The gut-brain axis in Binge Eating Disorder: From microbial dysbiosis to vagal dysfunction and therapeutic intervention

Binge Eating Disorder (BED), the most prevalent eating disorder worldwide, is characterized by recurrent episodes of uncontrolled food intake accompanied by marked psychological distress in the absence of regular compensatory behaviors. While behavioral and neurobiological frameworks have traditionally dominated research, converging evidence now positions the gut microbiota as a critical mediator of BED pathophysiology through bidirectional microbiota-gut-brain axis (MGBA) communication. This review synthesizes current knowledge of gut microbial remodeling in BED, elucidating how compositional alterations contribute to pathogenesis through disrupted satiety signaling, altered neurotransmitter metabolism, immune-inflammatory cascades, and vagal dysfunction. Recent evidence highlights BED-specific depletion of fermentative taxa, including Pediococcus, Catenibacterium, and Megasphaera, with depletion of Pediococcus correlated with reduced cardiac vagal tone. The mechanistic landscape encompasses short-chain fatty acid (SCFA)-mediated appetite modulation, α-MSH mimicry by bacterial caseinolytic protease B, serotonin and GABA pathways, and immune activation via lipopolysaccharide (LPS). Emerging microbiota-targeted therapeutic strategies, including prebiotics, probiotics, synbiotics, and fecal microbiota transplantation (FMT), are critically evaluated in light of current evidence from BED and related eating disorders. Despite the promising mechanistic rationale, rigorous clinical trials remain scarce. This review highlights several priorities for future research, and the development of precision medicine strategies integrating established therapeutic approaches with emerging microbiota-targeted interventions.