Copper is part of enzymes, which are proteins that help biochemical reactions occur in every cell. Copper is involved in the absorption, storage and metabolism of iron. The symptoms of a copper deficiency are similar to iron deficiency anemia. The liver makes a special protein, ceruloplasm, to transport copper and help convert iron to a form that can be used by other tissues.
Copper is utilized by most cells as a component of enzymes involved in energy production, protection of cells from free radical damage, strengthening connective tissue, and brain neurotransmitter function. Excess zinc intake can result in a copper deficiency when intake of copper is insufficient.
Copper is required for over 30 metalloproteins involved in oxidation-reduction reactions; neurotransmitter, energy, myelin, and bone or connective tissue production; immune function; and hematopoeisis.
An extensive body of evidence exists for copper deficiency associated with cardiovascular disease: aortic fissures and rupture, arterial foam cells and smooth muscle migration, cardiac enlargement and rupture, coronary artery thrombosis, and myocardial infarction.Mild copper deficiency can also contribute to elevated cholesterol, impaired glucose tolerance, and erythropoietin (= a hormone produced primarily by the kidneys) and iron resistant normocytic (= normal-sized red blood cells, but a low number of them) anemias, as well as neutropenia, thrombocytopenia, peripheral neuropathy, defective elastin, and bone demineralization. A type of myeloneuropathy similar to that seen in vitamin B12 deficiency, but responding to copper supplementation, has also been reported.
Menke’s disease is a copper deficiency condition. Dietary deficiency of copper is seen as low levels of erythrocyte copper even in early stages of copper depletion.
Chronically elevated plasma copper may result in elevation of erythrocyte copper levels as well, although the two specimens represent different copper utilization. Approxiamately 80% of erythrocyte copper is associated with superoxide dismutase (SOD), while most plasma copper is bound to ceruloplasmin. RBC copper appears to be closely associated with hepatic copper utilization.
Chronic copper exposure via copper piping or copper cooking utensils can lead to poisoning. Environmental and occupational exposures and excess supplementation can also lead to high copper. Symptoms include nausea, vomiting, and diarrhea.
High levels of copper can result in depression, irritability, muscle and joint pain, tremor, learning disabilities, behavioral disorders, and hemolytic anemia. Long term exposure to elevated copper can result in hepatic cirrhosis. Biliary obstruction is sometimes seen with high copper due to difficulty excreting copper. Renal dysfunction may be associated with high copper levels.
High blood levels of copper have been seen in Wilson’s disease and in the elderly. Autistic children have been shown to have high serum copper-zinc ratio and low ceruloplasmin. Copper dysregulation is present in some neurodegenerative conditions such as amyotrophic lateral sclerosis (ALS), Parkinson’s disease, Down’s syndrome, and idiopathic seizure disorder.