Here's background info:
Selective Estrogen Receptor Modulators (SERMS)
EVISTA® (raloxifene hydrochloride) is a selective estrogen receptor modulator (SERM) that belongs to the benzothiophene class of compounds.
The chemical designation is methanone, [6-hydroxy-2-(4-hydroxyphenyl)benzo[ b]thien-3-yl]-[ 4-[ 2-(1-piperidinyl) ethoxy] phenyl]-, hydrochloride. Raloxifene hydrochloride (HCl) has the empirical formula C28H27NO4S • HCl, which corresponds to a molecular weight of 510.05. Raloxifene HCl is an off-white to pale-yellow solid that is very slightly soluble in water. Raloxifene (Evista) has the ability to bind to and activate the estrogen receptor while exhibiting tissue-specific effects distinct from estradiol. As a result, raloxifene is the first of a benzothiophene series of antiestrogens to be labeled a SERM.
Raloxifene was specifically developed to maintain beneficial estrogenic activity on bone and lipids and antiestrogenic activity on endometrial and breast tissue. In December 1997, the U.S. Food and Drug Administration (FDA) labeled raloxifene for the prevention of osteoporosis.
Although the exact mechanism of action of raloxifene and other similar compounds has not yet been determined, it has been hypothesized that these agents work by inducing conformational changes in the estrogen receptor, resulting in differential expression of specific estrogen-regulated genes in different tissues. Activation of the estrogen receptor by these compounds may involve multiple molecular pathways that may result in gene expression of ligand-, tissue- and/or gene-specific receptors.
Because SERMs are capable of inducing specific changes in the estrogen receptor, it is not surprising that they may mediate specific pharmacologic activity through their unique agonist or antagonist properties. For example, the agonistic properties of raloxifene on bone tissue were recently demonstrated by the specific activation of the human transforming growth factor-b3 gene, which is an important regulator of bone remodeling.
Raloxifene also appears to have a favorable effect on lipid parameters in postmenopausal women. In the published European trial,13 treatment with raloxifene in a dosage of 30, 60 or 150 mg per day resulted in significant decreases in the serum concentrations of total and low-density lipoprotein (LDL) cholesterol over a 24-month period (P < 0.05 versus placebo). These decreases were evident during the first three months of therapy and were maintained thereafter. Notably, none of the treatment groups showed any changes in serum concentrations of high-density lipoprotein (HDL) cholesterol and triglycerides.
So you see:
BOTH Raloxifene and Tamoxifen are highly effective, with Raloxifene being definitively more effective. But both have been proven to work. So don't listen to your wanna-be internet gurus who say there's no way to reduce existing gyno. Nolva has been used for this in studies for years, and now we have an even stronger ally.
Here is a study regarding the effects of Raloxifene compared to Tamoxifen on gyno:
1: J Pediatr. 2004 Jul;145(1):71-6. Related Articles, Links
Comment in:
* J Pediatr. 2005 Apr;146(4):576; author reply 576-7.
* J Pediatr. 2005 Apr;146(4):576; author reply 576-7.
Beneficial effects of raloxifene and tamoxifen in the treatment of pubertal gynecomastia.
Lawrence SE, Faught KA, Vethamuthu J, Lawson ML.
Department of Pediatrics, University of Ottawa, Ontario, Canada.
[email protected]
OBJECTIVES: To assess the efficacy of the anti-estrogens tamoxifen and raloxifene in the medical management of persistent pubertal gynecomastia.
STUDY DESIGN: Retrospective chart review of 38 consecutive patients with persistent pubertal gynecomastia who presented to a pediatric endocrinology clinic. Patients received reassurance alone or a 3- to 9-month course of an estrogen receptor modifier (tamoxifen or raloxifene).
RESULTS: Mean (SD) age of treated subjects was 14.6 (1.5) years with gynecomastia duration of 28.3 (16.4) months. Mean reduction in breast nodule diameter was 2.1 cm (95% CI 1.7, 2.7, P <.0001) after treatment with tamoxifen and 2.5 cm (95% CI 1.7, 3.3, P <.0001) with raloxifene. Some improvement was seen in 86% of patients receiving tamoxifen and in 91% receiving raloxifene, but a greater proportion had a significant decrease (>50%) with raloxifene (86%) than tamoxifen (41%). No side effects were seen in any patients.
CONCLUSION: Inhibition of estrogen receptor action in the breast appears to be safe and effective in reducing persistent pubertal gynecomastia, with a better response to raloxifene than to tamoxifen. Further study is required to determine that this is truly a treatment effect.
PMID: 15238910 [PubMed - indexed for MEDLINE]
