Background: Stress and compromised parenting often place children at risk of abuse and neglect. Child maltreatment has generally been viewed as a highly individualistic problem by focusing on stressors and parenting behaviors that impact individual families. However, because of the global coronavirus disease 2019 (COVID-19), families across the world are experiencing a new range of stressors that threaten their health, safety, and economic well-being. Objective: This study examined the effects of the COVID-19 pandemic in relation to parental perceived stress and child abuse potential. Participants and Setting: Participants included parents (N = 183) with a child under the age of 18 years in the western United States. Method: Tests of group differences and hierarchical multiple regression analyses were employed to assess the relationships among demographic characteristics, COVID-19 risk factors, mental health risk factors, protective factors, parental perceived stress, and child abuse potential. Results: Greater COVID-19 related stressors and high anxiety and depressive symptoms are associated with higher parental perceived stress. Receipt of financial assistance and high anxiety and depressive symptoms are associated with child abuse potential. Conversely, greater parental support and perceived control during the pandemic are associated with lower perceived stress and child abuse potential. Results also indicate racial and ethnic differences in COVID-19 related stressors, but not in mental health risk, protective factors, perceived stress, or child abuse potential. Conclusion: Findings suggest that although families experience elevated stressors from COVID-19, providing parental support and increasing perceived control may be promising intervention targets.

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In the past 25 years research on the hypothalamic-pituitary-adrenocortical (HPA) axis has emerged as a vital area within the field of developmental psychopathology. 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 lifespan in both 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. Importantly, knowledge gained over the past 25 years has been translated to both 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.

Objective The current study investigated mediators between childhood/adolescent adversities (e.g., dating violence, maltreatment, homelessness, and parental death), low socioeconomic status (SES) during adolescence, and cardiovascular disease (CVD) risk in young adulthood. The purpose of these analyses was to understand whether SES during adolescence and childhood/adolescent adversities affect CVD risk through similar pathways, including maternal relationship quality, health behaviors, financial stress, medical/dental care, educational attainment, sleep problems, and depressive symptoms. Methods Using the National Longitudinal Study of Adolescent to Adult Health (N = 14,493), which has followed US adolescents (Wave 1; M = 15.9 years) through early adulthood (Wave 4; M = 28.9 years), associations were examined between childhood/adolescent adversity and SES to 30-year CVD risk in young adulthood. The outcome was a Framingham-based prediction model of CVD risk that included age, sex, body mass index, smoking, systolic blood pressure, diabetes, and antihypertensive medication use at Wave 4. Path analysis was used to examine paths through the adolescent maternal relationship to young adult mediators of CVD risk. Results Childhood/adolescent adversity significantly predicted greater adult CVD risk through the following pathways: maternal relationship, health behaviors, financial stress, lack of medical/dental care, and educational attainment; but not through depressive symptoms or sleep problems. Lower SES during adolescence significantly predicted greater adult CVD risk through the following pathways: health behaviors, financial stress, lack of medical/dental care, and educational attainment, but not maternal relationship, depressive symptoms, or sleep problems. Conclusions Childhood/adolescent adversities and SES affected CVD risk in young adulthood through both similar and unique pathways that may inform interventions.