Background Exposure to elevated levels of inflammatory markers during pregnancy has been suggested as possible aetiologic factor in the occurrence of autism spectrum disorder (ASD). In this study, we investigated the prospective relation between maternal C-reactive protein (CRP) during early pregnancy and children's autistic traits in the general population. Methods In a large population-based cohort in the Netherlands, we measured maternal CRP levels before 18 weeks of gestation (N = 4165). Parents reported on their children's autistic traits at age 6 years using the Social Responsiveness Scale, and the Pervasive Developmental Problem scale. Regression models were used to examine the relation between maternal CRP levels and autistic traits in children. Results Compared with the reference group (CRP < 2.3 mg/L), elevated levels of CRP (>7.8 mg/L) in pregnant women were associated with higher Social Responsiveness Scale scores in children [β = 0.055, 95% confidence interval (CI) 0.033, 0.078]; however, the effect was strongly attenuated after adjustment for several socioeconomic factors and in particular by maternal health-related factors including body mass index (fully adjusted model β = 0.018, 95% CI -0.005, 0.042). We found no relation between maternal CRP levels and pervasive developmental problem. Conclusions Our results suggest that the association between elevated levels of maternal CRP in pregnancy and autistic traits in children is confounded by maternal health-related and socioeconomic factors. Further studies are needed to explore whether other maternal inflammatory markers during pregnancy, as a response to maternal inflammation, are associated with the development of autistic traits in the offspring.

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Paediatric and Perinatal Epidemiology (Print)
Generation R Study Group

Koks, N., Ghassabian, A., Greaves-Lord, K., Hofman, A., Jaddoe, V., Verhulst, F., & Tiemeier, H. (2016). Maternal C-Reactive Protein Concentration in Early Pregnancy and Child Autistic Traits in the General Population. Paediatric and Perinatal Epidemiology (Print), 30(2), 181–189. doi:10.1111/ppe.12261