Bruce J. Ellis

Biological sensitivity to context: I. An evolutionary–developmental theory of the origins and functions of stress reactivity

Biological reactivity to psychological stressors comprises a complex, integrated, and highly conserved repertoire of central neural and peripheral neuroendocrine responses designed to prepare the organism for challenge or threat. Developmental experience plays a role, along with heritable, polygenic variation, in calibrating the response dynamics of these systems, with early adversity biasing their combined effects toward a profile of heightened or prolonged reactivity. Conventional views of such high reactivity suggest that it is an atavistic and pathogenic legacy of an evolutionary past in which threats to survival were more prevalent and severe. Recent evidence, however, indicates that (a) stress reactivity is not a unitary process, but rather incorporates counterregulatory circuits serving to modify or temper physiological arousal, and (b) the effects of high reactivity phenotypes on psychiatric and biomedical outcomes are bivalent, rather than univalent, in character, exerting both risk-augmenting and risk-protective effects in a context-dependent manner. These observations suggest that heightened stress reactivity may reflect, not simply exaggerated arousal under challenge, but rather an increased biological sensitivity to context, with potential for negative health effects under conditions of adversity and positive effects under conditions of support and protection. From an evolutionary perspective, the developmental plasticity of the stress response systems, along with their structured, context-dependent effects, suggests that these systems may constitute conditional adaptations: evolved psychobiological mechanisms that monitor specific features of childhood environments as a basis for calibrating the development of stress response systems to adaptively match those environments. Taken together, these theoretical perspectives generate a novel hypothesis: that there is a curvilinear, U-shaped relation between early exposures to adversity and the development of stress-reactive profiles, with high reactivity phenotypes disproportionately emerging within both highly stressful and highly protected early social environments.

Differential susceptibility to the environment: an evolutionary--neurodevelopmental theory.

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 x 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.

Timing of pubertal maturation in girls: An integrated life history approach

Life history theory provides a metatheoretical framework for the study of pubertal timing from an evolutionary-developmental perspective. The current article reviews 5 middle-level theories--energetics theory, stress-suppression theory, psychosocial acceleration theory, paternal investment theory, and child development theory--each of which applies the basic assumptions of life history theory to the question of environmental influences on timing of puberty in girls. These theories converge in their conceptualization of pubertal timing as responsive to ecological conditions but diverge in their conceptualization of (a) the nature, extent, and direction of environmental influences and (b) the effects of pubertal timing on other reproductive variables. Competing hypotheses derived from the 5 perspectives are evaluated. An extension of W. T. Boyce and B. J. Elliss (in press) theory of stress reactivity is proposed to account for both inhibiting and accelerating effects of psychosocial stress on timing of pubertal development. This review highlights the multiplicity of (often unrecognized) perspectives guiding research, raises challenges to virtually all of these, and presents an alternative framework in an effort to move research forward in this arena of multidisciplinary inquiry.

The Adaptive Calibration Model of stress responsivity

This paper presents the Adaptive Calibration Model (ACM), an evolutionary-developmental theory of individual differences in the functioning of the stress response system. The stress response system has three main biological functions: (1) to coordinate the organisms allostatic response to physical and psychosocial challenges; (2) to encode and filter information about the organisms social and physical environment, mediating the organisms openness to environmental inputs; and (3) to regulate the organisms physiology and behavior in a broad range of fitness-relevant areas including defensive behaviors, competitive risk-taking, learning, attachment, affiliation and reproductive functioning. The information encoded by the system during development feeds back on the long-term calibration of the system itself, resulting in adaptive patterns of responsivity and individual differences in behavior. Drawing on evolutionary life history theory, we build a model of the development of stress responsivity across life stages, describe four prototypical responsivity patterns, and discuss the emergence and meaning of sex differences. The ACM extends the theory of biological sensitivity to context (BSC) and provides an integrative framework for future research in the field.

Biological Sensitivity to Context

Conventional views suggest that exaggerated biological reactivity to stress is a harmful vestige of an evolutionary past in which threats to survival were more prevalent and severe. Recent evidence, however, indicates that effects of high reactivity on behavior and health are bivalent rather than univalent in character, exerting both risk-augmenting and risk-protective effects depending on the context. These observations suggest that heightened stress reactivity may reflect increased biological sensitivity to context, with potential for negative health effects under conditions of adversity and for positive effects under conditions of support. From an evolutionary perspective, the developmental plasticity of the stress-response systems, along with their structured, context-dependent effects, suggests that variation in these systems has been adaptively patterned to increase the capacity of children to match their stress-response profiles to anticipated developmental environments. Taken together, these theoretical perspectives generate a novel hypothesis: that there is a curvilinear, U-shaped relation between early exposures to adversity and the development of stress-reactive profiles, with high-reactivity phenotypes disproportionately emerging within both highly stressful and highly protected early social environments.

Fundamental Dimensions of Environmental Risk : The Impact of Harsh versus Unpredictable Environments on the Evolution and Development of Life History Strategies.

The current paper synthesizes theory and data from the field of life history (LH) evolution to advance a new developmental theory of variation in human LH strategies. The theory posits that clusters of correlated LH traits (e.g., timing of puberty, age at sexual debut and first birth, parental investment strategies) lie on a slow-to-fast continuum; that harshness (externally caused levels of morbidity-mortality) and unpredictability (spatial-temporal variation in harshness) are the most fundamental environmental influences on the evolution and development of LH strategies; and that these influences depend on population densities and related levels of intraspecific competition and resource scarcity, on age schedules of mortality, on the sensitivity of morbidity-mortality to the organism’s resource-allocation decisions, and on the extent to which environmental fluctuations affect individuals versus populations over short versus long timescales. These interrelated factors operate at evolutionary and developmental levels and should be distinguished because they exert distinctive effects on LH traits and are hierarchically operative in terms of primacy of influence. Although converging lines of evidence support core assumptions of the theory, many questions remain unanswered. This review demonstrates the value of applying a multilevel evolutionary-developmental approach to the analysis of a central feature of human phenotypic variation: LH strategy.

Does father absence place daughters at special risk for early sexual activity and teenage pregnancy

The impact of father absence on early sexual activity and teenage pregnancy was investigated in longitudinal studies in the United States (N = 242) and New Zealand (N = 520), in which community samples of girls were followed prospectively from early in life (5 years) to approximately age 18. Greater exposure to father absence was strongly associated with elevated risk for early sexual activity and adolescent pregnancy. This elevated risk was either not explained (in the US. study) or only partly explained (in the New Zealand study) by familial, ecological, and personal disadvantages associated with father absence. After controlling for covariates, there was stronger and more consistent evidence of effects of father absence on early sexual activity and teenage pregnancy than on other behavioral or mental health problems or academic achievement. Effects of father absence are discussed in terms of life-course adversity, evolutionary psychology, social learning, and behavior genetic models.

The evolutionary basis of risky adolescent behavior: implications for science, policy, and practice.

This article proposes an evolutionary model of risky behavior in adolescence and contrasts it with the prevailing developmental psychopathology model. The evolutionary model contends that understanding the evolutionary functions of adolescence is critical to explaining why adolescents engage in risky behavior and that successful intervention depends on working with, instead of against, adolescent goals and motivations. The current article articulates 5 key evolutionary insights into risky adolescent behavior: (a) The adolescent transition is an inflection point in development of social status and reproductive trajectories; (b) interventions need to address the adaptive functions of risky and aggressive behaviors like bullying; (c) risky adolescent behavior adaptively calibrates over development to match both harsh and unpredictable environmental conditions; (d) understanding evolved sex differences is critical for understanding the psychology of risky behavior; and (e) mismatches between current and past environments can dysregulate adolescent behavior, as demonstrated by age-segregated social groupings. The evolutionary model has broad implications for designing interventions for high-risk youth and suggests new directions for research that have not been forthcoming from other perspectives.

Impact of Fathers on Daughters' Age at Menarche: A Genetically and Environmentally Controlled Sibling Study.

Girls growing up in homes without their biological fathers tend to go through puberty earlier than their peers. Whereas evolutionary theories of socialization propose that this relation is causal, it could arise from environmental or genetic confounds. To distinguish between these competing explanations, the authors used a genetically and environmentally controlled sibling comparison design to examine the effects of differential exposure to family disruption/father absence in a community sample of sister pairs. As specified by evolutionary causal theories, younger sisters had earlier menarche than their older sisters in biologically disrupted families (n = 68) but not biologically intact families (n = 93). This effect was superseded, however, by a large moderating effect of paternal dysfunction. Younger sisters from disrupted families who were exposed to serious paternal dysfunction in early childhood attained menarche 11 months earlier than either their older sisters or other younger sisters from disrupted families who were not exposed to such dysfunction. These data suggest that early exposure to disordered paternal behavior, followed by family disruption and residential separation from the father, can lead to substantially earlier menarche.

Differential susceptibility to the environment: toward an understanding of sensitivity to developmental experiences and context.

Science, like evolution, is often remarkably convergent in itsgenerativityofnewideasanditsexplorationofnovelconcep-tualterritory.Justasevolutionhasrepeatedlyconvergeduponcommon phenotypic solutions to problems of survival andreproduction among species of differing lineage (Morris,2010), the history of scientific inquiry, and that of develop-mentalscienceinparticular,hasalsobeenmarkedbyconcur-rent and homologous discovery by a sometimes striking si-multaneity in its arrival at shared theoretical insights alongpaths of differing origins and trajectories. Thus, it has beenwith the emergence of “differential susceptibility to the envi-ronment”: a construct—really, a shared solution to a set ofcompelling conceptual and empirical dilemmas—that formsthe centerpiece of this Special Section of Development andPsychopathology.Inspired by a provocative and broadly attended sympo-sium (“Do Children Vary in Their Plasticity? DifferentialSusceptibility to Rearing Experiences”) at the 2009 AnnualMeeting of the Society for Research in Child Development(SRCD), the Special Section explores the convergence oftwo theories conceptualizing reactivity to environmentalstimuli as an indicator of sensitivity or susceptibility to envi-ronmental influence. The “biological sensitivity to context”theory advanced by Boyce and Ellis (2005; see also Boyceet al., 1995) originated in empirical observations of differ-ences in children’s autonomic and adrenocortical reactivityto challenge and posited a context-sensitive endophenotyperendering a subset of children unusually susceptible to therisk-inducing and development-enhancing influences of bothnegative and positive early social environments. At the sametime, the “differential susceptibility” theory posed by Belsky(1997,2005)startedwiththequestion“Whyshouldchildhoodexperiences influence later development?” Based on reflec-tions prompted by this question, it hypothesized that childrenshould differ in their susceptibility to rearing environments asabet-hedgingstrategyagainstanuncertainfuture.Boththeoriesconverged on evolutionaryexplanationsofwhyandhow indi-viduals vary systematically in their sensitivity or “permeabil-ity” to experiential and contextual influences on developmentand health.Moststudentsofchilddevelopmentdonotpresumethatallchildrenareequallysusceptibletorearingandothercontextualexperiences; a long history of research on Parenting Temp-erament interactions clearly suggests otherwise. Nevertheless,muchworkstillfocusesoncontextualeffectsthatapplyequallyto all children and thus fails to consider the possibility thatwhether, how, and to what degree early experiences influencechilddevelopmentmaycriticallydependuponindividualchar-acteristics. All four empirical papers presented at the SRCDsymposiumexaminedtheextenttowhichsuchchildcharacter-istics moderate effects of early rearing experiences on chil-dren’s adjustment and development. Drawing on biologicalsensitivity to context or differential susceptibility theory, eachpaper focused on a phenotypic, endophenotypic, or genotypicmarker of reactivity as a moderator of susceptibility to rearinginfluence. In the first two papersthe moderator was biological