All The PCT You Need is RIGHT HERE!

[Nelson Montana]

This is factually incorrect. There are a number of studies showing that treatment with Nolva does increase serum testosterone levels in men. It also shows a positive effect on lipids with very little sides in most users so I am always at a loss when you condemn Nolva.

Would you mind posting a couple of those studies? Because the one's I've seen are more than a little sketchy in accuracy. And dex isn't that bad with lipids at that dosage. aromasan is a good substitute. And both increase FREE T while Nolva lowers IGF. Just a few reasons to condemn Nolva.

 

[access]

Would you mind posting a couple of those studies? Because the one's I've seen are more than a little sketchy in accuracy. And dex isn't that bad with lipids at that dosage. aromasan is a good substitute. And both increase FREE T while Nolva lowers IGF. Just a few reasons to condemn Nolva.

That's hardly a few reasons Nelson. In fact it's not even one when you consider Nolva does increase serum Test levels as shown in a lot of studies. Actually any anti-e be it an AI or SERM should have somewhat of a positive impact on test levels due to the estrogen inhibition/supression.

Stimulation of calcitonin secretory capacity by increased serum levels of testosterone in men treated with tamoxifen

ABSTRACT

Previous studies have suggested that sex steroids, including both oestrogen and testosterone, influence calcitonin secretion. However, a negative effect of gonadotrophins on calcitonin has not been excluded. Twelve men with infertility and low-normal serum levels of testosterone were studied before and during tamoxifen therapy. Increases in the serum levels of LH, FSH, testosterone and calcitonin were observed after treatment. Our findings suggest that testosterone has a direct influence on calcitonin secretion.


Improvement in semen quality in infertile males after treatment with tamoxifen.

Lewis-Jones DI, Lynch RV, Machin DC, Desmond AD.
Department of Human Anatomy, University of Liverpool, U.K.

The effect of the anti-oestrogen Tamoxifen on the seminal quality of 131 men was studied. Parameters studied before and after treatment were sperm density, total ejaculate count, percentage progressive motility, progressively motile ejaculate count, percentage total motility and total motile ejaculate count. In a group of 38 males, the effect on serum LH, FSH, testosterone, oestradiol and prolactin was also studied. Tamoxifen significantly improved (p less than 0.05) the progressive motility in all patient groups where there was reduced pretreatment motility. Sperm density was also significantly improved in oligozoospermic patients. Elevations in the basal serum levels of FSH was noted, even in those patients where the basal level was elevated before treatment. Increases were also observed in the serum levels of the four other hormones studied.

Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.

Vandekerckhove P, Lilford R, Vail A, Hughes E.
St Mary's Hospital, IOW Healthcare NHS Trust, Parkhurst Road, Newport, Isle of Wight, UK PO30 5TG. Patrick.Vandekerckhove@iow.nhs.uk

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. AUTHORS' 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.

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.

Effect of lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men.

Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.

Administration of the antiestrogen tamoxifen for one month to 12 patients with idiopathic oligozoospermia significantly increased the mean basal testosterone (T) level and the responses of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to constant luteinizing hormone releasing hormone (LHRH) infusion but did not significantly influence the mean oestradiol (E2) levels or the E2 over testosterone ratio. Mean sperm concentration and total sperm output increased by about 70% after a mean treatment period of 5.5 +/- 0.4 months. No statistically significant difference was found between the two subgroups of patients treated with either the lower (5 or 10 mg once daily) or higher dose of tamoxifen (10 mg twice daily) with respect to basal or LHRH stimulated gonadotropin and testosterone response or the E2/T ratio and the effect on sperm density and total sperm output. In both subgroups the sperm motility and morphology remained unchanged. In conclusion higher doses of tamoxifen in this study prove not to be superior to lower doses in improving mean sperm density and total sperm output. The relative small percentage of patients achieving normalisation of only these sperm parameters pleads for further search for more effective selection of patients and other more effective treatment modalities in patients with idiopathic oligozoospermia.

Selection of oligozoospermic men for tamoxifen treatment by an antiestrogen test.

Schill WB, Schillinger R.

In a retrospective study 46 men with idiopathic normogonadotropic oligozoospermia were treated by 20 mg Tamoxifen daily for a period of 6 months. A significant improvement of sperm count, total sperm output, total and progressive motility as well as sperm morphology was observed. In 25 men before initiation of treatment a short-term antiestrogen test with daily 40 mg Tamoxifen for a period of one week was performed with assessment of serum levels of testosterone, LH and FSH before and afterwards. Considering hormonal response in those patients who showed a more than 50% increase of sperm count (responders), FSH levels after Tamoxifen administration were unaffected. In contrast, a significant increase of the FSH level was observed in the group of the non-responders. Serum testosterone and LH levels increased in both groups, but showed no obvious differences. A similar hormonal pattern was found in father's and nonfather's concerning the response of FSH after Tamoxifen administration. It is concluded that the response of FSH towards Tamoxifen may be of use to predict improvement of semen parameters and therefore seems to be suitable to select patients for Tamoxifen therapy.

Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.

Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.

Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.

 

[Nelson Montana]

That's hardly a few reasons Nelson. In fact it's not even one when you consider Nolva does increase serum Test levels as shown in a lot of studies. Actually any anti-e be it an AI or SERM should have somewhat of a positive impact on test levels due to the estrogen inhibition/supression.

................................................

I HAVE TO TAKE EACH STUDY IN PART TO SHOW HOW IT DOESN'T PROVE A THING. STICK WITH ME,.

.....................................................................................


Stimulation of calcitonin secretory capacity by increased serum levels of testosterone in men treated with tamoxifen

ABSTRACT

Previous studies have suggested that sex steroids, including both oestrogen and testosterone, influence calcitonin secretion. However, a negative effect of gonadotrophins on calcitonin has not been excluded. Twelve men with infertility and low-normal serum levels of testosterone were studied before and during tamoxifen therapy. Increases in the serum levels of LH, FSH, testosterone and calcitonin were observed after treatment. Our findings suggest that testosterone has a direct influence on calcitonin secretion.

.....................................................

ALL THIS REALLY SAYS IS THAT INFERTILE MEN SHOWED IMPROVEMENT IN CALCITONIN SECRETION WHICH MAY HAVE SOME EFFECT ON TREATING INFERTILITY. THAT REALLY HAS NOTHING TO DO WITH RECOVERING FROM STEROIDS.


.............................................


Improvement in semen quality in infertile males after treatment with tamoxifen.

Lewis-Jones DI, Lynch RV, Machin DC, Desmond AD.
Department of Human Anatomy, University of Liverpool, U.K.

The effect of the anti-oestrogen Tamoxifen on the seminal quality of 131 men was studied. Parameters studied before and after treatment were sperm density, total ejaculate count, percentage progressive motility, progressively motile ejaculate count, percentage total motility and total motile ejaculate count. In a group of 38 males, the effect on serum LH, FSH, testosterone, oestradiol and prolactin was also studied. Tamoxifen significantly improved (p less than 0.05) the progressive motility in all patient groups where there was reduced pretreatment motility. Sperm density was also significantly improved in oligozoospermic patients. Elevations in the basal serum levels of FSH was noted, even in those patients where the basal level was elevated before treatment. Increases were also observed in the serum levels of the four other hormones studied.

...................................................................

ANOTHER POORLY EXECUTED STUDY. IT SAYS THINGS "WERE NOTED" BUT IT DOESN'T CLARITY. THE ONLY IMPROVEMENT WAS ON OLIGOOSPERMIC PATIENTS AND DOESN'T SAY HOW MUCH OF AN IMPROVEMENT WAS NOTED. CURIOUSLY, IT MENTIONS AN INCREASE IN "SPERM DENSITY" BUT I'M NOT SURE WHAT THAT MEANS. SOME PEOPLE CLAIM BIG LOADS ON THE STUFF WHEREAS OTHERS, SUCH AS MYSELF, DRY UP. THAT'S DEPENDENT ON A LOT OF THINGS. FOR NOW, LET'S SAY THIS JUST VALIDATES THAT NOLVA AND CLOMID ARE "CRAP-SHOOTS" AS I'VE SAID MANY TIMES.

......................................................................


Clomiphene or tamoxifen for idiopathic oligo/asthenospermia.

Vandekerckhove P, Lilford R, Vail A, Hughes E.
St Mary's Hospital, IOW Healthcare NHS Trust, Parkhurst Road, Newport, Isle of Wight, UK PO30 5TG. Patrick.Vandekerckhove@iow.nhs.uk

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. AUTHORS' 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.

.....................................

DID YOU READ THIS ONE? IT ESSENTIALLY SAID THERE NOT MUCH OF DIFFERENCE. THE "AUTHOR" "CONCLUDES" THERE WAS SOME IMPROVEMENT IN SOME CASES BUT THAT COULD OCCUR OVER TIME ANYWAY.


........................................................

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.


..........................................

THIS ONE SAYS THERE WAS A "MODERATE" INCREASE IN HORMONES (THOUGH UNSTATED) AND THAT CLOMID ACTUALLY DECREASED LH. IT ALSO CLAIMS THE FFECTS TOOK PLACE AFTER 6-9 MONTHS. WHO DOES PCT FOR THAT LONG?


..................................................................

Effect of lower versus higher doses of tamoxifen on pituitary-gonadal function and sperm indices in oligozoospermic men.

Dony JM, Smals AG, Rolland R, Fauser BC, Thomas CM.

Administration of the antiestrogen tamoxifen for one month to 12 patients with idiopathic oligozoospermia significantly increased the mean basal testosterone (T) level and the responses of luteinizing hormone (LH) and follicle stimulating hormone (FSH) to constant luteinizing hormone releasing hormone (LHRH) infusion but did not significantly influence the mean oestradiol (E2) levels or the E2 over testosterone ratio.


..................................................................

Mean sperm concentration and total sperm output increased by about 70% after a mean treatment period of 5.5 +/- 0.4 months. No statistically significant difference was found between the two subgroups of patients treated with either the lower (5 or 10 mg once daily) or higher dose of tamoxifen (10 mg twice daily) with respect to basal or LHRH stimulated gonadotropin and testosterone response or the E2/T ratio and the effect on sperm density and total sperm output. In both subgroups the sperm motility and morphology remained unchanged. In conclusion higher doses of tamoxifen in this study prove not to be superior to lower doses in improving mean sperm density and total sperm output. The relative small percentage of patients achieving normalisation of only these sperm parameters pleads for further search for more effective selection of patients and other more effective treatment modalities in patients with idiopathic oligozoospermia.

..............................................

this seems to suggest there isn;t much difference between those who were treated and that dosage didn't matter. And again, variables occurred after 5 months. The supps and arimidex will raise FREE T in 5 hours!


..................................................................

Selection of oligozoospermic men for tamoxifen treatment by an antiestrogen test.

Schill WB, Schillinger R.

In a retrospective study 46 men with idiopathic normogonadotropic oligozoospermia were treated by 20 mg Tamoxifen daily for a period of 6 months. A significant improvement of sperm count, total sperm output, total and progressive motility as well as sperm morphology was observed. In 25 men before initiation of treatment a short-term antiestrogen test with daily 40 mg Tamoxifen for a period of one week was performed with assessment of serum levels of testosterone, LH and FSH before and afterwards. Considering hormonal response in those patients who showed a more than 50% increase of sperm count (responders), FSH levels after Tamoxifen administration were unaffected. In contrast, a significant increase of the FSH level was observed in the group of the non-responders.

.................................................
THIS IS INTERESTING. IN SOME, FSH WENT UP BUT NOTHING ELSE. YET IN THOSE WHO EXPERIENCED A HIGHER SPERM COUNT, FSH WAS UNAFFECTED. SPERM COUNT ISN;T TESTOSTERONE. AND IT ALSO TOOK 6 MONTHS.



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Serum testosterone and LH levels increased in both groups, but showed no obvious differences.


..................................

NO OBVIOUS DIFFERENCE AFTER 6 MONTHS. THERE YOU HAVE IT.


.......................................................................



A similar hormonal pattern was found in father's and nonfather's concerning the response of FSH after Tamoxifen administration. It is concluded that the response of FSH towards Tamoxifen may be of use to predict improvement of semen parameters and therefore seems to be suitable to select patients for Tamoxifen therapy.

Increased sperm count in 25 cases of idiopathic normogonadotropic oligospermia following treatment with tamoxifen.

Buvat J, Ardaens K, Lemaire A, Gauthier A, Gasnault JP, Buvat-Herbaut M.

Twenty-five subfertile men, all presenting with idiopathic normogonadotropic oligospermia, were treated with tamoxifen (20 mg/day) for 4 to 12 months. Semen analysis was performed twice before treatment and at least twice after 3 to 12 months of treatment. In 14 patients, serum luteinizing hormone (LH), serum follicle-stimulating hormone (FSH), and plasma testosterone (T) were assayed before treatment, then again after 2 weeks and 12 weeks of treatment. Semen volume, sperm motility, and sperm morphologic characteristics were not modified by tamoxifen. Conversely, a twofold increase of both the mean sperm concentration and the mean total sperm count per ejaculate was observed during treatment (P less than 0.001). Mean values of T, LH, and FSH increased during treatment, but the difference was only significant for T (P less than 0.001) and FSH (P less than 0.05). Ten pregnancies (40% of cases) were reported during the 161 months of treatment.

..........................................

VERY UNCLEAR. WHAT WERE THE NUMBERS? I HAVE TO DOUBT STUDIES THAT USE TERMS LIKE " INCREASED SIGNIFICANTLY" AS A SCIENTIFIC ASSESSMENT. THEN AGAIN, WHO ARE THESE PEOPLE?

..

 

[access]

Holy shit Nelson now your just losing credibility and showing no formal objectivity here at all. You can't take one study that showed IGF was lowered when taking Nolva as it suits your argument then condemn every other one even when your clearly in the wrong. These are just some there are many more but I see no point in posting endlessly study after study when there is more than enough empirical evidence in these alone that shows the benefit Nolva has for any individual looking for a med that would assist with recovery after a steroid cycle when the objective is to increase Test levels.

Your arguments against these studies are jokes for the most part. Just because you don't believe what is written there does not make it untrue or that you question the results based on study participants or elapsed time of those same studies because they don't fall into a time line of typical steroid cycle and PCT. You would be better served taking the time to read the whole study rather then just the abstract and attempt then to make an informed judgement rather than trying to undo the study with a few choice and meaningless words in a vein attempt to proffer your argument. I mean we are unlikely to actually see any studies based on what we do specifically and that is inject exogenous hormones into ourselves for several weeks or longer. Some of what we do needs to be based on information gleamed from between the lines of these same studies and anecdotal evidence. In both cases Nolva is a winner. I actually do not know of anyone who has used Nolva and has not benefited from it excepting maybe you if in fact that is the case. I am sure there are maybe a few but I am also sure there are a lot more who have used Nolva with a positive experience.

I would ask you show me a study where are an individual injected several milligrams of testosterone per week for 12 weeks and then used Nolva as a PCT and it didn't work. Of course your not going to be able to so please at least be somewhat unbiased. On the other hand I can show you several like individuals that did the same thing and did recover but this is anecdotal. We need to rely on anecdotal as it is a means to increase all of our knowledge and please don't get me wrong as I know Nolva is not for everyone just like anything we do but I do know it works to increase serum test levels and I religiously have blood work done after all my cycles to keep track of this along with what I did exactly for PCT.

I know from my own personal expereinces that Nolva is not the only answer here and I am not making an argument for that being the case but it is certainly a very beneficial part of PCT. I have had my best recoveries where Nolva has been included as part of PCT.

 

[Nelson Montana]

Holy shit Nelson now your just losing credibility and showing no formal objectivity here at all.

..........................................
I DISAGREE. I'M SHOWING THE FLAWS IN THESE STUDIES. I GAIN NOTHING FROM THAT. IT'S TOTALLY OBJECTIVE.


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You can't take one study that showed IGF was lowered when taking Nolva as it suits your argument then condemn every other one even when your clearly in the wrong.

...............................


YOU'RE CLEARLY CONFUSED. FIRST OF ALL, THIS HAD NOTHING TO DO WITH IGF-- THAT'S ANOTHER ARGUMENT. I JUST SPENT 20 MINUTES ADDRESSING WHAT YOU PRESENTED AND YOU'RE OFF ONTO SOMETHING ELSE NOW.



.......................................................................................................
These are just some there are many more but I see no point in posting endlessly study after study when there is more than enough empirical evidence in these alone that shows the benefit Nolva has for any individual looking for a med that would assist with recovery after a steroid cycle when the objective is to increase Test levels.

..........................................................

THERE IS NO POINT IS PRESENTING STUDY AFTER STUDY THAT IS FLAWED. THIS IS THE PROBLEM WITH MESSAGE BOARDS. IT REMINDS ME OF THE OLD DAYS WHERE AS LONG AS SOMEONE CUT AND PASTED A STUDY THEY WIN! IN THE RESL WORLD IT'S NOT THAT SIMPLE. I'M ACTUALLY READING THESE SO CALLED STUDIES. I STILL DON;T SEE ANY NUMBERS CONDUCTED BY A REPUTABLE MEDICAL ASSOCIATION. AS FOR EMPIRICAL EVIDENCE, THERE'S PLENTY THAT NOLVADEX KILLS LIBIDO.



...................................................

Your arguments against these studies are jokes for the most part.

.........................................
TELL ME WHAT'S SO FUNNY. I COULD USE A GOOD LAUGH.


.................................................................

Just because you don't believe what is written there does not make it untrue or that you question the results based on study participants or elapsed time of those same studies because they don't fall into a time line of typical steroid cycle and PCT.

.........................................

THAT'S COMPLETE PROJECTION AND ASSUMPTION ON YOUR PART. YOU'RE ENTITLED TO YOUR OPINION, AS ERRONEOUS AS IT MAY BE.



.............................................................................................
You would be better served taking the time to read the whole study rather then just the abstract and attempt then to make an informed judgement rather than trying to undo the study with a few choice and meaningless words in a vein attempt to proffer your argument.

..........................................................
BACK ATCHA BRO.



...........................................................

I mean we are unlikely to actually see any studies based on what we do specifically and that is inject exogenous hormones into ourselves for several weeks or longer. Some of what we do needs to be based on information gleamed from between the lines of these same studies and anecdotal evidence.

..........................................

I AGREE. BUT I'M NOT GOING TO CONCLUDE WHAT I WANT IT TO BE. BELIEVE ME, I'D LOVE FOR NOLVADEX TO WORK GREAT. BUT WHEN YOU SEE TIME AND TIME AGAIN THAT IT DOESN'T, YOU HAVE TO WONDER. IN MY PESONAL EXPERIENCE I FOUND IT KILLED LIBIDO. THEN THOUGH FURTHER INVESTIGATION I REALIZED MANY OTHERS HAD THE SAME EFFECT. THAT MAKES ME GO BACK AND LOOK AT SOME OF THESE STUDIES. WHY? WHY IS THIS HAPPENING. THEN YOU CAN SEE IT. THESE STUDIES ARE VERY SPECULATIVE AND IN SPOTS, FLAT OUT WRONG. BUT THEY'RE STUDIES! THEY'RE ON THE INTERNET! THEY'RE WRONG AND IF YOU LOOK CLOSELY AND TRY TO UNDERSTAND HOW THEY'RE CONDUCTED YOU'LL SEE THAT I'M HELPING YOU BY SHOWING HOW THEY ARE MISCONSTUED.


............................................

In both cases Nolva is a winner.

.............................................
THAT'S ABSOLUTELY NOT TRUE. IN BOTH CASES THERE WAS NOMINAL EFFECT, ONLY ON SOME, AND IT TOOK 6 MONTHS. SOUNDS LIKE A LOSER TO ME, ESPECIALLY WHEN THE ALTERNATIVE IS SO MUCH BETTER.


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I actually do not know of anyone who has used Nolva and has not benefited from it excepting maybe you if in fact that is the case.

............................
WELL, YOU OBVIOUSLY DON'T DO THIS AS MUCH AS I. I'VE BEEN AT THIS FOR OVER 30 YERAS, I'VE SPOKEN TO THE TOP PEOPLE IN THE INDUSTRY. I KNOW HUNDREDS OF PEOPLE WHO HATE NOLVA. IGNORANCE OF THE FACTS DOESN;T CHANGE THEM IN YOUR FAVOR.



.............................

I am sure there are maybe a few but I am also sure there are a lot more who have used Nolva with a positive experience.

.........................................

IN SOME CASES IT MAY HELP. I'D SAY 75% OF THE TIME NOLVA DOES NOTHING, WHICH IF FINE BECAUSE NOTHING WAS NEEDED. IT HELPS WITH GYNO. IN THE REST OF THE CASES IT SUPPRESSES RECOVERY.



............................................................

I would ask you show me a study where are an individual injected several milligrams of testosterone per week for 12 weeks and then used Nolva as a PCT and it didn't work.

...............................
WORK IN WHAT WAY? HOW IS THAT GAUGEABLE? THEY RECOVERED? FUCK DUDE, GUYS RECOVERED BEFORE ANYONE EVER KNEW WHAT NOLVADEX EXISTED.




.........................


Of course your not going to be able to so please at least be somewhat unbiased. On the other hand I can show you several like individuals that did the same thing and did recover but this is anecdotal. We need to rely on anecdotal as it is a means to increase all of our knowledge and please don't get me wrong as I know Nolva is not for everyone just like anything we do but I do know it works to increase serum test levels and I religiously have blood work done after all my cycles to keep track of this along with what I did exactly for PCT.

.............................

SO YOUR ANECDOTAL EVIDENCE IS MORE IMPORTANT THAN MINE?



.................................................................................


I know from my own personal expereinces that Nolva is not the only answer here and I am not making an argument for that being the case but it is certainly a very beneficial part of PCT. I have had my best recoveries where Nolva has been included as part of PCT.

...................................

THE USE OF NOLVADEX WAS INITIATED BY DAN DUCHAINE WHO HIMSELF ADMITTED IT KINDA SUCKED. IF IT WORKS FOR YOU, GREAT. BUT WHY SHOULD SOME NEWBIW TAKE A CHANCE WHEN THERE ARE LESS CHANCY, SAFER, HEALTHIER AND MORE RELIABLE ALTERNATIVES.

..

 

[access]

The IGF issue was first raised by you and not me and that is why I bought it up again and shows who is actually confused here Nelson. You seem to make these weird and sometimes absurb accustaions against products either for or against and then forget what you wrote in a short period of time. For the most part it is amusing and does make for some interesting debate but at least keep up on this one.

I am not going to back and forward on this with you and will leave the readers of this thread to make up their own minds. Several studies were presented showing Nolva in a positive light. Your attempts to discredit those studies were feeble and almost pathetic at best as was obvious you tried to construe the studies into soemthing they weren't. It's seems alomst unreasonable why you want to discredit a product that does so much for ones recovery but then I have to ask why would someone who is on HRT even know anything about Nolva in anyway personally. Perhaps that is the main problem here? You claim to have talked to top pros and know of many who will not use Nolva but where the hell are these people? I don't see them expressing that opinion in any collective way, it's in fact exactly the opposite. There are littlerally thousands out there using Nolva to great effect either alone or in combination with other meds.

Your original claim that Nolva is mass placebo is just irrational but does show your at least aware it is being used by masses and yet your way to discredit it is to say it's a pacebo..wow! Then you go on to state that it's site specific for breast tissue only shows you don't really understand in any conclusive way what Nolva does. It's an antagonist and mild estrogen and does little to effect actual estrogen levels but acts a substrate for the Estrogen Receptor. Nolva is not selective in how it binds to the Estrogen Receptor but rather selective in the way it is altered by the Estrogen Receptor and therfore will bind to any available Estrogen Receptor. It's quite potent in the liver for example and why it has a positive effect on lipids but resists conversion in breast tissue but will bind equally to either.

Now why wouldn't Nolva be great for PCT knowing the above? You have a product which stops any adverse effects from circulating estrogen which is rising coming off of cycle and simultaneously assisting with natural Testosterone production and all this with virtually no sides in nearly all users. Has to make one wonder.

 

[Nelson Montana]

The IGF issue was first raised by you and not me and that is why I bought it up again and shows who is actually confused here Nelson. You seem to make these weird and sometimes absurb accustaions against products either for or against and then forget what you wrote in a short period of time. For the most part it is amusing and does make for some interesting debate but at least keep up on this one.


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PLENTY OF INFO ON THAT. DO A SEARCH. ONE OF THE REASONS TAMOXIFIN SLOWS TUMOR GROWTH IS BY SUPPRESSING IGF-1



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I am not going to back and forward on this with you and will leave the readers of this thread to make up their own minds. Several studies were presented showing Nolva in a positive light. Your attempts to discredit those studies were feeble and almost pathetic at best as was obvious you tried to construe the studies into soemthing they weren't. It's seems alomst unreasonable why you want to discredit a product that does so much for ones recovery but then I have to ask why would someone who is on HRT even know anything about Nolva in anyway personally.

.............................................

SO YOUR ASSUMING THAT MY KNOWLEDGE OF STEROIDS IS BASED SOLELY ON MY EXPERIENCE ON HRT?!? YOU'RE SO OFF BASE YOU DON;T EVEN KNOW HOW OFF BASE TOU ARE.


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Perhaps that is the main problem here? You claim to have talked to top pros and know of many who will not use Nolva but where the hell are these people?

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WHAT DO YOU WANT -- THEIR PHONE NUMBERS? OR MAYBE I SHOULD ASK THEM TO COME ON HERE TO PROVE IT TO YOU. GEEZUS. GET REAL DUDE.


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I don't see them expressing that opinion in any collective way, it's in fact exactly the opposite. There are littlerally thousands out there using Nolva to great effect either alone or in combination with other meds.

.........................................


REALLY? AND WHERE THE HELL ARE THOSE PEOPLE?



...............................................

Your original claim that Nolva is mass placebo is just irrational but does show your at least aware it is being used by masses and yet your way to discredit it is to say it's a pacebo..wow!

................................................

YOU'RE CONFUSED AGAIN. IT ISN'T PLACEBO IN TREATING BREAST TUMORS. IT'S SIMPLY CAN'T BE GAUGED AS TO HOW MUCH BENEFIT IT HAD IN RECOVERY.

.....................................................................


Then you go on to state that it's site specific for breast tissue only shows you don't really understand in any conclusive way what Nolva does. It's an antagonist and mild estrogen and does little to effect actual estrogen levels but acts a substrate for the Estrogen Receptor. Nolva is not selective in how it binds to the Estrogen Receptor but rather selective in the way it is altered by the Estrogen Receptor and therfore will bind to any available Estrogen Receptor.

.......................................

YOU'RE SAYING THE SAME THING IN A DIFFERENT WAY. BECAUSE NOLVA AND CLOMID ARE MILD ESTROGENS IS WHY, IN PART, WHY IT BACKFIRES IN SO MANY CASES. BUT THAT'S ANOTHER ISSUE AND I HAVEN;'T GOT THE INCLINATION TO EXPLAIN IT TO YOU.


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Now why wouldn't Nolva be great for PCT knowing the above?


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FOR THE REASONS I'VE ALREADY EXPLAINED.


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You have a product which stops any adverse effects from circulating estrogen which is rising coming off of cycle and simultaneously assisting with natural Testosterone production and all this with virtually no sides in nearly all users. Has to make one wonder.
...................................................

LET ME GUESS -- YOU HAVEN'T USED IT? I THOUGHT SO.

..

 

[needtogetaas]

This is factually incorrect. There are a number of studies showing that treatment with Nolva does increase serum testosterone levels in men. It also shows a positive effect on lipids with very little sides in most users so I am always at a loss when you condemn Nolva.

Why nolva is sub par.

1. Nolva's primary mechanism of action is to compete with estrogen at the estrogen receptor. Not to lower estrogen. Its a (Selective Estrogen Receptor Modulator)

Nolvadex does not decrease estrogen production and that it simply blocks estrogen receptors.In fact total body estradiol increases with use of tamoxifen!! For this reason the sudden discontinuance of Nolvadex will allow the increased level of circulating estrogen to merge with the newly freed receptors and perhaps cause the feminizing side effects to become more apparent

This is why many people you use nolva for pct will have a (estrogen rebound) and end up with gyno months after that cycle. Believe me I get the pm's about this all day long. Tapering down and switching to a anti estrogen can help with this. Then again why not take the anti-e or other product in the first place.


SO yes well using it may work to raise your levels of testosterone, LH, and FSH back to normal you it is not with out its problems. You can have a rebound after using it for pct and may end up with higher estro then when you started. This in turn of course can have some problems. As we know higher levels of estro (when not on cycle) means lower levels of test. Rebound effects and so forth.

2. Now that we know estrogen in not really lowered but rather selectively blocked from different receptors when using nolvadex(and in some causes higher during the use and often after) this leaves us with.

Free estrogen no longer going into the receptors that its being blocked from? Where does it go? Well we all know the ( why you acting like a bitch bro you on nolve/clomid?) yup we all know it. You're a walking ball of estrogen acting like a little girl.


1. Klin Padiatr. 1987 Nov-Dec;199(6):389-91.
2. Stimulation of calcitonin secretory capacity by increased serum levels of testosterone in men treated with tamoxifen. Int J Androl. 1987 Dec;10(6):747-51.
3. Hormonal changes in tamoxifen treated men with idiopathic oligozoospermia Exp Clin Endocrinol. 1988 Dec;92(2):211-6.
4. 2 Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9
5. Fertil Steril. 1978 Mar;29(3):320-7.

SERMs (Selective Estrogen Receptor Modulators)
Maxim Health System [Powered by Invision Power Board]
Nolvadex tamoxifen citrate - Anabolic SteroidProfiles - Steroid . com

 

[access]

Ok needto, you I don't mind further responding to.

The problem with your argument against Nolva is primarily directed at it not being able to lower circulating estrogen coming off cycle. Firstly if you do preceive this as a problem then your best option is to commence Aromasin late in the cycle and then continue for a short period after and before commencing Nolva. This will have an effect of lowering the total amount of estrogen as I totally agree Nolva (or clomod for that matter) will not do this with them being SERMs.

The reason I prefer Nolva over an AI for PCT is that it acts much faster at blocking the estrogen at the receptor than an AI will do stopping the conversion process and ideally that is what we want. Something that acts quickly when we enter PCT. Now we should be running Nolva for 4 weeks and if you do then there will be no rebound as over that 4 week period circulating estrogen is continously lowering as we have stopped all exogenous injections of AAS and this then negates your argument of any rebound.

 

[Nelson Montana]

So if needto has an argument against nolva it's okay? WTF? So it's ME! lol.

Forgot about the rebound issue. Thanks needto. But you're wrong access -- again -- that there won;t be any rebound sfter only 4 weeks. That one you pulled out your ass, ya gotta admit.

Bottom line. Nolva isn't needed. The recommended PCT is better. End of story.