I love his fail at reverse psychology thinking I am thin skinned and he “got to me” or what ever lol. He’s really not that important, just got me more shocked than anything of his existence.
Thank you for this. I really appreciate your contributions, this is incredibly valuable information.
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Lmfao the anti ai brigade just got smashed again.
Why is this the case? I don’t follow that logic.
Let’s say you need X pg/mL of E2 systemically for all your tissues to function optimally.
Now let’s say you actually have X + 30 pg/mL systemically on TRT. You take an AI and drop 20pg/mL. You still have more than any of your tissues needs.
Your point is only valid if your levels are currently at the exact cutoff of what your tissues need and the AI takes you down from there.
The premise of using an AI is that there’s more E2 than you need, which is creating problems, and you’re trying to get rid of that extra E2. As long as you don’t drop more than that extra E2 with the AI, no tissue in your brain or body is being short changed.
The idea (not saying yours) that everyone’s body will perfectly regulate E2 to optimal levels given enough time is so stupid and contrary to everything we observe in science that I can’t understand how anyone with any scientific training could embrace it.
Not everyone is Michael Jordan or Einstein. Most people are far from being optimized in any area of athletic, intellectual or artistic performance. Very, very far.
Where does this idea come from that somehow when it comes to E2 conversion however, everyone’s endocrine system will just magically find the perfect conversion rate that makes them feel amazing without any additional tinkering?
It’s such a lazy idea. It’s using a binary model on something with a million variables. It’s worse than astrology
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Like I pointed out too, if the E2 overwhelmingly got short changed in just a certain tissue it would be a pain in the ass to crash our levels. If it was truly just being selective in one tissue you would get all sorts of problems wayyyyy before the crash. Not to mention then you still argue about circulating E2 going back to the tissue anyways.
It’s like you said in another thread it’s insane how they flip flop their judgements on what to do with TRT, because so far in this thread it’s a bunch of hypotheticals which honestly eventually has them saying “we just don’t know and because i said so”. Honestly it’s like you pointed out look how comfortably that statement was made “something has to be getting short changed”, like why? How do we know? Just because you said so?
That’s how this fad works, they make statements so confidently and comfortably without ever questioning each other. Newer guys come in doing their research see it that way and don’t bother to do any other research and assume like oh well it must be that way! Look at the groups those guys admire, people get blocked there so easy simply for asking questions. Look at here how some of them are throw hissy fits and insults simply because they are being questioned, they aren’t used to it because it doesn’t happen in the other groups I speak of. Even in this forum like I said things always come full circle and people are finally standing up and speaking out more and more, it’s driving them nuts.
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You go on TRT/TOT because your body is not functioning properly (hypothesis) but your aromatase function is perfect everywhere(for everyone) and would not suffer any dysfunction. Makes sense? If you don’t agree then you are banned from the inbred intelluctual ecosystem. Wash rinse repeat. Actually worse than that since they tout supra then tell you not to touch an AI (really cruel).
You have too much IQ and critical thinking ability/analytical skill @disciplined_trt. You are hereby banned from TOT/+++E2 Nation. Whaz up with that high aflutin fancy lad talk? E2 at any and all levels good for ya…it’s got electrolytes. Just like 2000 ng/dl TT / 40 ng/dl fT ya fool.
I will watch Idiocracy again this weekend in your honor.
Sorry for the sarcasm [tired of using science, logic, peer reviewed scientific literature, history of human knowledge in physiology, endocrinology, medicine, etc.].
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A lot is going on during aromatization, like creating fatty esters for your cardiovascular system, and using an AI is counter productive to that process.
You can see this in your lipids when taking an AI.
Now let’s say we have the same guy on two different protocols with the same or similar E2 levels, protocol #1 on an AI, the other not.
The lipids will not look the same because AI’s affect lipids negatively independent of E2 levels.
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Haha, thanks for the laughs.
Please, that was great. It’s good to laugh at all this sometimes. Trying to figure out how this ridiculously complex stuff works gets exhausting, especially given how much is at stake.
Is there any evidence of this? Any studies supporting this claim?
Or even rigorously recorded anecdotal evidence? I’m talking for example one guy with E2 at 70pg/mL taking 0.25mg/week of Adex and lowering his E2 to 35pg/mL, subsequently showing significantly worse lipids?
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Dose response of anastrozole, arimidex, letrozole vs lipids over time?
Effect of AI on lipids through direct E2 reduction or another mechanism?
Shall we take a walk down the literature?
I will post up my 6 week experiment with 0.5 mg anastrozole twice weekly [1 mg per week].
Good questions.
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Baseline:
6 weeks at 0.5 mg anastrozole twice E3.5D (sorry Endo wouldn’t give me the sensitive E2 test again, wasting resources that could go to the Pediatric patients 
):
Ignore the LCL,calc as it is wrong for low triglyceride folks.
Trig/HDL-c ratio took a hit.
I would have to show you the time series of my lipid profile and do some more math to see if +adex result was different than history of lipids without adex. Need replicates etc to show any statistical differences, etc.
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Definitely, that’s interesting.
Also noteworthy that the E2 range on the second lab says 0 - 42 pg/mL but your result is < 20 pg/mL. 0 - 20 pg/mL is a pretty wide range, you could’ve crashed your E2.
From what I’ve read anecdotally, 1mg/week of Anastrozole is a lot for TRT dosages of Test. What was your protocol?
Subjectively, how did you feel on with that AI dose?
I just started running 50mg E3.5D (100mg/week) of Test C. I’m going to give it 6-8 weeks and then add 0.125mg E3.5D of Anastrozole (0.25mg/week), see how that goes.
I’ll test TT/FT/E2 at peak and trough levels both with and without the AI. I’ll post the results.
If you have the time/courage, that would be great to see if the drop is statistically significant
0.0625 mg arimidex eod. E2 was measured at 28 at the moment bloods were done, not sure what the average would be. It’s sensitive E2 with a range of 8-35.
Here are 2 different bloodwork’s with out AI, I can’t find E2 for the second blood work but the first one E2 is at 20.3 on the same sensitive scale.
Baseline pre TRT, the document is from a different facility and not screen shot friendly so I will type it, E2 was untraceable at <12 on a NON sensitive reading with scale of 0-40.
Total cholesterol 154
LDL 87.6
HDL 44
VLDL 22.4
Triglycerides 112
Found one more blood work in where my E2 was the highest it ever was when I was really really getting into the E2 loving fad. My E2 was 48 on a NON sensitive reading on a scale of 0-40. Same thing about this one and not being screen shot friendly so typing it.
Total cholesterol 141
LDL 84.4
HDL 45
VLDL 11.6
Triglycerides 58
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I have a confession for the last few weeks I went back to higher dosing with AI 
I know it’s only me but I would love to update with blood work and protocol next time I get it. Then 6 months after that and again 6 months after that. I really want to put this to the test. Let’s see what a year of 0.125 - 0.25 mg of arimidex a week does to my lipids and liver.
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I will add to what i wrote above to make more compete. I would bet not much WRT to your experiment. I will add my liver values above.
7 mg week vs 0.25 mg/week. Factor of ~30.
Risk/reward and dose response with everything. Even Testosterone.
That’s an unusually low dose, definitely not typical. Perhaps long term things may change.
Nice, let’s walk through these when I get proper time. Did you read the first one?
That’s over 0.2mg per week.
0.25mg one week and 0.1875 the other.
Maybe I am wrong but I would think majority of TRT users are doing 0.5mg per week or less with a select few on 1 whole mg per week.
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Yeah, the after point was RIA E2 so 20 or less is below LOQ. Crappy test and no idea what my E2 was. Sorry
I felt fine on that dose and that was AI monotherapy before starting TRT.