Post cycle therapy (pct) when????

gotenks004

gotenks004

New member
PCT when????

My freind is on a Test Enanthate cycle of 500mgs a week and he wants to know when would be the best time to start the post cycle therapy (pct) he is only 22. He is on a 10 week cycle, I always start 3 weeks after the last inj. using clomid and tamoxifen and run it for 3 weeks but I'm hearing other people say it is better to start 2 weeks after the last injection what do you guys usually do?

And what would be the best dosage for clomid throughout the post cycle therapy (pct).

Thanks
 
PCT

post cycle therapy (pct) AKA post cycle recovery is a misnomer. That is old school and nowadays there is a much improved way to allow for total post cycle therapy (pct).
Your post cycle therapy (pct) should start 2 weeks into our cycle running Human Chorionic Gonadotropin (HCG) 500IU 2 days per week until 1 week post. Also, run nolva 20mg per day concurrently and 4-5 weeks post.Clomid is unnecessary and if run longer tern is actually quite dangerous. The effects of SERM's such as Clomid and Nolvadex are quite similar, but with Nolvadex having much more beneficial secondary effects..ie lipid profile satablization.
If you follow this your recovery will be cut in half if not more and muscle retained will be much higher...not to mention restoration of endogenous testosterone production.
P
 
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Re: PCT

Praetorian said:
post cycle therapy (pct) AKA post cycle recovery is a misnomer. That is old school and nowadays there is a much improved way to allow for total post cycle therapy (pct).
Your post cycle therapy (pct) should start 2 weeks into our cycle running Human Chorionic Gonadotropin (HCG) 500IU 2 days per week until 1 week post. Also, run nolva 20mg per day concurrently and 4-5 weeks post.Clomid is unnecessary and if run longer tern is actually quite dangerous. The effects of SERM's such as Clomid and Nolvadex are quite similar, but with Nolvadex having much more beneficial secondary effects..ie lipid profile satablization.
If you follow this your recovery will be cut in half if not more and muscle retained will be much higher...not to mention restoration of endogenous testosterone production.
P
Click to expand...


I agree with some of that - Human Chorionic Gonadotropin (HCG) throughout the cycle & the fact that Nolva is benificial for the lipid profile.

I disagree with - Clomid is unnecessary and if run longer tern is actually quite dangerous.

Although Clomid & Nolva are both SERMs, Clomid is clearly the better choice for restoring one's HPTA.
 
Cloid and nolvadex do little to restore endogenous testosterone production...what they do is provide an estrogen reduced environment that allows for quicker restoration of endogenous production. There also have been many studies done comparin gthe two and little significant difference is seen. Except of course the true possibility of sides with clomid...which in fact has been documented medically. Here is an excerpt from "Swale" of Cutting edge muscle...he is a medical doctor and has numerous high level athletes who use his post cycle therapy (pct) methods to great success.

My current best thoughts.

I advise my Anabolic Androgenic Steroids (AAS) patients to use small amounts of Human Chorionic Gonadotropin (HCG) (250IU to 500IU) on two consecutive days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

Any more than 500IU of Human Chorionic Gonadotropin (HCG) per day causes too much aromatase activity, and results in destruction of Leydig cells. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when Human Chorionic Gonadotropin (HCG) is so inexpensive.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of Anabolic Androgenic Steroids (AAS) (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

I want my patients to stop taking Human Chorionic Gonadotropin (HCG) within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.

I like Arimidex during the cycle (in fact, consider use of an Aromatase inhibitor (AI) while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.


Peace,
P
 
Praetorian said:
Cloid and nolvadex do little to restore endogenous testosterone production...what they do is provide an estrogen reduced environment that allows for quicker restoration of endogenous production. There also have been many studies done comparin gthe two and little significant difference is seen. Except of course the true possibility of sides with clomid...which in fact has been documented medically. Here is an excerpt from "Swale" of Cutting edge muscle...he is a medical doctor and has numerous high level athletes who use his post cycle therapy (pct) methods to great success.

My current best thoughts.

I advise my Anabolic Androgenic Steroids (AAS) patients to use small amounts of Human Chorionic Gonadotropin (HCG) (250IU to 500IU) on two consecutive days each week, right from the beginning of the cycle. This serves to maintain testicular form and function. It makes more sense to me to keep the horse in the barn, so to speak, then to have to chase it across three counties later on. I am also a big fan of maintaining estrogen within physiological ranges. Both therapies have been shown to hasten recovery.

Any more than 500IU of Human Chorionic Gonadotropin (HCG) per day causes too much aromatase activity, and results in destruction of Leydig cells. You are then inducing primary hypogonadism (which is permanent) while treating steroid-induced secondary (hypogonadotrophic) hypogonadism (which is temporary--hopefully).

If 250IU or 500IU on two days each week isn’t enough to stave off testicular atrophy, then I recommend using it more days each week (as opposed to taking larger doses). In fact, I wouldn’t mind having a guy use 250IU per day ALL THROUGH the cycle. Those that have tell me they thus avoid that edgy, burned-out feeling they usually get. They also say they simply feel better each day. Subjective reports, to be sure, but they are hard not to appreciate. Especially when Human Chorionic Gonadotropin (HCG) is so inexpensive.

The testes are then ready, willing and able to again produce testosterone at the end of the cycle. LH levels rise fairly rapidly, but endogenous testosterone production is limited by lack of use. I also want to make sure a SERM, such as Clomid or Nolvadex, is at effective serum dosage (around 100mg QD for Clomid, 20-40mg QD for Nolvadex) when serum androgen levels drop to a concentration roughly equal to 200mg of testosterone per week. That is when androgenic inhibition at the HP no longer dominates over estrogenic antagonism with respect to inducing LH production. Of course, if the fellow has been doing Clomid or Nolvadex all along the way (and I now prefer Nolvadex over Clomid, due to the possibility of negative sides from the Clomid), he is all set to simply continue it at the end (no need to switch from one to the other). BTW, I see no evidence of any benefit in using BOTH SERM’s at the same time. I used to think a couple of weeks of the SERM was enough; now I like to see an entire month after the last shot of Anabolic Androgenic Steroids (AAS) (and migration of long to short esters as the cycle matures). Tapering the SERM is probably a good idea during the last week, as well.

I want my patients to stop taking Human Chorionic Gonadotropin (HCG) within a week after the end of the cycle. The testosterone production it induces will further inhibit recovery, as will using Androgel, or any other testosterone preparation, while in recovery. There is no escaping this, as there is no such thing as a “bridge”. Just because you are not inhibiting the HPTA for the entire 24 hours does not mean you are not suppressing it at all. IOW, you can’t “fool” the body—it is smarter than you are.

I like Arimidex during the cycle (in fact, consider use of an Aromatase inhibitor (AI) while taking aromatisables a necessity) but it ABSOLUTELY should not be used post cycle (even though it has been shown to increase LH production) because the risk of driving estrogen too low, and therefore further damaging an already compromised Lipid Profile, is too great (this also drives libido back into the ground—and we don’t want that, do we?).

All this is meant to get my guys through recovery as fast as possible (the real goal, yes?). So far, all of them who have tried it have reported they are recovering faster than when they have tried other protocols.


Peace,
P
Click to expand...


Swale is a member here and that same post is in our archives.

Swale is actually my HRT doc.

Clomid is much better at stimulating the HPTA.

SERMs do have a direct effect on the HPTA.
 
LAWNSAVER said:
Swale is a member here and that same post is in our archives.

Swale is actually my HRT doc.

Clomid is much better at stimulating the HPTA.

SERMs do have a direct effect on the HPTA.
Click to expand...


Damn! That just COMMANDS respect.........short, concise, and to the point!

Semper Fi
 
LAWNSAVER said:
Swale is a member here and that same post is in our archives.

Swale is actually my HRT doc.

Clomid is much better at stimulating the HPTA.

SERMs do have a direct effect on the HPTA.
Click to expand...

Well Swale definitley is the man when it comes to post cycle therapy (pct). His help has improved mine dramatically...much thanks. On the other hand the debate on SERM's continues and we may have to agree to disagree...from anecdoatal evidence to my own experimentation i ahev found nolvadex much better.
I was able to dig up an article that may shed some light perhaps.
P


Clomid, Nolvadex and Testosterone Stimulation
by William Llewellyn

I have received a lot of heat lately about my preference for Nolvadex over Clomid, which I hold for all purposes of use (in the bodybuilding world anyway); as an anti-estrogen, an HDL (good) cholesterol-supporting drug, and as a testosterone-stimulating compound. Most people use Nolvadex to combat gynecomastia over Clomid anyway, so that is an easy sell. And for cholesterol, well, most bodybuilders unfortunately pay little attention to this important issue, so by way of disinterest, another easy opinion to discuss. But when it comes to using Nolvadex for increasing endogenous testosterone release, bodybuilders just do not want to hear it. They only seem to want Clomid. I can only guess that this is based on a long rooted misunderstanding of the actions of the two drugs. In this article I would therefore like to discuss the specifics for these two agents, and explain clearly the usefulness of Nolvadex for the specific purpose of increasing testosterone production.



Clomid and Nolvadex


I am not sure how Clomid and Nolvadex became so separated in the minds of bodybuilders. They certainly should not be. Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that Clomid is the only drug good at stimulating testosterone. What you will find with a little investigation however is that not only is Nolvadex useful for the same purpose, it should actually be the preferred agent of the two.

Studies conducted in the late 1970's at the University of Ghent in Belgium make clear the advantages of using Nolvadex instead of Clomid for increasing testosterone levels (1). Here, researchers looked the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts (oligospermia). For our purposes, the results of these drugs on hormonally normal men are obviously the most relevant. What was found, just in the early parts of the study, was quite enlightening. Nolvadex, used for 10 days at a dosage of 20mg daily, increased serum testosterone levels to 142% of baseline, which was on par with the effect of 150mg of Clomid daily for the same duration (the testosterone increase was slightly, but not significantly, better for Clomid). We must remember though that this is the effect of three 50mg tablets of Clomid. With the price of both a 50mg Clomid and 20mg Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the Nolvadex side.



Pituitary Sensitivity to GnRH


But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosterone and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say Clomid won't increase testosterone if taken for the same 6 week time period. Quite the opposite is true. But we are, however, noticing an advantage in Nolvadex.



The Estrogen Clomid


The above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers' clearly support this theory when commenting in their paper, "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested itself by an increase in transcortin and testosterone/estradiol-binding globulin [SHBG] levels; this increase was not observed after tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of Clomid which is practically absent in Tamoxifen seems the most probable explanation".

Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of Clomid and Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol. Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.

The Role of Anti-estrogens


It is important to understand that anti-estrogens alone do not do much to restore endogenous testosterone release after a cycle. Normally they only foster LH by blocking the negative feedback of estrogens, and we now see that LH rebounds quickly without help anyway. Plus, post cycle there is not an elevated level of estrogen for anti-estrogens to block, as testosterone (now suppressed) is a major substrate used for the synthesis of estrogens in men. Serum estrogen levels will actually be lower here as a result, not higher. Any estrogen rebound that occurs post-cycle likewise happens concurrently with a rebound in testosterone levels, not prior to it (note there is an imbalance in the ratio post cycle, but this is another topic altogether). We are seeing no mechanism in which anti-estrogenic drugs can really help here. We can see why this fact would not be difficult to overlook, however. The medical literature is filled with references showing anti-estrogenic drugs like Clomid and Nolvadex to increase LH and testosterone levels, and in normal situations these drugs do indeed increase endogenous androgen production by blocking the negative feedback of estrogens. Combine this with the fact that just as many studies can be found to show that steroid use lowers LH levels when suppressing testosterone, and we can see how easy it would be to jump to the conclusion that post-cycle we need to focus on restoring LH. We would miss the true problem of testicular desensitization unless we were really looking into the actual recovery rates of the hormones involved. When we do, we immediately see little value in using anti-estrogenic drugs.



Conclusion


To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables Nolvadex to offer the male bodybuilder certain advantages over Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of Clomid in order to get the same level of LH stimulation.

Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosterone levels to warrant using as anabolics. Here Nolvadex would seem to provide a better and more stable increase in testosterone levels, and likely will offer a similar or greater effect than Clomid for considerably less money. The potential rise in SHBG levels with Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosterone compared to Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.

In next month's follow-up article I will be discussing the role anti-estrogens play in post-cycle testosterone recovery. Most specifically, I will be detailing what a proper post-cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.


References:

1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7

2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30

3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45
 
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Again, an old article that really doesnt touch on "real world" experiences.

for the people who have used both, me as one of them, find that although the side effects are more pronouced with Clomid, the recovery and stimulation of the HPTA is better with clomid.

Lets think about it another way. Most urologist and endocrinologists I have consulted with have said that clomid have a must greater effect on stimulation of LH, and FSH. This will have a more postitive effect on natural test production.

For every article you find on N-dex being a better choice, we can throw 4 more that says clomid is better.

I will say that n-dex is the best when blood lipids are a problem.
 
My post cycle therapy (pct) in the past year has been much improved mostly due to the fact of Human Chorionic Gonadotropin (HCG) usage during my cycles. As well my lipid profile has been much more stable with the use of tamoxifen. It is inconsistent to say one or the other SERM's is superior based solely on anecdotal evidence. Also, although true you may be able to find studies to the contrary, this is indicative of almost any study attempting to prove a hypothesis. For any study proving one thing there are many proving the opposite. However, I can say that the improved post cycle therapy (pct) may be due more to the use of Human Chorionic Gonadotropin (HCG) than the use of tamox over clomid...but i cannot say it with scientific accuracy. I have found more info however which does support your claims and may shed some more light on the subject. Keeping in mind this is a constant learning game and i for one am always open to criticism and contrary opinion.

Posted by Pheedno @ Anabolicreview


My post cycle therapy consists of a three compound administration which is designed so that there is a primary and secondary LH stimulator which both are maximizing potential early in the duration; with the primary being phased out in extended protocol. With the addition of an Aromatase Inhibitor, which makes the above possible, the individual will also endure less of an increase in Sex Hormone Binding Globulin, which allows free testosterone levels to reach base line at a much quicker pace. The individual will also see less of a problem in most cases with sexual libido as the bounding SHBG is controlled(to an extent). Below you will find my suggested bare minimum, as well as a sample of an extended protocol. Extended post cycle therapy (pct) protcol is cycle length dependant so the below is not the standard for all cycles


post cycle therapy (pct) for cycles 8-16wks:
Day 1-30- .25mg L-dex + 100mg Clomid + 20mg Nolva

Extended protocol sample for a 12+ month cycle:
Day 1-15_ .25mg L-dex + 100mg Clomid + 20mg Nolva
Day 16-45_.25mg L-dex + 75mg Clomid + 20mg Nolva
Day 46-65_.25mg L-dex + 20mg Nolva
Day 66-80_.25mg L-dex

Now IMO, selective estrogen receptor modulators(SERMs) such as Clomiphine and Tamoxifen are selective to which tissues they bind too. Clomid being selective to the suprapituitary, while Tamox is selective to breast, bone, and liver ERs. I've come to this conclusion based on the comparison of studies on both SERMs. In every study showing benefit to HPTA from tamoxifin, the duration of the administration is 3-12months(This includes studies cited by William Llewellyn in his Nolva vs Clomid article). In studies showing levels of LH, FSH, and Testosterone checked after short durations of tamox, they were either insignificant, or their was an actual drop. I believe this is because tamox selectively works at the mammery(as well as bone and liver), thus taking longer for LH stimulation to occur.
With clomid, benefit to gonadotrophin concentrations, LH, FSH, and serum testosterone can be seen in short periods of 2-6wks. Because of the apparent selective nature of the two, and given our usual post cycle therapy (pct) duration, clomid is by far superior at LH stimulation than Nolva. Now both is the wise choice for a couple of reasons:

1. Nolva acts as the preventive measure to the estrogen flux
occured PC while clomid is the primary LH stimulator(Even more so in the case an Aromatase inhibitor (AI) is not used).
2. If your running a longer post cycle therapy (pct), clomid needs to be discontinued after a while as it has been shown to desensitize GnRH, this due, IMO, to it's selective nature to the suprapituitary. In the longer forms of post cycle therapy (pct), the clomid will be phased out, leaving Nolva and L-dex

Arimidex(or L-dex)
Estrogen is the main inhibitence of restoring HPTA, and Aromatase inhibitor (AI) administration has been shown to increase gonadotrophin concentrations and serum Testosterone by up to 50%. In addition, by adding L-dex, the inhibitence of excess estrogen allows Tamox to work greater at LH stimulation in the begining stages of post cycle therapy (pct), since the need to prevent binding in the mammery is lessened by the reduction in estrogen biosynthesis



Tamox vs Clomid

Am J Physiol 1983 Feb;240(2):E125-30

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro.

Adashi EY, Hsueh AJ, Bambino TH, Yen SS.

The direct effects of clomiphene citrate (Clomid), tamoxifen, and estradiol (E2) on the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) were studied in cultured anterior pituitary cells obtained from adult ovariectomized rats. Treatment of pituitary cells with Clomid or enclomid (10(-8) M) in vitro for 2 days resulted in a marked sensitization of the gonadotroph to GnRH as reflected by a 6.5-fold decrease in the ED50 of GnRH in terms of LH release from 2.2 x 10(-9) M in untreated cells to 3.6 x 10(-10) M. Treatment with E2 or Clomid also increased the sensitivity of the gonadotroph to GnRH in terms of FSH release by 4.3- and 3.3-fold respectively. Tamoxifen, a related antiestrogen, comparable to Clomid in terms of its ability to compete with E2 for pituitary estrogen receptors, was without effect on the GnRH-stimulated LH release at a concentration of 10(-7) M. Furthermore, tamoxifen, unlike Clomid, caused an apparent but not statistically significant inhibition of the sensitizing effect of E2 on the GnRH-stimulated release of LH. Our findings suggest that Clomid and its Enclomid isomer, unlike tamoxifen, exert a direct estrogenic rather than an antiestrogenic effect on cultured pituitary cells by enhancing the GnRH-stimulated release of gonadotropin.

__________________________________________________
_________

Br J Pharmacol 1978 Apr;62(4):487-93

Differential depletion of cytoplasmic high affinity oestrogen receptors after the in vivo administration of the antioestrogens, clomiphene, MER-25 and tamoxifen.

Kurl RN, Morris ID.

1 The in vivo actions of the oestrogen antagonists, MER-25 and tamoxifen upon the cytosol oestrogen receptors prepared from amygdala, hypothalamus, pituitary and uterus of rats were studied 24 h after drug administration. 2 There was a dose-related depletion of cytosol oestrogen receptors. However, the uterine and pituitary receptors were consistently affected at a lower dose than were those from the brain. 3 The ratios of the combined central ED50 to the combined peripheral ED50 were clomiphene 169 greater than MER-25 19.2 greater than tamoxifen 2.13. 4 The receptor changes were not related to biological activity monitored by serum luteinizing hormone levels and uterotrophic response. 5 The possible role of these drug effects in the induction of ovulation and future developments are discussed.

__________________________________________________
__________

the following study was not available in my library, so i wasn't able to obtain the article or abstract. it may have to be purchased, so if someone is interested, here's the title and authors of the research.

Nippon Funin Gakkai Zasshi 1978 Oct;23(4):398-404

[The hormonal dynamics picture of tamoxifen treatment cases, in comparison of clomid treatment cases]

__________________________________________________
_______

Cochrane Database Syst Rev 2000;(2):CD000151

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.








Join Date: Jan 2004
Location: South Florida
Posts: 1,436 Posted by Pheedno @ Anabolicreview


Case for Clomid

J Clin Endocrinol Metab 1985 Nov;61(5):842-5

Evidence for a role of endogenous estrogen in the hypothalamic control of gonadotropin secretion in men.

Winters SJ, Troen P.

To examine the mechanism by which endogenous estrogens inhibit gonadotropin secretion in men, blood samples were drawn every 10 min for 12 h in five men before and at the completion of 3 weeks of treatment with the estrogen antagonist clomiphene citrate (50 mg twice daily). Samples were analyzed for LH and alpha-subunit by RIA. Clomiphene produced a 3-fold rise in circulating LH levels, which was associated with a 80% increase in pulse frequency and a 70% increase in pulse amplitude. Immunoreactive alpha-subunit secretion was also pulsatile before and after clomiphene treatment. Mean alpha-levels rose 70%, together with a 39% increase in pulse frequency and a 41% increase in pulse amplitude. Circulating testosterone and estradiol levels increased 2-fold and FSH levels increased 3-fold after clomiphene treatment. Insofar as each LH and uncombined alpha-subunit pulse reflects a LHRH secretory episode, our data indicate that endogenous estrogens tonically restrain the hypothalamic release of LHRH. From these results and those of previous studies, we conclude that estrogens as well as androgens are important in the testicular feedback inhibition of the hypothalamic oscillator that governs pulsatile gonadotropin secretion.


J Androl 1991 Jul-Aug;12(4):258-63

The effects of normal aging on the response of the pituitary-gonadal axis to chronic clomiphene administration in men.

Tenover JS, Bremner WJ.

Department of Medicine, University of Washington School of Medicine, Seattle.

Serum androgens decline with age in normal men, despite normal or elevated bioactive serum gonadotropins, suggesting that primary testicular dysfunction occurs with aging. The authors further assessed the question of age-related testicular dysfunction by evaluating whether raising serum gonadotropins above the normal serum range for an extended time in healthy elderly men might result in bringing their gonadal function to a level similar to that found in young adult men. Five elderly (65 to 85 years old) and five young adult men (26 to 33 years old) were given 50 mg of clomiphene citrate (CC) twice a day for 8 weeks to stimulate gonadotropin production. During that time, testosterone (T), non-sex hormone-binding globulin bound T, and estradiol increased significantly in both age groups, while serum inhibin increased significantly only in the young adult men. The increases in serum androgens with CC administration were significantly greater in the young adult men than in the elderly men. These hormone changes occurred in the setting of serum gonadotropins that increased significantly in both age groups, although there was a tendency for the elderly men to have a smaller increase in luteinizing hormone. Despite 8 weeks of stimulation of the pituitary-gonadal axis by CC administration, the elderly men demonstrated significantly diminished testicular responses compared with the young adult men. Sertoli cell function, as determined by inhibin production, was more diminished in the elderly men than was Leydig cell function. These data strengthen the hypothesis that normal aging in men is accompanied by a decline in testicular function.


Urology 1991 Oct;38(4):317-22

Possible hypothalamic impotence. Male counterpart to hypothalamic amenorrhea?

Guay AT, Bansal S, Hodge MB.

Section of Endocrinology, Lahey Clinic Medical Center, Burlington, Massachusetts.

Twenty-one men with erectile complaints who were found to have a low level of serum testosterone without a reciprocal elevation of the serum levels of luteinizing hormone were evaluated to identify whether the defect was of hypothalamic or of pituitary origin. Patients underwent a luteinizing hormone (LH)-follicle-stimulating hormone (FSH)-releasing hormone stimulation test that showed a normal but sluggish increase in LH and FSH levels, thus ruling out a pituitary defect and suggesting a suprapituitary abnormality. This was confirmed when, in response to clomiphene, patients had a normal increase in gonadotropin and testosterone levels. Although the basal as well as clomiphene and gonadotropin releasing hormone-stimulated levels of total testosterone and gonadotropins were identical in men less than and more than fifty years old, the elevation of free testosterone levels in response to clomiphene was higher in patients younger than fifty. This suggested that although the primary abnormality found in these patients is altered secretion of gonadotropin hormone-releasing hormone from the hypothalamus, an age-related decline in the responsivity of Leydig cells to LH may make it more manifest in older patients. Elevation of testosterone levels from a subnormal to a normal range in response to clomiphene administered for seven days suggests that the defect is functional and reversible and that the drug may be useful in treatment of sexual dysfunction in this group of patients.
Nephron 1993;63(4):390-4

Effect of clomiphene citrate on hormonal profile in male hemodialysis and kidney transplant patients.

Martin-Malo A, Benito P, Castillo D, Espinosa M, Burdiel LG, Perez R, Aljama P.

Department of Nephrology, Hospital Universitario Reina Sofia, Cordoba, Spain.

The aim of this study was to evaluate the role of clomiphene citrate (CC) therapy in the hypothalamus-pituitary-gonadal axis of male uremic subjects. Thirty-four patients on hemodialysis (HD) and 8 successful kidney transplant subjects (RT) were evaluated. Nine healthy males were used as controls (C). At baseline, zinc, testosterone (TEST), prolactin (PRL), FSH, LH and estradiol plasma concentrations were measured. All subjects were treated with CC (100 mg/day) for a week. The aforementioned parameters were determined again on the seventh day of CC therapy, and 3 days after drug withdrawal. Following CC, there was a rise in FSH, LH and TEST levels in all subjects (p < 0.05); it is interesting to stress that TEST became normal in HD. In addition, we observed a decrease of PRL after CC only in HD patients (p < 0.01). In summary, CC was able to partially correct most of the




Join Date: Jan 2004
Location: South Florida
Posts: 1,436 Posted by Pheedno @ Anabolicreview

Tamoxifen

nolvadex aka tamoxifen studies:

Arch Gynecol Obstet 1993;252(3):143-7

Tamoxifen treatment of oligozoospermia: a re-evaluation of its effects including additional sperm function tests.

Sterzik K, Rosenbusch B, Mogck J, Heyden M, Lichtenberger K.

Abteilung Frauenheilkunde, Geburtshilfe der Universitat, Ulm, Germany.

Because of previous contradictory results, we reevaluated the effects of tamoxifen on 29 men presenting with idiopathic oligozoospermia. To determine whether a possible increase in sperm concentration might be correlated with an improvement of sperm quality, the hamster ovum penetration (HOP) test and the hypo-osmotic swelling (HOS) test were included as additional tests of sperm function. Patients were treated with tamoxifen (20 mg/day) for 3 months. From 4 weeks until the end of the study, tamoxifen had no significant effect (P > 0.05) on blood levels of luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone (T), or estradiol (E2). There was no significant improvement (P > 0.05) of conventional semen parameters (volume, concentration, motility, morphology), and of HOP and HOS test results. The lack of correlation between a rise in hormone levels and improvement of sperm quality suggests that tamoxifen is of questionable value in men with idiopathic oligozoospermia.


Asian J Androl 2001 Jun;3(2):115-9

Effect of intermittent treatment with tamoxifen on reproduction in male rats.

Gill-Sharma MK, Balasinor N, Parte P.

Department of Neuroendocrinology, Institute for Research in Reproduction, ICMR, Parel, Mumbai, India. dirirr@vsnl.com

AIM: To identify the antifertility effect of intermittent oral administration of tamoxifen in male rat. METHODS: Tamoxifen was administered orally at a dose of 0.4 mg x kg(-1) x d(-1) with an intermittent regime for 120 days. Treated and control rats were mated with cycling female rats on days 60, 90 and 120 of treatment. The mated males were sacrificed and the weights of reproductive organs were recorded, and the serum levels of LH, FSH, testosterone and estradiol estimated by radioimmunoassay. In the female rats, the numbers of implantation sites, corpora lutea, and numbers of normal and resorbed foetuses were recorded on d 21 of gestation. The potency, fecundity, fertility index, litter size and post-implantation loss were then calculated. RESULTS: The fecundity of male rats was completely suppressed by tamoxifen while the potency was maintained at the control level. The fertility index was significantly decreased. No viable litters were sired. Post implantation loss, indicative of non-viable embryos, was observed but was not significantly increased above the control level. The weights of the testes, epididymides, ventral prostate and seminal vesicles were significantly reduced. The blood LH and testosterone levels were significantly decreased, but not FSH and estradiol. CONCLUSION: Intermittent oral tamoxifen administration completely suppressed the fecundity of adult male rats with reserved potency.


Case study showing benefit to FSH, LH, and testosterone from tamox- Notice administration duration

Treatment of idiopathic and post varicocelectomy oligozoospermia with oral tamoxifen citrate.
BJU Int 1999 Apr; 83: 646-8
Kadioglu TC Köksal IT Tunç M Nane I Tellaloglu S

[see related articles]

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--------------------------------------------------------------------------------

Affiliation
Department of Urology, Faculty of Medicine, Istanbul University, Istanbul, Turkey.

Abstract
OBJECTIVE: To identify a subgroup of men who may benefit from tamoxifen citrate (a widely prescribed drug for male infertility) among those with normogonadotrophic and hypergonadotrophic oligozoospermia, either idiopathic or after varicocelectomy. PATIENTS AND METHODS: The study included infertile men with oligozoospermia, 136 referred to our outpatient clinic and 84 infertile after varicocelectomy. All patients received tamoxifen citrate (10 mg twice daily); semen analysis and hormone tests were repeated at the end of 3 and 6 months of treatment, the values being compared with those before treatment. RESULTS : The levels of follicle-stimulating hormone, luteinizing hormone and testosterone increased in all groups receiving tamoxifen citrate. Normogonadotrophic patients had a significant increase in sperm count and concentration, while the slight increase detected in the hypergonadotrophic group was statistically insignificant. CONCLUSION: In patients with normogonadotrophic oligozoospermia, tamoxifen citrate may be offered as a practical and economic alternative before using any assisted reproduction techniques. However, double-blind placebo-controlled trials are needed to confirm the findings of this preliminary study.



Study between tamox administration and placebo- attention to highlighted

Int J Androl. 1992 Feb;15(1):14-8. Related Articles, Links


Comment in:
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.(ABSTRACT TRUNCATED AT 250 WORDS)


Also notice levels were checked at 2wks-12wks, but it is not specified when increased levels of FSH, LH, and T were seen at maximized effect. Levels of T and FSH are only significant, with T at miniscuel proportions

Fertil Steril. 1983 May;39(5):700-3. Related Articles, Links


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.


Peace,
P
 
fellas this is a constructive,informational and kick ass debate .
glad your here praetorian:)
 
DADAWG said:
fellas this is a constructive,informational and kick ass debate .
glad your here praetorian:)
Click to expand...

No shit, praetorian has added a nice side to this ongoing debate.

I will say that with my experience I have noticed that Clomid brought my levels back 'faster' than Nolva, but of course I got the sides with that. I guess it will continue to be preferential.

Honestly, I can't do Clomid because it makes me cry when I watch dumb chic commercials!!!LOL

:crying:
 
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