Many people have posted that their gynecomastia has decreased due to using the product Epistane/Havoc.
On Epistane.com: "Epistane™ works by binding and deactivating the ERβ so that no estrodiol-elicited effects can be carried out in the cell. In the case of breast tissue ERβ is the primary target receptor responsible for growth and proliferation. Epistane™ binds to the ERβ and not only disables the receptor from binding to estradiol, it actually puts the cell in an estrogen deprived state, which decreases the cells viability and leads to a decrease in size and eventual cell death."
Notice the part I selected in bold, the claim that ERβ is the primary target receptor responsible for growth and proliferation. After I did some googling, I found some studies that disagreed.
"Estrogen Receptor alpha, beta and Progesteron Receptor Expression in Gynecomastia Using Immunohistochemical Staining.
Department of Surgery, Uijongbu St. Mary's Hospital, The Catholic University of Korea, Uijongbu, Korea.
Department of Clinical Pathology, Uijongbu St. Mary's Hospital, The Catholic University of Korea, Uijongbu, Korea.
PURPOSE: Gynecomastia is a common male breast abnormality and primarily occurs in puberty and senescence. The obvious etiological role of hormonal changes in gynecomastia, plus the discovery of estrogen receptor in normal and neoplastic breast, has spurred several investigations of ER content in male gynecomastic tissues. The results have been inconsistent and the fraction of ER-positive specimens has varied from 0~90%. METHODS: Immunohistochemical hormonal receptor analysis using monoclonal estrogen receptor (ER) alpha, beta and progesteron receptor (PR) was performed on the breast tissues of 58 patients with gynecomastia between January 1995 and January 2000 in the Department of Surgery, Uijongbu St. Mary's Hospital. These results were statistically compared with clinical data. RESULTS: 48 cases (82.8%) were ERalpha positive and 55 cases (94.8%) were ERbeta positive and PR positivity was noted in 55 cases (94.8%). There was negative relationship between ERalpha and age, PR and location. CONCLUSION: This study demonstrates that intracellular steroid receptors are present in most gynecomastic tissues. Additionally, it supports the general assumption that estrogen and progesteron may be two of the hormones responsible for the development of gynecomastia."
This study shows that ERα and ERβ receptors are found in gynecomastic tissue, not just ERβ. Could this be why not everyone is seeing the gynecomastia reduction that others are seeing? Epistane/Havoc do a great job at blocking the ERβ, while the ERα is left unblocked. While the ERβ is blocked, perhaps Estradiol starts attaching to the ERα, keeping the gynecomastia alive. Even worse, continued use of a product blocking only ERβ, may cause the creation of more ERα sites, because Estradiol attaches to both. Don't get me wrong here, I am on Epistane right now and am enjoying it. I am just trying to figure out a better treatment for reducing and possibly eliminating gynecomastia for myself and others alike. Perhaps those who see the gynecomastic tissue reduction while using Epistane/Havoc have a higher density of ERβ instead of ERα. Perhaps those old studies we read about how Tamoxifen cured the gynecomastia in only a fraction of test subjects happend to have a higher density of ERα. In those same old studies, Tamoxifen caused partial regression in some of the test subejects. Maybe Tamoxifen did get rid of all the ERα rich tissue, while the ERβ tissue remained healthy, still functioning off of Estradiol. I'm not certain though of course. This is all just a somewhat educated guess.
Because we are not going to use Immunohistochemical hormonal receptor analysis to figure out the density of which type of estrogen receptor that we have in our breast tissue, why not use two medications, one that blocks ERα and Epistane/Havoc to effectively block ERβ?
I did somemore googling and found that Raloxifene binds preferentially to the ERα. (see study at the very bottom also wikipedia says this under the search term "estrogen receptor")
Estradiol binds to both the ERα and ERβ.
Using Raloxifene and Epistane or Havoc would block both types of estrogen receptors, the ERα and ERβ.
With both estrogen receptors blocked, I think the chances of defeating gynecomastia would be far greater.
I also came across this article below, that talks about Testosterone's role in mammary tissue. Now think about this. Being on Epistane/Havoc is going to cause eventual shutdown. Wouldn't it be wise to use Testosterone along with both the ERα and ERβ blockers, Raloxifen and Epistane/Havoc respectively? It makes sense to me. And also another note about the study below, it says that Progesterone did not alter Estradiol's effect of creating gynecomastia, well in monkeys at least.
"Testosterone inhibits estrogen-induced mammary epithelial proliferation and suppresses estrogen receptor expression
JIAN ZHOU, SIU NG, O. ADESANYA-FAMUIYA, KRISTIN ANDERSON and CAROLYN A. BONDY1
This study investigated the effect of sex steroids and tamoxifen on primate mammary epithelial proliferation and steroid receptor gene expression. Ovariectomized rhesus monkeys were treated with placebo, 17ß estradiol (E2) alone or in combination with progesterone (E2/P) or testosterone (E2/T), or tamoxifen for 3 days. E2 alone increased mammary epithelial proliferation by ~sixfold (P<0.0001) and increased mammary epithelial estrogen receptor (ER{alpha}) mRNA expression by ~50% (P<0.0001; ERß mRNA was not detected in the primate mammary gland). Progesterone did not alter E2’s proliferative effects, but testosterone reduced E2-induced proliferation by ~40% (P<0.002) and entirely abolished E2-induced augmentation of ER{alpha} expression. Tamoxifen had a significant agonist effect in the ovariectomized monkey, producing a ~threefold increase in mammary epithelial proliferation (P<0.01), but tamoxifen also reduced ER{alpha} expression below placebo level. Androgen receptor (AR) mRNA was detected in mammary epithelium by in situ hybridization. AR mRNA levels were not altered by E2 alone but were significantly reduced by E2/T and tamoxifen treatment. Because combined E2/T and tamoxifen had similar effects on mammary epithelium, we investigated the regulation of known sex steroid-responsive mRNAs in the primate mammary epithelium. E2 alone had no effect on apolipoprotein D (ApoD) or IGF binding protein 5 (IGFBP5) expression, but E2/T and tamoxifen treatment groups both demonstrated identical alterations in these mRNAs (ApoD was decreased and IGFBP5 was increased). These observations showing androgen-induced down-regulation of mammary epithelial proliferation and ER expression suggest that combined estrogen/androgen hormone replacement therapy might reduce the risk of breast cancer associated with estrogen replacement. In addition, these novel findings on tamoxifen’s androgen-like effects on primate mammary epithelial sex steroid receptor expression suggest that tamoxifen’s protective action on mammary gland may involve androgenic effects.—Zhou, J., Ng, S., Adesanya-Famuiya, O., Anderson, K., Bondy, C. A. Testosterone inhibits estrogen-induced mammary epithelial proliferation and suppresses estrogen receptor expression."
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I am on Epistane right now, 40mg a day. I have pubertal gynecomastia. There may be some reduction, as I have been on Epistane for about 10 days now, but nothing spectacular. I injected 100mg of Testosterone Prop. today and will continue every other day at the same dose. It is a low dose of Testosterone, but still high enough for this purpose. I am also going to use Raloxifene for the rest of the cycle. I will keep everyone updated with my results.
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To develop compounds that are antagonists on ER(alpha), but not ER(beta), we have added basic side-chains typically found in nonsteroidal antiestrogens to pyrazole compounds that bind with much higher affinity to ER(alpha) than to ER(beta). In this way we have developed basic side-chain pyrazoles (BSC-pyrazoles) that are high affinity, potent, selective antagonists on ER(alpha). These BSC-pyrazoles are themselves inactive on ER(alpha) and ER(beta), and they antagonize E2 stimulation by ER(alpha) only. We investigated seven basic side-chain substituents on various alkyl-triaryl-substituted pyrazoles, and the most ER(alpha)-selective compound was methyl-piperidino-pyrazole (MPP). ER(alpha)-selective antagonism was observed on diverse reporter-promoter gene constructs containing estrogen response elements that are consensus, nonconsensus (pS2), or comprised of multiple half-estrogen response elements (NHERF/EBP50) and on genes in which ER works indirectly by tethering to other DNA-bound proteins (TGF(beta)3). In contrast to these BSC-pyrazoles, the antiestrogens trans-hydroxytamoxifen, raloxifene, and ICI 182,780 suppress E2 activity via both ER(alpha) and ER(beta). The most effective BSC-pyrazole, MPP, fully antagonized E2 stimulation of pS2 mRNA in MCF-7 breast cancer cells, consistent with the fact that these cells contain almost exclusively ER(alpha). These compounds should be useful in studying the biological functions of ER(alpha) and ER(beta) and in selectively blocking responses that are mediated through ER(alpha).
and I dont feel like stirrung up old discussions.
