A new review provisionally out to describe the importance of T2.
MINI REVIEW ARTICLE
Front. Endocrinol. | doi: 10.3389/fendo.2018.00427
3,5-diiodothyronine: a novel thyroid hormone metabolite and potent modulator of energy metabolism
Rosalba Senese, Pieter de Lange, Giuseppe Petito, Maria Moreno, Fernando Goglia and ANTONIA LANNI*
I can't access it either. It looks interesting though and I look forward to reading it.
If there's difficulty, put Frontiers in Thyroid Endocrinology into Google, and access second item down. This article comes up.
Here is the link: frontiersin.org/articles/10...
What does it mean for us, however? Do we always make it automatically from our normal T4 activity? I am no scientist! Help please...
Yes it will come from either T4 or T3 you take in. But perhaps insufficient T4/T3 may reduce T2 production and lead to energy problems.
Thank you for your speedy response. That’s a relief then. One less issue to worry about.
Could this account for why Natural dessicated thyroid is preferred by users above synthetic T4/T3 and T4 monotherapy - as per a recently posted study from USA and my good self who can only compare it to levothyroxine - which I found worlds apart in efficacy, NDT winning hands down.
There are lots of things in NDT we know nothing about. I would love to see the pharmacodynamics of T3 and T4 uptake by NDT compared against pure T4 and T3. This would tell us a very great deal about uptake and use of the hormones.
Yes it sounds very interesting. I hope this research is undertaken to help elucidate matters pertaining to NDT
Thanks for all the info you share 🤗
Yes, they (Pharma funded) seem to veer round attempting to answer such questions…… makes you wonder why (or perhaps not)….
Yes, agreed. In Greg Kelly's paper: Peripheral Metabolism of Thyroid Hormones: A Review, figure 3, he explains that in the liver, T4 -> T3 (called the 5' deiodinisation process) then T3 -> T2 (called the 3' deiodinisation process) and both depend upon selenium as a catalyst. So, if you are not producing T3 in the liver (i.e. you are a bad converter) you are unlikely to be producing T2 for the same reason, that reason I propose is lack of selenium to produce the selenoenzyme.
I just did a quick search for 3,5-T2 and came across this :
sciencedirect.com/science/a...
Title : The classic pathways of thyroid hormone metabolism
A quote from this link on the subject of 3,5-T2 :
A recent study in critically ill patients found that circulating levels of 3-T1AM were decreased during NTIS, suggesting that the decarboxylation pathway is not responsible for the increased metabolism of TH observed during illness (Langouche et al., 2016). The same study did observe increased circulating 3,5-T2 levels in critically ill patients. The mechanism via which 3,5-T2 is produced in vivo, the cause of the increased levels during NTIS, and the biological significance of 3,5-T2 during illness are currently unknown.
I was not aware that there was an increase in metabolism of thyroid hormones during illness. In fact, I always thought it was supposed to be a good idea to very slightly reduce thyroid hormone intake during illnesses like flu (I never actually did this myself though). Obviously I've got my facts rather badly muddled.
Thanks for posting Diogenes. look forward to reading full paper. So there is a reason for T1 and T2 just the same as there is a reason for T3 in the body otherwise why would healthy individuals produce them. The fly in the ointment is getting Docs, endos to accept that TSH and T4 only are not the only things they should be looking at when treating imbalances of thyroid hormones.
Count me in on any research 😉although 2 of my family felt well on levothyroxine alone.
I am replying to your request for help in the thyroid world. Not sure how I can help you but if I can then i am happy to contribute to any further knowledge being found. Ann Simpson
Endo review... that's a new slant!
