Cy Willson was once a normal, rosy-cheeked youth that spent his days getting the heifers ready for the county fair. Then, one day, while plowing a neighbor girl in the barn, he was bitten in the ass by a radioactive cow. The bite transformed him, giving him strange powers. Most of them, like being able to sleep standing up, were pretty much useless, but for some reason, his intelligence doubled. He was now able to digest pharmaceutical texts at great speed, but he often read them first.

He became an expert on drugs of all kinds. What's more, after experimentation with some of them, he became more than human. He became a Cy-BORG, ready to answer almost any question about androgens or any other drug, for that matter.

Remember, resistance is futile!

Q: A couple of years ago, T-mag ran an article called "Steroids for Health." In it, the author prescribed a layman's steroid cycle; one that an average bodybuilder could maybe do once or twice a year, safely, and that would add at least 8-10 pounds of muscle. I imagine your take on the subject is very much different. As such, can you give me a minimalist cycle that's A) readily available, B) relatively safe, and c) relatively effective?

A: Hell yes my take is different! First off, the recommendations came from an individual who thinks that just because a drug is a "veterinary androgen," it's only effective in animals for the most part. That's ridiculous. Boldenone (EQ) and stanozolol (Winstrol) work in humans just as they do in animals. The label has nothing to do with whether it's effective in humans or animals. The molecules are exactly the same. Nothing is different except the label.

This person also talks about how their standards for quality are lower. Well, in a way he's correct because these companies don't have someone regulating them, but any shortcomings in quality aren't because they think they're making these drugs for animal consumption. Yeah, and I bet it's just a coincidence that these veterinary companies are bringing back every bodybuilder's favorite drugs, like Anadrol (oxymetholone), trenbolone acetate, etc. These companies know exactly who their market is, plain and simple.

Moving on, this person also uses a *La Chatelier-like principle to explain why only certain androgens allow a better retention of muscle after a cycle is over and others don't. Essentially, his thoughts were that since you gain too much muscle with a certain drug, your body strives to reach equilibrium, so your body just magically "loses" these gains because it's too "heavy" on the body. Um, that's taking things too far and sounds like a fourth grader's reasoning skills.

[Editor's note: La Chatier was a chemist, now dead, largely known for the following principle: "Any change in one of the variables that determines the state of a system in equilibrium causes a shift in the position of equilibrium in a direction that tends to counteract the change in the variable under consideration." So now you know.]

Drugs like Primobolan do tend to allow you to keep gains more so than others, but the reasons don't have much to do with "striving to reach equilibrium" and more to do with physiology and endocrinology. True, the body does have a response mechanism in cases where you cause an imbalance, but this can't be applied to every situation. He also throws in other thoughts left over from the 70's like letting your receptors "refreshen" or whatever, when evidence points to them actually up-regulating.

But enough of the original article. There are three key determinants of whether you keep a good portion of your "gains" after the cessation of a cycle. One is the degree of inhibition of your endogenous Testosterone production or effect on the HPTA. Two is the amount of water retention or edema caused by the drug during usage, and three is — this one being a little more on the "iffy" side — whether it causes simple hypertrophy of skeletal muscle or the activation of satellite cells, leading to the formation of new muscle fibers. This last one isn't totally solid, but there's evidence supporting it.(1,2)

In any event, here are some sample cycles that are relatively available, safe and effective:

500 mg/week any Testosterone ester combined with 50 mg/day stanozolol (Winstrol)

500 mg/week nandrolone (Deca) combined with 500 mg/week of any Testosterone ester

500 mg/week methenolone (Primobolan) with 50 mg/day stanozolol (Winstrol) or methandrostenolone (D-bol)

Each one of these (with the exception of nandrolone) aren't very suppressive in terms of allowing endogenous testosterone production to return. These steroids won't cause much water retention as well, and lastly, with the nandrolone and Testosterone stack, you're theoretically increasing IGF-1 levels to a very high level, which in theory would lead to satellite cell activation, forming "new muscle."

As far as length goes, I feel 5-6 weeks is totally fine. Whatever slight side effects you'd see at 3 weeks would be the same as those you'd encounter after 5-6 weeks, so there's no point in only doing a 2 or 3 week cycle.

Q: With the advent of things like MAG-10, will there come a day when conventional steroids become passe'?

A: To be totally honest, yes, I do. Now I know some guys are going to argue with me here, but let's look at the facts. Most guys think that there are only a handful or two of androgens that have anabolic activity; in other words, those that are on the market like boldenone, Testosterone, nandrolone, stanozolol, oxymetholone, methandrostenolone, methenolone, oxandrolone, trenbolone, etc.

However, what you have to realize is that by simply making one tiny chemical alteration to a molecule like these, you not only have a totally different androgen, but one that can have totally different effects. Scientists have discovered a myriad of androgens with anabolic activity in the past, but the majority of them weren't brought to the market. Why? Well, anabolic steroids aren't used enough today to warrant further research. In other words, there isn't really a legal market for them beyond their rare use in medicine today (In the US anyhow).

Anyhow, there are two things that need to happen, for the most part, in order to produce an effective androgen that's legal. One, you have to find a drug with past research that demonstrated anabolic or more specifically myotrophic activity, and then, the most important part, make sure it meets the requirements set by the dietary supplement act to qualify as a supplement and not a regulated drug.

Well, so far, we've found things like 4-AD and 5alpha-Androst-1-ene and I'm positive there are at least a dozen other androgens that fit the two previously mentioned prerequisites.

The only problem that skeptics may have is psychological. Bill Roberts has mentioned this before and I tend to agree. Most guys just can't get over the fact that a legal supplement can achieve the same results as an illegal drug. The fact is, however, that there is no difference here other than legality. Is nandrolone an androgen? Yes. Does it promote anabolic activity in muscle? Yes. Are 4-AD, Nor-4-AD, and 5alpha-Androst-1-ene androgens? Yes. Have they been shown to possess anabolic activity? Yes, in fact 5alpha-Androst-1-ene was shown to be 2 times as myotrophic (anabolic) as Testosterone propionate.(3)

They are all by strict definition, anabolic-androgenic steroids, but one group is legal and the other is not. The only thing left for the future is to find androgens which each possess unique properties. For example, finding an androgen that matches the increase in red blood cell count of Anadrol or Winstrol or the increased "well being" seen with D-bol. Maybe one that matches the amazing strength gains seen with trenbolone; the list goes on.

I'm convinced that this will all happen in due time as each one of those unique traits are simply occurring because of simple alterations involving a certain chemical group at a specific position; a double bond; the addition or removal of an atom at a certain position; etc.

Q: Dude, is a 1-inch needle long enough for injection in to my ass? Oh, and do you have any tips on injecting? I've done it a few times but I'm not even sure if I'm doing it right.

A: A study peformed about 5 or so years ago can provide at least a partial answer to this question. In this study, they used ultrasonography to measure the thickness of the fat pad above the deltoid muscle in 220 adults. What they found was that a 5/8 inch needle would not have allowed enough penetration for a true intramuscular injection in 17% of men and around 50% of the women.

The authors concluded that for men weighing 59-118 kg, or 130-260 lb (rounded), and for women weighing 60-90 kg, it may be better to use a 1-inch or 25mm needle. They also suggested that a woman over 90 kg use a needle 1 1/4 inches long, or 38mm.(15)

So, with these data in mind, I think it's safe to assume that a 1-inch needle is sufficient in all types of men for deltoid injections and the same can likely be said for injections in to the thigh. As for the buttocks, I'd say the safest bet is to go with a 1 1/2 inch needle. However, there are going to be plenty of guys who are lean enough to use a 1-inch in the buttocks and a 5/8 inch in the deltoid, and even a 1/2 inch needle in the thigh. To be 100% sure, however, use the lengths suggested above.

As far as "techniques" that may be useful, one is simply stretching the skin flat while injecting and thus allowing for an easier IM penetration (and this is only after you've thoroughly cleansed and disinfected the area). And, if you wish to keep any of the oil from seeping out just after injection (this would only be a small amount but if you want to be anal), you can use the "Z" track method which is done by simply pulling back on the skin while you inject (pulling with your thumb and fingers over to the side) and then of course, letting go once you've pulled the needle out.

This allows you to create a seal with your skin that will prevent any oil from coming back out just after injecting.

Q: I remember T-mag columnist Brock Strasser mentioning that not all androgens exert their effects via the same mechanism. Do you agree?

A: Yes, I agree totally with Brock on this subject. While androgens exert their effects primarily through the androgen receptor and by altering glucocorticoid function to some degree, there are certainly other factors responsible.

By simply viewing "real world" evidence, we can see that not all androgens work by one or two mechanisms. One such example would be the acclaimed classic of combining nandrolone and Testosterone together. Since both bind very well to the androgen receptor, in theory, you wouldn't get very spectacular results right? Well, with this next study, I'll demonstrate why this isn't necessarily true. What researchers did was give normal, healthy men either 300 mg of Testosterone enanthate or nandrolone decanoate per week for a total of 6 weeks. This was a randomized, double-blinded cross over study by the way.

Anyhow, what they found was that in those who received the Testosterone, IGF-1 levels rose significantly, while IGF-1 didn't rise in those receiving nandrolone. However, and this is very important, those who received nandrolone had a significant decrease in IGF-BP, which is the binding protein that essentially renders IGF-1 useless.

The less IGF-BP there is, the more "free" or bioavailable IGF-1 there is floating around. So what can we conclude from this? Simple, by combining Testosterone — which increases IGF-1 concentrations — with nandrolone, which "frees up" more IGF-1 so that it may be used, you get a one-two punch, so to speak. (4)

Along these same lines, I'd like to include some other data which supports the idea that androgens have a wide variety of effects in addition to simply binding to the AR (androgen receptor) or working through other mechanisms. One such thing would be why certain androgens are better for strength gains than others. Obviously, this has to do with the CNS (Central Nervous System), but the question still remains, "How?"

I think at least one of the factors influencing the degree that a certain androgen influences strength is its effect on benzodiazepines and GABA (A) receptors. What is GABA? It's a major inhibitory neurotransmitter. Benzodiazepines are thought to bind to these receptors and cause things such as sedation, inhibition of neuromuscular transmission, and things of that nature.

Well, recent evidence suggests that humans may have an endogenous ligand (a molecule that binds to macromolecule) which acts much the same as the class of drugs known as benzodiazepines. The idea here is that if you can prevent this ligand from binding to the GABA receptor, you can prevent the effects mentioned previously.

For instance, Testosterone and stanozolol have both been shown to inhibit the binding of benzodiazepines to receptor sites. With that in mind, you can see how they may bind to these natural ligands and allow a higher level of neuromuscular transmission than otherwise possible. (5,6,7,8)

Anyhow, you can see that different steroids have vastly different effects and they exert these effects through different mechanisms.

Q: Does the diabetes drug metformin increase body fat?

A: While there are some studies indicating that it may increase fat mass, I don't believe this to be true as the majority of evidence indicates that fat mass is either not affected or is actually decreased.

Researchers gave normoglycemic, but obese children, metformin or placebo in a randomized, double-blind placebo controlled study. They were all on a calorie restricted diet (1,500 calories for females, 1,800 for males) and those that received the metformin (850 mg twice/day) for a total of 8 weeks experienced greater weight loss, greater decrease in body fat, and had a greater increase in the fat-free mass (muscle) to body fat ratio than those who received a placebo.(9)

In yet another study, metformin was given to obese women and women with polycystic ovary syndrome while on a hypocaloric diet. The diet consisted of 1,200-1,400 calories per day. This was once again, a randomized, double-blind study. Anyhow, in those women who received metformin (850 mg twice/day), subcutaneous adipose tissue (the kind we care about) was reduced significantly when compared to placebo.(10)

Yet another study demonstrated metformin's ability to increase fat loss. An in vivo study confirmed this effect in human subcutaneous adipose tissue as well, showing that it did not increase glucose transport in to these fat cells.(11,12,13)

Finally, an extremely current study found that metformin (2,550 mg/day) decreased subcutaneous adipocyte size and wasn't shown to increase glucose transport in to these same fat cells.(14)

To sum things up, while the studies are inconclusive, I think the majority of them suggest that metformin is a pretty good drug for helping people lean out.

Got a question for Cy-BORG? Send it to us (cy@t-mag.com) and we'll make sure he gets it.

References

1. Kadi F, et al. "Effects of anabolic steroids on the muscle cells of stength-trained athletes." Med Sci Sports Exerc 1999 Nov;31(11):1528-34

2. Nnodim JO. "Testosterone mediates satellite cell activation in denervated rat levator ani muscle." Anat Rec 2001 May 1;263(1):19-24

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

4. Hobbs CJ, et al. "Testosterone administration increases insulin-like growth factor-I levels in normal men." J Clin Endocrinol Metab. 1993 Sep;77(3):776-9

5. Thiblin I, et al. "Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids." British J Pharmacol 1999 Mar;126(6):1301-6

6. Masonis AE, McCarthy MP. "Direct interactions of androgenic/anabolic steroids with the peripheral benzodiazepine receptor in rat brain: implications for the psychological and physiological manifestations of androgenic/anabolic steroid abuse." J Steroid Biochem Mol Biol 1996 Aug;58(5-6):551-5

7. Masonis AE, McCarthy MP. "Direct effect of the anabolic/androgenic steroids, stanozolol and 17 alpha-methyltestosterone, on benzodiazepine binding to the gamma-aminobutyric acid (a) receptor." Neurosci Lett 1995 Apr 7;189(1):35-8

8. Masonis AE, McCarthy MP. "Effects of the androgenic/anabolic steroid stanozolol on GABBA receptor function: GABA-stimulated 36Cl-influx and [35S] TBPS binding." J Pharmacol Exp Therap 1996 Oct;279(1):186-93

9. Kay JP, et al. "Beneficial effects of metformin in normoglycemic morbidly obese adolescents." Metabolism 2001 Dec;50(12):1457-61

10. Pasquali R, et al. "Effect of long-term treatment with metformin added to hypocaloric diet on body composition, fat distribution, and androgen and insulin levels in abdominally obese women with and without the polycystic ovary syndrome." J Clin Endocrinol Metab 2000 Aug;85(8):2767-74

11. Paolisso G, et al. "Effect of metformin on food intake in obese subjects." Eur J Clin Invest 1998 Jun;28(6):441-6

12. Cigolini M, et al. "Influence of metformin on metabolic effect of insulin in human adipose tissue in vitro." Diabete Metab 1984 Dec;10(5):311-5

13. Goo AKY, et al. "Metformin: A new treatment option for non-insulin dependent diabetes mellitus." J Fam Pract 1996;42:612-618

14. Ciaraldi TP, et al. "Regulation of glucose transport and insulin signaling by troglitazone or metformin in adipose tissue of type 2 diabetic subjects." Diabetes 2002 Jan; 51 (1):30-6

© 1998 — 2002 Testosterone, LLC. All Rights Reserved.

PUBLISHED 
Discuss | Rate | Add Favorite | Print Version