The focus, as so often, appears to be on cholesterol but knowing about ongoing research can have some interest.
Thyroid. 2020 Feb 26. doi: 10.1089/thy.2020.0071. [Epub ahead of print]
Thyroid hormone analogues: an update.
Zucchi R1.
Author information
Abstract
The development of thyroid hormone (TH) analogues was prompted by the attempt to exploit the effects of TH on lipid metabolism, avoiding cardiac thyrotoxicosis. Analysis of the relative distribution of the a and b subtypes of nuclear thyroid hormone receptors (TRa and TRb), showed that TRa and TRb are responsible for cardiac and metabolic responses, respectively. Therefore, analogues with TRb selectivity were developed, and four different compounds have been used in clinical trials: GC-1 (sobetirome), KB-2115 (eprotirome), MB07344/VK2809, and MGL-3196 (resmetirom). Each of these compounds was able to reduce LDL cholesterol, but a phase 3 trial with eprotirome was interrupted because of a significant increase in liver enzymes and the contemporary report of cartilage side effects in animals. As a consequence, the other projects were terminated as well. However, in recent years TRb agonists have raised new interest for the treatment of non-alcoholic fatty liver disease (NAFLD). After obtaining excellent results in experimental models, clinical trials have been started with MGL-3196 and VK2809, and the initial reports are encouraging. Sobetirome turned out to be effective also in experimental models of demyelinating disease. Aside TRb agonists, TH analogues include some TH metabolites that are biologically active on their own, and their synthetic analogues. 3,5,3'-triiodothyroacetic acid (Triac) has already found clinical use in the treatment of some cases of TH resistance due to TRb mutations, and interesting results have recently been reported in patients with the Allan-Herdon-Dudley syndrome, a rare disease caused by mutations in the TH transporter MCT8. 3,5-diiodothyronine (T2) has been used with success in rat models of dyslipidemia and NAFLD, but the outcome of a clinical trial with a synthetic T2 analogue was disappointing. 3-iodothyronamine (T1AM) is the last entry in the group of active TH metabolites. Promising results have been obtained in animal models of neurological injury induced by b-amyloid or by convulsive agents, but no clinical data are available so far.
PMID: 32098589
DOI: 10.1089/thy.2020.0071
Full paper not available, and will probbaly remain behind a paywall:
I agree with you Helvella . In addition with the current events that is taking place now I'm thinking going with synthetic T3 and T4 is the way to go now. Hopefully that doesn't change.
Much easier to dose with NDT and it’s the closest thing to what our thyroids once made - it should be a personal choice - like getting bits of pig in your heart if it fails and no warfarin or synthetic parts and warfarin for life. Why should synthetics be the way to go? Not for me.
I agree with you . I was dosing with NT for many years till they reformulated and back ordered . I then switched to NP which worked great till they reformulated even thou they denied it . But patients know better and labs confirmed it that NP was not working as well as it used to . Patients where getting hypo symptoms with NP . Having all across the board of NDT's being reformulated being back ordered complicates our thyroid meds reliability . Hopefully they won't reformulate the synthetic T4 /T3 . Our choices of NDT are very sadly becoming slim . It's very Shameful and Tragic . Thyroid meds are our *Life Line*.
Yes the reformulation of NDT is a big issue. I read something recently it was an old article (pre T4 monotherapy era), where they actually said patients preferred T3 monotherapy to NDT so you may be right that the synthetics are ultimately going to be the most controllable thyroid hormone therapy. I could revert to true vegetarianism if it became easily available and was well administered, which is very appealing. I was so happy when I thought I was on synthetic T4 for life until I still felt utterly dreadful two years later. I took NDT out of sheer desperation. It was a lifesaver...but not for the poor pigs from whom it was derived.
Yes ! Yes ! I too was on T4 thyroid meds only . I was very excited that this is it and no worries . Oh how wrong I was . At first it worked fine after my TT. I started having all sorts of symptoms after a few months of T4 only . Palpitations high BP anxiety etc. Not till some T3/NDT was added to a lowered T4 that I got relief . T3/NDT made a huge difference for me. I'm very grateful for it . I don't convert my T4 to T3 well . The heart has T3 receptor sights as does other organs as well.
We sound pretty similar but my thyroid was totally destroyed by the autoimmune process. Oddly what I had is sometimes called Graves hypothyroidism (atropic autoimmune thyroiditis) it was certainly not very standard for hypothyroidism symptom wise - a real mixed bag of hypo and hyper symptoms. My T4 to T3 conversión is woefully inadequate since the poor old glad croaked. Rest of the hypothyroid relatives have no problems on Levothyroxine.
I'm sorry you went through the gamut too. I'm sure it was very concerning and caused lots of anxiety along the way. I know it did for me too. Yet Dr/Endo know so very little about it . I'm sure there are many that feel great with T4 only . I'm just not as lucky and many are in the same camp too . I was very frightened that this is the new way I needed to resort to. I am so excited and grateful for the T3/NDT that pulled me out of this slump .
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