JCaesar
ascend or rope
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Many users here recommend aromatase inhibitors when someone is trying to “heightmax”, with the intention of delaying growth plate closure and allowing more time for the growth plates to remain open.
Problem is, the actual slowdown in bone age (BA) progression shown in clinical trials is often much smaller than people think. Even in well-controlled studies, aromatase inhibitors (AIs) like letrozole or anastrozole usually slow BA progression by around 30–50% at most — and that’s in children and teens who start treatment at the right stage of puberty. Some numbers from placebo-controlled trials:
Common misconception:
Some people believe that if your estradiol (E2) level is below a certain number — often quoted as 15 or 20 pg/mL — your growth plates “cannot” close. This is false. While estradiol is a key trigger for epiphyseal fusion, the closure process is more complex and depends on both cumulative estrogen exposure over time and local signaling in the growth plate.
In fact, cases of aromatase-deficient men — whose estradiol stays under ~4 pg/mL their entire lives — show severely delayed closure, but not an absolute prevention of closure forever. Bone age can still advance, just much more slowly, and other growth plate–affecting factors (like IGF-1, androgens, and mechanical maturation of cartilage) may still play a role.
If you’re considering AIs for “heightmaxing,” it’s important to understand the actual degree of which you can slow down your growth plate closure rate, and possibly accompany the process with x-rays of the growth plates every so often if you want to truly track how they're doing.
Problem is, the actual slowdown in bone age (BA) progression shown in clinical trials is often much smaller than people think. Even in well-controlled studies, aromatase inhibitors (AIs) like letrozole or anastrozole usually slow BA progression by around 30–50% at most — and that’s in children and teens who start treatment at the right stage of puberty. Some numbers from placebo-controlled trials:
- Letrozole + testosterone in delayed puberty boys: BA advanced 0.9 years in 12 months, compared to 1.7 years in placebo → ~47% slowdown.
- Letrozole in boys with idiopathic short stature: BA advanced 0.9–1.1 years in 12 months, vs 1.3–1.4 years in controls → ~20–35% slowdown.
- Anastrozole in GH-treated boys: BA advanced 1.1 years vs 1.8 years in placebo → ~39% slowdown.
Common misconception:
Some people believe that if your estradiol (E2) level is below a certain number — often quoted as 15 or 20 pg/mL — your growth plates “cannot” close. This is false. While estradiol is a key trigger for epiphyseal fusion, the closure process is more complex and depends on both cumulative estrogen exposure over time and local signaling in the growth plate.
In fact, cases of aromatase-deficient men — whose estradiol stays under ~4 pg/mL their entire lives — show severely delayed closure, but not an absolute prevention of closure forever. Bone age can still advance, just much more slowly, and other growth plate–affecting factors (like IGF-1, androgens, and mechanical maturation of cartilage) may still play a role.
If you’re considering AIs for “heightmaxing,” it’s important to understand the actual degree of which you can slow down your growth plate closure rate, and possibly accompany the process with x-rays of the growth plates every so often if you want to truly track how they're doing.
