Copper: The Maligned Mineral
Few dietary components are more misunderstood than copper. Although copper is the third most abundant essential trace mineral in the body, after iron and zinc, most people consider it unimportant. Even worse, many people have actually taken steps to exclude it from their diets and dietary supplements, believing it to be nothing more than a cause of free radical reactions. This is surprising, because copper has been recognized as an essential nutrient since the 1920’s.1 In the past seventy years, much has been learned about the important biological roles of copper and the copper-dependent enzymes. In fact, copper is emerging as one of the most important minerals in our diet. While unbound, free copper does generate free radicals in vitro, the relevance of this in the body has been called more imaginary than real.2 In fact, copper has an entirely different role in the body, being a component of two of our most important antioxidant enzymes, copper-zinc superoxide dismutase and ceruloplasmin.3
Unbound, free copper is not found in large quantities in the human body. Instead, almost all of the copper in our bodies is bound to either transport proteins (ceruloplasmin and copper-albumin), storage proteins (metallothioneins), or copper containing enzymes.4 A substantial number of copper metalloenzymes have been found in the human body. Copper is essential for the proper functioning of these copper-dependent enzymes, including cytochrome C oxidase (energy production), superoxide dismutase (antioxidant protection), tyrosinase (pigmentation), dopamine hydroxylase (catecholamine production), lysyl oxidase (collagen and elastin formation), clotting factor V (blood clotting), and ceruloplasmin (antioxidant protection, iron metabolism, and copper transport).5 Most features of severe copper deficiency can be explained by a failure of one or more of these copper-dependent enzymes. For instance, depigmentation can be explained by a tyrosinase deficiency, and the defects of collagen and elastin causing abnormalities in the connective tissue and vascular system can be explained by a lysyl oxidase deficiency.