Connecting chemicals and obesity

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I would agree with Michelle Obama that the problem of childhood obesity is solvable, and that we should address it on many fronts. One part of the solution, however, is so elusive that it is just reaching the radar screen of public health experts.

Obesity rates have risen dramatically in the industrialized world over the last three decades. In the United States, we have an obesity epidemic. More than 20 percent of adults are clinically obese, and an additional 30 percent are overweight. The linkage between obesity and other devastating and costly health problems, such as Type 2 diabetes, heart disease, asthma and kidney disease, is well documented. An estimated $3,400 average annual health care spending for a normal-weight adult grows to $4,870 for an obese adult.

Most perplexing to scientists and public health experts is the growth in obesity in a segment of the population that can’t be explained by overindulgence in fast food or a more sedentary lifestyle: infants. In 2006, the Harvard School of Public Health reported that obesity in infants under six months had risen 73 percent since 1980.

To explain this unexpected phenomenon, recent research has focused on the possibility that chemicals present in our environment, and especially prenatal exposures to those chemicals, up the ante for obesity risk. The regulation of weight, like all systems in our body, relies on a complex system of communication, activity, and feedback. In bodies evolutionarily designed to deliver relatively stable levels of energy and performance despite dramatically different daily caloric intakes, weight maintenance depends on delicate systems of self-regulation.

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Fat cells were once understood as simply a kind of bank, saving energy for later needs. Now we know that these cells actually communicate with the brain, which in turns affects behavior, regulating both appetite and basal metabolic rate. The messengers in this system are hormones secreted by the fat cells. The concern is that these and other messages regulating weight may be intercepted, and rewritten.

What happens when chemicals never before present in human bodies, but bearing close resemblances to natural hormones, invade our tissues, our bloodstream, or pass through the placenta to act on developing fetal organs?

What happens when those chemicals attach to the same receptors designed to control body weight, but send inaccurate messages about appropriate levels of appetite or metabolic rate?

This is the theory behind emerging research into chemical “obesogens.”

Dr. Retha Newbold of the National Institute of Environmental Health Sciences has given low doses of the hormone-mimicking chemical DES to newborn mice. In six months, the mice were 20 percent heavier and had 36 percent more body fat than unexposed mice. Even before increases in weight and body fat were detected, serum profiles indicated higher levels of weight-regulating hormones in the DES-fed mice.

Dr. Bruce Blumberg at the University of California, Irvine, who coined the term “obesogen,” has performed similar experiments with a class of chemicals called organotins, widely found in PVC plastics, in fungicides and pesticides, and as marine antifouling agents.

Researchers at Seoul National University College of Medicine, South Korea, have exposed the common herbicide atrazine to rats, resulting in decreased basal metabolic rates, increased body weight, increased intro-abdominal fat and insulin resistance, without any changes in food intake or physical activity level.

Those changes, often referred to as “metabolic syndrome,” are considered harbingers of Type 2 diabetes. These researchers suggest there may be a causal relationship between high usage of atrazine in the MidWest Corn Belt, consequent drinking water contamination, and high concentrations of individuals with a body mass index over 30 kg/m2 in the same region.

In a culture still bewitched by the slogan “Better living through chemistry,” government has moved all too slowly to address the problem of chemicals and their impact on human hormonal systems.

Nearly a half century ago, Rachel Carson called attention to this problem in her book about the risks of pesticides, “Silent Spring.” It took more than 30 years for Congress to respond. In 1996, in the Food Quality Protection Act, Congress called for pesticides to be evaluated for their hormone disrupting potential. It took another 13 years for the EPA to implement this directive. In October 2009, the agency issued the first orders for testing the hormone effects of 67 common pesticides.

As science converges from laboratories around the world, however, change may be imminent.

This year, Congress will undertake the first effort in 30 years to re-examine and reform our bankrupt federal system of chemical safety regulation.

The Congressional delegation from Maine should support strong and effective reform.

The problem of obesity is unquestionably multifactorial. But given its high personal and societal costs, we can’t afford to ignore the risk that silent chemical collaborators — “obesogens” — share responsibility for its rising incidence.

Sharon S. Tisher, J.D. teaches environmental law at the University of Maine.

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