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“Obesogens” in our environment: chemicals that can make us fat

This study by Wendee Holtcamp, published in the journal Environmental Health Perspectives, surveys environmental chemicals that can contribute to obesity.

Obesity is rising steadily around the world. Convincing evidence suggests that diet and activity level are not the only factors in this trend—chemical “obesogens” may alter human metabolism and predispose some people to gain weight. Fetal and early-life exposures to certain obesogens may alter some individuals’ metabolism and fat-cell makeup for life. Other obesogenic effects are linked to adulthood exposures.

Chemical pesticides in food and water, particularly atrazine and DDE (dichlorodiphenyldichloroethylene—a DDT breakdown product), have been linked to increased BMI in children and insulin resistance in rodents.

Most known or suspected obesogens are endocrine disruptors. Many are widespread, present in common consumer items such as handbags, wallpaper, vinyl blinds, tile, and vacuum cleaner dust.  Phthalates, plasticizers that also have been related to obesity in humans, occur in many PVC items as well as in scented items such as air fresheners, laundry products, and personal care products.

Animal studies have also implicated another suspected obesogen: bisphenol A (BPA), which is found in medical devices, in the lining of some canned foods, and in cash register receipts.

Many endocrine disruptors exhibit an inverted U-shaped dose–response curve, where the most toxic response occurs at intermediate doses.41 However, in a recent unpublished study, vom Saal found that BPA affected rodent fat cells at very low doses, 1,000 times below the dose that regulatory agencies presume causes no effect in humans, whereas at higher doses he saw no effect. Receptors typically respond to very low levels of hormone, so it makes sense that they may be activated by low levels of an endocrine mimic, whereas high levels of a chemical may actually cause receptors to shut down altogether, preventing any further response.41 This is known as “receptor downregulation.” As a result, some endocrine disruptors have greater effects at low than at high doses; different mechanisms may be operating.15