Arimidex
Anastrozole
Arimidex (Anastrozole) is what we call an aromatase inhibitor (AI). In clinical use, it´s used to halt the progression of Breast Cancer in women. It works by blocking the aromatase enzyme, which is responsible for the production of estrogen. In athletics and bodybuilding, it is used as an ancillary compound to be added to a cycle of Anabolic Steroids. In this respect it is also used for its estrogen reducing properties, but it has the additional benefit of increasing testosterone levels, as we´ll see...

Arimidex Side Effects
Many anabolic steroids aromatize (convert to estrogen via the aromatase enzyme), and this is responsible for many of the unwanted side effects found with anabolic steroid use (acne, gynocomastia, water-retention, etc...). In one study, both .5mg and 1mg doses of Arimidex were shown to decrease estrogen by roughly 50%. The 1mg/day dose also increased testosterone levels by 58% (1). In that same study, in both groups, LH and FSH also went up slightly.

Changes in testosterone and E2 concentrations in normal young men (15 22 yr old) before () and after 10 days of oral anastrozole at 0.5 and 1 mg.(1)

This would seem to suggest that for use during a cycle, a dose of .5mgs/day would be sufficient to combat estrogen-related side effects. It is, however, important to remember that some estrogen is necessary to obtain optimal muscle growth. The lower estrogen levels provided by ´dex seems, anecdotally at least, to produce a more "hard" and "quality" look for bodybuilders who have experimented with it´s use in either a cutting or bulking cycle.

I´d like to point out that the elevation in Testosterone provided by Arimidex is so large that it can be used as a "form" of testosterone replacement therapy for hypogonadal men (2). Clearly, this suggests its use in a post-cycle-therapy (as well as its previously discussed use within a cycle) to regain natural testosterone levels and full functioning of the HPTA (Hypothalamic-Testicular-Pituitary-Axis).

Literature provided by the original maker of Anastrozole (Arimidex, produced by Zeneca Pharmaceuticals) states that stable blood plasma concentrations of the compound are achieved after a mere 7 consecutive 1mg daily doses. Also, Arimidex is just over 80% effective at inhibiting aromatase (3). Thus, if you want to take it for the entire duration of a cycle of anabolic steroids, you can simply start taking it on the same day you begin your cycle. Those are some pretty good numbers, huh?

But can you use it for the entire duration of a cycle? Is it dangerous? Well, certainly reducing estrogen levels in your body is good from a body building point of view, as it reduces water-retention and the potential for gynocomastia (if there´s no estrogen in your body, you can´t get gyno, regardless of how much progesterone is floating around)(5). Luckily this stuff is very mild on blood lipids (cholesterol) and doesn´t affect them adversely (2), in the studies I´ve seen.

Arimidex and Cholestrol
As previously mentioned, those lowered estrogen levels could possibly (eventually) adversely affect your cholesterol and possibly even your immune function. I am, however, very comfortable recommending Arimidex for relatively long-term use. This should be the ancillary compound of choice for those on long and heavy cycles, especially since it also doesn´t inhibit igf like some other ancillary compounds (insulin-like-growth-factor is an important component of anabolism)(4).


Aromasin
Exemestane
Aromasin (Exemestane) is a steroidal suicide aromatase inhibitor, which means that it lowers estrogen production in the body by blocking the aromatase enzyme, the enzyme responsible for estrogen synthesization. (1)(2)(3)

This stuff was developed to fight breast cancer in post-menopausal women, who need a particularly aggressive therapy, and for whom first line defenses such as SERMS (Tamoxifen) have not worked. This should be our first clue in inferring that this stuff is pretty strong, or at least stronger than some of the other compounds which are used to fight breast cancer.

Aromasin and Side Effects
Aromasin averages an 85% rate of estrogen suppression (4), so it´s clearly a very effective agent for bodybuilders and other athletes wanting to avoid estrogen related side effects such as gyno, acne, or water-retention brought on by aromatizing steroids. Specifically, Exemestane dose this by selectively inhibiting aromatase activity in a time-dependent and irreversible manner (hence the "suicidal" portion of it´s name, I guess).(7)

As with most of the compounds in this class, it also causes a reasonable rise in testosterone levels (6), and as you may have guessed, this rise in testosterone means that Exemestane can also cause androgenic sides(8)(9)(10). exemestane is very effective at both lowering estrogen (estradiol) and raising testosterone:
Estrogen and androgen plasma levels after 10 d of daily exemestane (25 or 50 mg) in healthy young males (mean ± SD; n = 9-11). To convert to Systeme International units: estradiol, picomoles per liter (x3.671); estrone, picomoles per liter (x3.699); androstenedione, nanomoles per liter (*0.003492); and testosterone, nanomoles per liter (x0.03467). (13)

So we can see that 25mgs is a very effective dose from that chart, right? As an added benefit, exemestane not only increases testosterone and lowers estrogen, but it also increases IGF levels (11).Additionally Worth noting is that Aromasin may possibly be less harsh on blood lipids (14)than some of the other (similar) compounds we use in the world of bodybuilding or athletics (other AI´s). It also has, at best no effect on IGF, and at worst could lower (13) it. AI´s are very tricky with regards to inconsistencies in IGF levels.

Unfortunately, you need to take Exemestane for a week to reach steady blood plasma levels of it, and exemestane has a ½ life of 27 hours (12.).

The ability of exemestane to lower estrogen levels by the aforementioned 85% makes it a very nice choice for use in any cycle where aromatizing steroids are used. In addition, since it´s not too harsh at all on blood lipid profiles, it´s a very good choice for longer cycles. It´s ability to raise both testosterone levels also seem to suggest that it would be a very nice addition to a Post-Cycle-Therapy (PCT).

Clomid
Clomiphine Citrate
Clomid is a drug given to women for use as a fertility aid. It is a SERM (Selective Estrogen Receptor Modulator) which acts by actually binding to the estrogen receptor and thereby blocking estrogen from doing the same. Clearly, this is advantageous when it binds to breast tissue, and prevents estrogen from binding there to cause gynocomastia (although it is not nearly as effective as nolvadex for this purpose). It also opposes the negative feedback loop that the body has with regards to estrogen and the HPTA (Hypothalamic-Pituitary-Testicular-Axis), and this in turn stimulates LH (Leutenizing Hormone) and FSH (Follicle Stimulating Hormone). LH and FSH, in turn stimulate the release of testosterone. Clearly this is advantageous to bodybuilders and athletes coming off of a cycle, and beginning their post-cycle-therapy. What we have in Clomid is essentially a drug that acts as a preventative measure against gynocomastia, as well as a drug that acts to raise endogenous (natural) testosterone levels. Usually, it is compared with another SERM, Nolvadex, for those reasons.

Clomid, however, is much weaker than nolvadex in a mg for mg comparison, with roughly 150mgs of clomid being equal to 20mgs of nolvadex (1).It should be noted, however, that 150mgs of clomid will still raise testosterone levels to approximately 150% of baseline value(1). You don´t have to use 150mgs, however; in my research, I´ve found that doses as low as 50mgs will show improvements and elevations in testosterone levels (4). In fact, my original Post-Cycle-Therapy regime (as suggested by Dan Duchaine in the original Underground Steroid Handbook) was 100mgs per day for a week and 50mgs/day for a week. Don´t laugh& for the late 90´s, when most anabolic steroid users didn´t even know how to use Clomid, it was considered a "state of the art" PCT routine. I suspect that Duchaine originally introduced this compound to the steroid using community.

Clomid, just like nolvadex, is very safe for long term treatment of lowered testosterone levels (2), with some studies showing its safety and efficacy for up to four months. And post-cycle, when steroid users are suffering form lowered testosterone levels, is when clomid is most effective.

I used to run Clomid for about 3 weeks post cycle, at 100-150mgs. Any more than that, and I experience emotional side effects (no, really) due to the excess amount of circulating estrogen I have in my body. All of that extra estrogen tends to make me moody, and it gets hard to squeeze workouts and cardio in-between reruns of "Sex & the City" (ok, I´m exaggerating).

Clomid Side Effects
A problem arose during a very aggressive Clomid PCT routine once. I was taking pretty high doses (150mgs/day) of clomid for an extended time (over a month) and was having vision issues. When I looked into the subject more closely, this was a common occurrence with steroid.com members. Upon further investigation, I found out the optic neuropathy (a fancy way of saying "vision problems") was actually very common with clomid usage (5)(6).Since I already wear contact lenses, I´ve had to remove Clomid from my PCT routine.

Clomid Success
Clomid as of late has fallen out of favor for post-cycle routines, but if you aren´t prone to vision problems or emotional issues, then it is just as good as nolvadex for raising testosterone when appropriate doses are used. I recommend using 150mgs/day for ten days, and decreasing the dose by 50mgs every ten days until you´re finished at day 30. Many of the bodybuilders and athletes I´ve spoken to have used it in a similar fashion and found that it restores their testosterone levels to normal.


Cytadren
Aminoglutethimide
Cytadren (Aminoglutethimide) is one of the more interesting compounds found in the bodybuilder´s arsenal of Ancillaries. It´s really not too popular today, but a decade or two ago, it was considered state of the art, and was prized by bodybuilders for many of it´s properties.

Lets first consider it´s primary use, which is that of an Anti-Estrogenic compound. is able to produce highly significant (almost total) estrogen suppression (1), and this is of course of interest to athletes who are using steroids which convert to estrogen. Unfortunately, this suppression of estrogen is not followed by an increase in any of the other hormones (testosterone, LH, FSH, etc... ) that many other anti-estrogenic compounds will cause. Thus, Cytadren is probably not going to be anyone´s first choice for use in Post-Cycle-Therapy.

The thing which, in my mind, sets it apart from other ancillary compounds currently in use today is its unique ability to inhibit the production of cortisol. Cortisol, as you recall, is a catabolic hormone, and breaks down muscle. Cytadren inhibits the conversion of cholesterol to pregnenolone (2) as well as having an aromatase inhibiting effect. Thus, Cytadren is quite unique in having both of these abilities, and certainly none of the AI´s I´ve seen thus far has anything resembling such an effect on cortisol.

Cytadren is used, medically, to fight breast cancer and/or hyperadrenocorticism, and it is the only drug currently available (to my knowledge) that can be used successfully for both purposes (1)(3). It may even have anti-depressive properties (4)(5). During a cycle, it may be used to both lower cortisol levels from intense training, and to lower estrogen levels. Sounds almost perfect, right? It´s use would allow us to consider the use of Arimidex, Nolvadex, or a similar compound for strictly post cycle use, when an increase in test, LH, and FSH would be more necessary...

Well, it´s not quite perfect, as you´ll soon see. The first problem is that it (possibly) could reduce androgen levels. The best we could hope for is that it doesn´t have much of an effect on circulating androgen levels (1).

The next problem is that eventually your body, smart cookie that it is, will start to figure out ways to compensate for the reduction in cortisol, by either producing more, or inhibiting the Cytadren´s effects. Great... And while the cortisol isn´t present in your body, your joints will be aching. Yeah, I´ve actually used this stuff (the things I do in the name of science!), and it worked& made me look a bit "dryer" and more cut; but as I recall, it also made me sleepy. This could be due to its effects on the adrenal cortex, I don´t really know, but that´s a pretty good guess.

If you are thinking about using Cytadren for this purpose, I´d have to tell you to forget it. Three grams of Vitamin C lowers your Cortisol around as much as 1,000mgs of Cytadren, from the literature I´ve seen on both, and the Vitamin C doesn´t do it at the expense of your adrenal responsiveness (7). A gram of Vitamin C lowered cortisol by 1/3rd in UltraMarathon Competitors (8) (these are the people who apparently don´t have cars, so they feel compelled to run 90 kilometers at a time). I just can´t justify taking Cytadren for an extended period of time to reduce cortisol, when Vitamin can do the same thing, more cheaply, and has other added benefits.

Next, we have to deal with Cytadren´s liver toxicity (3). This stuff is pretty stressful on your liver. I guess we can use some milk thistle and such, but do we really want to risk it, when it´s effects on cortisol are short lived and it may reduce circulating androgen levels?

Maybe...

See you can use this stuff for (maybe) the last week or so while you are dieting for a bodybuilding contest, when your circulating androgens are being totally replaced by synthetic androgens, and you aren´t giving your adrenal-cortex much chance to shut down and make you lethargic, then I think it may be useful. Taking 500mgs/day for your last week of contest prep may help you to dry out that last little bit, and edge out that ever increasing specter of cortisol over production for long enough to do dial in for your contest. For athletes considering this compound in their cycles, I think this is not a viable option when you consider all of the other available options


Cyclofenil
Cyclofenil is the least popular of the three Selective Estrogen Receptor Modulators (SERM) being used in athletics today. I actually used this stuff about half a decade ago, when it was just as easy to get as Clomid, and a bit cheaper. As we already know, SERMs cause ovulation in women and (more importantly to us) increase testosterone and other beneficial hormones. This drug actually works by simulating the effects of testosterone via inhibiting the negative feedback loop caused by estrogen, with regards to testosterone production. This in turn causes the increased secretion of Gonadotropin Releasing hormone, which increases output of Luteinizing Hormone which (finally!) increases secretion of testosterone from your testes.

So what we have here is a compound which, being a SERM, will prevent gyno by binding to the estrogen receptor in breast tissue and thus preventing stronger estrogens from binding to those tissues. This should be familiar territory if you remember your facts on Clomid and Nolvadex.

The results indicate that cyclofenil, paradoxically, has two opposing actions on the hypothalamic-hypophyseal axis, one of them is estrogen-like, in that it depresses serum FSH levels and competitively binds to breast tissue (this is good, remember), and the other action is antiestrogen-like, in that it depresses serum PRL levels and raises LH levels (4). Overproduction of prolactin, as you recall will suppress Testosterone, and could induce lactation (gross!) in male breast tissue.

From the reading I´ve done on this compound, I think 400-600mgs/day would be an appropriate dose for use in Post-Cycle-Therapy, or during a cycle (4). Dan Duchaine estimated roughly the same, saying that twice as much is necessary when compared to Clomid, twice as often. Due to its relative expense and unavailability when compared to other SERMs, such as Nolvadex and Clomid, I can´t see this stuff making its way into many people´s ancillary regimen


Falsodex
Falsodex is an estrogen receptor antagonist, which has no agonist effects at all. What it does is downregulates Estrogen Receptors (kinda like how Clen DownRegulates your beta receptors....so you get decreased effects from the stuff). Basically, it binds to the Estrogen Receptor more strongly then Tamoxifen, but still has no estrogen agonist effects.

The resultant down regulation of your Estrogen Receptors from the use of Falsodex results in decreased expression of the Progesterone Receptor as well! Tamoxifen, as we all know, can increase the sides from progesteronic drugs because of an increase in progesterone receptor expression. You can take Falsodex as both an anti-estrogen and an anti-progestin. You do not need to buy Arimidex (or similar drugs), and Bromocriptine!

Falsodex is administered via an IM injection of 250mgs once per month! And at that dose, it has have most if not all of the same estrogen lowering effects of 1mg/day of Arim or 2.5mgs per day of Letrozole, but has the added benefits of lowering progesterone receptor expression.


LetrozoleFemara
Letrozole (Femara) is the chemical name of Novartis´ selective third generationAromatase Inhibitor (AI). This drug was developed to fight breast cancer by inhibiting the aromatization. It is usually used as a part of an aggressive treatment in post-menopausal women, to fight and reverse the spread of breast cancer after other treatments (such as Tamoxifen therapy) has failed. It´s probably the most efficient product on the market for this purpose currently (5) It is very similar in structure and action to it´s predecessor Arimidex.

Letrozole (Femara) also does quite a few things which would be of interest to both bodybuilders and athletes. Firstly, it has been shown to reduce estrogen levels by 98% or greater (1). In at least one documented incidence, Letrozole (Femara) reduced estrogen in the test subject to undetectable levels, and increased LH, FSH and SHBG (4). Clearly this is all of interest to bodybuilders, as less estrogen in the body means less chance of certain side effects such as water-retention, Gynocomastia, and acne. This makes Letrozole (Femara) an appropriate choice for even the heaviest bulking or cutting cycles including harsh androgens. Also, if you are a competitive bodybuilder, Letrozole (Femara) is a must have product for contest prep; no other Ancillary compound will produce a dry and tight look like Letro will.

An effective dose of Letrozole (Femara) is .25-.5mg/day (I use .25mgs/day), but be forewarned, if you go over that amount, it can kill your sex drive. Also worth noting is that there´s a rebound effect on your estrogen when you come off Letrozol. Maximum inhibition of the aromatase enzyme has been found to happen at doses as low as 100mcg! (2)

Letrozole (Femara)´s effects on serum lipids (cholesterol, both HDL and LDL) are, in the words of one researcher: "inconsistent. " Clearly, however, you´ll eventually suffer an impaired lipid profile and immune system if you keep your estrogen levels too low for too long. Your sex drive will also probably suffer from extraordinarily low levels of estrogen present.

As previously mentioned, Letrozole (Femara) can be used to raise LH and FSH (which are hormones which signal your testes to produce more testosterone). It also, of course, will raise your testosterone levels (6) via this mechanism. Again, this is of interest to athletes and bodybuilders for obvious reasons. Letrozole (Femara), of course, can be used for post-cycle-therapy (PCT) to raise test levels, but for various reasons, Tamoxifen may be a better choice. Still, I have successfully used Letrozole (Femara) for this purpose.

How good is this compared with Aromasin and Arimidex, it´s too other main rivals? Well, In non-cellular systems, Letrozole (Femara) is 2-5 times more potent than anastrozole and exemestane in its inhibition of the aromatase enzyme and activity, and in cellular systems it is 10-20x more potent! It also lasts quite a long time in your body,but takes awhile to get going& Letrozole (Femara) has a whopping 2-4 day (!) ½ life, and you need to take Letrozole (Femara) for 60 days to get a steady blood plasma level (8).

Those are impressive numbers, but here´s one of the most interesting things about Letrozole (Femara):

It may reduce/eliminate/reverse existing gynocomastia!

In a study conducted on mice (*no, I know it´s not perfect), gyno-like-changes in the mammary gland were totally destroyed! Here´s a direct quote from that study:

"Our results also indicate aromatase overexpression-induced changes in mammary glands can be abrogated [destroyed] with very low concentrations of the aromatase inhibitor, Letrozole (Femara)."(7)

In addition, I´ve used Letro to get rid of my own gyno, as has a friend of mine, and we both used it at a dose of 2.5mgs/day, tapering down to .25mgs/day, and then finally off..the gyno never returned in both our cases.

I´d say that this stuff is pretty great, considering its availability and cost (when you consider the fact that .25mgs/day is more than enough protection from estrogen-related sides on most cycles), not to mention it´s overall utility for a variety of functions (destroying gyno, preventing estrogenic sides, and for PCT).

Nolvadex
(Tamoxifen Citrate)
Nolcadex and Gynocomastia
This drug is used as a first line defense against breast cancer. In the late 80´s, Dan Duchaine speculated that it could also be used by bodybuilders to halt the development of another type of tumor in the mammary gland, Gynocomastia. He introduced this find to the Steroid-using-community in his "Contest Prep" issue of the UnderGround Steroid Handbook Update Newsletters (the contest prep-issue was actually 3 issues in one, for those who had a subscription to the newsletter).

Nolvadex is commonly referred to in quite a few ways: as a SERM (Selective Estrogen Receptor Modulator), as an anti-estrogen (that is actually incorrect, as we will later see), and finally as a triphenylethylene. I happen to stick with calling Nolvadex a SERM, because out of my three options, it happens to be correct (as we know that calling it an anti-estrogen is incorrect), and pronouncable (as we know that I have no idea how to say "triphenylethylene"). Selective estrogen receptor modulators (SERMs) act as either estrogen receptor agonists or antagonists in a tissue-selective manner, lets see what that means to us&

Nolvadex actually has quite a few applications for the steroid using athlete. First and foremost, it´s most common use is for the prevention of gynocomastia. Nolvadex does this by actually competing for the receptor site in breast tissue, and binding to it. Thus, we can safely say that the effect of tamoxifen is through estrogen receptor blockade of breast tissue (1), especially since total body estradiol increases with use of tamoxifen. Clearly, if you are on a cycle which includes steroids which convert to estrogen, you may want to consider nolvadex as a good choice to run along side them.

Nolvadex Cycle
Nolvadex, however, is not the most potent ancillary compound we can use on a cycle, but it is probably the safest considering it doesn´t actually reduce estrogen in your body keeping some estrogen floating around could have many benefits on muscle growth, as well. Estrogen is also important for a properly functioning immune system, and not only that, but your lipid profile (both HDL and LDL) should also show marked improvement with administration of tamoxifen (4). Many bodybuilders actually use this stuff during their cycle for the health benefits provided by it. If, however, you are preparing for a bodybuilding contest, you need to use something which will suck most (if not all) of the estrogen out of your body. I am speculating that you may be able to use Nolvadex for the majority of a contest prep cycle, to keep yourself relatively healthy, and then switch over to Letrozole for the last 8 weeks.

Nolvadex also has some important features for the steroid using athlete. In hypogonadic and infertile men given nolvadex, increases in the serum levels of LH, FSH, and most importantly, testosterone were all observed (2)(3). The best (rough) estimate I can give you from my research is that 20mgs of Nolvadex will raise your testosterone levels about 150% (5)...and this would of course greatly aid post-cycle-recovery. What this means to us is that if you take Nolvadex after a cycle, when you are trying to raise your levels of testosterone, LH, and FSH back to normal, it will greatly aid recovery. In fact, if I were limited to just one compound to aid me in post-cycle-recovery, Nolvadex would be my choice. If you want a comparison, it would require 150mgs of Clomid to accomplish that type of elevation in testosterone, but nolvadex also significantly increased the LH (Leutenizing Hormone) response to LHRL (5), after 6 weeks.

Some of the more harsh ancillary compounds available today will give you a more "dry" look that nolvadex can´t, but nolvadex is simply safer to use in long (over 16 week) cycles.

Nolvadex Side Effects
Unfortunately, Nolvadex isn´t perfect. Anecdotally, it has been linked to reduced gains in some bodybuilders. This isn´t due, as previously thought, to its reducing estrogen levels (which it doesn´t), but rather to it´s ability to possibly reduce IGF (Insulin-like-Growth-Factor) levels, which are important for muscle growth.

Proviron
Mesterolone
Proviron (mesterolone) is basically an orally active DHT (Dihydrotestosterone) preparation. For comparision, we can think of some other orally prepared DHT compounds like Winstrol, Anavar, etc& Those both act very similarly in mechanism to Proviron, but a more accurate way to think of this compound is as something like "Oral Masteron." As I´m sure you noticed, their anabolic/androgenic ratio is very similar.Remember, DHT is 3 to 4 times as androgenic as testosterone and is, of course, incapable of forming estrogen. Also, Proviron is quite unique in that a simple look at it´s 4-ring structure will show us that it is not going to be too liver toxic, since it is not c17-Alpha-Alkylated, as many orals are& this modification (lacking in Proviron) makes drugs more liver toxic. Proviron has a 1-metyhl group added, instead. Looks pretty great on paper, right? Well, as usual, things tend to look better on paper than they do in the body. Your body has a negative feedback loop which prevents your body from having too much DHT floating around(if you´ve been paying attention up to now from reading my other stuff, you already know this). An excess of DHT will eventually be changed into another (largely not anabolic) compound.

And of course, being a DHT-based compound, this stuff isn´t going to be great for female athletes to use. Virilization (development of male sexual characteristics) is going to be a concern for women daring enough to try this stuff. My advice is that there is much better, safer compounds for female athletes and bodybuilders to use.

So lets go back to the comparison with being some sort of "Oral Masteron"& basically since Proviron is 5-alpha reduced and not capable of forming estrogen, and also has a very high affinity for binding to the aromatase enzyme (the enzyme responsible for converting all that good testosterone in your body into all that nasty estrogen). That means if you choose to take proviron with testosterone (and I know you wouldn´t even be doing a cycle without including some form of testosterone) and/or any aromatizable steroid, it should actually serve to prevent estrogen build up by the aforementioned binding to the aromatase enzyme, which prevents aromatase from doing it´s dirty work and making a bunch of estrogen out of the other steroids you are taking. It should also be noted that Proviron also binds very well to SHBG (Sex Hormone Binding Globulin& a hormone responsible for reducing the amount of circulating free testosterone in your body)(1). As a matter of fact, in the last study I read, it bound to SHBG better than any other drug studied. Also, I´d like to note that Proviron bound to the Anabolic Receptor better than any oral anabolic (except for the insanely toxic MethylTrienolone), having an ability to bind to the AR better then testosterone, but not as well as Nandrolone (1). Unfortunately, as we know, DHT also has a high affinity for binding to receptors in the scalp and prostate, causing some possible nasty side effects, like male pattern baldness and prostate enlargement. It´s important to remember that DHT and DHT derived compounds are used quite successfully to treat gynocomastia, and in this area, Proviron is no different.

Let´s delve into some of the positive points of this drug before we go any farther. Androgen Receptors are found in fat cells as well as muscle cells(5), and whilethey act on the AR in muscle cells to promote growth, they also act directly on the AR in fat cells to affect fat burning.(9)(3) The stronger the androgen binds to the A.R, the higher the lipolytic (fat burning) effect on adipose (fat)tissue(6)(2). As if that´s not enough good news, some steroids (notably, testosterone) even increase the numbers of A.R. in muscle and fat (9)(7). Thus, if you are taking a simple stack of proviron and testosterone, you´ll have more of the test you shoot as free testosterone floating around building muscle (compliments of the Proviron), more androgen receptors to be bound to (compliments of your testosterone) by your Proviron, thus causing more fat loss. Testosterone and Proviron are a very nice synergistic stack, pretty nearly an "ideal" stack of an oral and injectable, because both drugs will actually act to enhance the effect of the other.

So what we have here is a steroid which can basically make other steroids more effective by preventing their conversion into estrogen, as well as increasing the amount of circulating free testosterone in your body. This of course all provides a more hardened and quality look to muscles. Proviron is very much a "synergistic" drug in this respect, and it´s inclusion in any cycle would definitely make all of the other steroids perform better, and provide better gains. This is all compounded by the fact that proviron is a very lipolytic (fat-burning) drug.

Now, as if all of this weren´t enough, let´s talk about how Proviron affects your HPTA (Hypothalamic-Pituitary-Testicular-Axis)& the thing that regulates the male hormonal system. When a reasonable dose of this stuff is given (100-150mgs/day), it had no depressing effect on low or normal serum FSH and LH levels (6). Follicle Stimulating Hormone (FSH) and Leutenizing Hormone (LH) are two hormones which send a signal to your testes to produce testosterone. Good news for people considering it for PCT is that it can even raise your LH (10)! Thus, by not suppressing those hormones and maybe even raising some, your normal testosterone levels will remain intact. This points to a novel use for this compound during Post-Cycyle-Therapy for a non-suppressive "bridge" between cycles. In fact, in yet another study, administration of Proviron (basically the same dose as in the last study) produced no changes in steroids, thyroid hormones, gonadotropins nor PRL (Prolactin Levels& you want those to remain low). (8).

Unfortunately, this stuff is not too hot on it´s own. It´s a good drug for inclusion in a cycle containing testosterone and other armoatizable steroids, and it´s a good drug for a possible "bridge" between cycles. Alone, however, as an androgenic or anabolic agent, it´s effects have been very weak in both studies (9), as well as in the experience of everyone I spoke to about it. This may be due to the addition of the 1-methyl-group to DHT, which makes this stuff orally active. Whatever the case, as a stand alone anabolic or androgenic compound, it´s not too impressive.

BROMOCRIPTINE
Bromocriptine mesylate tablets equivalent to Bromocriptine 2.5mg tablets USP
Presentation

Bromocriptine is a brominated ergot derivative that functions as a dopamine D2 receptor agonist and a dopamine D1 receptor antagonist. It imposes a direct dopaminergic effect on cells located within the basal ganglia, mesolimbic system and hypothalamus. It does not possess the uterotonic and vasoconstrictive properties associated with other ergot preparations.

Bromocriptine specifically inhibits the synthesis and secretion of prolactin from the anterior pituitary gland by dopaminergic stimulation of pituitary prolactin cells. Amenorrhoea, galactorrhoea and other endocrine processes associated with hyperprolactinaemia are consequently returned to physiological levels of activity. Bromocriptine also enhances the release of gonadotrophin and gonadal steroids that are suppressed in hyperprolactinaemia. Preclinical studies have reported that bromocriptine decreases dopamine turnover in the median eminence and dopaminergic tubero-infundibular region of the hypothalamus which may further regulate the synthesis and secretion of prolactin.

Bromocriptine reduces the elevated levels of growth hormone (GH) in acromegaly and may alleviate the clinical symptoms and glucose intolerance presented in this condition.

The dopaminemimetic activity of bromocriptine in the striatum may be responsible for the beneficial effects observed in selected cases of Parkinsons Disease.

Pharmacokinetics
Bromocriptine is rapidly absorbed after oral administration, but only 6% of the dose reaches the systemic circulation due to the high hepatic extraction rate and first pass metabolism. Maximum peak concentrations are obtained within 1 to 1.5 hours; serum prolactin decreases within 2 hours and is maximally decreased at 8 hours. Bromocriptine is highly distributed in the liver, stomach, and intestine, and plasma protein binding amounts to 96%.

Bromocriptine is extensively metabolised by the liver. The fate of bromocriptine primarily involves biliary excretion with renal excretion of two major metabolites accounting for only 6% of the total dose. It is not known whether these metabolites (2-bromolysergic acid and 2-bromoisolysergic acid) are pharmacologically active in humans. The elimination of the parent drug from plasma is biphasic, with a terminal half life of about 15 hours (range 8-20 hours). Multiple dosing may result in accumulation of bromocriptine to the extent that plasma levels may be almost double those observed following single doses.

Dosage and Administration
Bromocriptine tablets should always be taken with food.

Dosage of bromocriptine mesylate is expressed in terms of bromocriptine, and should be individualised.

Male hypogonadism:
Initial dosage 1.25mg 2 or 3 times a day gradually increasing to 5-10mg a day.

Prolactinomas:
1.25mg 2 or 3 times daily; this can be gradually increased as needed to suppress prolactin secretion.

Inhibition of lactation:
On day one take 1.25mg morning and night with food, increasing on day two to 2.5 mg twice daily. Therapy should be continued for 14 days to prevent rebound lactation. Treatment should be started as soon as possible after parturition or abortion.

Contraindications
hypersensitivity to ergot alkaloids
uncontrolled hypertension, hypertensive disorders of pregnancy, hypertension postpartum and in puerperium
coronary artery disease and other severe cardiovascular conditions
symptoms and/or history of serious psychiatric disorders.
Warnings and Precautions
Hypotension:
Blood pressure should be monitored periodically in all patients receiving bromocriptine. When used by women post-partum, it may induce hypotension, or more rarely hypertension, and should not be given for at least 4 hours post partum. Blood pressure must be monitored on several occasions initially, as development of hypertension may be delayed. Particular attention should be paid to patients who have used other drugs that can alter blood pressure.

Inhibition of Lactation:
Occasionally serious adverse reactions have been reported. These include seizures, strokes, myocardial infarction, hypertension and psychic disorders. Constant or progressively severe headache, which can be accompanied by visual disturbances, often precede by hours or days the occurrence of a seizure and/or stroke. Periodic monitoring of blood pressure is recommended in postpartum women receiving bromocriptine for the inhibition of lactation. Lactation inhibition therapy should not begin until the vital signs have stabilised and not before 4 hours after delivery, as bromocriptine may cause hypotension or sometimes hypertension in some patients. If hypertension, a severe progressive or unremitting headache (with or without visual disturbance), or the evidence of CNS toxicity develops, the drug therapy should be discontinues and the patient evaluated promptly.

Effect on ability to drive or operate machinery:
Patients should be warned that bromocriptine may cause dizziness and fainting during the first few days, and may impair their ability to drive a car or operate machinery.

Bromocriptine should be used with caution in patients with impaired liver, renal or severe cardiovascular dysfunction.


Adverse Reactions
Nausea is the most common side effect at the beginning of therapy with bromocriptine, but vomiting, dizziness, postural hypotension and fainting sometimes occur. Initial doses must be low, taken preferably at bedtime, and blood pressure should be monitored initially.

Gastrointestinal effects include abdominal cramps, epigastric pain, indigestion, constipation or diarrhoea. Occasionally, acromegalic patients on doses 10 to 60 mg bromocriptine have developed a peptic ulcer or gastrointestinal haemorrhage.

Temporary reduction of dose or administration with food may relieve these effects.

Additional side-effects include headache, nasal congestion or watery rhinorrhoea, dryness of mouth, and drowsiness.

Drugs which can increase prolactin levels, e.g. butyrophenones, phenothiazines, tricyclic antidepressants, reserpine, metoclopramide, methyldopa, pimozide, oestrogens and TRF, may reduce the efficacy of bromocriptine.


Concomitant use of bromocriptine and other ergot alkaloids is not recommended since the combination may cause potentially serious side effects such as myocardial infarction and hypertension.

Alcohol may decrease tolerability to bromocriptine.

Overdosage
Overdosage of bromocriptine may cause nausea, vomiting, dizziness, postural hypotension, sweating, drowsiness, and hallucinations. The management of acute intoxication is symptomatic. Metoclopramide may be indicated for the treatment of emesis or hallucinations.

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