| Cy-BORG Intelligent Drug and Nutrition Info by Cy Willson |
| Cy Willson was once a normal, rosy-cheeked youth who 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 on 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 others, like being able to digest pharmaceutical and nutrition texts at great speed, were pretty handy. Of course, he often read some of these texts before digesting them. He became an expert on nutrition and drugs of all kinds. What's more, after experimentation, he became more than human. He became a Cy-BORG, ready to answer almost any question you puny humans want to throw at him. Remember, resistance is futile!
Q: What's the deal with this yerba matè stuff? I thought it was just an alternative to coffee or tea, but some people are saying it has all sorts of benefits: allergy relief, increased mental clarity, improved sleep, appetite suppression, etc. What's the real scoop, science dude? A: The effects seen with yerba matè are essentially stemming from the fact that it contains xanthines or derivatives thereof. Yerba matè in particular contains around 0.2 to 2% caffeine, 0.1 to 0.2% theobromine (found in cocoa and chocolate), and 0.05% theophylline. In regard to allergy relief, I suppose that since bronchodilation is a possibility with the xanthine types found in yerba matè, it could provide some relief in terms of breathing. As for increased mental clarity, this is because of the caffeine. Essentially, you can say that virtually all of the benefits seen with yerba mate stem from that fact that it contains xanthines. As far as research, a reduction in appetite is something that's actually been documented with yerba matè. Overall, you’re better off consuming caffeine tablets as opposed to buying yerba matè. Or you could get the same effects by consuming kola nuts, tea, coffee, guarana, etc. (5-9)
Q: I'm more than a little confused about the supplement R-ALA. What does it do exactly and how do you use it? A: Alpha lipoic acid is typically found as a racemic mixture of the R-(+) and S-(-) enantiomers. The R-(+) enantiomer has been shown to be more effective than the S-(-) enantiomer. As for what it accomplishes, well, it has anti-oxidant properties, protecting the cell from free radicals and also acts as a coenzyme. Dihydrolipoic acid (ALA can be reduced to this form after administration) also scavenges superoxide radicals and hydroxyl radicals and prevents lipid peroxidation. So, in other words, it’s good for us. Now on to the things that really interest us: ALA decreases blood glucose by essentially allowing more glucose to enter skeletal muscle via a synergistic effect with insulin, resulting in more efficient glucose utilization. Plain and simple, it increases insulin sensitivity in skeletal muscle. It's also been shown to possess anti-viral, neuroprotective, hepatoprotective, and anti-inflammatory effects. Now let's look at the pharmacokinetic properties of R-ALA. It’s oral bioavailability in healthy humans is around 35.6% whereas the S enantiomer’s bioavailability is 25.5%. Peak blood levels are also 40-50% higher with the R enantiomer as compared to the S enantiomer. One thing people should keep in mind is that food has been shown to reduce absorption and thus bioavailability in healthy humans. Maximum blood concentrations were obviously lower because of this. So, R-ALA should be taken on an empty stomach. When I say empty stomach, I mean 45-60 minutes before a meal or 3-4 hours after a meal will suffice. If you don’t get those exact figures, it’s okay, just try to get as close as you can. As far as half-life, oral administration yields a half-life of .21 hours for both enantiomers, although when administered intravenously the half-life was longer with the R enantiomer as compared to the S enantiomer (.37 hr vs. .32 hr). That’s just a tidbit of info though, not a recommendation to inject it intravenously. As far as dosage is concerned, the most common amount used is 300-600 mg/day in divided doses. I personally recommend 100-200 mg, three times daily on an empty stomach. Oh, and as a side note, R-ALA may also reduce hepatic glucose production, which is similar to at least one of the mechanisms of action thought to be responsible for metformin’s effects. (15-44)
Q: Your colleague John Berardi already weighed in on this topic (issue #214), but I'd like to hear your opinion. Fasting. Any benefits? Does it really cleanse and detoxify the body? I know some old school bodybuilders used to do it, but then again they did a lot of stupid things they thought were beneficial. A: Well, as far as cleansing and detoxifying, no, this doesn’t occur. I suppose if you consumed a completely terrible diet, then you could technically consider a fast "detoxifying" as you're eliminating those foods for a brief period of time. However, when most people say and hear these terms, they tend to think the body has toxic chemicals built up and that by fasting, we can excrete them. Well, in reality, if anything, you might think the opposite. Lipophilic xenoestrogens and other carcinogenic compounds tend to accumulate in adipose tissue. When fasting, lipolysis allows for the release of these compounds into the bloodstream. This is most certainly not what you want. One benefit that does come to mind is that short-term fasting may increase insulin sensitivity in muscle tissue. This is probably the one thing a person could "feel" the aftereffects of and this may be why the old school bodybuilders did it. When I say "feel," I simply mean that glycogen and intramuscular triglyceride stores make a dramatic increase when going from a fasted to a fed state. Anyone who’s fasted or ever been on a severely calorie-restricted diet can confirm that upon reintroduction of food, the "pumped" feeling in muscle is amazing, vascularity is increased and you feel good in general. However, starving in order to make gains seems a wee bit counterproductive, so I can’t recommend fasting in good consciousness. (45-46)
Q: I've got this plan where I use the new encapsulated MAG-10 for long periods of time. I specialize on a body part, let's say arms, and I work them balls out twice a week while only doing maintenance for other body parts. BUT, I take MAG-10 on arm workout days and each day after. In other words, I'm on MAG-10 for four days out of every seven for the duration of this specialization program, say for five to six weeks. Smart or dumb? A: I don’t know if I’d say simply that it’s smart or dumb, but rather something that can only be left up to speculation. Steroid hormones, at the molecular level, are typically slow to act and long lasting in terms of gene expression. Long lasting, however, can be minutes to hours. In terms of LH suppression, this tends to occur rapidly and thus I doubt it will help too much in that regard, although it may be of some benefit. If you were talking about doing this for an extremely long time, I’d say no. However, if going five to six weeks, this would be an okay idea. Personally, I'd use a serving every day for five to six weeks instead of the method you propose.
Q: Your Battle of the Proteins article is a T-mag classic, but you didn't mention much about non-soy vegetable proteins such as rice protein. What's the scoop? A: The problem is that rice protein and other related proteins are generally incomplete. In other words, they’re lacking one or more of the essential amino acids. However, by combining one type of protein which lacks one amino acid with another protein which doesn’t lack that amino acid, they form a complementary protein. In other words, they make up for each other’s deficiencies. This is why you’d commonly see the government-issue foods where they combine beans, corn, rice, corn meal and peanut butter. People could also add a complete protein to an incomplete protein and again create a complementary protein of sorts. Cheese could be used for this, combining it with macaroni. Anyhow, what is the protein quality like even after creating a complementary protein? Well, for the sake of survival, I’d of course advocate such a strategy, but for bodybuilders and athletes, I'd suggest sticking to the best proteins, those being whey and casein. If you’re specifically speaking about just one protein like rice protein and not in combination, then it’s a non-issue as the protein isn’t complete and therefore inferior.
Q: I have a friend who's a model and she's been using/abusing Cytomel for a long period of time. I know a lot of fitness models who've done this and they always end up getting really fat when they finally drop the thyroid drugs. Any way for my friend to safely come off without blowing up like Oprah on a Krispy Kreme bender? A: I'd suggest she use the new supplement HOT-ROX. It'll allow for increased endogenous thyroid hormone production without causing further TSH suppression. HOT-ROX also allows for the loss of fat mass via other mechanisms. For more info, see the articles below: Cy-BORG, issue #255
Q: Hey Cy, what's the final word on that bromocriptine drug everyone was so excited about last year? From what I've heard, it was much ado about nothing and mostly hype. Was it a dud? A: Well, I think it may have some benefit in certain individuals; however, for most people who aren't diabetic and/or obese, I really don’t think it'll be of much benefit. Two studies have demonstrated a lack of effect when using bromocriptine. One involved 15 obese, type-II diabetics and they were given .8 mg the first week and then the dosage was progressively increased by that same amount, peaking at 4.8 mg/day after six weeks. The total length of the study was sixteen weeks. This was double-blinded and placebo controlled. What did they find? No change in body composition (measured via hydrostatic weighing and MRI for distribution of fat mass) in those taking bromocriptine as compared to placebo. Another study involved 13 subjects, nine men and four women, which were obese, type-II diabetics. They were given 5 mg/day for six to eight months. What did they find? No change in abdominal visceral and subcutaneous adipose tissue was seen after treatment as compared to baseline (measured via planimeter-assisted computed tomography). No change in body fat percentage was seen either. Now, to be fair, there were a few studies demonstrating a positive change when obese diabetics were given bromocriptine. However, the fact that there are also two studies which found no difference after bromocriptine use also makes a valid argument. So what's going on here? I personally think the only people who'll benefit from bromocriptine (and even then it won’t be all that spectacular) are those who are suffering from hyperprolactinemia (which is associated with insulin resistance and consequently a gain in fat mass) and/or those who are extremely obese which consequently, could possibly lead to up-regulation of prolactin receptors. In other words, I’m saying the two are fairly well-correlated and that those who are obese may have a higher number of prolactin receptors and/or higher prolactin levels. What does this elevation of prolactin do? Well, in general, it'll be lipogenic or more specifically, in those that are obese, it’s making it that much harder for them to reduce fat mass. Adding bromocriptine in, which reduces prolactin as well as prolactin receptor mRNA, will then allow the person to lose fat. This is the only plausible explanation I can come up with as the fact it’s a dopamine agonist doesn’t seem to explain why only a small percentage of people benefit from it. So, I think it’s something occurring downstream, which is prolactin levels. I honestly wouldn't use this drug as its side effect-to-benefit ratio, in my opinion, is far too high. (1-4)
Q: Some steroid users say trenbolone gives them a crazy sex drive. Others say they get "tren dick" like deca dick. Why the difference? A: Again, this is really left up to speculation but I'd suspect it’s either stemming from a decrease in estradiol levels (people often forget it too plays a role in sex drive) or that trenbolone has some progestational activity. As for why some people experience this and some don’t, well, if it’s a decrease in estradiol, some people may have higher aromatase levels and thus it’s not as much of an issue. Or if it’s due to some progestational activity, it could be a matter of some people having a higher receptor content than others. It’s tempting to side with the latter as there's some direct and indirect evidence supporting the idea that trenbolone may possess some progestational activity. However, it’s completely reasonable to suspect a combination of these two issues to cause the decrease in sex drive, since progestational activity coupled with avid binding to the androgen receptor both suppress LH and, as a consequence, endogenous Testosterone is suppressed, which is the substrate for estradiol formation. For those who don’t have issues in regard to sex drive or even get a sex drive boost, there would obviously be a lesser amount of progesterone receptor content. Or perhaps estradiol levels remain unaffected—meanwhile, the high androgenic molecule binds to the androgen receptor and we see an increase in sex drive. The sex drive in general has so many contributing factors, it’s really difficult to narrow it down to one cause. Fluctuations in monoamine levels, androgen and estrogen levels, progesterone, dopamine, prolactin, etc., all in one way or another play a role in sex drive. Aside from that there are still many aspects about the human sex drive which have yet to be figured out. (10-14)
Q: What ever happened to IGF-1? It was talked about in 'roid books in the early '90s but you don't hear much about it now, except for a few sleazy supplement companies who are using the name. A: IGF-1 can allow for hypertrophy of muscle. Will it do such a thing when administered to humans? Yes. However, the gains seen really aren’t spectacular. More often than not, they don’t even come close to gains seen using androgens. For the most part, people should realize that IGF-1 is primarily responsible for GH’s anabolic effects in skeletal muscle as well as cell proliferation, leading to enlarged internal organs and increasing the risk for cancer dramatically. Oh, and this most certainly includes Long R3 IGF-I as I know some people will try to argue that it's much safer. Well, in order to give you the total picture, I’m going to go over some basic molecular biology as well as list the direct evidence we have concerning the side effects of IGF-1 and yes, that includes Long R3 IGF-I. First, people should understand that in the human cell cycle, growth requires growth factors in general. Seems simple enough. The next thing people need to understand is that for a normal cell, death is something that'll inevitably occur via loss of telomerase or apoptosis (programmed cell death). Again, I can’t overemphasize enough that the default pathway in humans is death, not growth. (Reassuring, isn't it?) Now, when you hear of cancer, malignant cancer, people tend to think of uncontrolled cell division. Essentially though, these transformed cancerous cells are immortalized. Now, many changes are required for this to occur (i.e. increased telomerase, increased bcl-2, increased myc and decreased p53). In the development of cancer, we tend to think of carcingogens consisting of both initiators and promoters. For instance, some initiators are UV radiation and tobacco smoke, usually causing DNA damage or mutation, whereas promoters tend to stimulate cell division. A few examples are phorbol esters, hormones (e.g. estrogens) and yes, growth factors. Now, keep in mind both events, initiation and promotion, are required for the development of malignant cells. As a side note, viral infection can also lead to the two events, but I digress. Anyhow, normally a cell serves its purpose and then dies via apoptosis. However, malignant cells don’t undergo apoptosis. They are, as I said before, immortal. The normal triggers to apoptosis are DNA damage, loss of cell-matrix contact, loss of cell to cell contact, and last but most certainly not least, lack of growth factors. When you introduce growth factors, you’re providing the catalyst for cancer formation, so to speak. Let’s say, for instance, you get many sunburns during your lifetime. Now, let’s say that one cell has its DNA damaged or altered. This, in and of itself, isn’t too much of a concern as this is only one part of the equation, the iniation. The second part is the promoter (including growth factors). Well, let’s imagine we introduce growth factors to the cell which has damaged or mutated DNA and it then begins to divide at a more and more rapid rate until it won’t stop. Voila, you have a tumor, which is now capable of even faster growth as well as being invasive (able to invade surrounding tissues) and metastatic (able to cause growth in completely unrelated and distant tissues) in regard to other tissues. In other words, you now have a malignant tumor, which we commonly refer to as cancer. The fact is, cancer stems from just one cell, just one cell, which begins to divide uncontrollably. People often talk about GH and the side effects thereof, but what most don’t realize is that many of those side effects aren't necessarily mediated by growth hormone but by IGF-1. Many people may go their whole lives with some DNA damage (or mutation rather) and never have cancer, but with the addition of growth factors, you’re asking for trouble. Even more specifically, you can increase the risk of developing rare forms of cancer, like sarcomas, which are tumors commonly found in connective tissues (i.e. muscle, bone, cartilage, etc.) Okay, now on to the more cosmetic side effects. With Long R3 IGF-I, it was shown to stimulate growth of the gastrointestinal tract. IGF-1 actually had no effect on body weight and wet tissue weight of the small and large intestine, whereas Long R3 IGF-I resulted in a 20% increase in the weight of the small and large intestine. This is what's causing a "GH gut" although using Long R3 IGF-I is much, much worse than using GH. Something else to keep in mind is that Long R3 IGF-I was shown to be even more potent than IGF-1 in inhibiting apoptosis and thus its potential for causing cancer is many times greater. Another idea is that IGF-1 may also keep telomerase activity high, which as we noted previously is a contributing factor for the loss of regulation in terms of cell division. In other words, it again can substantially increase the risk for developing cancer. Long R3 IGF-I was shown to increase telomerase activity in human prostate cancer cells, whereas IGF-1 had no effect. So, when I tell you to stay away from IGF-1, I’m actually referring to Long R3 IGF-I as it’s what's most commonly circulated and used. Although both aren't something a person should use, Long R3 IGF-1 is probably the worst choice you can make. So, unless you’re an IFBB pro who consistently places in the top ten at popular contests, you should forget about using IGF-1, or specifically the analogue of IGF-1 called Long R3 IGF-I. It’s really not worth the risk. This, out of all the compounds that bodybuilders may use, is probably the worst in terms of potential side effects. If you want a true distended belly and increased risk of cancer, be my guest. (47-52)
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