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Background: Stress is a universal phenomenon and one of the most common precipitants of insomnia. However, not everyone develops insomnia after experiencing a stressful life event. This study aims to test aspects of Spielman's '3P model of insomnia' (during adolescence) by exploring the extent to which: (a) insomnia symptoms are predicted by polygenic scores (PGS); (b) life events predict insomnia symptoms; (c) the interaction between PGS and life events contribute to the prediction of insomnia symptoms; (d) gene–environment interaction effects remain after controlling for sex. Methods: The sample comprised 4,629 twins aged 16 from the Twin Early Development Study who reported on their insomnia symptoms and life events. PGS for insomnia were calculated. In order to test the main hypothesis of this study (a significant interaction between PGS and negative life events), we fitted a series of mixed effect regressions. Results: The best fit was provided by the model including sex, PGS for insomnia, negative life events, and their interactions (AIC = 26,158.7). Our results show that the association between insomnia symptoms and negative life events is stronger for those with a higher genetic risk for insomnia. Conclusions: This work sheds light on the complex relationship between genetic and environmental factors implicated for insomnia. This study has tested for the first time the interaction between genetic predisposition (PGS) for insomnia and environmental stressors (negative life events) in adolescents. This work represents a direct test of components of Spielman's 3P model for insomnia which is supported by our results. [ABSTRACT FROM AUTHOR]

Background: Due to different assessment modes employed, a clear picture of the prevalence of sleep bruxism across time cannot be formed. Moreover, studies on the persistent or fluctuating nature of sleep bruxism have yielded divergent and even contradictory results. The aim of the present study was to evaluate in a nationwide twin cohort whether self‐reported sleep bruxism was correlated longitudinally, pairwise and cross‐twin over a 20‐year period. Objectives: Self‐reported bruxism was assessed in 1990 and 2011 by mailed questionnaires in the Finnish Twin Cohort study of same‐sex twins born 1945–1957. Methods: We assessed the phenotypic stability over time for all participating individuals (n = 4992). Among zygosity verified pairs (n = 516 MZ and n = 837 DZ), we estimated the cross‐sectional zygosity correlations and the zygosity‐specific cross‐twin cross‐time correlations. Results: Reported bruxism appeared rather persistent over time without significant difference regarding zygosity. The overall phenotypic longitudinal correlation was 0.540 and somewhat higher in men (0.596) than in women (0.507). Pairwise trait correlations in 1990 and 2011 were higher in MZ than in DZ pairs. The cross‐twin cross‐time correlations were higher in MZ twins than in DZ twins, but less than the cross‐sectional MZ and DZ pairwise correlations. Conclusions: The higher correlation of reported sleep bruxism in the cross‐twin cross‐time analyses in MZ than in DZ pairs implies a genetic background for bruxism persistence. Also, bruxism over time in individual twins appears to be fairly persistent and somewhat higher in men than women. [ABSTRACT FROM AUTHOR]

Background: Emerging research suggests that attention-deficit/hyperactivity disorder (ADHD) increases the risk for cardiovascular (CVDs) and metabolic disorders (i.e., cardiometabolic disorders) in adulthood. Yet, available studies are scarce and have mainly been focused on individuals receiving clinical ADHD diagnoses. We aimed to investigate the prospective associations of ADHD symptoms in young and mid-adulthood with subsequent cardiometabolic disorders and the underlying mechanisms. Methods: We studied 10,394 twins from the Swedish Twin Registry (STR), born between 1958 and 1985 without previous medical history of cardiometabolic disorders. They provided self-assessment of ADHD symptoms (score range 0–36) via a validated, DSM-IV-based scale in a web-based questionnaire/telephone interview within the Study of Twin Adults: Genes and Environment (STAGE), in 2005–2006 (aged 19–47 years), and were followed until the end of 2018 (33–59 years) to identify incident clinical diagnoses/medication prescriptions for cardiometabolic disorders acquired from Swedish national registers. We used Cox regression models to investigate the associations between ADHD symptoms score and cardiometabolic outcomes, with and without adjustment for relevant covariates, and a co-twin control design to study familial confounding. Results: A one-unit increase in the level of ADHD symptoms was associated with a 2% increase in the rate of CVDs (hazard ratio [HR] = 1.02, 95% confidence interval 1.01–1.04) and a 3% increase in the rate of metabolic disorders (HR = 1.03, 1.02–1.05), after adjusting for birth year and sex. The associations were no longer significant after adjusting for educational attainment, lifestyle factors, and comorbid psychiatric disorders. The associations remained significant after adjusting for familial factors shared by dizygotic twin pairs but became nonsignificant after adjusting for factors shared by monozygotic twin pairs. However, the strength of the associations attenuated significantly in monozygotic twins compared to dizygotic twins for CVDs only, suggesting genetic confounding. Conclusions: ADHD symptom score is associated with a higher risk for cardiometabolic disorders, which may be explained by lower educational attainment, adverse lifestyle factors, and psychiatric comorbidities. Moreover, the associations appear to be partly confounded by shared genetic factors, especially for CVDs. Further research is needed to investigate the identified associations at the level of individual cardiometabolic disorders and to follow-up participants until a more advanced older age. [ABSTRACT FROM AUTHOR]

Background: Emotional symptoms, such as anxiety and depressive symptoms, are common during adolescence, often persist over time, and can precede the emergence of severe anxiety and depressive disorders. Studies suggest that a vicious cycle of reciprocal influences between emotional symptoms and interpersonal difficulties may explain why some adolescents suffer from persisting emotional symptoms. However, the role of different types of interpersonal difficulties, such as social isolation and peer victimisation, in these reciprocal associations is still unclear. In addition, the lack of longitudinal twin studies conducted on emotional symptoms during adolescence means that the genetic and environmental contributions to these relationships during adolescence remain unknown. Methods: Participants (N = 15,869) from the Twins Early Development Study completed self‐reports of emotional symptoms, social isolation and peer victimisation at 12, 16 and 21 years old. A phenotypic cross‐lagged model examined reciprocal associations between variables over time, and a genetic extension of this model examined the aetiology of the relationships between variables at each timepoint. Results: First, emotional symptoms were reciprocally and independently associated with both social isolation and peer victimisation over time, indicating that different forms of interpersonal difficulties uniquely contributed to emotional symptoms during adolescence and vice versa. Second, early peer victimisation predicted later emotional symptoms via social isolation in mid‐adolescence, indicating that social isolation may constitute an intermediate pathway through which peer victimisation predicts longer‐term emotional symptoms. Finally, individual differences in emotional symptoms were mostly accounted for by non‐shared environmental factors at each timepoint, and both gene–environment and individual‐specific environmental mechanisms were involved in the relationships between emotional symptoms and interpersonal difficulties. Conclusions: Our study highlights the necessity to intervene early in adolescence to prevent the escalation of emotional symptoms over time and to consider social isolation and peer victimisation as important risk factors for the long‐term persistence of emotional symptoms. [ABSTRACT FROM AUTHOR]

Objectives: Accumulating evidence has revealed that dental anxiety is robustly associated with dental care‐related pain and discomfort, but also with the personality trait of neuroticism (i.e. the relatively stable disposition to experience the world as distressing, threatening and unsafe). However, there is a near absence of research on these risk factors in samples for which genetic information is available. With the aim of arriving at a more refined understanding of dental anxiety, this twin cohort study assessed genetic and environmental influences on neuroticism, dental care‐related pain and dental anxiety, and the relation between these phenotypes. Methods: Participants were recruited from the Norwegian Twin Registry, and data collections were carried out in 1992–98 (Time 1) and 2011 (Time 2). Well‐validated questionnaires were used to assess the study variables, including Corah's Dental Anxiety Scale, the Numerical Pain Rating Scale, the NEO Personality Inventory Revised (Time 2) and Eysenck's Personality Questionnaire (Time 1). Pearson correlation analysis and generalized estimating equations (GEE) were used to investigate phenotypic associations. Analyses of genetic and environmental influences were performed using Cholesky modelling. Results: A total of 746 monozygotic (MZ) and 770 dizygotic (DZ) twins in the age group of 50–65 participated in the study. Moderate estimates of heritability for dental anxiety (0.29), treatment‐related pain (0.24) and neuroticism (0.45–0.54) were found. Cholesky modelling showed furthermore that neuroticism assessed at Time 1 and Time 2 was related to dental anxiety and pain via both genetic and individual‐specific environmental pathways, albeit not very strongly. The particularly high phenotypic correlation observed between dental care‐related pain and anxiety (r =.68) was explained by both overlapping genetic and individual‐specific environmental influences (the genetic and environmental correlations were.84 and.63 respectively). Conclusions: The findings provide deeper insight into the aetiology of dental anxiety and confirm that while it is strongly linked to treatment‐related pain experiences, this relation is to a considerable degree independent of general negative affectivity/neuroticism. [ABSTRACT FROM AUTHOR]

Background: Symmetry is critical in perceived attractiveness, especially in female faces. The palate determines the teeth' alignment and supports facial soft tissues. Therefore, the study aimed to assess the effects of sex, orthodontic treatment, age, and heritability on the directional, anti-, and fluctuational asymmetry in the digital palatal model. Methods: The palate of 113 twins, 86 female and 27 male subjects, with and without previous orthodontic treatment, were scanned by the Emerald (Planmeca) intraoral scanner. Three lines were constructed horizontally in the digital model, one between the right and left first upper molars and two between the first molars and incisive papilla. Two observers calculated the left and right angles between the mid-sagittal plane and molar-papilla lines. The intraclass correlation coefficient was used to assess the inter-observer absolute agreement. The directional symmetry was determined by comparing the mean left and right angles. The antisymmetry was estimated from the distribution curve of the signed side difference. The fluctuating asymmetry was approximated from the magnitude of the absolute side difference. Finally, the genetic background was assessed by correlating the absolute side difference between monozygotic twin siblings. Results: The right angle (31.1 degrees) was not significantly different from the left one (31.6 degrees). The signed side difference followed a normal distribution with a mean of -0.48 degrees. The absolute side difference (2.29 degrees, p < 0.001) was significantly different from zero and negatively correlated (r=-0.46, p < 0.05) between siblings. None of the asymmetries was affected by sex, orthodontic treatment or age. Conclusions: The palate illustrates neither directional asymmetry nor antisymmetry, indicating that most people's palates are symmetric. However, the significant fluctuating asymmetry suggests that some subject has considerable asymmetry but is not influenced by sex, orthodontic treatment, age, and genetics. The proposed digital method is a reliable and non-invasive tool that could facilitate achieving a more symmetrical structure during orthodontic and aesthetic rehabilitation. Trial registration: The Clinicatrial.gov registration number is NCT05349942 (27/04/2022). [ABSTRACT FROM AUTHOR]

Aims: To estimate the effect of recreational legalization on cannabis use frequency and sources of variance across legal environments. Design: Longitudinal discordant twin and gene–environment interaction models in twins recruited from birth records and assessed prospectively. Setting: The United States, including states with different recreational cannabis policies before and after 2014, when recreational cannabis was first legalized. Participants: Two longitudinal, prospectively assessed samples of American twins aged 24–47 (n = 1425 in legal states, n = 1996 in illegal states), including 111 monozygotic pairs discordant for residence. Measurements Current cannabis use frequency (measured continuously and ordinally) was the primary outcome, and the predictor was recreational status of cannabis (legal/illegal) in the participant's state of residence at the time of assessment. Covariates include age, sex and cannabis use frequency prior to 2014. Findings Accounting for pre‐2014 use, residents of legal states used cannabis more frequently than residents of illegal states (b = 0.21, P = 8.08 × 10−5). Comparing 111 pairs of monozygotic twins discordant for residence confirmed the effect (b = 0.18, P = 0.014). There was inconclusive evidence for genetic influences on cannabis use frequency that were specific to the legal environment [χ2 = 2.9 × 10−9, degrees of freedom (d.f.) = 1, P > 0.999]. Existing genetic influences were moderated by the legal environment, as the genetic correlation between marijuana use before and after legalization was lower in states that legalized (rgenetic = 0.24) compared with states that did not (rgenetic = 0.78, Pdifference = 0.016). Conclusions: In the United States, there appears to be a ~ 20% average increase in cannabis use frequency attributable to recreational legalization, consistent across increasingly rigorous designs. In addition, the heritability of cannabis use frequency appears to be moderated by legalization. [ABSTRACT FROM AUTHOR]

An enduring issue in the study of mental health is identifying developmental processes that explain how childhood characteristics progress to maladaptive forms. We examine the role that behavioral inhibition (BI) has on social anxiety (SA) during adolescence in 868 families of twins assessed at ages 8, 13, and 15 years. Multimodal assessments of BI and SA were completed at each phase, with additional measures (e.g., parenting stress) for parents and twins. Analyses were conducted in several steps: first, we used a cross-lagged panel model to demonstrate bidirectional paths between BI and SA; second a biometric Cholesky decomposition showed that both genetic and environmental influences on childhood BI also affect adolescent SA; next, multilevel phenotypic models tested moderation effects between BI and SA. We tested seven potential moderators of the BI to SA prediction in individual models and included only those that emerged as significant in a final conditional model examining predictors of SA. Though several main effects emerged as significant, only parenting stress had a significant interaction with BI to predict SA, highlighting the importance of environmental moderators in models examining temperamental effects on later psychological symptoms. This comprehensive assessment continues to build the prototype for such developmental psychopathology models. [ABSTRACT FROM AUTHOR]

Background: Intellectual disability (ID) aggregates in families, but factors affecting individual risk and heritability estimates remain unknown. Methods: A population‐based family cohort study of 4,165,785 individuals born 1973–2013 in Sweden, including 37,787 ID individuals and their relatives. The relative risks (RR) of ID with 95% confidence intervals (95% CI) were obtained from stratified Cox proportional‐hazards models. Relatives of ID individuals were compared to relatives of unaffected individuals. Structural equation modeling was used to estimate heritability. Results: Relatives of ID individuals were at increased risk of ID compared to individuals with unaffected relatives. The RR of ID among relatives increased proportionally to the degree of genetic relatedness with ID probands; 256.70(95% CI 161.30–408.53) for monozygotic twins, 16.47(13.32–20.38) for parents, 14.88(12.19–18.16) for children, 7.04(4.67–10.61) for dizygotic twins, 8.38(7.97–8.83) for full siblings, 4.56(4.02–5.16) for maternal, 2.90(2.49–3.37) for paternal half‐siblings, 3.03(2.61–3.50) for nephews/nieces, 2.84(2.45–3.29) for uncles/aunts, and 2.04(1.91–2.20) for cousins. Lower RRs were observed for siblings of probands with chromosomal abnormalities (RR 5.53, 4.74–6.46) and more severe ID (mild RR 9.15, 8.55–9.78, moderate RR 8.13, 7.28–9.08, severe RR 6.80, 5.74–8.07, and profound RR 5.88, 4.52–7.65). Male sex of relative and maternal line of relationship with proband was related to higher risk (RR 1.33, 1.25–1.41 for brothers vs. sisters and RR 1.49, 1.34–1.68 for maternal vs. paternal half‐siblings). ID was substantially heritable with 0.95(95% CI 0.93–0.98) of the variance in liability attributed to genetic influences. Conclusions: The risk estimates will benefit researchers, clinicians, families in understanding the risk of ID in the family and the whole population. The higher risk of ID related to male sex and maternal linage will be of value for planning and interpreting etiological studies in ID. [ABSTRACT FROM AUTHOR]

Genetic and early environmental differences including early health habits associate with future health. To provide insight on the causal nature of these associations, monozygotic (MZ) twin pairs discordant for health habits provide an interesting natural experiment. Twin pairs discordant for leisure‐time physical activity (LTPA) in early adult life is thus a powerful study design to investigate the associations between long‐term LTPA and indicators of health and wellbeing. We have identified 17 LTPA discordant twin pairs from two Finnish twin cohorts and summarize key findings of these studies in this paper. The carefully characterized rare long‐term LTPA discordant MZ twin pairs have participated in multi‐dimensional clinical examinations. Key findings highlight that compared with less active twins in such MZ twin pairs, the twins with higher long‐term LTPA have higher physical fitness, reduced body fat, reduced visceral fat, reduced liver fat, increased lumen diameters of conduit arteries to the lower limbs, increased bone mineral density in loaded bone areas, and an increased number of large high‐density lipoprotein particles. The findings increase our understanding on the possible site‐specific and system‐level effects of long‐term LTPA. [ABSTRACT FROM AUTHOR]

Background: Do drinking patterns in late adolescence/early adulthood predict lifetime childlessness and number of children? Research on this question has been only tangentially relevant and the results inconsistent. The designs used to date have been compromised by genetic and environmental confounds that are poorly controlled; covariate effects of smoking and education that are often ignored; males being understudied; population‐based sampling rare, and long‐term prospective studies with genetically informative designs yet to be reported. Method: In a 33‐year follow‐up, we linked the drinking patterns of >3500 Finnish twin pairs, assessed at ages 18–25, to registry data on their eventual number of children. Analyses distinguished associations of early drinking patterns with lifetime childlessness from those predictive of family size. Within‐twin pair analyses used fixed‐effects regression models to account for shared familial confounds and genetic liabilities. Childlessness was analyzed with Cox proportional hazards models and family size with Poisson regression. Analyses within‐pairs and of twins as individuals were run before and after adjustment for smoking and education, and for oral contraceptive (OC) use in individual‐level analyses of female twins. Results: Baseline abstinence and heavier drinking both significantly predicted lifetime childlessness in individual‐level analyses. Few abstinent women used OCs, but they were nonetheless more often eventually childless; adjusting for smoking and education did not affect this finding. Excluding childless twins, Poisson models of family size showed heavier drinking at 18–25 to be predictive of fewer children in both men and women. Those associations were replicated in within‐pair analyses of dizygotic twins, each level of heavier drinking being associated with smaller families. Among monozygotic twins, associations of drinking with completed family size yielded effects of similar magnitude, reaching significance at the highest levels of consumption, ruling out familial confounds. Conclusions: Compared to moderate levels of drinking, both abstinence and heavier drinking in late adolescence/early adulthood predicted a greater likelihood of lifetime childlessness and eventual number of children. Familial confounds do not fully explain these associations. [ABSTRACT FROM AUTHOR]

Feeling inhibited and socially not at ease is reflected in the trait social inhibition (SI). SI is associated with psychopathology that arises in young adulthood, such as anxiety. We aim for a better insight into the genetic and environmental contributions to SI across the life span, and as such examine their contributions to SI stability and change across adolescent and adult life span. We analyzed cohort-sequential longitudinal data from the Netherlands Twin Register (NTR), spanning a period of 25 years (Men (N, %): 17855,37.4%; Age (Median, IQR): 19 years, 16-26 years: 7474 complete MZ twins and 8799 complete DZ twins). The data were organized into 7 age groups: <14 (preadolescence), 15-16 (early adolescence), 17-18 (mid adolescence), 19-20 Cite adolescence), 21-30 (young adulthood), 31-40 (adulthood), 41+ (middle-age--older adulthood). SI was assessed with the ASEBA-based proxy questionnaire. Phenotypic stability was established across the entire age range. Next, a longitudinal genetic simplex model was fitted to estimate the genetic and environmental contributions to the observed phenotypic stability. Results showed SI correlated well across follow-up of a single decade (.44 ≤ r ≤ .59) and moderately across the 25 years (.23 - .32) from adolescence to middle-age and older. Broad-sense heritability (h² was between 40 and 48% across the 7 age groups, Additive and nonadditive genetic effects together explained most of the stability of SI across the life span (about 60-90% of the phenotypic correlation between ages), whereas environmental effects played a lesser role (about 10-40%). Concluding, SI, known to increase the risk of internalizing psychopathology, is phenotypically stable across the life span, which is largely attributable to genetic contributions to individual differences in SI. [ABSTRACT FROM AUTHOR]

Given the importance of writing for academic achievement, this study aimed to understand how early oral language contributes to later writing skills. The first objective was to determine if preschool language skills were associated with high school writing, and if so, whether they contributed directly or indirectly through school age language. The second aim was to explore the extent to which genetic and environmental factors explained these potential associations. The sample was drawn from the Quebec Newborn Twin Study, a longitudinal follow-up of twins born in the greater Montreal area, Quebec, Canada. Language skills were assessed when children were 1.5, 2.5, 6, 7, 10, and 12 years old. Writing skills were measured at 15 years old. Participants who completed the writing task in French were included in the study (n = 316 twin pairs: 46% males). Mothers of these participants self-identified mostly as White. About 74% of them had a postse-condary diploma or certificate, and 27% further had a university degree. Most families had an income higher than 30,000 CND. Results indicate that preschool language was modestly associated with high school writing (r = .25) and that school age language fully mediated this association. Genes explained 53% of the association between preschool language and school age language and 64% of the association between school age language and high school writing. These results highlight the developmental continuity from oral to written language from preschool to high school and show that genetic factors largely account for this continuity. [ABSTRACT FROM AUTHOR]

Aim: Our aim was to explore whether familial factors influence the risk of ischemic heart disease, stroke, and their co-occurrence. Methods: In total, 23,498 monozygotic and 39,540 same-sex dizygotic twins from the Danish Twin Registry were followed from 1977 to 2011 in the Danish National Patient Registry for ischemic heart disease and stroke. Time-to-event analyses accounting for censoring and competing risk of death were used to estimate familial risk (casewise concordance relative to the cumulative incidence) and heritability of ischemic heart disease, stroke, and the co-occurrence by age. Results: During follow-up, we observed 5561 and 4186 twin individuals with ischemic heart disease and stroke respectively, with 936 twin pairs concordant for ischemic heart disease and stroke. Familial risks were significant for both, with higher cumulative risks in monozygotic than in dizygotic twins. Estimates for heritability were significant for ischemic heart disease as well as for stroke diagnosed after the age of 80. The casewise concordance of ischemic heart disease in twins whose co-twin was diagnosed with stroke did not differ for monozygotic and dizygotic twins; however, from age 55 it was 10% higher than the cumulative risk in the overall twin cohort and was 25% higher at age 90. A similar pattern was seen for stroke following the co-twin's ischemic heart disease. Conclusions: As in previous studies, we found a higher heritability of ischemic heart disease than of stroke. There was a significant familial risk but no heritability for the co-occurrence of ischemic heart disease and stroke. The co-occurrence is therefore likely due to other shared familial than genetic factors, highlighting that preventive initiatives should target families rather than individuals. [ABSTRACT FROM AUTHOR]

It is unknown whether the built environment influences recovery from low back pain (LBP). Objective: To investigate whether neighbourhood walkability influences the recovery from LBP after adjusting for genetics and shared environmental factors. Study group: We conducted a longitudinal analysis of adult twins with LBP from the Washington State Twin Registry (average follow-up: 1.7 years). Methods: Walkability, assessed using the valid and reliable Walkscore®, was our exposure. Recovery from LBP (i.e., pain free for 3 months) at follow-up was our outcome. Multivariate logistic regression analyses were performed for the total sample (n = 1,299 twins) and for twin pairs discordant for recovery at follow-up (within-pair analysis, n = 240 twins), stratified by zygosity (dizygotic (DZ) twins, n = 138; monozygotic twins (MZ), n = 102). Results: 384 (29.6%) twins had recovered from LBP at follow-up. The total sample analysis showed no association between walkability and recovery from LBP (OR = 0.99, 95%CI: 0.99-1.00, n = 1,250 twins). There was also no association between walkability and recovery from LBP after controlling for genetics and shared environmental factors in the within-pair twin analysis of all twins (OR = 0.99, 95% CI: 0.98-1.02, n = 240 twins), DZ twins (OR = 0.99, 95% CI: 0.97-1.01, n = 138) and MZ twins (OR = 0.99; 95%CI: 0.98-1.02, n = 102). Conclusions: People with LBP who live in an environment that supports physical activity are not more likely to recover from LBP than those who live in an environment where it is more difficult to be active. Because these results did not change after adjusting for genetic and shared environmental confounding, we are more confident in these findings. [ABSTRACT FROM AUTHOR]

Background Early applications of metabolomics in nutrition and health research identified associations between dietary patterns and metabolomic profiles. Twin studies show that diet-related phenotypes and diet-associated metabolites are influenced by genes. However, studies have not examined whether diet–metabolite associations are explained by genetic or environmental factors and whether these associations are reproducible over multiple time points. Objective This research aims to examine the genetic and environmental factors influencing covariation in diet–metabolite associations that are reproducible over time in healthy twins. Methods The UCD Twin Study is a semi-longitudinal classic twin study that collected repeated dietary, anthropometric, and urinary data over 2 months. Correlation analysis identified associations between diet quality measured using the Healthy Eating Index (HEI) and urinary metabolomic profiles at 3 time points. Diet-associated metabolites were examined using linear regression to identify those significantly influenced by familial factors between twins and those significantly influenced by unique factors. Cholesky decomposition modeling quantified the genetic and environmental path coefficients through associated dietary components onto the metabolites. Results The HEI was associated with 14 urinary metabolites across 3 metabolomic profiles (r: ±0.15–0.49). For 8 diet–metabolite associations, genetic or shared environmental factors influencing HEI component scores significantly influenced variation in metabolites (β: 0.40–0.52). A significant relation was observed between dietary intakes of whole grain and acetoacetate (β: −0.50, P  < 0.001) and β-hydroxybutyrate (β: −0.46, P  < 0.001), as well as intakes of saturated fat and acetoacetate (β: 0.47, P  < 0.001) and β-hydroxybutyrate (β: 0.52, P  < 0.001). For these diet–metabolite associations a common shared environmental factor explained 66–69% of variance in the metabolites. Conclusions This study shows that diet–metabolite associations are reproducible in 3 urinary metabolomic profiles. Components of the HEI covary with metabolites, and covariation is largely due to the shared environment. [ABSTRACT FROM AUTHOR]

Mortality risk is known to be associated with many physiological or biochemical risk factors, and polygenic risk scores (PRSs) may offer an additional or alternative approach to risk stratification. We have compared the predictive value of common biochemical tests, PRSs and information on parental survival in a cohort of twins and their families. Common biochemical test results were available for up to 13,365 apparently healthy men and women, aged 17-93 years (mean 49.0, standard deviation [SD] 13.7) at blood collection. PRSs for longevity were available for 14,169 study participants and reported parental survival for 25,784 participants. A search for information on date and cause of death was conducted through the Australian National Death Index, with median follow-up of 11.3 years. Cox regression was used to evaluate associations with mortality from all causes, cancers, cardiovascular diseases and other causes. Linear relationships with all-cause mortality were strongest for C-reactive protein, gamma-glutamyl transferase, glucose and alkaline phosphatase, with hazard ratios (HRs) of 1.16 (95% CI [1.07, 1.24]), 1.15 (95% CI 1.04-1.21), 1.13 (95% CI [1.08, 1.19]) and 1.11 (95% CI [1.05, 1.88]) per SD difference, respectively. Significant nonlinear effects were found for urea, uric acid and butyrylcholinesterase. Lipid risk factors were not statistically significant for mortality in our cohort. Family history and PRS showed weaker but significant associations with survival, with HR in the range 1.05 to 1.09 per SD difference. In conclusion, biochemical tests currently predict long-term mortality more strongly than genetic scores based on genotyping or on reported parental survival. [ABSTRACT FROM AUTHOR]

Objective: The aims of this longitudinal analysis of untreated monozygotic and dizygotic twins were to investigate vertical changes of the craniofacial structures during growth, to determine the concordance between genetically twins and to assess the genetic component for the various aspects of vertical growth.Settings and Sample Population: The sample consisted of 34 pairs of untreated monozygotic twins (23 male, 11 female) and 30 untreated dizygotic siblings of multiple birth (8 male, 8 female and 14 mixed) from the Forsyth Moorrees Twin Study (1959-1975); lateral cephalograms taken from 6 to 18 years of age were analysed at 3-year intervals.Materials and Methods: Cephalograms were traced, and longitudinal changes between twins in six angular and proportional vertical cephalometric variables (SN-NL, ML-NL, SN-ML, y-axis, PFH/AFH and LAFH/AFH) were analysed with intraclass correlation coefficients and linear regression modelling.Results: The concordance between monozygotic/dizygotic twins at 18 years of age was moderate to high with intraclass correlation coefficient values between 0.51 and 0.66. Additionally, sex differences in concordance at 18 years of age were found for three variables. High heritability (66%-79%) was observed for 5 of the 6 variables (LAFH/AFH, ML-NL, y-axis, SN-ML, PFH/AFH), while SN-NL showed limited heritability (34%).Conclusions: Although monozygotic/dizygotic twins share at least part of their genetic material, differences in the vertical dimension were found. This supports the complex developmental mechanism of the human face and the varying influence of genetic and environmental factors. [ABSTRACT FROM AUTHOR]

Type 2 diabetes, which is caused by both genetic and environmental factors, may be diagnosed using the oral glucose tolerance test (OGTT). Recent studies demonstrated specific patterns in glucose curves during OGTT associated with cardiometabolic risk profiles. As the relative contribution of genetic and environmental influences on glucose curve patterns is unknown, we aimed to investigate the heritability of these patterns. We studied twins from the Danish GEMINAKAR cohort aged 18-67 years and free from diabetes at baseline during 1997-2000; glucose concentrations were measured three times during a 2-h OGTT. Heterogeneity of the glucose response during OGTT was examined with latent class mixed-effects models, evaluating goodness of fit by Bayes information criterion. The genetic influence on curve patterns was estimated using quantitative genetic modeling based on linear structural equations. Overall, 1455 twins (41% monozygotic) had valid glucose concentrations measured from the OGTT, and four latent classes with different glucose response patterns were identified. Statistical modeling demonstrated genetic influence for belonging to a specific class or not, with heritability estimated to be between 45% and 67%. During ∼12 years of follow-up, the four classes were each associated with different incidence of type 2 diabetes. Hence, glucose response curve patterns associated with type 2 diabetes risk appear to be moderately to highly heritable. [ABSTRACT FROM AUTHOR]

We aimed to investigate the associations of long‐term leisure‐time physical inactivity, body mass index (BMI) change, and education with sitting time in a 35‐year follow‐up based on self‐reports in surveys. Influences of working status in 2011 and familial confounding on the associations were tested. Data were based on the population‐based Finnish Twin Cohort of 5232 twins (53‐67‐year‐old, 41% men) with four surveys in 1975‐2011. Statistical analyses were performed using linear regression with several covariates. The effect of familial confounding (genetics and shared environment) was analyzed using a co‐twin control design which should be interpreted as if familial confounding plays a role, an association should be seen among all individuals but not in discordant twin pairs. Compared to those not at work, those at work had a longer total sitting time/d. For those at work, higher education was associated with more total sitting but with less non‐work sitting. Long‐term leisure‐time physical inactivity was associated with more non‐work sitting among those at work, whereas long‐term weight gain with more total and non‐work sitting regardless of working status. Familial confounding attenuated the associations, except for the association of increasing BMI with total and non‐work sitting among women at work. To conclude, total sitting time was longer among those still at work, but it was also influenced by long‐term leisure‐time physical inactivity, higher education, and an increase of BMI over the years. Public health efforts should be targeted to reduce sedentary behavior by promoting life‐long leisure‐time physical activity and weight control. [ABSTRACT FROM AUTHOR]

The purpose of this review is to provide a detailed and updated description of the FinnTwin16 (FT16) study and its future directions. The Finnish Twin Cohort comprises three different cohorts: the Older Twin Cohort established in the 1970s and the FinnTwin12 and FT16 initiated in the 1990s. FT16 was initiated in 1991 to identify the genetic and environmental precursors of alcoholism, but later the scope of the project expanded to studying the determinants of various health-related behaviors and diseases in different stages of life. The main areas addressed are alcohol use and its consequences, smoking, physical activity, overall physical health, eating behaviors and eating disorders, weight development, obesity, life satisfaction and personality. To date, five waves of data collection have been completed and the sixth is now planned. Data from the FT16 cohort have contributed to several hundred studies and many substudies, with more detailed phenotyping and collection of omics data completed or underway. FT16 has also contributed to many national and international collaborations. [ABSTRACT FROM AUTHOR]

Background Little is known about adolescent mental health problems, including social phobia, as risk factors for future work incapacity. The aim of this study was to investigate the association between social phobia in adolescence and unemployment and sickness absence (SA) in early adulthood, also evaluating the role of familial factors (genetics and shared environment). Methods A sample of 2845 Swedish twins born in 1985–86 in Sweden was followed longitudinally in the population-based and prospective Twin study of CHild and Adolescent Development. Information on twins' social phobia was collected at ages 13–4, 16–7 and 19–20 years. Logistic regression providing odds ratios (OR) with 95% confidence intervals (95% CI) was used to analyze the associations between social phobia, unemployment and SA during the follow-up 2006–12. The influence of familial factors was evaluated by conditional logistic regression. Results Presence of social phobia during adolescence was associated with increased odds for unemployment and SA in young adulthood. For unemployment, the highest OR was at the age of 13–4 years (1.58 [95% CI: 1.22–2.06]), and the associations became null after adjusting for familial factors. For SA, the highest OR was at the age of 19–20 years (1.73 [95% CI: 1.13–2.65]), and the estimates changed slightly after adjusting for familial factors. Conclusions : Results suggest that social phobia experienced in adolescence contribute to early adulthood unemployment and SA. Familial factors seemed to explain the association between social phobia and unemployment. [ABSTRACT FROM AUTHOR]

Study Design: A longitudinal cotwin control study of the Vietnam Era Twin Registry.Objective: The aim of this study was to examine the association of post-traumatic stress disorder (PTSD) symptoms with incident chronic back pain (CBP), while controlling for genetic factors and early family environment.Summary Of Background Data: It is unknown whether PTSD symptoms are associated with an increased incidence of CBP.Methods: In 2010 to 2012, a baseline survey was undertaken as part of a large-scale study of PTSD. Study participants completed the PTSD Symptom Checklist (PCL) and a self-report measure of CBP. In 2015 to 2017, a follow-up survey was sent to all 171 monozygotic (MZ) twin pairs (342 individuals) where both cotwins had no history of CBP at baseline, but only one cotwin in the pair met criteria for having current PTSD symptoms (one twin with PCL <30 and the cotwin with PCL ≥30). No other inclusion/exclusion criteria were applied. CBP at 5-year follow-up was defined as back pain of duration ≥3 months in the low back or mid/upper back. Covariates included age, race, education, income, Veterans Affairs health care use, disability compensation, smoking, body mass index, and depression. Statistical analysis estimated the cumulative incidence of CBP according to baseline PTSD symptoms. Risk ratios (RRs) and 95% confidence intervals (95% CIs) were estimated in matched-pair cotwin control analyses adjusting for familial factors.Results: Among 227 males completing 5-year follow-up, including 91 MZ twin pairs, the mean age was 62 years. Five-year incidence of CBP in those without and with baseline PTSD symptoms was 40% and 60%, respectively. Baseline PTSD symptoms were significantly associated with incident CBP in crude and multivariable-adjusted within-pair analyses (RR 1.6, 95% CI 1.2-2.1; P = 0.002).Conclusion: PTSD symptoms were associated with an increased incidence of CBP, without confounding by genetic factors or early family environment. PTSD symptoms may be a modifiable risk factor for prevention of CBP.Level Of Evidence: 3. [ABSTRACT FROM AUTHOR]

Introduction: The common genetic variant (rs1051730) in the 15q24 nicotinic acetylcholine receptor gene cluster CHRNA5-CHRNA3-CHRNB4 was associated with smoking quantity and has been reported to be associated also with reduced ability to quit smoking in pregnant women but results were inconsistent in nonpregnant women. The aim of this study was to explore the association between rs1051730 and smoking cessation during pregnancy in a sample of Dutch women.Methods: Data on smoking during pregnancy were available from 1337 women, who ever smoked, registered at the Netherlands Twin Register (NTR). Logistic regression was used to assess evidence for the association of rs1051730 genotype on smoking during pregnancy. In a subsample of 561 women, we investigated the influence of partner's smoking. Educational attainment and year of birth were used as covariates in both analyses.Results: There was evidence for a significant association between having one or more T alleles of the rs1051730 polymorphism and the likelihood of smoking during pregnancy (p = .03, odds ratio = 1.28, 95% CI = 1.02 to 1.61). However, this association attenuated when adjusting for birth cohort and educational attainment (p = .37, odds ratio = 1.12, 95% CI = 0.87 to 1.43). In the subsample, smoking spouse was highly associated with smoking during pregnancy, even when educational attainment and birth cohort were included in the model.Conclusions: Our results did not support a strong association between this genetic variant and smoking during pregnancy. However, a strong association was observed with the smoking behavior of the partner, regardless of the genotype of the women.Implications: The present study emphasizes the importance of social influences like spousal smoking on the smoking behavior of pregnant women. Further research is needed to address the role of rs1051730 genetic variant in influencing smoking cessation and the interaction with important environmental factors like the smoking behavior of the partner. [ABSTRACT FROM AUTHOR]

Symptoms of attention-deficit hyperactivity disorder, in particular inattention symptoms, are associated with academic achievement. However, whether and why the developmental course of inattention symptoms (i.e. systematic decreases or increases of symptoms with age) predicts academic achievement remains unclear. A total of 5634 twin pairs born in the UK were included in the current study. We used latent growth curve modelling to estimate the baseline level and the developmental course of inattention symptoms (assessed at ages 8, 11, 14 and 16 years) and test whether they predicted the General Certificate of Secondary Education scores (GCSE, at age 16 years). We then implemented multivariate twin modelling to determine the role of genetic and environmental factors in explaining the relationship between inattention symptoms and GCSE scores. Increasing inattention symptoms across childhood and adolescence predicted poorer GCSE scores independently of the baseline level of inattention. Genetic factors explained most of this relationship, i.e. genetic factors contributing to individual differences in the developmental course of inattention also influenced GCSE scores. In conclusion, our study demonstrates that genetic factors underlying the developmental course of inattention symptoms across childhood and adolescence also influence academic achievement. This may result from indirect mechanism, whereby genetic factors explain systematic changes in inattention levels with age, which in turn impact academic achievement. The shared genetic aetiology may also suggest common neurobiological processes underlying both the developmental course of inattention symptoms and academic achievement. [ABSTRACT FROM AUTHOR]

Aims: The aim of this study was to investigate whether sick leave due to different mental disorders increased the risk of reoccurring sick-leave, disability pension and unemployment, taking genetics and shared environment into account. Methods: This register-based cohort study contains 2202 discordant twin pairs 18–64 years old, where one twin had sick leave due to a mental disorder 2005–2006. The end of the sick-leave spell was the start of follow-up for both twins. The twins were followed up for reoccurring sick-leave, disability pension and unemployment (> 180 days in a year), until December 2012. Analyses were censored for disability pension, death, emigration and old-age pension. Cox proportional hazards models with time-varying covariates were used to calculate hazard ratios with 95% confidence intervals (CI). Results: Those with sick leave due to mental disorders had a 3.64 (CI: 3.24–4.08) times higher risk of reoccurring sick-leave within the first two years; after that, hazard ratios were attenuated and explained by genetic factors. The first year, they had 12.24 (CI: 8.11–18.46) times the risk of disability pension. The risk was attenuated but remained at 2.75 (CI: 2.07–3.65) after one year. The risk of unemployment was 1.99 (CI: 1.72–2.31) during the whole follow-up period. The risk of unemployment and disability pension was lower for those with stress-related than other mental disorders, this was less clear for recurrent reoccuring sick-leave. Conclusions: Sick leave due to mental disorders increased the risk of reoccurring sick-leave within two years, disability pension and unemployment, independent of genetics and shared environment. [ABSTRACT FROM AUTHOR]

Importance: Psychiatric traits associated with categorically defined psychiatric disorders are heritable and present to varying degrees in the general population. It is commonly assumed that diagnoses represent the extreme end of continuously distributed traits in the population, but this assumption has yet to be robustly tested for many psychiatric phenotypes.Objective: To assess whether genetic risk factors associated with psychiatric disorders are also associated with continuous variation in milder population traits.Design, Setting, and Participants: This study combined a novel twin analytic approach with polygenic risk score (PRS) analyses in a large population-based twin sample. Phenotypic and genetic data were available from the Child and Adolescent Twin Study in Sweden. Inpatient data were available for January 1, 1987, to December 31, 2014, and outpatient data for January 1, 2001, to December 31, 2013. The last day of follow-up was December 31, 2014. Data analysis was performed from January 1, 2017, to September 30, 2017.Main Outcomes and Measures: Questionnaires that assessed traits of autism spectrum disorder (ASD), attention-deficit/hyperactivity disorder (ADHD), learning difficulties, tic disorders (TDs), obsessive-compulsive disorder (OCD), anxiety, major depressive disorder (MDD), mania, and psychotic experiences were administered to a large Swedish twin sample. Individuals with clinical psychiatric diagnoses were identified using the Swedish National Patient Register. Joint categorical/continuous twin modeling was used to estimate genetic correlations between psychiatric diagnoses and continuous traits. The PRSs for psychiatric disorders were calculated based on independent discovery genetic data. The association between PRSs for each disorder and associated continuous traits was tested.Results: Phenotype data were available for 13 923 twin pairs (35.1% opposite sex and 31.7% same-sex females) at 9 years of age, 5165 pairs (36.9% opposite sex and 34.0% same-sex females) at 15 years of age, and 4273 pairs (36.5% opposite sex and 34.4% same-sex females) at 18 years of age. Genetic data were available for 13 412 individuals (50.2% females). Twin genetic correlations between numerous psychiatric diagnoses and corresponding traits ranged from 0.31 to 0.69. Disorder PRSs were associated with related population traits for ASD (β [SE] = 0.04 [0.01] at 9 years of age), ADHD (β [SE] = 0.27 [0.03] at 9 years of age), TDs (β [SE] = 0.02 [0.004] at 9 years of age), OCD (β [SE] = 0.13 [0.05] at 18 years of age), anxiety (β [SE] = 0.18 [0.08] at 9 years of age; β [SE] = 0.07 [0.02] at 15 years of age; and β [SE] = 0.40 [0.17] at 18 years of age), MDD (β [SE] = 0.10 [0.03] at 9 years of age; β [SE] = 0.11 [0.02] at 15 years of age; and β [SE] = 0.41 [0.10] at 18 years of age), and schizophrenia (β [SE] = 0.02 [0.01] at 18 years of age). Polygenic risk scores for depressive symptoms were associated with MDD diagnoses (odds ratio, 1.16; 95% CI, 1.02-1.32).Conclusions and Relevance: These results suggest that genetic factors associated with psychiatric disorders are also associated with milder variation in characteristic traits throughout the general population for many psychiatric phenotypes. This study suggests that many psychiatric disorders are likely to be continuous phenotypes rather than the categorical entities currently defined in diagnostic manuals, which has strong implications for genetic research in particular. [ABSTRACT FROM AUTHOR]

Background: Prior research has documented shared heritable contributions to non-suicidal self-injury (NSSI) and suicidal ideation (SI) as well as NSSI and suicide attempt (SA). In addition, trauma exposure has been implicated in risk for NSSI and suicide. Genetically informative studies are needed to determine common sources of liability to all three self-injurious thoughts and behaviors, and to clarify the nature of their associations with traumatic experiences. Methods: Multivariate biometric modeling was conducted using data from 9526 twins [59% female, mean age = 31.7 years (range 24–42)] from two cohorts of the Australian Twin Registry, some of whom also participated in the Childhood Trauma Study and the Nicotine Addiction Genetics Project. Results: The prevalences of high-risk trauma exposure (HRT), NSSI, SI, and SA were 24.4, 5.6, 27.1, and 4.6%, respectively. All phenotypes were moderately to highly correlated. Genetic influences on self-injurious thoughts and behaviors and HRT were significant and highly correlated among men [ r G = 0.59, 95% confidence interval (CI) (0.37–0.81)] and women [ r G = 0.56 (0.49–0.63)]. Unique environmental influences were modestly correlated in women [ r E = 0.23 (0.01–0.45)], suggesting that high-risk trauma may confer some direct risk for self-injurious thoughts and behaviors among females. Conclusions: Individuals engaging in NSSI are at increased risk for suicide, and common heritable factors contribute to these associations. Preventing trauma exposure may help to mitigate risk for self-harm and suicide, either directly or indirectly via reductions in liability to psychopathology more broadly. In addition, targeting pre-existing vulnerability factors could significantly reduce risk for life-threatening behaviors among those who have experienced trauma. [ABSTRACT FROM AUTHOR]

Identifying the cognitive capacities associated with the development of school readiness is indispensable to support children's successful school transition. It has been shown that executive function (EF) in preschoolers is associated with both concurrent preacademic and subsequent academic skills. However, most research has controlled for the effect of general cognitive ability (GCA), and little research has examined non-English speaking children, which hinders the understanding of the development of school readiness in culturally diverse contexts. In addition, behavioral genetic research on the genetic and environmental influences on this association has been conducted with school-age children. Thus, the genetic and environmental influences on associations between GCA, EF, and preacademic skills during preschool age are unknown. We conducted multivariate behavioral genetic analyses on two waves of longitudinal data at 42 and 60 months of age from 171 and 135 pairs of monozygotic and dizygotic Japanese twins. The findings suggested that a genetic factor influenced GCA at 42 months and mediated preacademic ability at 60 months. In addition, another genetic factor emerged by 60 months that genetically mediated EF and math ability, independent of GCA. Preacademic ability at 60 months was affected by shared environments that influenced EF, rather than GCA. at 42 months. Moreover, shared environments that influenced preacademic ability at 42 months affected later GCA at 60 months. Finally, nonshared environments that had emerged by 60 months mediated these relationships, though the magnitude of this effect was modest. [ABSTRACT FROM AUTHOR]

Background and aims: Cannabis is one of the most commonly used substances among adolescents and young adults. Earlier age at cannabis initiation is linked to adverse life outcomes, including multi‐substance use and dependence. This study estimated the heritability of age at first cannabis use and identified associations with genetic variants. Methods: A twin‐based heritability analysis using 8055 twins from three cohorts was performed. We then carried out a genome‐wide association meta‐analysis of age at first cannabis use in a discovery sample of 24 953 individuals from nine European, North American and Australian cohorts, and a replication sample of 3735 individuals. Results: The twin‐based heritability for age at first cannabis use was 38% [95% confidence interval (CI) = 19–60%]. Shared and unique environmental factors explained 39% (95% CI = 20–56%) and 22% (95% CI = 16–29%). The genome‐wide association meta‐analysis identified five single nucleotide polymorphisms (SNPs) on chromosome 16 within the calcium‐transporting ATPase gene (ATP2C2) at P < 5E‐08. All five SNPs are in high linkage disequilibrium (LD) (r2 > 0.8), with the strongest association at the intronic variant rs1574587 (P = 4.09E‐09). Gene‐based tests of association identified the ATP2C2 gene on 16q24.1 (P = 1.33e‐06). Although the five SNPs and ATP2C2 did not replicate, ATP2C2 has been associated with cocaine dependence in a previous study. ATP2B2, which is a member of the same calcium signalling pathway, has been associated previously with opioid dependence. SNP‐based heritability for age at first cannabis use was non‐significant. Conclusion: Age at cannabis initiation appears to be moderately heritable in western countries, and individual differences in onset can be explained by separate but correlated genetic liabilities. The significant association between age of initiation and ATP2C2 is consistent with the role of calcium signalling mechanisms in substance use disorders. [ABSTRACT FROM AUTHOR]

Background: Available evidence points towards lower birth weight as a risk factor for the development of attention deficit/hyperactivity disorder (ADHD) symptoms. We probed the causal nature of this putative effect of birth weight on ADHD symptoms using the twin differences design, which accounts for genetic and shared environmental confounds. Method: In a large population‐based twin sample – 3,499 monozygotic (MZ) and 6,698 dizygotic (DZ) pairs – parents, teachers or twins rated the twins’ ADHD symptoms at nine assessment waves (2–16 years). We implemented the twin differences design, which completely accounts for shared environmental and genetic confounding in MZ twins. We tested whether: (a) the lighter‐born twins had elevated ADHD symptoms compared to the heavier‐born twins, by regressing within‐pair differences of ADHD symptoms on within‐pair differences of birth weight among MZ twins; (b) the effect of birth weight on ADHD was moderated by gender, gestational age and low birth weight; (c) this effect changed with age at ADHD assessment using adapted latent growth curve models; and (d) results differed for inattention and hyperactivity/impulsivity. Results: Birth weight significantly predicted ADHD symptoms from early childhood to late adolescence. The lighter‐born twin had more ADHD symptoms than the heavier‐born cotwin among MZ twins across assessment waves and raters. No moderation effect was detected. The magnitude of the effect of birth weight decreased significantly across time for hyperactivity/impulsivity, but the decrease failed to reach significance for inattention. Estimates for inattention were significantly larger than for hyperactivity/impulsivity at each time point, implying stronger effect of birth weight on inattention symptoms. Conclusions: Our findings provide stringent evidence for environmental effect of lower birth weight on the causal pathway to elevated ADHD symptoms. Effect of birth weight persists across a 14‐year period from childhood into late adolescence, in particular for inattention symptoms. [ABSTRACT FROM AUTHOR]

Conduct problems in children and adolescents can predict antisocial personality disorder and related problems, such as crime and conviction. We sought an explanation for such predictions by performing a genetic longitudinal analysis. We estimated the effects of genetic, shared environmental, and unique environmental factors on variation in conduct problems measured at childhood and adolescence and antisocial personality problems measured at adulthood and on the covariation across ages. We also tested whether these estimates differed by sex. Longitudinal data were collected in the Netherlands Twin Register over a period of 27 years. Age appropriate and comparable measures of conduct and antisocial personality problems, assessed with the Achenbach System of Empirically Based Assessment, were available for 9783 9-10-year-old, 6839 13-18-year-old, and 7909 19-65-year-old twin pairs, respectively; 5114 twins have two or more assessments. At all ages, men scored higher than women. There were no sex differences in the estimates of the genetic and environmental influences. During childhood, genetic and environmental factors shared by children in families explained 43 and 44% of the variance of conduct problems, with the remaining variance due to unique environment. During adolescence and adulthood, genetic and unique environmental factors equally explained the variation. Longitudinal correlations across age varied between 0.20 and 0.38 and were mainly due to stable genetic factors. We conclude that shared environment is mainly of importance during childhood, while genetic factors contribute to variation in conduct and antisocial personality problems at all ages, and also underlie its stability over age. [ABSTRACT FROM AUTHOR]

Abstract: Aims: To investigate how use of alcohol, illicit drugs and tobacco come from substance‐specific pathways and from pathways general to all three substances through adolescent development. Design: Analysis of population‐based survey. Adolescent twins reported alcohol use (AU), tobacco use (TU) and illicit drug use (IDU) in three waves (2006, 2008, 2010). Restructuring data by age allowed for variance decomposition into age‐ and substance‐specific and common genetic and environmental variance components. Setting: Norway. Participants: Seven national twin birth cohorts from 1988 to 1994, totalling 1483 pairs (558 monozygotic; 925 dizygotic, same and opposite sex). Measurements: Six‐point Likert scores of AU, TU and IDU on items from the Monitoring the Future Study. Findings: Substance use was found to be highly heritable; a2 = 0.73 [95% confidence interval (CI) = 0.61–0.94] for AU, a2 = 0.36 (CI = 0.18–0.52); d2 = 0.49 (95% CI = 0.29–0.62) for IDU and a2 = 0.46 (95% CI = 0.23–0.54); d2 = 0.05 (95% CI = 0.00–0.07) for TU during the whole adolescence period. General substance use (GSU) was also highly heritable at each age and averaged a2 = 0.57 (95% CI = 0.48–0.66). There was a high genetic carry‐over from earlier age to later age. Genetic effects on GSU at ages 12–14 years were still detectable 4 years later. New substance (general and specific)‐genetic effects also appeared. IDU demonstrated significant non‐additive genetic effects (ages 12–14 years). Shared environment had a small impact on AU only. There was almost no non‐shared environmental carry‐over from age to age, the effect probably due partly to reliability deficiency. Common genetic effects among substance and substance‐specific genetic effects were observed at each age‐period. Conclusions: Among Norwegian adolescents, there appear to be strong genetic effects on both substance‐specific and comorbid use of alcohol, illicit drugs and tobacco; individual differences in alcohol use can be explained partially by family background. [ABSTRACT FROM AUTHOR]

Background and Aims The DSM-IV personality disorders (PDs) are comorbid with alcohol use disorder (AUD) and with each other. It remains unclear which PD criteria are most likely to drive onset and recurrence of AUD and which are merely confounded with those criteria. We determine which individual PD criteria predict AUD and the degree of underlying genetic and/or environmental aetiology. Design A prospective observational twin study. Setting Norway 1999-2011. Participants A total of 2528 and 2275 Norwegian adult twins in waves 1 and 2 variable-selection analyses, and 2785 in biometric analyses. Measurements DSM-IV PDs and their 80 criteria were assessed using a structured personal interview, and AUD using the World Health Organization's Composite International Diagnostic Interview. Findings In a variable-selection analysis, two PD criteria were associated with AUD even after taking all the other criteria into account: criterion 8 of antisocial PD (childhood conduct disorder) and criterion 4 of borderline PD (self-damaging impulsive behaviours). Adjusting for each other, their respective odds ratios were 3.4 [confidence interval (CI) = 2.1-5.4] and 5.0 (CI = 3.3-7.7). Endorsement strength of the criteria was associated with AUD in a dose-response manner and they explained 5.5% of variation in AUD risk-more than the full diagnoses of antisocial and borderline PDs together (0.5%). The association between borderline criterion 4 and AUD 10 years later derived mainly from their overlapping genetic factors, whereas the association between antisocial criterion 8 and AUD 10 years later was due to both genetic and non-genetic factors. Conclusions Conduct disorder and self-harming impulsivity are the foremost risk traits for alcohol use disorder among the 80 personality disorder criteria of DSM-IV, predicting alcohol use disorder more effectively than personality disorder diagnoses. The twin-study analysis suggested that conduct disorder represents a joint genetic and developmental risk for alcohol use disorder and that impulsivity is a genetic risk. [ABSTRACT FROM AUTHOR]

Purpose: There is a need for well-defined language phenotypes suitable for adolescents in twin studies and other large-scale research projects. Rice, Hoffman, and Wexler (2009) have developed a grammatical judgment measure as a clinical marker of language impairment, which has an extended developmental range to adolescence. Method: We conducted the first twin analysis, along with associated phenotypic analyses of validity, of an abridged, 20-item version of this grammatical judgment measure (GJ-20), based on telephone administration using prerecorded stimuli to 405 pairs of 16-year-olds (148 monozygotic and 257 dizygotic) drawn from the Twins Early Development Study (Haworth, Davis, & Plomin, 2012). Results: The distribution of scores is markedly skewed negatively, as expected for a potential clinical marker. Low performance on GJ-20 is associated with lower maternal education, reported learning disability (age 7 years), and low scores on language tests administered via the Twins Early Development Study (age 16 years) as well as General Certificate of Secondary Education English and Math examination performance (age 16 years). Liability threshold estimates for the genetic influence on low performance on GJ-20 are substantial, ranging from 36% with a lowest 10% criterion to 74% for a lowest 5% criterion. Conclusions: The heritability of GJ-20 scores, especially at more extreme cutoffs, along with the score distribution and association with other indicators of language impairments, provides additional evidence for the potential value of this measure as a clinical marker of specific language impairment. [ABSTRACT FROM AUTHOR]

Purpose: This study investigates the heritability of language, speech, and nonverbal cognitive development of twins at 4 and 6 years of age. Possible confounding effects of twinning and zygosity, evident at 2 years, were investigated among other possible predictors of outcomes. Method: The population-based twin sample included 627 twin pairs and 1 twin without a co-twin (197 monozygotic and 431 dizygotic), 610 boys and 645 girls, 1,255 children in total. Nine phenotypes from the same comprehensive direct behavioral assessment protocol were investigated at 4 and 6 years of age. Twinning effects were estimated for each phenotype at each age using general linear mixed models using maximum likelihood. Results: Twinning effects decreased from 4 to 6 years; zygosity effects disappeared by 6 years. Heritability increased from 4 to 6 years across all 9 phenotypes, and the heritability estimates were higher than reported previously, in the range of .44-.92 at 6 years. The highest estimate, .92, was for the clinical grammar marker. Conclusions: Across multiple dimensions of speech, language, and nonverbal cognition, heritability estimates are robust. A finiteness marker of grammar shows the highest inherited influences in this early period of children's language acquisition. [ABSTRACT FROM AUTHOR]

The aim of this study was to estimate the contribution of genetic and environmental influences on motives for engaging in leisure-time physical activity. The participants were obtained from the FinnTwin16 study. A modified version of the Recreational Exercise Motivation Measure was used to assess the motives for leisure-time physical activity in 2542 twin individuals (mean age of 34.1 years). Linear structural equation modeling was used to investigate the genetic and environmental influences on motive dimensions. The highest heritability estimates were found for the motive dimensions of 'enjoyment' [men 33% (95% CI 23-43%), women 53% (95% CI 45-60%)] and 'affiliation' [men 39% (95% CI 0.28-0.49%), women 35% (95% CI 0.25-0.43%)]. The lowest heritability estimates were found for others' expectations [men 13% (95% CI 0.04-0.25%), women 15% (95% CI 0.07-0.24%)]. Unique environmental influences explained the remaining variances, which ranged from 47% to 87%. The heritability estimates for summary variables of intrinsic and extrinsic motives were 36% and 32% for men and 40% and 24% for women, respectively. In conclusion, genetic factors contribute to motives for leisure-time physical activity. However, the genetic effects are, at most, moderate, implying the greater relative role of environmental factors. [ABSTRACT FROM AUTHOR]

Identity formation is a key developmental task in adolescence. Although many adolescents in modern societies face issues of identity, there are substantial individual differences in identity exploration and commitment. Little is known about the origins of these individual differences. The current study investigated the genetic and environmental contributions to identity formation. In total, 571 11-year-old twins (85 monozygotic complete pairs and 176 dizygotic complete pairs) reported on their identity formation, using the Dimensions of Identity Development Scale (DIDS; Luyckx, Schwartz. Berzonsky, et al., 2008), as part of the Longitudinal Israeli Study of Twins (LIST; Avinun & Knafo, 2013). Multidimensional scaling analysis and confirmatory factor analysis supported the presence of all 5 dimensions at this young age: commitment making, exploration in-breadth, ruminative exploration, identification with commitment, and exploration in-depth. However, a model where exploration in-depth was divided into two subscales had a better fit to the data. Monozygotic twins were more similar to each other than dizygotic twins on all dimensions, except for one of the exploration in-depth subscales, supporting the idea that individual differences in various dimensions of identity formation are at least partially influenced by genetics (18-45%). For these dimensions, the rest of the variance was explained by nonshared environment effects (55-82%). Only one of the exploration in-depth subscales, that is, the tendency to explore commitments through discussion with others, showed evidence for the influence of the environment shared by twins (21%) but no genetic effect. Implications of the findings regarding the role of genetics and environment to identity formation are discussed. [ABSTRACT FROM AUTHOR]

Background: We aimed to disentangle genetic and environmental causes in lung cancer while considering smoking status.Methods: Four Nordic twin cohorts (43 512 monozygotic (MZ) and 71 895 same sex dizygotic (DZ) twin individuals) had smoking data before cancer diagnosis. We used time-to-event analyses accounting for censoring and competing risk of death to estimate incidence, concordance risk and heritability of liability to develop lung cancer by smoking status.Results: During a median of 28.5 years of follow-up, we recorded 1508 incident lung cancers. Of the 30 MZ and 28 DZ pairs concordant for lung cancer, nearly all were current smokers at baseline and only one concordant pair was seen among never smokers. Among ever smokers, the case-wise concordance of lung cancer, that is the risk before a certain age conditional on lung cancer in the co-twin before that age, was significantly increased compared with the cumulative incidence for both MZ and DZ pairs. This ratio, the relative recurrence risk, significantly decreased by age for MZ but was constant for DZ pairs. Heritability of lung cancer was 0.41 (95% CI 0.26 to 0.56) for currently smoking and 0.37 (95% CI 0.25 to 0.49) for ever smoking pairs. Among smoking discordant pairs, the pairwise HR for lung cancer of the ever smoker twin compared to the never smoker co-twin was 5.4 (95% CI 2.1 to 14.0) in MZ pairs and 5.0 (95% CI 3.2 to 7.9) in DZ pairs.Conclusions: The contribution of familial effects appears to decrease by age. The discordant pair analysis confirms that smoking causes lung cancer. [ABSTRACT FROM AUTHOR]

Background: Several nonpsychotic psychiatric disorders in childhood and adolescence can precede the onset of schizophrenia, but the etiology of this relationship remains unclear. We investigated to what extent the association between schizophrenia and psychiatric disorders in childhood is explained by correlated genetic risk factors. Methods: Polygenic risk scores (PRS), reflecting an individual's genetic risk for schizophrenia, were constructed for 2588 children from the Netherlands Twin Register (NTR) and 6127 from the Avon Longitudinal Study of Parents And Children (ALSPAC). The associations between schizophrenia PRS and measures of anxiety, depression, attention deficit hyperactivity disorder (ADHD), and oppositional defiant disorder/conduct disorder (ODD/CD) were estimated at age 7, 10, 12/13, and 15 years in the 2 cohorts. Results were then meta-analyzed, and a meta-regression analysis was performed to test differences in effects sizes over, age and disorders. Results: Schizophrenia PRS were associated with childhood and adolescent psychopathology. Meta-regression analysis showed differences in the associations over disorders, with the strongest association with childhood and adolescent depression and a weaker association for ODD/CD at age 7. The associations increased with age and this increase was steepest for ADHD and ODD/CD. Genetic correlations varied between 0.10 and 0.25. Conclusion: By optimally using longitudinal data across diagnoses in a multivariate meta-analysis this study sheds light on the development of childhood disorders into severe adult psychiatric disorders. The results are consistent with a common genetic etiology of schizophrenia and developmental psychopathology as well as with a stronger shared genetic etiology between schizophrenia and adolescent onset psychopathology. [ABSTRACT FROM AUTHOR]

Twin studies have estimated the relative contribution of genes and the environment to variance in exercise behavior and it is known that parental education positively affects exercise levels. This study investigates the role of parental education as a potential modifier of variance in exercise behavior from age 7 to 18 years. The study is based on large datasets from the Netherlands Twin Register ( NTR: N = 24 874 twins; surveys around the ages of 7, 10, 12, 14, 16 and 18 years) and two Finnish twin cohorts ( FinnTwin12: N = 4399; 12, 14 and 17 years; FinnTwin16: N = 4648; 16, 17 and 18 years). Regular participation in moderate-to-vigorous exercise activities during leisure time was assessed by survey. Parental education was dichotomized ('both parents with a low education' vs 'at least one parent with a high education'). The mean in exercise behavior tended to be higher and the variance tended to be lower in children of high educated parents. Evidence for gene-by-environment interaction was weak. To develop successful interventions that specifically target children of low educated parents, the mechanisms causing the mean and variance differences between the two groups should be better understood. [ABSTRACT FROM AUTHOR]

Study Design: Longitudinal twin-cohort study.Objective: To investigate the effect familial aggregation of chronic low back pain (LBP) has on the recovery from chronic LBP.Summary Of Background Data: LBP is a worldwide problem, with pain and disability often becoming chronic. Genetics and familial behaviors could significantly affect the recovery from chronic LBP but have not been extensively investigated.Methods: A total of 624 Spanish twins from the Murcia Twin Registry reported experiencing chronic LBP within the past 2 years during the 2009/11 data collection wave and were followed up in 2013. Familial aggregation of chronic LBP was determined by the co-twin experiencing chronic LBP within the past 2 years at baseline. Twins reporting LBP "within the past 4 weeks" at follow-up were considered to have not recovered.Results: There were 455 twins with available data on LBP at follow-up and available data on LBP from their co-twin at baseline. Twins with an affected co-twin at baseline were significantly more likely to have not recovered from chronic LBP at follow-up (odds ratio [OR] = 1.6, 95% confidence interval [CI]: 1.0-2.4, P = 0.046). This relationship was stronger for monozygotic twins (OR = 2.5, 95% CI: 1.3-4.8, P = 0.006) (n = 172) but disappeared when considering only dizygotic twins (OR = 1.1, 95% CI: 0.6-2.0, P = 0.668) (n = 283). Sibling-relative recurrence risk (λ s) was 1.2 for the total sample, 1.5 for monozygotic twins, and 1.1 for dizygotic twins.Conclusion: Having a sibling with chronic LBP at baseline increased the likelihood of LBP at follow-up by 20%, with this likelihood increasing to 50% if the sibling was an identical twin. These results are novel and highlight the important influence genetics have on people's recovery from chronic LBP. Information regarding the presence of chronic LBP within a family is easy to obtain and has the potential to inform clinicians on which patients are less likely to recover when treatment implementation is not considered.Level Of Evidence: 3. [ABSTRACT FROM AUTHOR]

Background: Familial factors play an important role in the variation of risk factors of cardiovascular diseases (CVD), but less is known about how they affect the risk of death from CVD. We estimated familial aggregation of CVD mortality for twins offering the maximum level of risk due to genetic and other familial factors.Methods: Altogether, 132 771 twin individuals, including 65 196 complete pairs from Denmark, Finland and Sweden born in 1958 or earlier, participated in this study. During the register-based follow-up, 11 641 deaths occurred from coronary heart disease (CHD), including 6280 deaths from myocardial infarct and 4855 deaths occurred from stroke, with 1092 deaths from ischaemic stroke and 1159 deaths from haemorrhagic stroke. Relative recurrence risk ratios (RRRs) with 95% confidence intervals (95% CIs) for monozygotic and dizygotic twins were calculated.Results: In the analyses pooling men and women, the RRR for monozygotic twins was 1.49 (95% CI 1.40-1.57) for CHD and 1.81 for any stroke (95% CI 1.54-2.09). The highest RRR was found for haemorrhagic stroke (3.53 95% CI 2.01-5.04). For dizygotic twins, the RRRs were generally lower.Conclusions: Family aggregation was found for CHD and haemorrhagic stroke. Clustering of risk factors in families increases the risk of CVD. [ABSTRACT FROM AUTHOR]

Most research into the role of gene-environment interactions in the etiology of obesity has taken environment to mean behaviours such as exercise and diet. While interesting, this is somewhat at odds with research into the social determinants of obesity, in which the focus has shifted away from individuals and behaviours to the types of wider obesogenic environments in which individuals live, which influence and produce these behaviours. This study combines these two strands of research by investigating how the genetic influence on body mass index (BMI), used as a proxy for obesity, changes across different neighbourhood environments measured by levels of deprivation. Genetics are incorporated using a classical twin design with data from Twins UK, a longitudinal study of UK twins running since 1992. A multilevel modelling approach is taken to decompose variation between individuals into genetic, shared environmental, and non-shared environmental components. Neighbourhood deprivation is found to be a statistically significant predictor of BMI after conditioning on individual characteristics, and a heritability of 0.75 is estimated for the entire sample. This heritability estimate is shown, however, to be higher in more deprived neighbourhoods and lower in less deprived ones, and this relationship is statistically significant. While this research cannot say anything directly about the mechanisms behind the relationship, it does highlight how the relative importance of genetic factors can vary across different social environments, and therefore the value of considering both genetic and social determinants of health simultaneously. [ABSTRACT FROM AUTHOR]

Background Depression is already highly prevalent by late adolescence, indicating that research into its developmental emergence should consider earlier risk factors and environmental contexts. The home environment is a key context for children and adolescents throughout development. However, the nature of relationships that exist between aspects of the home environment and the development of depressive symptoms cannot be assumed. Genetically informative studies have been used to provide insights about the aetiology of such relationships, often finding them to be partly confounded by the influence of children's genes. Here, we investigate developmental change in the aetiology of the association between aspects of the home environment and depressive symptoms at the onset of adolescence. Methods We used longitudinal child- and parent-report data from >5,000 twin pairs enrolled in the UK-representative Twins Early Development Study. Multivariate, genetically sensitive structural equation models were used to decompose latent variance and covariance in depressive symptoms (measured at 12 and 16 years) and aspects of the home environment (at 9 and 14 years) into genetic and environmental influences. Results Going from childhood to adolescence, genetic influences accounted for an increasing proportion of the association [30% (16-42) of r = .44 in childhood; 40% (25-61) of r = .43 in adolescence], at the expense of shared environmental influences, which decreased from 70% (58-83) to 48% (29-62). Unique environmental influences accounted for a significant proportion of the association in adolescence only [12% (06-18)]. Developmental changes could largely be attributed to subtle shifts in the relative importance of stable aetiological factors, rather than the emergence of influences unique to adolescence. Conclusions These findings emphasise the importance of developmental and aetiological context in interpreting associations between aspects of the home environment and child emotional outcomes. [ABSTRACT FROM AUTHOR]

Smoking and caffeine consumption show a strong positive correlation, but the mechanism underlying this association is unclear. Explanations include shared genetic/environmental factors or causal effects. This study employed three methods to investigate the association between smoking and caffeine. First, bivariate genetic models were applied to data of 10 368 twins from the Netherlands Twin Register in order to estimate genetic and environmental correlations between smoking and caffeine use. Second, from the summary statistics of meta-analyses of genome-wide association studies on smoking and caffeine, the genetic correlation was calculated by LD-score regression. Third, causal effects were tested using Mendelian randomization analysis in 6605 Netherlands Twin Register participants and 5714 women from the Avon Longitudinal Study of Parents and Children. Through twin modelling, a genetic correlation of r0.47 and an environmental correlation of r0.30 were estimated between current smoking (yes/no) and coffee use (high/low). Between current smoking and total caffeine use, this was r0.44 and r0.00, respectively. LD-score regression also indicated sizeable genetic correlations between smoking and coffee use (r0.44 between smoking heaviness and cups of coffee per day, r0.28 between smoking initiation and coffee use and r0.25 between smoking persistence and coffee use). Consistent with the relatively high genetic correlations and lower environmental correlations, Mendelian randomization provided no evidence for causal effects of smoking on caffeine or vice versa. Genetic factors thus explain most of the association between smoking and caffeine consumption. These findings suggest that quitting smoking may be more difficult for heavy caffeine consumers, given their genetic susceptibility. [ABSTRACT FROM AUTHOR]

Background: Twin 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. Methods: Univariate 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). Results: Heritability 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%). Conclusions: Hoarding 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. [ABSTRACT FROM AUTHOR]

Objective. To provide population-based estimates of relative risk of SLE and other autoimmune diseases (ADs) in relatives of SLE patients. Methods. A cohort of 5 237 319 Danish residents identified through the Civil Registration System was coupled to their relatives through the parental link and followed for SLE and other ADs between 1977 and 2013 through linkage to the National Patient Register. Twin zygosity was established through the Danish Twin Registry. Hazard ratios (HRs) with 95% CIs were calculated using Cox proportional hazards regression analyses. Results. During 117.5 million person-years of follow-up, 3612 persons were hospitalized with SLE. HRs of SLE were high among first-degree (HR = 10.3; 95% CI: 8.25, 12.9; n = 80) and second- or third-degree relatives of SLE patients (HR = 3.60; 95% CI: 2.20, 5.90; n = 16). HRs for any AD were elevated in firstdegree (HR = 1.51; 95% CI: 1.41, 1.62; n = 785) and second- or third-degree relatives of SLE patients (HR = 1.28; 95% CI: 1.18, 1.39; n = 582). Among individuals with SLE-affected first-degree relatives, the risk was significantly increased for RA (HR = 1.64; 95% CI: 1.35, 1.99; n = 103), IBD (HR = 1.21; 95% CI: 1.02, 1.43; n = 130) and type 1 diabetes mellitus (HR = 1.23; 95% CI: 1.01, 1.48; n = 106). Risk of other ADs was significantly increased both among SLE-affected first-degree (HR = 2.08; 95% CI: 1.88, 2.31; n = 371) and second- or third-degree relatives (HR = 1.38; 95% CI: 1.23, 1.54; n = 313). Conclusion. Family history of SLE is associated with a clearly elevated risk of SLE and, to a much lesser degree, of RA and other ADs. [ABSTRACT FROM AUTHOR]

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. [ABSTRACT FROM AUTHOR]