History of Anabolic SteroidsAnabolic steroids are man-made substances related to male sex hormones. Doctors use anabolic steroids to treat some hormone problems in men, delayed puberty, and muscle loss from some diseases. Bodybuilders and athletes often use anabolic steroids to build who made anabolic steroids and improve athletic performance. Using them this way is not legal or safe. Abuse of anabolic steroids has been linked with many health problems. Anabolic Steroids Madf called: Anabolic-androgenic steroids, Performance-enhancing drugs.
CAMH: Do You Know Anabolic Steroids
Anabolic steroids , also known more properly as anabolic—androgenic steroids AAS ,  are steroidal androgens that include natural androgens like testosterone as well as synthetic androgens that are structurally related and have similar effects to testosterone. They are anabolic and increase protein within cells , especially in skeletal muscles , and also have varying degrees of androgenic and virilizing effects, including induction of the development and maintenance of masculine secondary sexual characteristics such as the growth of facial and body hair.
Androgens or AAS are one of three types of sex hormone agonists , the others being estrogens like estradiol and progestogens like progesterone. AAS were synthesized in the s, and are now used therapeutically in medicine to stimulate muscle growth and appetite , induce male puberty and treat chronic wasting conditions, such as cancer and AIDS. The American College of Sports Medicine acknowledges that AAS, in the presence of adequate diet, can contribute to increases in body weight , often as lean mass increases and that the gains in muscular strength achieved through high-intensity exercise and proper diet can be additionally increased by the use of AAS in some individuals.
Health risks can be produced by long-term use or excessive doses of AAS. Ergogenic uses for AAS in sports , racing , and bodybuilding as performance-enhancing drugs are controversial because of their adverse effects and the potential to gain unfair advantage in physical competitions. Their use is referred to as doping and banned by most major sporting bodies. Since the discovery and synthesis of testosterone in the s, AAS have been used by physicians for many purposes, with varying degrees of success.
These can broadly be grouped into anabolic, androgenic, and other uses. Most steroid users are not athletes. AAS have been used by men and women in many different kinds of professional sports to attain a competitive edge or to assist in recovery from injury.
These sports include bodybuilding , weightlifting , shot put and other track and field , cycling , baseball , wrestling , mixed martial arts , boxing , football , and cricket. Such use is prohibited by the rules of the governing bodies of most sports. AAS use occurs among adolescents, especially by those participating in competitive sports. It has been suggested that the prevalence of use among high-school students in the U.
The AAS that have been used most commonly in medicine are testosterone and its many esters but most typically testosterone undecanoate , testosterone enanthate , testosterone cypionate , and testosterone propionate ,  nandrolone esters typically nandrolone decanoate and nandrolone phenylpropionate , stanozolol , and metandienone methandrostenolone. Designer steroids are AAS that have not been approved and marketed for medical use but have been distributed through the black market.
There are four common forms in which AAS are administered: Oral administration is the most convenient. Testosterone administered by mouth is rapidly absorbed, but it is largely converted to inactive metabolites, and only about one-sixth is available in active form. This modification reduces the liver's ability to break down these compounds before they reach the systemic circulation.
Testosterone can be administered parenterally , but it has more irregular prolonged absorption time and greater activity in muscle in enanthate , undecanoate , or cypionate ester form. These derivatives are hydrolyzed to release free testosterone at the site of injection; absorption rate and thus injection schedule varies among different esters, but medical injections are normally done anywhere between semi-weekly to once every 12 weeks.
A more frequent schedule may be desirable in order to maintain a more constant level of hormone in the system. In addition, because estered testosterone is dissolved in oil, intravenous injection has the potential to cause a dangerous embolism clot in the bloodstream.
Transdermal patches adhesive patches placed on the skin may also be used to deliver a steady dose through the skin and into the bloodstream. There is also the risk that an intimate partner or child may come in contact with the application site and inadvertently dose himself or herself; children and women are highly sensitive to testosterone and can suffer unintended masculinization and health effects, even from small doses.
Injection is the most common method used by individuals administering AAS for non-medical purposes. The traditional routes of administration do not have differential effects on the efficacy of the drug. Studies indicate that the anabolic properties of AAS are relatively similar despite the differences in pharmacokinetic principles such as first-pass metabolism. However, the orally available forms of AAS may cause liver damage in high doses. Known possible side effects of AAS include: Depending on the length of drug abuse, there is a chance that the immune system can be damaged.
Most of these side-effects are dose-dependent, the most common being elevated blood pressure , especially in those with pre-existing hypertension. AAS have been shown to alter fasting blood sugar and glucose tolerance tests.
A number of severe side effects can occur if adolescents use AAS. For example, AAS may prematurely stop the lengthening of bones premature epiphyseal fusion through increased levels of estrogen metabolites , resulting in stunted growth.
Other effects include, but are not limited to, accelerated bone maturation , increased frequency and duration of erections, and premature sexual development. AAS use in adolescence is also correlated with poorer attitudes related to health.
Probably carcinogenic to humans. Other side-effects can include alterations in the structure of the heart , such as enlargement and thickening of the left ventricle , which impairs its contraction and relaxation , and therefore reducing ejected blood volume. AAS use can cause harmful changes in cholesterol levels: AAS use in adolescents quickens bone maturation and may reduce adult height in high doses.
There are also sex-specific side effects of AAS. Development of breast tissue in males, a condition called gynecomastia which is usually caused by high levels of circulating estradiol , may arise because of increased conversion of testosterone to estradiol by the enzyme aromatase.
This side-effect is temporary; the size of the testicles usually returns to normal within a few weeks of discontinuing AAS use as normal production of sperm resumes. Female-specific side effects include increases in body hair , permanent deepening of the voice, enlarged clitoris , and temporary decreases in menstrual cycles.
Alteration of fertility and ovarian cysts can also occur in females. Kidney tests revealed that nine of the ten steroid users developed a condition called focal segmental glomerulosclerosis , a type of scarring within the kidneys.
The kidney damage in the bodybuilders has similarities to that seen in morbidly obese patients, but appears to be even more severe. High doses of oral AAS compounds can cause liver damage.
A review in CNS Drugs determined that "significant psychiatric symptoms including aggression and violence, mania , and less frequently psychosis and suicide have been associated with steroid abuse. Long-term steroid abusers may develop symptoms of dependence and withdrawal on discontinuation of AAS". Recreational AAS use appears to be associated with a range of potentially prolonged psychiatric effects, including dependence syndromes, mood disorders , and progression to other forms of substance abuse, but the prevalence and severity of these various effects remains poorly understood.
Large-scale long-term studies of psychiatric effects on AAS users are not currently available. DSM-IV lists General diagnostic criteria for a personality disorder guideline that "The pattern must not be better accounted for as a manifestation of another mental disorder, or to the direct physiological effects of a substance e.
As a result, AAS users may get misdiagnosed by a psychiatrist not told about their habit. Affective disorders have long been recognised as a complication of AAS use.
From the mids onward, the media reported " roid rage " as a side effect of AAS. A review determined that some, but not all, randomized controlled studies have found that AAS use correlates with hypomania and increased aggressiveness, but pointed out that attempts to determine whether AAS use triggers violent behavior have failed, primarily because of high rates of non-participation.
Compared with individuals that did not use steroids, young adult males that used AAS reported greater involvement in violent behaviors even after controlling for the effects of key demographic variables, previous violent behavior, and polydrug use. The drug response was highly variable. The mechanism of these variable reactions could not be explained by demographic, psychological, laboratory, or physiological measures.
A study of two pairs of identical twins, in which one twin used AAS and the other did not, found that in both cases the steroid-using twin exhibited high levels of aggressiveness, hostility, anxiety, and paranoid ideation not found in the "control" twin.
The relationship between AAS use and depression is inconclusive. There have been anecdotal reports of depression and suicide in teenage steroid users,  but little systematic evidence. A review found that AAS may both relieve and cause depression, and that cessation or diminished use of AAS may also result in depression, but called for additional studies due to disparate data.
The pharmacodynamics of AAS are unlike peptide hormones. However, as fat-soluble hormones, AAS are membrane-permeable and influence the nucleus of cells by direct action. The pharmacodynamic action of AAS begin when the exogenous hormone penetrates the membrane of the target cell and binds to an androgen receptor AR located in the cytoplasm of that cell.
From there, the compound hormone-receptor diffuses into the nucleus, where it either alters the expression of genes  or activates processes that send signals to other parts of the cell.
The effect of AAS on muscle mass is caused in at least two ways: It has been hypothesized that this reduction in muscle breakdown may occur through AAS inhibiting the action of other steroid hormones called glucocorticoids that promote the breakdown of muscles. As their name suggests, AAS have two different, but overlapping, types of effects: Some examples of the anabolic effects of these hormones are increased protein synthesis from amino acids , increased appetite, increased bone remodeling and growth, and stimulation of bone marrow , which increases the production of red blood cells.
Through a number of mechanisms AAS stimulate the formation of muscle cells and hence cause an increase in the size of skeletal muscles , leading to increased strength.
The androgenic effects of AAS are numerous. Depending on the length of use, the side effects of the steroid can be irreversible. Processes affected include pubertal growth, sebaceous gland oil production, and sexuality especially in fetal development. Some examples of virilizing effects are growth of the clitoris in females and the penis in male children the adult penis size does not change due to steroids [ medical citation needed ] , increased vocal cord size, increased libido , suppression of natural sex hormones , and impaired production of sperm.
Men may develop an enlargement of breast tissue, known as gynecomastia, testicular atrophy, and a reduced sperm count. Compounds with a high ratio of androgenic to an anabolic effects are the drug of choice in androgen-replacement therapy e. This disassociation is less marked in humans, where all AAS have significant androgenic effects.
A commonly used protocol for determining the androgenic: The VP weight is an indicator of the androgenic effect, while the LA weight is an indicator of the anabolic effect.
Two or more batches of rats are castrated and given no treatment and respectively some AAS of interest. Animal studies also found that fat mass was reduced, but most studies in humans failed to elucidate significant fat mass decrements.
The effects on lean body mass have been shown to be dose-dependent. Both muscle hypertrophy and the formation of new muscle fibers have been observed. The hydration of lean mass remains unaffected by AAS use, although small increments of blood volume cannot be ruled out. The upper region of the body thorax, neck, shoulders, and upper arm seems to be more susceptible for AAS than other body regions because of predominance of ARs in the upper body.
After drug withdrawal, the effects fade away slowly, but may persist for more than 6—12 weeks after cessation of AAS use. Overall, the exercise where the most significant improvements were observed is the bench press.
The measurement of the dissociation between anabolic and androgenic effects among AAS is based largely on a simple although arguably unsophisticated and outdated model involving rat tissue bioassays.
The intracellular metabolism theory explains how and why remarkable dissociation between anabolic and androgenic effects can occur despite the fact that these effects are mediated through the same signaling receptor, and of course why dissociation is invariably incomplete. An animal study found that two different kinds of androgen response elements could differentially respond to testosterone and DHT upon activation of the AR. Changes in endogenous testosterone levels may also contribute to differences in myotrophic—androgenic ratio between testosterone and synthetic AAS.
Testosterone can be metabolized by aromatase into estradiol , and many other AAS can be metabolized into their corresponding estrogenic metabolites as well.