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Thread: Tren Question...
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05-20-2011, 02:31 AM #1New Member
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Tren Question...
Guys I have taken Tren enanthate along with test enanthate before and was looking into Parabolan . Before I was taking my tren with .5 of dostinex every 4 days. It seemed to have blocked out gyno and any sexual side effects that I was supposed to have gotten. My question is, would there be anything else that I could grab that would protect me from gyno instead of purchasing the caber? It is very pricey, hard to find, and does take a while to grab. Please help! Thinking of starting cycle in 2 weeks but just thought I'd get input before doing something I'd regret. Thanks!
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05-20-2011, 02:42 AM #3New Member
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Sorry I meant the prolactin-caused gyno from the tren , not from the test.
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Oh, I get it. I here guys say Prami is the same thing as caber but I don't know on that myself.
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05-20-2011, 03:29 AM #5New Member
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i just dont wanna go through the hassle of trying to get it again!
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05-20-2011, 04:10 AM #6
I got prami on hand for my tren cycle thank god I'm not gyno pron I tried it for a couple of days because of other issues I was trying to deter main the cause didn't know if it was elevated estro or prolactin giving me troubles. Either way give it a go it didn't seem to have any adverse effects on me. Good luck
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05-20-2011, 04:59 AM #7New Member
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I need help guys getting caber is a pain in the ass
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05-20-2011, 05:24 AM #8
You can fight gyno caused by progesterone by taking tamoxifen , progeterone is caused by response to the estrogen receptor and tamoxifen down regulates the estrogen receptor in the breast tissue, so to control progesterone related sides take tamoxifen. But if you already have issues with proesterone take caber etc to reduce these symptoms but prevention look at tamoxifen.
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05-20-2011, 05:32 AM #9New Member
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Really? Never knew that. I thought it would actually increase the secretion of prolactin. I didn't know u can take it while on Tren
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I got mine from Sten Labs.
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05-20-2011, 05:41 AM #11
Read this what was posted by D7M, it will explain it in detail for you:
More from Nandi....
PROGESTERONE AND PROLACTIN INDUCED GYNECOMASTIA
Before delving into this subject, I’d like to say first and foremost, that in users of anabolic /androgenic steroids (AAS) the first step in combating the development of gynecomastia, or male breast enlargement, is to eliminate the causative agent: the anabolic steroid . Drug-induced gynecomastia almost invariably resolves on its own when a person quits taking the drugs responsible for it, if caught before permanent fibrosis develops. Unfortunately, most AAS users don’t want to employ this simple approach, for obvious reasons, so the foregoing will all be under the assumption that a person wants to prevent or treat gyno and still continue steroid use .
In the belief that certain anabolic steroids increase prolactin levels as well as act as agonists at the progesterone receptor, some have advocated the use of antiprolactin agents, like bromocriptine, or progesterone receptor blockers like RU-486 to treat AAS related gynecomastia, in lieu of more traditional drugs like tamoxifen .
In truth, the etiology of gynecomastia is unknown and a number of agents including estrogens, progestins, GH, IGF-1, and prolactin may be involved. However, most authorities believe that a decreased (T+DHT)/E ratio is central to the development of gyno, and that blocking the effects of estrogen, or increasing T + DHT levels, is central to ameliorating the problem.
Regarding prolactin, androgens decrease prolactin levels whereas estrogens increase prolactin. Non-aromatizing androgens have never been shown to elevate prolactin levels in humans, but testosterone has, due to its aromatization to estradiol (19). Prolactin secreting tumors, or prolactinomas, are often associated with gyno. But in these cases the prolactin is believed to induce gyno by suppressing testosterone production: “Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism”. (20). However, this is a moot issue in AAS users whose gonadotropin secretion is already blunted.
According to research cited in (20), prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels:
The presence of mild hyperprolactinaemia is therefore not uncommon in patients with estrogen excess. Significant primary hyperprolactinaemia, on the other hand, may directly stimulate epithelial cell proliferation in an estrogen-primed breast, causing epithelial cell proliferation and gynaecomastia.
So rather than focusing solely on lowering prolactin levels which may be elevated in users of aromatizing androgens, attacking estrogen should be the first line of action.
GH and IGF-1 are considered critical to the proliferation of mammary tissue. An excellent review of the role played by these hormones, as well as a general overview of gynecomastia can be found here:
Since elevated GH and IGF-1 are considered important to the anabolic effect of AAS, it would be impractical and counterproductive to attempt to prevent gynecomastia by blocking GH/IGF.
Progesterone acts in concert with estrogen to promote breast development, and at least part of any role played by synthetic progestins may be to stimulate IGF-1 production in the breast. But again, blocking the action of progesterone or synthetic progestins is not practical. Specific progesterone receptor antagonists like RU-486 block not only the progesterone receptor, but the androgen receptor as well, and have actually been associated with the development of gynecomastia (21). In any case, progesterone is thought to act on the breast to enhance the effects of estrogen (22) so once again, attacking estrogen is the easiest and most logical approach.
DHT gel (Andractim) or a generic knockoff might help as well. DHT is thought to act as an aromatase inhibitor (23) and perhaps compete directly with estrogen for binding at the estrogen receptor (24). DHT has been used in several case reports and controlled trials to successfully treat gynecomastia. So perhaps a viable strategy would be to combine DHT gel with tamoxifen. I would recommend tamoxifen rather than an aromatase inhibitor due to the simple fact that tamoxifen has been widely used in numerous controlled studies to succesfully treat gynecomastia, whereas the evidence to support the efficacy of aromatase inhibitors is scanty at best.
References:
(1) Price TM, O'Brien SN, Welter BH, George R, Anandjiwala J, Kilgore M. Am J Obstet Gynecol 1998 Jan;178(1 Pt 1):101-7
(2) Bjorntorp P. Hum Reprod 1997 Oct;12 Suppl 1:21-5
(3) Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH Metabolism 1997 Feb;46(2):179-85
(4) Zmuda JM, Fahrenbach MC, Younkin BT, Bausserman LL, Terry RB, Catlin DH, Thompson PD. Metabolism 1993 Apr;42(4):446-50
(5) Tomita T, Yonekura I, Okada T, Hayashi E
Horm Metab Res 1984 Oct;16(10):525-8
(6) Mystkowski P, Seeley RJ, Hahn TM, Baskin DG, Havel PJ, Matsumoto AM, Wilkinson CW, Peacock-Kinzig K, Blake KA, Schwartz MW. J Neurosci 2000 Nov 15;20(22):8637-42
(7) Greer,M. N Engl J Med 244:385, 1951
(8) Vagenakis AG, Braverman LE, Azizi F, Portinay GI, Ingbar SH. N Engl J Med 1975 Oct 2;293(14):681-4
(9) Krugman LG, Hershman JM, Chopra IJ, Levine GA, Pekary E, Geffner DL, Chua Teco GN J Clin Endocrinol Metab 1975 Jul;41(1):70-80
(10) Liva SM, Voskuhl RR J Immunol 2001 Aug 15;167(4):2060-7
(11) Ulloa-Aguirre A, Blizzard RM, Garcia-Rubi E, Rogol AD, Link K, Christie CM, Johnson ML, Veldhuis J Clin Endocrinol Metab 1990 Oct;71(4):846-54
(12) Hochman IH, Laron Z Horm Metab Res 1970 Sep;2(5):260-4
.
(13) Steinetz BG, Giannina T, Butler M, Popick F
Endocrinology 1972 May;90(5):1396-8
(14) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7
(15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
Ferrando AA
J Clin Endocrinol Metab 1999 Aug;84(8):2705-11
(16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94
(17) Bricout VA, Germain PS, Serrurier BD, Guezennec CY.Cell Mol Biol (Noisy-le-grand) 1994 May;40(3):291-4
(18) Ferrando AA, Sheffield-Moore M, Yeckel CW, Gilkison C, Jiang J, Achacosa A, Lieberman SA, Tipton K, Wolfe RR, Urban RJ.
Am J Physiol Endocrinol Metab 2002 Mar;282(3):E601-7
(19) Nicoletti I, Filipponi P, Fedeli L, Ambrosi F, Gregorini G, Santeusanio F
Acta Endocrinol (Copenh) 1984 Feb;105(2):167-72
(20) Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607
(21) Grunberg SM, Weiss MH, Spitz IM, Ahmadi J, Sadun A, Russell CA, Lucci L, Stevenson LL J Neurosurg 1991 Jun;74(6):861-6
(22) Nomura K, Suzuki H, Saji M, Horiba N, Ujihara M, Tsushima T, Demura H, Shizume K
J Clin Endocrinol Metab 1988 Jan;66(1):230-2
(23) Perel E, Stolee KH, Kharlip L, Blackstein ME, Killinger DW
J Clin Endocrinol Metab 1984 Mar;58(3):467-72
(24) Casey RW, Wilson JD.
J Clin Invest 1984 Dec;74(6):2272-8
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05-20-2011, 05:42 AM #12
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05-20-2011, 05:45 AM #14New Member
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So guys, if estrogen is the cause of all gyno directly, how about arimadex while on cycle with Tren ?
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05-20-2011, 05:47 AM #15
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05-20-2011, 06:10 AM #16New Member
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Alright so I'll grab some tamoxifen . What would be the dosing for that?
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05-20-2011, 04:03 PM #17
I am also curious about dosing.
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05-20-2011, 04:05 PM #18
great info M...............
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05-20-2011, 05:29 PM #19New Member
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Yeah I'd really like to know the dosing and when to take it. Ed or eod. Thanks!
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