Zinc deficiency in women, infants and children.

Abstract

Zinc deficiency in humans is widespread and is more prevalent in areas where the population subsists on cereal proteins. Conditioned deficiency of zinc is seen in many diseased states. A mild deficiency of zinc in pregnancy is associated with increased maternal morbidity, abnormal taste sensation, prolonged gestation, inefficient labor, atonic bleeding, and increased risks to the fetus. Among the urban poor in the US, a marginal zinc intake during pregnancy was associated with increased risk of preterm and very preterm delivery. Factors responsible for zinc deficiency in premature infants include high fecal losses of zinc, low body stores of zinc at birth, and increased zinc requirement during rapid growth. Zinc supplemented infants demonstrated improved linear growth velocity and maximum motor development scores. Marginal and moderate growth impairment in children as a consequence of inadequate zinc intake has been reported from many developed and developing countries. In one study from Japan, 21 prepubertal children were diagnosed to have zinc deficiency. The caloric intake, growth velocity, serum zinc, and plasma insulin-like growth factor-1 increased significantly in the zinc supplemented group. The clinical manifestations of zinc deficiency include growth retardation, hypogonadism in males, neurosensory disorders, cell-mediated immunological dysfunctions, and skin changes. Approximately 300 enzymes are known to require zinc for their activities. Zinc is required for DNA synthesis, cell division and protein synthesis. Several hundreds of zinc containing nucleoproteins are probably involved in gene expression of various proteins. A deficiency of zinc also affects proliferation and maturity of lymphocytes adversely.