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]

@AtrophicPyra

 

[ascend.exe]

dont take steroids brah, idk what an androgen is but dont take them peptides n sheet

we wuz takin peptides n sheet

 

[chombo]

I cant justify it but hook a brother out with 50 usd

 

[Y̷a̶g̶a̷m̴i̸]

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 see

 

[Kojo]

I cant justify it but hook a brother out with 50 usd

loll

 

[yourtibawis]

Growth plates have androgen receptors

 

[Goy.boy.Hero]

dont take steroids brah, idk what an androgen is but dont take them peptides n sheet

we wuz takin peptides n sheet

Please be satire

 

[Goy.boy.Hero]

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.

A more accurate claim would be: "The overwhelming evidence is that estrogen signaling is the primary driver of epiphyseal (growth plate) fusion. Androgens such as testosterone mainly accelerate fusion after they're converted to estrogen by aromatase. There is little convincing evidence that androgen receptor signaling alone causes growth plate fusion in humans."

 

[Genio]

I remember this one retard telling me that Estrogen wasn't the only main driver of Epiphyseal Closure, and that Tren would cause Epiphyseal closure, just lol at him.

Hope Raffaini or Ratinan or whoever shithead he went give's him the Tufano treatment.
Just purge all the autism off this forum.

 

[Kojo]

Growth plates have androgen receptors

Zero correlation, growth plates have androgen receptors = fusion ig

 

[Kojo]

I remember this one retard telling me that Estrogen wasn't the only main driver of Epiphyseal Closure, and that Tren would cause Epiphyseal closure, just lol at him.

Hope Raffaini or Ratinan or whoever shithead he went give's him the Tufano treatment.
Just purge all the autism off this forum.

They're retards, that tren rat study shows that the height was that same and not statistically significant. There's also another group that did trenbolone + exercise, that group was literally the tallest group in the study. Dnr all the idiots

 

[AtrophicPyra]

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.

your biased to argue with

 

[Kojo]

your biased to argue with

I don't see an argument so far

 

[AtrophicPyra]

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.

studies shown animals growth plates esp rodents who r growing on tren have gotten they growth plates closed earlier than they should have and they were skeletally smaller than control group

we see the same thing in human adolescence taking anavar, one study showed that anavar gave them 7.5cm less on there pah

a specific study showing rodents taking 100mg nandrolone equivalent human doses we’re SIGNIFICANTLY shorter than control studies

i also made tons of other threads of niche studies where androgens closed rodents plates and how that was the studies conclusion

have an open mind abt this stop being biased

 

[AtrophicPyra]

They're retards, that tren rat study shows that the height was that same and not statistically significant. There's also another group that did trenbolone + exercise, that group was literally the tallest group in the study. Dnr all the idiots

fyi androgens express maturation genes hence why they can bias towards differentiation in bone, think a little more clearly abt this

if your growth plates have androgen receptors, and there r countless studies showing androgens made rodents AND kids have a lower fah, what could that conclude to?

“muh it increased velocity and didint decrease fah in some studies“

nice one jackass, you have less time to optimize your growth through advanved pharma now

 

[AtrophicPyra]

I remember this one retard telling me that Estrogen wasn't the only main driver of Epiphyseal Closure, and that Tren would cause Epiphyseal closure, just lol at him.

Hope Raffaini or Ratinan or whoever shithead he went give's him the Tufano treatment.
Just purge all the autism off this forum.

19nors are infamous in most rodent studies to close growth plates earlier or cuase a lower fah ur just not looking deep enough for the studies

dht derivatives HAVE been proven to lower fah, 7.5cm less fah in one study

also more velocity is bad, u have less tome to optimize growth, why would u want that dont be stupid now

 

[Kojo]

fyi androgens express maturation genes hence why they can bias towards differentiation in bone, think a little more clearly abt this

if your growth plates have androgen receptors, and there r countless studies showing androgens made rodents AND kids have a lower fah, what could that conclude to?

“muh it increased velocity and didint decrease fah in some studies“

nice one jackass, you have less time to optimize your growth through advanved pharma now

Bunch of gibberish, what senescence genes does ar signalling express inherently that doesn't involve er activity?

There's no studies showing androgens decrease fah even in rodents. The trenbolone group in your famous rat study was actually the tallest, including exercise.

It also says only the femur bone was bigger, it says nothing about any other bones.

 

[Kojo]

19nors are infamous in most rodent studies to close growth plates earlier or cuase a lower fah ur just not looking deep enough for the studies

dht derivatives HAVE been proven to lower fah, 7.5cm less fah in one study

also more velocity is bad, u have less tome to optimize growth, why would u want that dont be stupid now

Send a study, alongside that send a mechanism by which they mature chondrocytes without e2

 

[Kojo]

fyi androgens express maturation genes hence why they can bias towards differentiation in bone, think a little more clearly abt this

if your growth plates have androgen receptors, and there r countless studies showing androgens made rodents AND kids have a lower fah, what could that conclude to?

“muh it increased velocity and didint decrease fah in some studies“

nice one jackass, you have less time to optimize your growth through advanved pharma now

also bias towards differentiation? lmao this is another trash arg I've come across recently, there's 3 different forms of differentiation, you're making an argument of simplicity without clarifying which differentiation they push.

Asymmetrical
Symmetrical (2 rz cells)
Symmetrical (2 pz cells)

androgens prioritise on expansion and asymmetrical division. Not symmetrical loss.

That would be e2 lol

Also your shitty tren study verbatim clarifies that technically the femur was shorter in the Tren no exercise rodents, but there's no statistical significance. For you boneheads this as a real life example is like saying "this guy is 185.5 and this guy is 185.4" lol

 

[AtrophicPyra]

Send a study, alongside that send a mechanism by which they mature chondrocytes without e2

delepletes resting zone chrondrocytes and pushes those cells into hypertrophy, thats the mechanism in which androgens mature and close the plates early

pushing chrondrocytes into hypertrophy is what makes the velocity get sped up, the depletion of chrondrocytes in the resting zone contributes aswel

however the chrondrocyte getting pushed too early into hypertrophy before completely proliferating multiple times is what creates the shorter fah

 

[Kojo]

delepletes resting zone chrondrocytes and pushes those cells into hypertrophy, thats the mechanism in which androgens mature and close the plates early

Yeah another trash argument I've seen people that know nothing about growth plate histology talk about. Just completely wrong, zero evidence backing this mechanism, it actually does the opposite of resting zone depletion, that's e2's job

pushing chrondrocytes into hypertrophy is what makes the velocity get sped up, the depletion of chrondrocytes in the resting zone contributes aswel

however the chrondrocyte getting pushed too early into hypertrophy before completely proliferating multiple times is what creates the shorter fah

Zero evidence for these 2 interlinked claims too. There's no such thing as premature hypertrophic maturation from androgens when androgens directly stimulate proliferation through mrna upregulation lol

 

[AtrophicPyra]

Bunch of gibberish, what senescence genes does ar signalling express inherently that doesn't involve er activity?

There's no studies showing androgens decrease fah even in rodents. The trenbolone group in your famous rat study was actually the tallest, including exercise.

It also says only the femur bone was bigger, it says nothing about any other bones.

runx2 is the main one, nothing i said was gibberish once again a closed mindset

there r a bunch i dedicated hours looking through even german research sites to find this shit u just didnt look deep enough

saying the femur bone got “bigger” is extremely vague, did it get wider or actually grow in length? androgens WILL grow and lengthen ur growthplates aka the faster velocity, but that doesnt mean it isnt lowering ur fah

 

[AtrophicPyra]

Yeah another trash argument I've seen people that know nothing about growth plate histology talk about. Just completely wrong, zero evidence backing this mechanism, it actually does the opposite of resting zone depletion, that's e2's job

Zero evidence for these 2 interlinked claims too. There's no such thing as premature hypertrophic maturation from androgens when androgens directly stimulate proliferation through mrna upregulation lol

…

r u being deadass? androgens dont prematurely push cells into a hypertrophic stage making it reach terminal sencense faster? u have some learning to do

also you do realize estrogen AND androgens both have maturation genes right? dont be stupid now, a hormone isnt exclusive to a specific set of genes

 

[AtrophicPyra]

Yeah another trash argument I've seen people that know nothing about growth plate histology talk about. Just completely wrong, zero evidence backing this mechanism, it actually does the opposite of resting zone depletion, that's e2's job

Zero evidence for these 2 interlinked claims too. There's no such thing as premature hypertrophic maturation from androgens when androgens directly stimulate proliferation through mrna upregulation lol

androgens indirectly promote igf1r sensitization directly in the growthplate independent of gh production, they do increase proliferation for chrondrocytes u just dont have the full concept right

 

[Kojo]

runx2 is the main one, nothing i said was gibberish once again a closed mindset

lol? what about runx2 causes premature hypertrophic maturation? got any literature on this? Especially with androgens? Because they're Runx2 inhibitors

there r a bunch i dedicated hours looking through even german research sites to find this shit u just didnt look deep enough

Anything but sending the literature

saying the femur bone got “bigger” is extremely vague, did it get wider or actually grow in length? androgens WILL grow and lengthen ur growthplates aka the faster velocity, but that doesnt mean it isnt lowering ur fah

lol? it was femoral length. And I'm referring to YOUR study that you send to say that tren stunts height when only the femur and humerus were measured after tren and control. Zero statistical significance. It also was final adult height of the bones.

 

[Kojo]

…

r u being deadass? androgens dont prematurely push cells into a hypertrophic stage making it reach terminal sencense faster? u have some learning to do

Send the literature

 

[Kojo]

also you do realize estrogen AND androgens both have maturation genes right? dont be stupid now, a hormone isnt exclusive to a specific set of genes

I asked for the maturation genes they possessed? Zero answer

There's also a difference in maturation for hypertrophic zone and resting zone cell senescence which ultimately is what leads to growth plate closure

 

[Kojo]

androgens indirectly promote igf1r sensitization directly in the growthplate independent of gh production, they do increase proliferation for chrondrocytes u just dont have the full concept right

I've already said this

This has nothing to do with premature hypertrophic senescence (Nothing to do with gp fusion, just decreases growth velocity if anything)

Nothing to do with resting zone cell recruitment or senescence

 

[AtrophicPyra]

lol? what about runx2 causes premature hypertrophic maturation? got any literature on this? Especially with androgens? Because they're Runx2 inhibitors

Anything but sending the literature

lol? it was femoral length. And I'm referring to YOUR study that you send to say that tren stunts height when only the femur and humerus were measured after tren and control. Zero statistical significance. It also was final adult height of the bones.

dude there r DIRECT studies proving nandrolone deca decresed fah in rodents at around 100mg human converted doses

also that trenbolone study showed the tren and no excersie group had a shorter femur it was in the conclusions nigga, it was a shitty study imo very poorly done, 99% sure humans dont grow taller when they excerise with androgens

also i dont even wanna keep talking abt that runx2 shit u dont even know what the gene is responsible for no fucking way u said androgens r runx2 inhibitors dont even get me started nigga

 

[AtrophicPyra]

I asked for the maturation genes they possessed? Zero answer

There's also a difference in maturation for hypertrophic zone and resting zone cell senescence which ultimately is what leads to growth plate closure

i literally told u runx2 is the primary maturation gene they possess,

if u push prolifertive cells that havent proliferated to their full capabilites into a hypertrophic stage, its going to shorten ur fah regardless

 

[AtrophicPyra]

I've already said this

This has nothing to do with premature hypertrophic senescence (Nothing to do with gp fusion, just decreases growth velocity if anything)

Nothing to do with resting zone cell recruitment or senescence

?? i was referring to when u said how androgens promote chrondrocyte proliferation, i was pointing out how u had the concept wrong

 

[Niebvll]

Its not estrogen alone

 

[Kojo]

dude there r DIRECT studies proving nandrolone deca decresed fah in rodents at around 100mg human converted doses

Aromatising androgen

also that trenbolone study showed the tren and no excersie group had a shorter femur it was in the conclusions nigga, it was a shitty study imo very poorly done, 99% sure humans dont grow taller when they excerise with androgens

Didn't listen to what I said, trenbolone no exercise was lower, trenbolone with exercise was the highest of them all

Control sat at in the middle

femur isn't fah. Yes it's a shitty study

So send any literature please

also i dont even wanna keep talking abt that runx2 shit u dont even know what the gene is responsible for no fucking way u said androgens r runx2 inhibitors dont even get me started nigga

Aka dodging your burden. Yes androgen receptor signalling in chondrocytes inhibits runx2

 

[Kojo]

Its not estrogen alone

It is, we can debate on it lol

Of course excluding time based eventual apoptosis (Takes years and years to occur)

 

[AtrophicPyra]

Its not estrogen 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

 

[Kojo]

if u push prolifertive cells that havent proliferated to their full capabilites into a hypertrophic stage, its going to shorten ur fah regardless

Zero literature saying this is the case. Waiting for the literature

 

[Kojo]

?? i was referring to when u said how androgens promote chrondrocyte proliferation, i was pointing out how u had the concept wrong

?? What concept did I get wrong?

Androgen receptor signalling locally upregulates igf-1 and mrna expression

I think you're not understanding the distinction in an "androgen" mediated response and what the binding of said (or any) androgen produces downstream of the agonism of the androgen receptor.

 

[AtrophicPyra]

Aromatising androgen

Didn't listen to what I said, trenbolone no exercise was lower, trenbolone with exercise was the highest of them all

Control sat at in the middle

femur isn't fah. Yes it's a shitty study

So send any literature please

Aka dodging your burden. Yes androgen receptor signalling in chondrocytes inhibits runx2

dude im not sooonfeeding u studies go on chatgpt ask to find studies regardling nandrolone deca and rats and growth plates and try and find it, im also not leaking the russian research site i found it on

also androgens strongly express runx2 to chrondrocytes not sure what ur on abt

 

[AtrophicPyra]

?? What concept did I get wrong?

Androgen receptor signalling locally upregulates igf-1 and mrna expression

I think you're not understanding the distinction in an "androgen" mediated response and what the binding of said (or any) androgen produces downstream of the agonism of the androgen receptor.

doesnt do anything to igf1 it directly upregulates the igf1 RECEPTOR big difference

we see this in turner syndrome girls with good gh levels, when taking anavar they grow due to igf1r sensitization

 

[Niebvll]

It is, we can debate on it lol

Look up telomere shortening and hayflick limit
Sure estrogen pushes cells into hypertrophy but its not the reason why all chondrocytes enter senescence

Of course excluding time based eventual apoptosis (Takes years and years to occur)

Proliferation induced senescence

 

[Niebvll]

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

When did I mention anything about hormones?

 

[Kojo]

dude im not sooonfeeding u studies go on chatgpt ask to find studies regardling nandrolone deca and rats and growth plates and try and find it, im also not leaking the russian research site i found it on

also androgens strongly express runx2 to chrondrocytes not sure what ur on abt

"go on chatgpt" Already invalidating what you're saying

Nandrolone Deca is aromatising

No literature for your claims = dnr

Yes, runx2 is inhibited by ar

 

[Kojo]

doesnt do anything to igf1 it directly upregulates the igf1 RECEPTOR big difference

we see this in turner syndrome girls with good gh levels, when taking anavar they grow due to igf1r sensitization

You're not understanding. I know you haven't gotten past the physiology/endocrinology of androgens but that's okay.

So like I will repeat, there is a distinction in androgens and the downstream effects they produce by the receptors they bind to. Androgens bind to Androgen receptors intracellularly, the androgen receptor activation in the cell helps the mrna expression of igf-1 locally.

 

[Kojo]

Look up telomere shortening and hayflick limit
Sure estrogen pushes cells into hypertrophy but its not the reason why all chondrocytes enter senescence

Proliferation induced senescence

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. This process naturally takes **ages** to occur which is why we see in humans with cyp19a1 mutations, they grow to their late 20s with an unfused growth plate

E2 primarily drives the reservoir into senescence which causes eventual gp fusion.

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.

 

[AtrophicPyra]

You're not understanding. I know you haven't gotten past the physiology/endocrinology of androgens but that's okay.

So like I will repeat, there is a distinction in androgens and the downstream effects they produce by the receptors they bind to. Androgens bind to Androgen receptors intracellularly, the androgen receptor activation in the cell helps the mrna expression of igf-1 locally.

dude.. how the FUCK would an androgen make igf1 work “better” ur saying a hormone makes another hormone work better directly because it promotes the mrna expression that sounds pretty stupid considering turner syndrome girls have normal igf1 levels and shitty igf1r sensitivity

 

[Ahmed88]

Debateable

 

[AtrophicPyra]

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

Its not estrogen alone

When did I mention anything about hormones?

 

[AtrophicPyra]

"go on chatgpt" Already invalidating what you're saying

Nandrolone Deca is aromatising

No literature for your claims = dnr

Yes, runx2 is inhibited by ar

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

 

[Kojo]

doesnt do anything to igf1 it directly upregulates the igf1 RECEPTOR big difference

we see this in turner syndrome girls with good gh levels, when taking anavar they grow due to igf1r sensitization

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^