Should I fear the estrogen


What is the best time to take the AI (Aromasin) in your experience? Just after pinning Test E/C? 6 hours after the shot? A day after?

What would be "healthier" - taking 25 mg 2x week or 12.5 mg 4x week?

I know, take bloods and go from there, but i'm interested in personal experiences.
 
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Hanlon's razor is an adage that states basically: do not attribute to malice that which is adequately explained by stupidity, laziness, or ignorance. However, in the case of fitness professionals, do attribute to malice that which they market themselves on and derive income (e.g., their "pet concepts"; generating newsworthy content that drives ad revenue by clicks).

His point that caber is unnecessarily used by bodybuilders is correct in its conclusion though. People take this dopaminergic agent unnecessarily because they believe that it will forestall sexual dysfunction as a result of, e.g., trenbolone. However, since trenbolone reduces prolactin, all that they really end up doing is taking a drug that enhances sex by reducing the male refractory period.
ok fair enough, but some guys do have high progesterone on cycle or TRT, there are plenty of threads on this forum on this matter, but it does seem to be a minority just as the guys that don't get sides from E2 in the hundreds...thats where my idea came from that maybe there is a link but without doing some meta analysis of the anecdotal reports, I shouldn't have said anything.
Having said that I will check mine on the next bloods as I'm curious, I also do not get sides from high E2 but I prefer to keep it under control a little.
 
ok fair enough, but some guys do have high progesterone on cycle or TRT, there are plenty of threads on this forum on this matter, but it does seem to be a minority just as the guys that don't get sides from E2 in the hundreds...thats where my idea came from that maybe there is a link but without doing some meta analysis of the anecdotal reports, I shouldn't have said anything.
Having said that I will check mine on the next bloods as I'm curious, I also do not get sides from high E2 but I prefer to keep it under control a little.
They may... but not associated with AAS. It's possible that hCG increases progesterone by increasing side-chain cleavage of cholesterol via cyt. P450 (20-hydroxylase, 22-hydroxylase, 20,22-lyase activity), thereby increasing pregnenolone that via 3β-HSD yields progesterone.
 
Serum E2 ≥ 40 pg/mL for a TRT user is a far lower A/E ratio than two-fold greater E2 concentrations in a guy running above 1.5 g of weekly testosterone-equivalent androgen.
Very interesting and much discussed topic. What would be your current recommendation?

From what I have read so far, the dominant approach is to keep estradiol as much as possible in the normal reference range regardless of testosterone dosage and values to counteract the negative effects of estradiol. Even without having symptoms. So the reference should be observed, not a ratio.

For example if at 500mg testosterone per week the estradiol level is outside the reference, one should use an AI protocol to bring it into reference.
 
Very interesting and much discussed topic. What would be your current recommendation?

From what I have read so far, the dominant approach is to keep estradiol as much as possible in the normal reference range regardless of testosterone dosage and values to counteract the negative effects of estradiol. Even without having symptoms. So the reference should be observed, not a ratio.

For example if at 500mg testosterone per week the estradiol level is outside the reference, one should use an AI protocol to bring it into reference.
That sounds like it would work, but is an example of invalid reasoning, excluding the middle, or a false dichotomy, between either keeping in range or getting your E2 bloodwork levels cRuNk.

The reason that an AAS user might be comfortable with elevations above normal ranges on high doses of AAS is due to the antiestrogenic class effects of androgens (tissue-level blockade of estrogen action, pituitary-level antigonadotropic action), and the proxy of androgen/estrogen ratio for general systemic estrogenicity (effects associated with the two ERs).

Look forward to a forthcoming article I've submitted to Millard for the main site, titled tentatively (subject to change), "Primo & EQ Crashed my E2! Help!" It will delve into these as factors that influence AAS effects on estrogenicity, broadly, and then for the cases of EQ & Primo.
 
Where to begin, this touches on a nitpick I've had for a really long time. So, to each is own. But for me, the short answer is yes.

One of the most annoying things I see in the TRT community (particularly on Youtube) is bros spreading pro-estrogen dogma. Everything from "don't worry about E2," "aromatase inhibitors are toxic," to shit as bizarre as "estrogen is a systemic health hormone!"

I agree with essentially none of it, except for maybe the idea AI's are toxic. Half the risks from androgen therapy is due to the aromatization process. High blood pressure, edema, thrombosis and heart attacks, irritability, sexual dysfunction, and depression are all made worse when estrogen is out of control. Now, what constitutes as "out of control?" Smarter minds than me might could help answer that.

As a general rule of thumb I typically always question pre-designated reference ranges on labs. And estrogen is no exception. As long as nothing looks majorly out of whack, then I'm far more supportive of going by personal symptoms (or lack thereof).

I think overall androgenicity to estrogenicity ratio plays an important role. It's not uncommon for hypogonadal men to have low estrogen just as much as low testosterone. But their T:E2 ratio is what's damaged the most, leading to the adipose accumulation, lack of drive, sexual dysfunction, depression, etc. And since estrogen stimulates CRH and ACTH, it increases the level of cortisol being secreted, which can increase the depressive (glucocorticoid antagonists have been studied for possible treatment to depression) effects of estrogen dominance even more, while eliciting an irritable hostility.

Estrogen also increases the action of tryptophan hydroxylase, which creates higher amounts of serotonin, both estrogen and serotonin can synergize in suppressing gonadotropin and LH, while increasing prolactin. Which can contribute to a really nasty feedback loop keeping you stuck in this situation until you intervene and fix it.

The one thing I do happen to agree with is the toxic effect of many aromatase inhibiting drugs, like Arimidex. Which can increase autoimmunity. Exemestane can be bad as well if you fuck up and take too much, because being a suicidal inhibitor you'll be in a prolonged state of low estrogen until you can make more aromatase. Low estrogen is also bad, which I'm sure you're well aware of. But there's much safer ways to control estrogen than AI's anyway.

Lower more frequent dosages of T can help prevent the rise in estrogen. Fat soluble vitamins A, D, & E can help. Vitamin E is actually an antagonist at the estrogen receptor. Zinc and/or aspirin act as mild aromatase inhibitors. Various flavonoids have been used and being researched for aromatase antagonism, some of them being quite potent in fact (look up 7-hydroxy-4-imidazolylflavan). 5ar androgens such as DHT can also keep the lid on estrogen. Interestingly, another commenter mentioned cialis for helping with erection quality, it also seems to help with the testosterone:estradiol ratio, and the mechanism behind which is hypothesized to be aromatase inhibition! (R)

So if you ask me, yes I do fear estrogen. But this is a personal thing for me. I am also biased, and I deal with a condition that makes me more sensitive to estrogen and higher aromatase activity. When people like Derek get on Youtube and talk about the glories of estrogen, I think they forget they're talking to a much wider audience than just heavy cycle users who also use very potent and potentially toxic AI drugs that can easily crash E2. To those people, low estrogen is certainly a problematic situation. But to tell the "Average Joe" out here he shouldn't worry about estrogen is misleading and potentially dangerous advice.
Are the AIs themselves inherently detrimental, or is it the fact that they can lower estrogen too much if abused? And it is the low estrogen that causes the side effects?
 
That sounds like it would work, but is an example of invalid reasoning, excluding the middle, or a false dichotomy, between either keeping in range or getting your E2 bloodwork levels cRuNk.
What are practical recommendations here?

If I take my example again. At 500mg of tesosterone and 90pg/ml of estradiol, should one take an AI to get estradiol levels to 40pg/ml? In terms of long term health (avoiding BPH, negative cardiovasvular effects, etc.).

What is your opinion about this table which shows predicted values for estradiol at different testosterone levels?

I am looking forward to your article.
 
What are practical recommendations here?

If I take my example again. At 500mg of tesosterone and 90pg/ml of estradiol, should one take an AI to get estradiol levels to 40pg/ml? In terms of long term health (avoiding BPH, negative cardiovasvular effects, etc.).

What is your opinion about this table which shows predicted values for estradiol at different testosterone levels?

I am looking forward to your article.
That paper is cited by my article.

Practically, just treat symptoms of high estrogenicity rather than being driven by bloodwork, but if E2 is > 75 pg/mL, the benefits of an AI probably outweigh foregoing it.

My opinion is that the coefficients of variation (a measure of dispersion about the mean) are too high to use these data to "predict" total E2 or total DHT. CVs are 20% for total estrogen & 52% for total DHT.
 
I like what he did (I was thinking of doing it myself) from the perspective that this sort of table provides for values that will be useful to most people (those that aren't outliers).
 
Thank you for your comments.
Practically, just treat symptoms of high estrogenicity rather than being driven by bloodwork, but if E2 is > 75 pg/mL, the benefits of an AI probably outweigh foregoing it.
Thank you for this recommendation.

May I ask if there is a basis or specific indication for this number?

And do you refer to the values of a sensitive estradiol test?

Would you also lower estradiol if it is above 75 pg/ml, but Masteron is used, which decreases the uptake of estradiol in the tissue? I wonder if too high estradiol can have negative effects despite the Masteron.
 
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I like what he did (I was thinking of doing it myself) from the perspective that this sort of table provides for values that will be useful to most people (those that aren't outliers).


Sir, are you for or against AI use on high-dose testosterone cycles, even with added primo or masteron? 500mg+ protocols
 
What is the best time to take the AI (Aromasin) in your experience? Just after pinning Test E/C? 6 hours after the shot? A day after?

What would be "healthier" - taking 25 mg 2x week or 12.5 mg 4x week?

I know, take bloods and go from there, but i'm interested in personal experiences.

Anyone?
 
Thank you for your comments.

Thank you for this recommendation.

May I ask if there is a basis or specific indication for this number?

And do you refer to the values of a sensitive estradiol test?

Would you also lower estradiol if it is above 75 pg/ml, but Masteron is used, which decreases the uptake of estradiol in the tissue? I wonder if too high estradiol can have negative effects despite the Masteron.
It's based purely on my empirical observation of bloodwork from AAS-using bodybuilders.

You ask a lot of questions, if you want this kind of access, you can PM me about my consultation services.
 
@StayFly if you can't PM me because you're still a New Member, I think that Millard has this policy for a good reason. Stick around for a while and contribute, and you'll eventually be able to.
 
That paper is cited by my article.

Practically, just treat symptoms of high estrogenicity rather than being driven by bloodwork, but if E2 is > 75 pg/mL, the benefits of an AI probably outweigh foregoing it.

My opinion is that the coefficients of variation (a measure of dispersion about the mean) are too high to use these data to "predict" total E2 or total DHT. CVs are 20% for total estrogen & 52% for total DHT.
So since I’m on a blast and my e2 stays up around 90 if I were to take an ai how much weekly would get me into a normal range of day 40. I know I have to do bloods but I’m tryna see a starting dose for it. I am prescribed anastrozole 1mg tabs. So that’s all I have. If I take 1mg pill every Friday is that enough to keep me down or will I get big spikes since I pin twice a week ? I still have 0 sides and feel great but I am considering trying it if I don’t have to take much to see if I notice a difference.
 
So since I’m on a blast and my e2 stays up around 90 if I were to take an ai how much weekly would get me into a normal range of day 40. I know I have to do bloods but I’m tryna see a starting dose for it. I am prescribed anastrozole 1mg tabs. So that’s all I have. If I take 1mg pill every Friday is that enough to keep me down or will I get big spikes since I pin twice a week ? I still have 0 sides and feel great but I am considering trying it if I don’t have to take much to see if I notice a difference.
Half life of anastrozole is 40 to 50 hours (1.5-2 days)
once a week is a bit sparsely
So at least divide your tablet for twice a week
If having sides, usually start at half the tablet every other day
Steady levels of anastrozole are achieved within 7 to 10 days of continuous administration
Differences from one tablet a week probably can be seen only on blood tests after some considerable time of usage
 
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