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Thyroid UK
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What does Tsh respond to?

T3 or t4?

I've tried to find the answer to this on hu but struggled - I suspect it's not clear cut!!!

16 Replies

The TSH (Pituitary Gland)responds when the T4 level becomes too low.


Very superficially, pituitary takes in both T4 and T3 from the bloodstream. It then converts the T4 to T3 and produces TSH depending on the sum of the two lots of T3.

There are reasons that this is not as simple as my description seems to suggest.


Haggisplant, my understanding is that pituitary gland responds to circulating hormone (T3) and rises when it is low to stimulate the thyroid gland to produce more T4 for conversion and shuts off TSH when it detects sufficient T3..


Clutter, nah. The pituitary and hypothalamus have their own enzymes and minds of their own. I think other factors besides just T4 and T3 levels factor in. People can have a low TSH, low fT4 and low fT3 when there's something else wrong with the body. That's your euthyroid sick syndrome. emedicine.medscape.com/arti...


This sentence strikes a chord - "The probability of death correlates with the levels of T4. When serum total T4 levels drop below 4 mcg/dL, the probability of death is about 50%; with serum T4 levels below 2 mcg/dL, the probability of death reaches 80%"... I know I felt very poorly with T4 at 0.6!


Glad you are with us, Aurealis. Sheesh, that's terrifying.


Bear in mind that mcg/dL is not the unit you'd expect in the UK, Europe, or most of the rest of the world except the USA! :-)


Before people panic, if you are taking T3 your T4 can become very suppressed without being dangerous.


I have low TSH and low T3 but only low-ish T4, so it must be more complex.


It's clear cut! The pituitary responds to fT3. However, the pituitary is real good at converting T4 to T3 so it responds to T4 also. Research shows that serum fT3 is about 3x as potent in reducing TSH as serum fT4. (Serum fT3 and fT4 ratios, not the ratio of T3 and T4 you might take as medicine).

The pituitary is stimulated by TRH produced by the hypothalamus. If you have a pituitary or hypothalamus failure the TSH may be low regardless of fT3, fT4. Other conditions such as depression, starvation and other illnesses can also lower TRH and hence TSH.

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Your point about the difference between serum levels and ratios taken as medicine is absolutely wonderful to see. You are absolutely right to point that out.

One of the first things I ever read about thyroid was how the hypothalamus makes TRH... Since then it seems to have been forgotten by most of the universe.


Thanks ...! I knew it would be complicated!

Essentially I'd like to be able to explain my seemingly hypothyroid myopathy symptoms over the last year as an issue with comversion to t3 given it was never tested. And then potentially request t3 combo treatment in the future if I'm still having issues. But that conversion issue was due to sertraline somehow changing t3 levels but not t4. Or lack of good ferritin levels.

However, for this to be so I guess Tsh must reflect more about t4 but not t3 (which is what we all bang on about) for my argument to work for the gp! (Who admits gps aren't v good at managing thyroid stuff)


"Administration of sertraline in patients stabilized on Levothyroxine may result in increased Levothyroxine requirements." See drugs.com/pro/levothyroxine... .

Often antidepressants are refractive (i.e. don't work) in hypothyroidism, they often require the addition of T3, although nobody knows why. You may find that a lower dose of sertraline is effective if you take T3, you may not need the sertraline at all.

TSH reflects fT3 and fT4 levels very well. The pituitary can be better than peripheral tissues at converting T4 to T3 and so TSH can be normal when there are peripheral T4 to T3 conversion problems.


Thanks - I was on such a low dose and was still not getting better. I'm now getting better slowly whilst off it. I discovered a small study which showed patients needed to raise thyroxine from between 25-50% to meet base line levels while on Sertraline. Dose sizes made no difference.

Apparently they did test t3 in November (not sure if gp or endo) and it was 3.5 but stated in range, upper range was 6 ish. I don't recognise that range.

I've been told I have joint hypermobility syndrome today so I guess anything that affects muscles (thyroxine and iron included) is going to be tough on me.


it is believed that that the hypothalamus responds to T3, and releases TRH which the pituitary responds to, to releases TSH.

the reason for this belief is that if it was T4 related, then blood tests could be done within hours/days of taking thyroxine TRH has a half life of just 5 minutes and TSH only has a half life of one hour. meaning its production is very responsive to the bodies needs in a short time.

yet it takes 3-4 weeks for T4 to decay (convert) into T3,

meaning the reason why doctors wait weeks to retest, must be due to waiting for the conversion to then measure the response.

(my researched opinion, use only as a point of research)


A really interesting response, very reasoned, thank you. It would make sense to me - in that I've just learnt that beta blockers reduce the peripheral comversion of t4 to t3. I used to take these long term due to anxiety (orhininally triggered by terrible journey to dusgnosis, then just from being a teacher!!) and when I took the slow release ones daily, I had to raise my thyroxine by 12.5. It did show In my blood tests not just how I felt. This might be simplistic but I seems to make sense.

My only doubt about your reasoning is the assertion that if it relied on t4 you could test in days; t4 has a half life of 7-10 days so would take quite a while to build to desirable level? Or is it just the 7-10 days?


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