Supplements folates

Folate supplements will rectify the megaloblastic anemia of vitamin Bj2 deficiency but may hasten the development of the (irreversible) nerve damage found in B,2 deficiency. There is also antagonism between fohc acid and the anticonvulsants used in the treatment of epilepsy. 

Elevated homocysteine concentrations have been associated with an increased risk for cardiovascular disease in both epidemiologic and clinical studies.43 Several studies have evaluated the benefit of lowering homocysteine levels with folic acid supplementation. One study reported a reduction in major cardiac events with the combination of folic acid, vitamin B12, and vitamin B6 following PCI.44 However, a more recent study found an increased risk of instent restenosis and the need for target-vessel revascularization with folate supplementation following coronary stent placement.45 The role of folate in the management of IHD is currently unclear. 

Anti-epileptic drugs, such as phenytoin, carbamazepine and valproate, may lead to neural tube defects if administered during pregnancy. Concurrent administration of folate supplements, such as folic acid, is recommended. 

Folate supplementation of food in the United States is expected to reduce folate-associated birth defects by up to 70%. 

The treatment of choice for toxoplasmosis is pyrimethamine with sulfadiazine a folate supplement is also given to counteract the megaloblastic... 

Pregnancy the exact cause of malformations is difficult to establish as epilepsy itself may cause foetal malformations (neural tube, clef palate...). Folate supplementation is considered to have a preventive effect. 

At higher dosage, methotrexate may cause bone marrow depression, megaloblastic anemia, alopecia, and mucositis. At the doses used in the treatment of inflammatory bowel disease, these events are uncommon but warrant dose reduction if they do occur. Folate supplementation reduces the risk of these events without impairing the antiinflammatory action. 

Folic acid (or folate) deficiency, one of the most common vitamin deficiencies in the population consuming few dietary fruits and vegetables, causes chromosome breaks in humans,34 analogous to those caused by radiation. Folate supplementation above... 

Stulc T, Melenovsky V, Grauova B, Kozich V, Ceska R. Folate supplementation prevents plasma homocysteine increase after fenofibrate therapy. Nutrition 2001 17(9) 721-3. 

The availability of erythropoietin has had a significant positive impact for patients with chronic renal failure. Erythropoietin consistently improves the hematocrit and hemoglobin level and usually eliminates the need for transfusions in these patients. An increase in reticulocyte count is usually observed in about 10 days and an increase in hematocrit and hemoglobin levels in 2-6 weeks. Most patients can maintain a hematocrit of about 35% with erythropoietin doses of 50-150 IU/kg intravenously or subcutaneously three times a week. Failure to respond to erythropoietin is most commonly due to concurrent iron deficiency, which can be corrected by giving oral iron. Folate supplementation may also be necessary in some patients. 

The mechanism by which dietary folate supplementation prevents NTDs is not understood (Prevention of Neural Tube Defects Results of... 

Spiegelstein, O., Mitchell, L. E., Merriweather, M. Y., Wicker, N. J., Zhang, Q., Lammer, E. J., and Finnell, R. H. (2004). Embryonic development of folate binding protein-1 (Folbpl) knockout mice Effects of the chemical form, dose, and timing of maternal folate supplementation. Dev. Dyn. 231(1), 221-231. 

Q9 B12 is ineffective when given by mouth if there is deficiency of intrinsic factor, as it would not be absorbed. It must be given as a depot injection, which lasts a few months. Folate supplements can be given by mouth. However, if the patient has neurological symptoms, folic acid supplements alone are not adequate B12 must also be administered. So the two forms of therapy are not equally effective. 

Epidemiological smdies suggest that hyperhomocysteineima is most significantly correlated with low folate status, but there is also a significant association with low vitamin Bg status (SeUiub et al., 1993). Trials of supplementation have shown that whereas folate supplements lower fasting homocysteine in moderately hyperhomocysteinemic subjects, supplements of 10 mg per day of vitamin Bg have no effect, although supplements do reduce the peak plasma concentration of homocysteine after a test dose of methionine (Ubbink et al., 1994 Ubbink, 1997 Dierkes et al., 1998). This can probably be explained on the basis of the kinetics of the enzymes involved the of cystathionine... 

Early studies suggested that folate supplements exacerbate or hasten the development of the neurological damage in vitamin B12 deficiency. There is little evidence that this is so, but high intakes of folate will prevent the development of megaloblastic anemia in vitamin B12 deficiency. In up to one-third of... 

About30% ofvitamin Bi2-deficient subjects have elevated serum folate. This is mainly methyl-tetrahydrofolate, the result of the methyl folate trap (Section 10.3.4.1). About one-third of folate-deficient subjects have low serum vitamin B12 the reason for this is not clear, but it responds to the administration of folate supplements. 

About one-third of folate-deficient subjects have low serum vitamin B12 the reason for this is not clear, but it responds to the administration of folate supplements. 

Adverse effects. Any sulphonamide-induced allergic reactions can be severe, e.g. erythema multiforme, Stevens-Johnson syndrome and foxic epidermal necrolysis. Because of its antifoT action the combination should not be used by pregnant women imless they take a folate supplement. 

Other effects include Dupu5dren s contracture and pseudolymphoma. Some degree of macrocyto-sis is common but anaemia probably occurs only when dietary folate is inadequate. This responds to folate supplement (the requirement for folate is increased, as it is a cofactor in some hydroxylation reactions that are accelerated by enzyme induction by phenytoin). Osteomalacia due to increased metabolism of vitamin D occurs after years of therapy. 

Prevention of fetal neural tube defect (spina bifida). Folic acid supplementation taken before conception and during the early weeks of pregnancy has been shown in an 8-year trial to prevent the condition in pregnancies subsequent to an affected birth. Women hoping to conceive and who have had an affected child are advised to take folic acid 5 mg/day. To prevent a first occurrence 400 micrograms/day should be taken both before conception, or as soon as possible after diagnosis. In both cases folate supplement should be taken for the first 12 weeks of pregnancy. 

Folate Is a generic term referring to a family of related compounds. All of these compounds represent modifications of the simplest form of the vitamin, folic acid (pteroylglutamic add, PlcGlu). Folic add does not occur in nature in appreciable amounts, though it is readily assimilated by the body and converted to the active cofactor forms of the vitamin. Folic acid is the form of the vitamin used in folate supplements. Folates are modified by reduction and by a poly glutamyl chain or tail. The reduced folates include dlhydrofolate and tetrahydrofolate. 

A small fraction of epileptics treated with anticonvulsants dilantin, phenytoin, diphenylhydantoin) develop folate deficiency. Epilepsy is not a rare disease. Hence, there is an awareness of the possibility of the occurrence of megaloblastic anemia in epileptics treated with the aforementioned anticonvulsant. Supplementing epileptics with folate can alleviate the deficiency however, the supplements may also result in an increase in Ihe seizure rate. Thus, physicians must be prepared to halt folate supplementation of epileptics beuig treated for anemia. 

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