Commentary: Alcohol, coronary heart disease and public health: which evidence-based policy

In a comprehensive review of the evidence available in 1984, Marmot concluded that moderate alcohol intake was associated with decreased coronary heart disease (CHD) mortality while heavy drinking resulted in higher mortality compared to non-drinkers.1 The consistency of the findings across ecological, case-control and prospective studies and the availability of convincing data on plausible mechanisms suggested a cardioprotective effect of moderate alcohol consumption. However, Marmot warned that increased intake was not recommended in view of the social and medical consequences of an increase of alcohol consumption in the population. Epidemiological data published since this review support the original conclusions by Marmot and have provided further information to fine tune our understanding of the relation of alcohol to CHD and their relevance to policy. Large prospective cohort studies have provided further solid data since 1984. Cohorts among middle-aged or elderly people included, for example, 51 529 American male health professionals with information on alcohol consumption studied for 12 years,2 87 526 American female nurses followed for 4 years,3 276 802 men enrolled by the American Cancer Society followed for 12 years,4 490 000 American men and women from the American Cancer Study II followed for 9 years,5 123 840 American adults from a prepaid health plan followed for 8 years,6 12 321 British male doctors followed for 13 years,7 36 250 middle-aged French men followed 12–18 years8 or 13 285 Danish men and women followed for an average of 13.5 years.9 These and most other studies and reviews10–14 have consistently found that consumption of 1–6 drinks a day was associated with a 20–50% lower risk of CHD. (One 120–150 ml glass of wine, one 280–360 ml bottle/can of light beer or one 20–30 ml measure of spirit each typically correspond to one ‘unit’ or ‘drink’ and contain 10–17 ml alcohol or 8–15 g of alcohol). Moderate alcohol intake has also been associated with a 20–30% reduced risk of stroke and other cardiovascular diseases5,7 and a 20% reduced risk of sudden death.15 Consistency of results among various populations and analytical control for several potential confounders in many of these studies makes it very unlikely that the apparent inverse relation between alcohol intake and CHD results from selection biases or confounding factors. In particular, results were generally not substantially altered in analyses excluding people with illnesses or abnormal risk factor levels at baseline. This argues against the view that higher mortality in non-drinkers relates to the inclusion of sick people (including former drinkers) into the categories of non-drinkers.16 Although ethical and feasibility issues preclude the conduct of clinical trials of alcohol consumption, current epidemiological evidence supports, virtually irrefutably, that light-to-moderate drinking substantially reduces the risk of CHD.