Good Calories, Bad Calories

animal fat, twenty-five thousand years ago, when we developed the skills to hunt big game. If this was the case, then we could safely recommend, as Stamler did, that we eat a low-fat diet, and particularly low in saturated fats, because animal fats in any quantity were a relatively new addition to the diet and therefore unnatural.

This interpretation, shared by Rose, was established authoritatively in 1985, the year after the NIH Consensus Conference, when The New England Journal of Medicine published a quantitative analysis of hunter-gatherer diets by two investigators—Boyd Eaton, a physician with an amateur interest in anthropology, and Melvin Konner, an anthropologist who had recently earned his medical degree. Eaton and Konner analyzed the diets of hunter-gatherer populations that had survived into the twentieth century and concluded that we are, indeed, genetically adapted to eat diets of 20–25 percent fat, most of which would in the past have been unsaturated. Eaton and Konner’s article has since been invoked to support low-fat recommendations—in Diet and Health, for instance—as Rose’s argument suggests it should.

But Eaton and Konner “made a mistake,” as Eaton himself later said. This was only corrected in 2000, when Eaton, working now with John Speth and Loren Cordain, published a revised analysis of hunter-gatherer diets. This new analysis took into account, as Eaton and Konner’s hadn’t, the observation that hunter-gatherers consumed the entire carcass of an animal, not just the muscle meat, and preferentially consumed the fattest parts of the carcass—including organs, tongue, and marrow—and the fattest animals. Reversing the earlier conclusion, Eaton, Speth, and Cordain now suggested that Paleolithic diets were extremely high in protein (19–35 percent of calories), low in carbohydrates “by normal Western standards” (22–40 percent of energy), and comparable or higher in fat (28–58 percent of energy). Eaton and his new collaborators stated with certainty that those relatively modern foods that today constitute more than 60 percent of all calories in the typical American diet—cereal grains, dairy products, beverages, vegetable oils and dressings, and sugar and candy—“would have contributed virtually none of the energy in the typical hunter-gatherer diet.” This latest analysis makes it seem that what Rose and the public-health authorities considered biological normality in 1985—a relatively low-fat diet—would now have to be be considered abnormal.^*22

The third critical caveat of Rose’s logic is that it makes it effectively impossible to challenge the underlying science once it is invoked to defend a particular hypothesis, one that is said to benefit the public health. Policy and the public belief are often set early in a scientific controversy, when the subject is most newsworthy. But that’s when the evidence is by definition premature and the demand for clarification most urgent. As the evidence accumulates, it may cease to support the hypothesis, but altering the conventional wisdom by then can be exceedingly difficult. (The artificial sweetener saccharine is still widely considered unhealthy, despite being absolved of any carcinogenic activity in humans over twenty years ago.) Rose’s logic demonstrates why good science and public policy are often incompatible.

The fourth caveat is closely related. The philosophy of population-wide preventive medicine implies that the public health is not served by skepticism of the science or the reporting of contradictory evidence, both of which are essential to the process of science. A campaign to convince the public to embrace a public-health recommendation requires unconditional belief in the promised benefits. This was the motivation for creating the appearance of a consensus in the dietary-fat controversy and, as Arno Motulsky had told the Washington Post, for publishing the National Academy of Sciences Diet and Health report as well.

But if the underlying science is wrong—and that possibility is implied by the lack of a true consensus—then this tendency of public-health authorities to rationalize away all contradictory evidence will make it that much harder to get the science right. Once these authorities insist that a consensus exists, they no longer have motivation to pursue further research. Indeed, to fund further studies is to imply that there is still uncertainty. But the public’s best interest will be served only by the kind of skeptical inquiry and attention to negative evidence that are necessary to learn the truth. “If the public’s diet is going to be decided by popularity polls and with diminishing regard for the scientific evidence,” remarked Pete Ahrens in 1979, “I fear that future generations will be left in ignorance of the real merits, as well as the possible faults, in any given dietary regimen aimed at prevention of [coronary heart disease].”

Among the more conspicuous examples of the kind of scientific and social quagmire to which the logic of sick populations and preventive public health can lead is the proposition that dietary fat causes breast cancer. This possibility was suggested in 1976 in George McGovern’s “Diet and Killer Disease” hearings, and then was cited in Dietary Goals for the United States as one reason why Americans should eat a low-fat diet (30-percent fat calories) as opposed to a cholesterol-lowering diet, in which the total fat content itself doesn’t change. By 1982, the proposition that dietary fat causes cancer was considered so likely true that a National Academy of Sciences report entitled Diet, Nutrition, and Cancer not only recommended that Americans cut fat consumption to 30 percent, but noted that the evidence was sufficiently compelling that it “could be used to justify an even greater reduction.” In 1984, the American Cancer Society released its first cancer- fighting, low-fat-diet prescription, and then both The Surgeon General’s Report on Nutrition and Health and Diet and Health embraced the hypothesis.

The proposition had emerged originally from the same international comparisons that led to Keys’s fat/heart- disease hypothesis—in particular, low rates of breast cancer and low fat consumption in Japan compared with high breast-cancer rates and high fat consumption in the United States. Moreover, when Japanese women immigrate to the United States, their breast-cancer rates quickly rise and, by the second generation, are equal to those of other American ethnic groups. As fat consumption increased in Japan from the 1950s to the early 1970s, breast-cancer rates there increased. These associations were given substance by the observation, originally made in the 1940s, that adding fat to the diet of laboratory rats promotes the growth of tumors, a phenomenon known technically as fat-induced tumorigenesis.

Considerable evidence also argued against the hypothesis. As John Higginson, founding director of the International Agency for Research on Cancer, noted in 1979, the international comparisons were as contradictory as they were confirmatory. In urban Copenhagen, breast-cancer rates were four times higher than in rural Denmark, but fat consumption was 50 percent lower. Large-population studies in Framingham; Honolulu; Evans County, Georgia; Puerto Rico; and Malmo, Sweden, had all reported low cholesterol levels associated with higher cancer rates. Since low cholesterol is allegedly the product of low-fat diets, it was “difficult to reconcile” this evidence, as the Framingham investigators noted in 1981, with the hypothesis that high-fat diets cause cancer.

The publication of the National Academy of Sciences report Diet, Nutrition, and Cancer in 1982 prompted the National Cancer Institute and the NAS to make funding available to test the hypothesis. A critical test would come from the Nurses Health Study, led by the Harvard epidemiologist Walter Willett, which began tracking diet, lifestyle, and disease in nearly eighty-nine thousand nurses around the country in 1982. Such a prospective study is no substitute for a randomized clinical control trial, but it constitutes the best that observational epidemiology can do. Willett and his colleagues published his first report on fat and breast cancer in January 1987 in The New England Journal of Medicine. Over six hundred cases of breast cancer had appeared among the eighty-nine thousand nurses over the first four years of the study. If anything, the less fat the women confessed to eating, the more likely they were to get breast cancer. In a New York Times article reporting the results of the study, Peter Greenwald, director of the National Cancer Institute Division of Cancer Prevention, said that the Nurses Health Study was “a good study, but not the only one,” and so NCI would continue to recommend—despite what was then, by far, the best evidence available—that Americans eat less fat to prevent breast cancer. Eight months