Selenium

• Correcting documented selenium deficiency
• Preventing Keshan disease in selenium-poor regions (established, historical public-health use)
• Adjunct in Hashimoto's and autoimmune thyroiditis protocols, per clinician (modest, mixed evidence)
• Support in select critical-illness and burn settings (investigational)
• Meeting baseline needs in populations on selenium-poor soils (parts of UK, New Zealand, some of China)

Selenium is an essential trace mineral with one of the narrowest therapeutic windows in human nutrition, RDA of 55mcg/day, Upper Limit of 400mcg/day. The mineral functions almost entirely through incorporation into approximately twenty-five selenoproteins in the human proteome, where it appears as selenocysteine, sometimes called "the 21st amino acid", incorporated through specific UGA codon recoding mechanisms unique to selenoproteins. The selenoprotein families perform distinct biological functions: glutathione peroxidases (GPx 1-4) reduce hydroperoxides using glutathione as electron donor, providing first-line antioxidant defense in cytoplasm (GPx1), plasma (GPx3), GI tract (GPx2), and membrane lipids (GPx4 / phospholipid hydroperoxide glutathione peroxidase, with critical anti-ferroptosis function); thioredoxin reductases (TrxR1, TrxR2, TrxR3) regenerate reduced thioredoxin maintaining cellular redox balance and DNA synthesis; iodothyronine deiodinases (DIO1, DIO2, DIO3) convert T4 to active T3 (DIO1, DIO2) and inactivate excess T3 (DIO3), the entire peripheral thyroid hormone activation system depends on selenoproteins; selenoprotein P (SELENOP, the major plasma selenoprotein) serves as selenium transport and distribution to peripheral tissues; selenoprotein W has unclear function in muscle and brain; methionine sulfoxide reductase B1 (MSRB1) repairs oxidized methionine in proteins. The selenoprotein system explains essentially all of selenium's biological roles, antioxidant defense, thyroid hormone metabolism, immune function, redox signaling, sperm motility, and possibly cancer prevention biology. The geographic variation in dietary selenium intake is among the most dramatic of any essential nutrient. Selenium content in plant foods depends almost entirely on soil selenium levels, which vary by orders of magnitude across global regions. The US Northern Plains (Nebraska, Dakotas) contain selenium-rich soils producing high-selenium crops; parts of the UK, New Zealand, and large regions of China contain selenium-poor soils. The Chinese Keshan County endemic cardiomyopathy of the 1960s-70s, characterized by Keshan disease, a juvenile cardiomyopathy now known to involve selenium deficiency exacerbating Coxsackievirus infection, was successfully addressed through selenium supplementation programs in affected regions. The related Kashin-Beck disease (a chondropathy primarily affecting children in selenium-iodine co-deficient regions of China, Tibet, Siberia) represents another major selenium-deficiency clinical syndrome. The dietary selenium concern in selenium-poor regions persists today, with public health supplementation programs in Finland (since 1984, adding selenium to fertilizer), parts of China, and selected other regions. The Brazil nut natural variability deserves special mention, Brazil nuts (Bertholletia excelsa) are the most concentrated natural selenium source by far, but selenium content varies enormously between nuts (typical range 50-90mcg per nut, but some individual nuts approach 400mcg). This makes "one Brazil nut daily" a popular but unreliable supplementation strategy, most users get adequate selenium but some inadvertently approach the Upper Limit, while others remain below RDA. The narrow therapeutic window combined with this natural variability creates substantial dosing complexity. The SELECT trial story is among the most important examples of mechanism-translation failure in nutritional pharmacology. The Selenium and Vitamin E Cancer Prevention Trial (SELECT, Lippman 2009 JAMA) randomized 35,000+ men to selenium (200mcg/day as L-selenomethionine), vitamin E, both, or placebo for prostate cancer prevention. The trial was halted early, not for benefit but for futility and concerning signals: no prostate cancer prevention benefit, possible diabetes risk increase from selenium (subsequently confirmed by Stranges 2007 and other analyses), possible prostate cancer risk increase from vitamin E. The SELECT outcome substantially recalibrated expectations about selenium's cancer prevention potential, earlier optimism from the Clark 1996 NPC (Nutritional Prevention of Cancer) trial, which had suggested possible prostate cancer prevention, did not replicate at the larger SELECT scale. The mechanism-translation problem is instructive: selenoproteins provide important antioxidant and redox functions, glutathione peroxidases participate in detoxification, the in vitro and animal evidence for cancer prevention was substantial, yet the human cancer prevention translation failed in the most rigorous trial. The SELECT outcome reshaped clinical guidance toward AI-level intake for users without documented deficiency and modest cancer prevention claims for the supplement category.

Standard selenium supplementation aims to meet the RDA of 55mcg/day adult (60mcg pregnancy, 70mcg lactation, age-specific in pediatrics). The Upper Limit (UL) of 400mcg/day adults reflects selenosis risk at chronic high intake. The narrow therapeutic window (RDA 55mcg, UL 400mcg, approximately 7-fold range) is among the narrowest of any essential mineral. Typical Western dietary intake from selenium-rich US food supply provides 50-150mcg/day in most users; supplementation for healthy non-deficient users typically aims at 50-100mcg/day to ensure RDA without approaching UL. Higher-dose protocols (200mcg/day) are appropriate for specific clinical applications, Hashimoto's thyroiditis adjunctive treatment (Toulis 2010), Graves' orbitopathy (Marcocci 2011), HIV nutrition (Baum 1997 framework). The SELECT trial used 200mcg/day in healthy users and demonstrated diabetes risk; this dose should not be used routinely in non-deficient users for general health support. Form matters: L-selenomethionine (organic) provides excellent bioavailability and protein incorporation buffer; sodium selenite (inorganic) provides rapid repletion; selenium-enriched yeast provides food-form mixture; methyl-selenocysteine provides plant-source alternative. Take with food, absorption is acceptable either way but food administration is conventional. Geographic dietary intake variation is enormous: residents of selenium-rich Northern Plains US likely meet RDA through diet alone; UK and parts of China require dietary planning or supplementation. The Brazil nut natural variability (50-400mcg per nut) makes "one Brazil nut daily" unreliable as targeted supplementation, fine as occasional dietary inclusion but not predictable dosing strategy. Stack awareness matters: combining multivitamin selenium (~50mcg), Brazil nut consumption (variable but potentially substantial), and dedicated selenium supplement can inadvertently approach UL.

RDA adults

55mcg/day

Pregnancy RDA

60mcg/day

Lactation RDA

70mcg/day

Upper Limit (UL) adults

400mcg/day

Hashimoto's adjunctive (Toulis)

200mcg/day

Graves' orbitopathy (Marcocci)

200mcg/day x 6 months

HIV nutrition (Baum framework)

100-200mcg/day

SELECT trial dose (concerning)

200mcg/day chronic

• L-Selenomethionine (Organic Form)

  Rating: gold

  The organic selenium form found in foods (incorporated nonspecifically into proteins in place of methionine). Excellent bioavailability and tolerability; gradual accumulation in body protein pools providing buffer against intake variation. Used in SELECT trial and most modern clinical research. The Cytoplan, NOW Foods, Pure Encapsulations, and Thorne L-selenomethionine products are reliable choices. Premium relative to inorganic forms but generally justified by bioavailability.

• Sodium Selenite (Inorganic Form)

  Rating: good

  Inorganic selenium salt used in Chinese Keshan disease prevention programs and many older clinical applications. Lower cost than selenomethionine; somewhat lower bioavailability and shorter half-life (no protein incorporation buffer). Reasonable for users requiring rapid selenium repletion or in clinical contexts; less preferred than selenomethionine for general supplementation.

• Sodium Selenate (Inorganic Form)

  Rating: good

  Alternative inorganic selenium form. Similar pharmacology to selenite; less commonly used than selenite in commercial supplements. Acceptable bioavailability for general supplementation.

• Selenium-Enriched Yeast

  Rating: gold

  High-selenium yeast (Saccharomyces cerevisiae grown on selenium-enriched medium) provides a complex mixture of selenium forms primarily including selenomethionine. Used in NPC trial (Clark 1996) and various other clinical research. Pharmacologically similar to selenomethionine alone but with additional yeast-derived selenocompounds. Reasonable choice for users preferring food-source-like supplements.

• Methyl-Selenocysteine (Se-Methylselenocysteine)

  Rating: good

  Selenocompound found naturally in allium plants (garlic, onion) and selenium-accumulator plants (broccoli, Brazil nuts grown on certain soils). Different metabolic pathway than selenomethionine, bypasses protein incorporation, more rapid metabolism to active selenocompounds. Preliminary evidence for distinct biological effects; not widely available in consumer supplements. Reasonable alternative form for users preferring plant-derived selenium.

• Brazil Nuts (Whole Food)

  Rating: caution

  The most concentrated natural selenium source globally (Bertholletia excelsa). Typical content 50-90mcg per nut, but enormous variability between individual nuts (some up to 400mcg). The "one Brazil nut daily" supplementation strategy is popular but unreliable, most users get adequate selenium but some inadvertently approach the Upper Limit. Brazil nuts grown in selenium-rich Amazon Basin soils contain highest selenium; central Brazilian or lower-selenium-soil Brazil nuts contain less. Reasonable dietary inclusion but not reliable as targeted supplementation.

• Selenium Multivitamin (Low-Dose)

  Rating: good

  Most multivitamins include selenium at 50-200mcg providing AI-bridging contribution to total intake. Reasonable foundation; verify dose to avoid stacking with other selenium-containing products toward UL.

• High-Dose Selenium Products

  Rating: caution

  Products providing >200mcg/day selenium routinely. Approach the Upper Limit (400mcg/day) particularly with stacking from food sources (Brazil nuts, multivitamins). The narrow therapeutic window means high-dose selenium products warrant specific clinical indication; the SELECT trial diabetes signal supports caution about chronic high-dose supplementation without specific indication.

• Hashimoto's thyroiditis (autoimmune thyroid)

  Strength of evidence for this group: modest

  Toulis 2010 meta-analysis and Karp 2013 Cochrane review support modest reductions in TPO antibody levels with 200mcg/day selenium in Hashimoto's thyroiditis. Effect on clinical thyroid outcomes (need for levothyroxine, hypothyroid symptoms) less clear. Reasonable adjunct to standard Hashimoto's management; not substitute for levothyroxine in established hypothyroidism. Coordinate with endocrinology.

• Documented selenium deficiency (geographic, malabsorption)

  Strength of evidence for this group: strong

  Users with documented selenium deficiency from selenium-poor geographic regions, malabsorption syndromes (Crohn's disease, celiac disease), prolonged TPN without selenium supplementation, or strict restrictive diets warrant supplementation. AI-level repletion (55-100mcg/day) typically adequate; specialist coordination for severe deficiency.

• Graves' disease (hyperthyroid) thyroid eye disease

  Strength of evidence for this group: modest

  Marcocci 2011 NEJM trial supports selenium 200mcg/day (as sodium selenite) for 6 months in mild Graves' orbitopathy: significant improvements in quality of life and ophthalmologic outcomes versus placebo. Foundational evidence for endocrine ophthalmology adjunct use. Coordinate with ophthalmology and endocrinology.

• Pregnancy and lactation (geographic deficiency)

  Strength of evidence for this group: modest

  Pregnancy AI is 60mcg/day; lactation 70mcg/day. Selenium status affects pregnancy outcomes including preeclampsia risk and miscarriage in some populations. Reasonable supplementation for users in selenium-deficient regions; coordinate with OB-GYN. Avoid high doses given narrow therapeutic window.

• HIV (immune function support)

  Strength of evidence for this group: modest

  Baum 1997 and subsequent work supports selenium status as relevant to HIV disease progression. Modest selenium supplementation (~200mcg/day) reasonable adjunct in HIV nutrition; not substitute for established antiretroviral therapy. HIV specialist coordination.

• Healthy adults (general supplementation)

  Strength of evidence for this group: cautious

  AI is 55mcg/day. Many US adults achieve this through diet given selenium-rich US food supply; supplementation may be appropriate for users in selenium-poor regions, on restrictive diets, or with documented low intake. Routine high-dose supplementation in healthy non-deficient users is not warranted given SELECT trial diabetes signal. Modest doses (50-100mcg/day) reasonable foundational supplementation.

• Athletes (oxidative stress contexts)

  Strength of evidence for this group: cautious

  Endurance athletes have elevated oxidative stress and may benefit from comprehensive antioxidant nutrition including selenium. Effect sizes preliminary; reasonable component of comprehensive sport nutrition. Avoid high-dose chronic supplementation.

• Cancer prevention (general adult)

  Strength of evidence for this group: cautious

  SELECT trial demonstrated no prostate cancer prevention benefit at 200mcg/day; possible modest cancer prevention signal only in users with low baseline selenium status. Cancer prevention claims should be substantially calibrated post-SELECT; not adequate evidence for high-dose supplementation specifically for cancer prevention in well-nourished populations.

• Type 2 diabetes (caution)

  Strength of evidence for this group: cautious

  SELECT and Stranges 2007 demonstrated increased diabetes risk with chronic 200mcg/day selenium supplementation. Coordinate with endocrinology for users with established diabetes; avoid high-dose chronic supplementation without specific indication.

• Cardiovascular disease (caution)

  Strength of evidence for this group: cautious

  Mixed evidence, some observational evidence connecting selenium status with cardiovascular outcomes; SELECT and other interventional trials have not demonstrated cardiovascular benefit. Avoid high-dose supplementation without specific indication. Coordinate with cardiology for users with established CVD.

• Pediatric use

  Strength of evidence for this group: cautious

  Pediatric AIs are age-specific (15mcg ages 1-3, 20mcg ages 4-8, 40mcg ages 9-13, 55mcg ages 14-18). Routine pediatric supplementation outside specific clinical indication not warranted; severe acute and chronic toxicity concerns at higher doses. Pediatric specialist coordination only.

• High-dose / chronic supplementation (selenosis caution)

  Strength of evidence for this group: avoid

  Chronic intake >400mcg/day produces selenosis: hair loss, nail brittleness and breakage, garlic breath, fatigue, irritability, GI distress, peripheral neuropathy, and in severe cases acute respiratory distress and death. The narrow therapeutic window combined with Brazil nut variability makes this particularly important. Stay below 400mcg/day from all sources combined.

• Iodine

  Interaction: synergy

  Selenium and iodine work integratively in thyroid hormone metabolism, selenoprotein deiodinases (DIO1, DIO2) convert T4 to active T3. Iodine supplementation in selenium-deficient individuals can paradoxically worsen hypothyroidism; selenium adequacy required for proper iodine utilization in thyroid hormone synthesis and activation. Mechanistically integrated.

• Vitamin E

  Interaction: synergy

  Complementary antioxidant systems, selenium-dependent glutathione peroxidases reduce hydroperoxides; vitamin E intercepts lipid radicals in membranes. Schwarz 1957 foundational work characterized the selenium-vitamin E interaction. SELECT trial combined both with concerning results; mechanism-translation framework distinct from interaction biology.

• Glutathione / NAC

  Interaction: synergy

  Selenium-dependent glutathione peroxidases use glutathione as electron donor; NAC supports glutathione synthesis. Mechanistically integrated antioxidant system. Common combination in comprehensive antioxidant protocols.

• Zinc

  Interaction: synergy

  Both essential trace minerals with overlapping roles in immune function, antioxidant defense, and thyroid metabolism. Common combination in comprehensive trace mineral supplementation. Different metabolic pathways but complementary.

• Vitamin C

  Interaction: caution

  Reduces selenite (inorganic selenium) to less bioavailable elemental selenium when taken simultaneously at high doses. Separate doses by 2+ hours when combining high-dose vitamin C with sodium selenite supplements. Less relevant for selenomethionine form.

• Statins

  Interaction: caution

  Statins may affect selenoprotein synthesis pathways through mevalonate pathway inhibition (selenocysteine tRNA isopentenylation). Clinical relevance debated; coordinate with cardiology for users on chronic statin therapy.

• Chemotherapy

  Interaction: caution

  Theoretical interaction concerns, selenium's antioxidant function may interfere with chemotherapy oxidative damage mechanisms. Some specific protocols (selenite in head and neck cancer) have shown benefit. Coordinate with oncology; integrative oncology consensus generally recommends caution about routine high-dose selenium during active chemotherapy.

• Brazil Nuts (Dietary Source)

  Interaction: caution

  Variability concern, Brazil nuts naturally contain 50-400mcg selenium per nut. Combined with multivitamin selenium and dedicated supplementation, daily Brazil nut consumption can approach UL inadvertently. Verify total selenium intake from all sources.

• Pregnancy

  Interaction: caution

  Pregnancy AI is 60mcg/day. Beneficial supplementation in selenium-deficient regions; high-dose supplementation in pregnancy warrants OB-GYN coordination given narrow therapeutic window and limited high-dose pregnancy safety data.

Look for: specific selenium form disclosed (L-selenomethionine preferred for general use, sodium selenite for repletion contexts, selenium-yeast for food-form preference); explicit mcg selenium content per serving (not just compound weight); appropriate dose for intended use (50-100mcg general, 200mcg specific clinical indications only); USP or NSF third-party verification; reputable manufacturer with quality control disclosure. Avoid: products without specific form disclosure; very high-dose products (>200mcg per serving) without specific clinical indication; proprietary "antioxidant blends" obscuring selenium dose toward UL; combinations with vitamin E at SELECT-trial doses (200mcg Se + 400IU E) which produced concerning results; products marketed for cancer prevention given SELECT failure.

Selenium's discovery came in 1817 through Jöns Jacob Berzelius in Sweden, characterizing residue from sulfuric acid production. Berzelius named the element after Selene (Greek moon goddess), pairing with tellurium (named after Earth) given chemical similarity. The toxic properties of selenium were recognized early in industrial chemistry; selenium's essentiality in human nutrition remained ambiguous for nearly 150 years. The biological essentiality era began in 1957 with Klaus Schwarz at NIH characterizing "factor 3" preventing dietary liver necrosis in rats, selenium was identified as the active component. The complementary biology with vitamin E (Schwarz 1957) established the antioxidant framework. The Rotruck 1973 Science paper characterizing selenium as essential cofactor of glutathione peroxidase provided the foundational selenoprotein biology that has guided subsequent understanding. The Keshan disease era brought selenium deficiency clinical syndromes to global attention. Keshan disease (juvenile cardiomyopathy named after Keshan County, China) was characterized as endemic to selenium-poor regions of China through the 1960s-70s. Chinese public health programs of sodium selenite tablet supplementation in affected regions essentially eliminated Keshan disease incidence, providing unambiguous clinical evidence of selenium essentiality in human populations. The related Kashin-Beck disease (chondropathy affecting children in selenium-iodine co-deficient regions of China, Tibet, Siberia) extended the geographic deficiency syndrome framework. The US RDA establishment came in 1980 (initially), with refinement through subsequent DRI revisions. The Institute of Medicine 2000 DRI for selenium established the modern 55mcg/day RDA and 400mcg/day UL framework that has guided supplementation guidance since. The Finnish selenium fortification program began in 1984, adding selenium to fertilizers used in Finnish agriculture in response to documented low population selenium status. Subsequent monitoring has demonstrated successful population selenium status improvement and provides natural experiment data on population-level selenium adequacy. The NPC (Nutritional Prevention of Cancer) trial era brought selenium to substantial clinical research attention. Clark 1996 JAMA paper from the NPC trial in skin cancer prevention showed null skin cancer outcome but possible reductions in prostate, lung, and colorectal cancer, generating substantial optimism about selenium cancer prevention potential. The SELECT trial era (2001-2009) was designed to test the prostate cancer prevention hypothesis at scale, 35,000+ men randomized to 200mcg/day L-selenomethionine, 400IU vitamin E, both, or placebo. The trial was halted in 2008 for futility and concerning signals; the 2009 JAMA publication by Lippman documented no prostate cancer prevention benefit, increased diabetes risk from selenium, and increased prostate cancer risk from vitamin E. The SELECT outcome substantially recalibrated selenium clinical guidance, high-dose chronic supplementation for cancer prevention in non-deficient users became substantially less defensible. The modern thyroid adjunctive era developed through the 2000s-2010s with substantial evidence for selenium in autoimmune thyroid conditions. The Marcocci 2011 NEJM Graves' orbitopathy trial established selenium 200mcg/day x 6 months as effective adjunct in mild Graves' eye disease. The Toulis 2010 meta-analysis consolidated Hashimoto's thyroiditis evidence; subsequent Karp 2013 Cochrane review provided rigorous methodology assessment. The 2008 Total Body Formula liquid supplement contamination episode caused acute selenium toxicity in users, manufacturing error produced doses 200-fold higher than labeled. Foundational pharmacovigilance event illustrating quality control importance with narrow-therapeutic-window minerals. The modern consumer market has matured substantially. Most multivitamins now include selenium at 50-200mcg providing AI-bridging contribution. Brazil nuts remain widely marketed as natural selenium source despite variability concerns. The narrow therapeutic window framework has become more widely communicated in functional medicine and consumer nutrition guidance; the SELECT outcome has substantially calibrated expectations about high-dose supplementation.

1. 1817Berzelius discovers selenium in Sweden
2. 1957Schwarz NIH characterizes selenium-vitamin E interaction
3. 1960s-70sKeshan disease characterization in China
4. 1973Rotruck Science paper on glutathione peroxidase selenium
5. 1979-80Chinese selenium supplementation programs essentially eliminate Keshan disease
6. 1980First US RDA established for selenium
7. 1984Finnish selenium fertilizer fortification program
8. 1996Clark NPC trial preliminary cancer prevention evidence
9. 1997Baum HIV-selenium framework
10. 2000IOM DRI establishes modern 55mcg/day RDA, 400mcg/day UL
11. 2001-2008SELECT trial enrollment and follow-up
12. 2007Stranges reanalysis of NPC trial diabetes risk
13. 2008Total Body Formula contamination acute selenosis episode
14. 2009SELECT trial JAMA publication, null cancer; diabetes signal
15. 2010Toulis Hashimoto's selenium meta-analysis
16. 2011Marcocci Graves' orbitopathy trial (NEJM)
17. 2013Karp Cochrane autoimmune thyroiditis review

• Whether the modest cancer prevention signal in low-baseline-selenium users from SELECT subset analyses translates to actionable subpopulation guidance, current evidence supports AI-level intake but not high-dose chronic supplementation for cancer prevention in general populations.
• Whether the SELECT diabetes risk signal generalizes across forms (L-selenomethionine vs sodium selenite vs selenium-enriched yeast), most safety data is from L-selenomethionine form.
• Whether selenium has specific applications in autoimmune diseases beyond Hashimoto's thyroiditis where modest evidence supports adjunctive use, preliminary evidence for other autoimmune conditions.
• Whether selenium supplementation in selenium-deficient regions produces meaningful population-level cardiovascular and metabolic outcomes, Finnish selenium fortification provides natural experiment with mixed results.
• Whether the Brazil nut variability problem can be addressed through commercial supply chain standardization, currently no widely-implemented selenium content verification on retail Brazil nuts.
• Whether HIV-selenium evidence translates to modern combination antiretroviral therapy era, most HIV-selenium research predates modern HAART.
• Whether genetic variants affecting selenoprotein synthesis or selenium metabolism (SELENOP, GPX1, etc.) should be considered in clinical nutrition assessment, research is preliminary and not widely integrated.
• Whether selenium supplementation has specific applications in male fertility beyond the established role of selenoproteins in sperm motility, preliminary evidence for male infertility adjunctive use.

Widely available globally as dietary supplement, food fortification ingredient, and component of multivitamin formulations. Legal under DSHEA in the United States and equivalent supplement regulations in most jurisdictions. Not on WADA prohibited list. Major retail supplement brands include NOW Foods, Thorne, Pure Encapsulations, Designs for Health, Source Naturals, and most multivitamin manufacturers. Cytoplan and similar UK brands cater to selenium-deficient UK market segment. Brazil nut access is universal in developed markets. Pharmaceutical selenite preparations are available in some markets for clinical applications including head and neck cancer adjunctive use. Geographic supplementation programs: Finland has fortified fertilizer with selenium since 1984 with measurable population selenium status improvements; parts of China continue endemic Keshan disease prevention through selenium tablet programs in affected regions. Production sources include selenium recovery from copper refining (industrial selenium), sodium selenite synthesis (pharmaceutical/food grade), and selenium-enriched yeast cultivation. Quality variation across consumer supplements is modest given the well-established chemistry; third-party testing (USP, NSF) provides standard verification. The narrow therapeutic window combined with form considerations (selenomethionine preferred for general use) makes brand and form selection more important than for many supplements.

Status current as of July 2026. Regulatory positions change, sometimes quickly.

Class

Essential trace mineral

Discovery

1817 (Berzelius, Sweden; named after Selene)

Essentiality establishment

1957 (Schwarz, NIH)

Glutathione peroxidase identification

1973 (Rotruck, Science)

RDA adults

55mcg/day

Pregnancy RDA

60mcg/day

What follows is unfinished work on our side, not a finding about Selenium. A short entry is not a safe entry.

• Cost and market. We have not documented what it sells for or who sells it.
• Supply chain. We have not mapped where it is made.
• Who uses it. We have not documented the user groups.
• What could change. No forward-looking summary yet.
• How it compares. We have not set it against the alternatives.
• Children and teenagers. We have not checked what is known about younger people.
• Where we land. We have not taken a position on this yet.