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  1. #1
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    interesting read

    this is a good read, kinda long but not too bias.

    Anabolic Steroids
    A Review for the Clinician
    Eric C. Kutscher,1,2 Brian C. Lund2 and Paul J. Perry2,3
    1 Western Missouri Mental Health Center, Kansas City, Missouri, USA
    2 Clinical and Administrative Pharmacy Division, College of Pharmacy, University of Iowa,
    Iowa City, Iowa, USA
    3 Department of Psychiatry, College of Medicine, University of Iowa, Iowa City, Iowa, USA

    The number of athletes self-administering ergogenic pharmacological agents
    to increase their competitive edge continues to be a problem.Most athletes using
    anabolic steroids (AS) have acquired a crude pharmacological database regarding
    these drugs. Their opinions regarding steroids have been derived from their subjective
    experiences and anecdotal information. For this reason, traditional warnings
    regarding the lack of efficacy and potential dangers of steroid misuse are
    disregarded. A common widely held opinion among bodybuilders is that the anabolic
    steroid experts are the athletic guruswho for years have utilised themselves
    as the experimental participants and then dispensed their empirical findings. This
    review will address the common anabolic steroid misconceptions held by many
    of today’s athletes by providing an evaluation of the scientific literature related
    to AS in athletic performance.
    As athletic competition continues to intensify,
    athletes strive for higher levels of performance to
    achieve success. Many of these athletes, as well as
    their coaches, believe that one must do whatever is
    required to win. If this formula requires the use of
    performance enhancing substances, such as anabolic
    steroids (AS), this is an acceptable gamble. Thus,
    the number of athletes administering performance
    enhancing pharmacological agents to achieve their
    goals is no longer limited to elite athletes, but to all
    categories of athletes.[1]
    Being actively involved with the bodybuilding
    population, through various regional and national
    bodybuilding competitions as well as interviewing
    bodybuilders around the Midwest, the authors are
    aware of the use of various types of performance enhancing
    agents. These athletes have varying attitudes
    on the effects, mechanism of action, and adverse
    effects that are related to the use of these substances.
    AS are themost prevalent agents being used among
    this population. AS are also the most studied of all
    the performance enhancing agents. Although there
    are many AS studies, there is no consensus among
    researchers regarding their effectiveness as ergogenic
    agents. In contrast, bodybuilders eagerly postulate
    numerous potential mechanisms of action and
    endorse AS efficacy because of their first-hand experience.[
    2]
    The AS using athletes of today have a ‘sophisticated’
    steroid pharmacological knowledge, based
    on both their subjective experiences and anecdotal
    information, which in their minds surpasses the majority
    of healthcare providers.[1,3] For this reason,
    traditional warnings from healthcare providers regarding
    the lack of efficacy and potential dangers
    of steroid misuse are largely disregarded.[1] Today,
    it appears that the AS experts in athletic competition
    are not medical clinicians, but athletes and former
    athletes who dispense their anecdotal AS experience
    as dogma to anyone willing to listen. Healthcare
    professionals caring for these athletes need to
    have amore thorough understanding of theAS ergogenic
    literature to have legitimate dialoguewith these
    patients when caring for them. Clinicians run the
    risk of losing their credibility with patients because
    they are under-informed as to the efficacy and toxicity
    of the AS.[1]
    Unfortunately, based on the pattern of AS usage
    currently being practised in the US, past efficacy
    and toxicology studies are of limited value in delineating
    the benefits and hazards of these drugs in
    the common dosages used by today’s athletes. Due
    to the limitations among current studies on the effects
    of AS, and the lack of literature in athletic performance,
    understanding the beliefs of the user by
    the general practitioner may be difficult. The goal
    of this article is to provide an unbiased summary
    of the relevant literature relating to AS use, including
    epidemiology, pharmacology, efficacy, adverse
    effects and misconceptions common among bodybuilders.
    This review will also incorporate the anecdotal
    theories of bodybuilders relating to safety
    and efficacy and the relevant literature that rebuts
    or strengthens their arguments. The uses of nutritional
    AS, such as androstenedione, are not included
    in this review.
    1. Epidemiology
    The prevalence of AS use has been reported in
    several populations, but data on the exact prevalence
    are limited to surveys of students and athletes
    whomay be reluctant to admit actual usage of these
    controlled substances. There have been estimates of
    more than 1 to 3 million current or former AS users
    in the US. Many of these may be young adults.[4,5]
    The most recent estimates report that 4 to 12% of
    US high school boys have used AS at sometime in
    their life.[6] Arecent survey conducted by Blue Cross
    and Blue Shield Association[7] reported that AS were
    the second most common substances known to be
    used for athletic performance among 12- to 17-yearold
    people, second only to creatine (31 vs 57%,
    respectively). Sullivan et al.[8] reported that 65 to
    84% of adolescent AS users were participants in
    organised athletics.[8] On the other hand, other reports
    showed that 3.2% ofModesto, California 7th
    grade girls and 2.8% of Massachusetts 6th and 7th
    grade girls have reported using AS, respectively.[9,10]
    These reports of AS use may be confounded by false
    positive reports, consisting of over the counter AS
    supplements or failure to accurately answer survey
    questions correctly. Nonetheless, these numbers are
    worrisome, especially when considering the adverse
    growth suppressing effects of AS in young adults.[11]
    A recent National Collegiate Athletic Association
    survey[12] found that only 1.1% of college athletes
    surveyed reported AS use, and Yesalis et al.[13] reported
    29.3% of college football players and 20.6%
    of male track-and-field athletes reported AS use.
    Some of the highest estimates have come from Yesalis
    and Bahrke,[10] reporting that 78% of trackand-
    field athletes in 1972 had prior steroid use .
    After Olympic athletes, the second most prevalent
    group believed to misuse AS is the bodybuilding
    and/or weightlifting population. Yesalis et al.[14]
    reported that 55%of elite power lifters admit to AS
    usage. Tricker et al.[15] reported the same percentage
    among amateur competitive bodybuilders. These
    high numbers relate to the fact that many bodybuilding
    competitions do not actually test for AS
    usage among competitors.Many of the ‘natural bodybuilding’
    organisations provide the option of polygraph
    or urinalysis tests if a competitor stands out
    as an AS user. Most ‘major’ competitions such as
    those held by the National Physique Committee,
    state that athletes must be ‘drug free’but do not test
    the competitors. Additionally, athletes have found
    systems to work around the rules of competing ‘drug
    free’ and have actually challenged the credibility
    of drug testing in athletic competition.[16]
    Although these reports of AS usage seem high,
    our experience in surveying bodybuilders suggests
    that these numbers may be under estimated. Indeed,
    current methods of self-reporting and/or surveying
    AS usage may yield inaccurate estimates in this
    population. We have observed that since AS were
    286 Kutscher et al.
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    categorised by the US Congress as Schedule III
    (non-narcotic) class drugs of misuse in 1990,[10]
    AS users have become far less forthcoming about
    their use of these drugs. This makes identification
    of AS using athletes by the primary care practitioner
    as well as in epidemiology studies problematic.
    2. Physiology
    In general, the physiological mechanisms of AS
    are commonlymisunderstood and overstated in the
    bodybuilding population. Many beliefs are anecdotal
    at best, and not supported by the medical literature.
    The two most common AS questions posed by
    bodybuilders to physicians are, ‘How exactly do AS
    cause muscle growth,’ and ‘Is this a dose-dependent
    effect?’ AS have numerous proposed mechanisms
    of action related to athletic performance. These include:
    increased skeletal muscle protein synthesis
    and skeletal muscle hypertrophy;[17,18] a decrease
    in the rate of protein breakdown;[11] an increase in
    the number of mononuclei;[19] activation of satellite
    cells;[19] and an increase in the number of androgen
    receptors containing mononuclei.[19] However, the
    exact mechanism is not understood. Misconceptions
    among athletes regarding the effects of AS on
    physiology often occur, and may account for the
    increase in serious adverse effects seen in this population.
    The physiological function of satellite cells in
    muscle growth is a source of considerable confusion.
    The effects of AS on the satellite cells are
    commonly misunderstood by bodybuilders. During
    muscle growth, myoblasts (young muscle cells)
    proliferate to eventually form mononuclei (mature
    muscle cells) in skeletal muscle. There are a number
    ofmyoblasts that do not mature into mononuclei;
    these cells are labelled as satellite cells.[19] After
    injury, such as that related to athletic training, satellite
    cells are recruited as the primary vehicle in
    muscle repair. These cells are eventually incorporated
    into muscle fibres as mononuclei during the
    repair and growth process.[19] Strength training increases
    the number of satellite cells, thereby causing
    muscle growth.[19] When the stress from exercise
    or training does not inducemuscle injury there
    does not seem to be growth in the muscle. The number
    of satellite cells available for recruitment in AS
    users versus non-users does not differ.[19] Thus,AS
    do not affect muscular hypertrophy by increasing
    the number of satellite cells in the muscle after injury.
    Instead, training appears to be the dynamic parameter
    that governs satellite cell number. This finding
    contradicts the notion of most bodybuilders that
    AS increase muscle recovery after intense training.
    Themisconception of faster recovery during heavy
    training may be psychological and related to the
    AS-induced euphoria athletes experience during
    training. This issue will be discussed inmore detail
    in section 4.4.[20]
    Some bodybuilders have reported that AS will
    precipitate muscle growth without intense strength
    training. Thus, AS are hoped to be an antidote for
    the ‘ancient wisdom’ of ‘no pain no gain’. However,
    the available data suggest the opposite. Bhasin et
    al.[21] provided evidence that testosterone administration
    could increase muscle strength and size in
    males, but only in the presence of weight-training.
    Use of AS and exercising theoretically increases
    the number of mononuclei in the muscle that can
    be used to increase protein synthesis and hence repair
    injured muscle and increase muscle size and
    strength.[19] For muscle growth to occur, stress on
    the muscle is required. Thus, the idea of using AS
    without increased weight-training to increasemuscle
    size and strength is erroneous.
    Most bodybuilders believe that a high protein
    diet enhances muscle growth during training. This
    observation is true since athletic training causes the
    catabolic effects of the glucocorticoids to generate
    a negative nitrogen balance. The body responds to
    this negative nitrogen balance by utilising the protein
    stores of the body to revert to a positive balance.[
    20] AS are extremely anticatabolic and convert
    a negative nitrogen balance to a positive balance
    by improving the utilisation of dietary protein and
    increasing protein synthesis.[17,20] AS use in normal
    and catabolic (training) individuals precipitates
    protein synthesis within the muscle cell, which in
    Anabolic Steroids 287
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    turn results in a positive nitrogen balance. Since
    normal individuals are not in a negative nitrogen
    balance (catabolic state), the effects of ASwill only
    be short-lived.[20] This fact explains why AS users
    report that the more they train and ingest protein
    while using AS, the more they ‘grow’.
    AS oppose the effects of glucocorticoids, not only
    through a positive nitrogen balance, but also through
    competition for glucocorticoid binding sites.[18,22]
    This effect decreases the amount of cortisol and
    other glucocorticoids available in the body. Studies[
    22] show that testosterone and other AS compete
    with cortisol, dexamethasone and triamcinolone for
    glucocorticoid binding sites. This competition may
    help reverse the negative nitrogen balance induced
    by training. Hence, the belief of some athletes that
    AS have an anticatabolic effect that results in a
    positive nitrogen balance is correct.
    Most bodybuilders assume that there is a dosedependent
    effect of AS on androgen receptor formation
    and muscle mass increase (unpublished observations).
    This notion is not absolutely correct in the
    absence of strength training. Kadi[19] showed that
    androgen-receptor–containing muscle fibres ormononuclei
    are highly selective. Androgen receptor content
    of the muscle fibres is a function of the type of
    muscle. There can either be a receptor up-regulation
    (increase in receptors) or a down-regulation (decrease
    in receptors) depending on the type of skeletal
    muscle involved. This could explain the distinguishing
    features of most bodybuilders, such as large
    trapezius and deltoid muscles, which may result
    from greater AS receptor up-regulation in these two
    areas.[19]
    The significance of the AS-androgen receptor
    complex interaction is commonly misunderstood.
    When an androgen binds to the androgen receptor
    on the nucleus of a muscle cell, a receptor-androgen
    complex is formed that is then transferred into the
    nucleus of themuscle cell. Once in the nucleus, this
    complex binds to complementary regions on DNA
    to activate the transport-RNAand producemessenger
    RNAthat encode a variety of enzymes and proteins.[
    17,23] The action that eventually occurs is the
    up- or down-regulation of the androgen receptors,
    increased protein synthesis and possibly an increase in
    the number of mononuclei in a muscle fibre.[17,23]
    Hence, the effect of AS on muscle fibre androgen
    receptors is dependent on themuscle type and number
    of receptors present.
    Muscle fibres replicate after strenuous activity,
    which in turn increases the total number of androgen
    receptors in that muscle group. An increased
    number of androgen receptors provide additional
    functional binding sites for androgens, which in turn
    leads to an enlargement of that muscle group.[17]
    An opinion that transcends all the AS medical literature
    is that AS do not provide much benefit in
    the absence of strength training.[19,24-26] This opposes
    bodybuilders’ anecdotal observations that higher
    doses of AS are more effective for muscle growth
    in the absence of increased strength training. The
    only means by which excessive supraphysiological
    doses of AS can benefit an athlete is by there being
    a surplus of uninnervated AS receptors. However,
    the only means to achieve a surplus of AS receptors
    is by heavy training.[19]
    The final performance-enhancing effect of AS,
    which is less commonly known among bodybuilders,
    but well known by runners, is the resultant increase
    in erythropoietin synthesis. This increase in erythropoietin
    subsequently increases hematocrit and blood
    oxygen carrying capacity.[24] Because of these effects,
    AS have been used in the treatment of anaemia.[
    27] However, this indication has been largely
    forgotten after recombinant human erythropoietin
    (epoetin alfa) became commercially available. Although
    the increase in oxygen carrying capacity
    would be expected to increase athletic performance,
    it is partially offset by sodium retention and blood
    volume increase. This can result in potentially fatal
    sludging of blood should the hematocrit increase
    too much.[24] These haemodynamic alterations may
    contribute to some of the bodyweight gain observed
    byASusers.[24] Currently erythropoietin has replaced
    the use ofAS for ‘blood doping’where athletes transfused
    themselves with blood having a greater than
    normal content of red blood cells.
    288 Kutscher et al.
     Adis International Limited. All rights reserved. Sports Med 2002; 32 (5)
    3. Efficacy
    Reviews of the effect of AS on athletic performance
    suggest that there is only limited evidence
    to support the efficacy of these drugs in athletic
    performance.[10] Many studies[21,25,26,28] contain
    significant methodological flaws in dosage and administration
    strategies when compared with realworld
    use. Athletes ‘stack’ AS. The drugs are administered
    in cycles of gradually increasing doses
    and increasing numbers of agents combined together
    (stacked). The cycles used are generally between 7
    to 14 weeks in length and involve a combination
    of oral agents and long-acting injectable agents.[29]
    In contrast, for ethical reasons, clinical investigations
    have been restricted to single agent regimens.
    Athletes tend to use oral agents in doses that are
    similar to those of clinical studies, but typically use
    injectable steroids at doses 3 to 8 times those utilised
    in clinical trials.[29] Disconcerting to us are anecdotal
    reports of supraphysiological doses of themore
    hepatotoxic C-17 alkylated agents being used (table
    I). Because higher dosages of AS tend to be
    used by athletes, it is difficult to compare anecdotal
    reports of efficacy with findings of clinical trials
    evaluating AS as single agents administered at lower
    dosages.
    Currently available data suggest that AS cannot
    produce a significant effect on muscle strength unless
    they are combined with weight training. The
    most recent demonstration of AS ergogenic potential
    was documented by Bhasin et al.[21] Forty-three
    men were randomised into four groups: placebo and
    no exercise, testosterone and no exercise, placebo
    plus exercise, and testosterone plus exercise. Testosterone
    was administered as testosterone enanthate
    (TE) 600 mg/wk, defined as a supraphysiological
    AS dosage. The mean bodyweight in all participants
    who received TE increased significantly (p <
    0.001) greater than that noted in the placebo group.
    The TE and exercise group increased the most, with
    an average bodyweight gain of 6.1kg. Additionally,
    both TE groups had significant increases (p <
    0.001) in cross-sectional areas of the triceps and
    the quadriceps verses the placebo group, with the
    largest increase once again occurring in the TE plus
    exercise group. The greatest increases in bench press
    were observed in the TE plus exercise group (p <
    0.001), although the placebo and exercise group
    did increase to a lesser degree (p = 0.005). There
    were no significant muscle increases observed in
    the placebo and no exercise group.[21]
    Two additional studies[26,30] also observed increased
    strength with metandienone administration
    plus exercise over placebo groups, which supports
    the Bhasin et al.[21] findings. Hervey et al.[31] noted
    that high dosages (25 mg/day) did not produce obvious
    differences in strength over low dosages (10
    mg/day). Thus, these data suggest that AS augment
    exercise to produce muscle growth. Additionally,
    the larger dosages used did not produce obvious
    muscle gains over the lower dosages. Unfortunately,
    no conclusions can be drawn regarding the megadoses
    commonly utilised by today’s AS users, because
    of a lack of controlled clinical studies.
    There are many anecdotal and case reports of
    largemuscle and strength gains by the use of supraphysiological
    doses of AS. Perry et al.[29] reported
    bodyweight gains of an average of 19.9kg after AS

  2. #2
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    sorry, heres the rest of it.

    Currently available data suggest that AS cannot
    produce a significant effect on muscle strength unless
    they are combined with weight training. The
    most recent demonstration of AS ergogenic potential
    was documented by Bhasin et al.[21] Forty-three
    men were randomised into four groups: placebo and
    no exercise, testosterone and no exercise, placebo
    plus exercise, and testosterone plus exercise. Testosterone
    was administered as testosterone enanthate
    (TE) 600 mg/wk, defined as a supraphysiological
    AS dosage. The mean bodyweight in all participants
    who received TE increased significantly (p <
    0.001) greater than that noted in the placebo group.
    The TE and exercise group increased the most, with
    an average bodyweight gain of 6.1kg. Additionally,
    both TE groups had significant increases (p <
    0.001) in cross-sectional areas of the triceps and
    the quadriceps verses the placebo group, with the
    largest increase once again occurring in the TE plus
    the placebo and no exercise group.[21]
    Two additional studies[26,30] also observed increased
    strength with metandienone administration
    plus exercise over placebo groups, which supports
    the Bhasin et al.[21] findings. Hervey et al.[31] noted
    that high dosages (25 mg/day) did not produce obvious
    differences in strength over low dosages (10
    mg/day). Thus, these data suggest that AS augment
    exercise to produce muscle growth. Additionally,
    the larger dosages used did not produce obvious
    muscle gains over the lower dosages. Unfortunately,
    no conclusions can be drawn regarding the megadoses
    commonly utilised by today’s AS users, because
    of a lack of controlled clinical studies.
    There are many anecdotal and case reports of
    largemuscle and strength gains by the use of supraphysiological
    doses of AS. Perry et al.[29] reported
    bodyweight gains of an average of 19.9kg after AS
     Adis International Limited. All rights reserved. Sports Med 2002; 32 (5)
    use, and an increase in the mean maximal bench press
    of 47% (p < 0.0001). The authors hypothesised that
    the obvious individual benefits of the AS makes
    these drugs psychologically addictive in many users.
    Additionally, the expected doses used may not
    actually be the actual doses, because of the diluting
    of the AS by black-market retailers. This blackmarket
    quality control problem emphasises the importance
    of obtaining serum testosterone profiles
    (total, free and weakly bound serum testosterone
    concentrations) in determining the effects ofmegadoses
    of AS.
    Contrary to beliefs of athletes using AS, some
    investigators believe that AS induce their beneficial
    effects as a result of psychological rather than
    physiologic effects. Ariel and Saville[25] showed that
    an athlete’s expectation of strength gains from AS
    could causemuscle growth, independent ofAS use.
    Fifteen male participants were informed that some
    of them would be selected to receive AS; instead, all
    participants received placebo. The apparent psychological
    effects of AS on strength were observed
    in several participants who experienced significant
    strength gains due to the belief that they were receiving
    AS. This study emphasised the psychological
    aspect of human performance, and the potential
    benefits of placebo supplementation on psychological
    enhancement. This motivational effect may help
    athletes produce significant athletic improvements
    even in the absence of AS administration.
    In light of the quality of AS literature, there remain
    a number of issues that need to be resolved to
    completely discern the efficacy of AS. All of the
    studies reviewed used single agents, contrary to the
    commonly used ‘stacks’ among athletes. Typically
    the doses administered were much lower than the
    mega-doses used by present day athletes. Despite the
    unknown efficacy of stacking, many researchers
    have suggested that stacking is a non-issue formuscle
    growth.[19,24] This is logical because regardless
    of the number ofAS being used, the endpoint is still
    the same, that is an increase in the free,weakly bound,
    and total testosterone concentrations in the body.
    Thus, all future studies of AS ought to have in common
    these three clinical chemistry parameters. Additionally,
    if these parameters are routinely measured,
    clinical correlations between AS dose and
    strength gain, muscle mass increases and adverse
    effects can be made. This monitoring strategy is
    beneficial to the athlete in that it will probably result
    in the use of smaller doses of AS. It also benefits
    the healthcare practitioners who are attempting
    to monitor and treat these athletes as patients.
    Lack of a patient-physician relationship has lead
    athletes to following guidelines in lay publications
    such as those contained in theUnderground Steroid
    handbook.[1,32]
    4. Adverse Effects
    The adverse drug effects of AS can be divided
    into 5 general categories: hepatic, cardiovascular,
    reproductive/endocrine, dermatological and psychiatric
    (table II).
    4.1 Hepatic Effects
    The association between liver function tests
    (LFT) elevations and AS has been documented in
    the literature.[20,28,33] Bodybuilders are well versed
    and quite concerned about this adverse drug effect.
    Elevations in aspartate transaminase, alanine transaminase,
    lactate dehydrogenase and alkaline phosphatase
    have been reportedwithAS use.[20]Although
    weightlifting alone can elevate LFT, individuals usingAS
    are at a greater risk of having elevated LFT.[20]
    However, hepatic enzymes usually return to normal
    onceAS are discontinued. The reversible course of
    the LFT elevations explains why athletes administer
    AS in a cyclic pattern.[34] Consequently, if AS
    are administered continually for at least 1 month,
    but generally for greater than 2 to 5 months at supraphysiological
    doses, dose-dependent jaundice and
    hepatic dysfunction are likely to develop.[34] Death
    caused by AS hepatotoxicity is extremely rare.[34]
    Of the AS, the C-17 alkylated AS aremore often
    associated with liver toxicity.[34] The most common
    C-17 alkylated AS used by athletes are the oral
    agents such as methyltestosterone , metandienone,
    oxymetholone, oxandrolone and stanozolol . Nonalkylated
    intramuscular agents such as testosterone
    and nortestosterone aremuch less likely to produce
    290 Kutscher et al.
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    liver problems.[20,34] However,many AS usersmisuse
    other substances including alcohol, which could
    possibly compound hepatic adverse drug effects.
    There have been cases of carcinoma of the liver
    associated with either high dose AS, long periods
    of administration of AS or in AS users with predisposing
    medical conditions.[20,34] Cyclic administration
    of AS reverses the risk of liver toxicity.[3]
    Additionally, avoiding C-17 alkylated agents (oral
    agents) is another practice that decreases hepatotoxicity.
    The ultimate means of preventing liver
    toxicity are AS abstention and the avoidance of other
    potentially hepatotoxic agents, such as alcohol. Although
    accepting of these facts, athletes are not
    usually concerned since the benefits of increased
    muscle mass and strength overshadow the known
    risks.
    4.2 Cardiovascular Effects
    Use of AS can lead to detrimental changes in
    serum lipid profiles. Potential changes include increases
    in low-density lipoprotein (LDL) and decreases
    in high-density lipoprotein (HDL).[27,33,35]
    Bodybuilders are generally of the opinion that since
    steroids are chemically similar to cholesterol, they
    will affect lipids in the same way as eating too much
    cholesterol. For bodybuilders this effect is not harmful
    since many of them are on ketogenic diets, which
    emphasises moderate to high fat, and low to moderate
    complex carbohydrate foods, while consuming
    extremely high amounts of protein.[32] Lipid
    changes are typically unpredictable and are unrelated
    to dosage and agents administered. A metaanalysis[
    35] conducted in 1991 reported decreases
    in HDL of 39 to 70% (mean 52%). These changes
    generally occur within the first week of administration
    and normalise within 3 to 5 weeks after AS
    discontinuation. Conversely, reports of LDLelevations
    between 11 to 100% have been reported (mean
    36%).[35] Since HDL levels decrease and LDL levels
    increase, total cholesterol levels generally do not
    reflect these changes and the atherogenic potential
    of AS can often be overlooked.[35]
    Unfortunately, many bodybuilders seem to believe
    that cholesterol monitoring is all that it required
    to monitor their lipid status. Triglyceride
    levels are also decreased by the exogenous androgen
    administration.[3] The long-term impact on morbidity
    and mortality of labile lipid profiles is unknown.
    However, an increase in LDL levels might
    directly contribute to arteriosclerosis especially if
    Table II. Most common adverse effects of anabolic steroids
    Hepatic
    LFT elevations (hepatotoxicity)
    Liver cancer
    Cardiovascular
    Decreased HDL
    Increased LDL
    Increased total cholesterol
    Decreased triglycerides
    Fluid retention (elevated blood pressure)
    Cardiac hypertrophy
    Reproductive and endocrine
    Decreased LH
    Decreased FSH
    Decreased thyroid functioning
    Adverse effects in males
    decreased spermatogenesis
    abnormal sperm morphology
    feminisation in males
    decreased size of testes
    Adverse effects in females
    hirsuitism
    voice deepening
    clitoral hypertrophy
    decreased breast mass
    amenorrhoea
    male pattern baldness
    Dermatologic
    Oily hair
    Oily skin
    Alopecia
    Sebaceous cysts
    Increased incidence of acne
    Psychiatric
    Mood changes
    Possible aggression
    Possible hostility
    Dependence and/or addiction
    FSH = follicle-stimulating hormone; HDL = high-density lipoprotein;
    LDL = low-density lipoprotein; LFT = liver function tests; LH =
    luteinising hormone.
    Anabolic Steroids 291
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    these agents are used over long periods of time.[8]
    With an increased risk of cholesterol plaques in the
    coronary vessels, a subsequent thrombus may occur
    in athletes using AS.[8] AS also stimulate platelet
    aggregation, increase coagulation enzyme activity,
    and cause coronary artery vasospasm.[8] Thus,AS
    have the potential to predispose users to thrombus
    formation by reductions of HDL, increases in LDL,
    increased platelet aggregation, coronary artery vasospasm
    and enhanced coagulation enzyme activity.
    Elevations in blood pressure in AS users have
    been reported and most likely result from blood
    volume increases and fluid retention.[8,27] This effect
    has not been well studied in humans, although
    is well-documented in animal studies.[8,27] Anecdotally,
    bodybuilders will complain of feeling an
    increase of pressure in their head and body resulting
    from what they believe is elevated blood pressure.
    AS also increase heart rate, which may lead
    to hypertrophy of the left ventricle.[8,36] Case studies
    of AS users at autopsies have found cardiac hypertrophy
    in these patients.[8] The consequences of
    cardiac hypertrophy can lead to decreasedmaximal
    oxygen uptake, remodelling of the heart, myocardial
    ischaemia and cardiomyopathy.[8] These effects
    are serious and can lead to sudden cardiac arrest,
    and will persist well after cessation of AS.[8] Unfortunately,
    it is difficult to ascertain whether the
    effects of AS on the heart are independent of the
    other agents present in the polypharmacy regimens
    of many AS users such as amphetamines as weight
    loss agents, as well as alcohol and tobacco cigarettes.
    4.3 Reproductive/Endocrine Effects
    In men, AS administration produces a predictable,
    dose-dependent depression of luteinising hormone
    (LH), and follicle-stimulating hormone (FSH)
    via the negative feedback loop of the hypothalamicpituitary-
    gonadal (HPG) axis.[30,37,38] As both LH
    and FSH are required for spermatogenesis, AS administration
    can lead to hypogonadotropic hypogonadism.
    The resulting effects of these physiologic
    changes include declines in sperm density and
    sperm count, decreased sperm motility, abnormal
    spermmorphology, testicular atrophy, and no change
    in libido.[10,27,39,40] However, the observed effect
    on libido was based on testosterone doses not exceeding
    500 mg/wk. These effects generally worsen
    with increased use of AS, and severe oligospermia
    can lead to infertility.[41] Bodybuilders are usually
    aware of these effects and often use agents such as
    chorionic gonadotropin (hCG ) to stimulate LH production
    and testicular testosterone production.[32]
    Turek et al.[41] described a case report of an AS user
    who was administered hCG 2000 to 3000 units three
    times a week. Following 3 months of treatment, the
    patient’s wife became pregnant, reportedly due to
    LH and sperm normalisation. FSH activity is required
    for completion of spermatogenesis. However,
    FSH activity is not precipitated by hCG. This
    leads to the belief that sperm counts are increased
    by hCG, but they may not be 100% viable. Many
    athletes who discontinue AS have their sperm morphology
    normalise within 4 months. However, this
    is not necessarily always the case since normalisation
    is a function of both the magnitude and duration
    of AS exposure.[38] Some individuals required
    up to 1 year for normalisation of morphology and
    motility.[37,38]
    AS can also lead to feminisation in males from
    the conversion of testosterone to estrogen metabolites
    (aromatisation).[27] As a result,many AS users
    report increased voice pitch and gynaecomastia, although
    these effects are unpredictable. Our experience
    notes that many users of AS self-administer the
    antiestrogenic agent tamoxifen to antagonise these
    effects. Unsurprisingly, the efficacy and safety of
    this practice remains to be confirmed. Our experiences
    with AS-using bodybuilders indicate that hair
    loss is minimal with testosterone ester doses of less
    than 600mg/wk. The adverse effect is reversible on
    discontinuation of the AS.
    AS use in women can lead to hirsutism, acne,
    deepening of the voice, clitoral hypertrophy, decreased
    breastmass, decreased menstruation or amenorrhoea,
    increased appetite and male pattern baldness.
    Even after discontinuation of the causative
    agents, these effects are sometimes irreversible.[42]
    292 Kutscher et al.
     Adis International Limited. All rights reserved. Sports Med 2002; 32 (5)
    The willingness to tolerate any physical and/or reproductive
    adverse drug effect to achieve an athletic
    goal is unique among AS administrating athletes.
    Other endocrine effects include decreased thyroid
    function and decreased serum T-4 binding globulin
    concentrations.[3]AS is known to cause acne
    and other skin changes including, but not limited
    to, oily hair and skin, alopecia, sebaceous cysts and
    hypertrophy of sebacious glands.High doses ofAS
    increase the amounts of Propionibacteria acnes,
    free fatty acids and cholesterol in the skin, which
    lead to these dermatological changes.[3]
    4.4 Psychiatric Effects
    Aggressive behaviour and mood changes have
    been linked to use of AS in case reports, animal
    studies and controlled clinical trials.[43,44] Although
    these reports describe increases in aggression and
    violent behaviour with AS use, there are relatively
    few controlled studies relating aggressive behaviour
    and mood changes to AS use among a bodybuilding
    and/or weightlifting population. Despite the nature
    of various reports on mood changes with AS administration,
    many bodybuilders report that they
    feel AS elicit an antidepressant-like feeling. This
    observation was recently challenged when Seidman
    et al.[45] reported no antidepressant effects of testosterone
    replacement in men with major depressive
    disorder. Conclusions of this study are limited and
    future studies of AS use in depression are needed.
    Six randomised controlled studies have administered
    supraphysiologic doses of testosterone to
    healthy male participants and observed them for
    changes in their mental status.[40,46-50] In general,
    these studies indicate little risk of mood changes
    or aggressive behaviour with doses of up to 300
    mg/week. However, with larger doses, changes in
    various mood and aggression subscales have been
    observed.
    Pope et al.[48] described significant increases in
    the Point Subtraction Aggression Paradigm (PSAP),
    and theYoungMania Rating Scale (YMRS) among
    recipients of higher testosterone doses (600 mg/wk)
    compared with placebo.[48] While between-group
    differences were observed, the distribution of individual
    scores was also important. On average, the
    endpoint YMRS scores were 3 points higher in recipients
    of testosterone. However, this difference
    does not indicate that all participants had a 3-point
    increase, but rather that most participants experienced
    no change, while a few individuals experienced
    marked changes. While Pope et al.[48] was
    able to demonstrate significant alterations in aggression
    and mood endpoints, the majority of controlled
    studies have not. This may be because psychiatric
    adverse drug effects are dose-dependent and
    all of the negative studies did not expose the participants
    to large enough doses to induce a change
    in the participants’mental status. Additionally, the
    negative studies indicate that individuals with a positive
    psychiatric history including personality disorder
    may be more susceptible to changes in mood
    and aggression.[40,46,47,49,50]
    Although AS use promotes aggression and mood
    changes, there are several limitations to the data.
    First, many of the studies did not enrol bodybuilders
    and/or weightlifters as participants.[40,46,47,49,50] The
    inclusion of healthymale participants does not represent
    individuals who are likely to use AS such as
    weightlifters, bodybuilders and other athletes. The
    second limitation is the exclusion of individuals
    with psychiatric disorders, particularly personality
    disorders. Such individuals may be more susceptible
    to AS-induced psychiatric changes than normal
    control participants. Finally, AS regimens were limited
    to a single agent administered weekly at doses
    less than 600 mg/week.[40,46-50] These regimens do
    not represent the multidrug combinations (stacks)
    and/or mega-doses of AS used by bodybuilders. Furthermore,
    the maximum dose given in clinical trials
    was 600 mg/week for 2 weeks, which is far below
    the doses commonly used by bodybuilders.[46,48]
    Data regarding AS use in bodybuilders and/or
    weightlifters and associated psychiatric changes are
    limited. Yates et al.[6] compared weightlifters that
    were either AS users (n = 20) or non-AS users (n =
    20) to alcoholics (n = 20) and non-weightlifting
    community controls (n = 20). Personality disorders
    were assessed using the Diagnostic and Statistical
    Anabolic Steroids 293
     Adis International Limited. All rights reserved. Sports Med 2002; 32 (5)
    Manual of Mental Disorders (3rd edition, revised)
    [DSM-III-R] criteria for cluster A, B and C personality
    traits, and the self-report personality diagnostic
    questionnaire. Forty-five percent ofAS users demonstrated
    antisocial personality traits compared with
    0% of community controls (p < 0.001).[6] In a later
    study, Yates et al.[51] examined the Buss-Durkee
    Hostility Inventory (BDHI) scores for eight AS users,
    four previous AS users to 25 non-AS using
    weightlifters. There were no significant differences
    among AS users, non-AS users and previous users
    on overall BDHI scores, but there were significant
    elevations on the BDHI subscores of assault, indirect
    aggression and verbal aggression among AS
    users.[51]
    A more recent study by Pope and Katz[52] conducted
    interviews with weightlifters using AS (n =
    88) and non-users (n = 68). DSM-III-R criteria
    were applied to identify psychiatric syndromes.
    Twenty-three percent of AS users experienced major
    mood changes of mania, hypomania or major
    depression. In contrast, the rate of major mood
    changes was only 6% among non-AS users (p <
    0.07). Aggressive behaviour, including fights, domestic
    disrupts, assaults and arrests, was common
    among AS users. All participants denied previous
    behaviour of this type before AS use.[52]
    Our experienceswithAS users indicate that psychiatric
    effects are unique to each individual and
    overall conclusions are difficult tomake.However,
    there are data suggesting that AS administration
    may be addictive. In interviews with 49 AS users,
    at least one DSM-III-R symptom of dependence
    was reported by 94% of the sample, while three or
    more symptoms were reported by 57% of the sample.[
    53] Three symptoms are required for a diagnosis
    of drug dependence. Arecent article[54] reported
    that 23% of AS using participants met DSM-IV
    criteria dependence, while 25% met DSM-IV criteria
    for abuse. The authors concluded thatASwere
    addictive and suggested that dissatisfaction with
    body sizemight lead to dependent patterns of use.[33]
    Our experience with many athletes using AS suggests
    that dissatisfaction with their body size and
    increases in strength and size obtained from AS are
    the primary stimuli for continued usage of these
    agents. Although these observationsmay be related
    to an underlying body dysmorphic disorder diagnosis,
    and unrelated to AS usage, no studies have
    been conducted addressing this issue in this population.
    Clinicians should not discount the addictive
    potential of these agents, as competitive athletes are
    often willing to use any substance to obtain their
    goals.
    5. Conclusion
    Understanding how AS are used in the bodybuilding
    community merits more study. The desire
    among competitive athletes to succeed is a powerful
    stimulus and using legal substances for illegal
    purposes to obtain these goals has become an increasingly
    large concern for healthcare professionals.
    Healthcare professionals should be able to educate
    their patients regarding the risks of using these
    agents. Aclinician’s warnings will gain credibility
    if they have a sound understanding of the issues
    related to AS use so that they can have an informed
    conversation with the patient/user. Clinicians should
    impress upon their patients that, despite the cavalier
    use of AS among athletes, the long-termeffects
    are not well established and they ought to be cautious.
    This requires the clinician to obtain as much
    knowledge about AS as possible by reviewing not
    only the medical literature, but mass-media literature
    as well. Physicians must warn their patients
    who use AS that the effects of these agents on overall
    health have not been extensively studied, and
    encourage them to avoid these agents to prevent
    any future health risks.
    Acknowledgements
    The authors had no funding for this article and have no
    conflicts of interest that could affect its content.

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