The Man Who Ate Everything - Jeffrey Steingarten [84]
The antialcohol forces found it easy to challenge the earliest prospective studies, which typically failed to disentangle the effects of smoking, preexisting heart disease, diet, exercise habits, age, and gender from the effects of alcohol. What if moderate drinkers in America are also more health conscious than nondrinkers, take more exercise, eat less fat, or do not smoke? Most studies conducted after the mid-1970s made statistical adjustments for these baseline risk factors, and the correlation between moderate drinking and lower levels of coronary disease grew even stronger. This outcome should have been obvious from the start—if alcohol were not protective, drinkers would have more heart attacks than nondrinkers because drinkers also tend to smoke and to eat fat. So the neo-Prohibitionists were dealt a double blow: many evils that were once blamed on alcohol are, it was discovered, really connected with cigarette smoking.
In the mid-1980s, the antialcohol forces readied their final (one hopes) onslaught against the overwhelming weight of research. What if, they asked, people who never drink are unusual? What if some of the nondrinkers had quit drinking (or never started) for a good reason, such as a long family history of premature coronary disease or their own ill health? These unhealthy nondrinkers would drag down the odds for the entire population of nondrinkers and misleadingly make moderate drinkers look good.
For two or three years, the pro-alcohol camp was thrown into disarray. Some medical journals and newsletters—most already exceedingly uncomfortable with the notion that alcohol protects the heart—announced that the U-shaped curve was a myth. But soon enough, myth again became reality. The four largest prospective studies, all completed after 1987, were careful to separate unhealthy (or high-risk) former drinkers from the population of teetotalers, leaving healthy lifelong nondrinkers. And again, moderate drinkers had the fewest heart attacks. The U-shaped curve was intact.
The facts now seem airtight. The spiraling costs of American health care could be reduced by at least a few dollars a year if researchers no longer felt the need to investigate the issue. Then we could move on to the more interesting questions. Why does alcohol have this protective effect? Is wine better for you than spirits? And what should you do about it?
Remember a few years ago when we learned that cholesterol comes in two types, one good and one bad? HDLs, or high-density lipoproteins, are the good kind of cholesterol because they lift fatty deposits from the inner walls of your arteries, where they would otherwise cause you untold grief, and carry them to your liver for disposal. (LDLs, or low-density lipoproteins, are the bad kind because they deposit fat there in the first place.) In numerous studies, high levels of HDLs in the bloodstream have been associated with a reduced risk of coronary heart disease. Aerobic exercise increases your HDLs. There is general agreement that alcohol does, too.
But now we learn that HDLs come in at least three (and maybe more) types, or subfractions. The neo-Prohibitionists had been arguing for years that drinking increases only HDL type 3 in our bloodstreams, which performs none of the useful work on the arteries that HDL type 2 does. (The other HDLs are apparently irrelevant to this debate.) Now, to the good fortune of moderate drinkers, several recent studies have shown that alcohol raises the level of both HDL-2 and HDL-3—about 17 percent each. And, in any case, HDL-3 now seems far less lazy than people had once thought.
Just as HDLs were the trendy blood component of the 1980s, something called apolipoproteins will surely become the blood buzzword of the nineties. The latest research tentatively demonstrates that the level of certain apolipoproteins in your bloodstream predicts your chances of having a heart attack even more accurately than the HDLs do. Moderate drinkers can raise their glasses again: