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Selenium is an essential trace element whose antioxidant role is mediated through its incorporation into selenoproteins, most notably glutathione peroxidases (GPx) and thioredoxin reductases (TrxR). These enzymes neutralize reactive oxygen species (ROS) and regenerate key antioxidants, constituting a central pillar of the body's enzymatic antioxidant defense. Human clinical and observational studies consistently show that selenium deficiency reduces GPx activity and elevates oxidative stress markers, while supplementation in deficient populations restores these activities.
Selenium has the strongest single-supplement evidence for Hashimoto's autoimmune thyroiditis. A 2024 meta-analysis of 35 RCTs found consistent TPO antibody reductions of 20–40% over 6+ months. Selenium maintains glutathione peroxidase activity, supports T-regulatory cell function, and deficiency correlates with higher autoimmune incidence.
Selenium deficiency is documented in celiac disease patients on long-term gluten-free diet in a 2019 PMC systematic review of micronutrient deficiencies in compliant CeD patients. Whole grains are a primary dietary source of selenium, and their exclusion from the GFD reduces selenium intake. The 2023 Birmingham Gastroenterology Associates guidance identifies selenium deficiency in CeD as contributing to thyroid dysfunction and immune function impairment.
Selenium deficiency is inversely correlated with cervical dysplasia severity in multiple observational studies. A 2015 randomized double-blind placebo-controlled trial (n=58, biopsy-proven CIN1) found 200 mcg/day selenium yeast for 6 months produced significantly higher CIN1 regression (88% vs. 56% placebo; p=0.01). An expression of concern was later published for this trial; the 2023 MDPI micronutrients review identified selenium as having among the stronger evidence for a protective role in CIN.
Selenium is an essential trace element for antioxidant defense (glutathione peroxidases) and thyroid hormone metabolism, with IOM-established RDAs for children. NIH ODS-funded label analysis found selenium in the 13 core nutrients at or above RDA in most children's MVMs. It is a standard ingredient in pediatric multivitamin formulas.
Selenium is an essential trace element that exerts documented anti-inflammatory effects primarily through its incorporation into selenoproteins, which regulate oxidative stress and key inflammatory signaling pathways. Clinical evidence from randomized controlled trials and meta-analyses shows selenium supplementation can reduce circulating inflammatory markers—notably CRP and IL-6—particularly in populations with elevated baseline inflammation. Evidence strength varies by route of administration and population, with intravenous selenium showing more consistent CRP-lowering effects than oral supplementation in critically ill patients.
Observational studies link lower selenium status with cognitive decline and dementia risk, including Alzheimer's disease, supported by the brain's priority maintenance of selenium even during systemic deficiency. A systematic review and meta-analysis of 11 studies found some improvement in cognitive tests in MCI patients receiving selenium supplementation. However, the large PREADViSE RCT found no significant benefit of selenium supplementation for dementia prevention. Evidence remains inconsistent, with selenium status appearing relevant but supplementation not clearly beneficial in adequately nourished populations.
Selenium is an essential trace element critical for glutathione peroxidase activity, a key antioxidant enzyme in COPD airways. Multiple authoritative reviews identify selenium deficiency as a risk factor for COPD progression. A PMC review of vitamins, minerals, and antioxidants in COPD specifically lists selenium as protective against chronic lung disease. Dietary selenium intake is inversely associated with COPD risk in epidemiological studies.
Multiple observational studies link low selenium intake or status with increased depressive symptoms, and some clinical trials show improvement with supplementation. A 2022 systematic review and meta-analysis (20 studies) found mixed results: supplementation showed a positive effect in some RCTs but a neutral effect in others. An optimal serum range (~82–85 µg/L) was associated with reduced depressive symptomatology in a study of 978 young adults. The proposed mechanism involves selenium's role in antioxidant defense via glutathione peroxidase and redox homeostasis.
Selenium is an antioxidant trace mineral that protects the ocular surface and lacrimal gland from oxidative stress relevant to DED. It is included in validated DED multivitamin formulations showing significant clinical benefit. A 2024 Frontiers in Pharmacology systematic review confirmed selenium as one of ten evidence-supported nutrients for dry eye management.
Reduced selenium concentrations in blood, plasma, and white cells, along with decreased glutathione peroxidase activity, have been documented in atopic dermatitis patients. A 2020 systematic review and meta-analysis found significantly lower selenium levels in atopic dermatitis patients versus controls (SMD −2.62). However, a double-blind RCT in 60 adults found no significant clinical improvement in eczema severity after 12 weeks of selenium supplementation at 600 µg/day. Evidence links selenium deficiency to atopic dermatitis pathophysiology but supplementation trials have not demonstrated consistent clinical benefit.
Selenium is an essential trace mineral that serves as a cofactor for antioxidant selenoproteins (glutathione peroxidases). One single RCT confirmed selenium supplementation was effective in reducing endometriosis-associated pain. Lower selenium levels have been observed in women with endometriosis compared to controls.
Selenium is an essential trace element required for testosterone biosynthesis and the structural integrity of sperm via selenoproteins including PHGPx (expressed in sperm midpiece). RCTs show selenium supplementation (alone or combined with NAC) significantly improves sperm count, motility, and morphology in infertile men. A 2025 systematic review confirmed selenium improved sperm motility vs. placebo.
Selenium is a trace mineral critical for antioxidant defense via glutathione peroxidase (GPx). Low serum and follicular selenium levels are associated with higher infertility occurrence. A double-blind RCT of antioxidant supplementation including selenium improved viable pregnancy rates in women undergoing ICSI.
Selenium is an essential trace mineral incorporated into selenoproteins including glutathione peroxidase, which protects hair follicle cells from oxidative stress. Both deficiency and excess cause hair loss. Correcting deficiency restores hair growth; selenium is included in clinical combination supplements for androgenetic alopecia and telogen effluvium.
Selenium is a trace mineral essential for antioxidant selenoproteins (GPx, thioredoxin reductase) and immune function. NHANES data show each 20 µg/day increase in dietary selenium is associated with 0.42% longer telomere length in older adults. The PNAS longevity vitamins framework identifies selenium as a triage longevity mineral, and clinical trials support its role in reducing age-related oxidative damage.
Selenium is an antioxidant mineral whose deficiency is linked to increased hearing loss risk. Selenium, along with zinc, has been shown to exert a clinically favorable effect on tinnitus intensity in patients with low levels of these minerals. A 2019 PubMed review identified selenium deficiency as a risk factor for hearing loss.
Selenium has been studied for cardiovascular protection given its role as an antioxidant via selenoproteins, with evidence from observational studies and RCTs. A meta-analysis of prospective studies demonstrated a nonlinear association between blood selenium and cardiovascular disease risk, with benefit observed within a narrow selenium range (55–145 µg/L). The KiSel-10 RCT showed that combined selenium and CoQ10 supplementation significantly reduced cardiovascular mortality in elderly Swedes with low baseline selenium. Evidence from trials is inconsistent across populations with differing baseline selenium status.
Selenium is an essential trace element that forms an extremely stable, insoluble compound with mercury (mercury selenide), effectively sequestering it and relieving symptoms of mercury toxicity. Selenium supplementation has been shown to increase mercury excretion and is recognized by PMC reviews as an important adjunct in heavy metal (especially mercury) detoxification.
Selenium is an essential cofactor for selenoprotein-based deiodinases and glutathione peroxidases required for thyroid hormone activation and oxidative protection of thyroid tissue. Multiple meta-analyses of RCTs encompassing over 2,300 Hashimoto's patients demonstrate significant reductions in TPO antibody titers and TSH with supplementation. Typical doses studied are 100–200 µg/day of selenomethionine or sodium selenite.
Selenium is an essential trace mineral required for synthesis of glutathione peroxidase and thioredoxin reductase—key antioxidant enzymes protecting hepatocytes from oxidative damage. Selenium deficiency impairs liver detoxification capacity and is associated with worse outcomes in liver disease. Clinical studies show selenium supplementation reduces oxidative stress markers and liver enzymes in hepatitis patients.
Selenium is an essential trace mineral and cofactor for glutathione peroxidase (GPx), a primary antioxidant enzyme in the retina. Observational studies suggest that adequate dietary selenium intake may reduce AMD risk. A clinical study on AMD used a supplement combining melatonin, zinc, and selenium with documented benefit. Selenium is included in AMD-specific clinical trial supplement formulations, and the Cochrane antioxidant review lists it alongside zinc and vitamins as an antioxidant with observational AMD associations.
Selenium is incorporated into selenoproteins including mitochondrial thioredoxin reductase and glutathione peroxidase, which protect the ETC from oxidative damage. It is also involved in mitochondrial biogenesis. A 4-year RCT combining selenium and CoQ10 in elderly individuals showed improved vitality, physical performance, and quality of life.
Selenium deficiency has been identified in patients with chronic pancreatitis, and selenium-containing antioxidant combinations have been studied in multiple RCTs for chronic pancreatitis pain relief. A double-blind placebo-controlled RCT (n=36) using a combination including organic selenium showed significant pain reduction and quality of life improvement in chronic pancreatitis patients. The clinical evidence for selenium as part of antioxidant cocktails (with vitamins C, E, beta-carotene, methionine) is supported by systematic reviews.
Selenium supplementation has been studied in multiple RCTs for PCOS, showing reductions in testosterone, hirsutism, CRP, and oxidative stress markers. A 2023 systematic review and meta-analysis of RCTs confirmed selenium's effects in PCOS. It is listed among evidence-supported minerals in major PCOS supplement reviews.
Selenium is an essential trace mineral critical for glutathione peroxidase activity and thyroid function, both of which are impaired during illness. Deficiency is associated with more severe respiratory illness, and post-illness selenium restoration supports immune reconstitution.
Selenium is an essential trace element with antioxidant and immunomodulatory roles, and clinical evidence supports its use in post-viral recovery. A 2021 post-COVID observational study found selenium-containing supplementation reduced fatigue and improved quality of life. A 2024 review confirmed selenium among the most promising trace elements for COVID-19 rehabilitation.
Selenium is an essential trace mineral with critical roles in antioxidant defense via glutathione peroxidases, thyroid hormone metabolism, and immune function. Blood selenium levels decline during pregnancy without supplementation. Poor selenium status is associated with miscarriage, preeclampsia, preterm delivery, and gestational diabetes. Evidence-based prenatal supplement recommendations (PMC 8229801, 2021) specifically recommended selenium supplementation during pregnancy.
Selenium has been investigated for prostate cancer prevention based on strong preclinical evidence and an earlier observational study suggesting cancer-protective effects. The large SELECT trial (35,533 men) found neither selenium nor vitamin E reduced prostate cancer incidence after 7 years. Subsequent analysis suggests benefit may be restricted to men with low baseline selenium status. Selenium is included in authoritative prostate supplement reviews.
Selenium is an essential trace mineral forming selenoproteins that protect prostatic cells from oxidative damage. The PROCOMB multicenter RCT (n=225) found saw palmetto + lycopene + selenium combination improved IPSS and maximum urinary flow beyond single therapies at 12 months. The SPRITE non-inferiority study (n=404) found saw palmetto + selenium + lycopene was non-inferior to tadalafil for LUTS relief. A 2019 BPH nutraceutical review confirmed selenium reduces prostatic inflammation histologically.
Multiple case-control studies consistently document significantly lower selenium levels in blood and serum of psoriasis patients versus healthy controls, with the deficit correlating with disease severity scores. A large study of 336 psoriatic patients and 336 matched controls found psoriasis risk was highest at the lowest selenium concentrations (OR up to 10.3). A 2020 systematic review and meta-analysis also confirmed significantly lower selenium in psoriasis patients. Intervention data with selenium supplementation in psoriasis are sparse and no conclusive benefit from supplementation has been established.
Selenium deficiency has been linked to elevated osteopontin (OPN) levels, which can impair bone health. A study cited in a US patent (US10073101) for scoliosis prevention/treatment, and a Wiley InterScience-referenced study, found many idiopathic scoliosis patients have low selenium and high OPN. Supplementation with 200 mcg/day as L-selenomethionine has been proposed to lower OPN and slow curve progression, though a Chinese cohort study also found high environmental selenium was a risk factor, indicating a complex dose-dependent relationship.
Selenium is an essential trace mineral that functions as a component of antioxidant selenoproteins (glutathione peroxidase, thioredoxin reductase), contributing to protection of skin cells against UV-induced oxidative damage. A 7-week human study using a carotenoid/antioxidant complex including organic selenium significantly increased actinic erythema threshold by 20% (p=0.01) and reduced UV-induced p53 expression, sunburn cell count, and lipid peroxidation.
Selenium is incorporated into selenoproteins essential for thyroid function, including the three iodothyronine deiodinases (DIO1, DIO2, DIO3) that convert prohormone T4 to active T3, and glutathione peroxidases that protect thyroid tissue from oxidative damage. The thyroid contains the highest selenium concentration per gram of any human tissue. Selenium supplementation reduces thyroid peroxidase antibodies in Hashimoto's thyroiditis.
Selenium is an essential trace mineral that functions in antiviral immune defense through incorporation into selenoproteins including glutathione peroxidase and thioredoxin reductase. Selenium deficiency is associated with increased viral mutation rates and disease severity. Multiple studies link selenium status to viral infection outcomes including HIV, influenza, and COVID-19.
Selenium is an antioxidant trace element incorporated into combination supplementation protocols for vitiligo. An animal study in autoimmune vitiligo mice using zinc, selenium, vitamins A/C/E, and polyphenols produced 70% repigmentation. Selenium is listed among antioxidant vitamins and minerals studied for vitiligo in peer-reviewed literature including the Frontiers in Nutrition Mendelian randomization study (2023).
Selenium is an essential trace mineral incorporated into selenoproteins including thioredoxin reductase and glutathione peroxidase, which protect follicle cells from oxidative damage. Deficiency is associated with androgenetic alopecia in systematic reviews. However, excess selenium causes hair loss (selenosis), making the therapeutic window narrow.
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