The obesity epidemic as a result of maternal effects and phenotypic evolution (1179.3)

Abstract

Objective: This research provides a reinterpretation and synthesis of existing evidence for a novel theory of the etiology of the obesity epidemic and the increased prevalence of energy contingent chronic non‐communicable diseases.Theory: Over the past century, socio‐environmental evolution (e.g., decreased pathogenic load, thermoneutral environments, reduced physical labor, and enhanced nutrition) engendered decrements in maternal energy expenditure and metabolic control that increased the availability of energy substrates to the intrauterine milieu. This perturbation of mother‐conceptus energy partitioning resulted in population‐wide cumulative maternal effects and the consequent evolution of human energy metabolism (i.e., intensified fetal insulin production and increments in hyperplastic adiposity). With each successive generation, these anatomic and physiologic alterations led to increments in the competitive dominance of adipocytes over other tissues (e.g., myocytes) in the acquisition and sequestering of nutrient‐energy during post‐prandial periods. By the late 20th century, a metabolic tipping point was reached in which the post‐prandial insulin response was so intense (via enhanced beta‐cell mass and function), and the relative number of adipocytes so magnified, that the sequestering of nutrient‐energy as lipid was inevitable, and obesity unavoidable.