Environmental Chemical Obesogens

Understanding the myriad of factors contributing to obesity is essential for curbing its decade-long expansion. Recently, despite the evidence of traditional contributing factors, the role of environmental chemicals with endocrine disrupting activity has also been highlighted. Undeniably, even very small concentrations of these endocrine disrupting chemicals (EDCs) have the capacity to induce severe health damages. The “environmental obesogen” hypothesis associates EDCs to the disruption of energy homeostasis, in particular because of their ability to modulate adipocyte biology. Further studies have revealed numerous potential mechanisms, including modulation of nuclear hormone receptor function and modification of the epigenome. More recently, their involvement in exacerbating metabolic dysfunction in an obesity context reinforces the hypothesis that EDCs have an important “environmental dysmetabolic” effect. Besides adulthood exposure, the perinatal effects are very important since they may allow a change in metabolic programming, encouraging the further development of obesity. Consequently, additional research directed at understanding the nature and action of EDCs will illuminate the connection between health and environment as well as the possible effects triggered by these compounds in respect to public health. Nutrition is being further substantiated as an important modulator of inflammatory and antioxidant pathways, especially associated with environmental insult; nutrition is also emerging as a tool to address exposure toxicity of ECDs as both a sensing and remediation platform. Ultimately, improving EDC exposure measurement, reducing confounding bias, identifying discrete periods of vulnerability and quantifying the effects of EDC mixtures will enhance inferences originated from epidemiological studies.

Keywords: Adipose tissue, Adipocytes, Cardiometabolic disease, Endocrine disrupting chemicals, Epigenetics, Inflammation, Metabolic syndrome, Metabolism-disrupting chemicals, Microbiota, Nutrition, Obesity, Obesity paradox, Obesogens, Type 2 diabetes.