It seems that when using a long acting ester like enth or cyp, we have near the end of the lifecycle a zone where the HTPA is suppressed, and yet the receptors are not sufficiently saturated, a worst of both worlds scenario. What strategies are there to square the curve here by using short acting nAR or Ar receptor substances.
Specifically, would Androsol be a useful for this, by steadily increasing the dose near the end of the ester cycle , and would androsol sufficiently support AR receptors via its conversion to T to mitigate this dead zone, or can we expect that 4-AD will only support the nAR receptors sufficiently, and does it really matter if is nAR or AR as long as the tail is squared?