Good Calories, Bad Calories

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.