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Brain may sabotage efforts to lose weight

The sight of food turns different parts of the brain on in lean versus obese people, a new study finds

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5:50pm, September 19, 2011
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In obese people, even when the brain knows the body isn’t hungry, it responds to food as if it were, new brain-scan data show. That means that when obese people try to shed weight, they may find themselves on the losing side of a battle with neural centers that unconsciously encourage them to eat.

For instance, in normal-weight people a neural reward system that reinforces positive feelings associated with food turns off when levels of the blood sugar glucose return to normal after a meal — a signal that the body’s need for calories has been sated. But in obese people, that reward center in the central brain turns on at the sight of high-calorie food even when their blood sugar levels are normal.

The new findings show that “the regulatory role of glucose was missing in the obese,” says Elissa Epel of the University of California, San Francisco, an obesity researcher not involved with the new study. She says the data might “explain the drive to eat that some obese people feel despite how much they’ve eaten.”

For the study, nine lean and five obese adult volunteers viewed pictures of foods such as ice cream, french fries, cauliflower or a salad while undergoing brain scans. Throughout the procedure, researchers asked the recruits to rate their hunger and how much they wanted a particular item.

Volunteers arrived for their brain scans several hours after eating, and the researchers used insulin pumps to establish volunteers’ blood sugar levels at either normal background values (roughly 90 milligrams per deciliter), or at the “mild” end of low (around 70 milligrams per deciliter). That low value can occur briefly in some people during the day, especially in people with diabetes or metabolic conditions that precede diabetes, notes endocrinologist Robert Sherwin of Yale University, coauthor of the new study.

All volunteers reported wanting food, especially high-calorie fare, when blood glucose was low, Sherwin’s team reports online September 19 in the Journal of Clinical Investigation. Brain scans showed that parts of the brain that control reason and willpower, such as the prefrontal cortex, were relatively inactive when blood glucose was low, while regions that foster eating and offer positive reinforcement turned on. For lean people, the opposite trend emerged when blood glucose was normal.

The surprise, Sherwin says, was that the part of the brain that allows people to consciously exert willpower over food intake largely turns off in obese people. This suggests, he says, that their brain differences “may perpetuate obesity.”

Though small, this study was so well designed and controlled that it “lets us see some clean results in a relatively small cohort,” says obesity scientist Dianne Lattemann of the Veterans Affairs Puget Sound Health Care System in Seattle. The research team’s ability to discern differences in the desire for foods relative to body weight — and based on a not-too-dramatic drop in blood sugar — “is extremely interesting,” she adds. The results pull together trends seen in animals and findings reported in more limited human trials.

Citations

K.A. Page et al. Circulating glucose levels modulate neural control of desire for high-calorie foods in humans. Journal of Clinical Investigation. Published online September 19, 2011. doi: 10.1172/JCI57873 [Go to]
Further Reading

N. Seppa. Bypass’s Big Boon: Scientists spot key players in surgery’s surprising ability to reverse diabetes. Science News, Vol. 180, September 10, 2011, p. 26. Available online: [Go to]

J. Raloff. Obesity messes with the brain, Science News, Vol. 179, April 23, p. 11, p. 8. Available online: [Go to]

J. Raloff. Still Hungry? Fattening revelations—and new mysteries—about the hunger hormone. Science News, Vol. 167, April 2, 2005, p. 216. Available online: [Go to]

J. Raloff. The New GI Tracts: For preventing heart disease, diets that control insulin are all the buzz. Science News, Vol. 157, April 8, 2000, p. 236. Available online: [Go to]

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