The Hypothalamic Pituitary Adrenal (HPA) axis is the coordinator of adaptive responses to physical and psychological stress. The central nervous system plays a key role in modulation of both basal and adaptive HPA axis functions. In fact, since long ago, animal studies have shown that acute and chronic exposure to glucocorticoids (a stress hormone released due to HPA axis activation, cortisol in humans) affects the function and the morphology of brain areas such as the hippocampus and the cingulate cortex. This thesis is based on novel neuroimaging methodologies used to investigate the interactions of psychological stress, cortisol and the brain. It consists of three functional studies and a morphometric one. In the first functional study we show that the hippocampus (where glucocorticoid receptors are most abundant) plays a role in initiation of an HPA axis stress response. In the second study, we provide evidence that besides hippocampus, the neural activity in the so-called "default mode network" (DMN), especially the anterior cingulate cortex (ACC), relates to interindividual variations in HPA axis response to psychological stress. In the third study we have investigated the cortisol-modulation of the DMN. Again, we provide evidence for a role of the ACC and the orbitofrontal cortex in negative feedback inhibition of the HPA axis activity. Finally, we show a morphological link between the ACC and the cortisol response to awakening which is an index of basal HPA axis activity. Overall, our findings confirm the critical role of the ACC and mesolimbic system in HPA axis regulation. These findings also draw attention to the interactions between functional subregions of the medial prefrontal cortex and states of HPA axis function prior to stress onset---suggesting an interplay of the monitoring and the executive planning roles of the medial prefrontal cortex in behavioral adaptation to stress. Beyond stress research, our findings offer a framework for combining neuroimaging and neuroendocrinology to better understand the interindividual variances in behavior, and perhaps to better identify subgroups at risk of psychological disorders.

This study examined percent fat, fat distribution, and resting cortisol concentrations between personality types for coronary artery disease (CAD) risk. Males (n= 29, 43 ± 8.8 years) selected through the Jenkins Activity Survey, scoring >_ 75th percentile (Type A=15) or S 30th percentile (Type B=14), had the following measures: percent fat, lipid profile, and waist-to-hip ratio. Each hour, heart rate, blood pressure (SBP, DBP), and cortisol were measured. A prediction model determined risk of CAD. Type A had a tendency to have higher DBP, but was only significant at one time point (F= 3.390, p= .022). Type B showed significantly higher total (t= -2.688, p= .012) and LDL cholesterol (t= -3.612, p= .001). Although we did not show many significant differences between groups, within groups, many significant correlations were detected among the variables measured. Further studies will justify the associations between percent fat, fat distribution, and cortisol across personality types. / School of Physical Education

[Truncated abstract] Obesity is rapidly increasing in prevalence and has significant physical and mental health implications. Stress, a general term referring to factors indicative of psychological strain such as depression and anxiety, has been identified as both a cause and consequence of weight gain and obesity in some individuals. In previous research, overeating in response to stress has been investigated as either a means of mood regulation or as a response to strict dietary restraint. Cortisol, a steroid hormone that increases in response to stress, has also been linked with increased food intake in both animal and human studies. Thus, cortisol may be an additional factor contributing to overeating and weight gain in response to stress. If stress does lead to overeating and weight gain, it is also likely that stress will inhibit attempts made by obese individuals at weight loss. The first study of this thesis was a repeated measures treatment study in which the associations of stress and cortisol levels with baseline body mass index and subsequent weight loss were investigated among females participating in a cognitive behavioural weight management programme. A cross-sectional analysis prior to treatment commencement showed that the association of stress and depression with body mass index was moderated by the severity of obesity. Dichotomous thinking, a cognitive style in which events are viewed in polarised 'black and white' terms, mediated the associations of both depression and eating disorder symptomatology with BMI. ... The second study of this thesis was a controlled laboratory-based examination of food intake following an acute psychological stressor. It was hypothesised that high baseline levels of psychological stress, such as depression and anxiety, would be associated with greater increases in negative mood and cortisol levels in response to the acute stressor, both of which, in turn, would be associated with greater food intake. Contrary to the hypothesis, baseline levels of psychological stress were not associated with the extent to which negative mood and cortisol levels increased following the acute stressor. The extent to which negative mood, but not cortisol, increased following acute stress was significantly positively associated with food intake. The results do not support the hypothesis that high cortisol levels are predictive of increased food intake in human females, although the results may have been affected by the broad participant inclusion criteria. The results suggest that increases in negative mood lead to increases in food intake, although it is argued that this is unlikely to be a general effect and suggestions for future research are made. The overall aim of this research was to examine whether stress and cortisol were associated with weight status, acute changes in eating behaviour and changes in weight in the medium-term. The results are discussed in relation to this aim, wth particular focus on the differences between treatment-seeking and community samples, implications for the treatment of obesity (especially when the individual is also experiencing high levels of depression), prevention of weight gain and possible future studies of the effects of stress and depression on weight change and eating behaviour.

Thèse (M.Sc.)--Université Laval, 2007. / Bibliogr.: f. 66-72. Publié aussi en version électronique dans la Collection Mémoires et thèses électroniques.

Diss. (sammanfattning) Linköping : Linköpings universitet, 2008. / Härtill 5 uppsatser.

Diss. (sammanfattning) Linköping : Univ., 2002. / Härtill 5 uppsatser.

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 80-91).

Thesis (Ph.D.) -- University of Western Sydney, Hawkesbury, 1998. / Thesis submitted for the degree of Doctor of Philosophy. Includes bibliographical references (leaves 190-214).

Thesis (Ph.D.) -- University of Adelaide, School of Paediatrics and Reproductive Health, Discipline of Obstetrics and Gynaecology, 2008. / "March 2008" Bibliography: leaves xxvi-xliii. Also available in print form.

Thesis (Ph. D.)--University of Alabama at Birmingham, 2008. / Title from first page of PDF file (viewed Sept. 19, 2008). Includes bibliographical references (p. 117-128).