Two genetic diseases involving copper metabolism have been identified:
Menkes disease is an acquired condition and a recessive disorder that results in a kind of copper deficiency. The absorption and transportation of copper is altered, causing abnormal distribution of the mineral within cells and organs.
Wilson's disease is an autosomal recessive disorder that results in copper overload and toxicity. This impairment in copper metabolism causes the accumulation of copper mainly in liver and brain tissue.
Absorption of copper ranges from 15-97%, depending on intake.
It has been noted that the Western diet is low in copper.
Because milk is low in copper, infants comprise a risk group for copper deficiency. The bioavailability from human milk is much higher than cow milk and infant formula.
Copper has an essential role in the biochemistry of living organisms. It is required for:
normal infant development
red and white blood cell maturation
protection against oxidative stress
Absorbed copper is bound primarily by albumin and transported to the liver. Copper is mainly incorporated into ceruloplasmin (ferroxidase I) in the liver. Ceruloplasmin is necessary for the absorption of iron as well as the mobilization of iron from the liver. In addition, a portion of copper is also incorporated in bile. A third portion of copper is incorporated into intracellular enzymes, such as superoxide dismutase and cytochrome oxidase.
Signs/symptoms of a copper deficiency are anemia,
leukopenia, neutropenia, and osteoporosis. Other symptoms of copper deficiency
include general weakness, impaired respiration, skin sores, decreased immune
function, elevated LDL cholesterol and reduced HDL cholesterol. Some possible
manifestations of copper deficiency are: arthritis, arterial disease, loss of
pigmentation, myocardial disease, and neurological effects.
A mild copper deficiency due to marginal copper intake over a long period of time can also occur. In addition to possible signs and symptoms of copper deficiency listed above, abnormal glucose tolerance may be seen.
Copper status indicators such as serum copper and ceruloplasmin have been established to assess copper deficiency. In addition, metallothionein, a protein that is involved in the metabolism of zinc and copper, may also be a useful laboratory indicator of copper status.1
Copper is relatively non-toxic in most mammals, including humans, and toxicosis is considered rare.3 In the long to term, toxicity is typically manifested by cirrhosis of the liver, along with hemolysis and damage to renal tubules, brain and other organs.4
Supplemental copper is contraindicated in those with Wilson's disease.
Supplemental copper is contraindicated in those sensitive to any component of a copper to containing dietary supplement.
Excess copper may interfere with the absorption of
zinc. Consulting a physician is important if excess amount of copper is
Alcohol, eggs, and fructose can induce copper
deficiency. Consulting physician is important if special diet is required.
Excretion losses may be increased by molybdenum.
Copper absorption may be adversely affected by many
nutrients, including calcium, iron, manganese, tin, zinc, phytates, vitamin
B6, vitamin C (only high amounts), L-cysteine, and antacids (high amounts).
Penicillamine [Cuprimineâ] is used for copper toxicity and to treat Wilson's disease, which affects copper metabolism and causes cirrhosis and brain and eye problems from abnormal deposits of copper. Individuals with Wilson's disease should avoid taking supplements containing copper.
Zidovudine [AZTâ], an antiviral agent used to treat HIV infection, may deplete blood concentrations of many minerals, including copper. Taking supplements may be helpful.
Information on the relationship between substances and disease is provided for general information, in order to convey a balanced review of the scientific literature. In many cases the relationship between a substance and a disease is tentative and additional research is needed to confirm such a relationship.
Cardiovascular disease: Because copper is a metal that can potentially act as a pro-oxidant and cause oxidative modification and free radical formation, its effects on cardiovascular disease has been investigated.910 However, due to conflicting evidence, the role of copper in atherosclerosis remains controversial.
A large, prospective and population-based study, using the NHANES II Mortality Study data, examined the association of serum copper concentrations and coronary artery disease. After controlling for numerous confounding variables, results showed higher serum copper concentrations among those who died from coronary artery disease (CAD) versus those who survived. 10
Plasma copper and zinc concentrations were studied and monitored in patients with acute myocardial infarction for 10 days following the clinical insult. Copper was found to increase on the 5th day following the attack, while zinc concentrations decreased significantly. 11
A single cross-sectional study evaluating serum copper and zinc concentrations in cancer and cardiomyopathy patients, along with a control group, found no difference in serum copper concentrations among cancer and ischemic cardiomyopathy patients versus the control group.12 However, serum zinc concentrations between patient groups were significantly lower than controls.
A few theories have been proposed in the literature regarding elevated serum copper concentrations and its relation to CAD: 10
Copper, as a pro-oxidant, oxidizes low density lipoprotein cholesterol, thereby increasing the risk for CAD.
Copper, as a risk marker for various indicators of inflammation such as C to reactive protein and serum amyloid A protein, may predict future CAD risk.
One paper suggested that copper deficiency can contribute to the formation of atherosclerotic lesions through decreased activity of the copper to dependent enzymes: lysyl oxidase and superoxide dismutase. This deficiency is believed to cause impaired arterial elastin and collagen cross to linking, and a decrease in free radical defense, respectively.9
Immunity: The role of copper and immunity has been studied.13 The authors concluded that immune function may be compromised from either suboptimal copper intake or marginal deficiency, as demonstrated in T cells from animals and humans. Since iron is also immunosuppressive, it remains difficult to differentiate between the effects of inadequate copper and iron status on immune system function, although it has been established that copper deficiency is quite rare in humans.
Diabetes: The role of copper in glucose homeostasis has not been well defined.
A study on plasma concentrations of selenium, zinc, and copper in type1diabetes mellitus patients and healthy controls found a significant difference in plasma copper concentrations between male and female controls and diabetic patients. A decrease in plasma copper concentrations in diabetic patients with poor metabolic control was more pronounced in females than males. However, the correlation between plasma copper and HbA1c was not significant. 14
A study conducted on type 2 (non-insulin dependent diabetes mellitus) subjects examined the relationship between copper, zinc and magnesium, and diabetes mellitus. Results showed significantly elevated plasma copper concentrations in the type 2 group versus control group, which may or may not be a result from type 2, since other factors may have contributed to higher plasma copper concentrations.
Parkinson's Disease: Genetic and environmental factors are thought to play an important role in the development of Parkinson's disease (PD). Occupational exposure to specific metals, such as copper, lead, iron, manganese, zinc, and others may be a risk factor for developing PD.
A population-based case-control study assessing the exposure of certain metals, such as copper, as a risk factor for PD was conducted on non-demented men and women receiving primary medical care versus a control group.17 Occupational exposure for 20 years or more to copper or manganese, was associated with PD. In addition, chronic exposure to combinations of lead-copper and iron-copper were also associated with increased risk of the disease.
Rheumatoid Arthritis: It has been suggested that patients with active rheumatoid
arthritis (RA) are deficient in copper, along with other minerals. Nutrient
intakes in both men and women with RA were compared to the RDA's, as well as
intakes from the typical American diet. These findings were confirmed by a
previous study on RA patients supplemented with copper (2 mg/day) for 4 weeks.
Results showed an increased erythrocyte copper-zinc superoxide dismutase (SOD)
activity concentration in 18 of 23 RA patients, who demonstrated significantly
lower SOD concentrations than age and sex-matched controls before
supplementation. The effects of copper supplementation on erythrocyte SOD
activity suggested a trend toward marginal copper status in RA patients. 18
The dietary supplement information contained on this site has been compiled from published sources thought to be reliable, but it cannot be guaranteed. Efforts have been made to assure this information is accurate and current. However, some of this information may be purported or outdated due to ongoing research or discoveries. The authors, editors and publishers cannot accept responsibility for errors or omissions or for any consequences from applications of the information in this site and make no warranty, expressed or implied, with respect to the contents herein.