The German twin family study ‘TwinLife’ was designed to enhance our understanding of the development of social inequalities over the life course. The interdisciplinary project investigates mechanisms of social inequalities across the lifespan by taking into account psychological as well as social mechanisms, and their genetic origin as well as the interaction and covariation between these factors. Main characteristics of the study are: (1) a multidimensional perspective on social inequalities, (2) the assessment of developmental trajectories in childhood, adolescence, and young adulthood in a longitudinal design by using (3) a combination of a multi-cohort cross-sequential and an extended twin family design, while (4) capturing a large variation of behavioral and environmental factors in a representative sample of about 4,000 German twin families. In the present article, we first introduce the theoretical and empirical background of the TwinLife study, and second, describe the design, content, and implementation of TwinLife. Since the data will be made available as scientific use file, we also illustrate research possibilities provided by this project to the scientific community.

We have observed the inconsistent findings from various studies on twin pregnancy outcomes obtained by assisted reproductive technology and spontaneous conception. In most studies, however, the concrete chorionicity, regarded as a confounding factor for predicting the perinatal outcomes of twin pregnancies, has not been determined. The purpose of this study was to compare obstetric and perinatal outcomes of only the dichorionic twin pregnancies according to the methods of conception: spontaneous and in-vitro fertilization (IVF). The twin pairs with dichorionicity reported from 1995 to 2008 were investigated and we divided them into two groups which consisted of 286 and 134 twins by spontaneous conception and IVF, respectively. Odds ratios for associations between IVF and pregnancy outcomes were analyzed after adjustment for maternal age and parity. There were no risk differences between the two groups regarding the obstetric complications, which include preterm delivery, preterm labor, preterm premature rupture of membranes, preeclampsia, placenta previa, and abruption. Any differences were not shown in the two groups for the risk estimates of perinatal outcomes, such as low birthweight, very low birthweight, small for gestational age, Apgar scores of < 7 at 5 minutes, discordance in birthweights, congenital anomalies and mortality. However, twins conceived after IVF were less likely to be admitted to the neonatal intensive care unit than those conceived spontaneously (adjusted OR 0.488; 95% confidence interval 0.261–0.910). In the cases of dichorionic twins, IVF may not be associated with adverse perinatal and obstetric outcomes compared with spontaneous conception.

Adolescents are prone to risk-taking behaviors leading to adverse consequences such as substance abuse, accidents, violence, and victimization. However, little is known about the contribution of genetic and environmental factors to individual differences in the propensity for risk-taking. This study investigated developmental changes, longitudinal stability, and heritability of risk-taking using data from 752 adolescent twins including 169 MZ and 203 DZ pairs. The Balloon Analogue Risk Task (BART), an experimental behavioral measure of risk taking, was administered to the twins at age 12 and then re-administered to a part of this sample at age 14. Risk-taking increased with age, but individual differences showed a significant longitudinal stability. Genetic model fitting showed that at age 12, heritability of risk-taking was modest but significant in both sexes, whereas at age 14, heritability increased to 55% in males and became nonsignificant in females. The findings suggest that propensity for risk-taking as measured by BART can be a useful endophenotype for genetic studies of adolescent externalizing psychopathology, however, the utility of this measure may be limited by sex differences in heritability.

Female twin pairs were identified from birth records, and their families invited to participate in a prospective study of the determinants of alcohol problems in women. We investigated sampling biases arising because of failure to locate families, or non-cooperation of families. Out of 2644 families with a live-born pair (born between July 1975 and December 1986) who survived beyond infancy, contact was established and a brief screening interview completed with 90% (N = 2380). Fewer than 6% of located families declined to participate in the initial screening interview. Predictors of failure to locate a family or to obtain a screening interview were identified from information recorded in birth records, and from neighborhood characteristics identified from 1990 US Census block group data for the family residence when the twins were born. African-American families were under-represented in the final sample, but this effect was barely significant when other variables were controlled for. Under-represented were families where the mother was 19 or younger at the birth of the twins, where the mother herself was born out-of-state, or where information about biological father was not reported in the birth record. Non-participating families on average came from neighborhoods with a higher proportion of residents living in poverty, and with a higher proportion of African-American residents. Sampling biases were however small. The unusual cooperativeness in research of families with twins persists.

The purpose of this study was to clarify the genetic contribution to stuttering and tics in childhood using the largest databases of Japanese twins. The subjects were 1896 pairs of twin children consisting of 1849 males and 1943 females with a mean age of 11.6 years (3 years to 15 years). All data were gathered by questionnaire. The prevalence of stuttering was 6.7% in males and 3.6% in females (p < .0001). The prevalence of tics was 6.8% in males and 4.1% in females (p = .0021). Concordance rates and polychoric correlations were all higher in monozygotic pairs than in dizygotic pairs irrespective of sex combination. Structural equation modeling showed that the proportion of total phenotypic variance attributable to genetic influences was 80% in males and 85% in females for stuttering, and 28% in males and 29% in females for tics. Moreover, co-occurrence between stuttering and tics was observed in 0.8% of males (tetrachoric correlation: r = .18) and 0.5% of females (r = .31), which was attributed partly (nearly 10% of total genetic variance of each trait) to the common genetic factors, with genetic correlation of r = .32.

Genome-wide association studies (GWAS) of attention-deficit/hyperactivity disorder (ADHD) offer the benefit of a hypothesis-free approach to measuring the quantitative effect of genetic variants on affection status. Generally the findings of GWAS relying on ADHD status have been non-significant, but the one study using quantitative measures of symptoms found SLC9A9 and SLC6A1 were associated with inattention and hyperactivity–impulsivity. Accordingly, we performed a GWAS using quantitative measures of each ADHD subtype measured with the Strengths and Weaknesses of ADHD and Normal Behaviour (SWAN) scale in two community-based samples. This scale captures the full range of attention and kinetic behavior; from high levels of attention and appropriate activity to the inattention and hyperactivity–impulsivity associated with ADHD within two community-based samples. Our discovery sample comprised 1,851 participants (mean age = 22.8 years [4.8]; 50.6% female), while our replication sample comprised 155 participants (mean age = 26.3 years [3.1]; 68.4% females). Age, sex, age × sex, and age2 were included as covariates and the results from each sample were combined using meta-analysis, then analyzed with a gene-based test to estimate the combined effect of markers within genes. We compare our results with markers that have previously been found to have a strong association with ADHD symptoms. Neither the GWAS nor subsequent meta-analyses yielded genome-wide significant results; the strongest effect was observed at rs2110267 (4.62 × 10−7) for symptoms of hyperactivity–impulsivity. The strongest effect in the gene-based test was for GPR139 on symptoms of inattention (6.40 × 10−5). Replication of this study with larger samples will add to our understanding of the genetic etiology of ADHD.

Two major challenges to conducting a community-based twin study of pathological gambling (PG) disorder are that: (a) it is relatively rare, and (b) individuals with the disorder in the community may be difficult to locate and recruit. We describe a new study of 4,764 individuals recruited from the Australian Twin Registry in which we attempt to effectively deal with the first challenge and examine the impact of the second challenge. The lifetime prevalence of DSM-IV PG in this Australian twin sample was 2.2%, which is 400–500% higher than has been obtained in prevalence surveys conducted in the United States. A number of predictors of non-participation were identified, including a lifetime PG disorder diagnosis, but these did not have a large net effect on the estimated number of individuals with PG or related characteristics in the twin sample. Results of biometric modeling suggested that the effect of genetic, shared family environmental, and nonshared environmental influences on the propensity to engage in 11 different specific forms of gambling (e.g., playing the lottery, betting on horse or dog races, playing electronic gaming machines) were generally moderate, low, and moderate, respectively, with mean parameter estimates obtained of 43%, 10%, and 46%. An intriguing comparison with results from a 1963 US adolescent twin study conducted by Loehlin and Nichols (1976) suggests that: (a) propensity genes for gambling involvement may be more likely to be expressed in the heavy-gambling Australian culture, or that (b) the family environment has a transient effect on the gambling behavior of young people.

Conduct disorder (CD) symptoms and substance dependence commonly co-occur. Both phenotypes are highly heritable and a common genetic influence on the covariation has been suggested. The aim of this study was to determine the extent to which genes and environment contribute to the covariance between CD and drug dependence using twins from the Colorado Longitudinal Twin Sample and the Colorado Twin Registry. A total of 880 twin pairs (237 monozygotic [MZ] female, 195 MZ male, 116 dizygotic [DZ] female, 118 DZ male and 214 DZ opposite-sex) aged 13 to 18 (mean = 15.65) were included in the analysis. CD was assessed by lifetime Diagnostic and Statistical Manual of Mental Disorders (4th ed.; DSM-IV; American Psychiatric Association, 1994) symptom count and a polysubstance dependence vulnerability index was developed from responses to the Composite International Diagnostic Interview — Substance Abuse Module. A bivariate Cholesky Decomposition model was used to partition the cause of variation and covariation of the two phenotypes. No sex-limitation was observed in our data, and male and female parameter estimates were constrained to be equal. Both CD symptoms and dependence vulnerability were significantly heritable, and genes, shared environment and nonshared environment all contributed to the covariation between them. Genes contributed 35% of the phenotypic covariance, shared environment contributed 46%, and nonshared environmental influences contributed the remaining 19% to the phenotypic covariance. Therefore, there appears to be pleiotropic genetic influence on CD symptoms and dependence vulnerability.

Socioeconomic position, racial/ethnic minority status, and other characteristics of the macro-environment may be important moderators of genetic influence on a wide array of psychosocial outcomes. Designed to maximize representation of low socioeconomic status families and racial/ethnic minorities, the Texas Twin Project is an ongoing study of school-age twins (preschool through 12th grade) enrolled in public schools in the Austin, Texas and Houston, Texas metropolitan areas. School rosters are used to identify twin families from a target population with sizable populations of African American (18%), Hispanic/Latino (48%), and non-Hispanic White (27%) children and adolescents, over half of whom meet US guidelines for classification as economically disadvantaged. Initial efforts have focused on a large-scale, family-based survey study involving both parent and child reports of personality, psychopathology, physical health, academic interests, parent–child relationships, and aspects of the home environment. In addition, the Texas Twin Project is the basis for an in-laboratory study of adolescent decision-making, delinquency, and substance use. Future directions include geographic expansion of the sample to the entire state of Texas (with a population of over 25 million) and genotyping of participating twins.

This paper is the first in a series that aims to give an overview of existing twin registers worldwide. A short description of 16 registries in nine European countries is presented. These registries have access to over 350 000 pairs and a resource for genetic–epidemiological research.

Phenotypic research on leadership style has long considered the importance of individual differences in personality when identifying the behaviors associated with good leaders. Although leadership and many personality traits have been separately shown to be heritable, these constructs have not been examined with genetically informative data to identify common sources of heritability in the two domains. A logical extension to current research, therefore, is to examine the extent to which factors of personality are predictive of leadership dimensions and the extent to which unique genetic contributions to the relationship between personality and leadership style may be identified. Adult twin pairs (183 MZ and 64 same-sex DZ) completed the Multifactor Leadership Questionnaire (MLQ) and the Personality Research Form (PRF). Univariate analyses indicated that both leadership factors (transformational and transactional leadership) and all five of the “Big Five” factors (openness, conscientiousness, extraversion, disagreeableness, and neuroticism) were best fit by genetic models. Multivariate genetic analyses suggest that transformational leadership shows a statistically significant positive genetic correlation with conscientiousness, extraversion, and openness to experience. Transactional leadership shows a significant negative genetic correlation with conscientiousness and extraversion, and a significant positive genetic correlation with disagreeableness. These results underscore the importance of conscientiousness and extraversion in predicting leadership style, and illustrate important differences between transformational and transactional leaders.

Do women experience orgasm because this trait was shaped by natural selection to augment female fitness? Or are women merely the lucky recipients of developmental patterns favored by selection to produce orgasm in males? A recent and widely publicized book by Elisabeth Lloyd (2005a) contends that there is insufficient evidence to validate any of the adaptive explanations yet proposed for female orgasm. We agree. But our reading of the data differs from Lloyd's. In this essay, we outline why, unlike Caton (2006), whose review of Lloyd's book appeared previously in this journal, we are not persuaded by Lloyd's argument that female orgasm is a nonadaptive byproduct of orgasm in men. We hold this view because we disagree with the criteria Lloyd uses to evaluate evolutionary hypotheses, and because we believe Lloyd defines female orgasm too narrowly, ignoring critical information about its affective aspects.

Twin–twin transfusion syndrome (TTTS) is a severe complication of monochorionic (MC) twin pregnancies associated with high perinatal mortality and morbidity rates. Management in TTTS is a major challenge for obstetricians and neonatologists. Twins with TTTS are often born prematurely after an extremely distressing and highly hazardous fetal period. Follow-up studies report varying rates of cerebral palsy (CP) and long-term neurodevelopmental impairment (NDI). This review discusses the latest findings on the long-term outcome of TTTS survivors, possible risk factors for long-term impairment, and provides recommendations for future research.

In twin studies of cardiovascular disease biomarkers the dizygotic correlations are often estimated to be less than half of monozygotic correlations indicating a potential influence of nonadditive genetic factors. Using a large and homogenous sample, we estimated the additive and dominance genetic influences on levels of high density lipoprotein, low density lipoprotein, apolipoprotein A-I, apolipoprotein B, total cholesterol, triglycerides, glucose, hemoglobin Alc and c-reactive protein, all of which are biomarkers associated with cardiovascular disease. The blood biomarkers were measured on 12,000 Swedish twins born between 1911 and 1958. The large sample allowed us to obtain heritability estimates with considerable precision and provided adequate statistical power for estimation of dominance genetic components. Our study showed complete absence of the shared environment component for the investigated traits. Dominant genetic component was shown to be significant for low density lipoprotein (0.18), glucose (0.31), Hemoglobin Alc (0.55), and c-reactive protein (0.27). To our knowledge, this is the first statistically significant evidence for dominance genetic variance found for low density lipoprotein, glucose, hemoglobin Alc, and c-reactive protein in a population based twin sample. The study highlights the importance of acknowledging nonadditive genes underlying the risk of developing cardiovascular diseases.

Genetic and environmental sources of covariation among cognitive measures of verbal IQ, performance IQ (PIQ), academic achievement, 2-choice reaction time (CRT), inspection time (IT) and the 6 Openness facets of the NEO Personality Inventory-Revised (NEO PI-R) were examined. The number of twin and twin–sibling pairs ranged from 432 (182 MZ, 350 DZ/sibling) to 1023 (273 MZ, 750 DZ/sibling) for cognitive measures, and between 432 (90 MZ, 342 DZ/sibling) — 437 (91 MZ, 346 DZ/sibling) for Openness facets. Structural equation modeling best supported a model with a 3-factor additive genetic structure. A genetic general factor subsumed the 5 cognitive measures and 5 of the 6 Openness facets (Actions did not load significantly). A second additive genetic factor incorporated the 6 Openness facets, and a third additive genetic factor incorporated the 5 cognitive measures. Specific additive and dominance genetic effects were also evident, as were shared common and shared unique environmental influences, and specific unique environmental effects. The Openness facets of Ideas and Values evidenced the strongest phenotypic correlations with cognitive indices, particularly verbal measures. The genetic correlations among Openness facets and cognitive measures ranged from −.06 to .79. Results were interpreted as suggesting that Openness is related to general cognitive ability (g) through a genetic mechanism and that gengenders a minor but discernable disposition towards Openness for the majority of facets.

The population-based twin program of research at the Norwegian Institute of Public Health (NIPH) was begun in 1992. It consists of a number of questionnaire and clinical interview projects exploring a broad array of mental and physical health outcomes. This article provides a brief update summarizing our research activities, some research highlights, new developments and potentials for further developing the program of twin research. In the most recent years a large effort has concentrated on completing a mental health interview study of Axis I psychiatric and substance use disorders and Axis II personality disorders. Although still in the early planning phases, one of the most significant developments is that an agreement is now in place to centralize the Norwegian twin data into a national Norwegian Twin Registry. This new registry will include twin cohorts born from 1905 onwards. Other resources for building twin projects are described. Nationally, there is great potential for linking the NIPH twin data with other health registries and with information in a number of Norway's large population-based biobank studies. Internationally, platforms such as those developed within GenomEUtwin, for data standards and data sharing and access are greatly facilitating international collaborations in twin research.

Etiological factors for stability and change in symptoms of anxiety and depression, including sex differences, are largely unexplored in young adults. Using biometric modeling and two-wave longitudinal data from 4393 Norwegian twins aged 18 to 31 we explored (i) heritabilities of symptoms of anxiety and depression, (ii) effects of genetic and environmental factors on the stability and change of such symptoms, and (iii) sex-specific effects. The phenotypic cross-time correlations for symptoms of anxiety and depression were estimated to .54 and .49 for males and females, respectively. The best fitting longitudinal model specified additive genetic and individual environmental influences and emerging effects from the shared environment for females only. For both males and females, long-term stability was mainly attributable to stable additive genetic factors, whereas change was essentially related to environmental influences. Minor time-specific genetic effects were indicated, and some stable variance was due to the individual environment. Additive genetic risk factors explained 87% and 68% of the phenotypic cross-time correlation for males and females, with the unique environment accounting for the remaining covariance. The results provide strong evidence for the temporal stability of genetic risk factors for symptoms of anxiety and depression in young adults, and substantial sex-specific influences on heritability, stability and change.

Objectives: The aim of the present study was to examine the role of genetic and environmental factors in the phenotypic variance of bruxism in a large population-based cohort of young adult twins in Finland.

Methods: The material of the present study derives from the FinnTwin16 cohort study consisting of five birth cohorts of twin pairs born in 1975–1979 who completed a questionnaire (at mean age 24, range 23–27 years) with data on frequency of sleep-related bruxism in 2000–2002. We used quantitative genetic modeling, based on the genetic similarity of monozygotic and dizygotic twins, to estimate the most probable genetic model for bruxism, based on decomposition of phenotypic variance into components: additive genetic effects (A), dominant genetic effects (D), and non-shared environmental effects (E).

Results: On average, 8.7% experienced bruxism weekly, 23.4% rarely, and 67.9% never, with no significant gender difference (p = .052). The best fitting genetic model for bruxism was the AE-model. Additive genetic effects accounted for 52% (95% CI 0.41–0.62) of the total phenotypic variance. Sex-limitation model revealed no gender differences.

Conclusions: Genetic factors account for a substantial proportion of the phenotypic variation of the liability to sleep-related bruxism, with no gender difference in its genetic architecture.

To our knowledge, no comprehensive, interdisciplinary initiatives have been taken to examine the role of genetic variants on patient-reported quality-of-life outcomes. The overall objective of this paper is to describe the establishment of an international and interdisciplinary consortium, the GENEQOL Consortium, which intends to investigate the genetic disposition of patient-reported quality-of-life outcomes. We have identified five primary patient-reported quality-of-life outcomes as initial targets: negative psychological affect, positive psychological affect, self-rated physical health, pain, and fatigue. The first tangible objective of the GENEQOL Consortium is to develop a list of potential biological pathways, genes and genetic variants involved in these quality-of-life outcomes, by reviewing current genetic knowledge. The second objective is to design a research agenda to investigate and validate those genes and genetic variants of patient-reported quality-of-life outcomes, by creating large datasets. During its first meeting, the Consortium has discussed draft summary documents addressing these questions for each patient-reported quality-of-life outcome. A summary of the primary pathways and robust findings of the genetic variants involved is presented here. The research agenda outlines possible research objectives and approaches to examine these and new quality-of-life domains. Intriguing questions arising from this endeavor are discussed. Insight into the genetic versus environmental components of patient-reported quality-of-life outcomes will ultimately allow us to explore new pathways for improving patient care. If we can identify patients who are susceptible to poor quality of life, we will be able to better target specific clinical interventions to enhance their quality of life and treatment outcomes.

Twin registries form an exceptionally rich source of information that is largely unexploited for phenotypic analyses. One obstacle to straightforward phenotypic statistical analysis is the inherent dependency, which is due to the clustering of cases within families. The present simulation study gauges the degree of the bias produced by the dependency of family data on the estimates of standard errors and chi-squared, when they are treated as independent observations in a phenotypic model, and assesses the efficiency of an estimator, which corrects for dependency. When family-clustered data are used for phenotypic analysis, in treating individuals as independent, and using standard maximum likelihood estimation, there is a tendency for the chi-square statistic to be overestimated, and the standard errors of the parameters to be underestimated. The bias increases with family resemblance, due to heritability or shared environment. The source of family resemblance — either heritability (h2) and/or shared environment (c2) — interacts with the composition of the sample. In the absence of c2, samples with twins, parents and spouses show the lowest bias, whereas in the presence of c2 samples with only twins show the lowest bias. In all conditions the bias remained below 15%. The use of the ‘complex option’ available in Mplus (clustering corrected robust maximum likelihood estimation) reduces the bias to the levels observed when only independent cases are considered. Thus with the use of robust estimates the bias due to family dependency becomes practically negligible in all conditions of dependency. In conclusion, the present study shows that the bias due to dependency in family data does not form a serious obstacle to phenotypic data analysis.