56 research outputs found
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
Early Puberty Is Associated With Higher Academic Achievement in Boys and Girls and Partially Explains Academic Sex Differences
Purpose: On average, boys have lower academic achievement than girls. We investigated whether the timing of puberty is associated with academic achievement, and whether later puberty among boys contributes to the sex difference in academic achievement. Method: Examination scores at age 16 were studied among 13,477 British twins participating in the population-based Twins Early Development Study. A pubertal development scale, a height based proxy of growth spurt, and age at menarche were used as indicators of puberty. Associations between puberty, sex, and academic achievement were estimated in phenotypic mediation models and biometric twin models. Results: Earlier puberty was associated with higher academic achievement both in boys and girls. The exception was early age at menarche in girls, which associated with lower academic achievement. More than half of the sex differences in academic achievement could be linked to sex differences in pubertal development, but part of this association appeared to be rooted in prepubertal differences. The biometric twin modelling indicated that the association between puberty and academic achievement was due to shared genetic risk factors. Genetic influences on pubertal development accounted for 7%-8% of the phenotypic variation in academic achievement. Conclusions: Pubertal maturation relates to the examination scores of boys and of girls. This can give genes related to pubertal maturation an influence on outcomes in education and beyond. Sex differences in pubertal maturation can explain parts of the sex difference in academic achievement. Grading students when they are immature may not accurately measure their academic potential. (c) 2021 Society for Adolescent Health and Medicine. Published by Elsevier Inc. All rights reserved. This is an open access article under the CC BY license (http://creativecommons.org/licenses/by/4.0/).Peer reviewe
Caffeine Consumption, Toxicity, Tolerance and Withdrawal; Shared Genetic Influences With Normative Personality and Personality Disorder Traits
Public Health Significance Both the amount of caffeine people consume and their response to caffeine is heritable. A modest proportion of the genetic influences underlying caffeine use and response is shared with personality and personality disorder traits. Our main aim was to estimate the extent of overlapping etiology between caffeine consumption and response and normative and pathological personality. Linear mixed-effects models were used to identify normative personality domains and personality disorder (PD) traits for inclusion in multivariate twin analyses together with individual caffeine related measures. Data were obtained from Norwegian adult twins in a face-to-face interview conducted in 1999-2004 as part of a population-based study of mental health and through self-report in 2010-2011 and 2015-2017. Personality disorder data was available for 2,793 twins, normative personality for 3,889 twins, and caffeine for 3,862 twins (mean age 43.0 years). Normative personality was assessed using the self-reported Big Five Inventory, PD traits were assessed by the Structured Interview for DSM-IV Personality, and caffeine consumption, toxicity, tolerance, and withdrawal were assessed through a self-report questionnaire developed at the Norwegian Institute of Public Health. Caffeine measures were found to be moderately heritable, h(2) = 30.1%-45.0%. All normative personality domains and four PD traits, antisocial, borderline, dependent and paranoid, were significantly associated with at least one caffeine variable. A small proportion of variance in caffeine consumption was attributable to genetic factors shared with normative personality (1.3%) and personality disorders (11.4%). A modest proportion of variance in caffeine tolerance and toxicity was attributable to genetic factors shared with both normative personality (26.9%, 24.8%) and personality disorders (21.0%, 36.0%). The present study found caffeine consumption and response to be heritable and provides evidence that a small to-modest proportion of this genetic etiology is shared with both normative and pathological personality.Peer reviewe
How interactions between ADHD and schools affect educational achievement: a family-based genetically sensitive study
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Specific Antisocial and Borderline Personality Disorder Criteria and General Substance Use : A Twin Study
Antisocial (ASPD) and borderline (BPD) personality disorders (PDs) are associated with increased risk for substance use. They are "specific" risk factors among PDs in that they withstand adjusting for the other PDs, whereas the reverse does not hold. Specificity is a classic sign of causation. This empirical work addresses 3 further problems that can undermine causal inferences in personality and substance-use research: hierarchical nature of etiologic factors in psychiatry, imperfectly operationalized PD criteria, and possible genetic or environmental confounding, as seen in lack of "etiologic continuity." We used exploratory structural equation bifactor modeling and biometric models to mitigate these problems. The participants were Norwegian adult twins of ages 19-36 years (N = 2,801). Criteria for Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), PDs were assessed using a structured interview. General substance-use risk was indicated by World Health Organization Composite International Diagnostic Interviewed alcohol use disorder and illicit drug use, and by self-reported regular smoking. A general risk factor for all criteria of both ASPD and BPD was the strongest individual correlate of general substance use and showed etiologic continuity, though just 3 specific PD criteria could predict substance use to the same extent. The findings indicate that a broad latent factor for both ASPD and BPD may be a specific and a genetically and environmentally unconfounded risk factor for substance use. Substance-use treatment research might benefit from attending to transdiagnostic models of ASPD, BPD, and related behavioral disinhibition.Peer reviewe
Genetically Informative Mediation Modeling Applied to Stressors and Personality-Disorder Traits in Etiology of Alcohol Use Disorder
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Joint factorial structure of psychopathology and personality
Background Normative and pathological personality traits have rarely been integrated into a joint large-scale structural analysis with psychiatric disorders, although a recent study suggested they entail a common individual differences continuum. Methods We explored the joint factor structure of 11 psychiatric disorders, five personality-disorder trait domains (DSM-5 Section III), and five normative personality trait domains (the 'Big Five') in a population-based sample of 2796 Norwegian twins, aged 19-46. Results Three factors could be interpreted: (i) a general risk factor for all psychopathology, (ii) a risk factor specific to internalizing disorders and traits, and (iii) a risk factor specific to externalizing disorders and traits. Heritability estimates for the three risk factor scores were 48% (95% CI 41-54%), 35% (CI 28-42%), and 37% (CI 31-44%), respectively. All 11 disorders had uniform loadings on the general factor (congruence coefficient of 0.991 with uniformity). Ignoring sign and excluding the openness trait, this uniformity of factor loadings held for all the personality trait domains and all disorders (congruence 0.983). Conclusions Based on our findings, future research should investigate joint etiologic and transdiagnostic models for normative and pathological personality and other psychopathology.Peer reviewe
Modeling assortative mating and genetic similarities between partners, siblings, and in-laws
Assortative mating on heritable traits can have implications for the genetic resemblance between siblings and in-laws in succeeding generations. We studied polygenic scores and phenotypic data from pairs of partners (n = 26,681), siblings (n = 2,170), siblings-in-law (n = 3,905), and co-siblings-in-law (n = 1,763) in the Norwegian Mother, Father and Child Cohort Study. Using structural equation models, we estimated associations between measurement error-free latent genetic and phenotypic variables. We found evidence of genetic similarity between partners for educational attainment (rg = 0.37), height (rg = 0.13), and depression (rg = 0.08). Common genetic variants associated with educational attainment correlated between siblings above 0.50 (rg = 0.68) and between siblings-in-law (rg = 0.25) and co-siblings-in-law (rg = 0.09). Indirect assortment on secondary traits accounted for partner similarity in education and depression, but not in height. Comparisons between the genetic similarities of partners and siblings indicated that genetic variances were in intergenerational equilibrium. This study shows genetic similarities between extended family members and that assortative mating has taken place for several generations.publishedVersio
On the importance of parenting in externalizing disorders: an evaluation of indirect genetic effects in families
Background: Theoretical models of the development of childhood externalizing disorders emphasize the role of parents. Empirical studies have not been able to identify specific aspects of parental behaviors explaining a considerable proportion of the observed individual differences in externalizing problems. The problem is complicated by the contribution of genetic factors to externalizing problems, as parents provide both genes and environments to their children. We studied the joint contributions of direct genetic effects of children and the indirect genetic effects of parents through the environment on externalizing problems.
Methods: The study used genome-wide single nucleotide polymorphism data from 9,675 parent–offspring trios participating in the Norwegian Mother Father and child cohort study. Based on genomic relatedness matrices, we estimated the contribution of direct genetic effects and indirect maternal and paternal genetic effects on ADHD, conduct and disruptive behaviors at 8 years of age.
Results: Models including indirect parental genetic effects were preferred for the ADHD symptoms of inattention and hyperactivity, and conduct problems, but not oppositional defiant behaviors. Direct genetic effects accounted for 11% to 24% of the variance, whereas indirect parental genetic effects accounted for 0% to 16% in ADHD symptoms and conduct problems. The correlation between direct and indirect genetic effects, or gene–environment correlations, decreased the variance with 16% and 13% for conduct and inattention problems, and increased the variance with 6% for hyperactivity problems.
Conclusions: This study provides empirical support to the notion that parents have a significant role in the development of childhood externalizing behaviors. The parental contribution to decrease in variation of inattention and conduct problems by gene–environment correlations would limit the number of children reaching clinical ranges in symptoms. Not accounting for indirect parental genetic effects can lead to both positive and negative bias when identifying genetic variants for childhood externalizing behaviors.publishedVersio
On the importance of parenting in externalizing disorders: an evaluation of indirect genetic effects in families
publishedVersio
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