Read today in another thyroid forum:
"Taking T4 with a suppressed TSH will maximize RT3 output from the T4.
T4 can also attach to the receptor sites limiting the space for T3 to fully get in."
I would be interested in any opinions on these assertions.
High levels of fT4 increases type-1 deiodinase which converts T4 to equal quantities of T3 and rT3. Also type-3 deiodinase is increased which converts T4 to rT3 and T3 to T2. So, the first point is correct if a suppressed TSH implies high thyroid hormone levels.
T4 is able to bind to thyroid hormone receptors with an affinity of about one percent of that of T3. So, the second point is logically correct but perhaps irrelevant.
Thanks for commenting jimh111 Re. T4 binding to T3 receptors, if you've got a reference I could read, that would be great, but I'm perhaps more intrigued by the description that T3 some how can't "fully squeeze in" which conjures up an image of bits hanging out, like two people in a single bed! 🙂 I can't see that as other than thyroid folk law. Am I missing something?
Re. the mechanics of prioritisation of RT3 over T3 in the case of high thyroid hormone levels, yes we're familiar with that; but as we also know, TSH can generally be suppressed with the ingestion of T3, but in the absence of high FT3 and FT4 levels and indeed with low in range or even below range FT4. So I'm thinking that the statement is more accurately a 'may' not a 'will' maximise RT3 in the presence of a suppressed TSH.
It's a long time since I read about T4 activity. To be more precise the study I saw mentioned T4 had about 1% the activity of T3. So, I shouldn't have written about T4 binding to receptors, but I guess that is probably the way T4 has genomic effects. (Thyroid hormone principally has genomic effects, it binds to receptors that bind to part of the DNA. Thyroid hormone also has some minor non-genomic effects, it works by other mechanisms - I'm very rusty on this). The 'fully get in' bit is dribble but I sort of guessed they meant there were fewer available receptors.
Again, I interpreted 'taking T4 with a suppressed TSH' to actually mean 'taking sufficient T4 to suppress TSH'. I usually prefer to refer to a 'very low TSH' rather than 'suppressed TSH' because the latter is presumptious, I see many low TSHs on this forum that are not due to suppression by abnormally high hormone levels.
Interesting - 'I see many low TSHs on this forum that are not due to suppression by abnormally high hormone levels.' I agree. Sometimes I find this all mind boggling, TSH appears to be misunderstood, as far as I am aware the pituitary gland sets the levels for TSH if it thinks the Thyroid needs them so should we be looking at this mechanism in isolation? Having no thyroid and past cancer, my TSH is supposed to be supressed but taking relatively normal levels of T4, possibly not even high enough, I really don't see how it is suppressing TSH. Am I way off?
We are in danger of drifting away from the original post. Thyroid hormones lower TSH and larger doses will suppress TSH but TSH can be low if the pituitary is not as vigourous as it should be. If you want to go into more detail please set up a separate post and pm me to let me know.
Without definitions (what constitutes suppressed TSH?), without knowing if that is adding 5 micrograms of T4 to a huge dose of T3, or T4 only, it is easy to pick holes but difficult to be clear what is being said.
Not at all sure I can accept the concept of T3 getting half in. Sure, something could get in the way and stop it attaching to the receptor. But this idea of not being fully in gives rise to more questions than answers.
It was an answer to someone asking why adding T4 to a normally mono-T3 treatment regime would make them "hypothyroid very quickly", so no specifics given unfortunately.
Sounds like the usual Internet "I made it up but it sounds good so now lots of people will copy it" nonsense. As far as I know, T4, T3 and rT3 all have their own totally separate receptors.
It sounds logical that if TSH is low, free T4 would be high and therefore more T4 would be converted to rT3 than T3, but you can have low TSH without high free T4 - both of mine are under range - and my rT3 is low normal. So it really doesn't follow. Very high free T4 probably increases rT3 regardless of what TSH is doing. I don't think anyone has done the studies, so most of these people are just parrotting what they have misunderstood elsewhere on the web. However, there is probably little point taking more thyroxine if your free t4 is top of the range and free t3 low in range - you need a reduction in thyroxine and some T3, but you can't really assume anything from low TSH.
Well, my latest numbers support the first sentence:
TSH = .01 (0.40 - 12.0)mIU/L (i.e. suppressed)
FT3 = 3.6 (2.3 - 4.2)pg/mL
FT4 = 1.3 (0.8 - 1.8)ng/dL
rT3 = 24 (6 - 25)ng/dL (i.e. too high - but "normal")
I understand that these are not the theoretical optimal (for someone ex-TT) but I feel great and as much as I would love to increase my dose (of Armor NDT) even a little bit the T3 content sends my blood pressure up (within minutes of taking it).
I cannot speak to the second sentence except to say that my T3 seems to be doing it's thing - not very scientific, sorry. So presumably it's getting in to my cells.
Yes I realize this is purely anecdotal - but many, many anecdotes eventually becomes sample data.
Reduce T3/ keep T4 the same ?
Adding T3 to T4 
