From: caf@omen.UUCP (Chuck Forsberg WA7KGX)
Subject: Re: New Adiposity 101 2/2
Organization: Omen Technology INC, Portland Rain Forest
Date: Thu, 13 Aug 1992 07:34:53 GMT



                           - 29 -



loss as skeletal muscle.  (Internation Journal of Obesity
(1992) 16, 481)

Some studies on human diet cycling are tabulated below.
              Human Studies on Weight Cycling

__________________________________________________________________________
|Study      | Subjects   Sample     Results   WC>BMI    Health Outcome    |
|___________|_____________________________________________________________|
|(Dale)     | 20 f       SKEWED     FUDGED    matched   (short term)      |
|Wadden     | 50 f       selected   FUDGED    yes       unknown           |
|TRIM       | 88         SKEWED     FUDGED    yes       (short term)      |
|Jequier    | f          -          -         yes       slow metab.       |
|Baltimore  | 846 m      volun.     FUDGED    ?         glucose intol     |
|WECO       | 2107 m     all        true      yes?      CHD               |
|Gothenburg | 2317       random     true      n/a       CHD, diabetes     |
|___________|_____________________________________________________________|

  WC>BMI: Weight Cycling linked to increased fatness (BMI)
A sample was judged SKEWED if subjects were selectively
excluded from the cohort because they developed diabetes,
CHD, morbid BMI, or other negative health outcomes linked to
diet cycling, after the commencement of diet cycling.
Results were judged FUDGED if BMI was factored out, begging
the question that diet cycling may damage health because of
the increase in obesity from diet cycling.

A recent survey of European obesity experts showed they
consider repeated dieting a greater causative factor for
obesity than lack of will-power, physical inactivity, or
depression leading to overeating.

By considering the studies by Drenick et al, Lissner et al,
and Bjorntorp and Sjostrom, it appears that obese (BMI > 35)
individuals with childhood onset obesity (BMI > 20 at age 5)
who lose 12% or more of their weight are at the greatest
risk of gaining back more than they lose, with the attendant
bad health effects.  The risk is a serious one, a slope of
.5 to .9 BMI/year weight gain (higher in some) compared to
0.25 for normal adults.

As explained above, studies that do not report adverse
effects from diet cycling are flawed because they filter out
the effect of weight gain caused by diet cycling.  To
correct this flaw, studies must match dieters and non
dieters according to their physical characteristics *BEFORE*
their first diet.

Weight loss studies should report the number and size of
adipose cells before slimming, after slimming, and after
weight regain.



                       Adiposity 101







                           - 30 -



6.5.1  Artificial Sweeteners  There has been considerable
media coverage of claims that artificial sweeteners hamper
weight loss efforts.  These appear to result from an
American Cancer Society study that found a correlation
between overweight and the use of artificial sweeteners.
This correlation might better be explained by noting that
people without weight problems generally avoid artificially
sweetened products on account of cancer concerns, inferior
taste, and the lack of "sugar high". Thin people may read
labels on artificially sweetened products suggesting such
products be used only by those desiring to reduce their
caloric intake.

A University of Toronto study on the effects of Aspartame
sweetened diet soda on randomly assigned subjects found no
effect on food selection at a meal 60 minutes afterwards.
Subjects who consumed a half liter of diet pop experienced
reduced hunger for about 45 minutes.

A New England Deaconess Hospital (1F-16) study found that
aspartame facilitated greater weight loss among obese women
on a multidisciplinary balanced deficit diet that included
exercise.

A Harvard Medical School study indicated Aspartame
facilitated long term weight maintenance in a
multidisciplinary weight loss program.

6.6  High Fiber Diet

High fiber diets have been proposed for weight loss from
time to time.  According to Consumers Reports, increasing
fiber in one's diet does not induce long term weight loss.
Guar Gum, an agent for adding fiber to the diet, has been
banned by the FDA.

6.7  Low Fat Diets

Concerns about cholesterol levels have focused attention on
low fat diets.  The negligible long term success rate of
semistarvation diets has sparked interest in the weight loss
possibilities of low fat diets.

This interest springs from a number of observations.

   + High fat (>>40% fat) diets cause weight gain in
     research rats.  Low fat evangelists fail to note that
     high carbohydrate diets have proven even more fattening
     to research rats.  In addition, not all rats gain
     weight on the high fat diet, and most rats revert to
     normal weight when their diet is normalized.  All of



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     the high fat rat diets seen in the literature involve a
     profound increase in total energy intake, contrary to
     most obese humans who have depressed energy intake.

     Replacing mothers milk (8% of calories from
     carbohydrates) with a milk-substitute formula (56% of
     calories from carbohydrates) grew fatter rats.  (See
     "The Role of Baby's Diet", below.)

   + Obese subjects often exhibit a greater carving for fat
     than lean individuals.  Since fat craving is a common
     after effect of energy deprivation, and most fat people
     have been on numerous diets, fat craving may be the
     result of dietary restriction, not the initial fat
     inducing condition.  Studies show fat children obtain a
     slightly greater proportion of their energy input from
     fat than thin children do.  This slight increase is
     decisively overshadowed by their lower total energy
     intake.  Pre-obese children consume less energy (50
     calories/day average) than their lean counterparts.

   + Some studies suggest energy from fat additions to an
     otherwise neutral energy balance cause a weight
     increase short term, which may be more pronounced in
     the obese.  This effect has not been demonstrated
     outside the context of induced overfeeding.  In
     "Oxidative and nonoxidative macronutrient disposal in
     lean and obese men after mixed meals" (Am J of Clin
     Nut, 1992;55;630-6), Owen et al report "Significantly,
     there was no tendency for the obese men to have the
     defect in suppression of fat oxidation after mixed
     meals that had been reported by others".

Low fat diets come in two types, semistarvation and ad
libitum.  Most VLCD diets are low fat; the Cambridge Food
For Life Ultimate Weight Loss Formula provides 6% energy
from fat (3% by weight).  It has been argued that the
infamous Atkins Diet is also a low fat diet because many
(not all) people do not like fatty foods that are not also
high in carbohyrdrates.

A Rockefeller University study appearing in the American
Journal of Clinical Nutrition (1992;55;350-5) found no
significant variation in energy need as a function of
percentage of fat intake (0 to 70%), confirming a 1930
study.  The 1930 study found that the long-term effect on
body weight of any diet is related only to the total energy
content of the diet.  Other features of the diet such as
carbohydrate or fat content did not, in the long run, have
consequential effects on body weight.




                       Adiposity 101







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There is no epidemologic evidence indicating that total fat
intake per se, independent of total caloric intake, is
associated with increased adiposity in the population.
Obesity itself has not been found to be associated with
dietary in either inter- or intra- population studies.
("Diet and Health:  Implications for reducing chronic
disease risk"; Committee on Diet and Health Food and
Nutrition Board Commission on Life Sciences, National
Research Council; National Academy Council, Washington D.C.
1989.)

"There is some problem in reconciling the short-term studies
showing an association between high-fat diets and obesity
with longer-term trials where there is no really strong
evidence that hig-fat diets do cause massive weight gain.
There is the National Diet Heart Study in the United States,
which lasted one year, and had men on diets varying in fat
content from 40% to 20% of energy.  The differenced in body
weight gain between these men were really very small"
"Whatever happens to fat in terms of its being deposited
preferentially on short-term overfeeding, there seems to be
no difference between carbohydrate and fat supplements in
terms of energy balance when you look over a period of 50 to
80 days." "If [dietary] fat is a promoter of weight gain and
obesity, it is more likely to be through its effects on the
hedonic characteristics of the food source than because of
any mysterious effect on intermediary metabolism"
(Discussion, Nutrition Reviews, Vol. 50, No. 4)

6.7.1  The Cornell Low Fat Study  A Cornell University study
"Weight loss on a low fat diet" has been widely quoted by
low fat diet evangelists.  This study is interesting
primarily for what the mass media never reported about its
methods and results.

The Cornell study located 25 non-smoking women of greater
than ideal weight who were not cognitively restricting their
food intake to achieve weight control. "Unrestrained eaters
were desired as subjects".  Since the majority of overweight
women actively try to reduce their weight, this study's
sample is not representative of overweight women.  Of the 25
subjects that passed the initial screening, 9 were excluded
from the study for unstated reasons, and another 3 dropped
out during the low fat phase of the study, leaving only 13
subjects.  Why all the fuss about sample selection?  The
researchers undoubtedly wanted to use subjects who were not
truly obese (they don't respond to the food the same as
normalweights do).  Neither did the researches wish to risk
using women whose metabolisms had been depressed by previous
diets.




                       Adiposity 101







                           - 33 -



Subjects were randomly assigned to ad libitum diets with low
fat (20% calories from fat) or high fat (40% calories from
fat) foods.  Subjects were placed on one diet or the other
for 11 weeks.  After an 7 week "washout period" the subjects
switched diets.  Subjects who first lost weight on the ad
libitum 35-40% fat control diet subsequently failed to lose
more weight on the low fat diet.

Caloric intake on the low fat diet was markedly depressed at
the beginning, with an initial weight loss of almost a pound
a week.  Within 11 weeks, caloric intake on the low fat diet
was increasing.  The difference in calorie intake was cut in
half, and weight loss almost halted.

"We are unable to explain the minimal effect that the low
fat diet had in the second half of the study".  The study
paper also indicated that weight loss on the low fat diet
was much less than expected from the caloric difference
between the two diets.

In addition, the media failed to report that the subjects
regained twice as much weight in the 7 week period after the
low fat diet as did the subjects on the control diet.


In a study of 171 women on a two year low fat diet, maximum
weight loss of 3.2 kg was reported at 6 months.  (Am J Clin
Nutr 1991;54:821-8.) By year 2 some of the weight was
regained.  The standard deviation was more than twice the
average weight loss. In other words, quite a few actually
gained weight on the low fat diet, not counting the 13 that
dropped out of the program.

The Pritikin Institute promotes an ultra low fat diet to
improve cardiovascular health.  In a 1991 radio interview, a
Pritikin Institute official characterized the weight loss
effects of the Pritikin ultra low fat diet as "slight".  Ann
Louise Gittleman, Pritikin Longevity Center nutrition
director, reported in 1992 that weight loss on the Pritikin
diet was temporary for most.

A Rockefeller University study reported energy intake
required to maintain body weight is not affected by wide
variation in diet composition.  Even with extreme changes in
the percentage of energy from fat (0% - 70%) there was no
detectable evidence of significant variation in energy need
as a function of percentage fat intake.  (American Journal
of Clinical Nutrition 1992;55;350-5) "Sixty years ago, LH
Newburgh and his colleagues examined the possibility that
so-called endogenous obesity might be the result of special
metabolic factors unrelated to energy intake or physical



                       Adiposity 101







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activity.  They found no evidence for such purely endogenous
obesity and also demonstrated that the long-term effect of
any diet on body weight is related only to the total energy
content of the diet.  Other features of the diet such as
carbohydrate or fat content did not, in the long run, have
consequential effects on body weight."

The incidence of obesity does not necessarily follow the
amount of dietary fat.  The average U.S. daily fat
consumption is 2.52 ounces, with 10% of males obese; the
average Australian daily fat consumption is much less at
1.54, but 14% are obese.  (LONGEVITY, May 1992)

"There is evidence that altering the proportion of the
calories in the diet from fat, carbohyrdate, and protein can
have a limited effect on weight loss; however the effects
appear to be quite small" (Methods for Voluntary Weight loss
and Control, NIH Technology Assessment Conference Panel,
Annals of Internal Medicine June 1992, 116;11)

6.8  Low Carbohydrate Diets

Sugar consumption is lower, low carbohydrate diets are more
popular, and the reported incidence of hyperobese
individuals is lower in Europe than in the U.S.

A number of short term studies, mostly in the 50's and 60's,
showed a marked advantage in weight loss from low
carbohydrate diets compared to diets higher in carbohydrate.

Dr. Atkins' Diet Revolution put forth the most controversial
low carbohydrate diet in 1972.  The American Medical
Association Council on Foods and Nutrition blasted the
Atkins diet in the June 4 1973 Journal of the American
Medical Association.  While Atkins rebuts many of the
Council's points in his 1992 sequel "Dr. Atkins' NEW Diet
Revolution," the Council's observation that "It is
unfortunate that no reliable mechanism exists to help the
public evaluate and put into proper perspective the great
volume of nutritional information and misinformation" is,
sadly, as true in 1992 as it was in 1973.

Atkins claims that 95% of overweight is metabolic and not an
eating disorder.  His solution is to limit sugar and other
carbohydrates to the dietary levels man experienced before
the agricultural revolution.  Since the AMA Council on Foods
and Nutrition put the Atkins diet off limits, few
investigations of the Atkins diet have appeared in the
literature.  Consumer Reports' Rating the Diets has rated
Atkins as "absolutely not recommended"; ironically their top
rated diet (Nutri/Systems) was the first to make payments on



                       Adiposity 101







                           - 35 -



product liability lawsuits.

Critics blast the Atkins diet as a high-fat regimen that
increases serum lipids.  Atkins, trained as a cardiologist,
responds: ``Am I advocating a high-fat diet?  Not in the
long run.  As my critics twenty years ago were forced to
acknowledge when they looked into the matter, and as
Professor John Yudkin proved, this isn't a high-fat diet.
The average person on a low-carbohydrate diet eats less fat
than he was eating on his previous "balanced" diet - the
average diet in America today.''

``the AMA [Council on Foods and Nutrition] said they were
"deeply concerned about any diet that advocates the
unlimited intake of saturated fats and cholesterol-rich
foods." Then they scrutinized all the medical literature
they could bring to bear and came up with a single case
described in 1929.2

Let's look at their language: "Individuals responding to
such a diet with a rise in blood fat will have an increased
risk of coronary heart disease."  Absolutely, All I can say
is: "I agree, and individuals who jump off a curb with a
parachute and are thereupon attacked by an enraged bull will
have an increased risk of torn garments."

The AMA's ad hoc nutrition panel had to phrase it that way,
because they knew, of course, that they could not find any
evidence that would have allowed him to make a stronger
statement.

I think it is clear from their circumspect language that the
AMA was aware of the difference between the results when fat
and cholesterol are added to a high-carbohydrate diet and
the results that occur when they are added to a low-
carbohydrate lipolytic diet.  In the usual scenario, when
carbohydrates are a large part of the diet, the undesirable
lipid reading may get worse if there is an increased intake


__________

 2. See Atkins' footnote on this study.  "This was the study
    of the Arctic explorer, Vilhjalmur Stefansson, who,
    impressed with the health of the native Eskimos he
    observed, volunteered with an associate to be observed
    for a year on an all animal food diet.  In this study,
    one of the two subjects cholsterol levels did go up but
    the other's dropped.  The AMA inaccurately reported that
    both men had cholsterol increases."




                       Adiposity 101







                           - 36 -



of fat as well; on the Atkins diet, such a result is rare
indeed.'' (Chapter 15, Dr. Atkins NEW DIET REVOLUTION, 1992)

Problems reported with the Atkins diet include weakness,
palatability, inconvenience and expense of obtaining low-
carbohydrate foods.  Several net.people have reported
abandoning the Atkins diet as a result of the bad publicity.

Atkins' latest book claims "the 10,000 active patients at
the Atkins Center for Complimentary Medicine in New York are
living testimonials to the major health improvements derived
from a low-carbohydrate diet." Dr. Atkins advertises books
and vitamins on his nationally syndicated radio talk show
(1-800-2-ATKINS, 1-800-6-ATKINS).

A relatively recent paper appeared in the Feb 1973 American
Journal of Clinical Nutrition, "Response of body weight to a
low carbohydrate, high fat diet in normal and obese
subjects".  This paper is unusual for diet studies in that
it discloses the individual results of each of its obese
subjects instead of hiding them in the arithmetic mean.  "we
treated obese subjects with high fat, low carbohydrate
diets.  If the carbohydrate content of the diet was not more
than 50 to 60 g/day and the fat content approximately 150
g/day, an average daily weight reduction of 0.3 kg was
achieved.  The cholesterol and triglyceride concentrations
in the serum, which had been raised at the beginning of the
experiment, invariably showed a tendency towards
normalization under this dietary program."

Several recent papers have reported low carbohydrate to be
better than the generally accepted low fat diet for diabetic
control.

6.9  Diets - the BOTTOM LINE

An article by William Bennett in the Annals, New York
Academy of Sciences, (book length issue on Human Obesity)
gives the bottom line on diets.  "Data on the dietary
treatment of obesity have been accumulating since 1931.
Nothing in the chronicle suggests that worthwhile progress
has been made by pursuing efforts to teach people more
effective ways to restrict their food intake.  There now is
enough information to permit the prediction that results
will be mediocre in the short run and after several years
the results will be less than acceptable.  The burden should
now be on the investigator to establish a strong reason for
undertaking yet another study of intake restriction,
including studies employing behavior modification aimed
primarily at altering eating behaviors.




                       Adiposity 101







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Committees reviewing the use of human subjects in these
experiments should not assume that they are ethically
uncomplicated.  The low probability that information of
therapeutic value will result from such a study should weigh
heavily in any deliberation on whether to authorize it."

"I can see little reason for intake restriction to receive
continued support, either as a subject of research or as an
accepted therapy for obesity.  Bloodletting as a therapy for
pneumonia was abandoned about a century before penicillin
was discovered.  It required a modicum of courage and good
sense on the part of practitioners who turned away from the
practice, but there is no reason to believe their patients
suffered from this lack of therapy."

"A survey of studies published 1977-1986 and reporting on
dietary or behavioral treatment of obesity reveals that the
maximum percentage of body weight lost is, on average, 8.5
percent - no different from the value, 8.9% in similar
studies from 1966-1976, as reviewed by Wing and Jeffery."

"The goals and research methods of studies on dietary
treatments for obesity are overdue for ethical as well as
scientific reevaluation.  The same may be said for the
numerous programs providing such treatment outside the
context of research."

A final footnote on combining diets and exercise.  A Harvard
Health letter compared results of 1982 and 1991 surveys of
doctors' lifestyles.  Since 1982 the doctors reduced their
consumption of red meat, fat, and cholesterol.  They
increased their dietary fiber and exercised more.
Unfortunately, the increased attention to diet and exercise
did not produce leaner bodies; the proportion reporting
weight problems increased from 29 to 39 per cent.

While diet evangelists continually assert that new wrinkles
in 30+ year old treatments are improving weight loss
outcomes, the long term success rate of even the best
available weight loss programs using diet, exercise, and
behavior modification remains less than five per cent. (NIH
conference Mar 30-Apr 1 1992)


7.  FLAWED RESEARCH

The quality of diet research and media coverage on the
problem of adiposity often leaves much to be desired.  The
vast majority of this research is so sloppy it would never
be accepted by the FDA as proof of an ethical drug's
efficacy.



                       Adiposity 101







                           - 38 -



The reader should beware of two common flaws in popular
obesity studies:

7.1  Correlation .vs. Cause and Effect

A typical correlation study might show that joggers are
thinner than couch potatoes.  This is a *correlation*.  Such
data are generally accepted as proof that obesity is caused
by lack of exercise, with the implication that fat couch
potatoes will become thin if only they get off their lazy
butts and exercise.

What is the error in drawing such a conclusion?  The error
is the unstated assumption that the correlation proves a
particular cause and effect.  In fact, other cause and
effect relationships may be involved.  Conventional wisdom
concludes: Lack of exercise causes obesity.  The other
explanation for the observed correlation is: Obesity and
associated impaired muscle development makes sports
activities unpleasant and frustrating if not impossible.

"While the link between exercise and health in some large
epidemologic studies seems powerful, intervention and
outcome studies suggest a more qualified correlation. ...
Yet "we still have no clinical trial to demonstrate that
increasing activity in a group of sedentary people reduces
the rate of disease vs sedentary controls," says William
Haskell, PhD, also a member of the Stanford faculty." (JAMA
June 12, 1991)

Correlation studies that draw conclusions or make
recommendations without properly evaluating alternative
models of causality are fundamentally flawed and must be
treated with suspicion.

7.2  Flawed Sample Selection/Distribution

Non-random selection or partitioning of the sample
population flaws many studies that otherwise appear to be
well designed.

One cannot use people as their own controls.  One cannot
allow subjects to select which experimental group they will
join because the selection process may be stronger than the
experiment.  News media might not understand the
implications, but the study will be flawed.

For example, a study on the mortality effects of obesity was
based on patients who had repeatedly lost and regained
weight, compared to lean individuals.  Was the higher
mortality caused by obesity, by the dieting, or did diet



                       Adiposity 101







                           - 39 -



cycling cause both?

Diet studies typically exclude dropouts from their data.
This is not acceptable in weight loss research because
dropouts generally have lower weight loss and greater weight
regain.  Excluding even a few such data points distorts the
experiment because the variability between subjects is much
greater than the average weight loss (SD >> M).

Studies comparing the relative success of alternative
treatments rarely assign subjects to the alternatives at
random.  The factors that determined sample selection and
partitioning may be more important than the alleged
independent variable.


8.  TRUTH IN RESEARCH PAPERS

The honesty and integrity in life sciences research has
increasingly come under question.  In one case, a researcher
has used legal action to obstruct investigation of his
experimental procedures.

We can all understand the pressure on a corporation or trade
institute to manage information about the safety and
efficacy of its products and services.  Such pressures are
not limited to the corporate sector.  Weight loss
researchers live by the "publish or perish" syndrome.
Exaggeration of weak results is sometimes a necessary
expedient to secure continuing research funding.  The old
saw "When all you have is a hammer, everything starts to
look like a nail" applies to research projects.

"It is seldom necessary to list individual results in a
paper.  Data can usually be summarized by a measure of
location and a measure of dispersion.  A common practice is
to list the arithmetic mean, standard deviation (S.D.) and
the number of observations (n) used to estimate these
statistics.  If only a few observations are available the
dispersion is better indicated by the range.  If the
distribution is significantly skewed [not a "normal
distribution"] both the median [50th percentile] and range
[minimum and maximum] should be cited." (Journal of
Endochrinology, 1992)

How can one spot "fudged" research?  One way is to look at
the way data is presented.  If mean (average) values for the
experimental groups are presented, check the standard
deviation values.  The standard deviation must be small
compared to the reported differences between groups.  If the
standard deviation is comparable to the differences between



                       Adiposity 101







                           - 40 -



groups, the data can not be used to analyize individuals.

Diet evangelists dismiss or downplay the importance of
genetics and other inborn differences affecting the
development of obesity.  Large standard deviations highlight
the biological differences between fat and thin people.  If
the standard deviation is not disclosed, the researcher is
hiding something from the reader.


Any study that takes weight loss as a goal should include
the following information:

   + Weight, height, and Body Mass Index (BMI) for subjects
     at entry, then weight and BMI at each follow-up time.

   + When expressed as means, these values should be
     accompanied by the standard deviation, not the standard
     error.

   + Data for males and females should always be separated.

   + If the study contains more than one experimental group
     and/or a control group, subjects must be randomly
     assigned to each group.

   + If the study contains more than one experimental group
     and/or a control group, the data should be presented
     for each group.

   + Studies with 50 or fewer subjects should present
     individual data.

   + Data should include followup for a minimum of three
     years after treatment ends.

   + If there are drop-outs, the remaining number of
     subjects should be recalculated and reported along with
     the mean weight at follow-up.  Almost all drop-outs
     regain their weight loss or more, and must be
     calculated this way.

   + Weight loss studies should report the number and size
     of adipose cells before slimming, after slimming, and
     after weight regain.
(Based on recommendations by by William Bennett,  Harvard
Medical School Health Letter)







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                           - 41 -



9.  MEDIA DISTORTION

Heavy advertising, a "thin is in" ethic, media preoccupation
with unusually obese individuals, and built-in repeat
business have bloated the diet industry into a 33 billion
dollar a year enterprise.

As Professor Garner's 1990 testimony before the House of
Representatives indicated, false advertising is rampant in
the diet industry.  While an individual deceptive diet ad
may not be too misleading to the public at large, the
collective effect of such deception (Nazi Big Lie effect)
creates great damage.

False advertising is, unfortunately, normal for the diet
industry.  The majority of diet food products tested for the
New York state Consumer Protection Board contained more
calories than listed on their package labels.  80 percent of
the diet food products tested exceeded claimed calories,
some by as much as 73 calories per serving.  Oscar Meyer
Lean'N Tasty Breakfast strips are 80% fat.


10.  NEW TECHNOLOGY

10.1  MULTIMODAL INTERVENTION

"The genesis of this project was an invitation to discuss
anorexiant medications with the house officers in the
Medical CLinic as Strong Memorial Hospital.  The colleague
who invited me was dismayed that the treatment options used
in the medical clinic were not helping people lose weight."
Michael Weintraub, MD "both the medical profession and
society look with disfavor on obese people and obesity in
general. ... Obese people are treated negatively in cartoons
and in literature.  Many believe that obese people need only
to "close their mouths" and be more motivated to lose
weight.  The use of medications to correct a characterologic
defect is, in the opinion of physicians and the public,
deemed inappropriate.

Unfortunately, a lack of understanding of both the natural
history of obesity and its diversity adds to the perjorative
view of obese people and of anorexiants.  Some health
professionals are not aware of data concerning mechanisims
present in the human organism that act to contravene
pertubations in body weight and that may account for the
apparent failure of interventions, including medications."

To provide longer-term data, Weintraub et al developed a 4
year multimodal program using state-of-the-art behavior



                       Adiposity 101







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modification, caloric restriction, and exercise for the
duration of the four year study.  When reading reports on
The National Heart, Lung, and Blood Institute funded
Multimodal Intervention Study, please keep in mind that this
"state-of-the-art" treatment was the PLACEBO.  "From the end
of the second double-blind phase at week 190 through week
210, we monitored study participants to see what happened
without medication but with continuing behavior
modification, caloric restriction, and exercise therapy. ...
One measure of the excellence of the ancillary [PLACEBO]
therapy in this study was that it enabled participants
treated with placebo to lose just 0.01 kg/week less than
participants receiving active therapy in the 18 studies that
lasted at least 8 weeks reviewed by Scoville for the FDA."

121 subjects, 18 to 60 years old, mean BMI of 33.4 +- 2.2,
three fourths female, entered the medication phase of the
study after 6 weeks of behavior mod, diet and exercise.  69
per cent had been on six or more diets previously.

Subjects on medication lost about three times the weight as
those only receiving behavior modification, diet and
exercise.  There was no indication of tolerance or abuse
potential of the medication.  There was no indication that
use of anorexiant inhibits the learning of behavior
modification.

As reported by the New York Times New Service, Dr. Albert
Stunkard, an obesity researcher at the University of
Pennsylvania, said he knew of no other study that had
elicited such a dramatic and sustained weight loss. It
``points to the way things are going to go,'' he said.

The investigators found their patients could not maintain
their weight loss without the drugs.

The final 30 weeks of the program assessed what happened
when all the patients were weaned from the drugs, relying on
continued diet, exercise and behavior control. They
gradually regained almost all the weight they had lost,
despite the continuing program of diet, exercise and
behavior modification.  Lipid profiles indicated the weight
regain was not caused by cheating.

When the study was over, and subjects were nearly as fat as
they were initially, many tried to get the drug combination
from their private doctors and ran into skepticism over the
treatment.

Some experts on weight loss hailed the studies, saying they
could mark a pronounced shift in the way obesity is studied



                       Adiposity 101







                           - 43 -



and treated.

These experts said the results showed obesity could be
treated the way chronic diseases like high blood pressure or
arthritis are.  In those diseases, drugs must be taken
indefinitely to keep symptoms in check.

``This is a landmark study,'' said Dr. George Blackburn, an
obesity researcher at New England Deaconess Hospital in
Boston.

Study VI of the report discusses individual outcomes.  One
subject did not reach goal weight (120% of ideal) but he was
able to maintain his weight loss even after medication
ceased.  Some others did reach goal weight but gained it all
back, or more.  Most lost at least some weight but regained
it after medication ceased, despite continuing behavior
modification, diet and exercise.  Some lost little or no
weight, or gained weight.  Diet evangelists who minimize the
deep biological diversity of fat people should study this
paper carefully.

The mechanisms by which fenfluramine plus pentramine induce
weight loss in human is not well understood.  Fenfluramine
increases diet Induced Thermogenesis (DIT) in rat, but not
RMR.  Fenfluramine increases growth hormone (GH) levels
under some conditions.  Fluoxetine, another serotonin-
reuptake inhibiting against, has been shown to improve
insulin sensitivity and other metabolic actions.

This study maintains a level of experimental design,
reportage, disclosure and honesty that distinguishes it from
most "successful" studies of traditional weight loss
techniques.  It underscores the abject failure of
traditional weight loss technology to improve the quality of
life for most fat people.

Free reprints of this 65 page supplement are available.

10.2  STIMULATION OF THERMOGENISIS

Thermogenisis refers to the generation of body heat in
muscle and brown adipose tissue (BAT).3 Lean subjects
increase thermogenisis in response to meals, exercise, and


__________

 3. There is some controversy about the location of
    thermogenisis in adults (BAT or muscle tissue).




                       Adiposity 101







                           - 44 -



cold weather.  Obese subjects show less of each of these
responses than lean subjects.  Obese subjects are less
tolerant to long term cold exposure because of their
inferior thermogenisis capability.

These facts have prompted many investigations into the
possibility of reducing obesity by increasing thermogenisis
in the obese.

In their book "Life Extension Weight Loss", Pearson and Shaw
suggest thermogenisis enhancing drugs and cold exposure as
ways to burn up fat.

Caffeine, ephedrine, nicotine and other materials have been
shown to increase metabolism in humans.  Aspirin increases
the thermogenic effectiveness of ephedrine in obese but not
lean women.  Some are associated with weight loss during the
treatment period.  Common side effects of such treatment
include high blood pressure and heart palpitations.

A double-blind Danish study reported that ephedrine 20mg +
caffeine 200mg administered three times daily dramatically
increased fat loss and fat oxidation (see "fast fibres") and
reduced loss of fat-free mass.  Three of the 8 patients on
E+C complained of insomnia, palpitations, and tremor,
respectively.  (Metabolism, 41;7 July 1992)

Smokers gain weight when they quit smoking; their final
weight averages the same as that of non smokers.  This
suggests nicotine reversibly depresses weight, 6 to 7 per
cent according to University of Wisconsin researcher Richard
Keesey.  Nicotine reduces weight by increasing metabolism,
not by reducing appetite or food intake.  A growing number
of young women have discovered this, and cigarette smoking
is gaining popularity as a weight control measure.

Pearson and Shaw recommend nicotinic acid to increase
thermogenisis and as a recreational drug.

A study of obese women on a swimming program suggests their
heat loss to water had the opposite effect, increasing their
fat stores.  It's been reported that women gain 10 pounds in
less than a week's time when they move to Alaska; they lose
this weight when they move back to a warmer climate.

It has been suggested that early exposure to cold might
promote adult leaness.  (p. 75, Obesity and Leanness - Basic
Aspects) Improvements in household heating in this century
may account for an increase in obesity.





                       Adiposity 101







                           - 45 -



10.3  GROWTH HORMONE TREATMENT

The pituitary gland releases Human Growth Hormone (HGH) in
bursts, mostly during the early hours of sleep.  Human
Growth Hormone promotes muscle growth and fat loss.  The
obese produce much less HGH than normal.

Obesity is associated with reduced 24 hour integrated
concentrations of growth hormone (IC-GH) and elevated
concentrations of insulin (IC-I) compared to lean
individuals.  The difference in growth hormone levels is
greatest in childhood.  The difference in growth hormone
between lean and obese children that IC-GH of obese children
are typical of poorly growing  children with classical
growth hormone (GH) deficiency.  In contrast to children
with classical GH deficiency, obese children are generally
normal or above average for height, growth rate, osseous
maturation and IGF-1 levels.

A study reported in the Dec 3 1990 Wall Street Journal
reported that short children treated with growth hormone
lost a "drastic 76 per cent of body fat" while gaining as
much as 25% lean body mass (compared to untreated controls).

Obese individuals normally release very little or no
detectable HGH.  Even under the most strenuous exercise,
obese individuals release only a small fraction of the HGH
lean sedentary individuals release in normal sleep.

A study of lipid metabolism in lean and pre-obese swine
(pigs of normal weight which will become fat) indicated low
levels of growth hormone at least until sexual maturity, and
an enhanced deposition of blood lipids as fat compared to
lean subjects. (International Journal of Obesity 1990, 14,
21-29) This enhanced deposition is significant in two ways.
First there is the direct accumulation of fat.  Secondly
this deposition of fat "short circuits" metabolism of blood
lipids into cholesterol and steroid hormones.  This theory
helps explain why destruction of fat tissue allows animals
to grow up with more muscle mass than identical but
untreated controls.

In the future, high risk babies might be given lipid
tolerance tests, and pre-obese individuals treated with HGH
and DHEA to keep them from becoming fat.

In a recent study, administration of synthetic growth
hormone to elderly male patients to normalize their low HGH
levels resulted in significant muscle gain and fat loss.

A Dutch study 8 GH deficient patients reported that 6 months



                       Adiposity 101







                           - 46 -



GH therapy increased lean body mass and decreased fat mass.
The sense of well-being improved in most patients.
Cholesterol levels decreased.  (Clinical Endocrinology 1992
37, p. 79)

A study at St. Thomas' Hopsital in London found that
patients with hypopituitarism have altered body composition
and quality of life.  In comparison with a matched control
group such patients had considerably reduced lean body mass
and increased fat mass and waist to hip ratio.  A number
were significantly depressed, sufficient to justify therapy.
"We conclude that there is a morbid syndrome associated with
growth hormone deficiency in adult life which responds
dramatically to hormone replacement.  To be effective this
therapy has to be continued indefinitely."

Obese men manifest fewer GH secretory bursts per 24 h and
accelerated HGH disposal rates.  (Journal of Clinical
Endocrinology and Metabolism 72:1 p. 51)


HGH may be useful in reducing diet-induced loss of lean
tissue.

10.4  Growth Hormone Stimulation

HGH is expensive.  An alternative to HGH injection is to
stimulate the body to excrete HGH.

Pearson and Shaw recommend stimulation of human growth
hormone (HGH) excretion with arginine amino acid supplements
as a weight loss method.  Unfortunately, the references
given in their book indicate their recommended amino acid
megadosage is still orders of magnitude too small to cause
the obese to release detectable amounts of HGH.

The obese have a high threshold which must be surpassed by
strenuous exercise (to the point of exhaustion) or
"incredible" doses of amino acids (orders of magnitude more
than even Pearson&Shaw recommend) before any stimulation of
HGH release is noted.  HGH levels achieved under these
exceptional conditions are still only a fraction of what
lean subjects spontaneously produce in their sleep.

Long term propranolol therapy increases body weight in heart
attack patients (2P-14); this may modify some of Pearson and
Shaw's recommendations.

"Chronic ingestion of L-dopa (an HGH releaser) leads to
sustained but reversible weight loss in both lean and obese
Zucker rats."



                       Adiposity 101







                           - 47 -



10.5  DHEA TREATMENT

University of Wisconsin researchers treated normal and 19
spontaneously obese dogs with DHEA.  The normal weight dogs
did not reduce weight or energy intake.  Two-thirds of the
obese dogs lost 20 percent of their excess body weight and
dropped cholesterol levels by nearly 25 percent without
reduction in food intake.  (Int J of Obesity 1990, 14,95-
104)

The 1990 Journal of Nutrition reported that DHEA treatment
reversed dietary induced obesity (from a mixture of corn oil
and condensed milk) as well as genetically induced obesity
(fa/fa rat).

In premenopausal obese women, DHEA levels are inversely
proportional to BMI.  Adipose cells remove DHEA from the
bloodstream; enhanced removal of DHEA in severely obese may
account for their impaired sensitivity to caloric
restriction.  (Metabolism, Feb 91, p 187)

Pearson&Shaw claim the "DHEA" sold by health food stores is
bogus.  The author of "The Vitamin Bible" reports successful
personal weight loss with DHEA but gives no further
information.

10.6  RU-486 TREATMENT

RU-486 causes obese mice to lose weight by getting fat cells
to generate heat rather than store fat.  RU-486 also blocks
the effects of glucocorticoids.  Reportedly RU-486 can help
cure Cushing's syndrome, a gland disorder characterized by
obesity and hypertension.  "Potentially the most potent
anti-aging drug available." (Longevity, Jan 1991) The 1990
American Journal of Physiology reported that RU-486
effectively reversed the obesity of fa/fa rats.

A paper in the 1992 International Journal of Obesity reports
that Norepinephrine (the neural transmitter, not the asthma
drug) inhibits rat pre-adipocyte proliferation.














                       Adiposity 101







                           - 48 -



10.7  CoPP TREATMENT

The 1990 Pharmacology reported that injections of cobalt-
protoporphyrin completely reversed the obesity of Zucker
fa/fa fatty rats to normal.  Significantly, untreated rats
that were fed the same amount of food as the CoPP treated
rats for the first 42 days reverted to the same weight as
untreated fatty rats by day 60.  This indicates CoPP caused
a long term reduction in the rats' set point.

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Typical CoPP treated (left) and untreated (right) Zucker
fatty rats.  Look at this from a distance to get the best
effect.  (B/W Xerographic photocopy of original color plate
was scanned, converted to GIF format by XView, converted to
ASCII with ASCGIF.)

10.8  CIRCADIAN LIPOSTAT MANIPULATION

Obesity and associated type II diabetes may be the result of
defective circadian [daily cycle] neuroendocrine rhythms.
Meier, Cincotta and Lovell have dramatically reduced body
fat with oral bromocriptine taken orally at times calculated
to reset circadian hormone rhythms to phase relationships
that cause loss of body fat.  Bromocriptine is a dopamine
agonist used to suppress lactation and in treatment of
Parkinson's disease.




                       Adiposity 101







                           - 49 -



"The phase of the prolactin rhythm differs in lean and fat
sparrows, fish, rats, and humans.  Daily injections of
prolactin in animals at times when the daily peaks occur in
the plasma of lean and fat animals produce the appropriate
decrease or increase in fat stores within two weeks."

In early clinical trials, without food restriction, body fat
was reduced equivalent to a 420 calorie VLCD, but without
the loss of lean body mass caused by weight loss diets.
Studies with Syrian hamsters investigating whole body
protein turnover indicate this treatment enhances protein
synthesis, redirecting anabolic activities from lipid to
protein.  Apparently the timed bromocriptine treatment
alters the genetically controlled partitioning of nutrients
described in "The response to long-term overfeeding in
identical twins" discussed above.

In the second study reported in Experientia 48 (March 1992
p. 248-), 15 diabetic subjects were given timed
bromocriptine treatment.  As with the non-diabetic subjects,
all 15 diabetic subjects lost fat.4 Blood glucose dropped
significantly.  Oral hypoglycemic medication was was
discontinued in 3 participants, and glucose levels remained
near normal for at least two months after treatment.  Doses
of hypoglycemic drugs and insulin were reduced in three
other subjects during treatment.

Blood pressure was also reduced, allowing blood pressure
medication to be discontinued in several.

In a telephone conversation (June 1992) Dr. Meier reported
that a third series of clinical trials was underway as part
of the FDA process to approve the treatment as safe and
effective.  He strongly emphasized how critical TIMING is to
fat loss; correct dosage given in the wrong rhythm actually
increases body fat.



__________

 4. That *all* subjects lost fat is significant.  In energy
    deprivation diet studies, some subjects may fail to
    achieve weight loss.  In long term diet followup, the
    standard deviation is two or three times as great as the
    average weight loss because a large minority gain
    weight, sometimes a great amount.  Without individual
    data or standard deviation, one simply cannot judge the
    true effectiveness of the experimental intervention.
    Many diet studies suppress this information.




                       Adiposity 101







                           - 50 -



"Our studies also indicate that a cause-effect relationship
between overfeeding and obesity is oversimplistic and that
food intake and lipid synthesis may be regulated in a
concerted fashion by circadian neuroendocrine activities."

10.9  TESTOSTERONE TREATMENT

Men with abdominal obesity have low testosterone values.  An
8 month study at the Sahigren's Hospital in Goteborg, Sweden
tested 23 men aged 40-65 years in a double blind experiment
in restoring testosterone levels to normal.  The
testosterone treated group improved in waist size, blood
pressure, plasma lipids, fasting glucose, and insulin
sensitivity.  Normalization of testosterone levels reduced
many of the health warning signs associated with obesity.

10.10  BETA3-ADRENOCEPTOR AGONISTS

Animal studies on several Beta3-agonists show they fulfill
many of the properties of the ideal anti-obesity drug.
These compounds produce selective loss of body fat mass with
a preservation of lean tissue.  In addition, the changes in
body composition are accompanied by favourable metabolic
changes including improvement in glucose tolerance,
reduction of hyperinsulinemia and hyperlipidaemia.  (S18-3)

10.11  FAT CELL REMOVAL

10.12  Surgery

Surgery is the only currently available fat reduction
treatment that has demonstrated long term success in a
majority of patients.

Unfortunately, the amount of fat removed by currently
accepted surgical procedures is too small to be useful for
mainstream weight reduction purposes.

A newspaper recently reported an increase in breast size for
women who had "love handles" removed.  It is possible the
breast size was recovering from the effects of stringent
dieting undertaken in unsuccessful attempts to spot reduce
the "love handles".

A South African study of freely-eating, non-obese
liposuction patients showed no increase in fat cell size,
metabolic efficiency, or regional adipose distribution 1 to
2 months after surgery.

Surgical removal of fat in Cushing's Syndrome patients (4F-
21) resulted in an increase in lean tissue mass, and no fat



                       Adiposity 101







                           - 51 -



regain.

Diabetic patients receiving abdominal liposuction have
reduced insulin requirements (dose reduced from 20 to 10
units).  (Unpublished data)

Some efforts are underway to develop surgical procedures to
significantly normalize fat cell numbers.

10.13  Immunological Manipulation

The Hannah Research Institute in Scotland have developed a
treatment to reduce adiposity by targeting cytotoxic
antibodies to fat cells.  In early experiments, rat fat cell
plasma was injected into sheep. The resultant antibodies
were filtered and introduced into the rats.  The treated
rats lost fat.

The treated rats also had more lean tissue than untreated
controls.  This suggests fat cells deprive lean tissue of
nutrients necessary for growth.

After treatment ended, the rats gained fat in other areas,
restoring a normal amount of fat.  This suggests some higher
level mechanism prevents adipose mass from falling below
norms.  Normal weight rats were used in these experiments;
results may be better for obese humans.

In a telephone conversation in 1991 I was told Hannah's
research is proceeding very well toward its goal of
producing leaner animal meat.  Human application in the near
future is unlikely due to risk of malpractice lawsuits.

Other researchers, using monoclonal antibodies, report
success in longer term suppression of fat cell numbers.
(Private conversation, 1992)


11.  PREDICTIONS

A portion of the current obesity epidemic will be traced to
nutritional and hormonal problems during pregnancy and/or
infancy.  Pregnancies with gestational diabetes and other
problems that previously failed now produce preobese
children.  The introduction of of high carbohyrdate baby
formula and sugary baby foods in this century will also be a
factor.  Low fat high carbohydrate weight loss diets applied
early in life will also be implicated.






                       Adiposity 101







                           - 52 -



12.  RECOMMENDATIONS FOR ACTION

Popular attitudes on obesity are based on the notion that
obesity is caused by sloth and gluttony.  Recent research
has discredited this stereotype and suggested possibilities
for effective prevention or treatment in the future.

   + Truth in Advertising must be enforced on all weight
     loss claims.  Advertising must disclose long term
     results obtained by typical users, accurately reporting
     the prevalence of weight regain and overshoot.5

   + Diagnostic procedures are needed to identify the 5 per
     cent of overweight subjects for whom weight loss diets
     provide long term benefits.

   + Policies and public education are urgently needed to
     reduce diet induced adipocyte hyperplasia.  (In
     English: diets make some fatter and we need to do
     something about it!) This is an area where malpractice
     and product liability lawyers can do some good.  The
     recent lawsuit settlements by Nutri-System Weight Loss
     Inc. are a promising start, and a meeting on the
     subject at a recent Trial Lawyers' convention bodes
     well for the future.

   + Effective interventions to correct human obesity must
     be developed and deployed.  Candidates include surgery,
     immunization to fat cell plasma, CoPP, RU-486,
     correction of low EGF, testosterone, DHEA and Growth
     Hormone levels.  One hundred million American
     endomoprphs deserve more than a few dimes' worth of
     legitimate obesity research.

   + Doctors should properly diagnose and properly treat the
     medical conditions of their obese patients instead of
     insisting on unrealistic weight loss as an alternative
     or precondition to treatment.

   + Regulatory interference in the development and
     deployment of effective new treatments must abate.
     Public health would be better served if regulators
     shifted their attention to the abuses of the diet
     industry.


__________

 5. The Federal Trade Commission is preparing a crackdown on
    diet companies.  (Reuter, May 21 1992)




                       Adiposity 101







                           - 53 -



   + Mothers should limit carbohydrate and sugar consumption
     during pregnancy and lactation.

   + Mothers should breast feed the full recommended time.

   + Babies should not be fed a high carbohydrate diet.

"We recognize that the message we have for endocrinologists
and metabolic specialists is a somber one, difficult to the
sufferer from obesity.  On the other hand, it seems to us
most consonant with the true state of affairs.  Our
understanding of genetic mechanisms is progressing rapidly
and the interaction between genetic endowment and early
environment will be under intensive study in the next
decade.  This is the hopeful side of the problem." (CLINICAL
REVIEW 28: A Biological Basis for Human Obesity, Journal of
Clinical Endocrinology and Metabolism, 1991.)


13.  REQUIRED READING

Human Obesity: Exploding the Myths The Western Journal of
Medicine Oct 1990; 153;421-428

Annals, New York Academy of Sciences, book length issue on
Human Obesity

LONG TERM WEIGHT CONTROL:
The National Heart, Lung, and Blood Institute funded
multimodal intervention study, Clin Pharmacol Ther, May 1992
Reprints of the entire supplement are available at no
charge.  Direct requests to:  Michael Weintraub, MD,
Department of Community and Preventive Medicine, University
of Rochester School of Medicine, PO Box 644 Rochester NY
14642

OBESITY AND LEANNESS, Basic Aspects, ISBN 0 86196 0173

Never Say Diet? article by Ruth Papazian,  FDA CONSUMER,
article downloaded from the Food and Drug Administration
Bulletin Board.  For copies contact the FDA Publications
Staff at 301-443-3220.


14.  RECOMMENDED READING

References such as (4F-21) refer to paper designations in
the Tokyo Internationl Congress on Obesity abstracted in the
International Journal of Obesity.  Some of these papers
appear in Progress in Obesity Research 1990 (Proceedings of
the 6th International Congress on Obesity), John Libbey &



                       Adiposity 101







                           - 54 -



Sons ISBN 0 86196 274 5

"Recent Advances in Obesity Research: V" ISBN 0-86196-072-6

"CLINICAL REVIEW 28: A Biological Basis for Human Obesity",
Journal of Clinical Endocrinology and Metabolism, 1991.

"Obesity in Europe 88" ISBN 0-86196-167-6

International Journal of Obesity (Periodical)

"Fat Chance" Nova episode broadcast on PBS (1983)

Annals, New York Academy of Sciences, book length issue on
Human Obesity

The Callaway Diet, Bantam non fiction paperback, ISBN-0-
553-28708-7 (C Wayne Callaway, M.D. is the former director
of the Nutrition and Lipid Clinic at The Mayo Clinic, former
director of the George Washington University Medical Center
Center for Clinical Nutrition, and has held prominent
positions with the U.S. Department of Health and Human
Services, and the National Institutes of Health.)

"Diet and Health:  Implications for reducing chronic disease
risk"; Committee on Diet and Health Food and Nutrition Board
Commission on Life Sciences, National Research Council;
National Academy Council, Washington D.C.  1989.

Progress in Obesity Research 1990 (Proceedings of the 6th
International Congress on Obesity), John Libbey & Sons ISBN
0 86196 274 5

"Number and Size of Adipose Tissue Fat Cells in Relation to
Metabolism in Human Obesity" Page 703, Metabolism, Vol 20 No
7 July 1971.

"Lean Body Mass, Exercise and VLCD", International Journal
of Obesity (1989), 13 (suppl. 2), 17-25.

"Super Nutrition for Women", Ann Louise Gittleman, Santa
Monica Pritikin Longevity Center nutrition director, Bantam
Books, 1991











                       Adiposity 101











                          CONTENTS


 1.  FOREWORD...........................................   1

 2.  ROSETTA STONE......................................   1

 3.  THE BIOLOGY OF ADIPOSITY...........................   3
     3.1    SET POINT...................................   3
     3.2    Rats, Pigs and Blimps.......................   4
     3.3    Brown Adipose Tissue (BAT)..................   6
     3.4    White Adipose Tissue (WAT)..................   6
     3.5    Preadipocytes > Fat Cells...................   6
     3.6    Fat Cell Receptors..........................   7
     3.7    Fat and Carbohydrate Oxidation..............   7
     3.8    Muscle Fibre Type...........................   8

 4.  FORTUNE OF BIRTH...................................   8
     4.1    Types of Adiposity..........................   8
     4.2    GENETICS....................................   9
     4.3    Maternal Environment........................  11
     4.4    Baby's Diet.................................  13

 5.  EFFECTS OF OBESITY.................................  13
     5.1    Personality Problems........................  14
     5.2    Health Problems.............................  14

 6.  TRADITIONAL TREATMENT..............................  15
     6.1    EXERCISE....................................  16
     6.2    DIETS.......................................  20
     6.3    SLOW vs RAPID Weight Loss...................  21
     6.4    Diet Side Effects...........................  21
     6.5    Diet Cycling................................  25
     6.6    High Fiber Diet.............................  30
     6.7    Low Fat Diets...............................  30
     6.8    Low Carbohydrate Diets......................  34
     6.9    Diets - the BOTTOM LINE.....................  36

 7.  FLAWED RESEARCH....................................  37
     7.1    Correlation .vs. Cause and Effect...........  38
     7.2    Flawed Sample Selection/Distribution........  38

 8.  TRUTH IN RESEARCH PAPERS...........................  39

 9.  MEDIA DISTORTION...................................  41

10.  NEW TECHNOLOGY.....................................  41
     10.1   MULTIMODAL INTERVENTION.....................  41
     10.2   STIMULATION OF THERMOGENISIS................  43
     10.3   GROWTH HORMONE TREATMENT....................  45
     10.4   Growth Hormone Stimulation..................  46



                           - i -











     10.5   DHEA TREATMENT..............................  47
     10.6   RU-486 TREATMENT............................  47
     10.7   CoPP TREATMENT..............................  48
     10.8   CIRCADIAN LIPOSTAT MANIPULATION.............  48
     10.9   TESTOSTERONE TREATMENT......................  50
     10.10  BETA3-ADRENOCEPTOR AGONISTS.................  50
     10.11  FAT CELL REMOVAL............................  50
     10.12  Surgery.....................................  50
     10.13  Immunological Manipulation..................  51

11.  PREDICTIONS........................................  51

12.  RECOMMENDATIONS FOR ACTION.........................  52

13.  REQUIRED READING...................................  53

14.  RECOMMENDED READING................................  53





































                           - ii -




-- 
Chuck Forsberg WA7KGX          ...!tektronix!reed!omen!caf 
Author of YMODEM, ZMODEM, Professional-YAM, ZCOMM, and DSZ
  Omen Technology Inc    "The High Reliability Software"
17505-V NW Sauvie IS RD   Portland OR 97231   503-621-3406