A long time ago, in a galaxy far far away (on-line issue #18 to be precise), T-mag ran an article called "Steroids for Health." The idea behind the article was sound and quite revolutionary at the time: steroids, when used safely and sanely, will not adversely affect your health; in fact, they may even be healthy.
The idea made a lot of sense, but unfortunately, the author didn't know very much about steroids. Some of the info was incorrect. Still, the concept was a good one and the premise remains true: steroids, like all other drugs, can be used in either a healthful or hurtful manner.
Given the numerous myths, misconceptions and outright propaganda spewed out by the media lately, we thought it was time to update and revise the steroids for health concept. This time we tasked a real steroid expert with the job, T-mag columnist and graduate level pharmacy student, Cy Willson.
The Facts They Don't Want You to Know
There's a potentially dangerous drug out there of which you should be made aware. It can cause damage to the gastrointestinal system (gastric mucosal bleeding) and lead to ulcers even when used at very low dosages. This drug was implicated in death by medical examiners 101 times in 1998 and led to 12,815 hospital visits in that same year. In short, this stuff could kill you... and you probably have some in your medicine cabinet right now! The name of this potential killer? Aspirin.
Armed with this knowledge, it's easy to see why politicians are doing their best to ban this dangerous drug. After all, they must protect Americans from themselves, 'cause we ain't smart enough to know that taking a whole bottle of aspirin at one time is bad for us. Sure, aspirin can be an effective pain reliever when used wisely, but our politicians know best and that's why they're banning this murderous drug.
What's that? You mean they're not trying to remove aspirin from the shelves and make it a prescription-only drug? That's odd, because they're trying their best to ban ephedrine and prohormones, both of which can be argued as being as safe, if not safer, than aspirin. And steroids? Why, those "nasty" drugs were given the boot a long time ago.
The irony is obvious. When used in a safe manner, steroids like Testosterone have been shown to increase muscle, decrease fat, and counteract many of the effects of aging. Used intelligently, Testosterone has been shown to have no effect on prostate or cholesterol levels.
And what about "roid rage"? Well, in a double blind, placebo controlled study, 43 normal men (age 19-40) were given 600mg/week of this drug and evaluated for ten weeks. It was concluded that Testosterone had no effect on aggressive behavior in normal men, yet "roid rage" is one of the main scare tactics used by doctors and others to dissuade steroid usage. (29)
But steroids can kill you, right? Well, according to the DAWN (Drug Alert Warning Network) medical examiner data from 1998, Testosterone wasn't implicated in a single death during that year. Not even one. Similarly, according to the DAWN detailed emergency department tables of 1999, there wasn't even one mention or episode for hospital visits caused by Testosterone use. In short, it's practically impossible to overdose on steroids, making them safer, in that regard, than most of the drugs in your bathroom cabinet.
Yet despite all of this, steroids are put into the same category as crack cocaine in the minds of most people, the very same people who pop aspirin tablets like breath mints.
Steroids for Health: The Real Story
It's quite obvious to anyone with an inkling of steroidal knowledge that these drugs can be used in a safe and healthful manner. Are there side effects and can you screw up your health with steroids? Sure, just like with any other drug. But used wisely and not abused, these side effects can be circumvented or at least lessened.
I'm going to give you a way to use anabolic steroids in a rather safe manner, while retaining a high percentage of the gains you make upon cessation of use. Aside from that, I'm going to give the reasons and mechanisms involved in determining cycle length, androgens to be used, etc. And, I'll even give you some reasons why I think using steroids can actually make you healthier!
Let's begin by clearing up some misconceptions proliferated by the original "Steroids for Health" article. First, the idea that androgens manufactured for "veterinary use" aren't effective in humans is completely false. A molecule of nandrolone or stanozolol (Winstrol) works in humans just as it does in animals. The label has nothing to do with whether it's effective in humans or animals. The molecules are exactly the same. Nothing is different except the label (assuming, of course, you're using a legit and high quality "vet" drug).
Second, many seem to think that using weak cycles for short periods of time allows them to retain gains because they're only building a little muscle at a time. They use a La Chatelier-like principle to explain why only certain androgens allow a better retention of muscle after a cycle is over and others don't. Essentially, their thoughts are that since you gain too much muscle with a certain drug, your body strives to reach equilibrium. Then your body just magically "loses" these gains because it's too "heavy" on the body.
Um, that's taking things too far and, honestly, sounds like a fourth grader's reasoning skills.
Drugs like Primobolan do tend to allow you to keep gains more so than others, but the reasons don't have much to do with "striving to reach equilibrium" and more to do with physiology and endocrinology. True, the body does have a response mechanism in cases where you cause an imbalance, but this can't be applied to every situation. (Other "leftover" ideas from the 1970's include letting your receptors "refreshen" or whatever, when evidence points to them actually up-regulating.)
So, you ask, why is it that a drug like Primobolan (methenolone) allows you to retain gains after a cycle? Is it because of the various reasons above? Of course not. It's simply a matter of endocrinology and physiology. We must first understand the real reasons why we lose gains after a cycle.
There are three key determinants of whether or not you keep a good portion of your gains after coming off a steroid cycle:
1) The degree of inhibition of your endogenous Testosterone production or effect on the HPTA [hypothalamic pituitary testicular axis].
2) The amount of water retention or edema caused by the drug during usage. (Some people think they're losing muscle after a cycle, when much of it could be water loss, depending on the steroids used.)
3) Whether the drug causes simple hypertrophy of skeletal muscle or the activation of satellite cells, leading to the formation of new muscle fibers. (This last one isn't totally solid, but there's evidence supporting it.) (1,2)
I suppose I should actually say there are four determinants, the last consisting of finding something which will match or come close to matching the nutrient partitioning effects of androgens while returning endogenous Testosterone production to baseline levels. The ability to do this while also allowing for endogenous Testosterone production to return is very important. More on that later.
The first thing we should consider is cycle length. In the past, three week cycles have been recommended for safety. I think three weeks is being too conservative. I'd instead suggest five to six-week cycles with five to six weeks off following cessation of use.
Now, even with five to six-week cycles, I'm being rather cautious but not overly so, as it's been demonstrated that using Anadrol at even 100 mg daily in normal men didn't cause any significant alterations. (3) Those in the study used 50 to 100 mg of oxymetholone daily for twelve weeks and saw no significantly adverse side effects. Liver function (which I think is blown totally out of proportion) was fine.
One thing that confuses me is the fact that people consume various hepatotoxic (liver damaging) drugs like acetominophen, antibiotics, and last but not least, alcohol, and yet never give it a second thought. If you really want to upset me, sit in front of me with a beer in one hand, and wash your acetominophen (Tylenol) down with it, all the while saying, "I don't know about those orals, dude; they're hard on your liver." Oh, the irony!
Speaking of hepatotoxicity, I think I should pass along some info in that regard. One study addressed the fact that aminotransferase levels can rise when muscle tissue is damaged (exercise accomplishes this) and thus give a false indicator that the person is experiencing hepatoxicity. (4) Another study essentially demonstrated how widespread the lack of information is in terms of physicians differentiating hepatotoxicity from muscle damage induced from exercise. Here's the abstract:
The use of anabolic steroids among competitive athletes, particularly bodybuilders, is widespread. Numerous reports have noted "hepatic" dysfunction secondary to anabolic steroid use based on elevated serum aminotransferase levels. The authors' objective was to assess whether primary care physicians accurately distinguish between anabolic steroid-induced hepatotoxicity and serum aminotransferase elevations that are secondary to acute rhabdomyolysis resulting from intense resistance training.
Surveys were sent to physicians listed as practicing family medicine or sports medicine in the yellow pages of seven metropolitan areas. Physicians were asked to provide a differential diagnosis for a 28 year old, anabolic steroid-using male bodybuilder with an abnormal serum chemistry profile. The blood chemistries showed elevated aspartate aminotransferase (AST), alanine aminotransferase (ALT), and creatine kinase (CK) levels, and normal gamma-glutamyltransferase (GGT) levels.
In the physician survey (n = 84 responses), 56% failed to mention muscle damage or muscle disease as a potential diagnosis, despite the markedly elevated CK level of the patient. Sixty-three percent indicated liver disease as their primary diagnosis despite normal GGT levels.
Prior reports of anabolic steroid-induced hepatotoxicity that were based on aminotransferase elevations may have overstated the role of anabolic steroids. Correspondingly, the medical community may have been led to emphasize anabolic steroid-induced hepatotoxicity and disregard muscle damage when interpreting elevated aminotransferase levels. Therefore, when evaluating enzyme elevations in patients who use anabolic steroids, physicians should consider the CK and GGT levels as essential elements in distinguishing muscle damage from liver damage. (5)
So, keep in mind that even the supposed "liver destroyer" we call Anadrol is actually rather safe to use up to twelve weeks. Aside from that, even if aminotransferase levels had risen, it doesn't necessarily mean they were experiencing any liver toxicity.
There are also studies using 10 mg of oxandrolone daily for twelve week periods where no significant side effects were seen, with the exception of a decrease in HDL. Also, 600 mg/week of Testosterone enanthate for ten and twenty weeks has shown no significantly adverse side effects in normal men. Essentially, it's obvious that the side effects with anabolic steroids are blown completely out of proportion and can only be applied with long-term use. (6-8)
I'm not suggesting that you shouldn't pick an ultra safe cycle which consists of androgens which aren't 17-AA (the ones most often implicated in true liver damage) and which aren't as bad in terms of altering blood lipids, so with that said I'm going to give two options.
The first is a standard cycle which is fine for anyone; the second is for those who wish to be "ultra safe." These would be the same people who are scared to death they'll be screened for anabolic steroids, yet aren't athletes. They're also the same people who drive around in their cars with football helmets on their heads. (Kidding, only kidding.)
Along those same lines, I'm going to essentially "weed out" various androgens according to their ability to suppress LH and endogenous Testosterone. First, we need to consider how androgens are able to suppress endogenous Testosterone levels. As I explained in my Never Ending Cycle article, the main two mechanisms are via the androgen receptor (AR) and the estrogen receptor (ER). However, two other factors that can play a role, depending on the particular androgen, are the PR (Progesterone Receptor) and whether the androgen inhibits Testosterone production at the testicular level.
Nandrolone decanoate is one androgen which can suppress LH via more than one mechanism. It has the ability to interact with the PR in addition to its avid binding to the AR. While there's some evidence supporting the idea that it affects Testosterone production at the testicular level, the decrease in LH seen in various studies indicates that this probably isn't the case. This is essentially why deca is such a suppressive androgen in terms of endogenous Testosterone production. (9-11)
Obviously, we can't use androgens that bind extremely well to the AR, aromatize to estradiol, or inhibit Testosterone production at the testicular level, as this too will cause suppression. Essentially, the only androgen which I can say without a doubt inhibits endogenous Testosterone production at the testicular level is fluoxymesterone. This is simply because studies have demonstrated a reduction of Testosterone without any concurrent reduction or suppression of LH levels.
So, that leaves us with essentially two androgens for our "ultra safe" cycle, and those would be methenolone and 4-AD. The reason for this is that we ideally want an androgen that doesn't aromatize or is 17-AA, yet is able to bind well to the AR, yet not too well. Methenolone has been shown to bind less avidly than nandrolone (but more so than Testosterone), doesn't aromatize, and isn't 17-AA, nor is it thought to affect endogenous Testosterone production at the testicular level. It obviously fits the bill.
4-AD is thought to work via non-AR mediated mechanisms, and thus should also be used. It too doesn't aromatize nor is it 17-AA or thought to affect endogenous Testosterone production at the testicular level.
Both androgens also have quite a bit of anecdotal evidence supporting their lack of suppression upon LH secretion. However, if you wish to go with just a "safe" cycle instead of the aforementioned "ultra safe" cycle, then we can use any one, two, or three of the following steroids for five or six weeks. Simply pick and choose. (12-14) (I've chosen to group them simply for informational purposes.)
Binds Avidly to AR
Does Not Bind Well to AR
Binds to Microsomal AR
Considering that you'll be "on" for five to six weeks, I suggest the following dosing regimen:
Pick any combination of androgens you feel comfortable with (choosing at least two). For instance, you could choose methandrostenolone and Testosterone for one cycle. A common rule of thumb is to use 400-500 mg/week of any androgen that you choose.
You could stack 400-500 mg of nandrolone and 400-500 mg of Testosterone to take advantage of each androgen's ability to alter IGF-1 or IGF-BP and thus allow for rather high levels of bioavailable or "free" IGF-1. In other words, Testosterone will increase IGF-1 levels, while nandrolone reduces IGF-BP levels and thus allows for more "active" or "free" IGF-1 to be available for action. Of course, that may be getting a whole lot more technical than you want.
Anyhow, in addition to nandrolone and Testosterone, one could add in 400-500 mg of stanozolol since it seems to be the only androgen, aside from danazol, which can bind to microsomal AR. This seems like a rather large dosing regimen, but remember, you're only going to be doing this for a few short weeks.
What I do want to emphasize is that you should always pick at least two androgens to use for a cycle.(15-17)
End of Cycle Concerns
When it comes to maintaining gains, what you do at the end of your cycle is most crucial. First, we have to find a way to restore endogenous Testosterone production while fighting the catabolic effects of being in a hypogonadal state (which is the end result of sudden cessation of steroids).
It's been demonstrated in normal, healthy young men that suppression of endogenous Testosterone production leads to a marked decrease in muscle mass and an increase in fat mass, and this is the reason why we experience the "loss of gains" after cessation of use in addition to the "shitty" feeling in general. It has nothing to do with the body having a mind of its own and dictating exactly how much muscle mass it will and will not allow you to have. (18)
So, what do we do? Simple, we must first get T levels up to normal, while at the same time not suppressing endogenous Testosterone production. How can this be accomplished? Well, the best choice is Androgel since its pharmacokinetic properties allow for an increase in Testosterone yet no suppression of LH and endogenous Testosterone production.
The next best thing would be to use around 100 mg of Testosterone enanthate weekly as the peak seen is still very close to remaining within the physiological range. (19) In addition to this, you should be taking 50 to 100 mg/day of clomiphene so that you can restore endogenous Testosterone production quickly and thus wean yourself off of the Androgel.
While that will take care of steroid-induced low endogenous Testosterone levels, you'll still lose some muscle. After all, you weren't simply in normal physiological state while using androgens. We've lost the great nutrient-partitioning effects of androgens and thus need to make some quick adjustments.
Here's one way to think about it: If you were to be ranked on a 1-10 scale in terms of lipolysis and protein synthesis, 5 would be your average physiological state, 3 would be when you're hypogonadal (post cycle), and anything in the 6-10 range would be where you're at when using supraphysiological doses of Testosterone or other androgens. So, using Androgel and clomiphene will ensure that we at least get back to a 5 and thus minimize loss of gains, but the next step is necessary in order to keep us at a higher range and thus further minimize loss of gains.
We need to pick some compounds which also have nutrient partitioning effects yet don't affect hormonal levels. Biotest's Methoxy-7 and a beta-2 agonist like ephedrine are the perfect combination. Both compounds will allow for an increase in nitrogen retention, as well as an increase in lipolysis and/or inhibition of lipogenesis.
When these two compounds are added in, we're much closer to the range in which our gains were made and thus, we greatly minimize or completely prevent any loss of gains and prevent any fat gain. Similarly, you could also use forksolin along with Methoxy-7 and leave the ephedrine out. (20-23)
Okay, so how is all this healthy?
The entire premise behind occasionally using anabolic steroids is to accomplish permanent changes in body composition. Don't get me wrong, I'm not saying that this is easy or that it's simply a matter of using, then going off and resuming your lifestyle filled with terrible foods and little exercise. Instead, I'm talking about following a cycling pattern similar to what I've described above. By utilizing such a program, you'll be able to retain muscle as well as prevent body fat accumulation after you're finished using androgens.
Just to be sure we're on the same page here, you need to understand that we may have permanent gains in muscle mass due to satellite cell activation and consequently the formation of new muscle tissue. Aside from that, as I explained previously in the article, the majority of hypertrophic gains are lost due to a hypogonadal state upon cessation of use, as well as the loss of a nutrient partitioning compound. Well, that's now solved by using the plan I outlined above.
As for fat mass, the same thing applies. With newly accrued muscle mass, we're expending more energy at all times and thus it's easier to maintain a lower body fat percentage. Also, as I said before, the gain in fat mass at the end of a cycle is also due to a hypogonadal state and, to a lesser extent, the loss of a nutrient partitioning agent.
How does all this relate to good health? As we all know, the benefits of having more lean-body mass and less fat mass goes well beyond the aesthetic changes. Having more muscle mass and less body fat can lower your LDL, increase HDL, decrease triglycerides in addition to blood pressure, and even improve glycemic control, which results from an improvement of insulin sensitivity. It may also improve your sleep and mood, and you'll likely even feel more energetic!
Obviously, these changes will essentially lower your risk of developing heart disease, diabetes, hypertension, hyperlipidaemia, stroke, and even some major cancers. (24-26,10) Now, I'm not saying that you'll be "immune" to all metabolic diseases, but you'll have a much lower risk of developing them. Also, keep in mind that if you follow the normal aging pattern, you'll likely lose muscle and gain fat as you get older, thus increasing your chances of experiencing one of the above diseases or disorders. With the judicious use of androgens, we can prevent such a thing from occurring.
In general, you can expect to live a longer, happier life.
1) Kadi F, et al. "Effects of anabolic steroids on the muscle cells of stength-trained athletes." Med Sci Sports Exerc 1999 Nov;31(11):1528-34
2) Nnodim JO. "Testosterone mediates satellite cell activation in denervated rat levator ani muscle." Anat Rec 2001 May 1;263(1):19-24
3) Schroeder ET, et al. "Effects of an Oral Androgen on Muscle and Metabolism in Older, Community Dwelling Men." Am J Physiol Endocrinol Metab 2002 Sep 24; [epub ahead of print]
4) Dickerman RD, et al. "Anabolic steroid-induced hepatotoxicity: is it overstated?" Clin J Sport Med 1999 Jan;9(1):34-9
5) Pertusi R, Dickerman RD, McConathy WJ. "Evaluation of aminotransferase elevations in a bodybuilder using anabolic steroids: hepatitis or rhabdomyolysis?" J Am Osteopath Assoc 2001 Jul;101(7):391-4
6) Lovejoy JC, et al. "Oral anabolic steroid treatment, but not parenteral androgen treatment, decreases abdominal fat in obese, older men." Int J Obes Relat Metab Disord 1995 Sep;19(9):614-24
7) Bhasin S, et al. "The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men." N Engl J Med 1996 Jul 4;335(1):1-7
8) Bhasin S, et al. "Testosterone dose-response relationships in healthy young men." Am J Physiol Endocrinol Metab 2001 Dec;281(6):E1172-81
9) Couzinet B, et al. "The antigonadotropic activity of a 19-nor-progesterone derivative is exerted both at the hypothalamic and pituitary levels in women." J Clin Endocrinol Metab 1999 Nov;84(11):4191-6
10) Friedl KE, et al. "The administration of pharmacological doses of testosterone or 19-nortestosterone to normal men is not associated with increased insulin secretion or impaired glucose tolerance." J Clin Endocrinol Metab 1989 May;68(5):971-5
11) Reel JR, et al. "Competitive progesterone antagonists: receptor binding and biologic activity of testosterone and 19-nortestosterone derivatives." Fertil Steril 1979 May;31(5):552-61
12) Sawin CT, et al. "Effect of chronic administration of estrogen, androgen, or both on serum levels of gonadotropins in adult men." J Clin Endocrinol Metab 1978 Jun;46(6):911-5
13) Jones TM, et al. "The effects of fluoxymesterone administration on testicular function." J Clin Endocrinol Metab 1977 Jan;44(1):121-9
14) Hobbs CJ, et al. "Testosterone administration increases insulin-like growth factor-I levels in normal men." J Clin Endocrinol Metab. 1993 Sep;77(3):776-9
15) Steinsapir J, Muldoon TG. "Role of microsomal receptors in steroid hormone action." Steroids 1991 Feb;56(2):66-71
16) Boada LD, et al. "Identification of a specific binding site for the anabolic steroid stanozolol in male rat liver microsomes." J Pharmacol Exp Their 1996 Dec;279(3):1123-9
17) Saartok T, Dahlberg E, Gustafsson JA. "Relative binding affinity of anabolic-androgenic steroids: comparison of the binding to the androgen receptors in skeletal muscle and in prostate, as well as to sex hormone-binding globulin." Endocrinology 1984 Jun;114(6):2100-6
18) Mauras N, et al. "Testosterone deficiency in young men: marked alterations in whole body protein kinetics, strength, and adiposity." J Clin Endocrinol Metab 1998 Jun;83(6):1886-92
19) Sokol RZ, Palacios A, Campfield LA, et al. "Comparison of the kinetics of injectable testosterone in eugonadal and hypogonadal men." Fertil Steril 1982;37:425-430
20) Perez-Llamas F, Zamora S. "Influence of clenbuterol on the protein digestibility and on nitrogen balance in rats." Comp Biochem Physiol Comp Physiol 1992 Mar;101(3):619-23
21) Pasquali R, et al. "Effects of chronic administration of ephedrine during very-low-calorie diets on energy expenditure, protein metabolism and hormone levels in obese subjects." Clin Sci (Lond) 1992 Jan;82(1):85-92
22) Astrup A, et al. "Pharmacology of thermogenic drugs." Am J Clin Nutr 1992 Jan;55(1 Suppl):246S-248S
23) Medicine in Science Sports and Exercise 2001;33(5 Suppl): (2421)
24) Lean ME, et al. "Pathophysiology of obesity." Proc Nutr Soc 2000 Aug;59(3):331-6
25) Pasanisi F, et al. "Benefits of sustained moderate weight loss in obesity." Nutr Metab Cardiovasc Dis 2001 Dec;11(6):401-6
26) Muscelli E, et al. "Metabolic and cardiovascular assessment in moderate obesity: effect of weight loss." J Clin Endocrinol Metab 1997 Sep;82(9):2937-43
27) Lovejoy JC, et al. "Exogenous androgens influence body composition and regional body fat distribution in obese postmenopausal women – a clinical research center study." J Clin Endocrinol Metab 1996 Jun;81(6):2198-203
28) Marin P. "Testosterone and regional fat distribution." Obes Res 1995 Nov;3 Suppl 4:609S-612S
29) Tricker R, et al. "The effects of supraphysiological doses of testosterone on angry behavior in healthy eugonadal men – a clinical research center study." J Clin Endocrinol Metab 1996 Oct;81(10):3754-8