Obesity: A Chemical Connection?

Steve Heilig, MPH and W. Peterson Myers, PhD

One of the more interesting developing lines of research in the etiology of the obesity and diabetes epidemics focuses on the possible role of industrial chemicals—pollutants—on metabolism, endocrine function, and conditions such as diabetes.   This line of inquiry has accelerated in just the past few years, with a growing literature indicating that some of the chemicals widely found in human bodies can disrupt normal development and function.   The chemicals in question enter our bodies via food, water, air, and in utero.  Both animal and human studies are finding some striking leads when looking at chemicals widely present in our bodies at concentrations similar to those studied.  Most recent among these are a rodent study which found that fetal exposure to diethylstilbestrol (DES) can lead to grotesque obesity in adult mice.  In humans, studies of pesticide compounds and PCBs indicated a link with increased insulin resistance, as well as interacting with existing obesity to increase the risk of type 2 diabetes.  A link between PCBs and confirmed diagnosed diabetes was found in women in another recent study. 

Most recently, in March a study found a link between phthalates, a class of chemicals commonly found in plastics and other common products, and obesity and diabetes in men.  Spurred by the widely-observed severe declines in sperm count and testosterone levels ­ also linked to these chemicals - the researchers hypothesize that phthalates are likely just a part of the mutifactorial picture, which includes the widely-known issues of diet, lack of exercise, food industry practices, socioeconomic status, and so on. They tested their prediction using data from the CDC, and found the prediction confirmed by statistical analysis,  This one study with humans leaves much to be done, but their findings are also consistent with a growing consensus ­ and predictions going back well over a decade ­ that some widely-used and present chemicals can act as endocrine disrupters and via other pathways at concentrations far below earlier suspected, and that widely-accepted standards of risk assessment and regulation do not address such factors.

For more information see www.ourstolenfuture.org and www.healthandenvironment.org.