nolva vs clomid

[dbo]

i read this article and i was wondering what everyone thinks about it. it would be interesting to get Dr. Scally's feedback on this.

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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 [sex hormone binding globulin ] 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 - leutenizing hormone - 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 - leutenizing hormone - response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.



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 - (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 - hypothalamic-pituitary-testicular axis - , 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 - leutenizing hormone - 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 sex hormone binding globulin 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 gynecomastia 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


01-Oct-2003, 12:36 AM #20
PotatoHead Not trying to take over thi

 

[number11]

subscribed...

 

[bigrobbie]

i read this article and i was wondering what everyone thinks about it. it would be interesting to get Dr. Scally's feedback on this.

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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 [sex hormone binding globulin ] 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 - leutenizing hormone - 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 - leutenizing hormone - response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.



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 - (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 - hypothalamic-pituitary-testicular axis - , 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 - leutenizing hormone - 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 sex hormone binding globulin 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 gynecomastia 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


01-Oct-2003, 12:36 AM #20
PotatoHead Not trying to take over thi

How old is this article? Just wondering.....

 

[BarbellBeast]

I've read this article before. I'm pretty stuck on using both simultaneously for PCT instead of one or the other. In my experience clomiphene alone works better than tamoxifen alone, but both together is a slam dunk IMO.

 

[bigrobbie]

I've read this article before. I'm pretty stuck on using both simultaneously for PCT instead of one or the other. In my experience clomiphene alone works better than tamoxifen alone, but both together is a slam dunk IMO.

I agree, I think the hCG craze has taken people away from Clomid....I like hCG, I think it works wonders, but I also still, most the time, opt for Clomid/Nolva PCT. Whatcha think.....hCG on cycle then work a Clomid/Nolva PCT....talk about a quick recovery! You agree or disagree?

 

[bigslick]

I agree hCG durning cycle 100%, mid-cycle.depending on amount i use durning cycle, i may run upto 1000iu for up to 10 days at end of cycle.

clomid/nolva are staples of my pct. back in the day I was a strong believer of proviron durning and pct and still have a hard time getting away from it, but there are much better options these days

 

[bigrobbie]

I agree hCG durning cycle 100%, mid-cycle.depending on amount i use durning cycle, i may run upto 1000iu for up to 10 days at end of cycle.

clomid/nolva are staples of my pct. back in the day I was a strong believer of proviron durning and pct and still have a hard time getting away from it, but there are much better options these days

Yea, I like 1000iu/e.d. for 10 days /Clomid/Nolva PCT....I'm liking Clen as part of PCT also, help prevent you from going catabolic, lean you up also. IMO...

 

[BBC3]

Whats the point of this? The bottom line is that for the purpose of E feedback for purposes of signaling the HPTA, by whatever means. Whether it is a heavy circlating amount of E in the system, or the body's percieved lack there of, for SERM purposes here are the facts.

NOLVA is a chemical that just happens to like to bind to E receptors in certain areas (breast tissue, prostate, etc). NOLVA prefers some E receptors and not others.
**** CERTAIN AREAS OF E BLOCKING = less overall estrogen blockage = more overall circulating resulting in LESS uptaked E by means of deprivation of E to certain areas.

CLOMID is a chemical that more accurately resembles the natural Estrogen structure and binds with receptors due to this fact.
****GENERALIZED SYSTEMWIDE E BLOCKING = even more overall estrogen blockage = even more overall E left circulating, and THAT MUCH LESS uptaked E by means of a more overall systemwide blockade.

YOU have to weigh and balance the other (side) effects, and inherent dangers of the drug you are willing to take. Go to the manufacturer website and read what these drugs do to you!

FACT: Nolva only partially affects E, are you going to get as good an E related response, NO. You may also benefit in the fact that you may not go to sleep crying like a bitch every night as an added benefit of this fact. If partial E blockage is all it takes to get the HPTA back online, and you decide that the risk of the other affects of NOLVA are acceptable. Then take that one. I am guessing that while NOLVA only blocks E to certain areas, it is more of a complete block on those areas.

FACT: Clomid will bind to E receptors on a more systemwide basis. You will therefore have a much greater and overall E related response. With that said you will also wind up with more E floating around to make you cry, or cause other harm associated. While it would seem to me that this drug clearly will have the greatest effect on the HPTA, decide whether or not ALL of the affects are acceptable to you. And take that one. I am guessing that with clomid you have more of a "competition" for estrogen sites, and a more variable dose related blocking response.

BUT: Dont sit here saying that Nolva is a better drug for HPTA restoration due to the fact that it only takes 20mgs to get the same affect of more Clomid! They are apples and oranges with clearly different flavors. Who knows why they work, perhaps one crosses the blood/brain barier and the other doesn't. Perhaps one directly affects the pituitary by means of direct physical action and the other doesn't. Maybe while the NOLVA only blocks E uptake to limited areas, it blocks it more completely than CLOMID, and this complete blockage to only a few areas is more important than a partial blockage thougout. Who knows.

I am assuming, the means by which they stimulate the HPTA is by the deprivation of E's interaction with the body, thus signalling that there is not enough hormone being produced (Master T to convert to E). So now we make more T to give our body the proof thereof that lies within the again received presence of E by the receptors, hence telling the HPTA that there is again now T in the body. Who knows, SERMS could stimulate the HPTA due to the fact that the body now has an overwhelming proportion of E-to-T and is now trying to produce more T to counter, simply for the purpose of making T. NO ONE REALLY KNOWS FOR SURE.......NOW, CHOOSE YOUR POISON. Who gives a shit if it takes 1mg of cyanide or 100mgs of arsenic to effectively harm you. The effect is the same IN RELATION TO THE DRUG. I AM SO FUCKING SICK OF HEARING PEOPLE SAY THAT NOVLA IS THE BETTER OPTION BECAUSE IT ONLY TAKES 20MGS!!!!!!!! Get the point.

FORGET about the fact that pound for pound, NOLVA stimulates the HTPA better. WHO GIVES A SHIT IF ONLY 10mgs of NOLVA equals the action of 50mgs of CLOMID!!!?!?!?!?!? You have to choose which chemical you want to put in your body, and the consequences there of.

PERSONALLY, I feel that if one chooses to use either drug for the purpose of stimulating the HPTA, consider there are two options and diversify your risk. Use one this time, and the other next, etc.......

NOW HERE IS A QUESTION GENERATED FROM THIS BRIEF RANT....: If it is in fact the percieved lack of E2 uptake at receptor sites that stimulates the HPTA, then why does this not hold true to DHT?? It should. If there is no notable increase in HPTA activity by the blocking of DHT uptake then perhaps that theory is not true. Perhaps SERMS are simply stimulating Testosterone production as a means of creating more T to effect proper balance again. Or better yet, perhaps SERMS are having a direct affect of the hypothalmus, or pituitary, than currently believed. Does Finasteride stimulate the HPTA. If not, perhaps this is the proof that SERMS are acting in some other manner than currently thought. After all, Adex is not a good stimulator at all. Why would it not. Pehaps the DEGREE to which hormones are blocked is the key factor alone, and the number of areas, or overall area affected is not important. But only certain ones (breast, etc), the ones containing the most receptors, hold the power, and the importance is not in overall receptor interaction throughout the body, but the completeness of the action on key body parts......!

Food for thought. Eat up....

i read this article and i was wondering what everyone thinks about it. it would be interesting to get Dr. Scally's feedback on this.

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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 [sex hormone binding globulin ] 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 - leutenizing hormone - 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 - leutenizing hormone - response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.



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 - (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 - hypothalamic-pituitary-testicular axis - , 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 - leutenizing hormone - 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 sex hormone binding globulin 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 gynecomastia 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


01-Oct-2003, 12:36 AM #20
PotatoHead Not trying to take over thi

 

[Conciliator]

And here BBC3 goes talking out of his ass again.

Clomid "more accurately resembles the natural Estrogen structure?" Clomid "will bind to E receptors on a more systemwide basis" while "NOLVA only blocks E uptake to limited areas?" "SERMS are acting in some other manner than currently thought?"

Where the hell do you come up with all of this baseless nonsense? You do it over, and over, and over, in threads on all sorts of topics you know little about. Your unsupported ideas and hunches are not "facts". Most are clearly incorrect, so don't delude yourself.

Ridiculous.

 

[BBC3]

AHhhh.... He bites. I figured the "fact" would be irresistable.........

And here BBC3 goes talking out of his ass again.

Clomid "more accurately resembles the natural Estrogen structure?" Clomid "will bind to E receptors on a more systemwide basis" while "NOLVA only blocks E uptake to limited areas?" "SERMS are acting in some other manner than currently thought?"

Where the hell do you come up with all of this baseless nonsense? You do it over, and over, and over, in threads on all sorts of topics you know little about. Your unsupported ideas and hunches are not "facts". Most are clearly incorrect, so don't delude yourself.

Ridiculous.

 

[BBC3]

Conciliator = The Nolvanator = True proponent of Nolva. Did not mean to libel your precious commodity. I'm waiting. . . . . . . . . .

 

[BBC3]

Come on Conciboy. IS that the best you can do??? A simply slash on my track record. Personally I feel you rebuttal is bad, so I will do the same for you.

I know you are still upset because you became so rattled in one of out last engagements that you nearly pissed yourself trying to explain that you were just a tiny little man trying to make it in a big world, but come on. I played your SunTzu with you this time, and you fucked my from behind like the little coward you are.

You are well aware that my posts are based on emperical evidence and simple observation. They also ALWAYS serve the point to promote education and debate, never allowing the possibility of harm to othes. They usually also end with some pretty insightful questions resulting. IF THE BEST YOU CAN DO IS PROVIDE DISAPPROVAL OF MY THOUGHTS, THEN SHUT UP. You constantly provide data to prove what is already known. So why dont you prove that what I said is incorrect beyond a doubt?? Because you can't. It we went on your premise to the "T", so to speak, there would be no discussion regarding the use of SERMs as a means to stimulate HPTA, as they were not intended for such, period. It is not my intention to defend my statements to a wall, that a little sissy is hiding behind. I would merely like to point out that the world needs servants and slaves too. You are clearly on of them. Did you ever hear the teacher tell you that if you relied solely on your calculator, you would not know how to build one if they were all gone tomorrow?? You clearly missed that class. Its easy to go around quoting the work of others, isn't it.?? I am sure you take the safe road in all your walks as well. I am wondering, why is it that you never ask WHY?? You have a poor habit of always accepting the gospel for what it is. I am not even sure why you are accepted around here at this point. I AM CERTAIN, that back in the day, you would have been huddled around the fire burning witches with the ugliest nd most chickenshit souls alive.!! This society is the furthest thing from a group who walks the line.....

The reason you dont ask why, is because you dont have the intelligence to do so. You hide behind that weakness by preaching your bible full of dissertations, and accepted writings. I am betting that you would not even have the balls to preach the other's data on any level other than that of an anonymous forum! There is not a single creative thought in your simple little head. You will make a good servant to society. Perhaps an engineer, a social worker, or even a trash man; however you would still do a great degree of dishonor to those professions in many ways. Simply put, you are probably one of the most ignorant people here. You jump off bridges in a single file line. You never consider any possibiity other than what you are told to believe. You take certain data as gospel, without even considering to possibility of error or motive. You are simply too afraid to consider elsewise. What does a person such as yourself accomplish? You make a great human Wiki !!! There is no power in preaching the workings of another man, only false security. So dont try to act like you are the gospel on a subject. You are nothing more than an SS want-to-be. Sieg Heil to you!! I guess you win again.......

 

[big_tom]

Oh boy! I'm staying out of this debate but I liked your post BBC. Thanks for that, good analysis indeed!

 

[BBC3]

Thank you for the positive review of my slightly off center review.

Please remember not to let Conciliator worry you. I believe that he actually is Arnold as he exhibits the same IQ, thought process, etc... Who else could he be??? I mean, where did he get that pic for the avatar? If he is not, he must sit around and masturbate to a shrine full of it....

After all, Lou may be deaf, but I am thinking his brain may function on about 10 times the level... Only a total idiot would gobble Dbol to that degree...

Hey Conciboy, stick to your guvonatorial tutoring jerky, you dont want to blow a fuse or anything.

Oh boy! I'm staying out of this debate but I liked your post BBC. Thanks for that, good analysis indeed!

 

[Conciliator]

I guess if you want it that bad, BBC3, we can start going through your nonsense one item at a time, like I've done numerous times before. Are you sure you want to go there? You seem to forget that I always post references and back up what I say and in the end, you're always left standing like an asshat.

Lets start with this nugget of bullshit. You said "CLOMID is a chemical that more accurately resembles the natural Estrogen structure." And then lets take half a second to actually examine the chemical structures:
Embedded Image Unvailable

What do you know. Clomid and nolva are extremely similar in structure. Both are nonsteroidal, first generation, triphenylethylene SERMs. In contrast, estrogen (E2) is a steroid with a completely different structure. Tell us BBC3, where the hell do you come up with the bullshit that clomid "more accurately resembles the natural Estrogen structure" compared to nolva? Seriously. Look at the damn chemical structures. If anything, nolva is more similar, with a methyl side chain as opposed to clomid's chloride. I don't see how anyone can take you seriously when almost everything you say is based nowhere in reality but in the fantasy of your head. Stop making shit up and posting whatever pops into that broken head of yours.

Do you want more? We can go on...

 

[BBC3]

OK TittieLICK. I meant Clomid has a chemical structure that more accurately resembles the ACTION of the natural estrogen structure. I left out ONE WORD. Get a hold of yourself. The statement was intended to depict simply that, generally speaking, Clomid acts more like E2, than Nolva. You should know this already! CLIT....

ARTICLE -

Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro
E. Y. Adashi, A. J. Hsueh, T. H. Bambino and S. S. Yen


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.

Simply put. Clomid has BOTH estrogenic AND anti-estrogenic effects, whereas Nolva has, more primarily anti-estrogenic effects. The tendency of Clomid to actually trigger the intended response of the E2 molecule is more likely with the use of Clomid, rather than Nolva, which I am also guessing is why it is not also used to treat breast cancer.

THERE STILL REMAINS THE QUESTION AS TO WHAT THE E2 RESPONSE IS ACTUALLY TRIGGERED BY. No one knows for sure. Either SERM will result in an increase in curculating estrogen by means of (a) blocking the uptake, and (b) the increase in HPTA activity. I would also wager that the higher estrogenic activity of Clomid as compared to Nolva may be due to the fact that while it competes for E2 receptors, just like Nolva does, its binding effect while more generalized, may not be as difinitive.

ANOTHER THING: I dont think anyone has ever proven that the HPTA response to Clomid, for example, is not just a result of a DIRECT BLOCKADE of the Hypothalmus or Pituitary, and simply triggered by the inability of these glands to directly sense the presence, or lack thereof, of E2 in the blood.

Sidenote:
Heres one for your Nolva lovin pipe......
The triphenylethylene drug tamoxifen is a strong liver carcinogen in the rat
The triphenylethylene drug tamoxifen is a strong liver carcinogen in the rat -- Gary et al. 14 (2): 315 -- Carcinogenesis

I guess if you want it that bad, BBC3, we can start going through your nonsense one item at a time, like I've done numerous times before. Are you sure you want to go there? You seem to forget that I always post references and back up what I say and in the end, you're always left standing like an asshat.

Lets start with this nugget of bullshit. You said "CLOMID is a chemical that more accurately resembles the natural Estrogen structure." And then lets take half a second to actually examine the chemical structures:
Embedded Image Unvailable

What do you know. Clomid and nolva are extremely similar in structure. Both are nonsteroidal, first generation, triphenylethylene SERMs. In contrast, estrogen (E2) is a steroid with a completely different structure. Tell us BBC3, where the hell do you come up with the bullshit that clomid "more accurately resembles the natural Estrogen structure" compared to nolva? Seriously. Look at the damn chemical structures. If anything, nolva is more similar, with a methyl side chain as opposed to clomid's chloride. I don't see how anyone can take you seriously when almost everything you say is based nowhere in reality but in the fantasy of your head. Stop making shit up and posting whatever pops into that broken head of yours.

Do you want more? We can go on...

 

[Bill Roberts]

In fact both of you make good points (my saying so is not necessarily an endorsement of each and every statement) and I believe the discrepancy between Llewellyn's conclusions and the article he cites versus other conclusions and the article BBC3 sites are mostly (but not entirely) dosage related.

Very simply, the 150 mg/day dosing level was not optimal. If anyone in bb'ing recommends using that much as an ongoing dose, I hadn't heard of it. I have always recommended 50 mg/day myself for those for whom Clomid is a suitable drug.

It may well be the case that the estrogenic effect at the pituitary is overdone at the 150 mg/day level.

In doing PCT as I believe it should be done, estrogen levels should be low-normal in the first place, and it's entirely possible that the effect described in the second study is a useful one.

Furthermore there is preferably (for the sake of recovery) not heavy estrogenic suppression during the cycle.

One doesn't want to in fact overly reduce (to below normal) estrogenic activity at the pituitary, and in some instances Nolvadex may be yielding that effect if estrogen is fairly low or is moderate in level already.

In practice both can work well. Hypothetically it might be the case that if high estrogen levels are present during the PCT and perhaps particularly if there was heavy estrogenic suppression during the cycle Nolvadex might be the superior choice via reducing estrogenic effect at the pituitary to a more normal level. While in contrast if the reverse were the case Clomid may be the superior choice.

However I haven't done comparisons that demonstrate that, or refute it. It is the case the Clomid has worked well many times when there was estrogenic suppression during the cycle, although not having high estrogen during the PCT, so the above shouldn't be taken to mean Clomid can't work well in that situation.

If a person prefers one versus the other for whatever reason, there is I think no compelling reason to switch. It is possible though that there may be optimization according to the circumstances with one being a little better under some circumstances and the other under differing circumstances.

 

[BBC3]

MMM, hmmmmmmm.... What to do.......... Now he has a great opportunity to really roll around in the mud. Perhaps even make a name for himself !! But does he stay his course??? So much conjecture, can he tolerate it? How to come in for round 2 without alienating the big gun. Does he even care? The main problem that arrises from resting on the work of others, is know its limitations, isn't it now.?? I would certainly hate to see you extend yourself down a road that has no end, when your database does. The last thing he wants is to risk a loss and allow BBC3 to slide into a coveted seat next to The Master.!! The taunt was well issued. Clearly, he must have some opinions..... ! ?? I suspect so.. Just how to go about it is the question. We all know he is principled and greedily stubborn with the stock he holds so dearly. So how to play it. Come on now. His name, is ConciBoy. Let him go. Dont try it. Dont even think it. Just stick to me. Give yourself half a chance! AHHH, but the opportunity is too great. With that said, continue on loading your guns. Make it a good one.

 

[bigpapabuff]

there is always a debate about which chems to use, i started using both and they worked well, now I always use clomid and nolva together. For me that's all i know, but it has always worked.

 

[Michael Scally MD]

i read this article and i was wondering what everyone thinks about it. it would be interesting to get Dr. Scally's feedback on this.

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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 - leutenizing hormone - 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 [sex hormone binding globulin ] 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 - leutenizing hormone - 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 - leutenizing hormone - response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.

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 - (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 - hypothalamic-pituitary-testicular axis - , 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 - leutenizing hormone - 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 sex hormone binding globulin 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 gynecomastia and elevation of endogenous testosterone, however the above research provides enough evidence for me to choose Nolvadex every time.

In the beginning of my treatment of AIH, I had to research the literature high and how to determine what might restore the HPTA. In marked contrast to the armchair opinions I read, I had the solemn and real obligation to cure the patient, if possible. The complete lack or absence of any studies on HPTA restoration secondary to AAS was eye opening. For most physicians, even to this day, the standard of care is to ?do nothing? or ?watchful waiting.? It was my decision for a number of reasons, primarily the patient?s health & welfare, to develop a successful protocol to treat AIH. [Note: It was my stance to care for illicit AAS users, which led to my revocation.]

The administration of SERMs is a common treatment in attempts to restore the HPTA because they increase LH secretion from the pituitary that leads to increased local testosterone production (1). Most notably, Guay has used clomiphene citrate as therapy for erection dysfunction and secondary hypogonadism.

I initially used clomiphene for AIH with fair success. As the post above states, I suspected that the problem lie in the fact that clomiphene is a mixed agonist/antagonist. Clomiphene citrate is a selective estrogen receptor modulator (SERM) approved in 1967 for the treatment of female infertility. Clomiphene citrate tablets USP is a mixture of two geometric isomers [cis (zuclomiphene ? 38%) and trans (enclomiphene ? 62%)], which have opposite effects upon the estradiol receptor (2). Enclomiphene is an estradiol antagonist, while zuclomiphene is an estradiol agonist. Prior to this, I did try to use tamoxifen alone with fair success.

The addition of tamoxifen to clomiphene might be expected to increase the overall antagonism of the estradiol receptor. It is for this reason that I added the tamoxifen ? to counter the agonist effect of clomiphene. I reported on my experience within major medical conferences and in the peer reviewed literature. [Note: A quick read of the reports demonstrate the change in the protocol.]

I readily admit that well-controlled trials still need to be done. [For many, they are aware regarding my current endeavors for this goal. I am drawing closer to this achievement. As far as I know, I am the only physician working to bring proper medical care to AAS users, both prescription and nonprescription.] For all of the talk about which is better, the evidence is not there. The bottom line is the AAS user needs to check HPTA status after stopping!


(1) Gooren LJ, Van der Veen EA, van Kessel H, Harmsen-Louman W. Estrogens in the feedback regulation of gonadotropin secretion in men: effects of administration of estrogen to agonadal subjects and the antiestrogen tamoxifen and the aromatase inhibitor d1-testolactone to eugonadal subjects. Andrologia 1984;16:568 ?77. Guay AT, Jacobson J, Perez JB, Hodge MB, Velasquez E. Clomiphene increases free testosterone levels in men with both secondary hypogonadism and erectile dysfunction: who does and does not benefit? Int J Impot Res 2003;15:156-65.

(2) Turner RT, Evans GL, Sluka JP, et al. Differential responses of estrogen target tissues in rats including bone to clomiphene, enclomiphene, and zuclomiphene. Endocrinology 1998;139(9):3712-20.

(3) Scally MC, Kovacs JA, Gathe JC, Hodge AL Uncontrolled Case Study of Medical Treatment for Elimination of Hypogonadism After Androgen Cessation in an HIV+ Male with Secondary Polycythemia treated 2 years Continuously with Testosterone. Endocrine Practice 2003;9(Suppl 1). Vergel N, Hodge AL, Scally MC. HPGA Normalization Protocol After Androgen Treatment. 4th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV. Antiviral Therapy 2002;7:L53. Scally MC, Street C, Hodge A. Androgen Induced Hypogonadotropic Hypogonadism: Treatment Protocol Involving Combined Drug Therapy. The Endocrine Society 2001 Annual Meeting (Denver, CO) Abstract. Street C, Scally MC. Pharmaceutical Intervention of Anabolic Steroid Induced Hypogonadism - Our Success at Restoration of the HPG Axis. Medicine and Science in Sports and Exercise 2000;32(5)Suppl.