Zinc deficiency in pregnant rhesus monkeys: effects on behavior of infants

Sandstead, Harold H.; Strobel, David A.; Logan, George B.; Marks, E. O.; Jacob, Robert A.

doi:10.1093/ajcn/31.5.844

Cited by 81 publications

(22 citation statements)

References 21 publications

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“…In the rhesus monkey, offspring who were zinc deprived during the third trimester of pregnancy were not as active, and played and explored less than control infants (Sandstead et al, 1978). In addition to lethargy and reduced responsiveness, deficits in learning, attention, and memory characterized offspring who were exposed to suboptimal nutrition from conception (Golub et al, 1995(Golub et al, , 1996.…”

Section: Long-term Effects Of Gestational Zinc Deficiencymentioning

confidence: 99%

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Uriu‐Adams

Keen

2010

Birth Defects Research Pt B

118

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A large body of evidence supports the concept that human pregnancy outcome is significantly influenced by the nutritional status of the mother. The consumption of "poor diets" has been associated with an increased risk for pregnancy complications, including gross structural birth defects, prematurity, low birth weight, and an increased risk for neurobehavioral and immunological abnormalities after birth. Forty-four years ago, zinc deficiency in mammals was shown to be teratogenic. Maternal zinc deficiency produces effects ranging from infertility and embryo/fetal death, to intrauterine growth retardation and teratogenesis. Postnatal complications of maternal zinc deficiency can also occur, and include behavioral abnormalities, impaired immunocompetence, and an elevated risk for high blood pressure in the offspring. It has been suggested that developmental zinc deficiency in humans can present a significant challenge to the conceptus, increasing the risk for numerous defects. Developmental zinc deficiency can occur through multiple pathways, and the concept that acute phase response-induced changes in maternal zinc metabolism may be a common cause of embryonic and fetal zinc deficiency is presented. Potential mechanisms underlying the teratogenic effects of zinc deficiency are reviewed. The potential value of maternal zinc supplementation in high risk pregnancies is discussed.

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Section: Long-term Effects Of Gestational Zinc Deficiencymentioning

confidence: 99%

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Uriu‐Adams

Keen

2010

Birth Defects Research Pt B

118

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“…Research on a small number of nonhuman primates (rhesus) has shown that severe maternal zinc deprivation (<1 ppm dietary zinc) throughout most of the third trimester caused acrodermatitis in the dam and a subsequent reduction of exploration and play in infants during weaning (353). Later study of these animals found impaired ability to solve complex learning sets at 300 and 700 days, but not at 1000 days (354).…”

Section: Importance Of Zinc To Brain Devel-opment and Function: Animamentioning

confidence: 99%

Zinc: Health Effects and Research Priorities for the 1990s

Walsh¹,

Sandstead²,

Prasad³

et al. 1994

Environmental Health Perspectives

156

225

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This review critically summarizes the literature on the spectrum of health effects of zinc status, ranging from symptoms of zinc deficiency to excess exposure. Studies on zinc intake are reviewed in relation to optimum requirements as a function of age and sex. Current knowledge on the biochemical properties of zinc which are critical to the essential role of this metal in biological systems is summarized. Dietary and physiological factors influencing the bioavailability and utilization of zinc are considered with special attention to interactions with iron and copper status. The effects of zinc deficiency and toxicity are reviewed with respect to specific organs, immunological and reproductive function, and genotoxicity and carcinogenicity. Finally, key questions are identified where research is needed, such as the risks to human health of altered environmental distribution of zinc, assessment of zinc status in humans, effects of zinc status in relation to other essential metals on immune function, reproduction, neurological function, and the cardiovascular system, and mechanistic studies to further elucidate the biological effects of zinc at the molecular level. - There is considerable evidence that zinc deficiency in humans is a serious worldwide problem and outweighs the potential problem of accidental, self-imposed, or environmental exposure to zinc excess. Acute deficiency (1) and chronic deficiency (2) are well-known entities in human populations and are probably much more common than generally recognized. The importance of zinc for human health was first documented in 1963 (3) Telephone (617) (617) 638-4329. E-mail: ctwalsh~bu.edu renal disease, and other chronically debilitating diseases are now known to be predisposing factors for zinc deficiency in humans (4).Zinc deficiency is reflected in clinical syndromes which affect men and women of all ages and all socioeconomic and cultural classes in the United States. It is neither prevalent in any specific area of the United States nor associated with any specific or definitive biochemical marker, which can make its identification difficult and confusing. Its presence is manifested by a wide spectrum of symptoms, from acute, life threatening problems to mild subclinical or marginal disorders which may only vaguely disturb well being. The acute problems are often seen in profoundly ill patients treated in hospitals, whereas subclinical problems may be so vague that patients seek assistance outside traditional medical practice.Based upon clinical data and using traditional, epidemiologic techniques, Henkin and Aamodt (5) have reclassified zinc deficiency into three syndromes; these are a) acute, b) chronic, and c) subacute zinc deficiency. Acute zinc deficiency is relatively uncommon and follows parenteral hyperalimentation or oral L-histidine administration. Chronic zinc deficiency is more common, usually resulting from chronic dietary lack of zinc. Subacute or latent zinc deficiency is the most common of these syndromes. It is estimated that there are 4...

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“…In this respect. Pekarek et al [22] observed simi larly high hair zinc levels in a severely zincdeprived patient, and increases in hair zinc content during zinc deprivation have been found in monkeys [23], These results might be due to a high zinc release from tissues, since it is well known that 'stress' is sufficient to cause tissue catabo lism. Moreover, severe muscle catabolism leads to a substantial loss of zinc in the urine [24].…”

Section: Discussionmentioning

confidence: 96%

Zinc Status in Anorexia nervosa

Varela¹,

Marcos²,

Navarro³

1992

Ann Nutr Metab

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Some aspects of zinc nutritive status in patients suffering from anorexia nervosa were evaluated. Basic anthropometric measurements, Zn levels in serum, urine and hair as well as serum alkaline phosphatase (ALP) and lactate dehydrogenase (LDH; Zn-dependent enzymes) and delayed dermal hypersensitivity were tested both in patients and in control subjects. The patients showed higher Zn levels in serum (123%), hair (85%) and urine (215 %) than controls, whereas ALP and LDH values were 38 and 21 %, respectively, lower than those from the control group. Half of the patients showed hypoergy, and less than 50% of them were able to show a normal immune response. These results suggest that Zn-dependent functions may be impaired in anorexia nervosa as a consequence of Zn unavailability.

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Zinc deficiency in pregnant rhesus monkeys: effects on behavior of infants

Cited by 81 publications

References 21 publications

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Zinc and reproduction: effects of zinc deficiency on prenatal and early postnatal development

Zinc: Health Effects and Research Priorities for the 1990s

Zinc Status in Anorexia nervosa

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