecture Notes in Mathematics [**2075**]{} CIME Fundation subseries (2013) Springer Verlag, 1-93.* F. Berteloot, F. Bianchi, [*Perturbations d’exemples de Lattès et dimension de Hausdorff du lieu de bifurcation*]{}, to appear in [J. Math. Pures et Appl.]{} F. Berteloot, F. Bianchi, C. Dupont, [*Dynamical stability and Lyapunov exponents for holomorphic endomorphisms of ${\mathbb {P}}^k$*]{}, to appear in Ann. Sci. Ecole Norm. Sup. F. Berteloot, C. Dupont, L. Molino, [*Normalization of bundle holomorphic contractions and applications to dynamics*]{}, Ann. Inst. Fourier, [**58**]{} (2008), no. 6, 2137-2168. I. Binder, L. DeMarco, *[Dimension of pluriharmonic measure and polynomial endomorphisms of ${\bf C}^n$]{}, Int. Math. Res. Not., [**11**]{} (2003), 613-625.* J.Y. Briend, J. Duval, *[Exposants de Liapounoff et distribution des points périodiques d’un endomorphisme de ${\mathbb {C}}{\mathbb {P}}^k$]{}, Acta Math., **[182]{} (1999), no. 2, 143-157.*** I.P. Cornfeld, S.V. Fomin, Ya. B. Sinai, *[Ergodic theory]{}, Grund. Math. Wiss. No 245, Springer, 1985.* J.-P. Demailly, *[Complex analytic and differential geometry]{}, available at https://www-fourier.ujf-grenoble.fr/ demailly/documents.html.* H. de Thélin, *[Sur les exposants de Lyapounov des applications méromorphes]{}, Invent. Math. **[172]{} (2008), no. 1, 89-116.*** H. de Thélin, G. Vigny, *[On the measures of large entropy on a positive closed current]{}, Math. Z. **[280]{} (2015), 919-944.*** T.-C. Dinh, *[Attracting current and equilibrium measure for attractors on $\Bbb P\sp k$]{}, J. Geom. Anal. **[17]{} (2007), no. 2, 227-244.*** T.-C. Dinh, N. Sibony, *[Dynamics in several complex variables: endomorphisms of projective spaces and polynomial-like mappings]{}, Lecture Notes in Math. **[1998]{} (2010).*** C. Dupont, *[On the dimension of invariant measures of endomorphisms of ${\mathbb {P}}^k$]{}, Math. Ann. **[349]{} (2011), 509-528.*** C. Dupont, *[Large entropy measures for endomorphisms of ${\mathbb {C}}{\mathbb {P}}^k$]{}, Israel J. Math. **[192]{} (2012), 505-533.*** M. Guysinsky, A. Katok, *[Normal forms and invariant geometric structures for dynamical systems with invariant contracting foliations]{}, Math. Res. Lett., [**5**]{} (1998), no. 1-2, 149-163.* M. Jonsson, D. Varolin, *[Stable manifolds of holomorphic diffeomorphisms]{}, Invent. Math. [**149**]{} (2002), no. 2, 409-430.* A. Katok, B. Hasselblatt, *[Introduction to the modern theory of dynamical systems]{}, Cambridge Univ. Press, 1995.* A. Katok, R. Spatzier, *[Nonstationary normal forms and rigidity of group actions]{}, Electron. Res. Announc. Amer. Math. Soc., **[2]{} (1996), no. 3, 124-133.*** M. Lyubich, *[Entropy properties of rational endomorphisms of the Riemann sphere]{}, Ergodic Theory Dynamical Systems, **[3]{} (1983), no. 3, 351-385.*** R. Mañé, *[The Hausdorff dimension of invariant probabilities of rational maps]{}, Lecture Notes in Math., [**1331**]{}, Springer, 1988.* L.S. Young, *[Dimension, entropy and Lyapounov exponents]{}, Ergodic Theory & Dynamical Systems, **[2]{} (1982), no. 1, 109-124.*** [F. Berteloot]{}\ [Université Toulouse 3]{}\ [Institut Mathématique de Toulouse]{}\ [Equipe Emile Picard, Bât. 1R2]{}\ [118, route de Narbonne ]{}\ [F-31062 Toulouse Cedex 9, France]{}\ [berteloo@picard.ups-tlse.fr]{}\ [C. Dupont]{}\ [Université de Rennes 1]{}\ [IRMAR, CNRS UMR 6625]{}\ [Campus de Beaulieu, Bât. 22-23]{}\ [F-35042 Rennes Cedex, France]{}\ [christophe.dupont@univ-rennes1.fr]{}\

How Do You Find the Y-Coordinate of a Point on a Line If You Have a Graph? How Do You Find the Y-Coordinate of a Point on a Line If You Have a Graph? Note: Looking at the graph of an equation? Trying to figure out the y-value of a point on that graph? Learn how to answer that question by watching this tutorial! This tutorial shows you how to use the graph of a equation to find the y-value of a point. Working With Graphs Graphing a function? It would be really helpful if you had a table of values that fit your equation. You could plot those values on a coordinate plane and connect the point to make your graph. See it all in this tutorial! Graphing a function? It would be really helpful if you had a table of values that fit your equation. You could plot those values on a coordinate plane and connect the point to make your graph. See it all in this tutorial! Finding Slopes Trying to find the slope of a graphed line? First, identify two points on the line. Then, you could use these points to figure out the slope. In this tutorial, you'll see how to use two points on the line to find the change in 'y' and the change in 'x'. Then, you'll see how to take these values and calculate the slope. Check it out!

Henry Goodman Henry Goodman (born 23 April 1950) is a RADA trained English actor. He has appeared on television and radio, in film and in the theatre. Early life He attended the Central Foundation Boys' School and joined the Royal Academy of Dramatic Art, London, in 1969. Career Goodman has had an extensive acting career that includes a wide range of roles in theatre, on television and radio. He has won numerous awards for his theatre work. Television In 2013 he played the role of Sir Humphrey Appleby in the remake of Yes, Prime Minister which was launched on the Gold television channel. Theatre Goodman appeared on Broadway in three shows. He briefly replaced Nathan Lane in The Producers in 2002, but was fired after one month due to creative differences with Mel Brooks. The following year he returned to Broadway in Tartuffe. In 2010 he played the role of Sir Humphrey Appleby in the stage version of Yes, Prime Minister at the Chichester Festival Gielgud Theatre, in London's West End from 17 September 2010. In 2012 he played title role in The Resistible Rise of Arturo Ui in Chichester and then in the West End to critical acclaim. In 2015 he played the title role in Ben Jonson's Jacobean comedy Volpone at the Royal Shakespeare Company, directed by Trevor Nunn co-starring Matthew Kelly and Miles Richardson. His previous RSC appearance was in 2003 as Richard III. In 2017 he played Lucian Freud in Looking at Lucian, written by Alan Franks, at the Ustinov Studio at Theatre Royal, Bath. Of this part, he said "I share an intense hunger to want theatre to be as meaningful as he wanted painting to be." Film He portrayed a HYDRA doctor in the 2014 film Captain America: The Winter Soldier, though he was uncredited in the credits. He played the character again, now named Dr. List, on the second season of the TV show Agents of S.H.I.E.L.D., and in the 2015 film Avengers: Age of Ultron. Radio Goodman is also a respected radio actor. He portrayed Leopold Bloom in BBC Radio 4's all-day adaptation of James Joyce's Ulysses for 'Bloomsday' in 2012. He has also played author and chemist Primo Levi and a large number of other, often Jewish, characters on Radio 4. Awards and reputation His awards include the Olivier Award for Best Actor in a Musical playing Charles Guiteau in Assassins at the Donmar Warehouse directed by Sam Mendes in 1993, and the Olivier Award for Best Actor for Shylock in The Merchant of Venice at the National Theatre directed by Trevor Nunn in 2000. He has also been nominated for an Olivier Award for Best Actor in a Musical in 1998 for Chicago, London Critics Circle Theatre Award for Best Actor (The Merchant of Venice), and Theatre Awards UK for Best Performance in a Play in 2012 (The Resistible Rise of Arturo Ui). In his autobiography, Antony Sher says Goodman's Shylock is "quite simply the best". He reprised his role for a television film which was released in 2004. Personal life One of six children, Goodman is Jewish. He is married to Sue Parker, a choreographer and dance director. Filmography Television The Golden Bowl Bust This is David Lander London's Burning Three Up, Two Down Gentlemen and Players Rules of Engagement After the War Act of Will Capital City Screen Two El C.I.D. Chain The Bill The Gravy Train Goes East (1991) Maigret Zorro Lovejoy Rides 99-1 Performance, BBC — Measure for Measure, 1994 Smith & Jones Cold Lazarus (1996) American Voices Murder Rooms: Mysteries of the Real Sherlock Holmes Masterpiece Theatre — Broken Glass, TV film, 1996 Dalziel and Pascoe Spooks, (2002, "The Lesser of Two Evils") Trust Foyle's War (2003) Keen Eddie, (2004, Rabbi Mendelssohn, "Who Wants to Be in a Club That Would Have Me as a Member?", Episode 11) M.I.T.: Murder Investigation Team Murder in Suburbia , "The Wedding", Series 2 - Episode 3 Mumbai Calling, (2007, Pilot) Falcon Yes, Prime Minister, (2010) 6 episodes Midsomer Murders , (2013) New Tricks, (2013, "Cry Me a River", Series 10, Episode 5) Playhouse Presents , Nixon's the One, (2014) Penny Dreadful, (2014, "Grand Guignol") Agents of S.H.I.E.L.D. – Dr. List Snatch - Saul Gold Film Sources: Rotten Tomatoes TCM AllMovie Murderers Among Us: The Simon Wiesenthal Story Secret Weapon Son of the Pink Panther Degas and Pissarro Fall Out Mary Reilly Private Parts The Saint Notting Hill Arabian Nights Dirty Tricks The Final Curtain Hamilton Mattress The Mayor of Casterbridge The Life and Death of Peter Sellers Churchill: The Hollywood Years Green Street Shakespeare's Happy Endings Colour Me Kubrick: A True...Ish Story Out on a Limb The Damned United Taking Woodstock The Last Days of Lehman Brothers The Road to Coronation Street Codebreaker The Half-Light Wonder The Challenger Captain America: The Winter Soldier – Dr. List Woman in Gold Avengers: Age of Ultron – Dr. List De Surprise Altamira Love is Thicker Than Water El Elegido Their Finest (2016) The Limehouse Golem (2016) References External links Interview with Henry Goodman on SomethingJewish Category:1950 births Category:Living people Category:People from Whitechapel Category:Male actors from London Category:People educated at Central Foundation Boys' School Category:Alumni of the Royal Academy of Dramatic Art Category:English male musical theatre actors Category:English male stage actors Category:Critics' Circle Theatre Award winners Category:Laurence Olivier Award winners Category:Royal Shakespeare Company members Category:Jewish British male actors

The works represent an awareness of the power of image to engage and inform conversations about identity, self-discovery and personal histories. With skilled techniques and in collaboration the artists encourage each other and the viewer to take a journey of consciousness, challenging notions of reality and dystopia. It made me reflect on the philosophical question: Is kNOWing half the battle? Erin K. Hylton is a cultural organizer, social justice advocate, mentor, and artist who proudly hails from the Bronx, New York and currently works as Schools Programs Coordinator at The Studio Museum in Harlem. Her academic focus is on the importance of cultural access to community development (New School ’12, M.S. Nonprofit Management-Social Justice; Salem College ’10, B.A. Art History & American Studies, Magna Cum Laude). In practice she works on community efforts with youth using creativity and artistic expression. Erin’s personal mantra is to “Take Action, Create Change”, and she believes art is the tool that can create that change in the world. artedgenyc.wordpress.com Tomorrow, Sunday, November 13, KayLove and I will be painting a memorial mural for Maylin Reynoso thanks to Las Brujas. They were able to secure a wall in the LES, Rivington and Bowery, through the New Museum and the gallery On Stella Rays, during Scamming the Patriarchy: A Youth Summit. If you didn't know her, Maylin was part of Las Brujas, an all female skater group in The Bronx. She disappeared one night in July, her family reported her missing but not much was done. After a week, they figured out that a body that appeared floating in the Harlem River days before, was her. "Whereas white women are innocent victims in disappearance scenarios, the assumption with young black and Latina women is often that they were somehow involved in activities that led to their kidnapping or death. Fourteen young black and Latina girls in the Bronx have gone missing since July 2014 (9 have been found). According to Bitch Magazine, despite initial concerns that their disappearances were linked to a forced prostitution ring in New York City, all of the girls were labeled as “runaways” by the NYPD. The disappearance of 14 young girls from a single borough should have gotten more attention. Instead, their disappearances have been treated largely as a mundane reality. Would the same be the case for 14 young white girls disappearing in the suburbs?"- The Huffington Post​

588 Achilles Achilles, minor planet designation: 588 Achilles (and provisional designation ), is a large Jupiter trojan from the Greek camp. Archillies was the first Jupiter trojan to be discovered, and was discovered by Max Wolf at the Heidelberg Observatory in 1906. Wolf named the minor planet after the legendary hero Achilles from Greek mythology. The dark D-type asteroid measures approximately in diameter which makes it one of the 10 largest Jupiter trojans. It has a rotation period of 7.3 hours and possibly a spherical shape. Discovery Achilles was discovered on 22 February 1906, by the German astronomer Max Wolf at the Heidelberg-Königstuhl State Observatory in southern Germany. It was the first discovery of a Jupiter trojan, although had been observed as two years previously. This body, however, remained unconfirmed as the observation period was not long enough to calculate an orbit. August Kopff, a colleague of Wolf at Heidelberg, then discovered 617 Patroclus eight months after Achilles, and, in early 1907, he discovered the largest of all Jupiter trojans, 624 Hektor. Orbit and classification Achilles orbits the Sun at a distance of 4.4–6.0 AU in the Lagrangian point of the Sun–Jupiter System once every 11 years and 11 months (4,343 days; semi-major axis of 5.21 AU). Its orbit shows an eccentricity of 0.15 and an inclination of 10 degrees from the plane of the ecliptic. Achilles is the first known example of the stable solution of the three-body problem worked out by French mathematician Joseph Lagrange in 1772, after whom the minor planet 1006 Lagrangea is named. After the discovery of other asteroids with similar orbital characteristics, which were also named after heroes from the Trojan War (see below), the term "Trojan asteroids" or "Jupiter trojans" became commonly used. In addition, a rule was established that the point was the "Greek camp", whereas the point was the "Trojan camp", though not before each camp had acquired a "spy" (Hektor in the Greek camp and Patroclus in the Trojan camp). Physical characteristics Spectral type In the Tholen taxonomic scheme, Achilles is classified as a D-type asteroid with an unusual spectrum (DU). Its V–I color index of 0.94 is typical for most larger Jupiter trojans (see table below). Photometry Achilles rotation period of 7.3 hours is somewhat shorter than that of most other large Jupiter trojans but close to that of 911 Agamemnon, 3451 Mentor and 3317 Paris, which are similar in size (see table below). Its low brightness amplitude is indicative of a rather spherical shape. From July 2007 until September 2008, coordinated photometric observations were carried out by astronomers at Simeiz (Crimea), Rozhen (Bulgaria), Maidanak (Uzbekistan) and Kharkiv (Ukraine) observatories. Analysis of the obtained lightcurves determined a period of hours with a brightness amplitude of 0.02–0.11 magnitude (). Alternative period determinations by Cláudia Angeli (7.0 h), Robert Stephens (7.312 h), Stefano Mottola (7.32 h) and Vincenzo Zappalà (12 h) are mostly in good agreement (). Diameter and albedo According to the surveys carried out by the Infrared Astronomical Satellite, IRAS, the Japanese Akari satellite, and the NEOWISE mission of NASA's Wide-field Infrared Survey Explorer, the body's surface has a very low albedo in the range of 0.0328 to 0.043, making its absolute magnitude of approximately 8.57 correspond to a diameter of 130.1 to 135.5 kilometers. Achilles is the 6th largest Jupiter trojan according to IRAS and Akari, and the 4th largest based on NEOWISE data: Naming This minor planet's name was suggested by Austrian astronomer Johann Palisa. It was named after Achilles, the legendary hero from Greek mythology and central figure in Homer's Iliad which tells the accounts of the Trojan War (also see 5700 Homerus and 6604 Ilias). As an infant, Achilles was plunged in the River Styx by his mother Thetis (also see 17 Thetis), thus rendering his body invulnerable excepting the heel by which he was held. He slew Hector (see also 624 Hektor), the greatest Trojan warrior. He was eventually killed by an arrow in the heel by Paris (see 3317 Paris). References External links Asteroid Lightcurve Database (LCDB), query form (info) Dictionary of Minor Planet Names, Google books Discovery Circumstances: Numbered Minor Planets (1)-(5000) – Minor Planet Center Asteroid 588 Achilles, at the Small Bodies Data Ferret 000588 Category:Discoveries by Max Wolf Category:Minor planets named from Greek mythology Category:Named minor planets 000588 19060222

502 So.2d 959 (1987) ROLLINS BURDICK HUNTER OF NEW YORK, INC., Appellant, v. EUROCLASSICS LIMITED, INC., Appellee. Nos. 85-1326, 85-2698. District Court of Appeal of Florida, Third District. February 3, 1987. Rehearing Denied March 12, 1987. *960 McDermott, Will & Emery and Robert T. Palmer and Steven E. Siff, Miami, for appellant. Palmer & Lazar and Bruce Lazar, Miami, for appellee. Before HENDRY, NESBITT and FERGUSON, JJ. NESBITT, Judge. Rollins Burdick Hunter of New York, Inc. (RBH) appeals an amended final judgment for Euroclassics Limited, Inc. (Euroclassics) in Euroclassics' action to collect benefits under an insurance policy. RBH further appeals the denial of its motion for relief from judgment and new trial on the *961 ground of newly discovered evidence. The two appeals are consolidated. We reverse the trial court's judgment. Jack Kartee, Euroclassics' president and sole officer, retained RBH, an insurance broker, to procure coverage for Euroclassics' twin-engine airplane. The airplane later disappeared under mysterious circumstances in the Caribbean while the policy was in effect. The policy's underwriter, Federal Insurance Company (Federal), denied Euroclassics' subsequent claim for insurance benefits on the ground that the policy did not cover losses occurring in the Caribbean. Euroclassics sued both Federal and RBH, alleging that Federal breached its agreement to provide the coverage (count I), or that RBH breached its agreement to obtain a policy with the proper geographic scope (count II), or that RBH negligently failed to obtain a proper policy (count III). Federal's sole defense, consistent with its basis for denying the claim for benefits, was that the policy simply did not cover losses occurring in the Caribbean. RBH, however, interjected affirmative defenses which asserted that Euroclassics was not entitled to coverage because the plane was being used for illegal activities at the time of its disappearance and because Euroclassics had materially misrepresented its intended usage of the plane at the time it applied for the insurance coverage. During discovery RBH deposed Kartee. RBH asked Kartee whether he had ever been convicted of a crime. Kartee answered in the affirmative and revealed that he had been convicted of conspiracy. Kartee refused, however, to answer any further questions concerning his criminal activities and instead invoked his fifth amendment privilege against self-incrimination. RBH moved for an order to compel Kartee to answer the questions or to strike Euroclassics' pleadings on the ground that RBH's ability to prove its affirmative defenses based on the illegal use of the aircraft was thwarted by Kartee's refusal to answer. The trial court denied the motion. At the bench trial, RBH presented no evidence of the aircraft's alleged involvement in illegal activities, although reference to rumors of such involvement was made throughout the trial. On the evidence presented the court entered judgment against RBH for the insured value of the airplane, plus interest. The court found Federal not liable. Shortly after the trial, Kartee testified in a federal criminal case under a grant of immunity. His testimony revealed that the aircraft had been used continuously, from the approximate time of its purchase until it disappeared, to smuggle drugs. Based on this newly discovered evidence, RBH moved for relief from judgment. The motion was denied. On appeal RBH argues that any negligence on its part in failing to procure the proper insurance coverage was not the proximate cause of Euroclassics' loss. Instead, RBH contends, Kartee's use of the insured aircraft for drug smuggling would have precluded Euroclassics from obtaining insurance in the first place. RBH further contends that since its affirmative defenses relied upon proof of Kartee's illegal activity, the trial court's order denying RBH's motion to compel discovery was erroneous and effectively prevented RBH from proving at trial what would have amounted to a valid defense. We agree. Generally, the scope of discovery is broad with parties being entitled to discover "any matter, not privileged, that is relevant to the subject matter of the pending action ... [and] appears reasonably calculated to lead to the discovery of admissible evidence." Fla.R.Civ.P. 1.280(b)(1); see Simons v. Jorg, 384 So.2d 1362 (Fla.2d DCA 1980); Murray Van & Storage, Inc. v. Murray, 343 So.2d 61 (Fla. 4th DCA 1977); Spencer v. Spencer, 242 So.2d 786 (Fla. 4th DCA 1970), cert. denied, 248 So.2d 169 (Fla. 1971). The trial judge gave no reason for denying RBH's motion to compel. Even taking into account the broad discretion afforded the trial court in discovery matters, see, e.g., Dickinson v. Wells, 454 So.2d 758 *962 (Fla. 1st DCA 1984), when viewed in light of the above enunciated rule, the trial court abused its discretion in denying RBH's motion to compel. Not only did RBH's questions to Kartee appear to be reasonably calculated to lead to admissible evidence, but the answers they would have evoked were necessary for RBH to prove its defenses which had been validly raised in its answer to the complaint. It would appear that the trial judge relied on Kartee's fifth amendment argument in denying RBH's motion to compel. This was also error. A civil litigant's fifth amendment right to avoid self-incrimination may be used as a shield but not a sword. This means that a plaintiff seeking affirmative relief in a civil action may not invoke the fifth amendment and refuse to comply with the defendant's discovery requests, thereby thwarting the defendant's defenses. City of St. Petersburg v. Houghton, 362 So.2d 681, 683 (Fla.2d DCA 1978); see also Minor v. Minor, 240 So.2d 301 (Fla. 1970); Zabrani v. Riveron, 495 So.2d 1195 (Fla. 3d DCA 1986); Fischer v. E.F. Hutton & Co., 463 So.2d 289 (Fla.2d DCA 1984). See generally Annotation, Dismissing Action or Striking Testimony Where Party to Civil Action Asserts Privilege Against Self-Incrimination As to Pertinent Question, 4 A.L.R.3d 545 (1965). The proper sanction where the plaintiff does so is to dismiss the action or strike the pertinent portions of the pleadings. See Minor, 240 So.2d at 302; Houghton, 362 So.2d at 685. While plaintiffs cannot be compelled to incriminate themselves, when seeking affirmative relief they may not use the same right to avoid answering pertinent questions and thereby prevail in a civil suit. In the instant case the plaintiff, Euroclassics, has done precisely that. Kartee claimed to have a fifth amendment right to avoid answering questions involving his criminal activities. Once the trial court upheld this alleged privilege by denying RBH's motion to compel, RBH's ability to defend itself against Euroclassics' claim was severely hampered. It is clear that the trial court's denial of RBH's motion was harmful error. On appeal, RBH relies primarily on its assertion that Kartee's representation made at the time of application, that the plane would be used solely for pleasure trips, was a material misrepresentation which would have voided the policy. RBH claims, and the evidence supports the contention, that both RBH and Federal would have refused to contract with Kartee had he told them that he had been using the plane and planned to use it in the future for drug smuggling. Consequently, regardless of RBH's alleged negligence, Euroclassics would not have been entitled to insurance coverage because of Kartee's misrepresentation. This affirmative defense is valid and would have exonerated RBH of liability if proven at trial. See C.A. Hansen Corp. v. Aetna Ins. Co., 455 So.2d 1329 (Fla. 4th DCA 1984) (evidence held to amount to a material misrepresentation voiding insurance coverage on a vessel where insurer was told that vessel would be used for fishing trip but was actually used for smuggling); Northwestern Nat'l Ins. Co. v. General Elec. Credit Corp., 362 So.2d 120 (Fla. 3d DCA 1978) (vessel owners not entitled to recover proceeds of insurance policy on destroyed vessel where vessel was used for drug smuggling in contravention of a "pleasure boat" provision in contract), cert. denied, 370 So.2d 459 (Fla. 1979); see also Phillips v. Ostrer, 418 So.2d 1104 (Fla.3d DCA 1982) (insurance policy induced by misrepresentation is void), review denied, 429 So.2d 6 (Fla. 1983); § 627.409, Fla. Stat. (1985). Euroclassics cannot possibly be entitled to greater coverage because RBH failed to follow its instructions than it would have been had RBH followed them. Consequently, the error is not harmless. Furthermore, because the trial court's decision effectively deprived RBH of the opportunity to defend itself, the trial court's judgment must be reversed. See § 59.041, Fla. Stat. (1985); see also Saunders v. Florida Keys Elec. Coop. Ass'n, 471 So.2d 88 (Fla.3d DCA 1985) (judgment reversed where trial court *963 erroneously denied motion to compel discovery concerning prior similar accidents). Because we hold that the court committed reversible error in denying RBH's motion to compel, we do not deem it necessary to address RBH's contention that the trial court erred in denying its motion for a new trial based on newly discovered evidence. It is interesting to note, however, that had Kartee admitted the same facts in response to the questions asked during his deposition as he later testified to at the criminal trial he would have proven RBH's defenses. In view of the trial court's error, the judgment under review is reversed and the cause is remanded for a new trial.

18 WEEKS, 1 DAY 153 days to go... Your baby today Anchored to the placenta by the umbilical cord, your baby floats in amniotic fluid. Your uterus provides a warm, protective environment for your baby with lots of room to move in near weightless conditions. As you approach the halfway mark of your pregnancy, you'll continue to be astounded that there's a baby growing inside you! The further along the path of pregnancy you are, the more attached and protective you're likely to feel toward your baby. What was once a tiny bundle of cells now looks like an almost fully formed baby-and you will continue to be amazed that you and your partner have made that baby and that this incredible process is happening inside your body. Once you feel your baby move (see You are 19 Weeks and 3 Days) within the next few weeks, the attachment to him is likely to grow even stronger. While you may have some anxieties at times, try to relax and enjoy your pregnancy-it will be over before you know it. Focus On... Health It's all a blur Water retention in pregnancy can affect the eyes. Both the lens and cornea can become thicker, and there can be an increase in fluid in the eyeball, causing pressure and blurred vision. This usually resolves itself after the birth. Exercising to keep the fluid moving, and avoiding wearing contact lenses can help. Notify your doctor if you have vision problems. Ask A... Doctor I have a high-powered career and have hardly had any time to think about the baby since I've been pregnant. Will this stop us from bonding? Even if you work full time while you're pregnant, this doesn't have to have a negative effect on your relationship with your baby. As your baby grows, you will probably find that you start to develop a relationship with your "belly" as you anticipate your baby's movements and perhaps talk to him. Make sure you plan enough maternity leave before your due date since this gives you time for practical and emotional preparations, as well as time to rest. There's some evidence to suggest that too much stress in a mother can affect her unborn baby's brain development (see You are 16 Weeks and 3 Days). This highlights the importance of ensuring you have regular opportunities to relax during pregnancy and so, if your work is stressful, maybe this would be a good time to look at your priorities.

Corticorubral synaptic organization in Macaca fascicularis: a study utilizing degeneration, anterograde transport of WGA-HRP, and combined immuno-GABA-gold technique and computer-assisted reconstruction. The macaque red nucleus receives afferents from two major sources, the cerebral cortex and the deep cerebellar nuclei. Approximately 90% of the corticorubral afferent axons project to pars parvicellularis of the red nucleus, the neurons of which transmit information to the cerebellum by way of the inferior olivary nucleus. The remaining 10% project to pars magnocellularis of the red nucleus, the major projection of which is to the spinal cord. In this study, corticorubral terminations labeled following lesions or injections of wheatgerm agglutinin conjugated to horseradish-peroxidase into the topographically defined hand area of the primary motor cortex were quantitatively studied via electron microscopy. Cortical afferent terminals within pars parvicellularis and pars magnocellularis synapse upon all regions of the dendritic arbors of rubral projection neurons. However, the majority of these labeled afferents synapse upon thin-diameter shafts or presumed spinous processes of rubral distal dendrites as well as upon vesicle-containing profiles of presynaptic dendrites of local circuit interneurons that are gamma-aminobutyric acid-immunoreactive, as identified by postembedding immunohistochemistry. Synaptic contacts formed by the labeled cortical terminal were large in width and extended through several serial sections. Synaptic contacts formed by the presynaptic dendritic profiles, on the other hand, were more punctate and could be seen in only one or two serial sections. These latter synaptic interactions probably provide a modification of the effects of cortical input to rubral projection neurons as suggested by previous physiological studies that indicated the dominance of cortical input onto distal dendrites as well as involvement with inhibitory circuits. An example of the complexities of these synaptic interactions is further demonstrated by a three-dimensional computer reconstruction. This quantitative study of corticorubral afferents in the macaque monkey provides insight into the interactions of cerebral cortical afferents with rubral projection neurons and their relationship with local circuit inhibitory interneurons to elucidate the role played by the cortex in the activation of rubral neurons.