Here is the standard recovery cycle I recommend my clients. It is based on established standards used by Endocrinologists. Beginning the last week of Anabolic Androgenic Steroids (AAS) use or a week later (depending on convenience), use 2,000U of Human Chorionic Gonadotropin (HCG), IM, three times weekly, for a total of three weeks. At the same time, use 20mg Nolvadex daily, for a total of six weeks. Clomid is added--50mg daily for a total of six weeks--if you have been shut down for a long time. Bill Llewellyn summarizes the rationale pretty well.
Originally posted by w_llewellyn
Tamoxifen does NOT suppress LH and T! Keep looking and you will find human studies clearly showing this, and in fact its superiority over Clomid in stimulating both. I'm thinking of putting together a comprehensive article on this, so you guys understand how Clomid and Nolvadx work, and their differences, a little better. Plus, if any SERM has estrogenic effects in the AP it is Clomid, not Nolvadex, which is why I prefer tamoxifen (it is a technical advantage, not a big one in the real world though)..
ANd I say again, fostering a little extra LH post cycle with CLomid, Nolvadex or Arimidex doesn't do a whole hell of alot. The brain increases LH rapidly post-cycle anyway, the testes just don't respond to it well because they have lost mass. THis is why we need Bolus LH (HCG) plus an anti-estrogen.
Originally posted by w_llewellyn
I have tried Clomid alone a few times, years ago, but typically used Nolvadex and Human Chorionic Gonadotropin (HCG). I have always found it to work very well for me. As for Arimidex, no, I have not tried to use this in a post-cycle recovery program. Years ago I had a scare with EXTREMELY messed up cholesterol (all LDL, almost no HDL), and since have stayed away from aromatase inhibitors altogether. Consider this though:
Both Clomid, which mind you I have always contended works as a T stimulating drug just like Nolvadex (just technically not as good), and Arimidex counter HPTA suppression by blocking the negative feedback caused by estrogens. They support LH release obviously.
Now post cycle it has clearly been shown that LH levels rebound quickly, while T levels are much slower to return to normal. Why? The reason is that the testes, after a period of inactivity, have lost mass and are not able to respond as well to LH in terms of T output. If your recovery program only focuses on LH support it is missing the more important problem, testicular mass. Human Chorionic Gonadotropin (HCG), as you know, can provide an additional bolus dose of LH. It can essentially help shock them back into shape, whereas it will take many weeks relying on heightened endogenous LH alone.