Mavafanculo said:
1)
Prevention and management of bicalutamide-induced gynecomastia and breast pain: randomized endocrinologic and clinical studies with tamoxifen and anastrozole.
Saltzstein D, Sieber P, Morris T, Gallo J.
Urology San Antonio Research PA, Pasteur Medical Plaza, San Antonio, Texas, USA.
A randomized, double-blind, placebo-controlled multicenter trial involving 107 men receiving bicalutamide ('Casodex') 150 mg/day therapy following radical therapy for prostate cancer assessed tamoxifen ('Nolvadex') 20 mg/day and anastrozole ('Arimidex') 1 mg/day for the prophylaxis and treatment of gynecomastia/breast pain. Tamoxifen, but not anastrozole, significantly reduced the incidence of gynecomastia/breast pain when used prophylactically and therapeutically. Serum testosterone levels increased with tamoxifen relative to placebo but prostate-specific antigen levels declined in all treatment groups. Further studies are needed to define the optimum tamoxifen dose and to assess any impact on cancer control. The use of tamoxifen in this setting remains to be investigated
2)
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]
3)
Management of physiological gynaecomastia with tamoxifen.
Khan HN, Rampaul R, Blamey RW.
Professorial Unit of Surgery, Department of Surgery, Nottingham City Hospital, Nottingham NG5 1PB, UK.
AIMS: We aimed to confirm suggestions that tamoxifen therapy alone may resolve physiological gynaecomastia. METHODS: A prospective audit of the outcome of tamoxifen routinely given to men with physiological gynaecomastia was carried out at Nottingham. Men referred with gynaecomastia had clinical signs recorded, e.g., type (diffuse 'fatty' or retro-areolar 'lump'), size and possible aetiology. They were offered oral tamoxifen 20mg once daily for 6-12 weeks. On follow-up patients were assessed for complete resolution (CR), partial resolution where patient is satisfied with outcome (PR) or no resolution (NR). Success was either CR or PR. RESULTS: Thirty-six men accepted tamoxifen for physiological gynaecomastia. Median age was 31 (range 18-64). Tenderness was present in 25 (71%) cases. Sixteen men (45%) had 'fatty' gynaecomastia and 20 had 'lump' gynaecomastia. Tamoxifen resolved the mass in 30 patients (83.3%; CR=22, PR=8) and tenderness in 21 cases (84%; CR=0, PR=0). Lump gynaecomastia was more responsive to tamoxifen than the fatty type (100% vs. 62.5%; P=0.0041). CONCLUSIONS: Oral tamoxifen is an effective treatment for physiological gynaecomastia, especially for the lump type.
Yes tamofixen does reduce gyno lumps but look how long the treatment program was. It is much slower than an AI like letro & there is evidence that it can be very liver toxic & possibly carcinogenic -
"Clomid & Nolva; A closer look
The use of Clomid and Nolvadex, as Selective Estrogen Receptor Modulators (SERMs), has gradually become well established in the steroid using community. The popular push of these drugs has almost made them mandatory. They have essentially become hormonal vitamins – vitamins that can do no wrong and provide seemingly endless benefits of testosterone support, bloat reduction, gynecomastia prevention and cholesterol health. It seems that we are all well educated about the benefits of Clomid and Nolvadex, so in this segment, I will present the risks and consequences from the short and long term use of Clomid and Nolvadex.
Upon examination of the research available for Clomid (clomiphene) and Nolvadex (tamoxifen) we find that the research is quite extensive, and contradicting.21 We see many early studies with tamoxifen done on breast cancer patients, which show an acceptable "safety profile", with an apparent lack of adverse effects.22 On the other hand, many of the early in vivo animal studies showed severely toxic effects, with the development of cancer in the liver, uterus, or testes upon tamoxifen administration.30-34,41 However, this evidence was largely disregarded by ex vivo (test tube) research on human cell-lines which appeared to show a lack of toxic effects.
For example, tamoxifen was generally accepted as being non-toxic to human liver upon the conclusion that tamoxifen did not cause noticeable DNA adducts (damage) during short-term ex vivo studies with human liver cells. This was in contrast to the in vivo animal studies showing dramatic carcinogenic effects on the liver.30-34,41 As scientists learned that the toxic effects from tamoxifen are from the metabolism and buildup of the a-hydroxytamoxifen, 4-hydroxytamoxifen and N-desmethyltamoxifen metabolites. It became apparent that ex vivo research was largely flawed due to low-rate metabolism.21 The carcinogenic effects of tamoxifen proved to be even more unusual and elusive, when it was hypothesized that tamoxifen had both genomic and non-genomic toxicity, which affecting different animals, in different organs.21 This created an obvious clinical challenge for measuring genotoxicity in a test tube. Eventually, it was established that tamoxifen was a bona-fide carcinogen in all species, at least in one way or another. Recent human studies have shown tamoxifen treated women to have 3x the risk of developing fatty liver disease, which appeared as soon as 3 months into therapy at only 20mg/day.24-26 In some cases, the disease lasted up to 3 years, despite cessation from tamoxifen therapy. Five and ten year follow-ups with patients on long term tamoxifen therapy showed cases of deadly hepatocellular carcinoma.27-29 In a 2000 case study involving tamoxifen induced liver disease, D.F Moffat et al made a profound statement –
"In addition, hepatocellular carcinoma in tamoxifen treated patients may be under-reported since there may be reluctance to biopsy liver tumours which are assumed to be secondary carcinoma of the breast."
In other words, it appears that the liver carcinoma from a large number of breast cancer patients on tamoxifen therapy has been misdiagnosed as a metastasis infection from the breast cancer itself. Upon closer examination it was found that the cancerous lesions in the livers of the long-term tamoxifen therapy case studies were identical to those seen in the early animal studies showing tamoxifen to be a potent hepatotoxin.28-34 Although the effects took much longer to manifest, it became obvious that tamoxifen was toxic to the human liver.
Another well known risk of tamoxifen therapy is the increased risk of developing endometrial cancer (uterine cancer). This is due to tamoxifen actually acting as an estrogen agonist in the uterus, presumable from the 4-hydroxytamoxifen metabolite. This estrogenic metabolite triggers abnormal growth of the uterus and the formation of cancer causing DNA adducts.33 As male bodybuilders we assume this presents no risk. On the contrary, the implications are quite scary when we realize the male equivalent to the uterus is the prostate -- differentiating from the same embryonic cell line and sharing the same oncogene, Bcl-2, and high concentration of the estrogen receptor. It is likely that tamoxifen has the same estrogenic action, and DNA damaging effects within the prostate. It is no wonder that tamoxifen failed as a treatment for prostate carcinoma.
Aside from restoring testosterone levels post cycle, tamoxifen is often used to combat gyno during cycle when "flare ups" occur. While tamoxifen may provide immediate inhibition of growth, and serve as valuable tool, it also has the ability to up-regulate the progesterone receptor.54-56 This is a true contradiction, which dramatically increases your chances of bringing upon gyno in future cycles when utilizing Nandrolone (Deca) or Trenbolone, both of which act upon the progesterone receptor. It is interesting to speculate: is tamoxifen use directly related to the increased gyno occurrences seen with modern day steroid users?
When we bring our attention to Clomid, we find less research is available on long term human toxicity, probably because of the relatively short term (3-4 week) clinical application for ovarian stimulation,59 although long term follow ups with patients who received Clomid for ovulation induction have shown an increased risk of developing uterine cancer.74 This is to be expected, since many of the same carcinogenic tendencies found with tamoxifen are the same effects seen with clomiphene.44,45,57,58 Upon analysis of anecdotal reports from Clomid and nolva users, we see the typical short term side effects of low libido, erectile dysfunction, and emotional instability – despite many men showing normalized testosterone and estrogen levels during the use of these SERM’s. Research on male breast cancer patients also shows frequent reports of low libido, thrombosis (arterial blockage), and hot flashes with tamoxifen use.47 Another common side effect associated with both SERMs, but more common with Clomid, is the loss of visual accuracy and development of visual "tracers", due to the ocular toxicity.
As the medical community became more aware of the side-effects associated with clomiphene and tamoxifen treatment, newer and safer SERMs, such as toremifene and raloxifene hit the developmental fast track. Toremifene appears to be less liver toxic, but it is an analog of tamoxifen, so it also carries many of the related genotoxic effects. Raloxifene appears to be even safer by being the least liver toxic, and not having any potential issue with the uterus or prostate. Unfortunately, raloxifene has been associated with a higher incidence of thromboembolism52 (arterial blockage), and also has very low oral absorption, making it an expensive alternative at a typical 120mg/day dose. Still, raloxifene could presumably be equally effective as Clomid or Nolvadex at restoring HPTA function, while imparting less side effects. Newer SERMs are already being evaluated such as bazedoxifene, arzoxifene, and lasofoxifene, in hopes of reducing risk even further. "
Eric m Potratz - Primordial Performance (sorry I have lost the references)
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