Copper is an important mineral in antioxidant activity, bone formation, wound healing, melanin production, coagulation, and neurotransmitter synthesis. Sources of dietary copper include vegetables, legumes, grains, fish, poultry, and other meat. Copper deficiency is usually due to decreased absorption or excess ingestion of zinc, ascorbic acid, or iron, which can chelate copper. Copper is solubilized via interaction with gastric acid and then absorbed through the proximal small bowel. It is stored in the liver. Due to its widespread availability in food sources and the body's ability to maintain long-term copper storage, deficiency from decreased dietary ingestion is quite uncommon in the United States.

Patients who have undergone gastric surgery (either gastrectomy or gastric bypass) are at risk for copper deficiency as they may insufficiently mobilize copper from food sources due to limited acid exposure. Patients with small bowel malabsorption such as small bowel Crohn disease, celiac disease, or protein-losing enteropathies are also at an increased risk. Patients with cirrhosis may be at risk for copper deficiency as copper is stored in the liver. Patients on dialysis or parenteral nutrition, premature infants on supplementary formula with no added copper, and patients taking excess zinc or chelating agents are all at risk of copper deficiency. Penicillamine and excess oral zinc supplementation are iatrogenic causes of copper deficiency as these agents chelate copper, which results in excess excretion.

Copper deficiency may present with changes in the hair and skin. Hair changes include alterations in hair pigmentation, pili torti, and patchy alopecia. Cutaneous findings may be nonspecific and may include impaired wound healing, seborrheic dermatitis, and generalized leukoderma. Systemic findings include anemia and neutropenia. Fatigue may occur due to microcytic anemia as well as peripheral neuropathy.

See Menkes kinky hair syndrome for discussion of inherited copper deficiency.