Magnesium Metabolism in Chronic Alcohol-Use Disorder: Meta-Analysis and Systematic Review

Chronic alcohol-use disorder has been imputed as a possible cause of dietary magnesium depletion. The purpose of this study was to assess the prevalence of hypomagnesemia in chronic alcohol-use disorder, and to provide information on intracellular magnesium and on its renal handling. We carried out a structured literature search up to November 2020, which returned 2719 potentially relevant records. After excluding non-significant records, 25 were retained for the final analysis. The meta-analysis disclosed that both total and ionized circulating magnesium are markedly reduced in chronic alcohol-use disorder. The funnel plot and the Egger’s test did not disclose significant publication bias. The I2-test demonstrated significant statistical heterogeneity between studies. We also found that the skeletal muscle magnesium content is reduced and the kidney’s normal response to hypomagnesemia is blunted. In conclusion, magnesium depletion is common in chronic alcohol-use disorder. Furthermore, the kidney plays a crucial role in the development of magnesium depletion.

Relationships between hyperinsulinaemia, magnesium, vitamin D, thrombosis and COVID-19: rationale for clinical management

Risk factors for COVID-19 patients with poorer outcomes include pre-existing conditions: obesity, type 2 diabetes mellitus, cardiovascular disease (CVD), heart failure, hypertension, low oxygen saturation capacity, cancer, elevated: ferritin, C reactive protein (CRP) and D-dimer. A common denominator, hyperinsulinaemia, provides a plausible mechanism of action, underlying CVD, hypertension and strokes, all conditions typified with thrombi. The underlying science provides a theoretical management algorithm for the frontline practitioners.Vitamin D activation requires magnesium. Hyperinsulinaemia promotes: magnesium depletion via increased renal excretion, reduced intracellular levels, lowers vitamin D status via sequestration into adipocytes and hydroxylation activation inhibition. Hyperinsulinaemia mediates thrombi development via: fibrinolysis inhibition, anticoagulation production dysregulation, increasing reactive oxygen species, decreased antioxidant capacity via nicotinamide adenine dinucleotide depletion, haem oxidation and catabolism, producing carbon monoxide, increasing deep vein thrombosis risk and pulmonary emboli. Increased haem-synthesis demand upregulates carbon dioxide production, decreasing oxygen saturation capacity. Hyperinsulinaemia decreases cholesterol sulfurylation to cholesterol sulfate, as low vitamin D regulation due to magnesium depletion and/or vitamin D sequestration and/or diminished activation capacity decreases sulfotransferase enzyme SULT2B1b activity, consequently decreasing plasma membrane negative charge between red blood cells, platelets and endothelial cells, thus increasing agglutination and thrombosis.Patients with COVID-19 admitted with hyperglycaemia and/or hyperinsulinaemia should be placed on a restricted refined carbohydrate diet, with limited use of intravenous dextrose solutions. Degree/level of restriction is determined by serial testing of blood glucose, insulin and ketones. Supplemental magnesium, vitamin D and zinc should be administered. By implementing refined carbohydrate restriction, three primary risk factors, hyperinsulinaemia, hyperglycaemia and hypertension, that increase inflammation, coagulation and thrombosis risk are rapidly managed.

Mg II λ2797, λ2803 emission in a large sample of low-metallicity star-forming galaxies from SDSS DR14

A large sample of Mg II emitting star-forming galaxies with low metallicity [O/H] = log(O/H) – log(O/H)⊙ between –0.2 and –1.2 dex is constructed from Data Release 14 of the Sloan Digital Sky Survey. We selected 4189 galaxies with Mg II λ2797, λ2803 emission lines in the redshift range z ∼ 0.3–1.0 or 35% of the total Sloan Digital Sky Survey star-forming sample with redshift z ≥ 0.3. We study the dependence of the magnesium-to-oxygen and magnesium-to-neon abundance ratios on metallicity. Extrapolating this dependence to [Mg/Ne] = 0 and to solar metallicity we derive a magnesium depletion of [Mg/Ne] ≃ –0.4 (at solar metallicity). We prefer neon instead of oxygen to evaluate the magnesium depletion in the interstellar medium because neon is a noble gas and is not incorporated into dust, contrary to oxygen. Thus, we find that more massive and more metal abundant galaxies have higher magnesium depletion. The global parameters of our sample, such as the mass of the stellar population and star formation rate, are compared with previously obtained results from the literature. These results confirm that Mg II emission has a nebular origin. Our data for interstellar magnesium-to-oxygen abundance ratios relative to the solar value are in good agreement with similar measurements made for Galactic stars, for giant stars in the Milky Way satellite dwarf galaxies, and with low-metallicity damped Lyman-alpha systems.