Anabolic steroid

• 1. Introduction

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  Anabolic steroids sit at the intersection of medicine, sport, and controversy in ways few drug classes can match. In the 1930s, three competing research teams, backed by pharmaceutical companies in the Netherlands, Germany, and Switzerland, raced to isolate the primary male sex hormone from the testes. That race produced testosterone, a molecule that would go on to reshape athletics, endocrinology, and criminal law across the following century.

  The questions this story raises are not small ones. Who actually uses these drugs, and why? What does long-term use do to the heart, the liver, and the mind? How did a medically synthesized compound travel from burn wards and Olympic weight rooms to a Schedule III controlled substance with a black market spanning the globe? And what does the growing scientific debate about what we even call these drugs tell us about how medicine got here?

• 2. The Race to Testosterone

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  Adolphe Butenandt, a chemist working in Marburg, made the first concrete step in 1931 when he purified 15 milligrams of the male hormone androstenone from tens of thousands of litres of urine. That achievement was remarkable but incomplete. Scientists already suspected a more powerful androgen lurked inside the testes themselves.

  The identification of testosterone came in a May 1935 paper titled "On Crystalline Male Hormone from Testicles (Testosterone)," authored by Karoly Gyula David, E. Dingemanse, J. Freud, and Ernst Laqueur. They coined the name from the stems of testicle and sterol, plus the suffix of ketone. The chemical synthesis followed in August that same year, when Butenandt and G. Hanisch published a method for preparing testosterone from cholesterol. Only one week after that, Ruzicka and A. Wettstein filed a patent application for their own preparation method.

  Butenandt and Ruzicka were both offered the 1939 Nobel Prize in Chemistry, but the Nazi government forced Butenandt to decline the honor at the time. He did eventually accept the prize after the end of World War II. Clinical trials using either oral methyltestosterone or injected testosterone propionate began as early as 1937, and Adolf Hitler himself, according to his physician, received testosterone derivatives to treat various ailments. AAS were also used in experiments on concentration camp inmates, and later by allied forces attempting to treat malnourished survivors.

• 3. From Medicine to the Weight Room

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  After the war, Soviet and East German sports programs saw in testosterone a tool for producing stronger Olympic athletes, particularly in weightlifting. The U.S. Olympic Team physician John Ziegler watched Soviet weightlifters dominate and then worked with synthetic chemists to build an AAS that would retain muscle-building power while reducing the masculinizing side effects. The result was metandienone, which Ciba Pharmaceuticals brought to market as Dianabol. The U.S. Food and Drug Administration approved it in 1958, primarily for burn victims and elderly patients.

  Ziegler prescribed only small doses to athletes, but he soon discovered that those using metandienone developed enlarged prostates and atrophied testes. The drug's off-label users were mostly bodybuilders and weight lifters, groups that would remain central to non-medical AAS use for decades.

  The International Olympic Committee placed AAS on its banned substances list in 1976. A decade later, the committee introduced out-of-competition doping tests, because many athletes had shifted their use to training periods rather than competition windows. AAS remained by far the most commonly detected doping substances in IOC-accredited laboratories for many years. The controversy over Ben Johnson's victory at the 1988 Seoul Olympics eventually drove the U.S. Congress to act, adding AAS to Schedule III of the Controlled Substances Act in the Anabolic Steroids Control Act of 1990.

• 4. Medical Purposes, Carefully Weighed

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  Since their synthesis in the 1930s, physicians have drawn on AAS for a range of conditions. Bone marrow stimulation for hypoplastic anemias caused by leukemia, kidney failure, or aplastic anemia was for decades a primary application. Pediatric endocrinologists have used them for children with growth failure, though the availability of recombinant growth hormone, which carries fewer side effects, has made AAS a secondary option.

  Oxandrolone has a well-established record improving both short-term and long-term outcomes for people recovering from severe burns. Methyltestosterone is used in delayed puberty, hypogonadism, cryptorchidism, and erectile dysfunction in males, and in low doses for certain menopausal symptoms in women. Testosterone is used in masculinizing hormone therapy for transgender men and other transmasculine people, producing changes including deeper voice, increased bone and muscle mass, and alleviation of gender dysphoria.

  A 2006 placebo-controlled trial of low-dose testosterone supplementation in elderly men with low testosterone levels found no benefit on body composition, physical performance, insulin sensitivity, or quality of life. That finding underscores the distance between documented therapeutic gains in specific conditions and broader assumptions about what these compounds can do. Nandrolone decanoate carries specific approval for osteoporosis in postmenopausal women, though the virilizing side effects have limited actual use for that purpose. Researchers also continue to investigate testosterone derivatives as potential male hormonal contraceptives, an application still described as experimental.

• 5. Who Actually Uses Them

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  Between one million and three million people in the United States, roughly one percent of the population, are thought to have used AAS. Studies consistently find that most users are not competitive athletes. Research shows AAS users in the U.S. tend to be mostly middle-class men with a median age of around 25 who are noncompetitive bodybuilders using the drugs for cosmetic purposes.

  A survey found that 78.4% of steroid users were noncompetitive bodybuilders and non-athletes. A 2007 study found that 74% of non-medical AAS users had completed post-secondary education, and that this group had higher employment rates and higher household income than the general population. Non-medical AAS use among college students was at or below one percent in available studies, though the estimated prevalence among U.S. high-school students may be as high as 2.7%.

  Among 12- to 17-year-old boys, steroid use reportedly jumped 25% from 1999 to 2000, with 20% citing appearance rather than sports performance as the motivation, according to a study by insurer Blue Cross Blue Shield. Users tend to research their drugs more thoroughly than users of other controlled substances, but the sources they consult most often include friends, non-medical handbooks, internet forums, and fitness magazines, channels that can carry inaccurate information. A 2007 study found that 99% of non-medical AAS users felt the public held an exaggerated view of side effects, and 92% believed the medical community lacked adequate knowledge of non-medical use. A substantial majority also reported distrust of their own physicians, and 56% had not disclosed their use.

• 6. The Body Under Pressure

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  Long-term or high-dose AAS use produces changes across nearly every organ system. The cardiovascular effects are among the most serious. Alterations in the structure of the left ventricle, including enlargement and thickening of its walls, impair the heart's ability to contract and relax, reducing the volume of blood ejected with each beat. Possible consequences include hypertension, cardiac arrhythmias, congestive heart failure, heart attacks, and sudden cardiac death. AAS also cause harmful shifts in cholesterol levels, raising low-density lipoprotein while lowering high-density lipoprotein, and accelerating atherosclerosis.

  The kidneys face separate dangers. A study found that nine out of ten steroid-using bodybuilders developed focal segmental glomerulosclerosis, a form of scarring within the kidneys. The damage resembled that seen in morbidly obese patients but appeared to be even more severe. Oral AAS, particularly those modified through 17-alpha alkylation, carry significant liver risks; estimates of hepatotoxicity rates from different studies range from one to seventeen percent with prolonged use. The condition peliosis hepatis has been increasingly recognised in AAS users.

  In adolescents, AAS can prematurely close the growth plates in bones, stunting adult height at high doses. For women and girls, the masculinizing effects of AAS, including irreversible voice deepening, can be permanent. When taken during pregnancy, AAS can cause male features in female fetuses and female features in male fetuses. The World Health Organization's International Agency for Research on Cancer classifies AAS under Group 2A: probably carcinogenic to humans.

• 7. The Mind and the Muscle

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  A 2005 review published in CNS Drugs concluded that significant psychiatric symptoms, including aggression and violence, mania, and less frequently psychosis and suicide, have been associated with steroid abuse. Of 53 bodybuilders who had used AAS, 27, or 51%, reported unspecified mood disturbance.

  Research by Cooper, Noakes, Dunne, Lambert, and Rochford found that AAS-using individuals were more likely to score higher on borderline personality profiles at 4.7 times the rate of non-users, antisocial profiles at 3.8 times, paranoid profiles at 3.4 times, schizotypal profiles at 3.1 times, and histrionic profiles at 2.9 times, among others. A 2008 study on a nationally representative sample of young adult males in the U.S. found an association between AAS use and involvement in violent acts, even after accounting for prior violent behavior and use of multiple substances.

  High concentrations of AAS comparable to those sustained by many recreational users have been shown to produce apoptotic effects on neurons, raising the possibility of irreversible neurotoxicity. Dependence and withdrawal have been documented among weightlifters and bodybuilders who took supraphysiologic doses over extended periods, though no evidence links dependence to medically supervised therapeutic use. The DSM-IV guidelines for personality disorders exclude patterns caused by the direct physiological effects of a substance, which means users may receive inaccurate diagnoses from psychiatrists unaware of their AAS use.

• 8. A Debate Over the Name Itself

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  David Handelsman has argued in multiple publications that the terms "anabolic steroid" and "anabolic-androgenic steroid" are obsolete and should be abandoned entirely. His core objection is that the pharmaceutical industry originally promoted the idea of separable anabolic and androgenic effects in the mid-20th century to justify developing agents that could build muscle without masculinizing women and children. That effort was abandoned by the 1970s after the discovery that a single androgen receptor mediates the effects of AAS in both muscle and reproductive tissue.

  The original test for separating anabolic from androgenic effects, known as the Hershberger assay, measured changes in the levator ani muscle against changes in the rat ventral prostate. Handelsman has characterized this as a flawed model using an unrepresentative muscle. In practical terms, all AAS have essentially similar effects through the androgen receptor, even if some vary in potency in certain tissues like skin, hair follicles, and the prostate based on their susceptibility to reduction by the enzyme 5-alpha reductase.

  Handelsman also notes that the term anabolic steroid is easily confused with corticosteroids, a pharmacologically separate class. He proposes that all these compounds simply be called androgens. The term anabolic steroid can be traced back to at least the mid-1940s, when it described a then-hypothetical testosterone derivative with muscle-building effects and minimal masculinizing action. Norethandrolone, synthesized in 1953 at G. D. Searle and Company, was found in 1955 to have similar anabolic activity to testosterone but only one-sixteenth of its androgenic potency, making it the first compound described as the first anabolic steroid. Whether the label that grew from that discovery still serves science accurately remains an open question.