# The Estrogen Conundrum, a Full Report of the Basic Understanding



## Get Some

In my opinion, most people do not pay enough attention to estrogen levels because they are more concerned with testosterone. Even moer concerning is the people who don't pay much attention to estrogen while running a nandrolone or trenbolone because of the "prolactin" or porgesterone receptor related sides. Well, I'm here to hopefully clarify these things for some of you. This shoudln't take too long to read and it could save you some real trouble and hassle in the future. I tried to divide it up into basic sections if you are looking for something specific but don't want to read it all *(please at least read the portion toward the end about Progesterone interaction).*

Estrogen is commonly referred to as "E2" in many threads you will see and is actually a reading of one's "estradiol" levels. Estrogens are made up of Estr*one* (E1), Estra*di*ol (E2), and Es*tri*ol (E3) (though the one we're concerned with is E2 specifically). It is ok to simply refer to these as estrogen, but it's more important that you know how to control your own through a basic understanding of the topic. 

*Complexity and Sexual Makeup*
The mechanisms through which E2 interacts with sexual reproductive organs and other hormones in the male body is actually much more complex than in a woman's body. This is mainly because we have so little E2 compared to our counterparts. The same can be said of testosterone in women; a slight change in levels can trigger huge changes. A lot of people know the term "aromatase" or "aromatization" when it comes to testosterone vs estrogen levels. But, many don't know that the leydig cells in your testicles are responsible for the aromatase process which creates E2. Natural E2 in this instance is responsible for the prevention of sperm cell apoptosis (basically the death of that sperm cell through mutation). So, E2 plays an important role in maintaining healthy sexual function in your life.

*What is Normal?*  
The average human male E2 level will sit somewhere inbetween 15 - 60 pg/mL. The middle of this range is obviously ideal for several reasons, but both end of the spectrum need to be examined to better understand the effects it can have on your body. First of all, let's point out that these "normal" male levels are about the same as a post-menopausal female. So, it makes sense that the higher your levels go past that top number, the more female characteristics start to take shape (much like some post-menopausal women may lose some female characteristics and may even develop some testosterone related attributes such as hair on their face).  But what about the low end? Is that a graveyard for both sexes?

*What is Low and What are the Symptoms?*
Low can be described as anything lower than that 15 pg/mL benchmark. However, it is possible for your levels to drop dangerously close to ZERO. It's funny when we as a society think so much about testosterone as the driving force of sexual thought and action in males, but actually E2 levels are just as important in maintaining that sexual desire. And to go even further, it's a desire for life and the feelings and emotions that will propel you through life. With low E2 levels, much of this is lost and most individuals feel like "hope is lost" and experience a very downtrodden feeling. I have been there myself (confirmed labs of less than 10 pg/mL) and I can tell you it's no fun at all.

*How to Avoid Dropping Into the Danger Zone*
For awhile now in bodybuilding community we have been using SERMs and AIs to control our "estrogen" levels for fear of "bitch tits" or gynecomastia. Well, that is one of the side effects if you let the aromatase process get out of control. On the other end of the spectrum is the loss of sex drive and the previously discussed downtrodden feeling. The main way you find yourself on the low end of the spectrum is by overdoing it in the prevention department. Many men who have had any gyno symtoms at all are so afraid of getting it again that they will consistently use far too high of an AI or SERM dose far too often in an effort to keep it at bay. Knowing the function of these items you are using to combat additional aromatase production is crucial in controlling and stabilizing levels. Since I have found a nice routine, I am able to keep my levels between 20-25 pg/mL with little problem. 

Aromatase Inhibitors (AIs) - Dosage and Effective Action
The most common aromatase inhibitor you will hear of people using is Arimidex, which is actually just the name brand for the drug anastrozole.  The other two you commonly hear about are Aromasin (exemestane) and Femara (letrozole).

*Arimidex (anastrozole) * - Has a half life of about 3 days and a common dosage of 1mg per day or 1mg every other day. A more advisable dose is 1mg E3D or 0.5mg EOD. Being that arimidex has a longer half life, it's harder to see what dose will be right for you unless you guess right from the outset. Anastrozole works through competitive inhibition. Basically, this means it blocks androgens from finding the necessary enzymes to bond with and go through the aromatase process (see chart below for basic explanation).







*Femara (letrozole)* - Has a half life of about 2 days and a common dosage  of 2.5mg per day or EOD. A more adviasble dose would be 1.25mg  EOD if you are looking to use Letrozole throughout cycle. However, because Letro acts through BOTH competitive inhibition AND reversible binding, it's much better to just keep this one on hand for flare ups. What's reversible binding you may say? Well take a look back at that chart and imagine the "round-headed" peg has already found it's enzyme. While anastrozole will seek out open slots, letrozole rips out cells from their occupied slots and stops the conversion process. This sounds like the answer right? Well, it's still harder to control this mechanism of action because of the conversion rate of double action going on. Like I said, it is best to start use when you have a gyno flare up and then discontinue use a day or two after the symptoms subside (and go back to using either arimidex or aromasin). 

*Aromasin (exemestane)* - has a half life of about 23-27 hours or roughly one day, and a common dosage is 25mg EOD. A more suitable dosage would be 6.25 mg ED or 12.5mg EOD. Aromasin is a definitive *Suicide Inhibitor*, meaning it permanently and irreversibly binds to enzymes looking to convert androgens to aromatase. This sounds great on paper, like you would only need a few doses.... but the reality is that oru bodies are constantly upregulating the supply of available enzymes as others die. So, continued use througout cycle is needed. This is the one drug IMO that if you can find the sweet spot, you are in the money! 12.5mg EOD will be enough for most to keep a steady level going, or you can use 6.25 mg ED to keep levels steady because of the shorter half life (although either method will produce very similar levels in most). Aromasin also binds to SHBG, lowering the available amount to bind with free test, thus increasing free test levels (It's a much more complicated process than that and I'm sure I'll write in more detail about it soon). 

*Adex vs Asin*
The fundamental difference you need to understand about Arimidex and Aromasin (other than half-life) is the actual chemical structure itself. Aromasin is very similar in structure to Androstenedione (I'm sure you all know what that is) and actually fools the enzymes into thinking it is match and they are supposed to attach. By the time the aromasin latches on, it's too late for that enzyme....there is no going back. Arimidex can also occcupy that slot, but at some point will be kicked out because of competition and a low cellular structure match (almost like a human body sometimes rejects donor organs). In vitro studies suggest a 90+% protein binding rate for Aromasin, while it makes sense based on the previous comment that Arimidex only has a protein binding rate of about 40%. In addition, the reason that a much smaller dose of arimidex is needed is because the bioavailability is very high at 85-90%, while the bioavailability of Aromasin is near 60%. So, Arimidex is more efficient in doing it's job, but Aromasin appears to be more effective (especially on paper if you go by the numbers). 

*What about SERMs?*
SERMs or Selective Estrogen Receptor Modulators are basically estrogen receptor antagonists. The two most common that we talk about are *tamoxifen (Nolvadex) and clomifene (Clomid)*. Clomifene directs it actions only at the hypothalamus, not directly on breast tissue... so, this indirect approach is not nearly as effective as Tamoxifen. Tamoxifen does act directly on breast tissue but in a different way than the AIs we discussed earlier. While tamox also competitively binds to estrogen receptors/enzymes, it cannot remove or reverse any binding that has already occurred. In addition, it is incapapable of causing the "cell death" that AIs can create. This would make tamoxifen a poor choice for those who have experienced gynecomastia in the past or are currently experiencing symptoms. However, if a regimen of 10-20mg EOD is started JUST PRIOR to a cycle it can be effective in limiting the amount of conversion. The reason I use the words "just prior" is because the half life of Tamox is about 5-7 days; much longer than any AI. You want to start using the tamox a few days before your first injection in order to prep your receptors for the onslaught of androgens. 

*How about Progesterone?*
Progesterone and Estrogen are interrelated in the way that they are both byproducts of exogenous hormone adminstration. 19-nor compounds such as trenbolone and nandrolone will have a pronounced effect on progestenic activity and can stimulate prolactin overporduction in breast tissue. It is a very common mistake that people use "prolactin receptor" and "progesterone receptor" interchangeably. They are very different receptors found in different locations in the body. They can have pronounced effects on each other, but only through the key "bridge" that makes it happen.... estrogen. Look at the chart below to get a basic idea of how progesterone can convert to estradiol and other estrogens.






*So What's the Estrogen to Progesterone Connection Mean?*
As you can see in the chart, all roads lead to estrogen. However, the road also starts much the same. It is very hard for progesterone to do it's job without estrogen present. So, if you keep your estrogen levels under control, then there shouldn't be much of an issue. *This is the basic reason why the method of running testosterone higher than a nandrolone WILL NOT minimize any side effects*. Those who swear by this method are really just controlling their estrogen levels and giving credit to the higher dose of test. In reality, some people do not run an AI when they run lower levels of test, but they do run an AI or increase the dose with higher levels of test. This may account for the method working better even though the increase in testosterone is not directly attributable. 


*BOTTOM LINE SUMMARY*

1. Get regular blood tests done to check your levels and make sure you are doing a good job of stabilizing them

2. make sure you always have the necessary prevention items in place BEFORE you start your cycle

3. before you resort to using a prolcatin antagonist, make sure your estrogen levels are under control first (in fact, many people believe that letrozole is in fact an effective prolactin antagonist, however, it's just really effective at lowering high E2 levels quickly)

4. Experiment until you find what is right for you... don't just aim blindly, but dose based on what I've set forth in this article combined with what works well for others you know. Once you fidn the sweet spot, this is one less thing you need to worry about.

5. If you actually read this far, pat yourself on the back 


- Get Some


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## RowdyBrad

Unreal man. This is sticky material!


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## LeanHerm

Did you write that or copy n paste?  Bad ass read


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## HH

Very good shit


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## RowdyBrad

So do you advise just running even mg of test to deca, as long as you control the estrogen and nor-19 sides?


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## JOMO

Great write up Get Some! I like how you broke it down into sections and described the frontloading of SERMs prior to first inject for limiting conversion! Sticky Please!!


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## Pikiki

Good shit man...


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## Azog

Great post!

Btw, I didn't mean to dislike your post. My ham fingers slipped on my iPhone. I'm not sure how to get rid of the dislike, maybe a mod can help?


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## Get Some

To be clear on this subject and answer some questions....

I wrote this today as a culmination of knowledge I have picked up over the years (I write little mini-informational articles from tiem to time because I believe there aren't enough out there that combine science AND personal experience)

Running test and deca at the same dose is fine, but running test at a lower dose than your deca can be fine too. It's all about controlling the estrogen and in turn progesterone and prolactin. It can all be done with an AI if the timing is right, but you have to have letro and caber on hand just in case. B6 is a bit weak, but will work with regular doses in a preventative fashion.

I'll have more to follow soon, just wish I had more time to do these write ups


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## RowdyBrad

Awesome. I have the letro and caber ready. Also, I plan on taking the caber for an extra couple weeks to keep from rebounding with the nor-19, as Bullseye mentioned in his thread.

If you already have slight gyno, do you advise 2.5mg of letro until symptoms go away or longer?


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## Get Some

If you already have lumps from gyno the I would do at least 2.5mg for 3-4 days in a row and see if it dissipates. Normally for me, if it's estrogen induced then the lumps start to go away within 24 hours. With Tren and Deca, you may have to run it alongside Caber to get the job done.

And for the record... Prami works but I hate it! It made me physically ill each time I took it and it makes you fal asleep. I made the mistake of not knowing when to dose it the first time and fell asleep at my desk at work feeling like shit!



rowdybrad said:


> Awesome. I have the letro and caber ready. Also, I plan on taking the caber for an extra couple weeks to keep from rebounding with the nor-19, as Bullseye mentioned in his thread.
> 
> If you already have slight gyno, do you advise 2.5mg of letro until symptoms go away or longer?


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## PillarofBalance

Congrats on your first Sticky at SI Get Some... Excellent material.  Here is my question to you.

My current Cycle is:

Test PP 350mg EOD
Nandrolone PP 200 EOD
TNE on training days 100mg
Caber .5mg E3D

I have no gyno issues at all.  Oddly enough. On Test Cyp at 750mg alone I had itchy nips. On 20mg of dbol after a couple days I get itchy nips.  I hit the adex hard when that happens.

So while I have no gyno issues, no deca dick issues I would assume my E2 levels are in check. Should I consider adding aromasin or something at this point or ever? I will continue this cycle until Mid August or when I run out of gear 

What say you?

EDIT: Before you even say it... I'm pinning EOD with the PP esters to keep injection volume down. Yes I know I'm not reaching maximum blood plasma levels


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## DF

Very nice sticky info GS


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## grind4it

2x agreed. Great sticky right here.



rowdybrad said:


> Unreal man. This is sticky material!


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## beasto

Bad ass read thanks for the info...I enjoyed every minute. Big up's getsome!!!


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## grizzldsealpoacher

This was really help full thanks for taking the time


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## Jada

GEt some great sticky!!!!!


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## Bro Bundy

that was one excellent read get some, great sticky


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## Bevo

Informed all of us like a boss!!!!


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## cokezero

That was an awsome post. That answered questions that I didn't even have. Thanks gs. write more since your that knowledgable. this is how we learn.


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## gymrat827

nice work man


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## Lulu66

Thanx for the post. Very good info.


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## Get Some

POB.... sorry I didn't get to your question earlier bro

how long have you been running this current cycle? Also, I truly believe there is a link between the amount your test levels rise and fall in correlation with how much aromatization goes on. I don't have any scientific results to back this up at the moment, but I'm still researching as always  ... a number of guys I train say they have experienced the same thing. More frequent pins lower the risk of them developing gyno. However, like you stated, you don't ever reach those peak plasma levels you could achieve with strategic ester-related dosing. So, if you've been running this for awhile just keep some caber and letro on hand and you should be fine. Let me know how you progress.


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## AndroSport

Good Shit - Get Some!

Intricate yet easy to read with he break-outs per interest/topic.

Perfect item to keep as a sticky/reference point for anyone needing to check back to.

Thank you


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## Trust

Nice info- Thanks man!


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## Moppy1

Also high estrogen is linked to prostate cancer.  In fact, medical correlations are stronger with extended high estrogen than testosterone as an inducer of prostate cancer.  You have to keep your estrogen low!


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## pirovoliko

Awesome, awesome awesome thread on a much overlooked subject. Cleared up alot fo rme personally.  Thanks .


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## 63Vette

This is an excellent read my good man. 

Kudos and much respect,

Vette


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## NbleSavage

Wow, just today reviewing this. VERY well stated!! Thanks for the add!


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## IWannaGetBig

Really great read. Question I'm still a little unsure on, I read what you said about Progesterone and see that number on my Blood Work results. Aside from the sides, lactating nips as an indicator, is there a number I can look for after running blood work?


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## brown1106

I know you posted this a while back but it has helped me understand. I didn't have an idea before reading this. Thx for the help..


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## Big

Good read. Thanks!


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## Patriot1405

Excellent, excellent post!!!!


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## BigTruck

Get some I appreciate what u do bro I've learned immensely from your threads!


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## LeanHerm

I freaking miss get some. I miss his posts and his teaching lessons.  Hope all is well with his big ass. 

Love,
Herm


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## Bro Bundy

bump for the new guys


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## Get Some

I forgot about this thread!

I wish I had the time to copy it over to TID as well but since I log in from mobile most days that won't work. Dammit, ill have to figure it out somehow.


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## FreeBirdSam

Tons of great info in here I tend to just read the "new posts" and sometimes forget these long lost stickied threads.   We need more of these get some!  We're all very fortunate to have a member around like you


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## tony.ammar.71

I have a question towards anavar


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## j2048b

tony.ammar.71 said:


> I have a question towards anavar



Start a thread with that as ur title, ir u may get banned real fast! 2nd thread uv highjacked with the same line...


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## bvs

Absolutely brilliant write up


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## Darkhorse1

If I could applaud without my wife committing me, I WOULD!!
This is hands down the single BEST THREAD I've ever read on the topic of estrogen and progesterone!!


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## IronAthiest

Awesome post, enlightening read!


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## Rip

Valuable info. Thanks.


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## jsam

Good info thanks for the read


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## FreeBirdSam

Getsome...  I am about to start a blast with the following:

1g test/wk, 
100mg NPP/eod, 
200 trenE/wk, 
100mg anadrol/day ****

I am gyno prone, and in the past have kept it at bay with exemestane, and when sympytoms arise taking nolvadex for a couple days and it reverses it..   But since this is my first run with Anadrol, should I start the Nolvadex prior to the blast and every day of it?  or just when symptoms arise??

Thanks buddy!


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## DocDePanda187123

Sam, I wouldn't wait to use the nolva until symptoms arose. I'd use it from the beginning.


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## Bro Bundy

sam drol  is the only compound that made my nips sting a bit...I would go from day 1 with nolva..shit mayb start a week earlier even..


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## TheLupinator

Start it right away... Raloxifene works too, it's what I'm on now. Current cycle is 600 test / 450 tren / 50mg (daily) drol - nips are fine


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## FreeBirdSam

Thanks fellas! Will do!


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## Ascastlat

Good read, very useful info...


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## Hockeyplaya18

Awesome post!! I have boner issues now and again, this should help!


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## Bro Bundy

bump!! start learning


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## Musclehngry

Great post, thanks so much...a definite keeper.


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## gh0st

Good post!


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## serratus

Awsome post. Science and experience together : it's a must. I'll use this info for my next cycle (started to-day)


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## ComeBacKid85

Totally awesome. Will be using this as a guide for sure.


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## chenmomo

Nice. it's very helpful


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## DeplorableCracker

awesome read, and thanks as this is the one area I'm really digging into and trying to figure out. Been on TRT for a while now, and am just getting into my first blast (Test Cyp only for now, bumping up to 750mg/week). Have some Deca on hand too, but I feel like the safe play is to sit on that for the next go around and stick to Test only. I have Aromasin on hand if needed. I've read that being as tall and lean as I am (9% or so), that estrogen conversion should generally be less of an issue? Do you guys recommend no Aromasin til bloods in a few months and/or noticeable sides? Or should I start with something like the 12.5 EOD from the rip?

also, the one thing i didn't gleam from the write up is...obviously the AI is to bring your E2 down, but what if it is crashed at some point? what do you do to bring it back up instead? chill and let your body take care of it over time or is there something else? again, sorry If I missed that in here somewhere.

Thanks guys!


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## Sicwun88

Great post!
A must read for all!!!!


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## Oldbastard

Get Some said:


> In my opinion, most people do not pay enough attention to estrogen levels because they are more concerned with testosterone. Even moer concerning is the people who don't pay much attention to estrogen while running a nandrolone or trenbolone because of the "prolactin" or porgesterone receptor related sides. Well, I'm here to hopefully clarify these things for some of you. This shoudln't take too long to read and it could save you some real trouble and hassle in the future. I tried to divide it up into basic sections if you are looking for something specific but don't want to read it all *(please at least read the portion toward the end about Progesterone interaction).*
> 
> Estrogen is commonly referred to as "E2" in many threads you will see and is actually a reading of one's "estradiol" levels. Estrogens are made up of Estr*one* (E1), Estra*di*ol (E2), and Es*tri*ol (E3) (though the one we're concerned with is E2 specifically). It is ok to simply refer to these as estrogen, but it's more important that you know how to control your own through a basic understanding of the topic.
> 
> *Complexity and Sexual Makeup*
> The mechanisms through which E2 interacts with sexual reproductive organs and other hormones in the male body is actually much more complex than in a woman's body. This is mainly because we have so little E2 compared to our counterparts. The same can be said of testosterone in women; a slight change in levels can trigger huge changes. A lot of people know the term "aromatase" or "aromatization" when it comes to testosterone vs estrogen levels. But, many don't know that the leydig cells in your testicles are responsible for the aromatase process which creates E2. Natural E2 in this instance is responsible for the prevention of sperm cell apoptosis (basically the death of that sperm cell through mutation). So, E2 plays an important role in maintaining healthy sexual function in your life.
> 
> *What is Normal?*
> The average human male E2 level will sit somewhere inbetween 15 - 60 pg/mL. The middle of this range is obviously ideal for several reasons, but both end of the spectrum need to be examined to better understand the effects it can have on your body. First of all, let's point out that these "normal" male levels are about the same as a post-menopausal female. So, it makes sense that the higher your levels go past that top number, the more female characteristics start to take shape (much like some post-menopausal women may lose some female characteristics and may even develop some testosterone related attributes such as hair on their face).  But what about the low end? Is that a graveyard for both sexes?
> 
> *What is Low and What are the Symptoms?*
> Low can be described as anything lower than that 15 pg/mL benchmark. However, it is possible for your levels to drop dangerously close to ZERO. It's funny when we as a society think so much about testosterone as the driving force of sexual thought and action in males, but actually E2 levels are just as important in maintaining that sexual desire. And to go even further, it's a desire for life and the feelings and emotions that will propel you through life. With low E2 levels, much of this is lost and most individuals feel like "hope is lost" and experience a very downtrodden feeling. I have been there myself (confirmed labs of less than 10 pg/mL) and I can tell you it's no fun at all.
> 
> *How to Avoid Dropping Into the Danger Zone*
> For awhile now in bodybuilding community we have been using SERMs and AIs to control our "estrogen" levels for fear of "bitch tits" or gynecomastia. Well, that is one of the side effects if you let the aromatase process get out of control. On the other end of the spectrum is the loss of sex drive and the previously discussed downtrodden feeling. The main way you find yourself on the low end of the spectrum is by overdoing it in the prevention department. Many men who have had any gyno symtoms at all are so afraid of getting it again that they will consistently use far too high of an AI or SERM dose far too often in an effort to keep it at bay. Knowing the function of these items you are using to combat additional aromatase production is crucial in controlling and stabilizing levels. Since I have found a nice routine, I am able to keep my levels between 20-25 pg/mL with little problem.
> 
> Aromatase Inhibitors (AIs) - Dosage and Effective Action
> The most common aromatase inhibitor you will hear of people using is Arimidex, which is actually just the name brand for the drug anastrozole.  The other two you commonly hear about are Aromasin (exemestane) and Femara (letrozole).
> 
> *Arimidex (anastrozole) * - Has a half life of about 3 days and a common dosage of 1mg per day or 1mg every other day. A more advisable dose is 1mg E3D or 0.5mg EOD. Being that arimidex has a longer half life, it's harder to see what dose will be right for you unless you guess right from the outset. Anastrozole works through competitive inhibition. Basically, this means it blocks androgens from finding the necessary enzymes to bond with and go through the aromatase process (see chart below for basic explanation).
> 
> 
> 
> 
> 
> 
> 
> *Femara (letrozole)* - Has a half life of about 2 days and a common dosage  of 2.5mg per day or EOD. A more adviasble dose would be 1.25mg  EOD if you are looking to use Letrozole throughout cycle. However, because Letro acts through BOTH competitive inhibition AND reversible binding, it's much better to just keep this one on hand for flare ups. What's reversible binding you may say? Well take a look back at that chart and imagine the "round-headed" peg has already found it's enzyme. While anastrozole will seek out open slots, letrozole rips out cells from their occupied slots and stops the conversion process. This sounds like the answer right? Well, it's still harder to control this mechanism of action because of the conversion rate of double action going on. Like I said, it is best to start use when you have a gyno flare up and then discontinue use a day or two after the symptoms subside (and go back to using either arimidex or aromasin).
> 
> *Aromasin (exemestane)* - has a half life of about 23-27 hours or roughly one day, and a common dosage is 25mg EOD. A more suitable dosage would be 6.25 mg ED or 12.5mg EOD. Aromasin is a definitive *Suicide Inhibitor*, meaning it permanently and irreversibly binds to enzymes looking to convert androgens to aromatase. This sounds great on paper, like you would only need a few doses.... but the reality is that oru bodies are constantly upregulating the supply of available enzymes as others die. So, continued use througout cycle is needed. This is the one drug IMO that if you can find the sweet spot, you are in the money! 12.5mg EOD will be enough for most to keep a steady level going, or you can use 6.25 mg ED to keep levels steady because of the shorter half life (although either method will produce very similar levels in most). Aromasin also binds to SHBG, lowering the available amount to bind with free test, thus increasing free test levels (It's a much more complicated process than that and I'm sure I'll write in more detail about it soon).
> 
> *Adex vs Asin*
> The fundamental difference you need to understand about Arimidex and Aromasin (other than half-life) is the actual chemical structure itself. Aromasin is very similar in structure to Androstenedione (I'm sure you all know what that is) and actually fools the enzymes into thinking it is match and they are supposed to attach. By the time the aromasin latches on, it's too late for that enzyme....there is no going back. Arimidex can also occcupy that slot, but at some point will be kicked out because of competition and a low cellular structure match (almost like a human body sometimes rejects donor organs). In vitro studies suggest a 90+% protein binding rate for Aromasin, while it makes sense based on the previous comment that Arimidex only has a protein binding rate of about 40%. In addition, the reason that a much smaller dose of arimidex is needed is because the bioavailability is very high at 85-90%, while the bioavailability of Aromasin is near 60%. So, Arimidex is more efficient in doing it's job, but Aromasin appears to be more effective (especially on paper if you go by the numbers).
> 
> *What about SERMs?*
> SERMs or Selective Estrogen Receptor Modulators are basically estrogen receptor antagonists. The two most common that we talk about are *tamoxifen (Nolvadex) and clomifene (Clomid)*. Clomifene directs it actions only at the hypothalamus, not directly on breast tissue... so, this indirect approach is not nearly as effective as Tamoxifen. Tamoxifen does act directly on breast tissue but in a different way than the AIs we discussed earlier. While tamox also competitively binds to estrogen receptors/enzymes, it cannot remove or reverse any binding that has already occurred. In addition, it is incapapable of causing the "cell death" that AIs can create. This would make tamoxifen a poor choice for those who have experienced gynecomastia in the past or are currently experiencing symptoms. However, if a regimen of 10-20mg EOD is started JUST PRIOR to a cycle it can be effective in limiting the amount of conversion. The reason I use the words "just prior" is because the half life of Tamox is about 5-7 days; much longer than any AI. You want to start using the tamox a few days before your first injection in order to prep your receptors for the onslaught of androgens.
> 
> *How about Progesterone?*
> Progesterone and Estrogen are interrelated in the way that they are both byproducts of exogenous hormone adminstration. 19-nor compounds such as trenbolone and nandrolone will have a pronounced effect on progestenic activity and can stimulate prolactin overporduction in breast tissue. It is a very common mistake that people use "prolactin receptor" and "progesterone receptor" interchangeably. They are very different receptors found in different locations in the body. They can have pronounced effects on each other, but only through the key "bridge" that makes it happen.... estrogen. Look at the chart below to get a basic idea of how progesterone can convert to estradiol and other estrogens.
> 
> 
> 
> 
> 
> 
> *So What's the Estrogen to Progesterone Connection Mean?*
> As you can see in the chart, all roads lead to estrogen. However, the road also starts much the same. It is very hard for progesterone to do it's job without estrogen present. So, if you keep your estrogen levels under control, then there shouldn't be much of an issue. *This is the basic reason why the method of running testosterone higher than a nandrolone WILL NOT minimize any side effects*. Those who swear by this method are really just controlling their estrogen levels and giving credit to the higher dose of test. In reality, some people do not run an AI when they run lower levels of test, but they do run an AI or increase the dose with higher levels of test. This may account for the method working better even though the increase in testosterone is not directly attributable.
> 
> 
> *BOTTOM LINE SUMMARY*
> 
> 1. Get regular blood tests done to check your levels and make sure you are doing a good job of stabilizing them
> 
> 2. make sure you always have the necessary prevention items in place BEFORE you start your cycle
> 
> 3. before you resort to using a prolcatin antagonist, make sure your estrogen levels are under control first (in fact, many people believe that letrozole is in fact an effective prolactin antagonist, however, it's just really effective at lowering high E2 levels quickly)
> 
> 4. Experiment until you find what is right for you... don't just aim blindly, but dose based on what I've set forth in this article combined with what works well for others you know. Once you fidn the sweet spot, this is one less thing you need to worry about.
> 
> 5. If you actually read this far, pat yourself on the back
> 
> 
> - Get Some





fantastic post thanks for sharing this!!


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## pgc640

Oldbastard said:


> fantastic post thanks for sharing this!!


the only thing I can say about estrogen levels is I know for a fact that high testosterone plus high estrogen equals way more muscle growth than high testosterone and crushing your estrogen with an AI. you're going to do a whole lot better in your cycle if you use novel decks as a gyno blocker and leave the AI out completely. the only time I would ever use an AI is say two maybe three weeks out from a contest to crush my estrogen to nothing so I could look as hard as I possibly can other than that I think AI is a pretty much useless for bodybuilding. and all you really have to do to know that's true is go look at pictures from the 1996 Olympia I didn't come out to 99 I believe so there was no AI to use look how ripped Ronnie Coleman wasn't in 1996 Olympia to everybody was an AI is not necessary

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## pgc640

Get Some said:


> In my opinion, most people do not pay enough attention to estrogen levels because they are more concerned with testosterone. Even moer concerning is the people who don't pay much attention to estrogen while running a nandrolone or trenbolone because of the "prolactin" or porgesterone receptor related sides. Well, I'm here to hopefully clarify these things for some of you. This shoudln't take too long to read and it could save you some real trouble and hassle in the future. I tried to divide it up into basic sections if you are looking for something specific but don't want to read it all *(please at least read the portion toward the end about Progesterone interaction).*
> 
> Estrogen is commonly referred to as "E2" in many threads you will see and is actually a reading of one's "estradiol" levels. Estrogens are made up of Estr*one* (E1), Estra*di*ol (E2), and Es*tri*ol (E3) (though the one we're concerned with is E2 specifically). It is ok to simply refer to these as estrogen, but it's more important that you know how to control your own through a basic understanding of the topic.
> 
> *Complexity and Sexual Makeup*
> The mechanisms through which E2 interacts with sexual reproductive organs and other hormones in the male body is actually much more complex than in a woman's body. This is mainly because we have so little E2 compared to our counterparts. The same can be said of testosterone in women; a slight change in levels can trigger huge changes. A lot of people know the term "aromatase" or "aromatization" when it comes to testosterone vs estrogen levels. But, many don't know that the leydig cells in your testicles are responsible for the aromatase process which creates E2. Natural E2 in this instance is responsible for the prevention of sperm cell apoptosis (basically the death of that sperm cell through mutation). So, E2 plays an important role in maintaining healthy sexual function in your life.
> 
> *What is Normal?*
> The average human male E2 level will sit somewhere inbetween 15 - 60 pg/mL. The middle of this range is obviously ideal for several reasons, but both end of the spectrum need to be examined to better understand the effects it can have on your body. First of all, let's point out that these "normal" male levels are about the same as a post-menopausal female. So, it makes sense that the higher your levels go past that top number, the more female characteristics start to take shape (much like some post-menopausal women may lose some female characteristics and may even develop some testosterone related attributes such as hair on their face). But what about the low end? Is that a graveyard for both sexes?
> 
> *What is Low and What are the Symptoms?*
> Low can be described as anything lower than that 15 pg/mL benchmark. However, it is possible for your levels to drop dangerously close to ZERO. It's funny when we as a society think so much about testosterone as the driving force of sexual thought and action in males, but actually E2 levels are just as important in maintaining that sexual desire. And to go even further, it's a desire for life and the feelings and emotions that will propel you through life. With low E2 levels, much of this is lost and most individuals feel like "hope is lost" and experience a very downtrodden feeling. I have been there myself (confirmed labs of less than 10 pg/mL) and I can tell you it's no fun at all.
> 
> *How to Avoid Dropping Into the Danger Zone*
> For awhile now in bodybuilding community we have been using SERMs and AIs to control our "estrogen" levels for fear of "bitch tits" or gynecomastia. Well, that is one of the side effects if you let the aromatase process get out of control. On the other end of the spectrum is the loss of sex drive and the previously discussed downtrodden feeling. The main way you find yourself on the low end of the spectrum is by overdoing it in the prevention department. Many men who have had any gyno symtoms at all are so afraid of getting it again that they will consistently use far too high of an AI or SERM dose far too often in an effort to keep it at bay. Knowing the function of these items you are using to combat additional aromatase production is crucial in controlling and stabilizing levels. Since I have found a nice routine, I am able to keep my levels between 20-25 pg/mL with little problem.
> 
> Aromatase Inhibitors (AIs) - Dosage and Effective Action
> The most common aromatase inhibitor you will hear of people using is Arimidex, which is actually just the name brand for the drug anastrozole. The other two you commonly hear about are Aromasin (exemestane) and Femara (letrozole).
> 
> *Arimidex (anastrozole) * - Has a half life of about 3 days and a common dosage of 1mg per day or 1mg every other day. A more advisable dose is 1mg E3D or 0.5mg EOD. Being that arimidex has a longer half life, it's harder to see what dose will be right for you unless you guess right from the outset. Anastrozole works through competitive inhibition. Basically, this means it blocks androgens from finding the necessary enzymes to bond with and go through the aromatase process (see chart below for basic explanation).
> 
> 
> 
> 
> 
> 
> *Femara (letrozole)* - Has a half life of about 2 days and a common dosage of 2.5mg per day or EOD. A more adviasble dose would be 1.25mg EOD if you are looking to use Letrozole throughout cycle. However, because Letro acts through BOTH competitive inhibition AND reversible binding, it's much better to just keep this one on hand for flare ups. What's reversible binding you may say? Well take a look back at that chart and imagine the "round-headed" peg has already found it's enzyme. While anastrozole will seek out open slots, letrozole rips out cells from their occupied slots and stops the conversion process. This sounds like the answer right? Well, it's still harder to control this mechanism of action because of the conversion rate of double action going on. Like I said, it is best to start use when you have a gyno flare up and then discontinue use a day or two after the symptoms subside (and go back to using either arimidex or aromasin).
> 
> *Aromasin (exemestane)* - has a half life of about 23-27 hours or roughly one day, and a common dosage is 25mg EOD. A more suitable dosage would be 6.25 mg ED or 12.5mg EOD. Aromasin is a definitive *Suicide Inhibitor*, meaning it permanently and irreversibly binds to enzymes looking to convert androgens to aromatase. This sounds great on paper, like you would only need a few doses.... but the reality is that oru bodies are constantly upregulating the supply of available enzymes as others die. So, continued use througout cycle is needed. This is the one drug IMO that if you can find the sweet spot, you are in the money! 12.5mg EOD will be enough for most to keep a steady level going, or you can use 6.25 mg ED to keep levels steady because of the shorter half life (although either method will produce very similar levels in most). Aromasin also binds to SHBG, lowering the available amount to bind with free test, thus increasing free test levels (It's a much more complicated process than that and I'm sure I'll write in more detail about it soon).
> 
> *Adex vs Asin*
> The fundamental difference you need to understand about Arimidex and Aromasin (other than half-life) is the actual chemical structure itself. Aromasin is very similar in structure to Androstenedione (I'm sure you all know what that is) and actually fools the enzymes into thinking it is match and they are supposed to attach. By the time the aromasin latches on, it's too late for that enzyme....there is no going back. Arimidex can also occcupy that slot, but at some point will be kicked out because of competition and a low cellular structure match (almost like a human body sometimes rejects donor organs). In vitro studies suggest a 90+% protein binding rate for Aromasin, while it makes sense based on the previous comment that Arimidex only has a protein binding rate of about 40%. In addition, the reason that a much smaller dose of arimidex is needed is because the bioavailability is very high at 85-90%, while the bioavailability of Aromasin is near 60%. So, Arimidex is more efficient in doing it's job, but Aromasin appears to be more effective (especially on paper if you go by the numbers).
> 
> *What about SERMs?*
> SERMs or Selective Estrogen Receptor Modulators are basically estrogen receptor antagonists. The two most common that we talk about are *tamoxifen (Nolvadex) and clomifene (Clomid)*. Clomifene directs it actions only at the hypothalamus, not directly on breast tissue... so, this indirect approach is not nearly as effective as Tamoxifen. Tamoxifen does act directly on breast tissue but in a different way than the AIs we discussed earlier. While tamox also competitively binds to estrogen receptors/enzymes, it cannot remove or reverse any binding that has already occurred. In addition, it is incapapable of causing the "cell death" that AIs can create. This would make tamoxifen a poor choice for those who have experienced gynecomastia in the past or are currently experiencing symptoms. However, if a regimen of 10-20mg EOD is started JUST PRIOR to a cycle it can be effective in limiting the amount of conversion. The reason I use the words "just prior" is because the half life of Tamox is about 5-7 days; much longer than any AI. You want to start using the tamox a few days before your first injection in order to prep your receptors for the onslaught of androgens.
> 
> *How about Progesterone?*
> Progesterone and Estrogen are interrelated in the way that they are both byproducts of exogenous hormone adminstration. 19-nor compounds such as trenbolone and nandrolone will have a pronounced effect on progestenic activity and can stimulate prolactin overporduction in breast tissue. It is a very common mistake that people use "prolactin receptor" and "progesterone receptor" interchangeably. They are very different receptors found in different locations in the body. They can have pronounced effects on each other, but only through the key "bridge" that makes it happen.... estrogen. Look at the chart below to get a basic idea of how progesterone can convert to estradiol and other estrogens.
> 
> 
> 
> 
> 
> 
> *So What's the Estrogen to Progesterone Connection Mean?*
> As you can see in the chart, all roads lead to estrogen. However, the road also starts much the same. It is very hard for progesterone to do it's job without estrogen present. So, if you keep your estrogen levels under control, then there shouldn't be much of an issue. *This is the basic reason why the method of running testosterone higher than a nandrolone WILL NOT minimize any side effects*. Those who swear by this method are really just controlling their estrogen levels and giving credit to the higher dose of test. In reality, some people do not run an AI when they run lower levels of test, but they do run an AI or increase the dose with higher levels of test. This may account for the method working better even though the increase in testosterone is not directly attributable.
> 
> 
> *BOTTOM LINE SUMMARY*
> 
> 1. Get regular blood tests done to check your levels and make sure you are doing a good job of stabilizing them
> 
> 2. make sure you always have the necessary prevention items in place BEFORE you start your cycle
> 
> 3. before you resort to using a prolcatin antagonist, make sure your estrogen levels are under control first (in fact, many people believe that letrozole is in fact an effective prolactin antagonist, however, it's just really effective at lowering high E2 levels quickly)
> 
> 4. Experiment until you find what is right for you... don't just aim blindly, but dose based on what I've set forth in this article combined with what works well for others you know. Once you fidn the sweet spot, this is one less thing you need to worry about.
> 
> 5. If you actually read this far, pat yourself on the back
> 
> 
> - Get Some


I did read the whole post. I agree with some of it and I don't agree with some of it. first of all I'll give you my ideas on this whole subject. my ideas are leave the AIS alone entirely and use novel decks to prevent gyno it's what bodybuilders did for years and years and years before 1999 when a remodex came out in the pharmaceutical companies before that all we had was navodext and proviron.
it is correct however that tamoxifen will not get rid of gyno if you already have gyno you could take a ton of it and gyno is not going to go away.
to get rid of pre-existing gyno electro will do it in less than a week. just the fourth of a tablet probably for four or five days and it'll be gone then once it's gone just go back to the novel decks and don't let yourself get it again. the dose of navodex I'm fine with 10 mg a day some want 20 some say 10 every other day I have done 10 every other day and that works also. I'm very gyno prone if I don't use tamoxifen I will get gyno quickly.

AIs do have their uses but to use them as a gyno prevention estrogen level prevention drug everyday during cycle I don't think it's practical. those drugs are so strong especially letro I wouldn't even touch electro as a everyday drug I would use but they're so strong that they can mess with your estrogen so badly what you really would need is three blood tests a week which isn't really practical. also the problems caused by very low estrogen that could happen very easily from these AIS is not good I mean sexual dysfunction and depression and all kinds of other things why go through that when you can make sure you won't have to go through that by just using another substance.

the way navidex works is it basically there's at the breast I guess you would say there's a lock and key sort of thing and the novel decks will fit in the lock so it blocks the estrogen from getting into that lock and causing gyno so it's a blocker it does nothing to eliminate estrogen and it doesn't lower estrogen so you won't get gyno but your estrogen levels can still raise. there's debate whether estrogen raising is a good thing or bad thing personally I think it's a good thing I know for a fact that high estrogen and high testosterone lead to more gains than high testosterone and low estrogen or normal estrogen and I know that for a few reasons. but forget using an AI and getting your estrogen even lower than normal you're going to impede your gains tremendously.

the first AI came out in about 1999 so before that all bodybuilders had was tamoxifen and everybody lived and everybody did okay and nobody had any bad effects from high estrogen. other than guy I know which they controlled with tamoxifen. I haven't bodybuilding for 31 years and I've used nothing but tamoxifen and I've never had any issues from high estrogen any noticeable side effects from high estrogen. I've also never had low acrogen because I do not screw around with ai's.

the only time I would recommend someone using AI is if they're competing for the last three two weeks about 3 or 2 weeks out from a contest to add it in to cross your estrogen as low as possible because that will allow you to come into the contest looking as hard as you possibly can. yes you'll also get the symptoms the sky was describing of low estrogen but it's only going to be for a couple of days cuz as soon as the contest is over you're going to discontinue what you're doing. but that's the only time I feel it's beneficial and to get rid of gyno so two things it does that's beneficial but using it as an everyday drug to prevent gyno and prevent high estrogen it doesn't make sense. also the argument that AIS make you hold less water is ridiculous too. the water gained by higher estrogen is so negligible that it's barely even noticeable. what water from high estrogen is is bodybuilders blaming why they're fat and bloated on their estrogen being high when all it is is them being a pig eating junk food not being able to stop eating and turning into a fat bloated water log pig. it has nothing to do with estrogen it has to do with their own self control. I myself have a fast metabolism and I've been doing this so long I don't even think about buying junk food so I never cheat never to eat bad food my body fat never exceeds 7%, and I take drugs that most people think make you gain water by just taking them which is such a fallacy and I'll be shredded ripped on these drugs take them 4 weeks out from a contest and be ripped yes my estrogen is higher but like I said the water retention caused by estrogen is negligible it's your diet that determines how much water you're going to hold if you use a certain drug. it is true if you use Anadrol and after every workout you eat two Whoppers and fries and you eat like shit the rest of the day you're going to gain about 30 lb in 8 weeks you're going to look like shit a big round head look like you're going to burst then you're going to stop the onadral you're going to lose about 25 of those 30 pounds in about a week and a half and you're actually going to look 10 times better because you had you would have looked so bad with all that water weight on you. and that water weight has nothing to do with estrogen conversion.
it's just like the off season I hate that word offseason bodybuilders use that word to allow them to become fat bloated pigs cuz it's the offseason and I got to get big and strong and look like shit to do it so I could diet for 3 months so I'll only look good two months out of the year does that make any sense to anybody? why would you bust your ass in the gym take anabolics follow a certain diet make your life revolve around the sport just to look good two months out of every year and look like a fat waterlog pig the rest of the year? I can't answer that question cuz I don't do it myself but I know plenty of people that do. and again they'll blame estrogen for causing the water retention and it's nothing to do with that.
not disputing what this guy wrote it was very informative and it was a nice post I'm just saying he didn't cover everything and he didn't really put it in a way that touched on bodybuilding in particular because the way things are scientifically isn't always in a book isn't always the way it's going to play out in the bodybuilding world. and in my opinion just use novel decks to prevent gyno don't ever touch an AI to prevent gyno or to lower your estrogen unless you're competing you could do whatever you want but I'm telling you all it's going to cause this problems

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## BigBaldBeardGuy

God has entered the forum. 🙄


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## pgc640

BigBaldBeardGuy said:


> God has entered the forum.


I'm wondering what kind of comment that is was that directed at myself? because I do not claim to be God of any kind but everything I did right or talking to the phone I had a cornea transplant so I can't type I can't see very well so I talking to the phone but I did not give you any bad information at all hey guys are not a good thing to be using except for one's instance before a bodybuilding contest. if you're being a smart-ass and calling me God give me a fucking break go look at yourself in the mirror and see what you look like from what you're doing then look at me at 50 see what I look like and shut the fuck up.

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## pgc640

BigBaldBeardGuy said:


> God has entered the forum.


and actually instead of making a smart comment give me your take on AIS and drug like tamoxifen tell me what's better to use please I'd love to know what you think?

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