Random, interesting studies
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I remember Click saying that promoting butyrate-generating foods was just a way of recapitulating life as it was in selenium-rich soil, since selenomethionine is converted to α-keto-γ-methylselenobutyrate (KMSB) and works basically the same way as butyrate.
So supplementing selenomethionine mimics a Methionine restriction and also promotes an increase in keto acid similar to butyrate. Interestingly, consuming resistant starch increases butyrate production and also mimics Methionine restriction (and other amino acids like leucine, tryptophan, etc.).
Funny how it works haha
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@TexugoDoMel yo did you know there are other selenium type aminos and stuff in fish
there's one called selenoine or something like that, I probably spelled it incorrectly
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Selenoneine? I remember seeing some relation to mercury detoxification, but I don't know much about this one in particular.
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@TexugoDoMel said in Random, interesting studies:
Selenoneine
"In addition, protective roles of selenoneine as a radical scavenger in the heart and blood cells in humans might also be essential for the adaptation to low-oxygen environments at high altitudes.""
""In contrast, tilapia blood, porcine kidney, chicken heart, gizzard and liver, and squid hepatopancreas contained low levels of selenoneine and selenoproteins. Furthermore, porcine liver contained only selenoproteins and not selenoneine. In summary, selenoneine was found to be widely distributed in various animal tissues and occurred at especially high levels in tuna tissues. "
"This selenium compound has strong antioxidant capacity and binds to heme proteins, such as hemoglobin and myoglobin, to protect them from iron auto-oxidation"
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@cs3000 said:
something interesting,
when thyroid receptors aren't bound by the hormone / agonist they block DNA transcription. using HDAC. HDAC inhibition is 1 way to help the people who have receptor mutation / resistance, (sort of)
https://academic.oup.com/hmg/article/23/10/2651/614693#10263757
https://scholars.mssm.edu/en/publications/histone-deacetylase-inhibition-reduces-hypothyroidism-induced-neu
So basically people can get some of the gene effects from T3 activation if its lacking, without the t3 , by hdac inhibition . not full effects but someBam! So the working mechanism of T3 is not directly cellular stimulation, but inhibition of the inhibition of cell metabolism?
Therefore, vice versa, a practically hypothyroid state would be mimicked by overmethylation of the CpG sites on the DNA (blocking the translation of genes) or by deacetylated/dephosphorylated/demethylated/de-beta-hydroxybutyrylated sites of the lysine chains of the histones (compressing the histones which wrap the DNA strands which prevents DNA access)?To supplement thyroid hormones would work in such circumstances but be a kind of force-feeding, rawhiding override and circumvention of the actual underlying culprits?
But using other inhibitors of HDAC or DNMT could then be actually better and closer to the original cause and also effectively act like thyroid hormones?I used to think of HDACis only as some very beneficial class of substances in a vague context of cancer (even though even in that they are very restricted).
Now they appear much more crucial in all kinds of diseases and chronic impairments.
If I were casually being offered some pure quality HDAC inhibitors I would gladly take them and run a treatment course with them. -
@CrumblingCookie HDAC inhibition also increases expression of thyroid receptor itself.
