The World Until Yesterday: What Can We Learn from Traditional Societies? (76 page)

Although colonial European physicians on Nauru knew how to recognize diabetes and diagnosed it there in non-Nauruan laborers, the first case in a Nauruan was not noted until 1925. The second case was recorded in 1934. After 1954, however, the disease’s prevalence rose steeply, and it became the commonest cause of non-accidental death. One-third of all Nauruans over the age of 20, two-thirds of those over age 55, and 70% of those few who survive to the age of 70 are diabetics. Within the past decade the disease’s prevalence has begun to fall, not because of mitigation of environmental risk factors (obesity and the sedentary lifestyle are as common as ever), but presumably because those who are genetically most susceptible have died. If this interpretation should prove correct, then
Nauru would provide the most rapid case known to me of natural selection in a human population: an occurrence of detectable population-wide selection within less than 40 years.

Table 11.1
summarizes for comparison some prevalences of diabetes around the world. It’s obvious that there are big differences among countries in their national average prevalences, ranging from low values of 1.6% in Mongolia and Rwanda up to high values of 19% in the United Arab Emirates and 31% in Nauru. But
Table 11.1
also illustrates that these national averages conceal equally big differences within any given country related to differences in lifestyle: at least in developing countries, wealthy or Westernized or urban populations tend to have much higher prevalences than do poor or traditional or rural populations.

India provides excellent examples of those subnational differences. (For this information I am grateful to Professor V. Mohan, of the Madras Diabetes Research Foundation.) The average prevalence in India as of the year 2010 was 8%. But there was little diabetes in India until just a few decades ago. Surveys in 1938 and 1959, in large cities (Calcutta and Mumbai) that are today strongholds of diabetes, yielded prevalences of only 1% or less. Only in the 1980s did those numbers start to rise, first slowly and now explosively, to the point where India today harbors more diabetics (over 40,000,000) than any other nation. The reasons are essentially the same as those behind the diabetes epidemic around the world: urbanization, rise in standard of living, the spread of calorie-rich sweet and fatty fast foods cheaply available in cities to rich and poor people alike, and increased sedentariness associated with replacement of manual labor by service jobs, and with video games and television and computers that keep children (and adults) seated lethargically watching screens for hours every day. Although the specific role of TV has not been quantified in India, a study in Australia found that each hour per day spent watching TV is associated with an 18% increase in cardiovascular mortality (much of it related to diabetes), even after controlling for other risk factors
such as waist circumference, smoking, alcohol intake, and diet. But those factors notoriously increase with TV watching time, so the true figure must be even larger than that 18% estimate.

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 (pre-valence 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.”

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 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.”