Coming off a cycle Need urgent advice

Right, next week will be my last shots of test cypionate. I have been doing a 10 weeks cycle of 700 mgs of test cypionate weekly. In addition i have been taking 1 tab of propecia daily plus half a tab adex daily.

My problem is now i dont have HCG and as I am in Zambia at the moment i cannot get any gear here etc. I have loads of nolvadex and clomid though.

DJ did you manage to speak to conan or doc about that propecia and pct thing. At the moment im looking mean ive put on over 10 kgs of lean muscle and my power is off the roof there is hardly any water and i have not had one hair fall out. My nuts have shrinked quite badly though which is worrying me for recovery now. Im not sure if i should stop finasteride 2 weeks after my last cyp shot or should i go into PCT with it. Also maybe start cutting tabs in half and taper it down? Since i dont have HCG will the standard PCT protocol still go? Anyone has any advice to give?

The only advice I can give is use the clomid and nolva and see what happens, I doubt it will bring your balls back though. you might need to do an extended PCT when you get back.

DHT is a vital part of your bodys balance so I would stop the fina a week into the PCT that way you should be safe with conversion and shouldn't experience any hair loss. I wouldn't go further into the PCT as I'm unsure of how it would affect you and don't see a point to be honest.

00pump wrote:

The only advice I can give is use the clomid and nolva and see what happens, I doubt it will bring your balls back though. you might need to do an extended PCT when you get back.

DHT is a vital part of your bodys balance so I would stop the fina a week into the PCT that way you should be safe with conversion and shouldn't experience any hair loss. I wouldn't go further into the PCT as I'm unsure of how it would affect you and don't see a point to be honest.

thats what worries me too. I knew that i wont have hcg for this cycle but i was told that since im doing pure test cycle that nolva and clomid should do the trick. Do i follow a standard docs pct protocol without hcg or should i increase nolva and clomid dosages? Anybody tried to come off without hcg from test cycle? Any feedback ?

Not much point in going higher than 40 tamoxifen and 100 clomiphene if running simultaneously in my opinion. To be cautious I would run it at 20mg and 50mg during two weeks after your lst shot, then bump up to 40 and 100/150 for two weeks, then back back down to maintainance dose of 20 tamoxifen (and 50 for as long as clomiphene lasts) for at least four.

SERMs can be used alone in PCT but I have never used them alone in PCT following dosages over 500mg a week.

they can... that is true... and its very possible it could sort you out.. but normally when i'm very shut down it does take HCG to kick things back in...

I feel you shouldn't worry about stuff now as it would be pointless... rather just do your PCT and lets see how things go... if you cant get HCG you can't get it... so don't stress about things out of your control...

sweeet!

well i was planning on stopping adex 2 weeks after the last cyp shot and then starting nolva with clomid. So should i run adex and nolva simutaneously? So you think i should start nolva and clomid immediately after my last shot of cyp at 20 mgs nolva and 50 mgs clomid? Wont the cyp still be in my system?

No use Nolva/Clomid 2 weeks after last shot, run the adex up to the start of the PCT.

I usually start while the esters are clearing to build up drug stable drug levels for when the test is gone. I suppose using A-dex will help to bridge this time anyways and SERMs don't take that long to build up so its a personal choice.

Inja wrote:

Not much point in going higher than 40 tamoxifen and 100 clomiphene if running simultaneously in my opinion. To be cautious I would run it at 20mg and 50mg during two weeks after your lst shot, then bump up to 40 and 100/150 for two weeks, then back back down to maintainance dose of 20 tamoxifen (and 50 for as long as clomiphene lasts) for at least four.

SERMs can be used alone in PCT but I have never used them alone in PCT following dosages over 500mg a week.

so u reckon i should do 2 months of clomid/nolva?

2 months, if you starting from directly after your last shot... you can do this to get stable plazma levels allot sooner.

just remeber clomid/nolva are harsh on your liver, hence very toxic... make sure you keep yourself same with SAMe or Milk Thistle.

This is all you can pretty much do for now... if this doesn't resolve it I doubt extending the SERM's any longer will help at all. You will then need when coming back to ZA get some HCG and follow that up with a SERM again.

But you could be lucky.. as I said when I was younger I never needed HCG, but from 25 upward I did...

What he said

its not like i can do anything about it now well we will find out soon if it worked or not

After a lot of reading on other forums(since not too many ppl here actually speak from experience) ive noticed that a LOT of so called "vets" recommend usage of clomid ON cycle as well as in PCT to maintain nut size. Ofcourse this is a case when HCG is not available but seems highly interesting to me right now. I think im gonna take your advice inja and begin clomid and nolvadex during the cycle and ill start clomid one week before the last shot of cyp even. Got nothing to lose actually.

Also been reading some studies where its said that subjects taking a dex at 1 mg a day have had their estrogen conversion suppressed above 50 % and had their free test levels increase by 68%. Same estrogen conversion block has been seen on subjects taking 0.5 of adex ED but not significant test lvl increase has been shown on this dosage. Wonder if i should carry on with adex at 1mg ED during the PCT as well. :hmm

You can use a SERM on cycle to help with size maintainance but only if you cant get HCG. Remember with extended SERM use comes extended risk of cancer, liver stress, etc...
You can run the Adex into PCT but ensure you run a few weeks after SERM after stopping the Adex.

Inja wrote:

You can use a SERM on cycle to help with size maintainance but only if you cant get HCG. Remember with extended SERM use comes extended risk of cancer, liver stress, etc...
You can run the Adex into PCT but ensure you run a few weeks after SERM after stopping the Adex.

wait wait arent SERMS used to treat cancer etc. Isnt clomid and nolva used over months periods clinically? Now you starting to scare me

while tamoxifen helps aid in breast cancer is has been shown to cause other cancers aswell as blood clots, etc...

it has also been shown to cause cancer of the uterus and endometrial cancer.

its a highly scheduled drug not to be taken lightly...

00pump wrote:

while tamoxifen helps aid in breast cancer is has been shown to cause other cancers aswell as blood clots, etc...

it has also been shown to cause cancer of the uterus and endometrial cancer.

its a highly scheduled drug not to be taken lightly...

You saying that there is actualy evidence tamoxifen causes cancer? hmmm. Also is not used for prostate cancer treatments in males over a 6 month period. Toxicity of tamoxifen is there i fully agree but its nowehre near as toxic and dangerous for the liver as dbols or anapolon. Never the less i wont go over 45 days with it. Clomid is relatively safe for usage am i not right?

jeah, their is evidence that is causes other types of cancer... only the 2 stated above that i'm aware of and the blood clots, mainly in woman though..

here is a copy / paste that might be usefull

The use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs), has gradually become well established in the steroid using community. The popular push of these drugs has almost made them mandatory. They have essentially become hormonal vitamins – vitamins that can do no wrong and provide seemingly endless benefits of testosterone support, bloat reduction, gynecomastia prevention and cholesterol health. It seems that we are all well educated about the benefits of Clomid and Nolvadex, so in this segment, I will present the risks and consequences from the short and long term use of Clomid and Nolvadex.

...

For example, tamoxifen was generally accepted as being non-toxic to human liver upon the conclusion that tamoxifen did not cause noticeable DNA adducts (damage) during short-term ex vivo studies with human liver cells.35,36 This was in contrast to the in vivo animal studies showing dramatic carcinogenic effects on the liver.30-34,41 As scientists learned that the toxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen, 4-hydroxytamoxifen and N-desmethyltamoxifen metabolites. It became apparent that ex vivo research was largely flawed due to low-rate metabolism.21 The carcinogenic effects of tamoxifen proved to be even more unusual and elusive, when it was hypothesized that tamoxifen had both genomic and non-genomic toxicity, which affecting different animals, in different organs.21 This created an obvious clinical challenge for measuring genotoxicity in a test tube. Eventually, it was established that tamoxifen was a bona-fide carcinogen in all species, at least in one way or another.21,37-39 Recent human studies have shown tamoxifen treated women to have 3x the risk of developing fatty liver disease, which appeared as soon as 3 months into therapy at only 20mg/day.24-26 In some cases, the disease lasted up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy showed cases of deadly hepatocellular carcinoma.27-29 In a 2000 case study involving tamoxifen induced liver disease, D.F Moffat et al made a profound statement –


"In addition, hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast."

In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as a metastasis infection from the breast cancer itself.28 Upon closer examination it was found that the cancerous lesions in the livers of the long-term tamoxifen therapy case studies were identical to those seen in the early animal studies showing tamoxifen to be a potent hepatotoxin.28-34 Although the effects took much longer to manifest, it became obvious that tamoxifen was toxic to the human liver.

...

When we bring our attention to Clomid, we find less research is available on long term human toxicity, probably because of the relatively short term (3-4 week) clinical application for ovarian stimulation,59 although long term follow ups with patients who received Clomid for ovulation induction have shown an increased risk of developing uterine cancer.74 This is to be expected, since many of the same carcinogenic tendencies found with tamoxifen are the same effects seen with clomiphene.44,45,57,58 Upon analysis of anecdotal reports from Clomid and nolva users, we see the typical short term side effects of low libido, erectile dysfunction, and emotional instability – despite many men showing normalized testosterone and estrogen levels during the use of these SERM’s. Research on male breast cancer patients also shows frequent reports of low libido, thrombosis (arterial blockage), and hot flashes with tamoxifen use.47 Another common side effect associated with both SERMs, but more common with Clomid, is the loss of visual accuracy and development of visual "tracers", due to the ocular toxicity.46

As the medical community became more aware of the side-effects associated with clomiphene and tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is an analog of tamoxifen, so it also carries many of the related genotoxic effects.48,49 Raloxifene appears to be even safer by being the least liver toxic, and not having any potential issue with the uterus or prostate.50-52 Unfortunately, raloxifene has been associated with a higher incidence of thromboembolism52 (arterial blockage), and also has very low oral absorption, making it an expensive alternative at a typical 120mg/day dose.53 Still, raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects.53 Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further.

...

21. Understanding the genotoxicity of tamoxifen?
David H. Phillips
Carcinogenesis, Jun 2001; 22: 839 - 849.

22. A randomized clinical trial evaluating tamoxifen in the treatment of patients with node-negative breast cancer who have estrogen-receptor-positive tumors
B Fisher, J Costantino, C Redmond, R Poisson, D Bowman, J Couture, NV Dimitrov, N Wolmark, DL Wickerham, ER Fisher, and et al.
N. Engl. J. Med., Feb 1989; 320: 479 - 484

23. Tamoxifen treatment and its consequences
Adrian Shulman, Ilan Cohen, Ron Maymon, and Marco M. Altaras
Hum. Reprod., Aug 1995; 10: 2174 - 2175

24. Tamoxifen induced hepatotoxicity in breast cancer patients with pre-existing liver steatosis: the role of glucose intolerance.
Elefsiniotis et al.
European Journal of Gastroenterology and Hepatology 2004;16:593-598.

25. Incidence and risk factors for non-alcoholic steatohepatitis: prospective study of 5408 women enrolled in Italian tamoxifen chemoprevention trial
Savino Bruno el al.
BMJ 2005;330;932-; originally published online 3 Mar 2005;

26. Fatty liver and transaminase changes with adjuvant tamoxifen therapy.
Liu, Chien-Liang a c; Huang, Jon-Kway b; Cheng, Shih-Ping a
Anti-Cancer Drugs. 17(6):709-713, July 2006

27. The association between tamoxifen and the development of hepatocellular carcinoma: case report and literature review.
Law CH, Tandan VR.
Can J Surg 1999;42:211-4.

28. Hepatocellular carcinoma after long-term tamoxifen therapy
D. F. Moffat, K. A. Oien, J. Dickson, T. Habeshaw and D. R. McLellan
Volume 11, Number 9 / September, 2000

29. Tamoxifen-associated hepatocellular damage and agranulocytosis.
Ching,C.K., Smith,P.G. and Long,R.G. (1992)
Lancet, 339, 940.

30. Tamoxifen induces hepatocellular carcinoma in rat liver: a 1-year study with two antiestrogens.
Hirsimaki P, Hirsimaki Y, Nieminen L, et al.
Arch Toxicol. 1993; 67: 49–4

31. Epigenetic reprogramming of liver cells in tamoxifen-induced rat hepatocarcinogenesis.
VP Tryndyak, O Kovalchuk, L Muskhelishvili, B Montgomery, R Rodriguez-Juarez, S Melnyk, SA Ross, FA Beland, and IP Pogribny
Mol Carcinog, Mar 2007; 46(3): 187-97

32. Antiestrogens and the formation of DNA damage in rats: a comparison.
Kim SY, Suzuki N, Laxmi YR, Umemoto A, Matsuda T, Shibutani S.
Chem Res Toxicol. 2006 Jun;19(6):852-8.

33. Activation of 4-hydroxytamoxifen and the tamoxifen derivative metabolite E by uterine peroxidase to form DNA adducts: Comparison with DNA adducts formed in the uterus of Sprague-Dawley rats treated with tamoxifen
Deena N. Pathak, Krisztina Pongracz, and William J. Bodell
Carcinogenesis, Sep 1996; 17: 1785 - 1790

45. Teratogenic effects of clomiphene, tamoxifen, and diethylstilbestrol on the developing human female genital tract.
GR Cunha, O Taguchi, R Namikawa, Y Nishizuka, and SJ Robboy
Hum Pathol, Nov 1987; 18(11): 1132-43.

46. Tamoxifen-associated eye disease. A review
SG Nayfield and MB Gorin
J. Clin. Oncol., Mar 1996; 14: 1018 - 1026.

47. Tamoxifen administration is associated with a high rate of treatment-limiting symptoms in male breast cancer patients.Anelli TF, Anelli A, Tran KN, Lebwohl DE, Borgen PI.
Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.

48. DNA adducts caused by tamoxifen and toremifene in human microsomal system and lymphocytes in vitro.
Hemminki,K., Widlak,P. and Hou,S.-M. (1995)
Carcinogenesis, 16, 1661–1664.

49. Major difference in the hepatocarcinogenicity and DNA adduct forming ability between toremifene and tamoxifen in female Crl:CD(BR) rats.
GC Hard, MJ Iatropoulos, K Jordan, L Radi, OP Kaltenberg, AR Imondi, and GM Williams
Cancer Res., Oct 1993; 53(19): 4534-41.

50. Selective estrogen receptor modulators: mechanism of action and clinical experience. Focus on raloxifene.
D Thiebaud and RJ Secrest
Reprod Fertil Dev, January 1, 2001; 13(4): 331-6.

51. Raloxifene, an oestrogen-receptor-beta-targeted therapy, inhibits androgen-independent prostate cancer growth: results from preclinical studies and a pilot phase II clinical trial.
RL Shazer, A Jain, AV Galkin, N Cinman, KN Nguyen, RB Natale, M Gross, L Green, LI Bender, S Holden, L Kaplan, and DB Agus
BJU Int, Apr 2006; 97(4): 691-7.

52. Review on raloxifene: profile of a selective estrogen receptor modulator.
M Heringa
Int J Clin Pharmacol Ther, August 1, 2003; 41(: 331-45.

53. Comparison of effects of the rise in serum testosterone by raloxifene and oral testosterone on serum insulin-like growth factor-1 and insulin-like growth factor binding protein-3.
EJ Duschek, LJ Gooren, and C Netelenbos
Maturitas, July 16, 2005; 51(3): 286-93.

Taken from www.muscleandscience.com/forum/showthread.php?t=397

The research is on-going.

00pump wrote:

jeah, their is evidence that is causes other types of cancer... only the 2 stated above that i'm aware of and the blood clots, mainly in woman though..

here is a copy / paste that might be usefull

The use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs), has gradually become well established in the steroid using community. The popular push of these drugs has almost made them mandatory. They have essentially become hormonal vitamins – vitamins that can do no wrong and provide seemingly endless benefits of testosterone support, bloat reduction, gynecomastia prevention and cholesterol health. It seems that we are all well educated about the benefits of Clomid and Nolvadex, so in this segment, I will present the risks and consequences from the short and long term use of Clomid and Nolvadex.

...

For example, tamoxifen was generally accepted as being non-toxic to human liver upon the conclusion that tamoxifen did not cause noticeable DNA adducts (damage) during short-term ex vivo studies with human liver cells.35,36 This was in contrast to the in vivo animal studies showing dramatic carcinogenic effects on the liver.30-34,41 As scientists learned that the toxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen, 4-hydroxytamoxifen and N-desmethyltamoxifen metabolites. It became apparent that ex vivo research was largely flawed due to low-rate metabolism.21 The carcinogenic effects of tamoxifen proved to be even more unusual and elusive, when it was hypothesized that tamoxifen had both genomic and non-genomic toxicity, which affecting different animals, in different organs.21 This created an obvious clinical challenge for measuring genotoxicity in a test tube. Eventually, it was established that tamoxifen was a bona-fide carcinogen in all species, at least in one way or another.21,37-39 Recent human studies have shown tamoxifen treated women to have 3x the risk of developing fatty liver disease, which appeared as soon as 3 months into therapy at only 20mg/day.24-26 In some cases, the disease lasted up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy showed cases of deadly hepatocellular carcinoma.27-29 In a 2000 case study involving tamoxifen induced liver disease, D.F Moffat et al made a profound statement –


"In addition, hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast."

In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as a metastasis infection from the breast cancer itself.28 Upon closer examination it was found that the cancerous lesions in the livers of the long-term tamoxifen therapy case studies were identical to those seen in the early animal studies showing tamoxifen to be a potent hepatotoxin.28-34 Although the effects took much longer to manifest, it became obvious that tamoxifen was toxic to the human liver.

...

When we bring our attention to Clomid, we find less research is available on long term human toxicity, probably because of the relatively short term (3-4 week) clinical application for ovarian stimulation,59 although long term follow ups with patients who received Clomid for ovulation induction have shown an increased risk of developing uterine cancer.74 This is to be expected, since many of the same carcinogenic tendencies found with tamoxifen are the same effects seen with clomiphene.44,45,57,58 Upon analysis of anecdotal reports from Clomid and nolva users, we see the typical short term side effects of low libido, erectile dysfunction, and emotional instability – despite many men showing normalized testosterone and estrogen levels during the use of these SERM’s. Research on male breast cancer patients also shows frequent reports of low libido, thrombosis (arterial blockage), and hot flashes with tamoxifen use.47 Another common side effect associated with both SERMs, but more common with Clomid, is the loss of visual accuracy and development of visual "tracers", due to the ocular toxicity.46

As the medical community became more aware of the side-effects associated with clomiphene and tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is an analog of tamoxifen, so it also carries many of the related genotoxic effects.48,49 Raloxifene appears to be even safer by being the least liver toxic, and not having any potential issue with the uterus or prostate.50-52 Unfortunately, raloxifene has been associated with a higher incidence of thromboembolism52 (arterial blockage), and also has very low oral absorption, making it an expensive alternative at a typical 120mg/day dose.53 Still, raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects.53 Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further.

...

21. Understanding the genotoxicity of tamoxifen?
David H. Phillips
Carcinogenesis, Jun 2001; 22: 839 - 849.

22. A randomized clinical trial evaluating tamoxifen in the treatment of patients with node-negative breast cancer who have estrogen-receptor-positive tumors
B Fisher, J Costantino, C Redmond, R Poisson, D Bowman, J Couture, NV Dimitrov, N Wolmark, DL Wickerham, ER Fisher, and et al.
N. Engl. J. Med., Feb 1989; 320: 479 - 484

23. Tamoxifen treatment and its consequences
Adrian Shulman, Ilan Cohen, Ron Maymon, and Marco M. Altaras
Hum. Reprod., Aug 1995; 10: 2174 - 2175

24. Tamoxifen induced hepatotoxicity in breast cancer patients with pre-existing liver steatosis: the role of glucose intolerance.
Elefsiniotis et al.
European Journal of Gastroenterology and Hepatology 2004;16:593-598.

25. Incidence and risk factors for non-alcoholic steatohepatitis: prospective study of 5408 women enrolled in Italian tamoxifen chemoprevention trial
Savino Bruno el al.
BMJ 2005;330;932-; originally published online 3 Mar 2005;

26. Fatty liver and transaminase changes with adjuvant tamoxifen therapy.
Liu, Chien-Liang a c; Huang, Jon-Kway b; Cheng, Shih-Ping a
Anti-Cancer Drugs. 17(6):709-713, July 2006

27. The association between tamoxifen and the development of hepatocellular carcinoma: case report and literature review.
Law CH, Tandan VR.
Can J Surg 1999;42:211-4.

28. Hepatocellular carcinoma after long-term tamoxifen therapy
D. F. Moffat, K. A. Oien, J. Dickson, T. Habeshaw and D. R. McLellan
Volume 11, Number 9 / September, 2000

29. Tamoxifen-associated hepatocellular damage and agranulocytosis.
Ching,C.K., Smith,P.G. and Long,R.G. (1992)
Lancet, 339, 940.

30. Tamoxifen induces hepatocellular carcinoma in rat liver: a 1-year study with two antiestrogens.
Hirsimaki P, Hirsimaki Y, Nieminen L, et al.
Arch Toxicol. 1993; 67: 49–4

31. Epigenetic reprogramming of liver cells in tamoxifen-induced rat hepatocarcinogenesis.
VP Tryndyak, O Kovalchuk, L Muskhelishvili, B Montgomery, R Rodriguez-Juarez, S Melnyk, SA Ross, FA Beland, and IP Pogribny
Mol Carcinog, Mar 2007; 46(3): 187-97

32. Antiestrogens and the formation of DNA damage in rats: a comparison.
Kim SY, Suzuki N, Laxmi YR, Umemoto A, Matsuda T, Shibutani S.
Chem Res Toxicol. 2006 Jun;19(6):852-8.

33. Activation of 4-hydroxytamoxifen and the tamoxifen derivative metabolite E by uterine peroxidase to form DNA adducts: Comparison with DNA adducts formed in the uterus of Sprague-Dawley rats treated with tamoxifen
Deena N. Pathak, Krisztina Pongracz, and William J. Bodell
Carcinogenesis, Sep 1996; 17: 1785 - 1790

45. Teratogenic effects of clomiphene, tamoxifen, and diethylstilbestrol on the developing human female genital tract.
GR Cunha, O Taguchi, R Namikawa, Y Nishizuka, and SJ Robboy
Hum Pathol, Nov 1987; 18(11): 1132-43.

46. Tamoxifen-associated eye disease. A review
SG Nayfield and MB Gorin
J. Clin. Oncol., Mar 1996; 14: 1018 - 1026.

47. Tamoxifen administration is associated with a high rate of treatment-limiting symptoms in male breast cancer patients.Anelli TF, Anelli A, Tran KN, Lebwohl DE, Borgen PI.
Department of Surgery, Memorial Sloan-Kettering Cancer Center, New York, New York 10021.

48. DNA adducts caused by tamoxifen and toremifene in human microsomal system and lymphocytes in vitro.
Hemminki,K., Widlak,P. and Hou,S.-M. (1995)
Carcinogenesis, 16, 1661–1664.

49. Major difference in the hepatocarcinogenicity and DNA adduct forming ability between toremifene and tamoxifen in female Crl:CD(BR) rats.
GC Hard, MJ Iatropoulos, K Jordan, L Radi, OP Kaltenberg, AR Imondi, and GM Williams
Cancer Res., Oct 1993; 53(19): 4534-41.

50. Selective estrogen receptor modulators: mechanism of action and clinical experience. Focus on raloxifene.
D Thiebaud and RJ Secrest
Reprod Fertil Dev, January 1, 2001; 13(4): 331-6.

51. Raloxifene, an oestrogen-receptor-beta-targeted therapy, inhibits androgen-independent prostate cancer growth: results from preclinical studies and a pilot phase II clinical trial.
RL Shazer, A Jain, AV Galkin, N Cinman, KN Nguyen, RB Natale, M Gross, L Green, LI Bender, S Holden, L Kaplan, and DB Agus
BJU Int, Apr 2006; 97(4): 691-7.

52. Review on raloxifene: profile of a selective estrogen receptor modulator.
M Heringa
Int J Clin Pharmacol Ther, August 1, 2003; 41(: 331-45.

53. Comparison of effects of the rise in serum testosterone by raloxifene and oral testosterone on serum insulin-like growth factor-1 and insulin-like growth factor binding protein-3.
EJ Duschek, LJ Gooren, and C Netelenbos
Maturitas, July 16, 2005; 51(3): 286-93.

Taken from www.muscleandscience.com/forum/showthread.php?t=397

The research is on-going.

well that majorly sucks. Always read that there was no evidence that gear is associated with cancer. But now we see that SERMs are which you have to take which means gear is very much associated with cancer then. Anyhow dont have much of a choice now

The endometrial cancer has nothing to do with male BBers as this is a direct result of the estrogen agonising activity of Tamoxifen.

But like I said above the main problem lies with the ability of tamoxifen (and clomiphene since they are almost structurally identical) to bind and thus alter DNA during replicative cycles. This binding and mutation can occur in genes that regulate the cell cycle, thus causing cancer.

There are two types of carcinogens, one is the initiator, that actually creates the potential for cancer by permanently altering potential cancerous genes, of cancer suppressing genes. Tamoxifen and clomiphene are both examples of this. The second it the promotor compound, that puts the cell into a carcinogenic state by altering its morphology. This promotes the activity of cancerous genes. Upon removal of the promoter the cell may return to normal unless altered by an initiator towards cancer. Cigarette smoke is an example of a promoter...

As Mr. Pumper posted the big problem is liver tumours because of the buildup of SERM metabolites increasing the cahnces that essential genomic regions are affected. Longer the use, the worse the risk. This has been known for a very long time guys...

Inja wrote:

The endometrial cancer has nothing to do with male BBers as this is a direct result of the estrogen agonising activity of Tamoxifen.

But like I said above the main problem lies with the ability of tamoxifen (and clomiphene since they are almost structurally identical) to bind and thus alter DNA during replicative cycles. This binding and mutation can occur in genes that regulate the cell cycle, thus causing cancer.

There are two types of carcinogens, one is the initiator, that actually creates the potential for cancer by permanently altering potential cancerous genes, of cancer suppressing genes. Tamoxifen and clomiphene are both examples of this. The second it the promotor compound, that puts the cell into a carcinogenic state by altering its morphology. This promotes the activity of cancerous genes. Upon removal of the promoter the cell may return to normal unless altered by an initiator towards cancer. Cigarette smoke is an example of a promoter...

As Mr. Pumper posted the big problem is liver tumours because of the buildup of SERM metabolites increasing the cahnces that essential genomic regions are affected. Longer the use, the worse the risk. This has been known for a very long time guys...

Well not much i can do there im gonna do 2 weeks of nolva straight after my last shot with clomid. and then 4 weeks after cyp is out.