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     

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 causes of individual differences in daily life positive affect and reward experience and its overlap with stress-sensitivity

Momentary positive affect (PA) and reward experience may underlie subjective wellbeing, and index mental health resilience. This study examines their underlying sources of variation and the covariation with stress-sensitivity. The experience sampling method was used to collect multiple appraisals of mood and daily life events in 520 female twins. Structural equation model fitting was employed to determine sources of variation of PA, reward experience, and the association between reward experience and stress-sensitivity. PA was best explained by shared and non-shared environmental factors, and reward experience by non-shared environmental factors only, although the evidence was also suggestive of a small genetic contribution. Reward experience and stress-sensitivity showed no association. PA was not heritable. Most—if not all—variance of reward experience was explained by environmental influences. Stress-sensitivity, indexing depression vulnerability, and reward experience were non-overlapping, suggesting that resilience traits are independent from stress-sensitivity levels in a general population sample.     

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.     

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.     

Genetic and Environmental Vulnerabilities Underlying Adolescent Substance Use and Problem Use: General or Specific?

Are genetic and environmental risks for adolescent substance use specific to individual substances or general across substance classes? We examined this question in 645 monozygotic twin pairs, 702 dizygotic twin pairs, 429 biological sibling pairs, and 96 adoptive (biologically unrelated) sibling pairs ascertained from community-based samples, and ranging in age from 12 to 18 years. Substance use patterns and symptoms were assessed using structured psychiatric interviews. Biometrical model fitting was carried out using age- and sex-specific thresholds for (a) repeated use and (b) problem use, defined as one or more DSM-IV symptoms of abuse or dependence. We hypothesized that problem use would be more heritable than use in adolescence, and that both genetic and environmental risks underlying tobacco, alcohol, and marijuana use and problem use would be significantly correlated. Results of univariate analyses suggested significant heritable factors for use and problem use for all substances with the exception of alcohol use. Shared environmental factors were important in all cases and special twin environmental factors were significant for tobacco use, tobacco problem use, and alcohol use. Multivariate analyses yielded significant genetic correlations between each of the substances (for both levels studied), and significant shared environmental correlations among use variables only. Our results suggest that tobacco, alcohol, and marijuana problem use are mediated by common genetic influences, but shared environmental influences may be more substance-specific for problem use.     

The Genetic and Environmental Etiology of Antisocial Behavior from Childhood to Emerging Adulthood

Previous research suggests that both genetic and environmental influences are important for antisocial behavior across the life span, even though the prevalence and incidence of antisocial behavior varies considerably across ages. However, little is known of how genetic and environmental effects influence the development of antisocial behavior. A total of 2,600 male and female twins from the population-based Swedish Twin Registry were included in the present study. Antisocial behavior was measured on four occasions, when twins were 8–9, 13–14, 16–17, and 19–20 years old. Longitudinal analyses of the data were conducted using structural equation modeling. The stability of antisocial behavior over time was explained by a common latent persistent antisocial behavior factor. A common genetic influence accounted for 67% of the total variance in this latent factor, the shared environment explained 26%, and the remaining 7% was due to the non-shared environment. Significant age-specific shared environmental factors were found at ages 13–14 years, suggesting that common experiences (e.g., peers) are important for antisocial behavior at this age. Results from this study show that genetic as well as shared environmental influences are important in antisocial behavior that persists from childhood to emerging adulthood.     

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.     

High Heritability for a Composite Index of Children’s Activity Level Measures

Despite the high heritability of children’s activity level, which forms part of the core symptom domain of hyperactivity-impulsivity within attention deficit hyperactivity disorder (ADHD), there has only been a limited success with identifying candidate genes involved in its etiology. This may reflect a lack of understanding about the different measures used to define activity level across studies. We aimed to study the genetic and environmental etiology across three measures of activity level: parent and teacher ratings of hyperactivity-impulsivity and actigraph measurements, within a population-based sample of 463 7–9 year old twin pairs. We further examined ways in which the three measures could be combined for future molecular studies. Phenotypic correlations across measures were modest, but a common underlying phenotypic factor was highly heritable (92%); as was a simple aggregation of all three measurements (77%). This suggests that distilling what is common to all three measures may be a good method for generating a quantitative trait suitable for molecular studies of activity level in children. The high heritabilities found are encouraging in this respect. 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.     

Exploring the inter-relationship of smoking age-at-onset, cigarette consumption and smoking persistence: genes or environment?

BACKGROUND: We investigated the genetic and environmental contributions to covariation between smoking age-at-onset, cigarette consumption and smoking persistence. METHOD: Multivariate biometrical modelling methods were applied to questionnaire data from Australian twins and their siblings (14 472 individuals from 6247 families). The contributions of genetic and environmental factors to covariation between the three traits were estimated, allowing for sex differences in both trait prevalence and the magnitude of genetic and environmental effects. RESULTS: All traits were moderately heritable in males and females (estimates between 0.40 and 0.62), but there were sex differences in the extent to which additive genetic influences were shared across traits. Twin-specific environmental factors accounted for a substantial proportion of the variance in smoking age-at-onset in females (0.19) and males (0.12), but had little influence (<0.08) on other traits. Unique environmental factors were estimated to have a moderate influence on smoking age-at-onset (0.17 for females, 0.19 for males), but a stronger influence on other traits (between 0.39 and 0.49). CONCLUSIONS: These results provide some insight into observed sex differences in smoking behaviour, and suggest that searching for pleiotropic genes may prove fruitful. However, further work on phenotypic definitions of smoking behaviour, particularly persistence, is warranted.     

Estimation of Parental Effects Using Polygenic Scores

Offspring resemble their parents for both genetic and environmental reasons. Understanding the relative magnitude of these alternatives has long been a core interest in behavioral genetics research, but traditional designs, which compare phenotypic covariances to make inferences about unmeasured genetic and environmental factors, have struggled to disentangle them. Recently, Kong et al. (2018) showed that by correlating offspring phenotypic values with the measured polygenic score of parents’ nontransmitted alleles, one can estimate the effect of “genetic nurture”—a type of passive gene–environment covariation that arises when heritable parental traits directly influence offspring traits. Here, we instantiate this basic idea in a set of causal models that provide novel insights into the estimation of parental influences on offspring. Most importantly, we show how jointly modeling the parental polygenic scores and the offspring phenotypes can provide an unbiased estimate of the variation attributable to the environmental influence of parents on offspring, even when the polygenic score accounts for a small fraction of trait heritability. This model can be further extended to (a) account for the influence of different types of assortative mating, (b) estimate the total variation due to additive genetic effects and their covariance with the familial environment (i.e., the full genetic nurture effect), and (c) model situations where a parental trait influences a different offspring trait. By utilizing structural equation modeling techniques developed for extended twin family designs, our approach provides a general framework for modeling polygenic scores in family studies and allows for various model extensions that can be used to answer old questions about familial influences in new ways.

     

The Relationship Between the Genetic and Environmental Influences on Common Internalizing Psychiatric Disorders and Mental Well-Being

To determine the relationship between the genetic and environmental risk factors for common internalizing psychopathology (IP) and mental well-being (MWB), we examined detailed measures of emotional, social and psychological well-being, and a history of major depression (MD), generalized anxiety disorder (GAD) and panic attacks in the last year, in 1,386 twins from same-sex pairs from the MIDUS national USA sample assessed in 1995 and then again in 2005. Statistical analyses were performed with the Mx program. In the 1995 data, the best fit model contained one substantially heritable common factor for MD, GAD and panic attacks, and one strongly heritable common factor for the three well-being measures. Genetic and environmental risk factors for IP accounted for, respectively, 50 and 5%, of the genetic and environmental influences on MWB. We then constructed, using 1995 and 2005 data, two common factors that reflected temporally stable influences on (i) MD and GAD, and (ii) on emotional and psychological well-being. Genetic and environmental risk factors for the stable liability to IP accounted for 41 and 29% of the stable genetic and environmental influences, respectively, on MWB. This study suggests that genetic risk factors for IP make up 41–50% of the genetic influences on MWB. The overlap of environmental risk factors is more modest. Although low levels of IP on average reflect a high genetic propensity for MWB, other independent genetic influences play an important role in producing good mental health.     

Genetic and Environmental Influences on Schizotypy among Adolescents in Taiwan: A Multivariate Twin/sibling Analysis

This study aimed to examine the relative contribution of genes and environment to psychometrically measured schizotypy and the causes for the covariation between different dimensions of schizotypy in a total of 330 pairs of twins and 36 same-sex sib-pairs aged 12–16 and systematically recruited from junior high schools in Taipei. Twins’ zygosity was determined by a combination of DNA typing and physical similarity. Schizotypy was measured using the Perceptual Aberration Scale (PAS) as well as the Schizotypal Personality Questionnaire (SPQ) and its three factors (Cognitive-perceptual Dysfunction, Disorganization, and Interpersonal Dysfunction). Univariate analyses of structural equation modeling using Mx program showed that scores on these schizotypal measures were substantially heritable (h ² ranging from 41 to 49%), with some genetic effects being non-additive. Multivariate analyses revealed common genetic factors linking between various traits of schizotypy, with bivariate heritability ranging from 50 to 65%. The proportion of the genetic contributions not shared with the other measures of schizotypy ranged from 24% for the Disorganization to 49% for the PAS scores. We concluded that there exist both common and specific genetic factors between the various dimensions of schizotypy, and at least half of their correlations were genetic in nature. Edited by Peter McGuffin     

Overlaps Between Autism and Language Impairment: Phenomimicry or Shared Etiology?

Traditionally, autistic spectrum disorder (ASD) and specific language impairment (SLI) are regarded as distinct conditions with separate etiologies. Yet these disorders co-occur at above chance levels, suggesting shared etiology. Simulations, however, show that additive pleiotropic genes cannot account for observed rates of language impairment in relatives, which are higher for probands with SLI than for those with ASD + language impairment. An alternative account is in terms of ‘phenomimicry’, i.e., language impairment in comorbid cases may be a consequence of ASD risk factors, and different from that seen in SLI. However, this cannot explain why molecular genetic studies have found a common risk genotype for ASD and SLI. This paper explores whether nonadditive genetic influences could account for both family and molecular findings. A modified simulation involving G × G interactions obtained levels of comorbidity and rates of impairment in relatives more consistent with observed values. The simulations further suggest that the shape of distributions of phenotypic trait scores for different genotypes may provide evidence of whether a gene is involved in epistasis.     

For others: epistasis and the evolutionary survival of an extreme tail of the quantitative distribution of autistic assets

The ongoing paradigm shift from the traditional qualitative dichotomy concept to the quantitative framework increases the necessity of an evolutionary implication and interpretation of the presence of a hypo-reproductive behavioral extreme (autism) with strong genetic contribution. As a theoretical challenge to explain the survival of the dimensional distribution of autistic traits, an epistasis-associated oscillation of fitness outcomes is proposed. In this hypothesis, an allele could contribute to the existence of both phenotypic extreme tails and the hypothesized genetic machinery (quantitative trait loci) for autism would necessarily be common in the entire human population. The postulated autism genes would allow autistics to enjoy autistic traits and assets and all of the residual non-autistic individuals could owe their social skills and reproductive advantages to the same autism genes. Importantly, the reported modest correlations between core autistic dimensions can be illustrated using unsynchronized epistatic pleiotropy.     

Three Mutually Informative Ways to Understand the Genetic Relationships Among Behavioral Disinhibition, Alcohol Use, Drug Use, Nicotine Use/Dependence, and Their Co-occurrence: Twin Biometry, GCTA, and Genome-Wide Scoring

Behavioral disinhibition is a trait hypothesized to represent a general vulnerability to the development of substance use disorders. We used a large community-representative sample (N = 7,188) to investigate the genetic and environmental relationships among measures of behavioral disinhibition, Nicotine Use/Dependence, Alcohol Consumption, Alcohol Dependence, and Drug Use. First, using a subsample of twins (N = 2,877), we used standard twin models to estimate the additive genetic, shared environmental, and non-shared environmental contributions to these five traits. Heritabilities ranged from .42 to .58 and shared environmental effects ranged from .12 to .24. Phenotypic correlations among the five traits were largely attributable to shared genetic effects. Second, we used Genome-wide Complex Trait Analysis (GCTA) to estimate as a random effect the aggregate genetic effect attributable to 515,384 common SNPs. The aggregated SNPs explained 10–30 % of the variance in the traits. Third, a genome-wide scoring approach summed the actual SNPs, creating a SNP-based genetic risk score for each individual. After tenfold internal cross-validation, the SNP sumscore correlated with the traits at .03 to .07 (p < .05), indicating small but detectable effects. SNP sumscores generated on one trait correlated at approximately the same magnitude with other traits, indicating detectable pleiotropic effects among these traits. Behavioral disinhibition thus shares genetic etiology with measures of substance use, and this relationship is detectable at the level of measured genomic variation.     

Genetic etiology of stability of attention problems in young adulthood.

Variation in attention problems in children and adolescents from non-clinical samples is highly heritable. It is unknown how attention problems develop later in life and whether the heritability in the general adult population is the same as in children and adolescents. We assessed the heritability and stability of individual differences in attention problems in the general young adult population and explored to what extent the stability can be attributed to genetic or environmental factors. On one or more occasions, young adult twins (age range, 18-30 years, N = 4,245) from the Netherlands Twin Registry filled out the attention problems (AP) subscale of the Young Adult Self-Report [Achenbach, 1997]: in 1991, N = 1,755 (of which 842 complete pairs), in 1995, N = 2,428 (1156 complete pairs) and in 1997, N = 2,344 (958 pairs). There was only a slight decrease in the average level of attention problems during young adulthood. The heritability at each occasion was around 40%. The correlation of attention problems across a period of 6 years was 0.42, and 77% of this correlation could be ascribed to genetic influences. Thus, individual differences in attention problems in young adulthood are heritable, and stability in individual differences over time can largely be ascribed to genetic influences. Genetic correlations across time were high, suggesting that the genes that influence variability in attention problems in late adolescence are largely the same as those that influence variability in early adulthood.     

Bulimic Behaviors and Alcohol Use: Shared Genetic Influences

Bulimic behaviors are frequently associated with alcohol use disorders. However, extant family and twin study findings have been inconsistent with regard to whether these behaviors share etiologic influences. A sample of 292 young adult, female twins was used to examine genetic and environmental factors underlying the association between binge eating and compensatory behaviors (e.g., vomiting) and alcohol use. Binge eating and compensatory behaviors were assessed using the Minnesota Eating Behavior Survey. Alcohol use was measured using the Alcohol Use Disorders Identification Test. Univariate models indicated that the heritability of binge eating, compensatory behaviors, and alcohol use was 41, 28, and 78%, respectively, with the remaining variance due to nonshared environmental effects. Bivariate models indicated that there was a moderate-to-large degree of overlap (genetic correlation = 0.31–0.61) in additive genetic factors between alcohol use and binge eating and compensatory behaviors, and no overlap in environmental effects. Findings suggest that these phenotypes co-aggregate in families and that similar genes or heritable traits may be contributing to their co-occurrence.     

Factor Structure of Planning and Problem-solving: A Behavioral Genetic Analysis of the Tower of London Task in Middle-aged Twins

We examined the genetic architecture of a Tower of London test of planning and problem-solving in 690 middle-aged male twins. Phenotypic analyses revealed only one general factor, but the best-fitting genetic model indicated two correlated genetic factors: speed and efficiency. One variable—number of attempts required to mentally figure the puzzles—loaded on both factors. Shared environmental effects could be dropped with virtually no reduction in model fit. Despite significant nonshared environmental correlations across measures, there was no discernable nonshared environmental factor structure. The correlation between genetic factors (r = 0.46) and the variable loading on both factors could reflect modulation of planning, testing alternatives, and working memory that are required to perform the test. Such coordinated activity is consistent with the notion of a supervisory attentional system, a central executive, or metacognitive ability. The different phenotypic and genetic factor results suggest that relying solely on the former could obscure genetic associations.