Copper

What is copper and what does it do in the body?

Copper is an essential mineral. According to the NIH Office of Dietary Supplements, it is a cofactor of cuproenzymes involved in energy production, iron metabolism, neuropeptide activation, connective tissue synthesis, and neurotransmitter synthesis. Ceruloplasmin, the most abundant cuproenzyme, plays a role in iron metabolism and carries more than 95% of the copper in healthy human plasma. Copper also takes part in angiogenesis, neurohormone balance, regulation of gene expression, brain development, pigmentation, and immune function; defense against oxidative damage rests mainly on copper-containing superoxide dismutases. ^[1]

About two-thirds of the body’s copper is in the skeleton and muscle; total copper in an adult is 50–120 mg and only small amounts are stored. Most copper is excreted in bile; total fecal loss of bile-derived and unabsorbed dietary copper is about 1 mg per day. Copper level is kept in balance by absorption from the intestine and release by the liver into bile. ^[1]

Copper status is not routinely assessed in clinical practice, and no biomarker that measures copper status accurately and reliably has been identified; plasma copper and ceruloplasmin are affected by estrogen status, pregnancy, infection, inflammation, and some cancers. NIH gives normal serum copper as 10–25 µmol/L (63.5–158.9 µg/dL) and ceruloplasmin as 180–400 mg/L. ^[1]

That a mineral works in an enzyme does not mean that taking more than the requirement would make that enzyme work better. In this guide, “role in the body,” “deficiency,” and “effect of supplementation” are treated as separate questions.

How much copper is needed daily?

The US Food and Nutrition Board (FNB), on which NIH relies, has set a recommended dietary allowance (RDA) of 900 µg for adults; it is 1,000 µg in pregnancy and 1,300 µg in lactation. EFSA gives an “adequate intake” (AI) level for adults. TÜBER 2022 also lists copper as an AI. ^{[1] [3] [2]}

The NIH RDA for ages 14–18 is 890 µg. ^[1] The values of the institutions are the product of different types (RDA and AI) and derivation methods; they are intended for population-level planning and are not individual dose recommendations. ^[3]

Which foods contain copper?

According to NIH, the richest food sources are shellfish, seeds and nuts, organ meats, whole-grain products, whole grains, and chocolate. The bioavailability of copper depends on the amount in the diet: it is 75% in a diet containing 400 µg of copper per day and 12% in a diet containing 7.5 mg. Tap water and other beverages can also contain copper (0.0005–1 mg/L). ^[1] TÜBER Table 2.2 gives the sources of copper as “red meat, shellfish, dried legumes, whole grains, and nuts.” ^[2] According to NIH, the average copper US adults get from food is 1,400 µg per day in men and 1,100 µg in women; in NHANES 2009–2012, 6–15% of adults who did not use supplements and 2.2–7.2% of those who used supplements consumed copper below the estimated average requirement (EAR). ^[1]

According to NIH, the amount of copper in supplements varies from a few micrograms to 15 mg (about 17 times the Daily Value); forms such as cupric oxide, cupric sulfate, amino acid chelates, and copper gluconate are used, and there are no studies comparing the bioavailability of these forms. ^[1]

Who develops copper deficiency?

NIH states that copper deficiency is uncommon in humans; its effects include anemia, hypopigmentation, hypercholesterolemia, connective tissue disorders, osteoporosis and other bone defects, abnormal lipid metabolism, ataxia, and increased risk of infection. ^[1] TÜBER Table 2.2 also lists inadequacy as “elevated blood cholesterol, increased risk of infection, pigmentation disorder, anemia like iron deficiency.” ^[2]

The groups NIH lists as at risk of deficiency are as follows. In celiac disease, in one study of 200 adults and children (69.9% reported following a gluten-free diet), copper deficiency was found in 15% because of malabsorption due to changes in the intestinal surface; NIH reports that the American College of Gastroenterology’s 2009 celiac guideline states that people with celiac disease are at increased risk of copper deficiency and that copper levels returned to normal within a month after a gluten-free diet together with adequate copper supplementation. Menkes disease and high-dose zinc use are the other groups (below). ^[1]

The nervous system dimension of acquired copper deficiency has been described in a review: according to a 2010 review examining 55 case reports from the literature, copper deficiency myelopathy is a treatable non-compressive myelopathy closely resembling subacute combined degeneration in B12 deficiency; cases were seen mostly in the fifth and sixth decades and in women (F:M = 3.6:1); risk factors are previous upper gastrointestinal surgery, excess zinc, and malabsorption syndromes, and in 20% no cause could be identified. Cytopenia was found in 78% of cases and spinal MRI abnormality in 47%; the diagnosis was confirmed by low serum copper and ceruloplasmin levels. These findings rest on case reports. ^[5]

What is the relationship between zinc and copper?

According to NIH, high dietary zinc can block copper absorption and excess zinc supplementation can cause copper deficiency; even with a moderately high zinc intake such as about 60 mg per day, a decrease in erythrocyte copper-zinc superoxide dismutase, an indicator of copper status, has been reported for up to 10 weeks. People who regularly take zinc supplements at high doses or who overuse zinc-containing denture creams can develop copper deficiency; this is one of the reasons the FNB set the zinc UL for adults at 40 mg per day. ^[1]

In a report describing three cases, anemia and neutropenia (severe in two) developed in three men aged 47, 21, and 42, and progressive peripheral neuropathy in two cases; bone marrow examination suggested copper deficiency and it was determined to be due to excess zinc; the second case was taking zinc supplements because of acrodermatitis enteropathica. ^[6] These are isolated case reports; they do not show prevalence or a dose-response relationship.

Copper treatment in Menkes disease

Menkes disease is a rare X-linked recessive disorder caused by ATP7A mutations that disrupts copper homeostasis; copper absorption from the intestine is markedly reduced. According to NIH, if untreated most patients die by age 3; subcutaneous copper injections started in the first weeks after birth can reduce the risk of death and improve development. ^[1] In a prospective study published in NEJM, among 12 newborns in whom copper replacement was started within 22 days after birth, survival was 92% at a median follow-up of 4.6 years, while among 15 historical controls with late diagnosis and late treatment, survival was 13% at a median follow-up of 1.8 years; normal neurodevelopment and myelination were found in two of the 12 patients. The comparison was made with historical controls; the authors note that those carrying a mutation that does not completely abolish ATP7A function may respond particularly well to copper treatment. ^[7]

Is copper supplementation useful for Alzheimer’s and cardiovascular health?

According to NIH, the results of observational studies examining the relationship between copper and cardiovascular disease are mixed: in Italy, among 1,197 people aged 45–64, diastolic blood pressure and total and LDL cholesterol were significantly lower in the highest copper intake tertile (2.29 mg/day) than in the lowest tertile (1.12 mg/day), whereas in a second NHANES analysis of 4,574 participants, the risk of death from coronary heart disease was 2.87 times higher in the highest serum copper quartile (≥137 µg/dL) than in the lowest quartile. A few small studies examining the effect of copper supplementation on cardiovascular risk factors in healthy adults found very little effect, and no clinical trial of copper supplementation has been conducted in people at increased risk. NIH considers the evidence insufficient for any conclusion. ^[1]

In Alzheimer’s disease, NIH reports conflicting observations on copper: some reports found low copper and copper-dependent enzyme activity in the brains of patients, others found high copper; in meta-analyses, serum copper was found to be higher in people with Alzheimer’s than in controls. In a 12-month randomized, double-blind, placebo-controlled, pilot phase 2 study in 68 patients with mild Alzheimer’s, no significant difference was found in the primary cognitive endpoints (ADAS-Cog, MMSE) between the group given 8 mg of copper per day (copper orotate dihydrate) and placebo; the treatment was well tolerated, and the authors reported that oral copper intake had neither a negative nor an accelerating effect on disease progression. ^[8] The study is a single, small trial; the result points toward “no benefit shown.”

Is excess copper harmful?

According to NIH, long-term high copper exposure can cause liver damage and digestive complaints such as abdominal pain, cramps, nausea, diarrhea, and vomiting. Toxicity is rare in healthy people without an inherited defect of copper homeostasis; copper toxicity has been reported with water left standing in copper pipes and fittings. The US Environmental Protection Agency has set the recommended upper limit for public water systems at 1.3 mg/L. ^[1]

NIH’s tolerable upper intake level (UL) is based on levels associated with liver damage: it is 10,000 µg/day for ages 19 and over, including pregnancy and lactation (8,000 µg for ages 14–18). The UL does not apply to people taking copper supplements under medical supervision and is an upper limit for customary daily intake. ^[1] In EFSA’s 2025 UL summary (based on the Scientific Committee on Food 2003), the UL for adults is 5 mg/day; no UL is defined for pregnancy and lactation (ND). ^[4] TÜBER Annex 1.5.5 also lists 5 mg for adults. ^[2] The two figures come from different institutions and differ by a factor of two.

NIH states that there are no known clinically significant drug interactions for copper. ^[1]

What is Wilson disease?

Wilson disease is a rare autosomal recessive disorder caused by an ATP7B mutation that impairs copper excretion and leads to copper accumulation in tissues; liver and nervous system damage, cirrhosis, acute hepatitis, hemolytic crisis, and liver failure can develop. According to NIH, lifelong copper chelation therapy or high-dose zinc can prevent permanent organ damage. ^[1] The 2025 EASL-ERN guideline describes Wilson disease as an autosomal recessive disorder of copper metabolism affecting the liver, brain, and other organs; it states that pharmacological treatment includes chelators (penicillamine, trientine) and zinc salts, and that chelators alone are recommended in significant liver disease. ^[9] This treatment is managed by physicians and is unrelated to copper supplementation.

How are copper supplements and drinking water regulated in Türkiye?

Ministry of Agriculture and Forestry approval is mandatory for every food supplement to be placed on the market in Türkiye. ^[14] According to Article 5 of Communiqué 2013/49 as amended by 2015/44, vitamins and minerals can be used only if listed in Annex-1 and in the forms in Annex-2; daily maximum limits are determined in accordance with Annex-3 on the basis of the label declaration, and in products containing vitamins and minerals the amount stated on the label is at least 15% of the nutrient reference value for ages 11 and over. ^[11] Statements claiming to prevent, treat, or cure disease cannot appear in labeling, presentation, and advertising. ^[12]

The main table of the Ministry’s Restricted Substances List (September 21, 2026) does not contain a separate row with a daily amount limit for copper as a mineral; in the table “Sources Used Before December 31, 2025 for Vitamins and Minerals,” “chemical synthesis” is shown as the source for “Copper (µg).” The “Sodium Copper Chlorophyllin” row in the same list covers a separate compound and is not within the scope of the mineral copper. ^[13]

For drinking water, the chemical parameters list of the Regulation on Waters Intended for Human Consumption, published in the Official Gazette of February 17, 2005, contains a parametric value of 2 mg/L for copper. ^[10] The US public water system limit reported by NIH is 1.3 mg/L; the two values belong to different countries and regulations. ^[1]

Evidence table: claim, population, and limits

A personal dose or supplementation decision for copper is made by evaluating zinc use, conditions affecting absorption, liver status, and total intake together; this guide does not recommend personal doses.