COPPER

Copper (Cu) is a trace element that is essential for most animals, including humans. The influence of copper upon human health is due to the fact it 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. Copper may be absorbed by both the stomach and small intestinal mucosa, with most absorbed by the small intestine. Copper is found in the blood bound to proteins.

Copper is utilized by most cells as a component of enzymes involved in energy production (cytochrome oxidase) and in the protection of cells from free radical damage (superoxide dismutase). Copper is also involved with an enzyme that strengthens connective tissue (lysyl oxidase) and in brain neurotransmitters (dopamine hydroxylase and peptidyl alpha amidating monoxygenase). One of the proteins, ceruloplasmin, transports copper as well as helps convert iron to a form that can be transported to other tissues. The average level of copper stored in the body is from 50 to 120 mg, with most of this in the liver. Excess dietary copper can also lead to high copper levels in the kidney. However, under normal situations, not much copper is excreted via the urine. Most copper is excreted via bile that is released into the gastrointestinal tract, with minimal copper reabsorbed by intestinal cells. The uptake of copper and elimination through the bile allows copper to be conserved and tightly regulated.

Deficiencies: Animals that are fed diets deficient in copper often exhibit anemia, cardiac abnormalities such as blood vessel and heart rupture, abnormal EKG's and have elevated levels of serum cholesterol, triglycerides and glucose. A lifetime of marginal diet copper in humans is thought to lead to heart disease. Copper deficiency has been observed in premature infants and infants suffering from malnutrition. Overt symptoms in adults are rare, but may occur with long term shortage or, possibly, in those who consume zinc supplements for a period of time.

Diet recommendations: The estimated safe and adequate intake for copper is 1.5 - 3.0 mg/day. Many survey studies show that Americans consume about 1.0 mg or less of copper per day. Copper is found in foods such as nuts [0.2 to 0.5 mg/28 g (1 Tbsp.)], shellfish (1.0 to 3.7 mg/serving), organ meats (3.8 mg/serving of beef liver) and legumes (0.2 mg/serving). Grains, grain products and chocolate have appreciable levels of copper. While these food items are good to excellent sources of copper, the absolute amount of copper absorbed may be influenced by other dietary components.

Copper absorption may be decreased by excess dietary iron or zinc. Conversely, too much copper may cause an iron deficiency. Vitamin C supplementation results in decreased copper status. In rats, large doses of vitamin C can lead to copper deficiency. Other dietary components have an influence upon copper status, but not necessarily absorption. Feeding rats either sucrose or fructose, as opposed to glucose or cornstarch, decreases copper status and exacerbates the signs of copper deficiency.

Toxicity: Cases of copper toxicity are rare but may occur. Excess copper consumption may lead to liver damage. Intake of supplements exceeding 3 mg copper/day for a protracted period of time may be cause for concern. Doses of 10 mg/day over several weeks may lead to toxic symptoms, such as weakness and nausea.

Genetic Conditions relating to copper: There are two well known genetic diseases affecting copper metabolism. Menkes' kinky-hair disease is a problem with copper transport or absorption. Wilson's disease is characterized by increased liver copper content, leading to severe hepatic damage, followed by increased brain copper levels and neurological problems. Menkes' disease results in pathology resembling copper-deficiency, as opposed to the pathology of Wilson's disease, which resembles copper-toxicity. The Menkes' gene codes for a P-type ATPase that has a mutation that prevents copper absorption in the intestine.

For further information:

Klevay, L. M. & Medeiros, D. M. (1996) Deliberations and evaluations of the approaches, endpoints and paradigms for dietary recommendations about copper. J. Nutr. 126: 2419S-2426S.

Medeiros, D. M. & Wildman, R. (1997) New findings on a unified perspective of copper restriction and cardiomyopathy. Proc. Soc. Exp. Biol. Med. 215: 299-313.

Lei, K. Y. & Carr, T. P., eds. (1990) Role of Copper in Lipid Metabolism. CRC Press, Boca Raton, FL.

Prepared By:

Denis M. Medeiros, Ph.D.
Professor, Dept of Human Nutrition
Ohio State University
1787 Neil Avenue 347 Campbell
Columbus, OH 43210-1295
Phone: 614-292-5575
FAX: 614-292-8880
Email: mailto:medeiros.2@osu.edu

Susan S. Percival, Ph.D.
Associate Professor
Food Science and Human Nutrition
University of Florida
Gainesville, FL 32611
Phone: 352-392-1991
FAX: 352-392-9467
Email: ssp@GNV.IFAS.UFL.EDU