Just back from the endo who I got sent to, to try and hold on to my T3 which I have been on for 4 years (ie T3 only), following the CCG debacle telling our local GPs that they may not prescribe T3 any more.
Luckily this endo (happy to name him, but I think you prefer not to here?), is sympathetic to T3 users, and has done some useful research on the D102 enzyme. He had already written to the CCG who thankfully have now backed down as long as the T3 patients are reviewed.
Anyway, although all the rest of his patients are on a combo of T3/T4, and I am the only one T3 only (I originally saw a different endo, but he has moved on), he was happy for me to stay on T3 only but felt that my dose of 55mcg (spread over 3 doses) was too high because my TSH is below range. He said he was quite happy for it to be low but would prefer for it to be detectable, although he did say ultimately that the risk was mine (ie re osteoporosis and Atrial Fibrillation). As a result I am going to try to reduce it to 45 mcg (in 3 doses) and see how I do and be retested in a month's time.
Somehow I thought I had read here that with T3 the TSH was always suppressed, but I am not sure now, and if I did, why is it? I did challenge him on this but he said that he found the opposite, which rather threw me. What do people think about it being below range? I have recently worked out that I am Histamine Intolerant, and I am now thinking that some of my symptoms (I ended up with an ME/CFS diagnosis some 8 years ago on top of the hypothyroid one 20 years ago) are down to the histamine intolerance, so I may be OK on the lower dose anyway.
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Agapanthus
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T3 does suppress TSH if you take enough of it - and it doesn't take much to suppress the TSH. But that's because you don't need it.
TSH = Thyroid Stimulating Hormone. It has two jobs :
1) It stimulates the thyroid gland to make more hormone when he pituitary detects that levels are low. If your gland cannot respond, the TSH gest higher and higher. But, if the gland is never going to respond, for whatever reason - or if your gland has been removed/killed off - we need to take some form of thyroid hormone replacement to lower the TSH. And, when we're doing that, it doesn't matter how low the TSH goes, because it is now superfluous to needs.
2) TSH also stimulates conversion of T4 to T3. However, having a high TSH does not guarantee that we will be able to convert. And many of us can't do it very well. Which is why we need to take T3. And, when we're taking T3, we no-longer need the TSH to stimulate conversion. So, once again, TSH is superfluous to needs.
The TSH itself has not connection to bones or hearts. It does not come into contact with them. Therefore it cannot influence osteoporosis or heart attacks.
However, when you are hyper, as in Graves, your FT3 is very high, and thus your TSH is suppressed. And, it's the high FT3, over long periods, that increases the risk of osteoporosis and heart attacks. Not the lack of TSH. And, I think that is where doctors get confused. I have noticed that they always have difficulty distinguishing between cause and effect!
So, if you need to take 55 mcg T3 to be well, then take 55 mcg. No point in making yourself ill for a myth. It's very doubtful that reducing your dose by 10 mcg would raise your TSH, anyway. But it would probably have a huge effect on your symptoms.
TSH both stimulates thyroid hormone production and responds to thyroid hormone feedback on the pituitary. Providing the hypothalmic pituitary thyroid axis is working correctly TSH is an accurate measure of thyroid hormone levels in the blood. In this case T3 does not 'always suppress the TSH', it depends upon how much L-T3 is being taken ncbi.nlm.nih.gov/pmc/articl... .
(Greygoose as an aside TSH does come into contact with all tissues via the blood and has a direct effect on bone formation. Sorry I can't remember the exact reference, this is one I haven't read ncbi.nlm.nih.gov/pubmed/246... . In any event I think this is a minor effect compared to the effects of thyroid hormone).
TSH seems to promote type-2 deiodinase (D2) but of course if you are taking L-T3 you are bypassing the need for D2. However, as tissues have varying reliance on D2 the effect of taking L-T3 will not be uniform across all tissues. Some will be overstimulated and some understimulated. A suppressed TSH indicates your overall hormone level is higher than it was when you were healthy.
I can see two situations when you might need to suppress the TSH and take some L-T3:-
When your axis is down-regulated and so your TSH is coming out too low (along with reduced D2). In this case you should recover with your fT3 and fT4 around normal levels but TSH suppressed, maybe fT3 in upper half.
The other case is when there is some form of peripheral resistance to thyroid hormone. If you give large doses of L-T4 (levothyroxine) in these cases the deidinases will work as they should and reduce the rate of T4 to T3 conversion. You need to take some form of T3. In this case you may need supra-physiological doses of L-T3 which suppress the TSH. This carries risks of bone loss and atrial fibrillation which can lead to strokes. There are also cardiac risks from being hypothyroid. It's a matter of balancing the risks and taking action to mitigate them. As far as bones are concerned you can take load bearing exercise (which you may not be able to do if hypo) and vit D / calcium / magnesium if necessary. Cardiac risk can be minimised by aerobic exercise (just normal fast walking, playing sports) and possibly low dose beta blocker.
My approach is to take the lowest dose of L-T3 that works and to try reducing the dose by a tiny bit every few months, just to make sure I'm on the minimum. You can't just solely go by how you feel as it can be more difficult to treat the brain than the heart, the brain is very good at preventing an increase in T3 levels. So, you could still be hypo in some tissues whilst the heart is hyper.
It's quite reasonable for your endo to be concerned if your TSH is suppressed, this is an initial warning sign. However, there may be no choice if you cannot function without a suppressed TSH. It then comes down to determining the minimum effective dose and taking sensible steps to mitigate any risk. You can exercise and they can monitor your heart and possibly prescribe a small prophylactic dose of beta blocker if necessary. This approach happens in other branches of medicine all the time.
There's no point in the doctor or patient burying their head in the sand. The doctor has to accept that some patients need a suppressed TSH to function and to avoid risks of tissue hypothyroidism. The patient needs to accept there are risks of a suppressed TSH (which may be unavoidable) and take sensible steps to minimise and mitigate them.
Re your third reference. Carla Moran's paper refers to the alpha-1 receptor mutation which is incredibly rare (thankfully) and the patients don't survive more than a few years. There are mutations of the beta-1 receptor, these patients present with elevated fT3 or fT4 and non-elevated TSH. They may be OK and not treated or clinically hypothroid and treated with levothyroxine. I believe they would be better cared for if they received at least some liothyronine.
Both T4 and T3 control TSH levels. T3 is about 70% as powerful (weight for weight) as T4 in this. So the relationship between reducing TSH and T4 or T3 levels is roughly the same influence for both. So again, when choosing a dose that does or does not suppress TSH, the same sort of criteria work for either T3 or T4. In the healthy person of course, both T3 and T4 compete together for controlling TSH.
Diogenes, can you clarify 'T3 is about 70% as powerful (weight for weight) as T4 in this.'
I assume you are talking about T3 in the blood? In tablets L-T3 is about 3x as potent as L-T4 in suppressing TSH in terms of mcg taken. In blood fT3 is about 4x or 5x as potent as fT4 in suppressing TSH using the usual pmol/L units. T3 is obviously lighter than T4 but did you mean to say it is only 70% as potent? My chemistry is long forgotten so I don't remember the significance of the various units of measure. Also, I don't know what percentage of T4 the pituitary converts to T3 so this may add to the confusion if you are measuring action directly at the pituitary cells.
This is what we find: that TSH is controlled 60% by FT4 and 40% by FT3 on the average. The average FT3 is only 1/3 of the FT4 concentration, thus its real molar effect is 3.3 times the 40% or 132. Thus the actual molar effect of FT3 is 132/60 or about 2.2 times greater than T4. We don't agree with the higher T3 figures. Also we don't agree with the idea that the thyroid is a minor player in producing T3 direct. Our figures clearly show that on the average, direct T3 production from the average thyroid is about 36% of the total. I estimate that the range might lie from about 20% (good body converters) to nearly 50% (poor converters). This explains why poor converters cannot use T4 only to supply enough T3 to the cells. The low-ball estimates of 20% or less coming from the thyroid wouldn't allow for this phenomenon. Incidentally in the rat, 40-50% of T3 comes from the thyroid so I wouldn't think we as mammals would do significantly less.
Diogenes, Thank-you so much for this quick and insightful reply. I think we get confused between the relative potencies of T3 and T4 in the blood or in tablet form and the relative contribution of T3 and T4 in a healthy person.
I've always believed statements that the thyroid contributed around 6 or 7 mcg T3 and consequently providing 10 mcg L-T3 should make up for this. Clearly if the thyroid contributes much more then higher doses of L-T3 are necessary and the research studies that compare combined therapy with L-T4 only therapy in patients with primary hypothyroidism are invalid.
Sorry Agapanthus this has drifted away from your questions, if I have further questions I will raise them in a separate post.
Thank you so much for all those helpful replies. Unfortunately I have started the day with a migraine, (stressful day yesterday probably triggered it), so having skim read them so far I am going to read them all through slowly later and look at the references.
To be fair to this endo, I think he is being reasonably concerned for me, and ultimately going to leave it to me, but I am going to at least give the reduction of T3 a go and see how I am on that. It may be that it does need more finely tuning, and I am so grateful that he and the GP are not going to cut off my supply, that this seems a small price to pay. Of course if I find that I feel very much worse then I will need to think again about it.
One thing he did comment on was the fact that I told him that I didn't take my T3 before seeing him in case he did a blood test, and also that I never took it before a blood test in case it took me over the range of FT3. He looked surprised and clearly did not know that is what people like me did! Maybe I should have kept quiet, but I did show him a test I did last year which was sprung on me unexpectedly, and I was over range with t3, so I then tested after privately (and didn't take my T3 for 18 hrs before) and was under range. He said that those peaks and troughs would still have an effect on me over time and that being over range was not a good thing (even if it only happened for part of the time). I know that not all people here would agree with that, but I didn't have enough knowledge to counter it - other than to say that very little research has been done on people on T3 only.
Thank you Shaws. I will read with interest! I wondered about the research done on these 2 issues (the AF and the osteoporosis) as I wanted to check it out and see if it seemed believable or not. Good old Dr Lowe - if only he was still with us!
I get the impression that this endo is realising that he is under some pressure now with the CCGs behaving as they are, and so perhaps trying harder to toe the line for fear of repercussions. Actually he did say ultimately it was up to me, which was good of him.
This statement is too general. In many cases TSH is a meaningful marker for patients taking thyroid hormones but not all cases. In general a suppressed TSH is associated with an increased risk of atrial fibrillation and consequent stroke. This research just looks at a large group of patients wihout taking note of their individual response to hormone.
However, there are valid situations where the TSH may be suppressed, to prevent a reoccurance of thyroid cancer or if you need to suppress the TSH in order to resolve hypothyroid symptoms.
Many endocrinologists say the TSH should never be suppressed, some patients say a suppressed TSH never matters. My view is that both are wrong, it's a difficult issue but you have to look at the patient's history, blood tests, signs and symptoms and come to a sensible treatment option for that particular patient.
Having just received my own test results today, I find that my TSH is 0.53 mU/L (0.27 - 4.20). And I believe that is reasonably representative of my status. (All other test results were also boringly unexceptional.)
Perhaps, prior to anything being identified and treated, my TSH might have been a bit higher? Perhaps, in future, I will find I want to change my levothyroxine dosing? But for now and for me, I do agree that TSH can be useful. The trap is to assume it will be useful, and not to apply appropriate discrimination and thought when attempting interpretation.
And were my TSH to shoot up, or suddenly be totally suppressed, I'd really be asking questions. I would not just ignore it.
It can be very difficult to know how much attention to pay to the TSH, there are grey areas. If a patient has a TSH of 70 and moderate symptoms the TSH will probably be useful guide to initial treatment. If a patient has severe symptoms with a TSH of 1.0 (Iike I did) then it will probably need to be suppressed and extra care taken to look for signs of
If you have a situation in which you have seen TSH rise and FT4 fall, over a reasonable period, and the reverse happen with added levothyroxine, you have a reasonable basis for accepting TSH. For as long as the system works in that individual.
(Unfortunately, from a personal perspective, while I have the TSH results to back it up, along with most others, I don't have the set of corresponding FT4 results.)
If a patient has a TSH of 70, that almost certainly identifies significant hypothyroidism - and likely of prolonged duration. In that case I doubt you can ever again trust TSH.
And in your case, absolutely, you had no proved basis for believing TSH. Trouble is, we here see that all the time. The ones supposedly trusted with diagnosis and treatment tend to fail to see it even when right in front of their noses.
On the whole I agree except I think the higher the initial TSH the more reliable it is likely to be as you can be more sure the problem is primary hypothyroidism (provided the patient is not severely hypothyroid).
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