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BACKGROUND: The impact of digital device use on health and well-being is a pressing question. However, the scientific literature on this topic, to date, is marred by small and unrepresentative samples, poor measurement of core constructs, and a limited ability to address the psychological and behavioral mechanisms that may underlie the relationships between device use and well-being. Recent authoritative reviews have made urgent calls for future research projects to address these limitations. The critical role of research is to identify which patterns of use are associated with benefits versus risks and who is more vulnerable to harmful versus beneficial outcomes, so that we can pursue evidence-based product design, education, and regulation aimed at maximizing benefits and minimizing the risks of smartphones and other digital devices. OBJECTIVE: The objective of this study is to provide normative data on objective patterns of smartphone use. We aim to (1) identify how patterns of smartphone use impact well-being and identify groups of individuals who show similar patterns of covariation between smartphone use and well-being measures across time; (2) examine sociodemographic and personality or mental health predictors and which patterns of smartphone use and well-being are associated with pre-post changes in mental health and functioning; (3) discover which nondevice behavior patterns mediate the association between device use and well-being; (4) identify and explore recruitment strategies to increase and improve the representation of traditionally underrepresented populations; and (5) provide a real-world baseline of observed stress, mood, insomnia, physical activity, and sleep across a representative population. METHODS: This is a prospective, nonrandomized study to investigate the patterns and relationships among digital device use, sensor-based measures (including both behavioral and physiological signals), and self-reported measures of mental health and well-be

BACKGROUND: Adolescence is marked by an increasing risk of depression and is an optimal window for prevention and early intervention. Personalizing interventions may be one way to maximize therapeutic benefit, especially given the marked heterogeneity in depressive presentations. However, empirical evidence that can guide personalized intervention for youth is lacking. Identifying person-specific symptom drivers during adolescence could improve outcomes by accounting for both developmental and individual differences. OBJECTIVE: This study leverages adolescents' everyday smartphone use to investigate person-specific drivers of depression and validate smartphone-based mobile sensing data against established ambulatory methods. We describe the methods of this study and provide an update on its status. After data collection is completed, we will address three specific aims: (1) identify idiographic drivers of dynamic variability in depressive symptoms, (2) test the validity of mobile sensing against ecological momentary assessment (EMA) and actigraphy for identifying these drivers, and (3) explore adolescent baseline characteristics as predictors of these drivers. METHODS: A total of 50 adolescents with elevated symptoms of depression will participate in 28 days of (1) smartphone-based EMA assessing depressive symptoms, processes, affect, and sleep; (2) mobile sensing of mobility, physical activity, sleep, natural language use in typed interpersonal communication, screen-on time, and call frequency and duration using the Effortless Assessment of Risk States smartphone app; and (3) wrist actigraphy of physical activity and sleep. Adolescents and caregivers will complete developmental and clinical measures at baseline, as well as user feedback interviews at follow-up. Idiographic, within-subject networks of EMA symptoms will be modeled to identify each adolescent's person-specific drivers of depression. Correlations among EMA, mobile sensor, and actigraph measures of slee

BACKGROUND: Understanding the neurobiological underpinnings of childhood maltreatment is vital given consistent links with poor mental health. Dimensional models of adversity purport that different types of adversity likely have distinct neurobiological consequences. Adolescence is a key developmental period, during which deviations from normative neurodevelopment may have particular relevance for mental health. However, longitudinal work examining links between different forms of maltreatment, neurodevelopment, and mental health is limited. METHODS: In the present study, we explored associations between abuse, neglect, and longitudinal development of within-network functional connectivity of the salience (SN), default mode (DMN), and executive control network in 142 community residing adolescents. Resting-state fMRI data were acquired at age 16 (T1; M = 16.46 years, s.d. = 0.52, 66F) and 19 (T2; mean follow-up period: 2.35 years). Mental health data were also collected at T1 and T2. Childhood maltreatment history was assessed prior to T1. RESULTS: Abuse and neglect were both found to be associated with increases in within-SN functional connectivity from age 16 to 19. Further, there were sex differences in the association between neglect and changes in within-DMN connectivity. Finally, increases in within-SN connectivity were found to mediate the association between abuse/neglect and lower problematic substance use and higher depressive symptoms at age 19. CONCLUSIONS: Our findings suggest that childhood maltreatment is associated with altered neurodevelopmental trajectories, and that changes in salience processing may be linked with risk and resilience for the development of depression and substance use problems during adolescence, respectively. Further work is needed to understand the distinct neurodevelopmental and mental health outcomes of abuse and neglect.

BACKGROUND: Morning-evening preference is defined as an individual's preference for a morning- or evening-oriented rhythm. Across adolescence, a preference for eveningness becomes more predominant. Although eveningness is cross-sectionally associated with internalizing and externalizing psychopathology, few studies have examined developmental changes in eveningness and its potential biological substrates. Here, we investigated the longitudinal relationships among the trajectory of eveningness preference, internalizing and externalizing psychopathology and white matter development, across adolescence. METHODS: Two-hundred and nine adolescents (49% male) were assessed longitudinally at four separate time points between 12 and 19 years of age. Morning-evening preference and internalizing and externalizing symptoms were assessed at each time point. Diffusion-weighted images were acquired on a subset of participants at the final two time points to estimate changes in global mean fractional anisotropy (FA). Linear mixed models were performed to estimate the change in eveningness over time. A series of linear regression models assessed the influence of change in eveningness on psychopathology and white matter development at age 19. RESULTS: Across the sample, a preference for eveningness became more predominant by 19 years of age. Greater individual-level change towards eveningness significantly predicted greater severity in externalizing, but not internalizing, symptoms at 19 years of age. In contrast, change in psychopathology from 12 to 19 years of age was not associated with morning-eveningness at age 19. A change towards eveningness predicted an attenuated increase in FA between 17 and 19 years of age. CONCLUSIONS: This study suggests that developmental changes in morning-evening preference may predict both neurodevelopmental and psychological outcomes in adolescents.

Depression affects neural processing of emotional stimuli and could, therefore, impact parent-child interactions. However, the neural processes with which mothers with depression process their adolescents' affective interpersonal signals and how this relates to mothers' parenting behavior are poorly understood. Mothers with and without depression (N = 64 and N = 51, respectively; Mage = 40 years) from low-income families completed an interaction task with their adolescents (Mage = 12.8 years), which was coded for both individuals' aggressive, dysphoric, positive and neutral affective behavior. While undergoing fMRI, mothers viewed video clips from this task of affective behavior from their own and an unfamiliar adolescent. Relative to non-depressed mothers, those with depression showed more aggressive and less positive affective behavior during the interaction task and more activation in the bilateral insula, superior temporal gyrus and striatum but less in the lateral prefrontal cortex while viewing aggressive and neutral affect. Findings were comparable for own and unfamiliar adolescents' affect. Heightened limbic, striatal and sensory responses were associated with more aggressive and dysphoric parenting behavior during the interactions, while reduced lateral prefrontal activation was associated with less positive parenting behavior. These results highlight the importance of depressed mothers' affective information processing for understanding mothers' behavior during interactions with their adolescents.

The negative impact of adverse experiences in childhood on neurodevelopment is well documented. Less attention however has been given to the impact of variations in "normative" parenting behaviors. The influence of these parenting behaviors is likely to be marked during periods of rapid brain reorganization, such as late childhood. The aim of the current study was to investigate associations between normative parenting behaviors and the development of structural brain networks across late childhood. Data were collected from a longitudinal sample of 114 mother-child dyads (54% female children, M age 8.41 years, SD = 0.32 years), recruited from low socioeconomic areas of Melbourne, Australia. At the first assessment parenting behaviors were coded from two lab-based interaction tasks and structural magnetic resonance imaging (MRI) scans of the children were performed. At the second assessment, approximately 18 months later (M age 9.97 years, SD = 0.37 years) MRI scans were repeated. Cortical thickness (CT) was extracted from T1-weighted images using FreeSurfer. Structural covariance (SC) networks were constructed from partial correlations of CT estimates between brain regions and estimates of network efficiency and modularity were obtained for each time point. The change in these network measures, from Time 1 to Time 2, was also calculated. At Time 2, less positive maternal affective behavior was associated with higher modularity (more segregated networks), while negative maternal affective behavior was not related. No support was found for an association between local or global efficacy and maternal affective behaviors at Time 2. Similarly, no support was demonstrated for associations between maternal affective behaviors and change in network efficiency and modularity, from Time 1 to Time 2. These results indicate that normative variations in parenting may influence the development of structural brain networks in late childhood and extend current knowledge about envir

An increased prevalence of duplicated Heschl's gyrus (HG) has been repeatedly demonstrated in various stages of schizophrenia as a potential neurodevelopmental marker, but it remains unknown whether other neuropsychiatric disorders also exhibit this macroscopic brain feature. The present magnetic resonance imaging study aimed to examine the disease specificity of the established finding of altered HG patterns in schizophrenia by examining independent cohorts of bipolar disorder (BD) and major depressive disorder (MDD). Twenty-six BD patients had a significantly higher prevalence of HG duplication bilaterally compared to 24 age- and sex-matched controls, while their clinical characteristics (e.g., onset age, number of episodes, and medication) did not relate to HG patterns. No significant difference was found for the HG patterns between 56 MDD patients and 33 age- and sex-matched controls, but the patients with a single HG were characterized by more severe depressive/anxiety symptoms compared to those with a duplicated HG. Thus, in keeping with previous findings, the present study suggests that neurodevelopmental pathology associated with gyral formation of the HG during the late gestation period partly overlaps between schizophrenia and BD, but that HG patterns may make a somewhat distinct contribution to the phenomenology of MDD.

BACKGROUND: A growing body of evidence suggests that parenting behaviors may affect child mental health via altering brain development. There is a scarcity of research, however, that has investigated associations between parenting behavior and brain structure using longitudinal magnetic resonance imaging. This study aimed to investigate associations between parenting behaviors and structural brain development across the transition from childhood to adolescence. METHODS: Participants were 246 children who provided 436 magnetic resonance imaging datasets covering the age range from 8 to 13 years. Parents (94% mothers) completed self-report measures of parenting behavior, and both children and parents reported on child mental health. Factor analysis was used to identify dimensions of parental behavior. Linear mixed-effects models investigated associations between parenting behaviors and age-related change in cortical thickness and surface area and subcortical volume. Mediation models tested whether brain changes mediated associations between parenting behaviors and changes in internalizing/externalizing symptoms. RESULTS: Hypothesized associations between parenting and amygdala, hippocampal, and frontal trajectories were not supported. Rather, higher levels of parent harsh/inconsistent discipline were associated with decreases in surface area in medial parietal and temporal pole regions and reduced cortical thinning in medial parietal regions. Some effects were present in female but not male children. There were no associations between these neurodevelopmental alterations and symptoms. CONCLUSIONS: This study provides insight into the links between parenting behavior and child neurodevelopment. Given the functions of implicated regions, findings may suggest that parental harsh/inconsistent discipline affects the development of neural circuits subserving sensorimotor and social functioning in children.

BackgroundThere is increasing evidence that patterns of pubertal maturation are associated with different patterns of health risk. This study aimed to explore the associations between anthropometric measures and salivary androgen concentrations in pre-adolescent children.MethodsWe analysed a stratified random sample (N=1151) of pupils aged 8–9 years old from 43 primary schools in Melbourne, Australia from the Childhood to Adolescence Transition Study. Saliva samples were assayed for dehydroepiandrosterone (DHEA), DHEA-sulfate and testosterone. Anthropometric measures included height, weight, body mass index (BMI) and waist circumference. Associations between (1) anthropometric measures and each androgen, and (2) hormone status with obesity and parental report of pubertal development were investigated using linear regression modelling with general estimating equations.ResultsGreater height, weight, BMI and waist circumference were positively associated with higher androgen concentrations, after adjusting for sex and socioeconomic status. Being overweight or obese was associated with higher testosterone and DHEA concentrations compared with the normal BMI category. Those who were obese were more likely (OR=2.7, 95% CI 1.61 to 4.43, p<0.001) to be in the top tertile of age-adjusted androgen status in both sexes.ConclusionThis study provides clear evidence for an association between obesity and higher androgen levels in mid-childhood. The adrenal transition may be a critical time period for weight management intervention strategies in order to manage the risk for metabolic problems in later life for high-risk individuals.

Adolescence is a period of dramatic developmental transitions-from puberty-related changes in hormones, bodies, and brains to an increasingly complex social world. The concurrent increase in the onset of many mental disorders has prompted the search for key developmental processes that drive changes in risk for psychopathology during this period of life. Hormonal surges and consequent physical maturation linked to pubertal development in adolescence are thought to affect multiple aspects of brain development, social cognition, and peer relations, each of which have also demonstrated associations with risk for mood and anxiety disorders. These puberty-related effects may combine with other nonpubertal influences on brain maturation to transform adolescents' social perception and experiences, which in turn continue to shape both mental health and brain development through transactional processes. In this review, we focus on pubertal, neural, and social changes across the duration of adolescence that are known or thought to be related to adolescent-emergent disorders, specifically depression, anxiety, and deliberate self-harm (nonsuicidal self-injury). We propose a theoretical model in which social processes (both social cognition and peer relations) are critical to understanding the way in which pubertal development drives neural and psychological changes that produce potential mental health vulnerabilities, particularly (but not exclusively) in adolescent girls.

BACKGROUND: A substantial body of research has emerged suggesting that depression is strongly linked to poor physical health outcomes, which may be partly due to increased allostatic load across stress response systems. Interestingly, health risks associated with depression are also borne by the offspring of depressed persons. Our aim was to simultaneously investigate whether maternal depression is associated not only with increased allostatic load across cardiac control, inflammation, cellular aging, but also if this is transmitted to adolescent children, possibly increasing the risk for early onset of psychiatric conditions and disease in these offspring. METHODS: A preregistered, case-control study of 180 low-income mothers (50% mothers depressed, 50% mothers nondepressed) and their adolescent offspring was conducted to determine how depressed mothers and their adolescent offspring systematically differ in terms of autonomic, sympathetic, and parasympathetic cardiac control; inflammation; cellular aging; and behavioral health in offspring, which are indicators suggestive of higher allostatic load. RESULTS: Findings indicate that depressed mothers and their adolescent offspring differ in terms of comorbid mental and physical health risk profiles that are suggestive of higher allostatic load. Findings indicate that depressed mothers exhibit elevated resting heart rate and decreased heart rate variability, and adolescent offspring of depressed mothers exhibit greater mental health symptoms, elevated heart rate, and accelerated biological aging (shorter telomeres). These effects persisted after controlling for a range of potential covariates, including medication use, sex, age, and adolescents' own mental health symptoms. CONCLUSIONS: Findings indicate that maternal depression is associated with increased allostatic load in depressed women and their adolescent children, possibly increasing risk for early onset of psychiatric conditions and disease in these offspring.

Parenting behavior has a vital role in the development of the brain and cognitive abilities of offspring throughout childhood and adolescence. While positive and aggressive parenting behavior have been suggested to impact neurobiology in the form of abnormal brain activation in adolescents, little work has investigated the links between parenting behavior and the neurobiological correlates of cognitive performance during this age period. In the current longitudinal fMRI study, associations between parenting behaviors and cognitive performance and brain activation across mid- and late-adolescence were assessed. Observed measures of maternal aggressive and positive behavior were recorded in early adolescence (12 years) and correlated with fMRI activation and in-scanner behavioral scores on the multi-source interference task (MSIT) during mid- (16 years; 95 participants) and late-adolescence (19 years; 75 participants). There was a significant reduction in inhibitory-control-related brain activation in posterior parietal and cingulate cortices as participants transitioned from mid- to late-adolescence. Positive maternal behavior in early-adolescence was associated with lower activation in the left parietal and DLPFC during the MSIT in mid-adolescence, whereas maternal aggressive behavior was associated with longer reaction time to incongruent trials in late-adolescence. The study supports the notion that maternal behavior may influence subsequent neurocognitive development during adolescence.

Gender-related differences in the susceptibility, progression and clinical outcomes of alcohol dependence are well-known. However, the neurobiological substrates underlying such differences remain unclear. Therefore, this study aimed to investigate gender differences in the neuroanatomy (i.e. regional brain volumes) of alcohol dependence. We examined the volume of a priori regions of interest (i.e., orbitofrontal cortex, hippocampus, amygdala, nucleus accumbens, caudate, putamen, pallidum, thalamus, corpus callosum, cerebellum) and global brain measures (i.e., total grey matter (GM), total white matter (WM) and cerebrospinal fluid). Volumes were compared between 660 people with alcohol dependence (228 women) and 326 controls (99 women) recruited from the ENIGMA Addiction Working Group, accounting for intracranial volume, age and education years. Compared to controls, individuals with alcohol dependence on average had (3-9%) smaller volumes of the hippocampus (bilateral), putamen (left), pallidum (left), thalamus (right), corpus callosum, total GM and WM, and cerebellar GM (bilateral), the latter more prominently in women (right). Alcohol-dependent men showed smaller amygdala volume than control men, but this effect was unclear among women. In people with alcohol dependence, more monthly standard drinks predicted smaller amygdala and larger cerebellum GM volumes. The neuroanatomical differences associated with alcohol dependence emerged as gross and widespread, while those associated with a specific gender may be confined to selected brain regions. These findings warrant future neuroscience research to account for gender differences in alcohol dependence to further understand the neurobiological effects of alcohol dependence.

Puberty triggers a period of structural "re-organization" in the brain, when rising hormone levels act via receptors to influence morphology. However, our understanding of these neuroendocrine processes in humans remains poor. As such, the current longitudinal study characterized development of the human subcortex during puberty, including changes in relation to pubertal (Tanner) stage and hormone (testosterone, dehydroepiandrosterone [DHEA]) levels. Beyond normative group-level patterns of development, we also examined whether individual differences in the rate of pubertal maturation (i.e., "pubertal/hormonal tempo") were associated with variations in subcortical trajectories. Participants (N = 192; scans = 366) completed up to three waves of MRI assessments between 8.5 and 14.5 years of age. Parents completed questionnaire assessments of pubertal stage at each wave, and adolescents provided hormone samples on a subset of waves. Generalized additive mixture models were used to characterize trajectories of subcortical development. Results showed that development of most subcortical structures was related to pubertal stage, although findings were mostly non-significant when controlling for age. Testosterone and DHEA levels were related to development of the amygdala, hippocampus and pallidum in both sexes, and findings in the amygdala remained significant when controlling for age. Additionally, we found that variability in hormonal (specifically testosterone) tempo was related to right hippocampal development in males, with an accelerated pattern of hippocampal development in those with greater increases in testosterone levels. Overall, our findings suggest prominent hormonal influences on the amygdala and hippocampus, consistent with the prevalence of androgen and estrogen receptors in these regions. We speculate that these findings are most likely reflective of the important role of adrenarcheal processes on adolescent brain development.

Males and females show different patterns of cannabis use and related psychosocial outcomes. However, the neuroanatomical substrates underlying such differences are poorly understood. The aim of this study was to map sex differences in the neurobiology (as indexed by brain volumes) of dependent and recreational cannabis use. We compared the volume of a priori regions of interest (i.e., amygdala, hippocampus, nucleus accumbens, insula, orbitofrontal cortex (OFC), anterior cingulate cortex and cerebellum) between 129 regular cannabis users (of whom 70 were recreational users and 59 cannabis dependent) and 114 controls recruited from the ENIGMA Addiction Working Group, accounting for intracranial volume, age, IQ, and alcohol and tobacco use. Dependent cannabis users, particularly females, had (marginally significant) smaller volumes of the lateral OFC and cerebellar white matter than recreational users and controls. In dependent (but not recreational) cannabis users, there was a significant association between female sex and smaller volumes of the cerebellar white matter and OFC. Volume of the OFC was also predicted by monthly standard drinks. No significant effects emerged the other brain regions of interest. Our findings warrant future multimodal studies that examine if sex and cannabis dependence are specific key drivers of neurobiological alterations in cannabis users. This, in turn, could help to identify neural pathways specifically involved in vulnerable cannabis users (e.g., females with cannabis dependence) and inform individually tailored neurobiological targets for treatment.

BACKGROUND: Use of social networking in later childhood and adolescence has risen quickly. The consequences of these changes for mental health are debated but require further empirical evaluation. METHODS: Using data from the Childhood to Adolescence Transition Study (n = 1,156), duration of social networking use was measured annually at four time points from 11.9 to 14.8 years of age (≥1 h/day indicating high use). Cross-sectional and prospective relationships between social networking use and depressive and anxiety symptoms were examined. RESULTS: In adjusted (age, socioeconomic status, prior mental health history) cross-sectional analyses, females with high social networking use had greater odds of depressive (odds ratio [OR]: 2.15; 95% confidence interval [CI]: 1.58-2.91) and anxiety symptoms (OR: 1.99; 95% CI: 1.32-3.00) than those that used a few minutes at most, while males with high social networking use had 1.60 greater odds of reporting depressive symptoms (95% CI: 1.09-2.35). For females, an increased odds of depressive symptoms at age 14.8 was observed for high social networking use at one previous wave and at two or three previous waves, even after adjustment (OR: 1.76; 95% CI: 1.11-2.78; OR: 2.06, 95% CI: 1.27-3.37, respectively) compared to no wave of high use. CONCLUSIONS: Our results suggest weak to moderate increased odds of depression and anxiety in girls and boys with high social networking use versus low/normal use. These findings indicate that prevention programs for early mental health problems might benefit from targeting social networking use in early adolescence.

The brain undergoes extensive structural changes during adolescence, concurrent to puberty-related physical and hormonal changes. While animal research suggests these biological processes are related to one another, our knowledge of brain development in humans is largely based on age-related processes. Thus, the current study characterized puberty-related changes in human brain structure, by combining data from two longitudinal neuroimaging cohorts. Beyond normative changes in cortical thickness, we examined whether individual differences in the rate of pubertal maturation (or "pubertal tempo") was associated with variations in cortical trajectories. Participants (N = 192; scans = 366) completed up to three waves of MRI assessments between 8.5 and 14.5 years of age, as well as questionnaire assessments of pubertal stage at each wave. Generalized additive mixture models were used to characterize trajectories of cortical development. Results revealed widespread linear puberty-related changes across much of the cortex. Many of these changes, particularly within the frontal and parietal cortices, were independent of age-related development. Males exhibiting faster pubertal tempo demonstrated greater thinning in the precuneus and frontal cortices than same-aged and -sex peers. Findings suggest that the unique influence of puberty on cortical development may be more extensive than previously identified, and also emphasize important individual differences in the coupling of these developmental processes.

A substantial body of knowledge suggests that exposure to adverse family environments - including violence and neglect - influences many aspects of brain development. Relatively less attention has been directed toward the influence of "normative" differences in parenting behaviors. Given the rapid brain reorganization during late childhood, parenting behaviors are particularly likely to impact the structure of the brain during this time. This study investigated associations between maternal parenting behaviors and the organization of structural brain networks in late childhood, as measured by structural covariance. One hundred and forty-five typically developing 8-year-olds and their mothers completed questionnaire measures and two observed interaction tasks; magnetic resonance imaging (MRI) scans were obtained from the children. Measures of maternal negative, positive, and communicative behavior were derived from the interaction tasks. Structural covariance networks based on partial correlations between cortical thickness estimates were constructed and estimates of modularity were obtained using graph theoretical analysis. High levels of negative maternal behavior were associated with low modularity. Minimal support was found for an association between positive maternal behaviors and modularity and between maternal communicative behaviors and modularity. Our findings suggest that variation in negative maternal behavior is associated with the structural organization of brain networks in children.

BACKGROUND: There is increasing evidence that patterns of pubertal maturation are associated with different patterns of health risk. This study aimed to explore the associations between anthropometric measures and salivary androgen concentrations in pre-adolescent children. METHODS: We analysed a stratified random sample (N=1151) of pupils aged 8-9 years old from 43 primary schools in Melbourne, Australia from the Childhood to Adolescence Transition Study. Saliva samples were assayed for dehydroepiandrosterone (DHEA), DHEA-sulfate and testosterone. Anthropometric measures included height, weight, body mass index (BMI) and waist circumference. Associations between (1) anthropometric measures and each androgen, and (2) hormone status with obesity and parental report of pubertal development were investigated using linear regression modelling with general estimating equations. RESULTS: Greater height, weight, BMI and waist circumference were positively associated with higher androgen concentrations, after adjusting for sex and socioeconomic status. Being overweight or obese was associated with higher testosterone and DHEA concentrations compared with the normal BMI category. Those who were obese were more likely (OR=2.7, 95% CI 1.61 to 4.43, p<0.001) to be in the top tertile of age-adjusted androgen status in both sexes. CONCLUSION: This study provides clear evidence for an association between obesity and higher androgen levels in mid-childhood. The adrenal transition may be a critical time period for weight management intervention strategies in order to manage the risk for metabolic problems in later life for high-risk individuals.

Background: Despite recent studies linking pubertal processes to brain development, as well as research demonstrating the importance of both pubertal and neurodevelopmental processes for adolescent mental health, there is limited knowledge of the full pathways and mechanisms behind the emergence of mental illnesses such as depression and anxiety disorders in adolescence. The Transitions in Adolescent Girls (TAG) study aims to understand the complex relationships between pubertal development, brain structure and connectivity, the behavioral and neural correlates of social and self-perception processes, and adolescent mental health in female adolescents.     Methods: The TAG study includes 174 female adolescents aged 10.0 to 13.0 years, recruited from the local community in Lane County, Oregon, USA. The participants, along with a parent/guardian, will complete three waves of assessment over the course of 3 years; the third wave is currently underway. Each wave includes collection of four saliva samples (one per week) and one hair sample for the assessment of hormone levels and immune factors; an MRI session including structural, diffusion, resting-state functional and task-based functional scans; the Kiddie Schedule for Affective Disorders and Schizophrenia (K-SADS), a diagnostic interview on current and lifetime mental health; production of a short self-narrative video; and measurement of height, weight, and waist circumference. The functional MRI tasks include a self-evaluation paradigm and a self-disclosure paradigm. In addition, adolescents and their parents/guardians complete a number of surveys to report on the adolescent's pubertal development, mental health, social environment and life events; adolescents also report on various indices of self-perception and social-emotional functioning.   Discussion: The knowledge gained from this study will include developmental trajectories of pubertal, neurological, and social proce

COVID-19 emerged in November 2019 leading to a global pandemic that has not only resulted in widespread medical complications and loss of life, but has also impacted global economies and transformed daily life. The current rapid response study in a convenience online sample quickly recruited 2,065 participants across the United States, Canada, and Europe in late March and early April 2020. Cross-sectional findings indicated elevated anxiety and depressive symptoms compared to historical norms, which were positively associated with COVID-19 concern more strongly than epidemiological data signifying risk (e.g., world and country confirmed cases). Employment loss was positively associated with greater depressive symptoms and COVID-19 concern, and depressive symptoms and COVID-19 concern were significantly associated with more stringent self-quarantine behavior. The rapid collection of data during the early phase of this pandemic is limited by under-representation of non-White and middle age and older adults. Nevertheless, these findings have implications for interventions to slow the spread of COVID-19 infection.

Both depression and substance use problems have their highest incidence during youth (i.e., adolescence and emerging adulthood), and are characterized by emotion regulation deficits. Influential neurodevelopmental theories suggest that alterations in the function of limbic and frontal regions render youth susceptible to these deficits. However, whether depression and substance use in youth are associated with similar alterations in emotion regulation neural circuitry is unknown. In this systematic review we synthesized the results of functional magnetic resonance imaging (fMRI) studies investigating the neural correlates of emotion regulation in youth depression and substance use. Resting-state fMRI studies focusing on limbic connectivity were also reviewed. While findings were largely inconsistent within and between studies of depression and substance use, some patterns emerged. First, youth depression appears to be associated with exaggerated amygdala activity in response to negative stimuli; second, both depression and substance use appear to be associated with lower functional connectivity between the amygdala and prefrontal cortex during rest. Findings are discussed in relation to support for existing neurodevelopmental models, and avenues for future work are suggested, including studying neurodevelopmental trajectories from a network perspective.

BACKGROUND: Although early life adversity (ELA) increases risk for psychopathology, mechanisms linking ELA with the onset of psychopathology remain poorly understood. Conceptual models have argued that ELA accelerates development. It is unknown whether all forms of ELA are associated with accelerated development or whether early maturation is a potential mechanism linking ELA with psychopathology. We examine whether two distinct dimensions of ELA - threat and deprivation - have differential associations with pubertal timing in girls, and evaluate whether accelerated pubertal timing is a mechanism linking ELA with the onset of adolescent psychopathology. METHODS: Data were drawn from a large, nationally representative sample of 4937 adolescent girls. Multiple forms of ELA characterized by threat and deprivation were assessed along with age at menarche (AAM) and the onset of DSM-IV fear, distress, externalizing, and eating disorders. RESULTS: Greater exposure to threat was associated with earlier AAM (B = -0.1, p = 0.001). Each 1-year increase in AAM was associated with reduced odds of fear, distress, and externalizing disorders post-menarche (ORs = 0.74-0.85). Earlier AAM significantly mediated the association between exposure to threat and post-menarche onset of distress (proportion mediated = 6.2%), fear (proportion mediated = 16.3%), and externalizing disorders (proportion mediated = 2.9%). CONCLUSIONS: Accelerated pubertal development in girls may be one transdiagnostic pathway through which threat-related experiences confer risk for the adolescent onset of mental disorders. Early pubertal maturation is a marker that could be used in both medical and mental health settings to identify trauma-exposed youth that are at risk for developing a mental disorder during adolescence in order to better target early interventions.

INTRODUCTION: No prospective studies have examined the prevalence, antecedents or concurrent characteristics associated with self-harm in non-treatment-seeking primary school-aged children. METHODS: In this cohort study from Melbourne, Australia we assessed 1239 children annually from age 8-9 years (wave 1) to 11-12 years (wave 4) on a range of health, social, educational and family measures. Past-year self-harm was assessed at wave 4. We estimated the prevalence of self-harm and used multivariable logistic regression to examine associations with concurrent and antecedent factors. RESULTS: 28 participants (3% of the 1059 with self-harm data; 18 girls [3%], 10 boys [2%]) reported self-harm at age 11-12 years. Antecedent (waves 1-3) predictors of self-harm were: persistent symptoms of depression (sex-age-socioeconomic status adjusted odds ratio [aOR]: 7.8; 95% confidence intervals [CI] 2.6 to 24) or anxiety (aOR: 5.1; 95%CI 2.1 to 12), frequent bullying victimisation (aOR: 24.6; 95%CI 3.8 to 158), and recent alcohol consumption (aOR: 2.9; 95%CI 1.2 to 7.1). Concurrent (wave 4) associations with self-harm were: having few friends (aOR: 8.7; 95%CI 3.2 to 24), poor emotional control (aOR: 4.2; 95%CI 1.9 to 9.6), antisocial behaviour (theft-aOR: 3.1; 95%CI 1.2 to 7.9; carrying a weapon-aOR: 6.9; 95%CI 3.1 to 15), and being in mid-puberty (aOR: 6.5; 95%CI 1.5 to 28) or late/post-puberty (aOR: 14.4; 95%CI 2.9 to 70). CONCLUSIONS: The focus of intervention efforts aimed at preventing and reducing adolescent self-harm should extend to primary school-aged children, with a focus on mental health and peer relationships during the pubertal transition.

Abnormal melatonin secretion has been demonstrated in patients with affective disorders such as major depressive disorder (MDD) and bipolar disorder (BD). However, magnetic resonance imaging (MRI) studies that previously investigated the volume of the pineal gland, which regulates circadian rhythms by secreting melatonin, in these patients reported inconsistent findings. The present study employed MRI to examine pineal gland volumes and pineal cyst prevalence in 56 MDD patients (29 currently depressed and 27 remitted patients), 26 BD patients, and matched controls (33 for MDD and 24 for BD). Pineal volumes and cyst prevalence in the current MDD, remitted MDD, and BD groups did not significantly differ from those of the healthy controls. However, pineal gland volumes were significantly smaller in the current MDD subgroup of non-melancholic depression than in the melancholic MDD subgroup. Interestingly, pineal volumes correlated negatively with the severity of loss of interest in the current MDD group. Medication and the number of affective episodes were not associated with pineal volumes in the MDD or BD group. While these results do not suggest that pineal volumes reflect abnormal melatonin secretion in affective disorders, they do point to the possibility that pineal abnormalities are associated with clinical subtypes of MDD and its symptomatology.

Peers become increasingly important during adolescence, with emerging gender differences in peer relationships associated with distinct behavioral and emotional outcomes. Males tend to socialize in larger peer groups with competitive interactions, whereas females engage in longer bouts of dyadic interaction with more intimacy. To examine gender differences in neural response to ecologically valid displays of positive affect and future social interactions, 52 adolescents (14-18 years old; female = 30) completed a social reward functional magnetic resonance imaging (fMRI) task with videos of a same-gender best friend (BF) or unfamiliar peer (UP) expressing positive (versus neutral) affect. Participants completed ecological momentary assessment of social experiences for two 5-day intervals. Compared with females, males more often reported that their happiest experience in the past hour occurred with class/teammates. Females and males displayed greater fusiform gyrus (FG) activation during BF and UP conditions, respectively (pvoxel<0.0001, pcluster<0.05, family-wise error). Compared with males, females exhibited greater nucleus accumbens (NAcc)-precuneus functional connectivity to BF Positive> UP Positive. An exploratory analysis indicated that the association of male gender with a greater proportion of positive experiences with class/teammates was statistically mediated by greater NAcc-precuneus functional connectivity. Gender differences in positive social experiences may be associated with reward and social cognition networks.

The quality of early caregiver-infant relationships has powerful implications for health trajectories across the lifespan, including associations with adult inflammation. However, because relatively few studies have examined this association during infancy, it remains unclear when this impact occurs and whether it is associated with longitudinal changes in salivary concentrations of inflammation across infancy. In 45 infants, we investigated whether the quality of infant-caregiver attachment (secure vs. insecure) was associated not only with levels of salivary C-reactive protein (sCRP) cross-sectionally, but also with changes in sCRP across 6 months. Interestingly, while there were no cross-sectional associations between infant-caregiver attachment and inflammation at 12 months of age, infant-caregiver attachment security predicted lower levels of sCRP 6 months later. In addition, attachment security predicted decreasing levels of sCRP from 12 months to 18 months of age. Implications for understanding the influence of the quality of early relationships on biological mechanisms related to disease are discussed.

BACKGROUND: Young people experiencing mental health problems are often reluctant to seek help, particularly from professionals (i.e., doctors or mental health workers). MAKINGtheLINK is a school-based intervention that aims to help adolescents overcome barriers to seeking professional help for mental health and substance use problems. METHODS: A cluster randomised controlled trial was conducted to evaluate the 12-month outcomes of MAKINGtheLINK among 2447 participants (Mean age=14.9 years, SD=0.5 years, 50% male). Randomisation resulted in 1130 students from 11 schools allocated to receive the intervention, and 1317 students from 10 schools allocated to the wait-list control group. After the baseline assessment, follow-ups were conducted at 6-weeks (n = 2045), 6-months (n = 1874), and 12-months (n = 1827). The primary outcome measure was help-seeking behaviour, from both formal (e.g., health professionals) and informal (e.g., friends, family members) sources. The trial was registered with the Australia and New Zealand Clinical Trials Register (ANZCTR) on the 27th of February 2013 (registration number ACTRN12613000235707). FINDINGS: The intervention was not associated with overall help-seeking at the 12-month follow-up (p = 0.99, odds ratio [OR]=1.00, 95% CI for OR = 0.70-1.42), or help-seeking for depression (p = 0.28, OR = 1.21, 95%CI =0.86-1.69), stress and anxiety (p = 0.73, OR = 1.04, 95%CI = 0.74-1.47), or alcohol/other drugs (p = 0.84, OR=1.12, CI=0.37-3.37). However, the intervention was associated with increased help-seeking from formal sources (compared to informal sources) both overall (p = 0.005, OR = 1.81, 95%CI = 1.19-2.75), as well as for depression (p = 0.01, OR=2.09, 95%CI=1.19-3.67), and stress and anxiety (p < 0.006, OR = 1.72, 95%CI = 1.17-2.54). INTERPRETATION: Rates of help-seeking remained unchanged following the intervention. However, MAKINGtheLINK effectively improved the quality of adolescent help-seeking behaviour by increasing help-seeking

Neuroscientific tools and approaches such as neuroimaging, measures of neuroendocrine and psychoneuroimmune activity, and peripheral physiology are increasingly used in clinical science and health psychology research. We define translational neuroscience (TN) as a systematic, theory-driven approach that aims to develop and leverage basic and clinical neuroscientific knowledge to aid the development and optimization of clinical and public health interventions. There is considerable potential across basic and clinical science fields for this approach to provide insights into mental and physical health pathology that had previously been inaccessible. For example, TN might hold the potential to enhance diagnostic specificity, better recognize increased vulnerability in at-risk populations, and augment intervention efficacy. Despite this potential, there has been limited consideration of the advantages and limitations of such an approach. In this article, we articulate extant challenges in defining TN and propose a unifying conceptualization. We illustrate how TN can inform the application of neuroscientific tools to realistically guide clinical research and inform intervention design. We outline specific leverage points of the TN approach and barriers to progress. Ten principles of TN are presented to guide and shape the emerging field. We close by articulating ongoing issues facing TN research. (PsycINFO Database Record (c) 2019 APA, all rights reserved).

Early adolescence is marked by puberty, and is also a time of flux in self-perception. However, there is limited research on the neural correlates of self-evaluation in relation to pubertal development. The current study examined relationships between neural activation during self-evaluation of social traits and maturation (age and pubertal development) in a community sample of female adolescents. Participants (N = 143; age M = 11.65, range = 10.0-13.0) completed a functional MRI task in which they judged the self-descriptiveness of adjectives for prosocial, antisocial and social status-related traits. Pubertal development was based on self-report, and was also examined using morning salivary testosterone, dehydroepiandrosterone, and estradiol. Contrary to preregistered hypotheses, neither age nor pubertal development were related to neural activation during self-evaluation. We further examined whether activation in two regions-of-interest, the ventromedial prefrontal cortex (vmPFC) and perigenual anterior cingulate (pgACC), was associated with trial-level self-evaluative behavior. In line with preregistered hypotheses, higher vmPFC and pgACC activation during self-evaluation were both associated with a higher probability of endorsing negative adjectives, and a lower probability of endorsing positive adjectives. Future studies should examine neural trajectories of self-evaluation longitudinally, and investigate the predictive value of the neural correlates of self-evaluation for adolescent mental health.

Researchers have increasingly begun to use consumer wearables or wrist-worn smartwatches and fitness monitors for measurement of cardiovascular psychophysiological processes related to mental and physical health outcomes. These devices have strong appeal because they allow for continuous, scalable, unobtrusive, and ecologically valid data collection of cardiac activity in "big data" studies. However, replicability and reproducibility may be hampered moving forward due to the lack of standardization of data collection and processing procedures, and inconsistent reporting of technological factors (e.g., device type, firmware versions, and sampling rate), biobehavioral variables (e.g., body mass index, wrist dominance and circumference), and participant demographic characteristics, such as skin tone, that may influence heart rate measurement. These limitations introduce unnecessary noise into measurement, which can cloud interpretation and generalizability of findings. This paper provides a brief overview of research using commercial wearable devices to measure heart rate, reviews literature on device accuracy, and outlines the challenges that non-standardized reporting pose for the field. We also discuss study design, technological, biobehavioral, and demographic factors that can impact the accuracy of the passive sensing of heart rate measurements, and provide guidelines and corresponding checklist handouts for future study data collection and design, data cleaning and processing, analysis, and reporting that may help ameliorate some of these barriers and inconsistencies in the literature.

Sexual minority adolescents (SMA) are more likely to suffer from depression, putatively through experiences of social stress and victimization interfering with processing of social reward. Alterations in neural reward networks, which develop during adolescence, confer risk for the development of depression. Employing both social and monetary reward fMRI tasks, this is the first neuroimaging study to examine function in reward circuitry as a potential mechanism of mental health disparities between SMA and heterosexual adolescents. Eight SMA and 38 heterosexual typically developing adolescents completed self-report measures of depression and victimization, and underwent fMRI during monetary and peer social reward tasks in which they received positive monetary or social feedback, respectively. Compared with heterosexual adolescents, SMA had greater interpersonal depressive symptoms and exhibited blunted neural responses to social, but not monetary, reward in socioaffective processing regions that are associated with depressive symptoms. Specifically, compared with heterosexual adolescents, SMA exhibited decreased activation in the right medial prefrontal cortex, left anterior insula (AI), and right temporoparietal junction (TPJ) in response to being liked. Lower response in the right TPJ was associated with greater interpersonal depressive symptoms. These results suggest that interpersonal difficulties and the underlying substrates of response to social reward (perhaps more so than response to monetary reward) may confer risk for development of depressive symptoms in SMA.

In threatening environments, the short (S) allele of 5-HTTLPR is proposed to augment risk for depression. However, it is unknown whether 5-HTTLPR variation increases risk for depression in environments of deprivation, lacking positive or nurturant features. Two independent longitudinal studies (n = 681 and 176, respectively) examined whether 5-HTTLPR moderated associations between low levels of positive parenting at 11-13 years and subsequent depression at 17-19 years. In both studies only LL homozygous adolescents were at greater risk for depression with decreasing levels of positive parenting. Thus, while the S allele has previously been identified as a susceptible genotype, these findings suggest that the L allele may also confer sensitivity to depression in the face of specific environmental challenges.

Children from highly disadvantaged families tend to experience worse health, educational, and job outcomes than less disadvantaged peers. However, the mechanisms underlying these relationships remain to be explicated. In particular, few studies have investigated the relationships between the psychosocial influences that children are exposed to early in life and longer term cortisol output. This study aims to contribute to the literature by exploring how disadvantaged young children's experiences of family adversity, and parenting and family functioning, are related to their long-term cortisol levels. A sample of 60 children (26 males, mean = 4.25 years, SD = 1.68) and their mothers (mean = 34.18 years, SD = 7.11) from a low-income population took part in a single assessment. Mothers completed questionnaires on the family environment, parenting practices, and child behaviour. Children provided a hair sample for cortisol assay and anthropometric measures. A parsimonious multivariate regression model (including potential predictors identified by a selection algorithm) was used to investigate the correlates of hair cortisol concentration (HCC) in children. Higher levels of social exclusion, being male, and younger age were each associated with higher HCC. Maternal nurturing and emotion coaching were associated with lower HCC. Findings suggest that chronic stress may underlie relationships between adversity and its long-term effects and that HCC offers a promising method for examining chronic stress in children and evaluating interventions by which it can be ameliorated.

Background: Parenting a toddler is a challenging experience for many parents with times of emotional dysregulation in both parent and child. Parenting interventions may be useful for parents to improve their ability to regulate emotions and respond to children's emotions in a way that assists the child to understand and regulate emotions (emotion competence). Tuning in to Toddlers (TOTS) is a new parenting program that aims to improve parents' emotion regulation, emotional responsiveness, and emotion coaching (aspects of emotion socialization) to promote optimal emotional development in toddlers, and prevent social and behavioral difficulties. This paper outlines the rationale, methodology, intervention, and recruitment used in a trial to establish program efficacy. Methods/Design: Parents of toddlers aged 18-36 months old were recruited through child care centers (CC) and maternal child health (MCH) centers in Melbourne, Australia and were allocated to either intervention or a 15-month wait-list control condition in a cluster-randomized controlled design. Inclusion criteria were a child in the age range at baseline attending one of the CC or MCH centers. Exclusion criteria were if the parent/carer had insufficient English to attend the intervention and complete measures. Parents in the intervention condition participated in the 6-session group TOTS program delivered by two facilitators using a structured manual and measures of program fidelity and acceptability. Participants in the wait-list control condition received the intervention after a 15-month waiting period. Participants completed measures at baseline, post-intervention (intervention participants only) and 15-month follow-up. Primary outcome measures included parent emotion socialization (parent-report and observed). Secondary outcomes included parent-reported parent functioning (emotion regulation and mental health), toddler social, emotional and behavioral functioning, and parent and toddler systemic cor

Hormone analysis is a valuable tool for understanding how physiology and behavior interact. Cortisol in hair has recently been examined as a measure of longer-term hormone output. The aim of this study was to investigate the relationships between other androgens in hair and anthropometric measures. In a child sample (n = 114, mean age: 8.5 years, 66 females) levels of cortisol, dehydroepiandrosterone (DHEA) and testosterone were assayed in the 0-3 cm section proximal to scalp. The 3-6 cm segment within a subsample of female participants (n = 35) was examined and compared. Results showed that testosterone strongly correlated with DHEA, and moderately correlated with cortisol (0-3 cm only). Higher hormone concentrations were present in the 3-6 cm segment. Finally, there was a weak positive association between DHEA and height. The replication of previously identified associations between androgens, particularly testosterone-DHEA, and with developmental measures suggests hair may offer a valid method of hormone measurement for DHEA and testosterone.

Levels of the adrenal hormones dehydroepiandrosterone (DHEA), its sulfate (DHEAS), and testosterone, have all been linked to behavior and mental health during adrenarche, and preclinical studies suggest that these hormones influence brain development. However, little is known about how variation in these hormones is associated with white matter structure during this period of life. The current study aimed to examine associations between DHEA, DHEAS, and testosterone, and white matter microstructure during adrenarche. To avoid the confounding effect of age on hormone levels, we tested these associations in 87 children within a narrow age range (mean age 9.56 years, SD=0.34) but varying in hormone levels. All children provided saliva samples directly after waking and completed a diffusion-weighted MRI scan. Higher levels of DHEA were associated with higher mean diffusivity (MD) in a widespread cluster of white matter tracts, which was partially explained by higher radial diffusivity (RD) and partially by higher axial diffusivity (AD). In addition, there was an interaction between DHEA and testosterone, with higher levels of testosterone being associated with higher fractional anisotropy (FA) and lower MD and RD when DHEA levels were relatively high, but with lower FA and higher MD and RD when DHEA levels were low. These findings suggest that relatively early exposure to DHEA, as well as an imbalance between the adrenal hormones, may be associated with alterations in white matter microstructure. These findings highlight the potential relevance of adrenarcheal hormones for structural brain development.

OBJECTIVE: Temperament has associations with later physical health outcomes, yet there is a dearth of research exploring the connection between temperament and mechanisms that have known associations with these health outcomes. Recent research has delineated a connection between personality and inflammation during adulthood, but this association has not yet been studied in adolescent samples. DESIGN: We investigated whether stable adolescent temperament (averaged over two years), specifically effortful control and negative emotionality, provided a more robust prediction of inflammation as measured by salivary C-reactive protein (sCRP), than depressive symptoms. METHODS: Temperament and depressive symptoms were measured in a sample of sixty-three adolescents (37 males) when they were approximately 12 years old (mean age = 12.30, SD = 0.69) and again when they were approximately 14 years old (mean age = 14.84, SD = 0.49). Levels of sCRP were determined approximately 7 months later (mean = 6.77, SD = 2.99) when participants were approximately 15 years old (mean age = 15.49, SD = 0.49). RESULTS: Regression analyses revealed that effortful control (EC) was significantly associated with lower sCRP levels, while higher negative emotionality (NE) was significantly associated with higher sCRP levels. Furthermore, these associations were larger than those for depressive symptoms and were differentially impacted by the addition of covariates. Implications for the role of stable risk and protective factors in inflammatory processes are discussed. CONCLUSIONS: These findings are the first to show associations between adolescent temperament and inflammation. Furthermore, these findings extend previous personality research to temperamental research in a younger sample of adolescents. Statement of contribution What is already known? There is a large extant literature on the association between depressive symptoms and inflammation. There is a smaller extant literature on the associa

Adolescents are notorious for engaging in risky, reward-motivated behavior, and this behavior occurs most often in response to social reward, typically in the form of peer contexts involving intense positive affect. A combination of greater neural and behavioral sensitivity to peer positive affect may characterize adolescents who are especially likely to engage in risky behaviors. To test this hypothesis, we examined 50 adolescents' reciprocal positive affect and neural response to a personally relevant, ecologically valid pleasant stimulus: positive affect expressed by their best friend during a conversation about past and future rewarding mutual experiences. Participants were typically developing community adolescents (age 14-18 years, 48.6% female), and risky behavior was defined as a factor including domains such as substance use, sexual behavior and suicidality. Adolescents who engaged in more real-life risk-taking behavior exhibited either a combination of high reciprocal positive affect behavior and high response in the left ventrolateral prefrontal cortex-a region associated with impulsive sensation-seeking-or the opposite combination. Behavioral and neural sensitivity to peer influence could combine to contribute to pathways from peer influence to risky behavior, with implications for healthy development.

INTRODUCTION: Working Memory and Task-Switching are essential components of cognitive control, which underlies many symptoms evident across multiple neuropsychiatric disorders, including psychotic and mood disorders. Vulnerability to these disorders has a substantial genetic component, suggesting that clinically unaffected first-degree relatives may carry some vulnerability-related traits. Converging evidence from animal and human studies demonstrates that dopamine transmission, striatal and frontal brain regions, and attention and switching behaviors are essential components of a multilevel circuit involved in salience, and disruptions in that circuit may lead to features of psychosis. Yet, it is possible that unaffected relatives may also possess characteristics that protect against development of illness. We hypothesized that reduced switch cost in a cued task-switching task, may be a behavioral expression of this "resilience" phenotype that will be observable in unaffected relatives. METHODS: We tested a large community sample (n = 536) via the web, to assess different subcomponents of cognitive control, including task-switching and working memory, as well as risk-taking, among individuals who report having an affected relative with a psychotic or mood disorder. RESULTS: Healthy individuals with suspected genetic risk due to a self-reported familial history of a psychotic disorder demonstrated better task-switching performance compared to healthy people without a psychiatrically ill relative and those with a relative with a mood disorder. This result was specific to illness status and task domain, in that individuals with a personal history of depression or anxiety did not show improved task-switching performance, and this improvement was selective to task-switching and not seen in other putative cognitive control domains (working memory or risk taking). CONCLUSIONS: Although this study has limitations and independent replication is needed, these preliminary fin

OBJECTIVE: The transition from childhood to adolescence is a vulnerable period for the development of anxiety symptoms. There is some evidence that hormonal changes occurring during adrenarche, an early pubertal phase, might play a role in this increased vulnerability. Little is known about underlying brain mechanisms. Given the role of the amygdala-based fear circuit in anxiety, the current study aimed to investigate whether children's adrenarcheal hormone levels were associated with functional connectivity of the amygdala while processing fearful facial expressions, and how this in turn related to anxiety symptoms. METHOD: Participants were 83 children (M age 9.53 years) who completed two morning saliva collections to measure levels of dehydroepiandrosterone (DHEA), its sulphate (DHEAS), and testosterone. They also completed the Spence Children's Anxiety Scale (SCAS), and viewed fearful and calm facial expressions while undergoing a functional MRI scan. Psychophysiological interaction (PPI) analyses were performed to examine amygdala connectivity and significant clusters were fed into a bootstrapping mediation model. RESULTS: In boys, mediation analyses showed an indirect positive effect of testosterone on anxiety symptoms, which was mediated by amygdala-secondary visual cortex connectivity as well as amygdala-anterior cingulate connectivity. In girls, DHEAS showed a negative indirect association with anxiety symptoms mediated by amygdala connectivity to the fusiform face area and insula. CONCLUSION: The results indicate unique roles for adrenarcheal hormones in anxiety and suggest that amygdala connectivity may represent an important neural mechanism in these associations. Importantly, results reveal prominent sex differences in the biological mechanisms associated with anxiety in children undergoing adrenarche.