Is B6 efficient at preventing prolactin related sides?

[Cronos]

Hi, everyone. I was hoping I could get people's personal opinion on whether or not oral B6 is effective at preventing prolactin related sides, and at what dose? Specifically with a low dose of tren @ 200-300mg/wk.

Please only input if you have personally tried this.

Thanks!

P.s. I understand caber or prami is a solid option, but I have just been studying the last few hours about the effectiveness of oral B6.

[dec11]

an AI from the beginning will control all, you do not need prami

[Cronos]

an AI from the beginning will control all, you do not need prami

You're telling me an AI, such as arimidex, will control all, INCLUDING PROLACTIN RELATED SIDES? I've never heard of this, can you please elaborate, or point me in the direction of some literature which confirms this? I thought AI's were only for estrogen related sides???

[Sgt. Hartman]

Estrogen regulates PrL and PrG. You can keep a dopamine agonist on hand just in case. Read this by Karl Hoffman (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.

[Cronos]

Okay, wow lol. A lot of interesting info here. So, does the vast majority of INTELLIGENT tren users run a serm like nolva on cycle, or an AI and NOT something like caber?

My biggest concerns for myself regarding using tren are PROPERLY controlling the sides, and PROPERLY/FULLY recover upon completion of PCT. From what I've studied, the people that have the hardest time recovering from tren, are the ones that did not properly control their prolactin. Am I on the money with saying this?

I'm trying to get all my facts straight before I tackle tren in my next cycle. I'm honestly really confused and a little overloaded with information, but I'm trying my best to learn and sort it out. I want to know exactly what supports to have, if I should run them throughout, or only as needed, at what dosages etc.

As I stated above, my biggest concerns are efficiently controlling sides from tren, and PROPERLY recovering.