Patients prescribed iron supplements often expect relief from fatigue and weakness, yet some experience no improvement despite adequate iron levels on laboratory tests. The culprit may not be iron itself, but copper—an overlooked mineral essential for making iron biologically available.
Copper-dependent enzymes, particularly ceruloplasmin and hephaestin, catalyse the oxidation of iron from its inactive to active form, enabling it to bind to transferrin for transport through the bloodstream. Without sufficient copper, iron becomes functionally trapped in tissues, rendering even high iron stores useless for oxygen transport. This mechanism explains treatment-resistant anaemia in patients with ostensibly normal ferritin levels.
Clinicians are increasingly recognising that comprehensive anaemia assessment must extend beyond iron panels to include copper status evaluation, particularly in patients on high-dose zinc supplementation or following restrictive diets low in organ meats and shellfish—primary copper sources.
Read the full article on GMJ Newsroom.
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