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Calling Bill Llewellyn!!
- Thread starter Mr. Las Vegas
- Start date
I will have to disagree that hcg and novaldex will do more for hpta resoration than clomid. Hcg does not provide a bolus dose of LH, it mimics LH it is not LH. It will stimulate the production of testosterone for a short time, but will do nothing to restore the hpta. It may have it's use in making the testes more 'available' for Lh stimulation, however at the same time it will produce just as much estrogen in your body as it will testosterone.
The novaldex, was such a wonderful breast cancer drug, and was revolutionary in teh field when discovered becasue it's BREAT TISSUE SPECIFIC. Not all encompasing the way clomid is, hence it will not bind to the hypothalamus, as well as clomid, and stimulate natural LH productionl.
The novaldex, was such a wonderful breast cancer drug, and was revolutionary in teh field when discovered becasue it's BREAT TISSUE SPECIFIC. Not all encompasing the way clomid is, hence it will not bind to the hypothalamus, as well as clomid, and stimulate natural LH productionl.
Mr. Las Vegas
New member
I have been going with HCG post cycle and it works wonders over Clomid for me.
Hustler_dt
New member
bump for good info.....
I grazed over pub med for some studies trying to prove that nolvadex does in fact stimulate natural test production. I found conflicting ideas. My thoughts are either clomid or nolvadex would work fine at restoring HPTA. I don't see how one is really better than the other.
Both clomid and nolvadex stimulate test production
Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.
Vandekerckhove P, Lilford R, Vail A, Hughes E.
Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN. [email protected]
BACKGROUND: Oligo-astheno-teratospermia (sperm of low concentration, reduced motility and increased abnormal morphology) of unknown cause is common and the need for treatment is felt by patients and doctors alike. As a result, a variety of empirical, non-specific treatments have been used in an attempt to improve semen characteristics and fertility. The administration of anti-oestrogens is a common treatment because anti oestrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this has been claimed to lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of anti-oestrogens on testicular spermatogenesis or steroidogenesis. This review considers the available evidence of the effect of both Clomiphene citrate and tamoxifen, both of which have a predominant anti-oestrogenic effect, for idiopathic oligo and/or asthenospermia. OBJECTIVES: The objective was to assess the effects of treating subfertile men with anti-oestrogens (clomiphene or tamoxifen) on pregnancy rates among couples where subfertility has been attributed to idiopathic oligo- and/or asthenospermia. SEARCH STRATEGY: The Cochrane Subfertility Review Group specialised register of controlled trials was searched". SELECTION CRITERIA: Randomised trials of anti-oestrogen therapy for 3 months or more compared to placebo or no placebo for subfertile males among couples where subfertility is attributed to male factor. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers. Any differences were resolved with a third reviewer. MAIN RESULTS: Ten studies involving 738 men were included. Five of the trials did not specify method of randomisation. Anti-oestrogens had a positive effect on endocrinal outcomes, such as serum testosterone levels. In trials with secure randomisation there was no difference in the pregnancy rate between the anti-oestrogen groups and the control groups (odds ratio 1.26, 95% confidence interval 0.99 to 1.56). The overall pregnancy rate for these five trials was 15.4% compared to the spontaneous rate of 12.5% in the control groups. These odds increased to 1.56 (95% confidence interval 0.99 to 2.19) when all 10 trials were included, but this result is likely to be artificially inflated. REVIEWER'S CONCLUSIONS: Anti-oestrogens appear to have a beneficial effect on endocrinal outcomes, but there is not enough evidence to evaluate the use of anti-oestrogens for increasing the fertility of males with idiopathic oligo-asthenospermia.
Evidence of tamoxifen restoring HTPA, and shows no decrease in LH-releasing hormone as clomid does.
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.
Evidence against tamoxifen restoring HPTA consistently
Short- and long-term hormonal effects of a single dose of 50 mg tamoxifen administered to normal males.
Fauser BC, Dony JM, Doesburg WH, Thomas CM, Rolland R.
To five potentially fertile males, a single dose of 50 mg tamoxifen was administered orally to explore the short- and long-term hormonal effects on the hypothalamic-pituitary-gonadal axis. Blood specimens were obtained through an integrated sampling technique for the first two hours after the intake of the drug. Then, samples were taken daily throughout one week, and twice weekly for the next two weeks. Hormone measurements of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone and oestradiol were obtained by specific RIA. All the subjects showed different response patterns. No general characteristic of the hormonal changes in the investigated group could be given. A consistent correlation between the within-individual levels of gonadotrophin and sex steroid changes could not be observed. It is concluded, within the limits of the used experimental design, that in healthy males a single administration of tamoxifen does not result in consistent changes in serum levels of either gonadotrophins or sex steroid hormones.
As far as HCG goes, I don't see the point in using something that will keep you shut down post cycle.
Both clomid and nolvadex stimulate test production
Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.
Vandekerckhove P, Lilford R, Vail A, Hughes E.
Institute of Epidemiology, University of Leeds, 34 Hyde Terrace, Leeds, Yorkshire, UK, LS2 9LN. [email protected]
BACKGROUND: Oligo-astheno-teratospermia (sperm of low concentration, reduced motility and increased abnormal morphology) of unknown cause is common and the need for treatment is felt by patients and doctors alike. As a result, a variety of empirical, non-specific treatments have been used in an attempt to improve semen characteristics and fertility. The administration of anti-oestrogens is a common treatment because anti oestrogens interfere with the normal negative feedback of sex steroids at hypothalamic and pituitary levels in order to increase endogenous gonadotropin-releasing hormone secretion from the hypothalamus and FSH and LH secretion directly from the pituitary. In turn, FSH and LH stimulate Leydig cells in the testes, and this has been claimed to lead to increased local testosterone production, thereby boosting spermatogenesis with a possible improvement in fertility. There may also be a direct effect of anti-oestrogens on testicular spermatogenesis or steroidogenesis. This review considers the available evidence of the effect of both Clomiphene citrate and tamoxifen, both of which have a predominant anti-oestrogenic effect, for idiopathic oligo and/or asthenospermia. OBJECTIVES: The objective was to assess the effects of treating subfertile men with anti-oestrogens (clomiphene or tamoxifen) on pregnancy rates among couples where subfertility has been attributed to idiopathic oligo- and/or asthenospermia. SEARCH STRATEGY: The Cochrane Subfertility Review Group specialised register of controlled trials was searched". SELECTION CRITERIA: Randomised trials of anti-oestrogen therapy for 3 months or more compared to placebo or no placebo for subfertile males among couples where subfertility is attributed to male factor. DATA COLLECTION AND ANALYSIS: Data were extracted independently by two reviewers. Any differences were resolved with a third reviewer. MAIN RESULTS: Ten studies involving 738 men were included. Five of the trials did not specify method of randomisation. Anti-oestrogens had a positive effect on endocrinal outcomes, such as serum testosterone levels. In trials with secure randomisation there was no difference in the pregnancy rate between the anti-oestrogen groups and the control groups (odds ratio 1.26, 95% confidence interval 0.99 to 1.56). The overall pregnancy rate for these five trials was 15.4% compared to the spontaneous rate of 12.5% in the control groups. These odds increased to 1.56 (95% confidence interval 0.99 to 2.19) when all 10 trials were included, but this result is likely to be artificially inflated. REVIEWER'S CONCLUSIONS: Anti-oestrogens appear to have a beneficial effect on endocrinal outcomes, but there is not enough evidence to evaluate the use of anti-oestrogens for increasing the fertility of males with idiopathic oligo-asthenospermia.
Evidence of tamoxifen restoring HTPA, and shows no decrease in LH-releasing hormone as clomid does.
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.
Evidence against tamoxifen restoring HPTA consistently
Short- and long-term hormonal effects of a single dose of 50 mg tamoxifen administered to normal males.
Fauser BC, Dony JM, Doesburg WH, Thomas CM, Rolland R.
To five potentially fertile males, a single dose of 50 mg tamoxifen was administered orally to explore the short- and long-term hormonal effects on the hypothalamic-pituitary-gonadal axis. Blood specimens were obtained through an integrated sampling technique for the first two hours after the intake of the drug. Then, samples were taken daily throughout one week, and twice weekly for the next two weeks. Hormone measurements of luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone and oestradiol were obtained by specific RIA. All the subjects showed different response patterns. No general characteristic of the hormonal changes in the investigated group could be given. A consistent correlation between the within-individual levels of gonadotrophin and sex steroid changes could not be observed. It is concluded, within the limits of the used experimental design, that in healthy males a single administration of tamoxifen does not result in consistent changes in serum levels of either gonadotrophins or sex steroid hormones.
As far as HCG goes, I don't see the point in using something that will keep you shut down post cycle.
E2 said:
HCG mimics LH of course, which is why it is able to provide a bolus dose (of LH STIMULATION if you want to be pedantic). It allows the testes to notice a level of stimulation far greater than endogenous LH will do on its own. Plus you have to remeber that post cycle your body is already in a physiological state that favors heightened LH levels. Estrogen levels are lower than normal because you have shunted the normal T>E2 pathway, and androgen levels are in the toilet. Your body is already primed for ample levels of LH, and studies show that they do return to normal much more quickly than T does because of the atrophy issue (in fact we often see rebound overcompensation because at first T is not raised well to offer a counterbalance).
Clomid (or Nolvadex) alone is simply not capable of offering much benifit here. For too long people have been assuming that because they work well in the normal state that they must also in the recovery window, which is a MUCH different place to be.
Nolvadex is not specific to breast tissue, and acts as an anti-estrogen in many other tissues inclusing the pituitary and hypothalamus. Clomid acts as a weak estrogen at the Pituitary, which represents a slight although admittedly more technical disadvantage over the more pure AE tamoxifen.
5,000-7,000 U of HCG per week for three weeks ( I recommend 2,000 U three times per week, non consecutive days). Begin HCG during last week of cycle. Nolvadex 20mg daily for 6 weeks, beginning the last week of the cycle or continue Nolvadex if using it during the cycle. My $0.02
