Estrogen blocker cycle.....

[The Rob]

I know some people have tried this and have had some success with it, so just share the gains you made\how long you did the cycke\and so on.

 

[keith1569]

currently imjust takin clomid

i frontloaded my first day with bout 150mg and then after that im gonna go 25mg a day..if i dont notice anything i'll up it to 50mg a day

if u pm me i'll pm u back when i finssh it..bout 1 month away from bein done..just started so i dont konw how its gonna work yet

 

[DR.D]

If your new to the game, or under 21, this is the best way to start. It will work, probably for several cycles before you feel the need to use exogenous androgens.

You 2 fellas are smart! I wish I'd done it that way, but back when dinosaurs ruled the earth, you couldn't find clomid at the gym, and the internet wasn't here. Just a small grid of boards you could connect your 1200baud modem up to with your Commador64 PC! :rofl: No online clomid like today.

 

[hypo]

this is new to me... you just take an estrogen blocker (will nolva work as well as clomid?) by itself? What are the benefits? Also will the use of the PCT stuff mess up HPTA or sex hormones at all?

 

[boby-at]

the main benefit (theoretically) is the shift of the HPTA towards androgen production via the negative feedback (the estrogen level regulates the HPTA too and the receptors are blocked by an exogeneous substance like clomid), so, in theory, one should expect higher serum concentrations of testosteron. however, I am not quite sure if this is working properly IRL

 

[The Rob]

If your new to the game, or under 21, this is the best way to start. It will work, probably for several cycles before you feel the need to use exogenous androgens.

You 2 fellas are smart! I wish I'd done it that way, but back when dinosaurs ruled the earth, you couldn't find clomid at the gym, and the internet wasn't here. Just a small grid of boards you could connect your 1200baud modem up to with your Commador64 PC! :rofl: No online clomid like today.

Well this is going to be my first "cycle" so this was how I wanted to start out.... will clomid and nolva and 60X0 baically do the same thing? or if there are differences with each what are they?

And my brother who's 19 was looking to get into PH's (I made a thread about it last time) would also be able to do this safely? unlike PH where 21 is a "requirement"

 

[Matthew D]

personally I would wait.. his body is growing and going through a ton of changing STILL..

 

[wastedwhiteboy2]

dr d. what effects would an anti-estrogen cycle have on a female? would it be similar effects on a man? I know clomid and nolva were made for women. would their period be off?

 

[Nullifidian]

Clomid is a fertility drug for women. Don't give this to your girlfriend unless you like the idea of triplets.

Nolva is a breast cancer drug. Not sure what effect it would have but it certainly isn't all that nice. Women in general don't want to inhibit estrogen unless the estrogen is causing a health problem, like breast cancer. I imagine taking tamox might have a masculinizing effect on a woman. I could be wrong though.

 

[CDB]

Well this is going to be my first "cycle" so this was how I wanted to start out.... will clomid and nolva and 60X0 baically do the same thing? or if there are differences with each what are they?

Nolva and Clomid are SERMS, which I believe stands for Selective Estrogen Receptor Modifiers. They bind to the estrogen receptors within certain tissues and in so doing 'trick' the body into producing more testosterone to up the estrogen, which it sees as low. During PCT they have that effect plus the benefit of inhibitting the effects of any abnormally high estrogen levels until the body is back in balance. Look up HPTA axis for more detailed info on the negative feedback mechanism of the whole thing.

6oxo is a suicide inhibitor of the aromatase enzyme itself. That is it stops the production of estrogen rather than just blocking its effects, similar to Arimidex. AIs are used more often than not on cycle to prevent bloat and to make sure there aren't excessive amounts of estrogen in the body at the end of a cycle. Some steroids have a similar effect, like 4oht, which is why you'd sometimes see that stacked with aromatizing substances to help with bloat, gyno, etc.

 

[The Rob]

Nolva and Clomid are SERMS, which I believe stands for Selective Estrogen Receptor Modifiers. They bind to the estrogen receptors within certain tissues and in so doing 'trick' the body into producing more testosterone to up the estrogen, which it sees as low. During PCT they have that effect plus the benefit of inhibitting the effects of any abnormally high estrogen levels until the body is back in balance. Look up HPTA axis for more detailed info on the negative feedback mechanism of the whole thing.

6oxo is a suicide inhibitor of the aromatase enzyme itself. That is it stops the production of estrogen rather than just blocking its effects, similar to Arimidex. AIs are used more often than not on cycle to prevent bloat and to make sure there aren't excessive amounts of estrogen in the body at the end of a cycle. Some steroids have a similar effect, like 4oht, which is why you'd sometimes see that stacked with aromatizing substances to help with bloat, gyno, etc.

So in THEORY the Nolva would be a "safer" cycle than the 60X0 right?

 

[Lakevillethor]

So in THEORY the Nolva would be a "safer" cycle than the 60X0 right?

I disagree. There is some evidence out there that suggests (PA showed it to me when I was at Ergopharm as I had some simlar questions), that when you take things like nolva, that bond to the estrogen receptor with some affinity, that your body will recognize a lack of estrogen and produce more estrogen as a result. Additionally, 6-OXO is proven to raise testosterone levels quite well so I would just take that and forget the nolva.

-AT

 

[wastedwhiteboy2]

my wife had her tubes tied so I think I'm safe. I just thought reducing estrogen might help her lean up some and maybe put on a little lean muscle. I assumed her test would go up slightly? I could be wrong?

 

[The Rob]

I disagree. There is some evidence out there that suggests (PA showed it to me when I was at Ergopharm as I had some simlar questions), that when you take things like nolva, that bond to the estrogen receptor with some affinity, that your body will recognize a lack of estrogen and produce more estrogen as a result. Additionally, 6-OXO is proven to raise testosterone levels quite well so I would just take that and forget the nolva.

-AT

That was a TOTALLY unexpected answer... really insightful though thx.

 

[Enigma76]

That was a TOTALLY unexpected answer... really insightful though thx.

It makes sense though. Circulating free estrogen while on nolvadex is high, because the tamox binds to the receptors. The body sees low estrogen, and ups test production; the reason for increased test production is to convert to estrogen (because the body only "sees" a small amount...remember that what the body "sees" is what can bind to receptors). So obviously estrogen will be increased while on nolva; the key is that it wont be doing anything, because the nolva will be blocking the receptors.

 

[Lakevillethor]

Yes, but once the nolva is discontinued you will have high estrogen levels. The aromatase inhibitor will stop all estrogen production all together so I don't know how once could say nolva is better choice for this type of cycle. In all honesty, either way the estrogen will not be halted completely. Ergo has evidence that shows that 6-OXO raises test levels so why I fail to see how 6-OXO is not the best choice.

 

[CDB]

Yes, but once the nolva is discontinued you will have high estrogen levels. The aromatase inhibitor will stop all estrogen production all together so I don't know how once could say nolva is better choice for this type of cycle. In all honesty, either way the estrogen will not be halted completely. Ergo has evidence that shows that 6-OXO raises test levels so why I fail to see how 6-OXO is not the best choice.

It's relatively expensive for one, and leaving any doubt aside about what study does exist regarding 6oxo, there are well studied alternatives available with established safety profiles.

 

[chrisrico]

Yes, but once the nolva is discontinued you will have high estrogen levels. The aromatase inhibitor will stop all estrogen production all together so I don't know how once could say nolva is better choice for this type of cycle. In all honesty, either way the estrogen will not be halted completely. Ergo has evidence that shows that 6-OXO raises test levels so why I fail to see how 6-OXO is not the best choice.

Guys have been using Nolva successfully for years though. Kinda hard to argue with real world results. What looks true on paper isn't necessarily always accurate. But, I have taken Ergopharm's product and got excellent results, but I think Nolva will do just as well.

 

[DR.D]

my wife had her tubes tied so I think I'm safe. I just thought reducing estrogen might help her lean up some and maybe put on a little lean muscle. I assumed her test would go up slightly? I could be wrong?

Your safe, reducing estrogen is a real good idea usually. There is so much estrogen in the world these days from PCB's and pesticides and stuff, that women are getting breast cancer younger than they once did. Most docs will put a women on a SERM faster than estrogen replacement because of the breast cancer protection it provides after menopause. However, nolva is a bad choice. There are newer, safer ones now. It will promote strength gains in women and lean muscle from increased test, but also maybe some hot flashes and emotional instability in certain women too. The ovaries and endometrium can be stimulated also, even though the breast is not.

As for PCT, forget about nolva. 6-oxo may work, but clomid is still the most effective choice. You can double or triple you baseline test levels with clomid, especially if your young.

 

[TheManGuy]

How much nolva 6 oxo, would be optimal for a cycle like this? 600mg ed I'd assume.

Also, how would this work stacked with m4ohn, for the ultimate safe and effective cycle??

 

[BodyWizard]

Dr. D - I'd love to hear your comments on such a cycle for aging men.

Actually, I'd love to learn more about endo/exo-hormone issues for guys like me (ie, "old" :blink: ), so if you have any links, please share 'em!

While I have you here, I'd like to thank you for pointing out the dangers of tamoxifen - I'll treat it with the caution it deserves - and I hope others will, too.

Anyway, your comments on every topic are always welcome!

 

[DR.D]

Dr. D - I'd love to hear your comments on such a cycle for aging men.

Actually, I'd love to learn more about endo/exo-hormone issues for guys like me (ie, "old" :blink: ), so if you have any links, please share 'em!

While I have you here, I'd like to thank you for pointing out the dangers of tamoxifen - I'll treat it with the caution it deserves - and I hope others will, too.

Anyway, your comments on every topic are always welcome!

Thank you for the vote of confidence BodyWizard! I have a few PubMed links that may intrest you concerning your questions. One of these points to the effectiveness of clomiphene in boosting test levels in men over 50.

http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=1755138
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=6781360
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=pubmed&dopt=Abstract&list_uids=3101546

The 25 days @ 25mg Clomid w/ a 5 day break and then repeating the cycle for 4 to 6 months looks like an intresting, low toxicity approach. I think one of these links even has a few positive points about Tamox. Feel free to PM anytime with specifics. I'll offer any info I have.

 

[Dwight Schrute]

Yes, but once the nolva is discontinued you will have high estrogen levels. The aromatase inhibitor will stop all estrogen production all together so I don't know how once could say nolva is better choice for this type of cycle. In all honesty, either way the estrogen will not be halted completely. Ergo has evidence that shows that 6-OXO raises test levels so why I fail to see how 6-OXO is not the best choice.

There is absoletly no proof of this whatsoever. In fact, its the opposite. 6-oxo showed to raise testosterone in normal men, no hypogonadic men. There is big difference.

6-oxo also raised estrone levels in his study.

 

[Dwight Schrute]

While I have you here, I'd like to thank you for pointing out the dangers of tamoxifen - I'll treat it with the caution it deserves - and I hope others will, too.

The cautions are a bit overblown.

 

[Dwight Schrute]

As I said in the other thread, the issue is hardly conclusive as to which is better.


Take your pick:


Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism.

Weinstein RL, Reitz RE.

Clinical Investigation Center, Naval Hospital, Oakland, USA.

An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.



OR:




Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

Tan RS, Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. [email protected]

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.


Tkae note that after the intial treatment, T levels dropped when Cloomid was disconitued. It rose again once treatment continued and leveld off after 2 months of use and then Clomid was dropped.

 

[Dwight Schrute]

This one too:

Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

Vermeulen A, Comhaire F.

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.

 

[Dwight Schrute]

The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men.

Adamopoulos DA, Vassilopoulos P, Kapolla N, Kontogeorgos L.

The effect of clomiphene citrate (CG) on sex hormone binding globulin (SHBG) was studied in 10 oligozoospermic patients with varicocele and 6 normospermic men. Plasma SHBG, testosterone (T), oestradiol (E2), FSH, LH, Prolactin (Prl), thyroxine (T4) and 17-OH-progesterone (17-OH-P) were determined before and during medication. SHBG concentration rose from 38.1 +/- 18.3 to 54.3 +/- 16.0 nmol/l (P less than 0.01), while T and E2 showed significant increases from 31.2 +/- 10.8 nmol/l and 24.6 +/- 5.4 pg/ml to 52.0 +/- 3.6 and 43.3 +/- 14.9, respectively in the oligozoospermic patients, with similar rises noted in the normospermic men. FSH, LH and 17-OH-P were markedly elevated while on CC, but Prl and T4 remained unchanged. The findings of this study indicated the CC causes an increase of SHBG concentration, which is probably related to the rise of E2 concentration. This SHBG change, combined with the intrinsic oestrogenic activity of CC might be one of the factors responsible, through a decrease of free T and a T to E2 imbalance, for the lack of significant effect on parameters of seminal quality in so treated patients.

 

[Rogue Drone]

So, if we believe that Toxo is both potentially effective for PCT and potentially toxic, is there a supplement protocol that could accompany Toxo's use and possibly negate this toxicity?

 

[Dwight Schrute]

What toxicity?



I posted this in the other thread.


Andrew James Parker
Dept. Biomedical Science,
University of Sheffield,
Sheffield, England
Updated May 25, 2000

Generic Name : Tamoxifen

USA Brand Name: Nolvadex (Zeneca Pharmaceuticals)

Other Proprietary Names: Dignatomoxi, Emblon, Fentamox, Istubol, Kessar, Mamofen, Noltam, Novofen, Oestrifen, Tamaxin, Tamifen, Tamoplex, Tamoxen, Valodex, Zitazonium

Classification: Antineoplastic; Antiestrogen

BT Dosage: 200mg/day (f) 240mg/day (m) [Adult] 60 -100mg/day [Children] Dosage depends on weight, tolerance and toxicity and varies according to individual circumstances. Always take in consultation with a physician.

Delivery: Oral tablet

Potential Side Effects: Hot flushes; Vaginal bleeding; Early onset menopause; GI distress; Vomiting; cataracts; Visual disturbances; Dizziness; thrombosis

Availability: This drug is routinely prescribed, inexpensive and should be readily available.

Abstract: The drug tamoxifen is most commonly associated with chemotherapy of breast cancer but has been used recently to treat other cancers including brain tumors. The mechanism of its action is complex involving several sites in and on cells. Current opinion suggests that its key role in malignant glioma is to inhibit a cell signaling enzyme called protein kinase C. It does this in a dose-dependent manner and consequently is administered at a much higher dose for brain tumor sufferers than is given to breast cancer patients. It has a low toxicity and its side effects are minimal. There is evidence to suggest that it should not be used in conjunction with the anti-epileptic (anticonvulsant) phenytoin. It has been used on its own and in conjunction with other drugs (adjuvant chemotherapy). Although tamoxifen does not improve all instances of brain tumor, there is considerable evidence that it is of benefit to many.A new non-invasive procedure may be able to detect those patients who will respond to tamoxifen.
TAMOXIFEN MINIREVIEW


The drug tamoxifen was synthesised in 1962 by scientists at ICI working on a contraceptive pill. Since it blocks the natural hormone estrogen (a steroid), it was classified as a nonsteroidal estrogen antagonist (8) . It has been used in the treatment of breast cancer for over 20 years (16) , although its efficacy has often been controversial (63) . Articles in the Lancet in the spring (3) and summer (61, 79) of 1998 respectively supported then refuted the value of tamoxifen with breast cancer. Later that year, the FDA approved tamoxifen citrate for reducing the incidence of breast cancer in women at high risk for developing the disease. In May 2000, an extensive study reported by Professor Sir Richard Peto has found convincingly in favor of tamoxifen, with the death rate falling by a third over ten years (54) . In addition to breast cancer, tamoxifen has been used to treat other cancers such as melanoma (30, 65) , hepatocellular carcinoma (73) , ovarian cancer (81) and prostate cancer (10) . This short review considers its application to cancer of the brain.

The action of tamoxifen is now known to operate at several sites in the cell (e.g. as a channel blocker : 2, 36, 74) and to affect numerous genes (40) but early studies concentrated on its action as an antihormone, specifically an antiestrogen (33, 67, 83) . Antiestrogenic mechanisms have been studied for around 40 years 83) but are still not fully understood. One known mechanism is that the tamoxifen molecule competes with the natural female hormone (estrogen) for binding sites on the surface of cells (46) . Estrogens are known to promote the growth of breast cancer cells, so if an antiestrogen such as tamoxifen blocks those sites, the effect of estrogen is diminished. Experiments have shown that tamoxifen blocks the effect of estradiol in cultures of astrocytes (31) , but are related to the type of estrogen receptor (ER) present (41) . Although tamoxifen has been found to be effective in decreasing brain tumor proliferation, whether this is mediated via the ER remains controversial, despite evidence of such mechanisms with a glioblastoma cell line (43) and in meningiomas (25) . Other studies have shown a specific cell cycle action of tamoxifen, mediated by mechanisms other than estrogen inhibition (66). There is also an important interaction between the ER and an enzyme called protein kinase C (35) .

Protein kinase C (PKC) denotes a group of enzymes that regulate functions such as cell growth and differentiation. It is known to be involved in a process called signal transduction. This is a messenger system, which transfers a signal arriving at the cell surface (e.g. hormone or neurotransmitter) into a cellular response. Protein kinase C has been implicated in glioma invasion (18, 77) and its role in malignant glioma growth and proliferation has been reviewed (5, 12, 27, 60) . Tamoxifen has been shown to block cell growth in brain tumor cell lines (26, 49, 68) and inhibits PKC (10, 47) . Proliferative signal transduction in glioma cells has been shown to occur through a predominantly PKC-dependent pathway (6, 7) . One isoform of PKC (isoform A) may be of particular importance (6, 18) . In addition to tamoxifen's action against PKC in adult high-grade gliomas, it has been shown to inhibit proliferation of cell lines derived from both low- and high-grade pediatric glial tumor (56) . A model cell system has been constructed for the screening and identification of PKC inhibitors potentially active against astrocytoma cells in culture (69, 70) .

As well as tamoxifen, a number of other PKC inhibitors have been shown to be effective in glioma inhibition. These include calphostin C (38, 59) and UCN-01 (57) .Another PKC inhibitor, hypericin (derived from the herb St John's Wort) has been used with tamoxifen for adjuvant chemotherapy of malignant glioma. In a study of seven human malignant glioma cell lines it was found that hypericin and tamoxifen induce apoptosis in a concentration and time-dependent manner (80) . In one patient, hypericin was able to replace tamoxifen's growth inhibition after loss of sensitivity to tamoxifen after a 22-month period (34, 55, 85) . One study on the action of tamoxifen on PKC activity in glioblastoma tissue found the inhibitory effect arrested the cell in the G (1) phase of the cell cycle. However, this action was observed to occur in a dose-dependent manner (22) and it is apparent that to be effective against gliomas tamoxifen has to be administered in a high dose.

The dose of tamoxifen used in the treatment of breast cancer is in the range 20-40 mg/day. However, since it has been shown that tamoxifen inhibits PKC in a dose dependent manner (22, 39, 80) , investigators have used higher doses to treat brain tumors. A key worker in this area is William Couldwell who, in a pioneering study (21) , first gave tamoxifen in antiestrogen doses (40mg/day) to monitor possible side effects in a cohort of malignant glioma patients. Provided no adverse reactions were observed dosage was then increased to 160mg (female) and 200mg/day (male). A positive response was obtained with a minority of patients (3 out of 11). A later study using the same dosage also found a subgroup of patients responding or stabilizing with high-dose tamoxifen. (23) .

In a study using doses graded between 40, 80 and 120mg/day, it was found that the patients receiving the higher doses demonstrated a longer median survival (51) . One study using 240mg/m (2) observed a variation in tamoxifen metabolic profile (29) . If there is a variation in how individuals metabolize this drug this may partially explain the variation in response to tamoxifen. However at that same dosage [240mg/m (2) ] another group found that symptoms of neurotoxicity occurred when tamoxifen was given in conjunction with interferon alpha-2a (17) .

In childhood glioma (45) , tamoxifen has been shown to produce tumor reduction and halting of tumor progression (9) . Pollack et al (58) found stabilization in 4 of 14 patients previously exhibiting progressive disease. One group had received 60mg/m (2) and a second group 100mg/m (2) daily. This study concluded that tamoxifen's low toxicity and easy administration; its proven effectiveness with some patients merited further study. Furthermore it was suggested that in patients with malignant gliomas, tamoxifen could potentate the effects of conventional chemothrapeutic agents.

A drug is said to have a synergistic effect when its action in combination with another drug is greater than the action of the two drugs administered separately - a "gestalt" pharmacology. There is considerable support for this effect with tamoxifen. Experiments on a human glioblastoma cell line (39) found that tamoxifen or tumor necrosis factor alpha could each inhibit proliferation in a dose-dependent manner. However, when given together the inhibitory action was greater than either agent alone. It has also been shown to improve quality of life when used in conjunction with procarbazine (11) and hypericin (86) . Similarly, the antiestrogenic action of tamoxifen is potentiated by bepridil - a sodium-calcium exchange blocker - in experiments on human astrocytoma and neuroblastoma cells (42) . Synergism has also been reported with radiotherapy (13, 26, 28, 50) .

Not all of tamoxifen's interactions are beneficial. There is evidence to support an adverse reaction with phenytoin (32, 64) and care should be exercised if tamoxifen is being considered for patients receiving this anti-convulsant. One report suggests that it may protect glioma cells from the action of cytotoxins (72) . A study reporting risk of thrombosis with tamoxifen (71) requires examination. Out of 4095 patients, 21 incidences of thrombosis were observed (0.5%), only one of these cases occurred with a brain cancer sufferer. The age range was 29 - 75 years and no evidence is presented as to whether the reported incidence exceeds that of a normal population not receiving chemotherapy.

Tamoxifen is generally considered to be of low toxicity (14, 82) but some workers have expressed doubts as to whether tamoxifen may be carcinogenic (4, 75) . However, such evidence is less substantial than that for its beneficial effects and indeed many malignant brain tumor sufferers would consider a "long term " risk in a positive way. In terms of proven carcinogenicity, tamoxifen is considerably less harmful than many other chemothrapeutic agents (15) .

As the number of trials and treatments of brain tumors with tamoxifen increases, so do the analyses and statistical analyses of such protocols (20, 37, 48, 84) . A review of treatment of high-grade astrocytomas by all treatments (37) found in favor of the nitrosoureas and platinums in the treatment of this type of tumor but also highlights the many problems associated with such group comparisons. How are patients selected for treatment and inclusion in the study? Do they receive the same dose - for the same period, and are they stratified by histology? Because these surveys are derived from individual patients and each patient will have received the physician's best treatment it is impossible to determine a standard treatment, only overall trends. If there is a subset of patients who are particularly susceptible to one chemotherapy, their positive response may be diluted by many that are not. The laws of statistics forbid a researcher from subjective selection of sample.

Long term survival with tamoxifen has been reported with a woman who developed a solitary brain metastasis following cancer of the breast. Following surgery and radiotherapy, this patient received tamoxifen and is generally well 10 years after brain metastases (53) . A positive response to tamoxifen has been observed with other metastatic brain tumors (44, 78) . Indeed the point is made that tamoxifen offers the benefit of treating both the primary (extracranial) and secondary (intracranial) tumors (44) . A detailed report of long term survival with primary brain tumor and tamoxifen awaits collation and analysis (52)

In summary, the evidence for tamoxifen in chemotherapy of brain tumor, although by no means proven, is more than encouraging. As with many experimental chemotherapies, there is often more promise shown with in vitro tissue culture studies than are delivered in clinical trials. There are many reasons for such a difference in response (76) . It would seem that this drug is effective with a minority of malignant glioma sufferers (21, 23) . The reason for this may be attributable to individual variations in tamoxifen metabolism (29) or it may point to variations in brain tumor pathology or metabolism yet to be clarified. Use of screening assays to predict the action of tamoxifen (1, 69, 70) may give insights into variations amongst gliomas and their susceptibility to this agent. Even more promising is the use of proton magnetic resonance spectroscopic imaging to predict how malignant gliomas will react to tamoxifen chemotherapy (62) . This paper suggests that it is possible to accurately predict the response of the tumor to tamoxifen on the basis of noninvasively acquired in vivo biochemical information. Certainly tamoxifen's low toxicity (71, 82) and minimal side effects coupled with its ready availability and low cost, present strong arguments for its application. It may be given alone (53, 69) or in combination with other agents (39, 42, 80) which enhances its action. It has also shown promise in conjunction with other techniques such as stereotactic radiosurgery (24) and radiotherapy (26, 28)

The potential benefits of tamoxifen clearly outweigh possible deleterious effects in brain tumor patients. It may only achieve a positive effect in a minority of patients but that fortunate group should not be denied the benefit simply because the drug does not improve survival for all brain tumor sufferers. The very fact that its action may take a considerable time to be manifest (19) will be good news to many. Indeed, the reasons underlying tamoxifen's variability may well indicate further avenues of research and treatment and broaden our understanding of this pernicious disease.

 

[Rogue Drone]

Dr.d Opinioned on the Nolva-Clomid Thread

" It's well established just how toxic this stuff is. Thromboembolic issues are of primary concern, and your more likely to have a stroke the longer you use it. Ocular degeneration and retinopathy are also a problem. As are an increased association with need for cataract removal surgery in people who use it. Tamox also induces multinucleated giant cells and germinal epithelial sloughing in a dose-dependent manner and these changes are detrimental to male fertility. Ever notice libido issues on Tamox? As for the liver, memangiosarcoma, adenoma, fatty liver, and carcimona are long term effects that show up years after use. Desmosterol levels are also elevated showing direct interference with cholesterol biosynthesis. That may sound good but it's really not"

Me, I'm like The CIA, I can't confirm or deny said statement.

Bobo, got any Toxo studies on the effect of multiple use by healthy males?; that I've never seen, doubt they exist.

 

[Dwight Schrute]

About Toxicity:


ABSTRACT: Toxicity of Antiestrogens

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.

 

[Dwight Schrute]

Dr.d Opinioned on the Nolva-Clomid Thread

" It's well established just how toxic this stuff is. Thromboembolic issues are of primary concern, and your more likely to have a stroke the longer you use it. Ocular degeneration and retinopathy are also a problem. As are an increased association with need for cataract removal surgery in people who use it. Tamox also induces multinucleated giant cells and germinal epithelial sloughing in a dose-dependent manner and these changes are detrimental to male fertility. Ever notice libido issues on Tamox? As for the liver, memangiosarcoma, adenoma, fatty liver, and carcimona are long term effects that show up years after use. Desmosterol levels are also elevated showing direct interference with cholesterol biosynthesis. That may sound good but it's really not"

Me, I'm like The CIA, I can't confirm or deny said statement.

They labeled it a class 1 carcinogen. The same as cigarette smoke.

All those above could be said about a host of things after years of prolonged use. So my advice, don't take Nolvadex at high doses for years at a time.

For 3 weeks, you're fine.

 

[N4cer]

Isn't 6OXO just formestane? Or is it chrysin?

And I don't know the facts of it, but it makes sense that if using an AI to reduce circulatory estrogen levels via inhibition of aromatase enzyme activity, you will have slightly increased test levels for a period of time.

But we all know that if the body recognizes an abundance of testosterone, it compensates - usually in 2-3 weeks.

Would this compensation occur via over-production of SHBG, or would it be from decreased test production due to negative feedback?

 

[Dwight Schrute]

Isn't 6OXO just formestane? Or is it chrysin?

And I don't know the facts of it, but it makes sense that if using an AI to reduce circulatory estrogen levels via inhibition of aromatase enzyme activity, you will have slightly increased test levels for a period of time.

But we all know that if the body recognizes an abundance of testosterone, it compensates - usually in 2-3 weeks.

Would this compensation occur via over-production of SHBG, or would it be from decreased test production due to negative feedback?

1. No. They are completely different substances.

2. IT will help raise testosterone in normal men, but that is different from increasing testosterone in a hypogonadic man. The literature just isn't there. Its mostly theory (but I agree it probably works)

3. As for how, even Pat doens't fully understand.

 

[Rogue Drone]

Ergo/Proviant's 6-oxo is Androst-4-ene-3,6,17-trione, neither of those two. It's a forgotten AI from the 80's that Pat Arnold rediscovered.

The Ergopharm site has a .pdf on their limited study of 6-oxo's effects on Endocrine values, run on six nonanabolic using subjects at 300mgs twice a day.

Pat Arnold says they are planning a more indepth one in the near future.

 

[Dwight Schrute]

Its acually more of a suicide inhibitor.

 

[N4cer]

So Bobo, we agree that use of an AI to increase circulatory test would be short-lived in effectiveness, as the body will soon compensate?

 

[Dwight Schrute]

Not while still using the AI. But when you stop, the rebound could be severe. Hormones tend to rise above normal after they have been suppressed for a while before returning to normal. Testosterone has been shown to do this. I see no reason to use an AI during PCT anyway.

Plus lowering estrogen to subphysiological levels isn't healthy anyway,

 

[Dwight Schrute]

And using Nolva and Letro together isn't wise either.

Drug and hormone interactions of aromatase inhibitors.

Dowsett M.

Academic Department of Biochemistry, The Royal Marsden NHS Trust, London, UK.

The clinical development of aromatase inhibitors has been largely confined to postmenopausal breast cancer patients and strongly guided by pharmacological data. Comparative oestrogen suppression has been helpful in circumstances in which at least one of the comparitors has caused substantially non-maximal aromatase inhibition. However, the triazole inhibitors, letrozole and anastrozole, and the steroidal inhibitor, exemestane, all cause >95% inhibition. Comparisons between these drugs therefore require more sensitive approaches such as the direct measurement of enzyme activity by isotopic means. None of these three agents has significant effects on other endocrine pathways at its clinically applied doses.p Pharmacokinetic analyses of the combination of tamoxifen and letrozole have revealed that these drugs interact, resulting in letrozole concentrations approximately 35-40% lower than when letrozole is used alone.

 

[Rogue Drone]

True dat, I incorrectly use the term AI for this basic class of substances.

FWIW, I'll add my thumbs up to many positive feedback reports on it's effectiveness for PCT, but like almost every other supporter, I don't have blood values to support this belief, just a subjective impression that it works.

Problem with all these products(SERMs and AI) is that there is very little testing data avaliable on generally healthy male gearheads, word of mouth and female cancer patient studies is all that's avaliable.

 

[Dwight Schrute]

Well the problem is that LH returns very fast regardless of what you use (even nothing). The key is to increase the response of Leydig cells to LH pulses. This is why HCG is golden during a cycle.

 

[Lakevillethor]

As I said in the other thread, the issue is hardly conclusive as to which is better.


Take your pick:


Pituitary-testicular responsiveness in male hypogonadotropic hypogonadism.

Weinstein RL, Reitz RE.

Clinical Investigation Center, Naval Hospital, Oakland, USA.

An isolated deficiency of pituitary gonadotropins was demonstrated in six 46 XY males, 22 to 36 years of age, with and without anosmia. Undetectable or low levels of serum follicle-stimulating hormone (FSH) and luteinizing hormone (LH) clearly separated hypogonadotropic from normal adult males. Chronic (8-12 wk) administration of clomiphene citrate caused no increase in serum FSH or LH in gonadotropin-deficient subjects. However, the administration of synthetic luteinizing hormone releasing factor (LRF) resulted in the appearance of serum LH and, to a lesser degree, serum FSH in three subjects tested. While levels of plasma testosterone were significantly lower in gonadotropin-deficient subjects, plasma androstenedione and dehydroepiandrosterone were in a range similar to that of age-matched normal men. Treatment with human chorionic gonadotropin (HCG) increased levels of plasma testosterone to normal adult male values in all gonadotropin-deficient subjects. Cessation of treatment with HCG resulted in the return of plasma testosterone to low, pretreatment levels. That HCG therapy with resultant normal levels of plasma testosterone may somehow stimulate endogenous gonadotropin secretion in gonadotropin-deficient subjects was not evident. The adult male levels of serum FSH and LH after LRF, and plasma testosterone after HCG, confirm pituitary and Leydig cell responsiveness in these subjects.



OR:




Use of clomiphene citrate to reverse premature andropause secondary to steroid abuse.

Tan RS, Vasudevan D.

Department of Family and Community Medicine, University of Texas Health Sciences Center, Houston, Texas 77030, USA. [email protected]

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.


Tkae note that after the intial treatment, T levels dropped when Cloomid was disconitued. It rose again once treatment continued and leveld off after 2 months of use and then Clomid was dropped.

I am quite aware of the difference. And I also pointed out the increased estrone level to PA and he said that it was something else registering as estrone in the study. Was he spewing bullshit? Probably. However, I can say that from my own real world results, that 6-OXO works the best for me post cycle --- it seems as though I keep gaining when I use it --- However, I am also very sensitive to orals in general so perhaps this is why. While his study was conducted with normal men, the biochemistry would essentially be the same for raising test levels with men with temporary test shut down. It is known that clomid raises test in normal men as well? Additionally, in your study posted above, you even displayed that clomid did not work in men with hypogonadotropic hypogonadism --- however, it does work with men with temporary shut down. What I am getting at is this: 6-OXO ultimately works on the same mechanism as clomid/nolva to raise test levels. They both shut down estrogen (via different mechanisms but both do it), which leads to a increased testosterone output. Isn't it a stretch to say that 6-OXO doesn't work?

Additionally people that continually post pub med studies to back up everything they say annoys me. As an engineer myself, I also have to take the facts into consideration before making a conclusion about almost everything I do -- this is a given -- and, to some extent, I can appreciate a good pub med study here and there. The difference is though, in my field, things are known --- we don't deal with the human body where new things are being discovered daily. There is so much that is still unknown about all of the things that pertain to bodybuilding and all the pubmed studies don't really mean **** --- maybe 6-OXO is working on a seperate mechinam that isn't even known yet-- maybe it hinders myostatin temporarily, maybe it boosts IGF-1 levels, etc? My point is that there is so much going on that the pubmed studies do not indicate that it is almost better to take real world results than the data supplied in those studies. 20 years from now, many of these folks will look back and laugh at what they thought of as "fact" in this day and age. I know that I am not alone in this thinking too as the doctors at The Mayo Clinic even prescribe my mother (a cancer patient) things that seem to work on people although they have no conclusive data. Just my $.02

 

[Brodus]

Three questions:

1. As far as I can tell, the only way to administer HCG is through injection, correct?

2. I don't see how the studies don't help-->whatever the mechanism is, what matters is the increase in Test/LH repsonse post-cycle right? Isn't this data quite clear in the studies?

3. The fact that Nolva is the only one of the antiestrogen to be classified as a carcinogen is bothersome. Based on this board, I've been a Nolva user for the past three cycles, but now I'm having second thoughts. Don't you think exposing yourself to a Class 1 carcinogen is a bad idea, if alternatives exist? LIke 6-OXO?

 

[Lakevillethor]

Three questions:

1. As far as I can tell, the only way to administer HCG is through injection, correct?

2. I don't see how the studies don't help-->whatever the mechanism is, what matters is the increase in Test/LH repsonse post-cycle right? Isn't this data quite clear in the studies?

3. The fact that Nolva is the only one of the antiestrogen to be classified as a carcinogen is bothersome. Based on this board, I've been a Nolva user for the past three cycles, but now I'm having second thoughts. Don't you think exposing yourself to a Class 1 carcinogen is a bad idea, if alternatives exist? LIke 6-OXO?

This is the type of thing I am talking about -- I was not aware that it seriously was a carcinogen -- I have heard this mentioned before but I thought it was in jest. And let me say that the studies do help -- I just do not view them as the "end all" solution as many do. Who knows though -- maybe 6-OXO is a carinogen too? My point was there are are SO many unknowns that using only pub med studies to influence all the decisions you make is foolish; yes they have their place, but I don't live my life by pub med.

 

[Brodus]

Well, I'm glad I know its a carcinogen now, thanks to PubMed!

Anyone have an answer to my first question? Isn't there a research chem site that sells HCG powder? (yes/no or a PM, not fishing for sources here)

 

[Brodus]

Even Australia's conservative National Health and Medical Research Council (NHMRC) warned that no amount of tamoxifen is safe when it comes to carcinogenic effects. </B>
In California there is a law called "Proposition 65" that requires the state to publish and maintain a list of all known carcinogens. In May 1995, the state's Carcinogen Identification Committee voted unanimously to add tamoxifen to its list.</B>

[font=sans-serif, helvetica, Times New Roman, Times]Following suit, in 1996 the World Health Organization formally designated tamoxifen a human carcinogen, grouping it with 70 other chemicals — about one quarter of them pharmaceuticals — that have received this dubious distinction. </B>[/font]

Tamoxifen is toxic to the liver, and there have been reports of acute hepatitis in patients treated with tamoxifen. Liver damage has occurred in every animal given tamoxifen. According to Gary Williams, medical director of the American Heart Foundation, tamoxifen has been shown in animal studies to be a "rip-roaring" liver carcinogen, inducing highly aggressive cancers in about 12 per cent of rats.

http://www.all-natural.com/tamox.html

 

[Lakevillethor]

Even Australia's conservative National Health and Medical Research Council (NHMRC) warned that no amount of tamoxifen is safe when it comes to carcinogenic effects. </B>
In California there is a law called "Proposition 65" that requires the state to publish and maintain a list of all known carcinogens. In May 1995, the state's Carcinogen Identification Committee voted unanimously to add tamoxifen to its list.</B>

[font=sans-serif, helvetica, Times New Roman, Times]Following suit, in 1996 the World Health Organization formally designated tamoxifen a human carcinogen, grouping it with 70 other chemicals — about one quarter of them pharmaceuticals — that have received this dubious distinction. </B>[/font]

Tamoxifen is toxic to the liver, and there have been reports of acute hepatitis in patients treated with tamoxifen. Liver damage has occurred in every animal given tamoxifen. According to Gary Williams, medical director of the American Heart Foundation, tamoxifen has been shown in animal studies to be a "rip-roaring" liver carcinogen, inducing highly aggressive cancers in about 12 per cent of rats.

http://www.all-natural.com/tamox.html

Probably will never use it again.

-AT

 

[The Rob]

This one too:

Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men.

Vermeulen A, Comhaire F.

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.

can someone layman that for me plz?

 

[wastedwhiteboy2]

can someone layman that for me plz?

I'll give this a try. nolva will increase natural test and so will a larger amount of clomid. nolva increases sensitivity while clomid decreases sensitivity. which means you build up a tolerance to clomid and the opposite with nolva. this is not exactly correct but gives you the idea. does this sound close guys?

 

[PumpingBricks70]

Probably will never use it again.

-AT

What do you plan on using? :blink: