Where’s the evidence that local e2 cant be inhibited?

Zagro

Zagro

Roids over Foids
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It’s like everytime retards on tiktok make a claim it spreads everywhere

Yes local e2 exists and there’s also estrogen biosynthesis in the chondrocytes locally but where does it say that we cant inhibit it?

Local e2 partly depends on your systemic/serum e2, and even when dosing test high you can take potent aromatase inhibitors which are known to work insanely good intracellulary.

So someone tell me how it cant be blocked
 
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The evidence is retards shouting it, an even better piece of evidence that it can be inhibited is the brain as that can be looked at more easily, if ai's were not able to do this they also wouldnt make you retarded when used in high doses as the hypocampus mainly uses local e2 yet they time and time again reduce ltp, memory etc and same with the amygdala but with anxiety and such we can also se lower e2 levels locally when tedted
 
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The evidence is retards shouting it, an even better piece of evidence that it can be inhibited is the brain as that can be looked at more easily, if ai's were not able to do this they also wouldnt make you retarded when used in high doses as the hypocampus mainly uses local e2 yet they time and time again reduce ltp, memory etc and same with the amygdala but with anxiety and such we can also se lower e2 levels locally when tedted
B-but fletchzilla on tiktok said it’ll stunt my growth

Yeah decent comparison and we literally have studies where letrozole is used on pubertal boys and it slows down bone age maturation rate compared to the control group, although their t levels are exceptionally high because of the letro so with their logic it should stunt growth cus muhh substrates

@birthdefect
 
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B-but fletchzilla on tiktok said it’ll stunt my growth

Yeah decent comparison and we literally have studies where letrozole is used on pubertal boys and it slows down bone age maturation rate compared to the control group, although their t levels are exceptionally high because of the letro so with their logic it should stunt growth cus muhh substrates

@birthdefect
exactly
infact letrozole is best for this purpose as its shown to decrease intracellular and peripheral aromatisation, likely why it causes a surge in test so much higher than arimidex
saying this tho, this doesnt even get into the best drug for e2 but i doubt many are sourcing it, a serd
 
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I used to say it couldn’t until I looked further into it and low and behold aromatase inhibitors will work in every tissue including bone
 
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It’s like everytime retards on tiktok make a claim it spreads everywhere

Yes local e2 exists and there’s also estrogen biosynthesis in the chondrocytes locally but where does it say that we cant inhibit it?

Local e2 partly depends on your systemic/serum e2, and even when dosing test high you can take potent aromatase inhibitors which are known to work insanely good intracellulary.

So someone tell me how it cant be blocked
Do you take any things to combat the negative side effects on your neurology while on the ai?
 
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It’s like everytime retards on tiktok make a claim it spreads everywhere

Yes local e2 exists and there’s also estrogen biosynthesis in the chondrocytes locally but where does it say that we cant inhibit it?

Local e2 partly depends on your systemic/serum e2, and even when dosing test high you can take potent aromatase inhibitors which are known to work insanely good intracellulary.

So someone tell me how it cant be blocked
idk
 
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Update: it cant be inhibited


Do you take any things to combat the negative side effects on your neurology while on the ai?
No because it has no effect on "neurology"
 
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:lul::lul::lul::lul::lul::lul::lul::lul: YO IM CAGING THIS IS WHAT U WERE SAYING ON MY THREADS HHAHASDNASHDAHAHAHAH
That's why i told you to stop insulting me as I've made the same mistake as you have, it isn't that I'm stubborn or anything dude. I wish we could inhibit E2 locally in the growth plate with aromatase inhibitors as that would be fucking amazing, but it's simply not possible to make a decent budge in local E2 levels.

It's interesting how people think that it's some personal matter to debate your standpoint even though you're false, nobody will care and we will have the truth uncovered so others stop making the same mistake, but people like yourself confuse other users
 
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incredible how this dude changes his mind in a metter of days:feelskek:
 
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incredible how this dude changes his mind in a metter of days:feelskek:
1778925393764

1778925403214


+

1778925433224
 
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whatever g, remember you where the guy that until not long ago was arguiing with @Ahmed88 about the utility of heightmaxxing and you are more and more converting to his belief that its all about genetics and there's nothing you can do about it besides taking 100UI + of hgh cuz muh "healthy adolescents produce up to 20 UI by themselves naturally so under 50 UI is cope"
You're delusional and I've never implied such things, quote a single one.

Everything is genetic indeed, but genetics themselves and their expressions are easily changed meaning it being genetic doesn't matter if you're dedicated enough to modify particular ones for your own use-case.

You're another weird user
 
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That's why i told you to stop insulting me as I've made the same mistake as you have, it isn't that I'm stubborn or anything dude. I wish we could inhibit E2 locally in the growth plate with aromatase inhibitors as that would be fucking amazing, but it's simply not possible to make a decent budge in local E2 levels.

It's interesting how people think that it's some personal matter to debate your standpoint even though you're false, nobody will care and we will have the truth uncovered so others stop making the same mistake, but people like yourself confuse other users
Yeah i agree i dont attach myself personally to the arguments i hold obviously, just to me it seems frustrating that you seem to pushback on this matter when it seems as youre purely going off of speculations and blowing up inisignificant nuances.

Though this thread now confused me cause it seems you backtracked, what actually is your ultimatum? Because obviously i would benefit from the truth too, i have more hgh coming as well as letro and test. Will def be administering the letro but unsure about the test as of now. What is it that makes you believe that this local aromatisation poses such a problem, because from the study on the teens ( the one which you reffered to here) you yourself conceded that their test levels increased to 5x baseline yet the letro still made their plates age 0.5x the normal rate

Have you since fallen upon evidence that counters this? If so could you share because its interesting to get to the bottom of and not something anyone really speaks of. everyone just says 'do an ai with ur androgens and ur good' and theyre usually reffering to underdosed arimidex which is cagefuel tbh, anything apart from letro shouldnt even be considered if plates r open. But yeah this is largely unknown still and we are yet to have a black and white answer.
 
whatever g, remember you where the guy that until not long ago was arguiing with @Ahmed88 about the utility of heightmaxxing and you are more and more converting to his belief that its all about genetics and there's nothing you can do about it besides taking 100UI + of hgh cuz muh "healthy adolescents produce up to 20 UI by themselves naturally so under 50 UI is cope"
doing anythign above like 12-15ius will do the opposite of what u want if the goal is height. First of all its not like you have infinite receptors so once they r saturated all the rest goes to giving u diabetes or acro. And all that gh would cause plates to close so much faster than any ai would otherwise slow. I think the golden dosage is 8-10, done for atleast 12 months and ideally 24-36
 
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doing anythign above like 12-15ius will do the opposite of what u want if the goal is height. First of all its not like you have infinite receptors so once they r saturated all the rest goes to giving u diabetes or acro. And all that gh would cause plates to close so much faster than any ai would otherwise slow. I think the golden dosage is 8-10, done for atleast 12 months and ideally 24-36
there was a study on healthy kids doing 8iu and they lost potential height. no iss no anything.

“GHD: In pubertal patients, a weekly dosage of up to 0.7 mg/kg divided into daily doses may be used”

im about 65kg. i should be pinning 19,5ius a day👍
 
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there was a study on healthy kids doing 8iu and they lost potential height. no iss no anything.

“GHD: In pubertal patients, a weekly dosage of up to 0.7 mg/kg divided into daily doses may be used”

im about 65kg. i should be pinning 19,5ius a day👍
20 ius and ur plates will close in 3 weeks time geg

was that study done with letro as well or j hgh alone
 
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Where is the evidence that soy lowers testosterone :feelskek:
 
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20 ius and ur plates will close in 3 weeks time geg

was that study done with letro as well or j hgh alone
Im grey, please tell me through wich mechanism that happens or show me studies.

Ive only read studies proving the opposite.
 
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Im grey, please tell me through wich mechanism that happens or show me studies.

Ive only read studies proving the opposite.
probably because stimulating the igf-1axis upregulates ERa. thats why we use aromatase inhibitors or just use non aromatizing AAS
 
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Im grey, please tell me through wich mechanism that happens or show me studies.

Ive only read studies proving the opposite.
how much have you grown from the time u hopped on roids and at what age? r u doing tren? what dose hgh?
 
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how much have you grown from the time u hopped on roids and at what age? r u doing tren? what dose hgh?
10IU GH
35 Tren
140 Test
2mg AI
500mcg BPC
25 Meclizine
+ supps

I’ve grown more than 10cm officially now.
 
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10IU GH
35 Tren
140 Test
2mg AI
500mcg BPC
25 Meclizine
+ supps

I’ve grown more than 10cm officially now.
nicee but isnt 10iu gh too low? and why just 35 tren and why test in general.

dont do meclizine It was just a magnificent stroke of luck that the base molecule meclizine had the perfect polarity and structure to act on fgfr3, we have literally no clinical data on whether its metabolites would have the same effect. The only data showing mecs effect on fgfr3 was in Petri dishes where the meclizine wouldn’t be exposed to blood or liver enzymes
 
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nicee but isnt 10iu gh too low? and why just 35 tren and why test in general.

dont do meclizine It was just a magnificent stroke of luck that the base molecule meclizine had the perfect polarity and structure to act on fgfr3, we have literally no clinical data on whether its metabolites would have the same effect. The only data showing mecs effect on fgfr3 was in Petri dishes where the meclizine wouldn’t be exposed to blood or liver enzymes
Yeah, I ran out of gh 3 days ago, But m blast will be way higher dosed, dm if you wanna see.
 
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[Deleted]
 
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It’s like everytime retards on tiktok make a claim it spreads everywhere

Yes local e2 exists and there’s also estrogen biosynthesis in the chondrocytes locally but where does it say that we cant inhibit it?

Local e2 partly depends on your systemic/serum e2, and even when dosing test high you can take potent aromatase inhibitors which are known to work insanely good intracellulary.

So someone tell me how it cant be blocked
They cant cuz they are retarded lol debated one of those dumbasses yesterday and he kept repeating the same shi over and over with no evidence whatsoever
 
obv, wich mechanism though?
High local levels of igf1 triggers rapid hypertrophy n proliferation of the chondrocytes, essentialy exhausting the stem cells at an accelerated rate to the point the plate thins out and fuses

Also high dose hgh significantly upregulates the expression of estrogen receptor alpha, which u obv realise how that would close plates. Its why u basically have to do an ai with rhgh and how i kinda fucked up not having done so earlier.

Its genuinely not smart to go above 8-10ius a day, your receptors can only get so saturated and the rest will spill over and cause sides that wont help with height at all. Any dose above that and you are simply causing plates to close faster while also not gaining any more height than u wouldve at like 8ius

8-10ius + letrozole is a perfect combo that will still delay plate closure significantly while also fully saturating your receptors and not getting any diminishing returns.
 
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High local levels of igf1 triggers rapid hypertrophy n proliferation of the chondrocytes, essentialy exhausting the stem cells at an accelerated rate to the point the plate thins out and fuses

Also high dose hgh significantly upregulates the expression of estrogen receptor alpha, which u obv realise how that would close plates. Its why u basically have to do an ai with rhgh and how i kinda fucked up not having done so earlier.

Its genuinely not smart to go above 8-10ius a day, your receptors can only get so saturated and the rest will spill over and cause sides that wont help with height at all. Any dose above that and you are simply causing plates to close faster while also not gaining any more height than u wouldve at like 8ius

8-10ius + letrozole is a perfect combo that will still delay plate closure significantly while also fully saturating your receptors and not getting any diminishing returns.
So yuo think 13.33IUs are too much? I’m reaaaaly nuking my e2
 
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So yuo think 13.33IUs are too much? I’m reaaaaly nuking my e2
eh ur pushing it but should be fine just dont go higher and yeah make sure e2 is nuked

at that dose tho u NEED to have the right supps to mitigate senescense, heres a section of my thread on it explaining which supps r best and the mechanisms in which they mitigate it:


The most critical "bottleneck" in 24month+ protocol isn't just keeping the plates open; it’s preventing chondrocyte senescence—the biological exhaustion of the growth plate's stem cells.

Without a protection strategy, you might see fast changes 6 months and then "hit a wall" where the plates are still open, but the stem cells are gone.

The "Stem Cell Protection" solution

  • Quercetin (The Senolytic Janitor):
    • The Mechanism: Prevents the accumulation of "zombie" (senescent) cells in the resting zone of the growth plate.
    • Anti-Senescence Role: By clearing out old cells that no longer divide, Quercetin prevents them from secreting inflammatory signals that would otherwise "poison" the surrounding healthy stem cells and force them into early retirement. It effectively keeps the "nursery" healthy so the HGH-driven division can continue longer.
  • Boron (The Matrix Stabilizer):
    • The Mechanism: Enhances the density of chondrocytes in the proliferative zone and protects the "extracellular matrix" (the house the cells live in).
    • Anti-Senescence Role: Boron stabilizes the physical scaffold of the growth plate. If the scaffold breaks down, stem cells die off. By strengthening the matrix, Boron ensures the "resting zone" reservoir isn't physically crushed or degraded by the high-pressure growth you're forcing with HGH.
  • Vitamin D3 + K2 (The Quality Control):
    • The Mechanism: Regulates the transition from cartilage to bone.
    • Anti-Senescence Role: If mineralization is sloppy, the growth plate becomes disorganized (like Rickets). This chaos causes stem cells to exhaust faster. D3 and K2 ensure that as HGH creates new cells, they are "locked in" as solid bone efficiently, preventing the biological "friction" that leads to early senescence.
  • Zinc & Magnesium (The Engine Co-Factors):
    • The Mechanism: Direct fuel for DNA synthesis and alkaline phosphatase activity.
    • Anti-Senescence Role: Zinc is required for the actual division of chondrocytes. A deficiency forces the few remaining stem cells to "overwork," leading to rapid exhaustion. Ample Zinc/Mag ensures the work is distributed across the cell population, preserving the reservoir's lifespan.
 
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He uses gpt dude why are you still listening jfl

Will reply here and in other threads soon
Yeah would’ve done it either way lol

Not even showed any evidence.
 
t
High local levels of igf1 triggers rapid hypertrophy n proliferation of the chondrocytes, essentialy exhausting the stem cells at an accelerated rate to the point the plate thins out and fuses

Also high dose hgh significantly upregulates the expression of estrogen receptor alpha, which u obv realise how that would close plates. Its why u basically have to do an ai with rhgh and how i kinda fucked up not having done so earlier.

Its genuinely not smart to go above 8-10ius a day, your receptors can only get so saturated and the rest will spill over and cause sides that wont help with height at all. Any dose above that and you are simply causing plates to close faster while also not gaining any more height than u wouldve at like 8ius

8-10ius + letrozole is a perfect combo that will still delay plate closure significantly while also fully saturating your receptors and not getting any diminishing returns.
thoughts on this? @Zagro “exhausting stem cells”
 
10IU GH
35 Tren
140 Test
2mg AI
500mcg BPC
25 Meclizine
+ supps

I’ve grown more than 10cm officially now.
Dude I wish my growth plates had been open when I was on HGH

Now im stuck at 5'8ft and have to get LL in 2 years:feelsrope:
 
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Dude I wish my growth plates had been open when I was on HGH

Now im stuck at 5'8ft and have to get LL in 2 years:feelsrope:
Nah that’s brutal.

Nobody should be below 6ft as a male. Fr I think Gh and androgen therapy should be given to any boy below the 40th percentile.

And yeah I also can’t be happy enough about me doing this good of a progress.:Comfy:
 
Dude I wish my growth plates had been open when I was on HGH

Now im stuck at 5'8ft and have to get LL in 2 years:feelsrope:
I remember when we sent pics and shit back in the server, you put all your syringes vials etc on toilet paper and showcased that shit or something
 
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It’s like everytime retards on tiktok make a claim it spreads everywhere

Yes local e2 exists and there’s also estrogen biosynthesis in the chondrocytes locally but where does it say that we cant inhibit it?

Local e2 partly depends on your systemic/serum e2, and even when dosing test high you can take potent aromatase inhibitors which are known to work insanely good intracellulary.

So someone tell me how it cant be blocked
Its just idiots saying that shit, We have seen standalone ai treatments leading to delayed growth plate closure.
 
I remember when we sent pics and shit back in the server, you put all your syringes vials etc on toilet paper and showcased that shit or something
yeah I remember that

It was like the first month on HGH
 
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