Symptoms of major depression: Their stability, familiality, and prediction by genetic, temperamental, and childhood environmental risk factors

Background: Psychiatry has long sought to develop biological diagnostic subtypes based on symptomatic differences. This effort assumes that symptoms reflect, with good fidelity, underlying etiological processes. We address this question for major depression (MD). Methods: We examine, in twins from a population-based registry, similarity in symptom endorsement in individuals meeting criteria for last-year MD at separate interview waves and in concordant twin pairs. Among individuals with MD, we explore the impact of genetic-temperamental and child adversity risk factors on individual reported symptoms. Aggregated criteria do not separate insomnia from hypersomnia, weight gain from loss, etc. while disaggregated criteria do. Results: In twins with MD at two different waves, the mean tetrachoric correlations (+/- SEM) for aggregated and disaggregated DSM-IV A criteria were, respectively, + 0.31 +/- 0.06 and + 0.34 +/- 0.03. In monozygotic (MZ) and dizygotic (DZ) twin pairs concordant for last-year MD, the mean tetrachoric correlations for aggregated and disaggregated criteria were, respectively, + 0.33 +/- 0.07 and + 0.43 +/- 0.04, and + 0.05 +/- 0.08 and + 0.07 +/- 0.04. In individuals meeting MD criteria, neuroticism predicted the most MD symptoms (10), followed by childhood sexual abuse (8), low parental warmth (6), and genetic risk (4). Conclusions: The correlations for individual depressive symptoms over multiple episodes and within MZ twins concordant for MD are modest suggesting the important role of transient influences. The multidetermination of individual symptoms was further evidenced by their prediction by personality and exposure to early life adversities. The multiple factors influencing symptomatic presentation inMDmay contribute to our difficulties in isolating clinical depressive subtypes with distinct pathophysiologies

Evaluation of a new trauma-related drinking to cope measure: Latent structure and heritability

Posttraumatic stress disorder (PTSD) and alcohol use disorder (AUD) commonly co-occur, share latent genetic risk, and are associated with many negative public health outcomes. Via a self-medication framework, trauma-related drinking to cope (TRD), an unexplored phenotype to date, may help explain why these two disorders co-occur, thus serving as an essential target for treatment and prevention efforts. This study sought to create a novel measure of TRD and to investigate its indirect influences on the association between PTSD and AUD, as well as its potential shared molecular genetic risk with PTSD in a genetically-informative study of college students. A sample of 1,896 undergraduate students with a history of trauma and alcohol use provided genotypic data and completed an online assessment battery. The psychometric properties of TRD and how it relates to relevant constructs were examined using descriptive statistics and structural equation modeling. Results of a correlated multiple mediator model indicated that, while accounting for the effects of generalized drinking motives, TRD partially mediated the relation between PTSD and alcohol use problems (β = 0.213, p \u3c .001), consistent with the self-medication hypothesis, and that this relationship was stronger for males (β = 0.804, p \u3c .001) than for females (β = 0.463, p \u3c .001). Results were substantiated using longitudinal data. Genotypic analyses to be presented will include univariate genome wide complex trait analyses (GCTA) to establish SNP-based heritability associated with TRD and PTSD, separately, as well as bivariate GCTA to examine potential overlap in heritability between TRD and PTSD.https://scholarscompass.vcu.edu/gradposters/1047/thumbnail.jp

Genetic and Environmental Structure of DSM-IV Criteria for Antisocial Personality Disorder: A Twin Study

Results from previous studies on DSM-IV and DSM-5 Antisocial Personality Disorder (ASPD) have suggested that the construct is etiologically multidimensional. To our knowledge, however, the structure of genetic and environmental influences in ASPD has not been examined using an appropriate range of biometric models and diagnostic interviews. The 7 ASPD criteria (section A) were assessed in a population-based sample of 2794 Norwegian twins by a structured interview for DSM-IV personality disorders. Exploratory analyses were conducted at the phenotypic level. Multivariate biometric models, including both independent and common pathways, were compared. A single phenotypic factor was found, and the best-fitting biometric model was a single-factor common pathway model, with common-factor heritability of 51% (95% CI 40–67%). In other words, both genetic and environmental correlations between the ASPD criteria could be accounted for by a single common latent variable. The findings support the validity of ASPD as a unidimensional diagnostic construct

The structure of the symptoms of major depression:Factor analysis of a lifetime worst episode of depressive symptoms in a large general population sample

Background: A range of depressive symptoms may occur during an episode of major depression (MD). Do these symptoms describe a single disorder liability or different symptom dimensions? This study investigates the structure and clinical relevance of an expanded set of depressive symptoms in a large general population sample. Methods: We studied 43,431 subjects from the Dutch Lifelines Cohort Study who participated in an online survey assessing the 9 symptom criteria of MD (DSM-IV-TR) and additional depressive symptoms during their worst lifetime episode of depressive symptoms lasting two weeks or more. Exploratory factor analyses were performed on expanded sets of 9, 14, and 24 depressive symptoms. The clinical relevance of the identified symptom dimensions was analyzed in confirmatory factor analyses including ten external validators. Results: A single dimension adequately accounted for the covariation among the 9 DSM-criteria, but multiple dimensions were needed to describe the 14 and 24 depressive symptoms. Five dimensions described the structure underlying the 24 depressive symptoms. Three cognitive affective symptom dimensions were mainly associated with risk factors for MD. Two somatic dimensions –appetite/weight problems and sleep problems—were mainly associated with BMI and age, respectively. Limitations: Respondents of our online survey tended to be more often female, older, and more highly educated than non-respondents. Conclusions: Different symptom dimensions described the structure of depressive symptoms during a lifetime worst episode in a general population sample. These symptom dimensions resembled those reported in a large clinical sample of Han-Chinese women with recurrent MD, suggesting robustness of the syndrome of MD

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-S-Norwegian Brief Form (PID-5NBF). 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-S-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-S-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