@article {464, title = {Multivariate genetic structure of externalizing behavior and structural brain development in a longitudinal adolescent twin sample}, journal = {International Journal of Molecular Sciences}, volume = {23}, year = {2022}, pages = {3176}, abstract = {

Externalizing behavior in its more extreme form is often considered a problem to the individual, their families, teachers, and society as a whole. Several brain structures have been linked to externalizing behavior and such associations may arise if the (co)development of externalizing behavior and brain structures share the same genetic and/or environmental factor(s). We assessed externalizing behavior with the Child Behavior Checklist and Youth Self Report, and the brain volumes and white matter integrity (fractional anisotropy [FA] and mean diffusivity [MD]) with magnetic resonance imaging in the BrainSCALE cohort, which consisted of twins and their older siblings from 112 families measured longitudinally at ages 10, 13, and 18 years for the twins. Genetic covariance modeling based on the classical twin design, extended to also include siblings of twins, showed that genes influence externalizing behavior and changes therein (h2 up to 88\%). More pronounced externalizing behavior was associated with higher FA (observed correlation rph up to +0.20) and lower MD (rph up to -0.20), with sizeable genetic correlations (FA ra up to +0.42; MD ra up to -0.33). The cortical gray matter (CGM; rph up to -0.20) and cerebral white matter (CWM; rph up to +0.20) volume were phenotypically but not genetically associated with externalizing behavior. These results suggest a potential mediating role for global brain structures in the display of externalizing behavior during adolescence that are both partially explained by the influence of the same genetic factor.

}, keywords = {Adolescence, externalizing behavior, Genetic correlation, gray matter volume, heritability, longitudinal, magnetic resonance imaging, white matter integrity}, doi = {10.3390/ijms23063176}, author = {Teeuw, Jalmar and Klein, Marieke and Mota, Nina Roth and Brouwer, Rachel M and van {\textquoteright}t Ent, Dennis and Al-Hassaan, Zyneb and Franke, Barbara and Boomsma, Dorret I and Hulshoff Pol, Hilleke E} } @article {416, title = {The Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia: design, results and future prospects}, journal = {European Journal of Epidemiology}, volume = {34}, year = {2019}, pages = {279{\textendash}300}, abstract = {

The impact of many unfavorable childhood traits or diseases, such as low birth weight and mental disorders, is not limited to childhood and adolescence, as they are also associated with poor outcomes in adulthood, such as cardiovascular disease. Insight into the genetic etiology of childhood and adolescent traits and disorders may therefore provide new perspectives, not only on how to improve wellbeing during childhood, but also how to prevent later adverse outcomes. To achieve the sample sizes required for genetic research, the Early Growth Genetics (EGG) and EArly Genetics and Lifecourse Epidemiology (EAGLE) consortia were established. The majority of the participating cohorts are longitudinal population-based samples, but other cohorts with data on early childhood phenotypes are also involved. Cohorts often have a broad focus and collect(ed) data on various somatic and psychiatric traits as well as environmental factors. Genetic variants have been successfully identified for multiple traits, for example, birth weight, atopic dermatitis, childhood BMI, allergic sensitization, and pubertal growth. Furthermore, the results have shown that genetic factors also partly underlie the association with adult traits. As sample sizes are still increasing, it is expected that future analyses will identify additional variants. This, in combination with the development of innovative statistical methods, will provide detailed insight on the mechanisms underlying the transition from childhood to adult disorders. Both consortia welcome new collaborations. Policies and contact details are available from the corresponding authors of this manuscript and/or the consortium websites.

}, keywords = {Childhood traits and disorders, Consortium, genetics, longitudinal}, doi = {10.1007/s10654-019-00502-9}, author = {Middeldorp, Christel M and Felix, Janine F and Mahajan, Anubha and EArly Genetics Lifecourse Epidemiology (EAGLE) consortium and Early Growth Genetics (EGG) consortium and McCarthy, Mark I} } @article {406, title = {Do parental psychiatric symptoms predict outcome in children with psychiatric disorders? A naturalistic clinical study}, journal = {Journal of the American Academy of Child \& Adolescent Psychiatry}, volume = {57}, year = {2018}, pages = {669{\textendash}677.e6}, abstract = {

OBJECTIVE: Parental psychiatric symptoms can negatively affect the outcome of children\&$\#$39;s psychopathology. Studies thus far have mainly shown a negative effect of maternal depression. This study examined the associations between a broad range of psychiatric symptoms in mothers and fathers and the child\&$\#$39;s outcome.

METHOD: Internalizing and externalizing psychiatric symptoms were assessed in 742 mothers, 440 fathers, and their 811 children at the first evaluation in 3 child and adolescent psychiatric outpatient clinics and at follow-up (on average 1.7 years later). Predictions of child\&$\#$39;s symptoms scores were tested at follow-up by parental symptom scores at baseline, parental scores at follow-up, and offspring scores at baseline.

RESULTS: Children whose mother or father scored above the (sub)clinical threshold for psychiatric symptoms at baseline had higher symptom scores at baseline and at follow-up. Offspring follow-up scores were most strongly predicted by offspring baseline scores, in addition to parental psychiatric symptoms at follow-up. Offspring symptom scores at follow-up generally were not predicted by parental scores at baseline. Maternal and paternal associations were of similar magnitude.

CONCLUSION: Higher symptom scores at follow-up in children of parents with psychopathology were mainly explained by higher symptom scores at baseline. Continuing parent-offspring associations could be a result of reciprocal effects, ie, parental symptoms influencing offspring symptoms and offspring symptoms influencing parental symptoms. Nevertheless, the results show that these children are at risk for persisting symptoms, possibly indicating the need to treat maternal and paternal psychopathology.

}, keywords = {child psychopathology, longitudinal, Parent-offspring associations, Parental psychopathology}, doi = {10.1016/j.jaac.2018.05.017}, author = {Wesseldijk, Laura W and Dieleman, Gwen C and van Steensel, Francisca J A and Bleijenberg, Ellen J and Bartels, Meike and B{\"o}gels, Susan M and Middeldorp, Christel M} } @article {201, title = {Externalizing problems in childhood and adolescence predict subsequent educational achievement but for different genetic and environmental reasons}, journal = {Journal of Child Psychology and Psychiatry}, volume = {58}, year = {2017}, pages = {292{\textendash}304}, abstract = {

Background

Childhood behavior problems predict subsequent educational achievement; however, little research has examined the etiology of these links using a longitudinal twin design. Moreover, it is unknown whether genetic and environmental innovations provide incremental prediction for educational achievement from childhood to adolescence.

Methods

We examined genetic and environmental influences on parental ratings of behavior problems across childhood (age 4) and adolescence (ages 12 and 16) as predictors of educational achievement at age 16 using a longitudinal classical twin design.

Results

Shared-environmental influences on anxiety, conduct problems, and peer problems at age 4 predicted educational achievement at age 16. Genetic influences on the externalizing behaviors of conduct problems and hyperactivity at age 4 predicted educational achievement at age 16. Moreover, novel genetic and (to a lesser extent) nonshared-environmental influences acting on conduct problems and hyperactivity emerged at ages 12 and 16, adding to the genetic prediction from age 4.

Conclusions

These findings demonstrate that genetic and shared-environmental factors underpinning behavior problems in early childhood predict educational achievement in midadolescence. These findings are consistent with the notion that early-childhood behavior problems reflect the initiation of a life-course persistent trajectory with concomitant implications for social attainment. However, we also find evidence that genetic and nonshared-environment innovations acting on behavior problems have implications for subsequent educational achievement, consistent with recent work arguing that adolescence represents a sensitive period for socioaffective development.

}, keywords = {behavior problems, Education, genetics, longitudinal, Strengths and Difficulties Questionnaire, twin study}, issn = {1469-7610}, doi = {10.1111/jcpp.12655}, url = {http://dx.doi.org/10.1111/jcpp.12655}, author = {Lewis, Gary J. and Asbury, Kathryn and Robert Plomin} }