Sorry to bring it up again but can't find the last thread.
If we are 'seen' to be converting really well, e.g. a very low ft4 (11.7) but high ft3 (6) with TSH 2.4, is there any research that shows that this is a purely compensatory situation of an already failing thyroid and it will only get worse?
Have found only the merest info on this and I'm looking for something with a bit more meat!
The endo was really pleased with these figures.
P.S. I'm not 'on' anything at all currently.
Any input would be great.
Written by
tulula59
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Maintenance of a normal serum T3 concentration until a relatively late stage in the development of hypothyroidism obviously serves as an appropriate mechanism of the body to counteract the impact of diminishing production of T4. It is accomplished by a preferential thyroidal secretion of T3: the increased secretion of TSH enhances the synthesis of T3 more than that of T4 and stimulates thyroidal 5'-monodeiodination of T4 into T3 (4,5). It explains why sometimes a slightly elevated serum T3 is found in the early stage of development of hypothyroidism. About 80% of the daily production rate of T3 is generated in extrathyroidal tissues via the conversion of T4 into T3. The peripheral tissues also have a defense mechanism against developing hypothyroidism by increasing the overall fractional conversion rate of T4 into T3.
So am compiling my last notes of a 10 page reference schedule for my GP - lucky them.
My questions are now though are:
If the peripheral tissues are doing what might be considered a grand job in converting the dregs of my t4 into t3 so that these ft3 levels look pretty healthy why would I still be symptomatic (hair-loss, joint pains, coarse skin etc, cold and tired)?
Secondly, on what basis can I push for a trial of t4 apart from the physical symptoms?
Thirdly, does a failing production of t4 always lead onto a worse situation or is there evidence somewhere that will be thrown back at me that the thyroid can revive itself?
And lastly, if you supplement with t4 when the peripheral tissues are doing the job in compensation then don't we get overloaded with t3 as a consequence?
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