why take hgh if u can take igf1

AtrophicPyra

AtrophicPyra

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igf1 is cheaper and ultimately the byproduct of hgh that u want.

somebody explain srs answers
 
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Because pinning IGF-1 on it's own will not do anything lol
 
GH works via:
Direct GH receptor signaling (JAK2–STAT5 pathway)

Indirect IGF-1 production (systemic + local)

IGF-1 injection only activates the IGF-1 receptor pathway.

So GH stimulates more total signaling inside the growth plate.

As well as IGF-1 has a much shorter half life
 
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extremely short half life, IGF-1 really only works well when used with also very high amounts of gh just to name a couple
ohh ok ty for telling me :soy:
 
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GH works via:
Direct GH receptor signaling (JAK2–STAT5 pathway)

Indirect IGF-1 production (systemic + local)

IGF-1 injection only activates the IGF-1 receptor pathway.

So GH stimulates more total signaling inside the growth plate.

As well as IGF-1 has a much shorter half life
not that igf1 has a shorter life, if u inject it most will bind to igfbps quickly, but there wont be enough igfbps compared to gh mediated igf1 cuz gh doesnt only mediate igf1 synthesis but also binding proteins for the igf1, also gh induces local igf1 synthesis inside the gp whereas injectable igf1 wont penetrate gp too effectively
 
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igf1 is cheaper and ultimately the byproduct of hgh that u want.

somebody explain srs answers
Because pinning IGF-1 on it's own will not do anything lol
pinning igf1 is very effective, and the effects of igf1 binding to chondrocyte receptors are different to agonism of gh receptors
only downside is that you have to pin igf1 twice a day instead of once, and also its insanely expensive and fairly difficult to source

igf1 binds to igf1r, causes chondrocytes to proliferate and hypertrophy
gh binds to ghr, promotes production of local igf1 + induces differentiation of resting zone stem cells into new chondrocytes
GH works via:
Direct GH receptor signaling (JAK2–STAT5 pathway)

Indirect IGF-1 production (systemic + local)

IGF-1 injection only activates the IGF-1 receptor pathway.

So GH stimulates more total signaling inside the growth plate.

As well as IGF-1 has a much shorter half life
one could argue (i am that one) that gh's ability to induce differentiation in the resting zone is actually a downside
i postulate that if differentiation could be controlled, we could get all proliferating chondrocytes to proliferate as much as possible while still having the stem cell pool dividing, then send a signal to promote differentiation and hypertrophy for a bit, then repeat

i expect botb for my use of postulate tbh
 
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