Working Memory and Parent-Rated Components of Attention in Middle Childhood: A Behavioral Genetic Study

The purpose of the current study was to investigate potential genetic and environmental correlations between working memory and three behavioral aspects of the attention network (i.e., executive, alerting, and orienting) using a twin design. Data were from 90 monozygotic (39% male) and 112 same-sex dizygotic (41% male) twins. Individual differences in working memory performance (digit span) and parent-rated measures of executive, alerting, and orienting attention included modest to moderate genetic variance, modest shared environmental variance, and modest to moderate nonshared environmental variance. As hypothesized, working memory performance was correlated with executive and alerting attention, but not orienting attention. The correlation between working memory, executive attention, and alerting attention was completely accounted for by overlapping genetic covariance, suggesting a common genetic mechanism or mechanisms underlying the links between working memory and certain parent-rated indicators of attentive behavior.     

Etiology of Stability and Growth of Internalizing and Externalizing Behavior Problems Across Childhood and Adolescence

Internalizing and externalizing behaviors are heritable, and show genetic stability during childhood and adolescence. Less work has explored how genes influence individual differences in developmental trajectories. We estimated ACE biometrical latent growth curve models for the Teacher Report Form (TRF) and parent Child Behavior Checklist (CBCL) internalizing and externalizing scales from ages 7 to 16 years in 408 twin pairs from the Colorado Longitudinal Twin Study. We found that Intercept factors were highly heritable for both internalizing and externalizing behaviors (a2 = .61–.92), with small and nonsignificant environmental influences for teacher-rated data but significant nonshared environmental influences for parent-rated data. There was some evidence of heritability of decline in internalizing behavior (Slopes for teacher and parent ratings), but the Slope genetic variance was almost entirely shared with that for the Intercept when different than zero. These results suggest that genetic effects on these developmental trajectories operate primarily on initial levels and stability, with no significant unique genetic influences for change. Finally, cross-rater analyses of the growth factor scores revealed moderate to large genetic and environmental associations between growth factors derived from parents' and teachers' ratings, particularly the Intercepts.     

Genetic and Environmental Sources of Individual Religiousness: The Roles of Individual Personality Traits and Perceived Environmental Religiousness

In the current study, we examined the genetic and environmental sources of the links between individual religiousness and individual personality traits, perceived parental religiousness, and perceived peer religiousness. Data from 870 individuals (incl. 394 twin pairs) were analyzed. Variance in individual religiousness was significantly influenced by genetic effects, environmental influences shared by twins reared together, and individual-specific environmental influences. Individual religiousness showed significant associations with age, sex, specific personality traits (e.g., agreeableness, openness to values), and perceived religiousness of important social interaction partners, such as parents, best friends, and spouses. The links to personality traits were relatively small and primarily genetically mediated. The associations between individual religiousness and parental religiousness were substantial and mediated by shared environmental effects. These links significantly decreased across age accompanying a significant decrease of shared environmental influences on individual religiousness. The correlations between individual religiousness and perceived religiousness of spouses and best friends were relatively moderate but increased with age. These associations were mediated by genetic as well as nonshared environmental sources accompanying an increase of nonshared environmental influences on individual religiousness with age. The results suggest that inter-individual differences in religiousness are due to multiple sources.     

Genetic and environmental influences on birthweight in a sample of Korean twins

This study is the first report of genetic and environmental influences on birthweight using Korean twins. The sample consisted of 255 monozygotic (MZ) and 178 dizygotic (DZ) twin pairs drawn from the Seoul Twin Family Study. Intraclass twin correlations were computed for the twins' birthweights obtained from parents (typically mothers) of the twins. To estimate genetic and shared and nonshared environmental influences on birthweight, standard univariate model-fitting analyses were performed using a software, Mx. For each gender, MZ twin correlations were higher than DZ twin correlations, suggesting existence of genetic influences on birthweight; however, DZ twin correlations were higher than half the MZ twin correlations, indicating that shared environmental factors are also important. For each zygosity, twin correlations were not significantly different between males and females, implicating that genes and environments that cause individual differences in birthweight may not vary between males and females. Model-fitting analyses based on the data pooled across gender yielded estimates of 17% for genetic, 60% for shared environmental, and 23% for nonshared environmental influences on birthweight.     

Genetic and Environmental Influences on EEG Coherence

EEG coherence measures the covariation in electrical brain activity between two locations on the scalp and is used to study connectivity between cortical regions. The aim of this study was to determine the heritability of EEG coherence. Coherence was measured in a group of 213 16-yr-old twin pairs. By including male and female twin pairs in the sample, sex differences in genetic architecture were systematically examined. The EEG was obtained during quiet supine resting. Coherence was estimated for short and long distance combinations of electrode pairs along the anterior-posterior axis within a hemisphere for four frequency bands (delta, theta, alpha and beta). Averaged over all electrode combinations about 60% of the variance was explained by genetic factors for coherence in the theta, alpha and beta bands. For the delta band, the heritability was somewhat lower. No systematic sex differences in genetic architecture were found. All environmental influences were nonshared, i.e., unique factors including measurement error. Environmental factors shared by twin siblings did not influence variation in EEG coherence. These results suggest that individual differences in coherence form a potential candidate for (molecular) genetic studies on brain function.     

Genetic and Social Determinants of Initiation and Age at Onset of Smoking in Australian Twins

Retrospective data on age at onset of smoking, reported by 3810 adult Australian twin pairs, were analyzed to determine the role of genetic and environmental factors in the onset of smoking. Results of nonmetric multidimensional scaling supported a two-process model in which different etiologic factors determined which individuals were at risk of becoming smokers and the age at onset of smoking in those who were at risk. Parametric model-fitting confirmed this difference. For female twins and younger male twins (aged 30 years or less), the onset of smoking was strongly influenced by genetic factors, with shared and nonshared environmental effects having a more modest impact. For older male twins, shared environmental influences on onset of smoking were very important, and the influence of genetic predisposition was slight. The age at which smoking onset occurred, however, was influenced by both genetic and nonshared environmental effects, but not by shared environmental effects, in both sexes and both cohorts.     

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.     

Multivariate Behavior Genetic Analyses of Aggressive Behavior Subtypes

This study examined the genetic and environmental architecture underlying aggressive behavior measured by the Life History of Aggression Questionnaire (LHA; Coccaro et al. 1997a). Following preliminary phenotypic factor analysis procedures, multivariate behavioral genetics models were fit to responses from 2,925 adult twins from the PennTwins cohort on five LHA items assessing lifetime frequency of temper tantrums, indirect aggression, verbal aggression, fighting, and physical assault. The best-fitting model was a 2-factor common pathway model, indicating that these five aggressive behaviors are underpinned by two distinct etiological factors with different genetic and nonshared environmental influences. Although there was evidence of significant sex differences, the structure of the two factors appeared to be quite similar in males and females, where General Aggression and Physical Aggression factors emerged. Heritability of these factors ranged from .37 to .57, and nonshared environmental effects ranged from .43 to .63. The results of this study highlight the heterogeneous nature of the aggression construct and the need to consider differences in genetic and environmental influences on individual aggressive behaviors in a multivariate context.     

Covariation of psychosocial characteristics associated with cardiovascular disease: genetic and environmental influences

OBJECTIVE: Three psychosocial characteristics associated with cardiovascular disease (CVD)-depression, hostility, and social support-tend to correlate with one another. However, the causes of each characteristic and why they tend to co-occur are not completely understood. Therefore, the current study used a twin design to examine the relative contributions of genetic and environmental influences to the variation and covariation of these three psychosocial characteristics. METHODS: The sources of variation and covariation among the Beck Depression Inventory, the Cook-Medley Hostility Scale, and the Interpersonal Support Evaluation List were examined in a young adult community sample of 157 monozygotic and 75 dizygotic twin pairs. RESULTS: Phenotypic confirmatory factor analysis indicated that a single latent factor could account for their moderate intercorrelations. Twin analyses indicated that the Beck Depression Inventory and Interpersonal Support Evaluation List were each influenced by genetic and nonshared environmental factors, whereas the Cook-Medley Hostility Scale was influenced by familial (genetic and/or shared environmental) and nonshared environmental factors. Bivariate associations between these scales were largely determined by common genetic effects and, to a lesser degree, common nonshared environmental effects. Covariation among the three scales could be explained by a single common genetic factor and a common nonshared environmental factor. Environmental factors shared within families did not contribute to covariation among the psychosocial characteristics. CONCLUSIONS: The results challenge the conventional approach of examining these psychosocial variables as independent risk factors for cardiovascular disease and argue for the importance of investigating specific causes for their covariation.     

Stability of Genetic and Environmental Influences on Reading Performance at 7, 12, and 16 Years of Age in the Colorado Adoption Project

The etiology of the longitudinal stability of reading performance was assessed by analyzing data from adoptive and nonadoptive sibling pairs (206 pairs at age 7, 195 pairs at age 12, and 110 pairs at age 16) tested in the Colorado Adoption Project (CAP). Results of longitudinal behavioral genetic analyses confirmed previous findings of moderate genetic influence on individual differences in reading performance at 7 and 12 years of age (a ² = .44 and .38, respectively), with somewhat higher heritability at age 16 (a ² = .57). Corresponding shared environmental influences were negligible (c ² = .07, .09, and .07). Moreover, common genetic influences were responsible for 66% of the observed stability (r _p) between ages 7 and 12 (.62), 62% of that between ages 12 and 16 (r _p = .74), and 88% of that between ages 7 and 16 (r _p = .55). Of particular interest, no new heritable variation was detected at either 12 or 16 years of age, suggesting that genetic influences at 7 years of age are amplified at the later ages. In contrast, new nonshared environmental influences (including measurement error) were manifested at each age, suggesting the possible importance of nonshared environmental factors (e.g., instructional methods, teachers, peers) for the development of individual differences in reading performance between 7 and 16 years of age.     

Prenatal life and post-natal psychopathology: evidence for negative gene-birth weight interaction

BACKGROUND: Many studies suggest that pregnancy and birth complications (PBCs) are environmental risk factors for child psychopathology. However, it is not known whether the effects of PBCs occur independently of genetic predisposition. The current study examined the possibility of gene-environment interaction in a twin design. METHOD: The East Flanders Prospective Twin Survey prospectively records the births of all twin pairs born in East Flanders, Belgium. The current study included 760 twin pairs aged 6-17 years. Multilevel regression analysis was used to assess the effects of several PBCs collected around the time of birth. Using structural equation modelling, ACE models assuming additive genetic (A), shared environmental (C) and unique environmental (E) influences, were compared in order to examine whether the contribution of genetic factors to parent-rated child problem behaviour varied as a function of exposure to dichotomously and continuously defined PBCs. RESULTS: A main independent effect of lower birth weight, corrected for gestational age (small for gestational age--SGA), on child problem behaviour was found. In addition, there was an interaction between genetic influence and SGA, in that being smaller for gestational age resulted in less influence of additive genetic factors on individual differences in problem behaviour. CONCLUSIONS: Results are suggestive of negative gene-birth weight interaction. Children who are SGA are less sensitive to the genetic effects, and those with high genetic vulnerability are less sensitive to the effects of being SGA in bringing about post-natal mental health effects.     

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.     

Genetic and environmental contributions to cannabis dependence in a national young adult twin sample

BACKGROUND: This paper examines genetic and environmental contributions to risk of cannabis dependence. METHOD: Symptoms of cannabis dependence and measures of social, family and individual risk factors were assessed in a sample of 6265 young adult male and female Australian twins born 1964-1971. RESULTS: Symptoms of cannabis dependence were common: 11.0% of sample (15.1% of men and 7.8% of women) reported two or more symptoms of dependence. Correlates of cannabis dependence included educational attainment, exposure to parental conflict, sexual abuse, major depression, social anxiety and childhood conduct disorder. However, even after control for the effects of these factors, there was evidence of significant genetic effects on risk of cannabis dependence. Standard genetic modelling indicated that 44.7% (95% CI = 15-72.2) of the variance in liability to cannabis dependence could be accounted for by genetic factors, 20.1% (95% CI = 0-43.6) could be attributed to shared environment factors and 35.3% (95% CI = 26.4-45.7) could be attributed to non-shared environmental factors. However, while there was no evidence of significant gender differences in the magnitude of genetic and environmental influences, a model which assumed both genetic and shared environmental influences on risks of cannabis dependence among men and shared environmental but no genetic influences among women provided an equally good fit to the data. CONCLUSIONS: There was consistent evidence that genetic risk factors are important determinants of risk of cannabis dependence among men. However, it remains uncertain whether there are genetic influences on liability to cannabis dependence among women.     

A Twin Study of Competence and Behavioral/Emotional Problems Among Adolescents in Taiwan

This work reports on a study to evaluate the relative contributions of genetic and environmental factors to both competence scales and behavioral/emotional syndromes as assessed by the Child Behavior Checklist (CBCL). A total of 279 pairs of twins and same-sex sib-pairs aged 12-16 years were recruited from 51 junior high schools in Taipei City, Taiwan. Twins' zygosity was determined by a combination of DNA typing and physical similarity. The Mx program was used to estimate parameters for a full model that contains effects from sex-specific additive genes, shared environment, and nonshared environment for the majority of the scales. The shared environment in the full model was replaced with nonadditive genetic factors for some scales when indicated. All girls' competence and behavioral/emotional syndromes exhibited a substantial heritability (h2 > 0.4), except for Social Competence and Withdrawn. For boys, though the heritability was also >0.4 for some scales (Social and School Competence, Thought Problems, Attention Problems, Delinquent Behavior, and Total Behavior Problems), environmental influences, especially shared environment, were predominant for most of the scales (10 out of 15 scales). Genetic factors are important for explaining adolescent behavioral problems, especially for girls, while shared environmental influences cannot be ignored for boys. Gender differences in heritability exist for various CBCL-based competence and behavioral/emotional problems.     

Sex steroids at birth: genetic and environmental variation and covariation.

Three sex-steroids (estradiol, progesterone, & testosterone) were assayed from the umbilical cord blood of 58 same-sex twin pairs in an investigation of the effects of sex, as well as genetic and environmental factors, on neonatal hormone levels. Although significant mean differences were found between boys and girls for both testosterone and progesterone, sex appeared to account for very little of the total variation for any of the hormones. Results showed that genetic influences significantly affected within-sex variation in both estradiol and progesterone levels, while variations in the intrauterine (shared twin) environment accounted primarily for differences in levels of testosterone. Moderate correlations were also found among the three hormones. Multivariate biometrical analyses revealed these relationships to be explained by an underlying general factor of nonshared environmental influences affecting all three hormones. Genetic factors appeared to be specific to each hormone rather than correlated across hormones. These results suggest not only that genes are operating at this early age, but also that maternal and other prenatal factors (e.g., placental effects, uterine position) have a significant role in variations of sex-steroids and possibly on later behaviors.     

Genetic and environmental influences on the association between smoking and panic attacks in females: a population-based twin study

BACKGROUND: Clinical and epidemiological studies have reported an association between lifetime cigarette-smoking and panic attacks. Several explanations for this relationship have been proposed, mostly focusing on direct causal pathways. The objective of this study was to investigate a hypothesis of shared vulnerability by examining whether panic attacks and cigarette-smoking share genetic or environmental liability factors. METHOD: Questionnaire data on 3172 female-female twins (1409 complete pairs), aged 18-31 years, from a population-based Norwegian twin registry, were used to calculate the correlation between genetic factors and the correlation between environmental factors that influence lifetime measures of panic attacks and daily smoking. RESULTS: The best-fitting biometrical twin model suggested that genetic factors influencing panic and smoking were uncorrelated. Shared or familial environmental factors were perfectly correlated, and accounted for 75 % of the association between the phenotypes. The correlation between individual environmental factors influencing the phenotypes was 0.25 (0.07-0.44). In the full model, the genetic correlation was 0.17 (0.00-1.00), and genetic and shared environmental factors respectively accounted for 18 % and 61 % of the co-variance between panic and smoking. CONCLUSION: The results suggest that panic attacks and lifetime smoking have few or no genetic liability factors in common. The shared environmental factors that influence the two phenotypes are identical. Liability to panic attacks in females appears to be more influenced by shared environmental factors than previously indicated by univariate studies.     

Genetic and Environmental Influences on Gambling and Substance Use in Early Adolescence

This study examined the genetic and environmental architecture of early gambling involvement and substance use to determine whether genetic or environmental factors that contribute to substance use also put young adolescents at risk for early involvement in gambling. Self-reports of substance use and gambling involvement were collected at age 13 years from 279 Monozygotic and Dizygotic twin pairs. Univariate ACE modeling revealed that genetic and nonshared environmental factors almost equally accounted for gambling involvement, with no contribution from shared environmental factors. In contrast, both shared and nonshared environmental factors played important roles in substance use; the contribution of genetic factors was also substantial. Bivariate analyses identified a significant, albeit modest, overlap between the genetic influence on gambling involvement and the genetic influence on substance use. The results shed light on the etiology of early gambling involvement and substance use, suggesting that preventive interventions targeting common risk factors may also need to be complemented by modules that are specific to each behavior.     

Longitudinal Genetic Analysis of Menstrual Flow, Pain, and Limitation in a Sample of Australian Twins

Genetically informative longitudinal data about menstrual disorders allow us to address the extent to which the same genetic risk mechanisms are operating throughout the reproductive life cycle. We investigate the relative contributions of genes and environment to individual differences in menstrual symptomatology reported at two waves, 8 years apart, of a longitudinal Australian twin study. Twins were questioned in 1980–1982 and 1988–1990 about levels of menstrual pain, flow, and perceived limitation by menses. Longitudinal genetic analysis was based on 728 pairs (466 MZ and 262 DZ) who were regularly menstruating at both survey waves. A bivariate Cholesky model was fitted to the two-wave data separately for flow, pain, and limitation variables. The baseline model comprised common genetic and environmental factors influencing responses at both waves and specific effects influencing only the second-wave response. We also included age as a covariate in the model. Proportions of the longitudinally stable variance in menstrual flow, pain, and limitation attributable to genetic and individual environmental effects were calculated for the best-fitting models. Genetic factors accounted for 39% of the longitudinally stable variation in menstrual flow, 55% for pain, and 77% for limitation. The remaining stable variance was due to individual environmental factors (61, 45, and 23%, respectively). Therefore the stable variance over the 8-year interval was largely environmentally influenced for menstrual flow, was approximately equally determined by genetic and by nonshared environmental influences in the case of pain, and was due almost entirely to genetic influences for limitation by periods. We demonstrate for the first time that the same genetic influences are operative throughout the reproductive life span.     

Cognitive ability and academic achievement in the Colorado Adoption Project: A multivariate genetic analysis of parent-offspring and sibling data

To test the hypothesis that the etiology of covariation among measures of cognitive ability and academic achievement is due at least in part to shared genetic influences, data from 198 adoptive and 220 nonadoptive families participating in the Colorado Adoption Project were subjected to multivariate behavioral genetic analyses. Data on measures of cognitive ability (verbal comprehension and perceptual organization) and academic achievement (reading recognition and mathematics achievement) from related and unrelated sibling pairs tested at age 7, as well as from adoptive and nonadoptive parents, were analyzed. Phenotypic analyses confirmed previous findings of moderate correlations among measures of cognitive ability and achievement, averaging about .35. Although 54% of the covariation between reading and mathematics achievement was due to influences shared with verbal ability, a significant proportion of this covariation was independent of the cognitive ability measures. Heritabilities for the various measures were moderate, ranging from .21 to .37. Moreover, genetic influences accounted for 33–64% of their phenotypic covariation; for example, 33–60% of the observed correlations between verbal comprehension and the achievement measures, 64% of those between perceptual organization and the achievement measures, and 63% of that between reading recognition and mathematics achievement were due to shared genetic influences. Similar to the results of the phenotypic analysis, nearly half of the genetic covariance between reading and mathematics achievement was independent of cognitive ability. Their remaining covariance was due primarily to nonshared environmental influences.     

注意缺陷多动障碍与品行障碍共病机制的双生子研究

目的 研究遗传因素和环境因素的相互作用对于注意缺陷多动障碍和品行障碍共病的影响.方法 利用已经建立的西南地区双生子随访登记系统,采用定量行为遗传学研究方法,用《困难和长处量表》父母评定的注意缺陷多动和品行问题分量表分作为定量表型,收集140对6～16岁双生子的临床资料,构建双生子行为表型的单因素和二因素结构方程模型,分析变量内双生子间、变量间双生子内以及变量间双生子间的相关性,基于模型的似然值和拟合度寻找最优模型,阐明遗传因素、共享的环境因素以及非共享的环境因素对于注意缺陷多动障碍和品行障碍共病的影响.结果 注意缺陷多动和品行问题的表型相关性为0.44(95% CI:0.09～0.27),其中遗传因素在二者总的表型相关性中占70%,非共享的环境因素占30%.对相关变量构建二因素结构方程模型并进行多个模型拟合,对寻找出的最优模型分析发现,注意缺陷多动和品行问题遗传相关性为0.76(95% CI:0.31～1),而个体特异性环境相关性为0.28(95% CI:0.02～0.51).结论 儿童存在3种不同的遗传因素影响注意缺陷多动障碍和品行障碍的发生,即单纯影响注意缺陷多动障碍的遗传因素、单纯影响品行障碍的遗传因素和对二者同时发生作用的遗传因素.本研究结果提示大部分作用于注意缺陷多动障碍的环境因素不会导致品行障碍的发生,即二者缺乏共同的环境因素.