Thread: Deca Dosage? Advice Needed
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10-26-2008, 04:43 PM #41Scammer
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we need to see of oestradiol levels using only nandrolone .. fortunately oswaldosalcedo was kind enough to be a guinne pig at CEM when this topic came up.. ran 800mg of deca only.. blood test pre and post cycle.
the values.
....................before cycle---------on cycle (week 5)
estradiol--------30.2 pg/ml----------74.9 pg/ml
prolactin--------11.1 pg/ml----------11.2 pg/ml
free t4-----------1.2 ng/dl------------1.3 ng/dl
at the end of the month i will take a blood test again (i continue on cycle)
estradiol blood levels .. supraphysiological level.
Today.
estradiol------- 68.30-------pg/ml
prolactin--------.9.70-------pg/ml
free T4---------.1.10-------ng/dl
well, no prolactin increase, estradiol stabilized (but supraphysiological) and free T 4 normal.
gynaecomastia due to estradiol, is not the mechanism (in this case), is by progestogenic or prolactin action or nandrolone coupling to the estrogen receptor.
progestins are derived either from progesterone or from testosterone , testosterone-derived progestins have more androgenic properties than the progestins derived from progesterone.
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10-26-2008, 04:44 PM #42Scammer
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reason for this little experiment..
nandrolone and aromatase
here is a possible explanation for that "progestenic" gyno.
jb
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Can 19-nortestosterone derivatives be aromatized in the liver of adult humans? Are there clinical implications?Kuhl H, Wiegratz I.
Department of Obstetrics & Gynecology, J.W. Goethe University Frankfurt, Frankfurt am Main, Germany.
CONTEXT: Previous studies in postmenopausal women have demonstrated that, after oral administration of norethisterone, a small proportion of the compound is rapidly converted into ethinylestradiol. The shape of the concentration - time curve suggested that this occurred in the liver. The results were confirmed by in vitro investigations with adult human liver tissue. In 2002, it was shown that, after oral treatment of women with tibolone, aromatization of the compound occurred, resulting in the formation of a potent estrogen, 7 alpha-methyl-ethinylestradiol. The result has been called into question, because the adult human liver does not express cytochrome P450 aromatase, which is encoded by the CYP 19 gene. Moreover, it has been claimed that the serum level of 7 alpha-methyl-ethinylestradiol measured by gas chromatography/mass spectrometry was an artifact. REPLY: Aromatization of steroids is a complex process of consecutive oxidation reactions which are catalyzed by cytochrome P450 enzymes. The conversion of the natural C19 steroids, testosterone and androstenedione, into estradiol-17beta and estrone is dependent on the oxidative elimination of the angular C19-methyl group. This complex key reaction is catalyzed by the cytochrome P450 aromatase, which is expressed in many tissues of the adult human (e.g. ovary, fat tissue), but not in the liver. However, 19-nortestosterone derivatives are characterized by the lack of the C19-methyl group. Therefore, for the aromatization of these synthetic steroids, the action of the cytochrome P450 aromatase is not necessary and the oxidative introduction of double bonds into the A-ring can be catalyzed by other hepatic cytochrome P450 enzymes. The final key process in the formation of a phenolic A-ring, both in natural androgens and 19-nortestosterone derivatives, is the enolization of a 3-keto group to the C2-C3-enol or the C3-C4-enol moiety, which occurs without the action of enzymes. CONCLUSION: 19-nortestosterone derivatives (norethisterone, norethynodrel, tibolone) can readily be aromatized in the adult human liver. This leads to the formation of the potent estrogens ethinylestradiol from norethisterone or norethynodrel and 7 alpha-methyl-ethinylestradiol from tibolone. This may have clinical consequences, e.g. the elevated risk of venous thromboembolic disease in premenopausal women treated with high doses of norethisterone for bleeding disorders, or the elevated risk of stroke or endometrial disease in postmenopausal women treated with tibolone.
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10-26-2008, 04:45 PM #43Scammer
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there is no gyno from estradiol, cos there is very low estradiol, not gyno from nandro alone cycle.
3 options:
1.-progestogenic action,2.-prolactin action or 3.-direct binding of nor-derivatives to the estrogen receptor.
1.-Science. 2006 Dec 1;314(5804):1467-70.
Prevention of Brca1-mediated mammary tumorigenesis in mice by a progesterone antagonist.
Poole AJ, Li Y, Kim Y, Lin SC, Lee WH, Lee EY.
Department of Biological Chemistry, University of California, Irvine, CA 92697-4037, USA.
Women with mutations in the breast cancer susceptibility gene BRCA1 are predisposed to breast and ovarian cancers. Why the BRCA1 protein suppresses tumor development specifically in ovarian hormone-sensitive tissues remains unclear. We demonstrate that mammary glands of nulliparous Brca1/p53-deficient mice accumulate lateral branches and undergo extensive alveologenesis, a phenotype that occurs only during pregnancy in wild-type mice. Progesterone receptors, but not estrogen receptors, are overexpressed in the mutant mammary epithelial cells because of a defect in their degradation by the proteasome pathway. Treatment of Brca1/p53-deficient mice with the progesterone antagonist mifepristone (RU 486) prevented mammary tumorigenesis. These findings reveal a tissue-specific function for the BRCA1 protein and raise the possibility that antiprogesterone treatment may be useful for breast cancer prevention in individuals with BRCA1 mutations.
http://cuttingedgemuscle.com/Forum/...=&threadid=1642
2.-Oncogene. 2003 Jul 24;22(30):4664-74.
Prolactin induces ERalpha-positive and ERalpha-negative mammary cancer in transgenic mice.
Rose-Hellekant TA, Arendt LM, Schroeder MD, Gilchrist K, Sandgren EP, Schuler LA.
Department of Pathobiological Sciences, School of Veterinary Medicine, University of Wisconsin, 2015 Linden Dr., Madison, WI 53706, USA.
The role of prolactin in human breast cancer has been controversial. However, it is now apparent that human mammary epithelial cells can synthesize prolactin endogenously, permitting autocrine/paracrine actions within the mammary gland that are independent of pituitary prolactin. To model this local mammary production of prolactin (PRL), we have generated mice that overexpress prolactin within mammary epithelial cells under the control of a hormonally nonresponsive promoter, neu-related lipocalin (NRL). In each of the two examined NRL-PRL transgenic mouse lineages, female virgin mice display mammary developmental abnormalities, mammary intraepithelial neoplasias, and invasive neoplasms. Prolactin increases proliferation in morphologically normal alveoli and ducts, as well as in lesions. The tumors are of varied histotype, but papillary adenocarcinomas and adenosquamous neoplasms predominate. Neoplasms can be separated into two populations: one is estrogen receptor alpha (ERalpha) positive (greater than 15% of the cells stain for ERalpha), and the other is ERalpha- (<3%). ERalpha expression does not correlate with tumor histotype, or proliferative or apoptotic indices. These studies provide a mouse model of hormonally dependent breast cancer, and, perhaps most strikingly, a model in which some neoplasms retain ERalpha, as occurs in the human disease.
http://cuttingedgemuscle.com/Forum/...&threadid=19119
3.-J Steroid Biochem Mol Biol. 2006 May;99(2-3):108-14.
Synthetic 19-nortestosterone derivatives as estrogen receptor alpha subtype-selective ligands induce similar receptor conformational changes and steroid receptor coactivator recruitment than natural estrogens.
García-Becerra R, Borja-Cacho E, Cooney AJ, Smith CL, Lemus AE, Pérez-Palacios G, Larrea F.
Department of Reproductive Biology, Instituto Nacional de Ciencias Médicas y Nutrición Salvador Zubirán, Vasco de Quiroga No. 15, Mexico City 14000, Mexico.
The binding of estradiol (E(2)) to estrogen receptors (ER) is followed by conformational changes resulting in coactivator or corepressor recruitment that influences gene transcription. A series of synthetic A-ring reduced 19-nortestosterone-derived progestins has the capacity to selectively bind and activate transcription through the ERalpha. Herein, the molecular mechanisms involved in ER subtype-selective interactions of these compounds as assessed by their effects upon both ERalpha and ERbeta structural conformation and their ability to induce recruitment of steroid receptor coactivator-1 (SRC-1) to ERalpha were investigated. The results demonstrated that all synthetic A-ring 3beta,5alpha-tetrahydro-reduced derivatives of 19-nortestosterone induced an ERalpha trypsin digestion pattern similar to that seen with E(2), without effects upon ERbeta. In addition, these compounds had the ability to recruit SRC-1 to the ligand-binding domain of ERalpha similar to E(2). Our data indicate that A-ring 3beta,5alpha-tetrahydro-reduced 19-nortestosterone-derived progestins behave as selective ERalpha agonists with ligand-receptor structural and functional responses similar to those induced with natural E(2).
http://cuttingedgemuscle.com/Forum/...&threadid=17140Last edited by Mulciber; 10-26-2008 at 04:51 PM.
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10-27-2008, 12:10 PM #44Junior Member
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So should I take Nolva during, or just in pct? This Nolva seems to be an issue with Deca ..lol
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10-27-2008, 12:51 PM #45
IMO, don't run nolva, save it for PCT.
So if you think you might be gyno prone run a low dose AI throught.
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10-27-2008, 04:26 PM #46Junior Member
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From my past test only cycle's, Gyno was never an issue, never had itchy nips, or anything, I do have some chest fat, but I was chubby as a kid. After a chest workout, My chest looks like's Arnie's from Terminator 1. lol
What AI would you recommend, A-dex? and dosage you guy's usually run, on a Deca /Test Cyp cycle?
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10-27-2008, 04:34 PM #47
Just a low dose 0.25mg EOD.
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10-28-2008, 02:34 PM #48Junior Member
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thanks for the info
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10-28-2008, 07:25 PM #49New Member
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ok hcg should not be ran pct. it is to be ran throughout cycle or pre pct.
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10-28-2008, 07:28 PM #50New Member
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you can run a good cycle with test and deca, I have ran 750 test and 500 deca a week. what you need to add to it is proviron 50mg/day and hcg @ 250/500 iu per week. this will keep the boys happy.
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10-29-2008, 01:42 AM #51Junior Member
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Any reason why I can't run HCG in just PCT, or just start HCG in week 10, when I stop the deca , but keep test injections till week 12. I mean with the test/deca I am already going to be shutdown naturally, so HCG would be pointless right?, I mean it would probably keep my nut size normal, but they still wouldn't produce test due to the fact I am shotting synthetic test into myself that would exceed my natural test production. I mean I could be completely wrong.
Please comment, I am open to all advice. I am not an expert, so all advice is great. Thanks guy for all your comments, I am learning constantly from this site. I can't believe the bogus I hear from people in the gym, I'm glad I research if not I could of takin a deca only cycle if it weren't for this site. ThanksLast edited by locowhiteguy77; 10-29-2008 at 01:45 AM.
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10-29-2008, 01:30 PM #52Junior Member
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bump
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11-02-2008, 02:08 PM #53Junior Member
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bump
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12-30-2024, 06:57 AM in ANABOLIC STEROIDS - QUESTIONS & ANSWERS