Helps activate many
Acts as an
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Copper is usually found in foods containing iron. The liver and brain
contain the largest amounts of copper in the human body. However, other
organs contain smaller amounts.
Copper is classified as an essential mineral. If the body does not acquire a
sufficient amount of copper, hemoglobin production is decreased and copper
anemia can result. Various enzyme reactions require copper as well. In the
body, the liver and brain contain the largest amounts of copper with other
organs containing smaller amounts. Copper imbalances can produce various
symptoms, inefficient utilization of iron and protein, diarrhea, high
cholesterol, thyroid problems, stunted growth, mental and emotional
problems, just to name a few.
Nutritional copper is believed to be beneficial in helping overcome chronic
inflammation, grey hair, cancer, parasites, arthritis, skin wrinkles, and
joint problems such as arthritis, bursitis, and rheumatism.
The following information was
sourced from the
Linus Pauling Institute
Copper (Cu) 75ppm
is an essential trace element for humans and animals. In the body,
copper shifts between the cuprous (Cu1+) and the 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 the
scavenging of free radicals. Although Hippocrates is said to have
prescribed copper compounds to treat diseases as early as 400 B.C.,
scientists are still uncovering new information regarding the functions
of copper in the human body.
Copper is a
critical functional component of a number of essential enzymes, known as
cuproenzymes. Some of the physiologic functions known to be
copper-dependent are discussed below.
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
Connective tissue formation
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 plays a role in bone formation.
copper-containing enzymes, ceruloplasmin (ferroxidase I) and ferroxidase
II 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. Although the
ferroxidase activity of these two cuproenzymes has not yet been proven
to be physiologically significant, the fact that iron mobilization from
storage sites is impaired in copper deficiency supports their role in
Central nervous system
A number of
reactions essential to normal function of the brain and nervous system
are catalyzed by cuproenzymes.
Neurotransmitter synthesis: Dopamine-b-monooxygenase catalyzes the
conversion of dopamine to the neurotransmitter norepinephrine.
of neurotransmitters: Monoamine oxidase (MAO) plays a role in the
metabolism of the neurotransmitters norepinephrine, epinephrine, and
dopamine. MAO also functions in the degradation of the neurotransmitter
serotonin, which is the basis for the use of MAO inhibitors as
and maintenance of myelin: The myelin sheath is made of phospholipids
whose synthesis depends on cytochrome c oxidase activity.
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.
dismutase: 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. 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 in high levels in the lungs and low levels in blood plasma.
Ceruloplasmin: 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.
Regulation of gene expression
Copper-dependent transcription factors regulate transcription of
specific genes. Thus, cellular copper levels may affect the synthesis of
proteins by enhancing or inhibiting the transcription of specific genes.
Genes regulated by copper-dependent transcription factors include genes
for copper/zinc superoxide dismutase (Cu/Zn SOD), catalase (another
antioxidant enzyme), and proteins related to the cellular storage of
Adequate copper nutritional status appears to be 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 (probably in
the form of ceruloplasmin) is required for iron transport to the bone
marrow for red blood cell formation (see Iron Metabolism). 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.
Zinc: High supplemental zinc intakes of 50 mg/day or more for extended
periods of time may result in copper deficiency. High dietary zinc
increases 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 intestinal
copper absorption. High copper intakes have not been found to affect
zinc nutritional status.
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.
Although vitamin C supplements have produced copper deficiency in
laboratory animals, 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 2 months resulted
in a significant decline in ceruloplasmin oxidase activity. In the other
study, supplements of 605 mg of vitamin C/day for 3 weeks resulted in
decreased ceruloplasmin oxidase activity, although copper absorption did
not decline. Neither of these studies found vitamin C supplementation to
adversely affect copper nutritional status.
evident or frank copper deficiency is relatively uncommon. Serum copper
levels and ceruloplasmin levels may fall to 30% of normal in cases of
severe 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. The anemia is thought to result
from defective iron mobilization due to decreased ceruloplasmin
activity. Copper deficiency may also result in abnormally low numbers of
white blood cells known as neutrophils (neutropenia), a condition that
may be accompanied by increased susceptibility to infection.
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
Individuals at risk of deficiency
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.
High-risk individuals include: premature infants, especially those with
low-birth weight, infants with prolonged diarrhea, infants and children
recovering from malnutrition, individuals with malabsorption syndromes,
including celiac disease, sprue, and short bowel syndrome due to
surgical removal of a large portion of the intestine. Individuals
receiving intravenous total parenteral nutrition or other restricted
diets may also require supplementation with copper and other trace
elements. Recent research indicates that cystic fibrosis patients may
also be at increased risk of copper insufficiency.
Take the recommended dosage of water soluble minerals with a full glass
of water, juice or other liquid.
For best results refrigerate after opening and use within six months.
However you can keep in a cool and dry location and away from direct
light, but do not freeze. Keep safely away from children. Do not keep in
bathroom medicine cabinet. Heat and dampness may alter the action of the