A trace mineral that ties collagen together, helps you use iron, and protects your nerves. The usual way people run low is by taking too much zinc.
Mechanisms, studies and evidence grades for each claim above.
Copper's best-established mechanistic role in this series is as the cofactor for lysyl oxidase, the enzyme that cross-links collagen and elastin fibers into stable covalent bonds during connective tissue synthesis.1 Without those cross-links, newly made collagen is mechanically weak. This is the third cofactor in the collagen chain alongside vitamin C and iron — see Glycine / Collagen for the full pathway. (Strong — well-characterized enzymology)
↑ back to summaryCopper is the core of ceruloplasmin and hephaestin, the ferroxidase enzymes that oxidize iron so it can be loaded onto transferrin and moved out of storage and gut cells. When copper runs short, iron gets stranded: the result is an anemia (often with low white-cell counts) that looks like iron deficiency but doesn't respond to iron.2 The hematologic effects are fully reversible with copper replacement, typically over 4–12 weeks.2 (Strong — consistent clinical literature)
↑ back to summaryThe neurological side of copper deficiency was recognized only relatively recently. The most common presentation is a myelopathy — spinal cord damage causing a stiff, spastic gait and loss of position sense in the feet — that is clinically and on MRI almost indistinguishable from the subacute combined degeneration of vitamin B12 deficiency. The two deficiencies can coexist, and the nerve damage can appear without any anemia at all.3
The recognized causes are prior gastric surgery, malabsorption, and excess zinc.3 Zinc induces a copper-binding protein (metallothionein) in gut cells that traps dietary copper so it's shed rather than absorbed — which is why long-term high-dose zinc supplements (and even zinc-containing denture creams) show up repeatedly in case reports. Crucially, copper replacement fixes the blood picture completely but the neurological damage only partially: improvement, when it happens, is often limited to sensory symptoms.2,3 That asymmetry is the practical argument for pairing any long-term zinc supplement with a little copper rather than waiting for symptoms. (Strong for the syndrome; Moderate for the zinc mechanism) See Zinc.
↑ back to summaryCopper is required, with zinc, for cytosolic superoxide dismutase (Cu/Zn-SOD), one of the main enzymes that neutralizes superoxide radicals, and for cytochrome c oxidase, the final complex of the mitochondrial electron transport chain.4 Frank deficiency lowers SOD activity; whether intakes above adequacy improve antioxidant status in people who aren't deficient is not established. (Moderate for the requirement; Inferred for any benefit above adequacy)
↑ back to summaryThe U.S. RDA is 900 mcg/day for adults, with a tolerable upper intake level of 10 mg/day.5 National authorities disagree on the exact reference values, because copper status biomarkers are insensitive at the margins — serum copper and ceruloplasmin only fall clearly in outright deficiency.4 Diagnosis of deficiency uses serum copper, ceruloplasmin, and 24-hour urine copper.2