M
maintenanceman
jfl
- Joined
- Feb 16, 2026
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this is a simple "guide" I made cuz I saw a bunch of niggas saying bullshit how exe is the worst ai
most people who run an ai with gh for height pick letrozole or anastrozole because that's what the clinical trials used. the logic makes sense on the surface. but the choice of which ai matters more than whether to run one at all, and the trial data actually makes the case against both of them if you read it carefully.
the mechanism
e2 drives growth plate fusion through estrogen receptor alpha on epiphyseal chondrocytes. elevated e2 accelerates chondrocyte senescence, which mineralizes the plate. this is why an ai belongs in a height protocol. but e2 has a floor. below roughly 10-15 pg/ml, chondrocyte proliferation slows, bone mineral density drops, and joint health degrades. crashing e2 is not neutral. it works against the same goal you're running the ai for.
letrozole
the stanford rct (pmc11388000) that people cite to support ai use found letrozole crashed e2 to 2.6 pg/ml on average. at that concentration the predicted height gains did not hold past year one. combined three year gain versus baseline was approximately 1.3cm. the drug overshot the target and undercut itself by dropping e2 below the proliferation floor. too potent to control at meaningful doses.
anastrozole
competitive reversible inhibitor. it blocks aromatase but does not destroy it. when you stop the drug, aromatase activity rebounds and e2 spikes. if plates are still open during that spike you've partially reversed the protocol at the most important moment, which is the end of the run when the window is closing anyway.
exemestane
suicidal inhibitor. it permanently inactivates the enzyme it binds rather than just blocking it. no rebound on cessation because the enzyme itself is gone. the body replaces it gradually, which gives a smooth natural taper instead of a spike.
at 6.25mg eod without exogenous testosterone, endogenous t is the only aromatase substrate. lower substrate means the ai has less to work on per dose, so eod keeps e2 in the 15-30 pg/ml range. ed at this dose without test will crash e2 below the floor the same way letrozole does.
the comparison
letrozole: too potent, clinical evidence shows it overshoots and slows growth at the e2 levels it produces
anastrozole: reversible binding creates rebound risk at the exact moment you stop, trial data exists but the mechanism has a structural flaw
exemestane: irreversible, no rebound, controllable at low doses without test, e2 lands in the correct range for chondrocyte proliferation without fusion
check e2 at week 4. target is 15-30 pg/ml. adjust from there based on your number, not a fixed dose schedule.
most people who run an ai with gh for height pick letrozole or anastrozole because that's what the clinical trials used. the logic makes sense on the surface. but the choice of which ai matters more than whether to run one at all, and the trial data actually makes the case against both of them if you read it carefully.
the mechanism
e2 drives growth plate fusion through estrogen receptor alpha on epiphyseal chondrocytes. elevated e2 accelerates chondrocyte senescence, which mineralizes the plate. this is why an ai belongs in a height protocol. but e2 has a floor. below roughly 10-15 pg/ml, chondrocyte proliferation slows, bone mineral density drops, and joint health degrades. crashing e2 is not neutral. it works against the same goal you're running the ai for.
letrozole
the stanford rct (pmc11388000) that people cite to support ai use found letrozole crashed e2 to 2.6 pg/ml on average. at that concentration the predicted height gains did not hold past year one. combined three year gain versus baseline was approximately 1.3cm. the drug overshot the target and undercut itself by dropping e2 below the proliferation floor. too potent to control at meaningful doses.
anastrozole
competitive reversible inhibitor. it blocks aromatase but does not destroy it. when you stop the drug, aromatase activity rebounds and e2 spikes. if plates are still open during that spike you've partially reversed the protocol at the most important moment, which is the end of the run when the window is closing anyway.
exemestane
suicidal inhibitor. it permanently inactivates the enzyme it binds rather than just blocking it. no rebound on cessation because the enzyme itself is gone. the body replaces it gradually, which gives a smooth natural taper instead of a spike.
at 6.25mg eod without exogenous testosterone, endogenous t is the only aromatase substrate. lower substrate means the ai has less to work on per dose, so eod keeps e2 in the 15-30 pg/ml range. ed at this dose without test will crash e2 below the floor the same way letrozole does.
the comparison
letrozole: too potent, clinical evidence shows it overshoots and slows growth at the e2 levels it produces
anastrozole: reversible binding creates rebound risk at the exact moment you stop, trial data exists but the mechanism has a structural flaw
exemestane: irreversible, no rebound, controllable at low doses without test, e2 lands in the correct range for chondrocyte proliferation without fusion
check e2 at week 4. target is 15-30 pg/ml. adjust from there based on your number, not a fixed dose schedule.
