few weeks into fgfr inhibs with roids

ReformedChad

ReformedChad

Oldgen grandpa
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Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
 
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ive only noticed a night height difference of a cm which is honestly good in a few weeks
is this actually real?

I didn't even notice it during my cycle
 
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love ur mundo pfp
im thinking of running erda too what supplements are you taking??
 
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Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
how old?
 
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Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
Basically in the same position nd gonna hop on soon, have u noticed some sides for erda yet?
 
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Basically in the same position nd gonna hop on soon, have u noticed some sides for erda yet?
no sides at low dose is uncommon, u dont need to take cancer crushing doses for fgfr inhibition
 
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Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
Nigha running a height cycle on 500 test im crine and on only 7 ius and 250 iq on top @zennn
The tren is nice. Also mirin the fact that you actually found a solid FGFR3 inhib source:soy:
 
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Nigha running a height cycle on 500 test im crine and on only 7 ius and 250 iq on top @zennn
The tren is nice. Also mirin the fact that you actually found a solid FGFR3 inhib source:soy:
"reads height cycle"

500 test

Black Boy What GIF by NoireSTEMinist
 
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thats some bullshit mane, whats the point of an fgfr3 inhibitor iff you pin 500 test lololol
 
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Can’t prevent local aromatizion
How impactful is this?

Certain studies have seen w/ letzorole which increases testosterone by up to 5 times still slows down growth plate maturation

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Aromatase deficient men case studies have ran 300 or so mg yet they see no change of maturation
 
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Main concern is fgfr3 like you're gonna get deformed from underexpression of fgfr3, that exists for a purpose. You don't wanna look marfanoid
 
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Looksmax “roiders” when they don’t understand that EQ is an AI
even if you take 2.5 letro ed it wont do shit to the local aromatisation on 500 test blud,and eq will still close your plates
 
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How impactful is this?

Certain studies have seen w/ letzorole which increases testosterone by up to 5 times still slows down growth plate maturation

+

Aromatase deficient men case studies have ran 300 or so mg yet they see no change of maturation
What you said is true but then he would have to use letzorole as an ai instead of eq, even then he would have to crash his estrogen to 0 which can be dangerous and not worth the risk for a few cm of height
 
Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
Get rid of the EQ ASAP and LOWER THE TEST you WILL close your plates like this
 
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What you said is true but then he would have to use letzorole as an ai instead of eq, even then he would have to crash his estrogen to 0 which can be dangerous and not worth the risk for a few cm of height
any ai by itself is far from the most optimal solution of delaying growth plate closure,in the studies gnrh therapy was superior in slowing down ba advancement, and 0e2 is not that bad either
 
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Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
500 test :lul: road to stunted height
 
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What you said is true but then he would have to use letzorole as an ai instead of eq, even then he would have to crash his estrogen to 0 which can be dangerous and not worth the risk for a few cm of height
EQ decreases E2 by itself because of androgen dominance, its practically the same as letzorole except letzorole is a direct aromatase inibitor and eq is just an androgen

Plus, even if he crashed his e2, letzorole is a reversible steroid, and he can't crash to 0 e2, and neither is that dangerous nor impractical. There are people (aromatase deficient men) that have undetectable e2 amounts since birth, are they actively in danger until estrogen therapy? no
 
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even if you take 2.5 letro ed it wont do shit to the local aromatisation on 500 test blud,and eq will still close your plates
zagro... what have you done
 
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Looksmax “roiders” when they don’t understand that EQ is an AI
The EQ is not horrible. But nigha you are running A 500 test dose and 7 ius of GH a night. You are just gonna nerf yourself. Even with extreme AIs such as letrozole you won't be able to prevent local e2:feelsuhh:
 
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The EQ is not horrible. But nigha you are running A 500 test dose and 7 ius of GH a night. You are just gonna nerf yourself. Even with extreme AIs such as letrozole you won't be able to prevent local e2:feelsuhh:
Idk how some people genuinely run retarded bodybuilder stacks like this and expect good results
 
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Idk how some people genuinely run retarded bodybuilder stacks like this and expect good results
Literally:forcedsmile: So retarded.
 
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Us high iq chads get great results (my pah was 6,1 but now look at me :lul:
Im 5 foot 7 at 14:forcedsmile:.my PAH is 181 cms. Il get to 185 no matter what
 
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EQ decreases E2 by itself because of androgen dominance, its practically the same as letzorole except letzorole is a direct aromatase inibitor and eq is just an androgen

Plus, even if he crashed his e2, letzorole is a reversible steroid, and he can't crash to 0 e2, and neither is that dangerous nor impractical. There are people (aromatase deficient men) that have undetectable e2 amounts since birth, are they actively in danger until estrogen therapy? no
Bro you misunderstand the case studies on aromatase deficient men, Those guys are actually in huge medical danger without treatment because they develop severe osteoporosis, terrible cholesterol, and heart issues, which is exactly why doctors have to put them on estrogen therapy

Also, crashing your E2 to zero is definitely doable and dangerous and will ruin your joints and heart, so it's not practical at all for bodybuilding nor heightmaxxing

Finally, EQ doesnt lower estrogen through "androgen dominance", it just has a weak AI metabolite that wont be enough to stop local aromatization when youre blasting 500mg of Test
 
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Bro you misunderstand the case studies on aromatase deficient men, Those guys are actually in huge medical danger without treatment because they develop severe osteoporosis, terrible cholesterol, and heart issues, which is exactly why doctors have to put them on estrogen therapy
All of these are progressive and take a lot of time to develop. Your cholesterol, heart and bone health will be completely fine as you can't suppress your e2 as much as aromatase deficiencies and even if you do it'll take a lot of time.
Also, crashing your E2 to zero is definitely doable and dangerous and will ruin your joints and heart, so it's not practical at all for bodybuilding nor heightmaxxing
This assumes you'll crash your e2 practically everytime you use an AI.

Simply use a reversible AI, and your chance of crashing e2 will be not only lower but also more preventable.

Don't act like an acute crash will devastate your health
 
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Simply use a reversible AI, and your chance of crashing e2 will be not only lower but also more preventable.
so you say that letrozole has a lower chance of 'crashing' e2 rather then aromasin,how come?
 
so you say that letrozole has a lower chance of 'crashing' e2 rather then aromasin,how come?
reversible, so if you start feeling side efffects you just taper a bit down and they're gone pretty fast before crashing. only reason it's more potent is because it's used in a lower dose, once you crash exemestane bare the sides for a week and if you feel sides you will do the same for a week and previous aromatase destruction will stack as well
 
reversible, so if you start feeling side efffects you just taper a bit down and they're gone pretty fast before crashing. only reason it's more potent is because it's used in a lower dose, once you crash exemestane bare the sides for a week and if you feel sides you will do the same for a week and previous aromatase destruction will stack as well
for heightmax purposes you have to crash e2 regardless and letrozole is the best ai for that matter
 
Rn im only on

500 test
250eq
200 tren
7IU Gh (too poor)

but im running 3mg erda with it, ive only noticed a night height difference of a cm which is honestly good in a few weeks

weight has gone up by 6kg (mostly carb retention, water)
I HATE MUNDO GET THIS FUCKING PIECE OF SHIT OUT OF UR PFP
 
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EQ decreases E2 by itself because of androgen dominance, its practically the same as letzorole except letzorole is a direct aromatase inibitor and eq is just an androgen

Plus, even if he crashed his e2, letzorole is a reversible steroid, and he can't crash to 0 e2, and neither is that dangerous nor impractical. There are people (aromatase deficient men) that have undetectable e2 amounts since birth, are they actively in danger until estrogen therapy? no
I made a whole guide abt this on TikTok

Testosterone binds to the catalytic site of CYP19A1 (aromatase) which executes three which lead to aromatisation When needed the 17b-HSD enzyme converts E2 into E1 in local tissue (like the growth plate) but the 17b-HSD enzyme complex is a bi directional regulatory switch they controls estrogen, this means: E1 can also convert to E2 via the 17b-HSD enzyme

EQ is structurally very similar to testosterone, the only main difference is an “extra” double bond. Since EQ is derived form testosterone it passes the same “aromatisation” procces where aromatase attempts to break the molecule down to estrogen but since EQ has an extra double bond the aromatase enzyme can’t break the EQ down to E2 so it’s broken down to 1,2 dehydroestradiol which is almost molecularly identical to E2. It then converts back to E1 and because of a sudden spike in E1 that same enzyme will Convert it to E2 meaning u would have high levels of e2 in local tissue (like the growth plate) but ur bloodwork would show low e2
 
I made a whole guide abt this on TikTok

Testosterone binds to the catalytic site of CYP19A1 (aromatase) which executes three which lead to aromatisation When needed the 17b-HSD enzyme converts E2 into E1 in local tissue (like the growth plate) but the 17b-HSD enzyme complex is a bi directional regulatory switch they controls estrogen, this means: E1 can also convert to E2 via the 17b-HSD enzyme

EQ is structurally very similar to testosterone, the only main difference is an “extra” double bond. Since EQ is derived form testosterone it passes the same “aromatisation” procces where aromatase attempts to break the molecule down to estrogen but since EQ has an extra double bond the aromatase enzyme can’t break the EQ down to E2 so it’s broken down to 1,2 dehydroestradiol which is almost molecularly identical to E2. It then converts back to E1 and because of a sudden spike in E1 that same enzyme will Convert it to E2 meaning u would have high levels of e2 in local tissue (like the growth plate) but ur bloodwork would show low e2
dnr its the metabolites of eq that act as actual AIs and AIs affects all tissues, just dnr
 
I made a whole guide abt this on TikTok

Testosterone binds to the catalytic site of CYP19A1 (aromatase) which executes three which lead to aromatisation When needed the 17b-HSD enzyme converts E2 into E1 in local tissue (like the growth plate) but the 17b-HSD enzyme complex is a bi directional regulatory switch they controls estrogen, this means: E1 can also convert to E2 via the 17b-HSD enzyme

EQ is structurally very similar to testosterone, the only main difference is an “extra” double bond. Since EQ is derived form testosterone it passes the same “aromatisation” procces where aromatase attempts to break the molecule down to estrogen but since EQ has an extra double bond the aromatase enzyme can’t break the EQ down to E2 so it’s broken down to 1,2 dehydroestradiol which is almost molecularly identical to E2. It then converts back to E1 and because of a sudden spike in E1 that same enzyme will Convert it to E2 meaning u would have high levels of e2 in local tissue (like the growth plate) but ur bloodwork would show low e2
And how significant is this high local e2? As I said a letzrole study showed they almost 5fold their T yet they had a slower maturation than others.
aromatisation is a systemic thing
There's synthesising hormones in the growth plates which cant be reached by traditional inhibitors due to cartillage
 
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There's synthesising hormones in the growth plates which cant be reached by traditional inhibitors due to cartillage
what
 
Steroidegenesis happens in growth plates as well

These cannot be inhibitedby aromatase inhibitors
at what rate though lol, probably minuscule
 

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