Thyroid UK advisors have published papers showing that patients without a thyroid have lower T3 levels. A new paper jstage.jst.go.jp/article/en... shows that serum T3 levels are related to thyroid volume. Patients with little or no thyroid tissue left have lower T3 levels and so would benefit more from liothyronine.
This study is not paticularly good but is easier to follow that some of the more mathematical studies. It has two flaws: blood was taken after ingestion of levothyroxine and the patients have fT3 and fT4 levels that are a little below average suggesting they are undermedicated. i suspect that adequately medicated patients will show a greater difference in fT3 and fT4 levels but this study at least shows a trend. It clearly demonstrates that patients without a thyroid should receive T3 therapy.
My personal view is that we should look at where T3 is coming from. Does it come from type-2 deiodinase (D2) that takes place close to the cell nucleus (especially in the brain), or does it come from circulation in the blood via the thyroid and type-1 deiodinase (D1). Patients on levothyroxine monotherapy that restores blood fT3 will have a higher fT4 and lower TSH. High fT4 increases reverse T3 levels and rT3 is known to inhibit D2. Similarly, a lower TSH reduces D2 activity. I believe these mechanisms combine to reduce T3 levels at the receptors in tissues dependent upon D2 for local T3. This is a secondary consequence arising from the loss of thyroidal T3. The lower TSH and elevated fT4 necessitated by levothyroxine monotherapy produces a shift from D2 to D1 deiodinase and a resultant loss of T3 in D2 dependent organs such as the brain.
Hope I haven't lost everyone. If you have little or no thyroid tissue you will need some T3 to restore the thyroid axis back to normal.
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jimh111
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If you take sufficient levothyroxine to give a high or high normal fT4 you will get enough T3 from type-1 deiodinase which takes place in the liver and kidney (and thyroid if you have one). However, you will have reduced D2 activity and this may lead to cognitive problems because the brain is reliant on D2 for 80% of its T3.
A secondary issue is that if a patient is given a little T3 (preferably slow release) they should feel just as good, or even better with an average fT3 and fT4. This may have benefits in reducing cardiac risk. I know it's incredibly difficult to get T3 prescribed and we don't have a slow release form but my view is that it would be a better and safer option than levothyroxinie monotherapy.
My late husband was on T3 and I've contemplated trying it just to see what the effects may be but there's no way I can get it prescribed and I'm not going down the self med route as I have to many other medical problems to make it a safe experiment. My Cardiologist is pretty good on thyroid stuff so I might run it by him next appt.
Yes it’s a very bad state of affairs as it isn’t freely available here like it once was. I wonder if we will ever see it’s reintroduction, it ought to be a no brainer given all the new research clearly demonstrating the need for T3 options for our medication, but I have zero faith in it ever happening in my lifetime.
The 'professionals' took advantage of the huge rise in costs for liothyronine - so it isn't the fact that it wasn't available but the price.
Why should we, the patients, suffer due to the suppliers wanting the highest price for T3. Why cannot the NHS source elsewhere and they had the 'perfect' excuse as is stated below:-
"In 2016, the 28-day National Health Service (NHS) cost of liothyronine in the UK increased dramatically from about £4·50 to £258·19, resulting in widespread patient concern and media coverage.1 Jan 2019
Liothyronine cost and prescriptions in England - The Lancet ...
The panic this instant withdrawal caused is beyond belief and patients left high and dry and pushed into symptomatic ill-health again. Previously it was a shortage of T3.
I have no idea why they also removed Natural Dessicated Thyroid Hormones too (but they used mis-information to do so) as the proof of its safety was proven. It also saved lives (without blood tests but on symptoms alone) - from 1892 without blood tests (none available then) and it was all about patients' symptoms and small increases until symptom-free.
So, the professionals seem not to care at all and seemed to have no conscience of what happened to patients and probably doctors were afraid they'd lose their livelihood if they did not follow the changed guidelines.
It is an utter disgrace the way thyroid patients have been treated or rather ill treated. I see it as modern day misogyny of the very worst order. Why are we not worth the price of T3? If the commissioning fools at the NHS let those rascals use a loop hole to cheat the system, that should be their problem not ours, but they just let the situation persist and take it out on those that need the medication. The whole business is scandalous, I can’t see it changing in my life time short of a miracle. Someone needs to write a block buster novel (made into a similar film) that sets the record straight.
I absolutely agree with this and my liver enzyme ALT levels reflect this is what's going on in my body. I only have half a thyroid. Consistently my T4 levels were flagged 113% on the reference range for several years but anything less and I'm non functional. The higher the T4 the higher my enzymes. This put my T3 at 70% in the reference range, just enough to keep me above water but still suffering some cognitive issues. My TSH was always above 1 and close to 2, which I find unusual for someone with high T4 levels. What does a person do in this scenario? Dose up to 113% in T4 and then add on a little T3 or reduce T4 to somewhere around 80% and add T3? 80% T4 levels get me less than 40% T3. I feel like when I increase my percentage of T4 and try to add T3 I have stomach bloating and a low flat mood.
I would be tempted to lower your Levi and add in some liothyronine. I think raising fT4 is counterproductive, it increases reverse T3 and lowers T4 to T3 conversion rate (the rate not the total amount).
The higher T4 ratio to T3 is absolutely making me feel poorly and by adding a smaller amount of T3 to a higher amount of Levo seems counterproductive. When I go back to the higher dose of Levo plus T3 the sleep problems, lack of appetite, low mood, and extreme stomach bloating returns. It's just a matter of figuring out how much T3 to add to compensate for such a loss. My conversion is already so poor that even a reduction in 12.5 mcg of Levo results in disabling body weakness and fatigue. It's hard to know how to approach it but I'm trying to learn. The Levo clearly reduced my T4 to T3 conversion rate because my TSH was not suppressed and even with half a thyroid I function normally without Levo, despite some slight fatigue but it was much better than being on levo.
I'm with Graves post RAI in 2005 and there was a profound change in my health in around 2014:
I was only ever on monotherapy with Levothyroxine and dosed to keep my TSH in the range (at the bottom ) rather than my symptoms, and ran with a high T4 but found through a private blood test that my T3 was at just 25 % through the range.
Being dyslexic anyway this was crippling my cognitive functions as well as my salivary glands, drying up with no saliva for around 18 months and with what I can only describe as my whole body drying out - though I was found negative for Sjogren's Syndrome.
Two years on a NHS not so merry go round produced no answers except for a low ferritin:
I was refused NDT by my surgery and a year or two later refused a trial of T3 owing to my suppressed TSH and told to reduce down my Levothyroxine :
I started self medicating in 2018 and felt the immediate benefit of adding a little T3 x 6.25 to a 25mcg drop in dose of T4 : I have gone on to trial NDT and it is where I have stayed and am so much better and have my life back.
Thanks in the most part to reading a few books, and the support from this amazing forum.
I’ve seen many cases like yours on the forum. This study although not great is another piece of evidence that patients with little or no thyroid have a greater need for T3.
Pure speculation on my part, but I suspect many Graves’ patients do OK on levothyroxine for as long as they have elevated TSH receptor antibodies (TRAb). These antibodies mimic TSH and they may also have a stimulating effect on deiodinase just like TSH. Thus Graves’ antibodies could help patients on levothyroxine keep their T3 levels up. When the antibodies disappear the patient becomes T3 deficient. This is a hypothesis and would need to be investigated in a clinical trial.
That is very interesting as I had trouble understanding such a time lag from treatment.
I did contact Elaine Moore and she confirmed my symptoms so long after treatment not uncommon and put my mind at rest.
As being so ill and being told that I was a conundrum by my own doctor really didn't fill me with any hope of any resolve through conventional channels.
Any more food for thought will be gratefully received : thank you :
I was only ever ok on monotherapy when allowed to stay on 125 mcg T4 which took my TSH to 0.01 :
My T4 would then be dropped to 100 mcg T4 and I'd scrape in the bottom of the TSH range but feel unwell and prescribed anti depressants as the consolation prize :
This went on for several years seesawing between being in or out of the bottom of the TSH range :
Why are we trying to stimulate a thyroid gland that is full of antibodies and RAI and that we have deliberately decided to burn out and disable and not use anymore ?
I can't understand this thinking at all - am I missing something in all this ?
That is interesting. Could one then have no thyroid but still get excess T3 if these antibodies are still about, that’s when taking NDT? I had Atropic autoimmune thyroiditis with vacillation between over and under activity the latter becoming more prominent over time. I was initially diagnosed with Graves disease but was reassigned to AAT. I have genes for impaired DIO2 activity, thyroid hormone resistance and a higher likelihood of Graves’ disease but nothing for any other thyroid disorder. There is a strong family incidence of thyroid disorder in women on the maternal side.
We first need research to show TSH stimulating antibodies (TRAb) also stimulate deiodinase. Given they fool the thyroid into thinking they are TSH it’s likely they also stimulate deiodinase.
NDT has excess T3 but if you have elevated TRAb then they could theoretically at least increase your T3.
My symptoms at diagnosis were dry gritty eyes, exhaustion and insomnia.
Once on the Carbimazole these symptoms resolved and at times I did experience the usual hyperactive symptoms, so guess had I not been on the AT meds my symptoms would have become much more acute,
So, I guess it's all about timing, dose level and antibody interaction, which after diagnosis doesn't seem to be of much interest to the medics as they haven't the answer to the AI component of this disease.
Looking back at my 73 years I believe I've been hypothyroid for the majority of this time.
I did have a thyroid blood test when around age 54 as my sister- 13 years my junior, was diagnosed with hypothyroidism after the birth of her 4th child - I thought at last I'll be found with something wrong, but found negative for thyroid, and felt dejected, once again.
I've read on Tania Smith's post from the Canadian Thyroid Support Group of a subset of people being diagnosed as Hypo/Graves and have presumed I must be in this gang and that the antibody component of this disease scuppered my chances of a diagnosis with just a TSH measurement being taken ???
It's not that unusual for Graves' TRAb and TPO to occur together. I don't know the cost of the assays but it would seem reasonable to check every patient for TSH, fT3, fT4, TPO and TRAb just once at outset.
Thanks for this. I'm Graves, post RAI, I became very unwell on t4 monotherapy. Tried adding synthetic t3 but cant tolerate it. Get bad palpitations & insomnia. However, on NDT I'm so much better. Sleep well too. I think NDT acts a bit like a slow release t3 as it's a far more complex molecule than synthetic t3. Just wish I could get it on the NHS.
I don’t have Graves’ and have never tried NDT but I have heard it may be slow release and having the hormone mixed in with thyroid tissue suggests it will be slow release.
I take Thyroid S which I was given to understand is slow release - though I know some people disagree.
For me it is totally different to Liothyronine : it's like the difference between wearing shoes two sizes too small or slippers - and there's no contest :
I did read of the Thyroid S tablet breakdown and amazed at the long list of the compound.
I just hope it remains the same formula when this NDT manufacturer releases the new production.
I take thyroid s too. I did a 6 week trial on t4/t3 combo. The t3 (liothyronine) was prescribed by the nhs. I didn't sleep for 6 weeks! I tried different doses & times of taking it. I felt it peak after4 hours & always woke up. Totally different from NDT. I am convinced that NDT is a slower release. I hope I dont run out of Thyroid S!!
Will it be available as before (just more expensive, obviously) or in more limited quantities? I am asking as I have been considering giving it a try when it returns. It´s not as cost-effective as it once was, but if it works as great as many here claim it would be worth it. I would hate to go on it, do great on it, only to end up unable to source it. The only alternatives - Tru Thyroid and Real Thyroid - don´t seem to be working as well.
I'm sorry but I have no idea as all I'm doing is relaying comments I've read on other websites.
There was NDT in the USA whenI looked a few weeks ago, it was more expensive than the Thai NDT I purchased but in 2021 if price is the deciding factor, the States might be a option previously not considered.
I'm having this issue with synthetic T3. It feels nothing like when I take NDT. I feel immediate results with NDT but maybe it's because NDT is giving me less T4 and more T3.
I find liothyronine helps my sleep. If I take too much I can't get to sleep, too little and my sleep is shallow.
It's about time the companies selling NDT and physicians prescibing it got together to run a randomised trial to compare NDT with equivalent doses of L-T3 + L-T4, looking at symptoms and 24 hour fT3, fT4, TSH. This should have been done long ago, the manufacturers make a fortune out of it.
My guess is NDT releases T3 more slowly but even this hasn't been checked as far as I know.
I sleep better with liothyronine but only if my Levo is lowered but this requires a lot of T3 to make up for any loss in T4. I'm starting to question if the synthetic T3 dose is even equivalent to the T3 in NDT. I tried to take the same amounts on synthetics as on NDT and it didn't seem to be equivalent. I take one grain of NDT comfortably and feel good whereas 10mcg of Lio at once makes me feel terrible with zero benefit.
Yes. The combined effects of 38mcg t4 + 9 mcg t3. The 100 mcg L-T4 equivalence is according to the manufacturers of NDT and L-T3 is about 3x as potent as L-T4 on a mcg basis.
This is complex and messy. Levothyroxine is poorly absorbed (about 50% but studies differ a lot). NDT seems to release its T3 more slowly, at least according to patients who have taken it and I believe them.
So, as you can see it is very difficult to compare NDT with synthetic hormone. It may be that a slower release of T3 is more effective in vivo, the body may be able to use it better, receptors may have a more steady saturation, L-T3 peaks may distort TSH and perhaps reduce receptor expression. All the preceding sentence is speculation, absolutely not fact but it gives an impression of the sort of things that could go on.
I cannot take synthetic t3. It's like a different hormone for me. I add some t4 with my NDT as I cant tolerate too much t3 in any form. I take the majority of my NDT just before bed, & 2 smaller doses through the day. I dont even notice it. Synthetic t3 makes me feel very jittery.
It feels like two different types of medications. If I take one grain of NDT I feel my mood improve, my appetite is good and I can move around without stiffness. I felt like lowering my Levo and trying to add more Lio had no effect. If I try to take 10mcg of Lio at once I feel terrible. I've been giving high consideration to adding some Levo to NDT. How much Levo do you add to your NDT?
I tried Greek Uni Pharma T3 first and was very happy - immediate lift of brain fog :
I couldn't maintain supply so purchased bulk of Mexican T3 and couldn't tolerate it at all. I had such big headaches, like I've never experienced, and I was unable to even think of going anywhere, let alone drive my little car - so I gave away this big tub to someone who hasn't a problem with the Mexican stuff.
I then trialled the NDT and haven't looked back and really do hope I never have to shop around again.
I do believe we should have options available that we can trial if one of the available ones do not. NDT was withdrawn a few months ago.
Sometimes even the change of manufacturer can make a difference to how the person feels. Quote below:
"The researchers report that 49% of the patients preferred desiccated thyroid extract, 19% preferred levothyroxine and 23% had no preference. Desiccated thyroid extract use was also associated with more weight loss. There was no difference in the psychometric testing or in any symptoms. Both types of thyroid hormone were able to normalize the abnormal thyroid blood tests.
WHAT ARE THE IMPLICATIONS OF THIS STUDY?
Although desiccated thyroid extract is not widely used, this study showed that many patients preferred this option as compared with levothyroxine. This result was observed despite there being no differences in thyroid function blood test and psychometric test results, although use of desiccated thyroid extract was associated with some weight loss. These results suggest that there may be a certain number of patients in who desiccated thyroid extract might be a reasonable treatment option. Further research is needed on this topic to confirm which patients this might benefit the most form desiccated thyroid extract therapy.
I agree. Levothyroxine should not have been approved until it was shown to be equivalent to or better than NDT.
I can't believe the manufacturers did not do a trial, I suspect they buried it because if levo was found to be as good as or almost as good as NDT it's adoption would have been much quicker. At the time of its introduction levo would have high profit margins, so any study that could show it was as good as NDT would have generated large profits.
The situation is a bit better nowadays. Most journals will only publish trials if they have been given advance notice of the trial, no more doing dozens of trials and publishing the one that gives the 'right' answer.
I’d be sooo curious to know how big my thyriod is! Technically I have Ords instead of Hashi’s but that’s not as popular a term.
All of my blood tests going back 7yrs or more have shown 0% through range T3, with varying middle to higher, but not over 80% through range T4. And if my T4 is low then my T3 is below range.
This study shows the effects of a small or missing thyroid. A mild form of central hypothyroidism (I call it subnormal TSH secretion) can cause a low T3 because TSH is lower than it should be . TSH promotes T4 to T3 conversion, so if TSH is low or normal when it should be high then there will be insufficient T3.
Ultrasound would reveal how big it is. I was told mine was tiny, shrivelled up and unlikely to have any function whatsoever, by my endocrinologist from an ultrasound exam. Two close relatives had cancer of the thyroid so he was checking there was no sign of it. Sounded to me like there was no thyroid to gets any cancer in.
Can’t you ask for one? I suppose they would regard it as unnecessary unless there was a situation like mine. Lymphoma of the thyroid is very rare and to have two close relatives with it and another two dying of different lymphomas is not something easily dismissed as it’s clearly something genetic going on. I presume because I don’t have a thyroid worth writing home about I would be unlikely to get cancer of the thyroid.
It really would be a waste of NHS resources or mine to have a scan. My treatment wouldn’t change. However it probably would be good scientific knowledge to understand how autoimmune conditions work because these endos don’t seem to have a clue!
So if my Ords resulted in an ever shrinking thyroid then it seems obvious the output is not good, that combined with heterozygous DIO2 variant then this would be good info.
But the studies and interest is just not there is it, not when we (on this forum) seem to be the minority. The majority do well on Levo.
I’m not so sure the majority do well on it, their blood results are not always normal with lower than healthy individuals levels of T3 which simply cannot be good for long term health. I have atropic autoimmune thyroiditis which is like Ords but has an initial phase like Graves’ disease with thyroid stimulating antibodies but I think TPO antibodies eventually dominate along with hypothyroidism and sporadic hyper episodes whilst they completely destroy the gland. I was not diagnosed until I reached end stage it was truly awful. I have one bad conversion DIO2 gene which explains a lot, I was rubbish on Levo yet my relatives on it had/have no problems so I knew something was not right. I self medicated on NDT out of sheer desperation and it was like a miracle I suddenly started to feel much more like my old self and got better and better so it was deffo lack of T3. Imagine having to find all this out off your own feeling like pants whilst these endocrinologists do nothing and tell you you will just have to put up with it when there is an obvious solution. I feel very let down by the medical profession who allowed me to fester for decades with this illness I did repeatedly ask if it could be thyroid related they got out their crystal ball and assured me it wasn’t - no tests, no checking of symptoms just by magical non scientific diagnosis. I was thin I had no goitre end of story. Then they failed to fully inform me of my choices. I may well have got T3 back then had I known about it, but now there is no chance and NDT sources are rapidly evaporating as the prices sky rocket they tell you never to get medication on the internet whilst actively withholding it themselves - total hypocrisy. I bet if it were a primarily a male disease it would be a very different story.
I suppose you could work backwards and assume your thyroid is small and producesm too little T3 and see if your experience backs this up. If you have Ords and in the latter stages it seems very likely this would be the case. You’d think ultrasound of the thyroid if you are having problems would be routine I don’t think it would be a waste of resources it could be a very valuable diagnostic tool and it’s not a really high tech exam - jelly and a wand thing and a screen, it’s all over in a few minutes no anaesthetics or complex stuff like that and pretty safe too. Not exactly a lot to ask fir is it?
I don’t think that an ultra sound of my thyroid gland is a waste of resources, that’s what ‘their’ thinking would be. I must have Ords because I’ve never had any swelling as is typical of Hashi’s.
I too was let down badly for more than 10yrs, it’s horrendous. I do think though that most people do well on Levo alone. I don’t always think that they are treated optimally and could probably be on a higher dose in order to be optimal but still they’d be ok on Levo and not let need T3 or NDT. You said it yourself, members of your family have had ‘no problems’.
I'd really like to know what my thyroid looks like too, but like you i don't suppose NHS would consider it worth the price just for curiosity's sake . I think i must have Ords, and probably not Atrophic Autoimmune Thyroiditis AAT because TSH never went very high at all.
I had no swelling ever, but TPOab were >3000, and in hindsight i did have a clear hyper phase, but TFT's were not tested at that time. (I just though i'd gone a bit mad and kept my mouth shut about it)
I'm also interested in the fact that some of us might have TRab as well as TPOab, and i agree with Jimh111 that i think it might be worth the cost to test all of us for TPOab and Trab with TSH, fT4, fT3 just once at outset.
My gut feeling is that if we could separate hypothyroid patients into groups, of Ord's , Hashi's, AAT, those who had very high TSH, and ones who didn't etc. , it might prove useful to observe if these groupings related to treatment levels of ft3/ ft4/ TSH that relieved symptoms. or at least the data might prove helpful in diagnosing those who often struggle due to TSH'normal' and other anomalies.
If nothing else , it would be reassuring that somebody gave a ....
I'd do more research on myself , but i'd spent all my money on expensive things you can't see under the floorboards of my house before i realised how interesting thyroid disease is.
I find this all so fascinating! Just googled AAT. My TSH never rose significantly ever! I had my first TSH test in
2001 - 2.5
2004 -1.4
Dec 2008 -6.3
Feb 2008 - 11.1
So for more than 19yrs I’ve been feeling rubbish but my TSH has been in range or only slightly out. I’m fascinated when I read other results of posters who have an extremely high TSH, it used to make me feel like I was being a big drama Queen as my TSH rarely ever got to double digits. But that was my GP’s impressions not mine. I 100% know now that I am so so ill if my TSH is even at 1 or 2.
So whatever it is I have, I can never use TSH as a guide to my health. Only FT3/4. FT3 always sat at 0% through range even if I had good FT4.
Tpo and Tg ab have never been high either. I think at time of diagnosis TPOab was only 123 (>100). Over time these have increased, but only as high as about 300.
I 💯 agree with you that if we can separate and find and understand causes then the knowledge will improve and then the treatment.
I have spent so much money on testing and private treatment 😱 I also invest in my kids tests, psychologist, counsellors ect I have no money for under the floorboards! Lol (or even leaks and a dodgy heating system! Lol) my house is only have finished but heyho at least I work to live, before I couldn’t even get of the sofa! (Not the entire 19yrs, I had sporadic periods of being well, bouncy even and then I’d plummet and then 2018 I began to plummet and couldn’t get back up again ☹️)
It does also raise questions though about my sisters diagnosis/treatment of graves and now I’d say she was hypo, she’s gone from always being a size 8 to a size 16. I’ve always been a steady size 12, with periods of size 10 and periods when I may have been more comfortable in a size 14 but not quite a 14 IYSWIM
Let’s say they felt well on it and I definitely didn’t. Whether they’d have felt even better on NDT or T3 combination therapy I don’t know.Do you read Dr Tania Smiths blog? It’s excellent can be tough but worth the effort.
This one is about the different antibodies and the categories of thyroid disease each combination causes:
I know what you mean it’s hard sometimes with the NHS you don’t want to squander their precious resources but their priorities are sometimes hard to comprehend. They could have saved a fortune diagnosing me promptly and correctly and treating me with NDT. Multiply that up for the many who seem to go from pillar to post with thyroid issues and end up ill on Levothyroxine and that’s lot of lolly they could be saving
Always open to more enlightenment, never apologise for education 🤗
Agree with regards to myself and the amount of money that’s been wasted looking for something that was right there under their noses 😩 Nevermind, I am where I am now thanks to this lovely forum. Happy and healthy (well for the next 6mths anyway 😂)
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