Welcome to the December edition of Albion's "Minerals In the News", a compilation of recent studies on minerals from various peer reviewed publications. This is a monthly service from Albion Human Nutrition and is intended for the use of Albion’s customers and associates.
Zinc deficiency affects DNA damage, oxidative stress, antioxidant defenses, and DNA repair in rats.
Song Y, et al
J Nutr, Sept 2009: 139(9):1626-31.
(AA) Approximately 12% of Americans do not consume the Estimated Average Requirement for zinc and could be at risk for marginal zinc deficiency. Zinc is an essential component of numerous proteins involved in the defense against oxidative stress and DNA damage repair. Studies in vitro have shown that zinc depletion causes DNA damage. We hypothesized that zinc deficiency in vivo causes DNA damage through increases in oxidative stress and impairments in DNA repair. Sprague-Dawley rats were fed zinc-adequate (ZA; 30 mg Zn/kg) or severely zinc-deficient (ZD; <1 mg Zn/kg) diets or were pair-fed zinc-adequate diet to match the mean feed intake of ZD rats for 3 wk. After zinc depletion, rats were repleted with a ZA diet for 10 d. In addition, zinc-adequate (MZA 30 mg Zn/kg) or marginally zinc-deficient (MZD; 6 mg Zn/kg) diets were given to different groups of rats for 6 wk. Severe zinc depletion caused more DNA damage in peripheral blood cells than in the ZA group and this was normalized by zinc repletion. We also detected impairments in DNA repair, such as compromised p53 DNA binding and differential activation of the base excision repair proteins 8-oxoguanine glycosylase and poly ADP ribose polymerase. Importantly, MZD rats also had more DNA damage and higher plasma F(2)-isoprostane concentrations than MZA rats and had impairments in DNA repair functions. However, plasma antioxidant concentrations and erythrocyte superoxide dismutase activity were not affected by zinc depletion. These results suggest interactions among zinc deficiency, DNA integrity, oxidative stress, and DNA repair and suggested a role for zinc in maintaining DNA integrity.
Hair Tissue Mineral Analysis and Metabolic Syndrome.
Park SB, et al.
Biol Trace Elem Res; Sept 2009; 130(3):218-28..
(AA) Deficiency of minerals causes functional abnormality of enzymes, frequently resulting in metabolic disturbance. We investigated possible relationship between minerals and metabolic syndrome by analysis of hair tissue minerals. We selected 848 subjects older than 20 years of age at Ajou University Hospital from May 2004 to February 2007. We excluded the subjects who had cancers, steroid and thyroid medication, and incomplete record from the study. Finally, 343 subjects were eligible. We performed cross-sectional analysis for the relationship between minerals and metabolic syndrome. The contents of calcium, magnesium, and copper in the metabolic syndrome group were significantly lower than those of the normal group, whereas the amounts of sodium, potassium, and mercury in the metabolic syndrome group were significantly higher than those of the normal group. By dividing the subjects into quartile with the level of calcium, magnesium, and mercury concentrations, we carried out logistic regression analysis to study the subjects and found that the subjects in the third quartile of calcium and magnesium concentrations had significantly lower odds ratio (OR) of the metabolic syndrome compared with that of the lowest quartile group [OR = 0.30, confidence interval (CI) = 0.10-0.89; OR = 0.189, CI = 0.063-0.566] and that the subjects in the highest mercury quartile had significantly higher OR of the metabolic syndrome compared with that of the lowest mercury quartile group (OR = 7.35, CI = 1.73-31.1). As part of the metabolic syndrome, the optimal calcium and magnesium concentrations in hair tissue may reflect decreased risk of metabolic syndrome, whereas high mercury concentration in hair tissue may indicate increased risk of metabolic syndrome.
Efficacy of Zinc Supplements in Reducing Relapses in Steroid-sensitive Nephrotic Syndrome.
Arun S, et al..
Pediatr Nephrol; Aug 2009; 24(8):1583-6.
(AA) Relapses in steroid-sensitive nephrotic syndrome (SSNS) often follow infections of the respiratory or gastrointestinal tract. Based on data that zinc supplements reduce the risk of infections, we examined the efficacy of such supplements in reducing relapse rates in these patients. Eighty-one patients with SSNS (1-16 years old) were stratified into frequent (n = 52) and infrequent (n = 29) relapsers and randomized to receive 12-months of therapy with the recommended dietary allowance of zinc (10 mg/day) (n = 40) or placebo (n = 41). Patients with frequent relapses also received long-term, alternate-day prednisolone. Subjects receiving zinc showed a 20% lower frequency of relapses, with 44.7% of the patients having sustained remission compared to 27.5% in the placebo group (P > 0.05). Patients with frequent relapses receiving zinc showed a 28% reduction in relapse rates and a significantly higher likelihood of sustained remission (P = 0.02). Findings from this double blind, randomized study suggest that zinc supplementation results in trends towards remission and reduced relapses, especially in patients with frequent relapses. Prospective, adequately powered studies are required for confirmation of these findings.
Antenatal Supplementation with Folic Acid + Iron + Zinc Improves Linear Growth and Reduces Peripheral Adiposity in School-age Children in Rural Nepal
Stewart CP, et al
Am J Clin Nutr; July 2009; 90(1):132-40.
(AA) We previously reported that a randomized controlled trial of antenatal micronutrient supplements in rural Nepal decreased the risk of low birth weight by approximately 15%. The objective was to examine the effects of micronutrient supplementation on growth and body composition in children of supplemented mothers through school age. Mothers received 1 of 5 micronutrient supplements daily: folic acid, folic acid + iron, folic acid + iron + zinc, multiple micronutrients, or a control. All of the supplements contained vitamin A. Children born during this trial were revisited at age 6-8 y to measure height, weight, mid upper arm circumference, waist circumference, and triceps and subscapular skinfold thicknesses. Arm fat and muscle area were estimated by using standard formulas, and height-for-age, weight-for-age, and body mass index-for-age z scores were calculated by using the World Health Organization growth standard. Of the 3771 surviving children, 3324 were revisited and consented to anthropometric measurements. Maternal supplementation with folic acid + iron + zinc resulted in an increase in mean height (0.64 cm; 95% CI: 0.04, 1.25) and a reduction in mean triceps skinfold thickness (-0.25 mm; 95% CI: -0.44, -0.06), subscapular skinfold thickness (-0.20 mm; 95% CI: -0.33, -0.06), and arm fat area (-0.18 cm(2); -0.34, -0.01). No significant differences were found between groups in mean weight or body mass index-for-age z scores, waist circumference, or arm muscle area. Other micronutrient combinations including a multiple micronutrient formulation failed to show a growth benefit. Antenatal supplementation with zinc may benefit child growth, particularly in areas where a deficiency of this nutrient is common.
Application of the Dietary Reference Intakes in Developing a Recommendation for Pregnancy Iron Supplements in Canada
Cockell KA, et al.
Am J Clin Nutr; Oct 2009; 90(4):1023-8.
(AA) For many pregnant Canadian women, usual iron intakes from food appear to be inadequate compared with Dietary Reference Intake requirement estimates. Dietary intake modeling was undertaken to determine an amount of iron supplementation that would confer acceptably low prevalence of apparently inadequate and apparently excessive intakes. The distribution of usual dietary iron intakes was estimated with the use of 24-h recalls from pregnant women aged 19-50 y in the Canadian Community Health Survey, Cycle 2.2. The prevalence of usual intakes below the Estimated Average Requirement for pregnancy (22 mg/d) or above the Tolerable Upper Intake Level (45 mg/d) was estimated. Iterative modeling with incremental iron supplement was performed to determine a suitable supplement amount. Because the sample of pregnant women was small (148 day 1 recalls), estimates of the tails of the distributions had large SDs, and supporting analyses based on intake data from nonpregnant women (4540 day 1 recalls) were made. Daily supplementation shifted the intake distribution curve without changing its shape. Supplementation with 16 mg iron/d was consistent with low (<3%) prevalence of apparently inadequate intakes. This amount of supplementation should not be associated with an increase in apparently excessive intakes by pregnant women in this population. On the basis of Dietary Reference Intakes, an iron supplement of 16 mg/d throughout pregnancy is justified as both efficacious and safe for healthy women living in Canadian households. This does not preclude the need for therapeutic iron doses for some individuals on the basis of iron status. The method can be applied to other populations if suitable baseline iron intake data are available.
Skeletal and Hormonal Effects of Magnesium Deficiency
Rude RK, Singer FR, Gruber HE.
J Am Coll Nutr. 2009 Apr;28(2):131-41.
(AA) Magnesium (Mg) is the second most abundant intracellular cation where it plays an important role in enzyme function and trans-membrane ion transport. Mg deficiency has been associated with a number of clinical disorders including osteoporosis. Osteoporosis is common problem accounting for 2 million fractures per year in the United States at a cost of over $17 billion dollars. The average dietary Mg intake in women is 68% of the RDA, indicating that a large proportion of our population has substantial dietary Mg deficits. The objective of this paper is to review the evidence for Mg deficiency-induced osteoporosis and potential reasons why this occurs, including a cumulative review of work in our laboratories and well as a review of other published studies linking Mg deficiency to osteoporosis. Epidemiological studies have linked dietary Mg deficiency to osteoporosis. As diets deficient in Mg are also deficient in other nutrients that may affect bone, studies have been carried out with select dietary Mg depletion in animal models. Severe Mg deficiency in the rat (Mg at <0.0002% of total diet; normal = 0.05%) causes impaired bone growth, osteopenia and skeletal fragility. This degree of Mg deficiency probably does not commonly exist in the human population. We have therefore induced dietary Mg deprivation in the rat at 10%, 25% and 50% of recommended nutrient requirement. We observed bone loss, decrease in osteoblasts, and an increase in osteoclasts by histomorphometry. Such reduced Mg intake levels are present in our population. We also investigated potential mechanisms for bone loss in Mg deficiency. Studies in humans and and our rat model demonstrated low serum parathyroid hormone (PTH) and 1,25(OH)(2)-vitamin D levels, which may contribute to reduced bone formation. It is known that cytokines can increase osteoclastic bone resorption. Mg deficiency in the rat and/or mouse results in increased skeletal substance P, which in turn stimulates production of cytokines. With the use of immunohistocytochemistry, we found that Mg deficiency resulted in an increase in substance P, TNFalpha and IL1beta. Additional studies assessing the relative presence of receptor activator of nuclear factor kB ligand (RANKL) and its decoy receptor, osteoprotegerin (OPG), found a decrease in OPG and an increase in RANKL favoring an increase in bone resorption. These data support the notion at dietary Mg intake at levels not uncommon in humans may perturb bone and mineral metabolism and be a risk factor for osteoporosis.
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