I've been looking for people who have discovered pulsatile GnRH as an adjunct to TRT to keep the HPG axis running as I recently discovered this protocol which makes me feel worlds better on TRT. It was important to me to try to keep the factory running as I may want to discontinue TRT at some point in the future.
So I started looking for solutions and discovered hCG and GnRH thanks to some forum posts like these, and dove into the literature around hypogonadism and fertility treatments and compared them to the protocols from TRT clinics (which I am not convinced are evidence-based, the weekly high-dose GnRH does not seem like it would be very effective, IDK though). I wanted to avoid AIs and SERMs as well.
I found the hCG (500 IU q4d or 1000 IU q7d) with TRT (50mg q2d) seemed to increase my aromatization sides (acne, nipple swelling, tight prostate/slow urination, etc) but GnRH substantially decreased them. My theory is that the real LH/FSH in a pulsatile fashion diverts most of your aromatization to your testicles where it belongs instead of secondary tissues (why did this not happen with hCG? keep in mind hCG has a really long half-life so your leydig cells are constantly activated instead of pulsed like natural LH release - maybe that has something to do with it?).
Unfortunately the pulsatile GnRH protocol is really inconvenient - 10 mcg q2h, which is a lot of pokes per day, and overnight, your FSH producing mRNA will decay. Commercial fertility treatment pulsatile GnRH solutions like LutrePulse - which is based on the OmniPod insulin pump (looking into the open source artificial pancreas community to see what they have in this vein) - use gonadarelin _acetate_ in solution, not just gonadarelin. GnRH without the acetate is unstable and will hydrolize, oxidize, and break down in water within a couple of days and lose potency quickly. Many fertility clinics seem to prepare GnRH for pulsatile injection with a sterile 0.1M sodium acetate buffer at pH 5.0 and that seems to maintain potency for weeks or months, but still maintains short serum half-life needed for pulsatility (unlike modified GnRH like triptorelin).
I had also looked into kisspeptins, but like SERMs I was afraid of some of the cardiovascular possibilities seen in studies, and I also think based on my amateur endocrinologist understanding, stimulating the KNDy network directly with kisspeptins might be redundant with the pulsatile GnRH. I feel like based on the side reduction so far, I could potentially increase my TRT dose without getting into AI territory.
Anyways, sorry for necro-ing the thread, this is my first post on this forum so I'm not sure what the etiquette is but it looks like this thread was posted to several times over the years so hopefully I'm not committing a major faux pas and this information is useful to someone out there.