Are bottom-up and top-down traits in dual-systems models of risky behavior genetically distinct?
ABSTRACT: Numerous dual-systems models of personality have been posited, which propose that behavior is influenced by two complementary systems. A bottom-up system is characterized by emotion-based drive (e.g., urge for rewarding experience), and a top-down system is characterized by the ability to control those urges. Although evidence suggests that these two systems are distinct and may be important in explaining some behaviors, these constructs are also moderately correlated. Notably, there has been little molecular or behavior genetic research on the genetic distinctness of the two systems central to the dual-systems model. The current study used a national twin sample to investigate the degree to which bottom-up and top-down systems, measured here as personality traits of sensation seeking and lack of planning, respectively, covary through genetic and environmental influences. Whereas the overlap between these systems was primarily comprised of unshared environmental influences (e.g., measurement error and unshared systematic variation) in females, a statistically significant proportion of the overlap was accounted for by genetic factors in men. Further, the genetic factors for these systems were moderately to highly correlated in men (rG = 0.62-0.79). These results provide clear support for a dual-systems model in women; however, these systems appear to share some common genetic influences in men.
Project description:The goals of the study were to determine the extent to which the underlying structure of different types of well-being was multidimensional and whether well- and ill-being were influenced by similar or different genetic and environmental factors. Participants were 1226 male twins ages 51-60, from the Vietnam Era Twin Study of Aging. Measures included: psychological well-being, Multidimensional Personality Questionnaire Well-Being scale (MPQWB), life satisfaction, self-esteem, and depressive symptoms. A two-orthogonal-factor common pathway model fit the data well. Psychological well-being and self-esteem loaded most strongly on Factor 1, which was highly heritable (h(2) = .79). Life satisfaction loaded most strongly on Factor 2, which was only moderately heritable (h(2) = .32). Only MPQWB had measure-specific genetic influences. Depressive symptoms loaded on both factors, and only depressive symptoms had measure-specific common environmental influences. All measures had specific unique environmental influences. Results indicate that well-being is genetically and environmentally multidimensional and that ill-being has partial overlap with both latent factors.
Project description:Callous-unemotional (CU) traits, such as lacking empathy and emotional insensitivity, predict the onset, severity, and persistence of antisocial behavior. CU traits are heritable, and genetic influences on CU traits contribute to antisocial behavior. This study examines genetic overlap between CU traits and general domains of personality. We measured CU traits using the Inventory of Callous-Unemotional Traits (ICU) and Big Five personality using the Big Five Inventory in a sample of adolescent twins from the Texas Twin Project. Genetic influences on the Big Five personality dimensions could account for the entirety of genetic influences on CU traits. Item Response Theory results indicate that the Inventory of Callous and Unemotional Traits is better at detecting clinically relevant personality variation at lower extremes of personality trait continua, particularly low agreeableness and low conscientiousness. The proximate biological mechanisms that mediate genetic liabilities for CU traits remain an open question. The results of the current study suggest that understanding the development of normal personality may inform understanding of the genetic underpinnings of callous and unemotional behavior.
Project description:Sensation seeking and impulsivity are personality traits that are correlated with risk for antisocial behavior (ASB). This paper uses two independent samples of twins to (a) test the extent to which sensation seeking and impulsivity statistically mediate genetic influence on ASB, and (b) compare this to genetic influences accounted for by other personality traits. In Sample 1, delinquent behavior, as well as impulsivity, sensation seeking and Big Five personality traits, were measured in adolescent twins from the Texas Twin Project. In Sample 2, adult twins from the Australian Twin Registry responded to questionnaires that assessed individual differences in Eysenck's and Cloninger's personality dimensions, and a structured telephone interview that asked participants to retrospectively report DSM-defined symptoms of conduct disorder. Bivariate quantitative genetic models were used to identify genetic overlap between personality traits and ASB. Across both samples, novelty/sensation seeking and impulsive traits accounted for larger portions of genetic variance in ASB than other personality traits. We discuss whether sensation seeking and impulsive personality are causal endophenotypes for ASB, or merely index genetic liability for ASB.
Project description:Using data from a large Australian twin sample we examined the extent to which genetic variation in the Big Three personality dimensions (positive emotionality, negative emotionality, and constraint) and their lower-order components explained genetic variation in the risk for disordered gambling (DG) among men and women. Genetic influences contributing to individual differences in normal-range personality traits explained over 40% of the genetic risk for DG, with a larger contribution among women than among men. The largest and most robust contributions came from the higher-order personality dimension of negative emotionality and its two lower-order dimensions of alienation and aggression. Surprisingly, low self-control was associated with the genetic risk for DG only among women, and risk-taking/sensation-seeking did not explain genetic risk for DG in either sex. The results of this study have implications for the causes of comorbidity between DG and other psychiatric disorders, the search for genes associated with DG risk, and the possibility of sex differences in the etiology of DG. Using a broad-band inventory of personality supports the conclusion that there probably is a substantial proportion of genetic variation in DG that cannot be explained by individual differences in personality.
Project description:Neuroticism, a dispositional trait of heightened negative emotionality, is a vulnerability factor for psychopathology. Given neuroticism's strong association with rumination, a repetitive thought pattern that intensifies and prolongs emotions, some question whether these constructs capture the same or unique information about vulnerability for psychopathology. The present study examined whether neuroticism is genetically and environmentally distinct from two clinically relevant ruminative subtypes-anger and depressive rumination-and whether genetic and environmental influences specific to rumination versus shared with neuroticism overlap with internalizing and externalizing psychopathology. These analyses were conducted on 439 same-sex twin pairs in the Colorado Longitudinal Twin study. Rumination and neuroticism latent variables were created from multiple rumination questionnaires administered at age 23 and shortened Eysenck Personality Questionnaires administered at ages 17 and 21, respectively. Lifetime psychopathology symptoms, assessed by two structured clinical interviews, were used to create ordinal composite variables. Multivariate Cholesky decompositions indicated that neuroticism, anger rumination, and depressive rumination have common genetic and nonshared environmental influences but are differentiated by nonshared environmental influences specific to each ruminative subtype. Genetic influences common to rumination and neuroticism explained considerable variance in internalizing psychopathology, suggesting possible genetic mediation or common genetic causes. Genetic and environmental influences on externalizing psychopathology did not substantially overlap with those on neuroticism and rumination. These findings suggest that rumination and neuroticism share most genetic influences yet are influenced by distinct environmental influences. Furthermore, our results indicate that a comprehensive understanding of transdiagnostic risk factors must include an examination of both genetic and environmental influences. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
Project description:To examine the genetic overlap between borderline personality features (BPF) and substance use disorders (SUDs) and the extent to which variation in personality traits contributes to this covariance.Genetic structural equation modelling was used to partition the variance in and covariance between personality traits, BPF and SUDs into additive genetic, shared and individual-specific environmental factors.All participants were registered with the Australian Twin Registry.A total of 3127 Australian adult twins participated in the study.Diagnoses of DSM-IV alcohol and cannabis abuse/dependence (AAD; CAD) and nicotine dependence (ND) were derived via computer-assisted telephone interview. BPF and five-factor model personality traits were derived via self-report questionnaires.Personality traits, BPF and substance use disorders were partially influenced by genetic factors with heritability estimates ranging from 0.38 (neuroticism; 95% confidence interval: 0.30-0.45) to 0.78 (CAD; 95% confidence interval: 0.67-0.86). Genetic and individual-specific environmental correlations between BPF and SUDs ranged from 0.33 to 0.56 (95% CI = 0.19-0.74) and 0.19-0.32 (95% CI = 0.06-0.43), respectively. Overall, there was substantial support for genetic influences that were specific to AAD, ND and CAD (30.76-68.60%). Finally, genetic variation in personality traits was responsible for 11.46% (extraversion for CAD) to 59.30% (neuroticism for AAD) of the correlation between BPF and SUDs.Both genetic and individual-specific environmental factors contribute to comorbidity between borderline personality features and substance use disorders. A substantial proportion of this comorbidity can be attributed to variation in normal personality traits, particularly neuroticism.
Project description:Schizophrenia is characterized by neuropsychological deficits across many cognitive domains. Cognitive phenotypes with high heritability and genetic overlap with schizophrenia liability can help elucidate the mechanisms leading from genes to psychopathology. We performed a meta-analysis of 170 published twin and family heritability studies of >800 000 nonpsychiatric and schizophrenia subjects to accurately estimate heritability across many neuropsychological tests and cognitive domains. The proportion of total variance of each phenotype due to additive genetic effects (A), shared environment (C), and unshared environment and error (E), was calculated by averaging A, C, and E estimates across studies and weighting by sample size. Heritability ranged across phenotypes, likely due to differences in genetic and environmental effects, with the highest heritability for General Cognitive Ability (32%-67%), Verbal Ability (43%-72%), Visuospatial Ability (20%-80%), and Attention/Processing Speed (28%-74%), while the lowest heritability was observed for Executive Function (20%-40%). These results confirm that many cognitive phenotypes are under strong genetic influences. Heritability estimates were comparable in nonpsychiatric and schizophrenia samples, suggesting that environmental factors and illness-related moderators (eg, medication) do not substantially decrease heritability in schizophrenia samples, and that genetic studies in schizophrenia samples are informative for elucidating the genetic basis of cognitive deficits. Substantial genetic overlap between cognitive phenotypes and schizophrenia liability (average rg = -.58) in twin studies supports partially shared genetic etiology. It will be important to conduct comparative studies in well-powered samples to determine whether the same or different genes and genetic variants influence cognition in schizophrenia patients and the general population.
Project description:BACKGROUND:Numerous factors influence late-life depressive symptoms in adults, many not thoroughly characterized. We addressed whether genetic and environmental influences on depressive symptoms differed by age, sex, and physical illness. METHOD:The analysis sample included 24 436 twins aged 40-90 years drawn from the Interplay of Genes and Environment across Multiple Studies (IGEMS) Consortium. Biometric analyses tested age, sex, and physical illness moderation of genetic and environmental variance in depressive symptoms. RESULTS:Women reported greater depressive symptoms than men. After age 60, there was an accelerating increase in depressive symptom scores with age, but this did not appreciably affect genetic and environmental variances. Overlap in genetic influences between physical illness and depressive symptoms was greater in men than in women. Additionally, in men extent of overlap was greater with worse physical illness (the genetic correlation ranged from near 0.00 for the least physical illness to nearly 0.60 with physical illness 2 s.d. above the mean). For men and women, the same environmental factors that influenced depressive symptoms also influenced physical illness. CONCLUSIONS:Findings suggested that genetic factors play a larger part in the association between depressive symptoms and physical illness for men than for women. For both sexes, across all ages, physical illness may similarly trigger social and health limitations that contribute to depressive symptoms.
Project description:The present study examined the genetic and environmental etiology underlying the Big Five personality traits and perceived stress, concurrently and longitudinally. In study 1, we used the twin sample from the National Longitudinal Study of Adolescent to Adult Health (Add Health IV) data. The results indicated that about 70% of the association between the Big Five personality traits and perceived stress was due to genetic influences. In study 2, we used the twin sample from the Midlife in the United States Survey (MIDUS I and II) to examine the genetic and environmental influences underlying the longitudinal relations between the Big Five personality traits and perceived stress. The results suggested that continuity in perceived stress was primarily accounted for by genetic influences, and changes in perceived stress were mainly due to nonshared environmental influences. The continuity in the association between the five personality traits and perceived stress was largely accounted for by genetic factors, and nonshared environmental factors made greater contributions to changes in the association between personality traits and perceived stress. Among the Big Five personality traits, the genetic components in conscientiousness and neuroticism made substantial contributions to the genetic link between personality traits and perceived stress across both studies.
Project description:Major depressive disorder and the anxiety disorders are highly prevalent, disabling and moderately heritable. Depression and anxiety are also highly comorbid and have a strong genetic correlation (rg ≈ 1). Cognitive behavioural therapy is a leading evidence-based treatment but has variable outcomes. Currently, there are no strong predictors of outcome. Therapygenetics research aims to identify genetic predictors of prognosis following therapy. We performed genome-wide association meta-analyses of symptoms following cognitive behavioural therapy in adults with anxiety disorders (n = 972), adults with major depressive disorder (n = 832) and children with anxiety disorders (n = 920; meta-analysis n = 2724). We estimated the variance in therapy outcomes that could be explained by common genetic variants (h2SNP) and polygenic scoring was used to examine genetic associations between therapy outcomes and psychopathology, personality and learning. No single nucleotide polymorphisms were strongly associated with treatment outcomes. No significant estimate of h2SNP could be obtained, suggesting the heritability of therapy outcome is smaller than our analysis was powered to detect. Polygenic scoring failed to detect genetic overlap between therapy outcome and psychopathology, personality or learning. This study is the largest therapygenetics study to date. Results are consistent with previous, similarly powered genome-wide association studies of complex traits.