Junior Member
Aromatase blocker will compromise your gains ?
i've read
"Unfortunately, an aromatase blocker will compromise your gains since it literally stops estrogen from being made. Androgenic related problems can be reduced somewhat by the use of finasteride, which will stop the conversion of testosterone to its more androgenic component DHT. "
on bodybuildingpro.com
and thats seems true because everyone i know who don't used proviron and nolvadex have more mass
could someone explains me why i don't really understand?
Steroidpedia
Estrogen plays a huge role in building muscle..
Test effects on IGF and GH are dependant on the aromatization to estrogen..
Estrogen helps build muscle.
Too much or too little estrogen can cause problems..
Merc.
Associate Member
Merc, do you know the perfect ratio between the two? I'm about to get blood work back and i need to know what to work my numbers to.
Steroidpedia
Originally Posted by SuperK
Have you seen my bloodwork sticky??
Hormone info is towards the bottom of the article..
http://forums.steroid.com/showthread.php?t=254423
Merc.
Junior Member
Thanks again Merc, you are everywhere to help me thats cool
So using only nolvadex is better than proviron which is aromatase blocker?
and last but not least, in your opinion whats the best protection for antioestrogen?
thank you
Junior Member
whoooaaa..
first off i have never heard of finasteride- im guessing it is some mysterious bottle of tasty research chemical.. but i have before and i am currently taking pharm. grade arimidex (aromatase blocker) which does not comprimise your gains! it prevents you from looking like a cream puff like many steroid users. Using nolva will only block estrogen, and not all of it- remember; that estrogen is still floating around in your body. Taking arimidex (aromatase blocker) with something like a gram of test a week allows your testosterone to stay TESTOSTERONE instead of converting. It doesn't block all estrogen but it will block a significant amount whereby giving you the opportunity to take "that much"
example: i took 50 mgs of dbol a day for a month with 20 mgs of nolva a day- along with test and eq; and i got way puffier than when i was on arimidex- I find that when I dont take arimidex i get weaker/softer- for me, it is that drug that allows me to take the amount of test that I want without having to worry about estrogen where taking nolva and a gram of test a week is not going to prevent all of that test turning into estrogen. some estrogen isn't bad- in fact it is essential for muscle gains; but alot of it floating around isn't a good thing at all!
personally; i find the best results with 1 mg of arimidex (aromatase blocker) a day with 10 of nolva.
im sure people are going to dissagree with what i say but that is what works for me!
Steroidpedia
Keep in mind Nolva lowers Igf-1 ( which can effect gains)..
It depends what compond(s) are begin used.. Like if using a 19 nor I wouldnt use nolva with it because it increses PgR and can possibly increse your chances of getting gyno..
Merc.
Steroidpedia
Adex is an AI which lowers total estrogen... Nolva is a SERM which binds the receptor.. It does not stop the conversion of estrogen into test ..
Merc.
Last edited by Merc..; 10-22-2007 at 07:06 PM.
Junior Member
Ok Merc, i don't know before..
in a susta/deca cycle what's the best option to avoid gyno and maximize gains?
thanks
Steroidpedia
What are your stats and cycle history ??
Also can you lay out your cycle ??
Merc.
Junior Member
first cycle, deca : 200 + susta 250/500, i'm on week 8
but i think i'll do the same cycle for the second, thats why i asked
(i'm currently 189.59 lbs)
Steroidpedia
Oh Sust is best used EOD IMO..
You could look into using Adex...
Merc.
Junior Member
EOD IMO ? could you write in full words i don't know this (not used in my country)
Adex is a bit expansive, do you know about arimiplex from ****?
thanks again for your time
Steroidpedia
Sorry ...
EOD = Every other day
IMO = In My opinion
Arimiplex is Anastrozole , same as ADEX ( anastrozole) right ??
What country are your from?
Merc.
Associate Member
I used to worry about gyno alot before. SO i was always using anti estrogens. couldnt figure out why i wasnt responding well.
First cylce of test was 750mg a week running ai's Not much to speak about.
Then i did a cycle just experimenting with 250mg a week. I got better gains with the lower dose. No use of anti estrogens unless i needed.
Yes both tests were legit. Actually the same.
But i ONLY use the anti estrogens if i really need them. Usually only at the beginning of the cycle before your levels stable out. maybe a couple times mid cycle and towards the end. And at very small doses.
Thats my experience. take it as you will
Associate Member
I used to worry about gyno alot before. SO i was always using anti estrogens. couldnt figure out why i wasnt responding well.
First cylce of test was 750mg a week running ai's Not much to speak about.
Then i did a cycle just experimenting with 250mg a week. I got better gains with the lower dose. No use of anti estrogens unless i needed.
Yes both tests were legit. Actually the same.
But i ONLY use the anti estrogens if i really need them. Usually only at the beginning of the cycle before your levels stable out. maybe a couple times mid cycle and towards the end. And at very small doses.
Thats my experience. take it as you will
Associate Member
ok sorry about the double post.. thats never happened to me before here.
Junior Member
Yes Merc, Arimiplex is Anastrozole, cheaper than "arimidex" its from a-x-i-o labs do you think its good?
(i'm from france)
Steroidpedia
I dont know anything about them..
I am on hormone replacement through my doctor and only use FDA approved compounding pharmacies..
Merc.
Junior Member
yeah- i pretty much said that bud- the whole idea that nolva will not stop the conversion of estrogen- as far as it being a SERM i have no idea what in the hell you are talking about.. so uh, yeah..
Steroidpedia
Here Ya go .....
SERM/AI Definition
--------------------------------------------------------------------------------
Selective Estrogen Receptor Modulator (SERM) Compounds that bind with estrogen receptors and exhibit estrogen action in some tissues and anti-estrogen action in other tissues. The ideal SERM would deliver all the benefits of estrogen without the adverse effects. ex: Clomiphene Citrate (Marketed as Clomid or Serophene). Tamoxifen (Marketed as Nolvadex).
Aromatise Inhibitor (AI) Aromatase inhibitors exhibit a very different mechanism of action than SERM’s. Aromatase inhibitors prevent the conversion of androgens into estrogen in fat, muscle, breast, and brain. ex: Anastrazole (brand name Arimidex). FEMARA (letrozole tablets).
NOTE: Clomid and Nolvadex are both anti-estrogens belonging to the same group of triphenylethylene compounds. They are structurally related and specifically classified as selective estrogen receptor modulators (SERMs) with mixed agonistic and antagonistic properties. This means that in certain tissues they can block the effects of estrogen, by altering the binding capacity of the receptor, while in others they can act as actual estrogens, activating the receptor. In men, both of these drugs act as anti-estrogens in their capacity to oppose the negative feedback of estrogens on the hypothalamus and stimulate the heightened release of GnRH (Gonadotropin Releasing Hormone). LH output by the pituitary will be increased as a result, which in turn can increase the level of testosterone by the testes.
Although these two are related anti-estrogens, they appear to act very differently at different sites of action. Nolvadex seems to be strongly anti-estrogenic at both the hypothalamus and pituitary, which is in contrast to Clomid, which although a strong anti-estrogen at the hypothalamus, seems to exhibit weak estrogenic activity at the pituitary.
by William Llewellyn
SERM:
Clomid, stimulates the hypophysis to release more gonadotropin so that
a faster and higher release of follicle stimulating hormone aud
luteinizing hormone occurs. This results in an increase of the body's
own testosterone production. Clomid is a synthetic estrogen, however
it does also work as an anti-estrogen. How does it work? Because it is
a weak synthetic estrogen, it will bind to the estrogen receptor (ER)
and not cause any problems. At the same time the increase in estrogen
from steroids are blocked from attaching to the ER.
Nolvadex, is very comparable to Clomid, behaves in the same manner in
all tissues, and is a mixed estrogen agonist/antagonist of the same
type as Clomid. The two molecules are also very similar in structure.
It is not correct that Nolvadex reduces levels of estrogen: rather, it
blocks estrogen from estrogen receptors and, in those tissues where it
is an antagonist, causes the receptor to do nothing.
Cyclofenil, similar to HCG and Clomid in action. This drug is most
commonly used to increase endogenous testosterone levels after a cycle
in an attempt to avoid a hard crash while waiting for your hormone
levels to naturally balance. Similar to HCG and Clomid, cyclofenil
seems to quickly and effectively raise natural levels. Cyclofenil is
an estrogen that works as an anti-estrogen as well as a testosterone
booster.
AI:
Femara, (letrozole tablets) for oral administration contain 2.5 mg of
letrozole, a nonsteroidal aromatase inhibitor (inhibitor of estrogen
synthesis). Letrozole is a nonsteroidal competitive inhibitor of the
aromatase enzyme system; it inhibits the conversion of androgens to
estrogens.
Cytadren, (aminoglutethimide) at moderate doses, is a fairly effective inhibitor of aromatase and a weak inhibitor of desmolase (an enzyme needed for the
production of all steroids), and at higher doses becomes an effective
inhibitor of desmolase. It is therefore useful when using aromatizable
steroids, though it is not the drug of choice for this purpose.
Aromasin, tablets for oral administration contain 25 mg of exemestane,
an irreversible, steroidal aromatase inactivator. Exemestane is
chemically described as 6-methylenandrosta-1,4-diene-3,17 -dione.
Anastrozole,(Arimidex) is the aromatase inhibitor of choice. The drug
is appropriately used when using substantial amounts of aromatizing
steroids, or when one is prone to gynecomastia and using moderate
amounts of such steroids. It is manufactured by Zenica Pharmaceuticals
and was approved for use in the United States at the end of Dec 1995.
Proviron, is also an estrogen antagonist which prevents the
aromatization of steroids. Unlike the antiestrogen Nolvadex which only
blocks the estrogen receptors (see Nolvadex) Proviron already prevents
the aromatizing of steroids. Therefore gynecomastia and increased water
retention are successfully blocked. Since Proviron strongly suppresses
the forming of estrogens no re-bound effect occurs.
Teslac,is unique in its effectiveness as an antiestrogen. Like
Proviron, it prevents the aromatizing process of the steroids from the
basis. Thus, Teslac prevents almost completely the introduction of more
estrogens into the blood and subsequent bonding with the estrogen
receptors.
6-OXO, contains a naturally occurring aromatase inhibitor that is devoid of any direct hormonal or prohormonal activity (androgenic or estrogenic). It is what science refers to as a "suicide inhibitor" of aromatase.
L-Dex, same as arimidex or anastrozole; known as an AI and popular on chemical supply sites. This is the name given on chemical supply sites instead of it's original name. L-Dex meaning "Liquidex".
There are a number of chemical research sites that sell liquid products similar to the above mentioned items. These products are the same but in liquid form such as liquid clomid, liquid nolva, liquid femera, and liquid arimidex.
Dosage's are usually adminstered by droppers but dosage amounts per ml differ from site to site.
Also, even though bodybuilders resort to these products in paranoia of the affects of estrogen. It is important to remember, estrogen is necessary and must be balanced not completely inhibited in the system. Below is an excellent reading about the necessity of estrogen.
To much is bad, but estrogen in moderation is priceless!
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[i]. 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.
References
1. Hormonal effects of an antiestrogen, tamoxifen, in normal and oligospermic men. Vermeulen, Comhaire. Fertil and Steril 29 (1978) 320-7
2. Disparate effect of clomiphene and tamoxifen on pituitary gonadotropin release in vitro. Adashi EY, Hsueh AJ, Bambino TH, Yen SS. Am J Physiol 1981 Feb;240(2):E125-30
3. The effect of clomiphene citrate on sex hormone binding globulin in normospermic and oligozoospermic men. Adamopoulos, Kapolla et al. Int J Androl 4 (1981) 639-45
Last edited by Merc..; 10-22-2007 at 09:37 PM.
Member
Its best to try to use as low of a dose of the weakest AI you can get by on.
I used to be a fan of high test, but now I think I'll keep it to 500 or lower and keep the AI dose low as well. It's like starting a fire, then immediately throwing water on it
Associate Member
what about first time users of test e at 500mg which one is the best to use?
New Member
I'm planning on running a Dbol & TestE cycle. I havent decided whether or not to run Letro during cycle, though if I do, I will only take 0.25mg ED. Letro is however a very powerful anti-estrogen, so I might start my cycle without it and only take the Letro if I see signs of gyno.
Steroidpedia
You could just keep nolva and adex on hand in case sides occur...
Merc.
Banned
these sound like something i want to use,are they something i can buy over the counter.i live in the uk..thanks merc i hate to sound so dumb but you have given me great advice so i have to ask
Steroidpedia
No problem .. You dont sound dumb at all .. No question is a dumb question .. Its dumb to do something that might harm you without learning about it first..
Glad to see you taking the time to research so you do everything right..
They are prescription meds..
Merc.
Banned
thanks,im going off topic here-on my last cycle i injected the test and decca in my chest,tries,bies,delts,lats,delts,traps-pretty much all over..now what i would like to know can i do the same with the tren and test prop or am i restricted to where it can go ?
thanks merc
Member
you can inject tren wherever you can inject test . 1 question though.. why are you injecting in that many places? I am injecting ED and only need 7 places to shoot... you listed 14+ locations (assuming bilateral injections) sounds to me like you're trying for site growth which doesn't happen with most aas.
Banned
IM ONLY INJECTING MY THIGH AT THE MOMENT,I WAS JUST COVRING ALL MY BODY PARTS IN THE PREVIOUS QUESTION SO I NEW THAT IF I WANTED TO PIN ANY OF THEM I COULD DO.
on my last cycle i injected all over as i was advised to do so,thanks for your help bro
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