Reconceptualizing PDs in personality dimensional terms represents a good start on providing a solid empirical footing for future editions of the DSM. Yet certain conundrums will remain even if PDs are reconfigured in personality trait terms. These conundrums pertain to CDs, as DSM–defined PDs, as well as dimensional personality traits, are both closely connected with CDs (for recent reviews, see Clark, in press
; Krueger & Tackett, 2003
). What is ultimately needed is a model that can make sense of the connections linking all these domains (CDs, PDs, and the structure of normal and abnormal personality).
The beginnings of such a model are provided by work on the structure of common mental disorders. The motivation behind this work has been to provide an understanding of the reasons why the mental disorders defined in official nosological systems such as the DSM and ICD are frequently comorbid. Rather than viewing comorbidity as an artifact or a nuisance, this work approaches comorbidity as a reliable empirical observation in need of an explanatory model.
The focus of this work has been primarily on comorbidity among mental disorders commonly observed in epidemiological samples (unipolar mood, anxiety, substance use, and antisocial behavior disorders); in the DSM nosology, these disorders are mostly conceptualized as CDs (with the exception of Antisocial PD). These disorders represent key targets because of their prevalence and clear public health relevance. Our earlier work on the link between personality and these disorders in epidemiological samples (e.g., Krueger, 1999a
) yielded evidence of systematic links between “normal–range” personality constructs and these disorders, both cross–sectionally and longitudinally. Specifically, the mood and anxiety disorders were associated with high levels of neuroticism/negative emotionality, whereas the substance use and antisocial behavior disorders were associated with high levels of neuroticism/negative emotionality and high levels of disinhibition.
Given this pattern of findings, comorbidity among common mental disorders makes sense when thought of in terms of the personological underpinnings of these disorders. As described earlier, Krueger et al. (1998)
demonstrated that unipolar mood and anxiety disorders were indicators of a latent internalizing propensity, and substance dependence and antisocial behavior disorders were indicators of a latent externalizing propensity (see also Krueger, 1999b
). Moreover, these propensities were highly stable over time, a finding replicated by Vollebergh et al. (2001)
. Recent evidence indicates that the internalizing–externalizing structure can also be observed in the primary care setting in numerous countries around the globe, and that the internalizing spectrum also appears to encompass somatoform syndromes (Krueger, Chentsova-Dutton, Markon, Goldberg, & Ormel, 2003
Putting the personality findings together with the findings on the structure of mental disorders, neuroticism/negative emotionality appears to provide the personological basis for internalizing psychopathology, and negative emotionality paired with disinhibition appears to provide the personological basis for externalizing psychopathology. Thus, the connections between personality and psychopathology make psychological sense. Negative emotionality is internalized given normative levels of disinhibition and presents as unipolar mood and anxiety disorder. If negative emotionality is paired with high levels of disinhibition, the presentation tends more toward externalizing (substance use and antisocial behavior) problems.
These observations provide the outlines of a hierarchically organized spectrum model of common mental disorders that also extends to encompass the link between personality and psychopathology. The findings suggest that unipolar mood disorders, anxiety disorders, and negative emotionality form a coherent group of constructs, and substance use disorders, antisocial behavior disorders, and disinhibitory personality traits form a related (owing to the role of negative emotionality in both internalizing and externalizing problems) but also distinguishable (owing to the unique role of disinhibition in externalizing problems) group of constructs. This conceptualization is bolstered by research on the genetic underpinnings of the connections between psychopathological syndromes and personality traits. That is, unipolar mood and anxiety problems share significant genetic variance with the personality trait of neuroticism; in addition, substance use and antisocial behavior problems share significant genetic variance with an unconstrained, impulsive personality style (see Krueger & Tackett, 2003
for a review). This conceptualization is also bolstered by research on the genetic underpinnings of the structure of psychopathology.
Kendler, Prescott, Myers, and Neale (2003)
recently presented a study showing that the observed phenotypic structure of common mental disorders closely mirrors the underlying genetic architecture of these constructs. Kendler et al. (2003)
studied the genetic and environmental underpinnings of the comorbidity among seven syndromes (major depression, generalized anxiety disorder, phobia, alcohol dependence, other drug abuse or dependence, adult antisocial behavior, and conduct disorder) that delineate the internalizing and externalizing spectra. Two general genetic factors were found, the first related primarily to the internalizing disorders (major depression, generalized anxiety disorder, phobia) and the second related primarily to the externalizing disorders (alcohol dependence, other drug abuse or dependence, adult antisocial behavior, and conduct disorder). As noted by Kendler et al. (2003
, p. 935), “These results suggest strongly that genetic factors are largely responsible for the pattern of comorbidity that results in the 2 frequently co–occurring clusters of internalizing and externalizing disorders.”
In addition to these broad genetic factors, Kendler et al. (2003)
also documented specific etiologic contributions that distinguish disorders within the broad internalizing and externalizing spectra. For example, finer–grained modeling of the internalizing syndromes of major depression, generalized anxiety disorder, panic disorder, animal phobia, and situational phobia revealed evidence for genetically distinguishable (but correlated) subfactors within the broader internalizing domain, with one subfactor loading more on depression and generalized anxiety disorder (with panic disorder as a weaker marker), and the other loading more on animal phobia, and situational phobia (cf. Krueger, 1999b
; Watson, in press
). Specific genetic factors also contributed to alcohol and drug abuse/dependence, above and beyond the contribution of the overarching genetic externalizing factor. In addition, environmental factors were important contributors to distinguishing between closely related syndromes. For example, conduct disorder showed a unique contribution from the shared family environment (cf. Hicks, Krueger et al., 2004
; Krueger, Iacono, McGue, & Patrick, 2002
These specific etiologic contributions in the context of broad, genetically coherent spectra are important phenomena because they speak to the hierarchical organization of the structure of common mental disorders. The idea behind this work has never been that there are only two constructs of relevance in understanding common mental disorders (internalizing and externalizing). Rather, the idea is that the internalizing and externalizing constructs provide the broad organizational schema and sources of genetic coherence for this domain, and are therefore major sources of the comorbidity among common mental disorders; in addition to this, other constructs (e.g., unique genetic and environmental events) explain how syndromes closely connected by shared genetic etiology come to be distinguishable. Put somewhat differently, both “lumping” and “splitting” perspectives on the organization of psychopathology are partially correct, and they can be reconciled by adopting a dimensional–hierarchical model of etiologic contributions within this domain that recognizes etiologic factors at continually varying levels of specificity versus breadth (cf. Krueger & Piasecki, 2002
Integrating this ongoing work on the structure of mental disorders into the DSM system represents a complex challenge, but it is a challenge that seems worth pursuing if the goal is to place the organization of the DSM on solid empirical footing. One way in which the organizational structure of future editions of the DSM could reflect the empirical structure of mental disorders would be to organize the syndromes that have been studied to date into internalizing and externalizing sections. The organization of internalizing syndromes has been particularly problematic in the DSM (see, e.g., the previous discussion of Depressive PD). Watson (in press)
has recently articulated an approach to resolving some of these problems. Watson’s (in press)
approach focuses on delineating facets within the internalizing spectrum in terms of the distinction between disorders that are more distress–related (e.g., Major Depression and Generalized Anxiety Disorder), those that are more fear–related (e.g., Panic Disorder and Phobias), and those that involve bipolarity of mood (e.g., Bipolar I and II, Cyclothymia). As described earlier, this reorganization reflects current knowledge of the structure of internalizing syndromes better than the putative distinction between mood and anxiety disorders (cf. Kendler et al., 2003
; Krueger, 1999b
Organizing externalizing syndromes into a coherent section also requires rethinking some basic aspects of the current organization of the DSM. The externalizing spectrum encompasses problems that are currently spread throughout the DSM, across sections covering substance–related disorders; disorders usually first diagnosed in infancy, childhood, or adolescence (conduct disorder); and the section on PDs (Antisocial PD). Yet empirical evidence continues to speak to the coherence of the externalizing spectrum, as well as the dimensional nature of this spectrum. For example, Krueger, Markon, Patrick, & Iacono (in press)
studied the comorbidity among the syndromes of conduct disorder, adult antisocial behavior, alcohol dependence, marijuana dependence, and drug dependence in a large, representative sample of adults. A series of models were fit to the data to ask if the comorbidity among these syndromes could be better accounted for in terms of a set of categories versus in terms of a coherent dimension of liability to experience multiple disorders in the externalizing realm. The data better supported a dimensional conceptualization, with an overarching dimension of externalizing liability connecting the disorders. A model specifying five separate categories of substance disorders and antisocial behavior disorders was untenable.
Another challenging issue relates to disorders described in the DSM that have not been studied in the internalizing–externalizing framework. This framework provides only the beginnings of a comprehensive model of clinical psychopathology because many important forms of psychopathology have not been studied in its context. This owes primarily to the limitations of existing data. For example, data on psychotic disorders are collected in large–scale investigations of comorbidity, but these disorders are conceptualized in such a way that they have very little variance in the population at large. This makes studying relations between these disorders and common mental disorders infeasible because there are too few cases of less common disorders—much less observations of patterns of comorbidity linking less common disorders with more common disorders—to allow for reliable conclusions to be drawn regarding less common disorders.
Two strategies are likely to be productive in overcoming this obstacle to broadening the internalizing–externalizing framework. A first strategy would focus on integrating novel domains of psychopathology into the framework in samples where prevalence is enhanced (e.g., in samples from psychiatric clinics). For example, Krueger et al. (2003)
were able to broaden the internalizing spectrum to include somatoform disorders by studying the model in primary care samples. A second strategy would focus on broadening conceptualizations of less common syndromes. For example, rather than focusing on dichotomous CDs such as Schizophrenia, research could focus on dimensions of psychosis such as positive symptoms, negative symptoms, and disorganization. Emerging work on dimensional approaches to psychosis (e.g., van Os et al., 1999
) could be integrated with ongoing work on the internalizing and externalizing dimensions that appear to underlie common mental disorders.
Another issue relates to the placement of personality constructs in a system that recognizes the internalizing and externalizing spectra, as these spectra transcend personality and psychopathology. Also recall that the foregoing review of PDs and CDs found them to be more similar than different. In particular, the major bases for distinguishing between PDs and CDs in the DSM–IV–TR (stability and age of onset) are not very differentiating, as the propensities underling both PDs and CDs appear to be relatively stable, and both PDs and CDs seem to be prevalent in younger age groups. This suggests that it might make the most sense to ultimately focus not on the putative PD–CD distinction, but rather, on the generation of key facet–level constructs that cover the range of symptomatology and traits currently spread across Axes I and II of the DSM–IV–TR. This idea was well articulated by Widiger and Clark (2000
, p. 954) who wrote, “Ultimately, as one builds toward DSM–V, what may emerge is a structured set not of categorical diagnoses but of component dimensions, a set of symptom–cluster building blocks from which the panoply of diagnoses could be constructed.” Based on our current understanding, personality–related facets (building blocks) appear well organized by the FFM domains (although more work is needed to identify the most optimal facets for clinical purposes), and common psychopathological symptoms appear well organized by the internalizing–externalizing domains. With regard to the latter, the internalizing and externalizing domains have emerged from analyses of DSM categories, and hence, more work is needed that breaks these diagnoses down into their component symptom dimensions. As noted by Widiger and Clark (2000)
, models for the fundamental dimensions that constitute the internalizing domain continue to be developed (Mineka et al., 1998
; Watson, in press
), and efforts to delineate fundamental dimensions of externalizing are also underway (Krueger et al., in press
Clearly, however, much work is needed before a reorganization of the DSM along the lines adumbrated here is possible. Thus, for the time being, some intermediate steps can be suggested. First, as we build toward the DSM–V, we should consider converting the existing PD section to a system of facet-level constructs organized by the FFM domains, and pursue research and discussion on the most optimal facets, as well as the most optimal cut points on those facets to distinguish between personality and its pathological manifestations (cf. Livesley, 2001
). That is, adoption of a dimensional approach to the description of personality in the DSM does not mean abandoning a distinction between normality and abnormality. To the contrary, it sharpens discussions about how dimensions of symptoms and traits are related to concepts such as mental disorder and psychopathology. It necessitates research and discussion focused on the links between these concepts. For example, even if alcohol problems are dimensional in nature, such that there are no natural cutpoints demarcating heavy drinking, abuse, and dependence (Krueger et al., 2004
), there are levels of alcohol problems beyond which society and professionals would deem intervention warranted. Understanding where relevant cutpoints lie would involve research on the way in which symptomatology per se is linked to consequences (e.g., social and occupational dysfunction) and discussion with professionals and policymakers about levels of consequences that societies are unwilling to tolerate.
Second, we should consider reorganizing sections and disorders described in the DSM–IV–TR to recognize the internalizing and externalizing spectra, and pursue research and discussion on the most optimal organization of diagnoses within these spectra. Finally, we should encourage further research linking cutting-edge developments in methodology with novel ideas about how to describe and organize personality and psychopathology constructs. For example, Widiger and Clark (2000)
envisioned the creation of a “diagnostic table of the elements” for future editions of the DSM. What are the main dimensions that would organize such a table? Do these represent some meshing between the FFM and the internalizing and externalizing spectra? What are the quantitative properties that distinguish one “element of psychopathology” from another? Open-minded, creative research that asks probing and novel questions but sticks close to the data in pursuing these questions has real potential ultimately to result in a diagnostic system that is empirically supported, useful in the clinic, and inspires research that leads to better prevention and treatment of mental disorders.