A paper published last month in the journal Magnesium Research sheds light on the study reported in the last post offering evidence for the link between calcium supplementation and heart attacks. The authors investigated the role of magnesium deficiency in the calcium-activated inflammation of metabolic syndrome.

“The concept that metabolic syndrome is an inflammatory condition may explain the role of Mg [magnesium]. Mg deficiency results in a stress effect and..activates the hypothalamic-pituitary-adrenal axis (HPA) axis and the sympathetic nervous system. The activation of the renin-angiotensin-aldosterone system is a factor in the development of insulin resistance by increasing oxidative stress [and]…leads to an inflammatory phenotype.”

They further describe how this develops an inflammatory milieu in blood vessels:

“One of the earliest events in the acute response to stress is endothelial [blood vessel 'lining'] dysfunction…Experimental Mg deficiency in rats induces a clinical inflammatory syndrome characterized by leukocyte and macrophage activation, synthesis of inflammatory cytokines and acute phase proteins, extensive production of free radicals. An increase in extracellular Mg concentration decreases inflammatory effects, while reduction in extracellular Mg results in cell activation. The effect of Mg deficiency in the development of insulin resistance in the rat model is well documented.”

They then elucidate how magnesium deficiency promotes atherosclerosis with the vascular inflammation characteristic of cardiovascular diseases including heart attacks:

“Inflammation occurring during experimental Mg deficiency is the mechanism that induces hypertriglyceridemia and pro-atherogenic changes in lipoprotein metabolism. The presence of endothelial dysfunction and dyslipidemia triggers platelet aggregability [stickiness], thus increasing the risk of thrombotic events [blood clots]. Oxidative stress contributes to the elevation of blood pressure. The inflammatory syndrome induces activation of several factors, which are dependent on cytosolic [inside the cell] Ca [calcium] activation. Recent findings support the hypothesis that the Mg effect on intracellular Ca 2+ homeostasis may be a common link between stress, inflammation and a possible relationship to metabolic syndrome.“

In other words, as calcium goes up in ratio to magnesium cardiovascular inflammation develops. This is important in light of the previous post on calcium supplementation and heart attacks.

The author of a review in the same issue of Magnesium Research notes:

“Hypomagnesemia is associated with an increased incidence of diabetes mellitus, metabolic syndrome, mortality rate from CAD [coronary artery disease] and all causes. Magnesium supplementation improves myocardial metabolism, inhibits calcium accumulation and myocardial cell death; it improves vascular tone, peripheral vascular resistance, afterload and cardiac output, reduces cardiac arrhythmias and improves lipid metabolism. Magnesium also reduces vulnerability to oxygen-derived free radicals, improves human endothelial function and inhibits platelet function, including platelet aggregation and adhesion, which potentially gives magnesium physiologic and natural effects similar to adenosine-diphosphate inhibitors such as clopidogrel [blood clot prevention].”

If you’re reading this, whether you are a man or woman it is highly likely that you have a functional deficiency of magnesium and should not be taking calcium.