Good Calories, Bad Calories

Finally, Himsworth had to deal with the reported absence of diabetes among the Inuit. He acknowledged that his hypothesis implied that the Inuit should have an extremely high incidence of diabetes, which they did not. (There were three reported cases of confirmed diabetes among a population of sixteen thousand Alaskan Eskimos in 1956.) Rather than suggest that the Inuit died too young to get diabetes—Ancel Keys used the early-death rationale a quarter-century later to explain away their reported freedom from heart disease and cancer—Himsworth suggested they did not actually eat high-fat diets, despite all reports to the contrary. He cited two journal articles. One, he wrote, implied that the Inuit on Baffin Island ate a diet of only 48 percent fat calories, not that much higher than the average Englishman. The other, from 1930, reported that the “fisherfolk” of Labrador and northern Newfoundland subsisted on a diet of 21 percent fat calories and 70 percent carbohydrates, which meant a diet only slightly higher in fat than those eaten in Southeast Asian countries. (Himsworth did both these authors a disservice by suggesting that they believed that the Eskimo diets were carbohydrate-rich rather than fat-rich. The former article noted that the Eskimo “in his natural state eats practically only flesh,” of which “in cold weather…one-third to one-half [by serving, not calories] may be taken as fat.” The “fisherfolk” discussed in the latter article were not Eskimos, as Himsworth assumed, but those “of English and Scotch descent.” Half of their daily calories came from white flour purchased at the local trading post, the author reported. Another quarter came from hard bread, rolled oats, molasses, and sugar.) “It would thus appear,” Himsworth concluded, “that the most efficient way to reduce the incidence of diabetes mellitus amongst individuals predisposed to develop this disease would be to encourage the consumption of a diet rich in carbohydrate and to discourage them from satisfying their appetite with other types of food.”

Once Joslin embraced Himsworth’s fat hypothesis, it became the conventional wisdom among diabetologists and the mainstream medical community in the United States. In the 1946 and 1959 editions of his textbook, Joslin allotted the suggestion that sugar and refined carbohydrates play a role in diabetes less than a page and a half. In the 1971 edition, edited by Joslin’s colleagues a decade after his death and renamed Joslin’s Diabetes Mellitus, the subject had vanished entirely.

Oddly, Himsworth himself acknowledged that his own hypothesis was difficult to defend. In a 1949 lecture to the British Royal College of Physicians, Himsworth described the “paradox” of his fat hypothesis: “Though the consumption of fat has no deleterious influence on [the ability to metabolize glucose], and fat diets actually reduce the susceptibility of animals to diabetogenic agents, the incidence of human diabetes is correlated with the amount of fat consumed.” Himsworth even suggested that dietary fat might not be the culprit after all, or that perhaps “other, more important, contingent variables” tracked with fat in the diet. He suggested that total calories played a role, because of the intimate association of diabetes and obesity, and because “in the individual diet, though not necessarily in national food statistics, fat and calories tend to change together.” He did not mention sugar, which tends to change together with fat in both national food statistics and individual diets.

Despite Joslin’s unconditional rejection of the hypothesis, investigators outside the United States continued to publish reports that implicated sugar specifically in the etiology of diabetes. In 1961, the Israeli diabetologist Aharon Cohen of Hadassah University reported that this was the best explanation for the pattern of diabetes seen in Jews who had immigrated to Israel from Yemen. In 1954, Cohen had spoken with Joslin, who had argued that diabetes was primarily caused by an inherited predisposition. Cohen, however, had spent the preceding years studying the dramatic differences in diabetes incidence among Native American tribes, and also treating diabetes among the refugees who had flooded into Israel with the end of World War II, and believed otherwise. As Cohen recalled the conversation, Joslin had effectively challenged him to test his belief by systematically examining the Israeli immigrant populations, and that’s what Cohen did. Over the next five years, Cohen and his collaborators examined fifteen thousand Israelis living in a belt from Jerusalem to Beersheba. He concentrated on Yemenite Jews, because he had two distinct, contrasting populations to work with. One had arrived in 1949, fifty-thousand strong, flown in a legendary yearlong airlift known as Operation Magic Carpet. The other had lived in Israel since the early 1930s. Cohen was “astonished” that he found only three cases of diabetes in his examinations of five thousand Yemenites who had come in 1949. The incidence of diabetes was nearly fifty times as great in the earlier arrivals, and comparable to other populations in Israel, New York, and elsewhere. Other studies had also demonstrated, as Cohen put it, “a significantly greater prevalence” of coronary heart disease, hypertension, and high cholesterol among the Yemenites who had been in Israel for a quarter-century or more.

Cohen and his collaborators interviewed the more recent immigrants about their diets, both in Israel and in Yemen. They concluded that sugar consumption was the one noteworthy difference that might explain the increased incidence of diabetes, and perhaps the coronary heart disease, hypertension, and high cholesterol, too. “The quantity of sugar used in the Yemen had been negligible,” Cohen wrote; “almost no sugar was consumed. In Israel there is a striking increase in sugar consumption, though little increase in total carbohydrates.”

In New Zealand, Ian Prior, a young cardiologist who would later become the nation’s most renowned epidemiologist, studied a population of five hundred Maoris living in an isolated valley of the North Island, thirty-five miles from the nearest town. Despite a physically active life—certainly by the standards of modern-day Europe or the United States—the Maoris, as Prior reported in 1964, had a remarkably high incidence of diabetes, heart disease, obesity, and gout. Sixty percent of the middle-aged women were overweight; over a third were obese. Sixteen percent had heart disease, and 11 percent had diabetes. Six percent of the men had diabetes. The staples of the Maori diet, Prior reported, were bread, flour, biscuits, breakfast cereals, sugar (over seventy pounds per person a year), and potatoes. There was also “beer, ice-cream, soft drinks, and sweets.” Tea was the common beverage, “taken with large amounts of sugar by the majority.”

In South Africa, George Campbell, who began his career as a general practitioner in Natal and then ran the diabetic clinic at the King Edward VIII Hospital in Durban, focused on a population of Indian immigrants living in the Natal region and on the local Zulu population. In the early 1950s, according to Campbell, his patients fell into two distinct categories of disease. The local whites suffered from diabetes, coronary thrombosis, hypertension, appendicitis, gall-bladder disease, and other diseases of civilization. The rural Zulus did not. In 1956, Campbell spent a year working at the Hospital of the University of Pennsylvania in Philadelphia and was “absolutely staggered by the difference in disease spectrum” between the black population in Philadelphia and the rural Zulus. Among the blacks of Philadelphia, he saw the same disorders that characterized his white patients in Durban.

After returning to South Africa, Campbell went to work at the King Edward VIII Hospital, which served exclusively the “non-white” population, and admitted some sixty thousand patients a year while administering to six hundred thousand outpatients. Once again, says Campbell, he was struck by the “remarkable difference in the spectrum of disease,” in this instance between the urbanized Zulus, who were appearing with the same spectrum of diseases he had seen among the blacks of Philadelphia, and what he called their “country cousins” who still lived in rural areas. The Natal Indian population became the primary subject of Campbell’s research when he realized that four out of every five of his diabetic patients came from that impoverished Indian community.

The ancestors of these Natal Indians had arrived in South Africa in the latter half of the nineteenth century to work as indentured laborers on the local sugar plantations. When Campbell began studying them in the late 1950s, over 70 percent lived below the poverty line, and many still worked for the sugar industry. Campbell and other researchers carried out half a dozen health surveys of this Natal Indian population. The incidence of diabetes among middle-aged men in some of the villages ran as high as 33 percent. It was nearly 60 percent among the ward patients and outpatients at the King Edward VIII Hospital. In ten years of operation, Campbell’s clinic treated sixty- two hundred Indian diabetics, out of a local Indian population of only 250,000. A “veritable explosion of diabetes is taking place in these people,” Campbell wrote, “in whom the incidence of the disease is now almost certainly the highest in the world.” Campbell contrasted this with the numbers in India itself, where the average incidence of diabetes across the entire country was approximately 1 percent. This disparity between the incidence of diabetes in India and the incidence among the Indians of Natal ruled out a genetic predisposition to diabetes as a meaningful