Guided by concepts from life history (LH) theory, a large human research literature has tested the hypothesis that exposures to extrinsic mortality (EM) promote the development of faster LH strategies (e.g., earlier/faster reproduction, higher offspring number). A competing model proposes that, because EM in the past was intimately linked to energetic constraints, such exposures specifically led to the development of slower LH strategies. We empirically address this debate by examining (1) LH variation among small-scale societies under different environmental conditions; (2) country-, regional- and community-level correlations between ecological conditions, mortality, maturational timing, and fertility; (3) individual-level correlations between this same set of factors; and (4) natural experiments leveraging the impact of externally-caused changes in mortality on LH traits. Partially supporting each model, we found that harsh conditions encompassing energetic stress and ambient cues to EM (external cues received through sensory systems) have countervailing effects on the development of LH strategies, both delaying pubertal maturation and promoting an accelerated pace of reproduction and higher offspring number. We conclude that, although energetics are fundamental to many developmental processes, providing a first tier of environmental influence, this first tier alone cannot explain these countervailing effects. An important second tier of environmental influence is afforded by ambient cues to EM. We advance a 2-tiered model that delineates this second tier and its central role in regulating development of LH strategies. Consideration of the first and second tier together is necessary to account for the observed countervailing shifts toward both slower and faster LH traits.

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.

Differential susceptibility theory stipulates that individuals vary in their susceptibility to environmental effects, often implying that the same individuals differ in the same way in their susceptibility to different environmental exposures. The latter point is addressed herein by evaluating the extent to which early-life harshness and unpredictability affect mother's psychological well-being and parenting, as well as their adolescent's life-history strategy, as reflected in number of sexual partners by age 15 years, drawing on data from the National Institute of Child Health and Human Development (NICHD) Study of Early Child Care and Youth Development. Results indicated that mothers whose well-being and parenting proved more susceptible to harshness also proved somewhat more susceptible to environmental unpredictability, with the same being true of adolescent sexual behavior. Nevertheless, findings caution against overgeneralizing sample-level findings to all individuals.

Although early-life adversity can undermine healthy development, children growing up in harsh environments may develop intact, or even enhanced, skills for solving problems in high-adversity contexts (i.e., “hidden talents”). Here we situate the hidden talents model within a larger interdisciplinary framework. Summarizing theory and research on hidden talents, we propose that stress-adapted skills represent a form of adaptive intelligence that enables individuals to function within the constraints of harsh, unpredictable environments. We discuss the alignment of the hidden talents model with current knowledge about human brain development following early adversity; examine potential applications of this perspective to multiple sectors concerned with youth from harsh environments, including education, social services, and juvenile justice; and compare the hidden talents model with contemporary developmental resilience models. We conclude that the hidden talents approach offers exciting new directions for research on developmental adaptations to childhood adversity, with translational implications for leveraging stress-adapted skills to more effectively tailor education, jobs, and interventions to fit the needs and potentials of individuals from a diverse range of life circumstances. This approach affords a well-rounded view of people who live with adversity that avoids stigma and communicates a novel, distinctive, and strength-based message.

Indicators are necessary to monitor national progress toward commitments made to the Convention on Biological Diversity (CBD), but countries often struggle to mobilize quantitative indicators for many biodiversity targets. Assessing the extent to which countries are using measurable indicators from global and national sources by surveying 5th National Reports to the CBD, we found that nationally generated indicators were used 11 times more frequently than global indicators and only one-fifth of indicators matched those recommended by the CBD, suggesting that countries and indicator experts should work more closely to agree upon measurable, scalable, fit-for-purpose indicators for the next generation of CBD targets.

We conducted signal detection analyses to test for curvilinear, U-shaped relations between early experiences of adversity and heightened physiological responses to challenge, as proposed by biological sensitivity to context theory. Based on analysis of an ethnically diverse sample of 338 kindergarten children (4–6 years old) and their families, we identified levels and types of adversity that, singly and interactively, predicted high (top 25%) and low (bottom 25%) rates of stress reactivity. The results offered support for the hypothesized U-shaped curve and conceptually replicated and extended the work of Ellis, Essex, and Boyce (2005). Across both sympathetic and adrenocortical systems, a disproportionate number of children growing up under conditions characterized by either low or high adversity (as indexed by restrictive parenting, family stress, and family economic condition) displayed heightened stress reactivity, compared with peers growing up under conditions of moderate adversity. Finally, as hypothesized by the adaptive calibration model, a disproportionate number of children who experienced exceptionally stressful family conditions displayed blunted cortisol reactivity to stress.

This study used a combination of microlevel observation data and longitudinal questionnaire data to study the relationship between differential reactivity and differential susceptibility, guided by three questions: (a) Does a subset of children exist that is both more likely to respond with increasingly negative emotions to increasingly negative emotions of mothers and with increasingly positive emotions to increasingly positive emotions of mothers (“emotional reactivity”)? (b) Is emotional reactivity associated with temperament markers and rearing environment? (c) Are children who show high emotional reactivity “for better and for worse” also more susceptible to parenting predicting child behavior across a year? A total of 144 Dutch children (45.3% girls) aged four to six participated. Latent profile analyses revealed a group of average reactive children (87%) and a group that was emotionally reactive “for better and for worse” (13%). Highly reactive children scored higher on surgency and received lower levels of negative parenting. Finally, associations of negative and positive parenting with externalizing and prosocial behavior were similar (and nonsignificant) for highly reactive children and average reactive children. The findings suggest that children who are emotionally reactive “for better and for worse” within parent-child interactions are not necessarily more susceptible to parenting on a developmental time scale.

Pepper & Nettle's paper exemplifies an emerging resistance against an exclusive focus on deficits in people who come from harsh environments. We extend their model by arguing for a perspective that includes not only contextually appropriate responses but also strengths – that is, enhanced mental skills and abilities. Such a well-rounded approach can be leveraged in education, jobs, and interventions.

The adaptive calibration model (ACM) is a theory of developmental programing focusing on calibration of stress response systems and associated life history strategies to local environmental conditions. In this article, we tested some key predictions of the ACM in a longitudinal study of Dutch adolescent males (11–16 years old; N = 351). Measures of sympathetic, parasympathetic, and adrenocortical activation, reactivity to, and recovery from social–evaluative stress validated the four-pattern taxonomy of the ACM via latent profile analysis, though with some deviations from expected patterns. The physiological profiles generally showed predicted associations with antecedent measures of familial and ecological conditions and life stress; as expected, high- and low-responsivity patterns were found under both low-stress and high-stress family conditions. The four patterns were also differentially associated with aggressive/rule-breaking behavior and withdrawn/depressed behavior. This study provides measured support for key predictions of the ACM and highlights important empirical issues and methodological challenges for future research.

How do exposures to stress affect biobehavioral development and, through it, psychiatric and biomedical disorder? In the health sciences, the allostatic load model provides a widely accepted answer to this question: stress responses, while essential for survival, have negative long-term effects that promote illness. Thus, the benefits of mounting repeated biological responses to threat are traded off against costs to mental and physical health. The adaptive calibration model, an evolutionary–developmental theory of stress–health relations, extends this logic by conceptualizing these trade-offs as decision nodes in allocation of resources. Each decision node influences the next in a chain of resource allocations that become instantiated in the regulatory parameters of stress response systems. Over development, these parameters filter and embed information about key dimensions of environmental stress and support, mediating the organism's openness to environmental inputs, and function to regulate life history strategies to match those dimensions. Drawing on the adaptive calibration model, we propose that consideration of biological fitness trade-offs, as delineated by life history theory, is needed to more fully explain the complex relations between developmental exposures to stress, stress responsivity, behavioral strategies, and health. We conclude that the adaptive calibration model and allostatic load model are only partially complementary and, in some cases, support different approaches to intervention. In the long run, the field may be better served by a model informed by life history theory that addresses the adaptive role of stress response systems in regulating alternative developmental pathways.

The biological sensitivity to context hypothesis posits that high physiological reactivity (i.e., increases in arousal from baseline) constitutes heightened sensitivity to environmental influences, for better or worse. To test this hypothesis, we examined the interactive effects of family cohesion and heart rate reactivity to a public speaking task on aggressive/rule-breaking and prosocial behavior in a large sample of adolescents (N = 679; M age = 16.14). Multivariate analyses revealed small- to medium-sized main effects of lower family cohesion and lower heart rate reactivity on higher levels of aggressive/rule-breaking and lower levels of prosocial behavior. Although there was some evidence of three-way interactions among family cohesion, heart rate reactivity, and sex in predicting these outcome variables, these interactions were not in the direction predicted by the biological sensitivity to context hypothesis. Instead, heightened reactivity appeared to operate as a protective factor against family adversity, rather than as a susceptibility factor. The results of the present study raise the possibility that stress reactivity may no longer operate as a mechanism of differential susceptibility in adolescence.

Girls receiving lower quality paternal investment tend to engage in more risky sexual behavior (RSB) than peers. Whereas paternal investment theory posits that this effect is causal, it could arise from environmental or genetic confounds. To distinguish between these competing explanations, the current authors employed a genetically and environmentally controlled sibling design (N = 101 sister pairs; ages 18–36), which retrospectively examined the effects of differential sibling exposure to family disruption/father absence and quality of fathering. Consistent with a causal explanation, differences between older and younger sisters in the effects of quality of fathering on RSB were greatest in biologically disrupted families when there was a large age gap between the sisters (thus maximizing differential exposure to fathers), with greater exposure within families to higher quality fathering serving as a protective factor against RSB. Further, variation around the lower end of fathering quality appeared to have the most influence on RSB. In contrast, differential sibling exposure to family disruption/father absence (irrespective of quality of fathering) was not associated with RSB. The differential sibling-exposure design affords a new quasi-experimental method for evaluating the causal effects of fathers within families.

Guided by evolutionary–developmental theories of biological sensitivity to context and reproductive development, the current research examined the interactive effects of early family environments and psychobiologic reactivity to stress on the subsequent timing and tempo of puberty. As predicted by the theory, among children displaying heightened biological sensitivity to context (i.e., higher stress reactivity), higher quality parent–child relationships forecast slower initial pubertal tempo and later pubertal timing, whereas lower quality parent–child relationships forecast the opposite pattern. No such effects emerged among less context-sensitive children. Whereas sympathetic nervous system reactivity moderated the effects of parent–child relationships on both breast/genital and pubic hair development, adrenocortical activation only moderated the effect on pubic hair development. The current results build on previous research documenting what family contexts predict variation in pubertal timing by demonstrating for whom those contexts matter. In addition, the authors advance a new methodological approach for assessing pubertal tempo using piecewise growth curve analysis.

Two extant evolutionary models, biological sensitivity to context theory (BSCT) and differential susceptibility theory (DST), converge on the hypothesis that some individuals are more susceptible than others to both negative (risk-promoting) and positive (development-enhancing) environmental conditions. These models contrast with the currently dominant perspective on personal vulnerability and environmental risk: diathesis stress/dual risk. We review challenges to this perspective based on emerging theory and data from the evolutionary, developmental, and health sciences. These challenges signify the need for a paradigm shift in conceptualizing Person × Environment interactions in development. In this context we advance an evolutionary–neurodevelopmental theory, based on DST and BSCT, of the role of neurobiological susceptibility to the environment in regulating environmental effects on adaptation, development, and health. We then outline current thinking about neurogenomic and endophenotypic mechanisms that may underpin neurobiological susceptibility, summarize extant empirical research on differential susceptibility, and evaluate the evolutionary bases and implications of BSCT and DST. Finally, we discuss applied issues including methodological and statistical considerations in conducting differential susceptibility research; issues of ecological, cultural, and racial–ethnic variation in neurobiological susceptibility; and implications of differential susceptibility for designing social programs. We conclude that the differential susceptibility paradigm has far-reaching implications for understanding whether and how much child and adult development responds, for better and for worse, to the gamut of species-typical environmental conditions.

Del Giudice's model of sex-specific attachment patterns demonstrates the usefulness of infusing life history theory with principles of sexual selection. We believe a full synthesis between the two theories provides a foundation for a comprehensive model of alternative reproductive strategies. We extend Del Giudice's ideas based on our own program of research, focusing specifically on the importance of intrasexual competition and the individual phenotype during development.