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Early maternal prenatal vitamin intake associated with reduced risk for autism

May 26, 2011 23 comments

This post is by Guest Blogger Rebecca Schmidt, Ph.D., Assistant Professor, Department of Public Health Sciences, UC Davis and first author on the research described below.

UC Davis researchers conducted a study comparing children with autism to children without autism, all aged 24-60 months, to see whether their mothers differed in terms of taking prenatal vitamin supplements before and during pregnancy. Combined effects of maternal vitamin intake and genotypes affecting a key metabolic pathway known as one-carbon metabolism were also examined.

In this retrospective study, mothers of  children with autism were significantly less likely than those of typically developing children to report having taken prenatal vitamins during the three months before and the first month of pregnancy. Prenatal supplement use was similar across the other months of pregnancy. Maternal education and the child’s birth year were accounted for; however, because the mothers were asked about their vitamin use years after their pregnancy, and after their child’s developmental status was known, recall bias could have influenced the results.

The researchers postulate that folic acid, the synthetic form of folate or vitamin B9, and the other B vitamins in prenatal supplements, are probably protecting against deficits in early fetal brain development. Folate is known to be critical for proper neurodevelopment and studies have found that supplemental folic acid has the potential to prevent up to 70 percent of neural tube defects.

Interaction effects were also observed between periconceptional prenatal vitamin intake and maternal and child genotypes. When a mother did not report taking prenatal vitamins and she or her child had genotypes associated with less efficient folate-dependent one-carbon metabolism, the child was at much greater risk for autism. These findings demonstrate gene/environment interactions in autism.

Maternal genes involved in significant interaction effects included the well-studied methylenetetrahydrofolate reductase (MTHFR) folate metabolism gene and vitamin B6-dependent cystathionine-beta-synthase (CBS), which is an enzyme involved in metabolizing protein building-blocks that contain sulfur. The child’s catechol-O-methyltransferase (COMT) gene was associated with more than seven times the risk for autism when in combination with no maternal periconceptional prenatal vitamin intake, compared to children with other genotypes whose mothers did report periconceptional prenatal vitamin intake. The COMT enzyme, responsible for the degradation of the neurotransmitter dopamine and well-known for its association with schizophrenia, is active during early neurodevelopment. Structural and functional brain differences have been described across COMT genotypes, particularly in the hippocampus and prefrontal cortex, regions previously shown to be affected in individuals with autism.

These findings are the first to suggest a concrete step women can take that may reduce the risk of having a child with autism. Future research is warranted to replicate these findings and enhance understanding of potential mechanisms.


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