1. I tihnk exemestane is worse than all of them. Also you can't compare lipid profiles of 6-OXO to other AI's because the study was done on normal men for only 3 weeks. Hardly conclusive in anything other than it raises testosterone. These are not the effects that would be seen in hypogonadal state (mainly estrogen levels)
I agree that exemestane is a poor choice, but only because of its minor androgenic effect.
Maybe I wasn't clear in my previous post, or you didn't understand what I tried to explain. That because 6-OXO is raising T so much despite normal plasma E levels, and because it showed no ill effects regarding the lipid profile, and because the research on steroidal A.I.'s (like 6-OXO is) have shown no ill effects on the lipid profile of subjects despite significantly lowered plasma E values, it is quite reasonable to conclude that 6-OXO does not have the potential health problems regarding the lipid profile -- that are surely found with non-steroidal A.I.'s.
In other words, 6-OXO should not be condemned as unhealthy because people are improperly associating it with non-steroidal A.I.s (which is what Swale uses). And as I said before, one explanation for the ability for steroidal A.I.'s to not cause lipid profile problems despite decreased estrogen levels/action is that they are somehow filling the protective role of estrogen, either directly or though unknown metabolites. So yes, while plasma E levels will be quite low post cycle when using 6-OXO (most likely), that does not at all mean you are going to experience lipid profile problems.
And as said before, on top of all of this -- even if I'm wrong, i just find it strange that people use the lipid profile risks as a reason to use Nolva, after using things like M1T alone (where their lipid profile is getting wrecked).
2.If it impaired action in the other tissues such as the brain, there would be a decrease in libido most likely and that hasn't been reported in most cases.
Not necessarily, but yes I do find it strange that there are not more reports of libido problems with 6-OXO... might be due to increased DHT action. Good point to raise though.
3. Plasma levels could remaine somewhat normal because these drugs do not block ALL aromatiziation not to mention circulating estrogen levels that were present before the study started. This is why it would have been better if it was on hypogonadal men and many conclusion on 6-OXO are just specualtion. THe only real thing the study proved was that it raised test in normal men.
Yes, but if they used a higher dose, as stated, I would guess that the plasma levels would drop... because the T would peak from direct AR mediated negative feedback and the aromatase levels would be so low that there is not enough substrate to bring the levels back up (like there is with the normal doses, as seen in the study).
And yes, ideally the study would be on hypogonadal men, but that doesn't mean its not useful for supporting reasoned conclusions indirectly, in conjunction with other knowledge/studies on steroidal A.I.s.
4. Estrogen rebound has nothing to do with upregulating recpetors IMO, it has everything to do with the amount and length of being suppressed. The analogy is that of test production usually rises to a higher than normal levels post cycle (documented in a number of cases) before returning to normal because of the strong suppression. If you do this to estrogen (suppress it strongly) you could have a much nastier rebound and levels could rise above natural levels before returning to normal. I think the whole arguemenet that SERMS are more likley to do that is complete bunk or you would have a number of cases of people developing gyno after using Nolva for extened peroids of time and they just don't exist in any significant numbers.
Well "estrogen rebound" is sort of used as a misnomer. More technically ppl should say "estrogen action rebound"... its all about whats happening in the tissues. Yes, the ER upregulation is probably not that big a factor in the big picture, I agree with that.
The reason that I feel SERMs have more potential for this effect is that upon cessation plasma T/E ratio will be low. With A.I.'s, the ratio will normalize as the drug's effect will slowly decrease after the last dose -- so despite a very high amount of substrate, plasma E levels won't rebound above normal because it takes time to produce aromatase protein because suicidal A.I.'s when bound remove the enzyme completely. Thus you get a sort of automatic tapering effect. I do think there is rebound potential with the non-steroidals though, as they upregulate aromatase and only competitively inhibit (not destroy).
As for Nandi and Swales theory, Pat wouldn't respond when I asked him about it on bb.com. Its not that I don't think he could at all its just the majority of stuff is just unknown and nobody know WHY certain things happen. Even Clomid isn't fully understood and they have studies clinically proving to reverse andropause from steroid abuse.
Yes, the SHBG/Total-T theory is interesting.. I don't really agree with it, but I'm not ready to argue against it at this point.
We know that SERMs work, I'm not contesting that. I just think that 6-OXO is at least equally effective (and safe), based on the on-paper mechanisms, and could also have some minor advantages over the SERMs...
