By Eric Crampton 01/10/2015 4


The correlation between alcohol consumption and any particular disorder matters a lot less than the link between alcohol consumption and overall mortality.

Anti-alcohol folks like to talk a lot about that alcohol consumption increases cancer risk (while ignoring that moderate consumption reduces stroke and heart disease); the other side downplays the cancer link while highlighting the cardiovascular benefits.

They’re both real, but what matters is the net effect: the J-curve. People who drink about a standard drink per day are about 14% less likely to die than are never-drinking teetotallers, and the benefits of moderate consumption wash out by the time you’re consuming about 3-4 standard drinks per day. And the risks mount from there.

Another study is out on the cardiovascular benefits of moderate drinking. There are some oddities in there, like finding differences across different types of alcohol. Rimm & Moats’ 2007 study remains the most convincing: they restrict things to a sample of healthy adults with few potential unobserved confounds and find that moderate drinkers’ relative risk of chronic heart disease was 0.38. Drinkers’ chances of getting chronic heart disease are less than half of abstainers’ risk. They conclude:

The evidence discussed above provides substantial support for the hypothesis that moderate drinking reduces the risk of CHD. Beer, wine, and spirits all have demonstrated significant benefits. These benefits are likely mediated through strong and lasting effects of alcohol on HDL cholesterol, fibrinogen, and glycemic control. The ‘‘sick-quitter’’ hypothesis and the concern that moderate drinkers lead a healthier lifestyle may explain a small proportion of the benefit attributed to alcohol in some studies, but recent studies which have removed sick quitters, updated alcohol and covariate information on diet and lifestyle factors, and separately documented benefits of alcohol among healthy and unhealthy populations further add to the evidence that moderate alcohol consumption is causally related to a lower risk of CHD.

So it is interesting that the New Zealand Heart Foundation’s Heart Age Forecast Tool doesn’t ask about your alcohol consumption. If you can cut your risk of chronic heart disease by more than half by drinking moderately, shouldn’t that be in the Forecast Tool? The Heart Foundation tries to downplay the effects of moderate alcohol consumption on CHD, saying that the benefits don’t hold for everyone. But if most of the benefits come from drinking in middle age, and the forecast tool asks your age.


4 Responses to “Alcohol heartbreaker”

    • They’ll typically use 10 grams, but they’ll typically say. The Di Castelnuovo and Donati metastudy on the J-curve (which I like best as it separates former drinkers from never drinkers) uses 10 grams per drink.

  • Hi Eric,

    The reason the Heart Foundation doesn’t include alcohol consumption in its heart age forecast tool is because the relationship between alcohol and cardiovascular disease is so complex. Our general advice is not to consume alcohol as a way of lowering your risk of heart disease. Although the most up to date scientific research suggests there may be some benefits of alcohol for reducing heart disease for some people, this is not the case for everyone, even when consumption is low or moderate. For most people there will be little, or no, overall benefit. Because the research is inconclusive, we don’t include alcohol consumption in our forecast tool.

    However, there are many other things with a much stronger evidence base that people can do to reduce their risk of heart disease. These include giving up smoking, eating a healthy diet and exercising regularly. More advice is available here http://www.heartfoundation.org.nz/healthy-living

    Kind regards,

    Heart Foundation

    • There will always be one or two studies that can mean any science isn’t settled, but the vast preponderance of the evidence points to strong cardiovascular benefits from light to moderate drinking. They’ve identified physiological pathways through which it’s strongly plausible, mostly through cholesterol ratios. A few recent ones:

      Ronksley et al, BMJ: Metastudy of 84. “Light to moderate alcohol consumption is associated with a reduced risk of multiple cardiovascular outcomes.” http://www.bmj.com/content/bmj/342/bmj.d671.full.pdf

      Arranz et al 2012, Nutrients. Summarises pathways through which alcohol consumption reduces heart risk.
      http://www.mdpi.com/2072-6643/4/7/759/htm

      Chiva-Blanch et al. 2013, Alcohol & Alcoholism. Systematic review of studies and metastudies 2000-2012. Moderate consumption provides protective effects in patients with documented CVD and in healthy subjects.
      http://alcalc.oxfordjournals.org/content/48/3/270.short

      Matsumoto et al, 2014. J Cardiopulmonary Rehabilitation and Prevention. Summaries existing lit, notes lowest risk for CVD among light to moderate drinkers.
      http://journals.lww.com/jcrjournal/Abstract/2014/05000/An_Expanding_Knowledge_of_the_Mechanisms_and.1.aspx

      Pai, Mukamal & Rimm. 2012. European Heart Journal. U-shaped relation between alcohol consumption and survival among male health professionals who had suffered myocardial infarction.
      http://eurheartj.oxfordjournals.org/content/33/13/1598.short

      O’Keefe et al 2014. Mayo Clinic Proceedings. Moderate alcohol use provides cardio benefits, but doctors should be careful in recommending it because some people will go and drink way too much. Daily low-to-moderate drinking, particularly with the evening meal, is most beneficial.
      http://www.sciencedirect.com/science/article/pii/S0025619613010021

      The *only* reasonable critiques I’ve seen thus far are:
      1) Confounding of non-drinkers with sick quitters matters. But this was entirely answered by Rimm & Moats 2007 and in the Di Castelnuovo & Donati metastudy. People who continue citing this, in my view, do so dishonestly.

      2) If light drinkers drink moderately because of a genetic variant that makes them both have better hearts and suffer quicker adverse experiences from heavier drinking, then the observed relationship could be an artefact of the underlying genetics. See Holmes et al, BMJ, 2014. http://www.bmj.com/content/349/bmj.g4164 . I note though that while one of the established paths by which alcohol affects CVD is through cholesterol ratios, they didn’t find any effect of their genetic variant on HDL. Further, there are some rather important critiques here that I’d want to see answered by the authors. http://www.bmj.com/content/349/bmj.g4164/rapid-responses

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