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Anabolic Discussion Board I need REAL SCIENTIFIC ifo on anabolic-androgenic steroids (chemists, doctors, ect)
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Author | Topic: I need REAL SCIENTIFIC ifo on anabolic-androgenic steroids (chemists, doctors, ect) | ||
Amateur Bodybuilder Posts: 88 |
I have chossen to write a paper on whether or not juice should be legal. Now personally, i believe that it should be up to the person, but i need real hard core unbiased data on its effects to back the sides for and against. Anyone know any good medical journal findings or reports i could use. Thanks. Tryin to let people the steroid truth. BIGRAND | ||
Amateur Bodybuilder Posts: 88 |
this fell quick Well, im gonna go see what i can find at my Library(i bet it wont be much) | ||
Amateur Bodybuilder Posts: 199 |
There was an interesting post from a bro (that's right, 1911, good post bro), which contained the following article. I cut it to give to a classmate for a community health presentation with a similar goal to yours. Clinics in Sports Medicine Volume 18 � Number 3 � July 1999 Copyright � 1999 W. B. Saunders Company STEROIDS AND STEROID-LIKE COMPOUNDS Jeffrey G. Blue 2 MD John A. Lombardo 1 2 MD 1 Department of Family Medicine, Ohio State University College of Medicine (JAL) 2 Ohio State University Sports Medicine Center (JGB, JAL), Columbus, Ohio Address reprint requests to John A. Lombardo, MD Ohio State University Sports Medicine Center 2050 Kenny Road Columbus, OH 43221 For years, athletes have turned to ergogenic agents in an attempt to gain the edge that could make the difference between winning and losing. Anabolic-androgenic steroids (AASs), with their inherent muscle-building capacity, have been the drug of choice for many of these athletes. Although AASs are still widely used, recent developments have had an impact on their use by athletes. First, the Anabolic Steroids Control Act of 1990 reclassified AASs as controlled drugs, making them more difficult to obtain and use. Second, the United States Dietary Supplement Health and Education Act of 1994 opened the door for many steroid supplements to be easily purchased over the counter. Finally, sports organizations have continued to add more drugs to their lists of banned substances and detection methods for illicit drugs have improved. This article attempts to review the recent data on AASs and other steroid compounds. ANABOLIC STEROIDS AASs are synthetic derivatives of the hormone testosterone. As their name suggests, they have both anabolic and androgenic properties. It is the anabolic effects, such as anticatabolism, increased skeletal muscle mass, and increased aggressiveness, that are desired by those who use them. The androgenic properties are responsible for many of the undesirable side effects. Testosterone is the primary and prototypical AAS hormone. It is produced endogenously and is responsible for the normal growth and development of the male sex organs and for maintenance of secondary sex characteristics. These effects include the growth and maturation of the prostate, seminal vesicles, penis, and scrotum; development of male hair distribution, such as facial, pubic, chest, and axillary hair; laryngeal enlargement; vocal cord thickening; and alterations in body musculature and fat distribution. [68] AASs are produced synthetically and have their base steroid structure altered to minimize the adverse side effects. The actions of AASs are similar to those of male sex hormones and can cause serious disturbances of growth and sexual development if given to young children. AASs can suppress the gonadotropic functions of the pituitary and may exert a direct effect on the testes. History That castration results in the loss of certain secondary male sex characteristics has been known for centuries. Early scientists proposed a neurologic explanation as the mechanism of action. In 1849, Berthold [50] experimented with cockerels and provided the first inkling as to the cause of these changes. Removal of the testicles from these birds caused comb shrinkage and loss of color and sexual function. Reimplantation of the testicles into the abdomen, however, prevented this regression. The results were correctly interpreted that the testis secreted a substance into the blood to regulate the development and maintenance of the male characteristics. From this work, the field of endocrinology was born as well. The first active extract of testis was not prepared until 1927. Shortly thereafter, in 1929, a similar type of activity was found in men's urine, which was followed in 1931 by the isolation of a pure substance, androsterone. A substance with the properties of the testis extract was synthesized in 1935 and proved to be identical to a pure substance, testosterone, obtained almost simultaneously from testis extract. Testosterone was found to influence the growth, development, and function of practically every organ in the body. Chemically synthesized steroids and endogenously modified steroids were found to have different effects on biologic tissue than testosterone. During the late 1940s and early 1950s, an attempt was made to synthesize a steroid compound that would be anabolic without exhibiting the unwanted androgenic side effects. In 1955, AASs with less, but still some, androgenic properties were developed. Today, no purely anabolic steroids are available. All steroids developed to date have some propensity to show androgenic effects. [50] Mechanism of Action AASs exert their main effect by increasing protein synthesis in skeletal muscles and inhibiting catabolic processes. The exact nature of the anabolic action on muscle is currently unclear but likely involves effects exerted through the androgen receptor and other lesser well-known mechanisms. AASs a can be taken orally or parenterally. After an AAS is administered orally, a rapid increase occurs in its concentration in the blood over the following few hours. Excretion of the compound and its metabolites usually takes several days to completely pass through the system. Parenteral preparations, such as microcrystal suspensions, implants, and ester solutions in vegetable oil, are absorbed slowly. The absorption of esters from the site of injection is a logarithmic process and depends on the nature of the ester concerned. The longer the fatty acid chain is in the ester, the slower the absorption rate. The rate of absorption is important regarding the duration of the action and is also relevant for the compound's pharmacodynamic pattern. [102] Once in serum, AASs bind with high affinity to sex hormone-binding globulin and with low affinity to albumin. A small amount, approximately 1% to 2%, is free. The free and albumin-bound portions represent the biologically active hormones. Metabolism of AASs takes place mainly in the liver and involves reduction, hydroxylation, and the formation of conjugates. The enzymes that bring about these changes and the metabolic pathways involved are similar to endogenous steroids. Testosterone is metabolized in the liver to various 17-keto steroids through two different pathways, and the major active metabolites are estradiol and dihydrotestosterone (DHT). DHT binds with greater affinity to sex hormone-binding globulin than does testosterone. In reproductive tissues, DHT is further metabolized to 3-alpha and 3-beta androstenediol. In many tissues, the activity of testosterone seems to depend on reduction to DHT, which binds to an androgen receptor in the cytoplasm. The steroid-androgen receptor complex is transported to the nucleus, where it initiates transcription events and cellular changes related to androgen action. At the cellular level, AASs can affect mitochondrial and sarcotubular enzymes in skeletal muscle, and these effects seem to be muscle-type specific. In fact, AAS may have deleterious effects on muscles of the respiratory system, decreasing capillary density and cause swelling and disruption in mitochondria. [91] Do They Work? At therapeutic dosages, AASs enhance neither muscle strength nor competitive performance. Endogenous androgen secretion is inhibited, and the net effect is negligible. The dosages taken by athletes and bodybuilders are 10-fold to 50-fold greater than are the therapeutic dosages and give rise to hyperandrogenic conditions. Although this improves endurance, strength, and muscle development, at the same time a hormone disturbance is developed, with a variety of consequences. Early studies on AASs were of poor quality and had mixed results. Athletes believed that AASs worked and continued to use them despite the lack of quality medical research supporting their efficacy. Criticisms from the medical community about AASs not being efficacious only further distanced the athletes who used them. A few well-controlled studies have been published supporting the anabolic role of AASs. In a meta-analysis of the studies from 1966 to 1990 assessing the effects of AASs on human muscle strength, 30 studies were reviewed in which subjects received more than one dose of the study steroid and in which changes in muscular strength were measured. Of the 30 studies, 14 were determined to be of poor quality. The remaining studies showed that AASs might slightly enhance muscle strength in previously trained athletes. No firm conclusions were made concerning the efficacy of anabolic steroids in enhancing overall athletic performance. Of note, most studies used low steroid dosages, and the authors recommended that the results should not be generalized to athletes using megadose regimens. [24] More recent evidence supports the view that supraphysiologic doses of anabolic steroids do have a definite, positive effect on muscle size and muscle strength. In a study of 43 healthy men, the group receiving injections of testosterone enanthate showed an increase in strength and muscle size compared with a control group receiving placebo. Changes in strength and muscle size were even more pronounced in the group receiving the steroid combined with strength-training exercises. [6] An examination of cellular changes induced by AASs showed that needle biopsies from 13 experienced male bodybuilders treated with AASs for 8 weeks had an increase in muscle fiber cross-sectional area. No significant changes were found in fibers, capillary ultrastructure, or capillary supply. [54] Whether or not scientific evidence supports the efficacy of AAS use, many athletes believe they do work and enhance their performance. Athletes using AASs report changes in muscle size, strength, and density, faster recovery from workouts and injuries, as well as increases in enthusiasm and aggression. [2] How Are They Used? AASs can be taken orally or injected. A typical dosage is approximately 250 to 3200 mg/wk, and users often "stack," or use more than one AAS at a time to achieve these doses. Athletes also "pyramid" their doses, referring to the pattern of changing dosages. Injectable and oral preparations are used in cycles that typically last 4 to 12 weeks. [26] Injection is a popular route of administration, and most users inject themselves, although some allow friends to do it for them. [52] Classification The use and abuse of AASs throughout the 1980s had escalated such that in 1990 the United States Congress enacted the Anabolic Steroids Control Act requiring that anabolic steroids be added to Schedule III (nonnarcotic) of the Controlled Substances Act. This action placed AASs in the company of other controlled substances, such as amphetamines, barbiturates, and narcotics. Prevalence Many recent epidemiologic studies have been conducted to determine the current usage patterns of AAS use in the United States. In a study of 1881 adolescents in Georgia, 6.5% of boys and 1.9% of girls reported using AASs without a doctor's prescription. Of ninth-grade students in that study, 5.4% of boys and 1.5% of girls reported using AASs. [23] In Arkansas, among 1492 adolescents, 7.6% of male adolescents and 1.5% of female adolescents admitted AAS use. [51] In Denver, Colorado, 6930 high school students were surveyed, and the prevalence of AAS use was 4.0% for male adolescents and 1.3% for female adolescents. AAS use was slightly higher in sports participants than nonparticipants. The mean age of starting AASs was 14 years. [98] Among 4722 Nebraska students in grades 7 to 12, 2.5% reported having used AASs in the preceding 30 days. A total of 4.5% of all of the male adolescents were steroid users, versus 0.8% of the female adolescents, and 73% of AAS users participated in school sports. Students who participated in school-sponsored sports were more likely than nonparticipants to use AASs. [87] In a large study by the Centers for Disease Control and Prevention, of 12,272 9th- through 12th-grade students, the prevalence of AAS use was found to be 4.08% among male adolescents and 1.2% in female adolescents. [22] In one of the largest cross-sectional studies of AAS use, 32,594 people aged 12 years and older living in households in the United States participated in the 1991 National Household Survey on Drug Abuse. Investigators estimated that more than 1 million current or former AAS users exist in the United States, with more than half of the lifetime user population being 26 years of age or older. More than 300,000 individuals used AASs in the past year, and 0.9% of males and 0.1% of females used AASs at least once in their lifetime. The median age of first use of AASs for the study population was 18 years. In 12- to 17-year-olds, the median age of initiation was 15 years. [109] Outside of the United States, fewer studies on the extent of AAS use are available, but prevalence rates are similar. In one survey of 16,119 Canadian students in the sixth grade and above, 2.8% reported using AASs in the year before the survey. Of those taking such drugs, 29.4% reported that they injected them. [64] In Great Britain, the statistics are similar to that in the United States. In a survey of 687 students at a college of technology, 4.4% of the men and 1.0% of the women used AASs. Of the users, 56% had first used AASs at age 15 years or less. AAS users were more likely to be male, less than 17 years of age, and participating in bodybuilding, weightlifting or rugby. [106] In another survey of 1667 workout-facility users, the lifetime prevalence of AAS use was 9.1% in men and 2.3% in women, and current use was 6% in men and 1.4% in women. The type of gym surveyed was related to AAS use, with three of the gyms reporting no use and one with 46% use. [52] In a study of 13,355 Australian high school students, 3.2% of male and 1.2% of female adolescents reported using AASs at some point in their lives, and 1.7% of male and 0.4% of female adolescents had used AAS in the previous month. [38] Among 2742 high school students in Uppsala, Sweden, 2.7% of male and 0.4% of female adolescents used doping drugs at some time in their lives. In this study, knowledge of how to get doping drugs far exceeded use, and the main reasons for using doping drugs were to improve appearance and to enhance performance in sports. [48] In Falkenberg, Sweden, 1383 students had a prevalence of AAS use of 5.8% among males. Among 15- to 16-year-old male adolescents, misuse of AASs was as high as 10% and of these, 50% also injected the drugs. [72] In a study of doping practices among athletes in Italy, 1015 Italian athletes and 216 coaches, doctors, and managers were surveyed. A total of 30% of athletes, managers, and coaches and 21% of doctors indicated that drugs or other doping practices could enhance athletic performance. A total of 62% of athletes who acknowledged doping reported pressure to do so from coaches and managers. According to more than 70% of athletes, access to illegal substances was not difficult. [85] Interestingly, among elite players of Australian Rules football, drug doping is not a problem. The results of 900 randomized, unannounced, prospective urine testing over 6 years showed no positive results for AASs, diuretics, caffeine, or peptide hormones. The low incidence of drug doping was believed to be the result of the fact that no doping method is considered to be of value to Australian Rules football. Also, an educational program is run by football authorities, and random testing for drugs occurs both during the season and off-season. [39] Although AAS use has decreased somewhat among adolescents, many still use them. A long-term comparison of AAS use from 1989 to 1996 indicated that use among male and female adolescents had decreased significantly. For female adolescents, the low point in lifetime steroid use was reached in 1991. Among male adolescents, after declining sharply between 1989 and 1991, steroid use has generally been stable since 1991. Based on the 1995 estimates of high school students and Youth Risk and Behavior Surveillance System data, approximately 375,000 male adolescents and 175,000 female adolescents in public and private schools in the United States used AASs at least once in their lives. [108] Finally, in considering the prevalence of AAS use, self-reporting may be inadequate to differentiate reliably between users and nonusers. In a study designed to determine the validity of self-reporting of AAS use among weightlifters, self-reporting was compared with assay results of simultaneous urine samples from 48 male weightlifters. The sensitivity of self-reporting in the detection of urinary AASs was 74%, and specificity was 82%. In addition, 22 of 23 participants who declared current use had at least one undeclared AAS identified in their urine; however, 15 participants reported at least one drug that was not detected in the urine. Furthermore, 3 of 17 declared nonusers had objective evidence of steroids in their urine. [27] User Profile The appetite for AASs has been created predominantly by our societal fixations on winning and physical appearance. Because AAS use often starts in adolescence, an examination of factors leading to AAS use during this time period is important so that interventions can be designed to decrease use in the future. Use of AASs may start quite early in life--as early as junior high school. In one survey of seventh-grade students, 4.7% male students and 3.2% of female students admitted to using steroids. The typical adolescent AAS user is likely to be engaged in strength training [22] and may know less than nonusers about the effects of AASs on the body. [79] In a study of adolescents in Arkansas, AAS users were more likely than nonusers to approve of AAS use in sports and to believe that AASs use could improve one's health. Knowledge of beneficial side effects and knowing other AAS users were related to AAS use. Information about the effects of AASs rarely came from physicians but often came from peers, and AAS use was strongly motivated by social influences, some knowledge of beneficial effects, and denial of adverse effects. [51] Dissatisfaction with body size and weight is one of the major reasons for using AASs. AAS users have a good body image and are less likely to be satisfied with their current weight. [25] In a study of 3403 male 12th-grade students, 47% reported the desire to gain weight. The perception of AAS use in these adolescents showed that 24% were not sure about the most dangerous health risks associated with AAS use, and 16% did not want to see the use of AASs in sports stopped. [104] In a survey of 404 male weightlifters, nearly three fourths of men who were thinking about using steroids felt "not big enough" compared with 21% not considering using steroids and 38% of steroid users. [9] Users of AAS also have been shown to exhibit greater pathologic narcissism and significantly lower empathy. [78] As a group, bodybuilders may exhibit certain personality traits that put them at risk for using AASs. In one study, compared with control groups of runners and martial artists, bodybuilders reported significantly greater body dissatisfaction, with a high drive for bulk, high drive for thinness, and increased bulimic tendencies than the control groups. In addition, bodybuilders reported significant elevations on measures of perfectionism, ineffectiveness, and lower self-esteem. AAS users reported that the most significant reason for using them was to improve appearance. [7] In another study, compared with nonusers, bodybuilders using AASs believed that the drugs enhanced physical strength, athletic ability, confidence, assertiveness, sexuality, and optimism. [86] Socioeconomic factors may play a role in AAS use. Among Australian high school students, factors associated with AAS use were truancy, unsupervised recreation, speaking only a non-English language at home, aboriginality, higher student income, birth overseas, and low level of social support. [38] In a survey of 1638 Division 1 athletes, those with a lower grade point average were less likely to believe that AASs are a threat to health, are a problem in their sport, or are addictive. Also, they were more likely to believe that AASs enhance performance. [74] A greater percentage of AAS users report family histories of abuse of alcohol and other drugs. [62] Affluence may affect AAS use, too. In a study of high school students, 10.2% of relatively affluent school district male students used AASs compared with 2.8% of less-affluent male students. [107] Another study of 3900 male high school students showed that the prevalence of AAS use is apparently similar in predominantly rural and metropolitan areas, finding no significant difference in the rate of steroid use by school enrollment or by city population size. [105] Other factors found in the typical user may include higher levels of alcohol and marijuana use, hostility, impulsivity, and a win-at-all-costs attitude. AAS users have greater peer tolerance of drug use and less parental influence not to use drugs. They also have less ability to refuse an offer of steroids. [25] The typical AAS user is likely different than the user of other psychoactive substances of abuse and dependence. In a survey of 175 inpatient substance abuse treatment directors, only 19% of centers responding had treated at least one individual using AASs. Facilities that had encountered AAS users reported a prevalence of less than 1% among all admissions. Treatment directors rarely found that AAS use was acknowledged as a problem by users. [11] Polypharmacy Adolescent AAS users in the United States are more likely to engage in injected drug use and the use of multiple drugs. [22] AAS users, whether they participate in sports or not, are more likely to use alcohol, tobacco, and other drugs than were nonusers. [87] High-risk behavior, including injecting the drugs with shared needles, also occurs with AAS users. In a study of 1881 adolescents in Georgia, the frequency of AAS use was associated with the frequency of use in the previous 30 days of other drugs, including cocaine, alcohol, marijuana, cigarettes, smokeless tobacco, and other injectable drugs. 25% of AAS users in the study reported sharing needles for injections. [23] In a study of 3900 male high school students in rural areas, the prevalence of illicit drug use was significantly higher among steroid users than nonusers, and the findings were similar with cigarette use. [105] Among 1422 ninth-grade students, AAS users were more likely to have used cocaine, injectable drugs, alcohol, marijuana, cigarettes, and smokeless tobacco in the previous month. [21] Finally, among 12- to 34-year-old people, AAS use was significantly and positively associated with the use of other illicit drugs, cigarettes in 12- to 17-year-olds only, and alcohol. [109] Of 175 AAS users identified from a cohort of 58,625 college students from 78 institutions, AAS users reported consuming dramatically more alcohol and demonstrated higher rates of binge drinking than nonusers. In addition, a significantly higher percentage of AAS users reported using tobacco, marijuana, cocaine, amphetamines, sedatives, hallucinogens, opiates, inhalants, and designer drugs. [62] In Great Britain, in a study of AAS use at gyms, interviewees took 16 different drugs during their present or previous cycle. [52] In another survey, 86% of users admitted to the regular use of drugs other than AASs for various reasons, including additional anabolic effects, the minimization of steroid-related side effects, and withdrawal symptoms. [26] What You See Is Not Always What You Get AASs are controlled substances in the United States and need to be obtained with a doctor's prescription or through the "black market." As such, these products may contain a variety of other substances. In one study, 15 of 42 products found on the black market in Germany were analyzed by gas chromatography or mass spectrometry and shown to not even contain the expected ingredients. [70] Another study documented two patients hospitalized with clenbuterol poisoning, which occurred with a falsification of the expected AAS. [101] Physician Perceptions Many physicians have limited knowledge about AASs and their effects. The most common medical contact for the AAS user is with the general practitioner--the family physician, pediatrician, or internist. In general, the knowledge in the medical community about AASs is poor, and credibility with AAS users is often lost because of this. A study examining the knowledge of 280 French physicians found the questioned physicians had little knowledge about doping practices in sports. Only 50% thought that doping could concern children, and just 34% had to face this problem within the 12 months before the survey. A total of 83% of them did not feel sufficiently knowledgeable about doping to participate in educational programs. [57] In a survey of 517 family physicians and pediatricians in Texas, just 55% reported being asked about AASs or seeing possible AAS users in their practices during the previous 5 years. High school-aged male adolescents were the subject of 60% of all inquiries, 26% of which were made by parents and were exclusively related to sports. In 62%, football and athletics in general were the most common reasons for inquiry, but 36% of the adolescents were interested in AASs for psychosocial reasons. [84] Among general practitioners in Great Britain, 12% incorrectly believed that medical practitioners are allowed to prescribe AASs for nonmedical reasons. Physician knowledge of which substances are prohibited in sports was poor. [37] Information about the side effects and risks involved with AAS use is usually obtained from peers rather than physicians. In AAS-using adolescents in Colorado, only 18% of students claimed to have been informed about AASs by physicians. [98] Side Effects A wide range of temporary and permanent adverse effects can occur with AAS administration, and many of these have been well documented in the literature. These effects can be short term and last as long as AASs are used, for a short time thereafter, or permanently. They may develop rapidly within several weeks or less or require up to several years of intake. For the most part, the side effects of AAS use are transient and reverse or upon cessation of use. Two groups that are particularly prone to the irreversible effects of AASs are women and children. AASs may cause no side effects at all, or they may cause fatalities as a result of suicides, homicides, liver disease, heart attacks, or cancer. The reported incidence of acute, life-threatening events associated with AAS abuse is low, but the actual risk may be underrecognized or underreported. Some authors argue that the side effects of AASs have been greatly overstated. They contend that the incidence of severe health problems associated with the use of AASs by athletes is low and that the use of moderate doses results in side effects that are largely benign and reversible. [93] The detection AAS users is often difficult. Often, the only visible physical signs associated with AAS use are skeletal muscle hypertrophy, acne, striae, and gynecomastia. [26] The typical side effects seen in adolescent users are quite similar to many of the physiologic changes that occur in normally in puberty. Cardiovascular Over the past several years, evidence has accumulated that associates AAS use with sudden cardiac death, myocardial infarction, altered serum lipoproteins, hematocrit, and clotting factors, hypertensive diseases, and cardiac hypertrophy. Research does not directly link AASs with cardiovascular diseases, but AAS use can significantly increase risk factors for atherosclerotic cardiovascular disease. Even though some experimental data from animals correlates well with the human findings, the adverse cardiovascular effects of AAS use are poorly understood. Possible explanations for the adverse cardiovascular effects seen with AAS use include (1) an atherogenic model involving the effects of AASs on lipoprotein concentrations, (2) a thrombosis model involving the effects of AASs on clotting factors and platelets, (3) a vasospasm model involving the effects of AASs on the vascular nitric oxide system, and (4) a direct myocardial injury model involving the effects of AASs on individual myocardial cells. [63] Lipids. Androgens and estrogens are modulators of plasma lipoprotein metabolism. In general, steroids with estrogenic activity increase plasma levels of high-density lipoproteins (HDL) and reduce levels of low-density lipoproteins (LDL). Those with androgenic activity have the opposite effect. This is consistent with the sex difference in HDL and LDL levels. Triglyceride levels are decreased by the exogenous administration of androgens and are elevated by oral estrogens, contrary to the observed sex difference in this lipid. The impact on the lipids is modified by factors such as dosage and chemical structure, with synthetic steroids having a more pronounced effect than natural hormones. Orally administered hormones have a greater metabolic effect than those given parenterally. The exact effects of these steroids are variable and may depend on the pretreatment lipoprotein pattern and endocrine status. The lipoprotein profile induced by AASs could have a significant impact on the risk for atherosclerosis and coronary artery disease. [68] The lipoprotein changes with AAS use have been studied extensively. In a review of the literature linking AASs to atherogenic changes in serum lipid levels, AASs decreased HDL levels by 52% and elevated LDL levels by 36%. [32] The depression in HDL levels can persist for several weeks after discontinuation of the drug. In a study of male bodybuilders using AASs, the 25% to 27% decrease in HDL was virtually reversed 6 weeks after cessation of drug use. [55] In another study that used only modestly supraphysiologic doses of AASs, the depression of HDL persisted for several weeks as well. [53] Atherogenic changes in the lipid-lipoprotein balance are related to the type of AAS studied. Numerous studies have shown that the 17 alpha-alkylated AASs depress HDL levels by the typical average of 50%. [30] In contrast, the existing studies of 17 beta-esterified AASs have shown mild or absent lipid effects, with HDL levels decreasing 0% to 16%. The potential effects on serum lipids of individual AASs are an important clinical consideration. In a study of the AAS nandrolone, a 17 beta-esterified AAS, 21 men and 3 women were administered the drug for 6 weeks. There was no significant change was found in HDL, LDL, total cholesterol, triglycerides, total cholesterol-to-HDL ratio, or the LDL-to-HDL ratio, and only small trends toward HDL depression and LDL elevation were noted. [33] Although most of the research has been performed on male subjects, females show similar changes. In a study of nine female weightlifters using AASs, a 39% decrease in HDL was observed. [59] In premenopausal women with endometriosis treated with the AAS danazol, HDL decreased 46%, and LDL increased 36%. [16] Blood Pressure. AASs can increase systolic and diastolic blood pressure. These changes are seen at rest and during exercise and during weightlifting and aerobic exercise. [80] The elevation in blood pressure lasts for the duration of action of the AAS and for a short time thereafter. In a study of male bodybuilders, the AAS-induced increase in diastolic blood pressure returned to pre-anabolic values approximately 6 weeks after cessation of drug administration. [55] Structural Effects. AASs may induce changes in the structure of the heart. Cardiac hypertrophy and resulting dysfunction can result. Echocardiographic studies have shown that AASs can induce an unfavorable enlargement and thickening of the left ventricle, which loses its diastolic properties with the mass increase. The changes tended to persist following a short period of drug withdrawal. [17] Competitive heavyweight bodybuilders using AASs were found to have concentric increases in left ventricular wall thickness and decreased ventricular compliance compared with controls. Despite these changes, however, they had no evidence of diastolic dysfunction. [19] In a study comparing AAS users when they were "on-cycle" (using AASs) to when they were "off-cycle" (not using AASs) showed that left ventricular mass and interventricular septum thickness were greater during AAS use. [83] In another study, no significant difference was found in left ventricular diastolic cavity diameter, septal thickness, posterior wall thickness, and myocardial mass between a group of AAS weightlifters and matched controls. [99] The cause of the structural changes is unclear. Endomyocardial biopsy of AAS users has revealed increased fibrosis in the myocardium in some users. [71] Animal studies of the combination of endurance training with AAS use have shown increased activity of lysosomal hydrolytic enzymes in the heart. [97] Thrombosis. Some recent evidence shows that AAS users may be subject to an increased risk for thromboembolism. Such a causative link has been proposed in reports of acute myocardial infarction and stroke in several athletes using androgens. No direct evidence shows that androgens are thrombogenic in humans, however. Indirect experimental data suggests that androgens affect platelet aggregation, coagulation proteins, and the vascular system in ways that facilitate thrombosis. Androgens also increase several anticoagulant and fibrinolytic proteins but have not been shown to protect thrombosis from occurring in high-risk patients. [28] [58] The results of coagulation assays do not support the presence of a hypercoagulable state. If AASs do produce a thrombotic tendency, they may do so through alterations in other hemostatic mechanisms or changes in lipid fractions, or more sensitive coagulation assays may be required for detection. [1] Another effect of AASs is their ability to stimulate the production of red blood cells by enhancing erythropoietin production. Endocrine During exogenous administration of androgens, endogenous testosterone release is inhibited through feedback inhibition of pituitary luteinizing hormone. With large doses of exogenous androgens, spermatogenesis may also be suppressed through feedback inhibition of pituitary follicle-stimulating hormone secretion. The result is the development of hypogonadotropic hypogonadism, characterized by low levels of gonadotropins, suppression of testosterone production, and azospermia. If testosterone is used alone or in combination with synthetic AASs, the circulating levels of testosterone are normal or high. Estrogen levels may be elevated because of the aromatization of testosterone. The level of sex hormone-binding globulin is suppressed. These endocrine parameters are of practical use in evaluating patients misusing androgenic anabolic steroids. [68] The endocrine manifestations concern particularly, but not exclusively, women and children. Signs of virilization, ranging from slight voice disturbances to severe derangement of reproduction, can develop with the use of AASs, and these changes may be permanent. In men, AASs can result in significantly reduced percentages of motile and normally formed sperm. In a study of bodybuilders, sperm levels depended on the duration of AAS use and the period since the last AAS use. In those who had stopped consumption of AASs more than 4 months previously, sperm numbers were in the normal range. Even after prolonged use of extremely high doses of AASs, sperm production may return to normal. [49] Other endocrine effects include gynecomastia, male-pattern baldness, and testicular atrophy. In one study of male bodybuilders, 56% reported testicular atrophy and 52% noted gynecomastia. [52] Older patients using AASs may be at an increased risk for prostatic hyperplasia and prostatic carcinoma. In women, side effects included virilization, menstrual irregularities, clitoral enlargement, and decreased breast size. [52] In a study of nine female weightlifters using AASs, thirtyfold elevations of serum testosterone were noted in the women injecting testosterone. In three of these women, serum testosterone levels exceeded the upper limits for normal male testosterone concentrations. [59] Postmenopausal women treated with nandrolone for osteoporosis had a lower fundamental frequency during speech, a loss of high frequencies, and an increase in voice instability and creakiness. Failure to adapt to the histologic changes in the vocal cords caused the changes. [31] The available data are often inconsistent and inconclusive concerning possible effects of AASs on libido in men and women. They may affect libido differently in men and women. In one study, male AAS users had a significantly higher coital and orgasmic frequency than did comparison athletes. They also reported a significantly higher incidence of erectile difficulties during the past month. [69] Studies of the effects of AASs on libido in women are limited. Other endocrine effects of AASs may include significantly decreased serum T4-binding globulin concentrations and a relative impairment, but still within the normal range, of thyroid function. [18] Hepatic Hepatic alterations are caused almost exclusively by the 17 alpha-alkylated AASs and can range from abnormal liver function tests to life-threatening liver tumors. AASs can cause development of peliosis hepatis, subcellular changes of hepatocytes, hepatocellular hyperplasia, and hepatocellular adenomas. On the other hand, it has not been convincingly proved that AASs can cause development of hepatocellular carcinomas when used in the usual therapeutic doses. Tumors reported as hepatocellular carcinomas caused by AASs are likely benign hyperplastic lesions that regress with withdrawal of the putative agent. The effects of nontraditional combinations and high-dose AASs are not yet known, leaving the possibility of a carcinogenic effect in those cases. [92] Peliosis hepatis is an unusual condition in which the liver is replaced with blood-filled cysts within the hepatic parenchyma. It usually occurs with chronic wasting conditions but has been reported in AAS users, sometimes associated with minimal hepatic dysfunction, but at other times associated with liver failure. It may not be recognized until life-threatening hemorrhage occurs. Withdrawal of the offending agent usually results in a complete disappearance of these lesions. [68] AASs may alter the ultrastructure of hepatocytes without affecting biochemical markers. In a study of male rats given AASs, no elevation of typical liver function tests occurred. Electron microscopic examination of hepatic tissue from treated animals, however, revealed swelling of mitochondria and a marked increase in the number of lysosomes. [36] The capacity of the liver to metabolize drugs may also be altered by high doses of AASs. In rats, AAS use modified the capacity of rat liver to metabolize drugs without affecting classic serum indicators of hepatic function. [82] Musculoskeletal Androgens are responsible for the growth spurt of adolescence and for the eventual termination of linear growth, which is brought about by the fusion of the epiphyseal growth centers. In children, exogenous androgens accelerate linear growth rates but may cause disproportionate advancement in bone maturation. Use over long periods may result in fusion of the epiphyseal growth centers and termination of the growth process. The resulting short stature is permanent. Another possible side effect of AAS abuse is abnormal form and function of connective tissue in athletes who abuse these drugs. AAS use, when coupled with exercise, may lead to dysplasia of collagen fibrils, which can decrease the tensile strength of tendon. Changes in tendon's crimp morphology have also been shown to occur, which may alter the rupturing strain of tendon and the normal biomechanics of the extremities. Given the large forces incurred by power-trained musculature, the integrity of tendinous tissue in these athletes may be at significant risk for compromise if steroids do, in fact, exert a destructive effect. [56] Both systemic AASs and local injections may predispose tendons to rupture. The research supporting these views is mostly from studies on animals. Results of biomechanical tests on rat tendons suggest that AASs produce a stiffer tendon, which fails with less elongation. [66] In another study, rats treated with AASs had Achilles tendons that were stiffer, absorbed less energy, and failed with less elongation. Tendon strength was unaffected, and the effects were entirely reversible upon discontinuation of the offending agent. Light microscopic, electron microscopic, and biochemical analysis were unable to elucidate the cause. [43] Finally, studies in male rats show that enzymes of collagen biosynthesis in muscle and tendon may be transiently affected. [45] Skeletal changes can occur with AAS use. Some AASs have approved indications for the treatment of established osteoporosis by their ability to increase bone density through a stimulation of bone formation. In postmenopausal women, AASs can stimulate type III collagen synthesis. [41] An interesting study in rats given high-dose AASs showed that changes other than increases in bone density can occur. In that study, craniofacial growth was altered, producing overt shape changes, notably a maxillomandibular, anteroposterior jaw discrepancy caused by maxillary excess. [5] Metabolic Androgens promote retention of nitrogen, sodium, potassium, and phosphorus and decreased urinary excretion of calcium. They can increase protein anabolism and decrease protein catabolism. Nitrogen balance is improved only with sufficient intake of calories and protein. They can abolish a negative nitrogen balance brought about by the administration of corticosteroids and antiandrogens and thus possess anticatabolic properties. Nitrogen loss after surgical procedures and following accidental trauma can be significantly reduced by preoperative or postoperative treatment with anabolic agents. [103] In supraphysiologic doses, AASs can create a prediabetic condition. Glucose metabolism is significantly altered and includes peripheral insulin resistance, hyperinsulinemia, and attenuated responses to glucagon. Hypercalcemia was present in 42% of AAS-using male bodybuilders in one study. [46] Skin Acne, oily hair and skin, sebaceous cysts, hirsutism, androgenic alopecia, striae atrophicae, seborrheic dermatitis, and secondary infections, including furunculosis, may occur in persons using AASs. Examination of skin biopsy specimens from persons using AASs demonstrates dramatic hypertrophy of the sebaceous glands. High doses of AASs can increase skin-surface lipids, the cutaneous population of Propionibacteria acnes, and the cholesterol and free fatty acids of the skin-surface lipids. [88] Psychiatric Endogenous testosterone has been linked to aggressive behavior in animals and humans. Studies using moderate doses of exogenous testosterone result in essentially no adverse effects on male sexual and aggressive behavior. In fact, the influence of AASs on psyche and behavior in normal doses is mostly positive, rendering the drugs useful for adjuvant therapy in patients whose general condition is poor, irrespective of the origin; however, investigations and case reports of athletes, usually involving higher doses, demonstrate an association between AAS use and affective and psychotic syndromes and psychological dependence. The psychological and behavioral effects of AAS use are variable. Most are transient and resolve upon discontinuation of the drugs. They seem to be related to the type (17 alpha-alkylated rather than 17 beta-esterified), but not dose, of AASs administered. Typical mental status changes that can occur include symptoms of depression, hostility, aggression, and paranoia. The difficulty in studying the psychological impact of AAS use is caused by the fact that, because of the psychological changes that occur, users often know when they are using AAS. A recent review of the psychological impact of AAS use found only three prospective, blinded studies demonstrating aggression or adverse overt behavior. Investigators estimated that only an extremely small percentage of individuals using AASs likely experience mental disturbances sufficiently severe to result in clinical treatment. Many times, the roles of previous psychiatric history, genetic susceptibility to addictions or mental disorders, environmental and peer influences, and individual expectations were not clearly determined. [4] The most commonly cited psychiatric side effect is aggressiveness, but acute affective and paranoid psychoses have also been reported. Other risk factors, such as abuse of alcohol and other drugs and psychological susceptibility, may contribute to the risk for personality changes or violent behavior that has been attributed to AAS use. AASs have been shown to acutely cause adverse and activating mood and behavioral changes in healthy men. In a placebo-controlled prospective study of 20 men at an inpatient facility, significant increases in positive mood (e.g., euphoria, energy, and sexual arousal), negative mood (e.g., irritability, mood swings, violent feelings, and hostility), and cognitive impairment (e.g., distractibility, forgetfulness, and confusion) occurred in AAS users. An acute manic episode was observed in one subject, and an additional subject became hypomanic. In this study, baseline characteristics, including family psychiatric history or previous drug abuse, did not predict symptom changes. [96] Major mood syndromes--mania, hypomania, or major depression--have been associated with AAS use. Hypomania has been correlated with AAS use, and major depression with AAS discontinuation. In a study comparing 88 athletes using AASs with 68 nonusers, AAS users displayed mood disorders during steroid exposure significantly more frequently than in the absence of steroid exposure and significantly more frequently than did nonusers. [75] AASs are not euphorigenic or mood-altering immediately following administration, as are other illicit drugs, but their use may result in psychological dependence. In a survey of 49 male weightlifters using AASs, 57% reported symptoms consistent with a diagnosis of dependence. Dosage and dissatisfaction with body size were the best predictors of dependent use. [10] In another study, AAS dependence was seen in 12.9% of current users and 15.2% of past users. [60] Aggressive and violent behavior has been linked to AAS use. Although this can be advantageous when training for strength, it can cause problems during daily activities. Adolescents using AASs have been shown to be more likely to carry a weapon and commit assault [20] and vandalism. [109] AAS use has been associated with violent crimes in case reports and may be an uncommon, although occasionally significant, factor in criminal behavior. [14] [17] Wives and girlfriends of AAS users may be at risk for severe injury from users while users are taking the drug. In a study of 23 AAS-using strength athletes and 14 nonusing athletes, AAS users reported significantly more fights, verbal aggression, and violence toward their significant others when using AASs than when not using them. Interestingly, AAS off-drug users did not differ significantly from nonusers in aggressive and violent behavior. [12] The frequency of AAS use among adolescents may be part of a "risk behavior syndrome" rather than an isolated behavior. In a study of 3054 high school students in Massachusetts, the frequency of AAS use was associated with driving after drinking alcohol, carrying a gun, the number of sexual partners within the past 3 months, not using a condom during last intercourse, injury in a physical fight requiring medical attention, history of a sexually transmitted disease, not wearing a helmet on a motorcycle, not wearing a passenger seatbelt, and a suicide attempt requiring medical attention. [65] AAS use is associated with changes in personality, moods, and self-esteem. Significant disturbances are possibly the direct result of AAS use. [13] The fact that nearly all AAS users are also dedicated weight trainers has often been overlooked in studies examining the relationship between AAS use and behavioral change. A triad may exist between AAS use; weight training, and behavioral change, including dependence. In addition, changes frequently attributed to AAS use may also reflect changes resulting from the concurrent use of other substances, such as alcohol, and from dietary manipulation, including food supplements. Weight training and related practices may be potential confounding factors in studies that examine the psychological and behavioral effects of AASs. [3] AAS users are also more likely to use alcohol, tobacco, and other drugs than are nonusers. [87] Sharing of needles to inject AASs is likely to occur. 29.2% of Canadian students using AASs by injection reported sharing needles in the course of injecting. [64] Interestingly, in a study of 21 AAS users contacted at a needle and syringe exchange in Great Britain, none reported engaging in needle sharing. [67] Abusers, who typically inject illicit preparations themselves, are also at risk for hepatitis and HIV. A potential risk for crossover between the misuse of performance-enhancing drugs and the misuse of psychoactive drugs by injection exists. Investigators have reported that some AAS users use illicitly obtained nalbuphine hydrochloride, and this can lead to opioid dependence. [61] Disorders of body image have been reported with AAS use. Both anorexia nervosa and a "reverse anorexia" syndrome, in which men who lift weights regularly believed that they appeared small and weak even though they were actually large and muscular. Reverse anorexia could precipitate or perpetuate the use of AASs in some individuals. In a study comparing 55 AAS-using bodybuilders and 53 nonusing controls, 2.8% of all subjects reported a history of anorexia nervosa--a rate far higher than the 0.02% rate typically reported among US men. Nine subjects, all AAS users, reported reverse anorexia and reported that they declined social invitations, refused to be seen at the beach, or wore heavy clothes even in the heat of summer because they feared that they looked too small. Four even reported that their reverse anorexic symptoms contributed to their decision to start using steroids. [76] Long-Term Complications Although athletes contemplating the use of AASs may correctly perceive their risks for significant physiologic effects to be small if they use the steroids for brief periods of time, many of these same athletes are unaware of the potential for habituation to the use of anabolic steroids. The result may be incessant use of steroids by an athlete who previously considered only short-term use. As we see athletes taking anabolic steroids for more prolonged periods, we are likely to see severer medical consequences. [42] Few studies on the long-term complications of AAS use have been conducted. Some authors argue that, because androgens have been available for more than 50 years with only few reports of serious long-term problems, they are relatively safe. In a study of 16 long-term AAS-using bodybuilders after a 3-month drug-free period, abnormal blood pressure, lipoprotein profiles, and liver-enzyme measurements returned to normal. [40] A recent study of male mice demonstrated a dramatically decreased life span by exposing them for 6 months to the kinds and relative levels of anabolic steroids used by many athletes and body builders. One year after the termination of steroid exposure, 52% of the mice given a high dose of steroids had died compared with 35% of the mice given a low dose and only 12% of the control mice given no exogenous hormones. Autopsy of the steroid-treated mice typically revealed tumors in the liver or kidney, other kinds of damage to these two organs, broadly invasive lymphosarcomas, or heart damage, and usually more than one of these conditions. [8] Drug Interactions Potentially adverse interactions with AASs can occur with concurrent administration of oral anticoagulants and antidiabetic drugs because sensitivity to each of these drugs is increased. Monitoring patients who receive either oral anticoagulants or antidiabetic treatment concurrently with anabolic drugs is particularly important. Commonly Used Anabolic-Androgenic Steroids The AASs commonly used illicitly include nandrolone (Deca-Durabolin), stanozolol (Winstrol), methenolone (Primobolan), tibolone (Livial), and oxandrolone. Other agents more commonly used for medical reasons include testosterone cypionate, enanthate, and undecanoate, and dihydrotestosterone (Transdermal). [68] STEROID SUPPLEMENTS In 1998, the race between two US baseball players to achieve a record number of home runs in one season focused attention on the increasing use of performance enhancing dietary supplements by athletes. The enthusiastic endorsement of such substances by high-profile professional athletes has raised their popularity among teenagers, college athletes, and amateur athletes. [44] These "prohormones," as they are called, are believed to be converted in the body to either testosterone or other similar hormones. Side effects are minimized when small doses are used but can approximate the typical AAS effects when taken in larger doses. Theoretically, these compounds can increase testosterone levels and can cause positive urine drug test results. Little research has been done on the ergogenic properties of these products, including androstenedione, which has been available since the 1930s. Most of the extraordinary claims are based on poorly designed studies from many years ago, and recent evidence is sorely lacking. No evidence shows that any legal supplement can substantially alter performance to date in the same way as illegal drugs. [94] Regulation The United States Dietary Supplement Health and Education Act of 1994 has allowed a wide variety of substances to be sold for human consumption without approval from the US Food and Drug Administration (FDA) as long as they are sold as "dietary supplements" and the product labeling includes no "drug intent." Since then, many commercial steroidal hormone products have become available as so-called "dietary supplements." These are not food products and do not occur naturally in the human food chain, and no foodstuffs can mimic the physiologic or pharmacological consequences evoked by these products. As dietary supplements, these products do not require evaluation for safety and efficacy by the FDA. They do not have to be manufactured in compliance with the FDA's current Good Manufacturing Practices, nor do they have to meet quality control standards expected of approved drugs. [73] Content and purity of these products are not regulated and can vary widely from containing too much of the stated product to none at all. [90] Dehydroepiandrosterone Dehydroepiandrosterone (DHEA) is a hormone that is made in large quantities as the sulfated form (DHEAS) by the adrenal cortex. In humans, serum levels of DHEA and DHEAS are high prenatally, decrease to virtually undetectable levels after birth, increase sharply at puberty, reach high levels during young adulthood, and finally decrease progressively until only negligible levels are left in old age. The decreasing rate for both DHEA and DHEAS is relatively constant at approximately 2% per year. Preliminary studies have demonstrated that DHEA may have a broad range of clinical uses. It has been touted to help burn fat; build muscle mass; boost libido; strengthen the immune system; prevent heart disease, cancer, and non-insulin-dependent diabetes; retard memory loss; help in the treatment of systemic lupus erythematosus; and prevent or slow the progression of Alzheimer and Parkinson diseases, all despite the fact that not one of these benefits has yet been demonstrated in a large, randomized, placebo-controlled clinical trials. Some evidence suggests that higher serum levels of the hormone may even be associated with an increased risk for ovarian and perhaps prostate or other types of cancers. Long-term effects are unknown, and virtually nothing is known about the interactions of DHEA with other drugs. [47] [89] [90] Androstenedione Androstenedione, a potent anabolic steroid, is produced endogenously in small quantities in the adrenal glands and gonads. It is converted in the liver into testosterone, an even more potent androgen. Testosterone is available by prescription only, whereas androstenedione can be easily purchased over the counter. No long-term studies on androstenedione supplementation have been conducted, but that side effects would mirror those of testosterone seems likely. [15] Several athletic organizations, including the International Olympic Committee, the National College Athletic Association, and the National Football League, have banned the use of androstenedione by their members. But finding offenders is difficult because the steroid is not tested for in standard drug tests. Manufacturers of androstenedione claim that the steroid is safe and that it only transiently increases testosterone levels and by only as much as 15%. Users and manufacturers claim that it allows them to build muscle mass quickly and recover rapidly from injury. [44] Other Supplements Other steroidal supplements currently available include androstenediol, norandrostenedione, and norandrostenediol. Even less is known about these substances. Other drugs, such as ephedrine, caffeine, and saw palmetto, are often packaged with supplements to add desired side effects or counteract potential adverse effects. PREVENTION The lack of scientific information has impeded, if not precluded, the formulation of an effective health education strategy. Previously, the scientific community lost credibility with its "stop steroid use" campaigns based on the lack of steroid efficacy in bringing about desired results or on their dire consequences. Teaching models that emphasize only the untoward consequences of anabolic steroids have been shown to be ineffective, even in the short term. [34] The most potent deterrent to the use of steroid drugs by athletes must be the moral issue of fair play and maintaining a "level playing field." [81] A balanced education approach can improve understanding of the potential adverse effects of these drugs. Lectures and handouts of a balanced education program (i.e., potential risks and benefits) increased agreement of high school varsity football players compared with a risks-only (i.e., negative or "scare tactics") presentation. [34] Use of a lecture and a handout to varsity high school football teams increased awareness of the adverse effects of AASs but did not change attitudes toward the use of AASs. [35] Results of a 10-week drug education and prevention program given to Division 1 athletes showed significant improvements in knowledge, attitude related to performance-enhancing drugs and recreational drugs, and perceptions of drug education. At the end of the course, 88% of the participating athletes thought that drug education can be effective in preventing drug abuse among student athletes. [100] Any drug program should include a policy, education program, testing (preferably year-round random testing), discipline for violation of policy, and evaluation and treatment programs. Such a comprehensive program will offer the optimal opportunity for deterring and decreasing drug use. Recent recommendations include a reassessment of the prevention, intervention, and regulatory efforts to reduce steroid use at the local, state, and national levels and to focus these efforts more on female adolescent steroid use. [108] Others make use of the differences between athletes with more intent to use AASs and those who indicated no predisposition to use steroids. Because higher-intent athletes had higher levels of alcohol and marijuana use, these items might be tackled concurrently. These athletes had more hostility; impulsivity; win-at-all-costs attitudes; and, despite similar physical measures, a good body image but were less satisfied with their current weight. These findings underscore the importance of using nutrition and appropriate training as effective alternatives to AASs. Higher-intent athletes had greater peer tolerance of drug use and less parental influence not to use drugs, which implies that a peer-led, small-group format might be important to dispel the perceived peer tolerance. Including a parent-based component, one that emphasizes a disapproval of drug use could also be effective. Higher-intent athletes had less ability to refuse an offer of steroids. The dynamics of turning down steroids may differ from that of other illicit substances so that training in refusal skills specific to steroids is needed. [25] MANAGING PATIENTS Little data suggest how best to follow patients who use supraphysiologic doses of AASs. Common sense suggests that certain evaluations should be considered. Because of the hepatotoxicity associated with the use of 17alpha-alkylated androgens and the possibility of other AASs producing similar, albeit lesser, elevations, liver function tests should be obtained periodically. Because of the changes in lipoprotein patterns and their inherent risks, serum lipids and lipoproteins should be determined. Hemoglobin and hematocrit should be checked periodically for polycythemia. Prostate-specific antigen should be checked in elderly men. Finally, physicians should keep in mind that AASs can cause interference with some laboratory tests. AASs may decrease levels of thyroxine-binding globulin, resulting in decreased total T4 serum levels and increase resin uptake of T3 and T4 . Free thyroid hormone levels remain unchanged, however, and no clinical evidence of thyroid dysfunction has been found. If one is to follow up patients who are using AASs, blood tests should be performed 4 to 6 weeks after the use has been stopped. In this way, abnormal results caused by the presence of AAS are minimized, and more meaningful results can be obtained. 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J Drug Educ 26:159-181, 1996 abstract 101. van der Kuy PH, Stegeman A, Looij BJ Jr, et al: Falsification of Thai dianabol. Pharm World Sci 19:208-209, 1997 abstract 102. van der Vies J: Pharmacokinetics of anabolic steroids. Wien Med Wochenschr 143:366-368, 1993 abstract 103. van Wayjen RG: Metabolic effects of anabolic steroids. Wien Med Wochenschr 143:368-375, 1993 abstract 104. Wang MQ, Yesalis CE, Fitzhugh EC, et al: Desire for weight gain and potential risks of adolescent males using anabolic steroids. Percept Mot Skills 78:267-274, 1994 abstract 105. Whitehead R, Chillag S, Elliott D: Anabolic steroid use among adolescents in a rural state. J Fam Pract 35:401-405, 1992 abstract 106. Williamson DJ: Anabolic steroid use among students at a British college of technology. Br J Sports Med 27:200-201, 1993 abstract 107. Windsor R, Dumitru D: Prevalence of anabolic steroid use by male and female adolescents. Med Sci Sports Exerc 21:494-497, 1989 abstract 108. Yesalis CE, Barsukiewicz CK, Kopstein AN, et al: Trends in anabolic-androgenic steroid use among adolescents. Arch Pediatr Adolesc Med 151:1197-1206, 1997 abstract 109. Yesalis CE, Kennedy NJ, Kopstein AN, et al: Anabolic-androgenic steroid use in the United States. JAMA 270:1217-1221, 1993 abstract [This message has been edited by 1911 (edited October 04, 2000).] ------------------ | ||
Amateur Bodybuilder Posts: 88 |
damn, hello info(good info i might add) Thanx bro. Anyone else? | ||
Amateur Bodybuilder Posts: 203 |
wow!.. lots of info there.. i like posts like these | ||
Cool Novice Posts: 46 |
Here you can plagerize from a term paper I wrote back in my college days about steroids: "I lyke steroyds. They make me honry. I get big mussles. They say steroids make you stoopid, but I tell them fuck you" Thats all I got on paper before I got side tracked. Man, college. What a great time. All 1 1/2 semesters of it.
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Amateur Bodybuilder Posts: 199 |
Actually, 1911 got it from online jounal source. Rate I type that would be days. Peace! ------------------ | ||
Pro Bodybuilder Posts: 399 |
I wish I could just spout off the locations and names of the articles, but I can't. The first is a meta-analysis that was published in the Canadian Journal of Applied Physiology (1997, I think), and the other was the recent (1999-2000) study in the New England Journal of Medicine looking at the effects of SUPRAphysiological doses of steroids. | ||
Amateur Bodybuilder Posts: 88 |
good shit. What i really need is hard core proof (or lack thereof) of the really shity sides that can be caused bu juice (im talkin hepatocellular carcinomas and shit, being that it kills regardless). ( i would also be interested on the proof of sides of tren, since it is extreamly androgenic and androgens suck balls.) THANX COCK. What the hell are you anyway? Pharmacist, endocrineologist, pathologist? | ||
Pro Bodybuilder Posts: 399 |
Microbiologist. |
All times are ET (US) | |