A Review of the Phenomenon of Hysteresis in the Hypothalamus–Pituitary–Thyroid Axis

[PR4NOW]

This is a rather interesting article edited by Dr. Dietrich, Diogenes colleague. PR

journal.frontiersin.org/art...

[shaws Administrator]

Thanks for this PR4NOW. I look forward to reading it properly.

[radd]

PR4NOW,

Hysterical thyroid hormones… LOL …us Hashi sufferers all know that feeling....... BUT hysteresis actually means a lagging behind phenomenon ( we learn something new everyday.) . …. :o))) ...

It' s like our hypothalamus and glands have a brain (mind) of their own ... Cute .... and they're trying to teach us PATIENCE. The ridiculously long delays between our NH endocrine appointments allows for plenty of hysteresis .... ; o))) .....

As thyroid hormone levels are critical to survival and life threatening when excessive// deficient, it's no wonder that a TSH should remain suppressed for weeks//months//years as a protection against rebound hypothyroidism, should hormone become deficient again .... wish all endos knew this.

And we know there are many reasons for this happening without even reducing meds ..... and as this phenomenon is likely to happen in a multitude of other crucial genes (governed by thyroid hormones) no wonder it takes so bl**** long to get better.

Given the importance of T3 it is strange it is not included in the FT4 & TSH mean of an individual's optimal and physiological operating level … coz it sure as hell makes a difference ! ! ….

Interesting for those of us supplementing Biotin (B Vit) …. (How do know if we have [elevated] streptavidin ? ? ...)

…[ .. Patients taking biotin supplements can also face the issue of falsely elevated or suppressed [TSH] in biotin-streptavidin affinity-based assays .. ] …

online.liebertpub.com/doi/1...

(unfortunately full text is a “pay for” …. anybody ? ? ….) …

Finally ………. for those medicating only T4, this paper claims it is not necessary to withhold meds prior to a blood draw as the TSH secretion rate response is so insignificantly slow (long half life.) ….. uummm interesting. I don’t think I would chance it as any change could be the difference between a dose raise (or not ).

ncbi.nlm.nih.gov/pubmed?

(other supplied link is a “pay for”)

Very interesting article with loads of good points. Thank you for posting.

[helvella Administrator in reply to radd]

It isn't us that has the streptavidin - it is the actual testing process that uses streptavidin. (If I have understood properly.)

en.wikipedia.org/wiki/Strep...

You would have to ask the lab whether their testing process is sensitive to biotin.

[radd in reply to helvella]

helvella,

Yes, you are right. On further investigation streptavidin is used within the test that measures thyroid hormones & TSH, but this protein also happens to be an excellent binder with biotin. It appears if the patient has been supplementing biotin, the hormone results may be incorrect.

I wonder if the endo's//doctors ask the lab about the sensitivity of their testing process ? ? ...

Of course endos//doctors could advise patients to stop supplementing biotin two days before blood is drawn but I have never heard of this happening.

[helvella Administrator in reply to radd]

About three months ago...

healthunlocked.com/thyroidu...

[helvella Administrator]

Why anyone should be in the least surprised by this is a mystery. That it has now been subject to formal mathematical modelling, though, is an achievement. That the paper has been published is excellent news.

I have long suspected that if you took a healthy person and somehow removed all thyroid function, you would see TSH rise. In the beginning, it would rise to the maximum level the pituitary can achieve - I suggest something like 10. Over time, the pituitary itself would become able to produce more TSH so the level would keep rising - 20, 30, 40, 50, and so on. (Isn't this "why" pituitary hyperplasia has been documented in severe hypothyroidism?)

I suggest that very high TSH at diagnosis is likely to reflect how long the person has been hypothyroid, possibly even more so than the severity (i.e. how little thyroid hormone they have).

Upon restoration of thyroid function, the enlarged pituitary would be likely to continue producing too much TSH until it shrinks down again and behaves like a "normal" pituitary. (Though I suspect this never fully resolves and even the first steps might takes years.)

In the period of restored thyroid function, any time that thyroid levels reduce at all, the pituitary is likely to produce an excessively large increase in TSH.

Why on earth would this hair-trigger TSH level be a reliable way of managing thyroid hormone dosing?

At the same time, someone who is diagnosed and treated early might find everything so very much more like the text-books seem to say.

[Hillwoman]

A very interesting post which helps me to make more sense of recent remarks made by Diogenes on the subject of epigenetics, in response to another member's post.