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Review
. 2016 Nov;28(4pt1):987-1012.
doi: 10.1017/S0954579416000663.

Understanding comorbidity among internalizing problems: Integrating latent structural models of psychopathology and risk mechanisms

Affiliations
Review

Understanding comorbidity among internalizing problems: Integrating latent structural models of psychopathology and risk mechanisms

Benjamin L Hankin et al. Dev Psychopathol. 2016 Nov.

Abstract

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 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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Conflict of interest statement

The authors report no conflicts of interest.

Figures

Figure 1
Figure 1
Simplified schematic example of a p factor model (e.g., Caspi et al., 2014). Different forms of internalizing and externalizing psychopathology load onto (i.e., are considered to be caused by), both their specific internalizing and externalizing factors, as well as the p factor, which captures what is common across all forms of psychopathology in the model.
Figure 2
Figure 2
Heuristic conceptual model using multiple units of analysis to understand how risk traits interact with environmental stressors to confer risk for broad latent psychopathology dimensions (comorbidity and continuity) or specific symptom manifestations (specificity and discontinuity). This model is intended to be illustrative of some important risk pathways and not exhaustive in terms of either risk factors or pathways. Strength of the lines are roughly indicative of effect sizes based on existing literature. Dashed lines indicate areas where there is less existing evidence. (A) The top sections depict four units of analysis: (1) neural and endocrine systems implicated in internalizing psychopathology, (2) latent vulnerability traits, which are fairly stable individual differences in cognitive and affective vulnerabilities (these risk factors have their own latent structures, not shown here for simplicity, see Figure 3 for an example), (3) latent psychopathology liabilities, which are broad psychopathology liability dimensions that span disorders. Latent internalizing psychopathology is divided into fear and distress sub-factors in some models as shown here, but these sub-factors are not included in all models and have not been studied for many risk factors), and (4) symptom specific syndromes, which are specific constellations of internalizing symptoms that systematically and characteristically group together as part of a coherent pattern. These risk factors are likely to interact; only a few such posited interactions are shown here for simplicity. (B) The bottom section depicts stressors, from different domains and types of events, transpiring across the lifespan that may trigger symptom specific syndrome manifestations at particular points during development. Prenatal and early life stressors have enduring effects across development via neurodevelopmental processes (depicted with thick arrow at top). Family, peer interpersonal and achievement stressors change in frequency and salience across development, as illustrated with the stress curves at the bottom (which are not meant to represent exact time frames). Note especially the accumulation of multiple types of stressors in adolescence, which is posited to contribute to increasing rates and levels of internalizing psychopathology during that developmental period.
Figure 3
Figure 3
The relationship between latent bifactor models of cognitive risk and psychopathology. Preliminary findings showed a novel structure of cognitive risks including a general factor (Common Cognitive Risk) as well as Specific aspects of cognitive risk, not accounted for by the common factor. The common cognitive risk factor captures the shared variance across dysfunctional attitudes, negative inferential style, self-criticism, dependency, and rumination, whereas the specific cognitive risk factors represent unique variance captured by that construct. This is one example demonstrating that when bifactor dimensional models of risk and psychopathology are connected together, novel and potentially clearer patterns are revealed for risk factors and processes that underlie comorbidity within internalizing spectra as well as across psychopathology more broadly. It is also possible that specific aspects of risk could relate to unique behavioral syndromes and thus also help to explain discontinuity in psychopathology (although not depicted here).

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