One thing that I found interesting is the implication that a strong negative reaction to alcohol is something that evolved as a response to alcoholic beverages being first created in Asia.
Is there any way to study the prevalence of the ADH1B and ADH1C genes over time? e.g. to determine if they actually become more common as alcoholic beverages proliferated?
I was a bit bothered by this part, because the article didn't seem transparent in saying that this is only a hypothesis, and instead kind of talked about it as a well established proven fact.
In the grim far future, instead of an interlock device on your car after a DWI, how about some gene therapy to vaccinate against alcoholism via alcohol dehydrogenase?
I saw a post by a guy getting his masters in chemistry who mentioned two or three drugs that each mimicked part of the effects of alcohol. Week later he took the post down.
There are also attempts to specifically create drugs that will be identical to alcohol but without the negatives. Whether that will ever come to fruition, and be legal, I don't know. For example https://www.menshealth.com/uk/nutrition/a30117412/alcohol-ha...
GHB huh, yeah just try Gabapentin, start with 1.2 grams and adjust as needed. The effects take an hour or so to start showing, but they're pretty much the good effects of alcohol (relaxation, disinhibition, feeling good, sociable) with few of the bad ones (somewhat stupefying and the hangover).
Tolerance builds up fast, a couple of weeks at most for daily use, then you have to taper down or risk dealing with terrifying withdrawals (insomnia, vivid nightmares, anxiety), which are (somewhat ironically) diminished/eliminated by using alcohol.
Just to be clear, I wasn't recommending GHB as something people should try over alcohol :) It was just the first drug name that came to mind that has some similar effects and that's quite popular as a recreational drug.
Gabapentin I don't think is nearly as popular, though a couple of years ago I was told that it had become a hugely popular drug in UK prisons for some reason.
Eh, why not? Anything's better than alcohol. Gabapentin is probably popular because it's like alcohol without the negative effects and it's non-addictive. It works as an antidepressant even though not accepted by the healthscam industry.
IIRC, former UK drug-advisor, David Nutt (famed for his common sense approach that was at logger-heads with the UK govs political approach) was working on some kind of synthenol, which was rumoured to be based on GHB, and have an "antidote" so you could remove the effects.
Very interesting person indeed, though I've met two unrelated people who've worked with him and both had great things to say about his science, not so great things to say about his personality / ego / way of working. But I hope he succeeds in his mission, and I'm already grateful for his speaking truth to power back when he got fired by the government for telling people the actual facts about how dangerous different drugs are.
Yep, Nutt always made a lot of sense to me. I never got the point of having an independent drug advisory committee if the government wasn't going to listen to a single thing it said, lean on them to say what that wanted to hear instead, and indeed make policy completely at odds with the science.
I think another likely reason why disulfiram might not work is that the hypothesis is wrong, and the gene variant is only correlated with alcoholism, but might not be the cause of why there are lower rate of alcoholism in people with it.
1. People with the gene variant drink slightly less than people without it, but otherwise their drinking patterns follows everyone else's.
2. alcoholism does not cause the gene variant in individuals (obviously).
3. The gene variant is invisible. Within a reasonable population group, it seems basically random who carries it or not (I.e, you can predict that Koreans are more likely to carry it than Americans, but within a group of Americans, or a group of Koreans, it's basically impossible to guess who carries it or not). It's even been used for Mendelian randomization studies, because as far as we can tell, it affects nothing else than alcohol digestion.
A better explanation for the relative lack of success of disulfiram is that you don't take it from birth without choosing to. You have to want to take it to gain the benefit of it, but if you need it, you don't really want to take it. You want to drink. It's the big problem of addiction, you want things that contradict each other, and you want the bad things more.
The drug researcher and philosopher Ole-Jørgen Skog wrote a lot of interesting things on this topic, on "The weakness of will" and time preferences:
"If the consumer's sole motive for changing his level of patience is to escape an allocation that is dictated by his first order preference (including time preference), but that contradicts his second order preferences, he will not be able to achieve this by rational means. This is to put the cart before the horse." (But he thought that if you sought patience for its own sake, rather for the sake of not wanting to be an alcoholic, there was maybe a way. Since deciding to value patience for its own sake is not strictly speaking a rational decision.)
> A better explanation for the relative lack of success of disulfiram is that you don't take it from birth without choosing to. You have to want to take it to gain the benefit of it, but if you need it, you don't really want to take it. You want to drink. It's the big problem of addiction, you want things that contradict each other, and you want the bad things more.
I don't see what supports this being a better explanation, I feel at this point all explanation that fits the data are equally likely, otherwise it's just bias.
In fact, I would say the proposed model failed the first test, which is that a good model should be good at predicting outcomes. In this case, the model failed to predict the outcome, as causing the condition in people did not reduce their alcohol consumption as we expected from the model.
Sure, it could be that only some details of the model are wrong, like that the condition only works if established prior to a history of alcohol consumption, or that it only works if having no choice on the matter of the condition, etc. But at this point it seems just as likely that the condition might not be the cause, but only correlated in possibly another way.
For example, we might have it backwards, and it is the lower drive to consume alcohol which caused the gene variant in the fist place.
Summary: East asians are partially adapted against alcohol because they invented it first and alcohol reduces fitness. No evidence presented but it sounds cute. Presumably they are also adapted against milk because of reasons.
I think it's the other way around with milk. Almost all mammals lose the ability to digest lactose in adulthood. Europeans slowly evolved to tolerate it, presumably because of widespread reliance on cows, sheep, and goats. It's a beneficial adaptation; milk is super-nutritious, and those animals convert indigestible grasses into digestible milk in environments where crops only grow for half the year.
Milk is pretty big in India but I have read that majority of Indians are lactose intolerant. So its a bit weird that lactose intolerant population uses milk heavily in its diet.
I can't speak for milk itself, but ghee (which is often used in India), for instance, is virtually lactose-free, so even lactose intolerant people can eat it. That also happens with cheese and other dairy products; so they are not entirely incompatible.
Milk is available and regularly purchased in every Chinese store. More than 90% of them are lactose intolerant.
It's not entirely clear to me why they drink so much of it, but I believe they consider it health food. It probably comes from copying Europeans.
(Do note that milk is quite nutritious even when you can't digest the lactose. The problem isn't that the milk isn't nutritious -- the problem is that the lactose will cause you various problems, most notably diarrhea.)
I've wondered about this to. Milk seems more widely consumed here in Taiwan than in the US. Milk tea, milk/fruit smoothies, cream-filled pastries everywhere, cheese is a very popular fusion with local specialties like danbing. If Asian people are so lactose intolerant, is everyone secretly walking around battling diarrhea?
Cheese is not popular, as far as I'm aware, on the mainland. But even if it was, it contains almost no lactose. Milk is different.
I know the Chinese consume milk, but I don't think any individual person consumes very much. Some anecdotes:
- A coworker revealed to me once that he was buying milk to feed to his baby. The baby, of course, would be able to digest lactose in pretty much any quantity.
- I shocked a tutor of mine once by having a carton of milk for lunch. She told me it was very important not to drink milk on an empty stomach, or else "it will be diarrhea!" She didn't quite know what to make of my response that that wouldn't happen to me because I'm white.
- A friend of mine told me that her parents made her drink one glass of milk per day, which practice she still continues (into her 30s). This tends to imply that it's seen as a healthful practice.
- Another friend of mine, younger, spoke of milk explicitly in terms of its healthfulness, and when I asked if she drank a lot of milk herself, responded "maybe not a lot, but at least every 2-3 days".
I think people have different tolerances, my siblings and parents all eat some yogurt and milk with no symptoms unless they eat a lot. I on the other hand have a much lower tolerance and carry lactaid pills wherever I go.
Cheese is not necessarily lactose-free. It depends on the type of cheese.
tl;dr, cheese has less lactose than milk but not necessarily 0%. As a rule-of-thumb, softer, crumblier, fresher, tangier cheeses, and yogurt, should be expected to have less lactose than harder, longer-aged firm and elastic and sweeter cheeses, but again not necessarily 0%.
Now for the long version.
Fresh milk has a sweet taste thanks to the lactose it contains. Lactose is a complex sugar composed of two simple sugars, glucose and galactose. When cheese or yogurt are made, lactic acid bacteria (LAB) ferment the lactose in milk and produce lactic acid (hence their name). Lactic acid lowers the pH of the milk and so the cheese or yogurt ends up more acidic, therefore tasting tangier, than the milk used to make it. Lower pH also affects the texture of the cheese: as a rule, more acidic cheeses are softer and crumblier whereas less acidic cheeses are firmer and with a more elastic texture.
The cheesemaking process controls the extent to which fermentation is allowed to continue and acidity to develop. Some cheeses, like cheddar, are salted to stop (rather, slow down) the activity of LAB and arrest the development of acidity. Others, like fresh goat's cheeses, are left to ferment all the way. Yogurt is allowed to ferment all the way also.
LAB activity generally stops at a pH of 4.6, at which point most LAB become inactive, but that doesn't mean that all of the lactose is consumed when that pH is reached. It depends on how much lactose was in the milk to begin with and how fast the fermentation advanced during the making of the cheese. In making Italian Cacciota cheese, a warm-room technique is used to bring the curd to a temperature near the optimum of the LAB culture, so that all the lactose is consumed quickly and the cheese reaches its target pH of 5.2 (so higher than 4.6), in a relatively short time (hours rather than days). "Washed curd" cheeses like Gouda, have a step in their make where whey is replaced with water, to "wash out" the lactose and stop the fermentation, so that the cheese retains its milky sweeteness. Acidity can also decrease (pH increase) during ripening. Some bloomy rind type cheeses like camambert start out quite acidic, with a low pH under 5.0 but their pH increases while they age because the molds and yeasts on their rind (that give them their characteristic white coats) consume lactic acid and release ammonia (which, being basic, raises the pH back up).
So it's not always easy to know how much lactose is in cheese and yogurt and it's not even an absolute rule that more acidic taste means more complete fermentation and so less lactose. Certainly, cheese can still have lactose. Less than milk, but not 0%. The safest bet is to look at the ingredients listed on the packaging, which sometimes (but not always) will list the amount of lactose.
A2 milk is (was?) very popular in China, people bought it and shipped it back home so much that some stores had to implement quotas here in Aus. It supposedly has the same amount of lactose but fewer symptoms of intolerance.
A2 is one of the two most common variants of β-casein, the dominant type of protein in cow's milk (A1 is the other most common variant and they're named in the order in which they were identified). A2 has nothing to do with lactose, which is a sugar, not a protein.
So "A2 milk" is milk with a smaller amount of A2 β-casein than normal and it should make no difference to people who cannot digest lactose.
Be aware also that the health claims surrounding "A2 milk" are bunkum, much like the claims about "Real Water" [1] etc "health foods".
From wikipedia:
> The a2 Milk Company claims that milk containing A1 proteins is harmful, and some companies producing goat's milk products make similar claims,[5] but a 2009 European Food Safety Authority (EFSA) review found that it could not be established that bioactive peptides in milk containing both the A1 and A2 proteins have an adverse effect on health.
Yeah I assumed as much but didn't care to research for my own benefit because I buy something else. They're really into Manuka honey too, which AFAIK was proven to work but only for topical applications. They tend to chase these 'health' trends a lot with foreign products from what I've seen. The melamine milk scandal probably has a lot to do with it all.
There is a believe Europeans are taller because of drinking milk during childhood. Also milk is considered healthy. I think you can build up a little of lactose tolerance with moderate intake (and it seem you can loose it, happened to me after staying away from milk products due to living in Asia for a couple of years)
> I think you can build up a little of lactose tolerance with moderate intake (and it seem you can loose it, happened to me after staying away from milk products due to living in Asia for a couple of years)
There are three major strategies a human body may implement for lactase:
The first is that you produce lactase as an infant, and then you stop producing it. This is the mammalian norm.
The second is that you produce lactase as an infant, and then you never stop producing it.
But the third is that you produce lactase as an infant, and then you keep producing it so long as lactose is a regular part of your diet. You will permanently stop producing it if you ever go for a significant period without consuming lactose.
from my observation the chinese don't actually drink that much milk. they buy it for children, and the reason why you see lots of milk in the store is because there are a lot more people living there. they also like to buy in bulk as gift for relatives, and they usually buy heat-treated milk that doesn't need to be cooled either.
fresh milk is available, but compared to the size of the population, it's not as much as it seems. in the one million-people town where i live, i only know two supermarkets that stock fresh milk.
> fresh milk is available, but compared to the size of the population, it's not as much as it seems. in the one million-people town where i live, i only know two supermarkets that stock fresh milk.
I was aware of the availability of imported boxed UHT milk. My experience is that it shows up in supermarkets in an "imports" section. (I tried it and found it extremely unpalatable.)
Fresh milk is available much more widely (in Shanghai, which is large). It's in every supermarket and every convenience store. The most common brand is named "Fresh Milk" (blue carton), which I wasn't able to drink without becoming nauseated, but there is also a "locally produced" (whitish carton, I don't remember the actual brand name) brand which I consumed in very large amounts.
I am lactose intolerant just like my father and usually avoid milk, but traditionally my family did not avoid it.
I can increase my tolerance to milk gradually, but I find no benefit in doing so, because I can drink up to 200 ml of milk without major issues, I can eat cookies, icecream and so on without major problems.
The only time I had major problems was when I used milk protein powder, but I switched to whey protein at that time and learnt that I was lactose intolerant.
My point is lactose intolerance doesn't have to be all or nothing.
I come from Eastern Europe from a mountain village where cattle/sheep raising used to be a big thing and I'm lactose intolerant but not completely intolerant, I can gradually increase my tolerance.
People in my village didn't just drink a lot milk like town folks do today, they'd use mostly fermented milk, and a lot of cheese -- their favorite drink is wine.
They're "adapted against milk" because their ancestors left Africa, and milk-drinking developed either in European humans, or we got it from Neanderthals.
They're adapted against milk for the same reason everything else is: producing lactase has a cost, and it makes no sense to pay that cost when there is no lactose in your diet.
I think the common theory is that lactase production is stopped during early adolescence in mammals as a sort of safeguard to not compete with younger siblings for milk (when you're old enough you can get other food, while your younger siblings depend on milk).
Some human subgroups (e.g. Europeans) are different, as they mutated to produce lactase even in adulthood (an evolutionary advantage in farming societies).
Your characterization of the theory as “cute” is spot on. There should be a name for this type of theory - puts a nice tidy bow on an observation but isn’t based on science and falls apart upon inspection.
And in terms of lactose intolerance, I lived in Asia and milk is amazingly popular with young kids. And I’ve almost never heard of much lactose intolerance beyond what you’d hear in the west.
I've heard that type of thing referred to as "just so" stories. Typically they sound like something that Rudyard Kipling would have written but with a warm cloak of Science wrapped around them.
You got it there other way around. It was Europeans who evolved for the consumption of milk (likely due to the environment/diet) while the rest of the world didn't, like other mammals. The production of lactase to digest lactose drops as adolescence approaches.
I guess you could flip the hypothesis and suggest maybe East Asians didn't (have the time to) evolve to digest alcohol sufficiently and hence the Asian flush. /joke
No one invented alcohol. Drinking "alcohol" (wine, beer) in sub-drunken quantities carries no systemic risk, i.e. it doesn't reduce fitness by any meaningful amount (if you can even quantify "fitness"). This is evidenced by thousands of years of wine-drinking civilizations and cultures that still exist to this day. The cause for Asians "adapting against" alcohol is probably just randomness. A random mutation.
> Summary: East asians are partially adapted against alcohol because they invented it first and alcohol reduces fitness.
This seems super unlikely.
It is at least as likely that the mutation which causes the "Asian flush" is protective against something else while losing the ability to consume whopping quantities of alcohol is simply a side effect.
You are precisely right. It seems to have been protective against a disease found from mouldy rice:
Mycotoxins, from toxin-producing fungi found in moldy rice, can be converted by the host ALDH enzymes from protoxin to toxin, and the effects of mycotoxins can be further potentiated by ethanol. If the incidence of hepatic disease found in many East Asians, especially JPN, is related to the consumption of mycotoxins, then individuals carrying the deficient ALDH22 variant with lowered alcohol consumption would be selectively favored.*
Sure, maybe alcohol was invented first in China (that's the earliest we have found anyway).
But we have found usage in ancient Persia from less than 2000 years after China. If this gene is highly selective, why wasn't it also equally selective outside East Asia?
A more likely explanation is that it is a random variation and provides little to no evolutionary benefit.
If it was random, why did it become dominant if it provided no evolutionary advantage?
There’s variations going on all the time, maybe they’re random, maybe they’re not. But the ones that stick in a population are the ones that get selected by outcompeting hosts without the variation.
You could probably also ask why Temujin had many children.
Founder effects are a thing and a sufficient explanation. They hold even for relatively detrimental defects, and likely hold even better for something as silent as acetaldehyde metabolism.
> There’s variations going on all the time, maybe they’re random, maybe they’re not. But the ones that stick in a population are the ones that get selected by outcompeting hosts without the variation.
This is only true if there is correlation between the variation and survival in terms of breeding.
A good example is the high incidence of Haemophilia B in European royalty[1]. It certainly doesn't give any selective advantage, but the fact that royalty are more likely to get medical care means it doesn't have any selective disadvantage either.
There are plenty of other random variations that aren't selective. Eye colour, male pattern baldness, the range of earlobe attachedness[2] are all variations that don't have any selective pressure and so their appearance in various geographic areas is down to history rather genetics.
Edit: Another comment led me to a paper arguing compellingly that this gene provided some protection against diseases carried in mouldy rice, and that was selective in China. See further discussion here: https://news.ycombinator.com/item?id=27705633
Is it really required that these genes are equally selective everywhere? If the adaptation theory were true, that would depend on how widely available alcohol was, as well as how harmful it is to lose the extra calories from rotting fruit, etc. No particular reason to think it would be equal everywhere.
Thanks for this. That paper led me down a rabbit hole and I ended up with this:
Evidence of positive selection on a class I ADH locus
It seems unlikely that the selection was recent and associated with alcoholism, the modern phenotypic manifestation of the polymorphism.... Mycotoxins, from toxin-producing fungi found in moldy rice, can be converted by the host ALDH enzymes from protoxin to toxin, and the effects of mycotoxins can be further potentiated by ethanol. If the incidence of hepatic disease found in many East Asians, especially JPN, is related to the consumption of mycotoxins, then individuals carrying the deficient ALDH22 variant with lowered alcohol consumption would be selectively favored.*[1]
So it sounds like it isn't alcoholism that is being selected against, but instead resistance to mouldy rice born infections, which is correlated with this gene. That explains the geographic distribution quite well, too.
This feels completely anachronistic. For early humans to evolve genes that prevent them from getting drunk, you’d assume that a large proportion of people would have to die or become infertile from alcoholism.
Given the number of things people would die of, the slow speed of progression of alcohol-related diseases, and the difficulty of producing enough beer for it to become a evolution-wise health problem, the conclusion really sounds like a stretch.
Beer is pretty easy to make if you're in an early agrarian state with a modest surplus of cereals, not up to the standards of modern-day breweries, but good enough by a fair margin. IIRC if you were a temple worker in the ancient state of Uruk, your pay would have included a bowl of beer a day. Such arrangements weren't rare.
Historically, people have drunk surprising amounts of alcohol – we may not have been as collectively sober as today for millennia (depending on the exact location, to be sure); beer and wine have the big advantage that they're reasonably safe to drink even if the primary source of water isn't (due to the fermentation process and the alcohol content), and that it's easier to tell when they aren't (because if fermentation doesn't work right, you definitely notice). In some of the more remote areas in the alps, even children still drank lots of diluted wine as late as the 1950s, for precisely that reason. That sort of thing was the rule, not the exception, for Europe pre-industrialization.
Evolutionary pressure on humans also doesn't usually involve everyone with allele X dropping dead right away, because people are pretty creative at avoiding that outcome, and it's often (probably, likely) not about small-ish effects under good, stable conditions, but outsize ones in exceptional circumstances.
There have been bad years and very bad years all the time; even as late as the 19th century, agrarian societies were pretty much helpless if harvests failed on a large scale (think Irish Potato Famine), and that's after 6000-ish years of working on that existential problem. When bad years become bad decades, and lots and lots of people die, that's when things like alcohol tolerance and lactose tolerance can make a big difference.
Being able to tolerate alcohol may mean access to a cleaner source of fluid, less pathogens for weakened immune systems to deal with, and access to nutrients that store pretty well. There may have been a social component as well – getting drunk together has been an extremely important vehicle for networking and bonding for literal ages. Finally, being able to get drunk relatively safely may have kept people functioning through highly traumatic experiences as well. Not saying that's what happened for sure, but a few ways this could have played a decisive role.
I believe monks used to make and consume "beer" too, but it had a low alcohol content. I think this had something to do with preservation? - like the alcohol and/or yeast purified the water, or at least provided an indicator of bad water.
There used to be something called "small beer" that was also v low in alcohol content, made from the same grain as a regular beer, but mashed/drained a 2nd time to get any remaining sugars.
The brewing process itself, which involves holding the mash at a pretty high temperature, probably does more to purify the water than the small amount of alcohol.
You could--but without any theory of microorganisms, why would you? If anything, the water tastes slightly worse after boiling and sitting, but the beer tastes good!
More seriously, I bet alcohol and hops do play a role. The alcohol isn't enough to sterilize anything (which requires a much stronger concentration: ~70%, usually). However, it and the hops could help maintain sterility once the heat has done its job.
Bacteriostatic water is used to dilute drugs for injection, and it uses a similar principle: a small (0.9%) amount of alcohol is added to keep any bacteria from getting a foothold.
The owner of one of the oldest craft brewers in my area once told me that "nothing that can hurt you can grow in beer." I don't know if this is completely true, but this might render fresh water with many types of dangerous pathogens safe to drink.
One famous story of historical excess drinking is associated with the U.S. constitution...
Finally, there is an easy method for most people reduce their impulse to drink temporarily by the use of the opioid blockers naltrexone or nalmefene. These can be used either for a goal of reduced-compulsion abstinence or long-term controlled drinking.
It isn't the alcohol in beer which makes it safe, it's the brewing process. To brew beer, before fermentation you first have to boil the wort (water + malt + hops), and this kills all the pathogens in the water you brewed it from.
While copious amounts of alcohol were drunk, it wasn't hard liquor, "normal" wine or beer; mostly low alcohol, enough to sanitize and preserve it, not enough to get you pissed up.
That said, I'm sure being an alcoholic was much more accessible back when because of (relative) cost - alcohol is relatively expensive nowadays compared to food, water and other drinks.
Sure, but that's not what the article says... The article says that these genes appeared to prevent humans from getting wasted - as in becoming less tolerant to alcohol.
Unless there was an epidemic of people getting wasted - and dying from it - in the same decade as some other terrible event, the argument doesn't hold.
Tangent: a pet peeve of mine is plots of alcohol vs disease plots that suggest that one or two drinks a day is healthier than none. This is not the case.
The data sets that produce these plots almost never take into account why people stop drinking. When you do control for this, and in the process filter out people who stop drinking because of other severe health issues, it becomes obvious that not drinking at all is the healthiest option.
>The data sets that produce these plots almost never take into account why people stop drinking. When you do control for this, and in the process filter out people who stop drinking because of other severe health issues, it becomes obvious that not drinking at all is the healthiest option.
But many studies do account for that scenario of "sick quitters". The statistical correlation still showed that light moderate drinkers had lower mortality rates.
The study itself may still be flawed but the point is that the researchers were aware of "sick quitters" being categorized as "non-drinkers" and thus distorting the results.
>The greater proportion of surviving
participants in our study who reported not drinking at follow-up compared to baseline is
probably due to a combination of the cohort’s becoming older and drinking less, secular
changes in alcohol consumption with time, and survival selection effects. Decline in
consumption is also associated with the development of ill health, particularly
cardiovascular disease. This accumulation of ill health and higher mortality risk in ‘sick
quitters’ increases the observed benefit in drinkers if non-drinkers include these ex-drinkers
[6, 24, 26]. In addition, regular light drinkers tend to have characteristics advantageous to
health [26, 27]. Thus, controlling for baseline disease is important, particularly if alcohol
history is unknown. With adjustment for baseline medical history as well as body mass
index, exercise, and smoking, the lower risks of death among light and moderate alcohol
drinkers observed in our study did not change substantially and remained statistically
significant although those associated with heavier drinking were reduced.
Yes, it was back and forth many years whether the dip at the bottom (with very modest drinkers being slightly healthier than non-drinkers) was genuine, or whether there was some remaining effect which hadn't been appropriately controlled for.
But that was pretty much settled with Mendelian Randomization studies on exactly this gene. As the article says, some people have different versions of the alcohol dehydrogenase enzyme, which basically gives them a worse hangover, faster. People with this condition drink slightly less than they otherwise would, wherever they are on the consumption curve. Knowing that, and knowing that the gene is more or less randomly distributed in the population under study, and assuming the gene affects nothing else (a safe bet, since alcohol dehydrogenase is a fairly task-specific enzyme), we can disentangle the effect of the alcohol from all the other things that could cause you to drink more or less alcohol.
Now the consensus seems pretty solidly on that the apparent protective effect of moderate alcohol consumption on stroke, cancer or heart disease is non-causal.
My next door neighbor seems to be one of the most relaxed, healthy women I've ever met. She sits on her porch every evening for an hour and slowly drinks one large glass of wine. I feel like alcohol can complement a healthy lifestyle. If you're healthy, exercise, and want to use alcohol as a small portioned daily treat that makes you relaxed and happier, then I see that being downright healthy.
That being said, most drinkers -- at least in the US -- do not fit the above category at all.
This n=1 personal anecdatum does not fit well in this thread about longitudinal studies.
Alcohol’s potential role in someone’s preferences about how to enjoy life doesn’t have anything to do with the discussion of whether it has a biologically protective effect.
I know a few problem drinkers who are linearly killing themselves and they all grasp for this “scientists have proven alcohol is good for you” misinformation as a part of their excusing narrative.
I agree with this completely, and it's kind of my point: while there are anecdotes of people fitting alcohol into a healthy life (and maybe getting a tangible benefit), many don't.
There's no study that shows that more than 1-2 standard drinks at a time is good for you. Anyone in this category is almost certainly not a problem drinker.
However i'd be surprised if there was a positive biological effect from alcohol.
It's not unreasonable to presume that such moderate drinking probably correlates with all sorts of other health related lifestyle choices. From my entirely anecdotal world view the most healthy people i know still have a couple drinks every now and then (but dont drink excessively regularly). It's almost impossible to control for all these factors in a study
Most of the non-drinkers i know do so because they don't like the taste/have alcoholic parents/are teetotal due to addiction and have no correlation in terms of other behaviors.
This makes sense. My entire life, I have been badgered about my non-drinking. Apparently only religious zealots, severe former alcoholics, and terminally ill people, abstain from alcohol. No other response will satisfy a person with a drink in their hand. So the problem quitters must be a large category, whether it gets recorded that way or not. And frankly, if we’re talking about former alcoholics, we’re also talking about a lot of compulsive liars; there may be reason to distrust their survey results.
Use sports. I tell them that I'm a competing athlete and cannot break my sports regimen, which is technically true, but not really the reason--I grew up in the post-communist Europe of 90s witnessing rampant alcoholism and came to look at alcohol as something for people who are too weak to face the life, but too afraid to die. Never had an inkling to try the stuff.
I realized this early on. The simple way around it for me in college was to get a drink, pour out 2/3 of it and carry it around with me. As long as you have it with you, nobody tries to give you one.
If it’s a beer, you can easily turn down offers of other drinks just by saying you don’t want to mix alcohol.
Overall, a pretty simple solution to the social problem.
I think of it as a drug that addresses some mild social anxiety and has some social history behind it. Drugs are similar in certain social circles.
But basically when someone wants you to drink it's their social anxiety that is manifesting, not yours. They need other people to participate in the bonding ritual, part of which requires people letting their guard down, which alcohol helps with.
But I'm not sure it's the chemical pathway that does it. I mean yes, drink enough and you will feel different. But you open up socially over a beer before the beer has any effect, eg. while you're waiting in line at the bar chatting to someone, or while you have just a tiny dose in your blood. Likewise with drugs, I never thought I was getting especially high or changed somehow. So perhaps it's more like a Schelling point, people accept that alcohol/drugs at a social event means that you can relax.
I've also never felt that I became someone else when drinking. Even when so drunk I couldn't walk straight, I could still understand social cues and conventions, and I still knew what I desired. It's like the beer is an excuse for bad behavior rather than the cause.
Luckily as an adult with kids I don't get badgered into getting hammered anymore. But I did think of a good excuse after talking to a cardiologist: you can always say you have some sort of condition that makes it a bad idea for you to drink or do drugs.
It certainly does change who a person is. It damages virtually every part of the brain and directly causes anxiety disorder, mood swings, and a whole host of other unpleasant psychiatric disorders (to say nothing of the physiological disorders); and it causes this damage at doses that most people would consider "moderate", if the doses are administered consistently over a long enough period.
Disease is one thing, but I think social life is better for the average moderate drinker which makes drinking (moderately) the healthier life choice if you zoom out a bit.
I am not an apologist. I have come to dislike alochol, and I’m trying to cut it from my life. But, at least here in scandinavia, having work, a love life and friends can be dependant on you drinking.
A fun thing i’ve noticed though, is that Tinder has alleviated this dependancy on alcohol quite a bit.
You can be out and have a social life while drinking alcohol free drinks. I've been drinking alcohol free beers 90% recently, most of them aren't that tasty but a few of them are just as good as regular beers.
In my experience people don't care if you drink pints of vodka or orange juice, as long as you're physically here and engage socially. It's like being vegetarian, some friends might look at you funny for a bit but unless they're complete morons they won't actively judge you
I should probably say that I'm not one of these beer enthusiast who has a very deep knowledge of beer, try every kind of beer and know 250 types of IPAs &c.
I'm not particularly interested in the topic, that being said here are the ones I like the most: Stoertebeker alcohol free atlantic ale, Lammsbräu alcohol free, BRLO naked, Franziskaner alhocol free, Paulaner alcohol free, monschof alcohol free
The only alcohol I keep drinking are whisky and red wine in very moderate quantities.
I really like the beers from the Athletic Brewing Company (https://athleticbrewing.com/). Aside from being slightly less carbonated than alcoholic beer, it's hard to tell the difference between them. And more importantly: everything I've tried from them tastes good.
> ...An unexpected, highly significant finding was observed: the AA rats, bred for high voluntary ethanol drinking, lived much longer than the ANA rats, bred for ethanol avoidance. The death rate by 24 months in the AA line was less than one-third of that in the ANA line.
> Conclusions: Lifelong ethanol consumption increased neither the mortality nor the morbidity of AA and ANA line of rats. Genes selected in the development of the high drinking AA line have additional effects producing rats that are healthier and living longer than the ANA rats possessing genes resulting in alcohol avoidance.
So what if people who drank were simply _genetically_ healthier to begin with, and moderate drinking has no effect on health outcomes whatsoever? The study seems to suggest that.
So much negativity in the comments here on the subtopic on "what caused the evolution". Yes, we know that nobody really knows, the author doesn't really know either.
What the post conceptually centers on is best depicted in that chart in the middle. Also, if you read the entire thing you'd have found out that the author isn't trying to make any specific point, but rather is telling a story.
(author here) I did not know that, and I'm not sure how it fits in! All else being equal, more ADH would imply faster acetaldehyde buildup, meaning men would have more of a "flush" than women. I don't know if all else is equal, though. For example, if men also had more ALDH, then they'd also be able to break down that acetaldehyde into acetate faster.
Taking a quick glance at the literature, it's... super complicated. This paper (https://doi.org/10.1002/jcla.10076) suggests that women have lower gastric ADH but higher liver ADH. There's some animal studies that suggest men have higher ALDH, but also some contradictory human studies that suggest that everything is just the same.
I always though the basic hypothesis is the other way around: the populations with low alcohol tolerance used methods other than brewing to generate safe water (e.g., boiling as in tea) and hence no selection for alcohol tolerance.
If there really is a selection against alcohol, why did that not kick in outside Asia, too? The selection mechanism postulated would need to be fast... are 2k years or so really significant?
Cannot relate to people trying to "well, actually" this article based on their absolute certainty that evolution happened the way it did for a specific reason (a thing we can never actually prove). The point of the post is to tell an interesting story and the writing is fun and funny. Lighten up people, sheesh.
So many internet know-it-alls thinking they'll disprove the entire article all at once with their one-sentence intellectual zinger, and then we'll all bow down and praise them for their great cleverness. I despair of internet forums - some have better culture for a while, but as far as I've seen, Dunning-Kruger always wins in the end.
The thing is that too consume alcohol at a harmful level you pretty well need distillation, which only came in about eight hundred years ago, so this doesn't leave much room for evolution!
Intriguing idea but not sure if it holds up upon further scrutiny.
Alcoholic drinks have been around since at least as early as the Neolithic period (10,000BCE) and the earliest archaeological evidence shows that they have been around in China and Middle East/Mesopotamia around the same time (~7000BCE). So why did the East Asians evolved to have the "Asian flush" while the rest of the world didn't?
Someone mentioned that alcoholic drinks were safer to drink than water so people were drinking alcoholic drinks as a safer alternative. But we have to remember the various "cradles of civilizations"(Mesopotamia, Yellow river, Indus Valley etc) all evolved around rivers so access to clean water probably wasn't a major issue.
What's more likely is the effect is an unintended consequence. Other qualities "unique" to Asians or East Asians are a general lack of body hair and (more pronounced) neoteny. I don't think there are adequate theories for those quality either. There's still a long way to go to fully understand evolution and genetics.
China has had continuous organized civilization, and the alcohol it produces, at least as long as anywhere.
That makes a good environment for mutations that protect people from alcohol consumption, but such mutations still has to randomly appear, and that it happened to appear in East Asia is probably just random.
The fact that populations who have never had alcohol succumb to rampant alcoholism when first getting access implies that even the eurasian populations without the Asian Flush genes probably has some less obvious genetic protection. You can also think of it as the most alcoholic prone genes have been weeded out over the centuries.
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[ 1.7 ms ] story [ 271 ms ] threadReally? That's the simplest explanation?
https://royalsocietypublishing.org/doi/10.1098/rspb.1979.008...
Is there any way to study the prevalence of the ADH1B and ADH1C genes over time? e.g. to determine if they actually become more common as alcoholic beverages proliferated?
(I note that another article on the front page is entitled "The most precious resource is agency", though I haven' gotten to it quite yet).
There are also attempts to specifically create drugs that will be identical to alcohol but without the negatives. Whether that will ever come to fruition, and be legal, I don't know. For example https://www.menshealth.com/uk/nutrition/a30117412/alcohol-ha...
Tolerance builds up fast, a couple of weeks at most for daily use, then you have to taper down or risk dealing with terrifying withdrawals (insomnia, vivid nightmares, anxiety), which are (somewhat ironically) diminished/eliminated by using alcohol.
Gabapentin I don't think is nearly as popular, though a couple of years ago I was told that it had become a hugely popular drug in UK prisons for some reason.
Very interesting person indeed, though I've met two unrelated people who've worked with him and both had great things to say about his science, not so great things to say about his personality / ego / way of working. But I hope he succeeds in his mission, and I'm already grateful for his speaking truth to power back when he got fired by the government for telling people the actual facts about how dangerous different drugs are.
Yep, Nutt always made a lot of sense to me. I never got the point of having an independent drug advisory committee if the government wasn't going to listen to a single thing it said, lean on them to say what that wanted to hear instead, and indeed make policy completely at odds with the science.
25mg orally would feel like a mild alcohol buzz, and would last for up to 4 hours.
Around 10mg nasally (either as powder or as a nasal spray) would have a similar effect, but would only last up to 2 hours.
DISCLAIMER: I am not suggesting anyone try this, it's information for educational purposes only!
1. People with the gene variant drink slightly less than people without it, but otherwise their drinking patterns follows everyone else's.
2. alcoholism does not cause the gene variant in individuals (obviously).
3. The gene variant is invisible. Within a reasonable population group, it seems basically random who carries it or not (I.e, you can predict that Koreans are more likely to carry it than Americans, but within a group of Americans, or a group of Koreans, it's basically impossible to guess who carries it or not). It's even been used for Mendelian randomization studies, because as far as we can tell, it affects nothing else than alcohol digestion.
A better explanation for the relative lack of success of disulfiram is that you don't take it from birth without choosing to. You have to want to take it to gain the benefit of it, but if you need it, you don't really want to take it. You want to drink. It's the big problem of addiction, you want things that contradict each other, and you want the bad things more.
The drug researcher and philosopher Ole-Jørgen Skog wrote a lot of interesting things on this topic, on "The weakness of will" and time preferences:
"If the consumer's sole motive for changing his level of patience is to escape an allocation that is dictated by his first order preference (including time preference), but that contradicts his second order preferences, he will not be able to achieve this by rational means. This is to put the cart before the horse." (But he thought that if you sought patience for its own sake, rather for the sake of not wanting to be an alcoholic, there was maybe a way. Since deciding to value patience for its own sake is not strictly speaking a rational decision.)
I don't see what supports this being a better explanation, I feel at this point all explanation that fits the data are equally likely, otherwise it's just bias.
In fact, I would say the proposed model failed the first test, which is that a good model should be good at predicting outcomes. In this case, the model failed to predict the outcome, as causing the condition in people did not reduce their alcohol consumption as we expected from the model.
Sure, it could be that only some details of the model are wrong, like that the condition only works if established prior to a history of alcohol consumption, or that it only works if having no choice on the matter of the condition, etc. But at this point it seems just as likely that the condition might not be the cause, but only correlated in possibly another way.
For example, we might have it backwards, and it is the lower drive to consume alcohol which caused the gene variant in the fist place.
It's not entirely clear to me why they drink so much of it, but I believe they consider it health food. It probably comes from copying Europeans.
(Do note that milk is quite nutritious even when you can't digest the lactose. The problem isn't that the milk isn't nutritious -- the problem is that the lactose will cause you various problems, most notably diarrhea.)
I know the Chinese consume milk, but I don't think any individual person consumes very much. Some anecdotes:
- A coworker revealed to me once that he was buying milk to feed to his baby. The baby, of course, would be able to digest lactose in pretty much any quantity.
- I shocked a tutor of mine once by having a carton of milk for lunch. She told me it was very important not to drink milk on an empty stomach, or else "it will be diarrhea!" She didn't quite know what to make of my response that that wouldn't happen to me because I'm white.
- A friend of mine told me that her parents made her drink one glass of milk per day, which practice she still continues (into her 30s). This tends to imply that it's seen as a healthful practice.
- Another friend of mine, younger, spoke of milk explicitly in terms of its healthfulness, and when I asked if she drank a lot of milk herself, responded "maybe not a lot, but at least every 2-3 days".
That's my secret. I'm always clenching.
(Though see cheese_goddess's comment.)
tl;dr, cheese has less lactose than milk but not necessarily 0%. As a rule-of-thumb, softer, crumblier, fresher, tangier cheeses, and yogurt, should be expected to have less lactose than harder, longer-aged firm and elastic and sweeter cheeses, but again not necessarily 0%.
Now for the long version.
Fresh milk has a sweet taste thanks to the lactose it contains. Lactose is a complex sugar composed of two simple sugars, glucose and galactose. When cheese or yogurt are made, lactic acid bacteria (LAB) ferment the lactose in milk and produce lactic acid (hence their name). Lactic acid lowers the pH of the milk and so the cheese or yogurt ends up more acidic, therefore tasting tangier, than the milk used to make it. Lower pH also affects the texture of the cheese: as a rule, more acidic cheeses are softer and crumblier whereas less acidic cheeses are firmer and with a more elastic texture.
The cheesemaking process controls the extent to which fermentation is allowed to continue and acidity to develop. Some cheeses, like cheddar, are salted to stop (rather, slow down) the activity of LAB and arrest the development of acidity. Others, like fresh goat's cheeses, are left to ferment all the way. Yogurt is allowed to ferment all the way also.
LAB activity generally stops at a pH of 4.6, at which point most LAB become inactive, but that doesn't mean that all of the lactose is consumed when that pH is reached. It depends on how much lactose was in the milk to begin with and how fast the fermentation advanced during the making of the cheese. In making Italian Cacciota cheese, a warm-room technique is used to bring the curd to a temperature near the optimum of the LAB culture, so that all the lactose is consumed quickly and the cheese reaches its target pH of 5.2 (so higher than 4.6), in a relatively short time (hours rather than days). "Washed curd" cheeses like Gouda, have a step in their make where whey is replaced with water, to "wash out" the lactose and stop the fermentation, so that the cheese retains its milky sweeteness. Acidity can also decrease (pH increase) during ripening. Some bloomy rind type cheeses like camambert start out quite acidic, with a low pH under 5.0 but their pH increases while they age because the molds and yeasts on their rind (that give them their characteristic white coats) consume lactic acid and release ammonia (which, being basic, raises the pH back up).
So it's not always easy to know how much lactose is in cheese and yogurt and it's not even an absolute rule that more acidic taste means more complete fermentation and so less lactose. Certainly, cheese can still have lactose. Less than milk, but not 0%. The safest bet is to look at the ingredients listed on the packaging, which sometimes (but not always) will list the amount of lactose.
So "A2 milk" is milk with a smaller amount of A2 β-casein than normal and it should make no difference to people who cannot digest lactose.
Be aware also that the health claims surrounding "A2 milk" are bunkum, much like the claims about "Real Water" [1] etc "health foods".
From wikipedia:
> The a2 Milk Company claims that milk containing A1 proteins is harmful, and some companies producing goat's milk products make similar claims,[5] but a 2009 European Food Safety Authority (EFSA) review found that it could not be established that bioactive peptides in milk containing both the A1 and A2 proteins have an adverse effect on health.
https://en.wikipedia.org/wiki/A2_milk
______________
[1] https://www.theguardian.com/us-news/2021/may/21/real-water-a...
There are three major strategies a human body may implement for lactase:
The first is that you produce lactase as an infant, and then you stop producing it. This is the mammalian norm.
The second is that you produce lactase as an infant, and then you never stop producing it.
But the third is that you produce lactase as an infant, and then you keep producing it so long as lactose is a regular part of your diet. You will permanently stop producing it if you ever go for a significant period without consuming lactose.
It sounds like you were a type 3.
fresh milk is available, but compared to the size of the population, it's not as much as it seems. in the one million-people town where i live, i only know two supermarkets that stock fresh milk.
I was aware of the availability of imported boxed UHT milk. My experience is that it shows up in supermarkets in an "imports" section. (I tried it and found it extremely unpalatable.)
Fresh milk is available much more widely (in Shanghai, which is large). It's in every supermarket and every convenience store. The most common brand is named "Fresh Milk" (blue carton), which I wasn't able to drink without becoming nauseated, but there is also a "locally produced" (whitish carton, I don't remember the actual brand name) brand which I consumed in very large amounts.
I can increase my tolerance to milk gradually, but I find no benefit in doing so, because I can drink up to 200 ml of milk without major issues, I can eat cookies, icecream and so on without major problems.
The only time I had major problems was when I used milk protein powder, but I switched to whey protein at that time and learnt that I was lactose intolerant.
My point is lactose intolerance doesn't have to be all or nothing.
https://en.m.wikipedia.org/wiki/Lactase_persistence
People in my village didn't just drink a lot milk like town folks do today, they'd use mostly fermented milk, and a lot of cheese -- their favorite drink is wine.
Some human subgroups (e.g. Europeans) are different, as they mutated to produce lactase even in adulthood (an evolutionary advantage in farming societies).
And in terms of lactose intolerance, I lived in Asia and milk is amazingly popular with young kids. And I’ve almost never heard of much lactose intolerance beyond what you’d hear in the west.
I guess you could flip the hypothesis and suggest maybe East Asians didn't (have the time to) evolve to digest alcohol sufficiently and hence the Asian flush. /joke
This seems super unlikely.
It is at least as likely that the mutation which causes the "Asian flush" is protective against something else while losing the ability to consume whopping quantities of alcohol is simply a side effect.
Mycotoxins, from toxin-producing fungi found in moldy rice, can be converted by the host ALDH enzymes from protoxin to toxin, and the effects of mycotoxins can be further potentiated by ethanol. If the incidence of hepatic disease found in many East Asians, especially JPN, is related to the consumption of mycotoxins, then individuals carrying the deficient ALDH22 variant with lowered alcohol consumption would be selectively favored.*
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1821113/
Sure, maybe alcohol was invented first in China (that's the earliest we have found anyway).
But we have found usage in ancient Persia from less than 2000 years after China. If this gene is highly selective, why wasn't it also equally selective outside East Asia?
A more likely explanation is that it is a random variation and provides little to no evolutionary benefit.
There’s variations going on all the time, maybe they’re random, maybe they’re not. But the ones that stick in a population are the ones that get selected by outcompeting hosts without the variation.
Founder effects are a thing and a sufficient explanation. They hold even for relatively detrimental defects, and likely hold even better for something as silent as acetaldehyde metabolism.
This is only true if there is correlation between the variation and survival in terms of breeding.
A good example is the high incidence of Haemophilia B in European royalty[1]. It certainly doesn't give any selective advantage, but the fact that royalty are more likely to get medical care means it doesn't have any selective disadvantage either.
There are plenty of other random variations that aren't selective. Eye colour, male pattern baldness, the range of earlobe attachedness[2] are all variations that don't have any selective pressure and so their appearance in various geographic areas is down to history rather genetics.
Edit: Another comment led me to a paper arguing compellingly that this gene provided some protection against diseases carried in mouldy rice, and that was selective in China. See further discussion here: https://news.ycombinator.com/item?id=27705633
[1] https://en.wikipedia.org/wiki/Haemophilia_in_European_royalt...
[2] https://en.wikipedia.org/wiki/Earlobe#Genetics
Is it really required that these genes are equally selective everywhere? If the adaptation theory were true, that would depend on how widely available alcohol was, as well as how harmful it is to lose the extra calories from rotting fruit, etc. No particular reason to think it would be equal everywhere.
Evidence of positive selection on a class I ADH locus
It seems unlikely that the selection was recent and associated with alcoholism, the modern phenotypic manifestation of the polymorphism.... Mycotoxins, from toxin-producing fungi found in moldy rice, can be converted by the host ALDH enzymes from protoxin to toxin, and the effects of mycotoxins can be further potentiated by ethanol. If the incidence of hepatic disease found in many East Asians, especially JPN, is related to the consumption of mycotoxins, then individuals carrying the deficient ALDH22 variant with lowered alcohol consumption would be selectively favored.*[1]
So it sounds like it isn't alcoholism that is being selected against, but instead resistance to mouldy rice born infections, which is correlated with this gene. That explains the geographic distribution quite well, too.
[1] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1821113/
Given the number of things people would die of, the slow speed of progression of alcohol-related diseases, and the difficulty of producing enough beer for it to become a evolution-wise health problem, the conclusion really sounds like a stretch.
Historically, people have drunk surprising amounts of alcohol – we may not have been as collectively sober as today for millennia (depending on the exact location, to be sure); beer and wine have the big advantage that they're reasonably safe to drink even if the primary source of water isn't (due to the fermentation process and the alcohol content), and that it's easier to tell when they aren't (because if fermentation doesn't work right, you definitely notice). In some of the more remote areas in the alps, even children still drank lots of diluted wine as late as the 1950s, for precisely that reason. That sort of thing was the rule, not the exception, for Europe pre-industrialization.
Evolutionary pressure on humans also doesn't usually involve everyone with allele X dropping dead right away, because people are pretty creative at avoiding that outcome, and it's often (probably, likely) not about small-ish effects under good, stable conditions, but outsize ones in exceptional circumstances.
There have been bad years and very bad years all the time; even as late as the 19th century, agrarian societies were pretty much helpless if harvests failed on a large scale (think Irish Potato Famine), and that's after 6000-ish years of working on that existential problem. When bad years become bad decades, and lots and lots of people die, that's when things like alcohol tolerance and lactose tolerance can make a big difference.
Being able to tolerate alcohol may mean access to a cleaner source of fluid, less pathogens for weakened immune systems to deal with, and access to nutrients that store pretty well. There may have been a social component as well – getting drunk together has been an extremely important vehicle for networking and bonding for literal ages. Finally, being able to get drunk relatively safely may have kept people functioning through highly traumatic experiences as well. Not saying that's what happened for sure, but a few ways this could have played a decisive role.
There used to be something called "small beer" that was also v low in alcohol content, made from the same grain as a regular beer, but mashed/drained a 2nd time to get any remaining sugars.
More seriously, I bet alcohol and hops do play a role. The alcohol isn't enough to sterilize anything (which requires a much stronger concentration: ~70%, usually). However, it and the hops could help maintain sterility once the heat has done its job.
Bacteriostatic water is used to dilute drugs for injection, and it uses a similar principle: a small (0.9%) amount of alcohol is added to keep any bacteria from getting a foothold.
One famous story of historical excess drinking is associated with the U.S. constitution...
https://www.wearethemighty.com/mighty-history/george-washint...
Finally, there is an easy method for most people reduce their impulse to drink temporarily by the use of the opioid blockers naltrexone or nalmefene. These can be used either for a goal of reduced-compulsion abstinence or long-term controlled drinking.
https://en.m.wikipedia.org/wiki/Naltrexone#Alcoholism
That said, I'm sure being an alcoholic was much more accessible back when because of (relative) cost - alcohol is relatively expensive nowadays compared to food, water and other drinks.
Somehow I doubt it was cheaper in the past, maybe more people made it themselves.
Like, you can still get 1.5L of ~9% homemade wine or 0.5L of ~40% spirit for ~1 Euro in Romania/Moldova.
Unless there was an epidemic of people getting wasted - and dying from it - in the same decade as some other terrible event, the argument doesn't hold.
The data sets that produce these plots almost never take into account why people stop drinking. When you do control for this, and in the process filter out people who stop drinking because of other severe health issues, it becomes obvious that not drinking at all is the healthiest option.
But many studies do account for that scenario of "sick quitters". The statistical correlation still showed that light moderate drinkers had lower mortality rates.
The study itself may still be flawed but the point is that the researchers were aware of "sick quitters" being categorized as "non-drinkers" and thus distorting the results.
Excerpt from 90+ Study publication https://pubmed.ncbi.nlm.nih.gov/17350977/ :
>The greater proportion of surviving participants in our study who reported not drinking at follow-up compared to baseline is probably due to a combination of the cohort’s becoming older and drinking less, secular changes in alcohol consumption with time, and survival selection effects. Decline in consumption is also associated with the development of ill health, particularly cardiovascular disease. This accumulation of ill health and higher mortality risk in ‘sick quitters’ increases the observed benefit in drinkers if non-drinkers include these ex-drinkers [6, 24, 26]. In addition, regular light drinkers tend to have characteristics advantageous to health [26, 27]. Thus, controlling for baseline disease is important, particularly if alcohol history is unknown. With adjustment for baseline medical history as well as body mass index, exercise, and smoking, the lower risks of death among light and moderate alcohol drinkers observed in our study did not change substantially and remained statistically significant although those associated with heavier drinking were reduced.
But that was pretty much settled with Mendelian Randomization studies on exactly this gene. As the article says, some people have different versions of the alcohol dehydrogenase enzyme, which basically gives them a worse hangover, faster. People with this condition drink slightly less than they otherwise would, wherever they are on the consumption curve. Knowing that, and knowing that the gene is more or less randomly distributed in the population under study, and assuming the gene affects nothing else (a safe bet, since alcohol dehydrogenase is a fairly task-specific enzyme), we can disentangle the effect of the alcohol from all the other things that could cause you to drink more or less alcohol.
Now the consensus seems pretty solidly on that the apparent protective effect of moderate alcohol consumption on stroke, cancer or heart disease is non-causal.
That being said, most drinkers -- at least in the US -- do not fit the above category at all.
Alcohol’s potential role in someone’s preferences about how to enjoy life doesn’t have anything to do with the discussion of whether it has a biologically protective effect.
I know a few problem drinkers who are linearly killing themselves and they all grasp for this “scientists have proven alcohol is good for you” misinformation as a part of their excusing narrative.
However i'd be surprised if there was a positive biological effect from alcohol.
It's not unreasonable to presume that such moderate drinking probably correlates with all sorts of other health related lifestyle choices. From my entirely anecdotal world view the most healthy people i know still have a couple drinks every now and then (but dont drink excessively regularly). It's almost impossible to control for all these factors in a study
Most of the non-drinkers i know do so because they don't like the taste/have alcoholic parents/are teetotal due to addiction and have no correlation in terms of other behaviors.
If it’s a beer, you can easily turn down offers of other drinks just by saying you don’t want to mix alcohol.
Overall, a pretty simple solution to the social problem.
But basically when someone wants you to drink it's their social anxiety that is manifesting, not yours. They need other people to participate in the bonding ritual, part of which requires people letting their guard down, which alcohol helps with.
But I'm not sure it's the chemical pathway that does it. I mean yes, drink enough and you will feel different. But you open up socially over a beer before the beer has any effect, eg. while you're waiting in line at the bar chatting to someone, or while you have just a tiny dose in your blood. Likewise with drugs, I never thought I was getting especially high or changed somehow. So perhaps it's more like a Schelling point, people accept that alcohol/drugs at a social event means that you can relax.
I've also never felt that I became someone else when drinking. Even when so drunk I couldn't walk straight, I could still understand social cues and conventions, and I still knew what I desired. It's like the beer is an excuse for bad behavior rather than the cause.
Luckily as an adult with kids I don't get badgered into getting hammered anymore. But I did think of a good excuse after talking to a cardiologist: you can always say you have some sort of condition that makes it a bad idea for you to drink or do drugs.
The problem with that is a lot of polite society depends on said filters, the overwhelming majority of people quite simply can't handle the truth.
I am not an apologist. I have come to dislike alochol, and I’m trying to cut it from my life. But, at least here in scandinavia, having work, a love life and friends can be dependant on you drinking.
A fun thing i’ve noticed though, is that Tinder has alleviated this dependancy on alcohol quite a bit.
In my experience people don't care if you drink pints of vodka or orange juice, as long as you're physically here and engage socially. It's like being vegetarian, some friends might look at you funny for a bit but unless they're complete morons they won't actively judge you
I'm not particularly interested in the topic, that being said here are the ones I like the most: Stoertebeker alcohol free atlantic ale, Lammsbräu alcohol free, BRLO naked, Franziskaner alhocol free, Paulaner alcohol free, monschof alcohol free
The only alcohol I keep drinking are whisky and red wine in very moderate quantities.
A passable alcohol-free Islay whisky would be an amazing thing!
> ...An unexpected, highly significant finding was observed: the AA rats, bred for high voluntary ethanol drinking, lived much longer than the ANA rats, bred for ethanol avoidance. The death rate by 24 months in the AA line was less than one-third of that in the ANA line.
> Conclusions: Lifelong ethanol consumption increased neither the mortality nor the morbidity of AA and ANA line of rats. Genes selected in the development of the high drinking AA line have additional effects producing rats that are healthier and living longer than the ANA rats possessing genes resulting in alcohol avoidance.
https://pubmed.ncbi.nlm.nih.gov/14745306/
So what if people who drank were simply _genetically_ healthier to begin with, and moderate drinking has no effect on health outcomes whatsoever? The study seems to suggest that.
I don't drink, mostly due to not liking the taste. But I thought wine and whisky had something in there that is good for you / antioxidant?
What the post conceptually centers on is best depicted in that chart in the middle. Also, if you read the entire thing you'd have found out that the author isn't trying to make any specific point, but rather is telling a story.
https://sites.duke.edu/apep/module-1-gender-matters/content/....
I wonder how that fits into the author's narrative?
Taking a quick glance at the literature, it's... super complicated. This paper (https://doi.org/10.1002/jcla.10076) suggests that women have lower gastric ADH but higher liver ADH. There's some animal studies that suggest men have higher ALDH, but also some contradictory human studies that suggest that everything is just the same.
Argh, biology.
If there really is a selection against alcohol, why did that not kick in outside Asia, too? The selection mechanism postulated would need to be fast... are 2k years or so really significant?
Evolution isn't a perfect machine. If those variant genes don't pop up at the right place at the right time, they might just not happen to catch on.
Someone mentioned that alcoholic drinks were safer to drink than water so people were drinking alcoholic drinks as a safer alternative. But we have to remember the various "cradles of civilizations"(Mesopotamia, Yellow river, Indus Valley etc) all evolved around rivers so access to clean water probably wasn't a major issue.
What's more likely is the effect is an unintended consequence. Other qualities "unique" to Asians or East Asians are a general lack of body hair and (more pronounced) neoteny. I don't think there are adequate theories for those quality either. There's still a long way to go to fully understand evolution and genetics.
That makes a good environment for mutations that protect people from alcohol consumption, but such mutations still has to randomly appear, and that it happened to appear in East Asia is probably just random.
The fact that populations who have never had alcohol succumb to rampant alcoholism when first getting access implies that even the eurasian populations without the Asian Flush genes probably has some less obvious genetic protection. You can also think of it as the most alcoholic prone genes have been weeded out over the centuries.
Early European civilisations kept their water safe by making it lightly alcoholic - Early Asian civilizations just boiled their water to make tea.