Selenium is an essential trace mineral that serves as a cofactor for 25 selenoproteins, including glutathione peroxidase (GPx) and thyroxine deiodinase (thyroid hormone activation). Our research highlights a critical lesson: the NPC trial (1996) suggested selenium reduced prostate cancer by 63%, but the massive follow-up SELECT trial (35,533 men) found NO cancer prevention benefit — and actually showed a non-significant INCREASE in type 2 diabetes. The therapeutic window is narrow: deficiency impairs immunity and thyroid function, but excess (>400mcg/day) causes selenosis. Form matters enormously — selenomethionine is well-absorbed but can accumulate; selenite/selenate are better regulated.
Selenium is incorporated as selenocysteine (the "21st amino acid") into 25 selenoproteins: (1) glutathione peroxidases (GPx1-6) — the primary cellular antioxidant defense system; (2) thioredoxin reductases — redox regulation; (3) iodothyronine deiodinases — convert T4 (inactive) to T3 (active thyroid hormone) and deactivate excess T3; (4) selenoprotein P — selenium transport protein and antioxidant. In Hashimoto's, selenium supplementation may reduce autoimmune thyroid inflammation by reducing oxidative damage to thyroid tissue.
No critical interactions at standard doses.
Reviewed by the Scan Dose Research Team and Clinical Advisory Board | Last updated:
Not medical advice. Based on published clinical research and systematic reviews.