Treatment of anabolic-androgenic steroid dependence: Emerging evidence and its implications

Abstract

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.

Figure 1

A proposed theoretical model showing three hypothesized mechanisms by which anabolic-androgenic steroid (AAS) dependence may develop. Note that hypothesized predisposing factors are not assumed to be exclusively premorbid traits; as discussed in the text, evidence suggests that the association between these factors and AAS dependence may well be bidirectional in each case, in that AAS use may further exacerbate a premorbid trait. For example, the “impulsive delay-discounting risk-taking endophenotype” likely predisposes to AAS use as well as to conduct disorder and other forms of substance abuse. However, evidence suggests that AAS exposure may exacerbate impulsive and risk-taking symptoms by further increasing sensitivity to reward and decreasing sensitivity for punishment. These hypothesized bidirectional mechanisms are not shown in the figure for reasons of clarity.