But the answer's simple - you just need levothyroxine....One day - the truth will out. We know so little - which makes the 'levo fits all' answer so frustrating.
A little bit heavy for after dinner reading! They mention that local conversion of T4 to T3 happens in 'cold exposure or physical exercise without perturbing systemic TH levels'. This is done by type-2 deiodinase (D2) and it's interesting that the very large increase in D2 activity is not reflected in blood tests i.e. 'systemic TH levels'. D2 is the dominant T4 to T3 conversion mechanism when hormone levels are not excessively high. We know that some patients have abnormally low fT3 when TSH is insufficient. This raises the question of 'where does the T3 come from'. This paper reminds us that the D2 derived T3 we see in the blood is by and large not coming from brown fat or muscles. I have a sneaky suspicion it is coming from the brain. This would explain why patients with low normal TSH, fT3, fT4 do so badly. Unfortunately, I know of no evidence to confirm this.
The mystery (to me) of D2 effect on conversion of T4 to T3 is very interesting at my lower state of understanding of converting T4 to T3.
I am hoping there is a secret to be discovered which Endos don’t know or don't think Is important.
Almost as though Endos think your health is good enough for you now and that we don’t deserve or are being unrealistic to want to feel “perfect” again.
I will pursue this D2 and T4 to T3 secret, the brown fat and muscles aspect and the heat and cold effect (I suspect I’ve suffered from that this winter).
Thank you - a little heavy going as you say, but of interest, especially the comment:
At the cellular level, the classic, biologically active TH, 3,5,3′-triiodo-L-thyronine (T3), predominantly acts through thyroid hormone receptors (THRs), which are predominantly localized in the nucleus and, upon binding of T3, act as ligand-dependent transcription factors that regulate gene transcription through binding to thyroid hormone response elements (TREs).
I appear to have impaired THR receptor signalling, so this might explain persistently low FT3 levels, perhaps.
Very difficult - if your cells do not respond to current levels, you might expect your body to attempt to increase them. Therefore, end up with higher serum T3?
When I first started reading about thyroid and thyroid hormone, I could never find anything that identified the precise things that thyroid hormone does in our bodies, our cells. Just general "control metabolism" and similarly woolly phases.
Reading some of this, I realise that I was reading a decade before a lot of this had been identified.
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