What is the best aromatase inhibitor to take in puberty for growth plates?

[manuel355335]

Im 15 and my plates are still open I am on hgh already but I need an ai so my bones dont age faster which ai is the best in your opinion because too low estrogen or zero estrogen is also bad and what ai lowers it but not too low?

 

[i cant lie cant lie]

Mirin the ai but i am NOT talking abt genetic mutations

Its google ai you dumbass. It sumarizes what i got from the search so i dont have to skim articles to find proof.

(you just proved my point: iss children are NOT normal) The genetics which the ai is refering to are likely mutations (Source: https://ispae-jped.com/genetics-of-...ract,of comorbidities, and genetic counseling.)

Just read the shit you sent me bro. It literally says these things are correlated and is little evidence, not even an answer.

Idiopathic short stature (ISS) is characterized by a height more than two standard deviations below the corresponding mean height of a given age, sex, and population group without evidence of systemic, endocrine, nutritional, or chromosomal abnormalities, and normal stimulated growth hormone levels. While growth is influenced by genetic, nutritional, hormonal, and environmental factors, ISS remains a diagnosis of exclusion after ruling out systemic, endocrine, or chromosomal disorders. Although multiple genes have been linked to be associated with linear growth, they account only for a small proportion of cases of short stature. Advances in genetic testing, including whole-exome sequencing and copy number variant analysis, have improved diagnostic precision, yet the yield remains low. Mutations in genes SHOX, ACAN, natriuretic peptide receptor-B, and insulin-like growth factor 1 receptor along with epigenetic factors have been implicated in ISS. Identifying pathogenic variants aids in personalized management, early detection of comorbidities, and genetic counseling. This review compiles current insights into genetic basis of ISS, emphasizing the need for further research to unravel its complex etiology and improve management strategies for affected individuals.


They have no abnormalities or systemic issue or endocrine issue. The problem has nothing to do with HGH so it would be stupid to say they have a better reaction when they fucking have it worse

And jfl at the not normal. Obviously they are not normal, they are 2 standard deviations lower than the average person it terms of height.

And ofcourse people get differents amount of igf1, i am not denying that, i am looking at the reason most iss children have lower igf1 levels that being mutations in the IGF1R

Every person has different igf1r gene. some subtly. some a lot
And im gonna give you the source because "Muh you used ai!!" but you didnt disprove my fucking point, idiot.

Large-scale analysis of variation in the insulin-like growth factor family in humans reveals rare disease links and common polymorphisms

The insulin-like growth factors IGF1 and IGF2 are closely related proteins that are essential for normal growth and development in humans and other sp…

www.sciencedirect.com

But again, we should review
Its, not fucking genetic. Its around 20% of cases. That low number proves that its a mere correlation and not the final answer.

It doesnt matter how much you argue. Iss is Iss. Idiopathic short stature. Idiopathic. Any "Discovery" you make doesnt fucking matter because if it was one then it wouldnt be idiopathic, dumbass.

All you show is correlation as proof. Thats not an answer. That is dissonance. You just want to be right.

 

[i cant lie cant lie]

He needs to check bone Age, my nigger ass at 18 Is still growing, its very Person to Person till how late you can grow, also hgh can still help with face and clavs

Bruh thats what he said
Also how the fuck are you still growing? What is your height now and height at 14? This would indicate you have a delayed puberty of some sort, so you would still be prepubertal even at 13-14, even if puberty starts for the normal person in 10-12 [but obviously you arent a normal person ]

 

[i cant lie cant lie]

And no iss arent close to us, since they arent blasting HGH cause of their genetics but because most of them have unknown causes bzhind their short stature and that does include genetics

Blasting GH is also funny, thereputic doses are like 4iu

These niggas take like 30-40iu per week which is like 4-6 a day, not blasting [and for those who are 60-80kg, i'm being very generous here, cause we are using studies of iss, and these shortcels CANNOT be so heavy ]

You also produce 2iu bro average teen produces 700mcg gh everyday which is 2iu

 

[KB_maxxer]

Bruh thats what he said
Also how the fuck are you still growing? What is your height now and height at 14? This would indicate you have a delayed puberty of some sort, so you would still be prepubertal even at 13-14, even if puberty starts for the normal person in 10-12 [but obviously you arent a normal person ]

At 14 i was like 158 now 18 im 170cm(my personal trainer sayd that my posture Is so bad thats im likely 172cm), still short but ill see how It Will end, 3cm were gained in last 6-7months.
My Brother Is 6'0 dad 173-174cm.

 

[KB_maxxer]

13-14, even if puberty starts for the normal person in 10-12 [but obviously you arent a normal person ]

Hair started appening at 13, but proper puberty id Say started late 14 to 15, but It progresses slowly and steadily, but idk if Its how i am or becuse i was unheslthy

 

[xdam]

Armidex aka Anastrozole brutally moggs Aromasin, not even a debate anyone who promotes aromasin while not being on a cycle is fucking retarded, its a steroidal ai and the effects are irreversible so unless you want joint paints for the rest of ur life go on and nuke ur e2 levels

 

[i cant lie cant lie]

Armidex aka Anastrozole brutally moggs Aromasin, not even a debate anyone who promotes aromasin while not being on a cycle is fucking retarded, its a steroidal ai and the effects are irreversible so unless you want joint paints for the rest of ur life go on and nuke ur e2 levels

Bruh i support letz/anas over aromasin but that last part is stupid, your e2 goes back to stable in a week

And unless you truly raped your e2, you wont have the problems seen in the last 2 sentences

 

[Ahmed88]

Its google ai you dumbass

They have no abnormalities or systemic issue or endocrine issue. The problem has nothing to do with HGH so it would be stupid to say they have a better reaction when they fucking have it worse

Ofc they dont have a HGH problem because we don't know it? Whats your point? We do not know why they react to HGH and grow from it and im not saying its a definitive answer to the ISS problem im saying your AI (or summarized studies) most likely mean genetic mutations and not just merely short parents. All im saying is ISS studies do NOT apply to normal kids (and there is 0 evidence that HGH grows non ghd and non iss children, there are acc studies against it)

These niggas take like 30-40iu per week which is like 4-6 a day, not blasting [and for those who are 60-80kg, i'm being very generous here, cause we are using studies of iss, and these shortcels CANNOT be so heavy

While i do admit some study doses are comical most studies, do use two sets of weekly dosing for example on non-iss and non-ghd the dose was (0.5iu/kg/week and 1iu/kg/week)

 

[i cant lie cant lie]

most likely mean genetic mutations and not just merely short parents

Related, only.

most likely mean genetic mutations

They fucking dont bro

m im saying your AI (or summarized studies)

I gave you non ai source, bro you fucking rat dnrd me

All im saying is ISS studies do NOT apply to normal kids (and there is 0 evidence that HGH grows non ghd and non iss children, there are acc studies against it)

Then why the fuck would it be fda approced for iss dummy
4cm is pretty good and thats the low threshold

Also, people with iss are very similar to people with normal height. They have no syndrome. No issue, no gene. How the fuck does my ai source count genetic mutations if iss is not genetic mutation? Then if it was a mutation it wouldnt be fucking idiopathic?

Here is a source that isnt ai because you are so persistent:

People with Idiopathic Short Stature (ISS) are biologically very similar to people of "normal" or average height, as ISS is defined by a lack of underlying disease, hormonal deficiency, or chromosomal abnormalities. Their health and cognitive development are generally indistinguishable from their peers. The primary differences are physical (height is typically 2 standard deviations or more below the mean) and psychosocial, often stemming from social biases

Idiopathic Short Stature: Conundrums of Definition and Treatment - PMC

Children with idiopathic short stature (ISS) are statistically defined by height SDS < −2 for their bone age and should be distinguished from children with familial short stature for whom height SDS corresponds to mean parental SDS and from the most ...

pmc.ncbi.nlm.nih.gov

you have not GIVEN 1 sOURCE at all. Master's in bro science istg

 

[i cant lie cant lie]

AI (or summarized studies)

Like sure bro i used ai sorry that i didnt waste a fucking hour reading articles that are filled with jargon and impossible to understand words.

What's with looksmax.org issue with ai anyways, the whole fucking forum resents it

 

[Ahmed88]

Related, only.

View attachment 4682970


They fucking dont bro

I gave you non ai source, bro you fucking rat dnrd me

Then why the fuck would it be fda approced for iss dummy
4cm is pretty good and thats the low threshold

View attachment 4682981
Also, people with iss are very similar to people with normal height. They have no syndrome. No issue, no gene. How the fuck does my ai source count genetic mutations if iss is not genetic mutation? Then if it was a mutation it wouldnt be fucking idiopathic?

Here is a source that isnt ai because you are so persistent:

People with Idiopathic Short Stature (ISS) are biologically very similar to people of "normal" or average height, as ISS is defined by a lack of underlying disease, hormonal deficiency, or chromosomal abnormalities. Their health and cognitive development are generally indistinguishable from their peers. The primary differences are physical (height is typically 2 standard deviations or more below the mean) and psychosocial, often stemming from social biases

Idiopathic Short Stature: Conundrums of Definition and Treatment - PMC

Children with idiopathic short stature (ISS) are statistically defined by height SDS < −2 for their bone age and should be distinguished from children with familial short stature for whom height SDS corresponds to mean parental SDS and from the most ...

pmc.ncbi.nlm.nih.gov

you have not GIVEN 1 sOURCE at all. Master's in bro science istg

Bro i do NOT care wether you used ai ITS REASONABLE I GET IT AND I DO NOT CARE AND i do NOT care wether their igf1 levels are lower (mere correlation) thats not the point


YES HGH GROWS ISS BUT WE DONT KNOW WHY THATS MY MAIN POINT

MY OTHER MAIN POINT IS ISS ARE NOT SHORT DUE TO MANLET PARENTS BUT BECAUSE THEY HAVE NO IDENTIFIABLE REASON BEHIND IT AND THATS A FACT AND THERE IS NOT A MOLECULE OF EVIDENCE THAT HGH DOES GROW NORMAL CHILDREN

AS FOR THE STUDIES ALL U NEEDED TO DO WAS CLICK MY SIGNATURE

(It explains everything)

Why HGH is cope and will NOT work for you!!!! (HGH USERS GTFIH!!!)

A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections. It won’t. Why? Let’s get into this 1. How Growth Hormone Actually Works 2. What the Studies ACTUALLY Show 3. Why HGH does NOT work...

looksmax.org

 

[alikay]

Bro i do NOT care wether you used ai ITS REASONABLE I GET IT AND I DO NOT CARE AND i do NOT care wether their igf1 levels are lower (mere correlation) thats not the point


YES HGH GROWS ISS BUT WE DONT KNOW WHY THATS MY MAIN POINT

MY OTHER MAIN POINT IS ISS ARE NOT SHORT DUE TO MANLET PARENTS BUT BECAUSE THEY HAVE NO IDENTIFIABLE REASON BEHIND IT AND THATS A FACT AND THERE IS NOT A MOLECULE OF EVIDENCE THAT HGH DOES GROW NORMAL CHILDREN

AS FOR THE STUDIES ALL U NEEDED TO DO WAS CLICK MY SIGNATURE

(It explains everything)

Why HGH is cope and will NOT work for you!!!! (HGH USERS GTFIH!!!)

A lot of People continue to believe that healthy children who lack growth hormone deficiency will experience height increases through HGH injections. It won’t. Why? Let’s get into this 1. How Growth Hormone Actually Works 2. What the Studies ACTUALLY Show 3. Why HGH does NOT work...

looksmax.org

some guy was fryin yo shi

 

[Ahmed88]

some guy was fryin yo shi

How come

 

[alikay]

How come

they're saying ur shi is js chatgpt

https://looksmax.org/threads/ahmed88-intellectually-disabled-or-trolling.1889868/#post-26436174

 

[Ahmed88]

they're saying ur shi is js chatgpt

https://looksmax.org/threads/ahmed88-intellectually-disabled-or-trolling.1889868/#post-26436174

Yeah just put my shi through ai detector, every hero has his villains

 

[i cant lie cant lie]

YES HGH GROWS ISS BUT WE DONT KNOW WHY THATS MY MAIN POINT

No that is stupid
We literally do.
We have a good understanding of why recombinant human growth hormone (HGH or rhGH) works for children with idiopathic short stature (ISS), though it's not due to a classic deficiency.


ISS is defined as short stature (typically height more than 2–2.25 standard deviations below the mean for age and sex) with no identifiable medical cause after thorough evaluation—no growth hormone deficiency (GHD), chronic illness, genetic syndromes, malnutrition, etc. These kids have normal GH secretion in stimulation tests, but they still respond to exogenous (supplemental) GH therapy.

• Pharmacological (dose-dependent) effect: GH promotes linear growth primarily by stimulating the production of insulin-like growth factor-1 (IGF-1) in the liver and locally at the growth plate in bones. It also directly affects chondrocytes (cartilage cells) to increase proliferation and differentiation, leading to longer bones. In normal physiology, more GH generally means more growth—this is why conditions with GH excess (like gigantism) cause excessive height. In ISS, providing higher-than-normal doses overrides whatever subtle limitations exist in the natural GH/IGF-1 axis, accelerating growth velocity and increasing final adult height. Studies show this is largely a supraphysiological (above-normal) response rather than fixing a specific defect.
• Empiric evidence of efficacy: Multiple clinical trials, meta-analyses, and long-term studies (including FDA approval in 2003 for ISS) demonstrate that GH therapy reliably increases short-term growth rate (e.g., by ~2–3 cm/year initially) and adds modest adult height gain—typically 4–7 cm (about 1.5–3 inches) on average, though results vary by individual, dose, age at start, and duration (often several years of daily injections). For example, controlled studies show treated kids reach heights ~0.8–1 SD better than untreated peers or predictions.

Here it literally says it works on them. Explain why it wouldnt work on us.

MY OTHER MAIN POINT IS ISS ARE NOT SHORT DUE TO MANLET PARENTS BUT BECAUSE THEY HAVE NO IDENTIFIABLE REASON BEHIND IT AND THATS A FACT AND THERE IS NOT A MOLECULE OF EVIDENCE THAT HGH DOES GROW NORMAL CHILDREN

Yea its idiopathic. Its unknown what the cause is. Do you know why its unknown?
Because kids with ISS have no fucking difference between me and you. They have no syndromal issues. No chromosomal issues. No genetic issues. No mutations. They are normal like us.
HENCE. They are normal children. But they are short. That is literally the point of iss. They are short. We dont know why. It has nothing to do with growth hormones. YET, GROWTH HORMONEs DO WORK on them.

Does this not make sense? If it helps them then it helps us lol. Do you need a meta analysis on a non fda approved thesis?
The government cares only about insured and genetic issues. Why would they do a study on normal statured people? They dont have a reason to, JFL. Thats why they do it.



I read your thread:

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)
Are you fucking dumb? Who told you it is genetic? I literally showed you that only 20% of cases are genetic. Are you fucking dumb?
Why is all you do repeat the same points? Have you even refuted one thing?
Its not fucking genetic to have iss if its only 20% of patients.
And how does iss being genetic even affect the efficacy of HGH? You are literally making one loop argument.
This is a logical fallacy. You are begging the question
MUH ITs GENETIC! And? What does that even prove? What genetics affect HGH being better on people with iss? Retard.

 

[Ahmed88]

No that is stupid
We literally do.
We have a good understanding of why recombinant human growth hormone (HGH or rhGH) works for children with idiopathic short stature (ISS), though it's not due to a classic deficiency.


ISS is defined as short stature (typically height more than 2–2.25 standard deviations below the mean for age and sex) with no identifiable medical cause after thorough evaluation—no growth hormone deficiency (GHD), chronic illness, genetic syndromes, malnutrition, etc. These kids have normal GH secretion in stimulation tests, but they still respond to exogenous (supplemental) GH therapy.

• Pharmacological (dose-dependent) effect: GH promotes linear growth primarily by stimulating the production of insulin-like growth factor-1 (IGF-1) in the liver and locally at the growth plate in bones. It also directly affects chondrocytes (cartilage cells) to increase proliferation and differentiation, leading to longer bones. In normal physiology, more GH generally means more growth—this is why conditions with GH excess (like gigantism) cause excessive height. In ISS, providing higher-than-normal doses overrides whatever subtle limitations exist in the natural GH/IGF-1 axis, accelerating growth velocity and increasing final adult height. Studies show this is largely a supraphysiological (above-normal) response rather than fixing a specific defect.
• Empiric evidence of efficacy: Multiple clinical trials, meta-analyses, and long-term studies (including FDA approval in 2003 for ISS) demonstrate that GH therapy reliably increases short-term growth rate (e.g., by ~2–3 cm/year initially) and adds modest adult height gain—typically 4–7 cm (about 1.5–3 inches) on average, though results vary by individual, dose, age at start, and duration (often several years of daily injections). For example, controlled studies show treated kids reach heights ~0.8–1 SD better than untreated peers or predictions.

Here it literally says it works on them. Explain why it wouldnt work on us.


Yea its idiopathic. Its unknown what the cause is. Do you know why its unknown?
Because kids with ISS have no fucking difference between me and you. They have no syndromal issues. No chromosomal issues. No genetic issues. No mutations. They are normal like us.
HENCE. They are normal children. But they are short. That is literally the point of iss. They are short. We dont know why. It has nothing to do with growth hormones. YET, GROWTH HORMONEs DO WORK on them.

Does this not make sense? If it helps them then it helps us lol. Do you need a meta analysis on a non fda approved thesis?
The government cares only about insured and genetic issues. Why would they do a study on normal statured people? They dont have a reason to, JFL. Thats why they do it.



I read your thread:

Let’s clarify: ISS children are not short simply because of genetics. ISS is defined as short stature without a known cause, that INCLUDES GENETICS and many children diagnosed as having ISS have partial GH insensitivity (Evidence: Idiopathic short stature)
Are you fucking dumb? Who told you it is genetic? I literally showed you that only 20% of cases are genetic. Are you fucking dumb?
Why is all you do repeat the same points? Have you even refuted one thing?
Its not fucking genetic to have iss if its only 20% of patients.
And how does iss being genetic even affect the efficacy of HGH? You are literally making one loop argument.
This is a logical fallacy. You are begging the question
MUH ITs GENETIC! And? What does that even prove? What genetics affect HGH being better on people with iss? Retard.

You’re misunderstanding both ISS and how GH works. ISS (idiopathic short stature) is defined as being ≥2–2.25 SD below the mean without an identifiable medical cause, but that doesn’t mean these kids are biologically identical to average-height children. Many are at the extreme lower tail of the height distribution, often below what their genes predict. Their growth plates may respond less efficiently to GH/IGF-1, bone age can be slightly delayed, and there may be subtle inefficiencies in the GH–IGF-1 axis, no one actually knows. “Idiopathic” means no single obvious cause has been identified it does not mean there is no biological or genetic basis.

In contrast, children who are short purely due to short parents (like most of the people who blast chinese ratpiss HGH) are tracking along their genetic growth curve. Growth velocity, bone age, and hormone responses are normal. They are already reaching their genetically programmed height, which is why GH therapy usually has little or no effect in normal children this is backed up by multiple studies not just what someone named Ahmed88 or i cant lie cant lie on .org says.

GH works in ISS because supraphysiologic doses can push the underperforming growth system stimulating IGF-1 and chondrocyte proliferation to increase growth velocity and modestly improve adult height (typically 4–7 cm). It does not make someone taller than their genetic potential. That’s why it works in ISS but would generally not have the same effect in children who are short only due to genetics. I debunked most of this in my thread.

(i still don't understand what you want to prove with the ,,20% are genetic claim''


(+ rep me )

 

[i cant lie cant lie]

You’re misunderstanding both ISS and how GH works. ISS (idiopathic short stature) is defined as being ≥2–2.25 SD below the mean without an identifiable medical cause, but that doesn’t mean these kids are biologically identical to average-height children. Many are at the extreme lower tail of the height distribution, often below what their genes predict. Their growth plates may respond less efficiently to GH/IGF-1, bone age can be slightly delayed, and there may be subtle inefficiencies in the GH–IGF-1 axis, no one actually knows. “Idiopathic” means no single obvious cause has been identified it does not mean there is no biological or genetic basis.

In contrast, children who are short purely due to short parents (like most of the people who blast chinese ratpiss HGH) are tracking along their genetic growth curve. Growth velocity, bone age, and hormone responses are normal. They are already reaching their genetically programmed height, which is why GH therapy usually has little or no effect in normal children this is backed up by multiple studies not just what someone named Ahmed88 or i cant lie cant lie on .org says.

GH works in ISS because supraphysiologic doses can push the underperforming growth system stimulating IGF-1 and chondrocyte proliferation to increase growth velocity and modestly improve adult height (typically 4–7 cm). It does not make someone taller than their genetic potential. That’s why it works in ISS but would generally not have the same effect in children who are short only due to genetics. I debunked most of this in my thread.

(i still don't understand what you want to prove with the ,,20% are genetic claim''


(+ rep me )

Wow, fair enough

 

[cometohaunted]

Why?
You taking aromasin will increase testosterone
Testosterone directly speeds up growth plate closure
so unless you are on a cycle, it would make sense
Also letzorole is more potent and cheapre

Are you fucking retardedtestosterone only boosts growth plate fusion BECAUSE it aromatises into estradiol you dumbass

 

[i cant lie cant lie]

Are you fucking retardedtestosterone only boosts growth plate fusion BECAUSE it aromatises into estradiol you dumbass

..?
Only?!

 

[i cant lie cant lie]

Are you fucking retardedtestosterone only boosts growth plate fusion BECAUSE it aromatises into estradiol you dumbass

if you can give a source for this then go ahead, or rep my post!

 

[cometohaunted]

..?
Only?!

View attachment 4736870

Shut the fuck up retard

 

[i cant lie cant lie]

View attachment 4738650 Shut the fuck up retard

Can you show the full page I mean, tell me a source that tells you it doesn't, since this mostly talks about estradiol


"testosterones role: testosterone stimulates growth and MATURATION" the stimulus of maturation is the acceleration of the growth plates!

 

[i cant lie cant lie]

View attachment 4738650 Shut the fuck up retard

Your post to rep explains everything as you angrily call people retards while showing incorrect information... hence nobody reps your posts

 

[cometohaunted]

Can you show the full page I mean, tell me a source that tells you it doesn't, since this mostly talks about estradiol


"testosterones role: testosterone stimulates growth and MATURATION" the stimulus of maturation is the acceleration of the growth plates!

acceleration doesn't equate to fusion, acceleration is about chondrocyte proliferation because test boosts igf1 activity since testosterone is anabolic and so is igf1 lmfao i'm a grey and you have 4.7k posts and you're this much of a dumb retard. Once again proving my point that how much posts you have genuinely does not fucking matter. If you're a retard, you're a retard. caging at this shit rn

 

[cometohaunted]

Your post to rep explains everything as you angrily call people retards while showing incorrect information... hence nobody reps your posts

idgaf about rep at all, if you're a retard you're a retard most people here arent nice I'm just replicating the same energy. don't confidently be a retard then I can be nice you little soyboy

 

[i cant lie cant lie]

idgaf about rep at all, if you're a retard you're a retard most people here arent nice I'm just replicating the same energy. don't confidently be a retard then I can be nice you little soyboy

Nigga you are literally wrong, you have yet to prove me wrong. Now you resorted back to insulting rather than arguing. Your rep plays a big role and you're a big troll or have a lot to learn!

 

[i cant lie cant lie]

acceleration doesn't equate to fusion, acceleration is about chondrocyte proliferation because test boosts igf1 activity since testosterone is anabolic and so is igf1 lmfao i'm a grey and you have 4.7k posts and you're this much of a dumb retard. Once again proving my point that how much posts you have genuinely does not fucking matter. If you're a retard, you're a retard. caging at this shit rn

Slide the source bro testosterone hormone on its own without igf1 affect closure dude like what do. you not understand

 

[Jesus_ist_König]

Imo Exemestane due to no rebound effect

 

[cometohaunted]

Nigga you are literally wrong, you have yet to prove me wrong. Now you resorted back to insulting rather than arguing. Your rep plays a big role and you're a big troll or have a lot to learn!

you joined 5 months ago please stop the tone policing

 

[i cant lie cant lie]

you joined 5 months ago please stop the tone policing

right

 

[cometohaunted]

Slide the source bro testosterone hormone on its own without igf1 affect closure dude like what do. you not understand

That isn't true, also I just told you testosterone is an anabolic hormone like igf1 meaning it literally objectively leads to growth plate proliferation, that's what acceleration means. it accelerates growth by proliferating the growth plates due to it's anabolic quality. it's the same reason igf1 grows you lmao you dont need a source for that

 

[cometohaunted]

Slide the source bro testosterone hormone on its own without igf1 affect closure dude like what do. you not understand

 

[i cant lie cant lie]

View attachment 4739216

No igf1 mentioned!!

And testosterone, which, in elevated cases [like 60% elevation from aromasin] DOES speed up growth plates!
thanks for proving my point. The significance doesn't matter because these are baseline normal levels, which, when using aromasin isnt normal levels.
Do you not want to delay growth plate closure as far as possible? I mean it would be weird to decrease growth plate closure then to just speed it up marginally... In conclusion, anastrozole > aromasin [in terms of delaying growth plates fusing] which is the whole argument!!!

 

[cometohaunted]

No igf1 mentioned!!

And testosterone, which, in elevated cases [like 60% elevation from aromasin] DOES speed up growth plates!
thanks for proving my point. The significance doesn't matter because these are baseline normal levels, which, when using aromasin isnt normal levels.
Do you not want to delay growth plate closure as far as possible? I mean it would be weird to decrease growth plate closure then to just speed it up marginally... In conclusion, anastrozole > aromasin [in terms of delaying growth plates fusing] which is the whole argument!!!

You're actually a troll lol i understand it nowthat search wasnt about igf1 it was about testosterone not accelerating growth fusion also I didn't even type in significance it just says significance. meaning there's no meaningful increases in fusion, also with aromasin you can keep normal levels you iqlet which is why people cut the pills instead of taking the full 25mg to stay within normal levels and not nuke e2. there's a threshold for when your estradiol increases and starts fusing plates and there's also a lower range where it's unhealthy. people stay within the 11-19 pg range (preferably latter side) to stay healthy lol jfl

 

[i cant lie cant lie]

ep normal levels you iqlet which is why people cut the pills instead of taking the full 25mg to stay within normal levels and not nuke e2. there's a threshold for when your estradiol increases and starts fusing plates and there's also a lower range where it's unhealthy. people stay within the 11-19 pg range (preferably latter side) to stay healthy lol jfl

? people cut every type off pill, its not aromasin
And yes thank you for admitting the fact.. But above physiological ranges of testosterone is gonna increase closure no matter how you inhibit estrogen.Otherwise your plates would never fuse if you kept nuking e2. Also, aromasin is harder to dose, it's effect isnt linear

So doubling the dose of anastrozole would double the effects. But doubling aromasin doesn't double effects
Anastrozole is more potent that aromasin too. So unless you are a retard who misses his doses, there's no point in not picking anastrozole

 

[Zagro]

Its google ai you dumbass. It sumarizes what i got from the search so i dont have to skim articles to find proof.

Just read the shit you sent me bro. It literally says these things are correlated and is little evidence, not even an answer.

Idiopathic short stature (ISS) is characterized by a height more than two standard deviations below the corresponding mean height of a given age, sex, and population group without evidence of systemic, endocrine, nutritional, or chromosomal abnormalities, and normal stimulated growth hormone levels. While growth is influenced by genetic, nutritional, hormonal, and environmental factors, ISS remains a diagnosis of exclusion after ruling out systemic, endocrine, or chromosomal disorders. Although multiple genes have been linked to be associated with linear growth, they account only for a small proportion of cases of short stature. Advances in genetic testing, including whole-exome sequencing and copy number variant analysis, have improved diagnostic precision, yet the yield remains low. Mutations in genes SHOX, ACAN, natriuretic peptide receptor-B, and insulin-like growth factor 1 receptor along with epigenetic factors have been implicated in ISS. Identifying pathogenic variants aids in personalized management, early detection of comorbidities, and genetic counseling. This review compiles current insights into genetic basis of ISS, emphasizing the need for further research to unravel its complex etiology and improve management strategies for affected individuals.


They have no abnormalities or systemic issue or endocrine issue. The problem has nothing to do with HGH so it would be stupid to say they have a better reaction when they fucking have it worse

And jfl at the not normal. Obviously they are not normal, they are 2 standard deviations lower than the average person it terms of height.



Every person has different igf1r gene. some subtly. some a lot
And im gonna give you the source because "Muh you used ai!!" but you didnt disprove my fucking point, idiot.

Large-scale analysis of variation in the insulin-like growth factor family in humans reveals rare disease links and common polymorphisms

The insulin-like growth factors IGF1 and IGF2 are closely related proteins that are essential for normal growth and development in humans and other sp…

www.sciencedirect.com

But again, we should review
Its, not fucking genetic. Its around 20% of cases. That low number proves that its a mere correlation and not the final answer.

View attachment 4682785


It doesnt matter how much you argue. Iss is Iss. Idiopathic short stature. Idiopathic. Any "Discovery" you make doesnt fucking matter because if it was one then it wouldnt be idiopathic, dumbass.

All you show is correlation as proof. Thats not an answer. That is dissonance. You just want to be right.

Bro ignore him lol

 

[birthdefect]

Why?
You taking aromasin will increase testosterone
Testosterone directly speeds up growth plate closure
so unless you are on a cycle, it would make sense
Also letzorole is more potent and cheapre

letrozole SIGNIFICANTLY increases testosterone because its the best ai to lower peripheral aromatisation, twice as much as arimidex iirc
this doesnt necessarily lead to better results for height btw

arimidex is best for this purpose

 

[cometohaunted]

? people cut every type off pill, its not aromasin
And yes thank you for admitting the fact.. But above physiological ranges of testosterone is gonna increase closure no matter how you inhibit estrogen.Otherwise your plates would never fuse if you kept nuking e2. Also, aromasin is harder to dose, it's effect isnt linear
View attachment 4739572
So doubling the dose of anastrozole would double the effects. But doubling aromasin doesn't double effects
Anastrozole is more potent that aromasin too. So unless you are a retard who misses his doses, there's no point in not picking anastrozole

1. Never even said people only cut aromasin or dont cut every type of pill u idiot, 2. (Repeats claim that we've been debating on with 0 evidence) lol repeating your claim that higher test is gonna fuse no matter how you inhibit estradiol isn't evidence. dont go off topic about how to dose aromasin I really don't care for the whole anastrozole letrozole exemestane argument of what is better it doesn't change the core of the debate that test doesn't drive growth plate fusion without an estradiol threshold reached ts is cagefuel

 

[Zagro]

1. Never even said people only cut aromasin or dont cut every type of pill u idiot, 2. (Repeats claim that we've been debating on with 0 evidence) lol repeating your claim that higher test is gonna fuse no matter how you inhibit estradiol isn't evidence. dont go off topic about how to dose aromasin I really don't care for the whole anastrozole letrozole exemestane argument of what is better it doesn't change the core of the debate that test doesn't drive growth plate fusion without an estradiol threshold reached ts is cagefuel

Are you retarded?

You don't have to reach a "estradiol threshold" for testosterone to drive growth plate fusion, any amount of is is enough to start driving growth plate fusion

 

[cometohaunted]

Are you retarded?

You don't have to reach a "estradiol threshold" for testosterone to drive growth plate fusion, any amount of is is enough to start driving growth plate fusion

Are you retarded?

There is a threshold of estradiol necessary to drive complete growth plate fusion. Also testosterone does not drive growth plate fusion on its own lmfao you have one of the most reputable botb posts and you're saying this retarded shit lol estradiol is what causes plates to close it's as simple as that. Within estradiol though there is a critical number/threshold needed for plates to actually close.

it's a similar principle to the fact there are males with aromatase deficiencies and they just never stopped growing since their estradiol wasn't at this range, studies were done on these types of men by giving them transdermal estradiol and their plates only fused at 20 pg/ml. Free knowledge. So anything above 20pg will fuse and staying a good amount below that will not

 

[Zagro]

Are you retarded?

There is a threshold of estradiol necessary to drive complete growth plate fusion. Also testosterone does not drive growth plate fusion on its own lmfao you have one of the most reputable botb posts and you're saying this retarded shit lol estradiol is what causes plates to close it's as simple as that. Within estradiol though there is a critical number/threshold needed for plates to actually close.

it's a similar principle to the fact there are males with aromatase deficiencies and they just never stopped growing since their estradiol wasn't at this range, studies were done on these types of men by giving them transdermal estradiol and their plates only fused at 20 pg/ml. Free knowledge. So anything above 20pg will fuse and staying a good amount below that will not

This is funny i would want to teach you but not now wait for my reply in a bit

You are contradicting yourself multiple times in this reply that's even more hilarous, don't take my reply here as an insult

 

[cometohaunted]

This is funny i would want to teach you but not now wait for my reply in a bit

You are contradicting yourself multiple times in this reply that's even more hilarous, don't take my reply here as an insult

Sure, we'll see how I'm contradicting myself

 

[i cant lie cant lie]

1. Never even said people only cut aromasin or dont cut every type of pill u idiot, 2. (Repeats claim that we've been debating on with 0 evidence) lol repeating your claim that higher test is gonna fuse no matter how you inhibit estradiol isn't evidence. dont go off topic about how to dose aromasin I really don't care for the whole anastrozole letrozole exemestane argument of what is better it doesn't change the core of the debate that test doesn't drive growth plate fusion without an estradiol threshold reached ts is cagefuel

1. Idk then why the fuck did you mention this?

aning there's no meaningful increases in fusion, also with aromasin you can keep normal levels you iqlet which is why people cut the pills instead of taking the full 25mg to stay within normal levels and not nuke e2.

What's the point of not cutting pills? Are you just gonna put convenience over efficiency?
2. I am the only one who presented evidence, you make bizarre claims with no evidence which can be easily disputed due to that:
Testosterone doesn't drive growth plate fusion.
But that's beside the point. The fact that it affects epiphyseal growth plate fusion is enough to understand that, if you want to optimize delaying fusion, you must make sure to not elevate testosterone levels. Hence:
we got 3 aromatase inhibitor types:
Aromasin increases testosterone [hence it's suboptimal for delaying fusion]
So does letzorole!

Arimidex [anastrozole] doesn't increase testosterone. Hence it is the best for delaying growth plate closure. What else is hard to understand?
Why would you pick aromasin, a compound which is suboptimal in delaying closure, when you can pick arimidex, which is way more potent and doesn't increase testosterone?

Is it solely due to convenience? Really? Would you use Testosterone Undecanoate instead of Testosterone Propionate, just because of convenience? I mean, arimidex is cheaper, more potent, why else would you pick aromasin...

really don't care for the whole anastrozole letrozole exemestane argument of what is better

It proves to me you are a troll trying to bring me down or something. This thread is literally about what is the best AI, yet you don't care? you just want to argue????
You literally went to another thread and clowned me for a mistake [Mirin necropost, that shit was 3 weeks ago, I could get you.a warning]

it doesn't change the core of the debate that test doesn't drive growth plate fusion without an estradiol threshold reached ts is cagefuel

1. "it doesn't change the core of the debate that test doesn't drive growth plate fusion" I explained it in this reply so I assume if you will dispute this then read what I said a few sentences ago.
2. "without an estradiol threshold reached" what threshold? Growth plates work since infancy bro what are you even saying It's called bone age, E2 advances your bone age maturation, that's how your growth plates fuse, bro they dont start fusing after reaching a threshold What threshold? Only if you have 0pg/ml of E2 concentration in your blood [Which, in even aromatase deficient people, is impossible] will your bone age not mature [hence the only possible way is an impossible route, hence your threshold is literally B.S! I'd like you to provide a source]. Yet it will still advance because of testosterone....!

 

[Sayan.xdd]

..?
Only?!

View attachment 4736870

thats false since bone maturation only happens via the ERa pathway. androgens by themselves dont have the properties to mature bones. that process happens through aromatization to estrogen

theres also a study where high dose testosterone was given for 6 months to an aromatase deficient male and it didn’t advance his bone age or close his epiphyses. only when he was given estradiol did his growth plates fuse

similarly theres another study where 46,XY individuals with complete androgen insensitivity still achieve normal epiphyseal fusion because estrogen is produced peripherally and acts through ERa even though the androgen receptor doesnt function

 

[i cant lie cant lie]

ats false since bone maturation only happens via the ERa pathway. androgens by themselves dont have the properties to mature bones. that process happens through aromatization to estrogen

Completely false statement. I'd like you to back it up with proof

theres also a study where high dose testosterone was given for 6 months to an aromatase deficient male and it didn’t advance his bone age or close his epiphyses. only when he was given estradiol did his growth plates fuse

Link the study.
Also that's an aromatase deficient male. These niggas have 1 picogram of e2 in their blood. We can't compare it to us, what you could compare with, would be ISS kids who took Aromasin/Arimidex/Letzorole, since they are the closest to us normal people.

similarly theres another study where 46,XY individuals with complete androgen insensitivity still achieve normal epiphyseal fusion because estrogen is produced peripherally and acts through ERa even though the androgen receptor doesnt function

This is outright false too.
If you have androgen insensitivity, your epiphyses will be delayed!

 

[Sayan.xdd]

Also that's an aromatase deficient male. These niggas have 1 picogram of e2 in their blood. We can't compare it to us, what you could compare with, would be ISS kids who took Aromasin/Arimidex/Letzorole, since they are the closest to us normal people.

aromatase deficient patients are actually one of the most informative human models for studying the role of estrogen in skeletal maturation. because they cant convert testosterone to estradiol they allow us to observe what happens when androgen signaling is present but estrogen signaling is absent. this is literally the main point of the argument.

id link the studies but i dont know if its worth my time

This is outright false too.
If you have androgen insensitivity, your epiphyses will be delayed!

whats false? fusion can still occur in the absence of functional androgen receptors. the point is that androgen signaling itself is not required for the process.

i appreciate your response but i dont think you're grasping what im arguing for.

 

[i cant lie cant lie]

aromatase deficient patients are actually one of the most informative human models for studying the role of estrogen in skeletal maturation. because they cant convert testosterone to estradiol they allow us to observe what happens when androgen signaling is present but estrogen signaling is absent. this is literally the main point of the argument.

id link the studies but i dont know if its worth my time


whats false? fusion can still occur in the absence of functional androgen receptors. the point is that androgen signaling itself is not required for the process.

i appreciate your response but i dont think you're grasping what im arguing for.

Again, a google search is enough to disprove the androgen insensitivity and ER pathway...
so all im waiting for is the study..!

 

[Sayan.xdd]

obviously there are much more studies

Again, a google search is enough to disprove the androgen insensitivity and ER pathway...

theres something called epistemological evaluation. knowledge requires JTB based on observed cases. google saying x doesnt suffice

 

[i cant lie cant lie]

obviously there are much more studies

theres something called epistemological evaluation. knowledge requires JTB based on observed cases. google saying x doesnt suffice

this isn't clear evidence
Estrogen being the main driver of fusion does not prove anything about androgens
In the 2nd picture, it also never talks about the effect of androgens. Even though they reached average female height., this doesnt prove anything with androgens, since these people have the estrogens of a woman.I mean, you cant give an androgen to a woman and expect same effects with men...
Additionally, the third example is too nuanced... The aromatase deficient people already have very elevated levels of T, this doesn't apply to us