Parental Inflammatory Bowel Disease with Child Autism: A Comprehensive Review and Meta-Analysis.

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Bibliographic Details
Title: Parental Inflammatory Bowel Disease with Child Autism: A Comprehensive Review and Meta-Analysis.
Authors: Wang, Xingmu (AUTHOR), Qian, Chenfei (AUTHOR), Yao, Huanying (AUTHOR)
Source: Journal of Autism & Developmental Disorders. Oct2025, Vol. 55 Issue 10, p3662-3669. 8p.
Subjects: Autism risk factors, Risk assessment, Medical information storage & retrieval systems, CINAHL database, Meta-analysis, Descriptive statistics, Relative medical risk, Inflammatory bowel diseases, Systematic reviews, MEDLINE, Medical databases, Psychology of parents, Asperger's syndrome, Online information services, Confidence intervals, Psychology information storage & retrieval systems, Publication bias, Intergenerational relations, Children
Abstract: Inflammatory bowel disease (IBD) has been shown to be connected to a greater possibility of neurologically developed problems, such as autism spectrum disorders (ASDs). However, the proof linking parental IBD with ASD in offspring is inconclusive. Thus, we carried out a meta-analysis and comprehensive review to elucidate such linking. Prior research was identified through reviewing multiple internet-based sources, including Cochrane, Web of Knowledge, Embase, CINAHL, PubMed, and PsycINFO, from 1960 to December 2022. Pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) were determined employing random-effects models, in spite of the I2 statistic measurement of heterogeneity. Prediction intervals (PIs) have been presented to allow for more useful inferences and to indicate the range of genuine effects that might be predicted in future scenarios. Six studies (two case-control studies and four cohort studies) involving 3,200,199 participants were incorporated into the meta-analysis. The pooled RRs of ASDs among offspring of IBD parents were 1.15 (95% CI, 0.92 to 1.45, P = 0.226; I2 = 81.4%, P = 0.003; PI, 0.53–2.62), indicating no significant connection between parental IBD and the likelihood of ASDs in children. Type of IBD, and sex both also yielded no statistically significant results according to subgroup analysis. Our meta-analysis does not provide evidence that parental IBD is connected with the elevated likelihood of ASDs in their children. To confirm these results and understand their underlying mechanisms, additional research with larger sample sizes and improved study designs is required. [ABSTRACT FROM AUTHOR]
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Database: Psychology and Behavioral Sciences Collection
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Abstract:Inflammatory bowel disease (IBD) has been shown to be connected to a greater possibility of neurologically developed problems, such as autism spectrum disorders (ASDs). However, the proof linking parental IBD with ASD in offspring is inconclusive. Thus, we carried out a meta-analysis and comprehensive review to elucidate such linking. Prior research was identified through reviewing multiple internet-based sources, including Cochrane, Web of Knowledge, Embase, CINAHL, PubMed, and PsycINFO, from 1960 to December 2022. Pooled relative risks (RRs) and corresponding 95% confidence intervals (CIs) were determined employing random-effects models, in spite of the I2 statistic measurement of heterogeneity. Prediction intervals (PIs) have been presented to allow for more useful inferences and to indicate the range of genuine effects that might be predicted in future scenarios. Six studies (two case-control studies and four cohort studies) involving 3,200,199 participants were incorporated into the meta-analysis. The pooled RRs of ASDs among offspring of IBD parents were 1.15 (95% CI, 0.92 to 1.45, P = 0.226; I2 = 81.4%, P = 0.003; PI, 0.53–2.62), indicating no significant connection between parental IBD and the likelihood of ASDs in children. Type of IBD, and sex both also yielded no statistically significant results according to subgroup analysis. Our meta-analysis does not provide evidence that parental IBD is connected with the elevated likelihood of ASDs in their children. To confirm these results and understand their underlying mechanisms, additional research with larger sample sizes and improved study designs is required. [ABSTRACT FROM AUTHOR]
ISSN:01623257
DOI:10.1007/s10803-024-06458-4