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Department of Internal Medicine,
University Health Center,
Detroit, MI
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INTRODUCTION |
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 TOP INTRODUCTION REFERENCES |
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The consequences of zinc deficiency are several and they impact on human health severely [3]. Growth retardation, male hypogonadism, neuro-sensory changes (abnormal dark adaptation and changes in taste acuity), delayed wound healing, abnormal immune functions, and impaired cognitive functions are some of the major effects of human zinc deficiency which are reversible with zinc supplementation [3]. A mild deficiency of zinc in pregnant women is associated with increased maternal morbidity, abnormal taste sensation, prolonged gestation, inefficient labor, atonic bleeding, and increased risks to the fetus [3].
A meta-analysis of 25 studies of the effect of zinc supplementation on growth in children less than 13 years of age was reported recently [4]. Zinc supplementation showed a highly statistically significant effect on linear growth and weight gain. Children who were stunted at baseline had a larger effect of zinc supplementation on linear growth, while non-stunted children had no effect. With weight gain, the magnitude of the effect of zinc supplementation was inversely related to plasma zinc concentration at baseline. These results show that growth retardation which is widespread throughout the developing countries worldwide may indeed be due to zinc deficiency and that zinc supplementation corrects this problem.
During our studies in the Middle East, we observed that most of the zinc deficient dwarfs did not live beyond the age of 25 years. Parasitic, viral and bacterial infections were presumed to be the causes of death. Several studies have now demonstrated the benefits of zinc supplementation on infectious diseases in human populations. Double-blind placebo-controlled trials have shown that the incidence and duration of acute and chronic diarrhea [5], and of acute lower respiratory tract infections [6], decreased significantly following zinc supplementation. Recently it was shown in Papua, New Guinea, that zinc supplementation reduced malaria incidence by >35% as judged by health center attendance records [7]. Zinc supplementation also reduced the frequency of recurrent boils in hospital patients and decreased S. Mansoni egg counts in children given zinc supplementation [7]. Subjects suffering from acrodermatitis enteropathica, a congenital disorder of zinc deficiency, were completely cured of repeated infections following zinc supplementation [7].
Zinc affects multiple aspects of the immune system. Th1 cytokine production, development of B lymphocytes and Th1 production of antibodies, NK cell and cytolytic activity functions, are all affected adversely as a result of zinc deficiency [7]. Macrophage and neutrophil functions are affected adversely by zinc deficiency and apoptosis of lymphocytes and perhaps other cells are potentiated under conditions of zinc deficiency [7]. Zinc also functions as an antioxidant and thus can play a role in stabilization of cell membranes.
Recent studies from China showed that cognitive impairment were corrected by zinc supplementation in children who were zinc deficient [8]. Thus three major health problems in developing countries, namely growth retardation, susceptibility to infections and cognitive impairment may indeed be related to zinc deficiency and all three are reversible with zinc supplementation.
In this issue of the Journal of the American College of Nutrition, two papers on zinc have been published [9,10]. One paper concluded that lower consumption of zinc and low serum zinc levels in India were associated with the prevalence of coronary artery disease and diabetes. If this observation is confirmed, one would then consider the zinc status to be an extremely important risk factor for the above conditions. The other paper presents results of zinc metabolic studies in patients with exocrine pancreatic insufficiency. They observed decreased zinc absorption and increased urinary zinc excretion and suggested that these alterations may form the basis for zinc deficiency in patients with chronic pancreatic disease. Unfortunately they did not measure directly endogenous excretion of zinc, although they concluded indirectly that decreased loss of endogenously excreted zinc may have sustained borderline zinc balance and zinc sufficiency. We have shown earlier that in experimental human zinc deficient subjects, endogenous excretion of zinc plays a more important role in homeostasis of zinc than the intestinal absorption of zinc [11]. In the studies of Dutta et al [10], dermal loss of zinc was not considered in the balance data, thus their borderline zinc balance in patients with chronic pancreatic disease may in reality represent a negative zinc balance.
Besides nutritional deficiency of zinc there are many other clinical conditions which may result in zinc deficiency. These include other malabsorption syndromes, chronic alcoholic liver disease, chronic renal disease, sickle cell disease, total parenteral nutrition if zinc is not replaced adequately, following use of chelating agents such as penicillamine therapy in Wilson’s disease, and various chronic debilitating illnesses [3].
It should be clear from the above discussion that zinc deficiency is a common nutritional problem in developing countries. A conditioned deficiency of zinc in association with many diseased states is very prevalent not only in the developing countries but also in the developed world. There are several adverse consequences to health related to zinc deficiency, however, it continues to remain a neglected problem. We can only hope that someday this is corrected.
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REFERENCES |
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TOPINTRODUCTIONREFERENCES |
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This article has been cited by other articles:
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  M. H. Dabbaghmanesh, A. Sadegholvaad, F. Zarei, and G. Omrani Zinc Status and Relation to Thyroid Hormone Profile in Iranian Schoolchildren J Trop Pediatr, February 1, 2008; 54(1): 58 - 61. [Abstract] [Full Text] [PDF]
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K. E. Elizabeth, V. Krishnan, and P. Zachariah Auxologic, Biochemical and Clinical (ABC) Profile of Low Birth Weight Babies A 2-year Prospective Study J Trop Pediatr, December 1, 2007; 53(6): 374 - 382. [Abstract] [Full Text] [PDF]
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 L. Huang, C. P. Kirschke, Y. Zhang, and Y. Y. Yu The ZIP7 Gene (Slc39a7) Encodes a Zinc Transporter Involved in Zinc Homeostasis of the Golgi Apparatus J. Biol. Chem., April 15, 2005; 280(15): 15456 - 15463. [Abstract] [Full Text] [PDF]
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 D. K. Lee, J. Geiser, J. Dufner-Beattie, and G. K. Andrews Pancreatic Metallothionein-I May Play a Role in Zinc Homeostasis during Maternal Dietary Zinc Deficiency in Mice J. Nutr., January 1, 2003; 133(1): 45 - 50. [Abstract] [Full Text] [PDF]
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 B. H. Grahn, P. G. Paterson, K. T. Gottschall-Pass, and Z. Zhang Zinc and the Eye J. Am. Coll. Nutr., April 1, 2001; 20(2): 106 - 118. [Abstract] [Full Text] [PDF]
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G. K. Andrews and J. Geiser Expression of the Mouse Metallothionein-I and -II Genes Provides a Reproductive Advantage during Maternal Dietary Zinc Deficiency J. Nutr., September 1, 1999; 129(9): 1643 - 1648. [Abstract] [Full Text]
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