Please Scroll Down to See Forums Below
How to install the app on iOS

Follow along with the video below to see how to install our site as a web app on your home screen.

Note: This feature may not be available in some browsers.

napsgear
genezapharmateuticals
domestic-supply
puritysourcelabs
Peptide Pro
UGFREAK
napsgeargenezapharmateuticals domestic-supplypuritysourcelabsPeptide ProUGFREAK

1mg arimidex too much?

drrman

New member
Im on fina and just threw in sust at 500mg per week to add some test and to get my sex drive up to par. Now, im currently taking arimidex at .5mg per day, is 1mg per day too much? im on a diet and am trying to stay lean and keep my abs. Is there anything else you think i should add in?
 
DRR, I'm sure you will get a bunch of different opinions on this. IMO, doseage is related to how susceptible your are to estrogen related gyno. Some guys can get away with not taking arimidex at 500mg of test a week and some guys need up to 1mg a day. In general I think guys are taking too much now. For most people who are not on high doses of test .25mg a day will be enough. If you are susceptible to gyno I think it goes to .5mg a day. Remember that some estrogen is needed for the growth process to occur. Good luck
firstenrgy
 
Remember that some estrogen is needed for the growth process to occur. Show me proof, I think the amount of growth difference if any is very little. Back up what ya post . - Superfrk

firstenrgy said:
DRR, I'm sure you will get a bunch of different opinions on this. IMO, doseage is related to how susceptible your are to estrogen related gyno. Some guys can get away with not taking arimidex at 500mg of test a week and some guys need up to 1mg a day. In general I think guys are taking too much now. For most people who are not on high doses of test .25mg a day will be enough. If you are susceptible to gyno I think it goes to .5mg a day. Remember that some estrogen is needed for the growth process to occur. Good luck
firstenrgy
 
Superfrk said:
Remember that some estrogen is needed for the growth process to occur. Show me proof, I think the amount of growth difference if any is very little. Back up what ya post . - Superfrk


I have heard someone else post about this as well, and I think that the difference between growing with the estrogen compared to growing without it or with very little of it is so insignificant that it does not matter. Now, I do believe that if taking way too much of an estrogen blocker can work against you, but that is in excess of <i.e.> greater than 1mg of Arimidex/Liquidex. But other than that, I see no harm with blocking the receptors completely from estrogen. I would rather be safe than sorry with gyno.

I have spoken my mind.......like it-don't like->I do not care IMO.

barnes3
 
Why Billy has Breasts: The Story of Estrogen

Why Billy has Breasts: The Story of Estrogen
A Biochemical Over-View of Estrogen
By Grendel

Meet poor Billy. Billy stands over 6 feet tall and weighs around 270 pounds. Billy was born a healthy normal man, but now Billy has an exciting career as an exotic dancer thanks to his use of steroids without anti-estrogens. To understand what happened to poor Billy lets examine estrogen and its relationship to male use of anabolic steroids.

Estrogens regulate the growth, differentiation, and functioning of diverse target tissues, both within and outside of the reproductive system. Most of the actions of estrogens appear to be exerted via the estrogen receptor (ER) of target cells, an intracellular receptor that is a member of a large super family of proteins that function as ligand-activated transcription factors, regulating the synthesis of specific RNAs and proteins. This process is almost identical to the action by which anabolic steroids effect protein synthesis.

Estrogen is also a steroid hormone, although not used for athletic enhancement. However, estrogen plays a key role in the use of AAS. Certain steroids, at high enough dosages, can convert via the enzyme aromatase into other hormones; in the case of testosterone-based steroids this other hormone is usually estrogen. Steroids with a dihydrotestosterone (DHT) base are not subject to aromatization; as a metabolite of testosterone its structure is not affected by the aromatase. Steroids with 17-alkylated structures generally convert into weaker estrogens. Some steroids, such as nandrolone (deca-durabolin) or trenbolone (parabolan, or in most people's cases Finaplex) convert into progesterone.

High dosages of steroids for prolonged periods also shut down the body's natural production of certain hormones (particularly testosterone) when steroid therapy is stopped the body attempts to establish homeostasis by adjusting hormonal levels. The average ratio of testosterone to estrogen in a healthy male is 100:1. When drugs increase the testosterone in the body, the body will respond by increasing the estrogen in the body. Additionally, estrogen circulates in the body bound to the protein SHBG (sex hormone binding globulin) as does the testosterone. SHBG is produced in the liver and use of steroids increases the production of this protein; which has a very high receptor affinity for testosterone. With more SHBG in the body, more testosterone is bound, becoming inactive as only free testosterone can activate an androgen receptor. SHBG, however, has poorer receptor affinity for estrogen and more active free estrogen circulates in the body, further altering the hormonal balance. These effects of steroids (i.e. the potential for conversion into estrogen, as well as the disruption of the hormonal balance in the body) can cause serious side effects in male users Thus, steroid users seek ways to block this estrogen from affecting them.

That is all a very nice and formal way of saying that you need to be taking anti-estrogens when you are using steroids. See, without the anti-estrogens you get all sorts of pleasant side effects, not limited to a nice pair of breasts (with oh -so tender nipples) and extra body fat! Without anti-estrogens you will end up like poor Bobby, shaking his titties in the face of wealthy Japanese businessmen. No, seriously, this article will explore how to effectively use anti-estrogens to prevent many of the side effects that accompany anabolic steroid usage.

The Drugs Are Your Friends
Oral clomiphene citrate (Clomid) is an ovulation stimulant used to treat ovulatory failure in women. Oral tamoxifen citrate (Nolvadex) belongs to a class of antineoplastics called antiestrogens. It is used to treat breast cancer. Body builders use both of these drugs. Why on earth would they do that? The answer is that both of these drugs are anti-estrogens. The term anti-estrogen is a little inaccurate. This class of pharmaceutical does not engage in some sort of matter/anti-matter reaction, annihilating estrogen in a blinding burst of anabolic goodness. Rather, let us think of the classical anti-estrogen drugs (such as nolvadex and clomid) as estrogen receptor antagonists (ERA). These ERAs are chemicals that are close enough in structure to estrogen to fit into the estrogen receptor site; however these chemicals do not have the same chemical effect as estrogen. The result is that any estrogen produced by the body or exogenous estrogen cannot find an open receptor site to attach to. The free-floating estrogen then presents far less problems to homeostasis.

There is a lot of conflict over using nolvadex, clomid and other ERAs. The regulation of estrogen-induced cellular effects is a multi-step molecular process. The diversity of estrogen and anti-estrogen effects on cellular functions is also modulated by tissue and gene specificity. This diversity of reaction may be explained by different levels of molecular regulation, including the presence of two distinct estrogen receptor isoforms (ER alpha and ER beta), their binding to activator or co-repressor transcriptional proteins, and their affinity to different DNA binding domains of target genes (estrogen responsive element or API). These mechanisms may account for the specific responses to estrogens or anti-estrogens according to tissue, cell or gene level. Therefore, in English, a drug like nolvadex, which targets breast tissues, is going to do a better job of preventing gynocomastia than is clomid. However clomid has the benefit of boosting the levels of follicle stimulating hormone, which helps restore the bodies natural testosterone levels and protects against testicular atrophy. It also increases ejaculatory capacity; by the way, so it's best to be considerate to those you care about (or those you employ, I suppose). That was my public service message for the month, by the way. I imagine that this is has something to do with LSH and FSH production in the body triggering the production of more semen, but I am not sure. Ask Bill Roberts over at the mighty TOSSED-OFF-TERONE.NET, or better yet, contact Greg Zulak c/o MuscleMag.

Many people stop using their ERA drugs when they end the cycle. That is a terrible idea. Clomid, as we have already discussed, helps immensely with your recovery processes. But remember, there is almost always an estrogen backlash to having been using testosterone drugs for so long. Therefore, many symptoms of high estrogen levels appear after the cycle. I would continue to use both Clomid and Nolvadex for up to 3 weeks after the last of the drugs have left your body. Remember, if on Friday you take 500 mg of a longer acting drug like Sustanon, then don't consider the following few weeks are truly off time. That is why it is important to know how long the drugs are effective in your body and yet another reason to switch to faster acting drugs in the last few weeks of a cycle.

Effective dosages of these two drugs are debated. I would recommend that the two drugs be used together, Nolvadex at 20 mg per day, and clomid at 50 mg per day. If Nolvadex is used by itself, 20-40 mg are sufficient. 50-100 mg of clomid can be used if clomid is the only ERA drug. Clomid should be used for two weeks after the last steroid injection to help return your body to its natural hormonal state. Nolvadex and Clomid are mildly expensive, but very available because they are not scheduled drugs and can be legally imported. Check the Anabolic Extreme Forum for the email address of one Mr. SBC who can help obtain these vital drugs.

There is a second class of drug used to combat estrogen side effects from what is grandly called steroid therapy; there are aromatase inhibitors. As mentioned previously in this article, the body can convert testosterone into estrogen using the enzyme aromatase. This second group of drugs, which I will call the inhibitors, prevents this process from occurring at all. This class of medication is generally only prescribed for severe conditions and is generally more expensive then any of the ERA.

Teslac, (testolactone), has fallen out of favor for several reasons. First of all, almost one gram daily is needed to achieve sufficient estrogen synthesis inhibition. This makes this a very expensive drug to use. Also, it is currently a scheduled drug because it is a testosterone derivate. Cytadren (aminoglutethimide) is a better choice, requiring dosages of between 250-500 mg per day to suppress estrogen synthesis. 250mg cytadren doesn't cause significant desmolase inhibition, so there would still be cortisol and other steroids, while estrogen is minimized! Cytadren is used therapeutically to combat Cushing's syndrome because it also interferes with the body's ability to synthesis cortisol. Sounds like fun, huh…no cortisol, no estrogen. What a fantastic environment. Tell that to Andreas Munzer! Cytadren can cause cysts as well as effect things like blood clotting. It is reported that Munzer used 1-2g(!) of cytadren/day! Therefore cytadren use should be done with precision. Arimidex (anastrozole) is a drug designed to combat second stage breast cancer. It is an extremely potent drug; one pill per day is sufficient to almost entirely inhibit estrogen in the body. However, the draw back is that this one pill per day can cost you around ten dollars.

The final conclusion about inhibitors is that these are far more powerful drugs then the ERA. All the drugs listed above effect a much wider hormonal spread then the anti-estrogens and they are also going to cost you a lot more. Of all the drugs mentioned, I think that arimidex is the most useful drug for the body builder. Duchaine helped promote cytadren, particularly because of its anti-catabolic ability to suppress cortisol. But, even he acknowledged the double-edged sword that this drug was. Too little cortisol is painful to the joints and in the end, extremely dangerous. I would not recommend the use of cytadren, but I have provided the moderate dosage schemes. The bottom line: These are not drugs to pop like M&Ms.

The Argument Against Our Little Friends:
But these drugs decrease your gains right? Damn it. I hate hearing that phrase clutched to…you guessed it…peoples' breast like a mantra. First of all, there is no way of telling what your gains would have been like without nolvadex or clomid. The scientific evidence that gave rise to this whole dispute (which I believe Duchaine had a hand in too) is that in addition to its anti-estrogenic action requiring estrogen receptors (ER) and leading to growth arrest of breast cancers, studies have previously shown that the anti-hormone tamoxifen (nolvadex) is able to block EGF, insulin and IGF-I mitogenic activities in total absence of estrogens. Thus the excessive use of anti-estrogens will actually result in a loss of some of the most anabolic of hormones (insulin and insulin-like growth factor 1). Steroid antagonists can inhibit not only the action of agonist ligands of the receptors they are binding to, but can also modulate the action of growth factors by decreasing their receptor concentrations or altering their functionality.

Translation: Yes, you are probably compromising your anabolic state by using ERA. But does that mean they shouldn't be used? No. I have heard statements so ridiculous as "Don't use anti-estrogens, they cut into your gains and cost too much. Just get surgery". Lovely, just fucking brilliant. Sure, like surgery isn't going to cut into your workouts or your gains. If you are swayed by the logic of just getting the surgery, I have a recommendation. Go get a pair of kitchen scissors. Ok, now, pull down your pants exposing your atrophied testicles suspended in your pimpled scrotum. Place the base of the scrotum in-between the scissor blades and apply extreme force. Thank you, you have helped the human race by ensuring you cannot procreate and pass on your inferior genetics…if you already have children please place them in a sack and toss them into a lake to drown.

I hope this article has proved helpful to you. If only poor Billy had spent those extra dollars on some Nolvadex, then perhaps he would not be the top billing at the local titty bar. This article may have gotten a little heavy at times with the technical jargon, and I apologize for that. Certainly, its not as much fun as discussing getting huge or getting ripped so you can get laid. But this an important topic if you are going to responsibly use steroids. I do not think that anyone should take their first shot or pill before they have secured enough ERA and/or inhibitors. All you have to do is look at almost any message board to see a desperate plea for Nolvadex or clomid from someone who is mid-cycle and has started to feel the begins of a lump under his nipple. The telltale tumor, you got to love it, huh Ronnie Coleman. There are always those people who claim to never get any problems no matter how much they take, that's great. There are also people who get gyno from androstenediol. I wouldn't want to find out I was a member of the second group and not have the appropriate drugs on hand. How do you know if you are going to be effected? You really can't know until you have some experience with heavy androgens. If you were over-weight as a child (many men experience some degree of gyno in puberty) you have a higher risk. But the bottom line is that no one should begin a cycle without having these drugs nearby. Surgery is not a viable alternative to anti-estrogens.
 
OK, I will give you the proof to back up what I said.
Here is an article called
Just say no to E!!! by Animal Notice the study refs that are given.


The premise:
you've been duped into believing or at least, have entertained the idea is that E is necessary for protein synthesis and/or E makes a cycle much better. You will see how that is absolutely and totally wrong.

The study.

Estrogen suppression in males: metabolic effects.

Mauras N, O'Brien KO, Klein KO, Hayes V.

Nemours Research Programs at the Nemours Children's Clinic, Jacksonville, Florida 32207, USA. [email protected]

We have shown that testosterone (T) deficiency per se is associated with marked catabolic effects on protein, calcium metabolism, and body composition in men independent of changes in GH or insulin-like growth factor I production.


It is not clear,however, whether estrogens have a major role in whole body anabolism in males. We investigated the metabolic effects of selective estrogen suppression in the male using a potent aromatase inhibitor, Arimidex (Anastrozole).

First, a dose-response study of 12 males (mean age, 16.1 +/- 0.3 yr) was conducted, and blood withdrawn at baseline and after 10 days of oral Arimidex given as two different doses (either 0.5 or 1 mg) in random order with a 14-day washout in between. A sensitive estradiol (E2) assay showed an approximately 50% decrease in E2 concentrations with either of the two doses; hence, a 1-mg dose was selected for other studies. Subsequently, eight males (aged 15-22 yr; four adults and four late pubertal) had isotopic infusions of [(13)C]leucine and (42)Ca/(44)Ca, indirect calorimetry, dual energy x-ray absorptiometry, isokinetic dynamometry, and growth factors measurements performed before and after 10 weeks of daily doses of Arimidex. Contrary to the effects of T withdrawal, there were no significant changes in body composition (body mass index, fat mass, and fat-free mass) after estrogen suppression or in rates of protein synthesis or degradation; carbohydrate, lipid, or protein oxidation; muscle strength; calcium kinetics; or bone growth factors concentrations. However, E2 concentrations decreased 48% (P = 0.006), with no significant change in mean and peak GH concentrations, but with an 18% decrease in plasma insulin-like growth factor I concentrations. There was a 58% increase in serum T (P = 0.0001), sex hormone-binding globulin did not change, whereas LH and FSH concentrations increased (P < 0.02, both). Serum bone markers, osteocalcin and bone alkaline phosphatase concentrations, and rates of bone calcium deposition and resorption did not change. In conclusion, these data suggest that in the male 1) estrogens do not contribute significantly to the changes in body composition and protein synthesis observed with changing androgen levels; 2) estrogen is a main regulator of the gonadal-pituitary feedback for the gonadotropin axis; and 3) this level of aromatase inhibition does not negatively impact either kinetically measured rates of bone calcium turnover or indirect markers of bone calcium turnover, at least in the short term. Further studies will provide valuable information on whether timed aromatase inhibition can be useful in increasing the height potential of pubertal boys with profound growth retardation without the confounding negative effects of gonadal androgen suppression.

The proofs:

Let's first look elsewhere at another mechanism where we have an insulin rise after a workout from recovery drinks causing a DECREASE in blood levels of Testosterone.

Does that mean that the drink or workout is causing LOWER testosterone levels?

Hell NO! The insulin causes the T to clear from the blood faster after the workout and the very same could be true of the supposed drop in I with anastrozol use above!

Damn if it doesn't look like we can throw a lot of animal studies out as it's not so much contradictory about what hormone does what but it is well known that T causes a rise in H and T and T3 and H are closely related, too, so to say that 'androgens in animals' caused a lowering or rising of one thing or another CANNOT be extrapolated to humans.

So we don't know if the I is being used better or not, but it seems that IT MOST CERTAINLY IS because if H is the same, and I is going down in the blood, is the H not being converted to I any longer by the liver? I would say SAID scenario is not the case plainly if nothing more than because more H floating around would cause a REDUCTION in H production and we didn't see that, either.

And anyone will tell you that certain hormones make you incredibly hungry and when they try I, they found the same 'hunger'.

And in fact this study PROOVED that E is not needed for protein synthesis and the elimination of E did NOT show a reduction in protein synthesis, at all even with less E!

The presence of E causes addition of fat not only subq, organ, interorgan, but also intramuscularly! So that great bulking hormone you are taking which is adding so much muscle is just adding fat INTO the muscle and when you diet, that fat will be the first to go. That's why a user would believe they are getting bigger 'muscle' on 'bulking AS'.

The fat from the E is going to go around the waist, too which is the most detrimental and difficult to get rid of and all too many are forgetting about. In fact, there was a study in the paper telling of how many more people with 'waste' fat are substantially more likely to have health problems.

Ahh but what the hell, who wouldn't love to look like the worlds strongest man chief iron bear, right? Nothing like having a huge beer gut and you don't even get to drink the beer!

Again it's your choice, but there's a reason that as males age, they get fatter around the waist and it's due to lower Hgh and increased aromatization, so enjoy that E.

Yes, T definitely makes a difference as the study illustrated in the first paragraph, but less E didn't decrease protein synthesis. Now, if extra T is added as in a cycle and more T is produced, is the E coming from aromatization going to cause a NOTED amount of protein synthesis or is that E just going towards the addition of intramuscular fat? It's perception by the user if they think that is a good thing.

And as for the ho's, any woman can look like a man with proper amounts of T and hGH and they will then have the same fat distribution problems when they are done and you can look at Chyna now that she is off the circuit. Anybody see her on any of the talk shows lately? Makes me want all the E I could get!

Again, I'd say that if E were so great, it's promoters would be using and suggesting amounts of E to take during any AS cycle and they don't as we know full (fool?) well that the main side which is gyno can be blocked with nolvadex and/or clomid, right? So E it up?

The problem then becomes that Nolv blocks IGF-1 production which would reduce REAL protein synthesis, so do you want a 'suspected' increase in E protein synthesis at the loss of IGF-1 which is proven to work?

In the end it's going to be your choice on what you believe the mechanism to be, but if addition of fat in the muscle is going to make you feel and think you are bigger, then get all the E you can.

I again call you back to the study with arimidex and what the 'authors' of posts and mag articles don't tell you because they know nearly NOTHING!

Harper Biochemistry pg 544.

Estrogen causes a rise in SHBG! Bing-fucking-O!

Do you see it, yet?

The reason there is a rise in blood levels of T in the study subjects is because there is less E and therefore less SHBG!

You see, you gotta know more and look farther than just the abstract you are looking at.

SHBG is also increased by a state of hyperthyroidism also read as lots of T3.

SHBG is decreased by ANDROGENS and that is why people add different AS or stacks!

I don't know to what levels SHBG can rise, but the reason given levels of AS cease to work being due to SHBG rising as the body sees so much free T around is a very plausible scenario and I've written on that before. Women have 2x the SHBG as men, so male levels can go up at least that much farther.

Therefore, if you want your cycle to end quicker and you want to make your T less effective and waste your money and injections, then you get all that E you can!
 
Last edited:
Well, that's it! We can lock the post. Superfrk has solved the mystery. If you are age 15-22 and are not taking any anabolic steroids, there is no need for arimidex. Who would have known. :rolleyes:

Now that I got the sarcasm off my chest, I wrote SOME estrogen is needed for the growth process to occur. By taking 1mg of arimidex ed with 500mgs of test a week is a little much IMO. I put "IMO" in my original post because there aren't many studies looking at estrogen combined with AS issue.
firstenrgy
 
thanks for the input guys, and yes, im very suceptible to estrogen sides, especially face bloat. Im taking 1mg per day now, and i also have femara on the way, im gonna switch to it, i've taken 3 susty's so far and still lean.
 
Top Bottom