Aromasin Nukes Estrogen Permanently??

[Deleted member 24582]

In women who have gone through menopause, estrogen is mainly produced by the aromatase enzyme, which converts androgens (sex hormones produced by the adrenal glands) into estrogens. Exemestane binds to aromatase, changing the protein permanently. This change "turns off" aromatase so that it can no longer make estrogen.


Is this actually true? so if you take aromasin and it nukes your estrogen and you feel like shit youre basically fucked forever? Bone mass would be fucked too.

 

[DarkoTheNihilist]

In women who have gone through menopause, estrogen is mainly produced by the aromatase enzyme, which converts androgens (sex hormones produced by the adrenal glands) into estrogens. Exemestane binds to aromatase, changing the protein permanently. This change "turns off" aromatase so that it can no longer make estrogen.


Is this actually true? so if you take aromasin and it nukes your estrogen and you feel like shit youre basically fucked forever? Bone mass would be fucked too.

That info it’s slightly wrong. Its a competitive inhibitor so it binds to the active site, occupying the aromatase permanently. Btw dumbass that doesnt mean your body wont create new enzymes. Estrogen comes back it just takes a 3-5 days according to the literature due to Asin’s 1 day half life. Arimidex and letrozole bind to the an allosteric site and denature the enzyme reversibly but the have half life of 2 days. Like they teach you this shit In biology class thats why you dumbasses gotta pay attention. Mabye start brainmaxxing lol. Btw no your bone mass wont take hit until years of use and even then its not gonna be that significant. And why tf do you mfs care about bone mass anyway its not like you actually play sports you just sit in your room all day browsing these forums like a hermit.
Btw did I say youre a dumbass

 

[Osie]

In women who have gone through menopause, estrogen is mainly produced by the aromatase enzyme, which converts androgens (sex hormones produced by the adrenal glands) into estrogens. Exemestane binds to aromatase, changing the protein permanently. This change "turns off" aromatase so that it can no longer make estrogen.


Is this actually true? so if you take aromasin and it nukes your estrogen and you feel like shit youre basically fucked forever? Bone mass would be fucked too.

Nigga you constantly produce aromatase though, so you're good. However, I heard the suppressed E2 effect last longer in your body despite the drug having a shorter half-life. However, supplementing with Vitamin D3, K2, and Calcium reduces and inhibits bone effects.

 

[Osie]

That info it’s slightly wrong. Its a competitive inhibitor so it binds to the active site, occupying the aromatase permanently. Btw dumbass that doesnt mean your body wont create new enzymes. Estrogen comes back it just takes a 3-5 days according to the literature due to Asin’s 1 day half life. Arimidex and letrozole bind to the an allosteric site and denature the enzyme reversibly but the have half life of 2 days. Like they teach you this shit In biology class thats why you dumbasses gotta pay attention. Mabye start brainmaxxing lol. Btw no your bone mass wont take hit until years of use and even then its not gonna be that significant. And why tf do you mfs care about bone mass anyway its not like you actually play sports you just sit in your room all day browsing these forums like a hermit.
Btw did I say youre a dumbass

Does e2 actually come back in days, could you list the study where it says that? I'm not saying I don't believe you, I just thought that your E2 is suppressed for longer periods of time despite the drug leaving your system faster than both Letrozole and Arimidex.

 

[Gaygymmaxx]

Nah it doesn't fuck nigga

 

[DarkoTheNihilist]

Does e2 actually come back in days, could you list the study where it says that? I'm not saying I don't believe you, I just thought that your E2 is suppressed for longer periods of time despite the drug leaving your system faster than both Letrozole and Arimidex.

Suppression lasts several days after dosing with both competitive and non competitive inhibitors. Although aromasin has a shorter half-life, it's mechanism of action is more long-lasting. Nevertheless, their effect while and after dosing is the same (considering you're not on steroids).

Btw idk why tf all you guys think aromasin is inherently better than arimidex or letrozole. Estrogen rebound is only a concern in individuals artificially modulating their serum testosterone concentrations, essentially ignoring the HPTA feedback loop. If youre not fucking anabolic steroids, your testosterone proportionately decrease with E2 gradually returning to baseline, so that there is less substrate for the enzyme. Like do the fucking math: if the half life of arimidex is 2 days and you stop cold turkey, your blood E2 would go
to 0.5mg 2 days after ---> 0.25mg 4 days after ---> 0.125 mg 6 days after ---> and so on
It's not like you miss one day of dosing and all of a sudden you have an E2 of 80pg/mL appear outta nowhere. And it's not like the pharmakinetics of these drugs wasn't taken into considering while they were being developed. Like for fucksake these are third-generation aromatase inhibitors for treating estrogen-dependent breast cancer. They sure fucking accounted for this possibility.
Not to mention if wanna be ultra safe just taper the dosage like you're intended to do with almost every pharmaceutical drug ITS NOT FUCKING ROCKET SCIENCE

On top of that, there is not a single study in the academic literature that uses Aromasin/exemestane to treat children with idiopathic short stature or GH deficency. Like doctors are perscribing arimidex and letrozole to fucking 12 year olds. Do you think they didn't take estrogen rebound into consideration when these kids probably forget to dose a couple times every month. Additionally, its not like if your E2 goes over that supposed "20pg/mL threshold" for a short period of time that epiphyseal ossifcation immediatley occurs with days. Like no bro this process takes years of peaked E2 signaling to completely induce. Again THIS IS GIVEN TO 12 YEAR OLDS.

Like if you're not at least going to browse through a few pubmed studies to verify the knowledge you guys hold so true to your hearts, then you shouldn't be in this biohacking niche. Like it is baffling to me there are still motherfuckers who think "sleepstrecthing" or tibial microfractures work. Like is it that fucking difficult to watch a video or read a single article on the physiology on of hypertrophic GP chondrocytes and how growth actually occurs. SPOILER ALERT, bones don't actually grow by "stretching" they grow by BUILDING osteoblast along the resting region of the epiphysis. Like for fucksake did Tyler Davis write all those articles on heightquest.com for nothing. like read motherfucker READ!!!

note - i know this kinda turned into a rant but if you dumbasses ever ask a stupid ass question like this again, you deserve to publicly crucified and burned at the stake in the next life cuz I cant keep explaining this bullshit any more.

 

[longjohnmong]

imagine thinking you only have so much of some enzyme and can never get more lmao

 

[Osie]

Btw idk why tf all you guys think aromasin is inherently better than arimidex or letrozole. Estrogen rebound is only a concern in individuals artificially modulating their serum testosterone concentrations, essentially ignoring the HPTA feedback loop. If youre not fucking anabolic steroids, your testosterone proportionately decrease with E2 gradually returning to baseline, so that there is less substrate for the enzyme. Like do the fucking math: if the half life of arimidex is 2 days and you stop cold turkey, your blood E2 would go
to 0.5mg 2 days after ---> 0.25mg 4 days after ---> 0.125 mg 6 days after ---> and so on
It's not like you miss one day of dosing and all of a sudden you have an E2 of 80pg/mL appear outta nowhere. And it's not like the pharmakinetics of these drugs wasn't taken into considering while they were being developed. Like for fucksake these are third-generation aromatase inhibitors for treating estrogen-dependent breast cancer. They sure fucking accounted for this possibility.
Not to mention if wanna be ultra safe just taper the dosage like you're intended to do with almost every pharmaceutical drug ITS NOT FUCKING ROCKET SCIENCE

On top of that, there is not a single study in the academic literature that uses Aromasin/exemestane to treat children with idiopathic short stature or GH deficency. Like doctors are perscribing arimidex and letrozole to fucking 12 year olds. Do you think they didn't take estrogen rebound into consideration when these kids probably forget to dose a couple times every month. Additionally, its not like if your E2 goes over that supposed "20pg/mL threshold" for a short period of time that epiphyseal ossifcation immediatley occurs with days. Like no bro this process takes years of peaked E2 signaling to completely induce. Again THIS IS GIVEN TO 12 YEAR OLDS.

I did not say that Aromasin is better than Arimidex or Letrozole. You joined the site on the 17th of February and have probably been lurking on this site for months before. You are just regurgitating information already said here but saying it in long-form paragraphs. And no, not everybody is re-reading the 2012 forum posts made by "Tyler Davis." Obviously, those articles have it's purpose but his research was still largely unproven and not useful for teenagers on a forum like this. It does not take years for estradiol to peak for growth plate closure lol, you wanna know why because when they injected Aromatase deficient people (male or female) with estradiol, it took only half a year month for their plates to close.
"Transdermal estrogen therapy led to a closure of epiphyseal cartilage and to a slight increase in bone age (from a mean bone age of 15 yr before estradiol treatment to a mean bone age higher than 17 yr after at least 6 months of estradiol treatment) and height (with a mean gain of 1 cm in height) in all aromatase-deficient men."

" if you dumbasses ever ask a stupid ass question like this again, you deserve to be publicly crucified and burned at the stake in the next life cuz I can't keep explaining this bullshit anymore." - lol who are you bro, don't go around insulting people without listing a study first. Once your test and e2 are in adult ranges, your growth plates will begin rapidly aging for the context of most people on this site. Nobody on this site is 12, so getting off an AI for them is much worse than it would be for a 12-year-old. As the longer you are off an AI, the more the growth plate closes, and the less growth potential you can squeeze out of the growth plates. I DO AGREE though that people should stop being so scared of non-steroidal AIs, your e2 will be fine off it anyways and plates can not close that fast.

 

[Osie]

On top of that, there is not a single study in the academic literature that uses Aromasin/exemestane to treat children with idiopathic short stature or GH deficency. .

I don't know if it matters that Exemestane hasn't been used to treat children with ISS or GHD, as the case it has been used in shows its efficiency well enough. It also shows that Letrozole may block too much E2 leading to lower results of height.
They did a study on a At the age of 6 years and 3 months, a boy with salt-losing CAH presented with a BA 7 years in advance. Treatment with an AI (exemestane) was initiated to decelerate bone maturation. His PAH was 151cm but they put him on 25MG a day of Aromasin, and then he ended with a NAH of 177cm. His bone age only changed by 2 years in the nine years he was using Aromasin.

"His BA had increased to 13 years at age 6 years and 3 months, and For that reason, treatment was started with an AI, once daily 25 mg Aromasin (exemestane), to decelerate bone maturation. After 2.5 years of AI treatment, at the age of 8 years and 9 months bone maturation had decelerated and his BA had remained 13 years. At age 12 years and 6 months, BA had remained 13.5 years of age. At the age of 15 years and 9 months, BA was similar to the calendar age.

 

[TeenAscender]

I don't know if it matters that Exemestane hasn't been used to treat children with ISS or GHD, as the case it has been used in shows its efficiency well enough. It also shows that Letrozole may block too much E2 leading to lower results of height.
They did a study on a At the age of 6 years and 3 months, a boy with salt-losing CAH presented with a BA 7 years in advance. Treatment with an AI (exemestane) was initiated to decelerate bone maturation. His PAH was 151cm but they put him on 25MG a day of Aromasin, and then he ended with a NAH of 177cm. His bone age only changed by 2 years in the nine years he was using Aromasin.

"His BA had increased to 13 years at age 6 years and 3 months, and For that reason, treatment was started with an AI, once daily 25 mg Aromasin (exemestane), to decelerate bone maturation. After 2.5 years of AI treatment, at the age of 8 years and 9 months bone maturation had decelerated and his BA had remained 13 years. At age 12 years and 6 months, BA had remained 13.5 years of age. At the age of 15 years and 9 months, BA was similar to the calendar age.

Lifefuel

 

[Osie]

Lifefuel

literally, just use 25MG a day and the effects should be just as good if not better than non-steroidal AI's

 

[TeenAscender]

literally, just use 25MG a day and the effects should be just as good if not better than non-steroidal AI's

I was on 12.5mg every 1.5 days for 8 months like a year ago then took a 6 month hiatus, I just turned 17. Definetely need to hop in again ASAP to salvage extra fractions of an inch as I’ve only grown 1.5 inches in the past 12 months