Detroit, tell us how you really feel about Deca. Don't hold back. lol. You are absolutely right about one thing, though--people either love it or hate it. I'm a fan, but since I already have ED, losing libido isn't a concern for me.
Caber doesn't work for deca dick because there is a misconception that the nors (deca/tren) raise prolactin when they do not. They are progestins and progestins by nature cannot raise prolactin. I have an article on this, but I'm too new for the system to let me post links. At any rate, studies with bloodwork will confirm this.
They can however, affect E2 even though they do not aromatize, so having some potent anti-Es on hand is a good thing. An AI simply may not be up to the task. With the right ratio of E2 in the mix, you can keep your libido. Test/Deca at 400/400 will work well. Just keep your E2 in check.
It's good to see you over here, Burly.
You nailed it here as well. Prolactin and Progesterone
cannot cause gyno unless there is a hormonal environment already present with an excessive imbalance of E2. There is plenty of evidence to support that. Progesterone and Prolactin are both cofactors in the equation and can add insult to injury, but the E2 is the dominant hormone needed for glandular growth and proliferation of actual ductal breast tissue. If you control/block E2, you will control your risk of developing it. I should mention that GH/IGF-1 also play a major cofactor role in gyno development as well.
I've said it for years and I'll say it again...Cabergoline/Dostinex is bad sh*t; and people should steer clear of it. Anytime you play around with a potent dopamine receptor agonist you need to fully understand the potential risks/side effects involved. Essentially, the guys that try to mitigate every potential side effect of a cycle are the ones that have major issues in the end. The hormonal milieu is so fragile that even minor mitigations can cause detrimental changes in the short/long term. Just a little bit can go a long way, and I would always advise when making changes or taking steps to mitigate issues to start small and titrate/adjust as needed. Control the estrogen, and all should be well.
I absolutely agree that 400/400 should work out just fine as long as he keeps the E2 in check; not destroy it or allow it to become excessive . If all else fails at that point your would introduce a SERM and hit the problem directly by blocking E2 receptors in the breast tissue.
Here's an interesting little read to peruse:
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. -DZM
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