HPTA Restart Protocol

KSMan, you wrote the following on the HPTA restart protocol and I was hoping you could elaborate a bit.

“2a) Slowly taper off of the SERM, do not stop suddenly or your HPTA may shutdown.”
Could you define the taper? Reduce dosage daily, or maintain dosage and go from ED to EOD to E3D, etc? If the latter, how long should one continue the taper? Just looking for a general guideline.

“2b) You will want to be on 0.5 mg anastrozole and cruise on that for a few weeks, then taper.”
Same thing here.

“Labs [optional]: With SERM or hCG, your T and E2 levels should be uncreased [else do TRT]. If high normal, 1.0 mg anastrozole per week. If mid range, 0.5mg”
Are you recommending obtaining labs during the protocol to monitor the above, or complete the protocol and take labs a few months later to see if it took?

Lastly, I can’t figure out the relationship between E2 and LH. I read in the SERM sticky that E2 was part of the negative feedback loop so I thought that E2 would be indirectly proportional to LH. But you wrote, “If E2 is high, LH may be high, cut SERM by 50%, anastrozole can be ineffective” which seems to state the opposite. Not sure how to interpret the two.

Thank you.

There are two things going on and you are trying to put everything into one model when there are two. We have closed loop HPTA actions and SERM induced open loop HPTA actions. And high LH can lead to high E2 production inside the testes - not HPTA related.

You can do labs during SERM to check LH/FSH and T levels.

  • LH/FSH should be increased
  • if LH too high, E2 may be high and SERM dose would need to be reduced
    – this effect is outside of HPTA control loop!
    – SERM also substantially makes HPTA “open loop” which is the whole point of the SERM in a TRT context

SERM has a longer half life, take 2-3 weeks to taper. SERM’s increase by multiple methods and if SERM stops too fast, HPTA sees the residual E2 levels and may shutdown recovery before it starts. AI simply reduces this potential.

Related: When young virile males are given 1mg anastrozole per day [clinical research], their E2 levels do not go to zero as one might expect. LH is high and T levels increase significantly. But higher LH leads to significant T–>E2 inside the testes [where anastrozole is ineffective] that increased serum E2 levels; while the high anastrozole levels turn off most T–>E2 in peripheral tissues. E2 near 17 was observed [if I recall accurately]. The serum levels of E2 limit HPTA and the system’s set point is shifted, but the HPTA is not open loop.

This effect was never explained in the early Clomid research papers. But now the reason is obvious when you see the effects of high hCG or SERM dose effects in the TRT community.

In older males, the testicular response to AI is weak and HPTA response to is limited by age related secondary hypogonadism effects. E2 levels simply crash with higher amounts of anastrozole. Those who are anastrozole over-responders are easily affected.