Exploring Reward Sensitivity as a Central Mechanism in Binge-Eating Behavior

Binge eating, a transdiagnostic behavior present in both binge eating disorder (BED) and bulimia nervosa (BN), has increasingly been conceptualized as a manifestation of reward system dysregulation. Although BN is marked by compensatory behaviors and heightened emotional reactivity, BED is frequently associated with obesity, hormonal imbalance, and diminished inhibitory control. Despite their clinical relevance, the neurobiological substrates underpinning binge eating remain insufficiently integrated, particularly regarding the interplay between reward sensitivity, affective instability, and cognitive dysfunction.

The objective of this review was to propose an integrative theoretical model centered on reward sensitivity as a core mechanism underlying binge-eating behavior in BED and BN, synthesizing multidimensional evidence to support precision-based interventions across cognitive, emotional, neurobiological, and nutritional domains.

A comprehensive scoping review was conducted across PubMed, Web of Science, CrossRef, and Google Scholar, yielding 81 studies selected for methodological rigor, diagnostic specificity, and relevance to reward processing frameworks. Inclusion was guided by the Population, Intervention, Comparison, Outcome strategy and evaluated using the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system.

Evidence converges on a constellation of traits-impulsivity, negative urgency, and executive dysfunction-interacting with aberrant dopaminergic and serotonergic signaling. Reinforcement learning mechanisms, particularly model-free pathways, appear to mediate the transition from episodic to compulsive binge eating. Neuroimaging implicates frontostriatal and limbic circuits in reward anticipation and valuation.

The proposed integrative model identifies reward hypersensitivity as a central mechanism in binge-eating pathology, shaped by neurobiological, behavioral, nutritional, and environmental factors. Distinct profiles between BED and BN-especially in compensatory behaviors, hormonal signaling, and neuroplasticity-highlight the need for precision-based treatments, including neuromodulation, cognitive flexibility training, nutritional rehabilitation, and pharmacogenetic strategies.