The essentiality of
zinc in humans was established in 1963. During the past 50 y, tremendous advances in both clinical and basic sciences of
zinc metabolism in humans have been observed. The major factor contributing to
zinc deficiency is high
phytate-containing cereal
protein intake in the developing world, and nearly 2 billion subjects may be
zinc deficient. Conditioned deficiency of
zinc has been observed in patients with
malabsorption syndrome,
liver disease,
chronic renal disease,
sickle cell disease, and other
chronic illnesses. Major clinical problems resulting from
zinc deficiency in humans include growth retardation; cell-mediated immune dysfunction, and
cognitive impairment. In the Middle East,
zinc-deficient dwarfs did not live beyond the age of 25 y, and they died because of intercurrent
infections. In 1963, we knew of only 3
enzymes that required
zinc for their activities, but now we know of >300
enzymes and >1000
transcription factors that are known to require
zinc for their activities.
Zinc is a second messenger of immune cells, and intracellular free
zinc in these cells participate in signaling events.
Zinc has been very successfully used as a therapeutic modality for the management of acute
diarrhea in children,
Wilson's disease, the
common cold and for the prevention of
blindness in patients with age-related dry type of
macular degeneration and is very effective in decreasing the incidence of
infection in the elderly.
Zinc not only modulates cell-mediated immunity but is also an
antioxidant and
anti-inflammatory agent.