Plain language summary
Children with autism spectrum disorder (ASD) display high incidence of gastrointestinal (GI) co-morbidities. Growing evidence now shows an association between diet and ASD, demonstrating that impaired gut function may worsen both GI and behavioural symptoms associated with ASD. The aim of this review was to examine the existing literature to further understand the connection between gut structure and function and ASD. This review found children with ASD and gut co-morbidities exhibit poor protein digestion, impaired gut-barrier integrity and a compromised gut microbiome. A potential mechanistic explanation is that the elevated level of undigested proteins is negatively affecting the integrity of the gut. Based on these findings, the authors conclude it is urgent to perform more experimental and clinical research on the “fragile gut” in children with ASD in order to move towards advancements in individualised clinical practice.
Children with autism spectrum disorders (ASD), characterized by a range of behavioral abnormalities and social deficits, display high incidence of gastrointestinal (GI) co-morbidities including chronic constipation and diarrhea. Research is now increasingly able to characterize the "fragile gut" in these children and understand the role that impairment of specific GI functions plays in the GI symptoms associated with ASD. This mechanistic understanding is extending to the interactions between diet and ASD, including food structure and protein digestive capacity in exacerbating autistic symptoms. Children with ASD and gut co-morbidities exhibit low digestive enzyme activity, impaired gut barrier integrity and the presence of antibodies specific for dietary proteins in the peripheral circulation. These findings support the hypothesis that entry of dietary peptides from the gut lumen into the vasculature are associated with an aberrant immune response. Furthermore, a subset of children with ASD exhibit high concentrations of metabolites originating from microbial activity on proteinaceous substrates. Taken together, the combination of specific protein intakes poor digestion, gut barrier integrity, microbiota composition and function all on a background of ASD represents a phenotypic pattern. A potential consequence of this pattern of conditions is that the fragile gut of some children with ASD is at risk for GI symptoms that may be amenable to improvement with specific dietary changes. There is growing evidence that shows an association between gut dysfunction and dysbiosis and ASD symptoms. It is therefore urgent to perform more experimental and clinical research on the "fragile gut" in children with ASD in order to move toward advancements in clinical practice. Identifying those factors that are of clinical value will provide an evidence-based path to individual management and targeted solutions; from real time sensing to the design of diets with personalized protein source/processing, all to improve GI function in children with ASD.