View source for Anabolic steroid

{{Hatnote|This article is about androgens as medications. For androgens as natural hormones, see [[Androgen]].}}
{{Infobox drug class
| Name = Anabolic–androgenic steroids
| Image = Testosteron.svg
| Alt = 
| Width = 225px
| Caption = Chemical structure of the natural AAS [[testosterone (medication)|testosterone]] (androst-4-en-17β-ol-3-one).
| Pronounce = 
| Synonyms = Anabolic steroids; Androgens
<!-- Class identifiers -->
| Use = [[#Medical uses|Various]]
| ATC_prefix = A14A
| Mode_of_action = 
| Mechanism_of_action = 
| Biological_target = [[Androgen receptor]]
| Chemical_class = [[Steroid]]s; [[Androstane]]s; [[Estrane]]s
<!-- Clinical data -->
| Drugs.com = {{Drugs.com|drug-class|androgens-and-anabolic-steroids}}
| Consumer_Reports = 
| medicinenet = 
| rxlist = 
<!-- External links -->
| MeshID = D045165
}}

'''Anabolic steroids''', also known more properly as '''anabolic–androgenic steroids''' ('''AAS'''),<ref name="Kicman2008">{{cite journal |last1=Kicman |first1=A T |title=Pharmacology of anabolic steroids |journal=British Journal of Pharmacology |volume=154 |issue=3 |year=2008 |pages=502–521 |doi=10.1038/bjp.2008.165|pmid=18500378 |pmc=2439524}}</ref> are [[steroid]]al [[androgen]]s that include [[natural product|natural]] androgens like [[testosterone (medication)|testosterone]] as well as [[synthetic compound|synthetic]] androgens that are structurally related and have similar effects to testosterone. They are [[anabolic]] and increase [[protein]] within [[cell (biology)|cell]]s, especially in [[skeletal muscle]]s, and also have varying degrees of [[androgenic]] and [[virilization|virilizing]] effects, including induction of the development and maintenance of [[masculinity|masculine]] [[secondary sexual characteristic]]s such as the growth of [[facial hair|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 [[agonist]]s, the others being [[estrogen (medication)|estrogen]]s like [[estradiol (medication)|estradiol]] and [[progestogen]]s like [[progesterone (medication)|progesterone]].

AAS were synthesized in the 1930s, and are now used therapeutically in medicine to stimulate muscle growth and [[appetite]], induce male [[puberty]] and treat chronic [[wasting]] conditions, such as [[cancer]] and {{abbrlink|AIDS|acquired immunodeficiency syndrome}}. The [[American College of Sports Medicine]] acknowledges that AAS, in the presence of adequate diet, can contribute to increases in [[body weight]], often as lean mass increases and that the gains in [[muscular strength]] achieved through high-intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.<ref>{{cite book |first=Michael |last=Powers |title=Performance-Enhancing Drugs |editor-first1=Joel |editor-last1=Houglum |editor-first2=Gary L. |editor-last2=Harrelson | name-list-format = vanc |work=Principles of Pharmacology for Athletic Trainers |publisher=SLACK Incorporated |date=2011 |edition=2nd |isbn=978-1-55642-901-9 |p=345 |url=https://books.google.com/books?id=wbkoeZuwqjwC&pg=PA345}}</ref>

Health risks can be produced by long-term use or excessive doses of AAS.<ref name="BarrettConnor1995">{{cite journal | vauthors = Barrett-Connor EL |title=Testosterone and risk factors for cardiovascular disease in men |journal=Diabete Metab |volume=21 |issue=3 |pages=156–61 |year=1995 |pmid=7556805}}</ref><ref name="Yamamoto2006">{{cite journal |vauthors=Yamamoto Y, Moore R, Hess HA, Guo GL, Gonzalez FJ, Korach KS, Maronpot RR, Negishi M |title=Estrogen receptor alpha mediates 17alpha-ethynylestradiol causing hepatotoxicity |journal=J Biol Chem |volume=281 |issue=24 |pages=16625–31 |year=2006 |pmid=16606610 |doi=10.1074/jbc.M602723200}}</ref> These effects include harmful changes in [[cholesterol]] levels (increased [[low-density lipoprotein]] and decreased [[high-density lipoprotein]]), [[acne vulgaris|acne]], [[high blood pressure]], [[hepatotoxicity|liver damage]] (mainly with most oral AAS), and dangerous changes in the structure of the [[left ventricle]] of the [[heart]].<ref name="De1991">{{cite journal |vauthors=De Piccoli B, Giada F, Benettin A, Sartori F, Piccolo E |title=Anabolic steroid use in body builders: an echocardiographic study of left ventricle morphology and function |journal=Int J Sports Med |volume=12 |issue=4 |pages=408–12 |year=1991 |pmid=1917226 |doi=10.1055/s-2007-1024703}}</ref> Conditions pertaining to [[hormonal imbalance]]s such as [[gynecomastia]] and [[hypogonadism|testicular size reduction]] may also be caused by AAS.<ref name="pmid21443513" /> In women and children, AAS can cause irreversible [[masculinization]].<ref name="pmid21443513" />

[[Ergogenic aid|Ergogenic]] uses for AAS in [[sport]]s, [[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 [[Use of performance-enhancing drugs in sport|doping]] and banned by most major sporting bodies. For many years, AAS have been by far the most detected doping substances in [[IOC]]-accredited laboratories.<ref name="Hartgens and Kuipers 2004">{{cite journal |vauthors=Hartgens F, Kuipers H |title=Effects of androgenic-anabolic steroids in athletes |journal=Sports Med |volume=34 |issue=8 |pages=513–54 |year=2004 |pmid=15248788 |doi=10.2165/00007256-200434080-00003}}</ref><ref name=Kicman/> 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.

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==Uses==

===Medical===
[[File:Anabolicsteroids41.jpg|thumb|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.

====Anabolic====
* [[Bone marrow]] stimulation: For decades, AAS were the mainstay of therapy for [[hypoplastic]] [[anemia]]s due to [[leukemia]] or [[kidney failure]], especially [[aplastic anemia]].<ref name=Basaria>{{cite journal |vauthors=Basaria S, Wahlstrom JT, Dobs AS |title=Clinical review 138: Anabolic-androgenic steroid therapy in the treatment of chronic diseases |journal=J. Clin. Endocrinol. Metab. |volume=86 |issue=11 |pages=5108–17 |date=November 2001 |pmid=11701661 |doi=10.1210/jcem.86.11.7983}}</ref> AAS have largely been replaced in this setting by synthetic protein hormones (such as [[epoetin alfa]]) that selectively stimulate growth of [[Hematopoietic stem cell|blood cell precursors]].
* [[Human development (biology)|Growth]] stimulation: AAS can be used by [[pediatric endocrinology|pediatric endocrinologists]] to treat children with [[growth failure]].<ref>{{cite journal |vauthors=Ranke MB, Bierich JR |title=Treatment of growth hormone deficiency |journal=Clinics in Endocrinology and Metabolism |volume=15 |issue=3 |pages=495–510 |year=1986 |pmid=2429792 |doi=10.1016/S0300-595X(86)80008-1}}</ref> However, the availability of synthetic [[growth hormone treatment|growth hormone]], which has fewer side effects, makes this a secondary treatment.
* Stimulation of [[appetite]] and preservation and increase of [[muscle]] mass: AAS have been given to people with [[cachexia|chronic wasting conditions]] such as [[cancer]] and [[AIDS]].<ref>{{cite journal |vauthors=Grunfeld C, Kotler DP, Dobs A, Glesby M, Bhasin S |title=Oxandrolone in the treatment of HIV-associated weight loss in men: a randomized, double-blind, placebo-controlled study |journal=J. Acquir. Immune Defic. Syndr. |volume=41 |issue=3 |pages=304–14 |year=2006 |pmid=16540931 |doi=10.1097/01.qai.0000197546.56131.40}}</ref><ref>{{cite journal |vauthors=Berger JR, Pall L, Hall CD, Simpson DM, Berry PS, Dudley R |title=Oxandrolone in AIDS-wasting myopathy |journal=AIDS |volume=10 |issue=14 |pages=1657–62 |year=1996 |pmid=8970686 |doi=10.1097/00002030-199612000-00010}}</ref>
* Stimulation of lean body mass and prevention of [[bone resorption|bone loss]] in elderly men, as some studies indicate.<ref name="pmid11320105">{{cite journal |vauthors=Kenny AM, Prestwood KM, Gruman CA, Marcello KM, Raisz LG |title=Effects of transdermal testosterone on bone and muscle in older men with low bioavailable testosterone levels |journal=J. Gerontol. A Biol. Sci. Med. Sci. |volume=56 |issue=5 |pages=M266–72 |year=2001 |pmid=11320105 |doi=10.1093/gerona/56.5.M266}}</ref><ref name="pmid17824721">{{cite journal |vauthors=Baum NH, Crespi CA |title=Testosterone replacement in elderly men |journal=Geriatrics |volume=62 |issue=9 |pages=14–8 |year=2007 |pmid=17824721}}</ref><ref name="pmid11730258">{{cite journal | vauthors = Francis RM |title=Androgen replacement in aging men |journal=Calcif. Tissue Int. |volume=69 |issue=4 |pages=235–8 |year=2001 |pmid=11730258 |doi=10.1007/s00223-001-1051-9}}</ref> However, a 2006 placebo-controlled trial of low-dose testosterone supplementation in elderly men with low levels of testosterone found no benefit on body composition, physical performance, [[insulin sensitivity]], or [[quality of life]].<ref name="pmid17050889">{{cite journal |vauthors=Nair KS, Rizza RA, O'Brien P, Dhatariya K, Short KR, Nehra A, Vittone JL, Klee GG, Basu A, Basu R, Cobelli C, Toffolo G, Dalla Man C, Tindall DJ, Melton LJ, Smith GE, Khosla S, Jensen MD |title=DHEA in elderly women and DHEA or testosterone in elderly men |journal=N. Engl. J. Med. |volume=355 |issue=16 |pages=1647–59 |date=October 2006 |pmid=17050889 |doi=10.1056/NEJMoa054629}}</ref>
* Prevention or treatment of [[osteoporosis]] in [[postmenopausal]] women.<ref name="MangusMiller2005" /><ref name="London1999">{{cite book|author=Royal College of Physicians of London|title=Osteoporosis: Clinical Guidelines for Prevention and Treatment|url=https://books.google.com/books?id=ANyPYl4gboQC&pg=PA51|year=1999|publisher=Royal College of Physicians|isbn=978-1-86016-079-0|pages=51–}}</ref> [[Nandrolone decanoate]] is approved for this use.<ref name="pmid10418991">{{cite journal | vauthors = Davis SR | title = The therapeutic use of androgens in women | journal = J. Steroid Biochem. Mol. Biol. | volume = 69 | issue = 1-6 | pages = 177–84 | year = 1999 | pmid = 10418991 | doi = | url = }}</ref> Although they have been indicated for this indication, AAS saw very little use for this purpose due to their virilizing side effects.<ref name="MangusMiller2005" /><ref name="M.D.2002">{{cite book|author=William N. Taylor, M.D.|title=Anabolic Steroids and the Athlete, 2d ed.|url=https://books.google.com/books?id=OGcQ0Tp2AFcC&pg=PA193|date=16 January 2002|publisher=McFarland|isbn=978-0-7864-1128-3|pages=193–}}</ref>

====Androgenic====
* [[Androgen replacement therapy]] for men with [[hypogonadism|low levels of testosterone]]; also effective in improving libido for elderly males.<ref name="pmid17403329">{{cite journal |vauthors=Shah K, Montoya C, Persons RK |title=Clinical inquiries. Do testosterone injections increase libido for elderly hypogonadal patients? |journal=J Fam Pract |volume=56 |issue=4 |pages=301–3 |date=April 2007 |pmid=17403329}}</ref><ref name="pmid17367445">{{cite journal |vauthors=Yassin AA, Saad F |title=Improvement of sexual function in men with late-onset hypogonadism treated with testosterone only |journal=J Sex Med |volume=4 |issue=2 |pages=497–501 |date=March 2007 |pmid=17367445 |doi=10.1111/j.1743-6109.2007.00442.x}}</ref><ref name="pmid9497881">{{cite journal |vauthors=Arver S, Dobs AS, Meikle AW, Caramelli KE, Rajaram L, Sanders SW, Mazer NA |title=Long-term efficacy and safety of a permeation-enhanced testosterone transdermal system in hypogonadal men |journal=Clin. Endocrinol. |volume=47 |issue=6 |pages=727–37 |date=December 1997 |pmid=9497881 |doi=10.1046/j.1365-2265.1997.3071113.x}}</ref><ref name="pmid10619981">{{cite journal |vauthors=Nieschlag E, Büchter D, Von Eckardstein S, Abshagen K, Simoni M, Behre HM |title=Repeated intramuscular injections of testosterone undecanoate for substitution therapy in hypogonadal men |journal=Clin. Endocrinol. |volume=51 |issue=6 |pages=757–63 |date=December 1999 |pmid=10619981 |doi=10.1046/j.1365-2265.1999.00881.x}}</ref>
* Induction of male [[puberty]]: Androgens are given to many boys distressed about extreme [[delayed puberty|delay of puberty]]. Testosterone is now nearly the only androgen used for this purpose and has been shown to increase height, weight, and fat-free mass in boys with delayed puberty.<ref>{{cite journal |vauthors=Arslanian S, Suprasongsin C |title=Testosterone treatment in adolescents with delayed puberty: changes in body composition, protein, fat, and glucose metabolism |journal=J. Clin. Endocrinol. Metab. |volume=82 |issue=10 |pages=3213–20 |year=1997 |pmid=9329341 |doi=10.1210/jc.82.10.3213}}</ref>
* [[Masculinizing hormone therapy]] for [[transgender men]], other [[transmasculine]] people, and [[intersex]] people, by producing masculine secondary sexual characteristics such as a [[voice deepening]], increased bone and muscle mass, [[android fat distribution|masculine fat distribution]], facial and body hair, and [[clitoral enlargement]], as well as mental changes such as alleviation of [[gender dysphoria]] and increased sex drive.<ref>{{cite journal |vauthors=Moore E, Wisniewski A, Dobs A |title=Endocrine treatment of transsexual people: a review of treatment regimens, outcomes, and adverse effects |journal=J. Clin. Endocrinol. Metab. |volume=88 |issue=8 |pages=3467–73 |date=August 2003 |pmid=12915619 |doi=10.1210/jc.2002-021967}}</ref><ref>[http://darahoffmanfox.com/ask-gender-therapist-can-transition-im-non-binary-genderfluid/ Ask a Gender Therapist: Can I Transition if I’m Non-Binary or Genderfluid? – Dara Hoffman-Fox]. May 7, 2014. Retrieved November 17, 2014.</ref><ref>[http://ieet.org/index.php/IEET/more/notaro20131025 Genderqueer, Pansexual, LGBTQ: Will Gender Exist 100 Years From Now? – Rebooted]. October 24, 2013. Retrieved November 17, 2014.</ref><ref>[http://www.sfgate.com/health/article/Young-people-exploring-nonbinary-gender-roles-5225994.php Young people exploring nonbinary gender roles – SF Gate]. February 12, 2014. Retrieved November 17, 2014.</ref><ref>[http://tranifesto.com/2014/01/09/ask-matt-my-genderqueer-child-wants-to-use-testosterone/ Ask Matt: My Genderqueer Child Wants to Use Testosterone – Tranifesto]. January 9, 2014. Retrieved November 17, 2014.</ref><ref name="pmid15649098">{{cite journal | vauthors = Warne GL, Grover S, Zajac JD | title = Hormonal therapies for individuals with intersex conditions: protocol for use | journal = Treatments in Endocrinology | volume = 4 | issue = 1 | pages = 19–29 | year = 2005 | pmid = 15649098 | doi = 10.2165/00024677-200504010-00003| url = }}</ref><ref>[http://interactyouth.org/post/97343969730/support-the-intersex-youth-supporting-tvs-first What is Intersex – An Intersex FAQ by Inter/Act – Inter/Act Youth]. September 12, 2014. Retrieved December 5, 2014.</ref>

====Other====
* Treatment of [[breast cancer]] in women, although they are now rarely used for this purpose due to virilizing side effects.<ref name="PerryDoll2012">{{cite book|author1=Michael C. Perry|author2=Donald C. Doll|author3=Carl E. Freter|title=Perry's The Chemotherapy Source Book|url=https://books.google.com/books?id=My3SjQTguyYC&pg=PA409|date=30 July 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-4698-0343-2|pages=409–}}</ref><ref name="MangusMiller2005">{{cite book|author1=Brent C Mangus|author2=Michael G Miller|title=Pharmacology Application in Athletic Training|url=https://books.google.com/books?id=tV72AAAAQBAJ&pg=PA151|date=11 January 2005|publisher=F.A. Davis|isbn=978-0-8036-2027-8|pages=151–}}</ref>
* In low doses as a component of [[hormone replacement therapy|hormone therapy]] for [[postmenopausal women|postmenopausal]] and [[transgender women]], for instance to increase [[energy (psychological)|energy]], [[well-being]], [[libido]], and [[quality of life]], as well as to reduce [[hot flash]]es.<ref name="pmid10076169">{{cite journal | vauthors = Bachmann GA | title = Androgen cotherapy in menopause: evolving benefits and challenges | journal = Am. J. Obstet. Gynecol. | volume = 180 | issue = 3 Pt 2 | pages = S308–11 | year = 1999 | pmid = 10076169 | doi = | url = }}</ref><ref name="pmid17087613">{{cite journal | vauthors = Kotz K, Alexander JL, Dennerstein L | title = Estrogen and androgen hormone therapy and well-being in surgically postmenopausal women | journal = J Womens Health (Larchmt) | volume = 15 | issue = 8 | pages = 898–908 | year = 2006 | pmid = 17087613 | doi = 10.1089/jwh.2006.15.898 | url = }}</ref><ref name="pmid18488873">{{cite journal | vauthors = Garefalakis M, Hickey M | title = Role of androgens, progestins and tibolone in the treatment of menopausal symptoms: a review of the clinical evidence | journal = Clin Interv Aging | volume = 3 | issue = 1 | pages = 1–8 | year = 2008 | pmid = 18488873 | pmc = 2544356 | doi = | url = }}</ref><ref name="pmid16794424">{{cite journal | vauthors = Somboonporn W | title = Androgen and menopause | journal = Curr. Opin. Obstet. Gynecol. | volume = 18 | issue = 4 | pages = 427–32 | year = 2006 | pmid = 16794424 | doi = 10.1097/01.gco.0000233938.36554.37 | url = }}</ref> Testosterone is usually used for this purpose, although [[methyltestosterone]] is also used.<ref name="pmid16794424" /><ref name="pmid11304877">{{cite journal | vauthors = Davis S | title = Testosterone deficiency in women | journal = J Reprod Med | volume = 46 | issue = 3 Suppl | pages = 291–6 | year = 2001 | pmid = 11304877 | doi = | url = }}</ref>
* [[Male contraceptive|Male contraception]], in the form of [[testosterone enanthate]]; potential for use in the near-future as a safe, reliable, and reversible male contraceptive.<ref name="administration282"/><ref>{{cite journal |vauthors=Aribarg A, Sukcharoen N, Chanprasit Y, Ngeamvijawat J, Kriangsinyos R |title=Suppression of spermatogenesis by testosterone enanthate in Thai men |journal=Journal of the Medical Association of Thailand = Chotmaihet thangphaet |volume=79 |issue=10 |pages=624–9 |year=1996 |pmid=8996996}}</ref>

===Enhancing performance===
{{See also|Ergogenic use of anabolic steroids}}
[[File:Rawdealsteroids4.jpg|thumb|Numerous vials of injectable AAS]]

Most steroid users are not athletes.<ref>{{cite web |url=https://www.reuters.com/article/2007/11/21/us-steroid-users-idUSCOL17558920071121 |title=Most steroid users are not athletes: study |agency=Reuters |date=2007-11-21 |accessdate=2014-01-03 }}</ref> Between 1 million and 3 million people (1% of the population) are thought to have misused AAS in the United States.<ref>{{cite journal |vauthors=Sjöqvist F, Garle M, Rane A |title=Use of doping agents, in particular anabolic steroids, in sports and society |journal=Lancet |volume=371 |issue=9627 |pages=1872–82 |date=May 2008 |pmid=18514731 |doi=10.1016/S0140-6736(08)60801-6}}</ref> 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.<ref name="pmid8355384">{{cite journal |vauthors=Yesalis CE, Kennedy NJ, Kopstein AN, Bahrke MS |title=Anabolic-androgenic steroid use in the United States |journal=JAMA |volume=270 |issue=10 |pages=1217–21 |year=1993 |pmid=8355384 |doi=10.1001/jama.270.10.1217}}</ref> "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%.<ref name="pmid17512138">{{cite journal |vauthors=McCabe SE, Brower KJ, West BT, Nelson TF, Wechsler H |title=Trends in non-medical use of anabolic steroids by U.S. college students: Results from four national surveys |journal=Drug and Alcohol Dependence |volume=90 |issue=2–3 |pages=243–51 |year=2007 |pmid=17512138 |pmc=2383927 |doi=10.1016/j.drugalcdep.2007.04.004}}</ref> 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,<ref name="pmid16679978">{{cite journal |vauthors=Parkinson AB, Evans NA |title=Anabolic androgenic steroids: a survey of 500 users |journal=Med Sci Sports Exerc |volume=38 |issue=4 |pages=644–51 |date=April 2006 |pmid=16679978 |doi=10.1249/01.mss.0000210194.56834.5d}}</ref> though a 2007 study found that sharing of needles was extremely uncommon among individuals using AAS for non-medical purposes, less than 1%.<ref name="Cohen2007"/> 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.<ref name=Cohen2007>{{cite journal |vauthors=Cohen J, Collins R, Darkes J, Gwartney D |title=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 |journal=J Int Soc Sports Nutr |volume=4 |page=12 |year=2007 |pmid=17931410 |pmc=2131752 |doi=10.1186/1550-2783-4-12}}</ref> 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.<ref name="Cohen2007"/> 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.<ref name="Copeland2007">{{cite journal |vauthors=Copeland J, Peters R, Dillon P |title=A study of 100 anabolic-androgenic steroid users |journal=Med. J. Aust. |volume=168 |issue=6 |pages=311–2 |date=March 1998 |pmid=9549549}}</ref>

AAS users tend to be unhappy with the portrayal of AAS as deadly in the media and in politics.<ref>{{cite web |last=Eastley |first=Tony |title=Steroid study debunks user stereotypes |publisher=[[Australian Broadcasting Corporation|ABC]] |date=January 18, 2006 |url=http://www.abc.net.au/am/content/2006/s1550328.htm |accessdate=2014-01-03 }}</ref> According to one study, AAS users also distrust their physicians and in the sample 56% had not disclosed their AAS use to their physicians.<ref name="pmid15317640">{{cite journal |vauthors=Pope HG, Kanayama G, Ionescu-Pioggia M, Hudson JI |title=Anabolic steroid users' attitudes towards physicians |journal=[[Addiction (journal)|Addiction]] |volume=99 |issue=9 |pages=1189–94 |date=September 2004 |pmid=15317640 |doi=10.1111/j.1360-0443.2004.00781.x}}</ref> 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.<ref name="Cohen2007"/> 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.<ref name="pmid16585446">{{cite journal |vauthors=Kanayama G, Barry S, Hudson JI, Pope HG |title=Body image and attitudes toward male roles in anabolic-androgenic steroid users |journal=Am J Psychiatry |volume=163 |issue=4 |pages=697–703 |date=April 2006 |pmid=16585446 |doi=10.1176/appi.ajp.163.4.697}}</ref> A recent study in the Journal of Health Psychology showed that many users believed that steroids used in moderation were safe.<ref>{{cite journal |vauthors=Grogan S, Shepherd S, Evans R, Wright S, Hunter G |title=Experiences of Anabolic Steroid Use |journal=Journal of Health Psychology |volume=11 |issue=6 |pages=845–856 |date=Nov 2006 |pmid=17035257 |doi=10.1177/1359105306069080 }}</ref>

AAS have been used by men and women in many different kinds of professional sports to attain a competitive edge or to assist in recovery from injury. These sports include [[bodybuilding]], [[Olympic weightlifting|weightlifting]], [[shot put]] and other [[track and field]], [[cycling]], [[baseball]], [[wrestling]], [[mixed martial arts]], [[boxing]], [[football]], and [[cricket]]. Such use is prohibited by the rules of the governing bodies of most sports. AAS use occurs among adolescents, especially by those participating in competitive sports. It has been suggested that the prevalence of use among high-school students in the U.S. may be as high as 2.7%.<ref>{{cite journal |vauthors=Hickson RC, Czerwinski SM, Falduto MT, Young AP |title=Glucocorticoid antagonism by exercise and androgenic-anabolic steroids |journal=Medicine and science in sports and exercise |volume=22 |issue=3 |pages=331–40 |year=1990 |pmid=2199753 |doi=10.1249/00005768-199006000-00010}}</ref> Male students used AAS more frequently than female students and, on average, those that participated in sports used steroids more often than those that did not.

===Available forms===
[[File:Depo-testosterone 200 mg ml.jpg|thumb|upright|A vial of injectable testosterone cypionate]]

There are four common forms in which AAS are administered: oral pills; injectable steroids; creams/gels for topical application; and skin patches. Oral administration is the most convenient. Testosterone administered by mouth is rapidly absorbed, but it is largely converted to inactive metabolites, and only about one-sixth is available in active form. In order to be sufficiently active when given by mouth, testosterone derivatives are alkylated at the 17α position, e.g. [[methyltestosterone]] and [[fluoxymesterone]]. This modification reduces the liver's ability to break down these compounds before they reach the systemic circulation.

Testosterone can be administered [[Parenteral medication|parenterally]], but it has more irregular prolonged absorption time and greater activity in muscle in [[enanthate]], [[undecanoate]], or [[cypionate]] [[ester]] form. These derivatives are hydrolyzed to release free testosterone at the site of injection; absorption rate (and thus injection schedule) varies among different esters, but medical injections are normally done anywhere between semi-weekly to once every 12 weeks. A more frequent schedule may be desirable in order to maintain a more constant level of hormone in the system.<ref name=Chr/> Injectable steroids are typically administered into the muscle, not into the vein, to avoid sudden changes in the amount of the drug in the bloodstream. In addition, because estered testosterone is dissolved in oil, intravenous injection has the potential to cause a dangerous [[embolism]] (clot) in the bloodstream.

[[Transdermal patch]]es (adhesive patches placed on the skin) may also be used to deliver a steady dose through the skin and into the bloodstream. Testosterone-containing creams and gels that are applied daily to the skin are also available, but absorption is inefficient (roughly 10%, varying between individuals) and these treatments tend to be more expensive. Individuals who are especially physically active and/or bathe often may not be good candidates, since the medication can be washed off and may take up to six hours to be fully absorbed. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose himself or herself; children and women are highly sensitive to testosterone and can suffer unintended masculinization and health effects, even from small doses. Injection is the most common method used by individuals administering AAS for non-medical purposes.<ref name="Cohen2007"/>

The traditional routes of administration do not have differential effects on the efficacy of the drug. Studies indicate that the anabolic properties of AAS are relatively similar despite the differences in pharmacokinetic principles such as [[first-pass effect|first-pass metabolism]]. However, the orally available forms of AAS may cause [[hepatotoxicity|liver damage]] in high doses.<ref name=Kicman>{{cite journal |vauthors=Kicman AT, Gower DB |title=Anabolic steroids in sport: biochemical, clinical and analytical perspectives |journal=Ann. Clin. Biochem. |volume=40 |issue=Pt 4 |pages=321–56 |date=July 2003 |pmid=12880534 |doi=10.1258/000456303766476977}}{{closed access}}</ref><ref>{{cite journal | vauthors = Mutzebaugh C |title=Does the choice of alpha-AAS really make a difference? |journal=HIV Hotline |volume=8 |issue=5–6 |pages=10–1 |year=1998 |pmid=11366379}}</ref>

====Examples of AAS====
[[File:Metandienone.svg|thumb|right|Chemical structure of the synthetic steroid [[metandienone]] (Dianabol). 17α-Methylation (upper-right corner) enhances oral [[bioavailability]].]]
{{See also|List of androgens/anabolic steroids}}

The AAS that have been used most commonly in medicine are [[testosterone (medication)|testosterone]] and its many [[testosterone ester|ester]]s (but most typically [[testosterone undecanoate]], [[testosterone enanthate]], [[testosterone cypionate]], and [[testosterone propionate]]),<ref name="Becker2001">{{cite book | first = Kenneth L. | last = Becker | name-list-format = vanc |title=Principles and Practice of Endocrinology and Metabolism |url=https://books.google.com/books?id=FVfzRvaucq8C&pg=PA1185 |year=2001 |publisher=Lippincott Williams & Wilkins |isbn=978-0-7817-1750-2 |pages=1185–1186}}</ref> [[nandrolone]] [[nandrolone ester|ester]]s (typically [[nandrolone decanoate]] and [[nandrolone phenylpropionate]]), [[stanozolol]], and [[metandienone]] (methandrostenolone).<ref name="Kicman2008"/> 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]].<ref name="Kicman2008" /> [[Androstanolone|Dihydrotestosterone]] (DHT), known as androstanolone or stanolone when used medically, and its [[dihydrotestosterone ester|ester]]s are also notable, although they are not widely used in medicine.<ref name="Llewellyn2011" /> [[Boldenone undecylenate]] and [[trenbolone acetate]] are used in [[veterinary medicine]].<ref name="Kicman2008" />

[[Designer steroid]]s are AAS that have not been approved and marketed for medical use but have been distributed through the black market.<ref name="pmid25684733">{{cite journal|last1=Rahnema|first1=C. D.|last2=Crosnoe|first2=L. E.|last3=Kim|first3=E. D.|title=Designer steroids - over-the-counter supplements and their androgenic component: review of an increasing problem|journal=Andrology|volume=3|issue=2|year=2015|pages=150–155|issn=2047-2919|doi=10.1111/andr.307|pmid=25684733}}</ref> Examples of notable designer steroids include [[1-testosterone]] (dihydroboldenone), [[methasterone]], [[trenbolone enanthate]], [[desoxymethyltestosterone]], [[tetrahydrogestrinone]], and [[methylstenbolone]].<ref name="pmid25684733" />

{| class="wikitable sortable collapsible collapsed" style="<!--font-size:small;--> width:100%;"
! colspan="7" | Overview
|-
! Generic name !! Class !! Brand name(s) !! Route(s) !! Launch !! {{abbr|Hits|Google Search hits (December 2017)}}
|-
| [[Androstanolone]] || Dihydrotestosterone || Andractim, others || Many || 1953 || 125,000
|-
| [[Boldenone undecylenate]] || Testosterone; 17β-Esterified || Equipoise, Parenabol || {{abbr|IM|Intramuscular injection}} || 1960s || 544,000
|-
| [[Drostanolone propionate]] || Dihydrotestosterone; 17β-Esterified || Masteron || {{abbr|IM|Intramuscular injection}} || 1961 || 574,000
|-
| [[Fluoxymesterone]] || Testosterone; 17α-Alkylated || Halotestin, Ultandren || Oral || 1957 || 478,000
|-
| [[Mesterolone]] || Dihydrotestosterone || Proviron || Oral || 1934 || 528,000
|-
| [[Metandienone]] || Testosterone; 17α-Alkylated || Dianabol || Oral, {{abbr|IM|intramuscular injection}} || 1958 || 996,000
|-
| [[Metenolone acetate]] || Dihydrotestosterone; 17β-Esterified || Primobolan || Oral || 1961 || 224,000
|-
| [[Metenolone enanthate]] || Dihydrotestosterone; 17β-Esterified || Primobolan Depot || {{abbr|IM|Intramuscular injection}} || 1962 || 371,000
|-
| [[Methyltestosterone]] || Testosterone; 17α-Alkylated || Metandren || Oral || 1936 || 597,000
|-
| [[Nandrolone decanoate]] || 19-Nortestosterone; 17β-Esterified || Deca-Durabolin || {{abbr|IM|Intramuscular injection}} || 1962 || 926,000
|-
| [[Nandrolone phenylpropionate]] || 19-Nortestosterone; 17β-Esterified || Durabolin || {{abbr|IM|Intramuscular injection}} || 1959 || 395,000
|-
| [[Oxandrolone]] || Dihydrotestosterone; 17α-Alkylated || Oxandrin, Anavar || Oral || 1964 || 1,280,000
|-
| [[Oxymetholone]] || Dihydrotestosterone; 17α-Alkylated || Anadrol, Anapolon || Oral || 1961 || 902,000
|-
| [[Stanozolol]] || Dihydrotestosterone; 17α-Alkylated || Winstrol, Stromba || Oral, {{abbr|IM|intramuscular injection}} || 1962 || 1,790,000
|-
| [[Testosterone (medication)|Testosterone]] || Testosterone || Numerous || Many || 1937 || 12,700,000
|-
| [[Testosterone cypionate]] || Testosterone; 17β-Esterified || Depo-Testosterone || {{abbr|IM|Intramuscular injection}} || 1951 || 1,290,000
|-
| [[Testosterone enanthate]] || Testosterone; 17β-Esterified || Delatestryl || {{abbr|IM|Intramuscular injection}} || 1954 || 1,210,000
|-
| [[Testosterone propionate]] || Testosterone; 17β-Esterified || Testoviron || {{abbr|IM|Intramuscular injection}} || 1937 || 1,010,000
|-
| [[Testosterone undecanoate]] || Testosterone; 17β-Esterified || Aveed, Andriol, Nebido || Oral, {{abbr|IM|intramuscular injection}} || 1970s || 385,000
|-
| [[Trenbolone acetate]] || 19-Nortestosterone; 17β-Esterified || Finajet, Finaject || {{abbr|IM|Intramuscular injection}} || 1987 || 651,000
|-
|}

==Adverse effects==
Known possible [[side effect]]s of AAS include:<ref name="pmid21443513">{{cite journal | vauthors = Turillazzi E, Perilli G, Di Paolo M, Neri M, Riezzo I, Fineschi V | title = Side effects of AAS abuse: an overview | journal = Mini Rev Med Chem | volume = 11 | issue = 5 | pages = 374–89 | year = 2011 | pmid = 21443513 | doi = | url = }}</ref><ref name="pmid17723870">{{cite journal | vauthors = Casavant MJ, Blake K, Griffith J, Yates A, Copley LM | title = Consequences of use of anabolic androgenic steroids | journal = Pediatr. Clin. North Am. | volume = 54 | issue = 4 | pages = 677–90, x | year = 2007 | pmid = 17723870 | doi = 10.1016/j.pcl.2007.04.001 | url = }}</ref><ref name="pmid24423981">{{cite journal | vauthors = Pope HG, Wood RI, Rogol A, Nyberg F, Bowers L, Bhasin S | title = Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement | journal = Endocr. Rev. | volume = 35 | issue = 3 | pages = 341–75 | year = 2014 | pmid = 24423981 | pmc = 4026349 | doi = 10.1210/er.2013-1058 | url = }}</ref><ref name="pmid19028512">{{cite journal | vauthors = Fragkaki AG, Angelis YS, Koupparis M, Tsantili-Kakoulidou A, Kokotos G, Georgakopoulos C | title = 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 | journal = Steroids | volume = 74 | issue = 2 | pages = 172–97 | year = 2009 | pmid = 19028512 | doi = 10.1016/j.steroids.2008.10.016 | url = }}</ref><ref name="pmid25805894">{{cite journal | vauthors = Nieschlag E, Vorona E | title = MECHANISMS IN ENDOCRINOLOGY: Medical consequences of doping with anabolic androgenic steroids: effects on reproductive functions | journal = Eur. J. Endocrinol. | volume = 173 | issue = 2 | pages = R47–58 | year = 2015 | pmid = 25805894 | doi = 10.1530/EJE-15-0080 | url = }}</ref>

* [[Cutaneous condition|Dermatological]]/[[integumentary system|integumental]]: [[oily skin]], [[acne vulgaris]], [[acne conglobata]], [[seborrhea]], [[stretch mark]]s (due to rapid [[muscle hypertrophy|muscle enlargement]]), [[hypertrichosis]] (excessive body hair growth), [[androgenic alopecia]] (pattern hair loss; scalp baldness), [[water retention (medicine)|fluid retention]]/[[edema]].
* [[Reproductive system disease|Reproductive]]/[[endocrine disease|endocrine]]: [[libido]] changes, reversible [[infertility]], [[hypogonadotropic hypogonadism]].
* Male-specific: [[spontaneous erection]]s, [[nocturnal emission]]s, [[priapism]], [[erectile dysfunction]], [[gynecomastia]] (mostly only with [[aromatase|aromatizable]] and hence [[estrogen (medication)|estrogen]]ic AAS), [[oligospermia]]/[[azoospermia]], [[testicular atrophy]], [[intratesticular leiomyosarcoma]], [[prostate hypertrophy]], [[prostate cancer]].
* Female-specific: [[masculinization]], irreversible [[voice deepening]], [[hirsutism]] (excessive facial/body hair growth), [[menstrual disturbances]] (e.g., [[anovulation]], [[oligomenorrhea]], [[amenorrhea]], [[dysmenorrhea]]), [[clitoral enlargement]], [[breast atrophy]], [[uterine atrophy]], [[teratogenicity]] (in female [[fetus]]es).
* Child-specific: premature [[epiphyseal closure]] and associated [[short stature]], [[precocious puberty]] in boys, [[delayed puberty]] and [[contrasexual precocity]] in girls.
* [[Emotional and behavioral disorders|Psychiatric]]/[[Neurological disorder|neurological]]: [[mood swing]]s, [[irritability]], [[aggression]], [[violence|violent behavior]], [[impulsivity]]/[[recklessness (psychology)|recklessness]], [[hypomania]]/[[mania]], [[euphoria]], [[depression (mood)|depression]], [[anxiety]], [[dysphoria]], [[suicidality]], [[delusion]]s, [[psychosis]], [[drug withdrawal|withdrawal]], [[drug dependence|dependence]], [[neurotoxicity]], [[cognitive impairment]].<ref name="pmid16000671">{{cite journal | vauthors = Hall RC, Hall RC, Chapman MJ | title = Psychiatric complications of anabolic steroid abuse | journal = Psychosomatics | volume = 46 | issue = 4 | pages = 285–90 | year = 2005 | pmid = 16000671 | doi = 10.1176/appi.psy.46.4.285 | url = }}</ref><ref name="pmid15984895">{{cite journal | vauthors = Trenton AJ, Currier GW | title = Behavioural manifestations of anabolic steroid use | journal = CNS Drugs | volume = 19 | issue = 7 | pages = 571–95 | year = 2005 | pmid = 15984895 | doi = | url = }}</ref>
* [[Musculoskeletal disorder|Musculoskeletal]]: [[muscle hypertrophy]], [[strain (injury)|muscle strain]]s, [[tendon rupture]]s, [[rhabdomyolysis]].
* [[Cardiovascular disease|Cardiovascular]]: [[dyslipidemia]] (e.g., increased {{abbrlink|LDL|low-density lipoprotein}} levels, decreased {{abbrlink|HDL|high-density lipoprotein}} levels, reduced {{abbrlink|apo-A1|apolipoprotein A1}} levels), [[atherosclerosis]], [[hypertension]], [[left ventricular hypertrophy]], [[cardiomyopathy]], [[myocardial hypertrophy]], [[polycythemia]]/[[erythrocytosis]], [[arrhythmia]]s, [[thrombosis]] (e.g., [[embolism]], [[stroke]]), [[myocardial infarction]], [[sudden cardiac death|sudden death]].<ref name="pmid20020375">{{cite journal | vauthors = Vanberg P, Atar D | title = Androgenic anabolic steroid abuse and the cardiovascular system | journal = Handb Exp Pharmacol | volume = | issue = 195 | pages = 411–57 | year = 2010 | pmid = 20020375 | doi = 10.1007/978-3-540-79088-4_18 | url = }}</ref><ref name="pmid20816133">{{cite journal | vauthors = Achar S, Rostamian A, Narayan SM | title = Cardiac and metabolic effects of anabolic-androgenic steroid abuse on lipids, blood pressure, left ventricular dimensions, and rhythm | journal = Am. J. Cardiol. | volume = 106 | issue = 6 | pages = 893–901 | year = 2010 | pmid = 20816133 | pmc = 4111565 | doi = 10.1016/j.amjcard.2010.05.013 | url = }}</ref>
* [[Liver disease|Hepatic]]: elevated [[liver function test]]s ({{abbrlink|AST|aspartate aminotransferase}}, {{abbrlink|ALT|alanine aminotransferase}}, [[bilirubin]], {{abbrlink|LDH|lactic dehydrogenase}}, {{abbrlink|ALP|alkaline phosphatase}}), [[hepatotoxicity]], [[jaundice]], [[hepatic steatosis]], [[hepatocellular adenoma]], [[hepatocellular carcinoma]], [[cholestasis]], [[peliosis hepatis]]; all mostly or exclusively with 17α-alkylated AAS.<ref name="pmid28379599">{{cite journal | vauthors = Solimini R, Rotolo MC, Mastrobattista L, Mortali C, Minutillo A, Pichini S, Pacifici R, Palmi I | title = Hepatotoxicity associated with illicit use of anabolic androgenic steroids in doping | journal = Eur Rev Med Pharmacol Sci | volume = 21 | issue = 1 Suppl | pages = 7–16 | year = 2017 | pmid = 28379599 | doi = | url = }}</ref>
* [[Renal disease|Renal]]: [[renal hypertrophy]], [[nephropathy]], [[acute renal failure]] (secondary to rhabdomyolysis), [[focal segmental glomerulosclerosis]], [[renal cell carcinoma]].
* Others: [[glucose intolerance]], [[insulin resistance]], [[immune dysfunction]].<ref name="pmid21443507">{{cite journal | vauthors = Brenu EW, McNaughton L, Marshall-Gradisnik SM | title = Is there a potential immune dysfunction with anabolic androgenic steroid use?: A review | journal = Mini Rev Med Chem | volume = 11 | issue = 5 | pages = 438–45 | year = 2011 | pmid = 21443507 | doi = | url = }}</ref>

===Physiological===
Depending on the length of drug abuse, 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]].<ref>{{cite journal |vauthors=Grace F, Sculthorpe N, Baker J, Davies B |title=Blood pressure and rate pressure product response in males using high-dose anabolic-androgenic steroids (AAS) |journal=J Sci Med Sport |volume=6 |issue=3 |pages=307–12 |year=2003 |pmid=14609147 |doi=10.1016/S1440-2440(03)80024-5}}</ref> In addition to morphological changes of the heart which may alter cardiovascular inefficiency irreversibly.

AAS have been shown to alter fasting blood sugar and glucose tolerance tests.<ref>{{cite web |url=http://dailymed.nlm.nih.gov/dailymed/drugInfo.cfm?id=3607 |title=DailyMed: About DailyMed |publisher=Dailymed.nlm.nih.gov |accessdate=2008-11-03}}</ref> AAS such as testosterone also increase the risk of [[cardiovascular disease]]<ref name="BarrettConnor1995" /> or [[coronary artery disease]].<ref>{{cite journal |vauthors=Bagatell CJ, Knopp RH, Vale WW, Rivier JE, Bremner WJ |title=Physiologic testosterone levels in normal men suppress high-density lipoprotein cholesterol levels |journal=Annals of Internal Medicine |volume=116 |issue=12 Pt 1 |pages=967–73 |year=1992 |pmid=1586105 |doi=10.7326/0003-4819-116-12-967}}</ref><ref>{{cite journal |vauthors=Mewis C, Spyridopoulos I, Kühlkamp V, Seipel L |title=Manifestation of severe coronary heart disease after anabolic drug abuse |journal=Clinical Cardiology |volume=19 |issue=2 |pages=153–5 |year=1996 |pmid=8821428 |doi=10.1002/clc.4960190216}}</ref> [[Acne]] is fairly common among AAS users, mostly due to stimulation of the [[sebaceous gland]]s by increased testosterone levels.<ref name="Hartgens and Kuipers 2004"/><ref>{{cite journal |vauthors=Melnik B, Jansen T, Grabbe S |title=Abuse of anabolic-androgenic steroids and bodybuilding acne: an underestimated health problem |journal=Journal der Deutschen Dermatologischen Gesellschaft = Journal of the German Society of Dermatology : JDDG |volume=5 |issue=2 |pages=110–7 |year=2007 |pmid=17274777 |doi=10.1111/j.1610-0387.2007.06176.x}}</ref> Conversion of testosterone to DHT can accelerate the rate of premature [[baldness]] for males genetically predisposed, but testosterone itself can produce baldness in females.<ref name="pmid12870172">{{cite journal |vauthors=Vierhapper H, Maier H, Nowotny P, Waldhäusl W |title=Production rates of testosterone and of dihydrotestosterone in female pattern hair loss |journal=Metab. Clin. Exp. |volume=52 |issue=7 |pages=927–9 |date=July 2003 |pmid=12870172 |doi=10.1016/S0026-0495(03)00060-X |url=http://linkinghub.elsevier.com/retrieve/pii/S002604950300060X}}</ref>

A number of severe side effects can occur if adolescents use AAS. For example, AAS may prematurely stop the lengthening of bones (premature [[epiphyseal plate|epiphyseal fusion]] through increased levels of [[estrogen (medication)|estrogen]] [[metabolite]]s), resulting in [[stunted growth]]. Other effects include, but are not limited to, accelerated [[bone age|bone maturation]], increased frequency and duration of erections, and premature sexual development. AAS use in adolescence is also [[correlated]] with poorer attitudes related to health.<ref>{{cite journal |vauthors=Irving LM, Wall M, Neumark-Sztainer D, Story M |title=Steroid use among adolescents: findings from Project EAT |journal=The Journal of Adolescent Health |volume=30 |issue=4 |pages=243–52 |year=2002 |pmid=11927236 |doi=10.1016/S1054-139X(01)00414-1}}</ref>

====Cancer====
WHO organization [[International Agency for Research on Cancer]] (IARC) list AAS under [[List of IARC Group 2A carcinogens|Group 2A]]: Probably carcinogenic to humans.<ref name="url_ACS_known_carcinogens">{{cite web |url=http://www.cancer.org/cancer/cancercauses/othercarcinogens/generalinformationaboutcarcinogens/known-and-probable-human-carcinogens |title=Known and Probable Human Carcinogens |date=2011-06-29 |publisher=American Cancer Society}}</ref>

====Cardiovascular====
Other side-effects can include alterations in the structure of the [[heart]], such as [[left ventricular hypertrophy|enlargement and thickening of the left ventricle]], which impairs its contraction and [[diastolic|relaxation]].<ref name="De1991" /> Possible effects of these alterations in the heart are hypertension, [[cardiac arrhythmia]]s, [[congestive heart failure]], [[myocardial infarction|heart attacks]], and [[sudden cardiac death]].<ref>{{cite journal |vauthors=Sullivan ML, Martinez CM, Gallagher EJ |title=Atrial fibrillation and anabolic steroids |journal=The Journal of emergency medicine |volume=17 |issue=5 |pages=851–7 |year=1999 |pmid=10499702 |doi=10.1016/S0736-4679(99)00095-5}}</ref> These changes are also seen in non-drug-using [[sportsperson|athletes]], but steroid use may accelerate this process.<ref>{{cite journal |vauthors=Dickerman RD, Schaller F, McConathy WJ |title=Left ventricular wall thickening does occur in elite power athletes with or without anabolic steroid Use |journal=Cardiology |volume=90 |issue=2 |pages=145–8 |year=1998 |pmid=9778553 |doi=10.1159/000006834}}</ref><ref>{{cite journal |vauthors=George KP, Wolfe LA, Burggraf GW |title=The 'athletic heart syndrome'. A critical review |journal=Sports Medicine |volume=11 |issue=5 |pages=300–30 |year=1991 |pmid=1829849 |doi=10.2165/00007256-199111050-00003}}</ref> 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.<ref>{{cite journal |vauthors=Dickerman RD, Schaller F, Zachariah NY, McConathy WJ |title=Left ventricular size and function in elite bodybuilders using anabolic steroids |journal=Clin J Sport Med |volume=7 |issue=2 |pages=90–3 |year=1997 |pmid=9113423 |doi=10.1097/00042752-199704000-00003}}</ref><ref>{{cite journal |vauthors=Salke RC, Rowland TW, Burke EJ |title=Left ventricular size and function in body builders using anabolic steroids |journal=Medicine and science in sports and exercise |volume=17 |issue=6 |pages=701–4 |year=1985 |pmid=4079743 |doi=10.1249/00005768-198512000-00014}}</ref>

AAS use can cause harmful changes in [[cholesterol]] levels: Some steroids cause an increase in [[Low-density lipoprotein|LDL "bad" cholesterol]] and a decrease in [[High-density lipoprotein|HDL "good" cholesterol]].<ref name="mnt">{{cite web |last=Tokar |first=Steve |title=Liver Damage And Increased Heart Attack Risk Caused By Anabolic Steroid Use |publisher=University of California – San Francisco |date=February 2006 |url=http://www.medicalnewstoday.com/releases/38069.php |accessdate=2007-04-24}}</ref> 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|date=June 2016}}

====Growth defects====
AAS use in adolescents quickens bone maturation and may reduce adult height in high doses.{{citation needed|date=June 2016}} 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.<ref name="ShortStature2015">{{cite journal | vauthors = Wit JM, Oostdijk W | title = Novel approaches to short stature therapy | journal = Best Practice & Research. Clinical Endocrinology & Metabolism | volume = 29 | issue = 3 | pages = 353–66 | year = 2015 | pmid = 26051296 | doi = 10.1016/j.beem.2015.01.003 }}</ref>

====Feminization====
[[File:GynecomastiaFrontalAsymSevere.jpg|thumb|22-year-old man with gynecomastia not due to AAS use. Before and after gynecomastia surgery.]]
{{see also|Feminization (biology)}}

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]].<ref>{{cite journal |vauthors=Marcus R, Korenman SG |title=Estrogens and the human male |journal=Annu Rev Med |volume=27 |pages=357–70 |year=1976 |pmid=779604 |doi=10.1146/annurev.me.27.020176.002041}}</ref> Reduced [[sexual function]] and temporary [[infertility]] can also occur in males.<ref name="administration282">{{cite journal | vauthors = Matsumoto AM |title=Effects of chronic testosterone administration in normal men: safety and efficacy of high dosage testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production |journal=J. Clin. Endocrinol. Metab. |volume=70 |issue=1 |pages=282–7 |year=1990 |pmid=2104626 |doi=10.1210/jcem-70-1-282}}</ref><ref>{{cite journal |vauthors=Hoffman JR, Ratamess NA |journal=Journal of Sports Science and Medicine |title=Medical Issues Associated with Anabolic Steroid Use: Are they Exaggerated? |date=June 1, 2006 |url=http://www.jssm.org/vol5/n2/2/v5n2-2pdf.pdf |format=PDF |accessdate=2007-05-08 |archiveurl=https://web.archive.org/web/20070620160853/http://www.jssm.org/vol5/n2/2/v5n2-2pdf.pdf |archivedate=20 June 2007 |deadurl=no}}</ref><ref>{{cite journal |vauthors=Meriggiola MC, Costantino A, Bremner WJ, Morselli-Labate AM |title=Higher testosterone dose impairs sperm suppression induced by a combined androgen-progestin regimen |journal=J. Androl. |volume=23 |issue=5 |pages=684–90 |year=2002 |pmid=12185103}}</ref> Another male-specific side-effect that can occur is [[testicular atrophy]], caused by the suppression of natural testosterone levels, which inhibits [[spermatogenesis|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.<ref>{{cite journal |vauthors=Alén M, Reinilä M, Vihko R |title=Response of serum hormones to androgen administration in power athletes |journal=Medicine and science in sports and exercise |volume=17 |issue=3 |pages=354–9 |year=1985 |pmid=2991700 |doi=10.1249/00005768-198506000-00009}}</ref>

====Masculinization====
{{See also|Virilization}}

Female-specific side effects include [[hirsutism|increases in body hair]], permanent deepening of the voice, [[clitoral hypertrophy|enlarged clitoris]], and temporary decreases in [[menstrual cycle]]s. Alteration of fertility and ovarian cysts can also occur in females.<ref>{{Cite journal |pmid=9216474|url=http://clinchem.aaccjnls.org/content/43/7/1262|year=1997|author1=Franke|first1=W. W.|title=Hormonal doping and androgenization of athletes: A secret program of the German Democratic Republic government|journal=Clinical chemistry|volume=43|issue=7|pages=1262–79|last2=Berendonk|first2=B}}
</ref> 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.<ref name="pmid14576190">{{cite journal |vauthors=Manikkam M, Crespi EJ, Doop DD, Herkimer C, Lee JS, Yu S, Brown MB, Foster DL, Padmanabhan V |title=Fetal programming: prenatal testosterone excess leads to fetal growth retardation and postnatal catch-up growth in sheep |journal=Endocrinology |volume=145 |issue=2 |pages=790–8 |date=February 2004 |pmid=14576190 |doi=10.1210/en.2003-0478}}</ref>

====Kidney problems====
Kidney tests revealed that nine of the ten steroid users developed a condition called [[focal segmental glomerulosclerosis]], a type of scarring within the kidneys. The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe.<ref>{{cite conference |first1=Leal C. |last1=Herlitz |first2=Glen S. |last2=Markowitz |first3=Alton B. |last3=Farris |first4=Joshua A. |last4=Schwimmer |first5=Michael B. |last5=Stokes |first6=Cheryl |last6=Kunis |first7=Robert B. |last7=Colvin |first8=Vivette D. |last8=D'Agati | name-list-format = vanc |date=October 29, 2009 |title=Development of FSGS Following Anabolic Steroid Use in Bodybuilders |url=http://fitforin.it/images/stories/allegati/herlitzabstract.pdf |conference=42nd Annual Meeting and Scientific Exposition of the American Society of Nephrology |laysummary=http://www.sciencedaily.com/releases/2009/10/091029141202.htm |id="Bodybuilding With Steroids Damages Kidneys" |laysource=ScienceDaily |laydate=October 30, 2009}}</ref>

====Liver problems====
High doses of oral AAS compounds can cause [[hepatotoxicity|liver damage]].<ref name="Yamamoto2006" /> [[Peliosis hepatis]] has been increasingly recognised with the use of AAS.

===Neuropsychiatric===
<!-- "Roid rage" redirects here. If you change this headline, please edit "Roid rage" to point to the new article title. -->
[[File:Rational harm assessment of drugs radar plot.svg|thumb|Addiction experts in psychiatry, chemistry, pharmacology, forensic science, epidemiology, and the police and legal services engaged in [[Delphi method|delphic analysis]] regarding 20 popular recreational drugs. AAS were ranked 19th in dependence, 9th in physical harm, and 15th in social harm.<ref>{{cite journal | vauthors = Nutt D, King LA, Saulsbury W, Blakemore C | title = Development of a rational scale to assess the harm of drugs of potential misuse | journal = Lancet | volume = 369 | issue = 9566 | pages = 1047–53 | date = March 2007 | pmid = 17382831 | doi = 10.1016/S0140-6736(07)60464-4 }}</ref>]]
{{See also|Anabolic–androgenic steroids abuse}}

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 [[drug abuse|abuse]]. Long-term steroid abusers may develop symptoms of [[Substance dependence|dependence]] and [[Drug withdrawal|withdrawal]] on discontinuation of AAS".<ref name="pmid15984895" /> High concentrations of AAS, comparable to those likely sustained by many recreational AAS users, produce [[apoptotic]] effects on [[neuron]]s,{{Citation needed|date=August 2015}} 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 disorder]]s, and progression to other forms of substance abuse, but the prevalence and severity of these various effects remains poorly understood.<ref name=khp>{{cite journal |vauthors=Kanayama G, Hudson JI, Pope HG |title=Long-Term Psychiatric and Medical Consequences of Anabolic-Androgenic Steroid Abuse: A Looming Public Health Concern? |journal=Drug Alcohol Depend |volume=98 |issue=1–2 |pages=1–12 |date=November 2008 |pmid=18599224 |pmc=2646607 |doi=10.1016/j.drugalcdep.2008.05.004}}</ref> 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.<ref name="pmid12230967">{{cite journal | vauthors = Brower KJ |title=Anabolic steroid abuse and dependence |journal=Curr Psychiatry Rep |volume=4 |issue=5 |pages=377–87 |date=October 2002 |pmid=12230967 |doi=10.1007/s11920-002-0086-6}}</ref> 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.<ref name="Hartgens and Kuipers 2004"/>

Large-scale long-term studies of psychiatric effects on AAS users are not currently available.<ref name=khp/> 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.<ref name=Fudala>{{cite journal |vauthors=Fudala PJ, Weinrieb RM, Calarco JS, Kampman KM, Boardman C |title=An evaluation of anabolic-androgenic steroid abusers over a period of 1 year: seven case studies |journal=Annals of Clinical Psychiatry |volume=15 |issue=2 |pages=121–30 |year=2003 |pmid=12938869 |doi=10.3109/10401230309085677}}</ref> 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.<ref>{{cite journal |vauthors=Pagonis TA, Angelopoulos NV, Koukoulis GN, Hadjichristodoulou CS |title=Psychiatric side effects induced by supraphysiological doses of combinations of anabolic steroids correlate to the severity of abuse |journal=Eur. Psychiatry |volume=21 |issue=8 |pages=551–62 |year=2006 |pmid=16356691 |doi=10.1016/j.eurpsy.2005.09.001}}</ref>

====Diagnostic Statistical Manual assertion====
[[DSM-IV]] lists [[Personality disorder#Diagnosis|General diagnostic criteria]] for a personality disorder guideline that "The pattern must not be better accounted for as a manifestation of another mental disorder, or to the direct physiological effects of a substance (e.g. drug or medication) or a general medical condition (e.g. head trauma).". As a result, AAS users may get misdiagnosed by a psychiatrist not told about their habit.<ref name="Rashid et al 2007">{{cite journal |doi=10.1192/apt.bp.105.000935 |title=Anabolic androgenic steroids: What the psychiatrist needs to know |year=2007 |vauthors=Rashid H, Ormerod S, Day E |journal=Advances in Psychiatric Treatment |volume=13 |issue=3 |pages=203–211}}</ref>

====Personality profiles====
Cooper, Noakes, Dunne, Lambert, and Rochford identified that AAS-using individuals are more likely to score higher on [[Borderline personality disorder|borderline]] (4.7 times), [[Anti-social behaviour|antisocial]] (3.8 times), [[Paranoid personality disorder|paranoid]] (3.4 times), [[schizotypal personality disorder|schizotypal]] (3.1 times), [[Histrionic personality disorder|histrionic]] (2.9 times), [[Passive-aggressive personality disorder|passive-aggressive]] (2.4 times), and [[Narcissistic personality disorder|narcissistic]] (1.6 times) personality profiles than non-users.<ref name="pmid8889121">{{cite journal |vauthors=Cooper CJ, Noakes TD, Dunne T, Lambert MI, Rochford K |title=A high prevalence of abnormal personality traits in chronic users of anabolic-androgenic steroids |journal=Br J Sports Med |volume=30 |issue=3 |pages=246–50 |date=September 1996 |pmid=8889121 |pmc=1332342 |doi=10.1136/bjsm.30.3.246}}</ref> Other studies have suggested that antisocial personality disorder is slightly more likely among AAS users than among non-users (Pope & Katz, 1994).<ref name="Rashid et al 2007"/> [[Bipolar disorder|Bipolar]] dysfunction,<ref>{{cite web |url=http://www.vitalquests.org/publication2steroiduse.html |title=Dr. Ritchi Morris |publisher=Vitalquests.org |accessdate=2013-12-01}}</ref> [[substance dependency]], and [[conduct disorder]] have also been associated with AAS use.<ref name="pmid19922565">{{cite journal |vauthors=Kanayama G, Brower KJ, Wood RI, Hudson JI, Pope HG |title=Anabolic-androgenic steroid dependence: an emerging disorder |journal=Addiction |volume=104 |issue=12 |pages=1966–78 |date=December 2009 |pmid=19922565 |pmc=2780436 |doi=10.1111/j.1360-0443.2009.02734.x}}</ref>

====Mood and anxiety====
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.<ref name = "Eisenberg_Galloway_2005">{{cite book |vauthors=Eisenberg ER, Galloway GP |chapter=Anabolic androgenic steroids |title=Substance Abuse: A Comprehensive Textbook |veditors=Lowinson JH, Ruiz P, Millman RB |publisher=Lippincott Williams & Wilkins |asin=B0049VACMW}}</ref> Of 53 bodybuilders who used AAS, 27 (51%) reported unspecified mood disturbance.<ref name="Lindström_1990">{{cite journal |vauthors=Lindström M, Nilsson AL, Katzman PL, Janzon L, Dymling JF |title=Use of anabolic-androgenic steroids among body builders—frequency and attitudes |journal=J. Intern. Med. |volume=227 |issue=6 |pages=407–11 |year=1990 |pmid=2351927 |doi=10.1111/j.1365-2796.1990.tb00179.x}}</ref>

====Aggression and hypomania====
{{anchor|roid rage}}
From the mid-1980s onward, the media reported "'''roid rage'''" as a side effect of AAS.<ref name = "Lenahan_2003">{{cite book | last1 = Lenahan | first1 = Pat | name-list-format = vanc | title = Anabolic Steroids: And Other Performance-enhancing Drugs | date = 2003 | publisher = Taylor & Francis | location = London | isbn = 0-415-28030-3 }}</ref>{{rp|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.<ref>{{cite journal |vauthors=Thiblin I, Petersson A |title=Pharmacoepidemiology of anabolic androgenic steroids: a review |journal=Fundam Clin Pharmacol |volume=19 |issue=1 |pages=27–44 |date=February 2005 |pmid=15660958 |doi=10.1111/j.1472-8206.2004.00298.x}}</ref> 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.<ref name="pmid18923108">{{cite journal |vauthors=Beaver KM, Vaughn MG, Delisi M, Wright JP |title=Anabolic-Androgenic Steroid Use and Involvement in Violent Behavior in a Nationally Representative Sample of Young Adult Males in the United States |journal=[[Am J Public Health]] |volume=98 |issue=12 |pages=2185–7 |date=December 2008 |pmid=18923108 |pmc=2636528 |doi=10.2105/AJPH.2008.137018 |url=http://www.ajph.org/cgi/pmidlookup?view=long&pmid=18923108}}</ref> A 1996 review examining the [[Randomized control trial#Blind trials|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.<ref name="pmid8969015">{{cite journal |vauthors=Bahrke MS, Yesalis CE, Wright JE |title=Psychological and behavioural effects of endogenous testosterone and anabolic-androgenic steroids. An update |journal=Sports Medicine |volume=22 |issue=6 |pages=367–90 |year=1996 |pmid=8969015 |doi=10.2165/00007256-199622060-00005}}</ref>

A 1996 [[randomized controlled trial]], which involved 43 men, did not find an increase in the occurrence of angry behavior during 10 weeks of administration of [[testosterone enanthate]] at 600&nbsp;mg/week, but this study screened out subjects that had previously abused steroids or had any psychiatric antecedents.<ref name="Bhasin1">{{cite journal |vauthors=Bhasin S, Storer TW, Berman N, Callegari C, Clevenger B, Phillips J, Bunnell TJ, Tricker R, Shirazi A, Casaburi R |title=The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men |journal=N. Engl. J. Med. |volume=335 |issue=1 |pages=1–7 |date=July 1996 |pmid=8637535 |doi=10.1056/NEJM199607043350101}}</ref><ref name="pmid8855834">{{cite journal |vauthors=Tricker R, Casaburi R, Storer TW, Clevenger B, Berman N, Shirazi A, Bhasin S |title=The effects of supraphysiological doses of testosterone on angry behavior in healthy eugonadal men—a clinical research center study |journal=J. Clin. Endocrinol. Metab. |volume=81 |issue=10 |pages=3754–8 |date=October 1996 |pmid=8855834 |doi=10.1210/jcem.81.10.8855834}}</ref> A trial conducted in 2000 using [[testosterone cypionate]] at 600&nbsp;mg/week found that treatment significantly increased [[mania|manic]] scores on the [[YMRS]], and aggressive responses on several scales. The drug response was highly variable. However: 84% of subjects exhibited minimal psychiatric effects, 12% became mildly hypomanic, and 4% (2 subjects) became markedly hypomanic. The mechanism of these variable reactions could not be explained by demographic, psychological, laboratory, or physiological measures.<ref name="pmid10665615">{{cite journal |vauthors=Pope HG, Kouri EM, Hudson JI |title=Effects of supraphysiologic doses of testosterone on mood and aggression in normal men: a randomized controlled trial |journal=Arch. Gen. Psychiatry |volume=57 |issue=2 |pages=133–40; discussion 155–6 |date=February 2000 |pmid=10665615 |doi=10.1001/archpsyc.57.2.133 |url=http://archpsyc.jamanetwork.com/article.aspx?articleid=481565}}{{open access}}</ref>

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.<ref>{{cite journal |vauthors=Pagonis TA, Angelopoulos NV, Koukoulis GN, Hadjichristodoulou CS, Toli PN |title=Psychiatric and hostility factors related to use of anabolic steroids in monozygotic twins |journal=Eur. Psychiatry |volume=21 |issue=8 |pages=563–9 |year=2006 |pmid=16529916 |doi=10.1016/j.eurpsy.2005.11.002}}</ref> A small-scale study of 10 AAS users found that [[cluster B]] personality disorders were confounding factors for aggression.<ref name="pmid12762541">{{cite journal |vauthors=Perry PJ, Kutscher EC, Lund BC, Yates WR, Holman TL, Demers L |title=Measures of aggression and mood changes in male weightlifters with and without androgenic anabolic steroid use |journal=J. Forensic Sci. |volume=48 |issue=3 |pages=646–51 |date=May 2003 |pmid=12762541}}</ref>

The relationship between AAS use and depression is inconclusive. There have been anecdotal reports of depression and suicide in teenage steroid users,<ref>{{cite news |title=Teens & Steroids: A Dangerous Mix |date=2004-06-03 |publisher=CBS Broadcasting Inc. |url=http://www.cbsnews.com/stories/2004/06/03/eveningnews/main620967.shtml |accessdate=2007-06-27 |archiveurl=https://web.archive.org/web/20070710161708/http://www.cbsnews.com/stories/2004/06/03/eveningnews/main620967.shtml |archivedate=10 July 2007 |deadurl=no}}</ref> 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.<ref name="pmid1551042">{{cite journal | vauthors = Uzych L |title=Anabolic-androgenic steroids and psychiatric-related effects: a review |journal=Can J Psychiatry |volume=37 |issue=1 |pages=23–8 |date=February 1992 |pmid=1551042}}</ref> 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).<ref>{{cite web |url=http://thinksteroids.com/articles/anabolic-steroids-suicide/ |title=Anabolic Steroids and Suicide – A Brief Review of the Evidence |publisher=Thinksteroids.com |date=2005-07-12 |accessdate=2013-12-01}}</ref>

==Pharmacology==

===Mechanism of action===
{{See also|Steroid hormone}}
[[File:Steroid receptor.png|thumb|The human [[androgen receptor]] bound to [[testosterone]]<ref>{{cite journal |vauthors=Pereira de Jésus-Tran K, Côté PL, Cantin L, Blanchet J, Labrie F, Breton R |title=Comparison of crystal structures of human androgen receptor ligand-binding domain complexed with various agonists reveals molecular determinants responsible for binding affinity |journal=Protein Sci. |volume=15 |issue=5 |pages=987–99 |year=2006 |pmid=16641486 |doi=10.1110/ps.051905906 |pmc=2242507}}</ref> The protein is shown as a [[Secondary structure|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 [[cell nucleus|nucleus]] of target [[Cell (biology)|cells]] through their interaction with the cell’s surface [[Receptor (biochemistry)|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 [[gene expression|expression]] of [[gene]]s<ref>{{cite journal |vauthors=Lavery DN, McEwan IJ |title=Structure and function of steroid receptor AF1 transactivation domains: induction of active conformations |journal=Biochem. J. |volume=391 |issue=Pt 3 |pages=449–64 |year=2005 |pmid=16238547 |pmc=1276946 |doi=10.1042/BJ20050872}}</ref> or activates processes that [[signal transduction|send signals]] to other parts of the cell.<ref>{{cite journal | vauthors = Cheskis BJ |title=Regulation of cell signalling cascades by steroid hormones |journal=J. Cell. Biochem. |volume=93 |issue=1 |pages=20–7 |year=2004 |pmid=15352158 |doi=10.1002/jcb.20180}}</ref> Different types of AAS bind to the AAR with different [[Dissociation constant|affinities]], depending on their chemical structure.<ref name="Hartgens and Kuipers 2004"/> Some AAS such as metandienone bind weakly to this receptor ''in vitro'', but still exhibit AR-mediated effects ''in vivo''.{{Citation needed|date=December 2016}} The reason for this discrepancy is not known.<ref name="pmid9593936">{{cite journal | vauthors = Roselli CE |title=The effect of anabolic-androgenic steroids on aromatase activity and androgen receptor binding in the rat preoptic area |journal=Brain Res. |volume=792 |issue=2 |pages=271–6 |year=1998 |pmid=9593936 |doi=10.1016/S0006-8993(98)00148-6}}</ref>

The effect of AAS on muscle mass is caused in at least two ways:<ref>{{cite journal |vauthors=Brodsky IG, Balagopal P, Nair KS |title=Effects of testosterone replacement on muscle mass and muscle protein synthesis in hypogonadal men—a clinical research center study |journal=J. Clin. Endocrinol. Metab. |volume=81 |issue=10 |pages=3469–75 |year=1996 |pmid=8855787 |doi=10.1210/jc.81.10.3469}}</ref> first, they increase the [[Protein biosynthesis|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 [[glucocorticoid]]s that promote the breakdown of muscles.<ref>{{cite journal |vauthors=Hickson RC, Czerwinski SM, Falduto MT, Young AP |title=Glucocorticoid antagonism by exercise and androgenic-anabolic steroids |journal=Med Sci Sports Exerc |volume=22 |issue=3 |pages=331–40 |year=1990 |pmid=2199753 |doi=10.1249/00005768-199006000-00010}}</ref> AAS also affect the number of cells that develop into fat-storage cells, by favouring [[cellular differentiation]] into muscle cells instead.<ref>{{cite journal |vauthors=Singh R, Artaza JN, Taylor WE, Gonzalez-Cadavid NF, Bhasin S |title=Androgens stimulate myogenic differentiation and inhibit adipogenesis in C3H 10T1/2 pluripotent cells through an androgen receptor-mediated pathway |journal=Endocrinology |volume=144 |issue=11 |pages=5081–8 |year=2003 |pmid=12960001 |doi=10.1210/en.2003-0741}}</ref> AAS can also decrease fat by increasing [[basal metabolic rate]] (BMR), since an increase in muscle mass increases BMR. {{citation needed|date=January 2016}}

===Anabolic and androgenic effects===
{| class="wikitable" style="float:right; font-size:92%; margin-left:12px;"
|-
|+ Relative androgenic:anabolic<br />activity in animals<ref name=Chr/>{{rp|735}}
|-
! Preparation !! 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
|}

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.

Some examples of the anabolic effects of these hormones are increased [[Protein biosynthesis|protein synthesis]] from [[amino acid]]s, increased appetite, increased bone remodeling and growth, and stimulation of [[bone marrow]], which increases the production of [[red blood cell]]s. Through a number of [[Anabolic steroid#Mechanism of action|mechanisms]] AAS stimulate the formation of muscle cells and hence cause an increase in the size of [[skeletal muscles]], leading to increased strength.<ref>{{cite journal |vauthors=Schroeder ET, Vallejo AF, Zheng L, Stewart Y, Flores C, Nakao S, Martinez C, Sattler FR |title=Six-week improvements in muscle mass and strength during androgen therapy in older men |journal=J Gerontol a Biol Sci Med Sci |volume=60 |issue=12 |pages=1586–92 |year=2005 |pmid=16424293 |doi=10.1093/gerona/60.12.1586}}</ref><ref>{{cite journal |vauthors=Grunfeld C, Kotler DP, Dobs A, Glesby M, Bhasin S |title=Oxandrolone in the treatment of HIV-associated weight loss in men: a randomized, double-blind, placebo-controlled study |journal=J Acquir Immune Defic Syndr |volume=41 |issue=3 |pages=304–14 |year=2006 |pmid=16540931 |doi=10.1097/01.qai.0000197546.56131.40}}</ref><ref>{{cite journal |vauthors=Giorgi A, Weatherby RP, Murphy PW |title=Muscular strength, body composition and health responses to the use of testosterone enanthate: a double blind study |journal=Journal of science and medicine in sport / Sports Medicine Australia |volume=2 |issue=4 |pages=341–55 |year=1999 |pmid=10710012 |doi=10.1016/S1440-2440(99)80007-3}}</ref>

The androgenic effects of AAS are numerous. Depending on the length of use, the side effects of the steroid can be irreversible. Processes affected include pubertal growth, [[sebaceous gland]] oil production, and sexuality (especially in fetal development). Some examples of virilizing effects are [[clitoral hypertrophy|growth of the clitoris]] in females and the [[penis]] in male children (the adult penis size does not change due to steroids{{medcn|date=March 2013}} ), increased [[vocal cord]] size, increased [[libido]], suppression of [[endogenous|natural]] [[sex hormone]]s, and impaired [[spermatogenesis|production of sperm]].<ref name="DoirpMissing">{{cite journal | vauthors = Kuhn CM |title=Anabolic steroids |journal=Recent Prog. Horm. Res. |volume=57 |pages=411–34 |year=2002 |pmid=12017555 |doi=10.1210/rp.57.1.411}}</ref> Effects on women include deepening of the voice, facial hair growth, and possibly a decrease in breast size. Men may develop an enlargement of breast tissue, known as gynecomastia, testicular atrophy, and a reduced sperm count.<ref name=casapalmera>{{cite web |title=How Anabolic Steroids Alter Both Men And Women |url=http://casapalmera.com/types-symptoms-and-effects-of-anabolic-steroid-use/ |work=casapalmera.com|accessdate=2 January 2014 }}</ref>

The androgenic:anabolic ratio of an AAS is an important factor when determining the clinical application of these compounds. Compounds with a high ratio of androgenic to an anabolic effects are the drug of choice in androgen-replacement therapy (e.g., treating [[hypogonadism]] in males), whereas compounds with a reduced androgenic:anabolic ratio are preferred for anemia and osteoporosis, and to reverse protein loss following trauma, surgery, or prolonged immobilization. Determination of androgenic:anabolic ratio is typically performed in animal studies, which has led to the marketing of some compounds claimed to have anabolic activity with weak androgenic effects. This disassociation is less marked in humans, where all AAS have significant androgenic effects.<ref name="Chr">{{cite book | editor-last = Katzung | editor-first = Bertram G. |last=Chrousos |first=George P. |chapter=The Gonadal Hormones & Inhibitors |title=Basic & Clinical Pharmacology |publisher=McGraw-Hill Medical McGraw-Hill distributor |location=New York London |year=2012 |isbn=0071764011}}</ref>

A commonly used protocol for determining the androgenic:anabolic ratio, dating back to the 1950s, uses the relative weights of ventral [[prostate]] (VP) and [[levator ani]] muscle (LA) of male [[Laboratory rat|rats]]. The VP weight is an indicator of the androgenic effect, while the LA weight is an indicator of the anabolic effect. Two or more batches of rats are [[castrated]] and given no treatment and respectively some AAS of interest. The ''LA/VP ratio'' for an AAS is calculated as the ratio of LA/VP weight gains produced by the treatment with that compound using castrated but untreated rats as baseline: (LA<sub>c,t</sub>–LA<sub>c</sub>)/(VP<sub>c,t</sub>–VP<sub>c</sub>). The LA/VP weight gain ratio from rat experiments is not unitary for testosterone (typically 0.3–0.4), but it is normalized for presentation purposes, and used as basis of comparison for other AAS, which have their androgenic:anabolic ratios scaled accordingly (as shown in the table above).<ref name=pmid9593936/><ref name="pmid13064212">{{cite journal | vauthors = Hershberger LG, Shipley EG, Meyer RK | title = Myotrophic activity of 19-nortestosterone and other steroids determined by modified levator ani muscle method | journal = Proceedings of the Society for Experimental Biology and Medicine. Society for Experimental Biology and Medicine (New York, N.Y.) | volume = 83 | issue = 1 | pages = 175–80 | year = 1953 | pmid = 13064212 | doi = 10.3181/00379727-83-20301| url = }}</ref> In the early 2000s, this procedure was standardized and generalized throughout [[OECD]] in what is now known as the Hershberger assay.

====Body composition and strength improvements====
Body weight in men may increase by 2–5&nbsp;kg as a result of short-term (<10 weeks) AAS use, which may be attributed mainly to an increase of lean mass. Animal studies also found that fat mass was reduced, but most studies in humans failed to elucidate significant fat mass decrements. The effects on lean body mass have been shown to be dose-dependent. Both [[muscle hypertrophy]] and the formation of new [[muscle fibers]] have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out.<ref name="Hartgens and Kuipers 2004"/>

The upper region of the body (thorax, neck, shoulders, and upper arm) seems to be more susceptible for AAS than other body regions because of predominance of ARs in the upper body.{{Citation needed|date=December 2016}} The largest difference in muscle fiber size between AAS users and non-users was observed in type I muscle fibers of the [[vastus lateralis]] and the [[trapezius muscle]] as a result of long-term AAS self-administration. After drug withdrawal, the effects fade away slowly, but may persist for more than 6–12 weeks after cessation of AAS use.<ref name="Hartgens and Kuipers 2004"/>

Strength improvements in the range of 5–20% 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]].<ref name="Hartgens and Kuipers 2004"/> For almost two decades, it was assumed that AAS exerted significant effects only in experienced strength athletes.<ref name="pmid61389">{{cite journal |vauthors=Hervey GR, Hutchinson I, Knibbs AV, Burkinshaw L, Jones PR, Norgan NG, Levell MJ |title="Anabolic" effects of methandienone in men undergoing athletic training |journal=[[The Lancet|Lancet]] |volume=2 |issue=7988 |pages=699–702 |date=October 1976 |pmid=61389 |doi=10.1016/S0140-6736(76)90001-5 |url=http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(76)90001-5/abstract}}{{closed access}}</ref><ref name="pmid7018798">{{cite journal |vauthors=Hervey GR, Knibbs AV, Burkinshaw L, Morgan DB, Jones PR, Chettle DR, Vartsky D |title=Effects of methandienone on the performance and body composition of men undergoing athletic training |journal=Clin. Sci. |volume=60 |issue=4 |pages=457–61 |date=April 1981 |pmid=7018798}}</ref> A randomized controlled trial demonstrated, however, that even in novice athletes a 10-week strength training program accompanied by [[testosterone enanthate]] at 600&nbsp;mg/week may improve strength more than training alone does.<ref name="Hartgens and Kuipers 2004"/><ref name="Bhasin1"/> This dose is sufficient to significantly improve lean muscle mass relative to placebo even in subjects that did not exercise at all.<ref name="Bhasin1"/> The anabolic effects of testosterone enanthate were highly dose dependent.<ref name="Hartgens and Kuipers 2004"/><ref name="pmid11701431">{{cite journal |vauthors=Bhasin S, Woodhouse L, Casaburi R, Singh AB, Bhasin D, Berman N, Chen X, Yarasheski KE, Magliano L, Dzekov C, Dzekov J, Bross R, Phillips J, Sinha-Hikim I, Shen R, Storer TW |title=Testosterone dose-response relationships in healthy young men |journal=Am. J. Physiol. Endocrinol. Metab. |volume=281 |issue=6 |pages=E1172–81 |date=December 2001 |pmid=11701431}}</ref>

===Dissociation of anabolic and androgenic effects===
Endogenous/natural AAS like testosterone and DHT and synthetic AAS mediate their effects by binding to and activating the AR.<ref name="Kicman2008"/> On the basis of animal [[bioassay]]s, the effects of these agents have been divided into two partially dissociable types: anabolic (myotrophic) and androgenic.<ref name="Kicman2008" /> 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.<ref name="Kicman2008" /> Explanations for the dissociation include differences in [[intracellular]] [[metabolism]], [[functional selectivity]] (recruitment of [[coactivator (genetics)|coactivator]]s), and [[Nuclear receptor#Non-genomic|non-genomic]] mechanisms (i.e., signaling through non-AR [[membrane androgen receptor]]s, or mARs).<ref name="Kicman2008" /> Support for the latter two explanations is limited and more hypothetical, but there is a good deal of support for the intracellular metabolism explanation.<ref name="Kicman2008" />

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.<ref name="Kicman2008" /> It is referred to as the [[myotrophic–androgenic index]].<ref name="Kicman2008" /> In this model, anabolic (myotrophic) activity is measured by change in the weight of the rat [[bulbospongiosus muscle|bulbocavernosus]]/[[levator ani]] muscle and androgenic activity is measured by change in the weight of the rat [[prostate gland|ventral prostate]] (or, alternatively, the rat [[seminal vesicles]]) in response to exposure to the AAS, and the measurements are then compared and used to form a ratio.<ref name="Kicman2008" />

====Intracellular metabolism====
Testosterone is [[metabolism|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.<ref name="Kicman2008" /> 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 [[metabolite]]s with little or no AR affinity.<ref name="Kicman2008" /> 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.<ref name="Kicman2008" /> In contrast, expression of 5α-reductase in [[skeletal muscle]] is undetectable.<ref name="Kicman2008" /> Aromatase is highly expressed in [[adipose tissue]] and the brain, and is also expressed significantly in skeletal muscle.<ref name="Kicman2008" /> 3α-HSD is also highly expressed in skeletal muscle.<ref name="Llewellyn2011" />

Natural AAS like testosterone and DHT and synthetic AAS are analogues of each other and are very similar structurally.<ref name="Kicman2008" /> For this reason, they have the capacity to bind to and be metabolized by the same [[enzyme]]s.<ref name="Kicman2008" /> According to the intracellular metabolism explanation, the androgenic-to-anabolic ratio of a given AR agonist is based on its capacity to be transformed by the aforementioned enzymes in conjunction with the AR activity of any resulting products.<ref name="Kicman2008" /> As an example, 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 has already been 5α-reduced, such as DHT itself or a derivative (like mesterolone or drostanolone), would not undergo such potentiation in said tissues.<ref name="Kicman2008" /> 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.<ref name="Kicman2008" /> As so-called "androgenic" tissues such as skin/hair follicles and 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.<ref name="Kicman2008" />

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.<ref name="Kicman2008" /> 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).<ref name="Kicman2008" /> 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 like [[metenolone]], [[oxandrolone]], [[oxymetholone]], [[drostanolone]], and [[stanozolol]] are all poor substrates for 3α-HSD and are described as potent anabolics.<ref name="Llewellyn2011" />

The intracellular metabolism theory explains how and why remarkable dissociation between anabolic and androgenic effects can occur, but why dissociation is invariably incomplete.<ref name="Kicman2008" /> In support of the model is the rare condition [[congenital 5α-reductase deficiency]], in which the 5α-reductase enzyme is defective, production of DHT is impaired, and DHT levels are very low while testosterone levels are normal.<ref name="Imperato-McGinleyPeterson1979">{{cite journal | vauthors = Imperato-McGinley J, Peterson RE, Gautier T, Sturla E | title = Androgens and the evolution of male-gender identity among male pseudohermaphrodites with 5alpha-reductase deficiency | journal = The New England Journal of Medicine | volume = 300 | issue = 22 | pages = 1233–7 | date = May 1979 | pmid = 431680 | doi = 10.1056/NEJM197905313002201 }}</ref><ref name="pmid16985920">{{cite journal | vauthors = Marks LS |title=5α-reductase: history and clinical importance |journal=Rev Urol |volume=6 Suppl 9 |issue= |pages=S11–21 |year=2004 |pmid=16985920 |pmc=1472916 |doi=}}</ref> Males with this condition are born with [[ambiguous genitalia]] and a severely underdeveloped or even absent prostate gland.<ref name="Imperato-McGinleyPeterson1979" /><ref name="pmid16985920" /> 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 axilla), no incidence of [[pattern hair loss|male pattern hair loss]], and no prostate enlargement or incidence of [[prostate cancer]].<ref name="pmid16985920" /><ref name="Sloane2002">{{cite book | first = Ethel | last = Sloane | name-list-format = vanc |title=Biology of Women |url=https://books.google.com/books?id=kqcYyk7zlHYC&pg=PA160 |year=2002 |publisher=Cengage Learning |isbn=0-7668-1142-5 |pages=160–}}</ref><ref name="HannoGuzzo2014" /><ref name="JainSiddiqi2006">{{cite book | first1 = N. K. | last1 = Jain | first2 = Maqsood | last2 = Siddiqi | first3 = J. H. | last3 = Weisburger | name-list-format = vanc |title=Protective Effects of Tea on Human Health |url=https://books.google.com/books?id=aILVwQhjsBMC&pg=PA95 |year=2006 |publisher=CABI |isbn=978-1-84593-113-1 |pages=95–}}</ref><ref name="Harper2007">{{cite book | first = Catherine | last = Harper | name-list-format = vanc |title=Intersex |url=https://books.google.com/books?id=fM6vAwAAQBAJ&pg=PA123 |date=1 August 2007 |publisher=Berg |isbn=978-1-84788-339-1 |pages=123–}}</ref> They also notably do not develop gynecomastia as a consequence of their condition.<ref name="HannoGuzzo2014">{{cite book | first1 = Philip M | last1 = Hanno | first2 = Thomas J. | last2 = Guzzi | first3 = S. Bruce | last3 = Malkowicz | first4=Alan | last4 = J. Wein | name-list-format = vanc |title=Penn Clinical Manual of Urology |url=https://books.google.com/books?id=OQTbAgAAQBAJ&pg=PA782 |date=26 January 2014 |publisher=Elsevier Health Sciences |isbn=978-0-323-24466-4 |pages=782–}}</ref>

====Functional selectivity====
An animal study found that two different kinds of [[androgen response element]]s could differentially respond to testosterone and DHT upon activation of the AR.<ref name="pmid11701661">{{cite journal | vauthors = Basaria S, Wahlstrom JT, Dobs AS | title = Clinical review 138: Anabolic-androgenic steroid therapy in the treatment of chronic diseases | journal = J. Clin. Endocrinol. Metab. | volume = 86 | issue = 11 | pages = 5108–17 | year = 2001 | pmid = 11701661 | doi = 10.1210/jcem.86.11.7983 | url = | quote = [...] in a recent animal study, Hsiao et al. (10) found two different kinds of androgen response elements that could respond differentially to T and DHT. Therefore, it is possible that a selective androgen response element sequence may play a role in differential T vs. DHT AR trans-activation.}}</ref><ref name="pmid11343670">{{cite journal | vauthors = Basaria S, Dobs AS | title = Hypogonadism and androgen replacement therapy in elderly men | journal = Am. J. Med. | volume = 110 | issue = 7 | pages = 563–72 | year = 2001 | pmid = 11343670 | doi = | url = | quote = Although both testosterone and dihydrotestosterone activate the same androgen receptor, differences in the sequence of androgen response elements are responsible for differential regulation of these hormones (21).}}</ref>

====Non-genomic mechanisms====
Testosterone signals not only through the nuclear AR, but also through mARs, including [[ZIP9]] and [[GPRC6A]].<ref name="pmid25257522">{{cite journal | vauthors = Wang C, Liu Y, Cao JM | title = G protein-coupled receptors: extranuclear mediators for the non-genomic actions of steroids | journal = Int J Mol Sci | volume = 15 | issue = 9 | pages = 15412–25 | year = 2014 | pmid = 25257522 | pmc = 4200746 | doi = 10.3390/ijms150915412 | url = }}</ref><ref name="pmid28479083">{{cite journal | vauthors = Thomas P, Converse A, Berg HA | title = ZIP9, a novel membrane androgen receptor and zinc transporter protein | journal = Gen. Comp. Endocrinol. | volume = | issue = | pages = | year = 2017 | pmid = 28479083 | doi = 10.1016/j.ygcen.2017.04.016 | url = }}</ref> It has been proposed that differential signaling through mARs may be involved in the dissociation of the anabolic and androgenic effects of AAS.<ref name="Kicman2008" /> Indeed, DHT has less than 1% of the affinity for testosterone for ZIP9 and the synthetic AAS [[metribolone]] and [[mibolerone]] are ineffective competitors for the receptor similarly, indicating that AAS do show differential interactions with the AR versus mARs.<ref name="pmid28479083" /> However, women with [[complete androgen insensitivity syndrome]] (CAIS), who have a male [[genotype]] (46,XY) and a defect in the AR such that it is non-functional, show a perfectly female [[phenotype]] despite having high levels of testosterone.<ref name="pmid26303084">{{cite journal | vauthors = Mongan NP, Tadokoro-Cuccaro R, Bunch T, Hughes IA | title = Androgen insensitivity syndrome | journal = Best Pract. Res. Clin. Endocrinol. Metab. | volume = 29 | issue = 4 | pages = 569–80 | year = 2015 | pmid = 26303084 | doi = 10.1016/j.beem.2015.04.005 | url = }}</ref> In addition, these women show little or no [[sebum]] production, incidence of [[acne]], and body hair growth (including in the pubic and axillary areas).<ref name="pmid26303084" /> Moreover, CAIS women have [[lean body mass]] that is normal for females but of course reduced for males.<ref name="OrwollBilezikian2009">{{cite book|author1=Eric S. Orwoll|author2=John P. Bilezikian|author3=Dirk Vanderschueren|title=Osteoporosis in Men: The Effects of Gender on Skeletal Health|url=https://books.google.com/books?id=nfWNYFdOsCsC&pg=PA114|date=30 November 2009|publisher=Academic Press|isbn=978-0-08-092346-8|pages=114–}}</ref> These findings suggest that the AR is mainly or fully responsible for masculinization and myotrophy caused by androgens.<ref name="pmid26303084" /><ref name="OrwollBilezikian2009" /> In any case, the mARs have been found to be involved in some other effects of testosterone like modulation of prostate cancer risk and progression.<ref name="pmid28479083" /><ref name="pmid21681779">{{cite journal | vauthors = Pi M, Quarles LD | title = GPRC6A regulates prostate cancer progression | journal = Prostate | volume = 72 | issue = 4 | pages = 399–409 | year = 2012 | pmid = 21681779 | pmc = 3183291 | doi = 10.1002/pros.21442 | url = }}</ref>

====Antigonadotropic effects====
Changes in endogenous testosterone levels may also contribute to differences in myotrophic–androgenic ratio between testosterone and synthetic AAS.<ref name="Llewellyn2011" /> AR agonists are [[antigonadotropic]] – that is, they dose-dependently suppress gonadal testosterone production and hence reduce systemic testosterone concentrations.<ref name="Llewellyn2011" /> By suppressing endogenous testosterone levels and effectively replacing AR signaling in the body with that of the exogenous AAS, the myotrophic–androgenic ratio may be be further increased, and this hence may be yet an additional mechanism contributing to the differences in myotrophic–androgenic ratio among different AAS.<ref name="Llewellyn2011" /> In addition, some AAS, such as nandrolone, are also potent [[progestogen]]s, and activation of the [[progesterone receptor]] is antigonadotropic similarly to activation of the AR.<ref name="Llewellyn2011" /> As such, combined progestogenic activity might further increase the myotrophic–androgenic ratio for a given AAS.<ref name="Llewellyn2011" />

===GABA<sub>A</sub> receptor modulation===
Some AAS, such as testosterone, DHT, stanozolol, and methyltestosterone, have been found to modulate the [[GABAA receptor|GABA<sub>A</sub> receptor]] similarly to endogenous [[neurosteroid]]s like [[allopregnanolone]], [[3α-androstanediol]], [[dehydroepiandrosterone sulfate]], and [[pregnenolone sulfate]].<ref name="Kicman2008" /> It has been suggested that this may contribute as an alternative or additional mechanism to the neurological and behavioral effects of AAS.<ref name="Kicman2008" /><ref name="pmid8294123">{{cite journal |vauthors=Bitran D, Kellogg CK, Hilvers RJ |title=Treatment with an anabolic-androgenic steroid affects anxiety-related behavior and alters the sensitivity of cortical GABAA receptors in the rat |journal=Horm Behav |volume=27 |issue=4 |pages=568–83 |year=1993 |pmid=8294123 |doi=10.1006/hbeh.1993.1041 }}</ref><ref name="pmid7603620">{{cite journal |vauthors=Masonis AE, McCarthy MP |title=Direct effects of the anabolic/androgenic steroids, stanozolol and 17α-methyltestosterone, on benzodiazepine binding to the γ-aminobutyric acid<sub>A</sub> receptor |journal=Neurosci. Lett. |volume=189 |issue=1 |pages=35–8 |year=1995 |pmid=7603620 |doi= 10.1016/0304-3940(95)11445-3|url=}}</ref><ref name="pmid8858992"/><ref name="pmid16814373">{{cite journal |vauthors=Rivera-Arce JC, Morales-Crespo L, Vargas-Pinto N, Velázquez KT, Jorge JC |title=Central effects of the anabolic steroid 17alpha methyltestosterone in female anxiety |journal=Pharmacol. Biochem. Behav. |volume=84 |issue=2 |pages=275–81 |year=2006 |pmid=16814373 |doi=10.1016/j.pbb.2006.05.009 |url=}}</ref><ref name="pmid17433821">{{cite journal |vauthors=Henderson LP |title=Steroid modulation of GABAA receptor-mediated transmission in the hypothalamus: effects on reproductive function |journal=Neuropharmacology |volume=52 |issue=7 |pages=1439–53 |year=2007 |pmid=17433821 |pmc=1985867 |doi=10.1016/j.neuropharm.2007.01.022 |url=}}</ref><ref name="pmid19376158">{{cite journal |vauthors=Schwartzer JJ, Ricci LA, Melloni RH |title=Interactions between the dopaminergic and GABAergic neural systems in the lateral anterior hypothalamus of aggressive AAS-treated hamsters |journal=Behav. Brain Res. |volume=203 |issue=1 |pages=15–22 |year=2009 |pmid=19376158 |doi=10.1016/j.bbr.2009.04.007 }}</ref>

===Comparison of AAS===
{| class="wikitable floatright" style="font-size:small;"
<!--{| class="wikitable sortable collapsible collapsed" style="<!--font-size:small;--><!--"-->
|+ Comparison of AAS<ref name="Llewellyn2011" /><ref name="Kicman2008" /><ref name="pmid8674183">{{cite journal | vauthors = Schänzer W | title = Metabolism of anabolic androgenic steroids | journal = Clin. Chem. | volume = 42 | issue = 7 | pages = 1001–20 | year = 1996 | pmid = 8674183 | doi = | url = }}</ref>
|-
! Compound !! {{abbrlink|5α-R|5α-Reductase}} !! {{abbrlink|AROM|Aromatase}} !! {{abbrlink|3-HSD|3-Hydroxysteroid dehydrogenase}} !! [[Estrogen (medication)|{{abbr|Estr|Estrogenic}}]] !! [[Progestin|{{abbr|Prog|Progestogenic}}]] !! [[Oral administration|{{abbr|Oral|Orally active}}]] !! {{abbrlink|Hepat|Hepatotoxicity}}
|-
| [[Androstanolone]] || No || No || Yes || No || No || No || No
|-
| [[Boldenone]] || No || Yes || No || Yes || No || No || No
|-
| [[Drostanolone]] || No || No || No || No || No || No || No
|-
| [[Fluoxymesterone]] || No || No || No || No || No || Yes || Yes
|-
| [[Mestanolone]] || No || No || Yes || No || No || Yes || Yes
|-
| [[Mesterolone]] || No || No || Yes || No || No || Yes || Yes
|-
| [[Metandienone]] || No || Yes || No || Yes || No || Yes || Yes
|-
| [[Metenolone]] || No || No || No || No || No || Yes || No
|-
| [[Methyltestosterone]] || Yes (↑) || Yes || No || Yes || No || Yes || Yes
|-
| [[Nandrolone]] || Yes (↓) || Low || No || Low || Yes || No || No
|-
| [[Norethandrolone]] || Yes (↓) || Yes || No || Yes || Yes || Yes || Yes
|-
| [[Oxandrolone]] || No || No || No || No || No || Yes || Low
|-
| [[Oxymetholone]] || No || No || No || Yes || No || Yes || Yes
|-
| [[Stanozolol]] || No || No || No || No || No || Yes || Yes
|-
| [[Testosterone]] || Yes (↑) || Yes || No || Yes || No || No || No
|-
| [[Trenbolone]] || No || No || No || No || Yes || No || No
|- class="sortbottom"
| colspan="8" style="width: 1px;" | 5α-R = Metabolized by [[5α-reductase]]. (↑ = Potentiated. ↓ = Inactivated.) AROM = Metabolized by [[aromatase]]. 3-HSD = Metabolized by {{abbrlink|3α-|3α-hydroxysteroid dehydrogenase}} and/or {{abbrlink|3β-HSD|3β-hydroxysteroid dehydrogenase}}. Estr = [[Estrogen (medication)|Estrogen]]ic activity. Prog = [[Progestin|Progestogen]]ic activity. Oral = [[Oral administration|Oral]] activity. Hepat = [[Hepatotoxicity]].
|}

====5α-Reductase and androgenicity====
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.<ref name="Kicman2008" /> 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.<ref name="Kicman2008" /> 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.<ref name="Kicman2008" /> 19-Nortestosterone derivatives like [[nandrolone]] can be [[metabolism|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.<ref name="Kicman2008" /> 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.<ref name="pmid20599615">{{cite journal | vauthors = Attardi BJ, Hild SA, Koduri S, Pham T, Pessaint L, Engbring J, Till B, Gropp D, Semon A, Reel JR | title = The potent synthetic androgens, dimethandrolone (7α,11β-dimethyl-19-nortestosterone) and 11β-methyl-19-nortestosterone, do not require 5α-reduction to exert their maximal androgenic effects | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 122 | issue = 4 | pages = 212–8 | date = October 2010 | pmid = 20599615 | pmc = 2949447 | doi = 10.1016/j.jsbmb.2010.06.009 }}</ref> Conversely, certain 17α-alkylated AAS like methyltestosterone are 5α-reduced and potentiated in androgenic tissues similarly to testosterone.<ref name="Kicman2008" /><ref name="Llewellyn2011" /> 17α-Alkylated DHT derivatives cannot be potentiated via 5α-reductase however, as they are already 4,5α-reduced.<ref name="Kicman2008" /><ref name="Llewellyn2011" />

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.<ref name="Kicman2008" /> 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]],<ref>{{cite book|author1=Orwoll, Eric S. |author2=Bilezikian, John P. |author3=Vanderschueren, Dirk |title=Osteoporosis in Men: The Effects of Gender on Skeletal Health|url=https://books.google.com/books?id=nfWNYFdOsCsC&pg=PA296|date=30 November 2009|publisher=Academic Press|isbn=978-0-08-092346-8|pages=296–}}</ref> [[voice change|voice deepening]], and changes in [[sex drive]] show no difference.<ref name="Kicman2008" /><ref name="FillitRockwood2010">{{cite book|author1=Fillit, Howard M. |author2=Rockwood, Kenneth |author3=Woodhouse, Kenneth |title=Brocklehurst's Textbook of Geriatric Medicine and Gerontology|url=https://books.google.com/books?id=DPcUtY0kP7oC&pg=PA166|date=10 May 2010|publisher=Elsevier Health Sciences|isbn=1-4377-2075-7|pages=166–167}}</ref>

====Aromatase and estrogenicity====
Testosterone can be [[metabolism|metabolized]] by [[aromatase]] into [[estradiol]], and many other AAS can be metabolized into their corresponding [[estrogen (medication)|estrogen]]ic metabolites as well.<ref name="Kicman2008" /> As an example, the 17α-alkylated AAS [[methyltestosterone]] and [[metandienone]] are converted by aromatase into [[methylestradiol]].<ref name="ThiemeHemmersbach2009">{{cite book|author1=Thieme, Detlef |author2=Hemmersbach, Peter |title=Doping in Sports|url=https://books.google.com/books?id=R-hIC-caIn8C&pg=PA470|date=18 December 2009|publisher=Springer Science & Business Media|isbn=978-3-540-79088-4|pages=470–}}</ref> 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.<ref name="Kicman2008" /><ref name="pmid18555683">{{cite journal | vauthors = Attardi BJ, Pham TC, Radler LC, Burgenson J, Hild SA, Reel JR | title = Dimethandrolone (7,11β-dimethyl-19-nortestosterone) and 11β-methyl-19-nortestosterone are not converted to aromatic A-ring products in the presence of recombinant human aromatase | journal = The Journal of Steroid Biochemistry and Molecular Biology | volume = 110 | issue = 3–5 | pages = 214–22 | date = June 2008 | pmid = 18555683 | pmc = 2575079 | doi = 10.1016/j.jsbmb.2007.11.009 }}</ref> 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.<ref name="pmid18555683" /> 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.<ref name="Kicman2008" /><ref name="Llewellyn2011">{{cite book|author=Llewellyn, William |title=Anabolics|url=https://books.google.com/books?id=afKLA-6wW0oC&pg=PT533|year=2011|publisher=Molecular Nutrition Llc|isbn=978-0-9828280-1-4|pages=533–,402–412,460–467}}</ref> 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]],<ref name="ThiemeHemmersbach2009" /> and for this reason, 17α-alkylated AAS can actually have high estrogenicity and comparatively greater estrogenic effects than testosterone.<ref name="ThiemeHemmersbach2009" /><ref name="Llewellyn2011" />

The major effect of estrogenicity is [[gynecomastia]] (woman-like breasts).<ref name="Kicman2008" /> AAS that have a high potential for aromatization like testosterone and particularly methyltestosterone show a high risk of gynecomastia, while AAS that have a reduced potential for aromatization like nandrolone show a much lower risk (though still significant at high dosages).<ref name="Kicman2008" /> In contrast, AAS that are 4,5α-reduced, and some other AAS (e.g., 11β-methylated 19-nortestosterone derivatives), have no risk of gynecomastia.<ref name="Kicman2008" /> 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 [[gonad]]al testosterone production.<ref name="pmid19231088">{{cite journal | vauthors = Tan RS, Scally MC | title = Anabolic steroid-induced hypogonadism—towards a unified hypothesis of anabolic steroid action | journal = Med. Hypotheses | volume = 72 | issue = 6 | pages = 723–8 | year = 2009 | pmid = 19231088 | doi = 10.1016/j.mehy.2008.12.042 | url = | quote = Regulation of the secretion of GnRH, FSH, and LH occurs partially by the negative feedback of testosterone and estradiol at the level of the hypothalamo-pituitary. Estradiol has a much larger, inhibitory effect than testosterone, being 200-fold more effective in suppressing LH secretion [57–61].}}</ref><ref name="Suvisaari2000">{{cite book | last=Suvisaari | first=Janne | title=7α-Methyl-19-nortestosterone (MENT) Pharmacokinetics and Antigonadotropic Effects in Men | publisher=University of Helsinki | location=Helsinki | year=2000 | isbn=952-91-2950-5 | page=14 | url=http://ethesis.helsinki.fi/julkaisut/laa/biola/vk/suvisaari/7alphame.pdf | quote = Androgens, estrogens and progestins exert a negative feedback effect on the secretion of GnRH and LH by their actions on the pituitary and the hypothalamus. Most of the negative feedback effect of androgens is caused by their estrogenic metabolites produced by aromatization. 5α-Reduction does not seem to be necessary for the negative feedback effect of testosterone. (Rittmaster et al, 1992; Kumar et al, 1995a; Hayes et al, 2000).}}</ref>

====Progestogenic activity====
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 [[progestogen]]s in addition to AAS.<ref name="Kicman2008" /><ref name="pmid16497801">{{cite journal | vauthors = Attardi BJ, Hild SA, Reel JR | title = Dimethandrolone undecanoate: a new potent orally active androgen with progestational activity | journal = Endocrinology | volume = 147 | issue = 6 | pages = 3016–26 | date = June 2006 | pmid = 16497801 | doi = 10.1210/en.2005-1524 }}</ref> Similarly to the case of estrogenic activity, the progestogenic activity of these drugs serves to augment their antigonadotropic activity.<ref name="pmid16497801" /> This results in increased potency and effectiveness of these AAS as [[wikt:antispermatogenic|antispermatogenic agent]]s and [[male contraceptive]]s (or, put in another way, increased potency and effectiveness in producing [[azoospermia]] and reversible [[male infertility]]).<ref name="pmid16497801" />

====Oral activity and hepatotoxicity====
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.<ref name="Kicman2008" /> A notable exception to this are AAS that are androgen [[precursor (biochemistry)|precursor]]s or [[androgen prohormone|prohormone]]s, 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).<ref name="WarrenConstantini2000">{{cite book|author1=Warren, Michelle P. |author2=Constantini, Naama W. |title=Sports Endocrinology|url=https://books.google.com/books?id=HNJ9BwAAQBAJ&pg=PA458|date=1 May 2000|publisher=Springer Science & Business Media|isbn=978-1-59259-016-2|pages=458–}}</ref><ref name="GregoryTravis2015">{{cite book|author1=Haff, G. Gregory|author2=Triplett, N. Travis|title=Essentials of Strength Training and Conditioning 4th Edition|url=https://books.google.com/books?id=bfuXCgAAQBAJ&pg=PA233|date=23 September 2015|publisher=Human Kinetics|isbn=978-1-4925-0162-6|pages=233–}}</ref> AAS that are not orally active are used almost exclusively in the form of [[androgen ester|ester]]s administered by [[intramuscular injection]], which act as [[depot injection|depot]]s and function as long-acting [[prodrug]]s.<ref name="Kicman2008" /> Examples include testosterone, as [[testosterone cypionate]], [[testosterone enanthate]], and [[testosterone propionate]], and nandrolone, as [[nandrolone phenylpropionate]] and [[nandrolone decanoate]], among many others (see [[Androgen ester|here]] for a full list of testosterone and nandrolone esters).<ref name="Kicman2008" /> An exception is the very long-chain ester [[testosterone undecanoate]], which is orally active, albeit with only very low oral bioavailability (approximately 3%).<ref name="LemkeWilliams2012">{{cite book|author1=Lemke, Thomas L. |author2=Williams, David A. |title=Foye's Principles of Medicinal Chemistry|url=https://books.google.com/books?id=Sd6ot9ul-bUC&pg=PA1360|date=24 January 2012|publisher=Lippincott Williams & Wilkins|isbn=978-1-60913-345-0|pages=1360–}}</ref> 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.<ref name="Kicman2008" />

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%),<ref name="MDDrummer2001">{{cite book|author1=Karch, Steven B. |author2=Drummer, Olaf |title=Karch's Pathology of Drug Abuse, Third Edition|url=https://books.google.com/books?id=AUTWJwn8uOwC&pg=PA489|date=26 December 2001|publisher=CRC Press|isbn=978-1-4200-4211-5|pages=489–}}</ref><ref name="pmid20153798">{{cite journal |vauthors=van Amsterdam J, Opperhuizen A, Hartgens F |title=Adverse health effects of anabolic-androgenic steroids |journal=Regul. Toxicol. Pharmacol. |volume=57 |issue=1 |pages=117–23 |year=2010 |pmid=20153798 |doi=10.1016/j.yrtph.2010.02.001 |url=}}</ref> with hepatotoxicity.<ref name="Kicman2008" /><ref name="pmid3042375">{{cite journal | vauthors = Wilson JD | title = Androgen abuse by athletes | journal = Endocr. Rev. | volume = 9 | issue = 2 | pages = 181–99 | year = 1988 | pmid = 3042375 | doi = 10.1210/edrv-9-2-181 | url = }}</ref><ref name="JamesonGroot2015">{{cite book|author1=Jameson, J. Larry |author2=De Groot, Leslie J. |title=Endocrinology: Adult and Pediatric|url=https://books.google.com/books?id=xmLeBgAAQBAJ&pg=PA2391|date=25 February 2015|publisher=Elsevier Health Sciences|isbn=978-0-323-32195-2|pages=2391–}}</ref><ref>{{Cite journal|last=Bond|first=Peter|last2=Llewellyn|first2=William|last3=Van Mol|first3=Peter|date=2016-08-01|title=Anabolic androgenic steroid-induced hepatotoxicity|journal=Medical Hypotheses|volume=93|pages=150–153|doi=10.1016/j.mehy.2016.06.004|issn=1532-2777|pmid=27372877}}</ref> In contrast, [[testosterone ester]]s have only extremely rarely or never been associated with hepatotoxicity,<ref name="pmid20153798" /> and other non-17α-alkylated AAS only rarely,{{Citation needed|date=September 2016}} 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).<ref name="MDDrummer2001" /><ref name="NieschlagBehre2012">{{cite book|author1=Nieschlag, Eberhard |author2=Behre, Hermann M. |author3=Nieschlag, Susan |title=Testosterone: Action, Deficiency, Substitution|url=https://books.google.com/books?id=MkrAPaQ4wJkC&pg=PA374|date=26 July 2012|publisher=Cambridge University Press|isbn=978-1-107-01290-5|pages=374–}}</ref><ref name="Becker2001" />{{Additional citation needed|date=September 2016}} In accordance, D-ring [[glucuronide]]s of testosterone and DHT have been found to be cholestatic.<ref name="CameronFeuer2012">{{cite book|author1=Cameron, Ross |author2=Feuer, George |author3=de la Iglesia, Felix |title=Drug-Induced Hepatotoxicity|url=https://books.google.com/books?id=xZf-CAAAQBAJ&pg=PA166|date=6 December 2012|publisher=Springer Science & Business Media|isbn=978-3-642-61013-4|pages=166–}}</ref>

Aside from prohormones and testosterone undecanoate, almost all orally active AAS are 17α-alkylated.<ref name="pmid11589254">{{cite journal | vauthors = Shahidi NT | title = A review of the chemistry, biological action, and clinical applications of anabolic-androgenic steroids | journal = Clin Ther | volume = 23 | issue = 9 | pages = 1355–90 | year = 2001 | pmid = 11589254 | doi = 10.1016/s0149-2918(01)80114-4| url = }}</ref> A few AAS that are not 17α-alkylated are orally active.<ref name="Kicman2008" /> Some examples include the testosterone 17-ethers [[cloxotestosterone]], [[quinbolone]], and [[silandrone]],{{Citation needed|date=September 2016}} which are prodrugs (to testosterone, [[boldenone]] (Δ<sup>1</sup>-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),<ref name="Kicman2008" /><ref name="Becker2001" /> 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).<ref name="Kicman2008" /><ref name="pmid16497801" /> As these AAS are not 17α-alkylated, they show minimal potential for hepatotoxicity.<ref name="Kicman2008" />

====Neurosteroid activity====
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|GABA<sub>A</sub> receptor]].<ref name="Kicman2008" /> Testosterone, via conversion into DHT, also produces 3α-androstanediol as a metabolite and hence has similar activity.<ref name="Kicman2008" /> Some AAS that are or can be 5α-reduced, including testosterone, DHT, [[stanozolol]], and methyltestosterone, among many others, can or may modulate the GABA<sub>A</sub> 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.<ref name="Kicman2008" /><ref name="pmid8294123"/><ref name="pmid7603620"/><ref name="pmid8858992">{{cite journal |vauthors=Masonis AE, McCarthy MP |title=Effects of the androgenic/anabolic steroid stanozolol on GABAA receptor function: GABA-stimulated <sup>36</sup>Cl<sup>−</sup> influx and [<sup>35</sup>S] TBPS binding |journal=J. Pharmacol. Exp. Ther. |volume=279 |issue=1 |pages=186–93 |year=1996 |pmid=8858992 |doi= |url=}}</ref><ref name="pmid16814373"/><ref name="pmid17433821"/><ref name="pmid19376158"/>

==Chemistry==
{{See also|List of androgens/anabolic steroids|List of androgen esters}}

AAS are [[androstane]] or [[estrane]] [[steroid]]s. They include testosterone (androst-4-en-17β-ol-3-one) and [[chemical derivative|derivative]]s with various [[molecular modification|structural modification]]s such as:<ref name="Kicman2008" /><ref name="BüttnerThieme2009">{{cite journal|last1=Büttner|first1=Andreas|last2=Thieme|first2=Detlef|title=Side Effects of Anabolic Androgenic Steroids: Pathological Findings and Structure–Activity Relationships|volume=195|year=2009|pages=459–484|issn=0171-2004|doi=10.1007/978-3-540-79088-4_19}}</ref><ref name="Llewellyn2011" />

* [[17α-Alkylated anabolic steroid|17α-Alkylation]]: [[methyltestosterone]], [[metandienone]] (methandrostenolone), [[fluoxymesterone]], [[oxandrolone]], [[oxymetholone]], [[stanozolol]]
* [[19-Nortestosterone|19-Demethylation]]: [[nandrolone]], [[trenbolone]]
* [[Dihydrotestosterone|5α-Reduction]]: [[dihydrotestosterone|DHT]] (androstanolone, stanolone), [[drostanolone]], [[mesterolone]], [[metenolone]] (methylandrostenolone), [[oxandrolone]], [[oxymetholone]], [[stanozolol]]
* [[Androgen ester|3β- and/or 17β-esterification]]: [[testosterone enanthate]], [[nandrolone decanoate]], [[drostanolone propionate]], [[boldenone undecylenate]], [[trenbolone acetate]]

As well as others such as [[boldenone|1-dehydrogenation]] (e.g., [[metandienone]], [[boldenone]]), [[4-hydroxytestosterone|4-substitution]] (e.g., [[clostebol]]), and various other substitutions.<ref name="Kicman2008" /><ref name="BüttnerThieme2009" /><ref name="Llewellyn2011" />

===Detection in body fluids===
The most commonly employed human physiological specimen for detecting AAS usage is urine, although both blood and hair have been investigated for this purpose. The AAS, whether of endogenous or exogenous origin, are subject to extensive hepatic biotransformation by a variety of enzymatic pathways. The primary urinary metabolites may be detectable for up to 30 days after the last use, depending on the specific agent, dose and route of administration. A number of the drugs have common metabolic pathways, and their excretion profiles may overlap those of the endogenous steroids, making interpretation of testing results a very significant challenge to the analytical chemist. Methods for detection of the substances or their excretion products in urine specimens usually involve [[gas chromatography–mass spectrometry]] or liquid chromatography-mass spectrometry.<ref name="pmid18570179">{{cite journal |vauthors=Mareck U, Geyer H, Opfermann G, Thevis M, Schänzer W |title=Factors influencing the steroid profile in doping control analysis |journal=J Mass Spectrom |volume=43 |issue=7 |pages=877–91 |date=July 2008 |pmid=18570179 |doi=10.1002/jms.1457}}</ref><ref name="pmid19429460">{{cite journal |vauthors=Fragkaki AG, Angelis YS, Tsantili-Kakoulidou A, Koupparis M, Georgakopoulos C |title=Schemes of metabolic patterns of anabolic androgenic steroids for the estimation of metabolites of designer steroids in human urine |journal=J. Steroid Biochem. Mol. Biol. |volume=115 |issue=1–2 |pages=44–61 |date=May 2009 |pmid=19429460 |doi=10.1016/j.jsbmb.2009.02.016}}</ref><ref name="pmid19465014">{{cite journal | vauthors = Blackledge RD |title=Bad science: the instrumental data in the Floyd Landis case |journal=Clin. Chim. Acta |volume=406 |issue=1–2 |pages=8–13 |date=August 2009 |pmid=19465014 |doi=10.1016/j.cca.2009.05.016}}</ref><ref>{{cite book |first1=Randall Clint |last1=Baselt |title=Disposition of Toxic Drugs and Chemicals in Man |edition=8th |publisher=Biomedical Publications |location=Foster City, CA |year=2008 |pages=95, 393, 403, 649, 695, 952, 962, 1078, 1156, 1170, 1442, 1501, 1581 |isbn=978-0-9626523-7-0}}</ref>

==History==

===Isolation of gonadal androgens===
The use of [[gonadal]] [[steroid]]s pre-dates their identification and isolation. Medical use of [[testicle]] extract began in the late 19th century while its effects on strength were still being studied.<ref name="DoirpMissing" /> 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 [[chemical synthesis|synthesized]] in 1934 by [[Leopold Ružička]], a chemist in [[Zurich]].<ref name = "PMID7817189"/>

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.<ref name = "PMID7817189">{{cite journal |vauthors=Hoberman JM, Yesalis CE |title=The history of synthetic testosterone |journal=Scientific American |volume=272 |issue=2 |pages=76–81 |year=1995 |pmid=7817189 |doi=10.1038/scientificamerican0295-76}}</ref><ref name = "PMID11176375">{{cite journal |vauthors=Freeman ER, Bloom DA, McGuire EJ |title=A brief history of testosterone |journal=Journal of Urology |volume=165 |issue=2 |pages=371–373 |year=2001 |pmid=11176375 |doi=10.1097/00005392-200102000-00004}}</ref> 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)."<ref>{{cite journal |vauthors=David K, Dingemanse E, Freud J, Laqueur L |title=Uber krystallinisches mannliches Hormon aus Hoden (Testosteron) wirksamer als aus harn oder aus Cholesterin bereitetes Androsteron |journal=Hoppe-Seyler's Z Physiol Chem |volume=233 |pages=281–283 |year=1935 |doi=10.1515/bchm2.1935.233.5-6.281 |issue=5–6}}</ref> They named the hormone ''[[testosterone]]'', from the [[stem (linguistics)|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."<ref>{{cite journal |doi=10.1002/cber.19350680937 |title=Über die Umwandlung des Dehydro-androsterons in Δ4-Androsten-ol-(17)-0n-(3) (Testosteron); ein Weg zur Darstellung des Testosterons aus Cholesterin (Vorläuf. Mitteil.) |trans-title=On the conversion of dehydro-Δ4-androstene androsterons in-ol (17) 0n (3) (testosterone), a way to represent the testosterone from cholesterol (Vorläuf. msgs.) |language=de |year=1935 |vauthors=Butenandt A, Hanisch G |journal=Berichte der deutschen chemischen Gesellschaft (A and B Series) |volume=68 |issue=9 |pages=1859–62}}</ref> 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)."<ref>{{cite journal |vauthors=Ruzicka L, Wettstein A |title=Sexualhormone VII. Uber die kunstliche Herstellung des Testikelhormons. Testosteron (Androsten-3-one-17-ol.) |trans-title=Sex hormones VII About the artificial production of testosterone Testikelhormons (androstene-3-one-17-ol) |language=de |journal=Helvetica Chimica Acta |volume=18 |pages=1264–75 |year=1935 |doi=10.1002/hlca.193501801176}}</ref> Ruzicka and Butenandt were offered the 1939 [[Nobel Prize in Chemistry]] for their work, but the [[Nazi Germany|Nazi]] government forced Butenandt to decline the honor, although he accepted the prize after the end of World War II.<ref name = "PMID7817189"/><ref name = "PMID11176375"/>

Clinical trials on humans, involving either oral doses of [[methyltestosterone]] or injections of [[testosterone propionate]], began as early as 1937.<ref name = "PMID7817189"/> 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. [[Olympic weightlifting|weightlifting]] or [[bodybuilding]] magazine.<ref name = "PMID7817189"/> 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.<ref name = "Lenahan_2003"/>{{rp|6}} [[Adolf Hitler]] himself, according to his physician, was injected with testosterone derivatives to treat various ailments.<ref name=Taylor>{{cite book | vauthors = Taylor WN |title=Anabolic Steroids and the Athlete |publisher=McFarland & Company |date=January 1, 2009 |location= |page=181 |doi= |isbn=0-7864-1128-7}}</ref> AAS were used in experiments conducted by the Nazis on concentration camp inmates,<ref name=Taylor/> and later by the allies attempting to treat the malnourished victims that survived Nazi camps.<ref name = "Lenahan_2003"/>{{rp|6}} President [[John F. Kennedy]] was administered steroids both before and during his presidency.<ref name=NewsHour>{{cite web |url=https://www.pbs.org/newshour/bb/health/july-dec02/jfk_11-18.html |title=President Kennedy's Health Secrets |vauthors = Suarez R,((Senior Correspondent)), Kelman J,((physician)) |date=2002-11-18 |work=PBS NewsHour |publisher=Public Broadcasting System}}</ref>

===Development of synthetic AAS===
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 Games|Olympic]] and other [[amateur sports|amateur]] [[Olympic weightlifting|weight lifters]]. In response to the success of Russian weightlifters, the U.S. Olympic Team physician [[John Bosley Ziegler|John Ziegler]] worked with synthetic chemists to develop an AAS with reduced androgenic effects.<ref name="pedsreview">{{cite journal |vauthors=Calfee R, Fadale P |title=Popular ergogenic drugs and supplements in young athletes |journal=Pediatrics |volume=117 |issue=3 |pages=e577–89 |year=2006 |pmid=16510635 |doi=10.1542/peds.2005-1429}}</ref> 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 use]]rs 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.<ref>Justin Peters [http://www.slate.com/id/2113752/ The Man Behind the Juice], ''Slate'' Friday, Feb. 18, 2005. Retrieved 29 April 2008</ref> AAS were placed on the list of banned substances of the 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.<ref name="Hartgens and Kuipers 2004"/>

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.<ref name="Hartgens and Kuipers 2004"/>

==Society and culture==

===Legal status===
[[File:Compounds showing anabolic and androgenic effects.png|thumb|right|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<!--most--> 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.<ref>{{cite web|url=http://www.deadiversion.usdoj.gov/21cfr/21usc/844.htm |title=Title 21 United States Code (USC) Controlled Substances Act |publisher=US Department of Justice |accessdate=2009-09-07 |archiveurl=https://web.archive.org/web/20090724051512/http://www.deadiversion.usdoj.gov/21cfr/21usc/844.htm |archivedate=24 July 2009 |deadurl=no |df= }}</ref> In Canada, AAS and their derivatives are part of the [[Controlled Drugs and Substances Act]] and are [[Schedule IV (Canada)|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.<ref>{{Cite canlaw |short title=Controlled Drugs and Substances Act |abbr=S.C. |year=1996 |chapter=19 |section=4 |subsection=7 |link=http://laws-lois.justice.gc.ca/eng/acts/C-38.8/page-2.html#h-4 |linkloc=Department of Justice |wikilink=Controlled Drugs and Substances Act}}</ref> 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.<ref>{{cite journal |last=Deacon |first=James |title=Biceps in a bottle |journal=Maclean's |page=52 |date=2 May 1994}}</ref> AAS are also illegal without prescription in Australia,<ref>{{cite web|title=Steroids |publisher=Australian Institute of Criminology |year=2006 |url=http://www.aic.gov.au/research/drugs/types/steroids.html |accessdate=2007-05-06 |archiveurl=https://web.archive.org/web/20070405033442/http://www.aic.gov.au/research/drugs/types/steroids.html |archivedate=2007-04-05 |deadurl=no |df= }}</ref> Argentina{{Citation needed|date=May 2017}}, Brazil{{Citation needed|date=May 2017}} and Portugal{{Citation needed|date=May 2017}}, and are listed as Class&nbsp;C [[Controlled Drug]]s in the United Kingdom. AAS are readily available without a prescription in some countries such as Mexico and Thailand.

====United States====
[[File:SteroidpillsDEA.jpg|thumb|right |200px| 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 (sprinter)|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]].<ref name="congress">{{USBill|101|HR|4658}}</ref>

The same act also introduced more stringent controls with higher criminal penalties for offenses involving the illegal distribution of AAS and human growth hormone. By the early 1990s, after AAS were scheduled in the U.S., several pharmaceutical companies stopped manufacturing or marketing the products in the U.S., including Ciba, Searle, Syntex, and others. In the Controlled Substances Act, AAS are defined to be any drug or hormonal substance chemically and pharmacologically related to testosterone (other than [[estrogen (medication)|estrogen]]s, [[progestin]]s, and [[corticosteroid]]s) that promote muscle growth. The act was amended by the Anabolic Steroid Control Act of 2004, which added [[prohormone]]s to the list of [[controlled substance]]s, with effect from January 20, 2005.<ref name="usdoj">{{cite web |url=http://www.usdoj.gov/dea/pubs/cngrtest/ct031604.html |title=News from DEA, Congressional Testimony, 03/16/04 |accessdate=2007-04-24 |deadurl=yes |archiveurl=https://web.archive.org/web/20070206195542/http://www.usdoj.gov/dea/pubs/cngrtest/ct031604.html |archivedate=February 6, 2007}}</ref>

====United Kingdom====
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.

Part 1 drugs are subject to full import and export controls with possession being an offence without an appropriate prescription. There is no restriction on the possession when it is part of a medicinal product. Part 2 drugs require a Home Office licence for importation and export unless the substance is in the form of a medicinal product and is for self-administration by a person.<ref>{{cite web |title=Patient.info Controlled Drugs |url=http://patient.info/doctor/controlled-drugs |publisher=Egton Medical Information Systems Limited |accessdate=8 August 2013}}</ref>

===Status in sports===
{{See also|Use of performance-enhancing drugs in sport}}
[[File:Anabolic substances and their legal status in most Western countries.png|thumb|right|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]]<ref>{{cite web |url=http://es.fifa.com/mm/document/afdeveloping/medical/50/29/56/fifadocregulations_09.01.09_e.pdf |title=FIFA Anit-Doping Regulations |publisher=FIFA |accessdate=2013-12-01}}</ref> the [[Olympic Games|Olympics]],<ref>{{cite web |title=Olympic movement anti-doping code |publisher=International Olympic Committee |year=1999 |url=http://www.medycynasportowa.pl/download/doping_code_e.pdf |format=PDF |accessdate=2007-05-06}}</ref> the [[National Basketball Association]],<ref>{{cite web |title=The nba and nbpa anti-drug program |work=NBA Policy |publisher=findlaw.com |year=1999 |url=http://news.findlaw.com/legalnews/sports/drugs/policy/basketball/index.html |accessdate=2007-05-06}}</ref> the [[National Hockey League]],<ref>{{cite web |title=NHL/NHLPA performance-enhancing substances program summary |publisher=nhlpa.com |url=http://www.nhlpa.com/PerformanceEnhancing/index.asp |accessdate=2007-05-06 |archiveurl=https://web.archive.org/web/20070602113854/http://www.nhlpa.com/PerformanceEnhancing/index.asp |archivedate=2 June 2007 |deadurl=no}}</ref> [[World Wrestling Entertainment]] and the [[National Football League]].<ref>{{cite web |title=List of Prohibited Substances |publisher=nflpa.com |year=2006 |url=http://www.nflpa.org/pdfs/RulesAndRegs/ProhibitedSubstances.pdf | archive-url = https://web.archive.org/web/20070620160852/http://www.nflpa.org/pdfs/RulesAndRegs/ProhibitedSubstances.pdf | archive-date = 2007-06-20 | dead-url = yes |format=PDF |accessdate=2007-05-06}}</ref> 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.<ref>{{cite web |title=World anti-doping code |publisher=WADA |year=2003 |url=http://www.wada-ama.org/rtecontent/document/code_v3.pdf |format=PDF |accessdate=2007-07-10 |archiveurl=https://web.archive.org/web/20070807192944/http://www.wada-ama.org/rtecontent/document/code_v3.pdf |archivedate=7 August 2007 |deadurl=no}}</ref><ref>{{cite web |title=Prohibited list of 2005 |publisher=WADA |year=2005 |url=http://www.wada-ama.org/rtecontent/document/summary_2005.pdf |format=PDF |accessdate=2007-05-06}}</ref> Spain has passed an anti-doping law creating a national anti-doping agency.<ref>{{cite news |title=Spain's senate passes anti-doping law |agency=Associated Press |date=October 5, 2006 |work=Herald Tribune |url=http://www.iht.com/articles/ap/2006/10/05/sports/EU_SPT_Spain_Doping.php |accessdate=2007-05-06 |deadurl=yes |archiveurl=https://web.archive.org/web/20061012025245/http://www.iht.com/articles/ap/2006/10/05/sports/EU_SPT_Spain_Doping.php |archivedate=October 12, 2006}}</ref> Italy passed a law in 2000 where penalties range up to three years in prison if an athlete has tested positive for banned substances.<ref>{{cite news |last=Johnson |first=Kevin |title=Italian anti-doping laws could mean 3 years in jail |work=USA Today |date=2006-02-20 |url=https://www.usatoday.com/sports/olympics/torino/2006-02-19-anti-doping-laws_x.htm |accessdate=2007-05-06}}</ref> 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,<ref>{{cite web |title=Act on promotion of doping-free sport |publisher=kum.dk |year=2004 |url=https://english.kum.dk/uploads/tx_templavoila/Act%20on%20Promotion%20of%20Doping-free%20Sport.pdf |format=PDF |accessdate=2016-09-04}}</ref> France,<ref>{{cite web |title=Protection of health of athletes and the fight against doping |publisher=WADA |year=2006 |url=http://www.wada-ama.org/rtecontent/document/national_laws_sports_code_legislative_part_En.pdf |format=PDF |accessdate=2007-05-06}}</ref> the Netherlands<ref>{{cite web |title=Anti-doping legislation in the netherlands |publisher=WADA |year=2006 |url=http://www.wada-ama.org/rtecontent/document/Dutch_Legislation_Concerning_Doping_Jan_2007.pdf |format=PDF |accessdate=2007-05-06}}</ref> and Sweden.<ref>{{cite web |title=The Swedish Act prohibiting certain doping substances (1991:1969) |publisher=WADA |year=1991 |url=http://www.wada-ama.org/rtecontent/document/National_Laws_Swedish_Act.pdf |format=PDF |accessdate=2007-05-06}}</ref>

===Usage===
{{See also|Anabolic–androgenic steroids abuse}}

====Law enforcement====
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]].<ref>{{Cite news |url=http://www.annarbor.com/health/steroid-abuse-among-law-enforcement-a-problem-nationwide/ |title=Steroid abuse among law enforcement a problem nationwide |first=Juliana |last=Keeping |work=The Ann Arbor News |date=27 December 2010 |accessdate=1 December 2013}}</ref> 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".<ref>{{Cite news |url=http://www.policechiefmagazine.org/magazine/index.cfm?fuseaction=display_arch&article_id=1512&issue_id=62008 |title=Anabolic Steroid Use and Abuse by Police Officers: Policy & Prevention |work=The Police Chief |date=June 2008 |accessdate=1 December 2013}}</ref> 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====
{{main article|WWE#Wellness Program}}

Following the [[Chris Benoit double murder and suicide|murder-suicide of Chris Benoit in 2007]], the [[United States House Committee on Oversight and Government Reform|Oversight and Government Reform Committee]] investigated steroid usage in the wrestling industry.<ref name="greenwichtimecontroversy">{{cite web |url=http://www.greenwichtime.com/news/article/Sunday-subscriber-advantage-WWE-steroid-385857.php#page-1 |title=WWE steroid investigation: A controversy McMahon 'doesn't need' | first = Brian | last = Lockhart | name-list-format = vanc |publisher=Greenwich Time |date=2010-03-01 |accessdate=2010-03-01}}</ref> The Committee investigated [[WWE]] and [[Total Nonstop Action Wrestling]] (TNA), asking for documentation of their companies' drug policies. WWE CEO and Chairman, [[Linda McMahon|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.<ref>[http://oversight.house.gov/images/stories/documents/20081231141129.pdf documents] {{webarchive |url=https://web.archive.org/web/20101224020122/http://oversight.house.gov/images/stories/documents/20081231141129.pdf |date=December 24, 2010 }}</ref><ref>{{cite web |url=http://www.theday.com/article/20100609/NWS12/306099933/1019&town= |title=Deposition details McMahon steroid testimony &#124; News from southeastern Connecticut |publisher=The Day |date=2007-12-13 |accessdate=2010-08-14}}</ref>

===Economics===
{{Main article|Illegal trade in anabolic steroids}}
[[File:Rd17.jpg|thumb|Several large buckets containing tens of thousands of AAS vials confiscated by the [[Drug Enforcement Administration|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.<ref name=Assael>{{cite news |first=Shaun |last=Assael |title='Raw Deal' busts labs across U.S., many supplied by China |date=2007-09-24 |url=http://sports.espn.go.com/espn/news/story?id=3033532 |work=ESPN The Magazine |accessdate=2007-09-24 |archiveurl=https://web.archive.org/web/20071014050947/http://sports.espn.go.com/espn/news/story?id=3033532 |archivedate=14 October 2007 |deadurl=no}}</ref> In these countries, the majority of steroids are obtained illegally through [[black market]] trade.<ref name=cy>{{cite book |last=Yesalis |first=C |year=2000 |title=Anabolic Steroids in Sport and Exercise |isbn=978-0-88011-786-9 |url=https://books.google.com/?id=I7-D2jH-OJ4C&pg=PA3 |chapter=Source of Anabolic Steroids |publisher=Human Kinetics |location=Champaign, Ill.}}</ref><ref>{{cite web |last=Black |first=Terry |title=Does the Ban on Drugs in Sport Improve Societal Welfare? |publisher=Faculty of Business, Queensland University of Technology |year=1996 |url=http://irs.sagepub.com/cgi/content/abstract/31/4/367 |accessdate=2007-04-24}}</ref> These steroids are usually manufactured in other countries, and therefore must be [[smuggling|smuggled]] across international borders. As with most significant smuggling operations, [[organized crime]] is involved.<ref name=mafia>{{cite book |url=https://books.google.com/?id=2w-oAl42t5cC&pg=PT183 |page=175 |isbn=978-0-470-83733-7 |chapter=Organized Crime | first = Richard W. | last = Pound | name-list-format = vanc |year=2006 |publisher=Wiley |location=Mississaug, Ontario |title=Inside dope : how drugs are the biggest threat to sports, why you should care, and what can be done about them}}</ref>

In the late 2000s, the worldwide trade in illicit AAS increased significantly, and authorities announced record captures on three continents. In 2006, Finnish authorities announced a record seizure of 11.8 million AAS tablets. A year later, the DEA seized 11.4 million units of AAS in the largest U.S seizure ever. In the first three months of 2008, Australian customs reported a record 300 seizures of AAS shipments.<ref name=kanayama08>{{cite journal |vauthors=Kanayama G, Hudson JI, Pope HG |title=Long-term psychiatric and medical consequences of anabolic-androgenic steroid abuse: a looming public health concern? |journal=Drug Alcohol Depend |volume=98 |issue=1–2 |pages=1–12 |date=November 2008 |pmid=18599224 |pmc=2646607 |doi=10.1016/j.drugalcdep.2008.05.004}}</ref>

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.<ref>{{cite web|url=http://www.gdcada.org/statistics/steroids.htm |title=Steroids |accessdate=2007-09-13 |work=National Institute on Drug Abuse |publisher=GDCADA |archiveurl=https://web.archive.org/web/20070911222757/http://www.gdcada.org/statistics/steroids.htm |archivedate=2007-09-11 |deadurl=no |df= }}</ref> 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.<ref>{{cite web |url=http://www.justice.gov/oig/reports/DEA/a0719/app2.htm |title=The Drug Enforcement Administration's International Operations (Redacted) |date=February 2007 |accessdate=2014-01-02 |work=Office of the Inspector General |publisher=USDOJ }}</ref>

==See also==
{{Portal|Pharmacy and Pharmacology}}
* [[List of androgens/anabolic steroids]]
* [[Selective androgen receptor modulator]]
* [[Antiandrogen]]
* [[Androgen insensitivity syndrome]]
* [[Steroid rosacea]]
* [[Steroid use in Bollywood]]
* [[Bigger, Stronger, Faster]]
* [[Juiced: Wild Times, Rampant 'Roids, Smash Hits & How Baseball Got Big]]
* [[List of androgens/anabolic steroids available in the United States]]

==References==
{{Reflist|colwidth=30em}}

==Further reading==
{{Refbegin}}
* {{cite journal | vauthors = Schänzer W | title = Metabolism of anabolic androgenic steroids | journal = Clin. Chem. | volume = 42 | issue = 7 | pages = 1001–20 | year = 1996 | pmid = 8674183 | doi = | url = }}
* {{cite book | vauthors = Yesalis CE |title=Anabolic Steroids in Sport and Exercise |publisher=Human Kinetics |year=2000 |location= |pages= |doi= |isbn=0-88011-786-9}}
* {{cite book | vauthors = Daniels RC |title=The Anabolic Steroid Handbook |publisher=RCD Books |date=February 1, 2003 |location= |page=80 |doi= |isbn=0-9548227-0-6}}
* {{cite book | vauthors = Gallaway S |title=The Steroid Bible |publisher=Belle Intl |edition=3rd Sprl |date=January 15, 1997 |location= |page=125 |doi= |isbn=1-890342-00-9}}
* {{cite book | vauthors = Llewellyn W |title=Anabolics 2007 : Anabolic Steroid Reference Manual |edition=6th |publisher=Body of Science |date=January 28, 2007 |location= |page=988 |isbn=978-0-9679304-6-6}}
* {{cite book | vauthors = Roberts A, Clapp B |title=Anabolic Steroids: Ultimate Research Guide |publisher=Anabolic Books, LLC |date=January 2006 |location= |page=394 |doi= |isbn=1-59975-100-3}}
* {{cite journal | vauthors = Tygart TT |title=Steroids, the Media, and Youth |journal=Prevention Researcher Integrated Research Services, Inc. |volume=16 |issue=7–9 |date=December 2009 |publisher=SIRS Researcher |url=http://www.tpronline.org/download-free-article.cfm?id=548}}
* {{cite web |url=http://business.highbeam.com/435553/article-1G1-138418723/do-look-ok-question-many-teens-struggle-every-day-and | vauthors = Eisenhauer L |title=Do I Look OK? |publisher=St. Louis Post-Dispatch (St. Louis, MO) |date=Nov 7, 2005 |accessdate=25 Oct 2010}}
* {{cite journal | vauthors = Fragkaki AG, Angelis YS, Koupparis M, Tsantili-Kakoulidou A, Kokotos G, Georgakopoulos C | title = 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 | journal = Steroids | volume = 74 | issue = 2 | pages = 172–97 | year = 2009 | pmid = 19028512 | doi = 10.1016/j.steroids.2008.10.016 | url = }}
* {{cite journal | vauthors = McRobb L, Handelsman DJ, Kazlauskas R, Wilkinson S, McLeod MD, Heather AK | title = Structure-activity relationships of synthetic progestins in a yeast-based in vitro androgen bioassay | journal = J. Steroid Biochem. Mol. Biol. | volume = 110 | issue = 1–2 | pages = 39–47 | year = 2008 | pmid = 18395441 | doi = 10.1016/j.jsbmb.2007.10.008 | url = }}<!--Has relative AR and PR affinities/potencies for a series of AAS and progestogens-->
{{Refend}}

==External links==
* {{Commons category inline|Anabolic-androgenic steroids}}

{{Androgens and antiandrogens}}
{{Androgen receptor modulators}}
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