Thesis (M.Soc.Sc.)--University of Hong Kong, 2004. / Also available in print.

Thesis (Ph.D.)--University of Nevada, Reno, 1989.

Thesis (Ph. D.)--University of Canterbury, 2007. / Typescript (photocopy). Includes bibliographical references (leaves 140-159). Also available via the World Wide Web.

The problem examined in this study was the nature of compulsive purchasing behavior. Three proposed models depicting this behavior as a learned adaptive response to anxiety and/or depression, an addiction, and a personality disorder were introduced and discussed in Chapter I. Background information concerning the areas examined in the models was presented in Chapter II. The research methodology was discussed in Chapter III and the findings of the research presented in Chapter IV. A summary, conclusions, implications, and recommendations were presented in Chapter V.

Thesis (Ed. D.)--Harvard University, 1991. / Includes bibliographical references.

Thesis (Ph.D.)--University of Melbourne, Dept. of Psychology, 2004. / Typescript (photocopy). Includes bibliographical references (leaves 275-322).

Thesis (Ph.D.) - University of Queensland, 2005. / Includes bibliography.

Thesis (Ph.D.)--Loyola College in Maryland, 2001. / Adviser: Joseph Ciarrocchi. Includes bibliographical references.

Thesis (Ph.D.)--Boston University / PLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis or dissertation. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you. / Compulsive hoarding is a serious disorder that causes significant impairment in the home. While compulsive hoarding has been traditionally associated with obsessive-compulsive disorder (OCD), standard OCD treatments have been mostly ineffective for hoarding. Recent research has provided evidence that hoarding has a distinct profile that could indicate a separate disorder. Further understanding of hoarding may advance classification and treatment. One understudied aspect of hoarding is excessive acquisition. Acquisition behaviors in hoarding appear to share similarities with impulse control disorders. While preliminary research has suggested elevated impulsivity in those who hoard, prior studies have been inconsistent in their measurement of impulsivity. Also, the relationship between impulsivity and excessive acquisition behaviors remains unexplored. This study assessed impulsivity in hoarding (n = 32) and anxiety disorder (n = 32) participants using a multi-dimensional model of impulsivity. Participants underwent a diagnostic assessment and completed self-report forms and neuropsychological tasks measuring impulsivity. Participants also completed an experimental task to assess acquiring behaviors after a mood induction. Participants completed measures of affect and state impulsivity, before and after a negative or neutral mood induction. There were no significant differences between diagnostic groups on self-reported impulsivity levels. Significant between-group differences were found on several neuropsychological tasks. Those with hoarding had significantly poorer response inhibition and lowered levels of adaptive and maladaptive risk-taking than participants with anxiety disorders. A diagnosis of hoarding predicted these outcomes independent of social phobia, generalized anxiety disorder, and major depressive disorder. In the acquisition task, the hoarding group acquired significantly more items than the anxiety disorder group but there was not a significant interaction effect with mood induction condition. The hoarding group had a significantly greater increase in state impulsivity across time but there was also not an interaction effect with mood induction condition. An analysis designed to assess whether state impulsivity mediated the relationship between negative affect and acquisition behaviors failed to find a significant indirect effect. Overall, study findings suggest differences in impulsivity for those who hoard as compared to those with an anxiety disorder. A continued emphasis on understanding impulsivity in hoarding could further diagnostic classification and treatment development. / 2031-01-02

The studies in this thesis aimed to develop and characterise a rodent model of meal feeding that would mimic aspects of human eating behaviour, leading to the overconsumption of calories and ultimately to obesity. In seeking to identify potential mechanisms that might be involved in the initiation of meals, a palatable scheduled feeding regime was utilised to induce a substantial food intake over short periods of time in rodents. This was done by providing scheduled access to a palatable diet for a 2h-period each day without imposed caloric restriction during the remainder of the day. Initially, the effects of different palatable diets were examined. Three of the four palatable diets resulted in a rapid adaptation of feeding behaviour and induced the consumption of large, binge-type meals in both Sprague Dawley rats and C57BL/6 mice. Candidate gene expression analysis by in-situ hybridisation during the two hour period leading up to scheduled feeding suggested that homeostatic neuropeptide systems in the hypothalamus did not have a major role in driving the consumption of these meals. Further characterisation of the scheduled feeding model revealed that palatable scheduled feeding does not lead to a relative hypophagic phase or an increase in pre-meal secreted gut hormones in anticipation of the scheduled meals. Interestingly, schedule-fed animals exhibited food anticipatory activity during the same period. In addition, scheduled-fed animals displayed only a mild obese phenotype but their metabolic health was adversely affected. Again using in-situ hybridisation, candidate gene expression was assessed during the scheduled feeding period itself, revealing a relationship with adiposity level but not with immediate feeding behaviour. Finally, in a ‘hypothesis-free' approach, gene expression was analysed by microarray at the point of initiation of scheduled feeding, with no apparent changes in gene expression levels. In conclusion, palatable scheduled feeding in mice and rats induces large, binge-type meals that appear not to be directly regulated by homeostatic neuropeptides in the hypothalamus. Investigations into forebrain candidate gene expression by in-situ hybridisation suggested that measuring mRNA levels might not be the optimal analytical approach to demonstrate an involvement of the reward-related signalling system. Alternative strategies for identifying meal feeding mechanisms in the palatable scheduled feeding model could focus on approaches such as neurotransmitter release.