Everything You Never Needed to Know About Reverse T3


I’m kicking today off with a mea culpa.  Last year, I published The Ultimate Guide to Thyroid Function Testing – Hypothyroidism Edition.  In that post, I gave short shrift to a useless blood test called reverse T3 (rT3):

Forget you ever read about reverse T3, T0, T1, and T2.  End of story.


If you’re reading this site, it’s probably because you like to understand things – believe me, I get that.  I don’t ask for many favors, but I’m asking you to trust me this once…the above tests will add absolutely nothing to your medical care.  It is totally unnecessary to invest your ATP in figuring out how to use or interpret these tests.

In retrospect, that may not have been the best way to encourage you to ignore the copious internet nonsense regarding testing for rT3.  Over the last couple of years, my readers’ comments and emails have demonstrated that y’all are an intelligent and skeptical bunch.  When I ask you to believe something simply because I say it is so, the little hairs on the back of your neck stand in indignant piloerection.  In an attempt to make it right with you, I will address the myths out there about rT3, hopefully putting this issue to rest – for now.

Getting on the Same Page

As I’ve said before, this is not a medical-o-pedia site, so I assume you’ve already done the background, boring reading and have a certain level of familiarity with the subject.  But, to quickly make sure we’re starting from the same point: the thyroid gland makes predominantly T4, plus some T3.  Circulating T4 is  converted to “active” T3 in our tissues by deiodinase enzymes.  We have three types of deiodinase enzymes in different tissues, and their level of activity depends on the needs of that particular tissue at that moment.

When T4 is metabolized by Type 1 Deiodinase (D1) in our tissues to form active T3, some biologically inactive rT3 is also formed.  When T4 is metabolized by Type 3 Deiodinase (D3) in our tissues, it is inactivated to rT3.

The classic pathways of thyroid hormone metabolism – Scientific Figure on ResearchGate. 

rT3 and T2 have no known biologic function in humans, but rT3 has been investigated as a marker for distinguishing abnormal thyroid function tests seen in non-thyroidal illness from abnormal thyroid tests in the setting of an actual thyroid problem.  Most of this investigation has been in critically ill patients, who tend to have higher levels of rT3.  Because it is now well-established that this subset of patients has elevated rT3, it is extraordinarily rare for a physician to order the test, as it usually does not add any actionable information to the situation.

To the best of my knowledge, there are no data to guide the use of rT3 in the routine diagnostic workup of hypothyroidism in free-living (non-ICU dwelling) humans.  Further, I am unaware of any data regarding how to use rT3 to guide thyroid hormone replacement therapy in people with known hypothyroidism.  At best, it would appear difficult – at worst, impossible – to interpret a rT3 level in someone who takes levothyroxine (T4), as the drug itself may cross-react with the immunoassay, causing the rT3 level to be falsely high.  In addition, there are data suggesting that the mere presence of additional T4 substrate (levothyroxine) in the blood can lead to increased inactivation of T4 to rT3 (see above diagram, again).  In other words, if you load up the left side of the chemical equation, chemistry rules dictate that the reaction will be driven to the right.

Regular readers know that I often harp on the importance of knowing your assay.  In the case of rT3, there is a liquid chromatography/tandem mass spectrometry (LC-MS/MS) assay that is less prone to interference.  But who cares how good the assay is if we don’t know what to do with the results?  Besides having no known biologic function, it should also be noted that the half-life of rT3 in the blood is 4 hours.  Compare that to T3’s half-life of 1 day and T4 at 5-9 days, and you will appreciate another reason why doctors avoid placing much emphasis on the rT3 level.

So why is the alternative medicine world obsessed with esoteric testing that has no clinical value?  The most cynical explanation is that they appropriate and bastardize impenetrable concepts to lend an air of credibility to the nonsense they peddle.  Look, the regulation of deiodinase activity is extraordinarily complex.  Consider this sentence from Visser et al‘s treatise Metabolism of Thyroid Hormone, posted on my favorite, consistently updated online thyroid textbook, Thyroid Manager:

Whereas initial studies focused on the role of the deiodinases in maintaining normal serum T3 concentrations, the paradigm has evolved that these enzymes can locally modify TH [HD: thyroid hormone] bioactivity independent of serum TH concentrations.

Translation: there are a few things we can measure and a lot we can’t measure when it comes to the metabolism and action of thyroid hormone at the blood, tissue and cellular levels.  There are many moving parts here – so many that I wager there is much we still don’t understand about thyroid hormone metabolism.  But let’s be clear about one thing: admitting that we don’t understand everything about thyroid hormone metabolism ≠ rT3 testing has value.

Alternative Medicine makes it possible to diagnose just about anyone on the planet with hypothyroidism.  Don’t worry if your TSH, T4, and T3 are all normal.  If you test your reverse T3 level enough times, you’re bound to eventually get a high reading, thus securing your diagnosis.  With that, I will now debunk Alt Med’s claims about rT3 in Everything You Never Needed to Know About Reverse T3.

Claim: Elevated rT3 is the best marker for tissue hypothyroidism.

HD: False.  For the average person reporting fatigue and weight gain, a normal TSH alone will usually rule out hypothyroidism.  rT3 can be elevated in non-thyroidal illness (NTI).  NTI is any systemic disease process in which thyroid function tests change (usually lowish T4 and T3 with a normal TSH) as a physiologic reaction to the NTI.  In most diseases, treatment of the NTI itself will restore thyroid function tests to normal, and treatment with thyroid hormone is neither required nor advised.  In fact, it is quite possible that thyroid hormone levels are down-regulated in these scenarios, as a normal protective response.

Claim: Elevated rT3 indicates that T4 replacement alone will be ineffective.

HD: False.  Alternative Medicine appears to justify this by saying that high rT3 is a consequence of reduced uptake of T4 by the cell and reduced T4 to T3 conversion.  While there is some truth to their statement, there are no data suggesting this proves therapy with levothyroxine alone will be inadequate.  Once you give levothyroxine to such a person, there will be significantly more T4 substrate available.  This alone has the potential to drive more T4 to T3 conversion, as well as greater cellular uptake of T4 (remember the laws of chemistry).  The point here is, once you change the metabolic milieu by giving a therapeutic dose of T4, that initial elevation of rT3 doesn’t mean much.  And, as described earlier, once you give T4, it makes no sense at all to check rT3 again to guide replacement.  If you want a more nuanced discussion of whether to use T3 therapy in hypothyroidism, read T3 Or Not T3 – Exploring The Controversy.

Claim: The T3/rT3 ratio is the best marker of intracellular thyroid hormone levels.

HD: Mostly False.  The T3/rT3 ratio has been studied as a prognostic tool in critically ill patients and the elderly.  When it is very low, that’s bad.  This tends to happen in illnesses that cause D1 activity to go down (less T4 to T3 conversion) and D3 activity to go up (more T4 to rT3 inactivation).  The T3/rT3 ratio has not been found to be useful in assessing the average person with “hypothyroid” symptoms.

Claim: Elevated rT3 blocks T3 from binding to its receptors, causing tissue/cellular hypothyroidism.

HD: False.  There is no credible evidence that this occurs, while there is plenty of evidence that this does not occur.  rT3 does not bind to nor have transcriptional activity at the thyroid receptor.  It certainly doesn’t enter the nucleus of the cell.  Therefore, it has no effect on the ability of T3 to drive cellular metabolism, maintain body temperature, etc.  So why does Alternative Medicine make this claim?  The best I can figure is that there are data showing that rT3 binds to a specific thyroid hormone receptor in the cytoplasm of brain astrocytes, initiating actin polymerization.  This is important for the structural integrity and motility of the cell.  I think the next claim will demonstrate how Alt Med leaps from this to “blocking T3.”

Claim: Elevated rT3 decreases metabolic rate by decreasing T4 to T3 conversion.

HD: Mostly False.  I had fun researching this one, as Alt Med does have some science on its side.  However, as usual, they take an idea with a kernel of truth and extrapolate the heck out of it.  I had to dig deep into the literature to attempt this explanation, and it’s a little dense, so bear with me.  There are a bunch of papers from the 1970s through ’90s looking at the role of rT3, mostly in vitro studies using mouse cell lines or in vivo studies in animals (birds, mice, rats, dogs, lambs, oh my!).  For example, Okamoto R et al published “Adverse effects of reverse triiodothyronine on cellular metabolism as assessed by 1H and 31P NMR spectroscopy” in Research in Experimental Medicine in 1997.  The authors demonstrated that, in a culture of mouse cells, administering rT3 lowered the ATP/ADP ratio from 6.9 to 6.1.

What does that mean?  Well, I’m not quite sure, as I don’t know how to translate that ATP/ADP ratio into something that is clinically meaningful.  But Alt Med appears to know, as they cite this study to back up their claim.  The experiment was done at a pH of 7.4, which is around where humans live, so maybe there’s a kernel of something interesting here.  But, the more impressive ATP/ADP lowering effects were seen in part deux of that experiment, when the investigators subjected the cells to significant stress by lowering the pH to 6.7 – not something that human cells are likely to experience for very long.

In 1988, Sechman et al published “The Relationship Between Basal Metabolic Rate (BMR) and Concentrations of Plasma Thyroid Hormones in Fasting Cockerels.”  Before you jump down my throat for veering off into the realm of birds’ thyroids, I only mention this study because it’s another classic example of a study cited by Alt Med as supporting the notion that elevated rT3 is the best marker for diagnosing hypothyroidism in humans who have normal TSH, T4, and T3 levels (AKA normal people).

In case you’re wondering, I pulled the paper and read it, so you won’t have to – you’re welcome.  The investigators showed that withholding food from birds lowers both T3 and BMR and increases rT3 – a normal physiologic response to starvation.  Upon refeeding, they show that T3 and BMR go back up (duh).  They postulate that rT3 antagonizes the effect of T3, though I’m not sure why they felt the need to explain the lower BMR by invoking any mechanism other than that T3 production/conversion is reduced when the body is starving and needs to conserve energy.  Their data certainly do not prove any antagonistic effect of rT3 on T3.

I don’t want to give the false impression that all of Alt Med’s “data” is from 2-3 decades ago, performed in animals that bear little resemblance to humans.  They also cite a 1959 preliminary report by Pittman et al called “Antimetabolic Activity of 3, 3′, 5′-Triiodo-DL-Thyronine in Man.”  I love this one, as I suspect there is no way you could get their study protocol past an IRB (Internal Review Board) nowadays.

In an effort to not completely burn out the attention span of the few readers who have stuck with me to this point, I will stick to the highlight reel.  The investigators gave whopping doses of rT3 pills to a small group of hypothyroid, euthyroid, and hyperthyroid subjects.  BMR remained unchanged in euthyroid and hyperthyroid people, while it went down in three out of four hypothyroid people.  None of the hypothyroid people had any “hypothyroid” symptoms during the period of rT3 administration.

Putting the Nail in the Coffin

In my opinion, none of the above studies (or numerous similar ones) should be used to support Alt Med’s authoritative claim that elevated rT3 decreases metabolic rate in people.  Given how deep Alt Med had to dig for this data and the weakness of said data for supporting their argument, I can only assume that they ignored other data I found that contradicts their argument.  Or, they just have a very poor grasp of how to interpret these studies – could be that.

Before I get to the papers I discovered, let’s take a step back.  The studies Alt Med cites found a possible metabolism-reducing effect of rT3…by administering high doses of it to cell cultures, animals, and humans.  Giving a big dose of rT3 to a person and seeing what happens is completely different from observing what happens when rT3 is produced by the body in the course of normal thyroid hormone metabolism.

Think about it using this example: the adrenal glands secrete cortisol into the bloodstream.  In the course of normal human physiology, the adrenals make more or less cortisol depending on the needs of the body.  Now think about hydrocortisone, a medication used to replace cortisol in people who can’t make the hormone.  If you give someone very high doses (supraphysiologic) of hydrocortisone for long enough, you can suppress their immune system, thrash their bone density, and make them gain a bunch of weight.  Would you then say that the hormone cortisol is an immunosuppressant, decreases bone density, and causes weight gain?  Of course not!  I cannot emphasize this point enough: if you administer a pharmacologic dose of a naturally occurring substance, the reaction to that substance will probably be very different from what actually happens when the body produces it on its own.

When it comes to rT3, even many of the papers cited by Alt Med show that, when the molar ratio of T4:rT3 or T3:rT3 is high enough, any “negative” effect of rT3 disappears.  In the case of normal human physiology, there appears to be no evidence that naturally occurring molar ratios ever result in rT3 blocking T4 to T3 conversion by acting as a competitive inhibitor.

Studies that Refute Alt Med’s Claims

I’m only going to torture you with two examples, as I know your brain is starting to hurt…

Galton et al published “Life without Thyroxine to 3,5,3’-Triiodothyronine Conversion: Studies in Mice Devoid of the 5’-Deiodinases” in Endocrinology in 2009.  Although this is not a human study, at least it was done on live mice – not mouse cells.  This was a “knockout study” in which the investigators bred mice that couldn’t make the Type 1 Deiodinase enzyme (D1KO), the Type 2 Deiodinase enzyme (D2KO), or either enzyme (D1/D2KO).  You would think that D1KO and D2KO mice would have low T3 levels and stumble around their cages, unable to run through any of the tasks set up by the investigators, right?  Well, you’d be wrong.  They maintained normal T3 levels and had remarkably little impairment in locomotion, learning, and memory – all things that are impaired in hypothyroid mice.

Reverse T3 levels in D1KO mice were elevated two-fold over wild-type (WT) mice.  D2KO mice had no change in rT3, while D1/D2KO mice had a six-fold elevation in rT3.  If rT3 can decrease metabolic rate by impairing T4 to T3 conversion in a clinically meaningful way, you would expect the double-knockout mice to be fatter and have lower T3 levels.  Interestingly, the D1/D2KO mice weighed 5% less than WT mice by 8 weeks (statistically significant) and were able to maintain a normal serum T3 level.

In 2015, Lado-Abeal published “Thyroid hormones are needed to sustain ‘inappropriately’ normal TSH during non-thyroidal illness syndrome: a clinical observation in severely ill patients with primary hypothyroidism.”  The author studied seven critically ill patients who also had primary hypothyroidism that was un- or poorly-treated on admission to the ICU.  I cite this paper for a couple of reasons.  First, the pituitary-thyroid axis was found to be intact in these hypothyroid patients; in other words, the TSH was quite high and came down with appropriate levothyroxine treatment.  Even severe NTI (non-thyroidal illness) did not make the TSH unreliable in patients with true hypothyroidism.  So please stop telling me that we’re missing cases of primary hypothyroidism when people have mild forms of NTI.  Second, the author found that rT3 was normal or elevated at baseline and continued to increase with stepwise increases in the levothyroxine dose.  As stated earlier, this is totally expected.  When you load up the left side of the chemical equation with T4, you will drive the production of whatever is on the right side – in this case, T3 and rT3.  So, Alt Med, please stop checking rT3 in patients on thyroid hormone replacement therapy.


If you’ve hung in all the way to the end, congratulations!  You are officially an Endocrinology nerd.  If you’re a doctor, please feel free to print this out or link to it every time you get a request to add a reverse T3 to the next set of labs.  If you are a layperson who is just really, really interested in your thyroid health, hopefully this will steer you away from engaging in fruitless testing that will not make you feel any better.  Have any additional thoughts?  Comment below!

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Image Credit: Photo by Alok Sharma on Unsplash

92 Replies to “Everything You Never Needed to Know About Reverse T3”

  1. I cannot believe you went to the trouble of finding and analyzing those alt med citations. Incredible sleuthing. The best lies have a kernel of truth to them. Keep up the good work!

    1. Thanks, Mike. I can’t believe I burned this much ATP either. I had no idea how many rabbit holes I’d have to dive down when I started this post!

  2. Thank you so much for taking the time to write this out! You are truly doing the Lord’s work here. It’s very hard (at least in my experience) to convince a patient who has “done their research” that they don’t need every test with the word “thyroid” on it to be run every other week. “But what about my antibodies!?!”. Hopefully a few of these “informed” patients will stumble on your work!

    As an FYI the deiodination pathway image isn’t showing up for me… ?

    1. Good job MedHeadBen, keep doing your part to kick that autoimmune diagnosis down the road. Got to keep the women sick and gaslit, or they might rise up and take their fair share of the world. *Salute* ….

      I mean, YIKES. I’m a patient, I guess you’re a physician (?), and neither of us are God, so I acknowledge there’s a lot that I don’t understand and a lot that I’m not going to get out of a doctor’s appointment. But at the very least, respect your patients enough not to mock them online.

  3. More thanks from me, you are taking me to the edge of my understanding, very good for me, as well as providing a useful reference for future discussions with friends who have been convinced of the need for further testing by various alties.

  4. So happy I found your site. I really wish my Endocrinologist took the time to explain the complexities even to a tenth of the detail that you do. I think the problem is patients will believe whomever gives them the most attention & information and unfortunately that’s often the ND community, rather than specialists. But I’ll show her your blog next time I see her!

    1. Thanks, Clare. I wish we (Endos) had more time in the exam room, as the extra education time could prevent people from seeking out poor advice from alternative medicine practitioners.

  5. Thanks for the information, your explanations are incredibly informative and thorough.

    Your condescending tone and misrepresentation of what trained clinicians who practice what you refer to as “alt med” make it somewhat difficult to read.

    I’ve read a dozen books on the thyroid written by “alt med” clinicians and most of the claims that you address in this article are a gross exaggeration or misrepresentation of anything that I have ever read.

    I’m sure this garbage can be found somewhere on the internet, but anything can be.

    Excellent info though, so I’ll keep reading.

    PS: Would be nice to see some cooperation between “alt med” and “conv med”. Both camps are trying to accomplish the same goal.

    Conventional medicine just has more funding and therefore more research but the safety profile and utility of alternative approaches should entice any clinician who cares about his/her patients to want to see more research done in this area.

    1. Adrian, I’m pleased that you found this informative. I would agree that I often take a “tone” when referring to Alt Med because they do a lot of wacky things that don’t help patients – at best – or hurt them – at worst. I promise you that I’m not grossly exaggerating or misrepresenting any of the points I made in this post. Patients bring this information to me from the web, nearly every day. If there is good information out there in the Alt Med world, it unfortunately is being lost in the signal-to-noise ratio.

      That said, I don’t mean to paint all purveyors of Alt Med/Functional Medicine/Naturopathy in a negative light. I share patients with a couple of very reasonable naturopaths, in real life. On this site, a naturopath who goes by the handle Crusty the ND is someone to whom I would gladly refer my patients, as his focus is on healthy lifestyle counseling – not worthless testing and supplements. I even wrote a post called Can Medical Doctors and Naturopaths Work Together? in an effort to explore whether it’s possible to collaborate.

      I would also agree with you that conventional and alternative medicine’s goal should be the same: help the patient. The problem is that our approaches to achieving that goal are often at irreconcilable odds. I have to disagree with your suggestion that Alt Med approaches can be classified as safe or safer than conventional med. If you’re talking about healthy lifestyle counseling and a few benign supplements, then sure. But what I see (in my office and on the internet) is people spending hundreds to thousands of dollars out-of-pocket for worthless blood tests and supplements that can be frankly dangerous.

      To summarize: I’m happy to work with an Alt Med provider who is expert in diet, exercise, sleep, and mental health. That is a constellation of services that I do not have the time (or in some cases the expertise) to provide at a level that patients need. Once they veer off of that track into trying to “balance hormones,” however, that’s when I get my back up.

      One additional point: I am impressed that you could still hear my message, even though you found my writing a little too confrontational. We need more people in the world who can dialogue with people with whom they don’t agree.

    2. Well said! I almost quit reading merely because of the condescending tone. Glad I read it all the way through as it was informative. I also wish conventional med and alt med could collaborate on a professional level to provide optimal care.

      1. Glad it was helpful. I do realize that my tone can be off putting, but you just need to get used to me. 😉

        Unfortunately, close collaboration between CM and AM is almost impossible, given that what we do is usually based on evidence, and what they do is often based on magical thinking.

  6. TSH Test.
    Latest I heard (for patients showing hypothyroid symptoms) was that since TSH is produced by the pituitary gland, then the TSH level test is basically telling you how your pituitary gland is doing, but not much about your thyroid. To get a better picture of the thyroid you need to run a full thyroid panel test. All thyroid hormones TSH, FT4, FT3 plus Magnesium, Selenium, DHCA, Vitamin D 25.

    What say you?

    Thank you.

      1. Hey HD,

        What’s false?
        TSH is produced by the pituitary gland?
        TSH level test is basically telling you how your pituitary gland is doing, but not much about your thyroid?
        To get a better picture of the thyroid you need to run a full thyroid panel test?

        Thanks again.

        1. The second and third statements are false. If you provide me with the journal article that makes these claims, I can try to address further.

          1. Which part is incorrect specifically? Your rejection of the claim about FT3/FT4/rT3 et is the first thing I’ve read on your blog that made me question your expertise. Could you be a bit more precise in highlighting what you think is false?

      2. Yes, TSH is a pituitary hormone and tells how the pituitary is responding to the thyroid hormones. TSH does not tell you the what the thyroid is producing. Need to test the Free T3 and Free T4. I have hypothyroidism and my TSH prior to meds tested between 0.24 and 0.50.

        1. Joanne,

          In return for the hard work of the thyroid to the TSH level, what does the pituitary control?

  7. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5075641/ and Please read this . I am looking at PTSD related nonthyroidal illness syndrome (NTIS) and in particular PTSDs anti-NTIS. I find actual research to be less cut and dried about whether testing for T3/reverse T3 issues versus T4 is necessary for NTIS and anti NTIS . Looking back PTSD’s unique unusual pattern of thyroid alterations was established as early as 1994 and I find the non testing of reverse T3 ( to save a buck in research and medicine) and consideration of treating high reverse T3 levels with T3 instead of T4 to have maybe left PTSD sufferers medically neglected or to effectively stifled research on thyroid hormone alterations on quality of life and physical and psychological .Psychiatrists are treating PTSD patients with T3 with recognised improvement though they add that https://www.ncbi.nlm.nih.gov/pubmed/11305702 further research is needed – I say lets spend the money and test free and reverse T3 in patients with NTIS and anti NTIS and establish whether T3 supplementation helps remove the remarkably similar symptoms of thyroid disease – until PTSD’s biological dysfuntion has a cure we can only help to chip away at the myriad of comorbidities ( including NTIS and anti NTIS) that cause people with chronic PTSD and otherillnesses that effect the HPT

  8. i dont think its as simple as you have described .
    While RT3 might have a short half life if it is being replaced that is really more relevant .
    The thought that the body makes a particular hormone for no reason suggests that in fact there is a reason but medical science is yet to fully appreciate its importance .

    1. Simple? Not sure I agree with your premise. But please elaborate on what you mean by rT3 being “replaced.” Replaced by what?

      There are plenty of chemical reactions in the body that convert an active substance to an inactive substance, and I wouldn’t say that’s for “no reason.” The reason is to modulate levels of the active substance, make another substance that is easier to excrete or metabolize, etc etc.

      1. You have cited the half life of Rt3 as a reason why it is inconsequential .
        How ever if Rt3 levels are being kept constant by continued conversion to Rt3 there is a problem.

        1. The short half-life is not the reason why it is inconsequential; the short half-life is one of the reasons why measuring it is problematic. Unless it is being produced at a steady state by all tissues equally, that short half-life will lead to widely variable levels of rT3. So one may not be able to trust the actual lab value obtained as an accurate reflection of how much rT3 is actually being made.

          1. If one is to assume conversion to RT3 is constant testing over time will establish a baseline level of RT3.
            I think what you have cited might well be the case with many hormones .
            What im looking for is why you would not consider RT3 of some relevance , bearing in mind it does have an effect on ATP conversion as does T3.

          2. I would probably not make the assumption that conversion to rT3 is constant over time. But, for the sake of argument, let’s say you tested someone ten times over 2 months under a variety of circumstances, and you found a fairly consistent rT3 level in that person. That doesn’t really change what I addressed in my post as the “evidence” showing an effect of rT3 on the ATP/ADP ratio in mouse cells. I am unimpressed by that evidence, and until someone shows me more compelling data, I have no reason to think that rT3 is going to negatively affect human energy expenditure.

          3. Ok fair enough.
            im probably more convinced but I cant supply any data save the fact that if we looked at this from the opposite angle ,, its accepted that the effect of T3 on atp is ” profound ”
            however im finding your opinion within your site very informative and ill keep reading

      2. ” replaced ” or shall we say replenished by on going deiodinase of t4 to rt3
        You cited the short half life of Rt3 but if it is being replenished at a rate similar to its elimination, that actually proves little.
        There is a flaw with you description I feel.
        Not all patients given t4 thyroxine are well.
        there certainly is a significant number who are unwell and exhibit some of the symptoms of being hypothyroid .
        Unless it is possible to successfully treat these patients it would seem somewhat optimistic to consider we have explored and understand everything about the conversion of t4 to t3.
        The combination of t4/t3 therapy suggests there is definitely something inadequate in this deiodinase mechanism. ?

    2. ” The thought that the body makes a particular hormone for no reason suggests that in fact there is a reason but medical science is yet to fully appreciate its importance .”

      Thanks for that Steve. I’m a patient…..my thought as well and I’ve been trying to get to the bottom of that. This site is as close as I’ve gotten to an answer on that and many things.

      1. Except this site unfortunately has no answers, just insists on the same tired party line that TSH is all that matters in thyroid health and our bodies are making other thyroid-related hormones that don’t mean anything (???), and people continue to suffer because of this. Supplementing only T4 as most docs do does not raise T3, the actual active thyroid hormone, it only suppresses TSH and raises rT3. I see a regular doctor, not an alternative doctor, and even he recognizes this. My health continued to deteriorate despite being on T4, but the full thyroid panel shows that my body is not converting T4 to T3, as is what is supposed to happen. Saying T3 and rT3 have no bearing on thyroid health is willful ignorance that is driving people to naturopath quacks just selling supplements. Many with this conversion issue recover their health on T3-only.

  9. I’m one that was on T4 only for a year, was very fatigued, then on dessicated thyroid for 12 years, then recently added in extra T3. My fatigue finally went away, I felt great. But now I’m re-thinking and I’m carefully considering your article. My question: I was diagnosed with Hashimotos 14 years ago, ultrasounds show my thyroid is lumpy, bumpy, and scarred. You mention someone with their thyroid removed would benefit from adding in some T3. Is a Hashimoto’s thyroid in that category (like not having a thyroid), or should my thyroid be producing some hormone (and some T3) on it’s own?

    1. Although I can’t speak to your specific situation, I can say that I’ve seen very few people who have a durable response to adding T3 to their T4 therapy. The few people who tend to respond – in my experience – are those post thyroidectomy. However, there are some patients with Hashimoto’s, who have small, atrophic thyroids, who might respond.

      It should be noted, however, that adding extra T3 to pig thyroid is piling more T3 on top of a preparation that already provides supraphysiologic amounts of T3.

      For those reading this comment, please recognize that my post about T3 does not apply to people adding it to pig thyroid – only.

      1. Hi HD,
        I found your statement regarding “patients with Hashimotos who have small, atrophic thyroids” very interesting and was wondering if you could elaborate on the reason why this may happen? I have been hypo for years, negative antibodies so it doesn’t appear on labwork that I have Hashimotos, yet on a recent ultrasound my thyroid was found to be smaller than usual (and I stupidly did not ask my Endo to elaborate on this). Is there a reason for a shrinking, shriveled thyroid, or are some people born with smaller than usual thyroids, predisposing us to hypothyroidism? I can’t find much info on the internet about this, surprisingly. Thanks again for all your work.

        1. Most small, atrophic thyroids in hypothyroid people will be due to the long-term autoimmune attack on the thyroid. The thyroid tends to take on a swiss-cheesy, moth-eaten appearance; I think this is simply related to how the tissue responds to this attack over time. That is not to say that all small thyroids are due to autoimmune issues. Some people simply have smaller thyroids than others, and that does not always equate to having hypothyroidism. Those smaller – but normal – thyroids will have normal echotexture on ultrasound (i.e. smooth gray, not moth-eaten).

          1. You have to love posts like this again and again lots of very educated studies and big words. But yet people still are suffering and with no answers on how to treat many of these conditions.

            My partner was diagnosed with Hashimoto’s and the endo said pretty much nothing can be done other then treatment and its life time disease.

            As your probably going to guess, its cured she shows no antibodies and has a perfect normal functioning thyroid, how did this occur when science and well educated doctors cant help. Its was simple as removing Gluten, Dairy and taking high doses of selenium for 2 weeks and then introducing lugols iodine at a very slow rate. Endo’s comment was it was miracle from god! only kidding, the had no answers on why it was corrected.

            Posts like this does nothing for humanity only steps backwards.

            Anyone reading this Google, Hashimoto’s, Graves disease and many other thyroid diseases using the Selenium, Zinc and then Lugols iodine as a protocol. Remember lugols is very strong it needs to be introduced slowly with one suffering thyroid issues, normally one drop every week and increase slowly.


          2. Interestingly, I have a small, atrophic thyroid according to a recent ultrasound of my thyroid. My endo explained that it was most likely the result of long-term damage to the thyroid from Hashimoto’s Disease. I was diagnosed with hypothyroidism about 30 years ago. I am now 65 years old. I have been on as much as 150 mcg of Synthroid. But, mostly was taking 100 mcg for several years. Then, out of nowhere my TSH was 10.8. So, my dosage was increased again. Then, it dropped to .1. All the while, I never felt any better on Synthroid or Levo. Finally, I found my way to a doctor who tested more than TSH. Turns out my Free T3 is on the low side. So, it would appear I am not converting T4 to T3 (?) Ironically, supplementing with T3 (while reducing the dosage of T4) is still not doing much to raise my T3. Not only am I not converting. It seems like I can’t even absorb T3. I am now taking 5 mcg of Cytomel 3x/day. I am concerned about the potential cardiac risks. Not sure what I will do if my next blood work shows Free T3 is still low. BTW, I am exhausted all the time, despite eating a clean diet and getting 8-10 hours of sleep a night.

  10. A big question is how do you know that a patient can benefit from added t3?

    There is a valid testing aside from correct t4 dose, normal tsh, co-morbilities, etc ? Before a trial of added t3

    Also, great post, I made it to the end. The paper explanation clears the air

    1. It’s hard to know if a patient will benefit from added T3 without trying it. But as I’ve written before, most people will not benefit, long-term.

  11. As a curious patient, I thank you for your detailed and thorough debunking. I have read, on the internet, all the false statements to which you refer. I’m grateful to you.

  12. I’m a doctor. Rather than hand over your diatribe to the next patient who asks me to get those labs, I’ll happily get those labs for them and then proceed to do what I always do – get the data that will allow me to optimize their thyroid function… …and/or recognize when their hypothyroid symptoms are being caused by poor conversion, not by a problem with the thyroid gland itself. (What you call “NTI”). A pity that you’re SO CLOSE to seeing the truth but your hubris keeps you from putting it together because you’re convinced that Alt Med ™ always equals quackery. I doubt that this next bit will get through to you, but… I feel the need to try: Your quote: “When you load up the left side of the chemical equation with T4, you will drive the production of whatever is on the right side – in this case, T3 and rT3.” The point you seem to be missing is that that’s not what happens. Yes, rT3 goes up. The T3? That one tends to go DOWN, buddy. How do I know? Because I’ve been looking at these pattern over and over again, in real patients, with real symptoms. Why have I seen it and you haven’t? Because when I’m suspicious of thyroid problems I check TSH and Free T3 and Free T4 AND Reverse T3. I collect real data and make real adjustments to a number of things (sometimes thyroid medication, sometimes now) and I see real improvements. And yes, my MD and residency training is every bit as real as yours, and no, I’m not a kook who is in it for the money. I appreciate your frustration because I believe that you believe what you say, but… please hear my frustration: The arrogance of you self-described skeptics is stifling. I see patients the patients you guys don’t know how to help. And I make them better.

      1. Dr Stone,
        Thank you for your post! I was pretty saddened and discourage by “HD” post and arrogance. Please keep up the good work. Too often MD’s assume they know it all and don’t listen to the patient. It’s the curious Dr that truly helps their patient. The studies are out there supporting a full thyroid panel (with RT3) and how they can help save someone’s life. My symptoms and high RT3 lead me to dig further and eventually uncover that my thyroid was putting on the “emergency brakes” on my metabolism due to underlying genetic iron overload. On my way to recovery – but if my Dr had a closed mind (like HD) about the importance of a high RT3, who knows where I would be. I am thankful for her detective work and willingness to dig deeper into the underlying high RT3 cause.

        There are many published studies highlighting the significance RT3 as marker of critical illness and including this test may be a life saver for your patient…i.e see link below.


        1. See my previous reply to Dr. Stone. Questioning the validity of testing and using science to explain it does not imply a closed mind. By the way, your link to a paper about thyroid testing in heart failure does not apply to 99.99% of the people we actually see in the office.

    1. Ken, I checked out your practice web site, and I suspect there is much upon which we would agree. I appreciate you acknowledging that I believe what I say; FWIW, I think the same applies to you.

      You seem to view me and other science-based skeptics as arrogant, yes? OK, so what is my recourse if I think I can prove – using science – that perseverating on T3 and rT3 levels is simply spinning one’s wheels? If I claim it’s worthless and back it up – which I did – I’m full of misplaced hubris. If I say nothing, patients continue to waste time and money on testing I believe has no value. If I endorse it…well, that’s clearly not an option.

      If you’d like to discuss hubris and arrogance – and I’m not sure this will get through to you – I’d suggest you at least consider that the mainstream thyroidology community does not utilize this type of testing…but you do. I’m sure you are a capable internist, but what you appear to be saying is that you’ve cracked the code…while most of us in the Endocrinology world would not agree.

      Now, it’s not impossible for mavericks or Alt Med or functional med to be right about some things. Look at the contrarians advocating a low-carb, high-fat style of eating. 15-20 years ago, I would have thought that was insane; now, it seems like a pretty good idea. But I wonder if it bothers you at all that there are very few (if any) people within mainstream Endocrinology who would agree that your approach to thyroid care has merit. If it doesn’t make you second-guess yourself, at least a little, I’m pretty sure that’s the definition of hubris.

      You say that you are seeing the toughest cases and making them better. That’s awesome. I promise you, though, for every patient you make better, there are more you likely lose through attrition. How do I know this? They wind up in my office, with years worth of T3 and rT3 levels, still feeling like something is off. And then I have to tell them, It’s Not Your Thyroid.

      As for seeing lower T3 levels in patients on levothyroxine, I believe I addressed that common (but not ubiquitous) finding in either this rT3 post, or one of these:

      T3 Or Not T3 – Exploring The Controversy
      Is TSH the Best Test?

      The point is that there is no clear significance of this level, but I’ve always said it is reasonable to try a small dose of T3 in someone who doesn’t feel optimized on their T4 therapy.

      1. I struggled with tsh levels unstable(very high highs & very low lows) for 10 years no matter the amount of levothyroxine given.
        February my doc threw in the rt3 test in my labs. My rt3 was very high although all other levels were fine. I was feeling very symptomatic so he put me on a small dose of levothyroxine along with a small dose of levothyroxine. to see if that would help…it worked! I finally felt better! All my levels, including rt3 have remained stable with the new regimen.
        With that said. I do have a few autoimmune illnesses which I still get symptoms from though. Was the other diseases causing this???

    2. Dear Dr. Stone, thank you for your compassion an wisdom. I completely agree with your statement. I only wish You could be my doctor since nothing I have tried seems to help me feel better with my Hashimoto’s diagnosis.

  13. Thank you so much for writing this! I recently saw a naturopath who did a blood test, showed me lab work that said my rT3 levels were high, and explained this meant it was dampening my thyroid activity (“applying the brakes too hard” was roughly how it was explained). She diagnosed me with a “secondary form of hypothyroidism” and prescribed a thyroid medication. It felt very much like going to a traditional doctor and I trusted the diagnosis – I mean, the test came by high and all, so it must be real thing, right? However, while I am tired and cold all the time, I’ve always been told a hallmark of hypothyroidism is weight gain, something I’ve never struggled with. Taking thyroid hormones sounded pretty serious and I hesitated. Then I noticed the small print on the lab that said the test is not approved by the FDA. I’ve since been doing my own research and I’m grateful to stumble upon your blog. I still don’t know the cause of my chronic fatigue, but I’m glad to know it’s not a thyroid issue and I’m glad I didn’t take what could have been dangerous thyroid hormones.

  14. And when you tell them “it’s not your thyroid”, what happens next? Send them back to the PCP who may: 1. run more labs which are ignored unless results are WAY out of range indicating cancer or other crisis, 2. offer psychotropic meds?

    We spend a ton of money on chronic disease attempting to “treat” our conditions but not successfully feeling well. Why? Apparently, there are “real fixes” to Hashimoto’s and Graves. And they are not coming from the endocrinology training programs nor involve surgery/radiation/waiting for gland failure.

    Formal, traditional medical intervention wrecked my health. I was ignored, discounted, and mistreated. I was misdiagnosed. I was given the wrong treatment, bad treatment. All because I didn’t fit in some nice “normal” box of what is taught in medical school. Your profession should be ashamed of how myself and countless others have been treated. We rely on you guys knowing what to do but you fail us when we present as complex.
    And this is why people go to functional medicine, alt med.

  15. Personally found all of this condescending. What say you to someone with clearly LOW TSH.. like borderline out of range, who has borderline out of range low free t3, total t3 etc but high reverse t3? And who has had a history of pregnancy bleeds? What do you tell Sheehan’s patients? And oh.. the patient has EVERY symptom of HYPOthyroid while according to TSH, they should be hyper.

    Mind you there are loads of people ignoring everything you said.. self treating and feeling 100% better when they get free t3 UP and reverse t3 DOWN.

  16. I’m not one to argue or attempt to disagree with you BUT… The title of this article is horribly misleading. You should rename it. Call it something like “Why reverse t3 testing is useless”. I came to learn about reverse t3 based on the title of the article and got a thorough education about why its bullshit.

  17. Unfortunately to agree 100% with your appraisal of reverse t3 you would also have to accept it is a hormone that is completely without purpose and the body produces it for no reason,
    This logically is obviously wrong.
    While I have learnt a lot from your obvious technical background you still have not responded to a previous point .
    If 25% of thyroid patients are still u thyroid sick while their bloods tests fall within ” the normal range” it demonstrates our knowledge about thyroid function is incomplete .
    Reverse T3 must have a purpose , influence and in some cases it has an adverse influence .
    I think to a degree you are working backwards from your conclusion that any discussion about reverse T3 is flawed .
    I think in general terms not enough acknowledgement is given to the fact that average thyroid levels are exactly that and certainly some people feel better at various levels within the normal range .
    This suggests there is a degree of individuality with thyroid function within the context of wellness

    1. Steve, your contention that rT3 must have a purpose and positive/negative influence is flawed. The body metabolizes all sorts of hormones such that inactive byproducts are formed in that process. One cannot point to a quantifiable compound/molecule in the blood and claim that it must have a function just by nature of its existence.

      But, if you want to get metaphysical about it, you could claim that these inactive metabolites do have a purpose – their existence is the desirable end result of metabolizing/breaking down the parent hormone. If we didn’t have a way to inactivate parent or active hormones, we’d have levels that are too high.

      Now, I agree with you that our knowledge about thyroid function is incomplete. I also agree that many people with hypothyroidism don’t feel well despite normal blood work. In addition, I agree that some people will feel better with high-normal thyroid hormone levels, while others will feel best when they are low-normal.

      1. I think I will have to disagree,’ but more in the context of semantics ,
        To say something maybe the neutral by product of other processes might be correct , , it might be that we don’t fully understand its function,
        one thing we could postulate is that IF
        it is a neutral product, that neutrality is in itself its function .
        so we might disagree,
        finding the forum very interesting cheers steve

  18. Is there anything I can do to get my body temperature up? Any tests you recommend if Rt3 is not the cause? I constantly feel cold all year round and have a low body temperature.

    Age: 23, 5’11, 74 kilograms, male, no medication, non-smoker


    My other labs were fairly normal except for borderline low testosterone and slightly low magnesium.

  19. So can I just stop taking my Reverse T3 tablets and it won’t affect anything or should I come off them slowly?

  20. Hmmm alot of energy spent to be condescending. Quite the ego trip.
    I have now spent almost 7 yrs without a thyroid. The first year was hell with T4 meds. Had to PROVE my genetic DIO2 mutations to idiot traditional med drs I cannot convert T4 of any kind including NDT of pig thyroid.
    I have my new much healthier life back on a tiny bit of ndt and T3 dosed 4x a day because i treated my high Reverse T3 and YES RT3 is Real!! And I’m not alone.
    It’s a sad thing to waste a beautiful mind for an ego of an article. SMH.
    I’d be dead today following your ideas.
    Get back to me when you have no thyroid.

    1. Thank you so much for the justification I was about to go nuts. Still not working as my immunotherapy for cancer absolutely crashed my hormones etc, but so good to be validated by you. Thank you for taking the trouble to write. Thank you

    2. I do address the issue of a DIO2 mutation in: Is TSH the Best Test?

      I will excerpt the relevant section here:

      “The Thr92Ala change in the coding region of D2 does seem to be associated with slower T4 to T3 conversion. Studies in people with the SNP have shown a few interesting things:

      – A correlation between the SNP and TSH in healthy people, but not between the SNP and thyroid hormone levels.
      – A lower TSH in people with one copy of the SNP, when compared to people without the SNP and when compared to people with two copies of the SNP (surprising!).
      – Thyroidectomized people with the SNP may require a higher T4 dose to normalize the TSH.

      One study showed the SNP was not correlated with general condition, neurocognitive functioning, or response to combination T4/T3 therapy; a second study showed an impairment in well-being that was mildly improved with combination T4/T3 therapy.

      So what should we make of this? First, know that if you are euthyroid, you probably have nothing to worry about. Remember that the body is great at achieving homeostasis. If there is slightly sluggish T4 to T3 conversion in tissues that use D2, the body has many available tools to mitigate that. It can inactivate D2 more slowly, reactivate D2 faster, increase thyroid hormone transport into the cell, etc. Bottom line: if you ordered one of those DIY genetic profiles online and it says you have the SNP, relax.

      Second, if you’re hypothyroid because your gland doesn’t work great (as opposed to having had surgery to remove it), much of the above will still apply to you. But if you feel poorly on levothyroxine despite a normal TSH, then you may wish to broach the idea of adding in a small dose of liothyronine. Just keep your expectations low, as T3 is not the cure-all as Alt Med portrays it.

      Third, if your thyroid has been surgically removed and you still don’t feel well despite having “optimized” your TSH on levothyroxine, there is some credible evidence that you might feel better with the addition of T3 to your T4 therapy.”

    1. No. This study involves giving pharmacological doses of rT3 to rats to test a hypothesis about brain injury. The physiologic production of rT3 in the normal course of thyroid hormone metabolism in humans is a totally different situation.

      1. Right but if the action of rt3 on rat brains is hypometabolic, is it that farfetched to believe that high levels created endogenously in a human would have a similar effect? Some people do have high rt3 levels.

        1. It is totally farfetched, yes. Even granting that the pharmacologic doses of rT3 they administered to rats did have a hypometabolic effect on the rat brains, I can nearly guarantee you that a human would never achieve such high rT3 levels through endogenous mechanisms, like what the rats received as a medication. The body is way too good at maintaining equilibrium to achieve crazy, supraphysiologic levels of rT3 through endogenous pathways. I don’t care how high a person’s endogenously created rT3 is, it will never compare with a whopping dose from an rT3 pill, which is a totally different ballgame.

          1. Ok, thank you for helping me understand! How much does the body endogenously make of rt3? Is there any sources I can read about this?

  21. “The investigators gave whopping doses of rT3 pills to a small group of hypothyroid, euthyroid, and hyperthyroid subjects. BMR remained unchanged in euthyroid and hyperthyroid people, while it went down in three out of four hypothyroid people.”

    As far as I can tell this is the only study into the effects of reverse T3 on basal metabolic rate. I don’t understand why this isn’t further researched when so many people suffer from low basal metabolic rates and cold intolerance despite having a normal tsh.

    1. Probably because rT3 generated endogenously doesn’t do much of anything. And giving rT3 pills doesn’t seem to have a useful application in humans.

  22. I can have ideal free T3 and free T4 numbers but if my reverse t3 is high, I’m going to experience hypo symptoms. I won’t lose weight, my feet will be ridiculously cold and I won’t feel good. The only time this didn’t happen was when I was pregnant- the pregnancy caused the high reverse T3. There are things that can be done to lower reverse T3 but you wouldn’t be interested in that, seeing as you think you know absolutely everything there is to know. I pray you actually contract hypothyroidism and experience some of these things first hand. You’ll realize that what you learned in med school doesn’t go far enough and you’ll lose the attitude.

    1. “There are things that can be done to lower reverse T3”

      What are these things? I have cold intolerance and very cold feet.

      1. To lower RT3, lower levo dose and raise liothyroneine . This clearly works, but I don’t know if it has any utility.

  23. I need help, I’ve had elevated TSH only slightly 3.8, but because we wanted fertility help they treated me, within a month I had gained 20 lbs and my TSH was more around 5-6. After trying lots of different dosing and only getting worse I came across the rT3 alternative claims and wanted to try being treated with liothyronine instead of Levo. My TSH was back around 1 in about 4 wks and stayed there, but my T3 levels were high obviously I was on a lot of it, and my T4 was low, so we’re back in regular T4 with a small amount of T3, my TSH levels are rising, but they don’t want to put me back on lio instead of levo because my T3 levels are high, but it’s what was working. I was able to get pregnant after failed times, IUI, and IVF once I started on Liothyroinine. They have never actually tested my rT3 levels, but the Wilson’s temperature syndrome and rT3 symptoms lined up with what I was experiencing, low body temperatures 95.5 and low blood pressure. We are back to rising TSH 2.8 still in the normal range and high T3 with really love T4 which is where we started, and I Have to sleep in the day even though on the other treatment both pregnant and nursing(waking up multiple times at night) I had more energy than I do now. I don’t want to self diagnose, but it is what work, and conventional isn’t working, so all studies aside. How do you explain away a paradox reaction to levo like I experience.

  24. If rT3 is absolutely nothing to test for or worry about, why do I constantly keep gaining weight and feel no relief from my hypothyroid symptoms while taking 175 mcg of Levothyroxine?

    1. I’m sorry you are having this problem, but the premise of your question is faulty. Gaining weight and having symptoms does not = rT3 having any value.

  25. From what I understand it is not rT3 that is the actual problem but the increase in Type 3 Deiodinase (D3) associated with high rT3. When the D3 level rises in the blood to control the T4 to T3 level to prevent hyperthyroidism it will also turn more T3 into T2 before it can be used by cells, causing hypothyroid symptoms.

    As shown in this case: Severe Hypothyroidism Caused by Type 3 Iodothyronine Deiodinase in Infantile Hemangiomashttps://www.nejm.org/doi/full/10.1056/NEJM200007203430305

    It would be nice if you could address this in your post. More research needs to be done on the association between T4:D3:rT3 and T3:D3:T2, to see if a high rT3 could indicate excessive D3 causing a T3 to T2 conversion ratio that’s fast and high enough to leave tissue level hypothyroidism. This may indicate why patients have experienced results when adding T3 and then removing or lowering T4, or doing what Alt Med recommends to “flush out rT3”.

    1. The study you cite brings up a very interesting point, though I do need to explain why it isn’t relevant when dealing with the average adult with hypothyroidism. Certain tumors, including the hemangioma in the infant from this case study, can over-express type 3 deiodinase (D3), which can lead to a kind of “consumptive hypothyroidism,” in which T4 is excessively converted to biologically inert rT3, and T3 is excessively converted to biologically inert T2.

      This scenario, in which a highly vascular tumor is making large amounts of D3, is not at all analogous to normal, adult human physiology. Remember that D3 is present in high levels only in fetal tissues (placenta, for example), certain tumors, and during critical illness. There is some D3 activity in brain tissue as well. The average person, therefore, is not going to be walking around with D3 levels high enough to result in consumptive hypothyroidism. The only people who even might have this problem are going to be people with certain tumors.

      In addition, if someone does happen to be inactivating much of their T4 and T3 before it can be used, the TSH is going to go up, alerting the clinician to the fact that there’s a problem that needs to be addressed. So I don’t see why looking at rT3 levels (or T2 levels) would add any actionable information to this situation.

      If I am missing your point, please let me know. I just don’t quite see how the D3 activity issue could be the source of some patients’ dissatisfaction with their thyroid hormone therapy.

    1. The post you cite is a good example of what I’ve found on that particular website: there’s a fair amount of good, accurate, science-based information in there…but I disagree with most of the conclusions drawn. I think I’ve already explained in the comment immediately above this one why I am not impressed by any argument suggesting that D3 overactivity is likely to play a major role in explaining why the average person with hypothyroidism doesn’t feel well, nor do I think it will help determine who needs more or less T4/T3.

      In order for their argument to be more compelling, they would have to be able to show:

      – D3 is expressed in multiple tissues throughout the body (it isn’t).
      – D3 over-expression is common under ordinary (non-critical) physiological conditions (it isn’t).
      – The inactivation of T4 and T3 via D3 over-expression can’t be overcome by simply giving higher doses of T4, T3, or a combination thereof (it can).
      – The body can’t compensate for mild amounts of increased inactivation of T4 and T3 by increasing D1 and/or D2 activity, increasing intracellular transport of T3, and increasing binding of T3 to nuclear receptors (it can).

  26. I have a doc that believes that i should lower rT3 by taking T3 (cytomel). it doesnt seem to do much when i have tried this in the past, possibly due to NTI’s as the OP describes.

    Do you know of evidence that supports or refutes the idea that taking T3 will improve metabolic health and enable weight loss, or is the higher rT3 simply a marker of health because neurotransmitters are guiding that pathway to occur?

    1. When it comes to evidence for T3 improving metabolic health and weight loss, you won’t find a lot of strong evidence. Part of this is due to the fact that most RCTs show little difference between the experimental group and the control group.

      When looking at individuals, however, there will be some people who see a drop in cholesterol, an increase in metabolic rate, and a drop in weight with the addition of T3 to their T4 regimen.

      Unfortunately, the number of people who truly need and benefit from T3 is far smaller than the number of people who try it in the hope that it is “the answer.”

      As for rT3, I think I see what you’re getting at. But I wouldn’t ever recommend trying to use it as a marker of health.

    1. Any serious illness that lands someone in the ICU can cause the funky thyroid function test numbers seen in NTI (usually low FT4, low FT3, and low or low-normal TSH).

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