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

Association between maternal education and diet of children at 9 months is partially explained by mothers\u27 diet

Infants of mothers of low educational background display consistently poorer outcomes, including suboptimal weaning diets. Less is known about the different causal pathways that relate maternal education to infants\u27 diet. The present study aimed to test the hypothesis that the relationship between maternal education and infants\u27 diet is mediated by mothers\u27 diet. The analyses included 421 mother–infant pairs from the Melbourne Infant Feeding Activity and Nutrition Trial (InFANT) Program. Dietary intakes were collected from mothers when infants were aged 3 months, using a validated food frequency questionnaire relating to the past year, and in infants aged 9 months using 3 × 24-h recalls. Principal component analysis was used to derive dietary pattern scores, based on frequencies of 55 food groups in mothers, and intakes of 23 food groups in infants. Associations were assessed with multivariable linear regression. We tested the product ‘ab’ to address the mediation hypothesis, where ‘a’ refers to the relationship between the predictor variable (education) and the mediator variable (mothers\u27 diet), and ‘b’ refers to the association between the mediator variable and the outcome variable (infants\u27 diet), controlling for the predictor variable. Maternal scores on the ‘Fruit and vegetables’ dietary pattern partially mediated the relationships between maternal education and two infant dietary patterns, namely ‘Balanced weaning diet’ [ab = 0.11; 95% confidence interval (CI): 0.04; 0.18] and ‘Formula’ (ab = −0.08; 95%CI: −0.15; −0.02). These findings suggest that targeting pregnant mothers of low education level with the aim of improving their own diet may also promote better weaning diets in their infants

Breastfeeding and depression: a systematic review of the literature

Background: Research has separately indicated associations between pregnancy depression and breastfeeding, breastfeeding and postpartum depression, and pregnancy and postpartum depression. This paper aimed to provide a systematic literature review on breastfeeding and depression, considering both pregnancy and postpartum depression. Methods: An electronic search in three databases was performed using the keywords: “breast feeding”, “bottle feeding”, “depression”, “pregnancy”, and “postpartum”. Two investigators independently evaluated the titles and abstracts in a first stage and the full-text in a second stage review. Papers not addressing the association among breastfeeding and pregnancy or postpartum depression, non-original research and research focused on the effect of antidepressants were excluded. 48 studies were selected and included. Data were independently extracted. Results: Pregnancy depression predicts a shorter breastfeeding duration, but not breastfeeding intention or initiation. Breastfeeding duration is associated with postpartum depression in almost all studies. Postpartum depression predicts and is predicted by breastfeeding cessation in several studies. Pregnancy and postpartum depression are associated with shorter breastfeeding duration. Breastfeeding may mediate the association between pregnancy and postpartum depression. Pregnancy depression predicts shorter breastfeeding duration and that may increase depressive symptoms during postpartum. Limitations: The selected keywords may have led to the exclusion of relevant references. Conclusions: Although strong empirical evidence regarding the associations among breastfeeding and pregnancy or postpartum depression was separately provided, further research, such as prospective studies, is needed to clarify the association among these three variables. Help for depressed pregnant women should be delivered to enhance both breastfeeding and postpartum psychological adjustment.This research was supported by FEDER Funds through the Programa Operacional Factores de Competitividade – COMPETE and by National Funds through FCT – Fundaçãopara a Ciência e a Tecnologiaunder the project: PTDC/SAU/SAP/116738/2010. The sponsors had no further role in the study design; in the collection, analysis and interpretation of data; in the writing of the report; and in the decision to submit the paper for publication

Revisiting the Children-of-Twins Design:Improving Existing Models for the Exploration of Intergenerational Associations

Datasets comprising twins and their children can be a useful tool for understanding the nature of intergenerational associations between parent and offspring phenotypes. In the present article we explore structural equation models previously used to analyse Children-of-Twins data, highlighting some limitations and considerations. We then present new variants of these models, showing that extending the models to include multiple offspring per parent addresses several of the limitations discussed. Accompanying the updated models, we provide power calculations and demonstrate with application to simulated data. We then apply to intergenerational analyses of height and weight, using a sub-study of the Norwegian Mother and Child Cohort (MoBa); the Intergenerational Transmission of Risk (IToR) project, wherein all kinships in the MoBa data have been identified (a children-of-twins-and-siblings study). Finally, we consider how to interpret the findings of these models and discuss future directions.Keyword

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

Socioeconomic status and risk for child psychopathology:exploring gene-environment interaction in the presence of gene-environment correlation using extended families in the Norwegian Mother, Father and Child Birth Cohort Study

Background: Low socioeconomic status (SES) is associated with increased risk for emotional and behavioural problems among children. Evidence from twin studies has shown that family SES moderates genetic and environmental influences on child mental health. However, it is also known that SES is itself under genetic influence and previous gene-environment interaction (G×E) studies have not incorporated the potential genetic overlap between child mental health and family SES into G×E analyses. We applied a novel approach using extended family data to investigate the moderation of aetiological influences on child emotional and behavioural problems by parental socioeconomic status in the presence of modelled gene-environment correlation. Methods: The sample comprised &gt;28,100 children in extended-family units drawn from the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers reported children’s emotional and behavioural symptoms. Parents’ income and educational attainment were obtained through linkage to administrative register data. Bivariate moderation Multiple-Children-of-Twins-and-Siblings (MCoTS) models were used to analyse relationships between offspring outcomes (emotional and behavioural symptom scores) and parental socioeconomic moderators (income rank and educational attainment). Results: The aetiology of child emotional symptoms was moderated by maternal and paternal educational attainment. Shared environmental influences on child emotional symptoms were greater at lower levels of parents’ education. The aetiology of child behavioural symptoms was moderated by maternal, but not paternal, socioeconomic factors. Genetic factors shared between maternal income and child behavioural symptoms were greater in families with lower levels maternal income. Nonshared environmental influences on child behavioural symptoms were greater in families with higher maternal income and education. Conclusions: Parental socioeconomic indicators moderated familial influences and non-shared environmental influences on child emotional and behavioural outcomes. Maternal SES and child mental health share aetiological overlap such that shared genetic influence was greater at the lower end of the socioeconomic distribution. Our findings collectively highlight the role that family socioeconomic factors play in shaping the origins of child emotional and behavioural problems. <br/

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

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

Socioeconomic status and risk for child psychopathology: exploring gene–environment interaction in the presence of gene–environment correlation using extended families in the Norwegian Mother, Father and Child Birth Cohort Study

Background Low socioeconomic status (SES) is associated with increased risk for emotional and behavioural problems among children. Evidence from twin studies has shown that family SES moderates genetic and environmental influences on child mental health. However, it is also known that SES is itself under genetic influence and previous gene–environment interaction (G×E) studies have not incorporated the potential genetic overlap between child mental health and family SES into G×E analyses. We applied a novel approach using extended family data to investigate the moderation of aetiological influences on child emotional and behavioural problems by parental socioeconomic status in the presence of modelled gene–environment correlation. Methods The sample comprised &gt;28,100 children in extended‐family units drawn from the Norwegian Mother, Father and Child Cohort Study (MoBa). Mothers reported children's emotional and behavioural symptoms. Parents' income and educational attainment were obtained through linkage to administrative register data. Bivariate moderation Multiple‐Children‐of‐Twins‐and‐Siblings (MCoTS) models were used to analyse relationships between offspring outcomes (emotional and behavioural symptom scores) and parental socioeconomic moderators (income rank and educational attainment). Results The aetiology of child emotional symptoms was moderated by maternal and paternal educational attainment. Shared environmental influences on child emotional symptoms were greater at lower levels of parents' education. The aetiology of child behavioural symptoms was moderated by maternal, but not paternal, socioeconomic factors. Genetic factors shared between maternal income and child behavioural symptoms were greater in families with lower levels maternal income. Nonshared environmental influences on child behavioural symptoms were greater in families with higher maternal income and education. Conclusions Parental socioeconomic indicators moderated familial influences and nonshared environmental influences on child emotional and behavioural outcomes. Maternal SES and child mental health share aetiological overlap such that shared genetic influence was greater at the lower end of the socioeconomic distribution. Our findings collectively highlight the role that family socioeconomic factors play in shaping the origins of child emotional and behavioural problems