hgh,raised prolactin puffy nipples??

[ftony]

Hello all ,I posted here once awhile ago .I would like to thank all you guys that take the time to post your threads and replys,thanks you. I finished a cycle of eq 300 mg wk, 200 primo wk and 20 mg of var a day for six weeks back in may . I stopped the cycle because I was shedding hair and well I need my hair. my pct was- 500 iu hcg twice a week for the last two weeks of the cycle then waited a week and started 300 mg clomid first day 100 mg for 2 weeks dropped it to 50 mg for 3 more weeks also ran 20 mg nolva every day along side the clomid ,i started my 2iu a ady of hgh during my post cycle . boyz were full in size, blood test showed test levels of 467ng not great but running .But it seems I have a problem ,I have developed puffys nipples ,no lumps or anything just puffy and when erect seem pointy bigger, now I dropped the hgh as well ugh ! I'm pissed i mixed it and guess its no good now .when i noticed the puffy nipps i went with 40mg nolvaed and .50 arimidex ed to help out,but I have read it may be from high prolactin... I went on reading prolactin reduces androgens. so finally to my question... is it possible that the hgh indirectly caused me to shut down again due to reducing my androgens from raised prolactin levels, and causing high estrogen low test /dht ratio and cause gyno??i did notice my boyz did shrink a bit... i get my hgh from a doctor so I know its real. Also I am getting the blood work done this week to see whats up but I was hoping to bounce this off you guys to see what you think.. i have some cabergoline I started yesterday and it seemed to help already .Maybe it is prolactin??? dunno almost forgot im 6-0 235lbs 36 years young not sure what my body fat is but im pretty lean.any help greatly appreciated!

[ftony]

Anyone,Mods ,Vets i would love to finish my bottle i mixed already,but not if i grow a set of rockets....

[ftony]

I think i may have answered my own question finding this on another forum... i did not write this just copy paste,but just incase anyone was having the same problem and was interested here it is ..... From Avant Labs...by 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.

Undoubtedly, due to space limitations, I have left out a number of what are surely many readers’ pet myths. Perhaps in a future issue we can address more of these myths and questionable notions. Feedback is always welcome, and if readers wish to submit their ideas for myths that need to be examined in the future, please feel free to contact Mind & Muscle with your ideas.

just a side note the cabergoline has helped my boyz increase in size ,and sex drive is creeping up fast!!!! i think ill go wack 1 out about now...Man its good to choke the chicken again LOL

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