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.

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One puzzle in high worry and generalized anxiety disorder (GAD) is the heterogeneity in the level of autonomic arousal symptoms seen among affected individuals. While current models agree that worry persists, in part, because it fosters avoidance of unpleasant internal experiences, they disagree as to whether worry does so by suppressing activation of autonomic arousal or by fostering persistent autonomic hyperarousal. Our Cognitive Control Model predicts that which pattern of autonomic arousal occurs depends on whether or not a worrier has sufficient cognitive control capacity to worry primarily in a verbal versus imagery-based manner. Because this model has been supported by only one study to date, the present study sought to replicate and extend that study’s findings. Results from an online survey in an unselected sample of over 900 college students provide further support for our model’s central tenet and initial support for its prediction that higher effortful control is associated with a higher percentage of verbal thought during worry. Finally, we report tentative evidence that autonomic arousal symptoms in worry and GAD vary as a function of individual differences in cognitive control capacity because higher capacity is linked to a greater predominance of verbal thought during worry.