A deficiency of folate can occur when the body's need for folate is increased, when dietary intake or absorption of folate is inadequate, or when the body excretes (or loses) more folate than usual. Medications that interfere with the body's ability to use folate may also increase the need for this vitamin. Some research indicates that exposure to ultraviolet light, including the use of tanning beds, can lead to a<unk> . The deficiency is more common in pregnant women, infants, children, and adolescents. It may also be due to poor diet or a consequence of alcoholism. Additionally, a defect in homocysteine methyltransferase or a deficiency of vitamin B12 may lead to a so-called "methyl-trap" of tetrahydrofolate (THF), in which THF is converted to a reservoir of methyl-THF which thereafter has no way of being metabolized, and serves as a sink of THF that causes a subsequent deficiency in folate. Thus, a deficiency in B12 can generate a large pool of methyl-THF that is unable to undergo reactions and will mimic<unk> . Folate (pteroylmonoglutamate) is absorbed throughout the small intestine, though mainly in the jejunum. Important steps in the absorption are reduction of the polyglutamate chain by pteroylpolyglutamate hydrolase (gamma-glutamyl hydrolase) and then transport across the brush border membrane by the proton-coupled folate transporter (SLC46A1). Diffuse inflammatory or degenerative diseases of the small intestine, such as Crohn disease, celiac disease, chronic enteritis or the presence of an entero-enteric fistula may reduce absorption. Situational Some situations that increase the need for folate include: * bleeding * kidney dialysis * liver disease * malabsorption, including celiac disease and fructose malabsorption * pregnancy and lactation (breastfeeding) * tobacco smoking * alcohol consumption Medication Medications can interfere with folate metabolism, including: * anticonvulsant medications (such as phenytoin, primidone, carbamazepine or valproate) * metformin (sometimes prescribed to control blood sugar in type 2 diabetes) * methotrexate, an anti-cancer drug also used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis. * 5-fluorouracil * hydroxyurea * trimethoprim * sulfasalazine (used to control inflammation associated with Crohn disease, ulcerative colitis and rheumatoid arthritis) * triamterene (a diuretic) * birth control pills (also related to the duration use of birth control pills) may reduce serum folate levels but without inducing clinically significant<unk> . When methotrexate is prescribed, folic acid supplements are sometimes given with the methotrexate. The therapeutic effects of methotrexate are due to its inhibition of dihydrofolate reductase and thereby reduce the rate de novo purine and pyrimidine synthesis and cell division. Methotrexate inhibits cell division and is particularly toxic to fast dividing cells, such as rapidly dividing cancer cells and the progenitor cells of the immune system. Folate supplementation is beneficial in patients being treated with long-term, low-dose methotrexate for inflammatory conditions, such as rheumatoid arthritis (RA) or psoriasis, to avoid macrocytic anemia caused by<unk> . Folate is often also supplemented before some high dose chemotherapy treatments in an effort to protect healthy tissue. However, it may be counterproductive to take a folic acid supplement with methotrexate in cancer treatment. Cerebral<unk>  Cerebral<unk>  is when levels of 5-methyltetrahydrofolate are low in the brain as measured in the cerebral spinal fluid despite being normal in the blood. Symptoms typically appear at about five months of age. Without treatment there may be poor muscle tone, trouble with coordination, trouble talking, and seizures. The causes of cerebral<unk>  include mutations of genes responsible for folate metabolism and transport. Mutations of the SLC46A1 gene that encodes the proton-coupled folate transporter (PCFT) result in CFD syndromes with both systemic<unk>  and cerebral<unk> . Even when the systemic deficiency is corrected by folate, the cerebral deficiency remains and must be treated with folinic acid. Pregnancy<unk>  can occur during pregnancy as a result of the increasing number of cells of the growing fetus, decreased absorption and intake of folate, maternal hormones that mediate its metabolism, vascular circulation of maternal and fetal blood and an increasing amount of blood resulting in dilution. Sickle cell anemia and living in areas of malaria result in even higher folate needs for women who are pregnant. When supplemented with 450 micrograms of folic acid per day, the risk of developing birth defects, specifically neural tube defects, is decreased. Supplementation to prevent birth defects is most effective one month prior to and during the first twelve weeks of pregnancy. Utilization of folic acid supplementation before conception has shown to result in a decrease in neural tube defects by 70%.
Folate deficiency
Vitamin E deficiency
Properdin deficiency
Zinc deficiency
Hereditary folate malabsorption
Iron deficiency
Familial isolated vitamin E deficiency
Cerebral folate deficiency