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In the United States, most prescription drugs with abuse potential are classed as Schedule II, III or IV substances under the jurisdiction of the Drug Enforcement Administration (120). AAS are presently classed in Schedule III; interestingly, they represent the only class of substances in Schedules II or III that is not already specifically recognized in DSM-IV as causing a dependence syndrome (118). Unlike most other scheduled drugs, however, AAS are legally available over the counter in many countries, and they can easily be ordered over the Internet from overseas, making enforcement and interdiction difficult in countries where AAS are illegal (121). What causes AAS dependence? In conclusion, why do some 30% of AAS users progress from more benign casual AAS use to more chronic and malignant AAS dependence, while 70% do not? Unfortunately, as discussed above, current knowledge of human AAS dependence remains limited ‘ indeed, arguably more limited than for any other major form of substance dependence. However, several hypotheses deserve consideration. First, the progression to AAS dependence might be catalyzed by body image disorders such as “muscle dysmorphia” (17) ‘ a form of body dysmorphic disorder, sometimes called “reverse anorexia nervosa,” characterized by preoccupations that one does not look sufficiently muscular (8, 36, 122’129). Individuals with muscle dysmorphia may develop a maladaptive pattern of chronic AAS use because, paradoxically, they often become increasingly dissatisfied with their muscularity despite growing bigger on AAS (69, 123). But this hypothesis remains uncertain. In an analysis of preliminary data from an ongoing study of AAS users conducted by three of the present authors (see (8)), it appears that adolescent body image disorder is strongly associated with initiation of AAS use. However, among AAS users, those who progressed to AAS dependence did not show a greater level of body image disturbance than those who did not. In other words, concerns about muscularity may bring an individual to the threshold of initially using AAS, but beyond this effect, these concerns may not determine whether that individual progresses onward to AAS dependence (Kanayama G, Hudson JI, Pope HG Jr, 2009, unpublished data). A second possible hypothesis is that individuals who progress to AAS dependence are more biologically vulnerable to the dysphoric effects of AAS withdrawal. As noted, AAS produce a characteristic withdrawal syndrome, with both affective and hypogonadal symptoms (65, 130’132). Individuals with more severe withdrawal symptoms after initial cycles of AAS use might become increasingly prone to resume AAS to prevent these symptoms. As implied above, this possible biological vulnerability might be related to the HPT axis, to opioidergic pathways, or to other neurotransmitter mechanisms. A third possible hypothesis is suggested by the apparent overlap of AAS dependence with other forms of substance dependence and with conduct disorder. An evolving neuropsychological literature has shown that individuals with many other forms of substance dependence exhibit a cluster of cognitive attributes that might be summarized as ‘risk-taking/decision-making deficits,’ such as elevated rates of delay discounting (133, 134); increased impulsivity (135’137); and deficits in decision-making, as illustrated by performance on gambling tasks and other measures of risk-taking (135, 138’140). These deficits are also associated with antisocial or ‘psychopathic’ traits (141’144), including conduct disorder (145’147). Conduct disorder in turn appears to be associated with AAS dependence (8), and other studies have documented criminality and so-called Cluster B personality traits, including antisocial personality, among AAS users (121, 148’155). These features may collectively mark an endophenotype (156) that plays a causal role in the development of substance dependence (135), all steroids name list. With AAS, the direction of causality might well go both ways: in individuals with these hypothesized underlying deficits, use of testosterone and presumably other AAS may shift the balance even further towards an increased sensitivity for reward and decreased sensitivity for threat or punishment, as suggested by both animal (157, 158) and human studies (159, 160). No studies, to our knowledge, have assessed the possible role of such deficits in individuals with AAS dependence, but this possibility would seem to deserve further investigation. A growing literature of human and animal studies suggests that AAS dependence is a valid diagnostic entity, often associated with conduct disorder and other forms of substance abuse.
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