Selenium: A Comprehensive Reference
1. Identity and Chemical Characterization
Element and Chemical Nature
Selenium, discovered in 1817 by Jöns Jacob Berzelius, is known as an element with two faces in relation to human health: as a micronutrient essential for life and a potentially toxic trace element. He named selenium after the Greek goddess of the moon, Selene. Selenium (chemical symbol Se, atomic number 34) is a nonmetallic element belonging to Group 16 (chalcogens) of the periodic table, chemically analogous to sulfur. Selenium is a trace mineral that is essential to good health but required only in small amounts.
Chemical Forms
Selenium exists in both inorganic and organic forms, each with distinct biological properties and bioavailability profiles.
- Inorganic forms: Inorganic selenium exists in different forms, including selenate (SeO₄²⁻), selenite (SeO₃²⁻), selenide (Se⁻), and elemental selenium (Se⁰).
- Organic forms: Organic selenium is primarily represented by selenoamino acids, such as selenomethionine (SeMet) and selenocysteine (SeC), where selenium substitutes sulfur in the structures of methionine and cysteine, respectively. Additionally, methylselenocysteine (MeSeCys), which contains a methyl group along with selenium replacing sulfur, has been recognized as a major source of naturally occurring organic selenium in plant-based foods for over a quarter of a century.
- Selenomethionine (SeMet): Selenomethionine is a naturally occurring amino acid. The L-selenomethionine enantiomer is the main form of selenium found in Brazil nuts, cereal grains, soybeans, and grassland legumes.
- Selenocysteine (SeC): Selenocysteine is the 21st proteinogenic amino acid; selenoproteins contain selenocysteine residues. It is an analogue of the more common cysteine with selenium in place of the sulfur. Selenocysteine was discovered in 1974 by biochemist Thressa Stadtman at the National Institutes of Health.
Distribution in Foods
Soil and groundwater contain inorganic forms of selenium (e.g., selenites, selenates) that plants accumulate and convert to organic forms, mostly selenomethionine and selenocysteine and their methylated derivatives. In foods, selenium is present primarily as selenomethionine along with selenocysteine.
Various chemical forms of selenium are found in selenium accumulators, including selenate, selenomethionine, selenocysteine, selenium-methyl-selenocysteine, and γ-glutamyl-selenium-methyl-selenocysteine. Although the two latter compounds are predominant in plants of the Allium and Brassicaceae families (which include garlic, onion, and broccoli), wheat, other grains (including Brazil nuts), and soy are rich in selenomethionine and contain smaller amounts of selenocysteine and selenate.
Selenomethionine is the main form in plants, while selenocysteine is the main form in foods of animal origin. The richest food source of selenium is Brazil nuts; it is also found in organ meats, seafood, muscle meat, and mushrooms.
Soil Dependence
Certain groups of people may have trouble getting enough selenium, including those who eat diets that consist mostly of plant foods grown in local soils that are low in selenium, because the amount of selenium in soil affects the selenium content of foods. Selenium deficiency is very rare in the United States and Canada.
2. Historical and Traditional Context
Discovery and Early History
Selenium had a long road from its initial discovery to its recognition as an essential nutrient. It was first identified in 1817, when Swedish chemist Jöns Jacob Berzelius was trying to pinpoint a toxic substance that was causing illness among workers in a sulfuric acid plant—which turned out to be selenium.
This element has a long and unsavory history of use as a dietary component. Its first description as being deleterious for animals to ingest was reported by Marco Polo in the late 13th century. In his travels in Western China, Marco Polo wrote about an illness that his "beasts of burden" acquired wherein their hooves became brittle and fell off after eating certain plants. These plants most likely were seleniferous plants, which absorb large quantities of selenium from the soil and store the selenium in their tissues.
Our understanding of selenium's significance in human health has evolved over the past 200 years since its discovery in 1817. Previously considered a carcinogen, selenium is now recognized as a crucial nutrient with a narrow therapeutic-to-toxic range.
Recognition as an Essential Nutrient and the Keshan Disease Story
The basic importance of selenium in both normal growth and reproduction in animals was not discovered until the 1950s. The pivotal connection between selenium deficiency and human disease came from China, where endemic selenium-deficiency conditions were studied in the 20th century.
Keshan disease is an endemic congestive cardiomyopathy, characterized by cardiac insufficiency, heart enlargement, arrhythmia, and electrocardiographic modifications. It was first identified in 1935 in Keshan County, Heilongjiang Province, northeast China. Keshan disease is a type of congestive cardiomyopathy characterized by symptoms like heart failure, cardiac enlargement, ECG irregularities, gallop rhythm, and cardiogenic shock. This condition predominantly impacts children and women of reproductive age. Initially discovered in areas of China plagued by selenium deficiency, Keshan disease was associated with a significant morbidity rate of 50%, often accompanied by occurrences of mortality. Additional factors such as chemical exposure or the presence of Coxsackievirus frequently compounded the severity of the disease.
Extensive cross-sectional epidemiological studies showed that low selenium concentrations in cereal grains and low selenium status of local residents were associated with the occurrence of Keshan disease. Several large population-based intervention trials using oral administration of sodium selenite tablets showed significant reduction of Keshan disease incidence. Based on this evidence, it was concluded that selenium deficiency is the major cause of Keshan disease, although other etiological factors could not be ruled out.
In certain regions in rural China, where the soil is deficient in selenium, maladies such as Keshan disease, a cardiomyopathy primarily in children, were found. Similarly, Kashin–Beck disease, a chronic, endemic osteochondropathy, was found primarily in southwestern to northeastern China. Keshan disease has been virtually eradicated in China by supplementing the diets of the populations residing in specific rural areas where the soil selenium was deficient.
3. Common Forms and Preparations as a Dietary Supplement
Forms of selenium that are commonly found in dietary supplements include selenomethionine, selenium-enriched yeast, sodium selenite, and sodium selenate. Common forms include selenomethionine, selenium-enriched yeast (grown in a high-selenium medium, predominantly as selenomethionine), sodium selenite, and sodium selenate.
The doses of selenium in multivitamin/mineral supplements vary, but many contain 55 mcg. The amount of selenium is often higher in supplements with fewer ingredients. For example, supplements that combine selenium with vitamin E or other ingredients generally contain 50 to 200 mcg of selenium. Selenium-only supplements typically contain 100 to 400 mcg.
The human body absorbs up to about 90% of selenium from selenomethionine, selenium-enriched yeast, selenite, and selenate. Several studies have suggested that the organic form of selenium (i.e., selenomethionine) is more bioavailable and less toxic than its inorganic form (i.e., sodium selenite). It was determined in a clinical trial that selenomethionine is absorbed 19% better than selenite.
4. Key Constituents, Active Compounds, and Mechanisms of Action
The Selenoproteome
The human genome encodes 25 selenoprotein genes, which incorporate low-molecular-weight selenium compounds in the form of selenocysteine. Important biological functions of selenium are associated with selenoproteins that contain it in the form of selenocysteine (Sec), known as the 21st amino acid in the genetic code. The human selenoproteome contains 25 selenoproteins, including glutathione peroxidases, thioredoxin reductases, and iodothyronine deiodinases. As a component of selenoproteins, selenium participates in defence against oxidative stress, maintenance of cellular redox status, redox signaling, and thyroid hormone metabolism.
Selenium is incorporated into polypeptides such as selenocysteine (SeC) and selenomethionine (SeMet), two key amino acids involved in various biochemical processes. All living organisms can convert inorganic selenium into biologically active organic forms, with SeMet being the predominant form and a precursor for SeC production in humans and animals.
Glutathione Peroxidases (GPx)
Glutathione peroxidase (GPx) is a selenoenzyme that converts hydrogen peroxide to water. It can also convert other reactive oxygen species (ROS) to water. Selenium is incorporated into proteins to make selenoproteins, which are important antioxidant enzymes. The antioxidant properties of selenoproteins help prevent cellular damage from free radicals.
Selenocysteine is present in several enzymes, including glutathione peroxidases, tetraiodothyronine 5′ deiodinases, thioredoxin reductases, formate dehydrogenases, glycine reductases, selenophosphate synthetase 2, methionine-R-sulfoxide reductase B1 (SEPX1), and some hydrogenases.
Thioredoxin Reductases (TrxR)
In humans, selenium is a trace element nutrient that functions as cofactor for glutathione peroxidases and certain forms of thioredoxin reductase. Thioredoxin reductases are selenoenzymes that play central roles in maintaining cellular redox homeostasis. Thioredoxin reductase uses a cysteine-selenocysteine pair to reduce the disulfide in thioredoxin.
Iodothyronine Deiodinases (DIO)
The thyroid hormone deiodinases (DIO) consist of three selenoproteins (DIO1, DIO2, and DIO3) that are involved in the metabolism of thyroid hormones by iodothyronine deiodination. Like most selenoproteins, they are thioredoxin-like proteins. Thyroid hormones regulate a variety of processes, including growth, development, and metabolic rate.
To date, 25 genetically encoded selenoproteins have been identified in humans, including glutathione peroxidase (GPx), thioredoxin reductase (TXNRD), and iodothyronine deiodinases (DIOs), which have a wide range of functions, from anti-inflammatory and antioxidant activities to thyroid hormone metabolism.
Selenomethionine-Specific Actions
Selenomethionine's antioxidant activity arises from its ability to deplete reactive oxygen species. Selenium and methionine also play separate roles in the formation and recycling of glutathione, a key endogenous antioxidant in many organisms, including humans.
5. Scientific Evidence by Area of Use
5.1 Deficiency-Related Diseases: Keshan Disease and Kashin-Beck Disease
Evidence strength: Strong (established causal relationship).
Historically, selenium deficiency was associated with a type of cardiomyopathy known as Keshan disease, which was initially documented in China in the 1930s. The administration of selenium supplementation to individuals residing in areas where Keshan disease is endemic has demonstrated a significant reduction in the incidence of this condition, underscoring selenium's therapeutic potential. Chronic selenium deficiency can produce a form of cardiomyopathy called Keshan disease, and a chronic bone and joint condition called Kashin-Beck disease.
The evidence here is among the most robust in selenium research. Several large population-based intervention trials using oral administration of sodium selenite tablets showed significant reduction of Keshan disease incidence. Based on the above evidence, it was concluded that selenium deficiency is the major cause of Keshan disease, although other etiological factors could not be ruled out.
5.2 Cancer Prevention
Evidence strength: Mixed; the most definitive large RCT did not confirm preventive effects, and current evidence does not support supplementation for cancer prevention in selenium-replete populations.
Some epidemiological studies have suggested that people with higher selenium status have a lower risk of several types of cancer, and one randomized controlled trial reported that men who took selenium had a lower risk of prostate cancer over a multi-year follow-up period. However, subsequent randomized controlled trials have found that selenium supplementation does not reduce the risk of prostate cancer or other forms of cancer.
The Nutritional Prevention of Cancer (NPC) Trial
The NPC trial initially reported that prostate cancers were reduced 63%, colorectal cancers 58%, and lung cancers 48%. A subsequent analysis of the complete NPC trial data reported that selenium supplementation reduced total and prostate cancer incidence but did not reduce lung or colorectal cancer incidence significantly. In addition, NPC had two limitations: it involved a relatively small number of subjects (1,312) and was initially planned to examine the role of selenium in skin cancer prevention.
The Selenium and Vitamin E Cancer Prevention Trial (SELECT)
Enrollment for the SELECT trial began in 2001 and ended in 2004. More than 400 sites in the United States, Puerto Rico, and Canada took part in the study. Over 35,000 men, age 50 and older at the start of the trial, participated in SELECT.
Selenium or vitamin E, alone or in combination at the doses and formulations used, did not prevent prostate cancer in this population of relatively healthy men. Specifically, the large SELECT trial demonstrated that selenium (as 200 μg/day l-selenomethionine) did not reduce prostate cancer risk (HR: 1.04; 99% CI: 0.87, 1.24), but this study was carried out in a selenium-replete US population (median baseline serum selenium: 136 ng/mL) with no history of cancer.
This randomized, double-blind, placebo-controlled, 2 × 2 factorial design clinical trial found that neither selenium nor vitamin E reduced the incidence of prostate cancer after seven years. The null result was surprising given the strong preclinical and clinical evidence suggesting chemopreventive activity of selenium. Potential explanations for the null findings include the agent formulation and dose, the characteristics of the cohort, and the study design. It is likely that only specific subpopulations may benefit from selenium supplementation; therefore, future studies should consider the baseline selenium status of the participants, age of the cohort, and genotype of specific selenoproteins.
Regarding prostate cancer specifically, the NPC trial showed a significant decrease in prostate cancer risk (HR: 0.33; 95% CI: 0.13, 0.82), but only for those men who had a history of cancer and lower selenium status (<123.2 ng/mL) at the start of the trial. Both a systematic review as part of this analysis and a Cochrane review on selenium intake and cancer suggest that selenium supplements do not, in general, prevent prostate cancer, and that the effects are likely to be dependent on the form of selenium in the supplement, habitual baseline selenium intake, and baseline selenium status and health of the population.
Colorectal Cancer
In a randomized, placebo-controlled trial in 1,374 participants who had colonoscopic removal of at least one colorectal adenoma (the Selenium and Celecoxib trial), selenium supplementation (200 μg/day with selenized yeast) for a median of 33 months had no effect on colorectal adenoma recurrence. However, in a subanalysis of patients with advanced adenoma at baseline (n=161), selenium supplementation reduced adenoma recurrence by 18%. Outcomes from other smaller trials have suggested either a lack of an effect or the possibility of an increased risk of cancer.
Lung Cancer
There is conflicting evidence regarding the potential benefits of selenium for use in lung cancer chemoprevention. Evidence from the NPC trial suggests that selenium supplementation may be of benefit in the prevention of cancer in those with low selenium status (serum selenium <106 ng/mL), while supplementation may increase risk of diabetes among subjects in the higher ranges of baseline selenium status. Selenium may reduce toxicities associated with cisplatin chemotherapy and radiation therapy. Further research is required to clarify optimal dosing strategies and risks associated with use.
5.3 Thyroid Disease and Autoimmune Thyroiditis
Evidence strength: Moderate for reduction of autoantibody titers in Hashimoto's thyroiditis; limited evidence for clinically meaningful long-term outcomes.
The thyroid gland needs selenium to produce hormones and function properly. After entering the thyroid cells, iodine ions are activated by H₂O₂ under the action of thyroid peroxidase (TPO). The activated iodine binds to tyrosine residues on thyroglobulin molecules under the action of TPO to produce monoiodotyrosine (MIT) and diiodotyrosine (DIT), which are subsequently coupled to produce T3 or T4. Activation and deactivation of thyroxine need the participation of DIOs (iodothyronine deiodinases) to complete.
Selenium has been one of the most intensively studied micronutrients in thyroid disease, with multiple randomized controlled trials (RCTs) examining its effects in Hashimoto's thyroiditis and other autoimmune conditions. Supplementation at doses around 200 μg/day has consistently reduced thyroid autoantibody titers, and several studies have reported parallel improvements in fatigue, mood, and overall quality of life.
A 2024 systematic review and meta-analysis of RCTs in Hashimoto's thyroiditis patients found: this systematic review and meta-analysis showed a significant reduction in TSH levels following selenium supplementation in Hashimoto's thyroiditis patients without thyroid hormone replacement therapy, and these effects disappeared when including patients receiving THRT. Furthermore, selenium supplementation exhibited favorable results by reducing TPOAb and MDA levels, with no statistically significant effect on fT4, fT3, T4, T3, TGAb, thyroid volume, and IL-2 and IL-10. Selenium supplementation was well tolerated, as evidenced by the absence of significant differences in adverse events between the selenium and placebo groups. Overall, the certainty of evidence was moderate.
Specifically, the meta-analysis found: TPOAb was reduced (SMD −0.96 [CI −1.36 to −0.56]; 29 cohorts; 2358 participants; I² = 90%) and malondialdehyde (MDA; SMD −1.16 [CI −2.29 to −0.02]; 3 cohorts; 248 participants; I² = 85%) decreased in patients with and without THRT.
For Graves' disease without eye involvement, patients with selenium supplementation were more likely to show improved thyroid function and faster remission of hyperthyroidism, with decrease in the levels of free T3, free T4, and autoantibody titre, along with an increase in TSH levels. Whether these effects correlate with clinically relevant long-term outcomes remains to be demonstrated.
Notwithstanding, a subsequent systematic review and meta-analysis, including trials in chronic autoimmune thyroiditis, concluded that the evidence in clinical parameters, such as effects of selenium supplementation on disease remission, progression, lowered levothyroxine dose, or improved quality of life, are scarce.
5.4 Cardiovascular Disease
Evidence strength: Weak; observational data is inconsistent and clinical trials have not confirmed a protective benefit in selenium-sufficient populations.
Studies suggest that taking selenium supplements does not reduce the risk of heart disease, especially in people who get enough selenium from food.
A recent meta-analysis that pooled trials reported no association of single-nutrient selenium supplementation with cardiovascular disease (4 trials), coronary heart disease (3 trials), stroke (3 trials), or cardiovascular-related mortality (5 trials). Additional clinical trials are needed to better understand any contributions of selenium from food and dietary supplements to cardiovascular health.
One notable RCT conducted in elderly Swedes with low baseline selenium status examined selenium combined with coenzyme Q10. Supplementation diminished inflammation and oxidative stress, impaired the increase of NT-proBNP, and improved renal function in both sexes. The supplementation improved cardiovascular survival, especially in women. This trial is noteworthy for enrolling a population with demonstrably low selenium status, which may explain its positive direction; results from this single trial do not change the overall evidence base for selenium-replete populations.
5.5 Cognitive Decline and Alzheimer's Disease
Evidence strength: Weak; observational findings are mixed and clinical trial evidence does not support supplementation to prevent cognitive decline.
Researchers are investigating the role of selenium in maintaining cognitive function in older adults, because chronic selenium deficiencies have been linked to cognitive decline. The results from observational studies have been mixed, with some reporting an association between lower plasma selenium concentrations and neurological impairments or a higher risk of Alzheimer's disease and others finding no such association. The evidence from clinical trials does not support the use of selenium supplementation to reduce the risk of cognitive decline and dementia in older adults.
Selenoproteins have antioxidant and anti-inflammatory activities, and serum selenium concentrations decline with age.
5.6 Male Fertility and Reproductive Health
Evidence strength: Preliminary; clinical evidence is inconsistent due to heterogeneous study designs and small sample sizes.
Selenium, a component of selenoproteins and selenocompounds in the human body, is crucial for the development of male reproductive organs, DNA synthesis, thyroid hormone metabolism, and defence against infections and oxidative damage. In the testis, selenium must exceed a desirable level since either a shortage or an overabundance causes aberrant growth. The antioxidant properties of selenium are essential for preserving human reproductive health.
Studies in humans on seminal selenium levels show that, generally, infertile men tend to have lower levels of seminal plasma selenium; however, in some cases, significantly higher selenium levels have been observed, suggesting that excessive selenium may also be linked to infertility. Additionally, most studies demonstrate a positive correlation between selenium levels in both seminal plasma and blood with certain seminogram quality parameters, particularly sperm motility. These findings, along with most available clinical trials, support the potential benefits of selenium supplementation for improving male infertility. However, there are limited studies on selenium status or supplementation concerning in vitro fertilization outcomes and pregnancy.
The clinical trials that have evaluated the effects of selenium supplementation on sperm quality have had conflicting findings. As for the implication of selenium in fertility and reproduction in men, though a few clinical trials explore the effects of selenium supplementation on male fertility, due to inconsistencies in the recruitment of subjects and heterogeneity of designs, the comparison of such studies is still complicated and less clear. Therefore, further research focused on the roles of selenium and selenoproteins is awaited for validating the evidence at hand and outlining any therapeutic schemes intended for improving male fertility.
5.7 Type 2 Diabetes
Evidence strength: Concerning; some evidence suggests a U-shaped relationship between selenium status and diabetes risk, with both deficiency and excess potentially increasing risk.
Some research shows that people with low selenium levels have a higher chance of developing type 2 diabetes. However, other research shows that people who have high levels of selenium also have an increased risk of type 2 diabetes. Because some evidence suggests that high serum selenium concentrations may have adverse effects on glycemic control, individuals with high selenium status and/or those at risk for type 2 diabetes mellitus should avoid taking selenium supplements.
6. Body Systems Associated with Selenium
Based on the established roles of selenoproteins, selenium is associated with the following body systems:
- Antioxidant/Oxidative Stress Defense: Via glutathione peroxidases and thioredoxin reductases, selenium-dependent enzymes neutralize reactive oxygen species and prevent lipid peroxidation.
- Thyroid System: The thyroid gland needs selenium to produce hormones and function properly. Selenium is also needed for reproduction, to make DNA, and for activation and deactivation of thyroid hormones via iodothyronine deiodinases.
- Immune System: Selenium is an essential trace element crucial for human health that primarily functions as an immunonutrient.
- Cardiovascular System: Selenoproteins may protect against oxidative modification of lipids and reduce inflammation, with ongoing research into effects on cardiovascular outcomes.
- Reproductive System: Selenium-dependent selenoproteins are essential for spermatogenesis and sperm motility.
- Neurological System: Selenium plays a role in neurological function; deficiency has been linked to cognitive decline in observational studies.
- Musculoskeletal System: Severe selenium deficiency underlies Kashin-Beck disease, an osteochondropathy.
7. Recommended Intakes and Dosages Used in Studies
The US Department of Agriculture has an RDA of 55 μg/day for adults. Plasma and serum selenium concentrations are commonly used to assess selenium status, and concentrations of 8 mcg/dL or higher are usually considered sufficient in healthy people.
Across the clinical trial literature, a range of doses has been employed:
- Hashimoto's thyroiditis trials: Supplementation at doses around 200 μg/day has consistently reduced thyroid autoantibody titers in multiple RCTs.
- SELECT trial (prostate cancer): 200 μg/day of l-selenomethionine was used in the SELECT trial.
- Colorectal adenoma trial: Selenium supplementation was used at 200 μg/day with selenized yeast for a median of 33 months.
- Danish aging study: A five-year, randomized, double-blind, placebo-controlled trial in healthy Danish older people (ages at inclusion, 60–74 years) used selenium supplementation of 100–300 μg/day.
- Selenium-only dietary supplements: Selenium-only supplements typically contain 100 to 400 mcg.
- Multivitamin/mineral supplements: Many multivitamin/mineral supplements contain 55 mcg of selenium.
8. Safety Considerations
Tolerable Upper Intake Level (UL)
The Food and Nutrition Board of the US Institute of Medicine (now the National Academy of Medicine) set the tolerable upper intake level (UL) for selenium at 400 μg/day in adults based on the prevention of hair and nail brittleness and loss and early signs of chronic selenium toxicity. The UL for selenium is 400 μg/day for adolescents and adults and includes both selenium obtained from food, which averages about 100 μg/day for adults in the US, and selenium from supplements.
The European Food Safety Authority (EFSA) conducted a reassessment and arrived at a different figure: Alopecia, as an early observable feature and a well-established adverse effect of excess selenium exposure, is selected as the critical endpoint on which to base a UL for selenium. A lowest-observed-adverse-effect-level (LOAEL) of 330 μg/day is identified from a large randomised controlled trial in humans (SELECT), to which an uncertainty factor of 1.3 is applied. A UL of 255 μg/day is established for adult men and women (including pregnant and lactating women).
The IOM has established the Tolerable Upper Limit (UL), No Observed Adverse Effect Level (NOAEL) and the Lowest Observed Adverse Effect Level (LOAEL) for selenium at doses of 400, 800, and 913 mcg/day in adults, respectively.
Selenosis (Chronic Selenium Toxicity)
Chronic selenium toxicity (selenosis) may occur with smaller doses of selenium over long periods of time. The most common symptoms of selenosis are hair and nail brittleness and loss. Other symptoms may include gastrointestinal disturbances, skin rashes, a garlic breath odor, fatigue, irritability, and neurological disorders.
Symptoms of selenium toxicity include nausea; vomiting; nail discoloration, brittleness, and loss; hair loss; fatigue; irritability; and foul breath odor (often described as "garlic breath").
In an area of China with a high prevalence of selenosis, toxic effects occurred with increasing frequency when blood selenium concentrations reached a level corresponding to an intake of 850 μg/day.
Signs and symptoms of selenium toxicity, including alopecia, hair and nail changes, skin rash, gastrointestinal disturbances, "garlic" breath odor, electrocardiogram changes, and nervous system abnormalities, have been reported at doses greater than 1 gram. Cardiopulmonary arrest and death have been reported with oral ingestions of 10 grams.
Clinically significant selenium toxicity was reported in 13 individuals after taking supplements that contained 27.3 mg (27,300 μg) per tablet due to a manufacturing error.
Potential Adverse Effects Under Consideration
The following effects were prioritised by EFSA for risk assessment: selenosis (including biomarkers of effect of excess selenium intake), hypertension, Alzheimer's dementia, amyotrophic lateral sclerosis (ALS), impaired neuropsychological development in children, thyroid diseases, prostate cancer, skin cancer, type 2 diabetes mellitus (T2DM), and overall mortality.
Known Drug Interactions
Selenium supplements may interact with medications. In addition, certain medications, such as cisplatin, can affect selenium levels in the body. Selenium can interact with certain medications, and some medications can have an adverse effect on selenium levels.
- Cisplatin (chemotherapy): Cisplatin can reduce selenium levels in hair and serum, but whether these reductions have a clinically significant impact is not known. Some small studies have shown that selenium supplementation can reduce cisplatin's toxicity, but the authors of a Cochrane Review concluded that the evidence that selenium supplementation alleviates the side effects of chemotherapy is insufficient.
- Chemotherapy agents (general): Although selenium may help reduce side effects from drugs such as cisplatin, doxorubicin, and belomycin, it may also interfere with their cancer-fighting ability. If undergoing chemotherapy, consultation with an oncologist is advised before taking selenium or any other supplement.
- Statins and niacin combinations: Simvastatin and niacin have been shown to lower LDL ("bad") cholesterol and raise HDL ("good") cholesterol in people with heart disease. Taking antioxidants, including selenium, along with these drugs may reduce their effectiveness. Theoretically, selenium may also reduce the effectiveness of other statins, including atorvastatin (Lipitor), fluvastatin (Lescol), lovastatin (Mevacor), and pravastatin (Pravachol).
- Anticoagulant/antiplatelet agents: Selenium may increase the risk of bleeding when taken with anticoagulant or antiplatelet drugs like warfarin, heparin, and aspirin.
High Selenium Status and Diabetes Risk
Evidence from the NPC trial suggests that supplementation may increase risk of diabetes among subjects in the higher ranges of baseline selenium status. This observation, consistent across several studies, underscores the importance of assessing baseline selenium levels before initiating supplementation.
References
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