Andre Sourander1, Subina Upadhyaya2, Heljä-Marja Surcel3, Susanna Hinkka-Yli-Salomäki2, Keely Cheslack-Postava4, Sanju Silwal2, Minna Sucksdorff5, Ian W McKeague6, Alan S Brown7. 1. Research Centre for Child Psychiatry, Department of Child Psychiatry, University of Turku, Turku, Finland; INVEST (Inequalities, Interventions and a New Welfare State) Research Flagship, University of Turku, Turku, Finland; Department of Child Psychiatry, Turku University Hospital, Turku, Finland; New York State Psychiatric Institute, Department of Psychiatry, Columbia University Irving Medical Center, New York, New York. Electronic address: andsou@utu.fi. 2. Research Centre for Child Psychiatry, Department of Child Psychiatry, University of Turku, Turku, Finland. 3. Faculty of Medicine, University of Oulu, Oulu, Finland; Biobank Borealis of Northern Finland, Oulu, Finland. 4. New York State Psychiatric Institute, Department of Psychiatry, Columbia University Irving Medical Center, New York, New York. 5. Research Centre for Child Psychiatry, Department of Child Psychiatry, University of Turku, Turku, Finland; Department of Pediatrics, Turku University Hospital, Turku, Finland. 6. Department of Biostatistics, Columbia University Mailman School of Public Health, New York, New York. 7. New York State Psychiatric Institute, Department of Psychiatry, Columbia University Irving Medical Center, New York, New York; Department of Epidemiology, Columbia University Mailman School of Public Health, New York, New York.
Abstract
BACKGROUND: Findings from previous studies on maternal 25-hydroxyvitamin D [25(OH)D] levels during pregnancy and autism spectrum disorder (ASD) in offspring are inconsistent. METHODS: The association between maternal 25(OH)D levels during pregnancy and offspring ASD was examined using data from a nationwide population-based register with a nested case-control study design. The ASD cases (n = 1558) were born between 1987 and 2004 and received a diagnosis of ASD by 2015; cases were matched with an equal number of controls. Maternal 25(OH)D levels during pregnancy were measured using quantitative immunoassay from maternal sera collected during the first and early second trimesters and archived in the national biobank of the Finnish Maternity Cohort. Conditional logistic regression examined the association between maternal 25(OH)D levels and offspring ASD. RESULTS: In the adjusted model, there was a significant association between increasing log-transformed maternal 25(OH)D levels and decreasing risk of offspring ASD (adjusted odds ratio [aOR] 0.75, 95% confidence interval [CI] 0.62-0.92, p = .005). Analyses by quintiles of maternal 25(OH)D levels revealed increased odds for ASD in the 2 lowest quintiles, <20 (aOR 1.36, 95% CI 1.03-1.79, p = .02) and 20-39 (aOR 1.31, 95% CI 1.01-1.70, p = .04), compared with the highest quintile. The increased risk of ASD was observed in association with deficient (<30 nmol/L) (aOR 1.44, 95% CI 1.15-1.81, p = .001) and insufficient (30-49.9 nmol/L) maternal 25(OH)D levels (aOR 1.26, 95% CI 1.04-1.52, p = .01) compared with sufficient levels. CONCLUSIONS: This finding has implications for understanding the role of maternal vitamin D during fetal brain development and increased risk of ASD.
BACKGROUND: Findings from previous studies on maternal 25-hydroxyvitamin D [25(OH)D] levels during pregnancy and autism spectrum disorder (ASD) in offspring are inconsistent. METHODS: The association between maternal 25(OH)D levels during pregnancy and offspring ASD was examined using data from a nationwide population-based register with a nested case-control study design. The ASD cases (n = 1558) were born between 1987 and 2004 and received a diagnosis of ASD by 2015; cases were matched with an equal number of controls. Maternal 25(OH)D levels during pregnancy were measured using quantitative immunoassay from maternal sera collected during the first and early second trimesters and archived in the national biobank of the Finnish Maternity Cohort. Conditional logistic regression examined the association between maternal 25(OH)D levels and offspring ASD. RESULTS: In the adjusted model, there was a significant association between increasing log-transformed maternal 25(OH)D levels and decreasing risk of offspring ASD (adjusted odds ratio [aOR] 0.75, 95% confidence interval [CI] 0.62-0.92, p = .005). Analyses by quintiles of maternal 25(OH)D levels revealed increased odds for ASD in the 2 lowest quintiles, <20 (aOR 1.36, 95% CI 1.03-1.79, p = .02) and 20-39 (aOR 1.31, 95% CI 1.01-1.70, p = .04), compared with the highest quintile. The increased risk of ASD was observed in association with deficient (<30 nmol/L) (aOR 1.44, 95% CI 1.15-1.81, p = .001) and insufficient (30-49.9 nmol/L) maternal 25(OH)D levels (aOR 1.26, 95% CI 1.04-1.52, p = .01) compared with sufficient levels. CONCLUSIONS: This finding has implications for understanding the role of maternal vitamin D during fetal brain development and increased risk of ASD.
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