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Born to be fat

Does prenatal exposure to chemicals called ‘obesogens’ help explain the epidemic of obesity?


 
Born to be fat

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Why are babies growing fatter and more quickly these days? This question has been puzzling Michelle A. Mendez, an epidemiologist at the Centre for Research in Environmental Epidemiology in Barcelona. “What could make them less active or eat more at such early stages of life?” she ponders over the phone from her office. “Is it just that parents are suddenly stuffing their children with food or is something else increasing their susceptibility to gaining weight?”

There’s been a dramatic increase in obesity in all age groups all over the world, but especially among kids. Rates of overweight European schoolchildren, for example, shot up from nine per cent in the mid-1970s to 24 per cent in 2000. In Canada, more than a quarter of children aged 2 to 17 years are overweight or obese. So Mendez—like other scientists who believe there are other causes for the obesity epidemic besides too many french fries—began to explore potential triggers for the tipping scales. In particular, she looked at whether early-life exposure to small amounts of chemicals in our environment make babies fat, possibly predisposing them to weight gain throughout life.

Using data from 518 pregnant Spanish women, Mendez and other researchers measured chemicals in the moms’ blood, such as DDE (a by-product of the now widely banned pesticide DDT, which lingers in the environment decades later, and is still found in small amounts in many foods such as meat, dairy and fish), to see if they correlated with fatter and faster-growing babies. The result: children of normal-weight mothers who had elevated levels of DDE in their systems were twice as likely to grow quickly in their first six months, and have a high body mass index (BMI) at 14 months. And, says Mendez, “Rapid early growth is associated with obesity in childhood and adulthood.”

The study, published in the journal Environmental Health Perspectives, is the latest addition to the mounting body of evidence that endocrine disruptors—chemicals that can mimic and interfere with the body’s hormones—may have adverse effects on human and animal health, among other things, triggering obesity. Known colloquially as “obesogens,” these pollutants, like DDE, are believed to alter or block the activity of natural female  and male sex hormones, causing fat to store more efficiently, and spurring the creation of fat cells where cartilage or bone would have been. “In the last five years or so,” says Mendez, “we’ve been realizing there may be more to the obesity epidemic than just bad diet and not enough exercise.”

Studies on animals have shown that exposure around the time of birth to even trace amounts of everyday chemicals can predispose subjects to weight gain throughout life. Perfluorooctanoic acid, found in non-stick pans, microwave popcorn bags and pizza boxes, has been associated with obesity in female mice. Bisphenol A, used in plastics and recently declared a toxic chemical in Canada, is linked to obesity in rats. Similarly, triclosan, an ingredient in antibacterial hand soaps, dishwashing detergents and other body care products, has been correlated to faster growth in frogs. Caren Helbing, a researcher at the University of Victoria who worked on the triclosan study, notes, “It’s critical to realize that some of the manufactured chemicals that have been important for protecting people, like flame retardants, were designed without thinking about how they would change the way hormones in humans work.”

The grandfather of the obesogen studies is Bruce Blumberg, a cell biologist at the University of California, Irvine. He coined the term “obesogen,” and has focused on mice and how they are affected by tributyltin (TBT), a pesticide added to paint used on ships to prevent the growth of marine organisms like barnacles and algae, which enters underwater environments and ends up in our seafood. “We found that if we treat pregnant mice with tributyltin, the pups in their womb will be predisposed to getting fat later in life,” Blumberg says. “They make more fat cells, and that appears to lead them to be heavier.”

These changes in animals are thought to be indicative of changes in humans, and the idea of obesogens as the new weight threat has caught on. Some folks, like the authors of a 2009 book The New American Diet, are even trying to capitalize on the notion that you can undo “the obesogen effect” through a special diet. But Blumberg says more empirical data is needed to understand how these chemicals work on humans at all stages in life, and whether the effects of early exposure can be reversed.

In the meantime, most scientists working on endocrine disruptors agree that staying away from chemicals, wherever possible, is a good idea. That means opting for glass or stainless steel instead of plastic, avoiding scented and anti-bacterial products, seeking out cosmetics and body products with fewer ingredients, and, perhaps, eating organic foods and wild fish instead of farmed varieties, which contain more pesticides. “Obesity correlates with lots of things, not just plastic,” Blumberg says, “but if it were as easy as just balancing your caloric chequebook, would anyone be obese?”


 

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