Benefits
Antioxidant defense
Selenoproteins including glutathione peroxidases (GPx1–4) neutralize hydrogen peroxide and lipid hydroperoxides, protecting cell membranes and DNA from oxidative damage.
Thyroid hormone metabolism
Iodothyronine deiodinases are selenoenzymes that convert inactive T4 to active T3. Selenium deficiency impairs thyroid hormone activation and may accelerate autoimmune thyroid disease.
Immune function
Selenium enhances proliferation of T and NK cells, promotes cytokine production, and supports the oxidative burst in macrophages. Deficiency is associated with increased susceptibility to viral infections.
Cancer risk reduction
Epidemiological studies suggest inverse relationship between selenium status and cancer incidence, particularly colorectal and prostate cancers. Mechanism involves DNA repair and apoptosis induction.
Mechanism of action
Selenoprotein synthesis
Selenium is incorporated as selenocysteine (the 21st amino acid) into over 25 selenoproteins via a unique UGA codon recoding mechanism. These proteins serve antioxidant, anti-inflammatory, and metabolic functions.
Glutathione peroxidase activation
Selenium is the catalytic center of GPx enzymes that reduce hydrogen peroxide and organic hydroperoxides to water and alcohols using glutathione as the electron donor, directly protecting against oxidative cell damage.
Thioredoxin reductase activity
Selenium-containing thioredoxin reductases maintain thioredoxin in its reduced state, enabling DNA synthesis, peroxiredoxin recycling, and transcription factor regulation.
Clinical trials
RCT of 200 µg/day selenomethionine vs placebo in 70 patients with autoimmune thyroiditis (Hashimoto's) for 3 months. Outcomes: anti-TPO antibodies, thyroid ultrasound. (Gärtner et al. 2002, J Clin Endocrinol Metab)
70 Hashimoto's patients.
Selenium reduced anti-TPO antibody titers and improved thyroid ultrasound echogenicity vs placebo. Note: subsequent CATALYST trial (2019) and other replications have shown mixed effects on clinical outcomes (overt hypothyroidism prevention not clearly established). Modest evidence; ATA does not strongly endorse selenium for routine Hashimoto's management.
Large RCT (SELECT — Selenium and Vitamin E Cancer Prevention Trial) of selenium (200 µg/day selenomethionine) and/or vitamin E in 35,533 men. (Lippman et al. 2009, JAMA — or related)
35,533 men. Long-term follow-up.
PRIMARY ENDPOINT NEGATIVE: neither selenium, vitamin E, nor combination reduced prostate cancer incidence vs placebo. Secondary findings: vitamin E ALONE INCREASED prostate cancer risk (~17%); selenium showed potential harm signal in subgroups (T2DM risk). CRITICAL CONTEXT: this large rigorous trial reversed earlier enthusiasm for selenium chemoprevention. Selenium supplementation in selenium-replete populations may HARM rather than help.