Cycle - Putting It All Together

Cycle - Putting It All Together Question: I have read all your articles on growth hormone, insulin, and finally igf, but I am still having a hard time putting all three together in a protocol for bulking. Can you outline a simple program for me, something that lists dosages, timing, and optimal use? I have done many cycles of anabolics, as well as insulin and gh, but now I am looking forward to adding in some igf to the mix. Thanks in advance for helping a guy out. Answer: I am happy to help you out bro as it is critical to get the timing sequence down for optimal growth. I have been personally testing different protocols with igf use, having done over 20 different cycles and timing schedules. I also have a few competitive bodybuilders and test subjects off-season testing my new protocols. I have nailed down what I feel is the best protocol at this time, though everything is subject to change as I keep researching. For now I have found that less is more. I highly recommend using a minimal schedule for all short chain sequence peptides, which include igf, insulin and even gh. I recommend using no more than 3 days per week, 2 days is fine, but no more than 3. The reason for this is that we are trying to prevent cell over-saturation and closure. All three products should be used in a similar manner. The protocol is as follows; inject all products post workout, preferably after training large muscle groups which cause the most glycogen depletion, hence providing faster uptake of peptides. A sample layout is to inject Monday, Wednesday, and Friday. Immediately post-workout inject 10-15iu of growth hormone IM, using a insulin pin and inject in any small muscle group such as delts, triceps, or biceps. Wait 20 minutes for the half-life clearance and conversion to igf to begin its sequence from the growth hormone and then inject a small dose of igf to create a synergistic super charge of the conversion process. I would recommend no more than 30mcg at this time. 10 minutes later you will take Humalog insulin only, and inject 5iu. I recommend starting with 5iu because Humalog has a very rapid onset and is easy to control with sugar. In conjunction with igf, you will be hyper-sensitive to insulin so start small and slowly work your way up to a maximum dose of 12iu post-workout. You will want to have around 80-100 grams of simple sugars such as dextrose and grape juice and an additional 60 grams of whey protein at the same time as your insulin. You will then eat another moderate glycemic index meal one hour after your high glycemic shake. The reason for the high dose growth hormone is to take what would normally be your one week intake of gh and spread it out into 3 equal doses, injected pwo. This will create a truly anabolic rich environment and you will also benefit from full uptake due to your pwo depleted state. So there is our post-workout regime, 3 days per week. Certainly you should take more than this, shouldn’t you? For most lifters, this protocol will be sufficient for growth. For someone with at least 6 months of gh use, 5 or more cycles of insulin and who no longer responds to typical igf protocols, the following regime may be followed: In addition to the above outline post-workout method, you may add additional doses of igf as well as insulin on the same day as your post-workout injection. I would highly recommend you take 15mcg igf an additional two times per day. By taking less igf more often you will prevent cell over-saturation as well as receptor down-regulation. Creating a cell rich environment that saturates the cells infrequently will target massive cell proliferation. In addition you will take insulin 20 minutes after the igf on those 2 additional injections creating an anabolic rich environment that will last all day, 3 days per week. For a sample protocol for someone that works out after work, I would recommend you do the following: Take 15mcg upon rising in the morning, followed by 10iu Humulin R or Humalog 20 minutes later. Immediately eat a carbohydrate rich meal with quality protein and low fat such as bananas, oatmeal and egg whites. For lunch, take another 15mcg igf with 10iu insulin and have another moderate glycemic carbohydrate meal and protein with minimal fats. Follow the above listed pwo protocol to complete your three time injection schedule which will be used three times per week. If you follow the outline laid out for you above to the letter, you will put on a massive amount of lean mass with a minimal amount of fat. You will need an anabolic and androgen rich environment to complete the schedule such as testosterone and tren in addition to the peptide products. T3 and T4 will not be necessary on this schedule as your thyroid levels will not be affected.

Clomid: Frequently Asked Questions

Clomid: Frequently Asked Questions Something I put together that may help some of the new comers out there as well as some of the more experienced. Question: What is Clomid? Answer: Clomid is a synthetic estrogen and is generally prescribed by doctors to trigger ovulation in females. Question: Why Should Bodybuilders use Clomid? Answer: Almost all anabolic androgenic steroids will cause an inhibition of the bodies own testosterone production. When he comes off the steroids he has no natural test production and no more steroids. The body is left in a state of catabolism (catabolic hormones are high and anabolic hormones are low) and as a result much of the muscle tissue that was gained on the cycle is now going to be lost. Clomid stimulates the hypophysis to release more gonadotropin so that a faster and higher release of follicle stimulating hormone aud luteinizing hormone occurs. This results in an increase of the body's own testosterone production. Question: Does Clomid also work as an anti estrogen? Answer: Clomid is a synthetic estrogen, however it does also work as an anti-estrogen. How does it work? Because it is a weak synthetic estrogen, it will bind to the estrogen receptor (ER) and not cause any problems. At the same time the increase in estrogen from steroids are blocked from attaching to the ER. Question: How effective is Clomid as an anti-estrogen? Answer: It is very weak and should not be relied upon if you are going to be using steroids that aromatise at any rapid rate, or if you are pre disposed to gyno. arimidex, Proviron and Nolvadex will all make better choices for this purpose. Question: Some say Clomid during a cycle is a waste, is this true? Answer: Lets first examine what happens when someone is using anabaolic androgenic steroids. When the level of androgens in the body get too high, the androgen receptor becomes more highly activated, and the hypothalamus stops sending a signal to the pituitary. In short the signal tells our body to stop producing testosterone. During a cycle the body has higher levels than normal of androgens and as long as this level is high enough Clomid will not help to keep natural test production up. It will be almost all but completely shut off. The only purpose of Clomid during a cycle is as an anti-estrogen. Question: When do I start Clomid? Some say 2 weeks others 3. Answer: When you start using your Clomid all depends on what steroids you were using during your cycle. Different steroids have different half lifes and you should adjust your Clomid intake accordingly. As we have seen above, if we take Clomid when the androgen levels in our body is still high it will be a waste. We need to wait for androgen levels to fall before implementing our Clomid therapy. However if we take it too late we could possibly lose gains. Look at the list below to determine when you should start Clomid therapy. By selecting from the list all the steroids you used in your cycle and which ever one has the latest starting point then go with that. For example if I cycled dbol, sustanon and winstrol I would use sustanon as it remains active in the body for the longest period of time. Anadrol/Anapolan: 8 - 12 hours after last administration Deca: 3 weeks after last injection and Clomid for 4 weeks Dianabol: 4 – 8 hours after last administration Equipoise: 3 weeks after last injection Fina: 3 days after last injection Primobolan depot: 10 – 14 days after last injection Sustanon: 3 weeks after last injection Testosterone Cypionate: 2 weeks after last injection Testosterone Enanthate: 2 weeks after last injection Testosterone Propionate: 3 days after last injection Testosterone Suspension: 4 – 8 hours after last administration Winstrol: 8 – 12 hours after last administration Question: What is the most effective way for Clomid therapy. Answer: Clomid has a long half life and as such there is no need to split up doses throughout the day. I read some where that it was 5 days (any feedback on this). Now if we used sustanon and we start using Clomid 3 weeks after our last injection we anticipate that androgen levels are low enough to start sending the correct signals. If androgen levels are still a little high then the normal 50mgs/day of Clomid for 1 week is not going to be effective. We need to start at a high enough amount that will work or help even if androgen levels are still a little high. 300mgs on day 1. I know I said don’t split it up due to its long half life but try and split this up 2 tabs 3 times a day. After we have finished this first day we seek to use 100mgs for 10 days and then followed by 50mgs for 10 days. Question: Do I need to use Clomid for 3 weeks? Answer: Why don’t you want too? It is very cheap, very effective and can mean the difference between maintaining gains and losing them. Question: How cheap is Clomid? Answer: Clomid normally comes in 50mg tablets but also comes in capsule form of 25mgs. A 50mg tablet can be anywhere between 25 cents and $2.50. (15 pence and 75 pence in England). Question: Do all steroids cause shut down of the hpta. Answer: Not all steroids do. Everyone is different and you must also take into account how long you have been using a certain steroid and at what dose in order to determine if you need Clomid or not. However as the price is so cheap, why risk not using it.

Clenbuterol

Clenbuterol Let me just start by saying that this is the single most mis-understood compound in use for athletics and bodybuilding today. Most of the information out there is ½ truths and conjecture. Ok…having said that, I’m going to make an effort to dispel some myths and give everyone a better understanding of Clen.
First, lets plow quickly through some of the basics: Clenbuterol (Clen) is a beta-2 agonist/antagonist bronchodilator. What this means, is that it stimulates your beta-2 receptors. And this in turn stimulates you (clen has stimulant effects which will make you feel….well…stimulated). All of this serves to increase your body temperature a bit, increase your basal metabolic rate, and decrease your appetite (Int J Obes Relat Metab Disord. 1994 Jun;18(6):429-33.). Clen also can decrease insulin sensitivity (Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E146-53.). Clen is a very effective repartitioning agent, and this is what it’s most often used for. What this means is that it will increase your ratio of Fat Free Mass (FFM) to Fat Mass, by decreasing your Fat and possibly increasing your FFM (J Appl Physiol. 2001 Nov;91(5):2064-70). Want me to quantify that a bit? In one study, horses given a reasonable dose of clen (slightly over 1mcg/lb) and excercised for 20mins, 3x a week ( I suppose they were Mentzer disciples) had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen given to horses who didn’t excercise; however, the excercised group had a different FFM response, which significantly increased (+4.4%) at week 6. Week 6! Clen and clen+excercise produce roughly the same results for the first 2 weeks! Remember the old 2 weeks-on/2weeks-off schedule? It’s officially dead and buried. If you want the quasi-anabolic effect from the clen, it’ll take more than 2weeks on (6 weeks apparently). And in fact, since clen alone is similar to clen+excercise for those first 2 weeks...why would you ever use a 2on/2off protocol? Keep in mind that animal responses to beta-agonist/antagonists differ a bit from ours…but you get the picture. 2on/2off? Ha ha... Clen has a biphastic elimination, which means that it is technically reduced in your body in 2 different stages. This isn’t particularly important, as a recent study has shown that for most intents and purposes, clen concentrations in the body decline with a ½ life (approximately) equivalent to 7-9.2hours and again up to as much as 35 hours later(J Anal Toxicol. 2001 May-Jun;25(4):280-7. and J Vet Pharmacol Ther. 2004 Apr;27(2):71-7. and J Pharmacobiodyn. 1985 May;8(5):385-91. ). If you’re really interested, though, clen technically declines biphastically at 10 and then 36 hours. But really, in our little world, where we use ½ life to tell us when to take our next dose, who the hell is going to take clen, then a dose 10 hours later, then a dose 36 hours later. We’ll stick with the earlier 7-9 hour ½ life for dosing purposes, and take our clen every 3.5-4.5 hours that we’re awake, stopping early enough to still be able to get to bed. Clen can, in some people, cause insomnia (and as with all stimulants, can cause anxiety in some). Clenbuterol can also cause a downregulation in testicular androgen receptors and in pulmonary, cardiac and central nervous system beta-adrenergic receptors(J Anim Physiol Anim Nutr (Berl). 2004 Apr;88(3-4):94-100.)…possibly making steroids less effective while you are on clen, but definitely making clen less effective as time goes on and you keep taking it. To counteract this, you can take some ketotifen or periactim every 3rd or 4th week that you remain on clen. Both of these are prescription anti-histimines, so they’ll make you drowsy (take before bedtime). Basically, the way both of these work is to reduce beta-2 receptor activity. A lot of people claim that clen is quite anti-catabolic and/or anabolic. This hasn’t been confirmed in human studies (Ann Pharmacother. 1995 Jan;29(1):75-7.). And the doses given to the animals in these studies where clen is shown to be very anticatabolic or highly anabolic are so absurdly high that no human could ever take them (1mg/kg of bodyweight and higher). The best you can hope for is the very mild anabolic effects I cited earlier. Oh yeah…I guess I should get around to the proper dosing of clen. My recommendations are the same for both men and women. You’ll need to take 20mcgs upon rising, and then repeat that same dose again later in the day, and then once again in that day (if you find you can tolerate the effects). So you’ll start with 20mcgs, and then repeat that dose 2 more times that same day if you can tolerate it (side effects will determine this…hand shaking, sweating, etc…classic stimulant sides). Then you can start increasing the dose gradually. Personally, I wouldn’t work my way up to more than 200mcg/day. 60-120mcg/day is an average dose. Also, bear in mind that clen isn’t great for your heart, and can cause some issues there (enlargement of ventricles, etc…) but most studies showing clen to cause heart problems are with animals, and even though the dosing is similar to what humans take (in some studies) it’s important to remember that animals have more beta-2 receptors and they cause certain event chains that humans’ beta-2 receptors may not. Clen causes cardiac hypertrophy to some degree, in some cases. Again though, many studies showing more significant heart problems are with mg dosing. We humans take clen in mcg doses. If we want to duplicate the “theraputic” levels of clen in the more conservative studies, we’d be taking just over 1mcg/lb of bodyweight. I’d suggest a bit less, though. Performance issues with clen also vary. Some studies show reduced exercise (cardiovascular) performance with clen (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.), while some show that clen can alleviate exercise induced asthma (Respiration. 1987;51(3):205-13.)! Sometimes you feel like a nut…sometimes you don’t, I guess. What this means, to me, is that you’ll need to figure out how clen affects your performance individually. Which brings me to the issue of cramps while on clen. I don’t get them. My friends don’t get them. Most of us are athletes who use clen during the season as well as the off season, and one of my friends even claims that it gives him more “wind” (cardiovascular stamina). Take on enough water every day and you should be fine. If you’re really concerned, you can take some extra minerals and taurine, since clen depletes taurine (Adv Exp Med Biol. 1996;403:233-45) as do most if not all beta-agonists. I don’t take anything more than my usual vitamins and minerals. Well…there it is…pretty much all I know about clen. I hope this answers some questions and clears up some misconceptions.

History of Anabolic-Androgenic Steroid Use in Competitive Sports and Medicine

History of Anabolic-Androgenic Steroid Use in Competitive Sports and Medicine The primary use of anabolic-androgenic steroids is in replacement therapy for male hypogonadism; other medical uses of anabolic-androgenic steroids include growth promotion in various forms of stunted growth, osteoporosis, mammary carcinoma, anaemias and hereditary angioneurotic oedema. Observation and clinical trials indicate that adjuvant therapy with anabolic-androgenic steroids can be supportive in the treatment of conditions characterised by a negative nitrogen balance: major surgery, cachexia of various origins, burns, traumata, convalescence from illness, injuries and immobilisations, as well as during radiotherapy and therapy with cytotoxic drugs (Kochakian 1976; Kopera 1976, 1985; Kruskemper 1968). Unfortunately, research concerning additional legitimate applications of anabolic-androgenic steroids has most likely been impeded by the existing emotional polarisation of anabolic-androgenic steroid supporters and opponents. As Kochakian (1990) has pointed out, the frequent and often hysterical references in the popular press to unsubstantiated adverse effects of anabolic-androgenic steroids has often resulted in the loss of both media and medical/scientific credibility, deterring research on beneficial and legitimate medical uses, and as a stimulus and encouragement for litigation against physicians. The use of various physical and chemical aids in performance enhancement is not a novel problem but has been a feature of athletic competition since the beginning of recorded history (Csaky 1972; Strauss & Curry 1987). Ancient Greeks ate sesame seeds, bufotenin was used by the legendary berserkers in Norwegian mythology, and the Andean Indians and the Australian aborigines chewed, respectively, coca leaves and the pituri plant for stimulating and antifatiguing effects (Csaky 1972; Williams 1974). Anabolic steroids have been used by athletes to enhance appearance and performance for many years. The first ergogenic use of anabolic-androgenic steroids was reported to have occurred in the 1950s among weightlifters and bodybuilders (Wright 1978). Since that time their use has permeated a myriad of sports (Anderson & McKeag 1985, 1989; Buckley et al. 1988; Gilbert 1969; Starr 1981; Todd 1987; Wade 1972; Yesalis et al. 1990a). Payne (1979) suggested that the use of anabolic-androgenic steroids was a significant problem at the 1964 Olympic Games. Ljungqvist (1975) reported that one-third of a sample of elite track and field athletes in Sweden; surveyed admitted to systematic anabolic-androgenic steroid use by 1972. Silvester (1973) reported that 68% of a sample interviewed at the 1972 Olympic Games from 7 countries, and who were competing in such diverse activities as throwing, jumping, vaulting, sprinting, and running up to 5000m, admitted having used anabolic-androgenic steroids. Although it was suggested as early as 1973 (Frazier 1973) and reiterated later (Wright 1978, 1980, 1982), it is now evident that the use of anabolic-androgenic steroids is not limited to elite amateur and professional athletes. It has trickled down from the professional and college levels to the high schools and junior high schools (Buckley et al. 1988; Yesalis et al. 1989a, 1990a). The estimated prevalence of nonmedical anabolic-androgenic steroid use and the implications for society and public health have also prompted several scientific meetings, including a technical review at the National Institute on Drug Abuse in 1989, and both federal and state investigations and efforts to reclassify anabolic-androgenic steroids as controlled substances (Government Accounting Office 1989; Halligan et al. 1989; Taylor 1987a,b; Yesalis 1989; Yesalis et al. 1990a) despite nonconcurrence from the American Medical Association (AMA 1989). Patterns of anabolic-androgenic steroid use among athletes have been determined from several surveys. Burkett and Falduto (1984) interviewed 24 weight-training athletes at a gymnasium in a metropolitan area of the southwestern United States. Subjects surveyed took a combined steroid does of 4 to 8 times the recommended medical does, used more than one anabolic-androgenic steroid at a time (‘stacking’), combined use of injectable and oral anabolic-androgenic steroids, and used the drugs frequently, usually in cycles (an episode of use from 6 to 12 weeks or more). Although Burkett and Falduto questioned a very specific sample of anabolic-androgenic steroid users, they concluded that their subjects seemed to be representative of the type of athletes who used anabolic-androgenic steroids. Cohen et al. (1988), in a study of hypercholesterolaemia in 21 male powerlifters using various anabolic-androgenic steroids, reported significantly higher levels of anabolic-androgenic steroid use in their subjects than Burkett and Falduto (1984), with daily dosages ranging from 60 to 400mg. Pope and Katz (1988) have also reported daily dosages between 10 and 200mg (of various anabolic-androgenic steroids) for anabolic-androgenic steroid users in their investigation of affective and psychotic symptoms associated with anabolic-androgenic steroid use. Frankle et al. (1984) found that 110 of 250 weightlifters they interviewed in several gymnasia in the metropolitan Chicago area, many of whom were noncompetitive lifters, also used a variety of anabolic-androgenic steroids. 50 weightlifters were interviewed in detail; a majority (56%) had no competitive intents in weightlifting, bodybuilding or any other athletic events, a proportion that substantially exceeds that found by Buckley et al. (1988) in a nation-wide survey of male high school seniors. Frankle et al. (1984) concluded that anabolic-androgenic steroid abuse had reached alarming proportions in noncompetitive athletes. The Buckley et al. (1988) survey suggests that one-quarter to one-half million adolescents in the United States have used or are currently using anabolic-androgenic steroids. Anderson and McKeag (1985) reporting on a nation-wide survey of alcohol and drug use among college athletes indicated that anabolic-androgenic steroids were used in all men’s sports, one women’s sport, and that the sport with the greatest admitted use (9%) was football. The overall anabolic-androgenic steroid use rate in all sports nationally was 4%. Anderson and McKeag (1989) replicated their original study 4 years later and although they found that overall use rates for anabolic-androgenic steroids had remained stable, anabolic-androgenic steroids were now being used in 2 additional women’s sports. A survey and follow-up telephone interview by Yesalis et al. (1988) following the 1987 US Powerlifting Federations’ National Championship found 33% of the initial respondents and 55% in a follow-up subsurvey of the same group, admitting previous anabolic-androgenic steroid use. Since athletes may have a propensity to underreport of disguise their actual anabolic-androgenic steroid use for various reasons, caution must be used when interpreting values concerning the prevalence of anabolic-androgenic steroid use by athletes

Supplement Performance - Creatine Plus Phosphate

Supplement Performance - Creatine Plus Phosphate

Creatine Supplementation

Creatine is a naturally occurring amino acid that is obtained from the diet
and/or synthesized endogenously (within the body) from the amino acids glycine,
arginine and methionine. Creatine has become a popular nutritional supplement
among athletes. The most commonly used protocol is to ingest a daily total of 20 to
30 grams of creatine, usually creatine monohydrate, in four equal doses of five to
seven grams dissolved in fluids over the course of day. (For a detailed review on
creatine supplementation strategies, see my article Creatine Loading Strategies in
November issue of MD).
Although not all studies report significant results, the preponderance of
scientific evidence indicates that creatine supplementation appears to be a generally
effective nutritional ergogenic aid for a variety of exercise tasks in a number of
athletic and clinical populations.1
For example, short-term creatine supplementation has been reported to
improve maximal power/strength (5-15%), work performed during sets of maximal
effort muscle contractions (5-15%), single-effort sprint performance (1-5%) and work
performed during repetitive sprint performance (5-15%).1 Moreover, creatine
supplementation during training has been reported to promote significantly greater
gains in strength, fat-free mass and performance, primarily of high- intensity
performance tasks.1
In the 1970s, Soviet scientists showed that creatine supplementation
improved athletic performance in short, intense activities such as sprints.2 According
to Dr. Michael Kalinski, a former Chairman of the Exercise Biochemistry Department
in the Kiev State Institute of Physical Education (Kiev, Ukraine, USSR), the Central
Institute of Physical Culture (CIPC) in Moscow initiated a long-term research
program to characterize the role of creatine in muscular performance and its use to
enhance muscle function. Also, Soviet scientists redirected their research from
academic studies on creatine metabolism in animals to applied studies on the
effects of creatine supplementation on human physical performance.2
For example, members of the USSR national track and field team who took
creatine supplements improved their performance in the 100-meter dash by one
percent and in the 200-meter sprint by 1.7 percent.2 As a result of these studies,
the CIPC officially recommended use of creatine supplements to enhance physical
capacity and the efficacy of exercise training. In additon, USSR national athletes
were routinely given these supplements.2
Some clinicians have expressed concern about the effects of creatine on
renal function. Drs. Pritchard and Kaira reported a case study of renal dysfunction
associated with creatine,3 but their conclusion that creatine was responsible for the
renal dysfunction is clouded by previous history of renal nephritic syndroma that was
stabilized by cyclosporine. It was unclear whether the observed improvement in
renal function following creatine withdrawal was due to adverse effects of creatine
itself, impurities in the creatine products, creatine/drug interactions and/or other
factors.
In three small studies, no adverse effects of creatine on renal function were
reported following either short-term4,5 or long-term supplementation of two to 30
grams per day for up to five years.6 Moreover, Dr. Richard Kreider and co-workers
recently reported that long-term creatine supplementation (up to 21 months) does
not appear to adversely affect markers of health status (metabolic markers, muscle
and liver enzymes, electrolytes, lipid profiles, etc.) in athletes undergoing intense
training in comparison to athletes who do not take creatine.7 There have also been
anecdotal reports of muscle cramping and strains associated with creatine
supplementation. However, Dr. Greenwood and colleagues recently reported that
creatine supplementation does not appear to increase the incidence of injury or
cramping in Division IA college football players.8
Phosphate Supplementation
Among the inorganic elements, phosphorous is second only to calcium in
abundance in the human body. Approximately 85 percent of the body´s
phosphorous is in the skeleton, one percent is found in the blood and body fluids,
and the remaining 14 percent is associated with soft tissue such as muscle.9
Phosphorous is of vital importance in intermediary metabolism of the energy
nutrients, contributing to the metabolic potential in the form of high-energy
phosphate bonds, such as ATP, and through phosphorylation of substrates.
Phosphate also functions in acid-base balance. Within cells, phosphate is the main
intracellular buffer.
Further, phosphate is involved in oxygen delivery. In red blood cells,
synthesis of 2,3-diphosphoglycerate requires phosphorus. Decreased 2,3-
diphosphoglycerate diminishes release of oxygen to tissues. Phosphorous is widely
distributed in foods. The best food sources are meat, poultry, fish, eggs and milk
products. Nuts, legumes, cereals, grains and chocolate also contain phosphorous;
however, animal products are superior sources of available phosphorus compared
with cereals and soy-based foods. Many phosphate-containing supplements are
available commercially, including K-Phos® and Neutra-Phos K®, which also provide
potassium. For maximum bioavailability, these supplements should not be ingested
with zinc, iron, or magnesium.9 Calcium (as calcium acetate or calcium carbonate)
also inhibits phosphorous absorbtion.9
Phosphate supplementation (“phosphate loading”) has been proposed as an
aid to athletic performance (Table 1).10 Studies investigating the ergogenic value of
phosphate supplementation date back to the 1920s. Early studies suggested that
phosphate salt supplementation could be used to increase physical working
capacity.10
Much of the contemporary interest in phosphate supplementation as a
potential ergogenic aid emanated from a report by Dr. Cade and colleagues in the
early 1980s.11 Results revealed that phosphate supplementation significantly
increased resting serum phosphate and red cell 2,3-diphosphoglyserate levels. In
addition, phosphate supplementation decreased submaximal lactate while
increasing maximal oxygen uptake. The greatest increase in maximal oxygen
uptake occurred in subjects ingesting sodium phosphate for two consecutive testing
trials.
Dr. Richard Kreider and co-workers conducted the most extensive study to
date to evaluate the ergogenic value of phosphate supplementation.12 In this study,
six highly trained male cyclists participated in a placebo-controlled, double blind
crossover study to determine the effects of sodium phosphate supplementation on
metabolic and myocardial adaptations to maximal exercise and 40-km time trial
performance. Subjects ingested either four grams per day of tribasic sodium
phosphate or a glucose placebo for five days. On the fourth day, subjects performed
either an incremental maximal cycling test or a 40-km stimulated time trial under
controlled laboratory conditions using the subjects’ racing bicycle attached to a
computerized race stimulator.
Analysis of maximal test results revealed that phosphate supplementation
significantly increased pre-max serum phosphate levels (17%), maximal oxygen
uptake (9%), minute ventilation (8%), ventilatory anaerobic threshold (10%),
echocardiographically-determined mean ejection fraction (4%) and myocardial
fractional shortening (8%). During the 40-km time trial, phosphate loading
significantly increased mean power output (17%), oxygen uptake (18%), ventilation
(15%), heart rate (8%), ejection fraction (13%) and fractional shortening resulting in
an eight percent reduction in performance time. These findings provide evidence
that sodium phosphate supplementation provides ergogenic value to highly trained
athletes.
According to recent review with Dr. Kreider, “Most studies investigating the
effects of sodium phosphate supplementation (three or four grams per day for three
or four days) on maximal aerobic capacity and/or endurance exercise performance
have reported ergogenic benefit… On the other hand, it appears that acute and/or
chronic calcium phosphate supplementation provides little ergogenic value.”10
Table 1. Proposed Theoretical Ergogenic Value of Phosphate
Supplementation
• Elevates extracellular and intracellular phosphate concentration
• Stimulates glycolysis and energy metabolism
• Increase the availability of phosphate for oxidative phosphorylation
and creatine phosphate synthesis
• Increases 2,3-diphosphoglycerate synthesis and peripheral extraction
of oxygen.
• Enhances myocardial and cardiovascular responses to exercise
• Serves as a metabolic buffer
• Increases anaerobic threshold and maximal oxygen uptake
• Improves exercise performance and/or efficiency
• May enhance psychological responses to exercise
Data from Kreider, 1999
Creatine Phosphate Supplementation
In their recent book Supplements for Strength-Power Athletes13, Drs. Jose
Antonio and Jeffrey Stout quoted results by Dr. Wallace and colleagues published in
Coaching and Sports Science Journal and unpublished results by Dr. Eckerson. Dr.
Wallace and co-workers investigated the effect of supplemental creatine alone
versus creatine plus phosphate on muscle power. Male and female subjects were
given either five grams of creatine four times per day or five grams of creatine plus
one gram of phosphate four times per day for five days. The combination of creatine
plus phosphate resulted in a significantly higher muscle power output, suggesting
performance benefits more from a combination of phosphates and creatine than
from creatine alone.
Dr. Eckerson and colleagues examined the effects of creatine alone versus
creatine plus phosphate on anaerobic working capacity. Male subjects were
randomly put into one of three treatments: placebo, five grams of creatine, or five
grams of creatine plus one gram of phosphates. Each subject was asked to dissolve
the supplement in 16 ounces of water and ingest it four times per day for six
consecutive days. The subjects performed a cycle ergometry test to determine
anaerobic working capacity. The placebo and creatine groups increased anaerobic
working capacity by –3.0 percent and 16.0 percent, respectively. The creatine plus
phosphate group increased anaerobic working capacity by 49 percent.
Phosphate and Resting Metabolic Rate
Phosphate supplementation has also been suggested to affect energy
expenditure. For example, Dr. Kaciuba-Uscilko and colleagues reported that
phosphate supplementation during a four-week weight loss program increased
resting metabolic rate.14 Further, Dr. Nazar and co-workers reported that phosphate
supplementation during an eight-week weight loss program increased resting
metabolic rate by 12-19 percent and prevented a normal decline in thyroid
hormones.15 Consequently, it’s possible that phosphate could serve as a potential
thermogenic nutrient in diet supplements.
Summing Up
The preponderance of scientific evidence indicates that creatine
supplementation appears to be a generally effective nutritional ergogenic aid for a
variety of exercise tasks in a number of athletic and clinical populations. There is
some evidence suggesting that sodium phosphate supplementation may enhance
aerobic capacity. Recent data suggest that combined creatine and phosphate
ingestion improves anaerobic working capacity more than creatine ingestion alone.
According to Drs. Jose Antonio and Jeffrey Stout, take a one-gram serving
phosphates (preferably a sodium-potassium mix) with every serving of creatine
during the loading phase, which would be four times daily for six days.

Side Effects of Steroids

Side Effects of Steroids Most of the time, when steroids are mentioned, they´re brought up as the reason a particular athlete can run so fast, hit so many home runs, or make so many tackles. They are also claimed to have extraordinarily harsh side effects and for causing severely unforgiving and permanent damage. Everybody´s seen movies like "The Program" where steroids ruin a young athlete´s life, or perhaps "The Aaron Henry Story" on HBO, where a young athlete suffers lifelong problems from his steroid abuse. Most recently, I saw the movie "Spiderman" where the villain, the Green Goblin, admits to having his superhuman strength and psychotic personality from using "performance enhancers"! I´m here to assure you that those types of horror stories are few and far between, and after consulting with literally hundreds of athletes and bodybuilders, I´ve almost never heard of anything even remotely resembling the popular "horror stories" we see in the media almost daily. I´ve certainly never seen anyone become the Green Goblin from using them, either.. By reading this article, coaches, athletes, parents and teachers will know the truth about anabolic steroid side effects and will be able to make their own informed decisions as to how bad they are. But I suspect that after reading what I have to say, as well as what the scientific literature says, the question of how bad steroids are will be a different question entirely; the only question remaining will be "why didn´t anyone tell me this before?" When I initially started research for this piece, I consulted not only real-life athletes who had vast experience with anabolic steroid use, but also scientific and medical journals. The picture that unfolded before me was very different than the one typically painted by the mass media, and certainly much different than the one I found on http://www.steroidabuse.org/, http://www.dea.org/, and http://www.drugabuse.gov/. In my research on the governmental sites, I found very little of use, to be perfectly honest. There were tons unfounded claims and talk of money being put into "studies." In reality, the government "studies" on anabolic steroids were not medical studies at all. They were surveys given to various age groups, on steroid use, in order to generate statistics. There was nothing of medical value or scientific merit on those sites, despite the endless parade of doctors that seemed to be against their use. Here´s an example of one of the more absurd claims made on one of those sites: "..[steroids] they are dangerous drugs, and when used inappropriately, they can cause a host of severe, long-lasting, and often irreversible negative health consequences. These drugs can stunt the height of growing adolescents, masculinize women, and alter sex characteristics of men. Anabolic steroids can lead to premature heart attacks, strokes, liver tumors, kidney failure and serious psychiatric problems. In addition, because steroids are often injected, users risk contracting or transmitting HIV or hepatitis.." This is the information found on a government website, in a piece written by a doctor. I´m surprised she didn´t mention turning into the Green Goblin in her list of possible health side effects. As you read what I have to say, I want you to keep this in the back of your head. I want you to remember this claim, made by a medical doctor, as you read the rest of this piece. All of the information here is exactly what has been reported to me by athletes, as well as what is found in credible scientific journals; then decide for yourself what the truth about steroid side effects is. -------------------------------------------------------------------------------- Anabolic Steroid Side Effects:1. Inhibition of Natural HormonesThe inhibition of natural hormones is probably the most common and probable side effect experienced from the use of anabolic steroids. In almost all cases, adding a hormone into your body will send a message to your endocrine system to stop producing it. This is because your body wants to remain in a very balanced state -- called "homeostasis," if I remember my high school biology class correctly. To maintain homeostasis, the body wants to avoid having too much of any particular hormone. To achieve this, the body sends a message to the testicles to slow down, or even stop producing testosterone when there is too much circulating. Unfortunately, this happens when any kind of hormone is added into the body, so even if an athlete is not using testosterone, but is using other anabolic steroids, the body will still send this signal 99% of the time. Of course different steroids cause varying degrees of inhibition ranging from total shut down of endogenous (natural) testosterone production, to very mild inhibition, where some natural hormones are still being produced and circulating. In almost all cases, this inhibition is over once the steroids aren´t active in the body anymore. In the following charts, we can see a mirror image of the level of steroid in the body (Nandrolone), compared with the level of natural testosterone being produced. In other words, as the level of steroid rises (chart 2), the level of testosterone falls (chart 1), and vice versa: Now, as that first chart shows, testosterone levels fell when Nandrolone (an anabolic steroid was administered, but interestingly, the following chart shows an almost identical mirror image, where the Nandrolone levels in the blood rise. What this indicates is that the amount of this particular steroid in the blood is directly and proportionately inhibiting natural testosterone production. Here´s the chart: Most athletes who use anabolic steroids accept all of this as a necessary price to pay in order to experience the benefits from using steroids. In an effort to combat this, athletes have experimented throughout the years with various compounds to avoid or at least limit this problem. Human Chorionic Gonadotropin, anti-estrogens, and Selective Estrogen Receptor Antagonists are all used during a cycle, or after (or both) with this goal in mind. The following is a table showing the various hormonal levels of former steroid users who haven´t used them for a year (*called "ex-abusers" by the nice people who funded the test) versus current users (*abusers): What we see in this chart is not surprising to anyone who is actually familiar with steroids, and not with media-hype. In people studied who haven t used steroids for a year, ALL of their measured hormones (testosterone, estrogen) were within the NORMAL RANGE! Clearly, the effects that steroids have on your hormones are reversible and the horror stories we ve all read in the media about people who never regained normal hormonal function after one cycle  are greatly exaggerated. I think anyone who is familiar with "After School Specials" about steroids will be very surprised at learning this fact. As for "The Aaron Henry Story" on HBO, I can t imagine how he has suffered side effects well into his 40âs when the steroid users in this study were totally fine after one year, and in some cases used more than he did! (*Journal of Steroid Biochemistry and Molecular Biology. 84 (2003) 369-375) 2. Steroid Effects and Liver DamageLiver damage is probably the most sensationalized of all side effects possible from steroid use. The media often focuses on this particular problem as if it occurs with every steroid, and in every person who takes them. Nothing could be further than the truth. Most anabolic steroids which are ingested orally pass through the liver, which functions as the body´s filtration system. When something goes through the liver, it is broken down by various enzymes, and passed along into the bloodstream. Most research on orally administered anabolic steroids focus on the fact that liver enzymes are elevated following ingestion. But does this necessarily mean that the liver is being damaged, does it? Of course not. Commonly, studies that focus on steroid toxicity often use absurd doses, or incorrectly focus on liver activity instead of damage. The liver functions as the filter for the human body.. it´s going to be activated whenever something (not just a steroid) passes through it. Does that show that steroids damage the liver? Let´s see what the scientists say.. There was an eight-week study done in 1999, which looked at the effects of an 8-week cycle of Oral steroids. The steroids examined were Halotestin (Fluoxymesterone), Dianabol (methylandrostanolone), or Winstrol (Stanozolol) on rats at the dose of 2mg/kg-body weight, administered five times a week for 8 weeks. That s almost 200mgs/day of any of those steroids, for a 200lb user. That is, I´ll speculate, much more than the average person would use on a cycle. In fact, I have never, in my years of researching steroids and speaking with athletes, heard of anybody using 200mgs/day of Halotestin, Winstrol, or Dianabol. Ever. And, at the end of that study, In vivo, each rat still had liver enzyme levels that were within normal range! (*Med Sci Sports Exerc. 1999 Feb;31(2):243-50, Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Molano F, Saborido A, Delgado J, Moran M, Megias A.) In another study, 16 bodybuilders using steroids were compared to 12 bodybuilders who were not. Then the bodybuilders who had used steroids stopped taking them for three months, at which points, the researchers found that liver enzymes had returned to the same levels as the non users. After only 3 months! (*Int J Sports Med 1996 Aug;17(6):429-33, Body composition, cardiovascular risk factors and liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. Hartgens F, Kuipers H, Wijnen JA, Keizer HA.) We can see from the chart below that ex-steroid users have totally normal liver enzymes one year after they stop using& .in fact, for some liver enzymes, even the current users have normal scores! (*Journal of Steroid Biochemistry and Molecular Biology. 84 (2003) 369-375) 3. Steroid Effects on Cholesterol (Blood Lipid Profile) Steroids can, in fact lower HDL cholesterol and raise LDL cholesterol. HDL (high density lipoprotein, commonly referred to as "good cholesterol") helps to protect the arteries by bringing unused cholesterol to the liver where it is broken down. LDL on the other hand has the opposite effect. Some steroids can therefore cause high cholesterol levels with low HDL and high LDL. Some steroids are, of course, very mild on blood lipids, while others are notably harsh. In both cases, however, it is likely that a return to within normal parameters would occur after steroids are not being taken. 4. Gynocomastia (Development of breast tissue in males)The development of gynecomastia or feminization of the breast tissue in males is possible with anabolic steroids. This is due to an excess of estrogen being present in the body, through a process known as "aromatization" whereby androgens like testosterone are converted to estrogen. This excess estrogen then finds its way to the receptors in breast tissue and binds to them. This results in the possibility of female-like breast tissue, which must sometimes be removed by surgery. Most athletes experience itchiness of the nipples, followed by pain. Since this develops over several days, usually, the athlete usually has more than enough time to discontinue the use of the compounds he´s taking, or to attempt to counteract the breast tissue development while remaining on the cycle. The two most common ways this is achieved by steroid users is either to use an anti-estrogen like Nolvadex or Arimidex in their cycle or to take Letrozole (*a very strong Aromatase Inhibitor and antiestrogenic compound) afterwards, to destroy the tissue that has developed. Male breast development occurs in basically the same way as female breast development, and the use of anabolic steroids can result in this happening at a later stage in life for males. At puberty a surplus of hormones all combine to stimulate the growth and development of breast tissue. The initiation and progression of breast development involves a variety of pituitary (and ovarian, in women) hormones, as well as various local mediators. As you can see from the following chart, testosterone has the ability to aromatize (convert to estrogen), and eventually become part of the cascade of hormones that eventually contribute to the development of breast tissue: (GYNECOMASTIA: ETIOLOGY, DIAGNOSIS, AND TREATMENT Chapter 14 - Ronald S. Swerdloff, MD, Jason Ng, MD, and Gladys E. Palomeno, MD, March 1, 2004) 5. Acne and Anabolic SteroidsAnabolic steroids can cause the Development of acne and the extent to which it is experienced can be due to a number of varying factors, with the particular steroids and exact dosages used being the two primary factors. The skin´s sebaceous glands have a particularly high affinity to Dihydrotestosterone, which is an androgen the body naturally produces from testosterone via the enzyme 5-alpha Reductase. Increased sebaceous gland activity can oily skin which can combine with bacteria and dead skin caused by normal wear and tear, eventually causing pores to become clogged more quickly than the body can remove them. This of course, is preventable by using only particular steroids, cleansing the skin regularly, and perhaps using a topical anti-androgen. (1. Am J Clin Dermatol. 2002;3(8):571-8. 2. Clin Dermatol. 2004 Sep-Oct;22(5):419-28. 3. Pol Merkuriusz Lek. 2004 May;16(95):490-2.) 6.  Roid Rage Increased aggressiveness is often claimed to occur with anabolic steroid use. Although it´s highly rare (less than 5%), significant psychiatric symptoms have been found in some steroid users, including aggression and increased violence, mania, and even psychosis. However, it must be noted that in the studies done without a control group, it can safely be assumed that naturally aggressive people simply just be more inclined to use steroids (type-A personalities, if you will). This would probably have an effect on possibly skewing the results. Certainly, if someone takes the risk to use steroids to improve their performance in a sport or their physique, they have certain aggressive traits. Can steroids enhance them? Possibly. Can steroids be to blame for anti-social, psychotic, "roid-rage" type behavior? Probably not. The evidence just isn´t there to support that. In fact, a landmark study was performed which examined different doses of testosterone administration on men aged 20-50, who had a variety of experience with steroids from having used them previously to not at all prior to the study. A variety of psychological tests were performed at the outset of the study as well as at the end. What was found was that no participant in the study had become violent as a result of the testosterone injections they had been receiving, although some said they  felt more aggressive. This clearly indicates that there is a high level of control over possible violent or aggressive behavior that can result from steroid use. The researchers also noted that in terms of the psychological tests performed, some subjects showed little or no response to testosterone, with regards to psychological measures, while others experienced significant changes. Thus, general temperment clearly plays a large role in how one responds psychologically to steroid administration. In addition, when this study was compared with others, similar results were found: Out of 109 cases studied, only 5 people exhibited Psychological (Manic or Hypomanic) effects. (*Archives of General Psychiatry, Volume 57, February 2000.) 7. Steroids and BaldnessSteroids can possibly cause men to start balding if they have a genetic predisposition towards Male Pattern Baldness. The gene for baldness is thought to reside in the X chromosome exclusively, so a good general indication of whether someone is genetically predisposed towards being bald is to look at the men on their mothers side. Chances are that if the majority of them are bald, then the person will be carrying that gene too. The reason steroids can cause premature balding is that the scalp reacts to Dihydrotestosterone (DHT) quite strongly, and many steroids can either convert to DHT or are derived from it. Of course, several anti-baldness medications can prevent this, such as Finasteride and Dutesteride. This is, of course, merely a cosmetic effect, and poses no real health issues. It could be catastrophic to a potential career with any one of a number of 80´s rock bands, but other than that, I can´t really see any real problems associated with hair loss; especially since it can be avoided when proper steps are taken and certain steroids are avoided. 8. Cardiovascular Problems from Anabolic SteroidsAnabolic steroids have been linked with cardiovascular issues. Part of this may be due to their effects on Blood Lipids (see above). But some of it is due to the fact that many steroid users have been found to have enlarged ventricles. This is actually very common in bodybuilders as well as powerlifters and other types of athletes, and is more indicative of the effect of weight training on the heart, rather than solely steroid use. 9. Virilization (Development of male characteristics in women)This term refers masculinization, or development of male sexual characteristics that females could potentially suffer from steroid use. This side effect on women is often reversible after the cycle has ended. Some typical signs of virilization are the development of a deeper voice, hirsuitism (growth of excess body hair), enlargement of external genitalia (clitoral enlargement), and possible male pattern baldness, or acne on the face or body. This is all dependent, of course, on the compounds used as well as the dosages employed. Personally, I have witnessed the most permanent of these effects to be the deepening of the voice due to the hypertrophy (growth) of the vocal chords. This is typically the most unwelcome side effect, as it makes it very obvious when a woman is using steroids. Of course, if this begins, the best course of action is to cease taking all steroids immediately. There are several ways to reverse this effect, the most common being to undergo a medical procedure known as vocal chord scraping. And yes, it´s exactly what it sounds like. 10. Stunted Growth (height)The use of some steroids can possibly stunt the growth potential of people who have not finished growing. This is only possible with certain steroids, and not with others. In fact, certain steroids have been used in clinical settings to improve growth rates in children. It is probable that the premature closure of the epiphysial cartilage, which is most likely caused by aromatizable steroids, will lead to a possible growth inhibiting effect, and could ultimately result in a shorter adult height. This most likely an irreversible side effect, as the growth plates would have sealed and can not "re-open". Anavar (Oxandrolone) has been used to improve the height of growth stunted children, and it is probable that most DHT-derived steroids could also be used for this purpose as could certain anti-estrogens. Speaking in broad terms, growth stops at the end of the teenage years...there is almost no chance to keep growing. This is because lengthening of a bone occurs at the epiphyseal growth plates (called the "growth plates" in common parlance), the remnant of the cartilage model. It's capable of proliferating. In 99.9% of humans, the process of bone elongation ends at around the mid to late teen years. At this point, the growth plates are obliterated and disappear, after which no more elongation (typified by an increase in limb length, height, etc...) can take place. Elongation of the bone occurs here and at a second epiphysis at the end. The proliferation of the cartilage happens very quickly, actually fast enough to keep ahead of the bone generation that´s "chasing" it, called ossification, which is just the replacement of cartilage by bone. As long as the cartilage growth "stays ahead" of the bone, you grow taller, as bone replaces cartilage. When the bone finally catches the cartilage (because the cartilage slows its growth rate, not the bone), it ossifies, and "seals" the growth plate. Here´s a growth plate picture, enhanced by radioactive dye (GP= Growth Plate), so you can sort of see the bone "catching" up with the cartilage. (Human Anatomy and Physiology, 6th Edition, John W. Hole jr., Wm. C. Brown Publishers.) 10. Prostate EnlargementOnce again, this is only a possibility that steroids could cause enlargement of the prostate. The media-perpetuated claim of possible prostate cancer seems to be wholly unfounded, according to most research. In many cases, this enlargement is quickly remedied upon cessation of anabolic steroid use. The first period of prostate Prostate growth, occurs first during puberty and is as a result of the testicular secretion of androgens. During adolescence to adulthood, the prostate stays at this stage, despite the relatively high levels of androgens found in the body. Then, much later on in life, there is often a second stage of growth. Although this was originally deemed to be a result of Dihydrotestosterone s actions in the body, it is more likely due to estrogen combined with a small amount of either DHT or Testosterone. Thus, it´s not hard to imagine that taking steroids can cause this type of prostate enlargement and caused trouble for a steroid taking athlete. Typically, a product such as Finasteride or Dutesteride is taken to avoid this problem, with a high degree of success. 11. High Blood PressureThis problem is possibly the most easily remedied of all steroid side effects. It s very common for steroid using athletes attempting to gain maximum bulk to abstain from all aerobic activity. This causes the body to work much harder to circulate blood. Also, the typical water and sodium retention induced by certain steroids can contribute to this. If blood pressure is measured regularly to ensure that the value is not higher than 140/90, there should be no problems. 12. Kidney ProblemsThe kidneys can undergo more possible strain during anabolic steroid intake. Kidneys are involved in some of the filtration and excretion systems of the body, and as such, when a foreign substance is administered, they necessarily work harder. Some steroid users have noticed very dark urine when on a cycle, and this is indicative of the kidneys working overtime to accomplish their goal. One of the major offenders of this seems to be Trenbolone, which turns the user s urine a very dark color unless enough water is taken in daily. Also, even though I know you re probably getting sick of hearing this from me, the possibility of side effects is dependant on both dose as well as compounds administered. Some steroids (Nandrolone) are even used to help treat people with Kidney problems! So clearly, they aren´t as bad as they´re made out to be with regards to possible kidney issues. 13. Immune System ChangesThere is a large amount of data indicating that anabolic steroids may have some effect(s) on modulating the immune system. As with most potential side effects, this is largely dose and compound dependant. There is strong evidence that different analogues produce vastly different effects on the immune system. Testosterone and certain analogues have been shown to be possibly immunosuppressive, while Nandrolone and other steroids are possibly immunostimulating. Both, however, have been found to be beneficial when given to AIDS patients, who clearly have an already compromised immune system. This is because the increase in lean body mass that those steroids can provide is consistent with an enhanced ability to fight off infections, enhanced survival rates, and a better quality of life. (1.Int J Immunopharmacol. 1995 Nov;17(11):857-63. 2. J Steroid Biochem Mol Biol. 1990 Sep;37(1):71-6 3. AIDS. 1996 Jun;10(7):745-52. 4. Journal of Neuroimmunology 83 1998, 162-67.) 14. Sterility in Males and FemalesIt´s a common side effect of steroids to cause temporary sterility in both males as well as females. In fact, anabolic steroids are so proficient at this that they have actually been studied and approved by the World Health Organization as a male contraceptive possibility. Steroids do this by disrupting the various hormones in women which potentiate the ability to have regular menstrual cycles. In men, steroids lower Follicle Stimulating Hormone to the point where normal production of sperm is not possible. This isn´t to say that nobody on a cycle has every conceived; quite the opposite, actually. There ve been legions of "happy accidents" reported to me by athletes who were on cycles and thought they couldn´t possibly conceive. Sterility caused by steroids is temporary, of course, and generally reversible by treatment with Selective Estrogen Receptor Modulators such as Nolvadex or Clomid, and/or Human Chorionic Gonadotropin. (1. Fertil Steril. 2004 Jan;81(1):226. 2. Urology. 2000 Oct 1;56(4):669.3. J Clin Endocrinol Metab. 1985 Oct;61(4):746-52 4. Fertil Steril. 1994 May;61(5):911-4. 5. Andrologia. 1985 Sep-Oct;17(5):497-501 6. Urol Clin North Am. 1986 Aug;13(3):455-63.) -------------------------------------------------------------------------------- Steroid Effects Myth: Believing Everything You HearOk, so this last side effect isn´t really a steroid effect at all. But it s true, nonetheless. It´s my hope that you read this entire article and were surprised and possibly even a little outraged. Maybe you were outraged with how casually I seem to treat a very serious topic& but more likely than not, you were outraged at the fact that most of you´ve come to think about steroids and their horrible side effects has been greatly exaggerated. The simple fact of the matter is that anabolic steroids, like any medication, can cause a host of unwanted side effects. I´m certainly not suggesting otherwise. What I am suggesting is that a more logical and rational view be taken of them. The literature suggests that these drugs are safe when used in a clinical setting; my numerous interviews and experience with athletes suggests that this also holds true outside the clinical setting. Please don´t misinterpret my position as being pro-steroid, anti-media, or anti-government. To do so would be to miss the point of this work entirely. I have the utmost respect for the media for providing the services that they do. I also have the utmost respect for the government and those who serve this country. Anabolic Steroid Side Effects are a very real and possible concern for those who decide to use them. My position, therefore, is one that I hope is consistent with both the media as well as the government s position: I simply wish to tell the truth, and allow my reader to make the best and most informed choice possible. In that regard, I think this article has served its purpose.
http://www.isteroids.com/

Steroids In Baseball and Sports

Steroids In Baseball and Sports
The story of steroid use in sports began just before the World Weightlifting Championships of 1954. The Soviets had made their Olympic debut in Helsinki in 1952, and made quite an impact, but nothing compared to the show they put on in 1954. That year, the Soviets easily dominated most of the weight classes. As the story goes, John Ziegler (team physician for the United States) questioned the soviet team´s doctor after the medals were given out, and the soviet doctor said that his team had been receiving testosterone injections. That, in all probability, was the first time anyone had ever used anabolic steroids to enhance performance in an athletic event. According to some unconfirmed sources, testosterone preparations were used by Germany´s Olympic team in 1936 for the Berlin Olympics. At that time, there were rumors that an Olympic medal winner had previously used oral Testosterone preparations, but the benefit to be had from them (due to the technology at the time regarding oral testosterone) would have been minor. In the case of the Soviets, however, rumors of discarded syringes in their dressing rooms made it clear that they were not using oral steroids, they were using something different. And everyone wanted to know what it was.
That wasn´t, however, the first time anabolic performance enhancement had been attempted. As far back as the original Olympic Games in ancient Greece, athletes ingested various herbs and foods with the hopes of improving their performance. The big winner in the 480 B.C. Olympic Games said he ate nothing but meat for 10 months prior to the Games. Now we know that meat is especially high in B vitamins and Creatine, both of which can enhance performance. Early attempts to increase Testosterone were documented as early as 776 BC andagain, by Olympic athletes´ ingested sheep´s testicles, which they knew to be a source of Testosterone production (3). Although it might seem extreme to us now, to eat meat for ten straight months (or to ingest sheep testicles), this was a small price to pay for the prize money that was offered back then & up to 1,200 days pay for winning an event was common. There were no participation medals; they did not compete for the love of the game, to give it their best shot, or even for pride. They competed for money and prestige, end of story (1). And that is why they sought out performance enhancers.
If that story sounds familiar, like perhaps one you´ve heard on TV or in magazines concerning modern-day steroid use in sports, it should. Athletes´ today- especially professional athletes- have very lucrative contracts and sponsorship deals, and steroids are known to enhance performance, reduce and repair injuries, and lengthen careers. So it should be no surprise to most people that when Dr.Ziegler returned from the World Weightlifting Championships, he immediately began researching testosterone and trying to develop something better for his Athletes.
What Dr. Ziegler developed, with the help of the Ciba pharmaceutical company was called "Methandrostenolone" or Dianabol. This was the creation of the first anabolic steroid that wasn´t simply testosterone. That was late in 1956. By the time the early 1960s rolled around, Ziegler´s weightlifters were dominating American weightlifting. And since then, many different steroids, each with their own different set of characteristics, have been developed.
By the late 1960´s the East Germans had also entered the fray and were giving steroids to their athletes as part of a state sponsored program to bolster national pride by winning Olympic Gold Medals. In 1968, Dr. Manfred Hoeppner, East Germany´s Chief Medical Officer, wrote and submitted a report to the government in which he recommended the total collective administration of steroids to the entire East German athletes (2). In the couple of decades that followed after this report, the East Germans´ presence was felt at every major world wide sporting event. From the Olympics to World Championships, they took home both medals as well as world records.
Of course, there have been other documented instances of athletes taking various drugs and other substances in an attempt to enhance their performance. Thomas Hicks, an American marathoner in the 1904 Olympics, had to be revived after he drank Brandy lased with cocaine and strychnine. He won the gold medal, although I believe the Brandy/Cocaine/Strychnine cocktail never really took off in popularity among his fellow athletes. His fellow runners, the sprinters attempted to use nitroglycerine a couple of decades later, to dilate (expand) their coronary arteries; they later switched to experimenting with Benzidrine, an amphetamine.
Many of such compounds had been used, but none are as powerful or provided such rapid increases in strength and powerful as anabolic steroids. For this reason, after its invention by Dr.Ziegler, Dianabol was quickly made available to anyone looking for an extra edge. It helped many bodybuilders, weightlifters, football players, and Olympic athletes train harder, longer, and more efficiently. As all steroids can do, it enhanced protein synthesis and allowed new muscle to be built at a rate that was much more rapid than would otherwise be possible. And that increased muscle power and strength translated into financial rewards for the athletes who were taking them.
If you were an athlete looking to take your career farther, Dianabol was going to be an indespensible part of your dietary intake. At this point, the "steroid arms-race" was in full swing. Athletes all over the world wanted to know where to get them and how to use them, and countries were scrambling to develop new steroids and protocols for using them. Then, oddly, in 1968 there was an official complaint about steroids made by the World Health Organization. This complaint wasn´t made by sports authorities, but by the World Health Organization. Steroids were being over produced by the major pharmaceutical firms, and were subsequently shipped to certain third world countries, where doctors would receive a kickback for prescribing large amounts of them. Kenya and Jamaica were the main countries where this was happening, and they (predictably) did very well for themselves at the Olympics that year.
At this time in the United States, professional sports were gaining prominence and athletes began to be able to support themselves by just playing their sport. Notably, at this time, there were no documented reports of athletes using steroids in sports other than Olympic competition. Nonetheless, at this time, a ban on Anabolic steroids was issued by the International Olympic Council, and in the coming decades, most professional sports organizations would follow suit. The original ban on anabolic steroids was enacted for ethical and moral concerns, not safety (as is often thought). Shortly after the first ban on performance enhancers came the first athlete caught breaking that ban. In the 1972, an American swimmer named Rick De Mont was found to be using a newly banned substance- ephedrine. At that time, ephedrine was an approved medication for asthma, and you guessed it- Mr. De Mont was an asthmatic with a prescription for it. Two years prior to that first the 1972 Olympics, Arnold Schwarzenegger won his first of seven Mr. Olympia titles, reportedly with the aid of Dr. Zeigler´s little blue Dianabol pills.
Steroid use in the Olympics went on, for the next couple of decades, in a game of Cat and Mouse between the athletes and the International Olympic Committee. For the most part, the athletes were very successful in avoiding positive drug tests. The East Germans developed several novel compounds to avoid detection, and were only caught when word leaked somehow. For the most part, the Russians and Americans were also very successful at this. Professional bodybuilding also marched onwards with competitors taking ever-increasing amounts of steroids and other drugs, without fear of testing positive.
By the 1990´s, Anabolic Steroids had been absorbed into society, and their use had penetrated every possible sport from the professional ranks down to the High-School level. There were the occasional scandals here and there, but nothing really captured the general public´s attention for very long. In 1987 the National Football League introduced it´s anti-steroid policy, and Major League Baseball was left as the most major sports organization in the world which still had no such policy.
Steroids in High School SportsSteroids in high-school have become an increasingly hot topic in both the media as well as at various levels of the government. This particular topic, of course is going to be at the forefront of many high-school athletes as well as their parents, coaches, and teachers. At this juncture, I think it´s important that I be crystal clear about my position on steroid use by high-school students/athletes and minors under the age of 18 in general. I do not endorse nor condone the use of any illegal substance by minors. However, I also feel it to be absurd to carry on allowing the campaign of misinformation on anabolic steroid use to be allowed to continue. I´ve personally been out of high-school for exactly a decade, and before I began writing about performance-enhancement full time, I worked with at-risk youths in a high-school. I believe this gives me a unique perspective to provide information from, as well as a certain degree of sensitivity to the current climate regarding this issue.
The first thing that I´m going to tell you is that "scare tactics" don´t work. Telling a high-school kid that steroids will kill you is silly; especially when he can turn on the television and look at ESPN and see Bill Romanowski setting NFL records, or Barry Bonds and Jason Giambi breaking home-run records. Scare-tactics and misinformation have failed miserably to stem the tide of anabolic steroid use by high-school students. My position therefore is that education and truth are the best ways to deal with the issue of steroids in high school sports.
First, let´s see where misinformation has gotten us, with regards to stopping high school students from taking steroids. Steroid "education" in schools started becoming widespread in the mid 1980. A quick look at the literature from this time shows that the position taken by the educational community was that steroids do not enhance athletic performance, and they carry with them the great probability of permanent health damage. I´m not really sure where to begin my comments on those particular positions, and still keep this article G-rated.
So let´s review the facts.
In 1988, a study published in the Journal of the American Medical Association examined Anabolic Steroid use patterns among the male adolescents. In this particular study, overall participation rate on a school-wide basis was 68.7% and on an individual basis was approximately half (just over 50%). The participants in this survey were 12th-grade male students in 46 high schools across the nation who completed a questionnaire which asked them several questions concerning their current or previous use of Anabolic Steroids. The results indicated that 6.6% of 12th grade male students use or have used AS and that over two thirds of the users were 16 years of age or younger when they did their first cycle (5).
The results of a 1990 survey of 2113 high school students show that Ninety-four (4.4%) of 2113 students admitted using anabolic steroids. When that is categorized further by gender, we find that 67 (6.5%) of 1028 males and 27 (2.5%) of 1085 females were users of steroids. Predictably, athletes had a statistically significant greater use of steroids (79 [5.5%] of 1436 subjects) than did non-athletes (15 [2.4%] of 636 subjects) (6). Still, the survey shows a total of roughly 4% of the surveyed high school population had used steroids.
Now, let´s fast forward a couple of years to examine a survey by the Center for Disease Control and Prevention. According to that survey, steroid use among high school students more than doubled between 1991 and 2003. Slightly over 6% of 15,000 students surveyed admitted trying steroid pills or injections. Huh? Wait and in 1988, 6% of the students in the survey had done steroids. Yet, in 2003 the number was still the same, though it had "doubled since 1991" according to the Center for Disease Control and Prevention. At this time, it should be noted that fewer than 4% of the nation´s high schools were testing for steroids, according to the National Federation of State High School Associations´ survey of athletic directors.
Are you confused yet? It seems that the rates of steroid use is holding relatively steady at between 4 and 6%, yet we´re being told that it´s an epidemic. So what´s the real story about steroids in high school?
In 2005, if we look at the Centers for Disease Control and Prevention Youth Risk Behavior Surveillance, 6.1% of students from grades 9 through 12 had taken anabolic steroids (7). Once again, we´re seeing about 6% or so of high school students are using anabolic steroids. Sorry, but that´s still basically the same rate as the previous two decades. Is this a "mounting problem" as many in the media would have us believe? Hardly. In fact, it´s holding steady.
So where is the media getting their information? Well, probably not from scientific journals or reliable sources for statistics. In fact, anecdotal evidence is frequently used in news reports, and that type of evidence typically greatly over estimates the widespread usage of anabolic steroids among athletes and often claims reach as high as 20-90%. On the other hand, scientific studies show a trend towards indicating that usage is actually rare and generally no higher than 6% (8). And, to look further into the hard scientific research instead of the soft anecdotal evidence, there is strong indications that suggest that anabolic steroid usage actually declines progressively from high school to college and beyond(8).
Should high school students be using anabolic steroids? No, definitely not. Is this the problem the media would have us believe it is? Again: no, definitely not. In fact, some estimates for 2004 even suggest that only 3.4% of 12th graders have used steroids (9). Let´s put that number in perspective, shall we? According to that xsame source, 76.8% of 12th graders have drank alcohol in their, and the rates of use for most other drugs by high school students (Marijuana, Cocaine, Ecstasy, etc...) are significantly higher than they are for steroid use. I don´t know if that eases the minds of most parents, but I think it ought to give some kind of perspective on exactly where the "steroid epidemic" ranks in importance.
Still for most parents, most memorable moment in the Congressional hearings on steroids was the testimony when the committee´s chairman, Rep. Tom Davis (R., Va.)claimed that there were in attendance "the parents of kids who have used steroids and committed suicide." Later, The New York Times published a story on a student who killed himself, Efrain Marrero, whose family said that his stopping anabolic steroid use provides a viable explanation for his suicide. The New York Times calls this "persuasive anecdotal evidence." Dr. Jack Darkes, who is an Assistant Professor in the Department of Psychology as well as the Director of Interventions, Alcohol and Substance Use Research Institute at the University of South Florida disagrees with the notion that steroids can be blamed for such instances, and instead cautions us to try to ascribe the tragic ending of a young life to just one factor. I would like to echo his sentiments and say that to attempt to overstate the issue of steroids in high school to only one factor, or overstate it´s importance is equally dangerous. Education at the high school level needs to be based in science and reason, and not simply be reactionary and emotional displays set into motion by the current media frenzy of attention to the issue. The first step is to educate the parents, coaches, and teachers with solid medically based and unbiased information, then to present it to adolescents through the high school education system they are enrolled in. Put simply, you wouldn´t let your children learn table manners from television, so why let them learn about steroids and other drugs from there?
Recent research strongly indicates that a prominent media outlet (a major magazine or television show, for example) can build an agenda for the entire media and thereby influence policy changes as far reaching as the national level of government (10). So if the general feeling we get from the media is that steroids are a rising problem and that steroid abuse is becoming more common in high schools  yet the hard scientific date suggests otherwis and who are we to trust? I think the answer is clear& personally, I would put my faith in science and scientific studies before the media. Unfortunately, it would appear that the former is not strongly influencing government policy, while the latter is (10). And that all started with steroids in baseball.
Steroids in Baseball
(Sports Illustrated, June 2002, as told by Ken Caminiti)
Major league baseball was the last major sports organization in the United States to implement a comprehensive drug testing policy. This all started with a bottle of a nutritional supplement seen in Mark McGwire´s locker. The bottle contained Androstendione, a prohormone, or a compound which can convert into another one inside the body. In this particular case, the compound in question converts to Testosterone once in the body. Unfortunately, at this time, McGwire was en route to breaking a home-run record that had been standing for decades. MGwire retired shortly after breaking that record, but the story of steroids in baseball and the Major League Baseball (MLB) organization went ahead at full speed. Just a few short years later, Ken Caminiti revealed to Sports Illustrated that he used anabolic steroids, and that he estimated roughly fifty percent of the players in the league were using them also. This admission opened the floodgates to the media to begin their full scale assault on MLB. Jose Canseco, in a book published during the height of the steroids in baseball media coverage, estimated that 85% of all players in MLB used steroids, and also admitted using them. Remember the difference between what has been found in scientific studies vs. anecdotal statistics? This is a prime example of one such difference. The players can´t even agree on a percentage, and they´re in the locker-rooms!
Although Caminiti´s story was the earliest major media admission of steroid use by a recently retired former MVP in baseball´s professional ranks, it was one of the most influential. The following is a chart illustrating media attention to steroids in baseball for the weeks preceding and following the Sports Illustrated piece on Caminiti. Week fourteen is when the piece was published. You can see that prior to that, only ten pieces were published in the mainstream media. In the same time (weeks-wise), you can see that hundreds of articles were put out after Caminiti admission:

The most famous story in the steroids in sports is that of Jason Giambi and Barry Bonds. Both of those players were suspected of using anabolic steroids when the BALCO scandal was exposed. Giambi, for his part, told a U.S. grand jury that he used a duo of undetectable steroids known respectively as "the cream" and "the clear," both of which he received from personal trainer Greg Anderson during the 2003 season. Bonds, on the other hand claimed that his trainer told him the substances were the nutritional supplement flaxseed oil and a pain-relieving balm for his arthritis.
There were also claims that a transcript of Bonds´ entire testimony was leaked to the press, and that according to a transcript of Bonds´ Dec. 4, 2003, testimony, he admitted the following were used by him: "the cream," "the clear," human growth hormone, Depo-Testosterone, insulin and a drug for female infertility that can be used to mask steroid use."
Bonds´ attorney, Michael Rains, said the leak of the testimony was simply engineered to discredit Mr. Bonds. However, it´s important to remember that at the time they were not banned by MLB.
So did all this media attention hurt baseball? The answer is a resounding "no". Baseball sales figures and attendance were in a slump before McGwire was en route to his home-run record, and they´ve been climbing ever since. But are all the additional home runs a result of steroid use? Well, it´s easy to say we need to put asterisks on every record set during the "steroid era" of baseball, but that would give too much credit to steroids alone. Of course training methods and nutrition are part of the puzzle, but the other piece is probably not as obvious. In the mid-´90s starting in the American League and in the late ´90s starting in the National League, home runs began to become more and more common.
Although steroids are often blamed, the construction of more "homer-friendly" ballparks also has something to do with it, no doubt. Coors Field, a recent addition to the MLB stable of fields has become the most prolific run-scoring park in the history of MLB. Enron Field was also built (reincarnated into the more media friendly "Minute Maid Park"), actually has a home-run friendly left field line that was (and still may be) a clear violation of major league rules. The Milwaukee Brewers, the Pittsburgh Pirates and Texas Rangers have all also built very homerun-friendly fields in recent years, as have the Arizona Diamondbacks. For their part, the Cardinals, Orioles, and White Sox have pulled in the distance from home-plate to their outfield fence. Need I also add that the strike zone has become much more beneficial to hitters since the era of Roger Maris? Still, the questions remain, about steroids in major league baseball. Do major league baseball players use steroids? Of course they do. Can we say that steroids are the reason for the inflated home-run statistics of recent years? Of course not.
With Multi-Million dollar contracts on the line every season, the only fact that we can be sure of is that steroids are being used in baseball, and they will continue to be used for as long as players can get away with it. Congress recently chimed in and pressured MLB into instituting a comprehensive testing policy for their athletes, but steroid use in baseball is unlikely to decline considerably as a result of it.
Steroids in FootballSteroid policy in football and the NFL as we know it began in 1987. But to understand the use of steroids in football, first we need to take a look at the emerging trends in the high school and collegiate ranks. So what´s going on in high school? Well, if we look at an examination of the heights and weights of members of the annual Parade Magazine´s High School All-American Football Teams from 1963-1971, we see no significant changes in the Body Mass Index of these elite high-school athletes. Now, if we take another look and examine those same players´ heights and weights but this time we compare 1972-1989, we see a clear trend towards an increased pattern in Body Mass Index (11). These are interesting results, to say the least. If we take a look at an elite collegiate program such as Michigan State University, we see this trend again. In 1975, their average player weighed 213lbs, and by 2005 that weight had jumped to 236lbs (12).
With regards to football, it would seem that current educational efforts are not working well, either. At the high school level education about steroids was studied on six different. Two football teams received a lecture on steroids and a four-page handout, two of them were given just the handout, and two teams were controls (and didn´t receive any education on steroids). Also, at this level of football, the incidence of self-report of current steroid use was 1.1%. After the education was given to the athletes, focusing of the adverse effects possible with anabolic steroid use, no differences in their attitudes toward the use of anabolic steroids occurred as compared to controls, at all (13). So that´s the starting point we have to look at anabolic use in professional football. Education, in its current form isn´t changing the attitudes of high-school players, and at the elite level of high-school and college, the players are getting significantly bigger. So what does the landscape of professional football look like? In a story that is very similar to its roots in high school and collegiate football, NFL linemen are weighing well over 300lbs on average today. Roughly 25 years ago, they weighed over fifty pounds less, on average (13).
The most famous story of steroid use in the NFL is that of Lyle Alzado. Seven years after having a successful career in the NFL, in 1992, Alzado died from brain lymphoma, a very rare form of brain cancer. He was 43 that year, but in the years preceding it, Alzado became an often used symbol of the dangers of steroid abuse. There is absolutely no medical link between steroids and brain lymphoma, and there is absolutely no reason for Alzado to believe his condition was related to steroid use.
The story of Bill Romanowski is probably the next most influential one concerning steroids in football. Although Bill Romanowski wasn´t indicted in the BALCO scandal, he later wrote a book, in which he admits that Victor Conte introduced him to several performance enhancing compounds, notably anabolic steroids (15).
Although he was a very good linebacker before he used steroids, people often attribute his tackling ability to them. He is probably most famous for his non-playing related antics, however. He spit in J.J. Stokes´ face, broke somebody´s finger at the bottom of a pile up, kicked a downed player in the head several times in one incident, broke a quarterback´s jaw with an illegal helmet to helmet hit, fought former boxer Charles Haley in training camp, often speared wide receivers illegally, broke another players´ ocular cavity, and was always involved in various shoving matches and on field altercations. Unfortunately, this has been attributed, post-facto, to his use of anabolic steroids.
Of course, football players use steroids, and of course this occurs at the high-school, collegiate, and professional levels. It´s a fact of the game that a very skilled but small player will usually get beaten by a very skilled but considerably larger player.
And once again, as long as there is prestige and money to be earned from playing football, there will be steroids in it.
Steroids in the OlympicsAnabolic steroid use in athletics, in all probability, began with the 1952 Olympics, as noted earlier in this article. Although not chronologically correct, I´m going to also finish this piece with the most famous case of sports doping in the world. Of course, I´m talking about the man who was considered the fastest man in the world: Ben Johnson. After breaking the world sprinting record in the 1988 Seoul Olympic Games, he tested positive for Winstrol (Stanozolol). For anyone who has never heard his coach tell the story, Charlie Francis has provided ample evidence for the test being somewhat unreliable (3). Briefly states, the accepted drug clearance time for Winstrol at that time was +/- three days for the oral form and +/- 14 days for the injectable. Ben had used the compound 28 days prior to the race, and the parent compound was still found. This is especially odd, since the parent compound only lasts for 45 minutes after administration. The testers, therefore, must be making the claim that Ben ingested it just prior to the actual race. Both he and his coach, Mr. Francis, denied this. In fact, it was later discovered that someone as lean as Johnson may have even been clear in less than 3 days! Some oral steroids at that time (Anavar, or Oxandrolone) couldn´t even be found on tests at that time.
So the test remains very suspect, although Ben Johnson was suspended and stripped of his Olympic Gold medal. He probably suffered the worst fate of all the people who have been caught using steroids either at the Olympics or otherwise.
So where does that leave us? Well certainly, the world of sports has embraced the use of steroids, or at least the athletes have... the use of steroids in sports is certainly visible but not as widespread as thought. It is not the problem that it is often made out to be, and it is not a problem that is easily defined or to put a number on. Statistically, it is a very elusive topic, and sources often present conflicting data. But one thing remains true, regardless of statistics, Congressional hearings, or admissions of guilt. Although some athletes still compete for the love of the game, prestige often accompanies success. And today, just as two millennia ago, athletes often find the opportunity to compete for both prestige as well as money. And that is why they sought out performance enhancers in the ancient Olympic Games, and that´s why athletes are using steroids in sports today.
By Anthony Roberts
References:
Wm. Blake Tyrrell, "The Smell of Sweat: Greek Athletics, Olympics, and Culture," Bolchazy-Carducci Publishers, Wauconda. 2004. "Hormonal Doping and Androgenization of Athletes: " Franke et. al "A Brief History of Drugs in Sport" by Charlie Francis "Speed Trap" by Charlie Francis JAMA 1988 Dec 16;260(23):3441-5. Am J Dis Child. 1990 Jan;144(1):99-103. J Sch Nurs. 2005 Dec;21(6):333-9. J Strength Cond Res. 2004 Nov;18(4):908-17. Monitoring the Future [MTF], n.d Journalism. 5(1). 51-68, 2004. Percept Mot Skills. 1993 Apr;76(2):379-83. (Michigan State University Dept. of Athletics) J Adolesc Health Care. 1990 May;11(3):210-4. (National Football League Statistics) "Romo My Life on the Edge: Living Dreams and Slaying Dragons."by Bill Romanowski et al. William Morrow Publishing co. 2005.

EPO (Erythropoietin)

EPO (Erythropoietin)

EPO gained notoriety in 1998 when a bunch of cyclists in the Tour de France got caught in posession of it.
EPO increases RBC in the blood. This will basically raise your energy levels (Cancer. 2003 Sep 1;98(5):1072-9), and thus will improve recovery, etc...A50 was developed for a very similar purpose as EPO, and I suspect that alot of the muscle enhancing effects/potency of A50 (increased muscle fullness, etc...) can be attributed to the much of same mechanisms which are at work in EPO. Its worth noting that EPO increases protein synthesis, just like A50 as well. Primarily, though, its effect is to increase RBCs.
Having more RBCs, thus having more oxygen delivered to muscle tissues is directly associated with a substantial improvement in athletic performance, i.e speed, endurance, strength, etc...(Sports Med. 2003;33(3):187-212.). EPO is associated with improved bodyweight, excercise capacity, oxygen uptake, respiration, whole body metabolism and energy efficiency (Semin Oncol. 2002 Jun;29(3 Suppl 8):69-74) In addition, cognitive function (learning, etc...)is also improved with EPO(Clin Breast Cancer. 2002 Dec;3 Suppl 3:S116-20).
Ok...so how much do you take? I'd say you'll need about 8,000-10,000IU for 2 weeks. Thats it. You take it all at once over 2 weeks (maybe a little over 1,000IU or so per day for 14 days) and then thats it. Then, sometime in week 3, you'll start feeling the results...which will last...for 3-6 months! Yeah, you read that right.
Watch your BP, and don't let it get out of hand, because that could mean your hematocrit is getting too high....and remember to keep well hydrated to avoid any possible issues with clotting & keep some aspirin on hand just in case you find that you need to thin your blood out a bit.

Clenbuterol

Clenbuterol

Let me just start by saying that this is the single most mis-understood compound in use for athletics and bodybuilding today. Most of the information out there is ½ truths and conjecture. Ok…having said that, I’m going to make an effort to dispel some myths and give everyone a better understanding of Clen.

First, lets plow quickly through some of the basics:
Clenbuterol (Clen) is a beta-2 agonist/antagonist bronchodilator. What this means, is that it stimulates your beta-2 receptors. And this in turn stimulates you (clen has stimulant effects which will make you feel….well…stimulated). All of this serves to increase your body temperature a bit, increase your basal metabolic rate, and decrease your appetite (Int J Obes Relat Metab Disord. 1994 Jun;18(6):429-33.). Clen also can decrease insulin sensitivity (Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E146-53.).
Clen is a very effective repartitioning agent, and this is what it’s most often used for. What this means is that it will increase your ratio of Fat Free Mass (FFM) to Fat Mass, by decreasing your Fat and possibly increasing your FFM (J Appl Physiol. 2001 Nov;91(5):2064-70). Want me to quantify that a bit? In one study, horses given a reasonable dose of clen (slightly over 1mcg/lb) and excercised for 20mins, 3x a week ( I suppose they were Mentzer disciples) had significant decreases in %fat (-17.6%) and fat mass (-19.5%) at week 2, which was similar to Clen given to horses who didn’t excercise; however, the excercised group had a different FFM response, which significantly increased (+4.4%) at week 6. Week 6! Clen and clen+excercise produce roughly the same results for the first 2 weeks! Remember the old 2 weeks-on/2weeks-off schedule? It’s officially dead and buried. If you want the quasi-anabolic effect from the clen, it’ll take more than 2weeks on (6 weeks apparently). And in fact, since clen alone is similar to clen+excercise for those first 2 weeks...why would you ever use a 2on/2off protocol? Keep in mind that animal responses to beta-agonist/antagonists differ a bit from ours…but you get the picture. 2on/2off? Ha ha...
Clen has a biphastic elimination, which means that it is technically reduced in your body in 2 different stages. This isn’t particularly important, as a recent study has shown that for most intents and purposes, clen concentrations in the body decline with a ½ life (approximately) equivalent to 7-9.2hours and again up to as much as 35 hours later(J Anal Toxicol. 2001 May-Jun;25(4):280-7. and J Vet Pharmacol Ther. 2004 Apr;27(2):71-7. and J Pharmacobiodyn. 1985 May;8(5):385-91. ). If you’re really interested, though, clen technically declines biphastically at 10 and then 36 hours. But really, in our little world, where we use ½ life to tell us when to take our next dose, who the hell is going to take clen, then a dose 10 hours later, then a dose 36 hours later. We’ll stick with the earlier 7-9 hour ½ life for dosing purposes, and take our clen every 3.5-4.5 hours that we’re awake, stopping early enough to still be able to get to bed. Clen can, in some people, cause insomnia (and as with all stimulants, can cause anxiety in some).
Clenbuterol can also cause a downregulation in testicular androgen receptors and in pulmonary, cardiac and central nervous system beta-adrenergic receptors(J Anim Physiol Anim Nutr (Berl). 2004 Apr;88(3-4):94-100.)…possibly making steroids less effective while you are on clen, but definitely making clen less effective as time goes on and you keep taking it. To counteract this, you can take some ketotifen or periactim every 3rd or 4th week that you remain on clen. Both of these are prescription anti-histimines, so they’ll make you drowsy (take before bedtime). Basically, the way both of these work is to reduce beta-2 receptor activity.
A lot of people claim that clen is quite anti-catabolic and/or anabolic. This hasn’t been confirmed in human studies (Ann Pharmacother. 1995 Jan;29(1):75-7.). And the doses given to the animals in these studies where clen is shown to be very anticatabolic or highly anabolic are so absurdly high that no human could ever take them (1mg/kg of bodyweight and higher). The best you can hope for is the very mild anabolic effects I cited earlier.
Oh yeah…I guess I should get around to the proper dosing of clen. My recommendations are the same for both men and women. You’ll need to take 20mcgs upon rising, and then repeat that same dose again later in the day, and then once again in that day (if you find you can tolerate the effects). So you’ll start with 20mcgs, and then repeat that dose 2 more times that same day if you can tolerate it (side effects will determine this…hand shaking, sweating, etc…classic stimulant sides). Then you can start increasing the dose gradually. Personally, I wouldn’t work my way up to more than 200mcg/day. 60-120mcg/day is an average dose.
Also, bear in mind that clen isn’t great for your heart, and can cause some issues there (enlargement of ventricles, etc…) but most studies showing clen to cause heart problems are with animals, and even though the dosing is similar to what humans take (in some studies) it’s important to remember that animals have more beta-2 receptors and they cause certain event chains that humans’ beta-2 receptors may not. Clen causes cardiac hypertrophy to some degree, in some cases. Again though, many studies showing more significant heart problems are with mg dosing. We humans take clen in mcg doses.
If we want to duplicate the “theraputic” levels of clen in the more conservative studies, we’d be taking just over 1mcg/lb of bodyweight. I’d suggest a bit less, though.
Performance issues with clen also vary. Some studies show reduced exercise (cardiovascular) performance with clen (Med Sci Sports Exerc. 2002 Dec;34(12):1976-85.), while some show that clen can alleviate exercise induced asthma (Respiration. 1987;51(3):205-13.)! Sometimes you feel like a nut…sometimes you don’t, I guess. What this means, to me, is that you’ll need to figure out how clen affects your performance individually.
Which brings me to the issue of cramps while on clen. I don’t get them. My friends don’t get them. Most of us are athletes who use clen during the season as well as the off season, and one of my friends even claims that it gives him more “wind” (cardiovascular stamina). Take on enough water every day and you should be fine. If you’re really concerned, you can take some extra minerals and taurine, since clen depletes taurine (Adv Exp Med Biol. 1996;403:233-45) as do most if not all beta-agonists. I don’t take anything more than my usual vitamins and minerals.
Well…there it is…pretty much all I know about clen. I hope this answers some questions and clears up some misconceptions.

Clomid: Frequently Asked Questions

Clomid: Frequently Asked Questions
Something I put together that may help some of the new comers out there as well as some of the more experienced.
Question: What is Clomid?

Answer: Clomid is a synthetic estrogen and is generally prescribed by doctors to trigger ovulation in females.

Question: Why Should Bodybuilders use Clomid?

Answer: Almost all anabolic androgenic steroids will cause an inhibition of the bodies own testosterone production. When he comes off the steroids he has no natural test production and no more steroids. The body is left in a state of catabolism (catabolic hormones are high and anabolic hormones are low) and as a result much of the muscle tissue that was gained on the cycle is now going to be lost. Clomid stimulates the hypophysis to release more gonadotropin so that a faster and higher release of follicle stimulating hormone aud luteinizing hormone occurs. This results in an increase of the body's own testosterone production.

Question: Does Clomid also work as an anti estrogen?

Answer: Clomid is a synthetic estrogen, however it does also work as an anti-estrogen. How does it work? Because it is a weak synthetic estrogen, it will bind to the estrogen receptor (ER) and not cause any problems. At the same time the increase in estrogen from steroids are blocked from attaching to the ER.

Question: How effective is Clomid as an anti-estrogen?

Answer: It is very weak and should not be relied upon if you are going to be using steroids that aromatise at any rapid rate, or if you are pre disposed to gyno. arimidex, Proviron and Nolvadex will all make better choices for this purpose.

Question: Some say Clomid during a cycle is a waste, is this true?

Answer: Lets first examine what happens when someone is using anabaolic androgenic steroids. When the level of androgens in the body get too high, the androgen receptor becomes more highly activated, and the hypothalamus stops sending a signal to the pituitary. In short the signal tells our body to stop producing testosterone. During a cycle the body has higher levels than normal of androgens and as long as this level is high enough Clomid will not help to keep natural test production up. It will be almost all but completely shut off. The only purpose of Clomid during a cycle is as an anti-estrogen.

Question: When do I start Clomid? Some say 2 weeks others 3.

Answer: When you start using your Clomid all depends on what steroids you were using during your cycle. Different steroids have different half lifes and you should adjust your Clomid intake accordingly. As we have seen above, if we take Clomid when the androgen levels in our body is still high it will be a waste. We need to wait for androgen levels to fall before implementing our Clomid therapy. However if we take it too late we could possibly lose gains. Look at the list below to determine when you should start Clomid therapy. By selecting from the list all the steroids you used in your cycle and which ever one has the latest starting point then go with that. For example if I cycled dbol, sustanon and winstrol I would use sustanon as it remains active in the body for the longest period of time.

Anadrol/Anapolan: 8 - 12 hours after last administration
Deca: 3 weeks after last injection and Clomid for 4 weeks
Dianabol: 4 – 8 hours after last administration
Equipoise: 3 weeks after last injection
Fina: 3 days after last injection
Primobolan depot: 10 – 14 days after last injection
Sustanon: 3 weeks after last injection
Testosterone Cypionate: 2 weeks after last injection
Testosterone Enanthate: 2 weeks after last injection
Testosterone Propionate: 3 days after last injection
Testosterone Suspension: 4 – 8 hours after last administration
Winstrol: 8 – 12 hours after last administration

Question: What is the most effective way for Clomid therapy.

Answer: Clomid has a long half life and as such there is no need to split up doses throughout the day. I read some where that it was 5 days (any feedback on this). Now if we used sustanon and we start using Clomid 3 weeks after our last injection we anticipate that androgen levels are low enough to start sending the correct signals. If androgen levels are still a little high then the normal 50mgs/day of Clomid for 1 week is not going to be effective. We need to start at a high enough amount that will work or help even if androgen levels are still a little high. 300mgs on day 1. I know I said don’t split it up due to its long half life but try and split this up 2 tabs 3 times a day. After we have finished this first day we seek to use 100mgs for 10 days and then followed by 50mgs for 10 days.

Question: Do I need to use Clomid for 3 weeks?

Answer: Why don’t you want too? It is very cheap, very effective and can mean the difference between maintaining gains and losing them.

Question: How cheap is Clomid?

Answer: Clomid normally comes in 50mg tablets but also comes in capsule form of 25mgs. A 50mg tablet can be anywhere between 25 cents and $2.50. (15 pence and 75 pence in England).

Question: Do all steroids cause shut down of the hpta.

Answer: Not all steroids do. Everyone is different and you must also take into account how long you have been using a certain steroid and at what dose in order to determine if you need Clomid or not. However as the price is so cheap, why risk not using it.

Nolva vs. Clomid for PCT

Nolva vs. Clomid for PCT
It seems like everyday questions concerning PCT pop up, and weather one should use either Clomid or nolva or a combo of both. I hope that this article written by BigCat may help to clear up some misconceptions.


While practically similar compounds in structure, few people ever really consider Clomid and nolva to be similar. Its not just a common myth in steroid circles, but even in the medical community. This misconception originates from their completely different uses. Nolvadex is most commonly used for the treatment of breast cancer in women, while Clomid is generally considered a fertility aid. In bodybuilding circles, from day one, Clomid has generally been used as post-cycle therapy and Nolvadex as an anti-estrogen.

But as I intend to demonstrate this is in essence the same. I believe the myth to have originated because nolva is clearly a more powerful anti-estrogen, and the people selling Clomid needed another angle to sell the stuff, so it was mostly used as a post-cycle aid. But few users really understand how Clomid (and also Nolvadex, logically) works to bring back natural testosterone in the body after the conclusion of a cycle of androgenic anabolic steroids. After a cycle is over, the level of androgens in the body drop drastically. The body compensates with an overproduction of estrogen to keep steroid levels up. Estrogen as well inhibits the production of natural testosterone, and in the period between the return of natural testosterone and the end of a cycle, a lot of mass is lost. So its in everybody's best interest to bring back natural test as soon as humanly possible. Clomid and Nolvadex will reduce the post-cycle estrogen, so that a steroid deficiency is constated and the hypothalamus is stimulated to regenerate natural testosterone production in the body. That's basically how the mechanism works, nothing more, nothing less.

Both compounds are structurally alike, classified as triphenylethylenes. Nolvadex is clearly the stronger component of the two as it can achieve better results in decreasing overall estrogen with 20-40 mg a day, than Clomid can in doses of 100-150 mg a day. A noteworthy difference. Triphenylethylenes are very mild estrogens that do not exert a lot, if any activity at the estrogen receptor, but are still highly attracted to it. As such they will occupy the receptor and keep it from binding estrogens. This means they do not actively work to reduce estrogen in the body like Proviron, Viratase or arimidex would (by competing for the aromatase enzyme), but that it blocks the receptor so that any estrogen in the body is basically inert, because it has no receptor to bind to.

This has advantages and disadvantages. The disadvantage is that when use is discontinued, the estrogen level is still the same and new problems will develop much sooner. The advantage is that it works much faster and has results sooner than with an aromatase blocker like Proviron or arimidex. Therefor, when problems such as gynocomastia occur during a cycle of steroids one will usually start 20 mg/day of nolva or 100 mg/day of Clomid straight away, in conjunction with some Proviron or arimidex. The proviron or arimidex will actively reduce estrogen while the Clomid or Nolvadex will solve your ongoing problem straight away. This way, when use is discontinued there is no immediate rebound.

So which one should you use? Well personally, I'd have to say Nolvadex. Both as an on-cycle anti-estrogen and a post-cycle therapy. As an anti-estrogen its simply much stronger, demonstrated by the fact that better results are obtained with 20-40 mg than with 100-150 mg of Clomid. For post-cycle, this plays a key role as well. It deactivates rebound estrogen much faster and more effective. But most importantly, Nolvadex has a direct influence on bringing back natural testosterone, where as Clomid may actually have a slight negative influence. The reason being that tamoxifen (as in Nolvadex) seems to increase the responsiveness of LH (luteinizing hormone) to GnRH (gonadtropin releasing hormone), whereas Clomid seems to decrease the responsiveness a bit1.

Another noteworthy fact about Nolvadex is that it acts more potently as an estrogen in the liver. As you remember, I mentioned that clomiphene and tamoxifen are basically weak estrogens. Well, tamoxifen is apparently still quite potent in the liver. This offers us the positive benefits of this hormone in the liver, while avoiding its negative effects elsewhere in the body. As such Nolvadex can have a very positive impact on negative cholesterol levels2 in the body, and therefore too should be considered a better choice than Clomid. It will not solve the problem of bad cholesterol levels during Steroid use, but will help to contain the problem to a larger degree.

Another reason why I promote the use of Nolvadex over Clomid post-cycle (as if being 3-4 times stronger and having more of a direct effect on restoring natural test wasn't enough) is because it's a lot safer. Not just because it improves lipid profiles, but also because it simply doesn't have the intrinsic side-effects that Clomid has. Clomid causes more acne for sure, but that's mainly because you need to use a 3-4 times higher dose. But Clomid seems to also affect the eyesight. Long-term Clomid therapy causes irreversible changes in eyesight3 in users. Irreversible. For me that alone is reason enough to prefer Nolvadex.

Lastly, one should be aware that use of these compounds can reduce the gains made on steroids. Nolvadex more so than Clomid, simply because it is stronger. Estrogen is responsible for a number of anabolic factors such as increasing growth hormone output, upgrading the androgen receptor and improving glucose utilization. This is why aromatizing steroids like testosterone are still best suited for maximum muscle gain. When reducing the estrogen levels, we therefore reduce the potential gains being made. For this reason one may opt to try Clomid during a cycle instead of Nolvadex. Although I would imagine that the problem that needed solved would be of more concern, in which case nolva remains the weapon of choice. It's a plain fact that there is a high correlation between gains and side-effects. Either you go for maximum gains and tolerate the side-effects, or you reduce the side-effects, and with it the gains. That's life, nothing is free.

Stacking and Use:

If problems of Gynocomastia or other estrogen related symptoms tend to pop up during a cycle the use of 20-30 mg of Nolvadex or 100 mg of Clomid daily should easily contain the problem, and be used until a few days after the problem subsides. For best results and the least amount of problems upon cessation it is best stacked with proviron (50 mg) or arimidex (0.5 mg) for this duration as well. Its not advised that these products be ran concomitantly with the steroid for the entire duration of the stack, as this will reduce your gains. Instead cease the usage of anti-estrogens once the problem is contained, and should the problem resurface, simply recommence the use of the products in the same manner as described above.

Once a cycle of steroids is concluded one should always initiate a post-cycle therapy to help bring back natural testosterone as soon as possible. This will help you to retain the mass you gained. How this is done depends highly on the type of steroid used. If only orals were used, therapy should start immediately, even the last day of the stack. If short-acting esters or water-based injectables were used, therapy should commence within 4-7 days after last injection, and if long-acting esters were used then it should commence 1.5 to 2 weeks after the last injection was given. The length of the therapy will vary as well, from 3-5 weeks. The longer acting the product was, the longer therapy should be continued to make sure all suppressive factors are cleared before use of Clomid/Nolvadex is discontinued.

The questions you will hear from athletes over and over is if they can get legal steroids clomid and nolvadex, is it possible?well I say yes you just have to look.
For best results, it is best stacked with HCG (Human Chorionic gonadotrophin), which functions as an LH analog and can help bring testicle size back up. HCG use starts the last week of a cycle, and on from there every 5-6 days (usually 1500-3000 IU) and discontinued 1.5 to weeks prior to the cessation of Nolvadex/clomid. The reason being that HCG itself is also suppressive of natural testosterone and should be out of the body before therapy is over, or it will inhibit natural testicle function. But I can not stress enough that HCG possibly plays a more important role in post-cycle therapy than clomid/Nolvadex. For Clomid and Nolvadex, doses are usually tapered down. Its best to start with 40-50 mg of Nolvadex or 150 mg of Clomid for the first week or the first two weeks, and then finish the program with 20-25 mg of Nolvadex or 100 mg of Clomid for an additional two weeks.

References

1 Vermeulen A., Comhaire F., Hormonal effects of an anti-estrogen, tamoxifen, in normal and oligospermic men, Fertil. Ster. 29 (1978) 320-27

2 Bruning PF, Bronfer JMG, Hart AAM, Jong-Bakker M, tamoxifen, serum lipoproteins and cardiovascular risk, Br. J. Cancer 1988 Oct, 58 (4) 497-9

Anabolic Workout Guide

You should take the following factors to heart since they are absolutely necessary for a successful training. What role does the use of anabolic/androgenic steroids play- Very simple: athletes who take steroids will make clearly faster, better, and greater progress than their natural colleagues. They will also obtain a much higher development stage than would have ever been possible without taking pharmaceutical compounds. Such stupid statements that one will achieve the same mass as a bodybuilder without taking steroids -it only takes longer- is nothing but a completely absurd publicity by the authorities who in their own interest conceal the truth. Read the following lines with an open-minded attitude and try to adapt this information for your own needs.
1. High-intensity training: The human organism vehemently refuses any unnecessary change since it feels best in a constant condition, a homeostasis. In order to lure it out of its passivity, several efforts and exertions must be made. The signal that the body needs in order to build up strength and muscle mass is triggered by heavy, hard, and intense training routines. These should consist of relatively few sets. Five to eight sets for large muscle groups and three to four sets for small muscle groups are completely sufficient when every set is carried out until muscle failure.
2. Training with relatively low repetitions: The body has two different types of muscle fibers: Since the muscle hypertrophy almost completely occurs in the fast-twitch white muscle fibers of type 2, a sensible bodybuilding workout must be developed in a way that these are sufficiently stimulated. For this purpose relatively few, heavy reps in the range of 6-10 are suitable.
3. Training with progressively heavier weights: In order to build up massive muscles they must be challenged and exposed to regular progressively-higher resistances. This can be achieved when the athlete continuously increases the weight during exercises. The stronger the muscles the larger their appearance. There is no mass without power. The basic exercises such as squats, bench presses, presses behind the neck, rows, barbell curls, dips, etc. are the most suitable.
4. Sufficient rest periods: The muscles are stimulated through training but only grow during their rest phase. The higher the intensity, the higher the damage of the muscle cell and the longer the resting phase. When you train with adequate intensity you simply cannot train each and every day nor should you attack a muscle twice a week. Learn to accept rest and recovery as important factors of your training success. Every day you train in the GYM should be followed by a complete off day. Bodybuilders who are interested in an optimal strength and muscle gain should train every muscle once very intensely every 7-8 days.
5. Plateau and phase training: The body can be put under maximum stress only for a limited time. If this time is exceeded, development comes to a stop and if continued the performance will regress. For this reason the intensity and extent of the training program should be changed every 12-14 weeks. The athlete should enjoy several days off training and then change to a several-week long maintenance training (plateau training).
The following training program considers all essential factors which are necessary for a quick buildup of strength and muscle mass. In combination with the nutrition tips included in this book its effectiveness can be considerably increased. Based on the high intensity it is not suitable for natural bodybuilders over a long time. This training schedule is obviously only intended as a suggestion and can be changed by every athlete to meet his individual needs, as long as the discussed principles are met.

Eight-Day Training Cycle: One day training, one day rest(One day on, one day off)Day 1: Chest, biceps Bench presses 3 sets 6- 8 reps Incline bench presses 2 sets 6- 8 reps Dips with added weights 2 sets 8-10 reps Barbell curls 3 sets 6-10 reps Dumbbell curls 2 sets 6-10 reps Day 3: Thighs Squats 3 sets 6-10 reps Leg presses 2 sets 8-10 reps Leg curls 2 sets 8-10 reps Day 5: Shoulder, triceps Presses behind neck 3 sets 6- 8 reps Upright row 2 sets 8-10 reps Side laterals 2 sets 8-10 reps Lying triceps presses 3 sets 6-10 reps Triceps pulley pushdown 2 sets 8-10 reps Day 7: Back. calves Chins with added weight 3 sets 8-10 reps Lat pull to neck 2 sets 8-10 reps Barbell bent-over row 2 sets 6-10 reps Seated cable row 2 sets 6-10 reps Standing calf raise 3 sets 8-12 reps Seated calf raise 2 sets 8-12 reps
Note: Training is only on uneven days, i.e. every 2nd, 4th, 6th, and 8th day is a complete rest day. The intervals between the various sets should be 3-4 minutes. The athlete should pay attention that the exercises -as much as possible- are carried out with free weights and not on machines. Every muscle is directly trained only once every eight days. It is important that every set is carried out until muscle failure meaning that the athlete is unable to do another rep-etition on its own. Only in this case are the relatively few sets and especially long rest periods justified. The muscle cell must be brought in a strongly catabolic condition since only then the distinct anticatabolic effect of anabolic/androgenic steroids develops fully. The required intensity of training, however, can only be achieved when you start (after a short warmup) with the heaviest weight possible and then decrease the weight in every following set because of the losing body strength so that the desired repetitions can still be obtained. In order to avoid any misunderstandings we would like to quickly explain this principle on an example. Our athlete is able to carry out a maximum of six repetitions with 300 pounds on bench presses.
1st warmup set: 10 reps with 140 pounds 2nd warmup set: 2 reps with 200 pounds 3rd warmup set: 2 reps with 240 pounds 1st working set: 6 reps with 300 pounds 2nd working set: 7 reps with 280 pounds 3rd working set: 7 reps with 260 pounds
The first warmup set serves to bring blood to the muscles and joints. The second and third warmup set are an approach to the weight of the first working set. The interplay between the muscle and nerve is stimulated, meaning the athlete gets a feeling for the heavy weights without wasting strength and energy at the same time. During the following chest exercises the warmup sets are completely omitted which means that they are only necessary for the first exercise of the muscle to be trained. Do not forget, however, that during every exercise or set you should try to squeeze out an additional one or two repetitions than during the previous training in order to in-crease training weights in the following week. This continuous tire-some struggle to increase repetitions and weight is the only way to a massive body. Always remember: HEAVY WEIGHTS BUILD BIG MUSCLES.

http://www.isteroids.com/

Side Effects of Steroids

Side Effects of Steroids
Most of the time, when steroids are mentioned, they´re brought up as the reason a particular athlete can run so fast, hit so many home runs, or make so many tackles. They are also claimed to have extraordinarily harsh side effects and for causing severely unforgiving and permanent damage. Everybody´s seen movies like "The Program" where steroids ruin a young athlete´s life, or perhaps "The Aaron Henry Story" on HBO, where a young athlete suffers lifelong problems from his steroid abuse. Most recently, I saw the movie "Spiderman" where the villain, the Green Goblin, admits to having his superhuman strength and psychotic personality from using "performance enhancers"!
I´m here to assure you that those types of horror stories are few and far between, and after consulting with literally hundreds of athletes and bodybuilders, I´ve almost never heard of anything even remotely resembling the popular "horror stories" we see in the media almost daily. I´ve certainly never seen anyone become the Green Goblin from using them, either..
By reading this article, coaches, athletes, parents and teachers will know the truth about anabolic steroid side effects and will be able to make their own informed decisions as to how bad they are. But I suspect that after reading what I have to say, as well as what the scientific literature says, the question of how bad steroids are will be a different question entirely; the only question remaining will be "why didn´t anyone tell me this before?"
When I initially started research for this piece, I consulted not only real-life athletes who had vast experience with anabolic steroid use, but also scientific and medical journals. The picture that unfolded before me was very different than the one typically painted by the mass media, and certainly much different than the one I found on www.steroidabuse.org, www.dea.org, and www.drugabuse.gov. In my research on the governmental sites, I found very little of use, to be perfectly honest. There were tons unfounded claims and talk of money being put into "studies." In reality, the government "studies" on anabolic steroids were not medical studies at all. They were surveys given to various age groups, on steroid use, in order to generate statistics. There was nothing of medical value or scientific merit on those sites, despite the endless parade of doctors that seemed to be against their use. Here´s an example of one of the more absurd claims made on one of those sites:
"..[steroids] they are dangerous drugs, and when used inappropriately, they can cause a host of severe, long-lasting, and often irreversible negative health consequences. These drugs can stunt the height of growing adolescents, masculinize women, and alter sex characteristics of men. Anabolic steroids can lead to premature heart attacks, strokes, liver tumors, kidney failure and serious psychiatric problems. In addition, because steroids are often injected, users risk contracting or transmitting HIV or hepatitis.."
This is the information found on a government website, in a piece written by a doctor. I´m surprised she didn´t mention turning into the Green Goblin in her list of possible health side effects. As you read what I have to say, I want you to keep this in the back of your head. I want you to remember this claim, made by a medical doctor, as you read the rest of this piece. All of the information here is exactly what has been reported to me by athletes, as well as what is found in credible scientific journals; then decide for yourself what the truth about steroid side effects is.
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Anabolic Steroid Side Effects:1. Inhibition of Natural HormonesThe inhibition of natural hormones is probably the most common and probable side effect experienced from the use of anabolic steroids. In almost all cases, adding a hormone into your body will send a message to your endocrine system to stop producing it. This is because your body wants to remain in a very balanced state -- called "homeostasis," if I remember my high school biology class correctly. To maintain homeostasis, the body wants to avoid having too much of any particular hormone. To achieve this, the body sends a message to the testicles to slow down, or even stop producing testosterone when there is too much circulating. Unfortunately, this happens when any kind of hormone is added into the body, so even if an athlete is not using testosterone, but is using other anabolic steroids, the body will still send this signal 99% of the time. Of course different steroids cause varying degrees of inhibition ranging from total shut down of endogenous (natural) testosterone production, to very mild inhibition, where some natural hormones are still being produced and circulating. In almost all cases, this inhibition is over once the steroids aren´t active in the body anymore. In the following charts, we can see a mirror image of the level of steroid in the body (Nandrolone), compared with the level of natural testosterone being produced. In other words, as the level of steroid rises (chart 2), the level of testosterone falls (chart 1), and vice versa:

Now, as that first chart shows, testosterone levels fell when Nandrolone (an anabolic steroid was administered, but interestingly, the following chart shows an almost identical mirror image, where the Nandrolone levels in the blood rise. What this indicates is that the amount of this particular steroid in the blood is directly and proportionately inhibiting natural testosterone production. Here´s the chart:

Most athletes who use anabolic steroids accept all of this as a necessary price to pay in order to experience the benefits from using steroids. In an effort to combat this, athletes have experimented throughout the years with various compounds to avoid or at least limit this problem. Human Chorionic Gonadotropin, anti-estrogens, and Selective Estrogen Receptor Antagonists are all used during a cycle, or after (or both) with this goal in mind. The following is a table showing the various hormonal levels of former steroid users who haven´t used them for a year (*called "ex-abusers" by the nice people who funded the test) versus current users (*abusers):

What we see in this chart is not surprising to anyone who is actually familiar with steroids, and not with media-hype. In people studied who haven t used steroids for a year, ALL of their measured hormones (testosterone, estrogen) were within the NORMAL RANGE! Clearly, the effects that steroids have on your hormones are reversible and the horror stories we ve all read in the media about people who never regained normal hormonal function after one cycle  are greatly exaggerated. I think anyone who is familiar with "After School Specials" about steroids will be very surprised at learning this fact. As for "The Aaron Henry Story" on HBO, I can t imagine how he has suffered side effects well into his 40âs when the steroid users in this study were totally fine after one year, and in some cases used more than he did!
(*Journal of Steroid Biochemistry and Molecular Biology. 84 (2003) 369-375)
2. Steroid Effects and Liver DamageLiver damage is probably the most sensationalized of all side effects possible from steroid use. The media often focuses on this particular problem as if it occurs with every steroid, and in every person who takes them. Nothing could be further than the truth. Most anabolic steroids which are ingested orally pass through the liver, which functions as the body´s filtration system. When something goes through the liver, it is broken down by various enzymes, and passed along into the bloodstream. Most research on orally administered anabolic steroids focus on the fact that liver enzymes are elevated following ingestion. But does this necessarily mean that the liver is being damaged, does it? Of course not. Commonly, studies that focus on steroid toxicity often use absurd doses, or incorrectly focus on liver activity instead of damage. The liver functions as the filter for the human body.. it´s going to be activated whenever something (not just a steroid) passes through it. Does that show that steroids damage the liver? Let´s see what the scientists say..
There was an eight-week study done in 1999, which looked at the effects of an 8-week cycle of Oral steroids. The steroids examined were Halotestin (Fluoxymesterone), Dianabol (methylandrostanolone), or Winstrol (Stanozolol) on rats at the dose of 2mg/kg-body weight, administered five times a week for 8 weeks. That s almost 200mgs/day of any of those steroids, for a 200lb user. That is, I´ll speculate, much more than the average person would use on a cycle. In fact, I have never, in my years of researching steroids and speaking with athletes, heard of anybody using 200mgs/day of Halotestin, Winstrol, or Dianabol. Ever.
And, at the end of that study, In vivo, each rat still had liver enzyme levels that were within normal range!
(*Med Sci Sports Exerc. 1999 Feb;31(2):243-50, Rat liver lysosomal and mitochondrial activities are modified by anabolic-androgenic steroids. Molano F, Saborido A, Delgado J, Moran M, Megias A.)
In another study, 16 bodybuilders using steroids were compared to 12 bodybuilders who were not. Then the bodybuilders who had used steroids stopped taking them for three months, at which points, the researchers found that liver enzymes had returned to the same levels as the non users. After only 3 months!
(*Int J Sports Med 1996 Aug;17(6):429-33, Body composition, cardiovascular risk factors and liver function in long-term androgenic-anabolic steroids using bodybuilders three months after drug withdrawal. Hartgens F, Kuipers H, Wijnen JA, Keizer HA.)
We can see from the chart below that ex-steroid users have totally normal liver enzymes one year after they stop using& .in fact, for some liver enzymes, even the current users have normal scores!

(*Journal of Steroid Biochemistry and Molecular Biology. 84 (2003) 369-375)
3. Steroid Effects on Cholesterol (Blood Lipid Profile) Steroids can, in fact lower HDL cholesterol and raise LDL cholesterol. HDL (high density lipoprotein, commonly referred to as "good cholesterol") helps to protect the arteries by bringing unused cholesterol to the liver where it is broken down. LDL on the other hand has the opposite effect. Some steroids can therefore cause high cholesterol levels with low HDL and high LDL. Some steroids are, of course, very mild on blood lipids, while others are notably harsh. In both cases, however, it is likely that a return to within normal parameters would occur after steroids are not being taken.

4. Gynocomastia (Development of breast tissue in males)The development of gynecomastia or feminization of the breast tissue in males is possible with anabolic steroids. This is due to an excess of estrogen being present in the body, through a process known as "aromatization" whereby androgens like testosterone are converted to estrogen. This excess estrogen then finds its way to the receptors in breast tissue and binds to them. This results in the possibility of female-like breast tissue, which must sometimes be removed by surgery. Most athletes experience itchiness of the nipples, followed by pain. Since this develops over several days, usually, the athlete usually has more than enough time to discontinue the use of the compounds he´s taking, or to attempt to counteract the breast tissue development while remaining on the cycle. The two most common ways this is achieved by steroid users is either to use an anti-estrogen like Nolvadex or Arimidex in their cycle or to take Letrozole (*a very strong Aromatase Inhibitor and antiestrogenic compound) afterwards, to destroy the tissue that has developed.
Male breast development occurs in basically the same way as female breast development, and the use of anabolic steroids can result in this happening at a later stage in life for males. At puberty a surplus of hormones all combine to stimulate the growth and development of breast tissue.
The initiation and progression of breast development involves a variety of pituitary (and ovarian, in women) hormones, as well as various local mediators. As you can see from the following chart, testosterone has the ability to aromatize (convert to estrogen), and eventually become part of the cascade of hormones that eventually contribute to the development of breast tissue:

(GYNECOMASTIA: ETIOLOGY, DIAGNOSIS, AND TREATMENT Chapter 14 - Ronald S. Swerdloff, MD, Jason Ng, MD, and Gladys E. Palomeno, MD, March 1, 2004)
5. Acne and Anabolic SteroidsAnabolic steroids can cause the Development of acne and the extent to which it is experienced can be due to a number of varying factors, with the particular steroids and exact dosages used being the two primary factors. The skin´s sebaceous glands have a particularly high affinity to Dihydrotestosterone, which is an androgen the body naturally produces from testosterone via the enzyme 5-alpha Reductase. Increased sebaceous gland activity can oily skin which can combine with bacteria and dead skin caused by normal wear and tear, eventually causing pores to become clogged more quickly than the body can remove them. This of course, is preventable by using only particular steroids, cleansing the skin regularly, and perhaps using a topical anti-androgen.
(1. Am J Clin Dermatol. 2002;3(8):571-8. 2. Clin Dermatol. 2004 Sep-Oct;22(5):419-28. 3. Pol Merkuriusz Lek. 2004 May;16(95):490-2.)
6.  Roid Rage Increased aggressiveness is often claimed to occur with anabolic steroid use. Although it´s highly rare (less than 5%), significant psychiatric symptoms have been found in some steroid users, including aggression and increased violence, mania, and even psychosis. However, it must be noted that in the studies done without a control group, it can safely be assumed that naturally aggressive people simply just be more inclined to use steroids (type-A personalities, if you will). This would probably have an effect on possibly skewing the results. Certainly, if someone takes the risk to use steroids to improve their performance in a sport or their physique, they have certain aggressive traits. Can steroids enhance them? Possibly. Can steroids be to blame for anti-social, psychotic, "roid-rage" type behavior? Probably not. The evidence just isn´t there to support that.
In fact, a landmark study was performed which examined different doses of testosterone administration on men aged 20-50, who had a variety of experience with steroids from having used them previously to not at all prior to the study. A variety of psychological tests were performed at the outset of the study as well as at the end. What was found was that no participant in the study had become violent as a result of the testosterone injections they had been receiving, although some said they  felt more aggressive. This clearly indicates that there is a high level of control over possible violent or aggressive behavior that can result from steroid use. The researchers also noted that in terms of the psychological tests performed, some subjects showed little or no response to testosterone, with regards to psychological measures, while others experienced significant changes. Thus, general temperment clearly plays a large role in how one responds psychologically to steroid administration. In addition, when this study was compared with others, similar results were found:

Out of 109 cases studied, only 5 people exhibited Psychological (Manic or Hypomanic) effects. (*Archives of General Psychiatry, Volume 57, February 2000.)
7. Steroids and BaldnessSteroids can possibly cause men to start balding if they have a genetic predisposition towards Male Pattern Baldness. The gene for baldness is thought to reside in the X chromosome exclusively, so a good general indication of whether someone is genetically predisposed towards being bald is to look at the men on their mothers side. Chances are that if the majority of them are bald, then the person will be carrying that gene too. The reason steroids can cause premature balding is that the scalp reacts to Dihydrotestosterone (DHT) quite strongly, and many steroids can either convert to DHT or are derived from it. Of course, several anti-baldness medications can prevent this, such as Finasteride and Dutesteride. This is, of course, merely a cosmetic effect, and poses no real health issues. It could be catastrophic to a potential career with any one of a number of 80´s rock bands, but other than that, I can´t really see any real problems associated with hair loss; especially since it can be avoided when proper steps are taken and certain steroids are avoided.
8. Cardiovascular Problems from Anabolic SteroidsAnabolic steroids have been linked with cardiovascular issues. Part of this may be due to their effects on Blood Lipids (see above). But some of it is due to the fact that many steroid users have been found to have enlarged ventricles. This is actually very common in bodybuilders as well as powerlifters and other types of athletes, and is more indicative of the effect of weight training on the heart, rather than solely steroid use.
9. Virilization (Development of male characteristics in women)This term refers masculinization, or development of male sexual characteristics that females could potentially suffer from steroid use. This side effect on women is often reversible after the cycle has ended. Some typical signs of virilization are the development of a deeper voice, hirsuitism (growth of excess body hair), enlargement of external genitalia (clitoral enlargement), and possible male pattern baldness, or acne on the face or body. This is all dependent, of course, on the compounds used as well as the dosages employed. Personally, I have witnessed the most permanent of these effects to be the deepening of the voice due to the hypertrophy (growth) of the vocal chords. This is typically the most unwelcome side effect, as it makes it very obvious when a woman is using steroids. Of course, if this begins, the best course of action is to cease taking all steroids immediately. There are several ways to reverse this effect, the most common being to undergo a medical procedure known as vocal chord scraping. And yes, it´s exactly what it sounds like.
10. Stunted Growth (height)The use of some steroids can possibly stunt the growth potential of people who have not finished growing. This is only possible with certain steroids, and not with others. In fact, certain steroids have been used in clinical settings to improve growth rates in children. It is probable that the premature closure of the epiphysial cartilage, which is most likely caused by aromatizable steroids, will lead to a possible growth inhibiting effect, and could ultimately result in a shorter adult height. This most likely an irreversible side effect, as the growth plates would have sealed and can not "re-open". Anavar (Oxandrolone) has been used to improve the height of growth stunted children, and it is probable that most DHT-derived steroids could also be used for this purpose as could certain anti-estrogens.
Speaking in broad terms, growth stops at the end of the teenage years...there is almost no chance to keep growing.
This is because lengthening of a bone occurs at the epiphyseal growth plates (called the "growth plates" in common parlance), the remnant of the cartilage model. It's capable of proliferating. In 99.9% of humans, the process of bone elongation ends at around the mid to late teen years. At this point, the growth plates are obliterated and disappear, after which no more elongation (typified by an increase in limb length, height, etc...) can take place. Elongation of the bone occurs here and at a second epiphysis at the end. The proliferation of the cartilage happens very quickly, actually fast enough to keep ahead of the bone generation that´s "chasing" it, called ossification, which is just the replacement of cartilage by bone. As long as the cartilage growth "stays ahead" of the bone, you grow taller, as bone replaces cartilage. When the bone finally catches the cartilage (because the cartilage slows its growth rate, not the bone), it ossifies, and "seals" the growth plate.
Here´s a growth plate picture, enhanced by radioactive dye (GP= Growth Plate), so you can sort of see the bone "catching" up with the cartilage.

(Human Anatomy and Physiology, 6th Edition, John W. Hole jr., Wm. C. Brown Publishers.)
10. Prostate EnlargementOnce again, this is only a possibility that steroids could cause enlargement of the prostate. The media-perpetuated claim of possible prostate cancer seems to be wholly unfounded, according to most research. In many cases, this enlargement is quickly remedied upon cessation of anabolic steroid use. The first period of prostate Prostate growth, occurs first during puberty and is as a result of the testicular secretion of androgens. During adolescence to adulthood, the prostate stays at this stage, despite the relatively high levels of androgens found in the body.
Then, much later on in life, there is often a second stage of growth. Although this was originally deemed to be a result of Dihydrotestosterone s actions in the body, it is more likely due to estrogen combined with a small amount of either DHT or Testosterone. Thus, it´s not hard to imagine that taking steroids can cause this type of prostate enlargement and caused trouble for a steroid taking athlete. Typically, a product such as Finasteride or Dutesteride is taken to avoid this problem, with a high degree of success.
11. High Blood PressureThis problem is possibly the most easily remedied of all steroid side effects. It s very common for steroid using athletes attempting to gain maximum bulk to abstain from all aerobic activity. This causes the body to work much harder to circulate blood. Also, the typical water and sodium retention induced by certain steroids can contribute to this. If blood pressure is measured regularly to ensure that the value is not higher than 140/90, there should be no problems.
12. Kidney ProblemsThe kidneys can undergo more possible strain during anabolic steroid intake. Kidneys are involved in some of the filtration and excretion systems of the body, and as such, when a foreign substance is administered, they necessarily work harder. Some steroid users have noticed very dark urine when on a cycle, and this is indicative of the kidneys working overtime to accomplish their goal. One of the major offenders of this seems to be Trenbolone, which turns the user s urine a very dark color unless enough water is taken in daily. Also, even though I know you re probably getting sick of hearing this from me, the possibility of side effects is dependant on both dose as well as compounds administered. Some steroids (Nandrolone) are even used to help treat people with Kidney problems! So clearly, they aren´t as bad as they´re made out to be with regards to possible kidney issues.
13. Immune System ChangesThere is a large amount of data indicating that anabolic steroids may have some effect(s) on modulating the immune system. As with most potential side effects, this is largely dose and compound dependant. There is strong evidence that different analogues produce vastly different effects on the immune system. Testosterone and certain analogues have been shown to be possibly immunosuppressive, while Nandrolone and other steroids are possibly immunostimulating. Both, however, have been found to be beneficial when given to AIDS patients, who clearly have an already compromised immune system. This is because the increase in lean body mass that those steroids can provide is consistent with an enhanced ability to fight off infections, enhanced survival rates, and a better quality of life.
(1.Int J Immunopharmacol. 1995 Nov;17(11):857-63. 2. J Steroid Biochem Mol Biol. 1990 Sep;37(1):71-6 3. AIDS. 1996 Jun;10(7):745-52. 4. Journal of Neuroimmunology 83 1998, 162-67.)
14. Sterility in Males and FemalesIt´s a common side effect of steroids to cause temporary sterility in both males as well as females. In fact, anabolic steroids are so proficient at this that they have actually been studied and approved by the World Health Organization as a male contraceptive possibility. Steroids do this by disrupting the various hormones in women which potentiate the ability to have regular menstrual cycles. In men, steroids lower Follicle Stimulating Hormone to the point where normal production of sperm is not possible. This isn´t to say that nobody on a cycle has every conceived; quite the opposite, actually. There ve been legions of "happy accidents" reported to me by athletes who were on cycles and thought they couldn´t possibly conceive.
Sterility caused by steroids is temporary, of course, and generally reversible by treatment with Selective Estrogen Receptor Modulators such as Nolvadex or Clomid, and/or Human Chorionic Gonadotropin.
(1. Fertil Steril. 2004 Jan;81(1):226. 2. Urology. 2000 Oct 1;56(4):669.3. J Clin Endocrinol Metab. 1985 Oct;61(4):746-52 4. Fertil Steril. 1994 May;61(5):911-4. 5. Andrologia. 1985 Sep-Oct;17(5):497-501 6. Urol Clin North Am. 1986 Aug;13(3):455-63.)
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Steroid Effects Myth: Believing Everything You HearOk, so this last side effect isn´t really a steroid effect at all. But it s true, nonetheless. It´s my hope that you read this entire article and were surprised and possibly even a little outraged. Maybe you were outraged with how casually I seem to treat a very serious topic& but more likely than not, you were outraged at the fact that most of you´ve come to think about steroids and their horrible side effects has been greatly exaggerated. The simple fact of the matter is that anabolic steroids, like any medication, can cause a host of unwanted side effects. I´m certainly not suggesting otherwise. What I am suggesting is that a more logical and rational view be taken of them. The literature suggests that these drugs are safe when used in a clinical setting; my numerous interviews and experience with athletes suggests that this also holds true outside the clinical setting.
Please don´t misinterpret my position as being pro-steroid, anti-media, or anti-government. To do so would be to miss the point of this work entirely. I have the utmost respect for the media for providing the services that they do. I also have the utmost respect for the government and those who serve this country.
Anabolic Steroid Side Effects are a very real and possible concern for those who decide to use them. My position, therefore, is one that I hope is consistent with both the media as well as the government s position: I simply wish to tell the truth, and allow my reader to make the best and most informed choice possible. In that regard, I think this article has served its purpose.

http://www.isteroids.com/

DNP (2,4-Dinitrophenol)

DNP (2,4-Dinitrophenol), an industrial chemical with various applications, has gained steady popularity as a fat loss tool. Boasting an astounding 50% increase in metabolic rate, it is able to contribute to reported fat losses of 10-12 pounds in 8 days of use. Classified as an "uncoupler of oxidative phosphorylation" medically, it is quite dangerous as there is no negative feedback system that may deal with overdoses. Specifically, there is no upper limit to the increase in body temperature that may be obtained with its use.
Introduction/History
Competitive bodybuilders and many others are continually on a quest for leanness. Used by the hardcore since Dan Duchaine's reporting of it a couple years ago, DNP (2,4-Dinitrophenol) has managed to steadily gain popularity as a powerful tool for weight loss. Interestingly, DNP was first used to ignite TNT in the early 1900’s. In 1931 a study released by Stanford University declared that DNP was able to cause amazing weight loss; subsequently it found its way into many diet potions and medications; regulation was much less strict during this time than the present, and many of these products were available over the counter. Two years later DNP was banned by the FDA as a dieting agent due to its inclusion in many OTC dietary supplements. The FDA was a new organization at this time and acted in a rather brazen manner, with the absence of any set procedures for taking substances off the market. Granted, there was only a 1% incidence of cataracts over a large population (around 100,000); nonetheless it happened (although interestingly, exclusively women). However, there are now ways to counter this which will be covered thoroughly.
The comparisons to the current drugs used for dieting are astounding, at least in terms of thermogenesis. While the ECA stack has been shown to provide approximately a 3% increase in metabolic rate, DNP can deliver a relatively controlled 50% elevation in resting metabolic rate. The thermogenic aspect of clenbuterol, while sometimes overestimated due to the high CNS stimulation that yields a "wired" feeling, can vary according to prior exposure to various amphetamine-like compounds and certainly is not much greater than that of ECA. DNP does not have the anorectic effects of ephedrine or other thermogenic agents; rather, it tends to increase hunger, particularly appetite for carbohydrates. This problem is easily solved with appetite suppressants, and one may even use ECA itself for this purpose while on DNP.
Molecular Basis for Efficacy
DNP accomplishes the astounding boost in metabolic rate via inhibition of the F0F1 ATP synthase molecule, located in the inner wall of each mitochondrion. While the electron transport chain still functions to pump hydrogen ions into the intermembrane space, the coupling of the proton gradient to ATP production is rendered impossible by DNP. As a result, ATP production is dramatically reduced, and the energy is instead thrown off as heat. This results in an astounding production of heat; when using dinitrophenol, the athlete will radiate so much heat that it is uncomfortable to be within any proximity of them. Luckily, this heat does not fully contribute to body temperature increases, and is instead thrown off from the entire body surface, particularly the head. As a result, adequate doses of DNP will usually only elevate body temperature by about 1-1.5ºC. This is a good thing for your central nervous system and other delicate tissues; if the heat produced by ATP contributed in a more direct matter to body temperature, effective doses for fat loss would cause supraphysiological body temperature increases on a level unwitnessed at this time. Nonetheless, overheating is a very real danger; this and other side effects shall now be addressed.
Risks/Side Effects
Hearing all of these wonderful things probably has you wondering what the side effects and risks are. They are quite formidable and contribute to making DNP one of the most intolerable (though effective) drugs used in bodybuilding. Starting with the most significant, and descending in importance, are the following risks and side effects of DNP use.
Risks:
Overheating - There is no upper limit to DNP's body temperature increase, meaning that one may literally "cook from the inside" if they take too much. Dosage considerations will be given later, but even an overdose of 4-6 times the recommended dosage may be lethal. Much smaller overdoses may result in damage to the brain and/or other body systems.
Carcinogenesis - Phenols in general are reputed to be carcinogenic. Although 2,4-dinitrophenol has never been implicated in a cancer diagnosis, some are nonetheless concerned, and understandably so. In addition to the inherent carcinogenic potential caused by its status as a phenol, production of free radicals and the release of various compounds stored in adipose tissue stores during DNP's rapid oxidation of fat may also potentially be harmful.
Death - This is self-explanatory and has occurred with several bodybuilders who chose to use this compound.
Side Effects:
Discomfort and sweating - This is the single most noticeable effect of DNP use, both by the user and those around him/her. Even in the winter, while indoors at ambient temperatures, one may expect his or her shirt to be completely soaked through with sweat. Those with jobs requiring formal or semi-formal apparel are advised to consider other means of fat loss (or a new job, if preferred). Other obvious considerations lie in the areas of social life, personal appearance, etc. and the user must prioritize.
Insomnia - Second in frequency of reports to sweating and discomfort is insomnia; this may be at least partially attributed to discomfort. Possible means of countering this include such supplements as Valerian root or melatonin. Alternatively, one may deal with this via prescription or OTC sleep medications or GHB-A precursors. However, these may be addictive if used on a regular basis and if their use may be avoided, by all means abstain from using them.
Yellow bodily fluids - Some don't notice this, but others find that all of their bodily fluids take on a yellowish appearance. Urine is a darker yellow, and even semen and vaginal secretions may be affected. According to current knowledge, this is not known to be harmful in and of itself.
Muscle Soreness - This is yet another thing that may be minimized via cerebral function. Dan Duchaine has recommended using a weight such as to allow no fewer than 15 reps per set of any weight training workout; judging from anecdotal reports and personal experience, this seems to be good advice. Low levels of ATP are a cause of muscle soreness in and of itself; the additional factor of encumbered recovery mechanisms make extreme soreness (and if not careful, catabolism) quite possible.
Allergic Reactions – These are highly individualized but may be summarily discussed. Various reactions are common with DNP use, and approximately 10% of users will be extremely allergic to it. Allergic reactions can include hives, blisters, and/or inexplicable rashes. If you suffer any of these side effects, and they are extremely bothersome, it is the recommendation of the author to cease usage immediately. If so desired, another trial may be made at a later date with a lower dosage, but do not attempt to continue the drug cycle at that point.
Carbohydrate Cravings - To counter this, some methods will be touched on later. As with most diets, willpower is sometimes the single most important factor.
Obtaining DNP and Making Capsules
If, given these considerations, you still are ready to take the plunge and use DNP, you will need to learn how to obtain and/or make your own capsules. DNP is shipped industrially in large metal tins holding a glass jar containing the wet DNP, which is wetted with enough water to total 15-35% of total mass to prevent explosion while in transit. Ample cushioning material around the glass jar is included to further prevent ignition of DNP (it is highly flammable) and the obvious possibility of breaking the jar. Chemical sellers will not sell this chemical to individuals or any other entity without an account. However, if you are resourceful enough to get some, the following are instructions on how to properly prepare capsules.
Extreme caution is necessary when making the caps. DNP is bright yellow and will even go through gloves. This stain will not go away for up to 2 weeks. If it does get on your hands or other parts of yoru house, you can usually get it off with 2(3H) Furanone dinitro (butyrolactone). It usually will come out of clothes with laundering. Care is of the utmost importance when measuring out the amount one would need. Dan recommends 5 to 8 mg/kg bodyweight in Dirty Dieting #0, assuming that the person is under 15% BF. He subsequently told me that he was really suffering on 6-8 mg/kg, and that is excessive in his opinion. Note that the calculation is bodyweight, not lean body mass. With the exception of obese persons, this method is sufficiently accurate. Obtain a reliable scale, a Cap M. Quik device, and some size "O" caps ($60-$200 minimum, approximately $10, and $2 respectively). Corn starch, available at the grocery, is also needed. Since DNP ships at about either 15% or 35% water by weight, it is necessary to dry out the material overnight before attempting to deal with it. No matter how dry it looks, this step is absolutely necessary for accurate dosing. The next day, mix 15 grams DNP with 10 grams corn starch, and pound it into a fine powder. Spread resulting mixture into the Cap M. Quik, finish the capping process, and you have 50 caps of 300mg potency. Repeat as above with 10 g DNP and 15 g corn starch in order to make 50 caps of 200mg each, or with 12.5g DNP and 12.5g corn starch to make the same number of 250mg caps. Bear in mind that the preparation process, in the absence of a laboratory equipped with a chemical hood, will destroy the immediate area. It gets in the air, and fine particles will stain everything. Wear clothes that are dispensable, at least 2 pairs of gloves, and a fume mask. Preferably, do this outside on an extremely calm day, or alternatively, place protective covering everything in sight if it is necessary to perform the encapsulation indoors.
Timetable of Effects and Symptoms
The following table describes the condition most users will find themselves in during a typical DNP cycle; it is by no means complete and mainly intended to drive home that users typically look at their best 3-5 days following cessation of DNP use.
Day(s) Effects 1 None; possibly elevated carbohydrate cravings and/or temperature elevation. 2 T4-T3 conversion has begun to decrease; lethargy possible. Temperature should be elevated, and radiation of heat is noticeable. 3-5 Body temperature is elevated, with all the effects that one expects from DNP use. In addition, water retention usually becomes manifest here. 6-8 Definite water retention, along with other symptoms of use; user most likely feels fatter due to having "flatter" muscles (mainly the result of glycogen depletion) and holding water. Final DNP dose taken in the evening of Day 8. 9-10 DNP is clearing the system slowly. All symptoms are still present. 11-12 Water should be gone by now, or getting there. Mild diuretics will expedite this. The user will probably notice perceived greater cardiovascular and muscular endurance. 13-14 This is when someone tends to look their best. Their glycogen stores are usually compensated at this point and the retained water should be gone.
Dosing Schedule
As touched on previously, getting the right dosage of DNP is rather easy to do although the importance of proper dosage cannot be overstated. It is far better for one to err on the side of too little rather than too much, certainly in the case of the novice who does not know if they are allergic to the substance. As stated before, the commonly used dosage by bodybuilders and other reasonably lean persons is 3-5mg/kg of bodyweight. This would mean that a 100-kilogram bodybuilder would use anywhere from 300-500mg per day. Experienced users commonly are found using up to 800mg/day relatively safely, and beginners sometimes find that they enjoy 3-5 pounds of fat loss per week with as little as 200mg/day. Dosing is highly individualized and most generalizations tend to collapse quite quickly; as a result, none will be attempted. Start on the low end of the scale and see how you react. It is not recommended to take more than 300mg at any one time; a larger man taking 600mg per day should divide the dose into a 5:00PM portion and another portion taken approximately 30 minutes before bedtime. Someone taking 300mg/day could easily take one dose in the evening. The typical cycling program is to do 7 or 8 days on, followed by 7 or 8 off; this should not decrease thyroid output dramatically and makes use of T3 (triiodothyronine, brand name Cytomel) unnecessary in most cases. T4-T3 conversion does decrease dramatically in the liver due to excessive heat; this begins within 24 hours of the first dose. However, there is usually adequate active thyroid hormone to make it through 8 days of using it while maintaining elevated body temperature. After approximately 3-5 days, the user may find themselves with a waking temperature that is no longer elevated, even though they are still using DNP. This is due to the decrease in T3 and may signal the necessity of either the use of exogenous T3 in subsequent cycles or shorter cycles of the drug. In addition, the schedule given works nicely because the user is able to enjoy the anabolic rebound effect on a relatively regular basis. Also, longer cycles might leave the muscle fibers in a state of relative dehydration and "starved" of ATP for too long; both of these readily contribute to catabolism.
Supplementation
While using DNP, supplements can greatly aid both in the effectiveness of the therapy and the comfort of the user. Of particular importance are antioxidants and the following quantities are recommended:
Magnesium (1500mg)* Vitamin C (3000mg in divided doses)* Vitamin E (1200 IU in divided doses)* Glutathione (200mg in divided doses)***) NAC (various amounts)** T3 (dose according to personal preference)** Calcium (2000mg not taken with the Magnesium) 5-HTP (if not on antidepressant medication) (various amounts)**** Meridia, Redux, or Fenfluramine (various amounts)**** Hydroxycitric Acid (particularly in the evenings to curb cravings)**** Pyruvate (2-6g/day in divided doses) Glycerol (3 tbsp/day in divided doses) Alpha-Lipoic Acid (500-1000mg daily in divided doses) Key:
* = Integral component of DNP program** = Of questionable (although possible) importance)*** = Of particular importance to women for prevention of cataracts**** = For the purpose of appetite suppression (may not be needed)
Practical Considerations
Given all of this information, there are nonetheless more things to know before you undertake your first DNP cycle. The following tips and tricks gathered from personal experience and consultations with users are presented for your aid:
Aim a fan at your head at night. Your head is the most precious thing on your body and is a prime site for heat loss. Any air flowing over it will aid in cooling via convection. Wash your bedding daily. It is a good idea to have some spare pillowcases on hand, if nothing else. Most likely, you will be sweating profusely while you sleep, and this will make your bed smell as enticing as a locker room. Cleanliness is also essential in the prevention of disease, not to mention the fact that you are breathing out DNP "fumes" all night and they collect on your bedding. Prevention of disease goes beyond washing your clothes, and includes all of the normal precautions that you would make to avoid infection, although in a more exaggerated way. DNP depletes your body of energy needed to battle pathogens and weakens your immune system, leaving you ripe for infection and incapable of fighting off most diseases once they have taken hold. This is rather intuitive, but be certain to wear loose, light clothing, preferably of a light color. Similarly intuitive is the desire to remain in a cool area … be CERTAIN not to overheat. Proper hydration is necessary – I have personally consumed up to 8 liters of water per day. Glycerol specifically aids in muscle hydration, so its use may be very important, particularly when considering that muscle cells in even a semi-dehydrated state are prime sites for catabolism. Cardiovascular work while on DNP – This is a strange issue that I have been asked about regularly, but am undecided in the direction to take and generally recommend that the user decide for themselves. My personal preference is to do cardio with a fan focused on me for 30-35 minutes at a relatively high intensity. This is an area for personal preference; barring other considerations, just see if you can handle it or not and go from there. Always be ready to stop if you feel yourself getting extremely overheated or weak. Diet - One may wonder why this issue receives such limited attention; after all, most methods of fat loss require a restrictive diet of some nature. However, there is no set diet that one must use to achieve good results with dinitrophenol, only certain factors that allow the user to decide intelligently how to eat: Insulin - DNP blunts the effects of insulin; this is a huge boon for dieters because insulin blocks lipolysis and causes the storage of adipose tissue. This means that carbohydrate intake does not need to be strictly limited, although it should stay reasonable for optimal results.
Body Temperature and Comfort - A general guideline is that the more carbohydrates eaten, the hotter the user will get while on DNP. Similarly, overfeeding also produces extreme heat; any excess calories are thrown off as heat quite readily. For this reason, along with certain hormonal factors, Duchaine espouses an Isometric diet while on DNP, and I have followed this personally with good results.
CKD's - These are extremely impractical while on a cyclical ketogenic diet (CKD), and are especially dangerous. This brings up blood glucose considerations; it is important to try to maintain relatively stable, or at least not severely depressed, blood glucose levels. If this guideline is not followed, the user may experience blurred vision and/or extreme fatigue possibly augmented by fainting or lightheadedness.
Anabolic rebound effect – I still remember the first time I spoke to Dan Duchaine regarding DNP, and he told me about what, at the time, seemed impossible. But I have experienced this phenomenon, and it indeed happens. Possible causes include, but are not limited to, either an anabolic effect from glycogen supercompensation-induced cellular expansion, or due to increased mitochondrial density. Increased mitochondrial density is an adaptive mechanism of the body and takes place surprisingly quickly in the presence of an uncoupler such as DNP (or anything else that inhibits oxidative phosphorylation). Whatever the mechanism of the anabolic rebound effect may be, the user can expect to gain about 5-7 pounds of intramuscular water or muscle and lose about the same amount of subcutaneous and intraperitoneal water within a week after their last DNP dose. This is probably the most pleasant aspect of using DNP; the user not only experiences unrivaled fat loss, but also enjoys a fair amount of hypertrophy without any other supplements or drugs. Muscle retention, and possibly gain, is improved with careful attention to several previously discussed considerations such as proper hydration and intelligent cycling. Conclusion
Currently, DNP is the most powerful weapon against fat loss in the bodybuilder's arsenal; however, this does not necessarily mean that it is right for everyone or is by any means safe. The possibility also exists that PGF2 may be better for some people, particularly when taking the fact that it may kill fat cells into consideration. However, the guidelines given here will allow the user unrivaled fat loss, and will do so quite safely provided that precautionary measures are taken. While certainly quite dangerous, it is nonetheless the most effective tool available today for the loss of bodyfat.

Its Game Day !!!

Its Game Day !!!

The game of the year is about here, tommorow is the big day. Hey, maybe you play flag football on the weekends and want to perform. The science is all the same. This article will teach you the important principles of game day nutrition.
These general guidelines can be used by those involved in team sports, or those that require moderate endurance with often bursts of power. Football or hockey would be perfect examples.
General Nutrition
Maintain a diet high in complex carbohydrates, moderate in protein and relative low in fat. Strive for a varied consumption of foods to ensure exposure to all the nutrients that the body’s cells need. Varying your intake also helps ensure that you don’t overexpose your cells to substances in foods that may be, with frequent exposure, harmful to general health.You should also try to avoid insoluble fiber the day before and day of the event as this may lead to gas and cramping.
Pre-exercise or pre-competition meal
Consume starchy, easy to digest, high carbohydrate foods. Consume plenty of fluids with meals and during the period between the meal and the exercise session or competition. When possible, consume a high carbohydrate meal about 3 hours before exercise.
During Exercise
Consume a sports drink that is approximately a 6 to 7 percent carbohydrate solution (Gatorade or Powerade). Drink 20 to 40oz (600 to 1200ml) of fluid per hour. This is determined by the environmental temperature, humidity, and your predisposition to sweating.
COACHES MUST ENSURE the players are sipping their drinks at the end of every shift when they get to the bench. During practice, every 7 to 10 minutes the players are given the opportunity to have a 15 second drink break. 2 to 4oz of fluid every 7 to 10 minutes is CRITICAL.
Post-exercise or post-competition replenishment
Drink a sports drink to ensure quick re-hydration and replenishment of depleted glycogen stores. Consume approximately 24oz (750ml) per pound of body weight lost during activity. Consume high-glycemic index foods (IE: foods high in natural sugars like fruit) directly after the exercise. Consume a well rounded meal within 2 hours.

Shoulder Injuries

Shoulder Injuries
Most everyone have at one time or another has tweeked their shoulder. Learn how this happens, and how to avoid it !!!
Shoulder injuries are very common around the weight lifting scene, especially in bodybuilding. Numerous repetitions are required by each individual deltoid head in the hopes of full and total development, all of which amplifies the risk of injury.
The hip and the shoulder work in a similar fashion, but are quite different in design. The head of the femur sits deep in the glenoid cavity of the pelvis, offering a wide range of motion but not as much as the shoulder. The shoulder is a “ball and socket” joint with the humerus held within the glenoid cavity of the scapula by a complex array of musculature and tendons.
Most weightlifting injuries occur when training shoulders, and believe it or not, rarely do the injuries result in muscle pulls or tears. Poor technique or over use of tendons which reinforce the articular capsule will lead to a condition of “entrapment” (when the supraspinatus tendon gets rubbed/compressed between the humerus and the top of the shoulder joint) and leads to inflammation. If this condition is not treated and/or the poor form corrected, the problem spreads, affecting the infraspinatus tendon and possibly the long head of the biceps brachii.
Everyone is different. Some people have full range of motion, while others can not raise their arms laterally without friction. Sorry to say there is nothing that can be done for those people as its simply genetic predisposition. They should avoid all back presses, all extensions from the neck and lateral raises that go too high. Barbell presses should never be performed from behind the neck, from the front only, as the risk far out weighs any benefit.
Muscular imbalances and misalignment can also put undue stress on the shoulder. A few visits per year minimum to an experienced sports massage therapist will help keep you properly aligned.
Treat your shoulders with respect, as they can be the weakest link in the weight lifting chain. If your shoulders are unhealthy, the remaining upper body parts will suffer as well.
Every experienced lifter will agree, treat your shoulders well if you want a lifetime of lifting.w

Cycle - Putting It All Together

Cycle - Putting It All Together
Question: I have read all your articles on growth hormone, insulin, and finally igf, but I am still having a hard time putting all three together in a protocol for bulking. Can you outline a simple program for me, something that lists dosages, timing, and optimal use? I have done many cycles of anabolics, as well as insulin and gh, but now I am looking forward to adding in some igf to the mix. Thanks in advance for helping a guy out. Answer:
I am happy to help you out bro as it is critical to get the timing sequence down for optimal growth. I have been personally testing different protocols with igf use, having done over 20 different cycles and timing schedules. I also have a few competitive bodybuilders and test subjects off-season testing my new protocols. I have nailed down what I feel is the best protocol at this time, though everything is subject to change as I keep researching.
For now I have found that less is more. I highly recommend using a minimal schedule for all short chain sequence peptides, which include igf, insulin and even gh. I recommend using no more than 3 days per week, 2 days is fine, but no more than 3. The reason for this is that we are trying to prevent cell over-saturation and closure. All three products should be used in a similar manner.
The protocol is as follows; inject all products post workout, preferably after training large muscle groups which cause the most glycogen depletion, hence providing faster uptake of peptides. A sample layout is to inject Monday, Wednesday, and Friday.
Immediately post-workout inject 10-15iu of growth hormone IM, using a insulin pin and inject in any small muscle group such as delts, triceps, or biceps. Wait 20 minutes for the half-life clearance and conversion to igf to begin its sequence from the growth hormone and then inject a small dose of igf to create a synergistic super charge of the conversion process. I would recommend no more than 30mcg at this time. 10 minutes later you will take Humalog insulin only, and inject 5iu. I recommend starting with 5iu because Humalog has a very rapid onset and is easy to control with sugar. In conjunction with igf, you will be hyper-sensitive to insulin so start small and slowly work your way up to a maximum dose of 12iu post-workout. You will want to have around 80-100 grams of simple sugars such as dextrose and grape juice and an additional 60 grams of whey protein at the same time as your insulin. You will then eat another moderate glycemic index meal one hour after your high glycemic shake.
The reason for the high dose growth hormone is to take what would normally be your one week intake of gh and spread it out into 3 equal doses, injected pwo. This will create a truly anabolic rich environment and you will also benefit from full uptake due to your pwo depleted state.
So there is our post-workout regime, 3 days per week. Certainly you should take more than this, shouldn’t you? For most lifters, this protocol will be sufficient for growth. For someone with at least 6 months of gh use, 5 or more cycles of insulin and who no longer responds to typical igf protocols, the following regime may be followed: In addition to the above outline post-workout method, you may add additional doses of igf as well as insulin on the same day as your post-workout injection.
I would highly recommend you take 15mcg igf an additional two times per day. By taking less igf more often you will prevent cell over-saturation as well as receptor down-regulation. Creating a cell rich environment that saturates the cells infrequently will target massive cell proliferation. In addition you will take insulin 20 minutes after the igf on those 2 additional injections creating an anabolic rich environment that will last all day, 3 days per week.
For a sample protocol for someone that works out after work, I would recommend you do the following: Take 15mcg upon rising in the morning, followed by 10iu Humulin R or Humalog 20 minutes later. Immediately eat a carbohydrate rich meal with quality protein and low fat such as bananas, oatmeal and egg whites.
For lunch, take another 15mcg igf with 10iu insulin and have another moderate glycemic carbohydrate meal and protein with minimal fats. Follow the above listed pwo protocol to complete your three time injection schedule which will be used three times per week.
If you follow the outline laid out for you above to the letter, you will put on a massive amount of lean mass with a minimal amount of fat. You will need an anabolic and androgen rich environment to complete the schedule such as testosterone and tren in addition to the peptide products. T3 and T4 will not be necessary on this schedule as your thyroid levels will not be affected.

The "Secret" to Getting Huge Revealed

The "Secret" to Getting Huge Revealed
Dave, what is the secret to getting huge? Does it mean taking huge amounts of steroids?
I am addressing this topic because this is the most prevalently asked question. My answer to you is in the form of the question, "how many people do you know who take large amounts of steroids yet look no better than they did before they started?" And the answer to that question is "TOO MANY!" The problem is that people think that if you take 1000mg of testosterone a week, you will get huge. What they forget is the most important part of the equation : THE FOOD! NO protein, NO carbs, and NO fat means NO muscle. If you are taking adequate amounts of "STUFF" and you still aren't growing, don’t assume that you need to take more stuff. EAT MORE FOOD (especially protein) and EAT MORE FREQUENTLY! I cant stress this enough. The difference between the massive bodybuilder and the mediocre bodybuilder is that the MASSIVE one views eating as a JOB (not as a luxury).
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Growth Hormone Vaccines
What's the deal with this new growth hormone vaccine that is being put out by Genentech? How does it last for up to a month?
According to my sources, Genentech’s new GH Vaccine is not actually growth hormone. Basically, upon injection, it blocks the hormone somatostatin. Somatostatin is the hormone responsible for inhibiting the production of growth hormone releasing hormone (GHRH) from the hypothalamus which in turn inhibits the release of GH from the pituitary gland. By blocking the Somatostatin hormone, you essentially enable the pituitary to produce unlimited amounts of GH (i.e. there is no shut off mechanism). The problem with this approach is that the amount of GH released is a very person-specific event. In other words, one individual may produce a lot of GH and another may produce very little (it becomes a genetic thing). I liken this product to attempting to increase testosterone levels using hCG. Why worry about how much GH the individual can produce naturally, when you can just administer the GH (in a known amount) using the current GH formulas that are out there? I don’t foresee that the bodybuilders will replace the use of GH with this new product. They will probably just add it into their stacks or they will use it when in an off cycle.
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Micronized Water-Based Steroids
What have you heard of the new "micronized" water-based steroids (Winstrol and testosterone suspension)? Is this a better formula? AND why doesn’t it settle out?
The term micronization refers to the crushing or pulverizing of the Winstrol or Test suspension powder into a very fine dust that once suspended in sterile water forms a milky looking colloidal mixture (i.e. the steroid tends to remain in suspension much longer without settling out).
Micronized creatine, on the market, is a similar theme to the micronized Winstrol and suspension we a talking about. It mixes in water more thoroughly, and thus is absorbed better through the GI tract thus causing less diarrhea and bloating.
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The Ultimate Precontest Stack for a Competitive Bodybuilder
Dave, what is the ultimate "STACK" for a precontest, dieting, bodybuilder? Please include dosages.
Given the current available anabolics (and starting from a point at around 8-10 weeks out), I would have to say that the following would be an ideal anabolic combination:
1000mg Sustanon per week (necessary to maintain base of muscle mass) 200mg Primobolan per week (great on low calorie diets) 50mg Winstrol every other day (hardening agent) 400mg Deca per week (keeps the joints feeling good) 50mg Anadrol per day (keeps the strength elevated, meanwhile, the hunger-blunting effect is welcome) 2-4 IU GH per day (fat burner and muscle preserver) 2-4 clenbuterol per day (fat burner and strength increaser)
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How to Kick My Nubain Addiction
I have a question, I use Nubain 4-6 times a day it is an addiction for me. I want to stop using it. I am also currently taking 4.5iu of Serostim a day and I use it yr round. I would be able to use 9iu of Serostim a day yr round if I could get off of Nubain. My question is will I be able to quit Nubain cold turkey? And will I see more of a significant result using 9iu of Serostim a day instead of 4.5? I don't want to waste my money if its not going to have more of a dramatic effect. What do you think?
Stick to the 4.5IU GH (Serostim) per day. That's plenty to grow with (with little side effects). IF you want to get off the Nubain as well, get down to small amounts (.15 cc) spaced every 3-5 hours. When you get to that point, switch to Ultram (they are pills). They will kill the withdrawal symptoms then and take Ativan or Valium for the anxiety. It should take about 1 week of doing this to be totally off (3 days for the physical withdrawal to go away and another 4 days for the mental desire to wane).
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How Do I Use Synthol?
What are the best bodyparts to inject Synthol into? How often and how many CCs per injection?
Synthol is used to enhance or augment a weak or lagging bodypart. The muscles that respond best are the small, rounder, muscle groups such as the biceps, triceps, and calves. Usually, 3cc amounts of Synthol are placed DEEP into the muscles 2-4 times per week for the first 3-4 weeks. Thereafter, 3cc amounts are injected on a once per week basis for the next 20-24 weeks until the size increase has become permanent.

Solid Cycles for Different Goals

Solid Cycles for Different Goals
Now before I get started, I have to emphisize that your diet, training, and rest is the key to achieving your goals. All cycles can be turned into a bulking cycle or cutting depending on your food consumption.
*Clomid therapy: 36 pills. 300mg day 1, 100mg next 10, 50mg final 10.**HCG therapy is instituted for the prevention of testicular atrophy. The old practice was effective, but I feel prevention is more productive than trying to revert the problem late in the cycle.
Solid first cycle
Week 1 to 10: 400mg of EQ ORWeek 1 to 10: 4-500mg of test Week 13 to 15: Clomid Therapy*
Bulking Cycle # 1
Week 1 to 16: .5mg of arimidex EODWeek 1 to 12: 300-500ius of HCG every 4th or 5th day**Week 1 to 6: 30mg of D-bol EDWeek 1 to 10: 600mg of EQWeek 1 to 10: 750mg of TestWeek 13 to 15: Clomid Therapy*
Bulking Cycle # 2
Week 1 to 16: .5mg of arimidex EODWeek 1 to 12: 300-500ius of HCG every 4th or 5th day**Week 1 to 5: 50mg of Anadrol EDWeek 1 to 6: 750mg of TestWeek 1 to 10: 400mg of DecaWeek 7 to 12: 75mg of Fina EDWeek 7 to 12: 100mg of Prop EDWeek 7 to 12: 50mg of Winny EDWeek 13 to 15: Clomid Therapy*
Cutting Cycle # 1
Week 1 to 8: 300-500ius of HCG every 4th or 5th day**Week 1 to 8: 50mg of Prop EDWeek 1 to 8: 75mg of Fina EDWeek 1 to 8: 50mg of winny EDWeek 1 to 10: 50mg of proviron EDWeek 13 to 15: Clomid therapy*
Cutting Cycle # 2
Week 1 to 16: .5mg of arimidex EODWeek 1 to 12: 300-500ius of HCG every 4th or 5th day**Week 1 to 10: 400mg of EQWeek 1 to 8: 40mg of Oxandralone EDWeek 4 to 12: 50mg of Prop EDWeek 7 to 12: 50mg of Winny EDWeek 13 to 15: Clomid Therapy*
Lean Mass Cycle
Week 1 to 16: .5mg of arimidex EODWeek 1 to 12: 300-500ius of HCG every 4th or 5th day**Week 1 to 12: 2ius of GH 5 on 2 offWeek 1 to 10: 500mg of TestWeek 1 to 12: 400mg of EQWeek 7 to 12: 40mg of Anavar Week 14 to 16: Clomid Therapy*
Basic bridge
Week 1 to 8: 30mg of Oxandralone EDWeek 1 to 8: 10 grams of creatine and 20 grams of glutamine Ed
Experienced Bridge
Week 1 to 8: 10ius of Insulin post workoutWeek 1 to 8: 10 grams of creatine and 20 grams of glutamine EdWeek 1 to 8: 100grams of Dextrose 10 minutes after slin shotWeek 1 to 8: 150grams( 3 shakes) of WPI during active time of slin.
There are many different combination that we can all use in the Iron Game. I have only used a few. These are basic cycles that will work well for many users. I have only included Deca in one cycle as I feel its negative effects on a HPTA are esaily avoided with the use of EQ. Some will say Fina will do the same thing, but because its ester works much faster, I believe it is not as suppressive as Deca.
Remember Diet is the key to all cycles. If you dont eat enough, you wont bulk, if you eat to much, you wont cut.

Steroid Side Effects and How to Stop them

Steroid Side Effects and How to Stop them - Part 1
This chapter, along with the chapter on the proper use of ancillary medications, are two of the most important chapters in this book. Why? Because AAS have side effects, and long-term use of AAS can have a profound effect on longevity and overall quality of life in later years if preventative measures are not taken. Having used steroids myself for over 10 years now, I have suffered through virtually ever side effect listed in this chapter, and have consequently educated myself on how to avoid them.
Regardless of your age, it’s important to always bear in mind that the use of AAS for the purposes of gaining an edge in sport can be an inherently unhealthy endeavor. There is a distinct difference between the doses of hormones or drugs that are used in slowing the aging process through hormone replacement therapy (hereafter referred to as HRT, please see the chapter on HRT by Dr. Ramon Scruggs for further clarification) and those that are used to enhance performance. If one is to properly use performance enhancing drugs, it is vital that they know the potential side effects of drugs they are using, know how to combat these side effects, and most importantly, actually implement the knowledge they have. Time and time again I’ve seen a bodybuilder develop gynecomastia (commonly referred to as “bitch tits” in the bodybuilding vernacular) despite the fact that the individual in question knew this was a possibility and also knew the preventative measures to take. One should not engage in the use of AAS or any other performance enhancing drug if the maintenance of proper health is not of primary concern.
Compounding the problem of treating the side effects of AAS is the hysteria surrounding their use in the first place. Many bodybuilders that use steroids find themselves to be social pariahs, muscular misfits if you will, and end up finding comfort in the company of others that engage in steroid use as well. Because a bodybuilder wears his sport, he’s branded a steroid user by many regardless of whether that’s the case or not. Often times, the shame one feels regarding their steroid use will cause them to suffer through the side effects associated with their use, rather than seeking competent medical help. Truth be told, it’s very difficult to find competent medical help to treat the side effects of steroids, as most doctors simply have no idea how to properly do so. More often than not, the physicians I worked with for most of my years on steroids were completely clueless as to how one might ameliorate the negative side effects of these drugs, and would simply tell me to “get off the steroids”. I say this not to dissuade those of you reading this from seeking out the advice of a doctor regarding the side effects of steroid use, just to prepare you for a probable response.
Most of the side effects related to steroids are cosmetic and will disappear when one discontinues their use. But those that aren’t are the most important to understand and treat as necessary. Most of these cannot be seen or felt, and all are related to issues of cardiovascular health. Steroids can adversely affect cholesterol levels, triglyceride levels, and hypertension, which over time can and will lead to an increase in heart disease. Always monitor your resting hear rate and blood pressure on a weekly basis when taking steroids and have your cholesterol and triglycerides checked every six months if you are using steroid consistently. These are not problems you can live with, ignore them and you may very well die much earlier than you would have otherwise. Ask yourself this question: “How much is every year of my life worth to me?” If you ignore the potential for an increased risk of heart disease when using anabolic steroids, you are essentially answering the question with, “Very little indeed.”
Before we begin a look at the actual side effects themselves and how to treat them, it’s important to note that not all AAS are created equal!! At times, for the sake of brevity, I will lump all AAS together, but the fact remains that some steroids will cause more negative side effects than others. One of the points of this book is to allow you to make that distinction, and walk away with the knowledge of how to use them as safely as possible. Below is a list of steroids most commonly associated with the side effects listed in this chapter:
Anadrol-50 (Oxymetholone)
Dianabol (Methandrostenolone)
Halotestin (Fluoxymesterone)
Testosterone and its various esters
Unfortunately for us, these also happen to be most of THE most effective AAS (with the exception of Halotestin) for building LBM. Generally, the maxim that the more effective a steroid is the more side effects it has holds true.
Finally, before we begin, readers will notice that I do not advocate the use of estrogen blockers such as Nolvadex, Clomid (I do post cycle, but not for the purposes of estrogen suppression), or Proviron. With anti-aromatases like arimidex (anastrazole), femara (letrozole), and to a lesser extent Cytadren (aminoglutethiamide) becoming cheaper and more readily available, use of estrogen blockers should be relegated to the bodybuilding archives. For a complete explanation as to why, read the chapter Proper Use of Ancillary Medications Both On and Off Cycle.
AAS Side Effects
Acne: One of the primary indicators of steroid use is acne, and I’m sure many of you reading this have either experienced acne caused by steroids or have seen someone who has. Like all steroid side effects, the degree to which someone will suffer from acne varies from individual to individual. The more androgenic a compound is, the more profound effect it will have on increasing oil production in the skin via stimulation of the sebaceous glands. Having said that, I’ve seen individuals use incredibly androgenic stacks and never have a hint or a pimple or blemish, and I’ve seen athletes (especially women) use very mild anabolics and suffer from horrible acne.
Treating acne is very important, both for physical and psychological reasons. Untreated acne can cause permanent scarring of the skin if it becomes severe enough, resulting in a pockmarked area that can only be smoothed through expensive plastic surgery. And acne can have a very powerful negative psychological effect on someone suffering from it, branding someone a steroid user and further isolating them from “normal” society. Severe acne can and will detract from the most aesthetic of physiques, and take away from ones overall presentation.
Depending on the severity, there are several options for the treatment of acne. Since acne is generally caused by the more androgenic steroids, there is always the option of switching to steroids that have few androgenic properties, such as nandrolone, oxandrolone, or primobolan. Light cases can commonly be controlled through frequent washings of the effected area (to remove excess dirt and oil before pores become clogged and infected) and the use of over the counter topical treatments. Moderate cases will generally respond to the use of Retin-A coupled with use of an antibiotic (such as tetracycline) which kills the bacteria which feeds off the oil created by the sebaceous gland. Severe cases of acne should be treated with Accutane, a prescription drug manufactured by Roche that is very effective at permanently eliminating acne. Accutane has a host of unpleasant side effects itself, and treatments are both lengthy and costly (health insurance is a must), but its use is much better than the possibility of permanent scarring from cystic acne. Fortunately, while acne is one of the most commonly seen side effects, it’s also the easiest to treat, as competent Dermatologists can easily be found.
It should also be noted that acne commonly become an issue for bodybuilders that do not cycle off steroids correctly, which will often cause a severe imbalance between levels of androgens and estrogens. Preparation for your off cycle period is equally important as the time spent on steroids, so use of an anti-aromatase both on and immediately following a cycle containing AAS that can convert to estrogen is a must.
Aggression: Men, due to their higher natural production of testosterone, are generally more aggressive than women. AAS, especially those that are extremely androgenic, will further increase aggression in both males and females. This can be beneficial as long as the individual in question can focus the aggression appropriately, such as the lifting of heavier weights during training. There often seems to be a direct correlation between ones ability to control aggression and ones intelligence.
There is nothing worse than an out of control steroid user who is unable or unwilling to control their aggression. Before beginning a cycle of AAS, especially one containing strong androgens, you must prepare yourself mentally for the fact that you are in all likelihood going to be more aggressive than normal, and consequently take the time to assess the nature of your reactions while using them.

clenbuterol FAQ

clenbuterol FAQ
Clenbuterol FAQ:
Everything you need to know about Clen I wrote this because of all the confusion that surrounds this drug. Enjoy.
What is Clenbuterol? Clenbuterol is a beta-2 agonist and is used in many countries as a broncodilator for the treatment of asthma. Because of it's long half life, Clenbuterol is not FDA approved for medical use. It is a central nervous system stimulant and acts like adrenaline. It shares many of the same side effects as other CNS stimulants like ephedrine. Contrary to popular belief, Clenbuterol has a half life of 35 hours and not 48 hours.
Dosing and Cycling Clenbuterol comes in 20mcg tablets, although it is also available in syrup, pump and injectable form. Doses are very dependent on how well the user responds to the side effects, but somewhere in the range of 5-8 tablets per day for men and 1-4 tablets a day for women is most common. Clenbuterol loses its thermogenic effects after 6-8 weeks when body temperature drops back to normal. It's anabolic/anti-catabolic properties fade away at around the 18 day mark. Taking the long half life into consideration, the most effective way of cycling Clen is 2 weeks on/ 2 weeks off for no more than 12 weeks. Ephedrine can be used in the off weeks. Clenbuterolvs Ephedrine vs DNP
Ephedrine will raise metabolic levels by about 2-3 percent and 200mg of DNP raises metabolic levels by about 30 percent. Clenbuterol raises metabolic levels about 10 percent and it can raise body temperature several degrees.
DNP is by far the most effective fat burner but many people will never use it because of the risks associated with it. It also offers no anti-catabolic benefit. Although it does have anti-catabolic effect, ephedrine short half life prevents it from being all that effective.
As far as side effects, Clenbuterol's are certainly milder than DNP's, and some would even say milder than an ECA stack. There is no ECA-style crash on Clenbuterol and many users find it easier on the prostate and sex drive. This may in part be due to the fact that Clen is generally used for only 2 weeks at a time.
Side effects
NAUSEANERVOUSNESSDIZZINESSDROWSINESSDRY MOUTHFACIAL FLUSHINGHEADACHEHEARTBURNINCREASED BLOOD PRESSUREINCREASED SWEATINGINSOMNIALIGHTHEADEDNESSMUSCLE CRAMPSTREMORSVOMITINGCHEST PAIN
The most significant side effects are muscle cramps, nervousness, headaches, and increased blood pressure.
Muscle cramps can be avoided by drinking 1.5-2 gallons of water and consuming bananas and oranges or supplementing with GNC potassium tablets at 200-400mg a day taken before bed on an empty stomach.
Headaches can easily be avoided with Tylenol Extra Strength taken at the first signs of a headache. You may need to take double the recommended dose.
Common Uses
Post-Cycle Therapy: Clen is used post cycle to aid in recovery. It allows the user to continue eating large amounts of food, without worrying about adding body fat. It also helps the user maintain more of his strength as well as his intensity in the gym. Diet: Roughly the same as on cycle.
Fat loss: The most popular use for Clen, it also increases muscle hardness, vascularity, strength and size on a caloric deficit. For the most significant fat loss, Clen can be stacked with t3. Diet: A high protein(1.5g per lb of bodyweight), moderate carb(0.5g to 1g per lb of bodyweight), low fat diet(0.25g per lb of bodyweight) seems to work best with Clen.
Alternative to Steroids: Clenbuterol has mild steroid-like properties and can be used by non AS using bodybuilder to increase LBM as well as strength and muscle hardness. Diet: A moderate carb, high protein, moderate fat diet work well.
Stimulant/Performance Enhancement: It can be used as a stimulant, but an ECA stack may be a better choice because of it's much shorter half-life. Diet: To take full advantage of the stimulatory effects of Clen, Carbs must be included in the diet. Keto diet do not work well in this case.
Precautions: Is Clen for you?
The same precautions that apply to Ephedrine must be applied to Clen, although some people find ECA stacks harsher than Clen. It should not be stacked with other CNS stimulants such as Ephedrine and Yohimbine. These combinations are unnecessary and potentially dangerous. Caffeine can be used in moderation before a workout for an extra kick, although its diuretic effects may shift electrolyte balance. Drink more water if you use Caffeine.
What else do I need to know?
Most users that report bad side effects and discontinue use are those who use high doses right at the start of the cycle. The worst side effects occur within the first 3-4 days of use.
A first time user should not exceed 40mcg the first day.
Example of a first cycle:
Day1: 20mcgDay2: 40mcgDay3: 60mcgDay4: 80mcgDay5: 80mcg(Note: Increase the dose only when the side effects are tolerable)Day6-Day12: 100mcgDay13: 80mcg (Tapering is not necessary, but it helps some users get back to normal gradually)Day14: 60mcgDay15: offDay16: offDay 17: ECA/ NYC stack
Example of a second cycle:
Day1: 60mcgDay2: 80mcgDay3: 80mcgDay4: 100mcgDay5: 100mcgDay6-Day12: 120mcgDay13: 100mcgDay14: 80mcgDay15: offDay16: offDay 17: ECA/ NYC stack
Do not take Clen Past 4pm and drink plenty of water: 1.5-2 gallons a day.
All brands are not equal when it comes to Clen, different brands will yield different results.
That about covers everything.

Hardcore Bulking (bodybuilding)

Hardcore Bulking

Off season is a bodybuilders favorite time of year and the favorite words whispered after a recent contest. So the time is here, what are you going to do about it?
First step is to determine what you want to do and set some goals. You cannot achieve anything without a plan. Those who fail to plan, plan to fail. So let’s set some clear cut goals. You are going to need all the tools at your disposal before you begin. You are going to work on written goals, nutrition, training, and finally the hardcore cycle.
Write down your goals. Have everything written down and in plain sight as a reminder of what you are trying to achieve. So write down your target weight, your training days, your daily calorie goals, your cycle, etc. Keep a master log book of everything you are trying to do. Like I stated, you must plan for success.
First thing is to determine your target weight and body fat goals. Don’t be overly concerned with fat. This is, after all, the off-season, but there is no need to go above 13-14%. At that point you can still see some abs if you flex them hard enough and you will have acquired the mass point necessary for massive gains. Picking a target weight is very dependent on your level of experience. Since this series of articles is targeted primarily at advanced lifters, I recommend trying to achieve 20lbs of pure mass; some fat, mostly muscle.
So now that you know you are trying to get another 20lbs of size, how do you go about doing this? First and foremost is diet. You cannot make gains if you are not feeding yourself at the goal you want to achieve. So since you know you are trying to get 20lbs, you are going to eat as if you you’re already at that weight. The best way to achieve this is to take in a total daily calorie intake of 30 kcals per pound of bodyweight for ectomorphs, 25 kcals for mesomorphs, and 20 for endomorphs. So for the 230lb average size ecto/meso bodybuilder, he is going to need to eat almost 7500 cals per day. Sounds incredible, I know, but it can be done quite easily. During the off-season you will eat calorie dense foods, some fast food, and some bulking shakes.
I am not going to outline an exact diet for you, but I will give some general guidelines that I highly recommend. Variety is very important in bulking, eating the same foods over and over is boring and there is no reason to. Save the tuna and rice for show time; you can get very creative when bulking and actually enjoy eating. So let’s look at some calorie dense foods that fall in the category of bulking and are acceptable bodybuilding foods.
I love cheese when bulking it is high in protein, goes on everything and it is a very easy way to add calories to every meal. I don’t mean Velveeta or cheese in a can here; I am talking about quality cheese, like Tillamook extra sharp. My other favorite is milk. I love milk with every meal and protein shake when bulking. Oh, and don’t forget my extra special, super bulking treat……natural peanut butter. Tons of calories, high in complete chain protein and essential fatty acids.
So now you have my favorites, let’s go shopping. Grab a pen and paper and write down a shopping list. Don’t just go in the store and wing it. Remember earlier I stated you are going to write everything down. This includes shopping. You write down your weekly shopping list, your training schedule, your cycles and your goals. So back to shopping, you are going to need a lot of food to get to 7500 cals per day. Here are my shopping list recommendations:
Breakfast ideas:7-10% lean ground beefHoney Nut Cheerios cerealOatmealBagelsWhole eggsCheeseBananas
Lunch ideas:TortillasGround beefSalsaCheeseBreadWhite rice Dinner ideas:FishBroccoliWhite riceGround beefBell peppersPotatoesSteak
Snack ideas:Roast beefBeef jerkeyNatural peanut butterGraham crackersString cheese
Now remember, I am not going to set up a diet for you, just give you some ideas of my favorite calorie dense foods. It is up to you to plan some meals and make sure to eat 5-6 meals per day. I don’t see a need to eat more than that because you are not trying to speed up your metabolism; you are trying to slow it down by eating more food at each meal and eating less often. I am a huge proponent of high calorie shakes during the off-season. I personally belong to Muscle Milk anonymous! All kidding aside, they have the most incredible flavors and are highly addictive. Instead of the usual 2 scoops, I use 4 scoops in 16oz 2% milk for a 900+ calorie shake. I have two of those per day, plus my 3 solid meals and then my night time snack.
My favorite night time bulking snack is 4 graham crackers spread with tons of natural peanut butter and then made into two sandwiches, 2 string cheese and a huge glass of milk. It is totally yummy, and I highly recommend it. You probably won’t wake up hungry in the middle of the night. The peanut butter will hold you over until you get up for breakfast.
People are always highly concerned about percentages of protein, carbohydrates, and fat. I am not so concerned, so long as I am getting 2 grams of protein per pound of body weight that I want to be, the rest will just naturally be carbs and fat. So for our hypothetical diet of 7500 calories per day to get to 250lbs, I need 500 grams of protein, which is 2000 calories of protein. That still leaves me 5500 calories of fat and carbs to enjoy. You must eat protein first in every meal, if you are going to get full while eating, it better be on protein and not anything else. It is always easy to squeeze in extra carbs, and needless to say, fat is too easy.
So for our 6 meals, of which 2 are already Muscle Milk and have 170 grams of protein, you don’t have far to go. The next 4 meals just have to have about 80 grams per meal. One glass of milk at each meal is 10 grams, so now you have just 70 grams. See how easy this is? Carbs add up real fast, especially with dense foods like cereal, bread, bagels, and rice / pasta.
Now you are beginning to see how easy bulking while eating clean is. A couple of days per week, I recommend you head over to McDonalds and get 2 or 3 Big Macs or double cheese burgers. Go to In and Out, Burger King, or whatever your favorite is, and do a major feast. You can easily get in 3000 cals in one sitting with 3 Big Macs, a large fry, and a shake. So if you do that 2 times per week, you are going to have two days of about 10,000 cals per day, something that is really going to help with the metabolism and bulking.We also need to address the very important issue of post-workout (pwo) nutrition. I cannot stress enough how important it is to consume the majority of your daily calories in the first 3 meals pwo on training days. The primary source of energy when training is the conversion of glycogenesis in the formation of glycogen from glucose. Glycogen is synthesized depending on the demand for glucose and ATP (energy). If both are present in relatively high amounts, then the excess of insulin promotes the glucose conversion into glycogen for storage in liver and muscle cells.
When you have completed a workout, your muscle cells are depleted of glycogen and it must be replenished as quickly as possible to promote recovery, and cell repair. Protein cannot be utilized for cell repair if we don’t first address the depletion of glycogen. The best way to replenish depleted glycogen stores is to use a very high glycemic carbohydrate in conjunction with a rapid and easily digested protein to shuttle into the cell for repair.
I personally use a custom made shake that costs me literally pennies to consume. I shop at the local beer brewer’s store and purchase bags of pure glucose or dextrose which they use for home beer brewing. I mix 40 grams of glucose with 16oz (84g) of grape juice and 3 scoops (66g) Nectar whey protein. Nectar is an ultra high quality, flavored whey isolate. This is one of the fastest digested proteins on the market, so in conjunction with my high glycemic pure glucose and grape juice, I have just made a super high quality, muscle repairing shake that costs literally nothing to make. I also recommend you throw in 10 grams of creatine and 10 grams of glutamine at this time. Your muscles are sponge’s pwo and this is the optimal time to feed them and prepare the tissue to utilize the nutrition for primary protein absorbtion instead of feeding the intestinal tract, a primary scavenger of ingested proteins, especially glutamine.
Your next two meals of extremely important because you are still within the so called “window of opportunity” for muscle repair with nutrition. Your pwo shake should not leave you feeling full for long; it is easily digested and is intended to be so. You are going to want to eat again one hour after you drink your shake. At this time, you still want an easily digested, low fat protein but you should move into moderate glycemic carbs as we are still “filling the tank” so to speak but no longer need fast carbs as most of our glycogen was replenished with the glucose.
This meal should be preferably a light, white fish, or chicken breast. I consume mahi-mahi, tuna, or chicken with broccoli and rice or a baked potato. Eat a large portion of protein, the carbs are just a means to an end to shuttle the protein, so fill up with protein first, then eat your carbs to shuttle the amino acid chain into muscle cells.
Our third and final pwo meal of importance while bulking will finally include some essential fatty acids which are also necessary for tissue repair, primarily tendon and ligament tissues. So now we get to really consume the calories and have fun with this meal. I like to eat 8-10 whole eggs, avocado, 6 pancakes, bacon and a glass of orange juice. Another favorite is 1lb lean ground beef in tortilla shells with avocado, salsa, cheese, a baked potato or rice and some milk.
So there you have the three most important meals of your day on training days. It is critical to watch your nutrition at this time, especially since you are trying to repair damaged muscle tissue, replenish glycogen stores, repair connective tissue, and cells. I cannot stress enough how important it is to eat, your body is willing and able to consume massive amounts of calories pwo without spilling into excess body fat storage.
Another critical issue we need to address is the use of insulin and nutrition pwo. The three meals I have outlined fall well within the acceptable specs for humalog use, not humulin-r so that cover pwo nutrition. I will cover the use of R in later articles, as well as proper eating if you choose to use it. For now just use 10-12iu humalog pwo only following the former meal guidelines and you will be utilizing proper protocol and nutrition to maximize your growth.
As stated, look for a future article on insulin use and proper nutrition with it for maximum off season bulking. Insulin is going to be one the greatest products we can use when bulking, especially since you really can’t go hypo if you are going to be eating that many calories each day. We will address multiple use per day on training days to maximize your gains, especially how to super-charge your diet.
I have said it before and I will say it a million more times until you get it through your thick heads. Without nutrition, no gains are possible. Bulking or dieting, it doesn’t matter what your goals are, nutrition is about 80% of our battle. Training and drugs are a means to an end. I can entirely change my physique from fat to lean, from thin to bulk all with diet manipulation. Try doing that with just training and a cycle but only eating 2 or 3 meals per day. Nutrition is your greatest anabolic agent, everything else is just the icing on the cake.
In the next installment of this series we are going to tackle hardcore training principles and eventually what you are all dying to know, the hardcore bulking cycle. For now, read and re-read the information presented before you. Learn to eat right and you can easily put on another 10lbs without even touching a weight or sticking a needle in your glute.

Guide to rHGH use

Guide to rHGH use

Disclaimer (warning): This information is for entertainment value only. I am not a medical doctor , therefore, I am not qualified to offer any medical advice nor advise you on how to take any substances. What follow is my experience and knowledge of HGH.
According to studies in the New England Journal of Medicine GH use will:
- Shed Bodyfat- Increase Muscle Tone- Boost your Energy, Strength, and Endurance- Reduce Wrinkles - Create Tighter, Smoother Skin- Help you Sleep Better- Improve Sex Drive and Performance- Improve Immune and Heart Function, Bone Density, Healing Time and Cholesterol, Improve Brain Function, Memory and Mental Focus
Wow! Sure sounds like a wonder drug to me! Yeah right, anyway here is some real world information for bodybuilders. Somatropin (rHGH) is produced by the pituitary gland and is responsible in adolescence for growth of tissues, protein deposition, and the breakdown of sub-q fat stores. As we age, growth hormone levels decrease but still remain active in the body, releasing in cycles during the day. Synthetic growth hormone used exogenously by bodybuilders is a 191 chain sequence of amino acids that replicates the bodies natural production of growth hormone.
Growth hormone has been in use by bodybuilders since the early 1980’s, though at this time, HGH was being extracted from the pituitary glands of cadavers and had enormous side effects, most prominently Creutzfeldt Jacob disease. This is a rare and fatal brain disease, it need not be discussed here since it is not possible in synthetic forms of HGH, but if you want more info just run a search in google. rHGH stimulates growth in most body tissues which is due to an increase in cell number rather than cell size. This includes muscle tissue as well as internal organs, hence the dreaded GH gut.
Use of growth hormone by bodybuilders will cause increased muscle size, localized and overall bodyfat loss, increased protein synthesis, increased glucose output by the liver, increased insulin resistance and lowered thyroid output. Stored fats will be used as a primary fuel source, thus the body fat loss.
So is rHGH the wonder drug everyone lusts after? It certainly is beneficial but not for everyone. You must be willing to take risks to achieve maximum benefits from its use, as well as substantial financial investment. Do it right the first time or don’t do it at all! You will achieve faster and greater growth from cycles of steroids than with GH, though once you reach a plateau, not many products work better.
Ok, so now you have decided that this is the drug for you and you are ready to try it, so what next? Well here are some general guidelines to follow for maximal results from GH use:
Daily injections are a must to maintain stable blood levels as GH has a very short life span in the body. It will peak almost immediately after injection and will clear the body with a half-life of only 20-30 minutes. It is best injected first thing in the morning upon rising to raise levels that are very low from sleeping, and immediately after training. I do not recommend injecting before bed as many bodybuilders do, since that is the time of day that your body will release naturally high levels of growth hormone, and exogenous use will only block that release. If you take it in the morning when levels are low, after training when levels are depleted and then let your body release while sleeping, you are getting one extra release for free! GH is best taken long term, short cycles do not maximize the benefits of muscle cell increase, only fat loss. Here is how I take my GH for maximum benefits:
6iu ed injected sub-q, preferably in the stomach (IM for certain brands)3iu injected upon rising, 3iu injected immediately post-workout10iu insulin taken 30 minutes after HGH injection25mcg cytomel eduse of androgens such as testosterone
The timing of GH and insulin injections is critical. If insulin is injected before the GH, your pancreas will stop release of insulin monitoring due to the exogenous source. GH when injected will mobilize stored glycogen release which will turn into glucose for energy. This will cause a rapid rise in blood sugar levels that will not shut down or stop rising due to the feedback loop being momentarily cut off. You will go hyperglycemic and end up in the hospital. You must first inject your GH, then the insulin; this will cause a rise in glucose release by the GH and will be controlled and shuttled into muscle tissue for repair by the later injection of insulin.Use of cytomel or some type of T3 hormone is critical since GH use will severely lower thyroid levels. Small exogenous sources are necessary to maintain normal levels and 25 mcg ed is sufficient. This will also aid in body fat loss by maintaining proper thyroid functioning.Use of androgens is also necessary due to the promotion of anabolism by increasing muscle size that benefits the new cell number increase by the GH. Remember GH will not directly cause muscle cell size increase, just the number of cells, therefore, androgens are necessary to increase size. Testosterone or trenbolone are both highly androgenic and perfect for out stack.
One myth that needs to be cleared up: high doses of GH use and the 5 on 2 off program. First, if you find that you are not achieving results off of 4-6iu ed, than something else is the problem, not your dose. The use of high doses if primarily cause by heat damage to the protein chain causing denatured proteins. This will decrease the effect and you must use higher doses to achieve the same effect. Other reasons for high dose use are; fake gh, not using insulin, cytomel or test, poor diet, improper timing schedule and the 5 on 2 off. This program was recommended by dealers as a way to move product by offering a lower cost cycle. No doctor in the world would recommend this protocol, Peak blood concentrations are reached in 2-6 hours after injection, and therefore, multiple daily injections are necessary to achieve stable release schedule and results. If you take your last injection Friday afternoon, and then not again till Monday morning, then you have negated all effects offered by the 6 hour concentration. Yes, you will achieve results using a 5 on 2 off program, but not as well as if you inject ed. It’s your money; I can only tell you how to optimize use.
Side effects of GH use include; carpal tunnel syndrome, tingling in the extremities, numbness in the hands and feet, increased organ growth, decreased insulin reception, acromegaly but only in extreme dose use, and decreased thyroid output causing fat accumulation. If you find that you are experiencing any of the above side effects, lower your dose immediately. This is especially important with carpal tunnel. If you feel like your wrists are hurting then lower the dose until pain subsides. You do not want to have that surgery, trust me.
GH is a fantastic product, beneficial for many reasons. Most people will experience thinning of the skin, increased vascularity, fat loss, permanent increases in muscle size due to the cell number increase, and overall feelings of wellness. You will probably need less sleep and feel supercharged all day long. I highly recommend HGH use, but only when you have the money to do it right. 4-6 month cycles are optimal, year round if you are over age 35.

Interleukin-6: Catabolic Agent or Growth Factor?

Interleukin-6 : Catabolic Agent or Growth Factor?

THE PROTEIN in our muscles undergoes a continual process of synthesis and degradation. Athletes and weightlifters know that after a strenuous workout, muscle tissue is damaged and needs time to regenerate and be repaired. If we provide sufficient rest and adequate nutrition, the body will usually overcompensate and produce stronger and larger muscles.
Most analyses of strength training are concerned with two phases: the work phase where we apply physical stress to our muscles to cause microtrauma and resulting overcompensation, and the anabolic phase in which we seek to enhance protein synthesis. But there's a third phase, a period of breakdown and recovery, which is rarely discussed. We are told to rest and to do what we can to avoid cortisol, but very seldom is there any mention of the signal molecules which accomplish the work of bringing the body back to a state of homeostasis.
Weightlifters talk of "destroying" their legs in a squat workout; of loading the muscles with weight and stressing them until they are barely able to function. What are the mechanisms that permit the body to recover from such punishment? Is it possible to optimize recovery so that less tissue is broken down, and we get into the anabolic phase more quickly?
The essay that follows will deal with some very technical concepts. I'm including a glossary containing brief definitions for the scientific terms used. The purpose of such a technical essay is twofold: First, it introduces some basic ideas in cell biology that will enable a better understanding of exercise physiology. Once the basic concepts are learned, one can view this area of science not as a collection of disparate facts, but as a coherent system that runs on a logical -- but complicated -- basis. Secondly, by going into detail concerning the stages whereby the body detects damage, disposes of damaged tissue, and ultimately replaces or strengthens the affected tissue, we can identify areas where we can intervene with nutrition or chemical agents to reduce damage and enhance our muscular gains. Also, it may be possible to take advantage of this intimate knowledge to design training protocols that coincide with the catabolic and anabolic stages that follow exercise.
Cytokines and Interleukins
There are four types of signaling molecules in the body: neurotransmitters, endocrine hormones, autacoids and cytokines. Cytokines are soluble proteins which act non-enzymatically to regulate cell function. There are various types of cytokines, among them being interleukins, hematopoietic regulators, interferons, growth and differentiation factors and chemotactic polypeptides. Interleukins (abbreviated IL) are cytokines that are produced by leukocytes (white blood cells) and that function during inflammatory responses. They may also be produced by other types of cells. Typically, interleukins have the twin properties of pleiotropy and redundancy. Pleiotropy means that an interleukin may have several different effects, depending on the environment and the tissue acted upon. Redundancy in this case refers to the ability of other cytokines (interleukins or not) to produce some of the same effects as the interleukin being studied. This redundancy can be due to the fact that receptors for interleukins often share common subunits, or it may also be caused by identical effects on transcription factors or on the DNA itself.
As of October 1998, eighteen different ILs have been described. We'll be focusing on interleukin-6 (IL-6), which has some special properties that make it interesting to bodybuilders. For those who might be curious, here is a brief survey of all the interleukins:

Figure 1.IL-6 molecule
Interleukin Description
IL-1 An inflammatory cytokine. One of the first cytokines to be secreted following trauma, infection, etc. Induces IL-6.
IL-2 Secreted by Type 1 T-helper cells (Th1) of the immune system. Stimulates cell-mediated (as opposed to antibody-mediated) immunity. Generally a beneficial cytokine. IL-2 levels decline with age, but are upregulated by DHEA.
IL-3 Growth factor for hematopoietic cells. Acts in a similar fashion as granulocyte-macrophage colony-stimulating factor (GM-CSF). Secreted by activated T lymphocytes, it induces formation of macrophages, neutrophils, etc. Also induces secretion of immunoglobulin from B cells.
IL-4 Anti-inflammatory cytokine. Related to IL-13. Released by activated T cells, it initiates the humoral response (antibodies).
IL-5 A B-cell growth and differentiation factor; also stimulates eosinophil precursor proliferation and differentiation. Secreted by activated T cells.
IL-6 Pro- (and sometimes anti-) inflammatory cytokine. Pleiotropic. The subject of this article. Main signal of cellular injury, and main mediator of the body's response to injury. Most important stimulator of acute phase proteins. Has an important role in hematopoiesis. Produced by a variety of cells.
IL-7 Growth factor produced by a number of different cells. Unlike other interleukins, IL-7 in not redundant, i.e. its function can not be duplicated by other cytokines. It is required for lymphocyte development.
IL-8 Pro-inflammatory. A chemokine. Can be induced by IL-1 and lipopolysaccharide from bacteria. Produced by many different cells.
IL-9 Cytokine produced by T cells, particularly when mitogen stimulated, that stimulates the proliferation of erythroid precursor cells. May act synergistically with erythropoietin. Synergizes with IL-4 to produce immunoglobulins.
IL-10 Anti-inflammatory. Produced by Th2 cells, plus some B cells and monocytes. Stimulates growth of stem cells and thymocytes. Stimulates B and T cell development. Suppresses cytokine production by macrophages.
IL-11 Pleiotropic cytokine originally isolated from bone marrow. Stimulates B cell maturation, and production of erythrocytes (red blood cells) and megakaryocytes. Synergizes with IL-3. Induces synthesis of acute-phase proteins in the liver.
IL-12 Formerly known as Natural Killer Cell Stimulatory Factor (NKSF). Produced by monocytes, macrophages, B cells, NK cells. Acts synergistically with IL-2 to transform T cells into cytotoxic T lymphocytes (CTLs). Stimulates the proliferation of activated T cells and NK cells and induces them to produce interferon-gamma.
IL-13 Anti-inflammatory. Related to IL-4. Produced by activated Th2 cells. Inhibits IL-6. Stimulates antibody production.
IL-14 A high molecular weight B lymphocyte growth factor. One of the least researched cytokines.
IL-15 Anabolic for skeletal muscle. IL-15 receptor contains some sub-units with the IL-2 receptor.
IL-16 Pro-inflammatory. Formerly called Lymphocyte Chemoattractant Factor.
IL-17 Pro-inflammatory. Produced by T cells. Activates NF-kappaB.
IL-18 Pro-inflammatory. Induces the cytokine interferon-gamma.
Interleukins and the Acute Phase Reaction
Fig. 2. Top mouse was continuously exposed to IL-6. Bottom mouse received antibodies against IL-6. From DeBenedetti1997.
EXERCISE modulates the immune system. Following even moderate exercise, there is an elevation in the number of neutrophils, the most common type of white blood cell (Boyum1996, Cannon1994, Tidball1995).
After acute or short-term exercise, the total number of lymphocytes increases, but if the exercise is intense and of long duration the number of lymphocytes decreases (Pedersen1997). A lack of glutamine resulting from exercise stress can impair the ability of lymphocytes to proliferate and to function (Sharp1992, Rohde1998).
Prolonged low intensity exercise may lower levels of interleukin-6 in the blood (Boyum1996), while intense or eccentric (negative) exercise causing muscle damage induces a dramatic rise in this cytokine (Bruunsgaard1997, Weinstock1997, Ullum1994).
In short, intense exercise increases cytokines which may act to break down muscle, while extensive exercise decreases cell- mediated immunity (i.e. the ability of Natural Killer cells, cytotoxic T lymphocytes, and phagocytes to eliminate potentially harmful cells and materials).
Massage therapy has been shown to increase cell-mediated immunity (Ironson1996), so there may be some benefits in combining massage with some forms of exercise.
The immune system
The human immune system is a network of active and passive defenses against substances and cells that would harm the body. It includes innate immunity from barriers like the skin, body temperature, pH (acidity) of the stomach, the inflammatory response and the action of phagocytic cells. It also includes acquired immunity, which is usually based on recognition and response to an antigen. This generally involves white blood cells called lymphocytes. There are two kinds: T cells (from the thymus) and B cells (from the bone marrow). Acquired immunity may be humoral, meaning it involves substances like antibodies and cytokines that are dissolved or suspended in the blood, or it may be cell-mediated, involving the cytotoxic activity of specialized cells.
Because the effects of exercise on the immune system do not involve antigens, such immune activity is fundamentally different from what you might read about in a text on immunology.
The Acute Phase Response
PARTS of the immune system are depressed following a workout. However, this is not to say that the body is defenseless. There is a "rapid deployment" system called the acute phase response that kicks in after trauma, and exercise is generally interpreted by the body as trauma. Exercise subjects the body to oxidative stress, and that generates reactive oxygen species and other free radicals that act as alarm molecules. Also, the body can sense potentially dangerous changes in osmolarity (e.g. swelling), hyperthermia (heat), hypoxia (oxygen starvation), pH (acidity) of the blood, ionic contents of cells, and a variety of other conditions.
Once initiated, the response is in the form of a cascade. Local to the injury there is acute inflammation and blood clotting. Systemically there is fever, leukocytosis (increased white blood cells), increased levels of hormones like cortisol, and in particular a major increase in synthesis of proteins called acute phase proteins (ACPs). Let's look at this process in more detail.
Initialization
During exercise, free radicals known as reactive oxygen intermediates (ROIs) and reactive nitrogen intermediates (RNIs) are formed. Additionally other reactive intermediates such as carbonyls may be produced. All these free radicals can signal and in some cases activate cells of the immune system.
When intense exercise causes damage to cells, the contents of the breached cell enters the surrounding lymph. This also has the effect of signalling that there has been damage.
Monocytes are white blood cells with a single nucleus that are formed in the bone marrow. When they arrive in the tissues of the body they may differentiate (mature) into macrophages, and lose some of their motility (ability to move independently). Muscle tissue contains a number of macrophages, and these are the first immune cells to react to exercise trauma. When a macrophage is activated, it undergoes a "respiratory burst" of oxidation, which produces even more ROIs, thus extending the signal to surrounding cells. Macrophages also secrete signal molecules like IL-8 which act as chemokines to attract other immune cells, in a process called chemotaxis.
Prostaglandins are secreted by macrophages as well. These, plus some metabolic byproducts of exercise like lactic acid, physical changes involved in pumping the muscle, and the effects of the first immune phenomena just described, combine to initiate inflammation in the effected muscles.
Neutrophils in the blood sense the alarm molecules and chemokines, and race to the defense of the injured tissue. The inflamed blood vessels are more permeable, and in a process called extravasation the neutrophils escape from the bloodstream, enter the muscles, and home in on the damage. They in turn are activated, undergo a respiratory burst, and begin secreting cytokines.
Cytokines
The first cytokines to be released as a result of exercise are the "pro-inflammatory" substances interferon-gamma (IFN-gamma), tumor necrosis factor (TNF) and interleukin-1 (IL-1). Also the chemokine IL-8 is released. IFN-gamma, TNF and IL-1 have a number of different effects on the body. They travel through the bloodstream and stimulate the liver to synthesize acute phase proteins like C-reactive protein, serum amyloid A and fibrinogen. They influence complement, which is yet another factor in the immune system, and kinins, which can produce vasodilation, pain, and may make you lose your lunch in the squat rack. They cause body temperature to increase. Most important for this article, all three act on T lymphocytes to cause them to secrete interleukin-6.
IFN-gamma, TNF and IL-1 all have the reputation of being catabolic cytokines which will reduce muscle mass. For example, IL-1 activates the enzyme "branched-chain alpha-keto acid dehydrogenase" to oxidize amino acids in the muscles (Cannon1991). However as we'll see below, at least part of the wasting effect may be mediated by IL-6, so that if the effect of IL-6 is blocked some of the catabolism is stopped.
T cell activation
A second part of the cytokine cascade derives from activated lymphocytes. As we've mentioned, under normal exercise conditions, immune cells are not activated by antigens. There are alternative methods by which they can be activated. For example, lymphocyte proliferation can be artificially stimulated with a chemical that increases the level of glutathione, an antioxidant (Berridge1997). Also it is known that reactive oxygen intermediates like hydrogen peroxide ( H2O2 ) can activate the nuclear transcription factor NF-kappaB. So there is good reason to expect that the reduction/oxidation changes resulting from exercise may result in T cell activation.
Also it is known that certain cytokines can activate lymphocytes. For example, IL-1 was originally called "Lymphocyte Activating Factor."
B lymphocytes are involved in antigen-based antibody formation, so although they also secrete some cytokines we won't consider them further. T cells differentiate under the influence of cytokines into cytotoxic T lymphocytes and T helper (Th) cells. We need only consider the latter. Th cells in turn differentiate into type 1 and type 2 T helper cells (Th1 and Th2). It is the Th2 cells that produce the bulk of the interleukin-6, although macrophages also produce it, and even muscle cells seem to produce some under stress. We'll cover IL-6 in detail below.
Termination of the acute phase
Cytokines and acute phase proteins have a brief half- life in the body, so even without anti-inflammatory signalling this phase would inevitably end. However a number of substances produced by the body have the effect of bringing it to a conclusion more quickly.
As we all know, cortisol is secreted as a result of exercise. A product of the adrenal glands, cortisol is a member of a class of compounds called glucocorticoids. We normally think of glucocorticoids as being catabolic, but they also has the effect of inhibiting the synthesis of all acute phase cytokines. Since many of those cytokines are catabolic, this is actually an anti-catabolic action of cortisol. To put this in another way: if you are successful in limiting cortisol production after a workout, you might find an increased level of cytokines, and thus no net prevention of muscle loss!
Cytokines sometimes have soluble receptors. One way these are produced is from membrane receptors that are cleaved and "shed" from cells. The receptors then circulate in the blood. Soluble receptors for IL-1, IL-4 and TNF have the effect of binding to and thus deactivating their cytokines. You might say they "mop up" the cytokine. The production of these soluble receptors is a second way in which the body limits the acute phase. On the other hand, soluble receptors for IL-6 have the opposite effect: they can cause IL-6 metabolic effects on cells with incomplete receptors that normally wouldn't be effected.
A protein called IL-1 receptor antagonist (IL-1Ra) binds to IL-1 receptors, blocking the effect of IL-1. IL-1Ra is secreted from cells upon stimulation by TNF, and its production is enhanced by IL-10 and IL-4. As levels of these last interleukins rise, IL-1 declines.
IL-10, IL-4 and IL-13 are anti-inflammatory cytokines. They inhibit the production of inflammatory cytokines and also reduce induction of cyclooxygenase-2 (COX2), an enzyme involved in inflammation which is the target of drugs like aspirin. Whereas IL-1 and TNF are produced early in the acute phase response, the anti-inflammatory cytokines come from activated T cells, so they are a way in which the body gracefully concludes the acute phase.
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IL-6
INTERLEUKIN-6 stands out among the interleukins in several ways. It is the main signal of tissue damage in the body (Sehgal1995). Although IL-1 and interferon initiate the synthesis of some acute phase proteins by the liver, IL-6 stimulates the liver to produce a larger and more complete set of these proteins (Hilton1992, Baumann1987). IL-6 is thought by many investigators to be the main factor in cachexia -- the wasting syndrome that accompanies AIDS, cancer, and some autoimmune diseases. Yet IL-6 is also a growth factor, intimately involved in the production of new cells, including new muscle cells.
A better understanding of the pleiotropic roles of interleukin-6 should provide insight into methods of improving physical development through training, nutrition and supplementation.
The IL-6 family of cytokines
IL-6 belongs to a family of physically similar or "homologous" cytokines, including Leukemia Inhibitory Factor (LIF), Ciliary Neurotropic Factor (CNTF), Granulocyte-Colony Stimulating Factor (G-CSF), IL-11, Oncostatin M (OSM), and Cardiotropin-1 (CT-1). IL- 6 type cytokines feature four anti-parallel helices, arranged as shown in Figure 1.

Receptors for IL-6 family cytokines are mulitimeric, having a specific component for binding with the cytokine, plus a transmembrane transducer protein called gp130 for delivering the signal to the nucleus of the cell. For example, the LIF receptor is composed of a gp130 molecule plus a specific component called LIFR-beta. IL-6 receptor is a trimer, with two gp130 molecules, plus a specific component called IL-6R-alpha. When IL-6 first contacts the cell, it binds with IL-6R-alpha. Then the gp130 molecules dimerize and bind with it to form the ligand-receptor complex.
While all this may appear a bit technical, study of the receptors and how they are bound tells us much about the actions of these cytokines. By means of this knowledge we can often block their effects.
Signal transduction
Once the IL-6 receptor complex is assembled and bound, chemicals within the cells called Janus kinases (JAK) phosphorylate the amino acid tyrosine on the gp130 molecules. We have an effective tyrosine kinase inhibitor (genistein) that can block this process. We'll return to genistein in the section on IL-6 blockers, below.
The phosphotyrosines link up with a substance previously termed "acute phase response factor" (APRF), but which is now called STAT3 (for "Signal Transducer and Activator of Transcription"). STAT1 and STAT3 become phosphorylated and dimerize. Then these dimers travel to the nucleus of the cell. Meanwhile the IL-6/IL-6R-alpha combination is taken into the cell ("endocytosed") and is broken down and destroyed. The gp130 units are recycled.
The STAT dimers bind with IL-6 response elements which then activate gene transcription factors.
NF-IL-6 (Nuclear Factor IL-6) is a member of the C/EBP (CAAT/Enhancer Binding Protein) family of transcription factors. It is almost undetectable in normal circumstances, but when cells are stimulated with IL-6 it is produced abundantly. C/EBP regulates fat tissue. It increases differentiation from pre-adipocytes to adipocytes, activates the glucose transporter GLUT4, etc. In short, it makes you fat. When adipose tissue is treated with TNF -- which reduces fat -- C/EBP is reduced, but NF-IL6 increases. It seems that the ratio of C/EBP to NF-IL-6 is a determinant of fatness. Both IL-6 and LIF are known to drastically reduce fat, so the activation of NF-IL-6 may be one of the mechanisms of that fat reduction.
STAT3 can also bind to the IL-6 response element of the junB gene (JRE-IL6).
Apart from the JAK/STAT pathway, there is a second pathway from the IL-6 receptor to the nucleus. It involves a protein called ras, and Mitogen Activated Protein Kinase (MAPK).
As a result of the alternate pathways, a variety of transcription factors can be activated, including AP-1 (Activator Protein-1) and NF-kappaB (Nuclear Factor kappa B).
NF-kappa B
NF-kappaB deserves special mention. The name derives from its discovery in B cells expressing kappa immunoglobulin. Subsequently it was found that NF-kappaB exists in nearly all mammalian cells. It regulates inflammation, immune reactions and acute phase response, and it is generally bad news for athletes. Elderly people and people with AIDS or chronic inflammation may have NF-kappaB almost permanently activated, which accounts for some of the tissue loss and poor health in those groups. On the other hand, NF-kappaB regulated genes encode hematopoietic growth factors, which can be useful to athletes.

Nuclear Factor kappa B
NF-kappaB is activity is low is a normal cell, due to an inhibitor named I-kappa-B. IL-1 and TNF act to degrade I-kappa- B, and by this means NF-kappaB is activated. As a result of transcription regulated by NF-kappaB, many cytokines -- including Il-6 -- are expressed. This is one way that IL-1 and TNF induce the secretion of Il-6. NF-kappaB can also be activated by reactive oxygen intermediates, and by IL-6 as described in the previous section.
There are several effective methods of inhibiting NF-kappaB, some of which will be described below.
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Effects of IL-6
MYOGENESIS -- the creation of new muscle tissue -- occurs when muscle satellite cells (also called sarcoplasts) or myoblasts (also called sarcoblasts) are activated. Often the terms "myoblast" and "satellite cells" are used interchangeably. Once activated, these cells proliferate, and then differentiate, and finally fuse with other cells to form myotubes or to join existing muscle fibers. The signal for these cells to proliferate is Hepatocyte Growth Factor (HGF). HGF is induced by heparin, which is liberated from the basal lamina of muscles when they are damaged. It is also induced by interferon-gamma, and is very potently induced by prostaglandin E2. All of these substances appear as a result of trauma to the muscle. In addition to activating the myoblasts, HGF increases their motility, so that they can migrate to the site of damaged muscle.
This same trauma results in the expression of IL-6, LIF, and Fibroblast Growth Factor (FGF). These three act as growth factors (yes, in this case IL-6 is a growth factor), increasing the proliferation of myoblasts. See Figure 3: response of IL-6 and LIF to muscle injury (source: Kurek1996). LIF is a stronger inducer of proliferation than IL-6, and whereas the effect of IL-6 is short-lived, a brief exposure to LIF will result in proliferation over an extended period. Injections of LIF have been suggested as a therapy for muscle trauma and disease (Kurek1996).
When cells divide, the telomeres at the end of their chromosomes shorten. Since the telomeres become shorter with each division, this sets a limit (the "Hayflick limit") on the number of times that a cell and its descendent cells can divide. This is particularly important in germ cells like myoblasts. An enzyme named telomerase can prevent the telomeres from shortening. Certain cytokines, including IL-6, can induce telomerase, hence increasing the number of times a cell can divide (Engelhardt1997). This appears to be a unique contribution made by IL-6 to the muscle regeneration system. IL-6 also has a similar effect in hemopoietic tissue.
Effect on Fat
Experiments on mice that were reported in 1989 and 1990 showed LIF inhibits the action of lipoprotein lipase (LPL), which is instrumental in uptake of fatty acids by adipose tissue (Hilton1992). A "dramatic and rapid loss of virtually all subcutaneous and abdominal fat" was reported. More recently, it has been shown that while administration of recombinant IL-6 to mice reduces LPL, it has almost no effect on fat reduction in mice (Fujita1996).
We've previously mentioned that IL-6 activates a regulator of fat tissue called NF-IL-6. NF-IL-6 is actually a repressed transcription factor which is normally inhibited. Signalling from IL-6 through the MAP kinase pathway overcomes the inhibition (Akira1995). In this way, while IL-6 may not be as successful at blocking fat uptake as LIF, it may decrease body fat by slowing the maturation of adipocytes.
Effect on Muscle
There are three main proteolytic pathways in skeletal muscle: cathepsins functioning in the lysosome, calpain proteases in the cell's cytosol, and the ATP-ubiquitin (Ub) pathway. IL-6 acts to destroy muscle through the cathepsin and ATP-Ub pathways. Fujita et al. showed that mice inoculated with a cancer (adenocarcinoma) developed high levels of IL-6 after 11 days: while untreated control mice had a level of 7.9 pg/ml of IL- 6, inoculated mice had an average of 1,142 pg/ml (Fujita1996). These inoculated mice had cathepsin B levels 236% higher, and cathepsin B levels 826% higher than controls. Tsujinaka et al. showed that in transgenic mice carrying DNA for human IL-6, treated mice had cathepsin B levels 20 times higher than controls (Tsujinaka1996).
IL-6 shortens the half-life of proteins in the myotubes that make up muscle fibers. It has been demonstrated that mRNA levels of proteosomes, which are involved with the ATP-Ub pathway, are increased by IL-6 (Ebisui1995, Tsujinaka1996). Strangely, TNF, which is often named as the main culprit in cachexia (wasting syndrome), has not been shown to have this effect. In fact, several studies have failed to show a direct effect by TNF on muscle proteolysis (reviewed in Fujita1996). Therefore it seems that the proteolytic action of TNF may actually be mediated through IL-6. In other words, without IL-6, TNF would not destroy muscle (although it would reduce fat). Therefore, IL-6 appears to be the primary agent in muscle wasting.
IL-6 is a catabolic agent in many disease states (Papanicolaou1998). It is present in rheumatism and other autoimmune type diseases, and is responsible for joint deterioration and muscle loss. DeBenedetti et al. found that transgenic mice with human IL-6 had stunted growth, attaining only about half the size of normal mice (Figure2). They also showed that in humans as well as mice, there is a negative correlation between IL-6 and IGF-1. In other words, the more IL-6 in the body, the less IGF-1. This relationship was unique to IL- 6: TNF and IL-1 were not correlated with IGF-1 (DeBenedetti1997).
In summary, the effects of IL-6 are mostly harmful for athletes. It plays beneficial roles in resisting infection, stimulating the acute phase response in case of trauma, and in hematopoiesis and production of stem cells. However, excessive IL-6 resulting from exercise or chronic inflammation will destroy muscle tissue and reduce IGF-1.
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Manipulation of IL-6
Now that we know the actions and effects of interleukin-6, let's consider ways to manipulate IL-6 secretion.
In the unlikely event that we'd want more IL-6, the method is obvious: just exercise. Any exercise that causes trauma to the muscles would suffice. If we want to start an acute phase response without the temporary immune suppression caused by exercise, there are herbs like Echinaceae and Rudbeckia speciosa that contain polysaccharides the body mistakes for bacteria, so that they can initiate an immune response (Bukovsky1995).
For inhibition of IL-6 and its effects there are many options. We'll first cover nutrition and supplements, and then drugs. Not all the options mentioned will be suitable for athletes; the goal here is to compile a comprehensive list from which people can choose according to their needs.
Nutrition and Supplements
Caloric restriction is perhaps the simplest method of reducing IL-6 (Volk1994). This is a technique employed by life- extensionists. It might have some application to dieting athletes, providing they don't use weight-loss drugs.
Oils and fatty acids.
oEicosapentaenoic acid (EPA) supplementation significantly reduced IL-6 ecretion from mononuclear cells in patients with cancer (Wigmore1997).
oSupplementation with docosahexaenoic acid (DHA) and EPA reduced production of IL-1, IL-6, TNF and IL-2 by mononuclear cells in normal individuals and in patients with Rheumatoid Arthritis and with Multiple Sclerosis (Calder1997).
o The fatty acids gamma linolenic acid (GLA), EPA and DHA reduce serum IL-1, IL-2, IL-4, IL-6, TNF alpha and IFN-gamma in cancer patients. Three months after cessation of fatty acid supplementation cytokine values returned to normal (Purasiri1994).
o In human endothelial cells, DHA decreased secretion of IL- 6, IL-1, IL-4, IL- 8 and TNF (DeCaterina1994).
o Blackcurrant seed oil rich in GLA reduced production of IL- 1 beta, TNF alpha IL-6 and PGE2 (Watson1993).
Sources of GLA: evening primrose oil, borage seed oil, blackcurrant seed oil.
Sources of EPA and DHA: fish oils (e.g. cod liver oil, salmon oil, etc.).
Lactoferrin (found in milk) reduces IL-6 (Mattsby1996).
Estrogen and androgens reduce IL-6 and block NF-kappaB. Therefore, foods like soy which are estrogenic and supplements like androstenedione would be expected to have a similar effect.
Since one of the signal pathways from the IL-6 receptor depends on tyrosine kinase, genistein, which is an effective tyrosine kinase inhibitor, should block it. Genistein is a component of soy, and can be purchased in purified form.
Zinc induces Heat Shock Protein HSP-70 and reduces cytokines and apoptosis (Klosterhalfen1997).
Antioxidants. Since antioxidants provide some of the initial signals in the acute phase response, and since NF-kappaB can be directly activated by reactive oxygen intermediates, antioxidants can prevent secretion of IL-6 and the effects of NF-kappaB transcription.
o Vitamin E supplementation (400 units twice per day) almost completely eliminated increased secretion of Il-6 in athletes following three 15 minute sets of downhill running (Cannon1991).

o L-ascorbic acid inhibits secretion of IL-1 and IL-6 (Tebbe1997).
o Black tea extract lowers concentrations of IL-6 (Amarakoon1995).
o Melatonin reduces oxidative stress, improves immune function. etc. (Reiter1997).
o Since expression of IL-6 mRNA is dependent on NF-kappaB binding to the IL-6 gene, supplementation with the antioxidant N-acetyl-L-cysteine (NAC) can block the process (Shibanuma1994).
o A number of experimental antioxidants have been employed in studies of NF-kappaB inhibition. They include glutathione, NADPH, pyrrolidine dithiocarbamate (PDTC), butylated hydroxyanisole (BHA), and various forms of superoxide dismutase.
Since IL-1, IFN-gamma, and TNF induce IL-6 production, any substances that inhibit them will usually have the effect of inhibiting Il-6.
NF-kappaB can be inhibited by nitric oxide (NO). One substance that induces NO is the amino acid arginine.
Aspirin and salicylate inhibit NF-kappaB. Also salicylate inhibits protein kinase activity, and so would prevent signalling by IL-6 via tyrosine kinase (Beauparlant1996). Since methyl salicylate is a common ingredient of ointments for sore muscles, this raises the possibility that a topical application could be effective against IL-6.
There is a negative correlation between dehydroepiandrosterone sulfate (DHEAS) and IL-6 in the blood (Straub1998). Therefore supplementation with DHEA will reduce IL-6.

Drugs for IL-6 reduction
Since IL-6 is a factor in many diseases, a number of drugs and pharmaceutical techniques have been investigated for lowering IL- 6 levels. Some of the substances mentioned below are experimental or unapproved.
Glucocorticoids like dexamethasone block transcription factors NF-kappaB and AP-1 (Brattsand1996). Unfortunately they are also catabolic to muscle, and so are of little use to the athlete, except in case of injury.
RU486 (mifepristone) can block NF-kappaB induced by TNF, although not as well as glucocorticoids (Beauparlant1996). It has the advantage that it also blocks glucocorticoid receptors, but unfortunately the receptors soon upregulate.
The immunosuppressant drugs FK506 and cyclosporin A will suppress T cells, but this would be an insane way to inhibit IL-6, due to the side effects.
Anti-inflammatory cytokines like IL-10, IL-4, IL-13, and Transforming Growth Factor beta (TGF-beta) will inhibit synthesis of IL-6 and other inflammatory cytokines. IL-10 also enhances synthesis of IL-1 receptor antagonist, downregulates TNF receptors and inhibits T cell proliferation (Koj1998, Xing1997, Dokter1996).
Soluble cytokine receptors and receptor antagonists are effective against IL-1 and TNF, which induce IL-6. Unfortunately, the IL-6 soluble receptor only increases the effect of IL-6. Enbrel, a soluble receptor for TNF made by Immunex, will be on the market soon for treatment of rheumatoid arthritis and similar inflammatory conditions.

Rolipram, an antidepressant sold in Europe by Schering, is also very effective at inhibiting TNF, and so has an indirect effect on IL-6.
Tenidap, a new anti-rheumatic drug, showed a great deal of promise against cytokines, but the FDA decided not to approve it because of problems with proteinuria (protein in the urine). This side effect may make it unsuitable for athletes. It is available from Europe (Breedveld1994, Bondeson1996).
Polymyxin B administration results in a prompt reduction in interleukin-6 levels in burn patients (Cone1997).
For women, medroxyprogesterone acetate has reduced IL-6 in breast cancer patients. Reduction was correlated with plasma levels of MPA, not dosage (Yamashita1996).
Use of a monoclonal antibody against CD-54 (ICAM-1) reduced IL-6 in rheumatoid arthritis (RA) patients (Schulze1996).
Antibodies against TNF have been used to reduce IL-6 (Fekade1996).
Indomethacin reduces Il-6 by inhibiting prostaglandin E2 (Hinson1996).
Tyloxapol, a potent anti-oxidant used in the treatment of cystic fibrosis and chronic bronchitis, inhibits NF-kappaB and IL-6 (Ghio1996).
The anti-rheumatic drug minocycline decreases serum levels of IL-6 (Kloppenburg1996).
The anti-rheumatic drug tepoxalin inhibits the production of IL-2, IL-6 and TNF alpha and inhibits activation of NF- kappaB (Ritchie1995).
Pentoxifylline is a methylxanthine derivative that acts as a phosphodiesterase inhibitor and is prescribed to improve capillary flow. It inhibits TNF and IL-6 and counteracts the respiratory burst of phagocytes that produces free radicals (Lundblad1995), Koj1998, Mandell1995).
Torbafylline, a xanthine derivative that suppresses TNF, has been used with some experimental success in the treatment of cachexia (Sinha1995).

The sex hormones estrogen and testosterone block IL-6 (Bellido1995, Vaananen1996, Stein1995). In fact, it seems that nearly any steroid inhibits IL-6: estrogen, testosterone, DHEA, glucocorticoids, and probably most androgenic/anabolic drugs.
Angiotensin Converting Enzyme (ACE) inhibitors decrease the levels of angiotensin II or limits its action, thereby interfering with the permissive effect of Angiotensin on IL-6 (Klahr1998).
Antibodies that destroy IL-6 receptors are effective at preventing muscle proteolysis caused by IL-6 (Fujita1996).
Conclusion
EXERCISE activates the immune system, which then cycles through an abbreviated version of the acute phase response. Damage to muscles results in IL-6 secretion, which signals the body to produce acute phase proteins. Depending on the amount of muscle damage, the acute phase response will terminate sooner or later, by the action of cortisol and anti-inflammatory cytokines.
IL-6 is the main mediator of muscle wasting. It may have some beneficial actions at the onset of the acute phase response, but chronically high IL-6 levels must be avoided for good health and optimum muscular development. We have a number of ways to accomplish that, from the simple use of antioxidants to specially designed antibodies. Through the use of these agents in coordination with training activity, we can effectively reduce the unnecessary muscle breakdown that normally follows intense exercise.
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Body Image, Bodybuilding, and Cultural Ideals of Muscularity

Body image is a term that has come to represent the "internal" image or representation that we have of our physical appearance (Thompson, Heinberg, Altabe, & Tantleff-Dunn, 1999). It is to be contrasted with the "outer" image or an objective view of attractiveness (i.e., a rating made by a supposedly unbiased observer). Although commonly thought of as overlapping substantially, in fact one’s inner view (body image) is only minimally correlated with actual ratings of attractiveness. The overlap is an astonishingly low 5%. Additionally, it appears that body image, rather than objective appearance, is more closely related to psychological factors and clinical conditions (e.g., eating disorders, depression, low self-esteem). For these reasons, research into a multitude of aspects of body image has mushroomed in recent years. One such active area of inquiry is the examination of exercise and body image. Within this general area, researchers have focused largely on the role of athletic status (sedentary, active), type of sport (running, bodybuilding), and contributing risk factors (media pressures). In this article, I outline some recent work that has focused on bodybuilding and evolving cultural standards of muscularity. I also briefly note the occurrence in recent years of a particular type of body image disorder, muscle dysmorphia, and offer some guidelines for dealing with problematic issues that might accompany an excessive focus on muscularity.
BackgroundOnly in the past 10-15 years have researchers actually given due attention to bodybuilding and body image. A primary reason is the greater prevalence of dissatisfaction with appearance that was initially documented in women, and the close connection between women’s body image problems and eating disorders (which occur roughly 10 times more often in women). However, beginning with a few studies in the mid-80s, a shift in attention to men’s appearance concerns began, and this was accompanied by a focus on bodybuilding. This was due largely to the finding that men’s dissatisfaction, when evident, was as often due to feeling too thin, small, or lacking in musculature as it was to a concern with excessive size or weight. In short order, researchers found that many individuals were quite unhappy with their lack of muscularity.
PrevalencePerhaps the best evidence of the increase in muscularity dissatisfaction comes from three general population surveys, covering 25 years (Cash, 1997). Two features relevant to this discussion were assessed (from a broader array of body sites): the upper torso (defined in these studies as the "chest" area) and "muscle tone." In 1972, 18% of men disliked their upper torso. By 1985 the percentage had risen to 28% and by 1996 it had reached 38% (surpassing, for the first time, women’s dissatisfaction with the breast body site). Percentages for "muscle tone" for men and women were: 1972 (M-25%; W-30%), 1985 (M-32%; W-45%), 1996 (M-45%; W-57%). Another survey by Jacobi and Cash (1994) provides some information on the muscularity satisfaction levels of a general (non-bodybuilding) sample. In a sample of college men and women, they found that 91% of the men and 78% of the women wanted to be more muscular. Clearly, there is a desire for a more muscular body present for both men and women.
It is also interesting to specifically evaluate bodybuilders, to determine if individuals who are objectively more muscular than average nonetheless experience body image problems (as noted above in the introduction, objective size may not translate readily into inner happiness). In our own investigation of this type, we found that both male and female bodybuilders/weightlifters (unfortunately, we did not differentiate in this study – a problem common to many investigations in this area) were more satisfied than runners and sedentary controls (Pasman & Thompson, 1988). In fact, there was no gender difference in the body image of male and female bodybuilders/weightlifters.
Much of the research in this area was recently reviewed by Goldfield, Harper, and Blouin (1998). They noted that bodybuilding appears to be gaining in popularity and estimate that 5 million participate in the USA alone. Their review combines an examination of body image concerns with data on risk for eating problems. Their analysis revealed that male bodybuilders had more severe body image disturbance and eating problems than a matched athletic control group (4 of 5 studies that met criteria for inclusion). Four other studies that did not include an athletic control group also indicated such eating and body image problems. The authors noted that there were fewer studies on which to base accurate conclusions for women, but did note that the available research suggests a similar link between bodybuilding, body image, and eating problems for females.
Goldfield et al. (1998) mentioned that the demands of competitive bodybuilding necessarily mandate such behaviors as weight loss prior to a contest and an excessive focus on body shape and body modification. In effect, it is part of the job. They caution, however, that some individuals who are unhappy with their size or have low self-esteem may "gravitate toward bodybuilding to achieve personal or societal standards of attractiveness" (150). Certainly, the decision to engage in bodybuilding to improve one’s appearance or to meet a personal goal of physical development should not be judged, either positively or negatively, by the professional or lay person. It is a personal and private matter. Indeed, there is no doubt that physical activity in its many and diverse forms may greatly contribute to enhanced self-esteem. In addition, aerobic and anaerobic exercise strategies are included as a primary component of almost all weight loss programs that are deemed optimal by nutritionists, exercise physiologists, psychologists, dieticians, and other professionals. The problem, and this is noted by Goldfied et al. (1998), is that preexisting eating or body image disturbances may be exacerbated by such involvement, possibly leading to clinically-severe disorders such as anorexia nervosa, bulimia nervosa, and body dysmorphic disorder. Ascertaining whether a bodybuilder is engaging in unhealthy behaviors along the path to a more muscular physique will be discussed shortly. First, however, I will review briefly some emerging research on risk factors that may help us understand the desire to add musculature.
Risk Factors and Associated FeaturesIt may be useful to understand whether there are specific interpersonal and/or societal factors that drive someone to be dissatisfied with muscularity and perhaps engage in extreme efforts to approximate a personal or sociocultural ideal. Our own research and that of others has begun to focus on two primary factors.
Teasing
Being teased or receiving negative comments about appearance is one risk factor that has received a great deal of empirical support (Heinberg, 1996; Thompson et al. 1999). A recent study by Pietrobelli and colleagues at the Obesity Research Center at St. Luke’s/Roosevelt Hospital (Columbia University) details the detrimental role of receiving teasing during physical activities (Pietrobelli, Leone, Heymsfield, & Faith, 1998). Subjects were 305 boys and 269 girls, grades 5-8, from a NY public middle school. The findings indicated that receiving teasing was associated with reduced participation in physical activities, reduced pleasure from exercise, and a lowered sense of control (defined as control related to the physical activity). There were no gender differences in the findings. The authors concluded that efforts to promote physical education in the school setting should contain a component related to awareness of teasing as a problematic interpersonal issue and strategies designed to help children cope with the teasing.
Media Images
A sociocultural component has long been blamed for the excessive concern with appearance found in women. Typically, the media are blamed for perpetuating an impossibly thin ideal as a model for women to emulate, and such images in magazines and on TV have been castigated as causing the widespread use of excessive dieting and bulimic behaviors to achieve the "unachievable." Interestingly, until very recently, almost no work has been conducted on an evaluation of the cultural images of appearance for men. Certainly, bodybuilding as a sport has been around for quite some time, and these images have been accessible. However, such exposure, via television and magazines, is less than that provided to other high-profile sports, such as football, baseball, and basketball. In addition, in recent years, a great deal of media attention has been devoted to the bodies of WWF wrestlers – there are currently three cable shows devoted to this "sport." Although there are no studies that have evaluated the evolving muscularity trends for men in the big three sports (baseball, football, basketball), it is generally conceded that, especially over the past 10 years, participants have increased in muscle mass. Indeed, the two highest profile current baseball icons (Mark McGuire, Sammy Sosa) have a high degree of muscle bulk and definition.
Recently, one study entered the void of research in this area, and generated a great deal of media attention and controversy. Pope, Olivardia, Gruber, and Borowiecki (1999) assessed the changing ideals of male body image by examining popular male action toys. They evaluated the changes in some toys over a 30 year period, and included in their analysis the following figures: GI Joe, Luke Skywalker and Hans Solo (from Star Wars), The Gold Ranger, Ahmed Johnson, Iron Man, Batman, and Wolverine). They measured the waist, chest, and bicep circumferences of the figures and scaled the measures using allometry to approximate the dimensions of a male of 70 in. (1.78m) in height. Much of their analysis focused on GI Joe, because of the availability of models from 1973 to 1998. The findings indicated a big increase in sizes for the measured body parts from GI Joe Land Adventurer (1973) to GI Joe Extreme (1998). The chest increased in size from 44.4 in. to 54.8 in. and the biceps increased from 12.2 in. to 26.8 in. The authors noted that, extrapolated to a 70 in. (height) male, "GI Joe would sport larger biceps than any bodybuilder in history" (p. 68). Although the waist increased in size also (31.7 in. to 36.5 in., the authors noted that the latter figure has "the sharply rippled abdominals of an advanced bodybuilder" (p. 67) whereas the early models have far less definition. The Stars Wars duo also acquired "particularly impressive gains in the shoulder and chest areas" (p. 69), however, the presence of clothing precluded the measurement of actual size changes over the years. There was only one "notable exception" to the trend of increased muscularity of models over time, "Mattel Company’s Ken, the boyfriend of Barbie" (p. 70).
These findings should, necessarily, be interpreted with some caution. Only a few action figures were examined. Second, as noted earlier, there is a lack of comparable data from other media models. Third, as always, it is impossible to determine cause and effect – there is no evidence that exposure to male action figures leads boys to develop a negative body image, or pursue a lifetime of bodybuilding. The authors do suggest that, anecdotally, their impression is that comic strip characters, male models in magazines and male movie actors have also become more lean and muscular in recent years. Follow-up studies should address these and other methodological weaknesses. Perhaps the timing was right for such an overreaction to a very small-scale study with so many limitations. For the past 20 years, researchers have focused on female dolls, primarily Barbie, as providing unrealistically thin body sizes for girls and women to emulate. Hopefully, the follow-up research will receive as much media attention.
Clinical Problems: Eating Disorders and Body DysmorphiaAs with any avocation that requires exacting standards for meeting an ideal physique (ballet, gymnastics, wrestling, horse jockeys, etc.), there is always the possibility that some individuals who engage in bodybuilding may engage in excessive behaviors or develop problematic traits. Restrictive intake of calories, especially before competition, may be a symptom that needs monitoring. Purging of food, via self-induced vomiting or laxative abuse, is often part of the bulimic cycle, and is a serious issue necessitating immediate counseling or intervention. A third, relatively new, clinical condition that has recently received a great deal of attention, is body dysmorphic disorder (Thompson et al., 1999). This is a disorder reserved for individuals who have the following characteristics: excessive preoccupation with an aspect of appearance, intense obsessive-compulsive activities centered around the site of concern (i.e., checking, weighing, grooming, etc.), and behavioral avoidant features (i.e., refusal to engage in social activities because of disparagement of the appearance feature. Research suggests that any aspect of appearance may become the focus of this level of dissatisfaction, leading to severe interference with social and occupational functioning. However, Pope, Phillips and colleagues have found a special type of BDD, which they term "muscle dysmorphia" (Phillips, O’Sullivan, & Harrison, 1997; Pope, Gruber, Choi, Olivardia, & Phillips, 1997). The central feature of this clinical syndrome is an individual who is preoccupied with muscularity, often believing that he or she is small, weak, or inadequate in this area – a belief that is commonly incorrect, in comparison to an objective rating. The individual may engage in compulsive bodybuilding, weightlifting, and consumption of bulking-up foods and other substances, yet maintain the elevated level of muscularity insecurity.
Research into the prevalence, assessment, and treatment of muscle dysmorphia is just beginning, and it would be premature to conclude that it occurs commonly. However, it may be important to be aware of warning signs. The primary symptom, as hinted at above, is a preoccupation with one’s muscular or size inadequacies, which simply does not fit with the views of others (the objective observer). The individual continues to maintain that he or she is not well-developed in the area of concern, and is truly distressed by this belief. Behaviorally, the person may engage in excessive and lengthy workouts, designed to "fix" the problem, express great irritation at others who disagree with his appraisal of his shortcomings, and avoid social activities and/or interpersonal commitments. In extreme cases, the obsession may produce such compulsive workout behavior that the individual may be fired from his occupation and/or lose close personal relationships.
Summary and RecommendationsClearly, work in this area is just emerging and much of the research has the "pathologizing" flavor of so much of mental health research (i.e., researchers focus on the psychological problems vs. the positive health associations). Nonetheless, it may be important to recognize potential problems related to an unhealthy focus on muscular development and the consequent undesirable behaviors such a desire may produce. Especially for adolescents, guidelines for early detection and sensible training need to be considered. Counselors, mentors, teachers and co-trainers might consider the following strategies:
Ensure that a non-toxic "teasing" environment exists for gym classes and intervene with both the teased and the perpetrator to resolve this negative type of interpersonal relationship.Use educational and "media literacy" strategies to inform children about the representativeness of body sizes perpetuated by toy action figures and sports icons.In any training program, for adults and adolescents, set realistic body shape and weight goals.Provide information regarding normal and healthy eating practices, as well as clear-cut definitions of the dangers of restrictive dieting and bulimic behaviors.In cases of low self-esteem, suggest alternative or complementary routes to building self-competence.Consider referral for a mental health evaluation if signs of muscle dysmorphia exists.

The Absurdity of the New Diet Drugs

The Quest for the New "Phen-Fen"
For a brief moment, obesity had the appearance of being cured. Doctors were getting rich doling out a combination of Phentermine and Fenfluramine dubbed Phen-Fen. While these drugs were only indicated for seriously obese individuals, almost anyone looking to lose a few pounds had no trouble getting a prescription. Of course, both of these drugs had been around for years. The positive results of the long-term Weintraub obesity studies (1) with this combination drove the American obesity industry into a frenzy. The combination was more effective then either drug alone. As an added plus, the mildly sedating and satiating properties of Fenfluramine seemed to partially negate the stimulating effects of Phentermine. Thus the combination apparently had fewer side effects than either alone as well (or so we thought). However, phentermine is still on the market and new combinations are being concocted with it.
We all know now that Phen-Fen proved to be a fiasco. Needless to say, this "cure" for obesity and the millions doctors were making could not go on forever. The revelation that Fenfluramine can cause pulmonary disease and heart problems has lead the medical establishment to start over again in its quest to find a new "cure", a new "Phen-Fen" that proves as effective (and profitable) as the original...
Attempt #1: Meridia (Sibutramine)
Meridia is an attempt to combine the properties of Fenfluramine and Phentermine in one pill. Phentermine is a stimulant, scientifically referred to as an adrenergic or catecholaminergic drug. A catecholanminergic drug increases brain levels of andrenaline and/or noradrenaline, your body's most stimulating neurotransmitters. Phentermine makes you stimulated and energized, thus reducing appetite, delaying time for food intake and increasing your metabolic rate . Fenfluramine, on the other hand, stimulates serotonin release. Serotonin is one of your brain's most sedating, satiating and relaxing neurotransmitters. Fenfluramine, by increasing serotonin levels, makes you feel less anxious, decreases carbohydrate cravings , and produces a feeling of rapid satiety - thus reducing food intake.
Meridia is a drug with both catecholaminergic and serotonergic properties. It works by blocking your brain’s reuptake of both serotonin and noradrenaline, thus prolonging and increasing the activity of these neurotransmitters (2). Theoretically at least, Meridia should be highly effective as it should help suppress appetite through two different pathways. So is Meridia theoretically should be the next Phen-Fen.
Early clinical trials do in fact did look impressive. Two separate year-long studies showed Meridia at recommended doses to produce much larger losses in weight than a placebo. At 10 mg per day, the Meridia group lost 4.8 kg over a year while the placebo group lost 1.8 kg. At 15 mg per day, the Meridia group lost even more weight - 6.1 kg while the placebo lost only 1.8 kg. (3)
However, Meridia is not exactly flying off the shelves like Phen-Fen. Very few of my patients have requested a prescription for Meridia, and many have told me that they have tried it and it didn't do anything for them. None of my medical colleagues have reported much success with Meridia either. So why is Meridia so effective in studies (funded by the pharmaceutical company that makes it), and yet apparently ineffective in the real world? I believe the studies mentioned above are somewhat misleading since the drop out rates were exceptionally high - around 50% in both studies. A common reason people drop out of diet drug studies is because they feel the drug is ineffective. Obviously, the people losing the most weight are most motivated to stay in the study. Thus the results are likely biased.
A survey by the newsletter Obesity Meds and Research News showed that of 248 people who had used Meridia for longer than four weeks, 45% were deemed "non-responders" - i.e. failed to lose more than one pound per week (4). While this survey was not scientific, it does parallel with my own observations that Meridia is not especially effective.
Meridia's apparent lack of efficacy may be due to its mode of action. Unlike Fenfluramine which stimulates the release of serotonin, Meridia is a serotonin reuptake inhibitor. Like Prozac and other anti-depressants, Meridia "recycles" your brain's serotonin instead of increasing serotonin production. Meridia and Prozac are safer than Fenfluramine, as the excess serotonin from Fenfluramine is what led to heart problems in Phen-Fen users. However, serotonin reuptake inhibitors are simply not as effective as Fenfluramine. Prozac might have some use for short-term weight loss, but in trials lasting longer than six months it is a failure. Patients might even gain more weight than a placebo when using Prozac (3). Since Meridia has similar properties as Prozac, its lack of success as a new Phen-Fen does not surprise me.
Attempt #2: Xenical (Orlistat)
This is an especially silly drug. Yes, clinical trials do show that patients on Xenical lose more weight than a placebo, and even keeps weight off longer than Meridia does when the drugs were terminated. Perhaps it was simply Pavlovian conditioning with the fear that when you eat fat you may leak stool and get stinky.
In the real world, I predict Xenical will be even more of a flop than Meridia. Unlike studies on Meridia, the Xenical studies controlled for diet. Both the Xenical and the placebo groups were put on restricted calorie diets. Strictly speaking, Xenical is not a classic anorectic drug like Meridia, phentermine, or fenfluramine. Xenical does not effect appetite much but prevents your body from processing dietary fat by blocking the digestive enzyme lipase. As a result up to one third of your dietary fat is excreted in your feces when you are on Xenical. So if you have two group of people each with consuming the same amount of calories, and the same dietary composition the group taking Xenical will lose more weight since they will be absorbing less calories from their dietary fat.
But let's look at real world conditions. Your average overweight person with a prescription for Xenical will not have his food intake monitored closely by a scientist. However, this patient will know that up to one-third of his fat calories will magically be gone. So do you think he will continue to eat as he was before, or might he be tempted to increase his fat intake by one-third? I'll let you be the judge, but I'm quite sure what the outcome will be. Since Xenical does not suppress appetite or increase metabolism, I really doubt it will have any long term effects on weight loss. Xenical requires strict adherence to a low fat diet to have any effect, but its use will likely encourage people to eat more high-sugar, high fat junk food instead of less. Xenical will also cause a few unfortunate "bathroom-related" side effects. Anything that causes you to excrete more fat--leaky stool will inevitably make going to the bathroom a less pleasant experience, and compound the social problems that the obese all ready have. Side effects of Xenical include liquid stools, fecal urgency, fecal leaking, and fecal incontinence. The last side effect can be especially embarrassing – fecal incontinence is just a polite, scientific way of saying that Xenical can make you "crap in your pants". Another problem is that the fat soluble vitamins--vitamin D, and the carotenes have been shown to be lowered in the Xenical studies. Researchers recommend daily multi-vitamin supplementation for those taking Xenical . Probably all fat soluble vitamin levels are ultimately affected—vitamin E, K etc.
I also don't like Xenical because it promotes the fallacy that fat is evil and responsible for obesity. As I'm sure most Meso-Rx readers know, no macronutrient is "evil". There are fats that can make you slimmer such as Omega-3 fatty acids, and those that can be fattening such as saturated fats and partially-hydrogenated fats. The key is to eat a diet balanced in proteins, fats, and carbohydrates with a good portion of the fat coming from Omega-3's. Someone who is eating a good, balanced diet should not take Xenical as it would mean less absorption of beneficial fatty acids for optimum human health. I really believe that the only people who can benefit from Xenical are those with simply atrocious eating habits who simply cannot stay away from potato chips, ice cream, and other such high fat, high starch foods. However, these are the last people who I would prescribe diet drugs to.
Xenical or Meridia for Athletes and Bodybuilders?
Both Xenical and Meridia are indicated for obese individuals (BMI greater than 30). So would an already lean bodybuilder trying to reduce his bodyfat even further have any use for either of these drugs? I have not heard of any burgeoning black market in Venice Beach or West Hollywood for either of these drugs, nor have any of my bodybuilding patients asked me for a prescription. Xenical is a big no-no for any bodybuilder, as most bodybuilders already eat relatively healthy and balanced diets. All Xenical will do for them is increase their time in the bathroom and make them lose weight in their wallets.
Meridia may have some hope for bodybuilders, although not much. A couple of studies have shown Meridia to have some thermogenic activity (2). Thus it is possible that Meridia has some muscle sparing activity similar to other thermogenics such as ephedrine. However, the studies on Meridia measure only total weight loss, with no distinction between fat loss and muscle loss. It is possible that Meridia could be used as a mild thermogenic by those who are overly sensitive to ephedrine, but at $100 per month Meridia is probably not worth it for most. This brings me to my next issue:
Cost Effectiveness of Xenical and Meridia
This is probably the most absurd aspect of these new diet drugs. In general, insurance companies will not "foot" the bill for anti-obesity drugs. Unless you are morbidly obese, you have to pay for these drugs out of your own pocket. The cost for a months supply of either Xenical or Meridia is roughly $100 per month or more.
Let's look at the economics of this. For Xenical, this is a ridiculous price. No trials have yet shown it to be effective in people whose diets are not closely monitored. My guess is that very few people will lose any weight at all from Xenical. So it is basically $100 down the toilet, quite literally considering some of the side effects of this drug.
Next, let's look at Meridia. Let's assume for a second that this drug is as effective as the studies say. Judging by two published studies mentioned above, taking 10-15 mg per day of Meridia for one year will produce anywhere from 6.6 to 9.46 lbs. greater weight loss than you would if you were given a placebo (3). Do the math yourself - at best you are paying $126.85 per pound of weight loss! To make matters worse, you don't know how much of this weight loss is actually from fat and not muscle. And this is all assuming of course that the these studies are actually representative of how well Meridia really works.
Another way to evaluate the cost effectiveness of Meridia is to compare it to other diet drugs. A 1973 review study funded by the FDA did a meta-analysis of 105 studies on various diet drugs. The conclusion of this review study was that these diet drugs available in 1973 (mostly amphetamine-like stimulants) induced patients taking the drugs to lose a half a pound a week more than the placebo group (5). Most of the studies reviewed were short term, none lasting more than a few months. Since this review study was completed, a half a pound a week more than the placebo group has become the standard to evaluate the scientific effectiveness of a diet drug in short term trials.
Short term trials may be the better way to evaluate a diet drug, as After 3-6 months of use a drug may lose its effectiveness. Just about all weight loss drugs and other methods lose their effectiveness after 6 months of use from a combination of lowered resting energy rates and from a decreased energy expended with exercise.
So does Meridia live up to this standard of .5 lbs. per week? Let's look at some of the shorter trials of Meridia to see how it compares to the classic stimulant drugs looked at in the 1973 review study. One of the largest short-term trials on Meridia on 1,047 total patients showed that this is not the case. At 10 mg per day, patients lost .32 pounds a week more than the placebo over 24 weeks. At 15 mg per day, this number moved up to .42 pounds a week more than the placebo - not quite up to par. Only at 30 mg per day did Meridia prove as effective as the "gold standard" of .5 pounds per week more than a placebo (2).
To be fair, some studies did show Meridia to induce a loss of more than .5 pounds a week more than the placebo, but these trials were very short term (12 weeks or less) and had lower sample sizes (1). However, the "kicker" in evaluating Meridia's cost effectiveness is comparing it to far cheaper over the counter diet drugs.
Let's look at phenylpropanolamine (PPA), commonly sold as Dexatrim or Accutrim. Short term trials have shown PPA to be about exactly as effective as Meridia - inducing anywhere from .3 to .5 pounds a week greater weight loss than a placebo (6). PPA cost just "pennies a day", and has an excellent safety profile as well. PPA is not a miracle worker, but will do the trick just as well as Meridia for a tiny fraction of the price.
Another drug to look at is ephedrine. This is a similar drug to PPA (also called norephedrine) which has never been approved as a diet drug. It is sold strictly as a decongestant, but this has not stopped bodybuilders from using it as an energizer and fat burner. When combined with caffeine, ephedrine is at least as effective as Meridia and plenty of trials have showed it to induce .5 pounds more weight loss per week than a placebo (7). Like PPA, it is also just pennies a day to use. More trials need to be done to compare its safety and efficacy compared to PPA.
Redirecting the Quest for the New Phen-Fen
The pharmaceutical industry has basically failed at finding effective new drugs for treating obesity so far. With the prevalence of cheap and effective drugs such as PPA and ephedrine available, there is really no point in paying $100 per month on drugs that are potentially even less effective. I believe obesity research should refocus itself dramatically to get serious about finding effective treatments.
The Amgen studies so far on Leptin are not that exciting from a fat loss point of view. But they are helping to open the scientific window on the Leptin Resistance Syndrome that the obese seem to have. The story is similar to the insulin resistance picture seen in some types of obesity. But leptin clearly won’t live up to the media’s hype as the new cure for obesity.
One absurd aspect of the research on diet drugs is that 99% of the studies only measure weight loss instead of fat loss. The key to long-term weight loss is keeping the muscle, so only measuring total weight loss is quite useless. New studies should measure both fat loss and muscle loss using new advances in body composition measurement. I believe ephedrine and/or PPA--the Beta adrenergic drug category will prove superior to most diet drugs in this aspect, as thermogenic drugs have been shown to have a strong muscle-sparing effect during dieting. The diet drug industry needs to radically refocus itself from weight loss to fat loss, a concept easily understood by bodybuilders but still somewhat mysterious to diet drug researchers.
Another aspect of diet drug research should be on how to "cycle" diet drugs for optimum effect. The concept of "cycling" drugs is old hat for bodybuilders. The idea is that the human body will adapt to most drugs if taken for too long, so you will get more effect from drugs if you take them intermittently rather than continuously. One study on Phentermine lasting nine months showed that a group taking this drug intermittently in a one-month on, one month off pattern actually lost slightly more weight than a group taking phentermine continuously (7). Since few diet drugs have been shown to induce weight loss for longer than six months, perhaps intermittent "cycles" could prolong the effects of these drugs. Future research should emphasize this concept.
These are just a few ideas for finding an effective treatment for obesity. In Part II of this series, I will go into more detail about what the research says about diet drugs and outline my personal suggestions for fat loss drugs and supplements.

History of Anabolic-Androgenic Steroid Use in Competitive Sports and Medicine

History of Anabolic-Androgenic Steroid Use in Competitive Sports and Medicine
The primary use of anabolic-androgenic steroids is in replacement therapy for male hypogonadism; other medical uses of anabolic-androgenic steroids include growth promotion in various forms of stunted growth, osteoporosis, mammary carcinoma, anaemias and hereditary angioneurotic oedema. Observation and clinical trials indicate that adjuvant therapy with anabolic-androgenic steroids can be supportive in the treatment of conditions characterised by a negative nitrogen balance: major surgery, cachexia of various origins, burns, traumata, convalescence from illness, injuries and immobilisations, as well as during radiotherapy and therapy with cytotoxic drugs (Kochakian 1976; Kopera 1976, 1985; Kruskemper 1968). Unfortunately, research concerning additional legitimate applications of anabolic-androgenic steroids has most likely been impeded by the existing emotional polarisation of anabolic-androgenic steroid supporters and opponents. As Kochakian (1990) has pointed out, the frequent and often hysterical references in the popular press to unsubstantiated adverse effects of anabolic-androgenic steroids has often resulted in the loss of both media and medical/scientific credibility, deterring research on beneficial and legitimate medical uses, and as a stimulus and encouragement for litigation against physicians.
The use of various physical and chemical aids in performance enhancement is not a novel problem but has been a feature of athletic competition since the beginning of recorded history (Csaky 1972; Strauss & Curry 1987). Ancient Greeks ate sesame seeds, bufotenin was used by the legendary berserkers in Norwegian mythology, and the Andean Indians and the Australian aborigines chewed, respectively, coca leaves and the pituri plant for stimulating and antifatiguing effects (Csaky 1972; Williams 1974). Anabolic steroids have been used by athletes to enhance appearance and performance for many years. The first ergogenic use of anabolic-androgenic steroids was reported to have occurred in the 1950s among weightlifters and bodybuilders (Wright 1978). Since that time their use has permeated a myriad of sports (Anderson & McKeag 1985, 1989; Buckley et al. 1988; Gilbert 1969; Starr 1981; Todd 1987; Wade 1972; Yesalis et al. 1990a). Payne (1979) suggested that the use of anabolic-androgenic steroids was a significant problem at the 1964 Olympic Games. Ljungqvist (1975) reported that one-third of a sample of elite track and field athletes in Sweden; surveyed admitted to systematic anabolic-androgenic steroid use by 1972. Silvester (1973) reported that 68% of a sample interviewed at the 1972 Olympic Games from 7 countries, and who were competing in such diverse activities as throwing, jumping, vaulting, sprinting, and running up to 5000m, admitted having used anabolic-androgenic steroids. Although it was suggested as early as 1973 (Frazier 1973) and reiterated later (Wright 1978, 1980, 1982), it is now evident that the use of anabolic-androgenic steroids is not limited to elite amateur and professional athletes. It has trickled down from the professional and college levels to the high schools and junior high schools (Buckley et al. 1988; Yesalis et al. 1989a, 1990a). The estimated prevalence of nonmedical anabolic-androgenic steroid use and the implications for society and public health have also prompted several scientific meetings, including a technical review at the National Institute on Drug Abuse in 1989, and both federal and state investigations and efforts to reclassify anabolic-androgenic steroids as controlled substances (Government Accounting Office 1989; Halligan et al. 1989; Taylor 1987a,b; Yesalis 1989; Yesalis et al. 1990a) despite nonconcurrence from the American Medical Association (AMA 1989).
Patterns of anabolic-androgenic steroid use among athletes have been determined from several surveys. Burkett and Falduto (1984) interviewed 24 weight-training athletes at a gymnasium in a metropolitan area of the southwestern United States. Subjects surveyed took a combined steroid does of 4 to 8 times the recommended medical does, used more than one anabolic-androgenic steroid at a time (‘stacking’), combined use of injectable and oral anabolic-androgenic steroids, and used the drugs frequently, usually in cycles (an episode of use from 6 to 12 weeks or more). Although Burkett and Falduto questioned a very specific sample of anabolic-androgenic steroid users, they concluded that their subjects seemed to be representative of the type of athletes who used anabolic-androgenic steroids. Cohen et al. (1988), in a study of hypercholesterolaemia in 21 male powerlifters using various anabolic-androgenic steroids, reported significantly higher levels of anabolic-androgenic steroid use in their subjects than Burkett and Falduto (1984), with daily dosages ranging from 60 to 400mg. Pope and Katz (1988) have also reported daily dosages between 10 and 200mg (of various anabolic-androgenic steroids) for anabolic-androgenic steroid users in their investigation of affective and psychotic symptoms associated with anabolic-androgenic steroid use.
Frankle et al. (1984) found that 110 of 250 weightlifters they interviewed in several gymnasia in the metropolitan Chicago area, many of whom were noncompetitive lifters, also used a variety of anabolic-androgenic steroids. 50 weightlifters were interviewed in detail; a majority (56%) had no competitive intents in weightlifting, bodybuilding or any other athletic events, a proportion that substantially exceeds that found by Buckley et al. (1988) in a nation-wide survey of male high school seniors. Frankle et al. (1984) concluded that anabolic-androgenic steroid abuse had reached alarming proportions in noncompetitive athletes.
The Buckley et al. (1988) survey suggests that one-quarter to one-half million adolescents in the United States have used or are currently using anabolic-androgenic steroids. Anderson and McKeag (1985) reporting on a nation-wide survey of alcohol and drug use among college athletes indicated that anabolic-androgenic steroids were used in all men’s sports, one women’s sport, and that the sport with the greatest admitted use (9%) was football. The overall anabolic-androgenic steroid use rate in all sports nationally was 4%. Anderson and McKeag (1989) replicated their original study 4 years later and although they found that overall use rates for anabolic-androgenic steroids had remained stable, anabolic-androgenic steroids were now being used in 2 additional women’s sports. A survey and follow-up telephone interview by Yesalis et al. (1988) following the 1987 US Powerlifting Federations’ National Championship found 33% of the initial respondents and 55% in a follow-up subsurvey of the same group, admitting previous anabolic-androgenic steroid use. Since athletes may have a propensity to underreport of disguise their actual anabolic-androgenic steroid use for various reasons, caution must be used when interpreting values concerning the prevalence of anabolic-androgenic steroid use by athletes

How to Make Anabolic Steroids Orally-Active?

The subject of androgenic / anabolic steroids, and the different ways that have been found to make them orally active, has been tossed around lately on the internet mags. This is an interesting topic to the science minded out there, but beyond that, it also has potential utility to the prohormone supplements. The following is my take on the subject, including scientific references and conjecture on my part.
The problem with natural androgens
Testosterone is the primary androgen in the human, and is the golden standard by which all other steroids are compared. Unfortunately, testosterone has very poor activity when taken orally. This necessitates that testosterone be administered by extra-oral means such by injection, subcutaneous pellet implant, and transdermal gel or patch.
17alpha alkylated steroids
Scientists have developed several synthetic testosterone derivatives that have increased oral bioavailability. The first synthetic alteration that scientists utilized is known as 17 alpha alkylation. 17a alkylation involves the addition of an alkyl group (methyl or ethyl) to the alpha position of the 17 carbon of the steroid backbone. The alkylation at this position prevents the major route of androgen deactivaton – oxidation to a 17-keto steroid - from taking place. This allows a large part of the steroid to avoid liver first pass metabolic degradation. Examples of 17a alkylated steroids are methyltestosterone and Norethandrolone (Nilevar)

While 17a alkylation is a very effective means of rendering steroids orally active, it suffers from a serious drawback. These steroids are all to some extent toxic to the liver. Some are more toxic than others, but they all have been associated with this problem. Jaundice is not completely uncommon with the usage of this stuff, although this condition is generally confined to individuals who are predisposed to liver problems. Several cases of liver cancer have supposedly been linked to 17a alkylated steroids, however, nothing definitive has been established in this regard. On the other hand, it is somewhat common to observe increases in blood test indicators of liver stress such as BSP retention, and intrahepatic cholestasis (a condition where bile clogs up and stops flowing from the liver).
While the dangers of 17a alkylated steroids are not trivial, they still comprise some of the most potent anabolic agents available, and therefore their use continues. Most smart bodybuilders are aware of the potential toxicities of these steroids, and therefore they are judicious with their use of them.
Lipophilic steroid derivatives
After ingestion, most steroids make their way to the intestines where they are absorbed into the portal circulation. The portal circulation carries the steroid directly to the liver, which is the workhouse of destructive metabolism and inactivation of drugs. As a result, if the steroid is not protected in some way, very little will make it through the liver and into the rest of the body where it can do its magic.
In addition to the portal route, there is another route through which substances can be absorbed into the body from the intestine. If a substance is lipophilic (fat like) enough it will be absorbed in the same manner that dietary fat is. Dietary fat is incorportated into chylomicra, which are small fat globules composed of protein and fat. These chylomicra are absorbed into the lymphatic circulation, which by passes the liver. If you make a steroid lipophilic enough by altering its structure, then it too will incorportate into chylomicra and absorb into the lymphatic system. Once in the lymphatic system it can cross over into the general blood circulation, making it there without being subjected to the massive metabolic breakdown in the liver.
Scientists have found that by adding lipophilic side chains to steroids, they will to some extent be absorbed into the lymphatic system. If the side chain is linked on in such a way that it can hydrolyze (break apart) easily after being absorbed, the steroid is essentially rendered orally active. Two side chains that have been utilized to increase the oral bioavailability of steroids through increased lymphatic absorption are long chain alkyl ester groups, such as is seen with testosterone undecanoate (andriol), and enyl ether groups, such as is seen with quinbolone (anabolicum vaster).

The term "orally active" is of course a relative term. Lipophilically modified steroids are more orally active than the free parent steroids, however, they are no where near as active as the 17alpha-alkylated steroids. Testosterone undecanoate (TU) is probably the most commonly known lipophilically modified androgen, and it is not considered a very potent compound (its recommended daily dosage is about 240mg). In fact, one study found the oral administration of testosterone undecanoate led only to an absolute testosterone bioavailability of 6.83 +/- 3.32%. That is very slight, especially considering the fact that in the same study they found the bioavailability of straight testosterone to be 3.56 +/- 2.45% (Eur J Drug Metab Pharmacokinet 1986 Apr-Jun;11(2):145-9). That means TU is just a little less than twice as orally active as free testosterone, which is unimpressive to say the least.
The other problem with lipophilic steroid preparations is the high variability in absorption from one person to another. In other words, one guy might absorb the stuff very well while the other guy might absorb very little. There is also high variation within individuals themselves, depending on their gastrointestinal condition when they take the stuff. In another study, ten post-menopausal women were given 40 mg of TU and their peak blood values were recorded. The values varied widely - more than ten fold (range: 5.8-64.0 nmol/L) - amongst the subjects (J Clin Endocrinol Metab 1998 Nov;83(11): 3920-4).
There is no specific data I can find on the bioavailabilty of enyl ether compounds, but since their mode of action is identical to long chain alkyl ester compounds like TU, it is a fair assumption that they too are not outstandingly high in oral bioavailability, or in consistency of absorption. What I do know is that the one and only enyl ether oral steroid on the market today (quinbolone) is generally regarded by european bodybuilders / athletes as too weak to even bother taking.
Ring A modified steroids
There is one more class of anabolic / androgenic steroids that are orally active. These have unique structural modifications in the steroid A ring. What these modifications do is help preserve the steroids 17beta hydroxyl group, and minimize oxidation to the inactive 17-keto form.
Androgens such as testosterone exist in the body in an equilibrium between their active 17beta hydroxyl form and the inactive 17-keto form.

Normally, the equilibrium lies pretty far to the right (formation of inactive 17 keto steroid), however some steroids have certain modifications made in the A ring that alter this equilibrium by shifting it heavily to the left (towards the formation of active 17beta hydroxyl steroid).
The most common A-ring modifications that shift the 17beta hydroxyl / 17-keto equilibrium to the left are methylation at the 1alpha position, and unsaturation (double bond) in the 1(2) position (Acta Endocr, 41, (1962) 494). Examples of orally active steroids that contain one or more these modifications include methenolone (Primobolan), mesterolone (Proviron), and 1-testosterone.

You probably have heard of mesterolone and methenolone, but it is doubtful you have ever heard of 1-testosterone. 1-testosterone is a very interesting compound, not just because it is orally active but also because it is very anabolic. It has been reported to be over 7 times as anabolic as testosterone in a study funded by the pharmaceutical giant Searle (J Org Chem, 27 (1962) 248). Furthermore, being a 5alpha reduced steroid, it should not aromatize to estrogens.

The History of Drug Testing in Sports & How Athletes Beat the Drug Tests

Drug Testing Nonsense
If I told you I was committed to an effort and was going to spend one million dollars of my money on a project, wouldn’t that seem like a sincere effort? Now let’s say you find out from a reliable source that the one million dollars represents mere pennies to me because I have tons of money. Then you find out that the project I was supposedly committed to is last on my funding list as far as financial commitment. Does it still seem like a high priority? This is the case with drug testing. In general, the International Olympic Committee (IOC) and other organizations talk a good game, but in reality, they are not sincere in their drug testing efforts. The historical evidence shows a repeating sequence of events since the implementation of drug testing: athletes take drugs, organizations develop tests, athletes beat tests, organizations come out with new tests, athletes beats tests, and so on. You get the point. Each time a new test is developed, drug testing officials release statements to the media indicating how sensitive the new techniques are. The tests get implemented and a very small percentage of athletes test positive for some type of banned substance. The drug testing officials then claim that based on their latest information, drug use is declining. This is comical, given all the data that indicates junior high school, high school, recreational, amateur and professional athletes are using steroids and other drugs. Yet somehow the IOC and other organizations want us to believe that they are cleaning things up based on the low number of positive drug test results. Given all the data that indicates drug use is prevalent, I feel that what the low numbers of positive drug tests actually indicate is how inadequate drug testing methods are.
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Prohibited and Restricted Drug Categories
Prohibited and restricted drugs fall into three main categories: (1) short- or immediate-acting stimulants and beta-blockers, (2) anabolic agents, and (3) masking agents. Stimulants and beta-blockers tend to affect performance only if taken just before the event. Drug testing for this category of drugs is believed to be very effective. Based on drug testing data, stimulant use has been essentially abolished from high-level sports because they are detected so easily. Anabolic agents usually require weeks to obtain the desired effect and are sometimes referred to as training drugs. The training drugs are inherently more difficult to detect and can be discontinued in time to pass an announced or anticipated test. Masking agents are drugs that affect the detectability of other drugs. Examples of masking agents are diuretics, probenecid, and epitestosterone. These drugs are only useful at the time of the test and, except for epitestosterone, are relatively easy to detect.
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Anabolic-Androgenic Steroids (AAS)
Of all the known drugs abused by athletes, anabolic-androgenic steroids (AAS) are probably the most widely publicized. Use of these agents is associated with side effects that have been reported in the literature. Reports from case studies by clinicians stir up the media, which always seem to somehow exaggerate the side effects. The clinical literature reports that AAS possible side effects include psychological and psychiatric disturbances, rupture of the myotendinous junctions, increased blood coagulation, an impaired blood lipid profile, gynecomastia, hypogonadism, cholestasis, skin disease, hypertension, stroke, and myocardial infarction. The negative consequences to the athlete’s health have not deterred the use of these substances, despite the drive to win.
Presently more than 100 different AAS are available. They can be taken either by mouth and swallowed, sublingually, injected, or from transdermal application. The basic chemical structures have been modified to increase the anabolic effects and reduce the androgenic effects. The anabolic effects of steroids lead to muscle-building and increased aggression, which enable people to train harder.
Originally, only power athletes, bodybuilders, and recreational weight trainers were believed to take AAS. Evidence accumulated that endurance athletes used them as a training aid by to improve recovery from high volume training loads. This was later confirmed by the positive tests of Chinese female distance runners for DHT, a topically applied androgen with a fairly short half-life in the blood. This has prompted some researchers to pose the following question: Since medical doctors and other health care professionals have consistently stated that steroids don’t enhance performance, why are we testing athletes for them? If they do work, then why are we telling athletes they don’t? The simple truth of the matter is that early studies on steroids used low dosages. To say that steroids didn’t work in general is based on the data from early research and leads one to draw an invalid conclusion. The more appropriate conclusion is that the particular substance administered did not prove to be anabolic at the dosage tested. However, the latest evidence published in the New England Journal of Medicine does indicate that AAS do work, and unlike what most people will tell you, they can also stimulate muscle growth without having to lift weights. Obviously though, lifting weights increases the potential for gains in muscle size and strength.
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Basic Overview of Drug Testing
On an annual basis, over 100,000 drug tests are conducted worldwide at a cost of $30 million. The drug tests are designed to detect and deter abuse of performance-enhancing drugs by competitors. The testing procedures for drug abuse in sport are strict and at times deemed unfair. They are deemed unfair because athletes are responsible for knowing what is banned despite the fact that additions are made almost daily to the list of banned substances. This has prompted researchers to recommend to athletes that the best possible solution is to avoid all drugs unless listed on the allowed substance list. The IOC has decided that drug tests will require confirmation, whenever possible, by gas chromatography and mass spectrometry, which define several chemical features of an abused drug, in effect producing a drug fingerprint. In addition, prior to the 1996 Olympic Games in Atlanta, the IOC required competitors to agree to a contract that prohibited them from taking any action beyond arbitration if they failed a drug test.
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Drug Test Timing
When athletes know when a drug test will occur, they can prepare for it and thereby neutralize the effects of drug testing on the use of performance enhancing drugs and/or masking agents. Year-round short-notice and no-notice testing are the most effective means to curtail the use of training drugs because they make athletes always at risk to be tested. Sports have recently begun to invest in this type of testing despite the high cost and difficulty in administration. Some countries claim to have achieved no-notice testing. The IAAF and international federations for swimming and weightlifting conduct year-round, short-notice testing. In the United States, the NCAA and the National Football League (NFL) have short-notice (1-2 days) programs, and the United States Olympic Committee (USOC) has approved the implementation of a no-notice program.
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Obtaining a Urine Sample
The drug testing procedure begins with taking a urine sample. While this sounds simple, it initiates a formal and highly regulated procedure to ensure that the urine sample that arrives at the laboratory actually comes from the athlete in question, with no opportunity to tamper with the sample. Why is urine used and not blood or other tissues? There are several reasons. Blood draws would require medical or paramedical staff and hence incur additional costs. Other tissues may not be valid for analysis under all conditions. Once selected for drug testing, the athlete is notified by an official and asked to sign a form acknowledging this notification. The athlete may or may not be accompanied by an official and must attend the testing station within the designated period. The testing station is supposed to be a private, comfortable place where plenty of drinks are available. Many times it is set up inside a specially designed mobile testing unit. Independent sampling officers, whom are trained and appointed by the respective governing body, carry out the collection of urine samples. Each officer carries a time-limited identity card and a letter of authority for the event to which they are allocated.
Before giving a urine sample, the athlete is told to select two numbered bottles. After providing the sample (about 100 ml), the athlete must voluntarily complete a form. The athlete declares any drug treatment taken in the previous seven days and must check and sign that the sample has been taken and placed in the bottles correctly. The urine sample is then sent for analysis to a laboratory currently accredited by the IOC. In the event of a positive test result, the laboratory will notify the governing body of the sport, who will then notify the athlete. The rules of the governing body of the particular sport determine what happens next. The rules vary across governing bodies, sports, and countries. An athlete is usually suspended while a positive result is investigated, but has the right to have a second analysis of the urine sample. This analysis may be observed directly by the athlete or by the athlete's representative. There follows a hearing, at which time the athlete’s case is presented. An appeal can be made, and there have been successful appeals both in the United States and other countries.
The testing procedure must be strictly adhered to so that all athletes receive the same treatment. Collection of the urine sample has to be observed because drug abusers may attempt to falsify the results by tampering with the samples. Volume, pH, and in some cases specific gravity and temperature of the sample are tested immediately. These simple tests check for some of the known methods of cheating the drug tests at this early stage. The urine pH is tested to detect attempts at changing the nature of the sample, which can affect the analysis of certain drugs, as well as their metabolism and clearance. Sodium bicarbonate, for example, can be taken by mouth in order to change urine pH. The pH is also tested to verify that the level of degradation, which a sample may have experienced by the time it is tested, is within acceptable limits. The specific gravity is checked for attempts to dilute the concentration of drugs, as is the case by deliberate diuretic use.
To ensure that the sample actually comes from the athlete, the testing officer must be able to see the urine flow from the athlete into the bottle. Male athletes are asked to strip to their waist and lower their shorts to their knees. Female athletes must also be observed very closely while they void a sample. This procedure can be very awkward, embarrassing, and humiliating. For a young athlete, giving a urine sample under these circumstances can be very traumatizing. Many people, regardless of age, are uncomfortable with the idea of being observed while giving a urine sample. The situation is further complicated if an athlete has been competing in an endurance sport and is dehydrated or competing at a weight category where they are reluctant to drink excess fluid.
At least 75 mL must be given under close scrutiny and the urine is split into 2 portions as "A" and "B" bottles. The athlete chooses the two coded bottles and the samples are sealed by the athlete. In most cases, only the athlete handles the urine and collection containers until sealed. The containers are sealed with tamper-proof strips, placed inside other sealed containers, wrapped in tamper-evident seals, and coded. The independent official observing the sample procedure records all of the information on a document. This initiates a chain-of-custody record to be continued by anyone who handles the specimen until the urine is used up or discarded in the laboratory. The laboratory staff never knows the athlete's name, only the bottle identification number. Everyone who handles the sample must understand the importance of the chain of custody and the essential role of maintaining it. The chain of custody guarantees that the sample content is protected and that the sample tested is from the correct athlete.
The possibility of sabotage of a urine sample has been raised many times by athletes. It is for this reason that that athletes should ensure that the testing procedure is observed rigorously for their own protection. Samples should be dispatched in the appropriate containers and all paperwork completed without any errors. After this the athlete is no longer part of the process and must rely on the integrity and accuracy of the system. The sample is then taken and sent by courier, along with a chain-of-custody document, to an accredited laboratory.
While the test protocol may seem excessive and violate certain rights of privacy and decency, there are important reasons for this protocol. There are many reports of athletes using elaborate arrangements of catheters to provide an alternative sample, bringing condoms filled with drug free urine to the testing station, and even catheterizing themselves and instilling drug free urine. If athletes go to these lengths to avoid detection, the testing protocol must be strict.
At the elite level, athletes are subject to year-round random testing. At any time, an independent sampling officer may call unannounced and request a urine sample. While this comes across straightforward on paper, in practice there are many difficulties. Frequently, athletes travel the world and finding the athlete can be difficult. After the independent sampling officer asks around to find the athlete in question, it is unlikely that the testing remains a surprise.
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Storing the Sample
The proper storage of samples is important to the reliability of the tests. Once collected, the sample must be protected so that the fluid, when tested in the laboratory, reflects the composition of the sample as it left the body of the person being tested. As part of sports doping policy, urine is not refrigerated or frozen until it reaches the laboratory. In a clinical setting, great care is taken to ensure that the sample tested is as near as possible to the condition in which it left the body. This is accomplished by adding a preservative or more often by refrigerating or freezing the sample. With worldwide testing in sports, samples are sent all over the world and there can be delays in delivering them to labs.
While refrigeration or freezing of the sample is the usual practice in the clinical setting, note that this is definitely not the case in sports. The addition of chemicals to prevent bacterial growth in the urine could preserve the specimen and may be a more practical alternative. Athletes, however, regard this method with some suspicion and think that this may introduce the possibility of tampering with the sample. Current scientific evidence indicates that their fears are misplaced. Urine contains thousands of bacteria from many different species. This is even more the case for a sexually active female. Urine collected from a female athlete will contain skin cells and microorganisms from the intestine flushed to the vaginal area by sweat. Many bacteria are ubiquitous and survive even in tap-water plumbing; if the water were used to wash any of the sample containers, other microorganisms could be added to the sample. Bacteria, in a container to which urine is added, will flourish in such a medium that is infinitely richer in nutrients than the water in which they have survived. Many constituents of urine support the growth of such bacteria, and metabolism presents a serious problem in drug testing because of the risk of falsifying doping test results. In this regard, urine contains several steroids that are utilized by bacterial enzymes that can interconvert endogenous steroids to the extent of producing testosterone in the urine. Because of the steroid concentrations in the urine, even a low conversion rate of steroids to T will produce a level of T sufficient to distort the test result. So athletes should be more concerned if officials don’t add something to the urine sample and not the other way around.
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Laboratory Protocols
Laboratories need to maintain high standards of practice in order to retain the respect of the sports community. In the event of an appeal for a positive test result, the data and procedures may have to withstand scientific and legal scrutiny. This makes accurate and complete presentation of the results essential. Accredited laboratories involved in drug testing may also exchange samples in a quality control program to confirm that they agree on the findings. If a lab comes up with results that are not consistent with other labs, they fail the quality control tests and accreditation can be withdrawn. While these quality control tests are not usually made public, some experts feel that they should be made available to all parties, especially in the case of legal disputes. Examples of quality controls include urine or water samples to which banned drugs have been added. In addition, urine samples from someone who has taken the banned drugs must also be taken. The reason for both procedures is that compounds can behave differently in urine samples derived from the body after drug administration. This procedure and the appropriate use of reference compounds is important for the interpretation of results from the drug tests.

Protein Bars Revealed

For those of us workout buffs and workaholics out there, a high protein bar can save the day (especially a very busy one—sometimes I find myself busier than a one legged man in a butt kicking contest!) The problem is there are so many protein bars out there it’s hard to sort through them all. There seems to be more new bars on the market than web sites going up. But which protein bars are the best? How can they be beneficial? What do you need to know before purchasing them? How about low carb protein bars vs. higher carb protein bars? Well, never fear, the answers you have been looking for are here. Let’s take a closer look at some of the ingredients found in protein bars.
Most of us know that quality nutrition and supplementation is the key to achieving athletic and physique success. It is important to eat 5-7 small meals daily to increase nutrient absorption, enhance metabolic rate, and help stabilize blood sugar (and insulin) levels. High protein meal replacement bars allow you to get all your meals in a convenient and generally tasty manner (I sure don't have the time to cook 6 food meals daily!). They help improve overall nutrition and give you key nutrients your body needs to improve health and physical performance.
Protein bars usually contain protein, carbohydrates, fat, vitamins and minerals, and additional functional ingredients. High protein/moderate to high carb bars are best suited for athletes and workout fanatics looking to get quality protein and carbs for increased energy. They are excellent for after a workout to enhance recovery and recuperation and enhance carbohydrate storage (glycogen) in muscle tissue.
Most protein bars usually start out with a "proprietary protein blend". Some bars may have only one protein source such as whey protein isolate but it is preferred to get a protein blend to utilize all the functional benefits of different proteins and help support lean muscle mass. Quality whey protein isolate has benefits including providing intact immunoglobulins to support immune function, providing the highest concentration of BCAA's (branched chain amino acids leucine, isoleucine, and valine which play a key role in the muscle building process-about 25%), it has a high biological value (BV) which means it is readily absorbed and utilized by human muscle tissue, and it may even support IGF-1 levels.
It is very important to look at the processing techniques of different whey proteins. The processing will determine whether the important protein microfractions (the compounds that give whey its functional benefits) are still intact and not. Look for ion exchange whey isolate. The ion-exchange process separates proteins based on their electric charge, which is controlled using various chemicals. Two other good choices are "ultrafiltered" or "cross flow microfiltered" whey. Both processes use a very high tech cold microfiltration process that utilizes ceramic filters to remove the fat and lactose thus separating out or "isolating" the protein without damaging it. Whey protein concentrate is a less processed and consequently less expensive form of whey protein. Whey protein concentrate is not as pure as whey isolate in that some fat, lactose and minerals are still left in the protein.
Casein is another milk protein that seems to have a timed-release effect as it forms a gel in the gut to slow the transit time of amino acids. This effect may enhance absorption. It has a very high natural glutamine content. Most of the glutamine in casein is found in the peptide form for better absorption (due to peptide transport systems in the digestive tract). Glutamine is a very important amino acid that has many benefits including supporting lean muscle mass. In a recent study published in the Annals of Nutrition and Metabolism, whey protein was compared with a casein protein hydrolysate (which contains about 20 % glutamine peptides) and a hypocaloric diet with regards to lean muscle mass, strength, and body fat. The results of this study showed that the casein protein hydrolysate group lost more body fat, gained more lean muscle mass, and had greater strength increases. The authors of the study stated that, "this significant difference in body composition and strength is likely due to improved nitrogen retention and overall anti-catabolic effects caused by the peptide components of the casein hydrolysate". Milk protein isolate contains both whey and casein and it is a decent source for these two proteins.
Soy protein isolate has been shown to enhance thyroid hormone output, which can increase metabolic rate to support fat loss. The isoflavones in soy have been shown to have numerous health benefits including cholesterol and triglyceride lowering effects. It contains an excellent ratio of glutamine, arginine, and the BCAA's. It is a fairly low priced protein source and can have positive benefits for women mainly, but men as well.
Egg albumin protein is the "regular old Joe" protein. It boasts a great amino acid profile but does not offer very many functional benefits. Hydrolyzed protein is also another source of protein found frequently in bars because it is inexpensive. This protein is heat-treated (and pre-digested) and most of the microfractions are destroyed. However, it does contain peptides that are easily absorbed in the body.
Most high protein bars on the market are not baked nowadays so if the raw materials were quality, then the protein microfractions stay intact. However, the raw material ingredients that make up a bar may have been subjected to heat. Ask manufacturers of bars to provide you with certificates of analysis for the proteins in the bar (and for the bar itself for that matter). This should give you peace of mind about the quality of the protein you are getting. Bars that contain rolled oats and some granola type bars are baked and the proteins in them lose the microfractions due to baking.
The basic bar making process from a quality manufacturer goes like this: first the main ingredients (including the proteins) are mixed together (manually or using an industrial sized mixer) with water, then the mixture is laid on a table evenly and goes through a "cooling" machine process using a cooling tunnel/extruder. Next, the bar is taken out of the cooling machine and enrobed (coated) with chocolate. Finally, the bar sheets are cut and ready to be wrapped. Keep in mind this is a greatly simplified explanation of the process.
Protein bars contain carbohydrates as well. Typically the main source is glycrerol (glycerine) which is a trihydric alcohol. Glycerol forms the backbone of triglycerides in the body. It is used in bars to help keep them soft and moist since glycerol is very good at drawing moisture. It also helps sweeten the bar. Although many companies do not list this as a source of carbohydrates, the FDA defines it as a carbohydrate. It has a very low glycemic index so it does not impact blood sugar levels greatly. Interestingly enough, there are ergogenic benefits associated with ingesting glycerol such as increasing the amount of water retained in the body and enhancing hydration (maybe even enhancing vascularity). Bars loaded with glycerol may cause stomach discomfort in some people so unless you want to hit the porcelain throne throughout the day, drink plenty of water with these protein bars. Corn syrup, high fructose corn syrup (dextrose), rice syrup, maltitol, honey (invert sugar), turbinado sugar, sucrose (which is glucose +fructose), crisp rice, and fructose are all used as carbohydrate sources in bars. Fructose is fruit sugar and is added to bars not only to provide a source of carbohydrates but also to sweeten the product as it has a very sweet taste. Fructose is mainly metabolized in the liver and therefore has a lower glycemic index. Consuming high amounts of fructose can lower metabolic rate and cause de-novo lipogenesis (the conversion of sugar into fat) since the liver can only metabolize limited amounts of fructose.
Protein bars also contain fat. The usual fats found in these bars are partially hydrogenated oils, fractionated vegetable oils, palm kernel oil, and peanut butter. A few bars have added essential fatty acids (EFA’s) but it is very difficult to preserve the quality due to their sensitivity to light, heat and oxygen. Most of the fat (especially the saturated fat) found in bars is in the coating. Saturated fats have been linked to many health problems including cardiovascular disease. Partially hydrogenated oils produce trans fatty acids (along with other altered fats) during the hydrogenation process. They are also very detrimental to health and have been known to increase cholesterol and interfere with the livers detoxification system. Hydrogenated oils increase shelf life of products, which is usually 9 months to 1 year for most protein bars. Fractionated oils seem to be better for you. Fractionation is the process of separating an oil into two or more different triglyceride fractions. In other words, it allows weaker oils to be changed into better oils.
Protein bars contain a blend of vitamins and minerals to support overall health and many chemical processes in the body. Pre-mixes from companies like Roche are usually added to formulas. Vitamins and minerals are usually ancillary items to bars and many minerals in the formulas actually compete for absorption like calcium and magnesium plus they are generally not in the higher absorbable chelated forms. Chromium is added to some bars (usually in the better polynicotinate form) to support optimal blood sugar levels and help aid in fat loss.
Some high quality bars on the market (for various purposes including post workout recovery, energy, and lower carb/high protein bars) include: LoCarb2 from BIOCHEM, Lean Body by Labrada, BioComplete by Bodylogix, Protein Plus from Powerbar, Lean Machine bars by GEN, Meso-Tech bars by MuscleTech, Met-Rx Food bars by Met-Rx, LoCarb sports bar by APT Nutrition, Myoplex Lite bars by EAS, and the Ultimate Protein Bar by BIOCHEM.
In the future, we will evaluate popular bars on the market and give them a rating based on various criteria.

Dan Duchaine - Interview with Hardcore Muscle

Dan Duchaine - Interview with Hardcore Muscle
HM: IGF-1 … Dan you seem to be standing back on this one. Colgan thinks it will bring on the age of the superfreak, while you have only spoken of its use in fat reduction. We know GH never panned out as incredible as everyone wanted it to. Do you want to make sure it is the real deal before you give it your stamp of approval? We keep hearing every imaginable scenario ranging from "the stuff is fantastic" to "didn't do anything for me." Do you have any opinions on how it is best used? It was reported to work a lot better with HGH in a study. Do you have any theories on how or what compounds (steroids, anticatabolics, insulin mimickers) could be used in a synergistic protocol for best results with IGF?
Dan: Well Colgan really calls it all the time, doesn't he? (laughs) Because he's always wrong - when Twinlabs changes their mind. Vanadyl sulfate is toxic but now that Twin is selling it, it's not toxic any more! But anyway, enough about Colgan. You know the thing is … I've never seen any real IGF-1. All the stuff I've seen pictures of and read about is the lab cell culture which is doctored not to bind on the carrier proteins. So it would probably be wonderful. You sent me a couple of reports and I read some others and if you look at the amounts they were using, it was quite high actually. Because of a four hour half-life they were using it twice a day, at a calculated dosage of 18mg a day. That's a very high amount. And these bodybuilders are taking 50 micrograms. And I find it hard to believe that 50 micrograms might do anything considering … God knows what they might have stacked on top of that. Maybe I'm wrong, but I think IGF will be terrific once it gets cheap enough to use. And you really want it to bind on the carrier proteins. You want it to last for the 4 hours. The cell culture stuff has a half life of 20 minutes, you don't want that. It's as short as growth hormone … you have to use the high amounts. Eventually someone will offer it either out of Russia or Australia. Of course you know, there were some side effects such as jaw pain and weird funky stuff. And it does work well with GH synergistically. They're just the opposite of each other. IGF-1 would lower your blood sugar and GH does the opposite. Together it stabilizes it. So the worst thing you could do is to use IGF-1 and insulin at the same time, you would conk out. I think it has a lot of potential. The only problem with all that stuff … if you remember back to the geriatrics using GH, when they stopped using GH, within a few weeks all the benefits ceased. At least when you stop steroids, it takes a year or more for all those gains to completely disappear. And I'm afraid for the high expense of IGF-1, that when you go off it, I wonder how long it will last.
HM: Yeah, a couple people told us they used it, and they said how awesome it worked and they weren't using anything else.
Dan: Over the phone…?
HM: Yeah.
Dan: Oh, yeah you know how that goes - "I'm 190 and ripped" and you see them in real life and it's a fat piece of shit. (We are all laughing hard.) It's like on the Internet, everybody is big and strong and ripped - on the computer and you meet them in real life and they are little dorks!
HM: (Laughing) Hypothetically, if you were going to use IGF-1, would you use it with…?
Dan: Oh yeah, steroids, GH, you would want to use it all for a synergistic effect. But definitely with growth hormone, all the studies say it's not only additive … put it this way … if you could get a ½ pound gain from IGF-1, and a ½ pound gain from growth hormone - if you put them together you wouldn't get just one pound, you would get much more, they are synergistic with the two added together … so yeah, go for it.
HM: Anything on the amounts of growth hormone?
Dan: Frankly, I think, nobody has used enough growth hormone because of the cost. The only guy I know of, the rumors were that (top WBF guy) was using like 12 IU's of GH a day. Every day. I don't know if that's true but that is pretty close to what someone should be using, for best results I would think. In the PDR, it's pretty cut and dry in what you should be using. The Genetech is not as efficient as the Lilly. It's microgram per kilogram - you can figure it out. It seems that a lot of bodybuilders are going low in dosage. In the early 80's it was worse, the recommended dosage was 2 IU's a week at $90 bucks a pop - like 2 IU's would even do anything. And people were wondering why it didn't work…
HM: Yeah, you might as well pound down some arginine. (joke)
Dan: I know the stunted growth children were taking it 3 times a week, but I don't know why only 3 times a week. Why not every day? It seems logical to me that it should be everyday. It's just like IGF-1 is supposed to be twice a day. And GH is even shorter acting so who knows.
HM: Maybe 4 times a day might do some good??!!
Dan: Yeah.
HM: Do you still feel Nolvadex can be put to good use - even though studies show it to decrease serum blood IGF levels in the body by 25%? Many have theorized that it lessens the muscle gains on a steroid cycle - do you agree?
Dan: Everyone said that even though they liked to use Nolvadex during dieting, they always found that during the off-season … they grew better without it. That was interesting. It might be the IGF-1. We somehow thought it was tied to estrogen but I don't know why. It depends. Past a certain age … like I'm 43 … if you measured my growth hormone and IGF-1 at middle age it is not very large. Would reducing it 25% make a major difference when it is so low to begin with? Probably not. It depends. As you get older, estrogen is more important to avoid for a lot of reasons, you know … prostate cancer, this and that. But when you're young, you could probably avoid Nolvadex. You know so many people have spent so much money on Nolvadex to combat gyno that they could have easily gotten the surgery for the same amount of money and cured the problem. Half of the people who go through puberty usually get some kind of gyno. They don't necessarily remember it, but it happens. And if you had gyno as an adolescent, you are going to get it if you use steroids - unless you totally avoid all the things that would cause it. And I don't know if Nolvadex will help those kind of people. I don't know if it is a real preventative. Close to two bucks a tab - get the surgery.
HM: How do you feel about Clomid's use as a prevention of gyno - overrated? Could a 2 on / 2 off program of Clomid be something in which gyno could be prevented in your opinion?
Dan: You know Teslac is an ideal antiestrogen but we could never find it out of the country, and we looked too. Clomid … inexpensive in Mexico but very expensive here. Everyone has done quite well with it for raising testosterone if you are young enough with 2 tabs a day. As far as an … they never approved it as an antiestrogen because it was more toxic than Nolvadex. Most people who use Clomid, they are not using it all year long. The problem is everyone's using so much testosterone - not a little but a lot! Back in the 80's we thought there was some kind of precision to anabolic use but now it is not quality but quantity…
HM: Have you had a chance to look at the other growth factors (EGF, fibroblast growth factor, nerve growth factor, TGF, etc.)… If so, do you feel any or all of these are interesting on a muscle-building standpoint?
Dan: Oh sure! There has been some research that the epidermal growth factor has been effective … but all the G.F.'s have been marketed at such a high price that people are unable to use high dosages. But who knows what's going to happen when prices come down and people are on some higher dosages. At the higher dosages, who knows what will be the outcome.
HM: Have you heard or have any insight on the new fat hormone drug in development?
Dan: Leptin … a few years ago we were talking about brown fat and having the beta 3 receptors and I believe they figured out that leptin is one of the naturally occurring beta 3 agonists in the body. The interesting thing about beta 3 receptors is that there's not many in the body, you got many more beta 2 receptors in the muscle. The beta 3's are only in small areas. However the nice thing about leptin is you don't need a lot and unlike clenbuterol, you don't down regulate the receptors. So for bodybuilding, it might be pretty good. However, for most of the obese people who think they are going to need it, some research has shown that they (obese) have genetically damaged beta 3 receptors that don't accept it. And many obese people have very high leptin levels already. The body is trying to compensate so it's not going to help them much. But it will be good for athletes because - clenbuterol is good but it only lasts 2-3 weeks at a time unless you jack up the dosage sky-high. As I mentioned on an audiotape a while ago, there is another thermogenic compound that I'll probably introduce at the end of the year. Even though I promised January 1. It is much more thermogenic than clenbuterol and doesn't even involve those receptors at all. It is much better and cheaper. More dangerous though because if you take too much you don't get sick … you die! Because you raise your body temp over 105 degrees and your cooked brain turns into poached eggs. So I have been hesitant introducing it or writing about it without some safeguards.

HM: To be blatantly honest with you, Dan, we have seen you come full circle on your diet theories. In your first book you recommended eating a lot and often. Now it seems you are approaching a nutrient density theory on diet. Low calories - high nutrients. Correct us if we are wrong. Even though nutrient density looks good on paper and looks like it will build the muscle desired, how come the guys (natural and unnatural) who really push the calories, really seem to be the ones putting on the greatest amount of muscle (and of course, extra bodyfat too)? i.e. … Yates, Sombaty versus Ray, Wheeler, etc. … Do you feel there is any possibility that the body can speed up with a more efficient anabolic effect with abundant calories - just as the metabolism slows down somewhat at deprivation of food? Couldn't the body adapt somewhat to a tremendous muscle building overload effect with food if a huge amount of demand (brutal workouts) is there?
Dan: Well … I don't think Yates and Sombaty get that fat actually. I must admit when I started out I wasn't the smartest guy in the world back then. I just had a knack with the words back in the early 80's. And I'm sure we were wrong on a lot of things. The thing is … there are a few individuals that can get up to 15-20% bodyfat, put on a lot of muscle and then be able to take it off. I have no problem getting that fat in off-season if they can prove to me they can get in shape. Obviously, like Rory Leidermeyer, he never got it right - he always fucked up. And most people who get that fat (15-20%) have trouble getting back down and even if they do, their vascularity and skin taughtness suffers.
HM: Do you feel it is a compromise though, not taking in enough food, with trying to maximize muscle mass?
Dan: You should always eat as much food as you can, but I think some people should spend the thirty bucks on calipers and keep the threshold of bodyfat at 12% or lower. Fifteen percent of bodyfat with a guy with a lot of muscle … he looks pretty fat. That's a bodybuilder who really is a powerlifter with a gut. Twelve percent isn't too sloppy and you can come down and up in bodyweight with some ease. But there are some people that can pull it off, but rarely have seen anyone going into a contest not fuck up on the way down.
HM: If you could pull it off, and eat a lot more food in the off-season, do you feel that you could gain more mass like that?
Dan: Sure, sure, but the secret is to keep it when you diet it off. First of let me say this. People lie. Vic Richards does not eat 15,000 calories. The guy pretty much can't count, he's so stupid. The guy wouldn't be able to count up the boxes with a calculator if the boxes were in front of him so I doubt 15,000. Very few people can hit 7,000. Strydom hit 7,000 but he had a lot of support to do that. People think if you eat so many calories you must be hotter. That's not true. An inch of fat all around the body will keep the heat in. If you have thin skin you are radiating heat out into the room so you can get away with taking in more calories.
HM: But let's say you have two twins. One of the twins says I'm going to get as big as I can while the other twin wants to build muscle but keep lean. Do you think that the guy who is taking in the gross amount of calories to build big time muscle (when they measure him in a water tank) will have a lot more muscle than the twin who tried to keep his bodyfat to a minimum?
Dan: Yes. Yes, but when they both come down to 6% bodyfat it will be very close because of the dieting. I think the high calorie guy will have a slight advantage in muscle mass but what is his skin and vascularity going to be like? But I must tell you, most bodybuilders I know eat more than 3,000 unless they lie around all day. Even I eat close to 3,000 but I … well I ride my bike quite a bit now. Most of those pros, of course, hold water but a lot of that fat is held under their abdominal wall in their viscera. That's not increase size of the gut from GH but a combination of high carbs, high insulin and high testosterone. All that fat in there is very sensitive to androgens especially DHT.
HM: Do you think they can ever get rid of that? The visceral fat?
Dan: They would lose a lot of muscle. Visceral fat is like the last fat to come off the body. Back in the old days when they weren't using a lot of androgens, you didn't have that. But now with everyone using so much testosterone, that gut is all over the place now. Pros, amateurs … you know.
HM: Wouldn't clenbuterol be at its most useful in these high density / calorie diets? Have you ever experimented with a clen / volume food intake protocol?
Dan: That's kind of like pointless, because many of these top pros use clen all year round unless they run out of it. And they are using 10-15 tablets a day. The problem is that it works 2 weeks and that's it. If you cycle it 2 weeks on and then three weeks off then … yeah it could work well. You could be precise about it but you'll never do it. (Dan was speaking of the thermometer method each morning as he has described in past articles.) It's so nice to eat so much shit on clen that people just don't get off it.
***
HM: You have spoken of a high fat diet. Is this different somewhat than DiPasquales'? If so, what are your basic recommendations?
Dan: First off, high fat diets have been around for quite awhile. I mean before Zumpano, there was the Atkins diet which was mostly low carbs all the time, which is not the healthiest thing in the world. Especially for athletes because it is too catabolic, over time. Both DiPasquales' and mine are based on the 7 day (5 on, 2 off) plan. I'm a little more precise. He doesn't care to get into ketosis, blood sugar, ketones in the urine and I do. Ketones are fractured fats and they are not as efficient as regular fats so you need more grams for the energy. Of course, it is a nice diet that he has done because it is just a rip-off of our stuff from the early 80's.
HM: He seems really vague about it.
Dan: The problem is I used that diet for a long time in the early 80's and most of the guys in prison were on it. You have to really do it yourself. He doesn't seem to have a lot of people on a one-to-one basis to really get the feedback. I doubt he has done it himself for a prolonged amount of time. He's armchair about it. People rebel against it and don't want to follow it. But you have to expect that.
HM: On your 33/33/33 diet are there any important do's and don'ts? Do you feel that the above diet is more beneficial dieting or can it be used ideally for muscle building too?
Dan: About 25% of the people in the U.S. wouldn't need that diet. They have really great insulin sensitivity. These people process carbs well and don't give a shit about aerobics and that would be fine. There are another 25% that are quite lousy at processing carbs like myself. And then there are about 50% that are somewhere in the middle. There is no such thing as an essential carbohydrate. There are essential amino acids, essential minerals / vitamins. There are essential fatty acids. There is no such thing as essential carbs. Protein can be turned into fat. Protein can turn into glucose. Past a certain point on many people, much of the protein and carbs that you eat are turned into fat right in the body - right in the liver and you have no control over it - and it is only one kind of fat. Saturated fat. Saturated fat really lowers insulin sensitivity. So if you just accept that your body is going to have some kind of fat in there, it is better to control it yourself than let the body do it.
***
HM: I have heard of some people still trying to crush up those Anadrol tablets and inject them.
Dan: Yeah, I remember one 50 mg shot injected seemed to feel like 3 orals. Hey, have you guys seen some of these guys with the instant calves? I talked to Nadler about that because some of these guys are way too poor for implants. I asked, could you do collagen there and he said, "Yeah, but it's 250 dollars a cc." But you can easily inject saline water in the muscle and it will swell up for a few days. You could do that for calves for a contest and it's a lot cheaper than Esiclene. It would swell up much better.
HM: Some people get nerve damage from …
Dan: Well, Nadler showed me step-by-step instructions on how to put silicone in your calves. Just long small amounts in your calves, not large amounts, and your muscle will encapsulate it. And you can keep building it up and building it up. You could do biceps too.
HM: How do you put the silicone in though?
Dan: A needle, but of course it is not legal to do it in this country. But you could easily do it in Tijuana.
HM: Could be dangerous with the silicone though - like it is with breast implants.
Dan: That's a little different; you're only using small amounts. When they originally did silicone in the 70's before they put it in the sac, they put a massive amount in the gland. But if you used a small amount and let the body encapsulate it, you could do it. I would do it.
HM: Will it move with the muscle though?
Dan: Yes it will. That's the nice thing about it. Nadler can't do it in this country but I could ask him - if he went to Tijuana, would he do it there? You would have to go back and forth because you couldn't do it all at once.
HM: Could someone do it themselves?
Dan: (Dan got a good chuckle out of that one.) I could probably do it. I have no fear of needles. I'll ask him.

DHT - Is It All Bad?

A considerable chunk of my work day is always spent answering people’s questions about prohormones and steroids. Of course, one of the biggest concerns people have is about estrogen and estrogen related side effects. Right behind that however are questions about DHT. It seems that people have the misconception that DHT is some evil androgen by product that serves no purpose in the body but to make our prostates blow up and our hair fall out.
The real situation is of course much more complex. DHT is one of those good guy / bad guy hormones that is sorely misunderstood. For many people, it is NOT something that you want to reduce or eliminate in the body. For some others though, keeping DHT levels under control is probably a prudent course of action. Knowing the facts about DHT will help you decide just which group you belong to.
Testosterone is a prohormone?
The main androgen secreted by the testes is of course testosterone. However, in most of the body, the androgenic signal is not carried through by testosterone. In these tissues, which include the brain (CNS), skin, genitals – practically everything but muscle – the active androgen is actually DHT. Testosterone in this case simply acts as a prohormone that is converted to the active androgen DHT by the action of the enzyme 5alpha reductase (5-AR).
5-AR is concentrated heavily in practically every androgen dependent area of the body except for skeletal muscle. This results in very little testosterone actually getting through to these parts of the body to bind to androgen receptors. Instead, it is quickly transformed into DHT, which then interacts with receptors.
This transformation serves a very important biological function in these tissues. You see, DHT is a much stronger androgen than testosterone – it binds about 3-5 times more strongly to the androgen receptor. If you took away 5-AR from these tissues and blocked the formation of DHT, then you would see some dramatic changes in physiology.
A good case in point is demonstrated in male pseudohermaphroditism due to congenital 5-AR deficiency. This is a relatively rare disorder, however it is actually quite common in the Dominican Republic. In this disorder, males are born with little or no 5-AR enzyme. They have ambiguous genitalia and are often raised as girls. When puberty occurs, their testosterone levels elevate normally although their DHT levels remain very low. Their musculature develops normally like that of other adults, however, they end up with little or no pubic / body hair and underdeveloped prostate and penis. Their libido and sexual function is often disrupted also.
Testosterone is the active androgen in muscle
Skeletal muscle is unique from other androgen dependent tissues in the body. It actually contains little or no 5-AR, so little or no DHT is actually formed in the muscle. In addition to this, any DHT that is formed, or that is already present in the blood and travels to the muscle, is quickly deactivated by an enzyme called 3alpha-hydroxysteroid reductase (3a-HSD).
So at least as far as muscle is concerned, testosterone is the primary active androgen. This is not to say that administering exogenous DHT is not without any anabolic effect. It actually does have some anabolic activity in the muscle, albeit significantly weaker than that of an equal amount of testosterone. This is due to its quick breakdown by 3a-HSD into the weak metabolite 5alpha-androstan-3a,17b-diol. If this enzyme were somehow blocked, it is likely that DHT would exhibit very potent anabolic effects on muscle.
It is important to understand that even though testosterone is the active androgen in muscle, and DHT exhibits relatively little direct anabolic effects on muscle in men, DHT is still very important for the full performance enhancement effects from testosterone. What I specifically mean here are the effects of DHT on the central nervous system, which lead to increased neurological efficiency (strength), and increased resistance to psychological and physical stress - not to mention optimal sexual function and libido.
I have heard several anecdotal reports of individuals who have stacked testosterone with proscar (a 5-AR inhibitor) and have noticed significantly reduced performance enhancement effects. What’s going on here? We know it couldn’t be due to the inhibition of the direct anabolic activity of testosterone on muscle anabolism. Most likely it is due to the reduction of androgenic effects in other parts of the body that contribute to the ergogenic effects, specifically the CNS, which is stimulated by androgens to increase neural output leading to greater strength and greater recoverability. Another possibility is a reduction in the production of androgen dependent liver growth factors (such as IGF-1), since DHT is an important androgen in the liver.
Anti – Estrogen effects of DHT
One important function of DHT in the body that does not get much discussion is its antagonism of estrogen. Some men that take Proscar learn this the hard way – by developing a case of gynecomastia. By reducing DHT’s protection against estrogen in the body, these men have fallen victim to its most dreaded ramification – bitch tits!
How does DHT protect against estrogen? There are at least three ways that this likely occurs. First of all, DHT directly inhibits estrogens activity on tissues. It either does this by acting as a competitive antagonist to the estrogen receptor or by decreasing estrogen-induced RNA transcription at a point subsequent to estrogen receptor binding.
Second of all, DHT and its metabolites have been shown to directly block the production of estrogens from androgens by inhibiting the activity of the aromatase enzyme. The studies done in breast tissue showed that DHT, androsterone, and 5alpha-androstandione are potent inhibitors of the formation of estrone from androstenedione. 5alpha-androstandione was shown to be the most potent, while androsterone was the least.
Lastly, DHT acts on the hypothalamus / pituitary to decrease the secretion of gonadotropins. By decreasing the secretion of gonadotropins you decrease the production of the raw materials for estrogen production – testosterone and androstenedione (DHT itself cannot aromatize into estrogens). This property of DHT comes into particular utility when it is administered exogenously, and this is to be discussed in further detail in the next section.
DHT, estrogen, and the prostate
When it comes to sex hormones, few things are as misunderstood by the general consumer as the relationship of the prostate to DHT. The inaccurate and overly simplistic attitude that DHT is responsible for prostate hypertrophy, and even prostate cancer predominates amongst most people.
The real situation is, of course, much more complex. One must understand that there are marked differences between healthy prostate growth (developmental growth), prostate growth due to BPH, and cancerous prostate growth.
The first period of prostate growth, deemed developmental growth, is connected to puberty and the testicular secretion of androgens. This takes the prostate from its prepubertal dormancy to the normal sized, healthy, and functional prostate gland of an adult. During the early and mid adult years the prostate stays at this stage, despite the constant high levels of androgens in the body. However, if androgens are blocked in the body then the adult prostate will shrink in size. This can occur by castration, or even by blockade of 5-AR (recall that DHT is the active androgen in the prostate).
Later in life, there is often a second stage of growth. This growth is deemed benign prostate hypertrophy (BPH) and this growth occurs in a wholly different hormonal environment than that of developmental growth. Evidence is mounting that the existence of a high estrogen / androgen ratio – a condition common in older men – is highly correlated to the development of BPH.
Experimental studies have shown the inability of androgens with saturated A rings (DHT related) to induce an initial condition of prostate hypertrophy. These compounds are non-aromatizable. Aromatizable androgens on the other hand, such as testosterone or androstenedione can induce hyperplasic modifications of the prostate of monkeys, but these effects are reversed by the addition of an aromatase inhibitor.
So apparently, estrogen is a causative factor in BPH or, probably more accurately, estrogen in the presence of a minimum, permissive amount of androgen.
None of this may come as news to many of you, but I bet that very few of you know that DHT can actually be used to treat BPH!! How can it do that? It basically does this by replacing the testosterone in the body, which then has the effect of reducing the amount of estrogen in the body. As I started to explain before, DHT is a strong androgen that will signal the pituitary to decrease the production of gonadotropins. The decrease in gonadotropins will then cause less testosterone to be produced which will in turn cause the estrogen levels to drop. The resulting change in the hormonal milieu (high DHT, low estrogen) then apparently results in a regression of BPH.
The clinical application of this theory is discussed in US patent 5,648,350 "Dihydrotestosterone for use in androgenotherapy". The following illustrates the results:
"In 27 subjects in which the plasma DHT level was controlled, so as to modulate the administered doses, said levels have been increased to 2.5 to 6 ng/ml. There resulted a decrease in gonadotrophy as well as in the plasma levels of testosterone which exceeded at least 1.5 ng/ml (from 0.5 to 1.4 according to the case); as to the estradiol plasma levels, these decreased by 50%.
Among this group of subjects, the volume of the prostate diminished significantly, as was evaluated by ultrasound and by PSA (Prostate Specific Antigen). The mean volume of the prostates was from 31.09.+-.16.31 grams before treatment and from 26.34.+-.12.72 grams after treatment, for a mean reduction of 15.4%, the treatment having a mean duration of 1.8 years with DHT (P=0.01)."
This kind of flies in the face of the traditional thinking concerning BPH now doesn’t it?
Conclusion
People have a natural tendency to classify things as either good or bad, with no gray areas. DHT (like estrogen) has recently been on everyone’s bad list, and is often considered to be a hormone that serves no function in the body except to cause harm. As you can see, this view is far from the truth. In my opinion, the widespread use of 5-AR inhibitors such as Proscar as a prophylactic agent for people that really don’t need it should be reconsidered. So give DHT a break.

Creatine: Not just a sports nutrition supplement

Creatine: Not just a sports nutrition supplement"
Readers of the March 2003 issue of Life Extension magazine should recall the long list of potential medical, performance and anti-aging effects of creatine. The article outlined the substantial body of research that found creatine may help with diseases effecting the neuro muscular system, such as muscular dystrophy and may have therapeutic applications in aging populations, wasting syndromes, muscle atrophy, fatigue, myopathies, Parkinson's disease, Huntington's disease and other mitochondrial cytopathies. Several studies have shown it may reduce cholesterol by up to 15% and has been used to correct certain inborn errors of metabolism, such as people born without the enzyme(s) responsible for making creatine.
The article also covered exactly what creatine is, how it works and how much is required to possibly treat the aforementioned pathologies. . In this article, we examine some additional properties of creatine, such as its effects on growth hormone release, homocysteine and chronic fatigue syndrome, as well as other important issues surrounding this supplement, such as its safety.
Although data is limited, some research suggests creatine can raise growth hormone equal to that of intense exercise. Growth hormone (GH) is known to play an essential role in the regulation of body fat levels, immunity, muscle mass, wound healing, bone mass and literally thousands of other functions both known and yet unknown. It is well established that GH levels steadily decline as we age and is partially responsible for the steady loss of muscle mass, loss of skin elasticity, immune dysfunction and many other physical changes that take place in the aging human body. Therefore, the possible effects of creatine on GH is worth exploring in aging populations.
One study found creatine could mimic the increased GH levels seen after intense exercise.1 In this comparative cross-sectional study, researchers gave six healthy male subjects 20 grams of creatine in a single dose at resting (non-exercising) conditions. The study found that all subjects showed a "significant" increase of GH in the blood during the six-hour period after creatine ingestion. However, the study also found "a large interindividual variability in the GH response." That is, there were wide differences among individuals in the levels of GH achieved from taking the creatine. For the majority of subjects the maximum GH concentration occurred between two and six hours after ingesting the creatine.
The researchers concluded "In resting conditions and at high dosages creatine enhances GH secretion, mimicking the response of strong exercise which also stimulates GH secretion." These researchers felt that the effects of creatine on GH could be viewed as one of creatine's anabolic properties with the lean mass and strength increases observed after creatine supplementation. Although creatine supplementation has been found to increase lean muscle mass and strength in many studies, the effects of creatine on those tissues via GH enhancement has yet to be elucidated.
Creatine may reduce homocysteine levels
Homocysteine has been recognized as an important independent risk factor of heart disease, more so than cholesterol levels according to some studies. Creatine biosynthesis has been postulated as a major effector of homocysteine concentrations,2 and oral creatine supplements may reduce levels of homocysteine. Many studies have found that methyl donors (such as trimethylglycine (TMG) reduce levels of homocysteine, which also reduces the risk of heart disease. Conversely, pathways that demand large amounts of methyl groups may hinder the body's ability to reduce homocysteine levels. The methylation of guanidinoacetate to form creatine consumes more methyl groups than all other methylation reactions combined in the human body.
Researchers have postulated that increasing or decreasing methyl demands on the body may increase or decrease homocysteine levels. In one study researchers fed rats either guanidinoacetate- or creatine-supplemented diets for two weeks.3 According to the researchers "plasma homocysteine was significantly increased (~50%) in rats maintained on guanidinoacetate-supplemented diets, whereas rats maintained on creatine-supplemented diets exhibited a significantly lower (~25%) plasma homocysteine level." These results suggest that homocysteine metabolism is sensitive to methylation demand imposed by physiological substrates such as creatine.
Creatine and chronic fatigue/fibromyalgia
Because of creatine's apparent abilities to improve the symptoms of other pathologies involving a lack of high energy compounds (e.g., congestive heart failure, etc.) as well as the aforementioned afflictions outlined in the introduction to this article, it has been suggested that creatine may help with chronic fatigue syndrome and fibromyalgia (some researchers now posit that they are in fact the same syndrome). Although the causes of both pathologies is still being debated, a lack of high energy compounds (e.g. ATP) at the level of the mitochondria and general muscle weakness exists. For example, people with fibromyalgia have lower levels of creatine phosphate and ATP levels compared to controls.4 No direct studies exist at this time showing creatine supplementation improves the symptomology of either chronic fatigue or fibromyalgia.
Considering, however, the other data that finds that creatine supplementation increases creatine and ATP levels consistently in other pathologies where low levels of creatine and ATP are found, it stands to reason that people suffering from either syndrome may want to peruse the use of creatine. Another similar syndrome to chronic fatigue and fibromyalgia, is Multiple Chemical Sensitivity Syndrome, which may also be potentially improved by the use of creatine supplements, though more research is clearly needed.
Creatine safety issues: fact or fiction?
After the first article in Life Extension magazine on the many potential medical and anti-aging uses of creatine, I received several letters and many e-mails that basically said "I would like to use creatine for the various reasons stated in the article, but I am worried about its safety." This fear over the safety of creatine was usually generated from some hysterical news report or poorly researched article. It's odd, but predictable that the media and conservative medical establishment have desperately tried to paint creatine as an inherently dangerous or "poorly researched" dietary supplement. The fact is, creatine may be the most extensively researched performance-enhancing supplement of all time, with a somewhat astounding safety record.
True to form, the "don't confuse us with the facts" media and anti-supplement conservative medical groups have had no problems ignoring the extensive safety data on creatine, or simply inventing safety worries where none exists. A perfect example of this was the news report that mentioned the deaths of three high school wrestlers who died after putting on rubber suits and riding a stationary bike in a sauna to lose weight. Amazingly, their deaths were linked to creatine by the media, rather than extreme dehydration! Even more amazingly, on further examination, it was found that two of the three wrestlers were not using creatine!
Creatine has been blamed for all sorts of effects, from muscle cramps to dehydration, to increased injuries in athletes. However, these effects have been looked at extensively by researchers without a single study reporting side effects among several groups taking creatine for various medical reasons over five years.5-8
In some, but not all people, creatine can raise a metabolic byproduct of creatine metabolism known as creatinine. Some people-including some medical professionals who should know better-have mistakenly stated that elevated levels of creatinine could damage the kidneys. Elevated creatinine is often a blood indicator, not a cause, of kidney dysfunction.
That's a very important distinction, and several short- and long-term studies have found creatine supplements have no ill effects on the kidney function of healthy people.9,10 Though it makes sense that people with pre-existing kidney dysfunction should avoid creatine supplements, it is reassuring to know that creatine supplements were found to have no ill effects on the kidney function of animals with pre-existing kidney failure, showing just how non toxic creatine appears to be for the kidneys.11 Bottom line, creatine safety has been extensively researched and is far safer than most over-the-counter (OTC) products, including aspirin.

The Thyroid Gland Part 1: Fat Loss, Muscle Growth, and Diet

The thyroid, how does it work? The thyroid gland is situated in the top part of the neck. It produces several hormones which are crucial for the appearance of the bodybuilder. It is not a question here of flaunting our science with complicated terms. I am concentrating on what is important for the bodybuilder in terms of leanness and muscles, but it is important to understand how the thyroid works and its mechanisms of action.
The thyroid gland produces a substance called T4 (thyroxine or tetra-iodothyronine). This T4 is called a pro-hormone, as the scientists haven't succeeded in demonstrating a direct action by it. Of course, a pro-hormone, is nonetheless a hormone. But its action is indirect, as it will, in part, be transformed into T3 (triiodothyronine) which is responsible for the actions of the thyroid. Not all the T4 is transformed into T3 -- it therefore constitutes a reserve of thyroid hormones in the blood. Its lifetime will thus be longer, the T3 being degraded more rapidly.
A portion of the T3 (20%) comes directly from the thyroid, the rest coming from the transformation of the T4. Tissues like the liver, the kidneys, the heart, the muscles or the central nervous system are the sites of this transformation.
The action of TSH TSH is a hormone that stimulates the thyroid (Thyroid Stimulating Hormone) to produce T4 and T3. When these two are elevated, they lower the level of TSH. On the other hand, when T3 and T4 are low, the level of TSH increases. In a blood analysis, a hypothyroid is therefore in theory characterized by a low T3 and T4 and a raised TSH, while a hyperthyroid is characterized by an elevated T3 and a low TSH.
In reality, many hypothyroids have not only a low TSH, but also a low T3. This is called having a "lazy" thyroid as the body does not react to the deficiency of thyroid hormones. Women often have this condition.
It is said that TSH determines the size of the thyroid gland. Those who take medications containing thyroid extracts lower the level of TSH, which means that they will atrophy their thyroid gland, sometimes even for a long time after the stopping of this medication. But why is this gland so important for the bodybuilder?
What are the effects of thyroid hormones? First of all, they are a determining factor for basal metabolism. The more the T3 is elevated, the more calories the body burns, particularly in the form of heat. Therefore the higher the level of these hormones is elevated, the more your body temperature will be elevated. In consequence, taking your temperature in the morning is a good indicator of the level of activity (or lack of activity) of your thyroid. Many women find that they are constantly cold, even in warm weather. This is often because they suffer hypothyroidism.
The thyroid hormones are also at once anabolic and catabolic. A weak level of T3 is mainly anabolic and very little catabolic. The higher this level gets, the more the catabolic action will predominate, while the anabolic activity reaches a ceiling quickly. The thyroid hormones also have indirect actions. For example: only the action of either epinephrine or norepinephrine on the beta receptors in the fat cells has lipolytic (fat loss) properties. So if one blocks these beta receptors, the increased caloric expenditure due to a high T3 level will be derived mostly from muscles (amino acids), and not from fat. On the other hand, thyroid hormones help to reduce fat (and to gain muscle) by increasing the number of beta receptors in the fat and muscle cells.
Moreover, thyroid hormones are indispensible for the production of IGF-1 by the liver. A large part of this permissive effect, other than a stimulation of the secretion of the secretion of GH, is due to the increase of the number of growth hormone receptors in the liver. Of course, all this works well if the thyroid gland functions normally. Unfortunately, this isn't always the case, especially during a diet poor in calories. We must therefore ask:
What are the effects of a diet on the thyroid gland? This is not a secret for anyone: the stricter and longer a diet is, the more the body adapts to the deficiency in calories and reduces its energy needs. Metabolism slows down and the body temperature is lowered. This action is essentially due to a reduction in the level of thyroid hormones in the blood. The lowering of thyroid hormones is produced not only directly by an atrophy of the gland but also by a lessening of the transformation of T4 to