Why HGH is actually worse than Ghs+Ghrp w Argenine (not clickbait)

[TheOsei]

Why GHS + GHRP w/ arginine >>>> exo hgh.

We know liver igf is near pointless and most of longitudinal growth occurs from autocrine GP igf produced.

More specifically there are two classes of igf-1 gene transcriptions

Exon 1 and exon 2

Exon 2 only accounts 5% igf gene transcription in chondrocytes outside of the liver (25%).

Study in knockout mice revealed that removing exon 2 does not affect development or postnatal growth. PMID: 20382057

Besides that. pulsatile gh given every 3hrs to rat showed 3-5x more activity in rib growth plates and other exon1 active tissue/muscle. PMID: 3197637.

This would be the end and we’ll settle for 4x daily hgh split, but rats have a much faster metabolism than us

Rhgh in humans peak in 4-6hrs, and igf sustains more, too long.
Does not mean it fails to raise igf just not the way it’s needed.

So theoretically ghrp2 would be far more ideal as it has a fast 30m onset and can be easily split to match and amplify 3-hourly igf release, targeting exon 1 better

Additionally ghs and ghrps are much better at not upregulating SOCS due to it not clinging onto GHR for long, modt under 45min.
Socs3 induces in only 30 minutes and returns to baseline in 2hrs

All ghs and ghrps are until this time threshold except for partislly ipamorelin

High dose arginine will also help lower somatostatin

In conclusion exogenous hgh is subpar due to favorism of exon2 igf transcription and SOCS induction. Ghs and Ghrps are superior due to shorter high impact gh/igf release while bypassing SOCS and inducing a greater level of exon1 mRNA activity as shown from shorter quicker pulsing.

 

[fraudster#1]

Why GHS + GHRP w/ arginine >>>> exo hgh.

We know liver igf is near pointless and most of longitudinal growth occurs from autocrine GP igf produced.

More specifically there are two classes of igf-1 gene transcriptions

Exon 1 and exon 2

Exon 2 only accounts 5% igf gene transcription in chondrocytes outside of the liver (25%).

Study in knockout mice revealed that removing exon 2 does not affect development or postnatal growth. PMID: 20382057

Besides that. pulsatile gh given every 3hrs to rat showed 3-5x more activity in rib growth plates and other exon1 active tissue/muscle. PMID: 3197637.

This would be the end and we’ll settle for 4x daily hgh split, but rats have a much faster metabolism than us

Rhgh in humans peak in 4-6hrs, and igf sustains more, too long.
Does not mean it fails to raise igf just not the way it’s needed.

So theoretically ghrp2 would be far more ideal as it has a fast 30m onset and can be easily split to match and amplify 3-hourly igf release, targeting exon 1 better

Additionally ghs and ghrps are much better at not upregulating SOCS due to it not clinging onto GHR for long, modt under 45min.
Socs3 induces in only 30 minutes and returns to baseline in 2hrs

All ghs and ghrps are until this time threshold except for partislly ipamorelin

High dose arginine will also help lower somatostatin

In conclusion exogenous hgh is subpar due to favorism of exon2 igf transcription and SOCS induction. Ghs and Ghrps are superior due to shorter high impact gh/igf release while bypassing SOCS and inducing a greater level of exon1 mRNA activity as shown from shorter quicker pulsing.

i writed about this some days ago
and some niggas said i was wrong

 

[italianltn]

Can one of the high IQ pharma guys confirm this? @Jason Voorhees You got a take?

 

[Jason Voorhees]

Can one of the high IQ pharma guys confirm this? @Jason Voorhees You got a take?

Im not very good at biology. @topology is expert in this topic

 

[fraudster#1]

here a complementation of this

may you guys here should learn somethings about pulsatile hgh
View attachment 4936560View attachment 4936563View attachment 4936565View attachment 4936568
gh administration lower endogenous production dose-dependitly via increasing circularting IGF-1 which in turn promotes more Somastostatin that directly affects Somatotrophes in the pituary. However, GHRELIN via GHS-R1A activation locally antagonizes Somastostatin in the pituary.

Additionally, it is common knowledge that GHRPs and GHRHs produce synergistic GH increases through different protein kinase pathways, but GHRH also decreases GHS-R1A desensitization.
Moreover, GHS-R1A and GHRH-R are present in muscle, bone and cartilage and have GH-R and IGF-1/2R sensitizing properties. GHRH-R also decreases the STAT5/3 transcription ratio in the liver which can keep syst. IGF-1 in the high phys/ low supra range even on high dose rHGH (anecdotally).
Therefore, not only is Somatostatin very effectively inhibited, but also disproportionally lower than with GH only which further spirals the cascade upwards because the GHS yield even more GH -> perpetuum mobile

1. The Synergistic Effect (1+1=3) (AI cover)
GHRPs (Growth Hormone Releasing Peptides) and GHRHs (Growth Hormone Releasing Hormones) work on different receptors in the pituitary gland.

• GHRH initiates the "pulse" of Growth Hormone.
• GHRP amplifies that pulse and inhibits Somatostatin (the hormone that tells your body to stop producing GH).
  By using both, you are simultaneously pressing the gas pedal and cutting the brake lines.

2. Preventing Desensitization
Usually, when you overstimulate a receptor, the body shuts it down to protect itself (desensitization). The text claims that GHRH actually helps keep the GHS-R1A receptors sensitive, meaning the drugs continue to work effectively for longer periods without needing higher doses.

3. Local Sensitivity in Tissues
The text mentions that these receptors are present directly in muscle, bone, and cartilage. This suggests that the substances don't just work through the liver; they make the target tissues themselves more "hungry" or sensitive to the IGF-1 and GH circulating in the blood.

4. The "Perpetuum Mobile" Cascade
By lowering Somatostatin levels disproportionately compared to using exogenous GH alone, the body stays in a state where it is constantly primed to release more of its own hormone. This creates a feedback loop (the "cascade") that keeps IGF-1 levels at the high end of the physiological range or even slightly above (supraphysiological), maximizing recovery and growth.

With regards to PK: In rat studies, pulsatile GH administration was superior (3-5x IGF-1mRNA). However, in human administration and pathophysiology (acromegaly), even physiological amounts of continuous GH yield higher hepatic and local IGF-1mRNA. My hypothesis is that ID8835 is a species-specific AUC integrater; in rats time-weighed (extended STAT5B is more detrimental than Cmax) and in humans amplitude-weighed, making the exactly opposite signaling patterns optimal for each species


As already implied, the goal is to create an insane AUC of GH with extremely potent, self-potentiating local IGF-1 signaling:

• rHGH >= 0,07 mg/kg/day (if allometrically scaled x<1; 80 kg bw -> 16,8 IU/day) showed statistically significant increases in under a year of administration of Tanner 3+ boys (Rothenbuhler et al 2015.). May be titrated to or over 0,1 mg/kg/day (e.g. 80 kg bw -> 24 IU/day)"

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View attachment 4936634

 

[TheOsei]

here a complementation of this

Nice

i writed about this some days ago
and some niggas said i was wrong

Jfl

 

[fraudster#1]

Nice

btw what dosage is considerated the minimum for argenine?

 

[topology]

Im not very good at biology. @topology is expert in this topic

Not this particular subject.. I've put off going into growth hormone as I've always thought it wasn't that nuanced. Seems I was wrong, I'll take a look at it soon.

 

[TheOsei]

btw what dosage is considerated the minimum for argenine?

Im gonna do high dose ghrp2 w cjc 4-5x a day with 3g arginine each