How Lab Rats Are Changing Our View of Obesity
Obesity stems primarily from the overconsumption of food paired with insufficient exercise. But this elementary formula cannot explain how quickly the obesity epidemic has spread globally in the past several decades nor why more than one third of adults in the U.S. are now obese. Many researchers believe that a more complex mix of environmental exposures, lifestyle, genetics and the microbiome ’s makeup help explain that phenomenon. And a growing body of work suggests that exposure to certain chemicals —found in nature as well as industry—may play an essential role by driving the body to produce and store surplus fat in its tissues. Evidence of that cause-and-effect relationship in humans is still limited, but in laboratory animals and in petri dishes data linking the chemicals to problematic weight gain are mounting. Moreover, the effects in animals appear to be passed on not just to immediate offspring but also grandchildren and great-grandchildren—potentially accounting for some multigenerational obesity.
The murkier picture for humans may become clearer in the next five years, says Jerry Heindel, a health science administrator at the National Institute of Environmental Health Sciences. His agency is now funding 57 grants related to obesity and diabetes, he said on March 2 at a meeting of the Institute of Medicine (IOM). The studies look at how chemicals, including those that appear to alter hormone regulation (such as the plasticizer bisphenol A and the antibacterial chemical triclosan), affect weight gain or insulin resistance. Thirty-two of the ongoing studies are in humans. And 20 of those will help assess the longer-term risks to children by tracking the youngsters' chemical levels in utero or as newborns and beyond.
Read article in Scientific American.
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