Good Calories, Bad Calories (16 page)

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 wel .

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 al contradictory evidence wil 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 stil uncertainty. But the public’s best interest wil 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 pol s and with diminishing regard for the scientific evidence,” remarked Pete Ahrens in 1979, “I fear that future generations wil be left in ignorance of the real merits, as wel 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 Kil er 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 compel ing 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 original y 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, original y made in the 1940s, that adding fat to the diet of laboratory rats promotes the growth of tumors, a phenomenon known technical y 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 Malmö, Sweden, had al reported low cholesterol levels associated with higher cancer rates. Since low cholesterol is al egedly 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 Wil ett, 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. Wil ett and his col eagues 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 later, NCI researchers themselves published the results of a study similar to the Nurses Health Study but smal er, also suggesting that eating more fat and more saturated fat correlated with less breast cancer. The NCI study went virtual y unnoticed, as Science later noted, “perhaps because no one wanted to hear the message that a promising avenue of research was turning into a blind al ey, and perhaps because it swam against the ‘medical y political y correct’ idea that fat is bad.”

In 1992, Wil ett published the results from eight years of observation of the Nurses cohort. Fifteen hundred nurses had developed breast cancer, and, once again, those who ate less fat seemed to have more breast cancer. In 1999, the Harvard researchers published fourteen years of observations. By then almost three thousand nurses had contracted breast cancer, and the data stil suggested that eating fatty foods (even those with copious saturated fat) might protect against cancer. For every 5 percent of saturated-fat calories that replaced carbohydrates in the diet, the risk of breast cancer decreased by 9 percent. This certainly argued against the hypothesis that excessive fat consumption caused breast cancer.

Despite this accumulation of contradictory evidence, Peter Greenwald and the administrators at NCI refused to let their hypothesis die. This was Rose’s philosophy at work. After Wil ett’s publication of the first Nurses Health Study results, Greenwald and his NCI col eagues had responded with an article in JAMA entitled “The Dietary Fat–Breast Cancer Hypothesis Is Alive.” The NCI administrators argued that any study that generated evidence refuting the hypothesis could be flawed. The existence of any positive evidence, they argued, even if it came from admittedly rudimentary studies—in other words, studies that almost assuredly were flawed—was sufficient to keep such a critical hypothesis alive.

The only evidence that Greenwald and his col aborators considered “indisputable” was that laboratory rats fed “a high-fat, high-calorie diet have a substantial y higher incidence of mammary tumors than animals fed a low-fat, calorie-restricted diet.” In this they were right, but they did not rule out the possibility that it was the calories or whatever caused weight gain (what they implied by the adjective “high-calorie”) and not the dietary fat itself that was to blame, which was very likely the case. Even in 1982, when the authors of Diet, Nutrition, and Cancer had reviewed the animal evidence for fat-induced tumor growth, it had been less than indisputable. Adding fat to the diets of lab rats certainly induced tumors or enhanced their growth, but the most effective fats by far at this carcinogenesis process were polyunsaturated fats—saturated fats had little effect unless “supplemented with” polyunsaturated fats. This raised questions about the applicability of these observations to Western diets, which were traditional y low in polyunsaturated fats, at least until the 1960s, when the AHA started advocating polyunsaturated fats as a tool to lower cholesterol. Adding fat to rat chow also caused the rodents to gain weight, which was among the foremost reasons why obesity researchers came to believe that dietary fat caused human obesity. But it was hard to determine in these experiments whether it was the fat or the weight gain itself that led to increased tumor growth.

This laboratory evidence that dietary fat caused breast cancer began to evaporate as soon as Diet, Nutrition, and Cancer was published, and researchers could get funding to study it. By 1984, David Kritchevsky, one of the authors of Diet, Nutrition, and Cancer, had published an article in Cancer Research reporting on experiments that had been explicitly designed to separate out the effects of fat and calories on cancer, at least in rats. As Kritchevsky reported, low-fat, high-calorie diets led to more tumors than high-fat, low-calorie diets, and tumor production was shut down entirely in underfed rats, regardless of how fatty their diet was. Kritchevsky later reported that if rats were given only 75 percent of their typical daily calorie requirements, they could eat five times as much fat as usual and stil develop fewer tumors. Mike Pariza of the University of Wisconsin had published similar results in 1986 in the Journal of the National Cancer Institute. “If you restrict calories just a little bit,” Pariza later said, “you completely wipe out this so-cal ed fat enhancement of cancer.” This observation has been confirmed repeatedly. Demetrius Albanes of the National Cancer Institute later described the data as “overwhelmingly striking.” And he added: “Those data have very largely been ignored and strongly downplayed.”

By 1997 when the World Cancer Research Fund and American Institute for Cancer Research released a seven-hundred-page report titled Food, Nutrition and the Prevention of Cancer, the assembled experts could find neither “convincing” nor even “probable” reason to believe that fat-rich diets increased the risk of cancer. A decade later stil , Arthur Schatzkin, chief of the nutritional epidemiology branch at the National Cancer Institute, described the accumulated results from those trials designed to test the hypothesis as “largely nul .”

Nonetheless, the pervasive belief that eating fat causes breast cancer has persisted, partly because it once seemed undeniable. Purveyors of health advice just can’t seem to let go of the notion. When the American Cancer Society released its nutrition guidelines for cancer prevention in 2002, the document stil recommended that we “limit consumption of red meats, especial y those high in fat,” because of the same epidemiologic associations that had generated the fat-cancer hypothesis thirty years earlier. By 2006, with the next release of cancer-prevention guidelines by the American Cancer Society, the ACS was acknowledging that “there is little evidence that the total amount of fat consumed increases cancer risk.” But we were stil advised to eat less fat and particularly meats (“major contributors of total fat, saturated fat and cholesterol in the American diet”), because “diets high in fat tend to be high in calories and may contribute to obesity, which in turn is associated with increased risks of cancers.” (Saturated fats, in particular, the ACS

added, “may have an effect on increasing cancer risk,” a statement that seemed to be based solely on the belief that if saturated fat causes heart disease it probably causes cancer as wel .)

Belief in the hypothesis persists also because of the time lag involved in research of this nature. In 1991, the National Institutes of Health launched the $700 mil ion Women’s Health Initiative to test the hypothesis (and also the hypothesis that hormone-replacement therapy protects against heart disease and cancer). The WHI investigators enrol ed forty-nine thousand women, aged fifty to seventy-nine. They randomly assigned twenty-nine thousand to eat their usual diets, and twenty thousand were prescribed a low-fat diet. The goal was to induce these women to consume only 20 percent of their calories from fat; to do this, they were told to eat more vegetables and fresh fruits, as wel as whole grains, in case fiber was beneficial as wel . If the diet succeeded in preventing breast cancer, or any chronic disease, the WHI investigators wouldn’t know if it was because these women ate less fat or because they ate more fruits, vegetables, and grains. It’s conceivable that a diet of fruits, vegetables, grains, and more fat, or of vegetables and fruits but less grains, could be even more protective. The women on the diet also consumed fewer calories—averaging 120 calories a day less than the controls over the eight years of the study.*23 So, similarly, if this diet appeared to prevent cancer, the WHI investigators wouldn’t know whether it did so because it contained less fat (or more fruits and vegetables) or fewer calories. To induce those on the diet to stick to it for the better part of a decade, the WHI investigators provided them with an intensive nutritional and behavioral-education program. The women assigned to eat their usual diets received no such attention, which means they would be considerably less likely to change their lives in other ways that might also have an effect on breast cancer—to exercise or maintain their weight, stay away from sweets, refined flour, fast-food joints, and smoky bars. This disparity in counseling is known as an intervention effect, and it is precisely to avoid such an effect that drug trials must be done with placebos and double-blind.

Al of these effects would be expected to bias the trial in favor of observing a beneficial effect where none exists, but the WHI trial stil came up negative.

In the winter of 2006, the WHI investigators reported that those women who were eating what we today consider the essence of a healthy diet—little fat, lots of fiber, considerable fruits, vegetables, and whole grains, fewer calories—had no less breast cancer than those who ate their typical American fare.

(The women on the diet had no less heart disease, colon cancer, or stroke, either.) The results confirmed those of every study that had been done on diet and breast cancer since 1982. This, however, was stil not general y perceived as a definitive refutation of the hypothesis. Rose’s logic of preventive medicine held fast (it stil does). In a press release on the findings, NHLBI Director Elizabeth Nabel stated, “The results of this study do not change established recommendations on disease prevention.” In editorials that accompanied the WHI articles in JAMA, in virtual y every press report, and even in the World Health Organization’s official statement on the trial, it was said that this particular study may have failed to show a beneficial effect of a low-fat, high-fiber diet on breast cancer (and heart disease, stroke, colon cancer, and weight), but that was not a reason to disbelieve the hypotheses. (The WHO press release was entitled “The World Health Organization Notes the Women’s Health Initiative Diet Modification Trial, but Reaffirms That the Fat Content of Your Diet Does Matter.”) Rather than enumerate the ways the WHI trial was biased to find a positive relationship, which was one facet of the controversy in the early 1990s over whether the trial should be funded to begin with, the WHI investigators and those like-minded now enumerated al the reasons why the study might have failed to find an effect.