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Medical Effects of PEDs

About This Page

This page is one of several each providing a detailed analysis of one or another of the chief claims about the use of PEDs (Performance-Enhancing Drugs) in baseball. Though each, including this one, can be read "stand-alone", you really should first read the main page here, which summarizes all of the findings and sets them out them in a coherent presentation.


Some Medical Background

lab test tube

Before examining in detail the various claims made about medical effects and side effects of steroids, it would be wise to understand what a steroid is. Explanations are available on line in many places, a representative one being the Wikipedia article Anabolic steroid (which, incidentally, "has been identified as one of the best articles produced by the Wikipedia community".) The article presents a good overview of both the chemistry involved and of many of the issues related to steroids, though not all assertions in it are supported by the scientific literature.

While an overview of steroids is useful, one must never forget that "steroids" is a word that encompasses a wide variety of individual substances. While they all belong to a single family, and thus have many similarities in their effects, there are important differences between them, such as the alkylation method used in making them. The differences can be important. For instance, so-called "17-α" alkylation was an early development that allowed steroids to be effective when ingested orally; when studies on the same general subject report significantly differing results, typically any negative findings are associated with a 17-α type of steroid, while other types, such as the 17-β class, rarely if ever produce negative results.

There are two medical questions about steroid use in baseball: What gains might it provide? What harmful side effects might there be? We will examine each question separately.

Normal Unaugmented Patterns

Before we look at whether performance might be abnormal, it is obviously essential to first know what normality is. One of the much-too-frequently heard claims about the performances of older players (those past their early 30s) is that stable or increasing power "must" signify "cheating". An old adage says that there is no harm in being a fool--harm is being a fool at the top of your lungs, and remarks like Anyone who's crossed the threshhold of 35 knows that you just don't get bigger and stronger with age--no matter how hard you work out (I won't attribute it, to save the man some embarrassment) rather prove it.

The simple, well-established scientific fact is that that's utter nonsense. Here are a few representative quotations from the literature:

In other words, it is commonplace medical knowledge that strength typically goes up till about age 40, then plateaus for another decade or two. Ballplayers don't drop out of the game before their mid-40s from lack of ability to power a baseball, but from declining ability to react quickly enough to meet the ball well (or to move well enough to play a position or run the bases) .

Anecdotal but interesting is the fact that Julio Franco's career Power Factor is 1.4, while in 2005, when he was 46, it was 1.64, following an age-44 P.F. of 1.53.

Gains From Steroids

As "masculinizing" substances, steroids tend to amplify biological factors associated with hormone-governed masculine qualities, one of which is muscle development. Although simple use of steroids will produce some modest increase in muscle mass, its real effects come into play when it is used in combination with substantial resistance training (weight lifting or comparable machine exercise). Steroids typically augment the muscle-building effects of such exercise. There are two critical points to be made about the effects of steroids in a muscle-development regimen.

Degree of Gain
comic of Superman lifting an authombile

The first critical point is that for every person there is an upper limit to the strength he or she can achieve. No amount of exercises or steroids (or both), over no matter how long a period, will ever enable anyone to throw automobiles around. That being so, the question devolves to whether any steroid can raise a person's upper limit beyond that obtainable only by exercise. No study can answer that question, because all studies are necessarily limited to some finite, reasonable time period.

freakishly developed musculature

But, as applied to baseball players--as opposed to bodybuilders or weight-lifters--that question is irrelevant. No ballplayer is developing his musculature to the absolute maximum possible, and the proof is that no ballplayer shows musculature remotely like the freakish over-development not uncommonly seen on avid bodybuilders. So the question cannot be "do steroids make a ballplayer stronger?" The question must further devolve to simply "how much faster might steroids enable a vigorously exercising ballplayer to reach a given level of strength?" That is, a ballplayer using steroids is never achieving any strength level that he could not reach by exercise alone; at most, he can be getting to a given level faster, and perhaps maintaining that level with shorter workouts, than without steroids.

Distribution of Gain

Different sports emphasize different muscles. The arm strength critical to a swimmer is much less important to a runner. But--and this seems inadequately appreciated outside the medical profession--steroids do not affect all muscles alike. There is a marked differential in their effects. The muscle groups that receive the lion's share of benefit from steroid use are those of the upper body. Steroidal effects on lower-body strength are far weaker:

  • The principal advantages ascribed to anabolic steroids are those associated with androgenicity, or masculine traits. Upper-body strength and muscularity are two such key traits. . . . anabolic steroids increase muscle mass and upper-body strength. Anabolic Steroids in Sport and Exercise, Charles E. Yesalis, ed.

  • Testosterone increases upper-body mass differentially, so performance in [upper-body] tasks like weight-lifting should improve more than lower-body tasks or tasks in which aerobic aerobic capacity rather than strength are assessed. As expected, the task in which increases have been reported most reliably are in the bench press. Recent Progress in Hormone Research 57:411-434 (2002), Cynthia M. Kuhn

  • [S]teroids increase muscle mass and upper-body strength . . . . The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. N Engl J Med 1996; 335: 1-7, Bhasin S, Storer TW, Berman N, et al.

  • [M]uscle deposition promoted by testosterone tends to be greater in the upper body; this provides the greatest effects (and therefore the greatest likelihood of abuse) for sports like swimming, which rely on upper-body strength. Buzzed: The Straight Facts about the Most Used and Abused Drugs, Cynthia Kuhn, Scott Swartzwelder, Wilkie Wilson (Duke University Medical Center)

  • Testosterone also produces characteristic body changes, Dr. Pope said, with the most marked muscle growth in the upper body and the biceps. Psychology: Concepts and Connections, Spencer A. Rathus

Because this matter is so important, I will present a couple of further quotations. First, let's see more from Dr. Karl Friedl, the author of the chapter in Anabolic Steroids in Sport and Exercise already quoted above:

Kochakian discovered early in his experiments that not all skeletal muscle responds to anabolic steroids equally. When he administered anabolic steroids to androgen-deficient guinea pigs, he found the predominant effect to be on upper-body muscles in the region of the shoulder girdle. . . . what Kochakian observed is consistent with the stereotypical body shape of normally virilized men . . . . In a study with a small number of men receiving testosterone or nandrolone injections for six weeks, we also found the main increases in body circumference in the shoulders and chest (Friedl, Dettori, Hannan, Patience, & Plymate, 1991).

Next, another quotation from Recent Progress in Hormone Research 57:411-434 (2002), also quoted from above, which makes clearer what is developed in other papers on this subject, the probable cause of the commonly observed differentials, namely differing densities of androgen receptors in different sets of muscles:

Androgen receptors are present in skeletal muscle of every mammalian species (Sar et al., 1990; Takeda et al., 1990). Levels of expression differ from muscle bed to muscle bed in a manner consistent with reported AAS effects on muscle strength in different tasks. For example, human muscle beds differ from each other, with expression higher in the muscles of the neck and chest girdle, in comparison to the limbs (Kadi et al., 2000).

That upper-body/lower-body differential effect will be of great significance when we evaluate actual, manifested effects putatively assigned to steroid use in baseball.

Augmented Playing Time

A different "gain" postulated by some for PED users is playing time. Its partisans argue that even if PEDs don't boost power rates, they distort power counts (that is, home-run totals, seasonal and career) by helping players to heal faster from injuries, and thus to get in more playing time than they could unaided.

Consideration of nothing else but the numerical fact that even the best home-run hitters produce an average of one home run every three games ought to discourage this belief, but a closer examination, as presented here on a separate page, PEDs as Healing Agents, more thoroughly dispels this folly. First, the consensus of medical opinion seems clearly to be that there is not a "healing effect" of the sort imagined by players and others, that is, some chemical magic that enables strained or torn muscles or ligaments to recover more quickly. Second, average playing time for regulars has decreased through the so-called "steroids era", the exact reverse of what the "more playing time" argument postulates.

Harmful Side Effects of Steroids

Overview of Steroid Side Effects
a bottle of testosterone

In everything to do with steroids, but most especially when examining claimed harmful side effects of steroids, it is necessary to pick sources with the greatest care. That goes beyond not using anecdotal or nonspecialist sources. If, for example, you choose to get your information from web sites with URLs like,, or, you may get claims that differ markedly from those to be found in the established literature of the medical community. A good part of the discrepancy derives from the difference between risks and consequences.

If you jump out of an airplane with a parachute, you are taking a risk; if you jump out of an airplane without a parachute, you encounter not risk but definite consequences. It is folly to confuse the two situations--but such confusion is what one sees in most nonspecialist articles about the supposed side effects of steroids. If one is intent, for whatever private reasons, on demonizing steroids, then it behooves one to blur or even erase the distinction between risks and definite consequences, and to present the risks as if they were definite consequences. So statements typified by "known side effects of  ——  include . . ." are misleading--whether by intent or not is immaterial--because they present possibilities as virtual certainties. Someone reading such a listing or tabulation is highly likely to conclude, wrongly, that using substance  ——  will bring on the entire (usually frightening) catalogue of woes set forth. The reality is that each of the side effects listed (well, not each--some are just made up) is a potential consequence: the degree of risk it represents needs to be evaluated on a three-dimensional matrix of actual probability of occurrence, severity of harm if it does occur, and transience (whether it goes away if the dosage is stopped). Such data are almost invariably lacking in most presentations.

Here are a few representative comments about steroid risks from credible, disinterested sources:

  • We know steroids can be used with a reasonable measure of safety. We know this because they're used in medicine all the time, just not to enhance body image or improve athletic performance. -- Dr. Charles Yesalis, Pennsylvania State university epidemiologist, steroid researcher for more than 25 years, and author of the 1998 book The Steroids Game, from the aptly titled article Pumped-Up Hysteria (Reason magazine).

  • There are also many popular misconceptions concerning their effects and side effects. One common misconception in popular culture and the media is that anabolic steroids are highly dangerous and users' mortality rates are high. -- from the "Misconceptions and controversies" section of the Wikipedia article Anabolic_steroid.

  • When examining the potential medical issues associated with anabolic steroid use, evidence indicates that most known side effects are transient. More so, few studies have been able to directly link anabolic steroids to many of the serious adverse effects listed. -- Hoffman and Ratamess, "Medical Issues Associated with Anabolic Steroid Use: Are They Exaggerated?", JSSM- 2006, Vol.5, Issue 2, 182 - 193; notable as the source George Mitchell suggested as an overview of current steroid medical knowledge.

  • Some members of the sports medicine community have, with the best intentions, adapted a conservative strategy and used strong, but often unfounded, pronouncements regarding the adverse effects of AAS. Athletes, on the other hand, have simply not witnessed long time AAS users 'dropping like flies'. This aggressive health education strategy does not seem to have had a major impact on use of AAS and has very likely added to the lack of credibility of the sports medicine and scientific communities in this area. "Problems with Current Information on Anabolic Steroids",

  • The only physical complication of AAS use that receives definitive support from . . . investigations is unfavourable changes in blood lipid profiles. -- "Pharmacoepidemiology of anabolic androgenic steroids: a review", Fundamental & Clinical Pharmacology, Volume 19 Issue 1 Page 27-44, February 2005.

Let's be clear here: no one says steroids are risk-free or anything like it: there is always risk when taking any medication. Again, the real questions are, for each purported risk, 1) is it serious? 2) is it likely? 3) is it reversible? Let us now turn to the specific individual issues.

"Psychiatric Effects"

The phrase 'roid rage is catchy (which is a clue to its origins), and thrown about quite a bit, but meaningless. Medically, what is being alleged is "mania", for which diagnostic tools are readily available (and which, in medical use, does not correspond to the everyday use of the word, which brings up images of madmen running amok with bloody axes). Curiously, another allegation against steroids is that they can cause suicidal depression, which is the direct opposite of mania. But before we look at the literature on these claims, we need to consider another issue.

Physiological effects of steroids can be estimated reasonably well because it can reasonably be supposed that few if any potential users are going to have significant pre-existing medical problems. But when trying to evaluate mental effects, that supposition has no basis. As Darkes (see farther below) and many others have pointed out, one of the chief failings of many studies of steroids and psychiatry is the failure to design the studies so that the cause-and-effect relationship is not tangled. While there are, in some reports, evidences of some possible correlation of steroid use and mental problems, what few if any of those studies address is which is cause and which effect.

It is a commonplace in medicine that persons with any of several mental problems tend to engage in a wide spectrum of reckless behaviors, usually including multiple simultaneous forms of substance abuse. Thus, a careless reckoning of whether a given set of users (or abusers) of a substance seem to have mental problems may not be at all indicative. This is sometimes called the "bread paradox": it is like saying that since well over 90% of convicted criminals confess to having eaten bread within hours of committing their crime, bread is clearly a psychoactive substance that induces criminal behavior.

An example of this--in this case recognized by the researchers--is found in Measures of aggression and mood changes in male weightlifters with and without androgenic anabolic steroid us [Perry et al, Journal of Forensic Sciences, Volume 48, Issue 3 (May 2003)]:

The subjective (BDHI) and objective (PSAP) assessments of aggression found that supranormal testosterone concentrations were associated with increased aggression. However, the [Personality Disorder Questionnaire] results suggest that this finding was confounded by the personality disorder profile of the steroid users, because steroid users demonstrated Cluster B personality disorder traits for antisocial, borderline, and histrionic personality disorder.

Other studies also strongly that the probable cause of the few percent of exceptions to be found are atypical idiosyncratic reactions--in layman's terms, the functional equivalent of an allergy. For instance, in 2000, Pope, Kouri, and Hudson, in "Effects of Supraphysiologic Doses of Testosterone on Mood and Aggression in Normal Men" (Arch Gen Psychiatry. 2000;57:133-140), a randomized, placebo-controlled crossover trial involving 50 subjects, found that--

[M]ost [subjects] showed little psychological change, whereas a few [4%] developed prominent effects. The mechanism of these variable reactions remains unclear.

Or again, we have An Evaluation of Anabolic-Androgenic Steroid Abusers Over a Period of 1 Year: Seven Case Studies [Fudala et al., Annals of Clinical Psychiatry, Volume 15, Number 2 (121-130)]:

Changes as measured by various behavioral rating scales were observed across time; however, these changes were not clearly related to periods of reported AAS use. Additional factors such as life events, subjects' other drug use, and the extended duration of activity of some of the AAS preparations probably influenced the results.

With that warning in mind, let us look at some of the findings in the literature.

About a decade ago, one of the first major medical investigations into steroidal effects, The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men (Bhasin, et al., N Engl J Med. 1996 Jul 4;335(1):1-7), while reporting general results added that Neither mood nor behavior was altered in any group. Dr. Charles E. Yesalis, one of the nation's best-known experts on steroids in sports (and no apologist for steroids, either) has many times written on the topic; in 1996, he and colleagues published an update to their 1990 paper "Psychological and Behavioural Effects of Endogenous Testosterone Levels and Anabolic-Androgenic Steroids Among Males: A Review" (Sports Med. 1996 Dec;22(6):367-90), in which update the Abstract states (emphases added):

With estimates of over 1 million past or current users in the US, an extremely small percentage of individuals using anabolic-androgenic steroids appear to experience mental disturbances severe enough to result in clinical treatment and medical case reports. Even among those so affected, the roles of previous psychiatric history, genetic susceptibility to addictions or mental disorders, environmental and peer influences, and individual expectations remain unclear.

That "extremely small" correlates with (as cited above) Pope's 4% (which was only two men); in general, the literature supports an estimate of 1% to a maximum of 4% of users having some sort of mental problems; but, as we have seen, whether that is correlation or actual cause-and-effect is unclear. Now let us further consult the professional literature by particular claim.


A representative finding is Tricker et al., The effects of supraphysiological doses of testosterone on angry behavior in healthy eugonadal men--a clinical research center study , Journal of Clinical Endocrinology & Metabolism, Vol 81, 3754-3758:

Anecdotal reports of "roid rage" and violent crimes by androgenic steroid users have brought attention to the relationship between anabolic steroid use and angry outbursts. . . . Conclusion: Supraphysiological doses of testosterone, when administered to normal men in a controlled setting, do not increase angry behavior.


Dr. Kirk Brower--noteworthy because George Mitchell cited him in connection with depression studies--has said that:

[T]o our knowledge no controlled studies have addressed specifically an association between anabolic androgenic steroid abuse and suicidal ideation.

A lengthy discussion of supposed steroid-caused depression--one too long to quote saliently here--but also including further references to and results from numerous of other medical studies, can be had in Anabolic-Androgenic Steroids and Suicide: A Brief Review of the Evidence by Dr. Jack Darkes, Assistant Professor, Department of Psychology Director of Interventions, Alcohol and Substance Use Research Institute, University of South Florida.

  Summing of "Psychiatric Effects":

The consensus findings in the scientific literature are that the incidence of nontrivial psychiatric effects in steroid users is a few percent, something from 1% to 4%--say around 2% as an average finding. But the literature also makes clear that in many of even those few instances--probably a clear majority of them--the subjects brought their own existing problems to the deal. The remaining fraction of users, those whose problems apparently arise chiefly or solely from the steroids, could reasonably be estimated at less than 1%, with those being the result of an atypical biochemical reaction (something comparable to an allergy).

To keep that in perspective, there is probably no substance, including common over-the-counter preparations, for which one cannot find a 1% or 2% fraction of the population having adverse reactions. (In fact, a Harris Poll found that about one-third of people taking a prescription medicine reported an adverse reaction--and that, remember, to a medication specifically prescribed for them; even in hospitals, serious adverse effects from prescribed drugs can run as high as nearly 7%.)

In short, as MythBusters would put it: Busted.

"Cardiovascular Effects"

From Hoffman and Ratamess, George Mitchell's preferred source of medical information on steroids:

  • [D]irect evidence showing cause and effect between anabolic steroid administration and myocardial infarction is limited.

  • [I]n most case studies the effects of diet or genetic predisposition for cardiovascular disease were not disseminated and could not be excluded as contributing factors.

  • [T]hese effects appear to be reversible upon cessation of the drug.

  • Sader and colleagues (2001) noted that despite low HDL levels in bodybuilders, anabolic steroid use did not appear to cause significant vascular dysfunction.

  • Interestingly, athletes participating in power sports appear to have a higher incidence of cardiovascular dysfunction than other athletes, regardless of androgen use (Tikkanen et al., 1991; 1998). Thus, a strength/power athlete with underlying cardiovascular abnormalities that begins using anabolic steroids is at a much higher risk for cardiovascular disease. However, anabolic steroid-induced changes in lipid profiles may not, per se, lead to significant cardiovascular dysfunction.

An extensive study by Hartgens, Cheriex, and Kuipers, Prospective Echocardiographic Assessment of Androgenic-Anabolic Steroids Effects on Cardiac Structure and Function in Strength Athletes (Int J Sports Med 2003; 24: 344-351), or rather pair of studies, found this:

Since the abuse of androgenic-anabolic steroids (AAS) has been associated with the occurrence of serious cardiovascular disease in young athletes, we performed two studies to investigate the effects of short-term AAS administration on heart structure and function in experienced male strength athletes, with special reference to dose and duration of drug abuse. . . . In Study 1 eight weeks AAS self-administration did not result in changes of blood pressure or cardiac size and function. Additionally, duration of AAS self-administration did not have any impact on these parameters. Study 2 revealed that eight weeks administration of nandrolone decanoate did not induce significant alterations in blood pressure and heart morphology and function. Short-term administration of AAS for periods up to 16 weeks did not lead to detectable echocardiographic alterations of heart morphology and systolic and diastolic function in experienced strength athletes. [Neither the] administration regimen used nor the length of AAS abuse [influenced] the results.

In fairness, it must be noted that some studies have found, variously, mild elevation of sleeping blood pressure, changes in the LDL/HDL cholesterol ratio, or slight enlargement of the left ventricular region of the heart. That is why the final point made by Hoffman and Ratamess, above (the Tikkanen result), is of particular note, in that it fits the discrepancy between studies that look at correlations as opposed to those that examine actual changes (or lack of them) from steroid use.

It is also important to understand that while left-ventricular hypertrophy (LVT) is associated with risk, that association seems to apply only to hypertension-caused LVT; in an article Can pathological left ventricular hypertrophy in arterial hypertension be distinguished from physiological hypertrophy caused by sports? (Schwanwell et al., Dtsch Med Wochenschr. 2001 Mar 9;126(10):263-7), we find:

In pathological left-ventricular hypertrophy due to hypertensive heart disease a pathological diastolic filling pattern was documented. In athletes with physiological left-ventricular hypertrophy a normal left ventricular diastolic filling pattern was revealed.

That is not an isolated finding. Another study, Left ventricular hypertrophy differences in male professional runners and in young patients suffering from mild hypertension (Palazzuoli et al., Blood Press. 2004;13(1):14-9), reported:

Our data indicate that LV concentric hypertrophy in sportsmen is associated with improvement of systolic and diastolic performance, whereas diastolic dysfunction can occurs even in the early stages of hypertension in young patients, in whom an alteration in the LV filling appears even in absence of systolic dysfunction and evident concentric myocardial hypertrophy.

The curious, preferring a longer laundry list of supporting citations, may examine the following:

Note also that even though the HDL/LDL ratio ("lipid profiles") is sometimes affected, Sader (as quoted by Hoffman and Ratamess) found no adverse effects from any such changes.

In short, the conclusion that seems to be in order are that steroid use by athletes can have some modest effects on the cardiovascular system, but that those effects are not notably severe or necessarily even dangerous--in fact, possibly beneficial.

"Liver Damage"

Let us first turn again to George Mitchell's recommended source of information, Hoffman and Ratamess:

Thus, some experts have questioned these criteria tools because of the difficulty in dissociating the effects of muscle damage resulting from training from potential liver dysfunction. This has prompted some researchers to suggest that steroid-induced hepatotoxicity may be overstated. . . . . No cysts or tumors have been reported in athletes using 17β-alkylated steroids. Thus, evidence appears to indicate that the risk for hepatic disease from anabolic steroid use may not be as high as the medical community had originally thought although a risk does exist especially with oral anabolic [17α-alkylated] steroid use or abuse.

As an example of the sort of "questioning" there mentioned, there is Dickerman et al, "Anabolic steroid-induced hepatotoxicity: is it overstated?" (Clin J Sport Med. 1999 Jan;9(1):34-9):

Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage.

So, first off, what we know is that even potential liver damage is uniquely associated with one specific sub-class of steroids, the 17-α-alkylated ones--as noted above, and, for further confirmation, as reported by Lowdell and Murray-Lyon, Reversal of liver damage due to long term methyltestosterone and safety of non-17 alpha-alkylated androgens [Br Med J (Clin Res Ed) v.291(6496)]:

We found no evidence of hepatic damage due to long-term treatment with non-17-α-alkylated androgens, which are traditionally regarded as free from hepatoxicity.

But even for the 17-α class, the seriousness can be over-estimated. In an experiment on mice with a particular 17-α steroid, A repeated 28-day oral dose toxicity study of 17a-methyltestosterone in rats, based on the 'Enhanced OECD Test Guideline 407' for screening the endocrine-disrupting chemicals [Okazaki et al., Archives of Toxicology, 75, Numbers 11-12 (635-642)], the authors reported that:

Based on these results, the no-observed-adverse-effect level (NOAEL) in the present study was estimated to be below 5 mg/kg per day.

Now extrapolating from rodents to humans is dicey, but those who demonize steroids do it all the time (and rarely--if ever--mention where their "data" came from), so let's do the same. A weight of 100 kg is 220 pounds, not unreasonable for a muscular ballplayer; based on that study, a man weighing 220 pounds could orally ingest 500 mg of a 17-α class steroid daily and still be clinically below the no-observed-adverse-effect level, which is merely a conservative threshold for a possible beginning of effects.

It is, of course, impossible to know what doses users are taking, since the use is banned; some reports (Bodybuilding Anabolic/Androgenic Steroid Practices) suggest that 500 mg would be a little above the average dose (476 mg). A 2006 report on 500 anonymous self-reporting users showed about 60% reported "using at least 1000 mg of testosterone or its equivalent per week"; 1000 mg a week is 143 mg a day, far under 500. A casual inspection of web sites recommending or selling steroids suggests lower dosages for oral steroids than those reported in the 1980 study. But given all the vagueness, the point still seems clear: for the one potentially liver-toxic steroid class known, typical user doses are around the bare minimum threshold for possible adverse effects.

Another critical fact in risk evaluation is reversibility: do the effects--if any--go away when the dosing is stopped? Yes, they do.

Body Composition, Cardiovascular Risk Factors and Liver Function in Long Term Androgenic-Anabolic Steroids Using Bodybuilders Three Months After Drug Withdrawal [Hartgens et al., Int J Sports Med 1996; 17: 429-433]:

In addition, no differences in fat mass, blood pressure, lipoprotein profiles, and liver enzymes exist between AAS users three months after interrupted drug use and their non-drug-using counterparts.

Reversal of liver damage due to long term methyltestosterone and safety of non-17 alpha-alkylated androgens [Lowdell and Murray-Lyon, Br Med J (Clin Res Ed) v.291(6496)]:

These results suggest that liver damage induced by methyltesterone is reversible, in agreement with occasional previous reports.

So as to potential harms to the liver from steroids: only one sub-class of steroids normally has any effect, the required dosage for effects is above what the typical user of that sub-class uses (though, in fairness, one must say there may be some using it at levels high even for covert users), and such harms as may occasionally occur are reversible.

Some further perspective wouldn't hurt here. Steroidal liver damage is unlikely and readily reversible. Yet "If you take Tylenol for four days as directed you may be at risk of [permanent] liver damage."; in more detail, studies show that Liver toxicity from acetaminophen poisoning is by far the most common cause of acute liver failure in the United States . . . The data suggest that consistent use of as little as 7.5 g/day of acetaminophen could lead to severe hepatic injury. So where is the outcry over Tylenol for ballplayers? Are players who take a Tylenol to reduce or get rid of a headache before a game to be banned? Ask Why not?, then plug your answer/s, unchanged, into the steroids debate.

"Reproductive-System Harm"

This catchall includes purported changes in libido; testicular shrinkage; and decreases in fertility.


There is some real irony here, in that anabolic steroids are often mentioned as cures for flagging libidos. Indeed, the literature reveals mixed results as subjectively reported, with increases outnumbering decreases (for what subjective reporting may be worth). Generally, "decreased libido" is associated with withdrawal from steroid use, amplifying the thesis that use typically increases libido. For instance, Moss et al., in 2006 in Sexual functioning of male anabolic steroid abusers [Archives of Sexual Behavior, Volume 22, Number 1 (1-12)] reported that:

Current anabolic steroid users had a significantly higher coital and orgasmic frequency than did comparison athletes.

Whether such an increase is regarded by a given user as an "adverse" effect will be a highly personal judgement; but the literature does not seem to suggest that any of these effects are exactly of life-altering magnitude.

Many scholarly papers concerning anabolic steroids found by internet search containing the word "libido" do not mention it in the abstracts or summaries available without payment of a fee, so it is hard to cite particulars. We may, however, turn to George Mitchell's recommended general source of steroids information, Hoffman and Ratamess; that paper caches reproductive-system effects under "Additional Adverse Effects", meaning they don't feel it deserves discussion as a full-fledged topic on its own. What they do have to say shows quite differing results from differing studies. For example:

  • Changes in libido appear to be the most common adverse event (approximately 61% of users) reported in a small sample of anabolic steroid users (O'Sullivan et al., 2000).

  • Other studies confirm unchanged libido following 10 weeks of anabolic steroid administration . . . (Schurmeyer, et al., 1984).

  • Decreases in libido as a result of hypogonadism appear to be a function of high baseline levels of sexual functioning and desire (Schmidt et al., 2004). This may explain the conflicting reports seen in the literature.

In English, that last means that the decreases are mostly in guys who were abnormally horny devils to begin with; with long-term steroidal use, such folk apparently get knocked back to more normal levels. More normal subjects tend to see the increases.

But, as the paper notes:

Regardless, changes in libido do appear to normalize once baseline endogenous testosterone concentrations return (Schmidt et al., 2004).

  Testicular Shrinkage:

There seems little doubt that some users do experience modest but perceptible shrinkage. Equally, though, there is no doubt that many others do not. Again, whether a possible mild shrinkage in testicle size is "adverse", and to what degree, is a highly personal judgement. In any event,

[T]esticular size is reduced within three months of androgen administration (Alen and Suominen, 1984). . . . However, the changes seen . . . in testicular volume . . . are reversible.

  Decreased Fertility:

There also seems little doubt that some users do experience some measurable loss of fertility.

[S]perm concentration and the number of spermatozoa in ejaculate may be reduced or eliminated by 7 weeks of administration (Schurmeyer et al., 1984). During this time risk for infertility is elevated. However, the changes seen in . . . sperm count and concentration are reversible.

And yet again, we need to recognize that a decreased likelihood of becoming a father while taking steroids may not be universally seen as an "adverse" side effect. And in no case (considering its ready reversibility) can it be considered a "significant" side effect.

  Summing Reproductive-System Effects:

Steroid use tends to "set" users' libidos, such that most will see an increase, while the minority with naturally extraordinarily high levels may see a decrease. Use also will, in some--possibly many--cases cause moderate testicular shrinkage. And it will very likely lower fertility. All of these effects are routinely reversible simply by ceasing use.

Demonizers can make what they will of this--indeed, they have--but it seems hard to see any of it, or all of it ensemble, as rising, even in worst cases, to a level above "annoying". Mai chacun a son goût.

"Musculoskeletal Problems"
Point one: This, for adolescents is a major, grave risk. But we are addressing possible effects on adult male professional athletes.

Point two: there is a substantial difference between the strains imposed on the musculoskeletal system by weight-lifters, who are the commonest study subjects, and by strength/speed athletes (like ballplayers).

Let us yet again fall back on our by-now old friends, George Mitchell's recommended Hoffman and Ratamess:

Anabolic steroids have been suggested to increase [sic] the risk of tendon tears in athletes (David et al., 1994; Stannard and Bucknell, 1993). . . . Evans and colleagues (1998) performed an ultrastructural analysis on ruptured tendons from anabolic steroid users. They concluded that anabolic steroids did not induce any ultrastructural collagen changes that would increase the risk of tendon ruptures. Although the incidences of tendon rupture in anabolic steroid users should not be discounted, it is important to consider it in relation to the mechanical stress encountered from the rapid increases in muscular performance.

If that sounds fuzzy, it's because for all the many oblique references to a supposed increase in tendon-rupture possibilities owing to steroid use, both clear examples and clinical indications seem determined to just not exist, naughty things that they are.

When we go looking for some hard-science results beyond the cited Evans, all we find are a few studies--often quite old now--done on mice and rats, and those scarcely conclusive (The overall picture and the architecture of the tendons provide tentative evidence . . . ); those rodent studies would seem to be the only possible basis for the occasional assertion that there "appears to be" a connection between steroids and musculoskeletal harms, even though the results are weak and and even though it is well-understood in science that extrapolating animal results to humans is quite dangerous.

There just is no literature of steroid-related tendon-damage studies because there isn't any history of such damages. The cynic is left to suspect that known musculoskeletal harms from steroid use by adolescents has been the basis used by demonizers for even mentioning "musculoskeletal problems".

(It is perhaps amusing that steroids in fact have an excellent medical reputation in curing torn tendons .)

Miscellaneous "Risks"

This hodgepodge category derives from that of the same name and composition in George Mitchell's lamentable catalogue of superstitions (discussed further elsewhere on this site); almost everything in it is classifiable as a "cosmetic" issue. We will look at its members individually.


While "steroid acne" is a well-known medical phrase, the term is associated with topical (rubbed-on) corticosteroids, not with oral or injected anabolic steroids. It does seem that anabolic steroids can also cause a form of acne, but--though the word is often seen in non-technical documents--I, at least, was unable to locate any medical reference to anabolic-steroid-caused acne being "serious".

The incidence rate is not often mentioned, but appears to be about half of users. In any event, drug-induced acne . . . heals without scarring on discontinuation of steroidal use.

Whether mild, or even moderate, reversible acne is significant is inherently a judgement that only the user can make; but it would be inordinately provocative to refer to it as a "health risk".

  Excess stimulation of sebaceous glands:

Sebum is a normal bodily excretion, being in plain English "oil"--an excess of sebum excretion might manifest as "oily hair" (of shampoo-type fame), or perhaps as an increase in ear wax. To categorize "excess" sebum secretion (and who separates "increased" from "excess" and how?) as a "significant health risk" would be--even more so than with acne--comic over-reaching.

  Increased body hair:

The few fleeting mentions of it in the literature seem all focussed on possible side effects of these male-hormone substances when taken by women. When MLB admits women to Organized Baseball, this might be an issue, however trivial; but don't set aside near-future time on your calendar for considering it.

  Male-pattern baldness:

From our old friends Hoffman and Ratamess:

Male-pattern baldness does not appear to be a common adverse effect, but is often discussed as a potential side effect associated with androgen use. . . . Thus, it is likely that androgenic alopecia observed as a result of exogenous androgen use is more prevalent in individuals that have a genetic predisposition to balding.

In English: well, no one has actually seen it, but men who are already balding just might find their balding accelerated. Darn, we're just sure we left that evidence lying around here somewhere . . . .

  Prostate enlargement:

George Mitchell's favorite source, Hoffman and Ratamess, does not even mention the prostate. But in the relatively recent "Circulating Steroid Hormones and the Risk of Prostate Cancer" (Cancer Epidemiology Biomarkers & Prevention Vol. 15, 86-91, January 2006), we find:

Epidemiologic studies have failed to support the hypothesis that circulating androgens are positively associated with prostate cancer risk and some recent studies have even suggested that high testosterone levels might be protective particularly against aggressive cancer. . . . None of the hormones was associated with nonaggressive prostate cancer . . . . High levels of testosterone and adrenal androgens are thus associated with reduced risk of aggressive prostate cancer . . . .

My, my.


Gynecomastia is a non-cancerous enlargement of the male breasts (gyneco, woman; mastos, of or like a breast), which can have many causes, of which steroid use is one. The severity of gynecomastia, natural or induced, can range from scarcely noticeable to grotesque. It is crucial to take note that this is perhaps the only steroid-induced side effect that does not necessarily go away when use of steroids is stopped. While it often does--

After suppression of anabolic steroid intake and treatment with tamoxifen, a high remission rate can be achieved ["Anabolic steroids and gynecomastia. Review of the literature", de Luis, Aller, Cuéllar, Terroba, and Romero; An Med Interna. 2001 Sep;18(9):489-91]

--often isn't always. Reports of the frequency of gynecomastia among steroid users vary in the literature; Hoffman and Ratamess say only 37%, quoting O'Sullivan (2000), but most sources say that roughly half of users develop at least detectable enlargement. Onset periods are also highly variable:

In some steroid users, gynecomastia may occur after the very first injection. In others, it may happen after many months of repeated use. And some users may never see as much as a single lump. ["Male Breast Reduction", Mordcai Blau, MD, PC]

For those cases in which discontinuation of the steroids is not followed by regression, supervised treatment with other substances (for example, tamoxifen or clomiphene) often eliminates the condition; but if it does not, surgery is required, and it is not necessarily simple:

Most body builders have very little body fat; therefore, the breast tissue that builds up is extremely firm and hard and presents a difficult surgical problem to remove. [Gynecomastia: Nashville, Tennessee Men's Cosmetic Procedures ]

One common consequence of gynecomastia in steroid users is that they turn to self-medication with other, additional substances in attempts to minimize or eliminate this side effect. Such self-medications can have yet other medical consequences, even if they do the intended job (for example, tamoxifen can boost triglyceride levels or cause fatty liver).

This is the first non-trivial issue medical-risk issue raised, and deserves thought from potential steroids users.

  Summing of "Miscellaneous Effects" Risks:

Most of these are both cosmetic only and not lifestyle-altering. Some, such as reduced fertility, may--though harmless and reversible--have significance for particular users. The sole exception, and arguably the only risk-significant medical side effect at all, is gynecomastia. Fortunately, it is an affliction that necessarily makes itself thoroughly obvious to the user right at onset. If there is anything further to be said about it, it is that it is critical to warn users and potential users of the special nature of this risk (not necessarily reversible or even necessarily correctable without non-trivial surgery).


First, we need to discriminate--as George Mitchell's favored source, Hoffman and Ratamess does--between the various sorts of folk indiscriminately lumped up as "users" in the quoted Mitchell text. Here are H & R's notes:

Anecdotally, it appears that a disproportionate magnitude of use and incidence of adverse effects are evident in bodybuilders (who are also known for consuming several other drugs that relieve some side effects but potentiate other risk factors as well, i.e. diuretics, thyroid hormones, insulin, anti-estrogens, etc.) compared to strength/power athletes. The mindset and motivation of these two types of athletes can be quite different. The strength/power athlete will typically use anabolic steroids to prepare themselves [sic] for a season of competition. They [sic] will generally cycle the drug to help them reach peak condition at a specific time of the training year. In contrast, bodybuilders use anabolic steroids to enhance muscle growth and definition. Their success is predicated on their aesthetic appearance. As a result many of these athletes may use anabolic steroids excessively for several years without cycling off or perhaps minimizing the length of "off cycles" depending on their competition schedule. Recent research has indicated that those athletes exhibit behavior that are consistent with substance dependence disorder (Perry et al., 2005). Although the medical issues associated with anabolic steroids may be quite different between these two types of athletes, the scientific literature generally does not differentiate between the two.

Let's be crystal-clear here: Hoffman and Ratamess are saying that bodybuilders, and not "strength/power athletes" (that is, sports athletes), are the users with reported dependency problems (few as those reports are). Bodybuilders are indeed the source of almost all the negative-effects reports of any kind that do exist, for several reasons (different goals, non-stop use, pure self-medication, and more: examine almost any bodybuilding or steroids-for-sale web site). Beyond what is quoted above, H & R says nothing whatever about addiction (which in itself is strongly indicative).

George Mitchell claimed that "some steroid users exhibit addictive behaviors identical to symptoms of addiction to other drugs of abuse", giving a footnote citation to support that claim. That footnoted reference is actually quoting another source, so let's turn to that root source (whose origin at the National Institute on Drug Abuse is itself suggestive of a less-than-disinterested approach):

An undetermined percentage of steroid abusers may become addicted to the drugs, as evidenced by their continued abuse despite physical problems and negative effects on social relations. Also, steroid abusers typically spend large amounts of time and money obtaining the drugs, which is another indication that they may be addicted. Individuals who abuse steroids can experience withdrawal symptoms when they stop taking steroids, such as mood swings, fatigue, restlessness, loss of appetite, insomnia, reduced sex drive, and steroid cravings. The most dangerous of the withdrawal symptoms is depression, because it sometimes leads to suicide attempts. If left untreated, some depressive symptoms associated with anabolic steroid withdrawal have been known to persist for a year or more after the abuser stops taking the drugs.

I have tried throughout to be dispassionate in analysis and presentation of evidence--but that is just a whacking great load of hot, smelly horseshit, and there's no other honest way to put it.

First off, it establishes no logical connection between its assertions that some "undetermined" fraction of users might be "addicted" and its statements about various symptoms that some users may experience when discontinuing steroids. The authors--notably anonymous, this being no piece of science--didn't have the guts to make a flat statement that discomfort on discontinuation demonstrates (much less proves) "addiction" because they'd have been horselaughed to the Moon if they did; so they try instead to get the reader to make that leap for them, by putting the two basically unrelated statements in one paragraph, in sequential sentences, as if the second claim somehow validated the first, instead of standing quite apart from it.

Second, it completely ignores all the literature--discussed farther above under "psychiatric" issues--that some small but definite percentage of steroid users are users exactly because they had mental problems of one sort of another coming into usage. Some of those problems are the sort that lead to a spectrum of high-risk activities in a manner that suggests "addiction" not to this or that activity but to risk itself. Others have personality problems of another sort, typically muscle dysmorphia, which is effectively the obverse of anorexia. Such persons will seem "addicted" to steroids (and, in the first sort, a collection of other things) for reasons totally unrelated to the effects or chemistry of steroids. To say steroids are "the problem" for such people is like saying food is "the problem" for an anorexic--and to imply otherwise is intellectual dishonesty of a high order.

Third, even the first two sentences, which basically say "they're addicted because a) they use it despite problems from it, and b) they spend time and money getting it", are beyond absurd. Part (a) assumes nontrivial problems that--as we have seen--are wildly unlikely to exist; it is classical begging of the question. Moreover, if they know so much about these people--that they are experiencing "physical problems" and "negative effects on social relations"--how come they don't know, and can't even estimate, how many of them there are? What, the authors read it in tea leaves?

And part (b) is so silly, one is left breathless: that users obtain what they use is proof that they're addicted to it? Egad.

To illustrate how half-witted all that is, consider the case that chocolate cake is addictive:

An undetermined percentage of chocolate-cake abusers may become addicted to the pastry, as evidenced by their continued abuse despite physical problems and negative effects on social relations (obesity, zits). Also, chocolate-cake abusers typically spend time and money obtaining the cake, which is another indication that they may be addicted. Individuals who abuse chocolate cake can experience withdrawal symptoms when they stop eating the cake, such as mood swings, fatigue, restlessness, loss of appetite, insomnia, reduced sex drive, and cake cravings. The most dangerous of the withdrawal symptoms is depression, because it sometimes leads to suicide attempts. If left untreated, some depressive symptoms associated with chocolate-cake withdrawal have been known to persist for a year or more after the abuser stops eating the cake.

That is neither less fact-based nor less logical than that ludicrous piece of NIDA propaganda, which is simply Reefer Madness all over again.

That George Mitchell elected to include that swill, which deeply insults the intelligence of anyone who might read and everyone who has read the so-called "Mitchell Report" is not surprising. Quite aside from the fact that the "Report" itself is in fact propaganda (as linked just above), and not a report in the normal sense, is the crucial fact that George Mitchell was a United States Senator from 1980 to 1995, during which time the Congress passed the legislation that classed steroids as controlled substances, to be exact, as Schedule III controlled substances, a finding that--under prior law--required that Abuse of the drug or other substance may lead to moderate or low physical dependence or high psychological dependence.

In sheer fact, steroids do not meet, or come close to, either criterion. But this is the same United States Senate that somehow reached this stunning conclusion:

Ultimately, the [Senate] Committee [on the Judiciary] concluded [in 1989] that steroids possessed the same abuse potential as cocaine hydrochloride, and should be regulated under the tight controls of Schedule II. -- Steroids Working Group United States Sentencing Commission, 2006 Steroids Report

At this point, you may be thinking that I've produced much indignation and little fact. Stand by. We had to visit fairyland before returning to the real world to see the nature and scope of the claims being asserted, and we needed to see it in a lot more detail than for most of the other farcical assertions because this is the keystone supporting the entire arch of illegality, without which people inclined to steroids could get sound medical advice, supervision, and treatment (and, for that matter, physicians could get reliable data on dosages and effects). Now back to Earth.

Perhaps the most persuasive argument that can be set forth here is the sum total of the testimony given before the Congress when it was considering the legislation that eventually made steroids taboo:

During deliberations, the AMA [American Medical Association], DEA [U.S. Drug Enforcement Agency], FDA [U.S. Food and Drug Administration] as well as the NIDA [National Institute on Drug Abuse] all opposed listing anabolic steroids as controlled substances, citing the fact that use of these hormones does not lead to the physical or psychological dependence required for such scheduling under the Controlled Substance Act. -- Wikipedia, "Anabolic steroid", Legal and sport restrictions

Between 1988 and 1990, congressional hearings were held to determine whether the Controlled Substances Act should be amended to include anabolic steroids. Significantly, medical professionals and representatives of regulatory agencies (including the Food and Drug Administration, the Drug Enforcement Administration, and the National Institute on Drug Abuse) testified against the proposed amendment to the law. Even the American Medical Association opposed it, maintaining that steroid abuse does not lead to the physical or psychological dependence required for scheduling under the Controlled Substances Act. But any "psychologically addictive" properties of steroids or public health dangers seemed to be secondary considerations to Congress. The majority of witnesses at the hearings were representatives from competitive athletics whose testimony, consistent with Congress's apparent main concern, focused on the purported need for legislative action to solve an athletic "cheating" problem. Congress decided that legislation could curtail sports cheating. -- Changing The Game: The Congressional Response to Sports Doping Via the Anabolic Steroid Control Act, R. Collins, Esq. [754 New England Law Review [Vol. 40:753 2006]

The American Medical Association and the U.S. Drug Enforcement Agency are not exactly wacky left-wing pinkos: they are bastions of conservatism, and they are entities that any sane person will grant have a considerably greater comprehension of both medicine and law enforcement than the average Congressperson.

Mind, as stated several times before, in a given individual anything can happen. Abnormal sensitivity to a relatively benign substance can exist--ask Bob Welch--and be deeply problematic for that individual, but that does not in itself justify some blanket prohibition against the substance. Most schoolchildren still eat peanut butter.

There has been some research using rodents that suggests that steroids can exhibit a very mild psychoactivity over prolonged exposure. Lest we seem to be sweeping that research under the rug, here is an extended quotation from the Abstract of a 2004 paper, Reinforcing aspects of androgens [Wood, doi:10.1016/j.physbeh.2004.08.012]:

[I]t is difficult in humans to separate direct psychoactive effects of AAS from the user's psychological dependence on the anabolic effects of AAS. Thus, studies in laboratory animals are useful to explore androgen reinforcement. Testosterone induces a conditioned place preference in rats and mice, and is voluntarily consumed through oral, intravenous, and intracerebroventricular self-administration in hamsters. Active, gonad-intact male and female hamsters will deliver 1 µg/µl testosterone into the lateral ventricles. Indeed, some individuals self-administer testosterone intracerebroventricularly to the point of death. Male rats develop a conditioned place preference to testosterone injections into the nucleus accumbens, an effect blocked by dopamine receptor antagonists. These data suggest that androgen reinforcement is mediated by the brain. Moreover, testosterone appears to act through the mesolimbic dopamine system, a common substrate for drugs of abuse. Nonetheless, androgen reinforcement is not comparable to that of cocaine or heroin. Instead, testosterone resembles other mild reinforcers, such as caffeine, nicotine, or benzodiazepines. The potential for androgen addiction remains to be determined.

That's about as up-to-date as there is: at worst, it's like a cup of coffee or a cigarette. When we see those things banned by Congress and MLB, we can re-visit steroids. But, very, very obviously, steroids are not in any realistic way "addictive".

Non-Steroidal PEDs

Some Medical Background

hGH molecule

Though in principle the list is huge, in practice we are talking about one substance: hGH, human growth hormone. As with steroids, a good introductory article is the one in Wikipedia, this titled Growth hormone.

In considering hGH, there are a few medical things to know. First, in some early work with the stuff--which started in the late 1950s--what was used was extracted from the pituitary glands of cadavers (one reason it was so rare and wildly expensive.) No such hGH has been in use since 1985; that is important because there were some issues raised concerning effects of that specific form of hGH, cadaveric hGH, issues totally unrelated to hGH in general. Second, some rumors about hGH have such ground as they do in studies relating to use in cows of bovine (cow-derived) GH, not human Growth Hormone--that is, hGH.

Since 1985, all hGH in general use has been artificial, synthesized hGH, which is significantly less expensive than "the real thing". But there are also in circulation a number of relatively inexpensive substances branded by their sellers in one way or another to suggest that they are hGH, but which are not; it is quite probable that many users of what they think is hGH are getting the imitation substances (one clue is price--even the synthesized "real" hGH is pretty expensive).

As with steroids, the key questions are: What gains might it provide? What harmful side effects might there be? We will again examine each question separately.

Gains From hGH

It's hard to believe at this point that there is anyone left who actually needs to be persuaded that hGH has zero effect on performance ability. Nonetheless, knowing that there are still both the innocently ignorant and the entrenched deniers, let's look. As to the "benefits", the Mitchell Report itself observes that A number of studies have shown that use of human growth hormone does not increase muscle strength in healthy subjects or well-trained athletes. Athletes who have tried human growth hormone as a training aid have reached the same conclusion.

If you want a pretty definitive summary of the case, try the article "I Don't Worry about HGH in Baseball, and Neither Should You", from the Sabernomics web site. It not only presents the points pithily, it even includes some further linked references that the really skeptical can follow out. But the conclusion, shown below, stands as today's consensus opinion.

With MLB's adoption of mandatory testing for steroids, many thought that home run rates would drop dramatically. They didn't, and many felt that the lack of a test for hGH could be part of the explanation. Well, it's time for the scientists working on such a test to start something else more important. Even if players are taking hGH, the drug is no more effective than ionized bracelets, magnets in your shoes, or jumping over the foul lines. The impact of hGH on home runs in today's game is zero. If a player is dumb enough to take this stuff, let him go right ahead.

Those wanting more scholarly citations will have no trouble finding them:

But if hGH does nothing for strength (or speed or endurance or anything of that sort), it may--emphasis on "may"--have some effect in promoting better or more rapid healing of actual injuries; George Mitchell remarks that because human growth hormone stimulates growth in most body tissues, athletes use it to promote tissue repair and to recover from injury. If that is some form of "cheating", perhaps we'd best also ban ice packs for pitchers arms, aspirin, maybe even soap for handwashing.

Some confusion in the popular mind doubtless arises because hGH can increase apparent muscle size; but for reasons best left to advanced biochemistry, the added muscle fiber does not in fact add any strength--and may even subtract a little. Dr. Marc R. Blackman, chief of the endocrine section at the National Institutes of Health's National Center for Complementary and Alternative Medicine and researcher on the use of growth hormone in healthy adults, has remarked that "Studies show that the amount of muscle increases, but not a single one shows an increase in strength or functional usefulness."

Also noteworthy is an article, "Growth Hormone Treatment of Tibial Fractures: A Randomised, Double-Blind, Placebo-Controlled Trial", in which the authors conclude that:

In closed tibial fractures separately, hGH treatment accelerated healing significantly, which may be of benefit in people with closed fractures. No new hGH safety issues were identified. So there is plenty of room for valid belief that hGH has significant and legitimate healing properties.

(Presumably healing bone fractures is allowed under MLB rules.)

Harmful Side Effects of hGH

First off, we must--as with steroids--take great care to note that we are addressing use by adults, and that use by adolescents carries a whole other set of potentially grave consequences.

Overview of hGH Side Effects

There is simply no plausible evidence of any sort of significant harm, or even much risk. Indeed, normal body amounts of hGH can vary by a ratio of at least 100:1.

Since growth hormone occurs naturally in the body, it is hard to distinguish between one's own growth hormone and the injected protein. The level of growth hormone varies widely through the course of a day--depending on nutrition, sleep and activity--making it almost impossible to set an amount that would be considered "too high" and indicative of doping -- BioMechanics, May 2006.

The Wikipedia article on Growth hormone remarks that Side effects in adults may include fluid retention, joint pain, and nerve compression symptoms. Besides those issues, others raised (by George Mitchell) include acromegaly, cancer, diabetes, impotence, cardiomyopathy, hypothyroidism, arthritis, and a few others. For completeness' sake, we will look more closely at each.


From an article (not a science study) in the May 2006 issue of Biomechanics:

Blackman's [2002] study [Blackman et al., JAMA. 2002;288:2282-2292] found a significant increase in . . . carpal-tunnel symptoms in men taking a combination of growth hormone and testosterone, and arthralgias [joint pains] in men taking growth hormone only. These side effects, which can be reversed by adjusting dosages and stopping use of the drug, have been found in previous growth hormone studies. More troubling, however, is a tendency toward a diabetic pattern in growth hormone users. The Blackman study detected a statistically significant increase in diabetes or fasting glucose intolerance in male subjects who received growth hormone compared to those who did not.

Yet a very recent (February 2007) publication, Care Report: Strong Diabetes [Young and Anwar, Br J Sports Med 2007;0:1-2. doi: 10.1136/bjsm.2006.030585], in which is reported an athlete apparently becoming diabetic from hGH, states expressly that:

It is believed that this is the first reported case of frank diabetes precipitated by supraphysiological recreational growth hormone misuse.

There have been no studies to monitor the chronic effects of growth hormone misuse in healthy young people who otherwise have no growth hormone deficiency. . . . Therefore, it is not known whether growth hormone misuse simply unmasks latent type 2 diabetes at an early stage, or whether it actually induces diabetes in an individual without diabetes otherwise.

If, by February of 2007 there has been but one case reported--as the authors noted, we see so little in the way of complications--scarcely suggests a significant likelihood of diabetes causation from hGH, which has been in relatively wide use for many years.


Acromegaly is a condition in which the human body itself produces a gross excess of hGH. It is not a condition plausibly caused by the taking of hGH, even at athlete levels: though athlete use is typically well beyond normal therapeutic levels (to the extent that there are such things for persons not suffering an hGH deficiency), acromegaly is thought to begin presenting at doses from 10 to 100 times therapeutic levels. To state that acromegaly is a "side effect" of hGH is like saying drowning is a side effect of drinking water.

That is not to say that there are no adverse growth effects: prolonged severe over-use could produce joint pain, or perhaps carpal-tunnel syndrome. But acromegaly per se is not a realistic risk--even the US Department of Health and Social Services agrees : excessive doses of GH . . . may theoretically cause acromegalic features . . . .

In clinical references, we find little. Perhaps the most relevant is "Acromegaly Induced by Growth Hormone Replacement Therapy" (B. Karges, Pfäfflec, Boehm, W. Karges; Hormone Research 2004;61:165-169), in which a single patient seriously deficient in hGH treated with what was retrospectively seen as an excess dose eventually developed, after 7 years, "clinically active acromegaly"; also, Upon GH dose reduction, the IGF-1 serum levels returned to normal, and the patient's clinical status stabilized. That is scarcely grounds for positing an implied strong correlation between hGH use and acromegaly. (No wonder the doctors laughed.)


There is occasional mention of potential cancer linkage--but at least some, and probably most or all, of the studies supposedly "linking" hGH and cancer can be discounted: one set derives from concerns of the effects of bovine growth hormone, given (in the U.S. only) to cows to increase milk secretion; another derives from that decades-old concerns about hGH taken from corpses. Neither is an issue here and now.

As one paper puts it, "data are limited and conflicting". Another study ( Growth Hormone-Deficient Dwarf Animals Are Resistant to Dimethylbenzanthracine (DMBA)-Induced Mammary Carcinogenesis [Ramsey et al., Endocrinology Vol. 143, No. 10 4139-4142]) showed that a modest decrease of a substance (IGF-1) that hGH boosts seemed to cause decreases in cancer rates; the implication is that hGH, by raising IGF-1 levels, might do the reverse, increase cancer rates, but that is not explicit in the study. It is perhaps noteworthy that the cancer most mentioned is breast cancer in females.

Another study, "Growth hormone treatment: cancer risk" [Sklar, Horm Res. 2004;62 Suppl 3:30-4], concluded that Overall, the clinical data are reassuring, but continued surveillance is mandatory. On the same note, Dr. Stanley Slater, associate director for geriatrics at the U.S. National Institute on Aging, remarked "There is no clinical evidence of it causing tumors to grow faster, but on biological grounds there is some suspicion. If you give someone growth hormone for 30 years, nobody knows what will happen."

As far back as 1960, Lipsett and Bergenstal [Lack of Effect of Human Growth Hormone and Ovine Prolactin on Cancer in Man, Cancer Research, Vol. 20, (1172-1178)] found that short-term hGH use did not appear to have any immediate carcinogenic effect, at least on breast or prostate cancers.

In sum, there are no data showing cancer risks from hGH use, but there are some preliminary animal studies that suggest that there might be some long-term risk. That is not to minimize the matter: the risk may be small and long-term, but the outcome is severe. But, again, data are limited and conflicting.


Curiously, many hGH users are taking it in an attempt to cure impotence, and science finds that reasonable. For example, there is Becker et al., Serum levels of human growth hormone during different penile conditions in the cavernous and systemic blood of healthy men and patients with erectile dysfunction [Urology, 2002 Apr;59(4):609-14]:

We believe our data provide strong evidence that GH may be of major importance in the maintenance of male erectile capability . . . .

Despite much diligent searching, I at least could find only a couple of passing references to hGH causing impotence, and none with any citations (save a reference to "Kieman and Cowan, 1992", which also I cannot locate). I daresay it is safe to write this one off as "silly".


Once again, we find hGH used as a treatment for the condition at issue. (See Pediatrics 2004 Oct;114(4):e452-8 or Z Kardiol 1998 Jun;87(6):425-35). Perhaps the simplest statement is in "Long-term stable expression of human growth hormone by rAAV promotes myocardial protection post-myocardial infarction" (Journal of Molecular and Cellular Cardiology Volume 42, Issue 2, February 2007, Pages 390-399):

It has been shown that growth hormone (GH) exerts a favorable effect on cardiovascular function in clinical and animal studies.

Another one busted.


And yet again: a condition for which hGH is generally regarded as a therapy, not a cause: it is normally a deficiency of hGH that causes or is associated with hypothyroidism. As to its effects when used for other conditions, it was reported in "Changes in Thyroid Hormone Levels during Growth Hormone Therapy in Initially Euthyroid Patients" (Wyatt, Gesundheit, and Sherman; Journal of Clinical Endocrinology & Metabolism Vol. 83, No. 10 3493-3497) that:

There were no clinical signs of hypothyroidism and no change in baseline or TRH-stimulated TSH levels or in cholesterol levels, and all patients grew at velocities expected for the treatment schedule. There is little evidence for the development of clinically significant hypothyroidism in the great majority of initially euthyroid patients after GH therapy is begun.

There are occasional mentions in the literature of hypothyroidism resulting from hGH, but I could not find any clear statement beyond such allusions; one source referred to it in a passing mention of "paradoxical" hGH effects, a term which is suggestive in the context. I am not a doctor, and don't even play one on TV, but it sounds to me as if a few particular individuals might respond in a way opposite to norms, and thus be at some risk. But, as noted here many times, there is no medication that does not carry some risks of unusual idiosyncratic responses. It seems--to borrow a term--paradoxical to list a condition that hGH normally improves as a specific "risk" from the substance.


Well, how familiar: hGH is often used to treat arthritis , notably juvenile rheumatoid arthritis. I, at least, found no references to hGH as a causative factor in arthritis.

It should be noted that gross overuse of hGH can cause some joint swelling and discomfort, owing to its, well, growth effects (as discussed above at acromegaly). That is unwanted, but is not itself arthritis, and normally reverts on cessation of use.

"Additional risks"

These arise from George Mitchell's ill-advised sortie into medicine. They include the "dangers" of using cadaver-extracted hGH, which ceased existence in 1985 (but sounds nice and creepy), and references to hGH "of unknown or questionable origin". Well, perhaps that is a risk, but it is not a risk of hGH per se, it is a risk with any substance not right out of the USP. And ironically it is only a risk because the useless and largely harmless hGH is a "banned substance". People died of poisoning drinking bad hooch during Prohibition: was prohibiting alcohol a wise idea?

Summing hGH Health Risks

The scientific literature supports very little concern--chiefly possible joint pain or, in the most serious realistic cases, carpal-tunnel syndrome. No other rumored risk is supported by the literature as plausible. Not a few of the loosely rumored "risks" are in reality conditions for which hGH is used as treatment.

And so, as Dr. Johnson so famously did say, "there's an end on't!"


This is only a very light skimming of this subject. It assumes that ballplayers a) are only using oral, not injected, amphetamines, and b) that they are not into such poisonous excesses as metamphetamines, which are highly addictive and generally toxic.

It has long been known in both theory and practice that amphetamines do have a positive effect on athletic performance. In 1981, Latles and Weiss, in "The amphetamine margin in sports" [Fed Proc. 1981 Oct;40(12):2689-92], reported that:

The amphetamines can enhance athletic performance. That much seems clear from the literature, some of which is reviewed here. Increases in endurance have been demonstrated in both humans and rats. Smith and Beecher, 20 years ago, showed improvement of running, swimming, and weight throwing in highly trained athletes. Laboratory analogs of such performances have also been used and similar enhancement demonstrated. The amount of change induced by the amphetamines is usually font, of the order of a few percent. Nevertheless, since a fraction of a percent improvement can make the difference between fame and oblivion, the margin conferred by these drugs can be quite important.

Their effects on fatigue were especially noted by, inter alia, Chandler and Blair, "The effect of amphetamines on selected physiological components related to athletic success", Medicine & Science in Sports & Exercise. 12(1):65-69, 1980:

The most revealing results were in the area of increased time to exhaustion during the Vo2max test presumably due to higher lactic acid tolerance, thus a possible rationale to substantiate the theory that this drug has the ability to mask fatigue. It may also be possible that the biochemical actions of the drug alter fatigue processes directly.
hGH molecule

Ballplayers do not appear to take amphetamine pills ("greenies" or "beans") so much for any boost as the obverse: to avoid a sag. The possibilities for sagging are obvious in a highly demanding sport played day in and day out for months on end, with frequent rravel, often cross-time-zone, thrown into the mix. Greenies are perceived as having an effect much like that of caffeine, that is, restoring alertness.

hGH molecule

Since players have always had copious amounts of coffee readily available, their resort to greenies signifies that they believe that the effects are either greater, more easily induced, longer lasting, or some combination of those things. I, at least, could not determine from a scan of the literature what the comparative effects of caffeine and amphetamines might be, and I suspect that they are not well quantified yet.

In any event, however, caffeine--as obtained in typical fashion, as by drinking coffee, is considered reasonably safe; amphetamines are emphatically not:

Addiction and dependency to [amphetamines] are extremely rapid. Side-effects include insomnia, exhaustion, violence and [possible] serious heart diseases.
    -- Pirnay, "Doping in sports" [Rev Med Liege. 2001 Apr;56(4):265-8]

Amphetamines redirect blood away from the skin, limiting the cooling of the blood. Therefore heatstroke is the most common side effect associated with amphetamines in sport, and has resulted in several deaths--often in cycling. This shift in blood volume, together with the other sympathomimetic effects of amphetamines, also presents a risk of cardiac arrest. Their ability to obscure painful injuries--although welcomed by some sportsmen--may result in players in contact sports carrying on long after their normal pain threshold would have removed them from the [field]. This can exacerbate serious injuries. There is also a very large risk of developing dependence to these drugs, both on the sports field and off.
    -- Rudge and Scifano, "The abuse of stimulants in sport" [Boll. Farmacodip. e Alcoolis., XXIV (4) 2001 (65-69)]

Greenies are long since banned by MLB, but conjecture is that their use continues to be widespread, if less open than formerly. The gross mistruths about steroids, hGH, and other PEDs that have been a staple of the "war against drugs" (aka Reefer Madness II) have, regrettably, made PED users so profoundly cynical about received wisdom that it may be very difficult to convince them that greenies are a real risk, and caffeine nearly as good (or, considering caffeine's remarkable effects, as good) as a substitute.

A Few Others

Let's just take a second for a brief look at a couple of other less-important PEDs.

Although [creatine] supplementation exhibits small but significant physiological and performance changes, the increases in performance are realized during very specific exercise conditions. This suggests that the apparent high expectations for performance enhancement, evident by the extensive use of [creatine] supplementation, are inordinate. -- The physiological and health effects of oral creatine supplementation [Terjung et al., Med Sci Sports Exerc. 2000 Mar;32(3):706-17]

We conclude that oral androstenedione does not increase plasma testosterone concentrations and has no anabolic effect on muscle protein metabolism in young eugonadal men. -- Androstenedione Does Not Stimulate Muscle Protein Anabolism in Young Healthy Men [Rasmussen et al., The Journal of Clinical Endocrinology & Metabolism Vol. 85, No. 1 55-59]

Of course, one paper per substance is not dispositive, but there are many more available. Regarding "andro", one might look at, for instance, Broeder, 2000; Brown, 2000; or Brown, 2001, all of which support the position, which seems nearly consensus, that andro is not particularly useful for athletic gains.

The take on creatine seems also generally in agreement with Terjung (above): mild enhancement. See, for example, Mihic, 2000; Persky, 2001; or Becque, 2000.


If we strip away the formalities and translate the abundant scientific evidence into plain talk, what we find about the risks of side effects from PEDs is this.

But we always have to keep in mind that as with anything one puts onto or takes into one's body, there can always be rare instances of individuals with thoroughly atypical responses, who thus might show unusually adverse reactions to this or that PED. That is not in itself a reason for considering such substances pernicious, much less for banning them, any more than it is for, say, sulfa drugs or acetaminophen or aspirin or, for that matter, coffee--which contains the potent narcotic caffeine.

PED Medical Effects on Performance

Steroids assist muscle development using resistance training. Other than some bodybuilders and weight-lifters, no athlete taking steroids is achieving his maximum possible strength, so steroid use does not actually augment strength, it simply reduces the total time and effort to reach and maintain a given level of strength. Steroids have a marked differential effect in muscle development, their effect being very much greater on upper-body musculature than on lower-body musculature; that is a crucial factor in baseball.

Human growth hormone somewhat increases muscle mass, but does not augment strength or any other athletic-performance measure. Other PEDs have either mild or no effects on athletic performance.

PED Side-Effect Risks

Excluding false or quite trivial factors, steroids appear to present the following risks: liver complications from massive doses of 17-α-alkylated type (reversible); lowering of fertility (reversible); and gynecomastia. Of those, only the last seems a true threat, in that it is not necessarily reversible merely on cessation of use, and in a few cases may not even respond to post-usage chemotherapy, requiring surgical intervention of a nontrivial nature. But it is also a risk whose appearance is immediately obvious to the subject.

Human growth hormone can, at high dose rates, cause joint discomfort, and possibly even carpal-tunnel syndrome. These effects are, however, reversible on cessation.

The Bottom Line

There are no significant long-term health risks associated with known PEDs that are not avoidable or reversible by cessation of use if symptoms present, and not many of any sort. Were the substances not illegal, which precludes reputable medical authorities from giving advice and supervision concerning their use, they would be considered altogether harmless. Even as it is, only the most uninformed users could be at any risk at all. To say--in flagrant despite of the collective opinion of the American Medical Association--that PEDs are a significant health risk to adults to the extent of justifying illegality or banning for that reason is sheer fabrication.

This page is one of several each providing a detailed analysis of one or another of the chief claims about the use of PEDs (Performance-Enhancing Drugs) in baseball. Though each, including this one, can be read "stand-alone", you really should first read the main page here, which summarizes all of the findings and sets them out them in a coherent presentation.

You loaded this page on Sunday, 26 May 2024, at 05:28 EDT.;
it was last modified on Sunday, 20 September 2020, at 00:36 EDT.


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Site Directory:

Search this site, or the web:

  • Overview and Summary
    a summary presentation of what appears in much more detail on the pages listed below

  • Actual Baseball Effects of PEDs
    two distinct, detailed analytic examinations of how PEDs might affect baseball statistics and of whether they have in fact done so, and why or why not, with links to several other such studies

  • Changes in the Baseball
    full discussions of the methods and results of two unrelated laboratory examinations of baseballs from several different years to see if there have been performance-affecting changes in the ball over time

  • The "Spliced" Power Factor
    a more detailed graphic explanation of what the "spliced" power factor graph is and how it is created

  • Medical Effects of PEDs
    comprehensive reviews of all the medical-side-effect claims about steroids, hGH, and other PEDs, supported by extensive citations from the established scientific literature of medicine

  • PEDs as Healing Agents
    looking into the claim that PEDs augment count-type records by allowing players to participate in more games than they could without chemical help

  • Adolescent Use of PEDs
    hard, scientific data from multiple extensive, long-term surveys of adolescent use of PEDs, detailing the actual extent of use, the established reasons for such use, and the true significance of "role models" in PED use

  • Ethical Issues in the Use of Performance-Enhancing Substances
    what professional medical ethicists have to say about how PED use in sports should be evaluated and why

  • Baseball and PEDs: Further Resources
    a select list of thought-provoking articles, essays, and books, a number of which are not cited elsewhere in these pages

  • Drugs in Sports: a Bookshop
    a collection of books relevant to drugs and sports, available for sale from this site

  • Eric Walker: Links
    baseball-related web pages by, about, or citing the webmaster of this site

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