Pros and cons of HCG

Discussion in 'Men's Health Forum' started by Structure, Apr 8, 2011.

  1. Structure

    Structure Member

    I was talking with my wife last night about some of the hcg questions that I've seen on the forum, and she stumped me with a question of her own: Why don't more men on TRT use HCG to prevent testicular atrophy and infertility?

    When I first started posting on Meso, I asked a similar question ("Is it possible to stay on a cycle indefinitely without suppressing if you took enough HCG, clomid and adex?"). However, I didn't have a good understanding of how HCG worked at that time; I mistakenly thought that HCG could be used to prevent hypothalamic / pituitary suppression, and that it would bring LH and FSH up.

    Since then, I've researched HCG in the journals, and I feel like I understand it pretty well at this point. Still, I was only able to answer her question partly.

    I explained to her that since HCG is similar to LH, HCG is only useful in men whose testes can respond to LH. This limits the usefulness of HCG to the group of men that have secondary hypogonadism. Still, I couldn't really explain why more men with secondary hypogonadism don't use HCG. I expect that some men on TRT are bothered by the shrinkage, but more still would be bothered by the infertility. HCG seems to take care of both problems.

    On the cons side, there's the hassle of having to give yourself shots, and there's the potential for high E2. However, it looks like if you use small, daily doses of HCG, you can pretty much avoid the E2 spike entirely (see Differential Effect of Single High Dose and Divided small Dose Administration of Human Chorionic Gonadotropin on Leydig Cell Steroidogenic Desensitization -- SMALS et al. 58 (2): 327 -- Journal of Clinical Endocrinology & Metabolism).

    On the pros side, it prevents testicular atrophy and infertility, and thus can make the transition from using TRT to not using TRT much less difficult --- atrophied testes don't respond right away to the body's own LH, so keeping them functional with HCG makes it so that they can "hit the ground running" so to speak.

    Am I missing something?
     
  2. LW64

    LW64 Member

    You're basically right, Structure.

    There are cases where even low-dose daily injections dont alleviate the E2 problem. I'm one of them. I was on hcg monotherapy for about 8 months and couldnt get my E2 low enough and I didnt like the idea of adding in an AI, even at low dose, so I stopped. Now I add it in (at 300 IU/week) with IM T injections and it still complicates things by contributing to an increase in E2.

    There are also some men who are secondary and dont care about shrinkage and/or fertility and cant be bothered to add one more drug to their TRT protocol, especially since it can raise E2 and have a negative effect on sexual ability.
     
    slick50 likes this.
  3. CubbieBlue

    CubbieBlue Member

    Not missing a thing. If it's not absolutely necessary, why use it?
     
  4. Structure

    Structure Member

    Thanks for the replies, guys.

    I assumed that I must have been missing something, because it sounds too good to be true: all the benefits of AAS without the consequences of atrophied testes. Take for example steroid abuse: occasionally, you'll see an AAS user post here that has developed hypogonadism from steroid abuse (e.g. long cycle, etc.). If they used a low dosage of hcg daily, then (at least in theory) they would they not suffer testicular atrophy, nor the slow HPT restart associated with atrophied testes.

    This kind of hearkens back to (what was meant by) my old post: if people are going to abuse steroids, why don't they use HCG to avoid the hypogonadal crash associated with atrophied testicles?

    I can understand that if you don't plan on having kids, you wouldn't want to bother with the shots. But for all others that are secondary, or for all athletes that plan on using their testicles when not on steroids, it doesn't make much sense to me that they would not incorporate daily HCG. After all, part of the reason why some athletes don't use steroids is because they don't want the shrunken testes. Is it just ignorance on their part, or (again) am I missing something?
     
  5. CubbieBlue

    CubbieBlue Member

    Testicular atrophy due to AAS is easily reversible. The hard part is getting the HPA to come back online.
     
  6. LW64

    LW64 Member

    [1] Not likely, but they may not be aware that something like HCG exists at all.

    [2] Very likey: they may not like the associated E2 rise and E2-related sides when they're trying to maximize the effect of their own T and intend to go to HCG 'later' to bring size/function back.
     
  7. Structure

    Structure Member

    (I assume you mean HPT axis) I was under the impression that the testes were the bottleneck in restarting the HPT axis; if you keep the testes functioning, then (unless I am mistaken) it is much easier to transition back to normal.

    Can any AAS users out there confirm / deny this?
     
  8. CubbieBlue

    CubbieBlue Member

    Actually, I meant the HPG Axis. I do not believe it is the testes that are the bottleneck, if not primary, they come back online rather easily with hcg.Now, many folks try this, and then get on clomid or tamoxifen to try and get their HP Axis to start pumping out hormones on its own volition. Most people try this with varying protocols and some end up failing and some end up succeeding. In secondary individuals it is often unclear why the HP is "underperforming".

    Keep in mind that hCG further suppresses the pituitary's natural release of hormones as well.
     
  9. Structure

    Structure Member

    I'm open to this, but it seems to contradict what I have heard in the past, including from Scally: http://forum.mesomorphosis.com/738910-post8.html

    On what are you basing your opinion?

    I understand that it suppresses the hypothalamus by reducing the amplitude and frequency of GnRH pulses, but I'm not aware of any direct suppression on the pituitary. Are there hormones other than LH and FSH that you had in mind? Again, I'm trying to learn here, so I don't assume I know all there is to know about this subject.
     
  10. LW64

    LW64 Member

    My own understanding is that it's not possible to generalize about what the bottleneck is as it varies from man to man.

    hcg may be suppressive, but it isnt as 'suppressive' as not having the H/P produce enough LH to keep your T in the normal range. In other words, you're already suppressed, but this way (say, clomid and HCG) you're starting up both ends of the HPTA.

    I've also always thought HCG was indirectly suppressive via the resulting E2 increase and subsequent down-regulation of the hypothalamus. I wasnt aware of any direct suppression on the pituitary from HCG itself.

    I just learned something in the response from Dr. Scally that you linked. I didnt know T itself is suppressive. What is the mechanism? I always thought the 'sensing device' is the hypothalamus and that it 'reads' E2, not T. The pituitary 'reads' T? I had no idea it could 'read' anything! Or does the hypothalamus 'read' E2 and T?


    I knew from my very good response to clomid that I was secondary and later found out when I used HCG only that my testicles are very capable of making T. What I tried to do when I was on clomid was [a] get the hypo/pit going and then gradually reduce the dose/frequency with the hope they would continue to run on their own. It didnt work; after about a year on clomid, my T levels started dropping.
     
    Last edited: Apr 8, 2011
  11. CubbieBlue

    CubbieBlue Member

     
  12. CubbieBlue

    CubbieBlue Member



    The body senses (or as you say, reads) testosterone. If it senses that there is enough testosterone in the body it will stop producing endogenous testosterone. Thus, T is suppressive. What
     
  13. Tyler81

    Tyler81 Member


    Yes you are.

    Most men do fine on just androgel or Testim. Which is one medication. By adding HCG, you often have to add in adex (to prevent high estrogen from HCG). So essentially you go from having one medication/variable to THREE medications and THREE variables.

    The challenge then becomes, if you don't feel good or have issues, is it the testosterone, HCG or adex causing the problem? And it's difficult to trouble shoot and find the proper balance.

    Another thing that my endocronologist explained to me about fertility: If a man goes through a normal puberty, if he want to have kids, he simply stops the testosterone and boosts with HCG as needed. He does NOT need to take HCG with the testosterone.

    So even for fertility purposes HCG is not needed until you actually want to have a baby.

    The exception is if you are young and have NOT gone through normal puberty or are an adult and did not go through normal puberty.
     
    Last edited: Apr 8, 2011
  14. Tyler81

    Tyler81 Member

    I also think the idea of T + hcg + adex protocol was made popular by Dr Crisler and guys who are on steriod cycles.

    When I used HCG for about a month last year, it felt like I was injecting water. I didn't feel any better or any worse. But I did experience some estrogenic sides like high anxiety and some mild gyno.

    In other words, HCG didn't make me feel any better and it maybe made me feel worse.

    And since I don't need it for fertility until I want to have a kid (explained by my endo, see previous post) I can't be bothered to use it.
     
  15. Structure

    Structure Member

    Scally wasn't exactly verbose in response to my question that time (and has so far remained silent this time), so it is difficult to say exactly what he meant. However, from my perspective it does not look as though the two of you are saying the same thing. I asked the following:

    This was his response:

    This seems to indicate that long-term usage of HCG does not result in a pituitary that is difficult to restore normal function in. On the contrary, you seem to indicate that while it is easy to get the testes functioning again, it is difficult to get the hypothalamic-pituitary-testicular axis working again:

    If the testes are easy to get up and running again, then the only parts remaining in this system are the hypothalamus and the pituitary. Thus, the two of you seem to be saying different things. This is an important distinction to make; on one hand, if AAS induced hypogonadism is as I see it, then the reason why AAS abusers have trouble is because the testes are so shut down that they no longer respond to LH, and must be brought back online with PCT. If HCG does not have any long term effect on the hypothalamus and the pituitary, then using HCG in conjunction with AAS would prevent testicular shut down, and would prevent post-AAS hypogonadism, since the testes would still be responsive to LH after the steroids were discontinued.



    This is similar to how I understand it. High E2 from larger doses of HCG are suppressive, and HCG inhibits the release of GnRH from the hypothalamus. High E2 can be addressed by lowering your dosage and using a daily injection schedule, but HCG in any non-trivial amount will suppress the release of GnRH from the hypothalamus. The question then becomes: are there consequences to the function of the hypothalamus from inhibiting GnRH long term? Does the hypothalamus have trouble "coming back online" as CubbieBlue has suggested, or is this not so, as I have interpreted Scally as having said?

    Is this in fact true? Or is it not true that some men have difficulty getting good sperm counts after having atrophied testicles for very long periods of time?
     
  16. m_ob

    m_ob Member

    I have found that 100 IU hcg daily works very well for the balance of T to E2. It keeps my leydig cells primed as far as sensitivity goes as well. I am extremely greatful that I was prescribed the HCG and not just the gel alone. The combo works well.
     
  17. LW64

    LW64 Member

    I want to be sure I understand you (and CubbieBlue) here, so I'll state my own (maybe flawed?) knowledge of how HCG suppresses the Hyp/Pit because, to me, [1] and [2] are the same thing.

    When using HCG it acts as an LH analogue and stimulates the testes to produce T. That T then eventually gets converted to various Es (with E2 being the main concern) and DHT. The receptors on the hypothalamus read E (not T) and since the amount of E is proportional to the amount of T, the amount of E 'seen' by the hypothalamus becomes the controlling variable for how much GnRH the hypothalamus 'decides' to send to the pituitary. When the hypothalamus 'reads' high E, it 'interprets' that as high T and turns down the GnRH to the pituitary resulting in less LH to the testes and lower T production. When the hypothalamus 'reads' low E, it 'interprets' that as low T and turns up the GnRH to the pituitary resulting in more LH to the testes and higher T production.

    The problem with HCG is that it causes higher E (by aromatase conversion of T to E) than with an equal amount of LH because of two unavoidable characteristics of HCG therapy:

    [1] You cant perfectly imitate the pulsatile nature of LH release from the pituitary, and

    [2] HCG has a much longer half-life than LH.

    So HCG's overall "MAKE T!" signal to the testes results in higher T and, in turn, higher E levels due to the testes being overstimulated - even (for some men) at a minimum level of HCG use.

    Now...Are you saying that, in addition to what I described, HCG itself interacts with the hypothalamus and/or pituitary directly and causes additional suppression, over and above the suppression due to higer E (aromatase converted T) that HCG unavoidably produces?


    I imagine that's a possibility. That's why a restart would use [1] HCG to kick-start the testes and [2] clomid to block the E receptors on the hypothalamus to fool it into 'thinking' there's litte or no T so it will send lots of GnRH to the pituitary resulting in more LH to the testes.


    The issue is what is meant by a 'long period of time' and how old and healthy is the individual thinking about this approach.
     
    Last edited: Apr 9, 2011
  18. Structure

    Structure Member

    That's great that the HCG and T combination has worked so well for you. It is situations like yours that makes me wonder why not all people with secondary hypogonadism are using both HCG and T. I'd be curious to hear how your dosages evolved; specifically: did you ever have problems with high E2 on HCG? Did you get lucky and just start off with 100IUs right off the bat, or did you have to do some tweeking? What are your numbers currently (TT / FT / E2), and how long have they been stable?

    Yes, this is exactly what I am saying. From my understanding, HCG (as well as other LH analogs) directly inhibit GnRH release. It is my understanding that this is how chemical castration drugs work.

    Your way of thinking makes sense to me. However, I feel like we are all just speculating. I'd love to concretely get to the bottom of this question ("are there consequences to the function of the hypothalamus from inhibiting GnRH long term from HCG use? Does the hypothalamus have trouble "coming back online" as CubbieBlue has suggested, or is this not so, as I have interpreted Scally as having said?"). However, I haven't seen anything in the journals that directly addresses this question. I wonder if the experts at the steroid forum have anything to contribute to the conversation. Bill Roberts? Scally? Millard?
     
  19. m_ob

    m_ob Member

    For me it was trial and error. I started out on 500IU e.o.d. This resulted in an annoying nipple pains, but some fast muscle gains as well. I then moved to 200 e.o.d and found this was a pretty good deal, but I got to thinking and decided that to maintain ultimate sensitivity, the lower, more frequent dose would be ideal.
     
  20. Structure

    Structure Member

    I took another look at chemical castration drugs. They are LH-RH agonists, not LH agonists; so my reasoning above can't be used. At first, the LH-RH agonist stimulates the release of LH and FSH, but it also desensitizes the pituitary to GnRH (much in the same way that too much HCG desensitizes the LH receptors in the testes). Thus the pituitary becomes oblivious to the GnRH secretions of the hypothalamus for X months thereafter, achieving "chemical castration".

    I'll take a quick look in the journals and see if I can find anything about LH receptors in the hypothalamus or pituitary; as far as I know, the only way that HCG is going to have a direct effect on either is through these receptors. Is anyone else any closer to finding a more definitive answer? I'm still under the impression that HCG will prevent the hypogonadism associated with the discontinuation of exogenous AAS.