HAHAHAHAHA!!!! I found them they were on wannabebig forum, well thanks anyways big guy, here are some stuides for you guys that I'll add to the anti-e thread:
Fertil Steril 1978 Mar;29(3):320-7 Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen A, Comhaire F
The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.
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Int J Androl. 1992 Dec;15(6):507-8
Treatment of idiopathic oligozoospermia with tamoxifen--a randomized controlled study.
Krause W, Holland-Moritz H, Schramm P.
Department of Andrology, Philipps-Universitat, Marburg, Germany.
There is no conclusive evidence of the usefulness of tamoxifen in the treatment of idiopathic oligozoospermia (OAT-syndrome), as it has been used mostly in uncontrolled studies. We herein report on the controlled treatment of OAT-syndrome with tamoxifen versus placebo following a randomized design. Seventy-six men with sperm counts of 2-20 x 10(6) ml-1, sperm motility of 20-50%, and sperm morphology (abnormal cells) between 50 and 80% were involved in the study. Patients with varicocele, a history of testicular maldescent or genital inflammation were excluded. Thirty-nine patients received tamoxifen (30 mg daily), 37 patients placebo. There was a statistically significant increase in the mean serum testosterone level after treatment in the tamoxifen-treated group (from 4.9 +/- 1.9 to 7.9 +/- 3.6 ng ml-1) in comparison to the placebo group (5.3 +/- 2.0 and 5.6 +/- 2.0 ng ml-1). Serum FSH levels increased slightly in the tamoxifen group (from 6.8 +/- 4.1 to 7.3 +/- 4.8 mU ml-1), but this was not statistically significant in comparison to the placebo group (from 5.9 +/- 3.9 to 5.2 +/- 3.5 mU ml-1). Serum levels of LH did not show any differences between groups. The sperm count increased during treatment from 9.3 +/- 11.7 to 11.4 +/- 13.7 x 10(6) ml-1 in the tamoxifen group and from 9.1 +/- 7.1 to 9.3 +/- 8.8 x 10(6) ml-1 in the placebo group; this difference did not reach statistical significance. The percentage of motile and abnormal sperm was not different between the two treatment groups
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Treatment of idiopathic oligozoospermia with tamoxifen.
Brigante C, Motta G, Fusi F, Coletta MP, Busacca M.
Eighteen subfertile men, with idiopathic normogonadotropic oligozoospermia were treated with an antiestrogenic compound, tamoxifen (Nolvadex), at the dose of 20 mg/day for four months. Hormonal parameters (LH, FSH, Testosterone, Prolactin) were evaluated before treatment and after 45 and 90 days of therapy. Serum LH, FSH and Testosterone increased significantly after 45 days of tamoxifen treatment. Seminal analyses, performed before and after three months of therapy showed improvements in sperm motility and in sperm density. By our clinical findings, tamoxifen can be considered a useful approach for an empiric treatment of idiopathic oligozoospermia.
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Both clomiphene citrate and tamoxifen are estrogen receptor blockers that have been suggested as empiric treatments for male infertility. By preventing the important negative feedback of estrogens to the pituitary and hypothalamus, LH/FSH pulsatile release and GnRH stimuli are augmented. Since FSH is important for spermatogenesis, it is possible that increased FSH release may further enhance sperm production. Increased LH release also results in higher serum testosterone levels that are converted peripherally as well as in the liver to estrogens. Since men with idiopathic infertility have normal testosterone levels, by definition, the increased FSH, LH and testosterone that result from clomiphene or tamoxifen treatment may boost testosterone and estrogen levels above normal levels. This increased estrogen production may be detrimental to normal sperm production and should be avoided. Therefore, all patients considered for empiric therapy should be counselled to have early and frequent testosterone and estradiol levels to monitor treatment.
Aromatase inhibitors block the conversion of testosterone to estrogen. Treatment with an aromatase inhibitor decreases estrogen levels, which leads to increased LH and FSH release from the pituitary, with a subsequent increase in testicular stimulation and serum testosterone levels without the usual increase in estrogen levels seen for anti-estrogens. Although one uncontrolled study suggested an increase in sperm concentration for nearly all patients treated (89%), other well-designed placebo-controlled studies have demonstrated no significant improvement in pregnancy rates for treated patients. Although many patients will have increased sperm concentration, no improvement in sperm motility was seen in these studies.
http://www.maleinfertility.org/new-therapy.html#anti
