How to Manage Anabolic Steroid Side Effects

[Nelson Vergel]

Anabolic Steroid Side Effects- Part 1
By Mauro DiPasquale, M.D.





As used by most athletes, the side effects of anabolic steroid use appear to be minimal. Even in those using large doses for prolonged periods of time, clinical evidence shows that any of the short term side effects are mostly reversible. As well, some of the more serious side effects such as hepatic toxicity and increased serum cholesterol, can be minimized by proper monitoring, changes in lifestyle, and if indicated, medication.

The absence of significant side effects to the long term use of low to moderate amounts of testosterone and some anabolic steroids has been shown in a series of clinical studies investigating the use of anabolic steroids and testosterone as male contraceptive agents. A considerable amount of research has been and is being carried out by the World Health Organization and independent researchers using combinations of testosterone, anabolic steroids (especially 19-nortestosterone) (1•2), medroxyprogesterone acetate and methyltestosterone (3), Gonadotropin Hormone Releasing Hormone agonists and antagonists. Several of these combinations have proven to significantly reduce the sperm count with no significant short or long term side effects (at least for as long as the various studies ran). In these studies, normal sperm production resumed shortly after discontinuation of the various compounds.

In general, anabolic steroid side effects can be separated into two groups. One group consists of side effects that are an exaggeration of the expected pharmacological properties of the anabolic steroids. Potential hormonally related side effects of anabolic
steroids in men include gynecomastia, fluid retention, acne, changes in libido, oligospermia and increased aggressiveness.

In women amenorrhea and other menstrual irregularities occur commonly. As well there is a possibility of virilizing effects from the use of anabolic steroids. Some of these effects, such as coarsening and eventually deepening of the voice, hirsutism, male pattern baldness, reduction of breast size, and clitoral enlargement, may or may not be partially reversed by the discontinuation of anabolic steroids and if needed the use of androgen antagonists such as cyproterone acetate.

In most men, however, once the anabolic steroids are discontinued, the hormonal parameters invariably return to normal, except perhaps in those athletes who have used large amounts of anabolic steroids for prolonged periods of time. In some of these athletes
testicular atrophy and refractiveness of the hypothalamic-pituitary-testicular axis. Occasionally the serum testosterone fails to returns to normal, and long term replacement therapy is necessary.

The other group of side effects are those which are not usually thought of as related to either the anabolic or androgenic properties of these compounds. These side effects, while controversial as to the role that anabolic steroids have in their genesis and development, result in more than just cosmetic changes, and include changes in serum cholesterol, cardiovascular disease, prostatic cancer, kidney dysfunction, disturbances in carbohydrate metabolism, emotional disturbances, increased incidence of musculoskeletal injuries, cerebrovascular accidents, and hepatic dysfunction (with rare instances of hepatic cirrhosis), hepatocellular carcinoma and peliosis hepatitis. This second group of side effects, while posing a serious threat to the athlete, has often been misrepresented and sensationalized in both the media and some of the scientific literature. As noted earlier we need better controlled long term studies to accurately determine the risk involved in the prolonged use of anabolic steroids.

To put these potentially life-threatening side effects in perspective, I have found it useful to compare the side effects of anabolic steroids to the side effects of oral contraceptives, especially prior to the 1980's when larger dosages of hormones were used. In general, the side effects of using low to moderate dosages of anabolic steroids are comparable to those seen in women using oral contraceptives. The risks inherent in this universally used and accepted method of contraception, which are well outlined in the Report on Oral Contraceptives, 1985 by the Special Advisory Committee on Reproductive Physiology to the Health Protection Branch, Health and Welfare, Canada, parallel in many ways the risks inherent in anabolic steroid use, although, of course, there are differences since it is mainly the male athletes who use anabolic steroids (although use among women is increasing in the power sports such as weightlifting, powerlifting, bodybuilding, and the track and field events that require explosive strength).

A search of the recent literature shows that the use of oral contraceptives is associated with similar side effects, such as hepatic disease, including hepatic cell adenomas and cancer of the liver (5•6) and changes in serum cholesterol. Even peliosis hepatitis, described primarily in patients on androgenic steroid medication and patients with tuberculosis, has recently been reported as a possible complication of the long-term use of oral contraceptives (7).

We can also separate side effects into the short term and long term consequences of using anabolic steroids. While many of the short term consequences are clinically clear (especially those resulting in changes in the female secondary sexual characteristics, and in feminization of the male) the long term consequences are more elusive. There is some speculation that chronic use of anabolic steroids may, in those genetically susceptible, cause hepatic cirrhosis, peliosis hepatitis, primary hepatoma, atherosclerosis and cardiac disease, diabetes, prostatic cancer, and cerebral vascular accidents.

There is, however, no solid clinical or experimental evidence to show that the use of anabolic steroids by healthy athletes has any effect on longevity, or that prolonged use leads to diseases of the various organs and systems mentioned above. I find it interesting that while substantial amounts of anabolic steroids have been used by athletes for over three decades, we are not seeing any significant long term effects on athletes who have used anabolic steroids in the fifties, sixties and seventies.

However, the changing pattern of anabolic steroids use over the past decade - anabolic steroids are being more widely, at higher dosages and for longer periods of time - may yet reveal more severe problems in the long term. There are some studies in progress now that may shed some light on the long term consequences of anabolic steroid use. One study, announced in 1987, proposed to examine football players and power lifters for possible long-term sequelae from anabolic steroid use in 1970s competition (8).

1- Schurmeyer T; Beliltien L; Knuth U A; Nieschl.aq B. Reversible azoospermia induced by the anabolic steroid 19-nortestosterone. Lancet . 1:417-420. Feb 25 1984 . LG Bn.

2 Schurmeyer T; Belkien L; Knuth U A; Ni eschlaq 8. Reversible azoospemia induced by the anabolic steroid 19-nortestosterone. Lancet . 1:417-420. Feb 25 1984.

3 Bashin J; Rachlis V; Robert B; Khai.t Z. caubined use of oral medroxyproqesterone acetate and methyltestosterone in a male contraceptive trial program. Contraception. 21:365-379. Apr 1980 .

4 Thomas DB. Steroid hormones and medications that al.ter cancer risks. Cancer (United States) Oct 15 1988, 62 (8 Supp1) p1755-67.

5 Forman D; Vincent TJ; Do11 R. Cancer of the 1iver and the use of oral. contraceptives. Br Med J [C1in Res] May 24 1986, 292 (6532) p1357-61.

6 Christoherson ; Mays BT; Barrows G. A study of steroid-related liver tumors. Am J Surq Patho1 Mar 1977, 1 (1) p31-41.

7 Janssens AR; Kreun.i.nq J; Ruiter DJ; Kroon JIM; Grond AJ. Generalized hepatiti after lonq-term use of oral contraceptives. Am J Gaatroenterol (United States) May 1988, 83 (5) p572-5.

8 Cowart vs. JAMA (Uni.ted States) Jun 12 1987, 257 (22) p3021, 3025,



For Part 2, click: Anabolic Steroid Side Effects- Part 2

 

[Nelson Vergel]

Part 2 of this article

 

[Nelson Vergel]

The results of the largest study among steroids users ever

Endocrinologists at Wake Forest University in the US have published the largest survey of steroids users ever. As many as 2385 men participated in the study, which will soon appear in the in the American Journal of Men's Health.

www.ergo-log.net

SAGE Journals: Your gateway to world-class research journals

Subscription and open access journals from SAGE Publishing, the world's leading independent academic publisher.

journals.sagepub.com

 

[Nelson Vergel]

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 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 rarer 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 that may not be immediately apparent to the user. The following is a summary of the biological systems and reactions affected by AAS use.





Cardiovascular System

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, 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.


*Cholesterol/Lipids

Anabolic/androgenic steroid 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.


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

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 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.93 After 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 for 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 antiestrogenic 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 the 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 nonsteroid-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.113 Another 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 on 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 affects 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.118 If 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 thrombin 119 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 prothrombic changes appear to overtake the anti-thrombic changes and physiology begin 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 events 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%.130 This level is considered clinically high and would increase blood viscosity enough to raise the risk of a 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.


*Homocysteine

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 events.133 134 135 The normal range for homocysteine levels 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 events is 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 hyperhomocysteinemia 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.





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.
[IMG alt="Screenshot (5041).png"]https://www.excelmale.com/forum/attachments/screenshot-5041-png.14669/[/IMG]




Numerous other potential side-effects of AAS use/abuse:

*Immune System

*Kidneys (Renal System)

*Liver (Hepatic System)


Physical
*Acne
*Hair Loss (Androgenetic Alopecia)
*Stunted Growth
*Tendon Injury
*Water and Salt Retention


*Virilization

Physical (Male)
*Dysphonia (Vocal Changes)
*Gynecomastia

Physical (Female)
*Birth Defects
*Dysphonia (Vocal Changes)
*Enlarged Clitoris (Clitoromegaly)
*Hair Growth (Hirsutism)
*Menstrual Irregularities
*Reduced Breast Size


Psychological
*Aggression
*Dependency/Addiction
*Depression/Suicide
*Insomnia


Reproductive (Male)
*Infertility
*Libido/Sexual Dysfunction
*Priapism
*Prostate Enlargement
*Testicular Atrophy

 

[Nelson Vergel]

Harm Reduction in Male Patients Actively Using Anabolics AAS and PEDs

Anabolic-androgenic steroid (AAS) and performance-enhancing drug (PED) use is a prevalent medical issue, especially among men, with an estimated 2.9–4 million Americans using AAS in their lifetime. Prior studies of AAS use reveals an association with polycythemia, dyslipidemia, infertility...

www.excelmale.com