Growth Plate Fusion through Androgens?

[Kojo]

If anyone can justify this retarded concept I'll give them 50usd

There's been way too much stupid low iq fear mongering about this, Eviscerate me if I don't give the 50usd I'm that confident

THERE IS NO GROWTH PLATE FUSION THROUGH THE USE OF ANDROGENS OR ANY ANDROGEN RECEPTOR SIGNALLING. EVERYTHING IS THROUGH ESTROGEN.

WHOEVER IS WILLING TO DISAGREE WITH THIS LETS TALK ABOUT IT BEFORE I LEAVE THE SITE AGAIN.

 

[Kojo]

??? im not asking u to get ur answers from gpt im asking u to get the study link for there

Yes, even ai is trash for studies. I've dabbled with ai before to assess it's consistency. Ai sucks and it's the reason why you're making stupid unjustifiable points rn. if you're gonna make a point justify it with some evidence/literature. You haven't done that a single time so far.

AI has also hammered down on a point, then conceded to me when I tried to debate it.

Ai also uploads completely random studies when you ask it for something. For example I asked it to send a study on era hypersensitivity as a positive feedback loop and it sent me an abstract on aromatase lol

 

[Niebvll]

I already know about telomere shortening and the hayflick limit. This doesn't come under the fusion of androgens which this thread is about

I've clarified time and time again that I'm not talking about telomere shortening or the hayflick limit. We already know resting zone chondrocytes have a finite limit of divisions.

Where did you clarify this?

I will definitely not read the whole thread before replying

THERE IS NO GROWTH PLATE FUSION THROUGH THE USE OF ANDROGENS OR ANY ANDROGEN RECEPTOR SIGNALLING.

Yes

EVERYTHING IS THROUGH ESTROGEN.

No
Not true
Thats all I said

Proliferation induced senescence isn't a thing nor is it induced by androgens, unless you're trying to articulate resting zone cell symmetrical division into the proliferative zone which is an anomaly.

Claims to know about telomere shortening
Doesnt know the resulting senescence process is called proliferation-induced/replicative senescence

 

[AtrophicPyra]

Yes, even ai is trash for studies. I've dabbled with ai before to assess it's consistency. Ai sucks and it's the reason why you're making stupid unjustifiable points rn. if you're gonna make a point justify it with some evidence/literature. You haven't done that a single time so far.

AI has also hammered down on a point, then conceded to me when I tried to debate it.

Ai also uploads completely random studies when you ask it for something. For example I asked it to send a study on era hypersensitivity as a positive feedback loop and it sent me an abstract on aromatase lol

ai is not shit for studies AT ALL, just keep writing a few more prompts till u find the study

yeah ik its very inconsistent but u just gotta be patient till u find it, it cant make up random study links via the pubmed site

 

[Niebvll]

@AtrophicPyra god youre dense

Its not estrogen alone

reply to the claim "everything is through estrogen"
no mention of any hormones that do what "estrogen doesnt do alone"

for nattys, estrogen is the main hormone responsible for gp closure but thats bec test isnt as anabolic as tren and its at natty levels of test

You coming up with random androgens

When did I mention anything about hormones?

Obvious confusion as I never mentioned any of those

 

[AtrophicPyra]

Androgens affect myogenesis in vitro and increase local IGF-1 expression - PubMed

Both T and IGF-1 increase myogenic commitment after 7-d exposure to a differentiation medium. With T causing a concomitant increase in IGF-1 mRNA underpinning IGF-1 as a central mediator in the cellular pathways associated with muscle hypertrophy, including those affected by androgens. The novel...

pubmed.ncbi.nlm.nih.gov

An example of what i'm talking about^

thats testosterone not tren or nandrolone or a dht derivative

they r all very different

 

[AtrophicPyra]

@AtrophicPyra god youre dense

reply to the claim "everything is through estrogen"
no mention of any hormones that do what "estrogen doesnt do alone"

You coming up with random androgens

Obvious confusion as I never mentioned any of those

i thought u were just responding in general to the thread

i meant that natty test levels isnt going to mature ur gp its only when its supraphysiological or if ur taking more potent androgens

 

[Niebvll]

i thought u were just responding in general to the thread

i meant that natty test levels isnt going to mature ur gp its only when its supraphysiological or if ur taking more potent androgens

They still aromatise

 

[AtrophicPyra]

They still aromatise

nandrolone barely aromatizes, i looked into it alot, it aromatises into a weaker form of estrogen not strong enough to cause plate closure, aromatizes 1/5th what test aromatizes

 

[Niebvll]

nandrolone barely aromatizes, i looked into it alot, it aromatises into a weaker form of estrogen not strong enough to cause plate closure, aromatizes 1/5th what test aromatizes

I mean natural testosterone

 

[Kojo]

ai is not shit for studies AT ALL, just keep writing a few more prompts till u find the study

yeah ik its very inconsistent but u just gotta be patient till u find it, it cant make up random study links via the pubmed site

I didn't say it makes things up. I said it sends the wrong things. Yeah You might have to prompt it 30 times but it doesn't change what I'm saying. It's interpretation of studies also sucks.

Not to mention, It's not my burden to find studies for YOUR claims when i'm the one asking you to prove them

 

[fraudster#1]

for anyone who thinks androgens would close growth plates, regardless ERa signalling, i ask to take a look at this
[https://www.nejm.org/doi/full/10.1056/NEJM199707103370204]

[https://pubmed.ncbi.nlm.nih.gov/8090165/

{https://pubmed.ncbi.nlm.nih.gov/37373981/}

{https://pubmed.ncbi.nlm.nih.gov/40048086/}

~Elevated levels of androgens in their body, yet undectetable levels of E2. Results? Still growing till 31 years old~​

 

[Kojo]

thats testosterone not tren or nandrolone or a dht derivative

they r all very different

They don't have to be identical compounds. They all bind to ar. This is a universal ar pathway lol

 

[Kojo]

for anyone who thinks androgens would close growth plates, regardless ERa signalling, i ask to take a look at this
[https://www.nejm.org/doi/full/10.1056/NEJM199707103370204]
View attachment 5467304​

[https://pubmed.ncbi.nlm.nih.gov/8090165/
View attachment 5467312
{https://pubmed.ncbi.nlm.nih.gov/37373981/}
View attachment 5467317

{https://pubmed.ncbi.nlm.nih.gov/40048086/}
View attachment 5467325
~Elevated levels of androgens in their body, yet undectetable levels of E2. Results? Still growing till 31 years old~

Yeah I use the cyp19a1 deficiency argument all the time. That dude keeps growing until e2 is injected

They never have an argument against it btw they just say "it's been debunked brooooo"

 

[AtrophicPyra]

I mean natural testosterone

yea if u take test at supraphysiological levels esp without an ai will close ur gp obv

but.. testosterone was injected directly into a clavicle causing it to grow, study never said anything abt its final adult length though thats the closest i got

 

[Niebvll]

yea if u take test at supraphysiological levels esp without an ai will close ur gp obv

but.. testosterone was injected directly into a clavicle causing it to grow, study never said anything abt its final adult length though thats the closest i got

Im saying natural testosterone aromatises into estrogen
Natural estrogen levels still have to come from somewhere
So is it really accurate to say natural testosterone levels dont work into plate fusion?

 

[AtrophicPyra]

Yeah I use the cyp19a1 deficiency argument all the time. That dude keeps growing until e2 is injected

They never have an argument against it btw they just say "it's been debunked brooooo"

once again he has normal physiological levels of androgens, testosterone is not as potent as trenbolone or nandrolone deca

 

[AtrophicPyra]

Im saying natural testosterone aromatises into estrogen
Natural estrogen levels still have to come from somewhere

what g

 

[fraudster#1]

Yeah I use the cyp19a1 deficiency argument all the time. That dude keeps growing until e2 is injected

They never have an argument against it btw they just say "it's been debunked brooooo"

not only, DHT treatment also didnt advanced bone age, even tho is a very potent androgen(same ar binding to tren)

YET no plate closure​

 

[DNRChampion]

If anyone can justify this retarded concept I'll give them 50usd

There's been way too much stupid low iq fear mongering about this, Eviscerate me if I don't give the 50usd I'm that confident

THERE IS NO GROWTH PLATE FUSION THROUGH THE USE OF ANDROGENS OR ANY ANDROGEN RECEPTOR SIGNALLING. EVERYTHING IS THROUGH ESTROGEN.

WHOEVER IS WILLING TO DISAGREE WITH THIS LETS TALK ABOUT IT BEFORE I LEAVE THE SITE AGAIN.

I understand where your coming from and your right BUT it’s depends on the situation with your body and what you take but if your estrogen sky rockets your plates will close earlier than usual

 

[Niebvll]

what g

My point is you said natty test isnt enough to close plates, but natty estrogen which leads growth plate senescence, comes from aromatised natty test
So it sort of is enough

 

[Niebvll]

I understand where your coming from and your right BUT it’s depends on the situation with your body and what you take but if your estrogen sky rockets your plates will close earlier than usual

Yeah and his point still stands, it all comes down to the estrogen

 

[fraudster#1]

once again he has normal physiological levels of androgens, testosterone is not as potent as trenbolone or nandrolone deca

nandrolone have the same androgenic binding as test btw
anyways. why DHT, a strong AR agonist,who don't aromatize, didn't affected bone age?

 

[AtrophicPyra]

They don't have to be identical compounds. They all bind to ar. This is a universal ar pathway lol

???bro different androgens express different genes and overall r just different

difference in potency
difference in binding

a testosterone derivative which is bioidenticial to dht is halotestin, halotestin has no buisness in growing ur muscles and is used to stimulaye the cns before a big lift, it also guarantees norwood 5, why? bec it expresses diff genes at more potent levels that nandrolone for example wouldnt even reach

same goes for cartilage and bone and every other part of the body androgens all express each part uniquely from each other

why does tren cause hairloss in some people but not high dose testosterone with dutasteride? because its potent at expressing certain genes, even towards growthplates, it can express maturation genes more strongly than testosterone ever will

 

[Kojo]

Where did you clarify this?

I will definitely not read the whole thread before replying

I've clarified this previously in my stance against androgens. i've also clarified this on this exact thread.

No
Not true
Thats all I said

Context clues is a thing, fusion relative to the hormonal axis, everything is estrogen.

Claims to know about telomere shortening
Doesnt know the resulting senescence process is called proliferation-induced/replicative senescence

You severely lack the capability to interpret implications, or it could be me not being clear enough

The proliferation of something in general just means it's division. I gave 2 kinds of applications for what you could mean by "proliferative fusion". "unless you're trying to articulate resting zone cell symmetrical division into the proliferative zone which is an anomaly."

This explanation is the hayflick limit/telomere shortening which does eventually happen, but takes a longer time to happen in conditions where e2 isn't prevalent as e2 directly decreases the hayflick limit capacity. This is exactly why the growth window is relatively restricted to adolescence. I said this on this exact thread lol

The other proliferation where I said it doesn't exist was me talking about proliferative cells specifically in the resting zone, not the proliferation of reservoir chondrocytes which is where the hayflick limit --> fusion idea links.

 

[AtrophicPyra]

nandrolone have the same androgenic binding as test btw
anyways. why DHT, a potent androgen,who don't aromatize, didn't affected bone age
View attachment 5467368

lmao dht does jackshit to bone and cartilage

one study was 2 twins were born one with no dht one with dht, both grew normally and had normal bmd

one just didnt have a dick

 

[AtrophicPyra]

I've clarified this previously in my stance against androgens. i've also clarified this on this exact thread.

Context clues is a thing, fusion relative to the hormonal axis, everything is estrogen.

You severely lack the capability to interpret implications, or it could be me not being clear enough

The proliferation of something in general just means it's division. I gave 2 kinds of applications for what you could mean by "proliferative fusion". "unless you're trying to articulate resting zone cell symmetrical division into the proliferative zone which is an anomaly."

This explanation is the hayflick limit/telomere shortening which does eventually happen, but takes a longer time to happen in conditions where e2 isn't prevalent as e2 directly decreases the hayflick limit capacity. This is exactly why the growth window is relatively restricted to adolescence. I said this on this exact thread lol

The other proliferation where I said it doesn't exist was me talking about proliferative cells specifically in the resting zone, not the proliferation of reservoir chondrocytes which is where the hayflick limit --> fusion idea links.

dude we ALL agree e2 matures ur gp and closes gp

 

[Kojo]

nandrolone barely aromatizes, i looked into it alot, it aromatises into a weaker form of estrogen not strong enough to cause plate closure, aromatizes 1/5th what test aromatizes

nandrolone barely aromatises relative to test sure, also I'm not sure where you got "weaker form of estrogen" from, it aromatises into e2. Sure at 1/5 what test aromatises, but using anything aromatisable whilst on a height stack with nuked e2 triggers a lot of feedback loops because of the body trying to reach homeostasis.

You could get local sulfation of estrogens within the growth plates that pretty much trap them inactively until they're desulfated and released back into the chondrocytes. Tissue estrogen levels are always much higher than serum due to it's local synthesis like how it works in the gp. It wouldn't matter how much nandrolone "aromatises" as long as it's statistically significant in which it is

 

[Niebvll]

I've clarified this previously in my stance against androgens. i've also clarified this on this exact thread.

But not in OP, you cannot expect me to read through all your replies before answering OP

Context clues is a thing, fusion relative to the hormonal axis, everything is estrogen.

Ok
I will pull the card that this is not my first language

You severely lack the capability to interpret implications, or it could be me not being clear enough


The proliferation of something in general just means it's division. I gave 2 kinds of applications for what you could mean by "proliferative fusion". "unless you're trying to articulate resting zone cell symmetrical division into the proliferative zone which is an anomaly."

Please show me where I mentioned proliferative fusion?
Its 4:30AM but Im fairly sure I never said this
I said proliferation induced senescence and I already explained what it is
You just didnt understand and assumed I mean something completely unrelated

This explanation is the hayflick limit/telomere shortening which does eventually happen, but takes a longer time to happen in conditions where e2 isn't prevalent as e2 directly decreases the hayflick limit capacity. This is exactly why the growth window is relatively restricted to adolescence. I said this on this exact thread lol

And I didnt read the thread are you stupid
I literally said that lol in my earlier post lol?
I read OP and answered OP

The other proliferation where I said it doesn't exist was me talking about proliferative cells specifically in the resting zone, not the proliferation of reservoir chondrocytes which is where the hayflick limit --> fusion idea links.

You said proliferation induced senescence doesnt exist
Yet it does, its just another name for replicative senescence
Takes one google search to confirm what it is

 

[AtrophicPyra]

nandrolone barely aromatises relative to test sure, also I'm not sure where you got "weaker form of estrogen" from, it aromatises into e2. Sure at 1/5 what test aromatises, but using anything aromatisable whilst on a height stack with nuked e2 triggers a lot of feedback loops because of the body trying to reach homeostasis.

You could get local sulfation of estrogens within the growth plates that pretty much trap them inactively until they're desulfated and released back into the chondrocytes. Tissue estrogen levels are always much higher than serum due to it's local synthesis like how it works in the gp. It wouldn't matter how much nandrolone "aromatises" as long as it's statistically significant in which it is

i lowk forgot the form it aromatises in but it aromatises into a weaker form of estrogen and
also a weaker form of dht which i also forgot the name of

either way, tamoxifen is literally a partial er activator and actually slows down gp maturation

 

[Kojo]

???bro different androgens express different genes and overall r just different

difference in potency
difference in binding

a testosterone derivative which is bioidenticial to dht is halotestin, halotestin has no buisness in growing ur muscles and is used to stimulaye the cns before a big lift, it also guarantees norwood 5, why? bec it expresses diff genes at more potent levels that nandrolone for example wouldnt even reach

same goes for cartilage and bone and every other part of the body androgens all express each part uniquely from each other

why does tren cause hairloss in some people but not high dose testosterone with dutasteride? because its potent at expressing certain genes, even towards growthplates, it can express maturation genes more strongly than testosterone ever will

lol? Of course different androgens express different genes with tissue dependance. Didn't say they're equivalent in potency or binding (affinity?)

Halotestins molecular structure is what makes it shit at hypertrophy, hypertrophy isn't the same as activating igf-1 mrna

It expresses different genes because it's molecular structure mimics dht.. (not exhaustively) all androgenic derivatives pretty much guarantee norwood 5

There's no such thing as "androgenic" or "anabolic" effects in growth plate cartilage which is why you're making a shitty equivocation. We just have ar signalling

You're also saying maturation genes (it has none)

Hypertrophic maturation =/= growth plate fusion

 

[Kojo]

lmao dht does jackshit to bone and cartilage

Dht actually mechanistically acts really good on on growth plate cartilage due to a theory I have is that it stimulates the pkc zeta isoform, but not enough evidence released publicly for that theory.

but we do know it leads to the health of the extracellular matrix of cartilage in the growth plates.

doesn't grow you more tho

 

[Kojo]

dude we ALL agree e2 matures ur gp and closes gp

Yes, and androgens do not

zero evidence

 

[AtrophicPyra]

lol? Of course different androgens express different genes with tissue dependance. Didn't say they're equivalent in potency or binding (affinity?)

Halotestins molecular structure is what makes it shit at hypertrophy, hypertrophy isn't the same as activating igf-1 mrna

It expresses different genes because it's molecular structure mimics dht.. (not exhaustively) all androgenic derivatives pretty much guarantee norwood 5

There's no such thing as "androgenic" or "anabolic" effects in growth plate cartilage which is why you're making a shitty equivocation. We just have ar signalling

You're also saying maturation genes (it has none)

Hypertrophic maturation =/= growth plate fusion

dht itself is extremely androgenic and very potent ar agonist, how come it doesnt do shit for bone and cartilage?

oh but apprently when we look at nandrolone and trenbolone studies they say that it made the mammal smaller skeltally than the control group?

why does anavar a DHT DERIVATIVE affect cartillage, when dht itself doesnt! its bec it had been modified to express as little androgenicity and as much anabolic gene expression as possible.

 

[AtrophicPyra]

Dht actually mechanistically acts really good on on growth plate cartilage due to a theory I have is that it stimulates the pkc zeta isoform, but not enough evidence released publicly for that theory.

but we do know it leads to the health of the extracellular matrix of cartilage in the growth plates.

doesn't grow you more tho

i mean they had the same bmd, idk i just wouldnt mess around dht for bone growth shits ass imo for anything involving dimo other than looking like a 55 y.o mexican dad

 

[AtrophicPyra]

Yes, and androgens do not

zero evidence

androgens proven to age bone and promote osteogenesis then that whole mechanism evaporates when it meets cartilage?

how could androgens promote differentiation and maturation genes like runx2 to osteoblasts, but not to cartilage?

yk what ill find you ONE study that proves that androgens WILL decrease fah give me a moment to find it

 

[Kojo]

But not in OP, you cannot expect me to read through all your replies before answering OP

Sure, this can be chalked up to a misunderstanding

Please show me where I mentioned proliferative fusion?
Its 4:30AM but Im fairly sure I never said this
I said proliferation induced senescence and I already explained what it is
You just didnt understand and assumed I mean something completely unrelated

"proliferation induced senescence" as a post to me talking about fusion, would be extension mean proliferation indued fusion.

Also again, I gave you a disjunct between two explanations for the words you've used yet you're saying I just didn't understand? lmao my response literally shows I understood, I said resting zone symmetrical proliferative division (Which is inherently telomere shortening)

You didn't explain what it was prior, you explained what it was after when you said telomere shortening/hayflick limits and THEN I said "well yes outside of those 2 there is no fusion that isn't mediated through e2"

And I didnt read the thread are you stupid
I literally said that lol in my earlier post lol?
I read OP and answered OP

Misunderstanding, I assumed you had read the entire thread and it's replies

You said proliferation induced senescence doesnt exist
Yet it does, its just another name for replicative senescence
Takes one google search to confirm what it is

Proliferation induced senescence does not exist given that we're talking about the proliferative zone of the chondrocytes. No, proliferation doesn't lead to senescence.

Proliferation symmetrically of the resting zone is what you're talking about.

If you had just listened to my clarifications/questions there'd be no confusion l o l

 

[Kojo]

i lowk forgot the form it aromatises in but it aromatises into a weaker form of estrogen and
also a weaker form of dht which i also forgot the name of

either way, tamoxifen is literally a partial er activator and actually slows down gp maturation

there's not enough evidence on tamox for slowing down gp maturation, also it activates era-af1 not 2 lol

there's 3 estrogens, e1 2 and 3. All of which can be converted into estradiol through dehydrogenase lmfao

 

[AtrophicPyra]

Yes, and androgens do not

zero evidence

https://www.sciencedirect.com/science/article/abs/pii/S0022347671802044

9 yr olds with very normal bone age, low igf1 probably didnt begin puberty yet all having lower fah? wonder why? maybe becuase the lack of igf1 failed to keep up with the maturation genes the anavar put up? instead of an increase in height velocity and maybe just speedrunning to the same fah u were always supposed to have, they had a negative fah

 

[Kojo]

androgens proven to age bone and promote osteogenesis then that whole mechanism evaporates when it meets cartilage?

There we go, ya getting there. You're losing the ai slop and you're actually being educated now.

Yes, tissues act completely different from each other, this is endocrinology 101, for example tamoxifen mimics estrogen in bone yet in cartilage it antagonises it via the receptor.

In joint tissues, androgen signalling can induce oxidative stress onto those chondrocytes yet this doesn't happen in the growth plates.

 

[Kojo]

how could androgens promote differentiation and maturation genes like runx2 to osteoblasts, but not to cartilage?

Different tissues act differently with different binding. Takes 85 iq to understand this concept, i mean it seems intuitive.

 

[AtrophicPyra]

there's not enough evidence on tamox for slowing down gp maturation, also it activates era-af1 not 2 lol

there's 3 estrogens, e1 2 and 3. All of which can be converted into estradiol through dehydrogenase lmfao

tamoxifen literally had a whole study conclusion done on how it slowed gp maturation fym nigga

once again i dont remember which one it converted to

 

[AtrophicPyra]

There we go, ya getting there. You're losing the ai slop and you're actually being educated now.

Yes, tissues act completely different from each other, this is endocrinology 101, for example tamoxifen mimics estrogen in bone yet in cartilage it antagonises it via the receptor.

In joint tissues, androgen signalling can induce oxidative stress onto those chondrocytes yet this doesn't happen in the growth plates.

no ai slop involved, aparently runx2 is inhibited through androgens

tamoxifen expresses estrogens gene expression partially thats why it had an affect on bone and indirectly on cartilage

kind of how tren is anticatabolic due to receptor competition, thats also why tamoxifen is slowing gp maturation except its via estrogen mediated gene experession where tamoxifen binds to the er instead of the estrogen

respond to the study i sent?

 

[Niebvll]

Sure, this can be chalked up to a misunderstanding

"proliferation induced senescence" as a post to me talking about fusion, would be extension mean proliferation indued fusion.

No it wouldnt
It means what its name is, by extension it contributes to fusion

Also again, I gave you a disjunct between two explanations for the words you've used yet you're saying I just didn't understand? lmao my response literally shows I understood, I said resting zone symmetrical proliferative division (Which is inherently telomere shortening)

It isnt telomere shortening, it just involves telomere shortening
The division itself is much more
And the proliferation induced senescence again is not telomere shortening or cell division, its the result of such
So you maybe didnt didnt understand, but atleast did misunderstand

You didn't explain what it was prior, you explained what it was after when you said telomere shortening/hayflick limits and THEN I said "well yes outside of those 2 there is no fusion that isn't mediated through e2"

I already explained what it was when mentioning the telomere shortening, I thought it wouldve been obvious that the senescence by cell division refers is the product of telomere shortening
The context maybe didnt make it as obvious as I thought

Proliferation symmetrically of the resting zone is what you're talking about.

No its not
Thats just rz depletion in a nutshell?? Not talking about the depletion
But whatever 5am i will probs sleep

 

[AtrophicPyra]

Different tissues act differently with different binding. Takes 85 iq to understand this concept, i mean it seems intuitive.

dude cartilage have androgen receptors too, they have both been proven to express the same runx2 maturation gene

 

[Kojo]

https://www.sciencedirect.com/science/article/abs/pii/S0022347671802044

9 yr olds with very normal bone age, low igf1 probably didnt begin puberty yet all having lower fah? wonder why? maybe becuase the lack of igf1 failed to keep up with the maturation genes the anavar put up? instead of an increase in height velocity and maybe just speedrunning to the same fah u were always supposed to have, they had a negative fah

"When oxandrolone medication was given to children whose bone age was at least 9 years, there was no evidence of a deleterious effect on predicted mature height."

Only 8 cohorts had a decrease in predicted adult height, out of 27.

study only measures predicted adult height not fah

Not enough of the study is available

 

[Kojo]

dude cartilage have androgen receptors too, they have both been proven to express the same runx2 maturation gene

I didn't say growth plate cartilage doesn't have androgen receptors, I've quite legitimately been saying the opposite.

Runx2 is a maturation gene for proliferative zone cells to mature into hypertrophic ones.

This process doesn't fuse plates, we wont over this before.

Also, no evidence ar signalling upregulates runx2, waiting for this

 

[AtrophicPyra]

I didn't say growth plate cartilage doesn't have androgen receptors, I've quite legitimately been saying the opposite.

Runx2 is a maturation gene for proliferative zone cells to mature into hypertrophic ones.

This process doesn't fuse plates, we wont over this before.

Also, no evidence ar signalling upregulates runx2, waiting for this

ok, when u deplete the proliferative zone mature it and push it strongly into hypertrophic cells, you are not letting the proliferative resting zone cells proliferate into their maximum capability, once they start hypertrophy, the growth has been hard set and u cannot alter it further aka the starting of plate closure

tons of evidence of ar signalling upregulating runx2, for instance the known mechanism of differentiation of osteoblats or osteogenesis

also respond to the study i have replied with

 

[AtrophicPyra]

"When oxandrolone medication was given to children whose bone age was at least 9 years, there was no evidence of a deleterious effect on predicted mature height."

Only 8 cohorts had a decrease in predicted adult height, out of 27.

study only measures predicted adult height not fah

Not enough of the study is available

pah is very good at predicting the fah, also look at the age group of the ppl who had a negative pah

7.5cm is pretty steep if u ask me and honestly i can probably link a thread i made wayyy more direct than this one give me a moment

 

[AtrophicPyra]

I didn't say growth plate cartilage doesn't have androgen receptors, I've quite legitimately been saying the opposite.

Runx2 is a maturation gene for proliferative zone cells to mature into hypertrophic ones.

This process doesn't fuse plates, we wont over this before.

Also, no evidence ar signalling upregulates runx2, waiting for this

The Effects of Trenbolone Supplementation on The Extremity Bones in Running Rats

Turkish Journal of Sport and Exercise | Volume: 21 Issue: 2

dergipark.org.tr

found one of the studies through one of my replies a few months ago with smth arguing the same exact thing

 

[Kojo]

No it wouldnt
It means what its name is, by extension it contributes to fusion

Just said this

No it wouldnt
It means what its name is, by extension it contributes to fusion

It isnt telomere shortening, it just involves telomere shortening
The division itself is much more
And the proliferation induced senescence again is not telomere shortening or cell division, its the result of such
So you maybe didnt didnt understand, but atleast did misunderstand

Sure, you're just being hyperspecific about it. Yes telomere shortening is a "result" of the division. I clump anything that is a direct result of something. This is like trying to say i'm wrong because I say "E2 closes plates" but really and truly it's e2 binding to era-af2 then triggering downstream genes like cxxc5-dvl and saying "well it's cxxc5 dvl that closes plates, not e2, cxxc5 dvl is just a RESULT of e2"

I hope you understand what I'm saying

No its not
Thats just rz depletion in a nutshell?? Not talking about the depletion
But whatever 5am i will probs sleep

rz depletion leads to reaching the hayflick limit through the fact that when resting zone cells divide, they're losing their telomere length individually for division. It's all intertwined.

Moral of this entire thing is yes things like telomere length/hayflick limit/rz depletion are always going to be naturally occuring things, however this is sped up through e2. You're not gonna fuse in your teens like how you usually do without e2 is the point of why I exclude these factors.

Same reason cyp19a1 men grow in their 30s