Thoughts on using Winstrol to combat Progesterone induced Gyno?

[Schutzhundk9]

Has anyone heard of using Winstrol to combat the gyno caused by deca, anadrol or tren? I've heard that winny is good at reducing progesterone induced gyno but I haven't seen any discussion on dosage.

Does anyone have any links to studies on this?

I understand that vitamin B6 can be used in dosages of around 600mg/day and I'm aware of bromocripine as well. What else is there?

What would the dosage of winny be to reduce progesterone gyno? Would it be greater or less than the common (non-therapeutic) 50-100mg/day?

 

[vadim_b1]

I heard of it, however it will not reduce already existing gyno.
It MAY help with controlling progesterone related side effects from compounds like deca and trenbolone.
Doses have to be quite high though, at least to match the doses of deca/tren.

Obviously there will be no studies on something like this, as they dont really stack compounds in medical practice.
And stanazolol dosages in medicine are around 50-100 mg/2 weeks.

If youre looking for something else theres always dostinex, and for more daring - mifepristone.

 

[KillerStack]

Has anyone heard of using Winstrol to combat the gyno caused by deca, anadrol or tren? I've heard that winny is good at reducing progesterone induced gyno but I haven't seen any discussion on dosage.

Does anyone have any links to studies on this?

I understand that vitamin B6 can be used in dosages of around 600mg/day and I'm aware of bromocripine as well. What else is there?

What would the dosage of winny be to reduce progesterone gyno? Would it be greater or less than the common (non-therapeutic) 50-100mg/day?

You can't find studies talking about "progesterone induced gyno" from anabolic steroids. There's really no such thing, scientifically speaking, to my knowledge. Not saying that progesterone isn't involved in breast development, but this term originates from the bodybuilding community.

Now as far as Winstrol, from what I remember the studies seem to say Winstrol is actually an agonist of the progesterone receptor, not an antagonist.

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.