Depressive Symptoms and Alcohol Use are Genetically and Environmentally Correlated Across Adolescence

Depressive symptoms and alcohol use are frequently positively associated during adolescence. This study aimed to assess the heritability of each phenotype across adolescence; to assess potential shared liabilities; to examine changes in the nature of shared liabilities across adolescence; and to investigate potential causal relationships between depressive symptoms and alcohol use. We studied a longitudinally assessed sample of adolescent Finnish twins (N = 1,282) to test hypotheses about genetic and environmental influences on these phenotypes within and across ages, using data from assessments at ages 12, 14, and 17.5 years. The heritability of depressive symptoms is consistent across adolescence (~40–50%), with contributions from common and unique environmental factors. The heritability of alcohol use varies across time (a² = .25–.44), and age 14 alcohol use is heavily influenced by shared environmental factors. Genetic attenuation and innovation were observed across waves. Modest to moderate genetic (r_A = .26–.59) and environmental (r_C = .30–.63) correlations between phenotypes exist at all ages, but decrease over time. Tests for causal relationships between traits differed across ages and sexes. Intrapair MZ difference tests provided evidence for reciprocal causation in girls at ages 14 and 17.5. Formal causal models suggested significant causal relationships between the variables in both boys and girls. The association between depressive symptoms and alcohol use during adolescence is likely due to a combination of shared genetic and environmental influences and causal influences. These influences are also temporally dynamic, complicating efforts to understand factors contributing to the relationship between these outcomes.     

Genetic and Environmental Influences on the Stability of Withdrawn Behavior in Children: A Longitudinal,Multi-informant Twin Study

We examined the contribution of genetic and environmental influences on the stability of withdrawn behavior (WB) in childhood using a longitudinal multiple rater twin design. Maternal and paternal ratings on the withdrawn subscale of the Child Behavior Checklist (CBCL) were obtained from 14,889 families when the twins were 3, 7, 10 and 12 years old. A longitudinal psychometric model was fitted to the data and the fit of transmission and common factor models were evaluated for each variance component. WB showed considerable stability throughout childhood, with correlation coefficients ranging from about .30 for the 9-year time interval to .65 for shorter time intervals. Individual differences in WB as observed by the mother and the father were found to be largely influenced by genetic effects at all four time points, in both boys (50–66%) and girls (38–64%). Shared environmental influences explained a small to modest proportion (0–24%) of the variance at all ages and were slightly more pronounced in girls. Non-shared environmental influences were of moderate importance to the variance and slightly increased with age, from 22–28% at age 3 to 35–41% at age 12 years. The stability of WB was largely explained by genetic effects, accounting for 74% of stability in boys and 65% in girls. Shared environmental effects explained 7% (boys) and 17% (girls) of the behavioral stability. Most shared environmental effects were common to both raters, suggesting little influence of rater bias in the assessment of WB. The shared environmental effects common to both raters were best described by a common factor model, indicating that these effects are stable and persistent throughout childhood. Non-shared environmental effects accounted for the remaining covariance over time. Edited by Hermine Maes.     

Heritability and Longitudinal Stability of Schizotypal Traits During Adolescence

The study investigated the genetic and environmental etiology of schizotypal personality traits in a non-selected sample of adolescent twins, measured on two occasions between the ages of 11 and 16 years old. The 22-item Schizotypal Personality Questionnaire- Child version (SPQ-C) was found to be factorially similar to the adult version of this instrument, with three underlying factors (Cognitive-Perceptual, Interpersonal-Affective, and Disorganization). Each factor was heritable at age 11–13 years (h ² = 42–53%) and 14–16 years old (h ² = 38–57%). Additive genetic and unique environmental influences for these three dimensions of schizotypal personality acted in part through a single common latent factor, with additional genetic effects specific to both Interpersonal-Affective and Disorganization subscales at each occasion. The longitudinal correlation between the latent schizotypy factor was r = 0.58, and genetic influences explained most of the stability in this latent factor over time (81%). These longitudinal data demonstrate significant genetic variance in schizotypal traits, with moderate stability between early to middle adolescence. In addition to common influences between the two assessments, there were new genetic and non-shared environmental effects that played a role at the later assessment, indicating significant change in schizotypal traits and their etiologies throughout adolescence.     

Genes and Developmental Stabiltiy of Aggressive Behavior Problems at Home and School in a Community Sample of Twins Aged 7–12

Though behavioral genetic studies of aggression have implicated heritable and environmental factors, there is limited understanding of how these factors influence aggression across different settings and over time. Ratings for 732 twins were collected from parents and teachers during middle childhood and early adolescence. Total aggression scores on the Child Behavioral Checklist (CBCL) and Teacher Report Form (TRF) were examined at each age, across both settings, and developmentally. In this sample, aggressive behavior was moderately to largely heritable at each age within the home (.76–.84) and school (.42–.61). Across each age, ratings by parents and teachers were moderately correlated (.19–.36). Genetic and environmental effects that were limited to a particular setting were important etiological factors for aggressive behavior consistently within each setting, while only genetic factors influenced levels of aggression across both settings. Stability during these ages was due to genetic effects common to each age and the persistence of child-specific environmental experiences within each setting. These results suggest that genetic and environmental influences on children’s aggressive behavior are largely setting specific. Levels of aggression seen consistently across both settings are due to genetic influences. Developmentally stable levels of aggressive behavior result from genetic influences common to all ages and individual environmental influences whose effects persist across ages.Edited by Danielle Posthuma     

Stable Genetic Effects on Symptoms of Alcohol Abuse and Dependence from Adolescence into Early Adulthood

Relatively little is known about how genetic influences on alcohol abuse and dependence (AAD) change with age. We examined the change in influence of genetic and environmental factors which explain symptoms of AAD from adolescence into early adulthood. Symptoms of AAD were assessed using the four AAD screening questions of the CAGE inventory. Data were obtained up to six times by self-report questionnaires for 8,398 twins from the Netherlands Twin Register aged between 15 and 32 years. Longitudinal genetic simplex modeling was performed with Mx. Results showed that shared environmental influences were present for age 15–17 (57%) and age 18–20 (18%). Unique environmental influences gained importance over time, contributing 15% of the variance at age 15–17 and 48% at age 30–32. At younger ages, unique environmental influences were largely age-specific, while at later ages, age-specific influences became less important. Genetic influences on AAD symptoms over age could be accounted for by one factor, with the relative influence of this factor differing across ages. Genetic influences increased from 28% at age 15–17 to 58% at age 21–23 and remained high in magnitude thereafter. These results are in line with a developmentally stable hypothesis that predicts that a single set of genetic risk factors acts on symptoms of AAD from adolescence into young adulthood.     

Exercise Participation in Adolescents and Their Parents: Evidence for Genetic and Generation Specific Environmental Effects

Individual differences in adolescent exercise behavior are to a large extent explained by shared environmental factors. The aim of this study was to explore to what extent this shared environment represents effects of cultural transmission of parents to their offspring, generation specific environmental effects or assortative mating. Survey data on leisure-time exercise behavior were available from 3,525 adolescent twins and their siblings (13–18 years) and 3,138 parents from 1,736 families registered at the Netherlands Twin Registry. Data were also available from 5,471 adult twins, their siblings and spouses similar in age to the parents. Exercise participation (No/Yes, using a cut-off criterion of 4 metabolic equivalents and 60 min weekly) was based on questions on type, frequency and duration of exercise. A model to analyze dichotomous data from twins, siblings and parents including differences in variance decomposition across sex and generation was developed. Data from adult twins and their spouses were used to investigate the causes of assortative mating (correlation between spouses = 0.41, due to phenotypic assortment). The heritability of exercise in the adult generation was estimated at 42%. The shared environment for exercise behavior in adolescents mainly represents generation specific shared environmental influences that seem somewhat more important in explaining familial clustering in girls than in boys (52 versus 41%). A small effect of vertical cultural transmission was found for boys only (3%). The remaining familial clustering for exercise behavior was explained by additive genetic factors (42% in boys and 36% in girls). Future studies on adolescent exercise behavior should focus on identification of the generation specific environmental factors.     

A common genetic factor explains the association between psychopathic personality and antisocial behavior

BACKGROUND: Both psychopathic personality traits and antisocial behavior are influenced by genetic as well as environmental factors. However, little is known about how genetic and environmental factors contribute to the associations between the psychopathic personality traits and antisocial behavior. METHOD: Data were drawn from a longitudinal population-based twin sample including all 1480 twin pairs born in Sweden between May 1985 and December 1986. The twins responded to mailed self-report questionnaires at two occasions: 1999 (twins 13-14 years old), and 2002 (twins 16-17 years old). RESULTS: A common genetic factor loaded substantially on both psychopathic personality traits and antisocial behavior, whereas a common shared environmental factor loaded exclusively on antisocial behavior. CONCLUSIONS: The genetic overlap between psychopathic personality traits and antisocial behavior may reflect a genetic vulnerability to externalizing psychopathology. The finding of shared environmental influences only in antisocial behavior suggests an etiological distinction between psychopathic personality dimensions and antisocial behavior. Knowledge about temperamental correlates to antisocial behavior is important for identification of susceptibility genes, as well as for possible prevention through identification of at-risk children early in life.     

The Genetic and Environmental Etiology of Sympathetic and Parasympathetic Activity in Children

The present study examines the genetic and environmental etiology of the associations among respiratory sinus arrhythmia (RSA), heart rate (HR), skin conductance level (SCL), and non-specific skin conductance responses (NS-SCR)—measures that purportedly index the parasympathetic and sympathetic branches of the autonomic nervous system. The sample was drawn from a cohort of 1,219 preadolescent twins (aged 9–10). Multivariate analyses of the data were conducted using structural equation modeling. Almost all genetic and environmental influences on the measures acted through two latent factors. The first latent factor was largely responsible for the variance in heart rate, SCL and NS-SCR, reflecting sympathetic activity, and its proportions of variance due to genetic and shared environmental influences were 27 and 28% in males, and 31 and 41% in females, respectively. The second latent factor accounted for the variance in RSA and heart rate, reflecting parasympathetic activity; genetic and shared environmental factors explained 27 and 23% of the variance in males, respectively, and 35 and 18% of the variance in females. Measurement-specific genetic effects accounted for 14–27% of the total variance in RSA and SCL, and measurement-specific shared environmental effects accounted for 10–12% in SCL. In general, the validity of separate sympathetic and parasympathetic constructs was supported.     

Thought Problems from Adolescence to Adulthood: Measurement Invariance and Longitudinal Heritability

This study investigates the longitudinal heritability in Thought Problems (TP) as measured with ten items from the Adult Self Report (ASR). There were ~9,000 twins, ~2,000 siblings and ~3,000 additional family members who participated in the study and who are registered at the Netherlands Twin Register. First an exploratory factor analysis was conducted to examine the underlying factor structure of the TP-scale. Then the TP-scale was tested for measurement invariance (MI) across age and sex. Next, genetic and environmental influences were modeled on the longitudinal development of TP across three age groups (12–18, 19–27 and 28–59 year olds) based on the twin and sibling relationships in the data. An exploratory factor analysis yielded a one-factor solution, and MI analyses indicated that the same TP-construct is assessed across age and sex. Two additive genetic components influenced TP across age: the first influencing TP throughout all age groups, while the second arises during young adulthood and stays significant throughout adulthood. The additive genetic components explained 37% of the variation across all age groups. The remaining variance (63%) was explained by unique environmental influences. The longitudinal phenotypic correlation between these age groups was entirely explained by the additive genetic components. We conclude that the TP-scale measures a single underlying construct across sex and different ages. These symptoms are significantly influenced by additive genetic factors from adolescence to late adulthood.     

Genetic and Environmental Causes of Variation in Trait Resilience in Young People

The aim of this multi-informant twin study was to determine the relative role of genetic and environmental factors in explaining variation in trait resilience in adolescents. Participants were consenting families (N = 2,638 twins in 1,394 families), from seven national cohorts (age 12–18 years, both sexes) of monozygotic and dizygotic twins reared together. Questionnaire data on the adolescents’ Ego-resilience (ER89) was collected from mothers, fathers and twins, and analysed by means of multivariate genetic modelling. Variance in trait resilience was best represented in an ADE common pathways model with sex limitation. Variance in the latent psychometric resilience factor was largely explained by additive genetic factors (77% in boys, 70% in girls), with the remaining variance (23 and 30%) attributable to non-shared environmental factors. Additive genetic sources explained more than 50% of the informant specific variation in mothers and fathers scores. In twins, additive and non-additive genetic factors together explained 40% and non-shared environmental factor the remaining 60% of variation. In the mothers’ scores, the additive genetic effect was larger for boys than for girls. The non-additive genetic factor found in the twins’ self ratings was larger in boys than in girls. The remaining sex differences in the specific factors were small. Trait resilience is largely genetically determined. Estimates based on several informants rather than single informants approaches are recommended.     

Genetic and Environmental Multidimensionality of Well- and Ill-Being in Middle Aged Twin Men

The goals of the study were to determine the extent to which the underlying structure of different types of well-being was multidimensional and whether well- and ill-being were influenced by similar or different genetic and environmental factors. Participants were 1226 male twins ages 51–60, from the Vietnam Era Twin Study of Aging. Measures included: psychological well-being, Multidimensional Personality Questionnaire Well-Being scale (MPQWB), life satisfaction, self-esteem, and depressive symptoms. A two-orthogonal-factor common pathway model fit the data well. Psychological well-being and self-esteem loaded most strongly on Factor 1, which was highly heritable (h² = .79). Life satisfaction loaded most strongly on Factor 2, which was only moderately heritable (h² = .32). Only MPQWB had measure-specific genetic influences. Depressive symptoms loaded on both factors, and only depressive symptoms had measure-specific common environmental influences. All measures had specific unique environmental influences. Results indicate that well-being is genetically and environmentally multidimensional and that ill-being has partial overlap with both latent factors.     

The Mediating Effect of Parental Neglect on Adolescent and Young Adult Anti-Sociality: A Longitudinal Study of Twins and Their Parents

The causes of correlation between parental treatment and offspring behavior are ambiguous since genetic and social factors are correlated in typical family studies. The problem is complicated by the need to characterize the effects of genes and environment on both juvenile and adult behavioral outcomes. A model is developed for the resemblance between juvenile and adult twins and their parents that allows some of these effects to be resolved. Data on childhood adversity, parental anti-social behavior, and longitudinal adult and juvenile anti-social behavior were obtained from 1,412 families of adolescent and young adult twins. A structural model is fitted that allows for the effects of genetic and social transmission of information from parents to children. Environmental effects of parents may be mediated through measured features of the home environment. Parameters were estimated by diagonal weighted least squares applied to the 33 distinct polychoric correlations between relatives and between variables within and between ages. Sub-hypotheses were tested. Results confirmed that effects of genes and environment were both highly significant. Genetic effects were large in juveniles and largely age and sex-specific. Approximately 30% of the variation due to the shared environment was due to the effect of childhood adversity. The remaining shared environmental effects are unexplained. Adversity is affected significantly by maternal anti-social behavior. The correlation between paternal ASP and adversity may be explained by antisocial fathers selecting (or creating) antisocial mothers. All significant environmental effects of parental ASP are mediated through the measure of adversity. Though transmission of ASP is both genetic and social, passive genotype–environment correlation is very small. Assortative mating for ASP has barely detectable consequence for the genetic correlation between siblings. The longitudinal study of twins and their parents makes it possible to demonstrate there is a direct causal effect of childhood adversity on child conduct disorder over and above any indirect genetic correlation.     

The Implications of Simultaneous Smoking Initiation for Inferences about the Genetics of Smoking Behavior from Twin Data

We examined early social influences across stages of smoking within the context of a twin study using an environmental exposure specific to smoking: whether twins started smoking at the same time (“simultaneous smoking initiation”: SSI). We expected that SSI would be a good index of shared social influences on smoking initiation. Rates of SSI were indeed significantly higher in MZ twins and in twins who shared peers and classes, as well as in male twins. With the exception of regular smoking in females, we found no significant difference in estimates of genetic and environmental parameters between SSI and non-SSI pairs for any of the smoking measures that we examined (DSM-IV and Fagerstrom HSI measures of nicotine dependence; DSM-IV nicotine withdrawal; heavy smoking; and in males, regular smoking). For regular smoking in females, allowing for additional shared environmental influences associated with SSI only modestly reduced our estimates of additive genetic variance (56% vs. 68%). These results indicate the important social influences that may occur for smoking initiation do not appear to seriously bias estimates of genetic effects on later stages of smoking.     

Genetic and Environmental Factors Influencing BMI Development from Adolescence to Young Adulthood

BMI increases progressively from adolescence to young adulthood. The aims of the present study were firstly, to investigate the extent to which genetic and environmental influences account for differences in BMI trajectories during this period, and secondly to examine whether boys and girls show divergences in these influences, as their BMI normally start differing across adolescence. The study sample consisted of 4,915 monozygotic and like- and unlike-sex dizygotic twins, born between 1975 and 1979. Data on BMI was gathered when twins were on average 16.1, 17.1, 18.6 and 24.4 years old. Genetic and environmental influences on the BMI trajectories were modeled using a latent growth curve approach. The results showed that the heritability of BMI decreased slightly after the adolescence period, from ≈80 to 70%. BMI transition from adolescence to young adulthood was best described by a quadratic trajectory that was highly accounted (61.7–86.5%) for by additive genetic influences. Genetic influences on BMI level showed a low correlation with those on the trend in BMI with age indicating that different sets of genes underlie the change of BMI during this period. Importantly, the analyses also evidenced that different genetic and environmental influences may underlie boys and girls evolution. In conclusion, our results suggested specific genetic influences accounting for the BMI rate-of-change from adolescence to young adulthood. This indicates that the specific genes behind BMI level may not be the same as the genes affecting BMI change which should be taken into account in further efforts to identify these genes.     

Age Differences in Genetic and Environmental Variations in Stress-Coping During Adulthood: A Study of Female Twins

The way people cope with stressors of day to day living has an important influence on health. The aim of the present study was to explore whether genetic and environmental variations in stress-coping differ over time during adulthood. The brief COPE was mailed to a large sample of the UK female twins (N = 4,736) having a wide range of age (20–87 years). Factor analyses of the items of the brief COPE yielded three coping scales: ‘Problem-Solving’, ‘Support Seeking’, and ‘Avoidance’. Monozygotic and dizygotic twin correlations tended to become lower with age for all three scales, suggesting that unique environmental factors may become more important with age during adulthood. Model-fitting results showed that relative influences of unique environmental factors increased from 60 % at age 20 years to 74% at age 87 years for ‘Problem-Solving’ and 56 % at age 20 years to 76% at age 87 years for ‘Avoidance’. During the same age period, genetic factors decreased from 40 to 26 % for ‘Problem-Solving’ and from 44 to 24 % for ‘Avoidance’. For ‘Seeking Support’, the magnitude of genetic and unique environmental factors was not significantly different across the adulthood. For all three scales, shared environmental effects were negligible. Overall, our findings implicate that the effects of environment that stem from idiosyncratic experience of stressful life events accumulate and become increasingly important in adulthood.     

Nonshared Environmental Influences on Sleep Quality: A Study of Monozygotic Twin Differences

Research has consistently demonstrated that environmental influences are important for explaining the variability in sleep quality observed in the general population. Although there is substantial evidence assessing associations between sleep quality and a host of environmental variables, it is possible that their effects are mediated by genetic influence. A monozygotic twin differences design was used to assess the specific contribution of nonshared environmental influences on sleep quality, whilst controlling for genetic and shared environmental effects in a sample of 380 monozygotic twins (mean age 19.8 years, SD = 1.26, range = 18–22 years). Participants completed the Pittsburgh Sleep Quality Index and questionnaires assessing several candidate “environmental” measures. When controlling for genetic and shared environmental effects, within monozygotic twin-pair differences in sleep quality were associated with within monozygotic twin-pair differences in general health for males (β = 1.56, p < 0.001) and relationship satisfaction for females (β = 1.01, p < 0.05). For the remaining environmental measures the results suggest that these seemingly “environmental” influences are actually in part dependent on genetics and/or the shared environment. These findings give insight into how specific environments affect sleep and the possible mechanisms behind these associations.     

Additional Evidence Against Shared Environmental Contributions to Attention-Deficit/Hyperactivity Problems

A recent meta-analysis “Burt (Psychol Bull 135:608–637, 2009)” indicated that shared environmental influences (C) do not contribute to Attention-Deficit/Hyperactivity Disorder (ADHD). Unfortunately, the meta-analysis relied almost exclusively on classical twin studies. Although useful in many ways, some of the assumptions of the classical twin model (e.g., dominant genetic and shared environmental influences do not simultaneously influence the phenotype) can artifactually decrease estimates of C. There is thus a need to confirm that dominant genetic influences are not suppressing estimates of C on ADHD. The current study sought to do just this via the use of a nuclear twin family model, which allows researchers to simultaneously model and estimate dominant genetic and shared environmental influences. We examined two independent samples of child twins: 312 pairs from the Michigan State University Twin Registry and 854 pairs from the PrE School Twin Study in Sweden. Shared environmental influences were found to be statistically indistinguishable from zero and to account for less than 5 % of the variance. We conclude that the presence of dominant genetic influences does not account for the absence of C on ADHD.     

The heritability of the skin conductance orienting response: a longitudinal twin study

The orienting response is a widely used experimental paradigm that reflects the association between electrodermal activity and psychological processes. The present study examined the genetic and environmental etiology of skin conductance orienting response (SCOR) magnitude in a sample of twins assessed at ages 9-10, 11-13 and 14-16 years. Structural equation modeling at each visit showed that genetic influences explained 56%, 83%, and 48% of the total variance in SCOR at visits 1, 2, and 3, respectively, with the remaining variance explained by non-shared environmental factors. SCOR was moderately stable across ages, with phenotypic correlations between time points ranging from .35 to .45. A common genetic factor explained 36%, 45% and 49% of the variance in SCOR magnitude across development. Additional age-specific genetic effects were found at ages 9-10 and 11-13 years, explaining 18% and 35% of the variance, respectively. The genetic correlations among the three time points were high, ranging from .55 to .73, indicating a substantial continuity in genetic influences from ages 9 to 16. These findings suggest that genetic factors are important influences in SCOR magnitude during late childhood and adolescence.     

A Bivariate Twin Study of Regional Brain Volumes and Verbal and Nonverbal Intellectual Skills During Childhood and Adolescence

Twin studies indicate that both intelligence and brain structure are moderately to highly heritable. Recent bivariate studies of adult twins also suggest that intelligence and brain morphometry are influenced by shared genetic factors. The current study examines shared genetic and environmental factors between brain morphometry and intelligence in a sample of children and adolescents (twins, twin siblings, and singletons; n = 649, ages 4–19). To extend previous studies, brain morphometric data were parsed into subregions (lobar gray/white matter volumes, caudate nucleus, lateral ventricles) and intelligence into verbal and nonverbal skills (Wechsler Vocabulary and Block Design subtests). Phenotypic relationships between brain volumes and intelligence were small. Verbal skills shared unique environmental effects with gray matter volumes while nonverbal skills shared genetic effects with both global and regional gray and white matter. These results suggest that distinct mechanisms contribute to the small phenotypic relationships between brain volumes and verbal versus nonverbal intelligence.