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

Type-IIx

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I've noticed a paucity of decent articles on T3/T4. I've also seen some mention of side effects like palpitations/heart rate that was not attributed to T3 use, when it probably should have been. So, I think a thread on T3 and T4, some ramifications, including rhGH, is a good idea.

Definitions:

T3: Triiodothyronine
T3 (exogenous) [Cytomel, LT3]: Liothyronine

T4: Thyroxine
T4 (exogenous) [Tiromel, LT4]: Levothyroxine

T4's effects on resting energy expenditure/body composition:
[Effects of Altering Levothyroxine Dose on Energy Expenditure and Body Composition in Subjects Treated With LT4]
A trend was also seen for a direct correlation between REE/LBM and increases in fT3 levels, with an average 0.11 kcal/kg/d increase in REE/LBM for each 10 pg/dL increase in fT3.

Tying this together with the pertinent Cytomel (Liothyronine) findings:

fT3-50mcg-dose-T3.png

This is the average time-course for fT3 in healthy euthyroid adults given a single 50µg oral dose of Cytomel (Liothyronine) [1].

This is just an average, one PK paper from Goede et al. shows how individualized responses are, see [2].

mean half-life (t1/2) ≈ 1 d (22 h [1])

Given a 50 µg Cytomel dose:
  • TSH change inverse to fT3, nadir 12 h, remained below baseline for ~ 72 h
  • TSH begins to escape from suppression at a T3 concentration ≈ 153 ng/dL with a gradual recovery over several days; about 96 h before TSH returns to baseline with a 100µg dose (18)
  • temp. increased insignificantly (p = 0.56)
  • mean HR ↑ 18 bpm within 12 h [1]

Dose-response
Given a 75 µg Cytomel dose (daily for 14 days):
- fT3 increased by 1.7-fold
- RMR increased by 15% (adjusted for LBM)
- UCP2 increased 1.7-fold and UCP3 increased 2.4-fold [4]

Mechanism of action
The primary mechanism by which T4 (exogenous, Tiromel) increases RMR in humans is through conversion to T3.

The primary mechanism by which T3 increases RMR in humans is not through transcriptional control of the genes encoding mitochondrial proteins [4]. In rats, it is clear that T3 works by uncoupling electron transport from ATP synthesis via increased mRNA expression and mitochondrial protein levels of UCP-3 [3]. UCP-3 is principally expressed in skeletal muscle and heart tissue (in addition to brown and white adipose tissue) [3].
... after T3 injection the variations with time in UCP3 mitochondrial protein content coincided closely with the induced changes in RMR [3].
In rats, evidence of mitochondrial uncoupling was an increase in the nonphosphorylating respiration rate accompanied by a decrease in membrane potential (ΔΨ) of 40% and 8%, respectively [3].

Conversely, in humans, T3 increases RMR/REE without altering the respiratory chain transcription program, as evidenced by a lack of COX2 and mtTFA mRNA induction [4]. It definitely increases mRNA expression of UCP3 and UCP2, and resulted in a significant (15% x 75 µg) RMR/REE increase [4].

Risks, complications
Liothyronine (Cytomel) & Levothyroxine (Tiromel) are associated with increased cardiac arrhythmia events; and may lead to (drug-induced) thyrotoxicosis.

Overt thyrotoxicosis is defined as elevated serum free thyroxine (FT4) and free triiodothyronine (FT3), and suppressed thyrotropin (TSH) concentrations. Thyrotoxicosis with TSH suppression only (TTSO), and normal thyroid hormone concentrations, is also defined as mild thyrotoxicosis. Both overt thyrotoxicosis and TTSO may be caused by the same thyroid disorders. The most common cause of thyrotoxicosis is the use of excessive doses of L-thyroxine for the treatment of hypothyroidism.
Classic symptoms of thyrotoxicosis include:
  • heat intolerance
  • palpitations
  • anxiety
  • fatigue
  • weight loss, and
  • tremor
In euthyroid persons (non-hypothyroid), higher fT4 levels are associated with higher risk of atrial fibrillation [5].

rhGH and T4
Though therapeutic use of rhGH does not cause central hypothyroidism, it may reveal it. A primary mechanism in rhGH's lipolysis is the peripheral conversion of T4 to T3. There are, also, no long-term studies of rhGH in supra-physiological doses. According to at least one well-respected bodybuilding coach ( @luki7788 ), symptoms of hypothyroidism do indeed present with chronic, supra-physiological administration.

The symptoms of hypothyroidism to watch for would be:
  • dry and scaly skin
  • sensitivity to cold
  • brittle hair and nails
  • slow movements and thoughts
  • depression
  • Only if not using clen, muscle cramps may be considered as an additional symptom

There are other symptoms of hypothyroidism; however, they are easily confused with primary effects of rhGH and/or AAS use.
_______________________________________
References:
[1] 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
[2] GOEDE, S. L., LATHAM, K. R., LEOW, M. K.-S., & JONKLAAS, J. (2017). HIGH RESOLUTION FREE TRIIODOTHYRONINE-THYROTROPIN (FT3-TSH) RESPONSES TO A SINGLE ORAL DOSE OF LIOTHYRONINE IN HUMANS: EVIDENCE OF DISTINCT INTER-INDIVIDUAL DIFFERENCES UNRAVELED USING AN ELECTRICAL NETWORK MODEL. Journal of Biological Systems, 25(01), 119–143. doi:10.1142/s0218339017500073
[3] De Lange, P., Lanni, A., Beneduce, L., Moreno, M., Lombardi, A., Silvestri, E., & Goglia, F. (2001). Uncoupling Protein-3 Is a Molecular Determinant for the Regulation of Resting Metabolic Rate by Thyroid Hormone. Endocrinology, 142(8), 3414–3420. doi:10.1210/endo.142.8.8303
[4] BARBE, P., LARROUY, D., BOULANGER, C., CHEVILLOTTE, E., VIGUERIE, N., THALAMAS, C., … LANGIN, D. (2001). Triiodothyronine-mediated up-regulation of UCP2 and UCP3 mRNA expression in human skeletal muscle without coordinated induction of mitochondrial respiratory chain genes . The FASEB Journal, 15(1), 13–15. doi:10.1096/fj.00-0502fje
[5] Baumgartner, C., da Costa, B. R., Collet, T.-H., Feller, M., Floriani, C., Bauer, D. C., … Rodondi, N. (2017). Thyroid Function Within the Normal Range, Subclinical Hypothyroidism, and the Risk of Atrial Fibrillation. Circulation, 136(22), 2100–2116. doi:10.1161/circulationaha.117.028753
 
Great post. I take 18.75mcg (12.5 when waking and 6.25 at 2pm) of T3 per day because I get severe brain fog symptoms without it. My FT3 was in the high 2s because I was converting to rT3 instead. I don't know what caused that for me (maybe high dose HGH use years ago) but I will be taking this the rest of my life.
 
Great post. I take 18.75mcg (12.5 when waking and 6.25 at 2pm) of T3 per day because I get severe brain fog symptoms without it. My FT3 was in the high 2s because I was converting to rT3 instead. I don't know what caused that for me (maybe high dose HGH use years ago) but I will be taking this the rest of my life.

How high was your “high dose” HGH use? And how long were you running those high doses??

I’ve always HGH and thyroid, so many contradicting opinions... I recents got my Total T-3, TSH and T4 tested, all within range... Would you recommend getting more in depth testing?? Also, there’s “in range” and “optimal” do you know what optimal numbers are for these tests??
 
How high was your “high dose” HGH use? And how long were you running those high doses??

I’ve always HGH and thyroid, so many contradicting opinions... I recents got my Total T-3, TSH and T4 tested, all within range... Would you recommend getting more in depth testing?? Also, there’s “in range” and “optimal” do you know what optimal numbers are for these tests??
If everything is in range, I wouldn't worry about it at all. No point in looking for trouble where there is none, right?
 
Maybe i can chime in on the "mild thyrotoxicose".
In germany this is called subclinical hyperthyreose. Ive suffered this one beginning of october for, to me, unknown reasons.
I am not sure if there where any interactions with the heart medication i take due to heart insufficiency or if maybe these heart issues are partly due to
a long existing subclinical hyperthyreose and was just now detected because the sides were enormous with my weak heart.
Maybe it was also due to my new multi that contained far more iodine for a full serving.
I am on T4 since 2012. Started out with 100µ and was increased to 150µ shortly after. Back then, my TSH was around 0,5 and my free T3 and T4 hormones were
in the middle.
At the beginning, we took blood tests every 6 months. Always in range. My doc did this until early 2016 and then told me that it seems "manifested" and we dont need to take routine BW for thyroid anymore.
Thinking back now, this was probably a mistake. I remember that since years (not sure when it started, maybe 2017 or 2018) i had an unbelievable thirst (some days ive downed 10 litres without issues), intolerance to heat and i had to shit more than twice a day eating 2500 kcal a day.
But back then i didnt think too much of it, many people cant stand heat and bodybuilders tend to drink a huge amount.
Now at the beginning of octobre all of the sudden my heart rate increased. I am on a hefty dose of betablocker (7,5mg nebivolol) and my usual resting heart rate during the day is high 50s low 60s, during the night around 50. From one day to another my Heart rate after my morning walk (it was a longer one) didnt go back to my baseline. It stayed around 75-80 the whole day. Also heart palpilations This night i didnt sleep very well, short bursts and my heart rate still was high.. low 70s. The next day same. I thought maybe i get ill and took another short walk to get fresh air. Heart rate did get incredible high (walking flat it was around 115, absolutely not normal for me) and also only dropped to low 80s after the walk.
The coming night was pure horror. I had cold sweats, brutal heart palpilations, didnt sleep a single minute and was out of breath doing barely anything but sitting.
Went to the doc the day after, got ecg done, got troponin test done and they took bloods. Sadly, they just did a few values because they assumed electrolyte imbalance due to my heart medications. All came back negative, ecg just showed high heart rate (low 90s at the docs office) and the heart palpilations which were said to be nothing dangerous.
I was at the docs office 3 times, monday, thursday and the monday of the following week and they had no clue. I googled alot at home and found the hyperthyreose, which absolutely fitted to my symptoms. Even stuff like very thin hear that fell out, diarrhea etc fit perfectly.
At the third appointment I had to tell them to please take blood and check the thyroid hormones and tsh.
TSH came back at 0,001, ft3 and ft4 were in range though. According to the web, this is called subclinical hyperthyreose and it can have the same or near same symptoms a full blown one. In my case, with my weak heart, the symptoms on my heart and cardiovascular system were immense..
we dropped down my dosage to 75µg and they injected something in my veins (forgot what exactly) and the next days the symptoms vanished.
 
Maybe i can chime in on the "mild thyrotoxicose".
In germany this is called subclinical hyperthyreose. Ive suffered this one beginning of october for, to me, unknown reasons.
I am not sure if there where any interactions with the heart medication i take due to heart insufficiency or if maybe these heart issues are partly due to
a long existing subclinical hyperthyreose and was just now detected because the sides were enormous with my weak heart.
Maybe it was also due to my new multi that contained far more iodine for a full serving.
I am on T4 since 2012. Started out with 100µ and was increased to 150µ shortly after. Back then, my TSH was around 0,5 and my free T3 and T4 hormones were
in the middle.
At the beginning, we took blood tests every 6 months. Always in range. My doc did this until early 2016 and then told me that it seems "manifested" and we dont need to take routine BW for thyroid anymore.
Thinking back now, this was probably a mistake. I remember that since years (not sure when it started, maybe 2017 or 2018) i had an unbelievable thirst (some days ive downed 10 litres without issues), intolerance to heat and i had to shit more than twice a day eating 2500 kcal a day.
But back then i didnt think too much of it, many people cant stand heat and bodybuilders tend to drink a huge amount.
Now at the beginning of octobre all of the sudden my heart rate increased. I am on a hefty dose of betablocker (7,5mg nebivolol) and my usual resting heart rate during the day is high 50s low 60s, during the night around 50. From one day to another my Heart rate after my morning walk (it was a longer one) didnt go back to my baseline. It stayed around 75-80 the whole day. Also heart palpilations This night i didnt sleep very well, short bursts and my heart rate still was high.. low 70s. The next day same. I thought maybe i get ill and took another short walk to get fresh air. Heart rate did get incredible high (walking flat it was around 115, absolutely not normal for me) and also only dropped to low 80s after the walk.
The coming night was pure horror. I had cold sweats, brutal heart palpilations, didnt sleep a single minute and was out of breath doing barely anything but sitting.
Went to the doc the day after, got ecg done, got troponin test done and they took bloods. Sadly, they just did a few values because they assumed electrolyte imbalance due to my heart medications. All came back negative, ecg just showed high heart rate (low 90s at the docs office) and the heart palpilations which were said to be nothing dangerous.
I was at the docs office 3 times, monday, thursday and the monday of the following week and they had no clue. I googled alot at home and found the hyperthyreose, which absolutely fitted to my symptoms. Even stuff like very thin hear that fell out, diarrhea etc fit perfectly.
At the third appointment I had to tell them to please take blood and check the thyroid hormones and tsh.
TSH came back at 0,001, ft3 and ft4 were in range though. According to the web, this is called subclinical hyperthyreose and it can have the same or near same symptoms a full blown one. In my case, with my weak heart, the symptoms on my heart and cardiovascular system were immense..
we dropped down my dosage to 75µg and they injected something in my veins (forgot what exactly) and the next days the symptoms vanished.
Thank you for your perspective, though I am sorry you had to experience hyperthyreose/thyrotoxicosis.
 
I hope this post helps provide the tools necessary to achieve goals while avoiding the risks/complications by knowing some of the signs. Optimal, clinically, would be defined as within range. Optimal, in physique enhancement may be defined as minimal effective dose for minimal duration without experiencing of the complications listed (inter-individual).
 
I wanted to ask you something @Type-IIx .

in europe cynomel (liothyronin sodique) is out of stock right now in so many countr

how much of a difference will be in the pharmacokinetics and dinamics changing from sodique to hydrochlorid??

i suppose none or little bit. I hope you know somethin absout it. Thanks
1636269763956.jpeg
 
I'm gonna pose this here, what time of day should we, as bodybuilders, take T3? I seem to remember Kikel having a very strong opinion on this, but I can't recall what time he was defending.
 
I'm gonna pose this here, what time of day should we, as bodybuilders, take T3? I seem to remember Kikel having a very strong opinion on this, but I can't recall what time he was defending.
I believe its on his Instagram and its in the middle of the night
 
Sure, the HPT axis is under circadian, pulsatile, ultradian, and circannual rhythmic regulation. But taking exogenous T3 kind of renders this regulation moot, no? By deciding to take exogenous T3 you are throwing a wrench into the regulatory system. So, you're going to take it between 0200 - 0400 hr during its natural peak because... this synchronizes with natural release? Can anyone expound on how this has clinical or practical relevance? There is simply no basis for a belief that HPT biorhythms are relevant once you start administering exogenous hormones. To disrupt sleep and wake up in the middle of the night to take something that you can just take whenever is... not necessary, and suboptimal.
 
I find if I take t3 an hour before waking. I wake up easier.. I read T3 and cortisone rise in the morning to wake you. So ive been doing this and feel more natural.
 
Sure, the HPT axis is under circadian, pulsatile, ultradian, and circannual rhythmic regulation. But taking exogenous T3 kind of renders this regulation moot, no? By deciding to take exogenous T3 you are throwing a wrench into the regulatory system. So, you're going to take it between 0200 - 0400 hr during its natural peak because... this synchronizes with natural release? Can anyone expound on how this has clinical or practical relevance? There is simply no basis for a belief that HPT biorhythms are relevant once you start administering exogenous hormones. To disrupt sleep and wake up in the middle of the night to take something that you can just take whenever is... not necessary, and suboptimal.
If the half life is 12 hrs (I'm not sure this is the case and am not stating that, just saw it in a number of threads) then I could almost argue for using the exogenous amount 12 hours AWAY from the natural release with an eye toward possibly retaining some of the natural release.

I never could find his post yesterday, I looked and even listened to a few podcast episodes that seemed like they may cover it, no dice.
 
I'm honestly questioning using it at all. I was unable to fill out like AT ALL last year at my show, and feel like I also lost a shitload of muscle and I wonder if it wasn't a lot to do with the T3 I ran the last 5 weeks or so.

plus this time around I have DNP to help with the fat loss piece (and help it fucking does)
 
If the half life is 12 hrs (I'm not sure this is the case and am not stating that, just saw it in a number of threads) then I could almost argue for using the exogenous amount 12 hours AWAY from the natural release with an eye toward possibly retaining some of the natural release.

I never could find his post yesterday, I looked and even listened to a few podcast episodes that seemed like they may cover it, no dice.
The half life is between 1 and 2 days (closer to 36 hours than 12). Multiple administration of 50 mcg of T3 provides a mean maximal plasma concentration of total T3 of 346 ng/dL in about 2.5 hours with an AUC of 4,740 ng * h/dL.
 

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