HCG~human chorionic gonadotropin

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    HCG~human chorionic gonadotropin

    HCG

    (human chorionic gonadotropin)

    Scientists first recognized a specific hormone now called Human Chorionic Gonadotropin (HCG) in the 1920´s (1). HCG is no doubt one of the most misused, misunderstood and underutilized tools in bodybuilding pharmacology we have available. HCG is not a steroid, but a naturally occurring peptide hormone, produced by the embryo in the early stages of pregnancy and later by the trophoblast (part of the placenta) to help control a pregnant woman´s hormones (1). This makes the uterine lining ready for implantation of the fertilized egg. HCG is a glycoprotein composed of 237 amino acids and has a mass of 36.7kDa. HCG basically "acts" as Leutenizing Hormone (LH) in your body. LH is a Gonadotropin. They were first extracted from the human in 1958; more precisely the pituitary glands. A gonadotropin is any substance that stimulates the gonads (ovary, testes). It is heterodimeric (initiates prophase of mitosis) with an alpha subunit identical to LH (luteinizing hormone), FSH (follicle stimulating hormone) and TSH (thyroid stimulating hormone). LH is as stated above is called a gonadotropin because it stimulates the gonads (testes). It is produced in the pituitary cells and is made up of a beta chain of 115 amino acids and an alpha chain of 89 amino acids. In the testes, the LH binds to receptors on the leydig cells which in turn stimulate the synthesis and secretion of testosterone. Like LH, FSH is also called a gonadotropin. It consists of a beta chain of 115 amino acids and an alpha chain of 89 amino acids, the same as LH. Production and release of FSH is controlled by GnRH (gonadotropin releasing hormone). FSH stimulates testicular growth and supports the function of sertoli cells, which are needed for sustaining maturing sperm cells. TSH is also known as a thyrotropin and is secreted by cells in the anterior pituitary glands. TSH is comprised of a beta chain of 112 amino acids and an alpha chain of 89 amino acids. The alpha chain is the same as that found in the two other pituitary hormones, LH and FSH, and HCG as well. TSH is produced when the hypothalamus releases TRH (thyrotropin releasing hormone). TRH then causes the pituitary gland to release.

    TSH. TSH makes the thyroid gland produce triiodothyronin (T3) and thyroxine (T4), which controls the body´s metabolism.

    HCG LEVELS & Pregnancy

    HCG is clinically used to induce ovulation and treat ovarian disorders in women, as well stimulate the testes hypogonadal (underproduction of testosterone) men. It is also used in the treatment of undescended testicles in young males. HCG offers no potential performance enhancement in female athletes, but does prove to be very useful in male athletes especially those that use AAS. As stated above HCG in males is similar to LH, because they are similar and LH binds to receptors on leydig cells stimulating synthesis and secretion of testosterone, the use of HCG would be an added bonus to ASS users even if there is a lack of endogenous LH. Since HCG increases the body´s natural testosterone levels its use during long or extremely high dosed cycles can be most beneficial were the effects on the hypothalamus causes a depressed signal to the testicles. The result of the depressed signal leads to what is known as testicular atrophy (shrunken nuts). The use of HCG will send an artificial signal to the testes (again, as if it were actually LH), thus preventing (to some degree) atrophy. It not only helps to maintain testicular size and condition but it will also help in restoring testicles back to their original size. At a time when below normal androgen levels (due to ASS use) could become costly. Restarting natural testosterone production as quickly as possible is of a special concern in males at the end of a cycle of AAS. The price paid by bodybuilders for failing to raise natural test levels is the loss of most if not all the hard earned muscle you have gained, the main cause is cortisol. Cortisol sends a message to the muscles that is opposite to that of testosterone. If cortisol is not dealt with (because of an extremely low testosterone level) it will quickly strip away the new and hard earned muscle you have just gotten.

    Some users find that they have better gains and quicker recovery while using HCG during a cycle of AAS. This first claim is more than likely due to the fact that the body has a high level of natural testosterone as well as that provided by the use of AAS, and the second may be somewhat justifiable, as stimulating the testes to secrete testosterone intermittently may aid recovery. Perhaps this is due to the maintenence of a higher level of Inter-Testicular-Testosterone (ITT) provided by the intermittent use of HCG, which should greatly aid recovery of the hypothalamic-testicular-pituitary-axis. An average dose of HCG during a cycle is between 500iu to 1000iu every week to every other week while on a cycle. In one study I looked at, a single injection of 6000IU of HCG elevated test levels for 6 days. That´s why a lot of people recommend taking it every 3-5 days. We´d have more stable blood levels, though if we shot it more frequently. Remember, it´s non-estrified and a water-based injectable, after all. In that same study I just spoke of, 1500IU of HCG shot test levels up between 250 and 300%. Taking it all at once however will cause an increase in estrogen levels caused by the aromatization of normal testosterone; the result may be a case of gynecomastia for the user (3).

    HCG CYCLES

    As regards HCG´s use of Post-Cycle-Therapy (PCT), smaller and more frequent doses after a cycle of AAS would give the best results with the least amount of side effects. A dose of 250iu to 500iu everyday (ed) for 2 to 3 weeks is plenty and should very little from person to person (3). The Physicians Desk Reference recommends 500iu/day, as did the late, great, Dan Duchaine. The smaller doses are sufficient enough to begin reversal of testicular atrophy and used in conjunction with nolvade, will help the already present problem of recovery without raising the levels of estrogen to high and increasing the risk of gynecomastia in the user. Lower doses of 250iu to 500iu also avoid the further risk of down regulating LH receptors in the testes. The old saying more is better definitely does not apply to the use of HCG. You don´t want to finish PCT after using too much HCG only to find out your back at the beginning again. Your best bet is to start at 250iu or 500iu ed for 5 or 6 days, and if you don´t notice anything happening (nuts dropping and getting bigger) up the dose slightly. Small doses like 500iu two days a week isn´t going to cut it like some people think. The only thing small doses of HCG ay be useful (sublingually) for is reducing symptoms of benign prostatic hyperplasia (7). Yeah, that´s right, you can probably reduce some symptoms of an enlarged prostate with the use of small doses of HCG.

    As stated above the cycles of HCG should be in the 2 to 3 week range with a least one month off in between, you could stretch your cycle out to four weeks without any major concern if you are using lower doses. One should however take care when using HCG as prolonged use could repress the body´s natural production of gonadotropins permanently, but this is mostly just pure speculation as it does not have yet to be reported nor has there been a case of an overdose. To be on the safe side shorter cycles of HCG seem to be that of the norm. Most users cycle HCG near the end of a steroid cycle, you should start your HCG therapy on the last week of your cycle. For best results you should also run nolva while you run HCG as taking HCG by itself will do little to nothing and gyno even though rare may also flair up. Once the HCG cycle is finished you continue with your usual clomid or nolvadex (preferably the latter) for pct as it is more effective when used in conjunction HCG for pct. With an AAS cycle of 6 to 10 weeks HCG may not be necessary unless extreme doses of AAS were used or there is an existing problem of testicular atrophy or you are running a heavy oral only cycle. AAS cycles of 12 or more weeks should have HCG as a part of post cycle plan.

    HCG SIDE EFFECTS

    Since HCG is used to stimulate testosterone production, side effects can be the same as those associated with AAS, although gyno may be more common. Possible side effects of HCG use are water and sodium retention after higher doses are used. This is usually a result of higher androgen production. It may cause gyno (again if doses are too high). Any athletes worried about failing urine test because of low levels of epitestosterone may find that using a dose of 500iu of HCG will increase epitestosterone levels. However the problem with HCG is that it is also banned by the IOC and can also be detected in a urine test, the half life of HCG is approximately 4 to 5 days. Another possible downside to HCG is that it to can be suppressive to natural testosterone because it takes the place of LH. Since LH is manufactured in the pituitary because of the response of GnRH (gonadotropin releasing hormone) which in turn is secreted by the hypothalamus. Because the HCG mimics LH and is being supplied exogenously the hypothalamus will be given a signal to still stop producing GnRH, so no natural LH will be produced (5). This is why it should always be used with a compound such as nolvadex. So although HCG is essential after long or heavy cycles, it should not be used without an ancillary such as (specifically) nolv. Also HCG therapy should be discontinued at least 2 weeks prior to stopping the use of nolva, or it may suppress natural testosterone itself (5). This should not be a problem if you are running it towards the end of your cycle of AAS and before pct.

    BUY HCG

    The average price to buy HCG is between 10$ to 40$ per 5000iu with solvent, it comes in doses of 100, 125, 250, 500, 1000, 1500, 2000, 2500, 3000, 5000, 10000, 20000 all iu (international units).

    HCG is readily available and can be found in almost all the places where you may find AAS. If you have a good source you should have no problems in obtaining this product. There are currently only a few fakes of HCG around, but most are few and far between. Since the powder of HCG is similar to the powder of somatropin often cheaper HCG is sold and marketed as the more expensive HGH (human growth hormone) on the black market.

    Anthony Roberts

  2. #2
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    This study demonstrates that around 300iu HCG every other day is needed to raise ITT levels to baseline while administering Testosterone. That's 1,050iu HCG weekly.



    Low-Dose Human Chorionic Gonadotropin Maintains Intratesticular Testosterone in Normal Men with Testosterone-Induced Gonadotropin Suppression

    Andrea D. Coviello, Alvin M. Matsumoto, William J. Bremner, Karen L. Herbst, John K. Amory, Bradley D. Anawalt, Paul R. Sutton, William W. Wright, Terry R. Brown, Xiaohua Yan, Barry R. Zirkin and Jonathan P. Jarow
    Center for Research in Reproduction and Contraception, Geriatric Research Education and Clinical Center, Veteran Affairs Puget Sound Health Care System (A.M.M.), and Department of Medicine, University of Washington School of Medicine (A.D.C., W.J.B., J.K.A., B.D.A., P.R.S.), Seattle, Washington 98195; Department of Medicine, Charles R. Drew University (K.L.H.), Los Angeles, California 90059; Department of Urology, Johns Hopkins University School of Medicine (X.Y., J.P.J.), Baltimore, Maryland 21287; and Division of Reproductive Biology, Department of Biochemistry and Molecular Biology Johns Hopkins University School of Public Health (W.W.W., T.R.B., X.Y., B.R.Z., J.P.J.), Baltimore, Maryland 21205

    Address all correspondence and requests for reprints to: Dr. Andrea D. Coviello, Feinberg School of Medicine, Northwestern University, Tarry 15-751, 303 East Chicago Avenue, Chicago, Illinois 60611-3008. E-mail: a-coviello@northwestern.edu.

    In previous studies of testicular biopsy tissue from healthy men, intratesticular testosterone (ITT) has been shown to be much higher than serum testosterone (T), suggesting that high ITT is needed relative to serum T for normal spermatogenesis in men. However, the quantitative relationship between ITT and spermatogenesis is not known. To begin to address this issue experimentally, we determined the dose-response relationship between human chorionic gonadotropin (hCG) and ITT to ascertain the minimum dose needed to maintain ITT in the normal range. Twenty-nine men with normal reproductive physiology were randomized to receive 200 mg T enanthate weekly in combination with either saline placebo or 125, 250, or 500 IU hCG every other day for 3 wk. ITT was assessed in testicular fluid obtained by percutaneous fine needle aspiration at baseline and at the end of treatment. Baseline serum T (14.1 nmol/liter) was 1.2% of ITT (1174 nmol/liter). LH and FSH were profoundly suppressed to 5% and 3% of baseline, respectively, and ITT was suppressed by 94% (1234 to 72 nmol/liter) in the T enanthate/placebo group. ITT increased linearly with increasing hCG dose (P < 0.001). Posttreatment ITT was 25% less than baseline in the 125 IU hCG group, 7% less than baseline in the 250 IU hCG group, and 26% greater than baseline in the 500 IU hCG group. These results demonstrate that relatively low dose hCG maintains ITT within the normal range in healthy men with gonadotropin suppression. Extensions of this study will allow determination of the ITT concentration threshold required to maintain spermatogenesis in man.

    full study;
    http://jcem.endojournals.org/cgi/content/full/90/5/2595

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    Contrary to what is posted on the net HCG does not promote weight loss at all.

    Ineffectiveness of human chorionic gonadotropin in weight reduction: a double-blind study.

    Stein MR, Julis RE, Peck CC, Hinshaw W, Sawicki JE, Deller JJ Jr.

    Our investigation was designed to retest the hypothesis of the efficacy of human chorionic gonadotropin (HCG) on weight reduction in obese women in a clinic setting. We sought to duplicate the Asher-Harper study (1973) which had found that the combination of 500 cal diet and HCG had a statistically significant benefit over the diet and placebo combination as evidenced by greater weight loss and decrease in hunger. Fifty-one women between the ages of 18 and 60 participated in our 32-day prospective, randomized, double-blind comparison of HCG versus placebo. Each patient was given the same diet (the one prescribed in the Asher-Harper study), was weighed daily Monday through Saturday and was counselled by one of the investigators who administered the injections. Laboratory studies were performed at the time of initial physical examinations and at the end of the study. Twenty of 25 in the HCG and 21 of 26 patients in the placebo groups completed 28 injections. There was no statistically significant difference in the means of the two groups in number of injections received, weight loss, percent of weight loss, hip and waist circumference, weight loss per injections, or in hunger ratings. HCG does not appear to enhance the effectiveness of a rigidly imposed regimen for weight reduction.

    PMID: 786001 [PubMed - indexed for MEDLINE]

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    This study on rats shows a refractory period of 60-96 hours after HCG administration. This may lend support to every 3-4 day injects of HCG rather than eod.



    Testicular steroidogenesis after human chorionic gonadotropin desensitization in rats.

    Chasalow F, Marr H, Haour F, Saez JM.

    When a single injection of 500 I.U. of human chorionic gonadotropin (hCG) is given to rats there is an initial acute rise of plasma testosterone and of testicular content for both cyclic AMP and testosterone. This response correlates with an increase in both lyase and 17 alpha-hydroxylase activities. Thereafter both plasma and testicular testosterone decline and do not increase after a second injection of hCG. During this period of desensitization, isolated Leydig cells were insensitive to the steroidogenic stimulatory effect of both hCG and dibutyryl cyclic AMP. The post-cyclic AMP block is not due to an alteration of the cyclic AMP-dependent protein kinase but it is correlated with a decrease in both lyase and 17 alpha-hydroxylase activities of the Leydig cell's microsomes. This decrease is not caused by the absence of the recently described cytosol activator of this enzyme because its addition did not restore the enzymatic activity. Within 60 to 96 h after hCG injection there was a spontaneous increase of both plasma and testicular testosterone and this parallels the recovery of lyase and 17 alpha-hydroxylase activities. These results suggest that both enzymatic activities are regulated, directly or indirectly, by hCG, and that this is partly responsible for the hCG-induced steroidogenic refractoriness of Leydig cells.

    PMID: 221476 [PubMed - indexed for MEDLINE]

    full study
    http://www.jbc.org/content/254/13/5613.full.pdf

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    The potential roles of estrogens in regulating Leydig cell development and function: A review

    References and further reading may be available for this article. To view references and further reading you must purchase this article.

    Tom O. Abney, , a

    a Department of Physiology and Endocrinology, Medical College of Georgia, Augusta, Georgia 30912, USA

    Available online 10 September 1999.

    Abstract
    It is generally agreed that estrogens, principally estradiol-17β, are synthesized by and act in the testis of mammals, including humans. The site of estradiol synthesis in the testis is generally believed to begin in the Sertoli cell and switch to the Leydig cell during neonatal development where a gonadotropin-regulated aromatase is present. Numerous studies suggest that the primary target cell of estradiol in the testis at all ages is the Leydig cell. In fact, the Leydig cell is known to possess an estrogen receptor that binds estradiol in the classic manner. The mechanism of estradiol action and the role of its receptor in the testis, however, remain unresolved. In Leydig cells, estradiol appears to induce several alterations that are dependent in large part on the developmental stage of the Leydig cell. In the fetal and neonatal testes, estradiol appears to block the ontogenic development of Leydig cells from precursor cells. There is also evidence that estradiol similarly blocks the regeneration of Leydig cells in the testis of mature, ethane dimethylsulfonate-treated animals. Evidence indicates that the precursor cell possesses high levels of estrogen receptors relative to that of the Leydig cell. It is postulated that estradiol is a paracrine factor involved in regulating the interstitial population of Leydig cells. Evidence also indicates that estradiol acts directly in the mature testis to block androgen production. It appears to do so by inhibiting the activities of several steroidogenic enzymes involved in testosterone synthesis. Although the more conventional receptor-mediated mode of action is feasible, several studies have suggested that this action might entail direct competitive inhibition of key steroidogenic enzymes by estradiol. In summary, the net biologic effect of estradiol in the testis appears to be inhibition of androgen production, either by limiting development and growth of the Leydig cell population or through direct action in the Leydig cell.

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