Evolution and ontogeny of stress response to social challenges in the human child

The stress response systems of the human child are highly sensitive to social challenges. Because stress hormones can have negative developmental and health consequences, this presents an evolutionary paradox: Why would natural selection have favored mechanisms that elevate stress hormone levels in response to psychosocial stimuli? Two complementary hypotheses are considered: (a) maladaptation to the novelty of chronic stress in social environments, and (b) adaptive neural reorganization that facilitates the ontogeny of social competencies. Data on salivary cortisol, morbidity, and social environment from an 18 year study of child health in a rural community on the island of Dominica are examined from the perspective of these alternative hypotheses. Results indicate that difficult family environments and traumatic events are associated with elevated cortisol levels and higher morbidity. The long-term effects of traumatic early experiences on cortisol profiles are complex and indicate domain-specific effects, with normal recovery from physical stressors, but heightened response to negative-affect social challenges.     

The Role of Neurobiological Deficits in Childhood Antisocial Behavior

ABSTRACT— Childhood-onset antisocial behavior is an important predictor of chronic and serious forms of antisocial behavior in later life. Both biological and social factors are involved in the development of abnormal behavior. We examine the underlying role of stress-response systems in the link between early social adversity and juvenile antisocial behavior, and propose that children with genetically and/or perinatally based neurobiological deficits have problems in activating these systems and therefore experience difficulties in regulating affect and behavior. Underactivity or attenuated reactivity of the stress-response systems may predispose antisocial individuals to seek out stimulation or take risks, and thereby explain deficits in learning and socialization. Further investigations of neurobiological functioning in antisocial children might not only indicate which children are more likely to persist in behaving antisocially but also guide the development of new interventions.     

Maternal Care and Individual Differences in Defensive Responses

Abstract— Familial transmission of mental illness is common. Recent studies in behavioral neuroscience and biological psychiatry reveal the importance of epigenetic mechanisms of transmission that center on the developmental consequences of variations in parental care. Studies with rats suggest that environmental adversity results in patterns of parent–offspring interactions that increase stress reactivity through sustained effects on gene expression in brain regions known to regulate behavioral, endocrine, and autonomic responses to stress. While such effects might be adaptive, the associated cost involves an increased risk for stress-related illness.     

Prescient human fetuses thrive

Fetal detection of adversity is a conserved trait that allows many species to adapt their early developmental trajectories to ensure survival. According to the fetal-programming model, exposure to stressful or hostile conditions in utero is associated with compromised development and a lifelong risk of adverse health outcomes. In a longitudinal study, we examined the consequences of prenatal and postnatal exposure to adversity for infant development. We found increased motor and mental development during the 1st year of life among infants whose mothers experienced congruent levels of depressive symptoms during and after pregnancy, even when the levels of symptoms were relatively high and the prenatal and postnatal environments were unfavorable. Congruence between prenatal and postnatal environments prepares the fetus for postnatal life and confers an adaptive advantage for critical survival functions during early development.     

The stress response systems: Universality and adaptive individual differences

Biological reactivity to psychological stressors comprises a complex, integrated system of central neural and peripheral neuroendocrine responses designed to prepare the organism for challenge or threat. Developmental experience plays a role, along with heritable variation, in calibrating the response dynamics of this system. This calibration occurs through setting of response thresholds in the regulatory mechanisms that coordinate the expression and use of trait-specific gene products and environmental elements that build alternative phenotypes. Whereas natural selection tends to favor developmental plasticity when the fitness of alternative phenotypes can be predicted from observable cues, genetic polymorphisms are most likely to be maintained when the advantages of niche specialization are high and organisms can evaluate and select their niches. Well-developed theories of both adaptive phenotypic plasticity and adaptive genetic variation in the stress-response systems have been advanced in the literature. Taken together, these theories strongly suggest that variation in stress-response phenotypes has been shaped by natural selection, is an adaptation to multiniche environments, and involves an integration of genetic influences and condition-sensitivity.     

Effects of stress across the lifespan

Stress is a known precipitant for metabolic and neurological diseases, with sensitive periods identified across the developmental continuum from conception to old age. However, the effects of stress may vary depending on the point or points along the developmental trajectory when adversity strikes. Past research has emphasized the consequences of stress on fully developed physiological systems in the brain and periphery, but more recent studies have explored the impact of stress on systems at different stages of maturation, with differential effects being revealed. This review provides an overview of the diverse effects of stress at critical developmental stages and the potential outcomes that may be associated with experiencing environmental adversity during ontogeny.     

Exploring the dynamics of development and evolution: comment on Blair and Raver (2012)

Blair and Raver (2012) have provided an organism-in-environment conceptualization of the development of stress response physiology and its relation to the development of self-regulation. They argue that we must consider the context in which self-regulation and stress reactivity occur to understand their implications for developmental outcome. More generally, they present a cogent argument for why it is necessary to think developmentally when considering the effects of early experience on subsequent physical, emotional, cognitive, and social development. Blair and Raver's article also highlights a persistent challenge for developmental theory--how to make sense of the relationship among the various timescales over which phenotypes develop and change occurs. Their efforts to identify the factors involved in the variability and stability of self-regulation over different timescales demonstrate the dividends of integrating developmental and evolutionary perspectives to better understand the malleability of phenotypic development.     

Altered stress responses in children exposed to early adversity: a systematic review of salivary cortisol studies

Pathological stress responses are implicated in numerous disorders. Hypothalamic-pituitary-adrenal axis function is influenced by gene-environment interaction, with early-life environmental adversity having long-lasting effects. We examine the evidence that, in humans, these effects are apparent from infancy. We systematically reviewed published findings on cortisol response to a stressor, in 0-5-year-olds already exposed to adversity. Adversity was defined as a negative environmental influence present post-conception. We searched Ovid MEDLINE (1950-May 2010), EMBASE (1980-May 2010) and PsychINFO (1806-May 2010). We included peer-reviewed, English language studies that analysed salivary cortisol before and after a standardised stressor. We identified 30 studies, of which 27 reported a significant effect of adversity on the cortisol response to stress. Six of these demonstrated an effect of prenatal substance exposure. Thirteen studies found that psychosocial adversity increased cortisol reactivity. Three studies reported that cortisol reactivity could be normalised by intervention programmes. The studies were heterogeneous, both in nature of adversity studied and in stressor used, precluding meta-analysis and assessment of publication bias. Our review presents evidence that adversity disrupts the stress response from an early age. Longitudinal studies are required to determine whether effects persist, alter with time, or are reversible with intervention.     

Women's mental health during pregnancy influences fetal and infant developmental and health outcomes

Women's mental health during pregnancy has important implications not only for the well-being of the mother, but also for the development, health, and well-being of her unborn child. A growing body of empirical evidence from population-based studies suggests that two indicators of women's mental health during pregnancy--psychosocial stress and social support--may exert a significant influence on fetal development and infant birth outcomes, such as birth weight and length of gestation, even after controlling for the effects of established sociodemographic, obstetric, and behavioral risk factors. This paper describes the role of three major biological systems involved in the physiology of pregnancy and stress physiology: neuroendocrine, immune/inflammatory, and cardiovascular systems. These systems have been hypothesized to mediate the effects of maternal mental health on fetal developmental and health outcomes, and a central role has been proposed for placental corticotropin-releasing hormone in this process. However, not all women reporting high prenatal stress and/or low social support proceed to develop adverse birth outcomes, raising the question of the determinants of susceptibility/vulnerability in the context of high stress and/or low social support. In this context, the role of race/ethnicity and genetic predisposition are discussed as two promising avenues of further investigation.     

Biopsychosocial Influences That Promote and Impede Social Brain Maturation

ABSTRACT

Social, emotional, and executive function systems of the brain change greatly during adolescence as the result of biopsychosocial influences. These factors alter the course of adolescent behavior through effects on the component processes of social behavior. Specifically, the influences of chronic stress, social and economic adversity, alcohol and drugs, and brain injury as well as parental buffering and support, increased neural connectivity and mentalizing resources, and enriched environments can impede or promote maturation of the social and executive brain networks that regulate social adjustment and emotional expression. Hence, there are many early “windows of opportunity” to affect the biological and neurocognitive foundations of adolescent social executive functions such as empathy, theory of mind, self-monitoring, and social emotions.     

Pathways to Lifespan Health Following Childhood Parental Death

The death of a parent is a profoundly stressful form of childhood adversity, increasing the short‐ and long‐term risk of mental health problems. Emerging research suggests it may also disrupt biological regulatory systems and increase the risk of long‐term physical health problems. This article presents a theoretical framework of the process by which the experience of parental death during childhood may influence mental and physical health outcomes over time. Drawing from a broad literature on adaptation following childhood parental loss, we focus on risk and protective factors in the childhood environment that are theoretically and empirically linked to emotional and biological regulatory responses to stress later in life, the effects of which may accumulate to impact long‐term health.     

Network structure reveals clusters of associations between childhood adversities and development outcomes

Exposure to childhood adversity is common and associated with a host of negative developmental outcomes. The most common approach used to examine the consequences of adversity exposure is a cumulative risk model. Recently, we have proposed a novel approach, the dimensional model of adversity and psychopathology (DMAP), where different dimensions of adversity are hypothesized to impact health and well‐being through different pathways. We expect deprivation to primarily disrupt cognitive processing, whereas we expect threat to primarily alter emotional reactivity and automatic regulation. Recent hypothesis‐driven approaches provide support for these differential associations of deprivation and threat on developmental outcomes. However, it is not clear whether these patterns would emerge using data‐driven approaches. Here we use a network analytic approach to identify clusters of related adversity exposures and outcomes in an initial study (Study 1: N = 277 adolescents aged 16–17 years; 55.1% female) and a replication (Study 2: N = 262 children aged 8–16 years; 45.4% female). We statistically compare our observed clusters with our hypothesized DMAP model and a clustering we hypothesize would be the result of a cumulative stress model. In both samples we observed a network structure consistent with the DMAP model and statistically different than the hypothesized cumulative stress model. Future work seeking to identify in the pathways through which adversity impacts development should consider multiple dimensions of adversity.     

How our work influences who we are: Testing a theory of vocational and personality development over fifty years

This study examines the developmental influences of occupational environments on personality traits from childhood to adulthood. We test aspects of a theory of vocational and personality development, proposing that traits develop in response to work experience following corresponsive and noncorresponsive mechanisms. We describe these pathways in the context of situations of vocational gravitation and inhabitation. In a sample from the Hawaii personality and health cohort (N = 596), we examined associations of childhood and adulthood personality traits, with occupational environments profiled on the RIASEC model. Mediations tests confirmed that work influenced personality development from childhood to adulthood for Openness/Intellect. We observed multiple reactivity effects of occupation environments on adulthood traits that were not associated with corresponding selection effects.     

Whatever does not kill us: cumulative lifetime adversity, vulnerability, and resilience

Exposure to adverse life events typically predicts subsequent negative effects on mental health and well-being, such that more adversity predicts worse outcomes. However, adverse experiences may also foster subsequent resilience, with resulting advantages for mental health and well-being. In a multiyear longitudinal study of a national sample, people with a history of some lifetime adversity reported better mental health and well-being outcomes than not only people with a high history of adversity but also than people with no history of adversity. Specifically, U-shaped quadratic relationships indicated that a history of some but nonzero lifetime adversity predicted relatively lower global distress, lower self-rated functional impairment, fewer posttraumatic stress symptoms, and higher life satisfaction over time. Furthermore, people with some prior lifetime adversity were the least affected by recent adverse events. These results suggest that, in moderation, whatever does not kill us may indeed make us stronger.     

创伤后心理复原的生理机制

心理复原是个体在经历对生命具有威胁的事件或严重的创伤后仍然能回复到良好适应状况的现象。对心理复原生理机制的研究存在两种研究取向：或从个人能力的角度,或从发展结果的角度。创伤记忆的抑制、大脑的可塑性、神经生物的调节以及基因、气质、情绪调节、认知过程、早期经验等保护因子的影响机制是研究的主要内容。文章最后对今后的研究进行了展望     

Infant Parasympathetic and Sympathetic Activity during Baseline,Stress and Recovery: Interactions with Prenatal Adversity Predict Physical Aggression in Toddlerhood

Exposure to prenatal adversity is associated with aggression later in life. Individual differences in autonomic nervous system (ANS) functioning, specifically nonreciprocal activation of the parasympathetic (PNS) and sympathetic (SNS) nervous systems, increase susceptibility to aggression, especially in the context of adversity. Previous work examining interactions between early adversity and ANS functioning in infancy is scarce and has not examined interaction between PNS and SNS. This study examined whether the PNS and SNS moderate the relation between cumulative prenatal risk and early physical aggression in 124 children (57% male). Cumulative risk (e.g., maternal psychiatric disorder, substance (ab)use, and social adversity) was assessed during pregnancy. Parasympathetic respiratory sinus arrhythmia (RSA) and sympathetic pre-ejection period (PEP) at baseline, in response to and during recovery from emotional challenge were measured at 6 months. Physical aggression and non-physical aggression/oppositional behavior were measured at 30 months. The results showed that cumulative prenatal risk predicted elevated physical aggression and non-physical aggression/oppositional behavior in toddlerhood; however, the effects on physical aggression were moderated by PNS and SNS functioning. Specifically, the effects of cumulative risk on physical aggression were particularly evident in children characterized by low baseline PNS activity and/or by nonreciprocal activity of the PNS and SNS, characterized by decreased activity (i.e., coinhibition) or increased activity (i.e., coactivation) of both systems at baseline and/or in response to emotional challenge. These findings extend our understanding of the interaction between perinatal risk and infant ANS functioning on developmental outcome.     

Telomeres in a Life-Span Perspective: A New "Psychobiomarker"?

ABSTRACT— In order to more fully understand associations between psychological stress and health, it is helpful for researchers to identify "psychobiomarkers," or biological measures that are regulated in part by psychological function and that predict longevity. Telomere length appears to be such a measure. Telomeres, the protective caps at the tips of chromosomes, shorten with age, and this shortening predicts disease and longevity. Leukocyte telomere length may be best viewed through a life-span approach, as it reflects in part the cumulative number of cell divisions that have occurred and the long-term biochemical environment. Recently, a critical mass of studies demonstrated that telomeres appear to shorten with chronic stress, although the mechanisms are unknown. This paper reviews what appear to be malleable determinants of rate of telomere attrition, focusing on early life chronic stressors and metabolic adversity (poor nutrition during development, and obesity). The next generation of research will benefit from experimental and longitudinal models integrating genetic variation, social environments, life experience, and health behaviors.     

Child development in the context of adversity: experiential canalization of brain and behavior

The authors examine the effects of poverty-related adversity on child development, drawing upon psychobiological principles of experiential canalization and the biological embedding of experience. They integrate findings from research on stress physiology, neurocognitive function, and self-regulation to consider adaptive processes in response to adversity as an aspect of children's development. Recent research on early caregiving is paired with research in prevention science to provide a reorientation of thinking about the ways in which psychosocial and economic adversity are related to continuity in human development.     

Depression and stress: a biopsychosocial exploration of evolved functions and mechanisms

Depression is a common and debilitating disorder linked to social adversity and stress. There have been many theories suggesting possible evolved functions of depression but few have explored evolved defensive mechanisms for coping with stressful events and how these maybe compromised in human depression. This paper will review some of the current evolutionary theories of depression and explore how major depression can arise when evolved defences to cope with adversity (e.g., fight, flight, disengage, submit and help-seeking) are aroused but blocked, arrested or ineffective. Psychosocial stressors can be seen as both activating,but also as arresting, evolved stress-coping defences leading to chronic states of stress with physiological effects on mood. This paper is set in the context of an evolution informed biopsychosocial approach.     

A systems view of psychological trauma: Developing post-traumatic stress response paradigms

This article traces the development of traumatic stress paradigms within the context of emerging psychological and organizational theories. It traces the evolution of the systems view of trauma from an early stimulus-response model using a biological perspective through the development of cybernetic, information-processing to the field systems perspectives of trauma. This article concludes by examining the evolutionary and contextualist paradigms of trauma theory and its value to the psychotherapist working with trauma victims.