Precious and not-so-precious metals have an interesting relationship with the human body. While some—such as gold silver and platinum—look nice on the body in the form of jewelry others have important roles in the body. For example silver is a broad-spectrum antimicrobial and antiviral agent. Gold is found in the body in miniscule amounts (one estimate puts it at about 0.000021 pounds) but nobody’s quite sure what it’s doing there if anything. But with copper now we’re talking. While silver can be beneficial for health in certain circumstances it’s not required in human physiology. This is where copper outshines its more lustrous cousin as copper is essential for human life.

Copper participates in a surprising array of enzymatic reactions that affect numerous tissues and systems but first and foremost owing to its role in facilitating the action of cytochrome c oxidase copper is essential for sustaining human life at the most basic and fundamental level – generation of ATP via the electron transport chain. Without that it wouldn’t much matter what else copper does in the human body.

Copper may be best known as part of the superoxide dismutase enzyme along with zinc. It’s also needed by dopamine β-hydroxylase which catalyzes the conversion of dopamine to norepinephrine. Beyond this one of copper’s big roles is in supporting the formation of healthy connective tissue. The enzyme lysyl oxidase is a copper-dependent enzyme (a.k.a. a “cuproenzyme”) required for the cross-linking of collagen and elastin the foundations of strong and flexible connective tissue. Owing to this lysyl oxidase and hence copper helps “maintain the integrity of connective tissue in the heart and blood vessels and also plays a role in bone formation.” Inborn errors of copper metabolism resulting in a severe reduction in lysyl oxidase activity are what underlie Ehlers-Danlos syndrome type IX and Menke’s syndrome. 

Copper has delicate relationships with two other metals critical for health namely zinc and iron. In the case of zinc high supplemental intakes for extended lengths of time may induce a copper deficiency. (In fact high dose zinc supplementation has been used as the sole therapy for reducing or preventing excess copper accumulation in some cases of Wilson’s disease.) According to the Linus Pauling Institute at Oregon State University “High dietary zinc intakes increase the synthesis of an intestinal cell protein called metallothionein which binds certain metals and prevents their absorption by trapping them in intestinal cells. Metallothionein has a stronger affinity for copper than zinc so high levels of metallothionein induced by excess zinc cause a decrease in copper absorption. In contrast high copper intakes have not been found to affect zinc nutritional status.”

As for iron copper may compete with iron for intestinal absorption. Beyond that the relationship between copper and iron is a bit more complicated than that between copper and zinc. The copper-containing enzyme ceruloplasmin is “a ferroxidase enzyme that has the capacity to oxidize ferrous iron (Fe²⁺) to ferric iron (Fe³⁺) which can be loaded onto the iron-transport protein transferrin.” Ceruloplasmin is required for iron transport to the bone marrow for red blood cell formation and as such anemia may be a sign of clinical copper deficiency. (Patients with anemia unresponsive to iron may benefit from supplemental copper.) Inadequate ceruloplasmin activity may result in hepatic iron overload due to impaired mobilization and transport of iron. Ceruloplasmin also functions as an antioxidant in two different ways. The first is related to its ferroxidase activity: by facilitating iron latching onto the transport protein transferrin it may prevent free ferrous ions from participating in free-radical-generating reactions. Second free copper ions are themselves drivers of free-radical damage. When bound to ceruloplasmin however copper ions are prevented from causing oxidative damage.

Copper status may also be affected by supplementation with alpha-lipoic acid or molybdenum. Alpha-lipoic acid is a known chelator of copper and has been used to this end for patients with Wilson’s disease. So it may be worth considering copper supplementation for patients without copper excess who are taking alpha-lipoic acid long term. Regarding molybdenum copper forms an insoluble complex with molybdenum in the GI tract and ingestion of large amounts of one of these nutrients may result in a deficiency of the other.

Foods rich in copper include liver shellfish beans whole grains nuts and seeds. However current copper intake in the industrialized world may be significantly lower than it was in the past. Up to 68% of the copper in whole wheat is lost during the refining process and as revealed by Alan Gaby MD in his seminal work Nutritional Medicine “The average copper content of fruits and vegetables declined by 81% between the years 1940 and 2000 presumably because of changes in farming methods that decreased the availability of copper in the soil.”

Future posts will explore some of these physiological roles for copper in more detail.