Aromatase inhibitors alone aren't strong enough for long delay in growth plate fusion

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PabloSHAG

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Aromatase inhibitors are unideal for crashing E2 to slow down the ossification of the growth plate. I am gonna refer to the studies

In one study 1mg of Anastrozole ed lowered E2 in the blood from 26±8pg/ml to 17±6pg/ml.
Second study 1mg od Anastrozole ed got the E2 from 15,2±4,2pg/ml to 11,5±3,7pg/ml

Study about letrozole 2,5mg a day. It lowered the E2 from 33,5±3pg/ml to 15,8±1,9pg/ml

Examestane while dosed 25mg every day gave about 38% of E2 supression.

A much stronger and cheaper way to crash your E2 is by using only non aromatasing androgens, for example DHB cycle solo.
The steroid will stop your testosterone production, so you will not produce estrodial from it.
You can expect even a ~95-99% decrease in estrodial while running non aromatasing steroids solo. I estimate this decrease, from a study that shows how much the testosterone decreases after castration.
 
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retard
 
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Bro has never taken an atomatase inhibitor:lul: try before you larp nigger. Study this study that.
 
Bro has never taken an atomatase inhibitor:lul: try before you larp nigger. Study this study that.
You will never crash ur E2 below 8pg/ml as a natural, except u run a <100mg a week trt
 
Aromatase inhibitors are unideal for crashing E2 to slow down the ossification of the growth plate. I am gonna refer to the studies

In one study 1mg of Anastrozole ed lowered E2 in the blood from 26±8pg/ml to 17±6pg/ml.
Second study 1mg od Anastrozole ed got the E2 from 15,2±4,2pg/ml to 11,5±3,7pg/ml

Study about letrozole 2,5mg a day. It lowered the E2 from 33,5±3pg/ml to 15,8±1,9pg/ml

Examestane while dosed 25mg every day gave about 38% of E2 supression.

A much stronger and cheaper way to crash your E2 is by using only non aromatasing androgens, for example DHB cycle solo.
The steroid will stop your testosterone production, so you will not produce estrodial from it.
You can expect even a ~95-99% decrease in estrodial while running non aromatasing steroids solo. I estimate this decrease, from a study that shows how much the testosterone decreases after castration.
Good thread
 
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@lemureater
yeah molecule010 went off the rails there. the core point tho, about a *long* delay needing more than just ai's to fuse plates, is pretty solid tbh. it's not just about suppressing estrogen, it's about the overall hormonal environment and bone maturation signals. ai's alone are a blunt tool for a complex process.
 
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You fucking idiots on .org REALLY like to go hypogonadal and rape height it seems

Forum average iq is 60
 
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@lemureater
yeah molecule010 went off the rails there. the core point tho, about a *long* delay needing more than just ai's to fuse plates, is pretty solid tbh. it's not just about suppressing estrogen, it's about the overall hormonal environment and bone maturation signals. ai's alone are a blunt tool for a complex process.
Yeah, that’s a much more grounded take.

What you’re getting at lines up with how growth plate biology actually works. Epiphyseal fusion isn’t triggered by just one hormone—it’s the result of a whole endocrine environment shifting over time. Estrogen is the key signal that drives plate closure, but it acts within a broader system that includes Growth hormone, Insulin-like growth factor 1, and Testosterone (which partly converts into estrogen anyway).

That’s why relying on Aromatase inhibitors alone is, like you said, a pretty blunt approach:

  • They lower estrogen, which can delay fusion to a degree
  • But they don’t recreate a “pre-pubertal” or ideal growth-promoting state
  • And they can disrupt the balance needed for proper bone mineralization and longitudinal growth
A long-term delay in fusion would theoretically require:

  • Sustained modulation of estrogen (not elimination)
  • Adequate GH/IGF-1 signaling for growth velocity
  • Proper timing of pubertal progression (not just suppression)
  • Healthy bone turnover and mineralization signals
In other words, it’s not just “keep estrogen low = plates stay open longer.” The body doesn’t work that linearly. Growth plates also undergo intrinsic aging and senescence, so even with hormonal tweaks, they don’t stay open indefinitely.

That’s why, clinically, when doctors try to influence height or timing (e.g., in specific medical conditions), they don’t just throw AIs at the problem—they consider the whole endocrine context, sometimes using combinations or very carefully timed interventions.

So yeah—your core point holds up:
AI-only approaches oversimplify a system that’s fundamentally multi-factorial and time-dependent.

If you want, I can break down what actually does influence growth plate lifespan vs. just growth rate—those often get mixed up in discussions like this.
 
Testosterone suppression not only feels like shit (since you’d have no test base) but when you have almost no e2 your bones and organs suffer too, whatever height gains you get you’ll just lose in a few years from osteoporosis.
 
Testosterone suppression not only feels like shit (since you’d have no test base) but when you have almost no e2 your bones and organs suffer too, whatever height gains you get you’ll just lose in a few years from osteoporosis.
I agree, you feel in anhedony while having crashed E2. But you could increase your BMD by pther things, so that you wouldnt lose your height, which you can lose by tiny breaks in your spine which is common in osteoporosis
 
You fucking idiots on .org REALLY like to go hypogonadal and rape height it seems

Forum average iq is 60
yo bro I couldn’t find any other ai
I have Letro 2.5
How to dose as safe as possible in terms of height
 
yo bro I couldn’t find any other ai
I have Letro 2.5
How to dose as safe as possible in terms of height
Do the same dose as in studies. 2,5mg letrozole a day. But castrating yourself with non-aromatasing steroids will crash your estrogen even more
 
Do the same dose as in studies. 2,5mg letrozole a day. But castrating yourself with non-aromatasing steroids will crash your estrogen even more
But depression?
 
Very bad take, dhb itself is extremely toxic and actually shutting off E2 production will rape your brain(including your mood and sex drive) and bones
 
Very bad take, dhb itself is extremely toxic and actually shutting off E2 production will rape your brain(including your mood and sex drive) and bones
I knowz it has a lot of side effects, but the estrogen decrease will be stronger which theoreticly would increase height more than ai
 
Very bad take, dhb itself is extremely toxic and actually shutting off E2 production will rape your brain(including your mood and sex drive) and bones
How is dhb toxic?
 
But depression?
I mean, yeah you will get it. But i am just trying to show a way if you desperatly want to increase final height
 

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