Good Calories, Bad Calories (22 page)

To defend his theory, Himsworth had to render irrelevant the conflicting evidence—the experience of isolated populations, for example, eating their traditional diets. “There appears to be unanimous agreement,” he wrote, “that the incidence of diabetes mel itus is very low in the lower social grades of coloured races resident in their native lands, but there is evidence that when these races are transplanted to westernized countries the diabetic mortality rate rapidly rises.” Himsworth’s interpretation was that the original diets of these populations were fat-poor and carbohydrate-rich and became higher in fat when these people moved into urban environments. Himsworth acknowledged that the Masai ate a diet that “contained the highest proportion of fat of any recorded diet” and did not appear to suffer from diabetes, but he considered this evidence “so scanty that no opinion can be expressed.”

Final y, 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 al 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 practical y 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, rol ed oats, molasses, and sugar.) “It would thus appear,” Himsworth concluded, “that the most efficient way to reduce the incidence of diabetes mel itus 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 al otted 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 col eagues 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 Col ege 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 actual y 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 al , 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 specifical y 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 I , and believed otherwise. As Cohen recal ed the conversation, Joslin had effectively chal enged him to test his belief by systematical y examining the Israeli immigrant populations, and that’s what Cohen did. Over the next five years, Cohen and his col aborators 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 col aborators 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 val ey of the North Island, thirty-five miles from the nearest town. Despite a physical y 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 Campbel , who began his career as a general practitioner in Natal and then ran the diabetic clinic at the King Edward VI I 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 Campbel , his patients fel into two distinct categories of disease. The local whites suffered from diabetes, coronary thrombosis, hypertension, appendicitis, gal -bladder disease, and other diseases of civilization. The rural Zulus did not. In 1956, Campbel 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, Campbel went to work at the King Edward VI I 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 Campbel , 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 cal ed their “country cousins” who stil lived in rural areas. The Natal Indian population became the primary subject of Campbel ’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 Campbel began studying them in the late 1950s, over 70 percent lived below the poverty line, and many stil worked for the sugar industry. Campbel 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 vil ages ran as high as 33 percent. It was nearly 60 percent among the ward patients and outpatients at the King Edward VI I Hospital. In ten years of operation, Campbel ’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,” Campbel wrote, “in whom the incidence of the disease is now almost certainly the highest in the world.” Campbel 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 explanation.

For the Natal Indians, working primarily in and around sugar plantations, Campbel considered sugar the obvious suspect for their diabetes. He reported that the per-capita consumption of sugar in India was around twelve pounds yearly, compared with nearly eighty pounds for these working-class Natal Indians. The fat content of the diet in Natal was also very low, which seemed to rule out fat as the culpable nutrient. Excessive calorie consumption couldn’t be to blame, according to Campbel , because some of these impoverished Natal Indians were living on as little as sixteen hundred calories a day—“a figure in many countries which would be regarded almost as a starvation wage”—and yet they “were enormously fat and suffered from undoubted diabetes proven by blood tests.”

Campbel also found the disparities in diabetes prevalence and sugar consumption between urban and rural Zulus to be tel ing. The urban Zulu population, as hospital records demonstrated, was beset by diabetes. But in “thousands” of physical examinations performed on rural Zulus, Campbel wrote, “no case of diabetes has ever been discovered in any of them.” Studies of a rural Zulu population in 1953 and an urban population in Durban in 1957, wrote Campbel , concluded that the former were eating six pounds of sugar a year each, compared with more than eighty pounds for the latter. The fat content of the diet in both populations was very low—less than 20 percent of the total calories—which again seemed to rule out fat as the culpable nutrient. By 1963, according to the South African Cane Growers Association, the urban Zulus were eating almost ninety pounds of sugar per person annual y, while the rural Zulus were eating forty pounds each (a sixfold increase in a decade).

“In the last few years sugar intake has risen drastical y in Natal,” wrote Campbel , “because of very efficient advertising and because sugar has obviously reached as high an addictive status in our non-White people as in the Whites…. Al [sugar]cane workers get a weekly ration of 1½ lb. Andit is estimated that they can augment this by chewing sugar cane to the extent of ½–1 lb. daily!”

These sugarcane cutters, in whom, as Campbel noted, “diabetes is virtual y absent,” turned out to be pivotal, in that later generations of diabetologists would cite them as compel ing evidence that diabetes was not caused by eating sugar. Campbel , however, believed it was the refining of the sugar, which al owed for its quick consumption and metabolism, that did the damage; chewing sugarcane resulted in a slow intake of sugar that he believed would be relatively benign. Moreover, cane cutters would cut and move by hand as much as seven tons of sugarcane each day, which required an extraordinary effort that suggested to Campbel —as it had to Frederick Al en a half-century before—that a physical y active lifestyle might ward off the danger of excessive sugar consumption, perhaps by burning the sugar as fuel to maintain the necessary “huge output of energy” before it could do its damage. “There are few occupations in the world,” Campbel wrote, “which entail such hard physical exertion as that involved in the cutting, moving, and stacking of sugar cane.”

Campbel also believed that diabetes required time to manifest itself. The cane cutters had been receiving their refined-sugar ration for only a decade at most. From his medical histories of the diabetic Zulus at his clinic, Campbel found what he cal ed a “remarkably constant period in years of exposure to town life” before rural Zulus who had moved permanently into Durban developed diabetes. “The peak ‘incubation period’ in 80 such diabetics,” he wrote, “lay between 18 and 22 years.” Thus, Campbel suggested that diabetes would appear in a population to any extent only after roughly two decades of excessive sugar consumption, just as lung cancer from cigarettes appears on average after two decades of smoking. He also suggested that, if international statistics were any indication, the kind of diabetes epidemic they were experiencing among Natal Indians—or, for that matter, most Westernized nations—required a consumption of sugar greater than seventy pounds per person each year.