Synopsis of our eBook: I said that when our eBook... - Thyroid UK

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Synopsis of our eBook

diogenes profile image
diogenesRemembering
27 Replies

I said that when our eBook was produced, I'd develop some kind of dialogue for doctor/patient based on its new findings. I've made a start and I append it below. It's a work in progress and if anyone has more ideas pls let me know:

A brief synopsis of our eBook Homeostasis and Allostasis of Thyroid Function

1)In health, each person has their own unique set of values for TSH, FT4 and FT3 which together interact to define their healthy state. T4 is the relatively inactive precursor of T3, the active hormone that defines health. Especially for FT4 and FT3 the values throughout life occupy a restricted region of the reference ranges typical of the individual, which are far more closely drawn within the range than the reference range that describes everyone. TSH is more variable, as throughout a day its values alter significantly, with a peak in the early hours of the night, thereafter declining through the day until the next peak.

2)Therefore, as nearly as possible, therapy in disease should attempt to regain the values (most importantly) for FT3 that originally applied in health.

3) But we have a problem, because we don’t know what that was, because it wasn’t measured when we were healthy.

4)Question for the doctor: If I had an FT3 and FT4 unique to myself in health, which we don’t know, how am I to regain this by therapy on T4? Surely only by trial and error and my response to therapy. But since we’ve agreed that my optimum values are not the same as the entire range, it can’t be logically right to just put me in the normal range for any parameter (TSH, FT4 or FT3) and say that I am properly treated. It’s more complicated than that (open-mouthed doctor stunned by irrefutable logic !).

5)Doctor, what I think you’ve been taught. That TSH from the pituitary stimulates the thyroid gland to produce T4. The T4 then goes into the circulation and is converted to T3 (the active hormone) as suitable for health. But my thyroid is damaged (lost). So you give me T4 to replace the lost T4 no longer supplied by the thyroid. In doing this you restore my TSH to what it was before I became ill. Therefore, get my TSH back somewhere in the normal range and all must be well (in ALL cases). Therefore all you need to measure is TSH.

6)Doctor, all that is completely wrong. First TSH stimulates the thyroid to produce BOTH T4 and some T3. Both enter the bloodstream and some T4 is converted to T3 as you were taught. But now the FT3 that governs my health is made up from two sources, the thyroid and body conversion.

7)The T3 produced by my thyroid direct is an important controller of the body’s conversion of T4. As my thyroid declines, it tries to keep its production of T3 as close to normal as possible, even though my T4 is lowered. So the level of FT3 from thyroid and body conversion is kept as close to natural as possible. Only when the thyroid has virtually gone, does the whole system collapse and body conversion of T4 by therapy has to take over completely.

8)So, we have two different situations: one where I’ve got some thyroid left, and another where I have none at all. The treatment of these situations is entirely different. But we don’t know which situation I’m in (for those who haven’t had their thyroid completely removed/destroyed). So once again treatment has not to be by rigid biochemistry, but by trial and error until I achieve something closer to original health.

9)We are all different. Our thyroids are different in size, and differ in their production of T4 and T3. Some people’s thyroids produce more T3 direct and others less. The combination of this T3 and body T4 conversion sum up to produce health FT3 levels. When we lose our thyroid, then we lose the T3 produced by it. This has to be made up by extra T4 conversion from T4 therapy. But to get to this state, more T4 has to be given than the thyroid produced in health, to force the body’s conversion to make up the difference. This, because T4 suppresses TSH, will give a lower TSH to achieve this than when in health. Therefore the TSH range suitable for health is unsuitable for therapy. Values lower than the healthy range are therefore suitable for treatment control. In certain cases, undetectable TSH may occur if the conversion capability of the patient is sufficiently restricted – but given normal range FT3 this does not matter. Suppressed TSH when one has some working thyroid left means something quite different (and undesirable) as opposed to those with no working thyroid at all.

10) If someone whose thyroid T3 constitutes a higher proportion of the total T3 loses their thyroid entirely, then the body T4 conversion from T4 mono therapy may not be able to make up for the loss of thyroid T3, however much T4 is offered. It is this minority of subjects who can never sufficiently recover using T4 alone. These are the patients who will need T3 in some form in therapy to restore the FT3 to their unique healthy level.

11) All these complications mean that simply using T4 therapy to put me somewhere in the "normal" range for TSH or FT4 is insufficient. FT3 is the measure to use in therapy control as you and I do not know the exact level of thyroid destruction (omit if not applicable to you). It really is a matter of trial and error and more liberalism in therapy choices.

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diogenes profile image
diogenes
Remembering
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27 Replies
dolphin5 profile image
dolphin5

That’s really helpful, thank you!!!

Musicmonkey profile image
Musicmonkey

This is looking good so far. Thank you! 😊

Hennerton profile image
Hennerton

A beautifully clear explanation for doctors. Thank you! Let us hope they read and remember, if ever they are lucky enough to see it. Will this eventually be distributed to GP practices?

diogenes profile image
diogenesRemembering in reply to Hennerton

Only patients can do that, and amaze their GP/endos by their detailed knowledge.

Hennerton profile image
Hennerton in reply to diogenes

You mean terrify them, don't you?

I had to correct a trainee GP last year at my practice. He asked me why I was taking T3, "as T4 is the active hormone". He was still looking puzzled when I left but at least he ordered me a special T3 blood test that the lab had refused to do.

Zephyrbear profile image
Zephyrbear in reply to diogenes

Does this mean I can supply them with a copy of this?

diogenes profile image
diogenesRemembering in reply to Zephyrbear

Yes if you want. I'll try and make it a little better as soon as I can get round to it.

Hoxo profile image
Hoxo

Excellent. One question - why is suppressed TSH an undesirable outcome if you have some thyroid remnant left ?

diogenes profile image
diogenesRemembering in reply to Hoxo

This is because the difference between having some (even down to 10%) of a working thyroid means that the remnant is working overtime to keep FT3 up as high as possible (not perfect, but trying). Therefore, together with body conversion the two sources of FT3 are nearly intact until the last vestige of working thyroid has gone - sudden collapse! If this is the case, then giving T4 with a working remnant will achieve adequate FT3 much more easily. So its easy to give too much, raise your FT3 above normal, overdose, and thus suppress TSH. With a poor converter who still has an active thyroid remnant the poor conversion is helped by the thyroid's T3 production, so in this case T4 therapy can again raise FT3 too high. So the indication for poor converters with some working thyroid left is very different from having none.

Winegum2 profile image
Winegum2 in reply to diogenes

I always assumed that our own production of T4 & T3 declined once on medication due to the fact that our Thyroids were no longer being stimulated into action due to a lowered TSH. Is this not the case?

diogenes profile image
diogenesRemembering in reply to Winegum2

There is an effect, but the point is that with a working thyroid remnant it is very easy to overdose on T4, giving a high FT3; a suppressed TSH is more likely to indicate that than if there was no thyroid working at all.

Pascha1 profile image
Pascha1 in reply to diogenes

So by me having sub thyroidectomy and being on T3 and T4 I should not have a supressed TSH, which happened after 14 years of T4 mono treatment.

does this mean I have to try find out if I have any working thyroid left or to see if all is destroyed now.. Really is not anything about out for us anywhere on the net on what happens to our thyroid after having a sub thyroidectomy,, I have searched high and low and nothing anywhere and was told nothing .

Drs know nothing as asked and Endo had no info to give me either ..

diogenes profile image
diogenesRemembering in reply to Pascha1

You simply canot know how much working thyroid is left unless a specific and expensive examination is done (which it won't be). Lacking that information, the only way forward is trial and error to achieve best health and place little trust in TSH levels.

Adam10 profile image
Adam10

Thanks Diogenes. So as “FT3 is the only measure to use in therapy control as you and I do not know the exact level of thyroid destruction” it is disappointing that endocrinologists including my new endo do not measure it but test only TSH and FT4. I will insist on FT3 being tested and will pay for it myself if necessary.

TSH110 profile image
TSH110

Excellent!

Pookie50 profile image
Pookie50

Thank you Diogenes! Is it also worth including that some people do not convert T4 to T3 as efficiently due to faulty gene(s)?

SlowDragon profile image
SlowDragonAdministrator

Can I ask, are you looking into why people with DIO2 gene variation react so badly to T4 mono therapy.....virtually regardless of how "well" their thyroid blood test results appear

Pascha1 profile image
Pascha1

Excellent!

Does reverse T3 actually mean anything ? isn't this the bad guy knocking good T3 down when on T4 mono ? ..if so why is this also not tested ?

susiemalc profile image
susiemalc

Thank you, Diogenes. This is very helpful and clear.

holyshedballs profile image
holyshedballs

Thanks Diogenes, this is very helpful in explaining the lack of logic in what doctors are taught or repeat in the surgery.

Would I be right in saying that current research has shown that TSH comes in different forms, the TSH alpha (I think) that stimulates the Thyroid is not the same as the TSH beta (I think) form and TSH alpha (I think) does not have a physiological effect on any peripheral tissues, even though some tissues have TSH receptors possibly for the beta form of TSH? see em-consulte.com/en/article/...

If this the case, then combined with your outline above, it is not logical to measure TSH at all or to base treatment on any value of TSH below the upper reference range, especially now that T4, FT4, T3 and FT3 can all be measured?

holyshedballs profile image
holyshedballs in reply to holyshedballs

Plus it is thought that bones and intestinal epithelial cells secrete TSH so adding to the TSH measurement conundrum.

Adam10 profile image
Adam10 in reply to holyshedballs

Would it be possible for someone to clarify the difference in testing T3 and FT3 and the importance of each please. I am 4 years into being a Hasimoto’s sufferer and I am still uncertain on these things. I hope this is not starting a new post.

diogenes profile image
diogenesRemembering in reply to Adam10

T4 and T3 circulate in blood almost completely stuck onto transport proteins. As these pass by cells that need T4 or T3 the cells take what they want through free T4 and free T3 and the transport proteins with their load carry on to the next tissue cells. The amount of T4 on these proteins is on average 5000 times the amount of free T4 and for T3 about 500 times FT3. But like T4 and T3 we each have different amounts of transport proteins. The reference range for the most important one is a factor of more than 2 from lowest to smallest, and a few people have none at all and some have 4 times the amount. So different T4/T3 loads in different people can give the same FT4 and FT3. This is why total T4 and total T3 are less accurate measures of thyroid function. In pregnancy the important transport protein level rises twofold and total T4 and T3 increase to match it but the FT4 and FT3 remain almost the same.

UrsaP profile image
UrsaP

Thanks diogenes Tagging linda96 to see if any further ideas.

Slabs profile image
Slabs

Is this related to this editorial? frontiersin.org/articles/10...

diogenes profile image
diogenesRemembering in reply to Slabs

It is. The editorial introduces the eBook contents.

humanbean profile image
humanbean in reply to Slabs

Slabs

Diogenes, who started this thread and just answered you, is John E.M. Midgley, one of the authors of the link you gave, and he is also one of Thyroid UK's advisors :

thyroiduk.org/tuk/About_Us/...

His co-authors are also advisors to Thyroid UK (who run this forum).

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