Tamoxifen citrate is a non-steroidal anti-estrogenic drug, used widely in clinical medicine. It is specifically a Selective Estrogen-Receptor Modulator (SERM) of the triphenylethylene family, and possesses both estrogen agonist and antagonist properties.
As such, it may act as an estrogen in some tissues while blocking the action of estrogen in others. In breast tissue tamoxifen citrate is a strong anti-estrogen. The primary worry among the athletic/bodybuilding population is gynecomastia, or the very unsightly development of female breast tissue in men. This can be first noticed by the appearance of swelling or a small lump under the nipple. If left to progress, this can develop into a large hard-tissue gynecomastia that may be an irreversible occurrence without surgery.
(Notice the word Selective.. What part of the body you think this drug was invented for?)
(Notice it says, If left to progress. So you can notice it when it starts and have those receptors release it before it becomes a problem.)
You can copy and paste all this until you're blue in the face, it doesn't make it correct.
http://www.drugsprofiles.com/anti-estrogens.html
Good copy paste job , nice to see you know how to copy and paste, but let's stick to authority website please.
I know it works and so do many others. Ask anyone what do you take when you feel a lump. So why are you questioning the medical study of it? Is it because its cheaper then Letro?
Yet again,
Tamoxifen upregulates the PgR, and can exacerbate existing gynecomastia conditions. You're forgetting that Tamoxifen is an ER agonist and via agonism it raises PgR expression. You can yell and scream all you want about price, but facts remain facts.
1: Cancer Res. 2002 May 15;62(10):2798-805.
Lack of ductal development in the absence of functional estrogen receptor alpha delays mammary tumor formation induced by transgenic expression of ErbB2/neu.Hewitt SC, Bocchinfuso WP, Zhai J, Harrell C, Koonce L, Clark J, Myers P, Korach KS.
Receptor Biology Section, Laboratory of Reproductive and Developmental Toxicology, National Institute of Environmental Health Sciences/NIH, Research Triangle Park, NC 27709, USA.
Expression of the mouse mammary tumor virus (MMTV) neu/erbB2 transgene in mice induces mammary tumors. To examine the effect of removing estrogen receptor alpha (ERalpha) signaling on the ability of an MMTV-neu/erbB2 transgene to induce mammary tumors, the neu transgene was expressed in the ERalpha knockout (alphaERKO) mouse, which lacks functional ERalpha. MMTV-neu females that lacked ERalpha still developed mammary tumors; however, tumor onset was significantly delayed. This study indicates that ERalpha is not required for mammary tumor induction by overexpression of neu/erbB2, but plays a role in the rate of tumor onset. The removal of ovarian steroid by ovariectomy in adults did not alter the onset rate. In contrast, prepubertal ovariectomy, which arrested mammary epithelial development, significantly delayed onset. In addition,
manipulations that increase progesterone also accelerate the tumor onset, indicating the slower onset in the alphaERKO is primarily attributable to the anovulatory phenotype resulting in lack of progesterone stimulation and a decreased abundance of target cells in the alphaERKO mammary gland.
Letrozole effectiveness on treating gynecomastia:
J Steroid Biochem Mol Biol. 2001 Dec;79(1-5):27-34. Aromatase overexpression transgenic mice model: cell type specific expression and use of
Letrozole to abrogate mammary hyperplasia without affecting normal physiology.
Mandava U, Kirma N, Tekmal RR.
Department of Gynecology and Obstetrics, Emory University, 4217 Woodruff Memorial Building, 1639 Pierce Drive, Atlanta, GA 30322-4710, USA.
Our recent studies have shown that
overexpression of aromatase results in increased tissue estrogenic activity and induction of hyperplastic and dysplastic lesions in female mammary glands and gynecomastia and testicular cancer in male aromatase transgenic mice. Both aromatase mRNA and protein are overexpressed in transgenic mammary glands and its expression is not limited to epithelial cells. However, it is more in epithelial than in stromal cells.
Our results also indicate aromatase overexpression-induced changes in mammary glands can be abrogated [destroyed] with very low concentrations of the aromatase inhibitor, Letrozole. Low concentration of
Letrozole had no effect on normal physiology as indicated by no significant change in the circulating levels of estradiol and follicle stimulating hormone as well as no change in estrogen responsive genes such as the progesterone receptor and lactoferrin in the uterine tissue. These observations indicate that the expression of aromatase in both epithelial and stromal cells can influence the complex interactions of biochemical pathways leading to mammary carcinogenesis and that the aromatase inhibitor,
Letrozole can be used as chemopreventive agents without affecting normal physiology.
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