I take 100mcg T4 and 20mcg T3. My last test with medichecks showed my TSH is slightly suppressed, TSH 0.084 mIU/L - range 0.27 - 4.20, but my T3 is normal, FT3 5.74 pmol/L - range 3.10 - 6.80 (FT4 a little low)
People on here kindly explained to me that I do not need to be concerned about the suppressed TSH (know my GP will be if she knew) as TSH will be low as am taking T3 and T4 so TSH doesn’t need to be active.
I got hold of the 2010 interview with Dr Tuft in Pulse Magazine as recommended on here and was surprised to see in his answer to question 6 that he said if taking T3 and T4 the serum TSH should be normal? In an earlier question he said slightly suppressed TSH on T4 levothryoxine only was ok. I was really surprised he said this and would appreciate any thoughts by anyone ? diogenes , hope to ok tag you as know you are good on this. Thanks in advance. This was his reply:
‘Even while taking the slightly higher dose of levothyroxine a handful of patients continue to complain that a sense of wellbeing has not been restored. A trial of levothyroxine and tri- iodothyronine is not unreasonable. The dose of levothyroxine should be reduced by 50μg daily and tri iodothyronine in a dose of 10μg (half a tablet) daily added.
While taking both hormones it is important serum TSH is normal and not suppressed. If the patient is still dissatisfied it should be made clear that the symptoms have nothing to do with thyroid disease or its treatment and perhaps issues at home and in the workplace should be addressed.’
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anniekims
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Dr Toft has always given precedence to blood tests over signs, symptoms and the responses to treatment. It's difficult to assess fT3 when patients are taking T3 so I suspect this underlies his emphasis on TSH. Although he has a recent change in emphasis he still holds to the same principles as a decade ago (he is entitled to). I think this is all wrong and lacks scientific method, the data (patient signs, symptoms and response) should override theory. The suggestion to replace 50μg levothyroxine with 10μg triiodothyronine (sic) is also wrong. Celi shows the ratio should be closer to 3:1, not 5:1 ncbi.nlm.nih.gov/pmc/articl... . This is not unusal, the large majority of endocrinologists are unable to grasp pharmacokinetics.
The last line of this made me smile as this is very nearly verbatim what he said to me at an appointment last September.
I was really disappointed as until sept 17, I was well. Fit, healthy, strong ( was working as a self employed gardener since I had kids) sensible diet, low stress (until that year but had passed) didn’t drink excessively or smoke.
Nothing in life should have been detrimental and the only thing that was wrong me me was hashis but yet he suggested other things may be to blame.
I am sorry. I hate that kind of thinking by docs that if the treatment isn’t working then it must be some psychological issue, stress. It’s fobbing the patient off and utterly demoralising when you know there are no work or home issues.
I may try gf. I don’t really see how it never affected me before, so why should it be now? My antibodies are quite low, a lot lower than when I was ill without any change in diet. I know they fluctuate though.
Murphysmum , it’s a fair point if gluten sensitivity is a problem why is it only affecting you in the last year when you have had thyroid problems for 13 years? I am not knowledgeable at all, so just thinking out loud could it be that before your body wasn’t wrongly reading gluten protein as something to attack but since your period of severe stress your body has got confused? Although you say your antibodies are relatively low currently. Sorry I am out of my depth here on gluten crosseover etc.
As always these statements are blanket ones. They apply to most people, even those on combination therapy. By that I mean from Ito's work, that TSH down to about 0.03 is no problem even for Toft. The trouble with undetectable TSH (really the amount below the sensitivity limit of the assay) is that from untreated hyperthyroidism, knowledge of undetectable TSH equates very firmly with overactivity of the gland and the resulting bad consequences. But undetectable TSH on treatment is not the same. In hyperthyroidism, virtually always FT3 is above normal, whether or not FT4 is. In treatment, the FT3 remains within the reference range with undetectable TSH, a very different thing. FT4 elevation to get adequate FT3 can suppress TSH. So, let's go back to simple questions. First what is the principal danger of hyperthyroidism? Answer high FT3, not particularly suppressed TSH, which is a response. What is the principal danger of over treatment? Answer, again high FT3. So what's sauce for the hyper goose is sauce for the overtreated gander. Suppressed TSH should be avoided if it is leading to overtreatment but not necessarily otherwise if it can't be helped. Why do we hear of patients longterm on either T4 monotherapy or combination or T3 only with never any readable TSH over decades and no ill effects? I'm married to one (50 years treatment and counting).
Thank you diogenes for your detailed reply and reiterating a suppressed TSH isn’t a problem when taking thyroid medication as long as T3 is in range and showing no clinical symptoms of being over medicated. This is evidenced by your partner and countless others who have a suppressed TSH for years on thyroid meds with no problems.
So to check I have understood you correctly probably the reason Tuft believes a suppressed TSH is ok if on T4 monotherapy is because for some patients to have sufficient levels of T3 converted by the body from T4 on T4 monotherapy the person might need high T4 levels which will of course suppress the TSH. However, if a patient is taking T3 and T4 there is no need to have the T4 high to make enough T3 as the patient is supplementing with oral T3 and in turn the TSH doesn’t need to be suppressed? Am I right to think if he is not worried the TSH is suppressed on T4 only it doesn’t make sense to be worried if it is suppressed also on T4/T3 as surely a suppressed TSH on medication - as long as FT3 is not above range - is either ok or not ok? Thank you.
Thanks for a clear description of what I believe is Dr Toft's view on why a suppressed TSH on L-T4 only therapy is OK. I believe it is essential to take the analysis a step further. We can't just measure fT3, we need to ask the question 'where is the T3 coming from?'. In my view not all T3 is equal. In the body T3 comes from thyroidal secretion and deiodinase in various tissues.
Type-1 deiodinase (D1) converts T4 to equal amounts of T3 and reverse T3. It is thus inefficient in that half of the T4 is converted to inactive rT3. D1 is up-regulated when thyroid hormone levels are high and takes place primarily in the liver and kidneys. It contributes to circulating T3 levels.
Type-2 (D2) converts T4 to T3, it is the major source of circulating T3. D2 is responsible for LOCAL regulation of T3 levels in organs such as the pituitary, brain, skeletal muscle, brown fat and possibly the heart. D2 is up-regulated when thyroid hormone levels are low and TSH is high. The exception is the pituitary where D2 activity has little variation.
If the thyroid starts to fail fT4 falls, TSH rises considerably and fT3 is maintained until thyroid failure is more severe. D2 activity is increased in an attempt to maintain T3 levels.
If high doses of L-T4 are given the pituitary is able to convert T4 to T3 efficiently using D2. The high doses of L-T4 will cause a shift from D2 to D1 in peripheral tissues. This has two effects: -
1. The conversion of T4 to T3 and rT3 by D1 in peripheral tissues is less efficient.
2. There will be less local T3 in tissues such as the brain that rely on TSH stimulating D2.
For patients who have straightforward primary hypothyroidism this may not be a problem, they may have sufficient flexibility that they can manage OK in this scenario.
But. Sometimes TSH is not truely suppressed. Sometimes patients have a low TSH with average or low normal fT3 and fT4, what is called a 'down-regulated hypothalamic pituitary thyroid axis'. This can happen during a period of thyrotoxicity or due to severe depression or starvation diets. We can predict what will happen in this patient group. If we give them L-T4 therapy their TSH will become suppressed much sooner than normal. As a consequence they will have much less D2 activity than normal patients and tissues that rely on D2, such as the brain, will have local hypothyroidism. If we give more L-T4 although D1 activity will increase circulating T3 levels D2 activity will reduce. Perhaps this is why some patients with low fT3, fT4 and normal TSH say they feel worse when given L-T4.
What if we give some L-T3? Enough to restore normal fT3 levels? This will help, but not make the patient well. The L-T3 will lower TSH and so reduce D2 activity. Those tissues that rely on D2 acitivity will still have local hypothyroidism. The brain gets 80% of its T3 from D2 conversion of T4 and 20% from circulating T3. Restoring circulating fT3 to normal will give the full 20% whack to the brain but the brain will not derive the full 80% from D2 due to the abnormally low TSH. This patient group responds to high doses of L-T3, doses that deliver above average fT3 levels. The patients feel well. However, with high circulating fT3 levels those tissues that are less reliant on D2 (such as the heart) will be thyroxtoxic.
It is not sufficient to observe circulating fT3 levels. We must try to deduce where the T3 is coming from.
Hi jimh111 thanks for your comment. I have been reading it multiple times but still do not understand it. This is due to me being really bad at science.
I will come back and try and read it again tomorrow but can I just ask you some things tonight please as the answers may help me understand? When you write in paragraph nine the sentence ‘sometimes TSH is not truly suppressed, sometimes patients have a low TSH’, does low TSH mean it is not quite suppressed but in a lab range the TSH would read at the lowest end of the normal range?
Also could you explain further what you mean by saying some people are flexible enough to manage not optimal DI or D2 enzyme activity when on LT4? By flexible do you mean they will still have enough circulating T3 in the brain and other peripheral tissses that they can manage with the reduced DI and D2 enzyme activity?
And are you concluding that Dr Tuft does not think the TSH should be suppressed when taking LT3 as well as LT4 (whilst being ok the TSH is suppressed when on LT4) because he is worried that certain tisssus such as the heart which don’t rely on D2 activity will end up thyrotoxic? However, if the person is taking just LT4 as less is needed there won’t be the risk of thyrotoxicity in tisssus that are not as reliant on D2 activity?
Finally, even though Dr Tuft prefers to not have the TSH suppressed whilst on L-T3, monotherapy or combo with L-24, for the fear of thyrotoxity in certain tissues, you still would argue that is the clinical symptpms that should be the deciding factor? Thank you!
anniekims, some clarification. If a TSH is very low or undectable it is described as 'suppressed'. This is a loaded term, the TSH should really be described as very low. TSH may be very low because it is truely suppressed, the patient has high thyroid hormone levels that have pushed the TSH all the way down. However, in some patients TSH is low or undetectable because the pituitary is underperforming, the patient may have averaging fT3 and fT4 but their TSH is really low instead of normal. In this case I believe they will not have normal deiodinase activity, due to the inappropriately low TSH.
In theory at least (and most likely in practice) a patient on L-T4 only therapy will have reduced T3 levels in some tissues. Many patients do well on L-T4. In real life we don't need perfect levels of every substance in the body. It seems that many patients can do well on L-T4 only even if their T3 levels is not ideal in all tissues. The body has built in flexibility. Some patients with the same thyroid disorder, perhaps with different genetic makeup, do not do well.
The above post from diogenes explains what I think is Dr Toft's objection to a 'suppressed' TSH when using combined therapy. i suspect Dr Toft is also looking at studies that show that a 'suppressed' TSH when on levothyroxine isn't associated with adverse outcomes whereas in hyperthyrodism, which usually produces high T3 levels, there are bad outcomes. Hence he is presumably concerned that giving T3 will be dangerous if it starts to suppress the TSH.
My point is that if you see a very low TSH you should try to work out is it due to suppression, a result of too much thyroid hormone or is the pituitaty underperforming. The latter situation disrupts the whole thyroid hormone system and presents difficult treatment challenges. My view is that in this situation we are forced to deliver higher circulating T3 levels to overcome hypothyroid signs and symptoms but that this carries risks. Having accepting the need for this therapy we should stike a sensible compromise between giving the patient a reasonable life and doing what we can to minimise risks. Endocrinologists tend to deny the existance of this form of hypothyrodism and patients tend to deny the risks.
I have a few problems with this. First when the thyroid is failing, the working remnant is very important in forcing production of T3 directly by the gland and not conversion changes so much. The gland is the conductor of the body's conversion through its direct T3 production and this will continue until the last moment, when the gland is now dead and there can be nothing other than using up the T4 supplies on the proteins, which will take about a week. When taking T4, conversion is indeed compromised because more T4 is needed to get a given T3 and this partly suppresses the conversion process. But therapy in any form is a compromise, and different from natural production, so the principal action is to keep FT3 normal within range and highish up in the range + patient presentation symptom analysis as an arbitrary diagnostic.
diogenes, I'm struggling to understand your comment. To simplify, maybe just consider the situation where the thyroid has completely packed in. For patients who have a fully functioning hypothalamic pituitary thyroid axis - i.e. their TSH is about where you would expect it for given hormone levels - the treatment you describe will work and is generally accepted by endocrinologists. That is, sufficient L-T4 is given to achieve a high normal fT4, an fT3 a little above average and a TSH that may be low.
In this scenario tissues that obtain their T3 from the blood will be slightly thyrotoxic and tissues reliant on D2 for local regulation will be slightly hypothyroid (the low TSH reducing D2 activity). By and large most of these patients will be fine.
If however, similar patients have an underperforming axis, an inappropriately low TSH will reduce D2 activity. This can be corrected by prescribing L-T3, sufficient to 'push' more T3 into those tissues such as the brain which rely on D2. If we do this circulating levels of T3 will be high, perhaps above the upper limit of the reference interval. This will be too much for tissues that do not express D2 and are reliant on circulating T3. These patients need high doses of L-T3 (e.g. 40 mcg daily) but there are risks. The trick is to be able to identify this patient group and ideally correct their pituitary function.
I think this group falls under T3 resistance in vairous forms. Resistance can come from problems with cell entry as well as problems with general response to a given dose. Furthermore, TSH in health can indulge in both feedback (HPT axis) and feedforward (the T3-TSH shunt in the thyroid itself).. You lose the thyroid and the feedforward part is lost.
I'll try a bit more clarification. I view the body as having organ-specific needs for T3. But D2 conversion + direct T3 supply from the thyroid together produce what I would call a "baseline" T3 production (cf a nuclear power station). This is set to supply adequately T3 for those tissues that don't convert. But overlying this are local extra needs supplied by appropriate extra controlled conversion eg brain. So I think it useful to know the baseline as a rough indicator of overall satisfaction. The baseline is of course represented in the blood. This is where T3-only therapy becomes tricky as without T4 at all, there is no method of locally fine-tuning. Wherever possible I would see even a smidgin of T4 being useful to help produce the extra local requirements, without overdosing elsewhere.
I agree, I take 50 mcg L-T4 even though I find marginal benefit. I'd rather have some T4 available just in case it is useful.
I plan to set up a website by the summer which will include these concepts, I hope the ability to include some diagrams will make it much easier to understand. I feel thyroid hormone therapy needs to go a step further, attempt to see and correct what is happening at tissue level.
Since patients on T3 only seem to "get along" OK with careful monitoring, I wondered if for them over the long term, the extra needs of the particular tissues could obtain this through increasing the local concentration of receptors in the cells. Input of T3 is given by K X P where K is the association constant and P the receptor concentration. There is a parallel in late pregnancy, where oestrogen-stimulated increases in receptor concentration occurs so that to get euthyroid uptake into the cells, there is a drop in FT4 levels that exactly balances out the increase in cell receptors.
Interesting. I must avoid the temptation to digress to far. It's also possible that tissues that are rendered thyrotoxic by this therapy reduce the concentration of receptors. This is a known problem in toxicology studies. Traditionally high doses of substances are given to rodents to look for poisoning or cancer risk. When testing potential endocrine disrupting chemicals (EDCs) this is a problem because the very high doses used suppress receptors and the endocrine disruption that occurs in real life is not detected in the study.
The ideal solution is to cure the source problem but until then we need higher doses of thyroid hormone to resolve signs and symptoms, an imperfect therapy.
diogenes , thinking about it further if I have understood you correctly if Dr Tuft is worried a suppressed TSH when taking T3/T4 could be a sign the person is over medicated, wouldn’t the solution be to test both FT4 and FT3 and if the levels are within range then he doesn’t need to worry the FT3 has got too high?
diogenes , sorry i forgot to ask above also, can you tell me what ‘“lto’ means in the sentence in your first reply to me that says ‘By that I mean from Ito's work, that TSH down to about 0.03 is no problem even for Toft.’ Thank you.
Ito is a Japanese scientist who has shown that biochemical euthyroidism on T4 alone is accompanied by reduced TSH - in his study 0.03-0.5. This is lower than the healthy range 0.5-4.0
‘Suppressed tsh should be avoided if it is leading to overtreatment’. Does this mean if overtreatment is leading to suppressed tsh, it should be avoided? I am confused by information on this forum, it seems to be very conflicting. Is this just because no one atually knows??? 😫
Sorry Hidden i don’t know. I presume same risks as if a hyperthyroid patient was untreated so googling that might give you some idea? I hope Diogenes may give you an informed answer as opposed to my ignorant one!
Ok thanks. If I take liothyronine and check my free T3 12 hours or so after my last dose as suggested on here and that is in range is that ok even if my tsh is below range? Or should I check it a few hours after dosing when levels might be higher? If my levels are above range after dosing, but then settle is this ok? Or do I run the risk of hyperthyroid type complications over a longer term?
Taking T3 is different from taking T4. With T4 only, the T4 rises a little after dosage but changes only slowly over the day and not by very much. With T3, this hormone only having a half-life of 1 day (50% lost in 1 day), you get spikes in FT3 levels immediately after taking a dose, so the "ride" throughout 24 hours is bumpier than with T4. This doesn't matter because the body's response is slow enough for the effect of the spikes to be evened out. The aim should be that the average FT3 through the day doesn't exceed the top end of the range. Momentary spikes don't really matter so long as they aren't hugely above normal.
I should add that Toft has come some way from his original stance, and has only a little further to go. But it's difficult to swallow all the unpleasant medicine in one go (admit fault). Academics/medics are as a class rather bad at that.
Thanks SlowDragon did he reply why he still believes TSH should not be suppressed on T3/T4 therapy when as you say most find on T3 meds their TSH is suppressed?
In the early 1990s I was involved in the initiation of guidelines in medicine, in the UK at least, when President of the Royal College of Physicians of Edinburgh. It was one of many errors of judgement in my long professional career. Their development was encouraged by government, during one of its recurrent financial difficulties, in order to deliver a higher level of healthcare throughout the country without having to replicate major teaching hospital services in smaller and often geographically remote hospitals. The unforeseen consequence is that guidelines have assumed a clinical and legal importance far beyond that which was ever intended by their protagonists.
I have read those words by Toft. I think he changed his mind since the early 90’s about some needing T3 but from what Slaydragon says it sounds like when quizzed last November he still isn’t keen on the TSH being suppressed when on T4/T3 therapy. But hear you lots of thinking can change over time.
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