Folic acid deficiency malformations

In addition to direct effects of chemical compounds on the fetus, metabolic disturbances in the mother, such as diabetes or hyperthermia, or deficiencies of calories or specific nutrients such as vitamin A, zinc, and folic acid may lead to teratogenesis. Compounds that inhibit placental functions may also induce malformations, e.g., by inhibiting placental circulation. For example, hydroxyurea disrupts the placental circulation and induces malformations. In addition, it also induces DNA damage. 

Reduced forms of folic acid are required for essential biochemical reactions that provide precursors for the synthesis of amino acids, purines, and DNA. Folate deficiency is not uncommon, even though the deficiency is easily corrected by administration of folic acid. The consequences of folate deficiency go beyond the problem of anemia because folate deficiency is implicated as a cause of congenital malformations in newborns and may play a role in vascular disease (see Folic Acid Supplementation A Public Health Dilemma). 

It appears reasonable to recommend supplementation with several B vitamins in physiological doses to many patients with epilepsy. Patients on inducer AEDs and VPA, and patients with an insufficient diet, are at risk for deficiency of several B vitamins. Moreover, the evidence that folic acid can prevent adverse effects in patients on AEDs is not much higher than the evidence for a protective effect of vitamins B2, Bg, B7 and B12 (Ranganathan and Ramar-atnam 2005). In animal studies, deficiency of vitamins B2 and Bg has been related to the occurrence of foetal malformations. Therefore, women of childbearing potential should supplement their diet with vitamin B2 and Bg, as well as folic acid. 

Malformation existing at birth acquired during development in the uterus and not through heredity. Sometimes, congenital defects in newborns are the result of (1) the administration of drugs during pregnancy, or (2) maternal deficiencies of nutrients such as folic acid. 

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