A highly mathematical paper by Uri Alon and coworkers has discovered the reason why, after a significant length of time in one state, TSH only responds to a change after a delay or even not at all. It is very complicated so I thought it useful to just pass on the essential findings. The reason is that say, in hypothyroidism that is countered by T4 dosing, and when TSH has been suppressed for a long time, the pituitary shrinks and the longer the time TSH is suppressed the harder and longer it takes to restore the gland, if indeed it could have shrunk so much over a long time as to be irreversible. In untreated hypothyroidism, the elevated TSH comes from an enlarged gland, so that reducing it to "normal" size takes time. In hyperthyroidism again the pituitary is suppressed, and treatment may normalise the thyroid hormones but the pituitary again shows a lag in normalising TSH by regrowing. This study again casts doubt on the value of TSH as an indicator of thyroid hormone sufficiency, especially in longterm therapy. These studies show what T4 longterm takers know well. And doctors ought to know.
Why TSH only responds to change of circumstance... - Thyroid UK
Why TSH only responds to change of circumstances after a long delay (if at all)
is this an example of neuroplasticity?
It is in effect a similar phenomenon, but with a whole gland rather than neurone connection readjustments.
I wonder if it matters that ones pituitary gland shrinks & stays shrunk for a long time? My TSH has been suppressed for years. First with Graves & now with NDT. What other functions may be affected?
Great question.
But I do know that if I wasn’t on some T3 with my T4 and my TSH was (almost) in range I wouldn’t be having so many good days. With more sedentary days and days with migraines I can see harm being done to other organs too.
I would prefer to be managing to have some life than have next to no life.
Hope someone answers your question though ☺️
Yes, I agree. When I had a bad batch of ndt my tsh went up to 2. I was very unwell, to the point were I was unable to function properly. I couldn't drive & felt severely depressed. However, I would be interested to know how my reduced pituitary function may be affecting other areas of my health. Thanks 🙂
Thank you so much for all yr input here. I had thyroidectomy 40 yrs ago (goitre+hashimotos)+I understand my TSH has been supressed for a number of years but over past 12 months new GPs panicking+telling me I'm over prescribed! I will have bone loss! No one listens regarding increased hypo symptoms, not even an Endo who said 'numbers not symptons'! How do we fight such ignorance when they choose to ignore both symptoms+ research evidence you provide? Thank you.
I've reduced my thyroxine dose by 100mcg over the last few years and my TSH has hardly moved. Yet my doctor still wants me to reduce my dose more to raise my TSH. They just don't understand. Karen
Maybe with his permission, print off Diogenes Post and show them that?
It's whether they will read and learn. I can but try, I suppose. Karen
"Nothing ventured...nothing gained."
And also....
"You can lead a horse to water, but you cannot make it drink".......mores the pity xx
Hi Kiri
Just a suggestion, but when I was requesting dose increases whilst in range and TSH heading below range, I produced hard copy “reports” with all my blood tests in a table (plotted on a graph) interpretation with references and request about a week before the telecon. Submitted report to surgery reception where upon the lovely receptionists would upload report onto patient access. It framed the whole appointment. They had to discuss the report, I made them work on refuting my research supporting references and symptoms! They couldn’t do it. I truly believe the written report fairly dispassionate, even when talking symptoms was key to getting my way. 😊👍
I think they would still just revert to saying I was on too much as that is what they did last time. It's an idea though. Symptoms don't seem to matter to doctors, only the TSH. Thanks for the suggestion though.
Karen
no worries 😊👍
If you want to see an example I uploaded onto a post and my bio is my journey more geared to helping others. On first principles using TSH makes absolutely no sense. I’ve posted the neighbours analogy several times. 😂👍
Thanks. I'll take a look.
This circumstance is no doubt where some endos are suggesting patients no longer need medication! They are no longer hypothyroid! In the U.S. I understand this has been happening for some time and patients are becoming very ill. However it’s being blamed on dementia and elderly patients with family watching are horrified. They are not told that their meds are being curtailed - unless they take an interest and then they can’t do anything about it. Families are frightened to step in and make a fuss and have little hope of helping with self medication. I discussed this with someone I know in the U.S. and they were of the opinion it was rife amongst those particularly in homes for seniors. I suspect wise endos (not) are doing similar here - particularly with the elderly. I think this probably breaks the law in this country and it surprises me that there has been no legal challenge.
Gosh, that's awful.
Most interesting - I had no idea the pituitary was affected like this, but it makes sense.
Thank you for that. Does it suggest anything regarding central/secondary type hypo where the TSH is already not reading appropriately for the low hormone levels (for example in chronic fatigue or fibromyalgia rather than a diagnoseable pituitary condition)? Or the effect of low B12 on pituitary function. Cheers
Ooo, it is complicated! Do you think that most endos would understand it? :-\
Here's the link for anyone who wants to give it a go - embopress.org/doi/epdf/10.1...
And here's the Abstract:
Thyroid disorders are common and often require lifelong hormone replacement. Treating thyroid disorders involves a fascinating and troublesome delay, in which it takes many weeks for serum thyroid- stimulating hormone (TSH) concentration to normalize after thyroid hormones return to normal. This delay challenges attempts to stabi- lize thyroid hormones in millions of patients. Despite its importance, the physiological mechanism for the delay is unclear. Here, we pre- sent data on hormone delays from Israeli medical records spanning 46 million life-years and develop a mathematical model for dynamic compensation in the thyroid axis, which explains the delays. The delays are due to a feedback mechanism in which peripheral thyroid hormones and TSH control the growth of the thyroid and pituitary glands; enlarged or atrophied glands take many weeks to recover upon treatment due to the slow turnover of the tissues. The model explains why thyroid disorders such as Hashimoto’s thyroiditis and Graves’ disease have both subclinical and clinical states and explains the complex inverse relation between TSH and thyroid hormones. The present model may guide approaches to dynamically adjust the treatment of thyroid disorders.
Does this mean we shouldn't rush into taking T3 too quickly, but wait to see how things are first on T4 only?
I would say that there will never be a position that doctors will treat by T3 at first. The rule will always be, T4 first, and if an unsatisfactory outcome then try T3.
Sorry, I meant, if on T4, wait and see for longer before adding T3
Baggiesfan
I've long thought that changes in pituitary size are important. "Pituitary hyperplasia" is a common enough term in thyroid literature.
Indeed, it seems very likely that enormously high TSH levels we see all too often can only be achieved if the person has been hypothyroid for long enough that the pituitary has enlarged.
Maybe in health an individual can only make enough TSH to reach 10.
It will take time for that person's pituitary to be able to make 60, 100 or more.
And pituitary hyperplasia has other impacts.
Pituitary Hyperplasia In Primary Hypothyroidism
If the pituitary becomes large enough, it may impinge on the optic chasm causing visual defects, including problems with visual fields and, ultimately, bilateral hemianopsia. In addition, as described above, patients may also get a paradoxical worsening of their vision with the initiation of treatment with thyroxine as a result of an imbalance of TSH production and release and increase in pituitary size.
Whole short paper is worth a look.
Thanks for breaking it down for us. I wonder how safe/healthy it is to have a shrunk pituitary from a suppressed TSH???
Unless it's hyperthyroidism then, where there is a potential health danger, then TSH suppression on T4 mono therapy is not so dangerous. Studies have tried again and again to quantify the dangers for Osteoporosis and AF of dose-repressed TSH. Always they come up with almost negligible effects, but the medical world has blown these up to a ridiculous and almost hysterical level (ie suppressed TSH = OP and AF). Always. Not so.
I assume that this only affects the TSH producing part of the pituitary Diogenes because that spells huge trouble if it covers its entire function!!!! ACTH in particular, I hope is not affected but it could add more evidence to the epidemic of low cortisol among Levothyroxine users.
Interested in your thoughts based on reading the paper.
Best wishes, Paul
That's correct. The pituitary is made up of different parts that produce different hormones.Only the TSH-producing part was studied here and the phenomenon doesn't necessarily affect other actions elsewhere.
I was thinking that too. It may be why some people have adrenal problems too?
Diogenes said that only the TSH producing part was studied. So, the study probably didn't exclude any effect on ACTH (cortisol) or LH/FSH (sex hormones) etc.
If they did not study it, then there might also be potential issues... or not?
It may be speculation but I would be interested in Diogenes's or others inputs.
Doctors only know what they want to know. Also by way of a question is the article an explanation for "downregulation of TSH" following Graves triggered by ,say anti thyroid antibodies or post partum thyroiditis ,which may or may not be the same thing .????
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