What you can use in addition to HGH, IGF-1, and aromatase inhibitors to ensure maximum growth during puberty

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7evenvox22

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Introduction:
Do you want to know what you can use in addition to HGH, IGF-1, and aromatase inhibitors to ensure maximum growth during puberty?

1754501760714
1754501732716
1754501753661




What is HGH?
If you are unfamiliar with HGH, I recommend checking out this thread before proceeding.
1754501802818


The understanding of growth plates:
Your growth plates can be divided into three zones: the resting zone, which contains small stem-like chondroprogenitor cells with slow replication; the proliferation zone, where chondrocyte divide rapidly and drive the linear expansion of bone; and lastly, the hypertrophic zone, where chondrocyte exit the cell cycle, undergo hypertrophy, and undergo apoptosis, enabling new bone to form.
Bones  growth  zones
Hypertophy    zone




HGH and IGF-1's effect on growth plates:
HGH and IGF-1 increase both proliferation and the process of hypertrophy.
Hgh igf1 proliferation  hypertorphy
Optimal profiferation


How to achieve optimal height growth:

For optimal height growth, we want to allow our cells to proliferate longer before hypertrophying, as this gives us a larger pool of cells that can convert later. If too many cells hypertrophy, you will quickly deplete your pool of cells ready to divide, which will leave you with fewer resources for bone growth and premature growth plate closure, effectively making you shorter with less bone built.
Effefctivly making u shorter


FGFR3's effect on bone development:

FGFR3 is a major negative regulator of bone development that inhibits proliferation and, therefore, acts as a brake for height growth.
Annotation 2025 08 06 080455


FGFR3 inhibition:

So to maximize our growth and the time our cells have to divide, we need to inhibit FGFR3 signaling in our growth plates. For this, we need a CNP analog like Vosoritide, which inhibits the MAPK pathway downstream of FGFR3 and therefore inhibits its signal, lifting its brake on proliferation and maximizing our resources for bone growth, while also avoiding premature growth plate closure. This could lead to significant increases in height, especially when combined with HGH and IGF-1.
Annotation 2025 08 06 080516
Annotation 2025 08 06 080528
Annotation 2025 08 06 080544


FGFR3's significance:

FGFR3's significance can be seen in achondroplasia, where FGFR3 overactivity leads to dwarfism, while the opposite can be observed in FGFR3-deficient people called Catchil syndrome, which most of the time results in gigantism.
Annotation 2025 08 06 080637
Annotation 2025 08 06 080654
Annotation 2025 08 06 080709


Theoretical combination of a CNP analog with a PTHRP agonist:

In theory, a cyclic use of a PTHrP agonist, which recruits HDAC4 into the nucleus and thus suppresses RUNX2, would additionally extend the proliferation phase and transiently slow differentiation. However, you shouldn't overdo it, since a complete absence of ossification will again lead to shorter bones and impair growth. Also note that this is purely theoretical, drawn from animal models, and no PTHrP analog is approved for height.
Annotation 2025 08 06 080750
Annotation 2025 08 06 080834


Final thoughts:

This is just one of many other very promising and potent possibilities to increase your height. Feel free to check the last thread I made about RANKL inhibition if you would like to dive deeper into how to simulate bone growth using pharmaceuticals.



https://looksmax.org/threads/how-to...ankl-inhibition-and-anabolic-support.1554299/



Thank you for reading, and I hope that I was able to help you with your bone growth journey. Have a blessed day. :)
 

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Introduction:
Do you want to know what you can use in addition to HGH, IGF-1, and aromatase inhibitors to ensure maximum growth during puberty?

If you are unfamiliar with HGH, I recommend checking out this thread before proceeding.
View attachment 3995998

The understanding of growth plates:
Your growth plates can be divided into three zones: the resting zone, which contains small stem-like chondroprogenitor cells with slow replication; the proliferation zone, where chondrocyte divide rapidly and drive the linear expansion of bone; and lastly, the hypertrophic zone, where chondrocyte exit the cell cycle, undergo hypertrophy, and undergo apoptosis, enabling new bone to form.


HGH and IGF-1's effect on growth plates:
HGH and IGF-1 increase both proliferation and the process of hypertrophy.
View attachment 3996009View attachment 3996008

How to achieve optimal height growth:

For optimal height growth, we want to allow our cells to proliferate longer before hypertrophying, as this gives us a larger pool of cells that can convert later. If too many cells hypertrophy, you will quickly deplete your pool of cells ready to divide, which will leave you with fewer resources for bone growth and premature growth plate closure, effectively making you shorter with less bone built.
View attachment 3996033

FGFR3's effect on bone development:

FGFR3 is a major negative regulator of bone development that inhibits proliferation and, therefore, acts as a brake for height growth.
View attachment 3996026

FGFR3 inhibition:

So to maximize our growth and the time our cells have to divide, we need to inhibit FGFR3 signaling in our growth plates. For this, we need a CNP analog like Vosoritide, which inhibits the MAPK pathway downstream of FGFR3 and therefore inhibits its signal, lifting its brake on proliferation and maximizing our resources for bone growth, while also avoiding premature growth plate closure. This could lead to significant increases in height, especially when combined with HGH and IGF-1.

FGFR3's significance can be seen in achondroplasia, where FGFR3 overactivity leads to dwarfism, while the opposite can be observed in FGFR3-deficient people called Catchil syndrome, which most of the time results in gigantism.
View attachment 3996020View attachment 3996019View attachment 3996018

Theoretical combination of a CNP analog with a PTHRP agonist:

In theory, a cyclic use of a PTHrP agonist, which recruits HDAC4 into the nucleus and thus suppresses RUNX2, would additionally extend the proliferation phase and transiently slow differentiation. However, you shouldn't overdo it, since a complete absence of ossification will again lead to shorter bones and impair growth. Also note that this is purely theoretical, drawn from animal models, and no PTHrP analog is approved for height.

This is just one of many other very promising and potent possibilities to increase your height. Feel free to check the last thread I made about RANKL inhibition if you would like to dive deeper into how to simulate bone growth using pharmaceuticals.



https://looksmax.org/threads/how-to...ankl-inhibition-and-anabolic-support.1554299/



Thank you for reading, and I hope that I was able to help you with your bone growth journey. Have a blessed day. :)
read every molecule son

shame such a high effort thread isn’t getting the attention it deserves
 
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