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Background: Parental criticism is correlated with internalising symptoms in adolescent offspring. This correlation could in part reflect their genetic relatedness, if the same genes influence behaviours in both parents and offspring. We use a Children‐of‐Twins design to assess whether parent‐reported criticism and offspring internalising symptoms remain associated after controlling for shared genes. To aid interpretation of our results and those of previous Children‐of‐Twins studies, we examine statistical power for the detection of genetic effects and explore the direction of possible causal effects between generations. Methods: Data were drawn from two Swedish twin samples, comprising 876 adult twin pairs with adolescent offspring and 1,030 adolescent twin pairs with parents. Parent reports of criticism towards their offspring were collected concurrently with parent and offspring reports of adolescent internalising symptoms. Children‐of‐Twins structural equation models were used to control for genetic influence on the intergenerational association between parental criticism and adolescent internalising. Results: Parental criticism was associated with adolescent internalising symptoms after controlling for genetic influence. No significant role was found for shared genes influencing phenotypes in both generations, although power analyses suggested that some genetic effects may have gone undetected. Models could not distinguish directionality for nongenetic, causal effects between generations. Conclusions: Parental criticism may be involved in psychosocial family processes in the context of adolescent internalising. Future studies should seek to identify these processes and provide clarity on the direction of potential causal effects. [ABSTRACT FROM AUTHOR]

Background: Low self-worth during adolescence predicts a range of emotional and behavioural problems. As such, identifying potential sources of influence on self-worth is important. Aspects of the parent-child relationship are often associated with adolescent self-worth but to date it is unclear whether such associations may be attributable to familial confounding (e.g. genetic relatedness). We set out to clarify the nature of relationships between parental expressed affection and adolescent self-worth, and parent-child closeness and adolescent self-worth. Methods: We used data from the Twin and Offspring Study in Sweden, a children-of-twins sample comprising 909 adult twin pairs with adolescent children. Using these data we were able to apply structural equation models with which we could examine whether associations remained after accounting for genetic transmission. Results: Results demonstrated that parent-child closeness and parental-expressed affection were both phenotypically associated with adolescent self-worth. Associations could not be attributed to genetic relatedness between parent and child. Conclusions: Parent-child closeness and parental affection are associated with adolescent self-worth above and beyond effects attributable to genetic relatedness. Data were cross-sectional, so the direction of effects cannot be confirmed but findings support the notion that positive parent-child relationships increase adolescent self-worth. [ABSTRACT FROM AUTHOR]

Background Although many children with autism spectrum disorders ( ASDs) experience difficulties with anxiety, the manifestation of these difficulties remains unresolved. The current study assessed anxiety in a large population-based twin sample, aged 10-15 years. Phenotypic analyses were used to explore anxiety symptoms in children with ASDs, their unaffected co-twins and a control sample. Methods Participants included 146 families from the Twins Early Development Study ( TEDS) where one or both children had a suspected ASD. Eighty control families were also included. The Revised Child Anxiety and Depression scale (Chorpita, Yim, Moffitt, Umemoto & Francis, 2000) was completed (self- and parent-report), along with diagnostic and cognitive tests. Children were categorized into four groups (a) ASD (b) Broader Autism Phenotype ( BAP: mainly co-twins of children with ASDs, with high subclinical autistic traits) (c) unaffected co-twins (with neither ASDs nor BAP) (d) controls. Results Children in the ASD and BAP groups scored significantly higher than controls for all parent-rated (although not child-rated) anxiety subscales. There were no significant differences between the ASD and BAP groups for any of the parent-rated anxiety subscales. Compared with controls, unaffected co-twins showed significantly heightened Social Anxiety, Generalized Anxiety, and Panic symptoms. Significant associations were observed between certain anxiety subscales and both IQ and ASD symptoms. For example, greater parent-rated Social Anxiety was associated with higher IQ and increased social and communicative impairments. Significant interrater correlations were observed for anxiety reports in children with ASDs ( r = .27-.54; p < .01), their unaffected co-twins ( r = .32-.63; p < .01) and controls ( r = .23-.43; p < .01) suggesting that children in this sample with and without ASD symptoms were able to report on their anxiety symptoms with some accuracy. Conclusions These findings support previous reports of heightened anxiety in children with ASDs, at least on parent-reported measures. Unaffected co-twins of children with ASDs also showed increased anxiety, generating questions about the potential etiological overlap between ASDs and anxiety. Progress in this area now depends on more refined anxiety measurement in ASDs and continued investigation of interrater differences. [ABSTRACT FROM AUTHOR]

Multivariate genetic studies have revealed genetic correlations between antisocial behavior ( ASB) and substance use ( SU). However, ASB is heterogeneous, and it remains unclear whether all forms are similarly related to SU. The present study examines links between cannabis use, alcohol consumption, and aggressive and delinquent forms of ASB using a behavioral genetic approach. Participants were 1,688 adolescents (482 monozygotic twins, 852 dizygotic twins, and 354 nontwin siblings) aged 15-23 years old ( M = 16.91), sampled from the community in the U.K. Multivariate model fitting revealed that the genetic components of alcohol consumption and cannabis use correlated with those of both aggression (.21 and .49, respectively) and delinquency (.35 and .69, respectively). Results suggest that both aggression and delinquency have genetic effects in common with alcohol consumption and cannabis use. [ABSTRACT FROM AUTHOR]

Alcohol use motives are closely associated with specific profiles of alcohol use and reflect a subjectively derived decisional framework based on a motivational style of responding. Adult twin studies typically estimate the heritability of alcohol use motives to be between 7 and 42%, although relatively little is known about genetic and environmental influences upon alcohol use motives in adolescence. Latent class analysis (LCA) models containing 1 through 5 classes were fitted to the data derived from 1,422 adolescent twin and siblings self-reported alcohol use motives. Using twin models, we estimated the genetic, shared, and nonshared environmental influences to the class membership data derived from the LCA. Four drinking motives classes were identified (family-oriented, social, enhancement/social, and coping/social). The coping/social and enhancement/social classes were differentiated from the social class on measures of depression, delinquency, and aggressive behavior. Analyses indicated that nonadditive genetic factors accounted for 76% of the variance in the coping/social motives class and additive genetic influences accounted for 66% of the variance in the social motives class. There was a moderate contribution of genetic factors and shared environmental factors influencing class membership of enhancement/social motivated drinkers (28 and 20% explained variance, respectively). Substantial shared environmental influences were revealed for membership of the family-oriented class (75%). Heritable influences may predispose individuals to drink to cope with negative affect, for social reasons, and to a lesser extent for enhancement. Familial environmental influences shape family-oriented motives for drinking in adolescents. [ABSTRACT FROM AUTHOR]

Altruistic behaviour raises major questions for psychology and biology. One hypothesis proposes that human altruistic behaviour evolved as a result of sexual selection. Mechanisms that seek to explain how sexual selection works suggest genetic influence acting on both the mate preference for the trait and the preferred trait itself. We used a twin study to estimate whether genetic effects influenced responses to psychometric scales measuring mate preference towards altruistic traits (MPAT) and the preferred trait (i.e., 'altruistic personality'). As predicted, we found significant genetic effects influencing variation in both. We also predicted that individuals expressing stronger MPAT and 'altruistic personality' would have mated at a greater frequency in ancestral populations.We found evidence for this in that 67% of the covariance in the phenotypic correlation between the two scales was associated with significant genetic effects. Both sets of findings are thus consistent with the hypothesized link between sexual selection and human altruism towards non-kin. We discuss how this study contributes to our understanding of altruistic behaviour and how further work might extend this understanding. [ABSTRACT FROM AUTHOR]

Background: Antisocial behaviour is often comorbid with depressed mood but is itself a collection of heterogeneous behaviours. Using a genetically informative design, we examine heterogeneity in antisocial behaviour and overlaps between different forms of antisocial behaviour with depressed mood. Methods: Data were drawn from the G1219 large-scale community sample containing self-report questionnaire data from 941 twin pairs and 328 sibling-pairs aged 12–21 years. Results: Inter-correlations among oppositionality, physical aggression and delinquency, and between the antisocial subscales and depressed mood, were mediated by genetic and non-shared environmental influences. Genetic factors generally contributed more to the correlations than the non-shared environment. Conclusions: These results indicate that many genetic and non-shared environmental influences were common to all the traits studied, but there was also evidence for trait-specific effects. [ABSTRACT FROM AUTHOR]

Imitation, vocabulary, pretend play, and socially insightful behavior were investigated in 5,206 same- and opposite-sex 2-year-old twin pairs in the United Kingdom. Individual differences in imitative ability were due to modest heritability (30%), while environmental factors shared between twins (42%) and unique to each twin (28%) also made significant contributions to the variance. Imitation correlated significantly, although modestly, with vocabulary, pretend play, and socially insightful behavior, and the strongest relationship was with vocabulary. A model that represented the covariance between the variables as being due to correlated latent genetic and environmental factors fitted the data well, with shared environmental factors influencing most of the covariance. Parents who encourage imitation may also tend to foster the development of language, pretence, and socially insightful behavior. [ABSTRACT FROM AUTHOR]

Background: Early childhood antisocial behaviour is a strong prognostic indicator for poor adult mental health. Thus, information about its etiology is needed. Genetic etiology is unknown because most research with young children focuses on environmental risk factors, and the few existing studies of young twins used only mothers' reports of behaviour, which may be biased. Method: We investigated genetic influences on antisocial behaviour in a representative-plus-high-risk sample of 1116 pairs of 5-year-old twins using data from four independent sources: mothers, teachers, examiner-observers previously unacquainted with the children, and the children themselves. Results: Children's antisocial behaviour was reliably measured by all four informants; no bias was detected in mothers', teachers', examiners', or children's reports. Variation in antisocial behaviour that was agreed upon by all informants, and thus was pervasive across settings, was influenced by genetic factors (82%) and experiences specific to each child (18%). Variation in antisocial behaviour that was specific to each informant was meaningful variation, as it was also influenced by genetic factors (from 33% for the children's report to 71% for the teachers' report). Conclusions: This study and four others of very young twins show that genetic risks contribute strongly to population variation in antisocial behaviour that emerges in early childhood. In contrast, genetic risk is known to be relatively modest for adolescent antisocial behaviour, suggesting that the early-childhood form has a distinct etiology, particularly if it is pervasive across situations. [ABSTRACT FROM AUTHOR]

A correction to the article "Infants' Use of Shared Linguistics Information to Clarify Ambiguous Requests," that was published in the May/June 2007 issue is presented.

Previous studies have found heterogeneous association between DAT1-3'-UTR-VNTR and attention deficit hyperactivity disorder (ADHD). Various proportions of conduct disorder (CD) comorbidity in their ADHD samples may partially explain the observational discrepancies. Evidence for this comes from family and twin studies which found ADHD probands with CD (ADHD + CD) are genetically different from those without CD (ADHD - CD). Genotypes of 20 DAT1 markers were analyzed in 576 trios, consisting of 141 ADHD + CD and 435 ADHD - CD. In addition to the classical TDT test, a specific genetic heterogeneity test was performed to identify variants that have different transmission patterns in the two phenotypic subgroups. After multiple-test correction, rs40184 and rs2652511 were significant in TDT tests. Further heterogeneity test found the two SNPs had a significant transmission pattern difference between ADHD + CD and ADHD - CD children, indicating that DAT1 has a significantly greater genetic influence on ADHD without CD. Although the result needs further replications, it does highlight the importance of selecting genetically homogeneous samples for molecular genetic analyses of ADHD., (Copyright 2007 Wiley-Liss, Inc.)

We are taking a quantitative trait approach to the molecular genetic study of attention deficit hyperactivity disorder (ADHD) using a truncated case-control association design. An epidemiological sample of children aged 5 to 15 years was evaluated for symptoms of ADHD using a parent rating scale. Individuals scoring high or low on this scale were selected for further investigation with additional questionnaires and DNA analysis. Data in studies like this are typically complicated. In the study reported on here, individuals have from 1 to 4 questionnaires completed on them and the sample is composed of a mixture of singletons and siblings. In this paper, we describe how we used a genetic hierarchical model to fit our data, together with a twin dataset, in order to estimate genetic factor loadings. Correlation matrices were estimated for our data using a maximum likelihood approach to account for missing data. We describe how we used these results to create a composite score, the heritability of which was estimated to be acceptably high using the twin dataset. This score measures a quantitative dimension onto which molecular genetic data will be mapped., (Copyright 2003 Wiley-Liss, Inc.)