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.