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Positive effects of excess Estrogen

ledom

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Estrogen, a good thing
by William Llewellyn

Can estrogen work to augment muscle growth? Is this hormone always unwanted when we are taking anabolic steroids? Anecdotal reports from athletes suggest that the use of estrogen maintenance drugs such as tamoxifen (anti-estrogen) or aminoglutethimide (anti-aromatase) may slightly hinder muscle mass gains during steroid therapy. An explanation or even clarification for this observation has not been easy to come by. Here I would like to take a look at the comparative effectiveness of certain aromatizable and non-aromatizable drugs, as well as the possible mechanism in which estrogen can play a beneficial role to the athlete.

The Androgen Receptor
All anabolic/androgenic steroids promote muscle growth primarily via the cellular androgen receptor (abbreviated as AR in this article). The steroid attaches to and activates the androgen receptor, which ultimately gives the cell an order to increase protein synthesis. This process is well understood. But it has been suggested that other mechanisms may foster muscle growth during steroid therapy as well, which lie outside of the androgen receptor. One way this is evidenced is by the fact that steroids displaying a high affinity for the AR in muscle tissue do not always promote an equally high level of muscle growth. In other words, anabolic potency does not always correspond perfectly to receptor affinity. Clearly there are some disparities that lead into question whether or not the androgen receptor is the only thing at work concerning growth.

Testosterone, Nandrolone and Methenolone
Testosterone is without question one of the most effective steroids for building muscle mass available to athletes. However it does not have the highest affinity for the androgen receptor compared to some other steroids. For example, it has been shown that by eliminating the 19-methyl group (nandrolone) the affinity of the steroid for the androgen receptor is greatly enhanced. Nandrolone thus displays approximately 2-3 times greater affinity for the androgen receptor compared to testosterone, yet its ability to promote muscle growth seems to be considerably lower than testosterone at an equal dosage. One discussed possibility for this occurrence is the reduced androgenic potency of nandrolone. While testosterone converts to the more active steroid dihydrotestosterone (3-4 times greater AR affinity) upon interaction with the 5-alpha reductase enzyme in various androgenic target tissues such as the skin, scalp, prostate, CNS and liver, nandrolone drops to a third of its original potency by converting to the weak steroid dihydronandrolone[ii]. However this action is very site specific, and in muscle tissue nandrolone dominates as the active form of the steroid. Therefore this explanation may not suffice.

Nandrolone also differs from testosterone in its ability to be converted by the aromatase enzyme to estradiol (an active estrogen). In comparison, nandrolone aromatizes at approximately 20% of the rate testosterone does, and as such is not known as a very estrogenic steroid. It is likewise favored when reduced estrogenic side effects such as water retention, fat deposition and gynecomastia are desired. However athletes know that there is a trade off with the reduced tendency for nandrolone to promote side effects, in that it is a less anabolic steroid. With its known high affinity for the AR in muscle tissue, could this suggest that estrogen may also be a key mediator of muscle growth?

When we look at Primobolan® (methenolone) we see a similar trend. Methenolone is at least as good a binder of the androgen receptor as testosterone. By some accounts it is on par with nandrolone[iii]. However it is known to be much weaker than both steroids at promoting muscle growth. We know that methenolone does not interact with 5-alpha reductase, and as such its affinity for the AR does not increase or decrease in androgen target tissues. This would logically seem like a more favorable trait for anabolism over the weakening we see with nandrolone. However methenolone is a markedly weaker anabolic, and requires relatively high doses to promote growth. This also brings into question the role of 5-alpha reductase in promoting an anabolic state. Perhaps the fact that Primobolan® is a non-aromatizable steroid is more relevant.

Estrogen and GH/IGF-1
To date the most common explanation for why anti-estrogens may be slightly counterproductive to growth in the sports literature has been the suggestion that estrogen plays a role in the production of growth hormone and IGF-1. IGF-1 (insulin like growth factor 1, formerly known as somatomedin C) is of course an anabolic product released primarily in the liver via GH stimulus. IGF-1 is responsible for the growth promoting effects (increased nitrogen retention, cell proliferation) we associate with growth hormone therapy. We do know that women have higher levels of growth hormone than men, and also that GH secretion varies over the course of the menstrual cycle in direct correlation with estrogen levels[iv]. Estrogen is likewise often looked at as a key trigger in the release of GH in women under normal physiological situations.

It is also suggested that the aromatization of androgens to estrogens in men plays an important role in the release and production of GH and IGF-1. This was evidenced by a 1993 study of hypogonadal men, comparing the effects of testosterone replacement therapy on GH and IGF-1 levels with and without the addition of tamoxifen[v]. When the anti-estrogen tamoxifen was given, GH and IGF-1 levels were notably suppressed, while both values were elevated with the administration of testosterone enanthate alone. Another study has shown 300mg of testosterone enanthate weekly (which elevated estradiol levels) to cause a slight IGF-1 increase in normal men, whereas 300mg weekly of nandrolone decanoate (a poor substrate for aromatase that caused a lowering of estradiol levels in this study) would not elevate IGF-1 levels[vi]. Yet another study shows that GH and IGF-1 secretion is increased with testosterone administration on males with delayed puberty, while dihydrotestosterone (non-aromatizable) seems to suppress GH and IGF-1 secretion, presumably due to its strong anti-estrogenic/gonadotropin suppressing action[vii]. All of these studies seem to support a direct, estrogen-dependant mechanism for GH and/or IGF-1 release in men. It is difficult to say at this point just how important estrogen is to IGF-1 production as it relates to the promotion of anabolism in the steroid using athlete, however it remains an interesting subject to investigate.

Glucose Utilization and Estrogen
Estrogen may play an even more vital role in promoting an anabolic state by affecting glucose utilization in muscle tissue. This occurs via an altering the level of available glucose 6-phosphate dehydrogenase. G6PD is an important enzyme in the support anabolism, as it is directly tied to the use of glucose for muscle growth and recuperation[viii] [ix]. During the period of regeneration after skeletal muscle damage, levels of G6PD are shown to rise dramatically. G6PD enzyme plays a vital role in what is known as the pentose phosphate pathway, and as such this rise is believed to enhance the PPP related process in which nucleic acids and lipids are synthesized in cells; fostering the repair of muscle tissue.

A 1980 study at the University of Maryland has shown that levels of glucose 6-phosphate dehydrogenase rise after administration of testosterone propionate, and further that the aromatization of testosterone to estradiol is directly responsible for this increase.[x] In this study neither dihydrotestosterone nor fluoxymesterone could mimic the affect of testosterone propionate on levels of G6PD, an affect that was also blocked by the addition of the potent anti-aromatase 4-hydroxyandrostenedione to testosterone. 17-beta estradiol administration caused a similar increase in G6PD, which was not noticed when its inactive estrogen isomer 17-alpha estradiol (unable to bind the estrogen receptor) was given. An anti-androgen could also not block the positive action of testosterone. This study provides one of the first palatable explanations for a direct and positive effect of estrogen on muscle tissue.

What does this all mean?
It is a long held belief among athletes that estrogen maintenance drugs can slightly hinder muscle gains during steroid therapy with a strong aromatizable steroid such as testosterone. Whether or not we have plausibly explained this remains to be seen, however the above evidence certainly does provide strong support for a direct and positive affect of estrogen on growth. Does this mean we should abandon estrogen maintenance drugs? I don’t think that should be the case. It is important to remember that estrogen can deliver many unwanted effects such as increased water retention, fat deposition and the development of female breast tissue when it becomes too active in the male body. Clearly if we plan a high-dose cycle with an aromatizable steroid, anti-estrogens will be an important inclusion. However we cannot ignore the suggestion of using estrogen maintenance drugs only when they are necessary to combat visible side effects during mild to moderately dosed cycles, especially if bulk is the ultimate goal of the athlete.
 

edarrin

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No is the short answer. Some estrogen is required to maintain healthy LDL:HDL ratios. Steriods have what is known as anabolic/androgenic ratio with testosterone (#1) being 50:50. Both Deca and Primo (others discussed) have a higher anabolic to androgenic ratio. Anabolic refers to muscle gain qualities while androgenic refers to the masculine effects(lower voice,facial hair growth etc)Weight gain does not always equate to lean muscle gain. Estrogen contibutes to water retention and fat gain (female type). That is why BBer's use the anti estrogens. I don't care what your fat lab coated asspicks think. If you want real usable info you need to educate yourself and also gain experience on how your body responds to different compounds. However, there is some very interesting and valuable info for beginners there. Estrogen is involved with IGF-1 levels which is important for muscle growth. Generally speaking the more androgenic roids(test, trenboloneetc) tend to be the strongest but also have the highest side effect profile. Dbol has very low receptor affinity but really causes rapid weight and strength gains (much of which is lost afterwards because it is due to water retention) probably indicating other methods as suggested in the article. Dbol also has an enormous capacity to aromatise into estrogen. Trenbolone is pretty much considered the strongest steroid in use today. It gives incredible strength and lean muscle gain with increased vascularity. Does not convert to estrogen however, it can give some people progesterenic side effects (which can cause gyno and temporary erectile dysfunction). So there is much to learn.
 

ledom

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Are you sure?

Bullshit. Without excess estrogen your body cannot fully utilize the excess androgens in your system. True, Tren is excellant overall LBM but combined with a goodlong acting test and the increased estrogen produced will enhance gains over tren alone anyday. Only safe ancillarie to use would be Arimidex while your on.

Feel like a debate? My scientific evidence has been evaluated in front of peers and published and on EVERY power-lifting to bodbuilding program out there. It's in the science bud. TW- The "Fat" scientist in my lab coat weighs 248lb @ 6% BF @ 6F 1. Proofs in the pudding.
:)
 

5alphareductase

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I would be very interested in doing a debate sort of thing with you, as I am with the estrogen=bad crowd. I dont think that all estrogen is bad obviously, but I have never seen anything that would lead me to beleive that lowering estrogen is somehow making you grow less.

We have had some debates on here and they got a bit out of hand with the name calling and shit, so lets keep this cival if it does happen. Thanks
 

ledom

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All I'm saying that to inhibit estrogen t o the levels of while being "off" WILL NOT beefit the user whohas EXCESS AAS in ther system. To FULLY utilize the excess androgens in the body who need to have somewhat elevated estrogen to assist in growth. Face it, in order to get big "no holds bar" you're going to get somewhat fat with your newly accumalted body weight. This is why mosy choose to do a cutter after a bulking cycle. If by all means the excess estrogen caused by your influx of hormones in your body is causing you trouble then by all means maybe nolva would be a good choce to use or to put your cycle on the back burner. Arimidex is one of the only ancillaries to use while on, other than RU482. Now once off, to keep the estrogen and progesterone in check is to use nolva,clomid (yes this also aids in the reduction of excess estrogen), Drol (for the progesterone) POST cycle. But to try to effectivelyhinde most of th estrogecaused while on your cycle that is heavy in androgens is simply..................well............luducrais. Which is to say somewhat counter-productive. If your going to us AAS, learn and wegh the risks, benefits and milk everything you can from it and do it right. Just read the original post again, it's logical AND proven.
 

5alphareductase

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I think that we need to separate the goal of having a good, muscular body and the goal of being the biggest person you can be. Being as big as possible definately requires more extreme measures with everything (training, food, supplements, drugs) and health can not be a primary concern. Health is still a concern, but getting as big as possible sometimes requires us to forego this concern for a bit. Being as big as possible isnt even healthy to begin with really. If you want to be muscular, but not as big as possible, health can still be a primary concern and most people can get as pretty big (225 lean or so on a 5'10 frame) without going to extreme measures.

I am a big beleiver in the set point theory, and estrogen is very important if being as big as possible is your goal. The extra water that you carry will allow you to expand your set point, as the body has built the support systems like nervous tissue, vascular tissue, and many more to allow it to support the extra weight. When you come off, or switch to other, less aromatizing drugs, the support systems are still there, so muscle will most likely replace the water that was once there. This could obviously be done with a fat person to, but it would take a lot longer.

If your goal is just to be muscular, then I dont see the point in going through the estrogen effects like water retention and female fat gain patterns for no real benefit, or a small one. The person isnt going to be using a ton of drugs anyways, so aromatization shouldnt be a huge problem, of course it will be in some people though and other measures have to be taken for that. To expose them to the high bp, from the estrogen water retention and in addition to the higher bp that some have from AS from increased hematocrit or something else, for long periods of time just doesnt seem to fit with me.

Since we are probably going to get in to the whole igf-1 thing to and how estrogen is involved I will say this, to my knowledge estrogen will only lead to an increase in hepatic igf-1 which is not very important in hypertrophy, as muscle igf-1 is for actual hyperplasia. This is why gh isnt great for mass, as it releases hepatic igf-1. You might get leaner from gh, but it wont have a huge anabolic effect. Even if estrogen does keep up hepatic igf-1, then that effect is negated by the female fat patterns that estrogen can produce. It is like going one step forward, then going one step back, you know.

I am not aware of any synergy between estrogen and AS, but I do not know everything about AS either. If you have a study showing the synergy, or the inability of the body to fully use AS without increased estrogen, then I would be glad to see it. Not being a dick, but I have never seen a study saying that.

Also, using anadrol for post cycle is not going to work. Anadrol is going to shut your HPTA down, or keep it down, no matter what amount of clomid or nolvadex you use. It gives plenty of androgenic quality for the body to still not produce its own test for the duration that you use it. If you are using it for the progesterone qualities, why not just use progesterone itself. Also, we have plenty of other anti aromotase drugs that are stronger than arimidex, like femara (letrozole), aromasin (exemestane), and the yet to be released because it is still only injectable formestane.

Lets keep up this debate as it is interesting to me. Thanks
 

ledom

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Concerning Anadrol.............We have our wires crossed. My meaning is during dieting Anarol shows it's superior structure by allowing the user to drop many calories and aid in the retention of LBM than without. Surely you agree with me on this subject. All you have to do is look at the structural activity of oxymethelone and you'll see that it is terrific for dieting.

Now concerning our estrogen debate. Again I believe that we have a common ground. What I am sayng is to those that combat excess estrogen while "on" are actually indering their growth from it's full potential. Your system is shutdown so why not do everything to it's full potential. If your stacking multiple items and/or large dosages (1 gram or more) of a long acting test per every 5 days, why not use the increased estrogen to your benefit. A litle bit of extra fat is a nominal price to pay when I know I'm carring around an extra 5 plus pounds of LBM made possible by the influx of ALL hormones in my body (including estrogen). The fact is the little extra weight/Fat storage is truly not harmful unless you have family issues with extra weight or something. If that is the case you shouldn't be using AAS to begin with.

As I' sure you know steroids are not a quick fix. But done correctly and with the proper training, diet and ancillaries in place it WILL super-charge you.

The extra weight is not from estrogen water. It's from it having a direct effect on the process of anabolism. A manifestation of GH secretion, glucose utilization and adrogen receptor proliferation. Concerning glucose utilization it increases gluose 6-phosphate dhydrogenae.........enzyme directly linked to muscle growth and recouperation(1)

1) The pentose phosphate pathway in regenerating skeletal muscle. Biochem J 170: 17 1978
 

5alphareductase

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Hey. I see that we have some agreements here on this issue. I totally agree with anadrol during dieting. The androgenic quality seems to really hold on to the muscle, and the common effect of no appetite from using the drug is actually a benefit during the diet.


With the estrogen issue, we are beginning to see some agreement here as well. I can agree that stopping estrogen production might be cutting gains a small bit short, but it comes down to what you want to do. To me, it isnt worth dealing with all of the estrogen shit just for an extra 5 pounds of muscle. To you it very well might be, and that is totally cool with me. I know the estrogen weight isnt all water, but that is the common thing that most people complain about with estrogen.

I wonder though how much estrogen actually plays a part in gluc 6-phos dehydrogenase as opposed to the different thyroid hormones. The different thyroid hormones also seem to increase the enzyme activity, but I wonder if this is due to a higher level of estrogen in the subjects naturally, or because of some other less understood cause.

I think that we can both agree that the knowledge of AS in the scientific area is very slim. We still dont even really understand non AR mediated anabolic effects which have to exist in some form, maybe as glucocorticoid production stopping or messing up the receptor for a time or something totally different.
 

ledom

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Very good. I enjoyed that. It's refreshing to know that there is another (you) out there who is knowledgable and always willing to learn (as I).
 

5alphareductase

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It is good for two people who have very different views at the start to debate the issue without to many insults (as I have been guilty of before).

This board has some pretty knowledgeable people on here so I am looking forward to some good topics of conversation in the future.
 

ledom

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I agree, 100%. I can talk about AAS or Structural activity relationships between the Delta's (THC's) ALLDAY!!!!!!
 

PottedMeat

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You guys do not know jack shit about estrogen levels vs. test. levels.

Unless you want to be sporting a pair of "bitch tits", do your fucking research.

Test. good, estrogen bad. Do your fucking research and determine the proper levels of each for your particular body type, goal etc.

I have NEVER taken or used anabolic roids and know more than most of you claim to on the matter. (I am 6'2, 230lbs. with 19 inch biceps).

To put it another way; if you do not know how to maintain an optimal insullin level throughout the day, skip the roids until you know up from down.
 

caizar

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nice attitude you have mate,hope you dont use gear for the safety of other's!
 

5alphareductase

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PottedMeat said:
You guys do not know jack shit about estrogen levels vs. test. levels.

Unless you want to be sporting a pair of "bitch tits", do your fucking research.

Test. good, estrogen bad. Do your fucking research and determine the proper levels of each for your particular body type, goal etc.

I have NEVER taken or used anabolic roids and know more than most of you claim to on the matter. (I am 6'2, 230lbs. with 19 inch biceps).

To put it another way; if you do not know how to maintain an optimal insullin level throughout the day, skip the roids until you know up from down.



Instead of coming on here and claiming how big and tough you are, and how much you know over us, why dont you just give us some reasons and good research behind why we are wrong here.

Just so you know, size doesnt mean everything man. Just because you are 230 doesnt mean that you know more than a guy who is 150. Some of the biggest guys are sometimes the stupidest.

This isnt a pissing match over who knows more or whatever, this is a board to exchange information and ideas, so explain your view and lets get on with it.
 

ledom

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Right on, Alpha. Post your info, preferably wth some sort of published report(s) backing them up or just plain logic and we'll take it into account. Were all trying to learn here. Take a valium/xanax, and chill. (sorry for the outburst, but an eye for an eye)

[ No name calling, please. - BA ]
 
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caizar

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well said you to guy's! he just wants a bloody argument which he aint going to get.
 

ledom

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I understand BA, I haven't said chump in years, so it felt good. I apologize if it was out of place. But you must admit we've been very good in keepin this forum in check.
 

PottedMeat

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5alphareductase said:
Instead of coming on here and claiming how big and tough you are, and how much you know over us, why dont you just give us some reasons and good research behind why we are wrong here.

Just so you know, size doesnt mean everything man. Just because you are 230 doesnt mean that you know more than a guy who is 150. Some of the biggest guys are sometimes the stupidest.

This isnt a pissing match over who knows more or whatever, this is a board to exchange information and ideas, so explain your view and lets get on with it.

Just read Dan Duchaine's Steroid Handbook and you will have spelled out for you the relationship between test., est. and insulin production.

I can assure you that someone that is 6'2", 230lbs. with 19 inch (fully pumped) biceps knows a thing or two about the matter.
 
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