I would really value advice on how to deal with my GP/consultant. I was lucky enough to get agreement for an NHS T3 trial, which i started in August. It has been significantly helping with physical and mental energy levels. I am not fully better, but I also have Long Covid so the picture is a bit complex.
My latest bloods are back:
TSH 0.03 (0.27-4.2)
FT4 17 (12-22)
FT3 5.5 (3.1-6.8)
My consultant mentioned she wanted my TSH to remain above 0.1 and they don’t believe in testing ft4, ft3 in my area so I anticipate a battle ahead to avoid having my dose reduced. My FT3/4 are well within range, but I am just not sure this will be enough to convince them.
For info, my last dose of T3 was taken 11 hr before a 930 am test. Last levo dose 24 hr before. Ferritin was on the lower side at 44 (13-150) and folate could be improved at 7.4 (3.9-20). B12 was over 900. I am on 100 ug levo, 10 ug T3.
Thank you.
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Jasp6
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Thank you SlowDragon . I don’t have vitamin d this time, but it was 92 nmol/l in July. Yes, i split my T3 into 2 doses, one in the morning and one in the evening. I haven’t tried taking it in one go yet. It is so hard to know when i am optimal as i currently have Long Covid with PoTS type symptoms, but I definitely don’t feel overdosed. It would be interesting to experiment with a little more to see the effects. For the moment though i think the bigger battle will be how to hang on to what i have and get the go ahead to continue on T3 beyond the trial. It is so stressful that they put so much emphasis on TSH.
It may not tell us much as my ferritin has dropped since then. I haven’t had the full iron panel done this time. My ferritin seems to wander around between about 30 and 90, with no obvious reason that i have figured out.
At least your consultant understands that taking T3 suppresses TSH, which is a start. Ask her what the aim is of your dose - to make you feel well? And you are getting there, why stop?
The labs usually do test T4 if your TSH is this low, but try as I might, they will not test T3 even if the GP orders it. The only way is private testing, so you could try mentioning this as most consultants are against private testing and wont look a the results. Ask her what options do you have if the NHS will not give you the full picture.
Hope you fully recover from the long Covid soon. Hug.
Thanks serenfach . Sadly i don’t think the consultant will acknowledge that T3 can suppress TSH. I pre-empted a conversation in my last meeting before the trial began as i queried why they were only testing TSH. She doesn’t believe the other tests are particularly helpful. It is good advice to ask the aim of the trial and that it should focus on symptoms. I think i am going to have dig out what i can to link T3 treatment and suppressed TSH and that suppressed TSH on its own is not dangerous or indicative of over treatment.
I had hoped this would be the case. Sadly it doesn’t work in my area. It just gets over-ruled by the lab. They only tested my FT4 this time because my TSH was below range. Otherwise it is only ever TSH. Luckily the nurse at my surgery kindly agreed to take some extra blood for the medichecks thyroid panel at the same time.
I’ve read on this forum in other strings that T3 does suppress TSH. Well it would logically.
I think coffee does too and alcohol and probably a number of other things to a greater or lessers extent.
TSH is not a thyroid hormone. It is made by the pituitary - there is a feedback loop that the pituitary responds to. I’m still getting my head round this and others understand it in more detail - but! When Thyroid hormone levels in the blood are too low TSH is produced - a sort of a chemical kick up the ass for the thyroid to get working. If the thyroid can’t produce any, or produce enough thyroid hormone TSH keeps rising.
If levels of T3 in the blood are sufficient the pituitary stops or reduces the production of TSH, it regulating.
But what if the whole body is not working optimally? Will the pituitary’s response be appropriate and proportional? What if the pituitary out of kilter with the Thyroid?
When FT3 is in the blood why would the pituitary even bother to make TSH? If there are optimal levels of T3 in the blood surely it’s job done? Providing doses of synthetic hormone interrupts the natural feedback loop.
So using just TSH relies on an awful lot of assumptions and seemingly little understanding. Because if you understand only as little as I do (and it IS very little at this stage) you understand TSH is not a reliable measure and probably the least important of all. It should be T3 then closely followed by T4.
How you feel should be front and centre in your treatment.
Apparently TSH started out just as a diagnostic- makes sense - then some smart arse decided to use it to manage thyroid diseases and dosing. I personally have no doubt whatsoever the driving factor would have been financial.
There is nothing to stop you getting private finger prick tests done that give a more complete picture of your well-being.
I do this and it has helped me:
1). understand what’s going on and compare results to how I actually feel (cause let’s face it no one else will with the exception of the forum members). I turn all results, NHS and private, to percentages within range - makes them comparable- watch most doctors squirm, they don’t understand data 😂. We can help you with this.
2) Talk on a level with the Doctors who masquerade as experts, but seem unable to answer more probing questions - Or interpret data.
I’ve been reading on this forum pretty much daily for almost a year now to widen my understanding. I have been given some exceptional advice by members as well as access to a great number of bonafide peer reviewed scientific/medical papers and I am advocating for myself and getting better.
Really hard work at the start getting to grips with it all but so worth it.
Thank you for taking the time for your considered reply. I agree the advice on this forum has been great. I will look back over old posts and the thyroid canada blog for some useful info to arm my defence. I agree there may be various good reasons why TSH goes suppressed, but it doesn’t yet seem to be widely acknowledged in the medical profession. If anyone has any specific papers they would recommend that would be great. Over recent years, i have taken the decision to pay for thyroid bloods myself as I reluctantly accept this just isn’t possible where i live.
Click on members and then search Diogenes- then see posts - a few down the list is a post on suppressed TSH. I bet there will be more! Diogenes very knowledgeable - will discuss papers and often clarify things!
Also below your post are highlighted words they take you to lists on that topic. TSH is there so it will definitely take you to discussions and links to pertinent papers.
There is a lot of information on this site half the battle is knowing where to find it! 😂👍
I think the problem here is reference ranges and what the GP/endocrinologist tolerance levels are for out of range results. I use NDT and my TSH is 0.04 with the same reference range 0.27-4.2. My NHS Consultant accepts the below reference range result. His view is that if it’s measurable it’s okay and latest research he was aware of indicated there was no evidence that cardiac issues or low density was caused by low TSH. My T3 and T4 are within reference ranges. He was very experienced and into partnership working with patients. He has since retired sadly. Other consultants will not operate much below the reference ranges as there is residual concerns about cardiac and bone density effects. Indeed my ill informed GP likes TSH to be midpoint of the reference range around 2. Needless to say my GP is not involved with my care and I self medicate. I wish you luck with this.
The issue may relate to reverse T3 which is a poorly understood entity. If the bulk of your T4 is converted to reverse T3 (due to ongoing illness) TSH will be suppressed but reverse T3 will block T3 from binding T3 receptors meaning that clinically you remain hypothyroid despite the suppressed TSH. So fatigue and weight gain will be present. I think you are very lucky to be in a T3 (liothyronine) trial!
Technical point , but it's not reverseT3 itself that blocks T3 getting to receptors... the deiodinase D3 converts T4 to reverseT3
When D3 action is upregulated (either due to excess T4 , or from a multitude of other potential causes), it catches T4 inside the cells (before it gets to receptors at the nucleus) and turns it to rT3 ,
meaning less T3 can get past the D3 guards to activate receptors in the cells nucleus.
but any T3 that gets past the D3 'guards' can still activate receptors.
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