Copper

Copper is an essential trace mineral. The NIH, the US National Institutes of Health, says enzymes called cuproenzymes need it. They use it to make energy, handle iron, build connective tissue and make nerve messengers. The body’s defense against oxidative damage depends mainly on the copper-containing superoxide dismutases (see antioxidants).

An adult body holds only 50 to 120 mg of copper, almost two-thirds of it in the skeleton and muscle. A carrier protein called ceruloplasmin holds more than 95% of the copper in blood plasma.

Most readers do not know how tightly the body steers its copper. In a 90-day study of 11 young men, the share absorbed was 55.6% on a low-copper diet (0.785 mg a day). It was 36.3% on an adequate one (1.68 mg) and 12.4% on a high one (7.53 mg).

Typical US diets meet or exceed the 900 mcg (microgram) allowance, and deficiency is uncommon. When it does happen, the causes are specific. They are stomach or bowel surgery, celiac disease, an inherited disorder called Menkes disease, and long-term high zinc intake, including zinc from some denture creams.

The evidence is lopsided. Deficiency is well documented in case series (reports on groups of patients). It causes anemia, low white blood cell counts and a spinal cord disease that can resemble vitamin B12 deficiency. Blood counts usually recover with copper.

Trials of copper supplements in healthy people are few and small. Studies of heart disease and Alzheimer’s disease disagree with each other. This page sets out what the studies show.

Health benefits of copper

• ★★★Eight approved EU health claimsThe EU allows copper claims such as normal connective tissues, nervous system and iron transport. They describe normal body function, not treatment.
• ★★Supplements did not change blood cholesterolIn 5 trials with 176 people, copper supplements did not clearly change total, LDL (“bad”) or HDL (“good”) cholesterol. A small effect cannot be ruled out.
• ★★Copper in drinking water upset stomachsIn 1,365 adults, water with 6 mg/L of copper caused more nausea, vomiting, diarrhea and stomach pain. In 60 women, nausea, pain or vomiting came at 3 mg/L or more.
• ★Copper supplement did not change thinking in Alzheimer’sIn 68 people with mild Alzheimer’s, a year of copper supplements (8 mg a day, as copper orotate) did not change thinking test scores. It was a small trial.
• ★Little change in heart-risk markers with copper supplementsIn middle-aged adults with moderately high cholesterol, 8 weeks of copper glycinate (2 mg of copper a day) did not clearly change cholesterol or homocysteine. In 16 healthy young women, 6 mg a day as copper sulfate cut PAI-1, a clotting-related factor, by about 30%.

Foods high in copper

Oysters lead the per-serving ranking on this page: 3 oz (85 g) holds 1.34 mg. That is 149% of the 0.9 mg Daily Value, the FDA label amount, and 100 g holds 1.58 mg. Next per serving come soybeans (0.7 mg per cup), adzuki beans, cashews and chickpeas.

Per 100 g the order changes, because seeds and nuts are dense but eaten in small portions. Sesame seeds (4.08 mg) and cocoa powder (3.79 mg) lead, followed by cashews, sunflower seeds, Brazil nuts and hazelnuts. The ranking below has the full list.

The NIH lists higher values for some foods than our ranking shows. Pan-fried beef liver holds 12.4 mg in 3 oz (1,378% of the Daily Value), and cooked wild eastern oysters 4.85 mg in 3 oz. Unsweetened baking chocolate has 0.938 mg in 1 oz, a medium cooked potato 0.675 mg and cooked shiitake mushrooms 0.65 mg per half cup. Beef liver is not among the foods ranked here.

Copper in food varies with growing conditions and processing. Tap water adds a variable amount (0.0005 to 1 mg/L, the NIH says).

Copper from plant foods is absorbed well. In rats, copper from sunflower seeds, peanuts, cooked shrimp and cooked beef was absorbed as well as copper sulfate. In a 63-day study of men, phytate and fiber did not change absorption. High-dose zinc supplements, on the other hand, can block it.

How copper works

Most of the biochemistry below is well established. But it comes from reviews, small isotope studies in people, and cell and animal work, not from trials of extra copper. Five ideas cover most of it.

Copper is built into enzymes, and the body tunes absorption to intake. The gut and liver pass it along, and two genes can fail. Copper lets iron move, and too much zinc blocks it. Here is each one, and what has been seen in people.

It is built into enzymes

Copper is a cofactor (a helper) for cuproenzymes, the NIH says. They work in energy production, iron metabolism, activating neuropeptides, building connective tissue and making neurotransmitters. Copper is also involved in blood vessel growth (angiogenesis), brain development, pigmentation and immune function. The body’s defense against oxidative damage depends mainly on the copper-containing superoxide dismutases.

That is why EU claims range from normal connective tissue and skin pigmentation to protection of cells from oxidative stress (see antioxidants). An excess of copper in cells can generate free radicals. So cells pass it on with chaperone proteins that deliver it to where it is used.

The body tunes absorption to how much you eat

Most copper is absorbed in the upper small intestine. A review puts absorption at 30% to 40% of the copper in typical diets of industrialized countries, through a carrier-mediated transport system. How much is absorbed depends strongly on how much is eaten.

In a 90-day isotope study of 11 young men, absorption fell from 55.6% on 0.785 mg a day to 36.3% on 1.68 mg. It was 12.4% on 7.53 mg. Most of the men reached copper balance on about 0.8 mg a day. The NIH describes the same pattern: about 75% at 400 mcg a day, falling to 12% at 7.5 mg a day.

Most copper leaves the body in bile, and total losses in the stool are about 1 mg a day.

Phytate holds back zinc, but it did not change copper absorption in a 63-day study of young men. Absorption was 35.0% from the basal diet, 31.4% with added phytate and 34.1% with added cellulose.

The gut and liver pass it along, and two genes can fail

Gut cells take in copper with a transporter called CTR1, and a pump called ATP7A moves it into the blood. In the liver, ATP7B puts copper onto ceruloplasmin for the blood or sends it into bile, according to a review of copper metabolism. Faults in these two pumps cause the two classic copper diseases.

Menkes disease is a rare X-linked recessive disorder caused by ATP7A mutations. Absorption of dietary copper drops sharply. The signs include failure to thrive, seizures and unusually kinky hair, and most children die by age 3 without treatment, the NIH says.

In Wilson disease, which is autosomal recessive, ATP7B mutations let copper pile up in the liver, brain and other organs. This causes liver disease and neurologic and psychiatric symptoms.

Both are treated by specialists. Copper injections started in the first weeks of life can improve survival in Menkes disease. Wilson disease is treated with chelation therapy (drugs that bind copper) or zinc salts, which reduce copper overload in different ways.

European liver guidelines note that no randomized trial in Wilson disease has had an optimal design, so advice rests on large case series. Neither disease is caused by diet, and people who have them need specialist care rather than the general advice on this page.

It lets iron leave cells

Iron leaves cells through the exporter ferroportin as Fe2+, but transferrin, the main iron carrier in blood, binds Fe3+ much better. Three copper-containing enzymes known in humans turn one into the other: ceruloplasmin, hephaestin and zyklopen. Hephaestin in gut cells lets dietary iron into the blood, and the release of iron from the liver relies on ceruloplasmin.

This is one way copper deficiency can disturb how the body handles iron. In 4 patients with acquired copper deficiency and liver abnormalities, 2 had cirrhosis or advanced fibrosis. The other 2 had iron overload in the liver, which the authors tie to the loss of ceruloplasmin. These are case reports, so the frequency of this problem is unknown.

Too much zinc blocks it

High zinc intake can interfere with copper absorption, and excessive use of zinc supplements can lead to copper deficiency, the NIH says. In perfused rat intestine, very high zinc in the gut lowered copper in the intestinal cells and the copper passed on to the blood. High-zinc diets raised the copper bound to metallothionein.

In people, 50 mg of zinc a day for 6 weeks lowered a copper enzyme in healthy men. The NIH notes similar falls at about 60 mg a day for up to 10 weeks.

In case series, people with copper deficiency often had high blood zinc. In a Scottish review, 12 of 16 did, and 9 used zinc-containing dental fixatives. The NIH names this as one reason the US upper limit for zinc is 40 mg a day.

What has been seen in people

The clearest findings are about deficiency. In case series, too little copper caused anemia, low white blood cells and spinal cord disease. In a national Scottish review, 93% of the blood count problems responded, but only 25% improved in nerve function, so early treatment matters. In Menkes disease, early copper injections raised survival.

Outside deficiency the results are thin or conflicting. Small trials in healthy adults raised copper enzymes without moving cholesterol, and a meta-analysis of five trials found no effect on blood lipids. The one Alzheimer’s trial found no effect on thinking.

Observational studies of heart disease point both ways. The studies of blood copper in Alzheimer’s disease cannot say whether copper is a cause or a result. All of these are among the study cards above.

How much copper do you need?

Adults need 900 mcg (0.9 mg) of copper a day in the US. That is the Recommended Dietary Allowance (RDA), which covers nearly all healthy people and is the same for men and women. EFSA sets adequate intakes of 1.6 mg a day for men and 1.3 mg for women.

Needs rise in pregnancy and breastfeeding. For ages 19 and older the US values are 1,000 mcg in pregnancy and 1,300 mcg while breastfeeding. For ages 14 to 18 they are 890 mcg, rising to the same 1,000 and 1,300 mcg. EFSA sets 1.5 mg a day for both.

Older adults have the same target as other adults: the US allowance does not change for ages 19 and up. Most people reach it. US adults eat about 1,400 mcg (men) and 1,100 mcg (women) a day from food.

In survey data from 2009 to 2012, 6% to 15% of adults who did not take a copper-containing supplement ate less than the average requirement. Among supplement users it was 2.2% to 7.2%.

Copper deficiency: signs and who is at risk

Copper deficiency is uncommon. Based on animal and human studies, the NIH lists many effects. They include anemia, loss of pigment, high cholesterol, connective tissue disorders, osteoporosis, unsteady walking and a higher risk of infection.

In case series the usual picture is a pair of problems. The first is blood changes: anemia, low white blood cell counts and sometimes low platelets. The second is a spinal cord disease with trouble walking. Both can be mistaken for other diseases, such as vitamin B12 deficiency or a bone marrow disorder called myelodysplastic syndrome.

• Stomach, bowel and weight-loss surgery. A Mayo Clinic review covered 40 patients with copper deficiency and blood abnormalities. Of them, 25% had had weight-loss surgery and 35% other stomach or bowel surgery. A meta-analysis put deficiency at 16% to 28% of patients 1 to 4 years after weight-loss surgery. A systematic review of 17 studies of the first 12 months judged most to be of low quality, so the true rate is uncertain.
• High zinc intake. People who regularly take high doses of zinc supplements or use excessive amounts of zinc-containing denture cream can develop copper deficiency, the NIH says. In a Scottish review, 12 of 16 people with copper deficiency had high blood zinc.
• Celiac disease. In a study of 200 adults and children with celiac disease, 15% had copper deficiency. The American College of Gastroenterology notes that copper levels normalize within a month of adequate supplementation on a gluten-free diet, the NIH reports.
• Menkes disease. This rare inherited disorder sharply reduces copper absorption (see how copper works above).

Copper status is not routinely checked, and the NIH says no biomarker assesses it accurately and reliably. Doctors usually measure serum copper (normal range 10 to 25 µmol/L, or 63.5 to 158.9 mcg/dL). They also measure ceruloplasmin (180 to 400 mg/L). Both can be changed by estrogen, pregnancy, infection, inflammation and some cancers, so results are read together with symptoms.

A review adds a 24-hour urine copper test. Copper deficiency anemia is treated with oral or intravenous copper. Blood changes are fully reversible over 4 to 12 weeks, but nerve damage is only partly reversible.

Forms of copper: absorption and effects

Copper supplements come as several compounds. The NIH lists cupric oxide, cupric sulfate, copper amino acid chelates and copper gluconate. It says no studies have compared the bioavailability (how well the body absorbs them) of these and other forms. The Linus Pauling Institute, in a page reviewed in July 2024, says the same.

Products range from a few micrograms to 15 mg of copper, which the NIH calls about 17 times the Daily Value.

The honest bottom line is that we found no trial in people that compared one copper form with another. We found none that tested a form for a health outcome either. The one form with a documented drawback is cupric oxide, which dissolves poorly. EFSA judged its bioavailability to be lower than that of other inorganic copper sources.

A 1999 commentary in the Journal of Nutrition argued that cupric oxide should not be used as a copper supplement for animals or humans. Claims that copper bisglycinate or other chelated forms are absorbed better have no human trial behind them that we found.

The forms used in the main trials on this page were:

• Alzheimer’s disease trial. Copper(II) orotate dihydrate, 8 mg of copper a day for 12 months.
• Heart-marker trials. Copper glycinate (2 mg a day for 8 weeks) and copper sulfate (3 and 6 mg a day for 4 weeks each).
• Drinking-water trials. Copper sulfate added to tap water in the trial of 60 women. The abstract of the 1,365-adult trial does not name the form.
• Deficiency treatment. A review names oral or intravenous copper as gluconate, sulfate or chloride. The case-series abstracts do not name the form.
• AREDS eye trial. 2 mg of copper as cupric oxide, together with 80 mg of zinc as zinc oxide.

Form	Share of copper by weight	What studies show	Source
Copper in food	Not applicable	The NIH lists shellfish, seeds and nuts, organ meats, wheat-bran cereals, whole grains and chocolate as the richest sources. People absorb 30% to 40% of the copper in typical diets, and the share falls as intake rises (55.6% to 12.4% in one isotope study). In rats, copper from several foods was absorbed as well as copper sulfate.	1, 5, 6, 7
Cupric oxide	About 80% (2 mg of copper = 2.5 mg of oxide, per EFSA)	Dissolves poorly. EFSA judged its bioavailability lower than other inorganic sources but expects some absorption, and the makers gave no specific data. A 1999 commentary argued against its use. The AREDS eye tablet used 2 mg as cupric oxide. We found no human absorption comparison.	3, 4, 15
Cupric sulfate	Not stated	Soluble. EFSA cites 25% to 60% absorption for mostly soluble copper salts such as sulfate. At 3 and 6 mg a day for 4 weeks, it raised serum copper and a copper enzyme in 16 women. In drinking water at 3 mg/L or more, it went with nausea or stomach pain. Named as a treatment form for deficiency.	3, 9, 12, 14
Copper gluconate	Not stated	In 7 adults, 10 mg of copper a day for 12 weeks changed no copper level and caused no more side effects than placebo. Named as a treatment form for deficiency. We found no absorption comparison with other forms.	8, 14
Copper glycinate and other amino acid chelates	Not stated	Glycinate at 2 mg a day for 8 weeks raised two copper enzymes against placebo in adults with moderately high cholesterol. No human trial compared a chelate with another form. In 2009 EFSA said it could not assess the safety of copper amino acid chelate in food supplements from the dossiers supplied.	1, 10, 16

Three studies bear directly on forms. None compares two supplement forms in people. They are an EFSA opinion on the oxide, a small trial of the gluconate form, and a rat study that compared foods with copper sulfate.

Is copper safe? Supplements, dose and interactions

Copper from food is not a concern for most people. The NIH says copper toxicity is rare in healthy people who do not have an inherited copper-handling defect. Cases have followed water that stood in copper pipes.

For adults, the US tolerable upper intake level (UL) is 10,000 mcg (10 mg) a day from food and supplements. The UL is the most a day unlikely to cause harm, and it was set to prevent liver damage.

It is 8 mg for ages 14 to 18, including pregnancy and breastfeeding at those ages. For younger children it is 5 mg at 9 to 13, 3 mg at 4 to 8 and 1 mg at 1 to 3. In pregnancy and breastfeeding at 19 and older it is 10 mg.

No limit is set for infants, who should get copper only from breast milk, formula and food. The limits do not apply to people given copper as treatment under a doctor’s care.

In the EU, the Scientific Committee on Food set an upper level of 5 mg a day for adults in 2003. EFSA adopted it in 2006, and EFSA’s August 2025 overview of upper levels still lists it.

EFSA’s Scientific Committee gave a new opinion in 2023, adopted in November 2022. It said the 10 mg a day used in earlier risk assessments can no longer be considered a no-effect level. It concluded that no copper build-up in the body is expected at 5 mg a day. It set an acceptable daily intake of 0.07 mg per kg of body weight, equal to 5 mg a day for adults.

That figure is an acceptable daily intake, not a formal upper level. The opinion says upper levels for each age group are to be set separately.

• Doses and side effects. Chronic high intake can cause liver damage and stomach and bowel symptoms such as abdominal pain, cramps, nausea, diarrhea and vomiting. In a 12-week double-blind trial, 7 adults on 10 mg a day as gluconate showed no change in copper levels. They had no more side effects than placebo. In 9 men who added 7 mg a day to their diet for 129 days, some copper and immune measures changed. They included a lower antibody response to an influenza vaccine, and the authors say the meaning is unknown.
• Drinking water. The WHO guideline value is 2 mg/L. It protects against acute stomach effects, with a margin of safety, in people with normal copper handling. Copper stains laundry above 1 mg/L, and the taste turns bitter above 2.5 mg/L. Standing or partly flushed water in copper plumbing is often above 1 mg/L, while running or fully flushed water tends to be low. Infants fed formula mixed with tap water are most exposed. The US EPA action level is 1.3 mg/L (1.3 ppm). If more than 10% of sampled taps exceed it, the water system must take steps to control corrosion. In trials, nausea or stomach pain rose at 3 mg/L or more in 60 women and at 6 mg/L in 1,365 adults.
• Inherited disorders. People with Wilson disease, biliary atresia or biliary cirrhosis should avoid supplemental copper, the Linus Pauling Institute advises. It says copper for infants should be approached with caution. Wilson disease needs lifelong specialist treatment.
• Zinc. Long-term high doses of zinc can cause copper deficiency, as described above. The AREDS eye tablet paired 80 mg of zinc with 2 mg of copper as cupric oxide.
• Alzheimer’s disease. The NIH reports that experts at a 2013 conference suggested people at higher risk of Alzheimer’s disease choose multivitamins without copper or iron. It adds that much more research is needed. Our study cards above show no benefit or harm from 8 mg a day in one small trial.
• Medicines. The NIH says copper is not known to have clinically relevant interactions with medications.

How to get more copper

• Best food. Oysters give 1.34 mg in 3 oz, 149% of the Daily Value, and the NIH lists pan-fried beef liver at 12.4 mg in 3 oz. Cashews give 0.62 mg per ounce and sunflower seeds 0.51 mg.
• Let absorption do its work. The body absorbed 55.6% of copper on a low-copper diet and 12.4% on a high one. Phytate and fiber did not change absorption in one trial. Zinc supplements of 50 mg a day for 6 weeks lowered a copper enzyme in healthy men.
• Food first, supplements for a reason. Most US adults reach the allowance from food. Supplements are mainly for deficiency found by a doctor, and total intake should stay under 10 mg a day (5 mg in the EU). After weight-loss surgery or long-term zinc use, ask your doctor whether to check copper.

History of copper

Two inherited copper diseases were described long before the nutrient role of copper was clear. In 1912 Kinnier Wilson published a long paper in the journal Brain on progressive lenticular degeneration. It described a familial nervous disease associated with cirrhosis of the liver. The disease now carries his name and is known to be caused by mutations in the gene ATP7B.

In 1962 Menkes and colleagues described a sex-linked recessive disorder with retardation of growth, peculiar hair, and focal cerebral and cerebellar degeneration. It is now called Menkes disease and is caused by ATP7A mutations.

The nutritional story starts in 1928. That year Hart, Steenbock, Waddell and Elvehjem published a paper titled “Copper as a supplement to iron for hemoglobin building in the rat” in the Journal of Biological Chemistry. Nutrition Reviews later listed it among its nutrition classics.

The modern reference values are recent. In 2008 a study reported that newborns with Menkes disease treated with copper in the first weeks had far better survival than late-treated patients. EFSA set European adequate intakes for copper in 2015, and in 2023 its Scientific Committee re-evaluated the existing guidance values for copper.

Frequently asked questions about copper

How much copper per day for a woman?

Adult women need 900 mcg (0.9 mg) of copper a day in the US, the same as men. The allowance rises to 1,000 mcg in pregnancy and 1,300 mcg while breastfeeding (ages 19 and older). EFSA gives 1.3 mg for adult women and 1.5 mg in pregnancy and while breastfeeding. The US upper limit is 10 mg a day from food and supplements.

Can too much zinc cause copper deficiency?

Yes: the NIH says high zinc intakes can interfere with copper absorption. A copper enzyme fell in healthy men taking 50 mg of zinc a day for 6 weeks. Case series describe anemia, low white blood cells and nerve damage. In a Scottish review, 12 of 16 people with copper deficiency had high blood zinc and 9 used zinc-containing dental fixatives. The US upper limit for zinc, 40 mg a day, was set partly for this reason.

Which foods are highest in copper?

The NIH lists pan-fried beef liver first, at 12.4 mg in 3 oz, ahead of cooked wild oysters (4.85 mg in 3 oz). In our USDA ranking, oysters lead per serving (1.34 mg in 3 oz), followed by soybeans, adzuki beans and cashews. Sesame seeds (4.08 mg) and cocoa powder (3.79 mg) lead per 100 g. Nuts, seeds, chocolate, mushrooms and potatoes add up over a day.

Is copper in drinking water a concern?

Usually not, but water that has stood in copper pipes can carry enough to upset the stomach. The WHO guideline value is 2 mg/L and the US EPA action level is 1.3 mg/L. In a trial of 60 women, 17% and 15% reported nausea, abdominal pain or vomiting at 3 and 5 mg/L. With no added copper it was 5%, and the WHO notes that running or fully flushed water tends to contain less.

Do copper supplements help heart health or Alzheimer’s disease?

No trial shows that they do. Small trials in healthy adults raised copper enzymes without changing cholesterol, and a meta-analysis of five trials found no effect on blood lipids. In 68 people with mild Alzheimer’s disease, 8 mg a day for a year did not change thinking scores. Observational studies disagree. Higher blood copper went with more coronary heart disease and with Alzheimer’s disease, while a US cohort linked higher dietary copper to lower death rates.

What is the best form of copper supplement?

No form has been shown to be better. The NIH and the Linus Pauling Institute say no human study has compared the bioavailability of cupric oxide, sulfate, gluconate and amino acid chelates. The one form with a documented drawback is cupric oxide, which dissolves poorly, according to EFSA. Supplements are mainly for deficiency found by a doctor.

Can copper deficiency be mistaken for vitamin B12 deficiency?

Yes. In 13 adults, copper deficiency caused a spinal cord disease that resembled the disease seen in vitamin B12 deficiency. Its blood changes can look like a bone marrow disorder, and a very low ceruloplasmin was the first clue. In a Scottish review, 93% of blood count problems responded to copper, but only 25% of patients improved in nerve function. So early diagnosis matters.

What are Menkes disease and Wilson disease?

Both are rare inherited disorders of copper handling. In Menkes disease (ATP7A), absorption is sharply reduced and the body runs short. Early copper injections raised survival to 92%, against 13% in late-treated patients. In Wilson disease (ATP7B), copper builds up in the liver and brain, and treatment is chelation or zinc. Neither is caused by diet, and people with Wilson disease should avoid supplemental copper.