Detained adolescents are at high risk for developing APD as they enter emerging adulthood. Nearly one-fifth developed APD, rates substantially higher than those in the general population (1%–4%) (Grant et al., 2004
; Lyons & Jerskey, 2002
; Robins et al., 1991
). Detained youth, similar to youth receiving mental health treatment (Loeber et al., 2002
; Robins, 1966
), demonstrate continuity of behavioral disorder from CD in adolescence to APD in emerging adulthood. CD was significantly associated with M-APD, and more than three quarters of the participants who developed M-APD reported a history of CD prior to age 15.
The hierarchical development model of APD proposes that youth with the most advanced and diversified symptoms of CD (e.g., rape, assault with a weapon, robbery) are at the greatest risk for developing APD (Loeber et al., 2003
). Findings from this and others studies (Lahey et al., 2005
; Satterfield & Schell, 1997
), however, suggest the accumulation of covert
symptoms increase the odds of developing APD. These findings are consistent with social interaction and coercive theories of delinquency, which propose that growth in covert antisocial behavior may mediate the progression from early overt antisocial behaviors to chronic adult antisocial behavior (Patterson & Yoerger, 1999
). Early overt antisocial behavior may lead to increased association with deviant peers and subsequent training and reinforcement in covert antisocial behavior (Patterson & Yoerger, 1999
). In addition, as children age into early adolescence, overt antisocial behavior is increasingly unacceptable to adults and peers, and either extinguishes or becomes more covert (Snyder, Reid, & Patterson, 2003
Post-hoc analyses found that the odds of developing M-APD significantly increased among youth with 5 or more symptoms of CD, regardless of the type of symptom. Taken together, these findings suggest that among detained youth, growth in covert CD symptoms may increase risk for APD, but only up to a specific number of symptoms. Once detained youth reach this threshold, the type of CD symptom may matter less than the sheer number of symptoms.
Despite the significant associations between CD or number of CD symptoms and M-APD, the utility of CD or number of CD symptoms for identifying which detained youth will develop M-APD is limited. Although Lahey et al. (2005)
found that 65% of low-income, clinic-referred youth with CD developed M-APD by age 18 or 19 years, only one third of detained youth with CD developed M-APD. Similar to general population youth, most detained youth appear to be characterized by Moffitt’s adolescent-limited antisocial pathway (Moffitt, 1993
), which proposes that youth engage in antisocial behavior for social and affiliative reasons during adolescence and desist from antisocial behavior in emerging adulthood. Our findings should not be interpreted, however, as suggesting that most detained youth desist from unlawful behavior. Even in the general population, youth characterized by adolescent limited antisocial behavior may continue to engage in unlawful behavior into young adulthood (Moffitt et al., 2002
). Our findings suggest instead that only a subset of detained youth with CD develop personality characteristics that facilitates the persistent violation of societal rules and norms (Loeber et al., 2003
In contrast to prior findings (Lahey et al., 2005
), the diagnosis of CD did not account for the association between ADHD and M-APD. This finding may reflect problems with the self-report measurement of ADHD in this study; however, it also may reflect how poorly CD predicts M-APD among juvenile detainees. Indeed, post hoc analyses showed that 5 or more symptoms of CD, a more robust predictor of M-APD in this sample, accounted for the association between ADHD and M-APD. This finding provides partial support for the theory that ADHD indirectly contributes to the development of APD through the development of CD symptoms in adolescence (Lahey et al., 2005
; Loeber et al., 2003
Comorbid ADHD and CD did not significantly increase the odds of developing M-APD after accounting for CD. Lahey et al. (2005)
explained similar findings in a sample of youth in treatment by noting that nearly all youth with CD had ADHD; however, fewer than half of detained youth with CD had comorbid ADHD. In contrast to Lynam (1996)
, these findings indicate that ADHD fails to contribute to the development of APD among detained youth.
The hierarchical developmental model proposes that a subset of children demonstrate continuity of antisocial behavior from ODD in childhood, to CD in adolescence, and to APD in young adulthood. The finding that ODD was not significantly associated with APD, even after excluding the contribution of CD, was unexpected, but not necessarily contradictory to the hierarchical developmental model. In contrast to prior research, ODD in this sample was assessed during adolescence rather than in childhood (Lahey et al., 2005
). ODD in childhood may contribute to later antisocial behavior in detained youth; however, these findings suggest covert antisocial symptoms in adolescence appear to contribute far more to the persistence of antisocial behavior than angry, aggressive, or oppositional behavior in adolescence (Loeber, Green, Lahey, Frick, & McBurnett, 2000
; Snyder et al., 2003
Heterotypic continuity of disorder was also found across categories of mental disorder. Even after accounting for CD symptoms or diagnosis, dysthymia, alcohol use disorder, and GAD were significantly associated with M-APD. Findings suggest that the relationship between these mental disorders and M-APD is complex; depression and alcohol use disorder increase the risk of developing M-APD, while anxiety decreases this risk.
Depressive symptoms in adolescence may manifest externally through antisocial behavior in emerging adulthood (Puig-Antich0, 1982
). Chronic symptoms of hopelessness, irritability, low self-esteem, and pessimism may contribute to a pattern of argumentativeness and interpersonal conflict (Kasen et al., 2001
). Impaired prosocial decision-making and coping skills associated with chronic depressive symptoms may further increase the risk for engaging in irresponsible behavior (Kasen et al., 2001
). In contrast to the greater level of impairment associated with acute depression, youth with more chronic depression may continue to associate with delinquent peers. They may be more willing than youth without depression to take risks and engage in self-destructive or reckless behavior than their peers, similar to the phenomenon of victim-precipitated suicide, or “suicide-by-cop” (Lindsay & Lester, 2004
In contrast to depression, anxiety disorders may protect against the development of APD by increasing fearfulness and behavioral inhibition (Frick et al., 1999
; Gray, 1982
). Although these traits were not examined in this study, the excessive worrying associated with GAD is conceptually inconsistent with the fearlessness and behavioral disinhibition found among the most severely antisocial adolescents and adults (Frick et al., 1999
). Anxiety may also increase social isolation and thereby decrease deviant peer association and opportunities for engagement in antisocial behavior (Farrington, Gallagher, Morley, St. Ledger, & West, 1988
; Moffitt et al., 2002
Alcohol use disorder was the only substance use disorder to significantly increase the odds of developing M-APD among detained youth. Loeber et al. (2002)
found an association between marijuana use – but not alcohol use – and APD in their sample of youth receiving mental health treatment. In contrast to youth receiving treatment, marijuana use and disorder may not represent an aberrant behavior among juvenile detainees; nearly all juvenile detainees have used marijuana at least once, more then three-quarters currently use marijuana (McClelland, Teplin, & Abram, 2004
), and nearly half have a marijuana use disorder (Teplin et al., 2002
). In contrast, alcohol use disorder is half as common as marijuana use disorder among juvenile detainees (Teplin et al., 2002
), and alcohol intoxication may increase volatility and impulsivity.
Significantly more males developed APD than females, as found in prior studies (Fazel & Danesh, 2002
; Kim-Cohen et al., 2003
; Lyons & Jerskey, 2002
). Gender also moderated some findings; dysthymia and GAD were significantly associated with APD for males but not females, and positive predictive values were substantially lower for females than males. Although the lower prevalence of APD among females may partially account for the weaker prediction of APD by mental disorders, unobserved factors are likely more predictive of APD for females. These findings suggest that future research consider a female-specific pathway in understanding the development of APD (Silverthorn & Frick, 1999
The lack of racial/ethnic differences in the development of APD is consistent with findings among youth receiving mental health treatment. Although Lahey et al., (2005)
found African Americans were more likely to develop APD than non-Hispanic Whites, this difference was accounted for by socioeconomic status (Lahey et al., 2005
). Most of our participants, regardless of race/ethnicity, were poor; approximately 10% earned annual incomes above the poverty level. A greater number of non-Hispanic Whites had risk factors for APD at baseline; however, they did not have an increased risk for APD at follow-up. Further research is necessary to understand the mediators of racial/ethnic differences and to specifically understand why greater risk for APD in adolescence among non-Hispanic whites does not result in a greater likelihood of developing APD in emerging adulthood.
It is important to consider these findings in the context of the limitations of this study. Our findings may apply only to youth from large urban areas who are detained. We examined youth only twice, three years apart, limiting the detection of mental disorders and APD. Many youth with CD experience brief periods of subthreshold symptoms and may not meet full criteria for the disorder at a given assessment (Lahey et al., 1995
). Consequently, we may have underestimated
the true continuity of antisocial behavior. Alternatively, we may have overestimated
the prevalence of APD because our assessment of APD occurred during an age at which APD diagnoses in the community are the most prevalent (Robins et al., 1991
This study is subject to the limitations associated with our use of the self-report versions of the DISC 2.3 and DIS-IV; unfortunately, obtaining collateral informants for most detained youth was not feasible (Teplin et al., 2002
). Because reliance on self-report is especially problematic for ADHD (Jensen et al., 1999
), our findings on ADHD must be considered preliminary at best. Assessing disorders in a correctional facility may alter the validity or reliability of the DISC 2.3 or DIS-IV. This study also did not examine other variables that may be important markers of APD, such as non-diagnostic psychosocial factors (Farrington, 2000
), or callous/unemotional or narcissistic traits (Frick et al., 1999
; Loeber et al., 2002
). The diagnosis of APD also is not synonymous with engagement in illegal behavior or other outcomes. Finally, the apparent association of 5 or more symptoms of CD with M-APD found in data-derived, post hoc analyses may be specific to this sample and needs to be confirmed by other studies.
Despite the limitations, the findings have clinical implications for the assessment and treatment of antisocial behavior among detained youth and for future research. The prevalence of APD in this population underscores the need for early intervention for youth at high risk for persistent antisocial behavior. Clinicians, researchers, and policy makers must collaborate to identify promising strategies to reduce the likelihood that detained youth will develop APD. Programs to prevent the initial onset of conduct problems are key to preventing persistent antisocial behavior (Loeber et al., 2002
); however, it is also important to alter the course of antisocial behavior among those youth already displaying conduct problems. Intervention studies need to examine if the symptoms of mental disorder, such as anxiety, depression, or alcohol use, are useful targets for prevention or intervention with detained youth.
Prevention and intervention programs targeted at the youth most at risk for developing APD make the best use of limited community and correctional resources; however, this requires accurate identification of youth at risk for APD. Unfortunately, while CD may adequately predict APD among youth in the general population (Lewinsohn, Rohde, & Farrington, 2000
) and treatment samples (Lahey et al., 2005
), findings from this study suggest that CD is a poor screener for identifying risk for APD among detained youth. Furthermore, the specificity of CD as a predictor, even in the general population, is not clear; a recent study found early conduct problems preceded nearly every mental disorder in adulthood (Kim-Cohen et al., 2003
Exploratory findings suggest that the predictive accuracy of individual
prognoses may be improved by examining multiple problem areas (e.g., dysthymia comorbid with 5 or more symptoms of CD). Reliance on combinations of disorders with a low prevalence in the population, however, will fail to identify the majority of detained youth who eventually develop APD. A similar problem arises when specific types of antisocial behavior are used for screening, such as psychopathy. Screeners for psychopathy may only identify a subset of youth at risk for APD, such as those at risk for future violent behavior (Gretton, Hare, & Catchpole, 2004
). Furthermore, the use of psychopathy measures as a clinical tool remains controversial (Seagrave & Grisso, 2002
). Better screening measures are needed to identify youth at risk for developing APD among youth already identified as delinquent by the juvenile justice system.
Future studies need to disentangle the pathways and mechanisms by which mental disorders and other psychosocial variables (e.g., callous/unemotional traits, parenting practices, peer influences) contribute to the development of APD among detained youth. Mental disorders may not directly influence the development of APD; instead, the associations may be due to correlations with underlying factors (McGue & Iacono, 2005
). For example, longitudinal studies have found a high degree of concurrent and prospective comorbidity among CD, depression, and anxiety from childhood to adolescence (Lahey, Loeber, Burke, Rathouz, & McBurnett, 2002
; Salekin, Leistico, Neumann, DiCicco, & Duros, 2004
), suggesting the possibility of underlying psychological processes, such as negative emotionality (Lahey et al., 2002
), or an interaction of neurobehavioral processes (Depue & Lenzenweger, 2006
It is unlikely that future research will be able to identify mental or other psychosocial factors that will prove to be adequate predictors of APD for all
detained youth. Because of the heterogeneity of detained youth and adults with APD (Loeber et al., 2003
), aggregated analyses likely obfuscate factors that may predict the development of APD in specific subgroups. Consequently, future studies should assess if and how the development of APD varies for specific subgroups of antisocial youth. Longitudinal studies should take advantage of analytic techniques that examine heterogeneity within samples and identify predictive factors that are specific to developmental trajectories of antisocial behavior.