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Neurosci Biobehav Rev. 2016 Apr;63:223-38. doi: 10.1016/j.neubiorev.2016.01.013. Epub 2016 Feb 2.

The neurobiological basis of binge-eating disorder.

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Department of Radiology, University of Alabama at Birmingham School of Medicine, 619 19th St. South, Birmingham, AL 35249, United States. Electronic address:
Shire, 300 Shire Way, Lexington, MA 02421, United States. Electronic address:
Shire, 300 Shire Way, Lexington, MA 02421, United States. Electronic address:
Department of Psychiatry, Department of Neurobiology, Child Study Center, CASAColumbia and Connecticut Mental Health Center, Yale University School of Medicine, 34 Park St., New Haven, CT 06519, United States. Electronic address:


Relatively little is known about the neuropathophysiology of binge-eating disorder (BED). Here, the evidence from neuroimaging, neurocognitive, genetics, and animal studies are reviewed to synthesize our current understanding of the pathophysiology of BED. Binge-eating disorder may be conceptualized as an impulsive/compulsive disorder, with altered reward sensitivity and food-related attentional biases. Neuroimaging studies suggest there are corticostriatal circuitry alterations in BED similar to those observed in substance abuse, including altered function of prefrontal, insular, and orbitofrontal cortices and the striatum. Human genetics and animal studies suggest that there are changes in neurotransmitter networks, including dopaminergic and opioidergic systems, associated with binge-eating behaviors. Overall, the current evidence suggests that BED may be related to maladaptation of the corticostriatal circuitry regulating motivation and impulse control similar to that found in other impulsive/compulsive disorders. Further studies are needed to understand the genetics of BED and how neurotransmitter activity and neurocircuitry function are altered in BED and how pharmacotherapies may influence these systems to reduce BED symptoms.


Binge-eating disorder; Cognition; Compulsivity; Impulsivity; Neuroimaging; Reward

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