Could someone please explain about a low TSH. Does your TSH become lowered by T3 or NDT? And then it simply remains low?
Set point for TSH: Could someone please explain... - Thyroid UK
Set point for TSH
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kmf0503
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If your TSH is suppressed for a period of time (several months?) the axis can become down-regulated. i.e. TSH becomes lower than it should be. Sometimes TSH recovers, sometimes it doesn't. Thus, it's important not to suppress TSH if you can avoid it.
in reply to jimh111
Mine is like that. What is the impact of having always low TSH for life?
jimh111 in reply to
A subnormal TSH means you will need full thyroid hormone replacement. Since TSH stimulates T4 to T3 conversion you may need some T3.
in reply to jimh111
Ah okay, thanks, that's exactly where I am right now - full replacement.
If you have no thyroid
function anyway due to total destruction does it matter any more? Mine is about 0.01 on NDT. I am not sure what counts as suppressed I presume it is anything under range.
This is very interesting information! I had a TT 5 months ago and was trying to assess where my TSH should be as I am on both T3 and T4. Do you have any info on optimal levels for TSH because some people on the forum say it should be less than 1. Any information would be greatly appreciated.
In healthy people TSH tends to cluster around 1.0 to 2.0. If treated with levothyroxine only TSH would need to be around 0.5 to give high normal fT4 and average fT3. However, many people have forms of hypothyroidism which require a lower TSH. Perhaps they have a TSH that is subnormal, i.e. when their fT3 and fT4 are normal their TSH is low. So in many cases a low or very low TSH is unavoidable.
A target TSH of 1.0 or a little lower is fine for an initial approach, or in those that cannot relate their symptoms e.g. infants or animals but ultimately you have to go by signs and symptoms. If this means getting a very low TSH then extra care is needed. In some cases a very low TSH cannot be avoided, I'm just saying don't ignore the fact that there is a risk. Lots of treatments carry risks, asperin can be very beneficial and harmful, we have to balance risks against benefits.
Thanks so much for this explanation. It will help to interpret my results. All the best.
I think you can forget TSH when you start supplementing with any Thyriod medication. This is how I view it, when my Thyriod began to fail my pituitary tried to send out more and more signal. It didn’t matter what amount of TSH it sent out my FT4 and FT3 just couldn’t get in range. So what’s the point of it? My Thyriod is broken. So I don’t care if my TSH is suppressed or not registering at all. My replacement thyroid meds have taken over and I feel good. If I were to listen to Medical people and try and keep my TSH in range I’d be very unwell (I have been, I know this to be a fact) I don’t know why people insist on using TSH range and say its best to try not to suppress TSH. That method just doesn’t work for many.
Not supressing TSH doesn't work for some patients but supressing TSH should be avoided if possible. A suppressed TSH carries risks and affects deiodinase. My TSH is almost suppressed, I'm aware of the risks and wish I had a higher TSH.
I wish I had known this little tip years ago. I wasn't put on NDT because the Levo had my levels out of whack. It was offered to me because he said some patients felt better on it. I was probably complaining about my ongoing hair loss and struggle with weight loss. He always said my TSH being suppressed was a result of the t3 in the Naturethroid and it was just a lab range and some patients had to be at the low end of the range so he wasn't concerned. I didn't think to question that advice as I understood lab ranges were just that- ranges- not exact science. I didn't know that it could be permanent. sigh
If I want to feel well I need my TSH suppressed - Graves disease post RAI - 2005.
Realistically the TSH is just one of 3 blood tests that need to be taken and should be looked at in conjunction with the T3 and T4 in order to monitor a persons dosage, whether that be T3, T4 or NDT.
The TSH was originally introduced as a diagnostic tool to identify hypothyroidism. It was never intended to be used as the sole measure of thyroid monitoring once the patient was on any form of thyroid hormone replacement.
Can you elaborate on this? What is deidoninase?? Thx
jimh111 what risks are you talking about and what info do you have that TSH is needed for conversion?
I'll try and answer the questions here. TSH doesn't just stimulate the thyroid it has other roles also. e. g. TSH plays a minor role in bone formation. TSH also stimulates deiodinase (converting T4 to T3). Studies show that a suppressed TSH is associated with atrial fibrillation and stroke. So, we want to avoid a very low TSH if we can. However, some of us only get better when our TSH is very low or undetectable. Furthermore, if TSH is suppressed for some time it can down-regulate our hypothalamic pituitary thyroid axis meaning our TSH is always lower than it should be. So it is wise to try and avoid a low TSH if possible.
I am writing a detailed description of this on my ibshypo.com website. I will put a post on this forum when it is available, probably in a few weeks time.
Can I ask for supporting documentation that shows your statement "Studies show that a suppressed TSH is associated with atrial fibrillation and stroke" please?
Atrial fibrillation is a stroke risk. I suspect patients who have been hypothyroid for some time (many of us) will be more susceptible because we might have suffered cardiovascular damage from our hypothyroidism. This is speculation but seems reasonable, ideally we would be diagnosed and correctly treated immediately.
There's a host of studies looking at TSH, thyroid hormones and atrial fibrillation. They are difficult to interpret because some studies are retrospective, some of the subjects may have parathyroid damage coinciding with thyroid damage and other issues. A further complication is the reason for TSH being abnormally low. Is it due to high levels of thyroid hormone (even if within their reference intervals)? Or is it due to insufficient TSH production (what I call 'subnormal TSH secretion').
For example, this study ahajournals.org/doi/10.1161... found no link between TSH and AF, provided fT4 was within its reference interval. At the other end of the spectrum this study nejm.org/doi/full/10.1056/N... found 'the relative risk of new atrial fibrillation in those in the low-serum-thyrotropin group was 3.1 (95 percent confidence interval, 1.7 to 5.5), significantly different (P<0.001) from that in the normal-serum-thyrotropin group' as illustrated in Figure 1. The risk of AF increases dramatically with age. There are also studies showing life expectancy correlates with TSH, within reason the higher your TSH the longer you live.
Note I am not saying patients should not let their TSH go low, just avoid it if possible. Being hypothyroid with a normal TSH is bad for the heart (and everything else). I'm writing a topic on subnormal TSH which will advocate T3 treatment (as being necessary). However, we cannot ignore the risks associated with such therapy. Unfortunately we need to face these risks to lead a normal life but that's no reason to bury our head in the sand. Acknowledge the risks, exercise to reduce them and keep an eye on your pulse, bp and hormone levels. The danger is that we believe the 'T3 always suppresses TSH' dogma (it doesn't) and take unnecessary risks. I advocate that we keep an eye on the risks and push for research into the underlying causes and development of better treatment strategies.
I've only quoted two studies because I'm short of time, if you trawl through PubMed you will find lots, they need to be interpreted in light of cohorts and counfouding issues.
Summary. A low TSH carries risk of AF and consequent stroke. Remaining hypothyroid carries similar risks. Try not to have a low TSH but if you have to minimise the risks by taking the lowest effective dose and excercise to keep the heart in good condition. Low dose beta blockers can be used in some cases.
Interesting as I always had palps when my numbers were off and on T4 only and now that I am on combo no more palps. But my TSH is almost undetectible and my FT4 is at bottom of range and FT3 is about midway. I personally feel better than I have for many many years.
Some patients have palps that resolve when they take thyroid medication, I've not researched this and don't know why it happens.
When I was on T4 only (20+ years) I had the palps all the time. Interestingly enough every time I wore one of those monitors it never showed up. Once I had the T3 added some 5 years ago they went away. I wonder what real damage was done to my heart because of those years of inadequate dose of thyroid hormones.
Look forward to reading it.
Medications and various supplements and vitamins that suppress TSH tend to be overlooked, as are others of the same that increase TSH. However, just because a substance causes TSH to be suppressed, it does not mean that your FT3 and FT4 increase as a result. The same applies for substances that increase TSH.
It took me awhile to discover why my TSH suddenly became <00.008 this spring. My TSH has been always below range, as I keep my FT3 and FT4 are where they should be for me, 65-75% range. Last year my TSH slowly became even lower. Then this spring it became the undetectable <00.008. My primary care urged me to see yet another endocrinologist. I think this was the 6th or 7th I’ve wasted my time and money on. I feel sorry for the patients who believe what these misinformed endocrinologists say. This endo was absolutely certain that I am “subclinical hypothyroid”, and that it’s not a pituitary problem as I have wondered. She makes this assumption because my TSH have been <00.008 the four times I’ve tested it this year, even though my FT3 and FT4 have been consistently ideal for me, 65-75% of range. I told her neither my FT3 nor FT4 has ever even been above 80% of range. 80% was too high for me, so I adjusted my meds. I told her that I have zero hyper symptoms. I barely have any symptoms but if I do, they are hypo symptoms (I have Hashi’s). I knew she was wrong that I am subclinical hyperthyroid and that there had to be a reason why my TSH is so low. So I researched until I discovered the answer, and I was right that there is a reason.
Over the last year I have taken 15 different medications, supplements and vitamins that increase dopamine, which in turn decreases TSH. These all influenced my TSH down to <00.008. These include 30 mg duluxetine for upper back pain, prednisone, curcumin, magnesium, ginkgo biloba, rhodiola and others I’ll have to add later. For smokers, nicotine also increases dopamine, which suppresses TSH. I have never been a smoker. ’ll have to post the list of substances and site references later. It’s 1:00 am here. I stopped taking most of the 15 substances five weeks ago. I will be retesting my bloods soon.
Had no idea that curcumin and magnesium would lower TSH. Interesting.
Hi guysgrams. They don't. 
To clarify, these supplements do not directly lower TSH. Curcumin and magnesium are indirect dopamine agonists. Meaning, they indirectly increase dopamine. If dopamine levels are increased enough cumulatively, they effect TSH production and conversion of T4 into T3. There are many other very common vitamins and supplements that increase dopamine besides curcumin and magnesium. B vitamins such as folate, B12 and B6 increase dopamine. So do vitamin D and Omega 3. Coffee, eggs, proteins, nuts, dairy, fruits and vegetables also increase dopamine. Taking curcumin, magnesium, other indirect dopamine increasing supplements or vitamins by themselves in standard doses will not indirectly increase your dopamine levels very much, nor would they likely decrease TSH. If you are taking a large enough group of other vitamins, supplements or medications that indirectly increase dopamine, and/or you are taking medications that are direct dopamine agonists, then this increase in dopamine reduces TSH.
I already had quite low TSH before starting thyroid medications. Over my life my TSH ranged from 0.7 to 1.8 TSH prior to being diagnosed with Hashimoto's. When diagnosed, my TSH was around 1.6, but my FT4 and FT3 were much too low. I had high TPOab over one thousand, so that confirmed my Hashimoto's. My lowish TSH confused doctors because all they saw was low TSH. They completely overlooked the one thing that matters in thyroid function: FT4 and FT3 levels. Taking thyroid medication suppressed TSH. T4 does so by itself; T3, even more so. Take both T4 and T3, which I do, and this suppressed already low TSH even more.
As an experiment and because I was curious as to if indirect dopamine agonists caused my TSH to suddenly drop to the extreme <0.008 consecutively for four consecutive 6 week lab tests, I stopped taking almost all of the indirect dopamine agonist medications, supplements, vitamins, as well as the topical cream I was using (prescription retinoid) for 6 weeks to see what would happen with my TSH and my FT4 and FT3. I stopped taking a brain-enhancing supplement that contained multiple indirect dopamine increasing ingredients. There were medications that I could not completely stop taking, such as my PRN prescription migraine medication. When I retested my 6 weeks later, my TSH increased. It went from <0.008 to 0.015, 0.24, 0.047. My conversion of T4 into T3 also improved a tiny bit. After my experiment, I went back to taking whatever supplements, vitamins, minerals, oral and topical medications as needed without a thought of how they'd effect my TSH because TSH does not matter, only FT4 and FT3 do.
However, I could care less about my TSH level because it's not TSH that causes any hypo or hyper symptoms, it's too high or too low levels of FT4 and FT3. In order for my FT4 and FT3 to be at my optimal levels, I must take both T4 and T3 at levels that greatly suppress my TSH. All that TSH is is a pituitary hormone that communicates with the thyroid to stimulate thyroid hormones. That is it. Nothing more. If you have a pituitary and/or hypothalamus problem (Central Hypothyroidism), then your pituitary gland will not release enough TSH to stimulate the thyroid to release enough T4. This could be why my TSH was already low prior to starting thyroid medication, as well as my FT4 and FT3.
Increasing dopamine to reduce TSH is not a good idea because this can result in inhibiting conversion of T4 into T3, which is even more of a problem. Reducing TSH by increasing dopamine does not increase FT4 and FT3 levels (Central Hypothyroidism).
pharmablog.eu/2015/01/drugs...
Look forward to seeing that list!
Yes, please let us know the list as I take a lot of vitamins as well as T4.
My Tsh is very low but to feel ok, I have to have a low Tsh, I had a TT in 2009
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