Overall, alcohol's anticlotting capacity is not as well established as its HDL effect, and some effects, such as platelet clumping, may be reversed by heavy or binge drinking. Nevertheless, anticlotting appears to have a role in the lower risk for heart attacks enjoyed by moderate drinkers. In addition, studies have shown a beneficial effect on CHD risk in people who have far fewer than two drinks a day--say, three or four drinks a week. Anticlotting could be a major factor in the protection accorded by alcohol in these small amounts, which seem insufficient to affect HDL levels greatly.
Although alcohol reduces heart disease risk mainly by raising HDL levels and reducing clotting, it probably acts in other ways as well. Moderate drinking may lessen CHD risk indirectly by decreasing the risk of type 2 (adult-onset) diabetes, which is a powerful predictor of CHD. This benefit appears to be related to enhanced insulin sensitivity, which promotes proper glucose usage. (Heavy drinking, however, has been connected to higher blood glucose levels, a marker for future diabetes.) Evidence is also growing that inflammation contributes to CHD, and alcohol's anti-CHD power may be related to an anti-inflammatory action on the endothelial tissue that lines blood vessels.
Before accepting alcohol's benefits, an epidemiologist attempts to locate hidden factors possibly at work. For instance, could lifelong abstainers differ from drinkers in psychological traits, dietary habits, physical exercise habits or other ways that might account for their higher CHD risk without the need to invoke the absence of alcohol? Were such traits to explain away alcohol's apparent protection, they would need to be present in both sexes, various countries and several racial groups. Considering that no such traits have been identified, the simpler and more plausible explanation is that light to moderate alcohol drinking does indeed enhance cardiovascular health.
In fact, the available evidence satisfies most standard epidemiological criteria for establishing a causal relation. The numerous studies examining light and moderate alcohol intake and health reach consistent conclusions. The prospective studies that exist have the correct temporal sequence--that is, individuals' habits of interest are identified, after which their health is monitored over the long term, and alcohol users have different health profiles than nondrinkers do. The positives associated with alcohol can be attributed to biologically plausible mechanisms. Alcohol offers specific enhancement of cardiovascular health, not general protection against all illness. And alcohol's effect can be identified independent of known "confounders," other alcohol-related factors that could be responsible for a subject's cardiovascular condition.
The 30 percent reduction in risk is, perhaps surprisingly to some, less convincing evidence than the arguments above, because a strong unknown confounder could still account for the connection. To take an extreme example, consider a hypothetical set of genes that confers on the possessor 60 percent less CHD risk and causes a strong predisposition toward liking moderate amounts of alcohol. The independent consequences of the genes could appear causally linked. In fact, however, no such confounder is known or likely.
Because heavy drinking is not more protective than lighter drinking, this absence of a clear dose-response relation is also a weakness. Nevertheless, the collected data make a strong case for the cardiac benefits of controlled drinking. I should note, however, that the kind of study considered to be the gold standard in human research--a prospective randomized blinded clinical trial--has not yet been done. Such a study might, for example, engage a large pool of nondrinkers, half of whom, chosen at random and without the knowledge of the researchers, would commence a moderate drinking regimen, while the other half remained abstainers. The two groups would be followed for years in a search for eventual differences in cardiovascular disease and heart-related deaths.