Study: Prenatal Vitamins Reduce the Risk of Autism
A study on prenatal vitamins and autism was conducted emphasizing the importance of proper nutrient intake before and during the early stages of pregnancy. This study in Epidemiology, lead by Rebecca Schmidt, found that women who did not take a prenatal vitamin 3 months prior and with the first month of pregnancy were twice as likely to have a child with autism. Of particular note was that certain maternal and child genetics put the child at much more significant risk of autism—a 7 fold increase in the risk of autism when women with particular gene variants did not supplement with a prenatal vitamin.
Of course it is important to first point out that I am not placing any blame on mothers. Since this supplementation is important before a woman knows she’s pregnant, unless someone was planning ahead, they would not have known to add a prenatal. Also, this discussion is to help support mothers and children. As we study more, we continue to learn what effects the risk of autism and what people can do to reduce that risk.
However, it does underscore the importance and benefit of preparing for pregnancy and conception through properly supplementation a minimum of 3 months ahead of trying conceive.
All women studied were at a greater autism risk in the child if no periconceptional prenatal vitamin supplementation was taken. However, mothers with the MTHFR and CBS genes were at significantly increased risk – 4.5 times and 7.2 times respectively, and children with the COMT gene were more likely to have increased risk of autism regardless of supplementation. The study highlighted that in order to reduce the risk, the prenatal needed to be taken 3 months prior and within the first month of pregnancy (before a woman is aware she’s pregnant).
Mothers with the MTHFR and CBS gene variant were more likely to have children with autism if they did not supplement with a prenatal vitamin. With MTHFR, women are less able to make the active form of folate (5 methyl tetrahydrafolate). Folate, as we know helps prevent spina bifida, a condition caused during development associated with folic acid deficiency during gestation. Folate is important for DNA methylation, an important process for regulating gene expression, so you can see how important this nutrient is for fetal/child development. While these women would benefit most from 5MTHF supplementation, it appears a prenatal with any form of folate was important for reducing the risk of autism.
CBS gene governs the production of cystathionine beta-synthase, an enzyme that uses vitamin B6 to convert homocysteine to a molecule called cystathionine a step toward the production of glutathione. The gene COMT affects the amount of dopamine and other neurotransmitters in the brain. Children with the COMT gene variant were more likely to have autism, with or without maternal supplementations—however, the risk was greater without supplementation.
This study is a huge step forward. It offers many clues to directions we should study further, and reinforces what we already know—that genetic and environmental factors both play a role in the development of autism.
We are beginning to understand the genetic and environmental components of autism more and more. This study showed us several genes (in the mother and child) that are factors in the risk for autism, and how maternal supplementation can support the development and health of the child and reduce the risk of autism. This study opens the door to understanding what children might be at greatest risk for developing autism, the benefits of proper and timely supplementation, even which children might be at greatest risk for harm from toxins.
For now we can say that prenatal and preconception nutrition is important for the health of babies in many areas of development and overall health, including reducing the risk of autism.
Schmidt RJ, Hansen RL, Hartiala J, Allayee H, Schmidt LC, Tancredi DJ, Tassone F, Hertz-Picciotto I. Prenatal Vitamins, One-carbon Metabolism Gene Variants, and Risk for Autism. Epidemiology. 2011; 22:476-485. [2011 May 23. Epub ahead of print]