some studies

[gynosucks1]

i always point these out, but found a nice thread from which i cut this out cuz i don't feel like piecing the stuff together myself...

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. slawrence@cheo.on.ca

OBJECTIVES: To assess the efficacy of the anti-estrogens tamoxifen and raloxifen 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.


Kuhn JM, Roca R, Laudat MH, Rieu M, Luton JP, Bricaire H.

We have studied clinical and endocrine parameters in a group (group A) of forth men referred to us because of persistent idiopathic gynaecomastia (of more than 18 months duration), before and during the administration of percutaneous dihydrotestosterone (DHT). The endocrine parameters (testosterone (T), 17 beta-oestradiol (E2), DHT, gonadotrophins (FSH and LH) and prolactin (PRL), were compared to those of control groups of 12 healthy men on DHT therapy (group B) and 10 on placebo (group C). Local administration of DHT was followed by the complete disappearance of gynaecomastia in 10 patients, partial regression in 19 and no change in 11 patients after 4 to 20 weeks of percutaneous DHT (125 mg twice daily). Before treatment the T + DHT/E2 ratio was significantly (P less than 0.001) lower in group A 244 +/- 21 (SEM) than in groups B and C (361 +/- 21) while T, DHT and E2 concentrations were all within the normal range. During DHT treatment plasma hormone levels were measured in 26 patients from group A: DHT levels increases significantly (day 0: 1.63 +/- 0.14 nmol/l; day 15: 12.8 +/- 1.6 nmol/l, P less than 0.001) while T and E2 levels fell significantly (T: day 0: 22.6 +/- 1.2 nmol/l; day 15: 11.0 +/- 1.5 nmol/l, P less than 0.001; E2: day 0: 110.5 +/- 7.12 pmol/l; day 15: 86.79 +/- 9.4 pmol/l, P less than 0.01). The T/E2 ratio decreased from 231 +/- 20 to 164 +/- 27 (P less than 0.05) while the T + DHT/E2 ratio increased significantly (P less than 0.02) to a normal mean value (day 15: 354 +/- 57).(ABSTRACT TRUNCATED AT 250 WORDS)"


For instance here is one where men received 120mg daily:
Effects of raloxifene on gonadotrophins, sex hormones, bone turnover and lipids in healthy elderly men.
Duschek EJ, Gooren LJ, Netelenbos C.
Department of Endocrinology, VU University Medical Centre, Amsterdam, The Netherlands.

OBJECTIVE: To explore effects on serum lipids, pituitary-gonadal axis, prostate and bone turnover of the administration of the mixed oestrogen agonist/antagonist raloxifene in healthy elderly men. PARTICIPANTS: Thirty healthy men aged 60-70 years randomly received raloxifene 120 mg/day (n=15) or placebo (n=15) for 3 months. MEASUREMENTS: In this double-blind, placebo-controlled study, serum gonadotrophins, sex hormones, prostate specific antigen (PSA), a marker of bone turnover, urinary hydroxyproline (OHPro) and cholesterol were measured at baseline and after 3 months. RESULTS: Raloxifene significantly increased serum concentrations of LH and FSH (by 29% and 21%), total testosterone (20%), free testosterone (16%) and bioavailable testosterone (not bound to sex hormone-binding globulin (SHBG; 20%). In parallel with testosterone, 17 beta-oestradiol also increased by 21%. SHBG increased by 7%. Total cholesterol (TChol) decreased significantly, from 5.7 to 5.5 mmol/l (P=0.03). Low-density lipoprotein cholesterol (LDL-c) and high-density lipoprotein cholesterol (HDL-c) showed a trend to decrease. Overall, there was no change in urinary OHPro/creatinine ratio as a marker for bone resorption. However, the raloxifene-induced increases in both serum testosterone and 17 beta-oestradiol were significantly related to a lower OHPro/creatinine ratio. Total PSA increased by 17% without significant changes in free PSA or free/total PSA ratio. Participants reported no side effects and raloxifene was well tolerated. CONCLUSION: In healthy elderly man, raloxifene 120 mg/day for 3 months increased LH, FSH and sex steroid hormones. Potentially beneficial effects were the small but significant decrease in TChol and the trend towards a decrease in LDL-c. Negative effects were the trend towards a decrease in HDL-c and the significant increase in serum PSA. A decrease in markers of bone resorption during raloxifene treatment was found only in men with relatively high increases in serum testosterone and 17 beta-oestradiol. Overall, there were no clear beneficial effects of administration of raloxifene to ageing men in this preliminary investigation.

Then this one uses 60mg:
Raloxifene to prevent gonadotropin-releasing hormone agonist-induced bone loss in men with prostate cancer: a randomized controlled trial.
Smith MR, Fallon MA, Lee H, Finkelstein JS.
Division of Hematology and Oncology, Massachusetts General Hospital, Boston, Massachusetts 02114, USA.

GnRH agonists decrease bone mineral density and increase fracture risk in men with prostate cancer. Raloxifene increases bone mineral density in postmenopausal women, but its efficacy in hypogonadal men is not known. In a 12-month open-label study, men with nonmetastatic prostate cancer (n = 48) who were receiving a GnRH agonist were assigned randomly to raloxifene (60 mg/d) or no raloxifene. Bone mineral densities of the posteroanterior lumbar spine and proximal femur were measured by dual energy x-ray absorptiometry. Mean (+/-se) bone mineral density of the posteroanterior lumbar spine increased by 1.0 +/- 0.9% in men treated with raloxifene and decreased by 1.0 +/- 0.6% in men who did not receive raloxifene (P = 0.07). Bone mineral density of the total hip increased by 1.1 +/- 0.4% in men treated with raloxifene and decreased by 2.6 +/- 0.7% in men who did not receive raloxifene (P < 0.001). Similar between-group differences were observed in the femoral neck (P = 0.06) and trochanter (P < 0.001). In men receiving a GnRH agonist, raloxifene significantly increases bone mineral density of the hip and tends to increase bone mineral density of the spine.




Good for the bones too-

[SERMs: an update for clinicians]

[Article in Japanese]

Ohta H.

Department of Obstetrics and Gynecology, Tokyo Women's Medical University, Japan.

With the successful manipulation by molecular pharmacological technology of the estrogenic properties of selective estrogen receptor modulators (SERMs) that are highly organ- and tissue-specific, SERMs have now become available for the management of osteoporosis, as they did for breast cancer earlier. This presentation focuses on raloxifene (RLX), a second-generation SERM and an agent of interest to clinicians engaged in the management of osteoporosis on a day-to-day basis. RLX is a unique agent, in that it exhibits similar but distinct effects on bone metabolism from those of estrogen. RLX also appears to exert milder inhibitory effects on bone resorption than bisphosphonates (BPs), another class of antiresorptive agents, while ample evidence suggests that RLX compares favorably with BPs in preventing a variety of non-traumatic fractures.