data constituted only half the evidence at best, and the other half did not support the hypothesis. As a result, “two strikingly polar attitudes persist on this subject, with much talk from each and little listening between,” wrote Henry Blackburn, a protege of Keys at the University of Minnesota, in 1975.
Confusion reigned. “It must still be admitted that the diet-heart relation is an unproved hypothesis that needs much more investigation,” Thomas Dawber, the Boston University physician who founded the famous Framingham Heart Study, wrote in 1978. Two years later, however, he insisted the Framingham Study had provided “overwhelming evidence” that Keys’s hypothesis was correct. “Yet,” he noted, “many physicians and investigators of considerable renown still doubt the validity of the fat hypothesis…. Some even question the relationship of blood cholesterol level to disease.”
Understanding this difference of opinion is crucial to understanding why we all came to believe that dietary fat, or at least saturated fat, causes heart disease. How could a proposition that incited such contention for the first twenty years of its existence become so quickly established as dogma? If two decades’ worth of research was unable to convince half the investigators involved in this controversy of the validity of the dietary-fat/cholesterol hypothesis of heart disease, why did it convince the other half that they were absolutely right?
One answer to this question is that the two sides of the controversy operated with antithetical philosophies. Those skeptical of Keys’s hypothesis tended to take a rigorously scientific attitude. They believed that reliable knowledge about the causes of heart disease could be gained only by meticulous experiments and relentlessly critical assessments of the evidence. Since this was a public-health issue, and any conclusions would have a very real impact on human lives, they believed that living by this scientific philosophy was even more critical than it might be if they were engaged in a more abstract pursuit. And the issue of disease prevention entailed an unprecedented need for the highest standards of scientific rigor. Preventive medicine, as the Canadian epidemiologist David Sackett had observed, targets those of us who believe ourselves to be healthy, only to tell us how we must live in order to remain healthy. It rests on the presumption that any recommendation is based on the “highest level” of evidence that the proposed intervention will do more good than harm.
The proponents of Keys’s hypothesis agreed in principle, but felt they had an obligation to provide their patients with the latest medical wisdom. Though their patients might appear healthy at the moment, they could be inducing heart disease by the way they ate, which meant they should be treated as though they already had heart disease. So these doctors prescribed the diet that they believed was most likely to prevent it. They believed that withholding their medical wisdom from patients might be causing harm. Though Keys, Stamler, and like-minded physicians respected the philosophy of their skeptical peers, they considered it a luxury to wait for “final scientific proof.” Americans were dying from heart disease, so the physicians had to act, making leaps of faith in the process.
This optimistic philosophy was evident early in the controversy. In October 1961,
This is among the most remarkable aspects of the controversy. Keys and other proponents of his hypothesis would often admit that the benefits of cholesterol-lowering had not been established, but they would imply that it was only a matter of time until they were. “The absence of final, positive proof of a hypothesis is not evidence that the hypothesis is wrong,” Keys would say. This was undeniable—but irrelevant.
The press also played a critical role in shaping the evolution of the dietary-fat controversy by consistently siding with proponents of those who saw dietary fat as an unneccessary evil. These were the researchers who were offering specific, positive advice for the health-conscious reader—eat less fat, live longer. The more zealously stated, the better the copy. All the skeptics could say was that more research was necessary, which wasn’t particularly quotable. A positive feedback loop was created. The press’s favoring of articles that implied Keys’s hypothesis was right helped convince the public; their belief in turn would be used to argue that the time had come to advise cholesterol-lowering diets for everyone, thus further reinforcing the belief that this advice must be scientifically defensible.
Believing that your hypothesis
In 1957, Keys insisted that “each new research adds detail, reduces areas of uncertainty, and, so far, provides further reason to believe” his hypothesis. This is known technically as
Keys, Stamler, and their supporters based their belief on the compelling nature of the hypothesis supplemented
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