Nonshared Environmental Influences Research Articles

Does the heritability of cognitive abilities vary as a function of parental education? Evidence from a German twin sample.

A well-known hypothesis in the behavioral genetic literature predicts that the heritability of cognitive abilities is higher in the presence of higher socioeconomic contexts. However, studies suggest that the effect of socioeconomic status (SES) on the heritability of cognitive ability may not be universal, as it has mostly been demonstrated in the United States, but not in other Western nations. In the present study we tested whether the importance of genetic and environmental effects on cognitive abilities varies as a function of parental education in a German twin sample. Cognitive ability scores (general, verbal, and nonverbal) were obtained on 531 German twin pairs (192 monozygotic, 339 dizygotic, ranging from 7 to 14 years of age; Mage = 10.25, SD = 1.83). Data on parental education were available from mothers and fathers. Results for general cognitive ability and nonverbal ability indicated no significant gene x parental education interaction effect. For verbal ability, a significant nonshared environment (E) x parental education interaction was found in the direction of greater nonshared environmental influences on verbal abilities among children raised by more educated parents.

A genetically informative analysis of the association between dyadic adjustment, depressive symptoms, and anxiety symptoms

BackgroundPrior research has found a reliable and robust association between poor dyadic (e.g., marital) adjustment and depression and anxiety. However, it is possible that this association may be due, at least in part, to confounding variables (i.e., variables that are causally associated both with marital adjustment and psychopathology and could account for their covariation). The present study was conducted using a genetically informative sample of twins to examine the association between dyadic adjustment and symptoms of depression and anxiety, accounting for unmeasured genetic and shared environmental confounds. MethodsA Swedish sample of monozygotic and dizygotic twins (218 female twin pairs and 321 male twin pairs) and their spouse or long-term partner completed self-report measures of dyadic adjustment, depressive symptoms, and anxiety symptoms. ResultsResults suggest that dyadic adjustment was significantly and negatively associated with depressive symptoms and anxiety symptoms in twins, and nonshared environmental influences largely accounted for this association. Furthermore, results obtained from partners’ reports of dyadic adjustment were largely consistent with those obtained from twins’ reports, suggesting that results were not a function of shared method variance. LimitationsLongitudinal research in genetically informative samples would provide a stronger test of the causal association between dyadic adjustment and psychopathology. ConclusionsThe pattern of findings suggest that common nonshared environmental influences, such as partners’ characteristics, may lead to poorer dyadic adjustment and depression and anxiety. Therefore, couple-based interventions that improve dyadic adjustment may be effective in preventing and treating psychopathology in relationship partners.

Etiology of Stability and Growth of Internalizing and Externalizing Behavior Problems Across Childhood and Adolescence.

Internalizing and externalizing behaviors are heritable, and show genetic stability during childhood and adolescence. Less work has explored how genes influence individual differences in developmental trajectories. We estimated ACE biometrical latent growth curve models for the Teacher Report Form (TRF) and parent Child Behavior Checklist (CBCL) internalizing and externalizing scales from ages 7 to 16years in 408 twin pairs from the Colorado Longitudinal Twin Study. We found that Intercept factors were highly heritable for both internalizing and externalizing behaviors (a2=.61-.92), with small and nonsignificant environmental influences for teacher-rated data but significant nonshared environmental influences for parent-rated data. There was some evidence of heritability of decline in internalizing behavior (Slopes for teacher and parent ratings), but the Slope genetic variance was almost entirely shared with that for the Intercept when different than zero. These results suggest that genetic effects on these developmental trajectories operate primarily on initial levels and stability, with no significant unique genetic influences for change. Finally, cross-rater analyses of the growth factor scores revealed moderate to large genetic and environmental associations between growth factors derived from parents' and teachers' ratings, particularly the Intercepts.

The etiology of social aggression: a nuclear twin family study.

Social aggression is a form of antisocial behavior in which social relationships and social status are used to damage reputations and inflict emotional harm on others. Despite extensive research examining the prevalence and consequences of social aggression, only a few studies have examined its genetic-environmental etiology, with markedly inconsistent results. We estimated the etiology of social aggression using the nuclear twin family (NTF) model. Maternal-report, paternal-report, and teacher-report data were collected for twin social aggression (N = 1030 pairs). We also examined the data using the classical twin (CT) model to evaluate whether its strict assumptions may have biased previous heritability estimates. The best-fitting NTF model for all informants was the ASFE model, indicating that additive genetic, sibling environmental, familial environmental, and non-shared environmental influences significantly contribute to the etiology of social aggression in middle childhood. However, the best-fitting CT model varied across informants, ranging from AE and ACE to CE. Specific heritability estimates for both NTF and CT models also varied across informants such that teacher reports indicated greater genetic influences and father reports indicated greater shared environmental influences. Although the specific NTF parameter estimates varied across informants, social aggression generally emerged as largely additive genetic (A = 0.15-0.77) and sibling environmental (S = 0.42-0.72) in origin. Such findings not only highlight an important role for individual genetic risk in the etiology of social aggression, but also raise important questions regarding the role of the environment.

Stability of Genetic and Environmental Influences on Female Sexual Functioning

BackgroundGenetic factors have been implicated in the etiology of female sexual dysfunction. Yet, how much the dynamic nature of sexual functioning is influenced by changes in genetic and/or environmental factors remains unknown. AimTo explore temporal stability of genetic and environmental influences on female sexual functioning over a 4-year period. MethodsData on desire, arousal, lubrication, orgasm, satisfaction, and pain were collected in 2009 and 2013 using the Female Sexual Function Index and were available for 1,209 British twin women. OutcomesTo track the stability of genetic influences the Female Sexual Function Index sub-domain and total scores were subject to multivariate twin analyses for repeated measures. ResultsDesire showed a lower heritability at follow-up (37% vs 14%) whereas for arousal and sexual pain the heritability at follow-up was higher compared to baseline (28% vs 34% and 30% vs 45%, respectively). The heritability of lubrication remained stable at 27%. According to the best-fitting additive environmental (AE) Cholesky model for all domains except for sexual pain there were no new genetic factors expressing themselves over the 4-year period, but an addition of new, unique environmental determinants could be observed. For sexual pain an additional genetic factor could be observed at follow-up, explaining 39% of the phenotypic variance. Clinical TranslationThe biological pre-disposition to sexual problems seems to remain relatively stable over time. ConclusionsThis is the first study to investigate the genetic stability of female sexual functioning in a large population sample of women. White ethnicity and the relatively high mean age of women asks for caution in extrapolating the findings to other ethnic and age groups. The findings highlight the value of more in-depth exploration of the non-shared environmental influences that could provide clues to the mechanisms behind remittance and/or persistence of sexual problems. Integration of these findings may provide a useful conceptual framework for the treatment and prevention of certain types of sexual problems.Burri A, Ogata S. Stability of Genetic and Environmental Influences on Female Sexual Functioning. J Sex Med 2018;15:550–557.

Sensitivity to Peer Evaluation and Its Genetic and Environmental Determinants: Findings from a Population-Based Twin Study

Adolescents and young adults are highly focused on peer evaluation, but little is known about sources of their differential sensitivity. We examined to what extent sensitivity to peer evaluation is influenced by interacting environmental and genetic factors. A sample of 354 healthy adolescent twin pairs (n = 708) took part in a structured, laboratory task in which they were exposed to peer evaluation. The proportion of the variance in sensitivity to peer evaluation due to genetic and environmental factors was estimated, as was the association with specific a priori environmental risk factors. Differences in sensitivity to peer evaluation between adolescents were explained mainly by non-shared environmental influences. The results on shared environmental influences were not conclusive. No impact of latent genetic factors or gene-environment interactions was found. Adolescents with lower self-rated positions on the social ladder or who reported to have been bullied more severely showed significantly stronger responses to peer evaluation. Not genes, but subjective social status and past experience of being bullied seem to impact sensitivity to peer evaluation. This suggests that altered response to peer evaluation is the outcome of cumulative sensitization to social interactions.

The gene-environmental architecture of the development of adolescent substance use.

Using a longitudinal twin design and a latent growth curve/autoregressive approach, this study examined the genetic-environmental architecture of substance use across adolescence. Self-reports of substance use (i.e. alcohol, marijuana) were collected at ages 13, 14, 15, and 17 years from 476 twin pairs (475 boys, 477 girls) living in the Province of Quebec, Canada. Substance use increased linearly across the adolescent years. ACE modeling revealed that genetic, as well as shared and non-shared environmental factors explained the overall level of substance use and that these same factors also partly accounted for growth in substance use from age 13 to 17. Additional genetic factors predicted the growth in substance use. Finally, autoregressive effects revealed age-specific non-shared environmental influences and, to a lesser degree, age-specific genetic influences, which together accounted for the stability of substance use across adolescence. The results support and expand the notion that genetic and environmental influences on substance use during adolescence are both developmentally stable and developmentally dynamic.

Genetic and Environmental Influences on Self-Control: Assessing Self-Control with the ASEBA Self-Control Scale

This study used a theoretically-derived set of items of the Achenbach System of Empirically Based Assessment to develop the Achenbach Self-Control Scale (ASCS) for 7–16 year olds. Using a large dataset of over 20,000 children, who are enrolled in the Netherlands Twin Register, we demonstrated the psychometric properties of the ASCS for parent-, self- and teacher-report by examining internal and criterion validity, and inter-rater and test–retest reliability. We found associations between the ASCS and measures of well-being, educational achievement, and substance use. Next, we applied the classical twin design to estimate the genetic and environmental contributions to self-control. Genetic influences accounted for 64–75% of the variance in self-control based on parent- and teacher-report (age 7–12), and for 47–49% of the variance in self-control based on self-report (age 12–16), with the remaining variance accounted by non-shared environmental influences. In conclusion, we developed a validated and accessible self-control scale, and show that genetic influences explain a majority of the individual differences in self-control across youth aged 7–16 years.

Genetic and environmental architecture of executive functions in midlife.

Research on executive functions (EFs) has revealed evidence for general abilities that underlie performance across multiple EF tasks and domains. This Common EF factor is highly stable in adolescence through young adulthood, correlates with other important cognitive abilities, and is explained largely by genetic influences. However, little is known about Common EF beyond young adulthood. This study examines 3 hypotheses regarding the latent structure, genetic/environmental etiology, and cognitive correlates of Common EF in middle age. We examined data from 1,284 middle-aged twins (51-60 years) in the Vietnam Era Twin Study of Aging who completed 7 neuropsychological measures of EFs, as well as measures of general cognitive ability and processing speed. Our confirmatory factor analysis indicated that Common EF explained variation across all 7 EF tasks. Inhibition and shifting were subsumed entirely under the Common EF factor, and there was an additional working memory span-specific factor. Common EF was heritable in midlife (a2 = .46), with additional evidence for both shared environmental influences (c2 = .41) and nonshared environmental influences (e2 = .13). Higher Common EF was moderately associated with higher general cognitive ability, measured both in early adulthood and midlife, and faster processing speed in midlife. These correlations were primarily driven by shared genetic influences. These results support the hypothesis that Common EF captures similar EF abilities in midlife as in adolescence and young adulthood. However, environmental influences may explain a larger portion of variance in this construct as individuals age. (PsycINFO Database Record

Genetic and Environmental Influences on Gambling: A Meta-Analysis of Twin Studies.

Disentangling the genetic and environmental influences of gambling is important for explaining the roots of individual differences in gambling behavior and providing guidance for precaution and intervention, but we are unaware of any comprehensive and systematic quantitative meta-analysis. We systematically identified 18 twin studies on gambling in the meta-analysis. The correlation coefficients within monozygotic (MZ) and dizygotic (DZ) twins, along with the corresponding sample size, were used to calculate the proportion of the total variance accounted for by additive genes (A), dominant genes (D), the shared environment (C), and the non-shared environment plus measurement error (E). We further assessed the moderating effects of gambling assessment (symptom oriented assessment vs. behavior oriented assessment), age, and sex. The whole sample analyses showed moderate additive genetic (a2 = 0.50) and non-shared environmental influences (e2 = 0.50) on gambling. The magnitude of the genetic influence (a2) was higher for disordered gambling assessed with symptom oriented assessment (53%) than for general gambling assessed with behavior oriented assessment (41%). Additionally, the magnitude of the genetic influence (a2) was higher for adults (53%) than adolescents (42%). Genetic influence (a2) was greater for male (47%) gambling than female (28%) gambling. Shared environment had noticeable effects on female gambling (c2 = 14%) but zero effect on male gambling. In conclusion, gambling behavior was moderately heritable and moderately influenced by non-shared environmental factors. Gambling assessment, age, and sex significantly moderated the magnitude of genetic and environmental influences on gambling. Note that the number of studies might serve as a limitation.

Differential environmental influences on the development of cognitive abilities during childhood

Twin studies have shown strong evidence that cognitive abilities are heritable. This longitudinal study examines genetic and environmental influences on distinct developmental patterns of verbal and non-verbal cognitive abilities from age 7 to 12 in 4718 British twins. Six subgroups with distinct patterns were identified with comparable heritabilities of group membership (ranging 0.37–0.62). Non-shared environmental influences that differentiate family members on group membership appear to be particularly strong in the three subgroups that demonstrated substantial developmental mean changes of cognitive abilities (ranging 0.51–0.54), compared to the other three subgroups with relatively stable mean levels (ranging 0.29–0.34). Shared environmental influences making family members similar for group membership were significant in only two subgroups – among the children with continuously low scores (0.20) and developmental early starters (0.28). These results suggest the existence of distinct developmental patterns of cognitive abilities. The impact of shared and non-shared environment on the membership of different developmental patterns may be greater for some children than others.

Do Genetic Factors Explain the Links Between Callous-Unemotional, Attention Hyperactivity and Oppositional Defiant Problems in Toddlers?

Research demonstrates that callous-unemotional (CU) behaviors, Attention Deficit Hyperactivity Disorder (ADHD) and Oppositional Defiant Problems (ODD) are related, but little is known about the sources of covariation among the three externalizing behaviors. The present study looked at genetic and environmental links between all three behavioral domains in twins at ages 2 and 3years (MZ=145, DZ=169), a time when CU behaviors are beginning to emerge. CU, ADHD, and ODD behaviors as assessed using the Child Behavior Checklist 1.5-5 (Achenbach and Rescorla 2000) were strongly interrelated at both ages. Genetic factors primarily explained the covariation among the three behavioral domains via a common externalizing factor; however, there were also genetic factors unique to each behavior. Furthermore, the majority of nonshared environmental influences on each externalizing behavior were behavior-specific. The heritable externalizing factor was highly stable across age, largely due to genetic factors shared across ages 2 and 3years. Despite their extensive phenotypic and genetic overlap, CU, ADHD, and ODD behaviors have unique genetic and nonshared environmental influences as early as toddlerhood. This supports phenotypic research showing that the three are related but distinct constructs in very young children.

The Impact of Variation in Twin Relatedness on Estimates of Heritability and Environmental Influences.

By taking advantage of the natural variation in genetic relatedness among identical (monozygotic: MZ) and fraternal (dizygotic: DZ) twins, twin studies are able to estimate genetic and environmental contributions to complex human behaviors. Recently concerns have been raised about the accuracy of twin studies in light of findings of genetic and epigenetic changes in twins. One of the concerns raised is that MZ twins are not 100% genetically and epigenetically similar because they show variations in their genomes and epigenomes leading to inaccurate estimates of heritability. This article presents findings from a simulation study that examined the degree of bias in estimates of heritability and environmentality when the genetic and epigenetic similarity of MZ twins differs from 1.00 and when the genetic and epigenetic similarity of DZ twins differs from 0.50. The findings suggest that in the standard biometric model when MZ or DZ twin similarity differs from 1.00 or 0.50, respectively, the variance that should be attributed to genetic influences is instead attributed to nonshared environmental influences, thus deflating the estimates of genetic influences and inflating the estimates of nonshared environmental influences. Although estimates of genetic and nonshared environmental influences from the standard biometric model were found to deviate from "true" values, the bias was usually smaller than 10% points indicating that the interpretations of findings from previous twin studies are mostly correct.

Genetic and Environmental Pathways Underlying Personality Traits and Perceived Stress: Concurrent and Longitudinal Twin Studies.

The present study examined the genetic and environmental etiology underlying the Big Five personality traits and perceived stress, concurrently and longitudinally. In study 1, we used the twin sample from the National Longitudinal Study of Adolescent to Adult Health (Add Health IV) data. The results indicated that about 70% of the association between the Big Five personality traits and perceived stress was due to genetic influences. In study 2, we used the twin sample from the Midlife in the United States Survey (MIDUS I and II) to examine the genetic and environmental influences underlying the longitudinal relations between the Big Five personality traits and perceived stress. The results suggested that continuity in perceived stress was primarily accounted for by genetic influences, and changes in perceived stress were mainly due to nonshared environmental influences. The continuity in the association between the five personality traits and perceived stress was largely accounted for by genetic factors, and nonshared environmental factors made greater contributions to changes in the association between personality traits and perceived stress. Among the Big Five personality traits, the genetic components in conscientiousness and neuroticism made substantial contributions to the genetic link between personality traits and perceived stress across both studies.

Adult Attention-Deficit/Hyperactivity Disorder (ADHD) and Insomnia: an Update of the Literature.

Insomnia is diagnosed when there is dissatisfaction with sleep quantity or quality. It has a prevalence in the general population ranging from 31 to 56%. Insomnia has previously been associated with adult attention-deficit/hyperactivity disorder (ADHD). In this review, we address three topics: (1) the cross-sectional relationship between ADHD and insomnia in adulthood, (2) the longitudinal relationship between ADHD and insomnia, and (3) insomnia as a side effect of pharmacological treatments for adult ADHD. Three cross-sectional, clinical, and population studies report a prevalence of insomnia in ADHD adults ranging from 43 to 80%. Longitudinal evidence for a link between childhood-onset ADHD and insomnia at later age is mixed, with one study confirming and another study not supporting such a longitudinal association. In randomized, placebo-controlled trials, insomnia is reported significantly more often in the treatment arm than in the placebo arm. In varying percentages of trial participants, insomnia is a treatment-emergent adverse effect in triple-bead mixed amphetamine salts (40-45%), dasotraline (35-45%), lisdexamfetamine (10-19%), and extended-release methylphenidate (11%). Ten to seventeen percent of subjects in placebo-controlled trials of atomoxetine report insomnia, possibly related to poor metabolizer status. The mechanisms explaining the relationship between ADHD and sleep problems are incompletely understood, but both genetic and non-shared environmental influences may be involved. Adults with ADHD should be assessed for insomnia, which is frequently comorbid, and both conditions should be treated.

Can flow experiences be protective of work-related depressive symptoms and burnout? A genetically informative approach

BackgroundGenetic research on depression and burnout has focused mostly on adverse factors, although various aspects in daily life related to positive coping and well-being have been shown to potentially be protective. Using a large genetically informative sample, we aim to explore the potential relationship between flow proneness and work-related depressive symptoms and burnout. MethodsAbout 10,000 Swedish twins filled in the Swedish Flow Proneness Questionnaire, a subscale of the Hopkins Symptom Checklist (SCL) depression scale, and the Emotional Exhaustion subscale of the Maslach Burnout Inventory-General Survey. A higher score indicated more flow, less emotional exhaustion and less depression. The classical twin design and co-twin control analyses were applied. ResultsPhenotypic correlations were .43 between depressive symptoms and flow proneness, .34 between burnout and flow proneness, and .62 between depressive symptoms and burnout. Broad-sense heritabilities (G) ranged between 33–35% for the three variables. Associations between the variables were due to significant genetic as well as non-shared environmental influences. Co-twin control analyses showed that associations remained significant when controlling for all genetic and shared familial factors, in line with a causal relationship. LimitationsAlthough the co-twin control design can test for consistency of associations with a causal relationship, it cannot unequivocally establish causality. ConclusionsGenetic liability has a substantial influence on associations between flow proneness and emotional problems at work (depression, burnout). However, the presence of significant environmental correlations is in line with a (partly) causal relationship between flow and work related depression and burnout, which in turn may suggest that interventions which increase flow could potentially reduce emotional problems at work.

Parental involvement as an etiological moderator of middle childhood oppositional defiant disorder.

The goal of this study was to investigate parental involvement as an etiologic moderator of oppositional defiant disorder (ODD) during middle childhood. Previous studies examining the influence of genetic and environmental factors on ODD have not considered whether and how these factors might vary by parental involvement. We thus conducted a series of "latent genetic by measured environmental" interaction analyses, in which measured parental involvement was allowed to moderate genetic, shared, and nonshared environmental influences on child ODD. Participants include 1,027 twin pairs (age ranged from 6 to 11 years old) from the Michigan State University Twin Registry. Results did indeed suggest that the etiology of ODD varies with maternal involvement, such that genetic influence on ODD became more prominent as maternal involvement decreased. However, these results were specific to children's perceptions of maternal involvement and did not extend to maternal perceptions of her involvement. There was no evidence that paternal involvement moderated the etiology of ODD, regardless of informant. The different results found in twins' and parents' data are consistent with those in previous research showing that children may have different perceptions from parents' about their family relationships and that this discrepancy needs to be taken into account in future research. (PsycINFO Database Record

Genetic and environmental influences on emotion regulation: A twin study of cognitive reappraisal and expressive suppression.

Previous studies have established that personality traits related to emotionality are moderately heritable. However, the relative heritability of the strategies people use to regulate emotions is unknown. The present study compared the magnitude of additive genetic, shared environmental, and nonshared environmental influences on 2 commonly used emotion regulation strategies: cognitive reappraisal and expressive suppression. In 743 twin pairs (1,486 twins), we replicated previous estimates of heritability of neuroticism (a2 = .41). Furthermore, cognitive reappraisal was significantly less heritable and more influenced by nonshared environment (a2 = .20; e2 = .80) than either neuroticism or suppression (a2 = .35; e2 = .65), another emotion regulation strategy. Finally, Cholesky decomposition modeling suggested that while there were common genetic and environmental influences on neuroticism, reappraisal and suppression, there were also significant nonshared environmental influences common between reappraisal and adaptive emotional functioning after controlling for neuroticism and suppression. These findings highlight that different aspects of emotional processing, even the use of different emotion regulation strategies, are differentially heritable. The importance of the nonshared environmental influences specific to reappraisal and adaptive emotional functioning speaks to the potential impact of social context, social partners, and psychosocial interventions on reappraisal habits. (PsycINFO Database Record

Genetic and environmental sources of covariation between early drinking and adult functioning.

The vast majority of individuals initiate alcohol consumption for the first time in adolescence. Given the widespread nature of its use and evidence that adolescents may be especially vulnerable to its effects, there is concern about the long-term detrimental impact of adolescent drinking on adult functioning. While some researchers have suggested that genetic processes may confound the relationship, the mechanisms linking drinking and later adjustment remain unclear. The current study utilized a genetically informed sample and biometric modeling to examine the nature of the familial influences on this association and identify the potential for genetic confounding. The sample was drawn from the Minnesota Twin Family Study (MTFS), a longitudinal study consisting of 2,764 twins assessed in 2 cohorts at regular follow-ups from age 17 to age 29 (older cohort) or age 11 to age 29 (younger cohort). A broad range of adult measures was included assessing substance use, antisocial behavior, personality, socioeconomic status, and social functioning. A bivariate Cholesky decomposition was used to examine the common genetic and environmental influences on adolescent drinking and each of the measures of adult adjustment. The results revealed that genetic factors and nonshared environmental influences were generally most important in explaining the relationship between adolescent drinking and later functioning. While the presence of nonshared environmental influences on the association are not inconsistent with a causal impact of adolescent drinking, the findings suggest that many of the adjustment issues associated with adolescent alcohol consumption are best understood as genetically influenced vulnerabilities. (PsycINFO Database Record

On the Heritability of Criminal Justice Processing

An impressive number of researchers have devoted a great amount of effort toward examining various predictors of criminal justice (CJ) processing outcomes. Indeed, a vast amount of research has examined various individual- and aggregate-level predictors of arrests, incarceration, and sentencing decisions. To this point, less attention has been devoted toward uncovering the relative contribution of genetic and environmental effects on variation in risk for CJ processing. As a result, the current study employs a behavioral genetic design to help fill this void in the existing literature. Using twin data from a national sample of youth, the current study produced evidence suggesting that genetic factors accounted for at least a portion of variance in risk for incarceration among female twins and probation among male twins. Shared and nonshared environmental influences accounted for the variance in risk for arrest among both female and male twins, probation among female twins, and incarceration among male twins. Ultimately, it appears that risk for contact with the CJ system and CJ processing is structured by a combination of factors beyond shared cultural and neighborhood environments, and appears to also include genetic factors. Moving forward, continuing to not use genetically sensitive research designs capable of estimating the role of genetic and nonshared environmental influences on CJ outcomes may result in misleading results.