Stress, Early Brain Development, and Behavior (original) (raw)
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Stress physiology and developmental psychopathology: Past, present, and future
Research on the hypothalamic–pituitary–adrenocortical (HPA) axis has emerged as a vital area within the field of developmental psychopathology in the past 25 years. Extensive animal research has provided knowledge of the substrates and physiological mechanisms that guide development of stress reactivity and regulation using methods that are not feasible in humans. Recent advances in understanding the anatomy and physiology of the HPA axis in humans and its interactions with other stress-mediating systems, including accurate assessment of salivary cortisol, more sophisticated neuroimaging methods, and a variety of genetic analyses, have led to greater knowledge of how psychological and biological processes impact functioning. A growing body of research on HPA axis regulation and reactivity in relation to psychopathology has drawn increased focus on the prenatal period, infancy, and the pubertal transition as potentially sensitive periods of stress system development in children. Theories such as the allostatic load model have guided research by integrating multiple physiological systems and mechanisms by which stress can affect mental and physical health. However, almost none of the prominent theoretical models in stress physiology are truly developmental, and future work must incorporate how systems interact with the environment across the life span in normal and atypical development. Our theoretical advancement will depend on our ability to integrate biological and psychological models. Researchers are increasingly realizing the importance of communication across disciplinary boundaries in order to understand how experiences influence neurobehavioral development. It is important that knowledge gained over the past 25 years has been translated to prevention and treatment interventions, and we look forward to the dissemination of interventions that promote recovery from adversity.
Development and Psychopathology, 2014
Despite widespread recognition that the physiological systems underlying stress reactivity are well coordinated at a neurobiological level, surprisingly little empirical attention has been given to delineating precisely how the systems actually interact with one another when confronted with stress. We examined crosssystem response proclivities in anticipation of and following standardized laboratory challenges in 664 4-to 14-year-olds from four independent studies. In each study, measures of stress reactivity within both the locus coeruleus-norepinephrine system (i.e., the sympathetic and parasympathetic branches of the autonomic nervous system) and the corticotrophin releasing hormone system (i.e., the hypothalamic-pituitary-adrenal axis) were collected. Latent profile analyses revealed six distinctive patterns that recurred across the samples: moderate reactivity (average cross-system activation; 52%-80% of children across samples), parasympathetic-specific reactivity (2%-36%), anticipatory arousal (4%-9%), multisystem reactivity (7%-14%), hypothalamic-pituitary-adrenal axis specific reactivity (6%-7%), and underarousal (0%-2%). Groups meaningfully differed in socioeconomic status, family adversity, and age. Results highlight the sample-level reliability of children's neuroendocrine responses to stress and suggest important cross-system regularities that are linked to development and prior experiences and may have implications for subsequent physical and mental morbidity.
Paediatric stress: from neuroendocrinology to contemporary disorders
European Journal of Clinical Investigation, 2017
Background Stress is defined as a state of threatened or perceived as threatened homeostasis. A broad spectrum of extrinsic or intrinsic, real or perceived stressful stimuli, called 'stressors', activates a highly conserved system, the 'stress system', which adjusts homeostasis through central and peripheral neuroendocrine responses. Inadequate, excessive or prolonged adaptive responses to stress may underlie the pathogenesis of several disease states prevalent in modern societies. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors and the timing of the stressful event(s), given that prenatal life, infancy, childhood and adolescence are critical periods characterized by increased vulnerability to stressors. Materials and methods We conducted a systematic review of original articles and reviews published in MEDLINE from 1975 through June 2016. The search terms were 'childhood stress', 'pediatric stress', 'stress and disorders' and 'stress management'. Results In this review, we discuss the historical and neuroendocrine aspects of stress, and we present representative examples of paediatric stress system disorders, such as early-life adversity, obesity and bullying. We also discuss the adverse impact of a socioeconomic crisis on childhood health. The tremendous progress of epigenetics has enabled us to have a deeper understanding of the molecular mechanisms underlying paediatric stress-related disorders. Conclusions The need for early successful stress management techniques to decrease the incidence of paediatric stress-related diseases, as well as to prevent the development of several pathologic conditions in adolescence and adulthood, is imperative.
Stress and development: Behavioral and biological consequences
Development and Psychopathology, 2001
Childhood abuse is an important public health problem; however, little is known about the effects of abuse on the brain and neurobiological development. This article reviews the behavioral and biological consequences of childhood abuse and places them in a developmental context. Animal studies show that both positive and negative events early in life can influence neurobiological development in unique ways. Early stressors such as maternal separation result in lasting effects on stress-responsive neurobiological systems, including the hypothalamic-pituitary-adrenal (HPA) axis and noradrenergic systems. These studies also implicate a brain area involved in learning and memory, the hippocampus, in the long-term consequences of early stress. Clinical studies of patients with a history of abuse also implicate dysfunction in the HPA axis and the noradrenergic and hippocampal systems; however, there are multiple questions related to chronicity of stress, developmental epoch at the time of the stressor, presence of stress-related psychiatric disorders including posttraumatic stress disorder and depression, and psychological factors mediating the response to trauma that need to be addressed in this field of research. Understanding the effects of abuse on the development of the brain and neurobiology will nevertheless have important treatment and policy implications.
Pediatric Stress: From Neuroendocrinology to Contemporary Disorders
European journal of clinical investigation, 2017
Stress is defined as a state of threatened or perceived as threatened homeostasis. A broad spectrum of extrinsic or intrinsic, real or perceived stressful stimuli, called "stressors", activates a highly conserved system, the "stress system", which adjusts homeostasis through central and peripheral neuroendocrine responses. Inadequate, excessive or prolonged adaptive responses to stress may underlie the pathogenesis of several disease states prevalent in modern societies. The development and severity of these conditions primarily depend on the genetic vulnerability of the individual, the exposure to adverse environmental factors and the timing of the stressful event(s), given that prenatal life, infancy, childhood and adolescence are critical periods characterized by increased vulnerability to stressors. We conducted a systematic review of original articles and reviews published in MEDLINE from 1975 through June 2016. The search terms were "childhood stress&q...
Ontogeny of Stress Reactivity in the Human Child: Phenotypic Flexibility, Trade-Offs, and Pathology
Adaptive and Maladaptive Aspects of Developmental Stress, 2012
We humans are highly sensitive to our social environments. Our brains have special abilities such as empathy and social foresight that allow us to understand each other's feelings and communicate in ways that are unique among all living organisms. Our extraordinary social minds, however, come with some significant strings attached. Our emotional states can be strongly infl uenced by what others say and do. Our hearts can soar, but they also can be broken. Our bodies use internal chemical messengers-hormones and neurotransmitters-to help guide responses to our social worlds. From romantic daydreams to jealous rage, from orgasm to lactation and parent-child bonding, the powerful molecules produced and released by tiny and otherwise seemingly insignifi cant cells and glands help orchestrate our thoughts and actions. Understanding this chemical language is important for many research questions in human health. Here we focus on the question of why social relationships can affect health-why it is that words can hurt children. Stress hormones appear to play important roles in this puzzle. The hypothalamic-pituitary-adrenal axis (HPAA) is highly responsive to traumatic experiences including social challenges. For the past 23 years we have conducted a fi eld study of child stress and family environment in a rural community in Dominica. The primary objective is to document hormonal responses of children to
Psychoneuroendocrinology, 2009
Early life stress (ELS) is expected to increase reactivity of the hypothalamic-pituitary-adrenocortical (HPA) axis; however, several recent studies have shown diminished cortisol reactivity among adults and children with ELS exposure. The goal of this study was to examine cortisol activity in 10-12year-old internationally adopted children to determine if moderate and severe ELS have different impacts on the HPA axis. Salivary cortisol and two measures of autonomic activity were collected in response to the Trier Social Stress Test for Children (TSST-C). Three groups reflecting moderate, severe, and little ELS were studied: early adopted children who came predominantly from foster care overseas (early adopted/foster care (EA/FC), n = 44), later adopted children cared for predominantly in orphanages overseas (late adopted/post-institutionalized (LA/PI), n = 42) and non-adopted (NA) children reared continuously by their middle-to upper-income parents in the United States (n = 38). Diminished cortisol activity was noted for the EA/FC group (moderate ELS), while the LA/PI group (severe ELS) did not differ from the NA group. Overall, few children showed cortisol elevations to the TSST-C in any group. The presence/absence of severe growth delay at adoption proved to be a critical predictive factor in cortisol activity. Regardless of growth delay, however, LA/PI children exhibited higher sympathetic tone than did NA children. These results suggest that moderate ELS is associated with diminished cortisol activity; however, marked individual differences in cortisol activity among the LA/PI children suggest that child factors modify the impact of severe ELS. Lack of effects of severe ELS even for growth delayed children may reflect the restorative effects of adoption or the generally low responsiveness of this age group to the TSST-C.
Factors promoting vulnerability to dysregulated stress reactivity and stress‐related disease
Journal of Neuroendocrinology, 2018
Effective coordination of the biological stress response is integral for the behavioral well-being of an organism. Stress reactivity is coordinated by an interplay of the neuroendocrine system and the sympathetic nervous system. The hypothalamus-pituitary-adrenal (HPA) axis plays a key role in orchestrating bodily responses to stress, and activity of the axis can be modified by a wide range of experiential events. This review will focus on several factors that influence subsequent HPA axis reactivity. Some of these factors include early life adversity, exposure to chronic stress, immune activation, and traumatic brain injury. The central premise is that each of these experiences serve as general vulnerability factors that accelerate future HPA axis reactivity in ways that make individuals more sensitive to stress challenges, and therefore feed forward into exacerbation of ongoing, or greater susceptibility toward, future stress-related disease states, especially as they pertain to negative affect and overall brain health.
Brain Research Bulletin, 2006
Recent evidence support the hypothesis that exposure to stress or trauma during early childhood may disturb the formation of functional brain pathways, in particular, of the limbic circuits. We examined the effects of exposure to early life trauma (juvenile stress) on emotional and cognitive aspects of behavior in adulthood as well as on dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) levels in relevant brain regions. Quantitative assessment of the effects of exposure to juvenile stress was made 1 month post-stress, and obtained by measuring: emotional (utilizing an open field and a startle response tests) and cognitive (Morris water-maze task) functions, as well as neurosteroids concentration (DHEA and its sulfate ester, DHEAS) in the hypothalamus and entorhinal cortex. We report here that an exposure to juvenile stress led to elevated levels of anxiety 1 month post-stress. Moreover, in a spatial learning task, the juvenile stress group performed poorer than the control group. Finally, an exposure to juvenile stress increased DHEAS but not DHEA concentrations both in the hypothalamus and the entorhinal cortex. These findings indicate that an exposure to juvenile stress has long-lasting effects on behavior and DHEAS levels in the hypothalamus and the entorhinal cortex. These effects may be of relevance to our understanding of early life stress-related disorders such as PTSD and major depression.