Here is a good read by William Llewellyn, comparing the 2 taken from the mind and muscle web page. Some good points here.
Clomid,
Nolvadex and testosteron
e Stimulation
By William Llewellyn
Editors Note: I am extremely pleased to have Bill Llewellyn contributing an article for us this week. For those who are unaware, he is the author of Anabolics 2000 and Anabolics 2002 and is one of the bodybuilding world's foremost experts on androgens and anabolics. He is also the President of Molecular Nutrition, one of the most innovative companies in this business. Along with Avant Labs and ErgoPharm, Molecular Nutrition is one of the few companies dedicated to putting forth only those products backed by legitimate research, rather than excessive hype and other such B.S. Two products, in particular, that deserve to be more well-known are Viritase, a potent anti-estrogen, and Boldione, a boldenone precursor. To find out more about these, and the rest of their products, I reccomend that you head over to their website -- but only after you have finsished reading big Mf'r and spent all of your money on our products, of course
Now, on to the article:
Introduction
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 testosteron
e-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 testosteron
e 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 testosteron
e production.
Clomid and
Nolvadex
I am not sure how
Clomid and
Nolvadex became so separated in the minds of bodybuilders. They certainly should not be.
Clomid and
Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosteron
e by the testes. Both drugs do this, but for some reason bodybuilders persist in thinking that
Clomid is the only drug good at stimulating testosteron
e. 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 testosteron
e 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 testosteron
e levels to 142% of baseline, which was on par with the effect of 150mg of
Clomid daily for the same duration (the testosteron
e increase was slightly, but not significantly, better for
Clomid). We must remember though that this is the effect of three 50mg tablets of
Clomid. With the price of both a 50mg
Clomid and 20mg
Nolvadex typically very similar, we are already seeing a cost vs. results discrepancy forming that strongly favors the
Nolvadex side.
Pituitary Sensitivity to GnRH
But something more interesting is happening. Researchers were also conducting GnRH stimulation tests before and after various points of treatment with
Nolvadex and
Clomid, and the two drugs had markedly different results. These tests involved infusing patients with 100mcg of GnRH and measuring the output of pituitary LH in response. The focus of this test is to see how sensitive the pituitary is to Gonadotropin Releasing Hormone. The more sensitive the pituitary, the more LH will be released. The tests showed that after ten days of treatment with
Nolvadex, pituitary sensitivity to GnRH increased slightly compared to pre-treated values. This is contrast to 10 days of treatment with 150mg
Clomid, which was shown to consistently DECREASE pituitary sensitivity to GnRH (more LH was released before treatment). As the study with
Nolvadex progresses to 6 weeks, pituitary sensitivity to GnRH was significantly higher than pre-treated or 10-day levels. At this point the same 20mg dosage was also raising testosteron
e and LH levels to an average of 183% and 172% of base values, respectively, which again is measurably higher than what was noted 10 days into therapy. Within 10 days of treatment
Clomid is already exerting an effect that is causing the pituitary to become slightly desensitized to GnRH, while prolonged use of
Nolvadex serves only to increase pituitary sensitivity to this hormone. That is not to say
Clomid won't increase testosteron
e 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 testosteron
e/estradiol-binding globulin [SHBG] levels; this increase was not observed after
Tamoxifen treatment". In reviewing other theories later in the paper, such as interference by increased androgen or estrogen levels, they persist in noting that increases in these hormones were similar with both drug treatments, and state that," …a role of the intrinsic estrogenic activity of
Clomid which is practically absent in
Tamoxifen seems the most probable explanation".
Although these two are related anti-estrogens, they appear to act very differently at different sites of action.
Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to
Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary. To find further support for this we can look at an in-vitro animal study published in the American Journal of Physiology in February 1981 (2). This paper looks at the effects of
Clomid and
Nolvadex on the GnRH stimulated release of LH from cultured rat pituitary cells. In this paper, it was noted that incubating cells with
Clomid had a direct estrogenic effect on cultured pituitary cell sensitivity, exerting a weaker but still significant effect compared to estradiol.
Nolvadex on the other hand did not have any significant effect on LH response. Furthermore it mildly blocked the effects of estrogen when both were incubated in the same culture.
Conclusion
To summarize the above research succinctly,
Nolvadex is the more purely anti-estrogenic of the two drugs, at least where the HPTA (Hypothalamic-Pituitary-Testicular Axis) is concerned. This fact enables
Nolvadex to offer the male bodybuilder certain advantages over
Clomid. This is especially true at times when we are looking to restore a balanced HPTA, and would not want to desensitize the pituitary to GnRH. This could perhaps slow recovery to some extent, as the pituitary would require higher amounts of hypothalamic GnRH in the presence of
Clomid in order to get the same level of LH stimulation.
Nolvadex also seems preferred from long-term use, for those who find anti-estrogens effective enough at raising testosteron
e levels to warrant using as anabolics. Here
Nolvadex would seem to provide a better and more stable increase in testosteron
e levels, and likely will offer a similar or greater effect than
Clomid for considerably less money. The potential rise in SHBG levels with
Clomid, supported by other research (3), is also cause for concern, as this might work to allow for comparably less free active testosteron
e compared to
Nolvadex as well. Ultimately both drugs are effective anti-estrogens for the prevention of gyno and elevation of endogenous testosteron
e, 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 testosteron
e recovery. Most specifically, I will be detailing what a proper post-
cycle ancillary drug program looks like, and explain why anti-estrogens alone are not effective during this window of time.
References:
1. Hormonal effects of an antiestrogen,
Tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7
2. Disparate effect of
Clomiphene and
Tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30
3. The effect of
Clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45
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