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Research on the hypothalamic–pituitary–adrenocortical (HPA) axis has emerged as a vital area within the field of developmental psychopathology in the past 25 years. Extensive animal research has provided knowledge of the substrates and physiological mechanisms that guide development of stress reactivity and regulation using methods that are not feasible in humans. Recent advances in understanding the anatomy and physiology of the HPA axis in humans and its interactions with other stress-mediating systems, including accurate assessment of salivary cortisol, more sophisticated neuroimaging methods, and a variety of genetic analyses, have led to greater knowledge of how psychological and biological processes impact functioning. A growing body of research on HPA axis regulation and reactivity in relation to psychopathology has drawn increased focus on the prenatal period, infancy, and the pubertal transition as potentially sensitive periods of stress system development in children. Theories such as the allostatic load model have guided research by integrating multiple physiological systems and mechanisms by which stress can affect mental and physical health. However, almost none of the prominent theoretical models in stress physiology are truly developmental, and future work must incorporate how systems interact with the environment across the life span in normal and atypical development. Our theoretical advancement will depend on our ability to integrate biological and psychological models. Researchers are increasingly realizing the importance of communication across disciplinary boundaries in order to understand how experiences influence neurobehavioral development. It is important that knowledge gained over the past 25 years has been translated to prevention and treatment interventions, and we look forward to the dissemination of interventions that promote recovery from adversity.

According to evolutionary life history models, environmental harshness and unpredictability can both promote a fast life history strategy characterized by increased risk taking and enacting short-term, opportunistic behaviors. The current longitudinal study tests whether environmental unpredictability during childhood has stronger effects on risky behavior during adolescence than harshness, and whether there may be an early “sensitive period” during which unpredictability has particularly strong and unique effects on these outcomes. Using data from the Minnesota Longitudinal Study of Risk and Adaptation, prospective assessments of environmental unpredictability (changes in residence, cohabitation, and parental occupation) and harshness (mean socioeconomic status) from birth into adolescence were used to predict self-reported externalizing behaviors and substance use at age 16 ( N = 220). Exposure to greater early unpredictability (between ages 0 and 5) predicted more externalizing behaviors as well as more alcohol and marijuana use at age 16, controlling for harshness and later unpredictability (between ages 6 and 16). Harshness predicted adolescent substance use, and later unpredictability predicted adolescent externalizing behaviors at the trend level. Early unpredictability and harshness also interacted, such that the highest levels of risk taking occurred in individuals who experienced more early unpredictability and lived in harsher environments. Age 16 externalizing behaviors, but not substance use, mediated the association between early unpredictability and externalizing/criminal behaviors at age 23. We discuss how exposure to early environmental unpredictability may alter biological and social–cognitive functioning from a life history perspective.

Background Although associations between cumulative risk, sleep, and overweight/obesity have been demonstrated, few studies have examined relationships between these constructs longitudinally across childhood. This study investigated how cumulative risk and sleep duration are related to current and later child overweight/obesity in families across the United States sampled for high sociodemographic risk. Methods We conducted secondary analyses on 3690 families with recorded child height and weight within the Fragile Families and Child Well-Being Study. A cumulative risk composite (using nine variables indicating household/environmental, family, and sociodemographic risk) was calculated for each participant from ages 3-9 years. Path analyses were used to investigate associations between cumulative risk, parent-reported child sleep duration, and z-scored child body mass index (BMI) percentile at ages 3 through 9. Results Higher cumulative risk experienced at age 5 was associated with shorter sleep duration at year 9, b = − 0.35, p  = .01, 95% CI [− 0.57, − 0.11]. At 5 years, longer sleep duration was associated with lower BMI, b = − 0.03, p  = .03, 95% CI [− 0.06, − 0.01]. Higher cumulative risk at 9 years, b = − 0.34, p  = .02, 95% CI [− 0.57, − 0.10], was concurrently associated with shorter sleep duration. Findings additionally differed by child sex, such that only male children showed an association between sleep duration and BMI. Conclusions Results partially supported hypothesized associations between child sleep duration, cumulative risk, and BMI emerging across childhood within a large, primarily low socioeconomic status sample. Findings suggest that reducing cumulative risk for families experiencing low income may support longer child sleep duration. Additionally, child sleep duration and BMI are concurrently related in early childhood for male children.

Adolescence is a crucial developmental period characterized by elevated stress and significant mental health challenges, including depression and anxiety. With barriers, such as stigma, accessibility, and cost hindering effective treatment, leveraging school systems for mental health interventions offers a strategic advantage due to their reach and potential for scalability. This study aimed to investigate the immediate impact of \"Project RE-THINK,\" a single-session, digital thought record intervention delivered in a school setting, on negative cognitions and overall emotional valence among adolescents. Project RE-THINK helps adolescents to identify, examine, and challenge negative cognitions to improve their mental health, as demonstrated through changes in negative cognition and overall emotional valence. Adolescents (N=1052) in grades 10-12 enrolled in high school during the 2023-2024 school year completed the digital thought record intervention activity. Using a quasi-experimental pre/post design, participants read through an example thought record and completed their own thought record, which involved identifying and describing a recent upsetting situation, answering a series of questions to challenge their negative cognition, and learning and using emotion regulation skills regarding the upsetting situation. Measures of pre- and postintervention overall emotional valence and negative cognition were collected to determine the intervention effect on participants' mental health. Descriptive statistics confirmed that smaller proportions of adolescents endorsed feeling negative emotions, such as anger, shame, anxiety, disgust, guilt, sadness, and fear, after the intervention. Paired samples t tests showed that adolescents experienced a significant reduction in their belief in their negative cognition from pre- to postintervention (t1051=27.71; P<.001; d=0.85, 95% CI 0.78-0.93), which demonstrates that the intervention helped them challenge their negative thoughts about their upsetting situation, as well as significant improvements to their overall emotional valence (t1051=-31.85; P<.001; d=-0.98, 95% CI -1.06 to -0.91), which demonstrates that the intervention helped them feel better about their upsetting situation. Findings also showed a significant correlation between change in negative cognition and change in overall emotional valence (r=0.25; P<.001), supporting our hypothesis that reducing the strength of belief in negative cognitions can help improve one's emotions. Finally, analysis of covariance (ANCOVAs) confirmed that there were no significant differences in intervention efficacy by gender, race and ethnicity, or socioeconomic status, suggesting broad intervention efficacy across adolescents from different backgrounds and experiences. Project RE-THINK effectively improved both cognitive and emotional outcomes among adolescents, demonstrating its potential as a scalable, low-cost intervention within school settings. Future studies should explore the longitudinal effects and potential integration of such interventions into regular school curricula to help adolescents learn effective emotions and coping skills as well as to help protect and sustain adolescent mental health.

Greater unpredictability in childhood from the level of the caregiver-child dyad to broader family, home, or environmental instability is consistently associated with disruptions in cognitive, socioemotional, behavioral, and biological development in humans. These findings are bolstered by experimental research in non-human animal models suggesting that early life unpredictability is an important environmental signal to the developing organism that shapes neurodevelopment and behavior. Research on childhood unpredictability has surged in the past several years, guided in part by theoretical grounding from the developmental psychopathology framework (shaped largely by Dr. Dante Cicchetti’s innovative work). The current review focuses on future directions for unpredictability research, including probing intergenerational effects, the role of predictability in resilience, cultural and contextual considerations, and novel developmental outcomes that should be tested in relation to childhood unpredictability. We urge the integration of multidisciplinary perspectives and collaborations into future research on unpredictability. We also provide ideas for translating this research to real-world practice and policy and encourage high-quality research testing whether incorporating predictability into interventions and policy improves developmental outcomes, which would support further dissemination of these findings.

Stressful experiences affect biological stress systems, such as the hypothalamic–pituitary–adrenal (HPA) axis. Life stress can potentially alter regulation of the HPA axis and has been associated with poorer physical and mental health. Little, however, is known about the relative influence of stressors that are encountered at different developmental periods on acute stress reactions in adulthood. In this study, we explored three models of the influence of stress exposure on cortisol reactivity to a modified version of the Trier Social Stress Test (TSST) by leveraging 37 years of longitudinal data in a high-risk birth cohort (N = 112). The cumulative stress model suggests that accumulated stress across the lifespan leads to dysregulated reactivity, whereas the biological embedding model implicates early childhood as a critical period. The sensitization model assumes that dysregulation should only occur when stress is high in both early childhood and concurrently. All of the models predicted altered reactivity, but do not anticipate its exact form. We found support for both cumulative and biological embedding effects. However, when pitted against each other, early life stress predicted more blunted cortisol responses at age 37 over and above cumulative life stress. Additional analyses revealed that stress exposure in middle childhood also predicted more blunted cortisol reactivity.

Greater childhood adversity predicts a higher likelihood of later self-injurious thoughts and behaviors (SITB). There is little research focused on whether the timing of childhood adversity predicts SITB. The current research examined whether the timing of childhood adversity predicted parent- and youth-reported SITB at age 12 and 16 years in the Longitudinal Studies of Child Abuse and Neglect (LONGSCAN) cohort (n = 970). We found that greater adversity at age 11–12 years consistently predicted SITB at age 12 years, while greater adversity at age 13–14 years consistently predicted SITB at age 16 years. These findings suggest there may be sensitive periods during which adversity may be more likely to lead to adolescent SITB, which can inform prevention and treatment.

Childhood adversity is associated with higher adult weight, but few investigations prospectively test mechanisms accounting for this association. Using two socioeconomically high-risk prospective longitudinal investigations, the Minnesota Longitudinal Study of Risk and Adaptation (MLSRA; N = 267; 45.3% female) and the Fragile Families and Child Wellbeing Study (FFCWS; n = 2,587; 48.5% female), pathways between childhood adversity and later body mass index (BMI) were tested using impulsivity, emotion dysregulation, and overeating as mediators. Childhood adversity from 0 to 5 years included four types of adversities: greater unpredictability, threat/abuse, deprivation/neglect, and low socioeconomic status. Parents reported on child impulsivity, emotion dysregulation, and overeating. Height and weight were self-reported and measured at 32 and 37 years in MLSRA and at 15 years in FFCWS. FFCWS results indicated that threat, deprivation, and low socioeconomic status predicted greater impulsivity and emotion dysregulation at 5 years, which in turn predicted greater overeating at 9 years and higher BMI z -score at 15 years. Early unpredictability in FFCWS predicted higher BMI through greater impulsivity but not emotion dysregulation at age 5. MLSRA regression results replicated the threat/abuse → emotion dysregulation → overeating → higher BMI pathway. These findings suggest that different dimensions of early adversity may follow both similar and unique pathways to predict BMI.

Psychosocial stress in childhood and adolescence is linked to stress system dysregulation, although few studies have examined the relative impacts of parental harshness and parental disengagement. This study prospectively tested whether parental harshness and disengagement show differential associations with overall cortisol output in adolescence. Associations between overall cortisol output and adolescent mental health problems were tested concurrently. Adolescents from the Fragile Families and Child Wellbeing Study (FFCWS) provided hair samples for cortisol assay at 15 years (N = 171). Caregivers reported on parental harshness and disengagement experiences at 1, 3, 5, 9, and 15 years, and adolescents reported at 15 years. Both parent and adolescent reported depressive and anxiety symptoms and antisocial behaviors at 15. Greater parental harshness from 1–15 years, and harshness reported at 15 years in particular, was associated with higher overall cortisol output at 15. Greater parental disengagement from 1–15 years, and disengagement at 1 year specifically, was associated with lower cortisol output. There were no significant associations between cortisol output and depressive symptoms, anxiety symptoms, or antisocial behaviors. These results suggest that the unique variances of parental harshness and disengagement may have opposing associations with cortisol output at 15 years, with unclear implications for adolescent mental health.

This study tested whether maternal responsiveness moderated or mediated pathways from iron deficiency (ID) at 12–18 months to adolescent behavior problems. Participants were part of a large Chilean cohort (N = 933). Iron status was assessed at 12 and 18 months. Maternal responsiveness was assessed at 9 months and 5 years. Parents reported their child’s symptomology at 5 years, 10 years, and adolescence (11–17 years; M = 14.4). Structural equation modeling identified a previously unrecognized pathway by which child externalizing problems and negative maternal responsiveness at 5 years mediated associations between ID at 12–18 months and adolescent internalizing, externalizing, and social problems. Positive maternal responsiveness in infancy did not buffer those with ID anemia from developing 5‐year internalizing problems.