“As measured here” encapsulates much of the challenge of scientific investigation, as well as the loophole that allowed the dietary-fat controversy to evolve into Henry Blackburn’s two strikingly polar attitudes. Perhaps the Framingham investigators failed to establish that dietary fat caused the high cholesterol levels seen in the local population because (1) some other factor was responsible or (2) the researchers could not measure either the diet or the cholesterol of the population, or both, with sufficient accuracy to establish the relationship.
As it turned out, however, the Framingham Study wasn’t the only one that failed to reveal any correlation between the fat consumed and either cholesterol levels or heart disease. This was the case in virtually every study in which diet, cholesterol, and heart disease were compared within a single population, be it in Framingham, Puerto Rico, Honolulu, Chicago, Tecumseh, Michigan, Evans County, Georgia, or Israel. Proponents of Keys’s theory insisted that the diets of these populations were too homogenous, and so everyone ate too much fat. The only way to show that fat was responsible, they argued, was to compare entirely different populations, those with high-fat diets and those with low-fat diets. This might have been true, but perhaps fat just wasn’t the relevant factor.
Ever since Sir Francis Bacon, in the early seventeenth century, scientists and philosophers of science have cautioned against the tendency to reject evidence that conflicts with our preconceptions, and to make assumptions about what assuredly would be true if only the appropriate measurements or experiments could be performed. The ultimate danger of this kind of selective interpretation, as I suggested earlier, is that a compelling body of evidence can be accumulated to support any hypothesis. The method of science, though, evolved to compel scientists to treat all evidence identically, including the evidence that conflicts with preconceptions, precisely for this reason. “The human understanding,” as Bacon observed, “still has this peculiar and perpetual fault of being more moved and excited by affirmatives than by negatives, whereas rightly and properly it ought to give equal weight to both.”
To Keys, Stamler, Dawber, and other proponents of the dietary-fat hypothesis, the positive evidence was all that mattered. The skeptics considered the positive evidence intriguing but were concerned about the negative evidence. If Keys’s hypothesis was incorrect, it was only the negative evidence that could direct investigators to the correct explanation. By the 1970s, it was as if the two sides had lived through two entirely different decades of research. They could not agree on the dietary-fat hypothesis; they could barely discuss it, as Henry Blackburn had noted, because they were seeing two dramatically different bodies of evidence.
Another revealing example of selection bias was the reanalysis of a study begun in 1957 on fifty-four hundred male employees of the Western Electric Company. The original investigators, led by the Chicago cardiologist Oglesby Paul, had given them extensive physical exams and come to what they called a “reasonable approximation of the truth” of what and how much each of these men ate. After four years, eighty-eight of the men had developed symptoms of coronary heart disease. Paul and his colleagues then compared heart disease rates among the 15 percent of the men who seemingly ate the most fatty food with the 15 percent who seemingly ate the least. “Worthy of comment,” they reported, “is the fact that of the 88 coronary cases, 14 have appeared in the high-fat intake group and 16 in the low-fat group.”
Two decades later, Jeremiah Stamler and his colleague Richard Shekelle from Rush–Presbyterian–St. Luke’s Medical Center in Chicago revisited Western Electric to see how these men had fared. They assessed the health of the employees, or the cause of death of those who had died, and then considered the diets each subject had reportedly consumed in the late 1950s. Those who had reportedly eaten large amounts of polyunsaturated fats, according to this new analysis, had slightly lower rates of coronary heart disease, but “the amount of saturated fatty acids in the diet was not significantly associated with the risk of death from [coronary heart disease],” they reported. This alone could be considered a refutation of Keys’s hypothesis.
But Stamler and Shekelle knew what result they should have obtained, or so they believed, and they interpreted the data in that light. Their logic is worth following. “Although most attempts to document the relation of dietary cholesterol, saturated fatty acids, and polyunsaturated fatty acids to serum cholesterol concentration in persons who are eating freely have been unsuccessful,” they explained, “positive results have been obtained in investigations besides the Western Electric Study.” They then listed four such studies: a new version of Keys’s study on Japanese men in Japan, Hawaii, and California; a study of men living for a year at a research station in Antarctica; a study of Tarahumara Indians in the Mexican highlands; and one of infants with a history of breast-feeding. To Stamler and Shekelle, these four studies provided sufficiently compelling support for Keys’s hypothesis that they could interpret their own ambiguous results in a similar vein. “If viewed in isolation,” they explained, “the conclusions that can be drawn from a single epidemiologic study are limited. Within the context of the total literature, however, the present observations support the conclusion that the [fat] composition of the diet affects the level of serum cholesterol and the long-term risk of death from [coronary heart disease, CHD] in middle-aged American men.”
The New England Journal of Medicine published Stamler’s analysis of the Western Electric findings in January 1981, and the press reported the results uncritically. “The new report,” stated the Washington Post, “strongly reinforces the view that a high-fat, high-cholesterol diet can clog arteries and cause heart disease.” Jane Brody of the New York Times quoted Shekelle saying, “The message of these findings is that it is prudent to decrease the amount of saturated fats and cholesterol in your diet.” The Western Electric reanalysis was then cited in a 1990 joint report by the American Heart Association and the National Heart, Lung, and Blood Institute, entitled “The Cholesterol Facts,” as one of seven “epidemiologic studies showing the link between diet and CHD [that] have produced particularly impressive results” and “showing a correlation between saturated fatty acids and CHD,” which is precisely what it did not do.*7
In preventive medicine, benefits without risks are nonexistent. Any diet or lifestyle intervention can have harmful effects. Changing the composition of the fats we eat could have profound physiological effects throughout the body. Our brains, for instance, are 70 percent fat, mostly in the form of a substance known as myelin that insulates nerve cells and, for that matter, all nerve endings in the body. Fat is the primary component of all cell membranes. Changing the proportion of saturated to unsaturated fats in the diet, as proponents of Keys’s hypothesis recommended, might well change the composition of the fats in the cell membranes. This could alter the permeability of cell membranes, which determines how easily they transport, among other things, blood sugar, proteins, hormones, bacteria, viruses, and tumor-causing agents into and out of the cell. The relative saturation of these membrane fats could affect the aging of cells and the likelihood that blood cells will clot in vessels and cause heart attacks.