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What Should We Do About rT3?

By Dr Barry Durrant-Peatfield

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.


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The late Dr John Lowe in his book the ‘ Metabolic treatment of Fibromyalgia ‘ states that the only treatment for ‘Euthyroid Hypometabolism ‘ are supraphysiological doses of T3. I interpret Euthyroid Hypometabolism as Thyroxine Resistant Hypometabolism (ref your article late 2013 ) which I also interpret as ‘poor conversion of t4 to T3. Is Dr Lowe’s recommendation on page 287 ( classification of forms of hypothyroidism.). is a sensible one………. I have 5 stepdaughters and 10 StepGrandchildren who I believe are poor converters . My wife died in 2012 whilst still under very early treatment from Dr Skinner, bless him. My two eldest stepdaughters became his patients during 2013 but they were ‘ shown the door ‘ by their GP’s. Immediately after Dr Skinner died. Sheila is familiar with our situation, Can you provide any guidance, please.

t 3 deficiency,