The Definitive Thyroid Hormone Thread (T3, T4, some implications for rhGH)

[Biggerp73]

5mcg thrice daily makes no sense at all, but e12h makes sense as fT3 peaks 12h post admin (nothing to do with half life). Again, 25mcg daily is replacement (makes sense if that's the objective), and note that this protocol would be the one you'd choose to most rapidly suppress TSH.

Let's hope @Stewie chimes in

 

[nothuman]

Did you drop the T3 without tapering and how long have you been off the T3? Your post makes me want to try dropping T3 from my thyroid med regimen to see how my body reacts.

I know you asked him but I had dropped T3 suddenly and my natural production came back within days. I would imagine he wouldn't need to taper off T3 if he's also on T4.

 

[Biggerp73]

I know you asked him but I had dropped T3 suddenly and my natural production came back within days. I would imagine he wouldn't need to taper off T3 if he's also on T4.

How long were you on t3 before dropping it? One thing that concerns me about using it is having a period of time after coming off where the metabolism is slow and you gain back the fat you lost

 

[nothuman]

How long were you on t3 before dropping it? One thing that concerns me about using it is having a period of time after coming off where the metabolism is slow and you gain back the fat you lost

I can't remember but it was several times. Only reason I stopped is because I couldn't get the right dose to fix my symptoms (it was medical use and not for bb purposes). Several months at a time and then my levels were back to where they were naturally. Nearly everyone's thyroid production returns after they stop taking it.

 

[danieltx]

Here's a question that hasn't been addressed in this thread so far.

Prevailing wisdom says T3 makes it hard to carb up. If one does a CKD with carbs on the weekend, is there benefit to cutting the T3 dose in half or dropping it altogether on those days? Or does the half life make that pointless?

 

[Biggerp73]

Here's a question that hasn't been addressed in this thread so far.

Prevailing wisdom says T3 makes it hard to carb up. If one does a CKD with carbs on the weekend, is there benefit to cutting the T3 dose in half or dropping it altogether on those days? Or does the half life make that pointless?

I used to have similar thoughts when I was dieting using DNP. I'd go PSMF as long as I could and then would eat a ton of zero fat carb foods (candies, fruits, rice, etc). I wouldn't feel like my muscles really got full the way they would normally from the carbs. In hindsight it would have been better to just not do the "carbups" at all, and just try to keep cals/carbs to a minimum.

But to answer your question, idk. Lol

 

[Type-IIx]

@need4tren I invite you - if you so choose (totally fine to ignore) - to make your case here (rather than cluttering luki's thread) for why PK/PD data in research subjects (e.g., Jonklaas, J., Burman, K. D., Wang, H., & Latham, K. R. (2015). Single-Dose T3 Administration. Therapeutic Drug Monitoring, 37(1), 110–118. doi:10.1097/ftd.0000000000000113) is irrelevant to enhanced bodybuilders due to absorption.

My contention is that despite the methods requiring that subjects are fasted, abstain from the use of hormones & vitamins, it does not follow that these factors affect Liothyronine (Cytomel, exogenous T3) absorption per se.

Are you able to provide any data to support the contrapositive: that being in the fed state, using hormones and/or vitamins (i.e., as an "enhanced bodybuilder"), alters the absorption of, and therefore pharmacodynamic increase to free T3, Liothyronine?

 

[OuchThatHurts]

When you talk about rhGH and hypothyroidism, that leaves me a bit confused bc I've always felt the increased T3 conversion was the cause of my increased RHR and lipolysis while administering GH. Hypothyroidism would seem to have the opposite effect. Are you saying it causes hypothyroidism or merely reveals if an individual was already hypo prior to use?

 

[need4tren]

@need4tren I invite you - if you so choose (totally fine to ignore) - to make your case here (rather than cluttering luki's thread) for why PK/PD data in research subjects (e.g., Jonklaas, J., Burman, K. D., Wang, H., & Latham, K. R. (2015). Single-Dose T3 Administration. Therapeutic Drug Monitoring, 37(1), 110–118. doi:10.1097/ftd.0000000000000113) is irrelevant to enhanced bodybuilders due to absorption.

My contention is that despite the methods requiring that subjects are fasted, abstain from the use of hormones & vitamins, it does not follow that these factors affect Liothyronine (Cytomel, exogenous T3) absorption per se.

Are you able to provide any data to support the contrapositive: that being in the fed state, using hormones and/or vitamins (i.e., as an "enhanced bodybuilder"), alters the absorption of, and therefore pharmacodynamic increase to free T3, Liothyronine?

Umm yeah my personal blood work from splitting dose. The pamphlet that comes with your t3 medication stating to keep away from food and a long list of micronutrients as it will impede absorption. Or a quick Google search will tell you the same thing

 

[The Runner]

@Type-IIx Have you seen any research that the use of exogenous T3 over multiple Cycles permanently slows one metabolism due to a reduction in thyroid hormones? I keep reading our bodies eventually bounce back once off T3 but I wonder If levels reduce with multiple Cycles over multiple years.

 

[Type-IIx]

When you talk about rhGH and hypothyroidism, that leaves me a bit confused bc I've always felt the increased T3 conversion was the cause of my increased RHR and lipolysis while administering GH. Hypothyroidism would seem to have the opposite effect. Are you saying it causes hypothyroidism or merely reveals if an individual was already hypo prior to use?

How are you measuring resting heart rate (i.e., device manufacturer & model) and comparing between rhGH and no rhGH (i.e., are you tracking values consistently & deriving a standard deviation)?

There is some evidence of an age-related increase to resting heart rate (RHR) in healthy elderly men by rhGH that is not evident in younger populations. I've never myself seen a case (outside of this data mentioned, a single study) of increased RHR by rhGH (but I do not doubt that you are experiencing it). There is RAAS activation (that can be blocked by a prostaglandin inhibitor like Ibuprofen) that typically persists for only 4 - 5 days at rhGH introduction or dose increase, then dissipates. It's possible that the age-related increase to RHR has a similar etiology as the age-related hemodynamic changes in response to T/androgen use (i.e., increased HCT/Hb).

RhGH induces lipolysis by several mechanisms:

A primary effect of rhGH is mobilization of body fat away from the abdominal region...

The primary effect of GH (in the basal state) is to promote lipid mobilization and oxidation as a means of switching substrate utilization from glucose and protein to lipid oxidation, [26]. The reduction in adipose-tissue mass from GH is due primarily to redistribution of intra-abdominal fat to peripheral depots [16]. Femoral depots certainly contribute, and there is evidence that long-term administration of rhGH results in a significant reduction of visceral adipose tissue [26]. The lipolytic effects are at least partly mediated by the hormone-sensitive lipase (HSL); direct oxidation of FFAs; and suppression of the lipoprotein lipase (LPL) in adipose tissue [26]. Further, GH likely via IGF-I, inhibits the conversion of cortisone to cortisol in adipose tissue from the abdomen by inhibiting the expression and activity of 11β-hydroxysteroid dehydrogenase 1 [26]. The resultant decrease in cortisol protects against central adiposity [26].

The lipolytic action of GH is primarily due to a permissive effect on catecholamine induced lipolysis [6]. GH exerts a marked increase in catecholamine sensitivity in human fat cells [6]. Whereas GH is directly lipolytic in rat adipocytes, this is not the case in humans.

Interestingly, another important means through which lipolysis is achieved is via increased resting energy expenditure (REE) of up to 20%. High GH levels stimulate REE independent of changes in LBM [26].

GH stimulates the peripheral conversion of T₄ to T₃ which is not enough to explain the 10-20% increase in REE from rhGH administration [26]. Administration of 3 IU (66 kg b.w.) daily increased 24 h EE by up to 24% while oxidized fat increased by up to 91% [42].

An increase in the mRNA expression for UCP 3 (an uncoupler) in skeletal muscle and fat after 4-months of GH substitution in hypopituitary patients has been observed [26]. The UCPs act by uncoupling oxidative phosphorylation resulting in heat production without ATP generation [26]. GH also increases resting cardiac output and blood flow in multiple organs including skeletal muscle (increasing REE) [26].

GH increases hormone-sensitive lipase (1-2 hr post-injection) activity, and increases HSL gene expression [40]. Increases the sensitivity of lipolysis to catecholamines [40].

GH binds directly to adipocytes, increasing the fat cell's sensitivity to catecholamines-- i.e., encouraging lipolysis. GH blocks differentiation of adipocytes (stops the formation of body fat). In already existing fat cells, GH inhibits glucose uptake and lipogenesis. IGF-I acts in a manner that actually increases the pool of undifferentiated cells that 'could' create fat cells, but hGH acts in opposition to both the formation of new fat cells and the storage of energy therein.

Excerpt from Bolus.

My view is that a decrement to sub-normal (hypothyroid) T4 levels after beginning a course of rhGH indicates pre-existing hypothyroidism (but does not cause it).

 

[Type-IIx]

Umm yeah my personal blood work from splitting dose. The pamphlet that comes with your t3 medication stating to keep away from food and a long list of micronutrients as it will impede absorption. Or a quick Google search will tell you the same thing

No evidence without a citation bro. "Let me Google that for you," or "muh bloodz" is troll shit.

 

[Type-IIx]

@Type-IIx Have you seen any research that the use of exogenous T3 over multiple Cycles permanently slows one metabolism due to a reduction in thyroid hormones? I keep reading our bodies eventually bounce back once off T3 but I wonder If levels reduce with multiple Cycles over multiple years.

No, the HPT (hypothalamo-thyroid) axis is resilient and not chronically suppressed (unlike the HPG [hypothalamo-gonadal] axis). The HPS (hypothalamo-somatotropic) axis is similarly resilient (such that rhGH does not chronically suppress GH secretion).

 

[Type-IIx]

No evidence without a citation bro. "Let me Google that for you," or "muh bloodz" is troll shit.

@need4tren humorously, I Googled it and the result was that "Thyroid hormones are well absorbed orally. From these hormones, liothyronine is almost completely absorbed and it does not present changes in the absorption rate due to concomitant administration of food."

 

[OuchThatHurts]

How are you measuring resting heart rate (i.e., device manufacturer & model) and comparing between rhGH and no rhGH (i.e., are you tracking values consistently & deriving a standard deviation)?

There is some evidence of an age-related increase to resting heart rate (RHR) in healthy elderly men by rhGH that is not evident in younger populations. I've never myself seen a case (outside of this data mentioned, a single study) of increased RHR by rhGH (but I do not doubt that you are experiencing it). There is RAAS activation (that can be blocked by a prostaglandin inhibitor like Ibuprofen) that typically persists for only 4 - 5 days at rhGH introduction or dose increase, then dissipates. It's possible that the age-related increase to RHR has a similar etiology as the age-related hemodynamic changes in response to T/androgen use (i.e., increased HCT/Hb).

RhGH induces lipolysis by several mechanisms:


Excerpt from Bolus.

My view is that a decrement to sub-normal (hypothyroid) T4 levels after beginning a course of rhGH indicates pre-existing hypothyroidism (but does not cause it).

This was 3 days after bumping up to 8iu but this is not entirely accurate because I normally like to rest for 15 to 20 minutes before doing AM and PM blood pressure daily (minimum is 5 minutes) but I was pressed for time and I just got done running laundry upstairs. God bless those that have a 2nd floor washer/dryer, seriously. So anyway, my heart rate hadn't quite settled back to 80. But prior to bumping up to 8iu, I was low 70's. So you can see here I'm 120 sys/84 dia, 93 BPM. My heart rate was never in those ranges around the house prior to GH. I'm a high 60's/70's guy. Almost my entire life. We talked about this tachycardia before. My doc thought nothing of it but did an ECG anyway and it was perfectly normal but even then I was 85 BPM.

I can go back on this device to my 2iu days where 72, 68, 75, et al was the norm. I would say, anecdotally of course, perhaps a 8-10% increase in RHR. I can say that with a high degree of confidence.

 

[need4tren]

@need4tren humorously, I Googled it and the result was that "Thyroid hormones are well absorbed orally. From these hormones, liothyronine is almost completely absorbed and it does not present changes in the absorption rate due to concomitant administration of food."

It's funny you try and sound so smart with everything and can't even legitimately Google something

Your the dude who likes to use the words "illicit hypertrophy" instead of grow and who we laugh at

 

[OuchThatHurts]

It's funny you try and sound so smart with everything and can't even legitimately Google something

Your the dude who likes to use the words "illicit hypertrophy" instead of grow and who we laugh at

View attachment 160414

So you decided you would spend time pulling an imgflip meme out of your ass to belittle someone for being articulate? Good for you.

 

[Type-IIx]

So you decided you would spend time pulling an imgflip meme out of your ass to belittle someone for being articulate? Good for you.

He's a troll brother, it's what trolls do.

 

[OuchThatHurts]

He's a troll brother, it's what trolls do.

He's coming after us normies. LOL

 

[Type-IIx]

This was 3 days after bumping up to 8iu but this is not entirely accurate because I normally like to rest for 15 to 20 minutes before doing AM and PM blood pressure daily (minimum is 5 minutes) but I was pressed for time and I just got done running laundry upstairs. God bless those that have a 2nd floor washer/dryer, seriously. So anyway, my heart rate hadn't quite settled back to 80. But prior to bumping up to 8iu, I was low 70's. So you can see here I'm 120 sys/84 dia, 93 BPM. My heart rate was never in those ranges around the house prior to GH. I'm a high 60's/70's guy. Almost my entire life. We talked about this tachycardia before. My doc thought nothing of it but did an ECG anyway and it was perfectly normal but even then I was 85 BPM.

I can go back on this device to my 2iu days where 72, 68, 75, et al was the norm. I would say, anecdotally of course, perhaps a 8-10% increase in RHR. I can say that with a high degree of confidence.

View attachment 160413

So it could likely be RAAS activation (was the doc visit showing 85 bpm more than a week after the bump to 8 IU?)

Anyway, consider tracking RHR in a spreadsheet if you do come off of rhGH completely (I believe cyclical use makes a lot of sense, so in my opinion you should do so [unless using agents that increase IGF-I bioavailability, e.g., slin] due to decreased GH response by 6 mo [due to binding protein dynamics, etc.]). Then treat any dose increase (including resumption after a period of cessation) as a second condition (permitting an increase in RHR that should dissipate in < a week). Then continue monitoring on rhGH (constant dose >= a week) as a third condition.