Selenium
Chemical formula Se (element); biological forms include selenomethionine and selenocysteine in proteins
Solubility Selenate and selenite salts are water-soluble; elemental selenium is insoluble
Bioavailability Seafood and organ meats supply selenoproteins; soil selenium varies by region
Dietary sources Seafood, Brazil nuts, liver, eggs, mushrooms; higher in sea-based diets
RDA (adults 19–50 y) ~55 µg/day (US adult)
Upper limit 400 µg/day (US adult supplemental UL)


Selenium is a trace mineral incorporated into selenoproteins including glutathione peroxidase. Mainstream nutrition treats deficiency as a cause of Keshan cardiomyopathy and immune impairment.

Ray Peat listed selenium among chain-breaking antioxidants that support respiration when oxygen delivery fails, alongside thyroxine, uric acid, vitamin A, Sodium, and Magnesium.[1] Seafood eaters get more selenium than land-only diets in his cholesterol writing.[2]

History

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Etymology

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The name comes from Selene, the Greek moon goddess, chosen because selenium was found alongside tellurium (named for tellus, "earth") and shares some of its chemical properties.

Jöns Jacob Berzelius discovered selenium in 1817 as a byproduct of sulfuric acid production.

Structure/Chemical properties

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Selenium (Se, atomic number 34) sits below sulfur in the periodic table. Biological activity is mainly through selenocysteine at enzyme active sites. Inorganic selenite and selenomethionine differ in metabolism but both can replete deficiency in mainstream nutrition.

The thyroid gland holds the highest selenium concentration per gram of any organ. Selenium is built into the iodothyronine deiodinases (DIO1, DIO2, DIO3) that activate and inactivate thyroid hormone, along with glutathione peroxidases and thioredoxin reductases that protect the gland from the hydrogen peroxide generated during hormone synthesis.[3]

Function/Mechanism of Action

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Many antioxidant nutrients act like a thyroid supplement did in the 1934 rabbit experiments, preventing atherosclerosis even when extra toxic cholesterol is given to the animals.

Peat grouped selenium with Vitamin E and saturated fats as defenses against PUFA-driven lipid peroxidation in heart-disease discussion; the medical establishment long opposed selenium and vitamin E for cardiovascular use while many physicians took vitamin E themselves in his account.[2]

If your liver isn't getting enough glucose or selenium, it is unable to convert thyroxine (T4) into T3. If you starve for 24 hours or exert too much energy, your liver isn't getting enough glucose to convert the T4 into active T3.

Peat repeated the same glucose-selenium dependency in later interviews: every tissue that converts T4 into locally active T3 needs both glucose and selenium to run the deiodinase reaction, not just the liver.[6] Glucose and selenium support T4-to-T3 conversion enzymes in Peat's thyroid article.[7] Riboflavin, coenzyme Q10, vitamin K, niacinamide, thiamine, and selenium support mitochondrial respiration in FPS compilations Peat endorsed.[8]

In animal models Peat cited, selenium supplementation protected against high-fat-diet atherogenic changes.[2] On mad-cow and amyloid topics selenium and vitamin E limit oxidant damage when PUFA and iron are high.[9]

Medical uses/Effects

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Exercise raised systemic selenium delivery to the hippocampus, activating neural stem cells and improving learning in aged mice; selenium supplementation alone replicated exercise-level neurogenesis and cognition gains.[10]

Low selenium status is associated with hypothyroidism, subclinical hypothyroidism, and autoimmune thyroid disease (Hashimoto's thyroiditis, Graves' disease); trials of selenium supplementation (commonly 100-200 µg/day) have reduced thyroid antibody levels in autoimmune thyroiditis and improved mild Graves' orbitopathy in some studies, though clinical outcomes vary by baseline selenium status.[3]

Mainstream medicine uses selenium repletion in deficiency. Peat's emphasis is dietary seafood and antioxidant context with lower PUFA and Iron, not megadose selenium pills as a primary strategy.[2] Rosacea writing names selenium among mitochondrial-support nutrients with riboflavin and thiamine.[11]

Side/Adverse effects

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Selenium toxicity (selenosis) causes garlic breath, nail changes, and neurologic symptoms at chronic high intake. Brazil nuts vary widely in selenium content. See Harm reduction before high-dose supplements.

Dosing

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Selenium, I think 100 micrograms is a safe supplement. And selenium is essential for the local production in the tissue.

Shellfish and varied whole foods match his seafood emphasis in cholesterol and iron articles.[2] Pair with adequate Vitamin E and thyroid support when addressing stored PUFA per his wider writing.

References

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  1. Iron's Dangers, Ray Peat article
  2. 2.0 2.1 2.2 2.3 2.4 Cholesterol, longevity, intelligence, and health, Ray Peat article
  3. 3.0 3.1 Ventura M, Melo M, Carrilho F. "Selenium and Thyroid Disease: From Pathophysiology to Treatment," International Journal of Endocrinology. 2017;2017:1297658. PMID: 28255299.
  4. Cholesterol and Longevity, Ray Peat newsletter
  5. Ray Peat, "EastWest Healing: The Thyroid", EastWest Healing, 35:32
  6. Ray Peat, "It's Time to Start Being Skeptical of the entire Medical System", One Radio Network, 50:41
  7. Thyroid: Therapies, Confusion, and Fraud, Ray Peat article
  8. Protect the Mitochondria, FunctionalPS compilation of Ray Peat material
  9. BSE - mad cow - scrapie, etc., Ray Peat article
  10. Leiter O, et al. "Selenium mediates exercise-induced adult neurogenesis and reverses learning deficits," Cell Metab. 2022. doi:10.1016/j.cmet.2022.01.005.
  11. Rosacea, inflammation, and aging: The inefficiency of stress, Ray Peat Newsletter
  12. Ray Peat, "Dr. Fauci's "Absolute or None" Approach Is Cult Thinking, Not Science", One Radio Network, 93:46