@article {274, title = {Aggressive behaviour in childhood and adolescence: the role of smoking during pregnancy, evidence from four twin cohorts in the EU-ACTION consortium}, journal = {Psychological Medicine}, year = {2018}, pages = {1{\textendash}9}, abstract = {

BACKGROUND:

Maternal smoking during pregnancy (MSDP) has been linked to offspring\&$\#$39;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.

METHODS:

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.

RESULTS:

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.

CONCLUSIONS:

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\&$\#$39; aggressive behaviour.

}, doi = {10.1017/S0033291718001344}, author = {Malanchini, Margherita and Emily Smith-Woolley and Ayorech, Ziada and Kaili Rimfeld and Eva Krapohl and Vuoksimaa, Eero and Korhonen, Tellervo and Meike Bartels and van Beijsterveldt, Toos C.E.M. and Richard J. Rose and et al.} } @article {259, title = {Differences in exam performance between pupils attending selective and non-selective schools mirror the genetic differences between them}, volume = {3}, year = {2018}, month = {2018/03/23}, pages = {3}, abstract = {

On average, students attending selective schools outperform their non-selective counterparts in national exams. These differences are often attributed to value added by the school, as well as factors schools use to select pupils, including ability, achievement and, in cases where schools charge tuition fees or are located in affluent areas, socioeconomic status. However, the possible role of DNA differences between students of different schools types has not yet been considered. We used a UK-representative sample of 4814 genotyped students to investigate exam performance at age 16 and genetic differences between students in three school types: state-funded, non-selective schools (\‘non-selective\’), state-funded, selective schools (\‘grammar\’) and private schools, which are selective (\‘private\’). We created a genome-wide polygenic score (GPS) derived from a genome-wide association study of years of education (EduYears). We found substantial mean genetic differences between students of different school types: students in non-selective schools had lower EduYears GPS compared to those in grammar (d\ =\ 0.41) and private schools (d\ =\ 0.37). Three times as many students in the top EduYears GPS decile went to a selective school compared to the bottom decile. These results were mirrored in the exam differences between school types. However, once we controlled for factors involved in pupil selection, there were no significant genetic differences between school types, and the variance in exam scores at age 16 explained by school type dropped from 7\% to \<1\%. These results show that genetic and exam differences between school types are primarily due to the heritable characteristics involved in pupil admission.

}, isbn = {2056-7936}, url = {https://doi.org/10.1038/s41539-018-0019-8}, author = {Emily Smith-Woolley and Pingault, Jean-Baptiste and Saskia Selzam and Kaili Rimfeld and Eva Krapohl and Sophie von Stumm and Asbury, Kathryn and Philip S. Dale and Young, Toby and Allen, Rebecca and Yulia Kovas and Robert Plomin} } @article {279, title = {The genetics of university success}, volume = {8}, year = {2018}, month = {2018/10/18}, pages = {14579}, abstract = {

University success, which includes enrolment in and achievement at university, as well as quality of the university, have all been linked to later earnings, health and wellbeing. However, little is known about the causes and correlates of differences in university-level outcomes. Capitalizing on both quantitative and molecular genetic data, we perform the first genetically sensitive investigation of university success with a UK-representative sample of 3,000 genotyped individuals and 3,000 twin pairs. Twin analyses indicate substantial additive genetic influence on university entrance exam achievement (57\%), university enrolment (51\%), university quality (57\%) and university achievement (46\%). We find that environmental effects tend to be non-shared, although the shared environment is substantial for university enrolment. Furthermore, using multivariate twin analysis, we show moderate to high genetic correlations between university success variables (0.27\–0.76). Analyses using DNA alone also support genetic influence on university success. Indeed, a genome-wide polygenic score, derived from a 2016 genome-wide association study of years of education, predicts up to 5\% of the variance in each university success variable. These findings suggest young adults select and modify their educational experiences in part based on their genetic propensities and highlight the potential for DNA-based predictions of real-world outcomes, which will continue to increase in predictive power.

}, isbn = {2045-2322}, url = {https://doi.org/10.1038/s41598-018-32621-w}, author = {Emily Smith-Woolley and Ayorech, Ziada and Philip S. Dale and Sophie von Stumm and Robert Plomin} } @article {198, title = {Weak associations between pubertal development and psychiatric and behavioral problems}, journal = {Translational Psychiatry}, volume = {7}, year = {2017}, month = {2017/04/}, pages = {e1098 - }, abstract = {

Pubertal development has been associated with adverse outcomes throughout adolescence and adulthood. However, much of the previous literature has categorized outcome variables and pubertal timing measures for ease of mean difference or odds ratio interpretation. We use a UK-representative sample of over 5000 individuals drawn from the Twins Early Development Study to extend this literature by adopting an individual differences approach and emphasizing effect sizes. We investigate a variety of psychiatric and behavioral measures collected longitudinally at ages 11, 14 and 16, for multiple raters and for males and females separately. In addition, we use two measures of pubertal development: the Pubertal Development Scale at each age, as well as the age of menarche for girls. We found that pubertal development, however assessed, was linearly associated with a range of psychiatric and behavioral outcomes; however, the effect sizes of these associations were modest for both males and females with most correlations between \−0.10 and 0.10. Our systematic analysis of associations between pubertal development, and psychiatric and behavioral problems is the most comprehensive to date. The results showing linearity of the effects of pubertal development support an individual differences approach, treating both pubertal development and associated outcomes as continuous rather than categorical variables. We conclude that pubertal development explains little variance in psychiatric and behavioral outcomes (\<1\% on average). The small effect sizes indicate that the associations are weak and should not warrant major concern at least in non-clinical populations.

}, isbn = {2158-3188}, url = {http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5416703/}, author = {Emily Smith-Woolley and Kaili Rimfeld and Robert Plomin} } @article {196, title = {Publication Trends Over 55 Years of Behavioral Genetic Research}, journal = {Behavior Genetics}, volume = {46}, year = {2016}, month = {Sep}, pages = {603{\textendash}607}, abstract = {

We document the growth in published papers on behavioral genetics for 5-year intervals from 1960 through 2014. We used 1861 papers published in Behavior Genetics to train our search strategy which, when applied to Ovid PsychINFO, selected more than 45,000 publications. Five trends stand out: (1) the number of behavioral genetic publications has grown enormously; nearly 20,000 papers were published in 2010\–2014. (2) The number of human quantitative genetic (QG) publications (e.g., twin and adoption studies) has steadily increased with more than 3000 papers published in 2010\–2014. (3) The number of human molecular genetic (MG) publications increased substantially from about 2000 in 2000\–2004 to 5000 in 2005\–2009 to 9000 in 2010\–2014. (4) Nonhuman publications yielded similar trends. (5) Although there has been exponential growth in MG publications, both human and nonhuman QG publications continue to grow. A searchable resource of this corpus of behavioral genetic papers is freely available online at http://www.teds.ac.uk/public{\_}datasets.html and will be updated annually.

}, issn = {1573-3297}, doi = {10.1007/s10519-016-9786-2}, url = {https://doi.org/10.1007/s10519-016-9786-2}, author = {Ayorech, Ziada and Saskia Selzam and Emily Smith-Woolley and Knopik, Valerie S. and Neiderhiser, Jenae M. and John C DeFries and Robert Plomin} }