Prenatal Nutrition and Risk of Child ASD: Findings and Updates from the Stockholm Youth Cohort

Oral Presentation
Thursday, May 10, 2018: 10:30 AM
Arcadis Zaal (de Doelen ICC Rotterdam)
B. K. Lee1, C. Dalman2, H. Karlsson3, E. A. DeVilbiss4, D. Rai5, C. J. Newschaffer6, J. McGrath7, D. Eyles8 and C. Magnusson9, (1)Epidemiology and Biostatistics, Drexel University, Philadelphia, PA, (2)Department of Public Health Sciences, Karolinska Institutet, Stockholm, Sweden, (3)Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden, (4)Drexel University, Philadelphia, PA, (5)Population Health Sciences, Bristol Medical School, Centre for Academic Mental Health, Bristol, United Kingdom, (6)AJ Drexel Autism Institute, Philadelphia, PA, (7)Queensland Brain Institute, University of Queensland, Brisbane, Australia, (8)Queensland Brain Institute, University of Queensland, St Lucia, Australia, (9)Karolinska Institutet, Stockholm, Sweden

Early life nutrition is critical for proper neurodevelopment. Whether this paradigm extends to risk of autism spectrum disorders (ASD) is not established.


Our goals were to assess whether prenatal nutritional factors, including 1) maternal body mass index (BMI) and gestational weight gain (GWG); 2) nutritional supplementation, and 3) gestational vitamin D were associated with risk of ASD in a population-based electronic register and biomarker study taking place in Sweden.


The Stockholm Youth Cohort is a total population register-based study consisting of all individuals born from 1984 onwards and resident in Stockholm County, Sweden for ≥4 years. ASD and intellectual disability (ID) diagnoses were extracted from electronic health and services registers using a validated approach covering all pathways to care in Stockholm County. Maternal sera and neonatal dried blood samples were available for a subsample of births. Data on maternal BMI at first antenatal visit, GWG, and nutritional supplementation were extracted from registers. Concentrations of total 25-hydroxyvitamin D (25[OH]D) were assessed from maternal and neonatal samples using a highly sensitive liquid chromatography tandem mass spectrometry method. The associations of prenatal nutritional factors and ASD, ASD without co-occurring ID, and ASD with ID were analyzed in logistic regression models adjusting for a large number of covariates, and odds ratios (ORs) and 95% confidence intervals (CI) were estimated. Sibling-matched samples of ASD cases and their unaffected siblings were analyzed to address potential familial genetic or environmental confounding.


We found in a sample of 333,057 individuals that maternal overweight/obesity and either insufficient or excessive GWG was associated with increased risk of child ASD. However, in sibling analyses, the relationship between elevated maternal BMI and ASD was not apparent, suggesting that maternal BMI may be a proxy for other risk factors. In a sample of 273,107 individuals, maternal multivitamin use with or without additional iron or folic acid was associated with lower odds of ASD with ID, when compared to mothers who did not use multivitamins, iron, and folic acid (OR: 0.69, 95% CI: 0.57-0.84).

In an analysis of 1,230 ASD cases and 1,500 controls. 25[OH]D deficiency (< 25 nmol/L serum equivalent) was associated with 1.35 times higher odds of ASD (95% CI: 1.04-1.75) as compared with 25[OH]D sufficiency (≥ 50 nmol/L serum equivalent). ORs were similar for associations of 25[OH]D deficiency with ASD without ID (1.36, 95% CI: 1.10-1.82) and ASD with ID (1.30, 95% CI: 0.87-1.96), although the latter was not statistically significant. Sibling-matched control analyses suggested these associations were not due to familial confounding. Maternal sera analysis is ongoing and results will be presented.


In epidemiological studies based in the Stockholm Youth Cohort, we found that diverse prenatal nutritional factors may be associated with later risk of child ASD.