What to do when T3 does not enter at the cell - what to do alternatively

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I have severe hypothyroidism for years [my age is over 70 years]. I fully follow R Peat's pro-metabolic diet. And I tried to use NDT \ T3 all this time, different brands, different ways.
No way out. I have cold feet and a low pulse and temperature, with or without NDT. Even using high doses of T3 [50 mcg some times] NOTHING happens; no answer to T3 at all.
The question I ask: perhaps you know ways to stimulate the metabolism through the use of substances other than T3, considering that I am absolutely resistant to T3. Salt, caffeine, milk, anything can raise metabolism EVEN when T3 won't be there in the mitochondria to generate energy. Here's the question. [Please: I´m not talking about thyroid problems directly; actually I am talking of a cell resistent to T3 and what to do by other ways].
 

youngsinatra

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I have severe hypothyroidism for years [my age is over 70 years]. I fully follow R Peat's pro-metabolic diet. And I tried to use NDT \ T3 all this time, different brands, different ways.
No way out. I have cold feet and a low pulse and temperature, with or without NDT. Even using high doses of T3 [50 mcg some times] NOTHING happens; no answer to T3 at all.
The question I ask: perhaps you know ways to stimulate the metabolism through the use of substances other than T3, considering that I am absolutely resistant to T3. Salt, caffeine, milk, anything can raise metabolism EVEN when T3 won't be there in the mitochondria to generate energy. Here's the question. [Please: I´m not talking about thyroid problems directly; actually I am talking of a cell resistent to T3 and what to do by other ways].
Low vitamin D is one factor that haidut mentioned in the past.
 

youngsinatra

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In this Danny Roddy podcast with Haidut, he says at 1:50:00 in, the following:

"vitamin D apparently is one of the key factors in allowing t3 to activate the thyroid receptor and basically cause many of these genomic effects, the transcription effects, that are relevant and expected to happen in a person with normal thyroid function. So if your vitamin D is low sometimes you know even taking very high amounts of t3 will not help because the body will quickly deactivate the t3 into T2 or even T1, if the vitamin D is insufficient. So somehow vitamin D and t3 have a very symbiotic relationship and if you know vitamin D is low, i think like almost everybody that tests, like 80 percent of the population is vitamin D deficient in Western countries, sometimes people don't get the benefit of even thyroid supplementation if their vitamin D levels are sub optimal or free fatty acids are high. So the functional hypothyroidism I would define as anything that basically if you do the three measurements pulse, temperature and Achilles tendon reflex. If even one of these is not working, it's not giving you the results that you want to see, that means either not enough t3 is being produced by the liver, probably because the liver is burdened with with excess estrogen and or something is interfering with the function of the thyroid hormone peripherally and that in most cases is either estrogen and/or low vitamin D."
 

cs3000

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Vitamin A receptor is related to Thyroid receptor also

idk exactly how it works looks complex , but T3 usually downregulates expression of thyroid receptors. & vitamin A can counter that effect.
does that indicate vitamin A is blocking t3 receptor activation?
deficiency isn't good for thyroid but maybe vitamin A levels too high can be a problem here
Yet the fact that T3 has a clear effect on TRP2 gene expression which is prevented in the presence of RA highlights the ligand-dependence of the effect we have described.

theres the role of MCT8 or MCT10 transporters which some things can compete with t3 at. e.g carnitine


edit found this Effect of vitamin A on the hypothalamo-pituitary-thyroid axis - PubMed
This study reports the effects of the administration of pharmacologic doses of vitamin A on multiple parameters of thyroid function. Vitamin A decreased total T4 and T3 levels. With vitamin A treatment, there was a marked increase in the percentage dialyzable T3 and T4 both in vivo and in vitro. The serum-free T3 and T4 levels as measured by dialysis were on the whole normal in vitamin A-treated rats.
Following thyroidectomy, the total T4 levels were still decreased, suggesting that vitamin A produced its effects by increasing peripheral clearance of thyroxine. Vitamin A did not alter basal thyroid stimulating hormone (TSH) or its response to thyroid releasing hormone, suggesting a relatively normal hypothalamic-pituitary-thyroid axis in vitamin A-treated animals.
Vitamin A may decrease tissue responsiveness to thyroid hormones as evidenced by the tendency to decreased Na-K-ATPase activity in the livers from vitamin A-treated rats and the decreased growth hormone response to T3 in GH3 pituitary cultures as shown in this study and by the decreased basal metabolic rate found after vitamin A in previous studies. Vitamin A decreased thyroid gland size and increases 125I thyroid uptake. In vitro, vitamin A enhanced T4 to T3 conversion in hepatic homogenates.
so along with helping t3 conversion the vit D effect on t3 responsiveness could be secondary, balancing excess vitamin A
 
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Jamsey

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That study is so ******* misleading do you guys even read what you are posting. If you look at the main treatment group, the human equivalent dosing is 4,516,129 iu 3 times a week, 6,774,193 iu 3 times a week, and 6,774,193 iu 5 times a week. And for their “mechanism of action testing,” they fed rats 2,258,064 iu for seven days straight and didn’t even achieve a significant difference Na-K-ATPase activity in the livers. But yeah let me make sure I don’t eat one too many eggs and accidentally ingest another million iu of vitamin a. It is very clear that in the vast majority of cases where scientists aren’t actively trying to murder rats, vitamin a works in a pro thyroid manner.


VAD = vitamin a deficient/deficiency
ID = iodine deficient

“A study in VAD mice showed that TSH levels had increased twice as much despite increasing total thyroxine levels, suggesting a role for VAD in creating a sort of resistance to thyroid hormones”

“In concomitant VAD and ID animal models, it was demonstrated that vitamin A supplementation (VAS), with or without iodine supplementation, was able to reduce thyroid volume and TSH serum levels and increase thyroid iodine uptake (10, 1416)”

“VAD reduces T3 binding and uptake by tissues and decreases hepatic conversion of T4 to T3, thus increasing the blood levels of both total and free T4 and T3 (10, 1618).”

“In the study carried out in South Africa (29), it was shown that iodine prophylaxis is effective in controlling ID independently of VAD, and that VA supplementation has an additional benefit for the thyroid, in addition to the treatment of VAD. In fact, VAS suppresses TSH-β gene expression, limiting TSH stimulation of the gland and thereby reducing the risk of goiter. The authors suggest that, as in the animal models (11, 1417), vitamin A nutritional status may modify thyroid sensitivity to TSH and/or the peripheral metabolism of thyroid hormones (10, 24, 29).”

“A relatively recent Iranian study by Farhangi et al. observed that, in healthy premenopausal obese and non-obese women, 4 months of VAS was able to reduce TSH and increase T3 levels (possibly due to a hepatic effect on the conversion of thyroid hormones), reducing the risk of subclinical thyroid dysfunction (32).”
Where are the sources that vitamin A contributes to hypothyroidism?

In poor countries, vitamin A intake as positively correlated with thyroid function again and again.

I posted this study in this thread. It is the only human RCT that I’m aware of. They used large doses, 25k IU a day of rentinyl palmitate, and essentially everyone’s thyroid improved sigificantly (lower TSH, higher T3, etc.):

The Effect of Vitamin A Supplementation on Thyroid Function in Premenopausal Women - PubMed

“Vitamin A caused a significant reduction in serum TSH concentrations in obese (p = 0.004) and nonobese (p = 0.001) groups. Serum T3 concentrations also increased in both obese and nonobese vitamin A-treated groups (p < 0.001).”

From the full text:

(The OA grounp [active group, obese] and the N group [non-obese, active group] both got the vitamin A. OP [Obese, placebo] got placebo)

View attachment 18514

View attachment 18511

View attachment 18512

View attachment 18513
 

Hugh Johnson

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I have severe hypothyroidism for years [my age is over 70 years]. I fully follow R Peat's pro-metabolic diet. And I tried to use NDT \ T3 all this time, different brands, different ways.
No way out. I have cold feet and a low pulse and temperature, with or without NDT. Even using high doses of T3 [50 mcg some times] NOTHING happens; no answer to T3 at all.
The question I ask: perhaps you know ways to stimulate the metabolism through the use of substances other than T3, considering that I am absolutely resistant to T3. Salt, caffeine, milk, anything can raise metabolism EVEN when T3 won't be there in the mitochondria to generate energy. Here's the question. [Please: I´m not talking about thyroid problems directly; actually I am talking of a cell resistent to T3 and what to do by other ways].
I suggest looking into Temperature Reset, there was a thread here. It is possible that your body does not consider 37C safe.

I found that my temperature only reached 37c after I forced it to. I also found that the only way I could maintain it was to force my temps up and then do hypoventilation practices. There is something about increasing co2 that drops my temps. It was excruciating, and I was sweating and wearing excessive clothing for a few years.
 
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I agree.

 

bell

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What you're describing sounds like RT3, which blocks the receptor to keep T3 from entering (one theory is that RT3 is made to slow the system down for hibernation)
Peat discusses it a little here, along with some other ideas about why T3 might fail -
View: https://www.youtube.com/watch?v=HynVEuBiCpM

On the hypoxia side, I wonder if you're getting enough B1 (Derrick Lonsdale writes about thiamine/B1 and "pseudo-hypoxia")
On RT3, you can check it with bloodwork. The T4 in your NDT might be the problem. IDK if this community talks about addressing that - if not, the STTM site has some good resources on how to interpret the labs and address it
 

bell

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What you're describing sounds like RT3, which blocks the receptor to keep T3 from entering (one theory is that RT3 is made to slow the system down for hibernation)
Peat discusses it a little here, along with some other ideas about why T3 might fail -
View: https://www.youtube.com/watch?v=HynVEuBiCpM

On the hypoxia side, I wonder if you're getting enough B1 (Derrick Lonsdale writes about thiamine/B1 and "pseudo-hypoxia")
On RT3, you can check it with bloodwork. The T4 in your NDT might be the problem. IDK if this community talks about addressing that - if not, the STTM site has some good resources on how to interpret the labs and address it


I can't find the original reference, but I also have a note that taking too much T3 at once will cause the body to produce RT3. And this is why Peat recommended taking it doses that were throughout the day, but tiny (5-10 mg)
 

youngsinatra

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I can't find the original reference, but I also have a note that taking too much T3 at once will cause the body to produce RT3. And this is why Peat recommended taking it doses that were throughout the day, but tiny (5-10 mg)
T3 cannot convert into rT3, only T4 can do that. But T3 can convert into T2 and T1 IIRC.

But high rT3 is definitely a big problem. Usually involves high stress/adrenal burden, iron deficiency or chronic systemic of intestinal infection. Sometimes a B vitamin deficiency can cause non-responsiveness, because they are needed as cofactors in energy metabolism and create bottlenecks.

rT3 will be high if the body feels unsafe or not well enough supported with a higher metabolic rate. For example if you are nutrient deficient and push the metabolic rate higher, your demand for those nutrients is even higher, so it’s like a protective slow-down.
 
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youngsinatra

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IDK = I don’t know
STTM = Stop The Thyroid Madness (A website dedicated to hypothyroidism therapies)
IIRC = If I Remember Correctly
 
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gilson d dantas
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I can't find the original reference, but I also have a note that taking too much T3 at once will cause the body to produce RT3. And this is why Peat recommended taking it doses that were throughout the day, but tiny (5-10 mg)
Yes. I thing you got the point. Yesterday I was thinking that it would be the problem: reverse T3. Now I have a new problem: how to heal that. I suppose many stressful situations and the use uf NDT are the cause. But now I must to discover what to do.
 

bell

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T3 cannot convert into rT3, only T4 can do that. But T3 can convert into T2 and T1 IIRC.

.
Yes - the body uses the pool of T4 to create RT3. But high T3 levels can be a cue that influences the body's decision to make RT3 instead of T3

Gilson, are you taking your T3 all in one go now or are you spreading it out? I'm attaching a link to an STTM resource, and it links to other resources that talk about how to address potential sources of RT3.

There are also several threads here that discuss RT3 too, I'm just not familiar with them

I would suggest testing for RT3 before working with this (that STTM article can help you clarify what to test) - this is one where the tests lose their value fast, once you start messing around
 

bell

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But high rT3 is definitely a big problem. Usually involves high stress/adrenal burden, iron deficiency or chronic systemic of intestinal infection. Sometimes a B vitamin deficiency can cause non-responsiveness, because they are needed as cofactors in energy metabolism and create bottlenecks.

rT3 will be high if the body feels unsafe or not well enough supported with a higher metabolic rate. For example if you are nutrient deficient and push the metabolic rate higher, your demand for those nutrients is even higher, so it’s like a protective slow-down.
These are great places to look. Anything that causes the body to "decide" it needs to down-regulate to protect itself, like how a machine is engineered to shut itself down if it's going beyond what is safe
 

youngsinatra

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These are great places to look. Anything that causes the body to "decide" it needs to down-regulate to protect itself, like how a machine is engineered to shut itself down if it's going beyond what is safe
Yeah. I know many have great success with treating their (functional) hypothyroidism without taking thyroid medications with Josh Rubin‘s RTN method, which is doing exactly that: supporting the metabolic needs and lowering the stress placed on our physiology by creating lifestyle and dietary changes.

He has YouTube videos about thyroid resistance / Wilson’s syndrome on his channel „EastWest Healing“

I believe he said that most (90%+) of thyroid problems have nothing to do with the thyroid.
 

bell

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Yeah. I know many have great success with treating their (functional) hypothyroidism without taking thyroid medications with Josh Rubin‘s RTN method, which is doing exactly that: supporting the metabolic needs and lowering the stress placed on our physiology by creating lifestyle and dietary changes.

He has YouTube videos about thyroid resistance / Wilson’s syndrome on his channel „EastWest Healing“

I believe he said that most (90%+) of thyroid problems have nothing to do with the thyroid.
THANK YOU!! I'll go look this up for myself too, this looks wonderful :)
 
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gilson d dantas
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Yeah. I know many have great success with treating their (functional) hypothyroidism without taking thyroid medications with Josh Rubin‘s RTN method, which is doing exactly that: supporting the metabolic needs and lowering the stress placed on our physiology by creating lifestyle and dietary changes.

He has YouTube videos about thyroid resistance / Wilson’s syndrome on his channel „EastWest Healing“

I believe he said that most (90%+) of thyroid problems have nothing to do with the thyroid.
Very good!!!!!!!!!!
 
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