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Two extant frameworks – the harshness-unpredictability model and the threat-deprivation model – attempt to explain which dimensions of adversity have distinct influences on development. These models address, respectively, why, based on a history of natural selection, development operates the way it does across a range of environmental contexts, and how the neural mechanisms that underlie plasticity and learning in response to environmental experiences influence brain development. Building on these frameworks, we advance an integrated model of dimensions of environmental experience, focusing on threat-based forms of harshness, deprivation-based forms of harshness, and environmental unpredictability. This integrated model makes clear that the why and the how of development are inextricable and, together, essential to understanding which dimensions of the environment matter. Core integrative concepts include the directedness of learning, multiple levels of developmental adaptation to the environment, and tradeoffs between adaptive and maladaptive developmental responses to adversity. The integrated model proposes that proximal and distal cues to threat-based and deprivation-based forms of harshness, as well as unpredictability in those cues, calibrate development to both immediate rearing environments and broader ecological contexts, current and future. We highlight actionable directions for research needed to investigate the integrated model and advance understanding of dimensions of environmental experience.

The literature on resilience and posttraumatic growth has been instrumental in highlighting the human capacity to overcome adversity by illuminating that there are different pathways individuals may follow. Although the theme of strength from adversity is attractive and central to many disciplines and certain cultural narratives, this claim lacks robust empirical evidence. Specific issues include methodological approaches of using growth-mixture modeling in resilience research and retrospective assessments of growth. Conceptually, limitations exist in the examination of which outcomes are most appropriate for studying resilience and growth. We discuss new research intended to overcome these limitations, with a focus on prospective longitudinal designs and the value of integrating these disciplines for furthering our understanding of the human capacity to overcome adversity.

Exposure to early life adversity (ELA) is associated with increased rates of psychopathology and poor physical health. The present study builds on foundational work by Megan Gunnar identifying how ELA results in poor long-term outcomes through alterations in the stress response system, leading to major disruptions in emotional and behavioral regulation. Specifically, the present study tested the direct effects of ELA against the role of parent socialization to shed light on the mechanisms by which ELA leads to emotion regulation deficits. Children ages 4–7 years (N = 64) completed interviews about their experiences of deprivation and threat, a fear conditioning and extinction paradigm, and an IQ test. Parents of the children completed questionnaires regarding their own emotion regulation difficulties and psychopathology, their children's emotion regulation, and child exposure to adversity. At the bivariate level, greater exposure to threat and parental difficulties with emotion regulation were associated with poorer emotion regulation in children, assessed both via parental report and physiologically. In models where parental difficulties with emotion regulation, threat, and deprivation were introduced simultaneously, regression results indicated that parental difficulties with emotion regulation, but not deprivation or threat, continued to predict children's emotion regulation abilities. These results suggest that parental socialization of emotion is a robust predictor of emotion regulation tendencies in children exposed to early adversity.

Several studies showed that adults who have experienced childhood adversity are more likely to develop alexithymia and low empathy. Therefore, this research aims to analyze the relationship between childhood adversity and alexithymia and empathy in adulthood and verify a predictive explanatory model of alexithymia. The sample comprised 92 adults who responded to the sociodemographic questionnaire, the Childhood History Questionnaire, the Interpersonal Reactivity Index, and the Alexithymia Scale of Toronto. Childhood adversity showed a positive relationship with alexithymia and a negative relationship with empathy. Predictive validity showed that marital status, adverse childhood experiences (ACEs), and empathic concern predicted higher alexithymia scores. These results show the impact of these childhood experiences on adult life, underlining the importance of developing intervention programs in this field.

Most developmental work regards adverse developmental experiences as forces that undermine well-being. Here, I present an alternative—or complementary—view, summarizing recent evidence on puberty, endocrinology, cellular aging, and brain connectivity that collectively reveals developmental acceleration in response to contextual adversity. Findings are cast in evolutionary-developmental terms, highlighting the trade-off between accelerated aging and (a) increased morbidity and (b) premature mortality.

Stress over the lifespan is thought to promote accelerated aging and early disease. Telomere length is amarker of cell aging that appears to be one mediator of this relationship. Telomere length is associated with early adversity and with chronic stressors in adulthood in many studies. Although cumulative lifespan adversity should have bigger impacts than single events, it is also possible that adversity in childhood has larger effects on later life health than adult stressors, as suggested by models of biological embedding in early life. No studies have examined the individual vs. cumulative effects of childhood and adulthood adversities on adult telomere length. Here, we examined the relationship between cumulative childhood and adulthood adversity, adding up a range of severe financial, traumatic, and social exposures, as well as comparing them to each other, in relation to salivary telomere length. We examined 4,598 men and women from the US Health and Retirement Study. Single adversities tended to have nonsignificant relations with telomere length. In adjusted models, lifetime cumulative adversity predicted 6% greater odds of shorter telomere length. This result was mainly due to childhood adversity. In adjusted models for cumulative childhood adversity, the occurrence of each additional childhood event predicted 11% increased odds of having short telomeres. This result appeared mainly because of social/traumatic exposures rather than financial exposures. This study suggests that the shadow of childhood adversity may reach far into later adulthood in part through cellular aging.

Although childhood adversity is a potent determinant of psychopathology, relatively little is known about how the characteristics of adversity exposure, including its developmental timing or duration, influence subsequent mental health outcomes. This study compared three models from life course theory (recency, accumulation, sensitive period) to determine which one(s) best explained this relationship. Prospective data came from the Avon Longitudinal Study of Parents and Children (n = 7476). Four adversities commonly linked to psychopathology (caregiver physical/emotional abuse; sexual/physical abuse; financial stress; parent legal problems) were measured repeatedly from birth to age 8. Using a statistical modeling approach grounded in least angle regression, we determined the theoretical model(s) explaining the most variability (r2) in psychopathology symptoms measured at age 8 using the Strengths and Difficulties Questionnaire and evaluated the magnitude of each association. Recency was the best fitting theoretical model for the effect of physical/sexual abuse (girls r2 = 2.35%; boys r2 = 1.68%). Both recency (girls r2 = 1.55%) and accumulation (boys r2 = 1.71%) were the best fitting models for caregiver physical/emotional abuse. Sensitive period models were chosen alone (parent legal problems in boys r2 = 0.29%) and with accumulation (financial stress in girls r2 = 3.08%) more rarely. Substantial effect sizes were observed (standardized mean differences = 0.22-1.18). Child psychopathology symptoms are primarily explained by recency and accumulation models. Evidence for sensitive periods did not emerge strongly in these data. These findings underscore the need to measure the characteristics of adversity, which can aid in understanding disease mechanisms and determining how best to reduce the consequences of exposure to adversity.

Children who have experienced environmental adversity—such as abuse, neglect, or poverty—are more likely to develop physical and mental health problems, perform poorly at school, and have difficulties in social relationships than children who have not encountered adversity. What is less clear is how and why adverse early experiences exert such a profound influence on children's development. Identifying developmental processes that are disrupted by adverse early environments is the key to developing better intervention strategies for children who have experienced adversity. Yet much existing research relies on a cumulative-risk approach that is unlikely to reveal these mechanisms. This approach tallies the number of distinct adversities experienced to create a risk score. This risk score fails to distinguish between distinct types of environmental experiences, implicitly assuming that very different experiences influence development through the same underlying mechanisms. We advance an alternative model. This novel approach conceptualizes adversity along distinct dimensions, emphasizes the central role of learning mechanisms, and distinguishes between different forms of adversity that might influence learning in distinct ways. A key advantage of this approach is that learning mechanisms provide clear targets for interventions aimed at preventing negative developmental outcomes in children who have experienced adversity.

School connectedness, a construct indexing supportive school relationships, has been posited to promote resilience to environmental adversity. Consistent with prominent calls in the field, we examined the protective nature of school connectedness against two dimensions of early adversity that index multiple levels of environmental exposure (violence exposure, social deprivation) when predicting both positive and negative outcomes in longitudinal data from 3,246 youth in the Fragile Families and Child Wellbeing Study (48% female, 49% African American). Child and adolescent school connectedness were promotive, even when accounting for the detrimental effects of early adversity. Additionally, childhood school connectedness had a protective but reactive association with social deprivation, but not violence exposure, when predicting externalizing symptoms and positive function. Specifically, school connectedness was protective against the negative effects of social deprivation, but the effect diminished as social deprivation became more extreme. These results suggest that social relationships at school may compensate for low levels of social support in the home and neighborhood. Our results highlight the important role that the school environment can play for youth who have been exposed to adversity in other areas of their lives and suggest specific groups that may especially benefit from interventions that boost school connectedness.

In psychological research, there are often assumptions about the conditions that children expect to encounter during their development. These assumptions shape prevailing ideas about the experiences that children are capable of adjusting to, and whether their responses are viewed as impairments or adaptations. Specifically, the expected childhood is often depicted as nurturing and safe, and characterized by high levels of caregiver investment. Here, we synthesize evidence from history, anthropology, and primatology to challenge this view. We integrate the findings of systematic reviews, meta-analyses, and cross-cultural investigations on three forms of threat (infanticide, violent conflict, and predation) and three forms of deprivation (social, cognitive, and nutritional) that children have faced throughout human evolution. Our results show that mean levels of threat and deprivation were higher than is typical in industrialized societies, and that our species has experienced much variation in the levels of these adversities across space and time. These conditions likely favored a high degree of phenotypic plasticity, or the ability to tailor development to different conditions. This body of evidence has implications for recognizing developmental adaptations to adversity, for cultural variation in responses to adverse experiences, and for definitions of adversity and deprivation as deviation from the expected human childhood.