Good Calories, Bad Calories

In 1972, Burkitt and Walker published an article in The Lancet supporting their theory and discussing their measurements of transit time and stool characteristics in twelve hundred human subjects. In rural areas, unaffected by industrialization, they reported, “diets containing the natural amount of fiber are eaten and result in large, soft stools that traverse the intestine rapidly. By contrast, the refined low-fiber foods of the economically-developed countries produce small firm stools which pass through the gut very slowly.” Thus, the relative constipation endemic in the developed world, they suggested, appeared to play a causative role in bowel- related disorders: appendicitis, diverticulitis, and both benign and malignant tumors of the colon and rectum, all of which showed the classic distribution of diseases of civilizations. “All these diseases are very closely associated epidemiologically,” Burkitt and Walker explained. “These diseases are still rare in developing countries and in rural Japan, where eating habits have changed but little, but they are all seen increasingly in Japanese who live in Hawaii and California and are increasing in Japan in those who have changed to a Western diet. In no country or region is one of these diseases common and the others rare save that appendicitis, which afflicts the young, appears about a generation before the other conditions.”

Within two years, Burkitt had extended his hypothesis from appendicitis, diverticulitis, and colon cancer to all chronic diseases of civilization. In the process, Cleave’s refined-carbohydrate hypothesis of saccharine diseases was transformed into Burkitt’s fiber hypothesis of Western diseases. This transformation of the causal agent of disease from the presence of carbohydrates to the absence of fiber may have been influenced by factors other than science—Burkitt’s close association with Harold Himsworth in particular. Himsworth had been secretary of the Medical Research Council when Burkitt was hired, and he had been publicly effusive about Burkitt’s contributions to modern medicine. It was Himsworth’s research that had been responsible for convincing diabetologists that sugar and other carbohydrates were not the cause of diabetes. Indeed, Cleave and Campbell had presented their saccharine-disease theory in the context of diabetes as a refutation of Himsworth’s scholarship as much as Joslin’s. That Burkitt would find Cleave’s general thesis compelling but the details unacceptable in light of Himsworth’s own work and beliefs is quite possible. Burkitt would often tell the story of how Himsworth had convinced him of the importance of paying attention to those factors that were absent in searching for the causative agents of disease. “Denis,” Burkitt recalled Himsworth telling him, “do you remember the story in Sherlock Holmes when Holmes said to Watson: ‘The whole clue, as I see it, to this case lies in the behavior of the dog.’ And Watson said: ‘But, sir, the dog did nothing at all.’ ‘That,’ said Holmes, ‘is the whole point.’ And it often is in medicine…. The clue can lie in what is not there rather than what is there.” In this case, fiber was not there. Burkitt also seemed motivated by the simple expediency of emphasizing the positive benefits of fiber rather than the negative effects of sugar and flour, which seemed like a hopeless cause. “[Sugar] is simply an integral part of the daily diet and emphatically is here to stay,” Burkitt’s collaborator Alec Walker said. Better to say Don’t Forget Fibre in Your Diet, which was the title of Burkitt’s 1979 diet book, than to say, Don’t eat sugar, flour, and white rice, and drink less beer.

The final transformation of Cleave’s refined-carbohydrate hypothesis into Burkitt’s fiber hypothesis came primarily through the efforts of Burkitt’s colleague Hugh Trowell, who had spent thirty years as a missionary physician in Kenya and Uganda, beginning in 1929. This had been a time, as Trowell 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 million men, women and children…emerge from pre-industrial life and undergo rapid westernization.” After Trowell 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.

Trowell’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 all 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 II, according to Trowell, 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,” Trowell recalled, “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 Trowell 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, Trowell returned to East Africa and described what he saw as “an amazing spectacle: the towns were full 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 Trowell 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 Trowell now called “Western diseases.”^*37 To explain how obesity could be induced by the fiber deficiency of modern refined-carbohydrate foods, Trowell 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, Trowell 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, Trowell 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 filling, 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, Trowell 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 full complement of dietary fiber.” Those “partially depleted” of fiber provide only “partial protection,” Trowell said; those fully depleted, sugar and white flour, offer no protection.

More attention would have been paid to Cleave’s hypothesis, Trowell 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.) Trowell didn’t make the same mistake. He accepted that diets rich in fat, especially 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 Trowell called their fiber hypothesis a “major modification” of Cleave’s ideas, but they never actually 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? Trowell 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 millennia ago to special diets, which in other groups, not adapted to these diets, might induce disease.” Trowell 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.