Researchers have found that women with a history of bulimia show key differences in their brain’s regulation of a hormone that controls mood and appetite, possibly suggesting an inherent susceptibility to the eating disorder.
“These alterations may make some women vulnerable for developing an eating disorder,” lead author Dr. Walter H. Kaye, of the University of Pittsburgh School of Medicine in Pennsylvania, told Reuters Health.
Kaye’s team studied nine women who have recovered from bulimia for at least one year. Bulimia nervosa is an eating disorder in which patients alternate between binge eating and purging. They suffer from a distorted body image and, often, mood disturbances such as depression.
All the women were scanned using positron emission tomography, or a (PET) scan, to gather images of brain activity. These were compared with brain scans from 12 women who had never had an eating disorder.
The researchers found that the bulimic patients’ brains showed a reduction in the ability of the chemical serotonin to bind to receptors in certain brain regions. They also found that these women did not show the normal decline in serotonin binding that comes with aging.
Serotonin is a neurotransmitter that helps regulate appetite, mood and impulse control. The findings are published in the July issue of the American Journal of Psychiatry.
“I suspect this finding suggests that there is a dysregulation of the serotonin system, which contributes to extremes of impulse control–undereating as well as overeating–both of which are often found in bulimia,” Kaye said.
He and his colleagues suspect the brain alterations were not a result of the bulimia, but a possible cause.
“While this finding could be a consequence of having bulimia, there is other data that suggests that certain traits, such as anxiety, may occur in childhood in people who later develop bulimia,” Kaye said. “Serotonin alterations could contribute to such traits.”
Previous research, he noted, has also found some evidence that bulimia has a genetic component.
SOURCE: American Journal of Psychiatry 2001;158:1152-1155.