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.     

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.     

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 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 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.     

Food Neophobia in Young Adults: Genetic Architecture and Relation to Personality,Pleasantness and Use Frequency of Foods,and Body Mass Index—A Twin Study

Food neophobia has been studied extensively in children, but its causal origins and relationship to eating behavior in adults are not well understood. We studied genetic and environmental effects on variation in food neophobia, measured using the Food Neophobia Scale, and explored associations between food neophobia and personality, pleasantness and use frequency of food groups, and body mass index in young adult twins (N = 1175, aged 20–25 years, 54.7% women). In women, additive genetic effects (heritability) accounted for 61% of variation in food neophobia, whereas in men, shared environmental effects explained 45% of the variation. Food neophobia negatively correlated with the personality trait Openness, corrected for the structural overlap (r = −0.23), and in women, these two traits had a genetic correlation (r _g = −0.39). In addition, food neophobia negatively correlated with pleasantness and use frequency of fruits and vegetables and of fish and with mean pleasantness of foods. Once evolutionarily important, food neophobia should at present be considered in nutrition counseling as a possible barrier to a balanced diet.     

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     

DeFries–Fulker Analysis of Longitudinal Reading Performance Data from Twin Pairs Ascertained for Reading Difficulties and from Their Nontwin Siblings

Reading difficulties are both heritable and stable; however, little is known about the etiology of this stability. Results from a preliminary analysis of data from 56 twin pairs who participated in the Colorado Longitudinal Twin Study of Reading Disability (Astrom et al., Twin Res Hum Genet 10:434–439, 2007) suggested that about two-thirds of the proband deficit at follow-up was due to genetic factors that also influenced deficits at their initial assessment. Although our proband sample is now nearly twice as large, it is still relatively small; thus, to increase power, we subjected data from probands, co-twins and their nontwin siblings to a novel extension of DeFries–Fulker analysis (DeFries and Fulker, Behav Genet 15:467–473, 1985; DeFries and Fulker, Acta Genet Med Gemellol, 37, 205–216, 1988). In addition to providing estimates of univariate and bivariate heritability, this analysis facilitates a test of the difference between shared environmental influences for twins versus siblings. Longitudinal composite reading performance scores at 10.6 and 15.5 years of age, on average, were analyzed from 33 MZ and 64 DZ twin pairs in which at least one member of each pair had reading difficulties, and from 44 siblings of the probands. Scores were highly stable (.86 ± .03, across probands, co-twins and siblings) and heritability of the group deficit at initial assessment was .67 ± .22. Longitudinal bivariate heritability was .59 ± .21, suggesting that nearly 60% of the proband reading deficit at follow-up is due to genetic factors that influenced reading difficulties at the initial assessment. However, tests for special twin environmental influences were nonsignificant.     

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.     

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.     

Changes in genetic and environmental influences on trait anxiety from middle adolescence to early adulthood

Background

Middle adolescence to early adulthood is an important developmental period for the emergence of anxiety. Genetically-influenced stable traits are thought to underlie internalizing psychopathology throughout development, but no studies have examined changes in genetic and environmental influences on trait anxiety during this period.

Method

A longitudinal twin study design was used to study same-sex twin pairs (485 monozygotic pairs, 271 dizygotic pairs) at three ages, 14, 18, and 21 years, to examine developmental shifts in genetic and environmental effects on trait anxiety.

Results

The heritability of trait anxiety increased with age, particularly between ages 14 and 18, no significant new genetic influences emerged after age 14, and the genetic influences were highly correlated across the three ages, supporting developmentally stable genetic risk factors. The environmental effects shared by members of a family decreased in influence across adolescence, while the influence of environmental effects unique to each individual twin remained relatively stable over the course of development and were largely age-specific.

Limitations

The twin study design does not inform about specific genes and environmental risk factors.

Conclusions

Genetic influences increased in importance from middle to late adolescence but common genetic factors influenced trait anxiety across the three ages. Shared environmental influences decreased in importance and demonstrated negligible influence by late adolescence/early adulthood. Nonshared environmental effects were almost entirely age-specific. These findings support the importance of developmentally-sensitive interventions that target shared environmental factors prior to middle adolescence and shifting non-shared environmental risks at each age.     

Genetic Covariation Between Brain Volumes and IQ,Reading Performance,and Processing Speed

Although there has been much interest in the relation between brain size and cognition, few studies have investigated this relation within a genetic framework and fewer still in non-adult samples. We analyzed the genetic and environmental covariance between structural MRI data from four brain regions (total brain volume, neocortex, white matter, and prefrontal cortex), and four cognitive measures (verbal IQ (VIQ), performance IQ (PIQ), reading ability, and processing speed), in a sample of 41 MZ twin pairs and 30 same-sex DZ twin pairs (mean age at cognitive test = 11.4 years; mean age at scan = 15.4 years). Multivariate Cholesky decompositions were performed with each brain volume measure entered first, followed by the four cognitive measures. Consistent with previous research, each brain and cognitive measure was found to be significantly heritable. The novel finding was the significant genetic but not environmental covariance between brain volumes and cognitive measures. Specifically, PIQ shared significant common genetic variance with all four measures of brain volume (r _g = .58–.82). In contrast, VIQ shared significant genetic influence with neocortex volume only (r _g = .58). Processing speed was significant with total brain volume (r _g = .79), neocortex (r _g = .64), and white matter (r _g = .89), but not prefrontal cortex. The only brain measure to share genetic influence with reading was total brain volume (r _g = .32), which also shared genetic influences with processing speed.     

The Etiology of Stability and Change in Religious Values and Religious Attendance

Studies have demonstrated little to no heritability for adolescent religiosity but moderate genetic, shared environmental, and nonshared environmental influences on adult religiosity. Only one longitudinal study of religiosity in female twins has been conducted (Koenig et al., Dev Psychol 44:532?C543, 2008), and reported that persistence from mid to late adolescence is due to shared environmental factors, but persistence from late adolescence to early adulthood was due to genetic and shared environmental factors. We examined the etiology of stability and change in religious values and religious attendance in males and females during adolescence and early adulthood. The heritability of both religious values and religious attendance increased from adolescence to early adulthood, although the increase was greater for religious attendance. Both genetic and shared environmental influences contributed to the stability of religious values and religious attendance across adolescence and young adulthood. Change in religious values was due to both genetic and nonshared environmental influences specific to early adulthood, whereas change in religious attendance was due in similar proportions to genetic, shared environmental, and non-shared environmental influences.     

A Multivariate Twin Study of Autistic Traits in 12-Year-Olds: Testing the Fractionable Autism Triad Hypothesis

Autistic traits—social impairment, communication impairment, and restricted and repetitive behaviors and interests—are heritable in the general population. Previous analyses have consistently reported limited genetic and environmental overlap between autistic trait domains in samples assessed in middle childhood. Here we extend this research to parent-report data for 12-year-olds. Data from 5,944 pairs in the Twins Early Development Study were analyzed to explore the domain-specific heritability and degree of shared genetic and environmental influences across different autistic traits in the general population and among individuals scoring in the top 5% of each domain. Sex differences in the etiological estimates were also tested in these analyses. Autistic traits were moderately to highly heritable (0.58–0.88) at age 12. Bivariate genetic correlations in the full sample (0.18–0.40) and the extremes (0.24–0.67), as well as even lower unique environmental correlations, all suggested considerable fractionation of genetic and environmental influences across autistic trait domains, in line with previous findings.     

Heritability, Assortative Mating and Gender Differences in Violent Crime: Results from a Total Population Sample Using Twin, Adoption, and Sibling Models

Research addressing genetic and environmental determinants to antisocial behaviour suggests substantial variability across studies. Likewise, evidence for etiologic gender differences is mixed, and estimates might be biased due to assortative mating. We used longitudinal Swedish total population registers to estimate the heritability of objectively measured violent offending (convictions) in classic twin (N = 36,877 pairs), adoptee-parent (N = 5,068 pairs), adoptee-sibling (N = 10,610 pairs), and sibling designs (N = 1,521,066 pairs). Type and degree of assortative mating were calculated from comparisons between spouses of siblings and half-siblings, and across consecutive spouses. Heritability estimates for the liability of violent offending agreed with previously reported heritability for self-reported antisocial behaviour. While the sibling model yielded estimates similar to the twin model (A ≈ 55%, C ≈ 13%), adoptee-models appeared to underestimate familial effects (A ≈ 20–30%, C ≈ 0%). Assortative mating was moderate to strong (r _spouse = 0.4), appeared to result from both phenotypic assortment and social homogamy, but had only minor effect on variance components. Finally, we found significant gender differences in the etiology of violent crime.     

Harsh Parenting and Serotonin Transporter and BDNF Val66Met Polymorphisms as Predictors of Adolescent Depressive Symptoms

Depressive symptoms are prevalent and rise during adolescence. The present study is a prospective investigation of environmental and genetic factors that contribute to the growth in depressive symptoms and the frequency of heightened symptoms during adolescence. Participants included 206 mother–father–adolescent triads (M age at Time 1 = 13.06 years, SD = .51, 52% female). Harsh parenting was observationally assessed during a family conflict paradigm. DNA was extracted from saliva samples and genotyped for the 5-HTTLPR and BDNF Val66Met polymorphisms. Adolescents provide self-reports of depressive symptoms annually across early adolescence. The results reveal Gene × Environment interactions as predictors of adolescent depressive symptom trajectories in the context of harsh parenting as an environmental risk factor. A BDNF Val66Met × Harsh Parenting interaction predicted the rise in depressive symptoms across a 3-year period, whereas a 5-HTTLPR × Harsh Parenting interaction predicted greater frequency in elevated depressive symptoms. The findings highlight the importance of unique genetic and environmental influences in the development and course of heightened depressive symptoms during adolescence.     

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.     

Elevated depressive symptoms and incident stroke in Hispanic, African-American, and White older Americans

Although depressive symptoms have been linked to stroke, most research has been in relatively ethnically homogeneous, predominantly white, samples. Using the United States based Health and Retirement Study, we compared the relationships between elevated depressive symptoms and incident first stroke for Hispanic, black, or white/other participants (N = 18,648) and estimated the corresponding Population Attributable Fractions. The prevalence of elevated depressive symptoms was higher in blacks (27%) and Hispanics (33%) than whites/others (18%). Elevated depressive symptoms prospectively predicted stroke risk in the whites/other group (HR = 1.53; 95% CI: 1.36–1.73) and among blacks (HR = 1.31; 95% CI: 1.05–1.65). The HR was similar but only marginally statistically significant among Hispanics (HR = 1.33; 95% CI: 0.92–1.91). The Population Attributable Fraction, indicating the percent of first strokes that would be prevented if the incident stroke rate in those with elevated depressive symptoms was the same as the rate for those without depressive symptoms, was 8.3% for whites/others, 7.8% for blacks, and 10.3% for Hispanics.     

Changes in genetic and environmental influences on the development of nicotine dependence and major depressive disorder from middle adolescence to early adulthood

This longitudinal study used a representative community sample of same-sex twins (485 monozygotic pairs, 271 dizygotic pairs) to study longitudinal changes in genetic and environmental influences on nicotine dependence (NicD) symptoms and major depressive disorder (MDD) symptoms and the longitudinal relationships between NicD and MDD symptoms at three relatively discrete ages spanning middle adolescence to early adulthood (ages 15, 18, and 21). Clinical interviews were used to assess NicD and MDD symptoms lifetime at age 15 and during the previous 3 years at the two subsequent assessments. Biometric models revealed similar patterns of findings for NicD and MDD. Heritability increased with age, particularly between ages 15 and 18. Shared environmental influences were small, and the proportion of variance attributed to shared environmental influences decreased with age. Nonshared environmental influences were moderate to large in magnitude and were entirely age specific. Both NicD and MDD symptoms showed considerable stability from age 15 to 21, and at each age those with one disorder showed elevated rates of the other. However, a cross-lagged model revealed no longitudinal predictive relationships between MDD symptoms and NicD symptoms after accounting for stability of symptoms within disorders. In summary, the transition between middle and late adolescence is a critical period for developmental shifts in the magnitudes of genetic and environmental influences on both MDD and NicD symptoms. Despite similarities in the development of genetic and environmental influences for the two phenotypes, the association between NicD and MDD reflects concurrent covariation rather than one phenotype being an antecedent influence on the subsequent development of the other.     

Stable Genes and Changing Environments: Body Mass Index Across Adolescence and Young Adulthood

The transition between adolescence and young adulthood is a developmentally sensitive time where children are at an increased risk for becoming overweight and developing obesity. Twin studies have reported that body mass index [BMI] is highly heritable, however, it remains unclear whether the genetic influences are sex-limited and whether non-additive genetic influences contribute to body mass index [BMI] during these ages. In the current report, we examined self-reported data on BMI in same [n = 2,744] and opposite-sex [n = 1,178] siblings participating in the National Longitudinal Study on Adolescent Health [Add Health]. To investigate whether the same or different genes contributed to BMI for both sexes, we fit quantitative sex-limited genetic models to three waves of data collection. At each of the three Waves of assessment, models that included additive genetic, individual-specific environment, and no sex-limited genetic influences fit the data most parsimoniously. Heritable effects on BMI at each of the three Waves were large for both sexes and ranged between .75 and .86. While genetic contributions across the ages were highly correlated, longitudinal analyses indicated that the relevant individual-specific environmental influences on BMI in adolescence and young adulthood change sizably. These results underscore the importance of understanding early genetic influences on BMI and highlight the role environmental experiences have at later ages when new genetic influences appear to make a small contribution to individual variation in BMI.