Sugar Addiction and BED: Elucidating Pathological Mechanisms and Therapeutic Strategies

Given the lack of systematic comparisons of neurobiological mechanisms and translatable therapeutic strategies between sugar addiction and binge eating disorder (BED), and the urgent need to address sugar-related metabolic and psychiatric comorbidities, this review aims to fill this gap and highlight the clinical and public health relevance of this comparison. This review examined the neurobiological parallels between sugar addiction and binge eating disorder (BED), highlighting shared dysregulations in dopaminergic, opioid, and GLP-1 systems, particularly within prefrontal-striatal-limbic circuits. Based on shared dysregulations in reward circuitry , opioid system downregulation , and hypothalamic POMC neuron dysfunction, we discussed the potential of repurposing investigational BED pharmacotherapies—such as lisdexamfetamine, naltrexone/bupropion, GLP-1 receptor agonists, and topiramate-for sugar addiction treatment. These agents are proposed to modulate neurotransmitter release, receptor activity, and neural network function to reduce cravings, impulsive feeding, and reward-seeking behaviors. Despite its high prevalence and significant adverse health consequences, sugar addiction remains unrecognized in major diagnostic systems (e.g., DSM-5 or ICD-11), limiting targeted therapeutic development. We underscore the necessity for additional mechanistic investigations and stringently designed clinical trials to transform these initial observations into validated, evidence-based treatment approaches. Future work should incorporate biotechnology-enabled approaches, such as neurocircuit-specific intervention strategies, biomarker-guided patient stratification, and rigorously designed clinical trials, to validate and translate these preliminary findings into evidence-based treatments.