Magnesium, Calcium and Inflammation

Magnesium and the inflammatory response: Potential physiopathological implications

Abstract:

The purpose of this review is to summarize experimental findings showing that magnesium modulates cellular events involved in inflammation. Experimental magnesium deficiency in the rat induces after a few days a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, release of inflammatory cytokines and acute phase proteins, excessive production of free radicals. Increase in extracellular magnesium concentration, decreases inflammatory response while reduction in the extracellular magnesium results in cell activation. Because magnesium acts as a natural calcium antagonist, the molecular basis for inflammatory response is probably the result of modulation of intracellular calcium concentration. The priming of phagocytic cells, the opening calcium channel and activation of N-methyl-d-aspartate (NMDA) receptors, the activation of nuclear factor-kappa B (NFκB) have been considered as potential mechanisms. Moreover, magnesium deficiency induces a systemic stress response by activation of neuro endocrinological pathways. As nervous and immune systems interact bidirectionally, the roles of neuromediators have also been considered. Magnesium deficiency contributes to an exaggerated response to immune stress and oxidative stress is the consequence of the inflammatory response. Inflammation contributes to the pro-atherogenic changes in lipoprotein metabolism, endothelial dysfunction, thrombosis, hypertension and explains the aggravating effect of magnesium deficiency on the development of metabolic syndrome. Further studies are still needed to assess more accurately the role of magnesium in immune response in humans, but these experimental findings in animal models suggest that inflammation is the missing link to explain the role of magnesium in many pathological conditions.

Source:

Archives of Biochemistry and Biophysics, Volume 458, Issue 1, 1 February 2007, Pages 48–56
Highlight Issue on Cellular Regulation of Magnesium, Andrzej Mazura, Jeanette A.M. Maierb, Edmond Rocka, Elyett Gueuxa, Wojciech Nowackic, Yves Rayssiguiera

a. Equipe Stress Métabolique et Micronutriments, Unité de Nutrition Humaine UMR 1019, Centre de Recherche en Nutrition Humaine d’Auvergne, INRA, Theix, St. Genès Champanelle, France
b. University of Milan, Department of Preclinical Sciences LITA Vialba, Via GB Grassi, 74 20157 Milan, Italy
c. Department of Veterinary Prevention and Immunology, Veterinary Faculty, Agricultural University, Norwida 31, 50-375 Wroclaw, Poland

Expert Commentary:

“As allopathic medicine realizes cholesterol is not the cause of heart disease, and their decades long attempt to treat this condition with statin drugs has failed, accusing fingers are pointing at inflammation.”

“According to a September 13, 2013 post on the American Heart Association website. “…clinical trials are ongoing to see if other medications might lower inflammation in arteries and reduce the risk of heart attack and stroke. More information on the role of inflammation should be available in the next few years.”

“We may not have years to find out but what we predict is that the use of drugs to treat inflammation will not work. Drugs actually create inflammation. What we do know is that enough research has been done to show that magnesium is a magnificent treatment for inflammation.”

“This paper is a review of findings showing that at the cellular level, magnesium modifies inflammation. In the animal model, magnesium deficiency is created when an inflammatory condition is created. Increasing magnesium decreases the inflammation response primarily by acting as a calcium channel blocker. Calcium in excess is one of the most pro-inflammatory substances in the body. With magnesium being actively required by 600-700 enzyme systems, more mechanisms of action to reduce inflammation are being proposed and found including activation of neuro endocrinological pathways and modulation of the immune response and dampening of oxidative stress.”

“The paper overviews the contribution of inflammation to the pro-atherosclerotic changes in lipoprotein metabolism, endothelial dysfunction, clot formation, and hypertension. It also explains the aggravating effect of magnesium deficiency on the development of metabolic syndrome.”

“The paper concludes that “ these experimental findings in animal models suggest that inflammation is the missing link to explain the role of magnesium in many pathological conditions.”

Carolyn Dean, MD, ND