Looksmax Water fact as to why reducing total aromatase activity won’t save fusion (1 Viewer)

[Mandy]

Niggas really don’t understand,that estradiol (E2) can be tissue localized or circulatory (systemic). A aromatase inhibitor will mainly target your circulatory estradiol or tissues such as adipose tissue,since it’s the easiest shot for antagonism rather than tissues that can’t be fully saturated with it such as the epiphyseal plate. And your body compensates,simply because your body doesn’t want to unnecessarily get rid of hormones so in theory:

-Circulatory estradiol downregulates. (via aromasin)
-Localized estradiol upregulates back to its normal level. (epiphyseal plate)

The aromatization happens locally,it doesn’t reach your blood first then gets transferred to tissue.

Even if you manage to inhibit the Aromatese enzyme locally,the co factor localized estradiol enzymes in the epiphyseal plate will upregulate and compensation for the lack of aromatization,such as HSD17B1, 7 and 4. This way the lack of Aromatese will be compensated by e1->e2 conversion. After a while this conversion can downregulate and eventually cause your chondrocytes to slow down proliferation.

E2 just finishes the plate fusion,inhibiting it won’t really cause it to grow for longer periods but rather just halt total growth till you have ideal levels again. The reason why I tell people to not play around with AI when they’re not on test is because they’re blindly lowering the levels,they don’t already know their natural baseline level which could lower e2 too much.

 

[bob08674]

Ok

 

[Razi]

ocean

 

[BastiHgH]

Niggas really don’t understand,that estradiol (E2) can be tissue localized or circulatory (systemic). A aromatase inhibitor will mainly target your circulatory estradiol or tissues such as adipose tissue,since it’s the easiest shot for antagonism rather than tissues that can’t be fully saturated with it such as the epiphyseal plate. And your body compensates,simply because your body doesn’t want to unnecessarily get rid of hormones so in theory:

-Circulatory estradiol downregulates. (via aromasin)
-Localized estradiol upregulates back to its normal level. (epiphyseal plate)

The aromatization happens locally,it doesn’t reach your blood first then gets transferred to tissue.

Even if you manage to inhibit the Aromatese enzyme locally,the co factor localized estradiol enzymes in the epiphyseal plate will upregulate and compensation for the lack of aromatization,such as HSD17B1, 7 and 4. This way the lack of Aromatese will be compensated by e1->e2 conversion. After a while this conversion can downregulate and eventually cause your chondrocytes to slow down proliferation.

E2 just finishes the plate fusion,inhibiting it won’t really cause it to grow for longer periods but rather just halt total growth till you have ideal levels again. The reason why I tell people to not play around with AI when they’re not on test is because they’re blindly lowering the levels,they don’t already know their natural baseline level which could lower e2 too much.

 

[Judenbänker]

stop destroying my copes

 

[Ascension]

Niggas really don’t understand,that estradiol (E2) can be tissue localized or circulatory (systemic). A aromatase inhibitor will mainly target your circulatory estradiol or tissues such as adipose tissue,since it’s the easiest shot for antagonism rather than tissues that can’t be fully saturated with it such as the epiphyseal plate. And your body compensates,simply because your body doesn’t want to unnecessarily get rid of hormones so in theory:

-Circulatory estradiol downregulates. (via aromasin)
-Localized estradiol upregulates back to its normal level. (epiphyseal plate)

The aromatization happens locally,it doesn’t reach your blood first then gets transferred to tissue.

Even if you manage to inhibit the Aromatese enzyme locally,the co factor localized estradiol enzymes in the epiphyseal plate will upregulate and compensation for the lack of aromatization,such as HSD17B1, 7 and 4. This way the lack of Aromatese will be compensated by e1->e2 conversion. After a while this conversion can downregulate and eventually cause your chondrocytes to slow down proliferation.

E2 just finishes the plate fusion,inhibiting it won’t really cause it to grow for longer periods but rather just halt total growth till you have ideal levels again. The reason why I tell people to not play around with AI when they’re not on test is because they’re blindly lowering the levels,they don’t already know their natural baseline level which could lower e2 too much.

I think this might be water

 

[Mandy]

I think this might be water

Maybe…

 

[h21ei]

idk bro don't ask me I'm just here for the free food

 

[Z1gler7]

Niggas really don’t understand,that estradiol (E2) can be tissue localized or circulatory (systemic). A aromatase inhibitor will mainly target your circulatory estradiol or tissues such as adipose tissue,since it’s the easiest shot for antagonism rather than tissues that can’t be fully saturated with it such as the epiphyseal plate. And your body compensates,simply because your body doesn’t want to unnecessarily get rid of hormones so in theory:

-Circulatory estradiol downregulates. (via aromasin)
-Localized estradiol upregulates back to its normal level. (epiphyseal plate)

The aromatization happens locally,it doesn’t reach your blood first then gets transferred to tissue.

Even if you manage to inhibit the Aromatese enzyme locally,the co factor localized estradiol enzymes in the epiphyseal plate will upregulate and compensation for the lack of aromatization,such as HSD17B1, 7 and 4. This way the lack of Aromatese will be compensated by e1->e2 conversion. After a while this conversion can downregulate and eventually cause your chondrocytes to slow down proliferation.

E2 just finishes the plate fusion,inhibiting it won’t really cause it to grow for longer periods but rather just halt total growth till you have ideal levels again. The reason why I tell people to not play around with AI when they’re not on test is because they’re blindly lowering the levels,they don’t already know their natural baseline level which could lower e2 too much.

 

[Godveil Heir]

doubt it'll be compensated fully
trials with AI say otherwise
no reason to not take ai as a teen 13-16

 

[Mandy]

doubt it'll be compensated fully
trials with AI say otherwise
no reason to not take ai as a teen 13-16

Blindly reducing estradiol? Also,I’m trying to figure out the trials,sounds low IQ but ye.

 

[Godveil Heir]

Blindly reducing estradiol? Also,I’m trying to figure out the trials,sounds low IQ but ye.

for a short time, as an early teen

other benefits are 0 risk of gyno and low risk of getting fat
and it does increase height somewhat.

ideally, you should be taking test & gh with it

 

[Mandy]

for a short time, as an early teen

other benefits are 0 risk of gyno and low risk of getting fat
and it does increase height somewhat.

ideally, you should be taking test & gh with it

Water,but SERMs work better for gyno in my opinion.

 

[Godveil Heir]

Water,but SERMs work better for gyno in my opinion.

agree, SERMs do mog for that
but might aswell just take AI, for added benefits
and it's giga cheap, will almost certainly eliminate gyno risk

 

[Synapzyzz]

u should make a yt/ tik tok account to upload this info, i got so entertained reading this and would've been even better if this had a minecraft parkour or background gameplay, this would be so good for individual retarded like me, please consider this!

 

[Mandy]

u should make a yt/ tik tok account to upload this info, i got so entertained reading this and would've been even better if this had a minecraft parkour or background gameplay, this would be so good for individual retarded like me, please consider this!

Bookmarked,I always thought of making videos on stuff like this on YouTube.

 

[oyopth31]

D17B1, 7 and 4. This way the lack of Aromatese will be compensated by e1->e2 conversion. After a while this conversion can downregulate and eventually cause your chondrocytes to slow down proliferation.

Aromatase is the only way to make E1 HSD needs E1 to make E2 without aromatase no estrogen therefore no E-2 or E-1

AIs are systemic and have successfully proven to delay bone maturation from quite a few clinical trials in ISS
Aditonally people with aromatase deficiency grow abnomally tall
Additionally, its a very well-known fact so beside all of this hypothetical sience just the real life evidences point to the fact that aromatase does delay bone maturation.
Clinical trials show that AIs increase the risk of bone loss and fractures. These trials specifically measure bone response.
If the drug didn't reach and saturate bone tissue, it wouldn't cause these side effects.

here are all the trials for those curious.
Hero et al. (2005): A randomized controll trial of 31 boys with ISS found that the boys who were treated with letrozole were able to achieve a 5.9 cm increase in PAH compared to the placebo group.

Mauras et al. (2008 & 2016): These trials studied the effect of anastrozole in boys with Growth Hormone Deficiency (GHD) and ISS.
In GHD patients, 36 months of anastrozole plus growth hormone (GH) resulted in a 6.7 cm increase in predicted adult height.
In ISS patients, those on the AI combination gained significantly more height than those on GH alone (22.5 cm vs 20.6 cm).
https://pubmed.ncbi.nlm.nih.gov/18165285/
https://pmc.ncbi.nlm.nih.gov/articles/PMC5155684/

Wickman et al. (2001): This trials were on boys with CDGP. treatment with letrozole effectively delayed the maturation of these bones, leading to a 5.1 cm increase in PAH after 18 months.
maturation and led to a 5.1 cm increase in predicted adult height after 18 months.
https://pubmed.ncbi.nlm.nih.gov/11403810/

Yackobovitch-Gavan et al. (2025): A recent retrospective study showed that mid-pubertal boys treated with an AI alone achieved a final adult height 3.2 cm taller than untreated controls (166.6 cm vs 163.4 cm).
https://pubmed.ncbi.nlm.nih.gov/40193585/
Haynes et al. (2003):This study showsthat letrozole achieves over 99% total body inhibition of aromatization. A 99% would be impossible if ais weere blocked from local tissues such as the growth plates.
https://pubmed.ncbi.nlm.nih.gov/14630089/
Across all trials, the most consistent finding is that AIs slow down bone age advancement height.
The conclusion is that ais still do work for height purposes

So that's really all I have to sayy however, if there is something I'm missing, please correct me. Cus I might just be spouting bs and have a great day. High Iq thoughts however

 

[oyopth31]

Aromatase is the only way to make E1 HSD needs E1 to make E2 without aromatase no estrogen therefore no E-2 or E-1

AIs are systemic and have successfully proven to delay bone maturation from quite a few clinical trials in ISS
Aditonally people with aromatase deficiency grow abnomally tall
Additionally, its a very well-known fact so beside all of this hypothetical sience just the real life evidences point to the fact that aromatase does delay bone maturation.
Clinical trials show that AIs increase the risk of bone loss and fractures. These trials specifically measure bone response.
If the drug didn't reach and saturate bone tissue, it wouldn't cause these side effects.

here are all the trials for those curious.
Hero et al. (2005): A randomized controll trial of 31 boys with ISS found that the boys who were treated with letrozole were able to achieve a 5.9 cm increase in PAH compared to the placebo group.

Mauras et al. (2008 & 2016): These trials studied the effect of anastrozole in boys with Growth Hormone Deficiency (GHD) and ISS.
In GHD patients, 36 months of anastrozole plus growth hormone (GH) resulted in a 6.7 cm increase in predicted adult height.
In ISS patients, those on the AI combination gained significantly more height than those on GH alone (22.5 cm vs 20.6 cm).
https://pubmed.ncbi.nlm.nih.gov/18165285/
https://pmc.ncbi.nlm.nih.gov/articles/PMC5155684/

Wickman et al. (2001): This trials were on boys with CDGP. treatment with letrozole effectively delayed the maturation of these bones, leading to a 5.1 cm increase in PAH after 18 months.
maturation and led to a 5.1 cm increase in predicted adult height after 18 months.
https://pubmed.ncbi.nlm.nih.gov/11403810/

Yackobovitch-Gavan et al. (2025): A recent retrospective study showed that mid-pubertal boys treated with an AI alone achieved a final adult height 3.2 cm taller than untreated controls (166.6 cm vs 163.4 cm).
https://pubmed.ncbi.nlm.nih.gov/40193585/
Haynes et al. (2003):This study showsthat letrozole achieves over 99% total body inhibition of aromatization. A 99% would be impossible if ais weere blocked from local tissues such as the growth plates.
https://pubmed.ncbi.nlm.nih.gov/14630089/
Across all trials, the most consistent finding is that AIs slow down bone age advancement height.
The conclusion is that ais still do work for height purposes

So that's really all I have to sayy however, if there is something I'm missing, please correct me. Cus I might just be spouting bs and have a great day. High Iq thoughts however

Shulman et al. (2008): A review of AI use in children that notes the primary mechanism of height gain is the direct inhibition of local estrogen production within the growth plate itself.
forgot this one