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I believe that you can go to or stay on a certain amount of androgens without negatively impacting the HPTA too much by including Serms and AI's to block the primary messanger (estrogen) to the HPTA. This does not work for your conventional cycles since the amount of androgens is high enough to become the secondary signal to the HPTA but could be used as a low dose HRT.
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Here is my theory: Estrogen, via aromatization acts as the first feedback after too much test has been produced (injected). At what level depends on the individual, but lets assume estrogen throttels the HP at 1,000 ng/dl of total testosterone. The second feedback is testosterone itself, but at higher levels (since the body assumes the estrogen feedback failed). We assume this number to be 2,000 ng/dl. So if we keep test from aromatizing and keeping estrogen at normal levels we can take enough test to reach 2,000ng/dl. How much test is that? That depends on blood tests.
Testosterone.net elaborates a little more in below article:
Androgel, Maintaining Gains and Message Board "Gurus"
Q: Concerning your ideas about maintaining gains from your Steroids for Health article, you said Androgel will work provided that an estrogen antagonist or aromatase inhibitor is used concurrently. But Androgel is nearly impossible for me to get, so what about the next best alternative you wrote about: 100 mg/week of Testosterone enanthate? Would propionate work as well? Also, where’s the data to shut those people up who insist it can’t be done?
A: Your alternative will still work well when you consider the peak concentration of Testosterone in the bloodstream. We have data supporting that suppression of LH can be prevented when elevating Testosterone up to a peak concentration of 2,044 ng/dl, provided that an estrogen antagonist or aromatase inhibitor is used.
When I recommended the 100 mg dose of Testosterone enanthate, I was basing that on the pharmacokinetic data which demonstrated that a 200 mg dose in seven eugonadal men resulted in a mean peak concentration of 1,965 ng/dl and 100 mg of enanthate given to seven eugonadal men resulted in a mean peak concentration of 1,181 ng/dl.
Oh, and before some genius decides to say "you can’t use that data because the person is in a hypogonadal state after a cycle and those people were eugonadal," I want to point out that the peak concentrations when administered to hypogonadal men would be even less, as common sense would tell you, so it makes an even better case for my 100 mg/week of enanthate.
If common sense isn’t enough, research has shown the mean peak Testosterone concentration following the administration of 200 mg of Testosterone enanthate to seven hypogonadal men was 1,233 ng/dl. As you can see, the peak concentration is nowhere near 2,044 ng/dl. So, you could technically use 200 mg/week with my post cycle protocol and still be fine, but I’m going to stick to my original recommendation of 100 mg/week.
As for using the propionate ester, I suppose you could but I don't have exact data on it. With what I do have, I'd say 25 mg every three days or so would be okay.
Lastly, as I've been saying to people for the past few years, I only recommend that you use Testosterone when employing such a protocol as it's the only androgen where we have data demonstrating that at a certain blood level (£ 2,044 ng/dl), LH isn't suppressed provided that an estrogen antagonist or an aromatase inhibitor is used concurrently. From this, we can then apply our pharmacokinetic data we have with administration of various forms of Testosterone and figure out a protocol.
These two key pieces of information aren't something that'll be easily located with other androgens. Fluoxymesterone (10 mg every six hours) may be an exception as we have data on that, but again, to make things less complicated, I suggest you only use Testosterone.
Oh, and administration of even 10 grams of Androgel won’t get total Testosterone past 1,100 ng/dl so considering that, I recommend only 5 grams. There’s no way that suppression is an issue provided an estrogen antagonist or aromatase inhibitor is used. I also go more in depth about the studies listed in the upcoming print issue, explaining why it was shown to work, as well as explaining the involvement of the AR (Androgen Receptor) and ER (Estrogen Receptor), so be sure to check it out.
The data I’ve presented here as well as that in the upcoming print issue of Testosterone will shut those people up once and for all. That and the fact that every person who’s used my protocol (and reported back to me) has retained or even made gains while recovering endogenous Testosterone production. I’ve presented both "real world" and scientific evidence so there’s no doubt in my mind it works. (19-24)
When I make recommendations, I’m not simply pulling things out of thin air; I’m basing them on some pretty solid data. Unfortunately, not everyone will simply take your word for it and that’s fine. To those who don’t believe me, look up the referenced studies in their full text yourself and then maybe we can drop the idea that our HPTA works via magical mechanisms, where it literally "senses" things and "can’t be tricked" as if it thinks or has cognitive abilities to begin with.
Of course, there will be those uneducated message board imbeciles (oops, I mean "gurus") who'll try to dissuade you from thinking this can be done despite the evidence demonstrating it can be done and the complete lack of evidence supporting the idea it can’t. To them, data is just a bunch of words on a piece of paper they don’t understand. They’d rather believe in magic or Jo-Jo the local gym clown instead of the principle matters and research involved with molecular biology and endocrinology.
So there.
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from
http://www.testosterone.net/nation_articles/296cy.jsp
BE OPEN MINDED TO THIS POSSIBILITY, BUT IT IS, AS EVERYTHING IN THIS FIELD, VERY INDIVIDUAL AND MAY NOT WORK FOR YOU
