Estrogen only "rebounds" based on the mechanism of suppression. SERM, for example, only masks estrogen expression by occupying receptors but estrogen production is left unchecked and actually increases as testosterone levels increase. AI's like letro inhibit inducible enzymes and just like a leaky faucet, they body will eventually try to balance the equation with increased aromatase activity. Steroidal AI's like Teslac, Exemestane, and ReboundXT will not result in 'rebound' phenomena because the inhibition is non-competitive and irreversible. They act as false substrates, so aromatase is still happy to act on them (instead of androstenedione) and the body keeps no record of an imbalance. There is no leaky faucet. In fact, after prolonged use, steroidal AI's often produce a protracted anti-e benefit even after being discontinued. This is why I suggest an inverse taper with SERM and RXT for post cycle therapy with an abrupt stoppage of RXT at the end. As the SERM elevates androgen/estrogen production, the AI dose is increased to compensate while the SERM is phased out. It works quite well to use this approach and rebound is not encountered. Adding LX and/or DHEA also really makes for a killer PCT in this scheme. This is a typical example of my PCT:
wk1: Clomid 150mg/d, RXT 25mg/d, DHEA 200mg/d, LX 75mg/d
wk2: Clomid 100mg/d, RXT 25mg/d, DHEA 200mg/d, LX 50mg/d
wk3: Nolva 60mg/d, RXT 50mg/d, DHEA 200mg/d, LX 25mg/d
wk4: Nolva 40mg/d, RXT 50mg/d, DHEA 100mg/d
wk5: Nolva 20mg/d, RXT 75mg/d, DHEA 100mg/d
wk6: RXT 75mg/d, DHEA 100mg/d
Notice I phase the Clomid out and introduce the Nolva later. This helps prevent sides from developing from accumulation of estrogenic metabolites from the Clomid and also acts to minimize the use of Nolva, which is more liver toxic than Clomid. Rebound is very unlikely and estrogen biosynthesis will likely be significantly lowered for 3+ wks even after the end of this PCT. I do long ones, as you can see.
