My questions are the following, vets please feel free to chime in with knowledge...
1) What's the difference between estrogen induced gyno and progesterone induced gyno?
2) What are the different symptoms of each?
3) Can one get progesterone induced gyno from running a beginner Test only cycle?
4) How do you combat the two after symptoms have arrived?
5) What things (foods, meds, env) should one avoid to help reduce the gyno (if this is even possible)?
Thank you for replying.
http://www.steroidology.com/forum/anabolic-steroid-forum/2525-understanding-roll-estrogen-progesterone-men.html
EDDYMERCKX said:
simple answer--you need high estrogen before you get gynecomastia. the etiology of gynecomastia a is really unknown but the cw is that a decreased (T+dihydrotestosterone)/E ratio is central to the development of gynecomastia, and that blocking the effects of estrogen, or increasing T + dihydrotestosterone levels, is central to ameliorating the problem.
prolactin may have a direct stimulatory effect on mammary tissue development, but only in the presence of high estrogen levels (see Ismail AA, Barth JH.Ann Clin Biochem 2001 Nov;38(Pt 6):596-607)
If aromatising steroids are to be included in the stack with progestagenic steroids, then the concurrent use of Competitive Aromatase Inhibitors, like Arimidex or Proviron, would also seem a sensible option. These can be incorporated to keep oestrogen levels low and avoid the activation of the progesterone. Although they will not help with already developed progesterone induced gynecomastia, they can certainly be emplo to avoid its development. As usual, the amount of aromatase inhibitor required increases with increasing dose of aromatising steroids used, but the best dose is still the minimum amount that can be got away with to produce the desired effect.
Not scientific studies but enough to get you started.
From my readings so far the difference between the two gyno a is that estrogen gyno is more lumpy tissue underneath the breast while progesterone gyno is more like flared and puffy nipples. Both can show elements of the other so sometimes its difficult to differentiate. Another factor to consider is that GH and IGF-1 are both necessary for the development of male gynocemastia. High estrogen, high progesterone, or estrogen dominance (high ratio of estrogen vs progesterone) cannot cause gyno in the absence of GH and IGF-1. That means if you're on a cycle of aromatizing compounds or 19-nors like deca and tren AND IGF-1 and/or GH you are at a much elevated risk to develop gyno.
Since the development of breast tissue in males occurs in an analogous manner to that in females, the same hormones that affect female breast tissue can cause gynecomastia. The testes secrete only 6-10 mg of estradiol and 2.5 mg of estrone per day. Since this only comprises a small fraction of estrogens in circulation (i.e. 15% of estradiol and 5% of estrone), the remainder of estrogen in males is derived from the extraglandular aromatization of testosterone and androstenedione to estradiol and estrone (45). Thus, any cause of estrogen excess from overproduction to peripheral aromatization of androgens can initiate the cascade to breast development.
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Another cause of gynecomastia from estrogen excess includes steroid displacement from sex-hormone binding globulin (SHBG). SHBG binds androgens more avidly than estrogen. Thus, any condition or drug that can displace steroids from SHBG, will more easily displace estrogen, allowing for higher circulating levels of estrogen. Drugs can cause gynecomastia by numerous mechanisms besides displacement from SHBG.
Breast development requires the presence of estrogen. Androgens, on the other hand oppose the estrogenic effects. Thus, equilibrium exists between estrogen and androgens in the adult male to prevent growth of breast tissue, whereby either an increase in estrogen or a decrease in androgen can tip the balance toward gynecomastia. Increased estrogen levels will increase glandular proliferation by several mechanisms. These include direct stimulation of glandular tissue and by suppressing LH, therefore decreasing testosterone secretion by the testes and exaggerating the already high estrogen to androgen ratio. Besides increased estrogen production, decreased testosterone levels can cause an elevation in the estrogen to androgen ratio, producing gynecomastia. Primary hypogonadism, with its reduction in serum testosterone and increased serum LH levels increases testicular estradiol production and is associated with an increased estrogen to androgen ratio. Klinefelter's syndrome, occurring in the 1 in 500 males who possess an XXY karyotype and primary testicular failure, features gynecomastia as well, again presumably secondary to decreased testosterone production, compensatory increased LH secretion, overstimulation of the Leydig cells and relative estrogen excess. In fact, androgen deficiency (hypogonadism) from whatever cause constitutes most cases of gynecomastia.
The androgen resistance syndromes, including complete and partial testicular feminization (e.g. Reifenstein's syndrome) are characterized by gynecomastia and varying degrees of pseudohermaphroditism. Kennedy Syndrome, a neurodegenerative disease, is also associated with decreased effective testosterone due to a defective androgen receptor (64). The gynecomastia is the combined result of decreased androgen responsiveness at the breast level and increased estrogen levels as a result of elevated androgen precursors of estradiol and estrone. As such, androgens in these diseases are not recognized by the peripheral tissues including the breast and pituitary. Androgen resistance at the pituitary results in elevated serum LH levels and increased circulating testosterone. The increased serum testosterone is then aromatized peripherally, promoting gynecomastia. Thus, gynecomastia is the result of increased estradiol levels that arise due to unopposed androgen unresponsiveness.
^^^ what I'm getting from that is androgens play a key part in inhibiting estrogen from causing gyno. Also an overstimulation of LH and high endogenous test (like that from Human Chorionic Gonadotropin (HCG) use) can lead to an Improper balance of estradiol to androgens. To me this suggests that an Aromatase inhibitor (AI) dose in cycle with Human Chorionic Gonadotropin (HCG) is a necessity. One should be using an Aromatase inhibitor (AI) already for various other reasons but especially with Human Chorionic Gonadotropin (HCG) since it stimulates LH production, it stimulates the Ledyig cells, and increases natural testosterone production all of which will lead to a more gyno friendly environment.
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: ***8220;Prolactinomas that are sufficiently large to cause gynecomastia do so as a result of impairment of gonadotropin secretion and secondary hypogonadism***8221;. (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.
Progestins & Gyno
Before you decide that blocking progesterone is the solution to gyno, consider a few things. There is not one case of progesterone induced gyno in the medical literature EXCEPT in those cases where strong synthetic progestins, like medroxyprogesterone, were administered. In these cases the gyno is due to suppression of LH and testosterone by the progestin, NOT by a direct effect on breast tissue. On a cycle your LH is already suppressed by the AAS anyway.
Breasts have two components: alveoli and ducts. The alveoli are what secrete milk; they drain into ducts. Gynecomastia is the result of ductal hyperplasia, not alveolar hyperplasia. Estrogen stimulates the ductal tissue, while progesterone stimulates the alveoli. Alveolar hyperplasia does not contribute to gyno. If you want to read more on breast development, I suggest visiting this site:
http://www.endotext.org/male/male14/male14.htm
In various tissues throughout the body, including cultured neoplastic breast tissue, progestins downregulate the estrogen receptor (1). Progesterone receptor blockers like RU-486 upregulate the estrogen receptor (1). This is consistent with the fact that RU-486 CAUSES gyno in patients in whom it is used to treat Cushing***8217;s disease and meningiomas (2).
Progestins are also anti-estrogenic in that they induce the enzyme 17-hydroxysteroid dehydrogenase, which catalyzes the oxidation of estradiol to the less potent estrone. Progestins also induce estrogen sulfotransferase, the enzyme which catalyzes the sulfation and inactivation of estrogens.
So do progestins contribute to gyno, and if yes, how so? If you visit the link above you will see that progestins increase IGF-1 levels. As that article indicated, IGF-1 is essential to the the development of mammary tissue. This is also how it is believed that progestins in Hormone Replacement Therapy (HRT) or oral contraceptives contribute to breast cancer: by increasing IGF-1 levels. But as bodybuilders we are always trying to maximize IGF-1. Hence the futility of trying to lower IGF-1 by blocking progestins. The other anabolics we use will elevate (hopefully) IGF-1, while blocking the progesterone receptor will only increase the levels and activity of estrogen by the mechanisms outlined above.
Two drugs have shown the greatest efficacy in treating gyno: Nolvadex, and Raloxifene, another SERM. Nolvadex has the longest track record, but a recent trial with Raloxifene showed it to be superior to Nolvadex. With these drugs you attack the problem at its source: the estrogen receptor. You get the added benefit of lowering IGF-1. Not a good thing for making gains, but important for treating gyno.
1) see above ^^^ Breasts have two components: alveoli and ducts. The alveoli are what secrete milk; they drain into ducts. Gynecomastia is the result of ductal hyperplasia, not alveolar hyperplasia. Estrogen stimulates the ductal tissue, while progesterone stimulates the alveoli. Alveolar hyperplasia does not contribute to gyno.
2) see above again. Puffy flared nipples, hard lumps underneath nipples, lactating nipples from elevated prolactin (only with previously elevated estrogen levels) and high progesterone will lead to this.
High estrogen can lead to high BP, low libido, weight gain, bloat/water retention, depression, prostate problems, anxiety/panic attacks, etc. low estrogen can lead to achy joints, loss of libido, ED that Viagra cannot help much with, bloating, fatty liver, insulin resistance, water retention (due to inability to hold NA+, and no pump in the gym (due to decreased NO production).
High progesterone sides include elevated estrogen levels (testicular release of progesterone leads to
Increase in estrogen levels), many of the sides of high estrogen, decrease in facial hair growth, prostate problems, difficulty urinating, ED, etc. Low progesterone (or estrogen dominance) can lead to
Prostate enlargement, smaller urethral, increased urination, depression fatigue, loss of libido, ED, hair loss, and bone and muscle loss.
Many of the symptoms over lap so its important to realize what compounds you're taking and to do a blood test during the cycle to figure out which is specifically causing your issues.
3) progesterone doesn't induce gyno on its own. It does so indirectly by promoting an increase of estrogen production. So if you get gyno on a test only cycle it's due to elevated estrogen and estrogen dominance OVER progesterone. Even with a 19-nor it's estrogen causing the gyno but high levels of progesterone lead to increased estrogen, prolactin levels, etc.
4) for symptoms of high estrogen you can use Arimidex, exemstane, letrozole, nolva (blocks the receptors in breast tissue from binding with estrogen but does not induce receptor activation), decrease alcohol consumption, increase vitamin B consumption, flaxseed, and chrysin (natural herb).
For high progesterone and prolactin you can take caber, prami, vitamin B6, bromocriptine, dostinex, and the best way to treat high progesterone is to lower estrogen.
