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Results for “disorders of gut-brain interaction”

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PubMed2026

Putting Globus Into Context: Prevalence, Characteristics, and Overlap With Other Disorders of Gut-Brain Interaction.

OBJECTIVE: Globus is characterized by the sensation of a lump in the throat without dysphagia or underlying structural abnormality or major motility disorder. Reported prevalences vary considerably across studies. Globus has been linked to both heartburn and affective disorders. This study aims to determine the global prevalence of globus, its association with heartburn, overlap with disorders of gut-brain interaction (DGBI) and psychosocial disorders, and its impact on health-related quality of life (HRQOL). METHODS: Internet surveys from the Rome Foundation Global Epidemiology study were used (N = 54,127). Rome IV criteria were used to identify globus and concurrent DGBI. Heartburn was defined as symptoms ≥ 2-3 days/week. Psychosocial co-morbidity and somatic symptom severity were assessed with PHQ-4 and PHQ-15, and HRQOL by PROMIS-10. RESULTS: The global prevalence of globus according to Rome IV criteria was 0.75%, representing 12.8% of esophageal DGBI and 1.86% of all DGBI. Prevalence was highest in Western Europe (0.94%) and Asia (0.90%), and lowest in the Middle East (0.31%). Globus was slightly more common in females (55.4%), and most affected individuals were aged between 40 and 64 years (46.6%). Coexisting heartburn was reported in 17.4% of cases, esophageal DGBI in 9.1%, and non-esophageal DGBI in 49.0%. Anxiety and/or depression was present in 60.5%. CONCLUSION: Global prevalence of globus is 0.75%, with a slight female predominance, and is most prevalent below 65 years. Overlap with non-esophageal DGBI was greater than with heartburn symptoms or esophageal DGBI, and most patients had anxiety and/or depressive symptoms.

Humans↗

PubMed2025

Psychological Resilience and Mental Wellbeing Mitigate the Risk of Irritable Bowel Syndrome.

INTRODUCTION: Comorbidities between mental disorders and irritable bowel syndrome (IBS) have been widely reported, yet associations between mental wellbeing and IBS, particularly regarding underlying genetic modification and proteomic signatures, remain underexplored. METHODS: This prospective cohort study analyzed 75,842 IBS-free participants aiming to investigate the prospective association between mental wellbeing and the risk of IBS in UK Biobank. Mental wellbeing was assessed through life satisfaction, positive affect, neuroticism, and depressive/anxiety symptoms. Cox models evaluate the hazard ratio (HR) for mental wellbeing and plasma proteome in relation to incident IBS during follow-up. Proteomic profiling identified mental wellbeing-associated proteins, with pathway enrichment analysis revealing biological mechanisms. Mediation and Mendelian randomization analyses further examine intermediate pathways and causality. RESULTS: With a 12.4-year follow-up period, 1,400 cases of incident IBS were documented. Better mental wellbeing mitigated IBS risk dose-dependently (low risk group: HR, 0.37; 95% confidence interval [CI]: 0.31-0.43). Higher life satisfaction (HR, 0.41; 95% CI: 0.30-0.56) and positive affect (HR, 0.50; 95% CI: 0.41-0.62) were inversely associated with IBS risk, whereas neuroticism (HR, 2.35; 95% CI: 1.92-2.88) and depressive/anxiety symptoms (HR, 3.09; 95% CI: 2.17-4.42) increased the risk. Findings remained consistent in across prevalent IBS and IBS subtypes. Mental wellbeing effects were independent of genetic predisposition. Mediation analyses revealed about 27% of protective effect of mental wellbeing were mediated through reduced depression and anxiety. Mendelian randomization supports causal protective effects of positive mental wellbeing on IBS. Proteomic profiling identified mental wellbeing-associated proteins mainly enriched in cytokine-cytokine receptor interactions. Chromogranin A and gastrin emerged as key protein biomarkers, showing significant associations with both mental wellbeing components and IBS risk. DISCUSSION: Our study demonstrates that enhanced mental wellbeing confers substantial protection against IBS development, highlighting psychological interventions as potential primary prevention strategies.

Humans↗

PubMed2026

Efficacy of pharmacological and microbiota-based therapies in preclinical models of autism spectrum disorder: a systematic review.

BACKGROUND: Autism spectrum disorder (ASD) is a multifactorial neurodevelopmental condition in which pharmacological and microbiota-targeted interventions are emerging as promising therapeutic avenues. Animal models are the main tool to investigate etiology, molecular mechanisms and screening for pharmacological therapies. Methodological differences, outcome measure variability, incomplete reporting, biological confounders, and overgeneralization of the results made evaluating innovative pharmacological agents challenging. These limitations in the field highlight a need for systematic and standardized research to reliably assess and translate pharmacological interventions from ASD animal models to human clinical relevance. SUBJECTS: This systematic review synthesized efficacy evidence for pharmacological and microbiota-based therapies across established ASD animal models. RESULTS: We identified 52 recent (2010-2025) studies that reported key ASD behavioral outcomes after pharmacological or microbiota-focused treatments. Interventions were grouped into therapeutic classes - including oxytocinergic agents, E/I balance therapeutic targets, metabolic drugs, cannabinoids, purine-based interventions and emerging targets - alongside microbiota-directed strategies such as probiotics, prebiotics, and fecal microbiota transplantation. By integrating effect directions and robustness across models, we identified most potential drug candidates, evaluated the efficacy of novel strategies, and recognized critical translational gaps. The reviewed studies demonstrate that ASD-like behavioral deficits in preclinical models can be modulated through interventions targeting diverse biological systems, including neurotransmission, neuroinflammation, metabolism, and the gut-brain axis. CONCLUSIONS: These findings support the multifactorial nature of ASD pathophysiology which arises from a network of interacting systemic processes rather than a single molecular defect. It could explain the limited success of traditionally narrowly targeted interventions and suggest a paradigm shift into a more systemic approach.

Animals↗