🧵 The Truth About Testosterone, DHT, and Growth Plate Closure (Even With Estrogen Controlled)

[Escanor1]

Growth plates (epiphyseal plates) are areas of cartilage at the ends of long bones that allow bones to grow. Once they “fuse,” height growth stops.


The main hormone responsible for this fusion is estrogen, not testosterone or DHT directly.

• Even in males, testosterone is converted (via aromatase) into estradiol, which triggers the closing process.

So if estrogen is suppressed, theoretically, growth plate fusion should be delayed — even if testosterone levels are high.

• This has been seen in some rare aromatase deficiency cases where men stayed tall and never fused until given estrogen.

However… DHT (dihydrotestosterone) can still play a role indirectly.

• While DHT itself doesn’t strongly affect growth plate closure, it can mature bone and cartilage in other ways, accelerating skeletal development.
• In short: it may not “close” the plates, but it can make the bone age advance faster.

Key point:

• Estrogen = closes the plates.
• Testosterone = provides substrate for estrogen (via aromatase).
• DHT = does not aromatize, but may still advance maturation in complex ways.

If you suppress estrogen completely, you might delay closure — but that’s not safe.

• Chronic low E2 impairs bone density, lipid health, brain function, and joint health.
• There’s a tradeoff between height and overall bone quality.

In summary:

• Testosterone → aromatized estrogen → closure
• DHT → speeds bone maturation, may indirectly hasten closure but not the direct cause
• Controlling estrogen can delay fusion

So the “test causes growth plates to close faster due to DHT” claim is mostly false.

• DHT isn’t the main culprit — estrogen is.
• But DHT can make your skeleton mature faster, which might look like early closure.

 

[psychopathic]

Never touching BOTB

 

[genetically fucked]

gptslop dogshit

 

[heinz_guderian]

chat gpt warrior

 

[Escanor1]

gptslop dogshit
View attachment 4236796

didnt have time to make it myself i have exams tmmrw lmao

 

[genetically fucked]

didnt have time to make it myself i have exams tmmrw lmao

then dont post it at all

 

[Apchun144]

This isn’t water this is vapor

 

[rotation]

Growth plates (epiphyseal plates) are areas of cartilage at the ends of long bones that allow bones to grow. Once they “fuse,” height growth stops.


The main hormone responsible for this fusion is estrogen, not testosterone or DHT directly.

• Even in males, testosterone is converted (via aromatase) into estradiol, which triggers the closing process.

So if estrogen is suppressed, theoretically, growth plate fusion should be delayed — even if testosterone levels are high.

• This has been seen in some rare aromatase deficiency cases where men stayed tall and never fused until given estrogen.

However… DHT (dihydrotestosterone) can still play a role indirectly.

• While DHT itself doesn’t strongly affect growth plate closure, it can mature bone and cartilage in other ways, accelerating skeletal development.
• In short: it may not “close” the plates, but it can make the bone age advance faster.

Key point:

• Estrogen = closes the plates.
• Testosterone = provides substrate for estrogen (via aromatase).
• DHT = does not aromatize, but may still advance maturation in complex ways.

If you suppress estrogen completely, you might delay closure — but that’s not safe.

• Chronic low E2 impairs bone density, lipid health, brain function, and joint health.
• There’s a tradeoff between height and overall bone quality.

In summary:

• Testosterone → aromatized estrogen → closure
• DHT → speeds bone maturation, may indirectly hasten closure but not the direct cause
• Controlling estrogen can delay fusion

So the “test causes growth plates to close faster due to DHT” claim is mostly false.

• DHT isn’t the main culprit — estrogen is.
• But DHT can make your skeleton mature faster, which might look like early closure.

nigga thought nobody would realise this is gpt

 

[amiok]

bhai’s repmaxxing