Posted by Anthony Brea D.C.

The concept of mineral imbalance as a major contributor to cardiovascular
disease has been elucidated in epidemiological, animal, and human
(clinical) studies. Not only has it been demonstrated, but a progressive
series of events has been clearly elucidated in HUMAN subjects at varying
degrees of magnesium (Mg) and potassium (K) deficiency.

When Mg intake is insufficient then tissue stores begin to suffer. There
are many places to get magnesium. Like platlets, red blood cells white
blood cells, smooth muscle cells of the arterial tree, heart muscle cells
etc... and this leaching causes havoc on the cardiovascular system. This
appears to be about nutritional deficiencies of minerals functioning as
electrolytes, not anti-oxidants. As magnesium levels start to decrease the
serum levels remains normal or close to it while the blood cells and
platlets start to become deficient. As Mg levels diminish K levels are
also reduced. Mg regulates the transport of K across cell membranes. K
deficiency on its own has been found to cause hypertension.

Generally, at the beginning stages of Mg++ deficiency, essential
hypertension is present with normal serum and intracellular Mg++ levels.
2) As the condition progresses the red blood cell Mg++ begins to decrease
while serum Mg++ remains normal 3)Finally, low serum and intracellular
Mg++ levels are found in the final stages.

Here are some studies that outline the progression of these stages.

(essential hypertension)
Normal serum and intracellular Mg++ levels.
Ozono R, Systemic magnesium deficiency disclosed by magnesium loading test
in patients with essential hypertension.

(vasospastic angina, ischemic heart disease)
Tanabe K , Magnesium content of erythrocytes in patients with vasospastic
angina.
Serum Mg++ Normal
Intracellular Mg++ significantly lower (1.59mg/dl) than healthy subject
(2.11 mg/dl)

(coronary heart disease, diminished left ventricular stroke volume [lower
than 55%])
Manthey J, Magnesium in serum of patients with coronary artery disease.
Lower Mg++ serum levels.

Generally as the levels of Mg++ decrease, first intracellularly (RBC) and
then in serum, the events commonly associated with progression of
cardiovascular disease occur.

Mg++ deficiency increase the vasospastic response of blood vessels to
stress-released hormones.

Animal studies show that Mg++ inhibits thrombus formation in arteries that
have suffered endothelial damaged by vasoconstriction(40-60% in
transluminal diameter). Untreated animals suffered marked platlet
deposition on exposed subendothelium, and microthrombi with a maximum
luminal protusion of 30% of the total luminal diameter. Animals
pre-treated with Mg++ showed platlet deposition restricted to 1-2
discontinuous layers.

Taking all these factors into account, it is my opinion that one
compelling theory arises as a major cause of cardiovascular disease.

1)That chronic increases in peripheral vasomotor tone secondary to Mg++
deficiency causes or exacerbates some cases of essential hypertension.

2)That as hypertension progresses in response to stresses (physical and
mental stress, K+/Mg++ deficiency etc...), endothelial damage occurs
and in the presence of diminished protective factors (eg.
anti-oxidants,Mg++,copper, essential fatty acids, B complex etc...)
atherosclerotic changes begin to occur.(plaque formation)

3) As the hypertension continues greater degrees of a) atherosclerosis,
b) Mg++/K+ deficiency and vasospasms eventually lead to vasospastic
angina, arrythmias, heart attack and finally sudden cardiac death.

Anthony Brea D.C.

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