CHICAGO — Certain brain areas are sluggish in people who eat too little and hyperactive in people who eat too much, a new study finds.
The results, presented April 3 at the annual meeting of the Cognitive Neuroscience Society, are based on brain activity in people who ranged from dangerously thin to morbidly obese. The findings help clarify the complicated relationship between the brain and food, and may even offer ways to treat conditions such as anorexia and obesity, said study coauthor Laura Holsen of Harvard Medical School and Brigham and Women’s Hospital.
Although scientists have looked for brain differences among particular groups of people with disordered eating habits, no previous study had compared responses to food across such a wide spectrum. “It’s important to study the extremes, because the biology is clearer in those individuals,” said psychologist Susan Carnell of the New York Obesity Nutrition Research Center, St. Luke’s-Roosevelt Hospital Center and Columbia University. “That helps us understand normal weight variation.”
One of five groups studied by the researchers consisted of people with anorexia, defined as being 85 percent or less of a healthy weight. A second group enlisted people who formerly had anorexia but had recovered to a healthy weight. Healthy people with a normal weight formed the third group; the fourth was composed of people who were obese.
At the far end of the scale and making up the final group were those with a disorder called Prader-Willi syndrome. A mutation on chromosome 15 leaves these people with developmental delays, mental deficits and an insatiable appetite. People with the syndrome often don’t feel full, leaving them vulnerable to extreme obesity. Some people with Prader-Willi have suffered stomach ruptures from extreme bouts of overeating, Holsen said. “They will eat as much as you will feed them and still not feel full.”
Holsen and her colleagues had participants come into the lab hungry and undergo fMRI brain scans while viewing pictures of high-calorie food. After eating a meal, the volunteers underwent another scan.
While hungry, volunteers with anorexia had lower than normal activity in brain areas associated with the rewarding feelings that food usually elicit: The hypothalamus, amygdala and hippocampus all showed lackluster responses to pictures of enticing food. At the other end of the spectrum, people with Prader-Willi had higher-than-normal activity in those brain regions. Volunteers in the middle three groups showed a similar trend, though less extreme.
After the meal, the pattern of activity in these reward areas didn’t change much, but the pattern in another brain area — a part of the outer layer of the brain called the dorsolateral prefrontal cortex — did. Brain activity there kicked on in most of the participants, except for those with Prader-Willi syndrome. This area might sense when the body is sated and curb further eating, Holsen said.
The results show that seemingly opposite eating disorders such as anorexia and the extreme overeating that accompanies Prader-Willi syndrome may share some common underlying brain circuits. “What’s interesting is that it seems to be the same structures that are involved in both extremes,” said Carnell. One day, these particular brain regions could be targeted in efforts to help treat obesity and anorexia by normalizing brain responses to food.