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Signs of folate deficiency anemia most of the time are subtle. [4] Anemia (macrocytic, megaloblastic anemia) can be a sign of advanced folate deficiency in adults. [1] Folate deficiency anemia may result in feeling tired, weakness, changes to the color of the skin or hair, open sores on the mouth, shortness of breath, palpitations, lightheadedness, cold hands and feet, headaches, easy bleeding ...
Folate in the form of folic acid is used to treat anemia caused by folate deficiency. [3] Folic acid is also used as a supplement by women during pregnancy to reduce the risk of neural tube defects (NTDs) in the baby. [3] [10] NTDs include anencephaly and spina bifida, among other defects.
As a consequence of the biochemical reactions in which homocysteine is involved, deficiencies of vitamin B 6, folic acid (vitamin B 9), and vitamin B 12 can lead to high homocysteine levels. [2] Other possible causes of hyperhomocysteinemia include genetics, excessive methionine intake, and other diseases. [3]
Folic acid should not be used for the treatment of HFM. Folic acid is not a physiological folate. It binds tightly to, and may impede, FRα-mediated endocytosis which plays an important role in the transport of folates across the choroid plexus into the CSF (see above). [30] [22] For a further consideration of treatment see GeneReviews. [5]
It has been thought that if someone is deficient in vitamin B 12 and folic acid, the vitamin B 12 deficiency must be treated first. However, the basis for this has been challenged, although due to ethical considerations it is no longer able to be tested if "neuropathy is made more severe as a result of giving folic acid to vitamin B 12 ...
At position 26 there is a change in the amino acid, from glutamic acid to lysine (E26K). Hemoglobin E is very common among people of Southeast Asian, Northeast Indian, Sri Lankan and Bangladeshi descent. [1] [2] The βE mutation affects β-gene expression creating an alternate splicing site in the mRNA at codons 25-27 of the β-globin gene.
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