Good Calories, Bad Calories

Four of these studies tried to establish relationships between dietary fat and health within populations—in Honolulu, Puerto Rico, Chicago (Stamler and Shekelle’s second Western Electric study), and Framingham, Massachusetts. None of them succeeded. In Honolulu, the researchers followed seventy-three hundred men of Japanese descent and concluded that the men who developed heart disease seemed to eat slightly more fat and saturated fat than those who didn’t, but the men who died seemed to eat slightly less fat and slightly less saturated fat than those who didn’t. This observation was made in Framingham and Puerto Rico as well. In 1981, investigators from the three studies published an article in the journal Circulation discussing the problem. They said it posed a dilemma for dietary advice, but not an insurmountable one. The fact that the men in Puerto Rico and Honolulu who remained free of heart disease seemed to eat more starches suggested that it might be a good idea to recommend that we all eat more starch, as McGovern’s Dietary Goals actually had. And because the advice should never be to eat more calories, we would have to eat less fat to avoid gaining weight.

When one is reading this report, it’s hard to avoid the suspicion that once the government began advocating fat reduction in the American diet it changed the way many investigators in this science perceived their obligations. Those who believed that dietary fat caused heart disease had always preferentially interpreted their data in the light of that hypothesis. Now they no longer felt obliged to test any hypothesis, let alone Keys’s. Rather, they seemed to consider their obligation to be that of “reconciling [their] study findings with current programs of prevention,” which meant the now official government recommendations. Moreover, these studies were expensive, and one way to justify the expense was to generate evidence that supported the official advice to avoid fat. If the evidence didn’t support the recommendations, then the task was to interpret it so that it did.^*16

The other disconcerting aspect of these studies is that they suggested (with the notable exception of three Chicago studies reported by Jeremiah Stamler and colleagues) low cholesterol levels were associated with a higher risk of cancer. This link had originally been seen in Seymour Dayton’s VA Hospital trial in Los Angeles, and Dayton and others had suggested that polyunsaturated fats used to lower cholesterol might be the culprits. This was confirmed in 1972 by Swiss Red Cross researchers. In 1974, the principal investigators of six ongoing population studies—including Keys, Stamler, William Kannel of Framingham, and the British epidemiologist Geoffrey Rose—reported in The Lancet that the men who had developed colon cancer in their populations had “surprisingly” low levels of cholesterol, rather than the higher levels that they had initially expected. In 1978, a team of British, Hungarian, and Czech researchers reported similar findings from a sixteen-thousand-man clinical trial of a cholesterol-lowering drug. By 1980, this link between cancer and low cholesterol was appearing in study after study. The most consistent association was between colon cancer and low cholesterol in men. In the Framingham Study those men whose total cholesterol levels were below 190 mg/dl were more than three times as likely to get colon cancer as those men with cholesterol greater than 220; they were almost twice as likely to contract any kind of cancer than those with cholesterol over 280 mg/dl. This finding was met with “surprise and chagrin,” Manning Feinleib, a National Heart, Lung, and Blood Institute (NHLBI) epidemiologist, told Science.