Biological Psychiatry Laboratory, McLean Hospital, Belmont, MA, USA.
Drug Alcohol Depend. 2010 Jun 1;109(1-3):6-13. doi: 10.1016/j.drugalcdep.2010.01.011. Epub 2010 Feb 25.
Currently, few users of anabolic-androgenic steroids (AAS) seek substance abuse treatment. But this picture may soon change substantially, because illicit AAS use did not become widespread until the 1980s, and consequently the older members of this AAS-using population - those who initiated AAS as youths in the 1980s - are only now reaching middle age. Members of this group, especially those who have developed AAS dependence, may therefore be entering the age of risk for cardiac and psychoneuroendocrine complications sufficient to motivate them for substance abuse treatment. We suggest that this treatment should address at least three etiologic mechanisms by which AAS dependence might develop. First, individuals with body image disorders such as "muscle dysmorphia" may become dependent on AAS for their anabolic effects; these body image disorders may respond to psychological therapies or pharmacological treatments. Second, AAS suppress the male hypothalamic-pituitary-gonadal axis via their androgenic effects, potentially causing hypogonadism during AAS withdrawal. Men experiencing prolonged dysphoric effects or frank major depression from hypogonadism may desire to resume AAS, thus contributing to AAS dependence. AAS-induced hypogonadism may require treatment with human chorionic gonadotropin or clomiphene to reactivate neuroendocrine function, and may necessitate antidepressant treatments in cases of depression inadequately responsive to endocrine therapies alone. Third, human and animal evidence indicates that AAS also possess hedonic effects, which likely promote dependence via mechanisms shared with classical addictive drugs, especially opioids. Indeed, the opioid antagonist naltrexone blocks AAS dependence in animals. By inference, pharmacological and psychosocial treatments for human opioid dependence might also benefit AAS-dependent individuals.
目前，很少有使用合成代谢雄激素类固醇（AAS）的人寻求药物滥用治疗。但这种情况可能很快会发生重大变化，因为非法使用 AAS 直到 20 世纪 80 年代才广泛出现，因此，使用 AAS 的较年长人群——那些在 80 年代作为年轻人开始使用 AAS 的人——现在才刚刚进入中年。这群人中的成员，特别是那些已经产生 AAS 依赖的人，因此可能会进入出现足以促使他们寻求药物滥用治疗的心脏和心理神经内分泌并发症的风险年龄。我们建议，这种治疗应该至少针对 AAS 依赖可能发展的三个病因机制。首先，患有“肌肉变形障碍”等身体意象障碍的个体可能会因为 AAS 的合成代谢作用而产生依赖；这些身体意象障碍可能对心理治疗或药物治疗有反应。其次，AAS 通过其雄激素作用抑制男性下丘脑-垂体-性腺轴，可能导致 AAS 戒断期间的性腺功能减退。因性腺功能减退而经历长期不愉快或明显重度抑郁的男性可能希望恢复使用 AAS，从而导致 AAS 依赖。AAS 诱导的性腺功能减退可能需要使用人绒毛膜促性腺激素或克罗米酚来重新激活神经内分泌功能，并且在仅对内分泌治疗反应不足的情况下可能需要抗抑郁治疗。第三，人和动物的证据表明，AAS 还具有愉悦效应，这可能通过与经典成瘾药物（尤其是阿片类药物）共享的机制促进依赖。事实上，阿片受体拮抗剂纳曲酮可以阻断动物的 AAS 依赖。推断起来，用于治疗人类阿片类药物依赖的药理学和心理社会治疗也可能对 AAS 依赖的个体有益。
