Intra- and extra-familial influences on alcohol and drug misuse: a twin study of gene-environment correlation.

AIMS: Genotype-environment correlation refers to the extent to which individuals are exposed to environments as a function of their genetic propensities. These correlations are important in the study of psychopathology because they identify environments that may maintain the expression of underlying genetic liabilities for a disorder. The present study examined the correlation between genetic liabilities for alcohol and drug misuse with perceptions of the social environments of the family of origin and the classroom. DESIGN: Postal survey data were collected from monozygotic and dizygotic twin pairs. SETTING: Twin pairs were recruited from Vancouver, British Columbia, Canada using newspaper advertisements and media stories. PARTICIPANTS: Eighty-five monozygotic and 77 dizygotic twin pairs were recruited from the general population. MEASUREMENTS: Twin pairs completed self-report measures of alcohol and drug misuse contained in the Dimensional Assessment of Personality Pathology, the Family Environment Scale, the Classroom Environment Scale, and the Traumatic Events Questionnaire. FINDINGS: Genetically indexed alcohol and drug misuse scores were regressed on the environmentally indexed FES and CES scales. Genetic liabilities for alcohol and drug misuse were associated with decreased perceived family moral-religious emphases, family cohesion and classroom task orientation and increased perceptions of classroom order and organization (strictness). CONCLUSIONS: Genotype-environment correlations, in particular, moral-religious emphases in the home, appear to be important in the development of substance misuse.

Sources of structure: genetic, environmental, and artifactual influences on the covariation of personality traits.

The phenotypic structure of personality traits has been well described, but it has not yet been explained causally. Behavior genetic covariance analyses can identify the underlying causes of phenotypic structure; previous behavior genetic research has suggested that the effects from both genetic and nonshared environmental influences mirror the phenotype. However, nonshared environmental effects are usually estimated as a residualterm that may also include systematic bias, such as that introduced by implicit personality theory. To reduce that bias, we supplemented data from Canadian and German twin studies with cross-observer correlations on the Revised NEO Personality Inventory. The hypothesized five-factor structure was found in both the phenotypic and genetic/familial covariances. When the residual covariance was decomposed into true nonshared environmental influences and method bias, only the latter showed the five-factor structure. True nonshared environmental influences are not structured as genetic influences are, although there was some suggestion that they do affect two personality dimensions, Conscientiousness and Love. These data reaffirm the value of behavior genetic analyses for research on the underlying causes of personality traits.

Covariance structure of neuroticism and agreeableness: a twin and molecular genetic analysis of the role of the serotonin transporter gene.

The Revised NEO Personality Inventory domains of Neuroticism and Agreeableness are considered factorially distinct despite several intercorrelations between these domains. The genetic correlation, an index of the degree to which these intercorrelations are caused by genetic influences, was estimated using data from 913 monozygotic and 562 dizygotic volunteer twin pairs from Canada, Germany, and Japan. The serotonin transporter gene, 5-HTTLPR, was assayed in a sample of 388 nontwin sibling pairs from the United States to determine the contribution of the serotonin transporter locus to the covariation between the Neuroticism and Agreeableness scales. In all four samples, genetic influences contributed to the covariance of Neuroticism and Agreeableness, with the serotonin transporter gene accounting for 10% of the relationship between these domains.

Commentary on reconceptualizing personality disorder categories using trait dimensions.

The ability of trait models of personality to account for categories of personality disorder is examined with particular reference to the five-factor approach. Although dimensional models are consistent with the evidence, and trait models can accommodate personality disorder categories, it is not clear that such models are directly applicable to clinical use. The lower-order or facet structure, in particular, needs further development to capture clinical concepts. It is also suggested that trait models do not account for all aspects of personality disorder-attention also needs to be paid to the organizing and integrative functions of personality.

Behavioural-genetic perspectives on personality function.

In the wake of the recent announcements that the human genome has been mapped, efforts to identify the genetic loci underlying personality function will grow and intensify. Much research has already been done in this area, but it has for the most part been limited to classical biometrical approaches designed to determine if personality has a heritable basis. These so-called "heritability" studies estimate how much of the individual differences in personality are attributable to genetic differences among people. Molecular-genetic approaches, on the other hand, are designed to identify specific putative loci, but have yielded mixed results. The inconsistency in research findings can be attributed in part to the lack of sufficient numbers of genetic markers in the chromosomal regions of interest--a problem that the creation of a map of the human genome will help to rectify. This map and its inevitable refinements, however, can only advance the search for the genes for personality to a limited degree. Serious unresolved problems in the conceptualization and definition of personality and its dysfunction remain, which will hamper the search for personality genes.

Personality disorder traits, family environment, and alcohol misuse: a multivariate behavioural genetic analysis.

AIMS: This study seeks to estimate the extent to which a common genetic and environmental basis is shared between (i) traits delineating specific aspects of antisocial personality and alcohol misuse, and (ii) childhood family environments, traits delineating broad domains of personality pathology and alcohol misuse. DESIGN: Postal survey data were collected from monozygotic and dizygotic twin pairs. SETTING: Twin pairs were recruited from Vancouver, British Columbia and London, Ontario, Canada using newspaper advertisements, media stories and twin clubs. PARTICIPANTS: Data obtained from 324 monozygotic and 335 dizygotic twin pairs were used to estimate the extent to which traits delineating specific antisocial personality traits and alcohol misuse shared a common genetic and environmental aetiology. Data from 81 monozygotic and 74 dizygotic twin pairs were used to estimate the degree to which traits delineating personality pathology, childhood family environment and alcohol misuse shared a common aetiology. MEASUREMENTS: Current alcohol misuse and personality pathology were measured using scales contained in the self-report Dimensional Assessment of Personality Pathology. Perceptions of childhood family environment were measured using the self-report Family Environment Scale. FINDINGS: Multivariate genetic analyses showed that a subset of traits delineating components of antisocial personality (i.e. grandiosity, attention-seeking, failure to adopt social norms, interpersonal violence and juvenile antisocial behaviours) are influenced by genetic factors in common to alcohol misuse. Genetically based perceptions of childhood family environment had little relationship with alcohol misuse. CONCLUSIONS: Heritable personality factors that influence the perception of childhood family environment play only a small role in the liability to alcohol misuse. Instead, liability to alcohol misuse is related to genetic factors common a specific subset of antisocial personality traits describing conduct problems, narcissistic and stimulus-seeking behaviour.

Toward an empirically based classification of personality disorder.

A framework for an empirically based classification of personality disorder is proposed that has two components: (a) a definition of personality disorder, and (b) a scheme for describing individual differences in personality disorder traits. It is suggested that the diagnosis process should begin by establishing the presence of personality disorder and then proceed to a description of the personality on a set of trait dimensions. It is argued that a definition of personality disorder should reflect an understanding of the nature of the "harmful dysfunction" implied by a diagnosis of personality disorder. With this approach, personality disorder is defined as the failure to solve life tasks involving the development of integrated representations of self and others, and the capacity for adaptive kinship and societal relationships. The second component of a classification is a system to describe individual differences. It is suggested that these should be based on taxonomies of normal and disordered traits, and that the classification incorporates both higher-order patterns and more specific basic traits. Given that personality appears to be inherited as a large number of genetic dimensions, it is suggested that the primary level for describing individual differences is that of the basic or lower-level traits rather than broader or higher-level traits used in descriptions of normal personality.

A practical approach to the treatment of patients with borderline personality disorder.

This approach to the treatment of BPD is part of a general framework for treating all forms of personality disorder. The therapeutic model has two components: (1) general strategies to manage core self and interpersonal pathology that characterizes all cases of personality disorder and (2) a specific or tailored component required to treat the problems of individual cases. The general strategies, derived from generic models of therapeutic change and self-psychology, emphasize the therapeutic relationship and the importance of a consistent treatment process, validation, and building motivation. A combination of specific interventions, including medication and psychotherapeutic strategies drawn from treatment approaches, is incorporated into this framework as required. The overall model is not an eclectic approach to treatment but an integrated framework based on an understanding of borderline pathology that emerges from recent research.

Why do measures of normal and disordered personality correlate? A study of genetic comorbidity.

The genetic and environmental correlations between measures of normal (NEO-FFI) and abnormal personality (Dimensional Assessment of Personality Pathology: DAPP-BQ) were estimated in a sample of 545 volunteer general population twin pairs (269 monozygotic and 276 dizygotic pairs). The largest genetic correlations were observed between the 18 DAPP-BQ dimensions and NEO-FFI neuroticism (range = .05 to .81; median = .48), extraversion (range = -.65 to .33; median = -.28), agreeableness (range = -.65 to .00; median = -.38), and conscientiousness (range = -.76 to .52; median = -.31). The smallest genetic correlations were found between the DAPP-BQ dimensions and NEO-FFI openness (range = -.17 to .20; median = -.04). The environmental correlations are lower in magnitude but show the same pattern of correlations between DAPP-BQ and NEO-FFI scales. These results indicate that these two scales share a common broad-based genetic architecture, whereas the environmental influences show greater scale specificity.

Dimensional assessment of personality pathology in patients with eating disorders.

This study examined patients with eating disorders on personality pathology using a dimensional method. Female subjects who met DSM-IV diagnostic criteria for eating disorder (n = 136) were evaluated and compared to an age-controlled general population sample (n = 68). We assessed 18 features of personality disorder with the Dimensional Assessment of Personality Pathology - Basic Questionnaire (DAPP-BQ). Factor analysis and cluster analysis were used to derive three clusters of patients. A five-factor solution was obtained with limited intercorrelation between factors. Cluster analysis produced three clusters with the following characteristics: Cluster 1 members (constituting 49.3% of the sample and labelled 'rigid') had higher mean scores on factors denoting compulsivity and interpersonal difficulties; Cluster 2 (18.4% of the sample) showed highest scores in factors denoting psychopathy, neuroticism and impulsive features, and appeared to constitute a borderline psychopathology group; Cluster 3 (32.4% of the sample) was characterized by few differences in personality pathology in comparison to the normal population sample. Cluster membership was associated with DSM-IV diagnosis -- a large proportion of patients with anorexia nervosa were members of Cluster 1. An empirical classification of eating-disordered patients derived from dimensional assessment of personality pathology identified three groups with clinical relevance.

Heritability of anxiety sensitivity: a twin study.

OBJECTIVE: In attempting to explain the familial predisposition to panic disorder, most studies have focused on the heritability of physiologic characteristics (e.g., CO2 sensitivity). A heretofore unexplored possibility is that a psychological characteristic that predisposes to panic-anxiety sensitivity-might be inherited. In this study, the authors examined the heritability of anxiety sensitivity through use of a twin group. METHOD: Scores on the Anxiety Sensitivity Index were examined in a group of 179 monozygotic and 158 dizygotic twin pairs. Biometrical model fitting was conducted through use of standard statistical methods. RESULTS: Broad heritability estimate of the Anxiety Sensitivity Index as a unifactorial construct was 45%. Additive genetic effects and unique environmental effects emerged as the primary influences on anxiety sensitivity. There was no evidence of genetic discontinuity between normal and extreme scores on the Anxiety Sensitivity Index. CONCLUSIONS: This study suggests that one psychological risk factor for the development of panic disorder-anxiety sensitivity-may have a heritable component. As such, anxiety sensitivity should be considered in future research on the heritability of panic disorder.

Gender differences in the etiology of anxiety sensitivity: a twin study.

OBJECTIVE: To estimate the magnitude of genetic and environmental factors on anxiety sensitivity by gender. DESIGN: Classic twins reared-together study design. PATIENTS: A community sample of 337 twin pairs, including 179 monozygotic (45 brother and 134 sister pairs) and 158 dizygotic (28 brother, 94 sister, and 36 brother-sister pairs). METHOD: Twin pairs completed the Anxiety Sensitivity Index (ASI) using a postal survey design. The ASI is composed of three factors: (1) fear of anxiety-related somatic sensations; (2) fear of cognitive dyscontrol due to beliefs that sensations like depersonalization are signs of mental illness (e.g., fear of concentration problems); and (3) fear of publicly observable anxiety reactions (e.g., fear of trembling). Biometrical modeling techniques were used to estimate heritability of the ASI dimensions by gender. RESULTS: ASI factors are heritable only in women, accounting for 37% to 48% of the total variance (median, 44.5%). Environmental factors accounted for all the variability in men. CONCLUSIONS: These findings have implications for understanding the etiology of panic disorder. Previous research suggests that anxiety sensitivity is a risk factor or diathesis for this disorder, and that panic disorder is more prevalent in women than men. Our findings suggest the hypothesis that the increased prevalence in women may occur because anxiety sensitivity is heritable in women.

Phenotypic and genetic structure of traits delineating personality disorder.

BACKGROUND: The evidence suggests that personality traits are hierarchically organized with more specific or lower-order traits combining to form more generalized higher-order traits. Agreement exists across studies regarding the lower-order traits that delineate personality disorder but not the higher-order traits. This study seeks to identify the higher-order structure of personality disorder by examining the phenotypic and genetic structures underlying lower-order traits. METHODS: Eighteen lower-order traits were assessed using the Dimensional Assessment of Personality Disorder-Basic Questionnaire in samples of 656 personality disordered patients, 939 general population subjects, and a volunteer sample of 686 twin pairs. RESULTS: Principal components analysis yielded 4 components, labeled Emotional Dysregulation, Dissocial Behavior, Inhibitedness, and Compulsivity, that were similar across the 3 samples. Multivariate genetic analyses also yielded 4 genetic and environmental factors that were remarkably similar to the phenotypic factors. Analysis of the residual heritability of the lower-order traits when the effects of the higher-order factors were removed revealed a substantial residual heritable component for 12 of the 18 traits. CONCLUSIONS: The results support the following conclusions. First, the stable structure of traits across clinical and nonclinical samples is consistent with dimensional representations of personality disorders. Second, the higher-order traits of personality disorder strongly resemble dimensions of normal personality. This implies that a dimensional classification should be compatible with normative personality. Third, the residual heritability of the lower-order traits suggests that the personality phenotypes are based on a large number of specific genetic components.

Twin study of dissociative experience.

The relative influence of genetic and environmental influences on measures of pathological and nonpathological dissociative experience was estimated using a classic twin-study design. Subjects were 177 monozygotic and 152 dizygotic volunteer general population twin pairs who completed two measures of dissociative capacity identified from the items comprising the Dissociative Experiences Scale (DES). Additive genetic influences accounted for 48% and 55% of the variance in scales measuring pathological and nonpathological dissociative experience, respectively. Heritability estimates did not differ by gender. The genetic correlation between these measures was estimated at .91, suggesting common genetic factors underlying pathological and nonpathological dissociative capacity. Genetic and environmental correlations between the DES scales and measures of personality disorder traits (Dimensional Assessment of Personality Pathology-Basic Questionnaire; DAPP-BQ) were also estimated. Significant genetic correlations (median = .38) were found between the DES scales and DAPP-BQ cognitive dysregulation, affective lability, and suspiciousness, suggesting that the genetic factors underlying particular aspects of personality disorder also influence dissociative capacity.

Heritability of facet-level traits in a cross-cultural twin sample: support for a hierarchical model of personality.

The common variance among personality traits can be summarized in the factors of the five-factor model, which are known to be heritable. This study examined heritability of the residual specific variance in facet-level traits from the Revised NEO Personality Inventory. Analyses of raw and residual facet scales across Canadian (183 monozygotic [MZ] and 175 dizogotic [DZ] pairs) and German (435 MZ and 205 DZ pairs) twin samples showed genetic and environmental influences of the same type and magnitude across the 2 samples for most facets. Additive genetic effects accounted for 25% to 65% of the reliable specific variance. Results provide strong support for hierarchical models of personality that posit a large number of narrow traits in addition to a few broader trait factors or domains. Facet-level traits are not simply exemplars of the broad factors they define; they are discrete constructs with their own heritable and thus biological basis.

Seasonal mood change and personality: an investigation of genetic co-morbidity.

Clinical observations and empirical studies suggest that Seasonal Affective Disorder (SAD) is related to personality. The present study estimates the genetic and environmental correlations between the Global Seasonality Score (GSS) from the Seasonal Pattern Assessment Questionnaire and personality measures, assessed using the NEO Five Factor Inventory (NEO-FFI) and the Dimensional Assessment of Personality Pathology (DAPP) in a volunteer sample of 163 monozygotic (MZ) pairs (102 female and 61 male pairs) and 134 dizygotic (DZ) pairs (70 female, 38 male and 26 opposite-sex pairs). Large genetic correlations were found between the GSS and NEO-FFI Neuroticism (0.52: 95% CI = 0.36-0.71) and DAPP-BQ Cognitive Dysregulation (0.50: 95% CI = 0.30-0.71), Affective Lability (0.49: 95% CI = 0.29-0.77), Anxiousness (0.37: 95% CI = 0.18-0.55) and Stimulus Seeking (0.45: 95% CI = 0.25-0.64) scales. The genetic correlations with the remaining scales, such as Extraversion (0.06: 95% CI = -0.16-0.26), Compulsivity (-0.09: 95% CI = -0.31-0.12) and Submissiveness (0.15: 95% CI = -0.05-0.34) were uniformly small. All environmental correlations between the GSS and personality scales were < or = 0.19. These results provide evidence that the observed correlations between these seasonality and personality dimensions are attributable to common genetic factors and that environmental influences are domain specific.

Suggestions for a framework for an empirically based classification of personality disorder.

BACKGROUND: The classification of personality disorder is one of the least satisfactory sections of contemporary psychiatric classification. Fundamental problems with current classifications include extensive diagnostic overlap, limited evidence of validity, and poor empirical support. METHODS: Conceptual analysis and the results of empirical studies are used to propose a framework for organizing an empirically based classification. RESULTS: First, personality disorder is a form of mental disorder and, therefore, should be classified as a single diagnostic entity on Axis I along with other mental disorders. A preliminary definition of personality disorder as a tripartite failure involving the self system, kinship relationships, and societal relationships is proposed. The evidence suggests that this definition can be translated into a reliable set of items. Second, the diagnosis of personality disorder should be separated from the assessment of clinically relevant personality traits. Given the consistent evidential support for a dimensional model of personality disorder, it is suggested that personality be coded on a set of trait dimensions selected to provide a systematic representation of the domain of behaviours represented by current diagnostic concepts. Third, given that personality traits are hierarchically organized, it is suggested that an axis for coding personality include basic or lower-order dimensions as the primary level of assessment and a few higher-order patterns to summarize information for some purposes. CONCLUSION: A preliminary list of 16 basic dispositional traits is proposed to describe the more specific components of personality disorder based, in part, on the convergence of evidence across studies: anxiousness, affective lability, callousness, cognitive dysregulation, compulsivity, conduct problems, insecure attachment, intimacy avoidance, narcissism, oppositionality, rejection, restricted expression, social avoidance, stimulus seeking, submissiveness, and suspiciousness. Three higher-order patterns were proposed: emotional dysregulation, dissocial behaviour, and inhibitedness, which may occur independently or in combination.

Personality disorder assessment: the challenge of construct validity.

We begin with a review of the data that challenge the current categorical system for classifying personality disorder, focusing on the central assessment issues of convergent and discriminant validity. These data indicate that while there is room for improvement in assessment, even greater change is needed in conceptualization than in instrumentation. Accordingly, we then refocus the categorical-dimensional debate in assessment terms, and place it in the broader context of such issues as the hierarchical structure of personality, overlap and distinctions between normal and abnormal personality, sources of information in personality disorder assessment, and overlap and discrimination of trait and state assessment. We conclude that more complex conceptual models that can incorporate both biological and environmental influences on the development of adaptive and maladaptive personality are needed.

The relationship between seasonal mood change and personality: more apparent than real?

A number of recent research reports have reported significant relationships between seasonal mood change (seasonality) and personality. However, some of the results are difficult to interpret because of inherent methodological problems, the most important of which is the use of samples drawn from the southern as opposed to the northern hemisphere, where the phenomenon of seasonality may be quite different. The present study examined the relationship between personality and seasonality in a sample from the northern hemisphere (minimum latitude = 49 degrees N). A total of 297 adults drawn from the general population (112 male and 185 female subjects) completed the Seasonal Pattern Assessment Questionnaire, and the results obtained confirmed most of the previously reported relationships and showed that these are reliable across (i) different hemispheres, (ii) different measures of personality and (iii) clinical and general population samples. However, the impact of the relationship seems to be more apparent than real, with personality accounting for just under 15% of the total variance.

Gender differences in the heritability of seasonal mood change.

The study estimated gender differences in the magnitude of genetic and environmental influence in seasonal mood change. The self-report Seasonal Pattern Assessment Questionnaire (SPAQ) was completed by 339 volunteer reared-together twinpairs (187 monozygotic pairs, 152 dizygotic pairs) and analysed using biometric genetic models. The SPAQ yields a global seasonality score (GSS) which is an index of change in sleep patterns, social activities, mood, weight, appetite, and energy level. The GSS was significantly heritable among males and females, estimated to account for 69% and 45% of the total variance, respectively. For the individual symptoms, changes in sleep patterns, social activities, mood, appetite, and energy levels were accounted for primarily by additive genetic effects in both males (median, 45.5%) and females (median, 30.5%). For both sexes, weight changes were not heritable. Sex-by-genotype analyses suggested that the genetic factors influencing female seasonality may not be the same as those influencing male seasonality.