Good Calories, Bad Calories (26 page)

The final transformation of Cleave’s refined-carbohydrate hypothesis into Burkitt’s fiber hypothesis came primarily through the efforts of Burkitt’s col eague Hugh Trowel , who had spent thirty years as a missionary physician in Kenya and Uganda, beginning in 1929. This had been a time, as Trowel later explained, when scores of British doctors working for the colonial service and missionary hospitals in the Kenyan highlands had the unprecedented experience of watching the native population of “three mil ion men, women and children…emerge from pre-industrial life and undergo rapid westernization.” After Trowel retired to England in 1959, he published Non-infective Disease in Africa, which was the first rigorous attempt to draw together the entire body of medical literature on the spectrum of diseases afflicting the native population of Africa.*36 The Western diseases—a list almost identical to Cleave’s—were conspicuous by their absence.

Trowel ’s experiences in East Africa had left him with the characteristic awareness of the diseases-of-civilization phenomenon. When he arrived in Kenya in 1929, he said, he had noticed that the Kenyans were al as thin as “ancient Egyptians,” yet when he dined with the native tribes, they always left food at the end of the meal and fed it to their domestic animals, which suggested that their relative emaciation was not caused by food shortages or insufficient calories. During World War I , according to Trowel , a team of British nutritionists was dispatched to East Africa to figure out how to induce the Africans in the British Army to put on weight, since they would not or could not do it. “Hundreds of x-rays,” Trowel recal ed, “were taken of African intestines in an effort to solve the mystery that lay in the fact that everyone knew how to fatten a chicken for the pot, but no one knew how to make Africans…put on flesh and fat for battle. It remained a mystery.” Nonetheless, by the 1950s, fat Africans were a common sight, and in 1956 Trowel himself reported the first clinical diagnosis of coronary heart disease in a native East African—a Banting-esque high-court judge (five foot two and 208 pounds) who had lived in England and had been eating a Western diet for twenty years. In 1970, Trowel returned to East Africa and described what he saw as “an amazing spectacle: the towns were ful of obese Africans and there was a large diabetic clinic in every city. The twin diseases had been born about the same time and are now growing together.”

Burkitt and Trowel had been friends since the late 1940s, when Burkitt first arrived in Uganda. In 1970 the two began working together on Burkitt’s fiber hypothesis and a textbook on diseases of civilization, which Burkitt and Trowel now cal ed “Western diseases.”*37 To explain how obesity could be induced by the fiber deficiency of modern refined-carbohydrate foods, Trowel reasoned that the causal factor was an increased ratio of energy to nondigestible fiber in the Western diet. Ninety-three percent of the nutrients in a typical Western diet were available for use as energy, Trowel calculated, compared with only 88 or 89 percent of those in a typical primitive diet containing copious vegetables, fruits, and wholemeal bread. The lower figure, Trowel wrote, is “the figure that is the natural, inherited evolutionary figure.” Over the course of a few decades, he said, we would unknowingly eat 4

percent more calories than would be evolutionary appropriate and therefore gain weight. (Later investigators would build on this idea by adding that fibrous foods were bulky, and thus more fil ing, and they also took longer to chew and digest, which supposedly led to an inevitable decrease in calories consumed, at least per unit of time.) As for heart disease, Trowel accommodated Keys’s logic: if the relevant epidemiology suggested that a low-fat, high-carbohydrate diet protected against heart disease, then carbohydrates obviously protect against heart disease, with the critical caveat that those carbohydrates must contain “their ful complement of dietary fiber.” Those “partial y depleted” of fiber provide only “partial protection,” Trowel said; those ful y depleted, sugar and white flour, offer no protection.

More attention would have been paid to Cleave’s hypothesis, Trowel explained, had Cleave accepted the validity of Keys’s research and “not dismissed completely the role of saturated animal fats” in heart disease. (Burkitt later said as much, too.) Trowel didn’t make the same mistake. He accepted that diets rich in fat, especial y saturated fat, raise cholesterol levels in the blood and so raise heart-disease risk, but then noted that the epidemiological evidence also implicated a low consumption of starchy high-fiber foods. So both fat and the absence of fiber could be blamed. (As Cleave and Yudkin had pointed out, exactly the same evidence can be used to implicate sugar and refined carbohydrates.) Burkitt and Trowel cal ed their fiber hypothesis a “major modification” of Cleave’s ideas, but they never actual y addressed the reasons why Cleave had identified refined carbohydrates as the problem to begin with: How to explain the absence of these chronic diseases in cultures whose traditional diets contained predominantly fat and protein and little or no plant foods and thus little or no fiber—the Masai and the Samburu, the Native Americans of the Great Plains, the Inuit? And why did chronic diseases begin appearing in these populations only with the availability of Western diets, if they weren’t eating copious fiber prior to this nutrition transition? Trowel did suggest, as Keys had, that the experience of these populations might be irrelevant to the rest of the world. “Special ethnic groups like the Eskimos,” he wrote, “adapted many mil ennia ago to special diets, which in other groups, not adapted to these diets, might induce disease.” Trowel spent three decades in Kenya and Uganda administering to the Masai and other nomadic tribes, Burkitt had spent two decades there, and yet that was the extent of the discussion.

Unlike the reaction to Cleave’s hypothesis, which garnered little attention even after Cleave testified to McGovern’s Select Committee, the media pounced on the fiber hypothesis almost immediately. After Trowel published a pair of articles on fiber and heart disease in The American Journal of Clinical Nutrition in 1972, Robert Rodale, a national y syndicated columnist, wrote a series of articles on the research, touting fiber as the answer to heart disease and obesity. Rodale was president of Rodale Press and the Rodale Institute, both dedicated to furthering the cause of organic foods and chemical-and pesticide-free “regenerative” agriculture. Rodale saw Burkitt and Trowel ’s fiber hypothesis as validation of the wisdom of organic foods and the agrarian lifestyle. “The natural fiber in whole processed foods may be instrumental in keeping cholesterol levels low and preventing the onset of heart disease,” he wrote.

Burkitt and Alec Walker fol owed up Trowel ’s articles with an August 1974 review in The Journal of the American Medical Association discussing the causal chain from fiber to constipation and “changes in gastrointestinal behavior” to the entire spectrum of Western diseases. The Washington Post wrote up the JAMA article on the day of its release, cal ing fiber “the tonic for our time.” That December, Reader’s Digest published an article on Burkitt and the fiber hypothesis; a year later, the magazine claimed that sales of fiber-rich products had more than doubled since the article. The breakfast-cereal industry, led by Kel ogg and General Foods, immediately started pushing bran and fiber as inherent heart-healthy aspects of their products. In 1975, Burkitt and Trowel published a book, Refined Carbohydrate Foods and Disease.

Burkitt then spent the next decade lecturing on the dangers of fiber-poor diets. He would condemn modern diets equal y for their “catastrophic drop in starch,” for their high fat content—“We eat three times more fat than communities with a minimum prevalence of [Western] diseases,” he would say; “We must reduce our fat!”—and for their lack of fiber, which he considered “the biggest nutritional catastrophe in [the United Kingdom] in the past 100 years.”

Not everyone bought into it. For public-health authorities and health reporters, dietary fat and/or cholesterol continued to be the prime suspects in chronic disease, and dietary fat had already been linked through international comparisons to colon cancer, as wel as breast cancer. Burkitt recal ed memorable disputes with researchers in the United States who blamed colon cancer on dietary fat, but he insisted that the absence of fiber was responsible. Eventual y, they compromised. His opponents, said Burkitt, conceded “that the fact that fat happened to be causative…did not preclude the possibility that fiber might be protective.” Harvard nutritionist Jean Mayer also discounted the significance of fiber, after Burkitt, Walker, and Trowel ’s early papers sparked the “furor over fiber” in the United States. But then Mayer, too, saw the wisdom of compromise. The ideal diet, he noted, would minimize the risk of both heart disease and cancer. It would be low in fat, or at least low in saturated fat, and so would be low in meat and dairy products. And it would be high in fiber. “A good diet,” Mayer wrote, “high in fruits and vegetables and with a reasonable amount of undermil ed cereals—wil give al you need of useful fiber.” The assumption that it would lead to long life and good health, however, was based more on faith and intuition than on science.

Over the last quarter-century, Burkitt’s fiber hypothesis has become yet another example of Francis Bacon’s dictum of “wishful science”—there has been a steady accumulation of evidence refuting the notion that a fiber-deficient diet causes colon cancer, polyps, or diverticulitis, let alone any other disease of civilization. The pattern is precisely what would be expected of a hypothesis that simply isn’t true: the larger and more rigorous the trials set up to test it, the more consistently negative the evidence. Between 1994 and 2000, two observational studies—of forty-seven thousand male health professionals and the eighty-nine thousand women of the Nurses Health Study, both run out of the Harvard School of Public Health—and a half-dozen randomized control trials concluded that fiber consumption is unrelated to the risk of colon cancer, as is, apparently, the consumption of fruits and vegetables. The results of the forty-nine-thousand-women Dietary Modification Trial of the Women’s Health Initiative, published in 2006, confirmed that increasing the fiber in the diet (by eating more whole grains, fruits, and vegetables) had no beneficial effect on colon cancer, nor did it prevent heart disease or breast cancer or induce weight loss.

“Burkitt’s hypothesis got accepted pretty wel worldwide, quite quickly, but it has gradual y been disproved,” said Richard Dol , who had endorsed the hypothesis enthusiastical y in the mid-1970s. “It stil holds up in relation to constipation, but as far as a major factor in the common diseases of the developed world, no, fiber is not the answer. That’s pretty clear.”

As we have seen with other hypotheses, the belief that dietary fiber is an intrinsic part of any healthy diet has been kept alive by factors that have little to do with science: in particular, by Geoffrey Rose’s philosophy of preventive medicine—that if a medical hypothesis has a chance of being true and thus saving lives, it should be treated as if it is—and by the need to give the public some positive advice about how they might prevent or reduce the risk of cancer. This was immediately evident in a New England Journal of Medicine editorial that accompanied back-to-back April 2000 reports on two major trials—one on fourteen hundred subjects of the Phoenix [Arizona] Colon Cancer Prevention Physicians’ Network, and one $30 mil ion trial from the National Cancer Institute—both of which confirmed that fiber had no effect on colon cancer. The editorial was written by Tim Byers, a professor of preventive medicine at the University of Colorado, who said that the two trials had been short-term and focused only on the early stages of cancer. For this reason, they should not be interpreted as “evidence that a high-fiber cereal supplement or a low-fat high-fiber diet is not effective in protecting against the later stages of development of colorectal cancer.” Byers was wrong, in that the results certainly were evidence that a high-fiber diet would not protect against the later stages of colorectal cancer; they simply weren’t sufficient evidence for us to accept the conclusion wholeheartedly as true.

Burkitt’s hypothesis lived on, and it would continue to live, as the fat/ breast-cancer hypothesis continued to live on, in part because the original data that led to it remained unexplained: “Observational studies around the world,” wrote Byers, “continue to find that the risk of colorectal cancer is lower among populations with high intakes of fruits and vegetables and that the risk changes on adoption of a different diet, but we stil do not understand why.” It would always be possible to suggest, as Byers had, that the trials could have been done differently—for longer or shorter duration, on younger subjects or older subjects, with more, less, or maybe a different kind of dietary fiber—and that the results would have been more promising. The American Cancer Society and the National Cancer Institute continued to suggest that high-fiber diets, high in fruits and vegetables, might reduce the risk of colon cancer, on the basis that some evidence existed to support the hypothesis and so a prudent diet would stil include these ingredients.

The media would also contribute to keeping the fiber hypothesis alive, having first played a significant role in transforming Burkitt’s hypothesis into dogma without benefit of any meaningful long-term clinical trials. “Scientists have known for years that a diet rich in vegetables, fruits and fiber, and low in fat, can greatly reduce—or eliminate—the chances of developing colon cancer,” as a 1998 Washington Post article put it—four years after the Harvard analysis of forty-seven thousand male health professionals suggested it was not true.

Although the New York Times ran articles on the negative results from the Nurses Health Study (by Sheryl Gay Stolberg) and the Phoenix and NCI fiber trials (by Gina Kolata), neither was written by the two reporters who had fol owed the subject for decades and traditional y wrote about diet and health for the paper: Jane Brody, who wrote the Times personal-health column, and Marian Burros, who had begun endorsing the benefits of fiber as a Washington Post reporter in the 1970s and had joined the Times in 1981. Rather, Burros and Brody chose to respond to the negative news about Burkitt’s hypothesis by continuing to defend it with the fal back position that it stil might be true in other ways. “If preventing colon cancer was the only reason to eat fiber,”