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- Irishriley
- Dec 3, 2010
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I dont believe it all though thats just my opinion.This has been debated often and I have yet to hear someone post that tamoifen has increased prolactin/progesterone sides.
here is an exert from a thread I made on 'ology about just this.
Increased susceptibility to gyno -
Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.
This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developming gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting 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?
here is an exert from a thread I made on 'ology about just this.
Increased susceptibility to gyno -
Tamoxifen is often used to combat gyno during cycle when “flare ups” occur. While tamoxifen may provide immediate inhibition of proliferation, and serve as valuable tool, it can actually increase future susceptibility to gyno.
This is caused by tamoxifen’s ability to up-regulate the progesterone receptor. (54-56) This can dramatically increase the chances of developming gyno in future cycles when utilizing progestin based anabolics such as Nandrolone (Deca) or Trenbolone (or any pro-hormone acting 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?
- Jan 19, 2011
- 494
- 117
Yes this is true. It is known that nandrolones bind to and activate PR. This is fact. It is also fact that tamoxifen increases PR, apparently albeit transiently. Put these two together and you can enhance PR signaling. Nandrolones also have activity at the estrogen receptor (ER). Estrogen signaling and progeterone signaling can lead to a nasty case of gyno. When using nandrolones it is best to use an aromatase inhibitor rather than a SERM to control estrogen effects.
- Dec 3, 2010
- 178
- 11
Yes I should have added that even with the debate there is just no reason to use a serm for estrogen control while running nandro's all ways use an AI.
But with that said and the evidence confirming the up-regulation of PR from serms a serm protocol is commonly used with out any reported problems that I know of for PCT.
Deca is know to still be detected 18 months after use there must be a missing variable in this or serms would not be viable and potentially hazardous to use for PCT.
But with that said and the evidence confirming the up-regulation of PR from serms a serm protocol is commonly used with out any reported problems that I know of for PCT.
Deca is know to still be detected 18 months after use there must be a missing variable in this or serms would not be viable and potentially hazardous to use for PCT.
- Jan 19, 2011
- 494
- 117
Metabolites of nandrolones are detected for 18 months. The drug levels fall precipitously well before then on the order of 2-3 1/2 lives. I know many that have had the problem when mixing tamox and nandrolones. To me there is no debate. Once I put together what I've seen in the literature about the 2 drugs and what I've seen from the mid 80s to present there is no doubt to me that the two shouldn't be mixed especially if one is prone to gynecomastia. But some will try anyway. A few will get away with it because we are not all clones. The debate will continue.
- Jan 19, 2011
- 494
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I think most would be OK with SERMs after a nandrolone cycle. Most will end nandrolones 2 weeks before stopping test. I use hCG thorughout but it's probably critical here to use hCG the last 2 weeks of test alone. Wait an additional 2 weeks before SERM addition and the nandrolones have diminished significantly. I would say start with clomid for the first 3 weeks alone. Then add in nolvadex keeping the clomid in for an additional week. Then end with 2 more weeks of nolvadex alone.
- Sep 9, 2010
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I think the more interesting question about Nolva is it's ability to suppress IGF-1 plasma levels. If you use Nolva almost ED or EOD to combat gyno during a cycle of 12 weeks plus take larger doses for 4 extra weeks during PCT, that could be detrimental to keeping your gains. The study below (although it was done with female subjects) states that after 4 months of daily usage (20mg ED) the effects of Nolva on IGF-1, and the GH response to GHRH are greatly magnified. This is enough for me NOT to use Nolva as an on cycle treatment for gyno prevention. I've not read any articles that show AIs having similar effects. 4 weeks of Nolva therapy during PCT seem to be much more reasonable in maintaining quality IGF-1 serum levels. Although, it does bring up the argument of whether or not it's a good idea to pin exogenous IGF-1 during PCT. If you're already running exogenous GH, this isn't really of concern. But, I think it's a valid consideration for those guys who cycle on and off.
Study on the Effects of Tamoxifen on GH and IGF-1 Levels
Effect of tamoxifen on GH and IGF-1 serum level in stage I-II breast cancer patients.
Mandala M, Moro C, Ferretti G, Calabro MG, Nole F, Rocca A, Munzone E, Castro A, Curigliano G.
Division of Medical Oncology, European Institute of Oncology, Via Ripamonti 435, 20141-Milan, Italy. [email protected]
OBJECTIVE: Tamoxifen suppresses insulin-like growth factor-1 (IGF-1) plasma levels in early and advanced breast cancer patients. Relationships between tamoxifen (GH) and IGF-1 are complex and not completely described yet. The present investigation was performed to evaluate the effect of acute and chronic tamoxifen administration on GH response to growth hormone-releasing hormone (GHRH),as well as on IGF-1 serum levels. MATERIALS AND METHODS: Evaluation of GH after administration of GHRH was performed (a) at baseline, (b) 3 hours after 20 mg oral administration of tamoxifen and (c) after 12 weeks of 20 mg a day oral tamoxifen treatment, in fifteen postmenopausal stage I-II breast cancer patients. IGF-I was measured at baseline and after chronic tamoxifen administration. RESULTS: The GH response to GHRH was significantly reduced after 12 weeks of tamoxifen 10 mg administered twice a day orally (mean peak 3.2 +/- 0.2 micrograms/l, mean AUC 261.3 +/- 18.2 micrograms/minute p < 0.01 versus basal AUC). A concomitant significant reduction of IGF-1 was observed after 3 months of tamoxifen treatment. Basal pretreatment levels of 113.2 +/- 15.5 micrograms/l were suppressed to 70 +/- 7.9 micrograms/l (p < 0.01). CONCLUSION: Our study confirm the inhibitory effect of tamoxifen on IGF-I and suggested, as shown in previous in vitro data, that its suppression could be directly related to GH reduction in response to GHRH stimulation.
Study on the Effects of Tamoxifen on GH and IGF-1 Levels
Effect of tamoxifen on GH and IGF-1 serum level in stage I-II breast cancer patients.
Mandala M, Moro C, Ferretti G, Calabro MG, Nole F, Rocca A, Munzone E, Castro A, Curigliano G.
Division of Medical Oncology, European Institute of Oncology, Via Ripamonti 435, 20141-Milan, Italy. [email protected]
OBJECTIVE: Tamoxifen suppresses insulin-like growth factor-1 (IGF-1) plasma levels in early and advanced breast cancer patients. Relationships between tamoxifen (GH) and IGF-1 are complex and not completely described yet. The present investigation was performed to evaluate the effect of acute and chronic tamoxifen administration on GH response to growth hormone-releasing hormone (GHRH),as well as on IGF-1 serum levels. MATERIALS AND METHODS: Evaluation of GH after administration of GHRH was performed (a) at baseline, (b) 3 hours after 20 mg oral administration of tamoxifen and (c) after 12 weeks of 20 mg a day oral tamoxifen treatment, in fifteen postmenopausal stage I-II breast cancer patients. IGF-I was measured at baseline and after chronic tamoxifen administration. RESULTS: The GH response to GHRH was significantly reduced after 12 weeks of tamoxifen 10 mg administered twice a day orally (mean peak 3.2 +/- 0.2 micrograms/l, mean AUC 261.3 +/- 18.2 micrograms/minute p < 0.01 versus basal AUC). A concomitant significant reduction of IGF-1 was observed after 3 months of tamoxifen treatment. Basal pretreatment levels of 113.2 +/- 15.5 micrograms/l were suppressed to 70 +/- 7.9 micrograms/l (p < 0.01). CONCLUSION: Our study confirm the inhibitory effect of tamoxifen on IGF-I and suggested, as shown in previous in vitro data, that its suppression could be directly related to GH reduction in response to GHRH stimulation.
