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Original Article |

Childhood and Adolescent Psychiatric Disorders as Predictors of Young Adult Disorders FREE

William E. Copeland, PhD; Lilly Shanahan, PhD; E. Jane Costello, PhD; Adrian Angold, MRCPsych
[+] Author Affiliations

Author Affiliations: Duke University Medical Center, Durham (Drs Copeland, Costello, and Angold), and University of North Carolina at Greensboro (Dr Shanahan).


Arch Gen Psychiatry. 2009;66(7):764-772. doi:10.1001/archgenpsychiatry.2009.85.
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Context  Most adults with a psychiatric disorder first met diagnostic criteria during childhood and/or adolescence, yet specific homotypic and heterotypic patterns of prediction have not been firmly established.

Objective  To establish which childhood and adolescent psychiatric disorders predict particular young adult disorders when accounting for comorbidities, disaggregating similar disorders, and examining childhood and adolescent predictors separately.

Design  Eleven waves of data from the prospective population-based Great Smoky Mountains Study (N = 1420) were used.

Setting  The Great Smoky Mountains Study is a longitudinal study of the development of psychiatric disorder and need for mental health services in rural and urban youth. A representative sample of children was recruited from 11 counties in western North Carolina.

Participants  Children in the community aged 9 to 16, 19, and 21 years.

Main Outcome Measures  Common psychiatric disorders were assessed in childhood (ages 9-12 years) and adolescence (ages 13-16 years) with the Child and Adolescent Psychiatric Assessment and in young adulthood (ages 19 and 21 years) with the Young Adult Psychiatric Assessment.

Results  Adolescent depression significantly predicted young adult depression in the bivariate analysis, but this effect was entirely accounted for by comorbidity of adolescent depression with adolescent oppositional defiant disorder, anxiety, and substance disorders in adjusted analyses. Generalized anxiety and depression cross-predicted each other, and oppositional defiant disorder (but not conduct disorder) predicted later anxiety disorders and depression. Evidence of homotypic prediction was supported for substance use disorders, antisocial personality disorder (from conduct disorder), and anxiety disorders, although this effect was primarily accounted for by DSM-III-R overanxious disorder.

Conclusions  Stringent tests of homotypic and heterotypic prediction patterns suggest a more developmentally and diagnostically nuanced picture in comparison with the previous literature. The putative link between adolescent and young adult depression was not supported. Oppositional defiant disorder was singular in being part of the developmental history of a wide range of young adult disorders.

More than three-quarters of young adults with psychiatric disorders first had a diagnosis between the ages of 11 and 18 years,18 indicating that we must consider childhood and adolescent mental illness as a key risk factor for later psychiatric problems. However, there remain important questions about diagnostic prediction from childhood and adolescence to adulthood. Herein, we present new evidence about which childhood and adolescent disorders reliably precede later disorders.

Homotypic prediction refers to a disorder predicting itself over time (eg, earlier depression predicting later depression). This supports the idea that a single disease process expresses itself robustly across developmental contexts. Homotypic prediction has been identified in most studies predicting from childhood to late adolescence913 and from childhood and adolescence to young adulthood.1,2,5,1419 Indeed, prior disorder status is typically the strongest predictor of having that disorder later.

Heterotypic prediction refers to different disorders predicting one another over time (eg, earlier oppositional defiant disorder [ODD] predicting later depression). Such patterns may suggest that the different disorders reflect a general disease process that has specific phenotypic expressions in different developmental contexts. Although typically less common than homotypic prediction, 2 patterns of heterotypic prediction have received consistent support. First, anxiety and depression tend to cross-predict from childhood/adolescence to adulthood (anxiety predicting depression: full support1,3,10,11,20; partial support9,13,16,19; depression predicting anxiety: full support1,3,10,11,20; partial support13,16). Second, childhood/adolescent conduct/oppositional problems tend to precede adult anxiety and depression,1,10,16,2123 but not vice versa1,11,13 (Hofstra et al17 present an exception).

Taken together, homotypic prediction appears to be common across a range of disorders, whereas heterotypic prediction is limited to a few specific pathways, but a number of substantive and methodological issues complicate the interpretation of this work. First, many studies collapse childhood and adolescent disorders to predict adult disorders, despite the fact that important changes in the prevalence of some disorders, such as depression and conduct disorder (CD), occur between childhood and adolescence.2426 Such changes could indicate that disorders at different ages result from different etiologic pathways2730 and so combining across childhood and adolescence could obscure important differences between childhood and adolescent prediction. Also, little attention has been paid to the fact that these developmental pathways may be different for males and females. For example, the prevalence of depression changes at puberty for girls but not for boys.31

Second, most studies collapse multiple, potentially heterogeneous disorders into more general diagnostic groupings. For example, all anxiety disorders tend to be combined into one category, which could mask differences in prediction between individual anxiety disorders. Furthermore, ODD and CD are often combined, despite the fact that they are distinct in factor analytic studies,32,33 in risk factors studies,34 and when tested as predicting later problems.35 Indeed, ODD may be as likely to be linked with emotional disorders as CD.10

Finally, studies of diagnostic predictors of later disorders have typically focused on pairwise associations: one earlier disorder predicting one later disorder. Yet, disorders tend to co-occur, and when comorbidity is not taken into account, pairwise associations may simply represent indirect effects rather than direct associations.36,37 For example, bivariate analyses may suggest that childhood anxiety disorders predict adolescent depression, but this association could be accounted for by comorbidity between childhood anxiety and depression.

Herein, we use Great Smoky Mountains Study (GSMS) data from middle childhood through young adulthood and stringent criteria to examine a broader range of patterns of homotypic and heterotypic prediction from middle childhood and adolescence to young adulthood.

SAMPLE AND PROCEDURES

The GSMS is a longitudinal study of the development of psychiatric disorder and need for mental health services in rural and urban youth.1419 A representative sample of 3 cohorts of children, aged 9, 11, and 13 years at intake, was recruited from 11 counties in western North Carolina. Potential participants were selected from the population of some 20 000 children using a household equal probability, accelerated cohort design.20 The accelerated cohort design means that over several years of data collection each cohort reaches a given age in a different year, thus controlling for cohort effects.21 Youth with behavior problems were oversampled. A screening questionnaire was administered to a parent (usually the mother) of the first-stage sample (n = 3896). The questionnaire consisted mainly of the Externalizing (Behavioral) Problems Scale of the Child Behavior Checklist22 and was administered by telephone or in person. All children scoring higher than a predetermined cut point (the top 25% of the total scores), plus a 1-in-10 random sample of the rest (ie, the remaining 75% of the total scores), were recruited for detailed interviews. Ninety-five percent of families contacted completed the telephone screen.

About 8% of the area residents and the sample were African American, and fewer than 1% were Hispanic. American Indian individuals made up only about 3% of the population of the study area, which is overwhelmingly white, but were oversampled from school records to constitute 25% of the study sample. This was done by using the same screening procedure but recruiting everyone irrespective of screen score. Of the 456 American Indian children identified, 96% were screened, and 81% (n = 350) participated in the study. All subjects were given a weight inversely proportional to their probability of selection so that the results presented are representative of the population from which the sample was drawn. Of all subjects recruited, 80% (n = 1420) agreed to participate.

Table 1 presents the study design and participation rates at each wave. Data were collected on 1 cohort at ages 9 and 10 years, 2 cohorts at ages 11, 12, and 13 years, and all 3 cohorts at ages 14, 15, 16, 19, and 21 years. This article presents data on 8806 parent/child pairs of interviews carried out across the age range 9 through 21 years. Participants were interviewed as closely as possible to their birthday each year. Funding constraints prevented our interviewing the youngest cohort from January 1997 through June 1998.

Table Graphic Jump LocationTable 1. Great Smoky Mountains Study: Data Collection by Cohort

Interviews were completed with the children and their primary caregiver at their home or a convenient location until age 16 years and with the young adults only thereafter. Before the interviews began, interviewees signed informed consent forms approved by the Duke institutional review board. Across waves, an average of 82% of all possible interviews were completed, ranging from 75% to 94% at individual waves.

MEASURES

Psychiatric disorders were assessed using (1) the Child and Adolescent Psychiatric Assessment (CAPA)3840 until age 16 years and (2) the upward extension of the CAPA, the Young Adult Psychiatric Assessment (YAPA)40 at ages 19 and 21 years. Scoring programs for the CAPA and YAPA, written in SAS,41 combined information about the date of onset, duration, and intensity of each symptom to create diagnoses according to the DSM-IV.29 With the exception of attention-deficit/hyperactivity disorder (ADHD), for which only parental reports were counted, a symptom was counted as present if it was reported by either the parent or the child until age 16 years or by the young adult at ages 19 and 21 years, as is standard clinical practice. Two-week test-retest reliability of CAPA diagnoses in children aged 10 to 18 years is comparable with that of other highly structured interviews (κs for individual disorders range from 0.6-1.0).39 To minimize recall bias, the time frame of both interviews for determining the presence of most psychiatric symptoms was the preceding 3 months. A previous publication suggested that there was little evidence of symptom attenuation (lower reported symptom levels in subsequent data waves), cohort differences, or differential dropout in this sample.11

In the current study, disorder status was aggregated across childhood (ie, ages 9-12 years), adolescence (ie, ages 13-16 years), and young adulthood (ie, ages 19-21 years). Childhood and adolescent diagnostic groupings included depression (including major depressive disorder [MDD], dysthymia, and depressive disorder, not otherwise specified), separation anxiety disorder in childhood, generalized anxiety disorder (GAD), CD, ADHD, and ODD. DSM-III-R overanxious disorder (OAD) was also included because we had previously found that it predicted several adolescent disorders when diagnosed in childhood.9 Disorders with a prevalence of less than 1% in a given developmental period were not included in analyses (eg, separation anxiety in adolescence, social phobia, posttraumatic stress disorder). Substance disorders (including those meeting abuse or dependence criteria) were only sufficiently common for inclusion beginning in adolescence. Young adult diagnostic groups included depression (same as childhood and adolescence groups), GAD, panic disorder without agoraphobia, agoraphobia without panic, and antisocial personality disorder (ASPD).

ANALYSES

Weighted logistic regression models were estimated using generalized estimating equations implemented by SAS PROC GENMOD. Sampling weights were inversely proportional to selection probability. Robust variance (sandwich-type) estimates were used to adjust the standard errors of the parameter estimates for the stratified design effects. Therefore, the resulting parameters are representative of the population from which the sample was drawn.

Ideally, all diagnoses from all developmental periods would be combined into a single path-type multivariate analysis. Because such complex models did not converge despite our reasonable sample size, we examined psychiatric status across 2 developmental periods at a time: from adolescence to young adulthood and from childhood to young adulthood. Homotypic and heterotypic patterns were determined by predicting each later disorder (eg, depression in young adulthood) from each earlier disorder in a series of 3 models. In the bivariate, unadjusted model, a prior disorder was the single predictor of the later diagnosis. The unadjusted odds ratios (ORs) resulting from model 1 are reported in Table 2 and Table 3. In the sex differences model, model 2, the prior disorder, sex, and the sex × prior disorder interaction were included (full results are available on request). In the final comorbidity or adjusted model, the prior disorder that corresponded to the outcome variable and all other prior disorders were included. For example, childhood depression and all other childhood disorders were entered to predict young adult depression in the childhood/young adulthood model. The adjusted ORs resulting from the final model are reported in Table 2 and Table 3. Inclusion of comorbid disorders provides a stringent test of homotypic and heterotypic prediction patterns. Where evidence of a sex × disorder interaction was detected, separate results for adjusted models were provided for males and females. Analyses involving childhood were based on 2 GSMS cohorts (n = 1008;<13 years at intake) and those involving adolescence were based on all 3 GSMS cohorts (N = 1420).

Table Graphic Jump LocationTable 2. Young Adult Diagnoses Predicted From Adolescent Diagnosesa
Table Graphic Jump LocationTable 3. Young Adult Diagnoses Predicted From Childhood Diagnosesa

As with any longitudinal study, not all assessments were completed at each data wave. Such missing assessments may affect prediction estimates if individuals with missing observations were more or less likely to have a psychiatric disorder than individuals with complete observations. To test for such effects, each individual's total number of missed assessments adjusted for the total number of expected assessments was predicted by the individual's psychiatric status at his or her first assessment (because all subjects had at least 1 assessment). Initial rates of psychiatric disorder did not predict the likelihood of missing assessments (z = 1.5; P = .23), suggesting no effect of differential dropout. Therefore, observations missing within a given developmental period were excluded from analyses involving that development period. Because subjects were interviewed multiple times within each developmental period, subjects could miss 1 interview and still be included in analyses for that period.

HOMOTYPIC PREDICTORS

Table 2 and Table 3 display the results from unadjusted and adjusted models for each pair of developmental groups (adolescence to young adulthood, childhood to young adulthood). Separate adjusted results are provided for males and females where a significant sex × disorder interaction was detected. Prediction between anxiety disorders, even if not the same disorder, is discussed as homotypic.

Adolescence to Young Adulthood

In unadjusted models, homotypic prediction was found for antisocial personality disorder (from adolescent CD), depression, and substance disorders (Table 2). Both generalized anxiety and panic disorders were predicted from OAD. The apparent association of adolescent depression with young adult depression was completely attenuated in adjusted models, whereas the homotypic prediction of ASPD, GAD, and substance and panic disorders was undiminished. Overanxious disorder predicted later GAD and panic disorders more strongly for males than females.

Because the attenuation of homotypic prediction of depression in the comorbidity-adjusted model was unexpected, possible informant effects were tested by running the adjusted models separately by parent and self-reports. The results were the same regardless of informant (parent report, OR, 0.6; 95% confidence interval [CI], 0.2-2.7; self-report, OR, 1.0; 95% CI, 0.4-3.1). To clarify whether homotypic prediction for CD predicting ASPD was an artifact of the diagnostic criterion for ASPD requiring prior evidence of CD before age 15 years, the adjusted model was rerun using an ASPD diagnosis in which subjects were not required to have displayed prior evidence of CD before age 15 years. Again, CD alone predicted ASPD (OR, 5.2; 95% CI, 1.4-19.1).

Childhood to Young Adulthood

As in the adolescence/young adulthood models, the link between CD and ASPD was also found after adjusting for comorbidity (Table 3). This link remained if the alternative form of the ASPD diagnosis (requiring no prior CD symptoms) was used (OR, 3.2; 95% CI, 1.0-9.6).

There was evidence of prediction between various anxiety disorders in unadjusted models, although only 3 associations were significant after adjustment: OAD predicted panic disorder, separation anxiety disorder predicted agoraphobia without panic disorder, and GAD predicted agoraphobia without panic disorder.

HETEROTYPIC PREDICTORS
Adolescence to Young Adulthood

In adjusted models, heterotypic patterns were found for depression and all anxiety disorders. Specifically, GAD and OAD predicted depression (in males for the depression-OAD link). Adolescent depression also predicted agoraphobia without panic disorder. Adolescent ODD predicted later GAD, panic disorder without agoraphobia (in males only), and depression. Finally, adolescent substance disorders predicted later depression.

Childhood to Young Adulthood

Compared with adolescent/young adulthood models, limited support for heterotypic prediction emerged in the childhood to young adulthood adjusted models: childhood ODD predicted young adult depression and childhood depression predicted panic disorder without agoraphobia and GAD.

A review of previous studies suggested the following conclusions with respect to the continuity of disorders from childhood and adolescence to young adulthood: (1) Homotypic prediction is the norm from childhood/adolescence to young adulthood. (2) Generalized anxiety and depression cross-predict. (3) Childhood/adolescent combined disruptive disorders (ODD and/or CD treated as a single entity) predict adult anxiety and depressive disorders in addition to ASPD. This study provided developmentally differentiated and stringent tests of these patterns by (1) separating childhood from adolescent diagnostic predictors, (2) disaggregating specific anxiety and disruptive disorders, and (3) adjusting for comorbid conditions. Our results indicate that prediction patterns are actually more developmentally and diagnostically nuanced than the previous literature suggests.

In summary, although homotypic patterns were common, the path from adolescent to young adult depression was entirely accounted for by other comorbidities. Of childhood and adolescent anxiety disorders, DSM-III-R OAD was most likely to predict later young adult anxiety disorders. Generalized anxiety and depression cross-predicted, although these effects were not uniform across childhood and adolescence. Finally, a single behavioral disorder, adolescent ODD, preceded anxiety and depressive disorders.

CAVEATS

Before considering these findings in more detail, the following methodological considerations should be kept in mind. First, the GSMS participants lived in a rural area, and the study oversampled American Indian children, with very few African American (8%) and no Latino or Asian American children. Thus, the sample is not representative of the US population. However, comparison of the GSMS with other studies indicates that there are similar rates of cumulative childhood disorders in representative samples from other counties, other regions of the United States, and samples involving higher levels of Hispanic and African American youth.42,43 While the subjects were followed up to 12 years (age 9-21 years), cases will have been missed because subjects may have met criteria for disorders prior to our study, between assessments, or after their last assessment.

Second, some associations of moderate to large magnitude were nonsignificant because of the limited number of youth with the particular disorder. However, studies of homotypic and heterotypic predictors from child to adult psychiatric disorder that deal with a range of disorders are rare because they depend on large, longitudinal community-based samples carefully characterized over many years. We are unaware of any currently existing studies with greater power to address these questions. Finally, our research aim was to determine which childhood and adolescent disorders reliably precede young adult disorders. This did not allow us to examine the chronological order of disorders within a developmental period. For the current analysis, the order of the disorders within a developmental period, however, had no effect on the strength of the association with the young adult outcome.

A terminological note is also in order. We have referred herein to homotypic and heterotypic prediction rather than continuity, despite the latter term's common usage. We believe that typical measurement schedules in prospective studies cannot adequately capture (dis)continuity, because observations of disorders tend to be intermittent (rather than continuous).

HOMOTYPIC PREDICTION

Although homotypic patterns were identified (eg, CD to ASPD and substance-related disorders), homotypic patterns were less common than previously reported by other studies when accounting for comorbidity between disorders. There was no evidence of homotypic prediction for depression and homotypic prediction of young adult anxiety disorders was primarily accounted for by DSM-III-R OAD, rather than by DSM-IV GAD.

In preparation for DSM-IV, Klein and colleagues44 reviewed taxonomic issues related to the DSM-III-R anxiety disorders. Overanxious disorder was the focus of particular attention because it included a group of heterogeneous worries (eg, about the future, academic performance, self-consciousness) and was highly comorbid with other anxiety disorders (particularly GAD). Despite these concerns, it was recommended that it be retained as a childhood anxiety disorder, but with modified criteria to reduce overlap with other disorders. Instead, it was eliminated with the rationale that these children would likely receive a diagnosis of DSM-IV GAD. In a prior study, our group compared the relative predictive validity of childhood OAD as compared with DSM-IV GAD in predicting adolescent disorders. Overanxious disorder not only predicted later anxiety disorders but also predicted adolescent depression and CD. In contrast, DSM-IV GAD only predicted later CD. In this study predicting young adult disorder status, OAD again predicted both anxiety disorders and depression. This is in line with findings from the New York Child Longitudinal Study in which OAD predicted young adult depression, social phobia, and generalized anxiety.3 Together, these findings suggest that the DSM-IV GAD criteria are insufficient for assessing the full range of “generalized anxiety” in children and adolescents and fail to identify anxious children at risk for a range of later disorders. It seems that Klein and colleagues were right to suggest that OAD should have been retained in the DSM-IV. We recommend its rehabilitation in the DSM-V.

The example of depression illustrates the importance of separating childhood from adolescent predictors and controlling for comorbidities. The significant bivariate prediction from adolescent to young adult depression (OR, 3.3) was entirely accounted for by comorbidity of adolescent depression with adolescent ODD, GAD, OAD, and substance disorders (OR for depression reduced to 0.8), whereas there was no direct prediction from childhood depression to young adult depression even in the bivariate models. This suggests that the apparent association between adolescent depression and young adult depression is epiphenomenal, resulting from the direct associations between comorbid adolescent disorders and later depression.

This may appear to be a clear departure from the consensus of previous research,45 but actually it is not. Many studies looking at the adolescence–young adult depression link have used highly selected or clinical samples and/or failed to account for common comorbid disorders.4650 While these studies can demonstrate that adolescent depression precedes young adult depression, they are insufficient, on their own, to provide evidence of direct prediction. Such evidence can only come from community samples that assess for a range of disorders, in addition to depression, at multiple points in both adolescence and young adulthood.

To date, 3 such studies have been published. The first, a community sample of adolescents followed up into young adulthood by Lewinsohn and colleagues, concludes that their results “clearly illustrate a strong pattern of continuity for depression.”5(p61) Their initial analyses demonstrate higher risk of later depression for a group of adolescents with MDD as compared with groups with either no depression or a nonaffective disorder. In this comparison, however, adolescent MDD cases were allowed to have other Axis I nonaffective disorders (and 51.0% did). A more stringent test compared risk for depression between a group with “pure” adolescent depression and a group with comorbid depression and found no difference. This might seem to suggest that even after controlling for comorbidity there is a link from adolescent to young adult depression, but rates of young adult depression are not provided for either of these 2 groups. It is entirely plausible then that the “pure” MDD group could both only be marginally associated (or not associated) with later MDD and, at the same time, not be statistically different from the comorbid MDD group. Without knowledge of the rates of young adult depression in these 2 groups, one cannot draw any conclusions about the role of comorbidity in the adolescent–young adult MDD link.

The second study tested this link in a birth cohort of 1265 children and concluded that there was a “direct and specific” link from adolescent depression to later depression.51 The study design provides a rather stringent test for the outcomes of adolescent depression by accounting for the effects of anxiety disorders, early cigarette smoking, CDs, alcohol abuse, and a range of other putative risk factors. At the same time, the negative outcomes (including depression) are assessed for ages 16 to 21 years and thus overlap both with late adolescence and young adulthood. If there were a rather punctuated shift in depression between adolescence and young adulthood, it would not be detected by this design. But is this likely? In fact, such a striking shift occurs in depression a few years earlier in the pubertal transition from childhood to adolescence,52 so this possibility cannot be rejected a priori. While the pubertal shift is associated with significant biochemical changes, the shift to young adulthood and the associated transition to independent living may be similarly substantial in the social domain.

The final study by Pine and colleagues3 found that the best-fitting multivariable prediction model of young adult depression did not include adolescent depression, after accounting for comorbidities. As with our findings, there was evidence of significant prediction from adolescent to adult depression in bivariate analyses. This significant effect was primarily attenuated by inclusion of CD in the best-fitting adjusted model; ODD was not included in their analysis.

We suggest, therefore, that the early conclusions about the link between adolescent and young adult depression may have been premature. This putative link may be attenuated by comorbid adolescent disorders, particularly anxiety and behavioral disorders. It may also be the case that there is a rather punctuated shift in the natural course of depression around age 17 or 18 years. This hypothesized shift is consistent with an emerging literature that suggests heterogeneity in childhood/adolescent and adult depressions with respect to biological correlates and psychosocial predictors.30,53

HETEROTYPIC PREDICTION

Each heterotypic pattern identified from previous research was extended by the current study. An emerging body of literature has suggested that generalized anxiety not only reliably precedes depression,3,5456 but vice versa.3 By disaggregating childhood and adolescent diagnoses, the current study found that this pattern was developmentally nuanced: only childhood depression predicted young adult GAD and only adolescent GAD predicted later depression. In addition, adolescent OAD was a stronger predictor of later depression in males than GAD. Furthermore, the cross-prediction was stronger than homotypic prediction for these 2 disorders (a finding also previously reported by Pine and colleagues3).

Together with evidence that GAD and depression co-occur more often with one another than with other disorders20,57 and have shared genetic etiology,58,59 this lends support to the notion of grouping these disorders more closely than is currently reflected in the DSM-IV. Cross-prediction (or sequential comorbidity) is not, however, very strong evidence of diagnostic unity. Childhood and adolescent GAD and MDD predicted different adult disorders and young adult GAD and MDD were predicted by different childhood and adolescent disorders. Our findings, together with those of other longitudinal epidemiologic samples,3,20 suggest that GAD and MDD, while closely related, are distinct both in terms of their natural courses and developmental histories.

A recent study by Kim-Cohen and colleagues found that CD/ODD “was a part of the developmental history of every adult disorder.”1(p713) Because CD and ODD were combined in that study, it was unclear, for any given outcome disorder, whether it was preceded by ODD, CD, or both. We found that young adult depression and anxiety disorders were preceded by adolescent ODD, but not CD. This finding is at odds with the traditional “failure model,”22,60 which suggests that depression results from the social and educational failures that often follow CD. As with homotypic patterns of depression, the bivariate link between adolescent CD and young adult depression in our study was entirely accounted for by comorbid disorders (here, adolescent GAD, ODD, and substance disorders). If it is indeed ODD, rather than CD, that predicts later depression, then this might suggest an amended failure model that emphasizes the social and emotional consequences of irritability and interpersonal difficultness rather than the legal and social sequelae of delinquency and overt aggression.

As part of the research agenda for DSM-V, questions have been raised about the diagnostic and predictive validity of ODD after accounting for comorbid disorders (eg, ADHD, CD).61 Our findings suggest that ODD is a singular disorder in being part of the developmental history of many young adult affective and anxiety disorders. No other childhood or adolescent disorder demonstrated such pleiotropic effects. In DSM-IV, ODD is ruled out if criteria for CD are met. In International Statistical Classification of Diseases, 10th Revision, ODD is a mere subtype of CD. Our data suggest that this subordination of ODD may be misguided. One accepted measure of the utility of a psychiatric diagnosis is the extent to which it predicts future psychiatric functioning.62,63 On this measure, ODD may be in a class by itself.

Correspondence: William E. Copeland, PhD, Center for Developmental Epidemiology, Department of Psychiatry and Behavioral Sciences, Duke University Medical Center, Box 3454, Durham, NC 27710 (william.copeland@duke.edu).

Submitted for Publication: September 21, 2008; final revision received January 25, 2009; accepted February 2, 2009.

Author Contributions: All authors had full access to all the data in this study and Dr Copeland takes responsibility for the integrity of the data and the accuracy of the data analysis.

Financial Disclosure: None reported.

Funding/Support: This work was supported by National Institute of Mental Health grants MH63970, MH63671, and MH48085, National Institute on Drug Abuse grant DA/MH11301, and the William T. Grant Foundation.

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Sourander  AMultimaki  PMDNikolakaros  GMDHaavisto  ARistkari  THelenius  HParkkola  KPiha  JTamminen  TMoilanen  IKumpulainen  KAlmqvist  F Childhood predictors of psychiatric disorders among boys: a prospective community-based follow-up study from age 8 years to early adulthood. J Am Acad Child Adolesc Psychiatry 2005;44 (8) 756- 767
PubMed Link to Article
Moffitt  TEHarrington  HCaspi  AKim-Cohen  JGoldberg  DGregory  AMPoulton  R Depression and generalized anxiety disorder: cumulative and sequential comorbidity in a birth cohort followed prospectively to age 32 years. Arch Gen Psychiatry 2007;64 (6) 651- 660
PubMed Link to Article
Zoccolillo  M Co-occurrence of conduct disorder and its adult outcomes with depressive and anxiety disorders: a review. J Am Acad Child Adolesc Psychiatry 1992;31 (3) 547- 556
PubMed Link to Article
Capaldi  DM Co-occurrence of conduct problems and depressive symptoms in early adolescent boys, II: a 2-year follow-up at grade 8. Dev Psychopathol 1992;4 (1) 125- 144
Link to Article
Loeber  RKeenan  K Interaction between conduct disorder and its comorbid conditions: effects of age and gender. Clin Psychol Rev 1994;14 (6) 497- 523
Link to Article
Rutter  M Adolescence as a transition period: continuities and discontinuities in conduct disorder. J Adolesc Health 1992;13 (6) 451- 460
PubMed Link to Article
Angold  ACostello  EJWorthman  CM Puberty and depression: the roles of age, pubertal status, and pubertal timing. Psychol Med 1998;28 (1) 51- 61
PubMed Link to Article
Costello  EJEgger  HLAngold  A The developmental epidemiology of anxiety disorders: phenomenology, prevalence, and comorbidity. Swedo  SPine  DChild and Adolescent Psychiatric Clinics of North America. Vol 14 New York, NY Elsevier2005;631- 648
Link to Article
Rice  FHarold  GTThapar  A Assessing the effects of age, sex, and shared environment on the genetic aetiology of depression in childhood and adolescence. J Child Psychol Psychiatry 2002;43 (8) 1039- 1051
PubMed Link to Article
Silberg  JPickles  ARutter  MHewitt  JSimonoff  EMaes  HCarbonneau  RMurrelle  LFoley  DEaves  L The influence of genetic factors and life stress on depression among adolescent girls. Arch Gen Psychiatry 1999;56 (3) 225- 232
PubMed Link to Article
Eley  TCStevenson  J Exploring the covariation between anxiety and depression symptoms: a genetic analysis of the effects of the age and sex. J Child Psychol Psychiatry 1999;40 (8) 1273- 1282
PubMed Link to Article
Kaufman  JMartin  AKing  RCharney  D Are child-, adolescent-, and adult-onset depression one and the same disorder? Biol Psychiatry 2001;49 (12) 980- 1001
PubMed Link to Article
Angold  AWorthman  CW Puberty onset of gender differences in rates of depression: a developmental, epidemiologic and neuroendocrine perspective. J Affect Disord 1993;29 (2-3) 145- 158
PubMed Link to Article
Lahey  BBRathouz  PJVan Hulle  CUrbano  RCKrueger  RFApplegate  BGarriock  HAChapman  DAWaldman  ID Testing structural models of DSM-IV symptoms of common forms of child and adolescent psychopathology. J Abnorm Child Psychol 2008;36 (2) 187- 206
PubMed Link to Article
Lahey  BBApplegate  BWaldman  IDLoft  JDHankin  BLRick  J The structure of child and adolescent psychopathology: generating new hypotheses. J Abnorm Psychol 2004;113 (3) 358- 385
PubMed Link to Article
Shanahan  LCopeland  WCostello  EJAngold  A Specificity of putative psychosocial risk factors for psychiatric disorders in children and adolescents. J Child Psychol Psychiatry 2008;49 (1) 34- 42
PubMed Link to Article
Rowe  RMaughan  BPickles  ACostello  EJAngold  A The relationship between DSM-IV oppositional defiant disorder and conduct disorder: findings from the Great Smoky Mountains Study. J Child Psychol Psychiatry 2002;43 (3) 365- 373
PubMed Link to Article
Angold  ACostello  EJErkanli  A Comorbidity. J Child Psychol Psychiatry 1999;40 (1) 57- 87
PubMed Link to Article
Ford  TGoodman  RMeltzer  H The British child and adolescent mental health survey 1999: the prevalence of DSM-IV disorders. J Am Acad Child Adolesc Psychiatry 2003;42 (10) 1203- 1211
PubMed Link to Article
Angold  ACostello  E The Child and Adolescent Psychiatric Assessment (CAPA). J Am Acad Child Adolesc Psychiatry 2000;39 (1) 39- 48
PubMed Link to Article
Angold  ACostello  EJ A test-retest reliability study of child-reported psychiatric symptoms and diagnoses using the Child and Adolescent Psychiatric Assessment (CAPA-C). Psychol Med 1995;25 (4) 755- 762
PubMed Link to Article
Angold  ACox  APrendergast  M  et al.  The Young Adult Psychiatric Assessment (YAPA).  Durham, NC Duke University Medical Center1999;
 SAS/STAT [computer program]. Version 9 Cary, NC SAS Institute, Inc2004;
Jaffee  SRHarrington  HCohen  PMoffitt  TE Cumulative prevalence of psychiatric disorder in youth. J Am Acad Child Adolesc Psychiatry 2005;44 (5) 406- 407
PubMed Link to Article
Roberts  REAttkisson  CRosenblatt  A Prevalence of psychopathology among children and adolescents. Am J Psychiatry 1998;155 (6) 715- 725
PubMed
Klein  RGTancer  NKWerry  JS Anxiety disorders of childhood or adolescence. Widiger  TAFrances  AJPincus  HARoss  RFirst  MBDavis  WDSM-IV Sourcebook. Vol 3. Washington, DC American Psychiatric Association1997;221- 239
Kessler  RCAvenevoli  SRies Merikangas  K Mood disorders in children and adolescents: an epidemiologic perspective. Biol Psychiatry 2001;49 (12) 1002- 1014
PubMed Link to Article
Garber  JKriss  MRKoch  MLindholm  L Recurrent depression in adolescents: a follow-up study. J Am Acad Child Adolesc Psychiatry 1988;27 (1) 49- 54
PubMed Link to Article
Harrington  RFudge  HRutter  MPickles  AHill  J Adult outcomes of childhood and adolescent depression. Arch Gen Psychiatry 1990;47 (5) 465- 473
PubMed Link to Article
Rao  URyan  NDBirmaher  BDahl  REWilliamson  DEKaufman  JRao  RNelson  B Unipolar depression in adolescents: clinical outcome in adulthood. J Am Acad Child Adolesc Psychiatry 1995;34 (5) 566- 578
PubMed Link to Article
Rao  UHammen  CDaley  S Continuity of depression during the transition to adulthood: a 5-year longitudinal study of young women. J Am Acad Child Adolesc Psychiatry 1999;38 (7) 908- 915
PubMed Link to Article
Weissman  MMWolk  SGoldstein  RBMoreau  DAdams  PGreenwald  SKlier  CMRyan  NDDahl  REWickramaratne  P Depressed adolescents grown up. JAMA 1999;281 (18) 1707- 1713
PubMed Link to Article
Fergusson  DMWoodward  LJ Mental health, educational, and social role outcomes of adolescents with depression. Arch Gen Psychiatry 2002;59 (3) 225- 231
PubMed Link to Article
Angold  AErkanli  ASilberg  JEaves  LCostello  E Depression scale scores in 8-17-year-olds: effects of age and gender. J Child Psychol Psychiatry 2002;43 (8) 1052- 1063
PubMed Link to Article
Jaffee  SRMoffitt  TECaspi  AFombonne  EPoulton  RMartin  J Differences in early childhood risk factors for juvenile-onset and adult-onset depression. Arch Gen Psychiatry 2002;59 (3) 215- 222
PubMed Link to Article
Breslau  NSchultz  LPeterson  E Sex differences in depression: a role for preexisting anxiety. J Psychiatr Res 1995;58 (1) 1- 12
Link to Article
Parker  GWilhelm  KMitchell  PAustin  M-PRoussos  JGladstone  G The influence of anxiety as a risk to early onset major depression. J Affect Disord 1999;52 (1-3) 11- 17
PubMed Link to Article
Lewinsohn  PMRohde  PSeeley  JRKlein  DNGotlib  IH Natural course of adolescent major depressive disorder in a community sample: predictors of recurrence in young adults. Am J Psychiatry 2000;157 (10) 1584- 1591
PubMed Link to Article
Kessler  RCChiu  WTDemler  OMerikangas  KRWalters  EE Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the national comorbidity survey replication [published correction appears in Arch Gen Psychiatry. 2005;62(7):709]. Arch Gen Psychiatry 2005;62 (6) 617- 627
PubMed Link to Article
Kendler  KSGardner  COGatz  MPedersen  NL The sources of co-morbidity between major depression and generalized anxiety disorder in a Swedish national twin sample. Psychol Med 2007;37 (3) 453- 462
PubMed Link to Article
Kendler  KSNeale  MCKessler  RCHeath  ACEaves  LJ Major depression and generalized anxiety disorder: same genes, (partly) different environments? Arch Gen Psychiatry 1992;49 (9) 716- 722
PubMed Link to Article
Capaldi  DMStoolmiller  M Co-occurrence of conduct problems and depressive symptoms in early adolescent boys, III: prediction to young-adult adjustment. Dev Psychopathol 1999;11 (1) 59- 84
PubMed Link to Article
Moffitt  TEArseneault  LJaffee  SKim-Cohen  JKoenen  KCOdgers  CLSlutske  WSViding  E Research review: DSM-V conduct disorder: research needs for an evidence base. J Child Psychol Psychiatry 2008;49 (1) 3- 33
PubMed Link to Article
Meehl  P Towards an integrated theory of schizotaxia, schizotypy, and schizophrenia. J Pers Disord 1990; (4) 1- 99
Kendell  RJablensky  A Distinguishing between the validity and utility of psychiatric diagnoses. Am J Psychiatry 2003;160 (1) 4- 12
PubMed Link to Article

Figures

Tables

Table Graphic Jump LocationTable 1. Great Smoky Mountains Study: Data Collection by Cohort
Table Graphic Jump LocationTable 2. Young Adult Diagnoses Predicted From Adolescent Diagnosesa
Table Graphic Jump LocationTable 3. Young Adult Diagnoses Predicted From Childhood Diagnosesa

References

Kim-Cohen  JCaspi  AMoffitt  THarrington  HMilne  BPoulton  R Prior juvenile diagnoses in adults with mental disorder: developmental follow-back of a prospective-longitudinal cohort. Arch Gen Psychiatry 2003;60 (7) 709- 717
PubMed Link to Article
Ferdinand  RFVerhulst  FCWiznitzer  M Continuity and change of self-reported problem behaviors from adolescence into young adulthood. J Am Acad Child Adolesc Psychiatry 1995;34 (5) 680- 690
PubMed Link to Article
Pine  DSCohen  PGurley  DBrook  JMa  Y The risk for early-adulthood anxiety and depressive disorders in adolescents with anxiety and depressive disorders. Arch Gen Psychiatry 1998;55 (1) 56- 64
PubMed Link to Article
Brook  JSCohen  PBrook  DW Longitudinal study of co-occurring psychiatric disorders and substance use. J Am Acad Child Adolesc Psychiatry 1998;37 (3) 322- 330
PubMed Link to Article
Lewinsohn  PMRohde  PKlein  DNSeeley  JR Natural course of adolescent major depressive disorder, I: continuity into young adulthood. J Am Acad Child Adolesc Psychiatry 1999;38 (1) 56- 63
PubMed Link to Article
Kessler  RCBerglund  PDemler  OJin  RMerikangas  KRWalters  EE Lifetime prevalence and age-of-onset distributions of DSM-IV disorders in the national comorbidity survey replication. Arch Gen Psychiatry 2005;62 (6) 593- 602
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Christie  KABurke  JD  JrRegier  DARae  DSBoyd  JHLocke  BZ Epidemiologic evidence for early onset of mental disorders and higher risk of drug abuse in young adults. Am J Psychiatry 1988;145 (8) 971- 975
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Burke  KCBurke  JD  JrRae  DSRegier  DA Comparing age at onset of major depression and other psychiatric disorders by birth cohorts in five US community populations. Arch Gen Psychiatry 1991;48 (9) 789- 795
PubMed Link to Article
Bittner  AEgger  HLErkanli  AJane Costello  EFoley  DLAngold  A What do childhood anxiety disorders predict? J Child Psychol Psychiatry 2007;48 (12) 1174- 1183
PubMed Link to Article
Burke  JDLoeber  RLahey  BBRathouz  P Developmental transitions among affective and behavioral disorders in adolescent boys. J Child Psychol Psychiatry 2005;46 (11) 1200- 1210
PubMed Link to Article
Costello  EJMustillo  SErkanli  AKeeler  GAngold  A Prevalence and development of psychiatric disorders in childhood and adolescence. Arch Gen Psychiatry 2003;60 (8) 837- 844
PubMed Link to Article
Fergusson  DMLynskey  MTHorwood  LJ Factors associated with continuity and change in disruptive behavior patterns between childhood and adolescence. J Abnorm Child Psychol 1996;24 (5) 533- 553
PubMed Link to Article
Orvaschel  HLewinsohn  PMSeeley  JR Continuity of psychopathology in a community sample of adolescents. J Am Acad Child Adolesc Psychiatry 1995;34 (11) 1525- 1535
PubMed Link to Article
Goodwin  RDFergusson  DMHorwood  L Early anxious/withdrawn behaviours predict later internalising disorders. J Child Psychol Psychiatry 2004;45 (4) 874- 883
PubMed Link to Article
Ferdinand  RFVerhulst  FC Psychopathology from adolescence into young adulthood: an 8-year follow-up study. Am J Psychiatry 1995;152 (11) 1586- 1594
PubMed
Hofstra  MBvan der Ende  JVerhulst  FC Child and adolescent problems predict DSM-IV disorders in adulthood: a 14-year follow-up of a Dutch epidemiological sample. J Am Acad Child Adolesc Psychiatry 2002;41 (2) 182- 189
PubMed Link to Article
Hofstra  MBvan der Ende  JVerhulst  FC Continuity and change of psychopathology from childhood into adulthood: a 14-year follow-up study. J Am Acad Child Adolesc Psychiatry 2000;39 (7) 850- 858
PubMed Link to Article
Newman  DLMoffitt  TECaspi  AMagdol  LSilva  PAStanton  WR Psychiatric disorder in a birth cohort of young adults: prevalence, comorbidity, clinical significance, and new case incidence from ages 11 to 21. J Consult Clin Psychol 1996;64 (3) 552- 562
PubMed Link to Article
Sourander  AMultimaki  PMDNikolakaros  GMDHaavisto  ARistkari  THelenius  HParkkola  KPiha  JTamminen  TMoilanen  IKumpulainen  KAlmqvist  F Childhood predictors of psychiatric disorders among boys: a prospective community-based follow-up study from age 8 years to early adulthood. J Am Acad Child Adolesc Psychiatry 2005;44 (8) 756- 767
PubMed Link to Article
Moffitt  TEHarrington  HCaspi  AKim-Cohen  JGoldberg  DGregory  AMPoulton  R Depression and generalized anxiety disorder: cumulative and sequential comorbidity in a birth cohort followed prospectively to age 32 years. Arch Gen Psychiatry 2007;64 (6) 651- 660
PubMed Link to Article
Zoccolillo  M Co-occurrence of conduct disorder and its adult outcomes with depressive and anxiety disorders: a review. J Am Acad Child Adolesc Psychiatry 1992;31 (3) 547- 556
PubMed Link to Article
Capaldi  DM Co-occurrence of conduct problems and depressive symptoms in early adolescent boys, II: a 2-year follow-up at grade 8. Dev Psychopathol 1992;4 (1) 125- 144
Link to Article
Loeber  RKeenan  K Interaction between conduct disorder and its comorbid conditions: effects of age and gender. Clin Psychol Rev 1994;14 (6) 497- 523
Link to Article
Rutter  M Adolescence as a transition period: continuities and discontinuities in conduct disorder. J Adolesc Health 1992;13 (6) 451- 460
PubMed Link to Article
Angold  ACostello  EJWorthman  CM Puberty and depression: the roles of age, pubertal status, and pubertal timing. Psychol Med 1998;28 (1) 51- 61
PubMed Link to Article
Costello  EJEgger  HLAngold  A The developmental epidemiology of anxiety disorders: phenomenology, prevalence, and comorbidity. Swedo  SPine  DChild and Adolescent Psychiatric Clinics of North America. Vol 14 New York, NY Elsevier2005;631- 648
Link to Article
Rice  FHarold  GTThapar  A Assessing the effects of age, sex, and shared environment on the genetic aetiology of depression in childhood and adolescence. J Child Psychol Psychiatry 2002;43 (8) 1039- 1051
PubMed Link to Article
Silberg  JPickles  ARutter  MHewitt  JSimonoff  EMaes  HCarbonneau  RMurrelle  LFoley  DEaves  L The influence of genetic factors and life stress on depression among adolescent girls. Arch Gen Psychiatry 1999;56 (3) 225- 232
PubMed Link to Article
Eley  TCStevenson  J Exploring the covariation between anxiety and depression symptoms: a genetic analysis of the effects of the age and sex. J Child Psychol Psychiatry 1999;40 (8) 1273- 1282
PubMed Link to Article
Kaufman  JMartin  AKing  RCharney  D Are child-, adolescent-, and adult-onset depression one and the same disorder? Biol Psychiatry 2001;49 (12) 980- 1001
PubMed Link to Article
Angold  AWorthman  CW Puberty onset of gender differences in rates of depression: a developmental, epidemiologic and neuroendocrine perspective. J Affect Disord 1993;29 (2-3) 145- 158
PubMed Link to Article
Lahey  BBRathouz  PJVan Hulle  CUrbano  RCKrueger  RFApplegate  BGarriock  HAChapman  DAWaldman  ID Testing structural models of DSM-IV symptoms of common forms of child and adolescent psychopathology. J Abnorm Child Psychol 2008;36 (2) 187- 206
PubMed Link to Article
Lahey  BBApplegate  BWaldman  IDLoft  JDHankin  BLRick  J The structure of child and adolescent psychopathology: generating new hypotheses. J Abnorm Psychol 2004;113 (3) 358- 385
PubMed Link to Article
Shanahan  LCopeland  WCostello  EJAngold  A Specificity of putative psychosocial risk factors for psychiatric disorders in children and adolescents. J Child Psychol Psychiatry 2008;49 (1) 34- 42
PubMed Link to Article
Rowe  RMaughan  BPickles  ACostello  EJAngold  A The relationship between DSM-IV oppositional defiant disorder and conduct disorder: findings from the Great Smoky Mountains Study. J Child Psychol Psychiatry 2002;43 (3) 365- 373
PubMed Link to Article
Angold  ACostello  EJErkanli  A Comorbidity. J Child Psychol Psychiatry 1999;40 (1) 57- 87
PubMed Link to Article
Ford  TGoodman  RMeltzer  H The British child and adolescent mental health survey 1999: the prevalence of DSM-IV disorders. J Am Acad Child Adolesc Psychiatry 2003;42 (10) 1203- 1211
PubMed Link to Article
Angold  ACostello  E The Child and Adolescent Psychiatric Assessment (CAPA). J Am Acad Child Adolesc Psychiatry 2000;39 (1) 39- 48
PubMed Link to Article
Angold  ACostello  EJ A test-retest reliability study of child-reported psychiatric symptoms and diagnoses using the Child and Adolescent Psychiatric Assessment (CAPA-C). Psychol Med 1995;25 (4) 755- 762
PubMed Link to Article
Angold  ACox  APrendergast  M  et al.  The Young Adult Psychiatric Assessment (YAPA).  Durham, NC Duke University Medical Center1999;
 SAS/STAT [computer program]. Version 9 Cary, NC SAS Institute, Inc2004;
Jaffee  SRHarrington  HCohen  PMoffitt  TE Cumulative prevalence of psychiatric disorder in youth. J Am Acad Child Adolesc Psychiatry 2005;44 (5) 406- 407
PubMed Link to Article
Roberts  REAttkisson  CRosenblatt  A Prevalence of psychopathology among children and adolescents. Am J Psychiatry 1998;155 (6) 715- 725
PubMed
Klein  RGTancer  NKWerry  JS Anxiety disorders of childhood or adolescence. Widiger  TAFrances  AJPincus  HARoss  RFirst  MBDavis  WDSM-IV Sourcebook. Vol 3. Washington, DC American Psychiatric Association1997;221- 239
Kessler  RCAvenevoli  SRies Merikangas  K Mood disorders in children and adolescents: an epidemiologic perspective. Biol Psychiatry 2001;49 (12) 1002- 1014
PubMed Link to Article
Garber  JKriss  MRKoch  MLindholm  L Recurrent depression in adolescents: a follow-up study. J Am Acad Child Adolesc Psychiatry 1988;27 (1) 49- 54
PubMed Link to Article
Harrington  RFudge  HRutter  MPickles  AHill  J Adult outcomes of childhood and adolescent depression. Arch Gen Psychiatry 1990;47 (5) 465- 473
PubMed Link to Article
Rao  URyan  NDBirmaher  BDahl  REWilliamson  DEKaufman  JRao  RNelson  B Unipolar depression in adolescents: clinical outcome in adulthood. J Am Acad Child Adolesc Psychiatry 1995;34 (5) 566- 578
PubMed Link to Article
Rao  UHammen  CDaley  S Continuity of depression during the transition to adulthood: a 5-year longitudinal study of young women. J Am Acad Child Adolesc Psychiatry 1999;38 (7) 908- 915
PubMed Link to Article
Weissman  MMWolk  SGoldstein  RBMoreau  DAdams  PGreenwald  SKlier  CMRyan  NDDahl  REWickramaratne  P Depressed adolescents grown up. JAMA 1999;281 (18) 1707- 1713
PubMed Link to Article
Fergusson  DMWoodward  LJ Mental health, educational, and social role outcomes of adolescents with depression. Arch Gen Psychiatry 2002;59 (3) 225- 231
PubMed Link to Article
Angold  AErkanli  ASilberg  JEaves  LCostello  E Depression scale scores in 8-17-year-olds: effects of age and gender. J Child Psychol Psychiatry 2002;43 (8) 1052- 1063
PubMed Link to Article
Jaffee  SRMoffitt  TECaspi  AFombonne  EPoulton  RMartin  J Differences in early childhood risk factors for juvenile-onset and adult-onset depression. Arch Gen Psychiatry 2002;59 (3) 215- 222
PubMed Link to Article
Breslau  NSchultz  LPeterson  E Sex differences in depression: a role for preexisting anxiety. J Psychiatr Res 1995;58 (1) 1- 12
Link to Article
Parker  GWilhelm  KMitchell  PAustin  M-PRoussos  JGladstone  G The influence of anxiety as a risk to early onset major depression. J Affect Disord 1999;52 (1-3) 11- 17
PubMed Link to Article
Lewinsohn  PMRohde  PSeeley  JRKlein  DNGotlib  IH Natural course of adolescent major depressive disorder in a community sample: predictors of recurrence in young adults. Am J Psychiatry 2000;157 (10) 1584- 1591
PubMed Link to Article
Kessler  RCChiu  WTDemler  OMerikangas  KRWalters  EE Prevalence, severity, and comorbidity of 12-month DSM-IV disorders in the national comorbidity survey replication [published correction appears in Arch Gen Psychiatry. 2005;62(7):709]. Arch Gen Psychiatry 2005;62 (6) 617- 627
PubMed Link to Article
Kendler  KSGardner  COGatz  MPedersen  NL The sources of co-morbidity between major depression and generalized anxiety disorder in a Swedish national twin sample. Psychol Med 2007;37 (3) 453- 462
PubMed Link to Article
Kendler  KSNeale  MCKessler  RCHeath  ACEaves  LJ Major depression and generalized anxiety disorder: same genes, (partly) different environments? Arch Gen Psychiatry 1992;49 (9) 716- 722
PubMed Link to Article
Capaldi  DMStoolmiller  M Co-occurrence of conduct problems and depressive symptoms in early adolescent boys, III: prediction to young-adult adjustment. Dev Psychopathol 1999;11 (1) 59- 84
PubMed Link to Article
Moffitt  TEArseneault  LJaffee  SKim-Cohen  JKoenen  KCOdgers  CLSlutske  WSViding  E Research review: DSM-V conduct disorder: research needs for an evidence base. J Child Psychol Psychiatry 2008;49 (1) 3- 33
PubMed Link to Article
Meehl  P Towards an integrated theory of schizotaxia, schizotypy, and schizophrenia. J Pers Disord 1990; (4) 1- 99
Kendell  RJablensky  A Distinguishing between the validity and utility of psychiatric diagnoses. Am J Psychiatry 2003;160 (1) 4- 12
PubMed Link to Article

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