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      Aggressive behaviour in childhood and adolescence: the role of smoking during pregnancy, evidence from four twin cohorts in the EU-ACTION consortium

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          Maternal smoking during pregnancy (MSDP) has been linked to offspring's externalizing problems. It has been argued that socio-demographic factors (e.g. maternal age and education), co-occurring environmental risk factors, or pleiotropic genetic effects may account for the association between MSDP and later outcomes. This study provides a comprehensive investigation of the association between MSDP and a single harmonized component of externalizing: aggressive behaviour, measured throughout childhood and adolescence.


          Data came from four prospective twin cohorts – Twins Early Development Study, Netherlands Twin Register, Childhood and Adolescent Twin Study of Sweden, and FinnTwin12 study – who collaborate in the EU-ACTION consortium. Data from 30 708 unrelated individuals were analysed. Based on item level data, a harmonized measure of aggression was created at ages 9–10; 12; 14–15 and 16–18.


          MSDP predicted aggression in childhood and adolescence. A meta-analysis across the four samples found the independent effect of MSDP to be 0.4% ( r = 0.066), this remained consistent when analyses were performed separately by sex. All other perinatal factors combined explained 1.1% of the variance in aggression across all ages and samples ( r = 0.112). Paternal smoking and aggressive parenting strategies did not account for the MSDP-aggression association, consistent with the hypothesis of a small direct link between MSDP and aggression.


          Perinatal factors, including MSDP, account for a small portion of the variance in aggression in childhood and adolescence. Later experiences may play a greater role in shaping adolescents’ aggressive behaviour.

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          Most cited references 42

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          Social-information-processing factors in reactive and proactive aggression in children's peer groups.

          We examined social-information-processing mechanisms (e.g., hostile attributional biases and intention-cue detection deficits) in chronic reactive and proactive aggressive behavior in children's peer groups. In Study 1, a teacher-rating instrument was developed to assess these behaviors in elementary school children (N = 259). Reactive and proactive scales were found to be internally consistent, and factor analyses partially supported convergent and discriminant validities. In Study 2, behavioral correlates of these forms of aggression were examined through assessments by peers (N = 339). Both types of aggression related to social rejection, but only proactively aggressive boys were also viewed as leaders and as having a sense of humor. In Study 3, we hypothesized that reactive aggression (but not proactive aggression) would occur as a function of hostile attributional biases and intention-cue detection deficits. Four groups of socially rejected boys (reactive aggressive, proactive aggressive, reactive-proactive aggressive, and nonaggressive) and a group of average boys were presented with a series of hypothetical videorecorded vignettes depicting provocations by peers and were asked to interpret the intentions of the provocateur (N = 117). Only the two reactive-aggressive groups displayed biases and deficits in interpretations. In Study 4, attributional biases and deficits were found to be positively correlated with the rate of reactive aggression (but not proactive aggression) displayed in free play with peers (N = 127). These studies supported the hypothesis that attributional biases and deficits are related to reactive aggression but not to proactive aggression.
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            The Child and Adolescent Twin Study in Sweden (CATSS).

            The Child and Adolescent Twin Study in Sweden (CATSS) is an ongoing longitudinal twin study targeting all twins born in Sweden since July 1, 1992. Since 2004, parents of twins are interviewed regarding the children's somatic and mental health and social environment in connection with their 9th or 12th birthdays (CATSS-9/12). By January 2010, 8,610 parental interviews concerning 17,220 twins had been completed, with an overall response rate of 80%. At age 15 (CATSS-15) and 18 (CATSS-18), twins and parents complete questionnaires that, in addition to assessments of somatic and mental health, include measures of personality development and psychosocial adaptation. Twin pairs in CATSS-9/12 with one or both twins screening positive for autism spectrum disorders, attention deficit/hyperactivity disorder, tic disorders, developmental coordination disorder, learning disorders, oppositional defiant disorder, conduct disorder, obsessive-compulsive disorder, and/or eating problems have been followed with in-depth questionnaires on family, social environment and personality, and subsequently by clinical assessments at age 15 together with randomly selected population controls, including 195 clinically assessed twin pairs from the first 2 year cohorts (CATSS-15/DOGSS). This article describes the cohorts and study groups, data collection, and measures used. Prevalences, distributions, heritability estimates, ages at onset, and sex differences of mental health problems in the CATSS-9/12, that were analyzed and found to be overall comparable to those of other clinical and epidemiological studies. The CATSS study has the potential of answering important questions on the etiology of childhood mental health problems and their role in the development of later adjustment problems.
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              The epigenetics of maternal cigarette smoking during pregnancy and effects on child development.

              The period of in utero development is one of the most critical windows during which adverse intrauterine conditions and exposures can influence the growth and development of the fetus as well as the child's future postnatal health and behavior. Maternal cigarette smoking during pregnancy remains a relatively common but nonetheless hazardous in utero exposure. Previous studies have associated prenatal smoke exposure with reduced birth weight, poor developmental and psychological outcomes, and increased risk for diseases and behavioral disorders later in life. Researchers are now learning that many of the mechanisms whereby maternal smoke exposure may affect key pathways crucial for proper fetal growth and development are epigenetic in nature. Maternal cigarette smoking during pregnancy has been associated with altered DNA methylation and dysregulated expression of microRNA, but a deeper understanding of the epigenetics of maternal cigarette smoking during pregnancy as well as how these epigenetic changes may affect later health and behavior remain to be elucidated. This article seeks to explore many of the previously described epigenetic alterations associated with maternal cigarette smoking during pregnancy and assess how such changes may have consequences for both fetal growth and development, as well as later child health, behavior, and well-being. We also outline future directions for this new and exciting field of research.

                Author and article information

                Psychol Med
                Psychol Med
                Psychological Medicine
                Cambridge University Press (Cambridge, UK )
                March 2019
                11 June 2018
                : 49
                : 4
                : 646-654
                [1 ]Social Genetic and Developmental Psychiatry Centre, King's College London , United Kingdom
                [2 ]Department of Psychology, University of Texas at Austin , United States
                [3 ]Institute for Molecular Medicine FIMM, University of Helsinki , Finland
                [4 ]Department of Biological Psychology, Netherlands Twin Register, Vrije Universiteit , Amsterdam, The Netherlands
                [5 ]Department of Psychological and Brain Sciences, Indiana University , United States
                [6 ]Centre for Ethics, Law and Mental Health and the Gillberg Neuropsychiatry Centre, Gothenburg University , Sweden
                [7 ]Department of Public Health, University of Helsinki , Helsinki, Finland
                [8 ]Department of Medical Epidemiology and Biostatistics, Karolinska Institutet , Sweden
                Author notes
                Author for correspondence: Margherita Malanchini, E-mail: m.malanchini@ , margherita.malanchini@
                S0033291718001344 00134
                © Cambridge University Press 2018

                This is an Open Access article, distributed under the terms of the Creative Commons Attribution licence (, which permits unrestricted re-use, distribution, and reproduction in any medium, provided the original work is properly cited.

                Page count
                Figures: 1, Tables: 2, References: 55, Pages: 9
                Original Articles


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