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

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

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

Justice sensitivity is undergirded by separate heritable motivations to be morally principled and opportunistic

Injustice typically involves some people benefitting at the expense of others. An opportunist might then be selectively motivated to amend only the injustice that is harmful to them, while someone more principled would respond consistently regardless of whether they stand to gain or lose. Here, we disentangle such principled and opportunistic motives towards injustice. With a sample of 312 monozygotic- and 298 dizygotic twin pairs (N = 1220), we measured people’s propensity to perceive injustice as victims, observers, beneficiaries, and perpetrators of injustice, using the Justice Sensitivity scale. With a biometric approach to factor analysis, that provides increased stringency in inferring latent psychological traits, we find evidence for two substantially heritable factors explaining correlations between Justice Sensitivity facets. We interpret these factors as principled justice sensitivity (h2 = 0.45) leading to increased sensitivity to injustices of all categories, and opportunistic justice sensitivity (h2 = 0.69) associated with increased sensitivity to being a victim and a decreased propensity to see oneself as a perpetrator. These novel latent constructs share genetic substrate with psychological characteristics that sustain broad coordination strategies that capture the dynamic tension between honest cooperation versus dominance and defection, namely altruism, interpersonal trust, agreeableness, Social Dominance Orientation and opposition to immigration and foreign aid

The genetic underpinnings of right-wing authoritarianism and social dominance orientation explain political attitudes beyond Big Five personality

Objective: Political attitudes are predicted by the key ideological variables of right-wing authoritarianism (RWA) and social dominance orientation (SDO), as well as some of the Big Five personality traits. Past research indicates that personality and ideological traits are correlated for genetic reasons. A question that has yet to be tested concerns whether the genetic variation underlying the ideological traits of RWA and SDO has distinct contributions to political attitudes, or if genetic variation in political attitudes is subsumed under the genetic variation underlying standard Big Five personality traits. Method: We use data from a sample of 1987 Norwegian twins to assess the genetic and environmental relationships between the Big Five personality traits, RWA, SDO, and their separate contributions to political policy attitudes. Results: RWA and SDO exhibit very high genetic correlation (r = 0.78) with each other and some genetic overlap with the personality traits of openness and agreeableness. Importantly, they share a larger genetic substrate with political attitudes (e.g., deporting an ethnic minority) than do Big Five personality traits, a relationship that persists even when controlling for the genetic foundations underlying personality traits. Conclusion: Our results suggest that the genetic foundations of ideological traits and political attitudes are largely non-overlapping with the genetic foundations of Big Five personality traits

Social inequalities in reception of social welfare support: A population based twin study

Social welfare support runs in families. Recent studies using Nordic registry data have found individual differences in genetic factors to be of substantial importance for medical benefits. However, to date there has been no genetically informative studies on receiving social welfare support. To prevent young adults to not drop out of the work life and become recipients of social welfare support, it is of substantial interest to clarify to what extent the familiarity of social welfare support is due to genetic or social differences between families. We used data from the Historical-Event Database on 7,698 Norwegian twins born 1967-1979 to estimate the relative contribution of genetic factors, the effective familial environment (i.e. the “shared environment”), and individual-specific environmental factors. We found that the two forms of familial risk, genetic and shared environmental, explained 39% and 45%, respectively, of the risk for receiving social welfare support among young Norwegian twins. Only 17% of the variance in risk factors could be explained by individual-specific risk factors. It appears that risk for receiving social welfare support can to a great extent be explained by environmental differences between families. Therefore prevention strategies targeting social inequalities between families would indeed be effective. Furthermore, genetic risk factors are also important in explaining risk for receiving social welfare support. These effects could be mediated through heritable traits related to substance abuse, psychiatric disorders, and personality. Individual-specific risk factors were of very little importance. Hence, with regard to receiving social welfare support, family matters

Prenatal smoking, alcohol and caffeine exposure and maternal-reported attention deficit hyperactivity disorder symptoms in childhood:triangulation of evidence using negative control and polygenic risk score analyses

Background and aims Studies have indicated that maternal prenatal substance use may be associated with offspring attention deficit hyperactivity disorder (ADHD) via intrauterine effects. We measured associations between prenatal smoking, alcohol and caffeine consumption with childhood ADHD symptoms accounting for shared familial factors. Design First, we used a negative control design comparing maternal and paternal substance use. Three models were used for negative control analyses: unadjusted (without confounders), adjusted (including confounders) and mutually adjusted (including confounders and partner's substance use). The results were meta-analysed across the cohorts. Secondly, we used polygenic risk scores (PRS) as proxies for exposures. Maternal PRS for smoking, alcohol and coffee consumption were regressed against ADHD symptoms. We triangulated the results across the two approaches to infer causality. Setting We used data from three longitudinal pregnancy cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC) in the United Kingdom, Generation R study (GenR) in the Netherlands and Norwegian Mother, Father and Child Cohort study (MoBa) in Norway. Participants Phenotype data available for children were: NALSPAC = 5455–7751; NGENR = 1537–3119; NMOBA = 28 053–42 206. Genotype data available for mothers was: NALSPAC = 7074; NMOBA = 14 583. Measurements A measure of offspring ADHD symptoms at age 7–8 years was derived by dichotomizing scores from questionnaires and parental self-reported prenatal substance use was measured at the second pregnancy trimester. Findings The pooled estimate for maternal prenatal substance use showed an association with total ADHD symptoms [odds ratio (OR)SMOKING = 1.11, 95% confidence interval (CI) = 1.00–1.23; ORALCOHOL = 1.27, 95% CI = 1.08–1.49; ORCAFFEINE = 1.05, 95% CI = 1.00–1.11], while not for fathers (ORSMOKING = 1.03, 95% CI = 0.95–1.13; ORALCOHOL = 0.83, 95% CI = 0.47–1.48; ORCAFFEINE = 1.02, 95% CI = 0.97–1.07). However, maternal associations did not persist in sensitivity analyses (substance use before pregnancy, adjustment for maternal ADHD symptoms in MoBa). The PRS analyses were inconclusive for an association in ALSPAC or MoBa. Conclusions There appears to be no causal intrauterine effect of maternal prenatal substance use on offspring attention deficit hyperactivity disorder symptoms

Maternal prenatal depressive symptoms and risk for early-life psychopathology in offspring: results from a genetically-informative, population-based sample

Background: Maternal prenatal depression is a known risk factor for early-life psychopathology among offspring; however, potential risk transmission mechanisms need to be distinguished. We aimed to test the relative importance of passive genetic transmission, direct exposure, and indirect exposure in the association between maternal prenatal depressive symptoms and early-life internalising and externalising psychopathology in offspring. Methods: We used structural equation modelling of phenotypic data and genetically informative relationships from the families of participants in the Norwegian Mother and Child Birth Cohort Study (MoBa). The analytic subsample of MoBa used in the current study comprises 22 195 mothers and 35 299 children. We used mothers' self-reported depressive symptoms during pregnancy, as captured by the Symptom Checklist, and their reports of symptoms of psychopathology in their offspring during the first few years of life (measured at 18, 36, and 60 months using the Child Behavior Checklist). Findings: Maternal prenatal depressive symptoms were found to be associated with early-life psychopathology primarily via intergenerationally shared genetic factors, which explained 41% (95% CI 36–46) of variance in children's internalising problems and 37% (30–44) of variance in children's externalising problems. For internalising problems, phenotypic transmission also contributed significantly, accounting for 14% (95% CI 5–19) of the association, but this contribution was found to be explained by exposure to concurrent maternal depressive symptoms, rather than by direct exposure in utero. Interpretation: Associations between maternal prenatal depressive symptoms and offspring behavioural outcomes in early childhood are likely to be at least partially explained by shared genes. This genetic confounding should be considered when attempting to quantify risks posed by in-utero exposure to maternal depressive symptoms. Funding: UK Economic and Social Research Council, Norwegian Research Council, Norwegian Ministries of Health and Care Services, and Education & Research, Wellcome Trust, Royal Society, and National Institute for Health Research

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

Maternal and offspring genetic risk score analyses of fetal alcohol exposure and attention-deficit hyperactivity disorder risk in offspring

Background: Studies investigating the effects of prenatal alcohol exposure on childhood attention-deficit hyperactivity disorder (ADHD) symptoms using conventional observational designs have reported inconsistent findings, which may be affected by unmeasured confounding and maternal and fetal ability to metabolize alcohol. We used genetic variants from the alcohol metabolizing genes, alcohol dehydrogenase (ADH) and aldehyde dehydrogenase (ALDH), as proxies for fetal alcohol exposure to investigate their association with risk of offspring ADHD symptoms around age 7–8 years. Methods: We used data from 3 longitudinal pregnancy cohorts: Avon Longitudinal Study of Parents and Children (ALSPAC), Generation R study (GenR), and the Norwegian Mother, Father and Child Cohort study (MoBa). Genetic risk scores (GRS) for alcohol use and metabolism using 36 single nucleotide polymorphisms (SNPs) from ADH and ALDH genes were calculated for mothers (NALSPAC = 8196; NMOBA = 13,614), fathers (NMOBA = 13,935), and offspring (NALSPAC=8,237; NMOBA=14,112; NGENR=2,661). Associations between maternal GRS and offspring risk of ADHD symptoms were tested in the full sample to avoid collider bias. Offspring GRS analyses were stratified by maternal drinking status. Results: The pooled estimate in maternal GRS analyses adjusted for offspring GRS in ALSPAC and MoBa was OR = 0.99, 95%CI 0.97–1.02. The pooled estimate in offspring GRS analyses stratified by maternal drinking status across all the cohorts was as follows: ORDRINKING = 0.98, 95% CI 0.94–1.02; ORNO DRINKING = 0.99, 95% CI 0.97–1.02. These findings remained similar after accounting for maternal genotype data in ALSPAC and maternal and paternal genotype data in MoBa. Conclusions: We did not find evidence for a causal effect of fetal alcohol exposure on risk of ADHD symptoms in offspring. The results may be affected by limited power to detect small effects and outcome assessment.publishedVersio