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    HCG and HMG 
    #1
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    Here's a thread I posted on another forum. Since practically nobody has used HMG I am posting it here to hopefully snag a person who has actually used or knows much about it. HMG mimics both LH and FSH. It is used in much lower doses than HCG (which solely mimics LH). HMG will drastically increase sperm count and has chance to bind to receptors in testicles that HCG alone will not bind to. The idea is using both at once will kickstart testosterone production better than just HCG along. PCT would still be normal nolvadex/aromasin (in our example below that would start week 15, I didn't list it for simplicity's sake).

    Here's the thread:

    I'm thinking about running HCG during my next 12 week Test E cycle (and during 2 weeks after last shot before PCT. During those 2 weeks I will also pin HMG alongside the HCG. I think 50-75IU alongside 250IU 3x/week (so that would be 6 doses of the HMG and 6 doses of the HCG for the 2 week interim between last test shot and PCT).

    During cycle I will run 250IU HCG 2x/week.

    So just to make sense of this:
    Test E 250mg 2x/week 1-12 (also some other stuff Dbol and EQ probably)
    HCG 250IU 2x/week 3-12
    HCG 250IU 3x/week 13-14
    HMG 50-75IU 3x/week 13-14

    Has anybody run HMG and did you notice quicker recovery?
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    #2
    Bluelight Crew Swerlz's Avatar
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    Human Menopausal Gonadotropins??
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    #3
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    yes sir

    you like that name
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    #4
    Bluelight Crew VictorZ06's Avatar
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    HMG is good stuff, but I don't think you need to include it in a test only cycle.

    It's fairly new, not as readily available, and somewhat expensive compared to HCG. I know of a few guys that used it, not really for PCT. They became infertile and wanted to have kids. Yeah, bad or no PCT can leave you infertile. You are correct though, both should be run at the same time for best results.

    I would use it if you were running a really heavy stack, in your case, I don't think recovery time would be very different.

    Some notes:

    HMG is typically used to treat infertility . Basically, long term use of HCG at doses of 1000 i.u. 3 or more times weekly causes suppresion or insensitivity of Luetinizing hormone (LH) and to some degree Follicle stimulating hormone (FSH).

    Body builders who dont respond to the classic PCT schemes of low dose HCG and clomid for a few weeks will definitley have a hard time with recovery and may encounter depression, a lacking sexual drive, low testicular weight along with low semen/sperm volume.

    HMG is Follicle stimulating hormone (FSH) and luetinizing hormone (LH). This simply stimulates your natural test production and keeps HCG working optimally. Your sex drive and sense of well being come back more rapidly then with other treatment as well as your potential for staying or becoming fertile.

    Luteinizing hormone (LH) and follicle-stimulating hormone (FSH) are called gonadotropins because stimulate the gonads - in males, the testes, and in females, the ovaries. They are not necessary for life, but are essential for reproduction. These two hormones are secreted from cells in the anterior pituitary called gonadotrophs. Most gonadotrophs secrete only LH or FSH, but some appear to secrete both hormones.

    As described for thyroid-simulating hormone, LH and FSH are large glycoproteins composed of alpha and beta subunits. The alpha subunit is identical in all three of these anterior pituitary hormones, while the beta subunit is unique and endows each hormone with the ability to bind its own receptor.

    In both sexes, LH stimulates secretion of sex steroids from the gonads. In the testes, LH binds to receptors on Leydig cells, stimulating synthesis and secretion of testosterone. Theca cells in the ovary respond to LH stimulation by secretion of testosterone, which is converted into estrogen by adjacent granulosa cells.

    As its name implies, FSH stimulates the maturation of ovarian follicles. Administration of FSH to humans and animals induces "superovulation", or development of more than the usual number of mature follicles and hence, an increased number of mature gametes.

    FSH is also critical for sperm production. It supports the function of Sertoli cells, which in turn support many aspects of sperm cell maturation.

    Diminished secretion of LH or FSH can result in failure of gonadal function (hypogonadism). This condition is typically manifest in males as failure in production of normal numbers of sperm. In females, cessation of reproductive cycles is commonly observed.

    Elevated blood levels of gonadotropins usually reflect lack of steroid negative feedback. Removal of the gonads from either males or females, as is commonly done to animals, leads to persistent elevation in LH and FSH. In humans, excessive secretion of FSH and/or LH most commonly the result of gonadal failure or pituitary tumors. In general, elevated levels of gonadotropins per se have no biological effect.



    /V
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    #5
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    good information. Victor, do you use HCG throughout the entire cycle or do you use it midway through or just right before PCT (or even during PCT)? So many people use HCG differently its quite confusing.

    I started it late in my cycle (2 weeks before the cycle ended). Testicular atrophy had already set in by that time of course (10 weeks on) and the HCG 'shocked' the testicles back and volume increased slowly (as did strength I believe I experienced a testosterone spike since I got a little acne and got maybe 10-15% stronger with lifts all of a sudden). When the HCG wore off and my PCT started I noticed a temporary decrease in testicle volume and then the nolva brought LH back to normal and finally the testicles stabilized at their average volume/size (after 2-3 weeks on nolvadex).

    So, now I'm thinking about running HCG during the entire cycle, but I also am afraid of desensitizing leydig cells. Don't want that to happen and then have a long time with low/abnormal LH levels. So I dont know what to do honestly. Keep researching and talking with people until August/September when I cycle again.

    One more question
    : Lots of websites say things about HCG and HMG like: "HCG is LH" and "HMG is LH and FSH". Do they mean "HCG mimics the action of LH" and "HMG mimics the action of LH and FSH". I mean, it has a different chemical structure right? HCG isn't identical with LH because then you would be injecting LH and not HCG. Or is it just another name for LH?
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    #6
    Bluelight Crew VictorZ06's Avatar
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    HMG is used to mimic FSH, and HCG mimics LH.

    I never had the need to use HMG, my recoveries are quick and easy. I usually start using HCG starting week 2 of my program, this way there is no hypogonadism. If I wait until the end to use it with PCT, my nuts would be the size of raisins and that doesn't float well in the bedroom.

    I have an article that helps better describe this, I'll see if I can dig it up.

    /V
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    #7
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    yes that makes sense to me (to use it before atrophy sets in).

    Have you had your LH levels checked after recovery to ensure they are normalized? I was recommended to get Test, Estrogen, Prolactin, LH, FSH levels checked after PCT is finished to ensure everything worked (and not just go by how I feel strong/sex drive up, etc)/.
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    #8
    Bluelight Crew VictorZ06's Avatar
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    I had it checked once a while back after running a rather heavy and long program, I can't recall the exact number but everything fell within normal. I want to say something like 14 mIU/ml, but I can't be sure.

    /V
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    #9
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    Wow I've never heard of this stuff but a way to increase FSH is a great advance...

    PCT's at the moment are pretty shit hot. If you're already running HCG and a serm AND an AI then its doubtful you'll need anything else.

    I've always been of the opinion that HCG should be reserved for the post cycle- pre PCT shots. I don't really understand why a postive LH signal would be a great idea (apart from in PCT). But people have been responding well in the past 3-4 years from a cycle that includes HCG from the start- to reduce atrophy before it begins. So I'm not one to piss on that parade. As for increasing FSH levels- I can again see why it might be useful post cycle but can't see the benefits during the cycle. But maybe there's something I'm missing....
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    #10
    Quote Originally Posted by sunyata View Post
    HCG 250IU 3x/week 13-14
    HMG 50-75IU 3x/week 13-14
    There isn't nearly as much literature on hmg as there is on hcg. Based on what has been written, 75ius EOD is the way I would try it. Is two weeks enough? I couldn't tell you for sure, but would be more apt to think a longer duration is necessary (3-4 weeks).

    As for your question regarding whether hmg will help you recover more quickly than hcg, it depends on your definition of recovery. HCG, which is synthetic LH (that answers another question), stimulates testosterone production. FSH is more important to sperm production. So, full recovery would be quicker with FSH. Testosterone recovery will not be markedly increased.

    Furthermore, I would not suggest the use of an AI post cycle due to possible detrimental effects on the heart (see the study below). Also, an AI post cycle may actually slow recovery by artificially lowering shbg. By lowering shbg, free testosterone levels are increased. Increasing free testosterone levels will inhibit the recovery of total testosterone recovery via negative feedback.

    http://www.pnas.org/content/98/6/3589.full
    Last edited by hiddenbeneathe; 01-06-2009 at 03:24.
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    #11
    Quote Originally Posted by VictorZ06 View Post
    Yeah, bad or no PCT can leave you infertile.
    Do you have anything other than anecdotal evidence to support this statement? Male contraceptive studies showed complete recovery of testosterone in 100% of subjects.

    Lancet. 2006 Apr 29;367(9520):1412-20.
    Rate, extent, and modifiers of spermatogenic recovery after hormonal male contraception: an integrated analysis.

    BACKGROUND: Hormonal methods for safe, reliable, and reversible contraception based on the suppression of spermatogenesis could soon become available. We have investigated the rate, extent, and predictors of reversibility of hormonal male contraception. METHODS: We undertook an integrated multivariate time-to-event analysis of data from individual participants in 30 studies published in 1990-2005, in which sperm output was monitored every month until recovery. The primary outcome was the time for the sperm concentration to recover to a threshold of 20 million per mL, an indicator of fertility. We undertook univariate and multivariate analyses, using Kaplan-Meier and Cox's methods. FINDINGS: 1549 healthy eugonadal men who were white (n=965), Asian (almost all Chinese men; n=535), or of other origins (n=49) and aged 18-51 years underwent 1283.5 man-years of treatment and 705 man-years of post-treatment recovery. These data represented about 90% of all published data from individuals using androgen or androgen-progestagen regimens. The median times for sperm to recover to thresholds of 20, 10, and 3 million per mL were 3.4 months (95% CI 3.2-3.5), 3.0 months (2.9-3.1), and 2.5 months (2.4-2.7), respectively. Multivariate Cox's analysis showed higher rates of recovery with older age, Asian origin, shorter treatment duration, shorter-acting testosterone preparations, higher sperm concentrations at baseline, faster suppression of spermatogenesis, and lower blood concentrations of luteinising hormone at baseline. The typical probability of recovery to 20 million per mL was 67% (61-72) within 6 months, 90% (85-93) within 12 months, 96% (92-9 within 16 months, and 100% within 24 months. INTERPRETATION: Hormonal male contraceptive regimens show full reversibility within a predictable time course. Various covariables affect the rate but not the extent of recovery, although their effect sizes are minor. These data are crucial for the further safe and practical development of such regimens.
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    #12
    Bluelight Crew VictorZ06's Avatar
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    Quote Originally Posted by hiddenbeneathe View Post
    Do you have anything other than anecdotal evidence to support this statement? Male contraceptive studies showed complete recovery of testosterone in 100% of subjects.
    I think you are assuming that I meant one could become PERMANENTLY infertile if proper measures are not taken.

    Long term testicular atrophy can cause you to become infertile permanently, this happens when the testicles die, and at that point they cannot be saved...leaving you infertile. Once the testis are dead, there is no coming back.

    Most AAS users who have shut down and become temporarily infertile can reverse. In some cases, this could take as long as two years.

    Here...I ran a real quick search and WikiAnswers (can't find that article/study) gave a brief explanation.

    http://wiki.answers.com/Q/Do_anaboli..._men_infertile

    "Proper post cycle therapy alleviates this in most cases, returning the body back to its normal state. However, in the long run, it is possible to cause testicular atrophy; a state in which the testicles literally die, and cannot be revived."

    /V
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    #13
    Quote Originally Posted by VictorZ06 View Post
    I think you are assuming that I meant one could become PERMANENTLY infertile if proper measures are not taken.

    Long term testicular atrophy can cause you to become infertile permanently, this happens when the testicles die, and at that point they cannot be saved...leaving you infertile. Once the testis are dead, there is no coming back.

    Most AAS users who have shut down and become temporarily infertile can reverse. In some cases, this could take as long as two years.

    Here...I ran a real quick search and WikiAnswers (can't find that article/study) gave a brief explanation.

    http://wiki.answers.com/Q/Do_anaboli..._men_infertile

    "Proper post cycle therapy alleviates this in most cases, returning the body back to its normal state. However, in the long run, it is possible to cause testicular atrophy; a state in which the testicles literally die, and cannot be revived."

    /V
    I hope you realize that anyone can answer those questions.
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    #14
    Bluelight Crew VictorZ06's Avatar
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    Quote Originally Posted by hiddenbeneathe View Post
    I hope you realize that anyone can answer those questions.
    I do realize that...I mentioned I couldn't find that article/study that I have. I also said I ran a quick search. None the less, I believe it's correct.

    Here is the question answered by a Physician:

    Can male steroid use cause permanent sterility?

    Answer: "Use of anabolic steroids while generally causing temporary infertility can sometimes even lead to testicular atrophy and permanent infertility."

    Source: http://www.justanswer.com/questions/...ause-permanent
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    #15
    Bluelight Crew VictorZ06's Avatar
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    As per your request for other than anecdotal evidence to support my statement, I'll provide you with that study I spoke of...

    Myostatin, Muscles and Bodyfat
    By: Jerry Brainium


    Myostatin is a protein discovered by researchers at Johns Hopkins University in 1997. The word myostatin means 'muscle stopper,' an accurate description of what it does in the body. Scientists aren't sure how myostatin works, but the leading theory is that it inhibits the involvement of satellite cells, or immature muscle cells, in muscle growth. That's the opposite of what several anabolic hormones, particularly insulinlike growth factor 1 (IGF-1), do.

    Animals born without the gene that codes for myostatin have two primary characteristics: They have much larger muscles than usual, and they have less bodyfat than usual. Other than that, they appear normal, with no obvious physical problems.

    Myostatin is a topic of enormous interest to bodybuilders, since, theoretically, if you can somehow block its effects, your muscles will grow like crazy. As noted previously in this space, weight training is an effective myostatin blocker, which accounts for some of the growth that comes from regular training. In animals, blocking myostatin activity or manipulating their genes so that they don't produce myostatin yields not only increased muscular growth but also a dramatic reduction in bodyfat. The theory is that the lack of myostatin produces a repartitioning effect, promoting muscle growth at the expense of bodyfat. In short, bodyfat is used as a source of energy to support muscle growth.

    A new study partially illuminates the relationship between myostatin and bodyfat levels.1 It involved six morbidly obese (a medical euphemism for 'very fat') subjects who underwent surgery to shorten their stomachs. That limits the amount of food they can eat without feeling full. The surgery is considered extreme and is a last resort for people with dangerously high bodyfat levels, people who, for some reason or other, will not or cannot diet and exercise. The side effects of the surgery can include death'but that's another story.

    As a result of the surgery, the patients lost 38.9 percent of their bodyweight. The researchers measured their myostatin levels before and after the weight loss and found a clear and significant decline in myostatin after the weight loss, which consisted mostly of bodyfat. The scientists suggest that the drop in myostatin was the body's way of preventing the loss of vital lean mass under rapid and extreme fat-loss conditions. The drop in myostatin apparently had the effect of preventing muscle loss and may have also helped the body actually reduce the size of fat cells, as it does in animals.

    Even though bodybuilders don't resort to stomach stapling as a fat-loss technique, the study has two implications for them. As you lose fat, myostatin levels will likely decline, helping you preserve muscle during a diet. The addition of a weight-training routine will no doubt amplify the effect. The other implication is that having excess bodyfat probably increases myostatin, making it harder to build muscle. That's been the case in a few studies of obese people who begin weight-training programs. They often start with considerable amounts of lean mass under the fat, but, compared to their leaner peers, they seen to have trouble adding muscle mass. Perhaps the higher levels of myostatin preclude significant muscle gains.

    Steroids, HCG and Fertility

    One of the more worrisome aspects of using high-dose anabolic steroid regimens is their effect on fertility. Many commonly used anabolic steroids exert a feedback mechanism on the pituitary gland in the brain, which responds by stopping the release of two hormones known as gonadotropins: luteinizing hormone and follicle-stimulating hormone. Interestingly, estrogen is even more potent than testosterone at inhibiting the release of LH and FSH. (Increased estrogen levels in male steroid users are the result of the conversion of testosterone or anabolic steroid drugs into estrogen through the activity of the ubiquitous enzyme aromatase.)

    The lack of gonadotropins lowers fertility, since those hormones are required for complete sperm development. Infertility is still often listed as a major side effect of anabolic-steroid use, though permanent infertility is rare among bodybuilders and other athletes. Cycling, or taking a break from all drug use, enables the body to bounce back from impaired fertility in most cases. Sometimes, however, that can take a while, depending on how much was used and the duration of the cycle.

    Athletes have well-known ways of offsetting the possible antifertility effects of high-dose anabolic-steroids. They turn to anti-estrogen drugs to prevent the rise in estrogen that results from aromatization. Such drugs include Nolvadex, clomiphene and lately, potent anti-aromatase drugs such as Arimidex and others in that category, which cripple the activity of aromatase, lowering estrogen levels.

    While blocking estrogen helps maintain fertility in men (although some estrogen is required for full sperm development), it doesn't affect the lack of gonadotropin secretion required for sperm development. For that purpose, bodybuilders and other athletes turn to human chorionic gonadotropin. HCG is the same hormone that shows up early in pregnancy. Male athletes are interested in the substance because it looks a lot like LH.

    Not only is LH needed for sperm development, but it's also the rate-limiting hormone for testosterone synthesis in the body. Athletes hope HCG will maintain the body's testosterone production, which would normally be suppressed by anabolic steroids. HCG also maintains the sperm count, offsetting infertility.

    Bodybuilders use HCG either during a steroid cycle or during the last two weeks of a cycle, when the drugs are tapered down to zero. Some have written that it's futile to use HCG during a cycle because the high steroid doses will overcome any effect of HCG. Others point out that HCG promotes not only testosterone synthesis but also estrogen. If the athlete doesn't also use an estrogen-blocking drug, estrogen-related side effects, such as gynecomastia, can quickly become apparent.

    A newly published study followed the use of HCG and steroids in 21 men, mostly bodybuilders, aged 24 to 42, for six years.2 The athletes used their own steroids; none were supplied by the researchers. As a result, the cycles of the subjects varied in dosages and time but were far higher than any doctor would prescribe. In short, they used real-world drug regimens. The average-length drug cycle was 138 days, while the average daily dose was 96 milligrams.

    As expected, all the subjects showed a decrease in sperm count while on a cycle. Within six weeks after getting off the drugs, nearly all had significant increases in sperm count. By the six-month mark most were back to normal, although one subject showed no sperm production at all at the end of his cycle. Nor did he recover after the six-month follow-up. Within five years, however, he and his wife had two healthy daughters.

    The study proved the long-held contention that injecting HCG (as a protein hormone, it must be injected) while on a high-dose steroid regimen does maintain sperm production. On the other hand, a novel finding was that using both high-dose anabolic steroids and HCG leads to abnormalities in sperm.

    What caused the abnormalities? Full sperm development requires not only LH, which is provided by the HCG, but also FSH. The men didn't use any type of FSH drug, although such drugs are available and are used to treat female infertility. The authors, however, suggest that HCG caused the abnormal sperm production all on its own.

    At first glance, this study appears to be alarming. Abnormal sperm is linked to male infertility and to possible birth defects. On the other hand, I know of not a single professional bodybuilder who's had a child born with any birth defect'and some of them used huge steroid cycles off and on for years. My guess is that somehow the body can tell which sperm are more effective at the job than others, and the superior sperm get to the goal first.

    One Reason to Steer Clear of Trucks

    Bodybuilders, particularly male bodybuilders, are acutely aware of the negative effects of excess estrogen, among them gynecomastia, or the development of excess glandular tissue in the breasts of men; increased subcutaneous fat deposits, or fat just under the skin; and excess water retention. Estrogen also sends potent feedback signals to the brain, which has the effect of shutting down testosterone synthesis.

    Bodybuilders are usually aware of adverse estrogen effects, and those who use drugs turn to aromatase-inhibiting drugs like Arimidex or Aromasin. There are, however, other sources of estrogen ubiquitous in the environment. In fact, environmental estrogens have become a major health concern.

    Some health authorities predict that if something isn't done about chemicals that produce environmental estrogens, the male sperm counts of the world are going to drop precipitously. Experimental animals exposed to environmental estrogens became infertile or were born with abnormal sex organs.

    If you're concerned about such estrogens, you may want to maintain a safe distance from trucks on the highway. That's because of research findings that diesel-fuel exhaust contains chemicals called alkylphenols, which interact with cellular estrogen receptors to exert potent estrogenic activity.3 Diesel exhaust particles have previously been linked to lung cancer, allergic rhinitis and asthma.

    Since the air around major highways contains tons of the stuff, what the effects are is anyone's guess.



    References
    1 Milan, G.,et al. (2004). Changes in muscle myostatin expression in obese subjects after weight loss. J Clin Endocrinol Metab. 89:2724-2727.
    2 Karila, T., et al. (2004). Concomitant abuse of anabolic androgenic steroids and human chorionic gonadotrophin impairs spermatogenesis in power athletes. Int J Sports Med. 25:257-63.
    3 Furuta, C., et al. (2004). Estrogenic activities of nitrophenols in diesel exhaust particles. Biol Repr. 70:1527-1533. IM



    /V
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    #16
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    thanks victor! nice stuff!

    *drools about myostatin inhibitors*

    Can't wait for those!
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    #17
    Bluelight Crew VictorZ06's Avatar
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    Quote Originally Posted by sunyata View Post
    thanks victor! Nice stuff!

    *drools about myostatin inhibitors*

    can't wait for those!
    .

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    #18
    I am on hcg course since 2 month and getting married in next 2 month, I read something about using hcg can defect our physical power. As it relates to weight loss and losing weight means depleting some of your power.. is this true.
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    #19
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    HCG and HMG for short cycles at reasonable dosages is not needed... Keep it simple people.
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