Sterility

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    Sterility


    Does test. treatment cause sterility? If so, is there anyway to prevent this?

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    Also interested in this...
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    Quote Originally Posted by krazy View Post
    Also interested in this...
    freeze it or hCG it. otherwise there is a risk.
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    Quote Originally Posted by krazy View Post
    Also interested in this...
    freeze your goo or hCG it. otherwise there is a risk.
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    You mean freezing the gel will prevent sterility?

    Huh? Does not compute.
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    Quote Originally Posted by krazy View Post
    You mean freezing the gel will prevent sterility?

    Huh? Does not compute.
    Your semen -- sorry.
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    Im 20 and doing TRT... can I expect sterility out of this even if my T levels arent in excessively high ranges?

    Is it permanent sterility or can I get virility back by stopping TRT? If permanent, how long does it take to become this way?
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    I'm going to post a few things in here and probably come back later and comment on them....just wanted to get them in here:


    If anyone has full access to these at this time it would help. In this first one I am curious how long this particular male had hypogonadotropic hypogonadism prior to his successful HCG treatment...(this should be particularly important to those on long term TRT/HRT treatment).


    1: Urology. 2000 Oct 1;56(4):669.Click here to read Links
    Acquired hypogonadotropic hypogonadism presenting as decreased seminal volume.
    Tash JA, McGovern JH, Schlegel PN.

    James Buchanan Brady Urology Foundation, Department of Urology, The New York Presbyterian Hospital-Weill Medical College of Cornell University, New York, New York, USA.

    A 32-year-old man with decreased ejaculatory volume was found to have acquired hypogonadotropic hypogonadism. Initial evaluation demonstrated castrate levels of testosterone with low serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) levels. Semen analysis revealed a volume of 0.35 cc and severe oligospermia. Administration of gonadotropin-releasing hormone (GnRH) did not effect an increase in LH or FSH, indicating a pituitary defect. Magnetic resonance imaging revealed a partially empty sella turcica. Treatment with human chorionic gonadotropin (hCG) alone resulted in normalization of testosterone levels, sperm concentration, and semen volume, as well as the successful conception and delivery of a healthy baby girl. The findings from this case demonstrate the importance of considering low serum testosterone levels in the evaluation of low semen volume, as well as the role of hCG alone as an infertility treatment for acquired hypogonadotropic hypogonadism.

    PMID: 11019338 [PubMed - indexed for MEDLINE]
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    Also promising (however old)......but unsure on dosing regimen. Interesting the HMG in there for FSH stimulation. Something not commonly used in steroid cyclers pct's:

    1: J Clin Endocrinol Metab. 1985 Oct;61(4):746-52.Links
    Male hypogonadotropic hypogonadism: factors influencing response to human chorionic gonadotropin and human menopausal gonadotropin, including prior exogenous androgens.
    Ley SB, Leonard JM.

    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.

    PMID: 3928676 [PubMed - indexed for MEDLINE]
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    Another old one. I'm assuming cryptorchidism is not really an issue for most, but for those who are this is probably somewhat relevant...


    1: N Engl J Med. 1985 Sep 12;313(11):651-5.Links
    Stimulation of spermatogenesis by gonadotropins in men with hypogonadotropic hypogonadism.
    Finkel DM, Phillips JL, Snyder PJ.

    We evaluated the efficacy of gonadotropin treatment in stimulating spermatogenesis in men with hypogonadotropic hypogonadism. When 21 men with hypogonadotropic hypogonadism were treated with human chorionic gonadotropin, the sperm count increased to within the normal range in the 6 in whom hypogonadism had begun after puberty, but in only 1 of the 15 in whom it had begun before puberty (P less than 0.002). When the remaining 14 men with prepubertal hypogonadism were treated with human menopausal gonadotropin in addition to human chorionic gonadotropin, the sperm count increased to normal in 5 of the 7 who had not had cryptorchidism, but in only 1 of the 7 who had (P less than 0.05). The need for human menopausal gonadotropin as a replacement for follicle-stimulating hormone could not be predicted by pretreatment serum and urinary levels of follicle-stimulating hormone. We conclude that gonadotropin treatment will usually increase the sperm count to normal in men with hypogonadotropic hypogonadism, unless cryptorchidism has occurred. The need for human menopausal gonadotropin treatment appears to depend on the time of onset of hypogonadism.

    PMID: 3927163 [PubMed - indexed for MEDLINE]
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    Again probably important to have HMG in there, also note the one individual who became azoospermic (unfortunate). I'd also be interested in ages of those involved:

    1: Eur J Endocrinol. 2002 Nov;147(5):617-24.Click here to read Links
    Maintenance of spermatogenesis in hypogonadotropic hypogonadal men with human chorionic gonadotropin alone.
    Depenbusch M, von Eckardstein S, Simoni M, Nieschlag E.

    Institute of Reproductive Medicine of the University, Domagkstr. 11, Munster D-48149, Germany.

    OBJECTIVE: It is generally accepted that both gonadotropins LH and FSH are necessary for initiation and maintenance of spermatogenesis. We investigated the relative importance of FSH for the maintenance of spermatogenesis in hypogonadotropic men. SUBJECTS AND METHODS: 13 patients with gonadotropin deficiency due to idiopathic hypogonadotropic hypogonadism (IHH), Kallmann syndrome or pituitary insufficiency were analyzed retrospectively. They had been treated with gonadotropin-releasing hormone (GnRH) (n=1) or human chorionic gonadotropin/human menopausal gonadotropin (hCG/hMG) (n=12) for induction of spermatogenesis. After successful induction of spermatogenesis they were treated with hCG alone for maintenance of secondary sex characteristics and in order to check whether sperm production could be maintained by hCG alone. Serum LH, FSH and testosterone levels, semen parameters and testicular Volume were determined every three to six Months. RESULTS: After spermatogenesis had been successfully induced by treatment with GnRH or hCG/hMG, hCG treatment alone continued for 3-24 Months. After 12 Months under hCG alone, sperm counts decreased gradually but remained present in all patients except one who became azoospermic. Testicular Volume decreased only slightly and reached 87% of the Volume achieved with hCG/hMG. During treatment with hCG alone, FSH and LH levels were suppressed to below the detection limit of the assay. CONCLUSION: Once spermatogenesis is induced in patients with secondary hypogonadism by GnRH or hCG/hMG treatment, it can be maintained in most of the patients qualitatively by hCG alone, in the absence of FSH, for extended periods. However, the decreasing sperm counts indicate that FSH is essential for maintenance of quantitatively normal spermatogenesis.
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