Anti AI crowd

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How's the protocol going for you?
I'm experimenting now with 70 mg twice weekly and no AI, after my E2 dropped lower than I expected (29 pg/mL) after a couple weeks where I took only 0.1 mg every six days. I also suspect that despite E2 levels in blood looking good, aromatase inhibition in the brain is maybe not the best thing for mood and libido.

I might just take the AI on an as-needed basis rather than a set schedule. It seems like the effects may be cumulative in surprising ways with regular dosing.
 
I'm experimenting now with 70 mg twice weekly and no AI, after my E2 dropped lower than I expected (29 pg/mL) after a couple weeks where I took only 0.1 mg every six days. I also suspect that despite E2 levels in blood looking good, aromatase inhibition in the brain is maybe not the best thing for mood and libido.

I might just take the AI on an as-needed basis rather than a set schedule. It seems like the effects may be cumulative in surprising ways with regular dosing.
I hear you. Erections quality improves for me with an AI or low dose protocol, but at the cost of libido. Low dose protocols make me feel worse across the board though so I'm trying to dial it in by adjusting the dose and AI to the right ratio. It's a tough balancing act.
 
I hear you. Erections quality improves for me with an AI or low dose protocol, but at the cost of libido. Low dose protocols make me feel worse across the board though so I'm trying to dial it in by adjusting the dose and AI to the right ratio. It's a tough balancing act.
I'm going to be experimenting next with some of the DHT derivatives I haven't tried yet (proviron, baby dose of masteron) to see if that might be a more effective way to counter excess E2 without the downsides of inhibiting aromatase in the CNS.
 
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.

Three things I don't discuss, religion, politics and estradiol. Might as well slam your pecker in a car door and get it over with if you go there.
 
Three things I don't discuss, religion, politics and estradiol. Might as well slam your pecker in a car door and get it over with if you go there.
I think you did make an excellent point in another thread however about the half life of AI not matching test esters and causing wild fluctuations in E2. At least I think it was your username.
 
Completely agree with this. I'm now also absolutely convinced "roid rage" is really Estrogen rage
If I remember correctly, this was shown in rats years ago, estrogen caused aggressive behavior, testosterone in the absence of estrogen (aromatase knockouts I believe) did not.
 
I think you did make an excellent point in another thread however about the half life of AI not matching test esters and causing wild fluctuations in E2. At least I think it was your username.
Yes that was me. A number of guys (former BBs) use low doses of drostanolone (Masteron enanthate) to mitigate higher E2 on HRT, methenolone (primobolan) is pretty suppressive as well, but it tends to knock down HDL even in low doses, drostanolone does not. Consider this, why do guys get gyno from finasteride or dutasteride? The effects on E2 are small 5 - 10% increase, but their DHT gets crushed. It is the E2/DHT ratio that matters. Masteron has been shown clinically to be effective in the treatment of gyno. Years ago, the DHT derived androgens were being developed for metastatic BC in women bc while test prop worked, it was too androgenic.
 
I tried primo for a short while and it caused significant joint pain and some prostate inflammation. I know some prefer to use DHT derivatives to control E2, but I honestly feel like microdosing anastrozole is more benign. At least, it feels healthier and more sustainable for me personally, based on my limited experience. I have yet to try another form of AI or DHT derivative. Maybe masteron or proviron would be friendlier?
Did you get your E2 measured on the methenolone?
 
I agree with this. That and guys being on tren lol. If u watch vids of guys talking about their experiences on high dose tren, it mimics what we view as “roid rage” to a T
19 nors are neurotoxic, tren probably the worst. Nandrolone will only yield about 10% of the estradiol that testosterone will mg/mg.
 
19 nors are neurotoxic, tren probably the worst. Nandrolone will only yield about 10% of the estradiol that testosterone will mg/mg.
Any idea how/ why nandrolone could be neurotoxic?

I’ve heard a few times over the years that nandrolone can be neurotoxic, but I’ve also heard that testosterone, without enough estrogen, can also be neurotoxic. And we know that nandrolone converts extremely extremely little into E2. Like for every 300mg of nandrolone, expect ur E2 level to go up around 4-6 points. So I would assume that any study done on nandrolone by itself, is going to show that it’s neurotoxic. Due to there not being enough E2, along with the androgens (from the nandrolone) in the person’s system. I would love to see a study where guys were put on nandrolone, as well as exogenous estradiol, so they had healthy E2 levels, while being on the nandrolone, and seeing then if nandrolone was still neurotoxic

I wonder if tren is neurotoxic for the same reason. Any study done on guys just taking tren, would have extremely low levels of estradiol as well, I would assume
 
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No. I have BPH, so any DHT agonist is only to going to worsen it.
Not so sure about that. Clinically guys were given DHT, increased circulating levels 7 fold but had no change in intraprostatic DHT over 28 days of treatment (Page et al 2011). A 2 year study increased circulating DHT by 10 fold, they had a slight decrease in PSA (Idan et al 2010). What occurs in circulation does not represent what is happening at the tissue level esp where 5AR is high. A low 50 mg dose of DHT or DHT analogue is unlikely to affect the prostate, but will likely suppress E2. Only way to know for sure is to have PSA and E2 checked. For all we know, the DHT analogue might improve BPH because it will lower circulating T and intraprostatic DHT. As far as prostatic inflammation, that can be caused by numerous things, just getting stressed can set it off.
 
Any idea how/ why nandrolone could be neurotoxic?

I’ve heard a few times over the years that nandrolone can be neurotoxic, but I’ve also heard that testosterone, without enough estrogen, can also be neurotoxic. And we know that nandrolone converts extremely extremely little into E2. Like for every 300mg of nandrolone, expect ur E2 level to go up around 4-6 points. So I would assume that any study done on nandrolone by itself, is going to show that it’s neurotoxic. Due to there not being enough E2, along with the androgens (from the nandrolone) in the person’s system. I would love to see a study where guys were put on nandrolone, as well as exogenous estradiol, so they had healthy E2 levels, while being on the nandrolone, and seeing then if nandrolone was still neurotoxic
There are numerous papers on the topic.
 
Did you get your E2 measured on the methenolone?
I did not. I actually persisted with the primo experimentation and had a couple weeks on it without joint pain or prostate issues, so that might have been a fluke or a temporary effect of starting it. It seemed to affect libido and mood negatively though, in a fashion similar to anastrozole. I read that primo forms an AI metabolite - if true, I guess it's unsurprising that it would feel similar to anastrozole, AR-related effects aside.

I'm hopeful masteron will be a more positive experience. It certainly gets better reviews than primobolan in the mood and libido department.
 
There are numerous papers on the topic.
Ya but what I’m saying is, are all the papers on guys taking nandrolone by itself? Because if so, I would assume that they would show nandrolone to be neurotoxic, due to there not being enough E2 in the guys system. Again, there’s papers showing that testosterone is neurotoxic if there’s not concurrently enough estrogen in the person’s system. Does that mean we should go around stating that testosterone is neurotoxic?

I’m not saying ur wrong. Again, I’ve heard that nandrolone is neurotoxic before. I’m just seeing if we can use some critical thinking skills to try and figure out why nandrolone is supposedly neurotoxic, and/ or see if you, or anyone else knew the exact mechanism why nandrolone causes neurotoxicity in these papers
 
I did not. I actually persisted with the primo experimentation and had a couple weeks on it without joint pain or prostate issues, so that might have been a fluke or a temporary effect of starting it. It seemed to affect libido and mood negatively though, in a fashion similar to anastrozole. I read that primo forms an AI metabolite - if true, I guess it's unsurprising that it would feel similar to anastrozole, AR-related effects aside.

I'm hopeful masteron will be a more positive experience. It certainly gets better reviews than primobolan in the mood and libido department.
I’ve had E2 tested numerous times on primo. It will absolutely lower E2 in the serum when u get ur blood tested. I’ve also had E2 tested on masteron. The difference between the two, E2 wise, is primo will lower E2 in the serum, masteron will not. e2 will be unchanged, on a blood test. But masteron also has E2 inhibiting effects. It’s just a different mechanism compared to primo. They both will inhibit E2 effects tho. For better or for worse. Just throwing that out there for anyone that gets their E2 checked while on masteron, and doesn’t see their E2 go down. Don’t want them to think that their masteron is bunk simply because their E2 didn’t go down on a blood test
 
I’ve had E2 tested numerous times on primo. It will absolutely lower E2 in the serum when u get ur blood tested. I’ve also had E2 tested on masteron. The difference between the two, E2 wise, is primo will lower E2 in the serum, masteron will not. e2 will be unchanged, on a blood test. But masteron also has E2 inhibiting effects. It’s just a different mechanism compared to primo. They both will inhibit E2 effects tho. For better or for worse. Just throwing that out there for anyone that gets their E2 checked while on masteron, and doesn’t see their E2 go down. Don’t want them to think that their masteron is bunk simply because their E2 didn’t go down on a blood test
I've seen Kurt Havens mention that masterons metabolites tend to function more as a SERM than an AI the way primo metabolites do, which could explain the E2 readings.
 
I've seen Kurt Havens mention that masterons metabolites tend to function more as a SERM than an AI the way primo metabolites do, which could explain the E2 readings.
Ya I remember watching the same video ur probably referring to. They go over the mechanisms by which each compound affects estrogen. Really good stuff. Saved it for future reference. Here it is if anyone wants to check it out

 
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.
 
It sounds like you are trying to make logical sense of their position which is not possible.

The actual E2 level does matter, because the circulating hormone you are measuring enters tissues and exerts effects. They tend to focus on the intracrine or paracrine functions of estradiol when formed by aromatase in tissues, which is a real aspect of our biology and a nugget of truth supporting their position. At the same time, they deny the reality that it is also an endocrine hormone, limiting the explanatory power of their belief system.
Where do you get it is an endocrine hormone that enters tissue and actually does something?
 
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