Interaction of the Gut Microbiota and the Enteric Nervous System: Implications in Gastrointestinal Disorders Associated With Autism Spectrum Disorder.
Baptiste Ganachaud, María José Mendoza-León, Justine Marchix and 7 others
A narrative review links gut bacteria and their chemical byproducts to the nerves controlling digestion, offering a possible explanation for the constipation and stomach pain common in autism.
The evidence is almost entirely from mice; no human gut nerve tissue has been examined yet.
Key findings
1Gastrointestinal disorders occur 4.4 times more frequently in autistic children than in neurotypical children, with constipation the most common symptom, yet no histopathological study to date has examined the enteric nervous system in intestinal biopsies from people with ASD.
2Fecal microbiota transfer in small groups of children with ASD reported roughly 80% reduction in GI symptoms and improvements in behavioral symptoms persisting at least 8 weeks, but the authors note these studies lack adequate placebo controls and larger cohorts are needed before the finding can be considered established.
3Multiple bacterial metabolites—short-chain fatty acids, succinate, steroid hormones, bile acids, tryptophan derivatives, and tetrahydrobiopterin—have been shown in animal work to directly alter enteric neuron activity, density, or neurochemical profile, but the specific molecules responsible for ENS changes in ASD patients have not been identified.
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What it does not show
No human intestinal biopsy data on the enteric nervous system in ASD exists; all ENS structural evidence comes from mouse or zebrafish models. Animal model findings are inconsistent: different ASD gene mutations produce different ENS phenotypes, and some models show no ENS change at all. Fecal microbiota transfer studies are small, lack placebo or sham controls, and the authors themselves call for larger well-controlled trials. Short-chain fatty acid levels in ASD are reported as both increased and decreased across studies, so the direction of the metabolic disturbance is unclear. No single consistent microbial signature specific to ASD has been identified across studies. The review is narrative rather than systematic; no formal quality assessment or risk-of-bias evaluation of included studies was performed.
Declared interests
The authors declare no conflicts of interest. Funding came from French and Chilean government research agencies (ANR, ECOS-Sud, Conseil Régional des Pays de la Loire, FHU Exac.t, FONDECYT, ANID). No commercial or pharmaceutical sponsor is named.
Summarised by AI from the full paper, without a clinician reviewing it. Check it against the source before it changes what you do. Read it on PubMed →