Does anyone know of published articles, papers, reports, etc., on how much T3 is produced by each of the body's organs?
I am aware that some T3 is generated by the Thyroid and the rest is as the result of conversions in the body's organs.
What i would like to know is how much T3 each organ is responsible for.
The reason for my question is that I have read that T3 is likely to be low in patients who have Chronic Kidney Disease.
I am interested to learn how much the kidneys normally contribute to the T3 pool and the significance of the loss of a kidney and/or a diseased kidney on FT3 blood levels.
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Parbrook
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No organ is responsible for producing T3. It is all to do with the Thyroid Gland producing both T3 and T4. hormones. To enable our metabolism to work perfectly there are billions of receptor cells in our bodies and each one needs only the Active T3 to saturate them.
These are a couple of excerpts:-
Dr. Lowe: In my book The Metabolic Treatment of Fibromyalgia, I refer to thyroid hormone receptors as "T3-receptors." I do so because evidence suggests that it is T3 and not T4 that binds to thyroid hormone receptors on genes within the nuclei of cells. In laboratory tests, T4 does bind to thyroid hormone receptors, but with far lower affinity than does T3.
1. It is debatable, however, whether T4 binds to thyroid hormone receptors in our bodies and exerts metabolic effects. Most thyroid researchers today argue that T4 is a storage form of T3. We believe that T4 exerts metabolic effects only after the enzyme 5'-deiodinase removes the fourth iodine atom from the T4 molecule. Removing the iodine atom, of course, converts T4 to T3.
PubMed (US National Libraries of Medicine) lists many review papers on thyroid hormone receptors. If you go to PubMed and type in the key words "thyroid hormone receptor and review," some 17 pages of abstracts will come up. You can then read the abstracts and find articles that you're interested in. If you have a medical library close to you, it will probably carry some journals that contain the articles.
2.You asked, if we don't have T4 receptors, "then why do we need T4 supplementation rather than just T3 alone?" With rare exception, we don't.
No one can rationally defend T4 supplementation on scientific grounds. I say this because the widespread use of T4 supplementation is not based on scientific studies that show it to be safer or more effective than the use of T3 alone. Instead, its widespread use is the result of a financial venture between the endocrinology specialty and corporations that profit from sales of the most commonly prescribed brands of T4.
Our long clinical experience shows that in general, patients respond far better to T3 alone than they do to T4 alone. Moreover, our safety monitoring of patients shows that the responsible use of T3 alone is as safe as the use of T4 or T4/T3. By "responsible use," of course, I mean employing the same precautions that are appropriate to the use of any thyroid hormone product.
"It is estimated that healthy adult subjects produce about 30 ug T3/day, of which about 5 ug are secreted directly from the thyroid and the rest is produced outside of the thyroid parenchyma via T4 deiodination."
In one of Dr. Bianco's videos it shows 5 from the thyroid, 5 from the liver and kidneys and 20 from deiodination in the rest of the body. All control of thyroid is local, in the tissues and organs throughout the human body. PR
CarolynB, yes this whole area of what the body produces and what actually returns us to a 'normal' state is a can of worms which is pretty much not understood by science. But then science is still pretty much clueless as to why we can react so differently to the different thyroid medications and why there always seems to be a persistent minority that needs T3 to return to 'normal'. Science is still years behind what thyroid patients have had to figure out in order to get our lives back. Science is a slow process. However, having said that, there are some encouraging signs, Dr. Midgley and his collaborators, Dr. Bianco and 'The biological imperative is to defend T3' (only took him 30 years), Dr. Hollenberg on the co-activators and co-repressors, and others doing good research, so there is hope. Dr. Bianco has a bunch of stuff on his website, you can download several papers. Also the videos from the 2013 spring symposium I posted about earlier are quite interesting. You might find DR. Celi's work on T3 of interest. PR
i am particularly interested in the affect on T3 levels in someone who only has one kidney and which is poorly functioning (CKD stage 4).
I have read in a couple of articles that T3 has been found to be low in patients with CKD 4 and 5, possibly due to reduced deiodination, or possibly as part of a mechanism that is designed to protect a diseased organ.
What I am trying to achieve is to establish whether I have a physiological case to put to my Endo for a higher dose of T3 to compensate for having a single kidney, which is CKD4.
I am currently taking 75mcg Levothyroxine and 20mcg Liothyronine. My FT3 has remained stubbornly low during the last 4 years and I still have some hypo symptoms. My initial thought was poor conversion, which is how I was able to justify a "trial" of Liothyronine, but I am now wondering if my low T3 is related to my renal condition.
Boy, that is a complicated question. I don't know if science knows enough to answer it. There is a fair amount about kidney problems and lower T3 maybe from NTI but this is not an area I have read a lot in. For us patients the goal is whatever mixture gets us back to 'normal' and the endos quite often aren't on the same page. Are you felling better with more T3? That should be the only thing that really counts, of course, it rarely is. PR
Over 4 years, I tried increasing doses of Levothyroxine up to 125mcg, on which I eventually felt Hyper, but never free of what I believe are Hypo symptoms.
On my current T4+T3 doses, some Hypo symptoms have improved, but have never completely resolved.
The complication is the impact of my CKD, which has resulted in me having low Iron for a few months (until an iron infusion) and low haemoglobin (which has not yet recovered to normal levels, so I know that these affect Thyroid hormone absorption.
Some Anaemia symptoms cross-over with Hypo Thyroid symptoms (tiredness, lethargy, etc.).
What I do know is that my FT3 has been hovering between 3.4 and 4.4 for the last 4+ years, which is why I am looking for a possible link with having a very limited renal function to support a case for increasing my T3 dose.
I wish I had something intelligent and useful to add, you are in uncharted territory. The good news is you are reading and researching and you seem pretty aware of the various factors involved. Hopefully you will keep us informed of your progress and what you learn. So many of us end up experimenting to find the solution. If you can slowly adjust the ratio of T3 upward it might be beneficial since you are still experiencing symptoms and adding T3 has already alleviated some symptoms. PR
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