Approximate dose-response bands. Individual response varies — these are starting points, not prescriptions.
Well below target. Risk of deficiency symptoms tied to iron metabolism.
Below the recommended daily target. Long-term adequacy not assured.
Daily target met. Standard nutritional support for iron metabolism.
Common for specific health goals. Check the evidence for your situation before sustaining this level.
Approaching the tolerable upper limit. Monitor and consider clinical guidance.
Above the tolerable upper limit. Risk of adverse effects — back off or consult a clinician.
You're at 0% of your copper target. The biggest single-serving sources to top it off:
Trace mineral required for iron metabolism, connective tissue, neurotransmitter synthesis, and antioxidant defence. Body content is small (~80 mg, mostly liver and brain). Most often discussed in the context of zinc supplementation — chronic high-dose zinc depletes copper, with consequences ranging from microcytic anemia to myelopathy.
Copper cycles between Cu+ and Cu2+ states, accepting and donating electrons in metalloenzymes. Ceruloplasmin uses copper to oxidise Fe2+ to Fe3+ for transport on transferrin — explaining why copper deficiency mimics iron deficiency anemia (refractory to iron alone). Wilson disease (ATP7B mutation) causes copper accumulation in liver and brain; Menkes disease (ATP7A) causes systemic copper deficiency.
Spontaneous deficiency is rare in unsupplemented adults but is increasingly recognised after gastric bypass, with long-term zinc supplementation, and in malabsorption.
Acute toxicity from copper-contaminated water or supplements causes GI distress; chronic excess (Wilson disease) drives hepatic and neurological damage.
Copper bisglycinate or copper sulfate at 1–2 mg/day is sufficient as a counterweight to zinc supplementation. A common ratio is 1 mg copper per 10–15 mg zinc when both are supplemented chronically.
~25–55% absorbed in proximal small intestine; absorption is upregulated when stores are low. High-dose zinc induces metallothionein in enterocytes, which traps copper and prevents transfer to blood — the mechanism behind zinc-induced copper deficiency.
Adequacy supports iron metabolism, antioxidant defence (Cu-Zn SOD), and connective tissue (lysyl oxidase). Modest deficiency is increasingly common in older adults on chronic zinc and may contribute to anemia and neurological symptoms typically attributed to other causes.
Cytochrome c oxidase, ceruloplasmin, iron transport.
The mechanisms and systems this nutrient feeds. Click any to drill into what runs on it.
Whole foods that contribute meaningfully (≥10% DV per 100 g serving). Click any food to see its full nutrient profile and what else it brings to the table.
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