Wondering if anyone here continually has a suppressed TSH?
I am on NDT for the last 7 yrs and whilst I understand that the TSH is usually low or suppressed on NDT I’m interested to hear about others experiences.
As we know the medics do not like a suppressed TSH and it gets blamed for cardiac problems and thinning bones to name but a few.
Recently because I was suffering from headaches and occasionally tachycardia my Endo suggested that it may be due to T3 and we agreed to lower the dose. I was willing to do this too as my FTF were at the higher range and so thought would give it a go. Also NDT is expensive so if I could reduce the cost that would be a bonus too.
I went for six weeks on a reduced dose of Erfa instead of 90 mgs I took 60mgs I also take Levothyroxine 25mcgs at night to keep my T4 up so I took that ever other night. What a disaster I let myself in for. I felt horrible and I have still not recovered.I didn’t imagine that the change would happen so fast. Interestingly despite the low FT’s my TSH stayed suppressed
My results were:
TSH 0.007. (0.27-4.20)
FT4. 13.00. (12.00-22.00)
FT3. 3.83. (3.10-6.80)
I am now back in my previous dose and waiting for things to improve.
Is there any literature about a suppressed TSH and low FT4 and FT3?
I’m thinking that maybe I have a pituitary problem here.
Would be really interested to hear your feedback and thank you in advance
Ali
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Alli1
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If you take sufficient thyroid hormone to suppress your TSH for a long time your ‘hypothalamic pituitary thyroid axis’ wil be down-regulated. This means your TSH will be lower than it should be. This has consequences,especially for T4 to T3 conversion. This happened to me when I needed high dose hormone treatment. The moral is to avoid suppressing your TSH if you possibly can.
Thank you for your reply. But the moral can’t be followed as in order to not have a suppressed TSH I would have to remain very ill because I would be trying to exist with an untreated hypothyroidism! What is the evidence for a poor T4-T3 conversion with a suppressed TSH I haven’t heard that before so would be interested to see any research on that
This is interesting after having my thyroid removed three years ago I was sent home with a letter from the surgeon who requested to my GP that my TSH should always be suppressed in the future.
That can happen, especially after thyroid cancer although now they are able to assess the need for TSH supression and back off a little after a year or two.
Hi, I take a combination of T3 and T4, and as soon as I started on the T3, even a small dose, my TSH was suppressed. If you look at my profile on here you will see I asked about this recently and had some helpful replies, including a link to a study which may help you (I'm typing this on my phone so can't copy and paste, but hopefully you'll find it)
My take on it is that, because I'm taking the active hormone in the form of liothyronine, my body realises it doesn't need to produce any more T3, so why would it generate TSH to do this?
For me it's a choice between a suppressed TSH and a life, or a higher TSH on thyroxine only and no life at all, so it's a no brainer.
What gets me about all research I see is "euthyroid control" subjects. Exactly how do they define "euthyroid"? From what I've seen it boils down to "TSH within standard range," which would be fine if that range had weeded out anyone having, let's say, 4 or more hypothyroid (or hyperthyroid for that matter) symptoms, and had also had verified the absence of all antibodies.
This does not surprise me: "Mean fT3 levels were lower in the LT4 euthyroid group compared with the other two groups." Maybe because their definition of "euthyroid" needs tweaking?
"fT3 levels were slightly below the reference range in four of the healthy control subjects, 41 of the LT4 euthyroid subjects, and five of the LT4-suppressed subjects."
So over half of the so-called euthyroid subjects needed more FT3.
"REE (REE/kg) was positively correlated with serum fT3 levels (p = 0.03), but not with fT4 or TSH levels." That makes perfect sense to me.
"Subjects lost 1.4 kg after 16 weeks of desiccated thyroid extract and 1.8 kg after six weeks of LT3, although there was no change in REE in the LT3 study (30). This raises the question of whether LT4-treated subjects with low T3 levels could benefit from low-dose LT3 therapy to assist with body weight regulation." Well, duh!
When I read this, I asked myself, precisely what are these known risks? "On the other hand, LT4 euthyroid women had lower REE than LT4-suppressed women had, as well as a trend toward lower REE than healthy controls. This group also had lower mean fT3 levels, raising the intriguing possibility that low-dose LT3 therapy might benefit the metabolic profile of these women. However, this possibility requires further rigorous interventional studies of metabolic function in LT4-treated subjects to establish the long-term balance between benefits and the known risks of LT3."
So, of course I googled it, and found this:
"Side Effects
With the exception of triggering hyperthyroid symptoms, side effects from Cytomel are rare. In such cases, skin reactions, generally mild, have been reported." verywellhealth.com/t3-natur...
Hmm.... seems to me that the medical world has been using scare tactics against hypothyroid patients who are sick and tired of feeling sick and tired.
Just to add I've had a suppressed TSH for about 7 years now, and like you was persuaded to try reducing my T3. All that happened was that I became very unwell, my free T3 dropped to the very bottom of the range, but my TSH remained suppressed. It was a completely pointless exercise that has cost me months of ill health!
You sound just like me Alison. My health is far from excellent on my thyroid meds anyway but when I tried reducing my dose I felt like I was dying with all sorts of symptoms I found a sore chest to be one of the main symptoms of reducing T3
Yes when I read your post it was so familiar I just had to reply. Just one last thing I forgot to mention is that, so far, I haven't had any problems with my heart or bones. In fact, my cholesterol readings are better than they ever were on levo alone. Don't let your doctor scare you!
Thank You Isn’t this a great forum for empowering people who are often let down by the professionals because thyroid is so poorly understood with little or no funding. I myself am a nurse of many years work in NHS for 30+ yrs and I know from my own training and working life the thyroid gland was barely mentioned .. so strange and it’s so significant. I’m careful not to let Drs scare me of course there’s an added problem for me as when they know I’m a nurse they can tend to want to let me know how informed they are!
I have a sister who like yourself was a nurse for over thirty years, imagine my surprise when after I had my thyroid removed she informed me that she had been taking Levo for over 8 years. I was devastated. If I had known beforehand I would have joined this site and raised my vitamins and minerals.
Alli1, I appreciate many patients have no choice but to suppress their TSH, I was in that situation. For those who can get by without a suppressed TSH (even if there are some minor symptoms) I would recommend they do not suppress their TSH. If they suppress their TSH for a long time their axis down-regulates, and they become dependent upon T3. They are no longer able to fully convert T4 to T3 because they have supressed their TSH.
There are studies that show TSH promotes type-2 deiodinase (T4 to T3 conversion) in various tissues. I don't have these to hand at the moment. Perhaps better evidence is the fact that for most patients in the early stages of primary hypothyroidism their TSH rises, fT4 falls but fT3 remains stable - the rate of T4 to T3 conversion increases - see p18 of this document acponline.org/system/files/... (I have not read this paper, just giving a reference to a graph).
I believe this is important because if a patient's TSH fails to increase when fT4 lowers (within the reference interval) their fT3 will also tend to fall (within interval). These patients have 'normal' blood test results, are not diagnosed but have quite severe symptoms because their D2 activity is lowered and tissues such as the brain which rely on D2 have local hypothyroidism. We see a lot of such cases on these forums.
Whoops! Sorry, I usually give the full term before the abbreviation. D2 is 'type-2 deiodinase' which converts T4 to T3 and regulates local levels of T3 as well as being the major source of circulating T3. Thus if D2 activity is reduced you not only get reduced serum T3 but some tissues have lower levels also.
If you are not taking any thyroid hormone and your fT3 is around mid-point with normal TSH / fT4 then it is likely tissues have normal lelels of T3. I don't like fT4/fT3 ratios because they are supposed to vary. If fT4 falls a little TSH rises and type-2 deiodinase increases to maintain fT3 levels. i.e. the fT4/fT3 ratio changes.
Being on levo only can disrupt this mechanism a bit. This is pointed out in some complex papers by the Thyroid UK advisors. The thyroid secretes some T3. The thyroid also converts some T4 to T3. So, if the thyroid is removed or diseased we end up with less T3 from thyroidal secretion and conversion. Giving levo only does not work for all patients although it does for many. If you give sufficient levo (L-T4) to normalise fT4 and TSH you find the patient's fT3 is a little low. So generally doctors prescribe a little more L-T4 so that TSH is a bit lower (e.g. 0.3), fT4 around 20.0 and this brings fT3 to around mid-interval. This works for many patients. However, the lower TSH reduces type-2 deiodinase (D2) and so tissues such as the brain which are dependant upon D2 become hypothyroid. These patients need some T3 medication. It's worse if the patient's TSH is too low to start with, by this I mean they have a low or normal TSH when their fT4 is low (even if within interval). When fT4 falls TSH should shoot up. This patient group will have insufficient D2 activity and giving them L-T4 will reduce their TSH even further making things worse. I believe this is an unrecognised form of hypothyroidism.
There are two issues. 1. Try to get better without suppressing your TSH if you can. 2. if a TSH becomes suppressed the doctor should ask 'is this reasonable?'. If fT3 and fT4 are mid-interval and TSH is very low then something is wrong with the axis and you can't rely on TSH (this assumes the patient in not fiddling the blood test results by having the blood taken a long time after taking their T3!).
"...the lower TSH reduces type-2 deiodinase (D2) and so tissues such as the brain which are dependant upon D2 become hypothyroid..."
Im still unclear what D3 really is but if its required for T4 to convert to T3 at cellular levels, including in the brain, or if its required for cells to utilise whatever FT3 is circulating, why isn't D2 given with LT4 to those of us with ablated Thyroids who have a necessarily broken feedback loop?
I thought at first that D2 was to do with vitamin D! But it is an enzyme that changes T4 (with 4 atoms of Iodine) to T3 (3 atoms of Iodine) by removing one iodine.
Minimol, unfortunately blood tests will only tell you how much hormone we have circulating in our blood. There is no test for hormone going into the cells (where it is actually used), short of some proxy tests used in research that measure metabolism as a whole.
There are quite a few reasons levels of hormones in the blood might not reflect hormone entering the cells
So, in layman's terms, downregulation of the axis is like having a product that nobody buys. After a while shops stop stocking it and the factory stops producing it.
Similarly, if there is no call for TSH for a long time, the pituitary stops making it, or makes very little.
I know this comment is much later but I'd be interested in your viewpoint... my understanding is that in central hypothyroidism where there is a reduced or absent TSH level, the recommendations are to never add t3. This would suggest that the preferred option would be to prescribe t4 only which these patients will struggle to convert? Therefore knowingly leaving them feeling unwell, or have I missed something somewhere?
I don't think you have missed anything. T3 will suppress TSH more than T4 simply because it is more potent but since a subnormal TSH will reduce T4 to T3 conversion it seems logical that these patients have a greater need for T3 than those with primary hypothyroidism. I don't see how patients with central hypothyroidism can do well without T3 although in general they are not given it. I feel the endocrinolgists haven't bothered to work out what will happen or simply asked the patients how they feel.
I was diagnosed 20+ yrs ago with hypothyroidism with a very high TSH and low below range FT4 I was on Levothyroxine for about 13 yrs and got on okish then I got very ill from what I realise now was from taking Teva brand Levo which was not ok I think they admitted to something being wrong with it at the time. Anyway it resulted in my thyroid becoming unstable and after several months of very poor health I saw an Endo who put me on Erfa Thyroid so that I could get some T3. My TSH has been suppressed since then really and anytime I try to lower my meds I suffer horrendous symptoms- they are by no means mild I can assure you! I would assume that most people with hypothyroidism experience many difficult symptoms on a day to day basis anyway and just have to tolerate them. health in my experience is never optimal again after a thyroid diagnosis. A suppressed TSH versus a living hell of existence... not much of a decision me thinks!
Adding T3 to one’s regimen, whether Cytomel or NDT, will drive down just about everyone’s TSH, by virtue of its potency, some 3 - 3.5 times stronger than T4. But doctors who blame suppressed TSH for heart and bone issues are not thinking things through. TSH is a pituitary hormone that rises and falls in an inverse response to circulating free T4 and free T3 levels. Metabolically, the thyroid hormones (thyroxine/T4 and triiodothyronine/T3) are what drive metabolism up or down and thereby affect heart and bone (and more) metabolism much more than TSH. Neither extreme of FT3/FT4 is desirable. Granted, severe suppression is probably not desirable, but suppression with well balanced, optimized free T’s should not be an issue.
There is no evidence to suggest that a lack of TSH causes Osteoporosis or Atrial Fibrillation.
Endos are being a bit lazy by insisting that they can determine the action of thyroid hormones by looking at TSH.
They then see a CORRELATION between low TSH and OP & AF but mistake that for CAUSATION.
Bernadette Biondi specialises in Thyroid and heart issues. She has done some work that is available on the internet that explains how excess thyroid hormone may cause AF in some patients.
Some of the other work that to suggest that high T4 causes AF is flawed by simplistic reasoning and mistaking correlation with causation.
I don’t have that to hand to quote it.
Nevertheless I monitor T4 and T3 and importantly my signs and symptoms to gauge how I am. I use an Omron blood pressure machine and a Kardia heart beat monitor to check for AF.
Hi Holyshedballs, I've really appreciated some of your posts recently! Thank you for the great information you share, it really benefits those of us too ill to do our own research.
Could you please say a bit more about the Kardia machine? I also use an Omron machine for blood pressure and pulse and would love to hear if there is other relevant machine I should get.
Maybe the drop from 90 to 60 NDT was too much a percentage fall. That’s 33% fall. Maybe try and drop by less. I know it’s difficult to measure NDT. I bite mine into quarters and keep the remaining tablet in a tissue. Then I know I’m not under or overdosing for that day/s. I have major issues if my dose or TSH goes under/over the range for just one day. Do you split your NDT throughout the day. As it has T3 in it with a short life I find it better to split my NDT dose morning and late afternoon. Otherwise you get a big hit in the morning and nothing late afternoon when T3 has virtually run out. If you get your bloods done in the morning with higher dose then your TSH could be suppressed. Try splitting your original dose, half morning then half afternoon, of 90 ref the T3 element. Not sure if you already do this? I started this after crashing out late afternoon most days then I felt much better and less yo yo ing. It’s the T3.
I agree it was a big decrease. Usually it's best to changes doses in small bites, like a quarter grain. Especially if having a decrease that might turn out to be painful.
Yes I have always split my dose as couldn’t tolerate the T3 hit all in one go I doubt my adrenals are strong enough for that! I agree that reducing by 30 was too much and I have like you varied my dose by breaking off bits of the tablet to titrate my dose. I never get my bloods tested after taking thyroid hormone always without.
It’s sometimes all trial and error and often a mastery!,
Hi. Thank you for your suggestion. Unfortunately when I use a razor blade they still crumble into tiny bits and powder leaving maybe one chunk that’s awkward to work out what it measured. Maybe your T3 are different and easier to manage. 👍😀
Hi, I am on Levo, 175 daily. My TSH has been supressed for years (0.02, 0.005). Doesn't seem to have any detrimental affect. My T4 is usually high, above the range, and my T3, quite normal in top part of range. I have to keep telling my GP that I feel absolutely fine. Any less Levo and I feel ill. My TSH seems irrelevant.
Hi Alli. I’m exactly the same. Total thyroidectomy nearly 11 years ago and even with T4 at 100mcg a day my TSH didn’t shift. I had pituitary scan which showed nothing. My family have a history of low pituitary hormones but the consultant wasn’t interested. He insisted I was over medicated. I didn’t take any replacement for months in frustration and had another blood test showing hardly any T3 or T4 in my blood. Again my TSH was 0.002. I had my thyroid removed due to benign nodules and a massive goitre. My bloods were ‘normal’. It really gets me down.
I stopped the T3 due to supply issues about 6 months ago and feel hypo most of the time despite having high T4 in my blood. I guess what I suspect is low pituitary hormones. I take HRT do to low estrogen and am not menopausal. My mother has been hospitalised for low growth hormone, my grandmother died from a brain haemorrhage and my male cousin was born with a pituitary rumour which mainly stunted his growth. This side of the family have had multiple none identical twins. My grandmother had 3 sets out of 9 children. We have a collagen disorder likely EDS and again despite major surgeries because of this I can’t get diagnosed. It’s just so frustrating. Sorry to ramble but hoping something might help !!!
Thank you. I found some old T3 a couple of weeks ago and that’s a temporary fix. It’s just so frustrating that doctors stick to their guidelines and never think outside the box 😢 x
I don't quite understand your comment. Suppressing TSH will run the risk of down-regulating the axis, whatever the cause of suppressed TSH. I appreciate many patients must take hormones that suppress TSH. The point I am making is to have a good go at getting better before you take suppressive doses of hormone. Once the axis has been down-regulated you are stuck with trying to get sufficient T3 into organs that rely on converting T4 to T3 (e.g. the brain) whilst not overloading other tissues such as the heart that are more reliant on circulating T3.
I have Graves, drank RAI in 2005 and a TSH for me to be ok on monotherapy has to be .001.with my T4 sitting on the very top of the range.
Consequently I only ever went from 125 down to 100 with my TSH coming in at .57 and being told I was " good to go " - and I was very ill, though told it wasn't anything to do with my thyroid.
At this point in time, through help from this site, I paid for blood tests and my T3 = 4 some 25% through the range with my T4 coming in at 80% through its range.
I now self medicating with NDT and am doing much better and getting my life back.
The thought of not being totally reliant on blood test results, very appealing !
I don't understand why there are no special guidelines for Graves patients.We have TSI antibodies that take control our TSH and continually stimulate our TSH -after all, that is why we went overactive in the first place.
When the thyroid is surgically removed or burnt out with RAI and disabled, the TSI antibodies are still there stimulating the TSH making us still appear overactive and we reach suppression on a much lower dose of T4 than people without Graves Disease.
I don't think TSH has any relevance without T3 and T4 results standing alongside.
If it is a cost cutting exercise not to take the 3 blood tests and just go with a TSH reading one might as well look into a crystal ball.
As T3 is now presumed a " banned substance " in all honesty why do the 3 blood tests ?
If a doctor takes all 3 readings, and wants to help you, how can he adjust, titrate, your dose, as needed, when not allowed to introduce T3 ?
I would have thought blood tests cost less than antidepressants let alone the add on business of chronic fatigue or pain relief clinic, or maybe even psychiatry.
Totally agree with you Pennyannie it just doesn’t make any sense. The common thread running through it all though is that Thyroid patients are left behind when it comes to treatment and investigation I often think it might take someone senior in Government to have the illness or have someone close to them with it in order for any real progress to be made
Why stay with the doctor, constrained with a TSH reading which isn't of any use to me. Without a T3 and T4 blood read which she refuses to do ?
I'm not going to get any better within the Nhs , in fact, I don't think they have any guidelines concerning autoimmune thyroid disease, and I don't want to listen to the dogma any longer.
I'm disillusioned and disappointed with the Nhs roundabout I've been on for almost two years, getting nowhere but keeping people in jobs in departments, justifying themselves but doing nothing to help me.
I am finding all the suppressed TSH comments very interesting and I think it would be good to combine these experiences to see it there is a common denominator. I have a suppressed TSH deliberately because of Thyroid cancer but wonder if it should be higher because of problems including heart and blood pressure, tachycardia, palpitations or, swop some T4 for T3, I take just Thyroxine. I have however, found that my Testosterone is raised and that is being investigated, this might be part of Netty888 's problem as well. It might of course, be that we just don't know the full science yet behind what the Thyroid does. fiftyone holyshedballs interesting.
Hi Annnsandell, I've had a thyroidectomy due to cancer, have a suppressed TSH, and have just found I may have high testosterone. I wonder if there's a pattern there or just a coincidence.
The only thing I've known about is facial hair. But I think that originally started when I was prescribed DHEA a few years ago, which is the precursor to cortisol and a few of the sex hormones. I've recently heard that some experts think women shouldn't have it, as it promotes testosterone.
I do gain weight easily, too, but I'm also still hypothyroid which causes that, too.
Hi, I was interested to know how much and type of DHEA you were taking. Also did it work well for you and make you feel better by increasing your hormones. Thanks for any information.
I was prescribed the DHEA by a private holistic doctor, primarily because of low cortisol and low DHEA. It was in tablet form, but I long time ago so I'm not sure of the dosage.
At the time I was given a cocktail of different adrenal support and felt a bit of improved. I think that was mainly due to Nutri adrenal (discussed on the forum quite a bit, most commonly as Nutri adrenal extra or NAX, a slightly different formula), and that the DHEA was probably a mistake.
Thanks so much for your speedy reply. Interesting that DHEA didn't help you so think I will research the adrenal support and go from there.Thanks again
Me too, just discovered that I have high testosterone and my tsh is at 0.07, so I am not sure if it’s because of the thyroid replacement or I had it all my life but haven’t been tested so far...
I am on T3 T 4 combination and my TSH is around the same as yours. My endocrinologist tests my SHBG sex hormone binding globulin as he says this indicates cell health. He says while this is in range there is no cause to worry about suppressed tsh. I had s total thyroidectomy and wasn’t converting T4 as shown by my very high T4 and below range T3 with high reverse T3. I had DIO2 gene test and inherited gene from both parents.
Once your TSH is suppressed, I don't know how it's possible for you to get it to be not suppressed, as suggested by jimh111.
I had my thyroid removed 20 years ago, was on thyroxine alone initially, but that didn't work, so was put on T3 which I have been on since.My TSH has always been 0.01.
A couple of years ago my Doctor wanted me to try thyroxine only because of the cost of T3.I agreed as long as I could go back on the T3 if it didn't work.,which it didn't.
The things is that even without the T3 my TSH was still supressed at the same figure,so how is it possible to get it to increase?
Maybe it's because I have no thyroid at all, I don't know.
Yea that’s my question really is how can we raise the TSH once it’s supressed as it seems impossible without becoming extremely ill. I wonder if having just taken T3 means that it never actually gets back to where it was when on T4 meds only - so much we don’t know and sadly neither do many medics!
Yes you're right.I couldn't take more than 75mcg of thyroxine, any more and I had high blood pressure and racing heart.But 75mcg on it's own wasn't enough without the T3.
When the endo prescribed it for me 20 years ago, there wasn't the question of price, so I was able to get it easily.
Whether they didn't know enough about it at the time to know the long term effects is another thing. But in Germany where my Sister lives, they automatically prescribe you T3 as well if you have your thyroid removed, and they are usually more advanced in treating health problems than they are here.
Alli1, there's also the fact that TSH response can be sluggish. This is effectively your pituitary shouting a message to the thyroid to make more hormone, and there is individual difference in how quickly it acts, and how loud the shouting.
This definitely gets worse as we age, so a person in their 20s would get a lovely loud shout, but it declines throughout life after that, and several decades later we will never get such a sensitive response again.
I believe lots of other things will impact the sluggishness, but it may be that the usual 6 week wait just isn't enough time to shake your pituitary into action.
Yes but six weeks is a very longtime when you feel so unwell! I understand the process of the TSH knocking at the door of the thyroid but then if that thyroid no longer exists or has shrivelled and atrophied then I guess it gets tired knocking and goes to sleep in a supressed state!
Yes, you probably don't want to wait any longer to find out if it will bounce back.
I am still on the journey. Diagnosed with "Subclinical" hypothyroidism (Hashimoto's). Eventually started on 25mcg Levo, then increased to 50, 75 and finally 100.
The last blood test on 100 mcg showed a TSH of 0.01, and T4 just below top of range. So I was put on 75/100 on alternate days. It's been 2 weeks now, and I am already starting to feel a bit worse, very tired and today seemed to have little strength in my legs while walking around town. So we will see. I suspect I'm not converting T4 to T3 properly, but of course can't have T3 tested unless done privately, which I may do if this continues.
But I just learned something important from this thread. jimh111 thank you so much for explaining downregulation of the axis I'm finally beginning to get it! I always had the impression that suppressed TSH was harmless if you feel well on it, as is T4 slightly over range. But it seems that, even if you feel well, long term TSH suppression is not a good idea if it can be avoided.
I am quite ashamed because I was very annoyed and frustrated with the medic who told me to decrease the Levo, and have been grumbling about it on here!
Does it mean that I am likely to have poor conversion and T3 would likely still be low if tested, (perhaps with too much rT3 s well)? My T4 was almost at the top of the range and TSH 0.01, and I still felt hypo.
You need to have fT3 measured. However, this may not tell all the story because possibly too much of the T3 might come from type-1 deidinase which doesn't help. I'd rather not go into this as I want to make time to write all this stuff up and put it on a webpage.
If you problem is pituitary, presumably your hypothalamus is already releasing as much Trh as it can, and the damaged pituitary can’t make any more Tsh however hard it tries- so in those circumstances downregulating would not happen?
I don't think it has been determined by any study but when high hormone levels down-regulate the axis it's not known whether the problem lies within the pituitary or hypothalamus. i.e. is TRH release from the hypothalamus reduced or is there insufficient response from the pituitary or both.
Alli1, I'm on NDT and my TSH bottoms out even with lower dose but my FT3 and FT4 are pretty low in the range and recent Endo visit said everything for me is fine. I still have hypo issues inspite my numbers being fine. My TSH was below normal while on Synthyroid alone and a combo of synthyroid and cytomel.
If you are on NDT, it is my understanding that it has T3, along with T1, 2, 4, 5 also. Any product with T3, will suppress your TSH because T3 is an active hormone. As far as I know the TSH (test) is your thyroid stimulating hormone and is produced when a gland (pituitary) in your brain sends a message to the thyroid to make and release thyroid hormones into your bloodstream. This means that the T4, the Levothyroxine, turns into T3 when it passes into & out of the liver. Being as you take a T3 pill, or even any pill, like NDT, which contains T3, this will, then, due to the active T3, suppress your Thyroid Stimulating Hormone, because the pituitary doesn't “need to” send a message to an already “converted” active pill. In other words, your TSH is irrevelant. Physicians, in fact in the 19th and early 20th century, only relied on asking the patient, “how they felt,” and went from there, judging their progress, or lack thereof, on their temperatures, taken the first thing each morning for a week or more and then averaged. This was known as the Basal Metabolic Temperature test. BTW, the only “cure” then was NDT, or you died.
Unfortunately, now, far too many physicians show little if any regard for their patients and simply write out a prescription for Levothroid, a generic brand of T4. I myself took this for over 20 years and was quite well on it, until, last year I had terrible headaches and a conversion problem converting T4 to T3. I am now on 50 mcg's of T4 and 30 mcg's of T3 and feel quite well but am still tweeking my dose(s), as my trust in doctors went from, let's say a 10 to a -1.
You will have to ask simple, direst questions, post a blood test with them on this, as well as any other, thyroid website you may choose to converse on, in order to learn as much as you can, as, virtually, your life and/or daily health may very well depend on it. I wish you the best and sincerely hope you find your way out of this thyroid maze. Sad to say I cannot recommend that you rely, solely, upon physicians, however, I know there are many good, well-meaning ones but, unfortunately, they are the few, whereas the others are merely clock-punchers. I will answer anything I can but I am only aware of most things my body relies upon and the first thing every human being has to understand is that we are all “different” and will, therefore, have bodies that respond to different doses. Peace be upon you and may you find your health solution and dose of thyroid all the sooner.
Hypopituitarism is the cause of my consistently suppressed TSH. You're right - the medicos hate it, yet they never seem to have any curiosity about what might be causing it, except the thyroid replacement therapy. Good luck. Wishing you well.
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