You get male dimo even when ur near ur 30’s and the threshold for male dimo is EXTREMELY low

[Paul.jnxy]

This is circular reasoning though, androgens don't deplete the zone, they stimulate the zone to produce cells for proliferation. I know it's a lot to take in but it's very easy to comprehend. E2 just kills of cells much earlier than they should. Normal growth doesn't, all cells die at some point, but E2 kills them before they even finish their job.

Hypertrophy kills them after finishing their job. If anything, more hypertrophy = more bone growth because there's more lacunae left to push into the diaphysis to lengthen the bone. Which makes people grow faster

So what you are basically saying is that androgens = help cell complete its job and e2 = kills cell before it completes its job leading to shorter FAH

 

[Kojo]

Chrondrocyte death after hypertrophy means it’s practically over and that cell is never gonna go back to cartilage or grow again

Huh? Chondrocyte death after hypertrophy doesn't mean it's over. The cycle literally just restarts again and you keep growing

 

[AtrophicPyra]

This is circular reasoning though, androgens don't deplete the zone, they stimulate the zone to produce cells for proliferation. I know it's a lot to take in but it's very easy to comprehend. E2 just kills of cells much earlier than they should. Normal growth doesn't, all cells die at some point, but E2 kills them before they even finish their job.

Hypertrophy kills them after finishing their job. If anything, more hypertrophy = more bone growth because there's more lacunae left to push into the diaphysis to lengthen the bone. Which makes people grow faster

Ya hypertrophy is good for bone growth but for cartilage it’s horrible.

They both express the same gene runx2 and that same gene does the same thing to to the same cell

Androgen is not as potent as estrogen at expressing this gene however, this means they both deplete the resting zone.

The problem isn’t even that androgens deplete the resting zone, it’s that they cause hypertrophy too fast AND deplete the resting zone too fast which ends up with unoptimal chrondrocyte proliferation,

In other words, u could have had more time to proliferate chrondrocytes and more chrondrocytes would have underwent hypertrophy leading to a greater FAH than if u took supraphysiological androgens

 

[Kojo]

So what you are basically saying is that androgens = help cell complete its job and e2 = kills cell before it completes its job leading to shorter FAH

Yes, this is bone growth histology 101

 

[AtrophicPyra]

Huh? Chondrocyte death after hypertrophy doesn't mean it's over. The cycle literally just restarts again and you keep growing

So then how does ur growth plate fuse?

 

[AtrophicPyra]

So what you are basically saying is that androgens = help cell complete its job and e2 = kills cell before it completes its job leading to shorter FAH

Androgens do the same thing since they both express runx2 at different potencies, they both accelerate cell sensence

 

[Paul.jnxy]

Androgens do the same thing since they both express runx2 at different potencies, they both accelerate cell sensence

Again no evidence runx2 even leads to closure

 

[Paul.jnxy]

Yes, this is bone growth histology 101

I summarised it for the other nga

 

[AtrophicPyra]

Again no evidence runx2 even leads to closure

Bro

That’s runx2’s purpose

 

[Kojo]

Mb my girl was mad I wasn't responding

Ya hypertrophy is good for bone growth but for cartilage it’s horrible.

Still missing the point

They both express the same gene runx2 and that same gene does the same thing to to the same cell

Runx2 expresses aromatase

Androgen is not as potent as estrogen at expressing this gene however, this means they both deplete the resting zone.

Not justified

The problem isn’t even that androgens deplete the resting zone, it’s that they cause hypertrophy too fast AND deplete the resting zone too fast which ends up with unoptimal chrondrocyte proliferation,

There's just no evidence of this, again you still don't understand what hypertrophy is

Nothing will ever deplete the resting zone because the resting zone duplicates for maintenance. There's zero evidence in the literature showing that the resting zone becomes depleted with a net negative of bone growth

In other words, u could have had more time to proliferate chrondrocytes and more chrondrocytes would have underwent hypertrophy leading to a greater FAH than if u took supraphysiological androgens

Just a conclusion from previous claims that show your lack of understanding

 

[Paul.jnxy]

Bro

That’s runx2’s purpose

Back up your claims

 

[Kojo]

Bro

That’s runx2’s purpose

No it isnt?? runx2's purpose is to induce chondrocytes into hypertrophy and ossify the lacunae left by hypertrophied cells, hypertrophy isn't plate closure

 

[Kojo]

So then how does ur growth plate fuse?

Because of estradiol bruhEstradiol rapes the resting zone and the proliferative zone

 

[Paul.jnxy]

Mb my girl was mad I wasn't responding

Still missing the point

Runx2 expresses aromatase

Not justified

There's just no evidence of this, again you still don't understand what hypertrophy is

Nothing will ever deplete the resting zone because the resting zone duplicates for maintenance. There's zero evidence in the literature showing that the resting zone becomes depleted with a net negative of bone growth

Just a conclusion from previous claims that show your lack of understanding

Bro

That’s runx2’s purpose

Its not brotato

 

[Kojo]

Androgens do the same thing since they both express runx2 at different potencies, they both accelerate cell sensence

runx2 doesn't promote cell senescence outside of e2

 

[Kojo]

@nwed I completely forgot about that bone growth histology thread I might have to really make it after this

I'm too lazy to make it super coordinated and fancy I'll just explain stuff and then use analogies and images to help the understanding

 

[AtrophicPyra]

Mb my girl was mad I wasn't responding

Still missing the point

Runx2 expresses aromatase

Not justified

There's just no evidence of this, again you still don't understand what hypertrophy is

Nothing will ever deplete the resting zone because the resting zone duplicates for maintenance. There's zero evidence in the literature showing that the resting zone becomes depleted with a net negative of bone growth

Just a conclusion from previous claims that show your lack of understanding

It depletes fast I never said it depleted 100% with barely any cells in the RZ

Androgens make chrondrocytes hypertrophy fast and deplete the RZ (rapidly)

That’s gonna lead to a net negative height there is literature abt this somewhere, + u can see this in real time with the higher arm Anavar dose that made patients have a shorter FAH

 

[AtrophicPyra]

Because of estradiol bruhEstradiol rapes the resting zone and the proliferative zone

And what genes does e2 express that the androgens don’t to cartilage?

They express similar maturation genes

 

[Kojo]

It depletes fast I never said it depleted 100% with barely any cells in the RZ

Androgens make chrondrocytes hypertrophy fast and deplete the RZ (rapidly)

Androgens don't really buffer hypertrophy, and even if it did it would have zero effect on growth. It'd be even better for growth actually since you'd leave an even bigger gap for ossification, resulting in growing even faster.

There's no link with hypertrophy and the resting zone, hypertrophy simply and literally is just the proliferated chondrocytes getting bigger in size then dying off. Proliferation has a direct link to the resting zone, not hypertrophy bhai

You keep repeating "androgens deplete the rz rapidly" but you're not giving any justification? This is literally circular reasoning. I keep challenging this claim by saying no, the resting zone cells simply maintain the pool by multiplying.

So there's no depletion it legit stays the same. And if the proliferative status goes up, so does the differentiation and multiplying status of the rz cells to keep up. You're forgetting that cells cannot proliferate that if rz cells aren't also providing the material for the

That’s gonna lead to a net negative height there is literature abt this somewhere, + u can see this in real time with the higher arm Anavar dose that made patients have a shorter FAH

Maybe because runx2 produces estrogen.. which goes back to the original convo, there's no androgenic mediated fusion outside of estrogen. Runx2 directly synthesises the aromatase enzyme which produces estrogen in the growth plate

 

[Kojo]

And what genes does e2 express that the androgens don’t to cartilage?

They express similar maturation genes

CYP19A1
You do know that even if the movers of fusion are the same and are both expressed, they give different signals.

Hormones are simply signals, 2 hormones can signal to the same gene transcriptor and still produce a different effect as they are 2 completely different signals that alter and determine how the gene transcriptor responds.

 

[AtrophicPyra]

Look it doesn’t just continue infinitely, it ends with fusion

 

[AtrophicPyra]

Androgens don't really buffer hypertrophy, and even if it did it would have zero effect on growth. It'd be even better for growth actually since you'd leave an even bigger gap for ossification, resulting in growing even faster.

There's no link with hypertrophy and the resting zone, hypertrophy simply and literally is just the proliferated chondrocytes getting bigger in size then dying off. Proliferation has a direct link to the resting zone, not hypertrophy bhai

You keep repeating "androgens deplete the rz rapidly" but you're not giving any justification? This is literally circular reasoning. I keep challenging this claim by saying no, the resting zone cells simply maintain the pool by multiplying.

So there's no depletion it legit stays the same. And if the proliferative status goes up, so does the differentiation and multiplying status of the rz cells to keep up. You're forgetting that cells cannot proliferate that if rz cells aren't also providing the material for the

Maybe because runx2 produces estrogen.. which goes back to the original convo, there's no androgenic mediated fusion outside of estrogen. Runx2 directly synthesises the aromatase enzyme which produces estrogen in the growth plate

How would androgens inducing hypertrophy be good in chrondrocytes in any way??

Proliferation zone, resting zone, hypertrophic zone are all connected, androgens stimulate all of them unequally, depleting the resting zone, and inducing hypertrophy upon chrondrocytes that have been proliferated making the cell die quicker and having a shorter FAH

 

[Kojo]

How would androgens inducing hypertrophy be good in chrondrocytes in any way??

Because hypertrophy is needed for you to even grow properly, one of the reasons people are taller than others is a genetic predisposition to more cell hypertrophy which leads to growing more

Proliferation zone, resting zone, hypertrophic zone are all connected, androgens stimulate all of them unequally, depleting the resting zone, and inducing hypertrophy upon chrondrocytes that have been proliferated making the cell die quicker and having a shorter FAH

They aren't connected, they're only connected in sequence not function. The proliferation zone is connected to the resting zone, the hypertrophic zone is connected to the proliferation zone. The hypertrophic zone isn't connected to resting zone because the hypertrophic zone doesn't demand anything of the resting zone. The proliferative zone demands cells to proliferative, the hypertrophic zone waits demands the proliferative cells so that they can grow and die.

I don't think you understand that chondrocyte death is literally a good thing? They need to die so that you can grow. If they never die then the cartilage can't add to your bone growth and you'd be a dwarf.

also, androgens induce proliferation and differentiation not hypertrophy lmao There's also no evidence it does this unequally, there's much more complex signalling that allows it to be equal. It's not "Androgen->hypertrophy, they have to act on chondrocytes and then signalling proteins and genes have to balance this out. This is why we have negative feedback loops.

 

[Kojo]

How would androgens inducing hypertrophy be good in chrondrocytes in any way??

Proliferation zone, resting zone, hypertrophic zone are all connected, androgens stimulate all of them unequally, depleting the resting zone, and inducing hypertrophy upon chrondrocytes that have been proliferated making the cell die quicker and having a shorter FAH

Again, cell death is a good thing. this allows bone to grow.

Active cell death is bad.

 

[AtrophicPyra]

Again, cell death is a good thing. this allows bone to grow.

Active cell death is bad.

Premature cell death is bad and this is all beneficial to bone and shit for cartilage

 

[AtrophicPyra]

Because hypertrophy is needed for you to even grow properly, one of the reasons people are taller than others is a genetic predisposition to more cell hypertrophy which leads to growing more

They aren't connected, they're only connected in sequence not function. The proliferation zone is connected to the resting zone, the hypertrophic zone is connected to the proliferation zone. The hypertrophic zone isn't connected to resting zone because the hypertrophic zone doesn't demand anything of the resting zone. The proliferative zone demands cells to proliferative, the hypertrophic zone waits demands the proliferative cells so that they can grow and die.

I don't think you understand that chondrocyte death is literally a good thing? They need to die so that you can grow. If they never die then the cartilage can't add to your bone growth and you'd be a dwarf.

also, androgens induce proliferation and differentiation not hypertrophy lmao There's also no evidence it does this unequally, there's much more complex signalling that allows it to be equal. It's not "Androgen->hypertrophy, they have to act on chondrocytes and then signalling proteins and genes have to balance this out. This is why we have negative feedback loops.

Yes it’s needed to grow but u wanna slow this process as much as possible so u can maximize proliferation and get more bang out of ur buck

Androgens promote differentiation hypertrophy wym

 

[Kojo]

Premature cell death is bad and this is all beneficial to bone and shit for cartilage

It's not "premature" there's no such thing as premature chondrocyte death if it reaches the hypertrophic zone, that QUITE LITERALLY means it's reached full maturation because hypertrophy is the LAST stage a chondrocyte goes through. Come on atrophic, just admit you're wrong because this is getting tiring man

 

[Kojo]

Yes it’s needed to grow but u wanna slow this process as much as possible so u can maximize proliferation and get more bang out of ur buck

Androgens promote differentiation hypertrophy wym

They promote differentiation and proliferation, they don't really target hypertrophy. Hypertrophy is just when chondrocytes absorb water. and subsequently grow. Hormones don't have much influence there

 

[AtrophicPyra]

It's not "premature" there's no such thing as premature chondrocyte death if it reaches the hypertrophic zone, that QUITE LITERALLY means it's reached full maturation because hypertrophy is the LAST stage a chondrocyte goes through. Come on atrophic, just admit you're wrong because this is getting tiring man

prematurely as in progresses into the hypertrophic zone too quickly and dies out too quickly making it fah shorter

 

[AtrophicPyra]

They promote differentiation and proliferation, they don't really target hypertrophy. Hypertrophy is just when chondrocytes absorb water. and subsequently grow. Hormones don't have much influence there

G terminal hypertrophy is right when the cell is gonna die and that all gets expressed through differentiation genes like runx2

 

[Kojo]

prematurely as in progresses into the hypertrophic zone too quickly and dies out too quickly making it fah shorter

there's no such thing as progressing into the hypertrophic zone to quickly, these are mediated by signals that you cannot change. Also if it goes into the hypertrophic zone too quickly, that allows the cycle to repeat itself again meaning you grow faster. If this entire process happens faster this actually means you get taller since you get to fill in more proliferative and hypertrophic actions to your chondrocytes before e2 comes in and rapes it at higher levels

 

[Nodal]

dimo doesnt even matter
only changes the age range attracted to you

 

[Kojo]

G terminal hypertrophy is right when the cell is gonna die and that all gets expressed through differentiation genes like runx2

????????????? Dude this literally means nothing, we know runx2 tells the chondrocytes to hypertrophy, runx2 has no impact on chondrocyte differentiation either I said this like an hour or 2 ago. It has no effects on cartilage outside of inducing hypertrophy to the cells and fusing the dead cells

 

[AtrophicPyra]

there's no such thing as progressing into the hypertrophic zone to quickly, these are mediated by signals that you cannot change. Also if it goes into the hypertrophic zone too quickly, that allows the cycle to repeat itself again meaning you grow faster. If this entire process happens faster this actually means you get taller since you get to fill in more proliferative and hypertrophic actions to your chondrocytes before e2 comes in and rapes it at higher levels

Yeah hence the increase in height velocity we see with anavar

However it also depletes the RZ and initiates cell sencense quicker leading to a net negative of FAH

 

[AtrophicPyra]

????????????? Dude this literally means nothing, we know runx2 tells the chondrocytes to hypertrophy, runx2 has no impact on chondrocyte differentiation either I said this like an hour or 2 ago. It has no effects on cartilage outside of inducing hypertrophy to the cells and fusing the dead cells

They promote differentiation and proliferation, they don't really target hypertrophy. Hypertrophy is just when chondrocytes absorb water. and subsequently grow. Hormones don't have much influence there

U said here they don’t target hypertrophy though

 

[Kojo]

Yeah hence the increase in height velocity we see with anavar

However it also depletes the RZ and initiates cell sencense quicker leading to a net negative of FAH

You keep repeating this, are you trolling me? Also anavar doesn't act on any of these zones, it just increases igf-1. All roids increase igf-1 and just add to proliferation as that's what igf-1 does. So yes anavar indirectly acts on differentiation and proliferation not hypertrophy

It does NOT DEPLETE THE RZ BRO The Resting zone cannot deplete without e2 or apoptosis bruh which happens in like your 30s

 

[Kojo]

U said here they don’t target hypertrophy though

I'm talking about androgens there, my response was to you questioning androgens and hypertrophy

Yes it’s needed to grow but u wanna slow this process as much as possible so u can maximize proliferation and get more bang out of ur buck

Androgens promote differentiation hypertrophy wym

 

[AtrophicPyra]

You keep repeating this, are you trolling me? Also anavar doesn't act on any of these zones, it just increases igf-1. All roids increase igf-1 and just add to proliferation as that's what igf-1 does. So yes anavar indirectly acts on differentiation and proliferation not hypertrophy

It does NOT DEPLETE THE RZ BRO The Resting zone cannot deplete without e2 or apoptosis bruh which happens in like your 30s

Bro Anavar doesn’t increase igf1 it increase igf1r sensitivity

On my life all androgens deplete the RZ its in literature

 

[Kojo]

Bro Anavar doesn’t increase igf1 it increase igf1r sensitivity

On my life all androgens deplete the RZ its in literature

Through e2, potentially, and if by deplete you mean premature depletion of the rz then no you are wrong. If you mean depletion as simply "using resting zone cells" then sure

also increasing igf-1r technically is increase in igf-1 but not literally. It doesn't change anything, just allows the receptors to use igf-1 better. I use these ideas interchangeably

 

[AtrophicPyra]

Through e2, potentially, and if by deplete you mean premature depletion of the rz then no you are wrong. If you mean depletion as simply "using resting zone cells" then sure

also increasing igf-1r technically is increase in igf-1 but not literally. It doesn't change anything, just allows the receptors to use igf-1 better. I use these ideas interchangeably

I mean both when talking abt RZ, it depletes too quickly inducing too much proliferative cells, this inturn makes those proliferative cells go into hypertrophic sequence faster since androgens induce hypertrophy and then the cell dies