Ai benefits for test

[hitch]

In adult men (usually middle-aged or older, often hypogonadal):

• Aromatase inhibitors (like anastrozole) ↓ estrogen
• That removes estrogen’s negative feedback on the brain
• → LH/FSH increase
• → Testosterone can rise a lot (e.g. ~400–500 → 1200–1500 ng/dL)
• Over short periods (6–12 months), some studies showed:
  • Spine bone mineral density increased ~1–2%
  • Hip BMD usually stayed the same (not always increased)

This happened despite estrogen being lower, because:

• Testosterone itself is anabolic to bone
• Androgen receptors in bone were strongly stimulated
• Estrogen was reduced but not eliminated

So yes — “+2% BMD” is a real finding in certain adult studies.














The critical part people miss








Those results do NOT generalize safely to teenagers.





Why?








1. Estrogen is essential during puberty





In adolescents:

• Estrogen is required for:
  • Normal bone mineralization
  • Growth plate maturation
  • Long-term peak bone mass
• 
  
• Suppressing estrogen too much can:
  • Impair trabecular bone formation
  • Reduce future peak bone density (even if short-term numbers look okay)

2. Adult bone ≠ growing bone

• Adults: bones are remodeling
• Teens: bones are modeling and growing
• Short-term gains can mask long-term structural deficits

3. Testosterone increase doesn’t fully replace estrogen

• Testosterone helps bone
• But estrogen is still required, even in males
• Men with aromatase deficiency (can’t make estrogen) develop severe osteoporosis, despite high testosterone

Why those studies still matter








They show:

• Estrogen is not the only driver of male bone health
• Testosterone can temporarily offset moderate estrogen reduction
• Complete estrogen suppression is harmful
• Context (age, duration, degree of suppression) is everything

1. Estrogen is the main feedback signal (not testosterone)








In males, the brain (hypothalamus + pituitary) mainly “listens” to estradiol (E2), not testosterone.

• Testosterone → converted to estradiol (via aromatase)
• Estradiol binds receptors in:
  • Hypothalamus
  • Pituitary
• 
  
• This suppresses GnRH → LH → testosterone

So under normal conditions:





More E2 = brain says “enough testosterone”














2. Aromatase inhibition removes that signal








When an aromatase inhibitor is used:

• Testosterone → cannot convert to E2
• Brain senses low estrogen
• Brain thinks the body is sex-hormone deficient

Result:

• ↑ GnRH
• ↑ LH (sometimes 2–3×)
• ↑ FSH
• Leydig cells are maximally stimulated

That’s why testosterone can jump:

• 450 → 900 → 1400+ ng/dL

This rise is endogenous (your own production), not external testosterone.














3. Why the rise can be huge (not just moderate)








Several amplifiers stack together:








A. Feedback loop sensitivity

• Estrogen feedback is very sensitive
• Small E2 drops → large LH increase

B. Less testosterone loss

• Less aromatization = more testosterone stays as testosterone

C. SHBG often drops

• Lower estrogen → ↓ SHBG
• → More free testosterone

So both total and free T rise.














4. Why this doesn’t keep climbing forever








Eventually:

• Androgen receptor signaling increases
• Other feedback mechanisms engage
• The system reaches a new (often unstable) equilibrium

That’s why many studies show:

• Big rise at 3–6 months
• Plateau or partial decline later

5. Why this is stronger in younger males








Younger males:

• Have very responsive hypothalamic–pituitary axes
• High baseline Leydig cell capacity
• Lower SHBG

So the same AI dose causes larger swings than in older men.














Key takeaway (important)








Testosterone rose because estrogen suppression tricked the brain into thinking testosterone was too low — even though it wasn’t.





That’s also why:

• Oversuppression causes side effects
• The system becomes unstable
• Bone, mood, lipids, and growth can be affected

If you want, I can also explain:

• Why too-low E2 eventually lowers testosterone
• Why libido can drop despite very high T
• Or why doctors aim for partial, not full, estrogen suppression

 

[birthdefect]

formatting fucked my brain more than -10 e2 levels