Zinc, Copper, and Selenium: The Trace-Mineral Hair Panel Decoded

Trace mineral deficiencies are a correctable cause of hair shedding that can coexist with AGA. The clinical utility of testing and the specific biology of each mineral.

Trace minerals are required as enzyme cofactors, structural components, and regulatory molecules throughout follicle biology. Unlike macronutrients where chronic deficiency is usually visible, trace mineral deficiencies can be subclinical — producing hair shedding as an early sign before other manifestations are obvious.

Zinc: the most clinically relevant

Zinc is the most studied trace mineral in hair loss. It is a cofactor for more than 300 enzymes, including RNA polymerase enzymes essential for follicle matrix cell proliferation. Zinc also modulates androgen receptor function — zinc finger domains in the androgen receptor require zinc for correct DNA binding. Interestingly, zinc inhibits 5-AR activity in vitro, though the in vivo relevance of this effect at physiological levels is unclear.

Clinical zinc deficiency presents with diffuse telogen effluvium that may be clinically indistinguishable from other TE causes. Resolution with zinc repletion is typically seen within three to six months. Serum zinc testing is the standard clinical assessment; zinc protoporphyrin is a more sensitive marker of functional zinc status. Food sources: red meat, shellfish (oysters highest), legumes, nuts, seeds.

Copper: structural cofactor

Copper-dependent enzymes are critical for hair shaft structural integrity. Lysyl oxidase (copper-dependent) cross-links keratin fibres in the hair cortex; deficiency produces structurally weak, lusterless hair that breaks easily. Tyrosinase (copper-dependent) catalyses melanin synthesis; copper deficiency contributes to loss of hair pigmentation. Copper deficiency in adults is uncommon but can occur with malabsorption, excessive zinc supplementation (zinc competes with copper for intestinal absorption via metallothionein), and post-bariatric surgery.

Selenium: narrow window

Selenium is incorporated into selenoproteins including glutathione peroxidases and thioredoxin reductases that protect follicle cells from reactive oxygen species. Selenium deficiency produces telogen effluvium. Selenium toxicity (selenosis) from excessive supplementation also causes diffuse hair loss — the same symptom as deficiency. This non-monotonic dose-response makes selenium supplementation without established deficiency genuinely risky. Confirm deficiency before supplementing. RDA is 55 mcg/day; toxicity threshold approximately 400 mcg/day.