Publications by Year: 2020

Platt, J. M., Bates, L. M., Jager, J., McLaughlin, K. A., & Keyes, K. M. (2020). Changes in the depression gender gap from 1992 to 2014: Cohort effects and mediation by gendered social position. Social Science & Medicine , 258, 113088. Publisher's VersionAbstract
The depression gap (i.e., higher rates of depression among women than men) represents an important mental health disparity in the US. Differences in gendered social position (i.e., the roles, responsibilities, and opportunities available to women and men), which have been changing since the mid-20th Century may contribute to this gender gap. The present study examined the evidence for a changing depression gap across birth cohorts and tested the extent to which any changes over time were mediated by changes in relative social position between women and men. Data were from the National Longitudinal Surveys. The depression gap was defined as differences in mean CESD scores for women vs. men. The analytic sample included 13,666 respondents interviewed from 1992 to 2014. Hierarchical mixed models estimated the magnitude of the gender depression gap over time, its association with 10-year birth cohort (range: 1957–1994), and whether any variation was mediated by ratios among women relative to men of obtaining a college degree, being employed full-time, and the average number of hours spent doing housework per week, three indicators of gendered social position. There was a linear decrease in the depression gap by 0.18 points across birth cohort (95% CI = −0.26, −0.10). The results of the mediation analysis estimated that an increasing ratio of college degree attainment mediated 39% of the gender depression gap across cohorts (95% CI = 0.18, 0.78). There was no evidence of mediation due to changing employment or housework ratios. These findings partially support the hypothesis that the depression gap is changing over time and is meaningfully related to the social environment. Understanding the social causes of the depression gap can illuminate the fundamental processes through which depression disparities may be perpetuated or attenuated over time and may aid in the identification of strategies to reduce them.
McLaughlin, K. A., Colich, N. L., Rodman, A. M., & Weissman, D. G. (2020). Mechanisms linking childhood trauma exposure and psychopathology: a transdiagnostic model of risk and resilience. BMC Medicine , 18 (1). Publisher's VersionAbstract
Transdiagnostic processes confer risk for multiple types of psychopathology and explain the co-occurrence of different disorders. For this reason, transdiagnostic processes provide ideal targets for early intervention and treatment. Childhood trauma exposure is associated with elevated risk for virtually all commonly occurring forms of psychopathology. We articulate a transdiagnostic model of the developmental mechanisms that explain the strong links between childhood trauma and psychopathology as well as protective factors that promote resilience against multiple forms of psychopathology. We present a model of transdiagnostic mechanisms spanning three broad domains: social information processing, emotional processing, and accelerated biological aging. Changes in social information processing that prioritize threat-related information—such as heightened perceptual sensitivity to threat, misclassification of negative and neutral emotions as anger, and attention biases towards threat-related cues—have been consistently observed in children who have experienced trauma. Patterns of emotional processing common in children exposed to trauma include elevated emotional reactivity to threat-related stimuli, low emotional awareness, and difficulties with emotional learning and emotion regulation. More recently, a pattern of accelerated aging across multiple biological metrics, including pubertal development and cellular aging, has been found in trauma-exposed children. Although these changes in social information processing, emotional responding, and the pace of biological aging reflect developmental adaptations that may promote safety and provide other benefits for children raised in dangerous environments, they have been consistently associated with the emergence of multiple forms of internalizing and externalizing psychopathology and explain the link between childhood trauma exposure and transdiagnostic psychopathology. Children with higher levels of social support, particularly from caregivers, are less likely to develop psychopathology following trauma exposure. Caregiver buffering of threat-related processing may be one mechanism explaining this protective effect. Childhood trauma exposure is a powerful transdiagnostic risk factor associated with elevated risk for multiple forms of psychopathology across development. Changes in threat-related social and emotional processing and accelerated biological aging serve as transdiagnostic mechanisms linking childhood trauma with psychopathology. These transdiagnostic mechanisms represent critical targets for early interventions aimed at preventing the emergence of psychopathology in children who have experienced trauma.
Colich, N. L., Platt, J. M., Keyes, K. M., Sumner, J. A., Allen, N. B., & McLaughlin, K. A. (2020). Earlier age at menarche as a transdiagnostic mechanism linking childhood trauma with multiple forms of psychopathology in adolescent girls. Psychological Medicine , 50 (7), 1090-1098. Publisher's VersionAbstract
{BackgroundAlthough early life adversity (ELA) increases risk for psychopathology, mechanisms linking ELA with the onset of psychopathology remain poorly understood. Conceptual models have argued that ELA accelerates development. It is unknown whether all forms of ELA are associated with accelerated development or whether early maturation is a potential mechanism linking ELA with psychopathology. We examine whether two distinct dimensions of ELA – threat and deprivation – have differential associations with pubertal timing in girls, and evaluate whether accelerated pubertal timing is a mechanism linking ELA with the onset of adolescent psychopathology.MethodsData were drawn from a large, nationally representative sample of 4937 adolescent girls. Multiple forms of ELA characterized by threat and deprivation were assessed along with age at menarche (AAM) and the onset of DSM-IV fear, distress, externalizing, and eating disorders.ResultsGreater exposure to threat was associated with earlier AAM (B = −0.1
Heleniak, C., & McLaughlin, K. A. (2020). Social-cognitive mechanisms in the cycle of violence: Cognitive and affective theory of mind, and externalizing psychopathology in children and adolescents. Development and Psychopathology , 32 (2), 735-750. Publisher's VersionAbstract
Children who are victims of interpersonal violence have a markedly elevated risk of engaging in aggressive behavior and perpetrating violence in adolescence and adulthood. Although alterations in social information processing have long been understood as a core mechanism underlying the link between violence exposure and externalizing behavior, scant research has examined more basic social cognition abilities that might underlie this association. To that end, this study examined the associations of interpersonal violence exposure with cognitive and affective theory of mind (ToM), core social-cognitive processes that underlie many aspects of social information processing. In addition, we evaluated whether difficulties with ToM were associated with externalizing psychopathology. Data were collected in a community-based sample of 246 children and adolescents aged 8–16 who had a high concentration of exposure to interpersonal violence. Violence exposure was associated with lower accuracy during cognitive and affective ToM, and the associations persisted after adjusting for co-occurring forms of adversity characterized by deprivation, including poverty and emotional neglect. Poor ToM performance, in turn, was associated with externalizing behaviors. These findings shed light on novel pathways that increase risk for aggression in children who have experienced violence.
Machlin, L., McLaughlin, K. A., & Sheridan, M. A. (2020). Brain structure mediates the association between socioeconomic status and attention-deficit/hyperactivity disorder. Developmental Science , 23 (1), e12844. Publisher's VersionAbstract
Low socioeconomic status (SES) is associated with greater risk for symptoms of attention-deficit/hyperactivity disorder (ADHD). One mechanism through which SES may confer risk for ADHD is by influencing brain structure. Alterations to cortical thickness, surface area and subcortical volume have been associated with low SES and with the presence of ADHD across multiple studies. The current study examined whether cortical thickness, surface area or subcortical volume mediate the associations between SES and ADHD in youth 3–21 years old (N = 874) from the Pediatric Imaging, Neurocognition and Genetics Study. Freesurfer was used to estimate cortical thickness, surface area and subcortical volume from structural magnetic resonance imaging. Parents reported on demographics, family SES, ADHD diagnoses and the presence of child attention problems. Statistical mediation was assessed using a bootstrap resampling procedure. Controlling for parental ADHD, child age, gender, birth weight and scanner, children in low SES families were more likely to be in the ADHD group. Consistent with previous reports in this sample, low SES was associated with reduced surface area across the frontal lobe and reduced subcortical volume in the amygdala, cerebellum, hippocampus and basal ganglia. Of these regions, a significant indirect effect of SES on ADHD status through subcortical volume was observed for the left cerebellum (95% confidence interval: 0.004, 0.022), the right cerebellum (95% confidence interval: 0.006, 0.025), and the right caudate (95% confidence interval: 0.002, 0.022). Environmentally mediated changes in the cerebellum and the caudate may be neurodevelopmental mechanisms explaining elevated risk of ADHD in children in low SES families.
Harkness, K. L., & Hayden, E. P. (2020). The Oxford Handbook of Stress and Mental Health (pp. 45-74) . Oxford University Press.Abstract
Decades of research have unequivocally shown that life stress is a central factor in the onset and course of almost every psychiatric disorder. However, the processes by which stress influences mental health are complex, and the integration of the myriad of biological and psychological systems involved requires a multidisciplinary perspective. Fortunately, scientists working from diverse vantage points have made huge advances in unpacking the complexities of stress-disorder relations. The Oxford Handbook of Stress and Mental Health provides a comprehensive, up-to-date overview of the science of stress and mental health. Topics covered include assessment issues, the role of stress in various mental disorders, developmental influences and individual difference factors that predict reactivity to stress, and treatment of stress-related mental health problems. Internationally recognized scholars in the field of stress and stress-related disorders have contributed their diverse expertise, providing both depth and breadth in terms of understanding stress and mental health. Chapters 1 to 4 provide a critical discussion of assessment issues in the domains of stress exposure and stress response. Chapters 5 to 14 review the relation of stress exposures to a broad range of mental health outcomes across the lifespan. Chapters 15 to 25 are concerned with understanding how the stress response unfolds at both psychological and neurobiological levels. Lastly, Chapters 26 to 33 addresses stress adaptation and resilience, as well as evidence-based treatments for stress and stress-related disorder. This volume will constitute an invaluable resource for students, established scientists, and clinicians looking for a comprehensive treatment of the topic of stress and mental health.