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Updated: Apr 3, 2026

Studying Food Reward and Motivation in Humans
Published on: March 19, 2014
The microbiome and eating disorders: a new framework at the interface of interoception and reward
Isabella Ziade1, Meghan M McDermott1, Kenneth J O'Riordan1
1APC Microbiome Ireland, University College Cork, Cork T12 Y120, Ireland.
Abstract:
Accumulating evidence suggests that the gut microbiome can modulate brain processes and behaviours relevant to eating behaviour and reward signalling through the dynamic communication pathways of the microbiota-gut-brain-axis. Emerging evidence links altered gut microbial composition to disordered eating patterns, implicating the gut microbiome as a possible mechanism underlying eating disorders, as well as a potential therapeutic target for these conditions. In this review, we synthesise evidence across preclinical and clinical research to propose an integrated framework wherein the gut microbiome, interoception and reward circuits may interact to shape disordered eating behaviours. We firstly explore how microbial signals modulate homeostatic and reward feeding systems via vagal afferents, neurotransmitter modulation and immune-neural pathways, and how these signals converge in brain regions implicated in reward systems and interoception. Particular attention is given to how these interactions may occur in under- and over-eating phenotypes of disordered eating. The therapeutic potential of microbiota-targeted interventions to modulate eating disorder-induced dysregulations in interoception and reward signalling is discussed. Combined evidence suggests a paradigm shift in the etiological considerations of eating disorders is warranted, taking into account dysregulations of gut microbiota and its effects on reward processing and interoceptive signalling. Specifically, we propose that EDs are underpinned by dysregulations of gut microbiota, reward processing and interoceptive signalling, rather than neurobehaviour alone. The novel, integrated, and transdiagnostic framework posited in this review could represent a conceptual shift in the aetiological understanding of eating disorders with the potential to derive new neurobiological targets for intervention.
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