Progesterone and Prolactin

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  1. so in crazy's case seth would you recomend a combination like adex/nolva in low doses?...or something elase entirely


  2. Quote Originally Posted by sethroberts View Post
    I would caution against "reducing" estrogen as I do think that AIs may be partially to blame. "Controlling" estrogen is preferable and I am partial to SERMS for this purpose. Especially for non-aromatizing or low aromatizing compounds because the reduction in SHBG and the increased "free" estrogens will not be helped by AI's.
    I got 2 small lumps under my nipple after a month of my PCT using Nolvadex. (cycle was tren/hdrol) I never been prone to gyno nor had it before. I have no clue what happened, but i just came up with my own conclusion that estrogen elevated again...

    So you think if i used a low dose of AI after i stopped that SERM would have brought me different results?
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  3. People started invoking "new" mechanisms for the induction of gyno in the late 1990's -- As far as I know, I was one of the first people proposing progesterone receptor activation as a potential cause of gyno back then. I have changed my mind since then as I have accumulated knowledge over the years. There is no evidence that progesterone or prolactin intitiate gynecomastia but plenty of evidence that estrogen does. All of this stemmed fro mthe fact that people were complaining of gyno from anadrol but also fron tren and nandrolone none of which were supposed to convert to estrogen. What I realized a while ago is that there is no need to invoke exotic mechanisms. Pher and superdrol do not convert to estrogen (nor does tren or anadrol) but they do suppress SHBG. SHBG is actually protective against breast tissue growth beyond just sequestering estrogens (you can read more about this in my book ). The removal of this protective effect as weel as the increase in "free" estrogen from the reduction in SHBG can explain some of the propensity for forming gyno with these compounds. With nandrolone, trenbolone, and other 19-norsteroids, there is also the added production of 5-alpha reduced metabolites that are weak androgens (there is some evidence that tren is metabolized in this fashion) which upstes the androgen to estrogen rati and further contributes to the ability to produce gyno.

  4. Quote Originally Posted by mooch2321 View Post
    so in crazy's case seth would you recomend a combination like adex/nolva in low doses?...or something elase entirely
    I am not a fan of AIs - they tend to suppress estrogen too low and SHBG with it not to mention the effects on cholesterol etc.

    In that situation, I would probably have used nolva throughout and into PCT.

  5. Quote Originally Posted by sethroberts View Post
    I doubt it is potent enough.

    what else can lower estrone sulfate levels....
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  6. When I was on a sust/deca cycle I had some first signs of gyno like symptoms. Note I say signs as there were never a lump or discharge that developed. What I do know is that nolva took care of ALL of the symptoms in quick fashion. I also used it along with clomid for pct. This was a year ago and never had issue since.

    That said I am week 3 into m-drol cycle and am using a-dex at very low dose and am taking low dose vitex and am have zero sensations in nipple area. I make sure bodyfat is always below 12 percent before starting any cycle as I think this helps.

    Just shows that there are a few ways to skin a cat.

  7. Quote Originally Posted by mooch2321 View Post
    we posted at the same time....i didnt see that last one....oh and im scrolling impaired..
    LOL!

    This thread is awesome BTW..

  8. what about the study showing nolva causes sperm damage? im still young when i recover i dont want that to recover and have poor sperm

  9. Quote Originally Posted by Problem View Post
    I got 2 small lumps under my nipple after a month of my PCT using Nolvadex. (cycle was tren/hdrol) I never been prone to gyno nor had it before. I have no clue what happened, but i just came up with my own conclusion that estrogen elevated again...

    So you think if i used a low dose of AI after i stopped that SERM would have brought me different results?
    You may have needed a longer course of nolva since your SHBG levels probably had not recovered by the time you came off. I doubt an AI would have helped since it was probably not production of estrogen that was the problem. I generally believe that 20 mg of nolva is enough but there are circumstances where 40 or 60 mg would be appropriate. These strong androgen cycles are sometimes worst than aromatizing androgens because they can suppress SHBG levels so low.

  10. Quote Originally Posted by crazyfool405 View Post
    what else can lower estrone sulfate levels....
    a sulfotransferase inhibitor or a 17 beta hydroxysteroid dehydrogenase inhibitor to prevent the back conversion of estrone to estradiol -- both of which are in development for breast cancer.

  11. Quote Originally Posted by sethroberts View Post
    People started invoking "new" mechanisms for the induction of gyno in the late 1990's -- As far as I know, I was one of the first people proposing progesterone receptor activation as a potential cause of gyno back then. I have changed my mind since then as I have accumulated knowledge over the years. There is no evidence that progesterone or prolactin intitiate gynecomastia but plenty of evidence that estrogen does. All of this stemmed fro mthe fact that people were complaining of gyno from anadrol but also fron tren and nandrolone none of which were supposed to convert to estrogen. What I realized a while ago is that there is no need to invoke exotic mechanisms. Pher and superdrol do not convert to estrogen (nor does tren or anadrol) but they do suppress SHBG. SHBG is actually protective against breast tissue growth beyond just sequestering estrogens (you can read more about this in my book ). The removal of this protective effect as weel as the increase in "free" estrogen from the reduction in SHBG can explain some of the propensity for forming gyno with these compounds. With nandrolone, trenbolone, and other 19-norsteroids, there is also the added production of 5-alpha reduced metabolites that are weak androgens (there is some evidence that tren is metabolized in this fashion) which upstes the androgen to estrogen rati and further contributes to the ability to produce gyno.
    I wonder about all these people claiming gyno while using Nolva, and how this would all change if people used PHARM GRADE medicines rather then these research chems.

  12. Quote Originally Posted by animaleater2 View Post
    When I was on a sust/deca cycle I had some first signs of gyno like symptoms. Note I say signs as there were never a lump or discharge that developed. What I do know is that nolva took care of ALL of the symptoms in quick fashion. I also used it along with clomid for pct. This was a year ago and never had issue since.

    That said I am week 3 into m-drol cycle and am using a-dex at very low dose and am taking low dose vitex and am have zero sensations in nipple area. I make sure bodyfat is always below 12 percent before starting any cycle as I think this helps.

    Just shows that there are a few ways to skin a cat.
    That is true and it is true that in men the majority of aromatase activity comes from adipose (but not all). I am concerned that opamine manipulation may be contributing to the increased incidence of "gyno" and "lactating" though.

  13. Quote Originally Posted by crazyfool405 View Post
    what about the study showing nolva causes sperm damage? im still young when i recover i dont want that to recover and have poor sperm
    It also inhibits cholesterol side chain cleavage. Don't you think androgens have the potential to cause sperm damage. There are risks involeved to using all of these medications.

  14. Quote Originally Posted by imprezivr6 View Post
    I wonder about all these people claiming gyno while using Nolva, and how this would all change if people used PHARM GRADE medicines rather then these research chems.
    Very good point. Even the "legal" OTC stuff has the potential to be contaminated. How many of these cases of tren gyno are the result of contamination or substitution?

  15. Quote Originally Posted by sethroberts View Post
    It also inhibits cholesterol side chain cleavage. Don't you think androgens have the potential to cause sperm damage. There are risks involeved to using all of these medications.
    o of course!!! but in recovery i dont want to be damaging my sperm i did enough on cycle.

  16. This thread is very informative and confusing at the same time. There are so many different theories that once you think you have a good understanding on how to prevent certain things, you read a different (yet still legit) opinion.

  17. Quote Originally Posted by crazyfool405 View Post
    o of course!!! but in recovery i dont want to be damaging my sperm i did enough on cycle.
    It's funny. I never worried about sperm damage. That is not to say that it can't happen but sperm are made constantly and I had 3 kids without issue.

  18. Quote Originally Posted by sethroberts View Post
    It's funny. I never worried about sperm damage. That is not to say that it can't happen but sperm are made constantly and I had 3 kids without issue.
    congrats man!

    when i get married thats the number im shooting for .

  19. Quote Originally Posted by sethroberts View Post
    1: J Agric Food Chem. 2001 May;49(5):2472-9. Links
    Evaluation of estrogenic activity of plant extracts for the potential treatment of menopausal symptoms.Liu J, Burdette JE, Xu H, Gu C, van Breemen RB, Bhat KP, Booth N, Constantinou AI, Pezzuto JM, Fong HH, Farnsworth NR, Bolton JL.
    Department of Medicinal Chemistry and Pharmacognosy, UIC/NIH Center for Botanical Dietary Supplements Research, College of Pharmacy, M/C 781, University of Illinois at Chicago, 833 South Wood Street, Chicago, Illinois 60612, USA.

    Eight botanical preparations that are commonly used for the treatment of menopausal symptoms were tested for estrogenic activity. Methanol extracts of red clover (Trifolium pratense L.), chasteberry (Vitex agnus-castus L.), and hops (Humulus lupulus L.) showed significant competitive binding to estrogen receptors alpha (ER alpha) and beta (ER beta). With cultured Ishikawa (endometrial) cells, red clover and hops exhibited estrogenic activity as indicated by induction of alkaline phosphatase (AP) activity and up-regulation of progesterone receptor (PR) mRNA. Chasteberry also stimulated PR expression, but no induction of AP activity was observed. In S30 breast cancer cells, pS2 (presenelin-2), another estrogen-inducible gene, was up-regulated in the presence of red clover, hops, and chasteberry. Interestingly, extracts of Asian ginseng (Panax ginseng C.A. Meyer) and North American ginseng (Panax quinquefolius L.) induced pS2 mRNA expression in S30 cells, but no significant ER binding affinity, AP induction, or PR expression was noted in Ishikawa cells. Dong quai [Angelica sinensis (Oliv.) Diels] and licorice (Glycyrrhiza glabra L.) showed only weak ER binding and PR and pS2 mRNA induction. Black cohosh [Cimicifuga racemosa (L.) Nutt.] showed no activity in any of the above in vitro assays. Bioassay-guided isolation utilizing ER competitive binding as a monitor and screening using ultrafiltration LC-MS revealed that genistein was the most active component of red clover. Consistent with this observation, genistein was found to be the most effective of four red clover isoflavones tested in the above in vitro assays. Therefore, estrogenic components of plant extracts can be identified using assays for estrogenic activity along with screening and identification of the active components using ultrafiltration LC-MS. These data suggest a potential use for some dietary supplements, ingested by human beings, in the treatment of menopausal symptoms.

    1: Pak J Biol Sci. 2007 Jul 15;10(14):2300-7.Links
    The effects of Vitex agnus castus extract and its interaction with dopaminergic system on LH and testosterone in male mice.Nasri S, Oryan S, Rohani AH, Amin GR.
    Department of Biology, Parand Branch, Azad University, Tehran, Iran.

    The purpose of this study was to evaluate the probable effects of Vitex agnus castus (Vac.) on the male reproductive physiology. It is a well known fact that LH secretion from the anterior pituitary of mammals is controlled by many neurotransmiters such as dopamine. In this experiment, we have studied the effect of Vac. extract on the LH and testosterone hormones and its interaction with the dopaminergic system on male mice. In order to evaluate these effects, we used the hydroalcoholic Vac. extract (for extraction we used percolation technique) injection with the following doses: 65, 165, 265, 365 and 465 mg kg-', bromocriptine as a dopamine receptor agonist (5, 10, 20 mg kg(-1)) and haloperidol as a dopamine receptor antagonist (1, 1.5, 2, 2.5, 3 mg kg(-1)). To study the interaction between Vac. extract and dopaminergic system, we injected the optimum doses of Vac. with bromocriptine or haloperidol at the same time. Intraperitoneal injections were applied in all experiments, once a day for 30 days. The control group remained intact and the sham group received vehicle. After the last injection, we collected the animal blood serums for hormonal assays. LH and testosterone were measured by Radio Immuno Assay (RIA). LH and testosterone, showed significant decrease in bromocriptine group and haloperidol increased these hormones. Vac. extract decreased significantly the LH and testosterone levels. The coadministration of Vac. extract and bromocriptine decreased LH and testosterone. Coadministration of Vac. extract and haloperidol decreased LH and testosterone levels. These results suggest: dopamine regulates the gonadotroph-leydig cells axis. It appears that Vac. exertes effects through dopaminergic system and other pathways. The findings of this study show we can use Vac. extract for pathological cases of increasing LH and testosterone.
    Interesting study. Sounds like vitex may even be an progesterone/estrogen antagonist in certain settings by competitively binding. (It certainly doesn’t look like it has any potency even remotely close to estrogen or progesterone itself)

    Im not sure the second study has much relevance. I’m not recommending vitex for PCT.

    -Eric

  20. Quote Originally Posted by sethroberts View Post
    Do you have any data to back up your assertion that the double bond in the 9th position prevents aromatization of dienolone? The 4,9,11 conjugated system makes it impossible for trenbolone to convert to estrogen but the lack of the 11 double bond in dienolone could allow the electron density of the double bond at the 9-position to actually aid in the formation of the conjugated a-ring system -- i.e. the formatin of estrogen.

    Your personal experience of the end effects means nothing in the face of binding data to the contrary. Anecdotal information is useful but does not trump controlled scientific data. Oh, so it has a yellowish hue and burns the musuc membranes -- you just described probably >10,000 unrelated compounds.
    Yeah, it should’nt be aromatizing. I’ll have to find a reference for this. Upon a quick search, I pulled this up –

    http://www.mesomorphosis.com/article...trenbolone.htm

    AR binding data is the ultimate tell all of a steroids effects eh? Interesting...

    -Eric

  21. Quote Originally Posted by sethroberts View Post
    You speak as if noone else has anecdotal information -- what you are also lacking is the education and experience in interpretting pharmacological data to formulate a hypothesis that is based on anything but conjecture. You company owners crack me up when you think that somehow you are qualified to make these determinations. If you knew anything about physiology and the action of estrogen you would know that endometrium and breast are very different tissues with very different responses to estrogens and SERMS. When those science type fellows talk about selective estrogen receptor modulators do you realize that they are talking about tissue selectivity and that while tamoxifen is used to fight breast cancer because it acts as an antagonist (with slight partial agonist activity) in the breast that those patients are at an increased risk of endometrial cancer because tamoxifen acts as an agonist in that tissue? You are certainly entitled to your opinion but just realize that it is an unqualified opinion of someone who is trying to defend a product that noone was bashing.
    Your right, I don’t know anything about science or SERMs…

    BTW, I notice you’re quick to recommend nolva. Here is a piece that some members might want to consider when choosing this drug for gyno related issues -

  22. Quote Originally Posted by sethroberts View Post
    I don't mean to be crabby, but my "interesting theory's" are built on 19+ years of personal experience combined with an extensive knowledge of physiology and pharmacology as well as 10+ years in the lab so when someone comes along asserting somethign to be fact based on personal experience alone and question my knowledge, I get a little miffed.

    quotes like this one "If you are referring to a stimulus effect at the female hypothalamus/pituitary of estrogen or progesterone, I hope you’re not assuming this stimulatory effect applies to males." don't help.

    I’m sorry your miffed and crabby… you shouldn’t be … ya know, with all this free advertising for your book you are getting.

    Anyway, Ive made the points I wanted to make.

    Good luck.

    -Eric

  23. Quote Originally Posted by Primordial Perf View Post
    Yeah, it should’nt be aromatizing. I’ll have to find a reference for this. Upon a quick search, I pulled this up –

    http://www.mesomorphosis.com/article...trenbolone.htm

    AR binding data is the ultimate tell all of a steroids effects eh? Interesting...

    -Eric
    So you reference an article about trenbolone as a support for dienolone not aromatizing?

    AR binding is not the ultimate tell all of a steroids effects, but it means a hell of a lot more than what you anecdotally "feel" from a steroid.

  24. Quote Originally Posted by Primordial Perf View Post
    Your right, I don’t know anything about science or SERMs…

    BTW, I notice you’re quick to recommend nolva. Here is a piece that some members might want to consider when choosing this drug for gyno related issues -
    Where was that paper published and who peer reviewed it?

  25. Quote Originally Posted by Primordial Perf View Post
    I’m sorry your miffed and crabby… you shouldn’t be … ya know, with all this free advertising for your book you are getting.

    Anyway, Ive made the points I wanted to make.

    Good luck.

    -Eric
    I have been posting on message boards since 1997 and have only had a book published for the past few months. Obviously my motivation for posting goes beyond advertising my book. Does yours go beyond selling/defending your products? I explained why I get crabby -- people who think that they are qualified to dispute the science because they own a supplement company. Does everyone know what qualifications it takes to start a supplement company and put products onto the market that you ingest?

  26. Quote Originally Posted by Primordial Perf View Post
    Your right, I don’t know anything about science or SERMs…

    BTW, I notice you’re quick to recommend nolva. Here is a piece that some members might want to consider when choosing this drug for gyno related issues -
    You may know something about SERMS but you lack the knowledge to understand something as basic as the fact that endometrium and breast are very different when it comes to estrogen response. That is probably the biggest problem on these boards is that people start reading articles in pubmed without the basic understanding of human physiology, pharmacology, pharmacokinetics and chemistry and start to make assertions that are dead wrong. And then they fight for these assertions to the death because their "guru"-hood is built on those assertions. Just like you cannot become a medical doctor by reading medical books, it is difficult if not impossible to become an expert in pharmacology or endocrinology by just reading books or articles - especially if you don't have the baseline education in the topics above.

  27. sethroberts said,

    Pher and superdrol do not convert to estrogen (nor does tren or anadrol) but they do suppress SHBG. SHBG is actually protective against breast tissue growth beyond just sequestering estrogens
    Other than keeping dosages and length of cycle reasonable, is there any way of limiting these sides while on a SD-clone?

    Or, in your opinion, what would be the best way to run an Mdrol cycle, including PCT?

  28. Quote Originally Posted by marco wolf View Post
    sethroberts said,



    Other than keeping dosages and length of cycle reasonable, is there any way of limiting these sides while on a SD-clone?

    Or, in your opinion, what would be the best way to run an Mdrol cycle, including PCT?
    whos seth roberts....

  29. Quote Originally Posted by mooch2321 View Post
    whos seth roberts....


    i must be scrollically impaired, though.

  30. Quote Originally Posted by sethroberts View Post
    You may know something about SERMS but you lack the knowledge to understand something as basic as the fact that endometrium and breast are very different when it comes to estrogen response. That is probably the biggest problem on these boards is that people start reading articles in pubmed without the basic understanding of human physiology, pharmacology, pharmacokinetics and chemistry and start to make assertions that are dead wrong...
    Seth, according to literature I've read in the past, tamoxifen increases PgRs initially, and then they go back to baseline after around 2 weeks. I was able to dig up a couple of the articles. I do not claim to be an expert in pharmacology or endocrinology, and would be interested in your input regarding my interpretation of these.


    (Full article attached)
    U. Karck and F. Kommoss
    Does tamoxifen change oestrogen and progesterone receptor expression in the endometrium and breast?
    Department of Obstetrics and Gynaecology, University of Freiburg, Hugstetter Straβe 55, 79106 Freiburg, Germany
    Institute of Pathology, University of Mainz, 55101 Mainz, Germany
    http://www.sciencedirect.com/science...9609ec32b2dc7c


    1: Cancer. 1993 Feb 15;71(4):1266-72.Links
    Up-regulation of estrogen receptor by tamoxifen in human breast cancer.
    Noguchi S, Motomura K, Inaji H, Imaoka S, Koyama H.
    Department of Surgery, Center for Adult Diseases, Osaka, Japan.
    http://www.ncbi.nlm.nih.gov/pubmed/8382104
    Attached Images Attached Images
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