The federal Centers for Disease Control and Prevention (CDC) has reported that obesity has been rising, even though Americans are consuming fewer calories. This seems puzzling to many. Changes in physical activity, the amount of calories burned, doesn’t appear to explain this discrepancy. As stated by the co-author of the study, Dr. William Dietz, former CDC director of Nutrition, Physical Activity and Obesity, “It’s hard to reconcile what these data show, and what is happening with the prevalence of obesity.”
However, evidence is growing that chemicals in our food, water, and environment may be changing our bodies’ hormonal balances and metabolism. Such chemicals are called endocrine disruptors. When linked to hormonal disorders linked to obesity they are called obesogens (literally, “causer of obesity”) — see here for more on the obesogen hypothesis.
A recent scientific review summarizes data from experimental animals and humans which support an association of endocrine disrupting chemicals, such as diethylstilbestrol, bisphenol A, phytoestrogens, phthalates, and organotins, with the development of obesity. The reviewers state, “The reasons for this sharp increase in overweight/obesity are not well understood but factors such as high fructose diets, genetics/epigenetics, increased maternal age, sleep debt, use of certain pharmaceuticals, and the built environment have all been proposed as playing a role.” They conclude:
“The data included in this review support the notion that brief exposure early in development to environmental chemicals with estrogenic activity increases body weight gain with age and alters markers predictive of obesity in experimental animals. Furthermore, epidemiologic studies support the findings in experimental animals and show a link between exposure to environmental chemicals (such as estrogenic chemicals, BPA, PCBs, DDE, and persistent organic pollutants and heavy metals) and the development of obesity.Importantly, the use of soy-based infant formula containing the estrogenic component genistein has been positively associated with obesity later in life. Using the DES animal model as an important research tool to study “obesogens”, the mechanisms involved in altered weight homeostasis (direct and/or through endocrine feedback loops, i.e., ghrelin, leptin, etc.) by environmental estrogens can be elucidated. In addition, this animal model may shed light on areas of prevention. Public health risks can no longer be based on the assumption that overweight and obesity are just personal choices involving the quantity and kind of foods we eat combined with inactivity. It is quite possible that complex events, including exposure to environmental chemicals during development, may be contributing to the obesity epidemic.”
For more on how our corporate economy is contributing to our living in a chemical soup which can alter our physiology and metabolism, check out: Obesogens & Canned Tales: Lessons in Corporate Social Responsibility.