Document Detail

Maternal periconceptional folic acid intake and risk of autism spectrum disorders and developmental delay in the CHARGE (CHildhood Autism Risks from Genetics and Environment) case-control study.
MedLine Citation:
PMID:  22648721     Owner:  NLM     Status:  MEDLINE    
BACKGROUND: Periconceptional folate is essential for proper neurodevelopment.
OBJECTIVE: Maternal folic acid intake was examined in relation to the risk of autism spectrum disorder (ASD) and developmental delay (DD).
DESIGN: Families enrolled in the CHARGE (CHildhood Autism Risks from Genetics and Environment) Study from 2003 to 2009 were included if their child had a diagnosis of ASD (n = 429), DD (n = 130), or typical development (TD; n = 278) confirmed at the University of California Davis Medical Investigation of Neurodevelopmental Disorders Institute by using standardized clinical assessments. Average daily folic acid was quantified for each mother on the basis of dose, brands, and intake frequency of vitamins, supplements, and breakfast cereals reported through structured telephone interviews.
RESULTS: Mean (±SEM) folic acid intake was significantly greater for mothers of TD children than for mothers of children with ASD in the first month of pregnancy (P1; 779.0 ± 36.1 and 655.0 ± 28.7 μg, respectively; P < 0.01). A mean daily folic acid intake of ≥600 μg (compared with <600 μg) during P1 was associated with reduced ASD risk (adjusted OR: 0.62; 95% CI: 0.42, 0.92; P = 0.02), and risk estimates decreased with increased folic acid (P-trend = 0.001). The association between folic acid and reduced ASD risk was strongest for mothers and children with MTHFR 677 C>T variant genotypes. A trend toward an association between lower maternal folic acid intake during the 3 mo before pregnancy and DD was observed, but not after adjustment for confounders.
CONCLUSIONS: Periconceptional folic acid may reduce ASD risk in those with inefficient folate metabolism. The replication of these findings and investigations of mechanisms involved are warranted.
Rebecca J Schmidt; Daniel J Tancredi; Sally Ozonoff; Robin L Hansen; Jaana Hartiala; Hooman Allayee; Linda C Schmidt; Flora Tassone; Irva Hertz-Picciotto
Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.     Date:  2012-05-30
Journal Detail:
Title:  The American journal of clinical nutrition     Volume:  96     ISSN:  1938-3207     ISO Abbreviation:  Am. J. Clin. Nutr.     Publication Date:  2012 Jul 
Date Detail:
Created Date:  2012-06-21     Completed Date:  2012-09-07     Revised Date:  2013-07-02    
Medline Journal Info:
Nlm Unique ID:  0376027     Medline TA:  Am J Clin Nutr     Country:  United States    
Other Details:
Languages:  eng     Pagination:  80-9     Citation Subset:  AIM; IM    
Department of Public Health Sciences, University of California Davis School of Medicine, Davis, CA 95616-8638, USA.
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MeSH Terms
California / epidemiology
Case-Control Studies
Child Development Disorders, Pervasive / epidemiology,  etiology*,  genetics
Child, Preschool
Confounding Factors (Epidemiology)
Developmental Disabilities / epidemiology,  etiology,  genetics
Diet / adverse effects*
Dietary Supplements / analysis
Folic Acid / administration & dosage*
Folic Acid Deficiency / physiopathology*
Food, Fortified / analysis
Genetic Association Studies
Maternal Nutritional Physiological Phenomena*
Methylenetetrahydrofolate Reductase (NADPH2) / genetics,  metabolism
Polymorphism, Single Nucleotide
Pregnancy Complications / physiopathology*
Pregnancy Trimester, First
Grant Support
K12-HD051958-06/HD/NICHD NIH HHS; P01-ES-11269/ES/NIEHS NIH HHS; R01-ES015359/ES/NIEHS NIH HHS; R01-ES015359-03S1/ES/NIEHS NIH HHS; T32-MH073124/MH/NIMH NIH HHS
Reg. No./Substance:
59-30-3/Folic Acid; EC protein, human; EC Reductase (NADPH2)

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