can anyone explain exactly what reverse t3 is?

had hypothyroid symptoms whilst living in usa -was prescribed slow release t3- came back to uk - doc and endo said to try t4 -made no difference -infact put on weight and symptoms got worse -can anyone help with their understanding of rev t3 in uk? presently desperate for doc in Scotland-thanks

20 Replies

  • should also have said that while on t3 in usa ALL my symptoms disappeared !!!

  • Welcome to the forum, Swkenzie.

    Email for a list of endos recommended by members. You can also post a question asking for endo recommendations but ask for responses to be sent to you via private messages.

    T4 is converted into something like 80% T3 and 20% rT3. rT3 is the body's brake on too much T3 being converted and causing hyperthyroidism. Excess rT3 can be caused by unconverted T4. It is almost impossible to get rT3 testing on the NHS, my London endo told me it isn't tested but I think Southamptom Hospital are trialling rT3 tests. Most people on the forum wanting rT3 testing use Genova via It takes 2/3 weeks to get results back as blood is sent to the USA for analysis.

    I can't tolerate T4 only but am fine on T4+T3 having cleared the buildup of T4 which is what I think people often mean by high rT3. What dose s/r T3 were you taking?

    ps type rT3 into the Search Unlocked box to find posts on rT3 and check out Paul Robinson's posts and his website and FB pages.

  • thank you clutter

  • This is a good explanation from ThyroidChange and Dr. Borenstein, MD.

    Unfortunately, it is very difficult to find this level of understanding in Scotland,

    good luck. When T4 is converted to T3 by removing one iodine atom if it is removed from the outer ring it is T3 and from the inner ring it becomes RT3.

    RT3 is natural in the body but can become problematic when levels increase. PR

  • Reverse T3 is an inactive form of T3 that does not deliver oxygen and energy to cells. Instead, it merely takes up space, and can in some cases actually block the cell's ability to take on active T3.

    I really don't like the above statement. Thyroid hormone is not an oxygen transporter, nor an energy transporter. Both rT3 and T3 get converted to T2. So even if we accept that rT3 is without any direct function, nevertheless its presence and eventual conversion affect T2 levels and availability.

    Although it might eventually be shown exactly what happens to rT3 and why it is claimed to block taking on T3, at present we do not appear to have a cast-iron proof that it is T3 receptors (alpha, beta, both or any other receptors) which, by getting blocked, prevent T3 having its function. Why not, for example, the cell membrane transporter mechanism? (That certainly seems to be allowed by some of Borenstein's language.)

    We regularly see that rT3 is a wastegate allowing us to get rid of excess T4. Why do we need to do that? There are perfectly functional sulphation and glucoronidation pathways that allow excretion of inactivated T4. It simply doesn't work for me to look at rT3 and believe that is why it is produced. Further evidence could, perhaps, persuade me that this is indeed the case, but for now my sceptics hat is well and truly stuck onto my head.

  • Rod, all good points which only serve to underscore how much is still debated and not agreed upon. PR

  • thank you pr4now


    Good website and rt3 info. here too!

  • thanks faith 63

  • As far as I understand it you don't have to worry about Reverse T3. Two Excerpts:

    1.Under normal conditions, cells continually convert about 40% of T4 to T3. They convert about 60% of T4 to reverse-T3. Hour-by-hour, conversion of T4 continues with slight shifts in the percentage of T4 converted to T3 and reverse-T3. Under normal conditions, the body eliminates reverse-T3 rapidly.

    2. Some have speculated that the elevated reverse-T3 is the culprit, continually blocking the conversion of T4 to T3 as a competitive substrate for the 5’-deiodinase enzyme. However, this belief is contradicted by studies of the dynamics of T4 to T3 conversion and T4 to reverse-T3 conversion. Laboratory studies have shown that when factors such as increased cortisol levels cause a decrease in T4 to T3 conversion and an increase in T4 to reverse-T3 conversion, the shift in the percentages of T3 and reverse-T3 produced is only temporary

    If you go to the date March 24, 1999 if you wish to read the whole answer:

  • But that wouldn't explain why so many ppl who end up using t3 only had enormous rt3 levels when tested. I've seen that on the rt3 FB group loads so evidently form one people it goes wrong and stays wrong

  • If I have a blood test and have just taken thyroid hormones about a couple of hours earlier. They will also show high.

    I think it might be the same with Reverse T3, i.e. 60% of T4 converts to Reverse T3 so we must have some RT3 in our bloodstream which isn't tested normally.

    I take T3 only, have never had a reverse T3. There is no need as I feel perfectly well. I have had problems with some T3 when it's the fillers/binders which cause me a problem. How do I know this - because when I change to another T3 symptoms go on the same dose I was taking before.

    This is another link, in more depth and an excerpt.

    Basically, we want to establish whether your body has about 20 times the amount of FT3 compared to the amount of rT3, as this has generally been found to be associated with good health. In essence, this is what makes the rT3 Ratio such a useful tool.


    Because labs use these two different ways of reporting their results, you may find your FT3 (free T3) reported as a figure in the hundreds, e.g. 325. Or it may be reported as a smaller figure, e.g. 3.2.

    In a similar fashion, the labs may present the rT3 figure as something like 220, or it may appear as 22.

    (Yes, I know; it's enough to drive you crazy! But, simply follow the formulas presented below, and hopefully most of you will be able to figure out your rT3 Ratio!)

    And, again from the excerpt in the other response:

    increased cortisol levels cause a decrease in T4 to T3 conversion and an increase in T4 to reverse-T3 conversion, the shift in the percentages of T3 and reverse-T3 produced is only temporary

  • High RT3 levels cause real problems as they block the receptor holes in the cells that the T3 needs to use. The conversion problems can be caused by adrenal fatigue, high iron, high ferritin, sex hormone imbalance etc. The cure for it is to drop the amount of T4 you are getting and replace it with T3. Eventually the RT3 will dissapate and the T3 can get into the cells whilst no more or very little RT3 is made. Whilst all this is going on try and find out what is causing the high RT3 and where possible sort it out.

  • I am interested in any decent research that identifies exactly what happens to rT3 in both healthy and unhealthy individuals. So far I have not found much which explains properly how rT3 blocks receptors. Can you point me at anything?

  • thanks hismum

  • You may be able to get answers on the STTM forums or the FTPO thyroid facebook page.

    All I know is that the RT3 is close enough in 'shape/ composition' to T3 to be able to enter the cells in place of T3. I have read that it can actually access the receptors easier than T3 so it blocks the T3 from getting in. It is no wonder it mimics so well, its only one ion different at the atomic level.

  • I have read similarly, but have never found any proper research to back it up. I remain sceptical.

    Sorry, I will not sign up to Facebook, and very much prefer sources which are open rather than closed. Everyone can respond to everything I post (unless the thread is restricted by its originator) and if I get something wrong, it can be pointed out to everyone. Closed groups/sites can end up being less scrutinised.

  • There isn't any evidence that rt3 blocks receptors is there? The problem presumably comes when rt3 pools or not enough t3 is available because our of balance ratio being converted to rt3. I am on FB group and have def seen rt3 results in people which are hugely outweighing t3 and t4

  • Worse than that, there is not even a clear identification of which receptors are being talked about.

    I think that rT3 might be very important, but we really don't understand it. Far too much seems to be on the basis of reasonable supposition (educated guesswork) rather than actual research.

  • thanks again hismum

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