MESO-Rx Exclusive The Most Effective Growth Hormone Protocol for Fat Loss

Endocrine IGF-1 levels will correlate with exogenous GH administration, as most already know. Once exogenous GH administration ceases, there will be about a 24-36 hour delay and then IGF-1 levels will fall to endogenous levels over the course of roughly 5-10 days, give or take.
That’s the answer I was looking for.
Thanks man..
 
Endocrine IGF-1 levels will correlate with exogenous GH administration, as most already know. Once exogenous GH administration ceases, there will be about a 24-36 hour delay and then IGF-1 levels will fall to endogenous levels over the course of roughly 5-10 days, give or take.
I would say you are being pretty conservative with endogenous IGF- 1 levels returning to normal in 5-10 days. I would venture to say 3-5 days would be sufficient, give or take.

mands
 
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I would say you are being pretty conservative with endogenous IGF- 1 levels returning to normal in 5-10 days. I would venture to say 3-5 days would be sufficient, give or take.

mands


IGF1 serum levels >500 ng/mL took up to 2 weeks to return “normal”

IGF1 serum levels <500 ng/mL took 10 Days or less

5-10 days (ChestRockwell) seems more accurate at the doses and levels we are using and achieving

This is all Approx. and based on actual blood results from myself and several others of course

3-5 days seems to reflex normal/lower doses and levels
 
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Thyroids and hgh natural production are one of the most resilient thing in the human body (hormones related).

No matter what i did i always went back to baseline. Ironically i have impaired my thyroids more with wrong diets or starving my body then with 100mcg t3 daily. Funny :)

That sounds reassuring - so what's your dosing regimen and results from the T3 (cytomel)?
 
IGF1 serum levels >500 ng/mL took up to 2 weeks to return “normal”

IGF1 serum levels <500 ng/mL took 10 Days or less

5-10 days (ChestRockwell) seems more accurate at the doses and levels we are using and achieving

This is all Approx. and based on actual blood results from myself and several others of course

1-3 days seems to reflex normal/lower doses and levels
I don't doubt you one bit. Seems that mine return around 96 hours after last injection.

This was the first one I found.

Recombinant human GH treatment (0.15 IU/kg x day) for 1 week increased serum total IGF-I, IGFBP-3, and ALS, exaggerating the responses to exercise. IGFBP-2 and IGFBP-1 were trivially suppressed. After GH withdrawal, the GH response to identical exercise was suppressed. Total IGF-I, IGFBP-3, and ALS returned to baseline over 3-4 days.

Responses of the growth hormone (GH) and insulin-like growth factor axis to exercise, GH administration, and GH withdrawal in trained adult males: ... - PubMed - NCBI

mands
 
I don't doubt you one bit. Seems that mine return around 96 hours after last injection.

This was the first one I found.

Recombinant human GH treatment (0.15 IU/kg x day) for 1 week increased serum total IGF-I, IGFBP-3, and ALS, exaggerating the responses to exercise. IGFBP-2 and IGFBP-1 were trivially suppressed. After GH withdrawal, the GH response to identical exercise was suppressed. Total IGF-I, IGFBP-3, and ALS returned to baseline over 3-4 days.

Responses of the growth hormone (GH) and insulin-like growth factor axis to exercise, GH administration, and GH withdrawal in trained adult males: ... - PubMed - NCBI

mands

When I was doing my GH/IGF1 serum testing and comparing it to quantitative (HPLC) results......it took quite awhile to return to normal when my IGF1 was 600-650+ ng/mL o_O

So I hear ya on the 96 hours

But when several others did similar blood work...

It took em quite awhile to get back to “normal baseline”

Some cases showed a slight elevation even after 10 days

But I’m sure it’s based on each individual, dose and serum levels
 
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When I was doing my GH/IGF1 serum testing and comparing it to quantitative (HPLC) results......it took quite awhile to return to normal when my IGF1 was 600-650+ ng/mL

:/

So I hear ya on the 96 hours

But when several others did similar blood work

It took em awhile to ge back to “normal baseline”

Some case showed a slight elevation even after 10 days
Seems on the lower end for myself and only a couple others. It's really hard for me to get anyone to get bloods when gathering data.

I wondering if any of the determining factors could attest to groups running AAS, PED's or meds? Would be cool to look at that's for sure.

mands
 
12,5 mcg t3 once a day, before bed on empty stomach.
You will not see any fat loss unless.you are dieting and i'm not atm. I'm using it for increased protein synthesis and maybe to help reduce the accumulation of fat during bulking.

Results? Hard to tell. I dont get pump in the gym unless I get at least 200+ carb a day for few days. That has always happened during t3 use for me, at higher level of t3 I cant get a pump even on 500gr of carbs.

I dont know if i'm getting something out of this, because there are too many variables. I believe in science more.or less... so I do blood test and if my FT3 is borderline high and my TSH is not completely shut down some good things are happening in my body.
If it's worth it... hard to tell.

I have tried 50mcg - 75mcg and even 100+ mcg a day.
Not worth it in my opinion. The risk of burning muscles and all the risks associated with iperthyroidism are not worth the benefit.

But 12,5mcg a day, is a nice boost without making a mess in your body.

Sorry for my very confused explanation


That sounds reassuring - so what's your dosing regimen and results from the T3 (cytomel)?
 
@ChestRockwell whats your opinion on splitting dosage to three times a day for fat loss? I know you mention 4iu split am and pm works well. I’m currently using 5iu a day split am and pre workout. I’m entering the last four weeks of my cycle and I’ve made great gains so far! I been eating at 800cals over maintenance but I’ve also added a little fat but not much.

My plan is to start this week at 300 cals over maintenance then drop cals 300g a week and to eventually get carbs down to 100g a day for the next four weeks. Would you suggest a more aggressive approach as far as dropping cals? Would this still be a beneficial Regiment for fat loss?

8:00am 2iu
Stay fasted until 11:00 am
11:00 am to 3:00 pm- Food and protein
4:00 pm 1.5iu pre workout
Stay fasted until 6:00pm
6:00pm to 11:00 pm- Food and protein
I work a erratic schedule but last shot 1.5iu will be right before bed sometime between 12:00 and 3:00 am but this is only for half the week. I know it last confusing but so is my life! Then obviously stay fasted until 11:00am.
What’s your opinion? Am I over thinking it?
 
What’s your opinion? Am I over thinking it?

You will still have a lipolytic advantage by injecting rHGH, even if you are not fasted. Of course, if you want to maximize your lipolytic potential then a truly fasted AM/PM (3-4IUs) might produce slightly more fat mobilization/oxidation potential than a non-or-partly fasted AM/Midday/PM protocol.

It comes down largely to budget a this juncture and whether or not it is "worth" the extra IUs each day working off the assumption you may not see much extra benefits from it.
 
You will still have a lipolytic advantage by injecting rHGH, even if you are not fasted. Of course, if you want to maximize your lipolytic potential then a truly fasted AM/PM (3-4IUs) might produce slightly more fat mobilization/oxidation potential than a non-or-partly fasted AM/Midday/PM protocol.

It comes down largely to budget a this juncture and whether or not it is "worth" the extra IUs each day working off the assumption you may not see much extra benefits from it.
Thanks for your feedback @ChestRockwell
I was only thinking about using the three times a day protocol for the next 4 weeks or until my cycle ends and then I go back into my normal trt regimen. After which I will definitely be dropping the mid day shot and just run my hgh am/pm. So the extra iu’s are not really an issue.

I have already been doing the pm fasting the whole cycle. Yet still have found ample time, 8 hours to hit my nutritional goals even with the short mid day fast in there also.

So it looks like its going be a short experiment to actually see for myself.
I want to try to maintain as much size and strength as possible while dropping cals.
I’ll also be dropping my test dose down and upping my Mast/NPP dose, also just starting the 3rd week on Var.

Thanks again man!!
 
Can anybody shed some light on this?
Strictly advising not to take t3, because the conversion of t4-t3 via d1/2 regulates fat-loss and with taking t3 you are creating a negative feedback loop and inhibiting the conversion process.

 
Can anybody shed some light on this?
Strictly advising not to take t3, because the conversion of t4-t3 via d1/2 regulates fat-loss and with taking t3 you are creating a negative feedback loop and inhibiting the conversion process.
That was written a very long time ago. Since then, there have been metaanalyses on the hGH-thyroid interactions. The findings are very disparate, but generally, even with long-term high dose administration of rhGH you are unlikely to see T4 out of range, and so don't need to worry about this. Also, it's normal for hGH to increase T3 significantly. I wouldn't worry about your thyroid levels whatsoever with hGH unless you get bloodwork back showing values out of range.
 
That was written a very long time ago. Since then, there have been metaanalyses on the hGH-thyroid interactions. The findings are very disparate, but generally, even with long-term high dose administration of rhGH you are unlikely to see T4 out of range, and so don't need to worry about this. Also, it's normal for hGH to increase T3 significantly. I wouldn't worry about your thyroid levels whatsoever with hGH unless you get bloodwork back showing values out of range.
As far as i understood it is not about the level but the actual conversion process and the effects of the enzymes. HGH increases the conversion process and therefore elevated levels of D2 (which seems to have interactions with metabolism/brown fat etc). This elevation of D2 does not happen if you supplement with T3.
 
As far as i understood it is not about the level but the actual conversion process and the effects of the enzymes. HGH increases the conversion process and therefore elevated levels of D2 (which seems to have interactions with metabolism/brown fat etc). This elevation of D2 does not happen if you supplement with T3.
D2? supplementing T3? I recalled that article pushing for T4 supplementing. Should I reread it, or was there a typo?
 
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D2? supplementing T3? I recalled that article pushing for T4 supplementing. Should I reread it, or was there a typo?
HGH increases the t4-t3 conversion via elevating the converting enzymes d1/d2. Those seem to have fat loss properties by them self. The conversion process does not happen if you supplement with t3, because of the negative feedback loop. You supplement with t4 to keep up with the increased demand. That was my understanding.

Role of d1/d2

Code:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141630/

BAT: D2-mediated TH activation regulates UCP1 expression and thermogenesis, adipocyte proliferation and differentiation and body weight.
 
HGH increases the t4-t3 conversion via elevating the converting enzymes d1/d2. Those seem to have fat loss properties by them self. The conversion process does not happen if you supplement with t3, because of the negative feedback loop. You supplement with t4 to keep up with the increased demand. That was my understanding.

Role of d1/d2

Code:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141630/
I'll reread a little later and give a reply if you want. I am certain that you don't have to worry about supplementing T4 unless hypothyroid or T4 is clinically out of range.
 
HGH increases the t4-t3 conversion via elevating the converting enzymes d1/d2. Those seem to have fat loss properties by them self. The conversion process does not happen if you supplement with t3, because of the negative feedback loop. You supplement with t4 to keep up with the increased demand. That was my understanding.

Role of d1/d2

Code:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6141630/

BAT: D2-mediated TH activation regulates UCP1 expression and thermogenesis, adipocyte proliferation and differentiation and body weight.
OK, I read about d1/d2. All very interesting minutae. However, you can disregard the recommendation to use T4 because as it turns out,

Now, as we’ve seen, GH is HIGHLY synergistic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body. As noted before, T3 enhances many effects of GH by several mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below: Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3) As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study which provided the graph above concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphysiological if we’re going to be using supraphysiological levels of GH, right?

Is wrong; at the very least, it is absurdly irrelevant minutae. The cited 1984 study that is the basis for the crux of Roberts' argument showed that thyroid hormone rapidly stimulates the rate of rat growth hormone [a different compound than 22 kda hGH] gene transcription which parallels the kinetics of binding of 3,5,3'-triiodo-L-thyronine (L-T3) to its nuclear receptor (Yaffe, B. M., and Samuels, H. H. (1984) J. Biol. Chem. 259, 6284-6291).

This is such tangential, unrelated minutae to supraphysiological rhGH use that it's baffling.

T3 increases with exogenous rhGH administration due to peripheral conversion of T4 to T3. Great. The increase in T3 contributes about 50% to GH's increase in REE. GH's primary lipolysis mechanisms have nothing to do with REE or thyroid. That alone should tell you the unbelievable irrelevance of this 2006 article today.

If you want to keep taking T4 with your rhGH, by all means! It's just unnecessary.
 
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OK, I read about d1/d2. All very interesting minutae. However, you can disregard the recommendation to use T4 because as it turns out,

Now, as we’ve seen, GH is HIGHLY synergistic with T3 in the body, and as a mater of fact, if you’ve been paying any attention up until this point, you’ll note that the limiting factor on GH’s ability to exert many of it’s effects, is mediated by the amount of T3 in the body. As noted before, T3 enhances many effects of GH by several mechanisms, including (but not limited to): increasing IGF-1 levels, IGF-1 mRNA levels, and finally by actually mediating the control of the growth hormone gene transcription process as seen below: Comparison of the kinetics of L-T3-receptor binding abundance to changes in the rate of transcription of the GH gene.(3) As you can see, T3 levels are directly correlative to GH gene transcription. The scientists who conducted the study which provided the graph above concluded that the amount of T3 present is a regulatory factor on how much GH gene transcription actually occurs. And gene transcription is what actually gives us the effects from GH. This last fact really seems to shed some light on why we need T3 levels to be supraphysiological if we’re going to be using supraphysiological levels of GH, right?

Is wrong; at the very least, it is absurdly irrelevant minutae. The cited 1984 study that is the basis for the crux of Roberts' argument showed that thyroid hormone rapidly stimulates the rate of rat growth hormone [a different compound than 22 kda hGH] gene transcription which parallels the kinetics of binding of 3,5,3'-triiodo-L-thyronine (L-T3) to its nuclear receptor (Yaffe, B. M., and Samuels, H. H. (1984) J. Biol. Chem. 259, 6284-6291).

This is such tangential, unrelated minutae to supraphysiological rhGH use that it's baffling.

T3 increases with exogenous rhGH administration due to peripheral conversion of T4 to T3. Great. The increase in T3 contributes about 50% to GH's increase in REE. GH's primary lipolysis mechanisms have nothing to do with REE or thyroid. That alone should tell you the unbelievable irrelevance of this 2006 article today.

If you want to keep taking T4 with your rhGH, by all means! It's just unnecessary.

Thanks for taking your time to dig deeper into it. Unfortunately it seems the article gives, T3 being a regulator for HGH transcription, the opposite of the optimal advice. Maybe these articles can get a [oudated] tag or sth.
 
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