Hi, there can be all sorts of things going wrong! Mysterious resistances, gland failures, conversion disorders, broken pituitary, broken hypothalamus, faulty deiodinase enzymes, etc. All potentially inherited or acquired. We really do seem to have no idea how this complicated system works or what it’s all for, or what can cause it to go wrong.
But I would have thought that if there was widespread ‘central hypothyroidism’, someone would have twigged by now, since that form does show up if you do a full panel of hormone tests.
Or I would have thought that when I wrote this. By now I am in such despair about the pitiful state of medical research that I wouldn’t be surprised if they’d never thought to look, so maybe it is all just perfectly obvious from blood tests and the fools have ignored it.
And the question of ‘what is the optimal treatment’ is bound to be tricky. I’m just trying to demonstrate that the problems exist and are widespread and thus worth looking at!
Although Skinner certainly thought ‘clinical hypothyroidism’ could usually be fixed by bunging enough T4 at the problem. He does mention in his book that he sometimes used T3 or NDT, but he doesn’t go into details. Various other people say ‘mostly T4 with a bit of extra T3’, but no-one has particularly clear ideas on what works and what doesn’t or why.
Thanks for the reference to Ray Peat, I hadn’t heard of him before. Can you link to the best expression of his thoughts?
But I would have thought that if there was widespread ‘central hypothyroidism’, someone would have twigged by now, since that form does show up if you do a full panel of hormone tests
Which tests? I am not aware of any simple blood test that measures the endpoint of thyroid activity on metabolic rate (except, arguably, cholesterol levels), rather than just the state of the T4->TRH->TSH->T4 feedback loop.
mostly T4 with a bit of extra T3′, but no-one has particularly clear ideas on what works and what doesn’t or why
The challenge with T3 is it has a very short half-life, one would need to take very small doses impracticably often to achieve stable levels. Taking mostly T4 with a bit of T3 helps compensate for the reduction in T3 production due to feedback without the problems caused by trying to obtain nearly all T3 directly from a supplement.
Thanks for the reference to Ray Peat, I hadn’t heard of him before. Can you link to the best expression of his thoughts?
His own essays at raypeat.com are the only accurate source, but can be challenging to read. Most of the summaries you will find online don’t do him justice.
Hi, there can be all sorts of things going wrong! Mysterious resistances, gland failures, conversion disorders, broken pituitary, broken hypothalamus, faulty deiodinase enzymes, etc. All potentially inherited or acquired. We really do seem to have no idea how this complicated system works or what it’s all for, or what can cause it to go wrong.
But I would have thought that if there was widespread ‘central hypothyroidism’, someone would have twigged by now, since that form does show up if you do a full panel of hormone tests.
Or I would have thought that when I wrote this. By now I am in such despair about the pitiful state of medical research that I wouldn’t be surprised if they’d never thought to look, so maybe it is all just perfectly obvious from blood tests and the fools have ignored it.
And the question of ‘what is the optimal treatment’ is bound to be tricky. I’m just trying to demonstrate that the problems exist and are widespread and thus worth looking at!
Although Skinner certainly thought ‘clinical hypothyroidism’ could usually be fixed by bunging enough T4 at the problem. He does mention in his book that he sometimes used T3 or NDT, but he doesn’t go into details. Various other people say ‘mostly T4 with a bit of extra T3’, but no-one has particularly clear ideas on what works and what doesn’t or why.
Thanks for the reference to Ray Peat, I hadn’t heard of him before. Can you link to the best expression of his thoughts?
Which tests? I am not aware of any simple blood test that measures the endpoint of thyroid activity on metabolic rate (except, arguably, cholesterol levels), rather than just the state of the T4->TRH->TSH->T4 feedback loop.
The challenge with T3 is it has a very short half-life, one would need to take very small doses impracticably often to achieve stable levels. Taking mostly T4 with a bit of T3 helps compensate for the reduction in T3 production due to feedback without the problems caused by trying to obtain nearly all T3 directly from a supplement.
His own essays at raypeat.com are the only accurate source, but can be challenging to read. Most of the summaries you will find online don’t do him justice.