Children with autism spectrum disorders (ASD) or autism are more prone to gastrointestinal (GI) disorders than the general population. These disorders can significantly affect their health, learning, and development due to various factors such as genetics, environment, and behavior. The causes of GI disorders in children with ASD can include gut dysbiosis, immune dysfunction, food sensitivities, digestive enzyme deficiencies, and sensory processing differences. Many studies suggest that numerous children with ASD experience GI problems, and effective management is crucial. Diagnosing autism is typically done through genetic, neurological, functional, and behavioral assessments and observations, while GI tests are not consistently reliable. Some GI tests may increase the risk of developing ASD or exacerbating symptoms. Addressing GI issues in individuals with ASD can improve their overall well-being, leading to better behavior, cognitive function, and educational abilities. Proper management can improve digestion, nutrient absorption, and appetite by relieving physical discomfort and pain. Alleviating GI symptoms can improve sleep patterns, increase energy levels, and contribute to a general sense of well-being, ultimately leading to a better quality of life for the individual and improved family dynamics. The primary goal of GI interventions is to improve nutritional status, reduce symptom severity, promote a balanced mood, and increase patient independence.

In relation to dietary intervention in individuals with autism spectrum disorder (ASD), certain food constituents especially gluten and casein are recognized to be challenging and should be restricted. In this study, levels of glutathione S-transferase, glutathione, lipid peroxides, serotonin (5-HT), interleukin-6 (IL-6), glutamate, and gamma aminobutyric acid (GABA) were measured in the brain homogenates of ASD rodent model. Rats were treated either with single dose clindamycin (30 mg/kg) or with propionic acid (PPA) (250 mg/kg) for 3 days and then fed a standard diet, casein-rich diet (CRD), or gluten-rich diet (GRD). The obtained data demonstrates that clindamycin and PPA induced oxidative stress, which was slightly affected by CRD. A marked increase in the proinflammatory cytokine (IL-6) concentration found in clindamycin- and PPA-treated groups was lower in CRD fed rats. Both CRDs and GRDs produced similar trends in glutamate levels. 5-HT levels were higher in the clindamycin- and PPA-treated groups and increased with a GRD but were less affected by a CRD. CRD could be less deleterious compared to GRD. Although the underlying cause of gastrointestinal symptoms in patients with ASD is not exactly known, the most widely accepted one is the opioid theory which is related to GRD and CRD.

An expanding body of literature is examining connections between Autism Spectrum Disorder (ASD) and dietary interventions. While a number of specialist diets have been suggested as beneficial in ASD, gluten has received particularly close attention as a potentially exacerbating factor. Reports exist suggesting a beneficial effect of the gluten-free diet (GFD) in ameliorating behavioural and intellectual problems associated with ASD, while epidemiological research has also shown a comorbidity between ASD and coeliac disease. However, both caregivers and clinicians have expressed an uncertainty of the value of people with ASD going gluten-free, and as the GFD otherwise receives considerable public attention a discussion which focuses specifically on the interaction between ASD and gluten is warranted. In this review we discuss the historical context of ASD and gluten-related studies, and expand this to include an overview of epidemiological links, hypotheses of shared pathological mechanisms, and ultimately the evidence around the use and adoption of the GFD in people with ASD.