Researchers Show that CRF in the Amygdala is Responsible for Compulsive Overeating

in Uncategorized
June 10th, 2013

Researchers from Laboratory of Addictive Disorders at Boston University School of Medicine (BUSM) have shown that direct injection in the amygdala, an area of the brain involved in anxiety, of a drug which inactivates corticotropin-releasing factor (CRF), a hormone key mediator of anxiety and stress, completely blocks both the compulsive overeating and the anxiety generated by abstinence from junk food. The results of this study were recently published in the journal Neuropsychopharmacology.

The researchers observed that “diet-cycling” increased CRF, a hormone key mediator of anxiety, in the amygdala, an area of the brain involved in processing of emotions and responses to stress.

Pietro Cottone

Pietro Cottone

“Diet-cycling produces an elevation of CRF in the amygdala; this hormone causes a negative emotional affect which in turn drives overeating” said senior study author Pietro Cottone, PhD, assistant professor of Pharmacology and Psychiatry at BUSM as well as co-director of the Laboratory of Addictive Disorders. “The changes we observe in the brain of diet cyclers are strikingly reminiscent of the ones seen in drug addicts.”

Attilio Iemolo

Attilio Iemolo

“In this study, we wanted to determine whether blocking one of the receptors to which CRF binds, CRF1, in the amygdala could block both the negative emotional response and the excessive eating of junk food” added Attilio Iemolo, postdoctoral fellow in the Laboratory of Addictive Disorder and first author of the study. Therefore, researchers administered a CRF1 blocker drug into the amygdala, and observed that the anxiety and compulsive eating of diet cyclers were gone.

Also contributing to this study were Angelo Blasio, PhD; Stephen St. Cyr, BA; Kenner Rice, PhD; Valentina Sabino, PhD. The Laboratory of Addictive Disorders at BUSM is continuing this line of research to better understand the neurobiology of compulsive eating, with the hope of ultimately developing new therapeutic agents for the treatment of eating disorders and obesity.

Funding for this study was provided by the National Institute of Mental Health, the National Institute on Drug Abuse and the National Institute on Alcohol Abuse and Alcoholism. In addition, funding was made available by the Peter Paul Career Development Professorship and by Boston University’s Undergraduate Research Opportunities Program.