Why you need to think twice about using clomid


New member
It seems like there is a lot of confusion about using clomid and/or Nolvadex post cycle. I came across this article and though you guys might like it. It was written by William Llewellyn.

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 other 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. 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, researches looked at the effects of Nolvadex and Clomid on the endocrine profiles of normal men, as well as those suffering from low sperm counts. For out 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.

But something more interesting is happening. Researchers were also conducting GnRH stimulation test before and after various points of treatment with Nolvadex and Clomid, and the two drugs had markedly different results. These test 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 test 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 significantly higher than pre-treated 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 that 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 above discrepancies are likely explained by differences in the estrogenic nature of the two compounds. The researchers's clearly support this theory when commenting in in their paper. "The difference in response might be attributable to the weak intrinsic estrogenic effect of Clomid, which in this study manifested inself 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 in 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 cultrued pituidary 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.

To summarize the above research succinctly, Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA 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 levelof 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 that 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.


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 mormospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45
Seen that article a kajillion times, this study seems to point to clomid as the better of the two

Am J Physiol 1981 Feb;240(2):E125-30 Related Articles, Links

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.

hhajdo said:
Actually, that study shows that Clomid is estrogenic in pituitary which doesn't have a negative effect on LH response to LHRH in vitro, but it does in vivo.
After several weeks of clomid use the LH response to LHRH was decreased (proving once again that Clomid is estrogenic in pituitary) while it was enhanced with Nolvadex.
That's important because estrogen has both a pituitary and a hypothalamic site of action.


"The mechanism proposed for this divergence between spontaneous pulse height and acute pituitary responsiveness to exogenous GnRH was that clomiphene was having tissue-specific mixed agonist/antagonist effects. The authors concluded that clomiphene was acting as an estrogen antagonist at the hypothalamus, resulting in an increase in endogenous GnRH secretion, but as an estrogen agonist at the pituitary, causing decreased responsiveness to exogenous GnRH"

..."This concept that E2 is a more potent suppressor of LH secretion than is T is supported by studies in both prepubertal boys (42, 43) and adult males (1, 2, 3, 7, 8, 41, 44), indicating that, on a molar basis, the steroid dose required to suppress gonadotropin secretion is approximately 200-fold less for E2 than for T..."

..."From these clinical investigative studies on the impact of aromatase inhibition in NL and GnRH-deficient men, employing frequent blood sampling combined with administration of a GnRH antagonist, we conclude that, in the human male, estrogen has dual sites of negative feedback, acting at the hypothalamus to decrease GnRH pulse frequency and at the pituitary to decrease pituitary responsiveness to GnRH..."
Ive about had it with that fucking article. I dont have anything nice to say about that article so I wont. Ill keep it to 2 points.

1) I dont give a shit about the neg-feed loop. Clomid is better because of other means, direct pituarty stimulation.

2) Dont believe me, think about this. Why are women seeking to get pregnant use Clomid and not Nolva?

I hate that fucking article!
Billy_Bathgate said:
Ive about had it with that fucking article. I dont have anything nice to say about that article so I wont. Ill keep it to 2 points.

1) I dont give a shit about the neg-feed loop. Clomid is better because of other means, direct pituarty stimulation.

2) Dont believe me, think about this. Why are women seeking to get pregnant use Clomid and not Nolva?

I hate that fucking article!

And I've had it w/ people posting an in vitro, rat pituitary cell-culture study to show the superiority of Clomid!
Ulter, hows it going? :)

Buff..me too! Im not a fan of studies really. Dime a dozen. Thats the first I seen on the Clomid though in vitro. Do you disagree about clomid or something or just busting my balls?

VB...I use both actually. But I dont use the nolva for htpa restoration, just as an anti-e. If it helps out though...well thats cool with me.
Actually, it seems that Clomid is estrogenic in pituitary which may leed to decreased LH response to LHRH with prolonged use.
As for the use of tamox in treatment of women infertility, it can be used with similar results.
There are some issues with its toxicity, although most info comes from rat studies.
An increased incidence of endometrial cancer among women taking tamoxifen was also noticed, so that's one reason for woman to avoid using it to treat infertility.
Slightly inferior results in treatment of infertility has little to do with its effect on Hypothalamus & pituitary but more to do with tamoxifen's effect on endometrium.

Antiestrogens as treatment of female and male infertilities.

Buvat J, Buvat-Herbaut M, Marcolin G, Ardaens-Boulier K.

...We have compared the results of clomiphene citrate (CC) to those of tamoxifen (TAM) in a randomized study including 66 infertile women presenting eugonadal anovulation (n = 26) or LPD (n = 40). Both drugs obtained the same pregnancy rate of 80% at 9 months in the anovulatory patients. Conversely, CC was superior to TAM in the LPD cases (pregnancy rates at 6 months of respectively 40 and 11%). The abortion rates were of 11% on CC versus 36% on TAM. Both drugs significantly increased the luteal phase length and plasma progesterone level to the same extent. The results of endometrial biopsies suggest that the difference in their effects on female fertility could result from a detrimental effect of TAM on endometrium. The rates of the side effects proved to be almost identical on both drugs. Thus the use of TAM is not justified as a first-step treatment in ovulation disturbances...
all this info is confusing, so are the ppls opinions on this.it would be great if i could use one or the other.

Billy_Bathgate said:
Ulter, hows it going? :)

Buff..me too! Im not a fan of studies really. Dime a dozen. Thats the first I seen on the Clomid though in vitro. Do you disagree about clomid or something or just busting my balls?

LOL. Naw, man. It wasn't even you who posted it. It's just that ppl throw around studies a lot; some more meaningful than others.
Actually, billy, for me the jury's still out on post cycle recovery. I just came off and seemed to do fine w/out Clomid, Nolva only, and herbs. But again, that's a series of one!
I'm off to Bermuda,
Later guys.
RoadHouse said:
i like a combo of HCG/Nolva/Clomid

As do I.

It is almost seeming pointless to me to even talk about this anymore. For every study, there is another showing something contradicting.


Personally, Ive done both and felt Clomid was much better than Nolva alone. That is enough for me to prefer it. But..I run both anyways.
I keep seeing that William L. article all over the Boards. The problem with the study on which he bases his conclusions is that it was so flawed in its design as to be laughable. Specifically, they used 3 times the normal dose of Clomid, compared to a common dose of Nolvadex. Perhaps the researchers from Belgium should have spent a little time on the Anabolic Androgenic Steroids (AAS) Message Boards before they wasted all that time and money!

I'm moving my Hormone Replacement Therapy (HRT) patients who use SERM's long term away from Clomid and into Nolvadex. There is some evidence (perhaps someone here has something to add) long-term use of Clomid may damage the eyes. Just in case, we're being prudent.
I like this article:

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.

Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case Nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.

Stacking and Use:

If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with Proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above.

Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued.

For best results, it is best stacked with Human Chorionic Gonadotropin (HCG) (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. Human Chorionic Gonadotropin (HCG) use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that Human Chorionic Gonadotropin (HCG) itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that Human Chorionic Gonadotropin (HCG) possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks.
I've used nolvadex alone post cycle. Compared to clomid? 6 of one and 1/2 dozen of the other. Toss it up. I plan to combine them and use Human Chorionic Gonadotropin (HCG) during cessation of androgens next cycle. Just to cover all bases so to speak. But either one will get the job done.
I have a couple observations t offer on the info Juice Authority posted. First, Clomid has never been marketed as an ancillary medication to Anabolic Androgenic Steroids (AAS) use, so it was not some sort of scam resulting in its promotion for post-cycle recovery. However, I do not know how it ever became popular over Nolvadex, causing Anabolic Androgenic Steroids (AAS) users to D/C Nolvadex at the end of a cycle just to start Clomid, when it would have been better to simply continue the Nolvadex right on through. Next, there is absolutely no factual basis for saying the body boosts estrogen levels at the end of the cycle to "keep steroid levels up". The body cannot produce estrogen without making testosterone first. Next, neither Clomid nor Clomid will "reduce the post-cycle estrogen". Estrogen levels can only drop by virtue of decreasing conversion from lower concentrations of testosterone and its own half-life. Saying that one medication is "stronger" than another because a lower dose is needed demonstrates a fundamental lack of understanding of pharmacokinetics. I'm more interested in the fact we are talking about 2-4 Nolvadex, compared to 2-3 Clomid, by your example. As they are basically the same price, I'd call that one a draw (or tipped toward Clomid). Now, it is incorrect to state that the SERM's are "mild estrogens", when in fact they act as estrogen antagonists at some tissues and estrogen agonists at others. That is what Selective Estrogen Receptor Modulation means. I'd have to say the jury is still out as to whether using an anti-estrogen actually reduces REAL muscle gains. But that is just my opinion. Nothing "deactivates rebound estrogen". Estrogen is broken down into its metabolites according to its half-life. Clomid absolutely does not "have a slight negative effect" on producing LH--it's efficacy is well-proven by multiple studies (again, more of the baloney from that study from Belgium). As for Human Chorionic Gonadotropin (HCG) use, none of my patients ever use more than 1000iu at a time. And 3000iu's has been shown to cause a 10-fold increase in aromatase activity--hardly what we are looking for. Some think aromatase is actually toxic to Leydig cells--we would then be causing permanent primary hypogonadism to go along with the temporary secondary (hypogonadotrophic) hypogonadism we have during and immediately after the cycle. Finally, it is absolutely untrue to say Human Chorionic Gonadotropin (HCG) is "more important" in post-cycle recovery than a SERM. Human Chorionic Gonadotropin (HCG) is ONLY for restoring testicular size (which somehow makes them come back on line sooner), and not restoration of the HPTA directly. It should not be used much after the cycle is over, as it is the falling serum androgen levels that alllow the SERM to take hold and induce LH production.

So, basically, this entire article is rubbish. It, like the William L. article, needs to be left behind. We just know better now.
"It, like the William L. article, needs to be left behind."

This is very good to know about you, there is at least one area where you and I are together. I only wish you would have been on the boards back when I was arguing this with Llewellyn a years ago. He is stuck in the 80's and as you said should be left behind.