Feeling much better, but have a Low TSH - Thyroid UK

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Feeling much better, but have a Low TSH

Blossom13 profile image

Hello all,

I recently had some bloods done, but the GP didn't do the FT3. I've now had some private tests done and wondered if I could get any feedback please:

FT4 - 18.5 (9.0 - 25.0)

FT3 - 5.2 (3.5 - 6.5)

TSH - 0.02 ( 0.50 - 5.0)

I am taking 100mcg T4 and 5mg T3 daily.

My GP wants me to reduce my T4 as he says I'm over-medicated, but I do not feel over-medicated at all, and in fact have been feeling much better overall. Him wanting me to reduce my T4 prompted me to get the tests done again including the FT3 and I thought they looked quite good.

So the low TSH strikes again! From all of my reading, it seems such a concern for so many, including myself. I know how I feel and I won't be reducing my T4, but there's just that underlying niggle going against the establishment. I would love to hear from any others with similar suppressed TSH who feel well. Thanks in advance.

22 Replies

I don't know, the whole TSH trip seems so irrational.

I think that the doctors interpret low TSH as automatically affirming that one is hyperthyroid, without examining other factors. Factors such as blood pressure, body temperature, pulse and just the way that the patient feels.

Low TSH could imply risk of hyperthyroidism which could have damaging effects but some of us just have freaking low TSH!

(Don't get me started on this! I'm so tired of the tyranny of Western medicine!)

The views I have shared are my anecdotal experiential crap your actual mileage may vary.

In the same boat could be my results . I also feel the best I have in years. Oh dear what to do . No idea against that which is spouted by doctors ☹️

yo'm at 100mg t4 and. 20mg t3. I feel better from monotherapy only t4. My tsh is 0.06. but doesn't matter. i feel ok.

Same boat here. I am on 100 / 87 mcg T4 ( alternate days) and 10 mcg T3 , FT4 and FT3 in range , actually Ft3 it's in range but not optimal and suppressed TSH 0.029. So frustrating to have conflicting information...makes you feel like you are damaging your health. Anyway I am not going to lower my meds, I don't feel it's the right thing to do.

My tsh is virtually unmeasurable it is so low as I take T3 only. I’ve learnt from reading posts on this forum for years to ignore the tsh and go by how I feel. This is easier for me to do as I do not get treatment on the nhs and don’t see a GP. I’m sure that some of the ‘experts’ on this forum will give you a link to articles which state that the tsh should not be used for dosage.

Resuktsare read differently when taking T3 in any form. TSH should be suppressed, FT4 can fall in its range but FT3 should be high but never over. With taking T3 you can no longer check that you are converting well as only the FT3 reading is accurate ( the FT4 reading CAN fall) as you can no longer compare the two reading as you would have done on T4 only so it would have been useful to check that before you added in the T3. However there isa way to aid conversation and that is by checking the levels of Vit D, B12, Folate and ferritin. These need to be optimal, not just in range so in your position if I didn't know if I was a good converter or not I would test and get these optimal. It's a bit of shutting the stable door after the horse has bolted but the best thing you can do to help.

Hi Blossom,

Doctors are still using TSH as the indicator of health and believe that a low TSH causes Osteoporosis and/or Atrial Fibrillation. There is no evidence to show that a lack of TSH causes either condition.I composed a letter for patients i n this situation. It is intended to cover most situations so it will probably need amending to suit your own circumstances. For example, the letter refers to a patient whose doctor has already reduced their dose of TSH.

Here it is:

Your Address here

no_reply@example.com

Date:

Dr’s name here

Surgery address here

Post code here

Dear Dr *********

Unilateral Reduction of my dose of thyroxine (T4)

Mental Capacity Act 2005

Good Medical Practice 2013

Good Medical Practice Consent: patients and doctors making decisions together 2008

Montgomery v Lanarkshire Health Board 2015

Bolitho v City and Hackney Health Authority 1993

I write following my appointment with you on ??/??/???? regarding your wish to reduce my ???mcg dose of T4.

During the appointment I told you that I did not want to reduce my dose of T4 because I feel good on this dose. I feel well, I can do my job to the best of my ability and I can contribute properly to my family life. I am not as irritable or fatigued. I can think clearer. I told you that my signs and symptoms return on a lower dose. You said that you wanted to reduce my dose because my Thyroid Stimulating Hormone (TSH) was too low and thereby there is of a risk of Osteoporosis (OP) and Atrial Fibrillation (AF). I showed/told you about research that shows that this not the case. (See appendix 1 attached.) I told you that you have no logical justification to reduce my dose of T4.

You did not carry out or refer me for an Electrocardiogram (ECG) test to establish a baseline or detect any abnormalities in my heart’s electrical activity despite your concerns about AF.

You did not refer me for a DEXA scan to establish a baseline or detect any abnormalities in my bone mineral density despite your concerns about OP.

You then reduced my dose of T4 to ??mcg.

Good Medical Practice

I am sorry to say that because you simply went ahead and reduced my dose against my wishes you did not comply with the preamble of the General Medical Council’s Guidance for Doctors Good Medical Practice 2013:

“The duties of a doctor registered with the General Medical Council”:

“Work in partnership with patients. Listen to, and respond to, their concerns and preferences. Give patients the information they want or need in a way they can understand. Respect patients’ right to reach decisions with you about their treatment and care.”

Mental Capacity Act 2005

During the appointment you did not assess me to determine if lacked Mental Capacity as laid out in section 3 of the Mental Capacity Act 2005. Therefore I am consider that you have assumed that I have mental capacity in accordance with section 1(2) of the Act.

Consent: patients and doctors making decisions together/Montgomery v Lanarkshire Health Board 2015

As I have, and you have assumed that I have, mental capacity to make decisions about my health, I am sorry to say that you did not follow the model in the General Medical Council’s Code of Practice Good Medical Practice Consent: patients and doctors making decisions together. This is important because the medical negligence case of Montgomery v Lanarkshire Health Board 2015 stated at paragraph 93 that following the model at paragraph 5 of Consent: patients and doctors making decisions together is a legal obligation.

The Guidance at paragraph 5 of Consent… states

If patients have capacity to make decisions for themselves, a basic model applies:

The doctor and patient make an assessment of the patient’s condition, taking into account the patient’s medical history, views, experience and knowledge.

The doctor uses specialist knowledge and experience and clinical judgement, and the patient’s views and understanding of their condition, to identify which investigations or treatments are likely to result in overall benefit for the patient. The doctor explains the options to the patient, setting out the potential benefits, risks, burdens and side effects of each option, including the option to have no treatment. The doctor may recommend a particular option which they believe to be best for the patient, but they must not put pressure on the patient to accept their advice.

The patient weighs up the potential benefits, risks and burdens of the various options as well as any non-clinical issues that are relevant to them. The patient decides whether to accept any of the options and, if so, which one. They also have the right to accept or refuse an option for a reason that may seem irrational to the doctor, or for no reason at all.2

If the patient asks for a treatment that the doctor considers would not be of overall benefit to them, the doctor should discuss the issues with the patient and explore the reasons for their request. If, after discussion, the doctor still considers that the treatment would not be of overall benefit to the patient, they do not have to provide the treatment. But they should explain their reasons to the patient, and explain any other options that are available, including the option to seek a second opinion.

With regard to part A

I told you about my condition and that it is my experience that on a reduced dose of T4, my signs and symptoms will return.

You did not assess me for signs of over treatment or refer to my blood tests for T4 and or T3 for to see if they were over their reference ranges.

I showed/told you that there is research that shows that low TSH does not cause OP.

I showed/told you that there is research that shows that OP and AF more likely when T4 and Liothyronine (T3) are too low or too high.

I told you that I do not have signs or symptoms of hyperthyroidism such as palpitations, tremor, or sweating.

I told you that I get some of my information from the internet and patient support groups. Their Lordships and Ladyship in the Supreme Court in Montgomery v Lanarkshire Health Board 2015 said at paragraph 76 of the judgement:

“it has become far easier, and far more common, for members of the public to obtain information about symptoms, investigations, treatment options, risks and side-effects via such media as the internet (where, although the information available is of variable quality, reliable sources of information can readily be found)3 (and) patient support groups…It would therefore be a mistake to view patients as uninformed, incapable of understanding medical matters, or wholly dependent upon a flow of information from doctors.

The idea that patients were medically uninformed and incapable of understanding medical matters was always a questionable generalisation, as Lord Diplock implicitly acknowledged by making an exception for highly educated men of experience. To make it the default assumption on which the law is to be based is now manifestly untenable”.

I told you that you had no logical justification to reduce my dose of T4.

With regard to part B

You simply said that there is a risk of OP and AF due to low TSH. It has been shown that the risks of OP or AF is due to either too much or too little for the individual patient’s T4 and T3.

You did not quantify the risk of OP or AF in a way I could understand or at all. Therefore you have no adequately explained the options to me and the possible risks or benefits of staying on my dose, raising my dose, changing to Liothyronine (T3) or having a mixture of T4 and T3.

By not quantifying the risks of the above options to me personally, you have not given me the opportunity to weigh the risks and benefits of each option as required in part C of the GMC’s model.

You did put pressure in me to accept your decision by simply saying that you are reducing my dose.

With regard to part C

I have the mental capacity to make decisions about my health. I have read the research referred to above. I understand that the risk of OP and AF is from having too much or too little T3 and/or T4 for me as an individual. I don’t have the signs or symptoms of too much T3 and/or T4. My blood tests show I am not outside the reference range for T3 and/or T4. I have weighed up the theoretical and mostly unfounded risks of staying on my dose against the actual risks of lowering my dose. I have also considered the non clinical factors of lowering or remaining on my dose, such as the impact on my family life and work life if my signs and symptoms recur, as they will do if my dose is reduced.

I have assessed the risks of OP and AF by lowering my dose to be much higher than remaining on my dose.

I have decided to remain on the dose I am on.

With regard to part D

Remaining on my dose is clearly of overall benefit to me. I feel well, I can do my job to the best of my ability and I can contribute properly to my family life. I am not as irritable or fatigued. I can think clearer. Reducing my dose will result in harm to my health by the return of my signs and symptoms. It will also negatively impact on my work, private and family life. Further, as described above, there is no reliable evidence that low TSH actually causes OP or AF.

If you are still of the opinion that you want to reduce my dose to ??mcg, please explain how remaining on my current dose would not be of overall benefit to me in writing. It is important that you quantify the risk of OP or AF to me as an individual in your written explanation. Good Medical Practice at paragraph 47 says that you must treat me an an individual. Please be aware that there is another body of responsible medical opinion that agrees with maintaining a dose of thyroid medication that suppresses TSH without causing thyrotoxicosis and had been recognised as such by the General Medical Council.

Lack of logic to reduce dose of T4

I am unaware of any guidance to unilaterally reduce a patients dose of T4 and/or T3. Such guidance does not appear in the British Thyroid Association’s statement on the management of primary hypothyroidism. Recommendation 7 states:

“Although fine tuning of serum TSH levels within the reference range may be indicated for individual patients, deliberate serum TSH suppression with high dose thyroid hormone replacement therapy (serum TSH <01 mU/L) should be avoided where possible as this carries a risk of adverse effects such as cardiac rhythm disorders including atrial fibrillation, strokes, osteoporosis and fracture (1/++0). As an exception, patients with a history of thyroid cancer may require deliberate suppression of serum TSH if there is a significant risk of recurrence”.

It does not recommend that ALL patients on thyroid hormone replacement therapy unilaterally have their dose reduced. It states “where possible”.

This recommendation is now out of date following research that low TSH is not a factor in OP or AF but excess or low T4 and/or T4 is. To blindly follow this out of date statement is in conflict with a doctors legal obligation to follow the model consultation in Good Medical Practice Consent: Patients and doctors making decisions together.

The Royal College of General Practitioners Curriculum states at 3.17 that a GP should:

“Recognise your central role as a primary care physician in managing diabetes mellitus and hypothyroidism”,

and

“Recognise the potential for abuse of thyroxine and propose strategies to reduce dosage”.

I can assure you that simply being on a dose that makes me well is not abusing thyroxine especially if my blood tests for T4 and T3 are within their reference ranges. Any strategy to reduce dosage must be logical. This is confirmed by the medical negligence case of Bolitho v City and Hackney Health Authority 1993 which states that a doctor’s actions must be logical even if it is supported by a responsible body of medical opinion. For the reasons above, I do not believe that your action to reduce my dose without any evidence or following the BTA statement contrary to my well evidenced and argued wishes to remain on my dose of T4/T3 is logical.

If you have concerns about me suffering from AF or OP please refer me to a cardiologist for an ECG test and an Orthopaedic specialist for a DEXA scan.

I hope you reconsider your decision to reduce my dose of T4 and/or T3 and restore it to the level that makes me feel well and contribute to my work and family life. I value my actual health more that an unfounded and unquantified potential risk in the future so much that if my dose is not maintained or restored, I will take this matter further by way of complaint to the Clinical Commissioning Group, the General Medical Council or by a claim for negligence.

Yours Sincerely

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Appendix 1

Thyroid Stimulating Hormone and Bone Mineral Density:

Journal of Bone and Mineral Research, Vol. 33, No. 7, July 2018, pp 1318–1325

DOI: 10.1002/jbmr.3426Evidence From a Two-Sample Mendelian Randomization Study and a Candidate Gene Association Study

Nicolien A van Vliet,1 Raymond Noordam,1 Jan B van Klinken,2 Rudi GJ Westendorp,1,3

JH Duncan Bassett,4 Graham R Williams,4 and Diana van Heemst1

1Department of Internal Medicine, Section of Gerontology and Geriatrics, Leiden University Medical Center, Leiden, the Netherlands

2Department of Human Genetics, Leiden University Medical Center, Leiden, the Netherlands

3Department of Public Health and Center for Healthy Aging, University of Copenhagen, Copenhagen, Denmark

4Molecular Endocrinology Laboratory, Department of Medicine, Imperial College London, London, UK

ABSTRACT

With population aging, prevalence of low bone mineral density (BMD) and associated fracture risk are increased. To determine whether low circulating thyroid stimulating hormone (TSH) levels within the normal range are causally related to BMD, we conducted a two-sample Mendelian randomization (MR) study. Furthermore, we tested whether common genetic variants in the TSH receptor (TSHR) gene and genetic variants influencing expression of TSHR (expression quantitative trait loci [eQTLs]) are associated with BMD. For both analyses, we used summary-level data of genomewide association studies (GWASs) investigating BMD of the femoral neck (n.32,735) and the lumbar spine (n.28,498) in cohorts of European ancestry from the Genetic Factors of Osteoporosis (GEFOS) Consortium. For the MR study, we selected 20 genetic variants that were previously identified for circulating TSH levels in a GWAS meta-analysis (n.26,420). All independent genetic instruments for TSH were combined in analyses for both femoral neck and lumbar spine BMD. In these studies, we found no evidence that a genetically determined 1–standard deviation (SD) decrease in circulating TSH concentration was associated with femoral neck BMD (0.003 SD decrease in BMD per SD decrease of TSH; 95% CI, –0.053 to 0.048; p.0.92) or lumbar spine BMD (0.010 SD decrease in BMD per SD decrease of TSH; 95% CI, 0.069 to 0.049; p.0.73). A total of 706 common genetic variants have been mapped to the TSHR locus and expression loci for TSHR. However, none of these genetic variants were associated with BMD at the femoral neck or lumbar spine. In conclusion, we found no evidence for a causal effect of circulating TSH on BMD, nor did we find any association between genetic variation at the TSHR locus or expression thereof and BMD. © 2018 The Authors. Journal of Bone and Mineral Research Published by Wiley Periodicals, Inc.

Appendix 2

Serum Thyroid-Stimulating Hormone Concentration and Morbidity from Cardiovascular Disease and Fractures in Patients on Long-Term Thyroxine Therapy

Robert W. Flynn, Sandra R. Bonellie, Roland T. Jung, Thomas M. MacDonald, Andrew D. Morris, and Graham P. Leese

Ninewells Hospital and Medical School (R.W.F., R.T.J., T.M.M., A.D.M., G.P.L.), University of Dundee, Dundee DD1 9SY, United Kingdom; and School of Accounting, Economics and Statistics (S.R.B.), Edinburgh Napier University, Edinburgh EH14 1DJ, United Kingdom

Context: For patients on T4 replacement, the dose is guided by serum TSH concentrations, but some

patients request higher doses due to adverse symptoms.

Objective: The aim of the study was to determine the safety of patients having a low but not suppressed serum TSH when receiving long-term T4 replacement.

Design: We conducted an observational cohort study, using data linkage from regional datasets between 1993 and 2001.

Setting: A population-based study of all patients in Tayside, Scotland, was performed.

Patients: All patients taking T4 replacement therapy (n 17,684) were included.

Main Outcome Measures: Fatal and nonfatal endpoints were considered for cardiovascular disease, dysrhythmias, and fractures. Patients were categorized as having a suppressed TSH (0.03 mU/liter), low TSH (0.04–0.4 mU/liter), normal TSH (0.4–4.0 mU/liter), or raised TSH (4.0 mU/liter).

Results: Cardiovascular disease, dysrhythmias, and fractures were increased in patients with a high TSH: adjusted hazards ratio, 1.95 (1.73–2.21), 1.80 (1.33–2.44), and 1.83 (1.41–2.37), respectively; and patients with a suppressed TSH: 1.37 (1.17–1.60), 1.6 (1.10 –2.33), and 2.02 (1.55–2.62), respectively, when compared to patients with a TSH in the laboratory reference range. Patients with a low TSH did not have an increased risk of any of these outcomes [hazards ratio: 1.1 (0.99 –1.123), 1.13 (0.88 –1.47), and 1.13 (0.92–1.39), respectively].

Conclusions: Patients with a high or suppressed TSH had an increased risk of cardiovascular disease, dysrhythmias, and fractures, but patients with a low but unsuppressed TSH did not. It may be safe for patients treated with T4 to have a low but not suppressed serum TSH concentration. (J Clin Endocrinol Metab 95: 186–193, 2010)

in reply to holyshedballs

Is it OK to copy this for future reference, holyshedballs? I won't know till March but think I might need the information :-)

holyshedballs profile image
holyshedballs in reply to

Absolutely, go ahead. Anybody can use or adapt it.

in reply to holyshedballs

Cheers and thank you. I didn't think you would refuse but it seemed polite to ask! x

in reply to holyshedballs

The worse mistake I've done through my 2.5 yr adventure without a thyroid is had a Dexa Scan, regret this everyday.

I'm a middle aged female with life long autoimmune disease that forced me into many,many years of steroid use to include injections and then surgical menopause early in my life. I had a Dexa Scan 2010 (6yrs) before thyroidectomy that showed I had mild osteopenia.....fast forward to (8yrs) from first dexa scan to 2nd dexa scan and the 2nd Dexa Scan still revealed mild osteopenia hardly changed.......Now I have to constantly deal with Endos trying to reduce my thyroid meds, they believe LOW TSH cause osteopenia and osteoporosis. If the endos had it their way I would be thyroidless, without meds.

I actually asked one Endo if her end game was to kill me by taking away all my thyroid meds based on TSH....she just looked at me like I was nutz.

Dexa scan = Endo battle, constantly.

holyshedballs profile image
holyshedballs in reply to

Yes that can be an issue also but bear in mind that there is no evidence to prove that OP is caused by low TSH, in fact the 1st article in the appendix proves there is no link between TSH and BMD. Here is the link so you can download it and give it to your Endo and GP. ncbi.nlm.nih.gov/pubmed/295...

I mentioned DEXA because GPs say they are worried about OP yet do nothing to determine a patients BMD before attempting to reduce their dose. it is to highlight their lack of logic.

Helvella, (I think) also posted an article about made up diseases particularly with regard to osteopenia. I also think that sub clinical hyperthyroidism is a made up disease, the clue being in the title. It's not to be poo pooed but kept an eye on until symptoms develop - in my view.

in reply to holyshedballs

Your absolutley right the tsh has nothing to do with osteopenia but, try telling the person that holds the prescription pad....not fun.

holyshedballs profile image
holyshedballs in reply to

We have to be resolute. Right is on our side. Make sure you have the support of your loved ones.

It is not logical to base therapy on TSH. The courts have said that any procedure followed by a doctor has to be logical - the Bolitho case.

Show them the paper that shows TSH has nothing to do with OP. Threaten to make formal complaints to the CCG and to the GMC if your dose is not maintained if necessary. That is why I wrote the letter - to provide the ammunition to educate the person who holds the prescription pad.

in reply to holyshedballs

"I also think that sub clinical hyperthyroidism is a made up disease, the clue being in the title."

I could barely function - sometimes unable to even string a sentence together - when my TSH was less than 6 and T4 still in range (No T3 test of course!) To call it "Subclinical" is a joke!!!

12-345 profile image
12-345 in reply to holyshedballs

Thank you so much for this.

Your results are within range so unless your have clinical signs such as palpitations, high temperature and pulse rates you are not over medicated. But I don’t expect you’ll be able to convince your doctor about that!

Thank you everyone for your feedback and stories - much appreciated!

I had my Levo reduced, although by half the usual amount, from 100mcg to 100/75 alternate days, because my TSH was 0.01. T4 was within range but only just under the top value. Not sure if I feel any better or not (Have been on this reduced dose for 5 and a half weeks). I didn't feel brilliant on 100mcg, though vastly better than when first started on Levo. My symptoms aren't obviously improved, but I'm not sure if they have got worse either. They are just different. I don't get as hot as before (had hot flushes for years, which slightly complicates things!) and my concentration ability is possibly slightly improved. But I also had an episode of irregular heartbeat last week, though it hasn't recurred so far and I felt fine otherwise.

The problem is that the one who is overseeing my treatment (the practice pharmacist not the doctor) says that the symptoms on 100mcg were due to overmedication because hypo and hyper symptoms do overlap a lot. Which is true. So I decided to wait till the next blood test in March (TSH only!) . I asked for a T3 test in case I wasn't converting properly, but the reaction was as if I had said a rude word! So I have ordered a Medichecks one as well

To be fair she has been good in other ways (such as giving a Levo increase based on symptoms even though TSH dropped within range. The problem is more to do with faulty training and perpetuation of medical myths in spite of the evidence. As well as the cost of T3

Excuse the long post above, but we all have different experiences and one thing or another might resonate with someone. Also when my concentration is poor I get even more long-winded than usual!!! :-D

I know exactly what you mean my TSH is this too , l use NDT and feel good but every time l

go to the doctors for other things and even when he said he would just observe l am dreading my app tomorrow

because l know he will ask me to have another blood test

What’s even more frustrating on their forms for bloods he states l take leverthyroxine?

Hi Blossom,

If you are taking T3 then your TSH will be supressed.

Mine is always supressed, I've just had a blood test done and it is 0.004. The NHS don't usually do the T4 and T3 these days, but I think they were so worried at this that they did the others! My T4 is 11.3(9-19) and the T3 3.5 (2.9-4.9).So looking at those two you can't say I am having too much medication!

My Doctor is used to it now as I have known her for years,so just accepts it is always very low and doesn't worry about it. I have no thyroid at all, so I think that as I have been on the T3 for 20 years my body has just stopped working properly.

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