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Supplemental material, sj-pdf-2-erp-10.1177_08902070211007666 for A person-centered approach to understanding child temperament at ages 3 and 6 by Mariah T Hawes, Megan C Finsaas, Thomas M Olino and Daniel N Klein in European Journal of Personality

Supplemental material, sj-pdf-1-erp-10.1177_08902070211007666 for A person-centered approach to understanding child temperament at ages 3 and 6 by Mariah T Hawes, Megan C Finsaas, Thomas M Olino and Daniel N Klein in European Journal of Personality

Additional file 1.

Supplemental material, sj-pdf-2-erp-10.1177_08902070211007666 for A person-centered approach to understanding child temperament at ages 3 and 6 by Mariah T Hawes, Megan C Finsaas, Thomas M Olino and Daniel N Klein in European Journal of Personality

Supplemental material, Supplementary_Materials_Table_S1_S2_3-15-20 for Using Item Response Theory to Compare Irritability Measures in Early Adolescent and Childhood Samples by Lea R. Dougherty, Maria M. Galano, Emma Chad-Friedman, Thomas M. Olino, Sara J. Bufferd and Daniel N. Klein in Assessment

Supplemental material, Supplemental_material for Factor Structure, Convergent, and Divergent Validity of the Prodromal Questionnaire–Negative Symptom Subscale by Katherine M. Pierce, Seth D. Maxwell, Thomas M. Olino, Shanna Cooper and Lauren M. Ellman in Assessment

Supplemental material, Supplemental_material for Factor Structure, Convergent, and Divergent Validity of the Prodromal Questionnaire–Negative Symptom Subscale by Katherine M. Pierce, Seth D. Maxwell, Thomas M. Olino, Shanna Cooper and Lauren M. Ellman in Assessment

Parent history of psychopathology is an established marker of children's own risk for later disorder and can therefore be used as a means of validating other risks, such as child temperament. While associations between children's temperament and parent psychopathology have been reported, few studies have used observational measures of child temperament or examined trait interactions, particularly between children's affective and regulatory traits such as effortful control (EC). In this bottom-up family study of 968 three-year-olds and their parents, we examined interactions between preschoolers' observed positive and negative affectivity (NA) and EC as predictors of a known marker of psychopathology risk: parent history of disorder. Children with lower positive affectivity had an increased probability of paternal depression history in the context of higher child NA. In addition, children with lower EC and higher NA had an increased probability of maternal anxiety. Findings shed new light on the main effects and interactions that account for associations between child temperament and parent history of disorder, one of the best-established markers of an individual's own risk for future disorder, implicating reactive and regulatory traits that merit special consideration in future longitudinal work. Copyright © 2017 John Wiley & Sons, Ltd.

Supplemental material, Mac_Giollabhui_Supplemental_Material for Is Worse Attention a Risk Factor for or a Consequence of Depression, or Are Worse Attention and Depression Better Accounted for by Stress? A Prospective Test of Three Hypotheses by Naoise Mac Giollabhui, Thomas M. Olino, Johanna Nielsen, Lyn Y. Abramson and Lauren B. Alloy in Clinical Psychological Science

Preliminary work indicates that cognitive vulnerability to depression may be associated with variants of the serotonin transporter promoter polymorphism (5-HTTLPR) and the valine to methionine at position 66 (val66met) polymorphism of the brain-derived neurotrophic factor (BDNF) gene; however, existing reports come from small samples. The present study sought to replicate and extend this research in a sample of 375 community-dwelling children and their parents. Following a negative mood induction, children completed a self-referent encoding task tapping memory for positive and negative self-descriptive traits. Consistent with previous work, we found that children with at least one short variant of the 5-HTTLPR had enhanced memory for negative self-descriptive traits. The BDNF val66met polymorphism had no main effect but was moderated by maternal depression, such that children with a BDNF methionine allele had a heightened memory for negative self-descriptive traits when mothers had experienced depression during children's lifetimes; in contrast, children with a methionine allele had low recall of negative traits when mothers had no depression history. The findings provide further support for the notion that the 5-HTTLPR is associated with cognitive markers of depression vulnerability and that the BDNF methionine allele moderates children's sensitivity to contextual factors.

ObjectiveS: Research implicates the A1 allele of the dopamine D2 receptor gene (DRD2) Taq1A polymorphism in the development of depression and anxiety. Furthermore, recent papers suggest that children with A1 allele of this gene may receive less positive parenting, and that the effects of this gene on child symptoms may be moderated by parenting. We sought to replicate and extend these findings using behavioral measures in a nonclinical sample of young children. Methods: In a sample of 473 preschool-aged children and their mothers, structured clinical interview measures and maternal reports of child symptoms were collected, and standardized observations of parent-child interactions were conducted. Results: An association was detected between the DRD2 A1 allele and symptoms of depression and anxiety indexed using interview and parent report methods. As found in previous reports, children with the DRD2 A1 allele received less supportive parenting and displayed higher levels of negative emotionality during parent-child interactions. Tests of mediation and moderation were conducted. Conclusion: We found associations between the DRD2 A1 allele and early-emerging anxious and depressive symptoms in a community sample of preschool-aged children, and evidence of a gene-environment correlation and moderation of the main effect of child genotype on child symptoms by parenting. © 2010 Wolters Kluwer Health | Lippincott Williams & Wilkins.

The ability to adaptively inhibit responses to tempting/distracting stimuli in the pursuit of goals is an essential set of skills necessary for adult competence and wellbeing. These inhibitory capacities develop throughout childhood, with growing evidence of important maturational changes occurring in adolescence. There also has been intense interest in the role of social adversity on the development of executive function, including inhibitory control. We hypothesized that the onset of adolescence could be a time of particular opportunity/vulnerability in the development of inhibition due to the large degree of maturational changes in neural systems involved in regulatory control. We investigated this hypothesis in a longitudinal study of adolescents by examining the impact of socioeconomic status (SES) on the maturation of inhibition and concurrent brain function. Furthermore, we examined gender as a potential moderator of this relationship, given evidence of gender-specificity in the developmental pathways of inhibition as well as sex differences in adolescent development. Results reveal that lower SES is associated with worse behavioral inhibition over time and a concurrent increase in anterior cingulate (ACC) activation, but only in girls. We also found that lower SES girls exhibited decreased ACC ↔ dorsolateral prefrontal cortex (dlPFC) coupling over time. Our findings suggest that female adolescents with lower SES appear to develop less efficient inhibitory processing in dlPFC, requiring greater and relatively unsuccessful compensatory recruitment of ACC. In summary, the present study provides a novel window into the neural mechanisms by which the influence of SES on inhibition may be transmitted during adolescence.

Growing evidence indicates that normative pubertal maturation is associated with increased threat reactivity, and this developmental shift has been implicated in the increased rates of adolescent affective disorders. However, the neural mechanisms involved in this pubertal increase in threat reactivity remain unknown. Research in adults indicates that testosterone transiently decreases amygdala-orbitofrontal cortex (OFC) coupling. Consequently, we hypothesized that increased pubertal testosterone disrupts amygdala-OFC coupling, which may contribute to developmental increases in threat reactivity in some adolescents. Hypotheses were tested in a longitudinal study by examining the impact of testosterone on functional connectivity. Findings were consistent with hypotheses and advance our understanding of normative pubertal changes in neural systems instantiating affect/motivation. Finally, potential novel insights into the neurodevelopmental pathways that may contribute to adolescent vulnerability to behavioral and emotional problems are discussed.

Evaluations of assessment instruments using classical test theory typically rely on indices of internal consistency, test-retest reliability, and construct validity. However, the use of models from item response theory (IRT) allows comparison of instruments (and items) in terms of the information they provide and where they provide it along the continuum of severity of the construct being assessed. Such results help to identify the measures most appropriate for specific clinical and research contexts. The present study examined the functioning of the Beck Depression Inventory (BDI), the Center for Epidemiologic Studies-Depression (CES-D) scale, and the nine primary symptoms from the depression module of the Schedule for Affective Disorders and Schizophrenia-Children (K-SADS) using IRT methods. A large sample of adolescents (n = 1709) completed the BDI, CES-D scale, and K-SADS. IRT calibration analyses demonstrated that the BDI and CES-D scale performed well in similar ranges of depressive severity (approximately -1 to +3 standard deviations [SDs]), although the BDI provided more information at higher severity levels and the CES-D scale at lower severity levels. The K-SADS depression items, which are dichotomous and focused on clinical disorder, provided the least information that was restricted to the narrowest range (approximately +1 to +3 SDs). This work finds consistency between past rationale for the use of the BDI in clinical samples while using the CES-D scale in epidemiological studies. The results for the K-SADS suggest that interview measures may benefit from increasing the number of items and/or response options to collect more psychometric information.

Although low positive affect (PA) and high negative affect (NA) have been posited to predispose to depressive disorders, little is known about the developmental trajectories of these affects in children at familial risk for mood disorders.We examined 202 offspring of mothers who had a history of juvenile-onset unipolar depressive disorder (n = 60) or no history of major psychopathology (n = 80). Offspring participated in up to seven annual, structured laboratory tasks that were designed to elicit PA and NA.Growth curve analyses revealed that PA increased linearly and similarly for all children from late infancy through age 9. However, there also were individual differences in early PA. Relative to control peers, offspring of mothers with lifetime unipolar depression had consistently lower levels of PA, and this association remained significant even when controlling for current maternal depression and maternal affect displays. Growth curve analyses also revealed a significant linear decrease in NA in children across time; however, there was no significant inter-individual variation either in early NA or rate of change in NA.Attenuated PA (rather than excessive NA) may be an early vulnerability factor for eventual unipolar depressive disorder in at-risk children and may represent one pathway through which depression is transmitted.

The brain-derived neurotrophic factor (BDNF) gene is a plausible candidate for early-emerging negative emotionality (NE), and evidence suggests that the effects of this gene may be especially salient in the context of familial risk for child maladjustment. We therefore examined whether the single-nucleotide polymorphism producing a valine-to-methionine substitution at codon 66 (val66met) of the BDNF gene was associated with childhood NE, in the context of parental depression and relationship discord. A sample of 413 three-year-old children was assessed for NE using standardized laboratory measures. The children's parents completed clinical interviews as well as a measure of marital satisfaction. Children with at least one BDNF methionine (met) allele exhibited elevated NE when a parent had a history of depressive disorder or when relationship discord was reported by a parent. In contrast, this allele was associated with especially low NE when parental depression was absent and when the parental relationship was not discordant. Our findings suggest that the BDNF met allele confers increased child sensitivity to both positive and negative familial influences.

Association studies of the serotonin transporter promoter polymorphism (5-HTTLPR) and negative emotionality (NE) are inconclusive. However, emerging evidence suggests that the association between this polymorphism and NE may be influenced by levels of another temperament trait, positive emotionality (PE). Therefore, this study examined whether the association between the 5-HTTLPR and NE was moderated by PE. A community sample of 413 three-year-old children completed a standardized battery of laboratory tasks designed to tap temperamental emotionality. Children were also genotyped for the 5-HTTLPR. No direct association between 5-HTTLPR genotype and NE was found. However, the interaction of child PE and NE predicted 5-HTTLPR genotype. Furthermore, children with a short allele who were also low in PE had significantly greater NE than children without a short allele or children with high PE. Our findings suggest that the short allele of the 5-HTTLPR is associated with NE only in the context of low PE. Inconsistent links between NE and this gene in previous research may stem from the failure to consider other temperament traits that moderate associations. © 2010 American Psychological Association.

Funder: Schweizerischer Nationalfonds zur F��rderung der Wissenschaftlichen Forschung; funder-id: http://dx.doi.org/10.13039/501100001711, Funder: Jacobs Foundation; funder-id: http://dx.doi.org/10.13039/501100003986, Funder: Swiss Federal Office of Public Health, Funder: Canton of Zurich Ministry of Education, Funder: Julius Baer Foundation, This study examined early external childcare in relation to development from age 7 to 20. A Swiss sample was used (N = 1,225; 52% male). Development included multi-informant-reported externalizing behavior, internalizing problems, prosocial behavior, delinquency, and substance use. Growth curve models revealed that, dependent on the informant, time in a daycare center was related to increased externalizing and internalizing problems until at least age 11. It was not related to delinquency. Roughly three days per week at a daycare mother or playgroup was related to increased externalizing behavior. External family care was associated with increased prosocial behavior. Finally, time in a daycare center was associated with fewer externalizing but more internalizing problems and substance use for children from vulnerable backgrounds. This relation with substance use lasted to age 20.

In school, shyness is associated with psychosocial difficulties and has negative impacts on children’s academic performance and wellbeing. Even though there are different strategies and interventions to help children deal with shyness, there is currently no comprehensive systematic review of available interventions. This systematic review and meta-analysis aim to identify interventions for shy children and to evaluate the effectiveness in reducing psychosocial difficulties and other impacts. The methodology and reporting were guided by the Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement and checklist. A total of 4,864 studies were identified and 25 of these met the inclusion criteria. These studies employed interventions that were directed at school-aged children between six and twelve years of age and described both pre- and post-intervention measurement in target populations of at least five children. Most studies included an intervention undertaken in a school setting. The meta-analysis revealed interventions showing a large effect in reducing negative consequences of shyness, which is consistent with extant literature regarding shyness in school, suggesting school-age as an ideal developmental stage to target shyness. None of the interventions were delivered in a classroom setting, limiting the ability to make comparisons between in-class interventions and those delivered outside the classroom, but highlighting the effectiveness of interventions outside the classroom. The interventions were often conducted in group sessions, based at the school, and involved activities such as play, modelling and reinforcement and clinical methods such as social skills training, psychoeducation, and exposure. Traditionally, such methods have been confined to a clinic setting. The results of the current study show that, when such methods are used in a school-based setting and involve peers, the results can be effective in reducing negative effects of shyness. This is consistent with recommendations that interventions be age-appropriate, consider social development and utilise wide, school-based programs that address all students.

According to the dual systems model of adolescent risk taking, sensation seeking and impulse control follow different developmental trajectories across adolescence and are governed by two different brain systems. The authors tested whether different underlying processes also drive age differences in reward approach and cost avoidance. Using a modified Iowa Gambling Task in a multinational, cross-sectional sample of 3,234 adolescents (ages 9-17; M = 12.87, SD = 2.36), pubertal maturation, but not age, predicted reward approach, mediated through higher sensation seeking. In contrast, age, but not pubertal maturation, predicted increased cost avoidance, mediated through greater impulse control. These findings add to evidence that adolescent behavior is best understood as the product of two interacting, but independently developing, brain systems. © 2016 The Society for Research in Child Development, Inc. J2: Child Dev.; Cited By :1; Export Date: 12 July 2017; Article in Press; CODEN: CHDEA; Correspondence Address: Icenogle, G.email: grace.icenogle@temple.edu