I've read 2 different articles on this site that say both are better at stimulating natural test after a cycle. I've heard pro's and cons on both. If I was to run a 6 week cycle of Epistane and 1-T which would be better for pct. I know nolva is used to combat gyno and there are stronger ones but I've seen to use it for pct too. But u just read that it doesn't help recovery and clomid does. This is a site to learn so how can u learn when u read two different things. Once and for all which is better
Clomid or nolva who really knows
- Thread starter maaan316
- Start date
g1234
Shut up and squat !
This is the never ending debate, but if you ask for opinions, I suggest nolvadex, read this profile from bigcat :
While practically similar compounds in structure, few people ever really consider Clomid and Nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while clomid is generally considered a fertility aid. In bodybuilding circles, from day one, clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.
But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because Nolva is clearly a more powerful anti-estrogen, and the people selling clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.
Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.
This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of Nolva or 100 mg/day of clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.
So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as clomid may actually have a slight negative influence. The reason being that Tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas clomid seems to decrease the responsiveness a bit1.
Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.
Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.
While practically similar compounds in structure, few people ever really consider Clomid and Nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while clomid is generally considered a fertility aid. In bodybuilding circles, from day one, clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.
But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because Nolva is clearly a more powerful anti-estrogen, and the people selling clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.
Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.
This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of Nolva or 100 mg/day of clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.
So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as clomid may actually have a slight negative influence. The reason being that Tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas clomid seems to decrease the responsiveness a bit1.
Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.
Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.
captain bj
New member
good read!
sorry, but this article clearly shows that big cat does not at all understand the mechanisms by which tamoxifen and clomiphene work. It has nothing to do with potency and everything to due with ER subtype affinity and action, as well as tissue affinity.
tamoxifen does NOT stimulate LH release. Its action, an ESTROGENIC ACTION BTW, on the HPG axis is to prime GnRh, if you are suppressed and not releasing significant LH, this is pretty much worthless. Clomiphene directly stimulates LH release, an ER ANTAGONIST action in the hypothalamus. Also contrary to popular belief, tamoxifen actually suppresses LH via estrogenic action-- AGAIN.
this is what happens when a northerner reads and fails to actually check the research by bill lewellyn's theories. Though believe that even bill and perhaps andy have even stepped away from the nolva only PCT.
J Endocrinol Invest. 2006 Jun;29(6):485-96. Links
Mechanism delineating differential effect of an antiestrogen, tamoxifen, on the serum LH and FSH in adult male rats.Balasinor N, Parte P, Gill-Sharma MK, Kini J, Juneja HS.
Division of Neuroendocrinology, National Institute for Research in Reproductive Health, Parel, Mumbai 400012, India. nafisabala@hotmail.com
Tamoxifen, a synthetic non-steroidal antiestrogen with residual estrogenic activity, administered to adult male rats reduces their fertility. A decrease in the circulating LH and testosterone levels with a transient rise or no change in circulating FSH levels was observed. The present study was carried out to delineate the mechanism causing the differential effect of tamoxifen on circulating gonadotropins by correlating it to changes in the hypothalamic LHRH, pituitary gonadotropins and testicular inhibin/activin. Hypothalamus, pituitary-hypothalamus complex (PHC) and intact pituitary (PI) from control and tamoxifen-treated male rats were superfused in vitro, and pulsatile release of LHRH by hypothalamus and that of LH and FSH by the PHC and PI were studied. Concomitantly, testicular immunoexpression of alpha and betaB subunits of inhibin/activin were studied by immunohistochemistry and enzyme-linked immunosorbent assays (ELISA). At 0.4 mg/kg/day dose of tamoxifen a decrease in mean hypothalamic LHRH and LH pulse frequency from PHC construct was observed. FSH pulse frequency was not affected under the same experimental conditions. At the same dose of tamoxifen, testicular expression of both alpha and betaB subunits of inhibin/activin was upregulated. The study demonstrated that reduced circulating LH levels were due to a decrease in hypothalamic LHRH concentration and in LH pulsatility following tamoxifen treatment. The lack of effect on circulating FSH under the same experimental conditions was likely due to its modulation by inhibin and activin.
Tamoxifen-induced light and electron microscopic changes in the rat testicular morphology and serum hormonal profile of reproductive hormones.Gopalkrishnan K, Gill-Sharma MK, Balasinor N, Padwal V, D'Souza S, Parte P, Jayaraman S, Juneja HS.
Institute for Research in Reproduction, Bombay, India.
The effects of oral administration of tamoxifen at doses of 40 and 200 micrograms/kg/day on testicular histology, testicular ultrastructure and serum hormonal profile were studied. The drug was administered to adult male rats over a period of 90 days and the effect was assessed at 10-day intervals. The morphometry, microscopic structures of the testis, including ultrastructure and daily sperm production rate, were evaluated. The hormone profiles of luteinizing hormone (LH), follice-stimulating hormone (FSH), testosterone, and estradiol were studied. The testes from treated animals showed disorganization of tubular elements with increased intercellular space. At day 50, the changes were extensive including presence of phagosomes. Morphometric studies showed a reduction in the spermatid and spermatozoan population (69.3%) with no changes in tubular diameter. The mean Leydig cell area was significantly lowered at day 50, at both doses. The daily sperm production rate was reduced as compared with controls. An array of degenerative changes were revealed by ultrastructural studies. The changes were extensive at day 50 at both doses. The characteristic features were lost in most of the cells with phagolysosomes becoming abundant. The cytoplasm of the cells was dense with poorly defined cytoplasmic organelles. Circulating LH levels were not modified at the 40 micrograms/kg/day dose but at 200 micrograms/kg/day, LH levels were significantly decreased. Initial transitory rise in FSH was seen with both doses. Both doses of tamoxifen decreased testosterone levels. Changes in the circulating estradiol levels were inconsistent, and no apparent relationship between dose and days of treatment was observed. Thus, this study supports our thesis of tamoxifen as a potential male contraceptive agent.
nolva after 1-t and perhaps even epistane , which is not and does not have the same activity as the studied epitiostanol, may be involved with the PgR and increases gyncomastia. Clomid and perhaps low dose AIFM or exemestane, supress E to much and you lose priming effect
tamoxifen does NOT stimulate LH release. Its action, an ESTROGENIC ACTION BTW, on the HPG axis is to prime GnRh, if you are suppressed and not releasing significant LH, this is pretty much worthless. Clomiphene directly stimulates LH release, an ER ANTAGONIST action in the hypothalamus. Also contrary to popular belief, tamoxifen actually suppresses LH via estrogenic action-- AGAIN.
this is what happens when a northerner reads and fails to actually check the research by bill lewellyn's theories. Though believe that even bill and perhaps andy have even stepped away from the nolva only PCT.
J Endocrinol Invest. 2006 Jun;29(6):485-96. Links
Mechanism delineating differential effect of an antiestrogen, tamoxifen, on the serum LH and FSH in adult male rats.Balasinor N, Parte P, Gill-Sharma MK, Kini J, Juneja HS.
Division of Neuroendocrinology, National Institute for Research in Reproductive Health, Parel, Mumbai 400012, India. nafisabala@hotmail.com
Tamoxifen, a synthetic non-steroidal antiestrogen with residual estrogenic activity, administered to adult male rats reduces their fertility. A decrease in the circulating LH and testosterone levels with a transient rise or no change in circulating FSH levels was observed. The present study was carried out to delineate the mechanism causing the differential effect of tamoxifen on circulating gonadotropins by correlating it to changes in the hypothalamic LHRH, pituitary gonadotropins and testicular inhibin/activin. Hypothalamus, pituitary-hypothalamus complex (PHC) and intact pituitary (PI) from control and tamoxifen-treated male rats were superfused in vitro, and pulsatile release of LHRH by hypothalamus and that of LH and FSH by the PHC and PI were studied. Concomitantly, testicular immunoexpression of alpha and betaB subunits of inhibin/activin were studied by immunohistochemistry and enzyme-linked immunosorbent assays (ELISA). At 0.4 mg/kg/day dose of tamoxifen a decrease in mean hypothalamic LHRH and LH pulse frequency from PHC construct was observed. FSH pulse frequency was not affected under the same experimental conditions. At the same dose of tamoxifen, testicular expression of both alpha and betaB subunits of inhibin/activin was upregulated. The study demonstrated that reduced circulating LH levels were due to a decrease in hypothalamic LHRH concentration and in LH pulsatility following tamoxifen treatment. The lack of effect on circulating FSH under the same experimental conditions was likely due to its modulation by inhibin and activin.
Tamoxifen-induced light and electron microscopic changes in the rat testicular morphology and serum hormonal profile of reproductive hormones.Gopalkrishnan K, Gill-Sharma MK, Balasinor N, Padwal V, D'Souza S, Parte P, Jayaraman S, Juneja HS.
Institute for Research in Reproduction, Bombay, India.
The effects of oral administration of tamoxifen at doses of 40 and 200 micrograms/kg/day on testicular histology, testicular ultrastructure and serum hormonal profile were studied. The drug was administered to adult male rats over a period of 90 days and the effect was assessed at 10-day intervals. The morphometry, microscopic structures of the testis, including ultrastructure and daily sperm production rate, were evaluated. The hormone profiles of luteinizing hormone (LH), follice-stimulating hormone (FSH), testosterone, and estradiol were studied. The testes from treated animals showed disorganization of tubular elements with increased intercellular space. At day 50, the changes were extensive including presence of phagosomes. Morphometric studies showed a reduction in the spermatid and spermatozoan population (69.3%) with no changes in tubular diameter. The mean Leydig cell area was significantly lowered at day 50, at both doses. The daily sperm production rate was reduced as compared with controls. An array of degenerative changes were revealed by ultrastructural studies. The changes were extensive at day 50 at both doses. The characteristic features were lost in most of the cells with phagolysosomes becoming abundant. The cytoplasm of the cells was dense with poorly defined cytoplasmic organelles. Circulating LH levels were not modified at the 40 micrograms/kg/day dose but at 200 micrograms/kg/day, LH levels were significantly decreased. Initial transitory rise in FSH was seen with both doses. Both doses of tamoxifen decreased testosterone levels. Changes in the circulating estradiol levels were inconsistent, and no apparent relationship between dose and days of treatment was observed. Thus, this study supports our thesis of tamoxifen as a potential male contraceptive agent.
nolva after 1-t and perhaps even epistane , which is not and does not have the same activity as the studied epitiostanol, may be involved with the PgR and increases gyncomastia. Clomid and perhaps low dose AIFM or exemestane, supress E to much and you lose priming effect
g1234
Shut up and squat !
I agree that the first part in bigcat's profile is outdated, this is how I think any SERM helps to restore testosterone production :
Clomiphene citrate or Tamoxifen citrate both bind with the estrogen receptor and causes the hypothalamus to sense a lack of estrogen, resulting in increased secretion of gonadotropins (FSH - follicle stimulating hormone - and lh - leutenizing hormone)
LH acts upon the Leydig cells of the testis and is responsible for the production of testosterone
FSH regulates the production of sperm
never ending debate...
Clomiphene citrate or Tamoxifen citrate both bind with the estrogen receptor and causes the hypothalamus to sense a lack of estrogen, resulting in increased secretion of gonadotropins (FSH - follicle stimulating hormone - and lh - leutenizing hormone)
LH acts upon the Leydig cells of the testis and is responsible for the production of testosterone
FSH regulates the production of sperm
never ending debate...
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well, lets just say that the real world data does not back that statement up. And given macro's contact with a very large number of persons, and theory preferably employed in practice. Most people do not use nolva alone, many do use the tamox + CLOM stack. Here there may be some synergy, though really depends on receptor isoforms and extent of actual binding as to which effect predominates. Certainly Clomid alone is superior to tamox.
people who swear by tamox, are also people that likely experience minimal suppression of LHRH. ie. people that would recover anyways, and people who are likely estrogen insensitive (pituitary/hypothalamically), or least with respect to tamoxifen.
lets just clear this up right now. there is not ONE estrogen receptor. There are two recognized ER's ERalpha and ERbeta, there are isoforms within those two classifications. Ratio's of these two receptors are what most important to how and what a SERM, or an estrogen for that matter will actually do.
note- there are a number of semi-recognized sub-types of each. This will also impact activity, lets say ERbeta(1a) is full agonized by tamoxifen. That does not mean that ERbeta(1b) will have either high affinity, strong binding, or even modulatory action on that recptor (generally because of also binding sites OTHER than the ER's and ER subtypes.
to address your final assertion. They do not at all act the same way, tamoxifen's action on GnRh is as an ER agonist. Clomid's action, stimulating LH release, is an ER blocking activity in the hypothalamus.
TheMilkMan
New member
I have used Nolva only and Nolva/Clomid... My PCT's with Nolva/Clomid were after much heavier cycles and I recovered much more easily/more quickly/better after them...
So from my personal experience, I would DEFINITELY incorporate Clomid whether you plan on using Nolva or not
So from my personal experience, I would DEFINITELY incorporate Clomid whether you plan on using Nolva or not
g1234
Shut up and squat !
Thanks a lot for these details, i read this with great interest.. makes me want to search for more..
g1234
Shut up and squat !
clomid 50mg + nolva 20mg for 3 weeks
StoneColdNTO
Administrator
Bump......you guys should pay close attention to what "macro" posted in here.
Ozzy27
Olympian Bodybuilder
Ya...I think I fall into the category of people who are estrogen insensetive. Could I use one sign as being able to withstand large doses of test (100-1200mg ew) without getting gyno?? Or am I way off??
I find it mind dumbing the debate between these for pct.. if your'e prone to gyno, should you use clomid, then??.. I have a ton of nolva.. and was going to run it pct, should I now go with clomid.. I had some issues lately with my eyesight and that is why I chose to go with nolva.(wonder if it was from clomid in my last pct a few yrs back?).plus i needed on hand in case of gyno anyway.. thought I'd be g2g..what dp ya' think.. man things change in six yrs being away from the gear scene.
