# Publications

2019
Vilsaint, C. L., NeMoyer, A., Fillbrunn, M., Sadikova, E., Kessler, R. C., Sampson, N. A., Alvarez, K., et al. (2019). Racial/ethnic differences in 12-month prevalence and persistence of mood, anxiety, and substance use disorders: Variation by nativity and socioeconomic status. Comprehensive Psychiatry , 89, 52–60. Publisher's VersionAbstract
Sumner, J. A., Colich, N. L., Uddin, M., Armstrong, D., & McLaughlin, K. A. (2019). Early Experiences of Threat, but Not Deprivation, Are Associated With Accelerated Biological Aging in Children and Adolescents. Stress and Fear , 85 (3), 268–278. Publisher's VersionAbstract
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.
Dennison, M. J., Rosen, M. L., Sambrook, K. A., Jenness, J. L., Sheridan, M. A., & McLaughlin, K. A. (2019). Differential Associations of Distinct Forms of Childhood Adversity With Neurobehavioral Measures of Reward Processing: A Developmental Pathway to Depression. Child Development , 90 (1), e96-e113.Abstract
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.
2018
Somerville, L. H., & McLaughlin, K. A. (2018). Normative trajectories and sources of psychopathology risk in adolescence . In A. S. Fox, R. C. Lapate, A. J. Shackman, & R. J. Davidson (Ed.), The nature of emotion: Fundamental questions (2nd ed. pp. 386-389) . Oxford University Press.Abstract

Adolescents are frequently portrayed as emotionally volatile, emotionally unhinged, emotionally clueless, and emotionally obsessed. Although these portrayals are overly dramatic, they are at least partially consistent with “storm and stress” theories of adolescence (Arnett, 1999). Although adolescents are overall more happy than unhappy (Larson et al., 2002), evidence does suggest that adolescents experience frequent and intense emotions that accompany a marked increase in their risk for mental disorders characterized by problems with emotion regulation. Here, we take a process-level perspective to evaluate why emotions “run hot” during adolescence.

Somerville, L. H., & McLaughlin, K. A. (2018). Normative trajectories and sources of psychopathology risk in adolescence . In A. S. Fox, R. C. Lapate, A. J. Shackman, & R. J. Davidson (Ed.), The nature of emotion: Fundamental questions (2nd ed. pp. 386-389) . Oxford University Press.Abstract

Adolescents are frequently portrayed as emotionally volatile, emotionally unhinged, emotionally clueless, and emotionally obsessed. Although these portrayals are overly dramatic, they are at least partially consistent with “storm and stress” theories of adolescence (Arnett, 1999). Although adolescents are overall more happy than unhappy (Larson et al., 2002), evidence does suggest that adolescents experience frequent and intense emotions that accompany a marked increase in their risk for mental disorders characterized by problems with emotion regulation. Here, we take a process-level perspective to evaluate why emotions “run hot” during adolescence.

Madhyastha, T., Peverill, M., Koh, N., McCabe, C., Flournoy, J., Mills, K., King, K., et al. (2018). Current methods and limitations for longitudinal fMRI analysis across development. Developmental Cognitive Neuroscience , 33, 118–128. Publisher's VersionAbstract
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.
Johnson, D. E., Tang, A., Almas, A. N., Degnan, K. A., McLaughlin, K. A., Nelson, C. A., Fox, N. A., et al. (2018). Caregiving Disruptions Affect Growth and Pubertal Development in Early Adolescence in Institutionalized and Fostered Romanian Children: A Randomized Clinical Trial. The Journal of Pediatrics , 203, 345-354.e3.Abstract
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.
Galbraith, T., Carliner, H., Keyes, K. M., McLaughlin, K. A., McCloskey, M. S., & Heimberg, R. G. (2018). The co-occurrence and correlates of anxiety disorders among adolescents with intermittent explosive disorder. Aggressive Behavior , 44 (6), 581-590.Abstract
Miller, A. B., Sheridan, M. A., Hanson, J. L., McLaughlin, K. A., E. Bates, J., E. Lansford, J., S. Pettit, G., et al. (2018). Dimensions of deprivation and threat, psychopathology, and potential mediators: A multi-year longitudinal analysis. Journal of Abnormal Psychology , 127 (2), 160–170.Abstract
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
Duffy, K. A., McLaughlin, K. A., & Green, P. A. (2018). Early life adversity and health-risk behaviors: proposed psychological and neural mechanisms. Annals of the New York Academy of Sciences , 1428 (1), 151-169.Abstract
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.
Platt, J. M., Keyes, K. M., McLaughlin, K. A., & Kaufman, A. S. (2018). Intellectual disability and mental disorders in a US population representative sample of adolescents. Psychological Medicine , 1–10.Abstract
King, K. M., McLaughlin, K. A., Silk, J., & Monahan, K. C. (2018). Peer effects on self-regulation in adolescence depend on the nature and quality of the peer interaction. Development and Psychopathology , 30 (4), 1389–1401.Abstract
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.
Platt, J. M., McLaughlin, K. A., Luedtke, A. R., Ahern, J., Kaufman, A. S., & Keyes, K. M. (2018). Targeted Estimation of the Relationship Between Childhood Adversity and Fluid Intelligence in a US Population Sample of Adolescents. American Journal of Epidemiology , 187 (7), 1456–1466.Abstract
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.
Jenness, J. L., Rosen, M. L., Sambrook, K. A., Dennison, M. J., Lambert, H. K., Sheridan, M. A., & McLaughlin, K. A. (2018). Violence exposure and neural systems underlying working memory for emotional stimuli in youth. Development and Psychopathology , 30 (4), 1517–1528.Abstract
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.
Heleniak, C., King, K. M., Monahan, K. C., & McLaughlin, K. A. (2018). Disruptions in Emotion Regulation as a Mechanism Linking Community Violence Exposure to Adolescent Internalizing Problems. Journal of Research on Adolescence: The Official Journal of the Society for Research on Adolescence , 28 (1), 229–244.Abstract
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.
Sheridan, M. A., McLaughlin, K. A., Winter, W., Fox, N., Zeanah, C., & Nelson, C. A. (2018). Early deprivation disruption of associative learning is a developmental pathway to depression and social problems. Nature Communications , 9 (1), 2216. Publisher's VersionAbstract
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.
Humphreys, K. L., Miron, D., McLaughlin, K. A., Sheridan, M. A., Nelson, C. A., Fox, N. A., & Zeanah, C. H. (2018). Foster care promotes adaptive functioning in early adolescence among children who experienced severe, early deprivation. Journal of Child Psychology and Psychiatry , 59 (7), 811–821. Publisher's VersionAbstract