Are the benefits of moderate drinking a myth? 

red-wine-505296_640I’ve been reviewing two questions in depth for the Open Philanthropy Project, my 75% employer: How much should we worry about geomagnetic storms? And do alcohol taxes save lives? I hope to share drafts on both soon.

In the meantime, I want to share what is for me a surprising discovery, assuming it is true. The idea that moderate drinking is better for your heart than abstention looks headed for the ash heap of history like so many upended lessons from observational epidemiology. (Years ago, I blogged a certain example of this trend, relating to hormone replacement therapy for post-menopausal women: roughly speaking, observational studies said it was good; randomized trials showed it was not just not good, but bad.)

Here’s a chunk from the draft text that explains how this issue relates to whether alcohol taxes save lives (net), and how I reached my current understanding. I emphasize that I based this write-up on a day or so of reading. That said, my priors about the reliability of studies of various types come from longer experience. I’d welcome critical reactions, and sharing of this post in order to provoke them.

The literature persuades me that raising alcohol taxes reduces deaths from alcohol-related diseases, notably cirrhosis. However, key studies such as Wagenaar, Maldonado-Molina, and Wagenaar (2009) on Alaska, Cook and Tauchen (1982) on US states generally, and Koski et al. (2007) on Finland persuade precisely by showing quick impacts. And their focus on the short-term leaves the long-term impacts less clear. This is not a criticism: as I have argued, long-term impacts are harder to prove (Shadish, Cook, and Campbell 2002, p.173).

In the absence of certainty, what is the most plausible prior? On the one hand, the benefits of an alcohol tax increase almost surely swell with time. Cirrhosis, for example, progresses over decades. If a higher price for alcohol slows the progression from near-death to death, which is what the studies are detecting, then it ought also to slow the progression at all stages. On the other hand, many studies suggest that moderate drinking, as compared to abstention, reduces coronary heart disease and other ailments (Fekjӕr 2013, p. 2015). Alcohol tax increases may well impede this apparently healthy moderation. The harm per person might be much smaller than the benefit per person among heavy drinkers of a tax hike, but the population harmed could be far larger. And this effect might play out purely in the long-term, so that it is missed in the studies favored here. In principle, this leaves the sign of net long-term impact ambiguous.

A full review of the relevant epidemiological literature on moderate drinking is beyond the scope of this document. However, an initial scan leaves me reasonably confident that tax increases save lives in the long run too. The reasons:

  • No randomized trials have checked on the benefits of moderate drinking how moderate drinking affects morbidity and mortality (Holmes et al. 2014, p. 4).
  • The belief in such benefits derives from non-experimental, observational studies, whose claims to causal identification make them akin to the alcohol tax studies passed over for low credibility in this review. In epidemiology, as in economics, observational studies have come under a shadow in the last decade or so, as randomized trials have upended established doctrines such as the belief that hormone replacement therapy reduces heart disease and cancer (Writing Group for the Women’s Health Initiative Investigators 2002).
  • A new generation of Mendelian randomization studies challenges the conventional wisdom on moderate drinking, albeit not with the overwhelming force that conventional randomized trials would (Davey Smith and Ebrahim 2003, p. 10). Mendelian randomization studies strive to exploit the randomness inherent in sexual reproduction as well as the now-low cost of gene sequencing, in order to fashion natural experiments. For example, if a mutation reducing the ability to metabolize alcohol, and thus the propensity to drink, is randomly distributed in a population, then whether one carries zero, one, or two copies of that gene can instrument for drinking in a study of drinking’s sequellae. In fact, genes are not distributed with perfect randomness, and can affect health through multiple pathways, so Mendelian randomization does not produce experiments as close to perfect as conventional randomized trial (Thomas and Conti 2004; Davey Smith and Ebrahim 2003, pp. 13–17). Nevertheless, that these studies have generally failed to find benefit from moderate drinking in comparison to no drinking creates serious doubts about traditional observational studies. A meta-analysis of Mendelian-randomized alcohol studies, aggregating data from 261,991 people of European descent, found that carriers of a particular variant gene for the alcohol dehydrogenase 1B enzyme drank 17% less (95% confidence interval 15.6–18.9%) and had 10% lower odds of coronary heart disease (95% confidence interval 4–14%; Holmes et al. 2014, p. 4). (The gene causes faster conversion of alcohol into aldehyde in the blood stream, so that people get drunk experience its toxic effects faster.) Restricting the analysis to low, moderate, or heavy drinkers did not change the apparent impact (Holmes et al. 2014, p. 7). Even at low levels, more drinking did at least modest harm. 1
  • A study based on a telephone survey of more than 200,000 people in the US checked whether self-reported drinking levels correlated with any of 30 demographic, social, and economic factors thought to contribute to cardiovascular disease, from age to poverty to less exercise to limited access to health care. Among light and moderate drinkers as a group, 27 of the 30 factors were correlated with drinking levels, and in the direction that could create a false appearance of moderate drinking leading to better health. For example, as people enter old age, they drink less and become more likely to die.2 (Naimi et al. 2005.) Presumably no observational study controls for all 27, and perhaps none needs to go quite that far since the factors are probably inter-correlated. Nevertheless, the study suggests that the endogeneity of moderate drinking to health is hard to eradicate from an observational study.

In light of these facts, Occam’s Razor argues for a simple theory: the net marginal impact of drinking on health is negative at all levels; and moderate drinking is a marker for relative youth, affluence, and healthy habits rather than a cause of good health (Chikritzhs et al. 2015). Pending high-quality evidence to the contrary, alcohol taxes should be presumed to save even more lives in the long run.

(If you want to read more on this issue, try the new Chikritzhs et al. editorial—hat tip to Alex Wagenaar—and Fekjӕr’s pointed piece.)


 

  1. After critiquing Mendelian randomization, VanderWeele et al. suggest relying on it more when it produces negative results, assuming the confidence intervals are narrow. I think that is what I am doing here, the negative result being no differential in impact by drinking level.  (back)
  2. The analysis excluded respondents reported to be in poor health, in order to prevent unhealthy former heavy drinkers from contaminating the sample of non-drinkers.  (back)
  • AlanSutton6

    You repeatedly mention age as a confound, implying that this obvious variable is not properly dealt with in studies that appear to show a protective effect of alcohol. Can you provide even a single example of a study claiming a protective effect of alcohol that did not adjust for age? I am really doubting that such studies would have been deemed publishable.

    • David Roodman

      Alan, I think all I say is that are a lot of potential confounders and probably no study controls for all of them, or comes close enough to rule out confounding in my mind. I see two mentions of age, one in a representative laundry list of factors, one as an example to provide intuition for the general idea.

  • Steven Berry

    I don’t understand how the “ability to metabolize alcohol” is properly “excluded” from the effect of drinking on health, and therefore available to be used as an “instrument” that effects the level of drinking but has no direct effect on health. This seems on first thought to be a really terrible instrument. Am I missing something?

    • David Roodman

      Hi Steven. It’s a good question. The biochemical idea is that people with certain variants of the enzyme alcohol dehydrogenase accumulate the toxic form of alcohol in their bodies more rapidly, and so stop drinking sooner. The statistical idea, which is certainly debatable, is that “ability to metabolize alcohol” affects health as measured in the studies only in this way–or at least only by changing the amount of drinking.

      Are you understanding yet doubting this assumption? Certainly a broad criticism of Mendelian randomization is that a given gene can affect health through many biochemical pathways. In this case maybe the gene also affects health through some pathway that does not involve how much people drink, violating the key statistical assumption. Is this your concern? In this particular case, I see that risk as lowish because I think alcohol metabolism is relatively well understood. But I’m no biochemist.

      More persuasive for me is footnote 1 above, where I invoke the idea that Mendelian randomization is more compelling when it produces negative results. If the assumption you question is in fact wrong–if the alcohol dehydrogenase 1B gene in fact affects health through pathways separate from amount drunk–then since the Mendelian studies return null results, the net effects of all these pathways is about zero. That would be something of a coincidence, so I would assign it lower probability.

      Am I understanding your question right?

      –David

      • Steven Berry

        Yes, I think I count as “understanding but doubting.” Wouldn’t how fast you metabolize alcohol have a direct effect on the alcohol-health relationship? This is your “multiple pathways” point, it just seems to me that there is surely a *direct* pathway here (I don’t know which way the bias is likely to go.)

        As for the “trust the negative,” I agree that it is unlikely that offsetting effects come out to exactly zero. But once you add statistical noise, it is not so simple. Offsetting effects can easily lead to a statistical inference that you cannot reject the null of zero effect.

        • David Roodman

          To be precise (and to approach the limits of my knowledge) just one step in alcohol metabolism is sped up resulting in more rapid accumulation of toxic aldehyde. But your point stands, yes, I suppose that in itself could effect health. My intuition is that the overall effect of reducing total intake would dominate the effect of quicker rise to toxicity. But the body is a complicated thing.

          I agree that the argument for greater weight on negative findings is not open and shut. Hopefully I didn’t phrase it that way. I argue only for greater weight, not all weight.

  • anonymous

    I think that the Mendelian critique may have a serious flaw if the causal path is “getting ‘buzzed’ releases stress – stress causes heart disease”. This means that it is not the amount of alcohol that matters, but the stress releasing effect.

    • David Roodman

      anonymous, are you suggesting that the ADH gene in question could affect how much people drink, if they drink, but not whether they drink, so it would be missing the action?

      • anonymous

        Yes. Suppose nonADH people need 2 drinks a day to get the stress-relieving benefits and people with the gene only need 1 drink per day. Then this would not be a proper instrument. Am I missing something?

        • David Roodman

          I think I understand, anonymous. I wrote before of the effect of the gene “whether” people drink, as distinct from how much. But since it is the rare human being who never drinks over a life time, I think a better way to phrase the distinction is between how often people drink and how much. Maybe, you suggest, people with the ADH1B gene drink just as often, as so get the full health benefit of moderation, even if they drink less in total. The comparison of those with and without the gene will then show no difference and lead us to wrongly conclude that moderate drinking does no good. In other words, the local average treatment effect in these studies is not representative for the question we care about.

          Which leads to an empirical question: does the gene have no effect on how often people drink? The Holmes et al study that I link to cites two studies apparently to the contrary:

          Macgregor S, Lind PA, Bucholz KK, Hansell NK, Madden PA, Richter MM, et al. Associations of ADH and ALDH2 gene variation with self report alcohol reactions,
          consumption and dependence: an integrated analysis. Hum Molecular Genetics
          2009;18:580-93.

          Bierut LJ, Goate AM, Breslau N, Johnson EO, Bertelsen S, Fox L, et al. ADH1B is associated with alcohol dependence and alcohol consumption in populations of European and African ancestry. Molecular Psychiatry 2012;17:445-50.

          I haven’t read them. Interestingly, they emphasize dependence, which reminds us of the potentially addictive nature of alcohol. Apparently people with the gene are less likely to become addicted. I’d expect less addiction would lead to drinking less often.

  • Alan Gunn

    Even if moderate drinking did improve people’s health, would it necessarily follow that raising alcohol taxes would reduce moderate drinking? While it would cause some moderate drinkers to stop drinking, wouldn’t it also cause some heavy drinkers to drink moderately? So the overall effect on health could be neutral, or even positive (if heavy drinking is worse than not drinking at all, which seems likely).

    • David Roodman

      Oh, very interesting, Alan. I suppose a do-no-harm dictum would be violated if moderate drinking is in fact good–some people helped and some hurt by a tax increase. But I think it’s a good point.

  • ThomasA

    Why is the goal of maximizing people-years lived the only outcome considered here? If moderate drinking shortens people’s lives, but makes those fewer years happier years, would that not be also be a reason to lower alcohol taxes?

  • Adam

    David – I really admire the way you respond to us in the comments. Thanks for caring about people enough to be so kind, and for caring about truth enough to keep pursuing it.

    • David Roodman

      Thank you, Adam. Much appreciated.

  • Sid

    “The gene causes faster conversion of alcohol into toxic aldehyde in the blood stream, so that people get drunk faster.”

    I believe this statement is precisely incorrect. One of us is confused about the metabolization of alcohol, and it may well be me, but my reading of the wikipedia page on alcohol dehydrogenase does seem to confirm me.

    My understanding is that the conversion of alcohol into acetaldehyde (the toxic aldehyde of which you speak) is not what causes drunkenness. Acetaldehyde causes hangovers. The transformation of alcohol to acetaldehyde conducted by alcohol dehydrogenase (ADH) is the first step in the process of sobering up: it is how the body clears alcohol from one’s system.

    It is alcohol, itself, good old C2H6O, which crosses the blood-brain barrier and causes drunkenness.

    The carriers of that particular variant gene for the alcohol dehydrogenase 1B enzyme who drank 17% less? Did so because their genes gave them a propensity for wicked hangovers, that start very soon after onset of intoxication. For people with that genetic constitution, drinking alcohol is not pleasant, but highly aversive. They weren’t getting drunk faster, they were getting hungover faster.

    • David Roodman

      Hi Sid,
      25 years ago, in college, my girlfriend spent inordinate amounts of time in a lab in the basement of a hospital, grinding up hamster livers and performing assays. Apparently hamsters *don’t* get drunk. So everything I thought I knew about alcohol dehydrogenase dates from then. She’s no longer my girlfriend, but fortunately she’s my wife.

      If “drunk” = cognitive impairment, which I think it basically does, then yes, it is true alcohol that causes drunkenness and those with the 1B variant would probably get drunk slower.

      What I had in mind when I tossed out the convenient word “drunk” was the non-cognitive toxic effects of aldehyde. Flushing is the most easily observed.

      I’ll adjust the wording. The epidemiological argument, such as it is, otherwise stands, right?

      –David

      • Sid

        No, on further reflection, I don’t think it does stand, but I confess I’m struggling to follow all the ramifications, so let me just share what I have.

        People who have the 1B variant are having less exposure to C2H6O than those who don’t, and they have more exposure to acetaldehyde than those who don’t, for the same volumes of alcohol imbibed.

        This means the difference is not merely that 1B variant people drink 17% less. The 1B variant people are having exposure rates to C2H6O equivalent to people who normals who drank even less than 17% below average, but acetaldehyde exposures equivalent to normals who drank more than 17% below average. It’s even possible that for 1B variants the acetaldehyde exposure per L of C2H6O ingested is so much higher than for normals, that even if they drink only 83% of normal, they getting more acetaldehyde exposure than normals drinking 100% of normal. I simply don’t know if that’s true.

        So the claim, “whether one carries zero, one, or two copies of that gene can instrument for drinking in a study of drinking’s sequellae”? I don’t buy it. You can’t treat the gene as a proxy for the behavior of drinking in a study of the health consequences of drinking, because it doesn’t code exclusively for the behavior of drinking, it also codes for variant health effects of drinking!

        This may clarify things a bit (or maybe not, it might muddy the waters). There’s this other gene that impacts the metabolic pathway of alcohol, one that doesn’t change the rate at which alcohol is metabolized into acetaldehyde, but which changes the rate at which acetaldehyde is metabolized into other things. It moderates how fast your hangover goes away.

        I, personally, apparently have an extra copy of that gene. Those of use with extra copies of that gene clear acetaldehyde from our systems faster than our systems can make it: we’re genetically immune from hangovers. Consequently, if there are any long-term morality consequences to acetaldehyde exposure (if, say, it causes cancer, or if it’s what reduces risk of heart disease), I will never be impacted by them, because no matter how much I drink, I will never have but trace amounts of acetaldehyde in my system. Acetaldehyde can’t build up in my system, because my system clears it so fast. So as far as acetaldehyde exposure is concerned, I’m a non-drinker.

        On the other hand, I am not as far as I know a 1B variant, so alcohol stays in my system perfectly typically. Alcohol, C2H6O, itself is a very powerfully bioactive chemical. It, not acetaldehyde, is the Central Nervous System depressant which impacts heart rate and breathing. It, not acetaldehyde, impacts activation of the HPA axis and the sensation of pain. And it, not acetaldehyde, is, I believe, the carcinogen that sharply inclines heavy drinkers to throat cancers.

        I hope it’s obvious from this that any study that attempts to use the impact of this other gene — which removes the negative consequence of hangovers from the behavior of drinking — as a way to operationalize rate of drinking with health consequences for drinking is clearly bogus: you can’t tell if any effect drinking has on me and my genetic cohort is because of our drinking more or our tee-totaler levels of exposure to acetaldehyde.

        Or worse, some as of yet undiscovered weird relationship between the extensive metabolization of acetaldehyde and some other part of the biopsychosocial system of drinking. Wouldn’t it be a hoot if it turned out that people who are extensive metabolizers of acetaldehyde also have different taste buds causing them to like alcohol more or less than those without that gene? Or if this absence of exposure to acetaldehyde causes something in the brain to upregulate in compensation?

        There’s so very much we still don’t know about alcohol and its pharmacokinetics and pharmacodynamics, but we already know that it’s quite complicated with many moving parts. So no, I don’t think the logic of “Mendelian randomization” holds for studies of the health consequences of drinking.

        • David Roodman

          Thanks, Sid. One thing: it’s not obvious to me that people with the 1B variant (meaning alcohol is converted faster to acetaldehyde) have more exposure to acetaldehyde, or at least not obvious that the difference is first-order. Every molecule of alcohol imbibed becomes aldedyhde at some point, right? Then people with 1B experience a lower lifetime dosage of acetaldehyde in volume terms. So: fewer molecules of exposure but perhaps more minutes of exposure per molecule. Maybe the net is positive, but relative to the unambiguous impact on alcohol exposure, that seems like the embodiment of second-order.

          I think your theoretical story illustrates the verity that there is no perfect Mendelian instrument. Human biochemistry is an extraordinary cobweb of pathways (about which I know little). Some of those pathways link any given instrument to any given outcome while bypassing the causal variable of interest. No argument there.

          I do think it is a mistake however, to speak of instruments in binarisms–bogus or not, valid or invalid–if only because we don’t have the luxury to do so. It seems to me that any standard that rules out Mendelian studies must also rule out all observational studies, in which the drinking level is its own instrument, and would seem to be at least as bad as any Mendelian instrument. Then we are left with nothing. Yet judgments must be made, about policy, lifestyle, etc., and so we ought to make the best use of the evidence we have, while of course not overstating our certainty. That’s what I see myself as trying to do.

  • Johan Sigfrids

    Have you seen http://www.ncbi.nlm.nih.gov/pubmed/25288221 ?
    It is a case-control study looking at how the CETP TaqlB genotype modifies the association between alcohol consumption and CHD. There are two alleles B1 and B2. Alcohole consumption does nothing for people that are B1B1 or B1B2, but moderate alcohol consumption is associated with a large reduction in CHD odds in people that are B2B2.

    • David Roodman

      Interesting, Johan. If I read it right the effect derives from observations of 13 “intermediate” drinkers with B2B2 and 27 “high” drinkers with B2B2. And the authors write, “our results can be contrasted to a meta-analysis of 7 studies…” That is, other studies have gotten different answers. That doesn’t make this one wrong, but I think it would be a mistake to draw much conclusion from one small, observational study in isolation.
      –David

  • Spencer

    Perhaps people who don’t drink use it as a way to separate themselves from social relations. One of the studies says that a very strong relationship exists between a network of social relationships and good health and long life. Light drinking may be only a marker and not a cause or, more likely, because it reduces inhibitions and feelings of awkwardness, it leads to more and better social relations. We could add that it could reduce tension thus allowing high achievers to operate under stress knowing that they will be able to decompress when they have wine with dinner or a before-dinner drink.

    Perhaps doctors should recommend moderate drinking because it is associated with (and is likely to cause) other behavior that actually does improve one’s health. I think it might be relatively easy to do controlled studies showing that moderate drinking actually causes more social interaction which leads to more and better social relationships.

    Personally, I find that non-drinkers tend to be rather critical of the relaxed behavior they observe among the drinkers. It may be an innocent remark such as “They were laughing but it wasn’t funny”, but critical comments are common. If the non-drinkers are marginalized because of their choice to abstain, then changing that choice and drinking with others would show alcohol to be a positive causal agent, though not directly through chemical effects on the body but indirectly by increasing one’s ability to develop social networks.

  • Jayson Lusk

    Logically, if there is no good evidence of the benefit of moderate drinking, there’s also no good evidence of harm from moderate drinking either. Taxes are likely to result in small or moderate reductions in consumption. Thus, it also seems we have weak evidence that such taxes will create much health benefit (at least among moderate drinkers)

    • David Roodman

      Hi Jayson. So when you imply there is no good evidence, you mean you don’t trust the Mendelian-randomized studies either?

      I’ve probed the evidence on the impacts of alcohol taxes on deaths from alcohol-linked diseases, notably cirrhosis, and found it persuasive. This presumably has to do with heavy drinkers, not moderate. E.g., see Cook & Tauchen (1982) on US states (which I have found to be robust to extension to 1960-2004) and Koski et al. (2007).

      My draft lit review is almost ready for sharing.

      • Jayson Lusk

        Thanks. Looking forward to seeing it

  • AlexWilliams

    I was with you until your logical jump in the last sentence. If it were true that people would spend precisely the same amount of money on the same concentration of alcohol, then increasing the cost of alcohol by x% would decrease consumption of it by (1 – 1/(1 + x))%. However, that’s a rather strong assumption and it isn’t sufficient to prove more lives will be saved in the long run.

    1. Poor people might spend more money on alcohol. Less disposable income might adversely affect their lives.
    2. People might just buy cheaper alcohol in higher concentrations. That might give their livers less time to process what they consume, which is worse for them.

    3. People might replace alcohol for worse vices.
    4. Tax money is used to fund questionable programs that harms and/or ends lives.

    • David Roodman

      Alex, this is a straw-man argument. The post does categorically assert that higher alcohol taxes save more lives in the long term. Therefore abstract arguments about possible alternative stories do not in themselves contradict the post. Evidence of some sort would required, in order to show that these stories are more than imaginable. Otherwise we get paralysis by analysis. It’s also possible that raising cigarette taxes kills children (maybe by funding child-killing government programs) and that air traffic controllers just get in the way. Possible.

      The post argues that the balance of the evidence together with Occam’s razor favors a straightforward theory, pending high-quality evidence to the contrary. It is also presented as an excerpt of a longer review of actual evidence, which unfortunately cannot be shared yet. Part of that evidence relates to a strong statistical link between alcohol taxes and cirrhosis, which itself goes against stories #1 and #2 in this comment.

      Since this is a disease that progresses over decades, it is reasonable to think that if the tax can slow the final stage toward death–as the data strongly suggest–then it slows the disease at all stages. The idea that moderate drinking is good for you does have a lot of evidence behind it–not sufficient to convince me now–but sufficient to make me research it.

      • AlexWilliams

        Since it seems your post has been considerably altered I have to retract “I was with you until your logical jump in the last sentence”. I agree that it’s most likely the case that alcohol consumption at any level is probably harmful to an individual.

        One that makes a positive claim (such as policy X saves lives) does not have logical luxury of being able to ignore unseen and/or secondary effects of the policy in question.

        We both agree that it is reasonable to think that if lower alcohol consumption can slow the final stage toward death. However, you can’t cite one study showing a statistical correlation and change “lower alcohol consumption” with “the tax” while maintaining the soundness of your argument.

        • David Roodman

          The post has not been altered except for the displayed strike-through of “get drunk.”

          There is no such stark claim in the post as “policy X save lives,” at least with regard to the long term.

          My review of the alcohol tax literature is extremely thorough. I’m sorry I cannot post it yet. (Open Philanthropy is overhauling its website now so posting a new page will just create another headache.) If you send me an email address, I’m happy to email it to you.

          • AlexWilliams

            The line I was referring to was “Pending high-quality evidence to the contrary, alcohol taxes should be presumed to save even more lives in the long run.” If that line wasn’t moved earlier, then I misspoke.

            I you’re not claiming “taxes saves lives in the long run”, then I don’t know why “taxes should be presumed to save even more lives in the long run”. I have a email account that I don’t mind receiving spam at [deleted].

          • David Roodman

            Alex, assertion and presumption are not the same. For me the latter, is about making the best call one can in the face uncertainty and the need to decide on practical action.

            Yeah, that line has not changed. I’ll send you the draft. Comments welcome. I’ll also delete your e-mail from this thread; let me know if you object to that.

          • AlexWilliams

            I don’t object to removing my email. I appreciate your clarification about attempting to make the best call. Because you at least admit there is uncertainty about the full nature of the effects of a tax policy, I hope you can have compassion for those that believe that a tax policy can cause more harm than good.

  • I still haven’t properly wrapped my head around the Mendellian papers. But out of the observational ones, these did seem pretty convincing:

    1. Rimm and Moats, 2007. They restricted their sample to men with healthy lifestyles: those who didn’t smoke, who exercised, who had a good diet, and who were not obese. Within that group, strong J curve on chronic heart disease. http://www.sciencedirect.com/science/article/pii/S104727970700004X .

    2. Di Castelnuovo and Donati’s metastudy, 2006. This one takes on the “sick-quitter” hypothesis fairly directly, splitting the sample between those that lumped sick-quitters in with abstainers and those that restricted things to never-drinkers. It makes the J-curve a bit shallower in all-source mortality, but it’s still rather strong.
    http://www.ncbi.nlm.nih.gov/pubmed/17159008

  • IOGT International

    Hi! This is an interesting exploration of evidence. You might find this additional evidence helpful, too. As the British Medical Journal wrote in an Editorial this year: the evidence for alcohol’s health benefits is evaporating.
    1) The effects of low-dose alcohol consumption: http://iogt.se/wp-content/uploads/Alkoholrapport-2014-ENG.pdf
    2) BMJ Editoarial (subscription needed): http://www.bmj.com/content/350/bmj.h407

    3) Alcohol taxation also (in addition to saving lives) does have a positive net benefit for job creation: http://www.iogt.org/policyofficerupdate/630/higher-alcohol-taxes-create-more-jobs/

    — Maik

  • anonymous

    You say “No randomized trials have checked on the benefits of moderate drinking (Holmes et al. 2014, p. 4).”, but I just learned from the Upshot website there seem to be a bunch of them – http://www.bmj.com/content/342/bmj.d636 . Were you aware of this meta-analysis?

    • David Roodman

      Hi anonymous. It looks to me like that BMJ review does not include randomized trials. But you’re right that the Upshot points directly to three randomized studies. Of these, two (here, here) appeared after I wrote this post. But one came out before, in 2013, so I stand (retroactively) corrected to that extent.

      Unfortunately, because of other priorities in my work, I don’t think I can devote the time now to doing full justice to these studies.

      I do worry about the combination of small samples and many hypotheses. The first study linked reports, “Across the 3 groups, no material differences were identified in blood pressure, adiposity, liver function, drug therapy, symptoms, or quality of life, except that sleep quality improved in both wine groups compared with the water group.” So it may be that the one outcome that showed a statistically significant difference is the one that got the headlines. Possibly the same goes for third one—the one I missed. Its pre-trial registration lists a rather long set of outcomes to be examined, but only a few seem mentioned in the abstract. The second study does not find a statistically significant effect, perhaps because of the small sample.

      These kinds of concerns could be dispelled by larger trials, which I hope are coming.

      • anonymous

        Thank you for your answer. I may be missing something obvious here, so I do apologize if that is the case, but I have the distinct impression that the BMJ review does include a bunch of randomized trials. When I searched for “random” within the references, I found a number of studies. Are you not considering them because they do not address mortality directly but other biomarkers?

        • David Roodman

          Hi anonymous. You are right again. On a skim I saw references to “random effects,” which is different. The point the authors are making in the papers making this assertion (Holmes et al. 2014; Chikritzhs et al. 2015) is that there have been no randomized trials with morbidity or mortality as the outcome, only biomarkers like cholesterol levels. I’ll edit the text above to clarify this.