This paper compares the QoL of patients who do not do well on T4 only, being given T3. The QoL signs definitely improve patients' wellbeing, but the common mutation variant of deiodinases doesn't seem to play a big role. No adverse effects found on giving T3. Downloadable:
Effect of Liothyronine Treatment on Quality of Life in Female Hypothyroid Patients With Residual Symptoms on Levothyroxine Therapy: A Randomized Crossover Study
February 2022
Frontiers in Endocrinology 13:1DOI: 10.3389/fendo.2022.816566LicenseCC BY 4.0
Betty Ann Bjerkreim, Sara Salehi Hammerstad, Hanne L Gulseth et al.
Written by
diogenes
Remembering
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We estimated the LT4 dose by calculating 15 μg of LT3 as equal to 50 μg of LT4, based on a pharmacoequivalence study which showed that the LT4/LT3 equivalence ratio is approximately 3:1
Treatment with LT3 monotherapy may therefore be an experimental treatment option in hypothyroid patients who suffer from residual symptoms despite LT4 treatment. However, long-term studies are needed to assess the long-term safety of this therapy regimen. Five patients on LT3 dropped out of the study due to side effects, which may indicate that some patients do not seem to tolerate LT3 monotherapy.
It's a pity medics lack open minds and are therefore skeptical about patient's experiences.
Instead they opine that T3-only causes ( serious) problems.
Some of us have already experimented with this therapy with very positive results....I, for one, have had to do this without NHS support but fear how I might be treated should I have to go into hospital or care!
I have the Dio2 snp/ homozygous but I rather doubt that this had a huge inpact on my thyroid health ...and certainly not the reason I need a supraphysiological dose to function. That, I'm convinced, is the result of ( as a geneticist suggested) an as yet unknown genetic variant which caused a form of Thyroid Hormone Resistance.
Try discussing that with an endo!!
I also wonder if some of the patients who dropped out of the study due to side effects may, instead, have needed more T3.
I was my own "guinea pig" so I had the fredom to experiment....based on various acquired sources of reliable information eg Dr John Lowe who needed high dose T3-only.
I was also well aware that T3 is a powerful hormone, and, of the "dangers" that were being touted, but decided that I had more to gain than I had to lose. A heart scan showed a healthy heart.
I did this in the full knowledge of my GPs but taking full, written, responsibility for the outcome. They now accept my use of T3 and leave me to it in the knowledge that they will not be seen as responsible should I drop dead from the effects of T3.. A sad reflection of NHS care from cradle to grave!
Without T3 I doubt I would be ranting regularly on the subject!!
It's high time the medical profession understood that as human beings we cannot be conveniently calibrated to specific set points like machines....
Hopefully this might allow a little light to enter through any tiny cracks in the current seemingly impenetrable thyroid wall raised by the thyroid care decision makers!
Well done you for bravely gong it alone.Its so sad that ,in the face of known medical evidence, you have to go solo.I too did this with Armour ndt when I was so angry at being refused t4 treatment with a t4 reading of 8 (12-22) .Sometimes anger is helpfull .
Ref the drop outs : ..but did they persevere? I've been prescribed antidepressants where they tell me that you need to persevere through initial symptoms to let body get used to it, ditto antibiotics ...so why not encourage people to press on through initial problems with t3? What's so dangerous about t3 or t4 that they don't give the same advice as with psychiatric ....but wait...... ,isn't thyroxine used by psychiatrists to augment their drugs ? So why this big fear of thyroxine meds ?
Interesting that they didn't rule out having a 'below range' TSH during treatment .. (TSH reference range: 0.5-3.6 mU/L)
"Thyroid function tests were performed every four weeks during the study period and treatment doses were adjusted, if necessary, aiming to achieve TSH levels 0.1-1.5 mU/L. "
Also interesting that despite the average TSH for the 'T3 group' being higher during the study than the average for the 'T4 group' (which suggest that the effective total hormone dose was bit 'less' in the T3 group ?) ..... they still got such significant improvements/ preference in QOL with T3 group .
" TSH in patients on LT3 was slightly higher (median 1.33 mU/L (interquartile range (IQR) 0.47-2.26)) than in patients on LT4 (median 0.61 mU/L (IQR 0.25-1.20; P<0.018)."
So clearly it IS possible to use T3 and maintain TSH in range for SOME people .
Makes me wonder why so many on the forum seem to find it impossible to achieve ?
seems the participants had TSH between 0.2 and 1.6 before the trial ,and all fT4 and fT3 were in range , and about half of them had positive TPOab
I’m one of those people who has managed to keep my TSH within range normally around 1.00. Last test in Dec was 0.89(0.35-5.50). My T3 and T4 levels are normally just below midway. I do my tests without taking medication that morning and always 9am ish blood draws. I believe I’ve managed to keep my TSH just about in range by reducing my levothyroxine dose down to a place where it’s low but not too low. I’ve never altered my T3 doses. I do feel extremely well and energetic mostly. My endocrinologists (NHS and private only) are both very interested how I achieved this each routine consultation I have with them and very pleased with my progress. I do feel very well and balanced, energised and happy mostly. Recently I had an issue and couldn’t obtain my liquid levothyroxine due to national stock outs. I was switched to tablets and my TSH went to 6.00 very quickly and T4 underage quickly also. T3 was ok. I felt very unwell. I’ve now managed to get my liquid again but it wasn’t easy, bloods due to be retested on 21st Feb. Hopefully all good again. Maybe my fine tuning of T4 levels has been helped by liquid form levo as you can tweak it so easily. Just a thought that it’s not always about T3 liothyronine doses and can be your levothyroxine dose that needs adjustment to bring your TSH from being suppressed whilst taking T3 liothyronine.
personally . i think your ability to stay with TSH 1 in range while using T3 has more to do how your TSH behaves .. (eg. the fact that your TSH went up so 'easily' to 6 in response to a T4 issue ) .. than it does with your fine tuning of T4 dose per se .. and i think your TSH response is fairly personal to you ..... basically think you just happen to be 'lucky ' in that department. and while it's always worth a try , and obviously a good aim to have ,, i just don't think your model can be translated to others as a way of keeping TSH in or near range if it doesn't want to play nice anyway.
many of us our TSH is just stubbornly lower than that ( or completely unpredicatable ) , even if we don't take any T3 at all.
For 15 years mine was routinely about 0.05 -0.2 with T4 60%-120% and fT3 30-50%
Then it lost the plot and decided to be 1.9 despite my fT4 being way over range 142%
( and the variations were not due to anything obvious like dose changes /time of last dose time of day )
I have occasionally used myself as guinea pig to try to learn about my own TSH response ( dangerous idea ~don't do this at home folks )....years ago i once got a TSH of 7 after i stopped all levo completely for 10 days so i thought .. ah ha! i think i understand my TSH.
since then i've tried taking just half my levo dose (50mcg ish ) for 10 days before testing TSH and got 2.7 .. so again i thought ah ha ! i definitely understand my TSH.
however, my ah ha!s were a bit premature . i did it again a year or so later (half dose for 10 days) , and got 0.5 which is just a tad under range .... oh ! maybe i don't understand my TSH after all.
So some of us have TSH's that just don't play as nicely as your does.
When i first started Levo , my TSH stayed stubbornly stuck at 2.9/2.5/2.7 when on doses of 50mcg / 100mcg / 150mcg (for several months each) I assume my GP was mightily confused by this.
i've got 20 years of TFT's and my TSH bears no (obvious) relationship whatsoever to my fT4 levels. ( or indeed to my fT3 levels on the 5 occasions they were tested )
The only one time my TSH level 'seemed' to be relevant to what was happening in real life was the time i actually had symptoms of overmedication , and then it had fallen lower than my 'usual ' to 0.018 .. sa again i thought ah ha! at least it does tell the truth about 'overmedication'.. anything lower than 0.05 ish means overmedication for me ! ...
But more recently i've accepted that i don't actually know what it's doing at all, or how to make it do anything at all... and even that low of 0.018 coinciding with my overmedication could have been nothing more than coincidence ... however i've no intention of becoming overmedicated again to prove that theory .. because being overmedicated is really horrible.
I know what you mean. I too had to play about and wait and see blood results. Since staring T3 medication I’ve got my bloods checked every 3 months without fail. I get my B12 injection and my bloods done on same day by same nurse. So it works like clockwork now. This has been going on for about 4 years now. Initially my TSH went suppressed. My NHS Endo had threatened me to withdraw T3 prescriptions if that happened! So I did my utmost to try and keep in range. And I reduced my levo ever so slightly so it wasn’t impacting in any way. Since then it’s always been in range ( except recently). When I was first diagnosed with Hashimotos some years earlier my TSH was 36! It does seem to respond quite quickly. Also if I go under or over medic I feel dreadful. So keeping it within range makes me feel normal. Over medication feelings are awful.
indeed .. i genuinely though i was dying of 'cancer of somewhere or other' when i was ovemedicated (and so did 2 doctors) . i've never been truly hyper . i think it must be terrifying if it happens to you .. not to mention feeling bloody awful.
p.s even at diagnosis my TSH was only 6.8 ,, despite having clear physical signs AND symptoms of being hypo for 4 years , and TPOab of >3000..
So i concluded (from the fact that it refused to shift from around 2.5 on levo for the first year and half , despite does of 50 - 150mcg levo) ... that mine is a bit like a heavy barn door on rollers that are a bit rusty and gummed up .. ie. it needs a massive shove applied to it for quite a long time with the full weight of the body before it moves.
Yours, on the other hand, i see as a lighter barn door, on well oiled rollers .. that you can open with one arm and a relatively light pressure.
But who know what's really going on ? .. just when you think you've understood your barn door ..a mouse comes along and make nest in the rollers.. or the hinge falls off..
Thank you diogenes . It is interesting to not, yet again, that it is based on a TSH in the reference range. Is it possible that people with a DIO2 polymorphism need a higher T3 and therefore lower TSH in order to benefit the most?
It wasn't based on 'TSH in ref range' though ... it said they "aimed to achieve a TSH between 0.1 and 1.5" and the ref range used was [0.5 -3.6].
So that implies they would have allowed TSH to be as low as 0.1 without reducing the dose .
~which doesn't undermine your point about DIO2 patients possibly needing it lower than that ,, but this study is an improvement on others that insist TSH must stay 'in range'
I’d be under medicated in their trial then. On T4 mono TSH needed to be approx 0.2 - 0.35 for me to function (crap function, but it was functioning). Then when T3 added (T4 lowered) my TSH dropped to 0.05
Hasn’t been higher since. And has been sitting at 0.01 for over a year now. My FT4 below 50%, my FT3 70% and I recon I’m needing a tad more of one of them, but doubt they will agree.
So a good trial, but I would be told off for my very low TSH and asked to leave 🚪 ……politely I hope 🙃
I know of two people that are homozygous for Dio2 and both need T3 to be dosed to a point that TSH is suppressed. This (very small) sample supports your theory.
I haven't had chance to read it all, but this bit stood outTSH in patients on LT3 was slightly higher (median 1.33 mU/L
I wonder if they would have got even better results if these patients were given more T3? Am I right in thinking that T3 has a more suppressive effect on TSH than T4? If so, it would suggest that these patients were under-medicated with T3.
With regards to the deiodinases. They only tested for Dio2 and found no difference. I'm not convinced they've got a valid comparison. There may well be other genetic factors at play that would make this comparison meaningless. For example, I have no Dio2 polymorphisms, but I am homozygous for Dio1. I do well on T3 and poorly on T4. If they had compared the people with Dio2 polymorphisms with me, they would have found no difference.
Is it because they are treating people as a homogenous group when in reality each person is their own discrete group. It reminds me of an average being meaningless when the underlying dataset is comprised of widely disparate results. For example, the average of the dataset 98, 2, 96, 4 is 50, but quoting an average of 50 is useless.
Thank you for making my point so much better than I did!
“I wonder if they would have got even better results if these patients were given more T3? Am I right in thinking that T3 has a more suppressive effect on TSH than T4? If so, it would suggest that these patients were under-medicated with T3.”
I totally agree about being treated as a homogeneous group…. We are clearly not!
I'm probably being a bit thick here but how did they achieve euthyroidism in patients on T3 (only)? My OH (who had a hemithyroidectomy over 13 years ago) has been on T3 only for many years and in all that time she has been TSH suppressed and her T4 has been way below the bottom of the "normal" range. Currently she takes between 50 and 70mcg T3 daily (split over 3 doses) depending on the demands of the day. Most days it's 55mcg but on a busy day she will raise it to 70mcg.
I think improved QoL was the paramount aim. You couldn'y say they were "euthyroid" in the sense that perfectly healthy people are, but only having "better treatment outcome"
A good treatment outcome surely needs to be the aim ...not just a "better"outcome.
One can feel better than when barely able to function but still far from "good". Been there!!
We therefore wanted to test the effects of LT3 monotherapy on QoL in hypothyroid patients with residual symptoms despite thyroid stimulating hormone (TSH) values within the reference range.
Were the patients who did not respond well to the T4/T3 treatment actually offered an adequate dose of T3, or...
Did focus on TSH prevent them reaching a therapeutic dose.
Maybe I'm missing something but it seems that we are still stuck here with TSH fixation.....the unreliable marker!
Treatment with LT3 monotherapy may therefore be an experimental treatment option in hypothyroid patients who suffer from residual symptoms despite LT4 treatment.
It's already been tried.....but strongly rejected by the powers that be.
And, already the choice of many patients who have to fly solo because the NHS reject the idea/T3 use.
Perhaps they will now open their minds and understand the value of T3-only treatment.
The doses of T3 used here were probably kept relatively smaller than the doses taken by most people who use T3 only ' in real life'
So that probably explains how the TSH was able to be kept 'more or less' in range. They did allow it to go a bit below range ~as low as 0.1 (when ref range was [0.5 -3.6] ...and obviously their fT4 WOULD have been very low (possibly below range) on T3 only, ( but they don't give the numbers so we can't see ) ...So whether or not they were kept 'euthyroid' rather depends how you define 'euthyroid'. ie "TSH in range" or "TSH, fT4 and FT3 in range" . or "TSH and FT3 in range when taking T3 only"
They used a ratio of (T3) 1:3 (T4) to estimate the equivalent dose of T3 for the levo dose they were taking previously.
Eg if someone was previously taking 100mcg Levo .. they would have been given 33.3mcg T3 to start off with .and then that dose adjusted to keep TSH between 0.1 and 1.5 as the trial went on.
"We estimated the LT4 dose by calculating 15 μg of LT3 as equal to 50 μg of LT4, based on a pharmacoequivalence study which showed that the LT4/LT3 equivalence ratio is approximately 3:1 (23). LT3 treatment was started at a dose of one third of the patient’s previous LT4 dose. ....
Thyroid function tests were performed every four weeks during the study period and treatment doses were adjusted, if necessary, aiming to achieve TSH levels 0.1-1.5 mU/L.......
All blood samples were collected in a fasting state in the morning before medication was ingested, approximately 24 hours after the last LT4 dose and 14 hours after the last LT3 dose."
My wife has been very fortunate in initially seeing Dr P who recognised that levo was causing her problems and that she needed T3. She also has an open-minded GP and happened to be referred to a likewise minded NHS endo who eventually suggested she should go T3 only.
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Patient's Perspective Paper: An Update
