Results 1 to 28 of 28
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05-08-2009, 02:13 PM #1
Starting Anavar Only Cycle at 40mgs?
6'4
250
20% BF
25 yrs old
Meal Plan for Today (Friday/just one piece of my diet):
10- 1 Whole Egg, 6 Egg Whites, 2 pieces of whole wheat toast, 12+ ounces of water
12- 8 Ounces of Grilled Chicken, 1 1/2 cups of Brocolli, 12+ ounces of water
2- 1 1/2 scoops of Max Pro Protein, with 1 cup of Fat free Milk, 1 tbsp of peanut butter
4- 1 Supreme Protein bar
4:30- NO Extreme Pre Workout Drink
5- 1 hour of lifting, 30 mins of cardio
6:30- 2 scoops of Matrix 5.0 with 1 cup of milk
7- 8 Ounces of (95% + lean) ground beef, 1 Full Artichoke, 1 full cucumber
9- 6 ounces of London Broil or 1 cup of Cottage Cheese
Now that we have the basic questions out of the way that EVERYONE asks, my question is, YES I am doing an Anavar only cycle and plan on taking it at 50mg ED and YES I know I am not at the 15% BF level everyone recomends. I was wondering if I should start the cycle straight out at 50 or start at 30 or 40 for the first few 3-4 days.
I have done one Anavar Only cycle about 2 years ago and started at 10 then to 20 then to 30 and felt that it was a complete waste, but it seems the Jury is still out on to start it straight at 50 or maybe at 40 if my main level will be 50mg a day. Also if anyone asks I will be taking all 50mgs in the morning because thats what has worked best for me.
So overall, start out at 40mg a day for the first 3 days or just go right with 50mg???
Thanks.........
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05-08-2009, 02:23 PM #2
waste of cash
Might as well go with Superdrol over Anavar if you are looking for gains. Only thing anavar is good for is probably briding between cycles IMO or as an addition to a cycle never a stand alone just for the shear fact that for the price you pay and the gains you get it isn't worth it.
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05-08-2009, 02:23 PM #3
Personally why not a test cycle of 500mgs ran for 10-12 weeks so you can bulk up a bit then cut yourself after awhile? If you are bend on using anavar then I see no reason as to pyramid it. Start right at 50mgs
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05-08-2009, 02:28 PM #4
I already have the Anavar , I prefer doing this Oral since the gains I saw last time were Tremendous with minimal side effects (lean muscle mass that is ~15lbs with a 30lb weight losss, especially the PITA trunk fat)
Thanks, I was thinking 50mg also from the start.
Also another question I had because everyone on here said you need some PCT for a anavar only cycle so I picked up some Clomid. But when talking to some guys local to me they said you dont need PCT since it doesnt shut you down and that the clomid may make me aromatize, any thoughts??
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05-08-2009, 02:35 PM #5
Anavar doesn't shut you down but it can suppress the HPTA by 30-40%, so a light PCT such as nolva or clomid dosed at 50/50/50/50 would be sufficent in opitimizing hormonal levels. As for clomid aromatizing, never heard that clomid it self is a SERM which means it selectivly blocks estrogen in certain parts of the body (namly the breast tissue) whle promoting the producting of LH and subsquent restart of the HPTA.
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05-08-2009, 02:46 PM #6
The one guy that said that doesn't even or have ever taken steroids but he was shooting the shit and I caught that because I thought the total opposite which is exactly what u said and I just didnt say anything without double checking.
So 50mg for a month for each day? I have the 50mg Clomid pills now, with a little extra surplus just incase i lost any god forbid when PCT came.......
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05-08-2009, 02:51 PM #7
Your HPTA is either shutdown (not producing ganadotropins) or inhibited (producing less ganadotropins).
Different AS will cause different effects to the HPTA.
And Clomid does not aromatize. Id use both Nolva and Clomid for PCT for about 4 weeks.
Clomid - 100/50/50/50
Nolva - 20/20/20/20Last edited by WARMachine; 05-08-2009 at 02:55 PM.
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05-08-2009, 02:57 PM #8
Why did you quote me and repeat basically everything I said
And Nolva/Clomid for anavar only at 50mgs is excessive IMO, and if you choose to go that route no need to have 100mgs the first week, the difference between 100mgs and 50mgs of clomid ED is negigible when taking into account the effect of anavar on the HPTA. At normal human dosages all anavar do is suppress the HPTA not shut it down, it is not that strong.
And both nolva and clomid block estrogen receptors, but both is not needed. Nolva is superior mg to mg so nolva at 20/20/20/20 is enough. But since he had clomid already I said that clomid could work. Look Superdrol is far more suppresive on the HPTA and can cause near shutdown in as little as a week and the standard PCT for Superdrol is 20/20/20/20 (nolva) OR clomid 50/50/50/50. So I don't buy into the notion that you need to both clomid and nolva for a compound as light as anavar.
Nolva and Clomid aren't wonder drugs, both have been linked to various forms of cancer at dosages as low as 20mg. So whenever you can limit your use of SERMS when not needed the better you are in the future.Last edited by Immortal Soldier; 05-08-2009 at 03:01 PM.
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05-08-2009, 03:02 PM #9
Cause obviously you dont read!
and if you choose to go that route no need to have 100mgs the first week, the difference between 100mgs and 50mgs of clomid ED is negigible when taking into account the effect of anavar on the HPTA
At normal human dosages all anavar do is suppress the HPTA not shut it down, it is not that strong.
Ill find the study in a minute.
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05-08-2009, 03:04 PM #10
Silly silly silly...
Clomid does things that Nolvadex cannot. And vise versa. Like i already mentioned...
Youre the particular reason why i wrote my thread on PCT.
I just finished it last night and will be adding it to my sticky.
Youve read too much of Pinnacle's work...
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05-08-2009, 03:06 PM #11
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05-08-2009, 03:07 PM #12
PCT and Anavar has had a big war back and forth as to if you need it or not. PCT is needed no doubt about it if you want to keep as much gains as possible!
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05-08-2009, 03:09 PM #13read my edit
Compared to what? 50mg? I'd like to see that study
Inhibited-to restrain, hinder, arrest, or check
Supress-To inhibit the expression of
Basically the same words
And im including the study in my sticky. You can read it there.
It should be posted by tonight, im waiting on some things for Admin to take care of first...
Now personally think that the whole 'standard' 4 week PCT needs to be trashed. The idea that 3-4 weeks is the standard of PCT retarts your natural test production, as many people who get bloodwork done on a regular basis can attest to, is not accurate. It can take months after PCT (or even years before full HPTA function is restored) and only in part in some cases. The idea of time on + PCT = time off is a sound one, but in truth, even that amount of time off is insufficient in many cases to restore full HPTA function. With that said, its important to remember to get blood tests done before you begin the cycle, during the cycle, and after PCT.
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05-08-2009, 03:11 PM #14
I am the particular reason you wrote your thread on PCT? That's great.
But in reality I will tell you most people will agree that nolva is enough for PCT for 50mg of low dosed anavar .
You want to add more fuel to fire? Go ahead, better be safe than sorry. Look this isn't an argument on nolva vs. clomid, it is what is a acceptable PCT for anavar. But you should also look into the fact of nolva and clomid use (in numerous studies) and how it has been linked to cancer in various parts of the body including prostate/breast/and tumors in the liver. While nolva and clomid are used in cancer thearpy they are carcinogenic.
And no, I don't read pinnacle's work.
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05-08-2009, 03:14 PM #15
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05-08-2009, 03:14 PM #16
Quote"You want to add more fuel to fire? Go ahead, better be safe than sorry"
^^^ Indeed always safer then sorry
Why go into war with guns and ammo and no medpack?
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05-08-2009, 03:15 PM #17
Agreed, but the point of PCT is not to bring your natural test production levels to baseline, that is wishful thinking. You do a 3-4 month cycle your body isn't going to bounce back in 3-4 weeks. I agree we are all different, but the main purpose of the PCT is to begin the process of natural testosterone production. However, it could take 6-7 months to reach pre-cycle hormonal levels for some people and some might never reach that level.
Now thats why the longer your on cycle, I feel the longer your PCT should be, nothing dramatic but instead of 4 week therapy you might have to extend it to 7 weeks, now that doesn't mean it will make your hormonal levels back to where they were in 7 weeks, but it starts the process and it sure as hell beats no PCT.
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05-08-2009, 03:17 PM #18
Isn't waiting a year before your next cycle common knowledge?
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05-08-2009, 03:17 PM #19
Tamoxifin is only considered carcinogenic if you have a UTERUS. I seriously doubt men have problems with uterine cancer!!
Crit Rev Toxicol 2000 Sep;30(5):571-94
"Chemoprevention of breast cancer by tamoxifen : risks and opportunities."
Smith LL, Brown K, Carthew P, Lim CK, Martin EA, Styles J, White IN
MRC Toxicology Unit, Leicester, UK.
The antiestrogen tamoxifen is widely used in the adjuvant therapy of breast cancers in women and helps to prevent the occurrence of breast tumors in healthy women. However, epidemiological studies have shown tamoxifen treatment to be associated with a 2- to 5-fold increased risk of endometrial cancer. In rats but not in mice, long-term administration of tamoxifen results in an increase in hepatocellular carcinomas. Mechanistically, this occurs through metabolic activation of the drug, mainly by the CYP3A family, to an electrophilic species, that causes DNA damage in target tissues, and subsequently leads to gene mutations. It is controversial whether low levels of DNA damage occur in human uterine tissues, and there is no evidence that this can be causally related to the mechanisms of carcinogenesis. In healthy women, the risk:benefits for the use of tamoxifen is in part related to the risk of developing breast cancer. The results from the carcinogenicity studies in rats do not predict the likelihood that women will develop liver cancer or indeed cancers in other organs. The mechanism of endometrial cancer in women remains unresolved, but the experience with tamoxifen has highlighted the potential problems that need to be addressed in the assessment of future generations of selective estrogen receptor modulators.
It seems that tamoxifen can be carcinogenic to endometrial tissue (uterine) and hepatic (liver) tissue, due to its ability to form DNA adducts. Another study stated that this effect is many times greater in the rat model, and may not be as problematic in humans. There is no clear cut answer for this, so everyone must weigh the odds on Nolvadex use.
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05-08-2009, 03:18 PM #20
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05-08-2009, 03:22 PM #21
Treating cancer with a carcinogen –
When research is done on anti-cancer drugs (such as SERMs), the aim is to find a drug that prolongs life, with the least amount of acute side-effects. In other words, the goal isn’t so much about finding a cure, as it is finding something that can alleviate the symptoms and/or prolong life.
For an estrogen dependant cancer, the idea was simple – Block the proliferative action of estrogen with an anti-estrogen and slow the cancer growth. What could be more appropriate than an already available, orally active, patentable synthetic estrogen such as tamoxifen ? It was a practical shoo-in.
Therefore, in 1971, when drug researchers decided to examine all of the historical anti-cancer SERM data, they found that all of the SERM’s showed anti-proliferative activity on estrogen dependant cancer, and all of them demonstrated some extent of toxicity. (10, 37-39) However, the SERM that happened to show the least amount of toxicity was tamoxifen. (clomiphene missed the mark by showing a high rate of cataract formation)
At the time, Pierre Blais, a well known drug researcher, commented on the finding (5) -
“Tamoxifen is a garbage drug that made it to the top of the scrap heap. It is a DES in the making."
In spite of the criticism from a number of researchers, the FDA approved tamoxifen as a cancer treatment in 1977, and in 1985 ICI was awarded a US patent for tamoxifen in the treatment of breast cancer. (5) Soon, tamoxifen would become the most popularity prescribed cancer drug.
“Its FDA approved for cancer treatment. It must be safe!”
It’s wrong to assume that an “FDA approved” drug has a proven safety profile. The FDA has continually issued stronger health warnings for tamoxifen over the years. For instance, in 1994 the FDA demanded that the tamoxifen manufacturer Zeneca (an ICI sub-division), issue warning letters to health care practitioners about the increased risk of endometrial and gastro-intestinal cancers with tamoxifen use. Zeneca also reported adverse effects similar to those seen with DES, such as reproductive abnormalities in the animals whose mothers received tamoxifen. (remember, DES was the original synthetic estrogen, and also an analog to tamoxifen)
A number of cancer researchers have pointed out the health risks too, such as Elwood et al (6) -
“[Tamoxifen], therefore, is not appropriate for use in the general population because of the known increased risk of endometrial cancer”
“So why is tamoxifen the most popularly prescribed cancer drug, if it’s so toxic?”
The answer is simple. Tamoxifen is the lesser of two evils.
Tamoxifen remains the most popularly prescribed drug because it is one of the few drugs that has shown a “statistically significant” improvement of the survival rate of breast cancer patients.* (Not to mention, tremendous financial motives and intraworking’s from its patent holder Zeneca)
Remember, the goal in cancer treatment is to prolong life -- even if it means committing to therapy that is potentially cancerous or injurious to future health (as confirmed in long-term follow up’s and close examinations of tamoxifen patients).
So, perhaps the risks are worthy for the cancer patient, but are they worthy for the health conscious male?
* Most research has shown tamoxifen to improve the survival rate by 4-14%. For instance, over a 5 year period, 74% of the women survived who used tamoxifen, compared to 70% of the women on placebo. Depending on the type of cancer, this may translate into an extra 2-3 years of life for a cancer patient. (9) Continuing tamoxifen therapy for more than 5 years, results in increased tumor recurrences and serious side effects. (8)
Translating the science, for men’s health -
Fast forward 30 years, through hundreds of human and animal trials and we find that the research is quite extensive, and contradicting. (21)
The damaging evidence from many early rat studies showed severely toxic effects, including the development of cancer in the liver, uterus, or testes upon tamoxifen administration. (30-34,41) However, this evidence was largely disregarded by further test tube studies on human cell-lines which appeared to show a lack of toxic effects. (21)
This misleading test tube data gave the green flag to perform large scale human studies with tamoxifen in the 80’s and 90’s. Even more misleading, was the majority of the human research described tamoxifen as having a “low incidence of troublesome side effects” and that the “side effects where usually trivial”. (22)
As science would uncover, the lack of human toxicity reported in original tamoxifen research was a result of insufficient study duration, inability to detect low level DNA damage with insensitive methodologies, and/or misdiagnosis of collateral cancers as metastasis infections from the breast cancer itself. (15, 21, 28-34)
A word on clomiphene (Clomid) –
Clomiphene (Clomid) consists of two stereoisomers which possess radically different pharmacodynamics. Zuclomiphene has predominantly estrogenic effects and slow clearance while the enclomiphene isomer has predominately anti-estrogenic effects and quick clearance. (9) This creates a dichotomy between estrogen blockage and estrogen stimulation and an acute imbalance once Clomid administration is discontinued. Bodybuilders will often complain of “estrogenic rebound” after stopping Clomid, which could be attributed to the lingering estrogenic isomer zuclomiphene as the anti-estrogenic enclomiphene has long cleared the system. (Recently, enclomiphene has been isolated by the pharmaceutical company Repros, for use in Androxal™.)
For all intents and purposes, tamoxifen is a superior SERM, simply for the fact that tamoxifen provides a purely anti-estrogenic isomer, whereas Clomid provides a mix of anti and pro estrogenic effects.
In regards to the health consequences about to be listed, it can be safely assumed that Clomid will share similar detrimental effects as tamoxifen, since it shares the same triphenylethylene backbone and carcinogenic tendencies. (44,45,57,58)
Liver cancer -
Originally, tamoxifen was accepted as being non-toxic to human liver upon finding that tamoxifen did not cause noticeable liver damage (DNA adducts) during short-term test tube studies with human liver cells. (35,36)
However, it became apparent that test tuberesearch was largely flawed due to the low rate of metabolism in such a superficial environment. (21) It was soon discovered that the hepatotoxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen and N-desmethyltamoxifen metabolites, which would only appear in an in vivo environment. (15) Surely enough, the results from the original rat studies showing dramatic carcinogenic effects on the liver, 30-34,41 soon correlated with human data when researchers found the same type of liver DNA adducts in tamoxifen patients. (15, 28-34)
More recent human research has reported tamoxifen treated women to have 3x the risk of developing fatty liver disease, which occurs as soon as 3 months into therapy at only 20mg/day. (24-26) In some cases, the disease lasts up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy shows cases of deadly hepatocellular carcinoma. (27-29)
In 2002, a bizarre study examined the use of tamoxifen for hepatocellular carcinoma treatment in humans. It was assumed that since tamoxifen could inhibit proliferation of breast cancer, it could offer the same benefit for liver cancer. The devastating results could not have been further indicative of tamoxifen’s hepatotoxic nature, as the tamoxifen treatment significantly increased the rate of death, compared to the group not receiving tamoxifen. (14)
Finally, in a case study reviewing tamoxifen induced liver disease; D.F Moffat et al made a profound statement –
“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 an infection from the breast cancer itself. (28)
Although tamoxifen induced liver cancer may take years to manifest in a healthy male, its damaging effects could easily be exaggerated by other popular hepatotoxic drugs, such as 17aa oral steroids . (15)
Prostate cancer -
In 1996, the International Agency for Research on Cancer (IARC) concluded that tamoxifen clearly promotes uterine cancer in humans – at a standard 20mg/day dose. (16,23,42) This is due to tamoxifen acting as an estrogen agonist in the uterus, presumably from the 4-hydroxytamoxifen metabolite, which triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts. (33, 40)
Contrary to popular thought, these implications are quite scary for a male when we realize the male equivalent to the uterus is the prostate – which differentiates from the same embryonic cell line, shares the same oncogene, Bcl-2, and high concentration of estrogen receptors. In fact, there is no reason to assume that tamoxifen would not initiate the same cancerous growth in the prostate. (60-62) It is no wonder that tamoxifen failed as a treatment for prostate carcinoma. (43)
Note: This same risk would be applicable to Clomid, which has also been linked to uterine cancer and ovarian hyper-stimulation. (18, 19, 57, 59)
Libido reduction & erectile dysfunction -
Erectile dysfunction, low libido, and general impotence are typical complaints from men recently discontinuing steroids or HRT therapy, which is often combated by Clomid or Nolvadex , paradoxically so.
Regardless of any positive effects on fertility or testosterone levels , Clomid and Nolvadex use is highly correlated with erectile dysfunction, libido suppression, and even emotional disorders. (10,47)
Research with male breast cancer patients has also reported decreased libido, and thrombosis associated with tamoxifen use. (47) The thrombotic effect (blood vessel clogging) could explain the mechanism by which SERM’s may inhibit erectile function, by reducing circulation to erectile tissue. (47, 52)
Increased susceptibility to gyno -
Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.
This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developming gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting upon the progesterone receptor).It is interesting to speculate. Is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?
Ocular toxicity –
Another possible side effect associated with SERMs is visual cloudiness, loss of vision and even cataract formation. Although this tends to be a more common side effect from high dosed SERM therapy, standard 20mg/day tamoxifen regimes have been reported to cause these symptoms of ocular toxicity. (17, 46)
Newer SERM’s -
As the medical community became more aware of the side-effects associated with 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 a closely related analog of tamoxifen, so it also carries many of the related genotoxic effects. (48,49)
Raloxifene is a newer SERM based off a benzothiophene structure, which appears to make it less toxic in the liver, uterus or prostate. (50-52) Unfortunately, Raloxifene has been associated with a higher incidence of thromboembolism (52), and also has very low oral absorption, making it an expensive alternative at a typical dose (120mg/day). (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. (further enumerating the evidence of toxicity with the tamoxifen generation of SERM’s)
What to do now?
Firstly, it should become a priority to create awareness about the possible side effects of SERMs. Once educated, users will be able to start reducing their requirements of these drugs, and begin adopting healthier, more responsible alternatives.
Carefully planned cycles, and the proper use of aromatase inhibitors (AIs) must pursue over haphazard combinations of excessively dosed aromatizing AAS’s -- which require high doses of SERM’s to reduce possible side-effects. Whereas avoiding SERM’s in HRT will involve the natural clearance and management of endogenous estrogens.
It will be important to maintain testicular function during cycle for a quick and efficient recovery of natural testosterone production for PCT – negating the need for high dose 2-3 month SERM based PCT’s. (For more information on the proper use of hCG during cycle, visit here)
Thus, abolishing the bad habit of SERMing will involve community wide enlightenment with careful, comprehensive planning of worthy alternatives.
References -
1. Drug Discovery
By Walter Sneader
2. D.E.S., the bitter pill.
Meyers, Robert (1983).
New York: Seaview/Putnam. ISBN 0-399-31008-8
3. Geometric isomers of substituted triphenylethylenes and antiestrogen action
VC Jordan, B Haldemann, and KE Allen
Endocrinology, Apr 1981; 108: 1353.
4. Antioestrogens: a review.
LUNAN, C.B. et al.
Clin. Endocrinol., 4, 551–572. (1975).
5. Patient No More: The Politics of Breast Cancer,
Batt, Sharon et al
Spinifex Press, Melbourne, Australia, 1994, page 118
6. The Estrogen Receptor: A model for molecular medicine
Elwood V et al.
Department of Cell Biology. Vol 9, 1980-1989
7. Tamoxifen (ICI46,474) as a targeted therapy to treat and prevent breast cancer
V Craig Jordan
British Journal of Pharmacology (2006) 147, S269-S276
8. Selective estrogen receptor modulation: concept and consequences in cancer.
VC Jordan
Cancer Cell, March 1, 2004; 5(3): 207-13.
9. A pharmacological review of selective oestrogen receptor modulators
Steven R. Goldstein, Suresh Siddhanti, Angelina V. Ciaccia, and Leo Plouffe, Jr
Hum. Reprod. Update, May 2000; 6: 212 - 224.
10. Clomiphene citrate (Clomid).
The Wm. S. Merrell Company
Clin. Pharmacol. Therap., 8: 891–897, 1967.
11. Cole, M. P., Jones, C. T., and Todd, I. D. A new anti-oestrogenic
agent in late breast cancer. An early clinical appraisal of ICI46474. Br. J.
Cancer, 25: 270–275, 1971.
12. Ward, H. W. Anti-oestrogen therapy for breast cancer: a trial of
tamoxifen at two dose levels. Br. Med. J., 1: 13–14, 1973.
13. Breast Cancer? Breast Health!
Weed, Susan S.,
Ash Tree Publishing, Woodstock, New York, 1996, page 203
14. High-dose tamoxfen in the treatment of inoperable hepatocellular carcinoma: A multiicenter randomized controlled trial.
Chow et al.
Hepatology, 36: 1221-1226, 2002
15. Liver Cancer: New Research
By Felix Lee
Publisher: Nova (2006)
16. IARC Tamoxifen: Monographs on the evaluation of carcinogenic risks to humans.
66: 253-365, 1996
17. Eye problems in breast cancer patients treated with tamoxifen
Paganini Hill et al.
Breast Cancer Res Treat, 60: 167-172 2000
18. Ovarian hyperstimulation and oophorectomy following accidental daily clomiphene citrate use over three consecutive months.
ES Sills, EA Poynor, and M Moomjy
Reprod Toxicol, Nov 2000; 14(6): 541-3.
19. Uterine Cancer after Use of Clomiphene Citrate to Induce Ovulation
Michelle D. et al
Am. J. Epidemiol., Apr 2005; 161: 607 - 615
20. Detoxifying Cancer Causing Agents to Prevent Cancer
Margaret Hanausek, Zbigniew Walaszek, and Thomas J. Slaga Integr
Cancer Ther, Jun 2003; 2: 139 - 144.
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, 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
34. Activation of the Tamoxifen Derivative Metabolite E to Form DNA Adducts: Comparison with the Adducts Formed by Microsomal Activation of Tamoxifen
Krisztina Pongracz, Deena N. Pathak, Takemichi Nakamura, Alma L. Burlingame, and William J. Bodell
Cancer Res., Jul 1995; 55: 3012 - 3015.
35. Activation of tamoxifen and its metabolite -hydroxytamoxifen to DNA-binding products: comparisons between human, rat and mouse hepatocytes.
Phillips,D.H., Carmichael,P.L., Hewer,A., Cole,K.J., Hardcastle,I.R., Poon,G.K., Keogh,A. and Strain,A.J.
Carcinogenesis, 17, 88–94. (1996)
36. Adjuvant tamoxifen in early breast cancer: occurrence of new primary cancers.
Fornander,T., Rutquist,L.E., Cedermark,B., Glas,U., Mattsson,A., Silfversward,C., Skoog,L., Somell,A., Theve,T., Wilking,N., Askergren,J. and Hjalmar,M.-L.
Lancet, i, 117–120.(1989)
37. Reduced genotoxicity of [D5-ethyl]-tamoxifen implicates -hydroxylation of the ethyl group as a major pathway of tamoxifen activation to a liver carcinogen.
Phillips,D.H., Potter,G.A., Horton,M.N., Hewer,A., Crofton-Sleigh,C., Jarman,M. and Venitt,S. (1994)
Carcinogenesis, 15, 1487–1492
38. Genotoxicity of tamoxifen, tamoxifen epoxide and toremifene in human lymphoblastoid cells containing human cytochrome P450s.
Styles,J.A., et al (1994)
Carcinogenesis, 15, 5–9.
39. Clastogenic and aneugenic effects of tamoxifen and some of its analogues in hepatocytes from dosed rats and in human lymphoblastoid cells transfected with human P450 cDNAs (MCL-5 cells).
Styles,J.A., et al. (1997)
Carcinogenesis, 18, 303–313.
40. Effect of tamoxifen on endometrial proliferation
A Decensi, et al.
J. Clin. Oncol., Feb 1996; 14: 434 - 440.
41. Safety Testing of New Drugs. Tamoxifen.
Lawrence,D.R., et al.
Academic Press, London, pp. 125–161. (1984)
42. Endometrial cancer in tamoxifen-treated breast cancer patients: findings from the National Surgical Adjuvant Breast and Bowel Project (NSABP) B-14.
Fisher,B et al.and other NSABP contributors (1994)
J. Natl Cancer Inst., 86, 527–537.
43. Phase II trial of tamoxifen in metastatic carcinoma of the prostate.
JH Glick, A Wein, K Padavic, W Negendank, D Harris, and H Brodovsky
Cancer, Apr 1982; 49(7): 1367-72.
44. Biotransformation of the Antiestrogen Clomiphene to Chemically Reactive Metabolites in the Immature Female Rat
Peter C. Ruenitz, et. al
Cancer Res., Aug 1987; 47: 4015 - 4019.
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, et al.
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, et al.
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, et al.
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(8): 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, et al
Maturitas, July 16, 2005; 51(3): 286-93.
54. Effects of tamoxifen on steroid hormone receptors and hormone concentration and the results of DNA analysis by flow cytometry in endometrial carcinoma.
M Nola, et al
Gynecol Oncol, Mar 1999; 72(3): 331-6.
55. Tamoxifen increases the plasma estrogen-binding equivalents and has an estradiol agonistic effect on histologically normal premenopausal and postmenopausal
Gorodeski, G.I., et al.
endometrium. Fertil. Steril, 57, 320-327. (1992)
56. Estrogen and progesterone receptor expressors oŁ decidual endometrium in a postmenopausal woman treated with tamoxifen and megestrol acetate.
Cohen, I., Shulman, A., Altaras, M., Tepper, R., Cordoba, M. and Beyth, Y.
Gynecol. Obstet. Invest., 38, 127-129. (1994)
57. Endometrial biopsy during induction of ovulation with clomiphene citrate in polycystic ovary syndrome.
R Homburg, H Pap, M Brandes, J Huirne, P Hompes, and CB Lambalk
Gynecol Endocrinol, September 1, 2006; 22(9): 506-10.
58. In vivo evaluation of the genotoxic effects of clomiphene citrate on rat reticulocytes: a micronucleus genotoxicity.
B Duran, I Ozdemir, Y Demirel, O Ozdemir, A Cetin, and A Guven
Gynecol Obstet Invest, Jan 2006; 61(4): 228-31.
59. Clomiphene citrate - end of an era? a mini-review
Roy Homburg
Hum. Reprod., Aug 2005; 20: 2043 - 2051
60. Selective estrogen receptor modulators: pharmacological profile in the rat uterus.
Bryant H. U., Wilson P. K., Adrian M. D., Cole H. W., Phillips D. L., Dodge J. A., Grese T. A., Sluka J. P., Glasebrook A. L.
J. Soc. Gynecol. Invest., 3: 152A 1996.
61. Molecular perspectives on selective estrogen receptor modulators (SERMs): progress in understanding their tissue-specific agonist and antagonist actions.
Lonard D. M., Smith C. L.
Steroid, 67: 15-24, 2002
62. Defining the "S" in SERMS.
Katznellenbogen B. S., Katznellenbogen J. A.
Science (Wash. DC), 295: 2380-2381, 2002
Just something I liked to share with you, you can draw your own opinions.Last edited by Immortal Soldier; 05-08-2009 at 03:25 PM.
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05-08-2009, 03:27 PM #22
Nice read...
Nothing new. All circumstantial evidence on cancer of the prostate. However likely it may be.
But good read for the newbies brutha.
Nicely done.
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05-08-2009, 03:31 PM #23
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05-08-2009, 03:34 PM #24
good debate. hijacked thread (lol) but very informative. thanks guys.
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05-08-2009, 03:35 PM #25
^ Indeed. I hate researching too. Part of it though, if it werent for guys like us, SWALE, and Swifto, we'd all still be running Deca only cycles with no PCT.
These new generation SERMs seem to be the new way.
I prefer Tamox and Clomid, but only because im yet to use Tormifene. From what i hear, Tormifene has recently been reported to be the best SERM at restarting an inhibited HPTA. (I will talk more about it in my sticky, just waiting on some info from Swifto.)
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05-08-2009, 03:35 PM #26
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05-08-2009, 04:57 PM #27
Holy Thread Jack BATMAN!!!!
Ok so I plan on taking the Clomid at 50mg a day for a month............
And I will start the Anavar on Monday at 50mg for the first day........
It was a while ago since the last time I did Anavar, but I should feel the "warmth" the first week but start to see true effects after a couple of weeks, correct?
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05-08-2009, 05:56 PM #28
In a few weeks yes you should start to feel strength gains and a somewhat veiny look.
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Zebol 50 - deca?
12-10-2024, 07:18 PM in ANABOLIC STEROIDS - QUESTIONS & ANSWERS