Seven Events That Made America America (18 page)

None of this concerned Ancel Keys, however. He had a powerful personality and an apparently novel argument, namely, that fats and meat were linked to cholesterol, and cholesterol to heart disease. His theory dated to a visit to Italy in 1951, where on the basis of noncontrolled (that is to say, unscientific) blood-serum measurements taken on a few hundred workers and Rotary Club members, he concluded that rich people had more heart disease simply because they ate more meat.
¹⁷
Even then, he had to admit, “Direct evidence on the effect of the diet on human arteriosclerosis is very little. . . .”
¹⁸
Over the next decade, Keys assembled his famous “six countries” study (later expanded to seven), claiming a consistent relationship between fat calories in the diet and heart disease. When other researchers examined his work, however, they found he had left out sixteen other countries, whose inclusion would disprove his hypothesis.
¹⁹
Similarly, in 1957 the American Heart Association sharply criticized Keys’s findings as “uncompromising stands based on evidence that does not stand up under critical examination,” and concluded that there wasn’t enough evidence to link food, especially fat, and heart disease.
²⁰
Only four years later, in 1961, the AHA made a U-turn, directed by a six-man committee including Keys and his chief supporter, Jeremiah Stamler, by issuing a report that contained only half a page of “recent scientific references,” many of which actually contradicted the 1957 report’s conclusions. The new AHA report cited the “best scientific evidence of the time” to link dietary fat and heart disease.
Time
quickly enshrined Keys as the heart guru of the age.

From 1961 to 1977, a tidal wave of research appeared on the causes of heart disease, diet, and cholesterol, yet none of it arrived at any clear conclusions. At best, two camps appeared—the Keys school, arguing that a high-fat diet led to heart disease, and a completely opposite school of thought comprising researchers who claimed that, in fact, fats and meat were not the problem, carbohydrates and insulin were. One protégé of Keys at Minnesota, Henry Blackburn, observed in 1975 that two “strikingly polar attitudes persist” while Thomas Dawber, who pioneered the Framingham Heart Study, flipped back and forth, admitting in 1978 that “the diet-heart relation is an unproved hypothesis,” then in 1980 insisting that the Framingham Heart Study proved the Keys hypothesis, before adding the caveat, “many physicians and investigators of considerable renown still doubt the validity of the fat hypothesis . . . [and] some even question the relationship of blood cholesterol level to disease.”
²¹
Research was showing fairly consistently that low-carbohydrate diets were optimal for losing weight, at which point the arguments usually shifted to the impact of high-fat diets on cholesterol, not weight.
²²

Despite the debate, the science was
never
settled. But there was a difference: the dietary-fat-equals-death group became utterly convinced of its certitude and acted like
activists
, while the other half of the researchers continued to act like
scientists
by suggesting nothing was proven on either side. Claude Bernard, in his
Introduction to the Study of Experimental Medicine
in 1865, warned that

Meyer Friedman, in 1969, labeled this tendency the “tyranny [of a] hypothesis once formulated,” noting that “to enthuse about one’s own theory or hypothesis is legitimate and even beneficial, but if presentation gives way to evangelistic fervor, emphasis to special pleading, and enthusiasm to bias, then progress is stopped dead.”
²⁴
Thomas Jefferson said it only slightly differently: “He who knows best knows how little he knows.”

Even as massive studies by the National Institutes of Health and the American Heart Association involving fifty thousand test subjects were being prepared in 1961—studies that would provide abundant evidence when the conclusions came in—the AHA was already preparing booklets emphasizing the importance of lowering cholesterol. Some of the researchers were already spinning the results in favor of the Keys hypothesis before the study was even under way. It made good press to say that fat caused heart disease, reinforcing the “truth” of the original hypothesis. Albert Einstein had categorically dismissed such an approach when, in 1919, two of his required three experiments proved his theory of relativity, saying only that until the “redshift” condition had been met, “the whole theory would have to be abandoned.”
²⁵
After the redshift was in fact confirmed empirically, philosopher Karl Popper remarked, “What impressed me most was Einstein’s own clear statement that he would regard his theory as untenable if it should fail in certain tests.”
²⁶
This was merely the theory of the universe, not a minor point about dietary fat—and yet Einstein was anything but dogmatic or proselytizing. Forty years later, not only did a large segment of heart researchers fail to wait for the results of a dietary /cholesterol version of a redshift, but there was no acknowledgment that the absence of such data would matter anyway!

Data that didn’t fit the Keys hypothesis was arbitrarily dismissed. This included evidence of Japanese men in California who had low cholesterol levels and still had higher rates of heart disease than relatives living in Japan. As the insightful historian of the diet debate Gary Taubes noted:

Among the various subgroups that began to stand out as more studies were conducted, the Masai nomads of Kenya had incredibly low blood-cholesterol levels, despite an almost exclusively fat/meat/milk diet; and other African tribes disproved the Keys hypothesis, despite his claims that they supported his conclusions.
²⁸

Supposedly, the Framingham Heart Study would provide definitive answers. Begun in 1952 in Framingham, Massachusetts, with 5,100 volunteers who were subjected to regular physicals and blood work—then reexamined every two years—the study initially included cholesterol among its risk factors, but as the evidence unfolded and as the participants in the study aged, low cholesterol was more closely linked to heart problems than high cholesterol!
²⁹
More important still, the Framingham dietary research disproved Keys, yet it was not published with the rest of the Framingham data until researchers dug it out in the late 1960s and it was finally included in the twenty-fourth volume of the study released in 1968. This data found no difference at all between the diets of high-cholesterol men and low-cholesterol men.
³⁰
In short, there was a significant amount of evidence that the fatcholesterol-heart disease links either did not exist or, in fact, were the opposite of what was being sold to the public by the American Heart Association and the government.

Over the next few years, studies examining the amount of fat consumed and correlating it with either cholesterol or heart disease proved remarkably
un
supportive of the Keys hypothesis. (Within particular populations in Puerto Rico, Honolulu, Chicago, Michigan, and Israel the results were the same, which is to say that there was no correlation.
³¹
) Then came the 5,400-strong Western Electric study in which, out of the 88 coronary cases, 14 were in the high-fat-intake group, 16 in the low-fat group. In 1977, researchers revisited the subjects and examined the cause of death, discovering that the “amount of saturated fatty acids in the diet was not significantly associated with the risk” of heart disease, and found no significant association of fatty acids in the diet with coronary disease.
³²
Despite a serpentine rationalization, the authors admitted that “most attempts to document the relation of dietary cholesterol, saturated fatty acids, and polyunsaturated fatty acids to serum cholesterol concentration . . . have been unsuccessful.”
³³

What followed is a case study in how data can be manipulated, regurgitated uncritically by the press, and turned into public policy. The update of the Western Electric study provided contrary evidence to the fat-heart disease hypothesis, so the authors of the study included four
other
studies whose evidence seemed to disprove their own results. Thus, they concluded that in fact a fatty diet affected serum cholesterol and long-term risk of death, and published this result in the
New England Journal of Medicine
in 1981. Jane Brody in
The New York Times
and
The Washington Post
slavishly reported these findings, which were then echoed in a report by the American Heart Association. To repeat: the Western Electric study did
not
show a correlation between risk of heart disease and a high-fat diet—it showed the opposite. Yet within four years after the publication of the study, virtually every major heart-related association had endorsed the false position.
³⁴

In fact, the only reliable method of arriving at medically and scientifically valid conclusions is to conduct double-blind, placebo-controlled clinical trials, and in fact, such trials are virtually impossible with food. Meat, butter, and cream, for example, have certain tastes that cannot be faked. Moreover, changing one aspect of a diet—fats—tends to change overall calories as well. Between 1950 and 1975, only about a dozen truly scientific trials of diet and heart disease were conducted. Only two of these actually examined low-fat diets and heart disease as opposed to cholesterol-lowering diets; and the two studies arrived at completely contradictory results.
³⁵
Or how about the New York Anti-Coronary Club, which examined 1,100 males beginning in the late 1950s? The researchers were so convinced that the fat/ heart disease link existed that as early as 1962 they leaked the interim results to
The New York Times
, which dutifully ran the headline “Diet Linked to Cut in Heart Attacks.”
³⁶
But there was a problem. The longer the study went, the more the data disproved the fat/heart disease link. In November 1966, another interim article appeared showing that 26 men on the low-fat diet had died, compared to only 6 on the high-fat diet. Seymour Dayton, in 1969, gave half of his test group a cholesterol-lowering diet and the other half a placebo: while only 66 of the lower-cholesterol group died from heart disease (compared to 96 in the placebo diet), the low-cholesterol group had higher death rates from cancer! A large study in Minnesota (the Minnesota Coronary Study) in 1968 found a cholesterol-lowering diet
increased
the risk of heart disease—but the results went unpublished for sixteen years, because, as one of the researchers said, “We were just disappointed in the way it came out.”
³⁷
In other words, the researchers were convinced that the science was “settled,” so their own results could not be valid.

Beneath the surface, those at the American Heart Association and the National Heart Institute knew there was a lack of support for their hypothesis in the data. In 1968, after six researchers had received large grants to confirm the fat/heart disease link, Pete Ahrens of Rockefeller University was tasked to examine the evidence of the studies. Even in 1968—six years after the AHA had already gone on record as touting the benefits of a low-fat diet—the report concluded, “it is not known whether dietary manipulation has any effect whatsoever on coronary heart disease.”
³⁸

At that point, the science—which was completely unsettled—became politicized by hysteria over population growth, exacerbated by the fear-mongering (and utterly wrong) book by Paul Ehrlich,
The Population Bomb
(1968). Concerns about growing worldwide population, along with the flawed notion that “not cleaning your plate” somehow caused “kids in China to starve,” allowed the antimeat activists to gain a foothold in policy making. This illogical association, used at countless dinner tables, took another turn when the diet radicals linked it to the production costs of meat as opposed to vegetables and fruits. Hence, the aforementioned Jean Mayer claimed in 1974 that the “enormous appetite for animal products” had caused more grain and soybeans to go into feeding cattle and hogs, “decreasing the amounts of food directly available for direct consumption by the poor.”
³⁹
In reality, it was the opposite: the more grain and soybeans that were needed for animals, the higher the demand, which meant the more likelihood farmers would grow even more—which they did. Such free-market logic didn’t faze Mayer, who concluded we needed “a shift in consumption in developed countries toward a ‘simplified’ diet containing less animal products, and, in particular, less meat.” (Though of course he failed to acknowledge that our predecessors ate a “simple” diet as well, but theirs was full of meat.) This view fit well with the new vegan movement, as argued in
Diet for a Small Planet
by Frances Moore Lappé.

One characteristic of all these works is the obsession with limits on resources, an economic zero-sum approach developed by Thomas Mun and the mercantilists, and proven wrong by two centuries’ worth of growing economies and vast new discoveries of resources. The buzzword was “small,” emphasizing the absence of a capacity for growth, only constant entropy to, presumably, a single pair of humans huddled around the last berry bush. Similarly,
Appetite for Change
by Warren James Belasco warned that shoppers in Indiana would affect food availability in India. The fact that the Left glommed on to the antifat/meat-kills mantra should not be surprising, nor should the notion that “Big Food” was somehow behind the fat-heavy shift in eating.