Had blood test last week
Results
FT3 4.4 pmol /L (3.8- 6.0)
FT4 18.3 pmol (7.5 -21.1)
TSH <0.01mu/L ( 0.35 - 3.5 )
Dr wants to reduce my dosage from 150 mcg. to 25 mcg.
I have a phone appointment on Friday.
Can anyone make suggestions as to how I fight to leave dose as it is as I still have many hypo symptoms.
Thanks. Janet
Refuse point blank
How much levothyroxine are you currently taking
Do you always get same brand of levothyroxine
Which brand
Ft4 is only 77% through range
Ft3 is extremely low at 27% through range
Helpful calculator for working out percentage through range
You have terrible conversion
First step is to Insist vitamin testing
Low vitamin levels results in poor conversion of Ft4 to Ft3
Presumably you have Hashimoto’s? ....Autoimmune thyroid disease diagnosed by high thyroid antibodies
All thyroid tests should be done as early as possible in morning before eating or drinking anything other than water and last dose levothyroxine 24 hours before test
Is this how you did this test?
When were vitamin D, folate, ferritin and B12 last tested?
What vitamin supplements are you currently taking?
Low Ft3 tends to lower vitamin levels
Low vitamin levels makes conversion of Ft4 to Ft3 worse and tends to lower TSH
Getting all four vitamins tested and OPTIMAL by supplementing may help improve Ft3 and TSH
The aim of levothyroxine is to increase dose upwards until Ft4 is in top third of range and Ft3 at least half way through range (regardless of how low TSH is)
EXTREMELY important to have optimal vitamin levels too as this helps reduce symptoms and improve how levothyroxine works
If Ft3 remains low once all four vitamins are optimal then, like many other people on levothyroxine you ar3 likely to need addition of small doses of T3 prescribed alongside levothyroxine
Email Thyroid UK for list of recommend thyroid specialist endocrinologists who will prescribe T3 .......NHS and Private
tukadmin@thyroiduk.org
I’m currently on150mcg.I’m sure no one should drop down from 150mcg to25mcg!
Test done according to guidelines on here.
I do have Hashimotos.
I’ve not had vitamins tested for at least 3 years.
I did buy some T3 in Crete, while on holiday a few years ago.
Made a big difference to symptoms.
I was told a couple of years ago , the last time they tried to reduce my levothyroxin, that I would get osteoporosis with a suppressed tsh.
I asked how they would know that as I have never had a bone density test.
I also pointed out that FT3 and FT4 were low in range!
I will check list for recommendation of endos.
Thanks for help
Janet.
Low Ft3 can cause osteoporosis
Many people find bone density IMPROVES with addition of T3
But TSH is almost always suppressed when taking any dose T3
T4 is biologically more suppressive of TSH than T3 in all physiological amounts In the healthy thyroid TSH induces faster rate of increase of T3 than T4 because it is the body’s fine tuning / urgent response to temporarily unmet thyroid hormone need and it is primarily a sustained systemic rise in T4 that eventually lowers TSH. Logically then and given normal blood levels of ft3, suppressed TSH probably indicates excess t4 and this may not need much of a reduction to ameliorate. Although TSH is likely going to run lower in thyroid hormone replacement than endogenous glandular supply there is a big question about how low exogenous thyroid should push TSH.... TSH does not only function on the thyroid gland, there are TSH receptors elsewhere, especially in bone marrow osteoblasts and evidence that it affects intra-cellular t4 t3 conversion which beg the question of what happens without normal circulating levels of TSH.... it seems a much safer bet to manage TSH to near or just under normal healthy levels by adjusting thyroid hormone replacement in combinations of t3 and t4 and by dose size and timing. Large single doses of levothyroxine, which are completely unphysiological by the way, are likely to be more suppressive of TSH than split dosing to mirror a more physiological thyroid output which is less likely to confuse the hypothalamus and pituitary response to circulating t4.
It’s interesting that splitting the dose of T 4 is suggested.
All thyroid output data from healthy individuals confirms the pulsitile production of TSH and T4 T3 response over 24 hrs while other research has shown that excess T4 has a primary negative feedback loop on T3 conversion. Furthermore, Levothyroxine is absorbed as free T4 whereas thyroidal T4 is protein bound for transport and storage so taking an entire 24hr supply of T4 in one go seems like complete madness! It’s only because it’s easy and more predictable from a pharmacological POV. But life is that simple!.....
Isn’t that simple!
Totally simple, I’mRight there with ya Hashihouseman lol
I presume you mean doc wants to reduce your dose to 125mcg rather than to 25, as this would be very ill advised! Anyway, he is going by your tsh rather than your t4/t3 levels, neither of which are particularly high...79%and 27% respectively through their ranges. Your conversion of t4 to t3 is not brilliant, and I would offer the thought that your lingering hypothyroid symptoms are as a result if this. However, getting liothyronine on the nhs is difficult. Perhaps one of the admin will suggest ways to improve your conversion by eg getting vitamins and minerals to an optimal level. In the meantime I’d try and resist that reduction in meds.
Thanks for reply. Dr wants to reduce to 25mcg!! Test was done as per guidelines on here. They all seem to be frightened by a suppressed tsh. One told me I’d get osteoporosis. My response to that was ‘ how will you check that as I’ve never had a bone density test?
Vitamins were probably checked 3-4 years ago.
I did buy liothyronine when on holiday in Crete a few years ago. It was €1 for 28 tablets. It was like a magic wand had been waved over me. Not sure why NHS can’t source it at a similar price.
I’m going to resist dropping down the levothyroxin at all. Not easy when doing it over the phone.
I may ask to see an endo that specialises in thyroid matters. Last one I saw was a diabetes specialist!
Thanks Janet.
Here's a link to a Thyroid UK page about the Myths of Hypothyroidism. The last one is "The Myth that a Suppressed TSH Leads to Osteoporosis".
thyroiduk.org/help-support/...
Would your doc take any notice if you emailed him/her that link before your appointment?
Thanks for link.
I’m not even sure that I’ll speak to a Dr. It could be a nurse practitioner!
So when did you last take any T3?
heart.bmj.com/content/84/4/...
Over replacement with thyroxine?
There is some concern that administering thyroxine in a dose which suppresses serum TSH may provoke significant cardiovascular problems, including abnormal ventricular diastolic relaxation, a reduced exercise capacity, an increase in mean basal heart rate, and atrial premature contractions.12 Apart from an increase in left ventricular mass index within the normal range, these observations have not been verified.13 Moreover, there is no evidence, despite the findings of the Framingham study, that a suppressed serum TSH concentration in a patient taking thyroxine in whom serum T3 is unequivocally normal is a risk factor for atrial fibrillation.
I last took T3 at least 3 years ago . I don’t have atrial fibrillation. My resting heart rate is around 55-60. Blood pressure 121/79.
So refuse to reduce dose
Ask/insist on vitamin testing
Ask for DEXA scan for osteoporosis, ultrasound scan of thyroid and referral to thyroid specialist endocrinologist
Get list of recommended endocrinologists from Thyroid U.K., and ideally have a name of endocrinologist you want to see at referral when talking to GP
Consider getting Dio2 gene test privately
(Not available yet on NHS)
thyroiduk.org/getting-a-dia...
Osteoporosis and LOW Ft3
Underline these results
Ft4 is only 77% through range
Ft3 is extremely low at 27% through range
These clearly show you are NOT over treated
Yes ask to see a new Endo. That advice is just odd. I'd push for T3 due to the poor conversion. Find the name of a friendly local one ftom Dionnes list and phone them up and see if they're taking on patients then suggests that to your doc. You'll be very poorly if you reduce that much - tell him you'd just have to self source if he does that but you'd prefer to remain under his care.
Great suggestion JAmanda.
Where can I find Dionne list please?
Email Thyroid UK for list of recommend thyroid specialist endocrinologists who will prescribe T3
...NHS and Private
tukadmin@thyroiduk.org
here is a letter I wrote for someone else with their T3 medication. you can replace T3 with T4.
please copy and paste in to you word/pages application and amend as appropriate. its slightly out of date but I don't have time to amend it at the moment,
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 liothyronine (T3)
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 T3.
During the appointment I told you that I did not want to reduce my dose of T3 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 T3.
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 T3 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:
A.The doctor and patient make an assessment of the patient’s condition, taking into account the patient’s medical history, views, experience and knowledge.
B.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.
C.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
D.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 T3, my signs and symptoms will return.
You did not assess me for signs of over treatment or refer to my blood tests for T3 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 T3 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 T3.
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 T3 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 T3 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 T3 for me as an individual. I don’t have the signs or symptoms of too much T3 and/or T3. My blood tests show I am not outside the reference range for T3 and/or T3. 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 T3
I am unaware of any guidance to unilaterally reduce a patients dose of T3 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 T3 and/or T3 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 T3 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 T3/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 T3 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
Sign here
Type your name here
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 T3 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 T3 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 T3 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 T3 to have a low but not suppressed serum TSH concentration. (J Clin Endocrinol Metab 95: 186–193, 2010)
WOW!! I wouldn’t want to mess with you. It would be easier just to prescribe the drug. Nic job
Having said that I could do what that type of letter as i would like to try PTU instead of carbimazole as I have Graves. carbimazole makes me really sick and I’ve had a psychiatrist appt to say I’m fully aware of my decisions of not taking the carbimazole and risking my health. Still no options forPTU
I pleased to report that I spoke to a locum doctor, by phone, yesterday. He told me that the lab report said I was over medicated as my TSH is suppressed! I pointed out that both T4 and T3 levels were not showing as over the recommended limit! He agreed and offered to leave me on my current dose of 150mcg! He also said he didn’t know much about Hypothyroidism! Hopefully he’s learnt a little more now, and knows to check other parameters as well as TSH!Thanks for all help.
Janet.
Blood Test results and the doctor is reducing my thyroxine.
Latest finger prick test
Oops on Lio dose - should I reduce?
Right Dose of Levothyroxine?
Thyroxine - GP wants to reduce dose!
