The neurobiological basis of binge-eating disorder

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...

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Published inNeuroscience and biobehavioral reviews Vol. 63; pp. 223 - 238
Main Authors Kessler, Robert M., Hutson, Peter H., Herman, Barry K., Potenza, Marc N.
Format Journal Article
LanguageEnglish
Published United States 01.04.2016
Subjects
Animals
Attention
Binge-Eating Disorder - genetics
Binge-Eating Disorder - physiopathology
Binge-Eating Disorder - psychology
Brain - physiopathology
Cognition - physiology
Decision Making - physiology
Dopamine - metabolism
Dopamine - physiology
Female
Humans
Impulsive Behavior - physiology
Male
Motivation
Receptors, Dopamine D2 - genetics
Receptors, Dopamine D2 - physiology
Reward
Compulsivity
Neuroimaging
Impulsivity
Cognition
Reward
Binge-eating disorder
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Summary: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.
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ISSN:0149-7634
1873-7528
DOI:10.1016/j.neubiorev.2016.01.013