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Copper : Side Effects and Interactions
(Page 4 of 4) Side Effects and Warnings Toxicity: Copper toxicity is rare in the general population. Excess copper consumption may lead to liver, kidney, or neurologic damage. Up to 3000-5000mcg daily appears to be safe for consumption in children older than three years, and up to 10,000mcg in adults. 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 (which can occur with ingestion of doses in the range of 1 gram of copper sulfate). Other medical problems associated with copper toxicity in studies or anecdotally include anxiety, depression, fatigue, 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. Exposure to copper (Cu) in drinking water results in gastrointestinal symptoms, which are modulated by Cu concentration, time, and sex. In the U.S., the health-based guideline for a maximum water copper concentration of 1.3mg/liter has been enforced by the Environmental Protection Agency. Liver damage may result from long-term exposure to lower doses of copper. The U.S. Food and Nutrition Board (FNB) has set the tolerable upper level of intake (ul) for copper at 10mg/day from food and supplements. | |||||||||||||||||
Genetic disordersaffecting 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 devicesare 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. Pregnancy and Breastfeeding Pregnancy: The U.S. Recommended Daily Allowance (RDA) is 1000mcg for pregnant women. It is unclear if copper supplementation is necessary during pregnancy to maintain adequate 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. Lactation: The U.S. Recommended Daily Allowance (RDA) is 1300mcg for nursing women. Copper is potentially unsafe when used orally in higher doses. Copper is present in breast milk. Interactions Most herbs and supplements have not been thoroughly tested for interactions with other herbs, supplements, drugs, or foods. The interactions listed below are based on reports in scientific publications, laboratory experiments, or traditional use. 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. Interactions with Drugs Antacids: Antacids may interfere with copper absorption. Ethambutol (Myambutol®): Ethambutol, 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. Oral contraceptives/estrogen replacement:Serum copper levels may be increased in women taking oral contraceptives, although the clinical significance of this observation is not clear. Penicillamine (Cuprimine®, Depen®): Penicillamine 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®): Trientine is a copper-chelating agent used in the management of Wilson's disease. Zidovudine (Retrovir®, AZT): Levels of copper may be reduced, although there is some evidence that this may be beneficial in HIV/AIDS patients, and therefore copper supplements may not be advisable. Interactions with Herbs and Dietary Supplements Boron: Boron has been reported to increase plasma copper levels, erythrocyte superoxide dismutase, and serum enzymatic ceruloplasmin in humans when co-administered with copper. Cadmium: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:Calcium may alter the metabolism of copper. Dehydroepiandrosterone (DHEA): Animal studies suggest that low copper levels may result in decreased serum DHEA levels, although it is unclear if increased copper intake increases DHEA levels. Fructose: High fructose diets have been shown to cause copper deficiency in rats, but not in pigs or humans. Iron: 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. Manganese: Manganese may reduce copper absorption and alter copper enzyme activities, particularly copper-zinc superoxide dismutase. Molybdenum: Molybdenum may reduce copper levels, possibly through an interaction in the intestines. Rapeseed oilmeal: Co-administration with copper may result in altered metabolism. Selenium: Animal studies suggest that copper may reduce serum selenium levels. Taurine: 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. Vitamin C: Vitamin C supplements appear to cause copper deficiency in laboratory animals, but effects in humans are not clear. Zinc: 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. Ahistologic study of the liver revealed that copper concentration in patients with Wilson's disease was reduced by treatment, suggesting that oral zinc was able not only to prevent further accumulation of copper but also to promote, at least in part, the depletion of its stores.
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