So, let's see if I understood you guys correctly, because I still feel like somewhere either my basic foundational information is wrong.
Austinite said:
I'm not sure what "all around SERM" means, but gynecomastia treatment with tamoxifen is certainly strong and effective. However, 2 to 6 weeks is merely impossible. This treatment generally takes longer.
Raloxifene: This one in particular is the weakest of the four SERMs at boosting testosterone recovery, but is allegedly (from all of the studies I have seen) the best candidate for blocking estrogen receptors at the breast tissue. Commonly dosed 60mg/day for the duration of PCT period (4-6 weeks) or gyno treatment (2-6 weeks) can be tapered down to 30mg daily for the final week. This one has also been effectively used to treat pubertal Gyno.
Agree that this is the most effective solution for gynecomastia, however, not in 2 to 6 weeks. Impossible in most cases. It's important to note that a 90 day dose of 60mg should be the maximum span, beyond that we risk bone demineralization. I will however,
disagree that raloxifene is weak at gonadotropin production. This is however, yet to be published so I have no documentation to provide at this time, so I will refrain from further comments.
What I meant by "all-around-SERM" is that it's multi-faceted, meaning not only is it effective at promoting healthy testosterone production through stimulating the HPT axis, but is also very effective at blocking estrogen from binding to estrogen receptors, and/or for treatment of gynecomastia.
The beneficial effects that tamoxifen has on testosterone production I deduced from this study, which I assume all of you have seen; 3 month greek study done on testosterone production with raloxifene,torem,and nolva
View attachment 554521
This is also why I mentioned that raloxifene does not seem to be a good candidate for the purpose of recovering testosterone levels solely; it simply is not as effective at doing so out of all of our other options. So, perhaps I don't have the most complete understanding of the functions of raloxifene in relation to gonadatrophin production, would welcome any enlightening input there.
Also, as far as this business of "rebound gyno", being on other boards I've seen virtually the same repetitive reaction of guys taking a PCT for a standard 4-6 week oral cycle with nonaromatizeable compounds, and then some time post SERM post cycle therapy (pct), say a month or two or three down the road, the end up getting symptoms of rebound gyno.... hence the development of the understanding that it must be caused by estrogen, and that running a mild suicidal Aromatase inhibitor (AI) with the SERM (something like 6-oxo, or Arimistane or even Aromasin) should basically get rid of this further development. Yet, you have stated;
It should never be done post cycle or when an individual is not on cycle. Please note, there would be no estrogen rebound in the presence or post presence of SERMs. No need for AI's. With some AI's, they can in fact induce a rebound. Always avoid AI's in cases mentioned.
Now, you specifically advise against the approach of running an Aromatase inhibitor (AI) outside of direct cycle use, and further state that Post Cycle recovery should only include SERM treatment (this, for the cases of short oral cycles, say 4-6 weeks, where Human Chorionic Gonadotropin (HCG) use would simply be impractical or unnecessary). Did I understand you correctly? And why is that?
Also, it has been my understanding that SERMs elevate circulating estrogen, so I don't see how the possibility of estrogen rebound post-SERM use is avoided if we only use SERM treatment during post cycle therapy (pct). Even on the basic level, SERMs artificially raise testosterone production to or slightly above baseline in most cases, which means more conversion to estrogen during a time when your T:E ratio is already off-balanced to favor Estradiol (in the cases when you have just finished a cycle and your endogenous T production is practically nil). So it makes sense to me that SERMs can potentiate further production of estrogen, bringing it further off balance, leading further into gynecomastia land. Or is my understanding somewhere flawed? Thanks.
Also, you had mentioned above that torem and tamox are not even close when it comes to comparison of function, yet their chemical structure is very similar, I understand they are not the same, but I assumed they were close given that fact. Also I've seen numerous studies where Torem ended up being slightly more effective than Tamox at reversing or regressing developing gyno. (hence my suggestion in the OP that Ralox, nolva and torem are practically interchangeable when it comes to the application of gyno treatment, ralox being the more favored one obviously) I can find some and post here for reference if want, or if you are also familiar with the general knowledge then I would appreciate a comment on Toremifene's proper use. For me personally I've noticed my body just takes well to it for PCT purposes, but didn't have it on hand when I had my gyno flare up so used nolva instead.
You also said Adex at 1mg daily is ludicrous.. I sort of understand that, but at the time it was corrective measure that was the issue. So I had been taking it at 1mg weekly as preventive measure, and then about 4 months down the road the lumps crept up. I waited another 2 months or so before I did anything about them. Here's another thing I'm fuzzy on; you said that SERM treatment for the purposes of gyno reversal would generally take longer than 2-6 weeks, but I was able to reverse my lumps with nolva/adex/lil bit of letro within a matter of 3 weeks completely. So I assume the responsible drugs were the adex and letro? and less so the nolva?
Those are the basic fuzzy misunderstandings and misconceptions that I can think of at the moment, thanks again for your time and input
