Selenium

Selenium is incorporated into proteins as the amino acid selenocysteine (the 21st amino acid), forming a class of enzymes called selenoproteins — 25 encoded in the human genome. Key members include the glutathione peroxidases (GPx1-GPx4), which neutralise reactive oxygen species, and the thioredoxin reductases (TxnRD1-3); three iodothyronine deiodinases (DIO1-3) regulate T4-to-T3 thyroid hormone conversion. The functional marker of adequacy is saturation of selenoprotein P (SELENOP) at plasma concentrations around 110 µg/L — the threshold used in the Nordic Nutrition Recommendations 2023 to define optimal intake (75-90 µg/day). A U-shaped dose-response is evident: deficiency (serum selenium below 90 µg/L) associates with accelerated epigenetic aging on DunedinPACE and GrimAge clocks in the Berlin Aging Study II (Vetter et al. 2025, n=1,568); excess carries independent risk — a case-control study (Le et al. 2024) identified a safe window of 111-124 µg/day with elevated cancer risk at both extremes. The SELECT trial (Klein et al. 2011, n=35,533) tested 200 µg/day L-selenomethionine in men with replete selenium; neither selenium nor vitamin E reduced prostate cancer incidence, showing supplementation in nutrient-replete populations does not extrapolate from deficiency-correction data.