Papua New Guinea, urban Wanigela 37
Aboriginal Australians
traditional ~0
Westernized 25–35
Native Americans
Chile Mapuche 1
U.S. Pima 50
The numbers in the right-hand column are prevalences of diabetes in percent: i.e., the percent of the population suffering from Type-2 diabetes. These values are so-called age-standardized prevalences, which have the following meaning. Because Type-2 prevalence in a given population increases with age, it would be misleading to compare raw values of prevalence between two populations that differ in their age distributions: the raw values would be expected to differ merely as a result of the different age distributions (prevalence would be higher in the older population), even if prevalences at a given age were identical between the two populations. Hence one measures the prevalence in a population as a function of age, then calculates what the prevalence would be for that whole population if it had a certain standardized age distribution.
Note the higher prevalences in wealthy, Westernized, or urban populations than in poor, traditional, or rural populations of the same people. Note also that those lifestyle differences give rise to contrasting low-prevalence and high-prevalence (over 12%) populations in every human group examined except Western Europeans, among whom there is no high-prevalence population by world standards, for reasons to be discussed. The table also illustrates the rise and subsequent fall of prevalence on Nauru Island, caused by rapid Westernization and then by the operation of natural selection against victims of diabetes.
Buried within that national average prevalence of 8% is a wide range of outcomes for different groups of Indians. At the low extreme, prevalence is only 0.7% for non-obese, physically active, rural Indians. It reaches 11% for obese, sedentary, urban Indians and peaks at 20% in the Ernakulam district of southwest India’s Kerala state, one of the most urbanized states. An even higher value is the world’s second-highest national prevalence of diabetes, 24%, on the Indian Ocean island of Mauritius, where a predominantly Indian immigrant community has been approaching Western living standards faster than any population within India itself.
Among the lifestyle factors predictive of diabetes in India, some are also familiar as predictors in the West, while other factors turn Western expectations upside down. Just as in the West, diabetes in India is associated with obesity, high blood pressure, and sedentariness. But European and American diabetologists will be astonished to learn that diabetes’ prevalence is higher among affluent, educated, urban Indians than among poor, uneducated, rural people: exactly the opposite of trends in the West, although similar to trends noted in other developing countries including China, Bangladesh, and Malaysia. For instance, Indian diabetes patients are more likely to have received graduate and higher education, and are less likely to be illiterate, than non-diabetics. In 2004 the prevalence of diabetes averaged 16% in urban India and only 3% in rural India; that’s the reverse of Western trends. The likely explanation for these paradoxes invokes two respects in which the Western lifestyle has spread further through the population and been practised for more years in the West than in India. First, Western societies are much wealthier than Indian society, so poor rural people are much better able to afford fast foods inclining their consumers towards diabetes in the West than in India. Second, educated Westerners with access to fast foods and sedentary jobs have by now often heard that fast foods are unhealthy and that one should exercise, whereas that advice has not yet made wide inroads among educated Indians. Nearly 25% of Indian city-dwellers (the subpopulation most at risk) haven’t even heard of diabetes.
In India as in the West, diabetes is due ultimately to chronically high blood glucose levels, and some of the clinical consequences are similar. But in other respects—whether because lifestyle factors or people’s genes differ between India and the West—diabetes in India differs from the disease as we know it in the West. While Westerners think of Type-2 diabetes as an adult-onset disease appearing especially over the age of 50, Indian diabetics exhibit symptoms at an age one or two decades younger than do Europeans, and that age of onset in India (as in many other populations as well) has been shifting towards ever-younger people even within the last decade. Already among Indians in their late teens, “adult-onset” (Type-2 or non-insulin-dependent) diabetes manifests itself more often than does “juvenile-onset” (Type-1 or insulin-dependent) diabetes. While obesity is a risk factor for diabetes both in India and in the West, diabetes appears at a lower threshold value of obesity in India and in other Asian countries. Symptoms also differ between Indian and Western diabetes patients: Indians are less likely to develop blindness and kidney disease, but are much more likely to suffer coronary artery disease at a relatively young age.
Although poor Indians are currently at lower risk than are affluent Indians, the rapid spread of fast food exposes even urban slum-dwellers in India’s capital city of New Delhi to the risk of diabetes. Dr. S. Sandeep, Mr. A. Ganesan, and Professor Mohan of the Madras Diabetes Research Foundation summarized the current situation as follows: “This suggests that diabetes [in India] is no longer a disease of the affluent or a rich man’s disease. It is becoming a problem even among the middle income and poorer sections of the society. Studies have shown that poor diabetic subjects are more prone to complications as they have less access to quality healthcare.”
Benefits of genes for diabetes
The evidence for a strong genetic component to diabetes poses an evolutionary puzzle. Why is such a debilitating disease so common among so many human populations, when one might have expected the disease to disappear gradually as those people genetically susceptible to it were removed by natural selection and didn’t produce children carrying their genes?
Two explanations applicable to some other genetic diseases—recurrent mutations and lack of selective consequences—can quickly be eliminated in the case of diabetes. First, if prevalences of diabetes were as low as those of muscular dystrophy (about 1 in 10,000), the genes’ prevalence could be explained as nothing more than the product of recurring mutations: that is, babies with a new mutation being born at the same rate as older bearers of such mutations die of the disease. However, no mutation occurs so frequently as to appear anew in 3% to 50% of all babies, the actual frequency range for diabetes in Westernized societies.
Second, geneticists regularly respond to the evolutionary puzzle by claiming that diabetes kills only older individuals whose child-bearing or child-rearing years are behind them, so the deaths of old diabetics supposedly impose no selective disadvantage on diabetes-predisposing genes. Despite its popularity, this claim is wrong for two obvious reasons. While Type-2 diabetes does appear mainly after age 50 in Europeans, in Nauruans and Indians and other non-Europeans it affects people of reproductive age in their 20s and 30s, especially pregnant women, whose fetuses and newborn babies are also at increased risk. For instance, in Japan today more children suffer from Type-2 than Type-1 diabetes, despite the latter’s name of juvenile-onset diabetes. Moreover (as discussed in Chapter 6), in traditional human societies, unlike modern First World societies, no old person is truly “post-reproductive” and selectively unimportant, because grandparents contribute crucially to the food supply, social status, and survival of their children and grandchildren.
We must therefore instead assume that the genes now predisposing to diabetes were actually favored by natural selection before our sudden shift to a Westernized lifestyle. In fact, such genes must have been favored and preserved independently dozens of times by natural selection, because there are dozens of different identified genetic disorders resulting in (Type-2) diabetes. What good did diabetes-linked genes formerly do for us, and why do they get us into trouble now?
Recall that the net effect of the hormone insulin is to permit us to store as fat the food that we ingest at meals, and to spare us the breakdown of our already accumulated fat reserves. Thirty years ago, these facts inspired the ge
neticist James Neel to speculate that diabetes stems from a “thrifty genotype” making its bearers especially efficient at storing dietary glucose as fat. For example, perhaps some of us have an especially hair-triggered release of insulin in rapid response to a small rise in blood glucose concentration. That genetically determined quick release would enable those of us with such a gene to sequester dietary glucose as fat, without the blood concentration of glucose rising high enough for it to spill over into our urine. At occasional times of food abundance, bearers of such genes would utilize food more efficiently, deposit fat, and gain weight rapidly, thereby becoming better able to survive a subsequent famine. Such genes would be advantageous under the conditions of unpredictably alternating feast and famine that characterized the traditional human lifestyle (Plate 26), 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 high-calorie meals day in and day out (Plate 27). Today, when many of us regularly ingest high-sugar meals and rarely exercise, a thrifty gene is a blueprint for disaster. We thereby become fat; we never experience famines that burn up the fat; our pancreas releases insulin constantly until the pancreas loses its ability to keep up, or until our muscle and fat cells become resistant; and we end up with diabetes. Following Arthur Koestler, Paul Zimmet refers to the spread of this diabetes-promoting First World lifestyle to the Third World as “coca-colonization.”
So accustomed are we in the First World to predictable amounts of food at predictable times each day that we find it hard to imagine the often-unpredictable fluctuations between frequent food shortages and infrequent gluts that constituted the pattern of life for almost all people throughout human evolution until recently, and that remain so in many parts of the world today. I’ve often encountered such fluctuations during my fieldwork among New Guineans still subsisting by farming and hunting. For example, in one memorable incident I hired a dozen men to carry heavy equipment all day over a steep trail up to a mountain campsite. We arrived at the camp just before sunset, expecting to meet there another group of porters carrying food, and instead found that they had not arrived because of a misunderstanding. Faced with hungry, exhausted men and no food, I expected to be lynched. Instead, my carriers just laughed and said, “Orait, i nogat kaikai, i samting nating, yumi slip nating, enap yumi kaikai tumora” (“OK, so there’s no food, it’s no big deal, we’ll just sleep on empty stomachs tonight and wait until tomorrow to eat”). Conversely, on other occasions at which pigs are slaughtered, my New Guinea friends have a gluttonous feast lasting several days, when food consumption shocks even me (formerly rated by my friends as a bottomless pit) and some people become seriously ill from overeating.
Table 11.2. Examples of gluttony when food is abundantly available
Daniel Everett (Don’t Sleep, There Are Snakes, pages 76–77). “They [the Piraha Indians of South America] enjoy eating. Whenever there is food available in the village, they eat it all…. [But] missing a meal or two, or even going without eating for a day, is taken in stride. I have seen people dance for three days with only brief breaks…. Pirahas [visiting] in the city for the first time are always surprised by Western eating habits, especially the custom of three meals a day. For their first meal outside of the village, most Pirahas eat greedily—large quantities of proteins and starch. For the second meal they eat the same. By the third meal they begin to show frustration. They look puzzled. Often they ask, ‘Are we eating again?’ Their own practice of eating food when it is available until it is gone now conflicts with the circumstances in which food is always available and never gone. Often after a visit of three to six weeks, a Piraha [originally weighing between 100 and 125 pounds] will return as much as 30 pounds overweight to the village, rolls of fat on their belly and thighs.”
Allan Holmberg (Nomads of the Long Bow, page 89). “The quantities of food eaten on occasion [by the Siriono Indians of Bolivia] are formidable. It is not uncommon for four people to eat a peccary of 60 pounds at a single sitting. When meat is abundant, a man may consume as much as 30 pounds within 24 hours. On one occasion, when I was present, two men ate six spider monkeys, weighing from 10 to 15 pounds apiece, in a single day, and complained of being hungry that night.”
Lidio Cipriani (The Andaman Islanders, page 54). “Cleaning themselves, to the Onges [of the Andaman Islands in the Indian Ocean], means painting themselves to ward off evil and to remove, so they said, the smell of pig fat after the colossal orgies which follow a particularly good hunt, when even they find the stench too much. These orgies, which give them appalling indigestion for days, are followed by an apparently instinctive variation of their diet to raw or cooked vegetable foods. On three occasions from 1952 to 1954 I was present at one of the solemn pork and honey orgies. The Onges ate almost until they burst, and then, hardly able to move, cleaned up by a grand painting session.”
Ditto, page 117. “As the tide goes down, the shoals [of fish called pilchards] are caught in the reefs stretching out to sea all around the island and the Onges leave everything to man-handle the canoes from pool to pool and fill them to overflowing. The water is almost saturated with fish, and the Onges go on and on until they have nothing more they can use to hold the catch. Nowhere else in the world have I seen anything like this wholesale slaughter. The pilchards of the Andamans are rather larger than usual, some weighing as much as half a kilogram or more…. Men, women and children work feverishly, plunging their hands into the heaving mass of fish so that they reek of it for days…. Everyone cooks and eats at the same time until (temporarily) unable to eat anymore, when the rest of the haul is laid on improvised racks with fires of green wood making smoke underneath. When, a few days later, all is gone, fishing begins again. And so life goes on for weeks, until the shoals have passed the islands.”
These anecdotes illustrate how people accommodate to the pendulum of feast and famine that swung often but irregularly through our evolutionary history. In Chapter 8 I summarized the reasons for the frequency of famine under traditional living conditions: food shortages associated with day-to-day variation in hunting success, short bouts of inclement weather, predictable seasonal variation in food abundance through the year, and unpredictable year-to-year variation in weather; in many societies, little or no ability to accumulate and store surplus food; and lack of state governments or other means to organize and integrate food storage, transport, and exchanges over large areas. Conversely, Table 11.2 collects some anecdotes of gluttony around the world at times when food becomes available in abundance to traditional societies.
Under these traditional conditions of starve-and-gorge existence, those individuals with a thrifty genotype would be at an advantage, because they could store more fat in surplus times, burn fewer calories in spartan times, and hence better survive starvation. To most humans until recently, our modern Western fear of obesity and our diet clinics would have seemed ludicrous, as the exact reverse of traditional good sense. The genes that today predispose us to diabetes may formerly have helped us to survive famine. Similarly, our “taste” for sweet or fatty foods, like our taste for salt, predisposes us to diabetes and hypertension now that those tastes can be satisfied so easily, but formerly guided us to seek valuable rare nutrients. Note again, just as we saw for hypertension, the evolutionary irony. Those of us whose ancestors best survived starvation on Africa’s savannahs tens of thousands of years ago are now the ones at highest risk of dying from diabetes linked to food abundance.
Thus, the starve-and-gorge lifestyle traditionally shared by all human populations resulted in natural selection of genes for a thrifty genotype that served us well under those starve-and-gorge conditions, but that has then caused virtually all populations to end up with a propensity for diabetes under modern Western conditions of unremitting food abundance. But why, by this reasoning, are Pima Indians and Nauruans unusual in their world-record diabetes prevalences? I think that’s because they were subjected in the recent past
to world-record strengths of selection for a thrifty genotype. The Pimas started out sharing with other Native Americans their exposure to periodic starvation. They then experienced a further prolonged bout of starvation and selection in the late 19th century, when white settlers ruined their crops by cutting off their sources of irrigation water. Those Pimas who survived were individuals who were genetically even better adapted than other Native Americans to survive starvation by storing fat whenever food had become available. As for Nauruans, they suffered two extreme bouts of natural selection for thrifty genes, followed by an extreme bout of coca-colonization. First, like other Pacific Islanders, but unlike the inhabitants of continental regions, their population was founded by people who undertook inter-island canoe voyages lasting several weeks. In numerous attested examples of such lengthy voyages, many or most of the canoe occupants died of starvation, and only those who were originally the fattest survived. That is why Pacific Islanders in general tend to be heavy people. Second, the Nauruans were then set apart even from most other Pacific Islanders by their extreme starvation and mortality during the Second World War, leaving the population presumably even more enriched in diabetes susceptibility genes. After the war, their newfound wealth based on phosphate royalties, their superabundant food, and their diminished need for physical activity led to exceptional obesity.
Three lines of human evidence and two animal models support the plausibility of Neel’s thrifty-gene hypothesis. Non-diabetic Nauruans, Pima Indians, African Americans, and Aboriginal Australians have postprandial levels of plasma insulin (in response to an oral glucose load) several times those of Europeans. New Guinea Highlanders, Aboriginal Australians, Maasai tribespeople of Kenya, and other peoples with traditional lifestyles have blood glucose levels far below those of white Americans. Given ample food, diabetes-prone populations of Pacific Islanders, Native Americans, and Aboriginal Australians do exhibit more propensity to obesity than do Europeans: first they gain weight, then they develop diabetes. As for animal models, laboratory rats carrying genes predisposing them to diabetes and obesity survive starvation better than do normal rats, illustrating the advantage of those genes under occasional conditions of famine. The Israeli sand rat, which is adapted to a desert environment with frequent scarcities of food, develops high insulin levels, insulin resistance, obesity, and diabetes when maintained in the laboratory on a “Westernized rat diet” with abundant food. But those symptoms reverse when the sand rat’s food is restricted. Hence diabetes-prone laboratory rats and Israeli sand rats serve as models both of the benefits of thrifty genes and of hair-triggered insulin release under “traditional rat conditions” of starve-and-gorge, and of the costs of those genes under “supermarket rat conditions.”
The World Until Yesterday: What Can We Learn From Traditional Societies? Page 54