Comorbidity and continuity of depression and conduct problems from elementary school to adolescence

Abstract

Despite nonoverlapping criterion sets, conduct disorder and depression co-occur at much higher rates than expected by chance. Contemporary model-based approaches to explaining heterotypic comorbidity use factor analysis and its variants to evaluate interrelations among symptoms in large population-based and twin samples. These analyses invariably yield broadband internalizing and externalizing factors, which load on a higher-order general liability factor-findings that are robust across age and informant. Although model-based approaches elucidate structural aspects of comorbidity, they are variable-centered, and usually cross-sectional. Most therefore do not assess developmental continuity of comorbidity, or whether noncomorbid individuals are prospectively vulnerable to heterotypic comorbidity. We use an accelerated longitudinal design to evaluate growth in parent-reported conduct problems (CPs) and depression among children, ages 8-15 years, who were recruited at study entry into depressed only (n = 27), CPs only (n = 28), comorbid (n = 81), and control (n = 70) groups based on levels of symptoms. Consistent with normative developmental trends across this age range, steep growth in depression was exhibited by all groups, including those who reported only CPs at study entry. In contrast, growth in CPs was restricted to those who reported high symptoms at intake (with or without comorbid depression), compared with low and stable among depressed only and control participants. To our knowledge, this is the first study to demonstrate, using carefully ascertained "pure" versus comorbid groups who were followed naturalistically, that comorbid depression is likely to develop among those with pure CPs, but comorbid CPs are not likely to develop among those with pure depression. (PsycINFO Database Record

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Figures

Figure 1

Effects of using statistical partialling techniques (e.g., ANCOVA, hierarchical regression, lag correlational designs) to evaluate heterotypic continuity of traits with shared etiologies. The left panel depicts the concurrent correlation (comorbidity) between depression and conduct problems (CPs) at age 8. The right panel depicts prospective prediction of CPs at age 12 by depression at age 8, controlling for CPs at age 8. Statistical partialling removes shared vulnerability (A in both the left and right panels), which (1) creates statistical entities (depression without vulnerability to CPs, CPs without vulnerability to depression) that misrepresent/distort etiological relations between disorders, and (2) under-estimate longitudinal associations by artificially attenuating common variance among predictors and outcomes (C, right panel). Despite recognition of these issues for decades (see Pedhazur, 1997), partialling procedures remain common in the psychopathology literature. Contrasted groups designs do not rely on statistical partialling and therefore offer advantages over research conducted with only comorbid samples.

Figure 2

Growth in depressive symptoms by group from ages 8–14 years. Age 15 data are omitted because only 13 participants were distributed across the four groups, so means are likely unreliable.

Figure 3

Growth in conduct disorder symptoms by group from ages 8–14 years. Age 15 data are omitted because only 13 participants were distributed across the four groups, so means are likely unreliable.

Figure 4

Growth in oppositional defiant disorder symptoms by group from ages 8–14 years. Age 15 data are omitted because only 13 participants were distributed across the four groups, so means are likely unreliable.