Although homotypic patterns were identified (e.g., 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 to 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 (e.g., about the future, academic performance, self-consciousness) and was highly comorbidity 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 of validity of childhood OAD as compared to DSM-IV GAD in predicting adolescent disorders. OAD not only predicted later anxiety disorders but also predicted adolescent depression and conduct disorder. In contrast, DSM-IV GAD only predicted later conduct disorder. 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 anxiety3
. 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 her 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 research45
, 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 disorders46-50
. 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 time points in both adolescence and young adulthood.
To date, three such studies have been published. The first, a community sample of adolescents followed into young adulthood by Lewinsohn and colleagues5 p.61
, concludes that their results “clearly illustrate a strong pattern of continuity for depression.” Their initial analyses demonstrate higher risk of later depression for a group of adolescents with MDD as compared to 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 two 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 two 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 depression51
. 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, conduct disorders, 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 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 adolescence52
, 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 colleagues found that the best-fitting multivariable prediction model of young adult depression did not
include adolescent depression after accounting for comorbidities3
. 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 (Pine, D., personal communication).
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. 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 predictors30, 53