Prepare the injection site. Testosterone injections are typically intramuscular — that is, given directly into a muscle. Two relatively easy and accessible sites for intramuscular injection are the deltoid upper arm or the glut upper back portion of the thigh, ie, the butt cheek. Whichever of these sites you choose, take a sterile alcohol pad and wipe the immediate area around where you intend to inject. This will kill bacteria on the skin, preventing infection. If injecting into the glute or buttocks, choose an injection site in the top outside section of the glute.
In other words, pick a site either in the top left corner of the left glute or the top right corner of the right glute. These site have the best access to muscle tissue and allow you to avoid hitting nerves and blood vessels in other parts of the glute. Hold your loaded syringe like a dart at a degree angle above the sterile injection site.
Quickly plunge it into the flesh. Before depressing the plunger, draw back on it slightly. Inject the medication at a steady, controlled pace. Care for the injection site post-injection. Once you have fully depressed the plunger, slowly pull the needle out. Press around the injection site with a sterile cotton swab as you do so — this prevents the emerging needle from pulling on the skin and causing extra pain.
Dispose of the used needle and syringe in a proper sharps container. If, after injection, you experience redness, swelling, or discomfort beyond that of normal soreness at the site of injection, call our office for an appointment and instructions. Precautions: Always store your medication at the recommended temperature, and always check the expiration date on the bottle.
Of course, keep all of your meds out of reach of children. Do not change your dose without consulting your provider. We encourage you to call the office if you have any questions. Anabolic-androgenic steroids AAS are synthetic compounds derived from testosterone, which is the main male hormone.
The binding of testosterone to androgen receptors has anabolic and androgenic effects. During puberty, the increase in testosterone levels contributes to linear growth augmentation, as well as muscle mass accumulation Bhasin et al. Testosterone also acts by increasing the number of muscle progenitor cells Sinha-Hikim et al.
Testosterone promotes mitochondrial biogenesis, improves net oxygen delivery to the tissue by increasing red cell mass and tissue capillarity, and facilitates oxygen unloading from oxyhemoglobin Coviello et al. The idea of designing and developing steroids with anabolic properties arose during the s soon after the identification and isolation of the hormone androsterone by the German investigator Butenandt, who collected this compound from thousands of liters of pooled human urine derived from a number of military service volunteers.
Most of the AAS used before the s were pharmacological agents approved for medicinal or veterinary use. By the s, various androgen precursors became nutritional supplements. Androgen precursors are either inactive or weak androgens that the body converts into potent androgens. These include naturally occurring precursors to testosterone, such as 4-androstenediol, 5-androstenediol, 4-androstenedione, and dehydroepiandrosterone, as well as precursors to synthetic AAS including 4-norandrostenedione, 4-norandrostenediol, and 5-norandrostenediol, which the body converts to nandrolone Pope et al.
Other synthetic AAS, such as desmethylstanozolol, methylclostebol, and methyltrienolone have been recently introduced into the market as dietary supplements. Thus, they potentially represent an even more serious health risk than the more traditionally used AAS.
From a clinical standpoint, AAS are commonly prescribed to treat several disorders, such as the androgen deficiency syndromes Conway et al. Less common medical uses of AAS deal with heart and renal failure Basaria et al. Contrasting data exists in the literature regarding the use of AAS in the treatment of androgen deficiency in aging males, infertility, sexual dysfunctions or impotence, as well as post-menopausal syndrome in women. Thus, while a review of Morley points toward therapeutic effects on libido and menopause-induced sarcopenia, Conway et al.
Hence, according to the state of the art presented in their review, they reported no indication for androgen therapy in male infertility because of its suppressing effect on spermatogenesis. Importantly, there is no evidence in available literature that AAS abuse or dependence might develop from the legitimate medical use of AAS. The use of AAS for non-medical intentions can easily determine abuse and lead to dependence.
When used by athletes, AAS can improve performance to levels obtainable by virtually any other combination of non-chemical solutions provided by modern sport techniques Noakes, Generally, supra-pharmacological doses of AAS act either by a direct mechanism, promoting an increase in mass, force, speed of muscular contraction, and recovery after intense physical exercise Tremblay et al.
Consumption of high doses of AAS typically consists in 6—12 week cycles, followed by a 6—12 week period of wash-out. These patterns of AAS use may easily precipitate in periods of continuous consumption without any AAS-free intervals due to the fact that abusers try to assure their muscle gains while avoiding withdrawal symptoms Brower, ; Kuhn, Several other drugs are frequently associated with the use of supra-pharmacological doses of AAS by abusers that are designed to increase their effects, diminish side effects or avoid detection by urine testing Wichstrom and Pedersen, The abuse of other illicit drugs, such as amphetamines and opioids, has also been shown to be strengthened by AAS use Arvary and Pope, Moreover, such abuse might reinforce the occurrence of adverse substance interactions.
In particular, in the case of AAS and amphetamine association, the overdose potential appears to be increased, due to cardiotoxicity Thiblin et al. The contemporary consumption of AAS and bromocriptine, used to rapidly reduce body fat and total weight, has been described as the cause of a syndrome characterized by syncopal episodes and atrial fibrillation Manoharan et al.
Populations of adolescents and young adults have been the subject of several clinical studies that explore the prevalence of AAS misuse and abuse. Irving et al. They observed that steroid use was more common in non-Caucasian males and in middle school students as compared to high school. In males, steroid use was associated with poor self-esteem, higher rates of depressed mood and attempted suicide, poor knowledge and attitudes about health, greater participation in sports emphasizing weight and shape, greater parental concern about weight, and higher rates of eating disorders and substance abuse.
In a study by Wichstrom and Pedersen , a representative sample of Norwegian youths 15—22 years of age was surveyed. Results showed that AAS use did not vary according to sport involvement or demographics. Moreover, AAS use was associated mainly with the abuse of marijuana, aggressive-type conduct problems and eating disorders.
The severity and impact of side effects induced by AAS abuse depend on a wide range of factors, such as dose, duration of administration, possible consumption of a combination of AAS, as well as gender and age of the abusers.
Data on the impact of sustained administration, failed to show any documented adverse events associated to a single episode of acute consumption of supra-pharmacological doses of AAS. Their abuse has been shown to be associated to greater effects on physical performance in younger individuals and women, together with increased incidence and risk of developing serious side events Kindlundh et al.
Few data exist on the risk of side effects linked to long-term use of high-dose of AAS for non-therapeutic purposes Parssinen and Seppala, Cardiovascular complications have been widely described in AAS abusers, including the occurrence of arrhythmic events Furlanello et al. In a recent post-mortem study that compared 87 deceased men positive for AAS with control subjects Far et al.
In another clinical investigation, ventricular hypertrophy, associated with fibrosis and myocytolysis, was detected after cardiac death in four AAS users Montisci et al. Also, controlled studies realized by echocardiography Krieg et al. Pathological effects on urogenital and reproductive systems have been reported.
In particular, hypogonadotropic hypogonadism with consequent testicular atrophy in men and development of inhibitory mechanisms for FSH and LH production in women have been described in selected populations of AAS abusers Anderson and Wu, ; Dohle et al. Increased virility and lowering of voice tone, irregular menstruation with infertility, decreased breast size, hypertrophic clitoris, and increased sexual desire have also been described in a population of female AAS abusers Franke and Berendonk, ; Kutscher et al.
Other complications include liver damage and hepatitis Tanaka et al. Although several studies point toward a reversibility of undesirable AAS-induced effects following suspension, they can become irreversible complications with prolonged AAS abuse Kutscher et al.
AAS are universally recognized to have psychoactive effects Yates, Although some spared studies have reported their therapeutic use in depression to improve mood and anergia Rabkin et al. Indeed, suicide and homicide have been shown to be the main cause of premature deaths among steroid users and, in particular, in the teen population Thiblin et al.
Although this does not imply that all steroid users will suffer crippling depression or homicidal rage, steroids appear to strongly contribute to psychiatric dysfunctions in susceptible individuals. Globally, the prevalence of AAS-induced psychiatric disorders has been hard to evaluate and determine, because of sampling biases in clinical case reports. In a review of Pope et al. However, this estimated percentage appears to be influenced by the fact that in most controlled trials, it is not possible to completely mimic the extreme doses and combinations of AAS taken by abusers for ethical reasons.
Thus, estimated rates of AAS-induced psychiatric alterations are probably even higher. This is also due to the fact that other factors can increase the likelihood of psychiatric consequences of AAS abuse, such as the presence of a positive psychiatric anamnesis, alcohol, or other drug use Dean, as well as other medical comorbidities.
For example, in a case-report of Morton et al. Psychological motivations contributing to anabolic steroid use and abuse have received little attention in psychiatric literature. Clinical studies demonstrate that steroids are used in part to deal with an earlier trauma, such as childhood physical or sexual abuse Porcerelli and Sandler, The data in the literature show no documented cases of dependence induced by AAS use at therapeutic doses.
This suggests that dependence is likely associated to the use of higher doses of AAS Long et al. However, molecular mechanisms leading to AAS-induced dependence are still unclear. In a review of the scientific literature published between and Brower, , AAS dependence was defined as a diagnosable mental disorder.
Between and , two more diagnostic studies of AAS dependence were published Midgley et al. In the s, Tennant et al. The initial phase of the AAS-induced withdrawal lasting for about 1 week seemed to be comparable to opioid-induced withdrawal, while the second phase was mostly characterized by clear depressive symptoms and craving Tennant et al.
Considerable evidence suggests that AAS dependence might share crucial mechanisms of opioid dependence in humans. In , Kashkin and Kleber posited that AAS dependence might partly arise via an opioidergic mechanism, through which AAS might enhance the activity of central endogenous opioids, and AAS withdrawal would lead to a decrease in this activity and a subsequent acute hyperadrenergic syndrome Kashkin and Kleber, This posited link between AAS and opioids was later confirmed by a large number of observations indicating that AAS users seem to be particularly at risk for developing opioid abuse or dependence McBride et al.
Additional clinical studies provided evidence that AAS might decrease the analgesic action of both metamizol and morphine Philipova et al. In , a study by Kanayama et al. In the population included in that study, opioid abuse or dependence began either before or after the onset of AAS use, suggesting the possibility that these forms of substance abuse might arise from a common molecular pathway Kanayama et al.
However, in a study of Negus et al. AAS seem to act through a more modest reinforcement mechanism compared to cocaine or heroin and resembles the reinforcement mechanism described for caffeine, nicotine, and benzodiazepines. In , Brower proposed a 2-stage model of steroid dependence. Stage 2 deals with consequent chronic use, following which physiological and psychological dependence may develop, thereby making it increasingly difficult for users to quit.
Psychoactive effects, such as mood changes and increases in aggressive behavior, characterize this stage of dependence. In Stage 2, addiction treatment may be required, especially when AAS abuse is associated with other substance dependence, such as alcohol, opioids, or amphetamine abuse Brower, Arvary and Pope investigated this phenomenon in a clinical study, including patients admitted to a private facility for dependence on heroin or other opioids. Results of this study strongly suggested that these patients were introduced to opioids through AAS use and bodybuilding physical activity.
A second model, explaining mechanisms leading to AAS dependence, has also been proposed Bahrke and Yesalis, This model holds that AAS-dependence development occurs specifically in socio-cultural contexts that are likely to motivate certain individuals, particularly men, to attain large and strong muscles by frequent and intensive training sessions. These training sessions also improve mood and self-esteem and are generally associated with very strict and controlled dietary regimens.
Thus, AAS-induced muscle-active effects might underlie the reinforcing actions of these compounds Midgley et al. Studies to elucidate mechanisms leading to AAS dependence have also included surveys of current and former AAS users, recruited from gyms, websites, and physicians. Brower et al. Specific dysfunctions of the various components of the brain reward system have been described in clinical studies.
For example, alterations in levels of monoamine metabolites, neurohormones, and neuropeptides, which play a crucial role in the reward mechanism, have been investigated in the cerebrospinal fluid of subjects who received methyltestosterone MT with respect to placebo-treatment Daly et al. In particular, changes in cerebrospinal fluid 5-HIAA significantly correlated with the activation of specific psychiatric symptom cluster scores.
In addition, according to this study, a decrease in cerebrospinal fluid MHPG may derive from reduced norepinephrine clearance, even though authors did not detect any significant correlations between changes in MHPG levels and the development of clear psychiatric symptoms, suggesting a less crucial role for noradrenergic changes in this process.
An increase in substance P levels and vasopressin Hallberg et al. Multiple factors have been associated with the induction of dependence in AAS users, such as low endogenous levels of testosterone. Indeed, it has been demonstrated that women, adolescents and elderly subjects have a lower probability of developing AAS dependence Wood et al. Among possible risk factors for dependence development, the most relevant appears to be participation in competitive sports with intense and repetitive physical exercise Kanayama et al.
Some investigators have also suggested that personality psychopathology may be a risk factor for AAS abuse. Yates et al. Although a growing number of reports, current knowledge of molecular mechanisms leading to AAS dependence in humans remains limited. In this regard, the reinforcing effects of AAS may also be biased by intensive physical exercise and by increased narcissistic self-esteem arising from the fulfillment of the desired body appearance. Preclinical studies have contributed in evaluating the impact of AAS exposure on neurochemical mechanisms underlying AAS-induced behavioral outcomes.
Animal studies offer a direct measure of behavioral parameters under conditions where age and sex of the subjects, along with AAS administration, are established by the investigator. In this section, we will focus our attention on the data in the literature from animal models employing different AAS exposure paradigms, frequently used to model human abuse patterns.
In particular, we will review laboratory animal research findings to assess AAS-induced behavioral effects, such as aggression and reward. Moreover, we will highlight studies that have reported neuronal pathways and signaling molecules involved in these behaviors. Behavioral human studies linking AAS abuse and aggression have confounding factors, such as regimen multiple steroids over a cycle of use , co-administration with other drugs of abuse and inaccurate measures of behavior simulated by subjective reports McGinnis, Conversely, experimental designs in animals that correlate AAS exposure and aggression are less equivocal.
The resident-intruder test is a common paradigm for assessing aggression. Initial studies on animal models have reported that long-term exposure to high doses of testosterone raised levels of aggression in gonadally intact rats and re-established aggression in castrated rats Lumia et al.
However, indices of aggressive responses depend on environmental context, social cues, sex and hormonal status of the intruder, age of exposure, physical provocation, and type of AAS administered Clark and Henderson, ; Lumia and McGinnis, Hence, studies in rats showed that AAS-treated males demonstrated a different predisposition for aggression when tested in three different environments home cage, opponent cage, or neutral cage Christie and Barfield, ; Lumia et al.
Adult male rats receiving high doses of AAS are more aggressive toward the intruder in their home cage and displayed lower levels of aggression in either opponents or neutral cages Breuer et al. Investigators extended their interest to other experimental factors demonstrating that AAS-treated rats are typically more aggressive toward intact rather than castrated rats, as well as toward ovariectomized rather than sexually receptive females Breuer et al.
McGinnis et al. Moreover, the environmental and social discriminating cues described above failed to alter testosterone-induced aggressive responses to physical provocation McGinnis et al. While testosterone clearly increases aggression, conflicting results have been reported in the literature concerning other commonly abused AAS stanozolol, nandrolone decanoate, boldenone undecylenate tested either in combination or individually.
Salas-Ramirez et al. Higher aggression levels were observed in male Syrian hamsters exposed to an AAS cocktail compared to controls, regardless of age treatment Salas-Ramirez et al. On the other hand, stanozolol failed to induce aggressive behavior in gonadectomized and intact rats and mice Clark and Barber, ; Martinez-Sanchis et al. More conflicting results have been reported by using nandrolone decanoate. Long et al.
Accordingly, adult rats exposed to mild physical provocation demonstrated decreased inter-male aggression when treated with stanozolol, while no effects of nandrolone have been reported Breuer et al. Regardless of the experimental methodologies employed to assess aggression, these findings suggest that strain, AAS chemical composition and regimen reflect the diversity of supra-therapeutic AAS exposure on behavioral responses in animals.
Several studies in preclinical models of aggression have investigated the AAS effects on the neurochemical changes in specific brain areas related to this behavior. High aggression is often associated to decreased serotonin 5-HT neurotransmission. Although this may account for high aggression as an individual feature, it has been suggested that serotonergic activity is probably higher during performance of aggressive behavior van der Vegt et al.
In particular, testosterone propionate exposure decreased both 5-HT and 5-HT metabolite, 5-HIAA, in the hippocampus but not in the striatum or in the frontal cortex of adult rats Bonson et al. A significant decrease in 5-HT 1A and 5-HT 1B receptors immunoreactive staining has been shown in the latero-anterior hypothalamus and amygdala of hamsters treated with a mixture of AAS Grimes and Melloni, ; Ricci et al.
However, no decrease in the number of 5-HT 1A receptor-expressing neurons and an increase in 5-HT 2A receptor immunoreactivity have been reported in the hypothalamus Ricci et al. Ambar and Chiavegatto have reported reduced 5-HT 1B mRNA levels in the hippocampus, hypothalamus, amygdala, and prefrontal cortex of nandrolone-treated mice suggesting that the serotonergic tone in these brain areas has a pivotal role for AAS-induced aggression in rodents Ambar and Chiavegatto, Nevertheless, it is difficult to separate the direct rewarding effects of AAS from the psychological dependence of users on their physical appearance, muscular strength, and athletic performance.
Hence, studies in animal models are a useful tool when examining androgen-reinforcing properties in conditions where anabolic effects and athletic performance are not relevant. Conditioned place preference CPP and self-administration are relevant experimental paradigms used to study reward in an experimental condition Wood, ; Koob, Several studies in adult rodents have reported that systemic testosterone injections induced CPP in male rats and mice de Beun et al.
In another animal model, it has been demonstrated that 15 days of administration of an AAS cocktail consisting of testosterone cypionate, nandrolone decanoate, and boldenone undecylenate, increased the rate of self-administration and enhanced the sensitivity to amphetamine challenge Clark et al. However, in the same study, a 2 week treatment with MT had no effect on reward or performance of intracranial self-stimulation.
In this light, Ballard and Wood have reported that in animals drostanolone and nandrolone tend to be self-administered Ballard and Wood, and can cause CPP Frye et al. Moreover, such effects can be prevented by dopaminergic antagonists Schroeder and Packard, indicating that dopaminergic pathways are necessary for these behavioral outcomes.
Indeed, the mesocorticolimbic circuitry, such as nucleus accumbens NAc and ventral tegmental area VTA are crucial for the reward system. Parrilla-Carrero et al. Very recently, the same research group has demonstrated nandrolone's failure to reward in adolescent mice Martinez-Rivera et al. Although the literature reports that the adolescent brain is more sensitive to the reinforcing effects of drugs of abuse, this study suggests that such sensitivity may be drug dependent Ernst et al.
Packard et al. Similarly, Frye et al. A growing body of evidence has shown the reinforcing effects of AAS using the experimental self-administration oral, intravenous iv, intracerebroventricular icv paradigm, which is considered as a model of addiction with the greatest face validity Johnson and Wood, ; Wood, ; Frye, ; Frye et al. Wood demonstrated that gonadally intact adult male hamsters preferentially self-administer testosterone orally by using a food-induced drinking model Wood, Although oral self-administration resembles oral AAS intake in humans, potential effects of taste solution or gut fill might present an inherent limitation on AAS oral consumption.
Thus, Wood et al. Moreover, Syrian hamsters voluntarily consume testosterone through icv self-administration, suggesting that testosterone-reinforcing effects are centrally mediated DiMeo and Wood, ; Wood, Ballard and Wood extended their research study on androgens and compared icv self-administration of four commonly abused AAS nandrolone, drostanolone, oxymetholone, stanozolol that differ in their method of administration, duration of action and metabolism.
Results from this study showed that male hamsters preferentially self-administered nandrolone or drostanolone, which are two of the mostly used injectable androgens in humans. Conversely, animals failed to self-administer the orally active androgens oxymetholone or stanozolol, suggesting that injectable androgens may be more reinforcing than orally active steroids Ballard and Wood, To better understand the behavioral outcomes described above, various neurochemical studies have examined AAS effects on the monoaminergic system by measuring neurotransmitter and metabolite levels or by detecting receptors and enzyme alterations in key brain areas linked to the reward pathway.
It has been reported that CPP induced by testosterone was blocked when adult male rats were directly injected into NAc with a D 1 -like or D 2 -like dopamine receptor antagonist SCH or sulpiride, respectively Schroeder and Packard, An up-regulation of the dopamine transporter DAT protein was observed in vivo by a binding study using positron emission tomography PET , in the striatum of male rat brain after chronic treatment with nandrolone Kindlundh et al.
Interestingly, Martinez-Rivera et al. Likewise, our research group showed a reduction in DA content in NAc of rats treated for 4 weeks with nandrolone, changes which were accompanied by reduced hedonic-related behavior Zotti et al. Furthermore, Birgner et al. In line with these results, nandrolone was shown to reduce type A and B activity of monoamine oxidase MAO Birgner et al. Further confirming the role of dopaminergic system in AAS effects on reward pathway, subchronic nandrolone has been shown to significantly down-regulate D 1 receptors in the NAc and caudate putamen of rats, and to up-regulate D 2 -like receptors in the NAc core and VTA Kindlundh et al.
In this regard, D 1 and D 2 receptors have been implicated in the reinforcing effects of drugs, as D 1 is necessary for the acquisition of the effect and D 2 crucial in mediating positive reinforcement Missale et al. On the other hand, we have previously reported that stanozolol had no effect on DA content in NAc Tucci et al.
Findings regarding the impact of different AAS on brain reward function are summarized in Table 1. Contradictory neurochemical results have been reported regarding AAS effects on the serotonergic system. In particular, intranasal administration of testosterone has been shown to increase dopaminergic and serotonergic systems in rat neostriatum and NAc de Souza Silva et al. Accordingly, nandrolone decanoate and oxymethenolone treatment enhanced 5-HT and 5-HIAA concentrations in rat cerebral cortex and hypothalamus, while decreased levels of 5-HT and 5-HIAA were observed in the striatum of nandrolone-treated rats Thiblin et al.
In particular, sub-chronic nandrolone administration down-regulates 5-HT 1B and up-regulates 5-HT 2 receptor density in rat brain Kindlundh et al. In addition, McQueen et al. On the other hand, several studies have associated the endogenous opioid system to behaviors linked to reward and reinforcement Gianoulakis, Thus, a number of experimental investigations have been carried out to ascertain whether AAS treatment modifies the levels of opioid peptides and their receptors in brain areas mediating reward.
Moreover, an increase in dynorphin converting enzyme-like activity was found only in the NAc of rats exposed to chronic nandrolone, suggesting an increased biosynthesis of dynorphin peptides, which, in turn, might affect basal DA levels in the NAc Spanagel et al. It is worth noting that AAS effects are commonly described after chronic or sub-chronic drug exposure.
Indeed, acute subcutaneous testosterone administration failed to influence accumbal DA release Triemstra et al. In this regard, it has been proposed that AAS effects on the reinforcement system may be DA-independent, as happens with other abuse substances such as ethanol and benzodiazepines. Moreover, AAS effects on mesolimbic dopamine might be indirect or rely on non-classic androgen-sensitive pathways. Thus, based on accumulated evidence, AAS have an addictive potential, especially in susceptible subjects.
As reported, many discrepancies need to be better clarified. First, it is important to clarify whether classic nuclear receptors are involved in these effects or if other mechanisms are also involved. Moreover, scientific evidence exists for fast actions of steroids acting on calcium channels, membrane receptors, second messengers and membrane fluidity for a review see Foradori et al. In this regard, a recent in vitro study has shown that testosterone, by acting on membrane receptors, was able to increase hippocampal plasticity within 2 h, leading to increased spine density Li et al.
Sato et al. In particular, their experiments demonstrated that animals, intact or carrying the testicular feminization mutation, preferentially self-administer dihydrotestosterone DHT and DHT conjugated to bovine serum albumin, DHT-BSA, which acts only on cell surface.
These observations prompted the authors to conclude that androgen self-administration may be mediated by plasma membrane receptors Sato et al. Accordingly, it has been postulated that classical genomic action of androgen may be not fast enough to assure reinforcement. Nonetheless, it is worth to note that further signaling systems, other than dopaminergic or opioidergic, can be implicated in reward.
This finding led the Authors to hypothesize that AAS may thus sensitize reward mechanisms. However, the number of studies investigating the effects of AAS on glutamatergic system in reward is still limited; hence, future investigations should be focused accordingly to clarify whether AAS reinforcement relies on non-classic pathways or on other signaling systems. Clinical and epidemiological data have reported that the abuse of AAS in humans is often associated with the abuse of psychotropic drugs, such as cocaine, opiates, alcohol, cannabis, amphetamine, and 3,4-methylenedioxy-methamphetamine MDMA.
These surveys have suggested a role of AAS as a gateway to other dependency-inducing drugs DuRant et al. Based on these findings, different animal paradigms have been used to investigate AAS pre-exposure effects on neurochemical and behavioral response to other addictive substances.
Consistent with reported higher alcohol intake in AAS abusers, increased voluntary alcohol consumption after cessation of AAS administration has also been observed in male adult rats Johansson et al. In line with these findings, corticotropin releasing factor modulation of GABAergic transmission in the amygdala seems to play a pivotal role in ethanol effects, suggesting that AAS might alter the sensitivity of these circuits and predispose to alcohol abuse Roberto et al.
Interestingly, nandrolone administration increased THC abstinence precipitated by the CB1 cannabinoid antagonist rimonabant Celerier et al. Administration of supra-pharmacological doses of nandrolone decanoate has been shown to decrease the hyper-locomotion and stereotyped behavior induced by amphetamine and MDMA, in a dose-dependent manner Kurling et al. Such behavioral outcomes have been corroborated by microdialysis results.
However, the higher dose of nandrolone decanoate has enhanced the acute effects of MDMA-induced release of 5-HT, followed by exhaustion of neuronal 5-HT stores. Likewise, it has been shown that pretreatment with nandrolone decanoate attenuates accumbal DA and 5-HT outflow, as well as the consequent stereotyped behavior induced by cocaine Kurling-Kailanto et al.
In these studies, the authors showed that changes in DA and 5-HT systems endure, even after a long recovery period from the last dose of nandrolone. This confirms the hypothesis that drug abuse causes long lasting changes in brain dopaminergic and serotonergic pathways Kurling et al.
These data are in line with earlier findings demonstrating that chronic cocaine and methamphetamine decreased D 2 -receptor and DAT expression during withdrawal and lasted up to 11 months after the last drug administration Volkow et al. Collectively, these results demonstrate that pre-treatment with nandrolone decanoate dose-dependently attenuates neurochemical and behavioral effects relating to the reward system induced by psychostimulant drugs.
These findings indicate that such reduced dopaminergic and serotonergic activity in brain regions strictly involved in the reward system might represent the neurochemical substrate that could underlie a higher prevalence of illicit drug use among AAS abusers.
Indeed, to achieve the desired effect of psychostimulant drugs, AAS users may require increased doses of these substances. On the other hand, testosterone has been hypothesized to act as a partial agonist on the opiod system considering that, depending on type of receptors involved, steroid effects are brain region specific Wood, However, contrasting data exist since no effects of AAS on morphine antinociception have been reported in other animal models Negus et al.
In fact, nandrolone pre-exposure has been shown to inhibit tolerance to antinociceptive properties of morphine and CPP induced by morphine in mice Celerier et al. Accordingly, pre-exposure to AAS has been shown to prevent morphine-induced striatal Fos expression Harlan et al. High variability is present in findings linking AAS to opiate withdrawal.
In monkeys no effect of AAS has been described for naloxone-precipitated morphine withdrawal paradigm, although Celerier et al. Moreover, the dysphoric effect mediated by nandrolone pre-treatment has been correlated to elevated striatal levels of dynorphin B, which in turn may account for the inhibition of dopaminergic activity in this brain region Steiner and Gerfen, ; Johansson et al.
Finally, testosterone has been shown not to increase motivation for morphine Cooper and Wood, Such discrepancies may rely on different AAS and schedule of treatment used, as well as different species or strain of animal used. Although literature has been populated by many clinical or preclinical reports, many knots in the unraveling of deleterious addictive effects of AAS still need to be untied.
Furthermore, taking into account that the use of these substances is becoming popular, especially among adolescents, a deeper knowledge of CNS effects of AAS is nowadays mandatory. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
Aitken, C. Pumping iron, risking infection? Drug Alcohol Depend. Alexander, G. Testosterone has rewarding affective properties in male rats: implications for the biological basis of sexual motivation. Ambar, G. Anabolic-androgenic steroid treatment induces behavioral disinhibition and downregulation of serotonin receptor messenger RNA in the prefrontal cortex and amygdala of male mice.
Genes Brain Behav. Anderson, R. Comparison between testosterone enanthate-induced azoospermia and oligozoospermia in a male contraceptive study. Pharmacokinetics and pharmacodynamics of once weekly administration of testosterone enanthate. PubMed Abstract Google Scholar. Arnedo, M. Rewarding properties of testosterone in intact male mice: a pilot study. Similar rewarding effects of testosterone in mice rated as short and long attack latency individuals.
Arvary, D. Anabolic-androgenic steroids as a gateway to opioid dependence. Baggish, A. Long-term anabolic-androgenic steroid use is associated with left ventricular dysfunction. Heart Fail. Bahrke, M. Weight training. A potential confounding factor in examining the psychological and behavioural effects of anabolic-androgenic steroids. Sports Med. Ballard, C. Intracerebroventricular self-administration of commonly abused anabolic-androgenic steroids in male hamsters Mesocricetus auratus : nandrolone, drostanolone, oxymetholone, and stanozolol.
Basaria, S. Clinical review anabolic-androgenic steroid therapy in the treatment of chronic diseases. Bhasin, S. The effects of supraphysiologic doses of testosterone on muscle size and strength in normal men. Testosterone dose-response relationships in healthy young men.
Birgner, C. The anabolic androgenic steroid nandrolone decanoate affects mRNA expression of dopaminergic but not serotonergic receptors. Brain Res. Altered extracellular levels of DOPAC and HVA in the rat nucleus accumbens shell in response to sub-chronic nandrolone administration and a subsequent amphetamine challenge. Reduced activity of monoamine oxidase in the rat brain following repeated nandrolone decanoate administration.
Bonson, K. Serotonergic control of androgen-induced dominance. Breuer, M. Aggression in male rats receiving anabolic androgenic steroids: effects of social and environmental provocation. Brower, K. Withdrawal from anabolic steroids. Anabolic steroid abuse and dependence. Psychiatry Rep. Symptoms and correlates of anabolic-androgenic steroid dependence.
Evidence for physical and psychological dependence on anabolic androgenic steroids in eight weight lifters. Psychiatry , — Influence of the anabolic-androgenic steroid nandrolone on cannabinoid dependence. Neuropharmacology 50, — Effects of nandrolone on acute morphine responses, tolerance and dependence in mice. Christie, M. Effects of aromatizable androgens on aggressive behaviour among rats rattus norvegicus.
Clark, A. Anabolic-androgenic steroids and aggression in castrated male rats. Behavioral and physiological responses to anabolic-androgenic steroids. Anabolic-androgenic steroids and brain reward. Conway, A. Use, misuse and abuse of androgens. The Endocrine Society of Australia consensus guidelines for androgen prescribing.
Cooper, S. Androgens and opiates: testosterone interaction with morphine self-administration in male rats. Neuroreport 25, — Coviello, A. Effects of graded doses of testosterone on erythropoiesis in healthy young and older men. Cunningham, R.
Physical provocation of pubertal anabolic androgenic steroid exposed male rats elicits aggression towards females. Factors influencing aggression toward females by male rats exposed to anabolic androgenic steroids during puberty. Daly, R. Cerebrospinal fluid and behavioral changes after methyltestosterone administration: preliminary findings.
Psychiatry 58, — Dean, C.
|Self administration of steroids||Kashkin, K. The effects of cocaine and nandrolone co-administration on aggression in male rats. Routledge handbook of drugs and sport. Severe intrahepatic cholestasis and liver failure after stanozolol usage - case report and review of the literature. Intravascular ultrasound and angiographic demonstration of left main stem thrombus-high-risk presentation in a young adult with anabolic steroid abuse.|
|El organon de aristoteles pdf||Examples of drugs serving as alternatives to anabolic steroids include clenbuterol, human growth hormone, insulin, insulin-like growth factor, and gamma-hydroxybutyrate GHB. J Health Psychol. Am J Public Health 0 :e1-e3. Some of these substances include androstenedione, androstenediol, norandrostenedione, norandrostenediol, and dehydroepiandtrosterone DHEAwhich can be converted into testosterone or a similar compound in the body. Aggression in why steroids are illegal rats receiving anabolic androgenic steroids: effects of social and environmental provocation. Spontaneous subdural haematoma in anabolic steroids dependent weight lifters: reports of two cases and review of self administration of steroids. Anabolic steroids are synthetically produced variants of the naturally occurring male hormone testosterone.|
|Taj samudra golden dragon||Homeopathy organon 6th edition|
|Can i take steroids to gain weight||Reversible anabolic androgenic steroid-induced cardiomyopathy. Med Sci Sports Exerc. Reprints and Permissions. Drug misuse prevention: targeted interventions NG Self-administration of 3alpha-androstanediol increases locomotion and analgesia and decreases aggressive behavior of male hamsters.|
|Gold network canada dragons den||Fastest way to make gold in dragon quest 4|
|Is testosterone ethanate a steroid||Forensic Sci. The idea of designing and developing steroids with anabolic properties arose during the s soon after the identification and isolation of the hormone androsterone by the German investigator Butenandt, who collected this compound from thousands of liters of pooled human urine derived from a number of military service volunteers. Steroids 77, — This confirms the hypothesis that drug abuse causes long lasting changes in brain dopaminergic and serotonergic pathways Kurling et al. Int J Drug Policy.|
Hold the syringe with its needle uncapped and pointing up in front of you. Look for air bubbles in the syringe. Flick the side of the syringe to get these bubbles to rise to the top. When your dosage is bubble-free, slowly depress the plunger to force the air at the top of the syringe out.
Stop when you see a tiny drop of medication come out of the tip of the syringe. Be careful not to squirt or spray a significant portion of your dosage onto the floor. Prepare the injection site. Testosterone injections are typically intramuscular — that is, given directly into a muscle.
Two relatively easy and accessible sites for intramuscular injection are the deltoid upper arm or the glut upper back portion of the thigh, ie, the butt cheek. Whichever of these sites you choose, take a sterile alcohol pad and wipe the immediate area around where you intend to inject. This will kill bacteria on the skin, preventing infection. If injecting into the glute or buttocks, choose an injection site in the top outside section of the glute.
In other words, pick a site either in the top left corner of the left glute or the top right corner of the right glute. These site have the best access to muscle tissue and allow you to avoid hitting nerves and blood vessels in other parts of the glute.
Hold your loaded syringe like a dart at a degree angle above the sterile injection site. Quickly plunge it into the flesh. Before depressing the plunger, draw back on it slightly. Inject the medication at a steady, controlled pace. Care for the injection site post-injection.
Once you have fully depressed the plunger, slowly pull the needle out. Press around the injection site with a sterile cotton swab as you do so — this prevents the emerging needle from pulling on the skin and causing extra pain. Testosterone dose-response relationships in healthy young men. Birgner, C. The anabolic androgenic steroid nandrolone decanoate affects mRNA expression of dopaminergic but not serotonergic receptors. Brain Res. Altered extracellular levels of DOPAC and HVA in the rat nucleus accumbens shell in response to sub-chronic nandrolone administration and a subsequent amphetamine challenge.
Reduced activity of monoamine oxidase in the rat brain following repeated nandrolone decanoate administration. Bonson, K. Serotonergic control of androgen-induced dominance. Breuer, M. Aggression in male rats receiving anabolic androgenic steroids: effects of social and environmental provocation. Brower, K.
Withdrawal from anabolic steroids. Anabolic steroid abuse and dependence. Psychiatry Rep. Symptoms and correlates of anabolic-androgenic steroid dependence. Evidence for physical and psychological dependence on anabolic androgenic steroids in eight weight lifters. Psychiatry , — Influence of the anabolic-androgenic steroid nandrolone on cannabinoid dependence. Neuropharmacology 50, — Effects of nandrolone on acute morphine responses, tolerance and dependence in mice.
Christie, M. Effects of aromatizable androgens on aggressive behaviour among rats rattus norvegicus. Clark, A. Anabolic-androgenic steroids and aggression in castrated male rats. Behavioral and physiological responses to anabolic-androgenic steroids. Anabolic-androgenic steroids and brain reward. Conway, A. Use, misuse and abuse of androgens. The Endocrine Society of Australia consensus guidelines for androgen prescribing.
Cooper, S. Androgens and opiates: testosterone interaction with morphine self-administration in male rats. Neuroreport 25, — Coviello, A. Effects of graded doses of testosterone on erythropoiesis in healthy young and older men.
Cunningham, R. Physical provocation of pubertal anabolic androgenic steroid exposed male rats elicits aggression towards females. Factors influencing aggression toward females by male rats exposed to anabolic androgenic steroids during puberty. Daly, R. Cerebrospinal fluid and behavioral changes after methyltestosterone administration: preliminary findings.
Psychiatry 58, — Dean, C. Prasterone DHEA and mania. Testosterone as appetitive and discriminative stimulus in rats: sex- and dose-dependent effects. Dopaminergic and serotonergic activity in neostriatum and nucleus accumbens enhanced by intranasal administration of testosterone. DiMeo, A. Circulating androgens enhance sensitivity to testosterone self-administration in male hamsters.
Dohle, G. Androgens and male fertility. World J. DuRant, R. Anabolic-steroid use, strength training, and multiple drug use among adolescents in the United States. Pediatrics 96, 23— Ernst, M. Neurobiology of the development of motivated behaviors in adolescence: a window into a neural systems model.
Far, H. Cardiac hypertrophy in deceased users of anabolic androgenic steroids: an investigation of autopsy findings. Farrell, S. Effects of pubertal anabolic-androgenic steroid AAS administration on reproductive and aggressive behaviors in male rats. Ferreira, I. Nutritional intervention in COPD: a systematic overview. Chest , — Foradori, C. Non-genomic actions of androgens. Franke, W. Hormonal doping and androgenization of athletes: a secret program of the German Democratic Republic government.
Frye, C. Some rewarding effects of androgens may be mediated by actions of its 5alpha-reduced metabolite 3alpha-androstanediol. Self-administration of 3alpha-androstanediol increases locomotion and analgesia and decreases aggressive behavior of male hamsters. The testosterone metabolite and neurosteroid 3alpha-androstanediol may mediate the effects of testosterone on conditioned place preference.
Psychoneuroendocrinology 26, — The nucleus accumbens as a site of action for rewarding properties of testosterone and its 5alpha-reduced metabolites. Furlanello, F. Arrhythmogenic effects of illicit drugs in athletes. Heart J. Galvan, A. Adolescent development of the reward system. Gianoulakis, C. Endogenous opioids and addiction to alcohol and other drugs of abuse.
Grimes, J. Serotonin-1B receptor activity and expression modulate the aggression-stimulating effects of adolescent anabolic steroid exposure in hamsters. Gupta, V. Effects of dihydrotestosterone on differentiation and proliferation of human mesenchymal stem cells and preadipocytes. Hallberg, M. Anabolic-androgenic steroids affect the content of substance P and substance P in the rat brain. Peptides 21, — Harlan, R. Androgenic-anabolic steroids blunt morphine-induced c-fos expression in the rat striatum: possible role of beta-endorphin.
Harrison, R. Chronic anabolic-androgenic steroid treatment during adolescence increases anterior hypothalamic vasopressin and aggression in intact hamsters. Psychoneuroendocrinology 25, — Hart, D. Anabolic effects of oxandrolone after severe burn. Hassan, N. Doping and effects of anabolic androgenic steroids on the heart: histological, ultrastructural, and echocardiographic assessment in strength athletes.
Haupt, H. Upper extremity injuries associated with strength training. Irving, L. Steroid use among adolescents: findings from Project EAT. Health 30, — Johansson, P. The effect on opioid peptides in the rat brain, after chronic treatment with the anabolic androgenic steroid, nandrolone decanoate. Anabolic androgenic steroids affects alcohol intake, defensive behaviors and brain opioid peptides in the rat.
Anabolic androgenic steroids increase beta-endorphin levels in the ventral tegmental area in the male rat brain. Johnson, L. Oral testosterone self-administration in male hamsters. Neuroendocrinology 73, — Kailanto, S.
Subchronic steroid administration induces long lasting changes in neurochemical and behavioral response to cocaine in rats. Steroids 76, — Kanayama, G. Past anabolic-androgenic steroid use among men admitted for substance abuse treatment: an underrecognized problem? Psychiatry 64, — Features of men with anabolic-androgenic steroid dependence: a comparison with nondependent AAS users and with AAS nonusers.
Risk factors for anabolic-androgenic steroid use among weightlifters: a case-control study. Kashkin, K. Hooked on hormones? An anabolic steroid addiction hypothesis. JAMA , — Kindlundh, A. Dopaminergic effects after chronic treatment with nandrolone visualized in rat brain by positron emission tomography. Psychiatry 26, — Adolescent use of anabolic-androgenic steroids and relations to self-reports of social, personality and health aspects.
Public Health 11, — Factors associated with adolescent use of doping agents: anabolic-androgenic steroids. Addiction 94, — The anabolic-androgenic steroid nandrolone decanoate affects the density of dopamine receptors in the male rat brain. Chronic administration with nandrolone decanoate induces alterations in the gene-transcript content of dopamine D 1 - and D 2 -receptors in the rat brain.
Koob, G. The neurobiology of addiction: a neuroadaptational view relevant for diagnosis. Addiction Suppl. Krieg, A. Cardiac tissue Doppler in steroid users. Kritzer, M. Region and sex differences in constituent dopamine neurons and immunoreactivity for intracellular estrogen and androgen receptors in mesocortical projections in rats.
Kuhn, C. Anabolic steroids. Recent Prog. Kurling, S. Sub-chronic nandrolone treatment modifies neurochemical and behavioral effects of amphetamine and 3,4-methylenedioxymethamphetamine MDMA in rats. Kurling-Kailanto, S. Subchronic nandrolone administration reduces cocaine-induced dopamine and 5-hydroxytryptamine outflow in the rat nucleus accumbens.
Psychopharmacology Berl. Kutscher, E. Anabolic steroids: a review for the clinician. Langer, C. Clinical significance of weight loss in cancer patients: rationale for the use of anabolic agents in the treatment of cancer-related cachexia. Nutrition 17, S1—S Li, S. Detecting the presence of hippocampus membrane androgen receptors in male SAMP8 mice and their induced synaptic plasticity. Lindqvist, A.
Anabolic androgenic steroid affects competitive behaviour, behavioural response to ethanol and brain serotonin levels. Long, S. The effects of nandrolone decanoate on cocaine-induced kindling in male rats. Neuropharmacology 39, — The effects of cocaine and nandrolone co-administration on aggression in male rats.
Psychiatry 20, — Luijkx, T. Anabolic androgenic steroid use is associated with ventricular dysfunction on cardiac MRI in strength trained athletes. Lumia, A. Impact of anabolic androgenic steroids on adolescent males. Effects of chronically high doses of the anabolic androgenic steroid, testosterone, on intermale aggression and sexual behavior in male rats.
Magnusson, K. Nandrolone decanoate administration dose-dependently affects the density of kappa opioid peptide receptors in the rat brain determined by autoradiography. Neuropeptides 43, — Enzymatic conversion of dynorphin A in the rat brain is affected by administration of nandrolone decanoate. Peptides 28, — Manoharan, G. Syncopal episodes in a young amateur body builder.
Martinez-Rivera, F. The effect of the anabolic steroid, nandrolone, in conditioned place preference and D 1 dopamine receptor expression in adolescent and adult mice. Processes , 81— Long-term chronic treatment with stanozolol lacks significant effects on aggression and activity in young and adult male laboratory mice. McBride, A. Three cases of nalbuphine hydrochloride dependence associated with anabolic steroid use.
McGinnis, M. Anabolic androgenic steroids and aggression: studies using animal models. Physical provocation potentiates aggression in male rats receiving anabolic androgenic steroids. Effects of withdrawal from anabolic androgenic steroids on aggression in adult male rats. McQueen, J. Menard, C. Androgenic-anabolic steroids modify beta-endorphin immunoreactivity in the rat brain.
Midgley, S. Dependence-producing potential of anabolic-androgenic steroids. Theory 7, — Missale, C. Dopamine receptors: from structure to function. Montisci, M. Anabolic androgenic steroids abuse and cardiac death in athletes: morphological and toxicological findings in four fatal cases. Forensic Sci. Morley, J. Testosterone replacement in older men and women. Morton, R. Psychiatric effects of anabolic steroids after burn injuries.
Psychosomatics 41, 66— Negus, S. Lack of evidence for opioid tolerance or dependence in rhesus monkeys following high-dose anabolic-androgenic steroid administration. Noakes, T. Tainted glory—doping and athletic performance. Oberlander, J.
Corticotropin-releasing factor modulation of forebrain GABAergic transmission has a pivotal role in the expression of anabolic steroid-induced anxiety in the female mouse. Neuropsychopharmacology 37, — Packard, M. Rewarding affective properties of intra-nucleus accumbens injections of testosterone. Parkinson, A. Anabolic androgenic steroids: a survey of users. Sports Exerc. Parrilla-Carrero, J.
The anabolic steroids testosterone propionate and nandrolone, but not 17alpha-methyltestosterone, induce conditioned place preference in adult mice. Steroid use and long-term health risks in former athletes. Peters, K. Androgen dependence in hamsters: overdose, tolerance, and potential opioidergic mechanisms. Neuroscience , — Philipova, T.
Polsky, B. Pope, H. Sadock, V. Sadock, and P. Effects of supraphysiologic doses of testosterone on mood and aggression in normal men: a randomized controlled trial. Psychiatry 57, — Adverse health consequences of performance-enhancing drugs: an Endocrine Society scientific statement. Porcerelli, J.
Narcissism and empathy in steroid users. Rabkin, J. A double-blind, placebo-controlled trial of testosterone therapy for HIV-positive men with hypogonadal symptoms. Ricci, L. Roberto, M. Corticotropin releasing factor-induced amygdala gamma-aminobutyric Acid release plays a key role in alcohol dependence. Psychiatry 67, — Increased GABA release in the central amygdala of ethanol-dependent rats.
Salas-Ramirez, K. Anabolic steroids have long-lasting effects on male social behaviors. Sato, S. Membrane androgen receptors may mediate androgen reinforcement. Psychoneuroendocrinology 35, — Adolescents and androgens, receptors and rewards. Schlussman, S. Effects of the androgenic anabolic steroid, nandrolone decanoate, on adrenocorticotropin hormone, corticosterone and proopiomelanocortin, corticotropin releasing factor CRF and CRF receptor1 mRNA levels in the hypothalamus, pituitary and amygdala of the rat.
Schroeder, J. Role of dopamine receptor subtypes in the acquisition of a testosterone conditioned place preference in rats. Schwartzer, J. Adolescent anabolic-androgenic steroid exposure alters lateral anterior hypothalamic serotonin-2A receptors in aggressive male hamsters. Shahidi, N. A review of the chemistry, biological action, and clinical applications of anabolic-androgenic steroids. Singh, R. Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors.
Endocrinology , — Sinha-Hikim, I. Testosterone-induced increase in muscle size in healthy young men is associated with muscle fiber hypertrophy. Testosterone-induced muscle hypertrophy is associated with an increase in satellite cell number in healthy, young men. Spanagel, R.
Opposing tonically active endogenous opioid systems modulate the mesolimbic dopaminergic pathway. Steiner, H. Role of dynorphin and enkephalin in the regulation of striatal output pathways and behavior. Tamaki, T. Nandrolone decanoate enhances hypothalamic biogenic amines in rats.
Tanaka, K. Serum testosterone:estradiol ratio and the development of hepatocellular carcinoma among male cirrhotic patients. Cancer Res. Tennant, F. Anabolic steroid dependence with opioid-type features. Thevis, M. Determination of the prevalence of anabolic steroids, stimulants, and selected drugs subject to doping controls among elite sport students using analytical chemistry.
Sports Sci. Thiblin, I. Increased dopaminergic and 5-hydroxytryptaminergic activities in male rat brain following long-term treatment with anabolic androgenic steroids. Cause and manner of death among users of anabolic androgenic steroids.
Anabolic androgenic steroids and suicide. Psychiatry 11, — Tremblay, M. Effect of training status and exercise mode on endogenous steroid hormones in men. Triemstra, J. Testosterone and nucleus accumbens dopamine in the male Syrian hamster.
Psychoneuroendocrinology 33, — Tucci, P. Neurochemical consequence of steroid abuse: stanozolol-induced monoaminergic changes. Steroids 77, — Activation of serotonergic neurotransmission during the performance of aggressive behavior in rats. Volkow, N. Low level of brain dopamine D2 receptors in methamphetamine abusers: association with metabolism in the orbitofrontal cortex. Loss of dopamine transporters in methamphetamine abusers recovers with protracted abstinence.
Effects of chronic cocaine abuse on postsynaptic dopamine receptors. Wichstrom, L. Use of anabolic-androgenic steroids in adolescence: winning, looking good or being bad? Alcohol 62, 5— Wines, J.