What about this?

[lisan1]

What do you think about this? She says that you need a normal TSH because it is a hormone that had effects in the body.

drchristianson.libsyn.com/w...

[jimh111]

Don't have time (or inclination) to read it but TSH like many hormones has other actions including a role in bone formation and stimulating deiodinase.

Some people have a subnormal TSH leading to low thyroid hormone levels and some need hormone doses that lower TSH. Not much you can do until the underlying causes are discovered and corrected, in the meantime you need to treat hypothyroidism.

[Sybilla14]

A great lecture linked by someone on the forum yesterday, you may wish to listen to: youtu.be/hWU2if9QQl0(Not working as expected?)

[helvella Administrator Thyroid UK]

Consider a typical TSH reference interval of 0.4 to 4.0.

When someone tells us that TSH is important (because of its effects on lipolysis, ATP and mitochondria function, skin health, etc.), ask this question:

Why does the reduction of TSH from 0.4 to zero matter? There is hardly a doctor on the planet who would argue that there is an issue with TSH being anywhere between 0.4 and at least 2.0, possibly all the way up to 4.0? We even see doctors refuse to treat hypothyroidism until TSH rises above 10.0!

• 0.0 to 0.4 is a range of 0.4.

• 0.4 to 2.0 is a range of 1.6.

• 1.6 is four times as big as 0.4.

We can sum this attitude up as:

The difference between 0.0 and 0.4 is vitally important.

Whereas the difference between 0.4 and 2.0 is entirely ignorable.

(Even worse, if we allow it to go up to 4.0, the range is 3.6 – or nine times 0.4. Possibly all the way up to 10.0 – or twenty-four times 0.4.)

Wouldn’t anyone expect more TSH to have a bigger effect? Yet in this situation we are told that the amount of TSH only really matters if it is below 0.4. Having several times that amount is totally unimportant and has no effect whatsoever.

Maybe having no TSH is significant? They have not convinced me.

The claim that TSH being within the reference interval indicates optimised dosing is also questionable. First, it is based on the assumption that the hypothalamus and pituitary are responding properly – as in healthy individuals with no thyroid disorder. (If that has not been demonstrated, it is an assumption. In thyroid disorders, the response of the hypothalamus and pituitary can be affected. Failure of that response, total or partial, might even be the cause of their thyroid disorder.)

[jrbarnes]

I laughed out loud at your response 🤪

[m7-cola in reply to jrbarnes]

Me too!!

[Honey1978]

My tsh is 1.29 is tha good

[helvella Administrator Thyroid UK in reply to Honey1978]

Honey1978,

I really recommend you start a brand new post. Click on the blue Write button near the top of the page.

Then tell a bit about yourself and put your questions together. I think you will find it much better to get replies all together, in one place.

[jimh111]

My prejudice but I'm always turned off at anything that refers to optimizing treatment, sounds too much like an introduction to marketing.

Without doubt TSH has effects beyond the thyroid and it makes sense to have a TSH if you can. Many tissues express TSH receptors including the brain, brown fat and skeletal muscles. There's an old song 'you gotta have a hat'. We could say 'you gotta have a TSH' except it's not possible for some patients.

For example bone has TSH receptors and TSH seems to promote bone turnover. We could speculate that during periods of iodine deficiency (as occurs in many countries and historically) there would be widespread hypothyroidism and TSH would shoot up. Perhaps the pituitary sends a TSH message to bone 'hey we're running out of thyroid hormone so don't rely on my T3 messages just keep turning over bone'. This would be cruical for children growing up. Perhaps this explains the bone loss seen in Graves', caused not just by high T3 but by Graves' antibodies pretending to be TSH and confusing the bone.

This subject is poorly understood so we certainly can't quantify the effects of TSH on tissues other than thyroid, how high or low TSH has to go before it upsets tissue homeostasis.

Another aspect is TSH regulates deiodinase, especially type-2 deiodinase which controls local T3 levels, especially in the brain. With a subnormal TSH the brain will be hypothyroid, the brain gets 80% of its T3 by D2 action on T4. If a subnormal TSH reduces T3 and T4 levels restoring normal serum T3, T4 will not work, the 80% T3 produced by TSH stimulated D2 will be reduced. If you boost serum T3 levels by taking lots of liothyronine (as I and others do) it will be a bit too much for the heart.

In times of trauma the hypothalamus tells the pituitary to reduce TSH which can be life saving. For example during brain injury low TSH and high reverse T3 combine to protect the brain.

So, although I don't plan to waste time reading this article (or any similar ones!) the point that TSH has important action outside the thyroid is valid. For this reason it's important that more research is done into why TSH secretion becomes subnormal and what if anything can be done to restore normal secretion.

Many of the more severe cases of hypothyroidism I see on this forum are associated with subnormal TSH, central hypothyroidism without a damaged pituitary. This can cause more severe symptoms than e.g. a pituitary adenoma. If the pituitary is damaged the hypothalamus picks up on low thyroid hormone levels and produces extra TRH. TRH increases the glycosylation of TSH, it makes it more potent thus reducing the effects of a low TSH. This appears not to happen when TSH is subnormal due to e.g. a down-regulated axis which happens after long term TSH supression by hyperthyrodism or excess thyroid hormone intake.

So, ignore articles like these but bear in mind TSH has actions outside the thyroid and ideally we would all have the right amount of TSH.

[lisan1 in reply to jimh111]

Thank you! Do you know which would raise TSH more lowering levo or lio?

[jimh111 in reply to lisan1]

The only study that has been done found that 10 mcg L-T3 had the same effect on TSH as 30 mcg L-T4. This might vary if fT3 or fT4 were high or low as T4 to T3 conversiosn would be affected. I'm afraid it gets very complicated and we don't really know what happens outside normal hormone levels.

[lisan1 in reply to jimh111]

Thank you! Do you have a link?

[jimh111 in reply to lisan1]

ncbi.nlm.nih.gov/pmc/articl...