Maternal zinc deficiency may be relatively common worldwide, but the public health importance of zinc deficiency is not well defined. The purpose of this review is to explain the potential public health importance of maternal zinc deficiency as it relates to fetal growth and development, complications of pregnancy, labor and delivery, and maternal and infant health

Although today severe zinc deficiency is considered rare, mild to moderate zinc deficiency may be relatively common throughout the world. Studies from developing countries report average usual zinc intakes of 5-11 mg/d, and zinc intakes of 8-14 mg/d in the U.S. and Europe. Considering how much zinc women need during pregnancy, it can be estimated that 82-100% of pregnant women worldwide likely have inadequate usual intakes of zinc. For this reason, in areas where improvements in zinc intakes are difficult, zinc supplements during pregnancy are probably needed.

Severe maternal zinc deficiency has been associated with spontaneous abortion and congenital malformations, such as anencephaly, whereas milder forms of zinc deficiency have been associated with low birth weight, intrauterine growth retardation and preterm delivery. Importantly, these same levels of zinc deficiency have also been related to complications of labor and delivery, including, prolonged or inefficient first-stage labor and protracted second-stage labor, premature rupture of membranes, and the need for assisted or operative delivery. These complications in turn impair maternal and perinatal health as they lead to increased risk of maternal lacerations, high blood loss, maternal infections, fetal distress, stillbirth, neonatal asphyxia (low APGAR scores), respiratory distress and neonatal sepsis.

Zinc is also a critical nutrient for central nervous system (CNS) development and function. As much of the development of the CNS occurs during pre- and post-natal life it is clear that maternal and early infant zinc deficiency are likely to adversely affect fetal and infant neurological and behavioral development. Further, it should be pointed out that dietary zinc insufficiency might not be necessary for adverse effects of zinc deficiency on CNS development to occur; maternal infections may remove zinc from the mother’s serum and make it unavailable to the fetus. Thus, one can think of primary zinc deficiency (due to inadequate diet) as well as zinc deficiency secondary to maternal morbidity. Defining the importance of secondary zinc deficiency is likely critical for designing interventions in developing country populations with high disease burdens.

Maternal zinc deficiency during pregnancy may result in problems for the infant during postnatal life as well. For example, effects from maternal zinc deficiency on growth and development in utero likely influence growth and development during postnatal life and beyond. Zinc is also important for the placental transfer of many substances critical for the young infant, including immunologic factors and vitamin A.

A major determinant of postnatal survival is the ability of the infant to resist infection by respiratory and diarrheal disease. Because specific protective immunity develops as a result of exposure to pathogens, the immunologically naive newborn is at particularly high risk for infection during the first six months of life, when adaptive immunity is still not fully functional, yet exposure to invading pathogens is significant. Two factors, however, provide the infant with protection against pathogens. First, the healthy infant develops natural immunity which consists of antibodies and T cells produced prior to infection which recognize common pathogens for respiratory and diarrheal disease. Second, the newborn has already received maternal antibodies during pregnancy. Perinatal zinc deficiency (PZD) can result in poor development of this natural immunity and decreased acquisition of maternal antibody. Thus, zinc deficiency in the mother may increase risk of illness in her baby during the year of life and beyond.

As described here, the mechanisms through which maternal zinc deficiency could influence health outcomes for the mother and her baby are well described. The results of studies in animals motivate concern about the potential health effects of mild to moderate maternal zinc deficiency. Observational studies in human populations have produced strong associations between poor maternal zinc status and various indicators of poor pregnancy outcome, but supplementation trials have not produced strong, or even consistent results. More supplementation trials are needed to define the public health importance of maternal zinc deficiency worldwide.