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TRT gurus promoting High E2

you guys can "believe" what you want, but the facts remain - the serum levels aren't driving e2's tissue action. block aromatase, block it EVERYWHERE that estradiol is needed and made. ;-) bone. brain. endothelium. penis. EVERYWHERE.

The body maintains its own balance of T:e2, VIA aromatase. it's how we're set up. same with 5 alpha reductase. You don't need to control e2 any more than you need to "control" DHT.

and again, symptoms typically come with hormonal fluctuations (bad protocols), OR high EVERYTHING. Many men feel worse when their T gets supraphysiologic. nothing to do with e2....Yet everyone wants to blame e2. It gets tiresome.
 
@thebigbus but your rule of thumb, just to be clear, is to use SERM (do you recommend raloxifene?) when you're on compounds that are causing gyno symptoms? Like say a guy was on trestolone or dianabol? Could he be advised to run raloxifene alongside this?

But if only on TRT, then ride out a little nipple sensitivity and let the body adjust on its own without a SERM?

Thanks for the information man, I wish you were my doctor lol :)
 
The body reacts to sudden spikes in hormones by countering their effects. Some of these "Counter hormones" cortisol, progest, prolactin, E... in addition to the elevated androgens can have undesirable effects.

I have a question for you or anyone else here regarding gear and cortisol. What actually happens to cortisol on gear, especially high doses over long periods. Could it be that cortisol is actually "too low" or if not low inhibited due to cortisol-antagonist action from gear like tren? Could the burned out feeling and joint pain you can get from a lot of gear be from too little cortisol action?

I remember reading that the Russians had a test to see if athletes were responsive to anabolics or if they were taking more than prescribed. They would administer dbol at night and measure cortisol in the morning. Ideally cortisol would be elevated. If not, it meant the athlete was probably abusing gear.

So the question is, is high cortisol a problem in juicers or could it be the opposite?
 
Nipple sensitivity is quite common, esp early in the TRT process, but almost always stops if you ride it out. I can't emphasize that enough. Guys jump on things too quickly, all for a little nip sensitivity and then they end up on the hamster wheel of symptoms.

As far as those on 500-1000mg, etc, who are sensitive to gyno, I'd prefer a SERM. I def still think nip sensitivity is not a "big deal". I have an old gyno lump, and occ sensitivity, but don't do anything about it. :)

one also has to take into account any other substances being taken. Things like nandrolone, which do not aromatize, but still convert to ESTROGENS (not estradiol, per se), can still affect E receptors and possibly gyno ( not to mention direct stimulation of progesterone receptors).

Thanks for the reply, bigbus.

So you are saying when somebody has nipple sensitivity they are exaggerating it, and it should go away on it's own ?

What if it doesn't?

I always used nolva for most of the 90's, and then a little bit in the 2000's, and eventually it got to the point where Nolva wasn't effective, so when I switched to Arimidex et al, it reduced the swelling. In 2006, I ran a cycle of Anadrol/Test Prop, and I developed gyno, and it was the one cycle I didn't use anything...it never went away. In 2007, I had to have the lumps surgically removed. Even after stopping the compounds all together, both AAS and AI's/Serms, it continued to get worse, which lead to the surgery.

Why would anybody be okay with having a lump, say for example like yours? Doing nothing didn't seem to help?

Not trying to be argumentative, i'm still learning all this like everybody else. It just seems like doing nothing didn't help many who used AAS over the years. I'm speaking in terms of those using doses higher than trt, of course. For trt, I could see using nothing would be probably a good thing if possible. However, a lot who used AAS in the 80's, and eventually the 90's, did get gyno from not using Nolva, and when introduced, it did help.

Wouldn't it smart to use 'something,' whether for estradiol or Estrogens, if it means it will not lead to gyno?

Again, just trying to learn for my own benefit, thanks:)

Again x2, I just wanted to acknowledge again, my concerns are for guys using more than trt...which I guess I swayed from the thread started of using trt doses.
 
Big Bus, reading over it again, maybe after separating trt vs. higher doses, we are more on the same page, in terms of action?
 
Big Bus, reading over it again, maybe after separating trt vs. higher doses, we are more on the same page, in terms of action?
yeah, re-reading his posts, he seems like he is talking more about TRT with the nipple sensitivity issue and resolving itself (its the original topic of the thread its just us deviants are always rotating back to talking about blasting lol)...
 
I dont buy it. You guys can go around with high estradiol(I know not everyone has issues), be lethargic, have brain fog, wonder why youre putting on so much fat, having trouble breathing, etc, me I'll continue using an ai. I've been doing this for 5-6 years now, anytime I've ever come off an ai or for that matter, had bunk ai, I have felt like complete dog shit.

The typical trt routine is pinning test cyp 2x/week. At one point I was using 150mg/week split into two 75mg injections. At the time, I was using a bunk ai, that took a long time to figure, wondered why stopping the ai wasnt helping, anyways, the only days I ever half decent was pin days, then the test would peak, followed by estradiol, and I'd feel miserable for the next few days. The ai was some bunk counterfeit pharma ai and every once in a while, I'd take a dose of some other stuff I had that I knew was good but at the time actually thought underdosed and I'd feel great the next day, go back to the bunk ai and crash right back out. Estradiol was directly responsible, period! Oh, and 3 days post pin, my test levels would be mid 700s.

And with the right ai protocol, I feel amazing on 500mg test.
 
I'm really tired of the high E crowd.

They are correct in stating that crashing estrogen is bad, and that AIs are easily overdosed, but they take things way too far in an attempt to reinvent the wheel and to make a name for themselves. Hell, they even go so far to suggest that gyno is not causes by excess Estrogens to defend their quackery :rolleyes:

Let's stick to the case of TRT. The goal that everyone agrees on is to reach a testosterone level in the high-normal range, and to keep blood levels as stable as possible with frequent injections. But when it comes to Estrogen levels, the high E crowd suddenly abandons that idea and claims that 'the more Estrogen the better, Estrogen is amazing and has only positive effects' (I'm exaggerating only slightly). Yes, Estrogen does have an important role in males. That's why we should strive to keep it in the normal range. But high Estrogen also has side effects, among them gyno, female-type body fat deposits (mostly around limbs), subcutenous water retention, prostatic hypertrophy, and more. Some of these side effects are especially prevalent when Estrogen/Androgen ratio is high, but high E even in combination with high androgen levels can cause side effects.

Hence, with Testosterone in the normal range, we also want Estrogen in the normal range. But this is far from guaranteed. Yes, most men on TRT with dialed in T levels will also have normal E2 levels. But for some (with certain genetic factors and lifestyles) E2 will be out of range. In that case, you should use an AI, BUT AT A DOSE THAT WILL NOT LOWER E2 TOO MUCH. That is, at a very, very low dose. Given the cumulative effects of suicidal AIs, the dose should even be tapered down to an even lower maintenance level. That way, AIs can in fact be used to achieve stable E2 levels in the normal range. Arguably, SERM use is a more foolproof way of controlling Estrogen, but long-term use is not something I would recommend given that there is a better alternative. I'm not gonna get into the moronic argument made here earlier about the distinction of tissue and serum Estrogen level. Let me just point out that the decrease of Aromatase activity with AIs is proportional to the prior Aromatase concentration in tissues. In general, the distinction between serum and tissue E2 levels is much less important that was suggested above. Anyway.

So the upshot is this: On TRT, get frequent blood work. If E2 is above range, use AIs, at an appropriate dose. The target for E2 should be in the high-normal range. However, some people (e.g. those with preexisting gyno) may be symptomatic in that range. For those people, the target E2 levels should be lower, but never below the normal range. In the rare case that E2 side effects cannot be controlled without crashing E2, then a SERM is a better alternative.
 


Diet could also play a role and if estro is not very high but slightly out of range I (an educated gym bro, not an endo) would highly suggest just munching more broccoli, drinking green tea etc before hitting even a low dose AI. Assuming it's in the case of monitoring and wanting to bring it down some and not way off range, so of course you would need to recheck the estro after the diet change if you went that rout . I would suggest most guys eat most the stuff on that list anyway but upping the dose of the 2 I mentioned (broccoli and green tea) seems to help me best..
 
I'm just a study of n=1 but I stick more by Dr. Rand MCClain's protocol off keeping e2 in the 15-20 range. On just 100mg of test my sensitive e2 is at 32pg/dl.... doesn't sound that bad but that level, my hot dog might as well be a rubber appendage. Doing an exeriment with 350 Test and 1 aromasin pill per day, I tanked by e2 to 4pg/dl. Guess what? Libido, energy and well-being were through the roof.... obviously I stopped because that low just isn't safe, but some people tend to do better on the lower side. Everyone talks about the 20-30 range, but if you look at bloodwork (in U.S. measurements), the low point is like 8 or so, the high point is around 35 ( don't have the papers in front of me)....a mid-level range really would be around 12-18.
 
All that SERM chat and how did nobody mention their negative effect on IGF-1 that would mean a definitive "no" if you are able to avoid
 
I'm really tired of the high E crowd.

They are correct in stating that crashing estrogen is bad, and that AIs are easily overdosed, but they take things way too far in an attempt to reinvent the wheel and to make a name for themselves. Hell, they even go so far to suggest that gyno is not causes by excess Estrogens to defend their quackery :rolleyes:

Let's stick to the case of TRT. The goal that everyone agrees on is to reach a testosterone level in the high-normal range, and to keep blood levels as stable as possible with frequent injections. But when it comes to Estrogen levels, the high E crowd suddenly abandons that idea and claims that 'the more Estrogen the better, Estrogen is amazing and has only positive effects' (I'm exaggerating only slightly). Yes, Estrogen does have an important role in males. That's why we should strive to keep it in the normal range. But high Estrogen also has side effects, among them gyno, female-type body fat deposits (mostly around limbs), subcutenous water retention, prostatic hypertrophy, and more. Some of these side effects are especially prevalent when Estrogen/Androgen ratio is high, but high E even in combination with high androgen levels can cause side effects.

Hence, with Testosterone in the normal range, we also want Estrogen in the normal range. But this is far from guaranteed. Yes, most men on TRT with dialed in T levels will also have normal E2 levels. But for some (with certain genetic factors and lifestyles) E2 will be out of range. In that case, you should use an AI, BUT AT A DOSE THAT WILL NOT LOWER E2 TOO MUCH. That is, at a very, very low dose. Given the cumulative effects of suicidal AIs, the dose should even be tapered down to an even lower maintenance level. That way, AIs can in fact be used to achieve stable E2 levels in the normal range. Arguably, SERM use is a more foolproof way of controlling Estrogen, but long-term use is not something I would recommend given that there is a better alternative. I'm not gonna get into the moronic argument made here earlier about the distinction of tissue and serum Estrogen level. Let me just point out that the decrease of Aromatase activity with AIs is proportional to the prior Aromatase concentration in tissues. In general, the distinction between serum and tissue E2 levels is much less important that was suggested above. Anyway.

So the upshot is this: On TRT, get frequent blood work. If E2 is above range, use AIs, at an appropriate dose. The target for E2 should be in the high-normal range. However, some people (e.g. those with preexisting gyno) may be symptomatic in that range. For those people, the target E2 levels should be lower, but never below the normal range. In the rare case that E2 side effects cannot be controlled without crashing E2, then a SERM is a better alternative.

this is the most sensible post I would say. My doc thinks people these days have a propensity to over amortise (due to environmental factors etc) which is why e is higher.He also points that the negative feedback loop for LH/FSH in the HPG is related to E. so obviously the body doesn’t want uncontrolled levels of high E by design.

high range free t and normal range e make sense
 
Along with the High E crowd is that if your genetically predisoped to gyno your going to get it. "Deal with it"

Not everyone wants to deal with $8k breast surgeries. Especially for the majority of us who dont compete and just want to look and feel good
 
I'm really tired of the high E crowd.

They are correct in stating that crashing estrogen is bad, and that AIs are easily overdosed, but they take things way too far in an attempt to reinvent the wheel and to make a name for themselves. Hell, they even go so far to suggest that gyno is not causes by excess Estrogens to defend their quackery :rolleyes:

Let's stick to the case of TRT. The goal that everyone agrees on is to reach a testosterone level in the high-normal range, and to keep blood levels as stable as possible with frequent injections. But when it comes to Estrogen levels, the high E crowd suddenly abandons that idea and claims that 'the more Estrogen the better, Estrogen is amazing and has only positive effects' (I'm exaggerating only slightly). Yes, Estrogen does have an important role in males. That's why we should strive to keep it in the normal range. But high Estrogen also has side effects, among them gyno, female-type body fat deposits (mostly around limbs), subcutenous water retention, prostatic hypertrophy, and more. Some of these side effects are especially prevalent when Estrogen/Androgen ratio is high, but high E even in combination with high androgen levels can cause side effects.

Hence, with Testosterone in the normal range, we also want Estrogen in the normal range. But this is far from guaranteed. Yes, most men on TRT with dialed in T levels will also have normal E2 levels. But for some (with certain genetic factors and lifestyles) E2 will be out of range. In that case, you should use an AI, BUT AT A DOSE THAT WILL NOT LOWER E2 TOO MUCH. That is, at a very, very low dose. Given the cumulative effects of suicidal AIs, the dose should even be tapered down to an even lower maintenance level. That way, AIs can in fact be used to achieve stable E2 levels in the normal range. Arguably, SERM use is a more foolproof way of controlling Estrogen, but long-term use is not something I would recommend given that there is a better alternative. I'm not gonna get into the moronic argument made here earlier about the distinction of tissue and serum Estrogen level. Let me just point out that the decrease of Aromatase activity with AIs is proportional to the prior Aromatase concentration in tissues. In general, the distinction between serum and tissue E2 levels is much less important that was suggested above. Anyway.

So the upshot is this: On TRT, get frequent blood work. If E2 is above range, use AIs, at an appropriate dose. The target for E2 should be in the high-normal range. However, some people (e.g. those with preexisting gyno) may be symptomatic in that range. For those people, the target E2 levels should be lower, but never below the normal range. In the rare case that E2 side effects cannot be controlled without crashing E2, then a SERM is a better alternative.

Love your posts brother !

Much respect
 
I'm really tired of the high E crowd.

So the upshot is this: On TRT, get frequent blood work. If E2 is above range, use AIs, at an appropriate dose. The target for E2 should be in the high-normal range. However, some people (e.g. those with preexisting gyno) may be symptomatic in that range.

Yes, however, @thebigbus indicated that serum E2 levels are largely meaningless, because tissue e2 levels are typically exponentially higher. Therefore, the use of an AI could misleadingly suggest that it is bringing 'e2' into a 'normal' range (while tissue levels may continue to soar). Meanwhile, the risk of AI neurotoxicity increases, without tangible benefit.
 
Yes, however, @thebigbus indicated that serum E2 levels are largely meaningless, because tissue e2 levels are typically exponentially higher. Therefore, the use of an AI could misleadingly suggest that it is bringing 'e2' into a 'normal' range (while tissue levels may continue to soar). Meanwhile, the risk of AI neurotoxicity increases, without tangible benefit.
He made that claim, yes. But it's hard to reconcile with basic physiology. Tissues are supplied with blood. Most of aromatase is located in tissues rather than the blood. Hence, the serum E2 levels are a result of tissue E2 levels. If you observe a decrease in serum E2 levels, this logically implies an (almost perfectly proportional) decrease in tissue E2 levels. At least in those whose gonadal Estrogen production is shut down.

Your idea that an AI could lower serum E2 levels while keeping tissue E2 levels almost unchanged is so ridiculous that it almost defies belief. Why do you think AIs are used in postmenopausal women with breast cancer? If, in fact, AIs didn't reliably lower tissue (here, the breast) E2 levels? (and yes, breast and tumor tissue do contain lots of aromatase: https://www.ncbi.nlm.nih.gov/pubmed/1954167)

Also, your last sentence is a complete non sequitur.

If left to their own devices, medical practitioners come up with the wackiest shit, it's like they never went to med school. That's why we have PhDs write medical guidelines for them to follow.
 
Your idea that an AI could lower serum E2 levels while keeping tissue E2 levels almost unchanged is so ridiculous that it almost defies belief.

That was your idea, not mine. To use a hypothetical, if there was a 30% decrease in both serum and tissue e2 levels, it is 'possibility' that serum e2 might be reduced to a 'normal' range, while tissue levels remain highly 'abnormal' (albeit also proportionally reduced).

Your disparaging suggestions about this medical practioner's motivation are also quite unfair and irrational.
 

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