Copper
Copper
Also known as: Cupric oxide, Copper gluconate, Copper sulfate, Ceruloplasmin-bound copper
Copper is an essential trace mineral required for iron metabolism, connective tissue formation, and energy production. Deficiency causes anemia and neurologic problems.
Introduction
Copper is an essential trace mineral known since ancient times for its use in tools and weapons. Its biological importance was recognized in the 1920s when anemia was discovered in copper-deficient animals fed milk diets.
Copper serves as a cofactor for numerous enzymes (cuproenzymes) involved in critical biological processes including iron metabolism, energy production, connective tissue synthesis, and neurotransmitter synthesis.
The balance between copper and zinc is particularly important - high zinc intake can induce copper deficiency by competing for absorption. This is why zinc supplements often advise taking copper as well.
Copper deficiency causes anemia (refractory to iron supplementation), neutropenia, and neurologic abnormalities including peripheral neuropathy and myelopathy. These can mimic vitamin B12 deficiency.
While deficiency is harmful, excess copper is also toxic and can cause Wilson's disease (genetic disorder) or liver damage. The therapeutic window is relatively narrow.
Most people obtain adequate copper from diet. Risk factors for deficiency include high zinc supplementation, malabsorption conditions, and Menkes disease (genetic copper transport disorder).
Main Benefits
Required for iron metabolism; deficiency causes anemia that does not respond to iron supplementation.
Essential for connective tissue formation through lysyl oxidase enzyme; supports bone, skin, and blood vessel health.
Required for energy production via cytochrome c oxidase, essential for mitochondrial function.
Supports immune function through copper-zinc superoxide dismutase and other cuproenzymes.
Required for neurotransmitter synthesis including dopamine and norepinephrine via dopamine beta-hydroxylase.
Mechanism of Action
Copper functions as an essential cofactor for numerous cuproenzymes:
Iron Metabolism: Ceruloplasmin (ferroxidase I) is a copper-containing enzyme that oxidizes ferrous iron (Fe2+) to ferric iron (Fe3+), enabling iron binding to transferrin for transport. Without copper, iron accumulates in tissues but cannot be utilized.
Connective Tissue Synthesis: Lysyl oxidase cross-links collagen and elastin, essential for blood vessel integrity, bone strength, and skin elasticity. Copper deficiency causes vascular fragility and bone abnormalities.
Energy Production: Cytochrome c oxidase (Complex IV) is the terminal enzyme of the electron transport chain, essential for ATP production. Copper deficiency impairs cellular energy production.
Antioxidant Defense: Copper-zinc superoxide dismutase (Cu/Zn SOD) converts superoxide radicals to hydrogen peroxide, protecting cells from oxidative damage. Extracellular SOD also requires copper.
Neurotransmitter Synthesis: Dopamine beta-hydroxylase requires copper to convert dopamine to norepinephrine. Tyrosinase (melanin synthesis) also requires copper.
Peptide Processing: Peptidylglycine alpha-amidating monooxygenase (PAM) requires copper for processing neuropeptides including oxytocin and vasopressin.
Natural Sources
Copper is found in a variety of foods. Organ meats, shellfish, nuts, and seeds are particularly rich sources.
Examples:
Beef liver
Oysters and shellfish
Cashews and other nuts
Sunflower seeds
Lentils and beans
Dark chocolate
Asparagus
Mushrooms
Whole grains
Widely available in foods; deficiency rare in well-nourished populations; vegetarians need attention to sources.
Deficiency Symptoms
Copper deficiency causes anemia, neutropenia, and neurologic abnormalities. Can mimic vitamin B12 deficiency.
Common Symptoms:
Anemia (microcytic, hypochromic, refractory to iron)
Neutropenia (low white blood cells)
Peripheral neuropathy
Myelopathy (spinal cord damage)
Osteoporosis and bone abnormalities
Skin and hair depigmentation
Vascular fragility
Rare in general population; risk with high zinc supplementation, malabsorption, Menkes disease; most people get adequate amounts.
Causes severe anemia and neurologic damage; can be disabling; neurologic damage may not fully reverse with treatment.
Recommended Daily Intake
RDA: adults 900 mcg/day. Upper Limit (UL) is 10,000 mcg (10 mg)/day due to toxicity risk.
Reference Values:
| Adult men | 900 mcg/day |
| Adult women | 900 mcg/day |
| Pregnancy | 1,000 mcg/day |
| Lactation | 1,300 mcg/day |
| Upper Limit (UL) | 10,000 mcg/day |
Sources for RDI/AI:
High zinc intake (>50 mg/day) can induce copper deficiency. Take copper with zinc supplements (typical ratio 10-15:1 zinc:copper).
Effectiveness for Specific Focuses
Required for superoxide dismutase and neutrophil function; deficiency causes neutropenia; supports immune function.
Essential for cytochrome c oxidase and ATP production; deficiency impairs energy metabolism.
Required for connective tissue synthesis and melanin production; deficiency affects skin and hair pigmentation.
Essential for blood vessel integrity via lysyl oxidase; deficiency causes vascular fragility; supports connective tissue.
Safety Information
Potential Side Effects
Nausea and vomiting
Abdominal pain
Diarrhea
Metallic taste
Liver damage (high doses)
Contraindications
Wilson's disease (genetic copper accumulation disorder)
Biliary cirrhosis
Copper toxicity
Overdose Information
UL 10 mg/day; excess causes GI symptoms and liver damage; narrow therapeutic window compared to some minerals.
Nausea, vomiting, abdominal pain, diarrhea, metallic taste, liver damage with chronic excess.
Documented Overdose Symptoms:
Gastrointestinal distress
Metallic taste
Liver damage
Toxicity Thresholds: UL: 10,000 mcg (10 mg)/day based on risk of liver damage.
Both deficiency and excess cause serious problems. Wilson's disease patients must avoid copper. High zinc intake can cause copper deficiency.
Interactions
Drug Interactions:
Zinc supplements (high doses compete for absorption)
Iron supplements (compete for absorption)
Penicillamine (chelation therapy for Wilson's disease)
High zinc strongly induces copper deficiency; must supplement copper with high-dose zinc; significant interaction.
Other Supplement Interactions:
Zinc - competitive inhibition of absorption; must balance intake
Iron - competes for absorption
Vitamin C - may enhance absorption
Critical to balance with zinc supplementation; high zinc without copper causes deficiency.
Do not take high-dose copper supplements unless zinc intake is also monitored. Wilson's disease patients must avoid copper supplements entirely. Take zinc and copper at different times if supplementing both.
Forms and Bioavailability
Copper supplements typically provide copper gluconate, sulfate, or oxide. Bioavailability varies by form.
Copper Gluconate
Organic salt form; good bioavailability; commonly used in supplements.
Well-absorbed; good bioavailability; standard form in quality supplements.
Preferred form for supplementation. Well-tolerated and effective.
Copper Sulfate
Inorganic salt form; well-absorbed but may cause more GI upset.
Good absorption; may be more irritating to stomach than gluconate.
Common form but gluconate generally preferred for tolerability.
Cupric Oxide
Inorganic form; poorer bioavailability than salts.
Poorer absorption; less bioavailable than gluconate or sulfate.
Sometimes used in multivitamins due to stability but not ideal for supplementation.
Warnings & Suitability
Did You Know...?
The Statue of Liberty's green color comes from copper oxidation - the statue contains about 179,000 pounds of copper.
Human blood is red from iron in hemoglobin, but some mollusks have blue blood because they use copper-based hemocyanin instead of iron.
Ceruloplasmin, the copper-containing protein that transports iron, is named from "caeruleus" (blue) because copper gives it a blue color.
The recommended ratio of zinc to copper in supplements is typically 10:1 to 15:1 to prevent copper deficiency from zinc supplementation.
General Scientific Sources
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Content Verification
Last Medical Review: 2/13/2026
Reviewed by: Editorial Team