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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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T3 to heal adrenals, Selenium, liver–all important info for thyroid patients!

Though this post was written in 2012, it has been updated to the current day and time and it still applicable. Enjoy!

HOW T3, DOSED A CERTAIN WAY, CAN REVERSE YOUR ADRENAL FATIGUE!

UK’s Hashimoto’s patient Paul Robinson has been a successful T3-only treated patient for more than 13 years, especially because he never did well on either synthetic T4, nor on the combination of T4/T3. And he learned so much about himself that he compiled all the information on T3 dosing in his book called Recovering With T3: My Journey from Hypothyroidism to Good Health Using the T3 Thyroid Hormone.

But what I especially find interesting is how he used T3 to cure his flagging adrenal function rather than HC (hydrocortisone).  And here is a short summary of key points. He calls this The Circadian T3 Method, aka the CT3M.

  1. Most of the day’s cortisol is made in the last four hours of sleep, which means your adrenals work their hardest during that time. And like any cell in your body which need T3 to function well, so do your adrenal cells…especially during the time they work the hardest.
  2. With the above in mind, it made sense to Paul that if adrenals are struggling with low cortisol, they clearly need T3 in that early morning 4-hour window in order to function better. How did he do it?  He moved his first T3 dose to one hour before he would normally wake up, held it for a few weeks to see the results, went earlier another half hour, held it for a few weeks to see the effect…and so on. He obtained a lot of data to ascertain what was happening–urine cortisol, blood pressure, pulse, etc. He found that the time which gave his adrenals the biggest boost, and thus better function, was 3 1/2 hours before he normally wakes up.  But he feels that others might find that anywhere in the first three hours of that four hour window, and it’s important to move slowly within that area to find the right time for you based on data.
  3. This protocol needs certain supplements, which include high potency B complex, B12, Vit. C, Vit. D and a good multi mineral. He goes into detail in his book.
  4. This protocol would not work if someone has Addison’s Disease, Hypopituitary or Diabetes…and may not work if you have pre-Diabetes blood sugar issues. It’s blood sugar in the cells that reacts positively with T3.

There is much more detail than the above. And Paul makes it clear that this treatment for adrenal fatigue and proven low cortisol should only be done in your relationship with your doctor. You can read more here on STTM.

UPDATE: many patients have reported that though the CT3M did wonders bringing up the morning cortisol, it didn’t help afternoon cortisol at all, and for some, didn’t help noon’s low cortisol. Yes, there are some who feel it’s helped all day, but also a large body who said it only helped morning. So we concluded that though it’s great for that low morning, you may have to use other supports for other low cortisol times. Also, the CT3M is excellent to help get off HC! Many are off in a month or less!

SELENIUM, EVEN WITH HIGH RT3, IS A MINERAL YOU NEED!

Check out what thyroid patient Cheryl Alvey has put together about selenium. This is a masterful page!

WHY THYROID PATIENTS NEED HEALTHY LIVER FUNCTION

What happens if your liver isn’t healthy?  Transportation is less optimal, and the deiodination type 1 will change to type 3, meaning T4 will convert to excess RT3! And guess what can make your liver unhealthy? Continued hypothyroidism, which happens to all too many who are on T4-only medications, or those left undiagnosed due to the TSH. Hypothyroidism is worsened with adrenal problems, and low iron.  And liver function can become unhealthy or stressed if you eat poorly  You can read more about all this here.

In the meantime, what can one do to promote better liver function? Milk thistle is one highly recommended way by many (use Milk Thistle supps from the seeds to avoid estrogenic affect). Also look into dandelion root /leaf, Sassafras, Burdock, Goldenseal and Yellow Doc root, Red Clover and Echinacea root. Ask someone knowledgeable at your local health food store.

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See thyroid patient Sam Aliyev’s latest YouTube video.  If you do one about the message of STTM, let me know and I’ll post about it.

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Why iron is so important, milk thistle for RT3, and send the revised STTM book as a Christmas present!

NOTE: though this post was originally written in 2012, it has been updated to the present day and time! Enjoy!

IRON AND ITS IMPORTANCE 

It all too common with hypothyroid patients: finding themselves with low iron levels.   I probably had insufficient iron my entire adult life, remembering that my doctors always told me I was borderline, yet nothing was done about it. So when I finally got on desiccated thyroid, and my iron needs increased due to better health, I finally fell into true anemia, and twice.  Miserable, let me tell you. I was breathless, achy, depressed and had horrific fatigue.

And why is iron so important?

  • Iron carries oxygen from your tissues to your lungs (so if iron is low, you can be breathless and your heartrate has to go up in response to less oxygen. Link here.)
  • Iron helps raise dopamine and serotonin in your brain (so if iron is low, you can feel depression or hyperactive i.e. attention-deficit hyperactivity disorder. Link here.)
  • Iron assists with the cortisol secretion after ACTH stimulation (so if your iron is low, the cortisol secretion is decreased, lowering glucose in your cells, and that might cause the pooling of T3 in your blood. Link here.)
  • Iron promotes good conversion of thyroid hormones T4 to T3 (so if iron is low, your storage iron T4 will build too high. Link here.)
  • Iron balances your autonomic nervous sytem (so if your iron is low, you can end up in a frequent state of fight-or-flight with accompanying adrenaline surges and nervousness due to heightened sympathic activity. Link here.)
  • Iron protects women from breast tumor growth (so if your iron is low, a benign tumor can become a malignant cancer tumor. Link here.) 
  • Iron improves your immune system (so if your iron is low, you are most susceptible to infections and illness. Link here.)
  • Iron supports brain cell health (so if your iron is low, you can have brain cell death contributing to dementia and possibly Alzheimers. Link here.)

How to discern if your iron is too low

We used to think testing one’s storage iron, ferritin, was enough. But it’s not. Your storage iron can look normal because of an ongoing inflammation, which tends to thrust iron into storage. So we learned that we need four labs at the minimum : ferritin, % saturation, serum iron, and TIBC.  Even low ferritin along with optimal results in the other labs have caused problems with T3 pooling in the blood.  Go here to read what we look for in our iron results.

Raising poor iron levels

Hypothyroid patients tend to “dry up” and that also causes lowered levels of hydrochloric acid in the stomach, which lowers absorption. For better absorption, try adding 1 tsp to 1 tbsp of Braggs Apple Cider Vinegar to each large glass of water or juice you use to swallow your iron pills, or use Betaine, which is an OTC hydrochloric acid supplement.

To learn more, go to the following page. And for even more details, read the Odds and Ends chapter in the revised STTM book.

CAN LIVER CLEANSES/SUPPORTS HELP IMPROVE YOUR RT3 RATIO??

Because of low iron or adrenal dysfunction, many thyroid patients have found themselves with high levels of Reverse T3…or more common, a poor RT3 ratio. And too much RT3 can mean the thyroid hormone T3 won’t adequately work in your cells, and you can feel miserable. The solution for most has been to switch to T3-only, but that can have a host of difficulties.  It’s not easy to dose with T3 alone.

Recently, though, patients are discovering an alternative way to lower one’s excess RT3: the use of a good liver cleanse/support product, and most especially those with the herb called Milk Thistle. It’s an herb which, for hundreds of years, has been used as a liver tonic.  In supplements, it’s the milk thistle seeds which are used because they contain silymarin–the powerful part of the herb which does the trick.  And doses in the 400 mg’s of milk thistle extract supplements seem to be doing the trick, say patients who are reporting on it, taking it twice a day at 200 and 200 minimum. Some studies state you can go higher, if needed. Be careful with its use, as it can lower ferritin levels to some degree. But as long as you keep your serum iron levels up, you can get by with the lowering of ferritin for the short while you may be on Milk Thistle to lower RT3.

HO! HO! HO! SEND THE REVISED STTM BOOK TO A FRIEND OR LOVED ONE FOR CHRISTMAS OR THE NEW YEAR!  It can be the BEST gift they will ever receive!  Go to the following page, and put in the name and address of the recipient, YOUR email, and the publishing company will get the book out to your special someone:  //www.laughinggrapepublishing.com/

 LISTEN TO ONE OF SEVERAL INTERVIEWS I’VE DONE LATELY…AND BOSTON IS NEXT! My next interview will be aired on WBZ-AM 1030 (Boston & New England) on the program called “Women’s Watch” with host Ellen Sherman. You can also listen live here: http://boston.cbslocal.com/station/wbz-news-radio/ No specific time as I am posting this, but it may happen next week. Watch the NTH Yahoo group, STTM Twitter and STTM Facebook groups for an announcement. And there are more to come thanks to a great publicist representing Stop the Thyroid Madness. Want to donate so she can continue helping us spread the word? Go here.  Janie can’t do it without you…and this is specifically to reach millions still on T4-only meds!

 STTM NOW HAS MANY FACEBOOK GROUPS!  See what Facebook has to offer you on top of already great Yahoo groups, here.

 

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Taking your temp, Selenium and RT3, TPA’s Autumn Newsletter, and HealthcheckUSA’s discount to STTM readers

NOTE: though this post was originally written in 2011, it can still contain relevant information for you today to consider, or do further research on. 

(Photo graphic by thyroid patient Sam Aliyev of Azerbaijan, Baku city.)

TAKING YOUR TEMPERATURE CORRECTLY?? Possibly not.

Thanks to Dr. Broda Barnes, informed thyroid patients know the importance of taking one’s temperature, especially just before we get out of bed in the morning. According to Barnes, we can suspect a thyroid problem if that temp is below 97.8. Conversely, healthy thyroid function (or adequate treatment) would  put our before-rising temp from 97.8 to 98.2. (Menstruating females would need to be aware of higher temps right after ovulation.).

Today, we favor the mercury thermometer over digitals for accuracy. But are we using the mercury thermometer correctly? Maybe not.

A discussion between thyroid patients recently underscored the need to leave it in the mouth longer than the 5 minutes we thought was adequate. Thyroid patient Jennifer states: At 5 minutes it read 97.6, at 10 minutes it read 97.8 and at 15 minutes it read 98 degrees. After that, it stayed 98 degrees.  We then discussed the fact that manipulating the muscle in the back of throat could have caused the final temp. But her experiment, as well as others, underscored that we need to be holding that mercury thermometer in our mouths no less than five minutes, and ten is probably better.

DOES SELENIUM REALLY CAUSE A RISE IN REVERSE T3 (RT3)?

The above statement about selenium causing excess RT3 has oft been repeated from group to group for a few years. But it may be very wrong.

For example, this study shows selenium did not cause a rise in RT3, and in fact, lowered  it. Here is one which shows LOW levels of selenium can result in increased RT3. This medical book states that though RT3 comes from T4, it also concludes that  low selenium increases RT3.

In other words,  though the enzymes that convert T4 to T3,  and convert T4 to RT3, are selenium dependent to do their job, that doesn’t mean that selenium is going to increase your RT3.  Bottom line, many thyroid patients love selenium, especially with its power to lower Hashimoto’s antibodies, and being anti-cancer. Suggested levels are no more than 400 mcg.

TPA’s AUTUMN NEWSLETTER IS OUT–many good articles!

TPA stands for Thyroid Patient Advocacy, and is a UK charity organization started by Sheila Turner. Check out the articles below in the latest newsletter.

Page 5: The Big Question – Is There an Anti-T3 Conspiracy.  Eric Prichard critically questions why those in Endocrinology need to cite numerous anti-T3 studies, in spite of many other studies which reveal the activeness and superiority of T3. Is the UK and other dark age countries ever going to get it?

Page 9:  Why I Believe T3 Should Be the Very Last Treatment that Thyroid Patients Consider.  Don’t let UK’s Paul Robinson’s title fool you. He believes in the efficacy of T3, but underscores why it can be complex to dose with just T3. Especially compelling are what follows Paul’s article, titled MEMBERS SUCCESS STORY.  Story 1 is about an individual who, when dosing T3 in the early morning hours, was able to get off all adrenal meds. Story 2 is about a gal’s successful transition from T4 to T3.

Page 15:  Thyroid Patients Have Come a Long Way, Baby….But We Still Have a Way to Go!  Though there are now numerous patient groups on the net and many lives have changed, Janie Bowthorpe (yes, me) explains how many doctors still have a long way to go in understanding how T4 and TSH fail patients, just as desiccated thyroid or T3 have turned miserable lives around.

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Thyroid Tidbits: Men with low iron, Reverse T4 (yes, I said it correctly), Inflammation in thyroid patients, plus more

(No, the tatoo isn’t mine. It belongs to a gal who says STTM helped changed her life. Amazing and brave! 🙂 )

MEN CAN HAVE LOW IRON, TOO:

I’ve seen a few hypothyroid men who have found themselves with low iron. In fact, either iron anemia is growing in men, or we’re just hearing from them more thanks to the internet.

And remarkably, it has become personal for me. Turns out my own husband is very low, which explains the fatigue he had been experiencing lately. Sadly, taking iron pills gives him a headache, so he will eat high-iron foods daily, and will be exploring Floradix, a liquid herb-based iron. Men, get all the needed iron labs!

REVERSE T4 (yes, I said it correctly)

I’ve been having an email chat with a scientifically-minded guy named Brian who also has a sister with a major in bio-chemistry. And something dawned on both of them concerning “levothyroxine” which is the synthetic term for T4.  The prefix LEVO means the “left-hand” version of a molecule, and thyroxine is the biological term for the real T4.  Says Brian: “Levo-thyroxine means it has exactly the same atoms in exactly the same order, but not the same shape (handedness), so if enzymes or proteins have to chemically “fit” it to work, they may not be able to. He concludes this can be one reason being on synthetic T4-only does not work, and knew it was alluded to by Dr. Mark Starr.

But Brian continues: In just the same way that levothyroxine is the mirror-image or “left-handed” version of regular thyroxin, RT3, or Reverse T3, is the mirror-image or “left-handed” version of T3.  If we were consistent with our terminology, in other words, levothyroxine would be known as “Reverse T4”. Says Brian, just as Reverse T3 is biologically inactive , so is Levothyroxine, thus “Reverse T4”. I love it!

CHECK OUT WHAT THIS MEDICAL TRANSCRIPTIONIST SAID:

In a facebook discussion,  a female medical transcriptionist has had a realization. Namely, in almost every report she is transcribing into text or digital format,  a patient with the diagnosis of hypothyroidism also has a medical history of depression and/or anxiety. You can read about depression & anxiety here. Of course, no patient who is informed is surprised! They are HYPOTHYROID symptoms.  And she then notes the prescription ordered by the doc: Synthroid.  WAKE UP DOCTORS. You are only dooming your patients to a lifetime of depression, anxiety and far more.

WHY MANY OF YOU HAVE INFLAMMATION (and don’t even know it), WHAT IT DOES, AND HOW TO TREAT IT

One thing I see a lot when doing phone consultations, as well as on thyroid patient groups, is evidence that someone has low-grade inflammation. In fact,  research has already shown that a large body of folks with hypothyroidism have higher levels of CRP (C-Reactive Protein) which is a lab test marker of inflammation.  That inflammation, in turn, puts you at a higher risk of heart disease.

Another clue that you have an inflammation problem is having higher ferritin levels (i.e. ferritin looks great, or is too high) along with poor iron serum/% saturation lab results.  In other words, in the presence of chronic inflammation, your iron will be diverted to your ferritin iron storage, and less will be in your serum and saturation.  You can also find yourself with very low TIBC (Total iron-binding capacity). The TIBC is measuring the protein “transferrin”, made in your liver, and which transports your iron through your body. If this is the case, you can’t take high levels of iron supplementation, as explained on the above ferrritin page and more in the book.

What do you do? 1) Treat your hypothyroidism properly–a huge step in lowering that inflammation–with desiccated thyroid, NOT Synthroid. (Read the Things We Have Learned page on STTM, or even more details in Chapter 3 in the new Revised STTM book). 2) Treat proven low cortisol with HC or hydrocortisone. Don’t guess! Do a saliva test!) If saliva testing reveals you have adrenal dysfunction, cortisol supplementation will help counter inflammation.   (Read the Adrenal Info and How to Treat page on STTM, or more details in Chapter 6 in the new Revised STTM book.) 3) Use Krill Oil as a supplement. Krill Oil is an even better marine fish oil with rich amounts of Omega 3 fatty oils,  and research with even a low dose of 300 mg proves that it does a bang-up job in reducing inflammation as well as pain in joints associated with rheumatoid and osteoarthritis.  My own husband is on 1000 mg a day.

HAVE THE REVISED SECOND EDITION OF THE STTM BOOK YET? IT’S WORTH IT.

I am frankly extremely proud of the Revised Second Edition of the STTM book.  In spite of being a lot of hard work, it is good to see all the additions, details and corrections throughout the entire book.  There is much more on labs and how to read them, ferritin and iron, adrenal dysfunction and how to treat it, reverse T3 and how to treat it, plus a completely new chapter on good supplements and foods.  I added a little more hidden humor, which was fun.  There are now 36 more pages, too, and at the same price.  You can see more about the book here.  The book is ideal since you can bring that right into the doctor’s office with the information highlighted and bookmarked. As far as Kindle or other readers, yes, I’m already aware that some of you have requested it. But right now, it’s the book only.  But I’ll make announcements in the future as to what might be coming up.

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