Sarah Blake, Hugo Cannon, Saran Shantikumar
ADHD is associated with a substantial increase in functional GI symptoms, distinct from organic gastrointestinal disease. Possible mechanisms include gut microbiome dysbiosis, vagal dysregulation and behavioural contributors. Future research should differentiate intrinsic biological pathways from medication-related effects to improve clinical management.
INTRODUCTION: Attention-Deficit/Hyperactivity Disorder (ADHD) is a neurodevelopmental condition with rising prevalence worldwide. Although alterations in the gut-brain axis have been implicated in its pathophysiology, underlying mechanisms remain unclear. An increase of gastrointestinal (GI) symptoms is well documented in autism spectrum disorder, but the extent of GI involvement in ADHD has not yet been systematically evaluated.
AIM: To determine whether individuals with ADHD exhibit a higher prevalence of GI symptoms compared with neurotypical controls.
METHODS: Following PRISMA 2020 guidelines (PROSPERO: CRD42024602363) (Blake et al., 2024), we searched MEDLINE, Embase and APA PsycInfo (all via Ovid) up to 12 May 2026. We included primary studies involving participants of any age with a DSM- or ICD-defined ADHD diagnosis and reporting GI symptoms. Studies involving formally diagnosed organic GI disease (e.g., IBD) were excluded. Two independent reviewers conducted screening and quality appraisal using Joanna Briggs Institute (JBI) tools. Where appropriate, random-effects meta-analyses were performed for individual and composite GI symptoms.
RESULTS: From 9,613 records, 23 studies met inclusion criteria, representing over 1.9 million participants. ADHD was associated with increased odds of every GI symptom investigated, including total GI symptoms (OR 1.48, 95% CI [1.35, 1.62]), irritable bowel syndrome (OR 1.58, 95% CI [1.39, 1.78]), constipation (OR 1.97, 95% CI [1.49, 2.61]) and encopresis (OR 4.32, 95% CI [2.50, 7.47]).
CONCLUSION: ADHD is associated with a substantial increase in functional GI symptoms, distinct from organic gastrointestinal disease. Possible mechanisms include gut microbiome dysbiosis, vagal dysregulation and behavioural contributors. Future research should differentiate intrinsic biological pathways from medication-related effects to improve clinical management.