Beyond emotional hunger: exploring the microbiota-gut-brain axis as a proposed mechanistic framework for emotional eating

Emotional eating (EE), characterized by food intake in response to affective states rather than physiological hunger, has traditionally been conceptualized through psychological models of stress, emotion dysregulation, and reward-driven behaviour. These frameworks, however, do not fully explain interindividual differences in vulnerability or the persistence of maladaptive eating patterns. This narrative review critically examines the microbiota–gut–brain axis as a potential mechanistic framework linking psychological, neurobiological, and nutritional determinants of emotional eating. Evidence from psychology, neuroscience, microbiology, and nutritional psychiatry is integrated to evaluate the roles of hypothalamic–pituitary–adrenal axis activation, reward processing, neurotransmitter metabolism, immune signaling, appetite-related hormones, and microbial metabolites. Emerging findings suggest that gut microbial composition and function may influence mood, stress responsivity, food craving, and eating behaviour through neural, endocrine, immune, and metabolic pathways. Most of this evidence, however, derives from animal models, mechanistic in vitro work, or human studies of stress, depression, obesity and general appetite regulation; comparatively few studies have measured emotional eating itself as an outcome, and the pathways described should therefore be read as candidate rather than established mechanisms. Dietary patterns may further modify these interactions by shaping microbial diversity, inflammatory tone, and metabolite production. Although current evidence is consistent with a plausible bidirectional relationship between gut–brain signaling and emotional eating, direct causal evidence in humans remains limited and the direction of the association is unresolved. EE should therefore be understood as a multidimensional biopsychological phenomenon. Future longitudinal and intervention studies are needed to clarify causal pathways and evaluate integrated psychological, nutritional, and microbiome-targeted strategies for personalized prevention and management in diverse clinical populations.