Progesterone and Prolactin

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  1. 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.


  2. 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.
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  3. 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 .

  4. 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

  5. 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
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  6. 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 -

  7. 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

  8. 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.

  9. 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?

  10. 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?

  11. 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.

  12. 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?

  13. 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....

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


    i must be scrollically impaired, though.

  15. 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

  16. I have a seemingly simple question in all this that I believe is the crux of the whole argument (at least it is for me, as I've researched this quite a bit). Maybe Seth can answer it.

    Does binding the progesterone receptor have any effect whatsoever on prolactin levels?

    Or even more simply: other than a concurrent rise in estrogen, what other stimuli can raise prolactin?

    If anyone can answer these, I think I'll have a pretty good grasp of what happens with so-called prolactin gyno.

  17. Quote Originally Posted by sethroberts View Post
    Where was that paper published and who peer reviewed it?
    And what peer reviewed journal published “anabolic pharmacology”?

  18. 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. 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.
    Anyway…

    You recommended Nolva for progestin based gyno. I’m sorry, but in my experience this doesn’t work. I’ve provided my recommendations for something that does work. No need for personal insults…

  19. Quote Originally Posted by Primordial Perf View Post
    And what peer reviewed journal published “anabolic pharmacology”?
    Ha ha. Touche.

  20. Quote Originally Posted by Primordial Perf View Post
    And what peer reviewed journal published “anabolic pharmacology”?
    Very true. However, I did not reference my book as support at any point in this discussion. You referenced a rather silly article written by yourself and posted on your company web site. Sorry if that doesn't carry much weight in my opinion. Nor does your personal experience.

  21. Quote Originally Posted by Primordial Perf View Post
    Anyway…

    You recommended Nolva for progestin based gyno. I’m sorry, but in my experience this doesn’t work. I’ve provided my recommendations for something that does work. No need for personal insults…
    Show me one shred of evidence that stimulation of the progesterone receptor causes gynecomastia.

  22. Quote Originally Posted by Mass_69 View Post
    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
    Those were the papers I was referring to when I mentioned in one of my posts that tamoxifen may cause a slight upregulation or no change in progesterone receptor.

  23. 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
    marco asked:

    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?
    I'm not trying to put you on the spot, or anything, but you've stated that you're "not a fan" of AI's. I was wondering what you would recommend instead of AI's, if anything at all.

  24. Quote Originally Posted by Dragon13 View Post
    I have a seemingly simple question in all this that I believe is the crux of the whole argument (at least it is for me, as I've researched this quite a bit). Maybe Seth can answer it.

    Does binding the progesterone receptor have any effect whatsoever on prolactin levels?

    Or even more simply: other than a concurrent rise in estrogen, what other stimuli can raise prolactin?

    If anyone can answer these, I think I'll have a pretty good grasp of what happens with so-called prolactin gyno.
    There are quite a few papers showing progesterone to reduce prolactin levels -- likely through its suppressive effects on estrogen receptor activation. I pasted abstracts from a couple below. Even medroxyprogesterone, a very potent porgesterone, causes a decease in prolactin receptor levels.

    Drugs that interfere with the production or release of dopamine. Antipsychotic medications are well known for causing increased prolactin levels.


    1: Biol Reprod. 1988 Dec;39(5):1067-73. Links
    Antagonism of estrogen-induced prolactin release by progesterone.Brann DW, Rao IM, Mahesh VB.
    Department of Physiology and Endocrinology, Medical College of Georgia, Augusta 30912-3000.

    Previous work from our laboratory has shown that during the process of nuclear occupancy of the progesterone receptor complex (1-2 h), nuclear estradiol receptors of the anterior pituitary are depleted. The purpose of this study was to determine whether the depletion of nuclear estradiol receptors by progesterone had functional biological significance. The ovariectomized (26 days of age) immature rat was used as the model for analysis of this question. The ability of estradiol to release prolactin from the anterior pituitary was the function chosen to determine the biological significance of the progesterone and estradiol interactions. In response to estradiol exposure (2 micrograms/rat), prolactin release reached peak values from 8 h to 12 h and returned to control levels by 24 h. A second injection of estradiol 13 h after the initial injection stimulated a second increase in serum prolactin at 25 h. This model of two injections of estradiol 13 h apart served to provide adequate levels of anterior pituitary progesterone receptors and elevated serum prolactin levels upon which superimposed progestin modulation could be examined. A single injection of progesterone (0.8 mg/kg BW) 1 h before the second estradiol injection blocked the increase in serum prolactin. This action was a receptor-mediated event because progesterone had no effect without estrogen priming or when the progesterone antagonist RU486 was used. Finally, when the interval between the progesterone and second estradiol injection was extended to 4 h, a time period when progesterone does not deplete pituitary nuclear estrogen receptors, the estrogen-induced increase in serum prolactin was not blocked.(ABSTRACT TRUNCATED AT 250 WORDS)

    1: Pharmacol Res Commun. 1988 Aug;20(8):719-30.Links
    Effects of medroxyprogesterone acetate on serum prolactin levels and liver prolactin binding capacity in the rat.Muccioli G, Racca S, Ricci Gamalero S, Di Carlo F.
    Institute of Pharmacology, Faculty of Medicine, University of Turin, Italy.

    Modifications in liver prolactin (PRL) receptor levels and serum PRL concentration induced by administration of medroxyprogesterone acetate (MPA) were investigated in rats of both sexes. MPA induced a reduction both of the levels of PRL in the serum and of liver PRL receptors in the female rat. The reduction of the number of PRL receptors caused by MPA was rapid and almost complete after 10 days of treatment and appeared earlier than that of serum PRL levels. Furthermore the MPA-induced decrease in PRL receptors was specific, since insulin binding to the same liver membranes was not affected. MPA given simultaneously with oestradiol (which increases both the number of liver PRL receptors and the serum PRL levels in the male rats) was able to counteract the increase in PRL binding induced by oestradiol. On the contrary, the oestrogen-induced increase in serum PRL was not affected by MPA treatment. Similar results were obtained using tamoxifen, a well known antioestrogenic drug. In conclusion, our results show that the reduction of PRL receptor levels induced by MPA in rat liver is specific, not correlated to serum PRL concentration, and seems to depend on the antioestrogenic activity of the drug.

  25. I got to say that I agree with Seth in everything he says, it make a lot a sense and for my research , experience and readings on anabolics its all true
    reps and I`M going to the store and buy the book, I`ll pay a lot in taxes but what the hell its well worth
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