Article Index

Written by Daniel Gwartney, M.D.
03 May 2018


Anabolic Steroids - What is the Right Dose?



One axiom ruled bodybuilding for decades as the elite explored the physiologic limits of growth: “More is better!” This can be naively applied to training volume, intensity or protein intake; frankly, the message most often refers to anabolic-androgenic steroids (AAS). The late Steve Michalik— 1970s bodybuilding legend who ran Mr. America’s Gym in Farmingdale, New York— reportedly had a sign prominently displayed that stated, “Message Of The Day: Up The Dosage!” above the image of a syringe.1


There was a gradual increase in AAS experimentation from the early days of the 1950s, when East Coast powerlifters followed the lead of Russian and East European Olympic lifters by ingesting tentative doses of methandrostenolone (Dianabol); West Coast bodybuilders were similarly developing physiques previously unseen at that time on Nilevar.2,3 Of course, many of the early misusers of AAS exceeded the suggested dosing proposed by individuals such as Dr. John Ziegler, who promoted the use of Dianabol among men training at the York Barbell Club in the 1950s and 1960.2 Both Ziegler and Michalik later voiced regret about their role in advocating AAS misuse.2,4


A Plethora of AAS

During the 1960s, a plethora of AAS were developed by some of the leading pharmaceutical companies. The hunt was on to find analogs (testosterone-derived drugs) that would provide increases in muscle mass without the side effects related to androgenic or estrogenic overstimulation (e.g., prostate enlargement, hair loss, gynecomastia, etc.). There was also a need to develop AAS that were not dependent upon 17-alpha alkylation, as that chemical modification induces hepatotoxic (liver damaging) effects in a large percentage of people. A number of agents were developed, some making it to market. Few remain available today for use in humans, as opposed to veterinary applications or simply being abandoned. Many readers are familiar with Anavar (oxandrolone), Winstrol (stanozolol) and Anadrol-50 (oxymetholone).


These AAS allowed men to use higher doses, combine drugs in stacks that complemented size and strength gains from aromatizable AAS with non-aromatizable AAS that increase vascularity and definition, or follow a bulking cycle with a cutting cycle with little or no break between. This led to increased size and definition among bodybuilders, such as that displayed by Arnold and his contemporaries. During the mid-1970s, definition became the focus of competitors, as more defined physiques such as Frank Zane gained favor with judges and the public. This temporarily limited the use of the AAS with greater size promotion, as they often held the undesirable effect of water retention, and potentially gynecomastia. Pre-contest cycles were highly dependent upon DHT-derived AAS, as they are protected from being aromatized. Parabolan, Primobolan, Winstrol, Anavar and Finaject were the most sought-after drugs by bodybuilders entering competition, though many still maintained a base of testosterone or nandrolone. The days of “Deca and D-bol” winning one a major title were gone.


Size Over Symmetry and Condition

Fans of the sport watched the images of professional bodybuilders grow on the covers of the magazine throughout the 1980s, until a sudden shift occurred. Like a glitch in the matrix, a near-overnight gap arose in the previously linear trend of bodybuilder size. This has been collected and presented on websites featuring photographs of bodybuilders, showing that up to the early 1990s, bodybuilders had been very gradually growing in size, from a BMI of just less than 31 to a BMI of just less than 32 over the course of almost 40 years.6 Then, a disjointed leap occurred, with the BMI magically (or chemically) going from less than 32 to well over 34, and continuing to increase at an accelerated rate to a BMI of almost 38— that is the average BMI! Some competitors are recorded above a BMI of 41 in show condition.


This huge, and it is HUGE, increase did not occur because someone discovered that syringes come in 10 cc volume, or the testosterone molecule was tweaked in an alchemical way, or even the accidental dripping of radioactive spider saliva into the vat at the pharmaceutical plant (Spider-Man reference). This new generation of bodybuilder was developed under the influence of the widespread use of peptide growth factors, including insulin, human growth hormone (hGH) and IGF-1.


It is worth noting that hGH and insulin were reported to have been used prior to the early 1990s, however, much like AAS, the limited access and absence of practical experience among bodybuilders kept the use of these hormones confined to a small number of men, likely using the drugs in limited amount and/or duration.


Insulin and hGH

The advent of recombinant technology opened the floodgates on the supply of insulin and hGH. Prior to the development of this technology, using bacteria to synthesize human hormones by inserting copies of DNA strands into the bacteria and stimulating production, insulin was often sourced from cows or pigs; hGH supply was reliant upon obtaining a regular supply of cadavers (dead people) and extracting hGH from the pituitary gland (a part of the brain). The recognition that dwarf children, the population that was receiving cadaveric hGH to treat growth retardation due to GH deficiency, were being diagnosed with a rare brain disorder caused scientists to develop hGH as the first recombinant hormone. This allowed a small test market prior to launching the resources necessary to meet the demand that recombinant insulin would generate. Unlike the experience with AAS, early adapters dove into hGH like pigs digging for truffles, using doses based upon the protocols designed for dwarf children. This resulted in immense growth, but not just of the muscles. The bones of the face, hands and feet all grew disproportionately, and the abdomen of these men became swollen like some Willy Wonka-esque special effect. It is likely that combined use of insulin with hGH exacerbated the abdominal presentation. Though use patterns vary, many now use hGH at a lower dose, and time insulin with meals and training.


So, it should be clear that the dosing of AAS has impressive but limited benefit as a monotherapy, (i.e., without stacking it with other classes of drugs such as hGH and/or insulin). From the onset, men have developed impressive physiques with muscular hypertrophy and strength gains using modest doses of AAS. The escalation of dosing regimens has resulted in a clearly evident, but not evolutionary increase in the muscle mass of the competitors. It also clearly aids in protecting against muscle loss during pre-contest dieting, as the mass of these men has increased concurrently with a reduction in body fat. Certain AAS have fat loss-enhancing properties, whereas others impede fat loss, but that is outside the scope of this article.


What Is the Right Dose?

The question arises, then, “What is the right dose?” This obviously is a question that does not have one right answer. First, it assumes that a person does not have a health condition that would increase the risk of an adverse (negative) side effect, potentially fatal in some cases. Though prostate cancer and heart disease were once dogmatically thought to be caused or worsened by testosterone replacement therapy (TRT) or AAS misuse, it appears that this is not the case in doses that are within or close to the upper physiologic limit. The greatest concern should lie in a history of blood clots (thrombophilic disease), which can be familial (relatives have a history of blood clots) or spontaneous. In fact, nearly all ischemic cardiovascular events reported in people receiving TRT occur in individuals with a thrombotic condition. At times, this does not manifest until the person goes on TRT, suggesting that it can “tip the scales” and lead to a life-threatening event (e.g., stroke, pulmonary embolism, coronary thrombosis, DVT).


Equally relevant, especially in adolescents and young adults, is the risk of a personality disorder or psychosis emerging. It is not only the grossly elevated levels of androgens circulating during cycles that may cause this, but also the rapid downward swing when going off-cycle. It is suggested that one highly publicized case involving a high school student who was taken off AAS abruptly (under the advice of a physician) contributed to his suicide. It is unclear how valid this opinion is, as the boy was also receiving psychiatric care and on some form of medication for a mental health condition.7


Though the existence of “roid rage” is contested, research does support that in predisposed individuals, supraphysiologic testosterone can increase the magnitude of response to provoked aggression, but does not increase spontaneous aggression.8 This means that if you upset an AAS user who is prone to losing his temper, he will react more angrily and/or violently. However, the person should not have outbursts without reason. Other potential risks (legal as well as health) exist, and should be understood before deciding to experiment with AAS.


Testosterone Threshold and Muscle Hypertrophy

Clearly, a healthy man will not want to use an amount of AAS that does no better than his natural levels of testosterone (or even worse). Thus, it is notable that research has shown that in both young adults and older men, testosterone is essentially maintained at baseline— with statistically significant changes in muscle mass and strength when dosed at 125 milligrams of testosterone enanthate weekly. Increasing this to 300 milligrams and even 600 milligrams weekly results in dose-dependent increases in both muscle mass and strength.9,10 Only in older men were any significant adverse effects noted, those being an increase in red blood cell mass, leg edema and prostate events.


Harrison Pope, who has been vigorously pursuing any association between AAS misuse and various psychopathologies, noted in a 2000 study that 600 milligrams of testosterone cypionate was well tolerated by the vast majority of subjects, with 12 percent experiencing an increase hypomanic scores on a survey and four percent showing more marked hypomania.11 No pathologic or criminal behavior was reported. It is interesting that the hypomanic scores reported in the study are considered to be in the normal range in other references, suggesting the sensitivity to change may have been slightly biased to over-reporting.


An interesting paper reported on the observed testosterone threshold necessary for skeletal muscle hypertrophy.12 The testosterone concentration needed to evoke an increase in muscle mass was at the top end of the physiologic range, actually slightly above, in this group of older men. The concentration of roughly 1,200 to 1,500 ng/dL correlates with the concentration produced by the men receiving 300 milligrams of testosterone ester weekly (1,345 ng/dL).9,12 This suggests that those seeking increases in muscle mass and strength might target 300 milligrams of testosterone ester weekly as a starting point. However, conversations with many men receiving TRT describe increases in strength and muscle mass equal to that achieved during young adult years at a dose of 200 milligrams of testosterone ester weekly. Topical formulations are generally found to be lacking in relevant changes in muscle mass in middle-aged men.


A dose range of 300 to 600 milligrams of testosterone ester weekly agrees with the field report of men self-administering AAS primarily for personal enhancement (i.e., personal satisfaction; 15% reported competition experience/plans). In a large survey of nearly 2,000 AAS users, the most common dose range was 200 to 600 milligrams of testosterone ester weekly (52%), with an additional 32 percent reporting a dose range of 600 to 1,000 milligrams weekly. Very few reported use above 1,400 milligrams of testosterone ester weekly.13 This suggests that in the “trial and error” lab of illicit use, AAS misusers find the “sweet spot” for AAS to be in the range denoted to increase muscle mass and strength with a minimal (or manageable) level of adverse effects— roughly 200 to 1,000 milligrams of testosterone ester weekly. The dosing studies reported earlier described an increase in fat-free mass of 7.9 kilograms in the men receiving the weekly dosing of 600 milligrams.9 This correlates to a 12.5 percent increase in six months (with a 10% decrease in fat mass). These results would be admirable for an amateur bodybuilder, and are consistent with the physiques seen in bodybuilders of the 1960s and 1970s.


Chemical Warfare

Obviously, the goal of the individual dictates the “right” dose. However, for the person considering AAS use, accounting for the potential for legal or health consequences, both scientific and “field” reports suggest that effects meeting the expectations of most non-competitive individuals can be met with a modest dosing schedule of 300 to 600 milligrams of testosterone ester weekly. Unfortunately, it is difficult to determine “right” dose for the infinite combinations of AAS. Further, those driven to compete will find that a weighting of risk tolerance versus desire to compete needs to be evaluated regularly, as many competitors are willing to accept dangerous and risky protocols of prolonged cycles with complex stacks including peptide hormones, stimulants, diuretics, insulin and other agents. At some point, it becomes chemical warfare, and war always has casualties.


If AAS misuse is your choice, consider the power and limitations of near-physiologic dosing, and understand that there is a ceiling to the amount of size AAS can provide. Unrealistic expectations will result in dissatisfaction and a temptation to push the boundaries of relative safety and tolerance to the point where adverse effects may affect your health, relationships or otherwise impact your life negatively.