The message of this paper is quite clear: low T3 is bad for your heart.
Yes, it was a study in rats, not humans.
They managed to induce the heart issues with just eight weeks of propylthiouracil (PTU). There are members who have had low thyroid hormone, including low T3, for years before receiving treatment. And all too many still have not got there.
Maybe, next time a medic suggests that it isn't worth testing T3, that low T3 isn't important, that T3 is too expensive to prescribe (or their hands are tied), look at this.
Triiodothyronine maintains cardiac transverse-tubule structure and function
Great Job Helvella as usual. Thank You for Bringing Great studies and findings to our Great Thyroid Forum.
WOW!!! It's indeed very impressive. Finally we as thyroid patients are being at last validated that T3 is important for our hearts. Great Start. What took this long for them to realise it. Perhaps the Endo/Dr's will get friendly with the idea if patients don't do well with T4 only that perhaps some T3 won't hurt in fact can help. Maybe now we won't need to beg and plead for the T3 and can be added to the T4 or even a step further to accept that some patients may do well with T3 sole. I'm sure many of us in thyroid land are applauding this major findings. Now we need to get Dr's on board and to implement T3 meds .
On levothyroxine alone I had severe palpitations and the cardiologist was puzzled with the overnight phone calls I had to make so that they could be recorded.
It wasn't until T3 was added to T4 that I got relief from palpitations which resolved altogether when I took T3 only. I am fortunate to have it prescribed for me but it took several years before they did prescribe it.
The angina I suffered on T4 was worse than when my TSH rocketed from zero to 110 and I was still untreated but finally got tested . It rapidly improved with NDT, after two years of t4 monotherapy heart pain hell and I never get it now at all.
You've gone through an awful lot and it is surprising that GPs cannot tell at the initital appointment that the patient has a problem with their thyroid gland.
Before blood tests were introduced all doctors could diagnose us upon our clinical symptoms alone and we got a trial of NDTs (the original thyroid hormone replacements).
I was very fortunate to consult with 'two of the "old school" doctors both of whom were pursued by the 'authorities' for treating hypo/hyper patients as they were taught whilst training. No blood tests were needed and patients were given NDTs (natural dessicated thyroid hormones) made from animals' thyroid glands.
My TSH was 100 and still GP phoned to tell me that I had no problems. I cried.
Thanks to Thyroiduk I found my way through the maze and am now well. Of course, we do need the correct thyroid hormone for us but most have now been withdrawn, i.e. Natural Dessicated Thyroid Hormones (first given in 1892) and T3 (liothyronine) . T4 (levothyroxine) is now prescribed but rarely T4/T3 combination.
At least the GP I eventually saw and listened realised a very low TSH then a jump to 110 a few weeks later was pretty serious stuff. Thank god I got him just in the nick of time. Small wonder you cried - it is stupifying and terrifying in equal measure that someone of that incompetence qualified as a doctor
I saw one a couple of weeks ago for a small mark on my leg, even though I sent pictures which surprised me (It was OK), and I saw a Gastroenterologist 3 months after Coeliac diagnosis, and had endoscope, chest x-rays, abdomen ultrasound, B12 injections, bloods taken at the path lab, but GP face to face....no.
I had AKI, and the GP called me to ask me to check my blood pressure while he was on the phone, stop some meds, sent me another blood form. Lots of phone calls, but face to face.......no.
"T-tubules (transverse tubules) are extensions of the cell membrane that penetrate into the centre of skeletal and cardiac muscle cells. ... Through these mechanisms, T-tubules allow heart muscle cells to contract more forcefully by synchronising calcium release throughout the cell." en.wikipedia.org/wiki/T-tub....
"calcium release" Is this tied up with.... T3 will cause osteoporosis?
Cardiac excitation-contraction coupling (Cardiac EC coupling) describes the series of events, from the production of an electrical impulse (action potential) to the contraction of muscles in the heart.
Calcium ions (Ca2+) contribute to the physiology and biochemistry of organisms' cells. They play an important role in signal transduction pathways, where they act as a second messenger, in neurotransmitter release from neurons, in contraction of all muscle cell types, and in fertilization. en.wikipedia.org/wiki/Calci...
The calcium ion is also known as Ca2+, meaning it has two less electrons than protons and is not stable in nature. As a pure element, it's a grey metal. study.com/academy/lesson/ca...
• STORM imaging shows reduced RyR2 cluster number and size in T3-deficient myocytes
Ryanodine receptor 2 (RYR2) is a protein found primarily in cardiac muscle. In humans, it is encoded by the RYR2 gene.[5][6][7] In the process of cardiac calcium-induced calcium release, RYR2 is the major mediator for sarcoplasmic release of stored calcium ions. en.wikipedia.org/wiki/Ryano...
Junctophilin-2 expression rescues atrial dysfunction through polyadic junctional membrane complex biogenesis. Then it gets far too complicated. ncbi.nlm.nih.gov/gene/57158
Makes me seriously wonder if patients with low T3 would be treated more appropriately if referred to cardiology rather than endocrinology?
Sometimes I think if we were referred to any other 'medical professional' that we might be diagnosed sooner. I also believe that many of our members - without any qualifications regarding a dysfunctional thyroid gland - know much more than the majority of GPs or Endos.
p.s. my GP told me that T3 converted to T4. (that was because my T3 was high and TSH low. He was aware I took T3 alone!
My GP thought erythropoietin (EPO) wasn't produced naturally. It is produced by the kidneys, but cyclists have been known to take synthetic injections developed for kidney disease (I think there was a scandal) because it increases red blood cells and therefore oxygen.
So many hypothyroid patients..........but so little knowledge is astounding.
Thanks Helvella. I am a cardiology research study subject studying the development of heart failure in those living with T2 diabetes, with no known cardiac challenges. My T2 has been in remission since 2014, so I am in a small sub-cohort reflecting that.
I've just had all manner of cardiac tests, including echos, exercise tests, CT, MRI and stressed MRI. Had I known of this paper, I would have been quizzing the researchers and medics looking after me.
I know for a fact that, for me, liothyronine was a blessing in that it enabled my whole body to be calm and relaxed, whereas with levothyroxine even the cardiologist was lost in that he couldn't figure out why I had such severe palps during the night.
Whatever caused the palps I still have to take a betablocker at bedtime - just in case I am plunged into a nightmare of trying to control heart rate.
I've taken a Betablocker for some years now at bedtime.
Thankfully on T3 alone everything is calm and relaxed. I also feel well and healthy.
Thank you helvella, much appreciated. I know the difference T3 made to me, [being left too long un_dx, 7 yrs with heart problems], hence Dr P saying "You'll need T3 for life" and that Armour wouldn't fix me... but considering how ill I'd been for so long, it certainly helped!
This article is so interesting. Last night I had quite severe palpitations and a raised heart rate which dropped within an hour of taking my T3. I think most doctors would assume it is caused by being overdosed….. my interpretation is that I need more T3 to cover the night time. I would be very interested in other people’s experiences.
I, too, found T3 calming and it enabled me to sleep throughout the night as well as being completely symptom-free during the day. What else could someone ask for - 'freedom'.
That would explain why I had chest pains for years prior to treatment with T4/T3, then they’ve come back since they took my T3 away! I told them there was a link between the two but they think I’m mad! What do I know?
Thank you for sharing this paper. I collect this kind of evidence. Unfortunately so far I have not found a physician who defines "low" in the context of ratio but only within range. Having a T3 level that is just so within (the low) range has so far not been considered low. Even when it slightly went below range it still was not considered low "because we don't know how much is actually in the cells" (was one argument). It seems that more and more research is being done, though, on thyroid function and there is hope that one day the importance of a healthy amount of T3 will be acknowledged and become part of routine testing and prescribing. In the meantime there is reason to be grateful for every (rare) doctor who is already aware of the importance of T3. As far as patients go maybe little strokes fell big oaks and persistence will get us somewhere.
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