I have been "on", blasting and cruising for about 3 years now. Well me and the lil lady have talked and are ready to have another kid. I have searched and seen some of the older protocols and will probably give them a shot... I was just curious if anyone has actual experience in any of the protocols and if there might be a more updated protocol?? Thanks for any help in advance.
swoleup57
took this from another forum which has some good points to think about:
i found this info .... hope you may find it useful
The Study: Two hypogonadal former anabolic steroid users were studied. Normal levels of LH are >3.6 IU/L and Testosterone are 300—1000 ng/dl. Former anabolic steroid users often have suppressed levels of both.
The Results: Subject #1 is a 6', 206lb former user of 500—2000+ grams per week of anabolics. His baseline numbers were: LH<1IU/L, Test=191ng/dl. This suject underwent a 32 day treatment of 2500 IU of HCG every 4 days, 50 mg of Clomid 2 times per day, and 10 mg Nolvadex per day. 15 days after treatment his numbers were: LH=5.2IU/L, Test=1072 ng/dl.
Subject #2 is a 5'10", 184lb male who used 400 mg per week of nandrolone. His baseline numbers were: LH<1IU/L, Test=45ng/dl. This subject's 32 day treatment consisted of 2500 IU of HCG every 4 days, 50 mg of Clomid 2 times per day, and 10 mg Nolvadex per day. There was no change. He underwent another treatment consisting of 60 days of 5000 IU of HCG every 4 days for 4 injections, then 2500 IU every 4 days for 4 injections, 50 mg of Clomid 2 times per day, and 10 mg Nolvadex per day. Still, no change. For the next 32 days, this subject received 5000 IU of HCG every other day for 6 injections, then 2500 IU every other day for 6 injections given with 150 IU of menotropins, 50 mg of Clomid 2 times per day, and 10 mg Nolvadex 2 times per day. 15 days after treatment his numbers were: LH=9.8IU/L, Test=507 ng/dl.(20)
Comments: The authors of this paper have presented some very interesting data that the medical community needs to learn from. When dealing with former androgen users, there may be better ways to increase Testosterone than the standard patch treatment (which will only prolong the problem of decreased T production.) Hypogonadal former androgen users need a treatment, not a band-aid. If you need to jump start your Testosterone after an androgen cycle, this combination of HCG, Clomid, and Nolvadex may be just what the doctor ordered.
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 treatmentsr 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.
Heres a quick study:
Ten typical cases of male eunuchoidism (two with anosmia) are reported. After administration of clomifene citrate to five patients, there is no change in blood levels of gonadotrophins in four cases; in the fifth, a small and transitory increase of LH is noted. The intravenous injection of LHRH (100 mug) to five patients induces an increase of serum LH in all cases and serum FSH in three cases. The initial site of the dysfunction is possibly hypothalamic with secondary gonadotrophic pituitary insufficiency. Among six patients anxious for paternity, prolonged treatment (for 36 to 98 weeks), with HCG (250-1 000 I.U. daily) +HMG (65-120 I.U. FSH daily) results in appearance of spermatozoa in the seminal fluid in five cases and a pregnancy was obtained in four cases. Comments are done upon methods of treatment."
"Ten typical cases of male eunuchoidism (two with anosmia) are reported. After administration of clomifene citrate to five patients there was no change in blood levels of gonadotrophins in four cases; in the fifth, a small and transitory increase of LH was noted. The intravenous injection of LHRH (100 mcg) to five patients induced an increase of serum LH in all cases and serum FSH in three cases. The initial site of the dysfunction is possibly hypothalamic with secondary gonadotrophic pituitary insufficiency. Among six patients desiring paternity, prolonged treatment (for 36 to 98 weeks), with HCG(1700-7000 I.U. weekly) + HMG (450-825 I.U. FSG weekly) resulted in the appearance of spermatozoa in the seminal fluid in five cases and a pregnancy was obtained in four cases. Methods of treatment are discussed."
"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."
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