Deca Dick - Advice urgently needed

[REK]

Are you using any AI? High estrogen=high prolactin. I've never had a problem with this and right now I'm running 300 test and 900 deca weekly.
Hcg and high test dosage will result in high estro...

Control your estrogen and you will control your prolactin bro. I will try to dig up an article from another board I found and post it.

Caber will help for sure as well, .5 mg 2x a week.

Deca dick has always been averted by using 2:1 ratio of test to nandrolone , long before all these other extras were marketed

YUP.

Cheers REK

 

[REK]

Here an article I found on another board, its about Gyno, but the principle of controlling Estrogen is relevant.


Progesterone and prolactin induced gynecomastia
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.
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(3) Ramirez ME, McMurry MP, Wiebke GA, Felten KJ, Ren K, Meikle AW, Iverius PH Metabolism 1997 Feb;46(2):179-85

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(5) Tomita T, Yonekura I, Okada T, Hayashi E
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(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

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(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

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(15) Sheffield-Moore M, Urban RJ, Wolf SE, Jiang J, Catlin DH, Herndon DN, Wolfe RR,
Ferrando AA
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(16) Doumit ME, Cook DR, Merkel RA..Endocrinology 1996 Apr;137(4):1385-94

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(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

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[ketsugo]

Overcomplicating over thinking

 

[SHINE]

REK I think that is an old Macro article on gyno. I still believe in using damn old nolva as first lines of defense if you start to get gyno. High doses of nolva not only stops estrogens actions at the site it kills the hell out of IGF which yes adds fibrous growth of your gyno.

 

[REK]

REK I think that is an old Macro article on gyno. I still believe in using damn old nolva as first lines of defense if you start to get gyno. High doses of nolva not only stops estrogens actions at the site it kills the hell out of IGF which yes adds fibrous growth of your gyno.

Yeah bro it's an older one for sure. I can't remember where I copied it from, I currently keep the authors names as to give the credit where its due, but this one was from a while back.

Cheers REK

 

[beetlejuice]

I dropped the deca to 300 and started feeling better although not 100%. Probably mentally related at this point. I elected to substitute the deca for tren this week. I've ran tren and test before and had no issues. Again, probably in my head but it just didn't feel right. I think I remember reading that the androgenic nature of tren might outweigh the 19-nor related effects.

I'm back to getting morning wood etc...

 

[KBD]

Deadweight- You don't take anything to reduce prolactin? I thought that was the cause for loss of libido from nandrolones? How much deca do you run? I'm 38 so no young stud here. But even on cialis or viagra they won't help your libido, right? Meaning your drive to have sex.

I once read a study that the prolactin "killing sex drive theory" is complete bullshit, as a matter of fact Bill Roberts over at meso explained this situation quite well. This is the reason i dont take deca, My dick means more than a extra 5-10lbs that can be gained by just simply upping your test dose and food intake. Get you some cialis, shit works amazing. Love it.

Test is my favorite AAS, its never let me "down" Lol.

 

[beetlejuice]

I once read a study that the prolactin "killing sex drive theory" is complete bullshit, as a matter of fact Bill Roberts over at meso explained this situation quite well. This is the reason i dont take deca, My dick means more than a extra 5-10lbs that can be gained by just simply upping your test dose and food intake. Get you some cialis, shit works amazing. Love it.

Test is my favorite AAS, its never let me "down" Lol.

I'm mid week on tren E 300 test E 750 and I'm feeling great. Hard all the time again.

Deca definitely doesn't agree with me.

Do you remember the essence of the study? If it's not prolactin what is it about deca that causes this?

 

[ketsugo]

Just control your estrogen with novaldex or letro, twice test dose to half deca, it's what has worked for 20 years before all this other stuff, only on these forums have I seen so much issues with deca, in the real world most that I know have never had an issue, test and deca and winny my favorite stack , over 20 + cycles never an issue. I use tren all three esters with nothing other than test and tamoxifen no issues ever. Test is the base of all cycles with deca double it