Estrogen - needed or not?

[Damios]

What do You Guys think about Estrogen and his impact on gain muscle mass or fat loss?

Estrogen is the second factor people often consider. Especially steroid and prohormone users are often plagues with a serious misunderstanding of estrogen and its effects on adiposity. Most are convinced that estrogen increases fat gain or retards fat loss, when in effect the opposite is true. Estrogens, and especially estradiol (E2), is probably a more effective fat loss aid than is testosterone. Although like testosterone, it may have certain anti-lipolytic effects by increasing a2 adrenoreceptors in specific female patterning (harder to lose fat in thighs and butt).



First of all, estradiol also reduces LPL (6), just like testosterone does, so uptake of fatty acids in adipocytes is reduced. Apart from that, its effects can be divided in three categories. Its effect on insulin-related events, its effects on Growth Hormone and its effects on reducing appetite.
Estradiol can cause a reduction in weight, with only a minimal effect in insulin itself (, but that does not mean it does not alter the body's reaction to insulin. Estradiol lowers insulin receptor number (9), and in very high doses even actual insulin sensitivity (10). It does so in various ways, not in the least by reducing GLUT4 recruitment and translocation in adipocytes (11), which results in less glucose uptake in fat cells.
This will result in a negative energy balance and a greater activation of lipolysis, right where we want it, in the fat tissue. The effect of estradiol on insulin is quite acute, and clearly evident in the fact that short-term modulation drastically reduces glucose appearance (release) and disappearance (uptake) (12), suggesting a dysfunctional glucose transport system.


The second way in which estradiol may increase fat loss, is its effect on growth hormone (13,14). Unlike testosterone, which stimulates the GH/IGF-1 axis, the effect of estrogen may actually be in reducing systemic (liver-derived) IGF-1 (13), which lowers inhibition of Growth Hormone.
In doing so it obviously reduces the anabolic capacity of the body (which is why we don't use estrogen to build muscle) but increases the fat burning capacity since whole-body IGF-1 is reduced, leading to a reduction in adipogenic markers (since IGF-1 and insulin activate the same cascades) and a concurrent increase in Growth Hormone, leading to further decreases in LPL and upregulation of beta-adrenoreceptors (cfr. Part 4). Estradiol may even reduce IGF-1, while increasing IGFBP-3 (15).
This may in effect be the reason why estradiol does not promote growth, since unbound IGFBP-3, which is under normal circumstances the main carrier or IGF-1 in circulation, has been attributed charachteristics that inhibit growth (16). It acts as a pro-apoptotic agent to activate cysteine proteases, much in the same manner that cortisol or TNFalpha would (cfr. Part 4).


This implies that as long as we are seeing an increase in estradiol accompanied by an equal or larger increase in testosterone, we are reaping positive effects, on both fat loss and muscle retention since testerone increases IGF-1, while estradiol prolongs the half-life and effect of the hormone by increasing IGFBP-3 and IGF1-receptor density (20). Without the testosterone increase, it may however increase muscle loss (and potentially increase fat loss further by enhancing apoptosis of fat cells ?).
A third way in which estradiol helps as a fat loss agent is by reducing appetite. It reduces sensations of hunger via modulation of melanin-concentrating hormone. We have discussed the role of orexigenic (hunger inducing) peptides once or twice previously, specifically NPY.


Obviously NPY isn't the only peptide involved. For instance Agouti-related peptide is also involved, as is melanin-concentrating hormone (MCH). When energy intake is restricted, MCH levels sky-rocket, leading to an increased sense of hunger. Estradiol was able to completely abolish this increase in MCH (17), making it a very potent appetite suppressor during low-calorie diets.


Lastly, estradiol increases both the release of arachiconic acid (18) and the actions of cyclo-oxygenase (19) in certain cell types. This results in a quick and effective increase in several prostaglandins, including PGF2 and PGI2, that are related to lower body-fat levels. Because these effects can be highly varying in different cell types it should not automatically assumed that these events do occur, or that they necessarily contribute to fat loss however.
Estradiol can also prevent muscle loss, once again only in the presence of testosterone, by blocking the low affinity glucocorticoid receptors (22), protecting against the effects of cortisol. Testosterone, or another blocker of the high affinity receptors must be present however, otherwise the blocking of the low affinity receptor would not yield very good results.


On a closing note, as with testosterone, the effects of estradiol are not uniformly positive. It has been shown to enhance PPARgamma (20), so modulation of testosterone/estradiol levels should occur in the presence of a PPARgamma blocker for maximal effects on fat loss. And lastly, estrogen increasing products are often omitted during diets for the simple reason that estradiol increases aldosterone (21), a hormone that increases sodium retention, and as a result water retention.


Excess levels of estrogen often lead to water retention and a puffed up look. While this does not affect fat loss one iota, and can be addressed quickly, in only 1 or 2 days, it does make it difficult for the dieter to judge his progress accurately.

These days, there probably isn’t a BB’r alive that hasn’t heard of trenbolone. In today’s drug circles, it has attained nearly super-hero status as an anabolic agent. “Nectar of the gods”…“A steroid on steroids”…and “indispensable” are just some of the terms which have been used to describe this highly desirable drug. There is no single characteristic responsible for Trenbolone’s unique effects on the musculature. Rather, it is a precise combination of attributes which provide such amazing results.



There are few non-methylated drugs capable of functioning as both a mass builder and cutter, while excelling at both. In fact, if pressed to name another non-methylated drug capable of duplicating trenbolone’s performance, I would be unable. Typically, trenbolone is known for its ability to generate substantial gains in dense, dry muscle tissue; a trait which has no doubt earned it a top spot in both contest prep and off-season programs alike. Likewise, its strength building and psyche altering capabilities have made it popular among strength-power athletes, but rather than re-hash these well known traits, I want to spend a bit of time talking about some of the less publicized qualities of trenbolone.


One often debated topic in the steroid world is the role of estrogen in the muscle growth process. Up until the last decade, many BB’rs were taught to avoid the use of anti-estrogenic drugs when in the off-season, as it was commonly believed that the elevated estrogen level achieved with aromatizable drugs was necessary for maximizing muscle growth. This belief was born out of real-world experience, with many BB’rs noting a reduction in overall weight gain when administering these drugs. Were these old-school BB’rs simply confusing estrogen induced water retention with genuine muscle growth, or was there more to the story?



In recent years, the phobia surrounding anti-estrogenic drugs has greatly diminished. While science has confirmed the importance of estrogen in the growth process, most steroid users now believe that keeping levels within the low-normal range is more than sufficient to obtain all its growth benefits. To this end, aromatase inhibitors such as Aromasin and Arimidex are freely employed in the programs of today’s steroid using BB’rs. So, how does this apply to trenbolone, a non-aromatizing steroid, you might ask?



Perhaps no other segment of our society has conducted more research on the anabolic effects of trenbolone than the meat industry. In a multi-billion dollar a year business, which relies on meat yield to turn profit, improving growth rate is priority #1. This has led to the development of long-standing products such as Revalor H; a combination hormonal preparation containing trenbolone acetate and estradiol in a 10:1 ratio. Why the addition of estradiol and more so, why such a high dose? When using a normal testosterone to estrogen ratio as a baseline for comparison, this formula is grossly lopsided in favor of estrogen. Other formulas, such as Revalor S, provide an even more exaggerated ratio, with 120 mg of testosterone for every 24 mg of estradiol. That is nearly a 5:1 ratio! Why is estrogen dosed so high? The answer is quite simple—because this combination results in a greater meat yield compared to using lower doses of estrogen or no estrogen at all.



In one particular study designed to examine the relationship between trenbolone and estrogen as it pertains to IGF-1 levels, 20 feedlot steers were randomly assigned into one of 4 groups and provided with varying combinations of these drugs. There 4 groups are as follows: 1) Control (received no trenbolone or estrogen). 2) Trenbolone only. 3) Estrogen only. 4) Trenbolone + estrogen. At the onset of treatment the animals were weighed and muscle biopsies were performed. This was repeated on days 7, 14, and 28.



In animals treated with estrogen only, IGF-1 levels increased by nearly 75% in only 28 days. Somewhat surprisingly, IGF-1 readings were nearly identical in the trenbolone + estrogen group, while the trenbolone only group experienced no increase in IGF-1 levels. These results indicate that estrogen alone was entirely responsible for mediating the increase in IGF-1 seen in the trenbolone + estrogen group. While animal studies are not always directly applicable to humans, this study strongly suggests that the anabolic effects of trenbolone are further enhanced in a high estrogen environment.



We find support for this position when evaluating the real-world results of the testosterone-trenbolone stack. Despite trenbolone’s much higher anabolic rating, superior gains in muscle mass are noted when trenbolone is combined with testosterone, compared to using trenbolone alone at an equal dosage. In this case it is testosterone, rather than synthetic estrogen as utilized in the study above, which supplies the necessary estrogenic component via aromatization. Although science has yet to uncover the ideal ratio of testosterone to estrogen in muscle seeking BB’rs, it is clear that estrogen amplifies the anabolic effects of trenbolone, as well as non-aromatizing AAS in general. More research is needed in this area.



Trenbolone may also stimulate growth through enhanced proliferation and differentiation of satellite cells, which may be mediated through an increase in IGF-1 sensitivity. In order to understand why this is important, let’s first look at the role of satellite cells in the muscle growth process. After a hard training session, the muscle cell proteins within muscle fibers sustain damage, which activates a special type of stem cell known as satellite cells. These cells, which are located between the basal lamina and plasma membrane (an area directly outside the muscle fibers), are quickly shuttled to the site of injury, initiating the muscle regeneration process. They then begin to multiple (proliferate) by fusing to other satellite cells and to existing muscle fibers. A portion of these satellite cells will remain as organelles, but the majority will differentiate (the process of turning immature stem cells into mature muscle cells) and fuse to muscle fibers, either creating new muscle protein stands (myofibrils) or helping to repair previously damaged muscle fiber. The formation of these myofibrils (muscle fibers) directly leads to an overall increase in the size of the muscle.



This muscle repair process is aided by numerous growth factors, such as testosterone, growth hormone, insulin, IGF-1, HGF, and FGF. These hormones influence the rate and amount of protein that is deposited in the muscle during the repair process, with higher levels speeding up the muscle growth process and lower levels slowing down the process. In particular, IGF-1 and FGF have a direct influence on the proliferative response of satellite cells. In multiple studies, trenbolone has been shown to enhance this proliferative response, which the researchers suggest is due to trenbolone’s ability to increase satellite cell sensitivity to IGF-1.



This research further supports the notion that trenbolone should be used in a high estrogen environment, as trenbolone’s likely ability increase satellite cell sensitivity to IGF-1 cannot be fully capitalized on without the additional increase in IGF-1 that only estrogen can provide. Together, trenbolone and estrogen work synergistically to promote an increased hypertrophic response. One of the most prized benefits of trenbolone is its ability to provide a hard, dense look to the muscles. This look is partially attributable to the reduction in subcutaneous water which accompanies trenbolone use, which many refer to as a ‘drying-out’ effect. Generally speaking, this reduction in sub-q water levels takes place relatively quickly–just 1-2 weeks, after which point water levels are maintained as long as trenbolone remains part of the program. However, many trenbolone users have noted an additional increase in muscle hardness and density which seems to take place in the months following this initial drying out phase.



One possible explanation for this effect is trenbolone’s ability to protect against intramuscular fat accumulation. While certain androgens, such as trenbolone and Oxandrolone, have been to shown to reduce visceral, as well as subcutaneous bodyfat levels, the potential for intramuscular fat reduction is less often discussed. In studies involving cattle, trenbolone has been shown to reduce intramuscular fat stores to a significantly greater degree than the control group. While there is no evidence demonstrating a connection between muscle composition (the proportion of I.M. fat to muscle fiber) and visual appearance, such a suggestion is not unreasonable. Muscle density is very closely associated with muscle hardness and in reality, the two terms are almost interchangeable, but there is a slightly different quality associated with muscle density that is somewhat difficult to explain. A dense muscle, in addition to displaying a hard appearance, appears as if the muscle fibers themselves are packed tightly together with no room left between them. The biceps of Lee Priest or Ronnie Coleman, when in competition shape, are excellent examples. Although heavy training has often been implicated in the creation of muscle density, heavy training alone, even when bodyfat and sub-q water are reduced to competition levels, does not guarantee muscle density. In fact, this effect can only be maximized through proper steroid selection and few steroids accomplish this better than trenbolone. Could it be that trenbolone, through its ability to alter muscle composition more profoundly than most other steroids, is partially responsible for the dense appearance it provides?



Another benefit associated with trenbolone is its nutrient repartitioning effect. A nutrient repartitioner is any substance which promotes the preferential use of nutrients for protein synthesis and glycogen restoration over the storage of adipose tissue. In other words, the food you eat is more likely to be used for muscle growth and less likely to be stored as fat. This nutrient repartitioning effect has a direct effect on food efficiency, as demonstrated in the study below. In an attempt to determine how effective trenbolone was for increasing food efficiency in cattle, 72 steers were separated into three groups of 24 according to breed, while controlling for food intake throughout. After slaughter, the carcasses were evaluated for net gain and feed efficiency, with treated steers showing an average increase of 17%, 26%, and 21%. Although food intake remained consistent between the treated and non-treated steers, lean mass increased substantially in the treated group. It is one thing to gain muscle when consuming a surplus of calories, but it is quite another to gain muscle on a number of calories that would normally be reserved for maintenance.



Trenbolone’s potent re-comping effect is a great example of this in the real-world, with many users claiming unrivaled results in this area. I can personally testify to this in my own life. There may be steroids that get you bigger and/or stronger, but nothing changes the body as comprehensively and quickly as trenbolone. Trenbolone is a complex steroid, having dozens of internal effects on our physiology. Many of them play a positive role in terms of physique & performance enhancement, but are largely unrecognized by the BB’ing community as a whole. In this article we touched on a few of these, which hopefully, has wetted your appetite for additional information on the subject.

[OTHstrong]

What do You Guys think about Estrogen and his impact on gain muscle mass or fat loss?

I don't know but I am pretty sure ''estrogen'' is a ''she' 

[Uncle Junior]

This is really confusing me now, so should I be taking an AI at all or not if only on between 500-750mg Test??

I currently take 0.25 dex EOD.

Also how does the relationship between Finsateride @ 1mg a day work with dex, do they counter act each other since I thought Finas makes your E2 go up and dex brings it down???

[nasht5]

This is really confusing me now, so should I be taking an AI at all or not if only on between 500-750mg Test??

I currently take 0.25 dex EOD.

Also how does the relationship between Finsateride @ 1mg a day work with dex, do they counter act each other since I thought Finas makes your E2 go up and dex brings it down???

do the AI only on mon and thur. estrogen is needed. just not to much of it, ergo the AI.

[OTHstrong]

This is really confusing me now, so should I be taking an AI at all or not if only on between 500-750mg Test??

I currently take 0.25 dex EOD.

Also how does the relationship between Finsateride @ 1mg a day work with dex, do they counter act each other since I thought Finas makes your E2 go up and dex brings it down???

Identify your problems and know what the compounds role is and you have your answer. You need to have a reason for taking AI not just because it is the norm.

I keep getting asked ---should I be doing AI?  If you do not have a problem with gyno and water retention then why bother

[trapz101]

i think you going to need estrogen to bulk? correct me if i'm wrong

[WillGrant]

This is really confusing me now, so should I be taking an AI at all or not if only on between 500-750mg Test??

I currently take 0.25 dex EOD.

Also how does the relationship between Finsateride @ 1mg a day work with dex, do they counter act each other since I thought Finas makes your E2 go up and dex brings it down???

Trying to grow it's needed , you only need an AI if susceptible to estrogen sides , blocking it disrupts the positive benefits on igf-1 production in the liver.

Your water issues are your bad diet , you don't need an AI on a low dose of test , (always keep one on hand though , just incase.)

[deadz]

Elevated Estro is not a good thing in the long-term. Keep it with-in range. As stated .5 of Adex Mon. and Thur.

[crazepharmacist]

This is really confusing me now, so should I be taking an AI at all or not if only on between 500-750mg Test??

I currently take 0.25 dex EOD.

Also how does the relationship between Finsateride @ 1mg a day work with dex, do they counter act each other since I thought Finas makes your E2 go up and dex brings it down???

Get off the finasteride. It can fuck with your androgen receptors. Tons of reports of guys having no response to hormones after using that drug. There's a clinical research study going on right now to try to find the mechanism of action.

[Fuzzy Nuts]

Trying to grow it's needed , you only need an AI if susceptible to estrogen sides , blocking it disrupts the positive benefits on igf-1 production in the liver.

Your water issues are your bad diet , you don't need an AI on a low dose of test , (always keep one on hand though , just incase.)

This became legend with nolvadex. Don't think it applies with other anti-e. I would try to keep E in normal range.