Nonshared Environment Research Articles

Evidence for distinct genetic and environmental influences on fear acquisition and extinction.

Anxiety disorders are highly prevalent with an early age of onset. Understanding the aetiology of disorder emergence and recovery is important for establishing preventative measures and optimising treatment. Experimental approaches can serve as a useful model for disorder and recovery relevant processes. One such model is fear conditioning. We conducted a remote fear conditioning paradigm in monozygotic and dizygotic twins to determine the degree and extent of overlap between genetic and environmental influences on fear acquisition and extinction. In total, 1937 twins aged 22-25 years, including 538 complete pairs from the Twins Early Development Study took part in a fear conditioning experiment delivered remotely via the Fear Learning and Anxiety Response (FLARe) smartphone app. In the fear acquisition phase, participants were exposed to two neutral shape stimuli, one of which was repeatedly paired with a loud aversive noise, while the other was never paired with anything aversive. In the extinction phase, the shapes were repeatedly presented again, this time without the aversive noise. Outcomes were participant ratings of how much they expected the aversive noise to occur when they saw either shape, throughout each phase. Twin analyses indicated a significant contribution of genetic effects to the initial acquisition and consolidation of fear, and the extinction of fear (15, 30 and 15%, respectively) with the remainder of variance due to the non-shared environment. Multivariate analyses revealed that the development of fear and fear extinction show moderate genetic overlap (genetic correlations 0.4-0.5). Fear acquisition and extinction are heritable, and share some, but not all of the same genetic influences.

Socioeconomic Background and Gene–Environment Interplay in Social Stratification across the Early Life Course

AbstractTo what extent are differences in education, occupational standing, and income attributable to genes, and do genetic influences differ by parents’ socioeconomic standing? When in a children’s life course does parents’ socioeconomic standing matter for genetic influences, and for which of the outcomes, fixed at the different stages of the attainment process, do they matter most? We studied these research questions using Finnish register-based data on 6,529 pairs of twins born between 1975 and 1986. We applied genetically sensitive variance decompositions and took gene–environment interactions into account. Since zygosity was unknown, we compared same-sex and opposite-sex twins to estimate the proportion of genetic variation. Genetic influences were strongest in education and weakest in income, and always strongest among those with the most advantaged socioeconomic background, independent of the socioeconomic indicator used. We found that the shared environment influences were negligible for all outcomes. Parental social background measured early during childhood was associated with weaker interactions with genetic influences. Genetic influences on children’s occupation were largely mediated through their education, whereas for genetic influences on income, mediation through education and occupational standing made little difference. Interestingly, we found that non-shared environment influences were greater among the advantaged families and that this pattern was consistent across outcomes. Stratification scholars should therefore emphasize the importance of the non-shared environment as one of the drivers of the intergenerational transmission of social inequalities.

Elucidating the Links Between Mother and Father Alcohol Use Disorder and Adolescent Externalizing Psychopathology: A Test of Transmission Specificity Within Competing Factor Structures and Genetic and Environmental Liabilities.

Parental alcohol use disorder (AUD) is a substantiated risk factor for adolescent externalizing psychopathology; however, the level of specificity at which risk from parental AUD is transmitted to adolescent offspring should be interrogated further. The current study modeled competing factor structures of psychopathology in a sample of 502 adolescent twin pairs (Mage = 13.24years) and tested associations with mother and father AUD. The bifactor model exhibited the best fit to the data when contrasted with correlated factors and general factor models. Paternal AUD predicted the externalizing and internalizing correlated factors, the adolescent P-factor but not the residual externalizing and internalizing factors, and the general factor. No significant associations with maternal AUD were noted. Lastly, the latent factors of adolescent psychopathology were all moderately heritable (h2 = 0.44-0.59) and influenced by the nonshared environment. Shared genetic factors primarily explained externalizing and internalizing covariance. Findings suggest that efforts to mitigate risk in offspring of fathers exhibiting AUD require broader approaches that address the full range of adolescent symptomology.

Behavioral and biological divergence in monozygotic twin pairs discordant for autism phenotypes: A systematic review.

Non-shared environment (NSE) effects account for around one-third of the etiology of autism spectrum disorder (ASD). However, the knowledge of mechanisms and phenotypic profiles associated with NSE in ASD is scarce. A systematic search was conducted using Embase, MEDLINE, and PsycINFO for studies published in English between 1990 and August 2020 using co-twin control design to compare behavioral and biological phenotypes among monozygotic (MZ) twin pairs concordant/discordant for ASD, clinical autism symptoms, or autistic traits. Risk of bias was assessed through a modified Newcastle-Ottawa Scale. Twenty six articles were included. Differential DNA methylation and gene expression were found among ASD discordant twins; however, genetic results were inconsistent. Neurological disorders and early medical events were associated with ASD and autistic traits, while no within pair differences were found for minor physical anomalies or head circumference. Structural and functional brain imaging studies and research on social and other cognitive/behavioral functions were inconclusive. Risk of bias assessment found that all studies used the same exposure (or outcome) measures to collect data for participants and most used either secure health-related records or structured interviews for ascertainment of exposure; however, only a handful of studies representative of the population from which they were drawn. Formal assessment of risk of publication bias (i.e., funnel plot) was not possible. Our results suggest that NSE in ASD could be associated with heterogeneous postzygotic genetic mechanisms and manifest as a range of biological and behavioral phenotypes. Extant findings were limited by relatively few studies, small sample sizes, and methodological diversity. More research is needed on co-occurring biological and behavioral phenotypes using a consistent format for designing, analyzing, and reporting MZ ASD discordant twin studies in order to further examine the role of NSE in the etiology of ASD.

The association between bullying-victimisation and sleep disturbances in adolescence: Evidence from a twin study.

Bullying-victimisation has been associated with sleep disturbances. This study investigated the degree to which subtypes of bullying-victimisation in adolescence are linked with sleep disturbances. Genetic and environmental contributions underlying bullying-victimisation and sleep disturbances were investigated. Participants (3,242-5,076 pairs) from a longitudinal community twin study reported on their bullying-victimisation at the age of 14years, and sleep quality and insomnia symptoms at age 16. Regression analyses were used, accounting for the role of individual and family factors. Structural equation twin model fitting was conducted. Bullying-victimisation was modestly associated with sleep quality and insomnia symptoms (r=0.22-0.23) and a similar strength of associations was found across bullying-victimisation subtypes (r=0.11-0.22). Bullying-victimisation, sleep quality and insomnia symptoms were predominantly influenced by genes (25-59%) and non-shared environments (40-62%). The association between bullying-victimisation and sleep quality was explained by genetic and non-shared environmental influences. For insomnia symptoms and sleep quality, the association with bullying-victimisation was in part explained by a genetic overlap. Associations between bullying-victimisation and sleep disturbances are not limited to specific aspects of bullying-victimisation but appear to exist for all subtypes. These findings stimulate research questions regarding the mechanisms underlying these links. For example, could certain heritable traits, such as temperament, increase vulnerability to experiencing sleep disturbances and being bullied? Research on bullying and sleep should aim to take the role of genetic predisposition into account, while also noting that it is not the only causal influence. Understanding more about these pathways could strengthen the development of techniques to prevent these difficulties from occurring.

Genetic and environmental influences on corticostriatal circuits in twins with autism

Corticostriatal circuits (CSC) have been implicated in the presentation of some restricted and repetitive behaviours (RRBs) in children with autism-spectrum disorder (ASD), and preliminary evidence suggests that disruptions in these pathways may be associated with differences in genetic and environmental influences on brain development. The objective of this investigation was to examine the impact of genetic and environmental factors on CSC regions in twins with and without ASD and to evaluate their relationship with the severity of RRBs. We obtained T1-weighted MRIs from same-sex monozygotic and dizygotic twin pairs, aged 6–15 years. Good-quality data were available from 48 ASD pairs (n = 96 twins; 30 pairs concordant for ASD, 15 monozygotic and 15 dizygotic; 18 pairs discordant for ASD, 4 monozygotic and 14 dizygotic) and 34 typically developing control pairs (n = 68 twins; 20 monozygotic and 14 dizygotic pairs). We generated structural measures of the orbitofrontal cortex (OFC), anterior cingulate cortex (ACC), caudate, putamen, pallidum and thalamus using FreeSurfer. Twin pair comparisons included intraclass correlation analyses and ACE modelling (a2 = additive genetics; c2 = common or shared environment; e2 = unique or nonshared environment). We also assessed correlations with RRB severity. Structural variation in CSC regions was predominantly genetically mediated in typically developing twins (a2 = 0.56 to 0.87), except for ACC white matter volume (a2 = 0.42, 95% confidence interval [CI] 0.08 to 0.77). We also observed similar magnitudes of genetic influence in twins with ASD (a2 = 0.65 to 0.97), but the cortical thickness of the ACC (c2 = 0.44, 95% CI 0.22 to 0.66) and OFC (c2 = 0.60, 95% CI 0.25 to 0.95) was primarily associated with environmental factors in only twins with ASD. Twin pair differences in OFC grey matter volume were also correlated with RRB severity and were predominantly environmentally mediated. We obtained MRIs on 2 scanners, and analytical approaches could not identify specific genetic and environmental factors. Genetic factors primarily contribute to structural variation in subcortical CSC regions, regardless of ASD, but environmental factors may exert a greater influence on the development of grey matter thickness in the OFC and ACC in children with ASD. The increased vulnerability of OFC grey matter to environmental influences may also mediate some heterogeneity in RRB severity in children with ASD.

Neighborhood Deprivation Moderates Shared and Unique Environmental Influences on Hazardous Drinking: Findings from a Cross-Sectional Co-Twin Study

Background: There has been increased interest in the interplay of genetic and environmental factors in the development of problematic alcohol use, including socioeconomic conditions of the neighborhood. Using a co-twin design, we examined the extent to which contributions of genetic, shared environmental, and unique environmental influences on hazardous drinking differed according to levels of neighborhood socioeconomic deprivation. Method: Data came from 1,521 monozygotic (MZ) and 609 dizygotic (DZ) twin pairs surveyed in Washington State. A measure of neighborhood deprivation was created based on census-tract-level variables and the Alcohol Use Disorders Identification Test 3-item instrument was used to assess level of hazardous drinking. We tested a series of nested structural equation models to examine associations among hazardous drinking, neighborhood deprivation, and the variance components (genetic [A], shared [C] and unique environmental [E] influences) of these two constructs, testing for both main effects and moderation by neighborhood deprivation. Results: Neighborhood deprivation was significantly associated with increased hazardous drinking, after accounting for A and C variance common to both phenotypes. Adjusting for within-pair differences in income and education, neighborhood deprivation moderated the magnitude of variance components of hazardous drinking, with the variance attributable to shared environment and non-shared environment increasing in more deprived neighborhoods. Conclusions: Findings point to amplification of early childhood as well as unique adulthood environmental risk on hazardous drinking in areas of greater deprivation.

6.59 PSYCHOSOCIAL ADVERSITY FACTORS AND NONSHARED ENVIRONMENTAL DIFFERENCES ASSOCIATED WITH ADHD IN A HIGH-RISK POPULATION

This poster presentation aims to describe the differences between an ADHD index sibling (AIS) and their high-risk siblings (HAS) with and without ADHD, with regard to their perception of nonshared environment and their psychosocial adversity factors.

Genetic and Environmental Influences on the Correlations between Traits of Metabolic Syndrome and CKD.

Metabolic syndrome is a cluster of risk factors associated with CKD. By studying the genetic and environmental influences on how traits of metabolic syndrome correlate with CKD, the understanding of the etiological relationships can be improved. From the population-based TwinGene project within the Swedish Twin Registry, 4721 complete twin pairs (9442 European ancestry participants) were included in this cross-sectional twin study. Metabolic syndrome-related continuous traits were measured, and the binary components as well as the status of metabolic syndrome were defined according to the National Cholesterol Education Program-Adult Treatment Panel III. The eGFR was calculated by cystatin C-based equations from the CKD epidemiology collaboration group, and CKD was defined by eGFR<60 ml/min per 1.73 m2. Genetic and environmental contributions to the correlations between traits of metabolic syndrome and CKD were estimated by using twin-based bivariate structural equation models. The correlation between metabolic syndrome and eGFR-defined CKD was 0.16 (95% confidence interval [95% CI], 0.12 to 0.20), out of which 51% (95% CI, 12% to 90%) was explained by genes, whereas 15% (95% CI, 0% to 42%) and 34% (95% CI, 16% to 52%) was explained by the shared and nonshared environment, respectively. The genetic and environmental correlations between metabolic syndrome and CKD were 0.29 (95% CI, 0.07 to 0.51) and 0.27 (95% CI, 0.13 to 0.41), respectively. For the correlation between abdominal obesity and eGFR, 69% (95% CI, 10% to 100%) was explained by genes and 23% (95% CI, 5% to 41%) was explained by environment. The genetic correlation between abdominal obesity and eGFR was -0.30 (95% CI, -0.54 to -0.06), whereas the environmental correlation was -0.14 (95% CI, -0.22 to -0.06). Both genes and environment contribute to the correlation between metabolic syndrome and eGFR-defined CKD. The genetic contribution is particularly important to the correlation between abdominal obesity and eGFR.

The relationship between independent and dependent life events and depression symptoms in Sri Lanka: a twin and singleton study

PurposeLife events have been associated with a variety of mental health conditions including depression. There is a scarcity of research in South Asia exploring the aetiology of independent and dependent life events and their relationship with depression symptoms. This study aimed, in a Sri Lankan population, to identify the socio-demographic correlates and genetic and environmental influences on independent and dependent life events and their relationship with depression.MethodsQuestionnaire data came from the Colombo Twin and Singleton Follow-up Study, CoTaSS-2 (N = 3969), a population study of Sri Lankan twins and singletons. Lifetime-ever independent and dependent life events were measured using a questionnaire and depressive symptoms using the Revised Beck’s Depression Inventory. Structural Equation Model-fitting analyses explored the genetic and environmental influences on life events and depression.ResultsLiving in a rural environment and financial hardship were associated with greater reporting of independent and dependent life events. Sex differences were evident in the aetiology of life events and depression symptoms. Independent and dependent life events, but not depression symptoms, were heritable in males. Independent life events and depression symptoms, but not dependent life events, were heritable in females. Non-shared environmental influences explained phenotypic associations between independent life events and depression symptoms in both males and females. Genetic and non-shared environmental influences explained the phenotypic associations between dependent life events and depression symptoms in males. Only non-shared environment explained the covariation between dependent life events and depression symptoms in females.ConclusionsSocio-demographic correlates of independent and dependent life events were similar to those reported in Western populations. Life events were associated with increased depression symptoms. Contrary to research in Western populations, we found that non-shared environmental, rather than genetic, influences explained much of the covariation between life events and depression symptoms. This suggests that whilst independent LEs may be heritable, the relationship is unlikely to be confounded by genetic influences and has significant implications for possible interventions for depression.

Deciphering the role of epigenetics in self-limited epilepsy with centrotemporal spikes

ObjectiveThe aetiology of self-limited epilepsy with centro-temporal spikes (SECTS) remains controversial and a strong genetic basis has long been presumed. The discordant monozygotic twin (MZ) model controls for shared genetic and environmental factors, enabling focus on the potential role of the non-shared environment. MethodsDNA methylation data was acquired from DNA extracted from three discordant MZ twin pairs, from both new born blood spots before epilepsy onset, and blood samples taken after epilepsy onset. An epigenome-wide analysis was performed, using the Illumina Infinium EPIC array. Differentially methylated regions (DMR) were identified using the bumphunter package in R. Comparative analyses were undertaken at the two different time points as well as a combined analysis independent of time. ResultsMany of the top DMR-associated genes have previously been described in neurodevelopmental disorders. The LYPD8 gene was associated with a top-ranked DMR both at birth and across the two time points. ConclusionWe have demonstrated the novel utility of the longitudinal, discordant MZ twin model, to facilitate a deeper appreciation of the complex neurobiology of SECTS. The genetic architecture of SECTS is complex and is likely to involve an interplay between genes and environment, in part mediated by epigenetics.

Physical activity and sedentary activity: population epidemiology and concordance in Australian children aged 11-12 years and their parents.

ObjectivesTo describe the epidemiology and parent–child concordance of objectively measured physical activity in a population-based sample of Australian parent–child dyads.DesignCross-sectional study (Child Health CheckPoint) nested within the Longitudinal Study of Australian Children.SettingAssessment centres in seven Australian cities and eight regional towns or home visits; February 2015–March 2016.ParticipantsOf all CheckPoint families (n=1874), 1261 children (50% girls) and 1358 parent (88% mothers) provided objectively measured activity data, comprising 1077 parent–child dyads.Outcome measuresActivity behaviour was assessed by GENEActiv accelerometer. Duration of moderate-to-vigorous physical activity (MVPA) and vigorous physical activity and sedentary behaviour (SB) were derived using Cobra custom software, along with MVPA/SB fragmentation and mean daily activity. Pearson’s correlation coefficients and linear regression estimated parent–child concordance. Survey weights and methods accounted for the complex sample design and clustering.ResultsAlthough parents had average lower accelerometry counts than children (mean [SD] 209 [46] vs 284 [71] g.min), 93% of parents met MVPA daily duration guidelines on published cutpoints (mean [SD] 125 [63] min/day MVPA), compared with only 15% of children (mean 32 [27] min). Parents showed less daily SB duration (parents: 540 [101], children: 681 [69] minutes) and less fragmented accumulation of MVPA (parents: α=1.85, children: α=2.00). Parent–child correlation coefficients were 0.16 (95% CI 0.11 to 0.22) for MVPA duration, 0.10 (95% CI 0.04 to 0.16) for MVPA fragmentation, 0.16 (95% CI 0.11 to 0.22) for SB duration and 0.18 (95% CI 0.12 to 0.23) for SB fragmentation.ConclusionsStandardised cutpoints are needed for objective activity measures to inform activity guidelines across the lifecourse. This may reflect large amounts of time in non-shared environments (school and work).

Comparing the genetic architecture of childhood behavioral problems across socioeconomic strata in the Netherlands and the United Kingdom

Socioeconomic status (SES) affects the development of childhood behavioral problems. It has been frequently observed that children from low SES background tend to show more behavioral problems. There also is some evidence that SES has a moderating effect on the causes of individual differences in childhood behavioral problems, with lower heritability estimates and a stronger contribution of environmental factors in low SES groups. The aim of the present study was to examine whether the genetic architecture of childhood behavioral problems suggests the presence of protective and/or harmful effects across socioeconomic strata, in two countries with different levels of socioeconomic disparity: the Netherlands and the United Kingdom. We analyzed data from 7-year-old twins from the Netherlands Twin Register (N = 24,112 twins) and the Twins Early Development Study (N = 19,644 twins). The results revealed a nonlinear moderation effect of SES on the contribution of genetic and environmental factors to individual differences in childhood behavioral problems. The heritability was higher, the contribution of the shared environment was lower, and the contribution of the nonshared environment was higher, for children from high SES families, compared to children from low or medium SES families. The pattern was similar for Dutch and UK families. We discuss the importance of these findings for prevention and intervention goals.

Sex differences in the etiology of disgust sensitivity: A preliminary behavioral genetic analysis

Evidence suggests that Disgust Sensitivity (DS) is a personality trait that may confer risk for the development of some anxiety-related disorders. To examine the origins of this trait we administered the DS subscale of the Disgust Propensity and Sensitivity Scale-Revised to 90 monozygotic and 90 dizygotic twin pairs, of which 55% were women. The DS subscale consists of two dimensions; Somatic Disgust and Ruminative Disgust. Biometrical modeling techniques were used to estimate heritability of the DS dimensions by sex. For women, each dimension was influenced by a combination of genetic and environmental factors. More specifically, 40.1% of the variance in DS was observed to be due to additive genetic factors and the remaining variance due to non-shared environment. Correlations among DS dimensions for women could be explained by genetic and environmental factors influencing the two dimensions. For men, the two dimensions were influenced by environmental but not genetic factors. These findings suggest that the etiology of DS is complex and arises as a function of dimension-specific and non-specific etiologic factors that vary as a function of sex. The implication of these findings for the sex differences in the etiology of some anxiety-related disorders are discussed.

Genetic and environmental influences on attention-deficit/hyperactivity disorder symptoms in Chinese adolescents: a longitudinal twin study.

Attention-deficit/hyperactivity disorder (ADHD) is a highly heritable neurodevelopmental disorder. However, no study has examined genetic and environmental influences in the longitudinal developmental course of ADHD symptoms in a non-Western population. This study investigated changes of genetic and environmental influences and their contributions to the stability and change of ADHD symptoms of hyperactivity/impulsivity and inattention in Chinese adolescent twins. A prospective sample of 602 twin pairs (48% male) self-reported both DSM-IV ADHD symptom subscales three times at the approximate age of 12, 13, and 15years. Longitudinal multivariate genetic analyses through structural equation modelling examined genetic and environmental contributions to the developmental course of ADHD symptoms. From early (time 1 and 2) to middle adolescence (time 3), both symptoms showed modest and non-significant genetic influences that became substantial and significant, whereas shared environmental influences were substantial and significant and became modest and non-significant. The same genetic factors influenced ADHD symptoms throughout adolescence, while shared and non-shared environmental influences largely came from new emerging factors. In early adolescence, genetic factor contributed to the stability of inattention, whereas shared environmental factor contributed to the stability of hyperactivity/impulsivity. Genetic influences of ADHD tended to be smaller, whereas shared environmental influences tended to be larger in Chinese than in Western populations. Genetic factors played a large role in the stability of ADHD throughout adolescence, while shared and non-shared environment primarily contributed to its change. Findings highlight the importance of shared family, neighbourhood, and community experiences on child psychopathology in a collectivistic culture such as the Chinese society.

Genetic and environmental sources of familial coaggregation of obsessive\u2212compulsive disorder and suicidal behavior: a population-based birth cohort and family study

Obsessive−compulsive disorder (OCD) is associated with high risk of suicide. It is yet unknown whether OCD and suicidal behaviors coaggregate in families and, if so, what are the mechanisms underlying this coaggregation. In a population-based birth cohort and family study, we linked individuals born in Sweden in 1967–2003 (n = 3,594,181) to their parents, siblings, and cousins, and collected register-based diagnoses of OCD, suicide attempts, and deaths by suicide and followed them until December 31, 2013. We also applied quantitative genetic modeling to estimate the contribution of genetic and environmental factors to the familial coaggregation of OCD and suicidal behavior. An elevated risk of suicide attempts was observed across all relatives of individuals with OCD, increasing proportionally to the degree of genetic relatedness, with odds ratios (OR) ranging from 1.56 (95% confidence interval (CI) 1.49–1.63) in parents to 1.11 (95% CI 1.07–1.16) in cousins. The risk of death by suicide also increased alongside narrowing genetic distance, but was only significant in parents (OR 1.55; 95% CI 1.40–1.72) and full siblings (OR 1.80; 95% CI 1.43–2.26) of individuals with OCD. Familial coaggregation of OCD and suicide attempts was explained by additive genetic factors (60.7%) and non-shared environment (40.4%), with negligible contribution of shared environment. Similarly, familial coaggregation with death by suicide was attributed to additive genetics (65.8%) and nonshared environment (34.2%). Collectively, these observations indicate that OCD and suicidal behaviors coaggregate in families largely due to genetic factors. The contribution of unique environment is also considerable, providing opportunities to target high-risk groups for prevention and treatment.

Genetic and environmental influences on the stability of psychotic experiences and negative symptoms in adolescence.

BackgroundPsychotic experiences (PEs) such as paranoia and hallucinations, and negative symptoms (NS) such as anhedonia and flat affect are common in adolescence. Psychotic experiences and negative symptoms (PENS) increase risk for later psychiatric outcomes, particularly when they persist. The extent to which genetic and environmental influences contribute to the stability of PENS in mid‐to‐late adolescence is unknown.MethodsUsing the Specific Psychotic Experiences Questionnaire (SPEQ) twice across ~9 months in adolescence, N = 1,448 twin pairs [M = 16.32 (0.68)] reported experiences of paranoia, hallucinations, cognitive disorganization, grandiosity and anhedonia, and their parents reported on a range of NS. Individuals were split into low‐scoring, decreasing, increasing and persistent groups for each subscale. Frequencies and mean differences in distress, depression traits and emotional problems were investigated across groups. Longitudinal structural equation modelling was used to estimate the aetiological components underlying the stability of PENS.ResultsPhenotypic stability was moderate for all PENS (r = .59–.69). Persistent PENS across 9 months were associated with greater levels of distress (V = 0.15–0.46, for PEs only), depression traits (d = 0.47–1.67, except grandiosity) and emotional problems (d = 0.47–1.47, except grandiosity and anhedonia) at baseline compared to groups with transitory or low levels of PENS. At both ages PENS were heritable and influenced by shared and nonshared environment. Genetic influences contributed 38%–62% and shared environment contributed 13%–33% to the stability of PENS. Nonshared environment contributed 34%–41% (12% for parent‐rated NS). There was strong overlap of genetic and shared environmental influences across time, and lower overlap for nonshared environment. Imperfect stability of PENS was at least partly due to nonshared environmental influences.ConclusionsWhen adolescent PENS persist over time, they are often characterized by more distress, and higher levels of other psychopathology. Both genetic and environmental effects influence stability of PENS.

The Problem of Non-Shared Environment in Behavioral Genetics.

The role of non-shared environment (NSE) in the development of psychological traits is usually comparable with that of the genotype. However, no specific factors of NSE with significant impact on such traits have been discovered so far. We propose that the current failures in understanding the origin of NSE are at least partly due to the fact that behavioral genetics has left out one of the key sources of phenotypic variation. This source is the intrinsic stochasticity of molecular processes underlying individual development. At the critical stages of ontogeny, even minor fluctuations in gene expression or gene-product functioning can remarkably affect the phenotype; this role is experimentally proved in multiple model organisms. In the present paper, several mechanisms of molecular stochasticity, which could affect the development of psychological traits, are discussed. We propose to distinguish external NSE (any external differences) and internal NSE (intrinsic molecular stochasticity). Available data indicate that the impact of external NSE is likely to be low, which makes the presumptive role of internal NSE rather decisive. If our assumption is true, the paradigm of behavioral genetics should be revised, and comprehensive analysis of molecular stochasticity during individual development is strongly required.

Associations between pre-sleep arousal and insomnia symptoms in early adulthood: a twin and sibling study.

This study examines the associations between overall pre-sleep arousal, its cognitive and somatic subscales and insomnia symptoms. Furthermore, the relative contribution of genetic and environmental influences on overall pre-sleep arousal, cognitive pre-sleep arousal, somatic pre-sleep arousal, and insomnia symptoms and the association between these variables is estimated. The cross-sectional data came from G1219 (wave 5), a twin/sibling study which comprised 862 individuals (aged 22-32 years, 34% males). Pre-sleep arousal was measured using the pre-sleep arousal scale and insomnia symptoms using the insomnia symptoms questionnaire. Both cognitive and somatic pre-sleep arousal were significant, independent factors associated with insomnia symptoms. Overall and somatic pre-sleep arousal showed a significant, substantial genetic influence (47% and 49% respectively) and non-shared environmental influence. For cognitive pre-sleep arousal and insomnia symptoms, non-shared environment appeared to be most important (74% and 61% respectively), and familiality was indicated. A strong, significant association of the genetic influences on overall pre-sleep arousal and insomnia symptoms was found (genetic correlation = .88). Strong, significant genetic correlations were found between cognitive pre-sleep arousal, somatic pre-sleep arousal and insomnia symptoms (genetic correlations .93 to 1). Non-shared environmental influences between these three variables were moderately, significantly correlated (non-shared environmental correlation .22 to .41). The large overlap of genetic influences between pre-sleep arousal and insomnia symptoms provides novel insight into the associations between these variables. The results indicate that those with cognitive and/or somatic pre-sleep arousal may also have a genetic vulnerability to insomnia symptoms.

Genetic and environmental influences on developmental trajectories of adolescent alcohol use.

Adolescent alcohol use demonstrates distinct developmental trajectories with different times of onset, levels, and rates of growth. Twin research on adolescent alcohol use has shown that genetic influences are consistent with a gradual growth of risks, whereas non-shared environmental influences are more consistent with an accumulation of risks over time. The current study investigated the relative contributions of genetic and environmental influences on shaping different developmental trajectories of alcohol use through adolescence. Self-reported past year alcohol use was collected from 877 Canadian twins (47.1% males) at age 13, 14, 15, and 17years. Growth mixture models were fit to examine different developmental trajectories of alcohol use, and biometric liability threshold models were fit to investigate genetic and environmental influences on the liability of belonging to identified trajectories. Three trajectories were identified: low (15.1%), early onset (8.2%), and normative increasing (76.7%). Memberships in the low and early-onset group were under genetic (27.6% and 34.7%), shared (42.4% and 21.5%), and non-shared environment influences (30.0% and 43.8%). Membership in the normative increasing group was under genetic (37.7%) and non-shared environment influences (62.3%). Non-shared environmental influences were significantly larger for the normative increasing trajectory than for the low trajectory. These findings provide a more refined picture of genetic and environmental influences in the development of alcohol use in subgroups of adolescents. Genetic and environmental influences both matter, but to different degrees in different trajectories. Future research should identify specific shared and non-shared environmental experiences that distinguish different trajectories.