Zinc deficiency in women, infants and
children.
J Am Coll Nutr 1996 Apr 15:2 113-20
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.