Aromatase Inhibitors are SHIT for Height (HIGH IQ ONLY)

Kojo

Kojo

18 | 160mg Isotret | 500mg Test
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Low effort Clickbait Shitpost, but Aromatase inhibitors are shit as a monotherapy for height increase and could actually work against you (though unlikely). STILL USE AI'S. CHECK "SOLUTION" AT THE BOTTOM OF THIS THREAD

If you don't know by now, basics of knowing/discussing or theorising about any hormone altering compounds is that feedack loops exist. You should also understand the concept of Ligands and receptors, binding(Binding affinity included) and competitive binding.

Ligands/Substrate are any molecule that binds to a binding site, Like enzymes or receptors which are proteins. Compounds you take into your system usually bind to the receptor it's designated to. Aromatase Inhibitors have to bind to aromatase and either deactivate it or kill it which comes under the umbrella term of "Antagonism".

Competitive binding is the process by which different ligands have to compete for the same binding site, only one thing can bind the site at once. The ligand that wins typically wins through having a higher binding affinity which is the strength at which it binds and takes over the binding site.

HOWEVER another factor matters like it's concentration, For example Endoxifen and 4-Hydroxytamoxifen have the same binding affinity, yet Endoxifen wins the binding race to estrogen receptors becaue it's concentration is much higher.


The relevance of all this is that testosterone and aromatase inhibitors exhibit the same effect as they both want to bind to aromatase, Testosterone wants to convert into E2 and AI's want to deactivate it. Now normally, AI's rape testosterone on binding affinity for this exact reason.

The Nuance comes in when you factor in the fact that Aromatase inhibitors like letrozole can give you disgusting surges of testosterone by 300% due to the negative feedback loop of the pituitary triggering more testosterone synthesis as the brain thinks estrogen is too low so it also thinks testosterone is too low.


This saturates the Aromatase Enzyme which leads to testosterone breaking through and outcompeting Letrozole for aromatase. This is why aromatase inhibitors as a monotherapy are dogshit for height and often do not produce any FAH additions, this also explains why we see insane growth velocity upregulations in kids using it
.

JUST TO BE CLEAR, I LOVE AROMATASE INHIBITORS (FUCK ANASTROZOLE, LETROZOLE SUPREMACY OVER BOTH OTHERS) BUT JUST DON'T USE IT ON IT'S OWN. ADD IN GROWTH BOOSTING COMPOUNDS WHILST DOING WHAT I SAID IN THE SOLUTION BELOW AND YOU HAVE YOUR IDEAL HEIGHT STACK.

Shut off the HPG-Axis;)

@Niebvll @Paul.jnxy @AtrophicPyra @avgsub5human @flowiza
 
Last edited:
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mirin high effort
enlightened me
 
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Mirin effort, I heavily agree
 
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Dnr, but bookmarked for later :feelshah:
 
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Low effort Clickbait Shitpost, but Aromatase inhibitors are shit as a monotherapy for height increase and could actually work against you (though unlikely).

If you don't know by now, basics of knowing/discussing or theorising about any hormone altering compounds is that feedack loops exist. You should also understand the concept of Ligands and receptors, binding(Binding affinity included) and competitive binding.

Ligands/Substrate are any molecule that binds to a binding site, Like enzymes or receptors which are proteins. Compounds you take into your system usually bind to the receptor it's designated to. Aromatase Inhibitors have to bind to aromatase and either deactivate it or kill it which comes under the umbrella term of "Antagonism".

Competitive binding is the process by which different ligands have to compete for the same binding site, only one thing can bind the site at once. The ligand that wins typically wins through having a higher binding affinity which is the strength at which it binds and takes over the binding site.

HOWEVER another factor matters like it's concentration, For example Endoxifen and 4-Hydroxytamoxifen have the same binding affinity, yet Endoxifen wins the binding race to estrogen receptors becaue it's concentration is much higher.


The relevance of all this is that testosterone and aromatase inhibitors exhibit the same effect as they both want to bind to aromatase, Testosterone wants to convert into E2 and AI's want to deactivate it. Now normally, AI's rape testosterone on binding affinity for this exact reason.

The Nuance comes in when you factor in the fact that Aromatase inhibitors like letrozole can give you disgusting surges of testosterone by 300% due to the negative feedback loop of the pituitary triggering more testosterone synthesis as the brain thinks estrogen is too low so it also thinks testosterone is too low.


This saturates the Aromatase Enzyme which leads to testosterone breaking through and outcompeting Letrozole for aromatase. This is why aromatase inhibitors as a monotherapy are dogshit for height and often do not produce any FAH additions, this also explains why we see insane growth velocity upregulations in kids using it
.

Shut off the HPG-Axis;)

@Niebvll @Paul.jnxy @AtrophicPyra @avgsub5human @flowiza
im so glad i dont have to deal with height

feel bad for ngas who crash e2 and other bullshit
 
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what do you suggest works?
 
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But what if you in response keep stacking the AI dose for a yet increased concentration:feelshah:
Does the feedback loop continue:feelswat:
 
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But what if you in response keep stacking the AI dose for a yet increased concentration:feelshah:
Does the feedback loop continue:feelswat:
feedback loop is based on your e2 levels so that would happen no matter what

If you mean to overpower test concentrations, you would need to hyper hyper dose letrozole which will just rape your health (excess ldl, liver enzymes etc) and it still doesn't work

There's a bunch of pharmacokinetic-related things that happen and are negative

Upping letrozole concentration doesn't make letrozole "bind more" you're just building up the compound in your body for zero reason because that additive letrozole can't even do anything since aromatase is already occupied
 
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Good thread:love:
 
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feedback loop is based on your e2 levels so that would happen no matter what
But at some point theyre gonna be 0? Or do you think localised aromatase will always keep them up to an extent:feelswat:
If you mean to overpower test concentrations, you would need to hyper hyper dose letrozole which will just rape your health (excess ldl, liver enzymes etc) and it still doesn't work

There's a bunch of pharmacokinetic-related things that happen and are negative
Yeah but this isnt what im talking about, Im talking just theory of the loop
Upping letrozole concentration doesn't make letrozole "bind more" you're just building up the compound in your body for zero reason because that additive letrozole can't even do anything since aromatase is already occupied
If its already occupied how does the extra test overtriumph letro in binding it? Occupied by the test through higher concentration, even higher concentratiln of letro should break through like the test did before no?
And if its occupied by the letro already I dont see the problem:feelswat:
 
But at some point theyre gonna be 0? Or do you think localised aromatase will always keep them up to an extent:feelswat:

Yeah but this isnt what im talking about, Im talking just theory of the loop

If its already occupied how does the extra test overtriumph letro in binding it? Occupied by the test through higher concentration, even higher concentratiln of letro should break through like the test did before no?
And if its occupied by the letro already I dont see the problem:feelswat:
I don't think localised aromatase is some separate thing that'll keep e2 up like a lot of people view it. When your e2 levels are 0 (which letrozole causes) that's what triggers the test, let me know if I'm misinterpreting something there

Even if it's already occupied, test is always going to try and compete for it no matter what. The same way estrogen is already occupying the estrogen receptors yet SERMs come in and take it over. It's because of mass action (Like what was explained in this thread)

Target site saturation also is a thing, alongside metabolic saturation which fucks up how you can metabolise the drug with your liver.
 
I don't think localised aromatase is some separate thing that'll keep e2 up like a lot of people view it.
Its not seperate but usually more inaccessible for aromatase inhibitors
When your e2 levels are 0 (which letrozole causes) that's what triggers the test, let me know if I'm misinterpreting something there
Yeah, so the test is up in concentration
You then up the letro again and my question was if the loop continues through that, you said it does as long as theres estrogen
There is already none
So loop ends there?
Even if it's already occupied, test is always going to try and compete for it no matter what.
yeah but the letro can outcompete it thats the point
The same way estrogen is already occupying the estrogen receptors yet SERMs come in and take it over. It's because of mass action (Like what was explained in this thread)
The thread explained it through concentration?
If you take the letro high enough it outcompetes the raised test from the earlier letro dose?
I dont think you get the principle
Im not saying anyone shoumd start raking 150mg letro ed, just that it would be possible to outcompete the test again
Target site saturation also is a thing, alongside metabolic saturation which fucks up how you can metabolise the drug with your liver.
Ok:feelswat:
 
Low effort Clickbait Shitpost, but Aromatase inhibitors are shit as a monotherapy for height increase and could actually work against you (though unlikely). STILL USE AI'S. CHECK "SOLUTION" AT THE BOTTOM OF THIS THREAD

If you don't know by now, basics of knowing/discussing or theorising about any hormone altering compounds is that feedack loops exist. You should also understand the concept of Ligands and receptors, binding(Binding affinity included) and competitive binding.

Ligands/Substrate are any molecule that binds to a binding site, Like enzymes or receptors which are proteins. Compounds you take into your system usually bind to the receptor it's designated to. Aromatase Inhibitors have to bind to aromatase and either deactivate it or kill it which comes under the umbrella term of "Antagonism".

Competitive binding is the process by which different ligands have to compete for the same binding site, only one thing can bind the site at once. The ligand that wins typically wins through having a higher binding affinity which is the strength at which it binds and takes over the binding site.

HOWEVER another factor matters like it's concentration, For example Endoxifen and 4-Hydroxytamoxifen have the same binding affinity, yet Endoxifen wins the binding race to estrogen receptors becaue it's concentration is much higher.


The relevance of all this is that testosterone and aromatase inhibitors exhibit the same effect as they both want to bind to aromatase, Testosterone wants to convert into E2 and AI's want to deactivate it. Now normally, AI's rape testosterone on binding affinity for this exact reason.

The Nuance comes in when you factor in the fact that Aromatase inhibitors like letrozole can give you disgusting surges of testosterone by 300% due to the negative feedback loop of the pituitary triggering more testosterone synthesis as the brain thinks estrogen is too low so it also thinks testosterone is too low.


This saturates the Aromatase Enzyme which leads to testosterone breaking through and outcompeting Letrozole for aromatase. This is why aromatase inhibitors as a monotherapy are dogshit for height and often do not produce any FAH additions, this also explains why we see insane growth velocity upregulations in kids using it
.

JUST TO BE CLEAR, I LOVE AROMATASE INHIBITORS (FUCK ANASTROZOLE, LETROZOLE SUPREMACY OVER BOTH OTHERS) BUT JUST DON'T USE IT ON IT'S OWN. ADD IN GROWTH BOOSTING COMPOUNDS WHILST DOING WHAT I SAID IN THE SOLUTION BELOW AND YOU HAVE YOUR IDEAL HEIGHT STACK.

Shut off the HPG-Axis;)

@Niebvll @Paul.jnxy @AtrophicPyra @avgsub5human @flowiza
thats why trenbolone plus ai to shit on negative feedback loop completely:feelshah:

makes me regret not hopping on tren and letrozole and erda when my plates were open:hnghn::hnghn:
 
Its not seperate but usually more inaccessible for aromatase inhibitors

Yeah, so the test is up in concentration
You then up the letro again and my question was if the loop continues through that, you said it does as long as theres estrogen
There is already none
So loop ends there?

yeah but the letro can outcompete it thats the point

The thread explained it through concentration?
If you take the letro high enough it outcompetes the raised test from the earlier letro dose?
I dont think you get the principle
Im not saying anyone shoumd start raking 150mg letro ed, just that it would be possible to outcompete the test again

Ok:feelswat:
dude..

only way to have zero and i mean ZEROOOOOO e2 is by having zero test..

2-3 years letrozole and tren only and forget:lul:
 
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He just said

Im just going off by his words

Omg bro i switched u up sorry
Its 6am no sleep
oh i didnt see..

btw indiamart trenbolone is coming soon:feelskek::feelskek:

health phase is OVERRR 50mg proviron and 100mg tren e with zero test base is gonna be what im running super soon:feelshah:

with 25mg aromasin ofc i cant show e2 any mercy
 
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oh i didnt see..

btw indiamart trenbolone is coming soon:feelskek::feelskek:

health phase is OVERRR 50mg proviron and 100mg tren e with zero test base is gonna be what im running super soon:feelshah:

with 25mg aromasin ofc i cant show e2 any mercy
Idrk about androgens
you do you on that I got no clue:feelswat:
 

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