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The aim of this study was to determine the effect of magnesium supplementation on the depression status of depressed patients suffering from magnesium deficiency. Sixty depressed people suffering from hypomagnesemia participated in this trial. The individuals were randomly categorized into two groups of 30 members; one receiving two 250-mg tablets of magnesium oxide (MG) daily and the other receiving placebo (PG) for 8 wk. The Beck Depression Inventory-II was conducted and the concentration of serum magnesium was measured. At the end of intervention, 88.5% of the MG and 48.1% of the PG (P = 0.002) had a normal level of magnesium. The mean changes of serum magnesium were significantly different across the two groups. After the intervention, the mean Beck score significantly declined. However, in the MG, this reduction was more significant than in the PG (P = 0.02), so that the mean changes in this group experienced 15.65 ± 8.9 reduction, but in the PG, it declined by 10.40 ± 7.9. Daily consumption of 500 mg magnesium oxide tablets for ≥8 wk by depressed patients suffering from magnesium deficiency leads to improvements in depression status and magnesium levels. Therefore, assessment of the magnesium serum and resolving this deficiency positively influence the treatment of depressed patients. •Magnesium is involved in the pathophysiology of some psychologic disorders including effective disorder such as depression.•In the majority of studies a significant relationship has been observed between magnesium deficiency and depression.•The result of 20-y follow-up study showed that magnesium intake may have an effect on the risk of developing depression.•When the patients suspected of depression are evaluated, it is recommended that they are evaluated their serum magnesium status.

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.

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.

Chronic exposure to insufficient levels of magnesium (Mg) in drinking water increases the risk of magnesium deficiency and its association with hypertension, dyslipidemia and type 2 diabetes mellitus. The aim of the study was to assess the potential association of mineral contents in drinking water with blood pressure and other components of metabolic syndrome (MetS) (BMI as measure of obesity, triglycerides, glucose, and insulin resistance, index-HOMA IR), in a healthy population. This study was conducted in three randomly selected municipalities (Pozarevac, Grocka and Banovci), and recruited 90 healthy blood donors, aged 20–50 years. The Pozarevac area had a four times higher mean Mg level in drinking water (42 mg L−1) than Grocka (11 mg L−1). Diastolic blood pressure was lowest in subjects from Pozarevac. Serum Mg (sMg) was highest, and serum Ca2+/Mg (sCa/Mg) lowest in subjects from Pozarevac, and after adjustment for confounders (age, gender, BMI), only total cholesterol and sMg levels were independent predictors of diastolic blood pressure, sMg levels were independent predictors of triglycerides, and sCa/Mg predicted glucose levels. These results suggest that Mg supplementation in areas of lower magnesium levels in drinking water may be an important measure in the prevention of hypertension and MetS in general.

Nutrients usually act in a coordinated manner in the body. Intestinal absorption and subsequent metabolism of a particular nutrient, to a certain extent, is dependent on the availability of other nutrients. Magnesium and vitamin D are 2 essential nutrients that are necessary for the physiologic functions of various organs. Magnesium assists in the activation of vitamin D, which helps regulate calcium and phosphate homeostasis to influence the growth and maintenance of bones. All of the enzymes that metabolize vitamin D seem to require magnesium, which acts as a cofactor in the enzymatic reactions in the liver and kidneys. Deficiency in either of these nutrients is reported to be associated with various disorders, such as skeletal deformities, cardiovascular diseases, and metabolic syndrome. It is therefore essential to ensure that the recommended amount of magnesium is consumed to obtain the optimal benefits of vitamin D.

Hypertension is a complex condition in which various actors and mechanisms combine, resulting in cardiovascular and cerebrovascular complications that today represent the most frequent causes of mortality, morbidity, disability, and health expenses worldwide. In the last decades, there has been an exceptional amount of experimental, epidemiological, and clinical studies confirming a close relationship between magnesium deficit and high blood pressure. Multiple mechanisms may help to explain the bulk of evidence supporting a protective effect of magnesium against hypertension and its complications. Hypertension increases sharply with advancing age, hence older persons are those most affected by its negative consequences. They are also more frequently at risk of magnesium deficiency by multiple mechanisms, which may, at least in part, explain the higher frequency of hypertension and its long-term complications. The evidence for a favorable effect of magnesium on hypertension risk emphasizes the importance of broadly encouraging the intake of foods such as vegetables, nuts, whole cereals and legumes, optimal dietary sources of magnesium, avoiding processed food, which are very poor in magnesium and other fundamental nutrients, in order to prevent hypertension. In some cases, when diet is not enough to maintain an adequate magnesium status, magnesium supplementation may be of benefit and has been shown to be well tolerated.

Abstract Context The association between magnesium status and metabolic syndrome (MetS) remains unclear. Objective This study aimed to examine the relationship between kidney reabsorption-related magnesium depletion score (MDS) and MetS among US adults. Methods We analyzed data from 15 565 adults participating in the National Health and Nutrition Examination Survey (NHANES) 2003 to 2018. MetS was defined according to the National Cholesterol Education Program's Adult Treatment Panel III report. The MDS is a scoring system developed to predict the status of magnesium deficiency that fully considers the pathophysiological factors influencing the kidneys' reabsorption capability. Weighted univariate and multivariable logistic regression were used to assess the association between MDS and MetS. Restricted cubic spline (RCS) analysis was conducted to characterize dose-response relationships. Stratified analyses by sociodemographic and lifestyle factors were also performed. Results In both univariate and multivariable analyses, higher MDS was significantly associated with increased odds of MetS. Each unit increase in MDS was associated with approximately a 30% higher risk for MetS, even after adjusting for confounding factors (odds ratio 1.31; 95% CI, 1.17-1.45). RCS graphs depicted a linear dose-response relationship across the MDS range. This positive correlation remained consistent across various population subgroups and exhibited no significant interaction by age, sex, race, adiposity, smoking status, or alcohol consumption. Conclusion Higher urinary magnesium loss as quantified by MDS may be an independent linear risk factor for MetS in US adults, irrespective of sociodemographic and behavioral factors. Optimizing magnesium nutritional status could potentially confer benefits to patients with MetS.

Magnesium (Mg2+) has many physiological functions within the body. These include important roles in maintaining cardiovascular functioning, where it contributes to the regulation of cardiac excitation–contraction coupling, endothelial functioning and haemostasis. The haemostatic roles of Mg2+ impact upon both the protein and cellular arms of coagulation. In this review, we examine how Mg2+ homeostasis is maintained within the body and highlight the various molecular roles attributed to Mg2+ in the cardiovascular system. In addition, we describe how nutritional and/or disease-associated magnesium deficiency, seen in some metabolic conditions, has the potential to influence cardiac and vascular outcomes. Finally, we also examine the potential for magnesium supplements to be employed in the prevention and treatment of cardiovascular disorders and in the management of cardiometabolic health.

So far, no coherent and convincing theory has been developed to fully explain the pathogenesis of migraine, although many researchers and experts emphasize its association with spreading cortical depression, oxidative stress, vascular changes, nervous excitement, neurotransmitter release, and electrolyte disturbances. The contribution of magnesium deficiency to the induction of cortical depression or abnormal glutamatergic neurotransmission is a likely mechanism of the magnesium–migraine relationship. Hence, there is interest in various methods of assessing magnesium ion deficiency and attempts to study the relationship of its intra- and extracellular levels with the induction of migraine attacks. At the same time, many clinicians believe that magnesium supplementation in the right dose and form can be a treatment to prevent migraine attacks, especially in those patients who have identified contraindications to standard medications or their different preferences. However, there are no reliable publications confirming the role of magnesium deficiency in the diet as a factor causing migraine attacks. It also seems interesting to deepen the research on the administration of high doses of magnesium intravenously during migraine attacks. The aim of the study was to discuss the probable mechanisms of correlation of magnesium deficiency with migraine, as well as to present the current clinical proposals for the use of various magnesium preparations in complementary or substitute pharmacotherapy of migraine. The summary of the results of research and clinical observations to date gives hope of finding a trigger for migraine attacks (especially migraine with aura), which may turn out to be easy to diagnose and eliminate with pharmacological and dietary supplementation.

Patients with mutations in Cyclin M2 (CNNM2) suffer from hypomagnesaemia, seizures, and intellectual disability. Although the molecular function of CNNM2 is under debate, the protein is considered essential for renal Mg 2+ reabsorption. Here, we used a Cnnm2 knock out mouse model, generated by CRISPR/Cas9 technology, to assess the role of CNNM2 in Mg 2+ homeostasis. Breeding Cnnm2 + /− mice resulted in a Mendelian distribution at embryonic day 18. Nevertheless, only four Cnnm2 −/− pups were born alive. The Cnnm2 −/− pups had a significantly lower serum Mg 2+ concentration compared to wildtype littermates. Subsequently, adult Cnnm2 + /− mice were fed with low, control, or high Mg 2+ diets for two weeks. Adult Cnnm2 + /− mice showed mild hypomagnesaemia compared to Cnnm2 + / + mice and increased serum Ca 2+ levels, independent of dietary Mg 2+ intake. Faecal analysis displayed increased Mg 2+ and Ca 2+ excretion in the Cnnm2 + /− mice. Transcriptional profiling of Trpm6 , Trpm7 , and Slc41a1 in kidneys and colon did not reveal effects based on genotype. Microcomputed tomography analysis of the femurs demonstrated equal bone morphology and density. In conclusion, CNNM2 is vital for embryonic development and Mg 2+ homeostasis. Our data suggest a previously undescribed role of CNNM2 in the intestine, which may contribute to the Mg 2+ deficiency in mice and patients.