T Nation

Nova vs Clomid post

From what I researched, Novadex and Clomid are basically interchangeable. What stands out is though that most people seem to use clomid for post cycle recovery…I hardly hear people saying they use, or recommend novadex post cycle. Clomid is always mentioned. Their drug profiles are basically the same ( but Nova is said to be a little stronger Anti-E)

Novadex is very easy for me to get at a great price, but clomid isn’t. I was just gonna run Nova throughout my cycle and a month after completion.

You guys see a problem with this? Am I missing something about clomid?

Yes my friend you are missing something about clomid big time. You see clomid is prescribed to woman as a fertility drug because it causes the hpta to increase secreation of LH which bolsters ovulation. This can result in quintuplets! In men it can do the same thing for endogenous test production. whereas Nolvadex is JUST an estrogen site antagonist. P-22

prisoner. clomid and nolvadex are both a mixed estrogen agonist/antagonist. let me give you an example. in breast tissue both are an antagonist as they occupy the estrogen receptor site thus preventing gyno. but, they are agonist of good cholestorol(sp?)causing an increase while on. clomid doesnt stimulate the hpta allowing for LH secretion. rather it again occupies the estrogen receptor at the hypothalimus thus preventing suppression and allowing normal LH recovery.

In anabolics 2004 it clearly states that Nova stimulates fsh production and is in fact stronger than clomid.

i just asked because no one usually posts that they use nova post. anabolics 2004 is a pretty creditable source to argue with.

i havent read 2004. but i can say that there was quite a few mistakes in the previous issue.

clomid is the preferred choice for recovery.it seems to stimulate endogenous levels better.although nolva may be better for gyno.clomid is what most all vets use.methoxy 7 is good in combination with clomid along with androgel and a beta antagonist seems to offer ecxcellent recovery results.

This topic is near and dear to my heart. Nolv can be used for recovery and is under rated for this purpose. Clomid is good to but Nolva at 40-80mg/day for recovery is good. I found this out cause I cannot take clomid. I must have a lot of estrogen receptors in my brain because clom acts and an agonist in brain tissue and makes me an emotional wreck. Some guys get it, some don’t. So don’t be afraid to use Clomid. Cy and many others have written about this. I am a huge nolv fan and hate Clomid because of that side effect. I think clomid may be stronger mg/mg at boosting LH but Nolv is a better anti e and is better with FSH I believe

drago1: yes you are correct in describing the precise mechanism of action in how clomid as I said “causes an increase in LH…” So I will agree with you as long as you retract your stimulation statement which I didn’t say.

As far as Nolvadex goes it stimulates estrogen receptors in some tissues and blocks them in other tissues. This has a duel benefit of targeting the breast yet sparing the bones from osteoporosis, and keeping the blood lipid levels healthy. It also can cause endometrial cancer in women. But does Nolvadex block the ER in the hypothalmus? I don’t have that data and I would seriously question an underground publication as being a credible resource. So unless someone can come up with something peer-reviewed, I’ll be still using clomid during recovery. P-22

I’d just like to say that Nolva took the puffiness out of my nips like Clomid never could.

P22 is correct in that clomid is better for recovery… I do not know the exact reason but it has been proven to be better in several studies. I would guess that clomid is simply better at bonding to the estogen receptors in the brain (as our depressed friend mentioned) therefore becoming more effecient at binding up estogen sites in the pituitary. Though novlidex is not JUST an estrogen “site binder” in breast tissue and whatnot… it’s abilities to stimulate LH production via the estrogen antagonist mechanism are much less significant than clomid’s ability to do so.

prisoner. agreed. good post.
horse. ditto here. nolva saved my ass, or should i say my tits, on my cycle just passed. i was on .5mgs/eod of adex too. i will always have nolva around for sure.

Hell why not just stack the shit out both and see what happens :)!

By William Llewellyn


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

Clomid and Nolvadex

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

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

Pituitary Sensitivity to GnRH

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

The Estrogen Clomid

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

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


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

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

well I didn’t take the time to read this because Mr William Llewellyn’s views tend not to be respected amoungst the BB/Steroid Community. This is the guy who prescribes HCG for endogenous testosterone recover post cycle, and He doesn’t just prescribe a little either:

Sample Post-cycle Plan:

Week 3: 5000IU HCG total + 20mg Nolvadex daily
Week 4: 5000IU HCG total + 20mg Nolvadex daily
Week 5: 2500IU HCG total + 20mg Nolvadex daily
Week 6: 20mg Nolvadex daily
Week 7: 20mg Nolvadex daily
Week 8: 20mg Nolvadex daily

Thanks P-22, good post. I respect Llewellyn very highly because he always has studies to back up what he says.

Survey says:

        N O V A D E X

It’s Nolvadex, not novadex.
I personally use nolvadex as my anti-e of choice because for that purpose, it is simply better! But for HPTA recovery, nolva will do nothing compared to clomid. So both have their strengths.

One little considered fact is that prolonged clomid usage has been demonstrated to have negative impacts on the eyesight of it’s users, which did not cease when usage was discontinued.

Additionaly, clomiphene citrate’s effects do diminish with continued usage, whereas tamoxifen’s do not.
For these reasons, I usually limit clomid use to the 3 weeks following a cycle - and why not?

I don’t get the guys who are all about the clomid, all the time. That’s you, Brock Strasser!

Lats2Dope = Learn2Spell


Archaic, where did you read that about Clomid?

And here I thought I’d spanked myself blind…

“One little considered fact is that prolonged clomid usage has been demonstrated to have negative impacts on the eyesight of it’s users, which did not cease when usage was discontinued.”

Excsqueeze me, pass the baking powder, so has Nolvadex. Look what I found on medline and there were many more than these.

Breast Cancer Res Treat. 2000 Mar;60(2):167-72.

Eye problems in breast cancer patients treated with tamoxifen.

Paganini-Hill A, Clark LJ.

Department of Preventive Medicine, Keck School of Medicine of the University of Southern California, Los Angeles, USA. annlia@juno.com

BACKGROUND: Tamoxifen is an oral anti-estrogen used in the treatment of breast cancer and recently approved to reduce the incidence of breast cancer in high risk women. As a large clinical trial of tamoxifen has reported an increased risk of cataract, we conducted a study of women with breast cancer to evaluate the association of tamoxifen with cataracts and other eye problems. METHODS: We attempted to recruit previously interviewed patients who were cases in a population-based case-control study of 2653 women with primary breast cancer diagnosed between 1987 and 1996 at ages 55-72 years in Los Angeles County, California, USA. In November 1997, each case was mailed a questionnaire to ascertain self-reported incidence of eye diseases and Amsler grid test scores. Information from 1297 women aged 57-75 years of age was analyzed. Women reporting treatment with tamoxifen were categorized as standard-term users (4-5 years), short-term users (<4 years), or long-term users (6+ years) and compared to non-users. All p-values, relative risks, and confidence intervals for differences in eye problems and grid test results are adjusted for age and stage of disease at diagnosis. FINDINGS: Standard-term and long-term users of tamoxifen more frequently reported developing cataracts than non-users (18.2%, 21.4% vs. 14.8%). The relative risk was 1.40 (95% confidence interval 0.94-2.10) for standard-term users and 1.70 (1.11-2.59) for long-term users. Tamoxifen use was unrelated to frequency of glaucoma or macular degeneration or to Amsler grid test results. INTERPRETATION: Our study suggests that five or more years of tamoxifen use increases risk of cataracts. Healthy women considering tamoxifen use to reduce risk of breast cancer should be advised of the possibility of cataract development. Women choosing such therapy should be diligent about receiving regular ocular exams.

PMID: 10845279 [PubMed - indexed for MEDLINE]
Eye. 1999 Dec;13 ( Pt 6):729-33.

Ocular toxicity in low-dose tamoxifen: a prospective study.

Noureddin BN, Seoud M, Bashshur Z, Salem Z, Shamseddin A, Khalil A.

Department of Ophthalmology, American University of Beirut, Lebanon. bndean@aub.edu.lb

PURPOSE: To look at the incidence, symptomatology, course and reversibility of low-dose tamoxifen ocular toxicity. METHODS: Sixty-five women with breast cancer, on tamoxifen oral therapy (20 mg/day), and a totally normal eye examination, were prospectively followed up. A full ophthalmic evaluation was done every 6 months, for a median of 30 months (range 4-79 months). Any sign of toxicity in the cornea, lens, retina or optic nerve was looked for, whether associated with a change in visual acuity or not. RESULTS: Ocular toxicity was documented in 8 patients, giving an incidence of 12%. Seven patients had keratopathy in the form of subepithelial deposits, whorls and linear opacities. Three of these patients had a concurrent symptomatic bilateral pigmentary retinopathy that warranted discontinuation of therapy. One patient developed bilateral optic neuritis that left her with optic nerve pallor and a decrease in vision. The patients who had the toxicity had a significantly higher tamoxifen cumulative dose (p = 0.03), and were longer on treatment (p = 0.04), than the non-affected ones. The keratopathy changes were reversible upon discontinuation of the drug. CONCLUSION: Prompt reporting of symptoms and yearly ophthalmic examinations are mandatory in patients on tamoxifen to detect toxic effects while these are still reversible.

Publication Types:
Clinical Trial

PMID: 10707134 [PubMed - indexed for MEDLINE]

Cancer Detect Prev. 1997;21(6):522-31.

Tamoxifen and ocular toxicity.

Ah-Song R, Sasco AJ.

Program of Epidemiology for Cancer Prevention, International Agency for Research on Cancer, Lyon, France.

Tamoxifen, widely used in the management of breast cancer, has been associated with a reduction of mortality and recurrence as well as occurrence of controlateral tumors. It is generally well tolerated, apart from certain well-documented adverse effects concerning mainly the reproductive organs, the most worrying being its carcinogenicity for the endometrium. Ocular toxicity has also been reported as one possible complication of the drug, with lesions described in the retina, the cornea, or the optic nerve, especially in women treated with high daily or cumulated doses of tamoxifen, although some cases have also been reported with standard doses. The incidence of such ocular complications is rather low considering the large number of patients receiving tamoxifen. The possible reversibility of these lesions, if discovered in time, emphasizes the need for clinicians to be aware of these ocular reactions and raises the question of periodic ophthalmological screening examinations among patients receiving tamoxifen.

Cancer. 1992 Jun 15;69(12):2961-4.

Clear evidence that long-term, low-dose tamoxifen treatment can induce ocular toxicity. A prospective study of 63 patients.

Pavlidis NA, Petris C, Briassoulis E, Klouvas G, Psilas C, Rempapis J, Petroutsos G.

Department of Medicine, Medical School, University of Ioannina, Greece.

The current study has prospectively investigated the incidence and course of ocular toxicity after low-dose tamoxifen treatment. Sixty-three patients with cancer who could be examined were analyzed. Tamoxifen was administered on a 20-mg daily dose. Median duration of treatment was 25 months. Median total tamoxifen dose was 14.4 gr. Four patients had retinopathy and/or keratopathy 10, 27, 31, and 35 months, respectively, after tamoxifen initiation (an incidence of 6.3%). Ophthalmologic findings consisted of decreased visual acuity, bilateral macular edema, yellow-white dots in the paramacular and fovea areas in all patients as well as corneal opacities in one patient. After tamoxifen withdrawal almost all ocular abnormalities were found to be reversible, except for the retinal opacities. This is the first prospective study in the literature indicating that even conventional low-dose tamoxifen treatment can induce ocular toxicity. In addition, the authors review and discuss the literature of the last decades.

Those poor women. If the cancer recurs, they’ll never see it coming.