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]

Human physiology has had several revisions in the past decade. I am not going to list them all, but science is always progressing. The biggest scientific breakthroughs are usually ones that were thought to be absolute law/definitive.

You can't name a singular physiological revision that wasn't already theory laden. Yes theories get revised, but objective and fully proven physiological states have NEVER been revised. For example:

It was a theory that testosterone did fuse the plates because they find that more testosterone lead to bone age advancements. However, it was discovered that growth plates actually depend on the aromatase enzyme converting into estrogen. Physiology didn't change it was just discovered. There was only a revision in the thesis (which really only added an extra step)

 

[Milktard]

I didn't say you AREN'T agreeing with me.

It doesn't matter if exogenous testosterone and dianabol are objectively androgens, it isn't a reasonable inference or interpretation to bring up ESTROGEN-INDUCING ANDROGENS because that would literally come under the category of fusion mediated by estrogen.

Context clues, the thread is about fusion mediated by ESTROGEN. There is something called exclusivity, it isn't broad because there's already analytical exclusions. A failure to recognise an analytical exclusion of a category is a failure of fluid reasoning. It is NOT a reasonable interpretation, do not convince yourself that it is.
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You're a pseudo-intellectual, get bitched

You're conflating lexical meaning with analytical categorization, lmfao. Your explicit claim is about the mechanism of GP fusion, not the chemical class of the drug. Are you dense?

Your entire objection depends on ignoring the analytical exclusion and reverting to a purely lexical definition of "androgen"

Your interpretation isn't reasonable; you didn't identify an ambiguity in the mechanism; you ignored the stated scope of this discussion.

You can't name a singular physiological revision that wasn't already theory laden. Yes theories get revised, but objective and fully proven physiological states have NEVER been revised. For example:

It was a theory that testosterone did fuse the plates because they find that more testosterone lead to bone age advancements. However, it was discovered that growth plates actually depend on the aromatase enzyme converting into estrogen. Physiology didn't change it was just discovered. There was only a revision in the thesis (which really only added an extra step)

I already said in my previous comment that this was all irrelevant to this topic; I was stating a fact.

To go on to your example, Exogenous testosterone was observed to accelerate bone age. Later, your research showed that the effect purely depends on aromatization to estradiol. The physiological outcome didn't change. This study is literally irrelevant for healthy individuals with no aromatase deficiency; it is still a good takeaway on why to run an AI on exogenous testosterone.

 

[cadee]

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

He is not saying that like wtf¿? IGF-1 is a 70 aminoacid polypeptide hormone and androgen receptor agonism promotes IGF-1 gene expression

 

[AtrophicPyra]

There's no contradiction, you can have a dual induced mechanism of fusion that's dependent on ONE thing but can influence the other things. AR signalling will put proliferative "stress" onto the chondrocytes to divide, but pairing that incentive to divide is what messes with the estrogenic environment already. This is just a steelman it isn't my actual position lol

If I was to humour your retarded unfounded position, I could simply say estrogen is already fusing plates and has a higher incentive to fuse plates when there is a higher incentive for division. It's called homeostasis

?? Where's the contradiction here? What are the literacy rates in your country

Controlling e2 from test aromatisation gets rid of tests local 300% surge from ai's. In which your bone age won't advance beyond it's normal rate.

For the second statement I said you can't EXHAUSTIVELY halt bone aging. It'll just be back on it's normal course. These are harmonious stipulations

you said that you can control e2 from test e and it wont mature ur gp

however i guarentee u support the idea that local aromatization will close your gp

so how does that contradiction work?

“Controlling e2 from test aromatisation gets rid of tests local 300% surge from ai's. In which your bone age won't advance beyond it's normal rate.”

thats not what u said before or atleast stood by

 

[Kojo]

you said that you can control e2 from test e and it wont mature ur gp

however i guarentee u support the idea that local aromatization will close your gp

so how does that contradiction work?

“Controlling e2 from test aromatisation gets rid of tests local 300% surge from ai's. In which your bone age won't advance beyond it's normal rate.”

thats not what u said before or atleast stood by

I didn't say controlling it with test won't mature your growth plates, I was saying you don't get the letrozole rebound effect on your growth plates. Letrozole slows it down but the intracrine aromatisation alongside the absurd test increase later down the line speeds it back up.

This is why controlling the HPGA gives you the delaying effect constantly. hpga shut off is necessary

Local aromatisation will still close your gp, I just don't think you understand what quantification is

Controlling test = Slowing fusion down (still eventual fusion just maybe 1-3 years later, never once said you will replicate the cyp19a1 mutation and never get maturation. Just slowed)

No test control = Slow fusion down temporarily, speed fusion back up later down the line due to feedback loops with aromatisation alongside 100-300% test increases. Resulting in normal gp closure and no additional adult height.