Please can someone give me a short explanation of RT3? I think I've read that it blocks the receptor cells...? But I can't remember much more.
I took 175 Levo for quite a few years, and my T4 test result was at top of range, but T3 was at the bottom, and I was very ill indeed. I wish I knew about RT3 then, as I would have got it tested.
I'd like to give a summary on RT3 to a forthcoming CCG meeting.
Thanks again
Not particularly short but I like Dr Peatfield's explanation in his book "Your thyroid and how to keep it healthy"
"You may remember that in order for thyroid hormone to work in controlling our metabolism it has to be converted from the basic, precursor hormone T4 to the active hormone T3. You will also remember that the amino acid thyronine (which is made by two tyrosine molecules coming together) when combined with four iodine atoms is how thyroxine is formed (which we know for short as T4). Then one of the three 5: deiiodinase enzymes removes one of the iodiio atoms and forms T3 (triiodothyronine or liothyronine), which does all the work of controlling our energy output. This it does by improving the capacity of the cell membrane to pass into the cell every chemical needed to make our metabolism work, and to fire up the capacity of the mitochondria within the cell to produce energy.
But circumstances may arise where the active T3 becomes unwanted by our metabolic chemistry. Then the T4 to T3 conversion is sabotaged, and the iodine atom removed from T4 is taken from a different site in the T4 molecule. So the chemistry is the same, but the layout is subtly different. This differed form of T3 is called reverse T3 (rT3). And reverse T3 doesnt have metabolic activity; it doesnt have any effect on the cell membrane or the mitochondria.
So, what is it for?
It turns out that this is a cunning way of removing excess thyroid hormone, and preventing too much active T3 from being made.
The reverse T3 rapidly breaks down to its component parts the thyronine and iodine, which are thus re-cycled and stored, until more thyroid hormone is required. So, you see rT3 is a way of disposing of excess thyroid hormone.
Certain circumstances can arrive when removal of excess thyroid hormone is helpful. Obviously, this process can remove excess T3 if the thyroid gland is producing too much. This happens in early hyperthyroidism, although the recycling is fairly limited, and with a thyroid gland thoroughly over the top, is only of modest effect.
Many authorities like to test for reverse T3. I dont find this a particularly helpful test, but perhaps we can look at how it can be interpreted. A low level is likely to be found with a hypothyroid state. If thyroid output is lower than it should be, then rT3 levels will be low since there is less T4 to be converted into either T3 or rT3. You can then conclude that primary thyroid output is below normal, or that conversion is limited.
Poor conversion relates to low adrenal function (adequate cortisone is needed for the conversion to work properly) or exhaustion or dysfunction of the 5 deiiodinaise enzyme itself. Diagnostically, poor conversion is usually evident in the serum tests or the 24-hour urinary thyroid hormone.
Treatment is of course obvious. Either the provisions of T4 or T3 or both; or the use of natural desiccated thyroid, once adrenal support is fully in place.
The pathological finding of increased rT3 means that either more thyroid hormone is being created than the system needs or can use: or, that there is some pathological process blocking adequate T3 uptake. Dieting or malnutrition will have this effect; chronic illness will do the same. Particularly one should mention the presence of cancer somewhere (especially metastatic cancer, i.e. when it spreads), a degree of liver or kidney failure, Cushings disease, insulin dependent diabetes, and the post operative state following surgery.
Treatment has to be, therefore, if appropriate, of the primary cause. Provision of extra T4 or T3 is not an option, because it will mearly create more rT3. High rT3 means that general health should be considered; and if all is well, one has to decide whether the provision of any thyroid replacement could be too much, or there is a processing factor causing a back up of T3 or T4.
Questions have been raised concerning the possible role of high rT3 in causing receptor resistance in fibromyalgia. My colleague John Lowe found no evidence of this, and nor have I. Receptor resistance may indeed occur, but it is due to other factors, most commonly adrenal insufficiency."
Anything helpful you can summarise there?
Dr Peatfields summary is very good. If thyroid hormone levels go high type-1 deiodinase which converts T4 to T3 and T4 to rT3 is increased. rT3 can also increase if there is some serious illness such as a cardiac problem or burns injury, what Dr P calls 'pathology'.
Dr P says provision of extra ...T3 is not an option. I believe he is restricting this comment to cases of T3 due to illness and that the causative illness shoud be sorted. If you have low fT3 even when fT4 is moderately high then it makes sense to prescribe T3 medication (Dr P does this in the form of NDT).
Having written all this I don't think a rT3 assay is much good in most cases, nobody really knows how to interpret the numbers. It's an expensive test and we should focus on the basic blood tests and give more attention to symptoms.
I think I've read that it blocks the receptor cells...
That is what used to be believed. Now, there is some evidence that it doesn't do that, and that it has its own receptors.
rT3 is inactive and inhibits T3 action. It used to be assumed this was through a 'dominant negative' action, bind to receptors in preference to T3. This is now known not to be so. rT3 inhibits T3 action but the mechanism is not known. rT3 could have its own receptors for other roles, I haven't seen any reference to this but it is perfectly possible. These receptors would be quite different in function to T3 receptors.
rT3 is inactive and inhibits T3 action
That sounds like a contradiction in terms. If it is inactive, how does it inhibit anything?
It was diogenes that posted about rT3 receptors, and he said that the purpose was not known.
Not a contradiction. rT3 is inactive, as far as we know it doesn't promote thyroid hormone action. rT3 is known to inhibit T3 action but not by competitive binding to thyroid hormone receptors. So we know it inhibits thyroid hormone action, we don't know how but we know it isn't by a dominant negative action (competitive binding to thyroid hormone receptors. There are a number of interactions when T3 binds to receptors and rT3 seems to inhibit this process but not by binding to the T3 receptors. Not a lot is known about rT3.
This diagram gives quite a good visualisation of what happens when the T4 bucket gets too full. goo.gl/images/tru6Bm
The diagram is likely to confuse. When fT4 is high type-1 deiodinase (D1) is increased. D1 converts T4 to T3 and rT3. Also with high hormone levels D3 increases, D3 converts T4 to rT3 and T3 to T2. So, in high hormone situations more rT3 is produced, presumably to try and prevent thyrotoxicity. In addition various illnesses lead to higher production of rT3.
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