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Share your labs of Tren’s effect on igf1 levels from hgh

The practical difficulty with determining Tren & rhGH dose/response vis-à-vis Δ IGF-I relates primarily to almost nobody having a true base-line serum IGF-I to refer to.

Some relevant posts/threads I have written on the topic:
Factors that Diminish GH Response (↓Δ IGF-I); The Purpose of the Serum IGF-I Test: A Revision (2.0) [Author: Type-IIx] – this is of the utmost importance for establishing meaningful bases to determine your dose/response.

https://www.professionalmuscle.com/...d-igf1-levels-blood-tests.166733/post-3062493 (thank you @SouthernMuscle for sharing this earlier in this thread) – this is a simplified explanation of the mechanisms. I also have written a detailed subsection, in the Reference portion of Bolus: A Practical and Reference Guide for the Use of Recombinant Human Growth Hormone (rhGH), under the section Interactions with other drugs or exogenous hormones – Trenbolone – that contains subsections (a) Enhanced insulin sensitivity & (b) Increased muscle and decreased fat mass, that explains all that we know about Trenbolone & rhGH synergy (greater than additive; 1 + 1 > 2).

To illustrate based on bloodwork from clients that I have been working with (note that even these guys don't have true base-line IGF-I values, there was always some confounding factor to their IGF-I values that I hope to correct by writing the above MesoRx quasi-article) how individual the apparent (though it cannot be quantified with reference to base-line, only by reference to the normal distribution of IGF-I values in a reference population) ↓Δ IGF-I & ↓ IGF-I (diminished increase to circulating liver-secreted IGF-I & diminished absolute circulating liver-secreted IGF-I) can be:

Example 1 has been running 100 mg trenbolone enanthate q.w., 300 mg testosterone cypionate q.w., anastrozole 0.25 mg t.i.w. & rhGH 5 IU q.d. or 6.i.w. (1.977 IU/BSA/day & 13.842 IU/BSA/week) on a long time-course and enjoys a 345 μg/L serum IGF-I.

Example 2 running 500 mg testosterone cypionate q.w., 350 mg methenolone enanthate q.w., 150 mg trenbolone enanthate q.w. & 5 IU q.d. rhGH (2.5 IU/m²/d & 17.5 IU/m²/w) after 6 weeks saw a paltry serum IGF-I of 246 μg/L. His rhGH dose has since been titrated up.

Other examples are confounded by the use of insulin & other agents that increase IGF-I bioavailability; these are recent, representative examples.

I have tons of baseline bloodwork on mine, and what seems to show is that instead of getting “lowered “ igf1. Rather it’s “capped” at my maximum of 244,244,272,275,261. Instead of going into the 500+ range. These were all while running tren with and without gh, some of them with mk677 even.

The only time I’ve gone over this very tight range is when trenbolone wasn’t in my protocol it seems like based on my notes.

Interestingly the highest igf1 reading I’ve ever gotten was while using no tren, and no gh. It’s possibly I was taking mk677 at some point around when I scored a 377 ng/ml last year, however it’s not listed as having been on mk677 in my notes. However around that time I do remember using it on and off sometimes. Most likely for this test, I was not using mk. However I am certain I wasn’t using tren for this record high reading I’ve gotten it 340ng/ml igf1.

Whenever I’m using gh, it’s during a cutting phase which is when I’m also likely to start adding tren at an increasing dose toward the completion of the cut.

As to what possible mechanism tren achieves this by, I have no idea at this point. I’m aware of the sensitization to Igf and increasing local Igf and its forms, but others such as test also do this but to varying degrees. I wonder why tren would actually result in lower numbers.

What I can say for certain, is that when I added in gh for the first time since last July- October- (4 weeks after starting tren) I visibly became more full in my muscles, my skin looked tighter, not watery and puffy, and my scale weight was about 4lb higher at my highest and lowest points of the week. So im assuming im still getting the effects of having higher igf1 activity. I’d already been dieting for 2 weeks averaging 650 under maintenance when I added in tren, it was Enanthate so I didn’t notice any drastic effect right away, what I did notice was that within 36 hours after adding in gh at 10 iu split 3x daily, my weight shot Up 4 lb. As I was approaching Sunday evening, my lowest weigh ins days for months now, I remained the same weight as I was on Tuesday- Wednesday. Later the next week my high weigh in day was Wednesday night which I weighed in at 4 lb over the previous Wednesday despite being in the same caloric deficit. Also I eat the same exact foods daily and measure my electrolyte intake. So those were kept constant.

Sorry for my long post. But if anything, since switching to igf1 lr3 over high dose gh, as my preferred source of igf1 receptor activity in the off-season for when I’m pushing food the highest, I’ve noticed a unique synergy between igf1 lr3 and Tren. When I I begin an lr3 bottle while taking even a low dose of tren, I’m able to keep using higher doses of lr3 for upward of 8 weeks continuously without any desensitization

In addition to the very distinct sensation and character the pump from lr3 produces, there is also a measurable aspect for me. That is that my blood glucose will run about 7-13 mg/dl lower regardless of my carbohydrate intake, regardless of my insulin dose/ ratio to carbs. This 7-13mg/dl stopped after about 3 weeks multiple times when using lr3 when not taking tren. While taking tren, the acute pump sensation stayed the same, and the objective measurement of blood sugar running lower by 7-13 points remained present longer when combined with tren.
 
I have tons of baseline bloodwork on mine, and what seems to show is that instead of getting “lowered “ igf1. Rather it’s “capped” at my maximum of 244,244,272,275,261. Instead of going into the 500+ range. These were all while running tren with and without gh, some of them with mk677 even.

The only time I’ve gone over this very tight range is when trenbolone wasn’t in my protocol it seems like based on my notes.

Interestingly the highest igf1 reading I’ve ever gotten was while using no tren, and no gh. It’s possibly I was taking mk677 at some point around when I scored a 377 ng/ml last year, however it’s not listed as having been on mk677 in my notes. However around that time I do remember using it on and off sometimes. Most likely for this test, I was not using mk. However I am certain I wasn’t using tren for this record high reading I’ve gotten it 340ng/ml igf1.

Whenever I’m using gh, it’s during a cutting phase which is when I’m also likely to start adding tren at an increasing dose toward the completion of the cut.

As to what possible mechanism tren achieves this by, I have no idea at this point. I’m aware of the sensitization to Igf and increasing local Igf and its forms, but others such as test also do this but to varying degrees. I wonder why tren would actually result in lower numbers.

What I can say for certain, is that when I added in gh for the first time since last July- October- (4 weeks after starting tren) I visibly became more full in my muscles, my skin looked tighter, not watery and puffy, and my scale weight was about 4lb higher at my highest and lowest points of the week. So im assuming im still getting the effects of having higher igf1 activity. I’d already been dieting for 2 weeks averaging 650 under maintenance when I added in tren, it was Enanthate so I didn’t notice any drastic effect right away, what I did notice was that within 36 hours after adding in gh at 10 iu split 3x daily, my weight shot Up 4 lb. As I was approaching Sunday evening, my lowest weigh ins days for months now, I remained the same weight as I was on Tuesday- Wednesday. Later the next week my high weigh in day was Wednesday night which I weighed in at 4 lb over the previous Wednesday despite being in the same caloric deficit. Also I eat the same exact foods daily and measure my electrolyte intake. So those were kept constant.

Sorry for my long post. But if anything, since switching to igf1 lr3 over high dose gh, as my preferred source of igf1 receptor activity in the off-season for when I’m pushing food the highest, I’ve noticed a unique synergy between igf1 lr3 and Tren. When I I begin an lr3 bottle while taking even a low dose of tren, I’m able to keep using higher doses of lr3 for upward of 8 weeks continuously without any desensitization

In addition to the very distinct sensation and character the pump from lr3 produces, there is also a measurable aspect for me. That is that my blood glucose will run about 7-13 mg/dl lower regardless of my carbohydrate intake, regardless of my insulin dose/ ratio to carbs. This 7-13mg/dl stopped after about 3 weeks multiple times when using lr3 when not taking tren. While taking tren, the acute pump sensation stayed the same, and the objective measurement of blood sugar running lower by 7-13 points remained present longer when combined with tren.
The practical difficulty with determining Tren & rhGH dose/response vis-à-vis Δ IGF-I relates primarily to almost nobody having a true base-line serum IGF-I to refer to.

Some relevant posts/threads I have written on the topic:
Factors that Diminish GH Response (↓Δ IGF-I); The Purpose of the Serum IGF-I Test: A Revision (2.0) [Author: Type-IIx] – this is of the utmost importance for establishing meaningful bases to determine your dose/response.

https://www.professionalmuscle.com/...d-igf1-levels-blood-tests.166733/post-3062493 (thank you @SouthernMuscle for sharing this earlier in this thread) – this is a simplified explanation of the mechanisms. I also have written a detailed subsection, in the Reference portion of Bolus: A Practical and Reference Guide for the Use of Recombinant Human Growth Hormone (rhGH), under the section Interactions with other drugs or exogenous hormones – Trenbolone – that contains subsections (a) Enhanced insulin sensitivity & (b) Increased muscle and decreased fat mass, that explains all that we know about Trenbolone & rhGH synergy (greater than additive; 1 + 1 > 2).

To illustrate based on bloodwork from clients that I have been working with (note that even these guys don't have true base-line IGF-I values, there was always some confounding factor to their IGF-I values that I hope to correct by writing the above MesoRx quasi-article) how individual the apparent (though it cannot be quantified with reference to base-line, only by reference to the normal distribution of IGF-I values in a reference population) ↓Δ IGF-I & ↓ IGF-I (diminished increase to circulating liver-secreted IGF-I & diminished absolute circulating liver-secreted IGF-I) can be:

Example 1 has been running 100 mg trenbolone enanthate q.w., 300 mg testosterone cypionate q.w., anastrozole 0.25 mg t.i.w. & rhGH 5 IU q.d. or 6.i.w. (1.977 IU/BSA/day & 13.842 IU/BSA/week) on a long time-course and enjoys a 345 μg/L serum IGF-I.

Example 2 running 500 mg testosterone cypionate q.w., 350 mg methenolone enanthate q.w., 150 mg trenbolone enanthate q.w. & 5 IU q.d. rhGH (2.5 IU/m²/d & 17.5 IU/m²/w) after 6 weeks saw a paltry serum IGF-I of 246 μg/L. His rhGH dose has since been titrated up.

Other examples are confounded by the use of insulin & other agents that increase IGF-I bioavailability; these are recent, representative examples.
Also do you have a mechanism for why high estrogen and especially exogenous will decrease igf1? Is it the increase in binding proteins you mean , or Igf1 serum itself ?
 
I have tons of baseline bloodwork on mine, and what seems to show is that instead of getting “lowered “ igf1. Rather it’s “capped” at my maximum of 244,244,272,275,261. Instead of going into the 500+ range. These were all while running tren with and without gh, some of them with mk677 even.
So, those aren't base-line ("all while running tren, with and without gh, some of them with mk677...") Base-line means after sufficient washout from rhGH & all agents that affect IGF-I. Base. Line.
The only time I’ve gone over this very tight range is when trenbolone wasn’t in my protocol it seems like based on my notes.

Interestingly the highest igf1 reading I’ve ever gotten was while using no tren, and no gh. It’s possibly I was taking mk677 at some point around when I scored a 377 ng/ml last year, however it’s not listed as having been on mk677 in my notes. However around that time I do remember using it on and off sometimes. Most likely for this test, I was not using mk. However I am certain I wasn’t using tren for this record high reading I’ve gotten it 340ng/ml igf1.
Not surprising, as mentioned [here], this demonstrates that Tren & excessive (especially exogenous) estrogens reduce IGF-I, and that insulin increases it (you left out your slin use here and since slin increases IGF-I potently, it's relevant).
Whenever I’m using gh, it’s during a cutting phase which is when I’m also likely to start adding tren at an increasing dose toward the completion of the cut.

As to what possible mechanism tren achieves this by, I have no idea at this point. I’m aware of the sensitization to Igf and increasing local Igf and its forms, but others such as test also do this but to varying degrees. I wonder why tren would actually result in lower numbers.
You'd understand the basics if you read the links [here].
What I can say for certain, is that when I added in gh for the first time since last July- October- (4 weeks after starting tren) I visibly became more full in my muscles, my skin looked tighter, not watery and puffy, and my scale weight was about 4lb higher at my highest and lowest points of the week. So im assuming im still getting the effects of having higher igf1 activity. I’d already been dieting for 2 weeks averaging 650 under maintenance when I added in tren, it was Enanthate so I didn’t notice any drastic effect right away, what I did notice was that within 36 hours after adding in gh at 10 iu split 3x daily, my weight shot Up 4 lb. As I was approaching Sunday evening, my lowest weigh ins days for months now, I remained the same weight as I was on Tuesday- Wednesday. Later the next week my high weigh in day was Wednesday night which I weighed in at 4 lb over the previous Wednesday despite being in the same caloric deficit. Also I eat the same exact foods daily and measure my electrolyte intake. So those were kept constant.

Sorry for my long post. But if anything, since switching to igf1 lr3 over high dose gh, as my preferred source of igf1 receptor activity in the off-season for when I’m pushing food the highest, I’ve noticed a unique synergy between igf1 lr3 and Tren. When I I begin an lr3 bottle while taking even a low dose of tren, I’m able to keep using higher doses of lr3 for upward of 8 weeks continuously without any desensitization
Who said LR3 is subject to significant tachyphylaxis on an 8 week time-course? It does rely on phosphorylation of IGF-I's downstream elements (Akt, PI3K, etc.) meaning that tachyphylaxis (desensitization) is likely; but not to a greater degree than rhGH.

LR3, Tren, & rhGH are synergistic, you got that right.
Also do you have a mechanism for why high estrogen and especially exogenous will decrease igf1? Is it the increase in binding proteins you mean , or Igf1 serum itself ?
Jesus man, I've only answered this a dozen fucking times for you. Why can't you just read and accept any new information? You are the most stubborn fucker I've ever met.

Remember this?
OK, @Para_33 I'm going to make one last ditch attempt to explain the phenomenon simply.

If a person takes nandrolone (Deca) only, an aromatizing androgen, and achieves sub-normal or low-normal E2, they will have significantly elevated IGF-I.

If you stop looking at the product (E2) as a positive factor (i.e., a primary variable that enhances IGF-I) - OK? If you can do that, it will begin to make sense.

I've seen it many times, I think falseprophet09 or has posted bloodwork that supports this here somewhat recently.

In fact, I am sure that E2 is a factor for IGF-I bioavailability - a negative one. That is, once aromatization is very high, E2 feeds back negatively on IGF-I levels because of IGFBP-1.

E2, then, is not a positive factor for enhancing IGF-I. Rather, aromatization as a process is.

If that thought exercise fails, I'm giving up on you.
Estrogens increase IGFBP-1, reducing IGF-I bioavailability and unleashing GH secretion by feedback withdrawal. It's why women have higher GH levels than men by body surface area and are less sensitive per-mg to rhGH.
 
Estradiol can lower IGF-1, especially oral, thanks to first pass metabolism effect. Since the liver is one of the main production sites for IGF-1, oral estradiol is know to decrease IGF-1 fairly reliably (and boost SHBG as well). Lower non-oral estradiol doses are much more mild on SHBG/IGF-1 levels. (gel, patches, injections) , but if the dose is high enough, non-oral will do the same.

I've seen data that trenbolone may even have some estrogen agonist effect. I think it was some fish study or something. It's actually a potent progestogen as well. So potentially it's an androgen/progestogen/estrogen all in one.

Androgens can be very weird. Nandrolone is the parent hormone for many forms of birth control hormones that are progestogens and DHT actually has a metabolite that is estrogenic (3b-diol)
 

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