Resilience, the capacity to maintain or regain functionality in the face of adversity, is a dynamic process influenced by individual, familial, and community factors. Despite its variability, distinct resilience trajectories can be identified within populations, yet the predictors defining these distinct groups remains largely unclear. Here, using data from the Avon Longitudinal Study of Parents and Children (ages 0-18), we quantify resilience as the remaining variance in psychosocial functioning after taking into account the exposure to adversity. Growth mixture modeling identified seven distinct resilience trajectories, with over half of the study population maintaining resilience throughout early life. Factors increasing the likelihood of resilient trajectory membership included a less emotional temperament, high cognitive abilities, high self-esteem, low levels of autistic social traits, strong sibling relationships, high maternal care, and positive school experiences. Among the socioeconomic factors considered, maternal education – a significant indicator of socioeconomic status – and birth-order were associated with resilient trajectories. Our findings underscore the importance of fostering cognitive abilities, self-esteem, social relationships, positive school experiences, and extracurricular engagement to bolster resilience in adversity-exposed individuals and communities. This research informs resilience-focused interventions in mental health, education, and social policy sectors, and prompts further exploration of socioeconomic influences on resilience trajectories.

Exposure to early-life adversity (ELA) and iron deficiency early in life are known risk factors for suboptimal brain and socioemotional development. Iron deficiency may arise from and co-occur with ELA, which could negatively affect development. In the present study, we investigated whether ELA is associated with iron deficiency in infants receiving no iron supplementation. This study is a secondary analysis of extant data collected in the 1990s; participants were healthy infants from working-class communities in Santiago, Chile (N = 534, 45.5% female). We measured stressful life events, maternal depression, and low home support for child development during infancy and assessed iron status when the infant was 12 months old. Slightly more than half of the infants were iron-deficient (51%), and 25.8% were iron-deficient anemic at 12 months. Results indicated that ELA was associated with lower iron levels and iron deficiency at 12 months. The findings are consistent with animal and human prenatal models of stress and iron status and provide evidence of the association between postnatal ELA and iron status in humans. The findings also highlight a nutritional pathway by which ELA may impact development and present a nutritionally-focused avenue for future research on ELA and psychopathology.

Early-life adversity is a major risk factor for psychopathology, but not all who experience adversity develop psychopathology. The current study evaluated whether the links between child and adolescent adversity and depression and anxiety were described by general benefits and/or buffering effects of interpersonal support. Data from 456 adolescents oversampled on neuroticism over a 5-year period were examined in a series of discrete-time survival analyses to predict subsequent disorder onsets. Models examined linear, quadratic, and interactive effects of interpersonal support over time, as measured by chronic interpersonal stress interview ratings. Results did not support buffering effects of interpersonal support against either child or adolescent adversity in predicting depression or anxiety. However, there was support for the general benefits model of interpersonal support as evidenced by follow-up analyses of significant quadratic effects of interpersonal support, demonstrating that higher interpersonal support led to decreased likelihood of depression and anxiety onsets. Secondary analyses demonstrated that effects of interpersonal support remained after accounting for baseline depression and anxiety diagnoses. Further, quadratic effects were driven by social domains as opposed to familial domains when considering child adversity. Implications for interventions and randomized controlled prevention trials regarding interpersonal relationships are discussed.

Environmental adversity increases child susceptibility to disrupted developmental outcomes, but the mechanisms by which adversity can shape development remain unclear. A translational cross-species approach was used to examine stress-mediated pathways by which poverty-related adversity can influence infant social development. Findings from a longitudinal sample of low-income mother–infant dyads indicated that infant cortisol (CORT) on its own did not mediate relations between early-life scarcity-adversity exposure and later infant behavior in a mother-child interaction task. However, maternal CORT through infant CORT served as a mediating pathway, even when controlling for parenting behavior. Findings using a rodent “scarcity-adversity” model indicated that pharmacologically blocking pup corticosterone (CORT, rodent equivalent to cortisol) in the presence of a stressed mother causally prevented social transmission of scarcity-adversity effects on pup social behavior. Furthermore, pharmacologically increasing pup CORT without the mother present was not sufficient to disrupt pup social behavior. Integration of our cross-species results suggests that elevated infant CORT may be necessary, but without elevated caregiver CORT, may not be sufficient in mediating the effects of environmental adversity on development. These findings underscore the importance of considering infant stress physiology in relation to the broader social context, including caregiver stress physiology, in research and interventional efforts.

Early-life adversity is a well-established risk factor for the development of depression later in life. Here we discuss the relationship between early-life adversity and depression, focusing specifically on effects of early-life caregiver deprivation on alterations in the neural and behavioral substrates of reward-processing. We also examine vulnerability to depression within the context of sensitive periods of neural development and the timing of adverse exposure. We further review the development of the ventral striatum, a limbic structure implicated in reward processing, and its role in depressive outcomes following early-life adversity. Finally, we suggest a potential neurobiological mechanism linking early-life adversity and altered ventral striatal development. Together these findings may help provide further insight into the role of reward circuitry dysfunction in psychopathological outcomes in both clinical and developmental populations.