Sources:
Legumes, mushrooms, chocolate, nuts and seeds, shellfish and liver are high in copper all greater than 2.4 µg per gram.
Food, water and air (via combustion and fossil fuels and agriculture) are sources of copper.
Copper pipes and fixtures in household plumbing may allow copper to leak into water.
Absorption factors:
Copper absorption occurs in the upper small intestine and compared to other elements, has a relatively high absorption rate at 55 to 75%. Copper levels in the body are homeostatically maintained by copper absorption from the intestine and copper released by the liver into bile to provide protection from copper deficiency and toxicity.
Most copper is excreted in bile/feces, and a small amount excreted in urine. Urinary copper declines only when dietary copper intake is very low. A 24 hour urinary copper provides a screening for suspected cases off toxicity or copper deficiency anemia. Correlation was seen in Wilson's disease using first morning or 24 hour urine. Grains contain phytates that may inhibit copper absorption in the intestines.
Intestinal iron absorption is a copper-dependent process. Iron, vitamin C, zinc, lead poisoning, hemachromatosis, excessive soft drink ingestion, bariatric surgery and zinc containing denture creams adversely affect copper bioavailability.
Cadmium exposure may result in increased urine excretion of copper due to possible renal tubular damage.
Increased molybdenum intake may elevate urinary copper excretion. Serum and 24 – hour urine copper excretion were similar in long-term copper IUD users as in a control group that did not have an IUD.
Biochemical actions:
Copper is a cofactor for more than 20 enzymes, particularly those involved in cellular, respiration and energy, metabolism, neurotransmitter and hormone biosynthesis, iron, metabolism, gene, transcription, melanin formation, and antioxidant defense. Copper is also involved in blood, coagulation and blood pressure control, myelination and connective tissue cross-linking.
Ceruloplasmin carries the predominance of copper in the blood, so alterations in blood copper, likely reflect the amount of circulating ceruloplasmin. Plasma copper and ceruloplasmin can increase during an acute phase response to infection and inflammation, pregnancy, and other hormonal perturbations, some carcinogenic phenotypes, and smoking. Plasma copper may be elevated in the states, while tissue copper could be low. Low plasma, copper indicates physiological impairment.
Symptoms of imbalance:
Copper deficiency is associated with osteoporosis, hypochromic, microcytic, anemia, impaired cholesterol and glucose metabolism, cardiovascular disease, connective tissue abnormalities, CNS disorders, and impaired immune function. Reductions in plasma copper and ceruloplasmin activity are noted in severely copper deficient individuals.
Copper toxicity is rare due to adequate homeostatic control, however, an upper tolerable intake level of 10 mg per day has been established. Wilson's disease is an inherited disease that results from decreased biliary copper excretion due to biliary atresia or biliary cirrhosis. Signs and symptoms include jaundice and abnormal LFTs, ascites, Kayser-Fleischer rings and neurological and psychiatric symptoms.
Copper dyshomeostasis involving either deficiency or excess, has been implicated in Alzheimer's disease and cognitive decline.
Copper
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