Environmental Estrogens and Obesity, Body Weight following DES Exposure

Environmental Estrogens and Obesity

Control-and-DES-treated-Mice image
Representative photograph of control and DES-treated mouse at ~ 6months of age. Image via NCBI.  Complex events including exposure to environmental chemicals during development may be contributing to the obesity epidemic.

2010 Study Abstract

Many chemicals in the environment, in particular those with estrogenic activity, can disrupt the programming of endocrine signaling pathways that are established during development and result in adverse consequences that may not be apparent until much later in life. Most recently, obesity and diabetes join the growing list of adverse consequences that have been associated with developmental exposure to environmental estrogens during critical stages of differentiation. These diseases are quickly becoming significant public health issues and are fast reaching epidemic proportions worldwide.

In this review, we summarize the literature from experimental animal studies documenting an association of environmental estrogens and the development of obesity, and further describe an animal model of exposure to diethylstilbestrol (DES) that has proven useful in studying mechanisms involved in abnormal programming of various differentiating estrogen- target tissues.  Other examples of environmental estrogens including the phytoestrogen genistein and the environmental contaminant Bisphenol A (BPA) are also discussed. Together, these data suggest new targets (i.e., adipocyte differentiation and molecular mechanisms involved in weight homeostasis) for abnormal programming by estrogenic chemicals, and provide evidence that support the scientific hypothesis termed “the developmental origins of adult disease”.

The proposal of an association of environmental estrogens with obesity and diabetes expands the focus on the diseases from intervention/treatment to include prevention/avoidance of chemical modifiers especially during critical windows of development.

Summary and Conclusions

The data included in this review supports the idea 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. Epidemiology studies support the findings in experimental animals and show a link between exposure to environmental chemicals (such as PCBs, DDE, and persistent organic pollutants) and the development of obesity. Furthermore, 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 endocrine feedback loops, i.e., ghrelin, leptin, etc.) by environmental estrogens can be elucidated. In addition, hopefully this animal model may shed light on areas of prevention. Public health risks can no longer be based on the assumption than overweight and obesity are just personal choices involving the quantity and kind of foods we eat combined with inactivity, but rather that complex events including exposure to environmental chemicals during development may be contributing to the obesity epidemic.

  • Environmental Estrogens and Obesity, Retha R. Newbold, Elizabeth Padilla-Banks, and Wendy N. Jefferson, NCBI PMCID: PMC2682588, 2010 May 25.
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