Evidence for Obesogens: Interpretations and Next Steps

Abstract

Traditionally toxicologists have embraced the presumption that “Alle Ding' sind Gift, und nichts ohn' Gift; allein die Dosis macht, das ein Ding kein Gift ist” or “All things are poison, and nothing [is] without poison; only the dose makes a thing not be poison”, as first proposed by Paracelsus in 1538, but hypothesized non-monotonic, low dose adverse effects of some substances challenge this premise. Three perspectives on environmental chemicals as ‘obesogens’ are presented in this issue. Schug and Heindel suggest there is compelling evidence demonstrating many industrial and agricultural chemicals act as obesogens and provide hypotheses on how endocrine disruption, particularly during early development, could lead to obesity later in life. On the other hand, Sharpe and Drake are skeptical of the current evidence linking environmental chemicals to obesity, emphasizing two primary criticisms: 1) Animal model studies have largely relied on high dose levels that do not reflect routes and magnitudes of exposures experienced by humans and 2) Epidemiological studies linking chemicals to obesity are likely confounded by high fat diets, since fat in the diet is the primary route of exposure for many of the lipophilic environmental chemicals considered obesogens, as well as total food intake which will increase obesity. Unwilling to draw conclusions on the current evidence, Legler stresses the need for further research and introduces the OBELIX (“OBesogenic Endocrine disrupting chemicals: LInking prenatal eXposure to the development of obesity later in life”) project, which is examining endocrine disrupters in the diet through a prospective birth cohort in four European countries and long-term animal studies using exposures that are comparable to those experienced in human populations.