Abstract:

Autism spectrum disorder (ASD) is a neurodevelopmental condition. In addition to core symptoms like social impairments and restricted repetitive behaviors, about half of individuals with ASD also experience gastrointestinal symptoms and inflammatory bowel disease (IBD). IBD is a kind of chronic disease associated with immune dysregulation, gut microbiome alterations, micronutrient malabsorption and anaemia, which may be perinatal factors associated with ASD. It's likely that comorbidities like IBD are diagnosed in children with ASD.

This article examines the relationship between IBD and ASD in children by analyzing the relevant domestic and foreign literature. Firstly, the results of the analysis indicate a considerable correlation between childhood IBD and ASD; nevertheless, the effect of ASD on IBD seems to be greater than that of IBD on ASD in children, necessitating more thorough study to substantiate this claim. Secondly, we provide explanations for the potential causes of the lack of a genetic correlation between juvenile ASD and IBD. Furthermore, we analyze the differences in the results between the two phases of the study from the perspective of parental IBD and childhood ASD, and we also suggest possible factors that might have affected this outcome. Finally, in terms of the therapeutic approach, we think that treating IBD in children can have an impact on ASD. To achieve this, we are attempting to implement a strategy that combines multiple therapeutic approaches, such as a combination of nutritional therapy and basic medication, treatment with biologics, and behavioral or psychological interventions.

The following aspects may need to be considered in future research: First, additional empirical evidence is required to support the claim that there is a causal association between ASD and IBD rather than reverse causality. The quantity of samples involved, age, ASD and IBD diagnosis criteria, severity, and analytic models employed will all affect the final experimental conclusions. Therefore, in order to get more persuasive results, it is important to make the elements impacting the confirmation of forward or reverse causality as consistent as feasible. Second, in order to avoid bias in experimental results caused by ignoring the influence of any of these components, the genetic association between IBD and ASD should be established by taking into account the roles of dominant genes, recessive genes, and environmental factors. Third, despite earlier research demonstrating a connection between ASD and IBD, the pathophysiological processes underlying the two conditions remain unclear. Using bioinformatics methods to explore potential regulatory factors, follow-up studies could examine the pathophysiology and common influencing factors of both disorders. Fourth, it's challenging to figure out if childhood ASD and parental IBD are causally related. In order to prove the association, further and more conclusive investigations will be required in the future due to the divergent opinions found in the present studies. Furthermore, while investigating this relationship, we should take into account the roles performed by the mother and father as well as control for or exclude out the influence of additional factors that may result in childhood ASD. Specific requirements for sample selection and classification should also be followed. Fifth, there's a possibility that clinicians' diagnosis of IBD symptoms in children's ASD and IBD research was inadequate. Future research may consequently require to develop a more objective way to diagnose IBD symptoms through clinical diagnosis, the use of Bristol Stool Scale and so on.

In conclusion, this article may offer novel ideas and approaches for investigating the etiology of ASD in children as well as for clinical therapy, since it examines the connection between IBD and ASD and offers some potential strategies for intervening in children's ASD through the treatment of IBD.

Key words: Autism spectrum disorder, inflammatory bowel disease, Crohn’s disease, ulcerative colitis