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Equate intake varies from 7.5 in high-income regions to 30 in South Asia

por Ethan Bayer (2020-05-15)


Equate intake varies from 7.5 in high-income regions to 30 in South Asia [16, 17]. Zinc intake is lower than recommended in more than 75 of pregnant women [18]. Zinc is a type 2 essential nutrient [19], as deficiency symptoms are rather nonspecific; response to repletion occurs very fast [20]. Deficiency determines growth retardation, male hypogonadism, delayed wound healing and cell-mediated immune dysfunction [21]. Reduced zinc is also associated with DNA damage, increased inflammatory status [22, 23] and represents a predisposing factor for malignant tumours development [24]. Some deficiency-associated conditions are partially explained considering zinc's role as a co-factor of enzymatic systems involved in nucleic acids replication, protein synthesis, and antioxidant defence. Disorders mainly related with CNS impaired function (behavioural changes, depression, emotional instability, anxiety, aggresivity, irritability, socializing deficits, impaired memory and learning, neurosensory alterations, anorexia etc.) are frequently associated with zinc deficiency in PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27309768 both humans and animal models [25, 26]. It is debatable, at least in case of some of these conditions, if decreased zinc is a consequence or a cause. Low zinc levels have been reported in autism spectrum disorders, attention deficit hyperactivity, schizophrenia, and Tapinarof spinocerebellar ataxia type 2 [27], underlining its importance in brain functioning. Under moderate zinc deficient diet in rats, brain zinc is maintained within normal limits, due to increased uptake [28], following transporters adaptation: the expressions of metallothionein-I and ZnT-1 are decreased, and that of LIV-1 is increased [29]; even so, subclinical deficiency affects human brain function [30]. Zinc salts are relatively nontoxic, particularly if taken orally. Symptoms including nausea, vomiting, epigastric pain, lethargy, and fatigue appear `at extremely high intakes (almost 100 folds above the recommended dietary allowance ?15 mg elemental zinc daily). Doses of 100300 mg zinc daily, which are high above recommended,determine induced copper deficiency, anaemia and neutropenia, immune dysfunction and increased lowdensity vs. high density lipoproteins ratio [31?3]. Zinc toxicity is also manifest at the CNS level, where zinc has an additional role in the death of seizures-damaged neurons [34]. In Alzheimer's disease, zinc has been shown to facilitate beta-amyloid aggregation [35]. In Parkinson disease, excessive hair zinc levels [36] and increased zinc exposure [37] are reported, but serum zinc is decreased [38]; substantia nigra zinc levels were found to gradually increase in rat model of parkinsonism [39]. A study of Larson et al., [40], evidenced increased withdrawal jumpings, but with no influence on acute dependence in conditions of zinc-chelator administration in mice. This is in accordance with preliminary data of ours showing a reduction of morphine dependence in rats by zinc PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/27909987 chloride (ZnCl2) (dose-dependent) [41]. A possible reasonable, yet partial explanation for these results can be given considering zinc ions effect of reducing -opioid agonists' binding to receptors [42, 43]. Taking into consideration zinc ability to reduce morphine-dependence intensity and the enhancement of withdrawal manifestations by zinc-chelators, we have formulated the hypothesis that zinc supplementation may reduce the risk of addiction in cancer-patients treated with opioids for chronic pain. The idea is reinforced by.