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 McGill study, published in 1994, concluded that reducing saturated fat in the diet to 8 percent of all 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 million 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 small 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 paradoxically 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 will actually 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 will 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 socially 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 killing 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 chronically overconsumes fat, and all of us have cholesterol levels that are unnaturally 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 wholly 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 will have little effect on a single individual—just as smoking sixteen or eighteen cigarettes a day instead of twenty will 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 compelling, but they come with four critically 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 controlled trials are necessary to determine which hypotheses are most likely true.

Second, as Rose observed, all public-health interventions come with potential risks, as well as benefits— unintended or unimagined side effects. Small or negligible risks to an individual will 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 called “unnatural factors” and restore “‘biological normality’—that is…the conditions to which presumably we are genetically 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 all 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 will 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 genetically 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 million 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 William 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 small game.” We only began consuming “substantial amounts of meat,” he explained, and thus substantial amounts of

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