Can we please stop with the borlore - Prolactin DOES NOT INCREASE GYNO
- 11-02-2009, 10:19 AM
- 11-02-2009, 11:26 AM
11-02-2009, 11:38 AM
11-02-2009, 11:40 AM
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.
11-02-2009, 11:41 AM
11-02-2009, 11:43 AM
11-02-2009, 11:47 AM
You clearly can't read...and obviously neither can Concilliator or whatever his name is...
He purposefully misuses the literature as usual. I've refuted everything he's said and yet crickets chirp...
The paper sited shows an affinity for the PR of 8-9% and we are splitting hairs on symantics, the net effect is the same. Additionally, the graph shows specifically that at lower concentrations the net effect of Deca is to NOT be as potent a progestin.
So, in a nutshell, Deca with a 8-9% affinity and a lower activity level up until high concentrations are reached is a full agonist (your two papers by the way) in your eyes. The net effect is going to be a partial agonist like I was saying in the first place.
Yes, this is BRINGING NOTHING. I always wonder why the world exists in the way it does, all I need to do is get back on these threads... Reading the papers, responding, showing how the data is being misinterpreted, yes, this is nothing...
11-02-2009, 11:52 AM
I get on showing a presentation and reference from a Doctor that says Prolactin has NO ROLE in gyno. So, it's not MY theory, it's the theory of a Doctor. Where did the other "theory" come from? A bunch of dudes that think progestins and prolactins are interchangable because they both start with P. When you take the counter point to the good Dr. you then take the burden of proving your argument.
Progesterone is the second or third (I believe the second) highest hormone in the MALE body after testosterone, so it seems pretty likely that it isn't the "progestational" effects.
11-02-2009, 11:56 AM
11-02-2009, 12:02 PM
You want the explanation?
Fine, as I've said numerous times. "heresay" isn't proof. Two things could be going on. All nipple tissue will produce fluid if squeezed, there are sweat and oil ducts that have fluid. Try it now, go squeeze your nipples for 2-3 minutes and see the fluid come out. How did I find this out, I got a panic stricken call from my sales rep saying that M1P caused a guy to leak. He was also on M1P and after squeezing his nips for a minute or two some fluid came out. So, then I for science sake squeezed mine (I was not taking M1P) and guess what? Yep, fluid.
Breast tissue in general is very sensitive. If you keep touching it and playing with it, they tend to get very irritated and sore. So, of course human nature is to keep playing with it to "check". This accounts for 99% of the pain, swelling that people feel.
Finally, I reread the posts and Concilliator said that Tren and Deca are not as strong progestins as Progesterone, then sites a study showing Tren to be as potent. This will be lost on the masses.
The point is to challenge the Dr. and the medical text book...great argument. I am officially done with this thread, it's clearly pointless.
11-02-2009, 12:06 PM
11-02-2009, 12:30 PM
I know from personal experience that prolactin causes gyno in me, I don't want to go into full detail but some Rec drugs lower dopamine and cause an increase in prolactin and they definitely cause gyno.
11-02-2009, 12:58 PM
Not sure about recreation drugs, so again anything is possible when you mess with your endocrine system and mix compounds. Also, it's not overactive sweat glands, it's normal oil ans sweat.
DAdams, since I might have been kind of a ****, let me send you some free products. I try to make amends when I am overly harsh. PM me your address and what you want to try...
11-02-2009, 01:10 PM
One thing I will say first. You can find one or two studies to backup basically anything you want to say. But if you have any experience in and have been around people who have you will know a few things to be true.
There are some who are sensitive to progesterone's and some who aren't. I myself, and many others that I know - and I would go as far as to say the majority get gyno while on things like Tren and Deca. That isn't ridiculous to say or some groundbreaking news - it's well known, and has been among people who don't sit behind a keyboard arguing on forums. Rather, the ones who are actually using these compounds and lifting weights to boot. I can also say that running dostinex while on either of these completely prevents it, and again that's not just me - a very widely known fact.
One thing I do know is that heavy doses of B6, Dostinex(Caber), p-5-p, dopamine (I think?), and a couple others all lower prolactin and all have been shown to help with things like Tren/Deca/etc...
So bring all your studies, everything else you need to make you feel better and I will find a couple bunk ones myself to "prove" the antithesis. Just goes to show you all these "scientists and doctors" really for the most part don't know wtf they are doing and have never actually got out there and tried anything for themselves. Its like a politician telling you what the war is like over in Afghanistan/Iraq, then the ACTUAL soldiers come back and are like wtf?...no - same concept.
11-02-2009, 01:17 PM
You bug-eyed, side-steppin' sand crab, you...
Let's have a go at it, I want some of those free samples, too.
11-02-2009, 01:21 PM
11-02-2009, 02:41 PM
Just because something is at a concentration that does not produce full activity does not make it a partial agonist. Those are two different things. Test is a full agonist of the AR. If you're taking 200mg/wk and getting less than full activity, it doesn't change the fact that test is still a full agonist, does it? Rather, something is a full agonist if it is capable of producing maximal activity when the receptor is saturated with the ligand, at whatever concentration that might be. All the data I provided shows that deca is a full agonist. Accordingly, it will NOT be blocking or reducing the effect of endogenous progesterone. It will only be adding to the overall progestational activity, which directly contradicts your unsupported argument earlier in this thread. The data shows that deca and tran have the same activity as progesterone, producing a 100% response. It just takes a higher concentration to saturate the receptor, since as ligands they have lower affinity.
11-02-2009, 03:38 PM
This study found that even a single, 100mg shot of deca produced plasma levels that high (>10 nM).
What we know is that there's definitely progestational activity from deca. The question is how much. We can only guess what happens in vivo, in cells that matter in human males.
11-02-2009, 03:39 PM
I actively posted and debated in that thread for pages and pages. Of course, you didn't like that thread because it exposed your marketing claims for what they clearly were, bull****.
11-02-2009, 04:04 PM
Not to mention that there are other references for nandrolone, showing that it may have a 20-30% RBA compared to progesterone. At 10%, it means that if you have 10x more nandrolone in your body than natural progesterone (which would be easy with the doses guys are injecting), you would double the progestogenic action in the body. If nandrolone has 30% the affinity of progesterone, that same dose would quadruple the progestogenic effects in the body. That could easily have physiological significance.
11-02-2009, 05:19 PM
As stated numerous times, increased AR's in immature cells would make logical sense since they are turning into androgen dependent cells.
There are conflicting papers on this subject and your paper doesn't even site the activity of Deca, it says "similar" results.
Fertil Steril. 1979 May;31(5):552-61.
Competitive progesterone antagonists: receptor binding and biologic activity of testosterone and 19-nortestosterone derivatives.
Reel JR, Humphrey RR, Shih YH, Windsor BL, Sakowski R, Creger PL, Edgren RA.
Testosterone and 19-nortestosterone derivatives were evaluated in a developmental scheme designed to identify competitive progesterone antagonists having abortifacient activity. Compounds that displayed significant binding to the rabbit uterine progesterone receptor were followed in biologic tests for progestational, antiprogestational, and abortifacient activities. Of the seven compounds tested for both progestational and antiprogestational activity, only one, 5 alpha-dihydronorethindrone, behaved exclusively as an antagonist. Five other 19-nortestosterones (19-nortestosterone, 17 beta-hydroxyestra-4, 9(10)-dien-3-one, norethindrone, norethindrone acetate, and R 2323) proved to be mixed agonists/antagonists. 5 alpha-Dihydronorethindrone, norethindrone, and 19-nortestosterone terminated pregnancy during the postnidatory period in rats; in addition, the latter two compounds inhibited progesterone-supported pregnancy in spayed rats and curtailed pregnancy during the postnidatory period in hamsters. These results demonstrate that several 19-nortestosterone derivatives bind to the uterine progesterone receptor and behave either as antagonists or mixed agonists/antagonists.
At some point it would seem that any concentration androgens can stimulate the PR, as shown in this article so, showing activity at a high concentration isn't reserved to deca.
Methods Find Exp Clin Pharmacol. 1997 May;19(4):215-22.
Estrogenic and progestagenic activities of physiologic and synthetic androgens, as measured by in vitro bioassays.
Markiewicz L, Gurpide E.
Mount Sinai School of Medicine (CUNY), Department of Obstetrics, Gynecology and Reproductive Science, NY, USA.
Estrogenic activities of testosterone (T) and 5a-dihydrotestosterone (DHT) were detected and measured by using their specific stimulatory effects on alkaline phosphatase (AP) activity in human endometrial adenocarcinoma cells of the Ishikawa Var-1 line. These two physiologic androgens were able to induce, at microM concentrations, estrogenic effect believed to be mediated by the estrogen receptor (ER) since the antiestrogens ICI-164384 and 4-hydroxytamoxifen (OHTam), but not the antiandrogens hydroxyflutamide (OHFl) or cyproterone acetate (CPA), reversed that effect. By using another in vitro bioassay, based on the progestin-specific stimulation of AP activity in cells of the T47D human breast cancer line, progestagenic activity was detected and measured in T, DHT and three synthetic androgens: nandrolone (19-nortestosterone). 7 alpha-methyl 19-nortestosterone (MENT) and mibolerone (7 alpha, 17 alpha-dimethyl 19-nortestosterone) (DMNT). While progestagenic effects of T and DHT required relatively high concentrations (microM levels), the synthetic androgens stimulated AP activity at nM or pM levels. These effects seem to be mediated by the progesterone receptor (PR), since they are completely abolished by the antiprogestins RU-486, ZK-98299 and ZK-112993, but not by the antiandrogen OHFl. These simple in vitro bioassays, expressing biological effects of the test compounds in human cells in culture, revealed dual or multiple hormonal activities coexisting in a single compound and provide quantitative information of considerable pharmacological importance concerning the complex actions of drugs.
Even so, where is the paper showing that progestational activity is partly the cause of gyno, even more so, where is the proof that normal prolactin levels or even higher than normal cause gynocomastia.
11-03-2009, 05:39 AM
What we do know is that there are newer papers from the same researcher. The lead author, J.R. Reel, is actually the author of the second paper I linked to here.
First, looking at progestational transcriptional activity, they found that nandrolone "at 10–8 M, increased transcriptional activity to the same extent as the progestin standard, R5020, at 10–8 M." Second, they performed a functional reporter assay and looked at alkaline phosphatase activity, which is produced in response to progestins in T47DCO cells. At 10-8 M, nandrolone "produced substantial increases in alkaline phosphatase activity." The conclusion states that "as we have shown here, 19-norandrogens exhibit considerable progestational activity both in vitro and in vivo."
11-03-2009, 05:42 AM
To add to that, I located a third study on nandrolone in which they performed a bioassay for transactivation of the human progesterone receptor. Again, this is a very recent study, 2007. It explains, "All steroids showed full agonist activity in the AR bioassay, reaching close to 100% of maximal T apart from nilutamide which was a partial agonist, reaching a plateau of 30% of maximal bioactivity (not shown). Significant deviation from maximum values in the PR bioassay was seen only with the PR antagonist, mifepristone (53% of maximal, Fig. 1B) and the prodrug, ethylestrenol (63% of maximal, not shown)." Here's a copy of figure 1. As you can see, nandrolone produced a full agonist response in both assays.
The paper also explains that "Currently marketed progestins fall into two main classes according to their structural relatedness to progesterone or 19-nortestosterone . Historically, this split arose from the finding that, whereas 19-nortestosterone (nandrolone) was a more potent androgen than testosterone, it was orally inactive and the introduction of a 17a-ethynyl group to render 19-nortestosterone orally active, as it does for estradiol, produced unexpected but highly potent progestin activity ." Historically, several synthetic progestins used for birth control have been 19-nortestosterone derivatives (which is their class name).
Based on these three studies I think it's safe to say that 1) nandrolone definitely has progestational activity, both in vitro and in vivo, and 2) nandrolone is likely a full agonist, capable of producing maximal bioactivity, as shown independently in 3 recent studies.
11-03-2009, 06:04 AM
"high concentration"? Hell no. It's says that nandrolone has progestational activity at 6 to 9 orders of magnitude lower than that of testosterone, mM (10-3) compared to nM (10-9) or pM (10-12). According to this paper, that means nandrolone produces progestational effects at one millionth to one billionth the concentration of testosterone. Yep, deca is just like test, lol.
To top it off, Nandi once referenced this study, saying "The second reason Deca may be so suppressive is that besides being an androgen, it also has progestigenic properties, meaning it binds to the human progesterone receptor at relatively low concentrations where it acts as an agonist (1)."
Who's "misusing the literature" now?
11-03-2009, 06:09 AM
11-03-2009, 07:54 AM
Your graph (full agonist) is a little misleading to your point, the transctivation graph is showing testosterone being a partial agonist at roughly 70% the activity. Additionally, it is showing that relative to progesterone Deca has lower activity which would make it a partial agonist. So, the data based on two graphs isn't conclusive by any stretch since "fullagonist.jpg" doesn't show deca (nortest) achieving the same levels of activation as progesterone. One can clearly see a large gap between progesterone and deca (nortestosterone) at almost every concentration, so to say that it has full agonist potential isn't 100% true based on this graph. In these experiments deca(nortestosterone) has a lower transcription activity level than progesterone.
However I would say you are probably right on this one, I reread the posts. I would agree with your statements that "Based on these three studies I think it's safe to say that 1) nandrolone definitely has progestational activity, both in vitro and in vivo, and 2) nandrolone is likely a full agonist, capable of producing maximal bioactivity, as shown independently in 3 recent studies." Looks like you found some good references to back up it being a full agonist. No one is denying that deca has progestational activity, the issue in question is whether it is a full agonist or partial agonist. Even then it isn't really at all part of the original discussion. So, ok it's looks like it has full transcription activity or pretty close to it. I am fine with being wrong occasionally, no big deal. It's cool to learn and I discovered something new, I had been under the impression that deca was not a full agonist, that it was only a partial agonist. I knew it had a low RBA, since the references were relatively obscure I hadn't bothered to look to see if it had full transcriptional activity. This is how we learn new things by discussing it. It's 100% not clear to me from your data that they do indeed have the same activity level but I would say it is probably the case.
11-03-2009, 09:20 AM
The original point is to A) not automatically lower prolactin when you have no reason to suspect prolactin is your issue other than you can "feel it". I never said that high prolactin is a good thing, just that it doesn't appear to cause gyno and that there is a need for it in the body. Finally, messing with every hormone in the body because you "feel" it is going to cause more problems. So, everyone running around saying "I need to lower prolactin because I can feel mine is elevated" is idiotic.
As for progesterone, ok I concede it might be a full agonist at high concentrations, yet that doesn't make it causative in gyno when in fact it may actually prevent gyno and four studies on it don't seem to be conclusive when the data is not precise.
This was a good discussion where recent research was brought to light showing Deca to be a full agonist vs. my belief that it was a partial agonist. So, I learned something and I think we've debunked some brolore here saying that prolactin has no role in males and should be beaten down.
11-03-2009, 06:29 PM
11-03-2009, 06:42 PM
11-03-2009, 07:16 PM
This is an interesting point about a possible cause for resistant tissues.
Anticancer Res. 2009 Jun;29(6):2167-71.
Differential effects of aromatase inhibitors and antiestrogens on estrogen receptor expression in breast cancer cells.
Smollich M, Götte M, Fischgräbe J, Radke I, Kiesel L, Wülfing P.
Department of Obstetrics and Gynecology, University of Münster, 48129 Münster, Germany.
BACKGROUND: Estrogen receptors (ER) alpha and beta play an important role in breast cancer. Recently, systemic adjuvant endocrine therapy with selective estrogen receptor modulator (SERM) tamoxifen has been challenged by aromatase inhibitors. Compared to antiestrogens, third-generation aromatase inhibitors (anastrozole and letrozole) exhibit an improved efficacy and tolerability. MATERIALS AND METHODS: Using real-time PCR analysis, 21 breast cancer tissue samples were analysed for a change of the ERalpha/ERbeta ratio during malignant progression. In stimulation experiments, differential effects of SERMs, ER antagonists and aromatase inhibitors have been investigated. RESULTS: Transition from normal breast to grade 1 tumors was characterized by down-regulation of ERbeta (relative quantification [RQ]=0.83, p=0.019), while transition from grade 1 to grade 3 tumors was associated with the decrease of ERalpha expression (RQ=1.14 vs. RQ=0.65, p<0.001). In stimulation assays, tamoxifen and fulvestrant increased ERalpha expression to RQ=1.51 (p=0.01) and RQ=1.42 (p<0.001), respectively, and left ERbeta unchanged. In contrast, aromatase inhibitors up-regulated ERbeta to RQ=1.23 (anastrozole, p=0.029) and RQ=1.38 (letrozole, p=0.048). CONCLUSION: Taken together, data indicate that SERMs/antiestrogens and aromatase inhibitors exhibit opposed effects on the ER expression of breast cancer cells: tamoxifen and fulvestrant up-regulate ERalpha expression, while aromatase inhibitors increase ERbeta expression, which may contribute to the aromatase inhibitors' therapeutic superiority over antiestrogens.
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