Apologies for the long post and apologies for any inaccuracies - I'm an engineer not an endocrinologist.
One of the reasons I went to the BTA conference was to try to understand why there is such a difference of opinion between endocrinologists as to the benefits of T3. Fundamentally, the current understanding is that the thyroid generates mainly T4 and some T3 and that this T4 is used elsewhere (the brain, liver, kidneys, skin etc) to convert the T4 into T3 for use by the cells through deiodinisation using D1 and D2. Each cell can then regulate the amount of T3 it needs by deactivating the T3 with D3 and there are several feedback loops in the various processes. So T3 is generated from T4 throughout the body. Treating hypothyroidism with T4 is just replacing the T4 not being generated by the thyroid and physiologically our body can use the synthetic T4 to create the T3 it needs. Dosage can be managed by TSH or by adjusting dosage and monitoring side effects.
In taking T3, we bypass this mechanism and the cells don’t get the choice to decide on how much T3 they receive. T3 therefore operates more ‘like a drug’. The dose can be too high (and make you feel good – but not do you good) because T3 delivery (through a tablet, no matter how many times a day you split the dose) does not mimic the body’s processes. (So, if it is to be used, endocrinologists think some sort of slow release T3 needs to be available).
I take T3 only 40 mcg once/day between 2am and 6am. I do not feel as though I get ‘a hit’ after taking it, my heart rate is constant etc and I would say I am ‘normally’ tired at the end of the day (ie in the same way that someone who doesn’t take T3 would be). I hover at the bottom of the T3 range and feel ok. I have tried splitting the dose but to me it was just a pain without any benefit. So clearly my own experience leads me to disagree with the opinion that current T3 formulation should not be used. However, I do still have a thyroid so I am still producing some T4 although the level is low. Recovering with T3 assures Pamela Risk that people with no thyroid can do well on T3 only.
There was mention of ‘intolerance’ to T4 treatment (USA 20-30%, UK10-15%?, Malaysia 0%) but not much discussion. In private discussion, colours, fillers, dosage were mentioned. There is work on genetic issues DIO2 etc, thyroid transporters/receptors MCT8 etc, work is starting on gut interactions and also on feedback mechanisms. But most of these are seen as peripheral to the fundamental mechanism.
My main issue is that the current BTA guidelines are inadequate for GPs and endos, particularly when the patient does not respond well to T4 treatment. My GP wasted multiple blood tests, MRI, lumbar puncture, nerve tests, respiratory consultant, rheumatologist on my analysis until using my own initiative I stopped taking T4 and found I improved in two days.
One of the most useful documents I’ve found this week is buried on the BTF website btf-thyroid.org/images/docu...
The American Guidelines (about 80 pages with 688 references) are also a good read liebertpub.com/doi/full/10....