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  • AI During PCT

    Any thoughts on this one?? I have read some articles recommending arimidex during PCT along with typical nolvadex/clomid therapy. They are recommending 0.25mg L-dex per day. Here is an excert...origianally posted by Pheedno on WCB.

    Arimidex(or L-dex)
    Estrogen is the main inhibitence of restoring HPTA, and AI administration has been shown to increase gonadotrophin concentrations and serum Testosterone by up to 50%. In addition, by adding L-dex, the inhibitence of excess estrogen allows Tamox to work greater at LH stimulation in the begining stages of PCT, since the need to prevent binding in the mammery is lessened by the reduction in estrogen biosynthesis.
    Last edited by Cmsmallzz; 10-02-04, 04:35 PM.

  • #2
    that is interesting to look into. . .I am using lentaron depot at the moment and this might be one of the reasons that it works so well. . .estrogen inhibition and stimulation of LH combo. . .

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    • #3
      Origional link used: http://anabolicminds.com/forum/show...swales+protocol

      Since this is the current hot topic, I figured I would post this:



      Since I've been hanging out here a bit lately, I've been getting quite a few emails from guys wanting individualized advice on their cycles. In the first place, I cannot design cycles, nor do I prescribe steroids (just ancillary medications). That would be a violation of my Oath as a physician, and DEA law to boot. Also, obviously I cannot afford to give away free Consultations. So, I'll post my PCT Protocols here, for anyone who may choose to use them.

      Also, I'm just running to catch a plane for Las Vegas, attending the American Academy of Anti-Aging Medicine International Conference. I guess they are supposed to publish an article I wrote on how to administer TRT for men. Wish me luck!

      Here it is:

      I advise my AAS patients to use small amounts of HCG (250IU to 500IU) two days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

      Any more than 500IU of HCG per day causes too much aromatase activity. Some feel aromatase is actually toxic to the Leydig cells of the testes. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

      If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when HCG is so inexpensive.

      The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of AAS (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

      I want my patients to stop taking HCG within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.

      I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).

      All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.

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      • #4
        I like Arimidex during the cycle (in fact, consider use of an AI while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).
        This is interesting...two opposing views from two good sources. I am wondering if maybe a dose of 0.25mg/day would be beneficial for LH production but not damaging to libido or lipid profile.

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        • #5
          Originally posted by Pheedno on WCB....

          Anastrozole supresses estrogen conversion at about 85% with a full clinical dose in a subject with normal levels of estrogen. We are males with supraphysiological levels of estrogen existing in the body post cycle, utilizing a 1/4 of the clinical dose(.25mg). At least thats the dose I recommend. You do need some estrogen to help with correlation to the AR(which is why I don't like letro) but estrogen is the main inhibitor of recovering HPTA. It needs to be controlled in order to prevent SHBG to accumilate and prolong F. Test reaching base line.

          Anastrozole doesn't effect my lipids to a great extent. This of course being individualistic but if concerns are warranted(which they should be if a person isn't getting blood work to thwart that concern) then both the SERMs(primarily nolva for selectivity to bone and liver ERs) aid in alleviating the lipid effect. You can aslo take it a step further and add 20mg of policosinol.

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