Vitamin D3 deficiency 5 times increases risk of having severe COVID-19. Vitamin K2 and Magnesium should be supplemented together with Vitamin D3, in order to prevent long-term health-risk and improve immunoregulatory effects based on a causal loop diagram, disclosed in Simon Goddek, “Vitamin D3 and K2 and their potential contribution to reducing the COVID-19 mortality rate,” International Journal of Infectious Diseases, 99 (2020) 286-290, https://doi.org/10.1016/j.ijid.2020.07.080, JIF 12.073 (top 14% journals in Infectious Diseases).
In SARS-CoV-2, magnesium (Mg) activates protein kinases, stimulates T-cell receptors and production by generating ATP, controls cell membrane inflammation, and has vasodilatory and antithrombotic effects. Is a modulator of the release of acetylcholine and histamine in the inflammatory cascade in viral infections, according to Theo A.T.G van Kempen et al., “SARS-CoV-2: Influence of phosphate and magnesium, moderated by vitamin D, on energy (ATP) metabolism and on severity of COVID-19,” American Journal of Physiology Endocrinology and Metabolism, 2021, 320, E2–E6, https://doi.org/10.1152/ajpendo.00474.2020, JIF 5.900 (top 16% journals in Physiology and top 25% journals in Endocrinology & Metabolism).
We found reduced maternal TNF-a and IL-6 production following in vivo MgSO4 treatment. In summary, MgSO4 reduced cytokine production in intrapartum women, term and preterm neonates, demonstrating effectiveness in those at risk for inflammation-associated adverse perinatal outcomes. By probing the mechanism of decreased cytokine production, we found that the immunomodulatory effect was mediated by magnesium and not the sulfate moiety, and it was reversible. Cellular magnesium content increased rapidly upon MgSO4 exposure, and reduced cytokine production occurred following stimulation with different TLR ligands as well as when magnesium was added after TLR stimulation, strongly suggesting that magnesium acts intracellularly. Magnesium increased basal IĸBa levels, and upon TLR stimulation was associated with reduced NF-kB activation and nuclear localization. These findings establish a new paradigm for innate immunoregulation, whereby magnesium plays a critical regulatory role in NF-kB activation, cytokine production, and disease pathogenesis, according to Jun Sugimoto et al., “Magnesium Decreases Inflammatory Cytokine Production: A Novel Innate Immunomodulatory Mechanism,” The Journal of Immunology, 2012 Jun 15;188(12):6338-46, https://doi.org/10.4049/jimmunol.1101765, JIF 5.430 (top 39% journals in Immunology / top 18% journals in Immunology in 2012).
Magnesium and vitamin D each have the possibility of affecting the immune system and consequently the cytokine storm and coagulation cascade in COVID-19 infections, according to James J. DiNicolantonio et al., “Magnesium and vitamin D deficiency as a potential cause of immune dysfunction, cytokine storm and disseminated intravascular coagulation in COVID-19 patients,” Missouri Medicine, 118(1), 68–73 (2021), https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7861592/pdf/ms118_p0068.pdf, JIF N/A.
Magnesium is an essential element required as a cofactor for over 300 enzymatic reactions and is thus necessary for the biochemical functioning of numerous metabolic pathways. Emerging evidence confirms that nearly two thirds of the population in the western world is not achieving the recommended daily allowance for magnesium, a deficiency problem contributing to various health conditions. Level I evidence supports the use of magnesium in the prevention and treatment of many common health conditions including migraine headache, metabolic syndrome, diabetes, hyperlipidemia, asthma, premenstrual syndrome, preeclampsia, and various cardiac arrhythmias. Magnesium may also be considered for prevention of renal calculi and cataract formation, as an adjunct or treatment for depression, and as a therapeutic intervention for many other health-related disorders, according to Gerry K. Schwalfenberg et al., “The Importance of Magnesium in Clinical Healthcare,” Scientifica, Volume 2017, Article ID 4179326, 14 pages, https://doi.org/10.1155/2017/4179326, JIF N/A.