Abstract
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.
Highlights
Autism spectrum disorder (ASD) is characterized by varying degrees of neural dysfunction that lead to behavioral abnormalities including: stereotyped/repetitive behaviors, impairments in social interaction, lack of verbal and nonverbal language skills, insistence on routines and intense or idiosyncratic interests [1,2,3]
Impaired gut immune and digestive function, high levels of circulating dietary peptides, presence of autoantibodies that cross react with dietary proteins, increased levels of putrefactive metabolites with potent actions on gut and behavior, and the microbial patterns associated with ASD, such as high prevalence of clostridial species and high ratios of Firmicutes to Bacteroidetes, suggest that protein-driven microbial dysbiosis exacerbates both gastrointestinal and ASD symptoms
Proteolytic microbes that thrive off of incompletely digested dietary proteins produce byproducts such as ammonia, amines, phenols, and sulfides that have a negative effect on gut health [102] and brain function [120]
Summary
Autism spectrum disorder (ASD) is characterized by varying degrees of neural dysfunction that lead to behavioral abnormalities including: stereotyped/repetitive behaviors, impairments in social interaction, lack of verbal and nonverbal language skills, insistence on routines and intense or idiosyncratic interests [1,2,3]. In vitro stimulation of peripheral blood mononuclear cells from children with ASD with certain dietary proteins (including β-lactoglobulin and α-lactalbumin from cow’s milk and gliadin from wheat but not casein cow milk protein or soy protein) resulted in elevated pro-inflammatory cytokine production when compared to healthy controls as well as non-ASD controls with non-allergic food hypersensitivity [33, 34] Together, these observations suggest that overall gut immune function is altered and food antigens may provide a pro-inflammatory stimulus in children with ASD and gastrointestinal symptoms. These observations suggest that overall gut immune function is altered and food antigens may provide a pro-inflammatory stimulus in children with ASD and gastrointestinal symptoms It has been unclear whether these manifestations co-occur with the disorder, are a result of the abnormal neural functions that characterize the disorder, or are contributing to the etiology of the disease state. There are no studies directly assessing the level and activity of proteolytic digestive enzymes
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