Biological sensitivity to context: I. An evolutionary–developmental theory of the origins and functions of stress reactivity
01 Jun 2005-Development and Psychopathology (Cambridge University Press)-Vol. 17, Iss: 2, pp 271-301
TL;DR: 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.
Abstract: 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.
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TL;DR: An ecobiodevelopmental framework is presented that suggests that many adult diseases should be viewed as developmental disorders that begin early in life and that persistent health disparities associated with poverty, discrimination, or maltreatment could be reduced by the alleviation of toxic stress in childhood.
Abstract: in fields of inquiry as diverse as neuroscience, molecular biology, genomics, developmental psychology, epidemiology, sociology, and economics are catalyzing an important paradigm shift in our un- derstanding of health and disease across the lifespan. This converging, multidisciplinary science of human development has profound impli- cations for our ability to enhance the life prospects of children and to strengthen the social and economic fabric of society. Drawing on these multiple streams of investigation, this report presents an ecobiodeve- lopmental framework that illustrates how early experiences and envi- ronmental influences can leave a lasting signature on the genetic predispositions that affect emerging brain architecture and long-term health. The report also examines extensive evidence of the disruptive impacts of toxic stress, offering intriguing insights into causal mech- anisms that link early adversity to later impairments in learning, be- havior, and both physical and mental well-being. The implications of this framework for the practice of medicine, in general, and pediatrics, specifically, are potentially transformational. They suggest that many adultdiseasesshouldbeviewedasdevelopmentaldisordersthatbegin early in life and that persistent health disparities associated with pov- erty, discrimination, or maltreatment could be reduced by the allevi- ation of toxic stress in childhood. An ecobiodevelopmental framework alsounderscoresthe needfornewthinking aboutthe focus andbound- aries of pediatric practice. It calls for pediatricians to serve as both front-line guardians of healthy child development and strategically po- sitioned, community leaders to inform new science-based strategies that build strong foundations for educational achievement, economic productivity, responsible citizenship, and lifelong health. Pediatrics
3,248 citations
Cites background from "Biological sensitivity to context: ..."
...Because the hippocampus and PFC both play a significant role in modulating the amygdala’s initiation of the stress response, toxic stress– induced changes in architecture and connectivity within and between these important areas might account for the variability seen in stressresponsiveness.(50) This can then result in some children appearing to be both more reactive to even mildly adverse experiences and less capable of effectively coping with future stress....
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TL;DR: It is proposed that temperament can and should be studied within an evolutionary ecology framework and provided a terminology that could be used as a working tool for ecological studies of temperament, which includes five major temperament trait categories: shyness‐boldness, exploration‐avoidance, activity, sociability and aggressiveness.
Abstract: Temperament describes the idea that individual behavioural differences are repeatable over time and across situations. This common phenomenon covers numerous traits, such as aggressiveness, avoidance of novelty, willingness to take risks, exploration, and sociality. The study of temperament is central to animal psychology, behavioural genetics, pharmacology, and animal husbandry, but relatively few studies have examined the ecology and evolution of temperament traits. This situation is surprising, given that temperament is likely to exert an important influence on many aspects of animal ecology and evolution, and that individual variation in temperament appears to be pervasive amongst animal species. Possible explanations for this neglect of temperament include a perceived irrelevance, an insufficient understanding of the link between temperament traits and fitness, and a lack of coherence in terminology with similar traits often given different names, or different traits given the same name. We propose that temperament can and should be studied within an evolutionary ecology framework and provide a terminology that could be used as a working tool for ecological studies of temperament. Our terminology includes five major temperament trait categories: shyness-boldness, exploration-avoidance, activity, sociability and aggressiveness. This terminology does not make inferences regarding underlying dispositions or psychological processes, which may have restrained ecologists and evolutionary biologists from working on these traits. We present extensive literature reviews that demonstrate that temperament traits are heritable, and linked to fitness and to several other traits of importance to ecology and evolution. Furthermore, we describe ecologically relevant measurement methods and point to several ecological and evolutionary topics that would benefit from considering temperament, such as phenotypic plasticity, conservation biology, population sampling, and invasion biology.
2,860 citations
Cites background from "Biological sensitivity to context: ..."
...…to social stress (Boissy & Bouissou, 1995; Le Neindre, Boivin & Boissy, 1996; Caspi et al., 1997; Grandin, 1998; Martin, 1998; Carlstead, Mellen & Kleiman, 1999; Trut, 1999; Malmkvist & Hansen, 2001; Boissy et al., 2005; Boyce & Ellis, 2005; Ellis, Jackson & Boyce, 2006; McDougall et al., 2006)....
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...Psychologists have long been interested in the study of human and animal temperament, which has led to significant theoretical and empirical developments (Wilson, 1994; Gosling, 2001; Boyce & Ellis, 2005)....
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TL;DR: Evidence consistent with the proposition that individuals differ in plasticity is reviewed, and multiple instances in which specific genes function less like "vulnerability factors" and more like "plasticity factors," thereby rendering some individuals more malleable or susceptible than others to both negative and positive environmental influences.
Abstract: Evolutionary-biological reasoning suggests that individuals should be differentially susceptible to environmental influences, with some people being not just more vulnerable than others to the negative effects of adversity, as the prevailing diathesis-stress view of psychopathology (and of many environmental influences) maintains, but also disproportionately susceptible to the beneficial effects of supportive and enriching experiences (or just the absence of adversity). Evidence consistent with the proposition that individuals differ in plasticity is reviewed. The authors document multiple instances in which (a) phenotypic temperamental characteristics, (b) endophenotypic attributes, and (c) specific genes function less like “vulnerability factors” and more like “plasticity factors,” thereby rendering some individuals more malleable or susceptible than others to both negative and positive environmental influences. Discussion focuses upon limits of the evidence, statistical criteria for distinguishing differential susceptibility from diathesis stress, potential mechanisms of influence, and unknowns in the differentialsusceptibility equation.
2,422 citations
Cites background from "Biological sensitivity to context: ..."
...Whereas one stipulated that there should be individual differences in developmental plasticity, not just vulnerability, and advanced no hypotheses concerning process (Belsky, 1997a, 1997b, 2005), the other highlighted physiological reactivity as a plasticity mechanism (Boyce & Ellis, 2005)....
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...Boyce and Ellis (2005) argued that for adaptive reasons, children in both especially supportive and especially unsupportive developmental contexts should develop or maintain high levels of physiological stress reactivity, which they regard as a susceptibility factor and thus plasticity mechanism…...
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...…itself forecasts elevated cortisol stress reactivity at age 3 months, illuminates at least one biological mechanism that may be central to such fetal programming of postnatal plasticity, in fact, the very one that Boyce and Ellis (2005) heralded in their biological-sensitivity-tocontext thesis....
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...For children fortunate enough to grow up in particularly supportive contexts, Boyce and Ellis (2005) contended, it would be adaptive to be maximally influenced by the developmental environment....
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TL;DR: A scientific consensus is emerging that the origins of adult disease are often found among developmental and biological disruptions occurring during the early years of life as mentioned in this paper, and that these early experiences can affect adult health in 2 ways: cumulative damage over time or by the biological embedding of adversities during sensitive developmental periods.
Abstract: A scientific consensus is emerging that the origins of adult disease are often found among developmental and biological disruptions occurring during the early years of life. These early experiences can affect adult health in 2 ways—either by cumulative damage over time or by the biological embedding of adversities during sensitive developmental periods. In both cases, there can be a lag of many years, even decades, before early adverse experiences are expressed in the form of disease. From both basic research and policy perspectives, confronting the origins of disparities in physical and mental health early in life may produce greater effects than attempting to modify health-related behaviors or improve access to health care in adulthood.
2,065 citations
Cites background from "Biological sensitivity to context: ..."
...Evidence for such effect modification has been derived from studies of gene-environment interaction in which allelic variations in neuroregulatory and transcription factor−encoding genes are associated with greater risks related to early stressors(71-74) as well as from studies showing that individual differences in neurobiological sensitivity to social environments can bias outcomes both positively and negatively, depending on the protective vs injurious nature of early exposures.(37,72,75-77) Biological Embedding....
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...These neurobiological responses are essential and generally protective, but when activated persistently under circumstances of chronic or overwhelming adversity, they can become pathogenic.(37,38) Within this context, extensive documentation of the disproportionate exposure of lowincomechildrentoenvironmental stressors, traumatic experiences, and family chaos(39-41) takes on a greater sense of urgency....
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TL;DR: Adverse childhood experiences induce significant biological changes in children (biological embedding), modifying the maturation and the operating balance of allostatic systems, and can exert long-term effects on biological aging and health.
1,513 citations
Cites background from "Biological sensitivity to context: ..."
...Because of the unpredictable and threatening context, the allostatic changes described in maltreated children could promote adaptation to the environment and, thus, be beneficial in the short-term [105]....
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References
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TL;DR: This review considers recent findings regarding GC action and generates criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stress-response or, as an additional category, is preparative for a subsequent stressor.
Abstract: The secretion of glucocorticoids (GCs) is a classic endocrine response to stress. Despite that, it remains controversial as to what purpose GCs serve at such times. One view, stretching back to the time of Hans Selye, posits that GCs help mediate the ongoing or pending stress response, either via basal levels of GCs permitting other facets of the stress response to emerge efficaciously, and/or by stress levels of GCs actively stimulating the stress response. In contrast, a revisionist viewpoint posits that GCs suppress the stress response, preventing it from being pathologically overactivated. In this review, we consider recent findings regarding GC action and, based on them, generate criteria for determining whether a particular GC action permits, stimulates, or suppresses an ongoing stressresponse or, as an additional category, is preparative for a subsequent stressor. We apply these GC actions to the realms of cardiovascular function, fluid volume and hemorrhage, immunity and inflammation, metabolism, neurobiology, and reproductive physiology. We find that GC actions fall into markedly different categories, depending on the physiological endpoint in question, with evidence for mediating effects in some cases, and suppressive or preparative in others. We then attempt to assimilate these heterogeneous GC actions into a physiological whole. (Endocrine Reviews 21: 55‐ 89, 2000)
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TL;DR: The long-term effect of the physiologic response to stress is reviewed, which I refer to as allostatic load, which is the ability to achieve stability through change.
Abstract: Over 60 years ago, Selye1 recognized the paradox that the physiologic systems activated by stress can not only protect and restore but also damage the body. What links these seemingly contradictory roles? How does stress influence the pathogenesis of disease, and what accounts for the variation in vulnerability to stress-related diseases among people with similar life experiences? How can stress-induced damage be quantified? These and many other questions still challenge investigators. This article reviews the long-term effect of the physiologic response to stress, which I refer to as allostatic load.2 Allostasis — the ability to achieve stability through change3 — . . .
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TL;DR: In connection with a study of various aspects of the modifiability of behavior in the dancing mouse a need for definite knowledge concerning the relation of strength of stimulus to rate of learning arose, the experiments which are now to be described arose.
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TL;DR: For centuries knowledge meant proven knowledge, proven either by the power of the intellect or by the evidence of the senses as discussed by the authors. But the notion of proven knowledge was questioned by the sceptics more than two thousand years ago; but they were browbeaten into confusion by the glory of Newtonian physics.
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