This study investigated the influences of neighborhood factors (residential stability and neighborhood disadvantage) and variants of the serotonin transporter linked polymorphic region (5-HTTLPR) genotype on the development of substance use among African American children aged 10-24 years. To accomplish this, a harmonized data set of five longitudinal studies was created via pooling overlapping age cohorts to establish a database with 2,689 children and 12,474 data points to span ages 10-24 years. A description of steps used in the development of the harmonized data set is provided, including how issues such as the measurement equivalence of constructs were addressed. A sequence of multilevel models was specified to evaluate Gene × Environment effects on growth of substance use across time. Findings indicated that residential instability was associated with higher levels and a steeper gradient of growth in substance use across time. The inclusion of the 5-HTTLPR genotype provided greater precision to the relationships in that higher residential instability, in conjunction with the risk variant of 5-HTTLPR (i.e., the short allele), was associated with the highest level and steepest gradient of growth in substance use across ages 10-24 years. The findings demonstrated how the creation of a harmonized data set increased statistical power to test Gene × Environment interactions for an under studied sample.
Dimensions of irritability and defiant behavior, though correlated within the structure of ODD, convey separable developmental risks through adolescence and adulthood. Irritability predicts depression and anxiety, whereas defiant behavior is a precursor to antisocial outcomes. Previously we demonstrated that a bifactor model comprising irritability and defiant behavior dimensions, in addition to a general factor, provided the best-fitting structure of ODD symptoms in five large datasets. Herein we extend our previous work by externally validating the bifactor model of ODD using multiple regression and multivariate behavior genetic analyses. We used parent ratings of DSM IV ODD symptoms, and symptom dimensions for ADHD (i.e., inattention and hyperactivity−impulsivity), conduct disorder (CD), depression/dysthymia, and generalized anxiety disorder (GAD) from 846 6−18-year-old twin pairs. We found that the ODD irritability factor was associated only with depression/dysthymia and GAD and the ODD defiant behavior factor was associated only with inattention, hyperactivity−impulsivity, and CD, whereas the ODD general factor was associated with all five symptom dimensions. Multivariate behavior genetic analyses found all five symptom dimensions shared genetic influences in common with the ODD general, irritability, and defiant behavior factors. In contrast, the defiant behavior factor shared genetic influences uniquely with inattention and hyperactivity−impulsivity, whereas the irritability factor shared genetic influences uniquely with depression/dysthymia and GAD, but not vice versa. This suggests that genes that influence irritability in early childhood also predispose to depression and anxiety in adolescence and adulthood. These multivariate genetic findings also support the external validity of the three ODD dimensions at the etiological level. Our study provides additional support for subtyping ODD based on these symptom dimensions, as in the revisions in the ICD-11, and suggests potential mechanisms underlying the development from ODD to behavioral or affective disorders.
Objective: The current study examined the prospective effects of exposure to stressful conditions in early childhood on physical health in young adulthood, and explored continuing exposure to stressors, as well as depression, in adolescence as possible mechanisms of this relationship.
Design: A prospective longitudinal design was used to examine 705 mother-child pairs from a community-based sample, followed from offspring birth through age 20.
Main Outcome Measures: Mothers provided contemporaneous assessments of early adverse conditions from offspring birth through age 5. Offspring responses to the UCLA Life Stress Interview, Structured Clinical Interview for DSM Disorders (SCID), Physical Functioning subscale of the SF-36 Health Survey, and questions about the presence of chronic disease were used to assess youth stress at age 15, depression from ages 15 to 20, and physical health at age 20.
Results: Early adversity conferred risk for elevated levels of social and non-social stress at youth age 15, as well as depression between ages 15 and 20. Social and non-social stress in turn had effects on physical health at age 20, directly and indirectly via depression.
Conclusions: Findings suggest that early adverse conditions have lasting implications for physical health, and that continued exposure to increased levels of both social and non-social stress in adolescence, as well as the presence of depression, might be important mechanisms by which early adversity impacts later physical health.
by
Maureen S. Durkin;
Mayada Elsabbagh;
Josephine Barbaro;
Melissa Gladstone;
Francesca Happe;
Rosa A. Hoekstra;
Li-Ching Lee;
Alexia Rattazzi;
Jennifer Stapel-Wax;
Wendy L. Stone;
Helen Tager-Flusberg;
Audrey Thurm;
Mark Tomlinson;
Andy Shih
Although offspring of depressed mothers are at an increased risk for depression themselves, not all of these children develop depression, highlighting the need to identify specific environmental and genetic moderators of risk. The goal of this study was to examine the aggregate influence of genetic polymorphisms associated with the regulation of the hypothalamic-pituitary-adrenal (HPA) axis as a potential moderator of the relation between environmental stress and prospective changes in depressive symptoms for offspring of depressed mothers. Participants were 238 mother- offspring dyads recruited from the community based on the mother's lifetime history of major depression during the youth's lifetime (present vs. absent). Mothers and youth completed assessments every 6 months for 2 years (5 total). Results indicated that offspring of depressed mothers showing the greatest increases in depressive symptoms during the follow up were those who had higher HPA multilocus genetic profile scores and who experienced the highest levels of interpersonal stress. These relations were significant for interpersonal stress and were not observed for noninterpersonal stress. These findings suggest that HPA multilocus genetic profile scores may be important genetic markers of stress reactivity and depression risk for offspring of depressed mothers. They also highlight interpersonal stress as a potentially modifiable risk factor for these high-risk youth.
Accumulating evidence suggests that males outperform females on mental rotation tasks as early as infancy. Sex differences in object preference have also been shown to emerge early in development and precede sex-typed play in childhood. Although research with adults and older children is suggestive of a relationship between play preferences and visuospatial abilities, including mental rotation, little is known about the developmental origins of this relationship. The present study compared mental rotation ability and object preference in 6- to 13-month-old infants. We used a novel paradigm to examine individual differences in infants’ mental rotation abilities as well as their differential preference for one of two sex-typed objects. A sex difference was found on both tasks, with boys showing an advantage in performance on the mental rotation task and exhibiting greater visual attention to the male-typed object (i.e., a toy truck) than to the female-typed object (i.e., a doll) in comparison to girls. Moreover, we found a relation between mental rotation and object preference that varied by sex. Greater visual interest in the male-typed object was related to greater mental rotation performance in boys, but not in girls. Possible explanations related to perceptual biases, prenatal androgen exposure, and experiential influences for this sex difference are discussed.
by
Lauren R. Doyle;
Eileen M. Moore;
Claire Coles;
Julie Kable;
Elizabeth R. Sowell;
Jeffrey R. Wozniak;
Kenneth L. Jones;
Edward P. Riley;
Sarah N. Mattson
Objectives: Caregivers of youth with heavy prenatal alcohol exposure report impaired communication, which can significantly impact quality of life. Using data collected as part of the Collaborative Initiative on Fetal Alcohol Spectrum Disorders (CIFASD), we examined whether cognitive variables predict communication ability of youth with histories of heavy prenatal alcohol exposure. Methods: Subjects (ages 10-16 years) comprised two groups: adolescents with heavy prenatal alcohol exposure (AE) and non-exposed controls (CON). Selected measures of executive function (NEPSY, Delis-Kaplan Executive Function System), working memory (CANTAB), and language were tested in the child, while parents completed communication ratings (Vineland Adaptive Behavior Scales - Second Edition). Separate multiple regression analyses determined which cognitive domains predicted communication ability. A final, global model of communication comprised the three cognitive models. Results: Spatial Working Memory and Inhibition significantly contributed to communication ability across groups. Twenty Questions performance related to communication ability in the CON group only while Word Generation performance related to communication ability in the AE group only. Effects remained significant in the global model, with the exception of Spatial Working Memory. Conclusions: Both groups displayed a relation between communication and Spatial Working Memory and Inhibition. Stronger communication ability related to stronger verbal fluency in the AE group and Twenty Questions performance in the CON group. These findings suggest that alcohol-exposed adolescents may rely more heavily on learned verbal storage or fluency for daily communication while non-exposed adolescents may rely more heavily on abstract thinking and verbal efficiency. Interventions aimed at aspects of executive function may be most effective at improving communication ability of these individuals. (JINS, 2018, 24, 1026-1037)
Background
Down syndrome (DS, OMIM #190685) is the most commonly identified genetic form of intellectual disability with congenital heart defect (CHD) occurring in 50% of cases. With advances in surgical techniques and an increasing lifespan, this has necessitated a greater understanding of the neurodevelopmental consequences of CHDs. Herein, we explore the impact of CHD on language development in children with DS.
Methods
Twenty-nine children with DS were observed systematically in parent–child interactions using the Communication Play Protocol to evaluate their language use; they also completed the Mullen Scales of Early Learning and MacArthur Communication Development Inventory. Mean ages were 31.2 months for children with DS and CHD (DS + CHD, n = 12) and 32.1 months for children with DS and a structurally normal heart (DS − CHD, n = 17).
Results
Compared with the DS − CHD controls, the DS + CHD group revealed lower scores in multiple areas, including fine motor skills and expressive and receptive vocabulary. Whereas most differences were not statistically significant, the Communication Development Inventory word count and symbol-infused joint engagement differed significantly (P < 0.01) and marginally (P = 0.09) between groups.
Conclusions
Finding that CHDs may account for part of the variation in language delay allows us to consider the specific mechanisms underlying the impact of CHDs on language acquisition in children with DS. Conclusions from this first study on early language outcomes of children with DS + CHD may be useful for clinicians in providing developmental surveillance and early intervention programmes with specific emphasis on language therapy as part of long-term follow-up for children with DS + CHD.
The notion that adolescence is characterized by dramatic changes in behavior, and often by emotional upheaval, is widespread and longstanding in popular western culture. In recent decades, this notion has gained increasing support from empirical research showing that the peri- and post-pubertal developmental stages are associated with a significant rise in the rate of psychiatric symptoms and syndromes. As a result, interest in adolescent development has burgeoned among researchers focused on the origins of schizophrenia and other psychotic disorders. Two factors have fueled this trend: 1) increasing evidence from longitudinal research that adolescence is the modal period for the emergence of “prodromal” manifestations, or precursors of psychotic symptoms, and 2) the rapidly accumulating scientific findings on brain structural and functional changes occurring during adolescence and young adulthood. Further, gonadal and adrenal hormones are beginning to play a more prominent role in conceptualizations of adolescent brain development, as well as in the origins of psychiatric symptoms during this period (Walker and Bollini, 2002; Walker et al., 2008). In this paper, we begin by providing an overview of the nature and course of psychotic disorders during adolescence/young adulthood. We then turn to the role of hormones in modulating normal brain development, and the potential role they might play in the abnormal brain changes that characterize youth at clinical high-risk (CHR) for psychosis. The activational and organizational effects of hormones are explored, with a focus on how hormone-induced changes might be linked with neuropathological processes in the emergence of psychosis.
While striving to succeed in the face of adversity may provide individuals with outward benefits, it may come at a cost to individuals' physical health. The current study examines whether striving predicts greater physiological or psychosocial costs among those who experienced child maltreatment, a stressor that disrupts the caregiving environment and threatens relationship security. Using data from the National Longitudinal Study of Adolescent to Adult Health, we tested whether greater striving after childhood maltreatment would come at a cost, increasing underlying cardiovascular disease (CVD) risk and depressive symptoms despite showing outward success via income and college degree attainment. The study included 13,341 Black, Hispanic, and White adolescents who self-reported striving and their experiences of childhood neglect, physical abuse, and sexual abuse. As young adults, participants reported depressive symptoms, income, and college degree attainment and completed a health assessment from which a 30-year Framingham-based CVD risk score was calculated. Higher striving was associated with lower CVD risk and depressive symptoms, and higher income and college degree attainment, regardless of maltreatment history. These findings highlight the potential for striving as a target for interventions and support the need to examine multiple biological and behavioral outcomes to understand the multifaceted nature of resilience.