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Evidence for Gestational Nutrition Influences On Autism Risk, with New Findings for Iron

Friday, 3 May 2013: 12:00
Auditorium (Kursaal Centre)
R. J. Schmidt, Public Health Sciences, University of California, Davis, Davis, CA; UC Davis MIND Institute, Sacramento, CA
Background: Gestational nutrition is known to influence child cognition and behavior due to the influence, during critical time windows, of nutrients such as folate, other B-vitamins, and iron, on brain, spinal cord, and neuron development.  Evidence is building for a role of gestational nutrition in the etiology of autism spectrum disorders (ASD).

Objectives: To review the research to date on the role of gestational nutrition in relation to risk for ASD in the child, discuss potential mechanisms, and present new findings in the CHARGE (Childhood Autism Risks from Genetics and Environment) case-control study on supplemental iron.

Methods: Children with a diagnosis of ASD or typical development (TD) confirmed at the UC Davis MIND Institute using standardized clinical assessments were included. We collected through structured telephone interviews maternal intake of multivitamins, prenatal vitamins, nutrient-specific vitamins, cereals, and other supplements for the three months before pregnancy, each month of pregnancy, and during breastfeeding (the index period). Data included whether or not each item was consumed, and if so, the brand, dose, frequency and months consumed. From this information, for each woman we calculated a total average value of selected nutrients (including iron) for each month.

Results: Mothers of children with ASD were significantly less likely than mothers of TD children to report taking an iron supplement at any point during the index period before and after adjustment for folic acid, maternal education, and child’s year of birth (odds ratio=0.7, 95% confidence interval: 0.5, 0.9, P=.015). Iron supplements were reported more often during the second and third trimesters, and lower use of iron supplements by ASD mothers during this time was driving the difference between case and control mothers observed for the index period. In addition, log-transformed mean (SD) total daily iron intake quantified from all sources for the index period was lower for mothers of children with ASD (3.7 (0.7) mg/d) than for mothers of children with TD (3.9 (0.7) mg/d, p=0.01), and ASD risk declined as iron increased (Ptrend=0.01).

Conclusions: Evidence for a role of nutrition in ASD etiology is similar to that observed for other neurodevelopmental conditions.  Maternal folic acid intake near conception was associated with decreased risk for ASD, especially in those genetically susceptible to inefficient metabolism. Though few women in the US are expected to be deficient in folate, supplemental folic acid could compensate for metabolic insufficiencies or increased demands.  In the case of iron, supplementation is more likely to be compensating for deficiencies. Iron deficiency affects 40-50% of pregnant women and can induce fetal iron deficiency because maternal circulation constitutes the only source of iron to the developing fetus.  Like other nutrients, iron plays a crucial role in early neurological development, and deficiencies early in life result in impaired cognition, motor development, social orientation and engagement, and language development. In the brain, iron contributes to neurotransmitter production, myelination, and immune function; dysregulation of all three of these pathways have been associated with ASD. Further investigations of nutritional contributions to ASD are needed to identify strategies for prevention.

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