What is it about?
Folic acid (vitamin B9) supplementation during pregnancy is used worldwide to prevent neural tube defects (NTDs). Although widely accepted, we only partially understand how this supplementation works. We show that folic acid promotes the production of the vitamin A derivative retinoic acid, thereby preventing NTDs. Eliminating the enzyme responsible for linking vitamin B9 to retinoic acid, ALDH1L1, abolishes the NTD-preventing effects of folic acid.
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Why is it important?
Our findings reveal a molecular link between folic acid and vitamin A, including the mechanism and the enzyme that connects these two metabolic pathways. The results show that ALDH1L1, the enzyme linking folic acid supplementation to retinoic acid production, requires the vitamin A derivative retinaldehyde. Optimal vitamin A levels enhance folic acid's ability to prevent neural tube defects, allowing a reduction in the folic acid dose.
Perspectives
The beneficial effects of folic acid supplementation are widely accepted, but dosage issues are widely discussed, as is the debate over folic acid enrichment of foods (flour, bread, cereals, etc.) in addition to supplementation. There are also reported cases of individuals who are insensitive to folic acid supplementation. Additional issues requiring extensive clarification concern the reported teratogenic effects of high and low folic acid levels in experimental models. To better understand these issues and others concerning folic acid, we need an in-depth understanding of its molecular and biochemical mechanisms of action.
Abraham Fainsod
Hebrew University of Jerusalem
Read the Original
This page is a summary of: Folic acid prevention of neural tube defects requires retinoic acid produced by ALDH1L1, Proceedings of the National Academy of Sciences, July 2026, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2616501123.
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