Cy-BORG
Intelligent Drug and Nutrition Info
by Cy Wilson
Street Gear
Q: Cy-Borg, heard of any new "street" steroids coming from the various bootleggers? Anything new and exciting coming from those naughty boys?
A: Well, Turinabol from Red Star is now out. It’s not really "new" but until now it wasn’t readily available to most people.
Trenbolone with an enanthate ester is also out now, being made by DPHARM. Extending the carbon chain length of the ester isn't a big deal, but with trenbolone enanthate it’s nice to only inject around every five to six days as opposed to every day or every other day with the acetate ester.
I honestly don’t think you’ll ever see many entirely "new" steroids on the market. Instead what you'll see is either those that were out of circulation being brought back, or the replacement of shorter carbon chained esters by longer chained esters in order to decrease injection frequency.
Going back to the Turinabol, I know there was some debate about what actual molecule Red Star was going to use. I want to point out that Turinabol itself is 4-chlorotestosterone 17-acetate, so it appears as though they're taking the original Turinabol (not be confused with "Oral Turinabol") and adding a more lipophilic ester—butyrate—in place of acetate.
The only problem I have is the general idea of a person calling a steroid the "oral version" after they've added a methyl group at the C-17. They assume it's the same molecule and exerts the same effects, the only difference being it's orally active. This is simply not true.
In doing such a thing, you're creating a molecule which can have completely different effects. So, comparing what they currently have to a product which was 17 alpha-alkylated wouldn't be accurate in terms of potency. However, I've seen Red Star make a note explaining that it's indeed less potent, yet less harmful than the 17 alpha-alkylated molecule. So, in all fairness, Red Star hasn't lied and has been very truthful.
Is it naive to assume it's 100% orally active? Yes. Is it naive to assume it has better oral bioavailability than a molecule with no 17 beta-esterfication (just a hydroxyl group) or a shorter chained ester? In most cases, no, not at all. If this proposed mechanism of delivery is via intestinal lymphatic transport, then this product could have a decent effect provided that one is taking enough of the product.
However, if this is indeed the proposed mechanism, it would be better to use an ester with a longer carbon chain (greater lipophilicity) and thus the molecules would have an easier time being incorporated in to chylomicrons during digestion in the intestine and would consequently be transported to systemic circulation via the intestinal lymphatic route.
Still, this doesn't allow the same extremely high bioavailability you'd get with an intramuscular injection. So, again, the molecule he's using will have very different effects as compared to its 17 alpha-alkylated counterpart, but Red Star has admitted this on various message boards so I see no problem since he's being honest.
Also, just so people aren’t confused, the alteration in terms of biological effects doesn’t apply with 17 beta-esterfication as the ester is typically cleaved prior to reaching systemic circulation. The same can’t be said with compounds having a methyl group at the C-17. I doubt many are interested, but this difference is due to a large variance in bond strength/stability and the fact that the esterase enzyme obviously won’t do anything to a methyl group.
Clear as mud? Sorry, I geeked out there for a minute!
Methyl 1-Test: The True Story
Q: What is Methyl 1-test? Is it potent? Is it legally sold as a supplement or what? I'm so confused!
A: First, Methyl 1-Test isn’t even proper nomenclature. As for it being potent, Counsell, et al., found that C-17 alkylation of 17B-hydroxy-5a-androst-1-en-3-one (also incorrectly referred to as 1-Testosterone) decreased anabolic and androgenic activity in bioassays. It had about one-fourth the anabolic potency of Testosterone propionate and about half the androgenic activity.
The androgen found in MAG-10, 5a-androst-1-ene (1-Testosterone), was shown to be as androgenic as Testosterone propionate but had twice the anabolic activity. So, in reality, with this so-called methyl-1-Testosterone, you're getting the potential liver toxicity while getting much less benefit.
I think people were excited when they first heard of it as they thought, "Oh, okay, well alkylating 1-Testosterone will solve the problem of oral bioavailability and thus we'll have one kick-ass compound." In reality, adding that methyl group creates not just a methylated version of the androgen, but an entirely different molecule, period!
People need to understand that adding a methyl group or a double bond (or really any number of functional groups and atoms) creates an entirely different androgen. For instance, methandrostenolone (D-bol) only differs from Testosterone by a methyl group at the C-17 and an additional double bond between the C-1 and C-2. But can you honestly say D-bol and Testosterone impart the same effects? Even disregarding bioassays, which have demonstrated substantial differences between the two androgens, it’s still obvious to anyone who’s used them.
Alterations such as these and others in a steroid ring system can easily change the shape or the way in which the steroid molecule interacts with a given receptor, thus we get drastically different effects. Once and for all, will people please understand that a methyl group at the C-17 creates an entirely new androgen and is different from 17 beta-esterifcation as those esters are generally cleaved prior to systemic circulation, whereas the methyl group can’t be cleaved via the esterase enzyme!
As for its legality, I wouldn’t think it would be legal. As far as I’ve always been told, C-17 alkylation isn't something our laws allow in terms of a legal steroid supplement. When I visited the various sites selling this product, it became clear that it likely isn’t legal. Every disclaimer stated that the product was for "research purposes only" and intended for animals, not humans.
They stated in no uncertain terms that if you buy and use the product they aren't liable as they're assuming you’re a licensed researcher using the compound on animals. I’m guessing people think that by claiming this "for research purposes only" they’ll evade the law. Well, unless the people who are buying this product have a DEA license to possess such materials, it's technically illegal. You can claim you’re a "researcher" all you want but without a DEA license, or a very close friend who has one, you don’t have much of a case.
I can’t see this stuff being around for long. Even if it is legal, this is most certainly not something our government agencies would look too highly upon, and in general it makes everyone else in the industry look bad.
The worst part is that it’s actually less potent than the parent steroid molecule! So, let’s see, you get all of these drawbacks and less benefit as compared to the parent molecule. Doesn’t make much sense to me. It’s lowlifes who bring out products like this that give the entire supplement industry a bad name. (15)
Herbs In The Hood
Q: I've read that something called Hoodia Gordonii is a good appetite suppressant. I think it comes from a cactus. Any science behind this stuff?
A: Hoodia Gordonii (a South African plant) was studied by a group called Phytopharm, a company who specializes in the development of botanic pharmaceuticals. Pfizer (yes, the same pharmaceutical company responsible for Viagra) formed a collaborative research agreement with Phytopharm. The agreement allowed Pfizer to license and develop the extract, which was called P57. In return, Phytopharm would receive up to $32 million dollars in licensing fees as well as royalties from the sale of it.
According to their preliminary data, the compound appeared to be effective. In one study (double-blind, placebo-controlled and randomized) 19 healthy, overweight men were given either P57 or a placebo twice daily for 15 days. Essentially, they found a reduction of appetite, which in turn reduced caloric consumption and body fat.
Now, in any other circumstance, I’d be very excited about this compound, but what happened next made me think twice. Pfizer announced they wished to discontinue development of P57 for the treatment of obesity and returned all the licensing rights back to Phytopharm. A partial reason given was that Pfizer closed their Natureceuticals portion of the company and thus they thought it would be best if the product were developed by another party.
I think that’s only a small reason as Pfizer went on to say that the data on P57 warranted further study. To me, this is a fair indicator that the product wasn’t what they thought it would be. Whether the data wasn’t entirely reflective of what happened or it was another issue, I don’t know. But when a company invests millions of dollars into the development of a product, only to back out without hesitation later down the line, this indicates that the product, in some way or another, wasn’t what they expected.
As many of you know, the treatment of obesity with drugs can easily yield a profit in the billion dollar range. For a company to simply ditch the project after having already invested millions, really makes me question the efficacy and/or safety of the product.
Consequently, you’re now seeing all of these Hoodia products circulating from various companies. Do I think this stuff is worthless? Maybe. I really can’t say as there really isn’t that much data to go on. And what Phizer did really makes me question the efficacy of the product. Until some more convincing data surfaces, I won’t recommend its use.
Best 'Roids?
Q: What are the best 'roids out there that balance effectiveness and health? It seems the really good ones also have the most negative side effects and the "safe" ones aren't very effective. Any recommended cycles for something in the middle of those two extremes?
A: I'd say androgens like methenolone, oxandrolone, and yes, Testosterone. With Testosterone, the nice thing is that we have so much data available on it demonstrating safety and efficacy. The fact that it’s an endogenous hormone also provides some comfort.
Aside from that, the side effects like gynecomastia (man boobs) and androgenic alopecia (hair loss) can both be circumvented with the use of an estrogen antagonist (or aromatase inhibitor) and a 5 alpha-reductase inhibitor like finasteride, respectively.
Oxandrolone’s only problem would be potential liver toxicity, but as I’ve stated in previous articles, this is completely overblown. Twenty mg/day wasn’t shown to be any different as compared to a placebo in terms of effects on hepatic function. Hey, it’s even shown some success in those with alcoholic hepatitis, improving long-term survival in those receiving 80 mg/day for 30 days and also demonstrating improvements in those taking 20 mg/day for 21 days. (1-4)
The Cure for Micro-Nuts
Q: I've been using steroids for a year straight. Obviously, I've experienced some testicular shutdown. How do I restore function? What do I need to take or do?
A: Well, first, don't use hCG. In short, it makes matters worse in terms of restoring HPTA functioning. See my previous column for more information.
What can you do? Clomiphene at 100 mg/day for at least eight weeks has a few case studies supporting the idea, and more recently I’ve had a number of people confirm the same thing anecdotally. I personally can confirm the efficacy of this protocol as I’ve used it many times.
In fact, I’ve had my blood drawn six times, a little over three and a half months after being "off" and a month and a half after discontinuing clomiphene therapy. Every time, my testicular size returns to normal and my total Testosterone has been anywhere from 511-700 ng/dl, and my free Testosterone in the range of 96.7-123 pg/ml.
What else can help? Well, the Eurycoma longifolia found in RED KAT has been shown to increase testicular steroidogenesis. In other words, it increases Testosterone levels at the testicular level, not requiring the hypothalamus or pituitary in order to exert its effects.
The Sclaremax in RED KAT is also a good idea as it directly increases cAMP formation in the Leydig cells, which in turn catalyzes the formation of Testosterone (steroidogenesis). The nice thing is that it accomplishes this without interacting with the LH/hCG receptors and thus the down-regulation of LH/hCG receptors isn’t an issue, whereas, it is with hCG. ZMA is also a good idea. (5)
Boobs for Boys: Not Good
Q: Is there a way to get rid of gyno that's already formed besides surgery? I've heard Nolva will do this. I've also heard rubbing DHT on the affected area works.
A: Well, if the gynecomastia has been there for any significant amount of time, it’s likely that tamoxifen and clomiphene will only help to a moderate extent and won’t completely get rid of the gyno. However, if caught early enough, you could expect a return to normalcy.
Aside from that, DHT has also been shown to be efficacious in the treatment of gynecomastia. Technically speaking, any androgen which doesn’t aromatize is a good candidate as androgen receptor binding seems to be the main mechanism behind these effects. You see, androgens themselves cause a down-regulation in ER (estrogen receptor) alpha expression as well as PR (progesterone receptor) expression.
Androgens are also thought to possess a growth-inhibitory effect on the breast, which is independent of the effects on ER and PR. In other words, it also has a direct effect. (6-14)
Pro-Steroids vs. The Real Deal
Q: Be honest. MAG-10 is damn good for over-the-counter stuff, but really, it can't compare with a true bootleg 'roid, can it?
A: I believe it can compare to pharmaceutical androgens and this has been shown time and time again. Is it more potent than a combination of, say, trenbolone, stanozolol and methandrostenolone in high dosages? I don’t think so. But is it efficacious to the point where it will outperform just about any lone androgen? I believe so.
People need to realize that biological functions/effects aren’t dictated by whether an androgen is produced by a pharmaceutical company or a supplement company.
The Scoop on THG?
Q: What's up with this THG stuff in all the newspapers? Some say it's not even a steroid; others are saying it'll only make you grow boobs. What's the real scoop?
A: THG (tetrahydrogestrinone), as indicated by the name, is a steroid. As far as separating an androgenic steroid from one that's anabolic, that's impossible. All androgens are at least somewhat anabolic and all anabolic steroids are at least somewhat androgenic.
I know of no data on this compound. Even if there were, it would be very difficult to locate as this THG name isn't even proper nomenclature, so it's impossible for me to predict what functional groups are where.
Tetrahydrogestrinone... okay, where in the hell are the 4 hydroxyl groups? I've heard people say it's similar to trenbolone, but trenbolone is, according to proper nomenclature, 17-beta-Hydroxyestra-4,9,11-trien-3-one.
First, it's obvious that whomever came up with this name (THG) didn't know about or care much for nomenclature. It looks like they just skimmed over the name and grouped things together. But even if it is similar to trenbolone, there's no specification as to where the double bonds (or anything else) are, so again, there's no way for me to give any info about it or confirm such a statement.
The fact is that when you have a steroid ring system, you can easily come up with a myriad of compounds. I mean, just alter one group or atom and you have an entirely new compound. You could go on forever, and that's not even taking into account stereoisomers, although stereoisomers are certainly limited biologically.
Everyone is getting a hard-on with this compound because it's "undetectable" but what they don't realize is that it was only "undetectable" because they didn't have an assay designed for it. Any compound is detectable, but you have to first be looking for it and then have a method of finding it with accuracy.
The funny thing is that now all of these guys are going to try and get a hold of this compound, and that's the first thing these organizations will start testing for after this publicity. Again, tetrahydroestrinone doesn’t really reveal much.
Insulin Advice
Q: I was thinking of using insulin for its anabolic effects. Any advice?
A: Well, unless you plan on gaining some fat mass in the process, be sure to use it with androgens, and in some cases, small amounts of GH. Other than that, I've always and will continue to recommend four IU’s twice daily, once in the AM and once after your workout. Some people may think eight IU’s isn’t much, but as with all things, I prefer to keep safety in mind as well.
As far as how long to use it, I don’t recommend any more than four to six weeks at a time. I have one friend who'll appear in the January issue of Muscle & Fitness who went from 265 at 8% body fat to 297 at 11% body fat in a matter of months using my protocol as far as androgen/GH/Insulin use goes.
OTC Drugs and Muscle Gains
Q: Are there any over-the-counter drugs out there that interfere with muscle gain? I've heard some anti-depressants can screw up your gains in the gym. Any truth to that?
A: If they do, in most cases it’s indirectly. For instance, a change in appetite, whether it be an increase or decrease, may be seen. Motivational factors may change and some may find that they're somewhat sedated (this is generally associated with SSRI’s).
When it comes to such medications, I suggest consulting your pharmacist or physician about a better alternative after describing your side effects. More often than not, there may be a different and/or more selective drug available that suits you better.
Discontinuing medication because it's affecting your workouts isn't something I’d recommend, but searching for an alternative is certainly fine.
Permanent Fat Loss?
Q: Okay, so you’ve established that androgens reduce fat mass in a direct manner. Anything else you can tell us that's exciting?
A: Sure! I have some data that supports the idea that androgens which bind avidly to the AR may cause a permanent reduction of fat mass. Stay with me here. First, I’m going to go over a study I reviewed and posted on the T-mag forum a while back. I think I explained things fairly well so I’m just going to paste what I wrote on the T-forum:
Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, Bhasin S.
Division of Endocrinology, Metabolism, and Molecular Medicine, Charles R. Drew University of Medicine and Science, Los Angeles, CA 90059.
Testosterone (T) supplementation increases skeletal muscle mass and decreases fat mass; however, the underlying mechanisms are unknown. We hypothesized that T regulates body composition by promoting the commitment of mesenchymal pluripotent cells into myogenic lineage and inhibiting their differentiation into adipogenic lineage.
Mouse C(3)H 10T1/2 pluripotent cells were treated with T (0-300 nM) or dihydrotestosterone (DHT, 0-30 nM) for 0-14 days, and myogenic conversion was evaluated by immunochemical staining for early (MyoD) and late (myosin heavy chain II: MHC) myogenic markers, and measurements of MyoD and MHC mRNA and protein. Adipogenic differentiation was assessed by adipocyte counting, and by measurements of PPARgamma2 mRNA, and PPARgamma2 and C/EBPalpha proteins.
The number of MyoD+ myogenic cells and MHC+ myotubes, and MyoD and MHC mRNA and protein levels increased dose-dependently in response to T and DHT treatment. Both T and DHT decreased the number of adipocytes and downregulated the expression of PPARgamma2 mRNA and PPARgamma2 and C/EBPalpha proteins. Androgen receptor (AR) mRNA and protein levels were low at baseline, but increased after T or DHT treatment. The effects of T and DHT on myogenesis and adipogenesis were blocked by bicalutamide.
Hence, T and DHT regulate lineage determination in mesenchymal pluripotent cells by promoting their commitment to the myogenic lineage and inhibiting their differentiation into the adipogenic lineage through an AR-mediated pathway. The observation that differentiation of pluripotent cells is androgen-dependent provides a unifying explanation for the reciprocal effects of androgens on muscle and fat mass in men.
This just provides more support for my idea that androgens allow for the reduction of fat mass and/or prevent fat accumulation. For some odd reason, many people still don't seem to believe me when I explain the idea.
Just to go over this quickly, pleuripotent cells are simply undifferentiated cells. In other words, cells that don't know what they're going to be. Now, these cells are a little more restricted as compared to totipotent cells (only found in embryos and can form any type of cell. These are the stem cells everyone gets in heated debates about.).
A good analogy would be best here instead of me going over every little detail. Essentially, totipotent cells would be like a kid who doesn't know what he wants to be when he grows up. He could be anything, a physician, a lawyer, a shoe salesman, etc.
Pleuripotent cells are like a kid who wants to be something in the general area of science, but doesn't know what exactly he wants to do—maybe be a chemist or maybe be a physician —still, they're technically related fields. At the same time, they're two completely different things in terms of what they do: they can form more than one type of lineage. Multipotent cells can form different types of cells but only from the same lineage. In other words, this is the kid who knows that he wants to be a physician, but doesn't know whether he wants to be an interventional radiologist or an endocrinologist.
Now, what androgens do is simply help to activate tissue specific genes. In other words, they promote the formation of muscle cells instead of fat cells. This was shown to be androgen receptor-dependent and thus, this again explains why compounds which bind avidly to the AR are great for fat loss: trenbolone, dromostanolone, A1-E, methenolone, oxandrolone, etc. Just further support for my thoughts in the Steroid Dieting article.
Now, before people start freaking out about my basing this idea on that single study, I want to also present a very interesting study which was published ahead of the print issue in the Journal of Applied Physiology. Essentially, they took 32 healthy males, ages 60-87, and randomized them to receive either 20 mg/day of oxandrolone or a placebo for twelve weeks. Neither diet and activity level was altered throughout the study. They were evaluated at baseline, after twelve weeks of treatment, and again at twelve weeks after cessation of treatment to see if there were any residual effects.
What did they find? Well, after twelve weeks, the group receiving oxandrolone as compared to placebo gained lean body mass, increased thigh muscle cross-sectional area, increased total body water and, last but not least, decreased total and trunk fat mass. Not very shocking right? Well, the interesting portion of the study was when they were evaluated twelve weeks after cessation of oxandrolone use. LBM returned back to baseline, but fat mass was still significantly lower as compared to baseline.
If you want exact figures, they found oxandrolone decreased whole body fat mass by -1.9± 1.0 kg, P<0.001 and trunk fat mass by -1.3± 0.6 kg, P<0.001 after twelve weeks. Placebo didn't experience a change in fat mass. Twelve weeks after discontinuing oxandrolone treatment, whole body fat mass was still less than baseline -1.5± 1.8 kg, P=0.001 and trunk fat mass was -1.0± 1.1 kg, P<0.001.
So, they actually maintained (approximately 80%) some of the effects on fat mass. This supports what I’ve been seeing anecdotally amongst myself and those around me. Over the years, cycle after cycle, it seems we have a lesser amount of fat mass and an easier time staying lean.
I have a friend who was using trenbolone and for the first time was able to see a six-pack. Four months after finishing the cycle, he’s lost some lean body mass, but he still has a six pack and his diet hasn’t changed one bit, in fact, his diet is much worse. This isn’t to say that you’re going to stay just as lean after every androgen cycle, simply because of the fact that if a person is on a hypocaloric diet and using androgens, it’s pretty difficult to differentiate fat lost from using androgens and fat lost due to the fact that you’re following a hypocaloric diet.
Obviously, we can assume that the hypocaloric diet will account for the majority of fat mass lost and thus when caloric intake returns back to baseline, that amount of fat lost due to the hypocaloric diet will return pretty close to baseline. However, the above data indicates that we may maintain a small amount of the fat lost directly due to the androgens, each time.
As indicated by the study (again diet and activity weren't altered) the amount of fat mass reduced which can be directly attributed to the use of androgens is relatively small (1.9 and 1.3 kilos over a twelve week period), but still significant. More importantly, if one can maintain even half of that amount lost, over time, cycle after cycle using androgens which bind avidly to the AR, one can expect an accumulative effect.
Again though, this maintenance of fat mass lost can only be applied to the amount of fat mass lost as a result of the use of androgens and not a hypocaloric diet. It would be a matter of years before one could say with certainty that they have an easier time maintaining a certain body fat percentage while keeping the same diet, but I think most who sit down and think about this will tend to agree. (16-18)
Pretty cool, huh?
Posted by: BUSTINOUT
Cool read. I had to print it up so I could take it to my "private library" to enjoy. Thanks for posting it.
what R U trying to say hmmm?? lol