Tren users, get in here.

[Bouncer]

what was your dose blm?

[blm]

200/ew. Just the feeling of power, growth, and pumps compared to when I was stacking is night and day. I could see how guys can hurt themselves physically (tendons, ligaments, muscle tears) running it at even higher doses based on how quickly and dramatically your strength unnaturally increases.

[rado]

What's your purpose for taking it? Bulk...Cutting...etc.

[Bouncer]

200/ew. Just the feeling of power, growth, and pumps compared to when I was stacking is night and day. I could see how guys can hurt themselves physically (tendons, ligaments, muscle tears) running it at even higher doses based on how quickly and dramatically your strength unnaturally increases.

you said it had actually made your joints feel better no?

[Bouncer]

What's your purpose for taking it? Bulk...Cutting...etc.

allow me to stay as lean as i am while putting on size.

[auri]

I'm shooting up to 400 next week.

[blm]

you said it had actually made your joints feel better no?

Absolutely, while I was on it. Now my joints are achey worse than they were before I started. Hence my comment about how people get hurt themselves because you're straight goes up so quickly.

[Bouncer]

you guys think i will get anything out of 100mg per week?

[blm]

Yes

[rado]

you guys think i will get anything out of 100mg per week?

Minimal and waste IMO.

[ROCKETW19]

you guys think i will get anything out of 100mg per week?

my opinion not alot but het you will or we will never know untill you try it.
it might be exactly what you are looking for or it might be just like the other times fuck you all up??????

[BEAST]

My test shot is due tomorrow I'll add 200mg of tren e to my 250mg test e.
I was taking 200 mg of mixed test and that fucker is painfull as hell. (remember my fat shot :( ) now I got a new bottle and suppose to be painless.

[jack tors]

i want to give it 1 more try before i totally write it off. have you ever run it at such a low dose as i am talking about?

i got good results from 150mg pw. bumped it up to 2cc's 300mg pw towards the end. started to feel neg. sides.

[jack tors]

Try TREN ACE (QUICK ACTING,,IN AND OUT) Use small dosages like 30-50mg ED or even EOD.

i think the quick in and out of Tren Ace is what gave me bad prolactin sides. hormones were all over the place and it was first run with tren. i def thought i was going to get gyno and all the nolva and adex wasnt stopping it. I took a ton of Nolva and it may have been luck but it stopped...at the time i didnt know why nolva didnt work

[StanG]

Here is a write up from the late Nandi ..it nails this issue right on the head. For those that remember him he isnt some Dr with textbook knowledge. The guy lived this lifestyle and was a fvcking genious. The only thing that has changed from the time he wrote this is that now ai's have proven themselves as an extremely effective method of estrogen mangement. You cannot get gyno is the absence of elevated estrogen ..period..end of story. There is no prolactin gyno or progesterone gyno without elevated estrogen, Progesterone can cause puffiness and nipple sensitivity but not gyno. RIP Nand:

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