Who Found the Role of Selenium, and How a Poison Became an Essential Mineral

Selenium was named in 1817, and its history covers two sides of one narrow margin: a Chinese heart disease tied to low intake and a toxicity whose early signs are hair loss and brittle nails. This page traces both, and the NIH limit between them.

The history of selenium is a story about a narrow margin. The element was named in 1817, and the research that followed covers two problems on either side of the safe range: a heart disease in China tied to low selenium, and a toxicity whose most common signs are hair loss and brittle nails. ## In this article - The 1817 mix-up that gave selenium its name - Keshan disease and the selenium trials - 1973: selenium's job in glutathione peroxidase - The narrow margin: soil, forms and the upper limit ## The 1817 mix-up that gave selenium its name Berzelius and Gahn roasted about 200 kg of sulfur from a Falun mine pyrite and obtained roughly 3 g of a precipitate that they first wrongly identified as tellurium. Berzelius doubted that result, repeated the analysis, and realized he had a new element ([PubMed](https://pubmed.ncbi.nlm.nih.gov/29207462/); [DOI](https://doi.org/10.3390/molecules22122124)). He named it selenium, from the Greek *Selene* for the moon, because it resembled tellurium, from the Latin *Tellus* for earth. The surprise is the pairing: the moon's name came from a comparison with the earth. A 2016 review in *ACS Chemical Biology* marks the bicentennial of that 1817 discovery and traces the biological discoveries that came after it ([PubMed](https://pubmed.ncbi.nlm.nih.gov/26949981/); [DOI](https://doi.org/10.1021/acschembio.6b00031)). The nutrition side came later, and it started with liver damage in rats and a heart disease in people. ## Keshan disease and the selenium trials Keshan disease is an endemic heart disease in China with a high case-fatality rate, according to a 2012 review by Junshi Chen. The review reports that low selenium in cereal grains and low selenium status in residents were associated with the disease. Several large population trials that gave sodium selenite tablets significantly reduced its incidence. Chen concludes that selenium deficiency is the major cause, while noting that other causes could not be ruled out ([PubMed](https://pubmed.ncbi.nlm.nih.gov/22705420/)). A 2018 meta-analysis by Zhou and colleagues pooled 41 studies of community trials. It found an overall risk ratio of 0.14 for the supplemented groups, and it says the disease was highly prevalent from the 1950s to the 1970s ([PubMed](https://pubmed.ncbi.nlm.nih.gov/29627894/); [DOI](https://doi.org/10.1007/s12011-018-1302-5)). Zhou's team concludes that selenium deficiency is a cause of the disease by the criterion of causation. The NIH lists Keshan disease among the conditions that selenium deficiency may trigger ([NIH ODS](https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/)). For how this fits the wider picture of selenium and immune research, see the [immune health guide](/health/immune-health). ## 1973: selenium's job in glutathione peroxidase The biochemical role came into focus in 1973. Rotruck and colleagues reported that erythrocytes from selenium-deficient rats were practically devoid of glutathione peroxidase activity, and that the selenium labeled in those cells went with the purified enzyme. They concluded that many nutritional effects of selenium "can be explained by its role in glutathione peroxidase" ([PubMed](https://pubmed.ncbi.nlm.nih.gov/4686466/); [DOI](https://doi.org/10.1126/science.179.4073.588)). A 1975 review credits that work with the discovery that selenium is a component of rat erythrocyte glutathione peroxidase ([PubMed](https://pubmed.ncbi.nlm.nih.gov/1100438/)). The earlier nutrition milestone is a paper by Klaus Schwarz and Calvin Foltz on selenium as part of "factor 3" against dietary liver degeneration. According to PubMed, a 1999 reprint in *Nutrition* lists it as a seminal article under that title. The reprint's title carries a date of 1951, which we could not reconcile with a primary source, so this page gives no year for the original ([PubMed](https://pubmed.ncbi.nlm.nih.gov/10408880/)). Today the NIH calls selenium an essential mineral and says it is a constituent of 25 selenoproteins, including glutathione peroxidases ([NIH ODS](https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/)). For the cell-level side of this story, the [mitochondrial health guide](/health/mitochondrial-health-complete-guide) is the place to start. ## The narrow margin: soil, forms and the upper limit Soil sets the starting point for plant foods. The NIH says the selenium content of plant-based foods varies by location, because the amount and form of selenium in the soil influence what plants contain. Animal products are steadier, since animals keep tissue selenium at predictable levels ([NIH ODS](https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/)). Seafood, meat and poultry are rich sources, and Brazil nuts carry particularly high amounts. The forms named in these sources are L-selenomethionine, selenium yeast and sodium selenite. A 2000 review in the *Journal of Nutrition* calls L-selenomethionine a major natural food form and says synthetic L-selenomethionine or selenium yeast are appropriate supplement forms. Ingested selenomethionine is either metabolized or stored in place of methionine in body proteins, and tissue levels reach a steady state at nutritional intakes ([PubMed](https://pubmed.ncbi.nlm.nih.gov/10867031/); [DOI](https://doi.org/10.1093/jn/130.7.1653)). The 2012 Lancet review by Margaret Rayman calls the link between selenium status and health U-shaped. Additional selenium may benefit people with low status, while people with adequate-to-high status might be affected adversely and should not take selenium supplements ([PubMed](https://pubmed.ncbi.nlm.nih.gov/22381456/); [DOI](https://doi.org/10.1016/S0140-6736(11)61452-9)). The adult upper limit is 400 mcg a day, and it covers selenium from food and supplements. The NIH bases it on hair and nail changes, which it names as the most common signs of chronically high intake. Early warnings include a garlic odor on the breath and a metallic taste, and the NIH also lists skin rash, nausea, diarrhea, fatigue, irritability and nervous system effects ([NIH ODS](https://ods.od.nih.gov/factsheets/Selenium-HealthProfessional/)). The adult RDA is 55 mcg, rising to 60 mcg in pregnancy and 70 mcg while nursing. We could not verify the livestock poisoning reports often told as selenium's origin story, so this page does not rely on them. The [history of iron supplements](/blog/history/history-of-iron-supplements-and-the-ferritin-test) covers the same poison-and-nutrient tension for another mineral. Our [selenium tablet](https://mtangelvitamins.com/products/selenium-200mcg-capsules-high?utm_source=learn_hub&utm_medium=content&utm_campaign=blog_post&utm_content=history-of-selenium-from-poison-to-keshan-disease) lists 200 mcg of selenium per tablet as L-selenomethionine, 363 percent of the Daily Value. The product page shows 60 tablets for $15.99, about $0.27 a day, and the directions say one tablet daily. That dose is half the adult upper limit, so add up food, multivitamins and any other supplement before you add it. ## Bottom line Count selenium from food before you add a tablet, and keep the total under the NIH's 400 mcg adult limit unless a clinician has set a different target. Seafood, meat, poultry and Brazil nuts are real sources, so a regular Brazil nut habit may already cover much of your intake. If your intake is already adequate, the 2012 Lancet review says extra selenium might affect you adversely. ## Frequently asked questions ### Why was selenium once known mainly as a poison? We could not verify the livestock poisoning reports that usually anchor this story in PubMed or NIH sources, so this page does not state them as fact. What the record supports is the toxicity side. The NIH describes chronically high intake, or selenosis, with hair loss, brittle nails, a garlic odor on the breath and a metallic taste, and it sets a 400 mcg adult upper limit. Read the poison label as a modern safety lesson, because the verified record gives the danger, not a settled origin story. ### Who named selenium, and why? Berzelius named it in 1817, working with Gahn. They first identified the precipitate as tellurium, but Berzelius repeated the analysis and found a new element. He named it for the Greek word for the moon, Selene, because it resembled tellurium, which takes its name from the Latin word for earth. ### What is Keshan disease, and how did it shape selenium research? Keshan disease is an endemic heart disease in China with a high case-fatality rate, according to a 2012 review. Low selenium in local grains and residents was associated with it, and trials that gave sodium selenite tablets significantly reduced its incidence. A 2018 meta-analysis of 41 studies found a pooled risk ratio of 0.14 for supplemented residents and calls selenium deficiency a cause of the disease. That body of trial evidence is why Keshan disease anchors selenium's nutrition history. ### When did researchers show selenium is essential? The NIH now calls selenium an essential mineral. The biochemical proof came in 1973, when Rotruck and colleagues reported selenium as a component of glutathione peroxidase in rats. The earlier liver-degeneration work by Schwarz and Foltz is a classic milestone, but we could not confirm its original publication year, so this page does not give one. ### Why is selenium toxicity a real risk with supplements? Chronically high intake causes selenosis. The NIH lists hair loss and nail brittleness as the most common signs, with garlic breath and a metallic taste as early warnings. The adult upper limit is 400 mcg a day from food and supplements combined. The organic and inorganic forms have similar effects at high intakes, so switching forms does not widen the margin. ### How do soil levels change the selenium in food? Soil sets the starting point for plant foods. The NIH says the selenium content of plant-based foods varies by geographic location, because the amount and form of selenium in soil influence what plants take up. Animal products are steadier, because animals hold tissue selenium at predictable levels. Seafood, meat and poultry are rich sources, and Brazil nuts carry particularly high amounts. ### Which selenium forms appear on supplement labels? The forms named in these sources are L-selenomethionine, selenium yeast and sodium selenite. A 2000 review calls L-selenomethionine a major natural food form and says synthetic L-selenomethionine or selenium yeast are appropriate supplement forms. The Chinese trials used sodium selenite tablets. The NIH says high intakes of the organic and inorganic forms have similar effects, so the label form matters less than the total amount you take. ## Next reads - [Mitochondrial health guide](/health/mitochondrial-health-complete-guide): the cell-level starting point for this story. - [The history of iron supplements](/blog/history/history-of-iron-supplements-and-the-ferritin-test): the same poison-and-nutrient tension, for a different mineral. ### Related reading - [The iodine origin story, from seaweed to iodized salt](/blog/history/history-of-iodine-from-seaweed-to-iodized-salt)