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Maternal pre-pregnancy body mass index and gestational weight gain with the risk of autism spectrum disorder and autistic traits among offspring
Dissertation   Open access

Maternal pre-pregnancy body mass index and gestational weight gain with the risk of autism spectrum disorder and autistic traits among offspring

Xi Wang
Doctor of Philosophy (Ph.D.), Drexel University
Jun 2018
DOI:
https://doi.org/10.17918/5g8c-th49
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Abstract

Autism spectrum disorders Pregnant women--Weight gain Autism--Etiology Body mass index Epidemiology
Objective: The objective of this project was to examine whether maternal pre-pregnancy body mass index (BMI) and gestational weight gain (GWG) are risk factors for autism spectrum disorders (ASD) and ASD-related symptoms (autistic traits) among offspring, and whether adverse obstetric outcomes can account for these associations. Methods: We used data from two population-based cohorts, the Avon Longitudinal Study of Parents and Children (ALSPAC) and the Stockholm Youth Cohort (SYC). The main-effect analysis included a sample of 11,199 mother-child pairs from the ALSPAC, a prospective cohort of births in the Bristol area of UK in 1991-1992. Children with ASD diagnosis were identified from multiple sources, including linkage to medical records, an educational database, and parental reports. The autistic traits included four individual measures (e.g., child's score of the Social and Communication Disorders Checklist) and seven standardized autistic factor scores that were derived from a previous factor analysis. The mediation analysis included a sample of 335,993 mother-child pairs from the Stockholm Youth Cohort, a record-linkage cohort comprising children born 1984-2007 and residing in Stockholm County, Sweden. ASD cases were identified from four national and regional registers. Potential mediators considered were adverse obstetric outcomes, including preterm birth, maternal complications during pregnancy (gestational diabetes, gestational hypertension, preeclampsia, eclampsia), cesarean section delivery, suction-assisted delivery, tongs-assisted delivery, and adverse neonatal outcomes (low birth weight, low Apgar score at 5 minutes after birth, small-/large-for-gestational-age). We used two mediation analysis methods under the counterfactual framework-G-computation method was used to analyze each mediator one at a time, and a weighting-based method was used to estimate the joint effect of multiple mediators. Results: In the ALSPAC, children born to obese mothers had lower (indicating worse performance and higher risk for ASD) mean factor scores of verbal abilities (beta estimate -0.11, 95% CI -1.19, -0.02), language acquisition (-0.09, 95% CI -0.18, -0.01) and semantic-pragmatic skills (-0.25, 95% CI -0.33, -0.17), compared to children born to normal-weight mothers. There was no evidence that maternal pre-pregnancy BMI was associated with other autistic trait measures nor the ASD diagnosis. In the SYC, we found that a small proportion of the total effect of insufficient GWG on offspring ASD was mediated by preterm birth, low birth weight, and small-for-gestational-age. For example, 15% of the total effect of insufficient GWG on ASD was mediated by low birth weight. There is no evidence showing that the total effect of pre-pregnancy overweight or obesity on offspring ASD risk were mediated by adverse obstetric outcomes. Conclusion: In a large population-based, birth cohort in the UK, we found weak associations between maternal pre-pregnancy overweight/obesity and offspring autistic traits that characterize the deficits in communication. We found no evidence supporting a relationship of maternal pre-pregnancy BMI and GWG with the risk of offspring ASD diagnosis. In a large prospective, register-based cohort in Sweden, we found some evidence that preterm, low birth weight, and small-for-gestational-age birth might partly account for the effect of insufficient GWG on offspring ASD risk. Given the complex manifestations of ASD, future studies on the relationship of maternal obesity and GWG with ASD should expand the outcome measures to dimensional autistic traits characterizing different components of ASD symptoms. It is also warranted for future studies on ASD etiology to apply mediation analysis methods under the counterfactual framework to explore the mechanisms underlying the effect of a risk factor for ASD.

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