We examined the lifetime prevalence of anxiety disorders (ADs) among adolescents with lifetime intermittent explosive disorder (IED), as well as the impact of co-occurring ADs on anger attack frequency and persistence, additional comorbidity, impairment, and treatment utilization among adolescents with IED. IED was defined by the occurrence of at least three anger attacks that were disproportionate to the provocation within a single year. Data were drawn from the National Comorbidity Survey-Adolescent Supplement (N = 6,140), and diagnoses were based on structured lay-administered interviews. Over half (51.89%) of adolescents with IED had an AD, compared to only 22.88% of adolescents without IED. Compared to adolescents with IED alone, adolescents with IED and comorbid ADs: (a) were more likely to be female; (b) reported greater impairment in work/school, social, and overall functioning; (c) were more likely to receive an additional psychiatric diagnosis, a depressive or drug abuse diagnosis, or diagnoses of three or more additional disorders; and (d) had higher odds of receiving any mental/behavioral health treatment as well as treatment specifically focused on aggression. Adolescents with IED alone and those with comorbid ADs did not differ in the number of years experiencing anger attacks or the highest number of anger attacks in a given year. ADs frequently co-occur with IED and are associated with elevated comorbidity and greater impairment compared to IED alone. Gaining a better understanding of this comorbidity is essential for developing specialized and effective methods to screen and treat comorbid anxiety in adolescents with aggressive behavior problems.
Prior research demonstrates a link between exposure to childhood adversity and psychopathology later in development. However, work on mechanisms linking adversity to psychopathology fails to account for specificity in these pathways across different types of adversity. Here, we test a conceptual model that distinguishes deprivation and threat as distinct forms of childhood adversity with different pathways to psychopathology. Deprivation involves an absence of inputs from the environment, such as cognitive and social stimulation, that influence psychopathology by altering cognitive development, such as verbal abilities. Threat includes experiences involving harm or threat of harm that increase risk for psychopathology through disruptions in social-emotional processing. We test the prediction that deprivation, but not threat, increases risk for psychopathology through altered verbal abilities. Data were drawn from the Child Development Project (N = 585), which followed children for over a decade. We analyze data from assessment points at age 5, 6, 14, and 17 years. Mothers completed interviews at age 5 and 6 on exposure to threat and deprivation experiences. Youth verbal abilities were assessed at age 14. At age 17, mothers reported on child psychopathology. A path analysis model tested longitudinal paths to internalizing and externalizing problems from experiences of deprivation and threat. Consistent with predictions, deprivation was associated with risk for externalizing problems via effects on verbal abilities at age 14. Threat was associated longitudinally with both internalizing and externalizing problems, but these effects were not mediated by verbal abilities. Results suggest that unique developmental mechanisms link different forms of adversity with psychopathology. (PsycINFO Database Record
Early life adversity (ELA) is associated with poorer health in adulthood, an association explained, at least in part, by increased engagement in health-risk behaviors (HRBs). In this review, we make the case that ELA influences brain development in ways that increase the likelihood of engaging in HRBs. We argue that ELA alters neural circuitry underpinning cognitive control as well as emotional processing, including networks involved in processing threat and reward. These neural changes are associated psychologically and behaviorally with heightened emotional reactivity, blunted reward responsivity, poorer emotion regulation, and greater delay discounting. We then demonstrate that these adaptations to ELA are associated with an increased risk of smoking cigarettes, drinking alcohol, and eating high-fat, high-sugar foods. Furthermore, we explore how HRBs affect the brain in ways that reinforce addiction and further explain clustering of HRBs.
BACKGROUND: Most research on the prevalence, distribution, and psychiatric comorbidity of intellectual disability (ID) relies on clinical samples, limiting the generalizability and utility of ID assessment in a legal context. This study assessed ID prevalence in a population-representative sample of US adolescents and examined associations of ID with socio-demographic factors and mental disorders. METHODS: Data were drawn from the National Comorbidity Survey Adolescent Supplement (N = 6256). ID was defined as: (1) IQ ? 76, measured using the Kaufman Brief Intelligence Test; (2) an adaptive behavior score ?76, and (3) age of onset ?18 measured using a validated scale. The Composite International Diagnostic Interview assessed 15 lifetime mental disorders. The Sheehan disability scale assessed disorder severity. We used logistic regression models to estimate differences in lifetime disorders for adolescents with and without ID. RESULTS: ID prevalence was 3.2%. Among adolescents with ID, 65.1% met lifetime criteria for a mental disorder. ID status was associated with specific phobia, agoraphobia, and bipolar disorder, but not behavior disorders after adjustment for socio-demographics. Adolescents with ID and mental disorders were significantly more likely to exhibit severe impairment than those without ID. CONCLUSIONS: These findings highlight how sample selection and overlap between ID and psychopathology symptoms might bias understanding of the mental health consequences of ID. For example, associations between ID and behavior disorders widely reported in clinical samples were not observed in a population-representative sample after adjustment for socio-demographic confounders. Valid assessment and understanding of these constructs may prove influential in the legal system by influencing treatment referrals and capital punishment decisions.General Scientific SummaryCurrent definitions of intellectual disability (ID) are based on three criteria: formal designation of low intelligence through artificial problem-solving tasks, impairment in one's ability to function in his/her social environment, and early age of onset. In a national population sample of adolescents, the majority of those with ID met criteria for a lifetime mental disorder. Phobias and bipolar disorder, but not behavior disorders, were elevated in adolescents with ID. Findings highlight the need to consider how behavioral problems are conceptualized and classified in people with ID.
Adolescence is a critical period for the development of self-regulation, and peer interactions are thought to strongly influence regulation ability. Simple exposure to peers has been found to alter decisions about risky behaviors and increase sensitivity to rewards. The link between peer exposure and self-regulation is likely to vary as a function of the type and quality of peer interaction (e.g., rejection or acceptance). Little is known about how the nature of interactions with peers influences different dimensions of self-regulation. We examined how randomization to acceptance or rejection by online "virtual" peers influenced multiple dimensions of self-regulation in a multisite community sample of 273 adolescents aged 16-17 years. Compared to a neutral condition, exposure to peers produced increases in cold cognitive control, but decreased hot cognitive control. Relative to peer acceptance, peer rejection reduced distress tolerance and increased sensitivity to losses. These findings suggest that different dimensions of adolescent self-regulation are influenced by the nature of the peer context: basic cognitive functions are altered by mere exposure to peers, whereas more complex decision making and emotion regulation processes are influenced primarily by the quality of that exposure.
Many studies have shown inverse associations between childhood adversity and intelligence, although most are based on small clinical samples and fail to account for the effects of multiple co-occurring adversities. Using data from the 2001-2004 National Comorbidity Survey Adolescent Supplement, a cross-sectional US population study of adolescents aged 13-18 years (n = 10,073), we examined the associations between 11 childhood adversities and intelligence, using targeted maximum likelihood estimation. Targeted maximum likelihood estimation incorporates machine learning to identify the relationships between exposures and outcomes without overfitting, including interactions and nonlinearity. The nonverbal score from the Kaufman Brief Intelligence Test was used as a standardized measure of fluid reasoning. Childhood adversities were grouped into deprivation and threat types based on recent conceptual models. Adjusted marginal mean differences compared the mean intelligence score if all adolescents experienced each adversity to the mean in the absence of the adversity. The largest associations were observed for deprivation-type experiences, including poverty and low parental education, which were related to reduced intelligence. Although lower in magnitude, threat events related to intelligence included physical abuse and witnessing domestic violence. Violence prevention and poverty-reduction measures would likely improve childhood cognitive outcomes.
Violence exposure during childhood is common and associated with poor cognitive and academic functioning. However, little is known about how violence exposure influences cognitive processes that might contribute to these disparities, such as working memory, or their neural underpinnings, particularly for cognitive processes that occur in emotionally salient contexts. We address this gap in a sample of 54 participants aged 8 to 19 years (50% female), half with exposure to interpersonal violence. Participants completed a delayed match to sample task for emotional faces while undergoing functional magnetic resonance imaging scanning. Violence-exposed youth performed worse than controls on happy and neutral, but not angry, trials. In whole-brain analysis, violence-exposed youth had reduced activation in the left middle frontal gyrus and right intraparietal sulcus during encoding and the left superior temporal sulcus and temporal-parietal junction during retrieval compared to control youth. Reduced activation in the left middle frontal gyrus during encoding and the left superior temporal sulcus during retrieval mediated the association between violence exposure and task performance. Violence exposure influences the frontoparietal network that supports working memory as well as regions involved in facial processing during working memory for emotional stimuli. Reduced neural recruitment in these regions may explain atypical patterns of cognitive processing seen among violence-exposed youth, particularly within emotional contexts.
Although community violence is an established risk factor for youth aggression, less research has examined its relation with internalizing psychopathology. This study examined associations of community violence exposure with internalizing symptoms, and state and trait emotion dysregulation as mechanisms underlying these associations, in 287 adolescents aged 16-17 (45.6% male; 40.8% White). Community violence exposure was associated with internalizing symptoms, negative affect during peer evaluation, trait emotional reactivity, and infrequent problem solving. Multiple emotion dysregulation indices were also associated with internalizing symptoms. In simultaneous multiple mediator models, indirect effects of community violence on internalizing problems were significantly explained by state and trait emotion dysregulation. Findings implicate emotion dysregulation as one mechanism linking community violence exposure to adolescent internalizing symptoms.
Early childhood deprivation such as institutionalization can greatly affect early development. Here, the authors study children who were raised in institutions but later randomly placed in foster care vs. not, to understand how early-life deprivation affects associative learning in adolescence.
Background Experiences in early life lay the foundation for later development and functioning. Severe psychosocial deprivation, as experienced by children in early institutional care, constitutes an adverse experience with long-term negative consequences. The Bucharest Early Intervention Project sought to examine the effects of foster care as an alternative to institutional care for abandoned infants in Romanian institutions. Methods At a mean age of 22 months, institutionalized children were randomized to foster care or care as usual. At age 12 years, we followed-up with 98 of these children (50 randomized to foster care), as well as assessed 49 never institutionalized comparison children. Adaptive functioning was assessed across seven domains—mental health, physical health, substance use, risk-taking behavior, family relations, peer relations, and academic performance. Children at or above the threshold for adaptive functioning in at least six of seven domains were classified as having overall adaptive functioning in early adolescence. Results Among all children who had experienced severe early deprivation, 40% exhibited adaptive functioning. Children randomized to foster care were significantly more likely to exhibit adaptive functioning at age 12 years than children in the care as usual condition (56% vs. 23%). In support of external validity, children who met the threshold for adaptive functioning at age 12 years had higher IQs and were more physiologically responsive to stress. Among children randomized to foster care, children placed prior to age 20 months were more likely to meet the threshold for adaptive functioning than those placed after this age (79% vs. 46%). Conclusions This study provides causal evidence that placing children into families following severe deprivation increases the likelihood of adaptive functioning in early adolescence.
Background Research on the neural correlates associated with risk for suicidal ideation (SI) has been limited, particularly in one increasingly at-risk group—adolescents. Previous research with adolescents indicates that poor emotion regulation skills are linked with SI, but these studies have not previously examined neural activation in service of emotion regulation between those with and without SI histories. Methods Here we examine whether SI is associated with neural responses during an emotion regulation functional magnetic resonance imaging task in a group of adolescents (N = 49) 13 to 20 years of age (mean = 16.95). Results While there were no differences between youths with and without SI in self-reported emotional responses to negative pictures, youths with SI activated the dorsolateral prefrontal cortex more than youths without SI on trials in which they attempted to regulate their emotional responses compared with trials in which they passively viewed negative pictures. In contrast, during passive viewing of negative stimuli, youths with SI activated the dorsolateral prefrontal cortex, temporoparietal junction, and cerebellum less than same-age control subjects. Conclusions These findings were robust to control subjects for depression and adversity exposure and are consistent with the idea that youths with SI have disrupted emotion regulation, potentially related to differences in recruitment of top-down control regions. In contrast, youths without SI activated regions implicated in emotion regulation even when not directed to effortfully control their emotional response. This is the first study to examine neural function during emotion regulation as a potential neural correlate of risk for SI in adolescents.
People differ in how specifically they separate affective experiences into different emotion types—a skill called emotion differentiation or emotional granularity. Although increased emotion differentiation has been associated with positive mental health outcomes, little is known about its development. Participants (N = 143) between the ages of 5 and 25 years completed a laboratory measure of negative emotion differentiation in which they rated how much a series of aversive images made them feel angry, disgusted, sad, scared, and upset. Emotion-differentiation scores were computed using intraclass correlations. Emotion differentiation followed a nonlinear developmental trajectory: It fell from childhood to adolescence and rose from adolescence to adulthood. Mediation analyses suggested that an increased tendency to report feeling emotions one at a time explained elevated emotion differentiation in childhood. Importantly, two other mediators (intensity of emotional experiences and scale use) did not explain this developmental trend. Hence, low emotion differentiation in adolescence may arise because adolescents have little experience conceptualizing co-occurring emotions.
Associative learning underlies the formation of new episodic memories. Associative memory improves across development, and this age-related improvement is supported by the development of the hippocampus and pFC. Recent work, however, additionally suggests a role for visual association cortex in the formation of associative memories. This study investigated the role of category-preferential visual processing regions in associative memory across development using a paired associate learning task in a sample of 56 youths (age 6-19 years). Participants were asked to bind an emotional face with an object while undergoing fMRI scanning. Outside the scanner, participants completed a memory test. We first investigated age-related changes in neural recruitment and found linear age-related increases in activation in lateral occipital cortex and fusiform gyrus, which are involved in visual processing of objects and faces, respectively. Furthermore, greater activation in these visual processing regions was associated with better subsequent memory for pairs over and above the effect of age and of hippocampal and pFC activation on performance. Recruitment of these visual processing regions mediated the association between age and memory performance, over and above the effects of hippocampal activation. Taken together, these findings extend the existing literature to suggest that greater recruitment of category-preferential visual processing regions during encoding of associative memories is a neural mechanism explaining improved memory across development.
Adolescence is a unique developmental period when the salience of social and emotional information becomes particularly pronounced. Although this increased sensitivity to social and emotional information has frequently been considered with respect to risk behaviors and psychopathology, evidence suggests that increased adolescent sensitivity to social and emotional cues may confer advantages. For example, greater sensitivity to shifts in the emotions of others is likely to promote flexible and adaptive social behavior. In this study, a sample of 54 children and adolescents (age 8–19 years) performed a delayed match-to-sample task for emotional faces while undergoing fMRI scanning. Recruitment of the anterior cingulate and anterior insula when the emotion of the probe face did not match the emotion held in memory followed a quadratic developmental pattern that peaked during early adolescence. These findings indicate meaningful developmental variation in the neural mechanisms underlying sensitivity to changes in the emotional expressions. Across all participants, greater activation of this network for changes in emotional expression was associated with less social anxiety and fewer social problems. These results suggest that the heightened salience of social and emotional information during adolescence may confer important advantages for social behavior, providing sensitivity to others’ emotions that facilitates flexible social responding.
Sexual minorities in the United States are at elevated risk of prejudice, discrimination, and violence victimization due to stigma associated with their sexual orientation. These stressors may contribute to physiological stress responses and changes in the regulation of the sympathetic nervous system (SNS). To date, no studies have examined the associations among minority sexual orientation, recent stressful events, and diurnal salivary alpha-amylase (sAA) patterns. The present study included 1663 young adults ages 18–32 years (31% men, 69% women) from the Growing Up Today Study, a prospective cohort of U.S. youth. Participants provided five saliva samples over the course of one day to estimate diurnal sAA patterns. Sexual orientation groups included completely heterosexual with no same-sex partners (CH; referent), mostly heterosexual/completely heterosexual with same-sex partners, and gay/lesbian/bisexual (LB or GB). Sex-stratified multilevel models were fit to evaluate the association of sexual orientation with diurnal patterns of log sAA. The association of recent stressful events was also evaluated. Among women, sexual minorities scored significantly higher than CH on perceived stress and number of stressful events in the past month (p \textless 0.05). Among men, sexual minorities scored higher than CH on perceived stress but not recent stressful events. In multivariable models, recent stressful events were not associated with sAA patterns, but significant sexual orientation group differences in sAA diurnal rhythm were observed among women though not among men. Compared to CH women, LB showed a blunted awakening response and elevated sAA levels across the day, both indicators consistent with SNS dysregulation. Findings suggest dysregulation of stress physiology in LB women, but not other sexual minority women or men, relative to same-sex heterosexuals. Observed dysregulation may relate to exposure among LB women to chronic stressors associated with sexual orientation stigma, although these relations and differences by sex warrant further study.
Many studies report smaller hippocampal and amygdala volumes in posttraumatic stress disorder (PTSD), but findings have not always been consistent. Here, we present the results of a large-scale neuroimaging consortium study on PTSD conducted by the Psychiatric Genomics Consortium (PGC)–Enhancing Neuroimaging Genetics through Meta-Analysis (ENIGMA) PTSD Working Group. We analyzed neuroimaging and clinical data from 1868 subjects (794 PTSD patients) contributed by 16 cohorts, representing the largest neuroimaging study of PTSD to date. We assessed the volumes of eight subcortical structures (nucleus accumbens, amygdala, caudate, hippocampus, pallidum, putamen, thalamus, and lateral ventricle). We used a standardized image-analysis and quality-control pipeline established by the ENIGMA consortium. In a meta-analysis of all samples, we found significantly smaller hippocampi in subjects with current PTSD compared with trauma-exposed control subjects (Cohen’s d = -0.17, p = .00054), and smaller amygdalae (d = -0.11, p = .025), although the amygdala finding did not survive a significance level that was Bonferroni corrected for multiple subcortical region comparisons (p \textless .0063). Our study is not subject to the biases of meta-analyses of published data, and it represents an important milestone in an ongoing collaborative effort to examine the neurobiological underpinnings of PTSD and the brain’s response to trauma.
Growing evidence suggests that childhood socioeconomic status (SES) influences neural development, which may contribute to the well-documented SES-related disparities in academic achievement. However, the particular aspects of SES that impact neural structure and function are not well understood. Here, we investigate associations of childhood SES and a potential mechanism—degree of cognitive stimulation in the home environment—with cortical structure, white matter microstructure, and neural function during a working memory (WM) task across development. Analyses included 53 youths (age 6–19 years). Higher SES as reflected in the income-to-needs ratio was associated with higher parent-reported achievement, WM performance, and cognitive stimulation in the home environment. Although SES was not significantly associated with cortical thickness, children raised in more cognitively stimulating environments had thicker cortex in the frontoparietal network and cognitive stimulation mediated the assocation between SES and cortical thickness in the frontoparietal network. Higher family SES was associated with white matter microstructure and neural activation in the frontoparietal network during a WM task, including greater fractional anisotropy (FA) in the right and left superior longitudinal fasciculi (SLF), and greater BOLD activation in multiple regions of the prefrontal cortex during WM encoding and maintenance. Greater FA and activation in these regions was associated higher parent-reported achievement. Together, cognitive stimulation, WM performance, FA in the SLF, and prefrontal activation during WM encoding and maintenance significantly mediated the association between SES and parent-reported achievement. These findings highlight potential neural, cognitive, and environmental mechanisms linking SES with academic achievement and suggest that enhancing cognitive stimulation in the home environment might be one effective strategy for reducing SES-related disparities in academic outcomes.
Childhood maltreatment is associated with posttraumatic stress disorder (PTSD) and elevated rates of adolescent and adult psychopathology including major depression, bipolar disorder, substance use disorders, and other medical comorbidities. Gray matter volume changes have been found in maltreated youth with (versus without) PTSD. However, little is known about the alterations of brain structural covariance network topology derived from cortical thickness in maltreated youth with PTSD. High-resolution T1-weighted magnetic resonance imaging scans were from demographically matched maltreated youth with PTSD (N = 24), without PTSD (N = 64), and non-maltreated healthy controls (n = 67). Cortical thickness data from 148 cortical regions was entered into interregional partial correlation analyses across participants. The supra-threshold correlations constituted connections in a structural brain network derived from four types of centrality measures (degree, betweenness, closeness, and eigenvector) estimated network topology and the importance of nodes. Between-group differences were determined by permutation testing. Maltreated youth with PTSD exhibited larger centrality in left anterior cingulate cortex than the other two groups, suggesting cortical network topology specific to maltreated youth with PTSD. Moreover, maltreated youth with versus without PTSD showed smaller centrality in right orbitofrontal cortex, suggesting that this may represent a vulnerability factor to PTSD following maltreatment. Longitudinal follow-up of the present results will help characterize the role that altered centrality plays in vulnerability and resilience to PTSD following childhood maltreatment.
The most comprehensive volume of its kind, The Oxford Handbook of Mood Disorders provides detailed coverage of the characterization, understanding, and treatment of mood disorders. Chapters are written by the world's leading experts in their respective areas. The Handbook provides coverage of unipolar depression, bipolar disorder, and variants of these disorders. Current approaches to classifying the mood disorders are reviewed and contemporary controversies are placed in historical context. Chapter authors offer a variety of approaches to understanding the heterogeneity of the experiences of those who meet criteria for mood disorders, both within and across cultures. The role of genetic and environmental risk factors as well as premorbid personality and cognitive processes in the development of mood pathology are detailed. Interpersonal, neurobiological, and psychological factors also receive detailed consideration. The volume reviews mood disorders in special populations (e.g., postpartum and seasonal mood disorders) as well as common comorbidities (e.g., anxiety, substance use disorders). Somatic and psychosocial treatment approaches receive in-depth coverage with chapters that describe and review empirical evidence regarding each of the most influential treatment approaches. The depth and breadth offered by this Handbook make it an invaluable resource for clinicians and researchers, as well as scholars and students.
Despite long-standing interest in the influence of adverse early experiences on mental health, systematic scientific inquiry into childhood adversity and developmental outcomes has emerged only recently. Existing research has amply demonstrated that exposure to childhood adversity is associated with elevated risk for multiple forms of youth psychopathology. In contrast, knowledge of developmental mechanisms linking childhood adversity to the onset of psychopathology—and whether those mechanisms are general or specific to particular kinds of adversity—remains cursory. Greater understanding of these pathways and identification of protective factors that buffer children from developmental disruptions following exposure to adversity is essential to guide the development of interventions to prevent the onset of psychopathology following adverse childhood experiences. This article provides recommendations for future research in this area. In particular, use of a consistent definition of childhood adversity, integration of studies of typical development with those focused on childhood adversity, and identification of distinct dimensions of environmental experience that differentially influence development are required to uncover mechanisms that explain how childhood adversity is associated with numerous psychopathology outcomes (i.e., multifinality) and identify moderators that shape divergent trajectories following adverse childhood experiences. A transdiagnostic model that highlights disruptions in emotional processing and poor executive functioning as key mechanisms linking childhood adversity with multiple forms of psychopathology is presented as a starting point in this endeavour. Distinguishing between general and specific mechanisms linking childhood adversity with psy- chopathology is needed to generate empirically informed interventions to prevent the long-term consequences of adverse early environments on children’s development.