Hypothesis paper proposes enteric neural contribution to food cravings, highlighting nutrient-gut-brain links.
This hypothesis paper explores whether enteric neural integration may contribute to the emergence of certain nutrient-specific food cravings. Current evidence indicates that the gastrointestinal tract is not merely a passive digestive organ. Enteroendocrine and neuropod cells can communicate rapidly with vagal afferents, different nutrients can engage partly distinct gut-brain pathways, and nutrient exposure can activate differentiated enteric neuronal ensembles. However, these findings do not demonstrate that the enteric nervous system independently generates conscious food cravings. The proposed model distinguishes between post-ingestive nutrient-linked appetitive drives and fasting-associated cravings. It suggests that enteric circuits may contribute to post-ingestive learning, physiological biasing, and the calibration of nutrient-related preferences. It further examines whether repeated nutrient exposure could induce nutrient-conditioned enteric plasticity, forming part of a distributed gut-brain memory mechanism that may influence cravings during fasting. The article presents testable predictions, experimental strategies involving blinded intragastric nutrient infusion, enteric neuronal mapping, vagal modulation, microbiome analysis, behavioural testing, and neuroimaging, as well as explicit conditions under which the hypothesis would be weakened or rejected.
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Narcis Somesfalean (2026) studied this question.
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