Developmental consequences of early life stress on risk for psychopathology: Longitudinal associations with children's multisystem physiological regulation and executive functioning

Abstract

The etiology of psychopathology is multifaceted and warrants consideration of factors at multiple levels and across developmental time. Although experiences of adversity in early life have been associated with increased risk of developing psychopathology, pathways toward maladaptation or resilience are complex and depend upon a variety of factors, including individuals’ physiological regulation and cognitive functioning. Therefore, in a longitudinal cohort of 113 mother–child dyads, we explored associations from early adverse experiences to physiological coregulation across multiple systems and subsequent variations in executive functioning. Latent profile analysis derived multisystem profiles based on children's heart rate, respiratory sinus arrhythmia, pre-ejection period, and cortisol measured during periods of rest and reactivity throughout a developmentally challenging protocol. Three distinct profiles of multisystem regulation emerged: heightened multisystem baseline activity (anticipatory arousal/ autonomic nervous system [ANS] responder), typically adaptive patterns across all systems (active copers/mobilizers), and heightened hypothalamic–pituitary–adrenal (HPA) axis activity (HPA axis responders). Path models revealed that children exposed to adversity before 18 months were more likely to evidence an anticipatory arousal/ANS responders response at 36 months, and children in this profile had lower executive functioning scores than the active copers/mobilizers. In sum, these findings provide important information about potential physiological associations linking early adversity to variations in children's task-based executive functioning.

PEP reward reactivity moderates the effects of RSA reactivity on antisocial behavior and substance use

“…We included age and race (1 = African American; 0 = not African American) as covariates because of their relationship with the behavior outcomes (Gray et al, 2017;Schilling et al, 2007;Vaughn et al, 2011) and with our main variables of interest (i.e., RSA and PEP) (Hinnant et al, 2011;Uchino et al, 1999). We included stress as a covariate because it was found to relate to ASB and substance use (Agnew, 2001(Agnew, , 2013Dariotis & Chen, 2020) and stress physiology (Dubow et al, 1997;Rudd et al, 2021;Stroud et al, 2016aStroud et al, , 2016b. We measured stress in early life and in recent times.…”

Early life stress lastingly alters the function and AMPA‐receptor composition of glutamatergic synapses in the hippocampus of male mice

“…While this period of rapid change shapes later cognitive and emotional development, it also renders the developing brain vulnerable to adverse experiences 1 . Accordingly, exposure to stress during early life (ELS) can disrupt neural development and increase the susceptibility to develop psychopathology and neurodegenerative disorders, and accelerate cognitive impairments and cognitive aging 7–10 . Despite the wide range of ELS‐induced effects reported by animal studies, the exact mechanisms as to how ELS exerts its enduring effects remain unclear.…”

Children’s executive function during the COVID-19 pandemic in Argentina: Associations with home literacy, reading, and screen times

“…It is generally accepted that stress interferes with cognitive functions, and, particularly, with EF (see Shields et al, 2015, 20167for meta-analyses), and it has been shown how environmental stressors, such as early life adverse experiences (Hostinar et al, 2012, Rudd et al, 2021, poverty-related factors (Haft et al, 2017), and natural disasters (Pfefferbaum et al, 2016) can have negative effects on children's EF development. Therefore, EF constitutes a relevant construct to examine when considering the potential impact of the COVID-19 pandemic, and the consequent changes in schooling and daily activities that took place during its first two years, on children.…”