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TRENBOLONE and igf1 levels - Blood tests

So, let me use this post to clarify things:
- Tren + rhGH ⇒ ↑mIGF-I (muscle isoform of IGF-I)
- Test + Tren + rhGH ⇒ ↑cIGF-I (systemic-liver IGF-I) & ↑mIGF-I

Whereas,
E2 (say, purposefully taking an estradiol pill) + Tren + rhGH ⇒ ↓cIGF-I (due to the absence of in situ aromatization + IGBP-1 negative feedback)

I have seen lots of evidence of rhGH ⇒ ↑cIGF-I, before "settling" at a much lower serum IGF-I after between 6 and 9 months of continuous use.
You realize your audience is a bunch of bodybuilders??? I mean thanks for clarifying its all so clear to me now....wtf??? It took me like a week to memorize these fucking pre and post and Intra carb shakes I gotta dial up my insulin and keep an eye on my gshock like my life depends on it because I'm all about what's cutting edge and you know what I'm pretty damn proud of my accomplishment and now you start posting some shit that is giving me flashbacks to genchem2 this is unreal but it's OK because you clarified the walls of text with hieroglyphics and indecipherable equations I've never even heard of but I appreciate the effort. I'll get back to you after I reread some calculus books.
 
I present it as a curiosity - my blood results and IGF serum
They are made over 2 weeks, the first without Trenbolone (300+) and the second after adding Trenbolone (the only change I made was switching from Nandrolone to Trenbolone, all other factors were exactly the same).
I have heard more than once that Trenbolone can lower IGF levels, but I thought that it only occurs with low estrogen levels and my estrogen is still between 50 and 80
Were u on gh/slin at the time? Those levels are low af, and ur a 110+ kg guy ur not small those levels are way low. My levels are double that even on 5iu hgh only.
 
You realize your audience is a bunch of bodybuilders??? I mean thanks for clarifying its all so clear to me now....wtf??? It took me like a week to memorize these fucking pre and post and Intra carb shakes I gotta dial up my insulin and keep an eye on my gshock like my life depends on it because I'm all about what's cutting edge and you know what I'm pretty damn proud of my accomplishment and now you start posting some shit that is giving me flashbacks to genchem2 this is unreal but it's OK because you clarified the walls of text with hieroglyphics and indecipherable equations I've never even heard of but I appreciate the effort. I'll get back to you after I reread some calculus books.
Hahah I really like your style bro, this post had be laughing out loud. Yeah I know it's chem nerd shit, but I always delve into the shit once I start learning about it. Don't have to memorize any formulas, just some rules of thumb are that tren does lower GH response (IGF-I), aromatizing androgens like test/deca/dbol synergize with GH, don't take estradiol pills like some people have started to do.
 
Hahah I really like your style bro, this post had be laughing out loud. Yeah I know it's chem nerd shit, but I always delve into the shit once I start learning about it. Don't have to memorize any formulas, just some rules of thumb are that tren does lower GH response (IGF-I), aromatizing androgens like test/deca/dbol synergize with GH, don't take estradiol pills like some people have started to do.
Now I think we are on the same Page and I feel good that I follow what you are saying. The thought of taking estradiol pills That is off the charts I never considered that. I do follow the rest of yiur recommendations tho just standard stuff. I don't add a bunch of stuff unless i have no choice because I've consistently seen guys come back with blood work proving time and again little things can and do impact the system overall big time. AIs serms and overall calories etc. It all matters.
 
Hepatic somatotroph quantity is genetically determined. To improve GH response (the increase in serum IGF-I), what you can control is body fat % (lower is better), liver health, keeping estradiol/estrogens under control, and if possible adding test or aromatizing androgen (300mg of test or 800+mg of deca weekly in the mix will markedly increase GH response).
Thanks man, do you have interests in Liver and Kidney health?

On a minimal regimen right now, might have had liver and kidney issues in the past (acute episodes), today I'm prettu carefu about it, right now taking 500mg TUDCA 1200mg NAC daily, as a general Liver health protocol.

kidneys you cannot do much with supplementation unfortunately, BP meds and astragalus might be our best bets here.
 
Thanks man, do you have interests in Liver and Kidney health?

On a minimal regimen right now, might have had liver and kidney issues in the past (acute episodes), today I'm prettu carefu about it, right now taking 500mg TUDCA 1200mg NAC daily, as a general Liver health protocol.

kidneys you cannot do much with supplementation unfortunately, BP meds and astragalus might be our best bets here.
I've got some interest in the issue of hepatoxicity (liver health) with AAS after reading the Bond, Llewelyn paper on their hepatotoxicity theory (potency to activate AR * resistance to hepatic breakdown). Basically, in addition to UDCA/NAC/silymarin, I'd recommend mitochondrial antioxidants like polyunsaturated phosphatidylcholine, B1/2/6/12. Sanofi-Aventi Esentiale/Forte is a good product to add for liver health while on orals.
 
I've got some interest in the issue of hepatoxicity (liver health) with AAS after reading the Bond, Llewelyn paper on their hepatotoxicity theory (potency to activate AR * resistance to hepatic breakdown). Basically, in addition to UDCA/NAC/silymarin, I'd recommend mitochondrial antioxidants like polyunsaturated phosphatidylcholine, B1/2/6/12. Sanofi-Aventi Esentiale/Forte is a good product to add for liver health while on orals.
That's really interesting, as I was currently researching polyenylphosphatidylcholine (PPC) supplements for liver and kidney health:

Polyenylphosphatidylcholine attenuates alcohol-induced fatty liver and hyperlipemia in rats

So far I'm on Nutrasal's patented PPC formulation, but I know about some products from Sanofi, didn't know about Essential Forte though; are you in Eastern Europe btw?
 
It means that T (or another aromatizing androgen) interacting with aromatase increases IGF-I, whereas the product of aromatization negatively feeds back. So you don't want to completely crush aromatization too much with an AI, but too much of its product (E2) can raise IGFBP-1 to blunt GH response.

So, I wouldn't say "higher is better" with E2, but rather that this does make an argument for some aromatization as an important factor in protein anabolism/growth.

Practically, it's an argument that T + GH > GH alone, or perhaps T + GH + Tren > GH +Tren^2 in terms of GH response (IGF-I levels).
Ok I'm not so much versed into those mechanisms at play in coordination there, but it's serum e2 levels sensing at systemic level, that you're saying is causing the negative feedback with IGF-1 there, and not the e2 sensing at hepatic level, so that occupying the e2 receptors with DHT derivatives (which would let overall e2 levels unchanged) as estrogen receptor antagonist (including ER in liver) wouldn't change the overall dynamic of the feedback loop here?

thank you for the clarification and all the valuable info you laid out here, really appreciated it.
 
Ok I'm not so much versed into those mechanisms at play in coordination there, but it's serum e2 levels sensing at systemic level, that you're saying is causing the negative feedback with IGF-1 there, and not the e2 sensing at hepatic level, so that occupying the e2 receptors with DHT derivatives (which would let overall e2 levels unchanged) as estrogen receptor antagonist (including ER in liver) wouldn't change the overall dynamic of the feedback loop here?

thank you for the clarification and all the valuable info you laid out here, really appreciated it.
Yes, in humans serum E2 at the systemic level increases IGFBP-1 concentrations, and higher IGFBP-1 levels reduce free IGF-I availability.

There is evidence in ruminants (cattle) that E2 may increase hepatic somatotroph quantity, but not in humans. Rather, in humans, in situ aromatization (aromatization, but not its estrogen products) augment GH pulse amplitude and duration at the pituitary.
 
Yes, in humans serum E2 at the systemic level increases IGFBP-1 concentrations, and higher IGFBP-1 levels reduce free IGF-I availability.

There is evidence in ruminants (cattle) that E2 may increase hepatic somatotroph quantity, but not in humans. Rather, in humans, in situ aromatization (aromatization, but not its estrogen products) augment GH pulse amplitude and duration at the pituitary.
Thank you for all the info you're providing, I'm trying to link what was mentioned in this thread here, with the results and conclusion of this study you might have come across earlier:

Effect of trenbolone acetate plus estradiol on transcriptional regulation of metabolism pathways in bovine liver

"[...] it can be assumed that regulation of IGF-1 levels really occurs on the level of transcription by directly affecting the IGF-1 gene. A higher synthesis of IGF-1 in the liver, which is the main source for IGF-1, could be partially responsible for the higher serum levels (32). Owing to the para- plus endocrine action of IGF-1, it can be assumed that the growth promoting effect of anabolics on muscle tissue is mediated by circulating IGF-1 produced in liver."

This particular conclusion here, also referring to the previous study:

Johnson BJ, White ME, Hathaway MR, Christians CJ, Dayton WR. Effect of a combined trenbolone acetate and estradiol implant on steady-state IGF-I mRNA concentrations in the liver of wethers and the longissimus muscle of steers. J Anim Sci 1998;76:491–7

I'm almost sure I've seen one of these studies above mentioned on another thread here on this forum, can't find it again though.
 
Thank you for all the info you're providing, I'm trying to link what was mentioned in this thread here, with the results and conclusion of this study you might have come across earlier:

Effect of trenbolone acetate plus estradiol on transcriptional regulation of metabolism pathways in bovine liver

"[...] it can be assumed that regulation of IGF-1 levels really occurs on the level of transcription by directly affecting the IGF-1 gene. A higher synthesis of IGF-1 in the liver, which is the main source for IGF-1, could be partially responsible for the higher serum levels (32). Owing to the para- plus endocrine action of IGF-1, it can be assumed that the growth promoting effect of anabolics on muscle tissue is mediated by circulating IGF-1 produced in liver."

This particular conclusion here, also referring to the previous study:

Johnson BJ, White ME, Hathaway MR, Christians CJ, Dayton WR. Effect of a combined trenbolone acetate and estradiol implant on steady-state IGF-I mRNA concentrations in the liver of wethers and the longissimus muscle of steers. J Anim Sci 1998;76:491–7

I'm almost sure I've seen one of these studies above mentioned on another thread here on this forum, can't find it again though.
Yes. TBA+E2 synergistically augments IGF-I in ruminants by this mechanism. It appears to not do so in humans. Rather, it seems the IGF-I function in humans is truly a dual effector vis a vis GH/IGF-I, with local mIGF (myokines) promoting a local effort for a global effect. That is, with respect to tren, by increasing muscle sensitivity to autocrine/paracrine IGF-I, there is signaling to the organism that compensatorily decreases circulating liver IGF-I secretion.

One anabolic mechanism I'm not clear on translation to humans is whether the increased serum concentration of adjunct anabolics (i.e., AAS or aromatizing androgen) occurs via E2 competition with hepatic tren metabolism (see TBA+E2) ("TB concentration in TBA + E2 treated steers was almost twofold higher than in steers implanted with TBA alone (Table 3) [1]). This observation may be attributed to E2 competition with hepatic TB metabolism. This action would cause a decrease in the formation of 17a-hydroxy- trenbolone, the major excreted urinary metabolite of TBA (Pottier et al., 1981)") [1]. Here, Tren is the primary and E2 is the "adjuvant" compound.

[1] Hayden, J. M., Bergen, W. G., & Merkel, R. A. (1992). Skeletal muscle protein metabolism and serum growth hormone, insulin, and cortisol concentrations in growing steers implanted with estradiol-17 β, trenbolone acetate, or estradiol-17β plus trenbolone acetate2. Journal of Animal Science, 70(7), 2109–2119. doi:10.2527/1992.7072109x

If you find any relevant basic science on hepatic metabolism in steers vs. humans I'd be interested. I'm happy to see you taking such an interest in this.
 
TREN has shown to improve insulin sensitivity andd reduce serum insulin so when serum insulin decreases igf 1bp1 increases which bind to igf 1 and breaks it so it'll be decreased
 
I present it as a curiosity - my blood results and IGF serum
They are made over 2 weeks, the first without Trenbolone (300+) and the second after adding Trenbolone (the only change I made was switching from Nandrolone to Trenbolone, all other factors were exactly the same).
I have heard more than once that Trenbolone can lower IGF levels, but I thought that it only occurs with low estrogen levels and my estrogen is still between 50 and 80
It's shown that tren improves insulin sensitivity and reduces serum insulin so when insulin decreased igf 1 bp1 will be increased which binds to igf 1 and breaks it so igf 1 will be decreased
 
Ok now I’m concerned. I’m about to add Tren E to my cycle. I don’t want it decreasing IGF from my HGH. Should I or shouldn’t I run Tren with HGH?
 
Tren use with HGH is a good topic. My igf and GH serum test were extremely low while taking tren even with added HGH. Is there a chance my GH wasn't bad and the Tren just killed my liver from converting HGH to igf?
 
Actually, yes, rhGH+tren is good with one other adjunct drug in particular with any longer cycle or blast (>8 weeks). The reason tren lowers serum IGF-I is because tren (dramatically) increases the responsiveness of skeletal muscle satellite cells to intramuscular IGF-I, and these myokines (mIGF-I splice variants) signal back to the IGF-I system to lower circulating/liver IGF-I production.

Still, circulating/liver IGF-I, increased by exogenous GH (rhGH) upregulates mIGF-I (e.g., IGF-IEa, -IEb). So, I suspect that the reduction in serum IGF-I with tren, then, is due to increased extrahepatic (inter- and intra-muscular) conversion of circulating/liver IGF-I to the more important anabolic intramuscular variants (mIGF-Is).
 
Actually, yes, rhGH+tren is good with one other adjunct drug in particular with any longer cycle or blast (>8 weeks). The reason tren lowers serum IGF-I is because tren (dramatically) increases the responsiveness of skeletal muscle satellite cells to intramuscular IGF-I, and these myokines (mIGF-I splice variants) signal back to the IGF-I system to lower circulating/liver IGF-I production.

Still, circulating/liver IGF-I, increased by exogenous GH (rhGH) upregulates mIGF-I (e.g., IGF-IEa, -IEb). So, I suspect that the reduction in serum IGF-I with tren, then, is due to increased extrahepatic (inter- and intra-muscular) conversion of circulating/liver IGF-I to the more important anabolic intramuscular variants (mIGF-Is).
Can you dumb that down a bit more for a idiot meathead
 
It's shown that tren improves insulin sensitivity and reduces serum insulin so when insulin decreased igf 1 bp1 will be increased which binds to igf 1 and breaks it so igf 1 will be decreased
I have only seen evidence of unchanged serum insulin in response to tren. I've seen a decreased GH pulse amplitude and duration, an increased insulin sensitivity (reduced glucose) primarily via decreased PPARγ.
 
Can you dumb that down a bit more for a idiot meathead
Yes, so:

tren lowers systemic/liver IGF-I (because it reduces natural GH release and does the next thing):
but tren dramatically INCREASES the actual muscle's response to that systemic IGF-I (it does this by making more efficient use of that IGF-I as a precursor for special subtypes of IGF-I that exist inside the muscle)
so, though tren lowers natural (endogenous) GH levels, if we force that GH into the body, it'll still increase that systemic IGF-I floating around and allow for more opportunities when that IGF-I that's floating around comes into contact with muscles to increase the muscle's growth.

Even if bloodwork for serum IGF-I is "low," on tren, be sure that tren is making better use of the IGF-I inside the muscles.
 
@Type-IIx earlier you mentioned “300mg test or 800mg+ Deca” I believe for aromatizing compounds, are those numbers you generalize or have found are dose to response specific?


Also, what in your findings or experience would the benefit of using trenbolone and nandrolone together with testosterone if any?
 

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