Nutrition and Disorders of Gut–Brain Interaction

Background: Disorders of gut–brain interaction (DGBIs) have a complex pathophysiology that is often characterized by a relationship between food ingestion and triggering of symptoms. Understanding of the underlying mechanisms and the role of nutrients as a therapeutic target are rapidly evolving. Ai...

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Bibliographic Details
Main Authors: Emidio Scarpellini, Lukas Michaja Balsiger, Bert Broeders, Karen Van Den Houte, Karen Routhiaux, Karlien Raymenants, Florencia Carbone, Jan Tack
Format: Article
Language:English
Published: MDPI AG 2024-01-01
Series:Nutrients
Subjects:
Online Access:https://www.mdpi.com/2072-6643/16/1/176
Description
Summary:Background: Disorders of gut–brain interaction (DGBIs) have a complex pathophysiology that is often characterized by a relationship between food ingestion and triggering of symptoms. Understanding of the underlying mechanisms and the role of nutrients as a therapeutic target are rapidly evolving. Aims and methods: We performed a narrative review of the literature using the following keywords, their acronyms, and their associations: nutrients, disorders of gut–brain interaction; functional dyspepsia; malabsorption; irritable bowel syndrome; diarrhea; constipation. Results: Functional dyspepsia displayed a significant correlation between volume, fat and/or wheat abundance, chemical composition of ingested food and symptoms of early satiety, fullness and weight loss. Carbohydrate malabsorption is related to enzyme deficiency throughout the GI tract. Food composition and richness in soluble vs. non-soluble fibers is related to constipation and diarrhea. The elimination of fermentable oligo-, di-, monosaccharides and polyols (FODMAPs) has a significant and non-unidirectional impact on irritable bowel syndrome (IBS) symptoms. Conclusions: Food volume, nutritive and chemical composition, and its malabsorption are associated with symptom generation in DGBIs. Further multicenter, randomized-controlled clinical trials are needed to clarify the underlying pathophysiology.
ISSN:2072-6643