Minerals

Copper

By All The Nutrients Editorial Team Published: 6 min read

Copper is an essential trace mineral that functions as a cofactor for over 30 enzymes involved in iron metabolism, oxidative stress defence, connective tissue synthesis, neurotransmitter production, and energy generation. Unlike many trace minerals, copper participates directly in electron transfer reactions — its ability to cycle between Cu²⁺ and Cu⁺ oxidation states makes it indispensable in the active sites of cuproenzymes. The RDA is 900 µg/day for adults (the same for men and women), rising to 1,000 µg/day during pregnancy and 1,300 µg/day while breastfeeding. Copper deficiency is more common than generally recognised, particularly in people with malabsorption conditions, high zinc supplement use, or poor dietary diversity. See the top food sources of copper ranked by µg per 100 g from USDA data.

Daily Value

0.900 mg

FDA 2020

Upper Limit

10.0 mg

per day

Top Source

Toddler drink, MEAD JOHNSON, PurAmino Toddler Powder, with ARA and DHA, not reconstituted

370 mg

What Does Copper Do?

  • Iron metabolism and prevention of anaemia — ceruloplasmin, the copper-containing ferroxidase enzyme, oxidises ferrous iron (Fe²⁺) to ferric iron (Fe³⁺), which is required for iron to be loaded onto transferrin for transport in the blood. Without adequate copper, iron cannot be exported from storage sites in the liver and intestinal cells — causing a secondary functional iron deficiency even when total body iron stores are adequate. This explains why copper deficiency anaemia closely resembles iron deficiency anaemia on laboratory tests.
  • Antioxidant defence via superoxide dismutase — copper-zinc superoxide dismutase (Cu/Zn-SOD, or SOD1) is the primary cytoplasmic antioxidant enzyme, catalysing the conversion of superoxide radicals (O₂⁻) — a damaging byproduct of cellular metabolism — to hydrogen peroxide and oxygen. This enzyme is critical for protecting cells from oxidative damage, particularly in neurons and red blood cells with high metabolic activity.
  • Connective tissue and bone integrity — lysyl oxidase (LOX), a copper-dependent enzyme, crosslinks collagen and elastin fibres in connective tissue, bone, blood vessels, and skin. Without adequate copper, collagen and elastin cannot form properly, leading to weakened connective tissue, fragile bones, and vascular instability. This is the mechanism underlying the aortic aneurysms and skeletal abnormalities seen in Menkes disease (genetic copper deficiency).
  • Neurotransmitter synthesis and neurological function — dopamine β-hydroxylase, a copper enzyme, converts dopamine to noradrenaline (norepinephrine) — a key neurotransmitter for attention, mood, and stress response. Copper is also required for cytochrome c oxidase (Complex IV of the mitochondrial electron transport chain), making it essential for ATP production in neurons and all metabolically active cells.

Signs of Copper Deficiency

Copper deficiency is underdiagnosed because serum copper levels are an insensitive marker (they remain normal until deficiency is severe) and symptoms overlap with iron deficiency and neurological conditions. The most common causes in high-income countries are: excessive zinc supplementation (zinc and copper compete for the same intestinal transporter, ZIP4/DMT1), gastric bypass surgery, prolonged total parenteral nutrition without copper, and malabsorptive conditions (coeliac disease, Crohn's disease).

  • Anaemia resistant to iron supplementation — hypochromic microcytic or normocytic anaemia caused by impaired iron export from cells
  • Neutropenia — low white blood cell count, increasing susceptibility to infection; often the first laboratory finding of copper deficiency
  • Neurological symptoms — subacute combined degeneration of the spinal cord (myelopathy) causing weakness, spasticity, sensory ataxia, and peripheral neuropathy; can be mistaken for vitamin B12 deficiency
  • Bone abnormalities — osteoporosis, fractures, and (in children) metaphyseal abnormalities resembling scurvy due to impaired collagen crosslinking
  • Hair and skin depigmentation — copper is required for melanin synthesis via tyrosinase; deficiency causes premature greying and pale skin
  • Cardiovascular abnormalities — weakened aortic walls from impaired elastin crosslinking; associated with cardiac arrhythmias in some cases
  • Menkes disease (genetic) — severe copper deficiency from birth causing progressive neurodegeneration, kinky hair, seizures, and death in early childhood

Upper Limit: The Tolerable Upper Intake Level (UL) for copper is 10 mg/day for adults. Excess copper from supplements causes nausea, vomiting, liver damage, and — at extreme doses — cirrhosis. Wilson's disease (genetic copper accumulation) causes severe liver and neurological damage from impaired copper excretion and requires lifelong medical management.

Consider supplementing

Copper supplement

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How to Get the Most from Copper

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Avoid high-dose zinc supplements unless medically indicated

Zinc and copper compete for absorption via the intestinal transporter metallothionein and the ZIP4 transporter. Supplemental zinc doses above 40 mg/day (the UL) chronically induce metallothionein in intestinal cells, which preferentially binds and retains copper, reducing its absorption significantly. Long-term zinc supplementation is a leading cause of acquired copper deficiency in adults — often presenting as anaemia and neurological symptoms years after starting zinc.

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Copper from shellfish and organ meats is the most bioavailable

Bioavailability of copper varies: shellfish (oysters, crab) and organ meats (beef liver) provide highly bioavailable copper with absorption rates of 25–50%. Nuts, seeds, and whole grains provide copper but also contain phytic acid, which reduces absorption to 15–25%. Cooking organ meats is one of the most efficient ways to correct copper deficiency.

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Vitamin C in very high doses may reduce copper status

High-dose vitamin C supplementation (>1,500 mg/day) has been shown in some studies to reduce ceruloplasmin activity and copper status, possibly by reducing Cu²⁺ to the less bioavailable Cu⁺ form in the gut. Dietary vitamin C from food at normal amounts does not pose this risk.

Common Copper Questions

What does copper do in the body?

Copper is a cofactor for over 30 enzymes. Key functions include: enabling iron transport via ceruloplasmin (preventing anaemia), antioxidant defence via superoxide dismutase (SOD1), connective tissue and bone synthesis via lysyl oxidase (LOX), neurotransmitter production (dopamine → noradrenaline), and energy production via cytochrome c oxidase in mitochondria.

What are the signs of copper deficiency?

The most common signs are anaemia that does not respond to iron treatment, low white blood cell count (neutropenia), and neurological symptoms resembling vitamin B12 deficiency — weakness, tingling, and balance problems from spinal cord damage. Bone fragility, premature greying, and pale skin are also associated. Copper deficiency is most common after gastric bypass surgery, with long-term high-dose zinc supplementation, or with malabsorption conditions.

Which foods are highest in copper?

The richest sources per 100g are: beef liver (12 mg), oysters (4–7 mg), shiitake mushrooms (1.3 mg), dark chocolate/cocoa (1.7 mg), cashews (2.2 mg), sunflower seeds (1.8 mg), sesame seeds (4.1 mg), and lentils (0.5 mg). Organ meats and shellfish are by far the most concentrated sources.

Can zinc supplements cause copper deficiency?

Yes — this is one of the most clinically important copper-mineral interactions. Long-term zinc supplementation at doses above 40 mg/day (the Tolerable Upper Intake Level) induces intestinal metallothionein, which binds copper and blocks its absorption. Cases of severe neurological copper deficiency caused by zinc supplements (including from denture adhesive creams containing zinc) are well-documented in medical literature. Anyone taking zinc supplements long-term should periodically check serum copper and ceruloplasmin levels.

How much copper do I need per day?

The RDA is 900 µg/day for adults, 1,000 µg/day during pregnancy, and 1,300 µg/day while breastfeeding. The Tolerable Upper Intake Level (UL) is 10,000 µg (10 mg)/day — much higher than dietary intake from food. Copper toxicity from diet alone is extremely rare; concerns relate primarily to high-dose copper supplements or occupational exposure.