Popular Links

Steroid Resources

Steroid Profiles

Using or dealing steroids can land you in jailDangers of Steroid Abuse (health risks, prison, death)

Permit me to begin by saying that I guarantee this article will not be the same repetitive laundry list of steroid horrors you’ve read in the media.  Nor will it be the type of medical journal article that only a small percentage of the population can comprehend.  Whenever a study refers to medical term, disease or procedure that’s unfamiliar I’ll define it in laymen’s terms.  I’m a guy who shoots straight, and wants you to fully understand the science behind the facts regarding several very real dangers faced when using anabolic androgenic steroids (AAS). 

Unfortunately, today’s youth are acquiring and taking AAS without any knowledge of these associated dangers.  Though the short-term adverse physical effects are fairly well known, many users both cycle and supplement AAS in such a way that they simply don’t suffer from negative effects.  It is because of this, that they fail to realize the seriousness of taking these drugs among which are the very harmful long-term physiological & psychological effects, and severe legal consequences. 

Do Kid's Really Use Steroids?

The public answer to this question is always a resounding “yes”, and depending on the source, you might be inclined to think that every 6th through 12th grader can bench press 225lbs.  This is however far from the truth, the benching that is.  According to the Center for Disease Control and Prevention’s (CDC) Youth Risk Behavior Surveillance—United States, the percentage of students who reported lifetime steroid use increased during 1991--2003 (2.7%--6.1%) and then decreased during 2003--2005 (6.1%--4.0%).  Although the declining trend is somewhat comforting, and the figures don’t seem staggering, I assure you they are both misleading.  Let’s crunch the numbers shall we?  The up to minute U.S. Census Bureau reports a total population of just over 301 million people, of which the National Center For Education Statistics estimates 16.5 million or 5.4% are public and private school children between 9th and 12th grade.  Using the CDC’s 4% current lifetime user’s stat, we get an estimated 660,000 students (14 to 17 years of age) who’ve admitted to steroid use as of the year 2005.  But that’s just the beginning, because as any researcher worth his paycheck will tell you, self-reports are notoriously underrepresented.  Sadder still is the fact that our 4% figure though reported in 2006 only used data through early 2005, which was just prior to the many recent professional sports scandals and subsequent resurgence of steroid popularity.  So what do all these numbers and dates mean?  Simply put, “The use of steroids among children is a REALLY BIG PROBLEM!”

Physiological Dangers

Steroid users are also vulnerable to a host of physiological side effects.  A quick review of high school science reminds us that physiology, in short, is the branch of biology that deals with the functions and activities of living organisms.  More specifically, it concerns the organs, tissues and cells, as well as the chemical reactions between them.  Believe me; you don’t want to damage this stuff.  Forget acne and excess body hair, physiological side effects are serious and if left untreated can take your life.

Here are some of the systems that AAS use directly impacts:

Gonad Effects:  Testosterone is essential for the production of sperm, the maintenance of sex drive, erectile potency, and the functioning of the prostate gland and other reproductive structures.  The natural production of testosterone is controlled by another set of hormones called gonadotrophins, which are released from the pituitary gland in the brain.  AAS use can throw this delicate system out of balance resulting in gonadotrophin suppression which can cause testicular atrophy (shrunken testicles), impotence, decreased sex drive, decreased mental and physical activity, infertility due to decreased sperm production and bone loss (1, 2, 3).  The reversibility of these effects varies and is largely dependent on the type, combination, amount and duration of AAS.  Some studies suggest that restoration of hormonal balance after discontinuation of AAS use allows testicular function to return to normal (4, 5), whereas other studies have shown the persistence of hormonal abnormalities even after discontinuation (6, 7).

Skeletal-Muscular Injury:  In spite of the apparent positive effects of AAS on bone and muscle strength, alterations in connective tissue structure induced by AAS therapy have been associated with a weakening of the tendons.  Further evidence suggests that AAS lead to abnormal growth or development (dysplasia) of collagen fibrils, and resulting decrease in overall tendon strength (8).  The risk of triceps tendon rupture, a relatively uncommon injury, is increased with AAS use (9). This problem is often seen with Winstrol a.k.a. Stanozolol usage, and is more pronounced in athletes who participate in sports that require hard starts and stops such as track runners and baseball players.  Though, clinical information on this particular topic is not abundant, the fact that “Winstrol weakens joints”, has long been part of gym lore.

Cholesterol & Lipoproteins:  Both recreational users and patients receiving AAS therapy often experience fluctuations in lipid profiles.  Palatini et al. (10) compared 14 non-AAS using bodybuilders to 10 users.  At study completion, the subjects taking AAS had lower high density lipoprotein (HDL, the good kind) cholesterol and elevated concentrations of low density lipoprotein (LDL, the bad kind).  Similarly, weekly administration of Nandrolone Decanoate a.k.a. Deca Durabolin (200 mg/wk) to 14 hemodialysis patients resulted in a significant decrease in HDL (11).
Simply put, everything we digest passes through the liver twice, and thus contributes to overall liver toxicity.  This is one of the reasons AAS users prefer to inject intramuscularly (into the muscle), a method that averts the first liver pass by going directly into the bloodstream.  The first liver pass filters nutrients in preparation for the bloodstream, while the second serves as a maintenance blood cleansing for continued service.  Oral steroids, known as 17aas, have been modified at the 17th position (hence the nickname) in order to survive the first liver pass in tact.  This allows for their properties to function as intended once inside the bloodstream (12, 13, 14).  Similarly, Testosterone (T) when compared to other AAS tends to have less of an effect on lipid profiles. Thompson et al. (15) in their six week cross-over trial of 11 male weight lifters, found that administration of oral Winstrol at a dose of 6 mg/d resulted in a more adverse lipid profile than a much greater and stronger intramuscular injection of T (200 mg/wk).  Serum HDL levels decreased by 33% during Winstrol treatment compared with a decline of 9% during T administration (15).  Try to commit this liver information to memory for later, when we more fully discuss its system.

Steroid abuse can lead to heart problemsCardiovascular:  Most people are aware of the fact that we study certain animals, mostly monkeys and mice, because of our distinct physiological similarities.  Well, T has been known to induce hypertension in animals for more than 6 decades (16).  Animal studies have shown that AAS increase water and inhibits the conversion mechanism that makes corticosterone, resulting in hypertension in rats (17).  Why does this matter to us?  Because fluid retention, a traditional AAS side effect, is a known contributing factor to hypertension.  Autoradiographic (a kind of X-Ray) and biochemical analyses (cell sample examinations) of the hearts of female rhesus monkeys and baboons indicate that arterial and ventricular heart cells contain androgen receptors, a primary absorption site for AAS.  The presence of this receptor suggests that sex steroid hormones may affect heart function directly, and may explain some of the peculiar differences in heart disease between men and women (18).

Cardiomegaly (an enlarged heart) has been reported in the preclinical studies of AAS (19, 20), and electron microscopy (an imaging technique that makes the picture larger and brighter) shows disintegration and swelling of heart tissue when AAS are given in conjunction with physical training (21).  The risk of arteriosclerosis (a progressive narrowing and hardening of the arteries) may also be increased with AAS use, as shown by an increase in aortic elastin and collagen content (additional and potentially obstructive materials within heart valves) with T administration to male rats.  Another study of male athletes found statistically significant greater cardiovascular risk factors in AAS users than nonusers (22).  Similar to my earlier citation, AAS users in this study also had high total cholesterol/HDL ratio, higher low density lipoprotein levels, and lower HDL levels compared to nonusers.

Hard evidence of cardiovascular morbidity (death caused by heart or artery problems) associated with AAS use, has been difficult to come by.  This is mostly due to the high level of secrecy observed by athletes and bodybuilders who use AAS, but here’s one to grow on.  Even under controlled, medically supervised conditions for patients undergoing therapeutic AAS treatment, there were 16 reported cases of morbid circulatory events (death caused by heart or artery problems) between 1976 and 1993 (23).  Only a true knucklehead would say that’s merely one death a year, plus one.  Remember, these were prescribed drugs and dosages, under the routinely monitored care of licensed, board certified physicians.  Would you care to venture odds for the personal user supervised by his source, a book he purchased, or some booming internet website?  You only have one heart, and nooo-body wants to be placed on that waiting list!

Hepatic:  Okay, let’s revisit our earlier liver information.  Studies have linked various abnormal liver function tests with the use of AAS (24, 25, 26).  Jaundice (the yellowing of the skin and whites of the eyes frequently due to liver problems) occasionally occurs in patients with a previously normal functioning liver due to hepatotoxicity (chemically caused liver toxicity or damage).  Cholestatic hepatitis is a condition where bile cannot flow from the liver to the duodenum (a hollow jointed tube) connecting the stomach to the jejunum (the central of the three divisions of the small intestine) has also been reported with the use of 17aas (27).  If jaundice occurs, it generally develops after 2-5 months of therapy or in AAS users on higher dosages or longer cycles of harsh orals like Dianabol (Methandrostenolone) or Andriol (Testosterone Undecanoate). 

In the majority of the patients, there is an elevation in transaminases (important enzymes in the production of various amino acids), with levels normalizing after a few weeks of discontinuation (28).  In athletes, particular care should be exercised when interpreting liver function tests, because the breakdown of skeletal muscle during intense training can also result in elevated transaminases.  For this reason liver values should not be the sole determinant of AAS abuse (29).  Some steroid users combine harsh and mild orals such as Andriol and Anavar (Oxandrolone), but HIV/Aids research informs us that combinations of this sort can still lead to a concentration of harmful levels. 

Peliosis hepatis (a disorder in which multiple blood-filled cystic spaces randomly ravage the liver) has also been reported with the use of AAS (30, 31, 32, 33).  Lastly, there have been isolated reports of AAS use resulting in carcinomas (any spreading cancer that arises from epithelial or compound layers of cells, that invades surrounding tissues and organs) of the liver (34, 35, 36, 37).  The majority of patients experiencing these conditions were taking compounds for approximately one to seven years, usually at high doses and/or untraditional combinations of 17aas (38, 39, 40, 41).

Psychiatric:  The effects of T on human aggression are controversial.  Anecdotal evidence supports the claim that AAS use results in a typical "roid rage" phenomenon, during which athletes experience an increase in aggression and irritability.  The scientific validity of this assertion is questionable in consideration of the fact that virtually all evidence supporting this behavior is based on either case reports or correlational studies (as byproducts of studies that sought other findings) (42).  However, a few well-controlled studies have demonstrated an association between AAS use and feelings of aggression, alertness, irritability, anxiety, suspiciousness, and other mood extremes (43, 44, 45).  Conversely, these results have been contradicted by further studies that found “absolutely no” evidence of aggressive behavior even when supraphysiological (this big word means amounts greater than normally found in the body) doses of T were administered (46). 

Wang et al. (47) recently reported that T administration to hypogonadal men (those with a defect in the reproductive system) resulted in a significant decrease in anger, sadness, irritability, and nervousness along with an increased sense of well-being, energy, and friendliness.  Cutting through the research here, it appears far more likely that increased aggression is partly a product of the type, amount and combination of substances used, and mostly a product of the user’s personality predisposition.

Steroid abuse can lead to court appearances and costsLaws and Penalties:  Concerns over growing illegal AAS abuse by teenagers, and many of the just discussed long-term effects, led Congress in 1991 to place the whole AAS class of drugs into Schedule III of the Controlled Substances Act (CSA).  Under this legislation, AAS are defined as any drug or hormonal substance, chemically and pharmacologically related to T (other than estrogens, progestins, and corticosteroids) that promotes muscle growth.  The possession or sale of AAS without a valid prescription is illegal.  Since 1991, simple possession of illegally obtained AAS carry a maximum penalty of one year in prison and a minimum $1,000 fine if this is an individual’s first drug offense.  The maximum penalty for trafficking (selling or possessing enough to be suspected of selling) is five years in prison and a fine of $250,000 if this is the individual’s first felony drug offense.  If this is the second felony drug offense, the maximum period of imprisonment and the maximum fine both double.  While the above listed penalties are for federal offenses, individual states have also implemented fines and penalties for illegal use of AAS.  State executive offices have also recognized the seriousness of AAS abuse and other drugs of abuse in schools. For example, the State of Virginia enacted a law that will allow student drug testing as a legitimate school drug prevention program (48, 49).

The International Olympic Committee (IOC), National Collegiate Athletic Association (NCAA), and many professional sports leagues (e.g. Major League Baseball, National Basketball Association, National Football League, and National Hockey League) have banned the use of steroids by athletes, both because of their potentially dangerous side effects and because they give the user an unfair competitive advantage.  Since the now infamous Mark McGuire incident, the IOC, NCAA, and NFL have also banned the use of steroid precursors (e.g. androstenedione) by athletes for the same reason steroids were banned.  The IOC and professional sports leagues use urine testing to detect steroid use both in and out of competition (48, 49).


  1. Jarow JP, Lipshultz LI 1990 Anabolic steroid-induced hypogonadotropic hypogonadism. Am J Sports Med 18:429[Medline]
  2. Kilshaw BH, Harkness RA, Hobson BM, Smith AWM 1975 The effects of large doses of the anabolic steroid, methandrostenolone, on an athlete. Clin Endocrinol 4:537[Medline]
  3. Knuth UA, Maniera H, Nieschlag E 1989 Anabolic steroids and semen parameters in bodybuilders. Fertil Steril 52:1041[Medline]
  4. Holma PK 1977 Effects of an anabolic steroid (metandienone) on spermatogenesis. Contraception 15:151[CrossRef][Medline]
  5. Lukas SE 1993 Current perspectives on anabolic-androgenic steroid abuse. Trends Pharmacol Sci 14:61[CrossRef][Medline]
  6. Turek PJ, Williams RH, Gilbaugh JH, Lipshultz LI 1995 The reversibility of anabolic steroid-induced azoospermia. J Urol 153:1628–1630[CrossRef][Medline]
  7. Martikainen H, Alen M, Rahkila P, Vihko R 1986 Testicular responsiveness to human chorionic gonadotropin during transient hypogonadotropic hypogonadism induced by androgenic/anabolic steroids in power athletes. J Steroid Biochem 25:109[Medline]
  8. Laseter JT, Russell JA 1991 Anabolic steroid-induced tendon pathology: a review of the literature. Med Sci Sports Exerc 23:1–3[Medline]
  9. Stannard JP, Bucknell AL 1993 Rupture of the triceps tendon associated with steroid injections. Am J Sports Med 21:482–485[Abstract]
  10. Palatini P, Giada F, Garavelli G, Sinisi F, Mario L, Michieletto M, Baldo-Enzi G 1996 Cardiovascular effects of anabolic steroids in weight-trained subjects. J Clin. Pharmacol 36:1132–1140
  11. Teruel J, Lasuncion M, Rivera M, Aguilera A, Ortega H, Tato A, Ortuno J 1997 Nandrolone decanoate reduces serum lipoprotein(a) concentrations in hemodialysis patients. Am J Kidney Dis 29:569–575[Medline]
  12. Glazer G, Suchman A 1994 Lack of demonstrated effect of nandrolone on serum lipids. Metabolism 43:204–210[CrossRef][Medline]
  13. Hendler E, Goffinet J, Ross S, Longnecker R, Bakovic V 1974 Controlled study of androgen therapy in anemia of patients on maintenance hemodialysis. N Engl J Med 291:1046–1051[Medline]
  14. Lippi G, Guidi G, Ruzzenente O, Braga V, Adam S 1997 Effects of nandrolone decanoate (Decadurabolin) on serum Lp(a), lipids, and lipoproteins in women with postmenopausal osteoporosis. Scand J Clin Lab Invest 57:507–512[Medline]
  15. Thompson P, Cullinane E, Sady S, Chenevert C, Saritelli AL, Herbert PN 1989 Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA 261:1165–1168[Abstract]
  16. Grollman A, Harrison TR, Williams Jr JR 1940 The effect of various sterol derivatives on the blood pressure of the rat. J Pharmacol Exp Ther 69:149–155[Abstract/Free Full Text]
  17. Brownie AC 1990 The adrenal cortex in hypertension. In: Laragh JH, Brenner BM, eds. Hypertension: pathophysiology, diagnosis, and management. New York: Raven Press; 64–77
  18. McGill Jr HC, Anselmo VC, Buchanan JM, Sheridan PJ 1980 The heart is a target organ for androgen. Science 207:775–777[Abstract/Free Full Text]
  19. Koenig H, Goldstone A, Lu CY 1982 Testosterone-mediated sexual dimorphism of the rodent heart. Circ Res 50:782–787[Abstract]
  20. Morano I, Gerstner J, Ruegg JC, Ganen U, Ganten D, Vosberg HP 1990 Regulation of myosin heavy chain expression in the hearts of hypertensive rats by testosterone. Circ Res 66:1585–1590[Abstract]
  21. Appell HJ, Heller-Umpfenbach B, Feraudi M, Weicker H 1983 Ultrastructural and morphometric investigations on the effects of training and administration of anabolic steroids on the myocardium of guinea pigs. Int J Sports Med 4:268–274[Medline]
  22. Kleiner SM, Calabrese LH, Fiedler KM, Naio HK, Skibinski CI 1989 Dietary influences on cardiovascular disease risk in anabolic steroid-using and nonusing bodybuilders. J Am Coll Nutr 8:109–119[Abstract]
  23. Rockhold RW 1993 Cardiovascular toxicity of anabolic steroids. Annu Rev Pharmacol Toxicol 33:497–520[CrossRef][Medline]
  24. Foss GL, Simpson LS 1959 Oral methyltestosterone and jaundice. Br Med J 1:259–263[Medline]
  25. Arias IM 1962 The effects of anabolic steroids on liver function. In: Gross F, ed. Protein metabolism. Berlin: Springer-Verlag; 434–445
  26. DeLorimier AA, Gordan GS, Lowe RC 1965 Methyltestosterone, related steroids, and liver function. Arch Intern Med 116:289–294[Medline]
  27. Ishak KG 1981 Hepatic lesions caused by anabolic and contraceptive steroids. Semin Liver Dis 1:116–128[Medline]
  28. Wewalka FG 1968 Anabolic steroids in the management of chronic wasting diseases. J Am Med Womens Assoc 23:339–345[Medline]
  29. Kibble MW, Ross MB 1987 Adverse effects of anabolic steroids in athletes. Clin Pharmacol 6:686–692[Medline]
  30. Sweeney EC, Evans DJ 1976 Hepatic lesions in patients treated with synthetic anabolic steroids. J Clin Pathol 29:626–633[CrossRef][Medline]
  31. Shapiro P, Ikeda RM, Ruebner BH, Connors MH, Halsted CC 1977 Multiple hepatic tumors and peliosis hepatis in Fanconi’s anemia treated with androgens. Am J Dis Child 131:1104–1106[Abstract]
  32. McDonald EC, Speicher CE 1978 Peliosis hepatis associated with administration of oxymetholone. JAMA 240:243–244[CrossRef][Medline]
  33. Arnold GL, Kaplan MM 1979 Peliosis hepatis due to oxymetholone: a clinically benign disorder. Am J Gastroenterol 71:213–216[Medline]
  34. Bernstein MS, Hunger RL, Yachnin S 1971 Hepatoma and peliosis hepatis developing in a patient with Fanconi’s andemia. N Engl J Med 284:1135–1136[Medline]
  35. Westaby D, Portmann B, Williams R 1983 Androgen related primary hepatic tumors in non-Fanconi patients. Cancer 51:1947–1952[CrossRef][Medline]
  36. Goodman MA, Laden AM 1977 Hepatocellular carcinoma in association with androgen therapy. Med J Austr 1:220–221
  37. Turani H, Levi J, Zevin D, Kessler E 1983 Hepatic lesions in patients on anabolic androgenic therapy. Isr J Med Sci 19:332–337[Medline]
  38. Ishak KG 1979 Hepatic neoplasms associated with contraceptive and anabolic steroids. Recent Results Cancer Res 66:73–128[Medline]
  39. Soe KL, Soe M, Gluud CN 1994 Liver pathology associated with anabolic androgenic steroids. Ugeskrift Leager 156:2585–2588
  40. Welder AA, Robertson JW, Melchert RB 1995 Toxic effects of anabolic-androgenic steroids in primary rat hepatic cell cultures. J Pharmacol Toxicol Methods 33:187–195[CrossRef][Medline]
  41. Cicardi M, Bergamaschini L, Tucci A, Agostoni A, Trnaghi G, Coggi G, Columbi R, Viale G 1983 Morphologic evaluation of the liver in hereditary angioedema patients on long-term treatment with androgen derivatives. J Allergy Clin Immunol 72:294–298[CrossRef][Medline]
  42. Morton R, Gleason O, Yates W 2000 Psychiatric effects of anabolic steroids after burn injuries. Psychosomatics 41:66–68[Free Full Text]
  43. Parrott AC, Choi PY, Davies M 1994 Anabolic steroid use by amateur athletes: effects upon psychological mood states. J Sports Med Physical Fitness 34:292–298[Medline]
  44. Cooper CJ, Noakes TD, Dunne T, Lambert MI, Rochford K 1996 A high prevalence of abnormal personality traits in chronic users of anabolic-androgenic steroids. Br J Sports Med 30:246–250[Abstract]
  45. Su TP, Pagliaro M, Schmidt PJ, Pickar D, Wolkowitz O, Rubinow DR 1993 Neuropsychiatric effects of anabolic steroids in male normal volunteers. JAMA 269:2760–2764[Abstract]
  46. Tricker R, Casaburi R, Storer TW, Clevenger B, Berman N, Shirazi A, Bhasin S 1996 The effects of supraphysiological doses of testosterone on angry behavior in healthy eugonadal men–a clinical research center study. J Clin Endocrinol Metab 81:3754–3758[Abstract]
  47. Wang C, Alexander G, Berman N, Salehian B, Davidson T, McDonald V, Steiner B, Hull L, Callegari C, Swerdloff RS 1996 Testosterone replacement therapy improves mood in hypogonadal men–a clinical research center study. J Clin Endocrinol Metab 81:3578–3583[Abstract]
  48. Steroid Abuse By School Age Children - A Guide for Parents and School Officials http://www.deadiversion.usdoj.gov/pubs/brochures/steroids/children/
  49. Greater Dallas Council On Alcohol & Drug Abuse - Steroids http://www.gdcada.org/statistics/steroids/scope.htm