Gut microbes reportsOct 28, 2026

Gut and brain links in Binge Eating Disorder: From unhealthy gut bacteria to nerve problems and possible treatments

Gut-Brain Axis Weekly Brief ↗PubMed ↗DOI ↗OA ↗

Updated Oct 29, 2026

Abstract

Binge Eating Disorder (BED) is characterized by recurrent episodes of uncontrolled food intake, with evidence suggesting that gut microbiota may play a critical role in its pathophysiology.

The gut microbiota is linked to BED through communication along the microbiota-gut-brain axis.
Alterations in gut microbial composition are associated with disrupted satiety signaling and changes in neurotransmitter metabolism.
Specific taxa such as Pediococcus, Catenibacterium, and Megasphaera are depleted in individuals with BED, with Pediococcus depletion linked to lower cardiac vagal tone.
Mechanisms involved include appetite modulation by short-chain fatty acids, mimicry of neuropeptides by bacterial proteins, and immune activation via lipopolysaccharides.
Current microbiota-targeted therapeutic strategies for BED include prebiotics, probiotics, synbiotics, and fecal microbiota transplantation, though clinical trial evidence is limited.

Simplified

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.

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Gut and brain links in Binge Eating Disorder: From unhealthy gut bacteria to nerve problems and possible treatments

Abstract

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