Copper (Cu) is a trace element that is essential for most animals,
including humans. The influence of copper upon human health is due to the
fact it is part of enzymes, which are proteins that help biochemical
reactions occur in every cell. Copper is involved in the absorption,
storage and metabolism of iron. The symptoms of a copper deficiency are
similar to iron deficiency anemia. Copper may be absorbed by both the
stomach and small intestinal mucosa, with most absorbed by the small
intestine. Copper is found in the blood bound to proteins.
Copper is utilized by most cells as a component of enzymes involved in
energy production (cytochrome oxidase) and in the protection of cells from
free radical damage (superoxide dismutase). Copper is also involved with
an enzyme that strengthens connective tissue (lysyl oxidase) and in brain
neurotransmitters (dopamine hydroxylase and peptidyl alpha amidating
monoxygenase). One of the proteins, ceruloplasmin, transports copper as
well as helps convert iron to a form that can be transported to other
tissues. The average level of copper stored in the body is from 50 to 120
mg, with most of this in the liver. Excess dietary copper can also lead to
high copper levels in the kidney. However, under normal situations, not
much copper is excreted via the urine. Most copper is excreted via bile
that is released into the gastrointestinal tract, with minimal copper
reabsorbed by intestinal cells. The uptake of copper and elimination
through the bile allows copper to be conserved and tightly regulated.
Deficiencies: Animals that are fed diets deficient in
copper often exhibit anemia, cardiac abnormalities such as blood vessel
and heart rupture, abnormal EKG's and have elevated levels of serum
cholesterol, triglycerides and glucose. A lifetime of marginal diet copper
in humans is thought to lead to heart disease. Copper deficiency has been
observed in premature infants and infants suffering from malnutrition.
Overt symptoms in adults are rare, but may occur with long term shortage
or, possibly, in those who consume zinc supplements for a period of time.
Diet recommendations: The estimated safe and adequate
intake for copper is 1.5 - 3.0 mg/day. Many survey studies show that
Americans consume about 1.0 mg or less of copper per day. Copper is found
in foods such as nuts [0.2 to 0.5 mg/28 g (1 Tbsp.)], shellfish (1.0 to
3.7 mg/serving), organ meats (3.8 mg/serving of beef liver) and legumes
(0.2 mg/serving). Grains, grain products and chocolate have appreciable
levels of copper. While these food items are good to excellent sources of
copper, the absolute amount of copper absorbed may be influenced by other
dietary components.
Copper absorption may be decreased by excess dietary iron or zinc.
Conversely, too much copper may cause an iron deficiency. Vitamin C
supplementation results in decreased copper status. In rats, large doses
of vitamin C can lead to copper deficiency. Other dietary components have
an influence upon copper status, but not necessarily absorption. Feeding
rats either sucrose or fructose, as opposed to glucose or cornstarch,
decreases copper status and exacerbates the signs of copper deficiency.
Toxicity: Cases of copper toxicity are rare but may
occur. Excess copper consumption may lead to liver damage. Intake of
supplements exceeding 3 mg copper/day for a protracted period of time may
be cause for concern. Doses of 10 mg/day over several weeks may lead to
toxic symptoms, such as weakness and nausea.
Genetic Conditions relating to copper: There are two
well known genetic diseases affecting copper metabolism. Menkes'
kinky-hair disease is a problem with copper transport or absorption.
Wilson's disease is characterized by increased liver copper content,
leading to severe hepatic damage, followed by increased brain copper
levels and neurological problems. Menkes' disease results in pathology
resembling copper-deficiency, as opposed to the pathology of Wilson's
disease, which resembles copper-toxicity. The Menkes' gene codes for a
P-type ATPase that has a mutation that prevents copper absorption in the
intestine.
