Background: Magnesium deficiency is associated with poor physical performance, but no trials are available on how magnesium supplementation affects elderly people's physical performance.Objective: ...The aim of our study was to investigate whether 12 wk of oral magnesium supplementation can improve physical performance in healthy elderly women.Design: In a parallel-group, randomized controlled trial, 139 healthy women (mean ± SD age: 71.5 ± 5.2 y) attending a mild fitness program were randomly allocated to a treatment group (300 mg Mg/d; n = 62) or a control group (no placebo or intervention; n = 77) by using a computer-generated randomization sequence, and researchers were blinded to their grouping. After assessment at baseline and again after 12 wk, the primary outcome was a change in the Short Physical Performance Battery (SPPB); secondary outcomes were changes in peak torque isometric and isokinetic strength of the lower limbs and handgrip strength.Results: A total of 124 participants allocated to the treatment (n = 53) or control (n = 71) group were considered in the final analysis. At baseline, the SPPB scores did not differ between the 2 groups. After 12 wk, the treated group had a significantly better total SPPB score (Δ = 0.41 ± 0.24 points; P = 0.03), chair stand times (Δ = −1.31 ± 0.33 s; P < 0.0001), and 4-m walking speeds (Δ = 0.14 ± 0.03 m/s; P = 0.006) than did the control group. These findings were more evident in participants with a magnesium dietary intake lower than the Recommended Dietary Allowance. No significant differences emerged for the secondary outcomes investigated, and no serious adverse effects were reported.Conclusions: Daily magnesium oxide supplementation for 12 wk seems to improve physical performance in healthy elderly women. These findings suggest a role for magnesium supplementation in preventing or delaying the age-related decline in physical performance. This trial was registered at clinicaltrials.gov as NCT01971424.
When magnesium is added to source-separated urine, struvite (MgNH4PO4·6H2O) precipitates and phosphorus can be recovered. Up to now, magnesium salts have been used as the main source of magnesium. ...Struvite precipitation with these salts works well but is challenging in decentralized reactors, where high automation of the dosage and small reactor sizes are required. In this study, we investigated a novel approach for magnesium dosage: magnesium was electrochemically dissolved from a sacrificial magnesium electrode. We demonstrated that this process is technically simple and economically feasible and thus interesting for decentralized reactors. Linear voltammetry and batch experiments at different anode potentials revealed that the anode potential must be higher than −0.9 V vs. NHE (normal hydrogen electrode) to overcome the strong passivation of the anode. An anode potential of −0.6 V vs. NHE seemed to be suitable for active magnesium dissolution. For 13 subsequent cycles at this potential, we achieved an average phosphate removal rate of 3.7 mg P cm−2 h−1, a current density of 5.5 mA cm−2 and a current efficiency of 118%. Some magnesium carbonate (nesquehonite) accumulated on the anode surface; as a consequence, the current density decreased slightly, but the current efficiency was not affected. The energy consumption for these experiments was 1.7 W h g P−1. A cost comparison showed that sacrificial magnesium electrodes are competitive with easily soluble magnesium salts such as MgCl2 and MgSO4, but are more expensive than dosing with MgO. Energy costs for the electrochemical process were insignificant. Dosing magnesium electrochemically could thus be a worthwhile alternative to dosing magnesium salts. Due to the simple reactor and handling of magnesium, this may well be a particularly interesting approach for decentralized urine treatment.
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► Electrochemical magnesium dosage is competitive with MgSO4 and MgCl2 dosage. ► To prevent passivation the anode potential has to be higher than −0.9 V vs. NHE. ► The average phosphate removal was 3.7 mg P cm−2 h−1 at −0.6 V vs. NHE. ► The energy consumption was low (max. 2.2 W h g P−1).
A direct, facile, and highly diastereo- and enantioselective dearomatization reaction of beta-naphthol derivatives with aziridines has been developed for the first time. A newly designed Box-OH ...ligand was employed for an insitu generated magnesium catalyst and proved to be efficient. The corresponding dearomatization product was transformed into a polycyclic scaffold and polyhydroxylated compound. 1HNMR studies revealed the activation mode of the dearomatization process of beta-naphthols, and a clear positive nonlinear effect was observed in the reaction, and provides insight into the coordination environment around the MgII center and the possible active species.
Magnesium is essential to the proper functioning of numerous cellular processes. Magnesium ion (Mg
2+
) deficits, as reflected in hypomagnesemia, can cause neuromuscular irritability, seizures and ...cardiac arrhythmias. With normal Mg
2+
intake, homeostasis is maintained primarily through the regulated reabsorption of Mg
2+
by the thick ascending limb of Henle’s loop and distal convoluted tubule of the kidney. Inadequate reabsorption results in renal Mg
2+
wasting, as evidenced by an inappropriately high fractional Mg
2+
excretion. Familial renal Mg
2+
wasting is suggestive of a genetic cause, and subsequent studies in these hypomagnesemic families have revealed over a dozen genes directly or indirectly involved in Mg
2+
transport. Those can be classified into four groups: hypercalciuric hypomagnesemias (encompassing mutations in
CLDN16
,
CLDN19
,
CASR
,
CLCNKB
), Gitelman-like hypomagnesemias (
CLCNKB
,
SLC12A3
,
BSND
,
KCNJ10
,
FYXD2
,
HNF1B
,
PCBD1
), mitochondrial hypomagnesemias (
SARS2
,
MT-TI
, Kearns–Sayre syndrome) and other hypomagnesemias (
TRPM6
,
CNMM2
,
EGF
,
EGFR
,
KCNA1
,
FAM111A
). Although identification of these genes has not yet changed treatment, which remains Mg
2+
supplementation, it has contributed enormously to our understanding of Mg
2+
transport and renal function. In this review, we discuss general mechanisms and symptoms of genetic causes of hypomagnesemia as well as the specific molecular mechanisms and clinical phenotypes associated with each syndrome.
Arterial hypertension is a disease with a complex pathogenesis. Despite considerable knowledge about this socially significant disease, the role of magnesium deficiency (MgD) as a risk factor is not ...fully understood. Magnesium is a natural calcium antagonist. It potentiates the production of local vasodilator mediators (prostacyclin and nitric oxide) and alters vascular responses to a variety of vasoactive substances (endothelin-1, angiotensin II, and catecholamines). MgD stimulates the production of aldosterone and potentiates vascular inflammatory response, while expression/activity of various antioxidant enzymes (glutathione peroxidase, superoxide dismutase, and catalase) and the levels of important antioxidants (vitamin C, vitamin E, and selenium) are decreased. Magnesium balances the effects of catecholamines in acute and chronic stress. MgD may be associated with the development of insulin resistance, hyperglycemia, and changes in lipid metabolism, which enhance atherosclerotic changes and arterial stiffness. Magnesium regulates collagen and elastin turnover in the vascular wall and matrix metalloproteinase activity. Magnesium helps to protect the elastic fibers from calcium deposition and maintains the elasticity of the vessels. Considering the numerous positive effects on a number of mechanisms related to arterial hypertension, consuming a healthy diet that provides the recommended amount of magnesium can be an appropriate strategy for helping control blood pressure.
•151 chemical compounds are tested towards their inhibiting effect on Mg alloys.•New inhibitors are tested on AZ31, AZ91, AM50, WE43, ZE41, Elektron 21 and three grades of pure magnesium.•The ...extensive database of magnesium corrosion inhibitors is set up.•A number of new inhibitors are discovered with efficiency exceeding that of chromate.•The salts of pyridinedicarboxylic and salicylic acids are the most efficient and universal Mg corrosion inhibitors.
This work presents the results of a systematic screening for magnesium corrosion inhibitors. The ability to form stable soluble complexes with Feii/iii was considered on first place when choosing the compounds for hydrogen evolution tests. Inhibiting effect of 151 individual compounds was tested towards six alloys (AZ31, AZ91, AM50, WE43, ZE41 and Elektron 21) and three grades of pure magnesium. Newly identified and previously reported inhibitors are ranked by their inhibiting efficiency and compared with Cr (VI) reference. A number of new inhibitors are discovered with efficiency exceeding that of chromate.
Magnesium (Mg(2+)) is an essential ion to the human body, playing an instrumental role in supporting and sustaining health and life. As the second most abundant intracellular cation after potassium, ...it is involved in over 600 enzymatic reactions including energy metabolism and protein synthesis. Although Mg(2+) availability has been proven to be disturbed during several clinical situations, serum Mg(2+) values are not generally determined in patients. This review aims to provide an overview of the function of Mg(2+) in human health and disease. In short, Mg(2+) plays an important physiological role particularly in the brain, heart, and skeletal muscles. Moreover, Mg(2+) supplementation has been shown to be beneficial in treatment of, among others, preeclampsia, migraine, depression, coronary artery disease, and asthma. Over the last decade, several hereditary forms of hypomagnesemia have been deciphered, including mutations in transient receptor potential melastatin type 6 (TRPM6), claudin 16, and cyclin M2 (CNNM2). Recently, mutations in Mg(2+) transporter 1 (MagT1) were linked to T-cell deficiency underlining the important role of Mg(2+) in cell viability. Moreover, hypomagnesemia can be the consequence of the use of certain types of drugs, such as diuretics, epidermal growth factor receptor inhibitors, calcineurin inhibitors, and proton pump inhibitors. This review provides an extensive and comprehensive overview of Mg(2+) research over the last few decades, focusing on the regulation of Mg(2+) homeostasis in the intestine, kidney, and bone and disturbances which may result in hypomagnesemia.
•Commonly encountered drug-induced hypomagnesemia is assessed by frequent monitoring of blood and urine magnesium levels.•The most common methods employed for measuring magnesium are dye binding and ...enzymatic methods which are not always traceable to the same standard reference materials.•Beyond serum measurements, calculated parameters such as fractional excretion of magnesium may be valuable, but are underutilized in assessing hypomagnesemia.
Magnesium is the fourth most abundant cation in the human body, essential for physiological processes and is the electrolyte with levels commonly deranged in critically ill patients. These derangements of magnesium imbalance can go unnoticed and result in poor clinical outcomes, requiring both worthy attention to abnormal values and accurate tools and methods to measure magnesium reliably. At present, clinical laboratories employ various methodologies for measuring magnesium in blood and urine. This review aims to address the role of magnesium from not only physiological and pathophysiological perspectives, but importantly to review the methods for measuring magnesium with relevant analytical considerations. Given the role of magnesium and drugs for various treatments, measuring magnesium has become more relevant as drugs can lead to magnesium imbalances. Clinical manifestations and etiology of magnesium imbalance as divided into hypomagnesemia and hypermagnesemia are also reviewed.
The 2015 Dietary Guidelines Advisory Committee indicated that magnesium was a shortfall nutrient that was underconsumed relative to the Estimated Average Requirement (EAR) for many Americans. ...Approximately 50% of Americans consume less than the EAR for magnesium, and some age groups consume substantially less. A growing body of literature from animal, epidemiologic, and clinical studies has demonstrated a varied pathologic role for magnesium deficiency that includes electrolyte, neurologic, musculoskeletal, and inflammatory disorders; osteoporosis; hypertension; cardiovascular diseases; metabolic syndrome; and diabetes. Studies have also demonstrated that magnesium deficiency is associated with several chronic diseases and that a reduced risk of these diseases is observed with higher magnesium intake or supplementation. Subclinical magnesium deficiency can exist despite the presentation of a normal status as defined within the current serum magnesium reference interval of 0.75–0.95 mmol/L. This reference interval was derived from data from NHANES I (1974), which was based on the distribution of serum magnesium in a normal population rather than clinical outcomes. What is needed is an evidenced-based serum magnesium reference interval that reflects optimal health and the current food environment and population. We present herein data from an array of scientific studies to support the perspective that subclinical deficiencies in magnesium exist, that they contribute to several chronic diseases, and that adopting a revised serum magnesium reference interval would improve clinical care and public health.
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