Therefore, magnesium helps to maintain the elasticity and stretchability of the vessels. [10]
Studies have shown that this effect is independent on the vasodilation caused by nitric oxide (NO). [11]
However, the production of NO is also dependent on magnesium. So you can’t even make enough NO to dilate your vessels and get you out of trouble when magnesium levels are too low.
In chronic magnesium deficiency it is common for the arterial walls to become more rigid and lose elasticity as more calcium precipitates out of the blood to harden the arterial linings.
The pressure of the circulation on the stiff arterial walls can cause tiny micro-splits at the places where the calcium has deposited, which turn into calcium lesions. The body then sends cholesterol bandages to plug up the holes. As electrons are lost from the good fluidic cholesterol (HDL) in the blood to the inflamed and acidic injury sites (calcium lesions), oxidised ‘bad’ cholesterol (LDL) forms and piles up in solid layers at those sites until the arterial passageway narrows and chokes off, resulting ischemia and heart attack.
The more oxidation and the less antioxidant presence, the more lipid peroxidation occurs – ie. fatty deposits.
“Magnesium deficiency potentiates free radical production and oxidative stress in endothelial cells through reduction in plasma antioxidants and increased lipid peroxidation.”[12]
Thrombosis and Stroke
In a dehydrated state of positive pH charge, platelet stickiness is triggered, causing a clumping together of blood cells, which can build up to form blood clots and thrombosis. If a clot lodges in the brain it becomes a stroke. Magnesium however promotes the release of prostacyclin, which reduces the platelet stickiness again to restore normal blood fluidity. Magnesium acts like an anti-coagulant!
Studies have confirmed that platelet-dependent thrombosis is significantly increased in patients with coronary artery disease and low intracellular magnesium. [13]
If you are getting calcium precipitation on the endothelial lining, that is because free calcium has moved into the blood stream, causing thickening and exacerbation of hypertension, as well as platelet aggregation. Magnesium is known to inhibit platelet activation by inhibiting Thromboxane A2 and interfering with the IIb-IIIa receptor complex. [14]
This condition is associated with a perfect storm coming together of 1) cellular acidosis (oxidative stress), 2) magnesium deficiency (= hypercalcemia) and 3) dehydration.