09-12-2004, 04:05 PM #1New Member
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- Sep 2004
Speech class: Arguing in favor of steroids
Hello all. I was referred to this forum from a message board for a great supplement company. On their forum I wrote this:
"So in speech class we have to pick a controversial issue. I'm arguing for the legalization of steroids . I haven't begun to research it yet, but I assume a major reason steroids are illegal is because they can lead to cancer. I plan to counter with statistics on cancer caused by smoking. One may argue that steroids cause 'roid rage , but I want to counter with violent crimes (assaults and murders) caused under the influence of alcohol. If there is a place I could view comparable statistics on crimes caused under 'roid rage, that would be a huge help. My arguement will be that if a person takes risks that only harm himself or herself, then the person should be free to have the right to pursue that venture, whether or not the person exercises that right. I may throw in accidental gun deaths as well. I might also want to mention the ephedra ban, the upcoming prohormone ban, and things like possible future bans of supplements. By the way, are there any future bans in the works? Statistics on deaths and health problems caused by ephedra and prohormones would be a help (although I'm unaware of any deaths caused by prohormones). Links to web sites, opinions, possible counter-arguements, and ect would be very greatly appreciated. I'm basically trying to prove that steroids only harm the user, when we have freedoms that can harm others, and that banning steroids is hypocritical. I NEED FEEDBACK!"
Anyway, I was told that there are a lot of knowledgable people on this forum that can help. It would be appreciated. Thank you. Sources would also be a major help.
09-12-2004, 04:11 PM #2
Wouldn't it be hard to argue something you've never personaly experianced
I mean thats like a virgin argueing that doggy style is the best position...
09-12-2004, 04:24 PM #3
ive never smoked but i can argue that its bad for u!
09-12-2004, 04:33 PM #4
09-12-2004, 04:33 PM #5Originally Posted by 1-Cent
thats funny sh_t but I think that it is verry possible to make a arguement about AS. There is so much information about AS, and AR is one of the best places to look. The main page of AR has tons of info about what they do to you and all of that good stuff. Also if you need something different just do a search on the forum and you should find everything you need. Just remember there is a ton of false info about AS and you need to sort through it.
search and ask questions
09-12-2004, 04:51 PM #6Originally Posted by BrianTKessler
09-12-2004, 05:01 PM #7Originally Posted by Flasher
09-12-2004, 05:11 PM #8
"I'm arguing for the legalization of steroids "
that right there is a terrible start. steroids ARE legal. they are not illegal substances, such as heroin. you may argue for the de-classification for steroids down to OTC, or the de-criminalization for them. Matter of sematics, but if I heard a speech start off like that, I would goto sleep.
secondly, your arguments are weak. you cant use that if tobaco and alcohol already do those things, then steroids will be ok. thats a bad idea. you need to use positive information, not negative association.
"risks that only harm himself or herself, then the person should be free to have the right to pursue that venture" wrong, it is technically illegal for one to intentionally harm themselves, and we actually dont have the right to harm...although, this obviously doesnt hold (tobaco, alcohol, high salt foods, etc etc)...however, I would not use this arguement at all
just some insite, i just took speech class last summer..its still fresh IMO, its a terrible topic. the evidence is not there well enough for long term of high doses on HUMAN subjects. the media propeganda will squash rat studeis and HRT studeis.
09-12-2004, 06:19 PM #9New Member
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- Sep 2004
First of all I'm not looking for sources on where to buy steroids . I meant web sites, research studies, magazine articles, ect. Let me state very clearly that while I may be a newbie on this message board, I'm not one of those newbies that are looking for places to buy steroids .
Second, yes it very well may be hard to argue about something I've never experienced. But I've neither confirmed nor denied that I've ever taken steroids. I would prefer not to be asked, either, and I would respectfully ask that if anyone has assumptions about whether I have or not, that you'd keep that assumption to yourself. I'm sure almost everyone on this forum would want that consideration, and everyone deserves it, including me. I've taken alcohol in my life, but that doesn't make me an expert on the legalities of Prohibition. I've smoked cigarettes, but I'm not an expert on tobacco settlements. There's a difference between putting a cycle together or knowing what to stack with Deca , as opposed to statistics on how many people were put behind bars for selling steroids for uses other than medical.
Third, my speech needs to be controversial. I don't want to pick something that everyone else is going to do, like abortion, gun control, stem cell, ect. I need to present steroids as a lesser evil, as opposed to pointing out its benefits. Its only benefit in the context of the speech would be huge muscles, or increased athletic performance. The audience and the teacher would crap all over that, since the vast majority aren't athletes or weight lifters. The public associates steroids as being muscle-headed 'roid rage freaks, pure and simple. Yes, there are positive uses for steroids, like medical, but those uses don't fit the arguement. I'm mainly going for the declassification angle. I'm trying to argue that a person should have the right to decide for himself or herself, whether or not they choose to exercise that right. Maybe its a bad topic, but that's the challenge. It's a hard sell, and I'm not afraid to try to sell it. I'll be graded more on presentation. Whether I'm right or wrong isn't as important as whether I've made valid points that provoke thought. Or whether I've spoken clearly and articulately. That doesn't change the fact that I need hard data to support my arguements, no matter how bad you may think that they are. Reading posted computer text is far different than listening to a live speech, where I can look you in the eye, or react to your responses. I think it's unfair to assume that I'd bore you. Besides, part of writing a good speech is knowing your audience. I may bore you because you're informed about steroids, and already know most of what I'll probably say. These are regular kids who are ill-informed, and I can take whatever facts I want, make them say what I want, and bull**** them into seeing things my way. But by all means, if you have a better arguement for declassifying them, then please share. I'd be more than grateful, and I truly mean that.
I hope none of you take this post as a flame on any of you. It may certainly look like it is when you read it, but I'm not directing hostility towards anyone. I'm just trying to work on a project I believe in. I lift weights, and I assume all of you do too. We're all brothers of iron and sisters of steel here. I would respectfully ask of anyone reading this to think twice before tearing into my posts, and if anyone has anything helpful, like where to find information on imprisonment or death from steroid abuse , or any of the other things I've mentioned (statistics on alcohol, tobacco, heart disease) in my original post, then your help would be very greatly appreciated. Thank you.
09-12-2004, 06:21 PM #10New Member
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- Sep 2004
- Long Island, NY
09-12-2004, 06:26 PM #11
HAHA!! For Nutrition Class I wrote a paper and gave a speech on the "Evils of Steroids ". The Prof had already made her position known (against, of course) so I spewed all the BS propaganda at the class to get my automatic A.
Also, we had to have a visual aid. Mine was a 3cc syringe with vet B-Complex in it!
09-12-2004, 07:50 PM #12Associate Member
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- Apr 2004
I like your topic bro....I did the same thing awhile back....I love how the media makes steroids out to be sooo much worse than they are (especially if you have the knowledge to use right)...GOD I REALLY HATE THAT who are they to judge. The whole topic really gets me going
09-12-2004, 08:16 PM #13
I was all fired up to do a speech on this topic for my COMS 100 class but we never had to do a controversial topic. I would have used some of your arguments, the smoking and alcohol ones mainly. And if done properly, a cycle of AAS can be very beneficial to the user. Roid rage is also a myth, its been discussed on here before, and it depends on the individual. I bet someone with roid rage would be just as aggitated off cycle as they are while on. The only time you hear about ephedra/PH/AAS in the news is when some idiot dies from them and they get a bad rap. You never hear about all the people who use them and have great results and know what theyre doing. The people who die from ephedra probably overdosed majorly cuz if 2 pills works, 6 must be waaay better. You can overdose and die from tylenol too.
The only difference from a legal drug and an illegal one is the law. MAO inhibitors are nasty drugs, very harmful to the user and they are prescribed to thousands of people. Many illegal drugs will not hurt the body at all, theyre illegal because when you are on them you can do something to hurt yourself or others or are addicting. The withdrawl symptoms of alcohol can and will kill you. Those of heroin WILL NOT kill you even though you feel like youre going to die. Bayer Asprin started in the 1930's as Bayer Heroin. They also made morphene, codene, and similar drugs. When people started getting addicted the govt steped in and made them illegal. As for causing cancer, everything causes cancer these days. Everyone has cancer cells in thier body, theyre just dormant and have to be activated by something outside, say cigarettes.
09-12-2004, 09:08 PM #14
Heres a reall nice article that sites about 6 studys that prooves some of the hype is wrong. If you want anymore or need anything else I will be happy to help you. Just so you know cancer isnt really one of the major concerns with steroids . Most of The National Health Institutes propaganda consists of Heart and cholesterol problems. WIN your debate and good luck!!!!
Testosterone and Your Ticker
The Positive Effects of Testosterone on the Heart
by Doug Kalman MS, RD
Steroids will cause your kidneys to implode, your heart to blow a ventricle, and your liver to squirt out of your arse, fly across the room, and knock the cat off the futon. We read it on the Internet and saw an after school special about it, so it must be true, right?
Actually, the more you learn about steroids, the more you come to realize that, like all drugs, there's a difference between their intelligent use and outright abuse. In this article, Doug Kalman takes a look at the effects of Testosterone on the heart. What he found may surprise you.
Over the years we've all heard the repeated mantra that anabolic steroids are bad for the heart. Some physicians will tell you that gear raises your risk of heart disease by lowering your good cholesterol (HDL) and raising your bad cholesterol (LDL). In fact, as some docs will tell you, steroids are known to even induce cardiac hypertrophy (enlargement of the heart). And since you can't flex your heart in an effort to woo women, who'd want that?
But, as in every story, there's more than one side. In fact, let it be said, the dangers of steroids are overstated and, hold onto your seats, may even be good for the heart. Let's examine some of the scientific studies on the positive effects of Testosterone on the heart.
What are the cardiovascular effects of steroids ?
Cardiologists at the Royal Prince Alfred Hospital in Australia recruited both juicing and non-juicing bodybuilders for a study. Each bodybuilder had various aspects of the heart measured (carotid intima-media thickness, arterial reactivity, left ventricular dimensions, etc.). These measurements indicate whether bodybuilding, steroid usage or both affect the function, size, shape and activity of the heart.
The doctors found some obvious and not so obvious results. Predictably, those bodybuilders who used steroids were physically stronger than those who didn't. What was surprising was that the use of steroids was not found to cause any significant changes or abnormalities of arterial structure or function.
In essence, when the bodybuilders (both groups) were compared with sedentary controls, any changes in heart function were common to bodybuilders. The take home message from this study is that bodybuilding itself can alter (not impair) arterial structure/function and that steroids do not appear to impair cardiac function. (1)
Does MRFIT need a T boost?
A famous cardiac study was published about 10 years ago. It soon became on ongoing study known as the Multiple Risk Factor Intervention Trial (MRFIT). The present study examined changes in Testosterone over 13 years in 66 men aged 41 to 61 years. The researchers determined if changes in total Testosterone are related to cardiovascular disease risk factors.
The average Testosterone levels at the beginning of the study were 751 ng/dl and decreased by 41 ng/dl. Men who smoked or exhibited Type A behavior were found to have even greater decreases in T levels. The change in Testosterone was also associated with an increase in triglyceride levels and a decrease in the good cholesterol (HDL).
The authors concluded that decreases in Testosterone levels as observed in men over time are associated with unfavorable heart disease risk. (2) Sounds to me like a good reason to get T support/replacement therapy in the middle age years!
In a similar study, researchers in Poland examined if Testosterone replacement therapy in aging men positively effected heart disease risk factors. Twenty-two men with low T levels received 200 mg of Testosterone enanthate every other week for one year. Throughout treatment, Testosterone, estradiol, total cholesterol, HDL and LDL were measured.
The researchers determined that T replacement returned both Testosterone and estradiol levels back to normal and acceptable levels. They also found that T replacement lowered cholesterol and LDL (the bad cholesterol) without altering HDL (the good cholesterol). Furthermore, there was no change in prostate function or size.
The take home message from this study is that T replacement doesn't appear to raise heart disease risk and it may actually lower your risk. (3) It appears that more physicians should be prescribing low dose Testosterone to middle age and aging men for both libido, muscle tone and for cardiac reasons.
What about younger men?
It's been long established that men have a higher risk of heart disease. One of the risk factors implicated is Testosterone. Reportedly, the recreational use of Testosterone can alter lipoprotein levels and, in fact, case reports exist describing bodybuilders who've abused steroids and have experienced heart disease or even sudden death. But the question remains, is the causal association one of truth or just an association?
To answer this, researchers at the University of North Texas recruited twelve competitive bodybuilders for a comprehensive evaluation of the cardiovascular effects of steroids. Six heavyweight steroid-using bodybuilders were compared with six heavyweight drug-free bodybuilders.
As expected, the heavy steroid users had lower total cholesterol and HDL levels as compared to the drug-free athletes. What was unexpected was that the steroid users also had significantly lower LDL (the bad cholesterol) and triglyceride levels as compared to the non-steroid users. In addition, the juicers also had lower apolipoprotein B levels (a marker for heart disease risk). Thus, the authors concluded that androgens do not appear to raise the risk of cardiovascular disease. (4) The take home message from this study is that the negative cardiac side effects of steroids are most likely overstated.
In a little more progressive study, researchers at the Albert Einstein College of Medicine in the Boogie Down Bronx (the BDB to those in the know) examined Testosterone as a possible therapy for cardiovascular disease. (5) The researchers note that T can be given in oral, injectable, pellet and transdermal delivery forms. It's noted that injections of Testosterone (100 to 200 mg every two weeks) in men with low levels of T will decrease total cholesterol and LDL while raising the HDL.
In fact, Testosterone therapy has been found to have antianginal effects (reduces chest pain). Low levels of Testosterone are also correlated with high blood pressure, specifically high systolic pressure. The researchers determined that returning T levels back to normal and even high-normal levels have positive cardiovascular effects and should be considered as an adjunctive treatment for maintaining muscle mass when someone has congestive heart failure.
Putting it all together
Strong research demonstrates that the risks of negative cardiovascular effects of steroids are overstated. In fact, a recent paper published in the Canadian Journal of Applied Physiology questioned the whole risk of using steroids. (6) Joey Antonio, Ph.D. and Chris Street MS, CSCS published strong data showing that the risks of steroid use are largely exaggerated, much like scare tactics used by your parents while you were a kid. Of course, it goes unsaid that abuse of anything will lead to unwanted consequences.
We know that as we age, circulating Testosterone levels naturally decrease. For most people the Testosterone decrease goes from high-normal to mid to low normal. Data shows that there's an inverse relationship between T levels and blood pressure as well as abdominal obesity (that paunch we see on so many middle age males).
Testosterone replacement lowers abdominal obesity and restores Testosterone back to normal levels. Restored Testosterone is correlated with better mood, better muscle tone, stronger sex drive, lower cardiovascular disease risks, stronger bones and better memory. It's important to note that while conservative use gives a pronounced positive health benefit, higher doses may not necessarily lead to further health benefits.
What to do
If you see your body composition changing (your gut starts looking like your Uncle Lester's), your strength or muscle tone diminishing despite your hard training and good diet, and your sex drive not matching up to TC's columns, have your Testosterone levels checked. The acceptable normal range for Testosterone to physicians is 300 mg/dl to 1100 mg/dl. Yes, that's a pretty wide range.
In the clinic, we see people with the complaints consistent with "andropause " (a term for male menopause) and/or increased cardiovascular risk having Testosterone levels between 300 mg/dl and 550 mg/dl. Bringing it up to the mid to high-normal level is what gives the health and "youthful" benefits. Traditionally 200 mg/dl of supplemental Testosterone given every one to two weeks improves body composition, lowers total cholesterol and LDL, while raising HDL.
It appears that supplemental T is a healthier and safer way to go than many of the drugs used to treat poor lipid profiles. The data presented in this article applies for males over 35, not those who are 18. If you think that you can benefit from Testosterone therapy look for physicians who market themselves as "anti-aging" or "longevity physicians" as well as the more progressive endocrinologists or cardiologists.
Long story short, used intelligently, Testosterone is good medicine!
About the author: Douglas S. Kalman MS, RD is a Director for Miami Research Associates (MiamiResearch.com) a leading pharmaceutical and nutrition research organization in Miami, Florida. Doug is also a national spokesperson for the American College of Sports Medicine and according to his latest test has high T levels. Doug can be reached at firstname.lastname@example.org.
1) Sader MA, Griffiths KA, McCredie RJ, et al. Androgenic anabolic steroids and arterial structure and function in male bodybuilders. J Am Coll Cardiol 2001;37(1):224-230.
2) Zmuda JM, Cauley JA, Kriska A, et al. Longitudinal relation between endogenous testosterone and cardiovascular disease risk factors in middle aged men. A 13 year follow-up of former Multiple Risk Factor Intervention Trial participants. Am J Epidemiol 1997;146(8):609-617.
3) Zgliczynski S, Ossowski M, Slowinska-Srednicka J, et al. Effect of testosterone replacement therapy on lipids and lipoproteins in hypogonadal and elderly men. Atherosclerosis 1996;121(1):35-43.
4) Diekerman RD, McConathy WJ, Zachariah NY. Testosterone, sex hormone-binding globulin, lipoproteins and vascular disease risk. J Cardiovasc Risk 1997;4(5-6):363-366.
5) Shapiro J, Christiana J, Frishman WH. Testosterone and other anabolic steroids as cardiovascular drugs. Am J Ther 1999;6(3):167-174.
6) Antonio J, Street C. Androgen use by athletes: A reevaluation of the health risks. Can J Appl Physiol 1996;21(6):421-440.
09-12-2004, 09:45 PM #15
Good luck bro, Not one I would do if it were me.
09-12-2004, 09:55 PM #16Originally Posted by BrianTKessler
09-12-2004, 10:08 PM #17New Member
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- Sep 2004
Anhydro78, this is a very good start. Thank you. I'm not very well versed in steroids , but I noticed that the tests involved 200mg doses of test eth, at 2 week intervals. I've heard that a good suggested minimum dosage for a beginner cycle would be 300mg at 2 week intervals. Does that sound about right? It might add a lot of credibility if I can mention that the men were getting doses 66% as high as bodybuilders who use steroids . Better yet would be to mention that a maximum steroid cycle would be maybe 10 weeks, as opposed to the 52 week study.
As for the people who are saying 'roid rage and cancer are overblown, it might be true and it might not... but I'll need something a lot better than "this dude on a message board told me so." No offense. I'd benefit on reading studies conducted on these issues. I'm in it to win it, and I don't want to give anyone room to doubt my arguement, so I need to show up and counter all the inevitable arguements. Part of my grade is taking possible questions from the audience and the teacher, and I know they'll all mention cancer and 'roid rage. I thank Anhydro78 once again for giving me a start at countering the heart attack angle. I think most people agree that knowing your limits and moderation are key, and that overdosing on any drug is usually what makes it dangerous. Now I'm able to formulate that thought more clearly.
This speech will mean a lot to me. I see it as an opportunity to inform the misinformed. So I need to know my sh*t.
09-12-2004, 11:49 PM #18Anabolic Member
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- Sep 2003
Well one place you can start is what steroid users in general think of steroids . For example MOST of us that have done steroids have never experienced roid rage . It is not a common side effect, rather a very rare one that mostly affects those with other issues like maybe they are a little scizzo to begin with. The media has played up roid rage as a serious problem, however I believe its a lot like in the 70's and 80's people were blaming the reason they killed someone was because they were on Angel Dust or LSD. Those arguments never held up in court against these very powerful mind altering drugs and they dont hold up against steroids either.
Also I should point out steroids are NOT illegal in this country. They are prescribed to many people as needed. Some people have hormone deficiency problems. Others might be on chemo therapy and get bad case of anemia and the steroids #1 thing they do to your body is increase red and white blood cell counts, effectively treating amenia. People with AIDS are commonly prescribed high doses of steroids that even the most competitive body builders would be scared to try. It seems steroids slightly weaken your immunity against bacteria but it vigorously strengthens your ability to fight viruses which is why steroids have become important with AIDS patients.
Above all else, this is the real reason guys do steroids. Its like this, women can get boob jobs, liposuction, etc. For guys to improve their body, surgury is not needed. All you need is take these drugs and you become big and handsome and then all the women want you. Its hard for a guy not to be motivated to improve his own looks and then reap the reward of getting lots of sex from the partners you are attracted to. Not only do you become all muscular but the steroids can also help you take inches off the fat belly at the same time. Most steroid users have a distinct impression they are becoming healthier and "more of a man" when they've taken steroids.
09-13-2004, 01:09 AM #19
Heres the thing about Roid Rage . If anyone would suffer from roid rage it would be me. I have Bi-Polar type 1 disorder with rapid cycling. And it doesnt even effect me. The only thing is if somehow someone is prone to blow up all the time, increased androgen levels would make the episode a little more intense. Thats all, your either an azzhole to begin with or not.
As for the study, that article sites 6 studys. not all the subjects where on just 200mgss of Tetosterone every week. ( By the way that is Hormone replacement therapy doses) the first couple in the study where done on admitted steroid users ( which they could have been on everything you can imagine) and they where compared to Non-steroid users.
What I got from this article is that many of the negative side effects that have been associated with steroid use , was actually common among steroid user and non steroid user athletes alike. The side effects may be caused by an athletes life style, workout program and diet.
Ive got a copy of a National Health Institute propaganda report. If you can tell this "study" was done without a control group and the athletes they picked to proove an increased mortality was Power lifters. Power Lifters are probally in worse health than any other athlete besides sumo wrestlers. LOL They dont even mention who or what type of athlete the other group was.
anyways heres the Bullsh!t. It reminds me of The Cops in the D.A.R.E. program telling all the kids Weed will kill you, or it is a gateway drug.
Increased premature mortality of competitive powerlifters suspected to have used anabolic agents.
Parssinen M, Kujala U, Vartiainen E, Sarna S, Seppala T.
National Public Health Institute, Laboratory of Substance Abuse, Helsinki, Finland. email@example.com
Misuse of supraphysiological doses of anabolic steroids is claimed to have serious side effects. The aim of the study was to determine the mortality, and the cause of premature deaths among a group of subjects who are strongly suspected to have used anabolic steroids for a non-medical purpose over several years. The mortality of 62 male powerlifters placed 1st-5th in weight series 82.5-125 kg in Finnish championships during 1977-1982 was compared with the mortality of population controls. The mortality during the 12-year follow-up was 12.9% for the powerlifters compared to 3.1% in the control population. By 1993 eight of 62 powerlifters and 34 of 1094 population controls had died, thus the risk of death among the powerlifters was 4.6 times higher (95% CI 2.04-10.45; p = 0.0002). The causes of premature death among the powerlifters were suicide (3), acute myocardial infarction (3), hepatic coma (1) and non-Hodgkin's lymphoma (1). These findings add to the growing amount of evidence of an association between anabolic steroid abuse and premature death, and support the view that measures to decrease AAS misuse among both competitive and amateur athletes are justified.
There is also growing evidence that steroid use increases the risk of suicide, depression, psychotic behavior and homicidal behavior and aggression among regular users. Steroid use among adolescents and young adults seems also correlated with poor self steam, problems with self image and parental over concern with body image. Steroid use is also likely to instigate regular users to experiment with other recreational illegal drugs, particularly opioids. Don't believe me? Check out those links:
09-13-2004, 01:19 AM #20
Here is an example of how to cycle safely. imnot sure how it will help you but it might show the theraputic benifits of steroids . The article is broken up and posted in three posts. It might help your cause to look into the theraputic benifits of Hormone Replacement Therapy.
SuperiorMuscle Archive > Superior Anabolic Section > Anabolic Articles
The Sane cycle : safe and effective use of steroids - Click HERE for Original Thread
The Sane cycle : safe and effective use of steroids
By Big Cat
This is my first outline, still very rough and basic and missing one or two essential elements, of the sane cycle. A project I have been working on in past months to outline a steroid /diet/supplementation plan that allows you to stay healthy, increase your health and still add a nominal amount of LEAN mass to your frame while maintaining of lowering fat.
Any and all comments are extremely welcome.
It has long been my goal to demonstrate that steroid use cannot only occur without causing any harm, it can actually benefit us in lengthening our life-span and increasing our quality of life. Since in essence, steroids have never led to the death of any person, and that they are far less lethal than most over the counter products, such as plain aspirin, they should really be legal. And since they are prescription medication, any use of these products should occur under medical supervision. But hey, some idiots did make them illegal and good luck finding a doctor that will help you, much less one that actually knows what he is talking about.
That is why I set out to write this. It is in no way complete, it is merely a quick rundown of several facts and the safest conclusions I could make based on them. But it should empower you to convince your health-care provider to help you, and educate him on how to do so.
Many people who have known me throughout my quest to refute the dangers of steroid use have asked me for help in proving these facts to sceptics and laymen, and this is EXTREMELY difficult because of the large amount of propaganda they have had to endure over past years. This may still be a tad too scientific for the dumber individuals, but may serve as a tool to educate smarter friends and relatives. And I hope that it may do so.
For cycle duration I have chosen 12 weeks. Its rather arbitrary and its certainly not something you should consider absolute fact. A cycle doesnít have to be 12 weeks to be safe. But we have ample evidence to suggest that with proper post-cycle, full HPTA recovery can be made in less than 50 days (1) , and since most people do not like to play pincushion and employ for the majority long-acting products, 12 weeks is sufficiently long to reap all the benefits of your cycle and get adequate gains.
As a rule we will use equal time off as on. So after the cycle (post-cycle not included) you will stay off 12 weeks. Recovery should be established in less than 50 days, so technically after 2 months you could already safely start another cycle, but since physiology is not linear math and not everyone will be able to complete the cycle and post-cycle as per the instructions, we should offer ourselves some leeway. So we will cycle on 12 weeks, then stay off 12 weeks before recommencing
We need to be realistic about the products we use as well. I could outline all sorts of magnificent exotic cycles, but chances that you will be able to find all the needed products without taking a second mortgage on your house or get swindled by less than reputable ******s is slim. Therefore we opt for the more available products. First of all we will exclude products that are no longer made or are extremely hard to find, that includes drostanolone (Masteron ), quinbolone (anabolicum vister ), mibolerone (cheque drops ), formebolone (esiclene ), clostebol (megagrisevit), MENT, methandriol, metribolone, furazabol (miotolan), Norethandrolone (Nilevar ), ethylestronol (orabolin), Stenbolone, oxabolone (steranabol), etc.
Of whatís left, we need to make a selection. Halotestin is out. Too androgen mediated, too liver toxic. Trenbolone and nandrolone (Deca -Durabolin , Laurabolin , Durabolin) are excluded because they are too suppressive. Andriol because it is ineffective, oxandrolone (Anavar ) because a useful dose (75+ mg per day) is too expensive, and Methenolone (Primobolan ) because of its price. Primo is a decent androgen, but seems to have no other mode of action.
Most of these products would have been excluded for other reasons anyway, with the possible exception of trenbolone and oxandrolone.
We will also exclude methandrostenolone (Dianabol ) and oxymetholone (Anadrol ). While these are useful drugs at the beginning of a cycle, especially as far as bulk and strength, they fall outside of what we are looking for : a long term cycling plan with relatively lean results. On top of that I want to make a case for stanozolol (Winstrol /Stromba) and I do not feel comfortable recommending the use of two orals, due to liver toxicity (eventhough liver toxicity is a tad exaggerated, but then that just allows us more leeway with the winny).
That leaves us with three products : testosterone , boldenone (equipoise ) and stanozolol (Winstrol/Stromba). Can you build an effective cycle with clean and proper results, with only these three substances ? Of course you can. But before we delve into that, let me defend my choice of products.
In defense of testosterone
Apart from being the most effective steroid, itís also the sanest choice with regards to health. It makes sense that by administering the exogenous variant of our prime androgen, we will not allow anything in the body that would normally occur to fall into disuse, nor allow anything that would normally not happen to occur. Because a lot of studies and conclusions are based on findings with testosterone, we can only safely make these assumptions about testosterone. That is why we not only use it, it will be the base for our cycle. And it should be for any health-conscious cycle.
Testosterone is the most effective steroid commercially available today. This observed in the real world, since even with the necessary bulk, testosterone increases lean body mass more than any other steroid we have access to. More than the stronger androgens, and more than the stronger estrogens. That is because testosterone has a very diverse mode of action. Testosterone is the most present androgen in the body. Its also the most important endogenous androgen in muscle tissue. But everywhere else in the body, that role is put aside for Dihydrotestosterone (DHT). Now DHT is a reduced version of testosterone with a saturated A-ring (steroids are lipophillic, 19-carbon, 4-ring structures made from cholesterol). These other tissues are rich in an enzyme called 5-alpha-reductase. When testosterone binds to this enzyme, its 4,5-double bond is broken and two hydrogen atoms (hence dihydro) attached to the spaces that are freed on the A-ring. DHT is a much more potent androgen, roughly three times the affinity of testosterone for the androgen receptor.
Many people regard DHT as the enemy, because among these androgen-specific tissues are the scalp (aggravating a genetic tendency to hair loss) and the skin (causing outbreaks of acne). But in fact DHT is more than that to us. Since it is the prime androgen in nerve tissue, it will be imperative to have ample DHT levels for optimal neuromuscular response. This is why many people taking the 5-alpha-reductase inhibitor finasteride (Proscar) find that their strength does not increase, or even decreases. Secondly we tend to forget that DHT is a potent anti-aromatase. The aromatase enzyme is the enzyme that converts testosterone to the estrogen estradiol (E2). As we will discuss next, E2 certainly has its benefits as well, but too high a concentration will result in excess adipose storage and more water retention (bloat). Certainly we donít need this if it can be avoided. Since this is a long term plan, we are in no way planning to walk around like the ďstay puffed marshmallow manĒ. By blocking the 5-alpha reductase we have a shift towards aromatization of testosterone, because there is more testosterone available (not converted to DHT) and there are more aromatase enzymes (not taken up by DHT). This could in turn lead to problems with feminization and gynocomastia (breast growth in men). So as you can see, DHT is quite important in this equation.
A more important issue is perhaps the prostate. Prostate cancer is a disease of modern society. And steroid use has been known to cause or aggravate Benign prostate hypertrophy, a growth stage of the prostate gland in middle-aged men. Because the prostate is androgen specific, DHT is often named as the culprit. But the latest research determines that estrogen is in fact the causative factor, although a level of androgenic action is required. Androgens have actually been proferred as a therapeutic means to treat BPH.
As we mentioned already, testosterone is a substrate for the aromatase enzyme and converts to E2. A female hormone. Here too demonisation has made E2 the enemy. And yet again we are overlooking several factors. First of all, bloat, fat gain and gyno occur only at very high concentrations of E2, something we should be able to avoid if we are sane with our doses. And if not, we have numerous anti-aromatase drugs at our disposal, of which I favour Mesterolone (Proviron ) as it is a DHT analogue, will increase free testosterone and does not block E2 entirely in low doses, so we still reap the benefits. So what are the benefits of E2 ? Well, estrogen enhances gluconeogenesis (use of glucose for tissue repair and energy storage) (2) , increases the release of human Growth Hormone (3) and can increase androgen receptor upregulation (E2 makes testosterone more effective as an androgen) (4).
Lastly we consider actions not mediated by either the androgen or the estrogen receptor. This could in large part explain why testosterone is still the greatest steroid available, despite there being more potent androgens and more estrogen mediated drugs. A combination of trenbolone, a much stronger androgen, and oxymetholone (which has direct estrogenic action, without requiring aromatisation) only yields roughly the same amount of mass as equipotent or even lesser doses of testosterone. Why ? Well this brings us back to the point I raised about using a base that is equal to the endogenous alternative. Because certain processes may not be activated by these bastard hormones. One study (5) showed that testosterone had more effect in ductal branching in prostate tissue than did DHT, which would indicate a non-AR mechanism, since DHT is more potent at the AR, especially in the prostate. Could it be the estrogen factor ? No, because the DHT prohormone 3-alpha (5-alpha-androstan-3a,17b-diol) had the same effect as testosterone, and 3-alpha does not aromatize. So there is another mechanism in play here, which certainly supports the thesis that there is more to testosterone than merely agonism of estrogen and androgen receptors. Another study demonstrated that testosterone may upgrade beta-adrenoreceptors in vivo, through a non-AR mediated mechanism (again testosterone outperformed DHT in this area), and since administration of estrogen receptor antagonists showed no significant changes, we can also state it was not ER-mediated. The relevance of this in regards to muscular hypertrophy may be a lot greater. This did in large part determine the diet I planned with this cycle and the use of beta-adrenergic agents. So testosterone has proven beneficial in three separate fashions, and easily allows a defense of its selection.
But safety played a factor in my decision as well. Many theories about the evils of steroids were debunked these past few years, and most of the studies that disproved this long-standing anti-steroid propaganda, used testosterone as a substrate. So the only safe conclusion as far as these studies go is that TESTOSTERONE, and not steroids in general, is safe and beneficial. That is not to say the others are not as safe, but there is no proof that gives us any certainty that they are. One of the main reasons against the use of steroids has been cardiovascular risk. Several studies have looked at this closely, and not only did they determine that testosterone did not pose a heart risk (6) , they also concluded that low testosterone levels induce cardio-vascular risk (7), whereas supraphysiological administration seemed to decrease the risk (8) (decreases in total cholesterol, HDL and LDL, LDL/HDL ratio and apoplipoprotein B, a marker for cardiovascular risk). In conclusion it is safe to state that testosterone is actually good for your ticker, and as normal levels of testosterone decrease with age, a good case is to be made for Hormonal Replacement therapy in the interest of cardiovascular health. Lastly testosterone was also shown to increase mental health (9), as it increased cognitive performances in older men. So testosterone cannot only promote more lean mass than any other steroid, it can also make you live longer by decreasing heart risk, and get better quality out of your remaining years by enhancing cognitive performance and fighting dementia.
Hence my case for using testosterone as a base of our safe cycle.
What type of testosterone ?
There are many different types of testosterone. Long esters, short esters, methyltest, andriol, and mixes like sustanon and omnadren . First of all we need to state that methyltest is not testosterone. The 17-alpha-methylation makes quite a few alterations. It will express less androgen binding, lower conversion to mestanolone (Methyl-DHT), and despite lower aromatization, also a heavier amount of estrogenic action because it converts to methyl-DHT, a much stronger and efficient type of estrogen. So methyltestosterone is not a valid choice. Andriol uses a rather ineffective delivery system based on lipophillic absorption in the ductus thoracicus of the lymphatic system. Fine in theory, but appears to be less effective than hoped, and the amounts needed to make andriol of use to us are not affordable.
We will also include sustanon and omnadren, these are combinations of long and short esters (structures attached to slow the release of the compound into the blood), usually injected over wide time-spans. This creates a very unstable blood-level, contrary to popular belief. Imagine if you will a product of 3 esters, one that releases over 3 days, one that releases over 6 days and one that releases over 9 days. 100 mg of each injected once every 9 days. The first three days the first ester would release 100 mg of testosterone. The second ester would release 50 mg and the last ester would release 33.3 mg of testosterone. The next three days the first is already gone, the second releases only 50 mg and the last only 33.3 mg. And on the last three days only 33.3 mg of testosterone from the last ester is released. At the beginning I have the massive dose of 183.3 mg in my blood, and at the end only 33.3 mg Ö you do the math.
The saner thing to do is to use a single ester and inject as soon as levels taper off to levels upon injection. The three most widely used esters and their frequency of injection are propionate (every 2 days), enanthate (every 6-7 days) and cypionate (every 7 days). There is also the longer undecanoate, but that is rather hard to find, and the esterless suspension. The latter is great for mass, but seems to cause a great deal of water retention and needs to be injected once or twice a day, which is not wishful for a long term plan. So which of these should we use ?
Well, the propionate is my first choice, because its release patterns seems to be the most beneficial in keeping water weight under control, and it clears faster than the other two allowing for faster recuperation. For lean gains, I would certainly make the choice for propionate, also because it has a lighter, shorter ester and thus more testosterone per mg. But not many people appreciate injecting every 2 days, and with the concomitant use of boldenone undecylenate the fast clearance time seems to be a non-factor. So if you can tolerate a little more water weight, enanthate or cypionate allow for weekly injections.
09-13-2004, 01:20 AM #21
In defense of boldenone
Boldenone differs from testosterone only in that it has an extra double-bond on itís a-ring at the 1 position. This changes the conformation of the A-ring and its affinity for certain structures. As such it is only half as androgenic as testosterone because of lower affinity to the androgen receptor, and it does not form a more potent androgen in androgen-specific tissue, because it has particularly low affinity for the 5-alpha-reductase enzyme (10) (that converts test to DHT). Eventhough its conversion product is quite potent (1-testosterone).
Boldenoneís affinity for the aromatase is roughly reduced by the same percentage, and so it only creates about half as much estrogen. So in essence, boldenone offers us many of the same characteristics that testosterone does, but because of its lessened affinity poses less of a threat for the acute, visible side-effects. So by dividing our doses over testosterone and boldenone, we can reduce both acute and long-term side-effects.
Boldenone is patented as a veterinary drug, but the high demand has made a wide range of affordable human grade products available to us and the use of boldenone is now quite wide-spread among recreational athletes. It is touted as the successor to the mighty Deca -Durabolin . Deca is nandrolone decanoate. Nandrolone has the benefit of being deactivated by the 5-alpha-reductase enzyme and being even less of a threat for acute androgenic side-effects. But alas, it is a very suppressive hormone that severely interferes with endogenous production of testosterone and it has been concluded that both nandrolone (11) and several of its metabolites (12) exhibit progestagenic activity (which causes gyno through estrogen mediated pathways) and seems to cause more bloat because it acts as an aldosterone agonist (13), resorbing more salts from the urinary tract. On top of that it seems to have a terrible effect on our libido (can you say limp dick ?).
Boldenone gives us none of the aforementioned problems, and despite being a much, much weaker androgen than nandrolone, it seems to exhibit the same level of anabolism in vivo. Which again points in the direction of the non-AR and non-ER mediated pathways to muscular hypertrophy we discussed with testosterone. Boldenone offers two other distinct benefits that have been noted by many a user, despite lack of scientific backing so far. The first is that boldenone seems to increase the appetite. This too is most likely a non-AR mechanism, since many of its inactive metabolites like androstadiendione exhibit the same property and to the same extent, but in low doses. This could be crucial since we steroids can build our muscles, but they need something to build with. That something is amino acids derived from our protein intake, hence our high-protein diets. But to have ample amino acids left to build muscle, we must first eat sufficient calories, more calories than our maintenance of metabolism requires. And in that case it can be of huge benefit to increase your appetite.
The second advantage is that it causes an uncharacteristic rise in aerobic fitness. It is well known that androgen binding increases Erythropoetin release from the kidneys, which increases red blood cell count. Red blood cells carry oxygen through the blood stream, so we have a greater aerobic capacity. But boldenone seems to exhibit an increase in aerobic capacity, far greater than its androgenic affinity would allow us to suspect. Which is probably why this veterinary hormone gained so much human attention in the first place. Along with the increase in respiratory capacity from beta-adrenrgic stimulation (discussed later in this article) could lead us to new heights in any type of sports we practice that require endurance.
So in light of its safety and efficacy, the choice for boldenone as our secondary drug is a quite easy one.
In defense of Stanozolol
Stanozolol is a methylated drug. That means it can be taken orally and be quite effective, but also displays a certain level of liver toxicity. We need to relativate these findings, toxicity is often overstated and it was found (14) that many cases where liver toxicity was determined based on aminotransferase levels were false positives when we looked at the CGT levels. Nonetheless some care should be taken. In general we advise no more than 6-8 weeks on any hepatoxic drug within normal doses (for stanazolol that is 50-100 mg per day) when taken orally and up to 10 weeks when injected (50-75 mg per day). After that ample time should be given to the liver to recover.
Stanozolol has no 3-keto group, which is in most cases essential for androgen binding. So it is far from the heavy androgen some would have you believe it is. But it does appear to exhibit good binding in some places. Like its parent, DHT, it seems to reduce some aromatase activity and it may guard against some progestagenic binding (15) as well (from nandrolone or trenbolone ) although it is unlikely its affinity for the PR is strong enough to play a crucial role in that. It has been suggested that stanozolol may have good binding to the microsomal AR, which may explain its benefits as far as energy utilization. Both aerobic and anaerobic, stanozolol seems to exhibit a large increase in performance. Strength and explosiveness increase, and athletes seem to tire less fast. It has therefore been a favourite of many runners, both in shorter and longer distances. The main use here for us will then also be to assist in the maintaining and gaining of strength, rather than sheer mass, although its light anti-aromatase properties will also aid us in attaining a more fat-free body.
One reason, with regards to safety, why I chose to include stanozolol and not a more potent bulk-up agent as the oral component of this cycle, is because of its effects on tendons. It has long been a concern that steroid usage causes tendon damage. Directly it doesnít of course, but as muscle size increases and strength increases, so does pressure on tendons. And since the tendons do not have a large degree of vascularity they cannot adapt as quickly as the muscle. Repeated strain causes microtraumata, and when enough microtraumata have built up, eventually the tendon will rupture. Stanozolol however, has been found to increase collagen synthesis (16) where testosterone did not. Collagen is a key component in fibrous tissue such as cartilage and tendons, and may therefore offer us the bonus effect of maintaining tendon health or even repairing damage of microtrauma, and keep our cartilage healthy so we can resist the pressure on our joints.
The Goal and the diet
The goal we are pursuing with this, is to create a stable long-term plan for cycling steroids that will not only not jeopardize our health, but actually improve it. The reason we choose to use steroids however is to look better or perform better. It would therefore be unwise for a long-term plan to include excess body-fat, too much water retention etc. On the other hand, muscle growth is reliant on sufficient calories.
Our primary goal is to eat enough. If we consider what we do in a day and the calories we need to achieve that, we need to eat at the very least 20% more to see sufficient growth. Preferably 30% more. Our secondary goal is to keep fat off. The prime mover there is insulin . Insulin stores glucose in the muscle as glycogen and increases the shuttling of nutrients into fat cells. So naturally our goal is to keep insulin low. Insulin is a very anabolic hormone, but that does not mean we cannot achieve growth without it. In order to keep insulin low, we need to eat as little as possible high-glycemic carbs. Any type of carbs that contain glucose (and can therefore increase insulin rapidly) must be avoided. That increases most types of pasta, white bread, an excess amount of starches like potatoes, anything that has added sugar in it, regular table sugar, dextrose, maltodextrin, maltose and several oligosaccharides. A little fruit here and there is fine, as fructose does not appear to be so drastic in insulin levels, and low Glycemic carbs are fine as well (such as the lactose in milk and such). Our diet will probably be moderate to low-carb because of this. More importantly our diet should be high protein. Because first of all protein is what we require to build muscle. Secondly because the body can burn protein, but most likely will not if other means are available. And since we will be manipulating our beta-adrenergic system, we will have plenty of free fatty acids at our disposal. That means the amount of protein in our diet needs to be so great that with it we are eating at least 20% above maintenance, and without it we are eating at least 20% below maintenance. I would keep fat around 20-25% of your diet (from clean sources of course) and then fill the rest in as you please : high-protein and no high GI carb sources.
Because this will allow us to keep insulin low, we cannot only keep fat off, we can also maximally manipulate the beta-adrenergic system, meaning we could potentially lose fat, or at least lower body-fat percentage by keeping fat off and increasing lean body mass.
The take home message : A high-protein diet that contains little or no high GI carb sources, and that meets the demand of being at least 20% over maintenance (around 18 kcals per pound of bodyweight, but that is just an estimate).
The actual cycle
Now we need to put the cycle together. Below I will outline one good way to use these products and then offer some explanations to my reasoning. I will also already include the post-cycle regimen, eventhough we will discuss that at a later point in time.
Week 1-12 : Testosterone enanthate / cypionate 400-500 mg/week
Or : Testosterone propionate 150 mg every other day
Week 1-2 : Boldenone Undecylenate 600-800 mg/week
Week 3-12 : Boldenone Undecylenate 300-400 mg/week
Week 6-13 : Stanozolol 50-100 mg/day
Week 12-14 : HCG 3000/3000/1500/1500 IU / 5days
Week 12-17 : Tamoxifen Citrate 20 mg/day
Week 14-15 : Clomiphene Citrate 100 mg/day
Week 16-17 : Clomiphene Citrate 50 mg/day
Week 14-15 : (Spironolactone) 50 mg/day
Week 7-18 : Beta-adrenergic mix with eph as described.
You may notice the dose of boldenone is larger the first two weeks, thatís because longer esters tend to need some time to accumulate before showing their best effects, and by front-loading with a higher dose, we can achieve accumulation faster and see results sooner. I ran the stanozolol a week longer in this example, which should be fine considering it would take at least 2 weeks after the cycle to clear all boldenone, so the stanazolol beyond this point should cause no further suppression.
The patterns for post-cycle will be discussed at a later time.
Post-cycle has been touted as critical in the process of complete and total recovery. Here too Iím basing myself on certainties from a few studies and making my conclusions accordingly. That is why I offer the advice I offer. This does not mean you should conclude that anything else will necessarily be detrimental, but I cannot guarantee as good an outcome.
[/b]The choice of a Tamoxifen/clomiphene/spironolactone combination[/b]
The choice for a tamoxifen/Clomiphene combo is primarily because of two factors. Only one relevant study (1) came up as far as recovery after a stack of products (testosterone and nandrolone) was used for twelve weeks, utilized HCG and both clomiphene and tamoxifen to achieve a complete recovery of the HPTA to acceptable levels in 45 days. The second reason is the raging war over which is the better post-cycle drug, clomiphene or tamoxifen has lead to several conclusions. The first is that while 150 mg of clomiphene and 20 mg of tamoxifen have lead to roughly a similar increase in LH levels (17) , but that with the high dosing of clomiphene over time there are certain disadvantages. Such as that it may damage eyesight and may act as a weak estrogen (18) in undesirable places (like the pituitary). So using tamoxifen alongside it will allow us to lower the dose and decrease the chance of these side-effects and add the distinct benefit that Tamoxifen (being the stronger of the two) will prevent the clomiphene from exerting any much influence at the pituitary, and that it will increase LH responsiveness to GnRH (17) where Clomiphene does not. Clomiphene is still used as it seems to offer other advantages, such as an increase in SHBG (19), which may seem like a bad thing at first, but which may decrease androgen-related negative feedback and may thus be in our advantage.
Regardless of the final outcome I feel I have settled the dispute, at least in my own head. Why bother figuring it out when we can use both, limit any negative effects and reap the proven benefits of full recovery ? I used to run tamoxifen slightly less long than clomiphene, but given the suppressive effects of the latter at the pituitary, I later decided it wiser to continue running tamoxifen as long as the clomiphene.
The addition of spironolactone is one of personal choice. It is a systemic anti-androgen that will reduce androgen-related negative feedback. Lack of androgens may also increase a loss of muscle tissue however, so whether or not you run it and for how long I leave up to you. I can only offer you personal findings, no studies. But in my experience the use of spironolactone during the first two weeks of clomiphene treatment offered a significant advantage in the amount of recovery post-cycle without any significant amount of muscle loss. But since I have no actual verifiable data on this, I will not attempt to push this too hard. The use of clomiphene alone should already aid in this by increase SHBG.
The use of HCG and the things you need to know
Human Chorionic Gonadotrophin acts as an LH analogue. That means it plays no active role in increasing hypothalamic or pituitary activity after suppression, but that it will act on LH receptors such as in the Leydig cells and activate the process of natural manufacture of testosterone and estrogen in the testes. This may counter or help quicker recovery of any testicular atrophy that may have occurred during a cycle, and since it increases the capacity to produce natural hormones, will also in the end speed up recovery because the response to increase LH will be greater.
What you do need to realize is that because it acts as LH, high doses of lengthy use will decrease receptor affinity for LH and increase negative feedback, thus countering the purpose of the post-cycle. For that reason it is not used during, but rather after the cycle, and intermittent rather than continually. Since it will also increase estrogen directly and via aromatase conversion, further shutdown may be created but this should in large part be covered by your co-administration of Tamoxifen and Clomiphene. Because of its inhibitory effects on the hypothalamic-pituitary axis, we will use it during the last part of the cycle and the weeks following, when the steroids have not yet cleared our body. And cease use several weeks prior to cessation of the Clomiphene/Tamoxifen combo so as not to let it interfere with our recovery at the hypothalamus and pituitary.
I should also inform you that practical experience has taught me that while most people respond better to the intermittent administration as described above, some have responded better to more frequent administration (ed to every three days).
Ephedrine and the point of beta-adrenergic stimulation
I have been referring to the beta-adrenergic system all throughout this article and I know a lot of you are dying to find out what the hell Iím talking about. Most of you who know the term beta-adrenergic have heard in relation to certain fat loss supplements. And that will be a key part of what we discuss here. But beta-adrenergic stimulation offers both catabolic benefits (lipolysis in adipocytes) and anabolic benefits (increased protein synthesis in muscle tissue). Naturally our high calorie diet will prohibit us from losing a great deal of fat and in most cases we may not lose any. But if we can prevent adding fat, the consequent increase in lean muscle tissue will lower our body-fat percentage favourably.
I will explain the mechanism of the beta-adrenergic system in a minute, but first we need to understand that we have beta-adrenoreceptors on fat cells, that will initiate the release of fatty acids for oxidation (fat loss) and that we also have them on muscle cells, where they will increase protein synthesis (20). That means muscular hypertrophy will be greater with adequate caloric intake while restricting fat loss. The combination should result in a lower body-fat percentage since lean body mass will increase and fat storage remains status quo.
The beta-adrenergic system in a nutshell
Imagine the end of a nerve, then a space and then a fat cell (adipocyte). The space between the nerve and the adipocyte is called the synapse or the synaptic space. The nerve stimulates the adipocyte via electrical charges (ion streams) or neurotransmitters. Among the neurotransmitters is a hormone called noradrenaline (NA). When NA is released into the synapse, it has several receptors it can bind to on the adipocyte. They are classified into two categories, alpha and beta. The alpha receptors will inhibit fat loss (or protein synthesis in the muscle cell) while the beta receptors will increase fat loss (or protein synthesis in the muscle cell).
09-13-2004, 01:22 AM #22
When a beta-receptor is engaged it will release a stimulatory G-protein into the cell, the alpha variation will release an inhibitory G-protein into the cell. These proteins will activate or deactivate the enzyme adenylate cyclase which splits ATP molecules into cyclic AMP (cAMP) molecules. cAMP is what we call the second messenger, the transporter of the signal in the cell. Without cAMP stimulation would not occur. cAMP activates the catalytic subunit of protein Kinase A, which activates Hormone sensitive Lipase (HSL) by phosphorylating it to HSL-P. HSL-P in turn will initiate a three step process by which it removes fatty acids that are bound to an alcohol function (normal storage of fat is triacylglycerides). These free fatty acids can be transported outside the cell by certain proteins and then used as fuel for the body, completing the oxidation of fat.
In muscle cells the process is similar, with stimulation, cAMP etc, but will obviously differ in the last few steps, leading to protein synthesis.
Beta agonists and the diet : losing fat AND gaining muscle ?
The main regulator of the system is insulin , which has the exact opposite effect as noradrenaline. So obviously we will have to keep insulin under control as much as possible. That will allow us to use the beta-adrenergic system to its maximum potential. Now noradrenaline has been touted as anti-catabolic, but this effect is observed because it causes protein synthesis and thus less protein is released from the cell to be burned. The effect is in other words anabolic . Which is why it may serve us as far as increasing lean muscle mass, especially since we have demonstrated effectively that testosterone and most likely boldenone will upregulate beta-adrenoreceptors. By using beta stimulators later in the cycle and post-cycle (provided adequate calories in diet) we can insure maximum muscle gain and muscle maintenance post-cycle, while keeping the fat off.
Because we need to eat a certain amount of calories to grow it is unrealistic to expect a great deal of fat loss capacity from the use of these products. But it should go a long distance in preventing the addition of further fat mass, which, combined with a significant increase in lean body mass, will decrease body-fat percentage. However, some fat loss is not unthinkable, since we are eating a high protein diet and the body will prefer the available free fatty acids, especially if we can bring them into circulation
Our first goal in this endeavour should be to have a product that stimulates noradrenaline. Now some may think it is wiser to opt for other methods of fat loss, but DNP , T3 and corticosteroids will make it increasingly difficult to preserve lean mass. Other still may profer that the use of stronger specific beta-2 or beta-3 agonists like clenbuterol , salbutamol, albuterol or octopamine should be used, but because of their potency they will quickly render the beta-adrenrgic system useless, and only make use of part of the available systems to us (either beta-2 or beta-3 instead of both). The beta-2 receptor is most certainly the prime mobilizer here, where the beta-3 only has minimal if any activity, but has been deemed crucial to continuation of cathecholamine responses under sustained sympathetic activity (21). Most likely it maintains a certain amount of beta-adrenergic stimulation, but without increasing metabolism, so as to spare calories but continue the use of fatty acids for survival. As much as 40% of the activity of ephedrine has been attributed to the beta-3 stimulatory effects (22).
Since ephedrine acts by increasing natural noradrenaline release, it serves our purpose the best. It is also the more natural approach and less taxing on our system than some other fat loss preparations (T3 causes rebound by TSH shutdown, clenbuterol is very strong in increasing heart rate, and the list goes on). As opposed to more specific beta-2 agonists such as the likes of clenbuterol, ephedrine actually seems to have improved effects on thermogenisis after continual use (23). Ephedrine Hcl is our best choice here, although some will no doubt opt for standardized preparations using ma huang. This herb, depending on preparation will contain more or less than the actual 8% ephedra from dose to dose and is hence unreliable. If this is the only thing available to you, it is better than nothing however, but pure ephedrine Hcl should be preferred.
Yohimbine is quite critical in the equation. It acts as a potent alpha-adrenoreceptor blocker (strong on alpha2, mild on alpha1). The alpha receptors inhibit adenylate cyclase activity in the cell, increase its breakdown and thus prohibit fat loss. In normal people with normal diets, there is a certain level of adrenergic action. But noradrenaline seems to have greater affinity for alpha receptors, so not enough beta receptors get filled to cause fat loss / protein synthesis. By increasing the noradrenaline release we have already filled all alpha receptors and a greater number of beta-receptors. But if we could block the alpha receptors, then that would lead not only to more potency from the existing noradrenaline / beta-latches, but it would create MORE noradrenaline / beta-latches since less NA is taken up by the alpha receptors. Thus a major strike in the right direction.
A second factor we need to consider is the alpha-2 receptor concentration on our nerve as well, which, when activated, will increase the re-uptake of noradrenaline into the nerve. By blocking this receptor we prevent re-uptake and again, more NA is available to us. So yohimbine interferes with the NAís auto-regulated negative feedback loop by acting as an alpha receptor antagonist, pre-synaptic and post-synaptic.
This is also very crucial in fat loss or prevention of fat gain in predisposed areas (abdomen and obliques in men, gluteo-femoral region in women), because these areaís have adipocytes that are extremely rich in alpha receptors, but rather poor in beta receptors (ever tried getting rid of those love handles ?).
Apart from the well-documented findings that the combination of ephedrine and caffeine far outperformed either alone (24) in terms of lipolysis, caffeine acts very distinctly as a phospho-diesterase inhibitor. PDEís are released in the cell as a response to continual beta-adrenergic stimulation and commences the breakdown of cAMP and creates adenosine from it. Adenosine travels outside the cell and has its own receptor, that acts very similarly to the alpha-receptor to block adenylate cyclase activity and stop fat loss. Caffeine has also been shown to prevent this process by blocking the adenosine receptor and seems to offer some benefit in preventing noradrenaline reuptake (25), like yohimbine does. Possibly via the same mechanism (adenosine receptor blockade).
Caffeine also decreases insulin sensitivity, further helping to assure maximal aid in preserving and enhancing the beta-adrenergic system, and possibly helping to prevent wrong doing from eventual lapses in our diet.
Lastly caffeine is a potent diuretic and will reduce water retention in the body, offering us a leaner and more striated appearance.
Forskolin is product derived from the coleus forskohlii plant that has been shown to upregulate the activity of the enzyme adenylate cyclase, which we have previously shown to be important as it creates cAMP accumulation needed for the second messenger response to beta-adrenergic stimulation. While forskolin by itself may have a null effect (it was previously used to lower blood pressure where beta-adrenergic stimulation should increase blood pressure), it should have various useful effects to us. In combination with these other products cAMP accumulation will further decrease any effect from prostaglandins and adenosine receptor stimulation, or alpha2-regulated inhibition. This allows a stable environment for second messenger transport.
Guggul sterones are an age-old ayurvedic medicine touted to increase thyroid activity. This has nothing to do with the beta-adrenergic system, and at first may seem rather obsolete. Continual fat loss and lower calorie diets have been known to cause a starvation response whereby T4 to T3 conversion is lowered and the opposite conversion increased to lower thyroid activity and thus slow metabolic rate. This occurs so that we do not use our entire fat supply in just a few days and can stay alive longer under starvation conditions. Now ephedrine has been shown to actually upgrade T4 to T3 conversion or at the very least lower the opposite reaction (23).
But this latter occurrence has been attributed to the continual alpha-receptor stimulation that ephedrine would display under normal conditions, but since we use an alpha-receptor blocker it is unlikely we will be able to make as much use of this benefit, and so the addition of Guggul is advisory, as it has been shown to increase T4 to T3 conversion (26).
Most likely, to avoid early beta-2 phosphorylation we will add yohimbine at a later stage, and should add guggul at the same time.
After HSL-P has released fatty acids they just sit there basically. They require protein transport to get them into circulation where they can be used as fuel. If not, and under the high caloric diet we have outlined this is most likely, they will simply be re-esterified again. This is why we do not expect any fat loss. But just to give nature a helping hand we might add some Acetyl-L-Carnitine (ALC), one of the proteins used to transport fatty acids. Adding too much has no use as supraphysiological amounts have shown little to no benefit, but adding some may increase any possible downregulation of the transport systems and increase the likelihood that some actual fat is used.
Putting it all together
So what sort of doses and what sort of dosing pattern do we need ? Well I wonít bore you with the details, but this particular mix has been most effective :
Product Per dose
Ephedrine Hcl 12.5 mg
Caffeine 100 mg
Yohimbine Hcl 3 mg
Forskolin 20-30 mg
Acetyl-L-Carnitine 200 mg
GuggulSterones 30 mg
You can opt to take 1 dose 6 times per day, roughly every 2.5 hours, or 2 doses 3 times per day, roughly every 5 hours. This is preferably taken between meals when it is most likely there is least insulin interference and most chance of any additional calories being burned that are not from food. For people who have a tendency to get jittery on ephedrine and are bothered by this, I suggest the first dosing pattern which has lower peak doses. For most people I would recommend the 3 a day dosing pattern however.
Use the Ephedrine/Caffeine/Forskolin/ALC combo for the full outlined twelve weeks, then add the yohimbine and guggul the last 6 weeks. For those wishing to do so, the last two weeks clenbuterol can be added to emphasize the fat loss effect.
More Dietary and supplementary Implications in regards to mass gain on-cycle and maintenance post-cycle.
It is imperative that the high-calorie diet is maintained at the very least through week 17. The chance of losing muscle when protein synthesis is kept high and no caloric deficit needs to be filled will severely decrease the chance of losing lean body mass. That goes without saying. It also goes without saying that this diet should be spread out over 5-6 meals daily in order to keep metabolism and nutrient supply high. But there are certain things we can do to enhance our chances as well.
Leptin has been hailed as the new miracle discovery in fat loss. Itís a hormone that seems to regulate the amount of fat to muscle that is burned when glycogen is not available to meet energy demands. Leptin seems to be exponentially higher in obese individuals than in leaner specimen. So being lean and staying lean, our leptin levels are not to our advantage. Leptin levels are marked by higher cAMP breakdown and greater adenosine interference. So thanks to caffeine and forskolin we can sort of inhibit the effect of our low leptin on interfering with the use of fat for fuel, but we can also implicate other measure of supplementation.
Normally I might recommend Vitamin E, which has been shown to elevate leptin levels (27) slightly. But since Vitamin E seems to lower blood clotting and this effect can be enhanced by steroid use , it is never advisory to take large amounts of vitamin E while on a steroid cycle. If you have some in your multi-vitamin, lets say no more than 30-40 units, I doubt it will be a problem, but more than that may not be safe.
That leaves only two other products proven to elevate leptin, and since nicotine (28) is highly addictive and goes against our health-conscious approach, that leaves us only with zinc (29) . The addition of the highly available zinc aspartate may offer us some benefits in keeping leptin levels higher and is worthwhile in our supplementation regimen.
This mineral is so versatile in its use to us, that it seems unlikely that I could mention it under anything other than its own paragraph. First of all it needs to be mentioned that many athletes are deficient in magnesium, and that this deficiency is hard to detect since magnesium is stored mostly in interstitial space and intracellularly (30), and not so much in blood where it is measured. Blood levels appear to be rather constant despite deficiency.
Now magnesium is necessary for proper muscle contraction (31), glycolysis (use of blood sugar, effectively lowering glycogen increasing efficiency of the beta-adrenergic system), protein synthesis, preventing cardio-vascular disease, improved cellular metabolism, and creatine storage. As such taking supplemental magnesium in a fairly large dose will be beneficial to us.
Since we recommend both the intake of zinc and magnesium, it may be wise to opt for a ZMA supplement, that contains 30 mg of chelated zinc and 450 mg of chelated magnesium. Since both can be hindered in absorption by calcium (32), and bodybuilders often eat calcium-rich foods, it is better to take them together during a time when the stomach is relatively empty (at least 60 minutes after the last meal) and without calcium present. The time of day preferentially near sleeping time as Zinc has beneficial effects in maintaining optimal testosterone levels and resting recovery, so this is the time of greatest activity.
Creatine has been the age-old supplement in bodybuilding, from high meat intake to the latest fad in creatine-enhancement supplementation. However, it appears plain old micronized creatine is still your best bet. The efficacy increase of most of these hyped up supplements is so small it in no way makes up for the price increase. Why do we recommend creatine here ? Well mostly energy supply during the late end of the cycle and the post-cycle. Glycogen will be low due to our low intake of high-GI carbs and enhanced glycolysis through supplementation. Therefore added creatine may be able to restore our ATP losses to some degree, at least for anaerobic activity like weight training, so we have ample energy at all times. By having increased magnesium intake we should be able to increase creatine storage as well. Transport of creatine into the cell will be somewhat limited in the absence of insulin, but should in no way be a problem. Considering the length of time we will use this and the minimal input we expect from it, it makes little sense to load the creatine. Taking 3 grams of creatine 45 minutes prior and again immediately after our workouts should be more than sufficient.
Vitamin B complex
Here too the benefits to be had are multiple. B-vitamins have common characteristics that include enhancing the circulation, allowing for a better oxygen supply and more energy, helps with blood formation and metabolizes carbohydrates. That means once again a valuable contribution to our goal of adding lean mass to the frame. B-vitamins are water-soluble and readily depleted, so making sure we have optimal levels on a daily basis is needed. A B-Vitamin complex that supplies a 100-1000% of the daily needed amounts is recommended.
Putting together supplementation
On workout days we will use 3 grams of creatine about 45 minutes before the workout, and again, with a post-workout protein shake (note : no weight gainers or added carbs) within 30 minutes of completing training, from week 1 through week 13.
The rest of our supplementation is taken throughout the cycle and post-cycle : 1 dose of B-vitamins with breakfast, 1 dose of ZMA on an empty stomach between before last and last meal of the day, in the absence of calcium. Last meal should be taken prior to bed.
Protein shakes should be used as deemed necessary to increase protein and/or calorie intake at any time during the day. Protein shakes are preferably a combination of casein and whey, mixed in milk.
Other worthwhile supplementation, but certainly not necessary, are dessicated liver tablets, CLA and omega-3 and 6 fatty acids to improve cholesterole profile.
The use of an anti-aromatase
Some may not be satisfied with just the lean results from using testosterone propionate , boldenone undecylenate, stanozolol and a beta-adrenergic cocktail on a low-carb, high protein diet. The aromatization from the testosterone/boldenone may still be too much to cope with. In that case an anti-aromatase drug can be added. But we should first point out that blocking the aromatization of these steroids will result in a lower HDL/LDL cholesterol ratio and thus has implications as far as cardio-vascular risk.
If an anti-aromatase product is used, I recommend proviron over femara or arimidex , eventhough the latter are stronger. Proviron is milder and does allow for some estrogen, which gives us the increased benefits mentioned under the header ďin defense of testosteroneĒ previously while still reducing over-all levels a bit which decreases water retention and visceral fat accumulation.
Now testosterone/boldenone lower subcutaneous fat primarily where the beta-adrenergic cocktail will reduce visceral fat first and then subcutaneous fat. So they are highly synergistic. By blocking the aromatase you will increase visceral fat burning because you stop estrogenís anabolic effect on visceral fat stores. I would only add Proviron if you note a tad too much water retention or if you experience signs of gynocomastia (male breast growth). Start with 25-50 mg and do not increase unless deemed absolutely necessary. At this dose you can run the proviron week 1-13, if you have to increase it, consider decreasing it again when problems desist.
What about the side-effects that will occur ?
Acute side-effects have been put into the background because they pose no threat to our health and existence per se. But since they are often visible, we still care to address them as best as we can :
When nipples get itchy or swollen and you fear gyno may begin to set in, you should use the proviron as outlined above. In the acute stage, running some 20-40 mg Nolvadex the first 3-4 days may offer relief as well. Again, any longer is not advisable since we do depend on estrogen for certain effects such as Growth Hormone increases and androgen receptor upregulation.
Hair loss via steroid use is a pre-existing genetic condition. If you do not have it all the steroids in the world wonít affect your hair. If you do have it however, then its an inevitable fact and sad to be the one to say it, but you might as well deal with it while you can still get the body to compensate for it.
I highly advise against the two standard treatments, which are the administration of either a 5-alpha-reductase blocker or an anti-androgen. That the latter is a bad idea I neednít point out. Using an anti-androgen would entirely defeat the purpose of using androgenic steroids. Among this class of drugs is spironolactone (aldactone). That the former is a bad idea may not be known to most. First of all since stanozolol is DHT derivative and boldenone has no high affinity for the 5AR, using a 5AR inhibitor would not affect these drugs. It would only stop the conversion of testosterone to DHT. Now we already mentioned the negative effects resulting from less DHT including less strength, lower neuromuscular response and increased chance of estrogenic side-effects (too much estrogen works against us because of its effects on gluconeogenisis).
So you might try topical remedies such as minoxidil hair sprays or something if you believe that sort of thing would work, but stay away from finasteride (proscar, propecia) and spironolactone (aldactone).
Liver damage is often overstated. We do use a liver taxing drug (stanozolol) so we do need to address this. Oftentimes the negative effect of oral steroids on the liver have been quoted because of elevated aminostransferase values, which are indeed a partial indicator for liver damage. However these levels will rise as a result of muscular damage from training as well and offer us no conclusion as to the actual negative effect. For that purpose it is essential that when you have bloodwork done, you ask the doctor to check creatine kinase and CGT levels as well. If the former is higher than normal and the latter remains unchanged then no liver damage has occurred. If the opposite is true and CK is normal and CGT is elevated, then liver damage has occurred.
If it does occur then the use of milk thistle (sylibum marianum) or Picrorohiza (33) is recommended. Both appear to have a good effect on liver regeneration. Because some of the activities of these products may be mediated by enhancing cytochrome P-450 activity, it Is not recommended that you take them as a precautionary measure. Instead, have blood levels checked for the aforementioned values once every 3 weeks while taking stanozolol and if deemed necessary, add them to your supplementation regimen
Loss of Libido
Since we use testosterone as a base, this will not be problem. Additional use of proviron would further stimulate libido, so it is actually possible your libido may be phenomenally higher than normal.
Get over yourself, these are zits, they pose no threat to your health. Proper skin care and OTC medication can be used if it makes you feel better, but avoid the use of prescription medication like anti-biotics and accutane at all costs, as these products are far more taxing on your liver than stanozolol. So in the interest of your health prescription medication for acne is not advisable.
If you get acne so bad that it really ruins your life : DONíT USE STEROIDS !!!!
If you are a a man : who cares ?
If you are a woman : DONíT USE STEROIDS !!!!
No link between steroids and prostate cancer has ever been demonstrated, however with age a condition known as benign prostate hypertrophy can occur. Since we previously determined estrogen to be the causative factor and that androgens can actually be used as therapy to counter BPH, adding proviron at 50 mg/day should limit your risk of this. If you already have BPH or other prostate problems : DONíT USE STEROIDS !!!!
Appendix : Working with your doctor
As we mentioned before, steroid use should occur under medical supervision. With this document you are capable of interpreting a lot of data. So this may be a good time to point out what sort of data you will need from your doctor. I would advise, as I do to all my athletes, that you have blood work done every 3 weeks while on and several weeks after the cycle, starting with the week before the cycle. The following data should be collected :
Supression and recovery are examined based on levels of LH, FSH, DHEA, androstenedione and testosterone. During the cycle blood levels of testosterone and androstenedione should rise, as other decline and post-cycle a reverse tendency should be noted.
Liver damage is based on aminotransferase values (ALT, AST) as well as Creatine Kinase (CK) and gamma-glutamyltransferase (CGT). When CGT is elevated we can speak of liver damage. If it is significantly elevated use of milk thistle and cessation of use for stanozolol is recommended. If CGT is not elevated, CK levels may explain why ALT and AST are elevated.
Thyroid activity is measured with levels of TSH, T4 and T3. TSH levels should not be affected at any time during this cycle since no exogenous thyroid hormone is used. The amount of T4 and T3 are crucial as both steroid use and yohimbine use will suppress T4 to T3 conversion, and guggul should counter that to some extent. This is why it may be wise to keep an eye on this as well. It canít hurt and if you are having blood checked anyway, canít see why you wouldnít have this checked
Lastly, cholesterol values. Total cholesterol and HDL/LDL ratio should be examined. During the cycle HDL/LDL-ratio should remain normal and total cholesterol should lower, unless you are using proviron, then HDL/LDL ratio may drop. After the cycle and complete recovery, values should restore themselves.
Peter "Big Cat" van Mol
09-13-2004, 01:24 AM #23
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Modulation of the cytosolic androgen receptor in striated muscle by sex steroids . Rance, Max. Endocrinol 115 (1984) 862-6
Foster BA, Cunha GR. Efficacy of various natural and synthetic androgens to induce ductal branching morphogenesis in the developing anterior rat prostate.
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Zmuda JM, Cauley JA, Kriska A, et al. Longitudinal relationship between endogenous testosterone and cardiovascular disease risk-factors in middle-aged men. Am J Epidemiol 1997; 146(8): 609-617 (13-year follow-up of former Multiple Risk Factor intervention Trial participants)
Diekerman RD, McConathy WJ, Zachariah NY. Testosterone , sex-hormone binding globuline, lipo-proteins and vascular disease risk. J Cardiovasc Risk 1997; 4(5-6): 363-366
Moffat SD, Zonderman AB, Metter EJ, Blackman MR, Harman SM, Resnick SM. Testosterone Supplementation Therapy for Older Men: Potential Benefits and Risks.J Am Geriatr Soc. 2003 Jan;51(1):101-115.
Schanzer, Donike , metabolism of boldenone in man : gas chromatographic/mass spectrometric identification of urinary excreted metabolites and determination of excretion rates, Bol Mass Spec 21, 1992, 3-16
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09-13-2004, 01:26 AM #24
Here is another article you may be able to use. I have no idea who wrote this one.
Nandrolone Decanoate (Deca Durabolin ) and Bone Density
A number of studies show that anabolic steroids can increase bone density.
The studies below showed that nandrolone decanoate does.
Nandrolone decanoate for men with osteoporosis.Hamdy RC, Moore SW, Whalen KE,
Landy C.Am J Ther. 1998 Mar;5(2):89-95.
To compare the efficacy and safety of nandrolone decanoate
and calcium (NDC) with those of calcium alone (CAL) in men with
idiopathic osteoporosis, a 12-month, randomized, prospective, controlled
study, was performed in an outpatient clinic. Twenty-one men with idiopathic
osteoporosis (as determined by radiological and dual energy x-ray
absorptiometry findings) were randomly allocated to either 50 mg nandrolone
decanoate intramuscularly (im) weekly and 1,000 mg oral calcium carbonate
daily (NDC group) or to 1,000 mg oral calcium carbonate daily (CAL group).
Bone densitometry (total body, left femur, and lumbar spine), serum, and
urine biochemical parameters were measured at 3-month intervals. In the NDC
group, bone mineral density initially increased, reached a plateau, and then
decreased to near baseline levels at 12 months. Increases in lean muscle mass
mirrored these changes. Free and total testosterone significantly decreased.
Hemoglobin increased in all patients in this group. Patients in the CAL group
exhibited no significant change in either total body or bone mineral density
or biochemical parameters. Thus, nandrolone decanoate, 50 mg im weekly,
transiently increases the bone mass of men with idiopathic osteoporosis in
this preliminary study. Careful monitoring is necessary.
Effects of nandrolone decanoate on bone mass in established osteoporosis.
Passeri M, Pedrazzoni M, Pioli G, Butturini L, Ruys AH, Cortenraad MG.
Maturitas. 1993 Nov;17(3):211-9.
A double-blind, randomized, placebo-controlled study was conducted in 46
postmenopausal women with established osteoporosis in order to assess the
long-term effects of nandrolone decanoate on the bone mineral density (BMD)
of the lumbar vertebrae and of the distal third of the radius and on the
biochemical markers of bone turnover. The patients received intramuscular
injections of placebo or 50 mg nandrolone decanoate every 3 weeks for 18
months. Thirty-two of the initial 46 patients completed 1 year of study and
25 completed the whole study period of 18 months. Overall, vertebral BMD
increased by 2.9% in the nandrolone decanoate group and fell by 2.3% in the
placebo group. Radial BMD showed a slight but transient improvement, with a
subsequent return to basal levels in the nandrolone decanoate group, whereas
there was a progressive decrease in the placebo group. Patients treated with
nandrolone decanoate also complained less of bone pain. Urinary
hydroxyproline decreased significantly in treated patients, whereas
osteocalcin tended to increase, but the change was not significant. HDL
cholesterol concentrations decreased only slightly and haemoglobin increased
significantly in the nandrolone decanoate group. Two patients treated with
nandrolone decanoate withdrew from the study because of hirsutism and
hoarseness. The results indicate that nandrolone decanoate exerts positive
effects on vertebral BMD and on bone pain in patients with established
Effects of nandrolone decanoate therapy on bone mass and calcium metabolism
in women with established post-menopausal osteoporosis: a double-blind
placebo-controlled study.Gennari C, AgnusDei D, Gonnelli S, Nardi P.Maturitas.
In many patients with involutional osteoporosis anabolic steroids may
produce a rapid subjective improvement and a pronounced reduction in the
frequency of complaints. Animal experiments have demonstrated that anabolic
steroids can also have an objective effect on bone tissue. Twenty (20) post-
menopausal osteoporotic patients were randomly assigned to 2 different treatment
regimens; 10 patients were treated with 50 mg i.m. of nandrolone decanoate
(ND) every 3 wk for 12 mth and 10 patients were treated with a placebo. Both
groups also received an oral calcium supplement (1 g/day). Bone mineral
content (BMC) was measured by dual photon absorptiometry before and after 1,
3, 6 and 12 mth of treatment. Plasma alkaline phosphatase (ALP) and urinary
hydroxyproline excretion were measured at the same time. Intestinal calcium
absorption was measured by the 47Ca oral test before and after treatment. A
transiliac bone biopsy was performed before and after treatment in 4 patients
in each group. After 1 yr there was a significant increase in lumbar spine
BMC in the group receiving calcium plus ND. A progressive increase in plasma
ALP was also observed in the group treated with ND but this was not
significant, whereas radiocalcium absorption did increase significantly in
this group. Histomorphometric study of bone samples demonstrated a
significant increase in trabecular bone volume (TBV) and in active osteoid
surface area in the patients treated with ND. Because plasma ALP tends to
increase when a small decrease in bone resorption occurs (as measured by
urinary hydroxyproline excretion) and the active osteoid surfaces also
significant augment, we concluded that ND therapy increases the bone
formation rate through inhibition of bone resorption. This interpretation
could explain the considerable increase in lumbar spine BMC and the
significant increase in TBV observed in patients treated with ND.
09-14-2004, 06:12 PM #25New Member
- Join Date
- Sep 2004
Awesome Anhydro. I only skimmed all that so far, but it looks great and I can't wait to use it. Thanks a lot. You really went above and beyond and I appreciate it a lot.
10-20-2004, 02:22 PM #26
. The withdrawl symptoms of alcohol can and will kill you. Those of heroin WILL NOT kill you even though you feel like youre going to die.
Withdrawal from alcohol can not kill you. FACT
10-20-2004, 03:22 PM #27Associate Member
- Join Date
- Nov 2003
"anyways heres the Bullsh!t. It reminds me of The Cops in the D.A.R.E. program telling all the kids Weed will kill you, or it is a gateway drug"
weed is a gateway drug
03-22-2005, 02:40 PM #28New Member
- Join Date
- Mar 2005
Info spotsOriginally Posted by BrianTKessler
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