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An hypothesis about RT3 – did you know you might have a hidden pool of it?

arrowPlease note this is a HYPOTHESIS, based on limited information, from 2014, and not to be taken as gospel.

Everyone makes Reverse T3 (RT3)–an inactive thyroid hormone. It’s a way to clear out excess T4 when your body isn’t needing that extra storage hormone. i.e. instead of the T4 converting to the active T3, your body (and specifically your liver), will convert it to RT3. If someone without a thyroid problem gets the flu, up goes the RT3 to conserve energy. If someone has a bodily injury, up goes the RT3 to conserve energy.

And thyroid patients seem to see their RT3 go up in the presence of low iron or a cortisol issue.

But if you think about it, why doesn’t it go down faster when we decrease our T4? T4 has a half life of one week, yet it can take 8 – 14 weeks for RT3 to go down. Hmmmmmm…

Thyroid patient Sebastian from Germany sent me this information about Reverse RT3 that I find fascinating. What do you think?

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I’m studying biology and chemistry and have Hashimoto’s Thyroiditis with high RT3. I just wanted to inform you about an interesting idea/hypothesis I have found.

There seems to be a “hidden pool” of RT3 in the human body. This RT3 pool can increase in size while enough T4 is available, and then secrete RT3 in times where the body needs it but hasn’t got enough T4 to produce it via deodination (the removal of an iodine molecule).

“It is concluded that a hidden pool of RT3 production exists in vivo in man.”
“It would appear that hypertrophy of this hidden pool of rT3 production occurs in high T4 states […]”

Source: LoPresti et al., “Does a hidden pool of reverse triiodothyronine (rT3) production contribute to total thyroxine (T4) disposal in high T4 states in man.”, J Clin Endocrinol Metab. 1990 May;70(5):1479-84. http://www.ncbi.nlm.nih.gov/pubmed/2335581

I have made observations regarding  my own thyroid blood tests and the blood tests of other patients that seem to support this hypothesis. I have been on T3-only for 6 weeks now, started with an RT3 of 330 pg/mL at approx. day 0, and now have measured a RT3 of 685 pg/mL (twice as much!), even though my TSH is low, FT4 has fallen rapidly to 0.5 ng/dL, and no T4 medication has been taken for full 6 weeks.
Another patient I know has also made interesting correlations between FT4 and RT3. He isn’t on T3-only, but observed a time-delayed (!) correlation between both values – which could be interpreted as an indicator for the presence of an RT3 storage pool in the body, that grows when enough T4 is available, and sets RT3 free in times when there is less T4 available.

I also found studies which found that RT3 has a 1000 times less feedback on the TSH than T3 has, and 100 times less than T4. This could explain any differences between TSH and symptoms, as the “RT3-system” seems to be almost completely isolated from the thyrotropic regulation system (the latter is that which directly influences the secretory activity of the thyroid gland).  RT3 can obviously rise and fall without having (almost) any effect on the TSH.

Source: Cettour-Rose et al.: “Inhibition of pituitary type 2 deiodinase by reverse triiodothyronine does not alter thyroxine-induced inhibition of thyrotropin secretion in hypothyroid rats”, European Journal of Endocrinology (2005) 153 429?434.

In combination, this could explain why the clearing process of RT3 takes approx. 8-14 weeks, although T4 has a plasma half-time of only 8 days, and rT3 only 4.5 hours!

The intracellular T3 receptors aren’t “clogged”, and then suddenly become free after that period of time has elapsed. Instead, RT3 is a competitive inhibitor of T3, meaning it constantly goes in and out of the T3 receptor. You probably know that already.

Patients report feeling well with T3 only dosages of approx. 80-120 µg T3 per day. According to Celi et al., 2010, this would be equal to 240-360 µg of T4. I always wondered why they don’t end up feeling hyper.

This all makes sense now under the assumption that a hidden RT3 storage pool exists somewhere in the body. Although there is no new T4 being produced or taken in, and although the remaining T4 and RT3 have both decayed rapidly after one starts with the T3 only method, there is still alot of RT3 being set free by the storage pool all the time. This storage pool might be big enough to last for several weeks to months. Since RT3 is the competitive inhibitor of T3, this might be why patients are able to tolerate (and even need) so very large amounts of T3.

Then, after the storage pool has been emptied, the remaining RT3 rapidly decays because of its short half-time and no new RT3 can be produced because no T4 is available in the body. Therefore, RT3 concentrations within blood and cells drop. Thus, the competitive inhibition gets a lot weaker at that point, and patients start feeling hyper because the same amount of thyroid hormones (T3) is now significantly increased in its effect, since it can stay much longer in the T3 receptors without being competitively inhibited (kicked out of the receptors) by RT3.

This process of totally emptying the RT3 storage might occur very quickly, therefore the drop in RT3 concentrations is very suddenly, all of which might happen within several days. And this is why patients then get hyper and have to reduce their dosage to half or less of what they’ve taken previously over the 8-14 weeks.

“Clogged receptors” don’t make sense because RT3 is a competitive inhibitor, capable of traveling in and out of the T3 receptor all the time.

“Clearance” occurring after 8-14 weeks, although both educt (T4) and product (RT3) have significantly (!) shorter lifetimes, doesn’t make sense either.  Neither does a totally defective TSH lab test, because in principle, it worked fine for all the patient’s lifetime before they got their thyroid disease; and because significant correlations between TSH and FT3 and FT4 can be observed.

This all makes sense to me now, based on two assumptions:

1. While T3 and T4 have a strong negative feedback effect on TSH secretion, RT3’s effect on the TSH secretion is minimal, being about a thousand times smaller in effect than that of T3, and about a hundred times smaller in effect than that of T4….as described in the study of Cettour-Rose et al., 2005, mentioned above.

2. The body has a large, previously unknown storage for RT3. This storage can grow while enough T4 is available, and the storage’s content can be set free when needed. As described in the study of LoPresti et al., 1990, mentioned above.

I hope you can use this information for further research. Thanks for reading.

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58 replies

Reverse T3–do you have this problem in excess? Let’s talk!

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This blog post has been updated to the current day and time. Enjoy!

Most thyroid patients have heard about T4…the thyroid storage hormone, also called a pro-hormone. You’ll see it in literature as “thyroxine” or “l-thyroxine”–the latter as the name for a man-made T4.

And many know about T3…the active thyroid hormone which rids us of hypothyroid symptoms.

And as patients become more informed, they learn that the body not only converts T4 to T3 through what is called deodination, it also provides some of that T3 directly. That is an important distinction! The latter fact can be why thyroid patients report getting far better results with natural desiccated thyroid (NDT) like Naturethroid, NP Thyroid or other brands.

Patients might also learn that there are actually five thyroid hormones made in your body, which is also what’s found in NDT: T4, T3, T2, T1 and calcitonin.

Reverse T3

But in every individual, whether a thyroid patient or not, a thyroid can also convert T4 to the inactive RT3 (reverse T3).  RT3 is an inactive thyroid hormone, as compared to T3 as the active thyroid hormone. And converting to RT3 is a natural and necessary process, even if there are consequences.(1)  The body might convert T4 to RT3 as a way to clear out excess T4, or as a way to reduce your metabolic rate.  It can happen if you go through any of the following:

  • surgery
  • a major physical accident
  • certain heart problems
  • intense chronic stress
  • restrictive low carbohydrate diets (2)
  • chronic inflammation

When Reverse T3 is a problem

Unfortunately, many thyroid patients make far too much RT3, as well, and patients with their open-minded doctors have been making cutting edge discoveries about this fact.  Many patients have seen that their high levels of RT3 can be found with the following conditions:

  • high cortisol
  • low cortisol
  • low iron levels
  • possibly low B12
  • lyme disease
  • gluten intolerance or Celiac
  • other undiscovered and untreated underlying issues that can go hand-in-hand with being hypothyroid.

Why is a high level of RT3 is problem? That excess RT3 is making itself lazily comfortable on your thyroid cell receptor sites, preventing the active T3 thyroid hormone from doing its job on that same receptor to get you out of your hypothyroid state.  It becomes akin to a clogged up drain to your organs and cells. So you stay hypo and symptomatic, in spite of seemingly “normal” other labwork.

The solution

Informed patients discovered they needed to discover and treat all the reasons contributing to their body converting to excess RT3.

Want to read more? All the below is based on patient experiences and wisdom to share and work with your doctor:

For those with the revised Stop the Thyroid Madness book, there is also more good detail in Chapter 12 called T3 is the Star of the Show, page 155, to continue your education. This is all good information to take into your doctor’s office.

JanieSignature SEIZE THE WISDOM

 

 

 

 

 

 

 

(1) http://press.endocrine.org/doi/abs/10.1210/jcem-41-6-1043

(2) http://press.endocrine.org/doi/abs/10.1210/jcem-42-1-197

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79 replies

Thank you to my doctor–what a BREATH OF FRESH AIR

Started with a new doc. He prescribes Armour and is reading the STTM book. That latter in itself is an eye-popping miracle.

And…as we were going over my extensive labwork, which he does for new patients, and as I was lamenting the way too many doctors put their patients on the lousy statins (when all they need to do is treat hypo CORRECTLY), he stated, with a sigh of dismay and humility, something to the effect of: We doctors are simply too busy to keep up with the latest good information that patients are finding out far ahead of us.

I nearly fell off my chair!! He was honestly and humbling admitting that patients are finding out good information far ahead of doctors! i.e. he was NOT dissing the internet; he was NOT dissing that a patient could actually be more informed than him; he was not dissing information that goes against the Big Pharma Con Job .

This doc is a keeper.

p.s. Think your doc is open-minded enough to read the STTM book?? You can have the publishing company send one directly to your doctor. Click on the SEND A BOOK TO YOUR DOCTOR.

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Oprah…you can save yourself a lot of problems….

….if you will take the time to read here of what thousands of patients have found out about the medication you will PROBABLY be put on, and about the lab you will PROBABLY be dosed by.

For those who haven’t heard, Oprah announced on September 10th during her Good Morning America interview that she “blew her thyroid out”. Now that also sounds suspiciously like she also has adrenal fatigue, but time will tell.

And Oprah will now join the club of an estimated “billions” worldwide with thyroid disease. But even worse, she may also be joining the club of those who for nearly 50 years, have been put on the lousy T4-only medications (Synthroid, Levoxyl, Levothyroxine and others) and who have been terrorized with the TSH lab and it’s dubious and pathetic “normal” range.

Yes Oprah, beginning in the 1960’s, doctors starting putting ALL of us on T4-only meds, and in the early 1970’s, dosing by the TSH lab. And NEITHER have worked. Sure, some will state they felt better. But many will tell you that NOTHING changed. And ALL, to one degree or another, have been left with a variety of hypothyroid symptoms while doctors have been proclaiming that those VERY symptoms had nothing to do with hypothyroid since we were now “adequately” treated.

But we have NEVER been “adequately” treated, Oprah. Doctors became cattle in the chutes of their pharmaceutically-financed medical schools, blindly believing that T4-only meds were working and that the man-made TSH was the gold standard of diagnosis and dosing…and ignoring clinical presentations which showed the opposite.

And when we still complained of symptoms, we have been put on anti-depressants, statins, anti-anxiety meds, and a variety of other pills to bandaid our continuing hypo symptoms.

And we finally fought back Oprah. For the last 7+ years, patients like myself found out that there has always been a MUCH better treatment (desiccated thyroid), MUCH better labs (free T3 and free T4) and much better dosing strategy (by symptom elimination). Our lives have become far better because of what we have learned.

This website represents the knowledge of a large and constantly growing body of patients worldwide, and some wise doctors, which goes totally COUNTER to nearly 50 LOUSY years of pitiful thyroid treatment.

You, Oprah, are a megaphone of influence. And if you can take the time to read this website, you might play a huge role in helping to change MILLIONS of lives. Because right now, the vast majority of the medical community does NOT get this, and is continuing to keep patients SICK and TIRED and/or with continuing hypothyroid symptoms of some kind. And YOU are going to be one, with your own continuing list of symptoms, if you don’t consider what thyroid patients are trying to tell you by nearly 50 years of LIVING it.

5 replies