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Copper is an essential trace element for human and animal life.

Copper is a cofactor of several important enzymes. It is required for the proper uptake and use of dietary iron in the body – and is therefore a critical factor in the prevention of anaemia. Date of preparation: December 2018.


Importance of copper for health

Copper is essential for human and animal life, though required in only trace amounts (1). Copper is a cofactor of several metalloenzymes that are oxidases for the reduction of molecular oxygen, e.g. the cytochrome c oxidase enzyme, the last enzyme in the electron transport chain (2). Copper is also critical for the use of dietary iron in the body, including the uptake of iron from the intestine, iron release from stores and the incorporation of iron into haemoglobin (2). Ferroxidases are cuproenzymes in the plasma, and function in ferrous iron oxidation that is needed to bind iron to transferrin (3).

Table 1: Roles of cuproenzymes and effects of copper deficiency
 Enzyme Function Effect of copper deficency
 Ceruloplasmin  Plasma multi-copper oxidase necessary for iron mobilisation  Iron-deficency anaemia
 Lysyl oxidase  Cross-links collagen and elastin  Weak-walled blood vessels
 Dopamine-β-hydroxylase  Catecholamine production  Neurological effects
 Cyochrome c oxidase  Electron transport chain  Decreased ATP synthesis
 Superoxide dismutase

 Superoxide radical scavenger 

Prevents lipid perodidation and membrane damage

 Tissue damage

Copper is a critical factor in the prevention of anaemia, and anaemia associated with hypochromic, microcytic erythrocytes is widely recognised (2). More recently, neuromuscular defects resembling pernicious anaemic have responded to copper supplementation rather than administration of vitamin B12 (2, 4).

Copper is required for numerous body processes (2):

  • Blood coagulation
  • Control of blood pressure
  • Cross-linking of connective tissue in bone, heart and arteries
  • Antioxidant defence
  • Energy transformation
  • Myelination of brain and spinal column
  • Reproduction
  • Hormone synthesis

Copper is absorbed mainly in the proximal part of the small intestine, followed by transport into the liver via the portal vein (1). The relative predictor of absorption is the copper content of the food consumed (2). Biliary excretion maintains plasma copper homeostasis, and urinary excretion is usually <0.1 mg/day over a wide range of dietary intakes (3). Homeostasis is influenced by interactions between other metals including zinc, iron, and molybdenum (3).

Important information

Foods high in copper include legumes, mushrooms, chocolate, nuts and seeds, and liver(2). Due to their relative abundance in the diet, bread, potatoes and tomatoes also make substantial copper contributions (2).

An inadequate copper intake has adverse effects on glucose and cholesterol metabolism, blood pressure control and heart function, immunity and bone mineralization (2). Low copper is associated with osteoporosis, also in infants and children (5, 6). It has been shown that copper administration can improve bone mineral density in post-menopausal women, though it is unknown whether the osteoporosis itself is due to copper deficiency (2).

Overt copper deficiency is rare in humans. Symptoms include normocytic, hypochromic anaemia, leucopoenia and neutropenia, and osteoporosis in children (3). The impact of diet may be particularly pronounced in neonates as digestive function and homeostatic regulation of biliary copper are immature (2).

Copper toxicity is relatively rare, since humans have evolved with precise homeostatic mechanisms for copper due to its reactivity (2). Copper exists almost always bound to proteins. People most at risk are those with a hereditary defect in copper homeostasis (Menkes’ disease), characterised by a reduced copper uptake and placental copper transport (3). Those with Wilson’s disease (see below) are also at higher risk of copper toxicity due to liver damage resulting from the disease (3).

Idiosyncratic copper toxicity is otherwise usually acute and has been associated with copper salts in supplements and drinking water (3); symptoms include gastrointestinal distress. Alternatively, exposure can be through metal fumes, bringing about an influenza-like syndrome (7).

is a rare autosomal-recessive disorder of a copper-transporting ATPase resulting in abnormal copper storage (5). Its global prevalence is estimated to be 1:30,000 (8). The defect results in a failure to excrete copper effectively in bile, and an impaired incorporation of copper into ceruloplasmin. Thus, copper is deposited in various tissues including the liver causing cirrhosis, the brain leading to neurological symptoms, the kidneys, and the eyes causing damage. Chelation therapy is very effective however liver cirrhosis and neurological damage are permanent.

Key info

Keywords: catalyst, serum copper, ceruloplasmin, cytochrome c oxidase, metalloenzymes, antioxidant, anaemia, vascular and skeletal problems, osteoporosis

Related nutrients/biomarkers:

  • iron
  • zinc
  • molybdenum
  • fructose
  • vitamin C

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