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2013-01-28

How Prenatal Folic Acid May Not Prevent Neural Tube Defects

Hot on the heals of another study on folic acid I covered a couple weeks ago, here is another one. Now, I rarely cover animal studies, but I think this new study is something I need to discuss. This is because it validates what I (and other NDs and healthcare practitioners) have been saying regarding the need to supplement directly with L-methylfolate (instead of folic acid).

A series of reactions, involving numerous enzymes, typically converts folic acid (the synthetic form of folate) into 5-methyltetrahydrofolate (5-MTHF, or more simply, L-methylfolate). However, a mind-boggling large percentage of the population are carriers of a genetic defect in which at least one of those enzymes don't function as it should. This has been theorized as one reason why some women will continue to have children with neural tube defects (NTDs, like spina bifida and anencephaly) despite seemingly adequate consumption of folic acid.

While folic acid supplements have reduced NTDs by as much as 70%, it's not good enough. Recently, it's been discovered that mutations in the human gene increase the risk of birth defects, and since humans share the same gene for the folic acid enzyme with mice (and all other mammals), a mouse model would provide researchers with great way to understand folic acid and its role in human birth defects.

Therefore, researchers at the University of Texas at Austin studied mice that lacked the critical enzyme in the folic acid metabolic pathway. What did they find? They found that a point mutation of a key folic acid enzyme causes NTDs in mice--just as expected.

"This is the clearest mechanistic link yet between folic acid and birth defects...and it may explain those 30 percent of neural tube defects [in humans] that cannot be prevented by folic acid supplementation" said the lead researcher.

So what should all those fertile women do? I would recommend L-methylfolate supplementation as mentioned above. This is the active form of folate, and bypasses the stage where that defective enzyme comes into play.

Source: Deletion of Mthfd1l causes embryonic lethality and neural tube and craniofacial defects in mice

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