
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.
bile acids, Lactobacillus, enterohepatic T3 recycling, intestinal permeability, secondary bile acids, gut-thyroid axis, selenoprotein axis, gut microbiome, selenium biotransformation, dysbiosis, Akkermansia, bacterial deiodinase, Hashimoto
bile acids, Lactobacillus, enterohepatic T3 recycling, intestinal permeability, secondary bile acids, gut-thyroid axis, selenoprotein axis, gut microbiome, selenium biotransformation, dysbiosis, Akkermansia, bacterial deiodinase, Hashimoto
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