Steroid Side Effects

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Cardiovascular System
Immune System
Kidneys (Renal System)
Liver (Hepatic System)
Physical (Both Sexes)
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Physical (Male)
Physical (Female)
Reproductive (Male)
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Steroid Side Effects

While anabolic/androgenic steroids (AAS) are generally regarded as therapeutic drugs with high safety, their use can also be associated with a number of adverse cosmetic, physical, and psychological effects. Many of these steroid side effects are often apparent during therapeutic-use conditions, although their incidence tends to increase profoundly as the dosages reach supratherapeutic ranges. Virtually everyone that abuses anabolic/androgenic steroids for physique- or performance-enhancing purposes notices some form of adverse effects from their use. According to one study, the exact frequency of tangible side effects in a group of steroid abusers was 96.4%. This shows very clearly that it is far more rare to abuse these drugs and not notice side effects than it is to endure them.90 In addition to the side effects that anabolic/androgenic steroids can have on various internal systems, there are others which may not be immediately apparent to the user. The following is a summary of the biological systems and reactions effected by AAS use.

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The use of anabolic/androgenic steroids in supratherapeutic (and often therapeutic) doses can have a number of adverse effects on the cardiovascular system. This may be noticed in several areas including unfavorable alterations in serum cholesterol, a thickening of ventricular walls, increased blood pressure, and changes in vascular reactivity. In an acute sense these drugs are admittedly very safe. The risk of an otherwise healthy person suffering a heart attack from an isolated steroid cycle is extremely remote. The risk of stroke is also extremely low. When these drugs are abused for long periods, however, their adverse effects on the cardiovascular system are given time to accumulate. An increased chance of early death due to heart attack or stroke is, likewise, a valid risk with long-term steroid abuse. In order to better understand this risk, we must look specifically at how anabolic/androgenic steroids affect the cardiovascular system in several key ways.


Anabolic/androgenic steroids use can adversely affect both HDL (good) and LDL (bad) cholesterol values. The ratio of HDL to LDL cholesterol fractions provides a rough snapshot of the ongoing disposition of plaque in the arteries, either favoring atherogenic or anti-atherogenic actions. The general pattern seen during steroid use is a lowering of HDL concentrations, which is often combined with stable or increased LDL levels. Triglyceride levels may also increase.The shift can be unfavorable in all directions. Note that in some cases, the total cholesterol count will not change significantly. The total cholesterol level can, therefore, give a false representation of uncompromised lipid health. Almost invariably the underlying HDL/LDL ratio will decrease. While this ratio should return to normal following the cessation of steroid intake, plaque deposits in the arteries are more permanent. If unfavorable shifts in lipids are exacerbated by the long-term use of steroidal compounds, significant damage to the cardiovascular system can result.[/vc_column_text][vc_single_image image=”1593″ alignment=”center” border_color=”grey” img_link_large=”yes” img_link_target=”_blank” img_size=”medium” css=”.vc_custom_1431008488379{padding-top: 30px !important;padding-bottom: 25px !important;}”][vc_column_text css=”.vc_custom_1428373788861{padding-bottom: 30px !important;}”]

Over time, plaque deposits may begin to narrow and clog arteries.

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Anabolic/androgenic steroids are most consistent in their lowering of HDL levels. This adverse effect is mediated through the androgenic stimulation of hepatic lipase, a liver enzyme responsible for the breakdown of HDL (good) cholesterol.91 With more hepatic lipase activity in the body, the favorable (anti-atherogenic) HDL cholesterol particles are cleared from circulation more quickly, and their levels drop. This is an effect that seems to be very pronounced at even modest supratherapeutic dosage levels. For example, studies with testosterone cypionate noted a 21% drop in HDL cholesterol with a dosage of 300 mg per week.92 Increasing this dosage to 600 mg did not have any significant additional effect, suggesting that the dosage threshold for strong HDL suppression is fairly low.

Oral steroids, especially c-17 alpha alkylated compounds, are particularly potent at stimulating hepatic lipase and suppressing HDL levels. This is due to first pass concentration and metabolism in the liver. A drug like stanozolol may, therefore, be milder than testosterone with regard to androgenic steroid side effects, but not when it comes to cardiovascular strain. A study comparing the effects of a weekly injection of 200 mg testosterone enanthate to only a 6 mg daily oral dose of stanozolol demonstrates the strong difference between these two types of drugs very well.93After only six weeks, 6 mg of stanozolol was shown to reduce HDL and HDL-2 cholesterol levels by an average of 33 and 71% respectively. HDL levels (mainly the HDL-3 subfraction) were reduced by only 9% in the testosterone group. LDL cholesterol levels also rose 29% with stanozolol, while they dropped 16% with testosterone. Esterified injectable steroids are generally less stressful to the cardiovascular system than oral agents.

It is also important to note that estrogens can have a favorable impact on cholesterol profiles. The aromatization of testosterone to estradiol may, therefore, prevent a more dramatic change in serum cholesterol. A study examined this effect by comparing the lipid changes caused by 280 mg of testosterone enanthate per week, with and without the aromatase inhibitor testolactone.94 Methyltestosterone was also tested in a third group, at a dose of 20 mg daily, to judge the comparative effect of an oral alkylated steroid. The group using only testosterone enanthate in this study showed a small but not significant decrease in HDL cholesterol values over the course of the 12-week investigation. After only four weeks, however, the group using testosterone plus the aromatase inhibitor displayed an HDL reduction of an average of 25%. The group taking methyltestosterone experienced the strongest HDL reduction in the study, which dropped 35% after four weeks. This group also noticed an unfavorable rise in LDL cholesterol levels.

The potential positive effect of estrogen on cholesterol values also makes the issue of estrogen maintenance something to consider when it comes to health risks. To begin with, one may want to consider whether or not estrogen maintenance drugs are actually necessary in any given circumstance. Are side effects apparent, or is their use a preventative step and perhaps unnecessary? The maintenance drug of choice can also have a measurable impact on cholesterol outcomes. For example, the estrogen receptor antagonist tamoxifen citrate does not seem to exhibit anti-estrogenic effects on cholesterol values, and in fact tends to increase HDL levels in some patients. Many individuals decide to use tamoxifen to combat estrogenic side effects instead of an aromatase inhibitor for this reason, particularly when they are using steroids for longer periods of time, and are concerned about their cumulative cardiovascular side effects.

Enlarged Heart

The human heart is a muscle. It possesses functional androgen receptors, and is growth-responsive to male steroid hormones. This fact partly accounts for men having a larger heart mass on average than women.95 Physical activity can also have a strong effect on the growth of the heart. Resistance exercise (anaerobic) tends to increase heart size by a thickening of the ventricular wall, usually without an equal expansion of the internal cavity. This is known as concentric remodeling. Endurance (aerobic) athletes, on the other hand, tend to increase heart size via expansion of the internal cavity, without significant thickening of the ventricles (eccentric remodeling). Even with concentric or eccentric remodeling, diastolic function usually remains normal in the athletic heart. The heart muscle is also dynamic. When regular training is removed from a conditioned athlete, the wall thickening and cavity expansion tend to reduce.

Anabolic steroid abusers are at risk for thickening of the left and right ventricular walls,96 known as ventricular hypertrophy. Hypertrophy of the left ventricle (the main pumping chamber) in particular is extensively documented in anabolic/androgenic steroid abusers.97 While left ventricular hypertrophy is, again, also found in natural power athletes, substance-abusing athletes tend to have a much more profound wall thickening. They also tend to develop pathological issues related to this thickening, including impaired diastolic function, and ultimately reduced heart efficiency.98 The level of impairment is closely associated with the dose and duration of steroid abuse. A left ventricle wall exceeding 13mm in thickness is rare naturally, and may be indicative of steroid-abuse or other causes.99 It may further suggest that pathological left ventricular hypertrophy has developed. Additional testing of such patients is recommended.

Left ventricular hypertrophy (LVH) is an independent predictor of mortality in overweight individuals with high blood pressure.100 It has also been linked to atrial fibrillation, ventricular arrhythmia, and sudden collapse and death.101 While LVH in non-steroid-using athletes tends to be without clinical significance, pathological increases in QT dispersion are noticed in steroid abusers with LVH.102 These changes tend to be similar to the increases in QT dispersion noted in hypertensive patients with LVH.103 Among other things, this could leave a steroid abusing individual more susceptible to a serious adverse event, including arrhythmia or heart attack. Isolated medical case studies of longtime steroid abusers support an association between LVH and related pathologies including ventricular tachycardia (arrhythmia originating in the left ventricle), left ventricular hypokinesis (weakened contraction of the left ventricle), and decreased ejection fraction (reduced pumping volume and efficiency).104

Heart mass can increase or decrease in relation to the current state of anabolic/steroid use, the average dosage, and duration of intake. Likewise, the heart usually begins to reduce in size once anabolic/androgenic steroids are no longer being used. This effect is similar to the way the heart will reduce in size once an athlete no longer follows a rigorous training schedule.105 Even with this effect, however, some changes in heart muscle size and function caused by the drugs may persist. Studies examining the effects of steroid use and withdrawal on left ventricular hypertrophy noted that athletic subjects who abstained from steroid abuse for at least several years still had a slightly greater degree of concentric left ventricular hypertrophy compared to non-steroid-using athletic controls.106 The disposition of pathological left ventricular hypertrophy following long-term steroid abuse and then abstinence remains the subject of investigation and debate.

Heart Muscle Damage

Anabolic/androgenic steroid abuse is suspected of producing direct damage to the heart muscle in some cases. Studies exposing heart cell cultures to AAS have reported reduced contractile activity, increased cell fragility, and reduced cellular (mitochondrial) activity, providing some support for a possible direct toxic effect to the heart muscle.107 108 Furthermore, a number of case reports have found such pathologies as myocardial fibrosis (scar tissue buildup in the heart), myocardial inflammation (inflammation of heart tissue), cardiac steatosis (accumulation of triglycerides inside heart cells), and myocardial necrosis (death of heart tissue) in long- term steroid abusers.109 110 111 112 A direct link between drug abuse and cardiac pathologies is assumed in these cases, but cannot be proven given the slow nature in which these cardiac pathologies develop, and the influence many other factors (such as diet, exercise, lifestyle, and genetics) can have on them. Individuals remain cautioned about the possibility of cardiac muscle damage with long-term steroid abuse.

Blood Pressure

Anabolic/androgenic steroids may elevate blood pressure. Studies of bodybuilders taking these drugs in supratherapeutic doses have demonstrated increases in both systolic and diastolic blood pressure readings.113Another study measured the average blood pressure reading in a group of steroid users to be 140/85, which was compared to 125/80 in weight lifting controls not taking steroids.114 Hypertension, or consistently high blood pressure at or above 140/90 for either systolic or diastolic measures, has been reported in steroid users,115 although in most cases the elevations are more modest. Increased blood pressure may be caused by a number of factors, including increased water retention, increased vascular stiffness, and increased hematocrit. Aromatizing or highly estrogenic steroids tend to cause the greatest influences over blood pressure, although elevations cannot be excluded with non-estrogenic anabolic/androgenic steroids. Blood pressure tends to normalize once anabolic/androgenic steroids have been discontinued.

Hematological (Blood Clotting)

Anabolic/androgenic steroids can cause a number of changes in the hematological system that affect blood clotting. This effect can be very variable, however. The therapeutic use of these drugs is known to increase plasmin, antithrombin III, and protein S levels, stimulate fibrinolysis (clot breakdown), and suppress clotting factors II, V, VII, and X.116 117 These changes all work to reduce clotting ability. Prescribing guidelines for anabolic/androgenic steroids warn of potential increases in prothrombin time, a measure of how long it takes for a blood clot to form.118If prothrombin time increases too greatly, healing may be impaired. The effects of anabolic/androgenic steroids on prothrombin time are generally of no clinical significance to healthy individuals using these drugs in therapeutic dosages. Patients taking anticoagulants (blood thinners), however, could be adversely affected by their use.

Conversely, anabolic/androgenic steroid abuse has been linked to increases in blood clotting ability. These drugs can elevate levels of thrombin119 and C-reactive protein,120 as well as thromboxane A2 receptor density,121 which can support platelet aggregation and the formation of blood clots. Studies of steroid users have demonstrated statistically significant increases in platelet aggregation values in some subjects.122 There are also a growing number of case reports where (sometimes fatal) blood clots, embolisms, and stokes have occurred in steroid abusers.123 124 125 126 127 Although it has been difficult to conclusively link these events directly to steroid abuse, the adverse effects of anabolic steroids on components of the blood coagulation system are well understood. These serious adverse effects are now regarded as recognized risks of steroid abuse among many that study these drugs.

In therapeutic levels, the anti-thrombic effects of anabolic/androgenic steroids seem to dominate physiology, and decreases in blood clotting ability may be noted. At a certain supratherapeutic dosage point, however, the pro-thrombic changes appear to overtake the anti-thrombic changes, and physiology begins to favor fast and abnormally thick clot formation (hypercoagulability). The exact dosage threshold or conditions required to increase blood clotting has not been determined, and some studies with steroid users taking supraphysiological doses fail to demonstrate increased coagulability.128 Individuals remain warned of the potential increases in thrombic risk with anabolic/androgenic steroid abuse. Blood clotting tendency should return to the pretreated state after the discontinuance of anabolic/androgenic steroids. point until the hematocrit issues have been corrected. Minor elevations in hematocrit may be addressed with phlebotomy. For this, 1 pint of blood may be removed periodically during steroid intake, often every two months. Proper hydration is also important, as dehydration can temporarily cause the hematocrit level to elevate, giving a false positive for polycythemia. The daily intake of aspirin is also commonly advised if the hematocrit is above normal, as this will reduce platelet aggregation, or the tendency for platelets to stick together and form clots. Individuals remain cautioned of the potential cardiovascular danger of high hematocrit levels associated with anabolic/androgenic steroid use.

Hematological (Polycythemia)

Anabolic/androgenic steroids stimulate erythropoiesis (red blood cell production). One potential adverse effect of this is polycythemia, or the overproduction of red blood cells. Polycythemia can be reflected in the hematocrit level, or the percentage of blood volume that is made up of red cells. As the hematocrit rises, so too does the viscosity of the blood. If the blood becomes too thick, its ability to circulate becomes impaired. This can greatly increase the risk of serious thrombic event including embolism and stroke. A high hematocrit level is also an independent risk factor for heart disease.129 The normal hematocrit level in men is 40.7 to 50.3%, and in women it is 36.1 to 44.3% (numbers may vary very slightly depending on the source). For the sake of scale, while a hematocrit of 50% may be normal, a hematocrit of 60% or above is considered critical (life threatening).

Anabolic/steroid administration tends to raise the hematocrit level by several percentage points, sometimes more. As a result, many steroid-using bodybuilders will have hematocrit levels that are above the normal range. For example, one study measured the average hematocrit in a group of steroid abusing competitive bodybuilders to be 55.7%.130This level is considered clinically high, and would increase blood viscosity enough to raise the risk of serious cardiovascular event. Although not likely to be an isolated cause, high hematocrit is believed to have been a contributing factor in the deaths of a number of steroid abusers, usually paired with high blood pressure, homocysteine, and/or atherosclerosis. The average hematocrit level in bodybuilders not taking anabolic/androgenic steroids was 45.6%, well within the normal range for healthy adult men.

Many physicians that specialize in hormone replacement therapy consider a hematocrit level of 55% to be an absolute cutoff point. At or above this point, and anabolic/androgenic steroid therapy cannot be continued safely. Drug intake would be ceased at this point until the hematocrit issues have been corrected. Minor elevations in hematocrit may be addressed with phlebotomy. For this, 1 pint of blood may be removed periodically during steroid intake, often every two months. Proper hydration is also important, as dehydration can temporarily cause the hematocrit level to elevate, giving a false positive for polycythemia. The daily intake of aspirin is also commonly advised if the hematocrit is above normal, as this will reduce platelet aggregation, or the tendency for platelets to stick together and form clots. Individuals remain cautioned of the potential cardiovascular danger of high hematocrit levels associated with anabolic/androgenic steroid use.


Anabolic/androgenic steroids may elevate homocysteine levels. Homocysteine is an intermediary amino acid produced as a byproduct of methionine metabolism. High levels of homocysteine have been linked to elevations in the risk for cardiovascular disease.131 It is believed to play a direct role in the disease, increasing oxidative stress, including the oxidation of LDL cholesterol, and accelerating atherosclerosis.132 Elevated levels of homocysteine may also induce vascular cell damage, support platelet aggregation, and increase the likelihood of thrombic event.133 134 135 The normal range for homocysteine levls in men aged 30 to 59 years is 6.3-11.2umol/L. For women of the same age the average is 4.5-7.9umol/L. Increased risk of heart attack, stroke, or other thrombic event are noted with even modest elevations in homocysteine. According to one study, a homocysteine level exceeding 15umol/L in patients with heart disease is associated with a 24.7% increased likelihood of death within five years.136

Androgens stimulate elevations in homocysteine,137 and men have an approximately 25% higher level on average than women.138 Anabolic/androgenic steroid abuse has been associated with hyperhomocysteinaemia, or consistent clinically high homocysteine levels.139 One study found that the average homocysteine concentration in a group of 10 men that had been self-administering anabolic/androgenic steroids (in a cyclic pattern) for 20 years was 13.2 umol/L.140 Three of these men died of a heart attack during the investigation, and had homocysteine levels between 15umol/L and 18umol/L. The average homocysteine level in bodybuilders who had never taken steroids was 8.7umol/L, while it was 10.4umol/L in previous steroid users (3 months abstinence). One study did show that administering 200 mg of testosterone enanthate (with and without an aromatase inhibitor) for three weeks failed to produce a significant elevation in homocysteine.141 It is unknown if the moderate dosage, drug type (esterified injectable vs. c17-aa), or short duration of intake were factors in the differing outcome from other studies. Individuals remain warned of the potential for elevations in the homocysteine level with steroid abuse.

Vascular Reactivity

The endothelium is a layer of cells that line the entire circulatory system. These cells are found on the inside of all blood vessels, and help increase or decrease blood flow and pressure by relaxing or constricting the vessels (referred to as vasodilation and vasoconstriction, respectively). These cells also help regulate the passage of materials in and out of blood vessels, and are involved in a number of important vascular processes including blood clotting and new blood vessel formation. Having a more flexible (reactive) endothelium is generally considered desirable for health, and, likewise, the endothelium is often compromised in individuals with cardiovascular disease. Patients with endothelial dysfunction tend to notice greater vasoconstriction, restricted blood flow, higher blood pressure, local inflammation, and reduced circulatory capacity.142 This may place them at greater risk for heart attack, stroke, or thrombosis (blood clot).

Endothelial cells are androgen responsive, which may partly account for men exhibiting less vascular reactivity than women.143 Similarly, anabolic/androgenic steroid use has been shown to impair endothelial activity and vascular reactivity. Studies at the University of Innsbruck in Austria compared the level of endothelial dilation in 20 steroid users to a group of control athletes.144 Those individuals using anabolic steroids noticed slight but measurably impaired vascular dilation and endothelial function. Additional studies at the University of Wales in Cardiff comparing vascular dilation in active, previous, and non-steroid users, also demonstrated anabolic steroids to cause a decline in endothelial-independent vasodilation.145 These effects leave the steroid user with more relative “stiffness” in the vascular system, which could increase the chance of an adverse cardiovascular event. In both studies, vascular reactivity improved after the discontinuance of anabolic/androgenic steroids.

Proving an Association

Direct links between steroid abuse and individual cases of stroke and heart attack have been difficult to prove. There are a number of things that have made this difficult. For one, cardiovascular disease is very common in men. It also usually takes decades to develop. This makes individual contributing factors (which include many things such as diet, lifestyle, health status, and genetic variables) extremely difficult to isolate. Data concerning the long-term use of steroids in physique- or performance-enhancing doses is also very limited. It would be unethical to conduct a controlled study where participants were given abusive doses of steroids for many years, so the data that is referenced tends to be from case studies. Individual case studies are important, but are usually considered too week to meet the requirements of statistical proof. Still, it would be a mistake to confuse this lack of proven association with proof of nonassociation. The cardiovascular risks of steroid abuse remain well supported by both documented acute changes in cardiovascular markers, and a growing body of case reports of injury or death. There are few medical experts close to the study of these drugs today that would actually deny their risks.[/vc_column_text][vc_single_image image=”1597″ alignment=”center” border_color=”grey” img_link_large=”yes” img_link_target=”_blank” img_size=”medium” css=”.vc_custom_1431008506423{padding-bottom: 25px !important;}”][vc_column_text css=”.vc_custom_1431012931354{padding-bottom: 25px !important;}”]

Anabolic/androgenic steroid abuse can produce changes in a number of areas of cardiovascular health that can work together to increase the risk of heart attack, stroke, or embolism.

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The human immune system is responsive to sex hormones. This results in functional differences in immunity between the sexes.Women tend to have a more active immune system compared to men, and are slightly more resistant to bacterial infection and other types of infection.146 The female immune system is also more prone to developing autoimmune diseases, which may be linked to its higher level of activity.147 The day-to-day activity of the immune system can also fluctuate throughout the menstrual cycle, further demonstrating the strong influence of sex steroids.148 The slightly weaker resistance to infection of men appears to be caused by testosterone, which is an immunosuppressive hormone.149 Androgens may modulate the immune system directly, through their conversion to estrogens,150 or by modifying glucocorticoid activity.151

Anabolic/androgenic steroids have displayed both immunostimulatory and immunosuppressive actions in animal models.152 Given that these drugs can influence the immune system through a variety of pathways, and anabolic steroids are a fairly diverse class of drugs, their effects on the immune system may vary depending on the particular conditions. When used therapeutically, changes in immune system functioning are usually minor, and have not amounted to strong immunostimulation or immunosuppression. Anabolic/androgenic steroids have also been used safely in many immunocompromised patients, such as those with muscle wasting associated with HIV infection, without any significant change in immune system or viral markers.153 154

The use of anabolic/androgenic steroids in supratherapeutic doses may slightly impair immune system functioning, reducing an individual’s resistance to certain types of infection. In one study, steroid abusers were shown to have lower serum levels of IgG, IgM, and IgA immunoglobulins (antibodies) compared to bodybuilding controls, consistent with immunosuppression.155 Although this may logically increase the chance of contracting certain types of illness, a significant increase in the history of illness could not be established in these same steroid abusers. Given the very random nature of illness, however, it may be difficult to establish such a link without extensive study. The effect of hormone manipulation on immunity should also be temporary, and return to a normal state once pre-treated hormonal chemistry is restored. Individuals remain warned of the potential for minor immunosuppression and increased chance of illness with steroid abuse.


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Anabolic/androgenic steroids are generally well tolerated by the renal system. These drugs are largely excreted from the body through the kidneys, although there is no inherent strong toxicity in this process. In fact, there are many instances in which these drugs may be used as supportive treatment in patients with compromised kidney function. For example, anabolic steroids have been prescribed to increase the production of red blood cells in patients with anemia related to various forms of kidney disease.156 157 They have even been used as general anabolic (lean body mass) support, and to treat hypogonadism, in patients undergoing dialysis.158 159 While care must be taken with such patients, therapy may often be conducted very safely. In otherwise healthy individuals, clinical renal toxicity caused by the short-term administration of anabolic/androgenic steroids is unlikely.

There have been isolated reports of severe kidney damage in steroid abusers. For example, a handful of individuals have developed Wilms’ Tumor (nephroblastoma),160 161 which is a rare form of kidney cancer usually found in children. Its appearance in adult steroid users is suspect, but not conclusive evidence that drugs were the actual cause. There have also been isolated reports of renal cell carcinoma in steroid abusers.162 163 Since this is the most common form of kidney cancer, however, conclusive links are again difficult to draw. There have additionally been case reports of combined liver and renal failure with steroid abuse.164 165 In these cases kidney failure may have been subsequent to steroid-induced liver toxicity, as cholestasis (bile duct obstruction) is known to cause acute tubular necrosis and renal failure.166

The use of anabolic/androgenic steroids in supratherapeutic doses may slightly impair immune system functioning, reducing an individual’s resistance to certain types of infection. In one study, steroid abusers were shown to have lower serum levels of IgG, IgM, and IgA immunoglobulins (antibodies) compared to bodybuilding controls, consistent with immunosuppression.155 Although this may logically increase the chance of contracting certain types of illness, Kidney health should be a concern for long-term steroid-using bodybuilders and power athletes. To begin with, excessive resistance training can produce some strain on the renal system. A condition called rhabdomyolysis is caused by the extreme damage of muscle tissue, which releases myoglobin and a number of nephrotoxic compounds into the blood.167 In high levels this can damage kidney tissue and even cause renal failure. There have been rare case reports of severe clinical rhabdomyolysis in bodybuilders, both with and without mention of steroid abuse.168 169 170 171 Steroid use may also cause hypertension, which can lead to kidney damage.172 While anabolic/androgenic steroids are generally not regarded as direct kidney toxic drugs, they may be used to support a lifestyle and long-term metabolic state characterized by extreme training, heightened daily muscle protein turnover, and elevated blood pressure. Over time this may compromise kidney health. Regular monitoring of kidney function is recommended.

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Many oral anabolic/androgenic steroids (or injectable forms of oral steroids) are toxic to the liver (hepatotoxic). These compounds can cause serious and sometimes life-threatening damage when abused, and occasionally even under therapeutic conditions. Those agents commonly associated with clinical hepatotoxicity include (but are not limited to) fluoxymesterone, methandrostenolone, methylandrostenediol, methyltestosterone, norethandrolone, oxymetholone, and stanozolol.173 174 175 176 177 These steroids all have either an ethyl or methyl group at carbon-17 (c-17alpha alkylation). All c-17alpha alkylated anabolic/androgenic steroids possess some level of hepatotoxicity. Liver strain, as assessed by elevated liver enzymes, has also been reported with non-alkylated esterified injectable steroids including nandrolone decanoate and testosterone enanthate in extremely rare instances.178 179 These steroids have never been associated with serious hepatic damage, however, and are not regarded as liver toxic.

Alkylation of c-17alpha specifically protects the steroid molecule from metabolism by the enzyme 17beta- hydroxysteroid dehydrogenase (17beta-HSD). This enzyme normally oxidizes a steroid’s 17beta-hydroxyl (17beta-ol) group, which must remain intact for the drug to impart any anabolic or androgenic effect. Oxidation of 17-beta-ol is one of the primary pathways of hepatic steroid deactivation. Without protection from this enzyme, very little active drug will survive the first pass through the liver and reach circulation after oral dosing. Alkylation of c-17alpha effectively protects the steroid from 17beta-HSD by occupying a hydrogen bond necessary for the breakdown of 17beta-ol to 17-keto. The compound must be metabolized through other pathways as a result, and immediate hepatic deactivation is prevented. The process allows a very high percentage of the steroid dose to pass into the bloodstream intact, but it also places some strain on the liver in the process.

Te exact mechanism of hepatotoxicity induced by alkylated anabolic/androgenic steroids remains unknown, but it is speculated to be due in large part to the natural activity of androgens in the liver. This liver possesses a high concentration of androgen receptors, and is responsive to these hormones.180 With hysiological androgens such as testosterone and dihydrotestosterone, however, only a moderate level of activity is permitted in this organ. This is because the liver is normally very efficient at metabolizing steroids, which mutes their local activity. But with the liver unable to easily deactivate alkylated steroids, however, a far greater level of hepatic androgenic activity is allowed. The concentration of steroid in the liver is also very high after oral administration, as the digestive tract delivers the drug directly to this organ before it can reach circulation. The fact that the most potent steroid ever given to humans on a mg-for-mg basis is also the most liver toxic, also supports a close association between androgenic potency and hepatotoxicity.181 182

Early liver toxicity is usually visible in blood test results for hepatic function before physical symptoms or dysfunction develop. This is most likely to include elevations in amino-transferase enzymes AST and ALT, also called serum glutamic-oxalocetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT), respectively. The cholestatic enzymes alkaline phosphatase (ALP) and gamma-glutamyltranspeptidase (GGT) may also be elevated, along with other markers (see: Understanding Blood Tests). Screening for abnormalities in hepatic markers is regarded as the most effective way of preventing liver damage from steroid administration. Should asymptomatic toxicity go unnoticed and without a change in drug intake, it is likely to progress to more severe hepatic strain, injury, or hepatic dysfunction. Immediate cessation of anabolic/androgenic steroid use and a full assessment of liver and full-body health is advised should any signs of unacceptable liver toxicity become apparent.

The most common form of actual liver dysfunction caused by the administration of oral anabolic/androgenic steroids is cholestasis.183 This describes a condition where the flow of bile becomes decreased, usually because of obstruction of the small bile ducts in the liver (intrahepatic). This causes bile salts and bilirubin to accumulate in the liver and blood instead of being properly excreted thorough the digestive tract. Inflammation (hepatitis) may also be present.184 Symptoms of cholestasis may include anorexia, malaise, nausea, vomiting, upper abdominal pain, or pruritus (itching). The stool may also change to a clay color (alcholic stool) due to the reduced excretion of bile, and the urine may become amber. Cholestatic jaundice may develop, which is characterized by a yellowing of the skin, eyes, and mucous membranes due to high levels of bilirubin in the blood (hyperbilirubinemia). Intrahepatic cholestasis may also coincide with hepatocellular necrotic lesions (death of liver tissue).

Intrahepatic cholestasis will usually resolve itself without serious injury or medical intervention within several weeks of discontinuing all hepatotoxic steroids. More serious cases may take several months before normal hepatic enzyme levels and functioning are restored. Hepatic lesions are likely to heal over time as well, at least partially. In some cases physicians have initiated supportive treatment with ursodeoxycholic acid (ursodiol), which is a secondary bile salt known to possess hepatoprotective and anti-cholestatic effects, in an effort to hasten recovery.185The exact value of using this medication to treat steroid-induced cholestatic jaundice remains unknown, however. The liver is highly resilient, and intrahepatic cholestasis is unlikely to continue degrading after drug discontinuance unless additional pathologies are present.

More serious hepatic complications are rare, but have included peliosis hepatis186 (blood-filled cysts on the liver), portal hypertension with variceal bleeding187 (bleeding caused by increased blood pressure in portal vein related to obstructed blood flow), hepatocellular adenoma188 (non-malignant liver tumor), hepatocellular carcinoma189(malignant liver tumor), and hepatic angiosarcoma190 (aggressive malignant cancer of the lining of blood vessels inside the liver). Some of these pathologies can be very insidious at times, developing quickly and without clear early symptoms. Although many of these potentially life-threatening side effects have often been attributed to very ill patients receiving steroid medications, a growing number of case reports are now involving otherwise healthy young bodybuilders abusing these drugs. Additionally, there are at least two case reports of a previously healthy bodybuilder developing liver cancer after taking high doses of oral anabolic/androgenic steroids, and one confirmed death.191 192

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Androgens stimulate the sebaceous glands in the skin to secrete an oily substance called sebum, which is made of fats and the remnants of dead fat-producing cells. Excess stimulation, as with steroid abuse, may also cause a significant increase in the size of the sebaceous glands.193 Sebaceous glands are found at the base of the hair follicles in all hair-containing areas of the skin. If the androgen level becomes too high and the sebaceous glands become overactive, the hair follicles may begin to clog with sebum and dead skin cells, resulting in acne. Acne vulgaris (common acne) is frequent in steroid users, especially when the drugs are taken in supratherapeutic levels. This often includes acne lesions on the face, back, shoulders, and/or chest.

A mild incidence of acne vulgaris is usually addressed with topical over-the-counter acne medications and a rigorous skin cleaning routine that removes excess oil and dirt. More serious acne may develop in sensitive individuals, including acne conglobata (severe acne with connected nodules under the skin) or acne fulminans (highly destructive inflammatory acne). Such incidences may require medical intervention, which usually involves treatment with isotretinoin. Topical anti-androgen drugs are also under investigation for the treatment of severe acne, and have shown a great deal of promise in early trials.194 Acne is typically resolved with the cessation of steroid use, although the overproduction of sebum may persist until the sebaceous glands have had time to atrophy back to original size. Serious forms of acne may produce lasting scars.[/vc_column_text][vc_single_image image=”1600″ alignment=”center” border_color=”grey” img_link_large=”yes” img_link_target=”_blank” img_size=”medium” css=”.vc_custom_1431008535613{padding-bottom: 25px !important;}”][vc_column_text css=”.vc_custom_1428374751884{padding-bottom: 25px !important;}”]

Acne on the chest caused by steroid use.

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Hair Loss (Androgenetic Alopecia)

Anabolic/androgenic steroids may contribute to a form of hair loss on the scalp known as androgenetic alopecia (AGA). This disorder is characterized by a progressive miniaturization of hair follicles, and a shortening of the anagen phase of hair growth, under androgen influence. The hair produced by affected follicles will progressively thin, covering the scalp less and less effectively. In men, the baldness produced is usually identified most simply as male pattern. This will initially include a receding hairline (fronto-temporal thinning) and thinning on the crown, areas where androgen receptor concentrations are high. In women, the balding usually takes on a more diffuse pattern, with thinning throughout the top of the head. Most women with androgenetic alopecia do not have a receding hairline.[/vc_column_text][vc_single_image image=”1601″ alignment=”center” border_color=”grey” img_link_large=”yes” img_link_target=”_blank” img_size=”medium” css=”.vc_custom_1431465211154{padding-bottom: 25px !important;}”][vc_column_text css=”.vc_custom_1428374838143{padding-bottom: 30px !important;}”]

With male AGA, hair loss is most pronounced on the temples and crown.

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Androgenetic alopecia is the most common form of hair loss in men and women alike. It is especially common in males, and more than 50% of the population will notice it by the age of 50.195 As its name signifies, androgenetic alopecia involves the interplay of both androgenic hormones and genetic factors. Individuals with this condition appear to be more locally sensitive to androgens, and have higher levels of androgen receptor protein and dihydrotestosterone in the scalp, in comparison to those unaffected.196 Although dihydrotestosterone is identified as the primary hormone involved in the progress of androgenetic alopecia, it does not possess a unique ability to influence this condition. All anabolic/androgenic steroids stimulate the same cellular receptor, and as a result are capable of providing the necessary androgenic stimulation. Baldness can result from steroid use, even in the absence of steroids that convert to, or are derived from, dihydrotestosterone.

The genetics of androgenetic alopecia are not fully understood. At one time it was believed this condition could be inherited solely from the maternal grandfather. More recent evidence contradicts this notion, however, showing strong support for father-to-son transmission in many cases.197 A number of genes have been identified as having a potential link to the disorder, including certain variants (polymorphisms) of the androgen receptor gene.198 199 No single genetic variant alone has yet been able to explain all cases of androgenetic alopecia, however. AGA is now believed to involve several genes (polygenic).200 The way these genes combine, and the level of androgens in the scalp, may ultimately work together to control the onset and severity of androgenetic alopecia. Estrogen is also known to lengthen the anagen phase,201and the pathogenesis of this condition may ultimately involve genes that alter both androgen and estrogen activity.

Treatment for androgenetic alopecia in men usually involves topical minoxidil and oral finasteride, a 5-alpha reductase enzyme inhibitor. Women are typically prescribed anti-androgens and estrogen/progestin drugs. The focus in both cases is on reducing relative androgenic action in the scalp, which may (at least temporarily) stall the condition. With this in mind, many steroid users concerned with hair loss will tailor their drug intake to minimize unnecessary androgenic activity. This usually involves moderate dosing and the careful selection of drugs with high anabolic-to-androgenic ratios, such as oxandrolone, methenolone, or nandrolone. Alternatively, some may choose to use injectable testosterone esters combined with finasteride to reduce scalp DHT conversion. These strategies are met with varying degrees of success.

There has been no study on the role of genetics in baldness linked to steroid abuse. Anecdotally, individuals with existing visible androgenetic alopecia appear to be those most susceptible to the effects of anabolic/androgenic steroids on the scalp. For many of these people, the loss of hair appears significantly accelerated when taking these drugs. On the other hand, this side effect is generally a much less significant issue with individuals that have not noticed thinning beforehand. Many go on to abuse steroids for years without any visible effect at all, making it clear that there is more to this disorder than local androgen levels. It is well understood that androgens play a role in the progression of androgenetic alopecia for those genetically prone. Steroid use can, therefore, coincide with the first noticeable onset of this condition. It is unknown, however, if anabolic/androgenic steroid abuse can cause baldness in an individual that does not carry any genetic susceptibility.

Stunted Growth

Anabolic/androgenic steroids may inhibit linear growth when administered before physical maturity. These hormones actually can have a dichotomous influence on linear height. On one hand, their anabolic effects may increase the retention of calcium in the bones, facilitating linear growth. A number of anabolic steroid programs have been successful in helping children with short stature achieve a faster rate of growth. At the same time, however, anabolic/androgenic steroid use may cause premature closure of the growth plates, which inhibits further linear growth. There have been a number of cases of noticeably stunted growth (short stature) in juvenile athletes that have taken these drugs.202 The specific outcome of steroid therapy depends on the type and dose of drug administered, the age in which it is administered, the length it is taken, and the responsiveness of the patient.

While androgens, estrogens, and glucocorticoids all inherently participate in bone maturity, estrogen is regarded as the primary inhibitor of linear growth in both men and women.203 Women are shorter on average than men, and also tend to stop growing at a slightly earlier age, due to the effects of this hormone. Anabolic/androgenic steroids that either convert to estrogen or are inherently estrogenic are, likewise, more likely to inhibit linear growth than other agents. Popular anabolic/androgenic steroids with estrogenic activity include (but are not limited to) boldenone, testosterone, methyltestosterone, methandrostenolone, nandrolone, and oxymetholone. These drugs must be used with additional caution in young patients due to their stronger potential for inducing growth arrest.

Estrogen acts directly on the epiphyseal growth plates to inhibit linear growth. These plates are located at the end of growing bones, and contain a collection of stem-like cells called chondrocytes. These cells proliferate and differentiate to form new bone cells, slowly expanding the length of the bones and the height of the individual. These cells have a finite life span, with programmed senescence (cell death). This will cause the rate of chondrocyte proliferation to slow over time, and eventually stop. The chondrocytes are replaced with blood and bone cells at the point of physical maturity, “fusing” the bones and inhibiting further linear growth. The stimulation of estrogen appears to accelerate bone age advancement by exhausting the proliferative potential of chondrocytes at an earlier time.204

Age will also influence a patient’s sensitivity to epiphyseal fusion. As young children are far from the point of bone maturity, the inhibitive effects of hormone therapy take longer to manifest in growth cessation. As the juvenile ages, they may become more sensitive to these effects. Studies treating teenage boys (average age 14 years) for tall stature, for example, found that six months of testosterone enanthate (500 mg every two weeks) was sufficient to reduce final height by almost three inches compared to the predicted outcome.205 This is a moderately supratherapeutic dose, underlining the fact that steroid intake during adolescence can have a very tangible impact on height. This issue may not be as simple as avoiding estrogenic steroids either, as non-estrogenic steroids have also induced skeletal maturation.206 Individuals remain warned of the potential for growth interruption when anabolic/androgenic steroids are used before physical maturity.

Tendon Injury

Anabolic/androgenic steroid use is sometimes associated with an increased incidence of tendon injury.207 208 There are a few potential causes for this. One of the most basic is the rapid growth of the muscles. Under the influence of anabolic/androgenic steroids, the muscles are capable of becoming significantly larger and stronger in a fairly short period of time. As the amount of weight lifted by the steroid user increases, so too does the load placed on the tendons. If the tendons are not given enough time to (or simply cannot) compensate for the added strain, they may rupture during training or athletic performance. Thus, anabolic steroids may indirectly lead to this type of injury in some users, essentially by making them too strong for their own connective tissues.

There may also be more direct mechanisms contributing to this type of injury. Similar to skeletal muscle tissue, the tendons are responsive to androgens. Studies show that under the stimulation of anabolic steroids, the tendons become more rigid.209 As tissue flexibility is reduced, so is the relative strength and forgiving nature of the tendons (essentially lowering the tearing point). Furthermore, while anabolic steroids are known to aid the healing process in the muscles, studies suggest that they may actually impair the healing of tendon injuries.210 While this is admittedly a post-injury event, one could speculate that smaller areas of damage might not repair properly, weakening the tissues. These factors, coupled with a rising workload due to expanded strength capacity, could explain a greater potential for tendon injury during anabolic/androgenic steroid use.

The data concerning the potential role of anabolic steroids in connective tissue injury is equivocal. Some studies find no association between AAS use and tendon injury.211 Overall, these types of injuries are still fairly uncommon. This could make proving an association with anabolic steroid use difficult. The level of AAS use is also undoubtedly a strong contributing factor in this type of injury. When we do see tendon ruptures, they tend to be reported in more advanced bodybuilders and steroid abusers. On the other hand, tendon injury (without a specific accident event) seems to be extremely uncommon in those that use AAS moderately and keep their body mass within reasonable levels. The potential for this type of injury is one reason many believe it is better to accumulate mass slowly and steadily with AAS, instead of rushing to put on the most bulk possible.

Water and Salt Retention

Anabolic/androgenic steroids may increase the amount of water and sodium stored in the body. This may include increases in both the intracellular and extracellular water compartments. Intracellular fluid refers to water that has been drawn inside the cells. While this does not increase the protein content of the muscles, it does expand the muscle cell, and is often calculated and viewed as a part of total fat free body mass. Extracellular water is stored in the circulatory system, as well as in various body tissues, in the spaces between cells (interstitial). Increases in interstitial fluid can be noticeable and troubling cosmetically. In strong cases this can bring about a very puffy appearance to the body (peripheral or localized edema), with bloating of the hands, arms, body, and face. This may reduce the visibility of muscle features throughout the physique. Excess fluid retention can also be associated with elevated blood pressure,212 which can increase cardiovascular and renal strain.

Estrogen is a regulator of fluid retention in both men and women.213 This effect appears to be mediated in part by changes in hypothalamic arginine vasopressin (AVP), the primary hormone involved in controlling water reabsorption in the kidneys.214 Increased levels of estrogen tend to increase AVP levels, which can promote the increased storage of water. Estrogen also appears to act on the renal tubes in the kidneys in an aldosterone- independent manner to increase the reabsorption of sodium.215 Sodium is the major electrolyte in the extracellular environment, and helps to regulate the osmotic balance of cells. Higher levels can significantly increase water in the extracellular compartment. Anabolic/androgenic steroids that either convert to estrogen, or possess inherent estrogenic activity, are, likewise, those steroids that are associated with increased extracellular water retention.216

Estrogenic anabolic/androgenic steroids are generally favored for mass gaining (bulking) purposes. A steroid user may ignore water retention during this phase of training, occasionally even finding the sheer increases in size to be a welcome benefit. Estrogenic steroids such as testosterone and oxymetholone are also regarded as the strongest mass- and strength-building agents, which may be caused in part by anabolic benefits of elevated estrogenic activity. The excess water stored in the muscles, joints, and connective tissues is also commonly believed to increase an individual’s resistance to injury. With the use of many strongly estrogenic anabolic/androgenic steroids, water retention can account for a large portion (35% or more) of the initial body weight gain during steroid treatment. This weight is quickly lost once the steroids are discontinued or estrogenic activity is reduced.

Non-aromatizing steroids such as oxandrolone and stanozolol have also been shown to promote increased water retention, so this effect is not entirely exclusive to aromatizable or estrogenic substances.217 218 Anabolic steroids with low or no estrogenic action tend to produce modest increases in whole body water and intracellular fluid retention, however, and not in the visible extracellular compartment.219 220 These steroids are considered to be more cosmetically appealing, and are generally favored by bodybuilders and athletes when looking to improve lean mass and muscle definition. Popular anabolic/androgenic steroids that are associated with low visible water retention include fluoxymesterone, methenolone, nandrolone, oxandrolone, stanozolol, and trenbolone.

Excess water retention may be addressed with the use of ancillary medications such as the anti-estrogen tamoxifen citrate, or an aromatase inhibitor such as anastrozole. By minimizing the activity of estrogens, these drugs can effectively reduce the level of stored water. In most cases where an aromatizable steroid is used, aromatase inhibitors prove to be significantly more effective at achieving this goal. A common practice among bodybuilders during competition is to also use a diuretic, which can shed excess water by directly increasing renal water excretion. This is regarded as the most effective method for rapidly improving muscle definition, but it can also be one of the most acutely risky practices as well. Water retention is not a persistent side effect of steroid use. Excess water is quickly eliminated, and normal water balance returned, once anabolic/androgenic steroid administration is halted.

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Dysphonia (Vocal Changes)

Although far less common than dysphonia in women, anabolic/androgenic steroids may alter vocal physiology in men. This may include a deepening of the voice.[/vc_column_text][vc_column_text css=”.vc_custom_1431013362716{padding-bottom: 30px !important;}”]

Dysphonia is most common when anabolic/androgenic steroids are administered during adolescence, as the deeper adult voice has not yet been established under the influence of androgens. The administration of anabolic/androgenic steroids before maturity can, likewise, cause a progressive lowering of the vocal pitch, and may trigger pubescent vocal changes in younger patients. Androgens have much less (often minimal) effect on vocal physiology in adulthood. Although a slight lowering of the voice may be noticed with androgen use in some cases, reports of clinically significant changes in the vocal quality of adult men are, likewise, very rare. There has also been an isolated report of stridor (vibrating noise when breathing) and vocal hoarseness in relation to anabolic/androgenic steroid abuse.221 This instance also involved smoking, however, making the direct influence of steroids more difficult to discern. In general, vocal physiology is well established by adulthood. Aside from very minor reductions in pitch, anabolic/androgenic steroids are not expected to have strong audible effects on the voice.


Anabolic/androgenic steroids with significant estrogenic or progestational activity may cause gynecomastia (female breast development in males). This disorder is specifically characterized by the growth of excess glandular tissue in men, due to an imbalance of male and female sex hormones in the breast. Estrogen is the primary supporter of mammary gland growth, and acts upon receptors in the breast to promote ductal epithelial hyperplasia, ductal elongation/branching, and fibroblast proliferation.222 Androgens, on the other hand, inhibit glandular tissue growth.223 High serum androgen levels and low estrogen usually prevent this tissue development in men, but it is possible in both sexes given the right hormonal environment. Gynecomastia is regarded as an unsightly side effect of anabolic/androgenic abuse by most users. In extreme cases the breast may take on a very female looking appearance, which is difficult to hide even with loose clothing.

Gynecomastia tends to develop in a series of progressive stages. The severity of this process will vary depending on the type and dose of drug(s) used, and individual sensitivity to hormones. The first sign is typically pain in the nipple area (gynecodynea). This may quickly coincide with minor swelling around the nipple area (lipomastia). This is sometimes referred to as pseudo-gynecomastia, as it primarily involves fat and not glandular tissue. At this stage, it may be possible to address mild nipple swelling by reducing or eliminating the offending steroidal compounds, and administering an appropriate anti-estrogenic medication for several weeks. If left untreated, however, this may quickly progress to clear gynecomastia, which involves significant fat, fibrous, and glandular tissue growth. The hard tissue growth may be easily felt in the early stages when pinching deeply around the nipple. Noticeable gynecomastia is likely to require corrective cosmetic surgery (male breast reduction).224

Although gynecomastia is one of the most common steroid side effects, given its clear association with certain drugs or practices, it is also an easily avoidable one. Careful steroid selection and reasonable dosing are usually regarded as the most basic and reliable methods for preventing its onset. Many steroid users also frequently take some form of estrogen maintenance medication, which may effectively counter the effects of elevated estrogenicity. Common options include the anti-estrogen tamoxifen citrate, or an aromatase inhibitor such as anastrozole. The use of a post-cycle hormone recovery program at the conclusion of steroid administration (which usually includes several weeks of anti-estrogen use) is also commonly advised, as gynecomastia is sometimes reported in the post-cycle hormone imbalance phase when steroids are not actually being taken.

It is important to note that progesterone can also augment the stimulatory effect of estrogen on mammary tissue growth.225 As such, progestational drugs may be able to trigger the onset of gynecomastia in sensitive individuals, even without elevating levels of estrogen. Many anabolic steroids, particularly those derived from nandrolone, are known to exhibit strong progestational activity. While gynecomastia is not a common compliant with these drugs, they are occasionally linked to this side effect in anecdotal reports. The anti-estrogen tamoxifen citrate is usually taken in such instances, as it can offset the effects of estrogen at the receptor, which are still necessary for progestins to impart their growth- promoting effects on the breast.

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Early gynecomastia.

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Birth Defects

Anabolic/androgenic steroid exposure to a woman during pregnancy can cause developmental abnormalities in an unborn fetus. Virilization of a female fetus is a particular concern, and may include clitoral hypertrophy or even the growth of ambiguous genitalia (pseudohermaphroditism). Reconstructive surgery will be required to correct these serious developmental abnormalities. Women who are pregnant, or are attempting to become pregnant, should not use or directly handle anabolic/androgenic steroid materials (raw powder, pills, crèmes, patches). Although anabolic/androgenic steroids can reduce sperm count and fertility in men, they are not linked to birth defects when taken by someone fathering a child.

Dysphonia (Vocal Changes)

Anabolic/androgen steroids are commonly linked to a deepening of the voice in females. This is caused by direct androgenic influence on the larynx and muscle tissues involved in vocal physiology, which (in females) are not normally exposed to high androgen levels. Early changes may include a light hoarsening of the voice, with audible shifts in pitch at the high and low end of the vocal spectrum (quiet speaking and voice projection).226 There is typically a lower general frequency during speech, a reduction of high frequency pitch, and voice instability and cracking. In many cases the changes caused by AAS drugs may resemble those of the pubescent male. If left to progress, these changes may go on to develop into a raspy and recognizable male-characteristic voice.

Deepening of the voice is defined as an androgenic or masculinizing effect. Anabolic/androgenic steroids with higher relative androgenicity such as testosterone, fluoxymesterone, and methandrostenolone, likewise, have a high tendency to produce voice changes when used in females.227 228 229 230 All anabolic/androgenic steroids are capable of altering the female voice given the right level of stimulation, however. To this point, vocal changes have been reported under therapeutic conditions with even mild anabolic substances such as oxandrolone and nandrolone.231 232 Care must be taken to monitor the voice during all AAS intake, as changes are often easily generated. Immediately discontinuing anabolic/androgenic steroids may reduce the severity of symptoms, although some changes are likely to persist. Anabolic/androgenic steroid use may, likewise, permanently alter vocal physiology in females.

Enlarged Clitoris (Clitoromegaly)

The male and female reproductive systems differentiate and develop under the influence of estrogen and testosterone. Even as an adult, the female reproductive system remains developmentally responsive to male sex hormones. An elevation of the androgen level in women may stimulate the growth of the clitoris (clitoral hypertrophy). If androgen levels are not abated quickly this may lead to virilization of the external genitalia, characterized by clinically abnormal enlargement of the clitoris (clitoromegaly). With clitoromegaly, the clitoris may begin to resemble a small penis, and may even visibly enlarge during sexual arousal (erection). In more serious cases its association to a male penis can be very striking and clear. Clitoromegaly can be a very embarrassing condition, usually prompting swift intervention when its onset is noticed.

Clitoromegaly is most commonly seen as a congenital disorder, although it may be caused by anabolic/androgenic steroid administration or other pathology in adulthood (acquired clitoromegaly). As a virilizing side effect, clitoromegaly tends to occur in a dose-dependant (androgenicity-dependent) manner. As such, higher doses and more androgenic substances (such as testosterone, trenbolone, and methandrostenolone) are more likely to trigger its onset. Primarily anabolic steroids such nandrolone, stanozolol, and oxandrolone are less androgenic and virilizing, and favored for the treatment of women for this reason. Clitoromegaly caused by steroid use is both avoidable and progressive. Mitigating excess androgenic action early when it is noticed is the most fundamental part of treatment. Reversal of significantly developed tissue, however, will require reconstructive surgery (clitoroplasty).233 Special care should be taken to preserve the dorsal and ventral neurovascular bundles and normal tissue sensation.234[/vc_column_text][vc_single_image image=”1605″ alignment=”center” border_color=”grey” img_link_large=”yes” img_link_target=”_blank” img_size=”medium” css=”.vc_custom_1431465188113{padding-top: 30px !important;padding-bottom: 25px !important;}”][vc_column_text css=”.vc_custom_1428375290516{padding-bottom: 30px !important;}”]

A photograph of distinct clitoromegaly.Here, the clitoris begins to resemble a penis-like structure under androgen influence. If left unabated, this may progress to a more defined phallic abnormality. Source: Copcu et al. Reproductive Health 2004 1:4 doi:10.1186/1742-4755-1-4.

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Hair Growth (Hirsutism)

Anabolic/androgenic steroids may cause male-pattern hair growth in females. Medically defined as hirsutism, this condition is characterized by the growth of hair in androgen sensitive areas of the body. With hirsutism, dark coarse hair (terminal hair) may develop on the face, chest, abdomen, and back, areas of the body normally associated with hair growth in men, not women. Treatment for hirsutism typically involves immediate abstinence from anabolic/androgenic steroid intake, and initiation of a strategy to minimize androgen action at the hair follicles. This may include the use of oral estrogens, anti-androgens (spironolactone), or finasteride. Topical ketoconazole, an antifungal agent, has also been used with some success. The response to medical treatments may be slow, and the changes caused by anabolic/androgenic steroid use may persist for a year or longer.235 Regular hair removal of the affected areas may be necessary. The severity of hirsutism will be related to the androgenicity of the drug(s) taken, the dosage and duration of use, and sensitivity of the individual.

Menstrual Irregularities

Anabolic/androgenic steroids may alter the menstrual cycle in females, resulting in infrequent or absent menses (amenorrhea). Fertility may also be interrupted. Normal menstruation is expected to resume after anabolic/androgenic steroids are discontinued, and the natural hormonal balance is restored. Complete recovery of the female hormonal axis and fertility can take many months in some cases, however, and long-term interruptions of fertility are possible, though unlikely.

Reduced Breast Size

Anabolic/androgenic steroids can inhibit the growth- supporting effects of estrogen on mammary tissues, and may cause a visible reduction in breast size (breast atrophy). Androgen use in females has specifically been shown to cause a reduction in glandular tissue size, and to promote an increase in fibrous connective tissue.236 These physiological changes are similar to those noted after menopause, when female sex steroids are very low. Reductions in breast size produced by AAS may be very persistent after the discontinuance of drug intake, as there can be substantial local tissue remodeling under excess androgen influence. Women are warned of the potential for substantial physical changes in the breasts with anabolic/androgenic steroid abuse.

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The effects of anabolic/androgenic steroids on human psychology are complex, controversial, and not fully understood. What is known for certain is that sex steroids influence human psychology. They play a role in an individual’s general mood, alertness, aggression, sense of well-being, and many other facets of our psychological state. There are known psychological differences between men and women because of differences in sex steroid levels, and, likewise, altering hormone levels with the administration of exogenous steroids may influence human psychology. The exact strength of this association, however, remains the subject of much research and speculation. In reviewing some of the more substantial data that has been presented thus far, we find a better (though incomplete) understanding of the effects of AAS in several key areas of psychological health.


Men tend to be more aggressive than women, a characteristic that has been partly attributed to higher androgen levels.237 Physiologically, androgens are known to act on the amygdala and hypothalamus, areas of the brain involved in human aggression. They also affect the orbitofrontal cortex, an area involved with impulse control.238Steroid abusers commonly report increases in aggression (irritability and bad temper) when taking anabolic/androgenic steroids. In fact, among the illicit steroid-using community, these drugs are often differentiated from one another with regard to their aggression-promoting properties. Many athletes in explosive strength sports even specifically favor highly androgenic drugs such as testosterone, methyltestosterone, and fluoxymesterone due to their perceived greater abilities to support aggression and the competitive drive.239 While some association between steroid use and aggression is understood, the magnitude of this association remains the subject of much debate.

The psychological effects of escalating dosages of testosterone esters have been examined in a number of placebo-controlled studies. At therapeutic levels, no adverse psychological effects are apparent. If anything, testosterone replacement therapy tends to improve mood and sense of well-being. When used at a contraceptive dosage (200 mg per week), again, no significant psychological effects are seen.240 241 As the dosage reaches a moderate supratherapeutic range (300 mg per week), psychological side effects such as aggression began to appear in some subjects, but these reports remain mild and infrequent.242 At a dosage of 500 to 600 mg per week (5 to 6 times the therapeutic level), mild increases in aggression and irritability are frequently reported. Approximately 5% of subjects displayed manic or hypomanic behavior in reaction to this much testosterone, although the vast majority of people still exhibited minor or no psychological change.243 244

One extensive placebo-controlled study furthers our understanding of the psychological effects of steroid abuse, often characterized by extreme doses and multi-drug combinations, through its examination of a group of 160 regular users before and during the self-administration of a steroid cycle.245 A placebo group was also examined, which consisted of 80 people that were unknowingly taking counterfeit medications. Extensive psychological evaluations were taken using System Check List-90 (SCL-90) and the Hostility and Direction of Hostility Questionnaire (HDHQ). Those using placebo steroids did not notice any significant psychological changes. Steroid abuse, however, was associated with higher levels of hostility in all HDHQ measures, with particular increases in acting out, criticism of others, paranoid hostility, guilt, self-criticism, blaming of others, blaming of self, and overall hostility. SCL-90 ratings were also high during steroid abuse for obsessive compulsiveness, interpersonal sensitivity, hostility, phobic anxiety, and paranoid ideation. Hostility measures tended to increase significantly as the level of abuse escalated from light to heavy, although no violent behavior was reported.

Criminality and Violence

Links between anabolic/androgenic steroid abuse and violence have been much more difficult to establish. Most papers suggesting such an association either used correlative data, or discussed individual case studies. These help broaden the scope of research, but are not reliable for proving causality. For example, one study questioned a group of 23 steroid abusing men, and reported that these men were involved in a significantly greater number of verbal and even physical fights with their girlfriends and wives during the times they were administering AAS drugs.246 With the known effects of anabolic/androgenic steroids on aggression, this finding is compelling. It may very well be that some men are more susceptible to this type of behavior when abusing AAS than others. A paper like this is not sufficient, however, to substantiate a violent “roid rage”. Further research is needed to determine if AAS can even trigger violent behavior in an extremely small minority of users, and if so, what trait(s) makes these individuals susceptible to this reaction when the vast majority of users are not.

Serious criminality has also been difficult to associate with steroid abuse. When discussed, we again tend to see weak correlative data and case studies. For example, one paper in Sweden reports an association between steroid abuse and weapons and fraud crimes.247 It is uncertain, however, if steroid abuse was actually responsible for this criminality, or just associated with it. It is simply possible these men were more exposed to, or more likely to use, illegal AAS for some unidentified reason. Another paper discussed three individuals with no prior criminal or psychiatric history that were arrested for murder or attempted murder after abusing anabolic/androgenic steroids.248While stories like these are interesting (and numerous), with millions of steroid users in the general population they are far from compelling. To date, there is no conclusive medical evidence that anabolic/androgenic steroid abuse can cause violent or serious criminal behavior in a previously mentally stable individual.


Anabolic/androgenic steroids are considered to be drugs of abuse. Although there is no universally accepted definition for this, abuse is commonly described as the continued use of a substance in spite of adverse consequences. Given the negative health consequences that are associated with supratherapeutic doses of AAS drugs, this classification is a difficult one to dispute. Drugs of abuse are very often also drugs of dependency, which in this context describes an impaired ability to control the use of a substance. There has been a longstanding debate over whether or not anabolic steroids also fit the definition of drugs of dependency. Furthermore, among those that support the notion of an anabolic steroid dependency, there is a split with regard to the nature of this dependency (psychological or physical).

Physical dependency is usually regarded as the most serious form of drug dependency, although both types can be very extreme and troubling depending on the situation. Physical dependency is defined as the need to administer a substance in order for the body to function normally. A physical dependency is usually characterized by drug tolerance, and withdrawal symptoms if the drug is discontinued abruptly. The most well known examples of drugs of physical dependency are opiates such as morphine, hydrocodone, oxycodone, and heroin. Opiates can be very difficult drugs for dependant individuals to quit using, since stopping their use tends to produce extreme withdrawal symptoms including physical pain, sweating, tremors, changes in heart rate and blood pressure, and intense cravings for the drug. The physical symptoms may last for days to weeks after the drug is discontinued, while the psychological symptoms can persist for months longer.

Anabolic/androgenic steroid abuse could be associated with many of the DSM-IV criteria necessary for a diagnosis of both psychological and physical drug dependency. For instance, it is not uncommon for someone to take the drugs in higher doses or for longer periods of time then they had initially planned (criteria #1). Many abusers also have a desire to cut down on their use of these drugs, but concerns over lost muscle size, strength, or performance may prevent this decision (criteria #2). Individuals often continue to abuse steroids in spite of negative health consequences (criteria #5). Steroid abuse is also associated with a diminishing level of effect and escalating dosages (criteria #6). Lastly, steroid discontinuance has been associated with withdrawal symptoms (criteria #7), including reduced sex drive, fatigue, depression, insomnia, suicidal thoughts, restlessness, lack of interest, dissatisfaction with body image, headaches, anorexia, and a desire to take more steroids.249

According to the American Psychiatric Association and its Diagnostic and Statistical Manual of Mental Disorders (DSMIV), three or more of the following criteria must be met for a diagnosis of psychoactive drug dependency.

  1. Substance is taken in higher doses or for longer periods than intended.
  2. Desire or unsuccessful efforts to cut down or control substance use.
  3. Excessive time spent obtaining, using, or recovering from the substance.
  4. Important activities are given up because of substance abuse.
  5. Continued substance use despite negative psychological or physical consequences.
  6. Tolerance, or the need for higher amounts of the substance to achieve desired effect.
  7. Withdrawal symptoms.

A drug dependency that is isolated to criteria #1 to #5 would be described as psychological. The meeting of criteria #6 or #7 indicates the dependency is also a physical one.

The physical benefits of anabolic/androgenic steroids complicate the matter of drug dependency a great deal. Unlike narcotics, the main motivator behind the use of steroids is their positive effect on muscle and performance. With this in mind, steroid addiction could actually be a misdiagnosis for muscle dysmorphia in many cases. This is a psychological disorder characterized by persistent feelings of physical inadequacy in spite of extreme muscular development. Steroid abuse (often extreme) is highly common in muscle dysmorphics, along with compulsive resistance training.250 But steroid abuse is regarded as a symptom of this disorder, not a cause. In a similar sense, the physique-, strength-, and performance-improving qualities of anabolic/androgenic steroids could be driving much or all of the abuse. An analogy would be the so-called addiction to chocolate. Some individuals develop tangible psychological issues surrounding the consumption of chocolate, with uncontrolled binging and negative social and health consequences.251 But we do not regard chocolate itself as a substance that causes dependency.

There is some evidence that the reinforcing qualities of steroid use go beyond an attraction to their physical benefits. Lab animals such as mice and hamsters will repeatedly self-administer testosterone and other anabolic/androgenic steroids for example, an effect that cannot be caused by a perception of physical change.252 Testosterone is also known to interact with the mesolimbic dopamine system, which is common with other drugs of abuse.253 254 Studies additionally suggest that anabolic/androgenic steroids influence dopamine transporter density and increase sensitivity of the brain reward system.255 Steroids are known to influence psychology, and abusers commonly report an increased sense of wellness, vitality, and confidence when taking AAS drugs. Some speculate this is due in part to an inherent psychoactive effect. Further research is needed to determine if anabolic/androgenic steroids are actually mild psychoactive drugs.

Anabolic/androgenic steroids are not drugs of marked intoxication,256 which makes them very different from other drugs and abuse or dependency. This makes diagnosing a drug dependency difficult. By definition, drug dependency is related to the abuse of a psychoactive substance, and it is unknown if AAS drugs can accurately be classified as psychoactive substances. At the present time, most experts do not regard anabolic/androgenic steroids as drugs of true physical dependency. It is difficult to correlate the post-cycle hormone imbalance with traditional withdrawal symptoms,and tolerance is really a function of metabolic limits on muscle growth, not necessarily a diminishing biological effect. Individuals remain warned, however, that steroid abuse is commonly associated with the signs of psychological dependency. Further research is needed to evaluate the biological and psychological nature of steroid abuse.


Anabolic/androgenic steroids abuse may be associated with bouts of depression. This is most common after the administration of AAS drugs has been discontinued, especially following high doses or long cycles. During the time that steroids are being administered, natural hormone production is diminished because the body recognizes the excess hormone levels. When the steroid drugs are abruptly discontinued, however, the body can enter a state of temporary hypogonadism (low androgen levels). This may be associated with a number of psychological symptoms including depression, insomnia, and loss of interest. This condition is usually referred to as anabolic steroid withdrawal depression, and can persist for weeks or even months as the body slowly resumes normal hormone production.257

The most common method of addressing anabolic steroid withdrawal depression in men is preemptively, with the implementation of an aggressive post-cycle hormone recovery program. These programs are typically based on the combined use of HCG (human chorionic gonadotropin) and anti-estrogenic drugs such as tamoxifen and clomiphene. They are used together in a way that can stimulate and sensitize the hypothalamic pituitary testicular axis, allowing natural hormone production to return more quickly. Alternately or concurrently, fluoxetine (or other antidepressant medications) may help alleviate symptoms of depression following steroid withdrawal, especially when this depression is prolonged or severe.258 These drugs must be used with caution, however, as they also have been linked with increased thoughts of suicide in some patients.259

Although less common, depression is sometimes reported during the active administration of anabolic/androgenic steroids. This may be caused by an imbalance of sex steroid levels, particularly with regard to relative androgenicity or estrogenicity. In more cases than not, it will involve a situation where sufficient androgenicity is not present, usually when primarily anabolic drugs are being taken alone. Given the diverse nature in which sex steroids interact with human psychology, however, it is difficult to clearly outline the parameters necessary for this type of depression to develop. Further confusing the issue is the fact that this depression can involve either elevated or suppressed levels of certain sex steroids. The addition of testosterone to an anabolic steroid cycle causing depression may alleviate the problem in many (but not all) instances, as it can provide both supplemental androgenic and estrogenic action.

Suicide has been linked to anabolic/steroid abuse in rare instances.260 Such reports are usually case studies, involving individuals that were believed to be psychologically stable before abusing AAS, and who committed suicide during or after use of the drugs. It is known that depression is a common complaint during anabolic steroid withdrawal. It is also known that a small percentage of users are especially sensitive to the psychological effects of anabolic/androgenic steroids, and notice dramatic mood swings, manic behavior, and/or severe depression with their use. It is unknown why these individuals have such extreme reactions, while the vast majority of users notice only mild or moderate changes to their psychological state. Further research is needed to identify and understand these individuals. Readers are cautioned that adverse psychological effects, including severe depression and suicidal thoughts, have been associated with steroid abuse in a small minority of users. Beyond this, there is no compelling evidence suggesting that anabolic/androgenic steroid abuse will lead to suicide in otherwise mentally stable users.


Anabolic/androgenic steroid use may be associated with insomnia. This adverse reaction appears to be related to an imbalance of hormone levels, and has been noticed during both excess and insufficient hormonal states. For example, insomnia is a common complaint among men suffering from low androgen levels (hypogonadism).261 It is also frequently reported by steroid abusers during the post-cycle refractory period, when endogenous androgen levels are also low due to steroid-induced suppression.262 At the same time, this side effect is also seen during active AAS administration,263 when androgen levels are very high. The full etiology of steroid-related insomnia is not fully understood, although increased cortisol or diminished estrogen is commonly blamed.264 265 Given the complex interactions between sex steroids and the human psyche, it is difficult to predict how and when this adverse reaction will appear. While insomnia may be frequently reported among steroid users, this side effect rarely reaches a clinically significant level.

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Anabolic/androgenic steroid use may impair fertility. The human body strives to maintain balance in its sex hormone levels (homeostasis). This balance is regulated largely by the hypothalamic-pituitary-testicular axis (HPTA), which is responsible for controlling the production of testosterone and sperm.The administration of anabolic/androgenic steroids provides additional sex steroid(s) to the body, which the hypothalamus can recognize as excess. It responds to this excess by reducing signals that support the production of pituitary gonadotropins luteinizing hormone (LH) and follicle-stimulating hormone (FSH). LH and FSH normally stimulate the release of testosterone by the testes (gonads), and also increase the quantity and quality of sperm. When LH and FSH levels drop, testosterone levels, sperm concentrations, and sperm quality may all be reduced.

When given in supraphysiological levels, anabolic/androgenic steroids commonly induce oligozoospermia. This is a form of reduced fertility characterized by having less than 20 million spermatozoa per ml of ejaculate. The quality of the sperm may also be impaired under the influence of AAS, as noted by an increase in the number of abnormal or hypokinetic (noticing reduced motion) sperm. Fertility is possible during oligozoospermia, however, as viable sperm are still made by the body. The odds of conception are just significantly lower than when sperm concentrations are normal. In many cases azoospermia is reached during AAS administration, which is defined as having no measurable sperm in the ejaculate. Conception is not possible with true steroid-induced azoospermia. Note that in some cases, fertility has been temporarily restored during active anabolic/androgenic steroid abuse with the use of human chorionic gonadotropin (HCG).266

Diminished fertility is considered a reversible side effect of anabolic/androgenic steroid abuse. Sperm concentrations usually return to normal within several months of discontinuing drug intake. A substantial post-cycle recovery program based on the use of HCG, tamoxifen, and clomiphene may significantly shorten the refractory period, and is highly recommended among those in the steroid-using community. In a small percentage of cases, particularly following long periods of heavy steroid abuse, recovery of the HPTA can be very protracted, taking up to a year or longer for full recovery.267 268 Given the undesirable psychological and physical symptoms that can be associated with a prolonged state of low testosterone levels, such a long recovery window is rarely regarded as acceptable. This will usually prompt an individual to seek medical intervention or initiate an aggressive HPTA recovery program.

The ability of anabolic/androgenic steroids to suppress LH, FSH, and fertility has initiated a great deal of research surrounding their use as male contraceptives. Injectable testosterone has been extensively studied by the World Heath Organization, for example, and was determined to be a safe and moderately effective method of male birth control. In studies which administered 200 mg of testosterone enanthate per week to healthy men, azoospermia was achieved in 65% of patients within six months.269 Most of the remaining patients were oligozoospermic. This diminished fertility was fully reversible, and baseline sperm concentrations returned within seven months on average after drug discontinuance. A state of full azoospermia is the desired endpoint of male contraception, however, and this has not been reliably achieved with AAS drugs alone, even in high doses.270 Anabolic/androgenic steroids have, likewise, are not approved for use as male contraceptives.

Libido/Sexual Dysfunction

Anabolic/androgenic steroids may alter sexual desire and functioning. The nature of their effects, however, can vary depending on the drug(s) and dosage(s) used, as well as the individual sensitivity of the user to hormonal manipulation. One of the most common responses is a stimulatory one. Testosterone is the primary male sex steroid. As such, it is responsible for increasing sexual desire and supporting many male reproductive-system functions.271Since all anabolic/androgenic steroids are derived from (and share similar action to) testosterone, use of these drugs is often linked to increases in sexual desire, as well as copulation and orgasm frequency.272 A significant increase in the frequency and duration of erections may also be noted. In most cases these side effects are not troubling, and may even be regarded as positive by the individual (some feel it improves their sex lives).

AAS use may also be associated with diminished libido and sexual functioning. This could be due to several factors. One is insufficient androgenic activity. This sometimes is noted with the use of primarily anabolic steroids such as methenolone, nandrolone, or oxandrolone, which may not provide sufficient androgenicity to compensate for suppressed endogenous testosterone.273 Studies also show that estrogen plays an important role in libido and sexual function in men.274 Therefore, the use of non-aromatizable steroids or aromatase-inhibiting drugs sometimes also causes interference. The addition or substitution of testosterone during a cycle is usually regarded as the most reliable way to correct issues with male sexual functioning, as it supplements the full spectrum of sex steroid activity. Note that sexual issues are also common after steroid discontinuance, when endogenous steroid levels are low.


In very rare instances, anabolic/androgenic steroids have been linked to priapism.275 276 277 This is a condition characterized by the development of an erection that will not return to its flaccid state within four hours. Priapism is a potentially very serious condition, which can require medical or surgical intervention. If left untreated, priapism can lead to permanent penile damage, erectile dysfunction, or even gangrene, which may necessitate removal of the penis. When priapism is linked to steroid use, testosterone is usually responsible. Furthermore, this condition appears to be more frequent in younger patients undergoing treatment for hypogonadism. This may be due in part to a rapid increase in androgenicity, in a male reproductive system that has not yet been exposed to high levels of stimulation. Priapism is very unlikely to develop in adult steroid abusers.

Prostate Cancer

Prostate cancer is dependent on androgens. This disease will not develop if androgens are eliminated from the body at a young age (as with castration),278 and abatement of androgenic activity in patients with active disease is regarded as a standard path of treatment. A complete picture of the involvement of androgens, however, remains unclear. Studies show there is no association between the testosterone level and likelihood of developing prostate cancer.279 On the same note, the administration of exogenous testosterone during androgen replacement therapy seems to have no effect on the risk for developing this disease.280 A review of the available medical literature also does not support an increased risk of prostate cancer in steroid abusers,281 which typically endure excessive levels of androgenic stimulation. The present model suggests that while testosterone is a necessary component of prostate cancer, it does not appear to be a direct trigger for its onset.282

New diagnoses of prostate cancer are sometimes reported during testosterone replacement therapy and steroid abuse.283 284 Such reports may be the result of a previously undiagnosed condition or unrelated development of this disease, with androgen stimulation assisting the tumor growth rate. Many forms of prostate cancer possess functional androgen receptors, and are highly androgen responsive. As such, they can be stimulated to grow under the influence of testosterone or other anabolic/androgenic steroids. Given this effect, AAS drugs are usually contraindicated in patients with a history of prostate cancer.285 While steroid administration appears unlikely to cause prostate cancer, individuals remain warned that the use of testosterone or other AAS drugs by someone with previously undiagnosed (latent) malignant prostate cancer could result in the more rapid advancement of this disease.286

Prostate Enlargement

Anabolic/androgenic steroids may influence the size of the prostate. Androgens are integral to the development of the prostate in early life, and are essential to maintaining prostate structure and function throughout adulthood. Increases in the androgen level often result in growth stimulation to this gland (prostate hypertrophy). For example, increased prostate volume has been reported in some patients receiving testosterone injections for the treatment of hypogonadism.287 While extreme prostate hypertrophy is not common under therapeutic conditions, prostate volume does tend to reach a size that is considered normal for a given androgen level.288 PSA (prostate-specific antigen) levels have also been shown to increase under the influence of exogenous testosterone in some patients,289 which is a diagnostic marker of prostate health often correlated with prostate volume.290 291 Additionally, reducing stimulation of the prostate by lowering the androgen level tends to reduce prostate volume.292

Anabolic/androgenic steroid abuse may result in significant increases in prostate volume. In more severe cases, this may lead to benign prostate hypertrophy (BPH). BPH is a common condition in older men, characterized by reduced urine flow, difficulty or discomfort urinating, and changes in urinary frequency. Anecdotal reports of BPH among steroid-using bodybuilders are not common, but do occur with enough frequency to warrant concern. Such reports are most often linked to more androgenic drugs such as testosterone and trenbolone, or the excessive dosing of AAS in general. One of the most extreme reports of prostate hypertrophy came from Dr. John Ziegler, the U.S. Olympic physician accredited with introducing Dianabol to sports.293 Dr. Ziegler noted that during the mid-1950s, many Russian weightlifters were abusing so much testosterone that they needed catheterization to urinate. Dianabol was released soon after, which is structurally a close derivative of testosterone with reduced androgenicity.

Studies of anabolic/androgenic steroid abusers show a preferential stimulation of the inner prostate under the influence of these drugs, in an area where benign prostate hypertrophy is known to originate.294 In contrast, prostate cancer usually develops in peripheral areas of the gland. Some association between BPH and prostate cancer is known to exist, however, although the exact nature and strength of this association remains uncertain.295 PSA values are often (although not always) elevated in both disorders, and serve as a marker of potential trouble. It is important for men to monitor prostate health regularly by digital rectal examinations and blood testing for PSA levels. Anabolic/androgenic steroid use is generally immediately discontinued if signs of BPH or elevated PSA values become apparent.

In addition to androgens, estrogens are also known to be involved in prostate growth and functioning.296 While androgens are generally stimulatory towards prostate growth, however, estrogen exerts both protective and adverse effects.297 On the beneficial side, stimulation of estrogen receptor (ER-beta subtype) may help protect the prostate from inflammation, cell hyperplasia, and carcinogenesis. Conversely, stimulation of the alpha subtype of the estrogen receptor is linked to abnormal cell proliferation, inflammation, and carcinogenesis. How the aromatization of testosterone and AAS (which will result in stimulation of both receptor subtypes) will effect prostate hypertrophy remains unclear. Prostate growth and elevated PSA values have been noted during steroid administration with both strongly and mildly estrogenic steroids.298 Furthermore, the administration of anastrozole (an inhibitor of estrogen synthesis) during testosterone administration does not appear to block stimulation of the prostate.299 Presently, the most successful strategy to minimizing prostate hypertrophy seems to be focused on reducing relative androgenic, not estrogenic, action.

Testicular Atrophy

Anabolic/androgenic steroids may produce atrophy (shrinkage) of the testicles. Testosterone is synthesized and secreted by the Leydig cells in the testes. Its release is regulated by the hypothalamic-pituitary-testicular axis, a system that is very sensitive to sex steroids. When anabolic steroids are administered, the HPTA will recognize the elevated hormone levels, and respond by reducing the synthesis of testosterone. If the testes are not given ample stimulation, over time they will atrophy, a process that can involve both a loss of testicular volume and shape. This atrophy may or may not be obvious to the individual. In some cases, the testes will appear normal even though their functioning is insufficient. In other cases, shrinkage is very apparent. Visible testicular atrophy is one of the most common side effects of steroid abuse, appearing in more than 50% of all anabolic/androgenic steroid abusers.300 301

Although testicular atrophy is very common in frequency, it is also regarded as a temporary reversible side effect.302The gonads, by their nature, will vary in size under hormonal influence. Atrophy should not produce permanent damage. Note, however, that it can be a somewhat persistent issue. It may take many weeks or months of sufficient LH stimulation after steroid discontinuance for original testicular volume to be restored. Likewise, testicular atrophy is usually the root cause of prolonged post-cycle hypogonadism. In extreme cases, full recovery can take more than 12 months, and may even require medical intervention. A post-cycle recovery program inclusive of HCG (which mimics luteinizing hormone activity) may be used to minimize this recovery phase.303 This drug is also frequently effective for maintaining testicular mass when used on a periodic basis during steroid administration.304 HCG must be used with caution, however, as overuse may cause desensitization of the testes to LH,305 complicating HPTA recovery.

Some of the more potent anabolic/androgenic steroids, including testosterone, nandrolone, trenbolone, and oxymetholone, appear to be more suppressive of testosterone release than many other AAS drugs. This may be explained in part by the additional estrogenic or progestational activity inherent in these steroids, as estrogens and progestins both also provide negative feedback inhibition of testosterone release.306 307 It is important to note, however, that all anabolic/androgenic steroids are capable of suppressing testosterone secretion. This includes primarily anabolic compounds such as methenolone and oxandrolone, which are normally regarded as milder in this regard. While these compounds may be less inhibitive of testosterone synthesis under some therapeutic conditions, when taken in the supratherapeutic doses necessary for physique- or performance-enhancement, significant atrophy and suppression are common, and distinctions less pronounced.

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Anaphylactoid Reactions

An anaphylactoid reaction is a serious and potentially life threatening allergic response to the administration of a foreign substance. Symptoms of this disorder include itching of the skin and eyes, swelling of the mucous membranes, hives, lowered blood pressure, abdominal pain, vomiting, and dilated blood vessels. The smooth muscles may also be stimulated to contract, thereby restricting breathing. Anaphylactic shock may develop in severe cases, which is marked by unconsciousness, coma, or death. The physical symptoms of this disorder are medicated by the release of histamine, leukotriene C4, prostaglandin D2, and tryptase. An anaphylactoid reaction has many of the same characteristics as anaphylaxis, although is not immune system mediated. Anaphylactoid reactions are highly uncommon with hormonal medications such as anabolic/androgenic steroids. Warnings of this reaction remain standard on many (often) injectable medications, however. Mild skin reactions may be effectively treated with an antihistamine. More serious manifestations may require IV epinephrine and other supportive care. Given the potential for rapid escalation of this condition, immediate medical attention should be sought if an anaphylactoid reaction develops.

Cancer, Brain

Anabolic/androgenic steroids are not associated with brain cancer. Complications relating to a rare and usually fatal form of cancer called primary central nervous system (brain) lymphoma caused the death of famous American football player Lyle Alzado. This type of brain cancer most commonly appears in immune-compromised patients, such as those suffering from Human Immunodeficiency Virus (HIV), or organ transplant recipients taking immunosuppressive drugs to prevent organ rejection.308 309 Before his death, Alzado had self-attributed his cancer to 14 years of anabolic/androgenic steroid abuse.310 While anabolic/androgenic steroids can be mildly immunosuppressive, these drugs are not associated with extreme clinical immunosuppression that could lead to brain lymphoma. Likewise, there is no clinical evidence or understood mechanism that suggests AAS abuse is responsible for Alzado’s death. Even though physicians say there is no proof of an association between performance-enhancing drug abuse and Alzado’s cancer,311 this story is frequently recounted in the media to convey the dangers of steroid abuse and steroid side effects.

Cancer, Breast

Although extremely rare, male breast cancer has been associated with the administration of testosterone.312 It is unknown, however, if the hormone therapy was related to the onset of this disease, or if it was just incidental to its progression and discovery. Androgens generally exhibit inhibitory effects on hormone-responsive breast cancers, and have actually been used in their treatment.313 Estrogens, on the other hand, can support the growth of many breast tumors. It is not uncommon for elevated estrogen levels to result from testosterone therapy, and at least a supportive role is plausible. The exact relationship between isolated cases of breast carcinoma and testosterone administration in men remains unclear. Testosterone is presently contraindicated in patients with breast cancer.

The data concerning the effects of anabolic/androgenic steroids on insulin sensitivity is difficult to interpret. It does appear that when these drugs are used initially, reductions in body fat are common, particularly visceral adipose tissue. This may actually improve insulin sensitivity and the overall metabolic state, and reduce certain specific risk factors for diabetes and cardiovascular disease. Beyond this, the effects of AAS on glucose metabolism are not fully understood, and difficult to predict. Studies using supratherapeutic doses of testosterone and nandrolone have failed to produce any negative changes, suggesting that moderate AAS abuse is probably not associated with impairments in insulin sensitivity. At the same time, studies do suggest that there could be concerns with heavy steroid abuse. Further research is needed is assess the impact of steroid abuse on metabolic health.

Insulin Resistance

Anabolic/androgenic steroids may alter insulin sensitivity, an important measure of metabolic health. The effect of these drugs may be variable, however. For example, testosterone administration may improve insulin sensitivity in men with hypogonadism.314 Oxandrolone (20 mg per day) has also been shown to improve insulin sensitivity in older men (60 to 87 years).315 These beneficial metabolic outcomes were correlated with reductions in visceral adipose tissue (VAT). This is a deep layer of fat that surrounds the abdominal organs, and is associated with insulin resistance.316 Insulin resistance may also lead to other health issues including hypertension, elevated triglycerides and cholesterol, and increased risk of diabetes and cardiovascular disease. By reducing VAT levels, testosterone and AAS may improve insulin sensitivity, and potentially metabolic health.

Conversely, anabolic/androgenic steroid abuse has been associated with impaired glucose metabolism.317 In one study, powerlifters that had abused AAS in high doses for up to seven years were shown to have diminished glucose tolerance and increased insulin resistance.318 In spite of a long history of resistance exercise, these subjects secreted more insulin in response to measured glucose ingestion than even obese sedentary control subjects. Additional studies with methandrostenolone demonstrated significantly increased insulin secretion and potential resistance.319A similar outcome is not found in all AAS studies, however. For example, testosterone enanthate in doses as high as 600 mg per week for 20 weeks failed to produce any changes in insulin sensitivity in healthy young men.320Nandrolone decanoate (300 mg per week) also did not impair glucose tolerance, and actually improved insulin independent glucose disposal.321 The data concerning the effects of anabolic/androgenic steroids on insulin sensitivity is difficult to interpret. It does appear that when these drugs are used initially, reductions in body fat are common, particularly visceral adipose tissue. This may actually improve insulin sensitivity and the overall metabolic state, and reduce certain specific risk factors for diabetes and cardiovascular disease. Beyond this, the effects of AAS on glucose metabolism are not fully understood, and difficult to predict. Studies using supratherapeutic doses of testosterone and nandrolone have failed to produce any negative changes, suggesting that moderate AAS abuse is probably not associated with impairments in insulin sensitivity.At the same time, studies do suggest that there could be concerns with heavy steroid abuse. Further research is needed is assess the impact of steroid abuse on metabolic health.


Anabolic/androgenic steroid use may be associated with periodic nosebleeds. According to one study, approximately 20% of illicit steroid users reported this side effect, making it fairly common.322 Nosebleeds are not a direct result of androgenic action, but are secondary to steroid-induced increases in blood pressure and/or reductions in blood clotting factors. Although they can be scary, most nosebleeds are harmless, and will not require emergency medical attention. When related to steroid use, however, they may reflect other more serious underlying health issues, particularly hypertension. Nosebleeds that occur under AAS influence usually stop reappearing shortly after drug discontinuance, as blood pressure and/or clotting factors return to their normal pre-treated state.

Sleep Apnea

Obstructive sleep apnea (OSA) is a disorder characterized by brief pauses in breathing during sleep, which occur when the soft tissues in the throat close and block the air passages. Sleep apnea may interfere with normal gas exchange, and can significantly reduce the productivity of sleep. It may also elevate the hematocrit, thicken the blood, and increase the risk of other health issues including hypertension and cardiovascular disease.323 Sleep apnea can sometimes go undiagnosed for years, as an individual may not be aware of the obstructions during sleep. Symptoms of OSA include daytime sleepiness, snoring, nocturnal awakenings, and morning headaches. Obstructive sleep apnea seems to occur most commonly in overweight individuals, and is related to a combination of hormonal, metabolic, and physical factors.324 325

Anabolic/androgenic steroids may be associated with the development of obstructive sleep apnea in a small percentage of individuals. The exact relationship between AAS and OSA, however, remains unclear. This adverse reaction seems to appear in some patients receiving testosterone drugs to treat hypogonadism.326 More detailed studies have shown that high does of testosterone can disrupt sleep and breathing, as well as increase sleep-related hypoxemia, effects that may precipitate obstructive sleep apnea.327 While OSA has not been clearly documented in steroid abusers, androgens have been shown to alter the structure and function of the oropharynx in ways that can predispose an individual to this disorder.328 More research is needed to determine if steroid abuse can trigger OSA in an otherwise healthy person. Individuals with a history of obstructive sleep apnea should not use anabolic/androgenic steroids. Physicians are advised to monitor their patients closely for signs of OSA during AAS therapy.[/vc_column_text][/vc_column][/vc_row][vc_row][vc_column width=”1/1″][vc_column_text css=”.vc_custom_1428565207685{padding-top: 25px !important;padding-bottom: 25px !important;}”]References:

90.Use of anabolic steroids and associated health risks among gay men attending London gyms.Bolding G,Sherr L,Elford J.Addiction.2002 Feb;97(2):195- 203. 91. Hepatic lipase activity influences high density lipoprotein subclass distribution in normotriglyceridemic men: genetic and pharmacological evidence. Grundy S et al. J Lipid Res 1999 40: 229-34.
92. Changes in lipoprotein-lipid levels in normal men following administration of increasing doses of testosterone cypionate. Kouri EM et al. Clin J Sport Med 1996 Jul;6(3):152-7.
93. Contrasting effects of testosterone and stanozolol on serum lipoprotein levels. JAMA 261:1165-8,1989
94. High-Density Lipoprotein Cholesterol Is Not Decreased if an Aromatizable Androgen Is Administered. Metabolism, 39:69-74,1990
95. Relationship of cardiac size to maximal oxygen uptake and body size in men and women. Hutchinson PL, Cureton KJ, Outz H, Wilson G. Int J Sports Med. 1991 Aug;12(4):369-73.
96. Androgenic anabolic steroids also impair right ventricular function. Kasikcioglu E et al. Int J Cardiol 2008 Feb 11 E Pub.
97. Cardiac effects of anabolic steroids. Payne J. et al. Heart 2004; 90:473-75.
98. Adverse effects of anabolic androgenic steroids on the cardiovascular, metabolic and reproductive systems of anabolic substance abusers. Tuomo Karila. Publications of the National Public Health Institute ISBN 951-740-388-2
99. Absence of left ventricular wall thickening in athletes engaged in intense power training. Pelliccia A et al. Am J Cardiol 1993; 72: 1048-54.
100. Left ventricular hypertrophy by Sokolow-Lyon voltage criterion predicts mortality in overweight hypertensive subjects. Antikainen RL, Grodzicki T. J Hum Hypertens. 2008 Aug 28. [Epub] 101. Hypertensive heart disease. A complex syndrome or a hypertensive cardiomyopathy? Lip GYH et al. Eur Heart J 2000; 21: 1653-65.
102. Adverse effects of anabolic androgenic steroids on the cardiovascular, metabolic and reproductive systems of anabolic substance abusers. Tuomo Karila. Publications of the National Public Health Institute ISBN 951-740-388-2
103. Left ventricular hypertrophy and QT dispersion in hypertension. Mayet J et al. Hypertension 1996; 28: 791-96.
104. Cardiac arrest following anaesthetic induction in a world-class bodybuilder. Angelilli A, Katz ES, Goldenberg RM. Acta Cardiol. 2005 Aug;60(4):443-4.
105. Effects of training on left ventricular structure and function. An echocardiographic study. Shapiro CM et al. Br. Heart J 1983; 50: 534-39.
106. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? Urhausen A, Albers T, Kindermann W. Heart. 2004 May;90(5):496-501.
107. The effects of anabolic-androgenic steroids on primary myocardial cell cultures. Melchert RB et al. Med Sci Sports Exerc 1992; 24:266-12
108. Cardiovascular effects of anabolic-androgenic steroids. Melchert RB et al. Med Sci Sports Exerc 1995;27: 1252-62
109. Cause and manner of death among users of anabolic androgenic steroids. Thiblin I et al. J Forensic Sci 2000;45:16-23
110. Anabolic steroid abuse and cardiac death. Kennedy MC et al. Med J Aust 1993; 158:346-48.
111. Serious cardiovascular side effects of large doses of anabolic steroids in weight lifters. Nieminen MS et al. Eur Heart J 1996; 17:1576-83.
112. Sudden cardiac death during anabolic steroid abuse: morphologic and toxicologic findings in two fatal cases of bodybuilders. Fineschi V et al. Int J Legal Med 2007 Jan;121(1):48-53.Epub 2005 Nov 15. Review.
113. Blood pressure and rate pressure product response in males using high-dose anabolic androgenic steroids (AAS). Grace F, Sculthorpe N, Baker J, Davies B. J Sci Med Sport. 2003 Sep;6(3):307-12.
114. Are the cardiac effects of anabolic steroid abuse in strength athletes reversible? A Urhausen et al. Heart 2004;90:496-501.
115. Cardiovascular side effects of anabolic-androgenic steroids. Herz. 2006 Sep;31(6):566-73.
116. Anabolic steroids and fibrinolysis. Lowe GD. Wien Med Wochenschr. 1993;143(14-15):383-5.
117. Effect of anabolic steroids on plasma antithrombin III. alpha2 macroglobulin and alpha1 antitrypsin levels. Walker ID, Davidson JF,Young P, Conkie JA. Thromb Diath Haemorrh. 1975 Sep 30;34(1):106-14.
118. Depo-Testosterone. Pharmacia. U.S. Prescribing Information. Revised August 2002.
119. Anabolic-androgenic steroid abuse in weight lifters: evidence for activation of the hemostatic system. Am J Hematol. Ferenchick GS, Hirokawa S, Mammen EF, Schwartz KA. 1995 Aug;49(4):282-8.
120. Raised concentrations of C reactive protein in anabolic steroid using bodybuilders. F M Grace, B Davies et al. Br J Sports Med 2004;38:97-98.
121. Testosterone increases human platelet thromboxane A2 receptor density and aggregation responses. Ajayi AA, Mathur R, Halushka PV. Circulation.
1995 Jun 1;91(11):2742-7.
122. Androgenic-anabolic steroid abuse and platelet aggregation: a pilot study in weight lifters. Ferenchick G, Schwartz D, Ball M, Schwartz K. Am J Med Sci. 1992 Feb;303(2):78-82.
123. Pulmonary embolism associated with the use of anabolic steroids. Liljeqvist S, Helldén A, Bergman U, Söderberg M. Eur J Intern Med. 2008 May;19(3):214-5. Epub 2007 Sep 19.
124. Coronary thrombosis and ectasia of coronary arteries after long-term use of anabolic steroids. Tischer KH, Heyny-von Haussen R, Mall G, Doenecke P. Z Kardiol. 2003 Apr;92(4):326-31.
125. Massive pulmonary embolus and anabolic steroid abuse. Gaede JT, Montine TJ. JAMA. 1992 May 6;267(17):2328-9.
126. Steroid anabolic drugs and arterial complications in an athlete–a case history. Laroche GP. Angiology. 1990 Nov;41(11):964-9.
127. Death caused by pulmonary embolism in a body builder taking anabolic steroids (metanabol). Siekierzyƒska-Czarnecka A, Polowiec Z, Kulawiƒska M, Rowinska-Zakrzewska E. Wiad Lek. 1990 Oct 1-15;43(19-20):972-5.
128. Coagulation abnormalities associated with the use of anabolic steroids. Ansell JE, Tiarks C, Fairchild VK. Am Heart J. 1993 Feb;125(2 Pt 1):367-71.
129. Hematocrit and the risk of cardiovascular disease–the Framingham study: a 34-year follow-up. Gagnon DR, Zhang TJ, Brand FN, Kannel WB. Am Heart J. 1994 Mar;127(3):674-82.
130. Homocysteine induced cardiovascular events: a consequence of long term anabolic-androgenic steroid (AAS) abuse. M R Graham, F M Grace et al. Br. J Sports Med. 2006;40:544-48.
131. Homocysteine and cardiovascular disease: time to routinely screen and treat? P. O’Callaghan et al. Br J Cario 2003; 10(2) 115-7.
132. Promotion of vascular smooth muscle cell growth by homocysteine: a link to atherosclerosis. Proc Natl Acad Sci 1994;91:6369-73.
133. Homocystinuria: metabolic studies on three patients. Brenton D et al. J Pediatr 1966;67-58-68.
134. Homocysteine, and atherogenic stimulus, reduces protein C activation by arterial and venious endothelial cell. Rogers G et al. Blood 1990;75:895-901.
135. Homocysteinethiolactone disposal by human arterial endothelial cells and serum in vitro. Dudman N et al. Atherioscler Thromb 1991;11:663-70.
136. Plasma homocysteine levels and mortality in patients with coronary artery disease. Nygard O et al. N Engl J Med 1997;337:230-6.
137. Effects of sex steroids on plasma total homocysteine levels: a study in transsexual males and females. Giltay EJ, Hoogeveen EK et al. J Clin Endocrinol Metab. 1998 Feb;83(2):550-3.
138. Homocysteine levels in men and women of different ethnic and cultural background living in England. Cappuccio FP, Bell R. et al. Atherosclerosis. 2002 Sep;164(1):95-102.
139. Hyperhomocysteinemia in bodybuilders taking anabolic steroids. Ebenbichler CF, Kaser S et al. Eur J Intern Med. 2001 Feb;12(1):43-47.
140. Homocysteine induced cardiovascular events: a consequence of long term anabolic-androgenic steroid (AAS) abuse. M R Graham, F M Grace et al. Br. J Sports Med. 2006;40:544-48.
141. The effect of supraphysiologic doses of testosterone on fasting total homocysteine levels in normal men. Zmuda JM, Bausserman LL, Maceroni D, Thompson PD. Atherosclerosis. 1997 Apr;130(1-2):199-202.
142. Hypertension, stroke, and endothelium. F. Consentino , M. Volpe. Cur Hypertension Rep. January 2005: 7(1); 68-71
143. Differences in Vascular Reactivity Between Men and Women. Bob J. Schank, MS et al. Angiology, Vol. 57, No. 6, 702-708 (2007)
144. Flow-mediated, endothelium-dependent vasodilatation is impaired in male body builders taking anabolic-androgenic steroids. Ebenbichler CF, Sturm W et al. Atherosclerosis. 2001 Oct;158(2):483-90.
145. Impaired vasoreactivity in bodybuilders using androgenic anabolic steroids. Lane HA et al. Eur J Clin Invest 2006 Jul; 36(7): 483-8.
146. The more effective immune system of women against infectious agents. Müller HE. Wien Med Wochenschr. 1992;142(17):389-95
147. Sex hormones, immune responses, and autoimmune diseases. Mechanisms of sex hormone action. Ansar AS et al. Human Repr Upd. 11(4) 411-23.
148. Sex hormones and the immune response in humans.A Bouman et al. Human Reprod Update 11(4) pp.411-23, 2005.
149. Effect of a single administration of testosterone on the immune response and lymphoid tissue in mice. Fuji H et al. Immunology 20:315-26. 1975.
150. Estrogens and health in males. Lombardi G, Zarrilli S et al. Mol Cell Endocrinol. 2001 Jun 10;178(1-2):51-5.
151. Dichotomy of glucocorticoid action in the immune system. Asadullah K, Schäcke H, Cato AC. Trends Immunol. 2002 Mar;23(3):120-2
152. Anabolic steroid effects on immune function: differences between analogues. Mendenhall CL, Grossman CJ, et al. J Steroid Biochem Mol Biol. 1990 Sep;37(1):71-6.
153. A trial of testosterone therapy for HIV-associated weight loss. Coodley GO, Coodley MK. AIDS. 1997 Sep;11(11):1347-52.
154. Effects of nandrolone decanoate compared with placebo or testosterone on HIV-associated wasting. J Gold,1 MJ Batterham et al. HIV Medicine (2006),
7, 146–155
155. The effect of anabolic steroids and strength training on the immune response. L Calabrese et al. Med and Sci in Sports and Exer. 21(4) pp. 386-92,
156. Androgens potentiate the effects of erythropoietin in the treatment of anemia of end-stage renal disease. Ballal SH, Domoto DT, Polack DC, Marciulonis P, Martin KJ. Am J Kidney Dis. 1991 Jan;17(1):29-33.
157. Use of androgens in patients with renal failure. Johnson CA. Semin Dial. 2000 Jan-Feb;13(1):36-9.
158. Anabolic effects of nandrolone decanoate in patients receiving dialysis: a randomized controlled trial. Johansen KL, Mulligan K, Schambelan M. JAMA.
1999 Apr 14;281(14):1275-81.
159. Testosterone metabolism and replacement therapy in patients with end-stage renal disease. Johansen KL. Semin Dial. 2004 May-Jun;17(3):202-8.
160. The effect of anabolic steroids on the gastrointestinal system, kidneys, and adrenal glands. Modlinski R, Fields KB. Curr Sports Med Rep. 2006 Apr;5(2):104-9.
161. Wilms tumor in an adult associated with androgen abuse. Prat J, Gray GF, Stolley PD, Coleman JW. JAMA. 1977 May 23;237(21):2322-3
162. Anabolic steroid abuse and renal cell carcinoma. Martorana G, Concetti S, Manferrari F, Creti S. J Urol. 1999 Dec;162(6):2089
163. Anabolic steroid abuse and renal-cell carcinoma. Bryden AA, Rothwell PJ, O’Reilly PH. Lancet. 1995 Nov 11;346(8985):1306-7
164. At what price, glory? Severe cholestasis and acute renal failure in an athlete abusing stanozolol.
Yoshida EM, Karim MA, Shaikh JF, Soos JG, Erb SR. CMAJ. 1994 Sep 15;151(6):791-3
165. Severe cholestasis with kidney failure from anabolic steroids in a body builder. Habscheid W, Abele U, Dahm HH. Dtsch Med Wochenschr. 1999 Sep
166. The incidence of post-operative renal failure in obstructive jaundice. Dawson JL. Br J Surg 1965; 52: 663-665.
167. Acute renal failure complicating muscle crush injury. Abassi ZA, Hoffman A, Better OS. Semin Nephrol. 1998 Sep;18(5):558-65
168. Rhabdomyolysis in a bodybuilder using anabolic steroids. Hageloch W, Appell HJ, Weicker H. Sportverletz Sportschaden. 1988 Sep;2(3):122-5.
169. Atraumatic rhabdomyolysis in a 20-year-old bodybuilder. Morocco PA. J Emerg Nurs. 1991 Dec;17(6):370-2.
170. Continuous veno-venous hemofiltration for the immediate management of massive rhabdomyolysis after fulminant malignant hyperthermia in a bodybuilder. Schenk MR, Beck DH, Nolte M, Kox WJ. Anesthesiology. 2001 Jun;94(6):1139-41.
171. Rhabdomyolysis in a bodybuilder using steroids. Daniels JM, van Westerloo DJ, de Hon OM, Frissen PH. Ned Tijdschr Geneeskd. 2006 May
172. Hypertension and the kidney. Hohenstein K, Watschinger B. Wien Med Wochenschr. 2008;158(13-14):359-64.
173. Hepatic effects of 17 alpha-alkylated anaboli-androgenic steroids. HIV Hotline. 1998 Dec;8(5-6):2-5.
174. Methyltestosterone, related steroids, and liver function. A deLorimier et al. Arch Inter Med Vol. 116 Aug 1965 p 289-94
175. Jaundice associated with norbolethone (Nilevar) therapy. Shaw R K et al. Ann Intern Med 52:428-34 1960.
176. Androgenic/Anabolic steroid-induced toxic hepatitis. Stimac D, Miliç S, Dintinjana RD, Kovac D, Ristiç S. J Clin Gastroenterol. 2002 Oct;35(4):350-2.
177. Review of oxymetholone: a 17alpha-alkylated anabolic-androgenic steroid. Pavlatos AM, Fultz O, Monberg MJ, Vootkur A, Pharmd. Clin Ther. 2001 Jun;23(6):789-801; discussion 771
178.A pilot study of anabolic steroids in elderly patients with hip fractures. Sloan JP,Wing P, Dian L,Meneilly GS. J Am Geriatr Soc. 1992 Nov;40(11):1105- 11.
179. Effects of long-term use of testosterone enanthate. II. Effects on lipids, high and low density lipoprotein cholesterol and liver function parameters. Tyagi A, Rajalakshmi M. et al. Int J Androl. 1999 Dec;22(6):347-55.
180. Cellular distribution of androgen receptors in the liver. Hinchliffe SA, Woods S, Gray S, Burt AD. J Clin Pathol. 1996 May;49(5):418-20.
181. Liver toxicity of a new anabolic agent: methyltrienolone (17-alpha-methyl-4,9,11-estratriene-17 beta-ol-3-one). Kruskemper, Noell. Steroids. 1966 Jul;8(1):13-24
182. T. Feyel-Cabanes, Compt. Rend. Soc. Biol. 157, 1428 (1963)
183. Anabolic-androgenic steroids and liver injury. M Sanchez-Osorio et al. Liver International ISSN 1478-3223 p. 278-82.
184. Androgenic/Anabolic steroid-induced toxic hepatitis. Stimac D et al. J Clin Gastroenterol. 2002 Oct;35(4):350-2.
185. Mechanisms and sites of action of ursodeoxycholic acid in cholestasis. Beuers U. Nat Clin Pract Gastroenterol Hepatol 2006; 3:318-28.
186. Peliosis hepatis in a young adult bodybuilder. Cabasso A. Med Sci Sports Exerc. 1994 Jan;26(1):2-4.
187. Bleeding esophageal varices associated with anabolic steroid use in an athlete. Winwood PJ et al. Post-Grad Med J 1990; 66:864-65.
188. Benign liver-cell adenoma associated with long-term administration of an androgenic-anabolic steroid (methandienone). Hernandez-Nieto L, Bruguera M, Bombi J, Camacho L, Rozman C. Cancer. 1977 Oct;40(4):1761-4
189. Hepatocellular carcinoma in the non-cirrhotic liver. Evert M, Dombrowski F. Pathologe. 2008 Feb;29(1):47-52
190. Intratesticular leiomyosarcoma in a young man after high dose doping with Oral-Turinabol: a case report.
Cancer. Froehner M, Fischer R, Leike S, Hakenberg OW, Noack B, Wirth MP. 1999 Oct 15;86(8):1571-5.
191. Hepatocellular carcinoma associated with recreational anabolic steroid use. Gorayski P, Thompson CH, Subhash HS, Thomas AC. Br J Sports Med. 2008 Jan;42(1):74-5; discussion 75.
192. Bodybuilder death steroids warning. Express and Star 2008 09/04. Epub.
193.Effect of testosterone and anabolic steroids on the size of sebaceous glands in power athletes.Kiraly CL et al.Am J Dermatopathol, 1987 Dec, 9:6, 515- 9.
194. RU 58841, a new specific topical antiandrogen: a candidate of choice for the treatment of acne, androgenetic alopecia, and hirsutism. Battmann T. et al. J Steroid Biochem Mol Biol. 1994 Jan;48(1):55-60.
195.Androgenetic alopecia and current methods of treatment. Bienová M, Kucerová R. et al. Acta Dermatovenerol Alp Panonica Adriat. 2005 Mar;14(1):5- 8.
196. Molecular mechanisms of androgenetic alopecia. Trüeb RM. Exp Gerontol. 2002 Aug-Sep;37(8-9):981-90.
197. The inheritance of common baldness: two B or not two B? Kuster W, Happle R. J Am Acad Dermatol 1984; 11: 921-26.
198. Polymorphism of the Androgen Receptor Gene is Associated with Male Pattern Baldness. Justine A Ellis, Margaret Stebbing and Stephen B Harrap. Journal of Investigative Dermatology (2001) 116, 452–455.
199. EDA2R is associated with androgenetic alopecia. Prodi DA, Pirastu N, et al. J Invest Dermatol. 2008 Sep;128(9):2268-70. Epub 2008 Apr 3.
200. Current understanding of androgenetic alopecia. Part I: Etiopathogenesis. Hoffmann R, Happle R. European Journal of Dermatology. Volume 10, Number 4, 319-27, June 2000
201. Estrogen and progesterone receptors in androgenic alopecia versus alopecia areata. Wallace ML, Smoller BR. Am J Dermatopathol. 1998 Apr;20(2):160-3.
202. Hormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government. Franke WW, Berendonk B. Clin Chem. 1997 Jul;43(7):1262-79.
203. Role of estrogen on bone in the human male: insights from the natural models of congenital estrogen deficiency.Faustini-Fustini, M. et al. Mol Cell Endocrinol. 2001 Jun 10;178(1-2):215-20.
204. Effects of estrogen on growth plate senescence and epiphyseal function. M Weise, S De-Levi et al. Proc Natl Acad Sci June 5,2001 pp. 6871-6876.
205. The results of short-term (6 months) high-dose testosterone treatment on bone age and adult height in boys of excessively tall stature. Brämswig JH, von Lengerke HJ et al.Eur J Pediatr. 1988 Nov;148(2):104-6.
206. Oxandrolone in constitutional delay of growth: analysis of the growth patterns up to final stature. Bassi F, Neri AS, Gheri RG, Cheli D, Serio M. J Endocrinol Invest. 1993 Feb;16(2):133-7.
207. Pectoralis maior tendon rupture and anabolic steroids in anamnesis–a case review. März J, Novotn˘ P. Rozhl Chir. 2008 Jul;87(7):380-3.
208. Successive ruptures of patellar and Achilles tendons. Anabolic steroids in competitive sports. Isenberg J, Prokop A, Skouras E. Unfallchirurg. 2008 Jan;111(1):46-9
209. Biomechanical responses of different rat tendons to nandrolone decanoate and load exercise. Marqueti RC, Prestes J, Wang CC, et al. Scand J Med Sci Sports. 2010 Jul 29.
210. The effect of local use of nandrolone decanoate on rotator cuff repair in rabbits. Papaspiliopoulos A, Papaparaskeva K, Papadopoulou E, et al. J Invest Surg. 2010 Aug;23(4):204-7.
211. Self-reported anabolic-androgenic steroids use and musculoskeletal injuries: findings from the center for the study of retired athletes health survey of retired NFL players. Horn S, Gregory P, Guskiewicz KM. Am J Phys Med Rehabil. 2009 Mar;88(3):192-200.
212. Salt, hypertension, and edema. Rössler R. Internist (Berl). 1976 Oct;17(10):489-93. Review.
213. Sex hormone effects on body fluid regulation. Stachenfeld NS. Exerc Sport Sci Rev. 2008 Jul;36(3):152-9.
214. Effect of ovarian steroids on vasopressin secretion. Forsling, M. L., P. Stromberg, and M. Akerlund. J. Endocrinol. 95: 147-151, 1982
215. Estrogen influences osmotic secretion of AVP and body water balance in postmenopausal women. Nina S. Stachenfeld, Loretta Dipietro, Steven F. Palter, and Ethan R. Nadel Am J Physiol Regul Integr Comp Physiol 274: R187-R195, 1998.
216. Independent and combined effects of testosterone and growth hormone on extracellular water in hypopituitary men. Johannsson G, Gibney J, et al. J Clin Endocrinol Metab. 2005 Jul;90(7):3989-94. Epub 2005 Apr 12.
217. Casner, S. W., Early, R. G., and Carlson, B.R. Journal of Sports Med and Phys Fitness, 1971 11,98.
218. The effects of anabolic steroids on growth, body composition, and metabolism in boys with chronic renal failure on regular hemodialysis. Jones RW, El Bishti MM et al. J Pediatr. 1980 Oct;97(4):559-66.
219. A randomized, placebo-controlled trial of nandrolone decanoate in human immunodeficiency virus-infected men with mild to moderate weight loss with recombinant human growth hormone as active reference treatment. Storer TW, Woodhouse LJ, J Clin Endocrinol Metab. 2005 Aug;90(8):4474-82. Epub 2005 May 24.
220. Bodybuilders’ Body Composition: Effect of Nandrolone Decanoate. VAN MARKEN LICHTENBELT, W. D., F. HARTGENS, N. B. J. VOLLAARD, S. EBBING, and H. KUIPERS. Med. Sci. Sports Exerc., Vol. 36, No. 3, pp. 484-489, 2004.
221. Severe laryngitis following chronic anabolic steroid abuse. Ray S, Masood A, Pickles J, Moumoulidis I. J Laryngol Otol. 2008 Mar;122(3):230-2. Epub
2007 May 14
222. Estrogen regulation of mammary gland development and breast cancer: amphiregulin takes center stage
Heather L LaMarca1 and Jeffrey M Rosen. Breast Cancer Res. 2007; 9(4): 304.
223. Androgens and mammary growth and neoplasia. Dimitrakakis C, Zhou J, Bondy CA. Fertil Steril. 2002 Apr;77 Suppl 4:S26-33.
224. Surgical treatment of gynecomastia in the body builder. Aiache AE. Plast Reconstr Surg. 1989 Jan;83(1):61-6.
225. Roles of estrogen and progesterone in normal mammary gland development insights from progesterone receptor null mutant mice and in situ localization of receptor. Shyamala G. Trends Endocrinol Metab. 1997 Jan-Feb;8(1):34-9.
226. A report on alterations to the speaking and singing voices of four women following hormonal therapy with virilizing agents. Baker J. J Voice 1999 Dec;13(4):496-507.
227. Fundamental voice frequence during normal and abnormal growth, and after androgen treatment.Vuorenkoski V, Lenko HL,Tjernlund P,Vuorenkoski L, Perheentupa J. Arch Dis Child. 1978 Mar;53(3):201-9.
228. Fluoxymesterone therapy in anemia of patients on maintenance hemodialysis: comparison between patients with kidneys and anephric patients. Acchiardo SR, Black WD. J Dial. 1977;1(4):357-66.
229. Testosterone therapy in women: its role in the management of hypoactive sexual desire disorder. Abdallah RT, Simon JA. Int J Impot Res. 2007 SepOct;19(5):458-63. Epub 2007 Jun 21.
230.Virilization caused by methandrostenolone-containing cream in 2 prepubertal girls. Sorgo W, Zachmann M. Helv Paediatr Acta. 1982 Sep;37(4):401- 6.
231. Change in speaking fundamental frequency in hormone-treated patients with Turner’s syndrome–a longitudinal study of four cases. AnderssonWallgren G, Albertsson-Wikland K. Acta Paediatr. 1994 Apr;83(4):452-5.
232. Virilization of the voice in post-menopausal women due to the anabolic steroid nandrolone decanoate (Deca-Durabolin). The effects of medication for one year. Gerritsma EJ, Brocaar MP, Hakkesteegt MM, Birkenhäger JC. Clin Otolaryngol Allied Sci. 1994 Feb;19(1):79-84.
233. Idiopathic isolated clitoromegaly: A report of two cases. Eray Copcu1, Alper Aktas et al. Reproductive Health 2004, 1:4.
234. Two Cases of Clitoromegaly. Clitoral Reduction Preserving Sensation of Clitoris. NODA KOJIRO (Chiba-ken Kodomo Byoin), UDAGAWA AKIKAZU (Chiba-ken Kodomo Byoin) et al. Journal of Japan Society of Aesthetic Plastic Surgery VOL.22;NO.3;PAGE.90-95(2000).
235. Evaluation and Treatment of Women with Hirsutism. MELISSA H. HUNTER, M.D., and PETER J. CAREK, M.D. Am Fam Physician 2003;67:2565-72.
236. Effects of long-term androgen administration on breast tissue of female-to-male transsexuals. M Slagter, L Gooren et al. J Histochem Cytochem. 54(8):
905-910, 2006.
237. Behavioural effects of androgen in men and women. Christiansen K. J Endocrinol. 2001 Jul;170(1):39-48.
238. Exogenous testosterone enhances responsiveness to social threat in the neural circuitry of social aggression in humans. Hermans EJ, Ramsey NF, van Honk J. Biol Psychiatry. 2008 Feb 1;63(3):263-70. Epub 2007 Aug 28.
239. Underground Steroid Handbook II. Daniel Duchaine. 1989. HLR technical books. Venice, CA.
240. Metabolic and behavioral effects of high-dose, exogenous testosterone in healthy men. Bagatell CJ, Heiman JR, Matsumoto AM, Rivier JE, Bremner WJ. J Clin Endocrinol Metab.1994 Aug;79(2):561-7.
241. The effects of exogenous testosterone on sexuality and mood of normal men. Anderson RA, Bancroft J, Wu FC. J Clin Endocrinol Metab. 1992 Dec;75(6):1503-7.
242. Psychological and serum homovanillic acid changes in men administered androgenic steroids. Hannan CJ Jr, Friedl KE, Zold A, Kettler TM, Plymate SR. Psychoneuroendocrinology. 1991;16(4):335-43.
243. Psychosexual effects of three doses of testosterone cycling in normal men. Yates WR et al. Biol Psychiatry. 1999;45:254-60.
244.Effects of supraphysiological doses of testosterone on mood and aggression in normal men. H Pope, E Kouri et al. Arch Gen Psychiatry. 2000;57:133- 140.
245. Psychiatric side effects induced by supraphysiological doses of combinations of anabolic steroids correlate to the severity of abuse. T Pagonis et al. Eur Psych 21 (2006) 551-62.
246. Violence toward women and illicit androgenic-anabolic steroid use. Choi PY, Pope HG Jr. Ann Clin Psychiatry. 1994 Mar;6(1):21-5.
247. Criminality among individuals testing positive for the presence of anabolic androgenic steroids. Klötz F, Garle M, Granath F, Thiblin I. Arch Gen Psychiatry. 2006 Nov;63(11):1274-9.
248. Homicide and near-homicide by anabolic steroid users. Pope HG Jr, Katz DL. J Clin Psychiatry. 1990 Jan;51(1):28-31.
249. Evidence for physical and psychological dependence on anabolic androgenic steroids in eight weight lifters. K Bower, G Eliopulos et al. Am J Psychiatry 1990; 147:510-12.
250. Muscle dysmorphia. An underrecognized form of body dysmorphic disorder. Pope HG Jr, Gruber AJ, Choi P, Olivardia R, Phillips KA. Psychosomatics.
1997 Nov-Dec;38(6):548-57.
251. “Chocolate addiction”: a preliminary study of its description and its relationship to problem eating. Hetherington MM, MacDiarmid JI. Appetite. 1993 Dec;21(3):233-46.
252. Reinforcing aspects of androgens. Wood RI. Physiol Behav. 2004 Nov 15;83(2):279-89.
253. Expression of testosterone conditioned place preference is blocked by peripheral or intra-accumbens injection of alpha-flupenthixol. Packard MG, Schroeder JP, Alexander GM. Horm Behav. 1998 Aug;34(1):39-47.
254. Role of dopamine receptor subtypes in the acquisition of a testosterone conditioned place preference in rats. Schroeder JP, Packard MG. Neurosci Lett. 2000 Mar 17;282(1-2):17-20.
255. Increased dopamine transporter density in the male rat brain following chronic nandrolone decanoate administration. Kindlundh AM, Rahman S, Lindblom J, Nyberg F. Neurosci Lett. 2004 Feb 12;356(2):131-4.
256. Abuse liability of testosterone. Fingerhood MI, Sullivan JT et al. J Psychopharmacol 1997; 11(1):59-63.
257. Anabolic steroid withdrawal depression: a case report. Allnutt S, Chaimowitz G. Can J Psychiatry. 1994 Jun;39(5):317-8.
258. The use of fluoxetine in depression associated with anabolic steroid withdrawal: a case series. Malone DA Jr, Dimeff RJ. J Clin Psychiatry. 1992 Apr;53(4):130-2.
259. New-generation antidepressants, suicide and depressed adolescents: how should clinicians respond to changing evidence? Dudley M, Hadzi-Pavlovic D, Andrews D, Perich T. Aust N Z J Psychiatry. 2008 Jun;42(6):456-66.
260. Anabolic androgenic steroids and suicide. Thiblin I, Runeson B, Rajs J. Ann Clin Psychiatry. 1999 Dec;11(4):223-31.
261. Testosterone deficiency and mood in aging men: pathogenic and therapeutic interactions. Seidman SN. World J Biol Psychiatry. 2003 Jan;4(1):14-20.
262. Treatment strategies of withdrawal from long-term use of anabolic-androgenic steroids. MedraÊ M, Tworowska U. Pol Merkur Lekarski. 2001 Dec;11(66):535-8. Review
263. Psychological moods and subjectively perceived behavioral and somatic changes accompanying anabolic-androgenic steroid use. Bahrke MS,Wright JE, Strauss RH, Catlin DH. Am J Sports Med. 1992 Nov-Dec;20(6):717-24.
264. Insomnia: pathophysiology and implications for treatment. Roth T, Roehrs T, Pies R. Sleep Med Rev. 2007 Feb;11(1):71-9. Epub 2006 Dec 18.
265. When does estrogen replacement therapy improve sleep quality? Polo-Kantola P, Erkkola R, Helenius H, Irjala K, Polo O. Am J Obstet Gynecol. 1998 May;178(5):1002-9.
266. Adverse effects of anabolic androgenic steroids on the cardiovascular, metabolic and reproductive systems of anabolic substance abusers. Tuomo Karila. Publications of the National Public Health Institute ISBN 951-740-388-2
267. Reversible hypogonadism and azoospermia as a result of anabolic-androgenic steroid use in a bodybuilder with personality disorder. A case report. Boyadjiev NP, Georgieva KN, Massaldjieva RI, Gueorguiev SI. J Sports Med Phys Fitness. 2000 Sep;40(3):271-4.
268. Conservative management of azoospermia following steroid abuse. M.R. Gazvani et al. Human Reprod 12(8) (1997) pp. 1706-08.
269. Contraceptive efficacy of testosterone-induced azoospermia in normal men. Lancet, 1990 20;336(8721):955-9.
270. Effects of chronic testosterone administraton in normal men: saferty and efficacy of high dose testosterone and parallel dose-dependent suppression of luteinizing hormone, follicle-stimulating hormone, and sperm production. Matsumoto AM. J Clin Endocrinol Metab 1990; 70:282-87.
271. Restorative increases in serum testosterone levels are significantly correlate to improvements in sexual functioning. A Seftel, R Mack et al. J Androl
25(6) 2004 pp.963-72.
272. Sexual functioning of male anabolic steroid abusers. Moss HB, Panzak GL, Tarter RE. Arch Sex Behav. 1993 Feb;22(1):1-12.
273. Low sex hormone-binding globulin and testosterone levels in association with erectile dysfunction among human immunodeficiency virus-infected men receiving testosterone and oxandrolone. Wasserman P, Segal-Maurer S, Rubin D. J Sex Med. 2008 Jan;5(1):241-7. Epub 2007 Oct 24.
274. Of mice and men: the many guises of estrogens. Simpson ER, Jones ME. Ernst Schering Found Symp Proc. 2006;(1):45-67.
275.Testosterone-induced priapism in Klinefelter syndrome. Ichioka K, Utsunomiya N, Kohei N, Ueda N, Inoue K, Terai A.Urology. 2006 Mar;67(3):622.e17- 8. Epub 2006 Feb 28.
276. Severe priapism as a complication of testosterone substitution therapy. Zelissen PM, Stricker BH. Am J Med. 1988 Aug;85(2):273-4
277. Testosterone induced priapism in two adolescents with sickle cell disease. Slayton W, Kedar A, Schatz D. J Pediatr Endocrinol Metab. 1995 JulSep;8(3):199-203.
278. Benign hypertrophy and carcinoma of the prostate. Moore RA. Surgery 1944;16:152-67.
279. Guilt by association: a historical perspective on Huggins, testosterone therapy, and prostate cancer. Morgentaler A. J Sex Med. 2008 Aug;5(8):1834-40. Epub 2008 Jun 10.
280. Testosterone therapy in hypogonadal men and potential prostate cancer risk: a systematic review. Shabsigh R, Crawford ED, Nehra A, Slawin KM. Int J Impot Res. 2008 Jul 17. [Epub ahead of print] 281. Long-term psychiatric and medical consequences of anabolic-androgenic steroid abuse: A looming public health concern? Kanayama G, Hudson JI, Pope HG Jr. Drug Alcohol Depend. 2008 Nov 1;98(1-2):1-12. Epub 2008 Jul 2.
282. The many faces of testosterone. Bain J. Clin Interv Aging. 2007;2(4):567-76.
283. Testosterone treatment in hypogonadal men: prostate-specific antigen level and risk of prostate cancer. Guay AT, Perez JB, Fitaihi WA,Vereb M. Endocr Pract. 2000 Mar-Apr;6(2):132-8.
284. Adenocarcinoma of prostate in 40 year old body-builder. Roberts TJ, Essenhigh DM. Lancet 1986;2:742.
285. Testosterone therapy for men at risk for or with history of prostate cancer. Morgentaler A. Curr Treat Options Oncol. 2006 Sep;7(5):363-9.
286. Testosterone replacement therapy and the risk of prostate cancer. Is there a link? Barqawi A, Crawford ED. Int J Impot Res. 2006 Jul-Aug;18(4):323-8. Epub 2005 Nov 10.
287. Volume change of the prostate and seminal vesicles in male hypogonadism after androgen replacement therapy. Sasagawa I, Nakada T, Kazama T, Satomi S, Terada T, Katayama T. Int Urol Nephrol. 1990;22(3):279-84.
288. A four-year efficacy and safety study of the long-acting parenteral testosterone undecanoate. Minnemann T, Schubert M, Hübler D, Gouni-Berthold I, Freude S, Schumann C, Oettel M, Ernst M, Mellinger U, Sommer F, Krone W, Jockenhövel F. Aging Male. 2007 Sep;10(3):155-8.
289. Effect of Testosterone Replacement Therapy on Prostate Tissue in Men With Late-Onset Hypogonadism
A Randomized Controlled Trial Leonard S. Marks, MD; Norman A. Mazer, MD, et al. JAMA. 2006;296:2351-2361.
290. Prognostic value of serum markers for prostate cancer. Stenman UH, Abrahamsson PA, Aus G, Lilja H, Bangma C, Hamdy FC, Boccon-Gibod L, Ekman P. Scand J Urol Nephrol Suppl. 2005 May;(216):64-81.
291. Relationship between prostate specific antigen, prostate volume and age in the benign prostate. Collins GN, Lee RJ, McKelvie GB, Rogers AC, Hehir M. Br J Urol. 1993 Apr;71(4):445-50.
292. Long-term treatment with finasteride results in a clinically significant reduction in total prostate volume compared to placebo over the full range of baseline prostate sizes in men enrolled in the MTOPS trial. Kaplan SA, Roehrborn CG,McConnell JD et al. J Urol. 2008 Sep;180(3):1030-2; discussion 1032- 3. Epub 2008 Jul 17.
293. Winning is the Only Thing. Randy Roberts, James S. Olson. JHU Press, 1991. ISBN 0801842409
294. Androgen or Estrogen Effects on Human Prostate. B. Jin, L Turner et al. J Clin Endocrinol Metab. 1996;81(12):4290-95.
295.Fingerprinting the diseased prostate: associations between BPH and prostate cancer. Shah US, Getzenberg RH. J Cell Biochem. 2004 Jan 1;91(1):161- 9.
296. Estrogen-regulated development and differentiation of the prostate. McPherson SJ, Ellem SJ, Risbridger GP. Differentiation. 2008 Jul;76(6):660-70. Epub 2008 Jun 28.
297.Estrogen action on the prostate gland: a critical mix of endocrine and paracrine signaling. G Risbridger, S Ellem et al. J Mol Endocrinol (2007) 39, 183- 88.
298. Effects of androgen therapy on prostatic markers in hemodialyzed patients. Teruel JL, Aguilera A, Avila C, Ortuño J. Scand J Urol Nephrol. 1996 Apr;30(2):129-31.
299. The role of aromatization in testosterone supplementation. Effects on cognition in older men. M.M. Cherrier, A.M. Matsumoto et al. Neurology
300. Use of anabolic steroids and associated health risks among gay men attending London gyms. Bolding G, Sherr L, Elford J. Addiction. 2002 Feb;97(2):195-203.
301. Indications of prevalence, practice and effects of anabolic steroid use in Great Britain. Korkia P, Stimson GV. Int J Sports Med. 1997 Oct;18(7):557-62.
302. A combined regimen of cyproterone acetate and testosterone enanthate as a potentially highly effective male contraceptive. C Meriggola et al. J Clin Endocrinol Metab 81(8) 3018-23, 1996.
303. HPGA normalization protocol after androgen treatment. N Vergel, AL Hodge, MC Scally. Program for Wellness Restoration.
304. An update to the Crisler HCG Protocol. John Crisler, DO. 2004.
305. Testicular responsiveness following chronic administration of hCG (1500 IU every six days) in untreated hypogonadotropic hypogonadism. Balducci R, Toscano V, Casilli D, Maroder M, Sciarra F, Boscherini B. Horm Metab Res. 1987 May;19(5):216-21.
306. Estrogen suppression in males: metabolic effects. Mauras N, O’Brien KO, Klein KO, Hayes V. J Clin Endocrinol Metab. 2000 Jul;85(7):2370-7.
307. Progesterone and testosterone in combination act in the hypothalamus of castrated rams to regulate the secretion of LH.Turner AI,Tilbrook AJ, Clarke IJ, Scott CJ. J Endocrinol. 2001 May;169(2):291-8.
308. Football; Alzado Tumor is Rare and Deadly. Elisabeth Rosenthal. NY Times. July 4, 1991.
309. Primary central nervous system lymphoma. O’Neill BP, Illig JJ. Mayo Clin Proc. 1989 Aug;64(8):1005-20.
310. Sports People: Football; Alzado Talks. NY Times. Associated Press Report. June 28,1991.
311. Alzado believed drug killed him – Ex-Raider star dead from brain cancer. Associated Press. May 15, 1992.
312. 54-year-old man with breast cancer after prolonged testosterone therapy. Sorscher S, Krause W. Clin Adv Hematol Oncol. 2005 Jun;3(6):475; discussion
313. Androgen therapy. Longson D. Practitioner. 1972 Mar;208(245):338-48.
314. Androgen treatment of middle-aged, obese men: effects on metabolism, muscle and adipose tissues. Mårin P, Krotkiewski M, Björntorp P. Eur J Med.
1992 Oct;1(6):329-36.
315. Effects of androgen therapy on adipose tissue and metabolism in older men. Schroeder ET, Zheng L, Ong MD, Martinez C, Flores C, Stewart Y, Azen C, Sattler FR. J Clin Endocrinol Metab. 2004 Oct;89(10):4863-72.
316. Insulin sensitivity, insulin secretion, and abdominal fat: the insulin resistance atherosclerosis study (IRAS) family study. Wagenknecht LE, Langerfeld CD et al. Diabetes 52:2490-2494.
317. Recent developments in the toxicology of anabolic steroids. Graham S, Kennedy M. Drug Saf. 1990 Nov-Dec;5(6):458-76.
318. Insulin resistance and diminished glucose tolerance in powerlifters ingesting anabolic steroids. Cohen JC, Hickman R. J Clin Endocrinol Metab. 1987 May;64(5):960-3.
319. Insulin action and dynamics modelled in patients taking the anabolic steroid methandienone (Dianabol). Godsland IF, Shennan NM, Wynn V. Clin Sci (Lond). 1986 Dec;71(6):665-73
320. The effects of varying doses of T on insulin sensitivity, plasma lipids, apolipoproteins, and C-reactive protein in healthy young men. Singh AB, Hsia S. et al. J Clin Endocrinol Metab. 2002 Jan;87(1):136-43.
321. Nandrolone, a 19-nortestosterone, enhances insulin-independent glucose uptake in normal men. Hobbs CJ, Jones RE, Plymate SR. et al. J Clin Endocrinol Metab. 1996 Apr;81(4):1582-5.
322. Indications of prevalence, practice and effects of anabolic steroid use in Great Britain. Korkia P, Stimson GV. Int J Sports Med. 1997 Oct;18(7):557-62.
323. Cardiovascular complications of respiratory diseases. Chowdhuri S, Crook ED, Taylor HA Jr, Badr MS. Am J Med Sci. 2007 Nov;334(5):361-80.
324. Obesity and hormonal factors in sleep and sleep apnea. Wittels EH. Med Clin North Am. 1985 Nov;69(6):1265-80.
325. Metabolic aspects of sleep apnea. Grunstein RR. Sleep. 1996 Dec;19(10 Suppl):S218-20.
326. Testosterone replacement therapy for older men. Borst SE, Mulligan T. Clin Interv Aging. 2007;2(4):561-6.
327.The Short-Term Effects of High-Dose Testosterone on Sleep, Breathing, and Function in Older Men Peter Y. Liu, Brendon Yee et al.The Journal of Clinical Endocrinology & Metabolism Vol. 88, No. 8 3605-3613
328. Induction of the obstructive sleep apnea syndrome in a woman by exogenous androgen administration. Johnson MW, Anch AM, Remmers JE. Am Rev Respir Dis. 1984 Jun;129(6):1023-5.

By | 2017-04-07T01:12:06+00:00 April 7th, 2015|Categories: Topics: Steroids|0 Comments

About the Author:

William Llewellyn is a researcher in the field of human performance enhancement. He is also author of the bestselling ANABOLICS book series, most recently the ANABOLICS 10th Edition. William is an active supporter of the harm reduction community, and currently serves as honorary lecturer at the Centre for Public Health at Liverpool John Moores University.

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