Here I am again. I'm not going to do the paste thing, either. Why? 'Ol Doc doesn't know how to. At any rate, here are my points:
Yes, I see almost complete suppression in many patients by the end of the second week (for logistical reasons, labs for Androgel patients are drawn at that point, before the patient has to buy another month's supply). That is a medical fact, with Third Generation FSH assays to prove it. As I'm sure you already know, LH is of no use in monitoring suppression because of its extremely short half-life and absolute pulsatile production (unless one has the time, and money, to undergo serial draws over an entire morning).
On the other hand, there are those individuals who maintain bountiful endogenous production on the usual 100mg per week testosterone replacement therapy (TRT) Upjohn test cyp dose. I have learned two things in my clinical experience: (1) You never know how a patient is going to react to a given dosage until to try, then do follow-up labs, and (2) NOTHING surprises me anymore.
And I do not ever want to say "no production". Constitutive production of LH and FSH can be expected, but not at any level which is supporting serum androgen levels to any appreciative degree.
Certainly, being a doctor does not automatically qualify me as an expert on this, or any other topic. Indeed, by my experience in trying to get other doctors to give their patients testosterone replacement therapy (TRT), it seems more that being a doctor precludes an individual from understanding this stuff! LOL. However, as far as "the finest minds" in this field go, I teach Endocrinologists how to administer TRT.
Duration is of very little influence where suppression is concerned. Once the HPTA is supprerssed, that is it. And it seems to make no difference how long the HPTA is supressed, if post cycle therapy (pct) is done correctly, then it regains form and fnction (in MOST cases--I do have quite a few patients who are former Anabolic Androgenic Steroids (AAS) users who then became hypogonadotrophic). Of course, appropriate post cycle therapy (pct) requires the use of Human Chorionic Gonadotropin (HCG), unless one wants to dramatically extend the time required for same, as testicular function is clearly the rate-limiting step in the process.
No one is recommending "chronic" HCG use. Minimal doses throughout the cycle do not qualify as same. Or, a short run at the end of the cycle should the patient fail to use it all along the way. But you are indeed correct that too much for too long is bad for you. This is something else entirely.
I would also add that a few of my Anabolic Androgenic Steroids (AAS) patients report they feel MUCH better on their usual heavy cycles when they add in regular injections of HCG along the way. Moreso, many tell me that my post cycle therapy (pct) protocols have allowed them to recover much faster, and with less annoyances along the way. They also say they are now avoiding that burned-out, edgy feeling one gets about half way into the cycle. I tend to value their opinions, as I always listen to my patients.
I have gravitated toward Nolvadex preferentially over Clomid for post cycle therapy (pct). But that is not because it does not work as well, but rather because there is some small evidence there may be a very small risk of permanent visual injury with it. And some, by experience, do not benefit from the possible emotional effects (although some do!). It's better to avoid the issue if we can. But Clomid is a tremendously useful and effective medication in the majority of individuals--or I wouldn't be using it at all. If you don't like it, fine, there's just that much more then for everyone else. LOL.
SHBG levels are of absoluely no consequence either in the intact HPTA, or on heavy steroid cycles. To learn why, study the feedback loops in the former example, and compare SHBG levels/endogenous production and the serum androgen levels of a heavy cycle in the latter example, AND any increase Clomid COULD induce. If you still don't understand, just let me know, and I'll be happy to flesh it out for you.
One must NEVER use an Aromatase inhibitor (AI) if they are not using a lot of aromatisable AAS. It would be ridicuously bad for your health to do so. As far as adding in a SERM under the same circumstances, I suppose there is no real danger from same, and there may actually be some benefit. But for those who willy-nilly add in anti-E when they are already not producing enough estrogen because their HPTA is suppressed by the cycle, that is a different matter.
There is some evidence that some Anabolic Androgenic Steroids (AAS) may have progesterone-like affects, and thus may induce gyno while operating in an environment of estrogen. I think the jury is still out on that one at this time, though.
