Attachment and Political Personality are Heritable and Distinct Systems, and Both Share Genetics with Interpersonal Trust and Altruism.

The attachment and caregiving domains maintain proximity and care-giving behavior between parents and offspring, in a way that has been argued to shape people's mental models of how relationships work, resulting in secure, anxious or avoidant interpersonal styles in adulthood. Several theorists have suggested that the attachment system is closely connected to orientations and behaviors in social and political domains, which should be grounded in the same set of familial experiences as are the different attachment styles. We use a sample of Norwegian twins (N = 1987) to assess the genetic and environmental relationship between attachment, trust, altruism, right-wing authoritarianism (RWA), and social dominance orientation (SDO). Results indicate no shared environmental overlap between attachment and ideology, nor even between the attachment styles or between the ideological traits, challenging conventional wisdom in developmental, social, and political psychology. Rather, evidence supports two functionally distinct systems, one for navigating intimate relationships (attachment) and one for navigating social hierarchies (RWA/SDO), with genetic overlap between traits within each system, and two distinct genetic linkages to trust and altruism. This is counter-posed to theoretical perspectives that link attachment, ideology, and interpersonal orientations through early relational experiences.

The p factor of psychopathology and personality in middle childhood: genetic and gestational risk factors.

BACKGROUND: A joint, hierarchical structure of psychopathology and personality has been reported in adults but should also be investigated at earlier ages, as psychopathology often develops before adulthood. Here, we investigate the joint factor structure of psychopathology and personality in eight-year-old children, estimate factor heritability and explore external validity through associations with established developmental risk factors. METHODS: Phenotypic and biometric exploratory factor analyses with bifactor rotation on genetically informative data from the Norwegian Mother, Father, and Child Cohort (MoBa) study. The analytic sub-sample comprised 10 739 children (49% girls). Mothers reported their children's symptoms of depression (Short Moods and Feelings Questionnaire), anxiety (Screen for Anxiety Related Disorders), attention-deficit/hyperactivity disorder inattention and hyperactivity, oppositional-defiant disorder, conduct disorder (Parent/Teacher Rating Scale for Disruptive Behavior Disorders), and Big Five personality (short Hierarchical Personality Inventory for Children). Developmental risk factors (early gestational age and being small for gestational age) were collected from the Medical Birth Registry. RESULTS: Goodness-of-fit indices favored a p factor model with three residual latent factors interpreted as negative affectivity, positive affectivity, and antagonism, whereas psychometric indices favored a one-factor model. ADE solutions fitted best, and regression analyses indicated a negative association between gestational age and the p factor, for both the one- and four-factor solutions. CONCLUSION: Correlations between normative and pathological traits in middle childhood mostly reflect one heritable and psychometrically interpretable p factor, although optimal fit to data required less interpretable residual latent factors. The association between the p factor and low gestational age warrants further study of early developmental mechanisms.

Associations between maternal depressive symptoms and risk for offspring early-life psychopathology: the role of genetic and non-genetic mechanisms.

BACKGROUND: Although maternal depressive symptoms are robustly associated with offspring early-life psychopathology symptoms, it is not clear which potential mechanisms are at play. We aimed to estimate the relative importance of genetic transmission and direct environmental exposure in these associations on three occasions in early childhood. METHODS: Biometric modeling of maternal sisters and their offspring from the Norwegian Mother and Child Cohort Study. The analyzed sample comprised 22 316 mothers and 35 589 offspring. Mothers reported their own depressive symptoms using the Symptom checklist, and offspring's concurrent symptoms of psychopathology using the Child Behavior Checklist at 1.5, 3, and 5 years postpartum. RESULTS: Associations between maternal symptoms of depression and offspring emotional problems were predominantly explained by passive genetic transmission at 1.5 and 3 years postpartum. At age 5, associations were more due to direct environmental exposure. For offspring behavioral problems, there was no net increase in the importance of direct environmental exposure across occasions. CONCLUSIONS: Associations between maternal depressive symptoms and offspring psychopathology symptoms remained after accounting for shared genes, consistent with a small, causal effect. For offspring emotional problems, this effect appeared to increase in importance over time. Our findings imply that treatment of maternal depressive symptoms could also benefit the offspring, and that genetic confounding should be considered in future studies of such mother-offspring associations.

How important are parents in the development of child anxiety and depression? A genomic analysis of parent-offspring trios in the Norwegian Mother Father and Child Cohort Study (MoBa).

BACKGROUND: Many studies detect associations between parent behaviour and child symptoms of anxiety and depression. Despite knowledge that anxiety and depression are influenced by a complex interplay of genetic and environmental risk factors, most studies do not account for shared familial genetic risk. Quantitative genetic designs provide a means of controlling for shared genetics, but rely on observed putative exposure variables, and require data from highly specific family structures. METHODS: The intergenerational genomic method, Relatedness Disequilibrium Regression (RDR), indexes environmental effects of parents on child traits using measured genotypes. RDR estimates how much the parent genome influences the child indirectly via the environment, over and above effects of genetic factors acting directly in the child. This 'genetic nurture' effect is agnostic to parent phenotype and captures unmeasured heritable parent behaviours. We applied RDR in a sample of 11,598 parent-offspring trios from the Norwegian Mother, Father and Child Cohort Study (MoBa) to estimate parental genetic nurture separately from direct child genetic effects on anxiety and depression symptoms at age 8. We tested for mediation of genetic nurture via maternal anxiety and depression symptoms. Results were compared to a complementary non-genomic pedigree model. RESULTS: Parental genetic nurture explained 14% of the variance in depression symptoms at age 8. Subsequent analyses suggested that maternal anxiety and depression partially mediated this effect. The genetic nurture effect was mirrored by the finding of family environmental influence in our pedigree model. In contrast, variance in anxiety symptoms was not significantly influenced by common genetic variation in children or parents, despite a moderate pedigree heritability. CONCLUSIONS: Genomic methods like RDR represent new opportunities for genetically sensitive family research on complex human traits, which until now has been largely confined to adoption, twin and other pedigree designs. Our results are relevant to debates about the role of parents in the development of anxiety and depression in children, and possibly where to intervene to reduce problems.

Mechanisms linking parental educational attainment with child ADHD, depression, and academic problems: a study of extended families in The Norwegian Mother, Father and Child Cohort Study.

BACKGROUND: Low educational attainment in parents is associated with child psychopathology. It is not clear whether the associations are due to risk factors that family members share or due to effects of maternal or paternal education on the offspring. We investigate whether associations between maternal and paternal educational attainment and child symptoms of attention deficit/hyperactivity disorder (ADHD), depression, and academic problems are due to shared genetic factors, shared family environmental factors, or effects of the parental phenotype educational attainment itself. METHODS: This study is based on the Norwegian Mother, Father and Child Cohort Study (MoBa). The sample comprised 34,958 children (17,128 girls) in 28,372 extended-family units. We used data from related nuclear families linked by siblings in the parent generation. We applied a quasi-experimental extended children-of-twins design that included siblings in both generations and took account of nonrandom mating by including partners. Educational attainment was self-reported by mothers and fathers. Mothers reported children's symptoms of ADHD, symptoms of depression, and academic problems by questionnaire when the children were 8 years old. RESULTS: Children of lowly educated parents scored higher on all outcomes and had an approximate doubling of the risk of high symptom levels. The association between maternal and paternal educational attainment and child symptoms of ADHD and academic problems persisted after controlling for shared genetic and family environmental factors. Phenotypic transmission to depression was weaker and in the best fitting model fully explained by genetic factors shared by the two generations. CONCLUSIONS: Associations between educational attainment of mothers and fathers and child symptoms of ADHD and academic problems could not be ascribed to shared familial risk factors, whereas associations with symptoms of depression could. Parental education or resources and behaviors resulting from low education might be targets of interventions aimed at reducing symptoms of ADHD and academic problems.

Maternal Perinatal and Concurrent Anxiety and Mental Health Problems in Early Childhood: A Sibling-Comparison Study.

Do associations between maternal anxiety symptoms and offspring mental health remain after comparing differentially exposed siblings? Participants were 17,724 offspring siblings and 11,553 mothers from the Norwegian Mother and Child Cohort study. Mothers reported anxiety and depressive symptoms at 30 weeks' gestation, and 0.5, 1.5, 3, and 5 years postpartum. Child internalizing and externalizing problems were assessed at ages 1.5, 3, and 5, and modeled using multilevel analyses with repeated measures nested within siblings, nested within mothers. Maternal pre- and postnatal anxiety were no longer associated with child internalizing or externalizing problems after adjusting for maternal depression and familial confounding. Maternal anxiety when the children were in preschool age, however, remained significantly associated with child internalizing but not externalizing problems.

A Life Course Study of Genetic and Environmental Influences on Work Incapacity.

Work incapacity is a major public health challenge and an economic burden to both society and individuals. Understanding the underlying causes is becoming ever more relevant as many countries face an aging workforce. We examined stability and change in genetic and environmental factors influencing work incapacity from age 18 until retirement, and sex differences in these effects. The large population-based sample comprised information from 28,759 twins followed for up to 23 years combined with high-quality national registry data. We measured work incapacity as the total proportion of potential workdays lost due to sickness absence, rehabilitation and disability benefits. Structural equation modeling with twin data indicated moderate genetic influences on work incapacity throughout life in both men and women, with a high degree of genetic stability from young to old adulthood. Environmental influences were mainly age-specific. Our results indicate that largely the same genetic factors influence individual differences in work incapacity throughout young, middle and older adulthood, despite major differences in degree of work incapacity and probable underlying medical causes.

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.

Development of ADHD symptoms in preschool children: Genetic and environmental contributions.

We examined genetic and environmental contributions to the development of symptoms of attention-deficit/hyperactivity disorder (ADHD) in preschool children. ADHD symptoms in siblings at 1.5, 3, and 5 years of age were investigated in a population-based sample from the prospective Norwegian Mother and Child Cohort Study. The longitudinal contributions of additive genetic, shared, twin-specific, and unique environmental influences were estimated using biometric structural equation models. Heritability of ADHD symptoms ranged from 54% to 70%. There was evidence of partially new genetic influences at successive ages, with genetic correlations ranging from .58 to .89. Contributions from shared environmental factors and twin-specific factors were minor. The importance of unique environmental effects appeared to increase across ages, and was mostly specific to a given age. There was no evidence suggesting that this pattern differs across males and females. Symptoms of ADHD are highly heritability in young children from as early as 1.5 years of age. Longitudinal stability of ADHD symptoms is mainly attributable to genetic influences, but there is also some evidence for age-specific genetic influences. These findings contribute to our understanding of development of ADHD early in life, and can guide future molecular genetics studies.

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.

Maternal perinatal and concurrent depressive symptoms and child behavior problems: a sibling comparison study.

BACKGROUND: Previous studies have found significant associations between maternal prenatal and postpartum depression and child behavior problems (CBP). The present study investigates whether associations remain in a prospective, longitudinal design adjusted for familial confounding. METHODS: The sample comprised 11,599 families including 17,830 siblings from the Norwegian Mother and Child Cohort study. Mothers reported depressive symptoms at gestational weeks 17 and 30, as well as 6 months, 1.5, 3, and 5 years postpartum. Fathers' depression was measured at gestational week 17. At the last three time-points, child internalizing and externalizing problems were concurrently assessed. We performed multilevel analyses for internalizing and externalizing problems separately, using parental depression as predictors. Analyses were repeated using a sibling comparison design to adjust for familial confounding. RESULTS: All parental depressive time-points were significantly and positively associated with child internalizing and externalizing problems. After sibling comparison, however, only concurrent maternal depression was significantly associated with internalizing [estimate = 2.82 (1.91-3.73, 95% CI)] and externalizing problems [estimate = 2.40 (1.56-3.23, 95% CI)]. The effect of concurrent maternal depression on internalizing problems increased with child age. CONCLUSIONS: Our findings do not support the notion that perinatal maternal depression is particularly detrimental to children's psychological development, as the most robust effects were found for maternal depression occurring during preschool years.

Pre-pregnancy mental distress and musculoskeletal pain and sickness absence during pregnancy - a twin cohort study.

Background: Sickness absence (SA) among pregnant women is high. The aim of this study was to examine whether factors known to predict SA in general also predict SA during pregnancy by estimating the association between prior mental distress and musculoskeletal pain and SA during pregnancy, and to assess the influence of familial (genetic and shared environmental) factors. In this prospective cohort study, data from 2076 female twins born 1967-79 who participated in a questionnaire study in 1998 were linked to register data on SA and childbirth during the years 1998-2008. Baseline measures included mental distress (symptoms of anxiety and depression; SCL-5) and musculoskeletal pain (lumbar spine, neck/shoulder and/or persisting muscular pain). SA was measured as a ratio of days on SA divided by potential working days. Negative binomial regression was performed for individual and within-pair effects. Musculoskeletal pain, but not mental distress, was prospectively associated with overall SA during pregnancy in the adjusted individual-level analyses. With each standard deviation increase in musculoskeletal pain, SA granted for any disorder increased with 12% (IRR 1.12, 95% CI = 1.07-1.17) and SA granted for pregnancy related disorders increased with 9% (IRR 1.09, 95% CI = 1.02-1.17). Within-pair estimates were similar, suggesting little or no familial confounding. Women with previous musculoskeletal pain are at increased risk of SA during pregnancy, whereas no increased risk in women with previous symptoms of mental distress could be demonstrated. SA during pregnancy seems partly to be associated with different factors than SA in general.

Does low alcohol use increase the risk of sickness absence? A discordant twin study.

BACKGROUND: Results from observational studies suggest that people who drink little or no alcohol are less healthy than medium drinkers. This has been demonstrated for many different measures of health, including sick leave. However, whether these associations are causal or due to confounding remains to be clarified. The aim of this study was to use a discordant twin design to determine whether the increased level of sick leave associated with a low level of alcohol consumption, as compared to those with a medium level of consumption, reflects a causal mechanism or is due to genetic or environmental confounding. METHODS: Six thousand seven hundred thirty-four young adult twins from the Norwegian Institute of Public Health's twin panel were in 1998 assessed for frequency of alcohol use and binge drinking. Data were linked to the Norwegian National Insurance Administration's recordings of sick leave over a 10 year period. The associations between alcohol consumption and sick leave were first estimated in the total study population, and then within di- and monozygotic twin pairs discordant for alcohol use. RESULTS: Compared to medium consumption, both low and high alcohol consumption was associated with increased risk of sick leave. When low level drinkers were compared to medium level drinkers in a discordant twin design, the results were consistent with the association being due to genetic confounding rather than a causal effect. CONCLUSIONS: The increased level of sick leave observed with low level drinkers seems to be mainly explained by confounding from genetic factors. In all observational studies of the relationship between alcohol consumption and health, one should be aware that important genetic confounders are likely to influence the results.

Mood, anxiety, and alcohol use disorders and later cause-specific sick leave in young adult employees.

BACKGROUND: Mental disorders strongly influence work capability in young adults, but it is not clear which disorders that are most strongly associated with sick leave, and which diagnoses that are stated on the sick leave certificates. Better knowledge of the impairments associated with different mental disorders is needed for optimal planning of interventions and prioritization of health services. In the current study, we investigate the prospective associations between eight mood, anxiety, and alcohol use disorders, and later sick leave granted for mental, somatic, or any disorder. METHODS: Lifetime mental disorders were assessed by structured diagnostic interviews in 2,178 young adults followed for eight years with registry data on sick leave. Relative risk ratios were estimated for the associations between each mental disorder and the different forms of sick leave. RESULTS: All included diagnoses were associated with later sick leave. In adjusted analyses, major depressive disorder and generalized anxiety disorder were the strongest predictors of sick leave granted for mental disorders, whereas social anxiety disorder and specific phobia were the strongest predictors of sick leave granted for somatic disorders. Specific phobia and major depressive disorder had the highest attributable fractions for all-cause sick leave. CONCLUSIONS: Mood and anxiety disorders constituted independent risk factors for all cause sick leave, whereas alcohol use disorders seemed to be of less importance in young adulthood. Disorders characterised by distress were most strongly associated with sick leave granted for mental disorders, whereas disorders characterised by fear primarily predicted sick leave granted for somatic conditions. A large part of all sick leave is related to specific phobia, due to the high prevalence of this disorder. The impairment associated with this common disorder may be under-acknowledged, and it could decrease work capacity among individuals with somatic disorders. This disorder has good treatment response and may be overlooked as a target for interventions aimed at prevention of sick leave.

Genetic and environmental contributions to the relationship between internalizing disorders and sick leave granted for mental and somatic disorders.

This study investigates the degree to which internalizing disorders (anxiety and mood disorders) are prospectively associated with sick leave granted for mental and somatic disorders, and the extent to which common genetic and environmental risk factors influence these relationships. Data include self-reported symptoms of psychological distress from 7,598 young adult twins and diagnostic interviews on a subsample of 2,766 adult twins, subsequently linked to registry data on sick leave. Regression analyses and multivariate twin models were used to investigate the relationship between internalizing disorders and sick leave. Internalizing disorders were associated with sick leave granted for both mental disorders and somatic disorders. The association between internalizing disorders and sick leave granted for mental disorders was influenced by genetic and non-shared environmental factors, while the association between internalizing disorders and sick leave granted for somatic disorders could be explained by common genetic factors alone. Monozygotic twins discordant for internalizing disorders differed significantly in rates of sick leave granted for mental but not somatic disorders. In conclusion, internalizing disorders in young adults predict sick leave granted for both mental and somatic disorders. Environmental risk factors for internalizing disorders seem to influence sick leave granted for mental disorders, but not sick leave granted for somatic disorders.

Personality disorders and long-term sick leave: a population-based study of young adult Norwegian twins.

Personality disorders (PDs) reduce global functioning, are associated with high levels of work disability, and are thus also likely to influence long-term sick leave (LTSL). Previous research has indicated significant genetic influence on both DSM-IV PDs and LTSL. To what degree genes contributing to PDs also influence LTSL has not been investigated. The aims of the current study were to investigate which PDs were significantly associated with LTSL, to what extent the genetic contributions to these PDs account for the heritability of LTSL, and to explore the hypothesis of a causal association between PDs and LTSL. The sample consisted of 2,771 young, adult Norwegian twins, born 1967-1979. PDs were assessed using the Structured Interview for DSM-IV Personality (SIDP-IV). The age range for the interview was 20-32. The data were subsequently linked to public records of LTSL (sick leave >16 days) up to 11 years later. The odds ratio for being in the highest LTSL category (>15% sick leave) when fulfilling the DSM-IV criteria for any PD diagnosis was 2.6 (1.8-3.8, 95% CI). Dimensional representations of schizotypal, paranoid, and borderline PD were independently and significantly associated with LTSL. The heritability of LTSL was 0.50. Genetic factors shared with the PDs accounted for 20% of this. The association between PDs and LTSL was due to shared genetic and not environmental influences, and was mainly explained by one common genetic factor. The hypothesis of a causal association was not supported, indicating that the association is explained by overlapping genetic liability between PDs and LTSL.

Personality disorders are important risk factors for disability pensioning.

PURPOSE: To determine whether personality disorders (PDs) are associated with increased risk of disability pensioning in young adults, independent of other common mental disorders. METHODS: 2,770 young adults from the general population were assessed for PDs by the Structured Interview for DSM-IV Personality, and for common mental disorders by the Composite of International Diagnostic Interview. These data were linked to the Norwegian National Insurance Administration's recordings of disability benefits for a 10-year period. Logistic regression analyses were applied to investigate the association between PDs and disability pensioning. The analyses were conducted for three types of PD measures: categorical diagnoses (any PD), dimensional scores of individual PDs and higher order components retrieved by principal component analyses. RESULTS: Having any PD was strongly associated with disability pensioning, regardless of disability diagnosis. The estimated odds ratio (OR) was substantially higher for PDs [OR 4.69 (95% confidence interval (CI) 2.6-8.5)] than for mood disorders [OR 1.3 (CI 0.7-2.3)] and anxiety disorders [OR 2.3 (CI 1.3-4.3)]. Measured dimensionally, all PD traits except antisocial traits were significantly associated with disability pensioning. After adjusting for co-occurring traits of other PDs, only schizoid, dependent and borderline PD traits showed a significant positive association with disability pension, while antisocial traits showed a significant negative association. The principal component analyses showed that negative affectivity, psychoticism, and detachment was associated with an increased risk of disability pensioning, while antagonism/disinhibition and obsessivity were not. CONCLUSIONS: PDs are strongly associated with disability pensioning in young adults, and might be more important predictors of work disability than anxiety and depressive disorders. Certain aspects of pathologic personalities are particularly important predictors of disability.

Bridging temperament and the Big Five in children: A genetically informative study.

Early temperament precedes children's emerging Big Five personality, but shared models of temperament and personality are scarce. We wanted to estimate the genetic factor structure underlying both temperament and the Big Five in children, employing a genetically informed study. Within the Norwegian Mother and Child Cohort Study, we selected 26,354 twins, siblings, and cousins. Mothers rated their children's temperament three times between the ages of 1.5 and 5 years, and the children's Big Five personality at the age of 8. We analyzed the data using biometric modeling. The mean heritability of single-time temperamental traits and Big Five personality traits was .48 and .45, respectively. The mean genetic correlations of temperament across time were .80. The genetic correlations of temperament at 5 years and the Big Five at 8 years revealed two factors, the first comprising reversed Big Five Neuroticism, Agreeableness, Conscientiousness, and reversed EAS Emotionality, the second comprising Big Five Extraversion, Openness to Experience, EAS Activity, Sociability, and reversed Shyness. A confirmatory factor analysis estimated the two factors showing heritabilities of .96 and .72, respectively. The two factors mirrored the metatraits Stability and Plasticity by John M. Digman. Temperament and personality in childhood can be meaningfully bridged using just two metafactors. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Genetic and environmental contributions to long-term sick leave and disability pension: a population-based study of young adult Norwegian twins.

Although exclusion from the workforce due to long-term sick leave (LTSL) and disability pension (DP) is a major problem in many Western countries, the etiology of LTSL and DP is not well understood. These phenomena have a strong association as most patients receiving DP have first been on LTSL. However, only a few of those on LTSL end up with DP. The present study aimed to investigate the common and specific genetic and environmental risk factors for LTSL and DP. The present study utilizes a population-based sample of 7,710 young adult twins from the Norwegian Institute of Public Health Twin Panel, which has been linked to the Historical-Event Database (FD-Trygd; 1998-2008). Univariate and bivariate twin models were fitted to determine to what degree genetic and environmental factors contribute to variation in LTSL and DP. The estimated heritabilities of LTSL and DP were 0.49 and 0.66, respectively. There was no evidence for shared environmental or sex-specific factors. The phenotypic-, genetic-, and non-familial environmental correlations between the variables were 0.86, 0.82, and 0.94, respectively. Our results indicate that familial transmission of LTSL and DP is due to genetic and not environmental factors. The risk factors contributing to LTSL and DP were mainly shared, suggesting that what increases risk for LTSL also increases risk for DP. However, a non-negligible part of the genetic variance was not shared between the variables, which may contribute to explaining why some progress from LTSL to DP, whereas others return to work.