I am mightily confused, including about debates about T3/4 and RT3
I gather many people on here do not think the RT3 measure is much use, can someone explain why?
I think others eg paul robinson, think that in a lot of cases, when T4 does not convert well it clogs things up and also goes into RT3 which than can have bad effect
I have no GP or endo so trying make sense of this so if anyone can point me to any useful research or ideas?
I was using T3 as my cortisol out of whack and thought the CT3 protocol might help
any thoughts/guidance gratefully received
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lauriegraham
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If RT3 is high you still do not know what has caused it. Only 1 of the reasons for high RT3 is thyroid related. The others are:
Chronic fatigue
Accute illness and injury
Chronic disease
Increased cortisol (stress)
Low cortisol (adrenal fatigue)
Low iron
Lyme disease
Chronic inflammation
Selenium deficiency
Excess physical, mental and environmental stresses
Long term use of certain betablockers
Physical injury
Illnesses like the flu
Starvation/severe calorie restriction
Poorly treated diabetes
Cirrhosis of the liver
Fatty liver disease
Renal failure
Fever of unknown cause
Detoxing of high heavy metals
It used to be thought that RT3 blocked the T3 receptors in cells but this has been shown not to be the case. RT3 has its own receptors and is converted to T2
RT3 is not as simple as "high rT3 = too much T4" .
Tania Smith on Thyroid Patients Canada has written several articles which largely or in part refer to rT3. I suggest finding a comfortable chair and a bit of time and doing a lot of reading.
You'll then know more than most of us!
Reverse T3 in the context of health status, dosages, and thyroid levels
Taking a closer look at the Dr Westin Childs website that @Carys21 linked to: "If reverse T3 levels build up in your body, then it doesn't matter how much free T3 is available.
Reverse T3 will act to block that free T3 and it will prevent your body from feeling better."
"Reverse T3 is an anti-thyroid metabolite that acts to completely BLOCK your thyroid from working. "
and they ALL relate to this passage ,, which is totally unrelated to his points about rT3 blocking T3 action:
"They believe that the only test necessary to evaluate the thyroid is the TSH and that all other additional tests provide no further useful information.
This mode of thyroid management is referred to as the "standard of care" (1).
And the standard of care is the methodology behind treating any given disease state.
It just so happens that the standard of care for thyroid management (treating low thyroid) is to test for the TSH (2) and provide treatment in the form of levothyroxine (3). "
Somebody asks him about this lack of relevant research references, in the readers comments :
"Lee
November 27, 2020 at 10:55 am
Your resource links, specifically the second one, go against what you have written. The first link is not about thyroid topic.
Reply"
Here's his reply:
Dr. Westin Childs
November 27, 2020 at 5:09 pm
"Hi Lee,
You are 100% correct which is why that second link is included 🙂 I’m illustrating the point that conventional doctors only believe in the TSH and this is what leads them to believe they don’t need to test for the reverse T3. The contradiction is the fact that so many thyroid patients continue to suffer from thyroid symptoms despite having a normal TSH which invalidates that point of view. If it were true that the TSH is the only thing needed then thyroid patients wouldn’t have a need to seek out further info or add additional tests.
The first link is included just to teach the reader about the standard of care so they understand what it actually means and how it drives pretty much all treatment in any given specialty. It’s not something specific to the thyroid but more general about all specialties within medicine. But the standard of care is what prevents doctors from being able to look beyond the TSH which is why it’s important to this conversation.
So, despite being asked .... he seems unable to offer any evidence to support his assertion that rT3 actually blocks T3 from getting into T3 thyroid hormone cell receptors and acting on them....which is not surprising , because whatever else rT3 does or doesn't do , it physically cannot fit onto T3 receptors in cells (the shape is just wrong .. it's the 'mirror image' of T3)
This is not an unknown new area of science .. plenty of evidence exists about what 'shape' rT3 is and what shape T3 is .... and there seems to be no evidence that rT3 can stop T3 from having an action on thyroid hormone receptors inside cells.
If he has some evidence that the rest of us haven't seen , why can't he produce a reference to the science of it when asked ?
Until proven otherwise , i'm sticking with what can be backed up be references.
It's curious he doesn't at least mention the many other causes of elevated rT3.
I think nearly everyone can agree that rT3 is an escape valve for safely getting rid of and recycling high T4 . even he acknowledges this :
"Reverse T3 is created by the body from T4. Your body can either turn T4 into T3 or into reverse T3 based on what it needs".
Perhaps if you run a website selling thyroid support 'bundles' for $224 a time , it's very useful to give readers the impression that rT3 is a problem that blocks T3 action.. since an awful lot of people will find some rT3 in their blood if they go looking.
that is so interesting, some of the canadian blogs recommended earlier in the thread similarly are very sceptical of his view .. what's a newbie to think? thanks again
If the science of something is 'over my head', i make my mind up who's opinion i trust more,, and go with that . The canadian blog always puts proper RELEVANT references, which pan out if you check up on them . The inventor of the fT3 and fT4 test has often posted on here to inform us of some of the best Thyroidpatients.Ca articles .. he seems to have a good opinion of lots of Tania S. Smiths work.. neither of them want to sell me anything ... i don't expect myself to be able to understand all the science .. i'm only good at making things .
But if someone doesn't provide references and and is selling something. i'm not likely to buy their sales pitch.
There did used to be an idea that ReverseT3 'blocked' the T3 receptors , but that is now years out of date, and some places like Stop The Thyroid Madness don't seem to have updated some of their writings on the subject . Since this piece by Dr Westin Childs has a recent date on it, it seem he doesn't want to update his thinking either.
Hmm I bought some 'stuff' from his site. It was supposed to be supplements to support your thyroid etc etc in capsule form.
I had to think very hard, but I decided to give it ago. It changed absolutely nothing, I might as well have donated it to ThUK, it would have definately have done more good.
Some things I read make sense, but since the supplements I don't really go there.
I have been reading some articles by Dr. Childs recently. Although he is an unconventional doctor and more open-minded than endos, he is a private practitioner selling his own supplements to improve T4 to T3 conversion and decrease rT3 production. So he also has in interest in making people believe they are suffering from high rT3 and therefore remain hypothyroid. I have noticed other articles where he is contradicted and not answers at all or just says something unrelated. I am always wary of doctors trying to sell their own supplements. For instance, one thyroid doctor writes about iodine deficiency and how hypothyroid patients may need twice the recommend amount (300 mg instead of 150 mg) daily of iodine. Then, this doctor goes on to say: if you buy my supplement XX, you will get that and much more. So they have an interest in making you believe you have rt3 dominance, iodine deficiency, and many other things, because they sell supplements to "cure" them...! Many thyroid patients on hormone replacement fail to make a complete recovery, and those doctors are then telling them they need supplements to get well. It´s very tempting to believe them and order their expensive products. But why take iodine if you are not sure you have a deficiency...?!
On the other hand, some people have high FT3 levels on levo, yet remain hypothyroid, so something must be causing this. If not rT3 dominance, then maybe pooling? That latter is said to be caused by cortisol dysregulation.
The fact that doctors contradict each other makes it worse for patients who end up not knowing whom or what to believe.
I know from my own experience that in the past when my RT3 was high my FT3 was at bottom of range or under. So I believe it blocks the T3. My own personal opinion.
Blocks T3 in what way? Stops it getting into the cells? Or stops T4 from converting into T3?
Absolutely no point in discussing rT3 without giving your FT4 level. You could just be under-medicated, and the high rT3 was due to one of the many other causes.
If rT3 simply blocked T3 receptors, wouldn't you expect T3 levels to remain the same or even rise?
After all, why would blocked receptors reduce the rate of conversion to T3? If the receptors are not getting enough T3, it would appear sensible for your body to make T3 levels rise. Or, if the control processes do not directly get affected by T3 receptors being blocked, it might be expected to remain the same.
Tania S Smith does discuss deiodinase activity in some detail.
I am convinced that the simple idea of rT3 blocking T3 receptors does not explain what is observed. But it is simple to say and imagine. Therefore the concept becomes lodged in the minds of those convinced by it.
When it comes to Dr. Childs, his theories are somewhat contradictory (I have read several of his articles about rT3 dominance...one of which is entitled "how to flush it out of your body").He claims that first of all, your body is turning most of the T4 into rT3, not FT3, leaving you hypothyroid. The cure is to lower or stop levo/NDT and go on T3 only drugs. No T4 = no rT3.
Then, he goes on to say that rT3 stops FT3 from getting into the cells. But, the problem here is that, if you have too little FT3 to begin with (due to impaired FT4 to FT3 conversion), how much FT3 is actually stopped from entering cells?!?! Since rT3 dominance (according to him) is the result of too little FT4 being converted to FT3, then the amount of FT3 would be insufficient already before it is stopped from entering the cells...or am I missing something?
And, surely, the question of what causes the balance to skew towards rT3 is fundamental? With the obvious and direct approach being to change that skew back rather than anything else.
If you used to convert perfectly well to an appropriate T3/rT3 balance, it rather suggests that it isn't a genetic issue (even if particular genetic make-ups tend towards or away from the problem).
If rT3 is so effective at blocking T3 receptors, why doesn't it block them most of them, most of the time? After all, the claim seems to be that a molecule of rT3 attaches to a T3 receptor and then remains in place for much longer than a molecule of T3. Even if the ratio of rT3 to T3 is relatively low, the extreme increase in time and strength of attachment to the receptor would tend to result in a very significant proportion of T3 receptors always being blocked by rT3. It is not as if any of us with working thyroids, or taking T4, wouldn't have a fair amount of rT3 sloshing around.
I have to admit I have problems following Dr. Child´s reasoning. He has written about patients whom he put on T3 because of high rT3, and they lost weight and all hypo symptoms disappeared. But he simultaneously put them on anti-obesity drugs such as Saxenda, which also decreases insulin resistance and leptin resistance (known to cause weight gain) and corrected other hormone imbalances such as low testosterone caused by estrogen dominance. So I am not sure how to know that going off T4 and taking T3 instead is the only reason those patients recovered? I mean, maybe they could have on levo/NDT as well, as long as other hormonal imbalances were corrected? He also claims in one of his article that conditions such as insulin and leptin resistance create a need for higher levels of FT3 in the body, making NDT an unsuitable form of treatment in these cases as it contains mostly T4 which is then converted to too much rT3 in insulin and leptin resistant people. But I have never seen this confirmed anywhere else, so not sure what to believe. He does not quote much research (if any).
He does claim that some drugs (such as anti-depressants, anti-seizure drugs, and blood pressure medication), chronic inflammation, and starvation diets cause rT3 dominance. But that would mean most people with Hashimoto´s have high rT3 levels, right? Not to mention patients with fybromyalgia, RA, etc...yet, it would seem Dr. Lowe did not believe in the rT3 dominance theory, and he was a fybromyalgia expert.
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