Good Calories, Bad Calories (15 page)

There is another way to interpret this statistical association between cholesterol, heart disease, and death. The association, as documented by Framingham, MRFIT, and other studies, only says that, the higher our cholesterol, the greater our risk of heart disease. It does not tel us whether the benefit from lowering cholesterol is shared by the entire population or only by a smal percentage. The latter is the implicit assumption of the above analysis. But what if the benefit of lowering cholesterol is indeed shared democratical y among al who do it? Perhaps we may al live longer by lowering our cholesterol. But how much longer?

Between 1987 and 1994, independent research groups from Harvard Medical School, the University of California, San Francisco, and McGil University in Montreal addressed the question of how much longer we might expect to live if no more than 30 percent of our calories came from fat, and no more than 10 percent from saturated fat, as recommended by the various government agencies. Al three assumed that cholesterol levels would drop accordingly, and that this low-fat diet would have no adverse effects, which was stil speculation rather than fact.

The Harvard study, led by Wil iam Taylor, concluded that men with a high risk of heart disease—such as smokers with high blood pressure—might gain one extra year of life by shunning saturated fat. Healthy nonsmokers, however, might expect to gain only three days to three months. “Although there are undoubtedly persons who would choose to participate in a lifelong regimen of dietary change to achieve results of this magnitude, we suspect that some might not,” the Harvard investigators noted.

The UCSF study, led by Warren Browner, was initiated and funded by the Surgeon General’s Office. This study concluded that cutting fat consumption in America would delay forty-two thousand deaths each year, but the average life expectancy would increase by only three to four months. To be precise, a man who might otherwise die at sixty-five could expect to live an extra month if he avoided saturated fat for his entire adult life. If he lived to be ninety, he could expect an extra four months.*20 The McGil study, published in 1994, concluded that reducing saturated fat in the diet to 8 percent of al calories would result in an average increase in life expectancy of four days to two months.

Browner reported his results to the Surgeon General’s Office, and only then submitted his article to JAMA. J. Michael McGinnis, the deputy assistant secretary for health, then wrote to JAMA trying to prevent publication of Browner’s article, or at least to convince the editors to run an accompanying editorial that would explain why Browner’s analysis should not be considered relevant to the benefits of eating less fat. “They would have liked it to come out the other way,” explained Marion Nestle, who had edited the Surgeon General’s Report on Diet and Health and had recruited Browner to do the analysis. This put Browner in the awkward position of protecting his work from his own funding agents. As he wrote McGinnis at the time, “I am sensitive to the needs of your office to put forward a consistent statement about what Americans should do, and to your dismay when a project that you have sponsored raises some questions about current policy. I am also concerned that the impacts of recommendations that apply to 240 mil ion Americans are clearly understood. This manuscript estimates the effects of one such recommendation—altering dietary fat intake to 30 percent of calories—based on the assumptions that underlie that recommendation. Shooting the messenger—or creating a smoke screen—does not change those estimates.” JAMA published Browner’s article—“What If Americans Ate Less Fat?”—without an accompanying editorial.

That cholesterol-lowering provides little benefit to the individual was not unknown to the authors of these expert reports. This rationale was elucidated in Diet and Health, which explained that the purpose of preventive medicine in public health was to achieve the greatest good by treating entire populations rather than individuals. In this case, that meant addressing the situation of the 85 or 90 percent of the population with normal or low cholesterol. Though the actual benefit to these individuals “might be smal or negligible,” as Diet and Health explained, “because these people represent the great majority of the population, the benefit for the total population is likely to be paradoxical y large.”

This strategy is credited to the British epidemiologist Geoffrey Rose, a longtime veteran of the dietary-fat controversy. “The mass approach is inherently the only ultimate answer to the problem of a mass disease,” Rose explained in 1981.

But, however much it may offer to the community as a whole, it offers little to each participating individual. When mass diphtheria immunization was introduced in Britain 40 years ago, even then roughly 600 children had to be immunized in order that one life would be saved—599 “wasted”

immunizations for the one that was effective…. This is the kind of ratio that one has to accept in mass preventive medicine. A measure applied to many wil actual y benefit few.

When it came to dietary fat and heart disease, according to Rose’s calculation, only one man in every fifty might expect to avoid a heart attack by virtue of avoiding saturated fat for his entire adult life: “Forty-nine out of fifty would eat differently every day for forty years and perhaps get nothing from it.”

And thus the dilemma: “People wil not be motivated to any great extent to take our advice because there is little in it for each of them, particularly in the short and medium term.”*21 The best way around this problem, Rose explained, is to create social pressure to change. Consider young women who diet, he suggested, “not for medical reasons but because thinness is social y acceptable and obesity is not.” So the task confronting public-health authorities is to create similar social pressure to induce “healthy behavior.” And to do that, the benefits—or the risks of “unhealthy” behavior—have to be made to seem dramatic. “The modern British diet is kil ing people in their thousands from heart attacks,” Rose told the BBC in 1984.

The assumption underpinning this public-health philosophy, as Rose explained in an influential 1985 International Journal of Epidemiology article entitled “Sick Individuals and Sick Populations,” is that the entire population chronical y overconsumes fat, and al of us have cholesterol levels that are unnatural y high. This is why attempts to uncover an association between fat consumption and cholesterol within a population like Framingham, Massachusetts, inevitably failed. Imagine, Rose suggested, if everyone smoked a pack of cigarettes every day. Any study trying to link cigarette smoking to lung cancer “would lead us to conclude that lung cancer was a genetic disease…since if everyone is exposed to the necessary agent, then the distribution of cases is whol y determined by individual susceptibility.” The only way to escape this misconception, as with dietary fat, cholesterol, and heart disease, is to study the “differences between populations or from changes within populations over time.” This “sick population” logic also explained why lowering cholesterol by 10 or 20 percent wil have little effect on a single individual—just as smoking sixteen or eighteen cigarettes a day instead of

twenty wil do little to reduce individual lung-cancer risk—but would significantly affect the burden of heart disease across the entire population, and so should be widely recommended.

The arguments on sick populations and preventive public health are compel ing, but they come with four critical y important caveats.

First, Rose’s logic does not differentiate between hypotheses. It would invariably be invoked to explain why studies failed to confirm Keys’s fat hypothesis, and would be considered extraneous when similar studies failed to generate evidence supporting competing hypotheses. It is precisely to avoid such subjective biases that randomized control ed trials are necessary to determine which hypotheses are most likely true.

Second, as Rose observed, al public-health interventions come with potential risks, as wel as benefits—unintended or unimagined side effects. Smal or negligible risks to an individual wil also add up and can lead to unacceptable harm to the population at large. As a result, the only acceptable measures of prevention are those that remove what Rose cal ed “unnatural factors” and restore “‘biological normality’—that is…the conditions to which presumably we are genetical y adapted.” “Such normalizing measures,” Rose explained, “may be presumed to be safe, and therefore we should be prepared to advocate them on the basis of a reasonable presumption of benefit.”

This facet of Rose’s argument effectively underpins al public-health recommendations that we eat low-fat or low-saturated-fat diets, despite the negligible benefits. It requires that we make assumptions about what is safe and what might cause harm, and what constitutes “biological normality” and

“unnatural factors.” The evidence for those assumptions wil always depend as much on the observers’ preconceptions and belief system as on any objective reality.

By defining “biological normality” as “the conditions to which presumably we are genetical y adapted,” Rose was saying that the healthiest diet is (presumably) the diet we evolved to eat. That is the diet we consumed prior to the invention of agriculture, during the two mil ion years of the Paleolithic era—99 percent of evolutionary history—when our ancestors were hunters and gatherers. “There has been no time for significant further genetic adaptation,” as the nutritionists Nevin Scrimshaw of MIT and Wil iam Dietz of the Centers for Disease Control noted in 1995. Any changes to this Paleolithic diet can be considered “unnatural factors,” and so cannot be prescribed as a public-health recommendation.

The Paleolithic era, however, is ancient history, which means our conception of the typical Paleolithic diet is wide open to interpretation and bias. In the 1960s, when Keys was struggling to have his fat hypothesis accepted, Stamler’s conception of the Paleolithic hunter-gatherer diet was mainly “nuts, fruits and vegetables, and smal game.” We only began consuming “substantial amounts of meat,” he explained, and thus substantial amounts of animal fat, twenty-five thousand years ago, when we developed the skil s 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, genetical y 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 preferential y 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 col aborators stated with certainty that those relatively modern foods that today constitute more than 60 percent of al calories in the typical American diet—cereal grains, dairy products, beverages, vegetable oils and dressings, and sugar and candy—“would have contributed virtual y 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 chal enge 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 stil 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.