how to run tren and keep growth plates open[gos into detail]

this is my first guide


tren is a Nor-9 and is not aromatizing meaning it doesn't turn to estrogen witch is why many greycells think that it wont stunt height and will even add does such as 200mg to height stacks although it does and that 200mg is acually decreasing alot same with halo btw this theoretically would work with halo but i did the research on tren i will make one on halo soon

ways it closes plates stunting height and how to counteract it

1. it directly signals Wnt/β-Catenin because of the androgen which causes the cartilage to convert to bone speeding up significantly plate closure
-how to solve: use a intracellular Wnt/β-Catenin inhibitors such as ICG-001 or PRI-724
-why it works: they disrupt the binding of β-Catenin to its co-activator CBP inside the nucleus therefore blocking the transcription of the RUNX2 gene which stop the cartilage cells converting to bone
-dangers/side effects: by blocking Wnt/β-Catenin it stops the body from producing new bone which causes rapid severe osteopenia therefore you have to utilize alternative pathways to keep bones growing dense and structurally sound(see 1.2 on how)

1.2.
-halting bone resorption for this we are going to use a RANKL inhibitor such as
denosumab cuz the body can't build new bone without Wnt signaling it must be forcefully stopped from destroying its own bone denosumab blocks the RANKL
protein stopping the progression of osteoclasts
-we will also use zoledronic acid which will shut down the bone breaking cells and allow your bones to become denser and stronger but because of the the other compounds it would maintain the density and strength of the bones
-Activating Non Wnt Anabolic Bone Pathways for this we will use ActRIIA-Fc Fusion Proteins and activin/myostatin inhibitors these compounds will stimulate bone mineral density through different pathways that work independently of the blocked Wnt/β-catenin providing an alternative bone-building signal

3.
-Prolactin and HPG Axis Management the compound we will use for this are caber(cabergoline) and HCG the caber will work with the pituitary gland to the prolactin surge that will cause progesterone therefore eliminating the risk of the progesterone causing an increase in estrogen because estrogen will close plates and if your on this form and researching doing tren you know what HCG is if not im JFL get of this thread

this was high effort and took a shit ton of reaserch so rep niggas
 
this is my first guide


tren is a Nor-9 and is not aromatizing meaning it doesn't turn to estrogen witch is why many greycells think that it wont stunt height and will even add does such as 200mg to height stacks although it does and that 200mg is acually decreasing alot same with halo btw this theoretically would work with halo but i did the research on tren i will make one on halo soon

ways it closes plates stunting height and how to counteract it

1. it directly signals Wnt/β-Catenin because of the androgen which causes the cartilage to convert to bone speeding up significantly plate closure
-how to solve: use a intracellular Wnt/β-Catenin inhibitors such as ICG-001 or PRI-724
-why it works: they disrupt the binding of β-Catenin to its co-activator CBP inside the nucleus therefore blocking the transcription of the RUNX2 gene which stop the cartilage cells converting to bone
-dangers/side effects: by blocking Wnt/β-Catenin it stops the body from producing new bone which causes rapid severe osteopenia therefore you have to utilize alternative pathways to keep bones growing dense and structurally sound(see 1.2 on how)

1.2.
-halting bone resorption for this we are going to use a RANKL inhibitor such as
denosumab cuz the body can't build new bone without Wnt signaling it must be forcefully stopped from destroying its own bone denosumab blocks the RANKL
protein stopping the progression of osteoclasts
-we will also use zoledronic acid which will shut down the bone breaking cells and allow your bones to become denser and stronger but because of the the other compounds it would maintain the density and strength of the bones
-Activating Non Wnt Anabolic Bone Pathways for this we will use ActRIIA-Fc Fusion Proteins and activin/myostatin inhibitors these compounds will stimulate bone mineral density through different pathways that work independently of the blocked Wnt/β-catenin providing an alternative bone-building signal

3.
-Prolactin and HPG Axis Management the compound we will use for this are caber(cabergoline) and HCG the caber will work with the pituitary gland to the prolactin surge that will cause progesterone therefore eliminating the risk of the progesterone causing an increase in estrogen because estrogen will close plates and if your on this form and researching doing tren you know what HCG is if not im JFL get of this thread

this was high effort and took a shit ton of reaserch so rep niggas
my dumbass made it in Google docs and forgot a section and alr deleted the Google doc so this parts simplified
1.1
Rapamycin
which is a mTORC1 Inhibitor or a IGF-1R Antagonists like Picropodophyllin which work cuz High-load trenbolone forces a massive local surge of IGF-1,which rapidly exhausts the growth plate's finite cell-division capacity. Dampening this pathway slows down the cellular clock stretching out the time cartilage cells have left to divide
 

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