Nonshared Environmental Factors Research Articles

Twin models of environmental and genetic influences on pubertal development, salivary testosterone, and estradiol in adolescence.

Research on sources of variation in adolescent's gonadal hormone levels is limited. We sought to decompose individual differences in adolescent testosterone, estradiol, and pubertal status, into genetic and environmental components. A sample of male and female adolescent twins from the greater Austin and Houston areas provided salivary samples, with a subset of participants providing longitudinal data at 2 waves. The sample included 902 adolescent twins, 49% female, aged 13-20years (M=15.91) from the Texas Twin Project. Thirty-seven per cent of twin pairs were monozygotic; 30% were same-sex dizygotic (DZ) pairs; and 33% were opposite-sex DZ pairs. Saliva samples were assayed for testosterone and estradiol using chemiluminescence immunoassays. Pubertal status was assessed using self-report. Biometric decompositions were performed using multivariate quantitative genetic models. Genetic factors contributed substantially to variation in testosterone in males and females in the follicular phase of their menstrual cycle (h2 =60% and 51%, respectively). Estradiol was also genetically influenced in both sexes, but was predominately influenced by nonshared environmental factors. The correlation between testosterone and estradiol was mediated by a combination of genetic and environmental influences for males and females. Genetic and environmental influences on hormonal concentrations were only weakly correlated with self-reported pubertal status, particularly for females. Between-person variability in adolescent gonadal hormones and their interrelationship reflects both genetic and environmental processes, with both testosterone and estradiol containing sizeable heritable components.

Heterogeneity in the development of proactive and reactive aggression in childhood: Common and specific genetic - environmental factors.

BackgroundFew studies are grounded in a developmental framework to study proactive and reactive aggression. Furthermore, although distinctive correlates, predictors and outcomes have been highlighted, proactive and reactive aggression are substantially correlated. To our knowledge, no empirical study has examined the communality of genetic and environmental underpinning of the development of both subtypes of aggression. The current study investigated the communality and specificity of genetic-environmental factors related to heterogeneity in proactive and reactive aggression’s development throughout childhood.MethodsParticipants were 223 monozygotic and 332 dizygotic pairs. Teacher reports of aggression were obtained at 6, 7, 9, 10 and 12 years of age. Joint development of both phenotypes were analyzed through a multivariate latent growth curve model. Set point, differentiation, and genetic maturation/environmental modulation hypotheses were tested using a biometric decomposition of intercepts and slopes.ResultsCommon genetic factors accounted for 64% of the total variation of proactive and reactive aggression’s intercepts. Two other sets of uncorrelated genetic factors accounted for reactive aggression’s intercept (17%) on the one hand, and for proactive (43%) and reactive (13%) aggression’s slopes on the other. Common shared environmental factors were associated with proactive aggression’s intercept (21%) and slope (26%) and uncorrelated shared environmental factors were also associated with reactive aggression’s slope (14%). Common nonshared environmental factors explained most of the remaining variability of proactive and reactive aggression slopes.ConclusionsA genetic differentiation hypothesis common to both phenotypes was supported by common genetic factors associated with the developmental heterogeneity of proactive and reactive aggression in childhood. A genetic maturation hypothesis common to both phenotypes, albeit stronger for proactive aggression, was supported by common genetic factors associated with proactive and reactive aggression slopes. A shared environment set point hypothesis for proactive aggression was supported by shared environmental factors associated with proactive aggression baseline and slope. Although there are many common features to proactive and reactive aggression, the current research underscores the advantages of differentiating them when studying aggression.

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.

Minority stressors, rumination, and psychological distress in monozygotic twins discordant for sexual minority status

Lesbian, gay, and bisexual (LGB) individuals report higher levels of depression and anxiety than heterosexual people. Genetic factors may be a 'common cause' of sexual minority status and psychological distress. Alternatively, these may be correlated because of non-genetic environmental factors (e.g. minority stressors). This study investigated minority stressors and distress in monozygotic twins discordant for sexual minority status. This design provides a test of the role of non-shared environmental factors while minimizing differences due to genetics. Thirty-eight twin pairs in which one was heterosexual and the other was LGB completed a survey. Differences between twin pairs in minority stressors, rumination, psychological distress, and gender non-conformity were examined. Associations between these variables were also tested. Although there were no significant group differences for distress, LGB twins had higher rumination, a vulnerability factor for distress, than heterosexual co-twins. LGB twins also had higher scores than heterosexual co-twins on expectations of rejection, active concealment, self-stigma, prejudice events, childhood gender non-conformity, and lower scores on sexual orientation disclosure. Differences between twin pairs in rumination were positively associated with differences in acceptance concerns and self-stigma. Finally, self-stigma was positively associated with rumination in the full sample of heterosexual co-twins and microaggressions were positively associated with rumination when looking at exclusively heterosexual co-twins. These results support environmental factors as a causal explanation for disparities in rumination between LGB and heterosexual individuals. These factors likely include minority stressors. Rumination may also be associated with minority stressors in heterosexual MZ co-twins of LGB individuals.

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.

Familial aggregation of myasthenia gravis in affected families: a population-based study.

IntroductionMyasthenia gravis (MG) is clinically heterogeneous and can be life-threatening if bulbar or respiratory muscles are involved. However, relative contributions of genetic, shared, and nonshared environmental factors to MG susceptibility remain unclear. The aim of this study was to examine the familial aggregation and heritability of MG and the relative risks (RRs) of other autoimmune diseases in the relatives of patients with MG.MethodsA population-based family study using the Taiwan National Health Insurance (NHI) Database was conducted. Participants included all individuals (N=23,422,955) who were actively registered in the NHI Database in 2013, 15,066 of whom had at least one first-degree relative with MG. We identified 8,638 parent–child relationships, 3,279 with an affected offspring, 3,134 with affected siblings, and 26 with affected twins. Prevalence and RRs of MG and other autoimmune diseases in the relatives of patients as well as the relative contributions of heritability, shared, and nonshared environmental factors to MG susceptibility were measured.ResultsRRs (95% confidence intervals [CIs]) for MG were 17.85 (8.71–36.56) for patients’ siblings, 5.33 (2.79–10.18) for parents, 5.82 (3.03–11.16) for offspring, and 1.42 (0.20–10.10) for spouses without genetic similarities. RRs (95% CIs) in individuals with a first-degree relative with MG were 2.18 (1.53–3.12) for systemic lupus erythematosus, 1.73 (1.09–2.74) for primary Sjögren’s syndrome, 1.90 (1.66–2.18) for autoimmune thyroid disease, and 1.68 (1.22–2.30) for rheumatoid arthritis. Accountability for the phenotypic variance of MG was 82.1% for familial transmission and 17.9% for nonshared environmental factors.ConclusionIndividual risks of MG and other autoimmune diseases are increased in the relatives of patients with MG. Familial transmission of MG was estimated to be 82.1%.

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.

Mental Toughness and Individual Differences in Learning, Educational and Work Performance, Psychological Well-being, and Personality: A Systematic Review.

Mental toughness (MT) is an umbrella term that entails positive psychological resources, which are crucial across a wide range of achievement contexts and in the domain of mental health. We systematically review empirical studies that explored the associations between the concept of MT and individual differences in learning, educational and work performance, psychological well-being, personality, and other psychological attributes. Studies that explored the genetic and environmental contributions to individual differences in MT are also reviewed. The findings suggest that MT is associated with various positive psychological traits, more efficient coping strategies and positive outcomes in education and mental health. Approximately 50% of the variation in MT can be accounted for by genetic factors. Furthermore, the associations between MT and psychological traits can be explained mainly by either common genetic or non-shared environmental factors. Taken together, our findings suggest a ‘mental toughness advantage’ with possible implications for developing interventions to facilitate achievement in a variety of settings.

Genetic and environmental influences on household financial distress

Heterogeneity of household financial outcomes emerges from various individual and environmental factors, including personality, cognitive ability, and socioeconomic status (SES), among others. Using a genetically informative data set, we decompose the variation in financial management behavior into genetic, shared environmental and non-shared environmental factors. We find that about half of the variation in financial distress is genetically influenced, and personality and cognitive ability are associated with financial distress through genetic and within-family pathways. Moreover, genetic influences of financial distress are highest at the extremes of SES, which in part can be explained by neuroticism and cognitive ability being more important predictors of financial distress at low and high levels of SES, respectively.

Alterations in resting state connectivity along the autism trait continuum: a twin study

Autism spectrum disorder (ASD) has been found to be associated with alterations in resting state (RS) functional connectivity, including areas forming the default mode network (DMN) and salience network (SN). However, insufficient control for confounding genetic and environmental influences and other methodological issues limit the generalizability of previous findings. Moreover, it has been hypothesized that ASD might be marked by early hyper-connectivity followed by later hypo-connectivity. To date, only a few studies have explicitly tested age-related influences on RS connectivity alterations in ASD. Using a within-twin pair design (N=150 twins; 8–23 years), we examined altered RS connectivity between core regions of the DMN and SN in relation to autistic trait severity and age in a sample of monozygotic (MZ) and dizygotic (DZ) twins showing typical development, ASD or other neurodevelopmental conditions. Connectivity between core regions of the SN was stronger in twins with higher autistic traits compared to their co-twins. This effect was significant both in the total sample and in MZ twins alone, highlighting the effect of non-shared environmental factors on the link between SN-connectivity and autistic traits. While this link was strongest in children, we did not identify differences between age groups for the SN. In contrast, connectivity between core hubs of the DMN was negatively correlated with autistic traits in adolescents and showed a similar trend in adults but not in children. The results support hypotheses of age-dependent altered RS connectivity in ASD, making altered SN and DMN connectivity promising candidate biomarkers for ASD.

Familial aggregation of nasopharyngeal carcinoma in Taiwan

BackgroundThe incidence of nasopharyngeal carcinoma (NPC) is higher in Chinese than in Caucasian populations. Genetic, viral, and lifestyle factors may explain these ethnic differences in the incidence of NPC. In the present study, we examined the familial aggregation, heritability, and relative risks (RRs) of NPC using a nationwide database in Taiwan. MethodsA population-based family study was conducted using the Taiwan National Health Insurance Research Database. Participants included all individuals (N=23,422,955) registered with that database in 2013; of these, 17,653 had NPC. Among them, 47.45%, 57.45%, 47.29%, and 1.51% had a parent, child, sibling, and twin, respectively, with NPC. ResultsAmong the approximately 23 million Taiwan NHI beneficiaries in 2013, the relative risks (RRs) (95% confidence intervals) for NPC were 34.46 (5.12–231.77) for twins of the patients, 9.23 (6.34–13.43) for siblings, 3.80 (2.97–4.86) for parents, 3.74 (2.60–5.37) for offspring, and 1.78 (1.16–2.74) for spouses without genetic similarity. The mean age of onset in first-degree relative-affected NPC patients was 35.5years compared to 39.0years for NPC patients without affected first-degree relatives (p≤0.0001). Using a threshold liability model, the accountability for phenotypic variance of NPC was estimated to be 61.3% for genetic factors (heritability), 13.9% for shared environmental factors, and 24.8% for non-shared environmental factors. The probability of a patient with NPC to be sporadic was 82.8%. ConclusionThis population-based analysis suggested a strong familial tendency in the development of NPC. Screening of first-degree relatives of NPC patients is recommended, particularly in endemic regions.

Association of a Family History of Atrial Fibrillation With Incidence and Outcomes of Atrial Fibrillation

The heritability of atrial fibrillation (AF), the contribution of genetic and environmental factors, and the association of a family history of AF with prognosis are unclear. To measure genetic and environmental factors in the familial aggregation of AF and to estimate the association of a family history of AF with major adverse cardiovascular events (MACE). In this Taiwanese nationwide population-based study among more than 23 million people, a custom data set was obtained using the data of all patients having a diagnosis of AF recorded between January 1996 and December 2013 in the Taiwan National Health Insurance Research Database. The study population comprised all 23 422 955 individuals registered with the database in 2013, of whom 177 770 had a diagnosis of AF and were included in the heritability estimation. From the latter, a subgroup of patients having newly diagnosed AF with a first-degree relative affected by AF between 2000 and 2010 were selected and matched 1:4 to controls without a family history for estimating MACE-free survival. The dates of analysis were January 2010 to December 2013. The prevalence and relative risk of AF in relatives of patients with AF, as well as the relative contributions of heritability and shared and nonshared environmental factors to AF susceptibility. Also measured was MACE-free survival after AF was diagnosed. In total, 1510 patients (204 [13.5%] female; mean [SD] age, 57.9 [9.2] years) had newly diagnosed AF with a first-degree relative affected by AF. Individuals with a first-degree relative affected by AF had a relative risk of 1.92 (95% CI, 1.84-1.99) for AF. The accountability for the phenotypic variance of AF was 19.9% for genetic factors (heritability), 3.5% for shared environmental factors, and 76.6% for nonshared environmental factors. After matching for age, sex, hypertension, type 2 diabetes, previous stroke, and anticoagulation, incident AF patients with vs without an affected first-degree relative had similar MACE-free survival. Genetic and environmental factors were associated with AF, with nonshared environmental factors accounting for three-fourths of the phenotypic variance in Taiwan. Patients having AF with a first-degree relative affected by AF did not have more MACE. Therefore, family history may not be particularly informative in the diagnosis or management of AF.

Heritability of hoarding symptoms across adolescence and young adulthood: A longitudinal twin study.

BackgroundTwin studies of hoarding symptoms indicate low to moderate heritability during adolescence and considerably higher heritability in older samples, suggesting dynamic developmental etiological effects. The aim of the current study was to estimate the relative contribution of additive genetic and environmental effects to hoarding symptoms during adolescence and young adulthood and to estimate the sources of stability and change of hoarding symptoms during adolescence.MethodsUnivariate model-fitting was conducted in three cohorts of twins aged 15 (n = 7,905), 18 (n = 2,495) and 20–28 (n = 6,218). Longitudinal analyses were conducted in a subsample of twins for which data on hoarding symptoms was available at both age 15 and 18 (n = 1,701).ResultsHeritability estimates for hoarding symptoms at ages 15, 18 and 20–28 were 41% (95% confidence interval [CI]: 36–45%), 31% (95% CI: 22–39%) and 29% (95% CI: 24–34%) respectively. Quantitative sex-differences emerged in twins aged 15 at which point the heritability in boys was 33% (95% CI: 22–41%) and 17% (95% CI: 0–36%) in girls. Shared environmental effects played a negligible role across all samples with the exception of girls aged 15 where they accounted for a significant proportion of the variance (22%; 95% CI 6–36%). The longitudinal bivariate analyses revealed a significant phenotypic correlation of hoarding symptoms between ages 15 and 18 (0.40; 95% CI: 0.36–0.44) and a strong but imperfect genetic correlation (0.75; 95% CI: 0.57–0.94). The bivariate heritability was estimated to 65% (95% CI: 50–79%).ConclusionsHoarding symptoms are heritable from adolescence throughout young adulthood, although heritability appears to slightly decrease over time. Shared environmental effects contribute to hoarding symptoms only in girls at age 15. The stability of hoarding symptoms between ages 15 and 18 is largely explained by genetic factors, while non-shared environmental factors primarily have a time-specific effect. The findings indicate that dynamic developmental etiological effects may be operating across the life span.

Genetic and environmental aspects in the association between attention-deficit hyperactivity disorder symptoms and binge-eating behavior in adults: a twin study.

Prior research demonstrated that attention-deficit hyperactivity disorder (ADHD) is associated with binge-eating behavior, binge-eating disorder (BED), and bulimia nervosa (BN). The aim of this study was to investigate these associations in an adult twin population, and to determine the extent to which ADHD symptoms and binge-eating behavior share genetic and environmental factors. We used self-reports of current ADHD symptoms and lifetime binge-eating behavior and associated characteristics from a sample of over 18 000 adult twins aged 20-46 years, from the population-based Swedish Twin Registry. Mixed-effects logistic regression was used to examine the association between ADHD and lifetime binge-eating behavior, BED, and BN. Structural equation modeling was used in 13 773 female twins to determine the relative contribution of genetic and environmental factors to the association between ADHD symptoms and binge-eating behavior in female adult twins. ADHD symptoms were significantly associated with lifetime binge-eating behavior, BED, and BN. The heritability estimate for current ADHD symptoms was 0.42 [95% confidence interval (CI) 0.41-0.44], and for lifetime binge-eating behavior 0.65 (95% CI 0.54-0.74). The genetic correlation was estimated as 0.35 (95% CI 0.25-0.46) and the covariance between ADHD and binge-eating behavior was primarily explained by genetic factors (91%). Non-shared environmental factors explained the remaining part of the covariance. The association between adult ADHD symptoms and binge-eating behavior in females is largely explained by shared genetic risk factors.

Genetic and other risk factors for suicidal ideation and the relationship with depression.

There is a genetic contribution to the risk of suicide, but sparse prior research on the genetics of suicidal ideation. Active and passive suicidal ideation were assessed in a Sri Lankan population-based twin registry (n = 3906 twins) and a matched non-twin sample (n = 2016). Logistic regression models were used to examine associations with socio-demographic factors, environmental exposures and psychiatric symptoms. The heritability of suicidal ideation was assessed using structural equation modelling. The lifetime prevalence of any suicidal ideation was 13.0% (11.7-14.3%) for men; 21.8% (20.3-23.2%) for women, with no significant difference between twins and non-twins. Factors that predicted suicidal ideation included female gender, termination of marital relationship, low education level, urban residence, losing a parent whilst young, low standard of living and stressful life events in the preceding 12 months. Suicidal ideation was strongly associated with depression, but also with abnormal fatigue and alcohol and tobacco use. The best fitting structural equation model indicated a substantial contribution from genetic factors (57%; CI 47-66) and from non-shared environmental factors (43%; CI 34-53) in both men and women. In women this genetic component was largely mediated through depression, but in men there was a significant heritable component to suicidal ideation that was independent of depression. These are the first results to show a genetic contribution to suicidal ideation that is independent of depression outside of a high-income country. These phenomena may be generalizable, because previous research highlights similarities between the aetiology of mental disorders in Sri Lanka and higher-income countries.

Counterproductive behaviors: Relations across life domains, etiology, and implications for applied practice

AbstractPrevious research on counterproductive work behavior (CWB) has shown that workplace deviance can be predicted from individual differences and environmental variables, but relatively little is known about CWBs’ relations with counterproductive behaviors in other domains of an individual's life. Data from 500 male twins were used to examine relations among counterproductive behaviors from several life domains, including school, non‐work, substance use, and work. The results supported the hypotheses that counterproductivity in work and a variety of personal life domains, previous and contemporaneous, are strongly and positively related. A general counterproductivity factor, giving rise to rule‐ and norm‐breaking behavioral repertoire of individuals, accounted for approximately half the variance across measures of counterproductivity in specific life domains. To inform theory and research, the etiology of inter‐individual differences in counterproductivity was examined. Biometric analyses revealed that most of the variance in the counterproductivity domains examined, including CWB, is attributable to genetic and unique (nonshared) environmental factors. The general counterproductivity factor spanning different counterproductivity domains was most influenced by genetic factors (75.4%), but was also influenced by unique environmental factors (24.6%). Biometric analyses indicated that 27% of the variance in CWB is attributable to genetic influences arising from the general factor of counterproductivity and 20% from genetic factors specific to CWB. Unique environmental influences associated with the work domain explained 12% of the variance in CWB. For the CWB criterion, regression analyses explored the usefulness of information from other counterproductivity domains for prediction and employee selection. Counterproductivity from academic and non‐work domains are potent predictors of counterproductivity at work (multiple Rs ranging between .50 and .54).

On the genetic and environmental reasons why intelligence correlates with criminal victimization

Researchers have expended considerable effort to understand the causes and correlates of criminal victimization. More recently, scholars have focused on identifying individual-level traits that increase the odds of victimization. Generally absent from this line of research, however, is examining the extent to which previously unmeasured genetic and environmental influences contribute to the covariation between victimization and individual-level risk factors. The current study aims to replicate and extend prior research by examining the contribution of genetic and environmental influences on the association between intelligence and victimization by analyzing twin and sibling data from two nationally representative samples of American youth. Quantitative genetic analyses indicate that common additive genetic factors, as well as non-shared environmental factors, explained the phenotypic association between intelligence and victimization. Finally, our results revealed that after correcting for possible familial confounding, the effect of intelligence on victimization experiences remained statistically significant. The findings of the current study replicate and extend prior research on the phenotypic association between indicators of general intelligence and the experience of victimization.

Commentary on Salvatore et al. (2017): Dyadic research can clarify non-shared environmental influences on alcohol use disorder and divorce.

Commentary on Salvatore et al. (2017): Dyadic research can clarify non-shared environmental influences on alcohol use disorder and divorce.

Chronic pain, depression and cardiovascular disease linked through a shared genetic predisposition: Analysis of a family-based cohort and twin study.

BackgroundDepression and chronic pain are the two most important causes of disability (Global Burden of Disease Study 2013). They occur together more frequently than expected and both conditions have been shown to be co-morbid with cardiovascular disease. Although shared socio-demographic risk factors (e.g. gender, deprivation) might explain the co-morbidity of these three conditions, we hypothesised that these three long-term, highly prevalent conditions co-occur and may be due to shared familial risk, and/or genetic factors.Methods and findingsWe employed three different study designs in two independent cohorts, namely Generation Scotland and TwinsUK, having standardised, validated questionnaire data on the three traits of interest. First, we estimated the prevalence and co-occurrence of chronic pain, depression and angina among 24,024 participants of a population-based cohort of extended families (Generation Scotland: Scottish Family Health Study), adjusting for age, gender, education, smoking status, and deprivation. Secondly, we compared the odds of co-morbidity in sibling-pairs with the odds in unrelated individuals for the three conditions in the same cohort. Lastly, examination of similar traits in a sample of female twins (TwinsUK, n = 2,902), adjusting for age and BMI, allowed independent replication of the findings and exploration of the influence of additive genetic (A) factors and shared (C) and non-shared (E) environmental factors predisposing to co-occurring chronic widespread pain (CWP) and cardiovascular disease (hypertension, angina, stroke, heart attack, elevated cholesterol, angioplasty or bypass surgery). In the Generation Scotland cohort, individuals with depression were more than twice as likely to have chronic pain as those without depression (adjusted OR 2·64 [95% CI 2·34–2·97]); those with angina were four times more likely to have chronic pain (OR 4·19 [3·64–4·82]); those with depression were twice as likely to have angina (OR 2·20 [1·90–2·54]). Similar odds were obtained when the outcomes and predictors were reversed and similar effects seen among sibling pairs; depression in one sibling predicted chronic pain in the other (OR 1·34 [1·05–1·71]), angina predicted chronic pain in the other (OR 2·19 [1·63–2·95]), and depression, angina (OR 1·98 [1·49–2·65]). Individuals with chronic pain and angina showed almost four-fold greater odds of depression compared with those manifesting neither trait (OR 3·78 [2·99–4·78]); angina showed seven-fold increased odds in the presence of chronic pain and depression (OR 7·76 [6·05–9·95]) and chronic pain nine-fold in the presence of depression and angina (OR 9·43 [6·85–12·98]). In TwinsUK, the relationship between CWP and depression has been published (R = 0.34, p<0.01). Considering the CWP-cardiovascular relationship, the most suitable model to describe the observed data was a combination of A, C and E, with a small but significant genetic predisposition, shared between the two traits (2·2% [95% CI 0·06–0·23]).ConclusionWe found an increased co-occurrence of chronic pain, depression and cardiovascular disease in two independent cohorts (general population-based cohort, twins cohort) suggesting a shared genetic contribution. Adjustment for known environmental influences, particularly those relating to socio-economic status (Generation Scotland: age, gender, deprivation, smoking, education; Twins UK: age,BMI) did not explain the relationship observed between chronic pain, depression and cardiovascular disease. Our findings from two independent cohorts challenge the concept of traditional disease boundaries and warrant further investigation of shared biological mechanisms.

The genetic and environmental aetiology of spatial, mathematics and general anxiety

Individuals differ in their level of general anxiety as well as in their level of anxiety towards specific activities, such as mathematics and spatial tasks. Both specific anxieties correlate moderately with general anxiety, but the aetiology of their association remains unexplored. Moreover, the factor structure of spatial anxiety is to date unknown. The present study investigated the factor structure of spatial anxiety, its aetiology, and the origins of its association with general and mathematics anxiety in a sample of 1,464 19-21-year-old twin pairs from the UK representative Twins Early Development Study. Participants reported their general, mathematics and spatial anxiety as part of an online battery of tests. We found that spatial anxiety is a multifactorial construct, including two components: navigation anxiety and rotation/visualization anxiety. All anxiety measures were moderately heritable (30% to 41%), and non-shared environmental factors explained the remaining variance. Multivariate genetic analysis showed that, although some genetic and environmental factors contributed to all anxiety measures, a substantial portion of genetic and non-shared environmental influences were specific to each anxiety construct. This suggests that anxiety is a multifactorial construct phenotypically and aetiologically, highlighting the importance of studying anxiety within specific contexts.