SOLVING the Omnivore's Dilemma

Newsweek Aritlce: Born to be Big

Early exposure to common chemicals may be programming kids to be fat.

By Sharon Begley | NEWSWEEKPublished Sep 11, 2009

“It’s easy enough to find culprits in the nation’s epidemic of obesity, starting with tubs of buttered popcorn at the multiplex and McDonald’s 1,220-calorie deluxe breakfasts, and moving on to the couch potatofication of America. Potent as they are, however, these causes cannot explain the ballooning of one particular segment of the population, a segment that doesn’t go to movies, can’t chew, and was never that much into exercise: babies. In 2006 scientists at the Harvard School of Public Health reported that the prevalence of obesity in infants under 6 months had risen 73 percent since 1980. “This epidemic of obese 6-month-olds,” as endocrinologist Robert Lustig of the University of California, San Francisco, calls it, poses a problem for conventional explanations of the fattening of America. “Since they’re eating only formula or breast milk, and never exactly got a lot of exercise, the obvious explanations for obesity don’t work for babies,” he points out. “You have to look beyond the obvious.”“

Scientists in Japan, whose work Heindel focused on, were also finding that low levels of certain compounds, such as bisphenol A (the building block of hard, polycarbonate plastic, including that in baby bottles), had surprising effects on cells growing in lab dishes. Usually the cells become fibroblasts, which make up the body’s connective tissue. These prefibroblasts, however, are like the kid who isn’t sure what he wants to be when he grows up. With a little nudge, they can take an entirely different road. They can become adipocytes—fat cells. And that’s what the Japanese team found: bisphenol A, and some other industrial compounds, pushed prefibroblasts to become fat cells. The compounds also stimulated the proliferation of existing fat cells. “The fact that an environmental chemical has the potential to stimulate growth of ‘preadipocytes’ has enormous implications,” Heindel wrote. If this happened in living animals as it did in cells in lab dishes, “the result would be an animal [with] the tendency to become obese.”

…”It took less than two years for Heindel’s “if” to become reality. For 30 years his colleague Newbold had been studying the effects of estrogens, but she had never specifically looked for links to obesity. Now she did. Newbold gave low doses (equivalent to what people are exposed to in the environment) of hormone-mimicking compounds to newborn mice. In six months, the mice were 20 percent heavier and had 36 percent more body fat than unexposed mice. Strangely, these results seemed to contradict the first law of thermodynamics, which implies that weight gain equals calories consumed minus calories burned. “What was so odd was that the overweight mice were not eating more or moving less than the normal mice,” Newbold says. “We meas-ured that very carefully, and there was no statistical difference.”“

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