In a recent paper, Dr. Edward Archer, a research fellow in the office of energetics and Nutrition Obesity Research Center (NORC) at the University of Alabama at Birmingham, investigated the evolutionary consequences of maternal inactivity and the increasing incidence of obesity in offspring. Over the past century, socioenvironmental evolution (e.g., reduced pathogenic load, decreased physical activity, and improved nutrition) led to cumulative increments in maternal energy resources (i.e., body mass and adiposity) and decrements in energy expenditure and metabolic control. These decrements reduced the competition between maternal and fetal energy demands and increased the availability of energy substrates to the intrauterine milieu.
This perturbation of mother-conceptus energy partitioning stimulated fetal pancreatic β-cell and adipocyte hyperplasia, thereby inducing an enduring competitive dominance of adipocytes over other tissues in the acquisition and sequestering of nutrient energy via intensified insulin secretion, altered myocyte development, and hyperplastic adiposity. During puberty in females, the competitive dominance of adipocytes was further amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in physical activity.
These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically compromised women produced progressively larger, more inactive, metabolically compromised children. Consequently, the evolution of human energy metabolism was markedly altered. This phenotypic evolution was exacerbated by increments in the use of cesarean sections, which allowed both the larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection was inadvertently rendered artificial selection, and the frequency of obese, inactive, metabolically compromised phenotypes increased in the global population.
Dr. Archer’s meta-theoretic analysis concluded that by the late twentieth century a metabolic tipping point was reached at which the postprandial insulin response was so intense, the relative number of adipocytes so large, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering of nutrient energy was inevitable and obesity was unavoidable.
“The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis” was published online in November in the medical journal Mayo Clinic Proceedings.