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

[Paul.jnxy]

There r 2 more keep searching, one of them directly says that androgens made them shorter textbook quotes

Link.

 

[AtrophicPyra]

Link.

Too far deep just search my name in search bar

And search in the search bar, androgen fph or androgen fah or androgen final predicted height etc.

 

[AtrophicPyra]

Back up your claims then.

RUNX2 is regulated by many pathways not soley by androgens + 0 evidence androgen receptor agonism leads to upregulated RUNX2.

Again back up your claims.

Most of the studies you linked are flawed. @Zagro debunked you on the tren one

??? Bro androgens directly express runx2??

Read any study showing this heck ask google

 

[Paul.jnxy]

I read the study up and down, if u actually saw the conclusion u would see that trenbolone group were smaller skeletally?

The nga zagro completely debunked your tren one? Didn't you read his reply. A lot of variables were not optimally altered for growth. No prolactin control at all leading to a skewed prolactin e2 ratio for example leading to being shorter stature due to high e2?

 

[Kojo]

Runx2 expression is massively upregulated in cartilage cells and some other downpath genes that’s also regulate differentiation

Runx2 isn't necessarily bad and is actually needed for proper bone growth.

Where does differentiation come into this? wnt works enough as a negative feedback loop on differentiation.

Also differentiation doesn't mean much for fusion, it's a common misconception that advanced differentiation causes fusion.

Rz cells will always leave a daughter cell behind to maintain the pool. This process only stops because E2 actually acts on those stem cells directly to decrease it's normal cell lifespan.

 

[avgsub5human]

honestly over if you need roids/trt for masculine features tbh, it should happen for most men in their puberty

I can respect kids wanna get on the upper limit of test and reap the benefits but again its not so black and white, trying to beat your genetics always results in some kind of drawback sadly you have to be well researched prior which these kids dont even do, who would at 14

 

[AtrophicPyra]

Runx2 isn't necessarily bad and is actually needed for proper bone growth.

Where does differentiation come into this? wnt works enough as a negative feedback loop on differentiation.

Also differentiation doesn't mean much for fusion, it's a common misconception that advanced differentiation causes fusion.

Rz cells will always leave a daughter cell behind to maintain the pool. This process only stops because E2 actually acts on those stem cells directly to decrease it's normal cell lifespan.

Well runx2 is the main gene there r downstream genes that also cause maturation in the gp

 

[AtrophicPyra]

The nga zagro completely debunked your tren one? Didn't you read his reply. A lot of variables were not optimally altered for growth. No prolactin control at all leading to a skewed prolactin e2 ratio for example leading to being shorter stature due to high e2?

He didn’t.

So ur saying high prolactin is what makes u shorter whilst taking tren and not the tren itself? Yk taking tren literally nukes ur e2 and test right

 

[Kojo]

There r 2 more keep searching, one of them directly says that androgens made them shorter textbook quotes

Just send them

I read the study up and down, if u actually saw the conclusion u would see that trenbolone group were smaller skeletally?

I did read it, the results literally show by technicality they were "smaller" but by marginal differences. The differences between the groups are literally there on the results graph in the bottom right corner lol

Literally every single chrondrocyte cell when it takes in an androgen, it will express maturation genes and downstream maturation genes, the main one is runx2, this will lead to premature closure.

Also where do we see androgens massively upregulating runx2? and what point is "too much" runx2 activity as it actually acts as a necessity for growth. Mice with low runx2 end up dwarfs.

Runx2 also directly produces aromatase (common knowledge)

Spoiler: Study

Role of RUNX2 in Breast Carcinogenesis - PMC

RUNX2 is a transcription factor playing the major role in osteogenesis, but it can be involved in DNA damage response, which is crucial for cancer transformation. RUNX2 can interact with cell cycle regulators: cyclin-dependent kinases, pRB and ...

pmc.ncbi.nlm.nih.gov

Studies also actually show androgens like DHT repress runx2

Spoiler: Study

Repression of Runx2 by Androgen Receptor (AR) in Osteoblasts and Prostate Cancer Cells: AR Binds Runx2 and Abrogates Its Recruitment to DNA - PMC

Runx2 and androgen receptor (AR) are master transcription factors with pivotal roles in bone metabolism and prostate cancer (PCa). We dissected AR-mediated repression of Runx2 in dihydrotestosterone (DHT)-treated osteoblastic and PCa cells using ...

pmc.ncbi.nlm.nih.gov

 

[Paul.jnxy]

He didn’t.

So ur saying high prolactin is what makes u shorter whilst taking tren and not the tren itself? Yk taking tren literally nukes ur e2 and test right

https://looksmax.org/threads/stack-for-height-and-dimo-gtfih.2165497/post-29793369

 

[Paul.jnxy]

Just send them

I did read it, the results literally show by technicality they were "smaller" but by marginal differences. The differences between the groups are literally there on the results graph in the bottom right corner lol

Also where do we see androgens massively upregulating runx2? and what point is "too much" runx2 activity as it actually acts as a necessity for growth. Mice with low runx2 end up dwarfs.

Runx2 also directly produces aromatase (common knowledge)

Spoiler: Study

Role of RUNX2 in Breast Carcinogenesis - PMC

RUNX2 is a transcription factor playing the major role in osteogenesis, but it can be involved in DNA damage response, which is crucial for cancer transformation. RUNX2 can interact with cell cycle regulators: cyclin-dependent kinases, pRB and ...

pmc.ncbi.nlm.nih.gov

Studies also actually show androgens like DHT repress runx2

Spoiler: Study

Repression of Runx2 by Androgen Receptor (AR) in Osteoblasts and Prostate Cancer Cells: AR Binds Runx2 and Abrogates Its Recruitment to DNA - PMC

Runx2 and androgen receptor (AR) are master transcription factors with pivotal roles in bone metabolism and prostate cancer (PCa). We dissected AR-mediated repression of Runx2 in dihydrotestosterone (DHT)-treated osteoblastic and PCa cells using ...

pmc.ncbi.nlm.nih.gov

Hey I wanted to say the aromatase one

 

[AtrophicPyra]

Just send them

I did read it, the results literally show by technicality they were "smaller" but by marginal differences. The differences between the groups are literally there on the results graph in the bottom right corner lol

Also where do we see androgens massively upregulating runx2? and what point is "too much" runx2 activity as it actually acts as a necessity for growth. Mice with low runx2 end up dwarfs.

Runx2 also directly produces aromatase (common knowledge)

Spoiler: Study

Role of RUNX2 in Breast Carcinogenesis - PMC

RUNX2 is a transcription factor playing the major role in osteogenesis, but it can be involved in DNA damage response, which is crucial for cancer transformation. RUNX2 can interact with cell cycle regulators: cyclin-dependent kinases, pRB and ...

pmc.ncbi.nlm.nih.gov

Studies also actually show androgens like DHT repress runx2

Spoiler: Study

Repression of Runx2 by Androgen Receptor (AR) in Osteoblasts and Prostate Cancer Cells: AR Binds Runx2 and Abrogates Its Recruitment to DNA - PMC

Runx2 and androgen receptor (AR) are master transcription factors with pivotal roles in bone metabolism and prostate cancer (PCa). We dissected AR-mediated repression of Runx2 in dihydrotestosterone (DHT)-treated osteoblastic and PCa cells using ...

pmc.ncbi.nlm.nih.gov

Well duh if ur deficient in runx2 ur gonna end up shorter because those cells won’t actually end up differentiating and make ur bones longer

In Anavar studies u can see high arm doses massively decrease fah by 1.5-7.5cm in one study compared to the control group that didn’t receive the anavar

Anavar is a dht deriv it 100% doesn’t not repress runx2

Also too much runx2 will make u shorter too

 

[Paul.jnxy]

Well runx2 is the main gene there r downstream genes that also cause maturation in the gp

You also did not account for the fact that AR signaling can affect RUNX2 through intermediates like IGF-1, nt/β-catenin pathway and the BMP pathway although there is still no real proof that runx2 directly leads to fusion either.

 

[Paul.jnxy]

You also did not account for the fact that AR signaling can affect RUNX2 through intermediates like IGF-1, nt/β-catenin pathway and the BMP pathway although there is still no real proof that runx2 directly leads to fusion either.

Why tf did I type like a kid with down syndrome

 

[AtrophicPyra]

You also did not account for the fact that AR signaling can affet RUNX2 thorugh intermediates like IGF-1, nt/β-catenin pathway and the BMP pathway although there is still no real proof that runx2 directly leads to fusion either.

There is proof

MANY MANY literature says it’s the main gene responsible for hyper trophy of chrondrocytes?

And that it’s main thing is differentiation

 

[Kojo]

Well duh if ur deficient in runx2 ur gonna end up shorter because those cells won’t actually end up differentiating and make ur bones longer

In Anavar studies u can see high arm doses massively decrease fah by 1.5-7.5cm in one study compared to the control group that didn’t receive the anavar

Send study

Anavar is a dht deriv it 100% doesn’t not repress runx2

I sent the study of dht having repressive effects on runx2, Unless you're agreeing it does by saying "doesn't not" or was that a typo?

Also too much runx2 will make u shorter too

Yeah but that's obvious, the question is there's no quantification of how much is "too much" and how you know if you even have "too much.

Also again, runx2 promotes aromatase.

Also send the anavar studies before I make a reply without the context

 

[Paul.jnxy]

There is proof

MANY MANY literature says it’s the main gene responsible for hyper trophy of chrondrocytes?

And that it’s main thing is differentiation

No actual proof. Back up your claims with papers then.

Its prooven to do only these.
Required for bone formation
drives chondrocyte hypertrophy
it regulates the cartilage bone transition

Nothing to do with fusion aka loss of the plate as the whole

 

[Kojo]

There is proof

MANY MANY literature says it’s the main gene responsible for hyper trophy of chrondrocytes?

And that it’s main thing is differentiation

It doesn't drive differentiation of msc's into chondroblasts so that's unrelated.

It does that for osteoblasts, being ready to calcify lacunae deposits post chondrocyte hypertrophy induction.

I can agree it induces hypertrophy too

 

[AtrophicPyra]

No actual proof. Back up your claims with papers then.

Its prooven to do only these.
Required for bone formation
drives chondrocyte hypertrophy
it regulates the cartilage bone transition

Nothing to do with fusion aka loss of the plate.

Bro..

If it causes hypertrophy to the chrondrocytes that’s gonna end up making u shorter..

After hypertrophy it goes into terminal hypetrophy and then cell sencense, why would u wanna speed that up???

 

[Paul.jnxy]

It doesn't drive differentiation of msc's into chondroblasts so that's unrelated.

It does that for osteoblasts, being ready to calcify lacunae deposits post chondrocyte hypertrophy induction.

I can agree it induces hypertrophy too

It does most probably induce hypertrophy but not plate closure

 

[AtrophicPyra]

Send study

I sent the study of dht having repressive effects on runx2, Unless you're agreeing it does by saying "doesn't not" or was that a typo?

Yeah but that's obvious, the question is there's no quantification of how much is "too much" and how you know if you even have "too much.

Also again, runx2 promotes aromatase.

Also send the anavar studies before I make a reply without the context

I’m not trying to be too lazy with the reply’s but I’m eating dominos rn and I already spent hours and days trying to figure this all out myself,

I already told u guys what I know it’s ur job to research and see if im right or wrong

 

[AtrophicPyra]

It does most probably induce hypertrophy but not plate closure

If it induces hypertrophy it’s gonna speed up the process to cell sencense???

That’s gonna lead to plate closure

 

[AtrophicPyra]

It doesn't drive differentiation of msc's into chondroblasts so that's unrelated.

It does that for osteoblasts, being ready to calcify lacunae deposits post chondrocyte hypertrophy induction.

I can agree it induces hypertrophy too

Runx2 isn’t just involved in osteoblasts it’s also involved in cartilage, it pushes both into hypertrophic sequence

 

[Kojo]

It does most probably induce hypertrophy but not plate closure

Yes, I'm not sure what the relevance of hypertrophy really is here.

As long as rz cells aren't being aged and chondrocytes aren't being ossified there's no closure.

Chondrocytes post hypertrophy just leave a bone model behind called lacunae for osteoblasts to turn into bone. This process doesn't effect any other chondrocytes in different growth plate zones

 

[Kojo]

I’m not trying to be too lazy with the reply’s but I’m eating dominos rn and I already spent hours and days trying to figure this all out myself,

I already told u guys what I know it’s ur job to research and see if im right or wrong

It is also your job to back up your claims on the subject though, I don't mind talking about it later, I kind of want to play FC26 rn anyways

 

[Kojo]

Runx2 isn’t just involved in osteoblasts it’s also involved in cartilage, it pushes both into hypertrophic sequence

You just repeated what I said..

 

[AtrophicPyra]

Yes, I'm not sure what the relevance of hypertrophy really is here.

As long as rz cells aren't being aged and chondrocytes aren't being ossified there's no closure.

Chondrocytes post hypertrophy just leave a bone model behind called lacunae for osteoblasts to turn into bone. This process doesn't effect any other chondrocytes in different growth plate zones

because hypertrophy in a cell leads to terminal hypertrophy and then cell death.

This is exactly what runx2 speeds up, sox9 does the exact opposite.

Why would u want tren to put ur cells in a post hypertrophic state? That’s gonna age ur bones and cartilage leading to premature ossification

 

[Kojo]

If it induces hypertrophy it’s gonna speed up the process to cell sencense???

That’s gonna lead to plate closure

What's the mechanistic link between rz cell senescene and and hypertrophy?? The process just continues to go on, where do the other cells get ossified that aren't ready for ossification

 

[Kojo]

because hypertrophy in a cell leads to terminal hypertrophy and then cell death.

Yes?? Of the cells that went through hypertrophy

the process still doesn't end there when it just continuously loops from rz->proliferation->hypertrophy and then it goes back to square 1. The hypertrophied chondrocytes leave bone formation behind for it's length to increase they don't just "die" off without gain. I'm not saying you said that if you didn't but i'm just clarifying.

Chondrocytes are meant to die off at some point through their maturation into bone. As long as you're getting a good rate of proliferation, the "excess" hypertrophy even if we granted that's the case, doesn't make any net negatives on bone growth.

The growth plate has 4 different functional zones which you obviously know. For growth to stop, the rz cells have to lose their capacity to differentiate and divide first. And then e2 fuses it from then on.

 

[AtrophicPyra]

What's the mechanistic link between rz cell senescene and and hypertrophy?? The process just continues to go on, where do the other cells get ossified that aren't ready for ossification

G..

The androgen depletes the resting zone of the chrondrocytes and speeds up hypertrophy of the chrondrocytes then the cell dies

The process doesn’t go on ur bones just end up shorter

 

[AtrophicPyra]

Yes?? Of the cells that went through hypertrophy

the process still doesn't end there when it just continuously loops from rz->proliferation->hypertrophy and then it goes back to square 1. The hypertrophied chondrocytes leave bone formation behind for it's length to increase they don't just "die" off without gain. I'm not saying you said that if you didn't but i'm just clarifying.

Chondrocytes are meant to die off at some point through that maturation into bone. As long as you're getting a good rate of proliferation, the "excess" hypertrophy even if we granted that's the case, doesn't make any net negatives on bone growth.

Bones can’t just grow g that’s what cartilage does, cartilage lengthens ur bones, once it turns into bone it won’t grow hence why u can’t grow after gp fused

Why would u want to speed up the death of the chrondrocyte through androgens?

 

[Kojo]

G..

The androgen depletes the resting zone of the chrondrocytes and speeds up hypertrophy of the chrondrocytes then the cell dies

The process doesn’t go on ur bones just end up shorter

Why would androgens deplete the resting zone of its chondrocytes........... The resting zone cells divide and leave another cell behind precisely so that DOESN'T happen. There are negative feedback loop signals in place so it puts a break on Resting zone chondrocyte differentiation. This isn't true whatsoever

It does go onto your bones.. I'm not sure if you understand how the bone growth process works brother bhai

The resting zone cells differentiate and LEAVE an identical resting zone cell behind to maintain the pool of the resting zone cells for further differentiation down the line. The resting zone cell that moves, goes into the proliferative zone where it divides even more.

These cells then move from the proliferative zone into the HYPERTROPHIC ZONE and then they start to swell in size (Hypetrophy). After this process, the cells die off in the calcification zone/process and leave behind bone formation (Lacunae) for osteoblasts to come in and replace those dead cells with bone in the diaphysis.

Which directly lengthens the diaphysis. We literally grow through chondrocyte hypertrophy

 

[user223]

I actually haven't seen his, a lot of people talk about him specifically. I'll have a look at it but people have said he was a late bloomer so I don't know his background there

he got fillers very clearly jfl op is a retard. roids are only good for the body halo.

 

[AtrophicPyra]

Why would androgens deplete the resting zone of its chondrocytes........... The resting zone cells divide and leave another cell behind precisely so that DOESN'T happen. There are negative feedback loop signals in place so it puts a break on Resting zone chondrocyte differentiation. This isn't true whatsoever

It does go onto your bones.. I'm not sure if you understand how the bone growth process works brother bhai

The resting zone cells differentiate and LEAVE an identical resting zone cell behind to maintain the pool of the resting zone cells for further differentiation down the line. The resting zone cell that moves, goes into the proliferative zone where it divides even more.

These cells then move from the proliferative zone into the HYPERTROPHIC ZONE and then they start to swell in size (Hypetrophy). After this process, the cells die off in the calcification zone/process and leave behind bone formation (Lacunae) for osteoblasts to come in and replace those dead cells with bone in the diaphysis.

Which directly lengthens the diaphysis. We literally grow through chondrocyte hypertrophy
View attachment 5275561 View attachment 5275562

Ye ik androgens go into ur bones

But once they turn from resting zone and proliferative to hypertrophic, it can’t go back and you’ll end up shorter since androgen speedrunned to cell sencense which would cause an increase of heaving velocity but decreased final adult height

The rate at which another resting zone cell get induced does not match the rate completely of the androgens hypertrophy to the chrondrocyte. That’s why androgens deplete the resting zone

 

[Kojo]

Bones can’t just grow g that’s what cartilage does, cartilage lengthens ur bones, once it turns into bone it won’t grow hence why u can’t grow after gp fused

Why would u want to speed up the death of the chrondrocyte through androgens?

Chondrocyte death directly produces growth, they literally die for a reason, so that the bone elongates by filling in the blank space (Lacunae again) with bone which legit makes the bone grow longer

I think you're confused by me saying "It leaves bone formation"

Bone formation isn't literal bone, it's like a blueprint for where bone is supposed to be added.

 

[AtrophicPyra]

Chondrocyte death directly produces growth, they literally die for a reason, so that the bone elongates by filling in the blank space (Lacunae again) with bone which legit makes the bone grow longer

I think you're confused by me saying "It leaves bone formation"

Bone formation isn't literal bone, it's like a blueprint for where bone is supposed to be added.

Ya ik cartilage gets replaced by bone which is why ur gp fuse

But u want to avoid premature cell sencense so it doesn’t get replaced by bone too fast hence a lower final adult height

 

[Kojo]

But once they turn from resting zone and proliferative to hypertrophic, it can’t go back and you’ll end up shorter since androgen speedrunned to cell sencense which would cause an increase of heaving velocity but decreased final adult height

It isn't supposed to go back, I think you're forgetting that bone growth is a cycle of this. Rz cell --> prolif --> hypertrophy. And you're missing the key that explains why this doesn't stunt you. It shows in your next reply

The rate at which another resting zone cell get induced does not match the rate completely of the androgens hypertrophy to the chrondrocyte. That’s why androgens deplete the resting zone

This isn't true or scientifically backed at all. Resting Zone Cells literally duplicate before leaving the resting zone. They won't leave the resting zone without duplicating. Also hypertrophy is the absolute last phase of growth, why would it have any effect on the resting zone lmao if anything you're better off arguing for proliferation depleting the resting zone. Hypertrophy just makes cells grow in size.

 

[AtrophicPyra]

It isn't supposed to go back, I think you're forgetting that bone growth is a cycle of this. Rz cell --> prolif --> hypertrophy. And you're missing the key that explains why this doesn't stunt you. It shows in your next reply

This isn't true or scientifically backed at all. Resting Zone Cells literally duplicate before leaving the resting zone. They won't leave the resting zone without duplicating. Also hypertrophy is the absolute last phase of growth, why would it have any effect on the resting zone lmao if anything you're better off arguing for proliferation depleting the resting zone. Hypertrophy just makes cells grow in size.

Androgens deplete RZ very rapidly and make them go proliferative for a bit but then massively undego hypertrophic Sequence which would then turn into cell death, that process happens too fast because it keeps depleting the RZ ur right they duplicate but at the end, its gonna result in the cell dying faster and making u shorter

 

[Kojo]

Ya ik cartilage gets replaced by bone which is why ur gp fuse

Yeah but this is the issue though you keep mixing up mechanisms, cartilage gets replaced by bone because of estrogen. The difference in what I'm explaining and what e2 does is,

e2 fuses active chondrocytes. It's like a construction team digging a hole and whilst they're digging the hole, people on the outside just fill the hole. The difference between what I'm explaining about hypertrophy and bone growth rn is, The diggers dug the hole, came out of it and then instructed people the fill the hole. That's why girls finish growing before boys. Simply because their chondrocytes don't get enough time to do what they're supposed to.

But u want to avoid premature cell sencense so it doesn’t get replaced by bone too fast hence a lower final adult height

There's no such thing as "getting replaced by bone too fast" in endochondral ossification. You're still confusing the 2 distinct pathways of ossification lol

e2 ossification = turning chondrocytes into bone = affects fah
growth ossification (Endochondral ossification) = turning lacunae into bone = doesn't affect fah

 

[AtrophicPyra]

Yeah but this is the issue though you keep mixing up mechanisms, cartilage gets replaced by bone because of estrogen. The difference in what I'm explaining and what e2 does is,

e2 fuses active chondrocytes. It's like a construction team digging a hole and whilst they're digging the hole, people on the outside just fill the hole. The difference between what I'm explaining about hypertrophy and bone growth rn is, The diggers dug the hole, came out of it and then instructed people the fill the hole. That's why girls finish growing before boys. Simply because their chondrocytes don't get enough time to do what they're supposed to.

There's no such thing as "getting replaced by bone too fast" in endochondral ossification. You're still confusing the 2 distinct pathways of ossification lol

e2 ossification = turning chondrocytes into bone = affects fah
growth ossification (Endochondral ossification) = turning lacunae into bone = doesn't affect fah

Don’t androgens and e2 express runx2 tho?

They both end up with the same result a shorter fah since the chrondrocytes turn into bone, ossification.

 

[Kojo]

Androgens deplete RZ very rapidly and make them go proliferative for a bit but then massively undego hypertrophic Sequence which would then turn into cell death, that process happens too fast because it keeps depleting the RZ ur right they duplicate but at the end, its gonna result in the cell dying faster and making u shorter

Androgens inducing proliferation just induces more differentiation. Which is equal. This entire process is synergistic, Everything starts at the resting zone so there's no way the proliferative and hypertrophic zone can sort of "leave the resting zone behind" or be too fast for it.

Chondrocytes in the proliferative zone are already proliferating, if the body wants to proliferate more cells, the resting zone simply pushes out more, and duplicates more. From then on, hypertrophy and the resting zone cells have zero link. That link happens with the proliferative zone and hypertrophic zone

Edit: If the body detects that this is happening way too fast for any cells to keep up, there are negative feedback loops in place that slow down differentiation, and that slow down proliferation which we all know is FGFR3. The body isn't retarded, it would never just run you into premature fusion or mess with cell synergy outside of e2.

 

[Paul.jnxy]

@AtrophicPyra @Kojo This is such an interesting convo. I left for like an hour now I don't even know where to continue.

 

[AtrophicPyra]

Androgens inducing proliferation just induces more differentiation. Which is equal. This entire process is synergistic, Everything starts at the resting zone so there's no way the proliferative and hypertrophic zone can sort of "leave the resting zone behind" or be too fast for it.

Chondrocytes in the proliferative zone are already proliferating, if the body wants to proliferate more cells, the resting zone simply pushes out more, and duplicates more. From then on, hypertrophy and the resting zone cells have zero link. That link happens with the proliferative zone and hypertrophic zone

Edit: If the body detects that this is happening way too fast for any cells to keep up, there are negative feedback loops in place that slow down differentiation, and that slow down proliferation which we all know is FGFR3. The body isn't retarded, it would never just run you into premature fusion or mess with cell synergy outside of e2.

Well it kind of is linked bec the resting zone induces more cells that can proliferate which would then hypertrophy except androgens deplete the zone which depletes the proliferation process whilst mildly stimulating it, and then undergoing massive hypertrophy and cell death

 

[AtrophicPyra]

@AtrophicPyra @Kojo This is such an interesting convo. I left for like an hour now I don't even know where to continue.

Where were u g

 

[Paul.jnxy]

Where were u g

history homework. Wanna see?

 

[AtrophicPyra]

history homework. Wanna see?

I have ptsd from history class

Am a victim to failing it so hard

 

[Kojo]

Don’t androgens and e2 express runx2 tho?

They both end up with the same result a shorter fah since the chrondrocytes turn into bone, ossification.

this is why you should nuke e2, and runx2 indirectly produces e2 by producing aromatase

E2 actually represses runx2

So do androgens. A lot of hormones have push pull effects on these genes which is why going so far down to the level of arguing with genes like runx2 doesn't get you anywhere. Androgens both upregulate and downregulate runx2. I sent the study earlier

Also no they don't both end up with the same result.. E2 decreases the lifespan of Resting zone cells and Chondrocytes. Hypertrophy doesn't affect the lifespan of these at all, they live for as long as they need to, to produce bone and then they die off since they've completed their function. Again you're confusing chondrocyte ossification with chondrocyte death, and lacunae ossification.

Chondrocyte death after hypertrophy practically means nothing because the resting zone simply continues to make more.

With e2, the resting zone struggles to make more because e2 is raping their life span. This should be comprehensive enough to understand

 

[AtrophicPyra]

this is why you should nuke e2, and runx2 indirectly produces e2 by producing aromatase

E2 actually represses runx2

So do androgens. A lot of hormones have push pull effects on these genes which is why going so far down to the level of arguing with genes like runx2 doesn't get you anywhere. Androgens both upregulate and downregulate runx2. I sent the study earlier

Also no they don't both end up with the same result.. E2 decreases the lifespan of Resting zone cells and Chondrocytes. Hypertrophy doesn't affect the lifespan of these at all, they live for as long as they need to, to produce bone and then they die off since they've completed their function. Again you're confusing chondrocyte ossification with chondrocyte death, and lacunae ossification.

Chondrocyte death after hypertrophy practically means nothing because the resting zone simply continues to make more.

With e2, the resting zone struggles to make more because e2 is raping their life span. This should be comprehensive enough to understand

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

With e2 the resting zone is also depleted just like androgens

And ye ik hypertrophy mainly is linked to proliferative phase not the resting zone

 

[Kojo]

Well it kind of is linked bec the resting zone induces more cells that can proliferate which would then hypertrophy except androgens deplete the zone which depletes the proliferation process whilst mildly stimulating it, and then undergoing massive hypertrophy and cell death

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

 

[Paul.jnxy]

TBF i agree with @Kojo. I believe he won the argument here.

Yeah but this is the issue though you keep mixing up mechanisms, cartilage gets replaced by bone because of estrogen. The difference in what I'm explaining and what e2 does is,

e2 fuses active chondrocytes. It's like a construction team digging a hole and whilst they're digging the hole, people on the outside just fill the hole. The difference between what I'm explaining about hypertrophy and bone growth rn is, The diggers dug the hole, came out of it and then instructed people the fill the hole. That's why girls finish growing before boys. Simply because their chondrocytes don't get enough time to do what they're supposed to.

There's no such thing as "getting replaced by bone too fast" in endochondral ossification. You're still confusing the 2 distinct pathways of ossification lol

e2 ossification = turning chondrocytes into bone = affects fah
growth ossification (Endochondral ossification) = turning lacunae into bone = doesn't affect fah