The Alcohol Effect

A discussion of moderate drinking requires a working definition of “moderate.” Simple definitions of light, moderate or heavy are somewhat arbitrary, but a consensus in the medical literature puts the upper limit for moderate drinking at two standard-size drinks a day. Studies show that drinking above that level can be harmful to overall health, although sex, age and other factors lower and raise the boundary for individuals.

The main medical benefit of reasonable alcohol use seems to be a lowering of the risk for coronary heart disease (CHD), which results from the buildup of atherosclerosis (fatty plaque) in the arteries. Atherosclerosis restricts blood flow to the heart and can promote the formation of vessel-blocking clots. It can thereby cause angina (chest discomfort resulting from low oxygen levels in the heart muscles), heart attack (the death of heart tissue that occurs when a blood clot or narrowing of the arteries prevents blood from reaching the heart) and death, often without warning. The condition usually starts at a young age but takes decades to blossom into overt CHD. The most common form of heart disease in developed countries, CHD causes about 60 percent of deaths from cardiovascular ills and about 25 percent of all deaths in those nations.

Pathologists uncovered the first clues to the value of alcohol in the early 1900s, noting that the large arteries of people who died of alcoholic liver cirrhosis seemed remarkably “clean”—that is, free of atherosclerosis. One explanatory hypothesis assumed that alcohol was a nebulous solvent, essentially dissolving the buildup in the arteries; another explanation held that heavier drinkers died before their atherosclerosis had a chance to develop. Neither idea truly explained drinkers’ unblocked arteries, however.

A more telling hint emerged in the late 1960s, when Gary D. Friedman of the Kaiser Permanente Medical Center in Oakland, Calif., came up with a novel idea: use computers to unearth unknown predictors of heart attacks. The power of computing could first identify healthy people who had risk factors similar to heart attack victims. Such factors include cigarette smoking, high blood pressure, diabetes, elevated levels of low-density lipoprotein (LDL, or “bad”) cholesterol, low levels of high-density-lipoprotein (HDL, or “good”) cholesterol, male gender, and a family history of CHD. Friedman then searched for predictors of heart attacks by comparing the patients and the newly found controls in hundreds of ways—for example, their exercise and dietary habits and their respective levels of various blood compounds. The computers spit out a surprising discovery: abstinence from alcohol was associated with a higher 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 addition, 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 it was for someone who did not drink at all. New data about alcohol protecting against death from CHD are even more impressive. At a meeting of the American Heart Association last November, it was announced 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 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. Alcohol seems to have 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 probably 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. 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. 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.

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 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.

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.

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