Researchers at the University of California, San Diego School of Medicine have pinpointed differences in brain function that may help to explain how people with anorexia nervosa can continue to starve themselves, even when already emaciated. The finding adds to growing evidence about the role of brain mechanisms in eating disorders and could lead to new treatment development efforts targeting specific brain pathways.
“When most people are hungry, they are motivated to eat,” said Christina E. Wierenga, PhD, the study’s first author and UC San Diego associate professor of psychiatry. “Yet individuals with anorexia can be hungry and still restrict their food intake. We wanted to identify brain mechanisms that may contribute to their ability to ignore rewards, like food.”
Wierenga said their study showed differences in brain response to reward in women recovered from anorexia. “They showed decreased response to reward, even when hungry. This is opposite of healthy women without an eating disorder, who showed greater sensitivity to rewards when hungry,” added Wierenga.
The study is published in the current issue of the journal
Walter H. Kaye, MD, a professor of psychiatry and director of the Eating Disorders Treatment and Research Program at UC San Diego and senior author, said the study’s results further support the view that neurobiology contributes to this disorder. “Our study suggests that brain circuitry differences in anorexics make them less sensitive to reward and the motivational drive of hunger. Put another way, hunger does not motivate them to eat.”
Anorexia nervosa is an eating disorder characterized by abnormally low body weight, fear of gaining weight and a skewed perception of body image. Up to 24 million Americans are estimated to suffer from anorexia and other eating disorders, including bulimia and binge-eating disorder. Women are much more likely to develop eating disorders, which are associated with many medical problems and can be life-threatening.
In their study, the research team analyzed brain function in 23 women who had recovered from anorexia and a control group of 17 healthy women who had never had the disease. Individuals were studied who had previously had anorexia nervosa and were at normal weight, rather than those in an active disease phase, to avoid the potential of malnutrition confounding their research results. Researchers analyzed participants’ brain circuitry related to motivation and reward during two distinct metabolic periods: when they were hungry and again when satiated.
Along with differences in brain response to reward, Kaye said the researchers saw greater activity in regions of the brain important for self-control among the recovered anorexics, regardless of metabolic state. This suggests these individuals may possess a higher degree of self-control than people without eating disorders, he said.
“We are using these new insights about brain mechanisms that contribute to disordered eating to guide the development of new treatment approaches in our Eating Disorders program at UC San Diego,” he said. “We’re very motivated to help advance efforts to better understand and address this life-threatening disorder.”
Co-authors include Amanda Bischoff-Grethe, A. James Melrose, Zoe Irvine, Laura Torres, Ursula F. Bailer, Alan Simmons, and Alice Ely, at UCSD; Julie L. Fudge, at the University of Rochester; and Samuel M. McClure at Stanford.
Funding for this research came, in part, from the National Institutes of Health (grants R01-MH042984-17A1, R01-MH042984-18S1) and the Price Foundation.