Doctor of Philosophy / A large number of neuroendocrine studies indicate a possible relationship between the Hypothalamo-Pituitary-Gonadal (HPG) axis and major depressive illness in men. This observation is not surprising, considering the similarities between the symptom profiles of depression and hypogonadism. However, owing to the strong likelihood that a number of other demographic, clinical and treatment covariates may potentially obscure a possible relationship between HPG and depression, studies in this area have produced somewhat inconsistent results. The main objective of the present study was to investigate the relationship between depression and HPG hormone levels in a population of hospitalised men. Another objective was to examine the relationship of a number of demographic, behavioural, clinical and treatment variables with HPG hormone levels and depression. METHOD: Serum hormones of the HPG axis (Luteinizing Hormone (LH), Follicle Stimulating Hormone (FSH), Free Testosterone (free T), Total Testosterone (total T) and Sex Hormone Binding Globulin (SHBG)) were compared between fifty-two male patients with Major Depressive Disorder (mean age = 42.04; SD = 14.1) and twenty-five male patients with other psychiatric conditions (mean age = 40.72; SD = 13.8) on admission into hospital. In addition, to elucidate the possible relationship between clinical outcome of depression and gonadal function, HPG parameters were measured in patients with depression 3 to 6 months following discharge. Based on their HDRS (Hamilton Depression Rating Scale) score, patients were categorised as remitters and non-remitters. Demographic, behavioral, clinical and treatment variables were also examined as possible correlates of hormone levels. RESULTS: Comparison between patients with depression and patients with other diagnoses indicated a significantly lower free T and total T in patients with depression. There were no differences in other hormone parameters between the two diagnostic groups. Correlational analyses indicated significant negative relationships between free T and total T and severity as well as duration of depression. Age was inversely correlated to both free T and total T, whereas BMI was negatively correlated with Total T and SHBG. There was a positive relationship between Total T as well as Free T and measures of sexual dysfunction. While no difference in hormone parameters was observed as a function of psychotic features, patients with melancholic features exhibited significantly lower levels of free T and total T compared to patients with no melancholic features. In the multiple regression analyses, age, duration and severity of depression were the strongest predictors of both free and total T. In separate regression analyses somatic features, over and above other features of depression were found to account most in the variability in free T and total T. Longitudinal analysis revealed significantly higher free T and total T levels on follow-up compared to baseline in the patients who remitted. There was no significant change in any of the hormones studies in the non-remitting group. CONCLUSION: The main findings of the present study support previous results that both total and free testosterone levels are lower during depression and that concentrations of free T and total T parallel changes in severity of depressive symptomatology. Further investigations into the mechanism for this observation, and perhaps examinations of testosterone supplementation for treatment of depression are in order.

Introduction A literature review of the evidence regarding aetiology, classification, epidemiology and treatment of depressive disorders was conducted. All of the domains that constitute the biopychosocial model were investigated as a basis for testing the hypothesis that a biomedical approach, or any domain in isolation, is inadequate for fully understanding depression. An integrative, explanatory, conceptual model was developed, based on supportive evidence that can better inform the clinical encounter. Methods A combination of manual and electronic searches were conducted. Medline, Psychlit, Sociofile and the Social Science index databases were accessed with multiple key words. The University of Queensland library catalogue was also searched. Part A - Historical and Philosophical Basis The limitations and challenges of the biomedical model are followed by suggested responses, in particular a biopsychosocial model applied within a patient-centred consultation style. Various methods of scientific enquiry are needed to develop a more complete understanding of depression. Part B - Assessing the Evidence Evidence from epidemiological, biological and psychosocial research is reviewed. Depressive illness tends to be a chronic or recurrent condition with multifactorial causation, and occurs on a complex spectrum of severity. There is emerging evidence for a chronic stress response being the initial biological dysfunction, This is consistent with the frequency of stressful life events that precipitate depressive episodes. There is convincing evidence for predisposing factors such as low self-esteem, poor interpersonal skills and deficiency of social support. A range of treatment modalities, for example pharmacotherapy and various psychotherapies, appear to have similar effectiveness, which suggests that recovery occurs when the perpetuating cycle is broken at different sites. Part C - Integrative Models. Available schematic integrative models are reviewed and most fall short of integrating the three domains of the biopsychosocial, or fail to illustrate the circular nature of causation. A model is proposed, based on the evidence reviewed in Part B, that addresses both considerations. Conclusion Some causal factors for depression are supported by evidence. Models that integrate these findings are necessary to more fully explain depression. When applied in conjunction with patient-centred consultation styles, improved clinical outcomes could be expected. There is the potential for further research to test out the benefit of such a biopsychosocial approach, and to better elucidate component causes and reversible risk factors. There is a need for narrative approaches to receive considerably greater attention.

Thesis (M.A.)--York University, 2005. Graduate Programme in Psychology. / Typescript. Includes bibliographical references (leaves 105-117). Also available on the Internet. MODE OF ACCESS via web browser by entering the following URL: http://gateway.proquest.com/openurl?url_ver=Z39.88-2004&res_dat=xri:pqdiss&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&rft_dat=xri:pqdiss:MR19652

Thesis (Ph. D.)--Virginia Commonwealth University, 2007. / Prepared for: College of Humanities and Sciences. Bibliography: leaves 142-158. Also available online.

Thesis (Ph. D.)--University of Texas at Austin, 2006. / Vita. Includes bibliographical references.

Thesis (Ph.D.)--University of Nebraska-Lincoln, 2006. / Title from title screen (site viewed Mar. 27, 2008). PDF text: 86 p. : ill. (some col.) ; 303 K. UMI publication number: AAT 3278160. Includes bibliographical references. Also available in microfilm and microfiche formats.

Thesis (Ph. D.)--University of Hong Kong, 2008. / Also available in print.

Thesis (Ph. D.)--Oregon State University, 2008. / Printout. Includes bibliographical references (leaves 109-127). Also available on the World Wide Web.

Thesis (Ph. D.)--Swinburne University of Technology, School of Social and Behavioural Sciences - 2000. / Submitted for the degree of Doctor of Philosophy, School of Social and Behavioural Sciences, Swinburne University of Technology - 2000. Typescript. Includes bibliographical references (p. 235-248).

Thesis (Ph.D.) -- University of Adelaide, Dept. of Psychiatry, 1974.