Hi,I've started seeing an Integrative doctor who has recommended I transition to T3 only after results indicated high RT3 (667 p/mol - ref 140-540 pmol). I've had longer term issues with fatigue after a virus, though since becoming sick I've realised my t4 and t3 levels have not been opt8since a total thyroidectomy in 2012. I'm on t4/t3 therapy, having just replaced my slow release t3 to normal t3, latest results were: t4- 18.6 pmol/L (ref 11-22), t3 - 5.1 pmol/l (ref 3.1-6.4), tsh 0.64 nU/L (ref 0.5-5).
My question is for those who are on T3 only and have had experience with addressing high RT3 through this method or have knowledge around whether this is a viable way to reduce RT3, what approach I should take if going down this route and if there are alternatives than T3 only. I did start to slowly reduce T4 and increase T3, but I have been back and forth on whether I should do it, partly due due to if it's safe and impact on my body. The doctor prescribed 40mcg t3 daily to replace my 100mcg t4 and 16.5 much t3.
Thanks
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Well, first of all, you do not need to 'address' high rT3. It is not the problem. There are many, many causes of high rT3 and only one of them has anything to do with thyroid. Yours is probably high because, as you said, you've had a virus. That is a natural reaction to a virus. Conversion of T4 to T3 is down-graded and more T4 is converted to rT3 than T3. This is to force you to rest while the body recovers.
High rT3 is a result, not a cause. It is inert and only stays in the body for about two hours before being converted to T2. It does not cause symptoms, it does not block T3 receptors - it has its own receptors - it doesn't do anything. Any symptoms you are experiencing are due to the low FT3 not rT3.
So, whilst there is no danger in T3 mono-therapy, changing to it just to bring down rT3 levels is a nonsense. I myself have been T3 only for many years, that's how I feel best. But I've never had my rT3 levels tested and I really don't care what they are. It's a totaly red herring. And T3 only doesn't suit everyone any more than T4 only does, or NDT. It might suit you, and you'll never know if you don't try. But it has nothing to do with rT3.
Thanks Greygoose, it's all rather confusing with the information I've received and read. I should clarify the virus I had was from 2022, so dealing with fatigue/brain fog for 2yrs, had lots of tests done, with thyroid hormones and the rt3 the outliers. As you have described the conversion in relation to t4 to rt3, is how the doctor sees my situation, with my body still being in rest mode from the virus - he suggested to remove t4 for a couple months and then reintroduce again. I might go back to my normal dosing of t3/t4 and try increasing t3 as needed first before committing to t3 only to see how that goes. It's just strange as before I got the virus, I did not have this fatigue even when my levels were not optimal, my vitamins are better now too.
Separately do you know much about t2? I've only just learnt about it in supplementation format (cream) and curious to know in what circumstances that would be useful for someone?
I would not advise messing around with your dose like that. It's never a good idea to chop and change doses, and you could end up feeling worse than you do now. And all for nothing! Because lowering your rT3 is not going to do anything for you. As I said, it's a total red herring. And as soon as you add back in the T4 the rT3 level will just go back to what it was before.
Try T3 mono-therapy if you wish, it might suit you better. But you'd have to stay on it for a lot longer than a couple of months to know if it does.
Quite frankly, your doctor's idea is stupid and only goes to show that he doesn't know much about treating hypo. I think he's just messing around and using you as a guinea pig.
No-one knows much about T2. There have been a few discussions about it on here, but no conclusions. This thread might start you off on a search but the HU search facility doesn't seem to be working very well at the moment:
Regarding T2. I have copied some claims and commented:
#1. There’s no reason to automatically assume that T2 is harmful because we know that it’s created naturally by the body.
That is obvious. We simply MUST not assume either that it is harmful nor that it is deleterious.
Assumptions in either direction are entirely inappropriate. But this warns only about assumptions of harmfulness. Assumptions of safety are far more dangerous.
#2. Thyroid patients have been using T2 for over 70 years because it’s naturally found (in small amounts) in NDT thyroid medications like Armour Thyroid and NP Thyroid.
This is a junk claim. If it were rationally based, it would tell us the approximate ranges of amounts of T2 that have been found in desiccated thyroid products. Who knows if the level is consistent, or can ever be zero?
It is also junk because if you are going down into the lesser constituents of desiccated thyroid, you absolutely must consider how much DIT (Diiodotyrosine) and MIT (Monoiodotyrosine) is contained.
Further, this mentions ‘These NDT thyroid medications contain a small amount of T2’ and then refers to people taking 50 to 300 micrograms of T2. That would be vastly more T2 than the T4 and/or T3 content of desiccated thyroid. The safety of any possible T2 in desiccated thyroid does NOT imply that much larger doses of T2, taken in tablet or topical forms, is safe.
#3. Over-the-counter T2 supplements have been available for a long time.
We can, therefore, assume that side effects would be even less pronounced in people who actually need it (e.g. hypothyroid patients) and this is exactly what we see.
Utter trash. We regularly see members struggling with small doses of T4 and/or T3 because their bodies are ill and often have been ill for years. This is at the extreme opposite end of any spectrum to healthy bodybuilders.
Only the most dangerous products (like DNP - 2,4-Dinitrophenol) cause the most serious issues, including deaths, in bodybuilders. And those are the ones we hear about.
#4. Studies show that doses of T2 less than 300 mcg per day do not impact thyroid lab tests and do not cause harmful side effects.
There are studies which show the safety of, say, 50 micrograms of Levothyroxine. That doesn’t mean that it is safe for everyone to take.
This is a sales patter, Not a scientific, logical discussion.
It does not explain why such high doses of T2 (compared to T4/T3) are required. Considering that our own T2 levels would be based on conversion of T3, there cannot be more T2 than T3 (molecule for molecule - assuming every T3 molecule gets converted to T2).
T2 might prove to be a major contribution to health in the fulness of time. This does not present that case.
In my view, these people are promoting T2 like crazy knowing full well that if it were to become an accepted medicine, it would become prescription only like T4 and T3. Making hay while the sun shines.
At present, we do not know enough. Anyone who tries it is placing trust in their supplier that the product is to some standard. And is volunteering to be a lab rat. Without the monitoring that formal experiments apply.
I have read over the years that there can be many causes for having high RT3; the link below gives several. For me, many years ago, it was low iron and high cortisol. I went on T3 monotherapy; it took 6 weeks after full transition, but I could tell when my T3 receptors were 'cleared' of RT3 as my heart began beating rapidly with me just lying on the couch. Don't want to contradict greygoose, who sounds very knowledgeble, but there are many reputable sources that say RT3 does compete with T3 for receptors, thereby keeping T3 out of the cells; my own experience corroborates this. I was on NDT until RT3 built up, transitioned to T3, then back to NDT after it cleared; did this twice, but then stayed on T3 to avoid the hassle.
Also at the link below, "“Many endocrinologists believe that reverse T3 (3,3’,5-triodothyronine) is only an inactive metabolite with no physiologic effect. This is an erroneous belief.....rT3 not just an inactive metabolite, but rather a potent inhibitor of tissue thyroid levels."
Thanks for your response, I was hoping someone with experience navigating high RT3 would chime in. How did you go about reducing your dosage, what symptoms should I be aware of as I do this and once dosed down? I'm a bit worried with reading the symptoms correctly, but also with not having the t4 as a reserve. I read through some of the info, I had sustained stress, low vitamins over a number of years which have now resolved, so hoping this will make permanent changes to the rt3 once cleared.
My doctor seems to think my body got stuck in high rt3 mode, which is what was mentioned in some of the resources shared, though in saying that there could be an underlying cause not seen atm, but from results etc nothing is obvious to me.
it's not as simple as rT3 'blocks' T3 receptors ... it's not rT3 itself that causes the problem , it's the deiodinase DIO3. Higher fT4 levels cause increased DIO3 , which lowers T4 levels by converting more of the T4 to rT3 ( and less to T3 ) and the result of that is higher rT3 ,it's complicated..... see details in links / replies in this post : healthunlocked.com/thyroidu....
the neuroendocrinology.org page uses an image taken from a marketing page by dr. westin childs as it's only refernce for 'rT3 blocking T3' ,
but the westin childs page in question blatantly misrepresents a very well known graph (it shows what happens to thyroid hormones in non- thyroidal illness) using it as his 'evidence' for what happens to thyroid hormones during thyroid illness .....making it hard to trust dr. westin childs level of understanding/ integrity on this issue
’What should stand out to you is the fact that reverse T3 (abbreviated as rT3) and T3 (abbreviated as T3) are the earliest markers of thyroid dysfunction.
They become abnormal much sooner than the other thyroid lab tests which makes these lab tests sensitive for diagnosing early thyroid problems”.
But rT3 is not a sign of thyroid dysfunction as it is produced outside the thyroid gland. Even euthyroid people can have high rT3.
but in primary hypothyroidism T3 is the last one to show a thyroid problem is developing .
In primary hypo, first ft4 level falls slightly , but not usually enough to go below range . TSH rises as a result of lower fT4 , and since TSH moves a lot in relation to relatively small ft4 changes , TSH is the first/ most obvious sign of a thyroid that is failing due to primary hypothyroidism. ft4 then falls further as thyroid can't produce enough T4 even with higher TSH.
In primary hypo The fT3 level is initially maintained (by the higher TSH increasing T3 production from thyroid , and also increasing T4 to T3 conversion by up regulating the deiodinases)
in that statement he's actually referring to what happens tp T3/ rT3 in severe non thyroidal illness so it's a rather misleading statement because he doesn't make this clear . He's using a graph showing what happens to thyroid levels in non thyroidal illness and presenting it as though the same thing happens in thyroid illness, but it's not the same at all.
Dr. Jacobs says: ”The important points are first to see if any of the above causes of high RT3 are present. However, if none are in play then the treatment to increase the T3/RT3 ratio must be with T3 only”.
So he seems to say that if you identify the cause(s) of high rT3, you don’t need to stop levo or NDT. But how many people can know for sure what caused it, as there can be several factors at play? You can have high or low cortisol, nutritional deficiencies and take several drugs known to raise rT3 all at the same time?
And, if you don’t know what caused high rT3 in the first place, how are you supposed to stop it from rising again once you have been on T3 for 12 weeks and then add T4?
So his reasoning does not sound entirely logic to me.
Other sites claim that, once rT3 levels are high they won’t come down unless you take T3 only for at least 12 weeks. So Dr. Jacob’s approach is more guarded as he says only people who cannot identify the reason for their high rT3 should be on T3 only. In other words, rT3 can normalise once you find the cause and correct it. This is the first time I come across that approach.
I would not put much faith in the STTM. For years, the blog owner has been going on and on about the FDA destroying NDT to force people on levo because they are paid by Big Pharma (no evidence of this), T3 pooling and rT3 dominance. She even comes up with the most incredible theory which defies logic; a hidden pool of RT3 in the body which lasts for up to 12 weeks and goes in and out of cells:
I don't know if it is because of big pharma (although I would not be a bit surprised; they spend billions on lobbying). But the FDA has been attacking NDT for a long, long time. anh-usa.org/fda-attacks-nat...
They are not alone in questioning the legitimacy of NDT. But I think it is T3 they are after, as they recommend T4 only and warn doctors not to routinely prescribe synthetic T3 either.
The first time I did the T3 to clear out RT3, I went back on NDT after 6 weeks; I didn't know enough at the time to address the underlying issues. The second time, I tried to address the low cortisol and iron, and thought I had, so after a few months I went back to NDT. All was well for about 3 years, then it hit again, but I was dealing with a whole new set of stressors by then. So, I've just stayed on T3 for years. I'm once again trying to address lower-than-optimal cortisol, iron, Mag, and B12 so I can go back to NDT.
I've never viewed RT3 as a villain; it's simply acting its part when a set of conditions exist. Dr. Fiona didn't address the underlying causes, which is something I'd like to know more about. It seems like walking a tightrope.
It was a good article, but I'm always a little suspect when medical professionals see a low-carb diet as causing illness, when it is actually high-carb diets that cause illnesses such as type 2 diabetes, PCOS, high blood pressure, heart disease, etc. I think what they're confusing is nutrition. A person eating low-carb can be adequately nourished if they eat enough protein and fat; just like a person eating low-carb can be malnourished if all they are eating is leafy greens and other low-carb plants. Our human ancestors ate low-carb out of necessity, but they were well-nourished with animal protein and fat, not sick, lethargic creatures. Anyway, I got off track.....it turns out I have one copy of the genetic variant for Thr92Ala-DIO2, which might explain my issues!
Many practitioners believe that low carb diets are harmful as it results in less T4 and T3, and (initially) more RT3. And that is true, but they fail to understand why. The reason is quite simple: as carbs are reduced, cells in the body become much more sensitive to all hormones, including thyroid hormones, so less of them is needed.
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