Good Calories, Bad Calories

“Although dietary habits vary widely amongst the African countries, tribes and villages,” wrote B. K. Adadevoh from Nigeria’s University of Ibadan in 1974, “it is generally established that the African diet is rich in carbohydrates. Caloric intake for most is low and protein falls short of the recommended allowance.”

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 all 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 25^th year of life and reaches enormous proportions from 30 onwards.”

The question of what causes obesity in these impoverished populations has typically 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 Gladwell 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—technically, 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, initially 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 million years of human evolution before the adoption of agriculture—a mode of life still 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 Kelly Brownell has called 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 called upon in a time of need. “Your genes match nicely with a scarce food supply,” Brownell 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 still 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 Gladwell 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 initially 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 stillbirths 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-cell anemia, normally 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 evolutionary history. Those same genes would lead to obesity and diabetes in an environment in which food was plentiful.

“If the considerable frequency of the disease is of relatively long duration in the history of our species,” Neel had asked to begin his discussion, “how can this be accounted for in the face of the obvious and strong genetic selection against the condition? If, on the other hand, this frequency is a relatively recent phenomenon, what changes in the environment are responsible for the increase?”

The thrifty gene could be the answer only if diabetes was of long duration in the species—and there is no evidence of that. The disease seems to appear only after populations have access to sugar and other refined carbohydrates. In the Pima, diabetes appeared to be “a relatively recent phenomenon,” as Neel himself later noted. When Russell and Hrdlika discussed the health of the Pima in the early 1900s, they made no mention of diabetes, even while noting the presence of such “rare” diseases as lupus, epilepsy, and elephantiasis.^*71 As late as 1940, when Elliott Joslin reviewed the medical records of the hospitals and physicians in Arizona, he concluded that the prevalence of diabetes was no higher among the Pima and other local tribes than anywhere else in the United States. Only in the 1950s, in studies from the Bureau of Indian Affairs, was there compelling reason to believe that diabetes had become common. When Neel tested adolescent Yanomamo for the condition known as glucose intolerance, which might indicate a predisposition to diabetes, he found none, so had no reason to believe that diabetes existed before such isolated populations began eating Western foods. The same was true of an isolated tribe of Pima, discovered living in the Sierra Madre Mountains of northern Mexico. “The high frequency of [Type 2 diabetes] in reservation Amerindians,” Neel later explained, “must predominantly reflect lifestyle changes.”

By 1982, Neel had come to side with Peter Cleave in believing that the most likely explanation for the high rates of obesity and diabetes in populations like the Pima that had only recently become Westernized was their opportunity to “overindulge in high sugar content foods.”

This left open the question of what biological factors or genes might determine who got obese and diabetic and who didn’t in the presence of such foods, but it eliminated any reason to suggest that thrifty genes had ever bestowed some evolutionary advantage. “The data on which that (rather soft) hypothesis was based has now largely collapsed,” Neel observed. He now suggested that either a tendency for the pancreas to oversecrete insulin and so cause hyperinsulinemia, or a tendency toward insulin resistance, which in turn would result in