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This chapter presents an interdisciplinary study on the effect of parental care on the psychology and biology of offspring. The research program, conducted with rodents, provides a detailed model of how early environmental influences can induce profound changes in the biology of the offspring at the level of gene expression. These changes in gene expression then have a cascading effect and alter the physiology of the offspring in ways that are enduring, probably lifelong.

This chapter focuses on the role children's physiological stress responses play in memory. It begins with a brief discussion of the rationale underlying the need to consider physiological stress responses when studying children's memory for emotional, primarily stressful, experiences. It then provides an overview of existing research that has included general measures of physiological arousal (i.e., heart rate), followed by a review of the biological systems that respond to stressful events and how arousal as driven by each of these specific systems may affect children's memory. The chapter concludes with a discussion of the need to consider developmental factors concurrent with physiological stress responses when studying children's memory for stressful events.

This chapter describes a dual-process model of responses to stress as a framework for understanding stress, coping, and memory. The model includes both automatic and controlled responses to stress that involve engagement with or disengagement from sources of stress and one's emotions. Controlled responses to stress, which are equated with the concept of coping, are considered within the broader cognitive processes of executive functions and memory. Two examples from research on children and adults with cancer are used to show the diverse relations among these processes—the relations between controlled, working memory processes and coping, and the interplay between disengagement coping and intrusive, automatic memories. Finally, directions for future research on the role of memory in coping with stress are outlined.

This chapter provides an overview of the long-term effects of early stress on the subsequent development of both physical and mental disorder. It then discusses the role of maternal care during pre- and postnatal periods as an early source of these effects, using research conducted in the laboratory with the rat. The chapter then reviews potential mediators of the effects of maternal behavior on gene expression. The chapter concludes with the questions that remain regarding the effects of early stress on pathology.

This chapter provides an overview of the brain's stress response system (the hypothalamic-pituitary-adrenal axis or HPA) and how early stressors can influence this system as the child develops. It reviews research suggesting that adverse effects on the stress response system produced by neglectful parenting can be reversed by subsequent more responsive care.

This chapter discusses how and why short-term changes in physiological state (i.e., the acute stress response) alter immune responsiveness in insects. It also explores the ramifications of these effects for ecological immunologists.

This chapter discusses the adverse effects of prenatal ethanol exposure on neuroendocrine and immune function, with particular emphasis on the concept of fetal programming in the hypothalamic-pituitary-adrenal (HPA) axis, a key player in the stress response. The HPA axis is highly susceptible to programming during fetal and neonatal development. Early environmental experiences, including exposure to ethanol, can reprogram to HPA axis such that HPA tone is increased throughout life. The chapter presents data showing that gestational ethanol exposure increases HPA activity in both the pregnant female and the offspring. Increased exposure to endogenous glucocorticoids over the lifespan can alter behavioral and physiological responsiveness and predispose the organism to the development of certain diseases later in life.

This chapter considers the relationships of stress to offensive and defensive aggression. It argues that stress defined in terms of hypothalamic-pituitary-adrenal (HPA) axis activity is relatively uninformative with reference to either the antecedents or the consequences of aggression. Stress defined in terms of threat is also insufficiently specific for understanding the two types of aggression. The incidence and specific elicitors of offensive aggression may be very different for mammalian species, depending on their social and physical environments. The prevalence of defensive threat/attack and their position in the defense pattern also change systematically with group social structure, environmental constraints, and the size and defensive capabilities of the animal relative to major predators for each species.

This chapter examines stress models in the rat using the biology of the rat and its natural defense mechanisms as a starting point. It focuses on tests that explore the capacity of rats to cope with ecologically relevant problems. Stress models challenge the natural defense mechanisms and hence call on the adaptive capacity of the animal. However, rather than pushing the animal toward a stress physiological ceiling, it might be far more informative to explore the natural factors that determine and modulate the individual adaptive capacity. These factors include not only perinatal and adult (social) experience but also factors that affect the speed of recovery after a stressor.

If we are to solve the multiple crises facing human service delivery we need a different way of understanding human nature and human dysfunction, one that incorporates 150 years of accumulated scientific knowledge and clinical wisdom. To understand what we are going to “diagnose” and “prescribe” for our troubled social service and mental health organizations, people need to have a working knowledge about the psychobiology of trauma and adversity, what it does to individuals, particularly when trauma is repetitive, occurs in early development, and is a result of interpersonal violence. Using a computer metaphor, this chapter discusses how attachment is the “operating system” for people, the master program that allows other human functions to work. Trauma disrupts attachment and like a computer virus, wrecks havoc in unpredictable ways, with the total life experience of the person involved. Creating trauma-informed cultures requires radical change in thinking, behavior, and attitudes.

Obesity, which is rising in affluent societies, is bad for health, expensive to treat and stigmatising. Its prevalence is higher in market-liberal societies than in those with a more extensive welfare state. This book explores the hypothesis that obesity is a response to stress, and that market-liberal societies are more stressful due to the greater intensity of economic and social competition, and to lower levels of social protection.

This chapter examines how environmental stressors lead to essential hypertension via the acute stress response. It focuses on research examining the physiological responses of heart rate and blood pressure reactions to stress. The chapter examines the measurement of acute stress responses such as anxiety and anger in response to standard environmental stressors or during daily life. Finally, behavioral lifestyle factors and interpersonal behaviors associated with risk for high blood pressure are also considered.

This chapter discusses various signal transduction pathways involved in the stress response, including stress-activated protein kinase signalling, heat shock protein induction, oxidative stress defence, metallothionein, and the mixed-function oxygenase system. It examines the key genes of these stress defence pathways, as well as the transcription factors regulating their expression (Mns2p, Mns4p, HSF, Nrf2, MTF-1, AhR, HIF 1α). These systems provide a basis for understanding genome-wide responses to stress. Examples are given for plant responses to drought, cold, and salt; abiotic stress responses in animals; and plant defence against herbivory. Studies show that a considerable part of the genome may be involved in temporary stress defence, and that there are both similarities and differences in the responses to different stress factors. A specific set of genes appears to be activated by nearly all stress factors, which leads to the definition of a ‘universal minimal stress proteome’. Finally, the chapter turns to the genomics of the innate animal immune system, as well as defence responses to heavy metals, pesticides, and endocrine disrupters. Genome-wide stress responses are particularly important in environmental physiology, since gene expression profiles are specific to the type of stress and may harbour important information for ecological risk assessment.

This chapter synthesizes the empirical evidence for reptiles on how environmental stresses can induce molecular stress pathways. In an evolutionary framework, it describes how these pathways can respond to natural selective forces to shape reproduction and aging. The chapter focuses on molecular pathways, including gene networks and DNA repair, enzyme and hormonal regulation, mitochondrial and cell function, that are induced by the stresses found in the natural environment: thermal, oxidative, caloric (prey abundance), predators/predation, social (mating systems), and immunological. Finally, it proposes areas of research that should be the focus of future studies to elucidate further the evolution of molecular mechanisms which determine life history traits in reptiles.

Organizations are living complex systems and as such are vulnerable to the impact of trauma and adversity. This chapter explores how groups respond to stress and suggests that as a result of acute and chronic organizational stress, destructive processes occur within and between organizations that mirror or “parallel” the processes for which clients seek help. The result for them is “sanctuary trauma”, while the result for providers of service is a collective maladjustments as the organizations within which we work cease fulfilling a fundamental social role, that of containing anxiety in the face of death, suffering, defeat, and uncertainty. In such cases, social defense mechanisms come to dominate whatever therapeutic activity is supposed to be occurring in the social service environment. However, these parallel processes can be named and understood within the context of present knowledge of individual and group psychology.

Chapter 3 describes infant brain development, the structures of the brain and the functions of brain regions, especially the limbic system and the orbitofrontal cortex. The brain’s response to stress and the developing stress response system of the young child is explained. Recent research on the neurobiological impact of trauma in infancy and its impact on the development of risk for psychopathology in childhood, adolescence, and adulthood is summarized for the reader. The chapter includes research on maltreatment and its relationship to the development of memory, affect regulation, and cognition in the first months and years.

This chapter presents three different models for how to think about stress. This is an exciting time for stress research. Until quite recently, the traditional model provided the only way to place empirical data into a theoretical context. The traditional model provided some help, but its many weaknesses, especially when applied to wild free-living animals, slowed progress considerably. An especially glaring weakness was the poor help the traditional model provided in generating testable predictions about what stimuli would be stressors to wild animals, what their stress responses would be, and how those stress responses would help wild animals survive in their natural habitats. The lack of testable predictions was especially problematic with the recent focus on anthropogenic stressors and their potential to cause chronic stress and conservation problems. This chapter discusses the traditional model and then presents allostasis and reactive scope, alternative models for stress that incorporate concepts from ecology.

This chapter explores avenues for future research in the area of religion, spirituality and psychoneuroimmunology. Recommendations are made based in part on a recent conference at Duke University Medical Center that brought together the world's leading experts in psychoneuroimmunology to discuss the future of research on religion and immune function. This chapter describes what went on during that conference and then discusses areas of research that conference participants and chapter authors felt should have the highest priority. Because the immune response is part of the “stress response”, one recurring theme was the need to study spirituality or religion as a potential moderator of the stress response in situations of high stress. This could include populations at risk for negative outcome from stress, such as Scandinavians at high risk for suicide or Irish Catholics at high risk for alcoholism. Other specific health effects might be studied as well, such as wound healing, responses to viral illness, or immune responses following administration of vaccines.

Chapter 7 considers stress as a modulator of adolescent development. It starts with an overview of the key hormones in the hypothalamic–pituitary–adrenal (HPA) axis and describes responses of the HPA axis and the sympathetic nervous system to stress. The HPA stress response is somewhat different in adolescents compared with adults; adolescents often show heightened stress reactivity and a protracted recovery period after psychological stressors compared to adults. The chapter then reviews research on chronic stress-induced anatomical and functional changes in the hippocampus, prefrontal cortex, and amygdala, three brain regions involved in regulation of the HPA axis and modulation of stress responses. Stress-induced changes in these brain regions include dendritic complexity of pyramidal cells, attenuated long-term potentiation, attention deficits, and changes in fear and depressive-like behaviors; these changes may be long-lasting. The perfect storm alludes to the alignment of three features of adolescence that together may render the adolescent brain especially vulnerable to effects of chronic stress: (a) The quality and quantity of stressors is different during adolescence than in adulthood; (b) stress reactivity is higher during adolescence; and (c) the hippocampus, prefrontal cortex, and amygdala are sensitive to stress hormones and are still developing during adolescence. However, the developing adolescent brain may be more resilient to insult, more responsive to interventions, and more buffered by social support systems.

Taking an ecological approach, the stress response is highly adaptive, allowing organisms to respond to stressful events with the emergency life-history stage (ELHS). This complex life-history stage serves to redirect an individual from its normal life cycle into an emergency coping mode, promoting survival in the best condition possible. After the perturbation passes, the normal life cycle can be resumed. This chapter disusses how the primary mediators of the stress response, especially the corticosteroids and catecholamines, help orchestrate the ELHS. The ELHS has four distinct components: the fight-or-flight response (to sudden threatening events such as an attack by a predator), reactive/proactive coping strategies (especially in response to social stress), preparations of the immune system for potential injury and infection, and facultative behavioral and physiological responses that potentiate avoidance of chronic stress.