With the development of large twin-family registers worldwide (see the December 2006 issue of Twin Research and Human Genetics for an overview) new options for research projects become feasible, including longitudinal studies. In this special issue on Longitudinal Twin and Family Studies, several aspects of longitudinal research are highlighted and an overview of results is given from European, Australian and United States twin studies. These studies deal with a time span from birth to adulthood and a wide range of phenotypes is covered. Data collection in some studies is age/cohort driven; in others, subjects are followed from different ages at regular time intervals. Most studies are based on data collection in twins, but adoption and parent–offspring data designs are described as well. The overview of results of current longitudinal projects makes this special issue a reference resource for longitudinal research in developmental behavior genetics.

The Netherlands Twin Register (NTR) was established around 1987 at the Vrije Universiteit in Amsterdam, the Netherlands. The current article summarizes the longitudinal genetic analyses of maternal and paternal ratings of twins' behavior as a function of the sex of the children for the traits of aggression (AGG), attention problems (AP), anxious/depression (ANX), internalizing behavior (INT) and externalizing behavior (EXT). We found that genetic influences are the most important factor in explaining individual differences in these traits. For most phenotypes, influences of genetic factors fluctuate throughout development, with the exception of AP, for which genetic influences remain of similar magnitude. Changes in genetic influences parallel those in shared environmental influences, while nonshared environmental influences remain relatively constant. Around 10% to 20% of the variance is accounted for by parent-specific shared environment, which includes rater bias. For all phenotypes, stability throughout childhood is accounted for by genetic and shared environmental factors, while nonshared environmental influences are mainly age/measurement specific. About 15% of the phenotypic stability is accounted for by rater-specific shared environmental influences, which include rater bias. In conclusion, between ages 3 and 12 genetic factors are the most important cause of individual differences in emotional and behavioral problems.

The study of twins and their families provides a highly useful tool for disentangling the genetic and environmental origins of traits. The Cardiff Study of All Wales and North West of England Twins (CaStANET) has followed children and adolescents over time into early adulthood, assessing a wide range of aspects of behavior and psychopathology using self-, parent and teacher reports. Four main waves of data collection have taken place to date, which have provided a wealth of information on the contributions of genetic and environmental risk factors to the psychological health of young people. This article first describes the CaStANET register and subsequently presents some of the findings that have emerged from this resource, with a focus on depression and anxiety, chronic fatigue, attention-deficit/hyperactivity disorder, conduct problems and prosocial behavior. We describe in somewhat more detail the 4th wave of data collection, which has recently been completed and has provided us with extensive information on substance use and problem use as well as associated risk factors in the twins and their families, including longitudinal data on conduct problems and the relations between family members. Because of the wealth of data already collected and the opportunity for genetically informative analyses over time, CaStANET provides a valuable resource for understanding the complexities of the psychological development of young people.

We enrolled more than 3500 same-sex twins from 5 consecutive Finnish birth cohorts into a longitudinal study as each cohort reached age 16. Twins completed the Psychopathic Deviate (Pd) Scale of the Minnesota Multiphasic Personality Inventory at baseline, Sensation Seeking Scale items as each cohort reached age 17, and later, at average ages 18.5 and 25, the Rutgers Alcohol Problem Index (RAPI). Using raw maximum likelihood estimation, we fit a Cholesky model to the 4 variables assessed at 4 ages across the 4 twin types; we estimated genetic and environmental influences on the stability of alcohol problems across development and the genetic and environmental contributions to predictive correlations between adolescent personality and later alcohol-related behavior problems. With one exception, the phenotypic, genetic, and environmental correlations were very similar for males and females. The exception was that the lagged associations of Pd and RAPI reflect a higher genetic correlation among males than females and a higher environmental correlation among females than males. Our analyses suggest that developmental changes underlying variation in alcohol problems from late adolescence to early adulthood differ for males and females. In males, the main change is decreased variation due to shared environmental effects; the magnitude of genetic effects is stable over time, and the high genetic correlation, .95, suggests that the same genetic influences are important at both ages. Among females, in contrast, genetic influences decline in magnitude from age 18 to 25, and at least part of the genetic effect evident at age 25 differs from the genetic effect evident at age 18.

There is significant covariation between internalizing and externalizing behavior, although there is also evidence that internalizing behavior is a protective factor against externalizing behavior. Several researchers have posited that the examination of the relationship between temperament or personality and behavior problems may help explain these seemingly contradictory results. Specifically, negative emotionality or neuroticism has been cited as a temperament characteristic that internalizing and externalizing behavior share in common, whereas behavioral inhibition may be related only to internalizing behavior. We examined the degree to which the covariation between internalizing and externalizing behavior assessed from age 4 to 12 years can be explained by temperament characteristics assessed from age 14 to 36 months. Additionally, we assessed the extent to which this relationship is due to genetic or environmental factors, analyzing data from 225 monozygotic and 185 dizygotic twin pairs assessed by the Colorado Longitudinal Twin Study. In males, a portion of the covariation between internalizing and externalizing behavior was explained by shared environmental influences in common with emotionality and shared environmental influences in common with shyness. In females, most of the covariation between internalizing and externalizing behavior was explained by shared environmental influences in common with emotionality. A possible limitation of this study is that the covariation between temperament and behavior problems may be due to shared measurement variance, as parent ratings were used to assess both temperament and behavior problems.

A prospective study of 692 male twins was undertaken to investigate the relationships among early adolescent problem behavior, contextual risk, and disinhibitory psychopathology. Early adolescent problem behavior was assessed by the number of the following behaviors engaged in by the time of the age-14 assessment: (1) tobacco use, (2) alcohol use, (3) marijuana use, (4) other illicit drug use, (5) sexual intercourse, and (6) police contact. Contextual risk was assessed as a composite of measures of peer models, parent-offspring conflict, and academic engagement from the age-14 assessment. Disinhibitory psychopathology was assessed by symptoms of nicotine dependence, alcohol dependence, drug dependence, and adult antisocial behavior at the age-18 assessment. Early adolescent problem behavior and contextual risk were strongly correlated (r = .53) and both were strongly and independently associated with symptoms of disinhibitory psychopathology (r from .35 to .60). The association of early adolescent problem behavior with both contextual risk and disinhibitory psychopathology was mediated entirely by genetic factors while the association between contextual risk and disinhibitory psychopathology was mediated by both genetic and nonshared environmental factors. The results are discussed in the context of emerging research on the prognostic significance of early adolescent problem behavior for risk of adult psychopathology.

To obtain a better understanding of how genetic and environmental processes are involved in the stability and change in problem behavior from early adolescence into adulthood, studies with genetically informative samples are important. The present study used parent-reported data on internalizing and externalizing problem behavior of adoptees at mean ages 12.4, 15.5 and 26.3. In this adoption study adopted biologically related sibling pairs shared on average 50% of their genes and were brought up in the same family environment, whereas adopted biologically unrelated sibling pairs only shared their family environment. The resemblance between these adopted biologically related (N = 106) and unrelated sibling pairs (N = 230) was compared and examined over time. We aimed to investigate (1) to what extent are internalizing and externalizing problem behavior stable from early adolescence into adulthood, and (2) whether the same or different genetic and environmental factors affect these problem behaviors at the 3 assessments. Our results show that both internalizing (rs ranging from .34 to .58) and externalizing behavior (rs ranging from .47 to .69) were rather stable over time. For internalizing and externalizing problem behavior it was found that both genetic and shared environmental influences could be modeled by an underlying common factor, which explained variance in problem behavior from early adolescence into adulthood and accounted for stability over time. The nonshared environmental influences were best modeled by a Cholesky decomposition for internalizing behavior, whereas a time-specific influence of the nonshared environment was included in the final model of externalizing behavior.

The Swedish Twin study of CHild and Adolescent Development (TCHAD) is a longitudinal study of how genes and environments contribute to development of health and behavioral problems from childhood to adulthood. The study includes 1480 twin pairs followed since 1994, when the twins were 8 to 9 years old. The last data collection was in 2005 when the twins were 19 to 20 years old. Both parents and twins have provided data. In this article we describe the sample, data collections, and measures used. In addition, we provide some key findings from the study, focusing on antisocial behavior, criminality, and psychopathic personality.

The Nonshared Environment in Adolescent Development (NEAD) project is a longitudinal study of twins/siblings and parents that has been assessed 3 times: middle adolescence, late adolescence and young adulthood (N = 720 families at Time 1). Siblings varied in degree of genetic relatedness including identical twins, fraternal twins, full siblings, half siblings and genetically unrelated (or step) siblings. There were also two family types: nondivorced and step. A multimeasure, multirater approach was taken in NEAD, with data collected from all participants (2 twins or siblings, mother and father) as well as from coded videotaped observations of family interactions. Detailed assessments of family relationships, adolescent adjustment and competence were collected at all 3 times. The original aim of NEAD was to identify systematic sources of nonshared environmental influences that contribute to differences among family members. Although systematic sources of nonshared environmental influences were not found in NEAD, three major sets of findings emerged: (1) genetic influences on family relationships and on associations between family relationships and adolescent adjustment; (2) genetic and environmental influences on adolescent adjustment, comorbidity and stability and change in adolescent adjustment from middle to late adolescence; and (3) genetic influences on relationships outside the family.

The Early Growth and Development Study is a prospective adoption study of birth parents, adoptive parents, and adopted children (N = 359 triads) that was initiated in 2003. The primary study aims are to examine how family processes mediate or moderate the expression of genetic influences in order to aid in the identification of specific family processes that could serve as malleable targets for intervention. Participants in the study are recruited through adoption agencies located throughout the United States, following the birth of a child. Assessments occur at 6-month intervals until the child reaches 3 years of age. Data collection includes the following primary constructs: infant and toddler temperament, social behavior, and health; birth and adoptive parent personality characteristics, psychopathology, competence, stress, and substance use; adoptive parenting and marital relations; and prenatal exposure to drugs and maternal stress. Preliminary analyses suggest the representativeness of the sample and minimal confounding effects of current trends in adoption practices, including openness and selective placement. Future plans are described.

The Twins' Early Development Study (TEDS) is a large-scale longitudinal study of twins from early childhood through adolescence. Since its conception, TEDS has had as its focus the study of problematic development within the context of normal variation, mainly in the development of language, cognitive and academic abilities and behavior problems from multivariate quantitative and molecular genetic perspectives. TEDS twins have been assessed at 2, 3, 4, 7, 9, 10 and (currently) 12 years of age, and DNA collected from more than 12,000 children. Identified from birth records of twins born in the United Kingdom between 1994 and 1996, more than 15,000 pairs of twins originally enrolled in TEDS, and well over 13,000 pairs — representative of the UK population — remain involved in the study to date. Similar to many other twin and adoption studies, TEDS data indicate that both genetic and environmental influences are important in nearly all areas of behavioral development. Multivariate genetic analyses allow researchers to go beyond this basic nature–nurture question, and TEDS results suggest that, especially in the area of learning abilities and disabilities, genes are generalists and environments are specialists. That is, genes largely contribute to similarity in performance within and between learning abilities and disabilities and across age, whereas the environment contributes to differences in performance. Quantitative genetic findings such as these chart the course for molecular genetic research. The TEDS dataset is proving valuable in genome-wide association research that tries to identify some of the many genes responsible for the ubiquitous heritability of behavior.

A previous publication reported the etiology of mathematics performance in 7-year-old twins (Oliver et al., 2004). As part of the same longitudinal study we investigated low mathematics performance and normal variation in a representative United Kingdom sample of 1713 same-sex 9-year-old twins based on teacher-assessed National Curriculum standards. Univariate individual differences and DeFries-Fulker extremes analyses were performed. Similar to our results at 7 years, all mathematics scores at 9 years showed high heritability (.62–.75) and low shared environmental estimates (.00–.11) for both the low performance group and the full sample. Longitudinal analyses were performed from 7 to 9 years. These longitudinal analyses indicated strong genetic continuity from 7 to 9 years for both low performance and mathematics in the normal range. We conclude that, despite the considerable differences in mathematics curricula from 7 to 9 years, the same genetic effects largely operate at the two ages.

The Wisconsin Twin Panel utilizes the resources of state birth records to study the etiology and developmental course of early emotions, temperament, childhood anxiety and impulsivity, the autism spectrum, and related psychobiological and behavioral phenotypes. The panel currently supports 5 active research studies which involve twins from birth to early adolescence. A range of research methods are employed, including questionnaires and structured interviews with caregivers, home and laboratory-based behavioral batteries, observer ratings, child self-report, psychophysiology, neuroendocrine measures, birth records, genotyping, and cognitive testing. The panel is in the early stages of generating longitudinal findings.

Plasma lipids such as high-density lipoprotein (HDL), low-density lipoprotein (LDL), total cholesterol and triglyceride levels contribute to variation in the risk of cardiovascular disease. The early stages of atherosclerosis in childhood have also been associated with changes in triglycerides, LDL and HDL. Heritability estimates for lipids and lipoproteins for adolescents are in the range .71 to .82, but little is known about changes of genetic and environmental influences over time in adolescence. We have investigated the contribution of genetic and environmental influences to variation in lipids in adolescent twins and their nontwin siblings using longitudinal twin and family data. Plasma HDL and LDL cholesterol, total cholesterol and triglycerides data from 965 twin pairs at 12, 14 and 16 years of age and their siblings have been analyzed. Longitudinal genetic models that included effects of age, sex and their interaction were fitted to assess whether the same or different genes influence each trait at different ages. Results suggested that more than one genetic factor influences HDL, LDL, total cholesterol and triglycerides over time at ages 12, 14 and 16 years. There was no evidence of shared environmental effects except for HDL and little evidence of long-term nonshared environmental effects was found. Our study suggested that there are developmental changes in the genes affecting plasma lipid concentrations across adolescence.

Considerable evidence from twin and adoption studies indicates that both genetic and shared environmental factors play a substantial role in the liability to antisocial behavior. Although twin and adoption designs can resolve genetic and environmental influences, they do not provide information about assortative mating, parent–offspring transmission, or the contribution of these factors to trait variation. We examined the role of genetic and environmental factors for conduct disorder (CD) using a twin–parent design. This design allows the simultaneous estimation of additive genetic, shared and individual-specific environmental effects, as well as sex differences in the expression of genes and environment in the presence of assortative mating and combined genetic and cultural transmission. A retrospective measure of CD was obtained from twins and their parents or guardians in the Virginia Twin Study of Adolescent Behavior Development and its Young Adult Follow up sample. Both genetic and environmental factors play a significant role in the liability to CD. Major influences on individual differences appeared to be additive genetic (38%–40%) and unique environmental (39%–42%) effects, with smaller contributions from the shared environment (18%–23%), assortative mating (~2%), cultural transmission (~2%) and resulting genotype-environment covariance. This study showed significant heritability, which is slightly increased by assortative mating, and significant effects of primarily nonparental shared environment on CD.

The primary aim of this study was to conduct a bivariate genetic analysis investigating the extent to which genetic and environmental factors contribute to stability and change in personality factors in the period from adolescence to young adulthood on a sample of Croatian twins. The sample used in this research was formed in 1992 based on a register of citizens of Zagreb and data was collected for 160 twin pairs (75 monozygotic and 85 dizygotic twin pairs). Twins were tested twice, 4 years apart with the Eysenck Personality Questionnaire (mean age at first time point was 17 years). Univariate analyses indicate that the best fitting model for extraversion, neuroticism, psychoticism and lie scale at both time points includes additive genetic (A) and nonshared environmental (E) influences, with heritability estimates in the .40 to .50 range. Longitudinal analyses using AE correlated factors model indicate that genetic factors contribute mainly to stability, while environmental factors contribute mainly to change in personality during that 4-year period of transition from adolescence to young adulthood.

We study the situation in which a cheap measure (X) is observed in a large, representative twin sample, and a more expensive measure (Y) is observed in a selected subsample. The aim of this study is to investigate the optimal selection design in terms of the statistical power to detect genetic and environmental influences on the variance of Y and on the covariance of X and Y. Data were simulated for 4000 dizygotic and 2000 monozygotic twins. Missingness (87% vs. 97%) was then introduced in accordance with 7 selection designs: (i) concordant low + individual high design; (ii) extreme concordant design; (iii) extreme concordant and discordant design (EDAC); (iv) extreme discordant design; (v) individual score selection design; (vi) selection of an optimal number of MZ and DZ twins; and (vii) missing completely at random. The statistical power to detect the influence of additive and dominant genetic and shared environmental effects on the variance of Y and on the covariance between X and Y was investigated. The best selection design is the individual score selection design. The power to detect additive genetic effects is high irrespective of the percentage of missingness or selection design. The power to detect shared environmental effects is acceptable when the percentage of missingness is 87%, but is low when the percentage of missingness is 97%, except for the individual score selection design, in which the power remains acceptable. The power to detect D is low, irrespective of selection design or percentage of missingness. The individual score selection design is therefore the best design for detecting genetic and environmental influences on the variance of Y and on the covariance of X and Y. However, the EDAC design may be preferred when an additional purpose of a study is to detect quantitative trait loci effects.

All psychological and psychophysiological traits vary, often widely, about their stable set-point values, due to transitory environmental influences. Because it is this stable set-point that embodies the genetically determined component of the trait, twin and family data based on one-time trait measurements must underestimate true trait heritability. The means of multiple measurements, taken months or years apart, then correlated within pairs of monozygotic twins, would yield an accurate estimate of the broad heritability of the set-point value, but such data are rare and expensive. Given just two measurements sufficiently far apart, the cross-twin cross-time correlation (RCT), divided by the retest or within-twin cross-time correlation (RWT), provides a valid estimate of set-point heritability. This article examines data from young and middle-aged twins who were tested twice, 3 or more years apart, on heart rate and blood pressure, personality traits, self-rating items, occupational and recreational interests, as well as on Wechsler Intelligence Scales. In every case, the disattenuated RCT revealed substantially higher heritability than indicated by correlations based on single measurements.

Problem (P) and pathological gambling (PG) symptoms wax and wane. Past symptoms are a risk for future symptoms even after controlling for familial influences. To address the genetic architecture of lifetime PG and current PG symptoms, we tested for common and unique genetic factors to lifetime PG symptoms at baseline and past year PG symptoms at 10-year follow-up. Diagnostic and Statistical Manual of Mental Disorders (3rd ed., Rev.; DSM-III-R; American Psychiatric Association, 1987) lifetime criteria of one or more PG symptoms were derived in 1992 and past year PG symptoms in 2002 from 1675 individual twins from the Vietnam Era Twin Registry. Cholesky decomposition models were fit to baseline and past year PG symptoms. Under the best fitting model we observed that 49% of the risk for one or more baseline PG symptoms in 1992 was due to a genetic factor and 51% of the risk was due to a unique environmental factor. All of the genetic variance (57.5%) in risk to past year PG symptoms in 2002 was common with baseline PG symptoms. Unique environment accounted for the remaining variance in past year PG symptoms with 13% common to baseline and 30% specific to past year PG symptoms. The genetic contributions to lifetime and past year gambling symptoms 10 years later are similar. There is no evidence for genetic contributions unique to past year PG symptoms. However, most of the unique environmental influences to past year PG are not shared with lifetime PG. This may reflect the changed social–cultural environment between 1992 and 2002, characterized by increasing access to legalized gambling.

The purpose of the present study was to examine genetic and environmental contributions to individual differences in maximal isometric, concentric and eccentric muscle strength and muscle cross-sectional area (MCSA) of the elbow flexors. A generality versus specificity hypothesis was explored to test whether the 4 strength variables share a genetic component or common factors in the environment or whether the genetic/environmental factors are specific for each strength variable. The 4 variables under study were measured in 25 monozygotic and 16 dizygotic male Caucasian twin pairs (22.4 ± 3.7 years). The multivariate genetic analyses showed that all 4 variables shared a genetic and environmental component, which accounted for 43% and 6% in MCSA (h2 = 81%), 47% and 20% in eccentric (h2 = 65%), 58% and 4% in isometric (h2 = 70%) and 32% and 1% in concentric strength (h2 = 32%) respectively. The remaining variation was accounted for by contraction type specific and muscle cross-sectional area specific genetic and environmental effects, which accounted for 38% and 14% in MCSA, 18% and 15% in eccentric, 12% and 26% in isometric and 0% and 67% in concentric strength respectively. This exploratory multivariate study suggests shared pleiotropic gene action for MCSA, eccentric, isometric and concentric strength, with a moderate to high genetic contribution to the variability of these characteristics.