Showing papers in "Magnesium Research in 2010"

Assessment of magnesium status for diagnosis and therapy

Abstract: Magnesium is an essential element needed for health. Even though only 1% of the total body magnesium is present in blood, the serum magnesium concentration (SMC) is the predominant test used by medicine to assess magnesium status in patients. The traditional method to establish a reference interval for the SMC is flawed by the large number of "normal" individuals who have a subtle chronic negative magnesium balance due to a significant decrease in magnesium intake over the past century. Evidence-based medicine should be used to establish the appropriate lower limit of the reference interval for health and I recommend 0.85 mmol/L based on current literature. The decrease in magnesium in the diet has led to chronic latent magnesium deficiency in a large number of people since their SMC is still within the reference interval due to primarily the bone magnesium supplementing the SMC. These individuals need adjustment of their diet or magnesium supplementation to achieve a normal magnesium status for health.

Magnesium and cardiovascular system

Abstract: Hypomagnesemia is common in hospitalized patients, especially in the elderly with coronary artery disease (CAD) and/or those with chronic heart failure. Hypomagnesemia is associated with an increased incidence of diabetes mellitus, metabolic syndrome, mortality rate from CAD and all causes. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially gives magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel. The data regarding its use in patients with acute myocardial infarction (AMI) is conflicting. Although some previous, relatively small randomized clinical trials demonstrated a remarkable reduction in mortality when administered to relatively high risk AMI patients, two recently published large-scale randomized clinical trials (the Fourth International Study of Infarct Survival and Magnesium in Coronaries) failed to show any advantage of intravenous magnesium over placebo. Nevertheless, there are theoretical potential benefits of magnesium supplementation as a cardioprotective agent in CAD patients, as well as promising results from previous work in animal and humans. These studies are cost effective, easy to handle and are relatively free of adverse effects, which gives magnesium a role in treating CAD patients, especially high-risk groups such as CAD patients with heart failure, the elderly and hospitalized patients with hypomagnesemia. Furthermore, magnesium therapy is indicated in life-threatening ventricular arrhythmias such as Torsades de Pointes and intractable ventricular tachycardia.

Oral magnesium supplementation improves vascular function in elderly diabetic patients.

Abstract: Magnesium (Mg) ions directly influence vascular tone and responsiveness and are cofactors for acetylcholine-induced endothelium-dependent relaxation. Alterations in extracellular Mg are able to modify the formation and release of nitric oxide (NO), altering arterial smooth muscle tone. Previous in vivo studies in humans have shown that parenteral or oral Mg supplementation increase endothelial-dependent vasodilation. The aim of the present study was to evaluate the effects of Mg oral supplementation on endothelial function in elderly diabetic and hypertensive subjects. Sixty elderly (≥ 65 years) diabetic patients were recruited (mean age: 71.1 ± 6.1 years; M/F: 35/25). Endothelial function, evaluated by non-invasive flow-mediated dilatation of the brachial artery, as well as anthropometric and laboratory data, including ionized Mg (Mg-ion), were measured in all patients before and after one-month. Thirty patients underwent oral Mg supplementation with 4.5 g/day of Mg pidolate (368 mg/day of Mg ion), while the rest were used as a control group. The usual management of diabetes and hypertension was not changed during the month of study participation for all the patients. In the group of patients that underwent Mg supplementation, Mg-ion concentration significantly increased from 0.42 ± 0.05 mmol/L to 0.49 ± 0.06 mmol/L; p < 0.05. Mg intervention resulted in a significant improvement of the post-ischemic endothelial-dependent flow-mediated dilation (from 3.3 ± 3.6% to 8.4 ± 3.9%; p < 0.05). No significant differences were found, either in ion-Mg or endothelial function, in the control group. In conclusion, the present study suggests that oral Mg improves endothelial function in diabetic elderly subjects.

Magnesium deficiency and metabolic syndrome: stress and inflammation may reflect calcium activation

Abstract: Magnesium (Mg) intake is inadequate in the western diet and metabolic syndrome is highly prevalent in populations around the world. Epidemiological studies suggest that high Mg intake may reduce the risk but the possibility of confounding factors exists, given the strong association between Mg and other beneficial nutriments (vegetables, fibers, cereals). The concept that metabolic syndrome is an inflammatory condition may explain the role of Mg.Mg deficiency results in a stress effect and increased susceptibility to physiological damage produced by stress. Stress activates the hypothalamic-pituitary-adrenal axis (HPA) axis and the sympathetic nervous system. The activation of the renin-angiotensin-aldosterone system is a factor in the development of insulin resistance by increasing oxidative stress. In both humans and rats, aldosteronism results in an immunostimulatory state and leads to an inflammatory phenotype. Stress response induces the release of large quantities of excitatory amino acids and activates the nuclear factor NFkappaB, promoting translation of molecules involved in cell regulation, metabolism and apoptosis. The rise in neuropeptides is also well documented. Stress-induced HPA activation has been identified to play an important role in the preferential body fat accumulation but evidence that Mg is involved in body weight regulation is lacking. One of the earliest events in the acute response to stress is endothelial dysfunction. Endothelial cells actively contribute to inflammation by elaborating cytokines, synthesizing chemical mediators and expressing adhesion molecules. Experimental Mg deficiency in rats induces a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, synthesis of inflammatory cytokines and acute phase proteins, extensive production of free radicals. An increase in extracellular Mg concentration decreases inflammatory effects, while reduction in extracellular Mg results in cell activation. The effect of Mg deficiency in the development of insulin resistance in the rat model is well documented. Inflammation occurring during experimental Mg deficiency is the mechanism that induces hypertriglyceridemia and pro-atherogenic changes in lipoprotein metabolism. The presence of endothelial dysfunction and dyslipidemia triggers platelet aggregability, thus increasing the risk of thrombotic events. Oxidative stress contributes to the elevation of blood pressure. The inflammatory syndrome induces activation of several factors, which are dependent on cytosolic Ca activation. Recent findings support the hypothesis that the Mg effect on intracellular Ca2+ homeostasis may be a common link between stress, inflammation and a possible relationship to metabolic syndrome.

The biochemical function of Mg²+ in insulin secretion, insulin signal transduction and insulin resistance.

Abstract: Insulin secretion is started by a Ca2+ influx that is competitively inhibited by extracellular Mg2+. This can explain the inverse correlation between serum Mg2+ and serum insulin concentration. After binding of insulin to its receptor, receptor tyrosine kinase is activated. The autophosphorylation of the receptor kinase and all protein kinases in the insulin signal transduction cascade are dependent on Mg2+. Besides MgATP as substrate, protein tyrosine kinases are activated by a second Mg2+. Other protein kinases and some protein phosphatases involved in insulin resistance are dependent on Mg2+ as well. In the complex action of Mg2+ on tyrosine protein kinases and serine/threonine kinases, which mediate or inhibit insulin signaling, the concentration of intracellular free Mg2+ ([Mg2+](i)) may have a permissive function. The secretion of various effectors such as adipokines, interleukin (IL)-1, IL-6, IL-8, IL-18, tumor necrosis factor-alpha (TNF-alpha), beta-adrenergics and reactive oxygen species (ROS) involved in insulin resistance is enhanced in Mg deficiency and obesity. Adipocytes produce chemotactic signals, leading to macrophage recruitment and in addition to adipocytes, to the production of proinflammatory cytokines. The concentration of free fatty acids (FFA), particularly palmitate, is increased in obesity and by the action of beta-adrenergics. The complex actions of adipokines, cytokines and palmitate in the induction of insulin resistance are reviewed. The concentration of extracellular and intracellular Mg2+ in patients and the experimental effects of insulin and catecholamines on [Mg2+](i) in various tissues are described. The controversial effects of different serum Mg2+ concentrations and Mg2+ supplementation on plasma glucose and insulin concentration in studies with human subjects and the controversial results of epidemiological studies are reported.

Magnesium supplementation improves indicators of low magnesium status and inflammatory stress in adults older than 51 years with poor quality sleep

Abstract: Low magnesium status has been associated with numerous conditions characterized as having a chronic inflammatory stress component. Some animal findings indicate that a moderate magnesium deficiency, similar to which apparently commonly occurs in humans, may enhance inflammatory or oxidative stress induced by other factors, including disrupted sleep/sleep deprivation. Thus, an experiment was performed with 100 adults (22 males and 78 females) aged 59 ± 8 years (range 51 to 85 years) with poor sleep quality revealed by a Pittsburg Sleep Quality Index (PSQI) score higher than five. The participants were randomly assigned to two groups matched by gender, age, and overall PSQI score. After baseline assessment (week one) of body mass index (BMI), diet, blood and urine biochemical variables, and sleep quality, one group was given a 320 mg magnesium/day supplement as magnesium citrate and the other group a sodium citrate placebo for seven weeks. Final assessments were made five and seven weeks (which were combined for statistical analysis to reduce intra-individual variation) after supplement initiation for the 96 participants who completed the study as designed. Based on food diaries, 58% of the participants were consuming less than the US. Estimated Average Requirement (EAR) for magnesium. Consuming less than the EAR was associated with a significantly higher BMI and plasma C-reactive protein (CRP) concentration. Only 40 participants had plasma CRP concentrations higher than 3.0 mg/L (an indication of chronic inflammatory stress). Overall PSQI scores improved (10.4 to 6.6, p 3.0 mg/L. The findings show that many individuals have a low magnesium status associated with increased chronic inflammatory stress that could be alleviated by increased magnesium intake. Because dietary magnesium intake did not change during the experimental period, another factor, possibly a placebo effect, improved sleep quality, which resulted in increased erythrocyte magnesium. This factor prevented the determination of whether magnesium deficiency contributes to poor sleep quality. The findings, however, suggest an association between magnesium status and sleep quality that needs further study to definitively determine whether a low magnesium status is a cause or an effect of poor sleep quality.

Rising Ca:Mg intake ratio from food in USA Adults: a concern?

Abstract: USDA food surveys from 1977 through 2007-8 show a rising food Ca:Mg ratio for all USA adult age-gender groups. Food Ca:Mg intake ratios rose from 2.3-2.9 in 1977 to 2.9-3.5 in 2007-8. The % rise in mean Mg intakes compared closely with % rise in mean energy intakes while % rise in mean Ca intakes were substantially higher in all groups, suggesting the rising Ca:Mg comes from higher Ca intakes via food selections, rising food Ca contents or both. Original intake data from these surveys need to be accessed to calculate each individual's Ca:Mg for statistical assessment of this ratio rise. Ca:Mg rose from largely below 3.0 in 1994-5 to generally above or approaching 3.0 after 2000, coinciding with a sharp 2% rise in type 2 diabetes incidence and prevalence in the USA population and a 1994-2005 rise in colorectal cancer incidence among young white, non-Hispanic adult men and women in the USA. The intracellular Ca activation response to low Mg is discussed as a possible mechanism linking metabolic and inflammatory syndromes with low dietary Mg and rising dietary Ca:Mg ratio. Adequacy of both Ca and Mg as well as the Ca:Mg ratio are important in assessing study outcomes. Health consequences should be considered for the USA's 64-67% adults not meeting their Mg requirement from foods, many also consuming below their Ca requirements, and their increasing Ca:Mg ratio from foods.

Antagonism between cadmium and magnesium: a possible role of magnesium in therapy of cadmium intoxication

Abstract: One of the important mechanisms of cadmium (Cd) toxicity is its interactions with bioelements, including magnesium (Mg). Exposure to Cd leads to disturbances in Mg metabolism in the organism, while Mg supplementation has an adverse effect on Cd absorption, accumulation and toxicity. According to the available results, which indicate a protective role of Mg against Cd toxicity, it remains to be seen whether magnesium may influence the important unsolved problem of Cd intoxication therapy. In this review, the interactions between the toxic metal Cd and the bioelement Mg are discussed on the basis of the available literature and our own results. We discuss these interactions mainly based on experimental data because data from human studies are scarce.

Vascular biology of magnesium and its transporters in hypertension

Abstract: Magnesium may influence blood pressure by modulating vascular tone and structure through its effects on myriad biochemical reactions that control vascular contraction/dilation, growth/apoptosis, differentiation and inflammation. Magnesium acts as a calcium channel antagonist, it stimulates production of vasodilator prostacyclins and nitric oxide and it alters vascular responses to vasoconstrictor agents. Mammalian cells regulate Mg2+ concentration through special transport systems that have only recently been characterized. Magnesium efflux occurs via Na2+-dependent and Na2+-independent pathways. Mg2+ influx is controlled by recently cloned transporters including Mrs2p, SLC41A1, SLC41A2, ACDP2, MagT1, TRPM6 and TRPM7. Alterations in some of these systems may contribute to hypomagnesemia and intracellular Mg2+ deficiency in hypertension and other cardiovascular pathologies. In particular, increased Mg2+ efflux through dysregulation of the vascular Na+/Mg2+ exchanger and decreased Mg2+ influx due to defective vascular and renal TRPM6/7 expression/activity may be important in altered vasomotor tone and consequently in blood pressure regulation. The present review discusses the role of Mg2+ in vascular biology and implications in hypertension and focuses on the putative transport systems that control magnesium homeostasis in the vascular system. Much research is still needed to clarify the exact mechanisms of cardiovascular Mg2+ regulation and the implications of aberrant cellular Mg2+ transport and altered cation status in the pathogenesis of hypertension and other cardiovascular diseases.

Magnesium supplements may enhance the effect of antihypertensive medications in stage 1 hypertensive subjects

Abstract: Comprehensive analytical review of 44 human studies in 43 publications of oral Magnesium (Mg) therapy for hypertension (HT) shows Mg supplements may enhance the blood-pressure (BP) lowering effect of anti-hypertensive medications (medications) in Stage 1 HT subjects. 9 studies conducted on subjects treated with medications continuously ≥ 6 months (with ≤ 2-wk washout) resulted in significant decreases in both SBP and DBP with oral Mg supplements as low as 230 mg (10 mmol) per day. Twice this oral Mg dose, i.e. 460 mg/day, was required to significantly lower both SBP and DBP in 18 of 22 studies conducted on Stage 1 HT subjects either treatment-naive or with their medication use interrupted ≥ 4 weeks within 6 months pre-study. Of the 4 remaining studies showing no BP change at these high Mg doses, two had large placebo effect, a third one had significant baseline discrepancies between Mg-test and placebo groups, and the fourth showed a significant decrease in DBP but not SBP. Thirteen studies on normotensive subjects, both treated and untreated with medications, showed no significant BP lowering effect with oral Mg therapy up to 25 mmol/day (607 mg). Conclusions: Mg supplements above RDA may be necessary to significantly lower high blood pressure in Stage I HT unless subjects have been continuously treated with anti-HT medications ≥ 6 months. Such medication use may lower by half the oral Mg dose needed to significantly decrease high blood pressure. Oral Mg therapy may have no effect in studies with normotensive subjects. Study of oral Mg therapy for severe or complicated hypertension has been neglected. Often the first cardiovascular risk factor to present, high blood pressure may be an early opportunity to correct poor Mg status and its possible complications including cardiovascular disease, respiratory diseases, and type 2 diabetes. Such preventive potential encourages quantification of these findings and testing of these hypotheses with a meta-analysis using categories elucidated by this preliminary study and finally would warrant a call for a prospective study.

Phagocyte priming by low magnesium status: input to the enhanced inflammatory and oxidative stress responses

Abstract: Epidemiological and experimental studies underline the role of magnesium in inflammation. Several data indicate an enhanced response of phagocytes (granulocytes, macrophages) derived from magnesium-deficient animals or cultured under low magnesium conditions to the inflammatory mediators' stimulation. On the contrary, it was pointed out that high extracellular Mg2+ concentration might partially attenuate the activation of phagocyte leukocytes. Thus, it is likely that magnesium-deficient conditions lead to the priming (pre-activation) of phagocytic cells. Magnesium status is an important modulator of the phagocyte response to immune stimuli and consequently could be implicated in a wide range of pathophysiological issues, e.g. those related to the production of radical oxygen species (ROS). It is likely that magnesium directly modulates phagocyte priming by its calcium antagonism and indirectly by its effect on the immunoinflammatory processes, the source of the priming mediators.

Splice-variant 1 of the ancient domain protein 2 (ACDP2) complements the magnesium-deficient growth phenotype of Salmonella enterica sv. typhimurium strain MM281.

Abstract: Evidence arguing for the existence of genes encoding for proteins directly involved in the transport of Mg 2+ through the cytoplasmic membrane have accumulated over the last few years. Gene ACDP2 (ancient conserved domain protein 2; old name CNNM2, cyclin M2) is one such gene. ACDP2 is a distant homologue of the bacterial gene corC, which is known to be involved in cobalt resistance. We have previously demonstrated that the over-expression of the human Mg 2+ carrier SLC41A1 partly complements the Mg 2+-dependent growth deficiency of Salmonella strain MM281 (triple disruptant in genes: mgtA, mgtB and corA) cultivated in media containing growth non-permissive [Mg 2+] e. We have used the same approach to examine whether over-expressed human ACDP2 has a similar efficacy to complement growth deficiency of the MM281 strain in media containing growth non-permissive [Mg 2+] e. Two splicing variants of the ACDP2 gene have been tested. Here, we show that over-expressed isomorph 1 is efficient in restoring growth of the MM281 strain in media containing growth non-permissive [Mg 2+] e, whereas isomorph 2 is not. Therefore, we conclude that ACDP2sp.v.1 is a functional Mg 2+-transporting entity per se. Our conclusion is supported by the measurable Mg 2+ influx seen in MM281 bacteria over-expressing ACDP2sp.v.1 but not in MM281 bacteria over-expressing ACDP2sp.v.2 or in cells transformed with the empty vector.

The role of magnesium deficiency in cardiovascular and intestinal inflammation

Abstract: Hypomagnesemia continues to cause difficult clinical problems, such as significant cardiac arrhythmias where intravenous magnesium therapy can be lifesaving. Nutritional deficiency of magnesium may present with some subtle symptoms such as leg cramps and occasional palpitation. We have investigated dietary-induced magnesium deficiency in rodent models to assess the pathobiology associated with prolonged hypomagnesemia. We found that neuronal sources of the neuropeptide, substance P (SP), contributed to very early prooxidant/proinflammatory changes during Mg deficiency. This neurogenic inflammation is systemic in nature, affecting blood cells, cardiovascular, intestinal, and other tissues, leading to impaired cardiac contractility similar to that seen in patients with heart failure. We have used drugs that block the release of SP from neurons and SP-receptor blockers to prevent some of these pathobiological changes; whereas, blocking SP catabolism enhances inflammation. Our findings emphasize the essential role of this cation in preventing cardiomyopathic changes and intestinal inflammation in a well-studied animal model, and also implicate the need for more appreciation of the potential clinical relevance of optimal magnesium nutrition and therapy.

Oral magnesium supplementation decreases alanine aminotransferase levels in obese women

Abstract: To evaluate the effect of oral supplementation with magnesium chloride on the systemic and hepatic inflammation, 38 non-hypertensive obese women aged 30 to 65 years were allocated into groups with and without hypomagnesemia. Hypomagnesemic women drank 50 mL of 5% solution of MgCl2 equivalent to 450 mg of elemental magnesium. Low-carbohydrate diets and physical activity were indicated for women in both groups. Chronic diarrhea, alcohol intake, use of diuretics, previous oral magnesium supplementation, hepatic disease, and renal damage were exclusion criteria. Hypomagnesemia is defined by serum magnesium concentrations or=40 U/L, and systemic inflammation by serum high-sensitivity C reactive protein (hs-CRP) concentration>or=3 mg/L. At baseline (p=0.06) and final of follow-up (p=0.80), there were no significant differences by body mass index between the groups in the study. In the same way, at baseline ALT (48.1+/-25.5 and 34.6+/-24.1 U/L, p=0.14) and hs-CRP (9.4+/-6.0 and 7.9+/-5.9 mg/dL, p=0.47) levels were similar in the supplemented and non-supplemented women. In the magnesium group, ALT (24.3+/-10.3 and 34.8+/-13.6 U/L, p=0.02) levels, but not hs-CRP (5.2+/-1.9 and 8.0+/-5.6 mg/L, p=0.08) reached significantly lower levels, in the fourth month of treatment, than in women in the control group. The adjusted odds ratios between the improvement in serum magnesium and reduction in ALT and hs-CRP levels were 0.56 (95% CI: 0.3-0.9) and 0.93 (95% CI: 0.6-29.9), respectively. Results of this study show that in hypomagnesemic obese women, oral supplementation with magnesium chloride reduces plasma ALT levels; hs-CRP levels only show a reduction trend.

Colon cancer and content of nitrates and magnesium in drinking water

Abstract: The objective of this study was to explore whether magnesium levels (Mg) in drinking water modify the effects of nitrate on colon cancer risk. A matched case-control study was used to investigate the relationship between the risk of death from colon cancer and exposure to nitrate in drinking water in Taiwan. All colon cancer deaths of Taiwan residents from 2003 through 2007 were obtained from the Bureau of Vital Statistics of the Taiwan Provincial Department of Health. Controls were deaths from other causes and were pair-matched to the cases by gender, year-of-birth, and year-of-death. Information on the levels of nitrate-nitrogen (NO 3-N) and Mg in drinking water were collected from Taiwan Water Supply Corporation (TWSC). The municipality of residence for cases and controls was assumed to be the source of the subject's NO 3-N and Mg exposure via drinking water. The results of our study show that there is a significant trend towards an elevated risk of death from colon cancer with increasing nitrate levels in drinking water. Furthermore, we observed evidence of an interaction between drinking water NO 3-N and Mg intake via drinking water. This is the first study to report effect modification by Mg intake from drinking water on the association between NO 3-N exposure and colon cancer risk.

Magnesium and strength in elite judo athletes according to intracellular water changes

Abstract: Magnesium (Mg) deficiency strongly affects muscle performance. In judo, many athletes often undergo impressive weight changes associated with severe dehydration. Common practices used by athletes to achieve a target weight can lead to Mg deficit. This study aimed to understand the impact of Mg changes on strength from periods of weight stability to prior to competition in a sample of elite judo athletes who differentially changed their intracellular water (ICW). The sample consisted of 20 elite male judo athletes. Subjects were divided according to ICW changes: losses below 2% and losses equal to or above 2%. Mg was measured in serum, red blood cells and urine by atomic absorption spectrophotometry. ICW was calculated as the difference between total-body water and extracellular water using dilution techniques. Maximal handgrip strength was evaluated using Jamar Hydraulic Hand Dynamometer. Upper-body power was determined in a bench press. Higher ICW decreases were associated with higher strength reductions, though our results suggest that an increase in red blood cell Mg might attenuate those strength reductions in athletes who decrease the ICW compartment. As Mg losses can be considerable and intake is frequently insufficient, athletes should consider supplementation, especially during periods of weight reduction.

The relationship between concentrations of magnesium and oxidized low density lipoprotein and the activity of platelet activating factor acetylhydrolase in the serum of patients with type 1 diabetes

Abstract: The study was aimed at comparing the concentration of metabolic parameters, the serum concentration of oxidized low density lipoproteins (oxLDL) and the activity of platelet activating factor acetylhydrolase (PAF-AH) in the relation to the serum concentration of magnesium (Mg) in patients with type 1 diabetes (DM1). DM1 patients (n=78) were divided into 2 groups: patients with low serum Mg concentration ( or=0.7 mmol/L, group 2, n=44). A control group (n=24) of healthy subjects was also recruited. Our results showed that DM1 patients had lower serum Mg concentrations than the control group. It was found that parameters of poor metabolic control and lipid profile are not related to the serum Mg concentration in DM1 patients. However, both the Mg concentration and the PAF-AH activity are independently related to the serum oxLDL concentration. In group 1 the oxLDL concentration and the PAF-AH activity were higher than in group 2, and the control group. Two groups of DM1 patients did not show any differences with regard to the metabolic control. Therefore, the oxidative modification of LDL and the higher activity of PAF-AH are related with the low Mg status; however, no relation has been observed between these parameters and the poor metabolic control in DM1 patients.

Vitamin B6-magnesium treatment for autism: the current status of the research.

Abstract: Auteur(s) : Kimberly A Murza, Stacey L Pavelko, Melissa D Malani, Chad Nye University of Central Florida, Center for Autism and Related Disabilities, Orlando, USA In 2005, a systematic review was published by the Cochrane Collaboration that reviewed the effects of vitamin B6-magnesium (vit B6-Mg) treatment for autism [1]. The focus of the review was to assess the impact of vit B6-Mg for improving the communication and behavioural responses of children and adults with [...]

Dietary magnesium supplementation suppresses bone resorption via inhibition of parathyroid hormone secretion in rats fed a high-phosphorus diet.

Abstract: This study examined the effects of dietary magnesium (Mg) supplementation on bone turnover and serum parathyroid hormone (PTH) levels in rats fed a high-phosphorus (P) diet. Male rats were randomized by weight into three groups, and fed a control diet (control), a high-P diet (HP) or a high-P and high-Mg diet (HPHMg) for 14 days. Serum osteocalcin levels were significantly higher in the HP and HPHMg groups than in the control group. Serum CTx levels were significantly higher in the HP and HPHMg groups than in the control group, while the levels in the HPHMg group were significantly lower than in the HP group. Serum PTH levels were significantly higher in the HP group than in the control and HPHMg groups. Dietary Mg supplementation had a significant influence on serum PTH levels in the HP and HPHMg groups. These results suggest that dietary Mg supplementation suppresses the high bone resorption induced by a high-P diet via inhibition of PTH secretion. Moreover, our results suggest that dietary Mg supplementation may be beneficial for the prevention of bone loss with high-P diet administration.

Plasma matrix metalloproteinase 9 correlates with disorders of brain magnesium homeostasis in patients undergoing coronary artery bypass surgery

Abstract: Background. Changes in plasma matrix metalloproteinase 9 (MMP-9) concentrations and parallel changes in brain magnesium homeostasis have not been examined in cardiac surgery patients. The purpose of the present study was to analyse these relationships in patients undergoing coronary artery bypass surgery (CABG) with extracorporeal circulation (ECC). Additionally, the effect of volatile anaesthetics was considered. Patients and methods. Adult patients undergoing CABG with ECC under general anaesthesia were studied. Plasma MMP-9 and total (tMg) and ionized (iMg) magnesium concentrations were measured during surgery and during the early postoperative period. The plasma arteriovenous (a-v) tMg and iMg differences in the brain circulation were considered to be markers for brain magnesium homeostasis. The Mini-Mental State Examination test and computer tomography were used to diagnose postoperative neuropsychological disorders (PNPDs). Results. In total, 92 patients were examined. PNPDs were noted in 17 cases. Cardiac surgery resulted in increased plasma levels of MMP-9. The highest MMP-9 concentrations were observed in patients with PNPDs. MMP-9 concentrations strongly correlated with a-v tMg and a-v iMg differences. Compared with arterial measurements, venous tMg and iMg concentrations were higher during and immediately after surgery and lower during the early postoperative period. The most severe differences in a-v tMg and iMg were noted in patients with PNPDs. Conclusion. 1. Cardiac surgery resulted in an increase in plasma MMP-9 concentrations. 2. This increase in MMP-9 was significantly greater in patients with PNPDs. 3. The plasma MMP-9 concentration was correlated with disorders of brain Mg homeostasis.

The influence of magnesium on morphine-induced stimulation of the reward system

Abstract: The present study was designed to assess the influence of magnesium (Mg) as MgCl 2 (10 or 40 mg/kg b.wt/day i.p.) and of its interaction with morphine on the reward system (RS) in Wistar rats. For this purpose, we evaluated conditioning place preference on a 12 day experiment schedule. Our data show that MgCl 2 (10 mg/kg b.wt/day) has moderate but significant effects on stimulating RS (increasing the time spent in associated conditioned compartment) (327.75 ± 11 s in the Mg (10 mg/kg b.wt) group vs 295.2 ± 8 s in the control (saline) group, p < 0.05) but not at higher Mg doses (40 mg/kg b.wt/day). We tested the influence of MgCl 2 (10 mg/kg b.wt./day i.p.) upon naloxone (2 mg/kg b.wt/ i.p.)-induced place aversion. Administrated alone, naloxone has an aversive effect on place preference. MgCl 2 (10 mg/kg b.wt/day i.p.) has a significantly decreased aversive effect of naloxone (280.7 ± 37 s in naloxone + MgCl 2 (10 mg/kg b.wt) group vs 189 ± 21 s in naloxone group, p < 0.05). MgCl 2 at both tested doses, added to morphine (3 mg/kg b.wt/day i.p), decreased the acquisition of morphine-induced place preference (262.2 ± 17 s) in morphine + MgCl 2 (40 mg/kg b.wt) group vs 462.15 ± 28 s in morphine group, p < 0.05). MgCl 2, 10 mg/kg b.wt/day i.p. decreased both morphine-induced place preference and naloxone-induced place aversion.

The frequency of magnesium consumption directly influences its serum concentration and the amount of elutable bone magnesium in rats.

Abstract: We investigated the influence of Mg feeding frequency on the variation in serum Mg concentration and tissue Mg levels in Mg-deficient rats Sprague-Dawley rats, which had been fed a Mg-deficient diet for 14 d, were divided into 3 groups that were kept on 3 diets differing in their Mg content The rats were fed 05-fold (Mg250 group), 1-fold (Mg500 group), or 15-fold (Mg750 group) the amounts of recommended Mg in their standard AIN-93G diet (Mg: 478 mg/kg diet) during the recovery period (12 d) The Mg500 and Mg750 groups were intermittently fed (Mg500, every 2 d; Mg750, every 3 d) so that their total intake of Mg during the recovery period could equal the Mg intake of the Mg250 group The serum Mg concentrations increased in the 3 groups after feeding with a Mg-containing diet However, serum Mg levels were only maintained within the normal range in the Mg250 group After feeding on the Mg-deficient diet, in the intermittently fed groups, serum Mg concentrations decreased Urinary Mg excretion was higher and Mg retention was lower in the Mg500 and Mg750 groups than in the Mg250 group Moreover, bone Mg, especially elutable bone Mg, was lower in the Mg500 and Mg750 groups than in the Mg250 group The elutable fraction of bone Mg correlated to the coefficient of variation of serum Mg concentration In conclusion, for the maintenance of serum Mg concentration, it is important to increase the amount of elutable bone Mg by frequent Mg consumption

Biochemical mechanisms of the metabolic syndrome and the role of magnesium

Abstract: Auteur(s) : Theodor Gunther Charite-Universitatsmedizin Berlin, Campus Benjamin Franklin, Institut fur Molekularbiologie und Biochemie, Berlin, Germany The metabolic syndrome is characterized by obesity, insulin resistance, dyslipidemia and hypertension [1-3]. Various hypotheses have been presented during the past as mechanisms of the metabolic syndrome: insulin hypothesis, glucose hypothesis, reactive oxygen species (ROS) hypothesis, ionic hypothesis [4-6]. The primary symptom in metabolic [...]

Downregulation of HD-PTP by high magnesium concentration: novel insights into magnesium-induced endothelial migration.

Abstract: Magnesium promotes endothelial migration, an event which is orchestrated by a complex interplay between protein tyrosine kinases and phosphatases. We found that high extracellular concentrations of magnesium do not modulate the levels and the activation of FAK and Src, two tyrosine kinases involved in driving cell migration. Interestingly, we show that magnesium induced-endothelial motility correlates with the downregulation of HD-PTP, a potential tyrosine phopshatase previously shown to be involved in modulating cell migration. The decreased amounts of HD-PTP are not dependent upon transcriptional mechanisms. In contrast to Fibroblast Growth Factor-induced HD-PTP downregulation, the proteasome seems not to be involved in regulating HD-PTP levels in endothelial cells cultured in high magnesium containing medium. Our results indicate that, in the presence of high magnesium concentrations, endothelial cells are stimulated to migrate through complex mechanisms involving also HD-PTP.

What about magnesium substitution in radiation oncology

Abstract: Auteur(s) : Oliver Micke1, Robert Hunger2, Jens Buntzel3, Ralph Mucke4, Klaus Kisters5 1Franziskus Hospital, Department of Radiotherapy and Radiation Oncology, Bielefeld, Germany 2Lurlibadstr. 80, Chur, Switzerland 3Sudharz Hospital, Department of Otolaryngology, Nordhausen, Germany 4Lippe Hospital, Department of Radiotherapy, Lemgo, Germany 5St. Anna Hospital, Department of Internal Medicine, Herne, Germany Dear Editor, We recently read with great interest the notable [...]

Significant first presence of Mg Symposium at Experimental Biology, a large USA conference.

Abstract: Auteur(s) : Andrea Rosanoff Center for Magnesium Education & Research, Hawaii USA Nutritional magnesium intake from foods in the United States of America (USA) is widely below individual daily requirements [1]. Magnesium in USA has been called the “orphan nutrient” by Robert Heaney due to its lack of attention by the USA nutrition research community during the 20th century – a time of prolific and varied nutrition research progress. USA's Dept. of Agriculture (USDA) first published [...]