AAS and growth plates

[micheal_2884]

(This was a reply but thought I’d make it a post since it’s something I’ve seen heavily debated)
To all the ppl saying that aromitizng AAS during puberty will accelerate growth plate closure despite the usage of Aromitase inhibitors here is what I have to say:


Aromatase inhibitors act within the bone tissue and growth plates aswell. Think about it, if AIs didn’t stop local aromitization why do they consistently yield a FAH that is greater than expected FAH in studies? Blood Serium estradiol levels are pretty indicative of local Estradiol levels in the bone and nearby tissues. Also, Androgens can cause some maturation of growth plates but cannot close the Epiphyseal plates on their own. This is why men with Aromitase enzyme defficiency continue to grow into adulthood aswell as males with estrogen receptor mutations. And this is despite them having normal to high testosterone levels. Their levels are sometimes higher than normal because their body produces more testosterone do to lack of estrogen or what seems like it (acting as a natural SERM).

TLDR: I do not belive when E2 is kept low that super physiological levels of testosterone or androgens accelerate Epiphyseal plate closure. If anything they can promote growth through androgenic activity (look at the study where boys were given halotestin and acheived a FAH greater than expected).

 

[smalldik97]

too much causes epiphyseal senescence

 

[davdon123678]

(This was a reply but thought I’d make it a post since it’s something I’ve seen heavily debated)
To all the ppl saying that aromitizng AAS during puberty will accelerate growth plate closure despite the usage of Aromitase inhibitors here is what I have to say:


Aromatase inhibitors act within the bone tissue and growth plates aswell. Think about it, if AIs didn’t stop local aromitization why do they consistently yield a FAH that is greater than expected FAH in studies? Blood Serium estradiol levels are pretty indicative of local Estradiol levels in the bone and nearby tissues. Also, Androgens can cause some maturation of growth plates but cannot close the Epiphyseal plates on their own. This is why men with Aromitase enzyme defficiency continue to grow into adulthood aswell as males with estrogen receptor mutations. And this is despite them having normal to high testosterone levels. Their levels are sometimes higher than normal because their body produces more testosterone do to lack of estrogen or what seems like it (acting as a natural SERM).

TLDR: I do not belive when E2 is kept low that super physiological levels of testosterone or androgens accelerate Epiphyseal plate closure. If anything they can promote growth through androgenic activity (look at the study where boys were given halotestin and acheived a FAH greater than expected).

AIs are amazing for stopping estrogen from closing the growth plates but running a heavy blast created a massive substrate diff that causes an E2 leak and that high androgen load leads to a growth plate burnout capping your height potential regardless of serum levels