Guest guest Posted November 11, 2011 Report Share Posted November 11, 2011 Do we really not know the answer to this basic question? Miriam > Is this the one you were referring to? It was me who picked out the > following sentence (from a letter by an endo)and asked if it was true. Unfortunately it went unanswered and is now on the third page somewhere, so if anyone does know the answer, I'm still interested - and so is Miriam [] > > " She is well informed over normal thyroid physiology and understands > that Tri-iodothyronine is the active thyroid hormone and that in > patients receiving Thyroxine exclusively, normal T3 levels are > maintained by peripheral conversion of Thyroxine. I have explained to her that the pituitary thyroid hormone receptor is a receptor > exclusively for T3 and that the maintenance of a normal TSH on Thyroxine replacement is therefore dependant on the conversion of T4 to T3. " > > Gill Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 11, 2011 Report Share Posted November 11, 2011 Hi Miriam and Gill, It was myself who was told this by an Endo a couple of weeks ago. While I am still learning about my thyroid and the (what seems like) vast amount of external factors which affect can affect so many different things, which in all honesty just totally confuse me. I have to keep reading and re-reading things in the hope that I manage to read it during an all too brief period of lucidity where my brain can actually absorb the information. I don't count myself knowledgable enough to be able to explain anything to do with the thyroid but I have come acroos the following link which even I managed to understand, a bit like a eureka moment it was to be honest.http://tiredthyroid.com/tsh.html One wee section I found especially interesting is the following: "Anyone with Graves' disease who has had radioactive iodine treatment (RAI), a thyroidectomy, or takes anti-thyroid drugs (ATD), and is now on thyroid medication, should not be dosed by TSH. Graves' is caused by TSH Receptor antibodies, and TSH can stay suppressed (near zero) for months or longer, even after treatment brings thyroid hormone levels down into the normal range or even below normal. [4] If they are unable to get adequate thyroid hormone replacement because of their suppressed TSH, these patients will suffer from hypothyroid symptoms. They would fare much better by adjusting their dose to Free T3 and Free and/or Total T4 levels, instead of the TSH." This is me - so why do the GP and Endo just look at TSH? I have never once had any form of testing whatsoever done regarding T3 and they refuse point blank to do these tests. It just proves that they really don't have any clue whatsoever sadly. Lynn >> Do we really not know the answer to this basic question?> Miriam > > "She is well informed over normal thyroid physiology and understands> > that Tri-iodothyronine is the active thyroid hormone and that in> > patients receiving Thyroxine exclusively, normal T3 levels are> > maintained by peripheral conversion of Thyroxine. I have explained to her that the pituitary thyroid hormone receptor is a receptor> > exclusively for T3 and that the maintenance of a normal TSH on Thyroxine replacement is therefore dependant on the conversion of T4 to T3." Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 11, 2011 Report Share Posted November 11, 2011 Thanks, that's a good article. This part seems particularly relevant: " One study determined that the relative potency of T3 to T4, in terms of its ability to inhibit TSH, was 100:12. [8] " That means a low TSH might reflect conversion of T4 to T3. But given that there are so many other factors which can lower TSH, it is not a reliable guide. Miriam > > It was myself who was told this by an Endo a couple of weeks ago. While I am still learning about my thyroid and the (what seems like) vast amount of external factors which affect can affect so many different things, which in all honesty just totally confuse me. I have to keep reading and re-reading things in the hope that I manage to read it during an all too brief period of lucidity where my brain can actually absorb the information. I don't count myself knowledgable enough to be able to explain anything to do with the thyroid but I have come acroos the following link which even I managed to understand, a bit like a eureka moment it was to be honest. > http://tiredthyroid.com/tsh.html <http://tiredthyroid.com/tsh.html> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 12, 2011 Report Share Posted November 12, 2011 hello lynn, gill and miriam i found the information about deiodinase enzymes to be absolutely crucial in understanding how the tsh works...and more particularly, understanding the knock on effect of too much stress (from any source, even too much fun!) i.e. initially to produce too much cortisol but after a prolonged period to not be able to produce enough cortisol...both situations impede thge use of t3 ...the way this occurs is by the body's changing production of these important enzymes in response to stress. i first came across this link about 15 months ago and it has probably taken me that long to really get to grips with what it is saying! http://nahypothyroidism.org/deiodinases/ " To accurately assess thyroid function, it must be understood that deiodinase enzymes are essential control points of cellular thyroid activity that determine intracellular activation and deactivation of thyroid hormones. This local control of cellular thyroid levels is mediated through three different deiodinase enzymes present in different tissues in the body; type I deiodinase (D1) and type II deiodinase (D2) increase cellular thyroid activity by converting inactive thyroxine (T4) to the active triiodothyronine (T3) while type III deiodinase (D3) reduces cellular thyroid activity by converting T4 to the anti-thyroid reverse T3 (reverse T3) (1-9) (see deiodinase figure). The activity of each type of deiodinase enzyme changes in response to differing physiologic conditions, and this local control of intracellular T4 and T3 levels results in different tissue levels of T4 and T3 under different conditions. Because it is the activity of these deiodinases and transport of T4 and T3 into the cell that determines tissue and cellular thyroid levels and not serum thyroid levels, serum thyroid hormone levels may not necessarily predict tissue thyroid levels under a variety of physiologic conditions. Depression Many depressed and bipolar patients have undiagnosed thyroid dysfunction as the underlying cause or major contributor to their depression that is not detected by standard thyroid tests (23-38). The dysfunction present with these conditions includes down regulation of D1 (reduced T4 to T3 conversion) and reduced uptake of T4 into the cell, resulting in increased serum T4 levels with low intracellular T3 levels (24-26,30,31,35,39-45) and upregulated D3, resulting in elevated reverse T3 (23,24,30,31), which blocks thyroid effect (147,184-194) and is an indicator of reduced transport of T4 into the cell (183,193). Additionally, studies show that depressed patients have reduced T4 transport across the blood brain barrier due to a defective transport protein, transthyretin, resulting in significantly reduced thyroid levels in the brains of depressed patients despite “normal†serum levels and standard thyroid tests (23,39,40) as well as a reduced TSH response to TRH (28-31,43-50). It is not surprising that T4 and T4/T3 combinations may have some benefit in depression; but due to the suppressed T4 to T3 conversion from suppressed D1(24-26,30) and reduced uptake of T4 into the cell and brain (25,31,39,40), timed-released T3 is significantly more beneficial than T4 or T4/T3 combination supplementation (25,41,202,225-227). " here's another link about these enzymes. trish > > Hi Miriam and Gill, > > It was myself who was told this by an Endo a couple of weeks ago. While > I am still learning about my thyroid and the (what seems like) vast > amount of external factors which affect can affect so many different > things, which in all honesty just totally confuse me. I have to keep > reading and re-reading things in the hope that I manage to read it > during an all too brief period of lucidity where my brain can actually > absorb the information. I don't count myself knowledgable enough to be > able to explain anything to do with the thyroid but I have come acroos > the following link which even I managed to understand, a bit like a > eureka moment it was to be honest. > http://tiredthyroid.com/tsh.html <http://tiredthyroid.com/tsh.html> Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 12, 2011 Report Share Posted November 12, 2011 this is the other link ....sorry! http://www.jci.org/articles/view/29812 > here's another link about these enzymes. Quote Link to comment Share on other sites More sharing options...
Guest guest Posted November 12, 2011 Report Share Posted November 12, 2011 Thanks. I'll have a look at those. Miriam > > here's another link about these enzymes. > Quote Link to comment Share on other sites More sharing options...
Recommended Posts
Join the conversation
You are posting as a guest. If you have an account, sign in now to post with your account.
Note: Your post will require moderator approval before it will be visible.