Various studies had missed the connection because they neglected to examine alcohol use as a behavior separate from smoking. We now know that because drinkers often also use cigarettes, the negative impact of smoking was masking the beneficial effect of alcohol. In 1974 my Kaiser Permanente colleagues Friedman and Abraham B. Siegelaub and I were the first, to our knowledge, to publish an examination of moderate drinking in the absence of smoking. We saw a clear connection between alcohol consumption and a decreased risk of heart attack.
Since then, dozens of investigations in men and women of several racial groups in various countries have correlated previous alcohol use with current health. These studies have firmly established that nondrinkers develop both fatal and nonfatal CHD more often than do light to moderate drinkers. In 2000 Giovanni Corrao of the University of Milan-Bicocca in Italy, Kari Poikolainen of the Järvenpää Addiction Hospital in Finland and their colleagues combined the results of 28 previously published investigations on the relation between alcohol intake and CHD. In this meta-analysis, they found that the risk of developing CHD went down as the amount of alcohol consumed daily went up from zero to 25 grams. At 25 grams--the amount of alcohol in about two standard drinks--an individual's risk of a major CHD event, either heart attack or death, was 20 percent lower than for someone who did not drink at all.
Recent data about alcohol protecting against death from CHD are even more impressive. At a meeting of the American Heart Association in November 2002 my Kaiser Permanente colleagues Friedman, Mary Anne Armstrong and Harald Kipp and I discussed an updated analysis of 128,934 patients who had checkups between 1978 and 1985, with 16,539 of them dying between 1978 and 1998. CHD was responsible for 3,001 of those deaths. We discovered that those who had one or two alcoholic drinks a day had a 32 percent lower risk of dying from CHD than abstainers did.
The possible mechanisms by which alcohol has such an apparently profound effect on cardiovascular health primarily involve cholesterol levels and blood clotting. Blood lipids, or fats, play a central role in CHD. Numerous studies show that moderate drinkers have 10 to 20 percent higher levels of heart-protecting HDL cholesterol. And people with higher HDL levels, also known to be increased by exercise and some medications, have a lower risk of CHD.
That lower risk stems from HDL's ability to usher LDL cholesterol back to the liver for recycling or elimination, among other effects. Less cholesterol then builds up in the walls of blood vessels, and so less atherosclerotic plaque forms. Alcohol has a greater influence on a different HDL subspecies (HDL3) than on the type increased by exercise (HDL2), although both types are protective. (The biochemical pathways in the liver that could account for alcohol's ability to raise HDL levels remain incompletely known; it is thought that alcohol affects liver enzymes involved in the production of HDL.) Three separate analyses aimed at determining specific contributions of alcohol all suggest that the higher HDL levels of drinkers are responsible for about half of the lowered CHD risk.
Alcohol may also disrupt the complex biochemical cascade behind blood clotting, which can cause heart attacks when it occurs inappropriately, such as over atherosclerotic regions in coronary arteries. Blood platelets, cellular components of clots, may become less "sticky" in the presence of alcohol and therefore less prone to clumping, although data on this question remain ambiguous. A 1984 study by Raffaele Landolfiand Manfred Steiner of Brown University's Memorial Hospital revealed that alcohol intake increases the level of prostacyclin, which interferes with clotting, relative to the level of thromboxane, which promotes clotting. Walter E. Laug of the University of Southern California Keck School of Medicine showed that alcohol raises levels of plasminogen activator, a clot-dissolving enzyme. Finally, several studies suggest that alcohol lowers levels of another promoter of blood clots, fibrinogen.