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.
The Helsinki Study was a strange and imaginative experiment. The Finnish investigators used two mental hospitals for their trial, dubbed Hospital K (Kellokoski Hospital) and Hospital N (Nikkila Hospital). Between 1959 and 1965, the inmates at Hospital N were fed a special cholesterol-lowering diet,†9 and the inmates of K ate their usual fare; from 1965 to 1971, those in Hospital K ate the special diet and the Hospital N inmates ate the usual fare. The effect of this diet was measured on whoever happened to be in the hospitals during those periods; “in mental hospitals turnover is usually rather slow,” the Finnish investigators noted.
The diet seemed to reduce heart-disease deaths by half. More important to the acceptance of Keys’s hypothesis, the men in the hospitals lived a little longer on the cholesterol-lowering diet. (The women did not.)
Proponents of Keys’s hypothesis will still cite the Helsinki Study as among the definitive evidence that manipulating dietary fats prevents heart disease
The Minnesota Coronary Survey was, by far, the largest diet-heart trial carried out in the United States, yet it played no role in the evolution of the dietary-fat hypothesis. Indeed, the results of the study went unpublished for sixteen years, by which time the controversy had been publicly settled. The principal investigator on the trial was Ivan Frantz, Jr., who worked in Keys’s department at the University of Minnesota. Frantz retired in 1988 and published the results a year later in a journal called
The Minnesota trial began in November 1968 and included more than nine thousand men and women in six state mental hospitals and one nursing home. Half of the patients were served a typical American diet, and half a cholesterol-lowering diet that included egg substitutes, soft margarine, low-fat beef, and extra vegetables; it was low in saturated fat and dietary cholesterol and high in polyunsaturated fat. Because the patients were not confined to the various mental hospitals for the entire four and a half years of the study, the average subject ate the diet for only a little more than a year. Average cholesterol levels dropped by 15 percent. Men on the diet had a slightly lower rate of heart attacks, but the women had more. Overall, the cholesterol-lowering diet was associated with an increased rate of heart disease. Of the patients eating the diet, 269 died during the trial, compared with only 206 of those eating the normal hospital fare. When I asked Frantz in late 2003 why the study went unpublished for sixteen years, he said, “We were just disappointed in the way it came out.” Proponents of Keys’s hypothesis who considered the Helsinki Mental Hospital Study reason enough to propose a cholesterol-lowering diet for the entire nation, never cited the Minnesota Coronary Survey as a reason to do otherwise.
As I implied earlier, we can only know if a recommended intervention is a success in preventive medicine if it causes more good than harm, and that can be established only with randomized, controlled clinical trials. Moreover, it’s not sufficient to establish that the proposed intervention reduces the rate of only one disease—say, heart disease. We also have to establish that it doesn’t increase the incidence of other diseases, and that those prescribed the intervention stay healthier
This point cannot be unduly emphasized. An unfortunate lesson came in the summer of 2002, when physicians learned that the hormone-replacement therapy they had been prescribing to some six million postmenopausal women—either estrogen or a combination of estrogen and progestin—seemed to be doing more harm than good. The parallels to the dietary-fat controversy are worth pondering. Since 1942, when the FDA first approved hormone replacement therapy (HRT) for the treatment of hot flashes and night sweats, reams of observational studies comparing women who took hormone replacements with women who did not (just as dietary-fat studies compared populations that ate high-fat diets with populations that did not) reported that the therapy dramatically reduced the incidence of heart attacks. It was only in the 1990s that the National Institutes of Health launched a Women’s Health Initiative that included the first large-scale, double-blind, placebo-controlled trial of hormone-replacement therapy. Sixteen thousand healthy women were randomly assigned to take either hormone replacement or a
