Minerals in the News Vol. 9, No. 10 (October 2011)

Houston MC.

Curr Hypertens Rep. 2011 Aug;13(4):309-17.

 

Blood pressure readings in hypertensive and non hypertensive patients have been seen to be reduced, as one increases the intake of dietary potassium in observational studies, clinical trials, and several meta-analyses. In hypertensive patients, the linear dose-response relationship is a 1.0 mm Hg reduction in systolic BP and a 0.52 mm Hg reduction in diastolic BP per 0.6 g per day increase in dietary potassium intake regardless of baseline potassium deficiency. The average reduction in BP with 4.7 g (120 mmol) of dietary potassium per day is 8.0/4.1 mm Hg, depending race and on the relative intakes of other minerals such as sodium, magnesium, and calcium. If the dietary sodium chloride intake is high, there is a greater BP reduction with an increased intake of dietary potassium. Blacks have a greater decrease in BP than Caucasians with an equal potassium intake. Potassium-induced reduction in BP significantly lowers the incidence of stroke (cerebrovascular accident, CVA), coronary heart disease, myocardial infarction, and other cardiovascular events. However, potassium also reduces the risk of CVA independent of BP reductions. Increasing consumption of potassium to 4.7 g per day predicts lower event rates for future cardiovascular disease, with estimated decreases of 8% to 15% in CVA and 6% to 11% in myocardial infarction.

 

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Moser AM, et al.

J Pediatr Hematol Oncol. 2011; 33(6):467-9

 

Globally, iron deficiency anemia (IDA) is the number one hematologic problem. Measures to prevent IDA in infants have not been well sustained. The aim was to evaluate the incidence of developing IDA in the second year of life, in infants who were nonanemic at the age of 1 year on routine blood test. Blood samples were obtained from 193, 24-month-old toddlers, from 2 large clinics of both main sectors in Southern Israel, comparable for lower economic status. IDA was defined as hemoglobin < 11 gr% and microcytosis as mean corpuscular volume < 70 fL. IDA was detected in 8 of 118 Bedouins (5 males) and in 10 of 75 Jewish (6 males) infants (P < 0.01). The probability of a nonanemic child to develop IDA in the second year of life for the whole study population was 9.3% (18 of 193 infants) and significantly higher in the Jewish population (13.3.0% vs. 6.8%, P < 0.01). Given the difficulty of toddlers to maintain a non-IDA status, and the very low probability of iron overload, the results clearly show the need to continue iron supplementation into the second year.

 

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Song M, et al.

J Hepatol; 2011 July 19; [Epub ahead of print].

 

Some manifestations of metabolic syndrome, like hyperlipidemia and fatty liver are associated with copper deficiency. Fructose intake has been reported to exacerbate complications of copper deficiency. This study investigated whether copper deficiency plays a role in fructose-induced fatty liver and explored the potential underlying mechanism(s). Male weanling Sprague-Dawley rats were fed an adequate copper or a marginally copper deficient diet for 4 weeks. Deionized water or deionized water containing 30% fructose (w/v) was also given ad lib. Copper and iron status, hepatic injury and steatosis, duodenum copper transporter-1(Ctr-1) were assessed. Fructose feeding impaired copper status, leading to iron overload. Liver injury and fat accumulation were significantly induced in marginal copper deficient rats exposed to fructose as evidenced by robust increased plasma aspartate aminotransferase and hepatic triglyceride. Hepatic carnitine palmitoyl-CoA transferase I expression was significantly inhibited, whereas hepatic fatty acid synthase was markedly up-regulated in marginal copper deficient rats fed with fructose. Hepatic antioxidant defense system was suppressed and lipid peroxidation was increased by marginal copper deficiency and fructose feeding. Moreover, duodenum Ctr-1 expression was significantly increased by marginal copper deficiency, whereas this increase was stopped by fructose feeding. Our data suggest that high fructose-induced nonalcoholic fatty liver disease may be due, in part, to inadequate dietary copper. Impaired duodenum Ctr1 expression seen in fructose feeding may lead to decreased copper absorption, and subsequent copper deficiency.

 

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Besecker BY, et al.

Am J Clin Nutr; 2011Jun; 93(6):1356-64.

 

Zinc deficiency is associated with immune dysfunction and infection. Previous human studies have shown that the acute phase response to sepsis caused plasma zinc to redistribute. Whether the alteration in zinc metabolism is predictive of disease severity in the setting of critical illness is unclear. The researchers investigated whether differences occurred in zinc metabolism at the start of critical illness between infected (septic) and noninfected subjects. They conducted this prospective study in an adult medical intensive care unit (MICU) at a tertiary care hospital. Subjects were enrolled within 24 h of intensive care unit admission. Subjects who did not meet sepsis criteria were considered for the critically ill control (CIC) arm. Blood was collected to measure plasma zinc and cytokine concentrations and zinc transporter gene expression in peripheral blood monocytes. Clinical data during the MICU stay were also recorded. A total of 56 patients were evaluated (22 septic, 22 CIC, and 12 healthy subjects). Plasma zinc concentrations were below normal in CIC patients and further reduced in the septic cohort (57.2 ± 18.2 compared with 45.5 ± 18.1 ?g/dL). Cytokine concentrations increased with decreasing plasma zinc concentrations (P = 0.05). SLC39A8 gene expression was highest in patients with the lowest plasma zinc concentrations and the highest severity of illness.The alteration of zinc metabolism was more pronounced in septic patients than in noninfected critically ill patients. Specifically, sepsis was associated with lower plasma zinc concentrations and higher SLC39A8 mRNA expression, which correlated with an increased severity of illness, including cardiovascular dysfunction.

 

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Chen Y, et al.

J Nutr. 2011 Jul;141(7):1225-32.

 

Even though chromium has been considered as an essential mineral for 50 years, possessing therapeutic impact in treating the symptoms of type 2 diabetes, its mechanism of action at a molecular level is unknown. One chromium-binding biomolecule, low-molecular weight chromium-binding substance (LMWCr or chromodulin), has been found to be biologically active in vitro assays and proposed as a potential candidate for the in vivo biologically active form of chromium. Characterization of the organic component of LMWCr has proven difficult. Treating bovine LMWCr with trifluoroacetic acid followed by purification on a graphite powder micro-column generates a heptapeptide fragment of LMWCr. The peptide sequence of the fragment was analyzed by MS and tandem MS (MS/MS and MS/MS/MS) using collision-induced dissociation and post-source decay. Two candidate sequences, pEEEEGDD and pEEEGEDD (where pE is pyroglutamate), were identified from the MS/MS experiments; additional tandem MS suggests the sequence is pEEEEGDD. The N-terminal glutamate residues explain the inability to sequence LMWCr by the Edman method. Langmuir isotherms and Hill plots were used to analyze the binding constants of chromic ions to synthetic peptides similar in composition to apoLMWCr. The sequence pEEEEGDD was found to bind 4 chromic ions per peptide with nearly identical cooperativity and binding constants to those of apoLMWCr. This work should lead to further studies examining a potential role for LMWCr in treating the symptoms of type 2 diabetes and other conditions resulting from improper carbohydrate and lipid metabolism.

 

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Aaron GJ, et al.

J Nutr. 2011 Jul;141(7):1225-32.

 

The effect of zinc fortification on plasma zinc is not certain. The objective in this study was to determine whether plasma zinc concentration changes in response to consuming zinc-fortified foods or liquid zinc supplements. Researchers conducted a 4-wk double-blind, randomized trial among 132 healthy Senegalese men ? 18 y. Participants received 1 of 4 interventions: 1) (control) 200 g/d of wheat bread fortified with iron and folic acid, but not zinc, and a liquid multivitamin supplement without zinc between meals; 2) (zinc supplement) the same bread and the same multivitamin supplement with 15 mg zinc as ZnSO(4) added; 3) (moderate zinc fortification) the same bread cofortified with 7.5 mg zinc as ZnO and the same multivitamin supplement without zinc; or 4) (high zinc fortification) the same bread cofortified with 15 mg zinc as ZnO and the same multivitamin supplement without zinc. Fasting blood samples were collected twice at baseline and at d 15 and 29 of the intervention. There was no significant interaction between group and study day (P = 0.11). However, at d 15, the mean change in plasma zinc concentration in the zinc-supplemented group was greater than in the placebo and fortification groups ( 0.72 ?mol/L vs. -0.09 to 0.03 ?mol/L; P = 0.05). At d 29 there were no significant group-wise differences. Across all time points, the zinc-supplemented group was the only group where plasma zinc concentration increased from baseline (P = 0.006). Plasma zinc concentration may not be a sufficiently sensitive indicator to evaluate short-term responses to zinc fortification.