Binge eating disorder and obesity are commonly approached through psychiatric, nutritional or metabolic frameworks, yet their clinical complexity increasingly suggests a deeper neurobiological dysregulation involving reward processing, interoceptive awareness, executive control and brain–body signaling. This Perspective proposes that binge eating and selected obesity phenotypes may be conceptualized as disorders of reward–interoception integration, in which highly salient food cues, dopaminergic motivational drive, altered hunger–satiety perception and impaired prefrontal inhibition may converge to increase vulnerability to loss-of-control eating. Within this framework, the insula, anterior cingulate cortex, salience network, mesolimbic reward circuitry and dorsolateral prefrontal cortex represent key neural nodes linking bodily signals, affective arousal, craving and behavioral regulation. Recent advances in glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic polypeptide/glucagon-like peptide-1 (GIP/GLP-1) receptor agonist therapies further support a brain–body model of ingestive behavior, suggesting that metabolic signals may be associated not only with appetite and satiety, but also with food craving, reward valuation and cue reactivity. In parallel, non-invasive neuromodulation, particularly prefrontal transcranial magnetic stimulation, offers a promising but still investigational strategy to potentially enhance inhibitory control and reduce craving-related vulnerability. The future treatment of binge eating and selected obesity phenotypes may benefit from an integrated neuropsychiatric approach combining incretin-based pharmacotherapy, neuromodulation, psychotherapy, clinical nutrition and digital craving monitoring. Moving beyond exclusively weight-centered models, this Perspective argues for a network-centered understanding of dysregulated eating as a condition of altered communication between reward, body, metabolism and executive control.