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DIET & DEFICIENCY

Food sources of copper

Richest sources of Cu contain 0.3-2 mg/100 g.

  • Wholegrain and wholegrain products
  • Nuts
  • Seeds (including cocoa beans), raisins
  • Legumes
  • Liver and other organ meats
  • Shellfish
https://studmed.uio.no/elaring/lcms16/ernaeringslaere/minerals-traceelements/illustrations/foods-high-in-copper.jpg

Photo Foods high in copper

Vegetarians tend to have a higher intake of copper than those who take a mixed diet.

Copper in drinking water:

Normally there is a low level (2-20 mg/litre of water). High levels can lead to diarrhoea. Copper pipes release more copper the more acid the water is. Copper cooking vessels can dissolve if used with acidic liquids (e.g. gløgg).

Absorption

About 30% of copper in the diet is absorbed.
Absorption is not controlled; a steady state is maintained by regulated excretion in bile.

Mo, Zn and Cd at high levels reduce uptake. High zinc induces intestinal metallothionein which binds Cu and prevents absorption.

Cu and Fe interact: excess copper can produce anaemia, while excess Fe can reduce Cu uptake.

Recommendations for copper intake

Calculated intake in Norway:

  • 1.2 mg/10 MJ/day

Recommended intake:

  • 1.2 mg/day

WHO estimated minimum requirements:

  • Women 0.6 mg/day,
  • Men 0.7 mg/day

Limits:

  • 10 mg/day (women),
  • 12 mg/day (men).

Cu deficiency is rare; may occur in infants recovering from malnutrition, in premature babies fed milk formula diets, and in patients undergoing total parenteral nutrition (so trace elements now added).

Symptoms of deficiency and toxicity

Ceruloplasmin concentration is the best marker of copper status.

Deficiency:

  • Anaemia
  • Changes in bone (osteoporosis)
  • Increase in serum cholesterol

Toxicity:

  • Vomiting
  • Diarrhoea

Genetic conditions

Wilson’s disease (toxicity)

Rare autosomal recessive copper storage disease. Defective catabolism and excretion of ceruloplasmin Cu in bile. Copper accumulates in liver and brain. Treated with chelators.

Menkes’ disease (deficiency)

Fatal X-linked disorder: mental retardation, poor pigmentation of skin and hair, hair ’kinky’. Low levels of available Cu, so synthesis of cuproenzymes is impaired, while Cu accumulates in certain tissues.