Androgenmaxxing + Aromatase Inhibitors Is Cope: Why It Doesn’t Increase Height or Bone Growth (GTFIH)

[currycel67]

Androgen-maxxing ≠ bone growth


Why serum estrogen numbers are cope, and why high androgens reduce height potential

There’s a persistent myth that “keeping blood estrogen low (via AI) while pushing testosterone” allows more bone growth and height. This is biologically incorrect.

Below is the actual endocrinology.


1. Growth plates respond to local estrogen, not serum estrogen

Growth plate closure is driven by estrogen action inside the growth plate, not by what you see on a blood test.


Key point:
Serum estradiol ≠ growth-plate estradiol


Even when blood E2 looks “normal” or “low,” estrogen can still be:


Produced locally in bone

Acting paracrinally inside the epiphyseal plate

Advancing growth plate senescence


Evidence

• Nilsson et al., Endocrine Reviews (2014)
  → Estrogen regulates growth plate fusion via local signaling, not circulating levels.
• Vanderschueren et al., JCEM (2004)
  → Growth plate maturation depends on intracrine estrogen conversion within bone.

This alone invalidates the idea that “E2 = 20–40 pg/mL means plates are safe.”




2. Testosterone itself advances growth plate maturation (even without estrogen spikes)


Another common mistake is assuming:

“Only estrogen closes plates — testosterone is safe.”
This is false.

Testosterone:

• Accelerates chondrocyte differentiation
• Advances bone age
• Shortens the proliferative phase of growth plates

This happens independently of serum estrogen levels.

Evidence

• Weise et al., JCEM (2001)
  → Androgens directly stimulate growth plate maturation.
• Mauras et al., JCEM (2008)
  → Higher androgen exposure → faster bone age advancement in adolescents.

So even if estrogen were perfectly suppressed (which it never is), high testosterone still shortens growth time.




3. Aromatase inhibitors do NOT “freeze” growth plates


AIs lower circulating estrogen, but:

• They do not fully block local aromatization in bone
• They do not stop androgen-driven maturation
• Long-term use impairs bone quality, not growth

Evidence

• Hero et al., JCEM (2005)
  → AI use in adolescent males increases predicted height short-term, but worsens bone microarchitecture.
• Shams et al., Bone (2019)
  → Estrogen suppression disrupts normal growth plate signaling and bone strength.

Translation:

AIs don’t “protect height” — they just distort development.



4. Why androgen-maxxing gives the
illusion of growth

People think it works because of:

• Early growth spurt


High androgens can cause:

Temporary height acceleration
Earlier pubertal peak


But:

Faster early growth = earlier stop

This is textbook endocrinology.

Evidence

• Karlberg, Hormone Research (2002)
  → Early puberty = shorter adult height
  → Delayed puberty = taller adult height

5. Craniofacial “bone growth” is also cope
Even during adolescence:

• Facial bones have limited growth windows
• Androgens mainly affect muscle, fat, skin
• Not skull size or jaw length

Changes people attribute to “bone growth” are:

• Masseter hypertrophy
• Fat redistribution
• Skin thickening

Not new bone.


6. Final summary (no cope)

• Serum estrogen levels do not reflect growth plate estrogen

• Testosterone + AI does not preserve height

• High androgens accelerate growth plate aging

• Androgen-maxxing trades future growth for early maturity

• Lost growth potential is permanent



Growth is about time, not hormone force.

Late bloomers win height.

Early androgen pushers finish early.


TL;DR

If your goal is height / frame:

• Androgen-maxxing is counterproductive
• Estrogen labs don’t tell the full story
• Biology doesn’t negotiate

and yeah I used ChatGPT to help me make this thread so stop saying ai slop because I don’t want to spend hours on making a thread cuz I have life

 

[DrMd]

dnr, all that just to prove a simple point

 

[currycel67]

dnr, all that just to prove a simple point

bump

 

[Dsm]

Bottom format oat

 

[wheyfart]

1. Growth plates respond to local estrogen, not serum estrogen

Growth plate closure is driven by estrogen action inside the growth plate, not by what you see on a blood test.


Key point:
Serum estradiol ≠ growth-plate estradiol


Even when blood E2 looks “normal” or “low,” estrogen can still be:


Produced locally in bone

Good thread
Not educated enough to fully debate you but this statement seems skewed to me, surely lower systemic estrogen should lead to lower estrogenic activity in the bones?
And even if that isn’t the case, how did you deduce that aromatization only happens for serum estradiol? This is the only thread where I’ve seen that statement, yet it is a very crucial point in deciding the usefulness of administering AIs.
Furthermore there IS clinical documentation on them delaying bone fusion, compared to the benefits from other compounds that are commonly discussed for heightmaxing here, which makes it more relevant to discuss (which isn’t the case on .org unfortunately)

 

[Micrognathic]

This thread is the definition of AI SLOP
OP GO KYS

and yeah I used ChatGPT to help me make this thread so stop saying ai slop because I don’t want to spend hours on making a thread cuz I have life

fair enough
If u "have a life," why even bother wasting ur time here

 

[currycel67]

Extremely low estrogen levels could delay temporarily but isn’t worth the sides and you’ll only gain 1-3 cm and the sides are brutal I do think the only height maxing methods are voxzogo and hgh

Good thread
Not educated enough to fully debate you but this statement seems skewed to me, surely lower systemic estrogen should lead to lower estrogenic activity in the bones?
And even if that isn’t the case, how did you deduce that aromatization only happens for serum estradiol? This is the only thread where I’ve seen that statement, yet it is a very crucial point in deciding the usefulness of administering AIs.
Furthermore there IS clinical documentation on them delaying bone fusion, compared to the benefits from other compounds that are commonly discussed for heightmaxing here, which makes it more relevant to discuss (which isn’t the case on .org unfortunately)