Neural tube defects spina bifida

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. 

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. 

Neural tube defects, characterized by a failure of the neural tube to close properly after conception, affect about one in 1000 live births in the USA. Periconceptional folic acid supplementation reduces the risk. To determine whether periconceptional exposure to folic acid antagonists might therefore increase the risk of neural tube defects, data from a case-control study of birth defects (1979-98) in the USA and Canada have been examined (14). Data on 1242 infants with neural tube defects (spina bifida, anencephaly, and encephalo-cele) were compared with data from a control group of 6660 infants with malformations not related to vitamin supplementation. Triamterene is a folic acid antagonist and in this series was associated with the development of neural tube defects, but there were too few cases to estimate an odds ratio. 

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. 

Women of childbearing age exposed to this agent should be counseled as to its possible teratogenic effects. One percent to 2% of fetuses exposed to VPA in the first trimester have developed neural tube defects and 1% spina bifida (77, 361,362 and 363). 

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. 

In reaching its conclusion about spina bifida, the IOM committee relied primarily on the results from the Ranch Hands. There was no difference in the frequency of all birth defects in the children of Ranch Hands and Comparisons.42 There were, however, four neural tube defects—three cases of spina bifida and one 59... 

Chance is a far more likely explanation for the occurrence of four cases of neural tube defects among the Ranch Hand children as compared to zero cases among the Comparison children, just as it is the most likely explanation for the occurrence of five cleft lip/cleft palate cases among the Comparison children and their absence from Ranch Hand children. The alternative explanation that herbicides cause spina bifida and prevent cleft lip/cleft palate is not at all credible. 

It s never too early to start taking a prenatal vitamin when attempting to conceive. If one makes you feel nauseated, keep trying others, as there is a large variety on the market. But be absolutely sure to take one that includes the maximum daily recommended dose of folic acid (important for helping prevent neural tube defects and spina bifida). Organic prenatal vitamins do exist. The main differences between these and more conventional vitamins is that they re vegetarian and include no filler, artificial color, or flavor. 

Exposure to retinoic acid, methylnitrosourea, and clomiphene during the early embryonic period, prior to the induction of the neural plate (before day 18 in the human), results in an increased incidence of neural tube defects and other malformations in experimental animal models (Bennett Finnell, 1998). In addition, exposure of rodents to teratogens such as retinoic acid, arsenic, and valproic acid during the period of neurulation results in neural tube defects such as spina bifida and encephaloceles (Adams Lammer, 1993 Bennett Finnell, 1998). Of these, therapeutic use of... 

The teratogenic syndrome of in utero VPA exposure in humans includes neural, craniofacial, cardiovascular, and skeletal defects. A similar teratology is exhibited in rodents, rabbits, and nonhuman primates. The most dramatic of malformations associated with gestational VPA exposure is spina bifida, a neural tube defect that is estimated to occur in 1-2% of VPA exposed infants. Mice are the only known animal model to exhibit a comparable effect of VPA on neural tube development. 

Q12 Yes, valproate increases the risk of giving birth to a baby with spina bifida or anencephaly since valproate antagonizes the effects of folic acid and causes these neural tube defects. Thus women who suffer from epilepsy and who are taking valproate should receive a much higher dosage of folic acid (5 mg daily) compared to healthy women, who are advised to take 400 J.g daily. 

Folate (pteroylglutamic acid) is essential for the synthesis and methylation of DNA during fetal and early postnatal development (Nunn et al., 1986). Folate deficiency may result from poor diet, malabsorption, from treatment with anticonvulsant drugs such as phenytoin or primidone, as well as from antifolate drugs such as methotrexate. Folate deficiency during pregnancy leads to an increased prevalence of fetal malformations such as spina bifida and related neural tube defects. Findings... 

Use during first trimester may raise risk of neural tube defects (e.g., spina bifida) or other congenital anomalies... 

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