Psychiatric and medical effects of anabolic-androgenic steroid use in women

BACKGROUND: Although numerous studies have documented the psychiatric and physiological effects of anabolic-androgenic steroids (AAS) in males, virtually no studies have investigated the effects of illicit AAS use in women. METHODS: We performed psychiatric and medical evaluations of 75 dedicated women athletes, recruited by advertisement primarily from gymnasiums in the Boston, Mass., area. RESULTS: Twenty-five (33%) of the women reported current or past AAS use. Users were more muscular than nonusers and reported use of many other 'ergogenic' (performance-enhancing) drugs in addition to AAS. Some described a frank syndrome of ergogenic polysubstance dependence, often with significant morbidity. Fourteen (56%) of the users reported hypomanic symptoms during AAS use and 10 (40%) reported depressive symptoms during AAS withdrawal, but none met full DSM-IV criteria for a hypomanic or major depressive episode. Nineteen (76%) users reported at least one adverse medical effect associated with AAS use. Perhaps the most interesting findings were several unusual psychiatric syndromes reported by both the AAS users and nonusers. These included rigid dietary practices (which we have termed 'eating disorder, bodybuilder type'), nontraditional gender roles and chronic dissatisfaction and preoccupation with their physiques (a syndrome which we have termed 'muscle dysmorphia'). CONCLUSIONS: Dedicated women athletes exhibit not only AAS abuse, but use of many other ergogenic drugs, sometimes associated with significant morbidity. In addition, these athletes frequently display several psychiatric syndromes which have not previously been well described.     

Impact of anabolic androgenic steroids on adolescent males

Anabolic androgenic steroid (AAS) use increased dramatically among adolescent males. This review focuses on studies using animal models of AAS exposure during adolescence which is a hormonally sensitive developmental period. AAS exposure during this critical period has wide-ranging consequences, including increased dendritic spine density, altered brain serotonin levels and escalated aggression in response to physical provocation. Human data suggest that AAS induces indiscriminate and unprovoked aggression often described as “'roid rage”. However, animal studies indicate that the behavioral impact of AAS is modulated by experiential and social contingencies, a perceived provocation, and the chemical composition of the AAS. The AAS, testosterone increases aggression in juvenile and adult male rats when physically provoked. In contrast, stanzolol, inhibits aggression in both juvenile and adult male rats, even when physically provoked. Nandrolone has minimal effects on aggression, unless preceded by attack training. Exposure to AAS during adolescence may have a host of unintended bio-behavioral consequences. Yet, the perception of harmlessness surrounds AAS use. The perception of harmlessness is promoted by the availability of AAS especially through internet pharmacies. The perception of acceptability is reflected in current cultural ethics that no longer condemn cheating to obtain personal achievement or success. A prevailing conviction is that although AAS are illegal they are not really bad. Reduction of the availability of AAS to adolescents requires ardent legislative and legal intervention. The problem of acceptability can be addressed by educating adolescents about the short-term and long-term effects of AAS on brain and behavior, to increase awareness of the potential consequences of AAS use that apply directly to them.     

Effects of anabolic androgenic steroids on sleep patterns of individuals practicing resistance exercise

Anabolic androgenic steroid (AAS) abuse has become a public health problem in many countries, and is associated with many psychiatric disorders. Epidemiological studies have also found increasing numbers of sleep disorders reported by individuals using AASs. The purpose of this study was to evaluate sleep patterns and disorders in anabolic androgenic users who practice resistance exercise. The sample comprised 58 males divided into three groups: (1) 20 current AAS users aged 26 ± 1.2, (2) 21 controls with no history of AAS use, aged 26 ± 1 and (3) 17 sedentary men with no sleep disorders aged 27.2 ± 0.34. The volunteers spent a night in the sleep laboratory for polysomnography. Comparing the three groups, the user group showed reduced sleep efficiency and more wakings after sleep onset than the sedentary group (P = 0.001). The sedentary group showed a higher percentage of stage 4 than the non-users group. We suggest that using of anabolic steroids reduced sleep efficiency and alters sleep architecture.     

What can allostasis tell us about anabolic-androgenic steroid addiction?

Anabolic-androgenic steroids (AASs) are synthetic hormones used by individuals who want to look better or perform better in athletics and at the gym. Their use raises an interesting paradox in which drug use is associated with a number of health benefits, but also the possibility of negative health consequences. Existing models of AAS addiction follow the traditional framework of drug abuse and dependence, which suggest that harmful use occurs as a result of the drug's ability to hijack the motivation-reward system. However, AASs, unlike typical drugs of abuse, are not used for acute intoxication effects or euphoria. Rather, AASs are used to affect the body through changes to the musculoskeletal system and the hypothalamic-pituitary-gonadal axis as opposed to stimulating the reward system. We offer an allostatic model of AAS addiction to resolve this inconsistency between traditional drug addiction and AAS addiction. This allostatic framework provides a way to (a) incorporate exercise into AAS misuse, (b) identify where AAS use transitions from recreational use into a drug problem, and (c) describe individual differences in vulnerability or resilience to AASs. Implications for this model of AAS addiction are discussed.     

Effects of pubertal anabolic-androgenic steroid (AAS) administration on reproductive and aggressive behaviors in male rats

Adolescence in human males is a hormonally sensitive period when many adult behaviors develop, including sexual and aggressive behaviors. Using a rat model, the authors examined the effects of three anabolic-androgenic steroids (AAS) during puberty: testosterone, nandrolone, and stanozolol. Copulation, vocalizations, scent-marking, and aggression were tested following AAS exposure. Relative to gonadally intact controls, rats injected with testosterone showed a significant increase in scent-marking and aggression in the opponent's home cage. Nandrolone had no effect. Stanozolol significantly inhibited all behaviors. Results suggest that depending on the chemical structure of the steroid, AAS exposure during puberty affects several androgen-dependent behaviors. Because adolescence in humans is a period of hormonal change, abuse of AAS, particularly stanozolol, during this time may disrupt the establishment of normal adult behavior patterns.     

Pubertal exposure to anabolic androgenic steroids increases spine densities on neurons in the limbic system of male rats

Human studies show that the number of teenagers abusing anabolic androgenic steroids (AAS) is increasing. During adolescence, brain development is altered by androgen exposure, which suggests that AAS may potentially alter central nervous system (CNS) development. The goal of the present study was to determine whether pubertal AAS exposure increased dendritic spine densities on neurons within the medial amygdala and the dorsal hippocampus. Pubertal gonadally intact male rats received the AAS testosterone propionate (5 mg/kg) or vehicle for 5 days/week for 4 weeks. To determine the long-term implications of pubertal AAS use, another set of males received the same AAS treatment and was then withdrawn from AAS exposure for 4 weeks. Results showed that pubertal AAS exposure significantly increased spine densities on neurons in the anterior medial amygdala, posterodorsal medial amygdala, and the cornu ammonis region 1 (CA1) of the hippocampus compared with gonadally intact control males. Spine densities returned to control levels within the anterior medial amygdala and the posterodorsal medial amygdala 4 weeks after withdrawal. However, spine densities remained significantly elevated after AAS withdrawal in the CA1 region of the hippocampus, suggesting that pubertal AAS exposure may have a long-lasting impact on CA1 hippocampal neuroanatomy. Since pubertal AAS exposure increased spine densities and most excitatory synapses in the CNS occur on dendritic spines, AAS may increase neuronal excitation. It is proposed that this increase in excitation may underlie the behavioral responses seen in pubertal AAS-treated male rats.     

Effects of anabolic androgenic steroids on the development and expression of running wheel activity and circadian rhythms in male rats

In humans, anabolic androgenic steroid (AAS) use has been associated with hyperactivity and disruption of circadian rhythmicity. We used an animal model to determine the impact of AAS on the development and expression of circadian function. Beginning on day 68 gonadally intact male rats received testosterone, nandrolone, or stanozolol via constant release pellets for 60 days; gonadally intact controls received vehicle pellets. Wheel running was recorded in a 12:12 LD cycle and constant dim red light (RR) before and after AAS implants. Post-AAS implant, circadian activity phase, period and mean level of wheel running wheel activity were compared to baseline measures. Post-AAS phase response to a light pulse at circadian time 15 h was also tested. To determine if AAS differentially affects steroid receptor coactivator (SRC) expression we measured SRC-1 and SRC-2 protein in brain. Running wheel activity was significantly elevated by testosterone, significantly depressed by nandrolone, and unaffected by stanozolol. None of the AAS altered measures of circadian rhythmicity or phase response. While SRC-1 was unaffected by AAS exposure, SRC-2 was decreased by testosterone in the hypothalamus. Activity levels, phase of peak activity and circadian period all changed over the course of development from puberty to adulthood. Development of activity was clearly modified by AAS exposure as testosterone significantly elevated activity levels and nandrolone significantly suppressed activity relative to controls. Thus, AAS exposure differentially affects both the magnitude and direction of developmental changes in activity levels depending in part on the chemical composition of the AAS.     

Anabolic steroid abuse and cardiac sudden death: a pathologic study

CONTEXT: Androgenic anabolic steroids (AAS) used for improving physical performance have been considered responsible for acute myocardial infarction and sudden cardiac death. OBJECTIVE: To establish the relationship between AAS and cardiac death. DESIGN: Case report. PATIENTS: Two young, healthy, male bodybuilders using AAS. MAIN OUTCOME MEASURES: Pathologic cardiac findings associated with AAS ingestion. RESULTS: The autopsy revealed normal coronary arteries. In one case, we documented a typical infarct with a histologic age of 2 weeks. A segmentation of myocardial cells at the intercalated disc level was observed in the noninfarcted region. This segmentation was the only anomaly detected in the second case. No other pathologic findings in the heart or other organs were found. Urine in both subjects contained the metabolites of nortestosterone and stanozolol. COMMENT: A myocardial infarct without vascular lesions is rare. To our knowledge, its association with AAS use, bodybuilding, or both lacks any evidence of a cause-effect relationship. The histologic findings in our 2 cases and in the few others reported in medical literature are nonspecific and do not prove the cardiac toxicity of AAS. A better understanding of AAS action on the neurogenic control of the cardiac function in relation to regional myocardial contraction and vascular regulation is required.     

Behavioural anxiolytic effects of low-dose anabolic androgenic steroid treatment in rats.

The use of anabolic androgenic steroids (AAS) in supratherapeutic doses has been associated with aggressive behaviour as well as with severe affective and psychotic symptoms. These symptoms usually follow a chronic exposure for several months. However, AAS also may have milder effects with hypomania-like features such as an increase in confidence, energy and self-esteem. We have studied the short-term effects on male rat behaviour in a modified open-field test of the AAS Metenolon administered three times at a low dose (0.01 mg/kg/week x 3). The control rats showed indications of increased timidity and aversive learning following retesting, a reaction that was absent in the AAS-treated rats. The AAS-treated rats showed less fear or anticipatory anxiety compared to control animals. Furthermore, the suppressed marking behaviour and altered morphological allometric relationships were compatible with a modified social and sexual competence in the AAS treated rats.     

Cardiac hypertrophy in deceased users of anabolic androgenic steroids: an investigation of autopsy findings

BackgroundThe use of anabolic androgenic steroids (AASs) has been associated with hypertrophy of the left cardiac ventricle (LVH) as diagnosed by echocardiography. Case reports suggest that AAS-related LVH may lead to sudden death. We performed an investigation of the gross cardiac pathological findings in deceased male AAS users in order to further elucidate the proposed role of AAS in cardiac hypertrophy.MethodsEighty-seven deceased males who tested positive for AAS at autopsy and 173 age-adjusted control deceased males without suspected AAS use were studied for cardiac hypertrophy. The AAS-positive subjects had been examined at any of the six departments of forensic medicine in Sweden during the period from 1989 to 2009. Data were assessed employing multivariate analyses controlling for body weight, height, age, bleeding after trauma, and the impact of weight training.ResultsThe analysis of the logarithm of heart mass by multivariate statistics implied that strong correlations existed between body mass and heart mass (P<.00001), height and heart mass (P<.02), age and heart mass (P<.00001), and trauma (bleeding) and heart mass (P=.00001). After controlling for these factors, a significantly higher heart mass (P=.0001) was found among the AAS-positive males.ConclusionOur findings suggest that use of AAS may lead to cardiac hypertrophy with a direct cardiotropic effect.     

改良阿氏评分结合血清C反应蛋白检测对儿童急性阑尾炎的临床应用价值

目的 探讨改良阿氏评分结合血清C反应蛋白(CRP)检测对儿童急性阑尾炎(acute appendicitis,AAS)的临床应用价值.方法 回顾性分析2015年11月至2016年11月期间我院儿科就诊的78例急性阑尾炎患儿为研究对象,单纯性AAS组32例,化脓性AAS组28例,穿孔性AAS组18例,选取同期体检的正常儿童10例为对照组,采用改良阿氏(Alvarado)评分结合血清CRP检测为受试患儿和正常对照组进行全面评估.结果 手术前单纯性AAS组、化脓性AAS组、穿孔性AAS组CRP参数水平依次上升,且显著高于对照组,组间比较差异有统计学意义(P＜0.05);单纯性AAS组、化脓性AAS组、穿孔性AAS组术后CRP参数均较术前明显下降(P＜0.05),然而依然高于对照组(P＜0.05).与单纯性AAS组、化脓性AAS组比较,穿孔性AAS组患儿手术前Alvarado评分、血清CRP阳性率及二者均阳性的百分比均明显提高(P＜0.05);化脓性AAS组的血清CRP阳性率与二者均阳性率明显高于单纯性AAS组(P＜0.05).结论 血清CRP检测有助于儿童AAS病情诊断、病理分型以及病情程度,改良Alvarado评分联合CRP对诊断AAS具有良好的互补性,能有效提高AAS术前诊断准确性,对临床科学治疗有指导作用,值得临床推广.     

Anabolic steroids induce region- and subunit-specific rapid modulation of GABA(A) receptor-mediated currents in the rat forebrain

Anabolic-androgenic steroids (AAS) have become significant drugs of abuse in recent years with the highest increase reported in adolescent girls. In spite of the increased use of AAS, the CNS effects of these steroids are poorly understood. We report that in prepubertal female rats, three commonly abused AAS, 17alpha-methyltestosterone, stanozolol, and nandrolone, induced rapid and reversible modulation of GABAergic currents in neurons of two brain regions known to be critical for the expression of reproductive behaviors: the ventromedial nucleus of the hypothalamus (VMN) and the medial preoptic area (mPOA). All three AAS significantly enhanced peak synaptic current amplitudes and prolonged synaptic current decays in neurons of the VMN. Conversely all three AAS significantly diminished peak current amplitudes of synaptic currents from neurons of the mPOA. The endogenous neuroactive steroids, 3alpha-hydroxy-5alpha-pregnan-20-one and 5alpha-androstane-3alpha,17beta-diol, potentiated currents in the VMN as did the AAS. In contrast to the negative modulation induced by AAS in the mPOA, the endogenous steroids potentiated responses in this region. To determine the concentration response relationships, modulation by the AAS, 17alpha-methyltestosterone (17alpha-meT), was assessed for currents evoked by ultrafast perfusion of brief pulses of GABA to acutely isolated neurons. Half-maximal effects on currents elicited by 1 mM GABA were elicited by submicromolar concentrations of AAS for neurons from both brain regions. In addition, the efficacy of 10(-5) to 10(-2) M GABA was significantly increased by 1 microM 17alpha-meT. Previous studies have demonstrated a striking dichotomy in receptor composition between the VMN and the mPOA with regard to gamma subunit expression. To determine if the preferential expression of gamma(2) subunit-containing receptors in the VMN and of gamma(1) subunit-containing receptors in the mPOA could account for the region-specific effects of AAS in the two regions, responses elicited by ultrafast perfusion of GABA to human embryonic kidney 293 cells transfected with alpha(2), beta(3), and gamma(2) or alpha(2), beta(3), and gamma(1) subunit cDNAs were analyzed. As with native VMN neurons, positive modulation of GABA responses was elicited for alpha(2)beta(3)gamma(2) recombinant receptors, while negative modulation was induced at alpha(2)beta(3)gamma(1) receptors as in the mPOA. Our data demonstrate that AAS in doses believed to occur in steroid abusers can induce significant modulation of GABAergic transmission in brain regions essential for neuroendocrine function. In addition, the effects of these steroids can vary significantly between brain regions in a manner that appears to depend on the subunit composition of GABA(A) receptors expressed.     

Reinforcing aspects of androgens

Are androgens reinforcing? Androgenic-anabolic steroids (AAS) are drugs of abuse. They are taken in large quantities by athletes and others to increase performance, often with negative long-term health consequences. As a result, in 1991, testosterone was declared a controlled substance. Recently, Brower [K.J. Brower, Anabolic steroid abuse and dependence. Curr. Psychiatry Rep. 4 (2002) 377-387.] proposed a two-stage model of AAS dependence. Users initiate steroid use for their anabolic effects on muscle growth. With continued exposure, dependence on the psychoactive effects of AAS develops. However, it is difficult in humans to separate direct psychoactive effects of AAS from the user's psychological dependence on the anabolic effects of AAS. Thus, studies in laboratory animals are useful to explore androgen reinforcement. Testosterone induces a conditioned place preference in rats and mice, and is voluntarily consumed through oral, intravenous, and intracerebroventricular self-administration in hamsters. Active, gonad-intact male and female hamsters will deliver 1 microg/microl testosterone into the lateral ventricles. Indeed, some individuals self-administer testosterone intracerebroventricularly to the point of death. Male rats develop a conditioned place preference to testosterone injections into the nucleus accumbens, an effect blocked by dopamine receptor antagonists. These data suggest that androgen reinforcement is mediated by the brain. Moreover, testosterone appears to act through the mesolimbic dopamine system, a common substrate for drugs of abuse. Nonetheless, androgen reinforcement is not comparable to that of cocaine or heroin. Instead, testosterone resembles other mild reinforcers, such as caffeine, nicotine, or benzodiazepines. The potential for androgen addiction remains to be determined.     

急性主动脉综合征的诊治

急性主动脉综合征包括一类严重的、危及生命的主动脉疾病,包括急性主动脉夹层(aortic dissection,AD)、壁内血肿(intramural haematoma,IMH)、主动脉穿透性溃疡(penetrating aortic ulcer,pAu),其中最常见的是主动脉夹层,其次为IMH、主动脉穿透性溃疡.先天性血管缺陷、遗传综合征和非遗传变异性综合征均是急性主动脉综合征的易患因素,可用CT、超声心动图、MRI等影像学方式来确诊.急性主动脉综合征的首要处理是控制血压以减少主动脉壁压力,其诊治往往需要一个多学科专家小组来评估并决定患者的治疗决策.急性主动脉综合征的最佳治疗方案仍然是一项具有挑战性的临床难题,需要进一步的研究来评价每种治疗方案的适用范围,制定以患者为本的精准治疗方案.     

Bibliometric and Altmetric Analysis of Retracted Articles on COVID-19

BackgroundWith greater use of social media platforms for promotions of research articles, retracted articles tend to receive approximately the same attention. We systematically analyzed retracted articles from retractionwatch.com to look at the Altmetric Attention Scores (AAS) garnered over a period of time in order to highlight the role of social media and other platforms in advertising retracted articles and its effect on the spread of misinformation.MethodsRetractionwatch.com was searched for coronavirus disease 2019 related retracted papers on November 6th, 2021. Articles were excluded based on lack of digital object identifier (DOI), if they were preprint articles, absent AAS, and incomplete AAS of pre retraction, post retraction, or both scores.ResultsA total of 196 articles were found on the Retraction Watch website of which 189 were retracted papers and 7 were expression of concern (EOC). We then identified 175 articles after excluding those that did not have a DOI and 30 preprint articles were also excluded giving 145 articles. Further exclusion of articles with absent AAS and incomplete AAS resulted in a total of 22 articles.ConclusionRetracted articles receive significant online attention. Twitter and Mendeley were the most popular medium for publicizing retracted articles, therefore more focus should be given by journals and their Twitter accounts to discredit all their retracted articles. Preprints should be reconsidered as a whole by journals due to the huge risk they carry in disseminating false information.     

The Amsterdam Alexithymia Scale: its psychometric values and correlations with other personality traits.

BACKGROUND: This article describes the construction and validation of the Amsterdam Alexithymia Scale (AAS) and explores some of the nomological net of alexithymia. METHODS: Four correlational studies are presented. The internal structure of the AAS is explored by factor analyses on items. Correlations of the AAS with sex and (Guilford) intellectual abilities are established. Mean scores of three different professional groups are compared. Correlations between the AAS and several clinical and personality scales are determined. Students served as subjects in all studies (347相似文献   

Developmental and withdrawal effects of adolescent AAS exposure on the glutamatergic system in hamsters

In the Syrian hamster (Mesocricetus auratus) glutamate activity has been implicated in the modulation of adolescent anabolic-androgenic steroid (AAS)-induced aggression. The current study investigated the time course of adolescent AAS-induced neurodevelopmental and withdrawal effects on the glutamatergic system and examined whether these changes paralleled those of adolescent AAS-induced aggression. Glutamate activity in brain areas comprising the aggression circuit in hamsters and aggression levels were examined following 1, 2, 3, and 4 weeks of AAS treatment or 1, 2, 3, and 4 weeks following the cessation of AAS exposure. In these studies glutamate activity was examined using vesicular glutamate transporter 2 (VGLUT2). The onset of aggression was observed following 2 weeks exposure to AAS and continued to increase showing maximal aggression levels after 4 weeks of AAS treatment. This aggressive phenotype was detected after 2 weeks of withdrawal from AAS. The time-course of AAS-induced changes in latero-anterior hypothalamus (LAH)-VGLUT2 closely paralleled increases in aggression. Increases in LAH-VGLUT2 were first detected in animals exposed to AAS for 2 weeks and were maintained up to 3 weeks following the cessation of AAS treatment. AAS treatment also produced developmental and long-term alterations in VGLUT2 expression within other aggression areas. However, AAS-induced changes in glutamate activity within these regions did not coincide with changes in aggression. Together, these data indicate that adolescent AAS treatment leads to alterations in the glutamatergic system in brain areas implicated in aggression control, yet only alterations in LAH-glutamate parallel the time course of AAS-induced changes in the aggressive phenotype.     

Prolonged alterations in the serotonin neural system following the cessation of adolescent anabolic-androgenic steroid exposure in hamsters (Mesocricetus auratus)

In hamsters (Mesocricetus auratus), anabolic-androgenic steroid (AAS) exposure during adolescence facilitates offensive aggression that is modulated, in part, by serotonin (5-HT) signaling and development and by signaling and expression of 5-HT1B receptors. To examine whether these effects are persistent or reversible, the authors administered AAS to hamsters, then examined them for aggression at 1, 4, 11, 18, or 25 days following cessation of AAS treatment. Then, 1 day later, hamsters were killed by transcardial perfusion and examined for 5-HT afferents to and 5-HT1B receptor-containing neuronal puncta and somata in areas of the brain altered by AAS, namely, the anterior hypothalamus, ventrolateral hypothalamus, and medial amygdala. Although aggression resulting from AAS exposure returned to control, nonaggressive levels by 18 days following cessation of AAS treatment, alterations in 5-HT afferent innervation and 5-HT1B receptor localization were observed throughout the extended time period examined. These data suggest that adolescent AAS exposure may have long-term, irreversible effects on 5-HT neural systems and that return to nonaggressive behavioral phenotypes following adolescent AAS exposure may not be a function of plasticity in central 5-HT systems.     

Alterations in anterior hypothalamic vasopressin, but not serotonin, correlate with the temporal onset of aggressive behavior during adolescent anabolic-androgenic steroid exposure in hamsters (Mesocricetus auratus)

In hamsters (Mesocricetus auratus), anabolic-androgenic steroid (AAS) exposure during adolescence facilitates offensive aggression that is correlated with the enhanced development of the arginine vasopressin (AVP) neural system and reduced development of the serotonin (5-HT) neural system in the anterior hypothalamus (AH). This study examined the temporal onset of these effects by measuring aggression and AH AVP and 5-HT during progressively shorter periods of AAS exposure during adolescent development. The authors tested adolescent hamsters that received AAS for 3, 7, 14, or 28 days for offensive aggression and then examined the hamsters for AVP/5-HT afferent innervation to the AH using immunohistochemistry. While reductions in AH 5-HT afferent innervation were detectable by 7 days of AAS exposure, no concomitant increases in offensive aggression were observed compared to oil-treated littermates. In contrast, by Day 14 of AAS treatment, AH AVP and offensive aggression were significantly higher than oil-treated controls. These data indicate that relatively short-term adolescent AAS exposure alters aggression and AH 5-HT and AVP development, yet only alterations in AH AVP development correlate with temporal onset of the aggressive behavioral phenotype during adolescent AAS exposure.