Good Calories, Bad Calories (45 page)

In April 1973, when the evils of dietary fat were stil widely considered hypothetical, the NIH epidemiologist Peter Bennett appeared before George McGovern’s Senate Select Committee on Nutrition and Human Needs to discuss diabetes and obesity on the Pima reservation. The simplest explanation for why half of al adult Pima were diabetic, said Bennett, was the amount of sugar consumed, which represented 20 percent of the calories in the Pima diet. “The only question that I would have,” Bennett had said, “is whether we can implicate sugar specifical y or whether the important factor is not calories in general, which in fact turns out to be real y excessive amounts of carbohydrates.” Bennett’s opinion was consistent with that of Henry Dobyns of the D’Arcy McNickle Center for the History of the American Indian, who is considered the foremost authority on Pima history. In 1989, Dobyns described obesity and diabetes in the tribe as being “to some extent a result of inadequate nutrition” and added that this inadequate nutrition had come about because “many of the poorer individuals subsist on a diet of potatoes, bread, and other starchy foods. Their traditional diet is beyond their reach, for they cannot catch fish in a dry riverbed and they cannot afford to buy much meat or many fresh fruits and vegetables.”

Studies of the Sioux of the South Dakota Crow Creek Reservation in the 1920s, Arizona Apaches in the late 1950s, North Carolina Cherokees in the early 1960s, and Oklahoma tribes in the 1970s al reported levels of obesity comparable to that in the United States today, but in populations living in extreme poverty. “Men are very fat, women are even fatter,” as the University of Oklahoma epidemiologist Kel y West said of the local tribes of the 1970s.

“Typical y, their lifetime maximum weight has been 185 percent of standard.”

The early study of the Sioux, by two investigators from the University of Chicago, is particularly interesting, because it was one of the few published studies of diet, health, and living conditions in such a population, and it appeared the same year that the U.S. Department of the Interior released the results of a lengthy investigation of Native American living conditions. “An overwhelming majority of the Indians are poor, even extremely poor,” the Interior Department reported, “living on lands from which a trained and experienced white man could scarcely wrest a reasonable living.” The University of Chicago report said most of the Sioux lived in one-or two-room shacks; 40 percent of the children lived in homes without toilet facilities; water had to be hauled from the river. Little milk was consumed, although canned milk was included in the government rations. Butter, green vegetables, and eggs were almost never eaten. No fruit was consumed.*70 Twenty-five to forty pounds of beef were issued per person as government rations each month, but this was “not an indication of the amount consumed by each person,” the report noted, “for the families who receive rations are not left alone to eat them. Issue day is visiting day for the families not on the ration rol , and often the visit lasts until the friends’ or relatives’ rations of meat are gone. The ration family, therefore, may be compel ed to live on bread and coffee for the remainder of the month.”

The staple of the Sioux diet on the reservation was “grease bread,” fried in fat and made from white flour, supplemented by oatmeal, potatoes, and beans, some squash and canned tomatoes, black coffee, canned milk, and sugar. “Almost two-thirds of the families, including 138 children, were receiving distinctly inadequate diets,” the report concluded. Fifteen families, with thirty-two children among them, “were living chiefly on bread and coffee.”

Nonetheless, 40 percent of the adult women, over 25 percent of the men, and 10 percent of the children “would be termed distinctly fat,” the University of Chicago investigators reported, whereas 20 percent of the women, 25 percent of the men, and a slightly greater percentage of the children were

“extremely thin.”

By the 1970s, when studies of obesity in populations began in earnest, the general attitude was that obesity was simply a fact of life in developed nations. “Even a brief visit to Czechoslovakia,” reported a Prague epidemiologist at the first International Conference on Obesity, in 1974, “would reveal that obesity is extremely common and that, as in other industrial countries, it is probably the most widespread form of malnutrition.”

The observation that this was also true in poor populations in nonindustrialized countries, that obesity frequently coexists side-by-side with malnutrition and undernutrition, shows up with surprising consistency. In a 1959 study of African Americans living in Charleston, South Carolina, nearly 30 percent of the adult women and 20 percent of the adult men were obese although living on family incomes of from $9 to $53 a week. In Chile in the early 1960s, a study of factory workers, most of whom were engaged in “heavy labor,” revealed that 30 percent were obese and 10 percent suffered from

“undernourishment.” Nearly half the women over forty-five were obese. In Trinidad, a team of nutritionists from the United States reported in 1966 that one-third of the women older than twenty-five were obese, and they achieved this condition eating fewer than two thousand calories a day—an amount lower than the United Nations’ Food and Agriculture Organization recommendation to avoid malnutrition. Only 21 percent of the calories in the diet came from fat, compared with 65 percent from carbohydrates.

In Jamaica, high rates of obesity, again among adult women in particular, were first reported in the early 1960s by a British Medical Research Council diabetes survey. By 1973, according to Rolf Richards of the University of the West Indies, Kingston, 10 percent of al Jamaican men and nearly two-thirds of the women were obese in a society in which “malnutrition in infancy and early childhood remains one of the most important disorders contributing to infant and childhood mortality.”

Similar observations were made in the South Pacific and throughout Africa. In Rarotonga in the South Pacific, for instance, in the mid-1960s, on a diet of only 25 percent fat, over 40 percent of the women were obese and 25 percent were “grossly obese.” Among Zulus living in Durban, South Africa, according to a 1960 report, 40 percent of adult females were obese. Women in their forties averaged 175 pounds. In a population of urban Bantu

“pensioners,” the mean weight of women over the age of sixty was reported in the mid-1960s to be 165 pounds. “Although dietary habits vary widely amongst the African countries, tribes and vil ages,” wrote B. K. Adadevoh from Nigeria’s University of Ibadan in 1974, “it is general y established that the African diet is rich in carbohydrates. Caloric intake for most is low and protein fal s short of the recommended al owance.”

It seems fair to assume that the lives of market women in West Africa in the 1960s or poor Jamaicans of the same era were nontoxic by any of the definitions that are commonly associated with the current obesity epidemic. The Sioux of the mid-1920s, or the Pima of the 1900s or 1950s, living on reservations and relying on government rations to survive, clearly lived in a state of poverty that most of us today would find almost unimaginable.

Obesity in Africa is not associated with prosperity. These photos from Nigeria, of market women and an obese eleven-year-old, date to the early 1970s.

So why were they fat? “It is difficult to explain the high frequency of obesity seen in a relatively impecunious society such as exists in the West Indies, when compared to the standard of living enjoyed in the more developed countries,” Rolf Richards wrote about Jamaica in the 1970s. “Malnutrition and subnutrition are common disorders in the first two years of life in these areas, and account for almost 25 per cent of al admissions to pediatric wards in Jamaica. Subnutrition continues in early childhood to the early teens. Obesity begins to manifest itself in the female population from the 25th year of life and reaches enormous proportions from 30 onwards.”

The question of what causes obesity in these impoverished populations has typical y been ignored by obesity researchers, other than to suggest that there is something unique about given groups of people that exacerbates the problem of obesity. The assumption, as The New Yorker writer Malcolm Gladwel wrote about the Pima in 1998, is that they are “different only in degree, not in kind.”

The idea of specific populations predisposed to obesity is encapsulated in a notion now known as the thrifty gene—technical y, the thrifty-genotype hypothesis—that is now commonly invoked to explain the existence of the obesity epidemic and why we might all gain weight easily during periods of prosperity but have such difficulty losing it. The idea, initial y proposed in 1962 by the University of Michigan geneticist James Neel, is that we are programmed by our genes to survive in the paleolithic hunter-gatherer era that encompassed the two mil ion years of human evolution before the adoption of agriculture—a mode of life stil lived by many isolated populations before extensive contact with Western societies. “Such genes would be advantageous under the conditions of unpredictably alternating feast and famine that characterized the traditional human lifestyle,” explained the UCLA anthropologist Jared Diamond in 2003, “but they would lead to obesity and diabetes in the modern world when the same individuals stop exercising, begin foraging for food only in supermarkets and consume three high-calorie meals day in, and day out.” In other words, the human body evolved to be what Kel y Brownel has cal ed an “exquisitely efficient calorie conservation machine.” And so, by this hypothesis, we suck up calories when they are abundant and store them as fat until they are cal ed upon in a time of need. “Your genes match nicely with a scarce food supply,” Brownel explains, “but not with modern living.” Such populations as the Pima and the descendants of African tribes, according to this logic, were until very recently stil trapped in this cycle of feast and famine and scarce food in general, and so their thrifty genes have yet to evolve to deal with times of continual plenty. The NIH

researchers who study the Pima, as Gladwel reported, “are trying to find these genes, on the theory that they may be the same genes that contribute to obesity in the rest of us.”

For the first few decades of its existence, this notion that we have evolved “thrifty mechanisms to defend energy stores during times of privation” was invariably referred to as a hypothesis. That qualification is now often dropped, but the thrifty gene remains only a hypothesis, and one that rests on many assumptions that seem unjustifiable.

James Neel initial y proposed the idea of a “thrifty genotype rendered detrimental by progress” to explain why diabetes was so prevalent in Western societies and yet apparently absent in primitive tribes, including the Yanomamo of the Brazilian rain forest, who were then the subject of Neel’s research.

Neel was addressing the diseases of civilization and the kind of observations that led Peter Cleave to propose his saccharine-disease hypothesis. (Neel was unaware of Cleave’s work at the time.) The enigma of Type 2 diabetes, Neel observed, is that it bestows significant evolutionary disadvantages upon anyone who has it. Diabetic women are more likely to die in childbirth and more likely to have stil births than healthy women; their children are more likely to be diabetic than those of healthy women. This implies that any genes that might predispose someone to become diabetic would evolve out of the population quickly, but this did not seem to have happened. One way to reconcile these observations is to imagine a scenario in which having a genetic predisposition to become diabetic is advantageous in some circumstances. (In a similar way, having the gene for sickle-cel anemia, normal y a disadvantage, provides protection against malaria, a major advantage in malarial areas, as Neel himself reported.) Since diabetic mothers are known to give birth to heavier children, Neel speculated that these diabetic genes bestowed an exceptional ability to use food efficiently, and thus an exceptional ability to convert calories into fat. Those with such thrifty genes, Neel explained, “might have, during a period of starvation, an extra pound of adipose reserve” that would keep them alive when those who failed to fatten easily would die of starvation. So it would be beneficial to have such genes in the event of famine or prolonged food deprivation, which Neel now assumed must have been the case throughout our