New Research - Triiodothyronine Secretion in Early Thyroid Failure
Here is a very important new research article.
In one of the co-authors own words, "The paper shows that during the course of thyroid decline from the start, increases in TSH resulting from the shortfall of T4 production has a stimulatory effect on thyroid direct T3 production, to make up as far as possible the shortfall in corporeal T4-T3 conversion caused by lack of enough T4. The feed forward TSH-T3 stimulation in the gland can go on for a long time, whereby at the end game when the gland finally dies, the T3 produced by the thyroid is greater than T4-T3 conversion in the body (because of the gross lack of T4). This can mean that the body tries to keep as stable as possible regarding T3 production until the thyroid is totally lost and this then enters an entirely new phase. It can be round about now when the patient feels hypo strongly."
It should be clear from the above description and from the article ihow important the thyroid gland actually is. It compensates for damage to itself so much that it can mask this for a long time. The article explains why so many patients that suffer from Hashimoto's thyroiditis feel well for such a long time due to the extra T3 production that the thyroid is capable of. Towards the end of the progression of Hashimoto's, when thyroid tissue damage has become very significant, severe symptoms can suddenly begin to appear. Lab testing at this stage often shows very high TSH, and very low FT4 and FT3 levels. This is exactly what happened to me. In the case of thyroidectomy patients, they are thrown into the state of thyroid tissue loss immediately, so getting their FT3 levels back up to a healthy level is very important (obviously the right level is very individual).
Please enjoy this - it is a very important article:
"Triiodothyronine Secretion in Early Thyroid Failure: The Adaptive Response of Central Feedforward Control"
December 2019 European Journal of Clinical Investigation. DOI: 10.1111/eci.13192
Rudolf Hoermann, Mark Pekker, John Edward M Midgley, Rolf Larisch Johannes W. Dietrich
The link to the article is: here
Note: in one place in the article is states:
"whereby at the end game when the gland finally dies, the T3 produced by the thyroid is greater than T4-T3 conversion in the body (because of the gross lack of T4)".
What the authors meant by this is that just before thyroid gland finally dies the T3 produced by the thyroid is greater than T4-T3 conversion in the body (because of the gross lack of T4). After this point the gland fails catestrophically and T3 levels plummet leaving the thyroid patient with low T3 and T4 levels.
In the words of another of the co-authors:
"Our data reveal that 1) there is a strong rescue mechanism based on direct thyroidal T3 secretion and activated on demand 2) this does not depend on conversion/ deiodinases and may explain 3) why experimental animals deficient in all three deiodinases, but with an intact thyroid were reported to survive and live well (they are not hypothyroid.).The thyroid gland and its massive ability to contribute T3 is crucial."
The article is saying that in a declining T3 environment (not a euthyroidal healthy state) the central role of the thyroid gland is paramount in maintaining healthy T3 levels. This is through the gland's ability to shift as much of its ability as possible into making T3. This is not controlled by TSH either. It is as another of the author's says, "Strong T3-protective mechanisms of the control system emerge with declining thyroid function, when glandular T3 secretion becomes increasingly influential over conversion efficiency."
They also conclude that this shows once again that the influence of TSH is being over estimated and the reliance on it to determine whether someone is properly treated or not is flawed.
All very interesting.