The first and most highly publicized was the Anti-Coronary Club Trial, launched in the late 1950s by New York City Health Department Director Norman Jolliffe. The eleven hundred middle-aged members of Jolliffe’s Anti-Coronary Club were prescribed what he called the “prudent diet,” which included at least one ounce of polyunsaturated vegetable oil every day. The participants could eat poultry or fish anytime, but were limited to four meals a week containing beef, lamb, or pork. This made Jolliffe’s prudent diet a model for future health-conscious Americans. Corn-oil margarines, with a high ratio of polyunsaturated to saturated fat, replaced butter and hydrogenated margarines, which were high in saturated fats. In total, the prudent diet was barely 30 percent fat calories, and the proportion of polyunsaturated to saturated fat was four times greater than that of typical American diets. Overweight Anti-Coronary Club members were prescribed a sixteen-hundred-calorie diet that consisted of less than 20 percent fat. Jolliffe then recruited a control group to use as a comparison.
Jolliffe died in 1961, before the results were in. His colleagues, led by George Christakis, began reporting interim results a year later. “Diet Linked to Cut in Heart Attacks,” reported the
The actual data, however, were considerably less encouraging. Christakis and his colleagues reported in February 1966 that the diet protected against heart disease. Anti-Coronary Club members who remained on the prudent diet had only one-third the heart disease of the controls. The longer you stayed on the diet, the more you benefited, it was said. But in November 1966, just nine months later, the Anti-Coronary Club investigators published a second article, revealing that twenty-six members of the club had died during the trial, compared with only six of the men whose diet had not been prudent. Eight members of the club died from heart attacks, but none of the controls. This appeared “somewhat unusual,” Christakis and his colleagues acknowledged. They discussed the improvements in heart-disease risk factors (cholesterol, weight, and blood pressure decreased) and the significant reduction in debilitating illness “from new coronary heart disease,” but omitted further discussion of mortality.
This mortality problem was the bane of Keys’s dietary-fat hypothesis, bedeviling every trial that tried to assess the effects of a low-fat diet on
Thirty-one of the men eating Dayton’s experimental cholesterol-lowering diet, however, died of cancer, compared with only seventeen of the controls. The risk of death was effectively equal on the two diets. “Was it not possible,” Dayton asked, “that a diet high in unsaturated fat…might have noxious effects when consumed over a period of many years? Such diets are, after all, rarities among the self-selected diets of human population groups.” Because the cholesterol-lowering diet failed to increase longevity, he added, it could not provide a “final answer concerning dietary prevention of heart disease.”
If these trials had demonstrated that people actually lived longer on cholesterol-lowering diets, there would have been little controversy. But almost four decades later, only one trial, the Helsinki Mental Hospital Study, seemed to demonstrate such a benefit—albeit not from a low-fat diet but from a high-polyunsaturated, low-saturated-fat diet.