Maternal and Neonatal Vitamin D Concentrations and Autism Spectrum Disorders: Findings from the Stockholm Youth Cohort

Poster Presentation
Thursday, May 2, 2019: 11:30 AM-1:30 PM
Room: 710 (Palais des congres de Montreal)
B. K. Lee1, D. Eyles2, C. Magnusson3, C. J. Newschaffer4, J. McGrath5, D. Kvaskoff6, P. Ko5, C. Dalman7, H. Karlsson8 and R. Gardner3, (1)Epidemiology and Biostatistics, Drexel University, Philadelphia, PA, (2)Queensland Brain Institute, University of Queensland, St Lucia, Australia, (3)Karolinska Institutet, Stockholm, Sweden, (4)AJ Drexel Autism Institute, Philadelphia, PA, (5)Queensland Brain Institute, University of Queensland, Brisbane, Australia, (6)University of Queensland, Brisbane, Australia, (7)Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden, (8)Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden
Background: Animal studies indicate that early life vitamin D is crucial for proper neurodevelopment. Few studies have examined whether maternal and neonatal vitamin D concentrations influence risk of autism spectrum disorders (ASD).

Objectives: Determine whether vitamin D concentrations assessed during pregnancy and the neonatal period were associated with risk of ASD in a population-based electronic register and biomarker study taking place in Sweden.

Methods: Participants were sampled from the Stockholm Youth Cohort, a register-based cohort in Stockholm County, Sweden. Concentrations of total 25-hydroxyvitamin D (25OHD) were assessed from neonatal dried blood and maternal sera samples using a highly sensitive liquid chromatography tandem mass spectrometry method. The neonatal analytic sample consisted of 1,399 ASD cases and 1,607 controls. The maternal analytic subsample consisted of 449 ASD cases and 574 controls. The maternal-neonatal analytic subsample consisted of 340 ASD cases and 426 controls.

Results: Neonatal 25OHD sufficiency (≥50 nmol/L) was associated with 0.75 times the odds of ASD (95% CI: 0.57, 0.98) as compared with 25OHD deficiency (<25 nmol/L). Sibling-matched control analyses indicated these associations were not due to familial confounding. Maternal 25OHD sufficiency was associated with 0.65 times the odds of ASD (95% CI: 0.43, 0.96) as compared with 25OHD deficiency. Children with both maternal 25OHD and neonatal 25OHD above the median had 0.56 (95% CI: 0.34, 0.90) times the odds of ASD compared to children with maternal and neonatal 25OHD both below the median. In all analyses, the association between higher 25OHD and lower risk of ASD was much more evident in children with mothers born in Nordic countries than in children with mothers from elsewhere.

Conclusions: Higher concentrations of maternal and/or neonatal vitamin D were associated with lower odds of ASD. Our results are consistent with an increasing body of evidence suggesting that vitamin D in early life may influence risk of neurodevelopmental disorders including ASD.