It is well known that comorbidity is the rule, not the exception, for categorically defined psychiatric disorders, and this is also the case for internalizing disorders of depression and anxiety. This theoretical review paper addresses the ubiquity of comorbidity among internalizing disorders. Our central thesis is that progress in understanding this co-occurrence can be made by employing latent dimensional structural models that organize both psychopathology as well as vulnerabilities and risk mechanisms and by connecting the multiple levels of risk and psychopathology outcomes together. Different vulnerabilities and risk mechanisms are hypothesized to predict different levels of the structural model of psychopathology. We review the present state of knowledge based on concurrent and developmental sequential comorbidity patterns among common discrete psychiatric disorders in youth, and then we advocate for the use of more recent bifactor dimensional models of psychopathology (e.g., p factor, Caspi et al., 2014) that can help to explain the co-occurrence among internalizing symptoms. In support of this relatively novel conceptual perspective, we review six exemplar vulnerabilities and risk mechanisms, including executive function, information processing biases, cognitive vulnerabilities, positive and negative affectivity aspects of temperament, and autonomic dysregulation, along with the developmental occurrence of stressors in different domains, to show how these vulnerabilities can predict the general latent psychopathology factor, a unique latent internalizing dimension, as well as specific symptom syndrome manifestations.

Multiple cognitive risk products (dysfunctional attitudes [DA], negative inferential style [NIS], self-criticism, dependency, rumination) predict internalizing disorders; however, an optimal structure to assess these risks is unknown. We evaluated the fit, construct validity, and utility of a bifactor, single, and correlated factor model in a community sample of 382 adolescents (age 11-15 years; 59% female). The bifactor, hierarchical single, and correlated factor models all fit well. The bifactor model included a common factor ( c), capturing covariance across all cognitive risk measures, and specific latent factors for DA, NIS, dependency and rumination. Construct validity of these factor structures was evaluated with external validators, including depression and anxious arousal (AA) symptoms, positive affect (PA) and negative affect (NA), and onset of depression diagnostic onset over 2 years. C was associated with higher depression, NA, and AA; lower PA; and predicted depressive episodes. Hierarchical single and correlated factor models also related to external validators.

Objective: Multiple cognitive risks from different theoretical paradigms (dysfunctional attitudes, negative inferential style, self-criticism, dependency, brooding) predict depression, but may be transdiagnostic vulnerabilities for multiple psychopathologies. Risk factors can be identified as broadly transdiagnostic and relatively specific to psychopathological outcomes by organizing the common and specific aspects of each respective construct using latent bifactor models, and by examining links between dimensions of risk and psychopathology. This study evaluated (a) whether a bifactor model of cognitive vulnerabilities, including a general cognitive risk dimension (c factor) and several specific dimensions replicated in early adolescents (M age ϭ 13.50 years) and extended to younger and older youth, and (b) how the general and specific cognitive risk dimensions related to the general psychopathology (p factor) and internalizingand externalizing-specific dimensions. Method: Community youth (N ϭ 571; 55% female) reported on cognitive risks; youth and a caregiver reported on psychopathologies (depression, anxiety, aggression, conduct, attention problems). Results: The cognitive risk bifactor model showed good fit and slight advantages over a correlated factors model. The bifactor model exhibited invariance across development and captured key associations that were identified when each individual cognitive risk was related to the bifactor model of psychopathology. The c factor strongly related to internalizing-specific, and moderately to the p factor and externalizing-specific dimensions. Specific cognitive risk dimensions (brooding, negative inferential style, dependency) related to all psychopathology dimensions. Conclusion: A general cognitive vulnerability (c factor) transdiagnostically associates with a breadth of psychopathologies and most potently to internalizing-specific among youth. What is the public health significance of this article?A common cognitive vulnerability representing general maladaptive thinking patterns (e.g., overly negative, self-focused beliefs) related to a breadth of mental health problems (depression, anxiety, aggression, conduct, attention issues), and particularly to symptoms that are specific to depression and anxiety among youth. This common cognitive vulnerability may be a transdiagnostic risk that informs transdiagnostic interventions.

Rumination, a thinking style characterized by a repetitive inward focus on negative cognitions, has been linked to internalizing disorders, particularly depression. Moreover, research suggests that rumination may be a cognitive vulnerability that predisposes individuals to psychopathology. Surprisingly little is known, however, about the etiology and development of rumination. The present study examined the role of specific components of child temperamental negative emotionality (sadness, fear, anger) and effortful control (inhibition), as well as parenting behaviors during early childhood on the development of rumination in middle childhood. Early childhood (age 3) temperament and parenting behaviors were assessed observationally and rumination was self-reported in middle childhood (age 9) in a large community sample (N = 425; 47.1% female). Two significant interactions emerged. First, temperamental anger interacted with inhibitory control (IC) such that high anger and low IC predicted higher levels of rumination, whereas low anger and low IC predicted lower levels of rumination. Second, IC interacted with parenting such that children with low IC and positive parenting had lower levels of rumination. In contrast, children with high IC reported similar levels of rumination regardless of parenting quality. Overall, these findings highlight the interplay of early IC with temperamental anger and positive parenting in the development of ruminative tendencies in middle childhood.

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