Article

Personality and comorbidity of common psychiatric disorders

Department of Psychiatry, Virginia Commonwealth University, Ричмонд, Virginia, United States
The British Journal of Psychiatry (Impact Factor: 7.34). 04/2005; 186:190-6. DOI: 10.1192/bjp.186.3.190
Source: PubMed

ABSTRACT We know little about the degree to which comorbidity, socommonly seen among psychiatric disorders, arises from variation in normal personality.
To study the degree to which variation in normal personality accounts for the comorbidity of eight common psychiatric and substance use disorders.
Internalising disorders (major depression, generalised anxiety and panic disorders, phobias), externalising disorders (alcohol and drug dependence, antisocial personality and conduct disorders) and personality dimensions of neuroticism, extraversion and novelty seeking were assessed in 7588 participants from a population-based twin registry. The proportion of comorbidity explained by each personality dimension was calculated using structural equation modelling.
Neuroticism accounted for the highest proportion of comorbidity within internalising disorders (20-45%) and between internalising and externalising disorders (19-88%). Variation in neuroticism and novelty seeking each accounted for a modest proportion (10-12% and 7-14%, respectively) of the comorbidity within externalising disorders. Extraversion contributed negligibly.
High neuroticism appears to be a broad vulnerability factor for comorbid psychiatric disorders. Novelty seeking is modestly important for comorbid externalising disorders.

0 Followers
 · 
89 Views
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: The study evaluated, among cocaine users, the hypothesized positive association of depression and concurrent cocaine use and impairment, alcohol use and impairment, and general drug use and impairment. The hypothesis that gender would moderate these associations, with women showing a stronger correlation between depression and measures of substance use and impairment, was also tested. Also examined was the association of depression with future cocaine use and impairment and substance use treatment participation. Empirical reports on adult cocaine users published in English in peer-reviewed journals since 1986 that contained data on depression and substance use outcome(s) were obtained using a systematic search. Studies that placed restrictions on range of depression scores to select the sample, experiments that administered cocaine to subjects, and trials of antidepressant medications were excluded. The search yielded 60 studies for the analysis including 53 reports that collected data from clinical venues and seven that were community-based. As hypothesized, the analyses showed that depression is associated with concurrent cocaine-, alcohol-, and general drug use and impairment. Effect sizes were small. Hypothesized moderating effects of gender were not supported. Depression was not associated, at a statistically significant level, with treatment participation or future cocaine use and impairment. Depression is consistently but modestly associated with measures of cocaine-, alcohol-, and general drug use and impairment among cocaine users. Associations of depression with treatment participation and with future cocaine use and impairment are not immediately evident, although limitations of data warrant cautious interpretation.
    Drug and Alcohol Dependence 07/2008; 98(1-2):13-23. DOI:10.1016/j.drugalcdep.2008.05.005 · 3.28 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Anxiety disorders are often comorbid with major depression (MD) and alcohol use disorders (AUD). Two common functional polymorphisms in catechol-O-methyltransferase (COMT Val158Met) and brain-derived neurotrophic factor (BDNF Val66Met) genes have been implicated in the neurobiology of anxiety and depression. We hypothesized that attentional response and working memory (auditory P300 event-related potential and Weschler Adult Intelligence Scale, Revised digit symbol scores) as well as genetic vulnerability would differ between pure anxiety disorders and comorbid anxiety. Our study sample comprised 249 community-ascertained men and women with lifetime DSM-III-R diagnoses. We analyzed groups of participants with pure anxiety disorders, pure MD, pure AUD, comorbid anxiety, and no psychiatric disorder. Participants were well at the time of testing; state anxiety and depressed mood measures were at most only mildly elevated. Individuals with pure anxiety disorders had elevated P300 amplitudes (P=0.0004) and higher digit symbol scores (P<0.0001) compared with all the other groups. Individuals with comorbid anxiety had the greatest proportion of COMT Met158 and BDNF Met66 alleles (P=0.009) as well as higher harm avoidance-neuroticism (P<0.0005) than all other groups. Our results suggest that there may be two vulnerability factors for anxiety disorders with differing genetic susceptibility: (a) heightened attention and better working memory with mildly elevated anxiety-neuroticism, a constellation that may be protective against other psychopathology; and (b) poorer attention and working memory with greater anxiety-neuroticism, a constellation that may also increase vulnerability to AUD and MD. This refinement of the anxiety phenotype may have implications for therapeutic interventions.
    Depression and Anxiety 05/2008; 25(5):383-92. DOI:10.1002/da.20378 · 4.29 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Prior research on the nature of the vulnerability of neuroticism to psychopathology suggests biases in information processing towards emotional rather than neutral information. It is unclear to what extent this relationship can be explained by genetic or environmental factors. The genetic relationship between a neuroticism composite score and free recall of pleasant and unpleasant words and the reaction time on negative probes (dot-probe task) was investigated in 125 female twin pairs. Interaction effects were modelled to test whether the correlation between neuroticism and cognitive measures depended on the level of the neuroticism score. The only significant correlation was between neuroticism and the proportion of recalled unpleasant words (heritability is 30%), and was only detectable at the higher end of the neuroticism distribution. This interaction effect seems to be due to environmental effects that make people in the same family more similar (e.g. parental discipline style), rather than genetic factors. An interesting sub-finding was that faster reaction times for left versus right visual field probes in the dot-probe task suggest that cognitive processing in the right hemisphere is more sensitive to subliminal (biologically relevant) cues and that this characteristic is under substantial genetic control (49%). Individual differences in reaction times on right visual field probes were due to environmental effects only. There is no evidence that the predisposition of individuals to focus on negative (emotional) stimuli is a possible underlying genetic mechanism of neuroticism.
    Psychological Medicine 05/2008; 39(1):45-54. DOI:10.1017/S0033291708003231 · 5.43 Impact Factor

Preview

Download
2 Downloads
Available from