Need help with my thryoid

[prodaf]

This is exactly what I wanted to hear since I’m in the same predicament. How low was your T3?

TSH = 3.9mUI/L
T3 = 1.04nmol/L
T4 = 102nmol/L

 

[saudades]

What a bunch of BS.

What do you think reverse-T3 does? It is inert and fits into the same receptor as T3 so if you have more of it floating around than you do normal T3, it will end up going into those receptors more than normal T3 and block it from working.

If that's BS, then pray tell us all why that is.

 

[saudades]

Taking T3 does lower T4 production though, right?

Yes, it will lower T4 production.

 

[MyNameIsJeff]

What do you think reverse-T3 does? It is inert and fits into the same receptor as T3 so if you have more of it floating around than you do normal T3, it will end up going into those receptors more than normal T3 and block it from working.

If that's BS, then pray tell us all why that is.

The “hibernation hormone” that isn’t
Technically, the term “hibernation hormone” is inappropriate to describe reverse T3. Reverse T3 can be elevated in conditions associated with a reduction in the metabolic rate, notably starvation, extreme carbohydrate restriction, chronic heart failure, and the non-thyroidal illness syndrome (also called “euthyroid sick syndrome” or “low T3 syndrome”) seen in critical illness, very elderly patients, chronic stress, myocardial infarction, and chronic inflammatory states. In these cases, the rise in rT3 is a consequence, not a cause, of the alterations in intracellular thyroid hormone metabolism directed by the deiodinase enzymes, the relative activities of which are affected by the condition itself.

What is Reverse T3? Reverse T3 (3,3’,5’-triiodothyronine, rT3) is a biologically inactive metabolite of thyroxine (T4) formed by selective deiodination; the active thyroid hormone T3 is formed by removal of an iodine atom in the outer ring of T4, while rT3 is formed by removal of an iodine atom in the inner ring of T4.
Relative amounts of each are determined by the activity of the respective deiodinase enzymes, which are regulated by hormonal and nutritional factors and physiological conditions.

Does rT3 really slow metabolism?
It is frequently claimed in articles published on the internet, but not in peer-reviewed papers, that rT3 blocks or “gets in the way of” the nuclear thyroid receptors. The nuclear thyroid receptors are the sites of action where the primary active thyroid hormone, T3, exerts its effects to drive cellular metabolism and maintain body temperature. There is no credible scientific evidence that rT3 enters the nucleus of the cell at all, and the bulk of the scientific literature states clearly that rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor. It is, however, known to have potent activity in the cytoplasm as an initiator of actin polymerization in astrocytes in the brain [7]. This is mediated in a non-genomic manner by its binding to a very specific thyroid receptor that exists only in the extranuclear compartment. Actin polymerization is important to cell structure and motility, and particularly important to normal brain development.

https://invivohealthcare.com/archiv...the-role-of-reverse-t3-in-thyroid-assessment/

You might think the following: "Oh, so based on the article, rT3 does activate a thyroid receptor in cytoplasm". Well yes, but as it turns out, this kind of thyroid receptor is only activated by T4 and rT3, but not by T3. So neither within the cell, nor outside the cell does rT3 compete with T3 for receptor binding.

Two well-characterized nongenomic actions of thyroid hormone in cultured brain tissues are: 1) regulation of type 2
iodothyronine 5
deiodinase (D2) activity and 2) regulation of
actin polymerization. In particular, the latter is likely to have
profound effects on neuronal migration in the developing
brain. In this study, we determined whether these nongenomic actions also occurred in vivo during brain development. Neonatal hypothyroidism was induced by propylthiouracil given to pregnant dams beginning on d17 of gestation
and continued throughout the neonatal period. On postnatal
d 14, rats were injected with either cold or [125I]-labeled iodothyronines and killed sequentially after injection. In contrast to reports in the adult rat, all three iodothyronines
readily and equally entered developing brain tissues. As expected, cerebrocortical D2 activity was markedly elevated in
the hypothyroid brain and both reverse T3 (rT3) and T4 rapidly
decreased D2 to euthyroid levels within 3 h. Furthermore,
cerebellar G-actin content in the hypothyroid rat was approximately 5-fold higher than in the euthyroid rat. Again, both rT3
and T4 rapidly decreased the G-actin content by approximately 50%, with a reciprocal increase in F-actin content to
euthyroid levels without altering total actin. Neither T3 nor
vehicle had any effect on D2 activity in the cortex or G- or
F-actin content in the cerebellum. The thyroid hormone-dependent regulation of actin polymerization in the rat brain
provides a mechanism by which this morphogenic hormone
can influence neuronal migration independent of the need for
altered gene transcription. Furthermore, these data suggest a
prominent role for rT3 during brain development.

https://www.ncbi.nlm.nih.gov/pubmed/16469804

 

[MyNameIsJeff]

Taking T3 does lower T4 production though, right?

Yes, but in a dose-dependent manner. 10mcg per day of T3 will nowhere near shut down your TSH and T4 production, as claimed by "saudades". For near-complete thyroid suppression you'd have to take 100mcg+ of T3.

 

[aphextwin]

That’s just common knowledge

T3 doesn't have to be taken on an empty stomach. Me and many others would wash it down with food all the time.

 

[nothuman]

T3 doesn't have to be taken on an empty stomach. Me and many others would wash it down with food all the time.

How do you know you're absorbing it when you do this?

 

[aphextwin]

I just know that my doc told me thyroid numbers were high. I told disclosed to her what I was using and she said she didn't prescribe it to patients and to be careful. Does that mean it's better to consume on an empty stomach? I can't say to be honest. I just know I know a well known bb from this site that does the same thing, but he's not on here much anymore but he does the same thing as me. I also know several local guys that take it with or without food. However the majority of the guys I know who use T3, tend to take it with food. Is it the correct way, I can't say.

 

[MyNameIsJeff]

T3 doesn't have to be taken on an empty stomach. Me and many others would wash it down with food all the time.

Can calcium supplements interfere with hypothyroidism treatment?
Answer From Todd B. Nippoldt, M.D.
Yes. Calcium supplements — or antacids containing calcium — can interfere with the absorption of thyroid hormone replacement medications, such as synthetic thyroid hormones levothyroxine (Synthroid, Unithroid, others) and liothyronine (Cytomel), as well as thyroid extract supplements.

This interference happens chiefly if you take thyroid hormone replacement and calcium supplements at or near the same time. You can avoid this problem with the following steps:

Don't take calcium supplements or antacids at the same time you take thyroid hormone replacement.
Take any products containing calcium at least four hours before or after taking thyroid hormone replacement.
Other supplements — especially those containing iron — also can interfere with absorption of thyroid hormone replacement, as can certain foods and medications. If your doctor prescribes thyroid hormone replacement, be sure to tell him or her about all the other drugs and supplements you're taking.

https://www.mayoclinic.org/diseases...sm/expert-answers/hypothyroidism/faq-20058536

 

[saudades]

Yes, but in a dose-dependent manner. 10mcg per day of T3 will nowhere near shut down your TSH and T4 production, as claimed by "saudades". For near-complete thyroid suppression you'd have to take 100mcg+ of T3.

I didn't mean to claim it would shut down TSH and T4 completely, but it will suppress to some degree, correct? I'm sorry I wasn't as accurate as you'd like. We all know that taking ANY hormone will suppress the body's production to a degree.

https://invivohealthcare.com/archiv...the-role-of-reverse-t3-in-thyroid-assessment/

You might think the following: "Oh, so based on the article, rT3 does activate a thyroid receptor in cytoplasm". Well yes, but as it turns out, this kind of thyroid receptor is only activated by T4 and rT3, but not by T3. So neither within the cell, nor outside the cell does rT3 compete with T3 for receptor binding.


https://www.ncbi.nlm.nih.gov/pubmed/16469804

Throw out a single study on rats to a doctor, and they'll just laugh at you and say it has no relevance to humans. Tried it myself, and that's what an actual thyroid doctor told me.

That article is confusing. rT3 is a consequence not a cause? Because of some underlying illness? It's not clear what they say high levels of rT3 relative to T3 indicate. They say, "There is currently no evidence for a clinical basis for the use of this ratio in routine thyroid function assessment." Obviously. If you're experiencing problems due to thyroid, then it isn't a routine assessment anymore, is it? You better get a complete picture of what's going on then and get everything tested if you're experiencing issues. The problem is that it's like pulling teeth to get a doctor to do that. I had a doctor tell me that he *could not* do a test for anything other than TSH and FT4.

So you seem pretty knowledgeable about thyroid. Why then, if you have high rT3, is the "accepted" remedy to take T3? This is what I've been told and what I've read in numerous places. Or is this not the case? If you can't tell, I've had my own problems with rT3, and that is what worked for me. I've heard so much conflicting information from nearly everywhere about thyroid, it makes it near impossible to know what's real. Especially when I try to post my own experience and someone flat out calls it BS.

 

[MyNameIsJeff]

I didn't mean to claim it would shut down TSH and T4 completely, but it will suppress to some degree, correct? I'm sorry I wasn't as accurate as you'd like. We all know that taking ANY hormone will suppress the body's production to a degree.





Throw out a single study on rats to a doctor, and they'll just laugh at you and say it has no relevance to humans. Tried it myself, and that's what an actual thyroid doctor told me.

That article is confusing. rT3 is a consequence not a cause? Because of some underlying illness? It's not clear what they say high levels of rT3 relative to T3 indicate. They say, "There is currently no evidence for a clinical basis for the use of this ratio in routine thyroid function assessment." Obviously. If you're experiencing problems due to thyroid, then it isn't a routine assessment anymore, is it? You better get a complete picture of what's going on then and get everything tested if you're experiencing issues. The problem is that it's like pulling teeth to get a doctor to do that. I had a doctor tell me that he *could not* do a test for anything other than TSH and FT4.

So you seem pretty knowledgeable about thyroid. Why then, if you have high rT3, is the "accepted" remedy to take T3? This is what I've been told and what I've read in numerous places. Or is this not the case? If you can't tell, I've had my own problems with rT3, and that is what worked for me. I've heard so much conflicting information from nearly everywhere about thyroid, it makes it near impossible to know what's real. Especially when I try to post my own experience and someone flat out calls it BS.

There is no need for a remedy for high rT3. High rT3 in and of itself does not have any deleterious effects. It is only an issue if it results from increased type 3 deiodinase activity such that T3 levels are decreased.

And clearly the remedy for low T3 is to take exogenous T3. Exogenous T3 will lower TSH and T4, thereby leading to an improved T3/T4 ratio. rT3 will usually go down together with T4, but this is just a side effect. What we really care about is T3.

 

[saudades]

There is no need for a remedy for high rT3. High rT3 in and of itself does not have any deleterious effects. It is only an issue if it results from increased type 3 deiodinase activity such that T3 levels are decreased.

And clearly the remedy for low T3 is to take exogenous T3. Exogenous T3 will lower TSH and T4, thereby leading to an improved T3/T4 ratio. rT3 will usually go down together with T4, but this is just a side effect. What we really care about is T3.

Then someone needs to tell all the doctors where I live that. Every doc I've been to focuses on T4 and don't want to touch T3.

Thanks for explaining it more thoroughly.

 

[nothuman]

I went back on the 5mcg T3 after two days off and it's not making me tired anymore.

Strange, but I'm happy. Less dizzy too so hopefully there is a connection. The whole point of this is to fix this issue that has tried hard to impact the last year and a half for me.

Should have my T4 soon so I can add 25mg to start and possibly work my way up to 10mcg and 50mcg depending on how I feel.

 

[nothuman]

I'm currently doing 10mcg T3 first thing in the morning and 50mcg T4 right before bed and so far, my dizzy/brain fog issues have been almost non existent. If it turned out that all this time, that debilitating feeling was because I'm hypothyroid...holy shit.

Praying I continue to feel this normal. Curious what blood tests will show when I get them checked eventually.

Thanks to those who recommended doses based on my individual numbers.

 

[deadliftsquates]

Not a fan of T3 only. Even twice a day dosing will lead to significant fluctuations in serum (free-) T3 levels and with it increased heart rate fluctuation etc. See https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5167556/

I'd instead suggest T3/T4 combination therapy. Something like 12.5mcg T3 and 50mcg T4 per day would be a good starting point. Ideally splitting the dose morning/evening, but only if you can then still take it on an empty stomach, away from coffee intake, etc. 10mcg of T3 only would almost certainly be too low.

Hello, can oyu explain this a bit. I thought our bodies made 25 mcg a day? Am I wrong? And if thats the case shouldnt you start out higher than what a person is already taking.

 

[Smack]

There is no need for a remedy for high rT3. High rT3 in and of itself does not have any deleterious effects. It is only an issue if it results from increased type 3 deiodinase activity such that T3 levels are decreased.

And clearly the remedy for low T3 is to take exogenous T3. Exogenous T3 will lower TSH and T4, thereby leading to an improved T3/T4 ratio. rT3 will usually go down together with T4, but this is just a side effect. What we really care about is T3.

Elevated RT3 is usually a result of some stress or illness no?

Other than being an indicator of something else do you think RT3 directly causes any negatives?

 

[Smack]

I'm currently doing 10mcg T3 first thing in the morning and 50mcg T4 right before bed and so far, my dizzy/brain fog issues have been almost non existent. If it turned out that all this time, that debilitating feeling was because I'm hypothyroid...holy shit.

Praying I continue to feel this normal. Curious what blood tests will show when I get them checked eventually.

Thanks to those who recommended doses based on my individual numbers.

Update this thread on your progress. Thyroid and adrenal issues goes hand in hand so that could be something to look into as well.

 

[nothuman]

Update this thread on your progress. Thyroid and adrenal issues goes hand in hand so that could be something to look into as well.

Still continue to feel much better!

I use 10mcg T3 (5 morning and 5 hours later) and 50mcg T4 before bed. If I start feeling a little of the fog, I will take another 5mcg of T3 (totaling 15mcg).

I am curious what my bloodwork is going to show when I get thyroid values tested.


Also, my endocrinolist fired me as a patient because I told him I am using thyroid hormones to fix how horrible I have felt. He said "there is no evidence that I am hypothyroid" despite my Free T3 testing at 2.6-2.9 depending on the test (this is actually called symptomatic subclinical hypothyroidism but what do I know). In other words, I can only continue to see him as long as I feel absolutely miserable. Clear example of some doctors not giving a shit how their patients feel.

 

[Smack]

Still continue to feel much better!

I use 10mcg T3 (5 morning and 5 hours later) and 50mcg T4 before bed. If I start feeling a little of the fog, I will take another 5mcg of T3 (totaling 15mcg).

I am curious what my bloodwork is going to show when I get thyroid values tested.


Also, my endocrinolist fired me as a patient because I told him I am using thyroid hormones to fix how horrible I have felt. He said "there is no evidence that I am hypothyroid" despite my Free T3 testing at 2.6-2.9 depending on the test (this is actually called symptomatic subclinical hypothyroidism but what do I know). In other words, I can only continue to see him as long as I feel absolutely miserable. Clear example of some doctors not giving a shit how their patients feel.

Subclinical aka I'm not knowledgeable so to sound like I am I throw out a label

I've gotten that before and walked out.

So what is the point in even having a normal range? Dr's love using the range to diagnose hypo/hyper with TSH but dismiss it when it comes to the actual levels of active hormone... Makes no sense. Amazing how these people who are supposed to be the smartest of us can be so narrow minded.

*End Rant*

 

[Smack]

despite my Free T3 testing at 2.6-2.9 depending on the test

Can you put the ranges in that were used? They're usually pretty close but some labs use different ranges.