# Activated Charcoal for Hangover Prevention: Way more than you wanted to know

Activated charcoal is charcoal that has been heated up a whole lot and then washed really hard, by water or acid. [This process](https://buyactivatedcharcoal.com/how_to_make_activated_charcoal/) is what "activates" it, and activating it increases the surface area by a lot. I think it prevents hangovers.

I won't spend too much time in this post arguing that activated charcoal works. Instead, I'll mostly take for granted that it does, then take a tour of the various things that might cause hangovers, stopping at each to look at why activated charcoal might or might not be likely to reduce them. So even if you're sure activated charcoal is just a hokey health craze thing I've tricked myself into believing, this post still has lots of interesting hangover science you might not have heard about.

***A quick warning***  
*Some sellers of activated charcoal say to take it every day. I don't think there's any reason to do this, and some people say it's bad to. This is because it's a great absorber - that's why it helps with hangovers! - but it's possible it absorbs things you want to keep, like nutrients from food, so there's a theory that daily use could result in nutrient deficiency. This post advises taking activated charcoal only on nights of heavy drinking. *

***Also, if you take medications, activated charcoal could make them less effective, by absorbing the active ingredient; this could be pretty bad, depending on how important the medications are to your health**.*  
  
*Don't take activated charcoal every day. If you take important medicines, do solid research or ask a professional before taking any charcoal.*

I used to suffer vicious hangovers pretty often - usually a headache and sometimes nausea - after nights of drinking with friends. This past spring, I started taking two 520mg capsules of activated charcoal before going to bed on these nights. Since then, I've had maybe 26 nights out with the level of drinking I'd expect to result in hangover, and had a headache twice and nausea just once. (Tiredness is still common). Based on past experience, without activated charcoal I would have had headaches 12-18 of these times and nausea 4-10 times. 

I recently convinced a friend to try a capsule before going to bed after a late night, after she'd insisted for months that there was no way this would work. The next morning she sent me a rave review, saying she'd expected to feel terrible after the number of drinks she'd had, but just felt a little tired. She's tried it a couple more times since and it seems like it worked those times too. I had another friend try it once and he said he thinks there was a 60% chance it helped; another friend's husband says it worked twice and didn't work once. I originally tried the stuff after I found [this article](https://www.byrdie.com/activated-charcoal-tablets-for-hangovers), by a woman who went to a bachelorette party. They were split into two hotel rooms, and she gave activated charcoal to the women staying in her room, but not to anyone in the other one. The next day, those in the other room were in much worse shape.

The idea that activated charcoal helps hangovers doesn't have much support in the first few pages of google results. If I'd stopped at those, I wouldn't think it does anything. But my personal experience with it is striking. So I'm confused. Let's look into it.

Why might activated charcoal prevent hangovers?
-----------------------------------------------

I mentioned activated charcoal (charcoal for short) has a lot of surface area. From US Poison Control:

> Activated charcoal is a special form of carbon that can bind other substances on its surface (adsorption). That is why it is used for water filtration. It is also used to adsorb drugs in the gut so the drugs don't enter the body. Activated charcoal is made by burning carbon-rich materials, such as wood, at very high temperatures to create charcoal. The resulting product is a black, odorless powder. The charcoal is then "activated" through a special process that makes lots of holes and crevices on the charcoal particles to increase surface area and available binding sites. One teaspoonful of activated charcoal has about the same total surface area as a football field!

They also [share](https://www.poison.org/articles/activated-charcoal) a story, back from the arsenic-drinking days of 1813, of a chemist drinking 5 grams (read: a whole lot) of arsenic trioxide mixed with activated charcoal and being fine.

So activated charcoal puts a whole lot of surface area into your body. All kinds of molecules are floating around in your body, and when they bump into the little granules of charcoal powder, they bind to them. Whether or not a particular molecule binds depends on its chemical properties. These molecules include those that might be poisoning you at the time. If a molecule does bind to the charcoal, it can no longer pass from the gut into the blood, because charcoal granules are too big. Instead, the toxin is stuck to the charcoal as it slowly makes its way through the gut, and out through poop.

Activated charcoal is [used in emergency rooms](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6620762/) to help victims of poisoning[^bujgo4xd4h]. (But not alcohol poisoning!) [One source](https://pubmed.ncbi.nlm.nih.gov/3710499/)[^6nhtih1b65s] says that it's a poor treatment for alcohol poisoning because alcohol is too rapidly absorbed by the gut; [another](https://michaelrucker.com/functional-supplements/activated-charcoal-hangover/) says it's poor because ethanol doesn't bind to AC as much as other poisons do; [this one](https://www.ncbi.nlm.nih.gov/books/NBK482294/#_article-17128_s3_)[^1io4qp7goxs] says that that low binding is due to the polarity of alcohols.

Does activated charcoal reduce blood alcohol levels?
----------------------------------------------------

After long nights of drinking, I usually take 1040mg of activated charcoal just before bed. This is usually around 2am, when my first drink might have been at 7 or 8pm. I have the sense these days to wind down my drinking as the night nears its end, so I usually do not even feel drunk when I take the charcoal. However, many of the studies on charcoal and alcohol give people charcoal right after giving them alcohol, and then measure their Blood Alcohol Content. I don't want to skip these, so let's spend some time on how charcoal interacts (or doesn't) with BAC. 

I looked at 4 or 5 studies on humans that gave the charcoal around the same time as the alcohol, waited a bit, then measured BAC. They all report not finding any lower BACs in people who took charcoal. Most were done in the 80's and are paywalled and were on less than 10 people, so I might say that there was plausibly an effect but the studies were underpowered. Except [this one](https://pubmed.ncbi.nlm.nih.gov/3723647/)[^26sir633xsy] measures slightly *higher* ethanol levels in the people who got the charcoal (p-value 0.08). I don't think charcoal actually raises ethanol levels, but the finding is at least evidence against a small-but-not-significant effect of charcoal on ethanol blood levels. That study also involved ludicrous amounts of the stuff - 60 grams of activated charcoal. That's 60 times what I take!

Then to confuse things, [this study on dogs](https://pubmed.ncbi.nlm.nih.gov/7246560/) finds an effect, saying "absorption of ethanol was significantly inhibited by activated charcoal during the first hour after administration. Blood ethanol levels remained significantly lower throughout the study"[^w80fnxfd1lj]. [This one](https://pubmed.ncbi.nlm.nih.gov/8442886/) finds the same in dogs and rats, though it's more complicated because they tried a couple different delivery methods and some worked and some didn't[^07fgstqb90gj]. I don't see any reason ethanol could bind to charcoal in dogs and rats but not humans, so I don't get this. Maybe there's something going on here, but no one can find it happening in humans, so action on ethanol probably isn't why activated charcoal works.

I mentioned earlier that top google results for searches like "does activated charcoal prevent hangovers" say it doesn't. Most of them are making the basic case I made here: they looked up whether activated charcoal binds to ethanol, found studies saying it doesn't, and rested their case. But this case is too basic. BACs and hangovers correlate - people who get more tanked have worse mornings - but there's a lot more going on with hangovers than just BAC levels. I'll get into some of the other compounds you get from alcoholic drinks next, and try and figure out whether activated charcoal might be acting on any of them. But first: if I take charcoal before bed, an hour after my last drink, does it even get a chance to meet those compounds in the body?

Can activated charcoal even meet alcohol when not taken at the same time? 
--------------------------------------------------------------------------

Some digestion happens in the stomach, but most of it happens in the small intestine. If I take charcoal an hour after my final drink, the night's alcohol is mostly gone from the stomach already, so they don't meet there. By the time the charcoal reaches the small intestine, the final drink has probably finished its initial pass through there too. 

Most ethanol metabolization happens in the liver, but same problem: the alcohol doesn't pause in the liver, politely waiting to move on until the activated charcoal catches up. So what gives? How can they ever meet? This goes for all drugs, not just alcohol - how can charcoal ever help with anything, unless it's taken right away? 

I was pretty confused by this, but it turns out the body digests drugs via [a cyclic process](https://en.wikipedia.org/wiki/Enterohepatic_circulation). From what I can tell, some volume of the drug is processed in the first pass through the liver, but if there's too much to process in one pass, the substance gets put back into the small intestine for another go-around. This explains why [this source](https://www.ncbi.nlm.nih.gov/books/NBK482294/#_article-17128_s3_) can recommend charcoal as possibly beneficial up to 4 hours after large ingestions of some toxins: the toxin or its metabolites might still be going through the cycle[^1io4qp7goxs]. If you're drinking a fair amount of alcohol, you'll need multiple go-arounds through this cycle of liver->intestine->back-to-liver to fully process it.

> *Side note: a quick review of the alcohol metabolism pathway here, to make the next paragraph make sense: Ethanol is converted into acetaldehyde (AcH), then AcH is converted into acetate, then acetate is converted into carbon dioxide and water. The ethanol->AcH and AcH->acetate steps are mostly done in the liver. I'll use the words "byproduct" and "metabolite" to refer to these intermediate chemical steps.*

So. Say I'm out drinking into the night - enough drinks to be at risk of hangover - and I get home at 2am and take activated charcoal. That liver->intestine->liver cycle is still going on: some ethanol has been converted into AcH, some AcH has been converted into acetate, and some acetate has been fully broken down into CO2 and water. The metabolites that the liver hasn't finished with are being periodically deposited back into the small intestine for another go. Charcoal makes it into the small intestine an hour or two after ingestion. So they meet!

But for how long? Things that don't get absorbed into the blood, like charcoal and food, spend hours in the stomach, then more hours in the small intestine. I did some squinting at a couple sources to try and nail down how long. Some doctor with Cleveland Clinic says it takes [40 minutes at quickest, up to 3-5 hours if you eat a lot](https://health.clevelandclinic.org/how-long-does-it-take-to-digest-food/), for food to leave the stomach; a paper says it takes [an hour for just 10%](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1383315/pdf/gut00511-0163.pdf)[^k5vw1i4erce] of food to pass the stomach (though no way it takes 10 hours for all of it to pass); someone at Mayo says it takes 6-8 for things to get through the stomach and the small intestine together; and another doctor says it could be [7 to 11](https://www.dailytelegraph.com.au/lifestyle/health/body-soul-daily/gut-transit-time-can-be-big-indicator-of-your-digestive-health/news-story/badc481cb67bc3bcb508e4ad93671132). These are all vaguely in line with each other, so I'm fine with taking 6-8 hours as a first approximation for the time from ingestion to small-intestine-exit. 

So, roughly, there's a 2 to 5 hour window where the charcoal is in your small intestine (6-8 hours minus the time it spends in the stomach), where it can meet the alcohol or alcohol byproducts. Some digestion happens in the large intestine, too, and stuff spends days in there, so maybe charcoal spends time with some of alcohol's byproducts there too.

But since charcoal doesn't do much to ethanol, knowing that charcoal and ethanol meet in the intestine isn't enough to tell us why charcoal might prevent hangovers. Who cares if they meet, if they don't bind? So let's look at the things ethanol breaks down into, as well as the other substances that come in alcoholic drinks, in search of something that binds.

On alcohol byproducts
=====================

Since you can go to bed at 3am and still be hungover at noon, the presence of ethanol probably isn't causing hangover directly - it's all been metabolized by noon! Plus, lots of ethanol in your system makes you feel drunk, not hungover; and being hungover doesn't feel like being drunk. So it must be something else. Our main suspects in this section will be the two byproducts of ethanol metabolization - acetaldehyde and acetate - and also methanol, since alcoholic drinks have small amounts of methanol in them. In high enough doses, methanol is definitely terrible for you; acetaldehyde is probably pretty bad; and acetate has been linked to headaches.

Acetaldehyde
------------

Everyone agrees that acetaldehyde (AcH) is pretty bad for you. Some evidence AcH is pretty bad: acetaldehyde dehydrogenase (ALDH) is the enzyme that breaks AcH down into acetate. If you give someone a drug to temporarily stop ALDH from working, then give them alcohol, they will probably be violently ill. The reason they get sick is because AcH builds up in their body. (Disulfiram is a drug that does just this, and is used to treat alcoholism by making alcohol just horribly unappealing.)

ALDH is involved in "Asian Glow" too - people that get Asian Glow get it because of problems with their ALDH enzyme. I don't think people with Asian Glow suffer near as badly as people on Disulfiram; I asked a friend who has it, and she said her face turns red after a drink or two but she doesn't feel sick at all. Probably most Asian Glow sufferers have an ALDH enzyme that's less efficient, but still mostly works. It could also be that each enzyme works fine, and just not enough of them are produced - similar to how lactose intolerance is usually caused by not having enough lactase.

Everyone says that in normal people (not on Disulfiram or anything), AcH is converted to acetate pretty darn quickly. By morning, there isn't any left. There might not even be much left by the time I take activated charcoal at the end of the night. So the timing doesn't line up here. Also, AcH doesn't really bind to charcoal. [This paper](https://pubmed.ncbi.nlm.nih.gov/28105888/)[^ptfxofrrz] tried using activated charcoal in the creation of alcohol, adding it to a "barley malt-based agricultural distillate". Of everything they tested, acetaldehyde had one of the lowest binding affinities to charcoal.

Acetaldehyde is pretty interesting, and a good thing to target if you're trying to prevent hangovers; more about it in the ZBiotics section below. But no way is activated charcoal working on it, so moving on for now.

Acetate
-------

[Acetate causes hangover headache in rats](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013144/)![^uo3voammz68] 

I'm not sure how you measure a rat headache. It sounds like the authors poked the rats in the face using a special rat-face-poking machine, and measured how strong a poke had to be to make the rat react.

Unlike AcH, which is converted to acetate quickly, acetate hangs around in the body for a while. The paper says that acetate levels are up for at least six hours after ethanol consumption, though I can't find any statement that direct in their citations for the claim. The whole quote is useful:

> Although... acetaldehyde levels are low and change minimally following ethanol intake, **acetate levels are significantly elevated for at least six hours**. Studies suggesting that acetaldehyde is responsible for hangover have not considered acetate, which increases to much higher levels in the circulation, even after moderate drinking, compared to acetaldehyde levels. Acetate alone may induce headaches at these elevated concentrations. This is supported by the clinical observation that **acetate given during kidney dialysis causes headache**.

These authors say a couple things throughout the paper suggesting they don't think AcH is very important in hangovers, though they don't go all-out, instead saying it's possible that AcH matters in addition to acetate:

> These data do not completely exclude the role of acetaldehyde in hangover... Acetaldehyde may still cause hangover symptoms in humans including headache. The data in this study demonstrate that acetate also contributes to the headache component of the hangover. 

Since Asian Glow symptoms are caused by AcH build-up, I don't think AcH is off the hook either. 

### Tangent: Acetate and caffeine

[This paper](https://pubmed.ncbi.nlm.nih.gov/8198211/)[^9f794furuf] has more bad things to say about acetate:

> Ethanol has been shown to increase markedly portal blood flow, primarily by increasing intestinal blood flow. This effect of ethanol is reproduced by acetate, infused at rates equivalent to those leading to endogenous acetate production following ethanol administration... adenosine is also known to increase markedly intestinal and portal tributary blood flow. We have shown that adenosine receptor blockade with 8-phenyltheophylline completely abolishes the effects of ethanol, acetate, and adenosine on intestinal and portal blood flow.
> 
> ... **acetate administration has marked effects on central nervous system function**. On two tests, motor coordination and anesthetic potency, both ethanol and acetate showed similar effects. **The effects of acetate were fully abolished by 8-phenyltheophylline**... Whereas ethanol at low doses increased locomotor activity in mice, acetate markedly reduced it.

No clue what 8-phenyltheophylline is. The important thing is it *blocks adenosine* \- just like coffee - and this improves symptoms! Also, the rat-headache people [found](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3013144/pdf/pone.0015963.pdf) that the rats they gave caffeine had less severe headaches. They say "acetate increases adenosine in many tissues, including the brain", so their model is basically that acetate causes adenosine, which causes headaches.

Caffeine doesn't have anything to do with activated charcoal, but people have been into treating hangovers with coffee forever: In 1768, the writer William Hickey wrote a whole lurid description of having a hangover. It's good stuff:

> My first return of sense or recollection was upon waking in a strange, dismal-looking room, my head aching horridly, pains of a violent nature in every limb, and deadly sickness at the stomach. From the latter I was in some degree relieved by a very copious vomiting. Getting out of bed, I looked out of the only window in the room, but saw nothing but the backs of old houses, from which various miserable emblems of poverty were displayed . . . . At that moment I do not believe in the world there existed a more wretched creature than myself. I passed some moments in a state little short of despair . . . .

Later in the same essay, he says "very strong coffee proved of infinite benefit"[^hq58q70bztt]. Sadly this doesn't work for me at all for some reason, but the acetate->adenosine angle gives a mechanism by which coffee might reduce hangovers.

### Does activated charcoal bind acetate?

[Wang 2005](https://pubs.acs.org/doi/10.1021/je049731v) looks at a bunch of different acetates (ethyl acetate, methyl acetate, butyl acetate...) and sees how much they're absorbed by different materials[^nw8cp2dx7ls]. This is again a study about air filtering, outside of any biological body, but they say that "In general, activated carbon has a greater affinity for \[these acetates\] because of the nonpolar nature of its surface compared to other solid sorbents." 

I'm not sure if the type of acetate matters here. Even [this paper](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3484320/) specifically on alcohol metabolism just calls the thing that AcH gets turned into "acetate"[^v6wm24fg0so]. Acetic acid is really similar to acetate, and [here's a source](https://link.springer.com/article/10.1007/s13201-016-0491-3) that says activated charcoal is good at binding acetic acid, so... that's suggestive?[^rup01cxolj] But me not knowing much chemistry is starting to be a problem here, and I don't know whether the difference between acetic acid and acetate would cause changes in the effectiveness of charcoal.

I also think this [extremely confusing abstract](https://journals.sagepub.com/doi/abs/10.1260/0263-6174.28.10.895) is saying that activated charcoal is good at absorbing ethyl acetate[^ckok5wxqjpa]. This still feels shaky, since I'm not sure if we're all talking about the same kind of acetate here. Also, like, Wikipedia says "In nature, acetate is the most common building block for biosynthesis". Does the most common building block for biosynthesis really cause hangover headaches? Sounds weird.

Methanol
--------

Methanol is present in all alcoholic drinks. It's produced naturally by the fermentation process (the step in alcohol production where sugar is broken down by microorganisms). Methanol is also added in large amounts to make denatured alcohol, but that's not what I mean here: it's present in small amounts in all alcoholic drinks, and most can be distilled out, but it's hard to completely remove. Methanol is often bound to pectin - a sugar molecule common in fruit - and fermentation frees methanol from pectin. The rough alcohol-creation/methanol model I have in my head is "more fruit = more methanol". But there's a little bit of methanol present even in things that don't seem fruity at all - for example, Budweiser, and Vodka too - because all plants have pectin.

Methanol is higher in wood-aged liquors than clear liquors. I only have rough numbers here, but the worst fruit brandies [can have as much ](https://www.ncbi.nlm.nih.gov/books/NBK531662/)as 4,000 mg of methanol per liter (mg/L) \[this seems high though - don't anchor to it!\], and Scotch whisky has 40-130 mg/L[^4yqxtwc0jah]. Vodka, much less: less than 2.5 mg/L in a survey of Brazilian vodkas, though higher in some vodkas in Eastern Europe - around 50 mg/L, and [this 1981 paper](https://pubmed.ncbi.nlm.nih.gov/7334803/)[^7au9dmen6v2][ ](https://pubmed.ncbi.nlm.nih.gov/7334803/)measured Smirnoff at 39 mg/L[^u1vrt26lupp]. (The Smirnoff number is more relevant to American drinkers, but it was the 80's, so let's discount it to 25 mg/L for no good reason). It's [present in wine](https://www.bio-conferences.org/articles/bioconf/pdf/2017/02/bioconf-oiv2017_02028.pdf), and red wines have more methanol than whites or rosés[^akuhmy7ei8s]. Reds have 60-280 mg/L, and whites, 40-120mg. Popular light beers had 6 - 20 mg/L in that same 1981 study.

These numbers are hard to compare as-is, since if you're drinking beer, you're drinking a whole lot more volume than if you're taking shots. What we want is methanol content per liter of ethanol, instead of per liter of liquid. Say the typical liquor is 50% ethanol, wine 15%, beer 5%. Then we get these rough ranges:

*   Scotch: 80-260 mg/L
*   Vodka: 50 mg/L
*   Red wine: 400 - 1850 mg/L
*   White wine: 250 mg/L - 800 mg/L
*   Light beer: 120 mg/L - 400 mg/L

(I'm worried about the beer numbers, because lots of soft sources online say beer has *no* methanol, and for some reason almost no scientists have ever published measurements of methanol in beer, so all I have is that one 1981 paper. I feel better about the other drinks, because I have a few sources for each that all hit around the same rough range. A friend who knows brewing points out that barley, used to make beer, has pectin, which explains how methanol can make it in.) 

Methanol is bad for you because of its byproducts: "[the products of](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf) methanol metabolism are extremely toxic and in high concentrations may cause blindness and death."[^hq58q70bztt] These two byproducts are formaldehyde and formic acid; it sounds like formic acid is the really bad one. (Though there is [an argument](https://www.lesswrong.com/posts/LfrNFfJFcqnG9WuFf/activated-charcoal-for-hangover-prevention-way-more-than-you?commentId=Ngxpe5LgBQp3do2PN) that formaldehyde is the worse one. Both are bad!)

There is a little bit of methanol in alcoholic drinks. It's so little that the papers I've seen so far just dismiss it; public health councils have looked into it a lot and don't think anyone is going to get proper methanol poisoning from properly-made alcoholic drinks. However, [for hangovers](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf):

> One specific congener implicated in hangover effects is methanol... Support for methanol’s contribution to hangovers comes from several sources. **For example, distilled spirits that are more frequently associated with the development of a hangover, such as brandies and whiskeys, contain the highest concentrations of methanol.** Moreover, in an experimental study with four subjects who consumed red wine containing 100 milligrams per liter (mg/L) of methanol, Jones (1987) found that **elevated blood levels of methanol persisted for several hours after ethanol was metabolized, which corresponded to the time course of hangover symptoms.** Methanol lingers after ethanol levels drop, because ethanol competitively inhibits methanol metabolism. The fact that **ethanol readministration fends off hangover effects** may be further evidence of methanol’s contribution to the hangover condition, given ethanol’s ability to block methanol metabolism and thereby slow the production of formaldehyde and formic acid.

(Notice the last sentence, where the authors take for granted that "ethanol readministration fends off hangover effects", i.e. that hair of the dog works! Also that dark liquors are probably worse for hangovers than light ones like vodka.)

The reason ethanol fends off methanol metabolization is that they're both processed by the enzyme alcohol dehydrogenase (ADH), but ADH really prefers to do ethanol first, for vague chemical reasons. I'm not sure if this means that all the ethanol in your body has to be broken down before methanol metabolization begins, or just that methanol metabolization is very slow while ethanol is still around, but either way, most of methanol metabolization occurs after ethanol has mostly been broken down. So as you sleep after a long drinking night, the concentration of ethanol is going down. This allows more methanol to be metabolized, and it breaks down into formaldehyde, then formic acid. This means your peak concentration of formaldehyde and formic acid happens hours after you finish drinking, either in the middle of the night or the next morning. 

So all over this post I've said (and will keep saying) stuff like "Methanol is important in hangovers", but I never actually mean the methanol is directly causing any of the symptoms - whatever effects it has are because of the formaldehyde and formic acid it turns into.

### Does activated charcoal bind methanol, formaldehyde, or formic acid?

Remember the paper from the acetaldehyde section that found it had one of the lowest affinities to activated charcoal? The other molecule they called out as having especially low binding was methanol. So direct action on methanol is out.

How about formic acid? [Adekola 2016](https://link.springer.com/article/10.1007/s13201-016-0491-3) (also done outside the body - in an "aqueous solution") says yes! "It is therefore established that \[activated charcoal\] has good potential for the removal of \[acetic acid\] and \[formic acid\] from aqueous solution"[^rup01cxolj]. [Another study too](https://www.tsijournals.com/abstract/study-of-the-adsorption-of-formic-acid-and-acetic-acid-on-activated-carbon-4282.html)[^i083aipwvg].

[Colgan 2016](https://pubmed.ncbi.nlm.nih.gov/27262203/) suggests using activated charcoal in drug packaging to stop formaldehyde and formic-acid degradation of the packaged drugs[^npykcvfk02]. I guess those two chemicals either leak in from the environment or are partly a result of the drugs themselves degrading over time. The study tried speeding up the drug-degradation process by some method, compared how fast drugs degraded with and without charcoal around, and found they degraded slower when there was charcoal present. 

Yet another finds that formic acid binds "much slower" to activated charcoal than acetic acid. But I'm not sure if this means that acetic acid gloms on super fast, and formic acid binds at a decent rate, or if it means that charcoal is bad at binding to formic acid. So there's decent evidence that charcoal has some decent action on formic acid.

Recall that the chain goes methanol->formaldehyde->formic acid. So adsorbing formaldehyde might also help with the possible toxic effects of the methanol metabolization pathway. [Here's a company](https://services.jacobi.net/formaldehyde-removal-from-air/) describing an air filter with activated charcoal in it that can remove formaldehyde from the air: "\[the design of our product\] ensures the efficient removal and retention of formaldehyde while retaining an excellent physical adsorption capacity." [Tanada 1999](https://pubmed.ncbi.nlm.nih.gov/10328902/) "aminates" activated charcoal - I don't know what that means (well, it means adding an amine group, but I don't know what *that* means) - and says that makes it effective at adsorbing formaldehyde[^bhe1et34u3]. 

And it's not just them - most hits for searches like "activated carbon formaldehyde" return results about air filtering. Even trying "activated carbon formaldehyde in the body" returns air filtering results! Trying a little harder, I find that activated charcoal administration is [one of the CDC's recommendations](https://wwwn.cdc.gov/TSP/MMG/MMGDetails.aspx?mmgid=216&toxid=39) for someone who's taken in too much formaldehyde. [Also](https://www.researchgate.net/publication/286274375_Development_of_Formaldehyde_Adsorption_Using_Modified_Activated_Carbon-A_Review) "Most researchers used activated carbon as an adsorbent for removal of formaldehyde because of its high adsorption capacity", though again with a focus on formaldehyde's gas form[^yl35wutnma8]. 

For a lot of things, action in the air is different than action within the body - but the narrow question "does formaldehyde bind well to activated charcoal" seems like a question about very local chemical properties, so I'm going to take these results as evidence that charcoal can bind formaldehyde effectively in the body too.

OK. Summarizing so far: 

*   Activated charcoal has little or no direct action on ethanol or methanol.
*   AcH, a byproduct of ethanol often implicated in hangovers, also is not much affected by charcoal.
*   Acetate, another alcohol byproduct, might cause headaches, and activated charcoal might bind acetate.
*   Methanol, present in small amounts in alcoholic drinks, has two toxic byproducts, and activated charcoal probably binds both.

I smell blood here. If methanol's byproducts really are implicated in hangovers, then we have our answer: charcoal binds its byproducts well, stopping them from being absorbed by the body, instead ferrying them out directly through poop. Above, I mentioned some reasons for thinking methanol is related to hangovers; let's go deeper into those reasons.

More on methanol and hangovers
==============================

Methanol definitely isn't the *only* cause of hangovers - you can get a hangover from pure ethanol administration (though [my source](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf)[^hq58q70bztt][ ](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf)doesn't cite a source). But looking at some hangover folk knowledge - things I've heard from friends and in random parts of the internet and in locations where alcohol is served, basically - gives hints that methanol might be involved:

### Folk knowledge #1: Clear liquors are less likely to cause hangovers than dark liquors

This one has to be true. 

[Rohsenow 2010](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674844/) gave bourbon to some people and vodka to others and compared how hungover they were by just asking them and rating their answers on some pre-established scale[^unjk61g61l]. Their ratings on the different alcohols looked like this:

![](https://39669.cdn.cke-cs.com/rQvD3VnunXZu34m86e5f/images/2ac377b7c5a754ac8b8c080e393333e33a15d442f7f6a36f.png)

This graph is kind of jank because I assumed a normal distribution and just plugged in their means and standard deviations.

[Chapman 2010](https://www.jsad.com/doi/abs/10.15288/qjsas.1970.s5.067) just gave people bourbon or vodka and then asked if they were hungover the next day, Yes or No[^i0jhlbwslva]. There were 30 people in each group; 13 of the vodka people were hungover, and 20 of the bourbon people. Those distributions look like this:

![](https://39669.cdn.cke-cs.com/rQvD3VnunXZu34m86e5f/images/2d752e2ea98a7426a84eac07acdff38f083206db55516f2f.png)

Bourbon definitely has more methanol than vodka, and bourbon causes more/worse hangovers than vodka. 

And another:

> [Pawan compared](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2125562/pdf/9001463.pdf) the hangover produced by different types of drink (but only one brand of each) in his study of 20 volunteers[^5yew8sgbfyc]. The severity of hangover symptoms declined in the order of brandy, red wine, rum, whisky, white wine, gin, vodka, and pure ethanol. Vodka and pure ethanol caused only mild headaches in two volunteers.

### Folk knowledge #2: Sugary drinks make for worse hangovers

I never really believed this one, but I hear it pretty often. I haven't looked into whether there might be mechanisms by which sugar causes hangovers, but fruit juice has methanol in it. [Orange juice has around 100 mg/L](https://www.researchgate.net/publication/287784314_Methanol_contents_of_fruit_juices_and_smoothies_in_comparison_to_fruits_and_a_simple_method_for_the_determination_thereof) \- fruit juices overall have [12 - 640mg ](https://inchem.org/documents/ehc/ehc/ehc196.htm)mg/L methanol, and the average juice has around 140 mg/L[^9urf4ffvk3v][^9e4uhus3fy]. Scotch whisky was 40-130 mg/L, so a "shot" of orange juice gives you as much methanol as a shot of whisky. This means if you mix your alcohol with orange juice all night, you're doubling up your methanol content. (Hopefully you're not drinking whisky-orange-juices, but you know what I mean).

Often, sugary drinks are sugary because they have fruit juice in them, so maybe it isn't the sugar, but instead the extra methanol, that makes sugary drinks give worse hangovers. And the reason you don't get hungover while drinking orange juice by itself is that your body starts on the methanol metabolization right away, instead of letting it store up. The only time the methanol from fruit has a chance to build up is when you consume it at the same time as ethanol.

**Bonded methanol?**

But actually, maybe most of the methanol in orange juice is still bonded to pectin. While it stays bound, it isn't an issue; this methanol only starts getting separated from pectin [once it reaches](https://cot.food.gov.uk/sites/default/files/cot/cotstatementmethanol201102revjuly.pdf) [the colon](https://www.yarchive.net/med/methanol_poisoning.html)[^6b5o582h9uw][^bt0zodr8d5]. The colon is later than the stomach and small intestine breakdown phases I've been talking about for most of this essay - juice reaches the colon maybe 6 - 15 hours after ingestion. So this is another delayed-effect kind of thing going on with methanol. 

### Folk knowledge #3: Hair of the dog works

Hair of the dog is the idea that having a drink or two while hungover makes you feel better. I mentioned this above too, but it's the biggest reason I think methanol is part of what causes hangovers, so let's go deeper into it.

[Jones 1987](https://pubmed.ncbi.nlm.nih.gov/3588516/) says that hair of the dog works ("The most effective treatment for hangover, at least for short periods, is to drink more ethanol")[^9iiq0cnjya]. [Swift 1998](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf) takes him at his word (also, I'm going to start using "F&F" to mean "formaldehyde and formic acid"): 

> Jones has suggested that it is the metabolism of methanol to F&F that causes symptoms of hangover, with quicker methanol metabolisers suffering more. The justification for this suggestion is threefold: the types of drink associated with more severe hangovers contain higher levels of methanol; the time course of methanol metabolism corresponds to the onset of symptoms; and a small dose of ethanol, which blocks the formation of F&F, provides an effective treatment for hangovers (“the hair of the dog”).[^hq58q70bztt]

Recall that the ADH enzyme is the main thing that processes both ethanol and methanol, but much prefers to do ethanol first. When methanol metabolization is inhibited because of this preference, its half life is long: [45 to 90 hours](https://www.ncbi.nlm.nih.gov/books/NBK482121/)[^9yxogbz0hdc]! When the ethanol is mostly gone, in the morning after a night of heavy drinking, methanol's half-life is just [2 to 3 hours](https://pubmed.ncbi.nlm.nih.gov/3588516/). 

Ethanol is so good at stopping methanol metabolization that it's [one of the main treatments for methanol poisoning](https://pubmed.ncbi.nlm.nih.gov/30864518/)[^zphx3sf0s3]. I think doctors still have to use other methods to get the methanol out once they've paused its metabolization; [Gonda 1978](https://pubmed.ncbi.nlm.nih.gov/645740/) recommends cleaning the blood with hemodialysis whenever a lethal dose of methanol has been ingested, while administering ethanol to give the patient more time[^04ghaymli3zt].  Some sources act like once you administer ethanol, you've cured the methanol poisoning - [Wikipedia](https://en.m.wikipedia.org/wiki/Methanol_toxicity#:~:text=Methanol%20poisoning%20can%20be%20treated%20with%20fomepizole%2C%20or,dehydrogenase%20on%20methanol%20by%20means%20of%20competitive%20inhibition.) calls ethanol an "antidote" - but I don't understand how this could be true. Won't the methanol still be around once the ethanol wears off?

Jones also measured methanol in people the day after drinking, and yup, it's still around: 

![](https://39669.cdn.cke-cs.com/rQvD3VnunXZu34m86e5f/images/7ea48642a9bffe4b54f0b8a321d4cfcb4456a2a80e6c5edf.PNG)

It's weird that there's so much ethanol left, relatively, at the beginning of the graph, and then it goes away so quickly. From some of the paper's language, it sounds like Jones might have intentionally started the graph at 100 mg/L blood ethanol, to investigate what's happening at low levels of these drugs. It's also weird that the methanol curve doesn't get steeper at around 10 or 11am - shouldn't the finishing-up of ethanol around that time free up ADH to metabolize methanol more quickly?

The reason for both of these weirdnesses: in Jones's view, ethanol levels under 100 mg/L is when ADH can really start working on methanol: "Below a blood concentration of about I00 mg/l, liver ADH is no longer saturated with ethanol as substrate and metabolism of methanol can therefore commence." So maybe the reason the methanol line doesn't bend is that you don't need *all* the ADH to metabolize methanol at the max rate, you just need enough of it, and "enough" happens at around 100 mg/L ethanol. I wish he'd measured the methanol levels before 9am, to see whether the methanol line is flat until that time. 

If Jones is correct here, taking activated charcoal in the morning should be good enough, as long as you wake up early enough to take it before your ethanol levels get this low. It also might explain a strange experience I had earlier this year. I woke up at 9am after a reallllly heavy night of drinking - my heaviest in years, and since - and felt perfectly fine up until around noon. I biked home! It was a beautiful day and I felt great; I felt industrious and started laundry. Then around noon, I got hit with one of the worst hangovers of my life and could barely walk. Unloading the dryer was a struggle. I'd never had a delayed-onset hangover like that before, and I could never figure out what caused it. Maybe it's because I drank so much the previous night that my ethanol levels didn't fall below the 100 mg/L dividing line until afternoon the next day? (This was before I'd ever taken activated charcoal. Actually, that day was so bad, it inspired me to start researching and trying to find hangover preventers. It was so bad, it eventually caused this post.)

**Hair of the dog as a methanol pause-button**

Lots of soft-science sources, like [this Healthline article](https://www.healthline.com/nutrition/hair-of-the-dog#what-it-is), warn things like "While \[hair of the dog\] may offer temporary relief, it only delays the inevitable, as the hangover will return once you stop drinking." 

This might make sense if hair of the dog worked by alleviating alcohol withdrawal. But if it works by arresting methanol metabolization, then this warning makes less sense. Let's call this latter view the pause-button view. 

In the pause-button view, when you wake up after a night of drinking and feel hungover, part of that is because you have F&F in your system. Taking another drink pauses methanol metabolization for the couple of hours it takes your body to process the new ethanol. While that's happening, your body is no longer making new F&F. Ethanol stops methanol from being converted by ADH, but since ADH doesn't do anything to F&F, focusing ADH back onto ethanol doesn't block or slow F&F breakdown at all. Your body gets a chance to clear them, without any more coming in. Their levels lower. Then, once the new ethanol has been metabolized, your system returns to metabolizing the remaining methanol, so your *peak* F&F level is lower than it would have been. This matches up with the ethanol-then-hemodialysis method of treating actual methanol poisoning.

**Or as staving off withdrawal?**

Or maybe part of being hungover is just minor & temporary alcohol withdrawal.

> [Several lines of evidence suggest](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf) that a hangover is a mild manifestation of the alcohol withdrawal syndrome in non-alcohol-dependent drinkers. First, the signs and symptoms of hangover and mild manifestation of the AW syndrome in non-alcohol-dependent drinkers overlap considerably... Several \[AW symptoms\] also are usually present during a hangover, including nausea and vomiting, tremor, sweating, anxiety, headache, and sensory disturbances.
> 
> Second, Begleiter and colleagues (1974) present evidence that the hangover condition is actually a state of central nervous system excitation, despite the perceived sedation and malaise. Support for this view comes from the research of Pinel and Mucha (1980), which shows that single doses of alcohol decrease seizure thresholds in animals several hours later. Their finding indicates rebound excitation, a phenomenon noted to occur after short-term administration of some sedatives that can quickly clear the body, including alcohol and certain benzodiazepine drugs.[^w7swq4iwyq8]
> 
> Third, the observation that alcohol readministration alleviates the unpleasantness of both AW syndrome and hangovers suggests that the two experiences share a common process.

This sounds very reasonable and could totally be true. Also, I asked my friend who's tried hair of the dog and she said she feels the benefits almost immediately, which makes sense under this theory but makes no sense under the methanol theory.

(I should probably mention here that I've never done hair of the dog, that it feels to me like the most alcoholism thing ever, and does seem like the kind of thing that could condition you into real no-shit alcoholic dependence. If this section has convinced you that methanol's byproducts are bad and inspired you to try hair of the dog to reduce their levels, don't - instead, first try dealing with those byproducts by taking activated charcoal!)

### Folk knowledge #4: Cheap swill gives worse hangovers

Cheaper liquor is less distilled, so less of the methanol has been removed. Of course, less of lots of stuff has been removed - distillation removes all kinds of things. So if this item of folk wisdom is true, it implicates methanol more than it implicates AcH or acetate. But there are all kinds of congeners in alcohol that distillation removes, and it could be one of those making it so that cheap swill gives worse hangovers. So this points toward methanol a little bit too, but is pretty weak evidence by itself.

(However, after I wrote this, I talked to a friend who knows brewing, and he says that additional distillation steps probably don't have a big effect on methanol concentrations. This section still feels true to me, but maybe it's not.)

### Folk knowledge #5: It doesn't seem like people get hangovers in the middle of long drinking binges 

I'm not sure if this is actually folk knowledge; it's just a vague feeling I have. I've never heard of people who pull all-nighters, drinking into the morning, being hit by hangover symptoms while still on their binge. I don't know enough people who drink through the morning often enough to have much of a sample size, but if continuing to drink does delay the hangover, that weakly suggests methanol is important in hangovers. (However, if this is true, staying awake *not* drinking should *not* delay the hangover, since it's only the continued presence of ethanol that delays methanol metabolism.) This would also fit with the alcohol withdrawal theory, though.

### Folk knowledge #6: Red wine gives bad hangovers

Red wine has more methanol than most other types of alcohol.

A test for the methanol theory of hangover
------------------------------------------

Drink 3 or 4 shots of vodka in the span of 5 minutes, then eat as much fruit and drink as much fruit juice as you can. Different fruits have different methanol contents, so use the highest *free* menthol fruit you can. It's important that it be free methanol, because methanol bound to pectin has to wait until it reaches the colon to be freed up. Since it takes 6-8 hours for food to reach the colon, the 3-4 hours it takes to metabolize the vodka isn't enough time to block the metabolization that starts 6-8 hours after you eat the fruit. To address this, you'd have to drink a lot more vodka, but that complicates the experiment. Monte 1984 is the source for the WHO's estimate[^9e4uhus3fy] of 12-640mg of methanol in fruit juices, and it sounds like he reports the methanol levels per fruit type, but I can't find his paper (book?) online, so I'm not sure which fruit is highest - maybe elderberry juice[^9urf4ffvk3v]?

The shots of vodka are enough to block methanol metabolization for a few hours, but not enough by themselves to make most people hungover. If you do start to get hangover systems 3-12 hours after the shots, then the free methanol in the fruit you ate & drank is probably causing it. (If you overdo it on the fruit, this might be dangerous.)

Other theories
--------------

[Verster 2008](https://academic.oup.com/alcalc/article/43/2/124/122754)[^kidjhqpnis] speculates that hangovers might have something to do with immune system activity. Sounds reasonable enough. I haven't touched on or looked into this angle at all. 

I mentioned the alcohol withdrawal theory[^w7swq4iwyq8] earlier (there's actually content in that footnote - read it!), while talking about hair of the dog. I think it's a solid idea.

Doesn't dehydration cause hangovers?
------------------------------------

Yes and no. Getting enough water is really important all the time. Alcohol makes you more dehydrated, and being low on water probably makes your body worse at processing alcohol and its byproducts, so not getting enough water on a night you're out drinking will make your hangover worse. But it's not the only factor. I've had nights where I knew I'd be having a lot of alcohol and so drank water like a fish throughout the day, all through the night, and when I got home afterward, and still got hungover. On the other hand, I once got too confident in the activated charcoal and had about one glass of water all night and had a pretty bad time the next day. 

Hydration is a key part of a good anti-hangover system. Eating enough is another part of that system, and for me and probably others, taking activated charcoal is a third leg of an effective system. For more on all the kinds of things that might cause hangovers, check out [this excellent review](https://pubs.niaaa.nih.gov/publications/arh22-1/54-60.pdf). I've cited it here like 5 times already. I read it hungover on New Year's Day 2019 and felt terrible the whole time and highly recommend it.

Other hangover prevention items
-------------------------------

### AfterEffect

I stumbled upon [Verster & Berthélemy 2012](https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3407600/) on something called AfterEffect. It doesn't have activated charcoal in it: "The ingredients of After-Effect comprise borage oil (gamma linolenic acid), fish oil (omega-3), vitamins B1, B6, and C, magnesium, *Silybum marianum* (silymarin), and *Opuntia ficus indica*."[^gsp7t5ipotc]

The study finds this drug reduces self-reported hangover symptoms by 2 to 3 points on all 8 symptoms they asked about, and overall, reduced hangover severity from 5.2 in the no-treatment group to 2.3 in the treatment group (standard deviations were 1.9 and 1.6). That's a lot!

The study was funded by the manufacturer, and Berthélemy is the founder and CEO. [Verster](https://www.uu.nl/en/research/pharmacology/research/joris-verster) runs a lab at a university, though, and has done [a million other hangover studies](https://pubmed.ncbi.nlm.nih.gov/?term=Verster+JC&cauthor_id=22852090), so he seems legit enough? There are probably other products like this out there too.

### ZBiotics

When I told a friend of mine I was writing this post, she sent me an Instagram ad for ZBiotics, an anti-hangover probiotic. (I haven't tried it). Their marketing material believes - and probably their core science staff believes too - that acetaldehyde is the main important thing to target to reduce hangovers. 

They [make a decent case](https://zbiotics.com/blogs/journal/what-is-acetaldehyde-and-why-does-it-matter) about how, yes, fine, AcH breaks down to acetate quickly *in the liver -* but there's a hitch in the stomach. In the stomach, there isn't much ADH or ALDH, so neither ethanol or acetaldehyde should be getting broken down until they reach the liver, where there's a lot of both enzymes. *But* there are also ethanol-metabolizing microbes in the stomach. These microbes turn some ethanol into AcH before it reaches the liver. There aren't any stomach bacteria that break down AcH, so the AcH that gets produced in the stomach just hangs around and builds up. 

I'm confused about this: don't non-afflicted drinkers make about the same amount of stomach AcH as people on Disulfiram do? And almost none of it gets broken down in the stomach, for either group? But people on Disulfiram get sick within [10 to 30 minutes](https://www.ncbi.nlm.nih.gov/books/NBK64036/) of drinking alcohol; I don't think that's enough time for the stomach AcH to have reached the liver. At 10 minutes, neither group has much ALDH in play to metabolize the stomach AcH, but people on Disulfiram have somehow built up more AcH than people not on it. I'm confused enough by this that I don't count it as a point against ZBiotics - after writing this paragraph, it seems to me like Disulfiram has no right to work on alcohol 10 minutes in, but it does, so I must have something wrong here.

Either way, [their solution](https://zbiotics.com/blogs/journal/engineering-zbiotics-part-1-what-we-did) is pretty cool: they bioengineered a bacteria, changing it in two ways. First, they made it produce acetaldehyde dehydrogenase instead of whatever it used to naturally produce, and second, they made it produce it all the time, instead of just sometimes. So you can basically buy and drink little biomachines that constantly pump out ALDH now. 

Theoretically, you could use this for Asian Glow symptoms too. But it could be pretty dangerous! Say you take ZBiotics before drinking, drink a lot because you feel fine, and then the ZBiotics wears off before you've cleared the ethanol. You'd have a bunch of acetaldehyde left to process, and not enough ALDH capacity to process it. So trying this is a good way to get acetaldehyde poisoning. I think this is an interesting avenue for research, but not something to try yourself, unless your doctor approves it.

For people with ALDH enzymes in good condition, trying to prevent hangovers, taking activated charcoal as well as something like this might be a good idea. Acetaldehyde is bad for you and charcoal does nothing to it, so seems good to target it with an additional thing. Bacteria and probably even ALDH enzymes are too big to be bound by activated charcoal, so I don't think they'd interfere with each other.

Maybe none of this works, and it's all placebo everywhere?
----------------------------------------------------------

I mean... maybe. Placebo treatments probably work [on nausea](https://pubmed.ncbi.nlm.nih.gov/25515086/) and [headache](https://jamanetwork.com/journals/jamainternalmedicine/fullarticle/1748829). But it's hard to express how bad my hangovers were before, compared to how mild they are on charcoal. It would be pretty surprising if a change that big was placebo. I should do a [gwern-style blinded self-experiment](https://www.gwern.net/zeo/Caffeine), but since I expect the fake-pill days to be spent hungover, it's hard to find the motivation.

Also, charcoal worked for one of my friends after she spent months saying it was fake bullshit, which isn't a great setup for an effective placebo effect. They worked on me after I read pages of results saying "no effect" & one page saying "eh I noticed an effect", and decided to try them anyway, which is also not very placebo-y. My vague impression of placebo is that a serious respectable scientist or doctor tells you "We think this will work." and then administers something that looks like Real Medical Treatment. Me & my friend's "I'm desperate so I might as well try this thing that probably doesn't work" approach was different. 

(Although it [worked at least once](https://journals.plos.org/plosone/article?id=10.1371/journal.pone.0015591) to give people bottles of sugar pills, where the bottles said "placebo" on them and recipients were told they were getting stuff "like sugar pills"[^jsj5f6wlceg]. So maybe you don't need the whole serious-administration-charade to get a placebo effect. A reviewer of this post said the same thing, that the charade isn't necessary.)

Sometimes when I recommend activated charcoal to people for hangovers, they say "PLACEBO!" right away, before asking me anything about what it is, what the mechanism might be, or anything. So I think there is just some subset of people who refuse to believe that anything except less drinking can help hangovers. Hopefully in this essay I've pointed out enough of the compounds in alcohol, and enough of why those might cause hangover symptoms, that you see hope in there being *some* treatment, even if you don't think the case for activated charcoal is convincing.

If activated charcoal actually doesn't work at all, there's a non-placebo possibility I might have fooled myself with: Maybe after the hellish hangover that caused me to go looking for cures, I moderated my drinking without realizing it, and that's why things have been better since then? The moderation part is a little bit true, at least compared to the night that caused that bad morning. But for 10 years I've been prone to hangovers, I've had cycles of \[bad hangover\] -> \[cut back\] before, and the difference this time is stark. Plus, the nights I've had this year are easily on the levels that have been giving me hangovers for years - yet I get very few of them now.

Is it bad to prevent hangovers?
-------------------------------

### The case for bad

Hangovers make excessive drinking less attractive. Maybe some people who would have become alcoholics are dissuaded by how bad hangovers are, and cut back on their drinking.

[Pristach 1983](https://pubmed.ncbi.nlm.nih.gov/6861616/) asked 26 alcoholics in rehab about their hangovers, and half of them said they hadn't had any hangovers in the past year[^fk8csam5pgb]. Only around [23% of the population](https://pubmed.ncbi.nlm.nih.gov/19630704/) is hangover-resistant, so twice the resistance in alcoholics is suggestive that there might be a link between hangover resistance and alcoholism. On the other hand, when Pristach asked who had ever been hungover, only 23% of the alcoholics said they'd never gotten one - in line with the population levels. (Also, some alcoholics drink so often that there's never a chance for a hangover. Like, if you drink all day, drink before you go to bed, and drink when you wake up, then you've always got some alcohol in your body). And [Piasecki 2005](https://www.researchgate.net/publication/7869765_Hangover_Frequency_and_Risk_for_Alcohol_Use_Disorders_Evidence_From_a_Longitudinal_High-Risk_Study) found that people with a family history of alcoholism got hungover more/worse[^yc54ftuxig]. So maybe there isn't much of a link.

### The case for good

If hangover is partially caused by buildup of methanol's toxic byproducts, then hangovers are partially you laying around being poisoned for a little while. A method that soaks up those poisons instead of letting them run around in your body is good for you. In this model, you get less severe hangovers because you're not being poisoned as severely. Same for acetaldehyde with a product like ZBiotics. The less time you lay around being low-grade poisoned, the better for your long-term health.

So it's a tradeoff. Preventing hangovers with these products might make you more likely to become a proper chronic alcoholic, but it might also mean you spend less time being poisoned on Sunday mornings.

Where to get and how to use activated charcoal
----------------------------------------------

I buy mine at Whole Foods. It's $8 for a bottle of 20 servings. They come in capsules, 520mg of charcoal per capsule. The bottle says take it every day - don't. I take two before bed if I think I'd otherwise have a hangover the next day. The exact timing isn't super important, nor is the exact dosage; just don't go overboard. The only ingredient in the stuff I buy is activated charcoal - like, literally, the ingredient list is one line long, and that line is "activated charcoal". I expect some sellers throw a bunch of other ingredients in there to make their product look better - I'd avoid those.

If you take important oral medications, don't take activated charcoal, or ask a pharmacist before doing so - it could absorb the active ingredient and make the medicine not work as well.

* * *

Thanks to Sophia Serafimov for helping me work out how to think about digestion pathways, Richard Perry for providing me with his views and experience on brewing & distillation and reviewing a draft of this post, and Kayla Nelson for reminding me that the liver is important in metabolization and cluing me in to ZBiotics.

[^bujgo4xd4h]: Zellner et al 2019: The Use of Activated Charcoal to Treat Intoxications. doi: 10.3238/arztebl.2019.0311 

[^6nhtih1b65s]: Hulten et al 1986: Does alcohol absorb to activated charcoal? DOI: 10.1177/096032718600500311 

[^1io4qp7goxs]: Silberman et al 2021: Activated Charcoal. PMID: 29493919 

[^26sir633xsy]: Minocha et al 1986: Activated charcoal in oral ethanol absorption: lack of effect in humans. DOI: 10.3109/15563658608990460 

[^w80fnxfd1lj]:  North et al 1981: Effect of activated charcoal on ethanol blood levels in dogs. PMID: 7246560 

[^07fgstqb90gj]: Erickson 1993: Lowering of blood ethanol by activated carbon products in rats and dogs. PMID: 8442886 DOI: 10.1016/0741-8329(93)90088-6 

[^k5vw1i4erce]: Degen & Phillips 1996: Variability of gastrointestinal transit in healthy women and men. PMID: 8977347 PMCID: PMC1383315 DOI: 10.1136/gut.39.2.299 

[^ptfxofrrz]: Balcerek et al 2017: Treatment with activated carbon and other adsorbents as an effective method for the removal of volatile compounds in agricultural distillates. PMID: 28105888 DOI: 10.1080/19440049.2017.1284347 

[^uo3voammz68]: Maxwell et al 2010: Acetate Causes Alcohol Hangover Headache in Rats. PMID: 21209842. (Candidate for best paper title) 

[^9f794furuf]: Israel et al 1994: Acetate-mediated effects of ethanol. PMID: 8198211 DOI: 10.1111/j.1530-0277.1994.tb00894.x 

[^hq58q70bztt]: Swift & Davidson 1998: Alcohol Hangover. PMID: 15706734 

[^nw8cp2dx7ls]: Wang et al 2005: Adsorption Equilibria of Acetate Compounds on Activated Carbon, Silica Gel, and 13X Zeolite. https://doi.org/10.1021/je049731v 

[^v6wm24fg0so]: Cederbaum: ALCOHOL METABOLISM. doi: 10.1016/j.cld.2012.08.002 

[^rup01cxolj]: Folahan 2016: Biosorption of formic and acetic acids from aqueous solution using activated carbon from shea butter seed shells. https://doi.org/10.1007/s13201-016-0491-3 

[^ckok5wxqjpa]: Branton et al 2010: Ethyl Acetate Adsorption onto Activated Carbon. https://doi.org/10.1260/0263-6174.28.10.895 

[^4yqxtwc0jah]: Chapter 3 of the book Alcohol Drinking (or is the book "IARC Monographs on the Evaluation of Carcinogenic Risks to Humans, No. 44"? I can't tell.) NBK531662. 

[^7au9dmen6v2]:  Greizerstein 1981: Congener contents of alcoholic beverages. PMID: 7334803 DOI: 10.15288/jsa.1981.42.1030 

[^u1vrt26lupp]: I'm halving the numbers from the linked paper in this sentence, because they report in terms of mg of methanol per liter of pure ethanol. Assuming all the liquors are 50% alcohol, halving the number gives the methanol content per bottle. This puts the numbers on the same scale as the wine/juice/beer numbers elsewhere in the post. 

[^akuhmy7ei8s]: Hodson et al 2017: Methanol in wine. Part of the "40th World Congress of Vine and Wine." DOI: 10.1051/bioconf/20170902028 

[^i083aipwvg]: Narges: Study of the adsorption of formic acid and acetic acid on activated carbon. From "Physical Chemistry: An Indian Journal. ISSN (PRINT): 0974-7524" 

[^npykcvfk02]: Colgan et al 2016: Use of Activated Carbon in Packaging to Attenuate Formaldehyde-Induced and Formic Acid-Induced Degradation and Reduce Gelatin Cross-Linking in Solid Dosage Forms. PMID: 27262203 DOI: 10.1016/j.xphs.2016.04.016 

[^bhe1et34u3]: Tanada et al 1999: Removal of Formaldehyde by Activated Carbons Containing Amino Groups. PMID: 10328902 DOI: 10.1006/jcis.1999.6176 

[^yl35wutnma8]: Rengga et al 2012: Development of Formaldehyde Adsorption Using Modified Activated Carbon - A Review. DOI:10.14710/ijred.1.3.75-80 

[^unjk61g61l]: Rohsenow et al 2010: Intoxication with Bourbon versus Vodka: Effects on Hangover, Sleep and Next-Day Neurocognitive Performance in Young Adults. doi: 10.1111/j.1530-0277.2009.01116.x 

[^i0jhlbwslva]: Chapman 1970: Experimental Induction of Hangover. https://doi.org/10.15288/qjsas.1970.s5.067 

[^5yew8sgbfyc]: I can't find the original (Pawan GLS: Alcoholic drinks and hangover effects. Proc Nutr Soc 1973; 32:15A), so the actual link is to a short letter that mentions Pawan's result. 

[^9urf4ffvk3v]: Possner et al 2014: Methanol contents of fruit juices and smoothies in comparison to fruits and a simple method for the determination thereof. 

[^9e4uhus3fy]: WHO 1997. Environmental Health Criteria 196. Methanol. Dr. L. Fishbein, Fairfax, Virginia, USA. 

[^6b5o582h9uw]: COMMITTEE ON TOXICITY OF CHEMICALS IN FOOD, CONSUMER PRODUCTS AND THE ENVIRONMENT. COT STATEMENT ON THE EFFECTS OF CHRONIC DIETARY EXPOSURE TO METHANOL. March 2011. 

[^bt0zodr8d5]: Jay_Mann@equinox.gen.nz. sci.med.nutrition newsgroup.  Jul 28 1995. Subject: Re: How Safe is Nutrasweet? 

[^9iiq0cnjya]: Jones 1987: Elimination half-life of methanol during hangover. PMID: 3588516 DOI: 10.1111/j.1600-0773.1987.tb01737.x 

[^9yxogbz0hdc]: Ashurst JV, Nappe TM. Methanol Toxicity. [Updated 2021 Jun 26]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan- 

[^zphx3sf0s3]: Pohanka 2019: Antidotes Against Methanol Poisoning: A Review. PMID: 30864518 DOI: 10.2174/1389557519666190312150407 

[^04ghaymli3zt]: Gonda 1978: Hemodialysis for methanol intoxication. PMID: 645740 DOI: 10.1016/0002-9343(78)90513-2 

[^w7swq4iwyq8]: I really like the part about hangovers being excitation. Basically, since alcohol is a downer, when you drink a ton of it, your body deploys uppers to counteract all the new downers. Maybe these uppers stick around longer than it takes for the ethanol to metabolize? Like, as an example (fake numbers!), say the uppers get deployed an hour after your first drink, and last 20 hours. And say the ethanol in the alcohol you drink only lasts until 14 hours. Then, if you start drinking at 8pm, you'll have the uppers around until until 4pm the next day, but the downers they're there to counter will only be around till 10am. Thus you're over-upped from 10am to 4pm, and this makes you hungover. (of course in real life it won't be a start-stop, single-deployment type of thing - the volumes you drink and when you drink them matter).I haven't looked into this theory enough to say much more about it, but the source[11] has a physical mechanism in mind, and also did I mention I love this theory? I might do a post on it someday. 

[^kidjhqpnis]: Verster 2008: The alcohol hangover–a puzzling phenomenon. https://doi.org/10.1093/alcalc/agm163 

[^gsp7t5ipotc]: Verster & Berthelemy 2012: Consumer Satisfaction and Efficacy of the Hangover Cure After-Effect. doi: 10.1155/2012/617942 PMCID: PMC3407600 PMID: 22852090 

[^jsj5f6wlceg]: Kaptchuk et al 2010: Placebos without Deception: A Randomized Controlled Trial in Irritable Bowel Syndrome. https://doi.org/10.1371/journal.pone.0015591 

[^fk8csam5pgb]: Pristach 1983: Alcohol withdrawal syndromes - prediction from detailed medical and drinking histories. PMID: 6861616 DOI: 10.1016/0376-8716(83)90078-9 

[^yc54ftuxig]: Piasecki et al 2005: Hangover Frequency and Risk for Alcohol Use Disorders: Evidence From a Longitudinal High-Risk Study. DOI:10.1037/0021-843X.114.2.223