No abstract

Maternal placentophagy, although widespread among mammals, is conspicuously absent among humans cross-culturally. Recently, however, advocates for the practice have claimed it provides human postpartum benefits. Despite increasing awareness about placentophagy, no systematic research has investigated the motivations or perceived effects of practitioners. We surveyed 189 females who had ingested their placenta and found the majority of these women reported perceived positive benefits and indicated they would engage in placentophagy again after subsequent births. Further research is necessary to determine if the described benefits extend beyond those of placebo effects, or are skewed by the nature of the studied sample.

The "thrifty genotype hypothesis" has become firmly entrenched as one of the orienting concepts in biomedical anthropology, since first being proposed by Neel (1962 Am. J. Hum. Genet. 14:353-362) over 40 years ago. Its influence on inquiries into the evolutionary origins of diabetes, lactose tolerance, and other metabolic disorders can hardly be underestimated, as evidenced by its continued citation in many top scientific and medical journals. However, its fundamental assumption, that foragers are more likely to experience regular and severe food shortages than sedentary agriculturalists, remains largely untested. The present report tests this assumption by making a cross-cultural statistical comparison of the quantity of available food and the frequency and extent of food shortages among 94 foraging and agricultural societies as reported in the ethnographic record. Our results indicate that there is no statistical difference (P < 0.05) in the quantity of available food, or the frequency or extent of food shortages in these reports between preindustrial foragers, recent foragers, and agriculturalists. The findings presented here add to a growing literature that calls into question assumptions about forager food insecurity and nutritional status in general, and ultimately, the very foundation of the thrifty genotype hypothesis: the presumed food shortages that selected for a "thrifty" metabolism in past foraging populations.

While there has been little success identifying the genetic bases of noninsulin-dependent (type-2) diabetes, current epidemiological data and animal models implicate fetal undernutrition in the development of type-2 diabetes. We examined the effects of fetal undernutrition on insulin responses and glucose tolerance in adulthood in genetically normal rats. Control rats were adequately nourished in utero and consumed nutritionally adequate (N) diets throughout life. Experimental rats (F1 generation) were undernourished in utero and consumed either N or high-energy, high-fat (HF) diets postweaning. The offspring of the experimental rats (F2 generation) received the respective diets of their parent. Body weights of experimental F1 rats at d 4 were 40% less than that of control pups, and they remained significantly smaller than controls throughout adulthood. The experimental F1 rats consuming N diets postweaning had a reduced insulin response (-30%) at 30-min postglucose challenge in adulthood (P > 0.05). However, their offspring (F2 generation) displayed a markedly elevated insulin response [+80% at 30 min (P < 0.05) and + 230% at 120 min (P < 0.001) postglucose challenge]. The insulin response of the F2 generation rats fed the high-energy, HF diet was even more pronounced [+130% at 30 min (P < 0.003) and + 250% at 120 min (P < 0.001) postglucose challenge]. Thus, undernourishment in utero produces striking insulin resistance in genetically normal, well-nourished second-generation rats.

Popular media reports concerning the causes of the current global obesity pandemic and its related sequelae-the cardiometabolic syndrome-are often couched in terms of dramatic changes in diet and lifestyle around the world; namely, drastically increasing dietary intakes of high energy foods and plummeting levels of daily physical activity-the hallmarks of the so called "nutrition transition." Far less attention is generally drawn to the important role phenotypic plasticity during early life (i.e., "developmental programming") plays in the cardiometabolic health crisis. Recently, however, researchers working within the field of the developmental origins of health and disease (DOHaD) and epigenetics have extended our understanding of the role played by these developmental processes and capacities in health and disease even further by investigating the transmissible nature of developmentally programmed cardiometabolic traits to subsequent generations. In this review, after briefly revisiting the fundamental discoveries of firstgeneration DOHaD research, I consider how recent discoveries regarding the transmissibility of developmentally acquired traits are providing new insights into the current global cardiometabolic pandemic, and how a better understanding of developmental programming-including transmissibility-are essential for the conceptualization and implementation of public health initiatives aimed at stemming this global health crisis. Am J Phys Anthropol 57:79-93,