From a blood-testosterone aspect this all seems okay to us, sure we have shut down natural testosterone production, but we still have testosterone in us; right? Well, one of the big problems with regards to fertility is that the testes do not work like that. The Leydig cells in the testes produce testosterone when stimulated by LH. Testosterone is released from these cells which are in close proximity to the Sertoli cells. When Sertoli cells see a high concentration of testosterone, they are stimulated to produce and mature sperm by the process of spermatogenesis. A high blood concentration of testosterone will not do this job. Thus administering anabolic androgenic steroids (AAS) will shut down natural testosterone production which will in turn slow down (and eventually near turn off) the proper formation and maturation of sperm. Thus infertility is a serious issue with use of anabolic steroids.
Classically, HCG has been seen to rectify this problem in males. HCG is an LH analogue – it 'looks' like LH to the body and so it can stimulate the Leydig cells to produce testosterone and in turn, hopefully, restore fertility. In some cases this will occur, and many people have had success from HCG therapy relating to infertility. However, the response is not robust and certainly with longer shut-down periods, many often find the use of HCG (even in combination with other post cycle therapy (PCT) medicines such as clomifene (aka clomid) and tamoxifen (aka nolvadex), etc) to not be effective at restoring fertility.
Furthermore, what HCG lacks is to produce the important effects that FSH inflicts upon fertility. FSH, despite its name, is important in male fertility in two main pathways. The first thing it does is to enhance the action of LH, by increasing the amount of protein that will 'see' testosterone in the Sertoli cells. The more easily these cells can see testosterone, the more likely spermatogenesis will occur. Secondly, FSH enhances the maturation of sperm by effects on their primary division. These are two important aspects of the role of FSH in the male testes that HCG is not optimal in promoting.
HMG, or its full name Human Menopausal Gonadotropin, bears similarities to HCG in that while HCG is similar to human LH, HMG contains actual LH. Additionally (and crucially) though, HMG also contains purified FSH. The combination of these two hormones perform the effects described above: induction of natural testosterone production by Leydig cells, and subsequent formation and maturation of sperm cells. The result is improved and potentially recovered fertility for the male concerned.
Does HMG really work?
So often we hear about various different drugs and the science for them is sound, but real world evidence is lacking. There are a few studies performed on HMG over the last 25 years, and I would like to draw your attention to two of these studies, pointing out a few key details. The first goes back to 1985 by Ley & Leonard and is an important study as it looks at males who had previously encountered anabolic steroids treatment (treatment for low hormone levels including mainly testosterone). This study is available online and I encourage you to read it in more detail than the brief summary I will provide here.
They looked at 13 hypogonadotropic men all of who had undetectable levels of LH/FSH, lower than normal levels of testosterone and azoospermia, thus were unable to currently conceive. Obviously with the low hormonal levels there were issues with libido as well. Furthermore, there were instances where upon testis biopsies, Leydig cells were completely absent. Despite this, all 13 men responded to treatment with HCG with increasing testosterone levels. However, upon addition of HMG treatment, most men saw a further increase in testosterone, sometimes very large. HCG was able to increase sperm counts in most men slightly; however, only upon addition of HMG were sperm counts above 'normal' fertility levels (i.e. 20 million per ml) observed. The study indicates that the addition of HMG therapy surpasses any level that HCG treatment could achieve alone. Admittedly this is a particular subset of men who have medical conditions and abnormal hormone issues, but the results are interesting nonetheless.
The second is more recent by Buchter et al in 1998. This is even more interesting from the point of view that it looks at three times the number of cases as the previous study and in a different manner. Again, this study can be found online and I encourage you to read it. The most interesting result you could take away from this study is that in the group of men treated who suffered from hypopituitarism, all 21 treated with HCG/HMG achieved spermatogenesis and a large proportion (81%) was able to successfully achieve pregnancies. The discussion of this article is most interesting as it raises the points from its own study and the literature that many in the field believe that to achieve spermatogenesis and pregnancy in a gonadotropin-compromised individual requires combinational therapy of HCG and HMG. The important point to note is that HCG is not sufficient alone in many cases.
Given the fact that other studies point to HMG increasing endogenous testosterone further than HCG can, as those who have relatively 'normal' pituitaries but have compromised their function due to AAS use, it would be wise to consider the use of HMG. This would not only be for purposes of fertility, but to induce natural testosterone levels back to normal values when they have been suppressed. Treatment in this latest study was the use of HCG twice per week at 1000-2500IU per dose (Mon-Fri) and HMG three times per week at 75-150IU (Mon-Wed-Fri). Thus for bodybuilders seeking to regain fertility, spermatogenesis and restore natural testosterone levels but wishing to keep costs down, a weekly dose of the lower ends should be employed for at least one month.
A schedule would involve:
Monday: 1000-1500IU HCG + 75IU HMG
Wednesday: 75IU HMG
Friday: 1000-1500IU HCG + 75IU HMG
Depending on the amount of suppression this cycle may need to be lengthened for a further period.
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