ALCOHOL AND CORONARY HEART-DISEASE - THE EVIDENCE FOR A PROTECTIVE EFFECT

There is a considerable body of evidence indicating that moderate alco hol intake is associated with a reduced incidence of, and mortality fr om, coronary heart disease (CHD). There is also substantial evidence t hat problem drinking (well beyond two drinks per day) is associated wi th increased cardiovascular mortality. However, the frequently reporte d harmful effect of alcohol abuse on CHD mortality rates could be a re sult of mislabeling as CHD conditions such as alcohol-induced dilated cardiomyopathy, dysrhythmias, and hypertensive cardiovascular disease. The combination of protective and harmful influences of alcohol consu mption results in a U-shaped mortality curve. A true protective effect of moderate intake of alcohol is likely, because of consistent findin gs in many large, well-conducted studies of diverse population samples and the apparent specificity of the protective effect for CHD and pos sibly atherosclerotic-thrombotic brain infarction. There are also biol ogically plausible mechanisms whereby the protection might be conferre d. Alcohol has been shown convincingly to raise HDL subfractions which have been found to be protective against CHD, and it may also provide protection by an antithrombotic effect. There is a suggestion that wi ne, and red wine in particular, may be more protective than other alco holic beverages. However, it is difficult to control adequately for co nfounding factors, since persons who prefer wine have been found to ha ve a more advantageous lifestyle, a better cardiovascular risk profile , are better educated, and smoke less. The evidence for a protective e ffect of moderate alcohol intake includes population studies of alcoho l and CHD mortality in 20 countries, case-control studies, prospective cohort studies, arteriographic studies, and animal experiments. Never theless, because there are no controlled trial data, it is possible th at some other factor may be responsible for the apparent protective ef fect of alcohol. The inclusion of former drinkers or sick individuals in the non-drinker category, and lack of control for cigarette smoking and other risk factors, have been excluded as reasons for higher CHD rates among individuals who do not consume alcohol. No alternative exp lanation for the protective effect has surfaced after two decades of i nvestigation of the alcohol-CHD relationship, yet, the penalties of he avy alcohol consumption are too large to ignore. Until we can be sure that advice that encourages the public to drink to avoid coronary hear t disease does not increase abuse, we must be cautious in making gener al recommendations.