These first two papers can be used to prove that on T4 monotherapy , a dose that is enough to 'satisfy' the hypothalamus /pituitary (ie. lowers TSH to the bottom end of the ref range) , does not necessarily provide 'enough' T3 to all the other tissues... some other tissues can remain hypothyroid despite TSH being in 'normal' range .
Just because the pituitary thinks that dose is 'enough' ... the heart / lungs/ muscles etc may not have 'enough' .
So some people need to take more T4 (to get enough T3 to those tissues) in order to feel well , and they then end up with a below range TSH and in a constant argument with their GP (who believes their pituitary's opinion on the matter).
( links to both were taken from this : bmcendocrdisord.biomedcentr...Time for a reassessment of the treatment of hypothyroidism John E. M. Midgley, Anthony D. Toft, Rolf Larisch, Johannes W. Dietrich & Rudolf Hoermann ~2019)
jci.org/articles/view/118353 Replacement therapy for hypothyroidism with thyroxine alone does not ensure euthyroidism in all tissues, as studied in thyroidectomized rats.
H F Escobar-Morreale, M J Obregón, F Escobar del Rey, G Morreale de Escobar (1995)
thelancet.com/journals/land...New insights into the variable effectiveness of levothyroxine monotherapy for hypothyroidism
A below range or supressed TSH in a patient taking Levo is usually taken to mean the patient is overmedicated/ Thyrotoxic (ie. the same as it means in people not taking any replacement thyroid hormone)
The following papers can be used to show why TSH level doesn't mean quite the same thing once on Levo. ~ fT4 is relatively higher / fT3 is relatively lower and TSH is relatively lower in patients on Levothyroxine monotherapy :
a previous reply from diogenes to someone else : "Your GP should realise that in T4 therapy a below-reference TSH doesn't often matter. Indeed this downloadable paper shows that in therapy TSH as low as yours (0.06) can still express the body as euthyroid. You could download it and show its basic conclusions."
(diogenes is an author in some of the papers below [JEM Midgley], also advisor to ThyroidUK ,and the inventor of one of the methods used for fT4/fT3 tests)
ncbi.nlm.nih.gov/pmc/articl... Biochemical Markers Reflecting Thyroid Function in Athyreotic Patients on Levothyroxine Monotherapy Mitsuru Ito, Akira Miyauchi, Mako Hisakado, et al. (2017)
onlinelibrary.wiley.com/doi...Homeostatic equilibria between free thyroid hormones and pituitary thyrotropin are modulated by various influences including age, body mass index and treatment Rudolf Hoermann, John E.M. Midgley, Adrienne Giacobino, Walter A. Eckl, Hans Günther Wahl, Johannes W. Dietrich, Rolf Larisch (2014) This study proves that once on Levo, the TSH level is shifted lower , and the fT4 is shifted higher ~ relative to the same amount of fT3. Therefore explaining why patients often need a lower than 'normal range' TSH to feel well on just levo. ( they need a higher fT4 to get the same amount of fT3 ~ and in order to get the same amount of fT3 they have a lower TSH)
fig. 2 ~ a graph showing the lower TSH / higher fT4 / same fT3 after levo ~ is accessible via the 'Supporting Information' dropdown at the end of the summary.
ncbi.nlm.nih.gov/pmc/articl...Increased fT4 concentrations in patients using levothyroxine without complete suppression of TSH (Heleen I Jansen, Marijn M Bult, Peter H Bisschop, Anita Boelen, Annemieke C Heijboer,and Jacquelien J Hillebrand 2023)
"Furthermore, a higher fT4/fT3 ratio was seen in patients using L-T4 compared to healthy controls (12, 21, 22). Hypothyroid patients receive L-T4 supplementation which replaces T4 only and thus these patients partially lack the active thyroid hormone triiodothyronine (T3) derived from the thyroid gland. This suggests a need for increased conversion of T4 into T3 in the peripheral tissues to reach adequate tissue T3 concentrations (21), resulting in the need for a higher L-T4 dosage to obtain a normal, or even somewhat lower, concentration of T3 (22, 23). Moreover, TSH is more sensitive to changes in T3 than in T4, clarifying the lack of negative pituitary feedback to increased fT4 concentrations leading to not (completely) suppressed TSH. This phenomenon may be more prominent in patient groups that are characterized by an even greater deficit of endogenous T3 production (e.g. athyroid patients). Even though in athyroid patients some T3 is still produced by deiodinases in several tissues, previous literature showed an outspoken dissociation between fT4 and fT3 concentrations in this group where even a higher L-T4 dosage did not lead to adequate fT3 concentrations (24). Thus, the adapted peripheral conversion of T4 into T3 in L-T4 users leads to an increased fT4 concentration combined with a not (completely) suppressed TSH, which is reflected in a higher fT4/fT3 ratio".
plus two more ... frontiersin.org/articles/10... Homeostatic Control of the Thyroid–Pituitary Axis: Perspectives for Diagnosis and Treatment Hoermann, Midgley ,Larisch, Dietrich (2015)
frontiersin.org/articles/10... Relational Stability in the Expression of Normality, Variation, and Control of Thyroid Function Hoermann, Midgley , Larisch , Dietrich (2016)
A defence i've often heard against the GP's accusation of 'overmedication' when we have a low/ supressed TSH is to say "well, my thyroid doesn't need stimulating anymore (or don't exist anymore) so it doesn't matter if i have 0 TSH , what do i need any any TSH for ? ... GP is an idiot"
..............but unfortunately that argument doesn't hold water , it would be nice and simple if it did, but it doesn't.
When we use this argument with a GP, it just confirms their opinion that we don't really understand what we are talking about and that they know best .
TSH has TWO roles in the HPT axis .. Feedforward and Feedback :
once a patient is taking thyroid hormone , GP's are not using TSH to see how much it is stimulating your thyroid ~ (the 'feedforward' role) ~ they DO know that role is now largely redundant.
They are using it as an index/ indicator to show the level of thyroid hormone in your body ~ (the feedback role) ~ and that role is NOT redundant.
Even with no thyroid at all , the TSH level is STILL a reflection of the amount/ effect of thyroid hormone action ON THE HYPOTHALMUS and PITUITARY .
As a result of the level of thyroid hormone action , the Hypothalamus makes TRH, which causes the Pituitary to make TSH...this is the "HPT axis" (Hypothalamus /Pituitary/ Thyroid axis).
The tricky part is to get your GP's to understand that once patients are taking thyroid hormone replacement, the hypothalamus /pituitary's OPINION about their dose can be INCORRECT because the HPT axis is effectively warped by monotherapy (using T4 only) .
When you give T4 only (as a replacement for the T4 AND the little bit of T3 MADE BY THE THYROID GLAND) .. you don't restore that patients ratio's of T4:T3 /TSH to quite the same as their previous healthy settings , and as a result their TSH INDICATOR (opinion) doesn't read quite the same as before.
.... the indicator still works , but the needle has moved~ it says you are doing 75mph (over the speed limit) , when you are only doing 69mph ....just the same as if you change the size of the wheels on a car , the speedo will display the speed incorrectly .
On levo only .... patients end up with relatively higher fT4 /relatively lower fT3 / and relatively lower TSH, than they had when their own thyroid was making a variable amount of ready made T3 .
This part can be proved, and i wrote this post to keep my links to the evidence/ explanation all in one place.
The TSH level is shifted downward a bit on 'levo only' .
Some patients need quite a lot of T4 to get enough T3 from conversion to satisfy ALL their organs and tissues to allow them to feel ok.
..... and this relatively higher level of T4 gives them a lower TSH than they had when they were healthy (because the pituitary is VERY VERY good at converting T4 to T3 ).
... but they haven't actually got as much T3 in the rest of their organs / tissues than they had when they were healthy, due to the loss of that little bit of 'ready made' T3 they used to get from their thyroid. The selfish and greedy pituitary thinks ..."if i've managed to make more than enough T3 from this amount of T4 , then everything else in this body has enough T3 too"
....... but something else in the body might not be as good at converting T4 to T3 as the pituitary is.
So for these patients, a low/ supressed TSH does not necessarily mean they are really overmedicated/ thyrotoxic... these patients are not overmedicated unless they have fT4 / fT3 results and or symptoms which also confirm overmedication.
They may need the higher fT4 (and therefore the lower TSH) to get the same level of T3 .. in order to feel well ~ or they might do better with a bit of added T3 and less T4 to even things up... because there is now some evidence that higher T4 levels can potentially be risky.
a link to my previous post with list of evidence re. Low vs. Supressed TSH / RISK (it includes a bit about potential risk of high fT4) healthunlocked.com/thyroidu... useful-evidence-that-tsh-between-0.04-0.4-has-no-increased-risk-to-patients-on-levothyroxine-updated-new-study-does-show-small-risk
(I intend to make another post with a list of collected evidence/ explanations showing how T3 lowers TSH relatively MORE than T4 does ~ for use when patients taking T3 need to have low TSH arguments with GP/Endo .. when i've done it i'll add a link to it here )
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tattybogle
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I intend to make another post with a list of collected evidence/ explanations showing how T3 lowers TSH relatively MORE than T4 does ~ for use when patients taking T3 need to have low TSH arguments with GP/Endo .
the stuff i've collected so far i have listed here:
added 11/09/2024 ~ recent research from Cardiff Endo's : healthunlocked.com/thyroidu... THYROID HORMONE PROFILES IN INDIVIDUALS ON NON STANDARD THYROID HORMONE REPLACEMENT (cardiff-study-about-t3-suppressing-tsh-more-than-t4)
Dual control of pituitary thyroid stimulating hormone secretion by thyroxine and triiodothyronine in athyreotic patients
Rudolf Hoermann , John E. M. Midgley**, Rolf Larisch July 13, 2017
"The present findings have several practical implications. (1) Conversion efficiency and the resulting FT3 play an important regulatory role in shaping the TSH–FT4 relationship in LT4-treated athyreotic patients. The data suggest a dual role of both thyroid hormones, FT4 and FT3, on hypothalamic–pituitary TSH control. This type of controlling of the controller is technically known under the term of cascade control. If the need arises, this provides mechanisms for the efficient adjustment of controlling elements. Clinically, the relatively strong additional direct and indirect influences of FT3 on TSH control demonstrate an important element in determining a suitable set point for adequate treatment......"
Q.from tuppence"... what puzzles me is how he intends to deal with TSH, whilst using T3. Perhaps my understanding is incorrect, but I understood any use of T3 will lower TSH? "
Diogenes replied... " It will do so, because molecule for molecule, T3 is about 3.5 times as potent as T4 in suppressing TSH"
reply by diogenes: The action of T3 and T4 on the pituitary and hypothalamus is roughly 50/50 for a healthy person. But since there's only about 1/3 the amount of FT3 compared with FT4, this means that one molecule of FT3 is 3 x more active than one molecule of FT4. Thus, if FT4 diminishes owing to thyroid loss, the more active FT3 takes over, and being more active suppresses the pituitary more than usual. This will happen with patients on combination or T3 therapy."
Re. T3 lowering TSH 'more' than T4 it's worth checking out this from Tania.S.Smith : thyroidpatients.ca/2019/01/... ... the-pituitary-response-is-abnormal-stop-tsh-worship/
( i haven't looked into her references for this comment ,but they are given.. she's usually pretty reliable with facts but you'll have to read the papers yourself to see if they really do contain the evidence for it ).
"HELLO, HYPOTHALAMUS?
Now consider how fickle the hypothalamus can be to T3 hormone dosing.
Look into the historic studies of T3 therapy and you will understand the unique effect oral dosing of T3 has on TSH. Oral T3 therapy is well known to be a TSH suppressant, much more so than T4 therapy.
Science has now given reason to believe that the early TSH suppression seen in T3-T4 combination therapy is very likely to be a side-effect and a localized hypothalamic bias (11, 12, 13).
The TSH is artificially suppressed post-dose long before FT3 levels rise to their post-dose peak, and the long-term TSH suppression remains in effect long after FT3 levels return to moderate or even low levels.
To put it plainly, the hypothalamus is hypersensitive to the quick rise in fT3 that will occur in T3 dosing, long before it has reached excess.
Why is the body doing this?
The hypothalamus is incorrectly assuming the T3 is coming in a steady stream from a hyperstimulated thyroid gland, rather than from a pulsed thyroid hormone dose. In response to the speed of the upward shift in FT3 level, it radically undercuts the pituitary’s ability to secrete TSH.......... "
just found another one to add to the list of references for T3 lowering TSH more than T4 does thyroidpatients.ca/2019/09/...a-dialogue-with-utiger-t3-over-suppresses-tsh/
To understand why TSH stays supressed for a long time after an episode of hyperthyroidism/ overmedication, (or ANY T3 use) has finished , you need to look up 'Hysteresis'
frontiersin.org/articles/10... A Review of the Phenomenon of Hysteresis in the Hypothalamus–Pituitary–Thyroid Axis Melvin Khee-Shing Leow
When you have a minute could you kindly give me your thoughts on Professor Toft's 2017 Thyroid Hormone Replacement - A Counterblast to Guidelines as I quote from page 3 :-
I am so concerned about the state of advice on the management of primary hypothyroidism that I am increasing reluctant to suggest ablative therapy with iodine -131 or surgery in patients with Graves disease irrespective of age or number of recurrencies of hyperthyroidism.
Treatment with a thionamide, in which the hypothalamic-pituitary-thyroid axis remains intact, making interpretation of thyroid status simpler, is currently a more attractive proposition.
I take the above to mean then, that currently, following iodine -131 or surgery in patients with Graves disease the hypothalamic-pituitary-thyroid axis is " not intact " and therefore this feedback loop broken and not a reliable measure of anything?
I'm sorry to give you more homework - but I have a supply of gold stars - and see this directly linking into what you have just posted.
i've always just assumed he just meant intact as in 'still physically intact cos the thyroid is still present' , which it is.... but just cos it's still physically intact , that doesn't mean the pituitary/ hypothalamus necessarily reads CORRECLY / EXACTLY same as it did before once on levo ( and he doesn't specifically state that it does)
to be honest i haven't ever though very hard about that particular part of what he wrote.
The counterblast article published in 2017 is around the same time as the papers showing the shift to higher T4 /lower T3/ lower TSH on levo .. perhaps he like so many others had a bit of blind spot for diogenes groups work and hadn't read it/ taken it seriously when he wrote 'counterblast' ?
So i dunno ... it would be good to be able to ask Toft himself for an explanation of what he meant .
I did and basically I outlined my thoughts to him, which have remained constant and what I always write on here in that after RAI/thyroidectomy the HPT axis is broken and you must be dosed and monitored on Free T3 and Free T4 readings.
I asked him if my understanding correct and my reply was :
You are indeed becoming very well informed :
Listening to all these professionals, especially those who are deemed at the top of their profession they seem to be the only ones to openly question their own knowledge and openly admit that they don't know everything and still questioning and learning :
It seems to me that this feedback loop must be broken especially if you have had a thyroidectomy as it is physically not there - and the feedback loop not complete but open as the thyroid is in a bucket on the floor !
I've never understood why we treat with RAI to kill the gland and then look for a TSH to even be working as though nothing had happened - and why would you want to stimulate, and kick start a gland you had just poisoned to disable and kill it off ?
i reckon we may be using the word 'feedback' to describe different parts/ functions of the HPT system .because i'm sure we agree on the end result .. ie. you can't trust TSH alone with a disabled / removed thyroid gland ... and so you need to look at T4 /T3 / and symptoms too.
regardless of the thyroid physically being there or not.... the hypothalamus and pituitary are still there and would still (eventually) respond to different fT4 and fT3 levels in the blood , so that link is not physically broken when the thyroid is removed /dead .. (this part is what i mean by 'Feedback' ....i mean the TSH level seen AS A REACTION TO the changing T4/T3 levels .
that function of the axis still 'happens' even with no thyroid present ... the levels of T4 and T3 (in the blood) will still act on thyroid hormone receptors in cells in the Hypothalamus (and Pituitary) , and together the Hypothalamus /Pituitary will still move the TSH level 'gauge' up and down in response to the changing T4 /T3 levels brought to the hypothalamus /pituitary via the blood .
However that TSH gauge clearly doesn't 'read' quite the same anymore :
....because thyroid hormone is being taken which alters the T4/T3 ratio's
....or because the thyroid isn't making any direct T3 anymore
....or sometimes because TRab are still at play
..... or sometimes due to Hysteresis, .... or a bit of all of them .
and then fT4 /fT3 tests and symptoms are needed to interpret the picture correctly.
The TSH level does still (eventually) move up and down to give it's 'feedback' on the thyroid hormone levels found in the hypothalamus / pituitary ... and this still happens even when there is no thyroid present .
But the AMOUNT of TSH produced by the pituitary as it's 'feedback' (it's response to the T4/T3 levels) can't be interpreted in the same way as when the person was healthy .
Even in someone with no thyroid, their TSH would (eventually) rise if they stopped taking thyroid hormone (apart from in circumstances like central hypo) , so the FEEDBACK part of their system still arguably 'functions' ... but it is now so warped/ broken / unreliable that they might be half dead before it managed to produce a TSH level over 2 .
(obviously without a thyroid or tablets they'd then die anyway because the FEEDFORWARD part of the axis is DEFINITELY BROKEN .. as you say ,their thyroid is now totally incapable of accepting or responding to a TSH signal.. because it's in a bucket, or totally shrivelled up )
The issue is that some GP's think TSH still reads/ means the same in all circumstances and that a below range TSH always means 'too much thyroid hormone' when we know from experience that it doesn't .
I re-wrote that so many times trying to clarify what i meant by 'feedback' that it probably makes less sense than when i started...but i'm fairly sure we are 'on the same page' as it were .
Thank you - am more confused now with this above - it's my dyslexia coming into play now as I'm tired.
I'll try again tomorrow when my T3 will be top of the range and my understanding as clear as it's ever going to be :
So, yes whilst Toft, and Bianco & Co openly admit that they don't fully have all the answers yet and that a TSH needs to be seen in conjunction with a FreeT3 and FreeT4 - primary care are able to know all the answers from the yearly thyroid function test which generally just consists of a TSH reading !!!
Maybe primary care doctors need to also be psychic - as currently they work ' blind ' and letting us all down.
Since primary doctors can't prescribe T3 maybe ignorance is bliss - for them alone - as they have no means of restoring thyroid hormonal balance nor a patients health and wellbeing.
putting T3 first in all circumstances would have the problem that in emerging hypothyroidism the body protects fT3 level for as long as it can when the thyroid is failing , so for 'diagnosis' purposes it is best to look at mainly TSH and fT4 ..because by the time fT3 is low most people will be in lots of trouble, and in most people their TSH / fT4 would have alerted them to the emerging problem much earlier than fT3 would .
But once someone is taking thyroid hormone replacement, then i think they should ROUTINELY do all three.
They've always tested my TSH and fT4 every blood test , (so i guess i'm lucky) , but they've only tested fT3 on 5 occasions in 20 yrs... and never when it would have been most interesting to know the result .. eg the time i was overmedicated on levo my TSH was a tiny bit lower than my usual , and my ft4 was over range 119% ... but it's been higher than that before and since ,without any overmedication symptoms .. so presumably my fT3 was higher at the time was suffering symptoms of overmedication, but i'll never know for sure.
i also think they should test all of us for all the antibodies at our annual review TPOab /TGab and TRab .,because even though it could be seen as a needles expense, i genuinely think the data produced would allow researchers to learn something interesting about how autoimmune thyroid disease works if they did so . So ideally some kind of govt 'thyroid disease research budget' could pay for it for a period of eg 10 yrs to get some proper data ... .....and then i woke up .....lol
But if we open our eyes beyond the individual's current state, it would be far preferable to always do all three.
For one thing, they'd have a huge collection of data for analysis. One of the issues we have is that FT3 test results are rarely available so can cannot contribute to research.
For another, many of us might have at least one, possibly more, FT3 tests from many years ago. When we might not have had any thyroid issues. To indicate where our personal levels might have been good.
You're right .. i was being too stingy .... yes, lets have "all of the results, all of the time ".. they can offset the cost against the money they saved by not letting anyone have anyT3 for the last 10 yrs.
exactly ... if it was a phone contract they would make a "bundle" and be promoting it heavily . I think we need some more business minded people in medicine. that bloke from Phones4U... or him that invented the Bank of Dave.
At the magic age of 65 - 7 years post RAI thyroid ablation for Graves my T4 was reduced because my TSH was low suppressed and for no other reason as I was doing ok and getting on with my life and hypothyroid as i had been all my life and saw this state of health as my normal.
Over 2 years my health fell away, I became virtually housebound, gave up volunteering at the Food Bank, gave up my little part time job, and could not play taxi to my nieces for school. football, netball and surfing competitions.
I had various O/P appointments over this 2 years for my symptoms and all were futile and no one joined up the dots and was eventually discharged but that I had a low ferritin, which I had before, and knew this wasn't that, and so my own research started in around 2015.
I fell into this forum researching low ferritin and the rest is history and on my bio.
I also forced myself to read Elaine Moore's first book on Graves Disease - and purchased a second copy for my doctor - lead balloon - I know - but thought naively that she too might find it interesting as i saw my symptoms detailed on the pages.
My doctor refused to test Free T3 and Free T4 and I refused to leave the room and then a phone call was made and the laboratory agreed they would run and Free T3 and a Free T4 for which I was invoiced and paid the Lab £34.00.
The imbalance of the T3/T4 was obvious to a blind man - and I was told I was very lucky to have any T3 at all - quite how this was meant to give me any confidence in this person purporting to be the thyroid lead in a group practise simply astounded me.
I fought for another 2years 2016/18 whilst building up all my vitamins and minerals and supplementing adrenal glandular to have either T3 prescribed or NDT on a named patient only prescription basis.
The NHS kept me on a piece of string, with letters not answered, and phone calls not replied to, and the stress of all this simply exacerbated my symptoms - maybe that was the plan, as I eventually gave up on the NHS ever helping me and I started self medicating and am much improved.
Not sure why I started to write all this now as I don't think I've added anything and gone off on a tangent !!
I'd be happy to pay the NHS for the correct thyroid blood tests, as long as someone is going to take the necessary action if the blood results corelate with what the patient is saying and experiencing.
I feel totally conflicted over paying extra like that.
Personally, at present, I'd be happy to pay. But the flip side is that those who can't pay will be refused and consigned to the dustbin. Which is (obviously) wrong and against the very basic rationale of the NHS.
Well yes of course, it goes straight against the grain - but so much does - doesn't it ?
We did at one time talk of funding some forum members when they couldn't afford the blood tests - didn't we ?
I'm only on a single person state pension though I paid a full stamp for over 40 years and live in shared ownership so, I'm not flush by any means but without health - wealth means very little.
All the time i was kept in a file on a desk somewhere - I was reading up and making sense so that I could be knowledgeable and once I realised I didn't have to rely on the system that broke me - I became much more able to get some distance and mend myself.
personally i've always thought that we should pay 'something' at the point of use (with an decently run 'income/ capital' based scheme for protecting those who really can't afford it).
I think people don't value it enough and tend to take it for granted , and i think paying a nominal fee would probably improve that situation.( and i say this as someone with an average annual income of well under 6K.. so i'm not loaded, but i'd manage £30 for a blood test and £20 to see the GP if i had to... i manage to find £20 -£50 to see the dentist when i need to ..( mind you i'll be stuffed if i ever need dentures).
..... but then i would think that, because i also think we should have to pay to get let out of the drunk tank if we get arrested for being Drink and Disorderly .. and if we need the RNLI to get us out of the poo when we crossed the road at high tide while ignoring the huge red sign .
Once you realise that you find yourself dust-binned and out of options going through the right channels and the right way -
you find out - and do what you need to do to get yourself out of the dustbin which in these particular circumstances probably means financing your own treatment.
During one's life there are various dustbins to be aware of - we all experience them in various guises - friendships, relationships jobs and the like - but I really didn't expect this of the NHS as I grew up believing that it was there for me at a time of need.
Disillusioned and disappointed doesn't come close.
i like it pennyannie .. not a tangent at all .. it's the entire reason most of us end up here:
we were trundling along ok .
GP says "TSH says you must do x , or else ".
So we do 'x '.
and as a result we end up watching our reasonably ok life going slowly down the pan.
And yes ...me too .. even though my disposable income has always been "slim to none" i'd have happily paid £30 a year to get fT3/fT4 TSH done every time consistently at the same NHS lab with proper venous blood draw. .. and i'd have happily paid another £50 a year to a fund some GP's to be trained PROPERLY in diagnosing and treating thyroid problems.. ( as long as they were the ones treating me ) and , i'd even be willing to be a guinea pig .
Why TSH remains lower for quite along while following episodes of hyperthyroidism / overmedication .... or any T3 use ** .
it is due (at least partly) to a mechanism called 'Hysteresis'.
"Hysteresis is a Greek term that means “shortcoming” and “to be late" ..... Although the phenomenon of persistent TSH suppression and elevation with consequent lagging of thyrotroph recovery following severe thyrotoxicosis and hypothyroidism had been observed for many years, the first formal description of hysteresis involving the HPT axis was enunciated in 2007" (Qoute from paper below)
healthunlocked.com/thyroidu... showing-the-delay-in-tsh-responses-to-thyroid-hormone-changes "a good paper showing that TSH delays its response to thyroid hormone changes, sometimes over a very long time indeed. Should be useful in demonstrating to GP's that suppressed TSH will not easily respond to T4 changes and that they should not expect to see changes in the medium term - ie don't further reduce doses just because the TSH hasn't changed".
healthunlocked.com/thyroidu... tsh-does-not-respond-quickly-to-changes-in-thyroid-hormone-levels "This paper demonstrates how TSH changes lag well behind changes in FT4/3 levels. The longer the dwell time of a particular set of FT4 and FT3 concentrations the longer the lag in TSH response. Useful to provide evidence that TSH is not a credible test if applied wrongly at the wrong time"
Both posts are discussing this same paper:
frontiersin.org/articles/10...A Review of the Phenomenon of Hysteresis in the Hypothalamus–Pituitary–Thyroid Axis Melvin Khee-Shing Leow
"2.5. Interpretation Errors from Physiological Memory Effects or Hysteresis
From clinical experience, we learned that healthy set points are expected in a certain area of the reference ranges of [FT4] and [TSH]. However, in cases of severe hyper- or hypothyroid conditions, the disordered physiology needs a significant amount of time to restore the system to normal system operation [4].
This “memory effect” in which a system is dependent not only on its current state but also on its former environment is recognized as hysteresis and is a phenomenon well characterized in many areas of physics such as what has been observed and analyzed in the magnetization curves of ferromagnetic materials. In the realm of physiology and medicine, hysteresis has also been encountered in pulmonary mechanics, bladder smooth muscle stretch, and even calcium-parathyroid hormone relationship [10–12].
With thyroid physiology, hysteresis causes a shift of the original characteristic over the horizontal axis, in this case the [FT4] axis. When the HPT axis encounters sustained elevated concentrations of [FT4] well above the extreme of the upper normal limit (i.e., thyrotoxicosis), it is consistently observed that the recovery response of [TSH] lags behind that of [FT4] with definitive treatment of the thyrotoxicosis before [TSH] will be detectable again even when [FT4] declines to subnormal levels. Evidently, the system “remembers” the huge amount of [FT4] and needs time to remove the effects. This is actually a beneficial adaptive feature that is evolutionarily conserved to protect the organism in case [FT4] should suddenly escalate rapidly without restraint, since the [TSH] will remain low and will not add undue further stimulation to the thyroid. When the [TSH] response is detectable again, we see a shift of the original HP characteristic to the lower end of the range of the [FT4] scale.
A similar effect is observable after a long standing hypothyroid condition with [FT4] concentrations depressed far below the lower normal limit. In this case, the [TSH] normalization response lags behind the recovery of [FT4] such that [TSH] may still remain in the supranormal levels despite [FT4] having achieved normal or even relatively high levels due to the HP curve being shifted to the higher range of the [FT4] values. Again, this hysteresis represents a protective mechanism as the persistently elevated [TSH] provides a “buffer” of additional thyroid stimulation in case [FT4] should suddenly diminish to negligible from an unpredictable loss of exogenous T4 supply."
~~
also .... the Pituitary can physically shrink if it hasn't been asked to make any TSH for along time .. it can take along time to get back to it's previous size, so even when it should be making more TSH , it can't , until it has got bigger again.
he gives links to studies showing how many months it can take TSH to recover, i have copied his reply and all it's links below .
(his reply starts:
"I will be away for a few weeks so //.......TSH Time to Recover studies:
TSH Receptor antibodies are known to suppress TSH so in the following studies it's important to look at the cohorts who do not have antibodies.
ncbi.nlm.nih.gov/pmc/articl... Factors Predicting Time to TSH Normalization and Persistence of TSH Suppression After Total Thyroidectomy for Graves' Disease
Shows a mean time of 17 months to TSH recovery.
~~
pubmed.ncbi.nlm.nih.gov/171... Behind a paywall. Study showed 73.5% of antibody negative patients recovered their TSH in three months and mean recovery times were: T3 2.1, T4 2.2 and TSH 6.0 months. You can get a glance of the recovery graph by using this google search google.com/search?q=Continu...
Note that most patients but not all recovered within 30 months . i.e. TSH, fT3, fT4 got somewhere within reference intervals.
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This pdf cimonline.ca/index.php/cim/... shows TSH recovers in about 80% of patients after 6 months. They also report atrophy of the pituitary
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plus a couple of other links in jims original reply which won't fit on here.
TSH is just the 'opinion' of your Pituitary about your dose ~ but your Pituitary's 'opinion' is a bit warped once you take Thyroid Hormone.
One thing I have found is that not everyone has a pituitary that is perfect and works well. Unfortunately, doctors are of the opinion that the pituitary is perfect in everyone and must be believed. My pituitary is as flat as a pancake in one direction and stretched in another. I've never had it tested to see if it actually produces what it should in the quantities it should.
I have discovered, thanks to this forum, that people can have FT4 and FT3 results similar to mine before I started thyroid hormones, when my TSH was between 5 and 6 (it has never actually reached 6) and others with similar FT4 / FT3 have a TSH of 10 in one case, and nearly 30 in another. I wish I'd kept links to those particular posts but I didn't used to be so obsessive about keeping links in the early days as I am now for things I think might be useful.
One thing I have found is that not everyone has a pituitary that is perfect and works well. Unfortunately, doctors are of the opinion that the pituitary is perfect in everyone and must be believed.
Yep—this! I really wish I know what my TSH was during pregnancy (and indeed, shortly afterwards). Alas, all those records are lost—I don’t seem to have a single TSH test prior to the period where I first started having it privately tested myself. All I know is, I’ve struggled to have as much energy as my peers since my mid to late teens onwards.
It’s funny how they refuse to accept that the there can be partial failure. Another is the idea that “adrenal fatigue” isn’t a real thing—I rather think it is.
‘’Contrary to all proclaimed efforts towards a more personalised medicine, this has become a regulated consumer mass market as with many other situations. This is of little benefit to patients who will continue to complain, and with some justification, that the medical profession is not listening, thereby abandoning one of its primary functions in the doctor-patient relationship.’’
From this patient's point of view if TSH tests were to be demoted and the focus to be on FT3 followed by FT4 then a competent medic should be better able to analyse lab results and to correctly diagnose and treat the majority of their patients.
However if the problem is cellular rather than glandular hypothyroidism the problem deepens and the use of blood tests has to give way to clinical evaluation.
Relying on TSH results has become a lazy and cheap way to test patients, and an unreliable one once medication has been initiated. We all know the outcome of that.
Doctors seem to think we are like machines that are similarly built, similarly function and can be similarly serviced. When it comes to treatment they further think we are like said machines that can be calibrated to a set point.
Time they understood that we are all different with different needs!
There seems to be a tendancy to rely on opinion rather than fact.....the facts that you are providing here
Those of us who ultimately depend on supraphysiological doses of T3 to function do not fit into the tidy round hole that patients are expected to inhabit...after taking " this little white pill which will make us well again".
We are square pegs that need to find an appropriate square hole..... which consists of a very specific dose of hormone not found acceptable to the decision makers.
Relying on TSH to provide that, is courting disaster....been there and paid the price.
for use when patients taking T3 need to have low TSH arguments with GP/Endo .
In an ideal world there should be no argument.
How do we get medics to understand and accept that they have been wrong for the best part of 50 years.
Until then patients are left either hitting their heads against a brick wall or going rogue and self medicating as many of us have had to do.
I would very likely be dead now if I had stuck with convention.....and the sound of TSH ringing in my ears
How do we fight this TSH obsession?
Knowledge is the best weapon, and we must be confident and brave enough to use it.
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CONTINUED ~ in my reply a LONG way further down this post.
