Your own words with my replies:
You claimed that "nandrolones are used as progestins in research," and that they "will stimulate the progesterone receptor." I asked for your evidence and you deflected with a weak ad hominem.
Since you seem unaware, nandrolone and trenbolone are 19-nors.
There is nothing wrong with my reading comprehension, bub, but there is something very wrong with your unsupported bullshit. And you've just been called on it.
Bullshit artists like you are a dime a dozen. We get them every couple of months and they all meet the same fate: they get exposed as the wannabe gurus they are and quickly head for the exit with their tail between their legs. You won't be the exception.
Twats like you ask others to do there research for them. You and your buddy have not advanced any theory that makes better sense that what I put up and neither of you have refuted it. You simply blat out nonsense and insult. I wonder if you even know what 19 nor means. I wonder if you know what the arcuate nucleus is or it's function. If you were at all intellectually curious you would have read my previous post and went on a hunt for more informatino rather than sit back and demand more evidence like a child asking for more ice cream. You and your buddy sword swallower need to stop smoking dope in his mom's basement and read a couple of text books. Rattling off a couple of scientific terms doesn't make you informed. Your behavior just makes you a spectacle and laughable.
While there are few articles in the scientific literature that directly address bodybuilder's concerns such as nandrolone's propensity to stimulate formation of gynocomastia or lead to erectile dysfunction, such literature should not be expected because as any
reasonable person knows that no university human studies approval board would approve a research protocol that comes close to duplicating the drug regimes used by bodybuilders.
To the other members, nandrolone has progestogenic activity. That is fact. In fact the large majority of synthetic progestins used in medicine and research are based on 19-nor testosterone (i.e. nandrolone). These two guys want to obscure the facts. Any of you can go to pubmed and use key words nandrolone and progestogenic. You will find over 300 hits. Scanning just a couple dozen of these you will glean more information about 19-nor testosterone compounds than these two twats have together in their collective doped up grayish brown matter between their ears. Below are a few examples. Happy reading and don't let twats like these two prevent you from digging in and figuring stuff out for yourselves.
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 L1,
Gurpide E.
Author information
Abstract
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.
.. and another 19-nor androgen analogue:
Endocrinology. 2006 Jun;147(6):3016-26. Epub 2006 Feb 23.
Dimethandrolone undecanoate: a new potent orally active androgen with progestational activity.
Attardi BJ1,
Hild SA,
Reel JR.
Author information
Abstract
Dimethandrolone (DMA), the 17beta-undecanoic acid ester of dimethandrolone (DMAU; 7alpha,11beta-dimethyl-19-nortestosterone) is a potent androgen currently in development for therapeutic uses in men. Cleavage of the 17beta-ester bond liberates the biologically active DMA. In this study we investigated the activity of DMAU and DMA both in vivo and in vitro. DMAU was active orally in castrate rat bioassays, and when administered sc, a single dose produced prolonged androgenic activity and suppression of LH with sustained circulating levels of DMA. DMA, other 19-norandrogens, and C-19 androgens bound to recombinant rat androgen receptor with high affinity and were equipotent in stimulating luciferase activity (EC50, 10(-10) -10(-9) M) in CV-1 cells cotransfected with a human androgen receptor expression vector and a luciferase reporter plasmid with three hormone response elements.
Because various 19-norandrogens are also known to bind to progestin receptors (PR) and to possess progestational activity in vivo, we evaluated the binding affinity of DMA for rabbit PR and recombinant human PR-A and PR-B and its ability to induce PR-mediated transcription and endogenous alkaline phosphatase activity in T47DCO human breast cancer cells. DMA and related
19-norandrogens bound with high affinity to both rabbit and human PR, whereas the less active 11alpha-methyl stereoisomer of DMA and C-19 androgens showed low or negligible binding to PR. In T47DCO cells, 10(-8) M DMA and other
19-norandrogens stimulated transcription of a progestin/glucocorticoid/androgen response element-thymidine kinase-luciferase reporter plasmid to the same extent as R5020, the potent progestin promegestone (EC50, approximately 10(-9) M), but C-19 androgens had no effect. Antiprogestins were potent inhibitors of transactivation and alkaline phosphatase activity induced by DMA and other 19-norandrogens in T47DCO cells, whereas antiandrogens were weak inhibitors. DMA and DMAU also exhibited dose-dependent progestational activity in the estrogen-primed immature female rabbit, as assessed by induction of endometrial gland arborization. The dual androgenic and progestational activities of DMA make it a potential candidate for a single-agent male contraceptive as well as for androgen therapy in men, pending a successful outcome of pharmacokinetic and toxicity studies currently in progress.
PMID:
16497801
[PubMed - indexed for MEDLINE]
...And for MENT, another 19 nortestosterone analog:
J Steroid Biochem Mol Biol. 1998 Nov;67(3):275-83.
Estrogenic and progestational activity of 7alpha-methyl-19-nortestosterone, a synthetic androgen.
Beri R1,
Kumar N,
Savage T,
Benalcazar L,
Sundaram K.
Author information
Abstract
Synthetic androgens exhibit estrogenic/antiestrogenic and progestational activities in addition to their androgenic effects. To investigate the pharmacological action of the synthetic androgen, 7alpha-methyl-19-nortestosterone (MENT), we examined its action in female rodents. The criteria employed for estrogenic/antiestrogenic effects were, uterine weight increase, vaginal cornification, induction of progesterone receptors (PR) synthesis and stimulation of peroxidase activity in the uteri of ovariectomized rats and mice. MENT increased uterine weight in a dose dependent manner, but did not cause vaginal cornification or stimulate PR synthesis in the uterus. The uterotropic activity of MENT was 200-fold lower than that of estradiol. Estrogen receptor (ER) bound [3H]-E2 was displaced by E2 and MENT with ED50 values of 70 pg and 250 ng, respectively, a 3,500 fold difference in their binding affinity. The low binding of MENT to ER, in contrast to its relatively high uterotropic action, suggested that receptors other than ER may be involved in its action on the uterus.
The progestational activity of MENT in immature rabbits using the McPhail index assay was comparable to that of progesterone. Binding affinities of MENT and progesterone to PR were also comparable. However, the action of MENT on the uterus does not seem to be a progestational effect since mifepristone, an antiprogestin, had no effect on MENT-induced uterine growth. Specific androgen receptors (AR) in uterine cytosol were demonstrated. The involvement of AR in MENT action was confirmed by using an antiandrogen (flutamide) and an antiestrogen (ICI-182) in ovariectomized mice. Although MENT did not block the uterotropic effect of E2, it inhibited the E2-induced cornification of vaginal epithelium, induction of uterine PR synthesis and increase in uterine peroxidase activity in ovariectomized rats. The antiestrogenic effect of MENT was also blocked by flutamide. These results suggest that the uterotropic and antiestrogenic effects of androgens are mediated via AR. It is concluded that the increase in uterine weight caused by MENT is attributable to its anabolic effects.
