Gestational Nutrition and Autism in the Charge Case-Control Study, with New Findings for Neonatal Vitamin D

Oral Presentation
Thursday, May 10, 2018: 10:55 AM
Arcadis Zaal (de Doelen ICC Rotterdam)
R. J. Schmidt1,2, Q. Niu3, D. Eyles4, R. L. Hansen3 and A. M. Iosif1, (1)Public Health Sciences, University of California Davis, Davis, CA, (2)MIND Institute, University of California, Davis, Sacramento, CA, (3)University of California Davis, Davis, CA, (4)Queensland Brain Institute, University of Queensland, St Lucia, Australia

Gestational nutrition has critical influences on neurodevelopment and evidence is building for a role in autism etiology; this includes associations with folate, iron, and potentially vitamin D.


To review findings from the population-based CHARGE (Childhood Autism Risks from Genetics and Environment) case-control study on gestational nutrients in relation to autism spectrum disorders (ASD) in the child, discuss potential mechanisms, and present new findings on neonatal vitamin D.


Children with clinically-confirmed diagnoses of ASD, developmental delay (DD), or typical development (TD) were included. We collected through structured telephone interviews maternal intake of supplements for the three months before pregnancy, each month of pregnancy, and during breastfeeding. We then calculated total average values of selected nutrients for each month. Total 25-hydroxyvitamin (25OHD) was measured using sensitive isotope dilution LC-MS/MS in archived newborn screening dried blood spots.


Maternal folic acid near conception was associated with decreased ASD, especially in those genetically susceptible to inefficient metabolism. Iron intake also was associated with decreased ASD especially in combination with conditions associated with functional iron insufficiency. Newborn 25OHD was associated with significantly reduced ASD only in females (ORadj=0.66; 95% CI: 0.48, 0.91, Pintxn=0.01). 25OHD was significantly associated with reduced DD (OR=0.84, 95%CI: 0.73, 0.97), cognitive and adaptive function prior to but not after adjustment for factors that contributed to vitamin D status (ORDD_adj=0.91, 95%CI: 0.78, 1.06). Significant interaction by race/ethnicity was observed (p=0.02), with an association between 25OHD and DD only in non-Hispanic white children (ORadj=0.76; 95% CI: 0.61, 0.95).


Evidence for a role of nutrition in ASD etiology is similar to that observed for other neurodevelopmental conditions. Maternal folic acid, iron, and vitamin D could potentially reduce ASD in certain genetically and environmentally susceptible subgroups. Further investigation of nutritional contributions and mechanisms are needed to identify targeted ASD prevention strategies.