I wanna take tren but im worried it could stunt my height

[Trerot]

Anyone have any experience with ts?

 

[krads]

dont take it, it will stunt your growth

 

[deaflty0323]

dont take it, it will stunt your growth

Do u know how it stunts it doesnt aromatise, so how. Is it just maturing bone age?

 

[AtrophicPyra]

Do u know how it stunts it doesnt aromatise, so how. Is it just maturing bone age?

overexpresses maturation genes such as runx2 which had been proven to push early proliferating chrondrocytes into hypertrophy and deplete the rz chrondrocytes

if u took smth like teriparatide with it, it could negate some of the rz depletion

 

[deaflty0323]

overexpresses maturation genes such as runx2 which had been proven to push early proliferating chrondrocytes into hypertrophy and deplete the rz chrondrocytes

if u took smth like teriparatide with it, it could negate some of the rz depletion

Would aboloperatide work?

 

[AtrophicPyra]

Would aboloperatide work?

yeah, if you want to hear the other side on why it may actually produce a positive fah or lead u with the same fah u can talk to @Kojo

 

[Trerot]

yeah, if you want to hear the other side on why it may actually produce a positive fah or lead u with the same fah u can talk to @Kojo

Whos that?

 

[AtrophicPyra]

Whos that?

a guy im debating whether or not androgens can make u lose out on some fah

 

[Kojo]

Would aboloperatide work?

Don't listen to things you hear on the internet, anyone that says something without citing the literature they get it from just ignore them.

 

[Kojo]

overexpresses maturation genes such as runx2 which had been proven to push early proliferating chrondrocytes into hypertrophy and deplete the rz chrondrocytes

No evidence for this claim, but **especially** the latter half about depleting the resting zone. Just a shitty understanding of growth plate histology and physiology

There's 3 different kinds of differentiation, AR signalling intracellularly promotes asymmetrical division, not proliferative symmetrical division. Zero evidence. Proliferation =/= proliferative symmetrical division, just clarifying that before you get this mixed up. Promote proliferation doesnt inherently mean promoting symmetrical proliferation of RZ recruitment.

if u took smth like teriparatide with it, it could negate some of the rz depletion

pth analogs do not fix this issue at all either, especially teriparatide. Teriparatide is a pth analog not a pthrp analog. It'll do nothing revolving chondrocytes or acting as a pthrp brake on differentiation.

Abaloparatide has more mechanistic backing because it's a pth analog that's supposed to act like pthrp, HOWEVER it's still inefficient at fully acting as pthrp because it detaches from it's binding site quicker than endogenous pthrp does.

Androgen signalling is good for acting as a brake on resting zone recruitment and resting zone expansion because it upregulates sox9, which upregulates ihh, which then upregulates pthrp activity as ihh acts on an axis with pthrp similar to other axis' like gh/igf-1 for example. pthrp influences the expansion of the resting zone and the breaking of those cells from dividing away.

 

[cowmuncher26]

Don't listen to things you hear on the internet, anyone that says something without citing the literature they get it from just ignore them.

Yo what do you think of this stack?:

0/30mg test pw
200mg tren pw
100 mast pw
10 winny eod (pwo) first half cycle
25 adrol eod (pwo) 2nd half cycle
erda 4mg ed cycled 2w on 2w off

 

[Kojo]

Yo what do you think of this stack?:

0/30mg test pw
200mg tren pw
100 mast pw
10 winny eod (pwo) first half cycle
25 adrol eod (pwo) 2nd half cycle
erda 4mg ed cycled 2w on 2w off

Sure it's good, no gh?

 

[Kojo]

Anyone have any experience with ts?

There's zero evidence trenbolone stunts final adult height.

 

[sub5skinnybum]

Anyone have any experience with ts?

fuck it bro take hgh and there you go

 

[AtrophicPyra]

Don't listen to things you hear on the internet, anyone that says something without citing the literature they get it from just ignore them.

oh yeah?

cite me proof androgens inhibit runx2
cite me proof androgens dont affect fah in adolescence (suprisingly didnt send me a single study btw)
cite me proof that androgens supposedly have no affect on your growth plate
cite me a study showing every gene expression you claim is expressed when a chrondrocyte meets an androgen receptor

you havent shown me anything either

 

[cowmuncher26]

Sure it's good, no gh?

If I had the money I would've

I might add some ghs/ghrps

ex. cjc no dac 300mg ed
ghrp2 150mg am pm ed
pyridostigmine before them

 

[AtrophicPyra]

No evidence for this claim, but **especially** the latter half about depleting the resting zone. Just a shitty understanding of growth plate histology and physiology

There's 3 different kinds of differentiation, AR signalling intracellularly promotes asymmetrical division, not proliferative symmetrical division. Zero evidence. Proliferation =/= proliferative symmetrical division, just clarifying that before you get this mixed up. Promote proliferation doesnt inherently mean promoting symmetrical proliferation of RZ recruitment.

pth analogs do not fix this issue at all either, especially teriparatide. Teriparatide is a pth analog not a pthrp analog. It'll do nothing revolving chondrocytes or acting as a pthrp brake on differentiation.

Abaloparatide has more mechanistic backing because it's a pth analog that's supposed to act like pthrp, HOWEVER it's still inefficient at fully acting as pthrp because it detaches from it's binding site quicker than endogenous pthrp does.

Androgen signalling is good for acting as a brake on resting zone recruitment and resting zone expansion because it upregulates sox9, which upregulates ihh, which then upregulates pthrp activity as ihh acts on an axis with pthrp similar to other axis' like gh/igf-1 for example. pthrp influences the expansion of the resting zone and the breaking of those cells from dividing away.

show me a few studies backing everything you just said up

ofc androgens promote both differentiation and proliferative gene expression, however they are more potent at promoting differentiation genes such as runx2 hence the matured bone age u see on ppl on androgens

also your completely wrong on pthrp analogs, it negates rz chrondrocyte depletion from androgens

androgens are notably efficient at depleting rz chrondrocytes bro rz recruitment?

 

[AtrophicPyra]

pthrp influences the expansion of the resting zone and the breaking of those cells from dividing away.

got one thing right, restores rz chrondrocytes and premature cell terminal sensence if u didnt know

 

[Kojo]

oh yeah?

cite me proof androgens inhibit runx2
cite me proof androgens dont affect fah in adolescence (suprisingly didnt send me a single study btw)
cite me proof that androgens supposedly have no affect on your growth plate
cite me a study showing every gene expression you claim is expressed when a chrondrocyte meets an androgen receptor

you havent shown me anything either

1. Your response is a tu quoque further proving your inability to black up any outlandish physiological claims you've made.

2. You didn't ask, ask and I'll surely provide with ease.

3. The specific claims "androgens don't affect fah in adolescence" is a negative claim, it's a claim by the assertion not the negation. Your claim is that they do, if there isn't evidence, they don't and we cannot say that they do. Also your own study says that oxandrolone doesn't have any affect on fah in any of those kids.

Bet ya ignored that though when I pointed that out to you, lolll

 

[AtrophicPyra]

1. Your response is a tu quoque further proving your inability to black up any outlandish physiological claims you've made.

2. You didn't ask, ask and I'll surely provide with ease.

3. The specific claims "androgens don't affect fah in adolescence" is a negative claim, it's a claim by the assertion not the negation. Your claim is that they do, if there isn't evidence, they don't and we cannot say that they do. Also your own study says that oxandrolone doesn't have any affect on fah in any of those kids.

Bet ya ignored that though when I pointed that out to you, lolll

??? bro ur the one that pinged me

my study showed a negative 7.5cm pah

also fda says on their site that oxandrolone shortens fah in growing kids, literally LOOK at the offical site

showed a study where rodents had signifcantly short enough femurs that it was included in the conclusion

pretty sure i showed another depicting the same outcome as the other rodent study too

craziest part about this all is that you cant find me ONE not EVEN ONE study of a child who is iss (not turner syndrome, that doesnt apply to us), (solely iss, that has had an improved fah due to aas) u cant find one bec it doesnt exist

you know why it doesnt exist? BECAUSE IM RIGHT

 

[Kojo]

oh yeah?

cite me proof androgens inhibit runx2
cite me proof androgens dont affect fah in adolescence (suprisingly didnt send me a single study btw)
cite me proof that androgens supposedly have no affect on your growth plate
cite me a study showing every gene expression you claim is expressed when a chrondrocyte meets an androgen receptor

you havent shown me anything either

https://pmc.ncbi.nlm.nih.gov/articles/PMC2718746/

Here's an example of runx2 actually being inhibited by ar signalling, though in osteogenic activity and prostate activity.

https://scholarlypublications.universiteitleiden.nl/access/item%3A2891711/view

This piece of literature talks about how the chondrocytes share identical genomic mapping as osteoblasts meaning it would function the same way in this tissue.

Your own study of oxandrolone already proves it has no effect on height, same with your tren study. The Tren+Exercise group was actually the tallest group in your study.

https://pmc.ncbi.nlm.nih.gov/articles/PMC8325743/ AR signalling and sox9

https://pmc.ncbi.nlm.nih.gov/articles/PMC2770942/ sox9 and pthrp

 

[Kojo]

show me a few studies backing everything you just said up

ofc androgens promote both differentiation and proliferative gene expression, however they are more potent at promoting differentiation genes such as runx2 hence the matured bone age u see on ppl on androgens

also your completely wrong on pthrp analogs, it negates rz chrondrocyte depletion from androgens

androgens are notably efficient at depleting rz chrondrocytes bro rz recruitment?

Still zero evidence of runx2

Jesus christ I really have to educate you like this? You're really showing your lack of knowledge here lol

"pthrp analogs" You mean pth analogs? There's only one pth analogs that's structurally modified to mimic pthrp and that's abaloparatide, teriparatide is just a pth analog.

Abaloparatide still doesn't function equivalently to native pthrp, it detaches from it's binding site too fast. I've already said before pthrp natively, slows down differentiation through expansion

"androgens are notably efficient at depleting rz chrondrocytes bro rz recruitment?" Clearly ignored everything I said about rz recruitment. Dude just admit you don't know a single fucking thing about this entire topic. You're so lost in the sauce it's insane, Rz recruitment depends on 3 aforementioned factors that you're ignoring.

If it is the case that androgens deploy rz recruitment, Which kind of rz differentiation are we talking about? Symmetrical expansion? Symmetrical proliferation? or asymmetrical division? if it's asymmetrical recruitment your rz literally does not get depleted, it gets maintained.

 

[Kojo]

got one thing right, restores rz chrondrocytes and premature cell terminal sensence if u didnt know

lol??? You're saying things I said like almost 2 days ago now I already knew pthrp negates both of these things, I have debates of me saying the exact same shit I'm saying to you to another shithead that believes in androgen induced fusion and he conceded

Rz restoration is called symmetrical expansion of the resting zone. I've explained this but of course you don't know anything about the physiology of this stuff ig

 

[mulattoviking]

Tren made me grow from 5'3 to 5'4.75 in a year. Just turned 48.

 

[AtrophicPyra]

Still zero evidence of runx2

Jesus christ I really have to educate you like this? You're really showing your lack of knowledge here lol

"pthrp analogs" You mean pth analogs? There's only one pth analogs that's structurally modified to mimic pthrp and that's abaloparatide, teriparatide is just a pth analog.

Abaloparatide still doesn't function equivalently to native pthrp, it detaches from it's binding site too fast. I've already said before pthrp natively, slows down differentiation through expansion

"androgens are notably efficient at depleting rz chrondrocytes bro rz recruitment?" Clearly ignored everything I said about rz recruitment. Dude just admit you don't know a single fucking thing about this entire topic. You're so lost in the sauce it's insane, Rz recruitment depends on 3 aforementioned factors that you're ignoring.

If it is the case that androgens deploy rz recruitment, Which kind of rz differentiation are we talking about? Symmetrical expansion? Symmetrical proliferation? or asymmetrical division? if it's asymmetrical recruitment your rz literally does not get depleted, it gets maintained.

i would look more into that however heres the thing

there is almost no point into looking this deep whether or not androgens negatively or positively affect fah

we have complete evidence it WILL fuck up your fah, i even made more threads abt nicher studies showing how trenbolone in various animals and nandrolone made them skeletally smaller in the conclusions

ill debate more abt the differentiation shit and the rz depletion tmrw bec i dont wanna spend all night explaining and finding the specific 2-3 studies showing androgens express runx2 on chrondrocytes just for you to completely ignore them


pthrp analogs as in abaloparatide

 

[Kojo]

show me a few studies backing everything you just said up

Sure? This is all water knowledge btw so I hope you're satire by calling what I'm saying into question..

Abalo -- https://pmc.ncbi.nlm.nih.gov/articles/PMC5119706/

Also abalo is water, I mean it literally isn't identical to pthrp so idk how you concluded that they function the same. It's just a synthetic version with only the first 34 amino acids, and only the first 22 are identical to pthrp. 12 of them aren't even identical let alone the entire structure

Symmetrical division -- https://pubmed.ncbi.nlm.nih.gov/30814736/

Asymmetrical division -- https://www.bioedonline.org/news/na...iscovered-stem-cell-that-keeps-bones-growing/

anything else?

 

[AtrophicPyra]

Sure? This is all water knowledge btw so I hope you're satire by calling what I'm saying into question..

Abalo -- https://pmc.ncbi.nlm.nih.gov/articles/PMC5119706/

Also abalo is water, I mean it literally isn't identical to pthrp so idk how you concluded that they function the same. It's just a synthetic version with only the first 34 amino acids, and only the first 22 are identical to pthrp. 12 of them aren't even identical let alone the entire structure

Symmetrical division -- https://pubmed.ncbi.nlm.nih.gov/30814736/

Asymmetrical division -- https://www.bioedonline.org/news/na...iscovered-stem-cell-that-keeps-bones-growing/

anything else?

bro

studies abt the literal topic we r arguing abt

studies of ppl growing with a POSITIVE fah

because if we r using pharma, the last thing we want is an increase in growth velocity just to ultimately reach the same fah, we want as much time to optimize growth as possible, so the only way to support ur claim that androgens will positively affect ur gp, it has to be an actual increase in fah

-rat studies can do too

 

[Kojo]

??? bro ur the one that pinged me

my study showed a negative 7.5cm pah

also fda says on their site that oxandrolone shortens fah in growing kids, literally LOOK at the offical site

showed a study where rodents had signifcantly short enough femurs that it was included in the conclusion

pretty sure i showed another depicting the same outcome as the other rodent study too

craziest part about this all is that you cant find me ONE not EVEN ONE study of a child who is iss (not turner syndrome, that doesnt apply to us), (solely iss, that has had an improved fah due to aas) u cant find one bec it doesnt exist

you know why it doesnt exist? BECAUSE IM RIGHT

I never said aas improve fah.. That would be a strawman

Firstly, you sent one singular study this entire 2-day debate, your own study says it didn't effect the fah of any children on oxandrolone. Your rodent study was on trenbolone, I've debunked this many times, you might be the only human on earth that gets debunked, completely ignores it and then continuously repeats their debunked claim. Ridiculous

Your study shows negative pah in 8 children out of 27. . . are we serious? A small minority had a negative pah

"there was no evidence of a deleterious effect on predicted mature height." -- this is your study btw https://www.sciencedirect.com/science/article/abs/pii/S0022347671802044

 

[Kojo]

i would look more into that however heres the thing

there is almost no point into looking this deep whether or not androgens negatively or positively affect fah

we have complete evidence it WILL fuck up your fah, i even made more threads abt nicher studies showing how trenbolone in various animals and nandrolone made them skeletally smaller in the conclusions

ill debate more abt the differentiation shit and the rz depletion tmrw bec i dont wanna spend all night explaining and finding the specific 2-3 studies showing androgens express runx2 on chrondrocytes just for you to completely ignore them


pthrp analogs as in abaloparatide

Just for you to ignore them? LMFAO You're genuinely ragebaiting, everything I've said so far you've completely ignored and I had to repeat it

You'll never win on anything to do with differentiation you'll genuinely get molested, you don't know anything about differentiation or the resting zone. Unless you're willing to learn of course? lmao

You KEEP bringing up this tren study oh my god the study fucking says they're statistically insignificant measurements, stop fucking ignoring this shit dude it's pissing me off now

You have not posted a SINGULAR study except an oxandrolone study that says nothing about the final adult height of the children

A tren study which itself concedes that the outcomes are not statistically significant, and the trenbolone group including exercise was literally the tallest fucking group there, not the control

You ignore everything I say and I'm genuinely tired of this. You're stamina debating, literally just waiting for me to give up lmao

Now you're mentioning roids that literally aromatise

 

[Kojo]

bro

studies abt the literal topic we r arguing abt

studies of ppl growing with a POSITIVE fah

because if we r using pharma, the last thing we want is an increase in growth velocity just to ultimately reach the same fah, we want as much time to optimize growth as possible, so the only way to support ur claim that androgens will positively affect ur gp, it has to be an actual increase in fah

-rat studies can do too

Are you fucking stupid Pyra? I didn't say androgens increase fah

Strawman of doom and despair

 

[AtrophicPyra]

Just for you to ignore them? LMFAO You're genuinely ragebaiting, everything I've said so far you've completely ignored and I had to repeat it

You'll never win on anything to do with differentiation you'll genuinely get molested, you don't know anything about differentiation or the resting zone. Unless you're willing to learn of course? lmao

You KEEP bringing up this tren study oh my god the study fucking says they're statistically insignificant measurements, stop fucking ignoring this shit dude it's pissing me off now

You have not posted a SINGULAR study except an oxandrolone study that says nothing about the final adult height of the children

A tren study which itself concedes that the outcomes are not statistically significant, and the trenbolone group including exercise was literally the tallest fucking group there, not the control

You ignore everything I say and I'm genuinely tired of this. You're stamina debating, literally just waiting for me to give up lmao

Now you're mentioning roids that literally aromatise

on my life if you find ONE study of an iss kid on androgens getting an increase of fah you win the debate

also i said ill argue that differentiation and rz depletion shit tmrw

look at the conclusion of the tren study

 

[AtrophicPyra]

Are you fucking stupid Pyra? I didn't say androgens increase fah

Strawman of doom and despair
View attachment 5472299

are you deadass? okay so what is your claim in this argument, that androgens just increase ur velocity to ur natural fah?

 

[Kojo]

on my life if you find ONE study of an iss kid on androgens getting an increase of fah you win the debate

also i said ill argue that differentiation and rz depletion shit tmrw

look at the conclusion of the tren study

Ah yes see this is what idiots that jump to the conclusion do. READ the study properly, read the measurements, the measurements have a 0.33 difference, the study objectively says the findings were not statistically significant. + IT LITERALLY ONLY MEASURES THE FEMUR??? NOT THE FINAL ADULT HEIGHT??

I didn't fucking say kids on androgens get a fah increase dude holy shit

 

[Kojo]

are you deadass? okay so what is your claim in this argument, that androgens just increase ur velocity to ur natural fah?

??????? The claim is androgens do not reduce your final adult height or fuse your growth plates

 

[Kojo]

are you deadass? okay so what is your claim in this argument, that androgens just increase ur velocity to ur natural fah?

TRENBOLONE + EXERCISE IS LITERALLY TALLER THAN THE CONTROL GROUP??

 

[AtrophicPyra]

I never said aas improve fah.. That would be a strawman

Firstly, you sent one singular study this entire 2-day debate, your own study says it didn't effect the fah of any children on oxandrolone. Your rodent study was on trenbolone, I've debunked this many times, you might be the only human on earth that gets debunked, completely ignores it and then continuously repeats their debunked claim. Ridiculous

Your study shows negative pah in 8 children out of 27. . . are we serious? A small minority had a negative pah

"there was no evidence of a deleterious effect on predicted mature height." -- this is your study btw https://www.sciencedirect.com/science/article/abs/pii/S0022347671802044

nigga why r u ignoring this? doing anything but addressing this?

acting like 8 children is nothing LMAO nigga thats like a 1/4 chance of getting raped by androgens pretty high chances

 

[AtrophicPyra]

View attachment 5472311 TRENBOLONE + EXERCISE IS LITERALLY TALLER THAN THE CONTROL GROUP??View attachment 5472317

bec rats gp grow under tension nothing like humans unless u refer to lsjl

 

[AtrophicPyra]

??????? The claim is androgens do not reduce your final adult height or fuse your growth plates

??? dude androgens COULD reduce your fah, its not gaurenteed it wont

androgens dont fuse your plates the same way estrogen does for ex, estrogen is guarenteed to shorten ur fah, androgens arnt, androgens push chrondrocytes into hypertrophic cells and deplete the rz SYMMETRICALLY causing a boost in velocity usually parallel to maturation, unless its potent enough to overexpress maturation genes such as runx2



ill find the runx2 studdy tmrw

 

[Kojo]

View attachment 5472312
nigga why r u ignoring this? doing anything but addressing this?

acting like 8 children is nothing LMAO nigga thats like a 1/4 chance of getting raped by androgens pretty high chances

How am I ignoring this?????? the conclusion literally says "there was no evidence of a deleterious effect on predicted mature height" on kids that were 9?? You do know the pah and height velocity of the other kids literally increased drastically right?? by your logic oxandrolone increases fah because pah increased. Pah is fucking irrelevant when using pharma because of it's easy HSDS alterations.

This literally goes to my theory that it's estrogen that is causing the deleterious pah because 9 year olds do not get these deleterious effects, meanwhile a small amount of older children do because their hormonal levels are shifting

Your own tren study LITERALLY says Group T was numerically higher than the other groups in ALL aspects of the study. The study still says it's insignificant

 

[Kojo]

bec rats gp grow under tension nothing like humans unless u refer to lsjl

It still says group T is the tallest overall in the conclusion.

It STILL says the findings comparatively are NOT statistically insignificant. they may as well be the same length.

They LITERALLY measure bones and not the full adult height

 

[AtrophicPyra]

How am I ignoring this?????? the conclusion literally says "there was no evidence of a deleterious effect on predicted mature height" on kids that were 9?? You do know the pah and height velocity of the other kids literally increased drastically right?? by your logic oxandrolone increases fah because pah increased. Pah is fucking irrelevant when using pharma because of it's easy HSDS alterations.

This literally goes to my theory that it's estrogen that is causing the deleterious pah because 9 year olds do not get these deleterious effects, meanwhile a small amount of older children do because their hormonal levels are shifting

View attachment 5472326
Your own tren study LITERALLY says Group T was numerically higher than the other groups in ALL aspects of the study. The study still says it's insignificant

your reading the study wrong 8 kids had a shitty fah

9 year olds r a whole diff category

It still says group T is the tallest overall in the conclusion.

It STILL says the findings comparatively are NOT statistically insignificant. they may as well be the same length.

They LITERALLY measure bones and not the full adult height

okay, well that wouldnt even make sense in humans, that whole study is dogshit imo which is why im referring to a study done ON HUMANS taking androgens when they r children now

 

[Kojo]

??? dude androgens COULD reduce your fah, its not gaurenteed it wont

Through which mechanism?????

??? dude androgens COULD reduce your fah, its not gaurenteed it wont

androgens dont fuse your plates the same way estrogen does for ex, estrogen is guarenteed to shorten ur fah, androgens arnt, androgens push chrondrocytes into hypertrophic cells and deplete the rz SYMMETRICALLY causing a boost in velocity usually parallel to maturation, unless its potent enough to overexpress maturation genes such as runx2

LMFAOOO There's literally ZERO evidence of this velocity boosts do not equate to resting zone depletion. Zero evidence

Hypertrophic cells =/= growth plate fusion. You still have a shit retarded comprehension of growth plate physiology. Go back to the drawing board

Deplete the rz symmetrically? There's zero evidence of this in the literature at all btw

I LITERALLY showed you the evidence that runx2 is inhibited by ar signalling..

Runx2 does not fuse plates, you pulled this idea out of your anal cavity

 

[AtrophicPyra]

Through which mechanism?????

LMFAOOO There's literally ZERO evidence of this velocity boosts do not equate to resting zone depletion. Zero evidence

Hypertrophic cells =/= growth plate fusion. You still have a shit retarded comprehension of growth plate physiology. Go back to the drawing board

Deplete the rz symmetrically? There's zero evidence of this in the literature at all btw

I LITERALLY showed you the evidence that runx2 is inhibited by ar signalling..

Runx2 does not fuse plates, you pulled this idea out of your anal cavity

through prematurely causing chrondrocytes to hypertrophy before fully proliferating, once cells start turning hypertrophic, it is only a matter of time before you reach your hardset fah, its practically plate closure bec ur not growing anymore eventually will reach terminal sensence and it will all be over

there is evidence of this in literature same with runx2 wait till tmrw or find the studies urself

also no u didnt show proof runx2 is inhibited by ar signalling its the complete opposite

runx2 doesnt fuse plates your right it was a vague explanation though

 

[Kojo]

your reading the study wrong 8 kids had a shitty fah

9 year olds r a whole diff category

But that's the point, 9 year olds have lower e2 which changes the reasoning behind the phenomenon

 

[AtrophicPyra]

But that's the point, 9 year olds have lower e2 which changes the reasoning behind the phenomenon

dude when ur on anavar u have less test and less free test esp on the higher doses like 0.2mg/kg/w

they would alr be in a low e2 environment

plus how the FUCK would anavar promote estrogen plate closure

 

[Kojo]

through prematurely causing chrondrocytes to hypertrophy before fully proliferating, once cells start turning hypertrophic, it is only a matter of time before you reach your hardset fah, its practically plate closure bec ur not growing anymore eventually will reach terminal sensence and it will all be over

there is evidence of this in literature same with runx2 wait till tmrw or find the studies urself

also no u didnt show proof runx2 is inhibited by ar signalling its the complete opposite

runx2 doesnt fuse plates your right it was a vague explanation though

Dude I've been trying to hammer this concept into you for months I don't know why you can't get it.

Lets say you did have premature maturation into hypertrophy, given that you have no estrogen, you already have enough time before you reach any hayflick limit, this is seen with estrogen deficiencies, they literally grow in their late 20s even tho naturally that's impossible.

This is because without estrogen the hayflick limit is damn near indefinite. Even if you was "losing out" on proliferation which is pretty much all your argument is coming down to, terminal senescence in the hypertrophic phase does NOT mean you can't grow anymore. it literally just means those specific chondrocytes can't proliferate anymore yes

The resting zone will just divide asymmetrically, and provide you with more chondrocytes.

But there is no evidence of anything that causes premature hypertrophy because there's pretty much almost no compound u can use that upregulates runx2

You do know the inhibition of runx2 is bad right? because you NEED runx2 to grow, Research

Cleidocranial dysplasia​

 

[Kojo]

through prematurely causing chrondrocytes to hypertrophy before fully proliferating, once cells start turning hypertrophic, it is only a matter of time before you reach your hardset fah, its practically plate closure bec ur not growing anymore eventually will reach terminal sensence and it will all be over

there is evidence of this in literature same with runx2 wait till tmrw or find the studies urself

also no u didnt show proof runx2 is inhibited by ar signalling its the complete opposite

runx2 doesnt fuse plates your right it was a vague explanation though

i literally showed you the proof? are we on the same forum?

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

I also then showed you the literature that shows runx2 and ar are identical in the growth plate as they are in osteoblasts which shows there would be no tissue distinctions

 

[AtrophicPyra]

Dude I've been trying to hammer this concept into you for months I don't know why you can't get it.

Lets say you did have premature maturation into hypertrophy, given that you have no estrogen, you already have enough time before you reach any hayflick limit, this is seen with estrogen deficiencies, they literally grow in their late 20s even tho naturally that's impossible.

This is because without estrogen the hayflick limit is damn near indefinite. Even if you was "losing out" on proliferation which is pretty much all your argument is coming down to, terminal senescence in the hypertrophic phase does NOT mean you can't grow anymore. it literally just means those specific chondrocytes can't proliferate anymore yes

The resting zone will just divide asymmetrically, and provide you with more chondrocytes.

But there is no evidence of anything that causes premature hypertrophy because there's pretty much almost no compound u can use that upregulates runx2

You do know the inhibition of runx2 is bad right? because you NEED runx2 to grow, Research

Cleidocranial dysplasia​

dude i know u need differentiation and proliferation to grow runx2 is very important

also going back to one of your claims on how you said we can NEVER replicate an aromatase mutation through ai’s, you said yourself its impossible to use ais to completely avoid having indefinite hayflick limit due to that

u also said how e2 would locally upregulate in tissues like the gp in a low systemic e2 environment, so if we used tren no test base, technically your growthplate would close prematurely and cause more bone age maturation than velocity like that anavar study right?

 

[AtrophicPyra]

i literally showed you the proof? are we on the same forum?
View attachment 5472361

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

I also then showed you the literature that shows runx2 and ar are identical in the growth plate as they are in osteoblasts which shows there would be no tissue distinctions

i literally showed you the proof? are we on the same forum?
View attachment 5472361

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

I also then showed you the literature that shows runx2 and ar are identical in the growth plate as they are in osteoblasts which shows there would be no tissue distinctions

im actually fucking crine nigga i cant

woahh runx2 is responsible for differentiation genes on chrondrocytes told you so,

 

[Kojo]

dude when ur on anavar u have less test and less free test esp on the higher doses like 0.2mg/kg/w

they would alr be in a low e2 environment

plus how the FUCK would anavar promote estrogen plate closure

I'll explain tomorrow, I gotta do something