Early-life adversity (ELA) is strongly associated with risk for psychopathology. Within adversity, deprivation and threat may lead to psychopathology through different intermediary pathways. Specifically, deprivation, defined as the absence of expected cognitive and social inputs, is associated with lower performance on complex cognitive tasks whereas threatening experiences, defined as the presence of experiences that reflect harm to the child, are associated with atypical fear learning and emotional processes. However, distinct associations of deprivation and threat on behavioral outcomes have not been examined in early childhood. The present study examines how deprivation and threat are associated with cognitive and emotional outcomes in early childhood. Children 4-7 years old (N=63) completed behavioral tasks assessing cognitive control and fear conditioning; deprivation and threat were assessed using child interview and parent questionnaires. Regression analyses were performed including deprivation and threat scores and controls for age, gender and IQ. Because this is the first time these variables have been examined in early childhood, interactions with age were also examined. Deprivation, but not threat was associated with worse performance on the cognitive control task. Threat, but not deprivation interacted with age to predict fear learning. Young children who experienced high levels of threat showed evidence of fear learning measured by differential skin conductance response even at the earliest age measured. In contrast, for children not exposed to threat, fear learning emerged only in older ages. Children who experienced higher levels of threat also showed blunted reactivity measured by amplitude of skin conductance response to the reinforced stimuli regardless of age. Results suggest differential influences of deprivation and threat on cognitive and emotional outcomes even in early childhood. Future work should examine the neural mechanisms underlying these behavioral changes and link changes with increased risk for negative outcomes associated with adversity exposure, such as psychopathology.
Exposure to childhood adversity is common and a powerful risk factor for many forms of psychopathology. In this opinion piece, we argue for greater translation of knowledge about the developmental processes that are influenced by childhood adversity into targeted interventions to prevent the onset of psychopathology. Existing evidence has consistently identified several neurodevelopmental pathways that serve as mechanisms linking adversity with psychopathology. We highlight three domains in which these mechanisms are well-established and point to clear targets for intervention: 1) threat-related social information processing biases; 2) heightened emotional reactivity and difficulties with emotion regulation; and 3) disruptions in reward processing. In contrast to these established pathways, knowledge of how childhood adversity influences emotional learning mechanisms, including fear and reward learning, is remarkably limited. We see the investigation of these mechanisms as a critical next step for the field that will not only advance understanding of developmental pathways linking childhood adversity with psychopathology, but also provide clear targets for behavioral interventions. Knowledge of the mechanisms linking childhood adversity with psychopathology has advanced rapidly, and the time has come to translate that knowledge into clinical interventions to prevent the onset of mental health problems in children who have experienced adversity.
Background Despite equivalent or lower lifetime and past-year prevalence of mental disorder among racial/ethnic minorities compared to non-Latino Whites in the United States, evidence suggests that mental disorders are more persistent among minorities than non-Latino Whites. But, it is unclear how nativity and socioeconomic status contribute to observed racial/ethnic differences in prevalence and persistence of mood, anxiety, and substance disorders. Method Data were examined from a coordinated series of four national surveys that together assessed 21,024 Asian, non-Latino Black, Latino, and non-Latino White adults between 2001 and 2003. Common DSM-IV mood, anxiety, and substance disorders were assessed using the Composite International Diagnostic Interview. Logistic regression analyses examined how several predictors (e.g., race/ethnicity, nativity, education, income) and the interactions between those predictors were associated with both 12-month disorder prevalence and 12-month prevalence among lifetime cases. For the second series of analyses, age of onset and time since onset were used as additional control variables to indirectly estimate disorder persistence. Results Non-Latino Whites demonstrated the highest unadjusted 12-month prevalence of all disorder types (p \textless 0.001), though differences were also observed across minority groups. In contrast, Asian, Latino, and Black adults demonstrated higher 12-month prevalence of mood disorders among lifetime cases than Whites (p \textless 0.001) prior to adjustments Once we introduced nativity and other relevant controls (e.g., age, sex, urbanicity), US-born Whites with at least one US-born parent demonstrated higher 12-month mood disorder prevalence than foreign-born Whites or US-born Whites with two foreign parents (OR = 0.51, 95% CI = [0.36, 0.73]); this group also demonstrated higher odds of past-year mood disorder than Asian (OR = 0.59, 95% CI = [0.42, 0.82]) and Black (OR = 0.70, 95% CI = [0.58, 0.83]) adults, but not Latino adults (OR = 0.89, 95% CI = [0.74, 1.06]). Racial/ethnic differences in 12-month mood and substance disorder prevalence were moderated by educational attainment, especially among adults without a college education. Additionally, racial/ethnic minority groups with no more than a high school education demonstrated more persistent mood and substance disorders than non-Latino Whites; these relationships reversed or disappeared at higher education levels. Conclusion Nativity may be a particularly relevant consideration for diagnosing mood disorder among non-Latino Whites; additionally, lower education appears to be associated with increased relative risk of persistent mood and substance use disorders among racial/ethnic minorities compared to non-Latino Whites.
Background Recent conceptual models argue that early life adversity (ELA) accelerates development, which may contribute to poor mental and physical health outcomes. Evidence for accelerated development in youths comes from studies of telomere shortening or advanced pubertal development following circumscribed ELA experiences and neuroimaging studies of circuits involved in emotional processing. It is unclear whether all ELA is associated with accelerated development across global metrics of biological aging or whether this pattern emerges following specific adversity types. Methods In 247 children and adolescents 8 to 16 years of age with wide variability in ELA exposure, we evaluated the hypothesis that early environments characterized by threat, but not deprivation, would be associated with accelerated development across two global biological aging metrics: DNA methylation (DNAm) age and pubertal stage relative to chronological age. We also examined whether accelerated development explained associations of ELA with depressive symptoms and externalizing problems. Results Exposure to threat-related ELA (e.g., violence) was associated with accelerated DNAm age and advanced pubertal stage, but exposure to deprivation (e.g., neglect, food insecurity) was not. In models including both ELA types, threat-related ELA was uniquely associated with accelerated DNAm age ($\beta$ = .18) and advanced pubertal stage ($\beta$ = .28), whereas deprivation was uniquely associated with delayed pubertal stage ($\beta$ = -.21). Older DNAm age was related to greater depressive symptoms, and a significant indirect effect of threat exposure on depressive symptoms was observed through DNAm age. Conclusions Early threat-related experiences are particularly associated with accelerated biological aging in youths, which may be a mechanism linking ELA with depressive symptoms.
Childhood abuse is a potent risk factor for psychopathology, including posttraumatic stress disorder (PTSD). Research has shown high resting vagal tone, a measure of parasympathetic nervous system function, protects abused youth from developing internalizing psychopathology, but potential mechanisms explaining this effect are unknown. We explored fear extinction learning as a possible mechanism underlying the protective effect of vagal tone on PTSD symptoms among abused youth. We measured resting respiratory sinus arrhythmia (RSA) and skin conductance responses (SCR) during a fear conditioning and extinction task in youth with variability in abuse exposure (N = 94; aged 6-18 years). High RSA predicted lower PTSD symptoms and enhanced extinction learning among abused youths. In a moderated-mediation model, extinction learning mediated the association of abuse with PTSD symptoms only among youth with high RSA. These findings highlight extinction learning as a possible mechanism linking high vagal tone to decreased risk for PTSD symptoms among abused youth.
Childhood adversity is associated with altered reward processing, but little is known about whether this varies across distinct types of adversity. In a sample of 94 children (6-19 years), we investigated whether experiences of material deprivation, emotional deprivation, and trauma have differential associations with reward-related behavior and white matter microstructure in tracts involved in reward processing. Material deprivation (food insecurity), but not emotional deprivation or trauma, was associated with poor reward performance. Adversity-related influences on the integrity of white matter microstructure in frontostriatal tracts varied across childhood adversity types, and reductions in frontostriatal white matter integrity mediated the association of food insecurity with depressive symptoms. These findings document distinct behavioral and neurodevelopmental consequences of specific forms of adversity that have implications for psychopathology risk.
The human brain is remarkably plastic. The brain changes dramatically across development, with ongoing functional development continuing well into the third decade of life and substantial changes occurring again in older age. Dynamic changes in brain function are thought to underlie the innumerable changes in cognition, emotion, and behavior that occur across development. The brain also changes in response to experience, which raises important questions about how the environment influences the developing brain. Longitudinal functional magnetic resonance imaging (fMRI) studies are an essential means of understanding these developmental changes and their cognitive, emotional, and behavioral correlates. This paper provides an overview of common statistical models of longitudinal change applicable to developmental cognitive neuroscience, and a review of the functionality provided by major software packages for longitudinal fMRI analysis. We demonstrate that there are important developmental questions that cannot be answered using available software. We propose alternative approaches for addressing problems that are commonly faced in modeling developmental change with fMRI data.
OBJECTIVES: To determine the effects of foster care vs institutional care, as well as disruptions in the caregiving environment on physical development through early adolescence. STUDY DESIGN: This was a randomized controlled trial of 114 institutionalized, though otherwise healthy, children from 6 orphanages and 51 never institutionalized control children living in birth families (family care group) in Bucharest, Romania. Children were followed from baseline (21 months, range 5-31) through age 12 years for caregiving disruptions and growth trajectories and through age 14 years for pubertal development. RESULTS: Children randomized to the foster care group showed greater rates of growth in height, weight, and body mass index (BMI) through age 12 years than institutionalized group. Tanner development was delayed in institutionalized group boys compared with foster care group and family care group boys at 12 but not 14 years. There were no differences in Tanner development and age of menarche among foster care group, institutionalized group, and family care group girls at ages 12 and 14 years. More disruptions in caregiving between 30 months and 12 years moderated decreases in growth rates of height in foster care group and weight in foster care group and institutionalized group across age. institutionalized group boys with >=2 disruptions showed lower Tanner scores at age 12 vs institutionalized group and foster care group boys with \textless2 disruptions. foster care group girls with >=2 disruptions had higher Tanner scores at age 14 vs foster care group girls with \textless2 disruptions. Age of menarche was not affected by caregiving disruptions. CONCLUSIONS: For children who experienced early institutionalization, stable placement within family care is essential to ensuring the best outcomes for physical developmental. TRIAL REGISTRATION: clinicaltrials.gov: NCT00747396.
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.