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Copper (Cu) is an essential trace element for humans and animals. In the body, copper shifts between the cuprous (Cu1+) and cupric (Cu2+) forms, though the majority of the body's copper is in the Cu2+ form. The ability of copper to easily accept and donate electrons explains its important role in oxidation-reduction (redox) reactions and in scavenging free radicals (1). Although Hippocrates is said to have prescribed copper compounds to treat diseases as early as 400 B.C. (2), scientists are still uncovering new information regarding the functions of copper in the human body (3).
The copper-dependent enzyme, cytochrome c oxidase, plays a critical role in cellular energy production. By catalyzing the reduction of molecular oxygen (O2) to water (H2O), cytochrome c oxidase generates an electrical gradient used by the mitochondria to create the vital energy-storing molecule, ATP (5).
Connective tissue formation
Another cuproenzyme, lysyl oxidase, is required for the cross-linking of collagen and elastin, which are essential for the formation of strong and flexible connective tissue. The action of lysyl oxidase helps maintain the integrity of connective tissue in the heart and blood vessels and also plays a role in bone formation (2).
Four copper-containing enzymes, known as multi-copper oxidases (MCO) or ferroxidases, have the capacity to oxidize ferrous iron (Fe2+) to ferric iron (Fe3+), the form of iron that can be loaded onto the protein transferrin for transport to the site of red blood cell formation. The MCO family comprises the circulating ceruloplasmin (which represents ~90% of plasma copper), the membrane-bound ceruloplasmin (called GPI-ceruloplasmin), and two proteins called Hephaestin and Zyklopen found in the intestine and the placenta, respectively (6). Interestingly, mice that do not express ceruloplasmin (Cp-/-) have normal copper metabolism but abnormal iron accumulation in the liver (7, 8). Similarly, individuals lacking ceruloplasmin display iron overload in selected tissues, including liver, brain, and retina (9). This supports the idea that the ferroxidase activity of ceruloplasmin is essential to the flux of iron in the body. Moreover, the fact that iron mobilization from storage sites is impaired in copper deficiency supports the role of MCO in iron metabolism (10).
Central nervous system
A number of reactions essential to normal function of the brain and nervous system are catalyzed by cuproenzymes.
Formation and maintenance of myelin
Superoxide dismutase (SOD) functions as an antioxidant by catalyzing the conversion of superoxide radicals (free radicals or ROS) to hydrogen peroxide, which can subsequently be reduced to water by other antioxidant enzymes (12). Two forms of SOD contain copper: (1) copper/zinc SOD is found within most cells of the body, including red blood cells; and (2) extracellular SOD is a copper-containing enzyme found at high levels in the lungs and low levels in plasma (2).
Ceruloplasmin may function as an antioxidant in two different ways. Free copper and iron ions are powerful catalysts of free-radical damage. By binding copper, ceruloplasmin prevents free copper ions from catalyzing oxidative damage. The ferroxidase activity of ceruloplasmin (oxidation of ferrous iron) facilitates iron loading onto its transport protein, transferrin, and may prevent free ferrous ions (Fe2+) from participating in harmful free-radical-generating reactions (12).
Regulation of gene expression
Cellular copper levels may affect the synthesis of proteins by enhancing or inhibiting the transcription of specific genes. Copper may regulate the expression of genes by increasing the level of intracellular oxidative stress. A number of signal transduction pathways are activated in response to oxidative stress and can lead to an increase in the expression of genes involved in the detoxification of reactive oxygen species (13).
Adequate copper nutritional status is necessary for normal iron metabolism and red blood cell formation. Anemia is a clinical sign of copper deficiency, and iron has been found to accumulate in the livers of copper-deficient animals, indicating that copper (via the copper-containing ceruloplasmin) is required for iron transport to the bone marrow for red blood cell formation (see Iron metabolism) (2). The connection between copper availability and iron metabolism has also been established in humans; copper deficiency can lead to secondary ceruloplasmin deficiency and hepatic iron overload and/or cirrhosis (10). Oral copper supplementation restored normal ceruloplasmin levels and plasma ferroxidase activity and corrected the iron-metabolism disorder in a copper-deficient subject (14). Moreover, infants fed a high iron formula absorbed less copper than infants fed a low iron formula, suggesting that high iron intakes may interfere with copper absorption in infants (15).
High supplemental zinc intakes of 50 mg/day or more for extended periods of time may result in copper deficiency. High dietary zinc intakes increase the synthesis of an intestinal cell protein called metallothionein, which binds certain metals and prevents their absorption by trapping them in intestinal cells. Metallothionein has a stronger affinity for copper than zinc, so high levels of metallothionein induced by excess zinc cause a decrease in copper absorption. In contrast, high copper intakes have not been found to affect zinc nutritional status (2, 15). Zinc supplementation (10 mg/day for eight weeks) was able to restore normal plasma copper/zinc ratios in 65 subjects on long-term hemodialysis who initially exhibited low zinc levels and elevated copper levels. Whether improving zinc and copper status of hemodialysis patients can impact their clinical outcomes needs to be assessed (16).
High fructose diets have exacerbated copper deficiency in rats but not in pigs whose gastrointestinal systems are more like those of humans. Very high levels of dietary fructose (20% of total calories) did not result in copper depletion in humans, suggesting that fructose intake does not result in copper depletion at levels relevant to normal diets (2, 15).
Although vitamin C supplements have produced copper deficiency in guinea pigs (17), the effect of vitamin C supplements on copper nutritional status in humans is less clear. Two small studies in healthy, young adult men indicate that the oxidase activity of ceruloplasmin may be impaired by relatively high doses of supplemental vitamin C. In one study, vitamin C supplementation of 1,500 mg/day for two months resulted in a significant decline in ceruloplasmin oxidase activity (18). In the other study, supplements of 605 mg/day of vitamin C for three weeks resulted in decreased ceruloplasmin oxidase activity, although copper absorption did not decline (19). Neither of these studies found vitamin C supplementation to adversely affect copper nutritional status.
Clinically evident or frank dietary copper deficiency is relatively uncommon. Serum copper and ceruloplasmin levels may fall to 30% of normal in cases of severe copper deficiency. Hypocupremia (low copper content in blood) is also observed in genetic disorders of copper metabolism, such as Wilson's disease and aceruloplasminemia, which are not linked to dietary copper deficiency. One of the most common clinical signs of copper deficiency is an anemia that is unresponsive to iron therapy but corrected by copper supplementation. Although the anemia is thought to result from defective iron mobilization due to decreased ceruloplasmin activity, the absence of ceruloplasmin in individuals with inherited aceruloplasminemia is not always associated with overt anemia (20). Copper deficiency may also lead to abnormally low numbers of white blood cells known as neutrophils (neutropenia), a condition that may be accompanied by increased susceptibility to infection. Copper depletion studies have suggested that reduced copper availability might affect erythroid and myeloid cell lineage, supporting a role for copper in the regulation of blood cell renewal (21, 22). More research is clearly needed to uncover the mechanisms underlying copper deficiency-induced anemia and neutropenia (4, 23). Osteoporosis and other abnormalities of bone development related to copper deficiency are most common in copper-deficient, low-birth-weight infants and young children. Less common features of copper deficiency may include loss of pigmentation, neurological symptoms, and impaired growth (2, 5).
Individuals at risk of deficiency
Cow's milk is relatively low in copper, and cases of copper deficiency have been reported in high-risk infants and children fed only cow's milk formula (24). High-risk individuals include premature infants (especially low-birth-weight infants); infants with prolonged diarrhea; infants and children recovering from malnutrition; and individuals with malabsorption syndromes, including celiac disease, sprue, and short bowel syndrome due to surgical removal of large portions of the intestine. Individuals receiving intravenous total parenteral nutrition lacking copper or other restricted diets may also require supplementation with copper and other trace elements (2, 5). Copper deficiency in infants with cholestasis (reduced biliary excretion of copper) has been linked to long-term parenteral nutrition lacking copper (25). Case reports indicate that cystic fibrosis patients may also be at increased risk of copper insufficiency (26). Finally, excessive zinc intake has led to secondary copper deficiency in individuals using zinc supplements or zinc-enriched dental creams (27, 28).
Acquired copper deficiency
A neurologic syndrome has been described in adults with acquired copper deficiency (29). The symptoms include central nervous system demyelination, polyneuropathy, myelopathy, and inflammation of the optic nerve. The etiology is unknown in absence of prominent risk factors (see risk factors in the above section: Individuals at risk of deficiency); case reports describe increased intestinal copper content suggesting a malabsorption syndrome like Menkes disease, but mutations in ATP7A gene were not linked to the condition (30) (see Inherited copper deficiency below). Oral copper replacement (2 mg/day of elemental copper) normalizes serum copper and ceruloplasmin concentrations, stabilizes the condition, and significantly improves the quality of life of affected subjects. However, the duration of copper supplementation has not yet been established, and dosing increments might be required in cases of relapse (29).
Copper trafficking within most cells except hepatocytes (liver cells) is facilitated by a Cu1+-transporting ATPase called ATP7A. Mutations in the ATP7A gene impair the transport of intracellular copper, which accumulates in the cytosol of enterocytes and vascular endothelial cells (31). This results in systemic copper deficiency and decreased cuproenzyme activity. Copper transport into the brain is also affected, leading to copper accumulation in the blood-brain barrier and reduced cuproenzyme activity in neurons. Affected individuals are diagnosed with Menkes disease (MD) or with a milder form of the disease called occipital horn syndrome (OHS). The clinical features of MD include intractable seizures, connective tissue disorders, subdural hemorrhage, and hair abnormalities ("kinky hair"). OHS patients exhibit muscular hypotonia and connective tissue abnormalities, including exostosis on occipital bones. Subcutaneous injections of copper-histidine are used to bypass the defective intestinal absorption and improve copper metabolic function in patients. However, copper entry into the brain remains limited (reviewed in 32).
A variety of indicators were used to establish the RDA for copper, including plasma copper concentration, serum ceruloplasmin activity, superoxide dismutase activity in red blood cells, and platelet copper concentration (15). The RDA for copper reflects the results of depletion-repletion studies and is based on the prevention of deficiency.
Recommended Dietary Allowance (RDA) for Copper
|Life Stage||Age||Males (mcg/day)||Females (mcg/day)|
|Infants||0-6 months||200 (AI)||200 (AI)|
|Infants||7-12 months||220 (AI)||220 (AI)|
|Adults||19 years and older||900||900|
While it is clear that severe copper deficiency results in heart abnormalities and damage (cardiomyopathy) in some animal species, the pathology differs from atherosclerotic cardiovascular disease that is prevalent in humans (15). Studies in humans have produced inconsistent results, and their interpretation is hindered by the lack of a reliable marker of copper nutritional status. Outside the body, free copper is known to be a pro-oxidant and is frequently used to produce oxidation of low-density lipoprotein (LDL) in the test tube. The copper-containing protein ceruloplasmin has been found to stimulate LDL oxidation in the test tube (33), leading some scientists to propose that increased copper levels could increase the risk of atherosclerosis by promoting the oxidation of LDL. However, there is little evidence that copper or ceruloplasmin promotes LDL oxidation in the human body. Additionally, the cuproenzymes, superoxide dismutase and ceruloplasmin, are known to have antioxidant properties, leading some experts to propose that copper deficiency rather than excess copper increases the risk of cardiovascular diseases (34).
Several epidemiological studies have found increased serum copper levels to be associated with increased risk of cardiovascular disease. A prospective cohort study in the US examined serum copper levels in more than 4,500 men and women 30 years of age and older (35). During the following 16 years, 151 participants died from coronary heart disease (CHD). After adjusting for other risk factors of heart disease, those with serum copper levels in the two highest quartiles had a significantly greater risk of dying from CHD. Three other case-control studies conducted in Europe had similar findings. One small study in 60 patients with chronic heart failure or ischemic heart disease reported that serum copper was a predictor of short-term outcome (36). Another prospective cohort study in 4,035 middle-aged men reported that high serum copper levels were significantly related to a 50% increase in all-cause mortality; however, serum copper was not significantly associated with cardiovascular mortality in this study (37). Additionally, serum copper has been found to be elevated in patients with rheumatic heart disease (38).
It is important to note that serum copper largely reflects serum ceruloplasmin and is not a sensitive indicator of copper nutritional status (39). Serum ceruloplasmin levels are known to increase by 50% or more under certain conditions of physical stress, such as trauma, inflammation, or disease. Because over 90% of serum copper is carried in ceruloplasmin, which is increased in many inflammatory conditions, elevated serum copper may simply be a marker of inflammation that accompanies atherosclerosis. In contrast to the epidemiological findings linking increased serum copper levels to heart disease, two autopsy studies found copper levels in heart muscle were actually lower in patients who died of CHD than those who died of other causes (40). Additionally, the copper content of white blood cells has been positively correlated with the degree of patency of coronary arteries in CHD patients (41, 42). Further, patients with a history of myocardial infarction (MI) had lower concentrations of extracellular superoxide dismutase (SOD) than those without a history of MI (43). Thus, due to a lack of a reliable biomarker of copper nutritional status, it is not clear whether copper is related to cardiovascular disease.
While studies in very small numbers of adults fed experimental diets low in copper have demonstrated adverse changes in blood cholesterol levels, including increased total and LDL-cholesterol levels and decreased HDL-cholesterol levels (44), other studies have not confirmed those results (45). Copper supplementation of 2-3 mg/day for four to eight weeks did not result in clinically significant changes in cholesterol levels (34, 46, 47). Further, research has failed to find evidence that increased copper intake increases oxidative stress. In a multi-center, placebo-controlled trial, copper supplementation of 3 or 6 mg/day for six weeks did not result in increased susceptibility of LDL to oxidation induced outside the body (ex vivo) by copper or peroxynitrite (a reactive nitrogen species) (48). Moreover, supplementation with 3 or 6 mg/day of copper decreased the in vitro oxidizability of red blood cells (49), indicating that relatively high intakes of copper do not increase the susceptibility of LDL or red blood cells to oxidation.
Although free copper and ceruloplasmin can promote LDL oxidation in the test tube, there is little evidence that increased dietary copper increases oxidative stress in the human body. Increased serum copper levels have been associated with increased cardiovascular disease risk, but the significance of these findings is unclear due to the association between serum ceruloplasmin levels and inflammatory conditions. Clarification of the relationships between copper nutritional status, ceruloplasmin levels, and cardiovascular disease risk requires further research.
Notably, it was suggested that elevated plasma copper concentrations could be linked to high homocysteine levels in individuals with vascular diseases (50, 51). Increased levels of homocysteine are associated with arterial wall lesions and increased risk of cardiovascular diseases (52). The interaction between homocysteine and copper was linked to impaired vascular endothelial function in animal models (53, 54). However, although copper restriction in animals has shown some beneficial effects on homocysteine levels and atherogenic lesions (55, 56), it is not known whether copper imbalance contributes to the atherogenic effect of homocysteine in humans.
Copper is known to play an important role in the development and maintenance of immune system function, but the exact mechanism of its action is not yet known. Neutropenia (abnormally low numbers of white blood cells called neutrophils) is a clinical sign of copper deficiency in humans. Adverse effects of insufficient copper on immune function appear most pronounced in infants. Infants with Menkes disease, a genetic disorder that results in severe copper deficiency, suffer from frequent and severe infections (57, 58). In a study of 11 malnourished infants with evidence of copper deficiency, the ability of certain white blood cells to engulf pathogens increased significantly after one month of copper supplementation (59). Moreover, 11 men on a low-copper diet (0.66 mg copper/day for 24 days and 0.38 mg/day for another 40 days) showed a decreased proliferation response when white blood cells, called monocytes, were isolated from their blood and presented with an immune challenge in cell culture (60). Recent mechanistic studies support a role for copper in innate immune response against bacterial infections (reviewed in 61). While severe copper deficiency has adverse effects on immune function, the effects of marginal copper insufficiency in humans are not yet clear.
The progressive loss of bone mineral density (BMD) leading to osteopenia (pre-osteoporosis) and osteoporosis is commonly observed in the elderly population. Women are more often affected by osteoporosis than men, (e.g., prevalence ratio is 5:1 in non-Hispanic whites) (62), primarily due to the postmenopausal reduction in estrogen production that is essential for maintaining strength of muscle, bone, and connective tissue (63). Osteoporosis is associated with an increased risk of falls, bone fracture, and mortality in individuals over 65 years of age (64). Osteoporosis has also been reported in infants with severe copper deficiency (65, 66), but it is not clear whether marginal copper deficiency during adulthood contributes to osteoporosis. While an increase in bone resorption (breakdown) was observed in 11 healthy adult males with a marginal copper intake of 0.7 mg/day for six weeks (67), the supplementation of 3 to 6 mg/day of copper for six weeks had no effect on biochemical markers of bone resorption or bone formation in two studies of healthy adult men and women (68, 69). However, it is possible that a reduction in copper intake and absorption in older people reduces the activity of the copper-dependent enzyme, lysyl oxidase, which is required for the maturation (cross-linking) of collagen—a key element in the organic matrix of bone.
Overall, research regarding the role of copper nutritional status in age-related osteoporosis is limited. An early study found that serum copper levels in 46 elderly patients with hip fractures were significantly lower than those of matched controls (70). However, another study found no differences in serum copper levels among postmenopausal women with normal BMD (N=40), osteopenia (N=40), or osteoporosis (N=40) (71). A small study in perimenopausal women, who consumed an average of 1 mg of dietary copper daily, reported decreased loss of BMD from the lumbar spine after copper supplementation of 3 mg/day for two years (72). Additionally, a two-year double-blind, placebo-controlled trial in 59 postmenopausal women found that a combination of supplemental calcium and trace minerals, including 2.5 mg of copper daily, resulted in maintenance of spinal bone density, whereas supplemental calcium or trace minerals, alone, were not effective in preventing loss of bone density (73). However, a more recent randomized, double-blind, placebo-controlled study, which initially enrolled 224 healthy, postmenopausal women aged 51 to 80 years, found daily supplementation with 600 mg of calcium, 2 mg of copper, and 12 mg of zinc for two years decreased whole-body BMD compared to supplemental calcium alone. Moreover, although BMD was clearly reduced in subjects with dietary copper intakes below the RDA (0.9 mg/day), supplemental copper did not prevent the progressive loss of BMD as well as the calcium regimen alone (74). Finally, several studies have suggested that tooth loss might be related to poor systemic BMD (75, 76). When compared with 20 healthy-matched controls, 50 patients (mean age 47.5 years) with low spinal BMD and advanced tooth wear were found with significantly lower copper content in tooth enamel. However, despite evidence suggesting bone demineralization, the serum copper levels in this population were similar to those of the healthy group (77). More research is required to draw conclusions regarding the effects of marginal copper deficiency and copper supplementation on bone metabolism and age-related osteoporosis.
Cognitive deterioration in individuals with Alzheimer's disease (AD) is linked to the presence of beta-amyloid plaques and abnormal Tau protein-forming aggregates. The possibility that copper imbalance is involved in the onset of AD is currently investigated. First, it appears that the fraction of 'free' copper (not bound to ceruloplasmin) is augmented in copper homeostasis disorders, as well as in AD individuals (78, 79). Moreover, AD patients appear to have higher levels of serum copper compared to healthy controls (80). Among the many hypotheses supporting a role for copper in AD onset or progression, it is suggested that copper could be involved in the formation of senile plaques through hypermetallation of the beta-amyloid peptides, possibly leading to zinc depletion, enhanced oxidative stress, and even brain damage (81, 82). Recent research has also identified genetic variations (polymorphisms) in the ATP7B gene that may modify the risk of developing AD (83). The protein, ATP7B, is responsible for the excretion of hepatic copper into the biliary tract, and its impairment in Wilson's disease results in increased 'free' copper level in blood and copper accumulation in liver and brain.
More research is needed to investigate whether genetic variants could influence the susceptibility of environmental exposure to high levels of copper. The addition of copper to drinking water has been associated with enhanced pathologic features in animal models of AD (84, 85). One study in a rabbit model reported that combining a high-cholesterol diet and copper (0.12 mg/L in drinking water) could impair cognition (84). A prospective cohort study in 3,718 elderly participants of the Chicago Health and Aging Project, followed for 5.5 years, evaluated the impact of fat and copper intakes using food frequency questionnaires and various cognitive assessments. For individuals with high intakes of saturated and trans fat, cognitive decline was greater for those in the highest quintile of total copper intake compared to the lowest quintile (median intake of 2.75 vs. 0.88 mg/day) (86).
Although a dysfunctional copper metabolism is suggested as a risk factor for AD, it could also be symptomatic of the disease. Moreover, it is still unclear whether copper supplementation or restriction could delay the progression of AD. A small, double-blind, placebo-controlled trial in 68 individuals with mild AD found that supplementation of 8 mg/day of copper for one year delayed the decrease of the beta-amyloid peptide Abeta42 in cerebrospinal fluid; a decrease in Abeta42 has been linked to cognitive deterioration (87). However, this delay was not associated with improved cognitive performance (88). Based on the utilization of copper-chelating agents in Wilson's disease, the recent use of slow-release zinc acetate (150 mg/day for six months) in a randomized, placebo-controlled study of 60 patients with mild to moderate AD resulted in a decrease in serum 'free' copper and stabilization of cognition deficits (81). Additional human studies are needed to clarify the role of copper in AD onset and progression, and to evaluate whether dietary copper might help prevent AD in high-risk individuals or manage the disease in AD patients.
Both neurologically presenting Wilson's disease and inherited aceruloplasminemia are characterized by copper accumulation in the brain, resulting in neurologic symptoms (dystonia and cognitive impairment) that resemble Parkinson's disease (PD) (89). The level of copper is diminished in brain regions of neuronal loss in PD patients (90). However, the recent meta-analysis of studies measuring copper levels in serum, plasma, and cerebrospinal fluid did not find any difference between PD patients and healthy elderly subjects (91).
Copper is found in a wide variety of foods and is most plentiful in organ meats, shellfish, nuts, and seeds. Wheat-bran cereals and whole-grain products are also good sources of copper. According to national surveys, the average dietary intake of copper in the US is approximately 1.0 to 1.1 mg (1,000 to 1,100 mcg) per day for adult women and 1.2 to 1.6 mg (1,200 to 1,600 mcg) per day for adult men (15). The copper content of some foods that are relatively rich in copper is listed in micrograms (mcg) in the table below. For more information on the nutrient content of foods, search the USDA food composition database.
|Liver (beef), cooked, pan-fried||1 ounce||4,128|
|Mollusks, oysters, eastern, wild, cooked, moist heat||6 medium oysters||2,397|
|Crab meat, Alaskan king, cooked||3 ounces||1,005|
|Crab meat, blue, cooked, moist heat||3 ounces||692|
|Mollusks, clams, mixed species, cooked, moist heat||3 ounces||585|
|Cashews nuts, raw||1 ounce||622|
|Sunflower seed kernels, dry roasted||1 ounce||519|
|Hazelnuts, dry roasted||1 ounce||496|
|Peanut butter, chunk style, without salt||2 tablespoons||185|
|Lentils, mature seeds, cooked, boiled, without salt||1 cup||497|
|Mushrooms, white, raw||1 cup (sliced)||223|
|Shredded wheat cereal||2 biscuits||167|
|Chocolate (semisweet)||1 ounce||198|
Copper toxicity is rare in the general population. Acute copper poisoning has occurred through the contamination of beverages by storage in copper-containing containers, as well as from contaminated water supplies (93). Guideline values for copper in drinking water have been set by the US Environmental Protection Agency (1.3 mg/liter) and by the World Health Organization (2 mg/liter) (94). Symptoms of acute copper toxicity include abdominal pain, nausea, vomiting, and diarrhea; such symptoms help prevent additional ingestion and absorption of copper. More serious signs of acute copper toxicity include severe liver damage, kidney failure, coma, and death. Of more concern from a nutritional standpoint is the possibility of liver damage resulting from long-term exposure to lower doses of copper. In generally healthy individuals, doses of up to 10,000 mcg (10 mg) daily have not resulted in liver damage. For this reason, the US Food and Nutrition Board set the tolerable upper intake level (UL) for copper at 10 mg/day from food and supplements (15). It should be noted that individuals with genetic disorders affecting copper metabolism (e.g., Wilson's disease, Indian childhood cirrhosis, and idiopathic copper toxicosis) may be at risk for adverse effects of chronic copper toxicity at significantly lower intake levels. There is some concern that the UL of 10 mg/day might be too high. In particular, men in a research study consumed 7.8 mg/day of copper for 147 days. They accumulated copper during that time, and some indices of immune function and antioxidant status suggested that these functions were adversely affected by the high intakes of copper (95, 96). However, another study did not report any adverse effects in individuals supplemented with 8 mg/day of copper for six months (88).
Tolerable Upper Intake Level (UL) for Copper
|Age Group||UL (mcg/day)|
|Infants 0-12 months||Not possible to establish*|
|Children 1-3 years||1,000|
|Children 4-8 years||3,000|
|Children 9-13 years||5,000|
|Adolescents 14-18 years||8,000|
|Adults 19 years and older||10,000|
*Source of intake should be from food and formula only.
Relatively little is known about the interaction of copper with drugs. Penicillamine is used to bind copper and enhance its elimination in Wilson's disease, a genetic disorder resulting in hepatic copper overload. Because penicillamine dramatically increases the urinary excretion of copper, individuals taking the medication for reasons other than copper overload may have an increased copper requirement. Additionally, antacids may interfere with copper absorption when used in very high amounts (2).
The RDA for copper (900 mcg/day for adults) is sufficient to prevent deficiency, but the lack of clear indicators of copper nutritional status in humans makes it difficult to determine the level of copper intake most likely to promote optimum health or prevent chronic disease. A varied diet should provide enough copper for most people. For those who are concerned that their diet may not provide adequate copper, a multivitamin/mineral supplement will generally provide at least the RDA for copper.
Older adults (> 50 years)
Because aging has not been associated with significant changes in the requirement for copper, our recommendation for older adults is the same as that for adults 50 and younger (97).
Written in April 2003 by:
Jane Higdon, Ph.D.
Linus Pauling Institute
Oregon State University
Updated in December 2013 by:
Barbara Delage, Ph.D.
Linus Pauling Institute
Oregon State University
Reviewed in January 2014 by:
Joseph R. Prohaska, Ph.D.
Professor of Biochemistry, Emeritus
University of Minnesota Medical School Duluth
Copyright 2001-2015 Linus Pauling Institute
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