Stop Me Before I Eat My Computer

Q: I have a problem maybe you can help me with — my ravenous appetite. Anything new out there in the drug world to really suppress the appetite? I need to get lean by summer!

A: I honestly don’t know of anything "new" on the market, nor do I know of anything that'll hit your local pharmacy any time soon.

Meridia (Sibutramine) is relatively new but really hasn’t been shown to be more effective than other anorectic compounds. Bontril (phendimetrazine), Tenuate (diethylpropion hydrochloride), Adipex and Fastin (both phentermine) are typically what'll be prescribed for those who have problems with excessive appetite. Phentermine is definitely the most popular simply because it’s cheap and most physicians are familiar with it.

While there are more mechanisms through which we may be able to suppress appetite, what we currently have on the market basically focuses on suppressing appetite via noradrenergic and/or serotoninergic manipulation. While there's ongoing research involving the use of drugs which focus on hypothalamic neuropeptide and other peptide system modulation, I don’t know of any that are readily available as of yet.

I’d suggest trying HOT-ROX. It may not kill the appetite as thoroughly as you’d like, but it’ll help lean you up by summer.

Origami for Gearheads

Q: My gym's resident steroid dealer offered me some "papervar." What the hell is that? Any good?

A: These products have been around for a good number of years. It's basically just an edible paper impregnated with a steroid. To get the right dose, you eat a certain size square of paper that usually has grids on it. This stuff was basically invented so that steroids could be sent through the mail and have a better chance of getting to the recipient than tablets, vials and bottles. It makes a good product in terms of concealment.

During my second year of undergraduate studies, I bounced at a local club and the guys in the back (other bouncers) would break off pieces of these "paper" products and continually suck all the powder out.

I remember there were products like papervar (containing oxandrolone), paperstrol (containing stanozolol), paperbol (containing methandrostenolone), and I’m sure someone has made some paper products that contain other 17 alpha-alkylated androgens.

As for them being good, I can’t say I’ve ever heard of any complaints.

'Roids to Avoid

Q: Are there any anabolic steroids out there you'd say to definitely stay away from? In other words, what's the worst 'roid on the market?

A: Methylandrostenediol or Methandriol is rather estrogenic and doesn’t really provide much of an anabolic effect to warrant its use. I believe some companies are even trying to sell this as a dietary supplement now. That’s idiotic regardless of which way you approach it!

Other than that, I can’t really say there are really any androgens you should avoid completely in every case. Nandrolone (Deca) probably isn’t the best choice in terms of an androgen, but for those who like it, more power to them.

On the Money

Q: I make porn movies. With drugs like Cialis and Viagra, I no longer have to worry about maintaining erections for long periods, but I’d really like to enhance my "money shot," if you know what I mean. What steroids will help me do this? Any other herbs or supplements that work to this end?

A: As far as androgens, I don’t think that’s the way you want to go. You may see a small increase initially, but it'll either return to normal quickly or after prolonged use of large dosages, seminal volume may even decrease.

Maca (Lepidium Meyenii), a Peruvian plant, is about the only non-prescription compound that I could find that effectively increased seminal volume in normal men. The drug clomiphene, anecdotally, has a great reputation for increasing seminal volume but I’ve yet to see any data supporting it.

Other than that, hCG could be used as it’s been shown to be effective in that regard, but that’s something I’d only recommend to someone whose livelihood depended on their "money shot."

Lastly, in animal models at least, it’s been shown that compounds that possess an anti-oxidative effect can benefit seminal volume. In any event, it certainly doesn’t hurt to continue taking your daily multivitamin and antioxidants. (6)

Steroids Like Pammy Anderson's Ta-Ta's

Q: What's the most faked steroid on the market?

A: From what I’ve seen, the rate of counterfeiting has gone down considerably. Why? The huge increase in the number of bootleggers as well as outfits that sell the various components needed to compound your own product have led to a drop in counterfeits.

When considering those two factors, it doesn’t really make sense to make counterfeit products. Back when you had only a few major brands around (Denkall, Loeffler, Tornel, etc.), it made sense for someone to pick out one brand and then begin making counterfeits. Now that people have the option of making their own or purchasing from one of the various bootleggers, the popularity of name brand products has gone down considerably.

This isn’t to say there aren’t any fakes out there, but the likelihood that someone has counterfeited a bootlegged product that has little popularity doesn’t make sense from a financial standpoint. Considering there are so many smaller bootlegging outfits, it’s nonsensical for someone to pick one out and begin making counterfeit products as it would only be a small matter of time before someone caught on and simply switched to another bootlegged product.

Aside from that, although I’m not one to investigate "what’s being faked" in depth, one thing I’ve always received many reports on were counterfeit Sustanon ampoules. If there were one thing I wouldn’t use, that’d probably be it.

Aside from that, more often than not, the guys who use it are only doing so because it’s one of the few products they actually know the name of. In other words, they’re usually the guys who're just starting out and the only things in their vocabulary are "Sostenon, Deca, and D-bol, dude."

If you want to use Testosterone, simply use Testosterone cypionate, enanthate or propionate. Many "powder" manufacturers also have Testosterone decanoate and undecanoate available.

MAG-10 for Dieting?

Q: What’s the wisdom of the following plan: I want to go on a relatively severe calorie restriction diet so I can get fairly cut up in about four weeks. I want to use MAG-10 during my diet phase — not to bulk up, but to preserve muscle mass. Is this shortcut wise or dopey?

A: I think it’s a great idea and I’ve gone over this plan in a detailed article here. Essentially, using androgens while dieting can allow you to preserve lean body mass and in some cases increase muscle while reducing fat mass.

Androgens and Protein

Q: A friend of mine who's done several cycles said you have to get at least two grams of protein for every pound of body weight if you want to maximize the steroid or pro-steroid cycle. Is that about right? Do I need that much protein when using something like MAG-10?

A: Yes, I believe you do. Anecdotally, I've found that one needs at least 1.5 to 2.0 grams of protein per pound of body weight to benefit the most while using androgens.

Androgens are always most beneficial when combined with a high-protein diet, whether you’re someone recovering from some trauma which caused a loss of lean body mass or you’re a bodybuilder who’s consistently training with weights and already has a great deal of LBM to support.

I can’t count how many times I’ve read letters from guys who have no clue what they’re doing. They’ll e-mail me saying the gear they’ve purchased must have been counterfeit "'cuz I only gained like three pounds in three weeks." But when I ask what their protein and overall caloric intake was, they have no idea. "You mean I have to eat a lot of food and protein to make gains? You mean muscle just doesn’t magically appear because I’m using steroids? You mean I’m not going to turn into that big guy from that Program movie?"

Yes, these are the people I’d like to bitch slap. Not surprisingly, I’ve seen the same exact letters from guys complaining that prosteroids "don’t work." When I ask them what their protein and overall caloric intake was, they again have no clue what I’m talking about. The simple fact is that you have to give the supplement or steroid something to work with, and that means getting a ton of protein!

Shady Science

Q: Hey, Cy-Borg, what's up with this Methyldienolone stuff? [17a-methyl-17b-hydroxyestra-4, 9(10)dien-3-one] It's supposed to be 1.1 times as anabolic as Methyl-1-Testosterone (according to those who sell it) while being only 15% as androgenic. What do you think?

A: What do I think? Well, I think the people selling it and the people in the community in general need to put down their copy of Vida’s book and realize some facts. The collections such as Vida’s which have bioassays used to measure anabolic/androgenic activity in rats, are at the very best inaccurate when applying the data to the same species.

Extrapolating from one species to another (in this case, a rat to a human) is a very big "no no" in any scientist's book. It’s just not something you do. When scientists see such things occurring in the supplement industry, it’s no wonder they don’t take most of the community seriously. Animals in general are merely research tools used as a rough model for study. Data obtained from such studies isn’t meant for direct extrapolation across species, and this case, to humans.

For those of you who don’t know why such a thing can’t be done, let me explain. First, it’s pretty well known that metabolism is quantitatively and/or qualitatively different in various animal species. For instance, from a toxicological standpoint, there are many compounds that humans can tolerate in large quantities whereas other animals could die from even a small amount.

The reverse is true as well. Humans can tolerate a large amount of ibuprofen, whereas even small amounts of ibuprofen can cause complete renal failure in dogs. Furosemide (Lasix) was found to cause liver damage in mice but has no effect on the liver in humans. Owls can consume cyanide and sheep can consume arsenic without any problems, but let a human try consuming those substances and there'll be side effects, like death! Rats can tolerate much larger quantities of nicotine before toxicity ensues as compared to mice, and mice can tolerate much larger quantities of carbon tetrachloride than rats. The list goes on and on.

You have to remember that a parent compound can be converted into other compounds that may be more powerful, less powerful, toxic or completely inactive. Let’s say you give compound X to a rat and he gets muscular, loses fat and gets a really hot rat girlfriend. When you give compound X to a human, there’s no effect, or worse yet, it’s highly toxic. Upon further investigation, it turns out the rat has an enzyme which humans lack or vice versa. See what I mean?

Along these same lines, I’m sure you’ve all seen the literature in the past in which beta 3-adrenergic receptor agonists had some significant effects in terms of reducing fat mass in rodents. Unfortunately, the same great results couldn’t be duplicated in humans. Why? A primary mechanism of action in rodents was beta 3-adrenergic receptor agonism and consequently, hypertrophy of BAT (Brown Adipose Tissue. Think "the brown fat that burns the white fat.") Unfortunately, we humans not only have lower levels of beta 3-adrenergic receptor mRNA in adipose tissue, but more importantly very little BAT as adults.

In many cases, it was this discrepancy that revealed why these compounds worked so well in rodents but not in humans. There were also pharmacological differences between human and rodent beta 3-adrenergic receptors. Oral bioavailability was an issue, too. In any event, this again demonstrates that a compound that was very effective in rodents had little effect in humans.

Anyhow, I’ve written all of that and I haven’t even begun to touch upon the validity of the bioassay used to gather the data found in Vida’s collection. Keep in mind all of these bioassays (commonly referred to as the Hershberger Assay or a modified version thereof) aren’t really accurate themselves.

Basically, what it involved was injecting a given androgen intramuscularly into castrated male rats and then measuring the effect on the growth of the seminal vesicles, ventral prostates and levator ani muscles. These values were then compared to the values found when the animals were administered Testosterone or another androgen of choice that had an established reference value.

What’s wrong with this? Where should I start!? First of all, let’s consider the idea of comparing equal dosages of one androgen that isn’t 17 alpha-alkylated nor 17 beta-esterified, to an androgen which is 17 alpha-alkylated. While parenteral administration eliminates the need for consideration of bioavailability differences, pharmacokinetic properties could be significantly different, perhaps the 17 alpha-alkylated molecule either taking longer to reach systemic circulation and/or having a longer elimination half-life than its non-17 beta-esterfied, non-17 alpha-alkylated counterpart.

Moving on, one should also consider that the "muscle" used to determine the anabolic effect of an androgen, called the levator ani muscle, isn't a skeletal muscle! The application of data obtained from it really isn’t possible within the same species (rats) let alone to humans!

The amount of androgen receptors in the levator ani of rats is about five times greater than the amount found in skeletal muscle. Think about that for a second. While you do, I’ll also point out that another problem with the Hershberger Assay is that the androgen portion is determined using the sex accessory organs (e.g., ventral prostate and seminal vesicles) contain the 5 alpha-reductase enzyme while the levator ani contains little to no 5 alpha-reductase. With that in mind, you then have to consider whether the androgen in question 5 alpha-reduces or not and if so, is the metabolite more or less potent than the parent steroid molecule?

If you take anything away from what I’ve said, it should be that these bioassays weren't meant to be interpreted literally. In other words, if one androgen was shown to cause twice as much growth of the levator ani as compared to Testosterone, does this mean it’s actually twice as potent as Testosterone? Not really. Does it mean it may be more potent than Testosterone? Perhaps, but again, these bioassays are anything but accurate and reliable.

It's getting to the point where things are really ridiculous. I’ll see one guy state that a certain androgen is ten times as potent as Testosterone, yet another androgen is ten times more potent than the first androgen and thus it’s 100 times more potent than Testosterone! Come on guys, you have to realize these bioassays are at the absolute best, rough figures even when applied to the same species (rat vs. rat).

Moving on, when people look at Vida’s book they tend to (for some reason which I’ve yet to understand) pick out the best figure they can find and only report that one. For instance, with the compound erroneously referred to as methyl-1-testosterone, you notice huge discrepancies between the various values given. You have M-1-T being anywhere from equipotent to twice as potent compared to Testosterone propionate in terms of an anabolic effect. When compared with methyltestosterone (taken orally) the values are 11 to 19 times greater for M-1-T as compared to methyltestosterone.

If you look over the data, even the control (Testosterone propionate) fluctuated greatly. You’ll even see that the anabolic potency varies from one group of M-1-T (910) to another (1600) by nearly twofold and the androgenic values go from 220 to 100 respectively.

Also, another fact to consider is the huge discrepancy in values with M-1-T being injected and given orally. This shouldn’t be the case. When injecting the compound you’re getting pretty close to 100% bioavailability, and when given orally, considering that the molecule is 17 alpha-alkylated, you’d expect a value that’s at the absolute very best, equivalent to the values with parenteral administration of the same 17 alpha-alkylated molecule. Instead, we see that oral adminstration of M-1-T produces significantly greater anabolic effects as compared to parenteral administration, which makes little sense.

A consideration of pharmacokinetics doesn’t account for the discrepancy either. This again points back to the fact that extrapolating animal data to humans is completely inaccurate and should never be done. What happens in one species, more often than not, will vary greatly from what happens in another.

What the general public doesn’t understand is that people selling you these products are simply gathering the figures that look best to them. In this case, it would be to tell you that M-1-T is 16 times more potent than Testosterone propionate and equipotent (if not less) in terms of being androgenic. If you get a chance to look at the reference values in Vida’s book you’ll get a better understanding of why it’s so inaccurate to apply this data to other rats, let alone humans!

Also, I want to again point out that Counsell, et al. found C-17 alkylation of 17b -hydroxy-5a -androst-1-en-3-one (incorrectly referred to as 1-Testosterone) forming what is now being called Methyl-1-testosterone (17a -Methyl-17b -hydroxy-5a -androst-1-en-3-one), decreased anabolic and androgenic activity in bioassays. It had about one-fourth the anabolic potency of Testosterone propionate and about half the androgenic activity.

Meanwhile, the parent steroid molecule, 17b -hydroxy-5a -androst-1-en-3-one (1-Testosterone) was found to be twice as anabolic as Testosterone propionate and equipotent in terms of androgenic activity. Now, if all of this conflicting data doesn’t convince you these bioassays aren’t meant to be interpreted literally and aren’t very reliable or accurate, I don’t know what will.

After seeing this data, I hope it becomes clear that this type of data really isn’t worth much. Does that mean it has no value at all? I wouldn’t say that. Instead, I think if you see a general trend with the androgen molecule in question, you can assume it may be a more or less potent androgen agonist in general.

For instance, if androgen X has been shown in bioassays to consistently have an effect upon both the sexual accessory organs and the levator ani which is many times greater than that of, say, Testosterone propionate, you can likely assume androgen X is indeed a more potent agonist at the AR.

Does this also mean it’ll be more effective in terms of muscle growth? In most cases I’d say yes, but then again, DHT is a rather potent androgen agonist and it isn't too impressive in terms of an anabolic effect.

Last, and just as important to keep in mind, is that although this particular bioassay may be generally effective in terms of assessing which compounds are or aren’t good androgen agonists, we must keep in mind that we don’t know all of the mechanisms involved when it comes to androgens and their effects upon muscle growth. There are indeed other mechanisms that are independent of the AR (androgen receptor) which allow for muscle growth, so using an assay which only assesses AR agonism is highly limited in terms of predicting the efficacy of an anabolic steroid.

In other words, more often than not, androgens that don’t bind well to the AR and primarily exert their effects via non-AR mediated mechanisms would be discounted due to a lack of effect in this particular bioassay, when in fact they're very potent. For example, steroids with a potent antiglucocorticoid effect, which don’t bind avidly to the AR, would be dismissed.

So, going back to the methyldienolone, it may be an effective product or it may not be, but stating that it’s so much more or less potent than another androgen according to bioassays isn’t accurate. In these cases, it’s basically up to what the "real world" results reveal.

The only problem with that is the psychological influence a person can experience when they’re being told a compound is so many more times potent than a compound they’ve already used. When you’re relying on subjective data, the placebo effect can play a significant role. This isn’t to say an androgen won’t be effective, but it could mean the difference between a person saying he made greater gains as compared to another product or not.

People all too often forget that many variables need to be taken into account, whether it be training, diet, compliance in terms of taking the compound regularly, etc., and while people always claim their diet and training are the same irrespective of whether they’re using androgens or not, this usually isn’t the case.

In other words, if you tell a person you have this super potent compound that’s 300% more potent than a compound he's already used and had success with, chances are he's going to make sure everything in his program is in line to maximize gains. On the flip side, you’ll also have guys who believe a compound is so powerful that they tend to let their diets go to crap as they rationalize that the compound will make up for it. (1-5)

In summary, buyer beware. Perhaps more importantly, be educated.

That’ll teach you to ask me a question like that!

References

1. Counsell RE, et al. "Anabolic agents. Derivatives of 5a-Androst-1-ene." J Org Chem 1962;27:248-251

2. Berti F, Gomarasca P, Frova C, d'Atri G. "Androstane derivative devoid of anabolic-virilizing effects and endowed with an antiglucocorticoid activity." Arzneimittelforschung. 1986 Sep;36(9):1369-71

3. Berti F, Frova C, Colonna G, Galimberti E. "Activity of a new androstane derivative on the nitrogen metabolism: antiglucocorticoid effects." Boll Chim Farm. 1985 Nov;124(11):469-76.

4. Vida, J.A. "Androgens and anabolic agents; chemistry and pharmacology." New York, Academic Press, 1969

5. Tremblay RR, Dube JY, Ho-Kim MA, Lesage R. "Determination of rat muscles androgen-receptor complexes with methyltrienolone." Steroids. 1977 Feb;29(2):185-95.

6. Gonzales GF, et al. "Lepidium meyenii (Maca) improved semen parameters in adult men." Asian J Androl. 2001 Dec;3(4):301-3.