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Journal of Nutrition 2003-May

Zinc supplementation and growth of the fetus and low birth weight infant.

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Carlos Castillo-Durán
Gerardo Weisstaub

Märksõnad

Abstraktne

Zinc deficiency limits growth in young children, and in animal models it also affects fetal growth. In animals, the effect of severe zinc deficiency on growth is evident. However, controlled trials of zinc supplementation during pregnancy in humans have not demonstrated consistent effects on weight at birth and/or duration of gestation. Those studies that have identified a positive effect of zinc on fetal growth were performed on low-socioeconomic or migrant groups in industrialized countries or in countries where diet and living conditions are improving. In contrast, in studies conducted either on populations with minimal risk of zinc deficiency or those suffering from multiple and severe nutritional deficiencies, no effects have been found. The potential confounding factors that may help explain the contradictory results include the following: age of pregnant women; presence of digestive diseases, other nutritional deficiencies, phytates or other factors that affect bioavailability; timing and duration of zinc supplementation and compliance with supplements. Few studies of zinc supplementation were conducted on infants that were born small for their gestational age or preterm; in this case, a positive effect on growth was shown. A study of zinc supplementation during pregnancy found reduced risk of diseases (diarrhea or impetigo) in small-for-gestational-age but not preterm infants. A second study demonstrated reduced mortality in small-for-gestational-age infants. We conclude that supplementation trials during human pregnancy do not provide conclusive evidence for a beneficial effect of zinc supplementation despite the experimental evidence that zinc deficiency may retard fetal growth or shorten pregnancy. However, early zinc supplementation in low birth weight or small-for-gestational-age infants reveals an effective improvement in growth, which suggests a prenatal depletion or insufficient zinc intake to support catch-up growth postnatally.

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