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I didn't write this to throw anyone off or be a hypocrite by any means, but to be aware of all the possible long-term side effects, so that if you are careful, can do your best to mitigate them. Not to mention it was pretty damn interesting reading into this stuff for school.
So to each their own, just be aware of the effects and stay safe if you choose to do so. This is especially important for younger guys that may not have fully developed brains - area in bold explains
*Note - I did have one study but can't find it, that suggests any of these effects are similar to that of alcohol and tobacco use in which it may or may not affect the individual ie. someone smoking a pack a day for 40 years and not getting cancer vs. someone that gets cancer smoking half that for 10 years.
Anabolic-Androgenic Steroids:
Long-Term Effects The User Needs to Know About
Abstract
The prevalence of anabolic-androgenic steroid (AAS) abuse amongst recreational users and adolescents has increased substantially over the past thirty years. Until recently, it was thought that the adverse side-effects of AAS abuse were reversible, however more recent research suggests that there may be long-term, irreversible effects on both the cardiovascular (CV) and nervous systems. AAS have been tested on animals and have been shown to display a level of neurotoxicity affecting various receptors in the brain in vitro and on animals including but not limited to gamma-aminobutyric acid (GABA)ergic, dopaminergic, and N-methyl-D-aspartate (NMDA) receptors, which may explain the neuropsychiatric effects experienced by human users. Research revealed a number of long-term neuropsychiatric effects of anabolic-androgenic steroid abuse, which include: cognitive deficits, behavioral changes, and increased prevalence of substance abuse, mania, hypomania, depression and suicide. Research also revealed that adolescents and young-adults are at greater risk of permanent changes in neurological development. Numerous etiological changes to the CV system were also revealed which include: decreased vascular reactivity, left ventricular hypertrophy, lower ejection fraction, polycythemia, cellular pathology, and subsequent cardiomyopathy. Athletes, recreational users, adolescents, and general practitioners should be educated further on the associated long-term, potentially life-altering effects of AAS abuse that may not be reversible upon cessation.
ANABOLIC-ANDROGENIC STEROIDS:
LONG-TERM EFFECTS THE USER NEEDS TO KNOW ABOUT
Introduction
The use of AAS by Olympic athletes has been documented as early as 1966 (Sjoqvist, Garle, & Rane, 2008) and has become a persistent issue in professional and amateur sport. However, AAS use in non-athlete populations is much more prevalent than one may suspect. In 1996, Melia, Pipe, and Greeburg surveyed over 16,000 school-aged students in grade six and above and found that 2.8% had used, or were using, AAS; it is estimated that over 83,000 young Canadians had used AAS at this time. Recent studies show that approximately 1.4% of high school students in the United States are using, or had used AAS, with estimates as high as 4.3% in 2009 according to the Center for Disease Control and Prevention (Cunningham, Lumia, & McGinnis, 2012; Johnston, O’Malley, Bachman, &, Schulenberg 2012; Lorang, Callahan, Cummins, Achar, & Brown, 2011). Because the use of performance-enhancing drugs by the general population did not become prevalent until the 1980’s, the long-term consequences of AAS abuse are just recently coming to light (Kanayama, Kean, Hudson, & Pope, 2012). Athletes and medical professionals are often aware of the many short-term risks and effects of AAS, which include: acne, aggression, reversible dyslipidemia, virilization, suppression of the hypothalamic-pituitary-testicular axis, and hypertension (Kanayama et al., 2012; Narayanan, Kahal, Mohammed, & Kilpatrick, 2012; Talih, 2007). 17alpha-alkylated – orally available – AAS may also cause significant liver dysfunction resulting in carcinoma and peliosis hepatis (Lamb, 1984). The long-term effects of AAS abuse however, are not commonly known among users and further investigation is warranted. This paper will discuss the potential long-term effects of AAS abuse in supraphysiological doses – primarily deleterious neuropsychiatric and cardiovascular effects.
Neuropsychiatric Effects
Numerous studies on animals show that AAS interact with the alpha-subunit of GABAergic receptors, which are the primary inhibitory neurotransmitter receptors in the brain (Masonis & McCarthy, 1996; McIntyre, Porter, & Henderson, 2002; Sigel & Steinmann, 2012; Yang, Jones, & Henderson, 2005). Dysfunction of GABAergic receptors is associated with major depressive disorder and anxiety, conditions that have also been associated with AAS abuse (Cryan & Kauppman, 2005; Lindqvist, 2012). Another link to the neuropsychiatric effects of AAS may be their interaction with dopaminergic receptors, which play important roles in many functions in the body from regulating blood pressure to voluntary movement (Beaulieau & Gainedtinov, 2011; Cunningham, Giuffrida, & Roberts, 2009; Kindlundh, Lindblom, & Nyberg, 2003; Birgner, 2008). Beaulieau and Gainedtinov (2011) found that dysfunction of dopaminergic receptors has been linked to attention deficit hyperactivity disorder (ADHD), Parkinson’s disease, and Tourette’s syndrome. Further more, an elevated level of testosterone has been shown to induce neuronal apoptosis , the long-term consequences of which remain to be determined (Estrada, Varshney, & Ehrlich, 2006). However, it should be noted that neural apoptosis has been linked to many neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s (Mattson, 2000). These findings are particularly startling considering the incidence of AAS use among adolescents.
The normal human brain reaches full size by 5 years of age, but its structure and biological makeup continue to change; some areas of the brain may not be fully developed until the ages of 21-25 years (Lebel, Walker, Leemans, Phillips, & Beaulieau, 2007; Pujol, Vendrell, Junque, Marti-Vilalta, & Capdevila, 1993). This may make younger AAS users, especially during adolescence, more vulnerable to long-term, permanent changes in brain development and possible neurological disorders (Cunningham et al., 2012). As previously stated, supraphysiological doses of AAS display some level of neurotoxicity in dopaminergic receptors, which are linked to ADHD; a study by Mueller et al. (2010) showed a higher incidence of psychiatric disorders – primarily ADHD and anxiety disorders – in children ages 8-18 years with genetic hyperandrogenism . These observations further reiterate the potential vulnerability of the approximately 1.4-4.3% of high school students using AAS.
Some neuropsychiatric effects of AAS are commonly known amongst users, including aggression, or “roid rage,” and changes in mood (Lumia & McGinnis, 2010). However, there are numerous effects of great concern that the average user or medical professional may not be aware of. Kanayama, Kean, Hudson, and Pope (2012) found that there might be irreversible cognitive deficits caused by long-term exposure to AAS. In a study of 22 long-term users and13 non-users, there were no differences in attention span, alertness, and motor speed; the long-term users however, showed significant deficits in immediate Pattern Recognition Memory (PRM) and impaired visuospatial working memory, both of which had a high correlation with the duration of exposure (Kanayama, et al., 2012). Cognitive deficits may not be of great concern to many AAS users because they do not pose any immediate health threat, however, there are more serious neuropsychiatric effects that may impact the users quality of life.
AAS have been shown to induce mania and hypomania, which may contribute to aggression, as well as mood and personality disorders, and major depressive disorder during and upon cessation of use (Pope, Kouri, & Hudson, 2000; Pope & Katz, 1994). AAS use may also lead to further substance abuse – particularly of opioids – as they have been shown to influence levels of endogenous opioid peptides in the brain – in regions responsible for dependence, emotion, and aggression – and may affect dopaminergic pathways responsible for the brain reward system as well as down-regulating the NR1 subunit of N-methyl-D-aspartate receptors (NMDA) ; the neuropsychiatric effects that may result in the changes in brain chemistry can be seen by the large amount of AAS users that have been shown to practice polypharmacy , as well as users suffering from AAS dependence (Kanayama, Hudson, & Pope, 2008; Nyberg & Hallberg, 2012; Kanayama, Brower, Wood, Hudson, & Pope, 2010; Kanayama & Pope, 2012; Ip, Barnett, Tenerowicz, & Perry 2011). Users may or may not attribute their psychiatric disorders to use of AAS but the evidence does support causation.
Even more troubling is the link between AAS and suicide. Case studies of 8 males, ages 21-33 years, showed that AAS may increase the incidence of completed suicide among predisposed individuals (Thiblin, Runeson, & Rajs, 1999). AAS have also been shown to increase impulsiveness among users, which is highly correlated with an increased risk of suicide among predisposed individuals (Galligani, Renck, & Hansen, 1996; Horesh et al., 1997).
A recent study by Lindqvist (2012) provides further evidence that the neuropsychiatric effects of AAS abuse may cause long-term, pathological changes in the brain. In 2012, a follow up study by Lindqvist was conducted on 668 Swedish power athletes who were surveyed – 20.9% of which admitted to using AAS between 1960-1979. Results showed that the AAS group was associated with a higher lifetime prevalence of illicit substance abuse and mental health disorders – primarily major depressive disorder and anxiety. Neuropsychiatric effects of AAS are not the only long-term health concern associated with AAS abuse.
Cardiovascular Effects
The effect of AAS on the cardiovascular system should be of great concern to users. A number of studies have shown that AAS cause hypertrophy of the left ventricular wall, and not until recently, have subsequently been shown to reduce left ventricular ejection fraction with long-term abuse (Achar, Rostamian, & Narayan, 2010; D’Andrea et al., 2007; Hassan, Salem, & Sayed 2009; Baggish et al. 2010). A lower ejection fraction strains the heart by forcing it to work harder to provide blood to the body. In the past, prior studies failed to show a change in ejection fraction; hence, the effects of AAS may have more implications on the CV system than previously thought (Achar et al., 2010; Baggish et al., 2010; D’Andrea et al., 2007; Hassan et al., 2009).
Not only do the dimensions of the heart change with AAS abuse but also there may be effects down to the cellular level that could be detrimental to cardiac function. AAS have been shown to cause disintegration of cardiac myocytes, loss of striations, dehiscent intercalated discs, and interrupted Z-bands (Hassan et al., 2009). Intercalated discs allow cardiac cells to communicate at the cellular level and act as a single unit, thus their impaired function could explain why Doppler echocardiogram results showed impaired function in the ST segment for one AAS user but function returned to normal upon cessation (Urhausen, Albers, & Kindermann, 2004). As such, some of the CV effects seem to be reversible, but some may not. Urhausen, Albers, and Kindermann (2004) examined 15 strength-trained athletes who had previously used AAS for a total of 26 weeks per year for 9 years on average, but discontinued use approximately 1 year before the study. As compared to a control group of strength trained athletes and bodybuilders, Urhausen et al. (2004) found that left ventricular wall thickness did not reverse completely upon cessation in the AAS group. Evidence from Sculthorpe, Fergal, Jones, and Davies (2010) showed that long-term – twenty or more years of use – could cause electrical instability in the myocardium, increasing the risk of malignant cardiac tachyarrhythmia.
Further evidence of left ventricular hypertrophy and cardiomyopathy has been found by examining the hearts of patients via biopsy or of deceased individuals via autopsy. Nieminen et al. (1996) studied 4 adult males with a history of AAS that had sought treatment for various heart conditions, with results showing that all four subjects had hypertrophied cardiac muscle; 2 of 3 males that underwent an endomyocardial biopsy showed fibrosis – connective tissue buildup – in the myocardium. Cardiac myopathy as a result of AAS is not something that should be taken lightly. Another study by Kanayama, Hudson, and Pope (2008) suggests that both psychiatric and medical side effects may persist long after the cessation of AAS use.
The heart is not the only part of the cardiovascular system that may be affected by AAS; pathological changes of other tissues may exist among users. A study by Lane et al. (2006) found that AAS use cause hypertrophy of smooth vascular tissue and increased vascular stiffness. Sader, Griffiths, McCredie, Handelsman, and Celermajer (2001) found that AAS use caused increases in arterial wall thickness, as well as inhibited vascular reactivity. Further evidence showed that AAS are associated with dysfunction of endothelial tissue – which comprises the inner layer of vascular tissue – as well as an increased level of atherosclerotic lipids; both factors may contribute to atherosclerosis, a risk factor for CV disease (Ebenbichler et al., 2001). The effects of inhibited vascular reactivity and increased vascular stiffness could contribute to hypertension by increasing vascular resistance, resulting in pathological changes to the heart (Karam, Lever, & Healy, 1989). Aside from monitoring atherosclerotic lipids, there are other biological markers that may be involved in CV disease that are affected by AAS.
C-reactive protein, a biomarker of inflammation, has been shown to increase the risk of heart disease by increasing oxidative stress and be increased levels may be a predictor of cardiovascular events in approximately 1-in-400 people (Hooten, Ejiogu, Zonderman, & Evans, 2012; Kaptoge et al., 2012). AAS have been shown to increase C-reactive protein in a number of studies (Grace & Davies, 2004; Sculthorpe, Grace, Angell, Baker, & George, 2012; Severo et al., 2013). McCarthy et al. (2000) studied a 31 year-old male with an 8-year history of AAS abuse that was admitted to hospital after experiencing unexplained leg pain. The only abnormal test during screening was elevated C-reactive protein and further tests revealed bilateral ischemic legs and a thrombus in the left ventricle that were attributed to AAS use.
Homocysteine, another biological marker that increases oxidative stress, has been found to inversely affect levels of high-density lipoprotein and is positively associated with CV disease and thrombosis (Coppola et al., 2000; Refsum, Ueland, Nygard, & Vollset, 1998; Wilcken & Wilcken, 1976). A number of studies have found that AAS increase levels of homocysteine (Angell et al., 2012; Luijkx et al., 2012; Sculthorpe et al., 2012). This evidence should encourage users to be very cautious of underlying mechanisms, that are not be commonly tested for otherwise healthy individuals, that may have deleterious effects on their health.
Further CV stress may be attributed to an elevated hematocrit and hemoglobin levels. Erythropoiesis is an effect of AAS that in theory would be of advantage for endurance athletes by increasing the amount of red blood cells in the body, providing more oxygen tissues for cellular metabolism (Coviello et al., 2008). However, there is evidence to suggest that endurance exercise is not affected by AAS (Hartgens & Kuipers, 2004). AAS increase erythropoiesis in a dose dependent matter, thus, when supraphysiological doses of AAS are used, whether erythropoiesis the main goal or not, the user is at risk of developing polycythemia (Coviello et al., 2008; Stergiopoulos, Brennan, Mathews, Setaro, & Kort, 2008). If the resulting increase in hematocrit is greater than 46% in males, evidence suggests a 240% increase in risk of unprovoked thrombosis in men; the risk for women was not as high (Braekken, Mathiesen, Njolstad, Wilsgaard, & Hansen, 2009).
Along side the increased prevalence of suicide, AAS have been associated with a number of CV effects that may increase the risk of life-altering cardiovascular events, and even death. The evidence presented earlier may contribute to a number of mechanisms in which the AAS user’s CV health is compromised, but more troubling is evidence that suggests AAS abuse could cause acute myocardial infarction as well as thromboembolenic events resulting in ischemic legs, brain injury, congestive heart failure, and stroke (Falkenburg, Karlsson, & Ortenwall, 1997; Laroche, 1990; Nieminen et al. 1996; Stergiopoulos et al., 2008; Wysoczanski, 2008; Youssef, Alqallaf, & Abdella, 2011).
Discussion
Athletes and recreational users alike, continue to use AAS for performance or body image enhancement despite knowledge of possible side effects, and may deprecate the possibility of these side effects affecting them (Anshel & Russell, 1997; Walker & Joubert, 2011). It is unlikely that they are aware of the extent of these effects, especially in the long-term, where research on the subject is limited. Though studies on patients with diseases such as HIV and cancer use physiological or moderately supraphysiological doses – 150-250mg per week, these may not be applicable to the approximately 59.6% of ergogenic AAS users who administer doses greater than 1000 mg per week (Strawford et al., 1999; Parkinson & Evans, 2006). As supraphysiological doses of exogenous testosterone may also cause dependence or addiction in susceptible individuals, thus the initial use of AAS may increase the prevalence of long-term abuse (Brower, 2002; Brower, Blow, Young, & Hill, 1991; Kanayama et al., 2008). It would be expected that the increased prevalence of AAS among recreational users would begin to take a toll on the users themselves as well as the health care system in the future.
Athletes who choose to use AAS for whatever reason, be it body image or performance-enhancement, should be further educated on the long-term implications of AAS abuse. The long-term effects of AAS on adolescents is particularly worrying and focus should be put on educating that age group, as they are more vulnerable to neurological effects. Knowledge about AAS and various effects they have on the body may also be limited among general practitioners (GPs) as compared to physicians who have been further educated about doping in sport, which was found to be the case among Irish and other European GPs; male GPs also had significantly more knowledge on the subject than their female counterparts (Woods & Moynihan, 2009). The education of athletes, adolescence, and average gym goers, about serious side effects may start by further educating GPs, allowing them to pass on that knowledge to patients.
Conclusion
In conclusion, there is strong evidence to suggest that AAS abuse may cause irreversible pathological changes to both the nervous and CV systems, and users should be aware of these effects before they choose to put themselves at risk.
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So to each their own, just be aware of the effects and stay safe if you choose to do so. This is especially important for younger guys that may not have fully developed brains - area in bold explains
*Note - I did have one study but can't find it, that suggests any of these effects are similar to that of alcohol and tobacco use in which it may or may not affect the individual ie. someone smoking a pack a day for 40 years and not getting cancer vs. someone that gets cancer smoking half that for 10 years.
Anabolic-Androgenic Steroids:
Long-Term Effects The User Needs to Know About
Abstract
The prevalence of anabolic-androgenic steroid (AAS) abuse amongst recreational users and adolescents has increased substantially over the past thirty years. Until recently, it was thought that the adverse side-effects of AAS abuse were reversible, however more recent research suggests that there may be long-term, irreversible effects on both the cardiovascular (CV) and nervous systems. AAS have been tested on animals and have been shown to display a level of neurotoxicity affecting various receptors in the brain in vitro and on animals including but not limited to gamma-aminobutyric acid (GABA)ergic, dopaminergic, and N-methyl-D-aspartate (NMDA) receptors, which may explain the neuropsychiatric effects experienced by human users. Research revealed a number of long-term neuropsychiatric effects of anabolic-androgenic steroid abuse, which include: cognitive deficits, behavioral changes, and increased prevalence of substance abuse, mania, hypomania, depression and suicide. Research also revealed that adolescents and young-adults are at greater risk of permanent changes in neurological development. Numerous etiological changes to the CV system were also revealed which include: decreased vascular reactivity, left ventricular hypertrophy, lower ejection fraction, polycythemia, cellular pathology, and subsequent cardiomyopathy. Athletes, recreational users, adolescents, and general practitioners should be educated further on the associated long-term, potentially life-altering effects of AAS abuse that may not be reversible upon cessation.
ANABOLIC-ANDROGENIC STEROIDS:
LONG-TERM EFFECTS THE USER NEEDS TO KNOW ABOUT
Introduction
The use of AAS by Olympic athletes has been documented as early as 1966 (Sjoqvist, Garle, & Rane, 2008) and has become a persistent issue in professional and amateur sport. However, AAS use in non-athlete populations is much more prevalent than one may suspect. In 1996, Melia, Pipe, and Greeburg surveyed over 16,000 school-aged students in grade six and above and found that 2.8% had used, or were using, AAS; it is estimated that over 83,000 young Canadians had used AAS at this time. Recent studies show that approximately 1.4% of high school students in the United States are using, or had used AAS, with estimates as high as 4.3% in 2009 according to the Center for Disease Control and Prevention (Cunningham, Lumia, & McGinnis, 2012; Johnston, O’Malley, Bachman, &, Schulenberg 2012; Lorang, Callahan, Cummins, Achar, & Brown, 2011). Because the use of performance-enhancing drugs by the general population did not become prevalent until the 1980’s, the long-term consequences of AAS abuse are just recently coming to light (Kanayama, Kean, Hudson, & Pope, 2012). Athletes and medical professionals are often aware of the many short-term risks and effects of AAS, which include: acne, aggression, reversible dyslipidemia, virilization, suppression of the hypothalamic-pituitary-testicular axis, and hypertension (Kanayama et al., 2012; Narayanan, Kahal, Mohammed, & Kilpatrick, 2012; Talih, 2007). 17alpha-alkylated – orally available – AAS may also cause significant liver dysfunction resulting in carcinoma and peliosis hepatis (Lamb, 1984). The long-term effects of AAS abuse however, are not commonly known among users and further investigation is warranted. This paper will discuss the potential long-term effects of AAS abuse in supraphysiological doses – primarily deleterious neuropsychiatric and cardiovascular effects.
Neuropsychiatric Effects
Numerous studies on animals show that AAS interact with the alpha-subunit of GABAergic receptors, which are the primary inhibitory neurotransmitter receptors in the brain (Masonis & McCarthy, 1996; McIntyre, Porter, & Henderson, 2002; Sigel & Steinmann, 2012; Yang, Jones, & Henderson, 2005). Dysfunction of GABAergic receptors is associated with major depressive disorder and anxiety, conditions that have also been associated with AAS abuse (Cryan & Kauppman, 2005; Lindqvist, 2012). Another link to the neuropsychiatric effects of AAS may be their interaction with dopaminergic receptors, which play important roles in many functions in the body from regulating blood pressure to voluntary movement (Beaulieau & Gainedtinov, 2011; Cunningham, Giuffrida, & Roberts, 2009; Kindlundh, Lindblom, & Nyberg, 2003; Birgner, 2008). Beaulieau and Gainedtinov (2011) found that dysfunction of dopaminergic receptors has been linked to attention deficit hyperactivity disorder (ADHD), Parkinson’s disease, and Tourette’s syndrome. Further more, an elevated level of testosterone has been shown to induce neuronal apoptosis , the long-term consequences of which remain to be determined (Estrada, Varshney, & Ehrlich, 2006). However, it should be noted that neural apoptosis has been linked to many neurodegenerative diseases such as Alzheimer’s, Parkinson’s, and Huntington’s (Mattson, 2000). These findings are particularly startling considering the incidence of AAS use among adolescents.
The normal human brain reaches full size by 5 years of age, but its structure and biological makeup continue to change; some areas of the brain may not be fully developed until the ages of 21-25 years (Lebel, Walker, Leemans, Phillips, & Beaulieau, 2007; Pujol, Vendrell, Junque, Marti-Vilalta, & Capdevila, 1993). This may make younger AAS users, especially during adolescence, more vulnerable to long-term, permanent changes in brain development and possible neurological disorders (Cunningham et al., 2012). As previously stated, supraphysiological doses of AAS display some level of neurotoxicity in dopaminergic receptors, which are linked to ADHD; a study by Mueller et al. (2010) showed a higher incidence of psychiatric disorders – primarily ADHD and anxiety disorders – in children ages 8-18 years with genetic hyperandrogenism . These observations further reiterate the potential vulnerability of the approximately 1.4-4.3% of high school students using AAS.
Some neuropsychiatric effects of AAS are commonly known amongst users, including aggression, or “roid rage,” and changes in mood (Lumia & McGinnis, 2010). However, there are numerous effects of great concern that the average user or medical professional may not be aware of. Kanayama, Kean, Hudson, and Pope (2012) found that there might be irreversible cognitive deficits caused by long-term exposure to AAS. In a study of 22 long-term users and13 non-users, there were no differences in attention span, alertness, and motor speed; the long-term users however, showed significant deficits in immediate Pattern Recognition Memory (PRM) and impaired visuospatial working memory, both of which had a high correlation with the duration of exposure (Kanayama, et al., 2012). Cognitive deficits may not be of great concern to many AAS users because they do not pose any immediate health threat, however, there are more serious neuropsychiatric effects that may impact the users quality of life.
AAS have been shown to induce mania and hypomania, which may contribute to aggression, as well as mood and personality disorders, and major depressive disorder during and upon cessation of use (Pope, Kouri, & Hudson, 2000; Pope & Katz, 1994). AAS use may also lead to further substance abuse – particularly of opioids – as they have been shown to influence levels of endogenous opioid peptides in the brain – in regions responsible for dependence, emotion, and aggression – and may affect dopaminergic pathways responsible for the brain reward system as well as down-regulating the NR1 subunit of N-methyl-D-aspartate receptors (NMDA) ; the neuropsychiatric effects that may result in the changes in brain chemistry can be seen by the large amount of AAS users that have been shown to practice polypharmacy , as well as users suffering from AAS dependence (Kanayama, Hudson, & Pope, 2008; Nyberg & Hallberg, 2012; Kanayama, Brower, Wood, Hudson, & Pope, 2010; Kanayama & Pope, 2012; Ip, Barnett, Tenerowicz, & Perry 2011). Users may or may not attribute their psychiatric disorders to use of AAS but the evidence does support causation.
Even more troubling is the link between AAS and suicide. Case studies of 8 males, ages 21-33 years, showed that AAS may increase the incidence of completed suicide among predisposed individuals (Thiblin, Runeson, & Rajs, 1999). AAS have also been shown to increase impulsiveness among users, which is highly correlated with an increased risk of suicide among predisposed individuals (Galligani, Renck, & Hansen, 1996; Horesh et al., 1997).
A recent study by Lindqvist (2012) provides further evidence that the neuropsychiatric effects of AAS abuse may cause long-term, pathological changes in the brain. In 2012, a follow up study by Lindqvist was conducted on 668 Swedish power athletes who were surveyed – 20.9% of which admitted to using AAS between 1960-1979. Results showed that the AAS group was associated with a higher lifetime prevalence of illicit substance abuse and mental health disorders – primarily major depressive disorder and anxiety. Neuropsychiatric effects of AAS are not the only long-term health concern associated with AAS abuse.
Cardiovascular Effects
The effect of AAS on the cardiovascular system should be of great concern to users. A number of studies have shown that AAS cause hypertrophy of the left ventricular wall, and not until recently, have subsequently been shown to reduce left ventricular ejection fraction with long-term abuse (Achar, Rostamian, & Narayan, 2010; D’Andrea et al., 2007; Hassan, Salem, & Sayed 2009; Baggish et al. 2010). A lower ejection fraction strains the heart by forcing it to work harder to provide blood to the body. In the past, prior studies failed to show a change in ejection fraction; hence, the effects of AAS may have more implications on the CV system than previously thought (Achar et al., 2010; Baggish et al., 2010; D’Andrea et al., 2007; Hassan et al., 2009).
Not only do the dimensions of the heart change with AAS abuse but also there may be effects down to the cellular level that could be detrimental to cardiac function. AAS have been shown to cause disintegration of cardiac myocytes, loss of striations, dehiscent intercalated discs, and interrupted Z-bands (Hassan et al., 2009). Intercalated discs allow cardiac cells to communicate at the cellular level and act as a single unit, thus their impaired function could explain why Doppler echocardiogram results showed impaired function in the ST segment for one AAS user but function returned to normal upon cessation (Urhausen, Albers, & Kindermann, 2004). As such, some of the CV effects seem to be reversible, but some may not. Urhausen, Albers, and Kindermann (2004) examined 15 strength-trained athletes who had previously used AAS for a total of 26 weeks per year for 9 years on average, but discontinued use approximately 1 year before the study. As compared to a control group of strength trained athletes and bodybuilders, Urhausen et al. (2004) found that left ventricular wall thickness did not reverse completely upon cessation in the AAS group. Evidence from Sculthorpe, Fergal, Jones, and Davies (2010) showed that long-term – twenty or more years of use – could cause electrical instability in the myocardium, increasing the risk of malignant cardiac tachyarrhythmia.
Further evidence of left ventricular hypertrophy and cardiomyopathy has been found by examining the hearts of patients via biopsy or of deceased individuals via autopsy. Nieminen et al. (1996) studied 4 adult males with a history of AAS that had sought treatment for various heart conditions, with results showing that all four subjects had hypertrophied cardiac muscle; 2 of 3 males that underwent an endomyocardial biopsy showed fibrosis – connective tissue buildup – in the myocardium. Cardiac myopathy as a result of AAS is not something that should be taken lightly. Another study by Kanayama, Hudson, and Pope (2008) suggests that both psychiatric and medical side effects may persist long after the cessation of AAS use.
The heart is not the only part of the cardiovascular system that may be affected by AAS; pathological changes of other tissues may exist among users. A study by Lane et al. (2006) found that AAS use cause hypertrophy of smooth vascular tissue and increased vascular stiffness. Sader, Griffiths, McCredie, Handelsman, and Celermajer (2001) found that AAS use caused increases in arterial wall thickness, as well as inhibited vascular reactivity. Further evidence showed that AAS are associated with dysfunction of endothelial tissue – which comprises the inner layer of vascular tissue – as well as an increased level of atherosclerotic lipids; both factors may contribute to atherosclerosis, a risk factor for CV disease (Ebenbichler et al., 2001). The effects of inhibited vascular reactivity and increased vascular stiffness could contribute to hypertension by increasing vascular resistance, resulting in pathological changes to the heart (Karam, Lever, & Healy, 1989). Aside from monitoring atherosclerotic lipids, there are other biological markers that may be involved in CV disease that are affected by AAS.
C-reactive protein, a biomarker of inflammation, has been shown to increase the risk of heart disease by increasing oxidative stress and be increased levels may be a predictor of cardiovascular events in approximately 1-in-400 people (Hooten, Ejiogu, Zonderman, & Evans, 2012; Kaptoge et al., 2012). AAS have been shown to increase C-reactive protein in a number of studies (Grace & Davies, 2004; Sculthorpe, Grace, Angell, Baker, & George, 2012; Severo et al., 2013). McCarthy et al. (2000) studied a 31 year-old male with an 8-year history of AAS abuse that was admitted to hospital after experiencing unexplained leg pain. The only abnormal test during screening was elevated C-reactive protein and further tests revealed bilateral ischemic legs and a thrombus in the left ventricle that were attributed to AAS use.
Homocysteine, another biological marker that increases oxidative stress, has been found to inversely affect levels of high-density lipoprotein and is positively associated with CV disease and thrombosis (Coppola et al., 2000; Refsum, Ueland, Nygard, & Vollset, 1998; Wilcken & Wilcken, 1976). A number of studies have found that AAS increase levels of homocysteine (Angell et al., 2012; Luijkx et al., 2012; Sculthorpe et al., 2012). This evidence should encourage users to be very cautious of underlying mechanisms, that are not be commonly tested for otherwise healthy individuals, that may have deleterious effects on their health.
Further CV stress may be attributed to an elevated hematocrit and hemoglobin levels. Erythropoiesis is an effect of AAS that in theory would be of advantage for endurance athletes by increasing the amount of red blood cells in the body, providing more oxygen tissues for cellular metabolism (Coviello et al., 2008). However, there is evidence to suggest that endurance exercise is not affected by AAS (Hartgens & Kuipers, 2004). AAS increase erythropoiesis in a dose dependent matter, thus, when supraphysiological doses of AAS are used, whether erythropoiesis the main goal or not, the user is at risk of developing polycythemia (Coviello et al., 2008; Stergiopoulos, Brennan, Mathews, Setaro, & Kort, 2008). If the resulting increase in hematocrit is greater than 46% in males, evidence suggests a 240% increase in risk of unprovoked thrombosis in men; the risk for women was not as high (Braekken, Mathiesen, Njolstad, Wilsgaard, & Hansen, 2009).
Along side the increased prevalence of suicide, AAS have been associated with a number of CV effects that may increase the risk of life-altering cardiovascular events, and even death. The evidence presented earlier may contribute to a number of mechanisms in which the AAS user’s CV health is compromised, but more troubling is evidence that suggests AAS abuse could cause acute myocardial infarction as well as thromboembolenic events resulting in ischemic legs, brain injury, congestive heart failure, and stroke (Falkenburg, Karlsson, & Ortenwall, 1997; Laroche, 1990; Nieminen et al. 1996; Stergiopoulos et al., 2008; Wysoczanski, 2008; Youssef, Alqallaf, & Abdella, 2011).
Discussion
Athletes and recreational users alike, continue to use AAS for performance or body image enhancement despite knowledge of possible side effects, and may deprecate the possibility of these side effects affecting them (Anshel & Russell, 1997; Walker & Joubert, 2011). It is unlikely that they are aware of the extent of these effects, especially in the long-term, where research on the subject is limited. Though studies on patients with diseases such as HIV and cancer use physiological or moderately supraphysiological doses – 150-250mg per week, these may not be applicable to the approximately 59.6% of ergogenic AAS users who administer doses greater than 1000 mg per week (Strawford et al., 1999; Parkinson & Evans, 2006). As supraphysiological doses of exogenous testosterone may also cause dependence or addiction in susceptible individuals, thus the initial use of AAS may increase the prevalence of long-term abuse (Brower, 2002; Brower, Blow, Young, & Hill, 1991; Kanayama et al., 2008). It would be expected that the increased prevalence of AAS among recreational users would begin to take a toll on the users themselves as well as the health care system in the future.
Athletes who choose to use AAS for whatever reason, be it body image or performance-enhancement, should be further educated on the long-term implications of AAS abuse. The long-term effects of AAS on adolescents is particularly worrying and focus should be put on educating that age group, as they are more vulnerable to neurological effects. Knowledge about AAS and various effects they have on the body may also be limited among general practitioners (GPs) as compared to physicians who have been further educated about doping in sport, which was found to be the case among Irish and other European GPs; male GPs also had significantly more knowledge on the subject than their female counterparts (Woods & Moynihan, 2009). The education of athletes, adolescence, and average gym goers, about serious side effects may start by further educating GPs, allowing them to pass on that knowledge to patients.
Conclusion
In conclusion, there is strong evidence to suggest that AAS abuse may cause irreversible pathological changes to both the nervous and CV systems, and users should be aware of these effects before they choose to put themselves at risk.
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