A more up to date/ accurate understanding of the process can be gained by reading the relevant articles on this site : thyroidpatients.ca/home/sit... Thyroidpatients.canada (full site list ~ i will add a link to the most relevant articles once i find them again)
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tattybogle
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Interesting articles and I wondered if anyone could anybody explain this to me please?
If ‘pooling’ doesn’t happen, why is it when initiating adrenal support we can have tissue overstimulation due to re-uptake? Where is this excess of T3 coming from if not the blood?
additionally, FT3 levels can drop on blood tests when cortex/HC is taken, which makes me more inclined to listen to the theory of pooling 🤔 Clarebear ’s bloods show this for example.
I agree, when my cortisol is low my T4 on 62.5mcg Thyroxine is 17.6 ( 12-22) when taking AC or HC it drops down to 12 (12-22) The same happens with Erfa..
Pooling was pushed by STTM and tied in with the myth concerning RT3 blocking receptors, and the fact that high RT3 and low FT3 often go together. A pool would need a damn or plug to accumulate but the body doesn’t allow large amount of hormone to sit around in a puddle.
Remember ‘pooling’ was used to relate to unusable thyroid hormone accumulating in the blood, which we now know can not happen. T3 is activated within the cell, it goes in and out on transporters regardless of RT3. Lowered FT3 levels result not from RT3, but from D3 blocking T3 from entering the cell’s nucleus and other means such as lowering activity of conversion enzyme D2.
Most thyroid hormone is bound with very little ‘free’. Any excess felt when starting adrenal supports would be resulting from improved usage and clearance, meaning for a short time you were possibly over medicated until you either reduced dose or systems readjusted to accommodate this improved new efficacy. All hormones work together and positively supporting one set will always influence others.
Courtesy of Tania Smith. Tatty has provided links above.
STTM are mistaken in saying it is rT3 that blocks T3 from entry, it’s actually the enzyme D3 (that happens to create rT3) that does the blocking?
FWIW, I never take “pooling” to imply a puddle of FT3 sat in the blood. If they genuinely meant that it was just a puddle of FT3 that is never excreted, you’d end up with FT3 of values like 1000s+ Because the puddle would just keep getting deeper. I take it to suggest that FT3 builds up outside the cell where it cannot be metabolised properly and is then excreted as you’d expect any unusable hormone to be - exactly the same way that Barry Peatfield describes being “thyrotoxic” when thyroid hormone accumulates in the body but can’t be used due to low cortisol, low iron etc.
i think the amount that is excreted is v small . Most of the process of dealing with unused thyroid hormone is by recycling of the iodine . the deiodinaes remove iodine atoms along the way to get from T4 to T3 /rT3 to T2 to T1 to T0. ( ish )
Not very much i don't think .. T2 (there's more than one sort of T2) get's turned into T1 , (then i think T '0' ?) i would need to ask a cleverer friend though ,i'm a bit hazy about some of this ..haven't paid enough attention in class lol. I just remember that recycling is the main thing rather than excreting . ie body trying to look after it's iodine supplies rather than wasting them...kinda thing .
(edited to correct typo )T3 and T4 get into the cells , once inside the cell wall , D3 turns some of the T4 into rT3 .. meaning it can't fit onto the T3 receptors . (T4 /T3 and rT3 can also leave the cell and return to the bloodstream)
as far as i understand it so far ~the main error in the way Sttm write about pooling , is they give people the impression that Reverse T3 is the thing that 'blocks' T3 from getting to the T3 receptors.. but it is not .. it is the action of the deiodinases which stop T3 from getting to the T3 receptors~ by catching T4 just inside the cell boundary and turning some of it into rT3 .
So high rT3 is the result of a problem , not the cause of it (i think)
so it’s this? STTM are mistaken in saying it is rT3 that blocks T3 from accessing cells, T3receptor sites inside the cells are blocked by the enzyme D3 that happens to create rT3.
T3 receptor sites inside the cells are blocked by the enzyme D3 that happens to create rT3.
technically nothing is blocking the T3 receptors... some T3 can still get to them and fit onto them .
Reverse T3 just can't fit onto the receptors that's all.
reverse T3 is the wrong 'shape' to fit into the keyhole , because it's 'reversed' ( like mirror image ).. it has had an iodine atom removed from the 'wrong' corner .. (if you remove an iodine atom from the 'right' corner you get T3 and that does fit onto T3 receptors)
as in 'block some of the T4 from being turned into T3 '
not
'block the receptors by bunging them up' ..
there is no 'blocking the keyhole '. there are just some really efficient defenders (D3) making some of the keys the wrong shape to fit the keyhole.
So ....same effect (not so many keys can get into T3 keyhole when D3 deiodinase is dominating that cell ) .. but different reason. (more keys are wrong shape to fit keyhole, not a bunged up keyhole.. the keyhole still works fine if any T3 gets to it )
rT3 has had an iodine atom removed from the 'wrong' place to make T3, but it's not exactly a mirror image.
Oh, and T0 is actually just tyrosine without any iodine because the last atom of iodine has been removed, to be recycled. The remaining tyrosine is 'disposed of' - perhaps excreted, I don't know, but it isn't recycled, I don't think. Doctors don't like calling it T0. I once mentioned it to a doctor in conversation (actually, he hadn't a clue what I was talking about) and he nearly had hysterics when I said T0, he thought it was very funny. Moron.
Cortisol action is a bit over my head , but i assume when trying to understand what happens to T3 levels here, you have to consider:
a) any changes in thyroid 'binding' in the blood TotalT4 / freeT3 TotalT3 /freeT3 .. any changes in the level of thyroid binding goblins ( thyroid binding globulins +2 others that i've forgotten ) will presumably affect the ratio of Total T3: FreeT3.
b) you also have to consider anything that affects the deiodinases .... if you change the level/ ratio/ efficiency of D1/ D2/ D3 then you change how much T4 goes to T3 or rT3 and how fast or slow T3 or rT3 goes to T2 etc etc ..
my knowledge is still very fuzzy , but deiodinases are up-regulated or down-regulated in different situations .. rather than me try to explain (badly) , start here:
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