Progesterone and Prolactin

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    Great post
    Everything I say is fictional and for entertainment purposes only. Do not ask me for sources. I dont have any.
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    Have to say I sub'd this thread for use later.

    Thanks.
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    i want to bump this for EVERYONE
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    Thanks! I knew I read this somewhere else by Seth a few years ago and I tried to tell people to just control estro to control prolactin issues. Not many took my advice seriously. It's nice to see an expert confirming it tho.
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    Nice revival bump.
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    Have to bump this... there's still so many discussions going on about progesterone and prolactin and designer tren gyno that it deserves to be re-read!

    Hats off to Seth and Eric, great discussion.

    BTW, for what it's worth... a low dose of .6mg Letro E3D and 1400mg of Vitex seems to help alleviate post-cycle gyno symptoms. Unusually the gyno reared it's ugly head during the third week of a 20mg ED Nolva pct which led me to believe that prolactin played a role. The gyno lump must have crept up on cycle but the puffy/enlarged nips (which I can only attribute to increased prolactin) def. arrived week 3 pct. FYI my cycle was a ph tren and 11-keto 8 week cut.
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    Quote Originally Posted by rokkus View Post
    Have to bump this... there's still so many discussions going on about progesterone and prolactin and designer tren gyno that it deserves to be re-read!

    Hats off to Seth and Eric, great discussion.

    BTW, for what it's worth... a low dose of .6mg Letro E3D and 1400mg of Vitex seems to help alleviate post-cycle gyno symptoms. Unusually the gyno reared it's ugly head during the third week of a 20mg ED Nolva pct which led me to believe that prolactin played a role. The gyno lump must have crept up on cycle but the puffy/enlarged nips (which I can only attribute to increased prolactin) def. arrived week 3 pct. FYI my cycle was a ph tren and 11-keto 8 week cut.
    throw in some p5p, more effective than vitex, imo.
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    Bumping this thread after having read through it in its entirety not least because it deserves to be seen but also because I'm hoping to get some insight into my own gyno troubles.

    I believe i developed a mild case of gyno at some point during puberty which never went away. I started cycling at age 21 about 1 year ago - first cycle was just basic test e with arimidex at 0.5mg ed. I was scared that the test would cause my pubertal gyno to flare up but it didn't, and so i thought hey maybe I'm not all that susceptible to it!

    Along comes my next cycle and I'm running Tren with a test base for a few months and everything seems fine. At this point I added 5iu ED of generic GH to my regiment and after about 2 weeks started to notice my nipples were puffier than usual . They have always been puffy to an extent I think and never looked quite right except when hard, but this was something else. I did some reading and what do you know it would appear that GH is known to cause gyno because it's structurally similar to prolactin (or something). I dropped the GH completely and within a few days things were back to "normal". I should note that i had been running caber at 0.5mg e3d all throughout this Tren cycle. I understand that caber won't do anything for gyno caused by GH but thought is I'd mention it anyway, especially due to what happened next..

    Everything seemed to be fine at this point and although my nipples were still naturally puffy this is how things have been since even my earliest recollections of life. So that's cool. Except for the fact that 2 weeks later gyno reared its head again. I figured this was Tren related so I dropped Tren and introduced superdrol. Since adding superdrol things have actually gotten a lot worse. I am taking 2.5mg letro and 0.5mg caber ED but it doesn't seem to be having an effect. My own thoughts and things I should note:

    - I've played around with AI's including letro at 2.5mg all throughout this cycle so that plus the fact that I've been running Tren all throughout I dare say that my SHBG levels are absolutely tanked? HOWEVER, I am currently not taking any exogenous testosterone whatsoever, and am relying on proviron for sex drive etc. I don't know how that affects things? Can there still be excess free floating estrogen due to low SHBG when there is no test being introduced or produced?

    - I figure that the cause of this is a mixture of the following:

    Tren for a long time = low SHBG so no protection from breast growth
    AIs for a long time = same as above
    GH use = caused gyno directly but also probably Igf levels are still raised anyway which is a factor for gyno in itself

    I'm still taking 2.5mg letro ed with no test whatsoever - is there any chance that SHBG could be low enough that estrogen could still be the issue?

    Perhaps it's because I've been running caber for so long with brief stints of up to 1mg per day - I read that too much for too long could have the opposite effect and cause raised prolactin levels?

    This post is a bit of a mess because its basically a splattering of my thoughts written down with no direction whatsoever. Doesn't help that I wrote this all on my phone either!

    I recognise that I can be reckless with the amount of hormones I use and seem to favour the shotgun approach, but please don't let that be the focus of your reply!

    Thanks!
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    So read the entire thread and made what I could of it; if my understanding is incorrect please correct me so others don't get the wrong idea. There are two approaches, the easiest of which would be to control estrogen from the get-go rather than fight off gyno with multiple other products [prevent the **** in the first place].

    My question is how much is enough in general terms (let's say no blood test).

    I'm about to start
    weeks 1-6: raw trenavar powder at 100mg/d
    weeks 3-6: DMZ 30mg/d
    weeks 1-6: MENT at 40mg pre-work out only.

    Some trusted scientist-folk have told me not to worry about anything in terms of ancilarries (for the trenavar), while 95% of the internet says to take everything under the sun, whereas this thread actually backs up their claims with evidence-based research and says to take a mild AI or possibly low-dose SERM.

    SO if the above was a cycle your client was going to take, what would you tell him, which AI and how much/ often, or which SERM and how much/ often. Assuming bloods are all WNL, and dose not currently have gyno.

    Thanks for all of the information regardless fellas... anyone/ everyone needs to read this thread; the conceptuals are extremely vital.
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    Why would a Suicide AI cause estrogen rebound? I had understood that it wouldn't and that the body would have to make more aromatase over a longer time period
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    Quote Originally Posted by ThyBroker View Post
    Why would a Suicide AI cause estrogen rebound? I had understood that it wouldn't and that the body would have to make more aromatase over a longer time period
    it doesn't matter if it binds to the ai perm or temp, it's going to cause rebound. you prob didn't understand incorrectly, just were misinformed.

    dont want the body trying to make things even, dont use a compound that will make it uneven. you have more test, you're going to have more aromatase to level the playing field and make more estrogen.
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    How does it rebound with a suicide inhibitor? My experience has been no rebound with it in the near term. Are you saying longer term rebound occurs like 4-8 weeks out due to the body over compensating? Any studies on this? Thxs!
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    as soon as your aromatase inhibitor, suicide or not, binds to the estrogen receptor, you are going to create an imbalance. how quickly the body responds to this is going to very person to person.

    I'm sure there are studies, feel free to look. it's how the body works, not brain surgery.

    the idea is a suicide inhibitor, or permanently binding to aromatase compound, will lower estrogen, and wont un bind causing that estrogen to become free again.

    how much this matters will be depending how how quickly estrogen is metabolized in ones body, and how many er sites are waiting to get hooked up.

    non non suicidal ai, or non permanently binding, will bind temporarily, then unbind, allowing estrogen to go about it's business. this may cause a rebound, maybe even higher one, in some people, esp those sensitive to the effects of estrogen.

    but it wont cause as much of an hpta disruption as a perm. binding ai, as you'll only temporarily have an inbalance of test to e ratio, so the responce to creast more aromatase wont be as much.

    stop taking an suicidal ai, (the dam is breaking basically) and you'll have all this aromatase that just can wait to bind to all this new test floating around.

    there is a trick to using ai's effectively, one will need to practice on themselves with various ai's to find what works best for them.

    if you focus on controlling estrogen, and not destroying it, rebound wont be a problem.
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    Respectfully, No. You state:

    "stop taking an suicidal ai, (the dam is breaking basically) and you'll have all this aromatase that just can wait to bind to all this new test floating around."

    That's just plain wrong. It takes a month to make aromatase and most of the other enzymes like 5 alpha so there is ample time for feedback and balance with the suicide AI and any rebound is likely slight or non-existent IMO. Enzymes by definition don't need to be rapidly made because they are resused so that's a longer process. On a long or heavy cycle your approach and advice could/would be disastrous IMO and result in someone getting Gyno or libido issues -- note.

    You state:

    "if you focus on controlling estrogen, and not destroying it, rebound wont be a problem."

    I assume you mean taper off of AI here, which really just prevents rebound with non-suicidal AI and results in more time so that the bound estrogen can slowly be released and or is metabolized or secreted -- if you do this with a suicide AI you will likely smash your libido for a month with longer term low estrogen. With suicide AI you just stop. If that's what you mean... IDK for sure. Anyway, good luck and that's my 2 cents.
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    I could be off on what im saying, but researching what patrick arnold has to say on the subject is what led me to my conclusion. I can tell you obviously know more about the subject than he does.

    btw, where did you learn/read about aromatase enzyme production taking 30 days to begin? I'd like to read more up on this subject, as it's caught my interest.
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    Best efforts jbryand101b, I have scoured the journals and I can't find the citation for turnover on 5 alpha reductase or aromatase... I can only say that I remember reading it, I believe in ncbi where it generally described enzyme turnover as being 30 days... I want to give you a cite and I want to know the exact number myself if anyone can help here it would be appreciated and please post it!
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    How do you know if something is prolactin or estrogen related? I've never had any gyno type symptoms but I'm just wondering.
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    Quote Originally Posted by ThyBroker View Post
    Best efforts jbryand101b, I have scoured the journals and I can't find the citation for turnover on 5 alpha reductase or aromatase... I can only say that I remember reading it, I believe in ncbi where it generally described enzyme turnover as being 30 days... I want to give you a cite and I want to know the exact number myself if anyone can help here it would be appreciated and please post it!
    i'll look, and i'll ask hen-v an pa if they have any info on the subject.
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    Quote Originally Posted by JD261985 View Post
    How do you know if something is prolactin or estrogen related? I've never had any gyno type symptoms but I'm just wondering.
    you dont.
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    That's a good question actually and I'll give you my best answer though it may not be as precise as some may want - bloods are helpful, but absent those:

    First, you should know what you are putting into your research "rat" so to speak and therefore be able to anticipate which problem your going to get. If you are putting in Test, well estrogen will result down the line. If you are putting in Tren/Deca too... well progestin receptors get stimulated and you get prolactin down the line. Other things and scenarios can cause imbalance too. You can end up high estrogen from 1) taking test, 2) pro-hormones, or 3) too much aromatase enzymes built up from past cylces ; 4) release of aromatase formerly tied up in a competitive AI like letro or anastrazole -- i.e., "rebound", 5) or other causes the list goes on, but those are typical scenarios.... Prolactin is raised by: 1) Progesterone/progestins(Tren/Deca); 2) built up progestin related receptors or reduced receptors in other areas from past cycles or other receptor imbalances in HPTA causing temporary or ongoing prolactin release loops; 3) stressed adrenals; 3) depressed L-Dopa receptors (this can happen from cocaine abuse, alcoholism, anti-depressants, etc.); 4) or other causes...

    Estrogen too high feels like, No libido, gyno, puffy skin excess water, emotional, awake but maybe little depressed, moody... Estrogen too low feels like, No Libido, really dry, dry joints, lethargic, fatigued, lethargic in bed all day...

    Prolactin High feels like: 1) No Libido and especially hard to orgasm, 2) some water retention, 3) tends toward gyno or even lactation in some with established gyno, 4) Little bit more depressed.... Prolactin too Low feels like: 1) Up and Down Libido and orgasm early/unfullfilling/incomplete; 2) anxious 3) skittish 4) little bit manic if L-Dopa ok or not suppressed, if L-Dopa suppressed or low L-Dopa while low Prolactin -- you feel really lame... feel nothing in these areas, no mania or energy either and no libido and no orgasm at all...

    That's a pretty good sketch IMHO and most if not all is backed up by the journals and real endocrinology.
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    i was getting ready to say this reminds me of seth's post from years ago.I'm on the am app and went back to the first page and see that it is.i enjoy reading seth's work. great discussion here fellas
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    Ya... you present some tough facts... I would think the letro and caber would have kept you safe... Areas to improve in would be that you have no no natural DHT... You need the DHT to help block and reverse the gyno... You need the Test to make DHT.... problem now is you been running some different stuff without Test while likely not making your own test and by not using your 5 alpha reductase system you have likely reduced your 5 alpha reductase capacity so that even when you take Test it will take a while to be able to make normal DHT -- cutting all test actually hurts you because you don't have natural DHT to help block/reverse the gyno -- I don't think the synthetic DHTs are doing you any good in this regard (i.e., the superdrol and proviron aren't blocking gyno like real in tissue DHT). So keep your test in there or make some with HCG/clomid if time for PCT for 10-30 days so that you can have natural DHT -- like that. So ONE - More real DHT!

    You would think its not estrogen because your taking all the letro... unless you have just built so much aromatase that even letro is doing you no good... its theoretically possible... that you can't competitively bind all the aromotase because there is just soo soo much and your cycles frankly look like the type that could do it... I mean your obviously fearlessly doing tren n superdrol and going for it... So, ya, your body is just made so much aromatase to combat and your aren't eliminating your just tying up a consistent same amount all the time and allowing it to build... I'd bet you have so much aromatase that maybe letro can't even do it. I'd take a suicide inhibitor instead to be sure and be sure that your estrogen is sufficiently low -- go exemenstane and be sure and then blood test just estrodiol to be sure. So TWO Suicide AI!

    Finally, I think you need to block at the receptors in the breast tissue with toremefine. I know people say that you shouldn't take nolva with tren/deca stacks and that's probably why it isn't in your set (fear of the progesterone receptor upregulation theory, which I think all must admit is partially true and though I can take nolva with tren most people can because the upregulation is temporary (2 weeks before back to normal and then maybe down regulates....), you probably shouldn't since your prone to gyno and next time you could take nolva with test 2 weeks prior to starting the tren and then avoid the upregulation issue while continuing the superior nolva (nolva is better then torem for HPTA) - and your gyno prone so it makes sense that you would subtract nolva out of your set described above though you haven't said so explicitly, but I think it's a mistake because you need those estrogen receptors blocked and the the progesterone receptor upregulate theory is not supported in the literature as the upregulation described down regulates within 2 weeks as described in this thread actually by Seth I think and though Eric disagrees, I think Seth is right, the upregulation is minor and temporary at most -- but you are very prone to Gyno at this point so then at least take the toremefine citrate to block estrogen receptors in the breast, though nolva is better for HPTA protection improvement which is the secondary benefit of these SERMS, though both are likely equal on gyno based on the study posted below). Ya... add... Toremefine for sure and next time do Nolva a few weeks prior to starting the tren and then keep on the nolva throughout... So THREE Toremefine!

    Ya, GH and IGF can contribute but those clear your system fast in like 3 days so pull em and that's all you can do and save for careful experimentation during PCT after you have control of the gyno.


    Article:

    Toremifene versus tamoxifen for advanced breast cancer.

    Source

    Division of Epidemiology, School of Public Health and Primary Care, The Chinese University of Hong Kong, Hong Kong, China.

    Abstract

    BACKGROUND:

    Toremifene (TOR) and tamoxifen (TAM) can both be used as treatments for advanced breast cancer.
    OBJECTIVES:

    To compare the efficacy and safety of TOR with TAM in patients with advanced breast cancer.
    SEARCH METHODS:

    The Cochrane Breast Cancer Group's Specialised Register was searched (1 July 2011) using the codes for "toremifene", "fareston", "tamoxifen, "nolvadex, and "breast cancer". We also searched MEDLINE (via PubMed) (from inception to 1 July 2011), EMBASE (via Ovid) (from inception to 1 July 2011), The Cochrane Central Register of Controlled Trials (CENTRAL) (The Cochrane Library, Issue 7, 2011), and the WHO International Clinical Trials Registry Platform search portal (1 July 2011). In addition, we screened the reference lists of relevant trials or reviews.
    SELECTION CRITERIA:

    Randomised controlled trials (RCTs) that compared the efficacy and safety, or both of TOR with TAM in women with advanced breast cancer. Trials that provided sufficient data on one of the following items: objective response rate (ORR), time to progression (TTP), overall survival (OS), and adverse events, were considered eligible for inclusion.
    DATA COLLECTION AND ANALYSIS:

    Studies were assessed for eligibility and quality. Two review authors independently extracted the following details: first author, publication year, country, years of follow-up, treatment arms, intention-to-treat (ITT) population size, menopausal status of patients, hormone receptor status, response criteria, efficacy and safety outcomes of TOR and TAM arms. Hazard ratios (HR) were derived for time-to-event outcomes, where possible, and response and adverse events were analysed as dichotomous variables. We used a fixed-effect model for meta-analysis unless there was significant between-study heterogeneity.
    MAIN RESULTS:

    A total of 2061 patients from seven RCTs were included for final analysis, with 1226 patients in the TOR group and 835 patients in the TAM group. The ORR for the TOR group was 25.8% (316/1226) whereas, the ORR for the TAM group was 26.9% (225/835). The pooled risk ratio (RR) suggested that the ORRs were not statistically different between the two groups (RR 1.02, 95% confidence interval (CI) 0.88 to 1.18, P = 0.83). The median TTP was 6.1 months for the TOR group and 5.8 months for the TAM group. The median OS was 27.8 months for the TOR group and 27.6 months for the TAM group. There were no significant differences in TTP and OS between the two therapeutic groups (for TTP: HR 1.08, 95% CI 0.94 to 1.24; for OS: HR 1.02, 95% CI 0.86 to 1.20). The frequencies of most adverse events were also similar in the two groups, while headache seemed to occur less in the TOR group than in the TAM group (RR 0.14, 95% CI 0.03 to 0.74, P = 0.02). There was no significant heterogeneity between studies in most of the above meta-analyses. Sensitivity analysis did not alter the results.
    AUTHORS' CONCLUSIONS:

    TOR and TAM are equally effective and the safety profile of the former is at least not worse than the latter in the first-line treatment of patients with advanced breast cancer. Thus, TOR may serve as a reasonable alternative to TAM when anti-oestrogens are applicable but TAM is not the preferred choice for some reason.
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    Wait -- more proof that tamoxifene is safe and doesn't upregulate progesterone receptors! Article added:

    Evaluation of estrogen and progesterone receptors in non-neoplastic breast tissue of women of reproductive age exposed to tamoxifen and raloxifene: a randomized, double-blind study.

    Source

    Department of Gynecology, Mastology Division, Getulio Vargas Hospital, Federal University of Piauí, Avenida Elias João Tajra, 1260, 64049-300, Teresina, Piauí, Brazil.

    Abstract

    The objective of the present study was to compare the effects of tamoxifen and raloxifene in non-neoplastic breast epithelium. A randomized, double-blind study was carried out in 57 ovulatory, premenopausal women of 18-40 years of age, who had been diagnosed with fibroadenoma of the breast. The patients were divided into three groups: Group A: placebo, n=20; Group B: tamoxifen 20 mg/day, n = 21; and Group C: raloxifene 60mg/day, n=16. The study medication was given for 22 days starting on the first day of the menstrual cycle. On the 23rd day, the fibroadenoma was removed and a sample of non-neoplastic breast tissue was collected for immunohistochemical evaluation of estrogen and progesterone receptors. Comparison between the mean percentages of stained nuclei in the three groups was performed by analysis of variance and multiple comparisons, using Tukey's method to compare pairwise means, with significance established at P < 0.05. Exposition to tamoxifen or raloxifene resulted in a significant and similar reduction in the mean percentage of stained nuclei for estrogen and progesterone receptors (P<0.0001). Tamoxifen and raloxifene reduce progesterone and estrogen receptor alpha expression significantly and to a similar extent in the non-neoplastic breast tissue of women of reproductive age.
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    Quote Originally Posted by jbryand101b View Post

    it doesn't matter if it binds to the ai perm or temp, it's going to cause rebound. you prob didn't understand incorrectly, just were misinformed.

    dont want the body trying to make things even, dont use a compound that will make it uneven. you have more test, you're going to have more aromatase to level the playing field and make more estrogen.
    Better to use a seerm and taper into something like erase in my opinion
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    I think based on everything out there in the journals and actual practice... Nolvadex should be the cornerstone of oncycle and pct estrogen control as well as HPTA support. The issue is that nolva and any other serm doesn't lower total estrogen, so ya, an erase or other AI is necessary, though erase doesn't work well with me, I end up with too much DHT and my rat starts to shed hair -- I don't know why, that's just my observance, that OTC anti-estrogens seem to reduce estrogen in part (irrespective of their claims that they competitively bind to aromatase) by reducing testosterone conversion into estrogen and facilitating 5 alpha reductase -- again, I don't know why and its just my observance with my "lab rat." Anastrazole works better for me and doesn't seem to have the same increase in 5 alpha reductase activity though I know testosterone is rising so some estra DHT increase occurs, just not as steep or pronounced - anastrazole needs to be tapered. Emenestane is my favorite though you need to use it very carefully because if you over do it... well takes a while to bring your estrogen back up.

    How does Erase work exactly? is it a competitive AI or does it claim suicide inhibition? Or does it just "exhibit" reduced estrogen as a consequence of facilitating test to dht... these are questions that I don't know because they don't really tell us what's in their product and then make touts and assertions trying to sell it... IF you have answers to these questions much appreciated.

    Here's another question for anyone who might know and I keep asking it... how long does it take to replenish your aromatase after you suicide inhibit it all? How long does it take to replenish your 5 alpha reductase after it is reduced from non use during say a tren only cycle? Anyone have any journal cites or cites with this information -- i.e., enzyme replenishment rates?
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