The recommended dietary allowance for copper is 0.9 mg per day for adults, yet many individuals following contemporary Western dietary patterns fall significantly short of this threshold. The problem intensifies in populations taking high-dose zinc supplements, which competitively inhibit copper absorption, or those avoiding organ meats and shellfish—foods that provide substantial copper bioavailability.
This nutritional gap carries metabolic consequences. Without adequate copper, iron mobilisation stalls, leading to functional iron deficiency characterised by fatigue, weakness, and cognitive impairment despite seemingly adequate iron stores. The deficit becomes particularly pronounced in refined-food-dominant diets, where micronutrient density is inherently compromised.
Clinical assessment of copper status—including serum copper, ceruloplasmin levels, and dietary history—should accompany iron studies when patients fail to respond to standard iron replacement therapy. Recognising and correcting copper insufficiency may unlock therapeutic efficacy in previously treatment-resistant cases.
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