Women and GH: dosages, effects of estradiol, IGFBP-1

[gains4000]

That's reasonable bro, especially because of the widespread confusion about estrogens & their attenuated link or association to IGF-I.

I've written elsewhere about the phenomenon of aromatization per se being what increases IGF-I, whereas estrogens (e.g., E2) actually negatively feed back. That is to say, while the process of aromatization – (3 steps, completed by cleavage of the bond between C10 and C19 to yield formic acid and the aromatized A-ring product with loss of the hydrogen atoms at the 1β and 2β positions) – increases IGF-I, its aromatic products (estrogens) reduce IGF-I. What this results in is a sort of parabolic shape to the aromatizing androgen (e.g., Test, Deca, MENT, Dbol, Methyltest, etc.) dose/IGF-I curve with an inflection point where blood concentrations of the aromatic product (e.g., E2) start to become high.

Here are some links where I discuss this:

https://www.professionalmuscle.com/forums/index.php?threads/trenbolone-and-igf1-levels-blood-tests.166733/post-3040740

https://www.professionalmuscle.com/forums/index.php?goto/post&id=3082951

https://www.professionalmuscle.com/...-dosages-effects-of-estradiol-igfbp-1.169919/ (the title post of this thread), specifically, the concepts demonstrating that estrogens increase IGFBP-1, reducing IGF-I bioavailability and unleashing GH secretion by feedback withdrawal. Hence, women have higher GH levels than men by body surface area and are less sensitive per-mg to rhGH.

is this how exemestane increases IGF-1? Excessive estrogen levels suppress IGF-1, therefore taking exemestane will bring it back up?

 

[Type-IIx]

is this how exemestane increases IGF-1? Excessive estrogen levels suppress IGF-1, therefore taking exemestane will bring it back up?

I don't know that exemstane does increase IGF-I. It has no effect on IGF-I at a dose of 50 mg daily, orally, for 10 days.

Exemestane's primary metabolite is 17-hydroxyexemestane, an androgen that may aromatize, so it's theoretically possible that it does increases IGF-I. I haven't modeled the metabolite for predicted target behavior, but I will when I get a chance.

 

[Type-IIx]

Apologies in advance if this is a dumb question, I'm trying to even word it in a non-dumbass way... and please redirect me if answered on another thread...

Can this study (you started the thread with) be applied to males taking highly aromatizable compounds? And if so, would the effect be moreso related to the total E level or the ratio of E:T?
Like if E levels were high and the ratio was also out of whack, would that male bodybuilder require more GH, like a female would?
If E levels were high but the ratio to androgens was appropriate would that be a different result in GH response?
Thanks

I'm reminded of the ancient adage, "There are no stupid questions, only stupid people who ask them."

Fortunately for both of us, you are not stupid bro. Any question that doesn't come in the form of self-aggrandized hostility directed at me with vitriol because I upset your preconceived notion is going to get a thorough and perfectly friendly answer.

Exogenous estrogens ≠ aromatizable androgen aromatic products (e.g., Exogenous E2 ≠ [{T ⇒ E2, Nand ⇒ E2, ...}].

• See: Why you should NOT take estrogens (Exogenous E2 ≠ Test's aromatic product) [MesoRx]

What I mean by this is that administering (e.g., by ingestion, orally; or by injection) estrogens, there are various unfavorable effects, that include:

• Increased SHBG (decreased free androgen index)
• Decreased IGF-I (due to increased IGFBP-1)
• Male reproductive pathologies (by corollary, far weaker & in low concentration, environmental estrogens cause these same maladies; so imagine what the highly potent estradiol [E2] user should expect when administering bioactive doses)

Whereas, aromatic products from androgens (E2 in the cases of testosterone [T] & nandrolone [Nand]; 17α-methylestrogen in the cases of metandienone [Dbol] & methyltestosterone [MT]; 7α-methylestradiol [7α-ME] in the case of MENT, etc.) are a result of the process of aromatisation (3 steps, completed by cleavage of the bond between C10 and C19 to yield formic acid and the aromatized A-ring product with loss of the hydrogen atoms at the 1β and 2β positions), that potently stimulates (circulating-liver-secreted) IGF-I.

But since estrogens per se exert a diminution of IGF-I increases, there must be some inflection point or a parabolic shape to the curve (i.e., an inverse-U shape) plotting ΔIGF-I on the y-axis vs. concentration of aromatic product (e.g., E2 pg/mL American units) on the x-axis where at high levels of estrogens (e.g., E2 > 75 pg/mL) further increases to IGF-I increase at a decreasing rate as a result of the negative feedback of estrogens (e.g., E2) on ΔIGF-I (GH response)... and this is consistent with what we see.

With exogenous estrogens, that same plot of ΔIGF-I on the y-axis vs. concentration of aromatic product (e.g., E2 pg/mL American units) would be visualised as a steep linear or even curvilinear decline (decreasing at an increasing rate).

 

[Type-IIx]

So to your question as to the extent of the influence, that is largely controlling, of A:E (androgen/estrogen ratio), there is still a direct effect of estrogens on side effects that include gynecomastia, edema (bloat), sexual dysfunction, etc.

See also https://thinksteroids.com/articles/primobolan-equipoise-crashed-my-e2-help/ – that despite its title is highly pertinent.

 

[Scorpyd]

So to your question as to the extent of the influence, that is largely controlling, of A:E (androgen/estrogen ratio), there is still a direct effect of estrogens on side effects that include gynecomastia, edema (bloat), sexual dysfunction, etc.

See also https://thinksteroids.com/articles/primobolan-equipoise-crashed-my-e2-help/ – that despite its title is highly pertinent.

Appreciate your link
Probably take a few readings to make full sense to me.

 

[Scorpyd]

Symptoms of Low Estrogenicity #6 - this part now makes sense.​

 

[Parabolic33]

No it's not possible.

What is the analogy between serum IGF-I & thyroid function that you are trying to make? Please explain.

That some tissue prefers to convert t4 into t3 locally. So the implication was a possibility that the same could be true with igf1 and however igf1 is produced locally- which brings me to a question…

Right, there is synergy. Because trenbolone increases muscle satellite cell responsiveness to autocrine/paracrine IGF-I, doing more with less. Do you happen to know to whom this idea of rhGH & trenbolone synergy came from, by chance? Did you happen upon that theory all by your lonesome bro?

Def not thought of only own,lol. I actually was a total newbie to this stuff when I first heard vigorous Steve talk about the synergy.

Then when I noticed on my own labs and others, that tren appears to lower the max ceiling on circulating igf1 levels achievable with hgh doses. I started to look into it more, and then I came across your article or one of your posts.

Trenbolone decreases endogenous (i.e., natural) GH secretion (i.e., pulse amplitude & duration).

So rhGH replaces that; and the muscle cells exert a "pull" on circulating IGF-I (cIGF-I), that is converted in the muscle cell to autocrine/paracrine IGF-IEa.

IGF-IEc is the mechanosensitive isoform ("MGF"), the activity of which is increased my resistance training (i.e., single fibre muscle tension).

Is cIGF-1 a different molecule than IGF-1Ea? Is it known if hgh can trigger igf1ea/igf1ec in a paracrine way ? In the actual muscle?

Or is the igf1 that’s ending up in the muscle only produced in the liver first, then ending up in muscle ?

Is that known at all ?

Then, Testosterone + Trenbolone + RhGH + Resistance Training are synergistic (greater than additive; 1 + 1 > 2) in their increases to muscle & total body size.


There's a pretty good theory about how this works.

I just gave it to ya in a very high level form. You're welcome.

Thanks for the input lol. You’re quite a catch

 

[Type-IIx]

That some tissue prefers to convert t4 into t3 locally. So the implication was a possibility that the same could be true with igf1 and however igf1 is produced locally- which brings me to a question…

It is indeed produced locally in an autocrine/paracrine fashion, in humans, as IGF-IEa & IGF-IEc (MGF; the mechanosensitive isoform, meaning sensitive to single muscle fibre pulling force, or loading).

Def not thought of only own,lol. I actually was a total newbie to this stuff when I first heard vigorous Steve talk about the synergy.

Then when I noticed on my own labs and others, that tren appears to lower the max ceiling on circulating igf1 levels achievable with hgh doses. I started to look into it more, and then I came across your article or one of your posts.

That's cool.

Is cIGF-1 a different molecule than IGF-1Ea? Is it known if hgh can trigger igf1ea/igf1ec in a paracrine way ? In the actual muscle?

It is different but almost identical, they are related. It is known, it does, via cIGF-I (circulating-systemic-liver-secreted endocrine IGF-I) in the actual muscle. I write alllll about this in the reference Theoretical section of Bolus. I'm not sure if you saw elsewhere, but it will be sold from https://ampouletude.com, my site, which is almost ready for an official launch, but is active/live already.

The book is not yet for sale, I'm preparing for that soon.

Or is the igf1 that’s ending up in the muscle only produced in the liver first, then ending up in muscle ?

Is that known at all ?

So autocrine means produced inside the muscle for local use and paracrine means produced peri- (around) the muscle for use inside. The local muscle IGF-I isoforms (IGF-IE -a & -c) are fed by anabolic stimuli including endocrine (c)IGF-I, androgens, resistance training (single-fibre muscle pulling force; tension), etc.

Thanks for the input lol. You’re quite a catch

Good man! Good questions here.