Copper

Copper is a trace mineral required for iron transport (via ceruloplasmin), mitochondrial cytochrome c oxidase, neurotransmitter synthesis, and connective tissue crosslinking. Both deficiency and excess have distinct clinical syndromes; the main real-world deficiency scenario is zinc-induced copper deficiency, which is under-recognised.

Daily requirements

Zinc-induced copper deficiency

Chronic zinc intake above ~50 mg/day induces metallothionein in the intestinal mucosa, which preferentially binds copper and prevents its absorption. Case reports abound of adults developing severe copper deficiency causing myelopathy (progressive spastic gait), sensory ataxia, and cytopenias after months to years of high-dose zinc — sometimes from denture-fixation creams that contained zinc, more commonly from OTC zinc lozenges taken for immunity. If you take zinc > 25 mg/day chronically, take a copper supplement too (1–2 mg copper per 15 mg zinc).

Copper deficiency signs

Wilson's disease

Autosomal recessive mutation of the ATP7B copper transporter causes copper accumulation in the liver, brain, and cornea. Presents with liver failure, movement disorders, and Kayser-Fleischer corneal rings. Treated with copper-chelation (penicillamine, trientine) or zinc (which blocks copper absorption — the same mechanism that causes iatrogenic deficiency in healthy adults).

Menkes disease

X-linked ATP7A mutation causing severe copper deficiency in infancy. Kinky-hair appearance, progressive neurologic decline, connective tissue defects; usually fatal in early childhood despite copper histidinate treatment. Very rare.

Food sources

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Not medical advice. New numbness, unsteady gait, or unexplained anaemia in someone taking chronic high-dose zinc — check serum copper, ceruloplasmin, and stop the zinc. Progression to myelopathy can be irreversible.

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