Folate neural tube defect

Folate deficiency The recommended dietary intake of folate has been increased (also protects against neural tube defects in the fetus), and additional folate is now added to flour (bread, pasta, and other products made liom flour)... 

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 deficiency during pregnancy is a major contributor to neural tube defects because of the critical role of folate in neuronal development. 

An important indication for folic acid has become the prevention of neural tube defects when given to women three months before conception and during the first trimester. The Recommended Dietary Allowance (RDA) for folate equivalents for pregnant women is 600-800 pg, twice the normal RDA of 400 pg for women who are not pregnant. 

Because both drugs may interfere with folic acid metabolism, their use during pregnancy is usually contraindicated by the potential for effects on the fetus, such as the development of neural tube defects associated with folate deficiency. The use of trimethoprim is contraindicated in patients with blood dyscrasias, hepatic damage, and renal impairment. 

Folic acid supplements are given to pregnant women to decrease the risk of neural tube defects such as spina bifida. Prenatal vitamin preparations that contain higher concentrations of folic acid must be dispensed under a health care worker s guidance because high folate intakes can mask the symptoms of pernicious anemia. 

Fleming A. The role of folate in the prevention of neural tube defects Human and animal studies. Nutr Rev 2001 58 S13. 

Folate deficiency is associated with the increased risk of neural tube defects (spina bifida, anencephaly), cardiovascular diseases, megaloblastic anemia, and some cancers (Bailey et al., 2003 Finglas et al., 2006 Scott et al, 1999). Unfortunately, folate intake is suboptimal in most of the world s populations, even in developed countries (Scott et al., 2000). Therefore there is an urgent need to increase folate content and bioavailability in staple foods. Because of its large consumption worldwide, potato is an appealing target for enrichment. 

If anticonvulsants are used, daily folate (1 mg per day) may decrease the risk of neural tube defects and vitamin K (20 mg per day) may prevent drug-induced bleeding. 

Folic acid deficiency, unlike vitamin B12 deficiency, is often caused by inadequate dietary intake of folates. Patients with alcohol dependence and patients with liver disease can develop folic acid deficiency because of poor diet and diminished hepatic storage of folates. Pregnant women and patients with hemolytic anemia have increased folate requirements and may become folic acid-deficient, especially if their diets are marginal. Evidence implicates maternal folic acid deficiency in the occurrence of fetal neural tube defects, eg, spina bifida. (See Folic Acid Supplementation A Public Health Dilemma.) Patients with malabsorption syndromes also frequently develop folic acid deficiency. Patients who require renal dialysis develop folic acid deficiency because folates are removed from the plasma during the dialysis procedure. 

C Bower. Folate and neural tube defects. Nutr Rev 53 S33-S38, 1995. 

D Rush. Periconceptional folate and neural tube defect. Am J ClinNutr59 511S-516S, 1994. 

Anyone taking diuretics for longer than six months may experience a folate, or folic acid, deficiency. Folic acid plays a part in the health and reproduction of virtually every cell in the body. It is responsible for protein metabolism, the prevention of neural tube defects in pregnancy, blood cell production, and the synthesis of neurotransmitters. Individuals with folate deficiencies may suffer from anemia, depression and other mood disorders, and may give birth to babies with neural tube defects. Supplementation with folic acid may be useful in reversing these effects. 

There has been an association between folate deficiency during the first weeks of pregnancy and neural tube defects, leading to a campaign to encourage folic acid intake. In as how much UV exposure might contribute to folate deficiency is still under discussion.126-128... 

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

Flansen, D. K., Streck, R. D., and Antony, A. C. (2003). Antisense modulation of the coding or regulatory sequence of the folate receptor (folate binding protein-1) in mouse embryos leads to neural tube defects. Birth Defects Res. Part A Clin. Mol. Teratol. 67(7), 475 487. 

Marasas, W. F., Riley, R. T., Hendricks, K. A., Stevens, V. L., Sadler, T. W., Gelineau-van Waes, J., Missmer, S. A., Cabrera, J., Torres, O., Gelderblom, W. C., Allegood, J., Martinez, C., et al. (2004). Fumonisins disrupt sphingolipid metabolism, folate transport, and neural tube development in embryo culture and in vivo A potential risk factor for human neural tube defects among populations consuming fumonisin-contaminated maize. J. Nutr. 134(4), 711-716. 

Rothenberg, S. P., Da Costa, M. P., Sequeira, J. M., Cracco, J., Roberts, J. L., Weedon, J., and Quadros, E. V. (2004). Autoantibodies against folate receptors in women with a pregnancy complicated by a neural tube defect. Obstet. Gynecol. Surv. 59(6), 410-411. 

Suarez, L., Hendricks, K. A., Cooper, S. P., Sweeney, A. M., Hardy, R. J., and Larsen, R. D. (2000). Neural tube defects among Mexican Americans living on the US-Mexico border Effects of folic acid and dietary folate. Am. J. Epidemiol. 152(11), 1017-10123. 

Valproate, carbamazepine, and other anticonvulsants pose teratogenic risks. Despite this, treatment should continue during pregnancy, as the potential threat to the fetus by a seizure is greater. However, it is mandatory to apply the lowest dose affording safe and effective prophylaxis. Concurrent high-dose administration of folate may prevent neural tube defects. 

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