Lowering reverse T3

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Vince

Super Moderator
TSH: 2.65 (.450-4.5)
T3 (Free): 3.8 (2.0-4.4)
T4 (Free): 1.58 (.82-1.77)
Reverse T3: 19.6 (9.2-24.1)
Thyroglobulin Antibody: 17.3 (0.9)
TPO Antibody: 75 (0-34)

I know the antibodies indicate Hashi's, but Defy is saying I don't need thyroid meds (yet) based off my other numbers. But I agree, I do have many low thyroid symptoms, and I'm not sure if doing TRT without addressing the thyroid at all is correct?
I would imagine over time your symptoms will get worse because of hashimoto's. Your numbers are good except for the reverse T3, you would like it below 15.
 
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Low doses of T3/Cytomel/liothyronine seemed to do the job for me, and correlated with improvements in motivation and a reduction in fatigue. Under guidance of Defy Medical I've titrated up to 10 mcg qd. Prior to treatment rT3 was 23. Under treatment it was 12 at last measurement. The nice thing about these low doses is that there's minimal suppression of natural production.
 
Low doses of T3/Cytomel/liothyronine seemed to do the job for me, and correlated with improvements in motivation and a reduction in fatigue. Under guidance of Defy Medical I've titrated up to 10 mcg qd. Prior to treatment rT3 was 23. Under treatment it was 12 at last measurement. The nice thing about these low doses is that there's minimal suppression of natural production.

Wow! You got your RT3 down to 12 just on 10mcg of T3? That’s awesome. What brand of T3 are you using? It’s not Empower’s SR T3 is it?
 
Déjà vu. I eventually figured out that it's Sigmapharm Laboratories.

Thanks. I have some of those in my drawer. Before getting prescribed T3 from Empower, that’s the brand Walgreens gave me.

So you’re clearly a smart and analytical guy, let me ask you, do you think thyroid medication is different than testosterone when it comes to suppression? With testosterone, my understanding is if you take a small dose of say 25mg/ week, that will completely suppress your endogenous T, and leave you with less T than before starting TRT. Is thyroid medication different? With a small dose of 10mcg of T3, do you think it’s the same, where it suppresses your system, and you’ll end up with less T3 than before starting thyroid treatment, or do you think it just adds onto whatever naturally free T3 production you already have?
 
T3 medication for suppression of T4. Suppression of T4 to reduce the amount that can convert to RT3. In the end even if your T3 is less more should be getting to the T3 receptor as its not full of RT3. That is if it is true that RT3 blocks the receptor.
 
T3 medication for suppression of T4. Suppression of T4 to reduce the amount that can convert to RT3. In the end even if your T3 is less more should be getting to the T3 receptor as its not full of RT3. That is if it is true that RT3 blocks the receptor.

Very good point. Didn’t even consider that even if free T3 stays the same, or goes down slightly, yet RT3 drops significantly, there could be more free T3 getting to the actual receptors. Again, if RT3 does in fact block the T3 receptors. Which I’ve heard varying things on, but to keep things simple, let’s just assume that’s what RT3 does.
 
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So you’re clearly a smart and analytical guy, let me ask you, do you think thyroid medication is different than testosterone when it comes to suppression? With testosterone, my understanding is if you take a small dose of say 25mg/ week, that will completely suppress your endogenous T, and leave you with less T than before starting TRT. Is thyroid medication different? With a small dose of 10mcg of T3, do you think it’s the same, where it suppresses your system, and you’ll end up with less T3 than before starting thyroid treatment, or do you think it just adds onto whatever naturally free T3 production you already have?
Keep in mind that I'm relatively new to thyroid issues, but my impression is that the negative feedback system is similar to what's seen in the HPTA. With testosterone, it's not true that a small exogenous dose causes complete suppression. Your example of 25 mg per week would probably result in a modest amount of suppression, but still some endogenous production. The key takeaway is that exogenous testosterone seems to be more suppressive than endogenous testosterone. This means that a combination of endogenous and exogenous testosterone always results in lower serum testosterone than with endogenous or exogenous alone.

Let's look at some sample numbers: A normal guy starts with total testosterone at 600 ng/dL. He takes 25 mg T cypionate over each week. I'll arbitrarily say that the stronger exogenous effect is linear, and a factor of 2. The guy is taking 25 * 0.7 = 17.5 mg pure testosterone, which by my assumption is equivalent to 35 mg (2 * 17.5) of endogenous testosterone. Let's say that his natural production is 60 mg per week. Therefore he has suppressed natural production to 25 mg per week (60 - 35), while replacing it with only 17.5 mg. So his total testosterone drops to about 425 mg/dL. This is undoubtedly an oversimplification, but I think it does give an idea of what's happening.

So returning to thyroid, going by only my numbers, it appears that exogenous T3 is only minimally more suppressive than endogenous T3, if at all; pre- and post-treatment free T3 are barely different. Rather, T4 is reduced by the amount needed to make the 10 mcg of T3 I've added exogenously.
 
T3 medication for suppression of T4. Suppression of T4 to reduce the amount that can convert to RT3. In the end even if your T3 is less more should be getting to the T3 receptor as its not full of RT3. That is if it is true that RT3 blocks the receptor.
I'm with you on the reduction of T4 and therefore rT3. But does rT3 actually block receptors? Many popular sites say so. But other reputable sites say not. E.g.:
Since high rT3 is linked with conditions associated with slow metabolism, it has been claimed in internet articles, but not in peer-reviewed papers, that rT3 causes a slowing in metabolism by blocking or obstructing the nuclear thyroid receptors. These receptors are the target sites where the primary active thyroid hormone, T3, binds, triggering its actions to drive cellular metabolism and maintain body temperature. Yet there is no credible scientific evidence that rT3 even enters the nucleus of the cell. While rT3 does not bind to, and has no known transcriptional activity at, the thyroid receptor, it does have potent non-genomic activity, mediated by binding to a specific thyroid receptor in the cytoplasm, as an initiator of actin polymerization in astrocytes in the brain [8][9].

So assuming my positive results are not placebo or coincidence, perhaps the "potent non-genomic activity" of rT3 is responsible for the problems being treated.
 
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Keep in mind that I'm relatively new to thyroid issues, but my impression is that the negative feedback system is similar to what's seen in the HPTA. With testosterone, it's not true that a small exogenous dose causes complete suppression. Your example of 25 mg per week would probably result in a modest amount of suppression, but still some endogenous production. The key takeaway is that exogenous testosterone seems to be more suppressive than endogenous testosterone. This means that a combination of endogenous and exogenous testosterone always results in lower serum testosterone than with endogenous or exogenous alone.

Let's look at some sample numbers: A normal guy starts with total testosterone at 600 ng/dL. He takes 25 mg T cypionate over each week. I'll arbitrarily say that the stronger exogenous effect is linear, and a factor of 2. The guy is taking 25 * 0.7 = 17.5 mg pure testosterone, which by my assumption is equivalent to 35 mg (2 * 17.5) of endogenous testosterone. Let's say that his natural production is 60 mg per week. Therefore he has suppressed natural production to 25 mg per week (60 - 35), while replacing it with only 17.5 mg. So his total testosterone drops to about 425 mg/dL. This is undoubtedly an oversimplification, but I think it does give an idea of what's happening.

So returning to thyroid, going by only my numbers, it appears that exogenous T3 is only minimally more suppressive than endogenous T3, if at all; pre- and post-treatment free T3 are barely different. Rather, T4 is reduced by the amount needed to make the 10 mcg of T3 I've added exogenously.

Interesting. So looks like the level of suppression might be similar to testosterone, but the way T3 suppressed the thyroid system could be a little different. If T3 suppresses T4, and maintains or improves free T3 levels, while lowering RT3, that could be good news for guys trying to use low dose T3, or low dose NDT. The moderators on the STTM FB group make you believe that low dose thyroid medication therapy isn’t possible, due to it shutting u down and your numbers eventually dropping lower than before treatment. So I’m really curious to learn more, and hear more about people’s experiences using low dose T3 or low dose NDT. I’m currently running an experiment with a 1/4 of a grain of NDT on myself, and will have results in about a month. There’s also a few guys on here, including yourself, that are using low dose thyroid medication, and I’m very curious to see how you all end up doing over the next couple months.
 
... There’s also a few guys on here, including yourself, that are using low dose thyroid medication, and I’m very curious to see how you all end up doing over the next couple months.
I'm just about at the four-month mark, and still happy with the results. Here's the dilemma: I'd like to try having fT3 and fT4 a little higher, but I don't see a practical way to do it without going the route of complete suppression, which I won't do just for the sake of "what if".
 
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I'm just about at the four-month mark, and still happy with the results. Here's the dilemma: I'd like to try having fT3 and fT4 a little higher, but I don't see a practical way to do it without going the route of complete suppression, which I won't do just for the sake of "what if".

What were your labs before T3, what are they after 10mcg of T3, and why would you be worried about 20mcg of T3 if 10mcg is working so well?
 
What were your labs before T3, what are they after 10mcg of T3, and why would you be worried about 20mcg of T3 if 10mcg is working so well?
There's room for improvement, and the thyroid sites claim optimal fT3 is the upper third or quarter of the reference range, while fT4 should be midrange. My numbers are lower. T4 has some importance on it's own, so I'd hesitate to push it lower with more T3, and that might not raise fT3 anyway until there's complete suppression of endogenous T3.
 
There's room for improvement, and the thyroid sites claim optimal fT3 is the upper third or quarter of the reference range, while fT4 should be midrange. My numbers are lower. T4 has some importance on it's own, so I'd hesitate to push it lower with more T3, and that might not raise fT3 anyway until there's complete suppression of endogenous T3.

You're concerns are very valid, and I agree. From what I know about treating the thyroid, I'd be worried about the exact same thing. I'd be worried that increasing your T3 dose will not start increasing free T3 until your endogenous production is completely suppressed, and you're 100% relying on exogenous T3.

Have you thought about trying to add in a very low dose of NDT, to keep free T4 in a healthy range, and try to increase free T3 some more? Then again, it's basically the same dilemma as above with the whole suppression thing, and then you have to worry about NDT possibly increasing RT3 back up, on top of having to worry about the whole suppression dilemma. You're definitely in a tough spot.

My personal recommendation, and if I were you, I would increase your T3 to either 15 or 20 mcg, and see how you feel, and then go from there.
 
Action of Reverse T3 on Cancer Cells

ABSTRACT

Background: Reverse T3 (rT3; 3,3',5'-triiodo-L-thyronine) is widely regarded as an inactive naturally occurring analog of thyroid hormone. rT3 is known to bind to the thyroid hormone analog receptor on plasma membrane integrin αvβ3. This integrin is generously expressed by tumor cells and is the initiation site for the stimulation by L-thyroxine (T4) at physiological free concentrations on cancer cell proliferation. Results: In the present studies, we show that rT3 caused increases of proliferation in vitro of 50% to 80% (P < 0.05–0.001) of human breast cancer and glioblastoma cells.

Conclusion: rT3 may be a host factor supporting cancer growth.

https://www.tandfonline.com/doi/abs/10.1080/07435800.2019.1600536?af=R&journalCode=ierc20
 
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Have you thought about trying to add in a very low dose of NDT, to keep free T4 in a healthy range, and try to increase free T3 some more? Then again, it's basically the same dilemma as above with the whole suppression thing, and then you have to worry about NDT possibly increasing RT3 back up, on top of having to worry about the whole suppression dilemma. You're definitely in a tough spot.

My personal recommendation, and if I were you, I would increase your T3 to either 15 or 20 mcg, and see how you feel, and then go from there.
We have similar thoughts on this. I probably will just try titrating a little higher with the T3 to see how it feels. And it is following the guidance of Defy.

This idea's a little out there, but I'm wondering if anyone has experimented with TRH injections? Might there be any benefits in this, or would it be no different than taking T4?
 
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There's room for improvement, and the thyroid sites claim optimal fT3 is the upper third or quarter of the reference range, while fT4 should be midrange. My numbers are lower. T4 has some importance on it's own, so I'd hesitate to push it lower with more T3, and that might not raise fT3 anyway until there's complete suppression of endogenous T3.

The longevity studies I have seen say ft3 in the lower 1/2 of the range is optimal. everyone seems to ignore this contradictory information, maybe confirmation bias?

Human longevity is characterised by high thyroid stimulating hormone secretion without altered energy metabolism

I don't know why alt-medicine wants optimal ft3 to be in the upper quarter. Don't know what they base this on. My rt3 was 16.4. but I tend be on the side that thinks it's not important as long as it isn't at an extreme.

My ft3 is 2.9 ft4 0.9 with 5 mcg T3 + 25mcg t4 twice a day, seems fine to me.

With out the meds, I was at 2.7 fT3, 0.97 ft4. Not a big difference, but a little higher fT3, but so small I wouldn't be surprised if it was 2.7 next time.

I had tried some natural desiccated thyroid, a smallish dose, I think 1 grain got my ft3 to 4.3, I could feel it but it wasn't totally positive, like an extra load of caffeine might feel. Kind of a buzzy feeling.

Main reason I went back on the T3/T4 was because I was taking some higher potency idodine, which had the biggest effect of pushing my TSH levels up and my ft3 down to 2.1 Likely that effect has gone away.

The most noticeable effect of the t3/t4 seems to be less constipation, but I would have to stop to see if it changes to be more fully convinced. I will likely try and see what happens without any t3/t4 meds sometime in the future.
 
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