Dr. Goldstein's observation (stated in his letter in the preceding group of letters) that cholesterol screening is not the issue is exactly right. The American College of Physicians' "evidence-based" guidelines [1] are based on the premise that screening leads inexorably to excessive drug prescription. The guidelines, however, present no evidence to support this premise. That is because available evidence shows the opposite to be true. In the United States, drugs are prescribed for only 3% of persons who have high cholesterol levels but no clinical coronary heart disease. Of all of the cholesterol-lowering drugs prescribed for patients without coronary heart disease, moreover, only 0.5% are for patients younger than 35 years of age (National Heart, Blood, and Lung Institute. Unpublished data). In Canada, lipid-lowering drugs are prescribed for only 8% of patients at high risk for coronary heart disease [2]. In the United Kingdom, only 16% of persons with cholesterol level between 250 and 320 mg/dL receive drugs [3]. Clearly, screening does not automatically lead to drug prescription.

The objective of measuring cholesterol levels in young persons is not only to prevent the relatively rare catastrophic events that can occur in young adults but to enhance the dietary, exercise, and weight control habits that prevent more serious disease later in life. If we were to follow the logic of Haq and associates, we would recommend that blood pressure not be measured until middle age because cerebrovascular as well as coronary catastrophes are rare in young adults.

It is probably true that modification of other risk factors, including those related to poorly understood cultural differences, may affect coronary disease. Dr. Ravnskov, however, missed the point of my citation of the Japanese migratory studies. These studies show the major effect that diet has independent of genetics or culture, and they indicate the effect that dietary changes can have if the dietary changes are large enough. In these studies, serum cholesterol was directly related to dietary saturated fat and cholesterol intake [4]. The authors of the paper cited by Dr. Ravnskoy, moreover, do not dismiss diet as a risk factor for coronary disease in these populations. Rather, they conclude that the observed coronary heart disease gradient is not "completely explained by differences in dietary intake, serum cholesterol, blood pressure or smoking" and offer acculturation as an additional hypothesis [5]. Dr. Ravnskov's unwavering quest for the "anything-but-cholesterol hypothesis" is ultimately futile. The molecular, pathologic, genetic, and clinical evidence showing that diets high in animal fat and elevated levels of cholesterol-laden atherogenic lipoproteins cause atherosclerosis is simply over-whelming. Lowering levels of these lipoproteins, moreover, prevents, arrests, and reverses both atherosclerosis and its clinical sequelae.

The College's guidelines [1] are based on the false and "evidence-poor" premise that cholesterol screening has no benefits and leads inexorably to drug intervention. In contrast, the National Cholesterol Education Program guidelines are conservative, thorough, and based on a broad array of scientific evidence showing that cholesterol causes atherosclerosis and that lowering cholesterol levels prevents it. We need fell no more forests, Dr. Goldstein, to show that.