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Objectives: To examine whether neighborhood income and neighborhood safety concerns influence multisystem physiological risk after adjusting for genetic and environmental selection effects that may have biased previous tests of this association., Methods: We used structural equation modeling with a genetically informed sample of 686 male and female twin pairs in the Midlife in the United States Study II (2004)., Results: Controlling for additive genetic and shared environmental processes that may have biased neighborhood-health links in previous examinations, higher neighborhood safety concerns were associated with less physiological risk among women but not men., Discussion: Our findings suggest a possible causal role of neighborhood features for a measure of physiological risk that is associated with the development of disease. Efforts to increase neighborhood safety, perhaps through increased street lighting or neighborhood watch programs, may improve community-level health., (© The Author(s) 2018. Published by Oxford University Press on behalf of The Gerontological Society of America. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.)

Background: Can the structure of genetic and environmental influences on normative personality traits (NPTs), abnormal personality traits (APTs), and DSM-IV criteria for personality disorders (PD) fit a high or low congruence model positing, respectively, close or more limited etiologic continuity?, Method: Exploratory factor analysis was applied to transformed correlation matrices from Cholesky twin decompositions obtained in OpenMx. In 2801 adult twins from the Norwegian Institute of Public Health Twin Panel, NPTs and APTs were assessed by self-report using the Big Five Inventory (BFI) and PID-5-Norwegian Brief Form (PID-5-NBF), respectively. PDs were assessed at interview using the Structured Interview for DSM-IV Personality (SIDP-IV)., Results: The best model yielded three genetic and three unique environmental factors. Genetic factors were dominated, respectively, by (i) high loadings on nearly all PDs and NPT/APT neuroticism and compulsivity, (ii) negative loadings on NPT agreeableness/conscientiousness and positive loadings on APT/PD measures of antisocial traits, and (iii) negative loadings on NPT extraversion and histrionic PD, and positive loadings on APT detachment and schizoid/avoidant PD. Unique environmental factors were dominated, by (i) high loadings on all PDs, (ii) high loadings on all APT dimensions and NPT neuroticism, and (iii) negative loadings on NPT extraversion and positive loadings on NPT detachment/avoidant PD., Conclusions: Two genetic and one environmental common factor were consistent with a high congruence model while one genetic and two environmental factors were more supportive of a low congruence model. The relationship between genetic and environmental influences on personality assessed by NPTs, APTs, and PDs is complex and does not fit easily into a low or high congruence model.

Psychologists using quantitative studies of the trait intelligence have established with much confidence that the impact of genes on intelligence increases with age, while the environmental effect of the family of origin declines. We examined the conjecture that a similar trend of increasing effect of genes/declining family environmental effect characterizes other status-related outcomes when arranged in typical age-graded sequence over adolescence and early adulthood. We used DeFries-Fulker (1985) (DF) analysis with longitudinal data on 1,576 pairs of variously-related young adult siblings (MZ twins; DZ twins; full siblings; half siblings; cousins; and nonrelated siblings; mean age 28) to estimate univariate quantitative genetic decompositions for fifteen status-related outcomes roughly ordered along the early life course: Verbal IQ, High school GPA, College plans, High school graduation, Some college, College graduation, Graduate school, Educational attainment, Occupational education, Occupational wages, Personal earnings, Household income, Household assets, Home ownership, and Subjective social status, with and without covariate controls for Age, Female gender, and Race/ethnicity (black, Hispanic, other; reference white). Results for successive outcomes did not support the conjecture of increasing heritability with maturity. Rather, the impacts of both the genes and the family environment tended to decline over the life course, resulting in a downward trend in family influences from all sources. There was some evidence of a recrudescence in relative influence of the family environment for outcomes related to the household that are often shared with a spouse, such as home ownership, suggesting a role of assortative mating in status reproduction. Other findings and limitations of the study are discussed., (Copyright © 2018 Elsevier Inc. All rights reserved.)

Adolescents and young adults are highly focused on peer evaluation, but little is known about sources of their differential sensitivity. We examined to what extent sensitivity to peer evaluation is influenced by interacting environmental and genetic factors. A sample of 354 healthy adolescent twin pairs (n = 708) took part in a structured, laboratory task in which they were exposed to peer evaluation. The proportion of the variance in sensitivity to peer evaluation due to genetic and environmental factors was estimated, as was the association with specific a priori environmental risk factors. Differences in sensitivity to peer evaluation between adolescents were explained mainly by non-shared environmental influences. The results on shared environmental influences were not conclusive. No impact of latent genetic factors or gene-environment interactions was found. Adolescents with lower self-rated positions on the social ladder or who reported to have been bullied more severely showed significantly stronger responses to peer evaluation. Not genes, but subjective social status and past experience of being bullied seem to impact sensitivity to peer evaluation. This suggests that altered response to peer evaluation is the outcome of cumulative sensitization to social interactions.

Callous-unemotional (CU) behaviors demonstrate meaningful individual differences in early childhood, even in nonclinical samples with low mean levels of CU, but the factors underlying this variation have not been examined. This study investigated genetic and environmental contributions to individual differences and to sources of continuity and change in CU in toddler twins (145 monozygotic, 169 dizygotic) assessed at ages 2 and 3 years. CU, as assessed by the Child Behavior Checklist 1.5-5 (Achenbach & Rescorla, 2000), was moderately stable across age (r = .45, p < .0001). Longitudinal biometric analyses revealed genetic and nonshared environmental influences on CU at both ages, with no significant contribution from shared environmental factors. Stability from age 2 to 3 was due to genetic factors, whereas change was due to both genetic and nonshared environmental influences. This genetic and nonshared environmental change was substantial, suggesting malleability of CU in early childhood. Over 50% of the genetic influences and 100% of the nonshared environmental influences on CU at age 3 were independent of those that operated at age 2. Implications of novel sources of variance across age are discussed.

The vast majority of individuals initiate alcohol consumption for the first time in adolescence. Given the widespread nature of its use and evidence that adolescents may be especially vulnerable to its effects, there is concern about the long-term detrimental impact of adolescent drinking on adult functioning. While some researchers have suggested that genetic processes may confound the relationship, the mechanisms linking drinking and later adjustment remain unclear. The current study utilized a genetically informed sample and biometric modeling to examine the nature of the familial influences on this association and identify the potential for genetic confounding. The sample was drawn from the Minnesota Twin Family Study (MTFS), a longitudinal study consisting of 2,764 twins assessed in 2 cohorts at regular follow-ups from age 17 to age 29 (older cohort) or age 11 to age 29 (younger cohort). A broad range of adult measures was included assessing substance use, antisocial behavior, personality, socioeconomic status, and social functioning. A bivariate Cholesky decomposition was used to examine the common genetic and environmental influences on adolescent drinking and each of the measures of adult adjustment. The results revealed that genetic factors and nonshared environmental influences were generally most important in explaining the relationship between adolescent drinking and later functioning. While the presence of nonshared environmental influences on the association are not inconsistent with a causal impact of adolescent drinking, the findings suggest that many of the adjustment issues associated with adolescent alcohol consumption are best understood as genetically influenced vulnerabilities. (PsycINFO Database Record, ((c) 2017 APA, all rights reserved).)

Background: Shared experiences within families play an important role in the initiation of cigarette use among adolescents. Behavioral genetic studies using various samples have implicated that the shared environment that twins experience is an important source of influence on whether adolescents initiate cigarette use. Whether the special twin environment, in addition to the shared environment, contributes significantly to making twin siblings more similar in cigarette initiation, and whether the influence of the special twin environment persists into adulthood, is less clear., Methods: Data for this study came from the National Longitudinal Survey of Adolescent Health. Twin, full-, and half-sibling pairs between the ages of 12 and 33 were separated into three age groups, with about 3,000 individuals in each age group. The proportion of variance in cigarette use initiation explained by genetic, shared, special twin, and unique environmental factors were examined., Results: The results of separate age-moderated univariate variance decomposition models indicate that the special twin environment does not significantly contribute to the variance in cigarette use initiation in adolescence or young adulthood., Conclusion: Factors shared by individuals in a family, but that are not specific to being a twin, are important in determining whether adolescents will initiate the use of cigarettes.

We studied developmental changes in infant positive affect from 6 to 12 months of age, a time marked by increasing use of positive vocalizations, laughter, and social smiles. We estimated the magnitude of genetic and environmental influences on observed and parent reported infant positive affect across development. Participants were drawn from a longitudinal twin study of infancy and toddlerhood (N = 536 twin pairs). Mothers and fathers reported on infant temperament and infants were videotaped during 2 observational tasks assessing positive affect. Parents also reported on their own affect and emotional expression within the family. Biometric models examined genetic and environmental influences that contribute to the developmental continuity of positive affect. Infant positive affect was associated with increased parent positive affect and family expressions of positive affect although not with family expressions of negative affect. In addition, the shared environment accounted for a large portion of variation in infant positive affect and continuity over time. These findings highlight the importance of the family environment in relation to infant positive emotional development. (PsycINFO Database Record, ((c) 2017 APA, all rights reserved).)

Gene × Environment interaction contributes to externalizing disorders in childhood and adolescence, but little is known about whether such effects are long lasting or present in adulthood. We examined gene-environment interplay in the concurrent and prospective associations between antisocial peer affiliation and externalizing disorders (antisocial behavior and substance use disorders) at ages 17, 20, 24, and 29. The sample included 1,382 same-sex twin pairs participating in the Minnesota Twin Family Study. We detected a Gene × Environment interaction at age 17, such that additive genetic influences on antisocial behavior and substance use disorders were greater in the context of greater antisocial peer affiliation. This Gene × Environment interaction was not present for antisocial behavior symptoms after age 17, but it was for substance use disorder symptoms through age 29 (though effect sizes were largest at age 17). The results suggest adolescence is a critical period for the development of externalizing disorders wherein exposure to greater environmental adversity is associated with a greater expression of genetic risk. This form of Gene × Environment interaction may persist through young adulthood for substance use disorders, but it appears to be limited to adolescence for antisocial behavior.

Behavioral traits generally show moderate to strong genetic influence, with heritability estimates of around 50%. Some recent research has suggested that trust may be an exception because it is more strongly influenced by social interactions. In a sample of over 7,000 adolescent twins from the United Kingdom's Twins Early Development Study, we found broad sense heritability estimates of 57% for generalized trust and 51% for trust in friends. Genomic-relatedness-matrix restricted maximum likelihood (GREML) estimates in the same sample indicate that 21% of the narrow sense genetic variance can be explained by common single nucleotide polymorphisms for generalized trust and 43% for trust in friends. As expected, this implies a large amount of unexplained heritability, although power is low for estimating DNA-based heritability. The missing heritability may be accounted for by interactions between DNA and the social environment during development or via gene-environment correlations with rare variants. How these genes and environments correlate seem especially important for the development of trust., Competing Interests: None.

To investigate familial influences on the full range of variability in attention and activity across adolescence, we collected maternal ratings of 339 twin pairs at ages 12, 14, and 16, and estimated the transmitted and new familial influences on attention and activity as measured by the Strengths and Weaknesses of Attention-Deficit/Hyperactivity Disorder Symptoms and Normal Behavior Scale. Familial influences were substantial for both traits across adolescence: genetic influences accounted for 54%-73% (attention) and 31%-73% (activity) of the total variance, and shared environmental influences accounted for 0%-22% of the attention variance and 13%-57% of the activity variance. The longitudinal stability of individual differences in attention and activity was largely accounted for by familial influences transmitted from previous ages. Innovations over adolescence were also partially attributable to familial influences. Studying the full range of variability in attention and activity may facilitate our understanding of attention-deficit/hyperactivity disorder's etiology and intervention.

Previous studies suggest strong associations between exposure to weight-conscious peer groups and increased levels of disordered eating. This association has been attributed to socialization effects (i.e., membership leads to disordered eating); however, selection effects (i.e., selecting into peer groups based on genetic and/or environmental predispositions toward disordered eating) could contribute to or even account for these associations. The current study was the first to use a co-twin control design to disentangle these types of selection factors from socialization effects. Participants included 610 female twins (ages 8-14) drawn from the Michigan State University Twin Registry. To comprehensively examine a range of eating pathology, several disordered eating attitudes and behaviors (e.g., body dissatisfaction, binge eating) were examined via self-report questionnaires. Questionnaires also were used to assess peer group emphasis on body weight and shape. Replicating previous results, significant individual-level associations were found between membership in weight-conscious peer groups and disordered eating. However, co-twin control analyses indicated that these associations were largely due to genetic and/or shared environmental selection factors rather than pure socialization effects. Importantly, results remained unchanged when controlling for pubertal status, suggesting that effects do not vary across developmental stage. Overall, these findings question whether associations between weight-conscious peer groups and disordered eating are due entirely to socialization processes. Future studies are needed to identify the specific genetic and/or shared environmental factors that may drive selection into weight-conscious peer groups., ((c) 2016 APA, all rights reserved).)

Background: Alcohol dependence is associated with increased levels of impulsivity, but the genetic and environmental underpinnings of this overlap remain unclear. The purpose of the current study was to investigate the degree to which genetic and environmental factors contribute to the overlap between alcohol dependence and impulsivity., Method: Univariate and bivariate twin model fitting was conducted for alcohol dependence and impulsivity in a national sample of 16 819 twins born in Sweden from 1959 to 1985., Results: The heritability estimate for alcohol dependence was 44% [95% confidence interval (CI) 31-57%] for males and 62% (95% CI 52-72%) for females. For impulsivity, the heritability was 33% (95% CI 30-36%) in males and females. The bivariate twin analysis indicated a statistically significant genetic correlation between alcohol dependence and impulsivity of 0.40 (95% CI 0.23-0.58) in males and 0.20 (95% CI 0.07-0.33) in females. The phenotypic correlation between alcohol dependence and impulsivity was 0.20 and 0.17 for males and females, respectively, and the bivariate heritability was 80% (95% CI 47-117%) for males and 53% (95% CI 19-86%) for females. The remaining variance in all models was accounted for by non-shared environmental factors., Conclusions: The association between alcohol dependence and impulsivity can be partially accounted for by shared genetic factors. The genetic correlation was greater in men compared with women, which may indicate different pathways to the development of alcohol dependence between sexes. The observed genetic overlap has clinical implications regarding treatment and prevention, and partially explains the substantial co-morbidity between alcohol dependence and psychiatric disorders characterized by impulsive behaviour.

We examined how genotype-environment correlation processes differ as a function of adolescent age. We tested whether adolescent age moderates genetic and environmental influences on positivity and negativity in mother-adolescent and father-adolescent relationships using parallel samples of twin parents from the Twin and Offspring Study in Sweden and twin/sibling adolescents from the Nonshared Environment in Adolescent Development Study. We inferred differences in the role of passive and nonpassive genotype-environment correlation based on biometric moderation findings. The findings indicated that nonpassive gene-environment correlation played a stronger role for positivity in mother- and father-adolescent relationships in families with older adolescents than in families with younger adolescents, and that passive gene-environment correlation played a stronger role for positivity in the mother-adolescent relationship in families with younger adolescents than in families with older adolescents. Implications of these findings for the timing and targeting of interventions on family relationships are discussed.

The genetic and environmental etiology of individual differences was examined in initial level and change in psychopathic personality from ages 9 to 18 years. A piecewise growth curve model, in which the first change score (G1) influenced all ages (9-10, 11-13, 14-15, and 16-18 years) and the second change score (G2) only influenced ages 14-15 and 16-18 years, fit the data better did than the standard single slope model, suggesting a turning point from childhood to adolescence. The results indicated that variations in levels and both change scores were mainly due to genetic (A) and nonshared environmental (E) influences (i.e., AE structure for G0, G1, and G2). No sex differences were found except on the mean values of level and change scores. Based on caregiver ratings, about 81% of variance in G0, 89% of variance in G1, and 94% of variance in G2 were explained by genetic factors, whereas for youth self-reports, these three proportions were 94%, 71%, and 66%, respectively. The larger contribution of genetic variance and covariance in caregiver ratings than in youth self-reports may suggest that caregivers considered the changes in their children to be more similar as compared to how the children viewed themselves.

Clinically significant anxiety symptoms are prevalent among the elderly, yet knowledge about the longitudinal course of anxiety symptoms in later life remains scarce. The goals of this study were to (a) characterize age trajectories of state anxiety symptoms in the second half of life, and (b) estimate genetic and environmental contributions to individual differences in the age trajectory of state anxiety. This study was based on data from 1,482 participants in the Swedish Adoption/Twin Study of Aging who were aged 50 and older at their first occasion (512 complete twin pairs, 458 singletons) and had up to 6 measurement occasions spanning 11 years. Consistent with life span developmental theories of age-related emotional change, anxiety symptom levels declined during the transition from midlife to the mid-60s, followed by a mild increase that gradually plateaued in the 80s. There were substantial individual differences in the age trajectory of anxiety. After accounting for effects of sex, cohort, mode of testing, and proximity to death, this longitudinal variation was partitioned into biometric sources. Nonshared environmental variance was highest in the late 60s and declined thereafter, whereas genetic variance increased at an accelerated pace from approximately age 60 onward. There was no evidence for effects of rearing or other shared environment on anxiety symptoms in later life. These findings highlight how the etiology of anxiety symptoms changes from midlife to old age., ((c) 2016 APA, all rights reserved).)

Factors underlying developmental delays and psychosocial risks are of interest to international adoption communities. The current study administered a Pre-Adoption Adversity (PAA) Questionnaire to mostly American parents raising (a) adopted Chinese twins or (b) same-age unrelated adopted siblings. A goal was to replicate earlier analyses of pre-adoption adversity/adjustment among adopted preschool-age Chinese girls. A second goal was to conduct genetic analyses of four content areas (Developmental Delays at Adoption, Initial Adaptation to Adoption, Crying/Clinging, and Refusal/Avoidance) derived from the PAA Questionnaire. A key finding was that age at adoption added less than other predictors to adoptees' externalizing and internalizing behaviors. Family factors (e.g., parental education) contributed significantly to behavioral outcomes among the adopted Chinese twins. Genetic effects were indicated for all four content areas, with shared environmental effects evident for Developmental Delays at Adoption and Crying/Clinging. Future investigators should consider incorporating genetically sensitive designs into developmental research programs., (Copyright © 2015 Elsevier Inc. All rights reserved.)

The current study investigated genetic and environmental influences on salivary testosterone during adolescence, using data from 49 pairs of monozygotic twins and 68 pairs of dizygotic twins, ages 14-19 years (M = 16.0 years). Analyses tested for sex differences in genetic and environmental influences on testosterone and its relation to pubertal development. Among adolescent males, individual differences in testosterone were heritable (55%) and significantly associated with self-reported pubertal status (controlling for age) via common genetic influences. In contrast, there was minimal heritable variation in testosterone for females, and testosterone in females was not significantly associated with pubertal status after controlling for age. Rather, environmental influences shared by twins raised together accounted for nearly all of the familial similarity in female testosterone. This study adds to a small but growing body of research that investigates genetic influences on individual differences in behaviorally relevant hormones., (© 2014 Wiley Periodicals, Inc.)

Parental psychopathology, parenting style, and the quality of intrafamilial relationships are all associated with child mental health outcomes. However, most research can say little about the causal pathways underlying these associations. This is because most studies are not genetically informative and are therefore not able to account for the possibility that associations are confounded by gene-environment correlation. That is, biological parents not only provide a rearing environment for their child, but also contribute 50% of their genes. Any associations between parental phenotype and child phenotype are therefore potentially confounded. One technique for disentangling genetic from environmental effects is the children-of-twins (COT) method. This involves using data sets comprising twin parents and their children to distinguish genetic from environmental associations between parent and child phenotypes. The COT technique has grown in popularity in the last decade, and we predict that this surge in popularity will continue. In the present article we explain the COT method for those unfamiliar with its use. We present the logic underlying this approach, discuss strengths and weaknesses, and highlight important methodological considerations for researchers interested in the COT method. We also cover variations on basic COT approaches, including the extended-COT method, capable of distinguishing forms of gene-environment correlation. We then present a systematic review of all the behavioral COT studies published to date. These studies cover such diverse phenotypes as psychosis, substance abuse, internalizing, externalizing, parenting, and marital difficulties. In reviewing this literature, we highlight past applications, identify emergent patterns, and suggest avenues for future research., (PsycINFO Database Record (c) 2014 APA, all rights reserved.)

The longitudinal rank-order stability of cognitive ability increases dramatically over the life span. Theoretical perspectives differ in their emphasis on genetic mechanisms in explaining the longitudinal stability of cognition and how stability changes with development. However, the patterns of stability of genetic and environmental influences on cognition over the life span remain poorly understood. We searched for longitudinal studies of cognition that reported raw genetically informative longitudinal correlations or parameter estimates from longitudinal behavior genetic models. We identified 150 combinations of time points and measures from 15 independent longitudinal samples. In total, longitudinal data came from 4,548 monozygotic twin pairs raised together, 7,777 dizygotic twin pairs raised together, 34 monozygotic twin pairs raised apart, 78 dizygotic twin pairs raised apart, 141 adoptive sibling pairs, and 143 nonadoptive sibling pairs, ranging in age from infancy through late adulthood. At all ages, cross-time genetic correlations and shared environmental correlations were substantially larger than cross-time nonshared environmental correlations. Cross-time correlations for genetic and shared environmental components were, respectively, low and moderate during early childhood, increased sharply over child development, and remained high from adolescence through late adulthood. Cross-time correlations for nonshared environmental components were low across childhood and gradually increased to moderate magnitudes in adulthood. Increasing phenotypic stability over child development was almost entirely mediated by genetic factors. Time-based decay of genetic and shared environmental stability was more pronounced earlier in child development. Results are interpreted in reference to theories of gene-environment correlation and interaction., (PsycINFO Database Record (c) 2014 APA, all rights reserved.)

Over the past decades, numerous twin studies have revealed moderate to high heritability estimates for individual differences in a wide range of human traits, including cognitive ability, psychiatric disorders, and personality traits. Even factors that are generally believed to be environmental in nature have been shown to be under genetic control, albeit modest. Is such heritability also present in social traits that are conceptualized as causes and consequences of social interactions or in other ways strongly shaped by behavior of other people? Here we examine a population-based sample of 1,012 twins and relatives. We show that the genetic influence on generalized trust in other people (trust-in-others: h2 = 5%, ns), and beliefs regarding other people's trust in the self (trust-in-self: h2 = 13%, ns), is virtually absent. As test-retest reliability for both scales were found to be moderate or high (r = .76 and r = .53, respectively) in an independent sample, we conclude that all variance in trust is likely to be accounted for by non-shared environmental influences. We show that, relative to cognitive abilities, psychiatric disorders, and classic personality variables, genetic influences are smaller for trust, and propose that experiences with or observations of the behavior of other people shape trust more strongly than other traits.

Objective: Using Swedish nationwide registry data, the authors investigated genetic and environmental risk factors in the etiology of drug abuse by twin sibling modeling. The authors followed up with epidemiological analyses to identify shared environmental influences on drug abuse., Method: Drug abuse was defined using public medical, legal, or pharmacy records. Twin and sibling pairs were obtained from the national twin and genealogical registers. Information about sibling pair residence within the same household, small residential area, or municipality was obtained from Statistics Sweden. The authors predicted concordance for drug abuse by years of co-residence until the older sibling turned 21 and risk for future drug abuse in adolescents living with parental figures as a function of family-level socioeconomic status and neighborhood social deprivation., Results: The best twin sibling fit model predicted substantial heritability for drug abuse in males (55%) and females (73%), with environmental factors shared by siblings operating only in males and accounting for 23% of the variance in liability. For each year of living in the same household, the probability of sibling concordance for drug abuse increased 2%-5%. When not residing in the same household, concordance was predicted from residence in the same small residential area or municipality. Risk for drug abuse was predicted both by family socioeconomic status and neighborhood social deprivation. Controlling for family socioeconomic status, each year of living in a high social deprivation neighborhood increased the risk for drug abuse by 2%., Conclusions: Using objective registry data, the authors found that drug abuse is highly heritable. A substantial proportion of the shared environmental effect on drug abuse comes from community-wide rather than household-level influences. Genetic effects demonstrated in twin studies have led to molecular analyses to elucidate biological pathways. In a parallel manner, environmental effects can be followed up by epidemiological studies to clarify social mechanisms.

The specificity of genetic and environmental risk factors for illicit substance use and substance use disorders (SUD) was investigated by utilizing self and co-twin reports in 1,791 male twins. There was a high rate of comorbidity between both use of, and SUD from, different classes of illicit substances. For substance use, the model that included one common genetic, one shared environmental, and one individual-specific (i.e., unique) environmental factor, along with substance-specific effects that were attributed entirely to genetic factors fit the data best. For illicit SUD, one common genetic and one common unique environmental risk factor, and substance specific shared environmental and unique environmental risk factors were identified. Risk factors for illicit substance use and SUD are mainly non-specific to substance class. Co-twin rating of illicit substance use and SUD was a reliable source of information, and by taking account of random and systematic measurement error, environmental exposures unique to the individual were of lesser importance than found in earlier studies.

We review the genetically informed literature on the genetics of personality. Over the past century, quantitative genetic studies, using identical and fraternal twins, have demonstrated that differences in human personality are substantially heritable. We focus on more contemporary questions to which that basic observation has led. We examine whether differences in the heritability of personality are replicable across different traits, samples, and studies; how the heritability of personality relates to its reliability; and how behavior genetics can be employed in studies of validity, and we discuss the stability of personality in genetic and environmental variance. The appropriate null hypothesis in behavior genetics is not that genetic or environmental influence on personality is zero. Instead, we offer a phenotypic null hypothesis, which states that genetic variance is not an independent mechanism of individual differences in personality but rather a reflection of processes that are best conceptualized at the phenotypic level.

In the past, shared environmental influences on personality traits have been found to be negligible in behavior genetic studies (e.g., Bouchard and McGue, J Neurobiol 54:4-45, 2003). However, most studies have been based on biometrical modeling of twins only. Failure to meet key assumptions of the classical twin design could lead to biased estimates of shared environmental effects. Alternative approaches to the etiology of personality are needed. In the current study we estimated the impact of shared environmental factors on adolescent personality by simultaneously modeling both twin and adoption data. We found evidence for significant shared environmental influences on Multidimensional Personality Questionnaire Absorption (15% variance explained), Alienation (10%), Harm Avoidance (14%), and Traditionalism (26%) scales. Additionally, we found that in most cases biometrical models constraining parameter estimates to be equal across study type (twins vs. adoptees) fit no worse than models allowing these parameters to vary; this suggests that results converge across study design despite the potential (sometimes opposite) biases of twin and adoption studies. Thus, we can be more confident that our findings represent the true contribution of shared environmental variance to personality development.

This study investigated the mean-level and individual-level trends as well as the genetic and environmental sources of rank-order continuity and change in temperament traits (Briskness, Perseveration, Sensory Sensitivity, Emotional Reactivity, Endurance, and Activity). We analyzed self-reports and peer ratings from 2 adult age groups of twins, aged 15-30 (n = 348; 113 monozygotic and 61 dizygotic twin pairs) and 31-67 (n = 352; 110 monozygotic and 66 dizygotic twin pairs), captured at 2 different points of time 13 years apart. Temperament traits were fairly stable accompanying high levels of heritability. However, they also undergo mean-level, individual-level, and rank-order changes. In young adulthood, rank-order change was due to both genetic and environmental factors, whereas in older adult years, rank-order change was predominantly attributable to environmental effects. Phenotypic rank-order continuity was larger for older adults due to higher genetic as well as environmental continuity. For specific temperament traits (e.g., Activity), environmental variance proportionally increased across adulthood compared with genetic variance resulting in decreasing levels of heritability, whereas the reverse was found for other traits (e.g., Endurance). Specifics regarding the traits studied were discussed. The results indicate a complex interplay between genetic and environmental sources resulting in continuity and change of temperament across adulthood., (PsycINFO Database Record (c) 2013 APA, all rights reserved.)

Background: Prior research has indicated that affiliation with delinquent peers activates genetic influences on delinquency during adolescence. However, because other studies have indicated that the socializing effects of delinquent peers vary dramatically across childhood and adolescence, it is unclear whether delinquent peer affiliation (DPA) also moderates genetic influences on delinquency during childhood. Method The current study sought to evaluate whether and how DPA moderated the etiology of delinquency in a sample of 726 child twins from the Michigan State University Twin Registry (MSUTR)., Results: The results robustly supported etiological moderation of childhood delinquency by DPA. However, this effect was observed for shared environmental, rather than genetic, influences. Shared environmental influences on delinquency were found to be several-fold larger in those with higher levels of DPA as compared to those with lower levels. This pattern of results persisted even when controlling for the overlap between delinquency and DPA., Conclusions: Our findings bolster prior work in suggesting that, during childhood, the association between DPA and delinquency is largely (although not solely) attributable to the effects of socialization as compared to selection. They also suggest that the process of etiological moderation is not specific to genetic influences. Latent environmental influences are also amenable to moderation by measured environmental factors.

Little is known about how genetic and environmental factors contribute to the association between parental negativity and behavior problems from early childhood to adolescence. The current study fitted a cross-lagged model in a sample consisting of 4,075 twin pairs to explore (a) the role of genetic and environmental factors in the relationship between parental negativity and behavior problems from age 4 to age 12, (b) whether parent-driven and child-driven processes independently explain the association, and (c) whether there are sex differences in this relationship. Both phenotypes showed substantial genetic influence at both ages. The concurrent overlap between them was mainly accounted for by genetic factors. Causal pathways representing stability of the phenotypes and parent-driven and child-driven effects significantly and independently account for the association. Significant but slight differences were found between males and females for parent-driven effects. These results were highly similar when general cognitive ability was added as a covariate. In summary, the longitudinal association between parental negativity and behavior problems seems to be bidirectional and mainly accounted for by genetic factors. Furthermore, child-driven effects were mainly genetically mediated, and parent-driven effects were a function of both genetic and shared-environmental factors.

This study assessed the genetic and environmental contributions to peer difficulties in the early school years. Twins' peer difficulties were assessed longitudinally in kindergarten (796 twins, Mage = 6.1 years), Grade 1 (948 twins, Mage = 7.1 years), and Grade 4 (868 twins, Mage = 10 years) through multiple informants. The multivariate results revealed that genetic factors accounted for a strong part of both yearly and stable peer difficulties. At the univariate level, the genetic contributions emerged progressively, as did a growing consensus among informants with respect to those who experienced peer difficulties. These results underline the need to intervene early and persistently, and to target the child and the peer context to prevent peer difficulties and their consequences., (© 2012 The Authors. Child Development © 2012 Society for Research in Child Development, Inc.)

Identical and fraternal twins (N=540, age 8 to 18 years) were tested on three different measures of writing (Woodcock-Johnson III Tests of Achievement-Writing Samples and Writing Fluency; Handwriting Copy from the Group Diagnostic Reading and Aptitude Achievement Tests), three different language skills (phonological awareness, rapid naming, and vocabulary), and three different reading skills (word recognition, spelling, and reading comprehension). Substantial genetic influence was found on two of the writing measures, writing samples and handwriting copy, and all of the language and reading measures. Shared environment influences were generally not significant, except for Vocabulary. Non-shared environment estimates, including measurement error, were significant for all variables. Genetic influences among the writing measures were significantly correlated (highest between the speeded measures writing fluency and handwriting copy), but there were also significant independent genetic influences between copy and samples and between fluency and samples. Genetic influences on writing were significantly correlated with genetic influences on all of the language and reading skills, but significant independent genetic influences were also found for copy and samples, whose genetic correlations were significantly less than 1.0 with the reading and language skills. The genetic correlations varied significantly in strength depending on the overlap between the writing, language, and reading task demands. We discuss implications of our results for education, limitations of the study, and new directions for research on writing and its relations to language and reading.

Numerous studies report gene-environment interactions, suggesting that specific alleles have different effects on social outcomes depending on environment. In all these studies, however, environmental conditions are potentially endogenous to unmeasured genetic characteristics. That is, it could be that the observed interaction effects actually reflect underlying genetic tendencies that lead individuals into certain environments. What is critical to move this literature forward is random environmental variation that we know is not correlated with innate characteristics of subjects. We exploit a natural experiment that randomizes a particular stressor-birth weight discordance within twin pairs-to address this challenge and ask: Do random differences in early environment (prenatal nutrition) moderate genetic effects on depression, delinquency, or GPA? Using Add Health data, the only consistently significant allele-birth weight interaction we reveal works in the opposite direction of Caspi et al.'s classic finding regarding the interaction of maltreatment with genetic variation in the serotonin transporter promoter. Less robust interactions found for DRD2 and MAOA are consistent with this pattern that reverses prior findings. These results do not necessarily overturn existing research but support our methodological point that gene-environment research must address endogeneity.

We used a longitudinal twin design to examine selection effects of personality traits at age 11 on high-risk environmental contexts at age 14 and the extent to which these contexts mediated risk for substance abuse at age 17. Socialization at age 11 (willingness to follow rules and endorse conventional values) predicted exposure to contextual risk at age 14. Contextual risk partially mediated the effect of socialization on substance abuse, though socialization also had a direct effect. In contrast, boldness at age 11 (social engagement and assurance, thrill seeking, and stress resilience) also predicted substance abuse directly but was unrelated to contextual risk. There was substantial overlap in the genetic and shared environmental influences on socialization and contextual risk, and genetic risk in socialization contributed to substance abuse indirectly via increased exposure to contextual risk. This suggests that active gene-environment correlations related to individual differences in socialization contributed to an early, high-risk developmental trajectory for adolescent substance abuse. In contrast, boldness appeared to index an independent and direct genetic risk factor for adolescent substance abuse.

Early disruptive behaviors, such as aggressive and hyperactive behaviors, known to be influenced by genetic factors, have been found to predict early school peer relation difficulties, such as peer rejection and victimization. However, there is no consensus regarding the developmental processes underlying this predictive association. Genetically informative designs, such as twin studies, are well suited for investigating the underlying genetic and environmental etiology of this association. The main goal of the present study was to examine the possible establishment of an emerging gene-environment correlation linking disruptive behaviors to peer relationship difficulties during the first years of school. Participants were drawn from an ongoing longitudinal study of twins who were assessed with respect to their social behaviors and their peer relation difficulties in kindergarten and in Grade 1 through peer nominations measures and teacher ratings. As predicted, disruptive behaviors were concurrently and predictively associated with peer relation difficulties. Multivariate analyses of these associations indicate that they were mainly accounted for by genetic factors. These results emphasize the need to adopt an early and persistent prevention framework targeting both the child and the peer context to alleviate the establishment of a negative coercive process and its consequences.

Depression is known to be associated with a wide array of environmental factors. Such associations are due at least in part to genetic influences on both. This issue has been little explored with preadolescent children. Measures of family chaos and parenting style at age 9 and child depressive symptoms at age 12 were completed by 3,258 twin pairs from the Twins Early Development Study and their parents. Quantitative genetic modeling was used to explore common and unique genetic and environmental influences on both family environment and later depressive symptoms. Depressive symptoms at age 12 were significantly heritable. Moderate genetic effects influenced parenting style and family chaos at the age of 9, indicating gene-environment correlation. There were significant genetic correlations between family environment and depressive symptoms. There was some evidence of a Gene × Environment interaction, with stronger genetic effects on depressive symptoms for children with more suboptimal family environment. There was an Environment × Environment interaction, with effects of nonshared environment on depressive symptoms stronger for twins with more adverse parenting experiences. There is some evidence for gene-environment correlation between aspects of family environment in middle childhood and subsequent depressive symptoms. This suggests that one of the mechanisms by which genes lead to depressive symptoms may be by themselves influencing depressogenic environments.

Biological parents pass on genotypes to their children, as well as provide home environments that correlate with their genotypes; thus, the association between the home environment and children's temperament can be genetically (i.e., passive gene-environment correlation) or environmentally mediated. Furthermore, family environments may suppress or facilitate the heritability of children's temperament (i.e., gene-environment interaction). The sample comprised 807 twin pairs (mean age = 7.93 years) from the longitudinal Wisconsin Twin Project. Important passive gene-environment correlations emerged, such that home environments were less chaotic for children with high effortful control, and this association was genetically mediated. Children with high extraversion/surgency experienced more chaotic home environments, and this correlation was also genetically mediated. In addition, heritability of children's temperament was moderated by home environments, such that effortful control and extraversion/surgency were more heritable in chaotic homes, and negative affectivity was more heritable under crowded or unsafe home conditions. Modeling multiple types of gene-environment interplay uncovered the complex role of genetic factors and the hidden importance of the family environment for children's temperament and development more generally.

Gene-environment correlation (rGE) exists both within and between families. Between families, accumulating rGE has been used to explain dramatic changes in phenotypic means over time. The Dickens and Flynn model of increases in cognitive ability over generational time, for example, suggests that small changes in phenotype can lead to subsequent reallocation of environmental resources. This process sets up a reciprocal feedback loop between phenotype and environment, producing accumulating rGE that can cause large changes in the mean of ability, even though ability remains highly heritable in cross-sectional data. We report simulations suggesting that similar processes may operate within twin and sibling pairs. Especially in dizygotic twins and siblings, small differences in phenotype can become associated with reallocations of environmental resources within families. We show that phenotype-environment effects can account for age-related increases in rGE, rapid differentiation of siblings raised together, and widely reported increases in the heritability of behavior during childhood and adolescence.

Background: Many psychological traits become increasingly influenced by genetic factors throughout development, including several that might intuitively be seen as purely environmental characteristics. One such trait is the parent-child relationship, which is associated with a variety of socially significant outcomes, including mental health and criminal behavior. Genetic factors have been shown to partially underlie some of these associations, but the changing role of genetic influence over time remains poorly understood., Method: Over 1000 participants in a longitudinal twin study were assessed at three points across adolescence with a self-report measure regarding the levels of warmth and conflict in their relationships with their parents. These reports were analyzed with a biometric growth curve model to identify changes in genetic and environmental influences over time., Results: Genetic influence on the child-reported relationship with parent increased throughout adolescence, while the relationship's quality deteriorated. The increase in genetic influence resulted primarily from a positive association between genetic factors responsible for the initial relationship and those involved in change in the relationship over time. By contrast, environmental factors relating to change were negatively related to those involved in the initial relationship., Conclusions: The increasing genetic influence seems to be due to early genetic influences having greater freedom of expression over time whereas environmental circumstances were decreasingly important to variance in the parent-child relationship. We infer that the parent-child relationship may become increasingly influenced by the particular characteristics of the child (many of which are genetically influenced), gradually displacing the effects of parental or societal ideas of child rearing.

The behavior genetic literature suggests that genetically influenced characteristics of the child elicit specific behaviors from the parent. However, little is known about the processes by which genetically influenced child characteristics evoke parental responses. Interpersonal theory provides a useful framework for identifying reciprocal behavioral processes between children and mothers. The theory posits that, at any given moment, interpersonal behavior varies along the orthogonal dimensions of warmth and control and that the interpersonal behavior of one individual tends to elicit corresponding or contrasting behavior from the other (i.e., warmth elicits warmth, whereas control elicits submission). The current study thus examined these dimensions of interpersonal behavior as they relate to the parent-child relationship in 546 twin families. A computer joystick was used to rate videos of mother-child interactions in real time, yielding information on mother and child levels of warmth and control throughout the interaction. Analyses indicated that maternal control, but not maternal warmth, was influenced by evocative gene-environment correlational processes, such that genetic influences on maternal control and child control were largely overlapping. Moreover, these common genetic influences were present both cross-sectionally and over the course of the interaction. Such findings not only confirm the presence of evocative gene-environment correlational processes in the mother-child relationship but also illuminate at least one of the specific interpersonal behaviors that underlie this evocative process.

Semantic fluency was examined in Hebrew-speaking 5-year-old monozygotic and dizygotic twins (N = 396, 198 pairs), 22% of them with mother-reported speech-related problems. There were positive correlations of similar magnitudes among monozygotic, same-sex dizygotic, and opposite-sex dizygotic twins. Analyses showed no genetic effects, alongside significant shared (39%) and non-shared environmental (61%) effects on fluency scores. The presence of speech-related problems in one twin affected the fluency score of the co-twin. A multivariate regression analysis revealed that parental education and length of stay at daycare significantly predicted fluency scores. We suggest that semantic fluency performance is highly affected by environmental factors at age 5 although genetic effects might emerge later on., (© 2012 Blackwell Publishing Ltd.)

The present study is the first to disentangle the genetic and environmental influences on personality profile stability. Spanning a period of 10 years, we analyzed the etiology of 3 aspects of profile stability (overall profile stability, distinctive profile stability, and profile normativeness) using self- and peer reports from 539 identical and 280 fraternal twins reared together. This 3-wave multirater twin design allowed us to estimate the genetic and environmental effects on latent true scores of the 3 aspects of profile stability while controlling for method effects and random error. Consistent biometric results were only found for profile normativeness, whereas overall and distinctive profile stability scores turned out to be biased. Over time, we found personality profile normativeness to be relatively stable. This stability was due to both stable genetic and nonshared environmental effects, whereas innovative variance was completely explained by nonshared environmental effects. Our findings emphasize the importance of distinguishing between the different aspects of profile stability, since overall and distinctive stability scores are likely biased due to the normativeness problem. Yet indicating a person's similarity to the average person, the normativeness of a personality profile itself has a psychological meaning beyond socially desirable responding., (© 2011 The Authors. Journal of Personality © 2011, Wiley Periodicals, Inc.)

Behavioral genetic research has consistently revealed that approximately one-half of the variance in antisocial behaviors is attributable to genetic factors. Even so, there is some reason to believe that different types of antisocial behaviors may have different developmental etiologies. The current study used this possibility as a springboard to examine the genetic and environmental influences on admission of drug-selling behaviors. Analysis of twin pairs drawn from the National Longitudinal Study of Adolescent Health revealed that 38% of the variance in a continuously coded drug-selling variable was accounted for by genetic factors and 69% of the variance in a dichotomously coded drug-selling variable was the result of genetic factors. The remaining variance for both measures was explained by nonshared environmental factors. The implications that these results have for drug research are discussed and avenues for future research are offered., (Copyright © 2012 Elsevier Ltd. All rights reserved.)

Background: Reading disability (RD) and attention deficit/hyperactivity disorder (ADHD) are comorbid and genetically correlated, especially the inattentive dimension of ADHD (ADHD-I). However, previous research indicates that RD and ADHD enter into opposite gene by environment (G × E) interactions., Methods: This study used behavioral genetic methods to replicate these opposite G × E interactions in a sample of same-sex monozygotic and dizygotic twin pairs from the Colorado Learning Disabilities Research Center (CLDRC; DeFries et al., 1997) and to test a genetic hypothesis for why these opposite interactions occur., Results: We replicated opposite G × E interactions for RD (bioecological) and ADHD-I (diathesis-stress) with parental education in the same sample of participants. The genetic hypothesis for this opposite pattern of interactions is that only genes specific to each disorder enter into these opposite interactions, not the shared genes underlying their comorbidity. To test this hypothesis, we used single models with an exploratory three-way interaction, in which the G × E interactions for each disorder were moderated by comorbidity. Neither three-way interaction was significant. The heritability of RD did not vary as a function of parental education and ADHD-I. Similarly, the heritability of ADHD-I did not vary as a function of parental education and RD., Conclusions: We documented opposite G × E interactions in RD and ADHD-I in the same overall twin sample, but the explanation for this apparent paradox remains unclear. Examining specific genes and more specific environmental factors may help resolve the paradox., (© 2011 The Authors. Journal of Child Psychology and Psychiatry © 2011 Association for Child and Adolescent Mental Health.)

A critique of research examining whether early experiences with primary caregivers are reflected in adaptation is that relevant longitudinal studies have generally not employed genetically informed research designs capable of unconfounding shared genes and environments. Using the twin subsample (N = 485 pairs) of the Early Childhood Longitudinal Study-Birth Cohort, the current study provides evidence that early parental support (derived from observations at 24 months and around age 4, in prekindergarten) is associated with academic skills (r = .32), social competence (r = .15), and externalizing behavior (r = -.11) in kindergarten. Crucially, the shared environment accounted for virtually all of the correlation between parenting and academic skills, roughly half of the association between parenting and social competence, and approximately one fourth of the correlation between parenting and externalizing behavior., (© 2012 The Authors. Child Development © 2012 Society for Research in Child Development, Inc.)

The Simple View of Reading (SVR) in Chinese was examined in a genetically sensitive design. A total of 270 pairs of Chinese twins (190 pairs of monozygotic twins and 80 pairs of same-sex dizygotic twins) were tested on Chinese vocabulary and word reading at the mean age 7.8 years and reading comprehension of sentences and passages one year later. Results of behavior-genetic analyses showed that both vocabulary and word reading had significant independent genetic influences on reading comprehension, and the two factors together accounted for most but not all of the genetic influences on reading comprehension. In addition, sentence comprehension had a stronger genetic correlation with word reading while passage comprehension showed a trend of stronger genetic overlap with vocabulary. These findings suggest that the genetic foundation of the SVR in Chinese is largely supported in that language comprehension and decoding are two core skills for reading comprehension in nonalphabetic as well as alphabetic written languages.

A meta-analysis of twin, family and adoption studies was conducted to estimate the magnitude of genetic and environmental influences on impulsivity. The best fitting model for 41 key studies (58 independent samples from 14 month old infants to adults; N=27,147) included equal proportions of variance due to genetic (0.50) and non-shared environmental (0.50) influences, with genetic effects being both additive (0.38) and non-additive (0.12). Shared environmental effects were unimportant in explaining individual differences in impulsivity. Age, sex, and study design (twin vs. adoption) were all significant moderators of the magnitude of genetic and environmental influences on impulsivity. The relative contribution of genetic effects (broad sense heritability) and unique environmental effects were also found to be important throughout development from childhood to adulthood. Total genetic effects were found to be important for all ages, but appeared to be strongest in children. Analyses also demonstrated that genetic effects appeared to be stronger in males than in females. Method of assessment (laboratory tasks vs. questionnaires), however, was not a significant moderator of the genetic and environmental influences on impulsivity. These results provide a structured synthesis of existing behavior genetic studies on impulsivity by providing a clearer understanding of the relative genetic and environmental contributions in impulsive traits through various stages of development., (Copyright © 2011 Elsevier Ltd. All rights reserved.)

The degree to which child temperament moderates genetic and environmental contributions to parenting was examined. Participants were drawn from the Nonshared Environment and Adolescent Development project and included 720 sibling pairs, ages 13.5 + 2.0 years (Sibling 1) to 12.1 + 1.3 years (Sibling 2). The sample consisted of 6 sibling types: 93 monozygotic twin pairs, 99 dizygotic twin pairs, and 95 full sibling pairs from never-divorced families and 182 full-sibling, 109 half-sibling, and 130 unrelated-sibling pairs residing in stepfamilies. Composite child temperament ratings (negative emotionality, activity, shyness, and sociability) were derived from mothers' and fathers' reports. Composite parenting ratings (negativity, warmth) for mothers and fathers were generated from children's and parents' reports. Analyses indicated that at higher levels of negative emotionality and sociability, child-based genetic contributions to mothers' and fathers' negativity increased, whereas the contributions of environmental factors declined. The opposite pattern was observed for child shyness. These same characteristics had less impact on parental warmth. For fathers only, nonshared environmental contributions to fathers' warmth increased in the presence of high child activity and sociability but declined when children were very shy. Overall these findings indicate that child-based effects on negative parenting are enhanced when children demonstrate potentially challenging characteristics but are weaker in the absence of such characteristics., ((c) 2011 APA, all rights reserved.)

Sex differences in the genetic and environmental influences on childhood conduct disorder and adult antisocial behavior were examined in a large community sample of 6,383 adult male, female, and opposite-sex twins. Retrospective reports of childhood conduct disorder (prior to 18 years of age) were obtained when participants were approximately 30 years old, and lifetime reports of adult antisocial behavior (antisocial behavior after 17 years of age) were obtained 8 years later. Results revealed that either the genetic or the shared environmental factors influencing childhood conduct disorder differed for males and females (i.e., a qualitative sex difference), but by adulthood, these sex-specific influences on antisocial behavior were no longer apparent. Further, genetic and environmental influences accounted for proportionally the same amount of variance in antisocial behavior for males and females in childhood and adulthood (i.e., there were no quantitative sex differences). Additionally, the stability of antisocial behavior from childhood to adulthood was slightly greater for males than females. Though familial factors accounted for more of the stability of antisocial behavior for males than females, genetic factors accounted for the majority of the covariation between childhood conduct disorder and adult antisocial behavior for both sexes. The genetic influences on adult antisocial behavior overlapped completely with the genetic influences on childhood conduct disorder for both males and females. Implications for future twin and molecular genetic studies are discussed.

Aims: Previous studies have found inverse associations between intelligence quotient (IQ) and cigarette smoking, but the causal pathways linking IQ with smoking status and nicotine dependence (ND) are not well understood. The aim of this study was to explore the associations between IQ and ND using a genetically informative twin design to detect whether any association is because of shared genetic or environmental factors., Design: A population-based twin cohort with IQ measured in adolescence and ND later in life, analysed by classical twin modeling based on linear structural equations., Setting: Swedish national registry data., Participants: A total of 5040 male twins born 1951-84., Measurements: IQ was measured at military conscription at a mean age of 18 years. ND was self-reported at the ages of 22-57 years using the Fagerström Test for ND scale (FTND). Both cigarette smoking and Swedish snus use were analysed., Findings: Both IQ and ND showed moderate heritability (0.58 and 0.39, respectively). The heritability of ND was similar for cigarette smoking and snus use. The phenotypic correlation between IQ and ND was weak: -0.11 (-0.16, -0.06) for total ND. Bivariate analysis revealed that this correlation was mainly because of genetic factors, but still the genetic correlation between IQ and ND from cigarette smoking was only -0.24., Conclusions: Nicotine dependence, as measured by the Fagerström Test for Nicotine Dependence, shows moderate heritability in both smokers and snus users but is only weakly associated with intelligence quotient; common genetic factors underlying nicotine dependence and intelligence quotient probably account for little of the observed association between smoking and intelligence quotient., (© 2011 The Authors, Addiction © 2011 Society for the Study of Addiction.)

In this first investigation of genetic and environmental influences on children's values, 271 German twin pairs (50.2% boys) reported their values at ages 7-11 years using the Portrait Values Questionnaire (Schwartz & Rubel, 2005). We distinguished between gender-neutral (conservation vs. openness to change) and gender-typed (self-transcendence vs. self-enhancement) values. Boys differed from girls in the importance given to gender-typed benevolence, achievement, and power values. Gender-neutral values showed moderate (.34) and gender-typed values showed higher (.49) heritability, with nonshared environment and error accounting for the remaining variance. For both sexes, substantial genetic effects accounted for the importance children gave to their respective gender-stereotypical end of the self-transcendence versus self-enhancement dimension. However, dramatic sex differences emerged in the gender-atypical end of the distribution. For girls, low self-transcendence (high gender-atypical values) showed a large (.76) group heritability. For boys, gender-atypical values (high self-transcendence) showed no heritability and a modest (.10) shared environment effect., ((c) 2011 APA, all rights reserved.)

Research has documented associations between family functioning and offspring psychosocial adjustment, but questions remain regarding whether these associations are partly due to confounding genetic factors and other environmental factors. The current study used a genetically informed approach, the Children of Twins design, to explore the associations between family functioning (family conflict, marital quality, and agreement about parenting) and offspring psychopathology. Participants were 867 twin pairs (388 monozygotic; 479 dizygotic) from the Twin and Offspring Study in Sweden, their spouses, and children (51.7% female; M = 15.75 years). The results suggested associations between exposure to family conflict (assessed by the mother, father, and child) and child adjustment were independent of genetic factors and other environmental factors. However, when family conflict was assessed using only children's reports, the results indicated that genetic factors also influenced these associations. In addition, the analyses indicated that exposure to low marital quality and agreement about parenting was associated with children's internalizing and externalizing problems and that genetic factors also contributed to the associations of marital quality and agreement about parenting with offspring externalizing problems., ((c) 2011 APA, all rights reserved.)