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Forskolin to delay plate closure theory? (2 Viewers)

Forskolin to delay plate closure theory?

fent

just hum bro!
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Quick theory dump before anyone asks how it works :

Forskolin spikes cAMP hard by hitting adenylate cyclase directly. PTHrP (the thing that keeps plates open) works the exact same way: Gs → cAMP → blocks chondrocyte hypertrophy → delays maturation/closure.


Cell studies show forskolin:
  • Kills collagen X expression (hypertrophy marker)
  • Keeps chondrocytes proliferative instead of blowing up into bone
  • Mimics PTHrP's anti-hypertrophy effect
  • :feelsokman::feelsokman::feelsokman:
In vivo rats: oral Coleus extract (forskolin source) made femurs longer in growing ones, better bone modeling, no early fusion reported.

So theoretically at 16 (plates probably still open), ~50 mg pure forskolin could mildly mimic PTHrP systemically → slow hypertrophy a bit → maybe buy a few extra months of growth before E2 seals it.

Other perks from adult studies: small BF drop, lean gain, free T up, bone mass increase.

But.... :
  • 0 human studies on height/plates in teens (or anyone)
  • Oral absorption sucks, probably barely reaches growth plates
  • High dose untested in puberty – could fuck BP, heart rate, stomach, hormones
  • T bump might raise E2 → faster closure risk lol
  • :feelsrope::feelsrope::feelsrope:
i already made a thread on this loser
 

gqq

Iron
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Quick theory dump before anyone asks how it works :

Forskolin spikes cAMP hard by hitting adenylate cyclase directly. PTHrP (the thing that keeps plates open) works the exact same way: Gs → cAMP → blocks chondrocyte hypertrophy → delays maturation/closure.


Cell studies show forskolin:
  • Kills collagen X expression (hypertrophy marker)
  • Keeps chondrocytes proliferative instead of blowing up into bone
  • Mimics PTHrP's anti-hypertrophy effect
  • :feelsokman::feelsokman::feelsokman:
In vivo rats: oral Coleus extract (forskolin source) made femurs longer in growing ones, better bone modeling, no early fusion reported.

So theoretically at 16 (plates probably still open), ~50 mg pure forskolin could mildly mimic PTHrP systemically → slow hypertrophy a bit → maybe buy a few extra months of growth before E2 seals it.

Other perks from adult studies: small BF drop, lean gain, free T up, bone mass increase.

But.... :
  • 0 human studies on height/plates in teens (or anyone)
  • Oral absorption sucks, probably barely reaches growth plates
  • High dose untested in puberty – could fuck BP, heart rate, stomach, hormones
  • T bump might raise E2 → faster closure risk lol
  • :feelsrope::feelsrope::feelsrope:
Why is your avi running at 1 frame per month
 

Dexter

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Forskolin spikes cAMP hard by hitting adenylate cyclase directly. PTHrP (the thing that keeps plates open) works the exact same way: Gs → cAMP → blocks chondrocyte hypertrophy → delays maturation/closure.
the mechanism is correct but application wise seems risky
PTHrP action in the growth plates is paracrine and not endocrine. its produced locally in the periarticular region. systemic administration of a cAMP inducer like forskolin is a blunt instrument that cant mimic the spatial and temporal regulation of PTHrP
In vivo rats: oral Coleus extract (forskolin source) made femurs longer in growing ones, better bone modeling, no early
seems misleading since rodent studies dont translate to human growth plate manipulation
rats GP stays open for much longer than it does in humans, rats dont undergo estrogen meditated GP closing. "no early fusion" is irrelevant since they dont undergo maturation like humans
the increased femoral length is prolly attributed to systemic anabolic effects like increased IGF1 or thyroid interaction
So theoretically at 16 (plates probably still open), ~50 mg pure forskolin could mildly mimic PTHrP systemically → slow hypertrophy a bit → maybe buy a few extra months of growth before E2 seals it
oral forskolin has a very low bioavailability in humans, like 20% iirc. not to mention the half life is 2 hours. to achieve a sustained cAMP elevation in chondrocytes deep within the epiphyseal plate, one would req a dose that would fuck up cardiovascular health long b4 it reaches the therapeutic threshold in the physis

mimicking PTHrP "systemically" is exactly the opposite of hiw the growth plate works. systemic cAMP elevation would affect every cell in ur body. PTHrP Works in a gradient.

by increasing cAMP, forskolin can increase aromatase activity and steroidogenesis. "T bump might raise e2" isn't a side effect but a direct consequence that would cause closure faster
 

Razi

Lamecel
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the mechanism is correct but application wise seems risky
PTHrP action in the growth plates is paracrine and not endocrine. its produced locally in the periarticular region. systemic administration of a cAMP inducer like forskolin is a blunt instrument that cant mimic the spatial and temporal regulation of PTHrP

seems misleading since rodent studies dont translate to human growth plate manipulation
rats GP stays open for much longer than it does in humans, rats dont undergo estrogen meditated GP closing. "no early fusion" is irrelevant since they dont undergo maturation like humans
the increased femoral length is prolly attributed to systemic anabolic effects like increased IGF1 or thyroid interaction

oral forskolin has a very low bioavailability in humans, like 20% iirc. not to mention the half life is 2 hours. to achieve a sustained cAMP elevation in chondrocytes deep within the epiphyseal plate, one would req a dose that would fuck up cardiovascular health long b4 it reaches the therapeutic threshold in the physis

mimicking PTHrP "systemically" is exactly the opposite of hiw the growth plate works. systemic cAMP elevation would affect every cell in ur body. PTHrP Works in a gradient.

by increasing cAMP, forskolin can increase aromatase activity and steroidogenesis. "T bump might raise e2" isn't a side effect but a direct consequence that would cause closure faster
Been typing all that time for this
Worth it nice read
 

EqBeliever

- Biased Misanthrope -
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the mechanism is correct but application wise seems risky
PTHrP action in the growth plates is paracrine and not endocrine. its produced locally in the periarticular region. systemic administration of a cAMP inducer like forskolin is a blunt instrument that cant mimic the spatial and temporal regulation of PTHrP

seems misleading since rodent studies dont translate to human growth plate manipulation
rats GP stays open for much longer than it does in humans, rats dont undergo estrogen meditated GP closing. "no early fusion" is irrelevant since they dont undergo maturation like humans
the increased femoral length is prolly attributed to systemic anabolic effects like increased IGF1 or thyroid interaction

oral forskolin has a very low bioavailability in humans, like 20% iirc. not to mention the half life is 2 hours. to achieve a sustained cAMP elevation in chondrocytes deep within the epiphyseal plate, one would req a dose that would fuck up cardiovascular health long b4 it reaches the therapeutic threshold in the physis

mimicking PTHrP "systemically" is exactly the opposite of hiw the growth plate works. systemic cAMP elevation would affect every cell in ur body. PTHrP Works in a gradient.

by increasing cAMP, forskolin can increase aromatase activity and steroidogenesis. "T bump might raise e2" isn't a side effect but a direct consequence that would cause closure faster
Thanks for the reply and in conclusion its not worth it at all right?
 

EqBeliever

- Biased Misanthrope -
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by increasing cAMP, forskolin can increase aromatase activity and steroidogenesis. "T bump might raise e2" isn't a side effect but a direct consequence that would cause closure faster
but looking back at the source it likely would have been noted(e2 spike), especially since the study tracked hormones and bone changes and its not noted
 

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