Stress And Child Development Research Paper

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Stressors that threaten well-being activate physiological systems that, while fostering immediate survival, can interfere with repair of the body, defense against illness, and development. Two systems play major roles in stress: the sympathetic adrenomedullary (SAM) system that produces adrenaline and other catecholamines, and the limbic–hypothalamic–pituitary–adrenocortical (LHPA) system that produces the steroid hormone cortisol in humans. Of these two systems, the LHPA system exerts slower, more persistent actions, and is often the focus of research on stress physiology. A growing literature indicates that conditions associated with stress, maltreatment and neglect during fetal and early development alter regulation of the LHPA system in ways that could heighten vulnerability later to stress-related disorders. During early life, individual differences in temperament interact with qualities of the caregiving environment to predict cortisol responses to psychosocial stressors. Combined, these growing literatures on normal and atypical development promise to explicate mechanisms through which early experiences affect physical and psychological health.

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1. Psychobiology Of The LHPA System

Animal studies constitute the bulk of research on this system. Determining their implications for human development is a major challenge. Current perspectives drawn from the animal research will be presented in this section.

Cortisol is the end product of a cascade of events that begins with stimulation of cells in an area of the brain called the hypothalamus. These cells secrete peptide hormones (CRH and AVP) that, in turn, cause cells in the pituitary gland (once thought of as the master endocrine gland) to produce yet another biochemical, ACTH. ACTH is secreted into the bloodstream where it is picked up by receptors on the cortex of the adrenal glands, stimulating the adrenal to secrete cortisol (Johnson et al. 1992). Humans produce cortisol even when they are not stressed. No stressed or basal cortisol production follows a daily rhythm. Like a thermostat, basal levels are maintained through negative feedback loops; the primary feedback sites are located in two areas of the brain, called the hypothalamus and hippocampus. Through multiple pathways in the brain, internal and external threats to well-being cause increased activity in this LHPA system that raise cortisol levels over baseline (de Kloet 1991). Responses to psychological stressors operate through pathways involving an area of the brain called the amygdala that also plays important roles in organizing behavioral reactions to threat. CRH, the peptide that begins the cascade of events that stimulates cortisol production, is produced in many brain areas, including sites such as the amygdala, where it is believed to play a major role in regulating threat reactive behavior and in stimulating both the LHPA and the SAM systems to react to psychological stressors. One major theory relating stress to depression focuses on repeated stressors and the orchestrating role of extra-hypothalamic CRH (Nemeroff 1996). The cumulative impact of stressors on health has been described as allostatic load, or the health impairing costs of survival-facilitating activity of the LHPA system (McEwen 1998).

Understanding how the LHPA system promotes both health and disease is a core problem in stress research. Both hypo and hyper-responsivity of the LHPA system are associated with disorder (de Kloet et al. 1998). Disorders of hypo-responsivity include those related to failure to contain immune inflammatory responses and to maintain the responsivity of areas of the brain involved in emotions and information processing; hyper-responsivity disorders include those related to immune suppression, cardiovascular disease, and affective psychopathology. One line of reasoning traces these contrasting impacts through the two types of receptors for cortisol that mediate two modes of the hormone’s effects (de Kloet et al. 1998). The first, a ‘proactive’ or ‘permissive’ mode, maintains basal activity of the system, regulates the threshold of the system’s response to stressors, promotes coordination of the daily rhythm in the hormone, and helps maintain the viability of brain systems involved in selective attention, sensory integration, and response selection. Low levels of circulating cortisol affect this mode through stimulating MR or Type I receptors in the central nervous system. The second, a ‘reactive’ or ‘suppressive’ mode, operates through GR or Type II receptors that mediate highly catabolic events promoting increases in energy availability, modulation of the immune system, and threat-related learning. GRs are occupied increasingly as cortisol rises above basal levels into stress ranges. Both proactive and reactive modes support health and survival. However, the reactive mode, if sustained, threatens health. In the hypothalamus and hippocampus, occupation of GR or Type II receptors also terminates the stress response, serving as a brake on the duration of the reactive/suppressive stress mode. In animals, early experiences appear to alter the balance of MRs/GRs, lowering the level of hormone at which the system shifts from proactive to reactive functioning and allowing the reactive, suppressive mode to continue for longer periods before cortisol returns to basal levels.

A recent line of developmentally relevant research focuses on mechanisms relating the LHPA system to systems involved in growth and development of the brain and body. Of particular note are studies examining the interaction of glucocorticoids, MR/GR balance and serotonin (5-HT) receptor activity in the hippocampus (Lopez et al. 1998), and studies examining the interaction of glucocorticoids, growth hormone, and insulin growth factors (e.g., IGF-1) (Johnson et al. 1992). In animals, conditions that elevate glucocorticoids chronically also increase basal glucocorticoid levels, affect MR GR ratios, and lower serotonin activity in the hippocampus. These conditions include stress during pre-and postnatal development. These changes are associated with heightened vulnerability to stressors later in life, as well as problems with behavior regulation, response inhibition, and sensitivity to self-administration of drugs of abuse (de Kloet et al. 1998). Critically, again in animals, conditions associated with responsive caregiving during postnatal development reduce the impact of prenatal stress and buffer the impact of postnatal stressors (Caldji et al. 1998, Levine 1994).

2. Studies In Infants And Young Children

2.1 Measurement Issues

Research in children has been stimulated by the development of cortisol assays that use samples of free-flowing saliva (Kirschbaum and Hellhammer 1994). Unfortunately, salivary sampling does not allow the assessment of activity higher in the system (i.e., at the pituitary and brain levels). Blood sampling is needed to assess ACTH concentrations, and a spinal tap is typically needed to measure CRH. Particular drugs are usually given to probe the physiology of the LHPA system in ways that bypass individual differences in how the person perceives and interprets events. Because of their invasiveness, none of these techniques is used typically with normally developing children.

In addition, the researcher who studies the LHPA system must attend to many confounding variables that constrain how studies can be conducted. Because of the daily rhythm in the hormones, all samples must be conducted at the same time of day. Careful attention needs to be given to the child’s health, what he or she has eaten and drunk recently, and the familiarity of the context (Kirschbaum and Hellhammer 1994). These constraints have limited the study of this system in children. Despite this, a literature is developing which promises to inform our understanding of early risks for later physical and emotional pathology.

2.2 Developmental Changes In Responsivity

Prenatally, the LHPA system produces cortisol by the beginning of the second trimester. In animals, the mother’s cortisol affects the fetus, resulting in the development of fewer MRs and larger LHPA responses to stressors (Barbazanges et al. 1996). In humans, fetal vulnerability (low birth weight, prematurity) increases with increased maternal psychosocial stress and LHPA activity (Sandman et al. 1997).

The full-term neonate exhibits robust, graded elevations in cortisol that sensitize to repeated pain-eliciting events (e.g., heel lances) and habituates to repeated handling stressors (e.g., physical examinations) (Gunnar 1992). Responsiveness to handling stressors appears to decrease at around 3 months of age, after which stressors such as physical examinations fail to provoke elevations in cortisol for most infants. An- other marked decrease in cortisol responsivity is observed between 6 and 12 months of age, after which during infancy it becomes difficult to provoke elevations in cortisol, on average, to many mild stressors (Gunnar 2000).

2.3 Relationships As Regulators Of The HPA System

By 6–12 months, social interactions with caregivers mediate cortisol responses. Thus, brief maternal separations fail to elevate cortisol if substitute caregivers are sensitive and responsive, while elevations are noted when substitute caregivers are not (Gunnar 2000). Similarly, the availability of the parent in secure attachment relationships buffers elevations in cortisol to events that elicit wariness and behavioral distress, while elevations are noted for toddlers exhibiting similar wariness distress if the attachment relationship is insecure (Spangler and Schieche 1998). Elevations in cortisol have also been noted for toddlers with the type of disorganized disoriented attachment more typically noted among infants of depressed and/or abusive parents. Higher home baseline levels of cortisol have also been reported among 3-year-olds whose mothers were clinically depressed during the child’s first year of life. These data are consistent with the literature in animals cited above relating maternal care to stress reactivity and regulation.

Social relations with peers are potent stimuli of the LHPA system in human adults and animals (Kirschbaum and Hellhammer 1994). For children, this appears true at least as early as the preschool years. For toddlers and preschoolers, childcare involving long hours of interaction with like-aged playmates produces elevations in cortisol for many children (Dettling et al. 1999). Even short periods of interaction in half-day preschool programs may elevate cortisol for some children. Children who show activation of the LHPA system in peer settings are those with problematic peer relations; peer rejection, low dominance status, and social withdrawal tend to characterize these children. Problematic styles of interacting (e.g., anger, aggression, and poor selfcontrol) that foster peer rejection also correlate with higher and more responsive patterns of cortisol production in preschool peer groups (Gunnar et al. 1997).

3. Temperament

Both extreme shyness and problems in effortful control have been associated with LHPA system activity in young children. Extreme shyness has been hypothesized to reflect altered thresholds for activation of stress physiology involving central fear circuits in the brain (i.e., amygdala–bed nucleus pathways). Thus, increased responsiveness of the LHPA system has long been hypothesized for extremely shy, socially anxious children (Kagan et al. 1987). Strong evidence for this hypothesis is largely lacking when children are assessed under conditions of social challenge (Gunnar et al. 1997); however, shyness, whether measured by teacher report or direct observation, has been found to correlate positively with cortisol sampled at home (de Haan et al. 1998). It is not clear why cortisol correlates more readily with shyness when home hormone concentrations are examined. It may be that under conditions of challenge, moderating factors such as coping strategies and social support need to be taken into account, while home levels are more reflective of tonic influences.

Rothbart has identified effortful control as a higherorder dimension of temperament that emerges from factor analyses of temperament questionnaires during the preschool years. Attention focusing and the capacity to inhibit prepotent responses form the core of this dimension, which Posner and Rothbart (1994) argue reflects the development of an attentional network involving the anterior cingulate gyrus which in animals also plays a role in containing the cortisol stress response (Diorio et al. 1993). In children, effortful control modifies relations between negative emotionality and behavior (Eisenberg et al. 1994). In preschool-aged children, parent and teacher reports of effortful control tend to be negatively correlated with cortisol levels and measures of cortisol responsivity in classroom settings (Gunnar et al. 1997). Whether these correlations reflect mechanisms linking the LHPA system to the neurobiology of effortful control or the impact of effortful control on the behaviors that create stressful social encounters has not been determined.

4. Neglect, Maltreatment, And Trauma

Based on the animal research, early neglect and abuse should alter the activity of the developing LHPA system. So far, there is only a small literature on this in humans. Because of the multiple genetic and experiential risk factors typically noted in children with maltreating backgrounds, isolating the impact of adverse early experiences on the human LHPA system promises to be difficult. A full discussion of this emerging literature is beyond the scope of this research paper. Two findings related to physical and sexual abuse seem consistent enough to mention. First, during periods of active abuse young children do exhibit elevated cortisol levels and heightened responsivity to CRH challenge suggestive of a hyper-responsive LHPA system. Once the child’s life circumstances are stabilized, however, for most children this hyperresponsiveness diminishes. The exceptions may be (a) depressed maltreated children who show a flattening of the daily rhythm in cortisol production (Hart et al. 1996), and (b) maltreated children with chronic posttraumatic stress disorder (PTSD) and who have higher baseline cortisol and catecholamine levels that are correlated with the duration of abuse (De Bellis et al. 1999).

In addition, the relations between growth failure, maltreatment, and LHPA system bear comment. Physical abuse and neglect sometimes produce significant growth delays due to reduced pituitary production of growth hormone (GH), cell insensitivity to GH, and blunted GH responses to provocative challenges, alterations that all revert to normal when the child is removed from the maltreating circumstances (Alanese et al. 1994). Theoretically, the LHPA system may be involved in the etiology of this syndrome, called variously psychosocial short stature or psycho-social dwarfism (Johnson et al. 1992). Children adopted from deprived, orphanage conditions exhibit growth failure, and six years after adoption have elevated baseline cortisol levels that were correlated with length of orphanage experience (Gunnar 2000).

5. Future Of Research

Psychobiological studies of stress in young children have burgeoned since the development of techniques to measure cortisol noninvasively in saliva. Community studies of children negotiating the normative stressors of childhood are beginning to make connection with studies of children from highly stressful, adverse life circumstances and those with clinical disorders. As in studies of adults and animals, individual differences in response to stressors are common and related to the child’s social circumstances and temperament. The challenge for the future is to determine the relation between LHPA function in early development and child outcomes and to explicate the relevant molecular processes.


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