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.”
Why is diabetes low in Europeans?
Diabetologists used to point to Pimas and Nauruans as the glaring exceptions of high diabetes prevalence, standing out from a world in which the relatively low diabetes prevalence of Europeans was taken as the norm. But the information that has become available in recent decades shows that, instead, Europeans are the exception in their low prevalence, contrasting with the high prevalence reached by Westernized populations of everyone else. Pimas and Nauruans are “merely” the highest of that normal high prevalence, already approached closely by some Aboriginal Australians and New Guinean groups. For every well-studied large non-European population grouping, we now know of some Westernized subgroup with a prevalence above 11%, usually above 15%: Native Americans, North Africans, sub-Saharan Black Africans, Middle Easterners, Indians, East Asians, New Guineans, Aboriginal Australians, Micronesians, and Polynesians. Compared to that norm, Europeans, and overseas Europeans in Australia, Canada, New Zealand, and the U.S., are unique among the modern world’s populations in their relatively low prevalence. All 41 national European values for the prevalence of diabetes (Table 11.1, first row) fall between 2% and 10%, with a mean value of only 6%.
That’s astonishing when one reflects that Europeans in Europe itself and overseas are the world’s richest and best-fed people, and the originators of the Western lifestyle. We refer to our indolent, obese, supermarket way of life as Western precisely because it arose first among Europeans and white Americans and is only now spreading to other peoples. How can we account for this paradox? Why don’t Europeans now have the highest, rather than the lowest, prevalence of diabetes?
Several experts in the study of diabetes have suggested to me informally that perhaps Europeans traditionally had little exposure to famine, so that they would have undergone little selection for a thrifty genotype. Actually, though, history provides abundant documentation of famines that caused widespread severe mortality in medieval and Renaissance Europe and earlier. Those repeated famines should have selected for thrifty genes in Europe, just as everywhere else. Instead, a more promising hypothesis is based on Europe’s recent food history since the Renaissance. The periodic widespread and prolonged famines that used to rack Europe, like the rest of the world, disappeared between about 1650 and 1900 at different times in different parts of Europe, beginning in the late 1600s in Britain and the Netherlands, and continuing into the late 1800s in southern France and southern Italy. With one famous exception, Europe’s famines were ended by a combination of four factors: increasingly efficient state intervention that rapidly redistributed surplus grain to famine areas; increasingly efficient food transport by land and especially by sea; increasingly diversified European agriculture after Columbus’s voyage of AD 1492, thanks to European voyagers bringing back many New World crops (such as potatoes and corn); and, finally, Europe’s reliance not on irrigation agriculture (as in many populous areas of the world outside Europe) but instead on rain agriculture, which reduced the risk of a crop failure too widespread to be solved by food transport within Europe.
The famous exception to the end of Europe’s famines was of course the Irish potato famine of the 1840s. Actually, that was the exception that proved the rule, by illustrating what happened even in Europe when the first three above-mentioned factors ending famines elsewhere in Europe didn’t operate. The Irish potato famine was due to a disease of a single strain of potato in an agricultural economy that was unusual in Europe in its reliance on that single crop. The famine occurred on an island (Ireland) governed by an ethnically different state centered on another island (Britain) and notorious for the inefficiency or lack of motivation of its response to the Irish famine.
These facts of Europe’s food history lead me to offer the following speculation. Several centuries before the advent of modern medicine, Europeans, like modern Nauruans, may have undergone an epidemic of diabetes that resulted from the new reliability of adequate food supplies, and that eliminated most diabetes-prone bearers of the thrifty genotype, leaving Europe with its low prevalence of diabetes today. Those gene-bearers may have been undergoing elimination in Europe for centuries, as a result of many infants of diabetic mothers dying at birth, diabetic adults dying younger than other adults, and children and grandchildren of those diabetic adults dying of
