Anabolic steroid

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Anabolic–androgenic steroids
Drug class
Chemical structure of the natural AAS testosterone (androst-4-en-17β-ol-3-one).
Class identifiers
SynonymsAnabolic steroids; Androgens
ATC codeA14A
Biological targetAndrogen receptor
Chemical classSteroids; Androstanes; Estranes
Clinical data
Drugs.comDrug Classes
External links
In Wikidata

Anabolic steroids, also known more properly as anabolic–androgenic steroids (AAS),[1] are steroidal androgens that include natural androgens like testosterone as well as synthetic androgens that are structurally related and have similar effects to testosterone. They are anabolic and increase protein within cells, especially in skeletal muscles, and also have varying degrees of androgenic and virilizing effects, including induction of the development and maintenance of masculine secondary sexual characteristics such as the growth of facial and body hair. The word anabolic, referring to anabolism, comes from the Greek ἀναβολή anabole, "that which is thrown up, mound". Androgens or AAS are one of three types of sex hormone agonists, the others being estrogens like estradiol and progestogens like progesterone.


Health risks can be produced by long-term use or excessive doses of AAS.[3][4] These effects include harmful changes in cholesterol levels (increased low-density lipoprotein and decreased high-density lipoprotein), acne, high blood pressure, liver damage (mainly with most oral AAS), and dangerous changes in the structure of the left ventricle of the heart.[5] These risks are only increased when, as they often do, athletes take steroids alongside other drugs, causing significantly more damage to their bodies.[6] The effect of anabolic steroids on the heart can cause myocardial infarction and strokes.[6] Conditions pertaining to hormonal imbalances such as gynecomastia and testicular size reduction may also be caused by AAS.[7] In women and children, AAS can cause irreversible masculinization.[7]

Ergogenic uses for AAS in sports, racing, and bodybuilding as performance-enhancing drugs are controversial because of their adverse effects and the potential to gain unfair advantage in physical competitions. Their use is referred to as doping and banned by most major sporting bodies. Athletes have been looking for drugs to enhance their athletic abilities since the Olympics started in Ancient Greece.[6] For many years, AAS have been by far the most detected doping substances in IOC-accredited laboratories.[8][9] In countries where AAS are controlled substances, there is often a black market in which smuggled, clandestinely manufactured or even counterfeit drugs are sold to users.



Various AAS and related compounds.

Since the discovery and synthesis of testosterone in the 1930s, AAS have been used by physicians for many purposes, with varying degrees of success. These can broadly be grouped into anabolic, androgenic, and other uses.




Enhancing performance[edit]

Numerous vials of injectable AAS

Most steroid users are not athletes.[49] In the United States, between 1 million and 3 million people (1% of the population) are thought to have used AAS.[50] Studies in the United States have shown that AAS users tend to be mostly middle-class heterosexual men with a median age of about 25 who are noncompetitive bodybuilders and non-athletes and use the drugs for cosmetic purposes.[51] "Among 12- to 17-year-old boys, use of steroids and similar drugs jumped 25 percent from 1999 to 2000, with 20 percent saying they use them for looks rather than sports, a study by insurer Blue Cross Blue Shield found."(Eisenhauer) Another study found that non-medical use of AAS among college students was at or less than 1%.[52] According to a recent survey, 78.4% of steroid users were noncompetitive bodybuilders and non-athletes, while about 13% reported unsafe injection practices such as reusing needles, sharing needles, and sharing multidose vials,[53] though a 2007 study found that sharing of needles was extremely uncommon among individuals using AAS for non-medical purposes, less than 1%.[54] Another 2007 study found that 74% of non-medical AAS users had post-secondary degrees and more had completed college and fewer had failed to complete high school than is expected from the general populace.[54] The same study found that individuals using AAS for non-medical purposes had a higher employment rate and a higher household income than the general population.[54] AAS users tend to research the drugs they are taking more than other controlled-substance users; however, the major sources consulted by steroid users include friends, non-medical handbooks, internet-based forums, blogs, and fitness magazines, which can provide questionable or inaccurate information.[55]

AAS users tend to be unhappy with the portrayal of AAS as deadly in the media and in politics.[56] According to one study, AAS users also distrust their physicians and in the sample 56% had not disclosed their AAS use to their physicians.[57] Another 2007 study had similar findings, showing that, while 66% of individuals using AAS for non-medical purposes were willing to seek medical supervision for their steroid use, 58% lacked trust in their physicians, 92% felt that the medical community's knowledge of non-medical AAS use was lacking, and 99% felt that the public has an exaggerated view of the side-effects of AAS use.[54] A recent study has also shown that long term AAS users were more likely to have symptoms of muscle dysmorphia and also showed stronger endorsement of more conventional male roles.[58] A recent study in the Journal of Health Psychology showed that many users believed that steroids used in moderation were safe.[59]



Medications and dosages used in masculinizing hormone therapy for transgender men

Medication Brand names Type Route Dosage
Testosterone undecanoate Andriol, Jatenzo Androgen Oral 40–80 mg/2–3x day (with meals)
Testosterone Striant Androgen Buccal 30 mg 2x/day
Natesto Nasal spray 11 mg 3x/day
AndroGel, others Transdermal gel 25–100 mg/day
Androderm, others Transdermal patch 2.5–10 mg/day
Axiron Axillary solution 30–120 mg/day
Testopel Subcutaneous implant 150–600 mg/3–6 months
Testosterone enanthate Delatestryl, others Androgen Injection (IM or SC) 50–100 mg/week or 100–250 mg/2–4 weeks
Testosterone cypionate Depo-Testosterone, others Androgen Injection (IM or SC) 50–100 mg/week or 100–250 mg/2–4 weeks
Testosterone isobutyrate Agovirin Depot Androgen Injection (IM or SC) 50–100 mg/week
Mixed testosterone estersa Sustanon 250, others Androgen Injection (IM or SC) 250 mg/2–3 weeks or 500 mg/3–6 weeks
Testosterone undecanoate Aveed, Nebido, others Androgen Injection (IM or SC) 750–1,000 mg/10–14 weeks
GnRH analogue Various GnRH modulator Parenteral (various) Variable
Elagolix Orilissa GnRH antagonist Oral 150 mg/day or 200 mg/twice a day
Medroxyprogesterone acetateb Provera, others Progestin Oral 5–10 mg/day
Depo-Provera, others Injection (IM) 150 mg/3 months
Depo-SubQ Provera 104 Injection (SC) 104 mg/3 months
Lynestrenolb Orgametril, others Progestin Oral 5–10 mg/day
Finasteridec Propecia, Proscar 5α-Reductase inhibitor Oral 1 mg/day
Dutasteridec Avodart 5α-Reductase inhibitor Oral 0.5 mg/day
Footnotes: a = Specifically 12% testosterone propionate, 24% testosterone phenylpropionate, 24% testosterone isocaproate, and 40% testosterone decanoate. b = For suppression of menses only. c = For prevention/treatment of scalp hair loss only. Sources: See template.

Androgen replacement therapy formulations and dosages used in women

Route Medication Form(s) Major brand name(s) Dosage
Oral Testosterone undecanoatea Capsule Andriol, Jatenzo 40–80 mg 1x/1–2 days
Methyltestosteroneb Tablet Metandren; Estratest 0.5–10 mg/day
Normethandronea,b Tablet Ginecoside 5 mg/day
Tibolonea Tablet Livial 1.25–2.5 mg/day
Prasterone (DHEA)c Tablet N/A 25–100 mg/day
Sublingual Testosteroned Tablet N/A 0.25–0.5 mg/day
Methyltestosterone Tablet Metandren 0.25 mg/day
Transdermal Testosteronea Patch Intrinsa 150–300 μg/day
Testosterone Cream; Gel AndroGel 5–10 mg/day
Vaginal Testosteroned Cream; Gel N/A ? mg 1x/1–3 days
Testosteroned Suppository N/A 1 mg 1x/2 days
Prasterone (DHEA) Insert Intrarosa 6.5 mg/day
Intramuscular Testosterone enanthateb Oil Delatestryl; Primodian Depot 25–100 mg 1x/4–6 weeks
Testosterone cypionateb Oil Depo-Testost.; Depo-Testadiol 25–100 mg 1x/4–6 weeks
Testosterone isobutyratea,b Water Femandren M, Folivirin 25–50 mg 1x/4–6 weeks
Testosterone EBHb,e Oil Climacteron 150 mg 1x/4–8 weeks
Nandrolone decanoate Oil Deca-Durabolin 25–50 mg 1x/6–12 weeks
Prasterone enanthatea,b Oil Gynodian Depot 200 mg 1x/4–6 weeks
Subcutaneous Testosterone Implant Testopel 50–100 mg 1x/3–6 months
Footnotes: a = Not available or no longer available in the United States. b = Alone and/or in combination with an estrogen. c = Over-the-counter. d = Compounded only. e = Discontinued. Sources: See template.

Androgen/anabolic steroid dosages for breast cancer

Route/form Androgen Dosage
Oral Methyltestosterone 30–200 mg/day
Fluoxymesterone 10–40 mg 3x/day
Calusterone 40 mg 4x/day
Normethandrone 40 mg/day
IM injection Testosterone propionate 50–100 mg 3x/week
Testosterone enanthate 200–400 mg 1x/2–4 weeks
Testosterone cypionate 200–400 mg 1x/2–4 weeks
Methandriol (aq. susp.) 100 mg 3x/week
Androstanolone (aq. susp.) 300 mg 3x/week
Drostanolone propionate 100 mg 3x/week
Nandrolone decanoate 50–100 mg 1x/1–3 weeks
Nandrolone phenylpropionate 50–100 mg/week
Notes: Dosages are not necessarily equivalent. Sources: See template.

Available forms[edit]

The AAS that have been used most commonly in medicine are testosterone and its many esters (but most typically testosterone undecanoate, testosterone enanthate, testosterone cypionate, and testosterone propionate),[61] nandrolone esters (typically nandrolone decanoate and nandrolone phenylpropionate), stanozolol, and metandienone (methandrostenolone).[1] Others that have also been available and used commonly but to a lesser extent include methyltestosterone, oxandrolone, mesterolone, and oxymetholone, as well as drostanolone propionate (dromostanolone propionate), metenolone (methylandrostenolone) esters (specifically metenolone acetate and metenolone enanthate), and fluoxymesterone.[1] Dihydrotestosterone (DHT), known as androstanolone or stanolone when used medically, and its esters are also notable, although they are not widely used in medicine.[62] Boldenone undecylenate and trenbolone acetate are used in veterinary medicine.[1]

Designer steroids are AAS that have not been approved and marketed for medical use but have been distributed through the black market.[63] Examples of notable designer steroids include 1-testosterone (dihydroboldenone), methasterone, trenbolone enanthate, desoxymethyltestosterone, tetrahydrogestrinone, and methylstenbolone.[63]

Major androgens/anabolic steroids marketed for clinical or veterinary use

Generic name Class Brand name(s) Route(s) Launch Status Hitsa
Androstanolone DHT Andractim, others Many 1953 Availableb 125,000
Boldenone undecylenate T; Ester Equipoise, Parenabol IM 1960s Veterinaryb 544,000
Danazol T; Alkyl Danocrine Oral 1971 Available 1,670,000
Drostanolone propionate DHT; Ester Masteron IM 1961 Discontinued 574,000
Ethylestrenol 19-NT; Alkyl Maxibolin, Orabolin Oral 1961 Availableb 117,000
Fluoxymesterone T; Alkyl Halotestin, Ultandren Oral 1957 Availableb 478,000
Mestanolone DHT; Alkyl Androstalone, Ermalone Oral 1950s Discontinued 278,000
Mesterolone DHT Proviron Oral 1967 Available 528,000
Metandienone T; Alkyl Dianabol Oral, IM 1958 Availableb 996,000
Metenolone acetate DHT; Ester Primobolan Oral 1961 Availableb 224,000
Metenolone enanthate DHT; Ester Primobolan Depot IM 1962 Availableb 371,000
Methyltestosterone T; Alkyl Metandren Oral 1936 Availableb 597,000
Nandrolone decanoate 19-NT; Ester Deca-Durabolin IM 1962 Available 926,000
Nandrolone phenylpropionate 19-NT; Ester Durabolin IM 1959 Availableb 395,000
Norethandrolone 19-NT; Alkyl Nilevar, Pronabol Oral 1956 Availableb 124,000
Oxandrolone DHT; Alkyl Oxandrin, Anavar Oral 1964 Availableb 1,280,000
Oxymetholone DHT; Alkyl Anadrol, Anapolon Oral 1961 Availableb 902,000
Prasterone (DHEA) T; Prohormone Numerous Many 1970s Available 11,600,000
Stanozolol DHT; Alkyl Winstrol, Stromba Oral, IM 1962 Discontinued 1,790,000
Testosterone T Numerous Many 1937 Available 12,700,000
Testosterone cypionate T; Ester Depo-Testosterone IM 1951 Available 1,290,000
Testosterone enanthate T; Ester Delatestryl IM 1954 Available 1,210,000
Testosterone propionate T; Ester Testoviron IM 1937 Available 1,010,000
Testosterone undecanoate T; Ester Aveed, Andriol, Nebido Oral, IM 1970s Available 385,000
Trenbolone acetate 19-NT; Ester Finajet, Finaject IM 1970s Veterinary 651,000
Footnotes: a = Hits = Google Search hits (as of December 2017). b = Availability limited / mostly discontinued. Class: T = Testosterone. DHT = Dihydrotestosterone. 19-NT = 19-Nortestosterone (nandrolone). Alkyl = 17α-Alkylated. Sources: See individual articles.

Routes of administration[edit]

A vial of injectable testosterone cypionate





Adverse effects[edit]

Known possible side effects of AAS include:[7][66][67][68][69]


Depending on the length of drug use, there is a chance that the immune system can be damaged. Most of these side-effects are dose-dependent, the most common being elevated blood pressure, especially in those with pre-existing hypertension.[76] In addition to morphological changes of the heart which may have a permanent adverse effect on cardiovascular efficiency.

AAS have been shown to alter fasting blood sugar and glucose tolerance tests.[77] AAS such as testosterone also increase the risk of cardiovascular disease[3] or coronary artery disease.[78][79] Acne is fairly common among AAS users, mostly due to stimulation of the sebaceous glands by increased testosterone levels.[8][80] Conversion of testosterone to DHT can accelerate the rate of premature baldness for males genetically predisposed, but testosterone itself can produce baldness in females.[81]



WHO organization International Agency for Research on Cancer (IARC) list AAS under Group 2A: Probably carcinogenic to humans.[83]


Other side-effects can include alterations in the structure of the heart, such as enlargement and thickening of the left ventricle, which impairs its contraction and relaxation, and therefore reducing ejected blood volume.[5] Possible effects of these alterations in the heart are hypertension, cardiac arrhythmias, congestive heart failure, heart attacks, and sudden cardiac death.[84] These changes are also seen in non-drug-using athletes, but steroid use may accelerate this process.[85][86] However, both the connection between changes in the structure of the left ventricle and decreased cardiac function, as well as the connection to steroid use have been disputed.[87][88]

AAS use can cause harmful changes in cholesterol levels: Some steroids cause an increase in LDL "bad" cholesterol and a decrease in HDL "good" cholesterol.[89] In addition, steroids provoke a rapid increase in body weight and an accompanying rise in blood pressure, both of which leave users more vulnerable to a cardiovascular event.[citation needed]

Growth defects[edit]

AAS use in adolescents quickens bone maturation and may reduce adult height in high doses.[citation needed] Low doses of AAS such as oxandrolone are used in the treatment of idiopathic short stature, but this may only quicken maturation rather than increasing adult height.[90]


22-year-old man with gynecomastia not due to AAS use. Before and after gynecomastia surgery.

There are also sex-specific side effects of AAS. Development of breast tissue in males, a condition called gynecomastia (which is usually caused by high levels of circulating estradiol), may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase.[91] Reduced sexual function and temporary infertility can also occur in males.[92][93][94] Another male-specific side-effect that can occur is testicular atrophy, caused by the suppression of natural testosterone levels, which inhibits production of sperm (most of the mass of the testes is developing sperm). This side-effect is temporary; the size of the testicles usually returns to normal within a few weeks of discontinuing AAS use as normal production of sperm resumes.[95]


Female-specific side effects include increases in body hair, permanent deepening of the voice, enlarged clitoris, and temporary decreases in menstrual cycles. Alteration of fertility and ovarian cysts can also occur in females.[96] When taken during pregnancy, AAS can affect fetal development by causing the development of male features in the female fetus and female features in the male fetus.[97]

Kidney problems[edit]


Liver problems[edit]

High doses of oral AAS compounds can cause liver damage.[4] Peliosis hepatis has been increasingly recognised with the use of AAS.


Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and legal services engaged in delphic analysis regarding 20 popular recreational drugs. AAS were ranked 19th in dependence, 9th in physical harm, and 15th in social harm.[99]

A 2005 review in CNS Drugs determined that "significant psychiatric symptoms including aggression and violence, mania, and less frequently psychosis and suicide have been associated with steroid abuse. Long-term steroid abusers may develop symptoms of dependence and withdrawal on discontinuation of AAS".[71] High concentrations of AAS, comparable to those likely sustained by many recreational AAS users, produce apoptotic effects on neurons,[citation needed] raising the specter of possibly irreversible neurotoxicity. Recreational AAS use appears to be associated with a range of potentially prolonged psychiatric effects, including dependence syndromes, mood disorders, and progression to other forms of substance abuse, but the prevalence and severity of these various effects remains poorly understood.[100] There is no evidence that steroid dependence develops from therapeutic use of AAS to treat medical disorders, but instances of AAS dependence have been reported among weightlifters and bodybuilders who chronically administered supraphysiologic doses.[101] Mood disturbances (e.g. depression, [hypo-]mania, psychotic features) are likely to be dose- and drug-dependent, but AAS dependence or withdrawal effects seem to occur only in a small number of AAS users.[8]

Large-scale long-term studies of psychiatric effects on AAS users are not currently available.[100] In 2003, the first naturalistic long-term study on ten users, seven of which having completed the study, found a high incidence of mood disorders and substance abuse, but few clinically relevant changes in physiological parameters or laboratory measures were noted throughout the study, and these changes were not clearly related to periods of reported AAS use.[102] A 13-month study, which was published in 2006 and which involved 320 body builders and athletes suggests that the wide range of psychiatric side-effects induced by the use of AAS is correlated to the severity of abuse.[103]

Diagnostic Statistical Manual assertion[edit]


Personality profiles[edit]

Cooper, Noakes, Dunne, Lambert, and Rochford identified that AAS-using individuals are more likely to score higher on borderline (4.7 times), antisocial (3.8 times), paranoid (3.4 times), schizotypal (3.1 times), histrionic (2.9 times), passive-aggressive (2.4 times), and narcissistic (1.6 times) personality profiles than non-users.[105] Other studies have suggested that antisocial personality disorder is slightly more likely among AAS users than among non-users (Pope & Katz, 1994).[104] Bipolar dysfunction,[106] substance dependency, and conduct disorder have also been associated with AAS use.[107]

Mood and anxiety[edit]

Affective disorders have long been recognised as a complication of AAS use. Case reports describe both hypomania and mania, along with irritability, elation, recklessness, racing thoughts and feelings of power and invincibility that did not meet the criteria for mania/hypomania.[108] Of 53 bodybuilders who used AAS, 27 (51%) reported unspecified mood disturbance.[109]

Aggression and hypomania[edit]

From the mid-1980s onward, the media reported "roid rage" as a side effect of AAS.[110]:23

A 2005 review determined that some, but not all, randomized controlled studies have found that AAS use correlates with hypomania and increased aggressiveness, but pointed out that attempts to determine whether AAS use triggers violent behavior have failed, primarily because of high rates of non-participation.[111] A 2008 study on a nationally representative sample of young adult males in the United States found an association between lifetime and past-year self-reported AAS use and involvement in violent acts. Compared with individuals that did not use steroids, young adult males that used AAS reported greater involvement in violent behaviors even after controlling for the effects of key demographic variables, previous violent behavior, and polydrug use.[112] A 1996 review examining the blind studies available at that time also found that these had demonstrated a link between aggression and steroid use, but pointed out that with estimates of over one million past or current steroid users in the United States at that time, an extremely small percentage of those using steroids appear to have experienced mental disturbance severe enough to result in clinical treatments or medical case reports.[113]


A 2006 study of two pairs of identical twins, in which one twin used AAS and the other did not, found that in both cases the steroid-using twin exhibited high levels of aggressiveness, hostility, anxiety, and paranoid ideation not found in the "control" twin.[117] A small-scale study of 10 AAS users found that cluster B personality disorders were confounding factors for aggression.[118]

The relationship between AAS use and depression is inconclusive. There have been anecdotal reports of depression and suicide in teenage steroid users,[119] but little systematic evidence. A 1992 review found that AAS may both relieve and cause depression, and that cessation or diminished use of AAS may also result in depression, but called for additional studies due to disparate data.[120] In the case of suicide, 3.9% of a sample of 77 those classified as AAS users reported attempting suicide during withdrawal (Malone, Dimeff, Lombardo, & Sample, 1995).[121]


Androgens such as testosterone, androstenedione and dihydrotestosterone are required for the development of organs in the male reproductive system, including the seminal vesicles, epididymis, vas deferens, penis and prostate.[122] AAS are testosterone derivatives designed to maximize the anabolic effects of testosterone.[123] AAS are consumed by elite athletes competing in sports like weightlifting, bodybuilding, and track and field.[124] Male recreational athletes take AAS to achieve an “enhanced” physical appearance.[125]

AAS consumption disrupts the hypothalamic–pituitary–gonadal axis (HPG axis) in males.[122] In the HPG axis, gonadotropin-releasing hormone (GnRH) is secreted from the arcuate nucleus of the hypothalamus and stimulates the anterior pituitary to secrete the two gonadotropins, follicle stimulating hormone (FSH) and luteinizing hormone (LH).[126] In adult males, LH stimulates the Leydig cells in the testes to produce testosterone which is required to form new sperm through spermatogenesis.[122] AAS consumption leads to dose-dependent suppression of gonadotropin release through suppression of GnRH from the hypothalamus (long-loop mechanism) or from direct negative feedback on the anterior pituitary to inhibit gonadotropin release (short-loop mechanism), leading to AAS-induced hypogonadism.[122]


Mechanism of action[edit]

The human androgen receptor bound to testosterone[127] The protein is shown as a ribbon diagram in red, green, and blue, with the steroid shown in white.

The pharmacodynamics of AAS are unlike peptide hormones. Water-soluble peptide hormones cannot penetrate the fatty cell membrane and only indirectly affect the nucleus of target cells through their interaction with the cell’s surface receptors. However, as fat-soluble hormones, AAS are membrane-permeable and influence the nucleus of cells by direct action. The pharmacodynamic action of AAS begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor (AR) located in the cytoplasm of that cell. From there, the compound hormone-receptor diffuses into the nucleus, where it either alters the expression of genes[128] or activates processes that send signals to other parts of the cell.[129] Different types of AAS bind to the AAR with different affinities, depending on their chemical structure.[8] Some AAS such as metandienone bind weakly to this receptor in vitro, but still exhibit AR-mediated effects in vivo.[citation needed] The reason for this discrepancy is not known.[130]

The effect of AAS on muscle mass is caused in at least two ways:[131] first, they increase the production of proteins; second, they reduce recovery time by blocking the effects of stress hormone cortisol on muscle tissue, so that catabolism of muscle is greatly reduced. It has been hypothesized that this reduction in muscle breakdown may occur through AAS inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles.[132] AAS also affect the number of cells that develop into fat-storage cells, by favouring cellular differentiation into muscle cells instead.[133] AAS can also decrease fat by increasing basal metabolic rate (BMR), since an increase in muscle mass increases BMR.[citation needed]

Anabolic and androgenic effects[edit]

Relative androgenic to anabolic
activity in animals

Medication Ratio
Testosterone 1:1
Testosterone cypionate 1:1
Testosterone enanthate 1:1
Methyltestosterone 1:1
Fluoxymesterone 1:2
Oxymetholone 1:3
Oxandrolone 1:3–1:13
Nandrolone decanoate 1:2.5–1:4
Sources: See template.

As their name suggests, AAS have two different, but overlapping, types of effects: anabolic, meaning that they promote anabolism (cell growth), and androgenic (or virilizing), meaning that they affect the development and maintenance of masculine characteristics.




Body composition and strength improvements[edit]



Strength improvements in the range of 5 to 20% of baseline strength, depending largely on the drugs and dose used as well as the administration period. Overall, the exercise where the most significant improvements were observed is the bench press.[8] For almost two decades, it was assumed that AAS exerted significant effects only in experienced strength athletes.[139][140] A randomized controlled trial demonstrated, however, that even in novice athletes a 10-week strength training program accompanied by testosterone enanthate at 600 mg/week may improve strength more than training alone does.[8][114] This dose is sufficient to significantly improve lean muscle mass relative to placebo even in subjects that did not exercise at all.[114] The anabolic effects of testosterone enanthate were highly dose dependent.[8][141]

Dissociation of effects[edit]

Endogenous/natural AAS like testosterone and DHT and synthetic AAS mediate their effects by binding to and activating the AR.[1] On the basis of animal bioassays, the effects of these agents have been divided into two partially dissociable types: anabolic (myotrophic) and androgenic.[1] Dissociation between the ratios of these two types of effects is observed in rat bioassays with various AAS relative to the ratio observed with testosterone.[1] Explanations for the dissociation include differences in intracellular metabolism, functional selectivity (recruitment of coactivators), and non-genomic mechanisms (i.e., signaling through non-AR membrane androgen receptors, or mARs).[1] Support for the latter two explanations is limited and more hypothetical, but there is a good deal of support for the intracellular metabolism explanation.[1]

The measurement of the dissociation between anabolic and androgenic effects among AAS is based largely on a simple although arguably unsophisticated and outdated model involving rat tissue bioassays.[1] It is referred to as the myotrophic–androgenic index.[1] In this model, anabolic (myotrophic) activity is measured by change in the weight of the rat bulbocavernosus/levator ani muscle and androgenic activity is measured by change in the weight of the rat ventral prostate (or, alternatively, the rat seminal vesicles) in response to exposure to the AAS.[1] Then, the measurements are compared and used to form a ratio.[1]

Intracellular metabolism[edit]

Testosterone is metabolized in various tissues by 5α-reductase into DHT, which is 3- to 10-fold more potent as an AR agonist, and by aromatase into estradiol, which is an estrogen and lacks significant AR affinity.[1] In addition, DHT is metabolized by 3α-hydroxysteroid dehydrogenase (3α-HSD) and 3β-hydroxysteroid dehydrogenase (3β-HSD) into 3α-androstanediol and 3β-androstanediol, respectively, which are metabolites with little or no AR affinity.[1] 5α-reductase is widely distributed throughout the body, and is concentrated to various extents in skin (particularly the scalp, beard-area of the face, pubic area, and genital area (penis and scrotum)), prostate, seminal vesicles, liver, and the brain.[1] In contrast, expression of 5α-reductase in skeletal muscle is undetectable.[1] Aromatase is highly expressed in adipose tissue and the brain, and is also expressed significantly in skeletal muscle.[1] 3α-HSD is highly expressed in skeletal muscle as well.[62]

Natural AAS like testosterone and DHT and synthetic AAS are analogues and are very similar structurally.[1] For this reason, they have the capacity to bind to and be metabolized by the same steroid-metabolizing enzymes.[1] According to the intracellular metabolism explanation, the androgenic-to-anabolic ratio of a given AR agonist is related to its capacity to be transformed by the aforementioned enzymes in conjunction with the AR activity of any resulting products.[1] For instance, whereas the AR activity of testosterone is greatly potentiated by local conversion via 5α-reductase into DHT in tissues where 5α-reductase is expressed, an AAS that is not metabolized by 5α-reductase or is already 5α-reduced, such as DHT itself or a derivative (like mesterolone or drostanolone), would not undergo such potentiation in said tissues.[1] Moreover, nandrolone is metabolized by 5α-reductase, but unlike the case of testosterone and DHT, the 5α-reduced metabolite of nandrolone has much lower affinity for the AR than does nandrolone itself, and this results in reduced AR activation in 5α-reductase-expressing tissues.[1] As so-called "androgenic" tissues such as skin/hair follicles and male reproductive tissues are very high in 5α-reductase expression, while skeletal muscle is virtually devoid of 5α-reductase, this may primarily explain the high myotrophic–androgenic ratio and dissociation seen with nandrolone, as well as with various other AAS.[1]

Aside from 5α-reductase, aromatase may inactivate testosterone signaling in skeletal muscle and adipose tissue, so AAS that lack aromatase affinity, in addition to being free of the potential side effect of gynecomastia, might be expected to have a higher myotrophic–androgenic ratio in comparison.[1] In addition, DHT is inactivated by high activity of 3α-HSD in skeletal muscle (and cardiac tissue), and AAS that lack affinity for 3α-HSD could similarly be expected to have a higher myotrophic–androgenic ratio (although perhaps also increased long-term cardiovascular risks).[1] In accordance, DHT, mestanolone (17α-methyl-DHT), and mesterolone (1α-methyl-DHT) are all described as very poorly anabolic due to inactivation by 3α-HSD in skeletal muscle, whereas other DHT derivatives with other structural features like metenolone, oxandrolone, oxymetholone, drostanolone, and stanozolol are all poor substrates for 3α-HSD and are described as potent anabolics.[62]

The intracellular metabolism theory explains how and why remarkable dissociation between anabolic and androgenic effects might occur despite the fact that these effects are mediated through the same signaling receptor, and why this dissociation is invariably incomplete.[1] In support of the model is the rare condition congenital 5α-reductase type 2 deficiency, in which the 5α-reductase type 2 enzyme is defective, production of DHT is impaired, and DHT levels are low while testosterone levels are normal.[142][143] Males with this condition are born with ambiguous genitalia and a severely underdeveloped or even absent prostate gland.[142][143] In addition, at the time of puberty, such males develop normal musculature, voice deepening, and libido, but have reduced facial hair, a female pattern of body hair (i.e., largely restricted to the pubic triangle and underarms), no incidence of male pattern hair loss, and no prostate enlargement or incidence of prostate cancer.[143][144][145][146][147] They also notably do not develop gynecomastia as a consequence of their condition.[145]

Relative affinities of nandrolone and related steroids at the androgen receptor

Compound rAR (%) hAR (%)
Testosterone 38 38
5α-Dihydrotestosterone 77 100
Nandrolone 75 92
5α-Dihydronandrolone 35 50
Ethylestrenol ND 2
Norethandrolone ND 22
5α-Dihydronorethandrolone ND 14
Metribolone 100 110
Sources: See template.

Functional selectivity[edit]

An animal study found that two different kinds of androgen response elements could differentially respond to testosterone and DHT upon activation of the AR.[148][149] Whether this is involved in the differences in the ratios of anabolic-to-myotrophic effect of different AAS is unknown however.[148][149][1]

Non-genomic mechanisms[edit]

Testosterone signals not only through the nuclear AR, but also through mARs, including ZIP9 and GPRC6A.[150][151] It has been proposed that differential signaling through mARs may be involved in the dissociation of the anabolic and androgenic effects of AAS.[1] Indeed, DHT has less than 1% of the affinity of testosterone for ZIP9, and the synthetic AAS metribolone and mibolerone are ineffective competitors for the receptor similarly.[151] This indicates that AAS do show differential interactions with the AR and mARs.[151] However, women with complete androgen insensitivity syndrome (CAIS), who have a 46,XY ("male") genotype and testes but a defect in the AR such that it is non-functional, are a challenge to this notion.[152] They are completely insensitive to the AR-mediated effects of androgens like testosterone, and show a perfectly female phenotype despite having testosterone levels in the high end of the normal male range.[152] These women have little or no sebum production, incidence of acne, or body hair growth (including in the pubic and axillary areas).[152] Moreover, CAIS women have lean body mass that is normal for females but is of course greatly reduced relative to males.[153] These observations suggest that the AR is mainly or exclusively responsible for masculinization and myotrophy caused by androgens.[152][153] The mARs have however been found to be involved in some of the health-related effects of testosterone, like modulation of prostate cancer risk and progression.[151][154]

Antigonadotropic effects[edit]

Changes in endogenous testosterone levels may also contribute to differences in myotrophic–androgenic ratio between testosterone and synthetic AAS.[62] AR agonists are antigonadotropic – that is, they dose-dependently suppress gonadal testosterone production and hence reduce systemic testosterone concentrations.[62] By suppressing endogenous testosterone levels and effectively replacing AR signaling in the body with that of the exogenous AAS, the myotrophic–androgenic ratio of a given AAS may be further, dose-dependently increased, and this hence may be an additional factor contributing to the differences in myotrophic–androgenic ratio among different AAS.[62] In addition, some AAS, such as 19-nortestosterone derivatives like nandrolone, are also potent progestogens, and activation of the progesterone receptor (PR) is antigonadotropic similarly to activation of the AR.[62] The combination of sufficient AR and PR activation can suppress circulating testosterone levels into the castrate range in men (i.e., complete suppression of gonadal testosterone production and circulating testosterone levels decreased by about 95%).[48][155] As such, combined progestogenic activity may serve to further increase the myotrophic–androgenic ratio for a given AAS.[62]

GABAA receptor modulation[edit]

Some AAS, such as testosterone, DHT, stanozolol, and methyltestosterone, have been found to modulate the GABAA receptor similarly to endogenous neurosteroids like allopregnanolone, 3α-androstanediol, dehydroepiandrosterone sulfate, and pregnenolone sulfate.[1] It has been suggested that this may contribute as an alternative or additional mechanism to the neurological and behavioral effects of AAS.[1][156][157][158][159][160][161]

Comparison of AAS[edit]

AAS differ in a variety of ways including in their capacities to be metabolized by steroidogenic enzymes such as 5α-reductase, 3-hydroxysteroid dehydrogenases, and aromatase, in whether their potency as AR agonists is potentiated or diminished by 5α-reduction, in their ratios of anabolic/myotrophic to androgenic effect, in their estrogenic, progestogenic, and neurosteroid activities, in their oral activity, and in their capacity to produce hepatotoxicity.[62][1][162]

Pharmacological properties of major anabolic steroids

Compound Class 5α-R AROM 3-HSD AAR Estr Prog Oral Hepat
Androstanolone DHT + *
Boldenone T ± ** ±
Drostanolone DHT ***
Ethylestrenol 19-NT; 17α-A + () ± *** + + + +
Fluoxymesterone T; 17α-A + () * + +
Mestanolone DHT; 17α-A + * + +
Mesterolone DHT + * ±
Metandienone T; 17α-A ± ** + + +
Metenolone DHT ** ±
Methyltestosterone T; 17α-A + () + * + + +
Nandrolone 19-NT + () ± *** ± +
Oxandrolone DHT; 17α-A *** + ±
Oxymetholone DHT; 17α-A *** + + +
Stanozolol DHT; 17α-A *** + +
Testosterone T + () + * + ±a
Trenbolone 19-NT *** +
Key: + = Yes. ± = Low. = No. = Potentiated. = Inactivated. *** = High. ** = Moderate. * = Low. Abbreviations: 5α-R = Metabolized by 5α-reductase. AROM = Metabolized by aromatase. 3-HSD = Metabolized by 3α- and/or 3β-HSD. AAR = Anabolic-to-androgenic ratio (amount of anabolic (myotrophic) effect relative to androgenic effect). Estr = Estrogenic. Prog = Progestogenic. Oral = Oral activity. Hepat = Hepatotoxicity. Footnotes: a = As testosterone undecanoate. Sources: See template.

Relative affinities (%) of anabolic steroids and related steroids

Compound Chemical name PR AR ER GR MR SHBG CBG
Androstanolone DHT 1.4–1.5 60–120 <0.1 <0.1, 0.3 0.15 100 0.8
Boldenone Δ1-T <1 50–75 ? <1 ? ? ?
Danazol 2,3-Isoxazol-17α-Ety-T 9 8 ? <0.1a ? 8 10
Dienolone 9-19-NT 17 134 <0.1 1.6 0.3 ? ?
Dimethyldienolone 9-7α,17α-DiMe-19-NT 198 122 0.1 6.1 1.7 ? ?
Dimethyltrienolone 9,11-7α,17α-DiMe-19-NT 306 180 0.1 22 52 ? ?
Drostanolone 2α-Me-DHT ? ? ? ? ? 39 ?
Ethisterone 17α-Ety-T 35 0.1 <1.0 <1.0 <1.0 25–92 0.3
Ethylestrenol 3-DeO-17α-Et-19-NT ? ? ? ? ? <1 ?
Fluoxymesterone 9α-F-11β-OH-17α-Me-T ? ? ? ? ? ≤3 ?
Gestrinone 9,11-17α-Ety-18-Me-19-NT 75–76 83–85 <0.1, 3–10 77 3.2 ? ?
Levonorgestrel 17α-Ety-18-Me-19-NT 170 84–87 <0.1 14 0.6–0.9 14–50 <0.1
Mestanolone 17α-Me-DHT 5–10 100–125 ? <1 ? 84 ?
Mesterolone 1α-Me-DHT ? ? ? ? ? 82–440 ?
Metandienone 1-17α-Me-T ? ? ? ? ? 2 ?
Metenolone 1-1-Me-DHT ? ? ? ? ? 3 ?
Methandriol 17α-Me-A5 ? ? ? ? ? 40 ?
Methasterone 2α,17α-DiMe-DHT ? ? ? ? ? 58 ?
Methyldienolone 9-17α-Me-19-NT 71 64 <0.1 6 0.4 ? ?
Methyltestosterone 17α-Me-T 3 45, 100–125 ? 1–5 ? 5–64 <0.1
Methyl-1-testosterone 1-17α-Me-DHT ? ? ? ? ? 69 ?
Metribolone 9,11-17α-Me-19-NT 208–210 199–210 <0.1 10–26 18 0.2–0.8 ≤0.4
Mibolerone 7α,17α-DiMe-19-NT 214 108 <0.1 1.4 2.1 6 ?
Nandrolone 19-NT 20 154–155 <0.1 0.5 1.6 1–16 0.1
Norethandrolone 17α-Et-19-NT ? ? ? ? ? 3 ?
Norethisterone 17α-Ety-19-NT 155–156 43–45 <0.1 2.7–2.8 0.2 5–21 0.3
Norgestrienone 9,11-17α-Ety-19-NT 63–65 70 <0.1 11 1.8 ? ?
Normethandrone 17α-Me-19-NT 100 146 <0.1 1.5 0.6 7 ?
Oxandrolone 2-Oxa-17α-Me-DHT ? ? ? ? ? <1 ?
Oxymetholone 2-OHMeEne-17α-Me-DHT ? ? ? ? ? ≤3 ?
RU-2309 (17α-Me-THG) 9,11-17α,18-DiMe-19-NT 230 143 <0.1 155 36 ? ?
Stanozolol 2,3-Pyrazol-17α-Me-DHT ? ? ? ? ? 1–36 ?
Testosterone T 1.0–1.2 100 <0.1 0.17 0.9 19–82 3–8
1-Testosterone 1-DHT ? ? ? ? ? 98 ?
Tibolone 7α-Me-17α-Ety-19-N-5(10)-T 12 12 1 ? ? ? ?
Δ4-Tibolone 7α-Me-17α-Ety-19-NT 180 70 1 <1 2 1–8 <1
Trenbolone 9,11-19-NT 74–75 190–197 <0.1 2.9 1.33 ? ?
Trestolone 7α-Me-19-NT 50–75 100–125 ? <1 ? 12 ?
Notes: Values are percentages (%). Reference ligands (100%) were progesterone for the PR, testosterone for the AR, estradiol for the ER, dexamethasone for the GR, aldosterone for the MR, dihydrotestosterone for SHBG, and cortisol for CBG. Footnotes: a = 1-hour incubation time (4 hours is standard for this assay; may affect affinity value). Sources: See template.

Anabolic and androgenic activities of anabolic steroids

Steroid Ref. /
Route Anabolic activity by Androgenic
Dissociation index by
Nitr. ratio Myotrophy Nitr. ratio Myotrophy
Androisoxazole T par. 2.1
Androisoxazole MT p.o. 1.7
Androisoxazole MT p.o. 1.55 0.22 7
Androstanolone TP par. 2.5 1.53 1.6
Androstanolone T par. 0.3
Androstanolone MT p.o. 0.8
Androstanolone MT p.o. 0.26 0.53 0.13
Bolasterone MT par. 5.75a 3 1.9
Bolasterone MT p.o. 4.2 1.3 3.2
Bolasterone MT par. 13.4 3.0 4.5
Bolasterone T par. 11.4 2.24–6.6 2–5
Clostebol acetate TP par. 0.68 0.14 5
Clostebol acetate TP par. 1.26 0.483 3
Clostebol acetate T par. 0.10 0.03 3
Drostanolone T par. 0.62–1.30 0.25–0.4 2.5–3.0
Ethyldienolone MT par. 1.0 0.1 10
Ethyldienolone MT p.o. 1.5 0.3 5
Ethylestrenol T par. 2.6
Ethylestrenol MT p.o. 4
Ethylestrenol MT p.o. 4.207 0.222 19
Ethylestrenol MT p.o. 1.7 0.21 8.1
Ethylestrenol MT p.o. 2.0 0.4 5
Ethylestrenol MT par. 0.4 0.17 2.3
Fluoxymesterone MT p.o. 20 9.5 2
Fluoxymesterone MT p.o. 28.2 4.5 6.3
Fluoxymesterone MT p.o. 0.9
Fluoxymesterone MT p.o. 3.8 1.5 2.7
Fluoxymesterone MT p.o. 0.72 0.46 1.5
Fluoxymesterone MT p.o. 1.75 0.93 1.9
Fluoxymesterone MT p.o. 5 9 0.55
Fluoxymesterone T par. 1.6
Fluoxymesterone T par. 17.45 1.18–7.51 –7.57 2.3–15
Mebolazine T par. 0.27 <0.06–0.12 >2
Mebolazine MT p.o. 3.3 2.1 0.15 14 22
Mestanolone MT p.o. 0.8 1.0 0.8
Metandienone T par. 0.5
Metandienone T par. 2.1 0.6 3.5
Metandienone T par. 2.25
Metandienone T par. 0.89 0.45 1.97
Metandienone MT p.o. 1.4
Metandienone MT p.o. 1.2 0.35 3.4
Metandienone MT par. 1.9 0.64 3
Metandienone TP par. 0.1 0.1 1.0
Metandienone TP par. 6.0 0.8 7.5
Metenolone MT p.o. 13
Metenolone T par. 16
Metenolone T par. 0.88 0.44–0.57 2
Metenolone TP par. 0.30 0.01–0.02 15–30
Metenolone acetate MT p.o. 0.86 0.12 7
Methandriol MT p.o. 0.70 0.78 0.9
Methandriol MT p.o. 0.8 0.68 1.8
Methandriol MT p.o. 0.70 0.46 1.1 0.7
Methandriol TP par. 0.067 0.025
Methylclostebol MT par. 0.85 0.1 8.5
Methylclostebol MT p.o. 0.5 0.1–0.15 3–5
Methylclostebol MT p.o. 0.65 0.32 0.12 5.4 2.7
Methylclostebol T par. 0.46 0.26–0.27 1.7–1.8
Methyldiazinol MT p.o. 3.0 0.2 15
Methyltestosterone T p.o. 1.14 0.94–1.03 1.1–1.2
Nandrolone MT p.o. 0.73 0.074 9.9
Nandrolone T par. 3.3
Nandrolone T par. 10
Nandrolone T p.o. 5
Nandrolone TP par. 16
Nandrolone TP par. 10
Nandrolone decanoate TP par. 3.29–4.92 0.41–0.31 12.1–10.6
Nandrolone phenylpropionate TP par. 2.2 0.14 16
Nandrolone phenylpropionate TP par. 2.05 0.18 11.1
Norboletone MT p.o. 16.3
Norboletone TP par. 3.4 0.15 20
Norclostebol acetate TP par. 1.12 0.25 4.5
Norclostebol acetate TP par. 0.57 0.04 14.2
Norethandrolone TP par. 1.0 0.06 16
Norethandrolone TP par. 0.8 0.12 6.6
Norethandrolone TP par. 0.77 0.38 2
Norethandrolone TP par. 3–4
Norethandrolone T par. 1.3
Norethandrolone MT p.o. 2 0.25–0.5 4–8
Norethandrolone MT p.o. 0.75 0.22 3.4
Norethandrolone MT p.o. 2
Norethandrolone MT p.o. 3.9 0.19 20
Norethandrolone MT p.o. 6.7
Norethandrolone MT p.o. 1.028 0.335 3.1
Normethandrone TP par. 1.0 0.06 16
Normethandrone T par. 4.5 0.37 12
Normethandrone T p.o. 14.2 6–1.92 2–7
Normethandrone T p.o. 0.60 0.25 2.4
Normethandrone MT p.o. 3.25 1.25 2.6
Normethandrone MT p.o. 4.6 1.1 4.2
Normethandrone MT p.o. 5.8 1.1 5.3
Oxabolone cipionate TP par. 1.2–1.6 0.25–0.4 3–6
Oxandrolone MT p.o. 6.3
Oxandrolone MT par. 3.22 0.24 13
Oxymesterone MT par. 3.3 0.48 6.9
Oxymesterone MT par. 3.3 0.5 6.6
Oxymesterone MT p.o. 1.34 0.42–0.61 2.2–3.2
Oxymesterone MT p.o. 4
Oxymesterone MT p.o. 1.8 0.36 5.0
Oxymesterone T par. 4.3
Oxymetholone MT par. 1.46 0.31 4.7
Oxymetholone MT p.o. 2.5
Oxymetholone MT p.o. 3.2 0.45 7.1
Oxymetholone MT p.o. 1.75 0.2 8.75
Oxymetholone MT par. 4.4 1.0 4.4
Oxymetholone T par. 4.3
Oxymetholone T par. 2.3 0.64–1.0 2.3–3.6
Oxymetholone T par. 2
Stanozolol MT p.o. 2 0.33 6
Stanozolol MT p.o. 2.2 0.33 7
Stanozolol MT p.o. 10 0.33 30
Stanozolol MT p.o. 3.2 0.3 10.6
Stanozolol MT par. 3.7 0.52 7.1
Stanozolol MT p.o. 2.5
Stanozolol MT p.o. 0.4
Stanozolol T par. 4.3
Stanozolol T par. 7.5 2.5 3
Stanozolol TP par. 0.13 0.03 4
Testosterone MT p.o. 0.6
Testosterone MT par. 2.0
Testosterone MT p.o. 0.36 0.28–0.50 0.7–1.3
Testosterone MT p.o. 0.38 0.57 0.67
Testosterone TP par. 0.17 0.63
Tiomesterone MT p.o. 4.65 0.61 7.5
Notes: All assays done with rodents, unless noted otherwise. Footnotes: a = Monkeys. Sources: See template.

Parenteral durations of androgens/anabolic steroids

Compound Brand name(s) Type Duration
Testosterone (aq. susp.) Andronaq, Sterotate, Virosterone Androgen 2–3 days
Testosterone propionate Androteston, Perandren, Testoviron Androgen 3–4 days
Testosterone phenylpropionate Testolent Androgen 8 days
Testosterone isobutyrate (aq. susp.) Agovirin Depot, Perandren M Androgen 14 days
Mixed testosterone estersa Triolandren Androgen 10–20 days
Mixed testosterone estersb Testosid Depot Androgen 14–20 days
Testosterone enanthate Delatestryl Androgen 14–20 days
Testosterone cypionate Depovirin Androgen 14–20 days
Mixed testosterone estersc Sustanon 250 Androgen 28 days
Testosterone undecanoate Aveed, Nebido Androgen 100 days
Testosterone buciclate (aq. susp.)d 20 Aet-1, CDB-1781e Androgen 90–120 days
Nandrolone phenylpropionate Durabolin Anabolic 10 days
Nandrolone decanoate Deca Durabolin Anabolic 21 days
Methandriol (aq. susp.) Notandron, Protandren Androgen 8 days
Methandriol bisenanthoyl acetate Notandron Depot Androgen 16 days
Metenolone acetate Primobolan Anabolic 3 days
Metenolone enanthate Primobolan Depot Anabolic 14 days
Note: All are via i.m. injection of oil solution unless noted otherwise. Footnotes: a = TP, TV, and TUe. b = TP and TKL. c = TP, TPP, TiCa, and TD. d = Studied, but never marketed. e = Developmental code names. Sources: See template.

Pharmacokinetics of testosterone esters

Testosterone ester Form Route of administration Elimination half-life Mean residence time
Testosterone undecanoate Oil-filled capsules Oral 1.6 hours 3.7 hours
Testosterone propionate Oil solution Intramuscular injection 0.8 days 1.5 days
Testosterone enanthate Castor oil solution Intramuscular injection 4.5 days 8.5 days
Testosterone undecanoate Tea seed oil solution Intramuscular injection 20.9 days 34.9 days
Testosterone undecanoate Castor oil solution Intramuscular injection 33.9 days 36.0 days
Testosterone buciclatea Aqueous suspension Intramuscular injection 29.5 days 60.0 days
Notes: Testosterone cypionate has very similar pharmacokinetics to TE. Footnotes: a = Never marketed. Sources: See template.

5α-Reductase and androgenicity[edit]

Testosterone can be robustly converted by 5α-reductase into DHT in so-called androgenic tissues such as skin, scalp, prostate, and seminal vesicles, but not in muscle or bone, where 5α-reductase either is not expressed or is only minimally expressed.[1] As DHT is 3- to 10-fold more potent as an agonist of the AR than is testosterone, the AR agonist activity of testosterone is thus markedly and selectively potentiated in such tissues.[1] In contrast to testosterone, DHT and other 4,5α-dihydrogenated AAS are already 5α-reduced, and for this reason, cannot be potentiated in androgenic tissues.[1] 19-Nortestosterone derivatives like nandrolone can be metabolized by 5α-reductase similarly to testosterone, but 5α-reduced metabolites of 19-nortestosterone derivatives (e.g., 5α-dihydronandrolone) tend to have reduced activity as AR agonists, resulting in reduced androgenic activity in tissues that express 5α-reductase.[1] In addition, some 19-nortestosterone derivatives, including trestolone (7α-methyl-19-nortestosterone (MENT)), 11β-methyl-19-nortestosterone (11β-MNT), and dimethandrolone (7α,11β-dimethyl-19-nortestosterone), cannot be 5α-reduced.[163] Conversely, certain 17α-alkylated AAS like methyltestosterone are 5α-reduced and potentiated in androgenic tissues similarly to testosterone.[1][62] 17α-Alkylated DHT derivatives cannot be potentiated via 5α-reductase however, as they are already 4,5α-reduced.[1][62]

The capacity to be metabolized by 5α-reductase and the AR activity of the resultant metabolites appears to be one of the major, if not the most important determinant of the androgenic–myotrophic ratio for a given AAS.[1] AAS that are not potentiated by 5α-reductase or that are weakened by 5α-reductase in androgenic tissues have a reduced risk of androgenic side effects such as acne, androgenic alopecia (male-pattern baldness), hirsutism (excessive male-pattern hair growth), benign prostatic hyperplasia (prostate enlargement), and prostate cancer, while incidence and magnitude of other effects such as muscle hypertrophy, bone changes,[164] voice deepening, and changes in sex drive show no difference.[1][165]

Aromatase and estrogenicity[edit]

Testosterone can be metabolized by aromatase into estradiol, and many other AAS can be metabolized into their corresponding estrogenic metabolites as well.[1] As an example, the 17α-alkylated AAS methyltestosterone and metandienone are converted by aromatase into methylestradiol.[166] 4,5α-Dihydrogenated derivatives of testosterone such as DHT cannot be aromatized, whereas 19-nortestosterone derivatives like nandrolone can be but to a greatly reduced extent.[1][167] Some 19-nortestosterone derivatives, such as dimethandrolone and 11β-MNT, cannot be aromatized due to steric hindrance provided by their 11β-methyl group, whereas the closely related AAS trestolone (7α-methyl-19-nortestosterone), in relation to its lack of an 11β-methyl group, can be aromatized.[167] AAS that are 17α-alkylated (and not also 4,5α-reduced or 19-demethylated) are also aromatized but to a lesser extent than is testosterone.[1][62] However, it is notable that estrogens that are 17α-substituted (e.g., ethinylestradiol and methylestradiol) are of markedly increased estrogenic potency due to improved metabolic stability,[166] and for this reason, 17α-alkylated AAS can actually have high estrogenicity and comparatively greater estrogenic effects than testosterone.[166][62]

The major effect of estrogenicity is gynecomastia (woman-like breasts).[1] AAS that have a high potential for aromatization like testosterone and particularly methyltestosterone show a high risk of gynecomastia at sufficiently high dosages, while AAS that have a reduced potential for aromatization like nandrolone show a much lower risk (though still potentially significant at high dosages).[1] In contrast, AAS that are 4,5α-reduced, and some other AAS (e.g., 11β-methylated 19-nortestosterone derivatives), have no risk of gynecomastia.[1] In addition to gynecomastia, AAS with high estrogenicity have increased antigonadotropic activity, which results in increased potency in suppression of the hypothalamic-pituitary-gonadal axis and gonadal testosterone production.[168]

Progestogenic activity[edit]

Many 19-nortestosterone derivatives, including nandrolone, trenbolone, ethylestrenol (ethylnandrol), metribolone (R-1881), trestolone, 11β-MNT, dimethandrolone, and others, are potent agonists of the progesterone receptor (AR) and hence are progestogens in addition to AAS.[1][169] Similarly to the case of estrogenic activity, the progestogenic activity of these drugs serves to augment their antigonadotropic activity.[169] This results in increased potency and effectiveness of these AAS as antispermatogenic agents and male contraceptives (or, put in another way, increased potency and effectiveness in producing azoospermia and reversible male infertility).[169]

Oral activity and hepatotoxicity[edit]

Non-17α-alkylated testosterone derivatives such as testosterone itself, DHT, and nandrolone all have poor oral bioavailability due to extensive first-pass hepatic metabolism and hence are not orally active.[1] A notable exception to this are AAS that are androgen precursors or prohormones, including dehydroepiandrosterone (DHEA), androstenediol, androstenedione, boldione (androstadienedione), bolandiol (norandrostenediol), bolandione (norandrostenedione), dienedione, mentabolan (MENT dione, trestione), and methoxydienone (methoxygonadiene) (although these are relatively weak AAS).[170][171] AAS that are not orally active are used almost exclusively in the form of esters administered by intramuscular injection, which act as depots and function as long-acting prodrugs.[1] Examples include testosterone, as testosterone cypionate, testosterone enanthate, and testosterone propionate, and nandrolone, as nandrolone phenylpropionate and nandrolone decanoate, among many others (see here for a full list of testosterone and nandrolone esters).[1] An exception is the very long-chain ester testosterone undecanoate, which is orally active, albeit with only very low oral bioavailability (approximately 3%).[172] In contrast to most other AAS, 17α-alkylated testosterone derivatives show resistance to metabolism due to steric hindrance and are orally active, though they may be esterified and administered via intramuscular injection as well.[1]

In addition to oral activity, 17α-alkylation also confers a high potential for hepatotoxicity, and all 17α-alkylated AAS have been associated, albeit uncommonly and only after prolonged use (different estimates between 1 and 17%),[173][174] with hepatotoxicity.[1][175][176] In contrast, testosterone esters have only extremely rarely or never been associated with hepatotoxicity,[174] and other non-17α-alkylated AAS only rarely,[citation needed] although long-term use may reportedly still increase the risk of hepatic changes (but at a much lower rate than 17α-alkylated AAS and reportedly not at replacement dosages).[173][177][61][additional citation(s) needed] In accordance, D-ring glucuronides of testosterone and DHT have been found to be cholestatic.[178]

Aside from prohormones and testosterone undecanoate, almost all orally active AAS are 17α-alkylated.[179] A few AAS that are not 17α-alkylated are orally active.[1] Some examples include the testosterone 17-ethers cloxotestosterone, quinbolone, and silandrone,[citation needed] which are prodrugs (to testosterone, boldenone1-testosterone), and testosterone, respectively), the DHT 17-ethers mepitiostane, mesabolone, and prostanozol (which are also prodrugs), the 1-methylated DHT derivatives mesterolone and metenolone (although these are relatively weak AAS),[1][61] and the 19-nortestosterone derivatives dimethandrolone and 11β-MNT, which have improved resistance to first-pass hepatic metabolism due to their 11β-methyl groups (in contrast to them, the related AAS trestolone (7α-methyl-19-nortestosterone) is not orally active).[1][169] As these AAS are not 17α-alkylated, they show minimal potential for hepatotoxicity.[1]

Neurosteroid activity[edit]

DHT, via its metabolite 3α-androstanediol (produced by 3α-hydroxysteroid dehydrogenase (3α-HSD)), is a neurosteroid that acts via positive allosteric modulation of the GABAA receptor.[1] Testosterone, via conversion into DHT, also produces 3α-androstanediol as a metabolite and hence has similar activity.[1] Some AAS that are or can be 5α-reduced, including testosterone, DHT, stanozolol, and methyltestosterone, among many others, can or may modulate the GABAA receptor, and this may contribute as an alternative or additional mechanism to their central nervous system effects in terms of mood, anxiety, aggression, and sex drive.[1][156][157][158][159][160][161]


AAS are androstane or estrane steroids. They include testosterone (androst-4-en-17β-ol-3-one) and derivatives with various structural modifications such as:[1][180][62]

As well as others such as 1-dehydrogenation (e.g., metandienone, boldenone), 1-substitution (e.g., mesterolone, metenolone), 2-substitution (e.g., drostanolone, oxymetholone, stanozolol), 4-substitution (e.g., clostebol, oxabolone), and various other modifications.[1][180][62]

Structural properties of major testosterone esters

Androgen Structure Ester Relative
mol. weight
T contentb
Position Moiety Type Lengtha Rank Group
1.00 1.00 11 Short
Testosterone propionate
Testosterone propionate.svg
C17β Propanoic acid Straight-chain fatty acid 3 1.19 0.84 10 Short
Testosterone isobutyrate
Testosterone isobutyrate.svg
C17β Isobutyric acid Aromatic fatty acid – (~3) 1.24 0.80 9 Moderate
Testosterone cypionate
Testosterone cypionate.svg
C17β Cyclopentylpropanoic acid Aromatic fatty acid – (~6) 1.43 0.70 8 Moderate
Testosterone phenylpropionate
Testosterone phenpropionate.svg
C17β Phenylpropanoic acid Aromatic fatty acid – (~6) 1.46 0.69 7 Moderate
Testosterone isocaproate
Testosterone isocaproate.svg
C17β Isohexanoic acid Branched-chain fatty acid – (~5) 1.34 0.75 6 Moderate
Testosterone caproate
Testosterone caproate.svg
C17β Hexanoic acid Straight-chain fatty acid 6 1.35 0.75 5 Moderate
Testosterone enanthate
Testosterone enanthate.svg
C17β Heptanoic acid Straight-chain fatty acid 7 1.39 0.72 4 Moderate
Testosterone decanoate
Testosterone decanoate.svg
C17β Decanoic acid Straight-chain fatty acid 10 1.53 0.65 3 Long
Testosterone undecanoate
Testosterone undecanoate.svg
C17β Undecanoic acid Straight-chain fatty acid 11 1.58 0.63 2 Long
Testosterone buciclated
Testosteronebuciclate structure.png
C17β Bucyclic acide Aromatic carboxylic acid – (~9) 1.58 0.63 1 Long
Footnotes: a = Length of ester in carbon atoms for straight-chain fatty acids or approximate length of ester in carbon atoms for aromatic fatty acids. b = Relative testosterone content by weight (i.e., relative androgenic/anabolic potency). c = Duration by intramuscular or subcutaneous injection in oil solution (except TiB and TB, which are in aqueous suspension). d = Never marketed. e = Bucyclic acid = trans-4-Butylcyclohexane-1-carboxylic acid. Sources: See individual articles.

Structural properties of major anabolic steroid esters

Anabolic steroid Structure Ester Relative
mol. weight
AAS contentb
Position Moiety Type Lengtha
Boldenone undecylenate
Boldenone undecylenate.svg
C17β Undecylenic acid Straight-chain fatty acid 11 1.58 0.63 Long
Drostanolone propionate
Drostanolone propionate.svg
C17β Propanoic acid Straight-chain fatty acid 3 1.18 0.84 Short
Metenolone acetate
Metenolone acetate.svg
C17β Ethanoic acid Straight-chain fatty acid 2 1.14 0.88 Short
Metenolone enanthate
Metenolone enanthate.png
C17β Heptanoic acid Straight-chain fatty acid 7 1.37 0.73 Long
Nandrolone decanoate
Nandrolone decanoate.svg
C17β Decanoic acid Straight-chain fatty acid 10 1.56 0.64 Long
Nandrolone phenylpropionate
Nandrolone phenylpropionate.svg
C17β Phenylpropanoic acid Aromatic fatty acid – (~6–7) 1.48 0.67 Long
Trenbolone acetate
Trenbolone acetate.svg
C17β Ethanoic acid Straight-chain fatty acid 2 1.16 0.87 Short
Trenbolone enanthated
Trenbolone enanthate.svg
C17β Heptanoic acid Straight-chain fatty acid 7 1.41 0.71 Long
Footnotes: a = Length of ester in carbon atoms for straight-chain fatty acids or approximate length of ester in carbon atoms for aromatic fatty acids. b = Relative androgen/anabolic steroid content by weight (i.e., relative androgenic/anabolic potency). c = Duration by intramuscular or subcutaneous injection in oil solution. d = Never marketed. Sources: See individual articles.

Detection in body fluids[edit]



Discovery of androgens[edit]

The use of gonadal steroids pre-dates their identification and isolation. Extraction of hormones from urines began in China c. 100 BCE.[citation needed] Medical use of testicle extract began in the late 19th century while its effects on strength were still being studied.[137] The isolation of gonadal steroids can be traced back to 1931, when Adolf Butenandt, a chemist in Marburg, purified 15 milligrams of the male hormone androstenone from tens of thousands of litres of urine. This steroid was subsequently synthesized in 1934 by Leopold Ružička, a chemist in Zurich.[185]

In the 1930s, it was already known that the testes contain a more powerful androgen than androstenone, and three groups of scientists, funded by competing pharmaceutical companies in the Netherlands, Germany, and Switzerland, raced to isolate it.[185][186] This hormone was first identified by Karoly Gyula David, E. Dingemanse, J. Freud and Ernst Laqueur in a May 1935 paper "On Crystalline Male Hormone from Testicles (Testosterone)."[187] They named the hormone testosterone, from the stems of testicle and sterol, and the suffix of ketone. The chemical synthesis of testosterone was achieved in August that year, when Butenandt and G. Hanisch published a paper describing "A Method for Preparing Testosterone from Cholesterol."[188] Only a week later, the third group, Ruzicka and A. Wettstein, announced a patent application in a paper "On the Artificial Preparation of the Testicular Hormone Testosterone (Androsten-3-one-17-ol)."[189] Ruzicka and Butenandt were offered the 1939 Nobel Prize in Chemistry for their work, but the Nazi government forced Butenandt to decline the honor, although he accepted the prize after the end of World War II.[185][186]

Clinical trials on humans, involving either oral doses of methyltestosterone or injections of testosterone propionate, began as early as 1937.[185] Testosterone propionate is mentioned in a letter to the editor of Strength and Health magazine in 1938; this is the earliest known reference to an AAS in a U.S. weightlifting or bodybuilding magazine.[185] There are often reported rumors that German soldiers were administered AAS during the Second World War, the aim being to increase their aggression and stamina, but these are, as yet, unproven.[110]:6 Adolf Hitler himself, according to his physician, was injected with testosterone derivatives to treat various ailments.[190] AAS were used in experiments conducted by the Nazis on concentration camp inmates,[190] and later by the allies attempting to treat the malnourished victims that survived Nazi camps.[110]:6 President John F. Kennedy was administered steroids both before and during his presidency.[191]

Development of synthetic AAS[edit]

The development of muscle-building properties of testosterone was pursued in the 1940s, in the Soviet Union and in Eastern Bloc countries such as East Germany, where steroid programs were used to enhance the performance of Olympic and other amateur weight lifters. In response to the success of Russian weightlifters, the U.S. Olympic Team physician John Ziegler worked with synthetic chemists to develop an AAS with reduced androgenic effects.[192] Ziegler's work resulted in the production of methandrostenolone, which Ciba Pharmaceuticals marketed as Dianabol. The new steroid was approved for use in the U.S. by the Food and Drug Administration (FDA) in 1958. It was most commonly administered to burn victims and the elderly. The drug's off-label users were mostly bodybuilders and weight lifters. Although Ziegler prescribed only small doses to athletes, he soon discovered that those having abused Dianabol suffered from enlarged prostates and atrophied testes.[193] AAS were placed on the list of banned substances of the International Olympic Committee (IOC) in 1976, and a decade later the committee introduced 'out-of-competition' doping tests because many athletes used AAS in their training period rather than during competition.[8]

Three major ideas governed modifications of testosterone into a multitude of AAS: Alkylation at C17α position with methyl or ethyl group created orally active compounds because it slows the degradation of the drug by the liver; esterification of testosterone and nortestosterone at the C17β position allows the substance to be administered parenterally and increases the duration of effectiveness because agents soluble in oily liquids may be present in the body for several months; and alterations of the ring structure were applied for both oral and parenteral agents to seeking to obtain different anabolic-to-androgenic effect ratios.[8]

Society and culture[edit]


Androgens were discovered in the 1930s and were characterized as having effects described as androgenic (i.e., virilizing) and anabolic (e.g., myotrophic, renotrophic).[62][1] The term anabolic steroid can be dated as far back as at least the mid-1940s, when it was used to describe the at-the-time hypothetical concept of a testosterone-derived steroid with anabolic effects but with minimal or no androgenic effects.[194] This concept was formulated based on the observation that steroids had ratios of renotrophic to androgenic potency that differed significantly, which suggested that anabolic and androgenic effects might be dissociable.[194]

In 1953, a testosterone-derived steroid known as norethandrolone (17α-ethyl-19-nortestosterone) was synthesized at G. D. Searle & Company and was studied as a progestin, but was not marketed.[195] Subsequently, in 1955, it was re-examined for testosterone-like activity in animals and was found to have similar anabolic activity to testosterone, but only one-sixteenth of its androgenic potency.[195][196] It was the first steroid with a marked and favorable separation of anabolic and androgenic effect to be discovered, and has accordingly been described as the "first anabolic steroid".[197][198] Norethandrolone was introduced for medical use in 1956, and was quickly followed by numerous similar steroids, for instance nandrolone phenylpropionate in 1959 and stanozolol in 1962.[197][198][199][200] With these developments, anabolic steroid became the preferred term to refer to such steroids (over "androgen"), and entered widespread use.

Although anabolic steroid was originally intended to specifically describe testosterone-derived steroids with a marked dissociation of anabolic and androgenic effect, it is applied today indiscriminately to all steroids with AR agonism-based anabolic effects regardless of their androgenic potency, including even non-synthetic steroids like testosterone.[62][1][195] While many anabolic steroids have diminished androgenic potency in comparison to anabolic potency, there is no anabolic steroid that is exclusively anabolic, and hence all anabolic steroids retain at least some degree of androgenicity.[62][1][195] (Likewise, all "androgens" are inherently anabolic.)[62][1][195] Indeed, it is probably not possible to fully dissociate anabolic effects from androgenic effects, as both types of effects are mediated by the same signaling receptor, the AR.[1] As such, the distinction between the terms anabolic steroid and androgen is questionable, and this is the basis for the revised and more recent term anabolic–androgenic steroid (AAS).[62][1][195]

Legal status[edit]

Various compounds with anabolic and androgenic effects, their relation with AAS

The legal status of AAS varies from country to country: some have stricter controls on their use or prescription than others though in many countries they are not illegal. In the U.S., AAS are currently listed as Schedule III controlled substances under the Controlled Substances Act, which makes simple possession of such substances without a prescription a federal crime punishable by up to one year in prison for the first offense. Unlawful distribution or possession with intent to distribute AAS as a first offense is punished by up to ten years in prison.[201] In Canada, AAS and their derivatives are part of the Controlled Drugs and Substances Act and are Schedule IV substances, meaning that it is illegal to obtain or sell them without a prescription; however, possession is not punishable, a consequence reserved for schedule I, II, or III substances. Those guilty of buying or selling AAS in Canada can be imprisoned for up to 18 months.[202] Import and export also carry similar penalties.

In Canada, researchers have concluded that steroid use among student athletes is extremely widespread. A study conducted in 1993 by the Canadian Centre for Drug-Free Sport found that nearly 83,000 Canadians between the ages of 11 and 18 use steroids.[203] AAS are also illegal without prescription in Australia,[204] Argentina,[citation needed] Brazil,[citation needed] and Portugal,[citation needed] and are listed as Class C Controlled Drugs in the United Kingdom. AAS are readily available without a prescription in some countries such as Mexico and Thailand.

United States[edit]

Steroid pills intercepted by the US Drug Enforcement Administration during the Operation Raw Deal bust in September 2007.

The history of the U.S. legislation on AAS goes back to the late 1980s, when the U.S. Congress considered placing AAS under the Controlled Substances Act following the controversy over Ben Johnson's victory at the 1988 Summer Olympics in Seoul. AAS were added to Schedule III of the Controlled Substances Act in the Anabolic Steroids Control Act of 1990.[205]


United Kingdom[edit]

In the United Kingdom, AAS are classified as class C drugs for their illegal abuse potential, which puts them in the same class as benzodiazepines. AAS are in Schedule 4, which is divided in 2 parts; Part 1 contains most of the benzodiazepines and Part 2 contains the AAS.


Status in sports[edit]

Legal status of AAS and other drugs with anabolic effects in Western countries

AAS are banned by all major sports bodies including Association of Tennis Professionals, Major League Baseball, Fédération Internationale de Football Association[208] the Olympics,[209] the National Basketball Association,[210] the National Hockey League,[211] World Wrestling Entertainment and the National Football League.[212] The World Anti-Doping Agency (WADA) maintains the list of performance-enhancing substances used by many major sports bodies and includes all anabolic agents, which includes all AAS and precursors as well as all hormones and related substances.[213][214] Spain has passed an anti-doping law creating a national anti-doping agency.[215] Italy passed a law in 2000 where penalties range up to three years in prison if an athlete has tested positive for banned substances.[216] In 2006, Russian President Vladimir Putin signed into law ratification of the International Convention Against Doping in Sport which would encourage cooperation with WADA. Many other countries have similar legislation prohibiting AAS in sports including Denmark,[217] France,[218] the Netherlands[219] and Sweden.[220]


Law enforcement[edit]

United States federal law enforcement officials have expressed concern about AAS use by police officers. "It's a big problem, and from the number of cases, it's something we shouldn't ignore. It's not that we set out to target cops, but when we're in the middle of an active investigation into steroids, there have been quite a few cases that have led back to police officers," says Lawrence Payne, a spokesman for the United States Drug Enforcement Administration.[221] The FBI Law Enforcement Bulletin stated that “Anabolic steroid abuse by police officers is a serious problem that merits greater awareness by departments across the country".[222] It is also believed that police officers across the United Kingdom "are using criminals to buy steroids" which he claims to be a top risk factor for police corruption.

Professional wrestling[edit]

Following the murder-suicide of Chris Benoit in 2007, the Oversight and Government Reform Committee investigated steroid usage in the wrestling industry.[223] The Committee investigated WWE and Total Nonstop Action Wrestling (TNA), asking for documentation of their companies' drug policies. WWE CEO and Chairman, Linda and Vince McMahon respectively, both testified. The documents stated that 75 wrestlers—roughly 40 percent—had tested positive for drug use since 2006, most commonly for steroids.[224][225]


Several large buckets containing tens of thousands of AAS vials confiscated by the DEA during Operation Raw Deal in 2007.

AAS are frequently produced in pharmaceutical laboratories, but, in nations where stricter laws are present, they are also produced in small home-made underground laboratories, usually from raw substances imported from abroad.[226] In these countries, the majority of steroids are obtained illegally through black market trade.[227][228] These steroids are usually manufactured in other countries, and therefore must be smuggled across international borders. As with most significant smuggling operations, organized crime is involved.[229]


In the U.S., Canada, and Europe, illegal steroids are sometimes purchased just as any other illegal drug, through dealers who are able to obtain the drugs from a number of sources. Illegal AAS are sometimes sold at gyms and competitions, and through the mail, but may also be obtained through pharmacists, veterinarians, and physicians.[231] In addition, a significant number of counterfeit products are sold as AAS, in particular via mail order from websites posing as overseas pharmacies. In the U.S., black-market importation continues from Mexico, Thailand, and other countries where steroids are more easily available, as they are legal.[232]


AAS, alone and in combination with progestogens, have been studied as potential male hormonal contraceptives.[48] Dual AAS and progestins such as trestolone and dimethandrolone undecanoate have also been studied as male contraceptives, with the latter under active investigation as of 2018.[233][169][234]

Topical androgens have been used and studied in the treatment of cellulite in women.[235] Topical androstanolone on the abdomen has been found to significantly decrease subcutaneous abdominal fat in women, and hence may be useful for improving body silhouette.[235] However, men and hyperandrogenic women have higher amounts of abdominal fat than healthy women, and androgens have been found to increase abdominal fat in postmenopausal women and transgender men as well.[236]

See also[edit]


  1. ^ a b c d e f g h i j k l m n o p q r s t u v w x y z aa ab ac ad ae af ag ah ai aj ak al am an ao ap aq ar as at au av aw ax ay az ba bb bc bd be bf bg bh bi bj bk bl bm bn bo Kicman, A T (2008). "Pharmacology of anabolic steroids". British Journal of Pharmacology. 154 (3): 502–521. doi:10.1038/bjp.2008.165. PMC 2439524. PMID 18500378.
  2. ^ Powers M (2011). Houglum J, Harrelson GL (eds.). Performance-Enhancing Drugs. Principles of Pharmacology for Athletic Trainers (2nd ed.). SLACK Incorporated. p. 345. ISBN 978-1-55642-901-9.
  6. ^ a b c Green GA (September 2009). "Performance-enhancing drug use". Orthopedics. 32 (9): 647–649. doi:10.3928/01477447-20090728-39. PMID 19751025.
  7. ^ a b c Turillazzi E, Perilli G, Di Paolo M, Neri M, Riezzo I, Fineschi V (2011). "Side effects of AAS abuse: an overview". Mini Rev Med Chem. 11 (5): 374–89. doi:10.2174/138955711795445925. PMID 21443513.
  11. ^ Ranke MB, Bierich JR (1986). "Treatment of growth hormone deficiency". Clinics in Endocrinology and Metabolism. 15 (3): 495–510. doi:10.1016/S0300-595X(86)80008-1. PMID 2429792.
  13. ^ Berger JR, Pall L, Hall CD, Simpson DM, Berry PS, Dudley R (1996). "Oxandrolone in AIDS-wasting myopathy". AIDS. 10 (14): 1657–62. doi:10.1097/00002030-199612000-00010. PMID 8970686.
  15. ^ Baum NH, Crespi CA (2007). "Testosterone replacement in elderly men". Geriatrics. 62 (9): 14–8. PMID 17824721.
  18. ^ a b c Mangus BC, Miller MG (11 January 2005). Pharmacology Application in Athletic Training. F.A. Davis. pp. 151–. ISBN 978-0-8036-2027-8.
  19. ^ Royal College of Physicians of London (1999). Osteoporosis: Clinical Guidelines for Prevention and Treatment. Royal College of Physicians. pp. 51–. ISBN 978-1-86016-079-0.
  20. ^ Davis SR (1999). "The therapeutic use of androgens in women". J. Steroid Biochem. Mol. Biol. 69 (1–6): 177–84. doi:10.1016/s0960-0760(99)00054-0. PMID 10418991.
  21. ^ William N. Taylor, M.D. (16 January 2002). Anabolic Steroids and the Athlete, 2d ed. McFarland. pp. 193–. ISBN 978-0-7864-1128-3.
  22. ^ a b "Oxandrolone Tablets, USP - Rx only" (PDF). Drugs@FDA. U.S. Food and Drug Administration. 1 December 2006. Retrieved 21 June 2016.
  23. ^ a b "Oxandrin (oxandrolone tablets, USP)" (PDF). Drugs@FDA. BTG Pharmaceuticals, U.S. Food and Drug Administration. 21 April 2003. Retrieved 21 June 2016.
  24. ^ Li H, Guo Y, Yang Z, Roy M, Guo Q (June 2016). "The efficacy and safety of oxandrolone treatment for patients with severe burns: A systematic review and meta-analysis". Burns. 42 (4): 717–27. doi:10.1016/j.burns.2015.08.023. PMID 26454425.
  25. ^ Rojas Y, Finnerty CC, Radhakrishnan RS, Herndon DN (December 2012). "Burns: an update on current pharmacotherapy". Expert Opinion on Pharmacotherapy. 13 (17): 2485–94. doi:10.1517/14656566.2012.738195. PMC 3576016. PMID 23121414.
  26. ^ Bork K (August 2012). "Current management options for hereditary angioedema". Current Allergy and Asthma Reports. 12 (4): 273–80. doi:10.1007/s11882-012-0273-4. PMID 22729959.
  27. ^ Choi G, Runyon BA (May 2012). "Alcoholic hepatitis: a clinician's guide". Clinics in Liver Disease. 16 (2): 371–85. doi:10.1016/j.cld.2012.03.015. PMID 22541704.
  28. ^ Manuchair Ebadi (31 October 2007). Desk Reference of Clinical Pharmacology, Second Edition. CRC Press. pp. 434–. ISBN 978-1-4200-4744-8.
  29. ^ Yagiela JA, Dowd FJ, Johnson B, Mariotti A, Neidle EA (19 March 2010). Pharmacology and Therapeutics for Dentistry - E-Book. Elsevier Health Sciences. pp. 569–. ISBN 978-0-323-07824-5.
  30. ^
  31. ^ Shah K, Montoya C, Persons RK (April 2007). "Clinical inquiries. Do testosterone injections increase libido for elderly hypogonadal patients?". J Fam Pract. 56 (4): 301–3. PMID 17403329.
  32. ^ Yassin AA, Saad F (March 2007). "Improvement of sexual function in men with late-onset hypogonadism treated with testosterone only". J Sex Med. 4 (2): 497–501. doi:10.1111/j.1743-6109.2007.00442.x. PMID 17367445.
  33. ^ Arver S, Dobs AS, Meikle AW, Caramelli KE, Rajaram L, Sanders SW, Mazer NA (December 1997). "Long-term efficacy and safety of a permeation-enhanced testosterone transdermal system in hypogonadal men". Clin. Endocrinol. 47 (6): 727–37. doi:10.1046/j.1365-2265.1997.3071113.x. PMID 9497881.
  34. ^ Nieschlag E, Büchter D, Von Eckardstein S, Abshagen K, Simoni M, Behre HM (December 1999). "Repeated intramuscular injections of testosterone undecanoate for substitution therapy in hypogonadal men". Clin. Endocrinol. 51 (6): 757–63. doi:10.1046/j.1365-2265.1999.00881.x. PMID 10619981.
  37. ^ Genderqueer, Pansexual, LGBTQ: Will Gender Exist 100 Years From Now? – Rebooted. October 24, 2013. Retrieved November 17, 2014.
  39. ^ Warne GL, Grover S, Zajac JD (2005). "Hormonal therapies for individuals with intersex conditions: protocol for use". Treatments in Endocrinology. 4 (1): 19–29. doi:10.2165/00024677-200504010-00003. PMID 15649098.
  40. ^ What is Intersex – An Intersex FAQ by Inter/Act – Inter/Act Youth Archived 2014-12-07 at the Wayback Machine. September 12, 2014. Retrieved December 5, 2014.
  41. ^ Perry MC, Doll DC, Freter CE (30 July 2012). Perry's The Chemotherapy Source Book. Lippincott Williams & Wilkins. pp. 409–. ISBN 978-1-4698-0343-2.
  42. ^ Allegra JC, Bertino J, Bonomi P, Byrne P, Carpenter J, Catalano R, Creech R, Dana B, Durivage H, Einhorn L (December 1985). "Metastatic breast cancer: preliminary results with oral hormonal therapy". Semin. Oncol. 12 (4 Suppl 6): 61–4. PMID 3909420.
  43. ^ Bachmann GA (1999). "Androgen cotherapy in menopause: evolving benefits and challenges". Am. J. Obstet. Gynecol. 180 (3 Pt 2): S308–11. doi:10.1016/S0002-9378(99)70724-6. PMID 10076169.
  44. ^ Kotz K, Alexander JL, Dennerstein L (2006). "Estrogen and androgen hormone therapy and well-being in surgically postmenopausal women". J Womens Health (Larchmt). 15 (8): 898–908. doi:10.1089/jwh.2006.15.898. PMID 17087613.
  45. ^ Garefalakis M, Hickey M (2008). "Role of androgens, progestins and tibolone in the treatment of menopausal symptoms: a review of the clinical evidence". Clin Interv Aging. 3 (1): 1–8. doi:10.2147/CIA.S1043. PMC 2544356. PMID 18488873.
  46. ^ a b Somboonporn W (2006). "Androgen and menopause". Curr. Opin. Obstet. Gynecol. 18 (4): 427–32. doi:10.1097/01.gco.0000233938.36554.37. PMID 16794424.
  47. ^ Davis S (2001). "Testosterone deficiency in women". J Reprod Med. 46 (3 Suppl): 291–6. PMID 11304877.
  48. ^ a b c Nieschlag E (2010). "Clinical trials in male hormonal contraception" (PDF). Contraception. 82 (5): 457–70. doi:10.1016/j.contraception.2010.03.020. PMID 20933120.
  49. ^ "Most steroid users are not athletes: study". Reuters. Reuters. 2007-11-21. Retrieved 2014-01-03.
  50. ^ Sjöqvist F, Garle M, Rane A (May 2008). "Use of doping agents, in particular anabolic steroids, in sports and society". Lancet. 371 (9627): 1872–82. doi:10.1016/S0140-6736(08)60801-6. PMID 18514731.
  51. ^ Yesalis CE, Kennedy NJ, Kopstein AN, Bahrke MS (1993). "Anabolic-androgenic steroid use in the United States". JAMA. 270 (10): 1217–21. doi:10.1001/jama.270.10.1217. PMID 8355384.
  52. ^ McCabe SE, Brower KJ, West BT, Nelson TF, Wechsler H (2007). "Trends in non-medical use of anabolic steroids by U.S. college students: Results from four national surveys". Drug and Alcohol Dependence. 90 (2–3): 243–51. doi:10.1016/j.drugalcdep.2007.04.004. PMC 2383927. PMID 17512138.
  53. ^ Parkinson AB, Evans NA (April 2006). "Anabolic androgenic steroids: a survey of 500 users". Med Sci Sports Exerc. 38 (4): 644–51. doi:10.1249/01.mss.0000210194.56834.5d. PMID 16679978.
  54. ^ a b c d e Cohen J, Collins R, Darkes J, Gwartney D (2007). "A league of their own: demographics, motivations and patterns of use of 1,955 male adult non-medical anabolic steroid users in the United States". J Int Soc Sports Nutr. 4: 12. doi:10.1186/1550-2783-4-12. PMC 2131752. PMID 17931410.
  55. ^ Copeland J, Peters R, Dillon P (March 1998). "A study of 100 anabolic-androgenic steroid users". Med. J. Aust. 168 (6): 311–2. doi:10.5694/j.1326-5377.1998.tb140177.x. PMID 9549549.
  56. ^ Eastley T (January 18, 2006). "Steroid study debunks user stereotypes". ABC. Retrieved 2014-01-03.
  57. ^ Pope HG, Kanayama G, Ionescu-Pioggia M, Hudson JI (September 2004). "Anabolic steroid users' attitudes towards physicians". Addiction. 99 (9): 1189–94. doi:10.1111/j.1360-0443.2004.00781.x. PMID 15317640.
  58. ^ Kanayama G, Barry S, Hudson JI, Pope HG (April 2006). "Body image and attitudes toward male roles in anabolic-androgenic steroid users". Am J Psychiatry. 163 (4): 697–703. doi:10.1176/appi.ajp.163.4.697. PMID 16585446.
  59. ^ Grogan S, Shepherd S, Evans R, Wright S, Hunter G (Nov 2006). "Experiences of Anabolic Steroid Use". Journal of Health Psychology. 11 (6): 845–856. doi:10.1177/1359105306069080. PMID 17035257.
  60. ^ Hickson RC, Czerwinski SM, Falduto MT, Young AP (1990). "Glucocorticoid antagonism by exercise and androgenic-anabolic steroids". Medicine & Science in Sports & Exercise. 22 (3): 331–40. doi:10.1249/00005768-199006000-00010. PMID 2199753.
  61. ^ a b c Becker KL (2001). Principles and Practice of Endocrinology and Metabolism. Lippincott Williams & Wilkins. pp. 1185–1186. ISBN 978-0-7817-1750-2.
  62. ^ a b c d e f g h i j k l m n o p q r s t Llewellyn, William (2011). Anabolics. Molecular Nutrition Llc. pp. 533–, 402–412, 460–467. ISBN 978-0-9828280-1-4.
  63. ^ a b Rahnema CD, Crosnoe LE, Kim ED (March 2015). "Designer steroids - over-the-counter supplements and their androgenic component: review of an increasing problem". Andrology. 3 (2): 150–5. doi:10.1111/andr.307. PMID 25684733.
  64. ^ a b Chrousos GP (2012). "The Gonadal Hormones & Inhibitors". In Katzung BG (ed.). Basic & Clinical Pharmacology. New York London: McGraw-Hill Medical McGraw-Hill distributor. ISBN 978-0071764018.
  65. ^ Mutzebaugh C (1998). "Does the choice of alpha-AAS really make a difference?". HIV Hotline. 8 (5–6): 10–1. PMID 11366379.
  66. ^ Casavant MJ, Blake K, Griffith J, Yates A, Copley LM (2007). "Consequences of use of anabolic androgenic steroids". Pediatr. Clin. North Am. 54 (4): 677–90, x. doi:10.1016/j.pcl.2007.04.001. PMID 17723870.
  67. ^ Pope HG, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S (2014). "Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement". Endocr. Rev. 35 (3): 341–75. doi:10.1210/er.2013-1058. PMC 4026349. PMID 24423981.
  68. ^ Fragkaki AG, Angelis YS, Koupparis M, Tsantili-Kakoulidou A, Kokotos G, Georgakopoulos C (2009). "Structural characteristics of anabolic androgenic steroids contributing to binding to the androgen receptor and to their anabolic and androgenic activities. Applied modifications in the steroidal structure". Steroids. 74 (2): 172–97. doi:10.1016/j.steroids.2008.10.016. PMID 19028512.
  69. ^ Nieschlag E, Vorona E (2015). "MECHANISMS IN ENDOCRINOLOGY: Medical consequences of doping with anabolic androgenic steroids: effects on reproductive functions". Eur. J. Endocrinol. 173 (2): R47–58. doi:10.1530/EJE-15-0080. PMID 25805894.
  70. ^ Hall RC, Hall RC, Chapman MJ (2005). "Psychiatric complications of anabolic steroid abuse". Psychosomatics. 46 (4): 285–90. doi:10.1176/appi.psy.46.4.285. PMID 16000671.
  71. ^ a b Trenton AJ, Currier GW (2005). "Behavioural manifestations of anabolic steroid use". CNS Drugs. 19 (7): 571–95. doi:10.2165/00023210-200519070-00002. PMID 15984895.
  72. ^ Vanberg P, Atar D (2010). "Androgenic anabolic steroid abuse and the cardiovascular system". Handbook of Experimental Pharmacology. 195 (195): 411–57. doi:10.1007/978-3-540-79088-4_18. ISBN 978-3-540-79087-7. PMID 20020375.
  73. ^ Achar S, Rostamian A, Narayan SM (2010). "Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm". Am. J. Cardiol. 106 (6): 893–901. doi:10.1016/j.amjcard.2010.05.013. PMC 4111565. PMID 20816133.
  74. ^ Solimini R, Rotolo MC, Mastrobattista L, Mortali C, Minutillo A, Pichini S, Pacifici R, Palmi I (2017). "Hepatotoxicity associated with illicit use of anabolic androgenic steroids in doping". Eur Rev Med Pharmacol Sci. 21 (1 Suppl): 7–16. PMID 28379599.
  75. ^ Brenu EW, McNaughton L, Marshall-Gradisnik SM (2011). "Is there a potential immune dysfunction with anabolic androgenic steroid use?: A review". Mini Rev Med Chem. 11 (5): 438–45. doi:10.2174/138955711795445907. PMID 21443507.
  77. ^ "DailyMed: About DailyMed". Retrieved 2008-11-03.
  78. ^ Bagatell CJ, Knopp RH, Vale WW, Rivier JE, Bremner WJ (1992). "Physiologic testosterone levels in normal men suppress high-density lipoprotein cholesterol levels". Annals of Internal Medicine. 116 (12 Pt 1): 967–73. doi:10.7326/0003-4819-116-12-967. PMID 1586105.
  80. ^ Melnik B, Jansen T, Grabbe S (2007). "Abuse of anabolic-androgenic steroids and bodybuilding acne: an underestimated health problem". Journal der Deutschen Dermatologischen Gesellschaft. 5 (2): 110–7. doi:10.1111/j.1610-0387.2007.06176.x. PMID 17274777.
  82. ^ Irving LM, Wall M, Neumark-Sztainer D, Story M (2002). "Steroid use among adolescents: findings from Project EAT". The Journal of Adolescent Health. 30 (4): 243–52. doi:10.1016/S1054-139X(01)00414-1. PMID 11927236.
  90. ^ Wit JM, Oostdijk W (2015). "Novel approaches to short stature therapy". Best Practice & Research. Clinical Endocrinology & Metabolism. 29 (3): 353–66. doi:10.1016/j.beem.2015.01.003. PMID 26051296.
  96. ^ Franke WW, Berendonk B (July 1997). "Hormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government". Clinical Chemistry. 43 (7): 1262–79. PMID 9216474.
  98. ^ Herlitz LC, Markowitz GS, Farris AB, Schwimmer JA, Stokes MB, Kunis C, Colvin RB, D'Agati VD (October 29, 2009). Development of FSGS Following Anabolic Steroid Use in Bodybuilders (PDF). 42nd Annual Meeting and Scientific Exposition of the American Society of Nephrology. Bodybuilding With Steroids Damages Kidneys. Lay summaryScienceDaily (October 30, 2009).
  100. ^ a b Kanayama G, Hudson JI, Pope HG (November 2008). "Long-Term Psychiatric and Medical Consequences of Anabolic-Androgenic Steroid Abuse: A Looming Public Health Concern?". Drug Alcohol Depend. 98 (1–2): 1–12. doi:10.1016/j.drugalcdep.2008.05.004. PMC 2646607. PMID 18599224.
  101. ^ Brower KJ (October 2002). "Anabolic steroid abuse and dependence". Curr Psychiatry Rep. 4 (5): 377–87. doi:10.1007/s11920-002-0086-6. PMID 12230967.
  102. ^ Fudala PJ, Weinrieb RM, Calarco JS, Kampman KM, Boardman C (2003). "An evaluation of anabolic-androgenic steroid abusers over a period of 1 year: seven case studies". Annals of Clinical Psychiatry. 15 (2): 121–30. doi:10.3109/10401230309085677. PMID 12938869.
  103. ^ Pagonis TA, Angelopoulos NV, Koukoulis GN, Hadjichristodoulou CS (2006). "Psychiatric side effects induced by supraphysiological doses of combinations of anabolic steroids correlate to the severity of abuse". Eur. Psychiatry. 21 (8): 551–62. doi:10.1016/j.eurpsy.2005.09.001. PMID 16356691.
  104. ^ a b Rashid H, Ormerod S, Day E (2007). "Anabolic androgenic steroids: What the psychiatrist needs to know". Advances in Psychiatric Treatment. 13 (3): 203–211. doi:10.1192/apt.bp.105.000935.
  105. ^ Cooper CJ, Noakes TD, Dunne T, Lambert MI, Rochford K (September 1996). "A high prevalence of abnormal personality traits in chronic users of anabolic-androgenic steroids". Br J Sports Med. 30 (3): 246–50. doi:10.1136/bjsm.30.3.246. PMC 1332342. PMID 8889121.
  106. ^ "Dr. Ritchi Morris". Archived from the original on 2013-12-03. Retrieved 2013-12-01.
  107. ^ Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG (December 2009). "Anabolic-androgenic steroid dependence: an emerging disorder". Addiction. 104 (12): 1966–78. doi:10.1111/j.1360-0443.2009.02734.x. PMC 2780436. PMID 19922565.
  108. ^ Eisenberg ER, Galloway GP. "Anabolic androgenic steroids". In Lowinson JH, Ruiz P, Millman RB (eds.). Substance Abuse: A Comprehensive Textbook. Lippincott Williams & Wilkins. ASIN B0049VACMW.
  110. ^ a b c Lenahan P (2003). Anabolic Steroids: And Other Performance-enhancing Drugs. London: Taylor & Francis. ISBN 0-415-28030-3.
  111. ^ Thiblin I, Petersson A (February 2005). "Pharmacoepidemiology of anabolic androgenic steroids: a review". Fundam Clin Pharmacol. 19 (1): 27–44. doi:10.1111/j.1472-8206.2004.00298.x. PMID 15660958.
  112. ^ Beaver KM, Vaughn MG, Delisi M, Wright JP (December 2008). "Anabolic-Androgenic Steroid Use and Involvement in Violent Behavior in a Nationally Representative Sample of Young Adult Males in the United States". Am J Public Health. 98 (12): 2185–7. doi:10.2105/AJPH.2008.137018. PMC 2636528. PMID 18923108.
  113. ^ Bahrke MS, Yesalis CE, Wright JE (1996). "Psychological and behavioural effects of endogenous testosterone and anabolic-androgenic steroids. An update". Sports Medicine. 22 (6): 367–90. doi:10.2165/00007256-199622060-00005. PMID 8969015.
  116. ^ Pope HG, Kouri EM, Hudson JI (February 2000). "Effects of supraphysiologic doses of testosterone on mood and aggression in normal men: a randomized controlled trial". Arch. Gen. Psychiatry. 57 (2): 133–40, discussion 155–6. doi:10.1001/archpsyc.57.2.133. PMID access
  117. ^ Pagonis TA, Angelopoulos NV, Koukoulis GN, Hadjichristodoulou CS, Toli PN (2006). "Psychiatric and hostility factors related to use of anabolic steroids in monozygotic twins". Eur. Psychiatry. 21 (8): 563–9. doi:10.1016/j.eurpsy.2005.11.002. PMID 16529916.
  119. ^ "Teens & Steroids: A Dangerous Mix". CBS Broadcasting Inc. 2004-06-03. Archived from the original on 10 July 2007. Retrieved 2007-06-27.
  120. ^ Uzych L (February 1992). "Anabolic-androgenic steroids and psychiatric-related effects: a review". Can J Psychiatry. 37 (1): 23–8. doi:10.1177/070674379203700106. PMID 1551042.
  122. ^ a b c d El Osta R, Almont T, Diligent C, Hubert N, Eschwège P, Hubert J (2016). "Anabolic steroids abuse and male infertility". Basic Clin Androl. 26 (2): 2. doi:10.1186/s12610-016-0029-4 (inactive 2019-08-18). PMC 4744441. PMID 26855782.
  123. ^ Kickman AT (2008). "Pharmacology of anabolic steroids". Br J Pharmacol. 154 (3): 502–521. doi:10.1038/bjp.2008.165. PMC 2439524. PMID 18500378.
  124. ^ Stromme SB, Meen HD, Aakvaag A (1974). "Effects of an androgenic-anabolic steroid on strength development and plasma testosterone levels in normal males". Med Sci Sports. 6 (3): 203–208. PMID 4437350.
  125. ^ Sagoe D, Molde H, Andreassen CS, Torsheim T, Pallesen S (2014). "The global epidemiology of anabolic-androgenic steroid use: a meta-analysis and meta-regression analysis". Ann Epidemiol. 24 (5): 383–398. doi:10.1007/s40279-017-0709-z. PMID 24582699.
  126. ^ Christou MA, Christou PA, Markozannes G, Tsatsoulis A, Mastorakos G, Tigas S (2017). "Effects of Anabolic Androgenic Steroids on the Reproductive System of Athletes and Recreational Users: A Systematic Review and Meta-Analysis". Sports Med. 47 (9): 1869–1883. doi:10.1007/s40279-017-0709-z. PMID 28258581.