ZINC AND GROWTH
In this issue of International Pediatrics, Dr. Kaji has written a Review Article entitled “Zinc in Endocrinology”. Zinc, although present in minute quantities in humans, is an essential nutrient and plays an important role as a component of many enzymes and the catalysts of enzyme systems regulating cell growth, DNA and protein synthesis, energy metabolism, regulation of gene transcription, hormone levels, and growth factor metabolism. Conversely, hormones influence zinc metabolism at several levels, including the excretion and transport of this metal.
In 1963, Prasad et al2 found that zinc deficiency was a cause of growth retardation and delayed sexual development in men. Since then this report has also shed light on the study of zinc metabolism and the role of this metal in the field of growth and sexual development in humans and other animals.
Growth hormone (GH) is a key hormone for growth and development. And zinc is also known to affect GH metabolism. Zinc ion induces the dimerization of GH in the way that two zinc ions associate per dimer of GH in a cooperative fashion. Formation of a zinc ion-GH diametric complex may be important for storage of GH in secretary granules.3 However, the biochemical and structural basis whereby zinc ion functions in storage or release of GH has not been elucidated.
The potential impact of zinc deficiency in infants, children, and maternal health in developing counties was not recognized by the United Nations until 1997, when zinc was included among the micronutrients deficiencies listed as a priority in the Third Report on the World Nutrition Situation.4 Zinc intake in insufficient quanties and/or of insufficient bioavailability, and various degrees of zinc deficiency, have been a public health problem in humans in both developed and developing countries.
Marginal zinc deficiency, as a consequence of inadequate zinc intake, causes growth retardation. We reported a boy with partial GH deficiency due to chronic mild zinc deficiency.5 When zinc administration was started, his growth rate, GH levels and plasma zinc concentrations increased significantly.5 Nakamura et al6 observed that zinc supplementation was effective for inducing growth and increasing IGF-I and osteocalcin concentrations in short children with zinc deficiency. Kaji et al7 also found that about 60% of short children had marginal zinc deficiency, and that oral zinc supplementation was effective on height gain in short boys with marginal zinc deficiency, but not in girls. The reasons for the difference in the effects between the sexes are not fully understood. These findings suggest that zinc deficiency should be considered as an etiologic factor in some children with unexplained short stature.
In general, some short children have poor appetites and dislike zinc-rich foods such as meats. Dr. Kaji reported that the recent prevalence of precooked foods, snacks and convenience foods is also the cause of marginal zinc deficiency. These inadequate dietary habits may be one of the factors for marginal zinc deficiency in some short children. In turn, marginal zinc deficiency can cause poor appetite, since zinc is also important for taste.
During the past few decades, many investigations have been performed to evaluate the association between maternal zinc nutrition and pregnancy outcome in humans and animals. In humans, however, a firm consensus has been in debate as to whether there is a positive association between maternal zinc nutrition and pregnancy outcome, including birth weight of infants and complications during pregnancy and delivery. Infant malnutrition and mortality rates are high, especially, in low birthweight infants in less-developed countries. Zinc deficiency is also widely prevalent in these circumstances. Recently, the effects of zinc supplements given to pregnant mothers during their infants’ growth and morbidity have been reported. In 2001, Osendarp et al8 reported that maternal zinc supplementation during pregnancy resulted in a reduction of the health risks in Bangladeshi low-birthweight infants in a randomized placebo controlled trial, although this intervention did not improve birth weight. On the contrary, in 1989 Mahomed et al9 found no effects on gestational age, birth weight, neonatal abnormalities, and complications of labor and delivery between mothers given a zinc supplement and those given a placebo in
Marginal zinc deficiency seems prevalent in infancy even in developed countries. In 2000, Umeta et al11 also observed that zinc supplementation can halt the stunting process in stunted infants in rural
Since 1963, zinc deficiency has also been reported to be a cause of hypogonadism. This observation led us to study the interrelationship between zinc and gonadal function. The zinc content of the prostate gland, the seminal fluid and ejaculated sperm are very high and testicular zinc is essential for spermatogenesis.13 Hunt et al14 observed the decreased testosterone level and seminal volume per ejaculation in healthy male volunteers who were fed a zinc-restricted diet for 35 days. Constitutional short boys at Tanner stages 1 and 2 had lower zinc levels in their serum and hair and lower testosterone levels than those at Tanner stages 3 to 5.15 These results suggest that the relative testosterone deficiency in constitutional delay may result in decreased zinc levels, which can cause further delay in sexual development and growth. Therefore, zinc therapy may be effective in some constitutional delay of growth and puberty.
As the public continues to explore zinc nutritional supplements for the prevention or treatment of various health problems, physicians need to inquire about the use of zinc and be aware of the possible side effects. Since a long-term zinc administration or a high dose of zinc can potentially induce antagonistic interactions with iron and copper, especially for catch-up growth in children with severe protein-energy malnutrition and an already compromised immune system, evaluation of both iron and copper status before and after intervention can provide reassurance that these status were not adversely affected. Porea et al16 reported an adolescent who developed anemia, leucopenia, and neutropenia after prolonged use of over-the-counter zinc for treatment of acne. Hypochromia and sideroblastic anemia may result from long-term or excessive exposure to zinc.
The interrelationships among zinc, growth, gonadal function, and GH-IGF-I axis appear to be complex and deserve further investigations.
References
Department of Pediatrics,
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