he increased requirements for most vitamins during pregnancy shown in Table 9-5 usually are supplied by any general diet that provides adequate calories and protein. he excep tion is folic acid during times of unusual requirements, such as pregnancy complicated by protracted vomiting, hemo lytic anemia, or multiple fetuses. hat said, in impoverished countries, routine multivitamin supplementation reduced the incidence of low-birthweight and growth-restricted fetuses, (Fawzi, 2007).
neural-tube defect risks (Chap. 13, p. 270). Namely, the CDC (2004) estimated that the number of afected pregnancies had decreased from 4000 pregnancies per year to approximately 3000 per year after mandatory fortiication of cereal products with folic acid in 1998. Perhaps more than half of all neural tube defects can be prevented with daily intake of 400 �g of folic acid throughout the periconceptional period. Evidence development (Ars, 2016). Putting 140 �g of folic acid into each 100 g of grain products may increase the folic acid intake of the average American woman of childbearing age by 1 00 �g/ d.
Because nutritional sources alone are insuicient, however, folic acid supplementation is still recommended (American
College of Obstetricians and Gynecologists, 20 16e). Likewise, the U.S. Preventive Services Task Force (2009) recommends that all women planning or capable of pregnancy take a daily supplement containing 400 to 800 �g of folic acid.
A woman with a prior child with a neural-tube defect can reduce the 2-to 5-percent recurrence risk by more than 70 percent with a daily 4-mg folic acid supplement taken during the month before conception and during the first trimester. As emphasized by the American Academy of Pediatrics and the American College of Obstetricians and Gynecologists (2017), this dose should be consumed as a separate supplement and not as multivitamin tablets. This practice avoids excessive intake of fat-soluble vitamins.
Vitamin A, although essential, has been associated with congeni tal malformations when taken in high doses (> 10,000 IU / d) during pregnancy. These malformations are similar to those produced by the vitamin A derivative isotretinoin (Accutane), which is a potent teratogen (Chap. 12, p. 245). Beta-carotene, the precursor of vitamin A found in fruits and vegetables, has not been shown to produce vitamin A toxicity. Most prenatal vitamins contain vitamin A in doses considerably below the teratogenic threshold. Dietary intake of vitamin A in the United States appears to be adequate, and additional supplementation is not routinely recommended. In contrast, vitamin A deiciency is an endemic nutritional problem in the developing world (McCauley, 2015). Vitamin A deficiency, whether overt or subclinical, is associated with night blindness and with an increased risk of maternal anemia and spontaneous preterm birth (West, 2003).
Vitamin BJ2 plasma levels drop in normal pregnancy, mostly as a result of reduced plasma levels of their carrier proteinstranscobalamins. Vitamin BJ2 occurs naturally only in foods of animal origin, and strict vegetarians may give birth to neonates whose BI2 stores are low. Likewise, because breast milk of a vegetarian mother contains little vitamin B12, the deiciency may become profound in the breastfed infant (Higginbottom, 1978). Excessive ingestion of vitamin C also can lead to a functional deiciency of vitamin B12. Although its role is still controversial, vitamin BI2 deiciency preconceptionally, similar to folate, may elevate the risk of neural-tube defects (Molloy, 2009).