The body of an adult contains an estimated 70 to 100 milligrams of copper — roughly the weight of a match. Around one third of it is in the liver and spleen, another third in muscle tissue, and the rest is distributed across brain, bone and blood. Compared with calcium, of which the body stores more than a kilogram, that is a tiny amount.
Even so, copper appears on almost every second page of biochemistry textbooks. The reason lies not in the quantity but in the design of some enzymes: they carry a copper ion in the active centre and cannot pass on electrons without this ion. There, a single atom determines whether a reaction proceeds or stalls.
This page collects what is documented about this one trace element — no more and no less. The European Commission has authorised four claims for copper on the basis of EFSA opinions; they appear here in their exact wording, each with the legal source stated.
Azuritsaum brings together reviewed knowledge on a single mineral. Four health claims are authorised for copper in the European Union. One of them reads:
“Copper contributes to normal iron transport in the body”
Under Regulation (EU) No 432/2012
To the guideCopper is one of the essential trace elements: the body does not produce it itself.
Each of the following claims stands on its own and rests on its own scientific opinion. The wording is legally prescribed and is reproduced here unchanged.
Iron does not travel freely in the blood but bound to the protein transferrin. Transferrin can only be loaded with trivalent iron, however. Ceruloplasmin — an enzyme carrying six copper atoms — performs the conversion of divalent into trivalent iron.
Under Regulation (EU) No 432/2012
In the nerve endings sits dopamine β-hydroxylase, a copper-containing enzyme that converts dopamine into noradrenaline. The formation of the myelin sheaths, that insulating layer around the nerve fibres, also proceeds via copper-dependent reaction steps.
Under Regulation (EU) No 432/2012
Superoxide radicals arise as a by-product of every round of cellular respiration. The superoxide dismutase in the cytosol carries one copper and one zinc atom each and converts these radicals into hydrogen peroxide, which is then broken down further.
Under Regulation (EU) No 432/2012
At the end of the mitochondrial respiratory chain sits cytochrome c oxidase. This enzyme complex has two copper-containing centres and transfers the electrons to oxygen — the step at which most of the energy in the cell is obtained.
Under Regulation (EU) No 432/2012
Copper from food is absorbed predominantly in the upper small intestine. The transporter CTR1 in the intestinal wall moves the ion into the cell; from there, specialised transport proteins known as chaperones take the copper to its precise destination. A free copper ion practically never remains unaccompanied inside the cell — the body keeps it bound at all times.
Most of it first reaches the liver via the portal vein. From there the paths diverge: incorporation into newly formed enzymes, storage in metallothioneins, or excretion via the bile. About 80 percent of excreted copper leaves the body by this route, with only a small share via the kidney.
Ceruloplasmin is a glycoprotein formed in the liver that carries around 90 percent of the copper circulating in blood plasma. Its ferroxidase activity consists in oxidising divalent iron to the trivalent form. Only in this form can iron bind to transferrin and be passed on in the blood.
At the cellular level a related enzyme, hephaestin, works directly in the membrane of the intestinal cells and performs the same oxidation step as iron leaves the cell. Both enzymes contain copper — this is where copper and iron metabolism touch each other directly.
This relationship is precisely the basis of the authorised claim: “Copper contributes to normal iron transport in the body” — Under Regulation (EU) No 432/2012.
In the brain the copper concentration is higher than in most other tissues. Two enzyme families largely explain this: the dopamine β-hydroxylase already mentioned, which catalyses the last step of noradrenaline formation, and cytochrome c oxidase, of which nerve cells need particularly large amounts because of their high energy turnover.
There is also peptidylglycine α-amidating monooxygenase, which converts numerous neuropeptides into their active form. It too works with copper in the active centre. The authorised claim summarises these findings: “Copper contributes to normal functioning of the nervous system” — Under Regulation (EU) No 432/2012.
Copper and zinc partly use the same binding partners in the intestinal wall. A very high zinc intake over a long period increases the formation of metallothionein in the intestinal cells; this protein binds copper particularly tightly, so that less of it passes into the blood. With a normal diet this effect plays no role; with high-dose single preparations it can become measurable.
Conversely, vitamin C in larger amounts can reduce copper in the intestine to the monovalent form and thereby affect its absorption. The evidence on this is inconsistent; the European authorities have so far derived no intake recommendation from it.
Two further claims round off the picture. The first reads: “Copper contributes to the protection of cells from oxidative stress” — Under Regulation (EU) No 432/2012. The second reads: “Copper contributes to normal energy-yielding metabolism” — Under Regulation (EU) No 432/2012.
The guide brings together what is documented about copper in the specialist literature and in the EU register: absorption routes, reference values, contents of individual foods and the four authorised claims in their exact wording.
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