Anthropology Archive

Thrifty Genotype or Starved Phenotype

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Native American populations suffer from extremely high rates of type 2 diabetes (adult onset), with an incidence of 40 percent or more in the adult population (such as the Pima of Arizona; Bennett, LeCompte, Miller, and Rushforth, 1976). This tendency to obesity and high incidence of diabetes in these populations has led biomedical researchers to postulate a genetic predisposition in a "thrifty genotype" (Neel, 1999). This postulated gene is hypothesized to have enhanced survival under conditions in which the availability of nutritional glucose was severely limited. The reasoning is that these populations evolved efficient metabolic systems as a consequence of a long-term adaptation to feast-or-famine cycles. A quick release of insulin more efficiently converts available glucose into fat stores. When these physiologies shaped by selective pressures of Arctic-sub-Arctic hunter-gatherer food strategies were exposed to the high carbohydrate, protein, and fat diets of the modern world, their "superefficient" metabolisms were then a detriment because they produced excessive storage of fats (see Diamond, 2006). Extensions of Neel's original hypothesis have pointed to the adaptive benefits of insulin resistance (a diabetes precursor) in populations with high-protein and low-carbohydrate diets and its maladaptive consequences when consuming energy-rich high-carbohydrate diets.

Population and clinical studies (see Martin, Johnston, Han, and Benyshek, 2000; Benyshek, Martin, and Johnston, 2001; Benyshek, Johnston, and Martin, 2004; McDermott, 2006, for reviews and discussion) call this genetic hypothesis into question and propose an environmental and nutritional alternative to the thrifty genotype hypothesis. Studies show that low birth weight, reflective of malnourishment in utero, is a strong predictor of adult diabetes. Severe famine in utero leads to abnormal insulin and glucose metabolism in adulthood, especially for the obese. This suggests that diabetes is a consequence of developmental acclimatization.

Native American groups with an excessive prevalence of diabetes were exposed to periods of near-starvation during the later nineteenth and early twentieth centuries (Benyshek et al., 2001). This period of deprivation was followed by dramatic increases in all aspects of diet, particularly carbohydrates and fats. This was partly produced by the high fat and carbohydrate content of the government rations, inducing basic changes in diet that made fry bread a new "traditional food." Initial Native American cohorts diagnosed with diabetes were children of those generations exposed to severe nutritional deprivation. Laboratory and clinical findings show that hyperglycemic conditions during gestation produce insulin and glucose abnormalities in subsequent generations. The role of the gestational environment in fostering these abnormalities is illustrated by the far greater importance of maternal than paternal diabetes as a risk factor.

Laboratory studies with rats exposed to similar conditions (maternal nutritional deprivation in utero followed by high-fat diets) demonstrate that diabetes can be induced by gestational nutritional deprivation and dramatic increases in nutrient supply from pregnancy to postweaning periods. Deprivation in utero, followed by excessive food energy sources, leads to elevated insulin-to-glucose ratios, glucose concentrations, and insulin resistance in adulthood. Fetal malnutrition in the females shaped their own glucose and insulin metabolism, which shapes the metabolic adjustments of their offspring. These elevated levels of insulin resistance were not improved by placement on an adequate diet after weaning. Subsequent studies by Martin and colleagues indicate that the thrifty-phenotype rats (thin at birth due to nutritional deprivation) that have low-protein diets are insulin-deficient as adults, but that those fed high-fat diets produce too much insulin (hyperinsulinemia) and develop adult insulin resistance.

This research indicates that epidemic levels of Native American diabetes are not genetic but, rather, a consequence of fetal malnutrition that is transmitted intergenerationally through the intrauterine environment affected by the mother's metabolic system. Diabetes was unknown in aboriginal populations, emerging as a health problem in these populations scarcely more than fifty years ago. Native American diabetes may be understood as a consequence of the intergener-ational transmission of disturbed insulin metabolism that began as protein and energy malnutrition during near-starvation in the early reservation period almost a century ago and was induced in subsequent generations from the high-energy diets that were subsequently available.

The implication of this model is that the Native American diabetes epidemic was produced by political and economic conditions, not genetic predispositions. Consequently, these populations are not doomed to a genetically determined susceptibility to diabetes but can reduce the incidence of diabetes through dietary manipulations, particularly during pregnancy. Glucose intolerance in the mother during pregnancy is a predisposing condition for later adult-onset diabetes in her offspring. Current high levels of carbohydrates in Native American diets reinforce these influences. Dietary change during gestation to reduce blood glucose levels is a possible intervention to interrupt the intergenerational transmission of susceptibility to diabetes.

Considerable difficulties impede achieving such changes in the current ideological, political, and economic environments that maintain the status quo, including the biomedical thrifty-genotype hypothesis. Additional challenges face this new thrifty-phenotype model that attributes the perpetuation of diabetes to the mother's gestational diet. Benyshek and coworkers (2001) emphasize the need to develop interventions that avoid blaming pregnant women and instead place their dietary behavior in the context of broader community influences and constraints. A community-level approach is consistent with the macrolevel political and economic forces that initiated the chain of events more than a century ago through famines. These political diseases produced through racist ideologies and their resultant social inequalities require political solutions that mend these intergen-erational disruptions in foodways. The persistence of the genetic model involved in the largely discredited thrifty-gene hypothesis is a form of reductionism characteristic of biomedical thought that ignores the determining causal factors involved in the interactions between the lifeways of groups and the macrosocial factors of the broader society.

temperature, humidity, nutrients, microorganisms, and toxic substances. These leave effects on the body, such as how access to nutrients has determinant effects on height and weight. Imagine how different you might look if you had eaten only half the food you have consumed across your life—or twice as much. Those differences would reflect phe-notypic variation made possible by your genetic characteristics.

McElroy and Townsend (1985) discuss three levels of physiological adaptation:

• Acclimation, a rapid, short-term adjustment to an environmental stressor
• Acclimatization, a pervasive but reversible response to exposure over a longer time
• Developmental (native) acclimatization, an irreversible adjustment to environmental stressors

Acclimation involves changes like feeling cold (or hot) when you first walk outside, but after a few days of similar temperatures, you may feel comfortable. Acclimatization will occur over longer periods of exposure, so that when you have spent two months of summer in the 110-degree (Fahrenheit) hot environment of Phoenix, a quick trip to San Diego where it is just 65 degrees might leave you feeling cold and shivering. However, in the winter, 65 degrees might feel like a hot day. Your temperature comfort zone undergoes regular shifts in acclimatization but establishes limits of flexibility early in life that involve developmental (native) acclimatization. For example, you could probably not do much physical work at 10,000 feet elevation or when it is minus 30 degrees Fahrenheit outside; this reflects your developmental acclimatization regarding lung capacity for low oxygen concentrations and temperature resistances that normally cannot be substantially changed once you are an adult.

Developmental acclimatization may affect not only individual metabolic development, for instance, where childhood obesity deposits fat cells for life. Acclimatization may also be passed from mother to embryo, as illustrated in the intergenerational transmission during gestation of disturbed metabolic effects that appear to underlie the diabetes epidemic in Native American groups.