Effect of alcohol on risk of coronary heart disease and stroke: causality, bias, or a bit of both?

Epidemiological studies of middle-aged populations generally find the relationship between alcohol intake and the risk of coronary heart disease (CHD) and stroke to be either U-or J-shaped. This review describes the extent that these relationships are likely to be causal, and the extent that they may be due to specific methodological weaknesses in epidemiological studies. The consistency in the vascular benefit associated with moderate drinking (compared with non-drinking) observed across different studies, together with the existence of credible biological pathways, strongly suggests that at least some of this benefit is real. However, because of biases introduced by: choice of reference categories; reverse causality bias; variations in alcohol intake over time; and confounding, some of it is likely to be an artefact. For heavy drinking, different study biases have the potential to act in opposing directions, and as such, the true effects of heavy drinking on vascular risk are uncertain. However, because of the known harmful effects of heavy drinking on non-vascular mortality, the problem is an academic one. Studies of the effects of alcohol consumption on health outcomes should recognise the methodological biases they are likely to face, and design, analyse and interpret their studies accordingly. While regular moderate alcohol consumption during middle-age probably does reduce vascular risk, care should be taken when making general recommendations about safe levels of alcohol intake. In particular, it is likely that any promotion of alcohol for health reasons would do substantially more harm than good.