First let me say that I do not claim to be an expert, so far I have not seen any juicing endocrinologist post on any boards anywhere. I also am not picking a fight with anyone that supports one way or the other. This is a bit of information to support the use of HCG/HMG.
The debate about taper vs. traditional PCT has been interesting and I may give it a shot some day. However what happens when the taper method fails after a heavy cycle? Or you testicles are like raisins as you taper down and stay that way? Or you want to go off for 6 months and desire to fully recover? There are plenty of guys that never fully recover from a cycle, after 3 months, 6 months or a year or longer.
There are no guarantees that as you taper down to nothing or run a conventional PCT that you still won?t be shut down to some degree. The literature in the endocrinology data base does not have many references on AAS induced hyopgonadism but the few that do exist are usually based on fertility studies of former users who can?t produce sperm or who?s testicles never recovered their normal size.
The point of the PCT is to recover back to baseline as quickly as possible. The conventional wisdom says the faster you recover the more of your gains that you keep. In my opinion and based on some of the studies listed below, thats where HCG comes into play.
If you search among the various boards, I think you?ll see that not many PCT strategies advocate HCG use in the PCT window, but right before the PCT starts. HCG is either used throughout the cycle in small doses of 500 ius 2X week, or 250 ius EOD. By using throughout the cycle the thought is to keep the testes from shrinking in the first place. If you wait until the end of the cycle you would start the HCG after the last shot of whatever it is your running at 500 ius a days for 10 days and then commence with the SERMS or AI or whatever it is you are using in the traditional PCT.
It appears in reading the literature that HCG is safe and does not come with any significant side effects, except bigger balls, a test increase and normal sperm production in most cases of hyopgonadism.
I have never used Pergonal, but in the spirit of research may add it in my next PCT its available if you look around. But in the following studies listed below it seems like Pergonal could be a great PCT tool if you want your sperm production to fully recover. I have had all the children I am going to have so it isn?t that big of a deal to me. But you younger guys may want to be dads someday.
The males listed in the studies that suffer primary or secondary hypogonadism, were able to conceive after treatment with HCG/HMG combination. In one study the HMG aided in testicular size increase in combination with the HCG.
I would also recommend that you check out Dr, Michael Scally over at Meso. There is an article he wrote that specifically addresses AAS Secondary Induced Hypogonadism. I posted it here a while back, but it?s a bitch to read in the board format.
The point is that there is a role for HCG as post cycle therapy tool for the recreational bodybuilder that would like to recover quickly with normal testicle size and does not want to stay on indefinitely.
This is an excerpt from Dr. Scallys article regarding AAS Secondary Induced Hypogonadisim
The normal operation of both the testicular and hypothalamic-pituitary regions is crucial in returning HPTA function to normal. Returning one component of the axis to normal without concurrently returning the other would sabotage and inhibit the operation of the entire HPTA. The ability to produce a cure whereby there is no longer a need for medication is small.
Discounting costs and focusing strictly on medicine reasons for this include inadequate stimulation for a critical part of the HPTA for full restoration, secondary inhibition of the HPTA, inadequate follow up and monitoring, and compliance due to the length of time the medicines are prescribed.
The individual use of human chorionic gonadotropin (hCG), clomiphene citrate, and tamoxifen citrate in the treatment of testicular sub-function and gonadotropin suppression, respectively, is well documented. The medicines utilized for the protocol used to normalize the HPTA come from the scientific literature detailing treatments of portions of the HPTA axis. In accordance with previous studies, each medication was used individually, and along with hCG, in initial trials.
The simultaneous use of clomiphene citrate and tamoxifen was determined through preliminary use of clomiphene citrate and tamoxifen, individually. It was discovered that although both clomiphene citrate and tamoxifen met with some success, when combined together they achieved a more significant increase in gonadotropin production. This clinical outcome resulted in the combination therapy of hCG, clomiphene citrate and tamoxifen.
These medicines hCG, clomiphene citrate and tamoxifen, with each being given over a defined period and for specific but related problems. The successful restoration of the HPTA requires the medications to be taken as prescribed. Every effort should be made to adhere to the schedule since the goal is to try and mimic the circadian rhythm that exists normally for the HPTA. hCG needs to be at a dose sufficient to stimulate testicular testosterone production.
Also, the schedule for hCG is determined by when your own body should be attempting to produce its own testosterone. This is the ideal situation when AAS cessation date is known along with the type and dose of AAS being prescribed.
In the case of decreased testicular function manifested by low testosterone levels, it is of primary importance to first return the normal function of the testicular cells. Long-term follow-up on HPTA restoration is necessary to ensure permanent reversal of hypogonadotropic hypogonadal conditions by the use of hCG, clomiphene citrate and tamoxifen.
Human Chorionic Gonadotropin (hCG) - hCG is a polypeptide hormone produced by the human placenta, is composed of an alpha and a beta sub-unit. The alpha sub-unit is essentially identical to the alpha sub-units of the human pituitary gonadotropins, luteinizing hormone (LH) and follicle-stimulating hormone (FSH), as well as to the alpha sub-unit of human thyroid-stimulating hormone (TSH). The beta sub-units of these hormones differ in amino acid sequence. The action of HCG is virtually identical to that of pituitary LH, although HCG appears to have a small degree of FSH activity as well. It stimulates production of gonadal steroid hormones by stimulating the interstitial cells (Leydig cells) of the testis to produce androgens and the corpus luteum of the ovary to produce progesterone.
hCG?s effect is centralized at the Leydig cells of the testicles and stimulates hormone function at the testicular level but does not reverse hypothalamic-pituitary suppression. Adequate stimulation from pituitary gonadotropins is required for the Leydig cells of the testicles to function independently in the body?s normal hormone axis. Clomiphene citrate and tamoxifen citrate seem to act upon the hypothalamic-pituitary region in stimulating gonadotropin production. It was with this understanding that hCG was eventually combined with clomiphene citrate and tamoxifen as attempted therapy to reverse gonadal function in hypogonadotropic hypogonadal males. hCG has been shown to significantly improve gonadal function in hypogonadotropic hypogonadal adult males [[54]]. Its use has proven beneficial in many clinical situations including stimulation of testosterone and sperm production. [[55]]. Recently, a case study report used hCG successfully in ASIH. [[56]]
[54] Okuyama A, Nakamura M, Namiki M, Aono T, Matsumoto K, Utsunomiya M, Yoshioka T, Itoh H, Itatani H, Mizutani S, et al. Testicular Responsiveness to Long-Term Administration of hCG and HMG in Patients with Hypogonadotrophic Hypogonadism. Hormone Research. 1986; 23(1): 21-30. Cisternino M, Manzoni SM, Coslovich E, Autelli M. Hormonal Replacement Therapy with hCG and HU-FSH in Thalassaemic Patients Affected by Hypogonadotropic Hypogonadism. Journal of Pediatric Endocrinology and Metabolism. 1998; 11 Suppl 3: 885-890. Burgess S, Calderon MD. Subcutaneous Self-Administration of Highly Purified Follicle Stimulating Hormone and Human Chorionic Gonadotrophin for the Treatment of Male Hypogonadotrophic Hypogonadism. Spanish Collaborative Group on Male Hypogonadotropic Hypogonadism. Human Reproduction. 1997 May; 12(5): 980-986. Martikainen H, Alen M, Rahkila P, Vihko R. Testicular Responsiveness to Human Chorionic Gonadotrophin During Transient Hypogonadotrophic Hypogonadism Induced by Androgenic/Anabolic Steroids in Power Athletes. Journal of Steroid Biochemistry. 1986 July; 25(1): 109-112. Barrio R, de Luis D, Alonso M, Lamas A, Moreno JC.
Induction of Puberty with Human Chorionic Gonadotropin and Follicle-Stimulating Hormone in Adolescent Males With Hypogonadotrophic Hypogonadism. Fertility and Sterility. 1999 Feb; 71(2): 244-248. D?Agata R, Heindel JJ, Vicari E, Aliffi A, Gulizia S, Polosa P. hCG-Induced Maturation of the Seminiferous Epithelium in Hypogonadotropic Men. Hormone Research. 1984; 19(1): 23-32. D?Agata R, Vicari E, Aliffi A, Maugeri G, Mongioi A, Gulizia S. Testicular Responsiveness to Chronic Human Chorionic Gonadotropin Administration in Hypogonadotropic Hypogonadism. Journal of Clinical Endocrinology and Metabolism. 1982 Jul; 55(1): 76-80. Burgess et al, 1997; Vicari E, Mongioi A, Calogero AE, Moncada ML, Sidoti G, Polosa P, D?Agata R. Therapy With Human Chorionic Gonadotrophin Alone Induces Spermatogenesis in Men With Isolated Hypogonadotrophic Hypogonadism- Long-Term Follow-Up. International Journal of Andrology. 1992 Aug; 15(4): 320-329. Ulloa-Aguirre A, Mendez JP, Diaz-Sanchez V, Altamirano A, Perez-Palacios G. Self-priming Effect of Luteinizing Hormone-Human Chorionic Gonadotropin (hCG) Upon the Biphasic Testicular Response to Exogenous hCG. I. Serum Testosterone Profile. Journal of Clinical Endocrinology and Metabolism. 1985 Nov; 61(5): 926-932. Liu L, Banks SM, Barnes KM, Sherins RJ.
Two-year Comparison of Testicular Responses to Pulsatile Gonadotropin-Releasing Hormone and Exogenous Gonadotropins from the Inception of Therapy in Men with Isolated Hypogonadotropic Hypogonadism. Journal of Clinical Endocrinology and Metabolism. 1988 Dec; 67(6): 1140-1145. Ley SB, Leonard JM. Male Hypogonadotropic Hypogonadism: Factors Influencing Response to Human Chorionic Gonadotropin and Human Menopausal Gonadotropin, Including Prior Exogenous Androgens. Journal of Clinical Endocrinology and Metabolism. 1985 Oct; 61(4): 746-752. Kelly WF, Kjeld JM, Mashiter K, Joplin GF. Reassessment of the Human Chorionic Gonadotropin Stimulation Test in Hypogonadal Males. Archives of Andrology. 1982 Feb; 8(1): 53-59. Dunkel L, Perheentupa J, Sorva R. Single versus Repeated Dose Human Chorionic Gonadotropin Stimulation in the Differential Diagnosis of Hypogonadotropic Hypogonadism. Journal of Clinical Endocrinology and Metabolism. 1985 Feb; 60(2): 333-337.
[55] See FN54. Burgess S and Calderon MD, 1997.
[56] Menon, D. K. (2003). Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin. Fertil Steril, 79 Suppl 3, 141-143.
Successful treatment of anabolic steroid-induced azoospermia with human chorionic gonadotropin and human menopausal gonadotropin.
Menon DK.
Department of Obstetrics and Gynecology, University Malaya Medical Centre, Kuala Lumpur, Malaysia.
OBJECTIVE: To document for the first time the successful treatment using human chorionic gonadotropin (hCG) and human menopausal gonadotropins (hMG) of anabolic steroid-induced azoospermia that was persistent despite 1 year of cessation from steroid use. DESIGN: Clinical case report. SETTINGS: Tertiary referral center for infertility. PATIENT(S): A married couple with primary subfertility secondary to azoospermia and male hypogonadotropic hypogonadism. The husband was a bodybuilder who admitted to have used the anabolic steroids testosterone cypionate, methandrostenolone, oxandrolone, testosterone propionate, oxymetholone, nandrolone decanoate, and methenolone enanthate. INTERVENTION(S): Twice-weekly injections of 10,000 IU of hCG (Profasi; Serono) and daily injections of 75 IU of hMG (Humegon; Organon) for 3 months. MAIN OUTCOME MEASURE(S): Semen analyses, pregnancy. RESULT(S): Semen analyses returned to normal after 3 months of treatment. The couple conceived spontaneously 7 months later. CONCLUSION(S): Steroid-induced azoospermia that is persistent after cessation of steroid use can be treated successfully with hCG and hMG.
Anabolic steroid induced hypogonadism treated with human chorionic gonadotropin
GV Gill
Endocrine Unit, Walton Hospital, Liverpool, UK.
A case is presented of a young competitive body-builder who abused anabolic steroid drugs and developed profound symptomatic hypogonadotrophic hypogonadism. With the help of prescribed testosterone (Sustanon) he stopped taking anabolic drugs, and later stopped Sustanon also. Hypogonadism returned, but was successfully treated with weekly injections of human chorionic gonadotropin for three months. Testicular function remained normal thereafter on no treatment. The use of human chorionic gonadotropin should be considered in prolonged hypogonadotrophic hypogonadism due to anabolic steroid abuse.
Male hypogonadotropic hypogonadism: factors influencing response to human chorionic gonadotropin and human menopausal gonadotropin, including prior exogenous androgens
SB Ley and JM Leonard
Although testosterone (T) therapy is sufficient for maturation and maintenance of secondary sex characteristics in hypogonadal men, gonadotropins are required for stimulation of spermatogenesis. Thirteen men with hypogonadotropic hypogonadism received treatment with hCG, followed in 12 by the addition of human menopausal gonadotropin (hMG). All initially had undetectable serum LH and FSH and low T levels and were azoospermic with small testes. During therapy, all achieved normal male levels of T. Twelve of 13 had marked and continuous increase in testicular volume. Three men had sperm in the ejaculate with hCG treatment alone. All but 1 patient developed sperm in their seminal fluid during combined hCG and hMG therapy. Two men achieved three pregnancies, and 2 more had semen that produced hamster oocyte penetration assays in the fertile range during the protocol period. Four of 5 who achieved sperm densities greater than 1 million/ml while receiving combined therapy maintained or increased sperm production while receiving continued hCG therapy after hMG was withdrawn. We examined the response to gonadotropin therapy of men who had received previous T therapy and those who had not. There were no differences in rapidity or degree of response, as assessed by rise in serum T, increase in testis volume, or maximal sperm density achieved. Multiple pituitary deficits and cryptorchidism were negative prognostic factors. In summary, the prognosis for successful stimulation of spermatogenesis in men with hypogonadotropic hypogonadism treated with hCG/hMG is good and not adversely affected by prior androgen treatment. Despite undetectable serum FSH levels, hCG treatment was sufficient to both initiate and maintain spermatogenesis in some patients.
European Journal of Endocrinology, Vol 131, Issue 4, 347-354
Copyright ? 1994 by Society of the European Journal of Endocrinology
________________________________________Clinical Studies
Serum inhibin concentrations before and during gonadotropin treatment in men with hypogonadotropic hypogonadism: physiological and clinical implications
RI McLachlan, DM Finkel, WJ Bremner and PJ Snyder
Medical Service, Veterans Administration Medical Center, Seattle, Washington 98108.
We measured by RIA the inhibin concentrations in the sera of 20 men with hypogonadotropic hypogonadism before and during treatment with gonadotropins in order to determine the role of gonadotropins in the control of inhibin secretion and the utility of the serum inhibin concentration in assessing the spermatogenic response to gonadotropin treatment in these patients. Before treatment the mean serum inhibin concentration in the 20 hypogonadotropic men as a group (391 +/- 49 U/L) was significantly lower (P less than 0.001) than that in 27 normal men (741 +/- 52 U/L). In the 7 men whose hypogonadism was of postpubertal onset, the mean serum inhibin concentration (559 +/- 69 U/L) was not significantly lower than that in normal men. In the 13 men whose hypogonadism was of prepubertal onset, the serum inhibin level was significantly lower [381 +/- 74 U/L (P less than 0.01) in the 7 without a history of cryptorchidism and 207 +/- 46 U/L (P less than 0.01) in the 6 with a history of cryptorchidism]. All 20 patients were azoospermic or severely oligospermic and had distinctly subnormal serum testosterone concentrations, even those whose serum inhibin values were normal. In the 7 patients with postpubertal hypogonadism, treatment with hCG alone for 6 months increased the serum testosterone concentration and maximum sperm count to normal, even though the previously normal inhibin concentration was not increased further. In the 13 patients with prepubertal hypogonadism, treatment with hCG alone increased the serum inhibin concentration, and combined treatment with hCG and human menopausal gonadotropin (hMG) increased inhibin further, to well within the normal range (742 +/- 143 U/L) in the patients without a history of cryptorchidism and to just within the normal range (487 +/- 96 U/L) in those with such a history. In the 7 patients with prepubertal hypogonadism but no history of cryptorchidism, treatment with hCG and hMG increased the maximum sperm count to normal in 5. In the 6 patients with prepubertal hypogonadism who did have a history of cryptorchidism, hCG and hMG treatment produced a normal sperm count in only 1. Of 12 patients whose serum inhibin level was more than 300 U/L before treatment, 11 developed a normal maximum sperm count in response to treatment, but of 8 patients whose inhibin concentration was less than 300 U/L before treatment, only 2 developed a normal sperm count in response to treatment (P less than 0.01).(ABSTRACT TRUNCATED AT 400 WORDS)
Therapy with human chorionic gonadotrophin alone induces spermatogenesis in men with isolated hypogonadotrophic hypogonadism–long-term follow-up.
Vicari E, Mongioi A, Calogero AE, Moncada ML, Sidoti G, Polosa P, D’Agata R.
Department, University of Catania Medical School, Italy.
The effects of long-term (14-120 months) hCG-treatment of 17 male patients affected by isolated hypogonadotrophic hypogonadism (IHH) on testicular volume, plasma testosterone levels, and sperm concentration were assessed. Mean testicular volume increased from 3.8 +/- 0.2 (Mean +/- SEM) ml to a maximal of 14.9 +/- 1.1 ml after 22.2 +/- 2.3 months of hCG treatment. Maximal testicular volume correlated positively with the volume recorded before the patients had undergone any previous treatment. Testicular growth was also analysed by sorting the patients into two sub-groups according to whether their initial testicular volume was less than 4 ml (small testis subset, STS) or greater than or equal to 4 ml (large testis subset, LTS), supposedly indicating complete or partial gonadotrophin deficiency, respectively. Testicular volumes in the LTS group were always greater than those of the STS. Plasma testosterone levels reached adulthood values during hCG treatment and no statistically significant difference was detected between LTS and STS patients with IHH. Thirteen patients (70%) became sperm-positive during treatment with hCG alone; five out of eight (60%) were STS patients and eight out of nine (90%) were LTS. In addition, LTS patients always had a greater sperm output than did STS patients. Sperm concentration correlated positively with maximal testicular volume, but not with patient age, length of treatment, or initial testicular volume. The administration of hMG to eight of these patients caused an increase in testicular volume in two patients but the mean volume was not statistically different from that recorded at the end of treatment with hCG alone. Similarly, sperm concentration improved in three patients but again it did not differ significantly from that achieved in the course of hCG treatment. It is noteworthy that one patient became sperm-positive after the addition of hMG to his therapeutic regimen. Among sperm-positive patients attempting conception, seven out of 10 succeeded, two of whom were from the STS group. In summary, this study indicates that hCG alone is an effective treatment to induce complete spermiogenesis in IHH patients regardless of their initial testicular volume. However, a number of IHH patients may benefit from the addition of hMG in terms of testicular volume, sperm output, and pregnancy outcome.
Recombinant human follicle-stimulating hormone and human chorionic gonadotropin for induction of spermatogenesis in a hypogonadotropic male.
Kliesch S, Behre HM, Nieschlag E.
Institute of Reproductive Medicine of the University, Munster, Germany.
OBJECTIVE: To determine the efficacy of recombinant FSH administration to induce spermatogenesis. DESIGN: Case report, clinical study. SETTING: Tertiary center for reproductive medicine of the university. PATIENT: A 44-year-old hypogonadal man with postpubertal pituitary insufficiency due to surgical removal of a prolactinoma. INTERVENTIONS: Recombinant FSH (150 IU three times weekly) was administered together with hCG (1,500 IU twice weekly). Control examinations were performed every 6 weeks, including hormone determinations, safety parameters, testicular volume measurements, and semen analysis. MAIN OUTCOME MEASURE: Semen parameters. RESULTS: After 18 weeks of treatment, first sperm were seen in the ejaculate and reached normal sperm concentrations after 24 weeks of treatment. Serum hormone levels were in the normal range and testicular volume increased. No adverse side effects were observed. CONCLUSIONS: Recombinant human FSH in combination with hCG can be used successfully for stimulation of testicular function in gonadotropin-deficient men.
Induction of testicular growth and spermatogenesis by pulsatile, intravenous administration of gonadotrophin-releasing hormone in patients with hypogonadotrophic hypogonadism.
Delemarre-Van de Waal HA.
Department of Pediatrics, Free University Hospital, Amsterdam, The Netherlands.
OBJECTIVE: To induce testicular growth including spermatogenesis, 38 patients with hypogonadotrophic hypogonadism were treated with long-term pulsatile GnRH administration. PATIENTS: The group of patients comprised 17 individuals with idiopathic hypogonadotrophic hypogonadism, 11 with Kallmann’s syndrome, four with multiple pituitary hormone deficiencies and six with a secondary hypogonadotrophic hypogonadism due to surgical removal of a brain tumour. Thirteen patients (seven with idiopathic hypogonadotrophic hypogonadism and six with Kallmann’s syndrome) had undescended testes, of whom six had undergone surgery on both testes and four on one testis. Sixteen of the 17 had previously received androgen therapy and six others had received gonadotrophin treatment, of whom three had long-term treatment to induce testicular development, without success.
TREATMENT: GnRH was administered intravenously in a dose of 2-20 micrograms per pulse every 90 minutes. After GnRH discontinuation, hCG treatment was instituted, 1500-3000 IU (i.m.) twice weekly.
RESULTS: During treatment plasma levels of LH, FSH and testosterone increased. In 35 out of the 38 patients plasma testosterone levels increased into the normal adult range. In all patients testicular volume increased. Mean pretreatment testicular volume per patient group ranged from 2.4 to 4.8 ml and increased to 11.5-18.1 ml by the end of treatment. There was a significant difference in the achieved testicular volumes between the patients with Kallmann’s syndrome and the brain tumour patients. GnRH treatment mean lasted between 46 and 75 weeks in the different groups. On hCG therapy, testicular development was either maintained or improved. Semen analysis revealed the presence of spermatogenesis in 31 out of the 38 patients (26 patients already on GnRH, and in another five patients on hCG therapy). All three patients pretreated with gonadotrophins as well as three patients with bilateral testicular surgery developed a detectable sperm count. In 19 adolescent patients with growth potential, an adequate height velocity was observed during GnRH treatment.
CONCLUSIONS: GnRH is a feasible way to induce testicular growth as well as spermatogenesis in hypogonadotrophic male patients, even in patients in whom gonadotrophin treatment has failed. After GnRH treatment, hCG alone can maintain or even improve testicular development, including spermatogenesis. GnRH treatment may also induce a physiological growth spurt in hypogonadotrophic adolescents
