Inherited Epigenetic Hallmarks of Childhood Obesity Derived from Prenatal Exposure to Obesogens

Abstract

Childhood obesity has reached epidemic levels in developed countries and is becoming a major cause for concern in the developing world. The causes of childhood obesity are complex and multifactorial, involving the interaction between individual genetics and environmental and developmental factors. Among the environmental factors, there is a growing interest in understanding the possible relationship between the so-called environmental obesogens and the development of obesity in children. Exposure to these obesogens such as phthalates, bisphenol A, or parabens, has been identified as a promoter of obesity through different mechanisms such as the alteration of adipocyte development from mesenchymal progenitors, the interference with hormone receptors, and induced inflammation. However, less attention has been paid to the inheritance of epigenetic modifications due to maternal exposure to these compounds during pregnancy. Thus, the aim of this review is to summarize the current knowledge of epigenetic modifications due to maternal exposure to those obesogens during pregnancy as well as their potential implication on long-term obesity development in the offspring and transgenerational inheritance of epiphenotypes.

Tackling obesity while preventing obesity stigma

“…Early life (especially the first 1000 days) represents a critical window for prevention, since it is then that nutritional and exercise patterns, and growth trajectories are set 2 5 8 9. But prevention is difficult given the potent obesogenic environments in which many children grow up and the influence of social determinants at many levels, from family to society at large 5 10. In fact, obesity is linked to poverty and disadvantage (in high-income countries) 11–13.…”

Transgenerational transmission of eating habits

“…Excess weight, nutrient deficiency, excessive weight gain, and exposure to obesogenic environments during pregnancy subject the sperm, ovum, and placenta to inflammation, oxidative stress, lipid accumulation, and insulin resistance, in addition to altering the epigenetics of breast milk and altering the mother’ energy and glucose metabolism. 9 , 30 …”