I think there is no purpose for the hcg if your on test replacement. Hcg can have a host of negative side effects. Unecessary
Not entirely true. Many practitioners consider this incredible hormone treatment of choice for hypogonadotropic (secondary) hypogonadism. Such certainly is intuitive, as supplementing with a LH analog indeed increases testosterone production in patients who do not concurrently suffer primary hypogonadism. But for some unexplained reason, while serum T levels may be adequately elevated, the patients simply do not report realization of the subjective benefits of TRT, when HCG is administered as sole TRT. You also run the risk of inducing LH insensitivity at higher dosages, and therefore may actually cause primary hypogonadism while attempting to treat secondary hypogonadism. HCG, especially at higher doses (defined as >500IU per shot), also dramatically increases aromatase activity, thus inappropriately elevating estrogens. Progesterone—a feminizing hormone in adult males—also elevates at those dosages. Personally, I recommend giving no more than 100IU of HCG per day, as starting dose. And please give it some time to work.
A real benefit of HCG is that it will prevent testicular atrophy. I do not think we should ignore the aesthetics of that consideration.
Now to address the nip issue.
you may need to address any side effects due to elevated estrogen levels which have occurred. I do not use an AI initially, even when E2 is elevated, because some patients will actually see a drop in estrogen over baseline on follow-up. We would have otherwise added an unnecessary (and relatively expensive) medication. Should the patient develop any “nipple issues” secondary to accelerating serum androgen levels and/or elevated estrogen, you cannot start them on a SERM right away because doing so will invalidate your estradiol assay at follow-up. Of note, males can experience said “nipple issues” even while estrogen levels are within physiological range, due to mere changes in hormone levels. A drug of the class SERM is treatment of choice in this case, until symptoms subside. I do not favor SERM’s long term, even though they have been shown to elevate T levels, because we simply do not know what they do long term. Reassure your patient he will not grow breasts in one month.
If a patient has “nipple issues”, even while estrogen is within normal range, then add a SERM, emergently. I prefer Nolvadex over Clomid. Clomid often induces untoward visual effects (i.e. “tracers”), and can cause emotional lability by virtue of its estrogen agonistic effects at the more peripheral (emotion) brain sites. Nolvadex is then initiated, should they experience nipple swelling or sensitivity, at 40mg per day until the symptoms abate, and then taper down 10mg every 10 days to discontinue.
My TRT male patients who suffer E2 elevations above the top of normal range are placed on between 0.25 and 0.5mg Arimidex every one to third day, depending upon the specific situation. It is possible to cut the tiny 1mg tabs into quarters, but here a compounded prep, to convenient dosing, makes a lot of sense. A month later I recheck E2, (as subsequently lowered SHBG will affect subjective response as well) and make further adjustment if necessary. Always remember it is important to not lower estrogen too far.
So now let’s say we have the patient in a state where Total Testosterone is in the upper quartile of “normal” range, Bioavailable Testosterone is nicely elevated, with E2 safely in check. At this point I offer the patient my HCG protocol. I add in 250-500IU of HCG, on day five, and day six, of the injection week, for those who use the IM injection. In other words, the two days prior to their test cyp shot. For those using a transdermal delivery system, 100-250IU SC (HCG is best administered subcutaneously) every one to third day. For the IM patients, this compensates for the drop off in serum androgen levels by the half-life of the test cyp.
Patients nearly always report they feel dramatically better once the HCG regimen is initiated (and they were properly tuned up on testosterone before they started it). HCG, as a LH analog, increases the activity of the P450 SCC enzyme, which converts CHOL to pregnenolone. Thus all three hormonal pathways are stimulated in patients who may be either entirely, or very nearly, HPTA suppressed. It is my belief this may be a factor in the heightened sense of well-being my patients report throughout the week—far in excess of what a nominal dose of HCG would produce by virtue of induced testosterone production.
Many TRT practitioners add in HCG for a short course every few months, to re-stimulate the testes. My opinion is that it is far better to keep them up to form and function all along the way. The physicians who intermittently use HCG also use it as a “break” in TRT, much the same way hormonally-supplemented athletes manage the typical anabolic steroid cycle. TRT should not be “cycled”. Once I get my patients properly tuned up, I want them to stay that way. They also erroneously believe this allows the HPTA to recover, when it clearly does not. The HCG-induced testosterone production is every bit as suppressive of the HPTA as the TRT, and the supplemented testosterone is still at suppressive serum levels during that time, anyway.
A good Dr will nearly always add HCG, DHEA and pregnenolone to the TRT regimen. Inserting these hormones helps restore natural hormonal pathways, "backfilling" them, if you will, once we have suppressed the HPTA with TRT. We will probably never know all the intermediary steps in these pathways, much less all the actions of each substance upon the body. In my professional opinion, this is the current state-of-the-art in TRT medicine.
