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How folic acid deficiency leads to Neural tube defects
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Folic acid deficiency is known to increase the risk of neural tube defects (NTDs), including spina bifida. Spina bifida is a congenital condition characterized by incomplete closure of the neural tube during fetal development, leading to malformation of the spinal cord and vertebrae. The exact mechanisms by which folic acid deficiency contributes to spina bifida are not fully understood, but there are several hypotheses:
1. Impaired DNA synthesis and cell division: Folic acid is essential for DNA synthesis and cell division, particularly during rapid fetal growth and development. A deficiency in folic acid can disrupt these processes, leading to abnormal cell proliferation and impaired closure of the neural tube.
2. Impaired methylation reactions: Folic acid is a precursor for the production of methyl groups, which are involved in numerous biochemical reactions, including DNA methylation. Methylation is an essential process for regulating gene expression and proper development. Folic acid deficiency can lead to reduced availability of methyl groups, which may result in altered gene expression patterns during neural tube closure.
3. Increased homocysteine levels: Folic acid is required for the conversion of homocysteine, an amino acid, to methionine. In the absence of adequate folic acid, homocysteine levels can increase. Elevated homocysteine has been associated with impaired embryonic development and an increased risk of neural tube defects.
It's important to note that folic acid supplementation is recommended for women of childbearing age, especially before and during early pregnancy, to reduce the risk of neural tube defects. By ensuring an adequate intake of folic acid, the risk of spina bifida and other NTDs can be significantly reduced.
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