Help - Search - Members - Calendar
Full Version: Clomid Effects in Men
Mind and Muscle Forums > Chemically Correct > Anabolics & Performance Enhancers
Pages: 1, 2, 3
Benson
I like clomid for lots of reasons, mainly because it lacks most of the toxicity issues of nolva and there is a decent amount of clinical data on its effectiveness in men, something largely lacking for tamoxifen.

I do think that it is often overdosed which is what leads to the emotionality, the primary complaint of most male users.

Here is an interesting study demonstrating that it is highly effective at raising T levels in hypogonadal men at just 25mg/day not the 150-300mg/day commonly advocated by steroid 'gurus'

Clomiphene Citrate Effects on Testosterone/Estrogen Ratio in Male Hypogonadism
J Sex Med 2005;2:716–721.

ABSTRACT

Aim. Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testostosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio.

Methods. Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed.

Results. The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 ± 39.8 ng/dL and 32.3 ± 10.9, respectively. By the first follow-up visit (4–6 weeks), the mean testosterone level rose to 610.0 ± 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P < 0.001). There were no side effects reported by the patients.

Conclusions. Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estadiol ratio in men with hypogonadism. This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway.
zuper1
QUOTE(Benson @ Apr 11 2007, 03:29 AM) [snapback]396705[/snapback]
I like clomid for lots of reasons, mainly because it lacks most of the toxicity issues of nolva and there is a decent amount of clinical data on its effectiveness in men, something largely lacking for tamoxifen.

I do think that it is often overdosed which is what leads to the emotionality, the primary complaint of most male users.

Here is an interesting study demonstrating that it is highly effective at raising T levels in hypogonadal men at just 25mg/day not the 150-300mg/day commonly advocated by steroid 'gurus'

Clomiphene Citrate Effects on Testosterone/Estrogen Ratio in Male Hypogonadism
J Sex Med 2005;2:716–721.

ABSTRACT

Aim. Symptomatic late-onset hypogonadism is associated not only with a decline in serum testosterone, but also with a rise in serum estradiol. These endocrine changes negatively affect libido, sexual function, mood, behavior, lean body mass, and bone density. Currently, the most common treatment is exogenous testostosterone therapy. This treatment can be associated with skin irritation, gynecomastia, nipple tenderness, testicular atrophy, and decline in sperm counts. In this study we investigated the efficacy of clomiphene citrate in the treatment of hypogonadism with the objectives of raising endogenous serum testosterone (T) and improving the testosterone/estrogen (T/E) ratio.

Methods. Our cohort consisted of 36 Caucasian men with hypogonadism defined as serum testosterone level less than 300 ng/dL. Each patient was treated with a daily dose of 25 mg clomiphene citrate and followed prospectively. Analysis of baseline and follow-up serum levels of testosterone and estradiol levels were performed.

Results. The mean age was 39 years, and the mean pretreatment testosterone and estrogen levels were 247.6 ± 39.8 ng/dL and 32.3 ± 10.9, respectively. By the first follow-up visit (4–6 weeks), the mean testosterone level rose to 610.0 ± 178.6 ng/dL (P < 0.00001). Moreover, the T/E ratio improved from 8.7 to 14.2 (P < 0.001). There were no side effects reported by the patients.

Conclusions. Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estadiol ratio in men with hypogonadism. This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway.

I don't know about the toxicity issues of Nolva but i would prefer it over Climid,even endos in Greece who don't know shit do not prescribe clomid.
Snip, Author Unknown but I suspect it is Anthony Roberts that might have posted it on his board.
Why don’t we use Clomid, another SERM? Well, basically because it takes much more to do the same thing. In comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but Nolvadex also has the added benefit of significantly increasing the LH (Leutenizing Hormone) response to LHRH (LH-releasing hormone) (6). This most likely indicates some kind of upregulation of the LH-receptors due to the anti-estrogenic effect Nolvadex has at the pituitary. Although both Nolvadex and Clomid are both SERMs, they are actually quite different. As you already know, Nolvadex is highly anti-estrogenic at the hypothalamus and pituitary, while Clomid exhibits weak estrogenic activity at the pituitary (7), which as you can guess, is less than ideal. It should be avoided for the PCT I’m suggesting…and in fact, avoided in general…it’s simply not as good as Nolvadex.
Need I even add that the 150mgs of Clomid you need to get the hormonal increase experienced with 20mgs of Nolvadex is much more expensive? So lets dump the Clomid…and no, using it along with Nolvadex will provide no “synergy” that I’ve ever seen in any relevant study.
SO how much Nolvadex should you use during PCT? I favor using 20mgs.day, although to be totally honest, you can probably even get away with far less than that.

Snipped from The A B C's of anti E's
Now dig this: According to William LLewellyn, studies conducted in the late 1970's at the University of Ghent in Belgium used Nolvadex for 10 days at a dosage of 20mg daily, which increased serum testosterone levels to 142% of baseline, on par with the effect of 150mg of Clomid daily for the same duration! Depending on what you read into this, I'd say that Nolvadex is a superior buy for post-cycle recovery. That being said, Nolvadex is good, but not quite perfect, as it lowers IGF-1 levels. Post-cycle, though, when I'm worried about returning test-levels to normal, I'm not too worried about IGF-1 levels. Though, personally, I've found testicular atrophy during a cycle is attenuated to a greater degree by Clomid. So besides competing with estrogen at the receptor, these drugs both increase serum test levels, and both drugs may also alter blood lipid profiles. I couldn't find the studies W.L. mentioned, but still found that 20mgs of tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but tamixifen did not decrease the LH response to LHRH (Fertil Steril. 1978 Mar;29(3):320-7.). Thus, I'd still reccomend Nolv over clomid. Actually, I think nolvadex is far superior to clomid for most purposes.
As Nolvadex isn't actually an anti-aromatase, but rather a competitor for the receptor site, and seeing as it increases test levels so much, I'd say that it's actually a better post-cycle drug than Clomid (which wreaks havoc on my eyesight, due to it's Occular Toxicity.and Nolvadex has some of that property, but in my experience doesn't mess with my eyesight as much).

Snipped from: Clomid, Nolvadex and Testosterone Stimulation
by William Llewellyn
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.

As you see above that after 10 days nolva increases pituitary sensitivity to GnRH while Clomid DECREASE pituitary sensitivity to GnRH.
Now I feel this is a real issue because most PCT should be run for a minimum of 30 days.
If this is fact the case then Clomid is by far inferior and might inhibit recovery.

Farther down in the article....snip.....

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.

In the article above it was also suggesting Clomid raised SHBG which is what binds to testoserone and allows for LESS free test:
"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".

Following so far, decrease pituitary sensitiviey (takes more to do less) to GnRH, which the hypothalamus tells the pituitary to release LH (which makes test) and FSH which makes sperm), increase in SHBG, which binds with test to allow less free test, which by the way is only 3% of the total test that actually is bioavailable.
virtualcyber
Also, Clomid doesn't kill estrogen levels, which is actually a GOOD thing.

PH use usually screws up one's lipid profile, partly due to lowering of estrogen levels.

So, guess what happens when you use a strong anti-aromatase during a PCT.

That is why I dislike compounds such as ATD.
ozzman
Here is another one, but with higher initial dosage, followed by a low dose for a while:

*******
Department of Endocrinology, Royal Victoria Infirmary and University of Newcastle-upon-Tyne, Newcastle-upon-Tyne, United Kingdom.

OBJECTIVE: Inhibition of pituitary gonadotropin secretion in men by T is principally mediated by aromatization to estrogen (E), which inhibits hypothalamic secretion of GnRH. We hypothesized that adult-onset isolated hypogonadotropic hypogonadism (IHH) might result from an altered central set-point for E-mediated negative feedback. DESIGN AND SETTING: Longitudinal clinical investigation unit-based evaluation of the clinical and biochemical response to E-receptor blockade. PATIENT(S): A 31-year-old man presenting with an 18-month history of sexual dysfunction resulting from severe adult-onset IHH (LH 1.7 U/L, FSH 2.0 U/L, T 3.5 nmol/L). INTERVENTION(S): Initial therapy with 50 mg of clomiphene citrate (CC) three times a day for 7 days, with overnight LH pulse profiling and 9 am T levels evaluated at baseline and on completion. A 2-month washout period, followed by low-dose maintenance therapy (25-50 mg/d) for 4 months. MAIN OUTCOME MEASURE(S): Baseline and stimulated T levels and LH pulsatility; effect on sexual function. RESULT(S): Clomiphene therapy resulted in complete normalization of pulsatile gonadotropin secretion, serum T level, and sexual function. CONCLUSION(S): Isolated hypogonadotropic hypogonadism may result from an acquired defect of enhanced hypothalamic sensitivity to E-mediated negative feedback. Whereas direct T replacement therapy can further suppress endogenous gonadotropin secretion, treating IHH men with gonadotropins can stimulate endogenous T secretion and enhance fertility potential. On theoretical grounds, reversal of gonadotropin deficiency with CC might be expected to have a similar biological effect.

**************
And another one used specifically after steroid use:




************

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. robert.s.tan@uth.tmc.edu

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH. RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.

zuper1
Yeah,but Nolva beats Clomid wink.gif
Benson
QUOTE(zuper1 @ Apr 11 2007, 04:31 PM) [snapback]396852[/snapback]
Yeah,but Nolva beats Clomid wink.gif


At what? Preventing gyno perhaps due to its affinity for breast tissue.

For restoring T production, there is really no clinical evidence that supports the contention that it is more effective than clomid.
zuper1
QUOTE(Benson @ Apr 11 2007, 10:15 PM) [snapback]396861[/snapback]
At what? Preventing gyno perhaps due to its affinity for breast tissue.

For restoring T production, there is really no clinical evidence that supports the contention that it is more effective than clomid.

I can guess you didn't read my post.
Clomid cause desensetization of pituitary to GNRH.
Clomid cause vision problems,sometimes irreversible.
Clomid cause emotionality.
Benson
QUOTE(zuper1 @ Apr 11 2007, 06:32 PM) [snapback]396886[/snapback]
I can guess you didn't read my post.
Clomid cause desensetization of pituitary to GNRH.
Clomid cause vision problems,sometimes irreversible.
Clomid cause emotionality.


I think you have your drugs mixed up. Tamoxifen is much more likely to cause permanent eye damage (PMID: 1591689) than clomid which (very rarely) causes transient visual disturbances that almost always go away once the drug is withdrawn. The visual disturbances are also dose-dependent.

And it only causes emotional disturbances when its overdosed...as I pointed out in my first post, the dose needed to restore testicular function in hypogonadal men is 1/10 the dose often suggested by steroid 'gurus' It should surprise nobody that it makes men weepy at 350mg/day, especially because it has a half-life measured in days...

Clomid has been studied over long periods in men and has demonstrated efficacy and safety....something that has never been done with nolva.
Benson
Toxicity of Antiestrogens
The Breast Journal
Volume 8 Issue 2 Page 92 - March/April 2002

The object of this article is to review briefly the preclinical and clinical safety of some antiestrogens. Tamoxifen, toremifene, droloxifene, and idoxifene are polyphenylethylene antiestrogens, whereas the pure antiestrogen, ICI 182,780 or faslodex, as well as raloxifene, is of a different structure. Tamoxifen has been shown to be genotoxic in several studies. It induces unscheduled DNA synthesis in rat hepatocytes and micronuclei in MCL-5 a cells in vitro. Tamoxifen also induces aneuploidy in rat liver in vivo and chromosome aberrations and micronuclei in mouse bone marrow. Toremifene has also shown to be genotoxic, but to a far lower extent, by inducing micronuclei in MCL-5 a cells in vitro and by inducing aneuploidy in rat liver in vivo. Tamoxifen has been shown to be hepatocarcinogenic in the rat in at least four independent long-term studies. The initiation of tumors in the rat is the result of metabolic activation by cytochrome P450 isoenzymes to an electrophile(s) that binds irreversibly to DNA. The other antiestrogens have not been shown to be carcinogenic in rodents. In several independent clinical studies, the risk of endometrial cancer has increased among tamoxifen-treated women. After reviewing the available data, the International Agency for Research on Cancer concluded that there was sufficient evidence to show that tamoxifen is a class I human carcinogen. The increased risk for endometrial cancer occurs predominantly among women who are 50 years old or older and who have been treated with tamoxifen. It is not yet clear whether the uterine tumor formation is a result of genetic mechanisms, analogous to those seen in the rat liver or due to the estrogen agonist action of tamoxifen. However, the other antiestrogens with a more or less similar intrinsic estrogenic potential have not been shown to be carcinogenic in humans.


Grassroots082
I noticed no eye disturbance/tracers with Clomid even at 100mg/day but with Nolva they are apparent at 40 and I swear my vision has not been the same since the use of Nolva (glad I sold that shit). The last SERM I tried was Toremifene and I was pretty happy with that, but from my experiences Clomid or Toremifene would be my SERM of choice.
Jay Black
What's the concensus on using both for PCT? I've seen it advocated several places.
Benson
QUOTE(Jeff @ Apr 11 2007, 10:39 PM) [snapback]396922[/snapback]
What's the concensus on using both for PCT? I've seen it advocated several places.


Unless you are especially concerned with gyno, I see no reason to use nolva with or ahead of either clomid or one of the newer SERMs that do not share its toxicity.
Redsky
I'm using both during my extensive PCT in high doses (Clomid 100mg/d, Nolva 40mg/d). I've not noticed any vision issues and minimal emotional issues. YMMV.
Redsky
Although I gotta admit I get weepy much easier within an hour after my dose. Fortunately, it's irrational and identifiable, so I laugh at it, like Clomid is a dog or something:
"Oh you silly clomid!"
Grassroots082
It has a half life of 5-7 days (source) so I would imagine that to be largely psychological, but perhaps there is some type of initial response. Are you taking liquid clomid or tabs?
Redsky
QUOTE(Grassroots082 @ Apr 17 2007, 05:47 AM) [snapback]397712[/snapback]
It has a half life of 5-7 days (source) so I would imagine that to be largely psychological, but perhaps there is some type of initial response. Are you taking liquid clomid or tabs?

Liquid, and I just notice it *more* in the bit of time after I take it. I have noticed being a bit more emotionally flighty over the past 3 weeks, but I imagined much of that was more of my test levels getting back to a normal level.
lepiricus
I am trying to figure out what Benson was gettting at in this thread.

Is he meaning to say that clomid might be a good thing to use at 25mg/day for sustained higher test levels rather than usage as a pct drug? In other words, you could use low dose clomid to be in the upper bound of testosterone to promote gains rather than running a true cycle where test levels are super human?

And, I am guessing that the down regulated gnrh system would be less pronounced at 25mg/day than at 150mg/day and shouldn't be a concern with prolonged use?
Benson
My main point was that the normal pct recomendations for clomid are way higher than they need to be to restore testicular output. And that when the dosage is kept at a reasonable level (50mg/day or so) clomid is almost entirely devoid of side effects.

As a corollary, low dose clomid would appear to be a decent way to make sure your production was optimized without incuring the risks of basement-level estrogen as you might get using an AI for the same purposes. The purpose of the study I posted was to evaluate the use of clomid as an alternative to HRT in hypogonadal men, something it appears to work decently for.

I have not studied the GNRH-sensitivity issue much but given that there are lots of studies of men using clomid at various doses for long periods and it doesn't seem to be a problem, my suspicion is that the effect is small.

Lastly, I wanted to point out once again that nolva is a moderately toxic drug and its use should be limited given the availability of other, SERMS.
lepiricus
ahhh, thanks for posting Benson.

Last year I was self medicating w/ 20mg/day of nolva for low-normal test and after 3 weeks I was high-normal in test and fsh/lh. I did this for about 3 months then tapered off. I did notice an improvement in my symptoms as well, no side effects to speak of. I did not have a blood test to look at after 3 months though.

I was thinking of a mimic of that using clomid at 25 mg/day, I was just worried a bit b/c of the reported gnrh sensitivity altering ability.

zuper1
QUOTE(lepiricus @ Apr 22 2007, 06:13 AM) [snapback]398478[/snapback]
ahhh, thanks for posting Benson.

Last year I was self medicating w/ 20mg/day of nolva for low-normal test and after 3 weeks I was high-normal in test and fsh/lh. I did this for about 3 months then tapered off. I did notice an improvement in my symptoms as well, no side effects to speak of. I did not have a blood test to look at after 3 months though.

I was thinking of a mimic of that using clomid at 25 mg/day, I was just worried a bit b/c of the reported gnrh sensitivity altering ability.

When you have cleared from Nolva haven't had any bloodwork?If not how were you feeling,better than on low to normal test?
lepiricus
QUOTE(zuper1 @ Apr 21 2007, 10:22 PM) [snapback]398488[/snapback]
When you have cleared from Nolva haven't had any bloodwork?If not how were you feeling,better than on low to normal test?


I didnt have bloodwork at the the end my run b/c I was doing it under the radar from my GP and endo, I did, however, feel better during the run and felt deflated a couple weeks after, but I am always wary of psychosomatic feelings.

When I do it with the clomid I wll have to time it right between my yearly physical and my endo appointment where my docs always run hormone tests as sop. I would be straight up with them but they times I have hinted at trying something both have said it wasn't necessary b/c my results are "completely normal"


what are people's thoughts on raloxifene or toremifene as serms?
Grassroots082
Benson knows best, you don't need to run 150/100/100/50 or whatever the "new" PCT plan is, unless you like fucking your vision up on purpose.

60mg Nolva is alot different than 20mg, obviously the higher you dose the more sides of any drug you will get so its no suprise you didn't get any sides. He's saying 150mg and 100mg of Clomid aren't needed, just like the general bro population telling people well you need 60mg Nolva for the first week, then 40/40/20 and taper off whatever. I gave my thoughts on Torm in the thread, based on this information..

QUOTE
Chem Res Toxicol. 2006 Mar 20;19(3):421-425. Related Articles, Links
Click here to read
Absence of DNA Adduct in the Leukocytes from Breast Cancer Patients Treated with Toremifene.

Umemoto A, Lin CX, Ueyama Y, Komaki K, Santosh Laxmi YR, Shibutani S.

Department of Oncological and Regenerative Surgery, Institute of Health Biosciences, The University of Tokushima Graduate School, Tokushima 770-8503, Japan, and Laboratory of Chemical Biology, Department of Pharmacological Sciences, State University of New York at Stony Brook, Stony Brook, New York 11794-8651.

Tamoxifen (TAM) causes cancer in rat liver and human endometrium, whereas the carcinogenicity of its chlorinated analogue toremifene (TOR) has not been observed. To elucidate the genotoxicity of TOR, the capability of forming DNA adducts by TOR was examined in the leukocytes of patients treated with TOR. Leukocytes were collected from 27 breast cancer patients (57.7 +/- 11.4 years old) taking TOR (40 mg/day for 25 patients, 80 mg/day for one patient, and 120 mg/day for one patient; average duration, approximately 12 months) and 20 untreated breast cancer patients (58.2 +/- 12.3 years old). The DNA extracted was analyzed by (32)P-postlabeling/high-performance liquid chromatography. No DNA adducts were detected in the leukocytes of either TOR-treated or nontreated patients. Our results contrast to the previous observation detecting TAM-DNA adducts in several patients treated with TAM, indicating that TOR is less genotoxic to humans.

PMID: 16544947 [PubMed - as supplied by publisher]


QUOTE
Bone mineral density and lipid changes during 5 years of follow-up in a study of prevention of breast cancer with toremifene in healthy, high-risk pre- and post-menopausal women.

Erkkola R, Mattila L, Powles T, Heikkinen J, Toivola B, Korhonen P, Mustonen M.

Department of Obstetrics and Gynaecology, Turku University Central Hospital, Turku, Finland.

A double-blind, randomised, placebo-controlled pilot study was initiated to evaluate the feasibility of chemoprevention with toremifene 60 mg/day in healthy women at high risk for breast cancer. Enrolment in the study was terminated earlier than planned because of slow patient accrual, although 13% of patients continued for 5 years. The revised efficacy outcomes were change in bone mineral density (BMD) from baseline at four skeletal sites, plus effects on serum lipids. In premenopausal women there was a trend for sustained increase in BMD during toremifene therapy after year 1 in lumbar spine. In postmenopausal women, toremifene had little or no effect on BMD trends. Levels of total and low-density lipoprotein (LDL) cholesterol were largely unchanged from baseline in premenopausal women treated with toremifene but were often slightly lower than in the placebo group during follow-up. Total and LDL cholesterol levels declined slightly from baseline in the postmenopausal women and were, at several points during the first 3 years, significantly lower than in the corresponding placebo group (p < 0.01). We conclude that: (a) assessment of toremifene 60 mg/day in chemoprevention will require further clinical trials; (cool.gif toremifene 60 mg/day has no substantive negative effects on BMD in pre- or postmenopausal women and may exert a minor favourable influence (in particular, the effects of toremifene 60 mg/day on BMD in premenopausal women may make the drug an attractive alternative to tamoxifen 20 mg/day for that patient subset); © lipid effects of toremifene 60 mg/day are, at minimum, neutral and may be modestly favourable for reducing cardiovascular risk.

Publication Types:

* Multicenter Study
* Randomized Controlled Trial

PMID: 16172794 [PubMed - indexed for MEDLINE]


QUOTE
Initiating activity of the anti-estrogen tamoxifen, but not toremifene in rat liver.

Williams GM, Iatropoulos MJ, Karlsson S.

American Health Foundation, Valhalla, New York, USA.

A striking difference between two structurally related anti-estrogen medicines is that tamoxifen is strongly hepatocarcinogenic in the rat, whereas toremifene lacks such activity. To study the basis for this difference, the initiating potential of tamoxifen and toremifene were studied by measurement of rapid induction of hepatocellular altered foci (HAF) that express placental-type glutathione S-transferase in the livers of female Sprague-Dawley (S-D) rats and female Fischer 344 (F344) rats. Both agents were administered by gavage at equimolar doses up to a dose that produced marked weight gain suppression. In rats given the high dose of 40 mg/kg per day tamoxifen continuously for 36 weeks, 75% of S-D rats developed liver neoplasms, in contrast to only 10% of F344 rats. In the S-D strain, tamoxifen produced a tendency to increased HAF at 2 weeks at the dose of 40 mg/kg per day and by 12 weeks, a dose-related increase was evident. In contrast, toremifene induced no HAF even at the equimolar high dose of 42.4 mg/kg per day for 12 weeks. The induction of HAF by tamoxifen was less in the F344 rats. Neither agent elicited increases in hepatocellular proliferation in S-D or F344 rats. When phenobarbital was administered for 24 weeks as a promoting agent after the anti-estrogens, S-D rats given tamoxifen at 20 mg/kg per day for 12 weeks, developed liver neoplasms, but not F344 rats or rats of either strain given even a higher dose (42.4 mg/kg) of toremifene. Thus, tamoxifen has initiating activity in these rat strains whereas toremifene does not.

PMID: 9395228 [PubMed - indexed for MEDLINE]


QUOTE
Comparison of DNA reactivity of the polyphenylethylene hormonal agents diethylstilbestrol, tamoxifen and toremifene in rat and hamster liver.

Montandon F, Williams GM.

American Health Foundation, Valhalla, NY 10595.

The polyphenylethylene estrogenic drug diethylstilbestrol and a structural analogue tamoxifen have been found to be hepatocarcinogenic in female rats, whereas another analogue, toremifene, did not induce liver tumors. The 32P post-labelling technique for detection of DNA adducts was used to investigate the DNA reactivity of these three hormonal agents in the livers of female Sprague-Dawley rats and Syrian hamsters. Adducts were quantified using a radioanalytic imaging system in comparison with the standard Cerenkov assay. With administration of the chemicals at several doses by daily gavage to rats for 10 days and to hamsters for 7 days, tamoxifen was found to produce five adducts in rat liver and six adducts in hamster liver. The amounts of adducts were dose related from 10 to 90 mumol/kg per day in rats and from 17 to 160 mumol/kg per day in hamsters. The two methods of quantification yielded comparable results. Under these conditions, neither toremifene nor diethylstilbestrol produced adducts in rats and diethylstilbestrol produced none in hamsters. We conclude that tamoxifen is highly DNA reactive in the species studied and that this is likely to be involved in its strong carcinogenicity in rat liver.

PMID: 8067901 [PubMed - indexed for MEDLINE]


QUOTE
Toremifene: An evaluation of its safety profile.

Harvey HA, Kimura M, Hajba A.

Division of Hematology/Oncology, Penn State College of Medicine, Penn State Milton S. Hershey Medical Center, 500 University Drive, Hershey, PA 17033, USA.

Toremifene has been in clinical use for 8 years for the treatment of advanced hormone-sensitive breast cancer and the adjuvant treatment of early breast cancer. More than 350,000 patient treatment years have accumulated, sufficient to allow evaluation of its longer-term safety profile in comparison with tamoxifen and, where possible, with raloxifene and aromatase inhibitors. We reviewed all preclinical and clinical safety data from 1978 to 2004 and comparative clinical safety data between October 1995 and the end of 2004. Secondary endometrial cancer incidence was lower with toremifene than with tamoxifen and was similar to that with raloxifene. It is speculated that toremifene may unmask existing endometrial tumors rather than induce new events. The risk of stroke, pulmonary embolism, and cataract may be lower with toremifene than with tamoxifen and the risk of pulmonary embolism and deep vein thrombosis lower than with raloxifene. Beneficial estrogen agonistic effects were equivalent to those of tamoxifen regarding bone mineral density and superior regarding lipid profiles.

PMID: 16289904 [PubMed - as supplied by publisher]


That's why I don't use Nolva, and why I never will (again).
djremix
arent the previous studies on women(post menopausal) and rats?

interesting arguments. i have to admit i have also bitten into the clomid is better argument, from vague first experiences to reasonings by DR. D from anabolicx.

i am now on pct from a cycle which was similar to the one i did a year ago.
what i changed in pct was mainly:

old cycle : tamox at 40, 30, 20, 20

this time : clomid at: day 1 to 12
1st day : 50mg
2nd : 100mg
3rd : 150mg
then i took 3 days off
repeat.
after starting day 13 to 27
nolva at 20mg/day

others include rebound reloaded, lean extreme and activate both times. and RYR first 2 weeks.

ill have another round of blood tests and hormone panel. should be interesting to see the results now.
as my previous cycle post pct results were nothing short of astounding...
smile.gif

snipit:
"** over 100% increase in total test from normal : 3.4 to 7.3!
(and 20,000% increase from last day of cycle.... 0.35 to 7.3)
** over 80% increase in free test from normal : 10.4 to 18.1
(and 170% increase from last day of cycle.... 3.1 to 18.1)
"
cycle details
Grassroots082
QUOTE
arent the previous studies on women(post menopausal) and rats?


Yes and your point?
zuper1
QUOTE(djremix @ Apr 23 2007, 03:04 PM) [snapback]398657[/snapback]
arent the previous studies on women(post menopausal) and rats?

interesting arguments. i have to admit i have also bitten into the clomid is better argument, from vague first experiences to reasonings by DR. D from anabolicx.

i am now on pct from a cycle which was similar to the one i did a year ago.
what i changed in pct was mainly:

old cycle : tamox at 40, 30, 20, 20

this time : clomid at: day 1 to 12
1st day : 50mg
2nd : 100mg
3rd : 150mg
then i took 3 days off
repeat.
after starting day 13 to 27
nolva at 20mg/day

others include rebound reloaded, lean extreme and activate both times. and RYR first 2 weeks.

ill have another round of blood tests and hormone panel. should be interesting to see the results now.
as my previous cycle post pct results were nothing short of astounding...
smile.gif

snipit:
"** over 100% increase in total test from normal : 3.4 to 7.3!
(and 20,000% increase from last day of cycle.... 0.35 to 7.3)
** over 80% increase in free test from normal : 10.4 to 18.1
(and 170% increase from last day of cycle.... 3.1 to 18.1)
"
cycle details

Where do you find this pct protocol,links?
oswaldosalcedo
i advocate clomid only pct plus a cortisol blocker or inhibitor just that.

Fertil Steril. 2006 Nov;86(5):1513.e5-9.

Complete reversal of adult-onset isolated hypogonadotropic hypogonadism with clomiphene citrate.


Ioannidou-Kadis S, Wright PJ, Neely RD, Quinton R.
Benson
Fertil Steril. 2003 Jan;79(1):203-5.
Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH. RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.

PMID: 12524089
Sub7
Benson,
So if someone wanted extra hormonal help but doesn't wish to mess with AAS, you are saying that using Clomid to achieve higher than normal (normal for that individual) T levels is a viable strategy???

If so how long can one stay on low dose Clomid and what is the best strategy to come off when so desired?
Benson
QUOTE(Sub7 @ Apr 24 2007, 06:02 PM) [snapback]398950[/snapback]
Benson,
So if someone wanted extra hormonal help but doesn't wish to mess with AAS, you are saying that using Clomid to achieve higher than normal (normal for that individual) T levels is a viable strategy???


I am.

QUOTE
If so how long can one stay on low dose Clomid and what is the best strategy to come off when so desired?


In several studies, men have been kept on 25-50mg/day for periods as long as a year without any reported negative effects. As for coming off, I would just stop taking it...clomid's long half-life will provide a sort of natural taper down to zero within a week after taking your last dose.
Jay Black
QUOTE(Benson @ Apr 24 2007, 05:52 PM) [snapback]398946[/snapback]
Fertil Steril. 2003 Jan;79(1):203-5.
Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

OBJECTIVE: To report a case of symptomatic hypogonadism induced by the abuse of multiple steroid preparations that was subsequently reversed by clomiphene. DESIGN: Case report. SETTING: University-affiliated andrology practice within family practice clinic. PATIENT(S): A 30-year-old male. INTERVENTION(S): Clomiphene citrate, 100-mg challenge for 5 days, followed by treatment at same dose for 2 months. MAIN OUTCOME MEASURE(S): Clinical symptoms, androgen decline in aging male questionnaire, total T, FSH, LH. RESULT(S): Reversal of symptoms, normalization of T levels with LH surge, restoration of pituitary-gonadal axis. CONCLUSION(S): Clomiphene citrate is used typically in helping to restore fertility in females. This represents the first case report of the successful use of clomiphene to restore T levels and the pituitary-gonadal axis in a male patient. The axis was previously shut off with multiple anabolic steroid abuse.

PMID: 12524089


This is excellent.
Benson
QUOTE(Jeff @ Apr 24 2007, 07:05 PM) [snapback]398963[/snapback]
This is excellent.


That's what I was thinking. Actual clinical data to support a PCT protocol...
zuper1
QUOTE(Benson @ Apr 24 2007, 11:11 PM) [snapback]398953[/snapback]
In several studies, men have been kept on 25-50mg/day for periods as long as a year without any reported negative effects. As for coming off, I would just stop taking it...clomid's long half-life will provide a sort of natural taper down to zero within a week after taking your last dose.
Iteresting,are you sure?Have you tried it,bloodwork?
Benson
QUOTE(zuper1 @ Apr 25 2007, 05:42 AM) [snapback]399031[/snapback]
Iteresting,are you sure?Have you tried it,bloodwork?


I am sure that there are a number of studies using clomid in men, some for periods as long as a year and I am also sure that the clinical effects of clomid in men include increasing testosterone.
zuper1
QUOTE(Benson @ Apr 25 2007, 11:02 PM) [snapback]399209[/snapback]
I am sure that there are a number of studies using clomid in men, some for periods as long as a year and I am also sure that the clinical effects of clomid in men include increasing testosterone.

But the issue here is if there evidence what happens after discontinuition on keeping levels in optimal range.
Benson
QUOTE(zuper1 @ Apr 26 2007, 10:37 PM) [snapback]399419[/snapback]
But the issue here is if there evidence what happens after discontinuition on keeping levels in optimal range.


Once you stop taking it, I suspect your levels would return to wherever they were before you started.
Benson
Finally...I found the study upon which all the PCT gospel is based.


Fertil Steril. 1978 Mar;29(3):320-7. Links
Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

The administration of tamoxifen, 20 mg/day for 10 days, to normal males produced a moderate increase in luteinizing hormone (LH), follicle-stimulating hormone (FSH), testosterone, and estradiol levels, comparable to the effect of 150 mg of clomiphene citrate (Clomid). However, whereas Clomid produced a decrease in the LH response to LH-releasing hormone (LHRH), no such effect was seen after the administration of tamoxifen. In fact, prolonged treatment (6 weeks) with tamoxifen significantly increased the LH response to LHRL. Treatment of patients with "idiopathic" oligospermia for 6 to 9 months resulted in a significant increase in gonadotropin, testosterone, and estradiol levels. A significant increase in sperm density was observed only in subjects with oligospermia below 20 X 10(6)/ml and normal basal FSH levels. When basal FSH levels were increased or oligospermia was moderate (greater than 20 X 10(6)/ml); no effect on sperm density was seen. As sperm density increased, FSH levels decreased, suggesting an inhibin effect. Sperm motility was not improved by tamoxifen treatment. In five boys with delayed puberty, tamoxifen treatment appeared to activate the pituitary-gonadal axis and pubertal development.

Now, this is fine but it appears that later research has largely debunked the LH desensitization claim...in fact some in vitro studies indicate that clomiphene produces significant sensitizing to the effects of GnRH...
Jay Black
More excellence displayed by B. Aye, mate.
Sub7
Gentlemen,

This is a tiny bit O/T but: If a moderately supressive AAS was used such as Pheraplex (DMT) would taking Clomid during the cycle prevent supression (I am not saying shutdown because with Pheraplex alone, you will likely not be totally shutdown)? If so, what dosage would be recommended before, during and after cycle? I am also saying "before" because I am hypothesizing that if your T production is higher than normal before the cycle, supression may be less severe -i.e. T levels at the end of the cycle may be higher in this scenario, as a % decline you will likely go down more.

Thanks

Sub
SupremeDan
AR activation still is the main factor on androgen negative feedback.....so clomid wont do much in this regards...
Benson
QUOTE(SupremeDan @ Apr 29 2007, 03:17 PM) [snapback]399661[/snapback]
AR activation still is the main factor on androgen negative feedback.....so clomid wont do much in this regards...


What he said. Clomid won't help on-cycle (hcg is the only thing that would) but post-cycle or as a standalone, I like it.
oswaldosalcedo
QUOTE(zuper1 @ Apr 26 2007, 06:37 PM) [snapback]399419[/snapback]
But the issue here is if there evidence what happens after discontinuition on keeping levels in optimal range.



it has to be diminished gradually (clomiphene).
and test levels are age dependent (and it can be supported according to).
oswaldosalcedo
cos clomiphene on withdrawal can increase estrogen production.
Benson
QUOTE(oswaldosalcedo @ May 2 2007, 09:42 PM) [snapback]400116[/snapback]
cos clomiphene on withdrawal can increase estrogen production.


How and why? Show your work wink.gif
zuper1
QUOTE(Benson @ May 3 2007, 03:08 AM) [snapback]400123[/snapback]
How and why? Show your work wink.gif

So yours that will not. wink.gif
Benson
QUOTE(zuper1 @ May 3 2007, 11:13 AM) [snapback]400179[/snapback]
So yours that will not. wink.gif


I made no such claim but there is no evidence that there is an estrogen rebound in men after discontinuation of clomid and there is no reasonable explanation I can think of for why it would.

oswaldosalcedo
Fertil Steril. 1980 Sep;34(3):285-6.

The occurrence of gynecomastia upon withdrawal of clomiphene citrate treatment for idiopathic oligospermia.


Lee PA.
Benson
QUOTE(oswaldosalcedo @ May 4 2007, 02:36 PM) [snapback]400300[/snapback]
Fertil Steril. 1980 Sep;34(3):285-6.

The occurrence of gynecomastia upon withdrawal of clomiphene citrate treatment for idiopathic oligospermia.


Lee PA.


Correlation does not equal causation. Clomid is a mildly effective treatment for gyno so the the fact that it occurred when the drug was withdrawn may simply mean that the guys estrogen levels were already high and the clomid was simply preventing the gyno.

OTOH, estrogen levels do go up when using clomid which makes sense because it increases LH and T levels.

Clomid along with a low dose AI would probably make the most sense if one were interested in using it to increase natural T production.

Grassroots082
Seems like Clomid, transdermal formestane and dhea would be great additions to PCT do you agree Benson?
Benson
QUOTE(Grassroots082 @ May 4 2007, 09:16 PM) [snapback]400350[/snapback]
Seems like Clomid, transdermal formestane and dhea would be great additions to PCT do you agree Benson?


Yes. Go easy on the latter two. More is not better.
Grassroots082
10-4
This is a "lo-fi" version of our main content. To view the full version with more information, formatting and images, please click here.
Invision Power Board © 2001-2008 Invision Power Services, Inc.