Anabolic Steroid Abuse Research Articles

Progressive idiopathic bilateral striato-pallido-dentate calcinosis (Fahr's disease) in a person with anabolic steroid abuse

A 33-year-old male black student suddenly died during a basketball game. His previous medical history, including his neurological status, was unremarkable, but he was known to take anabolic steroids for several years. At autopsy, the cause of death was due to a fresh myocardial infarction. On neuropathological examination, there was extensive bilateral symmetrical calcification involving the basal ganglia as well as the dentate nuclei and the white matter of the cerebellum (Fahr's disease). A possible correlation between anabolic steroid-induced hypercalcemia and brain calcification is discussed.

Anabolic-androgenic steroids induce apoptotic cell death in adult rat ventricular myocytes.

We tested whether exposure to anabolic-androgenic steroids (AASs) would induce apoptosis in adult rat ventricular myocytes in vitro. Myocytes were exposed to stanozolol (STZ), testosterone enanthate (TE) and testosterone (T) (0.1 micromol/L, 1 micromol/L, 10 micromol/L, and 100 micromol/L) for 20 h. The percentage of myocytes undergoing apoptosis was determined by terminal deoxynucleotidyl transferase-mediated nick end labeling (TUNEL) and was found to be increased when compared to control myocytes at STZ 10 micromol/L 12 +/- 2% (mean +/- SD), STZ 100 micromol/L 42 +/- 3%; TE 1 micromol/L 11 +/- 2%, TE 10 micromol/L 21 +/- 3%, TE 100 micromol/L 62 +/- 2%; T 10 micromol/L 11 +/- 2%, T 100 micromol/L 40 +/- 3% (P < 0.001 vs. CTL 2 +/- 2%). The STZ-, TE- and T-induced dose-dependent apoptotic cell death was corroborated by a significantly increased DNA laddering in myocytes exposed to STZ and T > or = 10 micromol/L and TE > or = 1 micromol/L. Notably, STZ, TE, and T exposure markedly increased the expression of the pro-apoptotic oncogene Bax-alpha, as assessed by reverse transcription-polymerase chain reaction. Taken together, these results clearly show for the first time that AASs induce apoptotic cell death in a dose-dependent manner. This finding may have important implications in understanding the pathogenesis of ventricular remodeling, cardiomyopathy, and sudden cardiac death associated with AAS abuse.

Ventricular thrombosis and systemic embolism in bodybuilders: etiology and management

Increased thrombogenicity and acute embolism are well-recognized complications of chronic anabolic steroid abuse. The following cases highlight such dangers in steroid-enhanced bodybuilders who developed intracardiac thrombosis that subsequently embolized. Systemic anticoagulation and surgical thrombectomy constituted the mainstay treatment. This represents the first report of such devastating cardiovascular complications after anabolic steroid abuse and their management.

Combined cardiac effects of cocaine and the anabolic steroid, nandrolone, in the rat

Despite reports of an increase in the incidence of simultaneous cocaine and anabolic steroid abuse, potential adverse interactions between these two drugs on the cardiovascular system are largely unquantified. Cocaine has been reported to induce coronary vasoconstriction, cardiac arrhythmias and conduction delays. Anabolic steroids have been associated with cardiac hypertrophy and hypertension. Utilising both in vivo (radiotelemetry) and in vitro (isolated Langendorff-perfused heart) techniques, our aim was to determine whether anabolic steroids cause cardiac hypertrophy and alter cardiac function, and consequently alter the response of the heart to cocaine. It was found that 15 days of treatment of rats with nandrolone decanoate (20 mg/kg, s.c.) was not sufficient to cause hypertrophy, alter cardiac function or the spread of electrical activity through the heart. However, nandrolone pretreatment was found to significantly potentiate the heart rate response to cocaine (45 mg/kg, i.p.) in vivo. This study indicates that nandrolone significantly elevates the heart rate response to high dose cocaine without changing heart morphology. The mechanism of this interaction remains uncertain.

Effects of the androgenic anabolic steroid, nandrolone decanoate, on adrenocorticotropin hormone, corticosterone and proopiomelanocortin, corticotropin releasing factor (CRF) and CRF receptor1 mRNA levels in the hypothalamus, pituitary and amygdala of the rat

There is increasing abuse of androgenic anabolic steroids (AAS) by non-athletes. AAS abuse has been associated with psychiatric symptoms such as mania, major depression and aggression and the development of dependence. Little is known about the effects of AAS on hypothalamic-pituitary-adrenal axis function or corticotropin releasing factor, which may be involved in mediating some of the psychiatric symptoms associated with AAS abuse. Male Sprague–Dawley rats received one daily intra-muscular injection of the AAS nandrolone decanoate (ND, 15 mg/kg) or vehicle for 3 days. Animals were sacrificed either 1 h or 24 h after the last injection, brain regions dissected and trunk blood collected. Corticotropin releasing factor (CRF), CRF receptor1 (CRF-R1) and proopiomelanocortin (POMC) mRNAs were measured with solution hybridization/RNase protection. Circulating levels of corticosterone and adrenocorticotropin hormone (ACTH) were determined using radioimmunoassays. One hour following the last injection, ND significantly increased circulating levels of both corticosterone and ACTH levels. In the amygdala, CRF mRNA levels were unchanged 1 h after the last injection of ND but were significantly reduced at 24 h. The same was found for hypothalamic POMC. No significant AAS effects were observed on: hypothalamic CRF mRNA; POMC mRNA in the amygdala or CRF R1 mRNA in the anterior pituitary.

Increased premature mortality of competitive powerlifters suspected to have used anabolic agents.

Misuse of supraphysiological doses of anabolic steroids is claimed to have serious side effects. The aim of the study was to determine the mortality, and the cause of premature deaths among a group of subjects who are strongly suspected to have used anabolic steroids for a non-medical purpose over several years. The mortality of 62 male powerlifters placed 1st-5th in weight series 82.5-125 kg in Finnish championships during 1977-1982 was compared with the mortality of population controls. The mortality during the 12-year follow-up was 12.9% for the powerlifters compared to 3.1% in the control population. By 1993 eight of 62 powerlifters and 34 of 1094 population controls had died, thus the risk of death among the powerlifters was 4.6 times higher (95% CI 2.04-10.45; p = 0.0002). The causes of premature death among the powerlifters were suicide (3), acute myocardial infarction (3), hepatic coma (1) and non-Hodgkin's lymphoma (1). These findings add to the growing amount of evidence of an association between anabolic steroid abuse and premature death, and support the view that measures to decrease AAS misuse among both competitive and amateur athletes are justified.

The effect on opioid peptides in the rat brain, after chronic treatment with the anabolic androgenic steroid, nandrolone decanoate

In recent years, an increase in abuse of anabolic androgenic steroids (AAS) has been seen among individuals not directly connected to sports. Clinical evidence suggests that abuse of these steroids may result in profound changes in personality, expressed by depressive symptoms, irritability and increased aggression. It is still unknown whether these alterations are related to changes in any particular transmitter system or whether they are persistent or reversible. In this study we focused on AAS effect on the endogenous dynorphin and enkephalin system in the brain. Male rats were given intramuscular injections of the AAS nandrolone decanoate (15 mg/kg), once daily for 2 weeks. The levels of the opioid peptide immunoreactivities (ir) were assessed by radioimmunoassay in two groups immediately after the treatment and in two other groups after additional 3 weeks without any drug treatment (recovery period). The result indicates that chronic AAS treatment increased the activity in the dynorphin B- and Met-enkephalin-Arg 6Phe 7-ir in the hypothalamus, striatum and periaqueductal gray (PAG) compared to controls. In addition, the steroid induced an imbalance between the dynorphin and the enkephalin opioid system in the nucleus accumbens, hypothalamus and PAG. This imbalance remained after the recovery period. Since increased peptide activity was found in brain regions regulating emotions, dependence, defensive reactions and aggression, it was suggested that the actual endogenous opioid systems are involved in previously reported AAS-induced changes in these behaviours.

Estudio de 43 ciclos de tratamiento con anabolizantes esteroideos en deportistas: usos y efectos secundarios

To know the actual abuse of anabolic steroids by amateur athletes in our environment as well as actions and secondary effects resulting from such abuse. Analytical observational study from May 1997 to November 1998. Forty-three therapy courses with anabolic steroids among 39 male athletes were studied. Diet and training were standardized for all participants. A verification was made that the test group started from a basal state. Duration of therapy was 6 weeks and the mean total dose was 2,928 mg. Significant differences were found in the test group regarding basal and post-therapy values for: transaminases (AST: 29.8 vs 45.0 IU/l, p < 0.001. ALT: 32.9 vs 51.4 IU/l, p < 0.01), cholesterol, HDL-cholesterol (31.4 vs 19.7 mg/dl, p < 0.01), LDL-cholesterol (145.9 vs 173.5 mg/dl, p < 0.01), LH (2.1 vs 0.2 U/l, p < 0.001), FSH (3.3 vs 0.4 U/l, p < 0.001), free testosterone (14.4 vs 34.0 pg/ml, p < 0.001), 17-beta-estradiol and arm muscular section (98.8 vs 103.7 cm2, p < 0.001). The inclusion of testosterone in therapy introduced a significant difference with respect to the use of synthetic anabolic agents alone, in total testosterone (4.5 vs 0.9 ng/ml, p < 0.001) and 17-beta-oestradiol, but neither with respect to free testosterone nor arm muscular section. An 84.6% of individuals in the problem group stated to complete two therapy courses in a year. The use of anabolic steroids increases the lean muscular mass. The most relevant secondary effects included: increased transaminase serum levels, change in the lipid profile and suppression of the hypothalamus-pituitary gland-gonad axis. The inclusion of testosterone did not increase the lean muscular mass.

Correlating testosterone and fighting in male participants in judo contests

The role of hormones in human aggression is open to debate, but takes on a new urgency owing to the alarming abuse of androgenic anabolic steroids by some sports participants. In this study, video-taped behavior exhibited by 28 male competitors during a judo fight was assessed to analyze its relation to serum testosterone and cortisol levels measured before and after the bouts. A positive relation between testosterone and offensive behaviors was obtained in the sense that the greater the hormonal titer, the greater the number of threats, fights, and attacks. These findings coincide with the pattern of relationships found using observational scales. Conversely, cortisol also presented positive correlations with some of these behavioral categories but did not moderate the relationship between testosterone and competitive behavior. The present results corroborate and extend earlier findings on the role of these hormones in human behavior, giving support to the view that testosterone can be linked to the expression of competitive aggression.

Temporal effects of testosterone propionate injections on serum lipoprotein concentrations in rats

The chronic abuse of androgenic anabolic steroids, a group of synthetic derivatives of testosterone, to improve athletic performance have demonstrated compromised serum lipoprotein concentrations reflecting an elevated risk for cardiovascular disease. While the detrimental alterations in the lipoprotein profile have been reported consistently for orally administered androgenic anabolic steroids, the reports examining the effects of parenteral administration of testosterone upon the lipid profile remain equivocal. The purpose of this study was to determine whether compromised serum lipoprotein concentrations would be manifest in rats receiving testosterone injections (twice per week) over the time course of 7 wk. Male rats were randomly assigned to either an experimental group (dose per injection, 3 mg x kg(-1) testosterone propionate solubilized in 1 mL of safflower oil) or a control group (injected with an isovolumic amount of safflower oil alone). The effects of the steroid regimen on the serum lipoprotein profiles were followed after 1, 3, 5, and 7 wk of injections. To assess the relative effects of testosterone propionate, testicular mass was determined at the time of sacrifice. Testicular mass (mean +/- SE) was significantly lower (P<0.01) in the experimental group, 3.08+/-0.03 g, compared with that in controls, 3.82+/-0.05 g, by week 3 and continued to decline for the remainder of the steroid regimen, reaching a nadir of 2.70+/-0.01 g at week 5. No significant differences were observed between groups for total serum cholesterol, serum triacylglycerols, or serum low density lipoprotein (LDL)-C at any time point. However, at week 7, serum high density lipoprotein (HDL)-C (mean +/- SE) was significantly lower (P<0.02) in the testosterone treated animals, 32+/-2 mg x dL(-1), compared with that in controls, 47+/-2 mg x dL(-1). As a result, the ratio of total cholesterol to HDL-C (mean +/- SE) significantly increased (P<0.02) by the seventh week in the testosterone treated group, 3.5+/-0.2, versus controls, 2.5+/-0.2. The results suggest that while testosterone propionate injections elicit a reduction in testicular mass within 3 wk, the lipoprotein profile is not altered until week 7. Further, the only compromised parameter under the conditions of this study is the decrease in serum HDL-C.

Large Hepatic Hematoma and Intraabdominal Hemorrhage Associated with Abuse of Anabolic Steroids

To the Editor: Hepatocellular neoplasms, peliosis hepatis, and hepatic necrosis have been reported to be complications of long-term therapy with androgenic anabolic steroids.1 We report a case of a large subcapsular hepatic hematoma and subsequent intraabdominal hemorrhage associated with the abuse of anabolic steroids by a bodybuilder. A 24-year-old man was admitted to the hospital with right-upper-quadrant pain, mild tachycardia, hypertension, and oliguria. The patient reported a 23-month history of polydrug abuse to enhance the results of his bodybuilding exercises. He had been taking mesterolone (50 mg) daily and nandrolone (400 mg), clomiphene (50 mg), and chorionic gonadotropin (1250 IU) . . .

Building the Agenda and Adjusting the Frame: How the Dramatic Revelations of Lyle Alzado Impacted Mainstream Press Coverage of Anabolic Steroid Use

This study addresses the manner in which a dramatic news event can impact mainstream press coverage of a social issue. In late June 1991, football player Lyle Alzado, in haggard condition, appeared on First Person with Maria Shriver and on the cover of Sports Illustrated and attributed his rare form of brain lymphoma to years of anabolic steroid abuse. Though scientific evidence of a relationship did not exist, a series of mainstream press reports did not hesitate in assuming a connection. The study provides an empirical analysis of (a) how a dramatic report in specialized print and broadcast media can build the agenda for mainstream journalism, and (b) how the report can help trigger a change in the way journalists address and frame issues. Methodologically, the study uses log-linear modeling to examine the relationships between a series of categorical variables, thus providing scholars with a framework for future content analyses on the subject.

Lack of effects of anabolic-androgenic steroids on locomotor activity in intact male mice.

Anabolic-androgenic steroid abusers have reported hyperactivity, euphoria, and decreased fatigue, among other behavioral effects. It has been suggested that the effects of these substances on the central nervous system are similar to those of psychostimulants; however, the influence of steroids on general locomotor activity in laboratory animals is not well understood, especially how noncastrated male rodents are affected. In this study, spontaneous locomotor activity displayed by gonadally intact male mice submitted to several experimental conditions was analyzed. Different housing conditions (individual or cohabiting with a female), diverse steroids (testosterone propionate, nandrolone decanoate, and a mixture of both steroids) and single or repeated injections were employed. At 24 hours after the injection (after the three last injections in the case of chronic treatment) spontaneous locomotor activity was registered on an activity recorder for one 15-min. period. No effects due to the treatment were found in almost every experimental condition. These results contrast with the dramatic decreases in activity described for female mice after treatment with such steroids. It seems that in intact males the steroids' influence on spontaneous locomotor activity may be more subtle than expected. These effects seem very complex depending on duration of treatment and specific situations (spontaneous or forced activity) as well as the interaction with endogenous androgen levels.

Anabolic-androgenic steroid use among high school football players.

Eight-hundred seventy-three Indiana high school football players were surveyed to investigate the use of anabolic-androgenic steroids (AAS). Subjects were varsity football players that were randomly selected from 27 high schools throughout Indiana. Out of a possible 1,325 subjects, 873 or 66% participated in the study. Subjects completed a 50 item questionnaire that measured demographic information, perceived use of AAS, reasons for use, and how AAS are taken. The results indicate that 6.3% of Indiana high school football players were current or former AAS users. The average age at time of first use of AAS was 14 years and 15% began taking before the age of ten. Almost half of respondents indicated they could obtain AAS if they so desired, and that other athletes, physicians, and coaches were listed as sources for AAS. Athletic trainers can play a vital role in disseminating accurate information about AAS abuse, including the long-term adverse health risks. These messages should begin with students and athletes as early as the fourth and fifth grades and delivered as often as possible throughout the school years.

Anabolic steroid-induced hepatotoxicity: is it overstated?

There have been numerous reports of hepatic dysfunction secondary to anabolic steroid use based on elevated levels of serum aminotransferases. This study was conducted to distinguish between serum aminotransaminase elevations secondary to intense resistance training and anabolic steroid-induced hepatotoxicity in elite bodybuilders. This was a case-control study of serum chemistry profiles from bodybuilders using and not using anabolic steroids with comparisons to a cohort of medical students and patients with hepatitis. The participants were bodybuilders taking self-directed regimens of anabolic steroids (n = 15) and bodybuilders not taking steroids (n = 10). Blood chemistry profiles from patients with viral hepatitis (n = 49) and exercising and nonexercising medical students (592) were used as controls. The focus in blood chemistry profiles was aspartate aminotransferase (AST), alanine aminotransferase (ALT), gamma-glutamyltranspeptidase (GGT), and creatine kinase (CK) levels. In both groups of bodybuilders, CK, AST, and ALT were elevated, whereas GGT remained in the normal range. In contrast, patients with hepatitis had elevations of all three enzymes: ALT, AST, and GGT. Creatine kinase (CK) was elevated in all exercising groups. Patients with hepatitis were the only group in which a correlation was found between aminotransferases and GGT. Prior reports of anabolic steroid-induced hepatotoxicity based on elevated aminotransferase levels may have been overstated, because no exercising subjects, including steroid users, demonstrated hepatic dysfunction based on GGT levels. Such reports may have misled the medical community to emphasize steroid-induced hepatotoxicity when interpreting elevated aminotransferase levels and disregard muscle damage. For these reasons, when evaluating hepatic function in cases of anabolic steroid therapy or abuse, CK and GGT levels should be considered in addition to ALT and AST levels as essential elements of the assessment.

ANABOLIC-ANDROGENIC STEROID ABUSE AND PSYCHOPATHOLOGY

Anabolic steroid abuse is a significant public health problem. There is evidence from both case reports and empirical studies that abuse of these drugs causes significant psychiatric and medical effects. There appears to be a relationship between increased dosages and severity of psychiatric symptomatology. Research is needed on the role of pathologic personality traits in the initiation and maintenance of anabolic steroid abuse.

Ultrastructural analysis of ruptured tendon from anabolic steroid users

Tendon rupture has been linked with anabolic steroid abuse on the basis of a small number of published case reports. Although experimental data from animal models suggest steroids alter the biomechanical properties of tendon, ultrastructural evidence to support this theory is lacking. Indeed, microscopic analysis of human tendon from steroid users has not previously been reported. In this study, specimens of ruptured human tendon from four patients were biopsied during surgical repair. Two of the subjects were anabolic steroid users, and two subjects were used as nonsteroid-user controls. Ruptured tendon from both groups was examined using electron microscopy. No differences in collagen fibril ultrastructure were seen. We conclude that anabolic steroids did not induce ultrastructural collagen changes that might predispose to tendon rupture in humans.

Growth hormone induced increase in serum IGFBP-3 level is reversed by anabolic steroids in substance abusing power athletes.

Body builders may use growth hormone (GH) and anabolic steroids to increase fitness and muscle mass. GH increases serum concentrations of IGF-I and IGFBP-3. The combined effects of GH and anabolic androgenic steroids on IGFBP-3 and IGF-I levels are not known under authentic substance-abusing conditions. The aim of this study was to investigate this in substance-abusing power athletes. Nine healthy, non-obese and non-competing male power athletes, all aggressive substance abusers, used GH and/or anabolic steroids independently of this study. Blood samples were taken both during and between the drug intake. Sixteen substance non-abusing wrestlers served as controls. Serum IGF-I concentration was measured by radioimmunoassay and the IGFBP-3 concentration was measured by two immunofluorometric assays, one detecting proteolytic fragments of IGFBP-3. The capacity of serum to proteolytically cleave IGFBP-3 was studied by the proteolysis assay. While growth hormone increased the IGFBP-3 and IGF-I concentrations, anabolic steroids decreased the same. Concomitant use of growth hormone and anabolic steroids decreased the IGFBP-3 concentration in five out of six abuse periods in spite of the fact that the IGF-I concentration remained elevated in four of them. However, in two men who were on low calorie diet both the IGF-I and IGFBP-3 concentrations decreased during combined GH/anabolic steroid abuse. No proteolytic fragmentation of IGFBP-3 was observed. Massive abuse of anabolic steroids decreases both the basal and GH-stimulated IGFBP-3 concentrations, whereas its effects on serum IGF-I concentration are variable and affected by low calorie diet. This study demonstrates that detection of GH doping by measuring the IGF-I and/or IGFBP-3 levels has notable confounding factors.

Left Ventricular Wall Thickening Does Occur in Elite Power Athletes with or without Anabolic Steroid Use

Reports on the occurrence of left ventricular wall thickening in resistance-trained athletes have rejected the possibility for this physiological adaptation to occur without concomitant anabolic steroid abuse. Others have concluded short bursts of arterial hypertension that occur with maximal weight lifting are not sufficient to induce left ventricular wall thickening, and left ventricular wall thickness ≥13 mm should not be found in pure resistance-trained athletes. Therefore, we examined 4 elite resistance-trained athletes by two-dimensional echocardiography. In addition, we retrospectively examined the individual left ventricular dimensions of 13 bodybuilders from our previous echocardiographic studies. All 4 elite resistance-trained athletes had left ventricular wall thicknesses beyond 13 mm. One of the elite bodybuilders has the largest left ventricular wall thickness (16 mm) ever reported in a power athlete. Retrospectively, 43% of the drug-free bodybuilders and 100% of the steroid users had left ventricular wall thickness beyond the normal range of 11 mm. In addition, 1 drug-free subject and 3 steroid users were beyond the critical mark of 13 mm. No subjects demonstrated diastolic dysfunction. In contrast to previous reports, we have demonstrated that left ventricular wall thicknesses ≥13 mm can be found routinely in elite resistance-trained athletes. The use of anabolic steroids concomitant with intensive resistance exercise does appear to augment left ventricular size without dysfunction. Anabolic steroids may accelerate left ventricular wall thickening indirectly by increasing strength, thus augmenting the pressor response.

Anabolic-Androgenic Steroid Abuse and Performance-Enhancing Drugs Among Adolescents

Adolescents use a wide variety of drugs and supplements, including anabolic steroids, to improve their sports performance and physical appearance. Prevalence rates for steroid use generally range between 4% and 12% among male adolescents and between 0.5% and 2% for female adolescents. Although the short-term health effects of anabolic steroids such as effects on the liver, serum lipids, reproductive and cardiovascular systems, and moods and behavior have been increasingly studied, the long-term health effects are not well known. Steroid users are more likely to be boys, participate in strength-related sports, and use other illicit drugs. The effects of many other potential risk factors have not been fully elucidated, however. Assessment of anabolic steroid abuse includes physical and mental status and laboratory examinations. Steroid cessation, supportive therapy, and adjunctive pharmacotherapies are all employed in treating steroid abuse and dependence.