Psychoneurometric assessment of dispositional liabilities for suicidal behavior: phenotypic and etiological associations.

BACKGROUND: Can core genetic liabilities for suicidal behavior be indexed using psychological and neural indicators combined? The current work addressed this question by examining phenotypic and genetic associations of two biobehavioral traits, threat sensitivity (THT) and disinhibition (DIS) - operationalized as psychoneurometric variables (i.e., composites of psychological-scale and neurophysiological measures) - with suicidal behaviors in a sample of adult twins. METHODS: Participants were 444 identical and fraternal twins recruited from an urban community. THT was assessed using a psychological-scale measure of fear/fearlessness combined with physiological indicators of reactivity to aversive pictures, and DIS was assessed using scale measures of disinhibitory tendencies combined with indicators of brain response from lab performance tasks. Suicidality was assessed using items from structured interview and questionnaire protocols. RESULTS: THT and DIS each contributed uniquely to prediction of suicidality when assessed psychoneurometrically (i.e., as composites of scale and neurophysiological indicators). In addition, these traits predicted suicidality interactively, with participants high on both reporting the greatest degree of suicidal behaviors. Biometric (twin-modeling) analyses revealed that a high percentage of the predictive association for each psychoneurometric trait (83% for THT, 68% for DIS) was attributable to genetic variance in common with suicidality. CONCLUSIONS: Findings indicate that psychoneurometric assessments of biobehavioral traits index genetic liability for suicidal behavior, and as such, can serve as innovative targets for research on core biological processes contributing to severe psychopathology, including suicidal proclivities and actions.

Declines in prevalence of adolescent substance use disorders and delinquent behaviors in the USA: a unitary trend?

BACKGROUND: Downward trends in a number of adolescent risk behaviors including violence, crime, and drug use have been observed in the USA in recent years. It is unknown whether these are separate trends or whether they might relate to a general reduction in propensity to engage in such behaviors. Our objectives were to quantify trends in substance use disorders (SUDs) and delinquent behaviors over the 2003-2014 period and to determine whether they might reflect a single trend in an Externalizing-like trait. METHODS: We analyzed data from 12 to 17 year old participants from the National Survey on Drug Use and Health, a representative survey of the household dwelling population of the USA, across the 2003-2014 period (N = 210 599). Outcomes included past-year prevalence of six categories of substance use disorder and six categories of delinquent behavior. RESULTS: Trend analysis suggested a net decline of 49% in mean number of SUDs and a 34% decline in delinquent behaviors over the 12-year period. Item Response Theory models were consistent with the interpretation that declines in each set of outcomes could be attributed to changes in mean levels of a latent, Externalizing-like trait. CONCLUSIONS: Our findings suggest that declines in SUDs and some delinquent behaviors reflect a single trend related to an Externalizing-like trait. Identifying the factors contributing to this trend may facilitate continued improvement across a spectrum of adolescent risk behaviors.

Deriving ICD-11 personality disorder domains from dsm-5 traits: initial attempt to harmonize two diagnostic systems.

OBJECTIVE: The personality disorder domains proposed for the ICD-11 comprise Negative Affectivity, Detachment, Dissociality, Disinhibition, and Anankastia, which are reasonably concordant with the higher-order trait domains in the Alternative DSM-5 Model for Personality Disorders. METHOD: We examined (i) whether designated DSM-5 trait facets can be used to describe the proposed ICD-11 trait domains, and (ii) how these ICD-11 trait features are hierarchically organized. A mixed Danish derivation sample (N = 1541) of 615 psychiatric out-patients and 925 community participants along with a US replication sample (N = 637) completed the Personality Inventory for DSM-5 (PID-5). Sixteen PID-5 traits were designated to cover features of the ICD-11 trait domains. RESULTS: Exploratory structural equation modeling (ESEM) analyzes showed that the designated traits were meaningfully organized in the proposed ICD-11 five-domain structure as well as other recognizable higher-order models of personality and psychopathology. Model fits revealed that the five proposed ICD-11 personality disorder domains were satisfactorily resembled, and replicated in the independent US sample. CONCLUSION: The proposed ICD-11 personality disorder domains can be accurately described using designated traits from the DSM-5 personality trait system. A scoring algorithm for the ICD-11 personality disorder domains is provided in appendix.

Do DSM-5 Section II personality disorders and Section III personality trait domains reflect the same genetic and environmental risk factors?

BACKGROUND: DSM-5 includes two conceptualizations of personality disorders (PDs). The classification in Section II is identical to the one found in DSM-IV, and includes 10 categorical PDs. The Alternative Model (Section III) includes criteria for dimensional measures of maladaptive personality traits organized into five domains. The degree to which the two conceptualizations reflect the same etiological factors is not known. METHODS: We use data from a large population-based sample of adult twins from the Norwegian Institute of Public Health Twin Panel on interview-based DSM-IV PDs and a short self-report inventory that indexes the five domains of the DSM-5 Alternative Model plus a domain explicitly targeting compulsivity. Schizotypal, Paranoid, Antisocial, Borderline, Avoidant, and Obsessive-compulsive PDs were assessed at the same time as the maladaptive personality traits and 10 years previously. Schizoid, Histrionic, Narcissistic, and Dependent PDs were only assessed at the first interview. Biometric models were used to estimate overlap in genetic and environmental risk factors. RESULTS: When measured concurrently, there was 100% genetic overlap between the maladaptive trait domains and Paranoid, Schizotypal, Antisocial, Borderline, and Avoidant PDs. For OCPD, 43% of the genetic variance was shared with the domains. Genetic correlations between the individual domains and PDs ranged from +0.21 to +0.91. CONCLUSION: The pathological personality trait domains, which are part of the Alternative Model for classification of PDs in DSM-5 Section III, appears to tap, at an aggregate level, the same genetic risk factors as the DSM-5 Section II classification for most of the PDs.

The association between personality disorders with alcohol use and misuse: A population-based twin study.

BACKGROUND: A clearer understanding of the etiological overlap between DSM-IV personality disorders (PDs) and alcohol use (AU) and alcohol use disorder (AUD) is needed. To our knowledge, no study has modeled the association between all 10 DSM-IV PDs and lifetime AU and AUD. The aim of the present study is to identify which PDs are most strongly associated with the phenotypic, genetic, and environmental risks of lifetime AU and AUD, and to determine if these associations are stable across time. METHODS: Participants were Norwegian twins assessed at two waves. At Wave 1, 2801 twins were assessed for all 10 DSM-IV PD criteria, lifetime AU, and DSM-IV AUD criteria. At Wave 2, six of the 10 PDs were again assessed along with AU and AUD among 2393 twins. Univariate and multiple logistic regressions were run. Significant predictors were further analyzed using bivariate twin Cholesky decompositions. RESULTS: Borderline and antisocial PD criteria were the strongest predictors of AU and AUD across the two waves. Despite moderate phenotypic and genetic correlations, genetic variation in these PD criteria explained only 4% and 3% of the risks in AU, and 5% to 10% of the risks in AUD criteria, respectively. At Wave 2, these estimates increased to 8% and 23% for AU, and 17% and 33% for AUD. CONCLUSIONS: Among a large Norwegian twin sample, borderline and antisocial PD criteria were the strongest predictors of the phenotypic and genotypic liability to AU and AUD. This effect remained consistent across time.

The Genetic and Environmental Sources of Resemblance Between Normative Personality and Personality Disorder Traits.

Recent work has suggested a high level of congruence between normative personality, most typically represented by the "big five" factors, and abnormal personality traits. In 2,293 Norwegian adult twins ascertained from a population-based registry, the authors evaluated the degree of sharing of genetic and environmental influences on normative personality, assessed by the Big Five Inventory (BFI), and personality disorder traits (PDTs), assessed by the Personality Inventory for DSM-5-Norwegian Brief Form (PID-5-NBF). For four of the five BFI dimensions, the strongest genetic correlation was observed with the expected PID-5-NBF dimension (e.g., neuroticism with negative affectivity [+], conscientiousness with disinhibition [-]). However, neuroticism, conscientiousness, and agreeableness had substantial genetic correlations with other PID-5-NBF dimensions (e.g., neuroticism with compulsivity [+], agreeableness with detachment [-]). Openness had no substantial genetic correlations with any PID-5-NBF dimension. The proportion of genetic risk factors shared in aggregate between the BFI traits and the PID-5-NBF dimensions was quite high for conscientiousness and neuroticism, relatively robust for extraversion and agreeableness, but quite low for openness. Of the six PID-5-NBF dimensions, three (negative affectivity, detachment, and disinhibition) shared, in aggregate, most of their genetic risk factors with normative personality traits. Genetic factors underlying psychoticism, antagonism, and compulsivity were shared to a lesser extent, suggesting that they are influenced by etiological factors not well indexed by the BFI.

Personality disorder in DSM-5: an oral history.

As the revision process leading to DSM-5 began, the domain of personality disorder embodied the highest aspirations for major change. After an initial prototype-based proposal failed to gain acceptance, the Personality and Personality Disorders Work Group (P&PDWG) developed a hybrid model containing categorical and dimensional components. A clash of perspectives both within the P&PDWG and between the P&PDWG and DSM-5 oversight committees led to the rejection of this proposal from the main body of DSM-5. Major issues included conflicting ways of conceptualizing validation, differences of opinion from personality disorder experts outside the P&PDWG, divergent concepts of the magnitude of evidence needed to support substantial changes, and the disagreements about clinical utility of the hybrid model. Despite these setbacks, the 'Alternative DSM-5 Model of Personality Disorder' is presented in Section III of the DSM-5. Further research should clarify its performance relative to the DSM-IV criteria reprinted in the main DSM-5 text.

The structure of adolescent psychopathology: a symptom-level analysis.

BACKGROUND: Most empirical studies into the covariance structure of psychopathology have been confined to adults. This work is not developmentally informed as the meaning, age-of-onset, persistence and expression of disorders differ across the lifespan. This study investigates the underlying structure of adolescent psychopathology and associations between the psychopathological dimensions and sex and personality risk profiles for substance misuse and mental health problems. METHOD: This study analyzed data from 2175 adolescents aged 13.3 years. Five dimensional models were tested using confirmatory factor analysis and the external validity was examined using a multiple-indicators multiple-causes model. RESULTS: A modified bifactor model, with three correlated specific factors (internalizing, externalizing, thought disorder) and one general psychopathology factor, provided the best fit to the data. Females reported higher mean levels of internalizing, and males reported higher mean levels of externalizing. No significant sex differences emerged in liability to thought disorder or general psychopathology. Liability to internalizing, externalizing, thought disorder and general psychopathology was characterized by a number of differences in personality profiles. CONCLUSIONS: This study is the first to identify a bifactor model including a specific thought disorder factor. The findings highlight the utility of transdiagnostic treatment approaches and the importance of restructuring psychopathology in an empirically based manner.

A longitudinal twin study of borderline and antisocial personality disorder traits in early to middle adulthood.

BACKGROUND: Antisocial personality disorder (ASPD) and borderline personality disorder (BPD) share genetic and environmental risk factors. Little is known about the temporal stability of these etiological factors in adulthood. METHOD: DSM-IV criteria for ASPD and BPD were assessed using structured interviews in 2282 Norwegian twins in early adulthood and again approximately 10 years later. Longitudinal biometric models were used to analyze the number of endorsed criteria. RESULTS: The mean criterion count for ASPD and BPD decreased 40% and 28%, respectively, from early to middle adulthood. Rank-order stability was 0.58 for ASPD and 0.45 for BPD. The best-fitting longitudinal twin model included only genetic and individual-specific environmental factors. Genetic effects, both those shared by ASPD and BPD, and those specific to each disorder remained completely stable. The unique environmental effects, however, changed substantially, with a correlation across time of 0.19 for the shared effects, and 0.39 and 0.15, respectively, for those specific to ASPD and BPD. Genetic effects accounted for 71% and 72% of the stability over time for ASPD and BPD, respectively. The genetic and environmental correlations between ASPD and BPD were 0.73, and 0.43, respectively, at both time points. CONCLUSION: ASPD and BPD traits were moderately stable from early to middle adulthood, mostly due to genetic risk factors which did not change over the 10-year assessment period. Environmental risk factors were mostly transient, and appear to be the main source of phenotypic change. Genetic liability factors were, to a large extent, shared by ASPD and BPD.

A longitudinal twin study of cluster A personality disorders.

BACKGROUND: While cluster A personality disorders (PDs) have been shown to be moderately heritable, we know little about the temporal stability of these genetic risk factors. METHOD: Paranoid PD (PPD) and schizotypal PD (STPD) were assessed using the Structured Interview for DSM-IV Personality in 2793 young adult twins from the Norwegian Institute of Public Health Twin Panel at wave 1 and 2282 twins on average 10 years later at wave 2. Using the program Mx, we fitted a longitudinal latent factor model using the number of endorsed criteria for PPD and STPD. RESULTS: The stability over time of the criteria counts for PPD and STPD, estimated as polychoric correlations, were +0.34 and +0.40, respectively. The best-fit longitudinal model included only additive genetic and individual-specific environmental factors with parameter estimates constrained to equality across the two waves. The cross-wave genetic and individual-specific environmental correlations for a latent cluster A factor were estimated to equal +1.00 and +0.13, respectively. The cross-time correlations for genetic and environmental effects specific to the individual PDs were estimated at +1.00 and +0.16-0.20, respectively. We found that 68% and 71% of the temporal stability of PPD and STPD derived, respectively, from the effect of genetic factors. CONCLUSION: Shared genetic risk factors for two of the cluster A PDs are highly stable in adults over a 10-year period while environmental risk factors are relatively transient. Over two-thirds of the long-term stability of the common cluster A PD liability can be attributed to genetic influences.

Examining the shared and unique relationships among substance use and mental disorders.

BACKGROUND: Co-morbidity among use of different substances can be explained by a shared underlying dimensional factor. What remains unknown is whether the relationship between substance use and various co-morbid mental disorders can be explained solely by the general factor or whether there remain unique contributions of specific substances. METHOD: Data were from the 2007 Australian National Survey of Mental Health and Wellbeing (NSMHWB). A unidimensional latent factor was constructed that represented general substance use. The shared and specific relationships between lifetime substance use indicators and internalizing disorders, suicidality and psychotic-like experiences (PLEs) were examined using Multiple Indicators Multiple Causes (MIMIC) models in the total sample. Additional analyses then examined the shared and specific relationships associated with substance dependence diagnoses as indicators of the latent trait focusing on a subsample of substance users. RESULTS: General levels of latent substance use were significantly and positively related to internalizing disorders, suicidality and psychotic-like experiences. Similar results were found when examining general levels of latent substance dependence in a sample of substance users. There were several direct effects between specific substance use/dependence indicators and the mental health correlates that significantly improved the overall model fit but they were small in magnitude and had relatively little impact on the general relationship. CONCLUSIONS: The majority of pairwise co-morbid relationships between substance use/dependence and mental health correlates can be explained through a general latent factor. Researchers should focus on investigating the commonalities across all substance use and dependence indicators when studying mental health co-morbidity.

Modeling and treating internalizing psychopathology in a clinical trial: a latent variable structural equation modeling approach.

BACKGROUND: Clinical trials are typically designed to test the effect of a specific treatment on a single diagnostic entity. However, because common internalizing disorders are highly correlated ('co-morbid'), we sought to establish a practical and parsimonious method to characterize and quantify changes in a broad spectrum of internalizing psychopathology targeted for treatment in a clinical trial contrasting two transdiagnostic psychosocial interventions. METHOD: Alcohol dependence treatment patients who had any of several common internalizing disorders were randomized to a six-session cognitive-behavioral therapy (CBT) experimental treatment condition or a progressive muscle relaxation training (PMRT) comparison treatment condition. Internalizing psychopathology was characterized at baseline and 4 months following treatment in terms of the latent structure of six distinct internalizing symptom domain surveys. RESULTS: Exploratory structural equation modeling (ESEM) identified a two-factor solution at both baseline and the 4-month follow-up: Distress (measures of depression, trait anxiety and worry) and Fear (measures of panic anxiety, social anxiety and agoraphobia). Although confirmatory factor analysis (CFA) demonstrated measurement invariance between the time-points, structural models showed that the latent means of Fear and Distress decreased substantially from baseline to follow-up for both groups, with a small but statistically significant advantage for the CBT group in terms of Distress (but not Fear) reduction. CONCLUSIONS: The approach demonstrated in this study provides a practical solution to modeling co-morbidity in a clinical trial and is consistent with converging evidence pointing to the dimensional structure of internalizing psychopathology.

Thought disorder in the meta-structure of psychopathology.

BACKGROUND: Dimensional models of co-morbidity have the potential to improve the conceptualization of mental disorders in research and clinical work, yet little is known about how relatively uncommon disorders may fit with more common disorders. The present study estimated the meta-structure of psychopathology in the US general population focusing on the placement of five under-studied disorders sharing features of thought disorder: paranoid, schizoid, avoidant and schizotypal personality disorders, and manic episodes as well as bipolar disorder. METHOD: Data were drawn from the National Epidemiologic Survey on Alcohol and Related Conditions, a face-to-face interview of 34 653 non-institutionalized adults in the US general population. The meta-structure of 16 DSM-IV Axis I and Axis II psychiatric disorders, as assessed by the Alcohol Use Disorder and Associated Disabilities Interview Schedule DSM-IV version (AUDADIS-IV), was examined using exploratory and confirmatory factor analysis. RESULTS: We document an empirically derived thought disorder factor that is a subdomain of the internalizing dimension, characterized by schizoid, paranoid, schizotypal and avoidant personality disorders as well as manic episodes. Manic episodes exhibit notable associations with both the distress subdomain of the internalizing dimension as well as the thought disorder subdomain. The structure was replicated for bipolar disorder (I or II) in place of manic episodes. CONCLUSIONS: As our understanding of psychopathological meta-structure expands, incorporation of disorders characterized by detachment and psychoticism grows increasingly important. Disorders characterized by detachment and psychoticism may be well conceptualized, organized and measured as a subdimension of the internalizing spectrum of disorders. Manic episodes and bipolar disorder exhibit substantial co-morbidity across both distress and thought disorder domains of the internalizing dimension. Clinically, these results underscore the potential utility of conceptualizing patient treatment needs using an approach targeting psychopathological systems underlying meta-structural classification rubrics.

Delineating physiologic defensive reactivity in the domain of self-report: phenotypic and etiologic structure of dispositional fear.

BACKGROUND: Individual differences in fear and fearlessness have been investigated at their extremes in relation to markedly different forms of psychopathology--anxiety disorders and psychopathy, respectively. A documented neural substrate of fear-related traits and disorders is defensive reactivity as reflected in aversive startle potentiation (ASP). METHOD: The current study extended prior work by characterizing, in a sample of adult twins from the community (n = 2511), the phenotypic and etiologic structure of self-report measures of fear and fearlessness known to be associated with ASP. RESULTS: Analyses revealed a hierarchical structure to the trait fear domain, with an overarching, bipolar fear/fearlessness dimension saturating each measure in this domain, and subfactors labeled 'distress,' 'stimulation seeking' and 'sociability' accounting for additional variance in particular measures. The structure of genetic and non-shared environmental associations among the measures closely mirrored the phenotypic structure of the domain. CONCLUSIONS: The findings have implications for proposals to reconceptualize psychopathology in neurobiological terms.

Initial construction of a maladaptive personality trait model and inventory for DSM-5.

BACKGROUND: DSM-IV-TR suggests that clinicians should assess clinically relevant personality traits that do not necessarily constitute a formal personality disorder (PD), and should note these traits on Axis II, but DSM-IV-TR does not provide a trait model to guide the clinician. Our goal was to provide a provisional trait model and a preliminary corresponding assessment instrument, in our roles as members of the DSM-5 Personality and Personality Disorders Workgroup and workgroup advisors. METHOD: An initial list of specific traits and domains (broader groups of traits) was derived from DSM-5 literature reviews and workgroup deliberations, with a focus on capturing maladaptive personality characteristics deemed clinically salient, including those related to the criteria for DSM-IV-TR PDs. The model and instrument were then developed iteratively using data from community samples of treatment-seeking participants. The analytic approach relied on tools of modern psychometrics (e.g. item response theory models). RESULTS: A total of 25 reliably measured core elements of personality description emerged that, together, delineate five broad domains of maladaptive personality variation: negative affect, detachment, antagonism, disinhibition, and psychoticism. CONCLUSIONS: We developed a maladaptive personality trait model and corresponding instrument as a step on the path toward helping users of DSM-5 assess traits that may or may not constitute a formal PD. The inventory we developed is reprinted in its entirety in the Supplementary online material, with the goal of encouraging additional refinement and development by other investigators prior to the finalization of DSM-5. Continuing discussion should focus on various options for integrating personality traits into DSM-5.

The structure of depression, anxiety and somatic symptoms in primary care.

BACKGROUND: Observed co-morbidity among the mood and anxiety disorders has led to the development of increasingly sophisticated dimensional models to represent the common and unique features of these disorders. Patients often present to primary care settings with a complex mixture of anxiety, depression and somatic symptoms. However, relatively little is known about how somatic symptoms fit into existing dimensional models. METHOD: We examined the structure of 91 anxiety, depression and somatic symptoms in a sample of 5433 primary care patients drawn from 14 countries. One-, two- and three-factor lower-order models were considered; higher-order and hierarchical variants were studied for the best-fitting lower-order model. RESULTS: A hierarchical, bifactor model with all symptoms loading simultaneously on a general factor, along with one of three specific anxiety, depression and somatic factors, was the best-fitting model. The general factor accounted for the bulk of symptom variance and was associated with psychosocial dysfunction. Specific depression and somatic symptom factors accounted for meaningful incremental variance in diagnosis and dysfunction, whereas anxiety variance was associated primarily with the general factor. CONCLUSIONS: The results (a) are consistent with previous studies showing the presence and importance of a broad internalizing or distress factor linking diverse emotional disorders, and (b) extend the bounds of internalizing to include somatic complaints with non-physical etiologies.

Meta-analysis of genome-wide association studies for personality.

Personality can be thought of as a set of characteristics that influence people's thoughts, feelings and behavior across a variety of settings. Variation in personality is predictive of many outcomes in life, including mental health. Here we report on a meta-analysis of genome-wide association (GWA) data for personality in 10 discovery samples (17,375 adults) and five in silico replication samples (3294 adults). All participants were of European ancestry. Personality scores for Neuroticism, Extraversion, Openness to Experience, Agreeableness and Conscientiousness were based on the NEO Five-Factor Inventory. Genotype data of ≈ 2.4M single-nucleotide polymorphisms (SNPs; directly typed and imputed using HapMap data) were available. In the discovery samples, classical association analyses were performed under an additive model followed by meta-analysis using the weighted inverse variance method. Results showed genome-wide significance for Openness to Experience near the RASA1 gene on 5q14.3 (rs1477268 and rs2032794, P=2.8 × 10(-8) and 3.1 × 10(-8)) and for Conscientiousness in the brain-expressed KATNAL2 gene on 18q21.1 (rs2576037, P=4.9 × 10(-8)). We further conducted a gene-based test that confirmed the association of KATNAL2 to Conscientiousness. In silico replication did not, however, show significant associations of the top SNPs with Openness and Conscientiousness, although the direction of effect of the KATNAL2 SNP on Conscientiousness was consistent in all replication samples. Larger scale GWA studies and alternative approaches are required for confirmation of KATNAL2 as a novel gene affecting Conscientiousness.

Genome-wide association study of conduct disorder symptomatology.

Conduct disorder (CD) is one of the most prevalent childhood psychiatric conditions, and is associated with a number of serious concomitant and future problems. CD symptomatology is known to have a considerable genetic component, with heritability estimates in the range of 50%. Despite this, there is a relative paucity of studies aimed at identifying genes involved in the susceptibility to CD. In this study, we report results from a genome-wide association study of CD symptoms. CD symptoms were retrospectively reported by a psychiatric interview among a sample of cases and controls, in which cases met the criteria for alcohol dependence. Our primary phenotype was the natural log transformation of the number of CD symptoms that were endorsed, with data available for 3963 individuals who were genotyped on the Illumina Human 1M beadchip array. Secondary analyses are presented for case versus control status, in which caseness was established as endorsing three or more CD symptoms (N = 872 with CD and N = 3091 without CD). We find four markers that meet the criteria for genome-wide significance (P<5 × 10(-8)) with the CD symptom count, two of which are located in the gene C1QTNF7 (C1q and tumor necrosis factor-related protein 7). There were six additional SNPs in the gene that yielded converging evidence of association. These data provide the first evidence of a specific gene that is associated with CD symptomatology. None of the top signals resided in traditional candidate genes, underscoring the importance of a genome-wide approach for identifying novel variants involved in this serious childhood disorder.

Borderline personality disorder co-morbidity: relationship to the internalizing-externalizing structure of common mental disorders.

BACKGROUND: Borderline personality disorder (BPD) shows high levels of co-morbidity with an array of psychiatric disorders. The meaning and causes of this co-morbidity are not fully understood. Our objective was to investigate and clarify the complex co-morbidity of BPD by integrating it into the structure of common mental disorders. METHOD: We conducted exploratory and confirmatory factor analyses on diagnostic interview data from a representative US population-based sample of 34 653 civilian, non-institutionalized individuals aged ≥18 years. We modeled the structure of lifetime DSM-IV diagnoses of BPD and antisocial personality disorder (ASPD), major depressive disorder, dysthymic disorder, panic disorder with agoraphobia, social phobia, specific phobia, generalized anxiety disorder, post-traumatic stress disorder, alcohol dependence, nicotine dependence, marijuana dependence, and any other drug dependence. RESULTS: In both women and men, the internalizing-externalizing structure of common mental disorders captured the co-morbidity among all disorders including BPD. Although BPD was unidimensional in terms of its symptoms, BPD as a disorder showed associations with both the distress subfactor of the internalizing dimension and the externalizing dimension. CONCLUSIONS: The complex patterns of co-morbidity observed with BPD represent connections to other disorders at the level of latent internalizing and externalizing dimensions. BPD is meaningfully connected with liabilities shared with common mental disorders, and these liability dimensions provide a beneficial focus for understanding the co-morbidity, etiology and treatment of BPD.

Contrasting prototypes and dimensions in the classification of personality pathology: evidence that dimensions, but not prototypes, are robust.

BACKGROUND: DSM-5 may mark the shift from a categorical classification of personality pathology to a dimensional system. Although dimensional and categorical conceptualizations of personality pathology are often viewed as competing, it is possible to develop categories (prototypes) from combinations of dimensions. Robust prototypes could bridge dimensions and categories within a single classification system. METHOD: To explore prototype structure and robustness, we used finite mixture modeling to identify empirically derived personality pathology prototypes within a large sample (n=8690) of individuals from four settings (clinical, college, community, and military), assessed using a dimensional measure of normal and abnormal personality traits, the Schedule for Nonadaptive and Adaptive Personality (SNAP). We then examined patterns of convergent and discriminant external validity for prototypes. Finally, we investigated the robustness of the dimensional structure of personality pathology. RESULTS: The resulting prototypes were meaningful (externally valid) but non-robust (sample dependent). By contrast, factor analysis revealed that the dimensional structures underlying specific traits were highly robust across samples. CONCLUSIONS: We interpret these results as further evidence of the fundamentally dimensional nature of an empirically based classification of personality pathology.