Copper is an essential trace mineral.
See Table 1 for Dietary Reference Values for copper.
In the UK, the average adult diet provides: for men, 1.82 mg daily; for women, 1.31 mg.
Copper functions as an essential component of several enzymes (e.g. superoxide dismutase) and other proteins. It plays a role in bone formation and mineralisation, and in the integrity of the connective tissue of the cardiovascular system. Copper promotes iron absorption and is required for the synthesis of haemoglobin. It is involved in melanin pigment formation, cholesterol metabolism and glucose metabolism. In the central nervous system (CNS), it is required for the formation of myelin and is important for normal neurotransmission. Copper has pro-oxidant effects in vitro but antioxidant effects in vivo; there is accumulating evidence that adequate copper is required to maintain anti-oxidant effects within the body.1
Table 1 Dietary Reference Values for copper (mg/day)
|EU RDA = none|
1≤18 years, 1.3 mg.
2≤18 years, 8.0 mg.
Note: No EAR, LRNI or FAO/WHO RNIs have been derived for copper.
EVM = Safe upper level from supplements alone.
TUL = Tolerable Upper Intake Level from diet and supplements.
See Table 2 for dietary sources of copper.
Table 2 Dietary sources of copper
|1 bowl All-Bran (45 g)||0.2|
|1 bowl Bran Flakes (45 g)||0.1|
|1 bowl muesli (95 g)||0.3|
|2 pieces Shredded Wheat||0.2|
|Bread, brown, 2 slices||0.1|
|white, 2 slices||0.1|
|wholemeal, 2 slices||0.2|
|Pasta, brown, boiled (150 g)||0.3|
|white, boiled (150 g)||0.1|
|Rice, brown, boiled (165 g)||0.5|
|white, boiled (165 g)||0.2|
|Meat, average, cooked (100 g)||0.2|
|Liver, lambs, cooked (90 g)||9.0|
|calf, cooked (90 g)||11.0|
|Kidney, lambs, cooked (75 g)||0.4|
|Chick peas, lentils, or red kidney||0.2|
|beans, cooked (105 g)|
|Potatoes, boiled (150 g)||0.1|
|Mushrooms, cooked (100 g)||0.4|
|Green vegetables (100 g)||0.02|
|2 handfuls raisins||0.1|
|8 dried apricots||0.2|
|10 Brazil nuts||0.4|
|Milk chocolate (100 g)||0.3|
|Plain chocolate (100 g)||0.7|
Excellent sources (bold); good sources (italic).
Copper is absorbed mainly in the small intestine, with a small amount absorbed in the stomach; absorption is probably by a saturable carrier-mediated mechanism at low levels of intake, and by passive diffusion at high levels of intake.
Copper is rapidly taken up by the liver and incorporated into caeruloplasmin. It is stored primarily in the liver. Copper is transported bound to caeruloplasmin.
Elimination is mainly via bile into the faeces; small amounts are excreted in the urine, sweat and via epidermal shedding.
Absorption may be reduced by phytate (present in bran and high-fibre foods) and non-starch polysaccharides (dietary fibre), but recommended intakes of fibre-containing foods are unlikely to compromise copper status.
Deficiency of copper is rare, but may lead to hypochromic and microcytic anaemias, leuco-penia, neutropenia, impaired immunity and bone demineralisation. Deficiency may also be caused by Menke’s syndrome (an X-linked genetic disorder in which copper absorption is defective); this disease is characterised by a reduced level of copper in the blood, liver and hair, progressive mental deterioration, defective keratinisation of the hair and hypothermia.
Marginal deficiency may result in elevated cholesterol levels, impaired glucose tolerance, defects in pigmentation and structure of the hair, and demyelination and degeneration of the nervous system. In infants and children, copper deficiency can lead to skeletal fragility and increased susceptibility to infections, especially those of the respiratory tract.
Copper deficiency has been linked to many of the processes, including atherosclerosis and thrombosis, associated with ischaemic heart disease. Whether this relationship is important in humans remains unanswered. More information is required concerning possible mild copper deficiency in human populations.
Copper has been claimed to be protective against hypercholesterolaemia. In various animal species, it has been demonstrated that feed-ing a copper-deficient diet results in increased serum cholesterol levels,1 but studies in humans have shown inconsistent results.1–3 A recent study in 16 young women (mean age 24 years) found that copper supplementation 3 or 6 mg daily improved copper status and that the concentration of fibrinolytic factor plasminogen activator inhibitor type 1 was significantly reduced by about 30% after supplementation with copper 6 mg daily.4
Claims for the value of copper supplements in rheumatoid arthritis and psoriasis have not been proved.
Copper should not be used in Wilson’s disease (the disorder may be exacerbated); or hepatic and biliary disease.
Pregnancy and breast-feeding
No problems have been reported with normal intakes.
With excessive doses (unlikely from supplements): epigastric pain, anorexia, nausea, vomiting and diarrhoea; hepatic toxicity and jaundice; hypotension; haematuria (blood in urine, pain on urination, lower back pain); metallic taste; convulsions and coma.
Copper toxicity may also occur in patients with Wilson’s disease (an inherited disorder in which patients exhibit a deficiency of plasma caeruloplasmin and an excess of copper in the liver and bloodstream). There is a theoretical possibility of copper toxicity in women who use copper-containing intrauterine contraceptive devices (further studies required).
Penicillamine: reduces absorption of copper and vice versa; give 2 h apart.
Trientine: reduces absorption of copper and vice versa; give 2 h apart.
Iron: large doses of iron may reduce copper status and vice versa; give 2 h apart.
Vitamin C: large doses of vitamin C (> 1 g daily) may reduce copper status.
Zinc: large doses of zinc may reduce absorption of copper and vice versa; give 2 h apart.
Copper supplements are available in the form of tablets and capsules, but mostly they are found in multivitamin and mineral supplements. The copper content of various commonly used salts is: copper amino acid chelate (20 mg/g); copper gluconate (140 mg/g); copper sulphate (254 mg/g).
There is no established use or dose for copper as an isolated supplement.
Upper safety levels
The UK Expert Group on Vitamins and Minerals (EVM) has identified a safe total intake of copper for adults from supplements alone of 5 mg daily.
The US Tolerable Upper Intake Level (UL) for copper, the highest total amount from diet and supplements unlikely to pose no risk for most people, is 10 mg daily for adults, 8 mg daily for youngsters aged 14–18, 5 mg daily for youngsters aged 9–13, 3 mg daily for children aged 4–8, and 1 mg daily for children aged 1–3.
There are no proven benefits in taking copper supplements unless there is a proven deficiency, which should be treated under medical supervision.
Klevay LM, Inman L, Johnson LK, et al. Increased cholesterol in plasma in a young man during experimental copper depletion. Metabolism 1984; 33: 1112–1118.
Medeiros D, Pellum L, Brown B. Serum lipids and glucose as associated with haemoglobin levels and copper and zinc intake in young adults. Life Sci 1983; 32: 1897–1904.
Shapcott D, Vobecky JS, Vobecky J, Demers PP. Plasma cholesterol and the plasma copper/zinc ratio in young children. Sci Total Environ 1985; 42: 197–200.
Bugel S, Harper A, Rock E, et al. Effect of copper supplementation on indices of copper status and certain CVD risk markers in young healthy women. Br J Nutr 2005; 94: 231–236.