Neurocircuit function in eating disorders
Article first published online: 9 MAY 2013
Copyright © 2013 Wiley Periodicals, Inc.
International Journal of Eating Disorders
Special Issue: Transformational Science, Transformational Practice: A Special Issue Dedicated to Michael Strober, Editor-In-Chief from 1983 to 2012.
Volume 46, Issue 5, pages 425–432, July 2013
How to Cite
Friederich, H.-C., Wu, M., Simon, J. J. and Herzog, W. (2013), Neurocircuit function in eating disorders. Int. J. Eat. Disord., 46: 425–432. doi: 10.1002/eat.22099
- Issue published online: 9 MAY 2013
- Article first published online: 9 MAY 2013
- Manuscript Accepted: 12 DEC 2012
- anorexia nervosa;
- bulimia nervosa;
- binge eating disorder;
- neural control of food intake;
- functional magnetic resonance imaging;
- positron emission tomography
Eating disorders are serious psychosomatic disorders with high morbidity and lifetime mortality. Inadequate response to current therapeutic interventions constitutes a challenging clinical problem. A better understanding of the underlying neurobiological mechanisms could improve psychotherapeutic and drug treatment strategies.
A review highlighting the current state of brain imaging in eating disorders related to the anxiety and pathological fear learning model of anorexia nervosa (AN) and the impulsivity model of binge eating in bulimia nervosa (BN).
Available neuroimaging studies in patients with acute AN primarily suggest a hyper-responsive emotional and fear network to food, but not necessarily to eating disorder-unrelated, salient stimuli. Furthermore, patients with AN show decreased activation in the ventral fronto-striatal circuits during the performance of a cognitive flexibility task. Results in patients with BN primarily suggest a hypo-responsive reward system to food stimuli, especially to taste reward. Additionally, patients with BN exhibit impaired brain activation in the inhibitory control network during the performance of general response–inhibition tasks.
Anxiety and pathological fear learning may lead to conditioned neural stimulus-response patterns to food stimuli and increased cognitive rigidity, which could account for the phobic avoidance of food intake in patients with acute AN. However, further neurobiological studies are required to investigate pathological fear learning in patients with AN. Patients with BN may binge eat to compensate for a hypo-responsive reward system. The impaired brain activation in the inhibitory control network may facilitate the loss of control over food intake in patients with BN. © 2013 by Wiley Periodicals, Inc. (Int J Eat Disord 2013; 46:425–432)