Stomach churning UK paper: This paper might well... - Thyroid UK

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Stomach churning UK paper

diogenes profile image

This paper might well stretch your digestive system.

This paper by Leese encapsulates what is wrong with British thyroidology. First it commits the sin of partiality - no mention of our paper on exactly the same topic published years ago. Second, it persists with faulty ideas - Weetman - a fan of alleging somatic disorder in patients that don't do well on T4 only. The group is now in this paper scratching its collective head about something being rotten in the state of Denamrk (to quote Shakespeare) but not having a clue about why and what to do about except fluttering its impotent wings. Thirdly it can't let go entirely of its old beliefs - they have to somehow be rationalised but have no idea how. Just rehash the old somatic argument -eg you are depressed so it can't be thyroid disease. Fourthly it still parrots the notion of normalisng TSH, when studies it apparently shrugs off that cold fact that healthy TSH range cannot be used in this way. Talk about Dick's days. Their idea are pre-Dick.

My Colleague Rudolf Hoermann expressed his surprise about Leese's position in view of his other paper on stable T3 therapy.

He did a good long-term study on LT3, so his comments really surprised me. If it does not fit, look for co-morbidities or something else to blame, rather than questioning whether something might be wrong with the approach.

Clinical Endocrinology

Time to Refresh thinking on the terminology and management of hypothyroidism

G Leese & E Soto-Pedre

doi: 10.1111/cen.14485

65 Replies

As you say sums up the failings... can’t even agree in their own heads!

"The control of tissue liothyronine concentrations involving membrane receptor uptake, de-iodination, nuclear thyroid receptor binding and other nuclear protein binding is complex.9 Pharmacological tools to manipulate these processes are currently lacking and it is not possible to fine-tune intracellular liothyronine concentrations, or its downstream intracellular effects". Didn't include antibodies for some reason?

😡 I think we should band together and present Drs Leese and Soto-Pedre a subscription to ThyroidUK via Health Unlocked. They need a dose of realism from better informed Endocrinologists and patients who are self treating and doing okay.

helvella profile image
helvellaAdministrator

Link to paper: onlinelibrary.wiley.com/doi...

PDF is available for download.

First paragraph starts:

Replacement therapy with L-thyroxine is not universally successful at reversing all symptoms for people with hypothyroidism. For such patients, current guidelines recommend looking for other co-morbidities including hypoadrenalism, celiac disease, anaemia, hypercalcaemia, sleep apnoea, renal failure and other conditions.

I'd like to ask if anyone - even a single member - here has actually had a doctor look for hypoadrenalism, celiac disease, hypercalcemia, sleep apnoea, renal failure and other conditions?

Some will have had some investigation but if they keep failing to explain, and don't lead to treatment, at what point does the investigator go back to thyroid?

Medics are so fond of the trite aphorism they keep coming up with: When you hear hoofs, think of horses, not zebras!

Why, when you have a thyroid patient in front of you, do you think of zebras (all these other disorders) rather than horses (the disorder the patient has already been diagnosed with)?

We all know that medics love their trite aphorisms, and some have a role as mnemonics, etc., but please don't keep turning them round and round such that you pick the one from the shelf that supports your prejudices.

Although liothyronine may not resolve ongoing adverse symptoms in the majority of people with hypothyroidism, it may be premature to dismiss it altogether.

How can they say this when we all know full well that endocrinology has stood almost 100% shoulder to shoulder in dismissing liothyronine for many years?

TSH110 profile image
TSH110 in reply to helvella

They investigated me for Myasthenia Gravis - I am sure I haven’t got it and never had it - my problems were due to hypothyroidism that was not being adequately treated on L4 monotherapy. Once I took NDT all those problems resolved. I was in need of higher levels of T3 it was as simple as that. I was never tested for any of those things in the list just labelled a head case and given antidepressants. No need of them anymore If there ever was a need for them in the first place. Mustering up the energy to read this paper and hoping I don’t blow a gasket in the process….

Localhero profile image
Localhero in reply to helvella

None of these things was ever considered for me when Levothyroxine on its own (compounded by too low a dose) didn’t work for me. I was offered antidepressants for depression/anxiety and told to use a laxative for constipation 🤷🏻‍♀️

TSH110 profile image
TSH110 in reply to Localhero

The rubbish in rubbish out school of medicine then.

Localhero profile image
Localhero in reply to TSH110

Exactly!!

nellie237 profile image
nellie237 in reply to helvella

I had a 24hr at home sleep monitor to test for sleep apnoea several years ago....my daughter heard me choking in my sleep (thankfully, I don't seem to do this now) I very much expect that I was undermedicated. The results were negative.........but the kit was so uncomfortable that I barely slept at all. I still don't sleep.

My liver was checked at Hashi's dx in 2007. Same with U&E.......then not for 5yrs

Never checked for hypoadrenalism.

Coeliac checked at Hashi's dx..........negative. Checked again 2020..........positive.

Calcium not tested prior to positive Coeliac dx.

TSH110 profile image
TSH110 in reply to nellie237

Before I was treated I could snore for Britain if not the World! Not sure if it was sleep anea but it was a terrible racket.

nellie237 profile image
nellie237 in reply to TSH110

Me too. 🤣🤣🤣 I think it is a bit better now.........I don't often wake myself up with the noise as I'm dozing off, like I used to.

TSH110 profile image
TSH110 in reply to nellie237

Yes that happened to me but in converse - I’d actually hear the snoring as I came round - it was terrible!

tattybogle profile image
tattybogle in reply to helvella

A GP once tested me for Myasthenia Gravis, when i described what happens to my face/eyelids/speech. ( i don't have it)

And i've had countless Full Blood Count's which showed low lymphocytes for years ,(that no one mentioned at the time)

But apart from the MG, no other suggestions have ever been made to investigate potential causes for my remaining issues .. in fact i always got the distinct impression GP's thought 'any other issues' were 'not real' .

Why were they so quick to believe i was suddenly making a fuss over nothing .. why would someone who's hardly ever been in the doctors surgery for the first 35yrs of life suddenly develop an liking for going in every month and 'moaning' once they are given Levo ....... oh .. unless it didn't actually restore my functioning as effectively as they told me it would.

Mr Weetman and others promoting this lazy ,unscientific , somatic ,'guff' have a lot to answer for.

A recent comment on my notes say's something like "we've done all we can for her 'fatigue' " really ?.... well.... they once sent me to see some ME therapists , because i asked to be , and referred me for some counselling, which i also asked for , they wouldn't have done either if i hadn't asked.

They've never tested any vitamins or done a full iron panel... in 18 yrs.

So, no ,i don't think they have looked very hard for any other co morbidities that would explain my remaining 'problems' .

nellie237 profile image
nellie237 in reply to tattybogle

Same here....loads of FBC's over the years. Had 6 tests for Folate and a couple of B12 over the years due to macrocytic anaemia. My only in range folate result was 3.6 (2.8 - 19) 3 weeks after having a drug eluding (incl folate) stent put in. Folate is vital for heart health, but of course women don't have heart attacks.....its all somatic.

I'm actually surprised that this guy didn't say 'hysteria'.....because he might as well do.

humanbean profile image
humanbean in reply to tattybogle

And i've had countless Full Blood Count's which showed low lymphocytes for years ,(that no one mentioned at the time)

I have had over-range lymphocytes in five Full Blood Counts since 2016. (Before that they were always mid-range.) But they are only just over the range by a tiny amount. All the tests I've had have been private ones paid for by me and they come out at, say 110% - 130% of the way through the range. I am absolutely convinced that if I got an NHS test it would promptly drop back into range and I would be told I am fine and that would be that. So I do nothing about it.

tattybogle profile image
tattybogle in reply to humanbean

i don't know how 'wrong' lymphocytes have to be before anyone says anything .. mine were 1 / 1.1 [1.5-4] for at least 5 yrs . could be much longer . and no comment was made.But you're right . if you go and ask em , they'll probably just write 'health anxiety' on your notes and still not be remotely interested in your lymphocytes.

humanbean profile image
humanbean in reply to tattybogle

i don't know how 'wrong' lymphocytes have to be before anyone says anything

I think the same thing about any blood test I have. If it is out of range (which, to be honest, is quite rare unless it is thyroid-related or lymphocytes) I don't know when that classifies as "a problem" for the vast majority of test results.

Is a result for X of 20 (ref range 10 - 18) a trivial or a serious problem? Or is a result for X of 2000 (ref range 10 - 18) a serious problem?

tattybogle profile image
tattybogle in reply to humanbean

Dunno .. getting a TPOab of >3000 [0-50] get's the doctor to say "oh...., i see.... your immune system's eating your thyroid.. have some Levo"

Can Wheetman explain why somatic disorder in hypothyroid patients seems to be miraculously cured by T3? Perhaps he can start a new branch of medicine Somtaticology where T3 is the first line treatment with 100% success rate in curing the patient.

greygoose profile image
greygoose in reply to TSH110

I wrote to him once, suggesting that somatic disorders were more than likely a symptom hypothyroidism, given that so many hypos - according to him - were suffering from them. Got an email back just saying 'Thank you for your opinions'. Just that. Nothing more. Sigh.

TSH110 profile image
TSH110 in reply to greygoose

I know whose opinion I would value and it certainly isn’t his!

greygoose profile image
greygoose in reply to TSH110

😁

diogenes profile image
diogenes in reply to TSH110

This is the heart of their dilemma. On the one hand Leese published a nice paper about controlled T3-only patients being satisfactorily dosed over several years. On the other they won't consider that some T4-only patients might be better on combination or T3, but ascribe their dissatisfaction to somatic influences. How, given the first paper, do they know which patients might benefit from some T3, if they dismiss those unhappily on T4 only as being depressive etc. as a group. The lack of logic is astounding.

TSH110 profile image
TSH110 in reply to diogenes

I wonder if he’s suffering from Multiple Personality Disorder or the two sides of his brain are not really communicating properly! He’s happy to write us off as a bunch of crazies, perhaps it’s just a case of projection!

nellie237 profile image
nellie237 in reply to TSH110

Yes!!!

I have recently been tested for celiac disease, but only because I have paid to see a private Endocrinologist who asked my GP to test for it and a full iron panel too. I don't know why they don't have a check list of what to test for, but that would mean they would have to use their funding for tests

Unable to work after fourteen years on T4 only, excrutiating depression, suicidal at times, zero energy. After three & a half decades, 42.5mcg of T3 only, decent folate, ferritin, vitamin D & Methylated multi B vitamins, sorted it out. I have two mutated genes- DIO2 and MTHFR. No thanks to three Professors of Endocrine, a multitude of endocrinologists and a gaggle of GP's; it was this amazing forum that sorted me out. I truly doubt any Endocrinologist could have sorted that lot out.

"Intriguing early data is presented that reducing the “inflammatory” load by thyroidectomy or selenium may help adverse symptoms."

Well it's very kind of Mr Leese to offer .... but i'm not sure that would help at all .., so No Thanks. (not until they can do a better job of treating those whose thyroid they've already whipped out for a good reason)

.... Am currently picturing a Quick Fit mechanic with his head under the bonnet of a Ferrari that won't run properly..

" Mmmm ..... i don't understand how this bit works ,... but it's squeeking a bit , so i'll just rip it out and the problem might be fixed.... "

Oh , and there he goes again ... pushing his new idea to re name it "pre-thyroid" instead of "subclinical hypothyroidism", .... which i think translates as "if nobody says the word 'Hypothyroidism' to them, they won't look it up " .

I don't see his new terminology catching on.. far too many of us have already looked it up . No point shutting the stable door after the hypo horse has crawled out.

He'd do better to 'grow a set' and admit he doesn't know all the answer's yet.. rather than keep publishing these articles that just get in the way of those who ARE trying to understand and improve the situation for thyroid patients.

nellie237 profile image
nellie237 in reply to tattybogle

"To avoid this issue, the term pre-thyroid could be used for what is currently called subclinical hypothyroidism and subclinical hyperthyroidism." Wow, because that's not going to cause confusion

Patient attending A&E whilst away from home

Dr: Please tell me about any other medical conditions you suffer from

Patient: Pre-thyroid

Dr: Hypo or Hyper?

Patient: I said Pre-thyroid????

It would be farcical if it wasn't so serious.

helvella profile image
helvellaAdministrator in reply to nellie237

May I join Club Cynical?

TSH110 profile image
TSH110 in reply to tattybogle

It’s a ridiculous term - we already have a thyroid, albeit faulty, how on earth can we be pre-thyroid? It’s incompatible with life.

tattybogle profile image
tattybogle in reply to TSH110

very good point .. he compares his term to the use of the term 'pre-diabetes' but by his logic pre-diabetes should actually be called 'pre-pancreas' ( remove the name of the disease and substitute the name of the responsible gland)

It's just a blatant attempt to remove 'the name' of a disease from public view , so that the public knowledge of the disease itself , also goes out of view.. which would of course make it even easier to say any symptoms are 'somatic'

Is the correct term for this sort of thinking 'pre-brain' .. or 'prehistoric' .. i can't decide....

helvella profile image
helvellaAdministrator in reply to tattybogle

Even pre-diabetes only means at a stage that treatment is going to be provided - not that there is nothing wrong.

And pre-pancreas would need to include Hyperinsulinemia. :-)

TSH110 profile image
TSH110 in reply to tattybogle

Tut tut tat - pre-varicating 🤣🤣🤣 I completely agree it’s an attempt at obfuscation but he won’t pull the pre-wool over our eyes! Or should it be wool over our pre-eyes?

tattybogle profile image
tattybogle in reply to TSH110

Weetman "NOO , not over your eyes... why don't these thyroid patients get it ? .. if their TSH is normal there is NO WOOL"

Sorry, I simply could not finish reading, as I feared I would explode with anger at the complete drivel written in all seriousness and being very aware that such drivel will cause problem for patients not yet diagnosed or already diagnosed and receiving the usual Levothyroxine only medication at low doses to appease the TSH blood test. I despair….

TSH110 profile image
TSH110 in reply to Hennerton

You missed the best bit at the end his new categories 😡🤯🤬

One doctor tested me for adrenal fatigue - prescribed HydroCortison - and low HGH - prescribed HGH injections. But, nothing else. I had to beg for nutrients tests, and only got the 15 years after being diagnosed hypo/Hashi's, and then all they would do was B12 and ferritin!

Aaargh ‘d like to classify that this has been written by a grade 1 NUT. It’s utter garbage.

FancyPants54 profile image
FancyPants54 in reply to TSH110

I guess it didn't work then. You couldn't help yourself. Your gasket is well and truly blown.

TSH110 profile image
TSH110 in reply to FancyPants54

…at a ballistic velocity!

I wonder if cardiology has completely abandoned T3 because “of the costs and unclear benefits”? Or are cardiologists canny enough to recognise its efficacy and keep using it? It would be interesting to know. As ever, I suspect we are the poor relative.

FancyPants54 profile image
FancyPants54 in reply to TSH110

The cardiologist I have been under for 3 years knows nothing about it at all. Just tries to scare me off it. He's hopeless. He's now left I think. However, Electrophyisists (don't know how to spell that, known as EPs) do understand it and help those who need it. They understand the heart's needs for T3. I've never seen an EP, I'm thinking of seeing one privately. Another huge expense. When I take T3 my arrhythmia calms down. Until the T3 wears off when it starts to make it's presence more known. I'm sure if I can only get on enough of it the arrhythmia will be very mild. It gives me fast heart rate. When I first started T3 with Levo it dropped the heart rate from mid to high 90's (resting) to low 80's. It's since gone back up. I think because I need more. At my last private endo appointment he prescribed me up to 40mcg a day and gave me a prescription big enough to try it. I've just started to try to work my way up there from 30mcg.

In the atrial fibrillation and arrhythmia world, cardiologists are referred to as plumbers and EPs as electricians (because arrhythmia is an electrical signalling issue) and no one has a lot of faith in the plumbers. Mine scanned me 3 years ago and said my heart was fine. I've not seen him since early 2019 due to pandemic so I have no idea if that still stands. I hope so.

TSH110 profile image
TSH110 in reply to FancyPants54

That’s interesting FancyPants54. I had terrible angina prior to diagnosis but it got even worse on Levothyroxine. I thought I was going to drop down dead of a heart attack (not unknown on both sides of my family). I gave up on it after two years, switching to NDT and experienced a remarkable improvement in the angina (along with a shed load of other symptoms T4 monotherapy never resolved) I haven’t suffered an attack of it for a long time now. I was told about 10 years before I was diagnosed with atropic autoimmune thyroiditis, that I had a problem that women of my age sometimes got to do with hormones and one chamber was not working properly but it was of no significance. He must have been a plumber not an electrician from what you’ve said…and I thought John Radcliffe was supposed to be top notch heart hospital, probably is for a man where they can’t start trying to blame the menopause for your heart not working properly 🙄. I bet it was a sign of the thyroid disorder. I had lots if other weird problems - frozen shoulder, piles, trouble with the ileum, depression, unexplained cramp…..blah blah blah - I bet they were all thyroid related.

FancyPants54 profile image
FancyPants54 in reply to TSH110

I bet they were too. The only endo I saw on NHS was at John Radcliffe. Useless.

Cardiologists fear T3 because they think too much of it will produce rapid heart rate. But so does too little. As it is we all know too much T3 makes us feel awful so we aren’t likely to do that to ourselves for long.

Levo hasn’t helped me. If I could be certain of a reliable source I would have gone to NDT by now. But it seems to be harder and harder to get.

TSH110 profile image
TSH110 in reply to FancyPants54

So JR might not be all it’s cracked up to be. Levo did help with the most overt symptoms but the important fine tuning as you get to more normal levels just didn’t happen with it for me. It looks like it has got a bit easier again to source NDT but the price has skyrocketed.

Very interesting. Yes my ticker evened itself out when I went onto a combo to include t3. Without t3 it’s a wild bucking bronco in my chest.

Or if Wheetman had his way - in your head!

Now that's very hopeful. Thank you. Mine is certainly much better behaved.

Fascinating that you find T3 calms your arrhythmia down. Can you say more?

Not really, because that's it. It's much calmer now, I don't know I have it most of the time. About the only time I'm aware of it is when I lie down in bed at night and turn into the pillow. I can hear my pulse then and it's AF. It used to be violent. Like a box of angry fogs leaping around inside my chest. Levo never helped anything. In fact I wonder if it's a hindrance, but I can test that later.

I feel we are being a little unfair to Leese. This document is reporting the Perros paper The enigma of persistent symptoms in hypothyroid patients

treated with levothyroxine: A narrative review . This is the one that will churn your stomach!

Much of what Leese has written is reportage although he places too much reliance on TSH and seems to view primary hypothyroidism as the only cause of hypothyroid symptoms.

When he writes "TSH between 4 and 10 mU/L and normal free thyroid hormone

concentrations, treatment is often started in an attempt to improve

symptoms which were unlikely to be due to thyroid dysfunction." he is correct! It IS unlikely their symptoms are due to thyroid dysfunction - due to their thyoid failing. If it were the problem a little homone would cure them. This doesn't happen. We need to accept that this form of hypothyroidism isn't due to mildly low hormone levels, an elevated TSH is coincidence, a red herring. More serious, those who aren't lucky enough to have an elevated TSH are completely ignored, even though they have the same signs and symptoms.

We need to focus on the forms of hypothyroidism that are not due to insufficient circulating hormone. This is completely ignored by the endocrine community and in many cases by thyroid advocates.

TSH110 profile image
TSH110 in reply to jimh111

Does Leese do this? What is the proof that Leese is right about those elevated levels having nothing to do with a problem with the thyroid? What exactly is causing it and why aren’t they testing for the other mystery things so people who don’t need hormone therapy don’t end up on it but those that do, get it? This implies to me that TSH testing is a complete waste of time for diagnosis as well as treatment. I’d be interested to read the research that proves the majority results with raised TSH have nothing to do with thyroid problems. I know of non thyroidal illness or are you thinking of central hypothyroidism? I think I may not have properly understood your point.

The elevated TSH reflects a minor problem with the thyroid but not the cause of the hypothyroidism. If it did giving a little T4 and a tiny bit of T3 would restore a normal TSH and the patient would be perfect. We know this doesn't happen.

Also, by relying on the elevated TSH we dump all the other patients with similar signs and symptoms. Indeed having a similar fT3, fT4 with a lower TSH is worse because TSH stimulates T4 to T3 conversion, especially in tissues that have local T3 regulation.

TSH is really useful for detecting thyroid gland failure and assisting monitoring. It saves thousands of babies from cretinism. TSH is a really useful tool but it is wrong to assume a normal TSH excludes hypothyroidism.

Certainly central hypothyroidism but also a mild form with a TSH lower than expected has I believe profound consequences. A lower TSH reduces thyroidal secretion and also T4 to T3 conversion. If the patient is treated with levothyroxine it lowers TSH even more and reduces T4 to T3 conversion even further thus initiating a vicious circle. There can be other forms of hypothyroidism such as endocrine disruption where environmental substances disrupt thyroid hormone action. Doctors never consider these possibilities.

TSH110 profile image
TSH110 in reply to jimh111

Thanks for the clarification it makes better sense now. I see that free T3 and free T4 ought to be looked at as well as TSH. I guess in my case I was so overt TSH (110) was enough to diagnose it, although just over a week before TSH was undetectable and they thought I had Graves - small wonder it was a bit of a rollercoaster ride. I presume antibody testing would still miss the other possibilities and some of those with autoimmune disease as they don’t always register on tests. From this am I right in understanding that these other causes are far more common than autoimmune thyroid disease itself?

jimh111 profile image
jimh111 in reply to TSH110

The relationship between TSH and thyroid hormones in healthy people is accurate allowing for individual variability. So, like the endocrine community we would expect TSH to be a very reliable marker for diagnosis and monitoring of therapy.

Whilst a high TSH / low fT4 is a very good indicator of primary hypothyroidism studies show that TSH has little or no correlation with symptoms in (levothyroxine) treated patients. The way I look at it is the effect of these other factors must therefore be of a roughly similar order to the TSH hypothyroidism relationship.

In other words it is likely that other forms of hypothyroidism are about as common as primary hypothyroidism. If these factors were not as strong we would see a better relationship between TSH and hypothyroid signs and symptoms. This is my logical reasoning of the situation.

diogenes profile image
diogenes in reply to jimh111

The problem for me of your thinking is that the individual solutions for thyroid and body health are overwhelmingly complex. The variations include: response of pitiuitary from hypothalamus (T4-primarily, but T3- stimulated if no or little T4): response of thyroid from pituitary (subject to feedforward control - if the thyroid starts to fail, then it maintains its direct T3 supply at the expense of T4: corporeal response to thyroid products - crosscontrol of body T4-T3 conversion versus thyroid production: and finally corporeal -hypothalamus control - by T4 and T3 in roughly a ratio 2/1. Mix all these up with individuality at each point and you have a recipe for a considerable variation in responses, disturbance of any one altering things in different ways for different people. For me this complexity simplifies to: treat the patient as an individual and consider patient response above biochemical evidence.

jimh111 profile image
jimh111 in reply to diogenes

I reflected on my comments and realised I left out an important factor, TSH has isoforms of varying potency. Since TSH has a role in regulating deiodinase these isoforms play a substantial role. Generally patients with an abnormally low TSH, insufficient feed forward, have TSH with reduced bioactivity. These patients cannot be expected to respond to levothyroxine monotherapy, even worse as the levothyroxine dose is increased their TSH falls reducing their T4 to T3 conversion rate.

However, all these variable factors should even out in a large study to give a good relationship between TSH and clinical response to levothyroxine therapy. There is little or no relationship between TSH and clinical response, even when averaged out amongst a group of patients. This leads me to believe there is a large body of patients whose hypothyroidism is not caused by a failing thyroid gland. The size of this patient group is subject to guesswork on my part.

helvella profile image
helvellaAdministrator in reply to jimh111

TSH is really useful for detecting thyroid gland failure and assisting monitoring. It saves thousands of babies from cretinism.

TSH is also liable not to identify issues in at least some groups. Such as those who are suspected of suffering from lack of oxygen (or did, even if not suspected) and at least some premature babies.

Timing of the blood sample is also critical with TSH often changing very rapidly in the hours after birth.

In line with what I think is a fairly general view here, I'd like to see TSH, FT4 and FT3 tested in every case that thyroid testing is done. Adult, child and neonate.

jimh111 profile image
jimh111 in reply to helvella

I am in essence agreeing with you. The general point I'm making is TSH is very useful for diagnosing primary hypothyroidism but misses many other forms. In statistical terms, contrary to endocrine properganda, TSH is not a sensitive marker for hypothyroidism. Sensitive means it detects most cases, TSH fails to detect a large number of cases.

helvella profile image
helvellaAdministrator in reply to jimh111

Maybe we could put in terms such as "High or low TSH = probable thyroid issue. But TSH in range does NOT demonstrate no thyroid issues." ?

diogenes profile image
diogenes in reply to helvella

Keep in mind the concepts described in this paper re ranges

dx.doi.org/10.1136/postgrad...

helvella profile image
helvellaAdministrator in reply to diogenes

One of my favourites - often posted by me! :-)

jimh111 profile image
jimh111 in reply to helvella

Yes, and by looking at fT3, fT4 also we can get some insight on whether TSH is at an appropriate level and pehaps a clue into its bioactivity (e.g a TSH of 1.0 with fT3 5.0, fT4 16.0 suggests it is much more bioactive than if fT3 4.0, fT4 12.0. The same number of TSH molecules but the second TSH having much less effect on the thyroid.

Im sorry to say nothing in that paper surprises me. Dundee thinks the TSH test is the gold standard in thyroid testing. They willrun every test that they can possibly think of to find another underlying cause for your symptoms. However they will prescribe T3 if they can find no other cause for your symptoms as long as your TSH stays in range. 🙄

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