HCG werking en gebruik

[Ramon1983]

Ik hoop eigenlijk dat de meer ervaren lui hun visie kunnen/willen geven in het onderstaande topic. Ik vermoed dat het onderwerp alsmede voor Ramon1983 erg leerzaam zou kunnen zijn. Overigens ook voor mezelf en de rest van het forum.

http://forum.bodynet.nl/anabolen/528...itor-ai-3.html

Dit is voor mij een zeer leerzaam topic inderdaad. Ik ben nu al een aantal weken hierover aan het lezen en ik zie bijna iedereen zeggen dat je te alle tijde HCG moet toevoegen aan een kuur. Dan zie ik weer tijdens PCT, dan weer de gehele kuur. Je ziet ontzettend veel verschillende hoeveelheden langskomen, dus ik zie soms door de bomen het bos niet meer. Zelf heb ik twee keer een injectiekuur gedaan, 1 keer test only en 1 keer test met primo en beide keren waren mijn ballen gekrompen, maar ook weer op normale grootte teruggekomen. Natuurlijk is dat minder prettig, maar ja, zolang ze maar terug groeien. Bij mijn volgende kuur, waarbij ik nog niet zeker weet wat het gaat worden, maar ik denk test e + Tren e wil ik HCG mee laten lopen. Toch weet ik het nog niet zeker, want ik lees ook weer dat het kan zorgen voor abnormale zaadjes!!??? In hoeverre moet je dit geloven, aangezien je de grootste onzin op internet ziet langskomen?

[Spuitelf11]

Ik heb nog een Engelse variant geschreven. Geen idee wat de status is omtrent hCG gebruik op de internationale fora (ik kom daar nooit), maar zal me niks verbazen als dat ook zo tegenstrijdig is als op de Nederlandse boards het geval is/was.

Unfortunately, a lot of bodybuilders to date still do not seem to appreciate the value of hCG usage during a cycle in regards of post cycle HPG axis recovery. For some it feels weird to use something, which serves the same goal as PCT, during a cycle instead of after. For others it is odd to use 'low dosages' of something they are used to inject after their cycle, instead of during. Allegedly they assume these 'low dosages' do not do anything at all, seemingly because their HPG axis is suppressed anyhow. Moreover, some claim it to be 'purely cosmetic', without any functional purpose.


If anything, and I would like to make this loud and clear, correct hCG usage is the absolute pinnacle of HPG axis recovery.


What is Human Chorionic Gonadotropin (hCG)?
As most do know, hCG is an endogeneous hormone. Normally hCG is solely produced by pregnant women and men do not usually produce it in signifcant amounts. The hormone has quite a lot in common with something both sexes produce, namely LH. LH is, as most of you reading this will know, secreted by the anterior pituitary in response to GnRH and binds to the LH Receptor (LHR) on Leydig cells to stimulate the steroidogenesis.


Structurally, both LH and hCG belong to a group of glycoproteins and exist out of two subunits, the alpha- and beta-subunit. LH and hCG share the same alpha-subunit, as do TSH and FSH. However, they differ in their beta-subunits. Nevertheless, LH and hCG are 80% homologous in their beta-subunit. Furthermore, they are ligands to exactly the same receptor, the LHR (also commonly dubbed the LHCGR). Since the LHR is a membrane bound receptor (more specific a G-protein coupled receptor), activating the LHR works much like an on/off switch, contrary to nuclear receptors which form a complex with their ligands and translocate to the nucleus to initiate gen transcription, and thus the response can be directly influenced by their ligands (be it by binding to a different hormone response element, recruiting different transcriptional cofactors, etc.). So unless hCG (or LH for that matter) also bind to other receptors with significant affinity, the two are biologically very much alike. Any difference would evolve from their pharmacokinetic differences. Notably, the big difference between the two is their half-lifes. Whereas hCG has a half-life of about 36 hours (depending on the literature source, I've also seen about 24 hours, but you'll get the point), the half-life of LH is less than half an hour.


So what would this imply? Well, for one instance, under physiological normal conditions, LH is secreted in pulses (as is GnRH). Most likely because this is efficient, as their receptors get temporarily desensitized. Mention the word 'temporarily'. Of most users concern is that, for some reason, the receptors get permanently desensitized, however this is not the case. The occuring desensitization is actually quite normal and is common among a lot of G-protein coupled receptors. As mentioned before, the LHR is a G-protein coupled receptor. G-protein coupled receptors exert their effects through G-proteins, activating a signaling cascade through several protein kinases fosforylating their downstream effectors. Now, this fosforylation can lead to (de)activation of the fosforylated molecule. The 'problem' is that the LHR also gets -temporarily- fosforylated due to its own cellular response, deactivating it, as it can not bind to a G-protein. Now, and I would lik to repeat this, this is a completely normal and commonly occuring biological process. It happens ALL the time.


Furthermore, if we were to look to a clinical study evaluating a rather high bolus of hCG through injection (Trinchard-Lugan et al. [2002]), we can see that, even on multiple injections, a strong steroidogenic response is retained. Implying this autofosforylation process probably is not of practical concern to us. For the ones wondering, we also see that SQ injection hardly differs from IM injection; SQ injection really is fine. Do not bother yourself with IM injections and suit yourself with SQ injections by means of a painless insulin needle.


Practical implications?
Now we get to the good part. As known, without a doubt, primary hypogonadism is the major obstacle in post-cycle recovery. Not secondary hypogonadism, as it usually resolves spontaneously and can be fastened by usage of SERMs (even leading to supraphysiological levels of the gonadotrophins). Now this is exactly where hCG is interesting, prevention of primary hypogonadism. Resolve this, and your only concern is secondary hypogonadism which is quickly recovered. As most readers know, when you apply AAS, you suppress your own endogeneous testosterone production due to suppression on level of the anterior pituitary as well as the hypothalamus, both of which is the result of the androgens and estrogens from AAS usage. Now, when the hypothalamus is suppressed concerning the secretion of GnRH, the anterior pituitary is strongly inhibited in its secretion of the gonadotropins: LH & FSH.


LH binds to the LHR on the Leydig cells and FSH binds to the FSHR on the Sertoli cells. The Leydig cells is where steroidogenesis take place, as they have all the machinery (steroidogenic enzymes) in place to do so. Binding of LH and LHR is a very potent signal to stimulate the steroidogenesis. In addition, some other factors also enhance this, this includes Sertoli derived factors working in paracrine manner (which are secreted on binding of FSH on the FSHR), as well as IGF-I, etc. But of primary concern is the activation of the LHR itself on the Leydig cell. If it not gets activated, testosterone production stalls and you'll be hypogonadal. As a result, intratesticulair testosterone levels drop immensly (normally they are roughly a 100 times higher than circulating androgens, hence why your exogeneous androgens do not matter concerning this), which is a prime paracrine regulator in the testes. As known, the testes experience, sometimes extremely severe, atrophy.


Now post-cycle, when your testes have shrunk, and you stimulate your gonadotrophins by means of a SERM, the hypothalamus and anterior pituitary part of the axis is OK. They'll even be heightened. But your testes fail to provide an adequate testosterone response! The steroidogenesis is impaired. This can take weeks or even months to recover, despite heightened gonadotropin levels. In some cases I have read this to be permanent.


Now, this is not what you want. So what you want is to maintain the internal milieu of the testes as much as possible, so recovery is quick after a cycle. By injecting hCG during a cycle (and I know this probably already made sense to a lot of you), you keep activating the LHR and the steroidogenesis will continue. You WILL continue producing testosterone during your cycle and you WILL maintain your intratesticulair testosterone (ITT) levels.


When we delve into the literature, a study by Coviello et al. (2005) provides us with some straight on directly useful results. In this study, they recruited healthy men and suppressed their HPG axis by means of testosterone injection (this is as close as to 'practical' for bodybuilders it will get). In addition, they seperated these men into groups, only varying in the amount of hCG they applied. They had a control group injecting no hCG, and three groups injecting 125 IU, 250 IU and 500 IU of hCG EOD. They measured, among other variables, LH, FSH and ITT. As expected, the gonadotropins were heavily suppressed. Now interestingly, the group applying 250 IU hCG EOD expressed ITT levels very similar to baseline. This implies that this amount of hCG was stimulating the steroidogenesis in the Leydig cells as LH would under physiological normal conditions!


Now, one drawback of this study is that it could have been that the injected testosterone, due to some unkown and mysterious mechanism, influenced the ITT (it is again, highly unlikely that it would, as ITT levels are roughly 100~ higher than circulating). So ok, in 2010, Roth et al. evaluated if the testosterone might have influenced the results by suppressing the HPG axis by means of an GnRH antagonist acyline. This was, as expected, not the case. Unfortunately, the highest dose evaluated in this particular study was 125 IU EOD, as the goal was not to provide juiceheads with valuable information, but rather from a fertility perspective (roughly about 20% of normal ITT is required to maintain normal spermatogenesis).


However, another drawback of this study, is that it evaluated the effects over 3 weeks. We do not know how this could evolve over a longer period of time. So unfortunately, this is the best we got and have to go with. Of course, other factors, besides activation of the LHR and its resulting signaling cascade, could play a part then. It is logically to assume that, if something like that was the case, addition of FSH could solve this. But data is lacking.


So it seems 250 IU hCG EOD is an adequate and valuable protocol, some might to dose it even higher due to interindividual variability. Besides, the underground manufactured hCG might be a (little) underdosed, adding to 'round up' this recommendation.


Of course we might evaluate anecdotical results from boards to conclude if hCG works as it should, however, how many users have actually applied a CORRECT protocol? Not underdosing it? And being consistent in their injections without 'forgetting' or omitting some? And was their HPG axis 'healthy' to begin with? Did they store it correctly? Exactly, it is thus hard to draw any conclusions from that. Might just want to evaluate this for yourself; test your total testosterone and LH on two seperate occasions before a cycle, accurately apply recommended protocol during a cycle, and evaluate it again, relatively shortly, after your PCT. Happy with the results? I certainly hope so.

[Dexie]

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