Wellness Professionals

Integrative • Comprehensive • Personalized

Magnesium, Copper and Cardiovascular Disease

By: Rick Buchikos

Two of the most important factors to consider in the treatment or prevention of heart disease are dietary copper and magnesium.

Absolute or relative copper deficiency may play a critical role in the development of coronary heart disease. As of 1983, it was estimated that at least 75% of American adults were not getting adequate amounts of copper in their diet (1). Two key enzymes, lysyl oxidase and superoxide dismutase, are both copper dependent and are of primary importance in cardiovascular health.  Decreased activity of lysyl oxidase results in decreased crosslinking of collagen and elastin, and decreased SOD results in increased susceptibility to damage from free radicals (2). In other words, a lack of bioavailable copper leads to  a weakening of arterial walls and an increased potential for damage, which can precipitate the onset of disease.

In animal models, copper deficiency has been shown to lead to aberrant connective tissue in hearts and arteries, hypercholesterolemia, lipid deposits, and inflammation.  Some of the animals die even suddenly due to ruptured hearts (1). Several species of animals deficient in copper were found to have “aortic fissures and rupture, arterial foam cell and smooth muscle migration, cardiac enlargement and rupture, coronary artery thrombosis and myocardial infarction (2).” Copper researcher Leslie M. Klevay maintains that there are at least 75 anatomical and biochemical changes common to both animals deficient in copper and humans with heart disease. According to Klevay, copper deficiency is the “simplest and most general explanation for ischemic heart disease (2).”

Saari (2000) states that copper deficiency is the cause of many cardiovascular defects including hypertension, inflammation, anemia, weakened structural integrity of the heart and blood vessels, impaired cardiac energy metabolism, reduced ability of the heart to contract, and an altered ability of blood vessels to dilate and contract. In addition to reduced enzyme function, other copper deficiency related mechanisms that may contribute cardiovascular defects include peroxidation, glycation and changes in nitric oxide-dependent processes (3).

Magnesium is another essential mineral in regards to preventing and/or treating heart disease. Hypomagnesemia is one of the most common electrolyte imbalances associated with chronic congestive heart failure, along with hypokalemia and hyponatremia, and is thought to be at least partly responsible for the high degree of mortality and sudden death characteristic of congestive heart failure (4).

Acute magnesium deficiency leads to arrhythmias and sudden death, and giving magnesium has been shown to reduce the incidence of arrhythmias as well as increase survivability in cases of myocardial infarction. Experimental models have shown that a lack of magnesium can cause evidence of cardiac failure, which again improves after giving magnesium.  Hypomagnesemia has also been shown to promote atherosclerotic lesions in animal experiments (5).

In the journal Circulation Research, Harvard heart physiologist Joanne S. Ingwall, PhD. discusses what is known as the “Starved heart hypothesis,” which is the idea that the heart requires adequate ATP to support its systolic and diastolic work, and that heart failure may be the result of insufficient energy, possibly due to lack of resources.   Given that the heart needs a constant supply of energy, and that ATP needs magnesium in order to be biologically active, I find it logical to conclude that an absolute deficiency of magnesium may in fact play a critical role in the onset of heart failure (6).


(1) Klevay, L.M. (1982). Copper and Ischemic Heart Disease. Biological Trace Element Research, 5, 245-255. (2) Klevay, L.M. (2000). Cardiovascular Disease from Copper Deficiency- A History. Journal of Nutrition, 130, 489S-492S.

(3) Saari, J.T. (2000). Copper deficiency and cardiovascular disease: role of peroxidation, glycation, and nitration. Can. J. Physiol. Pharmacol., 78, 848-855.

(4) Douban, S., Brodsky, M.A., Whang, D.D. & Whang, R. (1996). Significance of magnesium in congestive heart failure. American Heart Journal, 132(3), 664-671.  

(5) Efstratiadis, G., Sarigianni, M. & Gougourelas, I. (2006). Hypomagnesemia and cardiovascular system. Hiippokratia, 10(4), 147-152.

(6) Ingwall, J.S. & Weiss, R.G. (2004). Is the Failing Heart Energy Starved? On Using Chemical Energy to Support Cardiac Function. Circulation Research, 95, 135-145.