Low Fat / Low Cholesterol Study

In the January 4, 1985, issue of Science, Gina Kolata covered the 47th consensus panel report from the National Institutes of Health (NIH), published some three weeks earlier. Since 1961, the American Heart Association had asked Americans to reduce their intake of saturated fats and cholesterol and recommended its “prudent diet” emphasizing fruits, vegetables, and vegetable oils. The NIH had been hesitant to take a firm position on the diet-heart hypothesis, according to Kolata, because the scientific literature focusing on the connection between dietary cholesterol and saturated fatty acids (SFA) on the one hand, and heart disease on the other, did “not show that lowering cholesterol makes a difference” (Kolata 1985).

In 1990, the NHLBI held yet another meeting on the problem of “significantly increased” death rates from cancer and other noncardiovascular causes for people with low cholesterol. The lower the cholesterol, the worse it looked for cancer deaths, and damningly, it looked especially bad for healthy men who were actively trying to reduce their cholesterol through diet or drugs. But there was no follow-up to these meetings, and the results did not change the enthusiasm for the “prudent diet.” The effects of low cholesterol are still not well understood.

When I mentioned all this to Stamler, he didn’t remember any part of this cancer-cholesterol debate. In this way, he is a microcosm of a larger phenomenon that allowed the diet-heart hypothesis to move forward: inconvenient results were consistently ignored; here again, “selection bias” was at work.

Abstract

Our understanding of coronary artery disease risk and the atherosclerotic process has changed greatly in recent years. For example, it is now known that angiographically apparent coronary artery plaque is not the major cause of myocardial infarction (MI). Rather, it is unstable, soft plaque that cannot be seen angiographically that is prone to rupture and result in infarction. Also important are changes in vascular reactivity resulting from diet. Cholesterol levels by themselves reveal little about a patient's coronary artery disease risk. Most infarctions occur in patients who have normal total cholesterol levels. At-risk patients can be identified using the ratio of total-to-high-density lipoprotein (HDL) cholesterol levels. The ratio of triglyceride to HDL cholesterol levels is also important. Simple steps to assess patients' risk in practice are outlined. Primary prevention trials demonstrate that coronary artery disease risk can be lowered dramatically with diet and drug therapy.