Progesterone and Prolactin
- 04-21-2009, 09:32 PM
- 04-21-2009, 09:34 PM
- 04-22-2009, 05:42 AM
04-22-2009, 05:43 AM
04-22-2009, 05:47 AM
04-22-2009, 06:46 AM
04-22-2009, 08:47 AM
Other than keeping dosages and length of cycle reasonable, is there any way of limiting these sides while on a SD-clone?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
Or, in your opinion, what would be the best way to run an Mdrol cycle, including PCT?
04-22-2009, 10:10 AM
04-22-2009, 10:22 AM
04-22-2009, 01:50 PM
(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
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.
04-22-2009, 02:42 PM
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.
04-22-2009, 02:54 PM
04-22-2009, 02:55 PM
04-22-2009, 03:24 PM
04-22-2009, 04:16 PM
04-22-2009, 04:25 PM
04-22-2009, 04:28 PM
04-22-2009, 04:47 PM
marco asked: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
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.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?
04-22-2009, 05:04 PM
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.
04-22-2009, 05:05 PM
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
04-22-2009, 05:07 PM
04-22-2009, 05:15 PM
Seth- I know you don't agree with PP's article, but do YOU feel there is considerable risk using nolva for extended periods of time(ie.16-20wks)? Or are they over stated in that sort of time frame, and generally only an issue in prolonged use?
04-22-2009, 05:22 PM
04-22-2009, 05:37 PM
As for the 20wks, i was figuring if you ran a 14-16wk cycle while using nolva, then ran it for an additional 4wk pct, that would put you up in that range. Maybey longer factoring in any long esters clearing prior to PCT.
Even a 12wk cycle would put you at 16wk min.
04-22-2009, 05:47 PM
04-22-2009, 06:11 PM
Good thread. Good info. Cheers.
04-22-2009, 09:12 PM
04-22-2009, 09:21 PM
The dangers from Nolva are equally expressed by articles coming from peer reviewed journals too… Not just from my silly supplement company… the dangers are a reality.
Interesting that you say the “dangers are overstated”, yet you say “I would not use nolva for 20 weeks”…
Let me just ask..
Do you think Vitex is ineffective for combating gyno coming from the use of a progestin based anabolic?
04-22-2009, 09:22 PM
04-22-2009, 11:37 PM
statements like nolva makes gyno worse while on nandrolone are over all the boards. do you recommend using nolva if symptoms of gynecomastia appear while on nandrolone?
04-23-2009, 05:02 AM
Vitex does not carry the same toxic properties as nolva but that does not mean that it is free from potential side effects. Any substance that alters dopamine signalling has the potential to desensitive dopaminergic neurons to dopamine which could result in levated prolactin levels upon cessation due to the loss of inhibitory control.
Do you have any evdiece to the contrary?
04-23-2009, 05:13 AM
"The dangers are overstated" does not mean that there are not potential risks with its use. These risks increase with dose and duration as I have previously stated. The greatest dangers from nolva - in my opinion - are liver toxicity and endometrial cancer -- and I don't have a uterus.
I do not think vitex is effective for combating gyno coming from the use of progestin based anabolics because there is not evidence that it is the progesterone receptor activity or the prolactin that is causing the gyno. What are you proposing to be the mechanism of action of vitex efficacy in progestin based gyno? I am open to discussion and new evidence must always be considered if theories are to evolve over time but I am not going to go round and round with you in a circular argument -- either provide evidence outside of anecdotal observations or give us all a break.
04-23-2009, 05:31 AM
The statements about nolva are based on the following premises: 1) progesterone receptor stimulation causes gyno 2) nolvadex upregulates progesterone receptors. There is no evidence for #1 and although # 2 may occur in the short term, nolva has been shown to decrease progesterone receptor concentration in the longer term.
04-23-2009, 11:12 AM
dont we always use nolva short term anyway, so the long term decrease in PR concentration doesnt apply to how we use it correct?
04-23-2009, 11:23 AM
04-23-2009, 11:28 AM
A small study involving 20 healthy men showed increased prolactin levels in those receiving a low dose of chasteberry (120 mg per day) but a decrease of prolactin secretion with higher doses (480 mg per day).
Chasteberry also has been used to modify libido, most often to reduce sexual desire but sometimes to improve decreased libido.
Also, did you notice absolutely no mention of treatment of gynecomastia in that article. Additionally, there is no evidence in the scientiific/medical literature of its use for gynecomastia.
04-23-2009, 11:38 AM
Yea I just thought I'd put that out there because there was a small discussion on it and you can take from it what u can
04-23-2009, 11:43 AM
04-23-2009, 12:33 PM
I’d love to spend the next few hours of my day hunting down abstracts that show prolactin or progestin induce mammary gland growth… but I simply don’t have the opportunity at the moment. (pregnancy = prolactin = breast growth, hello!?)
Trenbolone would theoretically lower circulating estrogen during a cycle by way of negative feedback upon T production, yet gyno is a common occurrence with high doses of this Trenbolone. (obviously, I propose this is related to a direct action on the PR). I think your theory is that sulfate bound E2 is being released over the term of this cycle, and thus stimulating gyno by a lack of ER antagonism from trenbolone?
I suppose this is a possibility (and probably explains part of the problem), but you would be just as hard pressed to find a single silver bullet study to support that statement as I would have trying to find a study showing male gyno being induced by a progestin or a prolactin/progestin combination.
04-23-2009, 12:41 PM
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