One of the first articles I ever wrote which was widely circulated was about Clenbuterol. I wrote it partially to clear up some misconceptions about the drug, and partially because I got tired of answering the same questions over and over. Several years later, that article has been circulated on almost every anabolic steroid discussion board on the internet, and those boards who haven’t actually reposted the article still regularly discuss one of the concepts pioneered in the article… namely the use of Benadryl with Clenbuterol.

Now, its several years later, and I’ve mostly abandoned Clen for my own personal use, and actually recommend Albuterol (Salbutamol) as a much better alternative. Albuterol is a (relatively) selective beta-2 adrenoreceptor agonist, just like Clenbuterol. Honestly, I had pretty much given up on Clen a couple of years ago because for my own personal reasons (I had experienced much better results with Ephedrine and Caffeine). Then, a couple of weeks ago, I tried my first bottle of Albuterol, mostly out of curiosity…and wow! I like it much more than Clenbuterol. I mentioned this fact to my research assistant, and she told me that a lot of figure competitors also prefer Albuterol over Clenbuterol. I had no idea about that, but based on the effects I had with Albuterol I can see why. Clen is simply too harsh on most people; they get too jittery, too shaky, and too anxious. It’s a lot to go through to burn some fat.

But in my own personal experience, Albuterol produces a much “cleaner” type of stimulant effect than Clenbuterol. I don’t know how to really describe this other than to say that the “Clen-shakes” just aren’t as bad with Albuterol…in addition, I’m able to focus better on my work when I use Albuterol, while with Clen I’m stimulated but not really focused.

But even though Albuterol produces a much cleaner stimulant-type feeling in most people, the main question is “How well does it burn fat”? As far as fat-burning stimulants go, how does it stack up to Clenbuterol? Lets face it, most people are really only concerned with the end results, right? Well, at least in me and the people I’ve worked with, Albuterol seems to produce significantly better results than Clen in terms of fat burning effects…and it produces them just a bit more quickly too. This makes sense, if you think about it. Albuterol is often thought of as a “shorter acting” version of Clen…and, to draw an analogy, when we look at the steroids which are shorter acting versions (think about comparing something like Testosterone Propionate vs./ Cypionate, or NPP vs./ Deca)- they typically produce more dramatic results a bit quicker than their long acting cousins. I’m finding the same thing to be true with Albuterol. When we take a look at a medical study examining Clenbuterol vs. a beta-2 agonist which has an even longer half life (“Salmeterol”), we see that Clen out performs it in terms of anabolic effects (1). So I think it would only be logical to assume that something that was a shorter acting beta-2 agonist than Clen would likely outperform it, right?

Let me just restate that, to make sure we’re all on the same page, ok? Clenbuterol outperforms longer acting beta-2 agonists, in terms of anabolic effects. Albuterol is a beta-2 agonist with a shorter acting effect than Clenbuterol. Therefore, it’s only logical that Albuterol is going to be more anabolic than Clen, right? Ok, let’s move on…

To understand how Albuterol works, first we need to take a look at the Beta adrenergic system. This system is comprised of something called adrenoreceptors, and the most well known (to bodybuilders anyway) of the adrenoreceptors are the beta receptors. Beta receptors are embedded in the cell’s outer phospholipid membrane, and are stimulated by all the really popular stimulants…ephedrine, Clenbuterol, etc… These receptors can further be divided into three subtypes: 1, 2, & 3, (of which we are primarily concerned with type-2, because the type-3 variety seems to primarily be less relevant in humans than in other animals, and because Albuterol doesn’t stimulate the type-1 receptor). There also exists a type of receptor known as an alpha receptor, which isn’t relevant here, but warrants a brief explanation.

Alpha receptors differ from beta receptors in that they are activated at significantly lower catecholamine levels than are the beta receptors. A catecholamine is simply an organic compound that affects the sympathetic nervous system. For example, dopamine, norepinephrine and epinephrine are all catecholamines.

We are, as I said previously, mostly concerned with Beta-2 receptors, because those are what we see stimulated with Albuterol. It should come as no surprise to anyone who has used Clenbuterol as well as Albuterol is that when you stimulate your beta receptors, it causes something called vasodilatation (increased blood flow). Stimulation of these receptors also stimulates the break down of fatty acids into the blood stream for use as fuel, which causes a reduction in stored fat. Of course, this increased blood flow also comes with an increased heart rate.

This explains how Beta-2 adrenergic stimulation can also increase your body temperature a bit…however this isn’t something that’s too noticeable on a thermometer…most people will feel a bit hotter, and some will even break a sweat (I fall into the latter category). Beta-agonists work to do this by increasing heat production in the cell’s powerhouse, the mitochondria, which will also increase your basal metabolic rate, and decrease your appetite. Not too many people feel hungry after a whopping dose of stimulants.

There is also some evidence that Beta-Agonists are anabolic (more properly, however, this would actually be anti-catabolic). This is because Beta-agonists also act to initiate a hormonal cascade that involves the activation of a compound called cAMP (basically: cyclic-Adenosine Monophosphate). After this, cAMP activates calpistatin that is the inhibitor of calpain. Calpain works to degrade protein in skeletal muscle (among other functions). Therefore, we already saw that how stimulation of beta 2 receptors have the ability to increase energy expenditure and free up body fat to be used as fuel, and now we have some understanding of how that stimulation can also have the potential to be anti-catabolic as well .

Now that we’re all on the same page regarding the beta-adregenic system, and what sorts of effects we can expect when we stimulate it with beta-2 agonists…lets take a more specific look at Albuterol, and why I think it’s such a great compound.

When we take a look at Albuterol’s ability to burn fat, it’s clear that it has the ability to aid fat loss in both normal as well as obese men (2). That’s not very different from Clenbuterol, in any way. However, in my personal experience with it, I think that Albuterol really outperforms Clen in areas of strength gains as well as for athletic purposes….lets take a look at my claim and see how Albuterol performs in humans…

In one study, subjects were given Albuterol and performed 9 weeks of isokinetic knee extensions (there was also a group who performed the same exercise routine but were not given Albuterol). The Albuterol group, predictably, had better strength gains than the non-Albuterol group (only a therapeutic dose was given) (3). In my own experience, strength gains with Albuterol are much better and seen more quickly than I see them with Clen. In fact, while I don’t particularly experience much of a performance enhancing effect from Clen in the gym; on the other hand I see strength gains and muscular improvements within the first couple weeks of using Albuterol. Of course, this is likely a pure anabolic effect and probably not easily explained as a simple “enhanced” anti-catabolic effect, and likely can’t be explained away with the Calpain idea you read about earlier. I still think that I can take a pretty good shot at explaining why Albuterol is anabolic, though. strong body of evidence exists to suggest that Albuterol influences the release of cAMP. As you may know, cAMP also plays an important role in mediating certain catecholamines secreted by the adrenal medulla have an inhibitory effect on muscle dependent protein degradation, but in addition, norepinephrine released from adrenergic terminals may actually increase the rate of protein synthesis(not just decrease the rate of their degradation) in oxidative muscles, thereby leading to increased protein accretion (representing a true anabolic effect). That’s most likely the way that we receive part of the anabolic effect from Beta-stimulation. Another way is perhaps through the beta-adrenergic stimulated lowering of “Interleukin-6″ from fat cells (long story…).

Anecdotally, Clenbuterol and ephedrine have both shown themselves capable of temporarily increasing strength, and I would bet most beta-agonists have this effect, but I don’t think has been shown as conclusively in the medical literature as it has been with Albuterol. Albuterol has been shown to increase muscle size (3-6) as well as strength and endurance (3) (*while people have anecdotally reported that Clen seems to lower their aerobic capacity. Clenbuterol has a disadvantage when compared with Albuterol in the area of strength gains, probably due to the act that it use-dependently inhibits action potential firingin skeletal muscle fibers, which is not directly caused by inherent Beta-2 stimulant activities (7) . I think that’s the best quasi-scientific explanation I Again, my own personal experience and that of my research assistant(s) would also seem to strongly support this claim…all of us have gotten leaner, bigger and stronger with the use of Albuterol, while with Clen, we got more ripped but not really stronger (and certainly not much bigger). Anecdotally, we’ve seen Clenbuterol fall a bit flat when people use it for anabolic effects, although in animals it would appear to be highly anabolic, though human studies are a bit shaky (ha!) in this area.

One of the things I really like about Albuterol is that it has the potential to actually be used on my cycle to make it safer by improving my lipid profile (cholesterol)…or during PCT to help get my cholesterol levels back in check. This is because Albuterol shows significant benefits to cholesterol as it works to lower total cholesterol, specifically LDL (the bad stuff) while at the same time elevating HDL (the good stuff).(8)

In my own particular case, cholesterol never seems to be an issue, but now that I’m working with Oasis for HRT, it’s certainly in my best interests to show up every three months with nice looking blood work.

So now is the part you’ve been waiting for (*or the part you skipped to, ignoring the rest of the article…whatever…). How much of this should you take, and how often? Well, I can tell you that I have found the best results by working my way up from 4mgs taken once a day, up to 4-8mgs taken 3x a day. I know that some people will think that 24ms a day of this stuff is going to be too much (it is, after all, a stimulant). But I can tell you that I have a pretty good tolerance for stimulants (I’ve taken up to 200mcg/day of Clenbuterol, and some other pretty hefty stimulants that I probably shouldn’t mention in polite company). Most people are going to find their sweet spot at about 4mgs of Albuterol 3x a day or so…women will probably take about half that dose, and be fine with it.

I think that Albuterol is about to become very popular, very soon…and I, for one, am looking forward to seeing less of my old Clen article around the ‘net, and more of this one.

More Steroid Articles from MESO-Rx:

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Originally published at: Albuterol (Salbutamol)

Anabolicum Vister (quinbolone) is a prodrug of boldenone. It is the exact same molecule but with a cyclopentenyl ether modification at the 17beta hydroxy position. Unlike the ester modifications at the 17 position commonly used for injectable anabolic steroids, this modification provides enhanced oral bioavailability.

As with esterified compounds, the Anabolicum Vister molecule is not active in its modified form, and becomes effective only when the cyclopentenyl ether group is metabolically removed, yielding boldenone. At this point, properties are the same as boldenone delivered via de-esterification of injected boldenone undecylenate or other boldenone ester. The duration of action of this oral form is almost undoubtedly much shorter, however.

Quinbolone is not very potent (effective per milligram) compared to injected boldenone undecylenate (Equipoise) or any injected anabolic steroids, or to most oral anabolic steroids. I know of no athletes who use this product.

Quinbolone is the chemical name of active ingredient in Anabolicum Vister. Anabolicum Vister was a registered trademark of Parke Davis (Italy) in the United States and/or other countries prior to cancellation.

No related posts.

Originally published at: Anabolicum Vister (Quinbolone)

Anadrol (oxymetholone) is perhaps only second to Dianabol (methandrostenolone) in importance as an oral anabolic in bodybuilding. This is due to its undoubted efficacy. Like Dianabol, Anadrol does not bind strongly to the androgen receptor (AR). Most of the anabolism it provides is therefore presumably via non-AR-mediated effects.

When using either Anadrol or Dianabol at maximum recommended dose, adding more of the other seems to yield no additional effect. For this reason, generally one drug or the other is chosen, rather than taking both at the same time.

In contrast, combining Anadrol with even a very high dose of a Class I steroid such as trenbolone, Anavar, or Primobolan yields a large increase in effect Oxymetholone does not aromatize: there is no conversion to estrogen.

Contrary to what many bodybuilders expect of it, the drug can be mild in terms of side effects when no aromatizing steroids are present.

Nonetheless, when oxymetholone is used in a cycle yielding high estrogen levels, it is notorious for worsening apparently-estrogenic symptoms. This may be from its producing progestagenic symptoms which are easily confused as being estrogenic; from altering estrogen metabolism; by upregulating aromatase; or perhaps by increasing prolactin. The actual cause is not proven.

There is some indirect evidence that this may be from progestagenic activity, as in some cases concurrent use of Winstrol (stanozolol), which has some anti-progestagenic effect, can avoid the problem. Some have also reported Dostinex (cabergoline) usage, which reduces prolactin, to yield a remedy.

It is primarily in the context of usage in high-estrogen circumstances that Anadrol has earned a reputation of being a harsh drug. An example such use would be combination with high-dose testosterone without an aromatase inhibitor. Most do not find it harsh when there are no concurrent problems with high estrogen.

Regardless of being non-aromatizable, in those who have developed gynecomastia already Anadrol can be an aggravating agent, even with estrogen levels kept normal. It may also be a causative agent.

For those with gynecomastia problems who are considering Anadrol and are uncertain of their response to it, rather than rely on cabergoline and/or Winstrol for protection, I recommmend instead using Dianabol with an aromatase inhibitor or a selective estrogen receptor modulator (SERM) such as Clomid or Nolvadex.

Those not having pre-existing gynecomastia generally do well with Anadrol provided estrogen levels are not allowed to become excessive during the cycle. The above protective measures generally will not be required.

It is not unusual for a first time user to do quite well on an oxymetholone-only cycle, but the most effective use comes with stacking with a Class I steroid. Typical use is 50-150 mg/day, which is best divided into several doses per day. Higher daily doses have been used but it is not at all clear that there is any further anabolic effect from doing this. It seems to me that there is not.

When used alone, testosterone production may not completely suppressed, as there seems no indication that estrogen levels drop abnormally low, as occurs with completely suppressed testosterone production. If stacking with a non-aromatizing injectable, some amount of testosterone or other aromatizable steroid should also be used; or alternately the testosterone can be provided via low-dose HCG usage. If injectable testosterone is used, even 100 mg/week is sufficient for this purpose.

Because oxymetholone is 17-alkylated, it is stressful to the liver. It is better to limit use to no more than 6 weeks before taking a break of at least equal length.

While I cannot recommend anabolic steroid use for women at all, contrary to what many expect based on perception of men with regard to entirely differing side effects,

Anadrol has been shown medically to have a low rate of virilization at doses considerably higher than needed for non-extreme female bodybuilding or strength training. A total dosage of 25 mg/day is only half of the minimum medical dose ever routinely used, but is remarkably effective for muscle anabolism in women. Even 12.5 mg/day can be quite effective. As with any female use of oral anabolic steroids, divided doses across the day are probably safer than single-dose use for given total dosage per day, as peak levels will not be as high.

Oxymetholone is the name of active ingredient in Anadrol. Anadrol is a registered trademark of Unimed Pharmaceuticals in the United States and/or other countries.

Balkan Anapolon aka Anadrol (Oxymetholone)

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Originally published at: Anadrol (Oxymetholone)

Anadur (nandrolone hexylphenylpropionate) has a longer half life than Deca Durabolin (nandrolone decanoate). The claim that aromatization is less than with Deca Durabolin is unlikely to be correct. Because of the longer half life, for the same dose, there will be less drug in the blood during the first few weeks of use, thus creating this illusion. If blood nandrolone levels are the same, giving comparable effectiveness, rate of aromatization would be the same with Anadur or Deca.

This is true for all claims made for varying rates of aromatization according to ester. I do not think such claims are ever correct given equal blood levels of drug, and they certainly are not substantiated in the scientific literature.

The claim that 50-100 mg Anadur per 10 days will normally result in no virilization symptoms for women will be over-optimistic for many female users. Only a few weeks of such use will result in some irreversible virilization for some women. This is true for substantial doses of any anabolic steroid. If a drug is an agonist (activator) of the androgen receptor it will have virilization activity if given at a high enough dose. That dose will vary according to the individual’s susceptibility, and according to the specific tissue.

No related posts.

Originally published at: Anadur (Nandrolone Hexylphenylpropionate)

Anavar (oxandrolone), unlike most oral compounds is categorized as a Class I anabolic steroid, most efficiently stacked with Class II compounds such as Dianabol or Anadrol. It adds little if anything to high-dose use of Class I anabolic steroids such as trenbolone, or to high-dose testosterone, which is classified as having mixed activity. It can be an aid, albeit an expensive one, to moderate dose testosterone usage.

Anavar has often been called a weak steroid. Part of the reason for this is that use of a Class I steroid alone never is maximally effective. The other cause is that bodybuilders and authors in the field sometimes make unfortunate and unreasonable comparisons when judging anabolic steroids. If say 8 tablets per day does little, then a drug is pronounced useless or weak. And traditionally, oxandrolone was available in 2.5 mg Anavar tablets, proving only 20 mg daily with such usage, which totals to only 140 mg/week. For comparison, testosterone at that dose also gives little results. Indeed, few anabolic steroids give dramatic results at that dose, but they are not called weak on that account. The proper conclusion is that such Anavar tablets were individually weak, but not that the drug lacks potency.

As higher-dose Anavar tablets have become available, the oxandrolone’s reputation has improved. However, it still is not a particularly cost-effective Class I steroid, and if used alone cannot match the performance of a good stack.

Pharmacologically, it has been found that oxandrolone binds weakly to the androgen receptor. This seems inconsistent with the Class I / Class II system, but it is what has been found. Perhaps it is the case that what occurs in the body is not the same as occurs in in vitro study, or perhaps there is another interesting phenomenon occurring.

From the practical standpoint, however, oxandrolone’s stacking behavior requires that it be classified as a Class I steroid: it combines synergistically with those categorized as Class II, but only additively with Class I compounds. From the practical standpoint, it is a rather potent drug – that is to say, it has good effectiveness per milligram. Stacked with a Class II steroid, Anavar is quite effective at only 75 mg/day, or even 50.

Anavar does not aromatize or convert to DHT, and has an 8 hour half-life. Thus, a moderate dose taken in the morning is largely out of the system by night, yet supplies reasonable levels of androgen during the day and early evening.

One study found oxandrolone to be superior to testosterone and to Deca (nandrolone) for reducing abdominal fat in men, or at least in obese older men at the specific low doses studied, which were not necessarily equipotent. From this, some have made broad generalizations to bodybuilding. However, this does not necessarily carry over to anabolic steroid cycles at doses commonly used in bodybuilding. In the case of the study in question, I expect the difference in outcomes was dose-related.

In practice, at total androgen doses typically used, one can cut just as effectively without oxandrolone as with, given any of various possible substitutions for the oxandrolone. This is not to say this drug is ineffective, but rather that other androgens including testosterone are also effective at high dose for abdominal fat loss.

In the case of low-dose use however, I do think it is a correct conclusion that for most, low dose Anavar use is more effective for cutting than equal dosages of most other anabolic steroids. This may be partly or entirely from additive effect with natural testosterone: such oxandrolone use may not suppress such its production, the user may enjoy both the full effect of his natural testosterone and the effect of the oxandrolone. In contrast, low-dose testosterone or nandrolone use results in substantial suppression of natural testosterone, and so there is less total effect.

Oxandrolone, as with other 17-alkylated steroids, is hepatotoxic. At one time it was thought that it is not, but both clinical and practical experience with Oxandrin has shown that liver toxicity can indeed be an issue with prolonged use. I believe the usual principle of limiting 17-alkylated use to 6 weeks at a time should be applied when oxandrolone is used, just as with any alkylated oral.

Trenbolone or Primobolan are suitable substitutes for Anavar, without the liver toxicity issues. As a substitute, Primobolan shares the property of being low-suppressive, while trenbolone does not.

An interesting application of the drug that takes advantage of its oral administration is use as a morning-only bridging agent between cycles, which in my opinion should be done – if done – only after fully recovering normal testosterone production from the last cycle. At least 20 mg is usually acceptable in this application. Ideally, testosterone levels will be measured to monitor such bridging. A factor limiting to such bridging is the liver toxicity issue.

With regard to use by women, while there is a common belief that Anavar is minimally virilizing to female, in fact virilization is not unusual at 20 mg/day and can occur at considerably lower doses than that. Even 5 mg/day is not side-effect-free for all.

During a cycle, oxandrolone is not particularly recommended because there are more cost-efficient choices that will fully accomplish the same goals and do not add to liver toxicity.

The two best uses for Anavar are in optional bridging periods between cycles, if such are employed, while keeping care to avoid excessive duration of continuous 17-alkylated use; and, if short-acting injectables are not available, to supplement cycles as levels fall between the time of last injection and the start of post-cycle therapy so that that time period can remain effective for gains.

Oxandrolone is the chemical name of active ingredient in Oxandrin and Anavar. Anavar was originally the registered trademark of Searle Laboratories. Oxandrin is a registered trademark of Bio-Technology General Corp. in the United States and/or other countries.

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Originally published at: Anavar (Oxandrolone)

Andriol, is a unique version of testosterone undecanoate developed by Organon. This version of testosterone is based in oil and is sealed in a capsule to be taken orally. According to the manufacturer, this method bypasses the liver and enters the body as a fat through the lymphatic system.

In theory this seems quite interesting, however, athletes find Organon’s claims don’t hold up well. In doses of less than 240mg per day effects are generally non-existent. With higher doses, effects are small at best. This leads one to think most of the steroid is not making it to circulation.

Generally, steroid users experienced with any strong anabolics will be disappointed with Andriol’s results. Combined with other anabolics it may lend some effectiveness but should be questioned.

Testosterone undecanoate is the chemical name of active ingredient in Andriol. Andriol is a registered trademark of Organon Corporation in the United States and/or other countries.

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Originally published at: Andriol (Testosterone Undecanoate)

Androgel is the first testosterone gel approved by the FDA for hormone replacement therapy in men suffering from conditions involving low testosterone. Low testosterone, also known as hypogonadism, affects approximately four to five million American men. The condition is linked with diminished interest in sex, impotence, reduced muscle mass, decreased bone density and depressed mood and energy levels. 

Androgel’s unique transdermal delivery system offers many benefits. Those traumatized by needles will surely enjoy rubbing in testosterone to the skin, opposed to injecting it intra-muscularly. Although the therapeutic dose may fall short of being anabolic enough for bodybuilders and athletes.

Testosterone is the chemical name of active ingredient in AndroGel and Androderm. Androgel is a registered trademark of Unimed Pharmaceuticals. Androderm is a registered trademark of Watson Pharmaceuticals, Inc.

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Originally published at: Androgel (Transdermal Testosterone)

Arimidex (anastrozole) 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. Arimidex does not have the side effects of aminoglutethimide (Cytadren) and can achieve a high degree of estrogen blockade, much moreso than Cytadren. It is possible to reduce estrogen too much with Arimidex, and for this reason blood tests, or less preferably salivary tests, should be taken after the first week of use to determine if the dosing is correct.

As an aromatase inhibitor, Arimidex’s mechanism of action — blocking conversion of aromatizable steroids to estrogen — is in contrast to the mechanism of action of anti-estrogens such as clomiphene (Clomid) or tamoxifen (Nolvadex), which block estrogen receptors in some tissues, and activate estrogen receptors in others. During a cycle, if using Arimidex, there is generally no need to use Clomid as well, but (as mentioned in the section on Clomid) there may still be benefits to doing so.

Arimidex at 0.5 mg/day is usually sufficient for moderate dosages of testosterone and in some cases may be too much.

(Author note: Years back, aromatase inhibitors such as Arimidex and letrozole were much more expensive than Cytadren and much less available, so in the past Cytadren was often used as an aromatase inhibitor. That use is today obsolete.)

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Originally published at: Arimidex (Anastrozole)

Aromasin (Exemestane) is one of those weird compounds that nobody really knows what to do with. What we generally hear about it makes it very uninteresting…It’s a third generation Aromatase Inhibitor (AI) just like Arimidex (Anastrozole) and Femera (Letrozole). Both of those two drugs are very efficient at stopping the conversion of androgens into estrogen, and since we have them, why bother with Aromasin?

It’s a little harder to get than the other two commonly used aromatase inhibitors, because it’s not in high demand, and there’s never been a readily apparent advantage to using it. And I mean…lets face it: It’s awkward-sounding. Aromasin doesn’t have much of a ring to it, and exemestane is even worse. Arimidex has a bunch of cool abbreviations (“A-dex” or just ‘dex) and even Letrozole is just “Letro” to most people. Where’s the cool nickname for Aromasin/exemestane? A-Sin? E-Stane? It just doesn’t work. It’s the black sheep of AIs.

And why do we even need it when we have Letrozole, which is by far the most efficient AI for stopping aromatization (the process by which your body converts testosterone into estrogen)? Letro can reduce estrogen levels by 98% or greater; clinically a dose as low as 100mcgs has been shown to provide maximum aromatase inhibition (2)! So why would we need any other AIs?

Well, first of all, estrogen is necessary for healthy joints (3) as well as a healthy immune system (4). So getting rid of 98% of the estrogen in your body for an extended period of time may not be the best of ideas. This may be useful on an extreme cutting cycle, leading up to a bodybuilding contest, or if you are particularly prone to gyno, but certainly can’t be used safely for extended periods of time without compromising your joints and immune system.

So that leaves us with Arimidex, which isn’t as potent as Letrozole, but at .5mgs/day will still get rid of around half (50%) of the estrogen in your body. Problem solved, right? Use Arimidex on your typical cycles, and if you are very prone to gyno or are getting ready for a contest, use Letro.

But what about Post Cycle Therapy (PCT)?

I think at this point most people are sold on the use of Nolvadex (Tamoxifen Citrate) instead of Clomid for PCT, since both compete estrogen at the receptor site, both increase serum test levels, and both drugs may also alter blood lipid profiles favorably (6). But since 20mgs of Tamoxifen is equal to 150mgs of clomid for purposes of testosterone elevation, FSH and LH, but Tamoxifen doesn’t decrease the LH response to LHRH (6) I think most people agree to Nolvadex’s superiority for PCT.

I’ve always been in favor of using Nolvadex during PCT, along with an AI, because reducing estrogen levels has been positively correlated with an increase in testosterone (7) so in my mind, it’s be beneficial to increase testosterone by as many mechanisms as possible while trying to recover your endogenous testosterone levels after a cycle. SO which AI do we use? Letro or A-dex? Well, why don’t we just keep using whichever one we used during the cycle, and add in some Nolvadex? Unfortunately, Nolvadex will significantly reduce the blood plasma levels of both Letrozole as well as Arimidex (8). So if we choose to use one of them with our Nolvadex on PCT, we’re throwing away a bit of money as the Nolvadex will be reducing their effectiveness.

This, of course, is where Aromasin comes in, at 20-25mgs/day.

Aromasin, at that dose, will raise your testosterone levels by about 60%, and also help out your free to bound testosterone ratio by lowering levels of Sex Hormone Binding Globulin (SHBG), by about 20% (12)…SHBG is that nasty enzyme that binds to testosterone and renders it useless for building muscle. But what about using it along with Nolvadex for PCT?

To understand why Aromasin may be useful in conjunction with Nolvadex while both Letro and A-dex suffer reduced effectiveness, we’ll need to first understand the differences between a Type-I and Type-II Aromatase Inhibitor. Type I inhibitors (like Aromasin) are actually steroidal compounds, while typeII inhibitors (like Letro and A-dex) are non-steroidal drugs. Hence, androgenic side effects are very possible with Type-I AIs, and they should probably be avoided by women. Of course, there are some similarities between the two types of AIs…both type I & type II AIs mimic normalsubstrates (essentially androgens), allowing them to compete with the substrate for accessto the binding site on the aromatase enzyme. After this binding, thenext step is where things differ greatly for the two different types of AI’s. In the case of a type-I AI, the noncompetitive inhibitorwill bind, and the enzyme initiates a sequence of hydroxylation; this hydroxylation produces an unbreakable covalent bond betweenthe inhibitor and the enzyme protein. Now, enzyme activity is permanently blocked; even if all unattached inhibitor is removed.Aromatase enzyme activity can only be restored by new enzyme synthesis. Now, on the other hand, competitive inhibitors, called type II AI’s, reversibly bind to the active enzymesite, and one of two things can happen: 1.) either no enzyme activity is triggered or 2.) the enzyme is somehow triggered withouteffect. The type II inhibitor can now actually disassociate from the binding site, eventually allowing renewed competition between the inhibitor and the substratefor binding to the site. This means that the effectiveness of competitive aromatase inhibitors depends on the relative concentrations and affinitiesof both the inhibitor and the substrate, while this is not so for noncompetitive inhibitors. Aromasin is a type-I inhibitor, meaning that once it has done its job, and deactivated the aromatase enzyme, we don’t need it anymore. Letrozole and Arimidex actually need to remain present to continue their effects. This is possibly why Nolvadex does not alter the pharmacokinetics of Aromasin (11).

Before we close the book on Aromasin, it’s worth noting that you can (and should) still use one of the non-steroidal AIs during your cycle to reduce estrogen, if necessary. When you are ready for PCT, you can then switch over to Aromasin and still experience the full effects of an AI, since there is no cross-over tolerance experienced between steroidal and non-steroidal AIs (9). Since Aromasin is about 65% efficient at suppressing estrogen (10), it’s certainly a very powerful agent, especially considering you won’t experience reduced effectiveness because of your concurrent use of Nolvadex or from any sort of tolerance developed by using other AIs on your cycle(9). There is also a decent amount of preclinical data suggesting that Aromasin has a beneficial effect on bone mineral metabolism that isnot seen with non-steroidal agents, and it may also have beneficial effects on lipid metabolism that are notfound in the non-steroidal Letro and A-dex (9).

Finally, as we’re going to be using Nolvadex for PCT anyway, and we ought to be using an AI with it for maximum recovery…I think Aromasin- considering it’s compatibility with Nolvadex and beneficial effects on bone mineral content and lipid profile, has finally stopped being the black sheep of AIs and found a home in our Cycles.

More Steroid Articles from MESO-Rx:

• Nolvadex (Tamoxifen Citrate)
• Arimidex (Anastrozole)
• Clomid (Clomiphene Citrate)

Originally published at: Aromasin (Exemestane)

Dutasteride, along with Finasteride is a 5-alpha-Reductase inhibitor which are a group of drugs with anti-androgenic properties which inhibit the conversion of testosterone into dihydrotestosterone (DHT). This is the same chemical found in Proscar and Propecia and is used in the treatment hyperplasia and androgenic alopecia. Because these drugs reduce levels of dihydrotestosterone (DHT) they are used to prevent and treat hairloss. It is most commonly used to treat enlarged prostate glands.

Background

Dutasteride is marketed pharmaceutically as Avodart, Avidart, Avolve, Duagen, Dutas, Dutagen, Duprost. For unknown reasons, early clinical trials for dutasteride were abruptly ceased in 2002 (1), then continued later.

Action

Dutasteride is a 5-alpha-reductase inhibitor, meaning it blocks the action of the 5a-reducatse enzymes, that are responsible for 5a-reducing (converting) testosterone into dihydrotestosterone (DHT) by the addition of a double hydrogen bond.

Technical Data

Dutasteride inhibits both isoforms of 5a-reductase, therefore preventing the conversion of testosterone into dihydrotestosterone. This makes Dutasteride a reasonable treatment for Male Pattern Baldness (2). Of course, when you convert less Testosterone into Dihydrotestosterone, you increase testosterone levels by default (less conversion).

Dutasteride, at 2.5mgs/day is roughly 1.5x more effective than Finasteride at 5mgs/day, at treating hair loss (both halting it as well as regrowing it). In addition, Dutasteride can be used successfully at that same dose to treat prostate enlargement (3), and a lesser known effect of Dutasteride (again, at that same dose) use is to treat Acne (4) caused by an overabundance of androgens in the body.

User Notes

For the steroid using athlete suffering from DHT-related side effects, Dutasteride may be the answer. Hairloss, Acne, and prostate growth can all (potentially) be completely halted with the use of this product. Unfortunately, DHT is not all bad, and you potentially lose some muscle hardness (an amorphous quality if ever there is one), and even some of the other qualities we like from our androgen use.

Also…since this only prevents the 5a-reduction of the androgens subject to that conversion into a dihydro form of them…it will likely do nothing to stop hairloss or other symptoms caused entirely by the use of the androgens in the DHT family.

Dutasteride is the name of active ingredient in Avodart. Avodart is a registered trademark of GlaxoSmithKline in the United States and/or other countries.

References

• Am J Hum Genet. 2005 Jul;77(1):140-8. Epub 2005 May 18
• The importance of dual 5alpha-reductase inhibition in the treatment of male pattern hair loss: results of a randomized placebo-controlled study of dutasteride versus finasteride.J Am Acad Dermatol. 2006 Dec;55(6):1014-23. PMID: 17110217 [PubMed - indexed for MEDLINE]
• [Dihydrotestosterone and the role of 5 alpha-reductase inhibitors in benign prostatic hyperplasia]Urologe A. 2002 Sep;41(5):412-24. Review. German
• Testosterone metabolism in human skin cells in vitro and its interaction with estradiol and dutasteride.Skin Pharmacol Appl Skin Physiol. 2003 Nov-Dec;16(6):356-66. PMID: 14528059 [PubMed - indexed for MEDLINE]

More Steroid Articles from MESO-Rx:

• Proscar (Finasteride)
• DHT (Dihydrotestosterone)
• Primobolan Depot (Methenolone Enanthate)

Originally published at: Avodart (Dutasteride)