a minerals and electrolyte - treats Age-related macular degeneration, Menkes' kinky-hair disease, Alzheimer's disease prevention, Cardiovascular disease prevention / atherosclerosis, Dental conditions, Metabolic disorders, Immune system function, Marasmus, Neural-tube defect prevention, Osteoporosis / osteopenia, Copper deficiency, Cancer, Schizophrenia, Arthritis, Sideroblastic anemia, Plaque prevention, Systemic lupus erythematosus, and Childhood growth promotion
Interactions with Drugs
Antacids may interfere with copper absorption.
Several human studies indicate that taking certain antipsychotics (haloperidol and risperidone), 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.
Interactions with Herbs and Dietary Supplements
Several herbs and supplements, such as boron, vitamin C, selenium, molybdenum, 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.
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.