Thread: Caber Necessary?????

Ok so here is something written YEARS ago by the late Nandi. The man quite simply was a genius that was 10+ yrs ahead of his time easily. The smartest man on the subject of AAS & ancillary effects I have ever encountered,and he is sprely missed. RIP Karl. The thing is this, you have to do what works for you but physiology is physiology and this write up explains hormone relationships, effects and so on better than anything I ever read on the topic of prolactin or progesterone induced gyno. I a good read at the very leat and is right on topic here:

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

Originally Posted by Jimmyinkedup

Thats ok. Im sure we can both agreeably disagree man. Makes for good threads IMO. I will say this Im going to read back through this entire thread as the tren only question posted has me scratching my head a bit. Maybe I missed something.

Agreeably is the best way to disagree :-) Well said.

OP said nothing about running tren. I brought it up. And I am talking strictly about running Trenbolone solo, without testosterone. I was just making the point that Trenbolone does not convert to estrogen, but can, and often does, cause gyno. So I'm confused as to how controlling estrogen while running a drug that doesn't convert to estrogen prevents the development of gyno and lactation (the latter being wholly induced by prolactin).

Originally Posted by Largerthannormal

No not at all, who would run tren alone? why is tren in this post at all anyway? This post was about deca, they are not the same in many ways

I was saying i was agreeing with the androgen to estrogen relation meaning your test would have to be bunk " i did not mean run tren along, MY BAD"

I am saying if you are on any AAS as the first line of defense is E2 managament. and yes still keep caber on hand.

I think i have a good read on this somewhere. ill go look for it.

I put tren in this post, and I did it because its relevant. The mechanism through which trenbolone and nandrolone cause gynecomastia are the same (which, not coincidentally, is why caber works in both instances). I've run trenbolone solo, as have many many other people. Sometimes you just run what you have available to you.

I've read this before... Thanks for posting it, though. The problem is that it sounds good on paper, but doesn't work out in practical application (which is not uncommon). This proves my point, though. If non-aromatizing drugs don't increase prolactin, then one should not lactate while running trenbolone solo (again, I'm bringing trenbolone up because it causes gyno and does not aromatize). But lactation does occur with gynecomastia had through use of trenbolone.

Originally Posted by hunkstrum

Agreeably is the best way to disagree :-) Well said.


OP said nothing about running tren. I brought it up. And I am talking strictly about running Trenbolone solo, without testosterone. I was just making the point that Trenbolone does not convert to estrogen, but can, and often does, cause gyno. So I'm confused as to how controlling estrogen while running a drug that doesn't convert to estrogen prevents the development of gyno and lactation (the latter being wholly induced by prolactin).

I like this board already. Very cool..
Trens progestin effects work in concert WITH estrogen in the breast to promote tissue growth. The is no practical way to manage progesterone, so you MUST focus on estrogen. Of note you can add winstrol which actually will occupy but not activate the progesterone receptors to a degree.
Lactation is Prolactin and possibly oxytocin induced (patrick arnold speculation on the oxytocin). PRL can be managed like you aid with a dopamine agonist and should be if needed imo, but lowering prl isnt your gyno cure. The fact is as old school as it is if you take tamox or ralox you wont get gyno. What does that say? Well it says if e2 cant get to breast tissue, regardless of other hormone levels, gyno will not form. Thats huge and tell us a lot.

I'm loving the debate here!! A lot of good knowledge, experience, and perspective being talked about here. A lot of good points. I think the most important point here is that the smartest thing to do would be to have caber on hand and I think we can all agree on that.

Originally Posted by Jimmyinkedup

I like this board already. Very cool..
Trens progestin effects work in concert WITH estrogen in the breast to promote tissue growth. The is no practical way to manage progesterone, so you MUST focus on estrogen. Of note you can add winstrol which actually will occupy but not activate the progesterone receptors to a degree.
Lactation is Prolactin and possibly oxytocin induced (patrick arnold speculation on the oxytocin). PRL can be managed like you aid with a dopamine agonist and should be if needed imo, but lowering prl isnt your gyno cure. The fact is as old school as it is if you take tamox or ralox you wont get gyno. What does that say? Well it says if e2 cant get to breast tissue, regardless of other hormone levels, gyno will not form. Thats huge and tell us a lot.

ok.