Quote:
|
Originally Posted by Merpig
Clearly Synthroid seems to be the most common treatment of choice these days. Every single person I know in "real life" who has thyroid problems is on Synthroid (or generic). And all of them say it has turned their lives around! I find it hard to believe it works for no one. So does T4 work for 33% who take it? 75% 98%?
|
Deb, your question made me laugh. When I explain why, you're going to laugh too. It's the equivalent of someone who's been told they are diabetic (without being told if they have Type 1 or Type 2) -- saying "Well, why can't I just inject insulin? It works for every Type 1 diabetic I know!"
You've leapt to a very logical (but incorrect) conclusion: that "the thyroid" is a monolithic object rather than an entire metabolic system, and that "treating it" means treating the organ (the gland) rather than the hormones that support the gland.
The diabetes analogy is a good one, because it will hopefully help me to write about this in a way that will clarify the issue for you in a concrete way.
If it turns out that you have the thyroid equivalent of Type 1 diabetes (that is, you have a goiter, which means that there's a problem with the gland itself, or you are converting food into insufficient T4 in the gland) -- then you will indeed be put on Synthroid, and you will have to take it for life. As with Type 1 diabetes, there is currently no cure for a non-working Thyroid GLAND. And T4 is to a large extent, but not exclusively, made in the gland itself.
However, if you have the Type 2 diabetes thyroid equivalent -- it means you have a problem with the T1 or T2 or (in 99.9% of the cases) T3 hormones that support the gland.
But guess what? T1, T2 and T3 -- unlike T4 -- are not made in the gland!
T4 is NOT the physiologically active hormone. Instead it needs to be converted by an enzyme called 5'-deiodinase (the ' after the five means "prime") in order to become the active hormone T3 (liothyronine). At least 80% of the body's daily production of T3 is produced not in the thyroid gland, but in the tissues of your body (liver, kidney, etc.).
T3 IS the physiologically active thyroid hormone and is 4 times more potent, and 3 times shorter acting than T4. T3 is what goes to all the cells in the body and tells them how fast to operate, which determines the body temperature.
5' deiodinase has two jobs. It converts T4 to T3, and it converts RT3 to T2.
5 deiodinase (note, no "prime") is the enzyme that converts T4 to RT3.
The specific route by which this conversion happens:
5' deiodinase (5 "prime" deiodinase) plucks the iodine atom off the 5' position of T4 to make T3. It also converts RT3 to T2. T3 is 4 times more potent than T4 and is the primary agonist (stimulator) at the cell level.
But i
f the 5' deiodinase gets blocked at the cell receptor level, T4 gets converted by 5 (no prime) deiodinase into rT3 instead of T3.
It's exactly like becoming insulin resistant. Instead of glucose being taken up by insulin to the cells for food, the cells have blocked their insulin receptors and the insulin must then carry the glucose to the liver to be converted to adipose fat for storage.
The pancreas just thinks it's not producing enough insulin and makes even more, creating more blocked cell receptors. Would you tell someone in this condition to take insulin to fix the problem because after all, insulin works great for lots of diabetic folks? No, of course not. You would tell this person to begin making the dietary changes needed to slow down insulin production and increase insulin sensitivity.
If they don't listen, what will happen? Even the fat cells will become insulin resistant and then the pancreas will burn out, turning them from a Type 2 to a Type 1 diabetic. Then they'll be able to use insulin all right!
Well, having blocked T3 cell receptors because your T4 is converting not into T3 but into rT3 (not glucose into food, but into adipose fat storage) and pouring MORE T4 into your system will do the same thing: burn out your entire thyroid system. Then sure, you'll be on T4 forever, and T3 too.
"Under stress (and this can take many forms, including calorie and/or carbohydrate restriction over an extended period of time) the body converts T4 less to T3 and more to RT3 to conserve energy. With less T3, the cells of the body slow down. This makes it clear that there is a peripheral auto-regulatory mechanism as well as the glandular one that regulates T4 production. And there is a glandular auto-regulatory mechanism (negative feedback inhibition), that regulates the thyroid gland's T4 production. The amount of T4 that is converted peripherally to the active T3 can drop by 50%. And at the same time, the amount of T4 converted to the inactive RT3 can increase by 50%."
This understanding of the glandular problem (goiter, not enough T4 production in the gland) vs. the peripheral T4 to rT3 problem also answers SeeJay's question about why people stay on Synthroid forever, whereas that is not the case (or should not be the case) for Cytomel.
In the case of a Type 1 diabetes thyroid equivalent, the nature of the glandular problem is likely chronic and incurable (now, anyway), so synthetic T4 must, like insulin, be taken daily and forever.
In the case of a Type 2 diabetes thyroid equivalent, the problem lies in the peripheral tissue and organs, and a short course of the right amount of T3, given in the correct protocol, can drain the rT3 reservoir, unblock the T3 cell receptors and 'fix' the problem -- just as a change from a sugar and fructose-laden high carb diet to a sugar and fructose-free low carb, high fat diet can restore insulin sensitivity to cells. Unless one reverts back to old behavior and/or eating patterns, the fix should be permanent.
This also explains, btw, one noted 'marker' for an rT3 problem and what happens when you fix it: Total Cholesterol level changes.
People who eat a high fat, low carb diet should have very normal TC after one year. But because the 5' deiodinase -- in the liver, remember -- is one of the signals given to the liver that cholesterol levels are fine, and that signal is replaced by the inactive 5 (no prime) deiodinase molecule, the liver keeps churning out what it believes is missing but needed. Cholesterol. That's why mine has increased dramatically in the last two years (as my rT3 problem increased) despite extremely low risk markers for heart disease otherwise. Mine went from 200 to 381 in just 24 months. You didn't answer my question about whether yours was over 200, but I'm guessing it is.
Cytomel therapy has another 'side-effect' and you can probably guess now what it it: dramatic lowering of TC. And now you know why, and exactly how that works, and why every Medical Journal article on the subject specifically states that high TC caused by peripheral thyroid hormone problems be treated by thyroid medication (which you also now know must be T3, and not T4), and not statins. It's the only time I've ever seen statins not suggested by the statinators for curing anything.
With my T3 therapy, I expect my TC to, in the words of the Medical Journals -- drop like a rock.
So to answer your original question that made me laugh: "Does T4 work for 33% who take it? 75% 98%?" -- T4 therapy given to patients with a thyroid glandular problem (that is, the Type 1's of the thyroid world) should be 100% effective, 100% of the time.
Otoh, giving T4 therapy to patients who have peripheral thyroid hormone problems (the Type 2's of the thyroid world) is the same as giving them cotton candy, in ever increasing doses. It might make them feel better (high on the excess glucose) for a short while, and then it will, if not stopped, cause severe damage throughout the body.
At this moment you have no idea if you are Type 1 or Type 2 and speculating about what drug or drugs you will need is futile. You need to get the tests done -- all the tests -- that will tell you which type of thyroid problem you have, and that will tell you what specific drug you need, and in what dose and protocol, to take to help it.
Lisa
Full list of Hypothyroid symptoms -- in a 'range'
). 
Your Thyroid 'problem' -- Type 1 or Type 2?
Linear Mode
