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  1. #21
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    SERM's

    Tamoxifen Citrate (Novladex)
    Tamoxifen is without a doubt the most broadly used anti-estrogen therapy thanks to heavy marketing in the breast cancer campaigns. It was first synthesized in 1966 and initially developed as an oral contraceptive but was unfortunately found to INDUCE (rather than inhibit) ovuation, likely a side effect of its simultaneous anti- and pro-estrogenic activity. For four decades, tamoxifen has been studied and developed for use in various stages of breast cancer and most of the research we will explore in the next part of this article series actually centers on its most widespread use – palliative treatment of advanced breast cancer in postmenopausal women. It is a non-steroidal agent effective on oral administration. It is partially metabolized by the liver through both N-demethylation and 4-hydroxylation. Tamoxifen’s 4-hydroxylation metabolite (4-hydroxytamoxifen) is intrinsically 100 times more potent and is predominantly created by cytochrome enzyme 2D6 metabolism of tamoxifen. Human liver microsome studies showed that N-demethylation of tamoxifen by cytochrome enzyme 3A4 produces a less potent anti-estrogen (N-desmethyltamoxifen). Competitive partial agonist inhibition of estrogen binding to the estrogen receptor. There are 2 types of estrogen receptors (ER-α and ER-β), which have different tissue distributions and can either homodimerize or heterodimerize. Binding of estradiol and SERMs to the estrogen-binding sites of the ER’s initiates a series of events that includes alteration of the ER, dissociation of heat-shock proteins, and ER dimerization which facilitates the binding of the ER to specific estrogen-response elements (ERE’s) in the vicinity of estrogen-regulated genes. Many co-regulator genes interact with the receptor to act as co-responders or co-activators, while at least 50 transcriptional activating factors modulate the effects of estrogen on target genes. Differences in tissue distribution of ER subtypes, the function of co-regulator proteins, and the various transcriptional activating factors may explain the variable response of tamoxifen in different people and ER-positive tissues. Primary tissue types affected by tamoxifen (secondary to presence of ERs) include: breast, endometrium in women, the coagulation system (offering the potential for thromboembolism as a side effect of use), bone (modulation of bone mineral density, greater response from raloxifene), and liver (alteration of lipid profile).


    Clomiphene Citrate
    Clomiphene shares the triphenylethylene structure with tamoxifen and toermiphene, while raloxifene is a benzothiophene compound which we will see in our next discussion how this plays out in practice. We will also take a look via way of FSH stimulation how this compound stacks well with something like hCG (at least hypothetically) in various instances. Clomid carries the trans isomers of clomiphene and tamoxifen have more antiestrogenic activity than do the cis isomers. This plays a role as tamoxifen tends to be marketed as ONLY the trans isomer, whereas clomiphene is available as the racemic mixture (mixture of both cis and trans isomers). I bring these last couple of structural facts up because this tends to increased the required daily dose of clomiphene compared to tamoxifen for the same efficacy. Clomiphene works as a weak estrogen agonist and a moderate estrogen antagonist. It is believed to act through antagonizing estrogen receptors in the HPTA (or HPTO in the female). By blocking estrogen’s negative feedback inhibition of gonadotropin secretion, clomiphene increases FSH and LH secretion and thereby induces ovulation in the female (a more accurate depiction of the drug’s intention) and spermatogenesis in the male.
    Clomid has also been touted by many physicians as an HRT jumpstart or alternative to testosterone. Here is a well known study which engages on Clomid given to patients suffering from hypogonadism.
    “Clomiphene Citrate Effects on Testosterone/Estrogen Ratio in Male Hypogonadism

    Ahmad Shabsigh, MD 1 , Young Kang, MD 1 , Ridwan Shabsign, MD 1 , Mark Gonzalez, MD 1 , Gary Liberson, MD 1 , Harry Fisch, MD 1 , and Erik Goluboff, MD 1
    1 Department of Urology, NY Presbyterian Medical Center, New York, NY, USA
    Correspondence to Harry Fisch, MD, 944 Park Ave, New York, NY 10020, USA. Tel: 212-879-0800; Fax: 212-988-1634; E-mail: harryfisch@aol.com
    Copyright Blackwell Publishing Ltd 2005

    ABSTRACT

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

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

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

    Conclusions. Low dose clomiphene citrate is effective in elevating serum testosterone levels and improving the testosterone/estadiol ratio in men with hypogonadism. This therapy represents an alternative to testosterone therapy by stimulating the endogenous androgen production pathway. Shabsigh A, Kang Y, Shabsign R, Gonzalez M, Liberson G, Fisch H, and Goluboff E. Clomiphene citrate effects on testosterone/estrogen ratio in male hypogonadism. J Sex Med 2005;2:716–721.”

  2. #22
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    Raloxifene (Evista)
    Raloxifene is a New generation selective estrogen receptor modulator (SERM) of the benzothiophene family. This SERM is similar in its effects to the novladex in displaying estrogen receptor antagonist properties in some tissues while acting as an estrogen receptor agonist in others. The main difference between the two is the variation in their tissue selectivity. While raloxifene is a strong anti-estrogen in breat and uterine tissues, it been documented to be estrogenic in bone which is a good thing. This aspect allows it to protect bone mineral density, mimicking the effects of estradiol on bone marrow. In this regard it’s different from nolvadex, which has estrogen antagonist properties in both breast and bone. Raloxifene had a higher rate of effectively reducing the size of gynecomastia compared to novla when given to boys going through puberty. In other words, if you are developing gyno during a cycle, Raloxifene is clearly the choice to use, but I would suggest combining it with Clomid which has much more potent effects on LH which will help restore the HPTA more efficiently. Studies show that it will not boost testosterone like Tore/Clomid/Novla. Not only does it exert positive effects on the bones but has been recently shown to have positive effects on the lipids, another reason why it may be such a nice addition to post cycle therapy.
    Dosing: At least 60mgs a day, but many double that dosage, again I recommend stacking it with Clomid/Toremifene.

    It is a new generation SERM that acts in a manner similar to other various SERMs. There are, however, some molecular differences worth noting here which contribute to various tissue level effects seen with this molecule.



    Toremifene Citrate (Fareston)
    Toremifene is a triphenylethylene derivative of Novladex in which they share similar pharmacological profile. There have been several phase II and randomized trials have compared toremifene with tamoxifen mano to mano. The one that brings up a lot of attention shows that Novladex had the highest increase in testosterone levels in men suffering from hypogonadism when compared to Toremifene and Raloxifene. However after 3 months, the users with Novladex started to decline a bit, while both Toremifene and Raloxifene continued to rise steadily. Raloxifene was much lower than Novla and Tore when it came down to increases in testosterone. Toremifene was quite close according to the data that was displayed on a chart. Many people tend to experience very little sides which is more than likely because of the cholro bond added to it. The interesting aspect to Toremifene is that acts like both Clomid and Novladex in terms of its mechanisms. This could explain why lots of individuals experience such rapid recovery from it. Sort of like the best of 2 worlds, but because it can be estrogenic in certain tissues which also have shown to interfere with GnRH and LH, so I recommend that one take an AI with it to avoid potential issues. Another pro benefit of Toremifene compared to Nolvadex is that it's 8 times more androgenic than Nolvadex.

  3. #23
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    Did you guys mention Novaldex? I guess you did under another name. Sorry I'm a newbie. :-)

  4. #24
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    Post #21 shows it CLEARLY:
    Tamoxifen Citrate (Novladex)
    Tamoxifen is without a doubt the most broadly used anti-estrogen therapy thanks to heavy marketing in the breast cancer campaigns. It was first synthesized in 1966 and initially developed as an oral contraceptive but was unfortunately found to INDUCE (rather than inhibit) ovuation, likely a side effect of its simultaneous anti- and pro-estrogenic activity. For four decades, tamoxifen has been studied and developed for use in various stages of breast cancer and most of the research we will explore in the next part of this article series actually centers on its most widespread use – palliative treatment of advanced breast cancer in postmenopausal women. It is a non-steroidal agent effective on oral administration. It is partially metabolized by the liver through both N-demethylation and 4-hydroxylation. Tamoxifen’s 4-hydroxylation metabolite (4-hydroxytamoxifen) is intrinsically 100 times more potent and is predominantly created by cytochrome enzyme 2D6 metabolism of tamoxifen. Human liver microsome studies showed that N-demethylation of tamoxifen by cytochrome enzyme 3A4 produces a less potent anti-estrogen (N-desmethyltamoxifen). Competitive partial agonist inhibition of estrogen binding to the estrogen receptor. There are 2 types of estrogen receptors (ER-α and ER-β), which have different tissue distributions and can either homodimerize or heterodimerize. Binding of estradiol and SERMs to the estrogen-binding sites of the ER’s initiates a series of events that includes alteration of the ER, dissociation of heat-shock proteins, and ER dimerization which facilitates the binding of the ER to specific estrogen-response elements (ERE’s) in the vicinity of estrogen-regulated genes. Many co-regulator genes interact with the receptor to act as co-responders or co-activators, while at least 50 transcriptional activating factors modulate the effects of estrogen on target genes. Differences in tissue distribution of ER subtypes, the function of co-regulator proteins, and the various transcriptional activating factors may explain the variable response of tamoxifen in different people and ER-positive tissues. Primary tissue types affected by tamoxifen (secondary to presence of ERs) include: breast, endometrium in women, the coagulation system (offering the potential for thromboembolism as a side effect of use), bone (modulation of bone mineral density, greater response from raloxifene), and liver (alteration of lipid profile).

  5. #25
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    lot of great info. I'm a bit of a novice with the ancillaries. I'm looking for more info on dostinex vs. pramipexole used with a stack of test, win, and tren. I appreciate all the advise I can get.

  6. #26
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    Androst-3,5-dien-7,17-dione (3,7 Keto DHEA)
    3,7 Keto DHEA is a metabolite of 7-oxogeneated DHEA and is naturally occurring. Its a non-steroidal irreversible suicidal aromatase inhibitor that does not convert to any androgens, estrogen or progesterones, in other words it will NOT cause shutdown with prolonged usage. There is a study that shows the capabilities of this AI in regards to preventing 11-Beta-HSD1 to become active. 11-Beta-HSD1 is responsible for converting cortisone to unwanted cortisol which is the dreaded muscle killing hormone. Not to mention that same 11HSD enzyme is responsible for elevating harmful/inflammating cytokines which cause the immune system to drop. This in theory would suggest that this AI also has some slight porgensterone receptor/prolactin blocking capabilities, but warrants further research as its a fairly new compound. This compound shows great promise since it as a higher Ki value than Aromasin which is basically the ability of the compound to bind to the designated (aromatase) receptor. As you see this compound brings 1-2 punch with lowering cortsiol which brings a better test to cort ratio and lowers estrogen, again bringing a better test to estro ratio. Again this compound still warrants for further research. I know a chemist who said that 50mgs would be ideal in limiting cortisol and keeping ones immune system up. The basic dosing range is 50-125mgs from what people including myself have gathered. I suggest splitting the dosage from the first thing you do when you get up as cortisol levels are highest, followed with a dosage either after training or right before sleep.

    Whats going on fellas. Just wanted to put my .02 in here on this product. I am using this now. PES Erase. I love it. My cycle is 400mg and have since bumped it up to 600mg per week. When I started my cycle I did not want to suppress my estrogen to low, so I only took 1 cap. I started to get itch nips and was a little worried so I went to two caps and it has worked great. I have read of a guy on another forum who was taking 1gram of test and got blood work and , and the results were favorable that the product lowered his estrogen but did not crush it. Definitly something to look into if you can not get aromasin. And it's pretty cheap as well.

  7. #27
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    If the testes are already shrunken for years from steroid use without PCT in the past, will HCG help restore size of testes if used at 500IU twice a week? How long would it take for the effect of HCG on testicular size to take place?

  8. #28
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    Quote Originally Posted by vo2max View Post
    If the testes are already shrunken for years from steroid use without PCT in the past, will HCG help restore size of testes if used at 500IU twice a week? How long would it take for the effect of HCG on testicular size to take place?
    You might want to start a thread in the steroid section. But it depends bro. Each body is different. Plus depends on how long you were on? How old are you. What you used?

  9. #29
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    So Bromo would be good for a cycle of Primo correct?

    Im also confused. It says Bromo is used to treat acromegaly by suppressing GH, but then later says it Dopamine increase, increases GH, which is what gives Bromo its fat burning qualities?

    Am I understanding this correctly?

  10. #30
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    Sorry guys, still new to the board, have been doing research but Im still just a little fuzzy.

    What would be best for a 6 week Primo + DMZ the last 4 weeks as far as PCT?

    Im planning on some Nolva to help with HPTA, should I use HCG during for the same reason? Also is anything like Aromasin or Clomid needed for estrogen?

    I also read that adding Test to the end of a Primo cycle is good, which is why i asked if I should use HCG.

    Anyways thanks in advance, this board kicks ass

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    Arimadex & Letrozole great explination.

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    Good stuff. I had a lot of questions about aromasin and you just answered them all.

  13. #33
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    Great info in here guys.

    be running torem, aromasin on an upcoming cycle

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    Nicw


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