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An Article Mainly About The Side Effects Of Anabolic Steriods
Anabolic steroids (AS) are effective in enhancing athletic performance. The trade off, however, is the occurrence of adverse side effects which can jeopardize health.
AS may exert a profound adverse effect on the liver. This is particularly true for orally administered AS. The parenterally administered AS seem to have less serious effects on the liver. Testosterone cypionate, testosterone enanthate and other injectable anabolic steroids seem to have little adverse effects on the liver. However, lesions of the liver have been reported after parenteral nortestosterone administration, and also occasionally after injection of testosterone esters. The influence of AS on liver function has been studied extensively. The majority of the studies involve hospitalized patients who are treated for prolonged periods for various diseases, such as anemia, renal insufficiency, impotence, and dysfunction of the pituitary gland. In clinical trials, treatment with anabolic steroids resulted in a decreased hepatic excretory function. In addition, intra hepatic cholestasis, reflected by itch and jaundice, and hepatic peliosis were observed. Hepatic peliosis is a hemorrhagic cystic degeneration of the liver, which may lead to fibrosis and portal hypertension. Rupture of a cyst may lead to fatal bleeding.
Benign (adenoma's) and malign tumors (hepatocellular carcinoma) have been reported. There are rather strong indications that tumors of the liver are caused when the anabolic steroids contain a 17-alpha-alkyl group. Usually, the tumors are benign adenoma's, that reverse after stopping with steroid administration. However, there are some indications that administration of anabolic steroids in athletes may lead to hepatic carcinoma. Often these abnormalities remain asymptomatic, since peliosis hepatis and liver tumors do not always result in abnormalities in the blood variables that are generally used to measure liver function.
AS use is often associated with an increase in plasma activity of liver enzymes such as aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (AP), lactate dehydrogenase (LDH), and gamma glutamyl transpeptidase (GGT). These enzymes are present in hepatocytes in relatively high concentrations, and an increase in plasma levels of these enzymes reflect hepatocellular damage or at least increased permeability of the hepatocellular membrane.
In longitudinal studies of athletes treated with anabolic steroids, contradictory results were obtained on the plasma activity of liver enzymes (AST, AST, LDH, GGT, AP). In some studies, enzymes were increased, whereas in others no changes were found. When increases were found, the values were moderately increased and normalized within weeks after abstinence. There are some suggestions that the occurrence of hepatic enzyme leakage, is partly determined by the pre-treatment condition of the liver. Therefore, individuals with abnormal liver function appear to be at risk.
AS are derivatives of testosterone, which has strong genitotropic effects. For this reason, it will not be surprising that side effects include the reproductive system. Application of anabolic steroids leads to supra-physiological concentrations of testosterone or testosterone derivatives. Via the feed back loop, the production and release of luteinizing hormone (LH) and follicle stimulation hormone (FSH) is decreased.
Prolonged use of anabolic steroids in relatively high doses will lead to hypogonadotrophic hypogonadism, with decreased serum concentrations of LH, FSH, and testosterone.
There are strong indications that the duration, dosage, and chemical structure of the anabolic steroids are important for the serum concentrations of gonadotropins. A moderate decrease of gonadotropin secretion causes atrophy of the testes, as well as a decrease of sperm cell production. Oligo, azoospermia and an increased number of abnormal sperm cells have been reported in athletes using AS, resulting in a decreased fertility. After stopping AS use, the gonadal functions will restore within some months. There are indications, however, that it may take several months.
In bodybuilding, where usually high dosages are uses, after stopping steroid use, often choriogonadotropins are administered to stimulate testicular function. The effectiveness of this therapy is unknown.
The various studies suggest that using more than one type of anabolic steroid at the same time ("stacking") causes a stronger inhibition of the gonadal functions than using one single anabolic steroid. After abstention from anabolic steroids these changes in fertility usually reverse within some months. However, several cases of have been reported in which the situation of hypogonadism lasted for more than 12 weeks.
A well known side effect of AS in males is breast formation (gynecomastia). Gynecomastia is caused by increased levels of circulating estrogens, which are typical female sex hormones. The estrogens estradiol and estrone are formed in males by peripheral aromatization and conversion of AS. The increased levels of circulation estrogens in males stimulate breast growth. In general, gynecomastia is irreversible.
AS may affect sexual desire. Although few investigations on this issue have been published, it appears that during AS use sexual desire is increased, although the frequency of erectile dysfunction is increased. This may seem contradictory, but sexual appetite is androgen dependent, while erectile function is not. Since sexual desire and aggressiveness are increased during AS use, the risk of getting involved in sexual assault may be increased.
In the normal female body small amounts of testosterone are produced, and as in males, artificially increasing levels by administration of AS will affect the hypothalamic-pituitary-gonadal axis. An increase in circulating androgens will inhibit the production and release of LH and FSH, resulting in a decline in serum levels of LH, FSH, estrogens and progesterone. This may result in inhibition of follicle formation, ovulation, and irregularities of the menstrual cycle. The irregularities of the menstrual cycle are characterized by a prolongation of the follicular phase, shortening of the luteal phase or amenorrhea. Although these changes are generally more pronounced in younger women, large inter-individual responsiveness to anabolic steroids exists. The effects of AS dosages as generally used in sport, on the hypothalamic-pituitary-gonadal axis in females are hardly studied.
Other side effects of anabolic steroid use in females are increased sexual desire and hypertrophy of the clitoris. The few systematic studies that have been conducted suggest that the effects are similar to the effects in patients, treated with anabolic steroids.
Anabolic steroid use by pregnant women may lead to pseudohermaphroditism or to growth retardation of the female fetus. Anabolic steroid use may even lead to fetal death. However, these side effects have not been studied systematically. It is likely that the severity of the side effects is related to the dosage, duration of use and the type of the drug.
Additional side effects of anabolic steroids specifically in women are acne, hair loss, withdrawal of the frontal hair line, male pattern boldness, lowering of the voice, increased facial hair growth, and breast atrophy. The lowering of the voice, decreased breast size, clitoris hypertrophy and hair loss are generally irreversible. Females using AS may develop masculine facial traits, male muscularity, and coarsening of the skin.
When anabolic steroids are administered in growing children side effects include virilization, gynecomastia, and premature closure of the epiphysis, resulting in cessation of longitudinal growth.
AS also affect the cardiovascular system and the serum lipid profile. Relatively few studies have been done to investigate the effect of anabolic steroids on the cardiovascular system. No longitudinal studies have been conducted on the effect of anabolic steroids on cardiovascular morbidity and mortality.
Most of the investigations have been focused on risk factors for cardiovascular diseases, and in particular the effect of anabolic steroids on blood pressure and on plasma lipoproteins. In most cross-sectional studies serum cholesterol and triglycerides between drug-free users and non-users is not different. However, during anabolic steroid use total cholesterol tends to increase, while HDL-cholesterol demonstrates a marked decline, well below the normal range. Serum LDL-cholesterol shows a variable response: a slight increase or no change. The response of total cholesterol seems to be influenced by the type of training that is done by the athlete. When a great deal of the exercise consists of aerobic exercise, the increasing effect of AS is counterbalanced by an exercise-induced increasing effect, which may result in a net decline in total cholesterol. Aerobic training does not seem to be able to offset the steroid-induced decline in HDL-cholesterol and its subfractions HDL-2, and HDL-3.
The precise effect of anabolic steroids on LDL-cholesterol is unknown yet. It appears that anabolic steroids influence hepatic triglyceride lipase (HTL) and lipoprotein lipase (LPL). Males usually have higher levels of HTL, while females have higher LPL activity. HTL is primarily responsible for the clearance of HDL-cholesterol, while LPL takes care of cellular uptake of free fatty acids and glycerol. Androgens and anabolic steroids stimulate HTL, presumably resulting in decreased serum levels of HDL-cholesterol.
The effect of anabolic steroids on triglycerides is not well known. It is suggested that relatively low doses do not affect the serum triglyceride levels, while it cannot be excluded that higher doses elicit an increase.
No unanimity exists about the influence of anabolic steroids on arterial blood pressure. The response is most probably dose dependent. There is some data suggesting that high doses increase diastolic blood pressure, whereas low doses fail to have a significan
Most of the adverse effects of anabolic-androgenic steroid (AAS) use are dose dependent and are reversible with cessation of the offending agent or agents. This overview of side effects and interactions is just that, an overview, and is not meant to represent the full spectrum of potential side effects that may be seen with this class of agents. Vital signs, including heart rate and blood pressure, and basic chemistries, such as sodium, potassium, hemoglobin, hematocrit, BUN (blood urea nitrogen), creatinine, hepatic, and lipid profiles, must be monitored carefully. Monitoring these parameters will help the clinician to determine drug choice, treatment dose, and duration, and will help to alert the prescriber to potentially serious adverse effects that necessitate the discontinuation of therapy.
The most common deleterious effects of AAS use on the cardiovascular system include increased heart rate, increased blood pressure, and changes in lipid metabolism, including lowered high-density lipoprotein (HDL) and increased low-density lipoprotein (LDL). The increase in heart rate is thought to be more profound with the androgens, especially those resistant to aromatase, and is believed to be due to the inhibition of monoamine oxidase (MAO). This effect, when combined with the increased renal recovery of ions, such as sodium, causing subsequent fluid retention, can lead to dramatic increases in blood pressure. Combine this with a tendency to lower HDL and raise LDL, and the stage is set for untoward atherogenic and cardiac effects. Anabolic steroid users can have a lower left ventricle ejection fraction. Ananbolic steroid abuse has been associated with ventricular arrhythmias.
The changes made to C-17 to inhibit hepatic degradation make nearly all oral preparations hepatotoxic. The alanine aminotransferase/aspartate aminotransferase (ALT/AST) can be seen to rise, usually in a dose-dependent fashion. Levels approaching 2-3 times baseline are often set as upper limits of reference ranges when administering oral AASs, but the risk-to-benefit ratio must be constantly evaluated.
AAS use also results in suppression of clotting factors II, V, VII, and X, as well as an increase in prothrombin time. Another life-threatening, albeit rare, adverse effect that is seen in the liver and sometimes in the spleen is peliosis hepatitis, which is characterized by the appearance of blood-filled, cystic structures. These cysts, which may rupture and bleed profusely, have been found in patients with near-normal liver function test (LFT) values, as well as in individuals who are in liver failure. Fortunately, drug cessation usually results in complete recovery.
Primary liver tumors have been reported, most of which are benign, androgen-dependent growths that regress with the discontinuation of AAS therapy. Several case reports exist of young, healthy athletes who have died from primary malignant liver carcinoma, with the only identifiable risk factor being oral AAS use.
Anabolic steroid abuse has been considered a risk factor for nonalcoholic fatty liver disease.
The endocrine system has a remarkable array of checks and balances that ensure the human body is at or near homeostasis at any point in time. Interruption of one feedback system has been shown to produce changes in other hormone feedback systems via direct receptor changes, as well as through competition for common enzymes and metabolic pathways. Studies have shown that AASs bind to glucocorticoid, progesterone, and estrogen receptors and exert multiple effects. Discussions exist as to how the endogenous testosterone and spermatogenic functions of the testes are inhibited by the use of testosterone and AASs. By suppressing FSH, spermatogenic function should be reduced.
AASs have also been shown to alter fasting blood sugar levels and decrease glucose tolerance, presumably due to either a hepatic effect or changes in the insulin receptor. Thyroxine-binding globulin (TBG) may also be lowered by AASs and result in lowered total T4 levels, with free T4 levels remaining normal. An up-regulation of sex-hormone binding globulin, with a concomitant decrease in TBG, is thought to cause the changes in total T4 levels.
The aromatization of testosterone/AASs to estradiol and related compounds can render many adverse estrogenic effects. The most apparent and common adverse effect is the growth of tender, estrogen-sensitive tissue under the male nipple. This unsightly growth is termed gynecomastia and can be treated medically or surgically.
The male prostate is very sensitive to androgens, especially those that are reduced in prostatic tissue to dihydrotestosterone (DHT) or DHT analogs. In response to this stimulation, the prostate grows in size, potentially causing or exacerbating benign prostatic hyperplasia (BPH). Worsening BPH may indeed cause severe bladder and secondary renal damage. In addition, the use of AASs in patients with underlying carcinoma of the prostate is absolutely contraindicated due to the potential for hormone-sensitive tumor growth. However, a 3-year study of hypogonadal men on testosterone replacement therapy failed to show significant differences between the group and the controls in urinary symptoms, urine flow rate, or urine postvoid residual.
Direct clotting factors may be reduced with an increase in prothrombin time. In patients on concomitant anticoagulant therapy, this increase could cause bleeding. AASs cause increases in hemoglobin and hematocrit and are used in many cases of anemia, although the clinician must be aware of the potential for polycythemia.
Skin, especially the face and scalp, has a high degree of androgen receptors and 5AR. DHT is known to cause increases in sebum production, leading to clinical acne. Also, male pattern baldness is related to scalp DHT production and binding, along with genetic factors influencing hair growth. Male pattern baldness is greatly exacerbated by most AASs in susceptible individuals.
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