A significant body of research has identified the deleterious effects of stress on psychological well-being (e.g., Tataro, Luecken, & Gunn, 2004). Religiosity and religious coping have been identified as variables that may impact a person’s experience with stress (Ano & Vasconcelles, 2005). Aukst-Margetic and Margetic (2005) suggest that the connection between stress, religious variables, and well-being can be understood through the frame of psychoimmunodocrinological research, which examines the relationship between neurohormonal functioning (e.g., cortisol level) with psychological factors that may impact health. The purpose of this study was to investigate whether acute stress reactivity, as measured by changes in cortisol levels in response to a laboratory stressor, is related to religiosity, religious coping, and psychological well-being such as depression and anxiety. Another purpose of this study was to attempt to replicate and extend Tataro, Luecken, & Gunn (2005), which found evidence that higher religiosity and composite religiosity/spirituality was associated with lower cortisol level after exposure to acute stress. Results indicated that cortisol level was not significantly related to gender, self-rated religiousness, spirituality, frequency of prayer, or forgiveness. In addition, cortisol reactivity was not significantly related to measures of psychological well-being, although negative religious coping significantly predicted depression, and state and trait forms of anxiety. Limitations, practical implications, as well suggestions for future research are discussed.

Traditionally, it was believed that young children did not experience long-term negative effects resulting from a traumatic experience. Many professionals continue to assume that the effects of trauma on infants (0-3 years) are transient and that intervention is unnecessary. However, research has shown that infants and young children can develop posttraumatic stress disorder (PTSD; Scheeringa, Peebles, Cook, & Zeanah, 2001). Symptoms consistent with older children and adults (i.e., re-experiencing, avoidance/emotional numbing, and hyperarousal) have been found with infants and young children exposed to trauma. The purpose of this dissertation was to better understand the nature of trauma in early childhood using a multidimensional approach. Three studies were conducted to determine the effects of trauma and PTSD on young children. Study 1 considered the effectiveness of using the Child Behaviour Checklist (CBCL), a popular measure of childrens adjustment, to screen for PTSD symptoms in a sample of young children. Results suggested that the PTSD subscale of the CBCL correctly identified 71% of children with PTSD. Study 2 examined the role that potentially traumatic events, as well as family and child characteristics, play in the development of symptoms of PTSD by surveying a community sample. Results suggested that certain events were more likely to be associated with symptoms of PTSD and that children with younger mothers and higher rates of internalizing problems were more likely to experience symptoms of PTSD. Study 3 explored the effects of trauma on young childrens emotional, physiological and relational functioning, and was conducted in two phases: Phase I considered PTSD symptom expression, physiological stress-response (i.e., salivary cortisol) and quality of attachment in children recruited from a community sample; and Phase II considered PTSD symptoms, quality of attachment and maternal psychological distress in the development of PTSD in a clinical sample of young children. Results found that in Phase I PTSD symptoms were not associated with either cortisol level or quality of attachment, although effect sizes were moderate. Phase II results found a direct and significant association between quality of attachment and PTSD symptoms. A non-significant but moderate effect size was found for the link between maternal psychological distress and PTSD symptoms. Findings are discussed with regards to their implications for future research and clinical practice.

The role of mainstream media in women’s views of female beauty and body image has been well documented. However, few published studies have observed ethnic differences in physiological stress reactivity that may occur from pressures to comply with a particular image of beauty. This study examined whether the exposure to the mainstream ideal body image would negatively affect Latina women’s physiological and psychological functioning, and how their responses differed in comparison to their White counterparts. Participants included college-aged female students from Pitzer College who self-identified as Latina or Caucasian. Participants completed questionnaires assessing, body esteem (MSBRQ-AS; SATAQ; CDFRS), ethnic identity (SEE), state anxiety (STAI-State) and affect (PANAS) prior to and following exposure to Victoria’s Secret or Chrysler automobile commercials. Physiological stress reactivity was assessed through changes in systolic and diastolic blood pressure, as well as salivary cortisol. 3-way ANOVA tests indicated a significant 2-way interaction between condition and time on participants’ levels of diastolic blood pressure, F(1, 27) = 4.266, MSe = 29.803, p =.049, η2 =.136, as well as ratings of appearance evaluation, F(1,36) = 5.733, MSe = 3.692, p =.022, η2 =.137, and body satisfaction F(1,36) = 4.27, MSe = 4.747, p = .046, η2 =.106. Women who viewed the Victoria’s Secret commercials demonstrated increased levels of diastolic blood pressure and reported lower ratings of body esteem in comparison to women who viewed the Chevy Sonic commercials. Potential trends in anxiety reactivity and the internalization of mainstream female beauty in Latina women following exposure to the stimuli are further discussed.

Background: Studies have not examined the relationships between serum vitamin D (SVitD), serum cortisol (SCort), bone mineral density (BMD), and body fat percent (BF%) in elite figure skaters. However, studies of non-athletes have found that BMD is inversely related to SCort and directly related to SVitD, and BF% is inversely related to SVitD and directly related to SCort. It was, therefore, the purpose of this study to assess the relationships between SCort, SVitD, BMD, and BF% in elite figure skaters. Methods: U.S. national team figure skaters were assessed at a national training camp during the summer, 2012. BMD and body composition were measured by dual energy x-ray absorptiometry (DEXA). Blood chemistry values for SVitD and SCort were obtained via venous puncture after an overnight fast, the same morning as the DEXA measurement. Georgia State University Institutional Review Board approval was obtained for the assessment of data collected at this training camp. Results: 24 out of 39 training camp attendees (61.5%) volunteered to be assessed as part of this study. Subjects ranged from 17 to 34 years and included males (n=11) and females (n=12). In all skaters statistically significant negative correlations (2-tailed Spearman) were found between SCort and BMD of the spine (r=-0.458, p=0.032), pelvis (r=-0.532, p=0.011), ribs (r=-0.517, p=0.014), and trunk (r=-0.538, p=0.010). In females, SCort was negatively correlated with BMD of the pelvis (r=-0.664, p=0.026) and trunk (r=-0.609, p=0.047), and was positively correlated with total BF% (r=0.657, p=0.020) and trunk fat % (r=0.708, p=0.010). In males, SCort was significantly correlated with BMD of the ribs (r=-0.627, p=0.039). The 3 skaters (all female) with SCort > 28 mcg/dL had significantly lower mean BMD of the total body, left femoral neck, legs, trunk, and pelvis, and significantly greater BF% of the total body and trunk when compared to the 20 skaters with SCort 7-28 mcg/dL. No significant correlations between SVitD and BMD or BF% were found. A Mann-Whitney U test found no significant differences in BMD and BF% between the 8 skaters with SVitD ≥ 30 ng/mL compared to the 15 skaters with SVitD < 30 ng/mL (p>0.05). Females with SVitD ≥ 30 ng/mL had significantly higher BMD (p=0.041) of the right femoral neck when compared to those with lower SVitD. Conclusions: Correlations consistently found negative associations between SCort cortisol and BMD in multiple assessment areas, particularly those composed of trabecular bone. Higher SCort was also associated with higher BF% in female skaters. Despite spending a great deal of time in indoor facilities, limiting vitamin D creation through sunlight exposure, no significant correlation between SVitD and BMD was found. Female athletes in ‘appearance’ sports, may be predisposed to restrained eating behaviors, which may be associated with elevated SCort. These findings suggest a need for further study of the interaction between SCort, BMD, and BF% in these athletes. The lack of a statistically significant relationship between SVitD and BMD suggests the need to investigate additional factors associated with bone injury risk in athletes.

Some aspects of the stress response during acute intensive care for severe burns are described and quantified by measuring hormonal and neuroendocrine patterns and relating these to organ function in the short term. This includes an assessment of whether there are markers for the severity of stress that are better than conventional descriptors of the severity of a burn in predicting failing organ function. P-CgA after a major burn injury is an independent and better predictor of organ dysfunction assessed as SOFA score than the traditionally used TBSA% burned. The results also suggest that the extent of neuroendocrine activation is related to organ dysfunction, and this motivates a more extensive effort to evaluate P-CgA as a prognostic marker with respect to mortality and long-term outcome. P-NT-proBNP exhibited a complex pattern with considerable inter-individual and day-to-day variations. Values of P-NT-proBNP were related to size of burn, water accumulation and systemic inflammatory response. A considerable covariation with trauma response and SOFA scores was observed in day by day analyses, but with weight change only on day 2. Maximum P-NT-proBNP showed a stronger correlation with SOFA score on day 14, with mortality, and with LOS, than did age and TBSA% burned. High values were also independent predictors of all subsequent SOFA scores up to two weeks after injury. P-NT-proBNP and NT-proANP reflect and predict organ function after burn injury similarly, notwithstanding a significantly larger intra-individual variability for P-NT-proBNP. P-NT-proBNP, but not NT-proANP, reflects the systemic inflammatory trauma response. Free cortisol concentration was related to the size of burns, as was the circadian cortisol rhythm. This effect of burn size was, at least in part, related to its effect on organ function. This thesis points to the fact that the stress response is richly interwoven, and cannot be adequately assessed by one biomarker only. All biomarkers studied here can be viewed as representing efferent limbs of the stress reaction, and they would need to be supplemented by biomarkers representing individual physiologic responses that follow the stress signaling.

There is a need to understand how free-ranging animals respond and adapt to stress. However, little is currently known regarding the physiologic adaptations to stress in bears, and there are few tools available to wildlife managers to assess the health and stress status of free-ranging animals, including ursids. The hypothalamus-pituitary-adrenal (HPA) axis plays major roles in the physiological adaptation to stress, leading to the increased secretion of glucocorticoids (e.g. cortisol in most mammals) that mediate adaptive changes in physiology and behaviour. The vast majority of glucocorticoids are bound to its primary carrier protein, corticosteroid-binding globulin (CBG), in most animals, and only the unbound fraction is bioavailable. Thus, CBG plays a major role in modulating glucocorticoid dynamics, and this protein must be characterized to build a more complete understanding of the adaptive role that the HPA axis plays in mitigating stress in bears. The overall objective of this thesis was to characterize the HPA axis activity and CBG levels in bears, and develop tools targeted towards the monitoring of the health and stress status of American black bear (Ursus americanus), grizzly bear (U. arctos), and polar bear (U. maritimus). The binding characteristics of cortisol to CBG in bears were studied via saturation binding experiments, and this information was used to estimate free cortisol concentrations based on CBG concentrations. To quantify CBG concentrations in bears, an enzyme-linked immunosorbent assay (ELISA) was developed. Grizzly bear CBG cDNA was cloned and sequenced, and an antibody was developed against a peptide sequence of the deduced amino acid sequence. The antibody showed good cross-reactivity against black, grizzly, and polar bear CBG, and the ELISA based on this antibody found differences in the mean CBG levels between species. Using this data, free cortisol levels were estimated, and mean levels were elevated in polar bears relative to black and grizzly bears. Having developed these tools, the roles that corticosteroid-binding globulin (CBG) and bioavailable cortisol played in the physiological adaptation to major life history traits and environmental challenges faced by ursids were investigated. Importantly, CBG was not modulated by the acute stress of capture and handling, despite the large differences in the magnitude of acute cortisol responses that are induced by these methods, suggesting that CBG levels may reflect the chronic health and stress status of bears. Altogether, there were few changes in CBG levels throughout much of the annual life cycle of bears, implying that CBG does not play a major adaptive role in the life history traits of bears and, instead, metabolic and environmental factors may be the key modulators of cortisol dynamics. However, CBG was not significantly associated with our measures of dietary patterns and nutrition, including body condition, seasonal dietary patterns, and fasting. The majority of the observed variation in the levels of this protein in bears remains unexplained. However, stress-induced free cortisol levels were negatively associated with urea to creatinine ratio (an indicator of dietary protein content and fasting status in grizzly and polar bears, respectively) and positively associated with lactation in hibernating black bears, suggesting that the variation in adrenal function may be playing an important role in the adaptation to adverse environmental conditions and/or metabolic stress in bears. In addition to serum cortisol dynamics, other proteins were also hypothesized to play adaptive roles in maintaining the hibernating phenotype in bears. Changes in the serum proteome during hibernation in black bears were assessed as a means to discover novel proteins that may be indicative of metabolic stress in bears. The serum proteomes of active and hibernating black bears were compared and analyzed for significant changes by two-dimensional electrophoresis and tandem mass spectrometry. Proteins involved with immune-related function were significantly altered during hibernation, leading to the proposal that the serum protein changes are essential for maintaining immune competence, wound healing, and bone structure. Altogether, this thesis developed a method to quantify CBG and estimated free cortisol concentrations in bears, and characterized their roles in the physiological adaptations associated with the major life history traits and environmental challenges faced by ursids. Also, novel serum proteins were identified as potential markers of immune function and health status in bears. These tools may be tremendously useful for wildlife managers and conservationists in determining how chronic stressors, including anthropogenic activities and climate change, may impact the stress and health performances of individual and populations of free-ranging bears.

Recent research has suggested that boredom is a construct that can be distinguished from similar affective states including apathy, anhedonia, and depression, using self-reports. The current study investigated whether boredom and sadness (an analogue for depression) are distinct in terms of their physiological signatures. State boredom and sadness were induced in a group of healthy participants while their physiological parameters of heart rate (HR), skin conductance (SCL), and cortisol levels were monitored. Results indicated that the autonomic nervous system response for both states can be characterized by directional fractionation, with boredom resulting in increased HR but decreased SCL relative to sadness. Cortisol levels were higher after the boring induction than the sad induction, indicating increased hypothalamic-pituitary-adrenal axis activation for boredom. Overall, boredom appears to have a physiological signature that is distinguishable from a primary symptom of depression.

Municipal wastewater effluent (MWWE) is an important source of pollution in the aquatic environment impacting fish. MWWE is a complex mixture of chemicals including pharmaceuticals, personal care products, industrial chemicals and pesticides. A link between reproductive endocrine disruption and MWWE exposure has been established in fish, but less is known about the effects of MWWE on non-reproductive endocrine disruption. The overall objective of this thesis was to examine the impacts of MWWE exposure on the stress response and intermediary metabolism in rainbow trout (Oncorhynchus mykiss). In fish, the primary adaptive organismal stress response involves the activation of hypothalamic-sympathetic-chromaffin axis to produce catecholamines, predominantly epinephrine, and the hypothalamic-pituitary-interrenal (HPI) axis to produce cortisol. Both of these hormones play a key role in elevating plasma glucose levels that is essential to fuel the increased energy demand associated with stress. Along with the organismal stress response, the cellular stress response, involving the synthesis of a suite of heat shock proteins (hsps), also plays an important role in protecting cellular protein homeostasis in response to stressors, including toxicants. The impact of MWWE on stress-related pathways were identified using a low-density trout cDNA microarray enriched with genes encoding for proteins involved in endocrine-, stress- and metabolism-related processes. This was further confirmed by assessing plasma hormone and metabolite levels and stress-related targeted genes and proteins expression and enzyme activities in select tissues in rainbow trout. Studies were carried out in controlled field (caging) and laboratory experiments to examine the impacts of MWWE on stress and tissue-specific metabolic responses in rainbow trout. Further in vitro studies using rainbow trout hepatocytes in primary cultures were carried out to investigate the mechanism of action of two pharmaceuticals, atenolol and venlafaxine, found in relatively high concentrations in MWWE in impacting the stress-mediated glucose response. In caged fish, MWWE exposure significantly elevated plasma cortisol and glucose concentrations, and altered the mRNA abundance of a number of stress-related genes, hormone receptors, glucose transporter 2 and genes related to immune function. When fish were exposed to an acute handling stress following a 14 d exposure to MWWE, the cortisol response was abolished and the glucose response was attenuated. The effects on cortisol did not correlate with changes in the expression of genes involved in cortisol biosynthesis, but were associated with an increase in hepatic glucocorticoid receptor (GR) protein expression. Upon further investigation in controlled laboratory studies, MWWE exposure elevated constitutive hsp 70 and hsp90 expression after 8 d exposure, which correlated with a decrease in glycogen levels in the liver in fish exposed to a high concentration of MWWE compared to control fish, pointing to a MWWE-induced increase in liver energy demand. By 14 d, glycogen stores were replenished, and this was commensurate with increases in liver gluconeogenic capacity, including increases in the activities of phosphoenolpyruvate carboxykinase (PEPCK) and alanine aminotransferase (AlaAT), along with a decrease in liver GR expression. In the heart, GR protein expression increased in treated fish, and the activity of pyruvate kinase increased, indicating an increase in glycolytic capacity. Subjecting the MWWE exposed fish to a secondary handling disturbance (acute stress) led to an attenuated plasma cortisol and glucose response compared to the control group. This corresponded with a reduced liver gluconeogenic capacity and a lower liver and heart glycolytic capacities, reflecting a disturbance in the energy substrate repartitioning that is essential to cope with stress. While it is difficult to establish causative agents from a complex mixture such as MWWE, the two pharmaceutical that were tested impacted glucose production. Specifically, atenolol and venlafaxine disrupted the epinephrine-induced glucose production, but did not modify cortisol-mediated glucose production in trout hepatocytes. The suppression of epinephrine-mediated glucose production by atenolol and venlafaxine was abolished by cAMP analogue (8-bromo cAMP) or glucagon (a metabolic hormone that increases glucose production). This suggests that both drugs disrupt β-adrenoceptor signaling, while it remains to be determined if the response is receptor isoform-specific. Altogether MWWE exposure disrupts the organismal and cellular stress responses in trout. Key targets for MWWE impact leading to the impaired cortisol and metabolic responses to stress include liver and heart GR expression, liver gluconeogenic capacity, and liver, heart and gill glycolytic capacities. Most significantly, MWWE impairs the ability to metabolically adjust to a secondary acute stressor, which is an important adaptive process that is integral to successful stress performance. From an environmental stand-point, long-term exposure to MWWE will lead to reduced fitness and will compromise the capacity of fish to cope with additional stressor, including escape from predators.

Traditionally, it was believed that young children did not experience long-term negative effects resulting from a traumatic experience. Many professionals continue to assume that the effects of trauma on infants (0-3 years) are transient and that intervention is unnecessary. However, research has shown that infants and young children can develop posttraumatic stress disorder (PTSD; Scheeringa, Peebles, Cook, & Zeanah, 2001). Symptoms consistent with older children and adults (i.e., re-experiencing, avoidance/emotional numbing, and hyperarousal) have been found with infants and young children exposed to trauma. The purpose of this dissertation was to better understand the nature of trauma in early childhood using a multidimensional approach. Three studies were conducted to determine the effects of trauma and PTSD on young children. Study 1 considered the effectiveness of using the Child Behaviour Checklist (CBCL), a popular measure of childrens adjustment, to screen for PTSD symptoms in a sample of young children. Results suggested that the PTSD subscale of the CBCL correctly identified 71% of children with PTSD. Study 2 examined the role that potentially traumatic events, as well as family and child characteristics, play in the development of symptoms of PTSD by surveying a community sample. Results suggested that certain events were more likely to be associated with symptoms of PTSD and that children with younger mothers and higher rates of internalizing problems were more likely to experience symptoms of PTSD. Study 3 explored the effects of trauma on young childrens emotional, physiological and relational functioning, and was conducted in two phases: Phase I considered PTSD symptom expression, physiological stress-response (i.e., salivary cortisol) and quality of attachment in children recruited from a community sample; and Phase II considered PTSD symptoms, quality of attachment and maternal psychological distress in the development of PTSD in a clinical sample of young children. Results found that in Phase I PTSD symptoms were not associated with either cortisol level or quality of attachment, although effect sizes were moderate. Phase II results found a direct and significant association between quality of attachment and PTSD symptoms. A non-significant but moderate effect size was found for the link between maternal psychological distress and PTSD symptoms. Findings are discussed with regards to their implications for future research and clinical practice.

This study investigated the effect of chronic alcohol exposure on the responses of the maternal hypothalamus-pituitary adrenal axis (HPA-axis) and thyroid hormones throughout gestation using an ovine model. Maternal plasma concentrations of ACTH, cortisol and the thyroid hormones T3, free T4 and total T4 were determined in response to infusion of 0.75, 1.25 and 1.75 g/kg alcohol. Maternal endocrine responses to alcohol administration have been investigated before in rodent models. However, this is the first study using a large animal model (sheep), in which all three human trimester equivalents occur in utero. Different concentrations of alcohol were administered intermittently from gestational day 4 to 132 in a pattern that modeled human binge drinking during pregnancy. Maternal blood samples were collected on specific days (GD 6, 40, 90, 132) and at multiple time-points (0, 0.5, 1, 1.5, 2, 6, 24 hours) and were analyzed to determine blood alcohol concentrations (BACs) and ACTH, cortisol, free T4, total T4 and T3 plasma concentrations. Alcohol readily permeates the placenta and can directly affect fetal cells and tissues. Alcohol also causes endocrine imbalances in the mother and interferes with maternal-fetal hormonal interactions and the mother’s ability to maintain a healthy pregnancy, thus also indirectly affecting fetal development. Sheep receiving either 0.75, 1.25 or 1.75 g/kg alcohol achieved peak BAC values of 93 + 5, 126 + 5 and 183 + 5 respectively. Alcohol exposure resulted in increased plasma ACTH and cortisol concentrations peaking at 2 hours after beginning of the infusion and returning to baseline values at 6 hours after beginning of the infusion. There was no effect of alcohol on any of the plasma thyroid hormone concentrations. Thyroid hormone concentrations changed as a result of progressing pregnancy. Plasma concentrations of total T4 and free T4 were higher on gestational days 6 and 40 compared to GDs 90 and 132, and plasma T3 concentrations were highest on GD 6. The results of this study show that alcohol stimulates the HPA-axis in a dose dependent fashion in pregnant sheep. The response of the HPA-axis to repeated alcohol exposure throughout gestation remained unchanged. Alcohol exposure did not affect the release of thyroid hormones. Thyroid hormone concentrations changed during pregnancy in sheep in a manner similar to changes observed in pregnant women.