olkn2890
Iron
- Joined
- Feb 19, 2025
- Posts
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I’m currently taking 1 mg of anastrozole daily. When I asked an AI about this protocol, it warned of two critical risks:
1. Critically suppressed estrogen (likely <15 pg/mL), blocking osteoblast differentiation → impaired bone mineralization and accelerated bone loss.
2. Premature growth plate closure (6-12 months earlier than natural timing) – not during use, but upon discontinuation due to estrogen rebound.
The AI advised immediate tapering to avoid irreversible damage.
I countered with a study where a 14-year-old took the same dose + exogenous HGH for 2 years, achieving +12.5 cm height. The AI acknowledged this but emphasized:
→ Success required supraphysiological IGF-1 (500-600 ng/mL) from HGH to bypass estrogen-dependent osteoblast pathways
→ Without equivalent IGF-1 elevation, bone formation would be compromised
We compromised on a modified protocol:
→ Reduce to 0.5 mg/day
→ Add Ipamorelin if my IGF-1 is <300-400 ng/mL
→ Strictly monitor E2 (target: 20-35 pg/mL) and IGF-1
Questions for the community:
1. Is the AI’s claim about osteoblast differentiation failure at low E2 (<20 pg/mL) valid and what to do about it?
2. How real is the rebound-triggered growth plate closure risk?
3. Would this protocol genuinely maximize height with moderate risks?
4. What’s the best protocol to maximise height in your opinion?
1. Critically suppressed estrogen (likely <15 pg/mL), blocking osteoblast differentiation → impaired bone mineralization and accelerated bone loss.
2. Premature growth plate closure (6-12 months earlier than natural timing) – not during use, but upon discontinuation due to estrogen rebound.
The AI advised immediate tapering to avoid irreversible damage.
I countered with a study where a 14-year-old took the same dose + exogenous HGH for 2 years, achieving +12.5 cm height. The AI acknowledged this but emphasized:
→ Success required supraphysiological IGF-1 (500-600 ng/mL) from HGH to bypass estrogen-dependent osteoblast pathways
→ Without equivalent IGF-1 elevation, bone formation would be compromised
We compromised on a modified protocol:
→ Reduce to 0.5 mg/day
→ Add Ipamorelin if my IGF-1 is <300-400 ng/mL
→ Strictly monitor E2 (target: 20-35 pg/mL) and IGF-1
Questions for the community:
1. Is the AI’s claim about osteoblast differentiation failure at low E2 (<20 pg/mL) valid and what to do about it?
2. How real is the rebound-triggered growth plate closure risk?
3. Would this protocol genuinely maximize height with moderate risks?
4. What’s the best protocol to maximise height in your opinion?
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