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Copper

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Related terms
Background
Evidencetable
Tradition
Dosing
Safety
Interactions
Attribution
Bibliography

Related Terms
  • Copper 7, copper acetate, copper amino acid chelates, copper citrate, copper gluconate, copper glycinate, copper intrauterine device, copper sebecate, copper sulfate, copper T, Cu, Cu IUD, cuivre, cupric oxide, cupric sulfate, cuprum, CuSO4, elemental copper, inorganic copper, organic copper.

Background
  • Copper is a mineral that occurs naturally in many foods, including vegetables, legumes, nuts, grains, and fruits, as well as shellfish, avocado, and beef (organs such as liver). Because copper is found in the earth's crust, most of the world's surface water and ground water used for drinking purposes contains small amounts of copper.
  • Copper is involved in numerous biochemical reactions in human cells. Copper is a component of multiple enzymes, is involved with the regulation of gene expression, mitochondrial function/cellular metabolism, connective tissue formation, as well as the absorption, storage, and metabolism of iron. Copper levels are tightly regulated in the body.
  • Copper toxicity is rare in the general population. Wilson's disease is a genetic disorder in which the body cannot rid itself of copper, resulting in deposition in organs and serious consequences such as liver failure and neurologic damage. Obstruction of bile flow, contamination of dialysis solution (in patients receiving hemodialysis for kidney failure), Indian childhood cirrhosis, and idiopathic copper toxicosis are other rare causes of potentially dangerous excess copper levels. Such individuals should be followed closely by a physician and nutritionist.
  • Copper deficiency can occur in infants fed only cow-milk formulas (which are relatively low in copper content), premature/low-birth weight infants, infants with prolonged diarrhea or malnutrition, individuals with malabsorption syndromes (including celiac disease, sprue, or short bowel syndrome), cystic fibrosis, in the elderly, or those receiving intravenous total parenteral nutrition (TPN) or other restrictive diets.
  • Medicinal use of copper compounds dates to Hippocrates in 400 B.C. Bacterial growth is inhibited on copper's surface, and hospitals historically installed copper-alloy doorknobs and push-panels as a measure to prevent transmission of infectious disease.

Evidence Table

These uses have been tested in humans or animals. Safety and effectiveness have not always been proven. Some of these conditions are potentially serious, and should be evaluated by a qualified healthcare provider. GRADE *


Copper deficiency may occur in infants fed only cow-milk formulas (which are relatively low in copper content), premature/low-birth weight infants, infants with prolonged diarrhea or malnutrition, individuals with malabsorption syndromes (including celiac disease, sprue, or short bowel syndrome), individuals with cystic fibrosis, in the elderly, or in those receiving intravenous total parenteral nutrition (TPN) or other restrictive diets. Such individuals may require supplementation with copper (and other trace elements).

A


There is not enough scientific evidence available to determine if copper plays a role in this disorder.

C


Conflicting study results report that copper intake may either increase or decrease the risk of developing Alzheimer's disease. Additional research is needed before a recommendation can be made.

C


The use of copper bracelets in the treatment of arthritis has a long history of traditional use, with many anecdotal reports of effectiveness. There are research reports suggesting that copper salicylate may reduce arthritis symptoms more effectively than either copper or aspirin alone. Further study is needed before a firm recommendation can be made.

C


Preliminary research reports that lowering copper levels theoretically may arrest the progression of cancer by inhibiting blood vessel growth (angiogenesis). Copper intake has not been identified as a risk factor for the development or progression of cancer.

C


The effects of copper intake or blood copper levels on cholesterol, atherosclerosis (cholesterol plaques in arteries), or coronary artery disease remain unclear. Studies in humans are mixed, and further research is needed in this area.

C


Severe copper deficiency may retard growth. Adequate intake of micronutrients including copper and other vitamins may promote growth as measured by length gains.

C


Laboratory studies have shown that copper may help protect tooth enamel (the outer layer of the teeth). However, early human research suggests that copper may not be effective.

C


Copper is involved in the development of immune cells and immune function in the body. Severe copper deficiency appears to have adverse effects on immune function, although the exact mechanism is not clear.

C


Copper deficiency may occur with marasmus, and supplementation with copper may play a role in the nutritional treatment of infants with this condition. Infants with marasmus should be managed by a qualified healthcare professional.

C


Menkes' kinky-hair disease is a rare disorder of copper transport/absorption. Copper supplementation may be helpful in this disease, although further research is necessary before a clear recommendation can be made.

C


Trimethylaminuria (TMAU) is a metabolic disorder characterized by the inability to oxidize and convert dietary-derived trimethylamine (TMA) to trimethylamine N-oxide (TMAO). Preliminary evidence suggests that the use of copper chlorophyllin results in a reduced urinary-free TMA concentration and normalization of TMAO. Further research is required in this field before a strong recommendationscan be made.

C


Osteopenia and other abnormalities of bone development related to copper deficiency may occur in copper-deficient low-birth weight infants and young children. Supplementation with copper may be helpful in the treatment and/or prevention of osteoporosis, although early human evidence is conflicting. The effects of copper deficiency or copper supplementation on bone metabolism and age-related osteoporosis require further research before clear conclusions can be drawn.

C


Some studies of schizophrenic patients report high blood copper levels with low urinary copper (suggesting that copper is being retained), and low blood zinc levels. In some of these cases, zinc was observed to be helpful as an anti-anxiety agent. The role of copper supplementation is not clear.

C


Copper deficiency is one of the causes of sideroblastic anemia that should be considered when evaluating this condition, particularly when the anemia is unresponsive to iron therapy alone. This anemia appears to be caused by defective iron mobilization due to decreased ceruloplasmin activity.

C


Copper has been used to reduce wrinkles and skin appearance following laser skin resurfacing. Currently, there is not enough scientific evidence to make recommendations for or against this use.

C


A preliminary study suggests that copper offers no benefit to individuals with SLE. Further research is required before recommendations can be made.

C


The risk of neural-tube defects is decreased in women who take folic acid and multivitamins during the periconception period. Supplementation with trace-elements alone, such as copper, does not appear to prevent these defects.

D
* Key to grades

A: Strong scientific evidence for this use
B: Good scientific evidence for this use
C: Unclear scientific evidence for this use
D: Fair scientific evidence for this use (it may not work)
F: Strong scientific evidence against this use (it likley does not work)


Tradition / Theory

The below uses are based on tradition, scientific theories, or limited research. They often have not been thoroughly tested in humans, and safety and effectiveness have not always been proven. Some of these conditions are potentially serious, and should be evaluated by a qualified healthcare provider. There may be other proposed uses that are not listed below.

  • Aflatoxin toxicity, allergies, anemia, antibacterial, antioxidant, athletic performance, bone healing, bronchitis, cataracts (prevention/progression), cognition, cystic fibrosis, decreasing cadmium absorption, depression, ethambutol-induced optic neuropathy, fatigue, fetal development, high blood pressure, high cholesterol, Hodgkin's disease biomarker, hyperactivity, infertility, learning disabilities, muscle ache, muscle cramps, optic nerve damage (ethambutol-induced), oral deodorant, phenylketonuria, pneumonia, premenstrual syndrome, psoriasis, senility, skin problems (stretch marks), stomach ulcer, toxicity (pyrrolizidine alkaloid), vitiligo, weight gain, wound healing.

Dosing

Adults (18 years and older)

  • The daily U.S. Recommended Daily Allowance (RDA) is 900 micrograms for adults; 1,000 micrograms for pregnant women; 1,300 micrograms for nursing women; and 890 micrograms for adolescents 14-18 years old. Surveys suggest that most Americans consume less than the RDA for copper each day. Up to 10,000 micrograms daily appears to be safe for consumption in adults. Vegan diets appear to provide adequate amounts of copper.
  • In a number of clinical trials copper doses of 2-10 milligrams by mouth were safely used in patients. For plaque inhibition, a 1.1mM copper rinse has been used for four days. The appropriate application of ointment preparations containing copper in concentrations up to 20% has also been studied with no apparent toxic effects.

Children (younger than 18 years)

  • The daily U.S. Recommended Daily Allowance (RDA) for children is 890 micrograms for adolescents 14-18 years old; 700 micrograms for children 9-13 years old; 440 micrograms for children 4-8 years old; 340 micrograms for children 1-3 years old; 220 micrograms for infants 7-12 months old; and 200 micrograms for infants 0-6 months old. Surveys suggest that most Americans consume less than the RDA for copper each day. Up to 3,000-5,000 micrograms daily appears to be safe for consumption in children.
  • Copper deficiency may occur in infants fed only cow-milk formulas (which are relatively low in copper content) or synthetic low lactose diets, premature/low-birth weight infants, infants with prolonged diarrhea or malnutrition, malabsorption syndromes (including celiac disease, sprue, or short bowel syndrome), cystic fibrosis, or during intravenous total parenteral nutrition (TPN) or other restrictive diets. Such situations may merit copper supplementation (and other trace elements), which should be under the supervision of a healthcare professional. In the United States, copper is not available in infant supplements.
  • Management of marasmus should be under the supervision of a healthcare professional, although 20-80 micrograms per kilogram per day of copper sulfate supplementation by mouth has been reported as safe.

Safety

The U.S. Food and Drug Administration does not strictly regulate herbs and supplements. There is no guarantee of strength, purity or safety of products, and effects may vary. You should always read product labels. If you have a medical condition, or are taking other drugs, herbs, or supplements, you should speak with a qualified healthcare provider before starting a new therapy. Consult a healthcare provider immediately if you experience side effects.

Allergies

  • An allergic skin reaction, called contact dermatitis, has occurred after exposure to copper sulfate.

Side Effects and Warnings

  • Copper toxicity is rare in the general population. Excess copper consumption may lead to liver, kidney, or neurologic damage. Excess dosing may lead to toxic symptoms including weakness, abdominal pain, nausea, vomiting, and diarrhea, with more serious signs of acute toxicity including liver damage, kidney failure, pleural damage, coma, and death. Other medical problems associated with copper toxicity in studies or anecdotally include anxiety, depression, dizziness, fatigue, headache, learning disabilities, memory lapses, diminished concentration, insomnia, seizure, delirium, stuttering, hyperactivity, arthralgias, myalgias, hypertension, gingivitis, dermatitis, discoloration of skin/hair, preeclampsia, postpartum psychosis, weight gain, or transaminitis. Acute copper poisoning has occurred through the contamination of beverages by storage in copper containing containers as well as from contaminated water supplies. In the U.S., the health-based guideline for a maximum water copper concentration of 1.3 milligrams per liter has been enforced by the Environmental Protection Agency.
  • Genetic disorders affecting copper metabolism such as Wilson's disease, Indian childhood cirrhosis, or idiopathic copper toxicosis place individuals at risk of adverse effects of chronic copper toxicity at significantly lower intake levels. Trientine is a copper-chelating agent used in the management of Wilson's disease. Penicillamine has also been used to bind copper and enhance its elimination in Wilson's disease. Zinc in therapeutic dosages has been used to inhibit copper absorption in patients with Wilson's disease. Animal research suggests that supplementation with taurine may reduce toxic effects of copper when given in combination, although it is not clear if this is the case in humans.
  • Copper-T devices are a type of intrauterine devices (IUD) used for birth control which have been linked to the development of anemia and increased risk of pelvic infection in some users. Copper released from the IUDs may cause hormonal changes and alter the menstrual cycle in women. Other common side effects include pain/cramps, abnormal bleeding, and device expulsion. In some cases, pelvic inflammatory disease (PID) or anemia may develop.

Pregnancy and Breastfeeding

  • It is unclear if copper supplementation is necessary during pregnancy to maintain adequate copper levels. Copper is potentially unsafe when used orally in higher doses. Animal studies suggest that trace metal aberrations, including copper, may be related to disturbed fetal growth or teratogenicity, particularly in the setting of diabetic pregnancy.
  • Copper is potentially unsafe when used orally in higher doses than the RDA. Copper is present in breast milk.

Interactions

Interactions with Drugs

  • Antacids may interfere with copper absorption. Copper may alter cholesterol levels and interact with agents taken to reduce cholesterol.
  • Several human studies indicate that taking certain antipsychotics (haloperidol and risperidone), anticonvulsants (valproic acid), diuretics (water pills), nifedipine or birth control pills may alter copper levels in the body, although clinical significance is unknown. Copper levels should be monitored by a qualified healthcare professional.
  • Ethambutol (Myambutol®) and its metabolite chelate copper resulting in depleted levels. Copper chelation in the retina may contribute to ethambutol-induced optic neuropathy. Whether supplemental copper can prevent this adverse effect is not clear.
  • Penicillamine (Cuprimine®, Depen®) is used to bind copper and enhance its elimination in Wilson's disease. Because it dramatically increases the urinary excretion of copper, individuals taking penicillamine for reasons other than copper overload may have an increased requirement for copper.
  • Trientine (Syprine®, Trien®) is a copper-chelating agent used in the management of Wilson's disease.
  • Levels of copper may be reduced after zidovudine (Retrovir®, AZT), although there is some evidence that this may be beneficial in HIV/AIDS patients, and therefore copper supplements may not be advisable.
  • Although not well studied in humans, copper may also interact with antibiotics, blood thinning agents, anticancer agents, liver- or kidney-damaging agents or agents that affect the immune system, Caution is advised.

Interactions with Herbs and Dietary Supplements

  • Several herbs and supplements, such as boron, vitamin C, selenium, molybdenum, amino acids, and manganese, may alter (decrease or increase) copper levels in the body. Although copper may increase the concentration of cadmium in tissues based on animal research, cadmium supplementation does not appear to significantly alter copper levels. Calcium or rapeseed oil may alter the metabolism of copper. Magnesium may affect blood levels of copper or selenium.
  • Long-term, high-copper intake may cause decreases in plasma concentrations of folate.
  • Animal studies suggest that low copper levels may result in decreased serum dehydroepiandrosterone (DHEA) levels, although it is unclear if increased copper intake increases DHEA levels.
  • Adequate copper nutritional status appears to be necessary for normal iron metabolism, transport, and red blood cell formation. High iron intake may interfere with copper absorption. Copper deficiency is associated with retention of iron in the liver.
  • Animal research suggests that supplementation with taurine may reduce toxic effects of copper when given in combination, although it is not clear if this is the case in humans.
  • High levels of supplemental zinc intake over extended periods of time may result in decreased copper absorption in the intestines or copper deficiency possibly due to increased synthesis of the intestinal cell protein metallothionein, which binds some metals. This may be the mechanism by which zinc induces sideroblastic anemia. However, some animal research suggests that high dietary zinc may not interfere with tissue or plasma concentrations of copper.
  • Antacids may interfere with copper absorption. Although not well studied in humans, copper may also interact with herbs and supplements with antibacterial, blood thinning, anticancer, liver- or kidney-damaging, diuretic, hormonal or immune-altering effects. Caution is advised. Copper levels should be monitored by a qualified healthcare professional.

Attribution
  • This information is based on a systematic review of scientific literature edited and peer-reviewed by contributors to the Natural Standard Research Collaboration (www.naturalstandard.com).

Bibliography
  1. Abdullah AZ, Strafford SM, Brookes SJ, et al. The effect of copper on demineralization of dental enamel. J Dent Res 2006 Nov;85(11):1011-5.
  2. Araya M, Olivares M, Pizarro F, et al. Community-based randomized double-blind study of gastrointestinal effects and copper exposure in drinking water. Environ Health Perspect 2004;112(10):1068-1073.
  3. Behera C, Rautji R, Dogra TD. An unusual suicide with parenteral copper sulphate poisoning: a case report. Med Sci Law 2007 Oct;47(4):357-8.
  4. Bonham M, O'Connor JM, McAnena LB, et al. Zinc supplementation has no effect on lipoprotein metabolism, hemostasis, and putative indices of copper status in healthy men. Biol Trace Elem Res 2003;93(1-3):75-86.
  5. Bremner I. Manifestations of copper excess. Am J Clin Nutr 1998;67(5 Suppl):1069S-1073S.
  6. Donoso A, Cruces P, Camacho J, et al. Acute respiratory distress syndrome resulting from inhalation of powdered copper. Clin Toxicol (Phila) 2007 Sep;45(6):714-6.
  7. el Kholy MS, Gas Allah MA, el Shimi S, et al. Zinc and copper status in children with bronchial asthma and atopic dermatitis. J Egypt Public Health Assoc 1990;65(5-6):657-668.
  8. Ferretti G, Bacchetti T, Menanno F, et al. Effect of genistein against copper-induced lipid peroxidation of human high density lipoproteins (HDL). Atherosclerosis 2004;172(1):55-61.
  9. Gunay N, Yildirim C, Karcioglu O, et al. A series of patients in the emergency department diagnosed with copper poisoning: recognition equals treatment. Tohoku J Exp Med 2006 Jul;209(3):243-8.
  10. Jones AA, DiSilvestro RA, Coleman M, et al. Copper supplementation of adult men: effects on blood copper enzyme activities and indicators of cardiovascular disease risk. Metabolism 1997;46(12):1380-1383.
  11. Kessler H, Bayer TA, Bach D, et al. Intake of copper has no effect on cognition in patients with mild Alzheimer's disease: a pilot phase 2 clinical trial. J Neural Transm 2008;115(8):1181-1187.
  12. Klevay LM. Dietary copper and risk of coronary heart disease. Am J Clin Nutr 2000;71(5):1213-1214.
  13. Mellacheruvu S, Vergara C. A 32-year-old patient with hemolytic anemia and fulminant hepatic failure. Conn Med 2006 May;70(5):293-5.
  14. Oon S, Yap CH, Ihle BU. Acute copper toxicity following copper glycinate injection. Intern Med J 2006 Nov;36(11):741-3.
  15. Patterson RA, Lamb DJ, Leake DS. Mechanisms by which cysteine can inhibit or promote the oxidation of low density lipoprotein by copper. Atherosclerosis 2003;169(1):87-94.

Copyright © 2011 Natural Standard (www.naturalstandard.com)


The information in this monograph is intended for informational purposes only, and is meant to help users better understand health concerns. Information is based on review of scientific research data, historical practice patterns, and clinical experience. This information should not be interpreted as specific medical advice. Users should consult with a qualified healthcare provider for specific questions regarding therapies, diagnosis and/or health conditions, prior to making therapeutic decisions.

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