The Childhood Obesity Epidemic as a Result of Nongenetic Evolution: The Maternal Resources Hypothesis

Abstract

Over the past century, socio-environmental evolution (e.g., reduced pathogenic load, decreased physical activity [PA], improved nutrition) led to cumulative increments in maternal energy resources (i.e., body mass, 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 beta-cell and adipocyte hyperplasia, thereby inducing an enduring competitive advantage of adipocytes over other tissues in the acquisition and sequestering of nutrient-energy via intensified insulin secretion and hyperplastic adiposity. At menarche, the competitive dominance of adipocytes was further amplified via hormone-induced adipocyte hyperplasia and weight-induced decrements in PA. These metabolic and behavioral effects were propagated progressively when obese, inactive, metabolically compromised women produced progressively larger, more inactive and metabolically compromised children. Consequently, the evolution of human energy metabolism was significantly altered. This phenotypic evolution was exacerbated by increments in the use of Caesarian sections that allowed both the larger fetuses and the metabolically compromised mothers who produced them to survive and reproduce. Thus, natural selection was iatrogenically rendered artificial selection, and the frequency of obese, inactive, metabolically compromised phenotypes increased in the global population. By the late 20th century, a metabolic tipping point was reached in which the post-prandial insulin response was so intense, the relative number of adipocytes so magnified, and inactivity so pervasive that the competitive dominance of adipocytes in the sequestering of nutrient-energy was inevitable, and obesity was unavoidable.

Childhood obesity: Current and novel approaches

“…We [60] and many others [61] have shown the importance of maternal BMI in predicting later health problems in the offspring and there is growing interest in optimising maternal health to improve on childhood obesity outcomes. Most recently, this has elegantly been put forward as the 'Maternal Resources Hypothesis' which posits that the childhood obesity epidemic is the result of the evolutionary processes of maternal effects, phenotypic evolution and socio-environmental evolution, leading to a tipping point in human energy metabolism at which adipocytes outcompete other cell types in the acquisition and sequestering of nutrient energy [62].…”

Effects of Running on Chronic Diseases and Cardiovascular and All-Cause Mortality

“…[1][2][3]17 We have previously reported that a progressive decline in PA, especially in occupational and household PA, over the past 5 decades is a primary cause of the obesity epidemic that has been spreading in our society, and this also impacts the health of the next generation and contributes to many chronic diseases and adverse CVD outcomes. [18][19][20][21] Considerable evidence suggests that high levels of PA and ET are associated with improved clinical outcomes, beyond those expected on the basis of effects on traditional risk factors for CVD, suggesting that other factors (eg, autonomic function, preconditioning, and endothelial function) might also explain the marked benefits noted. [1][2][3]5 This evidence comes from studies evaluating the effects of both leisure time PA and occupational PA on subsequent prognosis.…”

Obesity: epigenetic regulation – recent observations

“…It is well known that the prenatal period is crucial in the establishment of the epigenome (21,(56)(57)(58). One of the most critical processes during pregnancy is the establishment of imprinted genes.…”