Can we please stop with the borlore - Prolactin DOES NOT INCREASE GYNO

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    Can we please stop with the borlore - Prolactin DOES NOT INCREASE GYNO


    Prolactin has NO effect on gyno according to:

    Anastassia Amaro, MD Fellow, Endocrinology and Metabolism
    Washington University School of Medicine December 15, 2005

    Sited also in Griffin and Wilson, Williams Textbook ofEndocrinology, Tenth Edition,18:709-769, 2003

    Also,

    I've never heard of prolactin being an issue with GH use EVER, so can we please stop the brolore already?

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    Quote Originally Posted by LegalGear View Post
    Prolactin has NO effect on gyno according to:

    Anastassia Amaro, MD Fellow, Endocrinology and Metabolism
    Washington University School of Medicine December 15, 2005

    Sited also in Griffin and Wilson, Williams Textbook ofEndocrinology, Tenth Edition,18:709-769, 2003

    Also,

    I've never heard of prolactin being an issue with GH use EVER, so can we please stop the brolore already?
    Funny you mention this, especially since decades of research shows androgens lower prolactin levels.

    I think many get progesterone and prolactin confused for some reason, and even then progesterone requires estrogen to induce gyno in the first place.

    So in the end.. blame it all on that evil estrogen.
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    ooops... meant to say one more thing.. Prolactin is a RESULT of gyno, not the other way around.

    Okay... carry on.
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    Progesterone REDUCES gyno. The thing about progesterone is that things like Deca are natural progesterone agonists, meaning they bind to the PR but only have 30% of the effect of pregesterone, which means that they LESSEN the progesterone effect being a possible CAUSE for gyno.

    Progesterone reduces estrogen receptor activity and something like Deca that reduces progesterone makes estrogen stronger.
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    Quote Originally Posted by LegalGear View Post
    Progesterone REDUCES gyno. The thing about progesterone is that things like Deca are natural progesterone agonists, meaning they bind to the PR but only have 30% of the effect of pregesterone, which means that they LESSEN the progesterone effect being a possible CAUSE for gyno.

    Progesterone reduces estrogen receptor activity and something like Deca that reduces progesterone makes estrogen stronger.
    Can you please reference in real life where this holds true? All my research disproves your fact.

    ESTROGEN, GH AND IGF-1, PROGESTERONE, & PROLACTIN

    Estrogen and progesterone act in an integrative fashion to stimulate normal adult female breast development. Estrogen, acting through its ER a receptor, promotes duct growth, while progesterone, also acting through its receptor (PR), supports alveolar development (18). This is demonstrated by experiments in ER knockout mice, which display grossly impaired ductal development, whereas PR knockout mice possess significant ductal development, but lack alveolar differentiation (31, 7).

    Although estrogens and progestogens are vital to mammary growth, they are ineffective in the absence of anterior pituitary hormones (15). Thus, neither estrogen alone nor estrogen plus progesterone can sustain breast development without other mediators, such as GH and IGF-1. This was confirmed by studies involving the administration of estrogen and GH to hypophysectomized and oophorectomized female rats, which resulted in breast ductal development. The GH effects on ductal growth are mediated through stimulation of IGF-1. This is demonstrated by studies of estrogen and GH administration to IGF-1 knockout rats that showed significantly decreased mammary development when compared to age-matched IGF-1- intact controls. Combined estrogen and IGF-1 treatment in these IGF-1 knockout rats restored mammary growth (26, 45). In addition, Walden et al. demonstrated that GH-stimulated production of IGF-1 mRNA in the mammary gland itself, suggesting that IGF-1 production in the stromal compartment of the mammary gland acts locally to promote breast development (55). Furthermore, other data indicates that estrogen promotes GH secretion and increases GH levels, stimulating the production of IGF-1, which synergizes with estrogen to induce ductal development.

    Like estrogen, progesterone has minimal effects in breast development without concomitant anterior pituitary hormones; again indicating that progesterone interacts closely with pituitary hormones. For example, prolonged treatment of dogs with progestogens such as depot medroxyprogesterone acetate or with proligestone caused increased GH and IGF-1 levels, suggesting that progesterone may also have an effect on GH secretion (36). In addition, clinical studies have correlated maximal cell proliferation to specific phases in the female menstrual cycle. For example, maximal proliferation occurs not during the follicular phase when estrogens reach peak levels and progesterone is low (less than 1 ng/mL [3.1nmol]), but rather, it occurs during the luteal phase when progesterone reaches levels of 10-20 ng/mL (31- 62nmol) and estrogen levels are two to three times lower than in the follicular phase (47). Furthermore, immunohistochemical studies of ER and PR showed that the highest percentage of proliferating cells, found almost exclusively in the type 1 lobules, contained the highest percentage of ER and PR positive cells (47). Similarly, there is immunocytological presence of ER, PR, and androgen receptors (AR) in gynecomastia and male breast carcinoma. ER, PR and AR expression was observed in 100% (30/30) of gynecomastia cases (48). Given these data and the fact that PR knockout mice lack alveolar development in breast tissue, it appears as if progesterone, analogous to estrogen, may increase GH secretion and act through its receptor on mammary tissue to enhance breast development, specifically alveolar differentiation (31, 21).

    Prolactin is another anterior pituitary hormone integral to breast development. Prolactin is not only secreted by the pituitary gland but may be produced in normal mammary tissue epithelial cells and breast tumors. (50, 28). Prolactin stimulates epithelial cell proliferation only in the presence of estrogen and enhances lobulo-alveolar differentiation only with concomitant progesterone. Recently, receptors for luteinizing hormone/ human chorionic gonadotropin have been found in both male and female breast tissues, though its function remains to be determined (11)
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    This is talking about NORMAL development of women in puberty. Not in men who are using steroids and have developed glandular systems. The gyno reference shows in increase in the receptors for progesterone, androgens and estrogens which isn't "normal".
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    Quote Originally Posted by LegalGear View Post
    Progesterone REDUCES gyno. The thing about progesterone is that things like Deca are natural progesterone agonists, meaning they bind to the PR but only have 30% of the effect of pregesterone, which means that they LESSEN the progesterone effect being a possible CAUSE for gyno.

    Progesterone reduces estrogen receptor activity and something like Deca that reduces progesterone makes estrogen stronger.
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    Quote Originally Posted by LegalGear View Post
    This is talking about NORMAL development of women in puberty. Not in men who are using steroids and have developed glandular systems. The gyno reference shows in increase in the receptors for progesterone, androgens and estrogens which isn't "normal".
    This whole article is all about MALE breast tissue development.

    Like I said, can you please show me some research to back up your statement? We are trying to keep the BroLore out of this. I am not discrediting that estrogen is the main player in gyno development, in fact I stated nothing can happen without the presence of estrogen, but ignoring hormonal imbalances of other hormones due to anabolic use is very tunnel vision.
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    LegalGear is getting his info from Seth Robets book Anabolic Pharmacology, i'm educationally guessing.

    Take trenbolone for example. I have seen a handful of peopl run fina-only cycles and develop gyno. Since tren is a 19-nor compound that doesnt aromatase, then there is no increased estrogen. Yet these people still are getting gyno.

    And don't tell me its from estrogen cleaving off from SHBG. That amount of estrogen is very minimal.

    You could argue that it is because progestins take a huge hit on the HPTA and shutdown testosterone production easily, then estrogen is increased, but that would contradict your point.

    Also, don't let 1-2 studies saying one thing make you assume it is fact. There's plenty of studies testing the same things giving opposite conclusions in science. Even Seth says in his section on pregestins that it is all relatively new research. He also only references 2 studies on this specific topic.

    Also, there are PR receptors in gynecomastia. So if you have even the slightest bit of pre-existing gynecomastia from puberty or a previous cycle, progestins can cause increased gyno growth.
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    I thought it was still considered an unknown when it came to gyno. Lots of theories but nothing completely conclusive?
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    Also there is a lot of real-worl evidence showing that people have greatly decreased gyno when adding cabergoline to their cycle, which in your theory should make it worse.
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    Quote Originally Posted by Jayhawkk View Post
    I thought it was still considered an unknown when it came to gyno. Lots of theories but nothing completely conclusive?
    That is correct
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    in doing research i found that when looking for causes of gyno, it is standard for doc's to check levels of estrogen AND PROLACTIN. it would appear that the medical profession considers elevated prolactin a legitimate cause for gyno.
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    Quote Originally Posted by LegalGear View Post
    Prolactin has NO effect on gyno according to:

    Anastassia Amaro, MD Fellow, Endocrinology and Metabolism
    Washington University School of Medicine December 15, 2005

    Sited also in Griffin and Wilson, Williams Textbook ofEndocrinology, Tenth Edition,18:709-769, 2003

    Also,

    I've never heard of prolactin being an issue with GH use EVER, so can we please stop the brolore already?
    Do you frequent board geared to steroid users? If so you would not be saying ANY of this. GH causes gyno is MANY people and so does prolactin.
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    That statement doesn't mean a high level of prolactin with the presence of gyno is necessarily a 'cause' per se. It could also be considered a result...

    All i know is that for every person saying they got gyno from "x" you have another saying they didn't. What makes this anecdotal evidence even more diluted is the fact that a lot of people do not really know what gyno is and confuse inflammation and/or irritation as a diagnosis of gyno.
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    Do you frequent board geared to steroid users? If so you would not be saying ANY of this. GH causes gyno is MANY people and so does prolactin.
    I think using a community of forum users is a good place to start when trying to figure out an answer. It by no means should be used as scientific or conclusive evidence of a result or lack thereof. Too many people ignore or simply refuse to acknowledge the many other variables that could be part of the problem.
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    Quote Originally Posted by Jayhawkk View Post
    I thought it was still considered an unknown when it came to gyno. Lots of theories but nothing completely conclusive?
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    'there are few outward signs of increased prolatin levels. however, some men do develop gynecomastia'. prolactin is considered a hormone, any time there is an imbalance of hormones the risks of gyno increase, at least imo.
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    Quote Originally Posted by thebigt View Post
    'there are few outward signs of increased prolatin levels. however, some men do develop gynecomastia'. prolactin is considered a hormone, any time there is an imbalance of hormones the risks of gyno increase, at least imo.
    Is lactation "outward" enough for you? ha
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    Quote Originally Posted by justreading View Post
    Is lactation "outward" enough for you? ha
    hahaha, yeah. but the quote was from a medical report.
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    Quote Originally Posted by andrew732 View Post
    VERY true!
    Man... you call LG 100% correct, then go on to agree everything on gyno is inconclusive... which is it?
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    I know the article is written about male breast tissue development, but it's also siting research clearly done on women and development.

    As for Finaplex, it is pretty easily explained that there are A LOT of idiots out there and Fina-H vs. Fina-S are very different, one contains estrogen one does not. One would think the Steer (male) Fina would be the one to get. I can see it now, walking into the farm supply and ask "I need some fina pellets" Do you need them for a steer or a heifer? Oh, a steer of course...

    I would agree that none of this is conclusive, however why then do you have people running around worried all day about their prolactin levels? It's your typical scare tactics. People think Creatine causes kidney damage still because of stupid scare tactics and EVERYONE has gyno. Drives me nuts...

    I just posted a link by a doctor specializing in this field who said in his presentation and cited an advanced medical text saying "prolactin has no effect on gynocomastia" in his presentation on the subject.

    Anecdotal information is the worst kind because juice heads are morons and the people making juice are even worse. You really think an underground lab that is a little low on a compound won't just throw in whatever they have laying around to get a run out?
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    Quote Originally Posted by LegalGear View Post
    I know the article is written about male breast tissue development, but it's also siting research clearly done on women and development.

    As for Finaplex, it is pretty easily explained that there are A LOT of idiots out there and Fina-H vs. Fina-S are very different, one contains estrogen one does not. One would think the Steer (male) Fina would be the one to get. I can see it now, walking into the farm supply and ask "I need some fina pellets" Do you need them for a steer or a heifer? Oh, a steer of course...

    I would agree that none of this is conclusive, however why then do you have people running around worried all day about their prolactin levels? It's your typical scare tactics. People think Creatine causes kidney damage still because of stupid scare tactics and EVERYONE has gyno. Drives me nuts...

    I just posted a link by a doctor specializing in this field who said in his presentation and cited an advanced medical text saying "prolactin has no effect on gynocomastia" in his presentation on the subject.

    Anecdotal information is the worst kind because juice heads are morons and the people making juice are even worse. You really think an underground lab that is a little low on a compound won't just throw in whatever they have laying around to get a run out?
    wow wow wow is all I can say! Juice heads are morons? What do you call supplement users? There are good and bad among all kinds but juice heads are some of the most intense, intelligent, type A personalities that I have ever met. They are driven to reach their goals and generally upstanding, intelligent people who know enough to resist the marketing gimmicks of supplement companies.

    There are studies and statistics that can prove anything you want to prove. I can care less if i have "proof" that prolactin causes gyno but this can be proven, many people have gotten gyno NOT attributed to estrogen and often while lactating. Even if you can't prove prolactin caused it, it certainly makes sense to assume so and act as if it is the case because inhibiting prolactin has solved many cases of gyno. It may be a co-factor but it IS a factor and has distinct signals that it is involved in many cases.
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    Really? How about all the ones (99% of them) that wouldn't touch Methyl 1-Test because it isn't as good as the "real" stuff. Please tell me why a compound being a schedule III steroid makes it "real"? Can any of them tell me structurally why Methyl 1-Test or Halodrol or Superdrol is inferior to D-Bol, Anadraul or Anavar? Ask them though and they are "experts".
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    google incresed prolactin in males and tell me why we SHOULDN'T be concerned about prolactin levels. infertility, low sex drive and gyno are a few of the symptoms. come on man, i can't believe you think prolactin is a good thing-hell i can't find one good thing about prolactin in men.
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    I think it can be argued both ways- and, from what I have seen, it is also dependant of the hormonal state of said individual. If your T levels are normal and you haven't done anything to throw the T:E ratio out of whack, PRL is probably something you don't need to worry about (much). However, someone who has come off a cycle is going to have low androgen levels, and higher E levels, and this is a good enviroment for male breast development. Throw IGF-1, GH, etc. into the mix, and it could be a real issue. Most of the studies affirming that prolactin may have a role in male breast development are in individuals who have already had issues from an endocrine standpoint:

    Histopathology. 2008 Jul;53(1):56-61.

    Prolactin receptor expression in gynaecomastia and male breast carcinoma.
    Ferreira M, Mesquita M, Quaresma M, André S.

    Serviço de Anatomia Patológica, Instituto Português de Oncologia de Lisboa Francisco Gentil, EPE, Lisboa, Portugal. marco_franco@sapo.pt

    AIMS: Despite the well-established function of prolactin (PRL) in normal breast development, its role in breast cancer pathogenesis is still controversial. PRL activity is dependent on the activation of a transmembrane protein, the PRL receptor (PRLR). The aim was to evaluate and compare PRLR expression in gynaecomastia and male breast carcinoma (MBC). METHODS AND RESULTS: PRLR expression was detected immunohistochemically in 30 cases of gynaecomastia and 30 cases of MBC. The whole series was also assessed for oestrogen receptors (ER), progesterone receptors (PR) and androgen receptors (AR). A cut-off of 10% was used as the criterion for positivity. Histological type and tumour differentiation were evaluated. Pathological stage was assessed [Tumour Node Metastasis (TNM)-International Union Against Cancer system]. Statistical analysis was performed with Fisher's exact test. PRLR positivity was seen in 20% of gynaecomastia cases and in 60% of MBC cases (P = 0.003). In gynaecomastia immunoreactivity was predominantly observed in luminal cell borders, whereas in MBC the reactivity was heterogeneous and mainly cytoplasmic. There was no statistically significant correlation between PRLR expression and ER, PR, AR, pTNM, or histological grade. CONCLUSIONS: PRLR is significantly more expressed in MBC than in gynaecomastia, and with different patterns of reactivity, suggesting a role for PRL in male breast carcinogenesis.




    Am J Pathol. 2008 Jan;172(1):194-202. Epub 2007 Dec 21.

    Prolactin drives estrogen receptor-alpha-dependent ductal expansion and synergizes with transforming growth factor-alpha to induce mammary tumors in males.
    Arendt LM, Schuler LA.

    Cellular and Molecular Biology Program, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Dr., Madison, WI 53706, USA.

    Male breast cancer is rare and has been the focus of limited research. Although the etiology is unclear, conditions increasing circulating prolactin (PRL), as well as estrogen, increase the risk of tumorigenesis. We modeled exposure to elevated PRL in transgenic mice, using the mammary-selective, estrogen-insensitive promoter neu-related lipocalin (NRL), to drive PRL expression. Male NRL-PRL mice did not develop mammary tumors. However, in cooperation with the well-characterized oncogene transforming growth factor-alpha (TGF-alpha), PRL induced mammary tumors in 100% of male bitransgenic mice. Similar to disease in human males, these tumors expressed variable levels of estrogen receptor-alpha (ER-alpha) and androgen receptors. However, carcinogenesis was not responsive to testicular steroids because castration did not alter latency to tumor development or tumor ER-alpha expression. Interestingly, both NRL-TGF-alpha/PRL and NRL-PRL males demonstrated increased ductal development, which occurred during puberty, similar to female mice. This outgrowth was diminished in NRL-PRL males treated with ICI 182,780, suggesting that PRL enhances ER-mediated growth. Treatment of MCF-7-derived cells with PRL increased phosphorylation of ER-alpha at residues implicated in unliganded ER-alpha activity. Together, these studies suggest that PRL expands the pool of cells susceptible to tumorigenesis, which is then facilitated by PRL and TGF-alpha cross talk. Activation of ER-alpha is one mechanism by which PRL may contribute to breast cancer and points to other therapeutic strategies for male patients.
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
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    Quote Originally Posted by LegalGear View Post
    Really? How about all the ones (99% of them) that wouldn't touch Methyl 1-Test because it isn't as good as the "real" stuff. Please tell me why a compound being a schedule III steroid makes it "real"? Can any of them tell me structurally why Methyl 1-Test or Halodrol or Superdrol is inferior to D-Bol, Anadraul or Anavar? Ask them though and they are "experts".
    Actually most won't touch m-1-t or superdrol because they are unproven and show signs of being more toxic than dbol. Track the history of these drugs and their analogs and you will know why real deal users are smart enough to not touch them, for their health.
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    any way you cut it, increased prolactin in males is not a good thing. rather or not it causes gyno we could argue about all day, but one thing we all should agree on prolactin is not a good thing for a male.
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    Quote Originally Posted by justreading View Post
    Actually most won't touch m-1-t or superdrol because they are unproven and show signs of being more toxic than dbol. Track the history of these drugs and their analogs and you will know why real deal users are smart enough to not touch them, for their health.
    All of the aforementioned compounds are considered steroids- they all come from the same base derviation and cholesterol backbone- when they were first synthed, it was for one purpose or another, with no classification that it was a PH/AAS/etc. We have put in all of the added terminology over the years, and, in reality, there is not a "better" compound than another- it really just depends on the desired method of application- for instance- Oxymethelone (Anadrol 50) is great for increasing RBC- but it is not great for building a lean, hard look, even though it is 5-alpha reduced. Bodybuilding applications do not necessarily translate over to other "real world" apps, and vice-versa....
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    No one is saying that prolactin is "good" however having people reduce aspects of their hormonal cascade when there is no indication of higher than normal levels is crazy and pointless. Like anything excess prolactin isn't a positive, but reducing it just because isn't good either.
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    Quote Originally Posted by justreading View Post
    Actually most won't touch m-1-t or superdrol because they are unproven and show signs of being more toxic than dbol. Track the history of these drugs and their analogs and you will know why real deal users are smart enough to not touch them, for their health.
    Ok, well it's your story, you tell it... I'd take my chance with a GMP certified facility making my M1T vs. a guy in his basement making D-Bol tabs any day. Additionally, that wasn't what I heard, it was that it wasn't "real gear". I think you are really stretching here...
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    Quote Originally Posted by LegalGear View Post
    No one is saying that prolactin is "good" however having people reduce aspects of their hormonal cascade when there is no indication of higher than normal levels is crazy and pointless. Like anything excess prolactin isn't a positive, but reducing it just because isn't good either.
    It's like anything else- you want to keep levels normalized, and not throw it out of whack- It is ok to lower E, Cortisol, and SHBG to a certain extent, but there is a rebound effect when you start messing around with these entities. Prolactin isn't "bad" in most contexts- but in an atypical state where the T:E or T:C ratio isn't where it should be, it could be an issue, just like decreasing it too much could be an issue as well.....homeostatic mechanisms are pretty delicate things
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    Some choice quotes:

    " Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome , arteriogenic ED , and premature ejaculation."

    That's right drive that prolactin into the ground! Erectile Dysfunction, Metabolic Syndrome, Premature Ejaculation. All great things for a guy.


    J Sex Med. 2009 May;6(5):1457-66. Epub 2009 Feb 10.
    Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction.

    Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, Boddi V, Bandini E, Balercia G, Forti G, Maggi M.

    Andrology Unit, Department of Clinical Physiopathology, University of Florence, Florence, Italy.

    INTRODUCTION: The physiological role of prolactin (PRL) in male sexual behavior is poorly understood. Conversely, the association between PRL pathological elevation in both reproductive and sexual behavior is well defined. AIM: The aim of the present study is to assess the correlates of normal PRL (PRL < 735 mU/L or 35 ng/mL), in male subjects consulting for sexual dysfunction. METHODS: A consecutive series of 2,531 (mean age 52.0 +/- 12.9 years) subjects was investigated. Patients were interviewed using the structured interview on erectile dysfunction (SIEDY), a 13-item tool for the assessment of erectile dysfunction (ED)-related morbidities. Middlesex Hospital Questionnaire was used for the evaluation of psychological symptoms. MAIN OUTCOME MEASURES: Several hormonal (testosterone, thyroid stimulation hormone, and PRL) and biochemical parameters (glycemia and lipid profile) were studied, along with penile Doppler ultrasound (PDU) and SIEDY items. RESULTS: After adjustment for confounders anxiety symptoms decreased across PRL quartiles (I: <113 mU/L or 5 ng/mL; II: 113-156 mU/L or 5.1-7 ng/mL; III: 157-229 mU/L or 7.1-11 ng/mL; IV: 229-734 mU/L or 11.1-34.9 ng/mL). Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome (MetS; odds ratio [OR] = 1.74 [1.01-2.99], P < 0.05), arteriogenic ED (peak systolic velocity at PDU < 35 cm/sec; OR = 1.43 [1.01-2.03], P < 0.05), and premature ejaculation (PE; OR = 1.38 [1.02-1.85]; P < 0.05). Conversely, comparing subjects with PRL-secreting pituitary adenomas (N = 13) with matched controls, no significant difference was observed, except for a higher prevalence of hypoactive sexual desire in hyperprolactinemia. CONCLUSIONS: Our findings demonstrate that, in subjects consulting for sexual dysfunction, PRL in the lowest quartile levels are associated with MetS and arteriogenic ED, as well as with PE and anxiety symptoms. Further studies are advisable in order to confirm our preliminary results in different populations.
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    Quote Originally Posted by LegalGear View Post
    Ok, well it's your story, you tell it... I'd take my chance with a GMP certified facility making my M1T vs. a guy in his basement making D-Bol tabs any day. Additionally, that wasn't what I heard, it was that it wasn't "real gear". I think you are really stretching here...
    M1T was a weird compound- I have worked with it some- and also used it- didn't really like working with it (really can irritate the nasal passages and eyes, even with protective garbing). As for using it- I have never had that dramatic an effect out of anything I have taken- it was too strong for me, even @ 10 mg/day
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    Quote Originally Posted by LegalGear View Post
    Some choice quotes:

    " Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome , arteriogenic ED , and premature ejaculation."

    That's right drive that prolactin into the ground! Erectile Dysfunction, Metabolic Syndrome, Premature Ejaculation. All great things for a guy.


    J Sex Med. 2009 May;6(5):1457-66. Epub 2009 Feb 10.
    Hypoprolactinemia: a new clinical syndrome in patients with sexual dysfunction.

    Corona G, Mannucci E, Jannini EA, Lotti F, Ricca V, Monami M, Boddi V, Bandini E, Balercia G, Forti G, Maggi M.

    Andrology Unit, Department of Clinical Physiopathology, University of Florence, Florence, Italy.

    INTRODUCTION: The physiological role of prolactin (PRL) in male sexual behavior is poorly understood. Conversely, the association between PRL pathological elevation in both reproductive and sexual behavior is well defined. AIM: The aim of the present study is to assess the correlates of normal PRL (PRL < 735 mU/L or 35 ng/mL), in male subjects consulting for sexual dysfunction. METHODS: A consecutive series of 2,531 (mean age 52.0 +/- 12.9 years) subjects was investigated. Patients were interviewed using the structured interview on erectile dysfunction (SIEDY), a 13-item tool for the assessment of erectile dysfunction (ED)-related morbidities. Middlesex Hospital Questionnaire was used for the evaluation of psychological symptoms. MAIN OUTCOME MEASURES: Several hormonal (testosterone, thyroid stimulation hormone, and PRL) and biochemical parameters (glycemia and lipid profile) were studied, along with penile Doppler ultrasound (PDU) and SIEDY items. RESULTS: After adjustment for confounders anxiety symptoms decreased across PRL quartiles (I: <113 mU/L or 5 ng/mL; II: 113-156 mU/L or 5.1-7 ng/mL; III: 157-229 mU/L or 7.1-11 ng/mL; IV: 229-734 mU/L or 11.1-34.9 ng/mL). Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome (MetS; odds ratio [OR] = 1.74 [1.01-2.99], P < 0.05), arteriogenic ED (peak systolic velocity at PDU < 35 cm/sec; OR = 1.43 [1.01-2.03], P < 0.05), and premature ejaculation (PE; OR = 1.38 [1.02-1.85]; P < 0.05). Conversely, comparing subjects with PRL-secreting pituitary adenomas (N = 13) with matched controls, no significant difference was observed, except for a higher prevalence of hypoactive sexual desire in hyperprolactinemia. CONCLUSIONS: Our findings demonstrate that, in subjects consulting for sexual dysfunction, PRL in the lowest quartile levels are associated with MetS and arteriogenic ED, as well as with PE and anxiety symptoms. Further studies are advisable in order to confirm our preliminary results in different populations.
    This relates to what I was saying before: anyone who tends to run into issues with PRL seems to have already had some endocrine disruptive issues- in this case the patients were coming in for erectile dysfunction- and it doesn't really give the #'s for the other hormonal profiles- but I would be willing to make a bet that they were out of whack as well....
    Dirk Tanis, BA, MSci
    Chief Operating Officer, Applied Nutriceuticals
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    Quote Originally Posted by LegalGear View Post
    Ok, well it's your story, you tell it... I'd take my chance with a GMP certified facility making my M1T vs. a guy in his basement making D-Bol tabs any day. Additionally, that wasn't what I heard, it was that it wasn't "real gear". I think you are really stretching here...
    Were you beaten up by a bodybuilder? Seriously, where did this hatred come from? You are supposed to be a professional in the athletic enhancement field, how can you know so little about something yet speak so definitively?
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    Quote Originally Posted by LegalGear View Post
    Some choice quotes:

    " Patients in the lowest PRL quartile showed a higher risk of metabolic syndrome , arteriogenic ED , and premature ejaculation."

    That's right drive that prolactin into the ground! Erectile Dysfunction, Metabolic Syndrome, Premature Ejaculation. All great things for a guy.
    Looks like somebody still needs to learn basic concepts, like correlation does not imply causation.
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    Quote Originally Posted by LegalGear View Post
    No one is saying that prolactin is "good" however having people reduce aspects of their hormonal cascade when there is no indication of higher than normal levels is crazy and pointless. Like anything excess prolactin isn't a positive, but reducing it just because isn't good either.
    there is not a single positive reason for a male to have prolactin at all, so what would be the negative of reducing it. it seems that bromo is popular for it's sex benefits as well as overall well being that users report. prolactin also reduces production of testosterone and dopamine, so i don't think there is a 'however'. prolactin is just plain bad for males period.
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    Quote Originally Posted by LegalGear View Post
    Prolactin has NO effect on gyno according to:

    Anastassia Amaro, MD Fellow, Endocrinology and Metabolism
    Washington University School of Medicine December 15, 2005

    Sited also in Griffin and Wilson, Williams Textbook ofEndocrinology, Tenth Edition,18:709-769, 2003
    Why don't you give a link to the PDF where you found this? http://endo.wustl.edu/conferences/PD...necomastia.pdf (slide 19)

    The basis of your argument is an appeal to authority (Dr. Amaro), who in turn appeals to another authority (Griffin and Wilson). What we need to know is what exactly it says in Williams Textbook of Endocrinology between pages 709 and 769. You need to investigate whether Dr. Amaro paraphrased correctly. Did Griffin and Wilson give primary references to support their claim? What were they and how strong are they? You've barely scratched the surface.
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    Quote Originally Posted by LegalGear View Post
    I just posted a link by a doctor specializing in this field who said in his presentation and cited an advanced medical text saying "prolactin has no effect on gynocomastia" in his presentation on the subject.
    First, you didn't post a link. You gave a reference. Second, you misquoted him, which is you just being lazy. Don't put quote marks around a paraphrase.
  

  
 

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