Good Calories, Bad Calories

The Masai nomads of Kenya in 1962 had blood-cholesterol levels among the lowest ever measured, despite living exclusively on milk, blood, and occasionally meat from the cattle they herded. Their high-cholesterol diets supplied nearly three thousand calories a day of mostly saturated fat. George Mann, an early director of the Framingham Heart Study, examined the Masai and concluded that these observations refuted Keys’s hypothesis. In response, Keys cited similar research on the Samburu and Rendille nomads of Kenya that he interpreted as supporting his hypothesis. Whereas the Samburu had low cholesterol—despite a typical diet of five to seven quarts of high-fat milk a day, and twenty-five to thirty-five hundred calories of fat—the Rendille had cholesterol values averaging 230 mg/dl, “fully as high as United States averages.” “It has been estimated,” Keys wrote, “that at the time of blood sampling the percentage of calories from fats may have been 20–25 percent of calories from fat for the Samburu and 35–40 percent for the Rendille. Such diets, consumed at a bare subsistence level, would be consistent with the serum cholesterol values achieved.” Keys, however, had no reason to assume that either the Samburu or the Rendille were living at a bare subsistence level. To explain away Mann’s research on the Masai, Keys then evoked more recent research suggesting that the Masai, living in nomadic isolation for thousands of years, must have somehow evolved a unique “feedback mechanism to suppress endogenous cholesterol synthesis.” This mechanism, Keys suggested, would bestow immunity on the Masai to the cholesterol-raising effects of fat.

To believe Keys’s explanation, we would have to ignore Mann’s further research reporting that the Masai indeed had extensive atherosclerosis, despite their low cholesterol, without suffering heart attacks or any other symptoms of coronary heart disease. And we’d have to ignore still more research reporting that when the Masai moved into nearby Nairobi and began eating traditional Western diets, their cholesterol rose considerably. By 1975, Keys had relegated the Masai, and even the Samburu and the Rendille, to the sidelines of the controversy: “The peculiarities of those primitive nomads have no relevance to diet-cholesterol-CHD [coronary heart disease] relationships in other populations,” he wrote.

Once having adopted firm convictions about the dangers of dietary fat based on his own limited research among small populations around the world, Keys repeatedly preached against the temptation to adopt any firm contrary convictions based on the many other studies of small populations that seemed to repudiate his hypothesis. “The data scarcely warrant any firm conclusion,” he would write about such contradictory evidence. When a 1964 article in JAMA, The Journal of the American Medical Association, for instance, reported that the mostly Italian population of Roseto, Pennsylvania, ate copious animal fat—eating prosciutto with an inch-thick rim of fat, and cooking with lard instead of olive oil—and yet had a “strikingly low” number of deaths from heart disease, Keys said it warranted “few conclusions and certainly cannot be accepted as evidence that calories and fats in the diet are not important.”

The Framingham Heart Study was an ideal example of this kind of selective thinking at work. The study was launched in 1950 under Thomas Dawber’s leadership to observe in a single community aspects of diet and lifestyle that might predispose its members to heart disease—risk factors of heart disease, as they would come to be called. The factory town of Framingham, Massachusetts, was chosen because it was what Dawber called a “reasonably typical” New England town. By 1952, fifty-one hundred Framingham residents had been recruited and subjected to comprehensive physicals, including, of course, cholesterol measurements. They were then re-examined every two years to see who got heart disease and who didn’t. High blood pressure, abnormal electrocardiograms, obesity, cigarette smoking, and genes (having close family with heart disease) were identified as factors that increased the risk of heart disease. In October 1961, Dawber announced that cholesterol was another one. The risk of heart disease for those Framingham men whose cholesterol had initially been over 260 mg/dl was five times greater than it was for men whose cholesterol had been under 200. This is considered one of the seminal discoveries in heart-disease research. It was touted as compelling evidence that Keys’s hypothesis was correct.