Associations between perinatal risk and physical health in pre-adolescence in the Adolescent Brain Cognitive Development (ABCD) Study®: the unexpected relationship with sleep disruption.

BACKGROUND: To investigate relationships among different physical health problems in a large, sociodemographically diverse sample of 9-to-10-year-old children and determine the extent to which perinatal health factors are associated with childhood physical health problems. METHODS: A cross-sectional study was conducted utilizing the Adolescent Brain Cognitive Development℠ (ABCD) Study (n = 7613, ages 9-to-10-years-old) to determine the associations among multiple physical health factors (e.g., prenatal complications, current physical health problems). Logistic regression models controlling for age, sex, pubertal development, household income, caregiver education, race, and ethnicity evaluated relationships between perinatal factors and childhood physical health problems. RESULTS: There were significant associations between perinatal and current physical health measures. Specifically, those who had experienced perinatal complications were more likely to have medical problems by 9-to-10 years old. Importantly, sleep disturbance co-occurred with several physical health problems across domains and developmental periods. CONCLUSION: Several perinatal health factors were associated with childhood health outcomes, highlighting the importance of understanding and potentially improving physical health in youth. Understanding the clustering of physical health problems in youth is essential to better identify which physical health problems may share underlying mechanisms. IMPACT: Using a multivariable approach, we investigated the associations between various perinatal and current health problems amongst youth. Our study highlights current health problems, such as sleep problems at 9-to-10 years old, that are associated with a cluster of factors occurring across development (e.g., low birth weight, prenatal substance exposure, pregnancy complications, current weight status, lifetime head injury). Perinatal health problems are at large, non-modifiable (in this retrospective context), however, by identifying which are associated with current health problems, we can identify potential targets for intervention and prevention efforts.

A Mixed-Methods Approach to Refining and Measuring the Construct of Positive Risk-Taking in Adolescence.

Adolescence is a peak period for risk-taking, but research has largely overlooked positive manifestations of adolescent risk-taking due to ambiguity regarding operationalization and measurement of positive risk-taking. We address this limitation using a mixed-methods approach. We elicited free responses from contemporary college students (N = 74, Mage  = 20.1 years) describing a time they took a risk. Qualitative analysis informed the construction of a self-report positive risk-taking scale, which was administered to a population-based sample of adolescents (N = 1,249, Mage  = 16 years) for quantitative validation and examination of associations with normative and impulsive personality. Sensation seeking predicted negative and positive risk-taking, whereas extraversion and openness were predominantly related to positive risk-taking. Results provide promising evidence for a valid measure of adolescents' engagement in positive risks.

Weak and uneven associations of home, neighborhood, and school environments with stress hormone output across multiple timescales.

The progression of lifelong trajectories of socioeconomic inequalities in health and mortality begins in childhood. Dysregulation in cortisol, a stress hormone that is the primary output of the hypothalamus-pituitary-adrenal (HPA) axis, has been hypothesized to be a mechanism for how early environmental adversity compromises health. However, despite the popularity of cortisol as a biomarker for stress and adversity, little is known about whether cortisol output differs in children being raised in socioeconomically disadvantaged environments. Here, we show that there are few differences between advantaged and disadvantaged children in their cortisol output. In 8-14-year-old children from the population-based Texas Twin Project, we measured cortisol output at three different timescales: (a) diurnal fluctuation in salivary cortisol (n = 400), (b) salivary cortisol reactivity and recovery after exposure to the Trier Social Stress Test (n = 444), and (c) cortisol concentration in hair (n = 1210). These measures converged on two moderately correlated, yet distinguishable, dimensions of HPA function. We tested differences in cortisol output across nine aspects of social disadvantage at the home (e.g., family socioeconomic status), school (e.g., average levels of academic achievement), and neighborhood (e.g., concentrated poverty). Children living in neighborhoods with higher concentrated poverty had higher diurnal cortisol output, as measured in saliva; otherwise, child cortisol output was unrelated to any other aspect of social disadvantage. Overall, we find limited support for alteration in HPA axis functioning as a general mechanism for the health consequences of socioeconomic inequality in childhood.

Adolescent girls' stress responses as prospective predictors of self-injurious thoughts and behaviors: A person-centered, multilevel study.

Adolescent risk for self-injurious thoughts and behaviors (STBs) involves disturbance across multiple systems (e.g., affective valence, arousal regulatory, cognitive and social processes). However, research integrating information across these systems is lacking. Utilizing a multiple-levels-of-analysis approach, this person-centered study identified psychobiological stress response profiles and linked them to cognitive processes, interpersonal behaviors, and STBs. At baseline, adolescent girls (N = 241, Mage = 14.68 years, Range = 12-17) at risk for STBs completed the Trier Social Stress Test (TSST), questionnaires, and STB interviews. Positive affect (PA), negative affect (NA), and salivary cortisol (SC) were assessed before and after the TSST. STBs were assessed again during 3, 6, and 9 month follow-up interviews. Multitrajectory modeling of girls' PA, NA, and SC revealed four profiles, which were compared on cognitive and behavioral correlates as well as STB outcomes. Relative to normative, girls in the affective distress, hyperresponsive, and hyporesponsive subgroups were more likely to report negative cognitive style (all three groups) and excessive reassurance seeking (hyporesponsive only) at baseline, as well as nonsuicidal self-injury (all three groups) and suicidal ideation and attempt (hyporesponsive only) at follow-up. Girls' close friendship characteristics moderated several profile-STB links. A synthesis of the findings is presented alongside implications for person-centered tailoring of intervention efforts.

Exploring joint HPA-inflammatory stress response profiles in adolescent girls: Implications for developmental models of neuroendocrine dysregulation.

Prior research has struggled to differentiate cortisol stress response patterns reflective of well-regulated versus dysregulated hypothalamic-pituitary-adrenal (HPA) axis function among adolescents. Here, we show how exploring profiles of joint HPA-inflammatory stress responsivity, and linking those profiles to pubertal development and peer stress exposure may aid such distinction. Adolescent girls (N = 157, Mage  = 14.72 years, SD = 1.38) at risk for psychopathology completed assessments of salivary cortisol and pro-inflammatory cytokines (i.e., tumor necrosis factor-α, interleukin-1ß, and interleukin-6) prior to and following the Trier Social Stress Test. Adolescents, a close friend, and a caregiver completed questionnaire measures of peer stress and pubertal status. Multitrajectory modeling of adolescents' cortisol and cytokine levels revealed three profiles: low cortisol response-stably low cytokine (n = 75), high cortisol response-stably moderate cytokine (n = 47), and low cortisol response-stably high cytokine (n = 35). Relative to low cortisol response-stably low cytokine, adolescents exhibiting the high cortisol response-stably moderate cytokine profile were more advanced in their pubertal development, but presented with similarly low levels of peer stress exposure. Despite showing cortisol responses that were indistinguishable from low cortisol response-stably low cytokine, adolescents exhibiting the low cortisol response-stably high cytokine profile were more pubertally advanced, but also more likely to have experienced chronic peer strain (self-report) and relational peer victimization (close friend-report). These findings thus illustrate the potential value of taking a multisystem approach to studying adolescent stress responsivity and underscore the importance of considering developmental and social factors when interpreting cortisol stress response patterns. Ultimately, such work may help inform developmental models of neuroendocrine dysregulation and related risk for psychopathology.

The Role of Social Support in Coping with Psychological Trauma: An Integrated Biopsychosocial Model for Posttraumatic Stress Recovery.

This theoretical review proposes an integrated biopsychosocial model for stress recovery, highlighting the interconnectedness of intra- and interpersonal coping processes. The proposed model is conceptually derived from prior research examining interpersonal dynamics in the context of stressor-related disorders, and it highlights interconnections between relational partner dynamics, perceived self-efficacy, self-discovery, and biological stress responsivity during posttraumatic recovery. Intra- and interpersonal processes are discussed in the context of pre-, peri-, and post-trauma stress vulnerability as ongoing transactions occurring within the individual and between the individual and their environment. The importance of adopting an integrated model for future traumatic stress research is discussed. Potential applications of the model to behavioral interventions are also reviewed, noting the need for more detailed assessments of relational dynamics and therapeutic change mechanisms to determine how relational partners can most effectively contribute to stress recovery.

Linking post-stressor interpersonal processes in adolescent girls' close friendships with acute HPA stress responses.

INTRODUCTION: For adolescent girls, close friendships may facilitate stress management and mitigate risk for internalizing psychopathology. However, little is known about how friendship processes may buffer (or potentially exacerbate) acute psychobiological responses to interpersonal stressors in ways that affect risk. METHODS: In a sample of 220 girls (ages 12-17 years) with a history of internalizing symptoms, this study investigated friendship dynamics following the Trier Social Stress Test (TSST) to evaluate associations between post-stressor friendship behaviors (expressions of vulnerability by the stressed teen; support offered by their close friend) and hypothalamic-pituitary-adrenal (HPA) axis stress responses. RESULTS: Multilevel regression modeling revealed that girls who displayed more pronounced cortisol reactivity expressed greater vulnerability to, and received greater support from, their close friend. Expressed vulnerability was associated with more efficient cortisol recovery. Close friend support was not significantly associated with cortisol recovery, nor did it influence the connection between expressed vulnerability and cortisol recovery. CONCLUSIONS: Findings suggest that HPA reactivity may prompt expressions of vulnerability to girls' close friends, and in this context, promote more efficient HPA recovery. Findings highlight the role friendship dynamics may play in HPA-related risk for internalizing symptoms and point to expressed vulnerability in adolescent girls' close friendships as a potential consideration for interpersonally-centered therapeutic approaches.

Twin models of environmental and genetic influences on pubertal development, salivary testosterone, and estradiol in adolescence.

OBJECTIVE: Research on sources of variation in adolescent's gonadal hormone levels is limited. We sought to decompose individual differences in adolescent testosterone, estradiol, and pubertal status, into genetic and environmental components. DESIGN: A sample of male and female adolescent twins from the greater Austin and Houston areas provided salivary samples, with a subset of participants providing longitudinal data at 2 waves. PARTICIPANTS: The sample included 902 adolescent twins, 49% female, aged 13-20 years (M = 15.91) from the Texas Twin Project. Thirty-seven per cent of twin pairs were monozygotic; 30% were same-sex dizygotic (DZ) pairs; and 33% were opposite-sex DZ pairs. MEASUREMENTS: Saliva samples were assayed for testosterone and estradiol using chemiluminescence immunoassays. Pubertal status was assessed using self-report. Biometric decompositions were performed using multivariate quantitative genetic models. RESULTS: Genetic factors contributed substantially to variation in testosterone in males and females in the follicular phase of their menstrual cycle (h2  = 60% and 51%, respectively). Estradiol was also genetically influenced in both sexes, but was predominately influenced by nonshared environmental factors. The correlation between testosterone and estradiol was mediated by a combination of genetic and environmental influences for males and females. Genetic and environmental influences on hormonal concentrations were only weakly correlated with self-reported pubertal status, particularly for females. CONCLUSIONS: Between-person variability in adolescent gonadal hormones and their interrelationship reflects both genetic and environmental processes, with both testosterone and estradiol containing sizeable heritable components.

Hair and Salivary Testosterone, Hair Cortisol, and Externalizing Behaviors in Adolescents.

Although testosterone is associated with aggression in the popular imagination, previous research on the links between testosterone and human aggression has been inconsistent. This inconsistency might be because testosterone's effects on aggression depend on other moderators. In a large adolescent sample ( N = 984, of whom 460 provided hair samples), we examined associations between aggression and salivary testosterone, hair testosterone, and hair cortisol. Callous-unemotional traits, parental monitoring, and peer environment were examined as potential moderators of hormone-behavior associations. Salivary testosterone was not associated with aggression. Hair testosterone significantly predicted increased aggression, particularly at low levels of hair cortisol (i.e., Testosterone × Cortisol interaction). This study is the first to examine the relationship between hair hormones and externalizing behaviors and adds to the growing literature that indicates that androgenic effects on human behavior are contingent on aspects of the broader endocrine environment-in particular, levels of cortisol.

Sensation seeking and impulsive traits as personality endophenotypes for antisocial behavior: Evidence from two independent samples.

Sensation seeking and impulsivity are personality traits that are correlated with risk for antisocial behavior (ASB). This paper uses two independent samples of twins to (a) test the extent to which sensation seeking and impulsivity statistically mediate genetic influence on ASB, and (b) compare this to genetic influences accounted for by other personality traits. In Sample 1, delinquent behavior, as well as impulsivity, sensation seeking and Big Five personality traits, were measured in adolescent twins from the Texas Twin Project. In Sample 2, adult twins from the Australian Twin Registry responded to questionnaires that assessed individual differences in Eysenck's and Cloninger's personality dimensions, and a structured telephone interview that asked participants to retrospectively report DSM-defined symptoms of conduct disorder. Bivariate quantitative genetic models were used to identify genetic overlap between personality traits and ASB. Across both samples, novelty/sensation seeking and impulsive traits accounted for larger portions of genetic variance in ASB than other personality traits. We discuss whether sensation seeking and impulsive personality are causal endophenotypes for ASB, or merely index genetic liability for ASB.

Developmental changes in genetic and environmental influences on rule-breaking and aggression: age and pubertal development.

BACKGROUND: Antisocial behavior (ASB) can be meaningfully divided into nonaggressive rule-breaking versus aggressive dimensions, which differ in developmental course and etiology. Previous research has found that genetic influences on rule-breaking, but not aggression, increase from late childhood to mid-adolescence. This study tested the extent to which the developmental increase in genetic influence on rule-breaking was associated with pubertal development compared to chronological age. METHOD: Child and adolescent twins (n = 1,031), ranging in age from 8 to 20 years (M age = 13.5 years), were recruited from public schools as part of the Texas Twin Project. Participants reported on their pubertal development using the Pubertal Development Scale and on their involvement in ASB on items from the Child Behavior Checklist. Measurement invariance of ASB subtypes across age groups (≤12 years vs. >12 years old) was tested using confirmatory factor analyses. Quantitative genetic modeling was used to test whether the genetic and environmental influences on aggression and rule-breaking were moderated by age, pubertal status, or both. RESULTS: Quantitative genetic modeling indicated that genetic influences specific to rule-breaking increased as a function of pubertal development controlling for age (a gene × puberty interaction), but did not vary as a function of age controlling for pubertal status. There were no developmental differences in the genetic etiology of aggression. Family-level environmental influences common to aggression and rule-breaking decreased with age, further contributing to the differentiation between these subtypes of ASB from childhood to adolescence. CONCLUSIONS: Future research should discriminate between alternative possible mechanisms underlying gene × puberty interactions on rule-breaking forms of antisocial behavior, including possible effects of pubertal hormones on gene expression.

An in-laboratory stressor reveals unique genetic variation in child cortisol output.

Dysregulation of biological stress response, as measured by cortisol output, has been a primary candidate mechanism for how social experiences become biologically embedded. Cortisol is the primary output of the hypothalamic pituitary adrenal (HPA) axis. Cortisol levels vary systematically across the day and change in response to both sudden, acute stress experiences as well as prolonged exposure to environmental stress. Using data from 8- to 15-year-old twins in the Texas Twin Project, we investigate the extent to which genetic influences are shared across different measures of cortisol output: chronic cortisol accumulations in hair (n = 1,104), diurnal variation in salivary output (n = 488), and salivary response to a standardized, acute in-laboratory stressor (n = 537). Multivariate twin models indicate that genetic factors regulating cortisol response to the in-laboratory stressor are separable from those regulating baseline cortisol levels, naturally occurring diurnal variation in cortisol, and hair cortisol levels. These findings illustrate that novel environments can reveal unique genetic variation, reordering people in terms of their observed phenotype rather than only magnifying or mitigating preexisting differences. (PsycInfo Database Record (c) 2022 APA, all rights reserved).

A Comprehensive Overview of the Physical Health of the Adolescent Brain Cognitive Development Study Cohort at Baseline.

Physical health in childhood is crucial for neurobiological as well as overall development, and can shape long-term outcomes into adulthood. The landmark, longitudinal Adolescent Brain Cognitive Development StudySM (ABCD study®), was designed to investigate brain development and health in almost 12,000 youth who were recruited when they were 9-10 years old and will be followed through adolescence and early adulthood. The overall goal of this paper is to provide descriptive analyses of physical health measures in the ABCD study at baseline, including but not limited to sleep, physical activity and sports involvement, and body mass index. Further this summary will describe how physical health measures collected from the ABCD cohort compare with current normative data and clinical guidelines. We propose this data set has the potential to facilitate clinical recommendations and inform national standards of physical health in this age group. This manuscript will also provide important information for ABCD users and help guide analyses investigating physical health including new avenues for health disparity research as it pertains to adolescent and young adult development.

Genetic Associations Between Executive Functions and a General Factor of Psychopathology.

OBJECTIVE: Symptoms of psychopathology covary across diagnostic boundaries, and a family history of elevated symptoms for a single psychiatric disorder places an individual at heightened risk for a broad range of other psychiatric disorders. Both twin-based and genome-wide molecular methods indicate a strong genetic basis for the familial aggregation of psychiatric disease. This has led researchers to prioritize the search for highly heritable childhood risk factors for transdiagnostic psychopathology. Cognitive abilities that involve the selective control and regulation of attention, known as executive functions (EFs), are a promising set of risk factors. METHOD: In a population-based sample of child and adolescent twins (n = 1,913, mean age = 13.1 years), we examined genetic overlap between both EFs and general intelligence (g) and a transdiagnostic dimension of vulnerability to psychopathology, comprising symptoms of anxiety, depression, neuroticism, aggression, conduct disorder, oppositional defiant disorder, hyperactivity, and inattention. Psychopathology symptoms in children were rated by children and their parents. RESULTS: Latent factors representing general EF and g were highly heritable (h2 = 86%-92%), and genetic influences on both sets of cognitive abilities were robustly correlated with transdiagnostic genetic influences on psychopathology symptoms (genetic r values ranged from -0.20 to -0.38). CONCLUSION: General EF and g robustly index genetic risk for transdiagnostic symptoms of psychopathology in childhood. Delineating the developmental and neurobiological mechanisms underlying observed associations between cognitive abilities and psychopathology remains a priority for ongoing research.

Genetic and Environmental Links between : General Factors of Psychopathology and Cognitive Ability in Early Childhood.

In adults, psychiatric disorders are highly comorbid, and are negatively associated with cognitive abilities. Individual cognitive measures have been linked with domains of child psychopathology, but the specificity of these associations and the extent to which they reflect shared genetic influences are unknown. This study examines the relation between general factors of cognitive ability (g) and psychopathology (p) in early development using two genetically-informative samples: the Texas "Tiny" Twin project (TXtT; N = 626 individuals, age range = 0.16 - 6.31 years) and the Early Childhood Longitudinal Study-Birth Cohort (ECLS-B; N ≈ 1,300 individual twins, age range = 3.7 - 7.1 years). The total p-g correlation (-.21 in ECLS-B; -.34 in TXtT) was primarily attributable to genetic and shared environmental factors. The early age range of participants indicates that the p-g association is a reflection of overlapping genetic and shared environmental factors that operate in the first years of life.

Genetic and Environmental Associations Between Child Personality and Parenting.

Parenting is often conceptualized in terms of its effects on offspring. However, children may also play an active role in influencing the parenting they receive. Simple correlations between parenting and child outcomes may be due to parent-to-child causation, child-to-parent causation, or some combination of the two. We use a multi-rater, genetically informative, large sample (n = 1411 twin sets) to gain traction on this issue as it relates to parental warmth and stress in the context of child Big Five personality. Considerable variance in parental warmth (27%) and stress (45%) was attributable to child genetic influences on parenting. Incorporating child Big Five personality into the model explained roughly half of this variance. This result is consistent with the hypothesis that parents mold their parenting in response to their child's personality. Residual heritability of parenting is likely due to child characteristics beyond the Big Five.

Genetic and environmental influences on internalizing psychopathology across age and pubertal development.

Symptoms of anxiety and depression are commonly comorbid and partially share a genetic etiology. Mean levels of anxiety and depression increase over the transition to adolescence, particularly in girls, suggesting a possible role of pubertal development in the activation of underlying genetic risks. The current study examined how genetic and environmental influences on anxiety and depression differed by chronological age and pubertal status. We analyzed composite scores from child self-reports and parent informant-reports of internalizing symptomology in a racially and socioeconomically diverse sample of 1,913 individual twins from 1,006 pairs (ages 8-20 years) from the Texas Twin Project. Biometric models tested age and pubertal status as moderators of genetic and environmental influences shared between and specific to anxiety and depression to determine whether etiology of internalizing symptomology differs across development as a function of age or puberty. Genetic influences did not increase as a function of age or puberty, but instead shared environmental effects decreased with age. In an exploratory model that considered the moderators simultaneously, developmental differences in etiology were reflected in genetic and environmental effects unique to depression. Results suggest that genetic variance in internalizing problems is relatively constant during adolescence, with environmental influences more varied across development. (PsycINFO Database Record

Developmental differences in reward sensitivity and sensation seeking in adolescence: Testing sex-specific associations with gonadal hormones and pubertal development.

Sensation seeking has been found to increase, on average, from childhood to adolescence. Developmental scientists have hypothesized that this change could be driven by the rise of gonadal hormones at puberty, which affect reward-related processing in the brain. In a large, age-heterogeneous, population-based sample of adolescents and young adults (N = 810; ages 13-20 years), we tested for sex-specific associations between age, self-reported pubertal development, gonadal hormones (estradiol and testosterone) as measured in saliva, reward sensitivity as measured by a multivariate battery of in-laboratory tasks (including the Iowa gambling task, balloon analogue risk task, and stoplight task), and self-reported sensation seeking. Reward sensitivity was more strongly associated with sensation seeking in males than females. For both males and females, reward sensitivity was unrelated to age but was higher among those who reported more advanced pubertal development. There were significant sex differences in the effects of self-reported pubertal development on sensation seeking, with a positive association evident in males but a negative association in females. Moreover, gonadal hormones also showed diverging associations with sensation seeking-positive with testosterone but negative with estradiol. Overall, the results indicate that sensation seeking among adolescents and young adults depends on a complex constellation of developmental influences that operate via sex-specific mechanisms. (PsycINFO Database Record

Genetic and environmental influences on pubertal hormones in human hair across development.

Puberty is a complex biopsychosocial process that can affect an array of psychiatric and medical disorders emerging in adolescence. Although the pubertal process is driven by neuroendocrine changes, few quantitative genetic studies have directly measured puberty-relevant hormones. Hair samples can now be assayed for accumulation of hormones over several months. In contrast to more conventional salivary measures, hair measures are not confounded by diurnal variation or hormonal reactivity. In an ethnically and socioeconomically diverse sample of 1286 child and adolescent twins and multiples from 672 unique families, we estimated genetic and environmental influences on hair concentrations of testosterone, DHEA, and progesterone across the period of 8-18 years of age. On average, male DHEA and testosterone were highly heritable, whereas female DHEA, progesterone, and puberty were largely influenced by environmental components. We identified sex-specific developmental windows of maximal heritability in each hormone. Peak heritability for DHEA occurred at approximately 10 years of age for males and females. Peak heritability for testosterone occurred at age 12.5 and 15.2 years for males and females, respectively. Peak heritability for male progesterone occurred at 11.2 years, while the heritability of female progesterone remained uniformly low. The identification of specific developmental windows when genetic signals for hormones are maximized has critical implications for well-informed models of hormone-behavior associations in childhood and adolescence.

Multivariate analysis of genetic and environmental influences on parenting in adolescence.

Adolescents whose parents are affectionate, maintain consistent rules, and are knowledgeable about their whereabouts tend to exhibit more adaptive levels of psychological functioning across multiple domains. Behavioral genetic research has documented the sensitivity of parenting to genetically influenced child characteristics and behaviors. Yet, the question of whether the correlations between parenting behaviors are driven by overlapping parent effects, overlapping child effects, or some combination of the two remains open. In a sample of N = 542 twins, ages 13.6 to 20.1 years, from the Texas Twin Project, we evaluated the extent to which adolescents' genetically influenced traits broadly affect multiple dimensions of parenting (maternal and paternal warmth and control, and parental monitoring). We found that shared environmental factors primarily accounted for the covariation among parental warmth, control, and monitoring. Child-driven genetic effects were primarily detected in parenting variance unique to fathers. These results indicate that adolescents' family-wide environmental contexts are general across multiple domains of parenting, whereas genetically influenced adolescent-driven effects are specific to particular aspects of parenting and to particular relationships. (PsycINFO Database Record