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 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     

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.     

Phenotypic and Genetic Analyses of the Wisconsin Card Sort

The present study assessed the factor structure and etiology of traditional perseverative and nonperseverative errors, and six narrowly defined errors that occur during the Wisconsin Card Sorting Task (WCST). A computer-administered version of the WCST, designed to maximize the variance in a nonclinical sample, was used. Phenotypic factor analysis and twin models were used to examine the structure and genetic and environmental etiology in 191 monozygotic and 165 dizygotic adolescent twin pairs. Factor analysis did not support the traditional division of errors into perseverative and nonperseverative errors. Heritability of individual indices was small to moderate (a² = 0.10 – 0.42), with varying significance. Estimates of shared environment (c² = 0.00 – 0.14) were not significant. The best fitting multivariate genetic model had one genetic factor, with specific variance and covariance due to nonshared environmental influences. These results suggest that there are common underlying genetic influences on WCST indices, along with index-specific environmental variance that does not correspond to the traditional division between perseverative and nonperseverative errors.     

Internalizing Behavior in Adolescent Girls Affects Parental Emotional Overinvolvement: A Cross-lagged Twin Study

The aim of this study was to examine the direction and the etiology of the association between different parenting styles (parental emotional overinvolvement [EOI] and parental criticism) and internalizing behavior from adolescence to early adulthood. A longitudinal genetically informative cross-lagged design was applied to a population-based sample of Swedish twins contacted at age 16–17 (n = 2369) and at age 19–20 (n = 1705). Sex-limitation modelling revealed different effects for boys and girls. For girls, genetic influences on internalizing problems at age 16–17 independently explained 2.7% of the heritability in parental EOI at age 19–20. These results suggest that emotionally overinvolved and self-sacrificing parental behavior stems in part from daughters (but not sons) genetic predisposition for internalizing behavior. These findings highlight the importance of genetically influenced child-driven effects underlying the parenting-internalizing association, and clarify that the role of such effects may differ depending on sex, type of parenting and developmental period.     

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.     

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.     

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.     

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.     

The Complexity of Personality: Advantages of a Genetically Sensitive Multi-Group Design

Findings from many behavioral genetic studies utilizing the classical twin design suggest that genetic and non-shared environmental effects play a significant role in human personality traits. This study focuses on the methodological advantages of extending the sampling frame to include multiple dyads of relatives. We investigated the sensitivity of heritability estimates to the inclusion of sibling pairs, mother–child pairs and grandparent–grandchild pairs from the German Socio-Economic Panel Study in addition to a classical German twin sample consisting of monozygotic- and dizygotic twins. The resulting dataset contained 1.308 pairs, including 202 monozygotic and 147 dizygotic twin pairs, along with 419 sibling pairs, 438 mother–child dyads, and 102 grandparent–child dyads. This genetically sensitive multi-group design allowed the simultaneous testing of additive and non-additive genetic, common and specific environmental effects, including cultural transmission and twin-specific environmental influences. Using manifest and latent modeling of phenotypes (i.e., controlling for measurement error), we compare results from the extended sample with those from the twin sample alone and discuss implications for future research.     

Variation in Attraction to Host Plant Odors in an Invasive Moth Has a Genetic Basis and is Genetically Negatively Correlated with Fecundity

Lepidopteran insects are major pests of agricultural crops, and mated female moths exploit plant volatiles to locate suitable hosts for oviposition. We investigated the heritability of odor-guided host location behavior and fecundity in the cosmopolitan oriental fruit moth Grapholita (Cydia) molesta, an oligophagous herbivore that attacks fruit trees. We used a full-sib/half-sib approach to estimate the heritability and the genetic correlation between these two traits. Results document a considerable genetic basis for olfactory attraction of females (h ²  = 0.37 ± 0.17) and their fecundity (h ²  = 0.32 ± 0.13), as well as a genetic trade-off between female attraction and fecundity (r _g  = −0.85 ± 0.21). These estimations were empirically corroborated by comparing two strains maintained in the laboratory for different numbers of generations. The long-term reared strain lost its olfactory discrimination ability but achieved significantly higher fecundity compared with the short-term reared strain. Our results highlight that genetic studies are relevant for understanding the evolution of odor-guided behavior in herbivore insects and for judging the promise of pest management strategies involving behavioral manipulation with plant volatiles.     

Catechol-<Emphasis Type="Italic">o</Emphasis>-Methyltransferase Genotype and Childhood Trauma May Interact to Impact Schizotypal Personality Traits

We attempt to identify gene by childhood abuse interactions which predispose to the development of schizotypal traits in a familial bipolar disorder (BD) sample. Self-report measures of schizotypal personality traits (Schizotypal Personality Scale) and childhood maltreatment (Childhood Trauma Questionnaire) were administered to 222 participants from 44 families with BD. Variants of catechol-o-methyltransferase (COMT) and four other dopamine pathway-related genes: DRD4, DRD2,MAOA, and SLC6A3, were typed. BD type I (BD I) subjects scored significantly higher than their unaffected relatives on the Schizotypal Personality Scale. The val allele of the Val158 Met polymorphism of the COMT gene was associated with increased schizotypal personality trait scores in individuals exposed to higher levels of self-reported childhood trauma (p < 0.05). There was no direct effect of the val158met polymorphism on schizotypal personality traits. Further, no passive correlation between COMT genotype and childhood trauma was found. We raise the possibility that genetically-driven variation in COMT may interact with childhood trauma to contribute to the risk of developing schizotypal personality traits.     

A Twin Study of the Genetics of High Cognitive Ability Selected from 11,000 Twin Pairs in Six Studies from Four Countries

Although much genetic research has addressed normal variation in intelligence, little is known about the etiology of high cognitive abilities. Using data from 11,000 twin pairs (age range = 6–71 years) from the genetics of high cognitive abilities consortium, we investigated the genetic and environmental etiologies of high general cognitive ability (g). Age-appropriate psychometric cognitive tests were administered to the twins and used to create g scores standardized within each study. Liability-threshold model fitting was used to estimate genetic and environmental parameters for the top 15% of the distribution of g. Genetic influence for high g was substantial (0.50, with a 95% confidence interval of 0.41–0.60). Shared environmental influences were moderate (0.28, 0.19–0.37). We conclude that genetic variation contributes substantially to high g in Australia, the Netherlands, the United Kingdom and the United States. Edited by Dick Rose.     

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.     

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.     

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.     

All night analysis of time interval between snores in subjects with sleep apnea hypopnea syndrome

Sleep apnea–hypopnea syndrome (SAHS) is a serious sleep disorder, and snoring is one of its earliest and most consistent symptoms. We propose a new methodology for identifying two distinct types of snores: the so-called non-regular and regular snores. Respiratory sound signals from 34 subjects with different ranges of Apnea-Hypopnea Index (AHI = 3.7–109.9 h⁻¹) were acquired. A total number of 74,439 snores were examined. The time interval between regular snores in short segments of the all night recordings was analyzed. Severe SAHS subjects show a shorter time interval between regular snores (p = 0.0036, AHI cp: 30 h⁻¹) and less dispersion on the time interval features during all sleep. Conversely, lower intra-segment variability (p = 0.006, AHI cp: 30 h⁻¹) is seen for less severe SAHS subjects. Features derived from the analysis of time interval between regular snores achieved classification accuracies of 88.2 % (with 90 % sensitivity, 75 % specificity) and 94.1 % (with 94.4 % sensitivity, 93.8 % specificity) for AHI cut-points of severity of 5 and 30 h⁻¹, respectively. The features proved to be reliable predictors of the subjects’ SAHS severity. Our proposed method, the analysis of time interval between snores, provides promising results and puts forward a valuable aid for the early screening of subjects suspected of having SAHS.     

Genetic and Environmental Influences on Risky Sexual Behaviour and its Relationship With Personality

Risky sexual behaviour is a major health issue in society, and it is therefore important to understand factors that may predispose individuals to such behaviour. Research suggests a link between risky sexual behaviour and personality, but the basis of this link remains unknown. Hans Eysenck proposed that personality is related to sexual behaviour via biological underpinnings of both. Here we test the viability of this perspective by analysing data from identical and non-identical twins (N = 4,904) who completed a questionnaire assessing sexual attitudes and behaviour as well as personality. Using genetic modelling of the twin data, we found that risky sexual behaviour was significantly positively correlated with Impulsivity (r = .27), Extraversion (r = .24), Psychoticism (r = .20), and Neuroticism (r = .09), and that in each case the correlation was due primarily to overlapping genetic influences. These findings suggest that the genetic influences that shape our personality may also predispose us to risky sexual behaviour.     

Differential Genetic Etiology of Reading Difficulties as a Function of IQ: An Update

In order to test the hypothesis that the genetic etiology of reading disability differs as a function of IQ, composite reading performance data from 308 pairs of identical (monozygotic, MZ) twins and 440 pairs of fraternal (dizygotic, DZ) twins (254 same-sex and 186 opposite-sex) in which at least one member of each pair was classified as reading-disabled were subjected to multiple regression analysis (DeFries and Fulker, Behav Genet 15:467–473, 1985; Acta Genet Med Gemellol 37:205–216, 1988). In the total sample, heritability of the group deficit in reading performance (h_g²) was .61 (±.06). However, results of fitting an extended regression model to reading performance and IQ data suggested that the genetic etiology of reading disability differs as a linear function of IQ (p ≤ .04). When the basic regression model was fitted separately to data from twin pairs with Wechsler (Examiner's manual: Wechsler intelligence scale for children—revised, 1974; Examiner's manual: Wechsler adult intelligence scale—revised, 1981) Full Scale IQ scores in the upper and lower 25% of the sample, resulting estimates of h_g² were .75 (±.12) and .50 (±.10), respectively (p ≤ .045). These results suggest that reading difficulties in children with a higher IQ are due substantially to genetic influences and may require intensive remediation efforts.     

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.