Copper (Cu) is an essential trace mineral to humans. The majority of the body’s copper is in the Cu2+ form. The human body contains about 1.4 to 2.1 mg of copper per kg of body mass.
Since the body cannot synthesize copper, a diet must supply steady amounts for absorption. Copper is absorbed in the small intestine and then transported to the liver bound to albumin. After processing within the liver, copper is propagated to other tissues in a second phase by protein ceruloplasmin, which carries the majority of copper in blood. In healthy individual, about 1 mg per day absorbed from foods and excreted from the body.
The importance of the functional quality of copper to accept and donate electrons explains its vital role in oxidation-reduction reactions (redox) and in scavenging free radicals. Copper fuses with specific proteins to produce enzymes that act as catalysts for a number of body functions, including energy production, transformation of melanin for pigmentation and to form cross-links in collagen and elastin which is extremely important for connective tissues maintenance and repairs.
Recent nutrition surveys have shown that the diets of 25% or more of adolescents, adults, and elderly, do not meet the recommended daily intake of copper [srs]. Additional copper supplementation is generally not needed for healthy adults, however, those who are affected by even minor in symptomathology digestive issues or use zinc supplements or zinc containing denture adhesives, may require additional supplementation.
If copper deficiency is present as determined via mineral hair analysis and 24-hour urine copper tests, the copper supplementation needs to be taken to normalize the copper stores first, then further maintained with 8:1 zinc/copper supplementation while monitoring the levels of both zinc and copper every 3-6 months via hair mineral analysis test.
The RDA for copper in healthy adults is up to 3mg per day. In individuals with digestive disorders, an additional copper supplementation may be required. The International Program on Chemical Safety, a World Health Organization-associated agency, stated in 1966 “there is greater risk of health effects from deficiency of copper intake than from excess copper intake.”
Copper toxicity does not normally occur in humans because of transport systems that regulate absorption and excretion. Chronic copper toxicity can mostly only occur due to autosomal recessive genes mutations such as seen in Wilson’s disease, which can also be confirmed via a high 24-hour urinary copper levels. A severe case of liver cirrhosis can also contribute to copper toxicity if the Wilson’s disease is present with two inherited genes mutations. Other causes of copper toxicity can be the continuous use of copper plumbing, pots, pans, utensils and inorganic molecules such as cupric oxide that present in vitamin supplements.
An example of chronic copper poisoning that lead to liver failure was in a young adult man with no known genetic susceptibility who consumed 30–60 mg/d of copper as a mineral supplement for 3 years [Eur. J. Med. Res. 4: 252]. On the other hand, no effects on liver enzymes, oxidative stress and other biochemical markers have been reported in healthy young volunteers given daily doses of 6 to 10 mg/d of copper for up to 12 weeks [srs].
However, it is important to understand that organic copper from foods and its free bio-inactive form accumulation are processed by liver, which also processes all other trace minerals. If the liver cannot process and excrete the excess minerals via bile, toxicity of MULTIPLE minerals will be present on the tests, and not necessarily the copper alone.
In healthy individuals, additional supplementation should not exceed 3mg/day for limited time unless provisioned by a doctor.
In mild or moderate cases of copper deficiency, mineral hair analysis and 24-hour urine copper test are most reliable. Serum copper levels may remain normal unless there is a severe copper deficiency, whereas the ceruloplasmin levels may be border low, indicating the presence of the condition.
Common causes of copper deficiency
If insufficient amounts of copper are present in the diet, copper stores in the liver will become depleted and a copper deficiency will lead to disease or tissue injury.
- Celiac disease or gluten intolerance
- Low stomach acid
- Intestinal dysbiosis
- H. Pylori overgrowth
- Pancreatic insufficiency or significant liver disorders
- Hypercalcemia leading to digestive disorders
- Menkes disease (starts in infancy)
- Nutritional imbalances including vegetarianism, low-birth-weight infants, infants fed cow’s milk instead of breast milk or fortified formula
- Zinc supplementation of 50 mg/day or more for extended periods of time
- Vitamin C (ascorbic acid) supplementation in high doses [srs]
- High fructose diet
Copper deficiency symptoms and conditions
- Susceptibility to fungal and bacterial infections due to transitional or sustained deficiency of neutrophils (neutropenia) [srs1] [srs2]
- General fatigue and sometimes poor motor coordination
- Weight gain
- Neurological dysfunctions
- Anemia is a clinical marker of copper deficiency, and iron has been found to build up in the liver with copper deficiency, indicating that copper is required for iron transport to the bone marrow for red blood cell formation
- Hypopigmentation [srs]
- Low or border low ceruloplasmin levels
- Connective tissues and bone disorders resulting in chronic pain
- Coronary heart disease
- Digestive disorders including pancreatic insufficiency
- Osteoporosis and osteoarthritis
- Rheumatoid arthritis
- Heart and cardiovascular disease
Copper rich foods
The best dietary sources of copper are liver (beef), other organ meats, seafood, whole grains, legumes, chocolate, nuts (especially brazils and cashews), seeds (especially poppy and sunflower), grains such as wheat and rye, fruits (including lemons, raisins, coconuts, papaya and apples), cereals, potatoes, peas, red meat, mushrooms and kale. Meat and fish may contain sufficient copper to provide up to 50% of the required copper intake in a balanced diet.