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 geneticist 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 ( |
Allan Holmberg ( |
Lidio Cipriani ( |
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