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I post a question about this in a different part of the forum. I botched the question and couldn't find this info.
So, this is on the website of a supplier:
"CAUTION: Tamoxifen on nandrolone cycles and on PCT (post cycle therapy) can strengthen progestogenic activity of nandrolone, so it should not be used. Clomid or toremifene are recommended for PCT after all 19-nor testosterone modifications."
Can anyone expand upon this?
Sounds more like broscience than anything - progestogenic activity in what regard? Prolactin? Gyno? HPTA suppression? Progesterone activity is ultimately allowed by estrogen and tamoxifen being a mixed agonist/antagonist at the ER can theoretically act in synergy with any progestin but not at the sites of our interest - it's showed to reduce prolactin, increases FSH/LH in both males/woman with intact HPTA and normal progesterone levels, and it blocks ER in the breast.
Thanks Biz,
My specific concern is with regard to PCT: not just the HPTA access but restoring normal hormonal levels. If Tamox prevents progesterone from going back to normal. The following articles suggest that Tamox has Progesterone activity. Does it take place outside of the tumors associated with breast cancer? IDK, I can't find anything on it. However, specifically in regard to PCT, I would like to find a substitute for Tamox.
The following info all relates to Tamoxifen in it's use for female breast cancer.
I did some research on this and may originate with breast cancer studies in which the progesterone activity of Tamoxifen resulted in desirable outcomes with regard to tumors having Progesterone positive nuclei.
"High progesterone receptor expression correlates to the effect of adjuvant tamoxifen in premenopausal breast cancer patients."
https://www.ncbi.nlm.nih.gov/pubmed/16899609
"RESULTS:
Our findings show a gradually increasing tamoxifen effect in tumors with >10% ER-positive nuclei. However, when analyzing tamoxifen response according to various PR fractions, we found that it was primarily patients with tumors showing >75% PR-positive nuclei that responded to tamoxifen treatment, with an improved recurrence-free [relative risk, 0.42 (0.25-0.70); P = 0.001] as well as overall [relative risk, 0.49 (0.28-0.84); P = 0.010] survival.
CONCLUSIONS:
Adjuvant tamoxifen improved recurrence-free and overall survival for premenopausal patients with tumors showing >75% PR-positive nuclei. No effect could be shown in tumors with fewer PR-positive nuclei. The PR was a stronger predictor of treatment response than the ER. Based on these findings, we suggest the implementation of a fractioned rather than dichotomized immunohistochemical evaluation of hormone receptors in clinical practice, possibly with greater emphasis on the PR than the ER."
AND
"High progesterone receptor expression correlates to the effect of adjuvant tamoxifen in premenopausal breast cancer patients."
https://www.ncbi.nlm.nih.gov/pubmed/16899609
"RESULTS:
Our findings show a gradually increasing tamoxifen effect in tumors with >10% ER-positive nuclei. However, when analyzing tamoxifen response according to various PR fractions, we found that it was primarily patients with tumors showing >75% PR-positive nuclei that responded to tamoxifen treatment, with an improved recurrence-free [relative risk, 0.42 (0.25-0.70); P = 0.001] as well as overall [relative risk, 0.49 (0.28-0.84); P = 0.010] survival.
CONCLUSIONS:
Adjuvant tamoxifen improved recurrence-free and overall survival for premenopausal patients with tumors showing >75% PR-positive nuclei. No effect could be shown in tumors with fewer PR-positive nuclei. The PR was a stronger predictor of treatment response than the ER. Based on these findings, we suggest the implementation of a fractioned rather than dichotomized immunohistochemical evaluation of hormone receptors in clinical practice, possibly with greater emphasis on the PR than the ER."
AND, this last one is more current, easier to read and well-illustrated.
Solving a breast cancer mystery ? why do ?double-positive? women do better? - Cancer Research UK - Science blog
However, the point here may be that Tamoxifen for breast cancer is different than Tamox for gynocomastia. If anything, Tamox might be better for Gyno because of its action on the PR receptors. But, I can't find enough, and I don't know enough to conclude that there is anything to worry about with regard to PCT. Perhaps someone who knows more will add to this, but maybe this is to technical to elicit comment?
OOPS! I guess I got so confused with the info that I posted the same article twice...
Tamoxifene has no intrinsic activity at the PR receptor, but the PR expression and regulation are indeed dependent by the ER. From the very article you linked:Quote:
Originally Posted by Quester
In the case of PR+ tumours, above research shows that ER blockade from tamoxifen alone is much more effective than ER+ tumours, case in which tamoxifen only serves as an adjunct to AI.Quote:
The PR is located downstream of the ER, and the prevailing theory has long been that the amount of PR in a tumor potentially reflects a functioning ER pathway, thereby predicting the effect of endocrine treatment. However, recent studies show that ER+/PR− tumors may be resistant to tamoxifen but respond to aromatase inhibitors (20), suggesting a still functioning ER mechanism. Instead, tamoxifen resistance has been attributed to cross talk between ER and growth factor signaling pathways that down-regulate PR while activating other ER functions.
You can easily guess tamoxifen will up-regulate PR at sites where it's an estrogen agonist (bone, liver, ?) and down-regulate in breast and hypothalamus, but if PCT is successful it's all going to crawl back to normal once the drug is discontinued.
In the male, most of the circulating progesterone comes from the Testes as stimulated by LH (and thus maintained by HCG also), together with other good stuff like pregnenolone and DHEA, and the remainder from the adrenals. It's a rather understudied and underrated hormone when it comes to males, it's so much more than a gestational hormone , both men and women display same very levels outside luteal phase so it's not even strictly a sex, female hormone.
It's not evil so to speak, but a factor in overall endocrine homeostasis.
Again , I don't see anything of concern after "alterations from 19-nors" when tamoxifen is used for PCT, but if anyone has any empirical evidence to show from personal experience he's welcome to chime in and share... I don't know much about toremifene and PCT but raloxifene is an effective substitute.
Perhaps it has something to do with the information coming from an online distributor, Pharmacom, that doesn't carry Nolvadex (Tamox).
Occam's razor then.
My opinion, I have used nolva to keep already developed gyno at bay on npp. I literally made a gyno knot disappear on cycle of npp ith nolva.