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Magnesium Suppresses Formation of Clogged Arteries - May 2014

The molecular biology and pathophysiology of vascular calcification.

Abstract Nutritional Magnesium Association
McCarty MF1, Dinicolantonio JJ, “The molecular biology and pathophysiology of vascular calcification.” Postgrad Med. 2014 Mar;126(2):54-64. doi: 10.3810/pgm.2014.03.2740.

Vascular calcification (VC), commonly encountered in renal failure, diabetes, and aging, is associated with a large increase in the risk for cardiovascular events and mortality. Calcification of the arterial media and of heart valves clearly plays a mediating role in this regard, whereas it is less clear how calcification of plaque influences atherogenesis and risk for plaque rupture. Vascular calcification is an active process in which vascular smooth muscle cells (VSMCs) adopt an osteoblastic phenotype and deposit hydroxyapatite crystals; apoptosis of VSMCs also promotes this deposition. Drivers of this phenotypic transition, which include elevated serum phosphate, advanced glycation end-products, bone morphogenetic proteins, inflammatory cytokines, and leptin, invariably induce oxidative stress in VSMCs, which appears to be a necessary and sufficient condition for induction of the runt-related transcription factor 2 gene (RUNX2) and the shift to osteoblastic behavior. Magnesium antagonizes the impact of phosphate on VSMC osteoblastic transition, both by a direct effect within VSMCs and by suppressing absorption of dietary phosphate. Antioxidants that suppress reduced nicotinamide adenine dinucleotide phosphate oxidase activity may have the potential to block the osteoblastic transition of VSMCs. Minimizing the absorption of dietary phosphate may also be helpful in this regard, particularly in renal failure, and it can be achieved with plant-based dietary choices, avoidance of phosphate additives, and administration of pharmaceutical phosphate binders, supplemental magnesium, and niacin. Good vitamin K status opposes VC by optimizing the γ-carboxylation of matrix Gla protein, a physiological antagonist of VC. Adequate but not excessive vitamin D status also appears to discourage VC. Etidronate, a structural analogue of pyrophosphate, has shown potential for blocking VC.
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Expert Commentary by Dr. Carolyn Dean, MD, ND

Typically, less than half of calcium intake is absorbed in the gut,1 the rest either being excreted or potentially forming kidney stones or being transported to soft tissues where it can harden (calcify).
• Adequate levels of magnesium are essential for the absorption and metabolism of calcium and vitamin D and according to this study, magnesium suppresses the absorption of dietary phosphate which is a factor in vascular calcification.
The study points out that adequate Vitamin D status also appears to discourage Vascular Calcification. Magnesium converts vitamin D into its active form so that it can aid calcium absorption. Magnesium also stimulates the hormone calcitonin, which helps to preserve bone structure and draws calcium out of the blood and soft tissues back into the bones, lowering the likelihood of osteoporosis, clogged arteries, some forms of arthritis, heart attack and kidney stones.
• There is a growing amount of scientific evidence pointing to high calcium–low magnesium intake leading to calcification, or hardening, of arteries (atherosclerosis—the number one cause of death in the US), osteoporosis and osteoporotic bone fractures.2,3

  • 1. National Institutes of Health, Office of Dietary Supplements. 2011. Dietary Supplement Fact Sheet: Calcium. “Calcium Intakes and Status.”
  • 2. Bolland, MJ, A Grey, A Avenell, GD Gamble, and IR Reid. 2011. “Calcium Supplements with or without Vitamin D and Risk of Cardiovascular Events: Reanalysis of the Women’s Health Initiative Limited Access Dataset and Meta-Analysis.” Epub BMJ (Apr 19): 342:d2040. doi:10.1136/bmj.d2040. PMID:21505219.
  • 3. Raggi, P, TQ Callister, and LJ Shaw. 2004. “Progression of Coronary Artery Calcium and Risk of First Myocardial Infarction in Patients Receiving Cholesterol-Lowering Therapy.” Arterioscler Thromb Vasc Biol 24:1272–77.

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Magnesium Counteracts Vascular Calcification - Passive Interference or Active Modulation? - 2017

Arteriosclerosis, Thrombosis, and Vascular Biology. 2017;37:1431–1445 https://doi.org/10.1161/ATVBAHA.117.309182
Anique D. ter Braake, Catherine M. Shanahan and Jeroen H.F. de Baaij

Over the last decade, an increasing number of studies report a close relationship between serum magnesium concentration and cardiovascular disease risk in the general population. In end-stage renal disease, an association was found between serum magnesium and survival. Hypomagnesemia was identified as a strong predictor for cardiovascular disease in these patients. A substantial body of in vitro and in vivo studies has identified a protective role for magnesium in vascular calcification. However, the precise mechanisms and its contribution to cardiovascular protection remain unclear.
There are currently 2 leading hypotheses:

  • first, magnesium may bind phosphate and delay calcium phosphate crystal growth in the circulation, thereby passively interfering with calcium phosphate deposition in the vessel wall.
  • Second, magnesium may regulate vascular smooth muscle cell transdifferentiation toward an osteogenic phenotype by active cellular modulation of factors associated with calcification.

Here, the data supporting these major hypotheses are reviewed. The literature supports both a passive inorganic phosphate–buffering role reducing hydroxyapatite formation and an active cell-mediated role, directly targeting vascular smooth muscle transdifferentiation. However, current evidence relies on basic experimental designs that are often insufficient to delineate the underlying mechanisms. The field requires more advanced experimental design, including determination of intracellular magnesium concentrations and the identification of the molecular players that regulate magnesium concentrations in vascular smooth muscle cells.
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Effects of Mg Citrate, Mg Oxide, and Mg Sulfate on Arterial Stiffness: RCT - March 2022

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