People with low testosterone from endogenous factors (elderly men, people with Klinefelter’s syndrome, etc.) invariably have high Luteinizing hormone. In fact, it is speculated that high LH because of low T could be a risk factor in Alzheimer’s. What has happened in these populations is a problem in their testes, not their HPTA axis. The high LH in people with low T shows an actual supercompensation of HPTA, which Bill Roberts used to get into years ago.
Bodybuilders who shut their testosterone down with anabolic steroids will eventually have their HPTA axis restored and even super compensated if they wait long enough. For a bodybuilder, 12 months is forever, however you are essentially starting puberty all over again. From the beginning of puberty, it could take several years for FSH and LH pulses from the pituitary to reach their maximum levels, and this is no different in bodybuilders.
I have attached a study on bodybuilders who had “permanent” low testosterone from years of steroid use, and after about 36 months, not only had the bodybuilders LH and FSH returned to normal, but they had higher LH and FSH than the control group, in fact shutdown bodybuilders had the highest LH in all study groups even though their testosterone was the lowest. HPTA axis can shut down for 12-36 months (or even longer) if you have been “on” for a long time. I hypothesize that if you are permanently “shut down”, you will eventually have a super compensated HPTA with your low T.
What has happened in terms of permanent shutdown is direct testicular damage, and I have included a few studies on this. The reason that HCG works is not only by mimicking LH and FSH, but because it is restoring the Leydig cell function in the testicles. It is no coincidence that HCG comes from pregnant women, because HCG is what develops the male fetuses’ Leydig cells during pregnancy, cells that will be used many years later to respond to puberty. But without the Leydig cells functioning, you can have all the LH you want, and it won’t help. I have attached other studies that show that bodybuilders can have permanent damage to their testicular function, not their HPTA axis. This may be why HCG is so effective in male fertility. It is restoring the testes’ ability to make sperm, the FSH and LH mimicking is not the direct benefit of HCG for men. Even women who have low estrogen have high LH, the problem is their ovaries not their pituitary.
So how does this affect PCT? The focus should be on restoring testicular function. HCG seems important, not because of the LH and FSH mimicking, but the restoration of Leydig cell function that is vital once HPTA is restored. Don't declare HCG ineffective if you don't get immediate rises in test. You may be helping your Leydig cells which will pay dividends down the road. I found research on other novel compounds that could also help. One is stem cell therapy to the testes. Another is Insulin Growth Factor 3(IGF-3). For male’s with Klinefelter’s syndrome or when the testes do not descend after puberty (your balls don’t drop) they have used both stem cells and IGF-3 successfully to restore testicular function.
But the future of PCT is restoring testicular function, not HPTA.
The idea that you have shut down your HPTA axis permanently I believe may be bro-science. If you are permanently shut down, it’s in your balls, not your pituitary.
However the testicular damage from long cycles
can be permanent if one is on long enough, which means along with your low T you may never have kids.
If we found effective ways to regenerate Leydig cells in the testes, we could help many people with low T, not just bodybuilders.A few of the studies I have referenced
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4988681/https://onlinelibrary.wiley.com/doi/pdf/10.1111/j.1365-2605.1987.tb00380.x https://www.endocrine.org/news-and-advocacy/news-room/2021/steroid-abuse-by-men-leads-to-long-lasting-impaired-testicular-functionhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5217336/#:~:text=In%20adult%20males%2C%20LH%20regulates,the%20male%20foetus'%20Leydig%20cellshttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5080638/