AURORA, Colo. – Bulimia nervosa is a severe
eating disorder associated with episodic binge eating followed by extreme
behaviors to avoid weight gain such as self-induced vomiting, use of laxatives
or excessive exercise. It is poorly understood how brain function may be
involved in bulimia.

A new study led by Guido Frank, MD, assistant professor, Departments
of Psychiatry and Neuroscience and Director, Developmental
Brain Research Program
at the University of Colorado Anschutz Medical
Campus, studied the brain response to a dopamine related reward-learning task
in bulimic and healthy women.

Dopamine is an important brain chemical or
neurotransmitter that helps regulate behavior such as learning and motivation. Frank
found that bulimic women had weakened response in brain regions that are part
of the reward circuitry. This response was related to the frequency of
binge/purge episodes. Overeating and purging episodes thus could cause such a
weaker response and set off a vicious cycle of altered brain function.

findings are important for several reasons.

First, they directly implicate the
brain reward system and related dopamine function in this disorder.

bulimic behavior appears to directly affect brain reward function and it is
uncertain whether such alterations return to normal with recovery or not.

Third, brain dopamine could be a treatment target in bulimia nervosa using
specific medication that targets those abnormalities.

“This is the first study that suggests that brain dopamine
related reward circuitry, pathways that modulate our drive to eat, may have a
role in bulimia nervosa. We found reduced activation in this network in the
bulimic women, and the more often an individual had binge/purge episodes the
less responsive was their brain. That suggests that the eating disorder
behavior directly affects brain function. These findings are important since the
brain dopamine neurotransmitter system could be an important treatment target
for bulimia nervosa,” said Frank.

This study was published in Biological
June 28, 2011.​

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