The Gut-Selenium-Thyroid Axis: Microbiome-Dependent Selenium Biotransformation, Bacterial Deiodinase Activity, and Dysbiosis as a Third Route to SIK Axis Failure Independent of Dietary Selenium or Iodine Status

This paper proposes that gut dysbiosis represents a third route to Selenoprotein Axis failure through three simultaneous mechanisms: (1) disruption of beneficial bacteria that convert dietary selenium to bioavailable selenomethionine, reducing effective selenium delivery even when dietary intake is adequate; (2) loss of bacteria with deiodinase activity that participate in enterohepatic T3/T4 recycling, reducing effective thyroid hormone activation independently of the hepatic deiodinase step; (3) increased intestinal permeability from dysbiosis allowing endotoxin to enter circulation, activating NF-kB and amplifying hepcidin elevation. A 2025 Nature npj Science of Food review confirmed that gut microbiota can metabolize and transform selenium. A 2025 Frontiers review confirmed that gut microbiome regulates thyroid hormones through its own deiodinase activity. All claims are hypothesis-level.