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Copper
Overview
Copper is essential in all higher plants and animals. Copper is the third most abundant trace mineral in the human body. Copper is carried mostly in the bloodstream on a plasma protein called ceruloplasmin. When copper is first absorbed in the gut it is transported to the liver bound to albumin. Copper is found in a variety of enzymes, including the copper centers of cytochrome c oxidase, the Cu-Zn containing enzyme superoxide dismutase, and is the central metal in the oxygen carrying pigment hemocyanin. The blood of the horseshoe crab, Limulus polyphemus uses copper rather than iron for oxygen transport. It is believed that zinc and copper compete for absorption in the digestive tract so that a diet that is excessive in one of these minerals may result in a deficiency in the other.

What is Copper?
Copper, in its many forms, is the third most common mineral in the body. In addition to being important for many enzyme systems, copper is found throughout the musculo-skeletal system, although the largest amounts are found in the brain and liver.

Copper, through its involvement in the formation of several key enzymes is not only involved in the release of energy inside the cell, but also contributes to the function of very many antioxidants, assisting the the "mopping up" of the free radicals that cause cell damage.

The formation and regulation of hormones such as melatonin is under the control of copper, via its role in the blood protein ceruloplasmin and copper enzymes are also responsible for the production of a wide range of neurotransmitters and other neuroactive compounds, including the catecholamines and encephalins.
Collagen production, formation of red blood cells and the oxidation of fatty acids are all highly dependent on copper concentration.

Thankfully, copper deficiency per se is rare. However, due to the intricate interaction with zinc (copper and zinc compete for the same absorption sites in the gut), high zinc levels can prevent proper absorption

Deficiency Symptoms
As suggested, copper deficiency is not common, but does occur. Symptoms largely reflect the systems which utilize copper and include collagen deficiency (poor bone and joint function as well as vascular disease). The involvement of copper in numerous hormonal systems means that those system can be severely affected. This may lead to brain dysfunction and somewhat altered levels of red blood cells and cholesterol.

Symptoms of Copper deficiency:
Immune system Dysfunction
Vascular Disease (haemorrhage in severe cases)
Brittle Bones (in children)
Oedema (swelling)
High cholesterol levels (see cholesterol)
Poorly pigmented skin
Anaemia

Where it is found

Source

mg/100g

Source

mg/100g

Oysters

7.6

Tuna

0.6

Whelks

7.2

Dried figs

0.6

Lamb liver

6.0

Sunflower oil

0.5

Crab

4.8

Butter / Rye grain / Barley /Prunes / cooked mushrooms

0.4

brewer's yeast

3.3

Olive oil

0.4

Brazil nuts

3.2

Carrots

0.4

Dry roasted cashews

2.2

Coconut

0.3

Olives

1.6

Garlic

0.3

Hazelnuts/ Almonds

1.4

Wholewheat bread

0.3

Walnuts / Pecans

1.3

Peas / Millet

0.2

Shrimps

0.8

Corn oil / ginger

0.2

Buckwheat

0.8

Molasses

0.2

Peanuts

0.8

Turnip

0.2

Chocolate (semisweet)

0.7

Papaya

0.1

Cod

0.6

Apple

0.1

 
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Copper

Benefits / uses
The body needs copper for normal growth and health. Copper is needed to help body use iron. It is also important for nerve function, bone growth, and to help body use sugar. Copper is a component of or a cofactor for approximately 50 different enzymes. These enzymes need copper to function properly. Copper is an essential nutrient that plays a role in the production of hemoglobin, myelin, collagen, and melanin. Copper also works with vitamin C to help make a component of connective tissue known as elastin. Copper is a critical functional component of a number of essential enzymes, known as cuproenzymes. Copper is an essential component of the natural dark pigment, melanin, that colors skin, hair, and eyes. The cuproenzyme, tyrosinase, is required for the formation of the pigment melanin. Melanin is formed in cells called melanocytes and plays a role in the pigmentation of the hair, skin, and eyes. Copper is a strong antioxidant. It works together with an antioxidant enzyme, superoxide dismutase (SOD), to protect cell membranes form being destroyed by free radicals. Copper is needed to make adenosine triphosphate (ATP), the energy the body runs on. Copper may play a role in staving off heart rhythm disorders (arrhythmias) and high blood pressure. Copper's anti-inflammatory actions may help in reducing arthritis symptoms.

Doses

Age

mg/day

Children (0-3 years)

0.3 - 0.4

Children (4-6 years)

0.6

Children (7-14 years)

0.7 - 0.8

15yrs+ (inc adults)

1.0 - 1.2

Lactation

1.5

 

Possible Side effects / Precautions / Possible Interactions:
All copper compounds, unless otherwise known, should be treated as if they were toxic. Symptoms of acute copper toxicity include abdominal pain, nausea, vomiting, and diarrhea, which help prevent additional ingestion and absorption of copper. More serious signs of acute copper toxicity include severe liver damage, kidney failure, coma, and death. 30g of copper sulfate is potentially lethal in humans. The suggested safe level of copper in drinking water for humans varies depending on the source, but tends to be pegged at 1.5 to 2 mg/l. The DRI Tolerable Upper Intake Level for adults of dietary copper from all sources is 10 mg/day. Supplemental copper is contraindicated in those with Wilson's disease (hepatolenticular degeneration), a disease of abnormal copper accumulation.

When To Take/Types To Take
Copper supplements are best taken with a meal. It is available in various salts as sulphate, gluconate, aspartate, citrate and picolinate etc as well as various amino acid Chelates.

Research studies / References

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arw Finley EB, Cerklewski FL. Influence of ascorbic acid supplementation on copper status in young adult men. Am J Clin Nutr. 1983;37(4):553-556.
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arw Percival SS, Kauwell GP, Bowser E, Wagner M. Altered copper status in adult men with cystic fibrosis. J Am Coll Nutr. 1999;18(6):614-619.
arw Fox PL, Mazumder B, Ehrenwald E, Mukhopadhyay CK. Ceruloplasmin and cardiovascular disease. Free Radic Biol Med. 2000;28(12):1735-1744.
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arw Kinsman GD, Howard AN, Stone DL, Mullins PA. Studies in copper status and atherosclerosis. Biochem Soc Trans. 1990;18(6):1186-1188.
arw Wang XL, Adachi T, Sim AS, Wilcken DE. Plasma extracellular superoxide dismutase levels in an Australian population with coronary artery disease. Arterioscler Thromb Vasc Biol. 1998;18(12):1915-1921.
arw Klevay LM. Lack of a recommended dietary allowance for copper may be hazardous to your health. J Am Coll Nutr. 1998;17(4):322-326.
arw Milne DB, Nielsen FH. Effects of a diet low in copper on copper-status indicators in postmenopausal women. Am J Clin Nutr. 1996;63(3):358-364.
arw Medeiros DM, Milton A, Brunett E, Stacy L. Copper supplementation effects on indicators of copper status and serum cholesterol in adult males. Biol Trace Elem Res. 1991;30(1):19-35.
arw Turley E, McKeown A, Bonham MP, et al. Copper supplementation in humans does not affect the susceptibility of low density lipoprotein to in vitro induced oxidation (FOODCUE project). Free Radic Biol Med. 2000;29(11):1129-1134.
arw Rock E, Mazur A, O'Connor J M, Bonham MP, Rayssiguier Y, Strain JJ. The effect of copper supplementation on red blood cell oxidizability and plasma antioxidants in middle-aged healthy volunteers. Free Radic Biol Med. 2000;28(3):324-329.
arw Failla ML, Hopkins RG. Is low copper status immunosuppressive? Nutr Rev. 1998;56(1 Pt 2):S59-64.
arw Percival SS. Copper and immunity. Am J Clin Nutr. 1998;67(5 Suppl):1064S-1068S.
arw Heresi G, Castillo-Duran C, Munoz C, Arevalo M, Schlesinger L. Phagocytosis and immunoglobulin levels in hypocupremic children. Nutr Res. 1985;5:1327-1334.
arw Kelley DS, Daudu PA, Taylor PC, Mackey BE, Turnlund JR. Effects of low-copper diets on human immune response. Am J Clin Nutr. 1995;62(2):412-416.
arw Conlan D, Korula R, Tallentire D. Serum copper levels in elderly patients with femoral-neck fractures. Age Ageing. 1990;19(3):212-214.
arw Eaton-Evans J, Mellwrath EM, Jackson WE, McCartney H, Strain JJ. Copper supplementation and the maintenance of bone mineral density in middle-aged women. J Trace Elem Exp Med. 1996;9:87-94.
arw Strause L, Saltman P, Smith KT, Bracker M, Andon MB. Spinal bone loss in postmenopausal women supplemented with calcium and trace minerals. J Nutr. 1994;124(7):1060-1064.
arw Baker A, Harvey L, Majask-Newman G, Fairweather-Tait S, Flynn A, Cashman K. Effect of dietary copper intakes on biochemical markers of bone metabolism in healthy adult males. Eur J Clin Nutr. 1999;53(5):408-412.
arw .Baker A, Turley E, Bonham MP, et al. No effect of copper supplementation on biochemical markers of bone metabolism in healthy adults. Br J Nutr. 1999;82(4):283-290.
arw Hendler SS, Rorvik DR, eds. PDR for Nutritional Supplements. Montvale: Medical Economics Company, Inc; 2001.
arw Bremner I. Manifestations of copper excess. Am J Clin Nutr. 1998;67(5 Suppl):1069S-1073S.
arw Fitzgerald DJ. Safety guidelines for copper in water. Am J Clin Nutr. 1998;67(5 Suppl):1098S-1102S.
arw Turnlund JR, Jacob RA, Keen CL, et al. Long-term high copper intake: effects on indexes of copper status, antioxidant status, and immune function in young men. Am J Clin Nutr. 2004;79(6):1037-1044.
arw Turnlund JR, Keyes WR, Kim SK, Domek JM. Long-term high copper intake: effects on copper absorption, retention, and homeostasis in men. Am J Clin Nutr. 2005;81(4):822-828.
arw Wood RJ, Suter PM, Russell RM. Mineral requirements of elderly people. Am J Clin Nutr. 1995;62(3):493-505.