The periconceptional use of folic acid-containing supplements reduces the first occurrence, as well as the recurrence, of neural tube defects. Women of populations in which adverse pregnancy outcomes are prevalent often consume diets that contain a low density of vitamins and minerals, including folate. Folate intake may need to be sustained after complete closure of the neural tube to decrease the risk of other poor pregnancy outcomes. A central feature of embryonic and fetal development is widespread cell division; folate is central because of its role in nucleic acid synthesis. During gestation, marginal folate nutriture can impair cellular growth and replication in the fetus or placenta. Folate deficiency can occur because dietary folate intake is low or because the metabolic requirement for folate is increased by a particular genetic defect or defects. During pregnancy, low concentrations of dietary and circulating folate are associated with increased risks of preterm delivery, infant low birth weight, and fetal growth retardation. A metabolic effect of folate deficiency is an elevation of blood homocysteine. Likewise, the presence of maternal homocysteine concentrations have been associated both with increased habitual spontaneous abortion and pregnancy complications (eg, placental abruption and preeclampsia), which increase the risk of poor pregnancy outcome and of decreased birth weight and gestation duration.