Anti AI crowd

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This thread is dead on and I can confirm the anecdotes mentioned.

Primo crashes my E2 every single time and it takes a really long time for the symptoms to go away. Jacks up my lipids horribly. Masteron doesn't seem to touch my E2 but I can definitely feel and see the hardening effects. It feels different than primo. Primo I'm like dead inside. Masteron it still feels like I have plenty of E2 working on my brain but physically I look different. In my experience primo works like an AI and masteron like a serm.

I also can't deal with the low dose TRT. When I am older I will revisit the low dose protocols but for now I'm trying to feel like a million bucks.

I also feel like the mismatched half lives of esterfied test and anastrozole causes problems. Why wouldn't it? Seems obvious.

I've been experimenting with a healthy dose of Test cyp 200-250 a week along with anastrozole ED at .125 and I am honestly feeling really good so far. Feels natural but good. Such a low ai dose a day, while substantial over the week doesn't seem to crash my estrogen. Much better than primo or masteron. I opted for anastrozole over exemastane because I wanted something non-steroidal. I didn't want any interference at the androgen receptor. No bloodwork yet but everything is going well.
How's the AI protocol treating you thus far?
 
Defy Medical TRT clinic doctor
If you deem your estradiol high, and you take anastrozole and feel great on it, then nothing studies say will convince you to leave estradiol alone.

Blocking estradiol is like blocking DHT. But what I have been saying for years does not really matter, no matter how much data we have on the subject. I give up.

So just to clarify your position, you're opposed to using an AI in most instances b/c it blocks a natural biological conversion process?
 
Wondering if anyone can clear up something for me about the anti AI crowd. You all know there are the guys that are not only against AI but that also say they don’t even check E2. They say they aren’t concerned about it and as long as your dose is right you don’t need to check it. But what they never say is “does the actual E2 level matter”. In other words, let’s say at your current dose, your T level is 1800 and your E2 is 90. And let’s say you don’t feel good. Would they say it’s nothing to do with estrogen since estrogen doesn’t matter? Or would they said “yes E2 matters but should be controlled by adjusting T dose?” In other words what im asking is do they say estrogen just doesn’t matter at all so don’t check it. Or are they saying estrogen definitely matters, and should be kept in range by adjusting T dose?
The E2 reference range doesn't account for TRT or natural test levels above 500. If your not feeling well lower your T dose
 
The E2 reference range doesn't account for TRT or natural test levels above 500.

I've read this many times on these forums especially and have asked for evidence supporting that statement. Never got any and I don't expect this will change, but please post it if you have it.
 
Beyond Testosterone Book by Nelson Vergel
I've read this many times on these forums especially and have asked for evidence supporting that statement. Never got any and I don't expect this will change, but please post it if you have it.
This may not answer your question but I believe is still relevant.


Our study did not link high estradiol levels with diminished sexual performance. Paradoxically, patients with low estradiol below 42.6 pg/ml had more patients complaining of low libido as defined by ICD-9 of 799.81 in the problem list. Patients with higher estradiol levels above 42.6 pg/ml had less sexual dysfunction problems identified by their providers. Of those that providers had identified as having low libido, 2,726 of 7,332 patients (31%) had higher estradiol levels and 4,606 patients (69%) had normal estradiol levels. In contrast to those who did not complain of low libido, 4,811 patients (28%) had high estradiol and 12,360 patients (72%) had normal estradiol levels. When the chi-square test was applied, the difference was statistically significant, p < .05; in other words, there is a real difference with those who complained of low libido and had high estradiol and those who did not complain of low libido and had normal or low estradiol.
 
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