TRENBOLONE and igf1 levels - Blood tests

[luki7788]

@luki7788 when you got this result were you on rhGH?

yeah i'm nonstop on gh

 

[TeaMan]

So the conclusion on this are simple - stop worreing about igf-1 serum level?

 

[NGL34]

Tren likely also lowers IGF-I (sans rhGH, rhIGF-I, LR3-IGF-I, etc.) via reduced hepatic somatotroph quantity and GH pulse amplitude and duration. Aromatizing androgens like T, due to aromatization or their structure, may ameliorate this.

It would be ever more curious if luki was on rhGH here.

I must of missed something in your posts, but why would you be surprised if Luki was on hgh?

 

[goback2013]

Tren the magic poison... that's all I can say. Well I'll also say this. If I dial it in I have low side effects and it works like crazy. If I overdose (for me) I feel like shit and look like shit, full of inflammation, water retention. That's got tb be having some sort of toxic effect on multiple systems in the body. I'm not shocked that IGF-1 is awry. Those studies I think were in cows that showed a rise in IGF-1. It would be interesting to know what the number would be using a therapeutic and not toxic dose.

What's considered a therapeutic dose ?
Maybe 30mg per week... break that up however you see fit.
I can dose 5mg( based on label claim) and next day look harder and more vascular.

 

[pickapeck]

What's considered a therapeutic dose ?
Maybe 30mg per week... break that up however you see fit.
I can dose 5mg( based on label claim) and next day look harder and more vascular.

If you were to base it on the original Parabolin which was tren hex, it would be 76 mg every 2 weeks so I would say for our purposes 100-150 mg/w roughly but testing, note taking and bloodwork will give you the correct answer or one close.

 

[Type-IIx]

I must of missed something in your posts, but why would you be surprised if Luki was on hgh?

188 ng/mL serum IGF-I. This could be a function of the IGF-I decrement that's usually seen around 6 mo. of continuous use. It may be, if anything, only party reflective of reduced GH response since luki says he's continuously been on rhGH, my interpretation is for years? But mainly, this shows a real effect of tren lowering serum IGF-I. I believe the latter does occur via reduced hepatic somatotroph quantity mostly. It's an untested hypothesis in humans but is seen in mammals. The addition of aromatizing androgen (i.e., test) increases GH response, i.e., should bring up the serum IGF-I. In humans it is in situ aromatization and NOT estradiol that augments GH response, due to E2's compensatorily increasing IGFBP-1.

 

[jaxino]

188 ng/mL serum IGF-I. This could be a function of the IGF-I decrement that's usually seen around 6 mo. of continuous use. It may be, if anything, only party reflective of reduced GH response since luki says he's continuously been on rhGH, my interpretation is for years? But mainly, this shows a real effect of tren lowering serum IGF-I. I believe the latter does occur via reduced hepatic somatotroph quantity mostly. It's an untested hypothesis in humans but is seen in mammals. The addition of aromatizing androgen (i.e., test) increases GH response, i.e., should bring up the serum IGF-I. In humans it is in situ aromatization and NOT estradiol that augments GH response, due to E2's compensatorily increasing IGFBP-1.

So is that true, that if we let E2 goes up high levels, the HGH response gets better and better?

how high E2 should be? 100, 50pg/ml?

 

[Type-IIx]

So is that true, that if we let E2 goes up high levels, the HGH response gets better and better?

how high E2 should be? 100, 50pg/ml?

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).

 

[luki7788]

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).

So my theory that the estrogen level in the normal range is the best and most beneficial in terms of muscle growth and both too high and too low levels have more negatives than positives ..?

 

[Type-IIx]

Of course, for muscle hypertrophy, tren greatly increases the muscle isoform of IGF-I (mIGF-I). Systemic-liver IGF-I (what I refer to usually as cIGF-I, i.e., serum IGF-I) is related to total-body protein balance, reducing chronic inflammatory response, increasing free fatty acid utilization and enhancing insulin sensitivity upon receptor binding and subsequent intracellular signaling, and glucose metabolism. In many ways, having a blunted cIGF-I response to rhGH worsens insulin sensitivity. Systemic (cIGF-I) also relates to decreased:

- total body fat
- abdominal fat mass
- fat mass of the upper extremities, and
- serum markers of bone metabolism
- total serum cholesterol
- LDL-cholesterol
- LDL/HDL ratio
- serum apolipoprotein B
- plasma activity of plasminogen activator inhibitor (PAI-1)

 

[Type-IIx]

So my theory that the estrogen level in the normal range is the best and most beneficial in terms of muscle growth and both too high and too low levels have more negatives than positives ..?

With higher doses of T, the inverse U-shaped curve likely shifts to the right if you plot growth vs. E2 as a product of T, if that makes sense. So, you still have an optimal range, but it likely increases in proportion to the absolute androgen concentration unbound and loosely bound (i.e., free- and albumin-bound T). Also, an important consideration is the saturation point for estradiol in the individual, it may be that at 750mg-1g you saturate aromatase, and after that there is no further increase in estradiol. Some people may "feel" good at higher doses because they have a low absolute aromatase.

Coming back to just speaking practically, I believe that E2 should not be high ever. I think it's best controlled wisely (I dislike this new "higher E2 is always better" mantra). But, it is an additional 'tick mark' for ways aromatization functions as a mechanism in anabolism.

 

[Type-IIx]

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.

 

[Soalian]

am interested since am on tren cycle atm

 

[Soalian]

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.

decreased GH/IGF-1 signalling has been shown to extend longevity in a wide variety of species including worms, fruit flies, yeast and mice.

So reduced hepatic somatotroph signaling and/or quantity might blunt the liver IGF-1 production from hepatocytes overall, and therefore reduce the circulating systemic levels of IGF-1 right?

Could tren then be used as a therapeutic in order to keep low IGF-1 signaling in certain circumstances, in order to try and avoid the deleterious, maybe pro-aging effects, of chronic high-IGF-1 signaling? (lol)

 

[Type-IIx]

decreased GH/IGF-1 signalling has been shown to extend longevity in a wide variety of species including worms, fruit flies, yeast and mice.

So reduced hepatic somatotroph signaling and/or quantity might blunt the liver IGF-1 production from hepatocytes overall, and therefore reduce the circulating systemic levels of IGF-1 right?

Could tren then be used as a therapeutic in order to keep low IGF-1 signaling in certain circumstances, in order to try and avoid the deleterious, maybe pro-aging effects, of chronic high-IGF-1 signaling? (lol)

Some of the worst research I've seen is on the IGF-I/longevity link. I have a collection of hilariously bad research.

You and I both know tren is not a longevity drug. But thank you for the laugh!

 

[montecresto]

Not mind blowing, tren chews up blood sugar and IGF is heavily stimulated by raising levels of BS.

In b4 someone posts a study on castrated steer on their way to slaughter.

nice post bro.

 

[Soalian]

Some of the worst research I've seen is on the IGF-I/longevity link. I have a collection of hilariously bad research.

You and I both know tren is not a longevity drug. But thank you for the laugh!

would love to hear your thoughts on the IGF-1 and aging debate here, honestly.

 

[Type-IIx]

would love to hear your thoughts on the IGF-1 and aging debate here, honestly.

I'm not tuned into that debate enough to know the current arguments or personalities, but I have just in my own research collected a small set of hilariously bad research on the subject since I am interested in the GH/IGF-I system a great deal. I'll just say that it's probably fair to correlate body mass/IGF-I/shortened life span given the disparate data points from various fields... but, epidemiology is far outside its area of expertise when it starts proposing mechanisms like "the body likely decreases its circulating IGF-I as an adaptive protective mechanism to increase longevity with age."

These correlations aren't even particularly strong. And I am opposed to the notion that living 120 years in a weakened vessel is preferable to living 3/4 that long with vigor.

 

[Soalian]

I'm not tuned into that debate enough to know the current arguments or personalities, but I have just in my own research collected a small set of hilariously bad research on the subject since I am interested in the GH/IGF-I system a great deal. I'll just say that it's probably fair to correlate body mass/IGF-I/shortened life span given the disparate data points from various fields... but, epidemiology is far outside its area of expertise when it starts proposing mechanisms like "the body likely decreases its circulating IGF-I as an adaptive protective mechanism to increase longevity with age."

These correlations aren't even particularly strong. And I am opposed to the notion that living 120 years in a weakened vessel is preferable to living 3/4 that long with vigor.

thanks man, appreciate it, would you know of ways of upregulating IGF-1 expression and/or density and/or quantity of receptors in the liver?

I'm not-so well-versed on it.

Thanks!

 

[Type-IIx]

thanks man, appreciate it, would you know of ways of upregulating IGF-1 expression and/or density and/or quantity of receptors in the liver?

I'm not-so well-versed on it.

Thanks!

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).