Microbiota-gut-brain axis in binge-eating disorder: Towards microbiome-based therapies

Abstract

Binge-eating disorder (BED) is the most common eating disorder, but the mechanisms that underlie this disorder are still largely unknown. There is tentative evidence to suggest that the gut microbiota, which communicates to the brain via the gut-brain axis, plays a role in the pathogenesis of BED. However, more mechanistic research is urgently required to gain greater clarity and inform the development of superior management strategies. In this review, we sought to develop a new conceptual model that incorporates the gut microbiota to provide valuable guidance for future research in this area. In BED, the large quantities of hyper-palatable, energy-dense foods rapidly consumed reduces microbial diversity and their associated metabolites alongside promotions in microbial volatility and inflammation. These dietary-induced effects on the microbiota alter pathways implicated in BED including satiety, reward, impulsivity, and mood. The biological mechanisms underpinning the psychological effects include actions of microbial components and metabolites, alongside effects on the hypothalamic-pituitary-adrenal axis and the dopaminergic and serotonergic systems. Importantly, individual baseline characteristics such as genetics and environmental stressors can moderate the relationship between one's diet, the gut microbiota, and BED. A growing body of evidence suggests that microbiota-targeted interventions, so called psychobiotics, may affect these pathways to modulate brain and behaviour. While further research is necessary to test this hypothesis, the gut microbiota represents a novel avenue for future BED therapeutics.

Keywords: Binge-eating disorder; Diet; Mechanisms; Microbiota-gut-brain axis; Psychology.

Graphical abstract

Fig. 1

Model of binge-eating disorder. Dietary behaviours observed in binge-eating disorder (BED) including increased consumption of high-fat, high-sugar, energy-dense foods eaten rapidly typically offset by periods of healthier eating disrupt gut microbial diversity and stability, in turn reducing beneficial bacteria and associated metabolites. Such perturbances to gut microbiota alters areas of the central nervous system (CNS) implicated in BED – satiety, reward, impulsivity, and negative affect – underpinned by inflammation and actions of microbial components and byproducts acting on the hypothalamic-pituitary adrenal axis (HPA), dopaminergic (DA), and serotonergic system (5-HT). Individual characteristics such as genetics and stress moderate the gut microbiota and BED relationship. SCFA: short-chain fatty acids, GLP-1: glucagon-like peptide 1, CCK: Cholecystokinin, GABA: Gamma aminobutyric acid.