Varying Degrees of Zinc Deficiency and Pregnancy Outcome in Experimental Animals

Zinc deficiency in pregnant experimental animals limits fetal growth and, if severe, causes teratogenic anomalies. Although the data from human studies are not consistent, similar outcomes have been observed and were associated with poor maternal zinc status. This paper reviews humans studies of zinc status and pregnancy outcome, describes the physiologic adjustments in zinc utilization during pregnancy to meet fetal needs while maintaining maternal status, and identifies dietary and environmental conditions that may override those physiologic adjustments and put the health of the mother and fetus at risk. Adjustments in intestinal zinc absorption appear to be the primary means by which zinc retention is increased to meet fetal demands. However, transfer of sufficient zinc to the fetus is dependent on maintenance of normal maternal serum zinc concentrations. Conditions that could interfere with zinc absorption include intake of cereal-based diets that are high in phytate, high intakes of supplemental iron, or any gastrointestinal disease. Conditions that may alter maternal plasma zinc concentrations and the transport of zinc to the fetus include smoking, alcohol abuse, and an acute stress response to infection or trauma. Supplemental zinc may be prudent for women with poor gastrointestinal function or with any of these conditions during pregnancy. Am J Clin Nutr 2000;71(suppl):1334S–43S.