Alterations in fear learning as a mechanism linking childhood exposure to violence with PTSD symptoms: a longitudinal study.

BACKGROUND: Fear learning is a core component of conceptual models of how adverse experiences may influence psychopathology. Specifically, existing theories posit that childhood experiences involving childhood trauma are associated with altered fear learning processes, while experiences involving deprivation are not. Several studies have found altered fear acquisition in youth exposed to trauma, but not deprivation, although the specific patterns have varied across studies. The present study utilizes a longitudinal sample of children with variability in adversity experiences to examine associations among childhood trauma, fear learning, and psychopathology in youth. METHODS: The sample includes 170 youths aged 10-13 years (M = 11.56, s.d. = 0.47, 48.24% female). Children completed a fear conditioning task while skin conductance responses (SCR) were obtained, which included both acquisition and extinction. Childhood trauma and deprivation severity were measured using both parent and youth report. Symptoms of anxiety, externalizing problems, and post-traumatic stress disorder (PTSD) were assessed at baseline and again two-years later. RESULTS: Greater trauma-related experiences were associated with greater SCR to the threat cue (CS+) relative to the safety cue (CS-) in early fear acquisition, controlling for deprivation, age, and sex. Deprivation was unrelated to fear learning. Greater SCR to the threat cue during early acquisition was associated with increased PTSD symptoms over time controlling for baseline symptoms and mediated the relationship between trauma and prospective changes in PTSD symptoms. CONCLUSIONS: Childhood trauma is associated with altered fear learning in youth, which may be one mechanism linking exposure to violence with the emergence of PTSD symptoms in adolescence.

Does reward processing moderate or mediate the link between childhood adversity and psychopathology: A longitudinal study.

Childhood adversity is common and associated with elevated risk for transdiagnostic psychopathology. Reward processing has been implicated in the link between adversity and psychopathology, but whether it serves as a mediator or moderator is unclear. This study examined whether alterations in behavioral and neural reward processing function as a mechanism or moderator of psychopathology outcomes following adversity experiences, including threat (i.e., trauma) and deprivation. A longitudinal community sample of 10-15-year-old youths was assessed across two waves (Wave 1: n = 228; Wave 2: n = 206). Wave 1 assessed adverse experiences, psychopathology symptoms, reward processing on a monetary incentive delay task, and resting-state fMRI. At Wave 2, psychopathology symptoms were reassessed. Greater threat experiences were associated with blunted behavioral reward sensitivity, which, in turn, predicted increases in depression symptoms over time and mediated the prospective association between threat and depression symptoms. In contrast, reward sensitivity moderated the association between deprivation experiences and prospective externalizing symptoms such that the positive association of deprivation with increasing externalizing symptoms was absent for children with high levels of reward sensitivity.

Maternal mental health mediates the effects of pandemic-related stressors on adolescent psychopathology during COVID-19.

BACKGROUND: This study examined whether COVID-19-related maternal mental health changes contributed to changes in adolescent psychopathology. METHODS: A community sample of 226 adolescents (12 years old before COVID-19) and their mothers were asked to complete COVID-19 surveys early in the pandemic (April-May 2020, adolescents 14 years) and approximately 6 months later (November 2020-January 2021). Surveys assessed pandemic-related stressors (health, financial, social, school, environment) and mental health. RESULTS: Lower pre-pandemic family income-to-needs ratio was associated with higher pre-pandemic maternal mental health symptoms (anxiety, depression) and adolescent internalizing and externalizing problems, and with experiencing more pandemic-related stressors. Pandemic-related stressors predicted increases in maternal mental health symptoms, but not adolescent symptoms when other variables were covaried. Higher maternal mental health symptoms predicted concurrent increases in adolescent internalizing and externalizing. Maternal mental health mediated the effects of pre-pandemic income and pandemic-related stressors on adolescent internalizing and externalizing problems. CONCLUSIONS: Results indicate that adolescent mental health is closely tied to maternal mental health during community-level stressors such as COVID-19, and that pre-existing family economic context and adolescent symptoms increase risk for elevations in symptoms of psychopathology.

Genome-wide association mapping of ethanol sensitivity in the Diversity Outbred mouse population.

BACKGROUND: A strong predictor for the development of alcohol use disorder (AUD) is altered sensitivity to the intoxicating effects of alcohol. Individual differences in the initial sensitivity to alcohol are controlled in part by genetic factors. Mice offer a powerful tool to elucidate the genetic basis of behavioral and physiological traits relevant to AUD, but conventional experimental crosses have only been able to identify large chromosomal regions rather than specific genes. Genetically diverse, highly recombinant mouse populations make it possible to observe a wider range of phenotypic variation, offer greater mapping precision, and thus increase the potential for efficient gene identification. METHODS: We have taken advantage of the Diversity Outbred (DO) mouse population to identify and precisely map quantitative trait loci (QTL) associated with ethanol sensitivity. We phenotyped 798 male J:DO mice for three measures of ethanol sensitivity: ataxia, hypothermia, and loss of the righting response. We used high-density MegaMUGA and GigaMUGA to obtain genotypes ranging from 77,808 to 143,259 SNPs. We also performed RNA sequencing in striatum to map expression QTLs and identify gene expression-trait correlations. We then applied a systems genetic strategy to identify narrow QTLs and construct the network of correlations that exists between DNA sequence, gene expression values, and ethanol-related phenotypes to prioritize our list of positional candidate genes. RESULTS: We observed large amounts of phenotypic variation with the DO population and identified suggestive and significant QTLs associated with ethanol sensitivity on chromosomes 1, 2, and 16. The implicated regions were narrow (4.5-6.9 Mb in size) and each QTL explained ~4-5% of the variance. CONCLUSIONS: Our results can be used to identify alleles that contribute to AUD in humans, elucidate causative biological mechanisms, or assist in the development of novel therapeutic interventions.

Social experiences and youth psychopathology during the COVID-19 pandemic: A longitudinal study.

The early stages of the COVID-19 pandemic and associated stay-at-home orders resulted in a stark reduction in daily social interactions for children and adolescents. Given that peer relationships are especially important during this developmental stage, it is crucial to understand the impact of the COVID-19 pandemic on social behavior and risk for psychopathology in children and adolescents. In a longitudinal sample (N=224) of children (7-10y) and adolescents (13-15y) assessed at three strategic time points (before the pandemic, during the initial stay-at-home order period, and six months later after the initial stay-at-home order period was lifted), we examine whether certain social factors protect against increases in stress-related psychopathology during the pandemic, controlling for pre-pandemic symptoms. Youth who reported less in-person and digital socialization, greater social isolation, and less social support had worsened psychopathology during the pandemic. Greater social isolation and decreased digital socialization during the pandemic were associated with greater risk for psychopathology after experiencing pandemic-related stressors. In addition, children, but not adolescents, who maintained some in-person socialization were less likely to develop internalizing symptoms following exposure to pandemic-related stressors. We identify social factors that promote well-being and resilience in youth during this societal event.

Multimodal mapping of the brain's functional connectivity and the adult outcome of attention deficit hyperactivity disorder.

We have a limited understanding of why many children with attention deficit hyperactivity disorder do not outgrow the disorder by adulthood. Around 20-30% retain the full syndrome as young adults, and about 50% show partial, rather than complete, remission. Here, to delineate the neurobiology of this variable outcome, we ask if the persistence of childhood symptoms into adulthood impacts on the brain's functional connectivity. We studied 205 participants followed clinically since childhood. In early adulthood, participants underwent magnetoencephalography (MEG) to measure neuronal activity directly and functional MRI (fMRI) to measure hemodynamic activity during a task-free period (the "resting state"). We found that symptoms of inattention persisting into adulthood were associated with disrupted patterns of typical functional connectivity in both MEG and fMRI. Specifically, those with persistent inattention lost the typical balance of connections within the default mode network (DMN; prominent during introspective thought) and connections between this network and those supporting attention and cognitive control. By contrast, adults whose childhood inattentive symptoms had resolved did not differ significantly from their never-affected peers, both hemodynamically and electrophysiologically. The anomalies in functional connectivity tied to clinically significant inattention centered on midline regions of the DMN in both MEG and fMRI, boosting confidence in a possible pathophysiological role. The findings suggest that the clinical course of this common childhood onset disorder impacts the functional connectivity of the adult brain.

Mapping the neuroanatomic substrates of cognition in familial attention deficit hyperactivity disorder.

BACKGROUND: While the neuroanatomic substrates of symptoms of attention deficit hyperactivity disorder (ADHD) have been investigated, less is known about the neuroanatomic correlates of cognitive abilities pertinent to the disorder, particularly in adults. Here we define the neuroanatomic correlates of key cognitive abilities and determine if there are associations with histories of psychostimulant medication. METHODS: We acquired neuroanatomic magnetic resonance imaging data from 264 members of 60 families (mean age 29.5; s.d. 18.4, 116 with ADHD). Using linear mixed model regression, we tested for associations between cognitive abilities (working memory, information processing, intelligence, and attention), symptoms and both cortical and subcortical volumes. RESULTS: Symptom severity was associated with spatial working memory (t = -3.77, p = 0.0002), processing speed (t = -2.95, p = 0.004) and a measure of impulsive responding (t = 2.19, p = 0.03); these associations did not vary with age (all p > 0.1). Neuroanatomic associations of cognition varied by task but centered on prefrontal, lateral parietal and temporal cortical regions, the thalamus and putamen. The neuroanatomic correlates of ADHD symptoms overlapped significantly with those of working memory (Dice's overlap coefficient: spatial, p = 0.003; verbal, p = 0.001) and information processing (p = 0.02). Psychostimulant medication history was associated with neither cognitive skills nor with a brain-cognition relationships. CONCLUSIONS: Diagnostic differences in the cognitive profile of ADHD does not vary significantly with age; nor were cognitive differences associated with psychostimulant medication history. The neuroanatomic substrates of working memory and information overlapped with those for symptoms within these extended families, consistent with a pathophysiological role for these cognitive skills in familial ADHD.

Genome-wide association for testis weight in the diversity outbred mouse population.

Testis weight is a genetically mediated trait associated with reproductive efficiency across numerous species. We sought to evaluate the genetically diverse, highly recombinant Diversity Outbred (DO) mouse population as a tool to identify and map quantitative trait loci (QTLs) associated with testis weight. Testis weights were recorded for 502 male DO mice and the mice were genotyped on the GIGAMuga array at ~ 143,000 SNPs. We performed a genome-wide association analysis and identified one significant and two suggestive QTLs associated with testis weight. Using bioinformatic approaches, we developed a list of candidate genes and identified those with known roles in testicular size and development. Candidates of particular interest include the RNA demethylase gene Alkbh5, the cyclin-dependent kinase inhibitor gene Cdkn2c, the dynein axonemal heavy chain gene Dnah11, the phospholipase D gene Pld6, the trans-acting transcription factor gene Sp4, and the spermatogenesis-associated gene Spata6, each of which has a human ortholog. Our results demonstrate the utility of DO mice in high-resolution genetic mapping of complex traits, enabling us to identify developmentally important genes in adult mice. Understanding how genetic variation in these genes influence testis weight could aid in the understanding of mechanisms of mammalian reproductive function.

A multicohort, longitudinal study of cerebellar development in attention deficit hyperactivity disorder.

BACKGROUND: The cerebellum supports many cognitive functions disrupted in attention deficit hyperactivity disorder (ADHD). Prior neuroanatomic studies have been often limited by small sample sizes, inconsistent findings, and a reliance on cross-sectional data, limiting inferences about cerebellar development. Here, we conduct a multicohort study using longitudinal data, to characterize cerebellar development. METHODS: Growth trajectories of the cerebellar vermis, hemispheres and white matter were estimated using piecewise linear regression from 1,656 youth; of whom 63% had longitudinal data, totaling 2,914 scans. Four cohorts participated, all contained childhood data (age 4-12 years); two had adolescent data (12-25 years). Growth parameters were combined using random-effects meta-analysis. RESULTS: Diagnostic differences in growth were confined to the corpus medullare (cerebellar white matter). Here, the ADHD group showed slower growth in early childhood compared to the typically developing group (left corpus medullare z = 2.49, p = .01; right z = 2.03, p = .04). This reversed in late childhood, with faster growth in ADHD in the left corpus medullare (z = 2.06, p = .04). Findings held when gender, intelligence, comorbidity, and psychostimulant medication were considered. DISCUSSION: Across four independent cohorts, containing predominately longitudinal data, we found diagnostic differences in the growth of cerebellar white matter. In ADHD, slower white matter growth in early childhood was followed by faster growth in late childhood. The findings are consistent with the concept of ADHD as a disorder of the brain's structural connections, formed partly by developing cortico-cerebellar white matter tracts.

An Ethics and Social-Justice Approach to Collecting and Using Demographic Data for Psychological Researchers.

The collection and use of demographic data in psychological sciences has the potential to aid in transforming inequities brought about by unjust social conditions toward equity. However, many current methods surrounding demographic data do not achieve this goal. Some methods function to reduce, but not eliminate, inequities, whereas others may perpetuate harmful stereotypes, invalidate minoritized identities, and exclude key groups from research participation or access to disseminated findings. In this article, we aim to (a) review key ethical and social-justice dilemmas inherent to working with demographic data in psychological research and (b) introduce a framework positioned in ethics and social justice to help psychologists and researchers in social-science fields make thoughtful decisions about the collection and use of demographic data. Although demographic data methods vary across subdisciplines and research topics, we assert that these core issues-and solutions-are relevant to all research within the psychological sciences, including basic and applied research. Our overarching aim is to support key stakeholders in psychology (e.g., researchers, funding agencies, journal editors, peer reviewers) in making ethical and socially-just decisions about the collection, analysis, reporting, interpretation, and dissemination of demographic data.

Psychology's Contributions to Anti-Blackness in the United States Within Psychological Research, Criminal Justice, and Mental Health.

The mass incarceration of Black people in the United States is gaining attention as a public-health crisis with extreme mental-health implications. Although it is well documented that historical efforts to oppress and control Black people in the United States helped shape definitions of mental illness and crime, many psychologists are unaware of the ways the field has contributed to the conception and perpetuation of anti-Blackness and, consequently, the mass incarceration of Black people. In this article, we draw from existing theory and empirical evidence to demonstrate historical and contemporary examples of psychology's oppression of Black people through research and clinical practices and consider how this history directly contradicts the American Psychological Association's ethics code. First, we outline how anti-Blackness informed the history of psychological diagnoses and research. Next, we discuss how contemporary systems of forensic practice and police involvement in mental-health-crisis response maintain historical harm. Specific recommendations highlight strategies for interrupting the criminalization of Blackness and offer example steps psychologists can take to redefine psychology's relationship with justice. We conclude by calling on psychologists to recognize their unique power and responsibility to interrupt the criminalization and pathologizing of Blackness as researchers and mental-health providers.

Differentiating Between Us & Them: Reduced In-Group Bias as a Novel Mechanism Linking Childhood Violence Exposure with Internalizing Psychopathology.

Strong in-group bonds, facilitated by implicit favoritism for in-group members (i.e., in-group bias), promote mental health across development. Yet, we know little about how the development of in-group bias is shaped by early-life experiences. Childhood violence exposure is known to alter social information processing biases. Violence exposure may also influence social categorization processes, including in-group biases, in ways that influence risk for psychopathology. We examined associations of childhood violence exposure with psychopathology and behavioral and neural indices of implicit and explicit bias for novel groups in children followed longitudinally across three time points from age 5 to 10 years old (n = 101 at baseline; n = 58 at wave 3). To instantiate in-group and out-group affiliations, youths underwent a minimal group assignment induction procedure, in which they were randomly assigned to one of two groups. Youth were told that members of their assigned group shared common interests (in-group) and members of the other group did not (out-group). In pre-registered analyses, violence exposure was associated with lower implicit in-group bias, which in turn was associated prospectively with higher internalizing symptoms and mediated the longitudinal association between violence exposure and internalizing symptoms. During an fMRI task examining neural responses while classifying in-group and out-group members, violence-exposed children did not exhibit the negative functional coupling between vmPFC and amygdala to in-group vs. out-group members that was observed in children without violence exposure. Reduced implicit in-group bias may represent a novel mechanism linking violence exposure with the development of internalizing symptoms.

Stress-related psychopathology during the COVID-19 pandemic.

The COVID-19 pandemic has introduced widespread societal changes that have required ongoing adaptation. Unsurprisingly, stress-related psychopathology has increased during the pandemic, in both children and adults. We review these patterns through the lens of several leading conceptual models of the link between stress and psychopathology. Some of these models focus on characteristics of environmental stressors-including cumulative risk, specific stressor types, and stress sensitization approaches. Understanding the specific aspects of environmental stressors that are most likely to lead to psychopathology can shed light on who may be in most need of clinical intervention. Other models center on factors that can buffer against the onset of psychopathology following stress and the mechanisms through which stressors contribute to emergent psychopathology. These models highlight specific psychosocial processes that may be most usefully targeted by interventions to reduce stress-related psychopathology. We review evidence for each of these stress models in the context of other widescale community-level disruptions, like natural disasters and terrorist attacks, alongside emerging evidence for these stress pathways from the COVID-19 pandemic. We discuss clinical implications for developing interventions to reduce stress-related psychopathology during the pandemic, with a focus on brief, digital interventions that may be more accessible than traditional clinical services.

Early-childhood temperament moderates the prospective associations of coping with adolescent internalizing and externalizing symptoms.

While appraisal and coping are known to impact adolescent psychopathology, more vulnerable or resilient responses to stress may depend on individual temperament. This study examined early life temperament as a moderator of the prospective relations of pre-adolescent appraisal and coping with adolescent psychopathology. The sample included 226 (62% female, 14-15 years) adolescents with assessments starting at 3 years of age. Adolescents were predominately White (12% Black 9% Asian, 11% Latinx, 4% Multiracial, and 65% White). Observed early-childhood temperament (fear, frustration, executive control, and delay ability) were tested as moderators of pre-adolescent coping (active and avoidant) and appraisal (threat, positive) on internalizing and externalizing symptoms during the pandemic. Interaction effects were tested using regression in R. Sex and family context of stress were covariates. Early-childhood temperament was correlated with pre-adolescent symptoms, however, pre-adolescent appraisal and coping but not temperament predicted adolescent psychopathology. Frustration moderated the relations of active and avoidant coping and positive appraisal to symptoms such that coping and appraisal related to lower symptoms only for those low in frustration. Executive control moderated the associations of avoidant coping with symptoms such that avoidance reduced the likelihood of symptoms for youth low in executive control. Findings underscore the role of emotionality and self-regulation in youth adjustment, with the impact of coping differing with temperament. These findings suggest that equipping youth with a flexible assortment of coping skills may serve to reduce negative mental health outcomes.

Contributions of Emotion Regulation and Brain Structure and Function to Adolescent Internalizing Problems and Stress Vulnerability During the COVID-19 Pandemic: A Longitudinal Study.

BACKGROUND: Adolescence is a period of increased vulnerability for internalizing problems, particularly following stressful life events. We examined how emotion regulation and brain structure and function were associated with internalizing problems during the COVID-19 pandemic and moderated the association between pandemic-related stressors and internalizing problems. METHODS: Data are from a longitudinal sample (N = 145, age range, 10-15 years) strategically assessed at 3 crucial time points: before the COVID-19 pandemic, early during the stay-at-home order period, and again 6 months later. We examined associations of amygdala and hippocampal volume and amygdala activation during an emotional processing task before the pandemic, examined use of emotion regulation strategies before and during the pandemic, and examined pandemic-related stressors with internalizing problems. RESULTS: Greater exposure to pandemic-related stressors was associated with higher internalizing problems both early and later in the COVID-19 pandemic. Youths who reported more frequent use of rumination before the pandemic and higher use of expressive suppression and lower use of cognitive reappraisal early in the pandemic had higher internalizing problems early in the pandemic. Higher left amygdala activation to neutral relative to fearful faces before the pandemic was associated with greater internalizing problems and a stronger link between pandemic-related stressors and internalizing problems early in the pandemic. CONCLUSIONS: Stressors related to the COVID-19 pandemic are strongly associated with adolescent internalizing problems, as are individual differences in emotional reactivity and regulation and their underlying neural mechanisms. Interventions that reduce pandemic-related stressors and foster adaptive emotion regulation skills may protect against adolescent psychopathology during this period of heightened exposure to stress.

Promoting youth mental health during the COVID-19 pandemic: A longitudinal study.

The COVID-19 pandemic has introduced novel stressors into the lives of youth. Identifying factors that protect against the onset of psychopathology in the face of these stressors is critical. We examine a wide range of factors that may protect youth from developing psychopathology during the pandemic. We assessed pandemic-related stressors, internalizing and externalizing psychopathology, and potential protective factors by combining two longitudinal samples of children and adolescents (N = 224, 7-10 and 13-15 years) assessed prior to the pandemic, during the stay-at-home orders, and six months later. We evaluated how family behaviors during the stay-at-home orders were related to changes in psychopathology during the pandemic, identified factors that moderate the association of pandemic-related stressors with psychopathology, and determined whether associations varied by age. Internalizing and externalizing psychopathology increased substantially during the pandemic. Higher exposure to pandemic-related stressors was associated with increases in internalizing and externalizing symptoms early in the pandemic and six months later. Having a structured routine, less passive screen time, lower exposure to news media about the pandemic, and to a lesser extent more time in nature and getting adequate sleep were associated with reduced psychopathology. The association between pandemic-related stressors and psychopathology was reduced for youths with limited passive screen time and was absent for children, but not adolescents, with lower news media consumption related to the pandemic. We provide insight into simple, practical steps families can take to promote resilience against mental health problems in youth during the COVID-19 pandemic and protect against psychopathology following pandemic-related stressors.

Reward processing modulates the association between trauma exposure and externalizing psychopathology.

Childhood adversity is common and strongly associated with risk for psychopathology. Identifying factors that buffer children from experiencing psychopathology following adversity is critical for developing more effective intervention approaches. The present study examined several behavioral metrics of reward processing reflecting global approach motivation for reward and the degree to which reward responses scaled with reward value (i.e., behavioral sensitivity to reward value) as potential moderators of the association of multiple dimensions of adversity-including trauma, caregiver neglect, and food insecurity-with depression and externalizing psychopathology in a sample of youth aged 8-16 years (n = 132). Trauma exposure and externalizing problems were positively associated at low and moderate levels of reward reactivity, but this association became non-significant at high levels of reward reactivity. Our findings extend prior work, suggesting that high behavioral sensitivity to reward value may buffer against externalizing problems following exposure to trauma.