Nonshared Environmental Correlations Research Articles

The genetics of intelligence and social outcomes in a Hungarian twin sample

Most previous research found that within-family resemblance on social outcomes and intelligence is mostly due to genetic factors with a limited role of the shared environment, with the exception of educational attainment. Hypotheses about a gene-environment interaction with SES, with a presumably smaller role of genetic factors in families with low social status, have been only partially confirmed. However, these results do not necessarily generalize to all societies, and data from Central or Eastern European countries is currently deficient. In the current work we replicate using data from the Hungarian Twin Registry that intelligence, income, and educational attainment are substantially heritable, with limited role of the shared environment. In contrast to studies in Anglo-Saxon or Western European countries, we found an influence of the shared environment on standardized high school test scores, especially history. Both genetic and shared environmental (but not nonshared environmental) correlations were substantial, in line with generalist genes and shared environments but specific nonshared environmental effects. The results show that the heritability of social traits is observable in Central/Eastern Europe, but they highlight a potentially problematic aspect of Hungarian high school final tests, as students' family of origin appears to be a potent determinant of grades.

A Genetically Informed Study of the Association Between Perceived Stress and Loneliness

Although research shows a strong positive association between perceived stress and loneliness, the genetic and environmental etiology underlying their association remains unknown. People with a genetic predisposition to perceived stress, for example, may be more prone to feeling lonely and vice versa. Conversely, unique factors in people’s lives may explain differences in perceived stress levels that, in turn, affect feelings of loneliness. We tested whether genetic factors, environmental factors, or both account for the association between perceived stress and loneliness. Participants were 3,066 individual twins (nFemale = 2,154, 70.3%) from the Washington State Twin Registry who completed a survey during April–May, 2020. Structural equation modeling was used to analyze the item-level perceived stress and loneliness measures. The correlation between latent perceived stress and latent loneliness was .68. Genetic and nonshared environmental variance components underlying perceived stress accounted for 3.71% and 23.26% of the total variance in loneliness, respectively. The genetic correlation between loneliness and perceived stress was .45 and did not differ significantly between men and women. The nonshared environmental correlation was .54 and also did not differ between men and women. Findings suggest that holding constant the strong genetic association between perceived stress and loneliness, unique life experiences underlying people’s perceived stress account for individual differences in loneliness.

EPIGENETIC AGE ACCELERATION AND IMMUNE CELL COUNT: A TWIN STUDY

Abstract Accelerated aging, as measured by epigenetic clocks, is associated with declines in immune system functioning. Investigating the causal basis of this association may provide mechanistic insight into the link between DNA methylation, on which epigenetic clocks are based, and age-related changes in immune cell composition. Using preliminary data from the Louisville Twin Study, this study examined the genetic and environmental sources of covariation between immune cell count (neutrophils, lymphocytes) and GrimAge Acceleration. GrimAge is a composite biomarker derived from 7 DNA methylation-based surrogates associated with mortality and smoking pack years. GrimAge Acceleration is the residual of GrimAge regressed onto chronological age. Participants consisted of 43 monozygotic twin pairs and 30 (18 same-sex) dizygotic twin pairs with a mean age of 54.5 years (sd = 5.27). Phenotypic analyses revealed that GrimAge Acceleration was significantly associated with neutrophil and lymphocyte count (r = 0.45 and -0.49, respectively). To examine the sources of covariation between these variables, biometric regression models were used to decompose the covariance between GrimAge Acceleration and neutrophils (and lymphocytes) into genetic and environmental components. Bivariate analyses revealed moderate, marginally significant genetic correlations between GrimAge Acceleration and immune cell count (rg = 0.32 and -0.38 for neutrophils and lymphocytes, respectively) and large, significant nonshared environmental correlations (re = .58 and -.54 for neutrophils and lymphocytes, respectively). Common genetic factors accounted for 39% of the phenotypic correlation in neutrophils and 43% in lymphocytes, whereas common nonshared environmental factors accounted for 61% and 57% of the correlation in these cell types, respectively.

A GENETICALLY INFORMED STUDY ON THE ETIOLOGICAL ASSOCIATIONS AMONG EPIGENETIC CLOCKS

Abstract Epigenetic clocks are believed to capture the molecular footprints of biological programs that subserve innate aging processes. Although epigenetic clocks can predict disease phenotypes and mortality with a high degree of accuracy, little is known about the extent to which they capture the same (or different) developmental and maintenance mechanisms. Quantitative genetic studies may provide useful information on the etiological links between epigenetic clocks, particularly pertaining to the question of whether they are influenced by a common set of genetic and environmental factors. Using preliminary data from the Louisville Twin Study, this study used a multivariate independent pathway model to examine the shared and unique genetic and environmental influences of three epigenetic clocks (GrimAge, HannumAge, PhenoAge). Participants consisted of 43 monozygotic pairs and 30 (18 same-sex) dizygotic twin pairs with a mean age of 54.5 years (sd = 5.27). Phenotypic analyses revealed significant correlations among the clocks (r = 0.63 - 0.78). Subsequent multivariate biometric analyses showed that there were common genetic and nonshared environmental influences across all three clocks (p < 0.001), with unique genetic and nonshared environmental influences specific to GrimAge and HannumAge (p < 0.001). To examine the sources of covariation between these variables, biometric regression models were used to decompose the covariance between each of the clocks (GrimAge and Hannum, Hannum and PhenoAge, PhenoAge and GrimAge) into genetic and environmental components. These analyses revealed large, significant genetic correlations (rg = 0.80-0.86) and medium to large, significant nonshared environmental correlations (re = 0.37-0.73) among the clocks.

Estimating the Genetic Contribution to Astigmatism and Myopia in the Mexican Population.

Astigmatism and myopia are two common ocular refractive errors that can impact daily life, including learning and productivity. Current knowledge suggests that the etiology of these conditions is the result of a complex interplay between genetic and environmental factors. Studies in populations of European ancestry have demonstrated a higher concordance of refractive errors in monozygotic (MZ) twins compared to dizygotic (DZ) twins. However, there is a lack of studies on genetically informative samples of multi-ethnic ancestry. This study aimed to estimate the genetic contribution to astigmatism and myopia in the Mexican population. A sample of 1399 families, including 243 twin pairs and 1156 single twins, completed a medical questionnaire about their own and their co-twin's diagnosis of astigmatism and myopia. Concordance rates for astigmatism and myopia were estimated, and heritability and genetic correlations were determined using a bivariate ACE Cholesky decomposition method, decomposed into A (additive genetic), C (shared environmental) and E (unique environmental) components. The results showed a higher concordance rate for astigmatism and myopia for MZ twins (.74 and .74, respectively) than for DZ twins (.50 and .55). The AE model, instead of the ACE model, best fitted the data. Based on this, heritability estimates were .81 for astigmatism and .81 for myopia, with a cross-trait genetic correlation of rA = .80, nonshared environmental correlation rE = .89, and a phenotypic correlation of rP = .80. These results are consistent with previous findings in other populations, providing evidence for a similar genetic architecture of these conditions in the multi-ethnic Mexican population.

Associations Between Adolescent Pain and Psychopathology in the Adolescent Brain Cognitive Development (ABCD) Study.

Pain and psychopathology co-occur in adolescence, but the directionality and etiology of these associations are unclear. Using the pain questionnaire and the Child Behavior Checklist from the Adolescent Brain Cognitive Development study (n = 10,414 children [770 twin pairs] aged 12-13), we estimated longitudinal, co-twin control, and twin models to evaluate the nature of these associations. In two-wave cross-lag panel models, there were small cross-lag effects that suggested bidirectional associations. However, the co-twin control models suggested that most associations were familial. Pain at age 12 and 13 was mostly environmental (A = 0-12%, C = 15-30%, E = 70-73%) and the twin models suggested that associations with psychopathology were primarily due to shared environmental correlations. The exception was externalizing, which had a phenotypic prospective effect on pain, a significant within-family component, and a non-shared environmental correlation at age 12. Environmental risk factors may play a role in pain-psychopathology co-occurrence. Future studies can examine risk factors such as stressful life events.

Environmental influences on the relationship between childhood conduct problems and prosocial behavior: A twin study

The mechanism explaining the relationship between prosocial behavior (PB) and conduct problems (CP) is unclear. This study aimed to examine whether common genetic and/or environmental factors mediate the PB–CP relationship. In total, 1198 South Korean children twins (Mean age = 8.51 ± 2.70 years), —485 monozygotic twins (239 complete pairs and 7 cotwin missing cases) and 713 dizygotic twins (355 complete pairs and 3 cotwin missing cases)—participated in this study. Mothers of these twins rated their children on the PB and CP scales of the Strengths and Difficulties Questionnaire via a telephone interview. The phenotypic correlation between PB and CP in the sample was −0.34 (95%CI = −0.39, −0.29). Bivariate model-fitting analysis suggests that environmental influences entirely explained the relationship and genetic influences were not significant. The shared and non-shared environmental correlations were −1.0 (95%CI = −1.0, −0.57) and −0.25 (95%CI = −0.33, −0.17), respectively, indicating that common family environmental factors of the two traits completely overlap.

Genetic and environmental correlations between the General Factor of Personality (GFP) and working memory

The present study examines the association between the General Factor of Personality (GFP) and working memory and its etiology with a behavioral genetic approach. The GFP, which explains the common variance among lower-order personality traits, is considered to reflect social effectiveness. Meanwhile, working memory also plays a significant role in social competence. Hence, we expected a substantial association between the GFP and working memory. A total of 253 Japanese twin pairs (124 monozygotic female; 52 monozygotic male; 28 dizygotic female; 17 dizygotic male; and 32 opposite sex twins) were included in the analyses. Phenotypic analyses confirmed a significant positive correlation between the GFP and working memory. Biometric analysis with a bivariate Cholesky decomposition model showed that the phenotypic correlation derived from additive genetic and non-shared environmental correlations. The present findings are in line with social effectiveness account of the GFP.

Genetic and environmental architecture of conscientiousness in adolescence

Using a genetically informative design (about 2000 twin pairs), we investigated the phenotypic and genetic and environmental architecture of a broad construct of conscientiousness (including conscientiousness per se, effortful control, self-control, and grit). These four different measures were substantially correlated; the coefficients ranged from 0.74 (0.72–0.76) to 0.79 (0.76–0.80). Univariate genetic analyses revealed that individual differences in conscientiousness measures were moderately attributable to additive genetic factors, to an extent ranging from 62 (58–65) to 64% (61–67%); we obtained no evidence that shared environmental influences were observed. Multivariate genetic analyses showed that for the four measures used to assess conscientiousness, genetic correlations were stronger than the corresponding non-shared environmental correlations, and that a latent common factor accounted for over 84% of the genetic variance. Our findings suggest that individual differences in the four measures of conscientiousness are not distinguishable at both the phenotypic and behavioural genetic levels, and that the overlap was substantially attributable to genetic factors.

Relationships between cognitive abilities and prosocial behavior are entirely explained by shared genetic influences: A Nigerian twin study

The relationship between prosocial behavior (PB) and cognitive abilities has been well documented. This study explored genetic and environmental overlaps in the relationship between PB and verbal and non-verbal abilities. Participants included 3179 twins attending public secondary schools in Lagos State in Nigeria (mean age = 14.6 years, SD = 1.7 years). The PB scale of the Strengths and Difficulties Questionnaire was used to measure PB. The set B of the Mill-Hill Vocabulary test (MHV) and Raven's Standard Progressive Matrices Plus (SPM) were used to measure verbal and non-verbal ability, respectively. The MHV-PB and the SPM-PB correlations were 0.29 (95%CI = 0.26, 0.32) and 0.19 (95%CI = 0.15, 0.23), respectively, indicating that PB is more strongly related to verbal than to non-verbal ability at the phenotypic level. Bivariate model-fitting analyses revealed that additive genetic correlations were 0.73 (95%CI = 0.59, 0.92) for MHV-PB and 0.55 (95%CI = 0.40, 0.82) for SPM-PB, respectively. Neither shared nor non-shared environmental correlations were significant. Bivariate heritability was estimated at 1.0 (95%CI = 0.65, 1.00 for MHV- PB and 95%CI = 0.60, 1.00 for SPM-PB), indicating that the relationships between PB and two cognitive measures were mediated entirely by common genes. Multivariate Cholesky model-fitting analysis showed that while MHV explained 10% of additional additive genetic variance of PB above and beyond the common genetic variance, SPM became non-significant after the common genetic variance was controlled. These results suggested that the relationship between cognitive abilities and PB may be largely driven by verbal ability.

Association of etiological factors across the extreme end and continuous variation in disordered eating in female Swedish twins.

Accumulating evidence suggests that many psychiatric disorders etiologically represent the extreme end of dimensionally distributed features rather than distinct entities. The extent to which this applies to eating disorders (EDs) is unknown. We investigated if there is similar etiology in (a) the continuous distribution of the Eating Disorder Inventory-2 (EDI-2), (b) the extremes of EDI-2 score, and (c) registered ED diagnoses, in 1481 female twin pairs at age 18 years (born 1992-1999). EDI-2 scores were self-reported at age 18. ED diagnoses were identified through the Swedish National Patient Register, parent-reported treatment and/or self-reported purging behavior of a frequency and duration consistent with DSM-IV criteria. We differentiated between anorexia nervosa (AN) and other EDs. The heritability of the EDI-2 score was 0.65 (95% CI 0.61-0.68). The group heritabilities in DeFries-Fulker extremes analyses were consistent over different percentile-based extreme groups [0.59 (95% CI 0.37-0.81) to 0.65 (95% CI 0.55-0.75)]. Similarly, the heritabilities in liability threshold models were consistent over different levels of severity. In joint categorical-continuous models, the twin-based genetic correlation was 0.52 (95% CI 0.39-0.65) between EDI-2 score and diagnoses of other EDs, and 0.26 (95% CI 0.08-0.42) between EDI-2 score and diagnoses of AN. The non-shared environmental correlations were 0.52 (95% CI 0.32-0.70) and 0.60 (95% CI 0.38-0.79), respectively. Our findings suggest that some EDs can partly be conceptualized as the extreme manifestation of continuously distributed ED features. AN, however, might be more distinctly genetically demarcated from ED features in the general population than other EDs.

Comorbidity of substance misuse with anxiety-related and depressive disorders: a genetically informative population study of 3 million individuals in Sweden.

Causes of the comorbidity of substance misuse with anxiety-related and depressive disorders (anxiety/depression) remain poorly known. We estimated associations of substance misuse and anxiety/depression in the general population and tested them while accounting for genetic and shared environmental factors. We studied individuals born in Sweden 1968-1997 (n = 2 996 398) with follow-up in nationwide register data for 1997-2013. To account for familial effects, stratified analyses were conducted within siblings and twin pairs. Substance misuse was defined as ICD-10 alcohol or drug use disorder or an alcohol/drug-related criminal conviction. Three dimensions of ICD-10 anxiety and depressive disorders and a substance misuse dimension were identified through exploratory factor analysis. Substance misuse was associated with a 4.5-fold (95% CI 4.50-4.58) elevated risk of lifetime generalized anxiety/depression, 4.7-fold (95% CI 4.63-4.82) elevated risk of panic disorder and agora/social phobia, and 2.9-fold elevated risk of phobias/OCD (95% CI 2.82-3.02) as compared to those without substance misuse. The associations were attenuated in within-family analyses but we found elevated risks in monozygotic twin pairs discordant for substance misuse as well as significant non-shared environmental correlations. The association between anxiety/depression and substance misuse was mainly driven by generalized anxiety/depression, whereas other anxiety/depression dimensions had minor or no independent associations with substance misuse. Substance misuse and anxiety/depression are associated at the population level, and these associations are partially explained by familial liabilities. Our findings indicate a common genetic etiology but are also compatible with a potential partially causal relationship between substance misuse and anxiety/depression.

A Meta-Analytical Review of the Genetic and Environmental Correlations between Reading and Attention-Deficit/Hyperactivity Disorder Symptoms and Reading and Math

ABSTRACTAccording to the Multiple Deficit Model, comorbidity results when the genetic and environmental risk factors that increase the liability for a disorder are domain-general. In order to explore the role of domain-general etiological risk factors in the co-occurrence of learning-related difficulties, the current meta-analysis compiled 38 studies of third- through ninth-grade children to estimate the average genetic, shared environmental, and nonshared environmental correlations between reading and attention-deficit/hyperactivity disorder (ADHD) symptoms, and reading and math, as well as their potential moderators. Results revealed average genetic, shared and nonshared environmental correlations between reading and ADHD symptoms of .42, .64, and .20, and reading and math of .71, .90, and .56, suggesting that reading and math may have more domain-general risk factors than reading and ADHD symptoms. A number of significant sources of heterogeneity were also found and discussed. These results have important implications for both intervention and classification of learning disabilities.

Dysfunctional beliefs about sleep and insomnia symptoms in early adulthood: A twin and sibling study.

This study examines the associations between dysfunctional belief about sleep (DBAS), its subtypes and insomnia symptoms and estimates the relative contribution of genetic and environmental influences to these variables and the associations between them. The data came from G1219, a twin/sibling study that comprises 862 individuals (aged 22-32years, 34% male). The Insomnia Symptoms Questionnaire was used to measure insomnia symptoms and a 10-item version of the Dysfunctional Beliefs and Attitudes about Sleep Scale was used to assess DBAS. A higher DBAS score was associated with more insomnia symptoms. Overall DBAS showed a mainly non-shared environmental influence (86%). The genetic correlation between overall DBAS and insomnia symptoms was large but not significant, the shared environmental correlation was very small, negative and not significant, whereas a moderate, significant overlap in the non-shared environmental influences was evident (non-shared environmental correlation=0.32). For the association between the subscales of DBAS and insomnia symptoms no significant overlap for genetic (weak to strong associations) or shared environmental factors (very weak negative to strong associations) was indicated. Most of the non-shared environmental influences on the four variables were significantly moderately correlated (non-shared environmental correlation=0.24-0.46). These findings help to deepen our understanding of cognitive theories of insomnia by dissecting one of its crucial elements and illuminating the factors involved in its association with insomnia symptoms.

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 Contributions to the Covariation Between Cardiometabolic Traits.

BackgroundThe variation and covariation for many cardiometabolic traits have been decomposed into genetic and environmental fractions, by using twin or single‐nucleotide polymorphism (SNP) models. However, differences in population, age, sex, and other factors hamper the comparison between twin‐ and SNP‐based estimates.Methods and ResultsTwenty‐four cardiometabolic traits and 700,000 genotyped SNPs were available in the study base of 10 682 twins from TwinGene cohort. For the 27 highly correlated pairs (absolute phenotypic correlation coefficient ≥0.40), twin‐based bivariate structural equation models were performed in 3870 complete twin pairs, and SNP‐based bivariate genomic relatedness matrix restricted maximum likelihood methods were performed in 5779 unrelated individuals. In twin models, the model including additive genetic variance and unique/nonshared environmental variance was the best‐fitted model for 7 pairs (5 of them were between blood pressure traits); the model including additive genetic variance, common/shared environmental variance, and unique/nonshared environmental variance components was best fitted for 4 pairs, but estimates of shared environment were close to zero; and the model including additive genetic variance, dominant genetic variance, and unique/nonshared environmental variance was best fitted for 16 pairs, in which significant dominant genetic effects were identified for 13 pairs (including all 9 obesity‐related pairs). However, SNP models did not identify significant estimates of dominant genetic effects for any pairs. In the paired t test, twin‐ and SNP‐based estimates of additive genetic correlation were not significantly different (both were 0.67 on average), whereas the nonshared environmental correlations from these 2 models differed slightly from each other (on average, twin‐based estimate=0.64 and SNP‐based estimate=0.68).ConclusionsBeside additive genetic effects and nonshared environment, nonadditive genetic effects (dominance) also contribute to the covariation between certain cardiometabolic traits (especially for obesity‐related pairs); contributions from the shared environment seem to be weak for their covariation in TwinGene samples.

Stability of genetic and environmental influences on executive functions in midlife.

Research on executive functions (EFs) has revealed that individual differences in general EF abilities are highly correlated across the first few decades of life, especially at the level of genetic influences. Our work has also provided evidence for substantial heritability of this Common EF factor in midlife, but it remains unclear whether individual differences in Common EFs continue to show strong stability in middle age. We examined data from 1,464 middle-aged twins from the Vietnam Era Twin Study of Aging, most of whom completed 7 neuropsychological measures of EFs at 2 points in middle age (Mages = 56 and 62). Confirmatory factor analysis indicated that individual differences in Common EF, a latent factor explaining variation in seven neuropsychological EF tasks, were highly correlated across this 6-year period (r = .97), and that the same genetic and environmental influences were operating across this interval (genetic and shared environmental correlations = 1.0, nonshared environment correlation = .95). Similar phenotypic and genetic stability was observed for a Working Memory (WM)-Specific latent factor, which explained additional variance in working memory span tasks not captured by Common EF (r = .98, genetic correlation = 1.0, nonshared environmental correlation = .88). There was a large mean-level performance decline in Common EF (d = -.60) but not WM-Specific (d = -.03). These results suggest that there is substantial decline in Common EF abilities across middle age but that individual differences are almost perfectly stable. (PsycINFO Database Record

A twin study of genetic and environmental influences on relationship between attention deficit and anxiety/depression in children and adolescents

Objective: To understand the genetic and environmental influences on the relationship between attention deficit and anxiety/depression in children and adolescents. Methods: A total of 1 062 same-sex twins aged 6-18 years were included in this study. A parent-rated child behavior checklist (CBCL) was used in the assessment. Software Mx was used to fit the univariate model of structural equation. The relationship between attention deficit and anxiety/depression was analyzed through bivariate genetic modeling. Results: The genetic factor had influence on the relationship between attention deficit and anxiety/depression (r(g)=0.48). Shared and non-shared environmental correlation scores of attention deficit and anxiety/depression were 0.86 and 0.14 respectively. Conclusion: Common genetic and shared environmental influences can explain the relationship between attention deficit and anxiety/depression in children and adolescents.

Familial Liability to Epilepsy and Attention-Deficit/Hyperactivity Disorder: A Nationwide Cohort Study

BackgroundEpilepsy and attention-deficit/hyperactivity disorder (ADHD) are strongly associated; however, the underlying factors contributing to their co-occurrence remain unclear. A shared genetic liability has been proposed as one possible mechanism. Therefore, our goal in this study was to investigate the familial coaggregation of epilepsy and ADHD and to estimate the contribution of genetic and environmental risk factors to their co-occurrence. MethodsWe identified 1,899,654 individuals born between 1987 and 2006 via national Swedish registers and linked each individual to his or her biological relatives. We used logistic regression to estimate the association between epilepsy and ADHD within individual and across relatives. Quantitative genetic modeling was used to decompose the cross-disorder covariance into genetic and environmental factors. ResultsIndividuals with epilepsy had a statistically significant increased risk of ADHD (odds ratio [OR] = 3.47, 95% confidence interval [CI] = 3.33–3.62). This risk increase extended to children whose mothers had epilepsy (OR = 1.85, 95% CI = 1.75–1.96), children whose fathers had epilepsy (OR = 1.64, 95% CI = 1.54–1.74), full siblings (OR = 1.56, 95% CI = 1.46–1.67), maternal half siblings (OR = 1.28, 95% CI = 1.14–1.43), paternal half siblings (OR = 1.10, 95% CI = 0.96–1.25), and cousins (OR = 1.15, 95% CI = 1.10–1.20). The genetic correlation was 0.21 (95% CI = 0.02–0.40) and explained 40% of the phenotypic correlation between epilepsy and ADHD, with the remaining variance largely explained by nonshared environmental factors (49%, nonshared environmental correlation = 0.36, 95% CI = 0.23–0.49). The contribution of shared environmental factors to the cross-disorder overlap was not statistically significant (11%, shared environmental correlation = 0.32, 95% CI = −0.16–0.79). ConclusionsThis study demonstrates a strong and etiologically complex association between epilepsy and ADHD, with shared familial factors and risk factors unique to the individual contributing to co-occurrence of the disorders. Our findings suggest that epilepsy and ADHD may share less genetic risk as compared with other neurodevelopmental disorders.

A longitudinal twin study of general cognitive ability over four decades.

In this longitudinal study we examined the stability of general cognitive ability (GCA), as well as heterogeneity and genetic and environmental influences underlying individual differences in change. We investigated GCA from young adulthood through late midlife in 1,288 Vietnam Era Twin Study of Aging participants at ages ∼20, ∼56, and ∼62 years. The correlations among the 3 occasions ranged from .73 to .85, reflecting substantial stability. The heritability was significant on each of the 3 occasions and ranged from .59 to .66. The influence of the shared environment was not significant at any of the ages. The genetic correlations across the 3 occasions ranged from .95 to .99 and did not differ significantly from 1.0. The nonshared environmental correlations ranged from .21 to .47. Latent growth curve analysis was applied to characterize trajectories over the 42-year period. Slope was significantly different from 0 and indicated that there was modest change over time. There was a significant genetic influence on initial level of GCA (h2 = .67), but not change (h2 = .23). Genetic factors primarily contribute to stability, while change reflects the influence of nonshared environmental influences. There was a significant negative correlation between initial level of GCA and change (r = -.31). Latent class growth analysis identified 4 trajectories. In general, the 4 groups followed parallel trajectories and were differentiated mainly by differences in AFQT performance level at the time of military induction. (PsycINFO Database Record