Are the cardiac effects of alcohol good, bad, or neither?

There are consistent observational data to indicate that the association between alcohol use and adverse cardiac outcomes as a whole is U-shaped; that low-moderate amounts of alcohol use (up to one drink or 12.5 g alcohol per day in women and up to two drinks or 25 g per day in men) are associated with a reduced risk of overall cardiovascular events and mortality (Figure 1) when compared with abstinence or heavy alcohol use. The U-shaped relationship between alcohol use and all-cause mortality. Reproduced with permission from Ref.1 However, this generalization masks important nuances that merit closer scrutiny. Patterns of drinking, the type of alcohol consumed, and factors associated with alcohol consumption, such as socio-economic status, education, and dietary patterns may be important modifiers of the cardiac effects of alcohol. Alcohol use may also have differing effects in healthy hearts, when compared with those with established cardiac disease, and in particular, left ventricular dysfunction; and alcohol’s effects on coronary outcomes may differ from its effects on arrhythmias, on heart failure risk, on atrial fibrillation, and on the risk of ischaemic stroke and intracerebral haemorrhage. It is important to acknowledge that even if there is a beneficial cardiac effect of a modest level of alcohol intake, the net health consequences may still be negative when we consider the risk of cancer, injury and cirrhosis associated with alcohol use. Finally, the observational data that have given rise to the popular tenet that modest amounts of alcohol may have beneficial cardiac effects are subject to the same limitations and potential for bias and confounding as any other observational data. We have repeatedly seen positive, biologically plausible associations that have been proven non-causal by subsequent randomized trials (e.g. vitamin D and cancer prevention; hormone replacement therapy and cardiovascular disease prevention). While tempting to point to the large number of individuals on whom the U-shaped relationship is based as evidence for the robustness of the association between low-moderate alcohol use and favourable cardiac outcomes, these large numbers may simply serve to make a biased or confounded relationship more precisely biased or confounded. For these reasons, restraint should be shown before endorsing the use of alcohol to reduce cardiovascular risk. An average of up to one drink per day in women and up to two drinks per day in men is considered moderate alcohol consumption, and this pattern is associated with lower cardiovascular outcome rates. If, however, this weekly quantity is consumed during a single day, the reverse is observed. Binge, or heavy episodic alcohol use, typically defined as the consumption of ≥5 drinks during any one day, is associated with an increased risk of adverse cardiovascular events (Figure 2) and all-cause mortality. Furthermore, heavy acute alcohol use may be a trigger that acutely precipitates myocardial infarction. Therefore, heavy episodes of alcohol use should be discouraged. The relationship between acute alcohol use and the risk of cardiovascular events. A heavy episode of alcohol consumption is associated with an increased acute risk of harmful cardiovascular events. Reproduced with permission from Ref.2 There remains uncertainty whether some types of alcohol are harmful (e.g. beer or spirits) and others protective (e.g. wine). Types of alcohol consumed are highly likely to be associated with potentially confounding factors, such as socio-economic status and pattern of drinking. In vitro, alcohol has demonstrated toxic effects on cardiomyocytes. In the CARDIA study, alcohol intake was associated with adverse cardiac remodelling during 20 years’ follow-up. Heavy alcohol use may be associated with the development of alcoholic cardiomyopathy. As the causal factor in this condition, abstinence should intuitively be recommended in those with non-ischaemic cardiomyopathy where alcohol use may play a causal role. It appears paradoxical that observational data on alcohol use in other populations with systolic left ventricular dysfunction (e.g. analyses from SOLVD) suggest that low-moderate alcohol consumption in these groups is associated with better cardiovascular outcomes than abstinence or heavy consumption. While this apparent paradox may be due to differences in the quantities of alcohol consumed between those who develop alcoholic cardiomyopathy and those with heart failure who have a better outcome at low-moderate consumption levels, it seems counter-intuitive to advocate the use of a potential myocardial toxin in those who exhibit significant myocardial injury. The relationship between alcohol use and cardiovascular outcomes does not appear homogeneous. Alcohol use has been associated with an increased risk of intracerebral haemorrhage, even at low-moderate levels of consumption. Also, there appears to be a continuous positive association between alcohol use and the risk of cancer. Consideration of non-cardiovascular effects must be made when evaluating the potential risks and benefits of alcohol use. Adequate randomized, controlled trials of alcohol use are lacking. Mendelian randomization is a genetic epidemiologic approach that leverages the assumed random assortment of genetic variants to evaluate the causal relationship between a risk/protective factor and clinical events. A major advantage of Mendelian randomization approaches are that genetics are not susceptible to reverse causation, unlike behavioural exposures. The available Mendelian randomization data are not consistent with a beneficial cardiovascular effect of alcohol. This new line of research adds to the uncertainty about the causal nature of the relationship between alcohol use and cardiovascular outcomes. The answer to the question, ‘Are the cardiac effects of alcohol good, bad, or neither?’ remains elusive because our best scientific tool to address this question—the randomized, controlled trial—has not been successfully implemented. While some cite ethical reasons for the paucity of randomized data, a larger barrier to the conduct of a trial randomizing adults to low-moderate alcohol use vs. abstinence is one of practicality. Funding such a trial would be challenging, a potentially prohibitively large sample size would be required, especially given anticipated cross-over rates, and masking is likely to be imperfect in the absence of a suitable placebo. Faced with the reality that we may never be able to answer the question posed in the title, a prudent approach would be to accept a low-moderate level of alcohol use in those without significant cardiomyopathy or cirrhosis. No matter how voluminous and consistent the observational evidence, it is not sufficient to justify recommending alcohol use for the prevention of adverse cardiovascular events. Conflict of interest: none declared. References are available as supplementary material at European Heart Journal online.

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