Thyroid UK
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TSH supressed again GP & Endo keep changing my dose

Hello good people, I need some clever minds to help me.

I am struggling to attain a euthyroid state as my GP and Endo keep changing my dose of combination therapy (without asking how I feel!) as they are reactive to the supressed TSH.

My previous NHS results 10/5/2017 TEVA Oral Solution LT4 65mcg (13ml)/Sigma Pharma LT3 15mcg

TSH *0.28 mu/L 0.4 -5.5

FT4 12.6 pmol/L 11.0 -26.0

FT3 4.2 pmol/L 3.0 - 6.0

My previous Medichecks results 14/12/2017 TEVA LT4 75mcg/Mercury Pharma LT3 25mcg:

TSH *0.027 mIU/L 0.27 - 4.20

FT4 *10.2 pmol/L 12.00 - 22.00

TOTAL THYROXINE (T4) *56.8 nmol/L 59.00 - 154.00

FT3 4.49 pmol/L 3.10 - 6.80

REVERSE T3 11 ng/dL 10.00 - 24.00

REVERSE T3 RATIO 26.57 15.01 - 75.00

These are my latest Medichecks results 6/3/18 with a current dose of LT4 50mcg/LT3 30mcg (…I ask for the LT3 to be increased by 5mcg, as the LT4 reduction of 25mcg made me feel terrible).

TSH *0.018 mIU/L 0.27 - 4.20

FT4 *7.92 pmol/L 12.00 - 22.00

TOTAL THYROXINE (T4) *51.0 nmol/L 59.00 - 154.00

FT3 5.32 pmol/L 3.10 - 6.80

THYROGLOBULIN ANTIBODY 108.000 IU/mL 0.00 - 115.00


ACTIVE B12 160.000 pmol/L 25.10 - 165.00

FOLATE (SERUM) 16.72 ug/L 2.91 - 50.00

25 OH VITAMIN D 158 nmol/L 50.00 - 200.00

CRP - HIGH SENSITIVITY 0.63 mg/l 0.00 - 5.00

FERRITIN *166 ug/L 13.00 - 150.00

I am on modified Paleo diet and am pleased about the auto antibody levels, as it is the first time I have got them in range. Also I am supplementing and all the vits/mins look good – need to tweak ferritin and possibly consider methyl folate instead of folic acid.

My FT3 at 5.32 is looking great and cognitively I feel much, much better although my energy levels are still low. I would guess (!) that symptomatically and getting the FT4 into the upper quarter that my optimal dose is 100mcg LT4 and 30mcg LT3… ignoring the suppressed TSH.

I remember someone on HU TUK saying that they had requested their HPs ignore the supressed TSH.

The only issue I am led to believe for supressed TSH is osteoporosis. I do weight bearing exercise to strengthen bone as best as I can and I supplement with Mg/CA/Vit D/Vit K and monitor my calcium levels (CORRECTED CALCIUM 2.31 mmol/L 2.20 - 2.60). I have not had a bone density DEXA scan. The other issue sometimes uttered by HPs is heart problem…my QRISK Cardiovascular Disease 10 year risk score is a 1.47%. And just my luck, my Endo has bizarrely stated suppressed TSH causes cognitive issues (see my previous post).

I have the GP next Tuesday and the Endo in April…I just don’t know how to approach this issue with my HPs, other than perhaps offering a patient letter confirming that I would like the TSH value to be disregarded, so that they are both ‘covered’.

Any thoughts /insights please? 

28 Replies

That is a myth. A suppressed TSH with FT3 in range, neither means that you are over-medicated, nor does it cause bone or heart problems.

Hope these links help. :)


Thank you greygoose :-)


You're welcome. :)


Hi greygoose,

I have had time now to digest this information you have kindly given me ... I don't know how to argue out with NHS HPs, whom I am reliant on for my medication, what my dose should be and why suppressed TSH is such an issue on combination therapy.

I am DIO2 gene heterozygous so any 'usual' LT4/LT3 ratio won't necessarily apply to me.

My rT3 is looking good (adrenals supported nicely now), so any unconverted 'surplus' FT4 doesn't seem to be an issue for me.

I am really stumped :-(


I can't tell you what your dose should be - neither can your doctors, if it comes to that. It's the dose you feel well on, but you can only find that by trial and error.

* Your TSH is low because you do not need it anymore. Thyroid Stimulating Hormone - you no-longer need to stimulate your thyroid because you are taking hormone exogenously - T4 and T3.

* In any case, there is not point in stimulating the thyroid because it cannot respond well enough to produce enough hormone to keep you well - which is why you are on thyroid hormone replacement.

* You have Hashi's. Every time the TSH tries to stimulate the thyroid, the activity stimulates the immune system to attack the thyroid and destroy it a little more. Then you have these distressing swings from hypo to 'hyper', as the dying cells dump their stock of hormone into the blood. This means that it is difficult to find a stable dose. Keeping your TSH suppressed, will even out those swings, so it will be easier to find the right dose, and lessen your symptoms.

* TSH just does what it says on the label. It stimulates the thyroid to make hormone - you don't need that. It also drives conversion, but not always very well - you don't need that because you're taking T3. TSH has nothing to do with heart or bones. Over-range FT3 could possibly increase the risk of osteoporosis and/or heart problems, but it would have to be over-range long-term as in Grave's Disease. And, even then, it's not a certainty, just a possibility.

* Over-range FT3 due to thyroid hormone replacement does not have the same possible consequences as over-range FT3 due to an over-active thyroid.

* Ipso facto, it really doesn't matter a damn if the TSH is suppressed, as long as the FT3 is in range.

That's all I can think of for the moment. Make notes, and adopt an air of authority. :)


Wow... thank you greygoose this is thoughtful info :-)


You're welcome. :) Hope it helps.

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Usual caveats apply, everyone unique, I’m not a doctor etcetc...... but, based on years of monitoring my bloods and t4 T3 doses and symptom diary if your indications and doses were mine (I’ve been there) I would not be content to let tsh go so low, none of the research papers I have seen for euthyroid levels of both healthy and treated hypothyroidism individuals have tsh suppressed, suppression is for other clinical purposes not a blow it away approach to treating hypo. If it were me I’d increase T4 and cut the T3 to about 10% of the T4 amount, gradually bringing them into that sort of ratio. From the sort of levels you’ve had and symptom improvement indicators I am getting stabilised on around 75-90 mcg levothyroxine and 7.5 mcg liothyronine. Incidentally I’m amazed you can cope with such big T3 doses, do you split them. I split my T3 and t4 into three doses during the circadian rythym for higher range tsh i.e. 11pm 4am 10am! It takes time to stabilises symptoms and blood levels but in trying to find the holy grail of my set point (dynamic equilibrium between TSH T4 T3) I aim at a TSH of about 1-1.5 T4 of 14-15 and T3 4.4-5.0. In my experience T4 levels have a much bigger affect than the clinicians acknowledge or understand. Dumping massive amounts of t4 once every 24 hrs seems brutal and medieval treatment, just for the sake of simplicity. The healthy thyroid gland does not give 100mcg of free T4 in one hit and maybe that’s why some patients don’t respond well and then under-medicate?!

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Hi Hashihouseman, thank you for your reply.

With my fatigue and poor cognition it is difficult to assimilate all the varying research information I have waded through in the past few years. I understand that patients on NDT dose regardless of TSH suppression.

When you say "suppression is for other clinical purposes" which ones are you alluding to? I am not quite sure why TSH suppression is such an issue for my dosing.

I am DIO2 gene heterozygous and have a T4 to T3 conversion issue, so I can't do the 'usual' ratio of LT4:LT3. I dose LT4 50mcg/LT3 15mcg 07:30 and LT3 15mcg 16:30...I take a lot of supplements and it is difficult to park everything in my day without causing absorption issues etc. You make an interesting point about splitting the LT4 in the day.

As a patient I am not sure now to argue this out with my HPs ... who I fear will simply reduce my dose and cause my symptoms to get worse. What I do know is that the LT3 is helping enormously. I long to find my holy grail of a set point :-) ...which will be easier I suppose now that I am managing the auto antibodies, healing my gut and have the vits/mins in range -ish. Perhaps I should negotiate with the HPs and request that my dose is changed to LT4 75mcg/LT3 20mcg ?? and test yet AGAIN!

I am still fighting to have the Liothyronine medication parked on my file as a clinical need.



I think he means he thinks it's OK to have suppressed TSH if you had thyroid cancer, but not for those who didn't. But I don't think any studies actually differentiated between those who had very low TSH because they were hyper (ie high thyroid hormones as well as low TSH) and those who had very low TSH because they were taking thyroid hormones (or had underfunctioning pituitary glands) and had in range thyroid hormones. I'd argue that I'd rather have slightly thinner bones and be able to function than have brain fog, fatigue, constipation and all the other hypo symptoms, as well as being at a higher risk of heart problems through being undermedicated.


Thank you Angel_of _the_North ... well said. I certainly do not want to go back to my hapless self with brain fog pre LT3! I just can't find the evidence that supports the HPs assertion that suppressed TSH causes heart,cognition and bone problems. It is frustrating and confusing, as I recognize that thyroid care is not fit for purpose especially in UK and that there is so much more research that needs to be just seems that HPs are making stuff up!


Ah yes me too on the T3 ‘parked’ on our patient records.... that seems an important milestone and one other clinicians should beware overruling..... we hope!

And me too on heterozygous DI02 polymorphism, but I still convert and I proved it with swapping out T3 for T4, which was mighty uncomfortable until I adjusted the T4:T3 dose and allowed my system to steady on a different (more T4) ratio. That said I have definitely observed a low T3 trend in bloods at T4 levels the reference data suggest give good fT3, so yes a poor converter, despite my endo saying everyone converts and not giving a........

I absolutely need T3 but the trick is as little as possible with not too much T4 and when I see stability happen and can narrow in a little bit more on the levels I dare to think I’m closer to holy grails and unicorns

However I am also certain that despite the side effects of too much T4 that I suffer I definitely need more than I was getting on a desiccated only replacement regime, which actually got me drug dependent on getting my next T3 fix and upped my pulse by 25% and suppressed my TSH.....

I don’t want to dose regardless of suppression because a) it’s uncomfortable b) it’s physiologically abnormal c) it’s uneccessary and extreme if there’s a balance that relieves symptoms and is somewhere around the median of the healthy population TSH T4 & T3 levels. If I remember right clinical suppression is a necessary evil for managing thyroid cancer risk.

I also suspect that suppression or even very low bottom of reference lab ranges is a result of chronic T4 overdosing, which could be reduced with physiologically normal amounts of a T3 ‘supplement ‘........... (and now I’ll duck beneath a parapet).

Our set points are worth discovering and fighting for, test and test again, it’s the only way:). I saw a good academic paper recently which talked about how hard it was in theory to find a set point, because so much data was necessary, a figure of around 200 samples was mentioned but the exact sampling regime wasn’t clear..... however I have actually got all day (rest of life!) and it doesn’t seem that much of a sacrifice or effort to see an actual unicorn.

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Thank you Hashihouseman... it is confusing because some people say LT4 causes TSH suppression, including my GP who was ok with me increasing my LT3 in response to the LT4 reduction, and others say it is LT3 medication that always suppress TSH.

I wonder whether I should be medicating at 16:30 LT3 the day before the blood draw and whether this has effected the TSH results which are lower than previously.

Lets raise a cup to finding the unicorns... :-)


I just read your main profile narrative, all thought provoking stuff, thank you for sharing. You seem much more switched on and rational than your sense of cognitive dysfunction makes you feel..... imagine how sharp you’d be if you were free of thyroid chaos. Anyway one thing in particular you said brought me to question it in case it helps: suppressed tsh even transient COULD be a cause of bad head effects...... I say this because when ever I get the adverse effects I associate with higher t4 doses there is a logical and partially observed suppression of tsh and I wonder whether some of us are sensitive to whatever brain chemistry is affected by higher or lower tsh levels beyond what or bodies were used to Before Hypothyroidism....... I used to blame levothyroxine and think it had bad side effects for me but maybe it’s not side effects per se but direct effects i.e t4 effect on TSH.

However, I also suspect unphysiological levels of free t4 in the gut and being absorbed through the gut may have true side effects from interference in gut tissue biochemistry e.g. enzyme metabolism .... since taking levo I realised many of the worst symptoms were almost dead ringers for histamine poisioning and there is some evidence that excessive levels of t4in the gut affect the neutralising capacity of what used to be called histaminease (DAO). And, more evidentially, I could reduce the symptoms by taking anti histamines and so the next logical step was taking a DAO supplement and then the next logical step a copper supplement (DAO is a copper dependent enzyme) . Of course the doctors all scoff and there is a real risk of copper toxicity but I’m careful and whether it is coincidence with better titration of my combined hormone replacement doses or real amelioration of ‘side effects’ I have felt a significant reduction of levothyroxine intolerance.......

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Good morning Hashihouseman,

I am sorry for the delay in reply. I have been to the GPs and its been really good to take along a new approach, helped by you all in this post. I have suggested that the dose be changed to LT4 75mcg/LT3 20mcg to begin this journey of finding the set point, as I have only two credible data points at the moment (due to change from LT4 oral solution and a 'Metavive mistake'). It is a a significant reduction in LT3 and I may go more foggy, but I want to be able to engage with the HPs as best as possible and present lab values/symptoms in a methodical way and I will split the dose in the day as you suggest ... the increments are so crude in tablet form.

I talked about getting LT3 clinical need on my file and he said it is already on! Wow. He said he will write a letter to me to confirm this. He explained that even though NE Derbyshire have black listed LT3 it exists in the BNF (check monthly drug tariff NHS BSA for updates) and GPs legally should follow their terms of service (which he wrote a long time ago apparently). So if secondary care aka Endo is saying prescribe LT3 then GPs are legally obliged to do so. It seems that there are a lot of GPs out there breaching their terms of service.

This is all very, very, very wrong!

Interesting point you make about histamines - I was preparing bone broth (good for gut repair) for too longer a period (24hr instead of ~14hr) as it produces lots of histamines - I have had wicked hay fever since 2009. So I shall investigate this further. I do go sublingual with both LT4 and LT3 ...due to my poor stomach acid and gut damage. Do you take zinc with the copper supplement? I had a hair mineral analysis done via my Nutritionist (ARL Labs) which showed a significant mineral depletion across the board.

Onwards and upwards hey!


You may suffer from the significant changes but hanging on in there to see what happens was worth it for me and coming down off too much T3 was hard because of it's highly addictive / high withdraw symptom effect !! if you can run to it try doing the finger prick TSH T3T4 test ASAP and then every 3-4 weeks to see how your bloods are responding. It's baloney this NHS view that bloods are only valid 6 or even 12 weeks from changes to dose etc. I found it especially helpful to track the trend, the rate of change and pinpoint different times in the circadian rythm, now I have a spreadsheet with loads of data and it all helps narrow in on the set point. The research I could find on combination therapy was informative but not as investigative as we need, we have to experiment on ourselves to a large extent but here's one nice quote from

2012 ETA Guidelines: The Use of L-T4 + L-T3 in the Treatment of Hypothyroidism

Wilmar M. Wiersinga a Mark P.J. Vanderpump, Leonidas Duntas, Valentin Fadeye, Birte Nygaard

Because of tissue heterogeneity, pituitary TSH secretion may not reflect what happens in other target tissues, and therefore serum TSH alone may not be a good marker for the adequacy of thyroid hormone replacement [67, 68, 70]. Theoretically, thyroid hormone replacement therapy should aim not only at normalization of serum TSH but also at normalization of serum free T4, free T3 and free T4/free T3 ratio.

The pharmacodynamic equivalence of L-T4 and L-T3 has been recently studied in a randomized, double-blind, cross-over study in 10 thyroidectomized patients [71]. The target (TSH 60.5^1.5 mU/l for at least 30 days) was reached by an average daily dose of 40.3 8 11.3 g L-T3 and 115.2 8 38.5 g L-T4 (L-T3:L-T4 ratio 0.36 8 0.06). It was concluded that therapeutic substitution of L-T3 for L-T4 was achieved at approximately 1:3 ratio. To some extent these data can be used to calculate the dose of L-T4 and L-T3 in L-T4 + L-T3 combination therapy as follows (table 6, method A):

So, I have tended to think that T3 replacement with T4, up to a certain level where the T3 itself is essential for some of us, needs 3 × the T4 in µg. So IF you found you could reduce your T 3 by another 5 µg for example then you would swap it for 15 µg of T4. And yes dividing pills is a pain, I use I super splitter and a jewelry scale ! The oral Levothyroxine was much easier but the cost too much for my GP!

How excellent you have your T3 need on record and how interesting all that stuff on GP terms of service and NHS drug lists, thank you!

And the Hay Fever ! me too ! yes that was the clue for me to investigate the histamine and thyroid medication links because I never had hay fever in my life before I was 51 and taking Levothyroxine ! Less Levothyroxine less hay fever!!! And it affects the gut histamine levels which Rinatdine controlled but I didn't want to take hence experimenting with DAO supplements and then copper.

And to prove there's move to this than meets the eye...

Effect of L-thyroxine and carbimazole on blood levels of biogenic amines in rat.

Upadhyaya L 1 , Agrawal JK, Dubey GP.

Author information Abstract

Circulating levels of 5-hydroxytryptamine (5HT), histamine, monoamine oxidase (MAO), histaminase, tri-iodothyronine (T3) and thyroxine (T4) were studied in L-thyroxine and carbimazole treated rats. Increased concentrations of 5-HT, histamine, glutamate, T3 and T4 were recorded in L-thyroxine-treated rats while plasma gamma-aminobutyric acid (GABA), MAO and histaminase levels were significantly decreased. Considerable reduction in 5-HT, glutamate, T3 and T4 with trend towards the rise in plasma levels of MAO and histaminase was noticed in carbimazole treated group. There was a significant correlation between these amines and thyroid hormone values. The findings suggest that alterations in the metabolism of thyroid hormones may have a link with the altered metabolism of biogenic amines.

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oh and there's this:

Brit. J. Pharmacol. (1961), 17, 137-143.




From the Department of Pharmacology, School of Pharmacy, University of London, Brunswick Square, W.C.J

(Received June 6, 1961)

Injections of thyroxine sodium increased the sensitivity of mice to histamine, the maximal effect occurring after 6 days.

During a study of the influence of the endocrine glands on the sensitivity of rats to an intraperitoneal injection of egg-white, LUger & Masson (1948) noted that injections of thyroid extracts produce a striking modification of the anaphylactoid reaction. This reaction in untreated rats is characterized by gross oedema of the extremities with recovery within 6 hr, but a shock-like condition is produced within a few minutes of the egg-white injection into thyroxine-treated rats and many of the animals die. Parratt & West (1960) confirmed this result, and showed that the cause of death is internal oedema and haemorrhage in the intestinal tract. These latter authors also found that after thyroxine treatment the histamine released by the injection of egg-white accumulates in the blood, possibly as a result of inhibition of histaminase, an enzyme responsible for its inactivation. Parratt & West (1957) had previously reported that egg-white releases both histamine and 5-hydroxytryptamine in the rat and that both amines play roles in producing the anaphylactoid reaction.

The mouse, like the rat, is resistant to the systemic effects of histamine and 5-hydroxytryptamine, but this resistance may be lowered by pre-treatment with Haemophilus pertussis vaccine (Parfentjev & Goodline, 1948; Kallos & KallosDeffner, 1957) or by adrenalectomy (Halpern & Wood, 1950; Munoz, 1957). It was of interest, therefore, to determine whether mice are rendered supersensitive to histamine and 5-hydroxytryptamine after treatment with thyroid hormones, and whether anti-thyroid drugs have the opposite effect.

... I asked my GP to refer me to immunology to investigate.... but both the GP and my endocrinologist clearly thought this was a neurosis too far, idiots!

If I was Bill Gates I would be doing primary research into this to get to the bottom of it since I suspect it could be a significant cause of lack of wellness in hypothyroid treated patients... that along with failure to establish each patients set point !

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Thank you so much Hashihouseman, this is invaluable information.

I appreciate your guidance and time :-)


All very interesting Hashihouseman. There is a great book about the mental effects of high copper/low copper; high/low histamine etc you might find interesting and helpful. I've lent it and can't remember the author or title, sorry, and it's American so refers to depression etc as 'schizophrenia' but as long as you know that in the USA schizophrenia covers many things we don't even consider mental ill-health, such as the histamine responses, it's a good informative read. Let me know if you'd like the title etc.

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Any T3 containing meds will always suppress TSH its the perfectly normal response of the thyroid pituarity feedback system which doctors refuse to learn


Hello reallyfedup123,

I had thought, from the swamp of confusing reading that I have done over the years and NOTABLY impaired by my cognitive issues, that it was T4 that was predominate in the feed back system to regulate the pituitary TSH secretion not T3?? Have I confused myself with this information?

Looking at Dr A Toft pulse magazine article again...he states that - "While taking both hormones it is important serum TSH is normal and not suppressed." with no explanation as to why this is important...and only states for the monotherapy not the combination therapy what TSH should be - "The appropriate dose of levothyroxine is that which restores euthyroidism and serum TSH tothe lower part of the reference range – 0.2-0.5mU/l. "

I really don't know how to go forward with this... in an empowered way and stop this cycle of dose change and testing that the HPs have me lock in...



We should clarify ‘any T3 will suppress TSH’ in this context, the thread seemed to be about a level of TSH that was referred to as suppressed rather than the negative feedback of t3 & t4 on tsh in general...... ? The clinical suppression of TSH seems to be regarded as that which is an order of magnitude less than even very low TSH e.g. 0.1-0.4 and which is required for managing thyroid conditions other than hypothyroidism?


Toft is wrong ....its T3 circulating in the body which suppresses the pituarity thyroid feedback system

I am aware that Levo T4 also affdcts TSH but its a false reaction and why GPs reliance on TSH is so so wrong

TSH is highest very early morning which is precisely why we always advise blood tests are very esrly morning and fasting and never take your thyroid meds in previous 24 hours

Once you are on a dose that resolves your symptoms ...thats exactly what you need and should stay on ...there should not normally be any reason to change the dose unless hashimotos has furthur damaged your thyroid and your hypothyroid symptoms return

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Ok thank you, please do you have any literature that I could show my HPs to counter Toft's statement and present the fact that FT3 suppresses TSH not FT4?

I have always done blood draw at ~08:00am and fasted...however the day before I have taken my dose as normal i.e. LT4 50mcg/LT3 15mcg 07:30 and LT3 15mcg 16:30. I wonder if I should not take the 16:30 LT3 dose and whether that has effected the results??

Oh poo... have I been stupid?



Apologies in case I'm 'teaching grandmother ....' but I'm feeling sympathy for you and would like to offer helpful advice.

Here's a link to an article I've forgotten but I noted as 'excellent' on T3, rT3 etc, hope it's still live.

I am under a Professor and a Consultant who take very good care of me on T3. My understanding from them is that T3 is short-lived so there is no problem with taking it before your blood tests - also the tests are marked to indicate whether the person tested is on thyroid medication or not - and the results must be read taking that into account.

Also, T3 is used up when we are active: I have to adjust my doses daily according to how much yoga I teach and whether or not I, for instance, take my daughter's dog for a walk. I think this is why finding the right balance is so tricky.

Also, if you are taking T4 (I'm not) which you know is converted into the T3 needed by the cells, then you need calories for that conversion, so how much you eat could also be affecting how you feel and your test results.

Hope that is of some help.

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Excellent article and sound info thank you thyr01d...this is quite a journey we are on ! :-/


In my opinion if you want Doctors off your back when forced to have a blood test i woukd actually avoid taking either t4 ir t3 in the 48 hours before

But thats my personal view a search on here for the research paper Dr Midgeley recently published they are a well respected researcher

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Thank you, I really appreciate you giving me your time reallyfedup123 :-)


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