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 limitedindeed, 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 [8,36,122129]. 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]. However, 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 associated strongly 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 (G. Kanayama, J. I. Hudson & H. G. Pope 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2009, unpublished data).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
[65,130132]. 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 [135137]; and deficits in decisionmaking, as illustrated by performance on gambling tasks
and other measures of risk-taking [135,138140]. These
pb]deficits are also associated with antisocial or psychopathic traits [/b][141144], including conduct disorder
[145147]. 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 [121,148155]. These features may, collectively,
mark an endophenotype [156] that plays a causal role in
the development of substance dependence [135]. 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
just to addon, here's a dope piece from an article I read a while back:
on the inside.
