Theses and Dissertations
This collection includes both ASU Theses and Dissertations, submitted by graduate students, and the Barrett, Honors College theses submitted by undergraduate students.
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Description
Fibromyalgia (FM) is a chronic musculoskeletal disorder characterized by widespread pain, fatigue, and a variety of other comorbid physiological and psychological characteristics, including a deficit of positive affect. Recently, the focus of research on the pathophysiology of FM has considered the role of a number of genomic variants. In the current manuscript, case-control analyses did not support the hypothesis that FM patients would differ from other chronic pain groups in catechol-O-methyltransferase (COMT) and mu-opioid receptor (OPRM1) genotype. However, evidence is provided in support of the hypothesis that functional single nucleotide polymorphisms on the COMT and OPRM1 genes would be associated with risk and resilience, respectively, in a dual processing model of pain-related positive affective regulation in FM. Forty-six female patients with a physician-confirmed diagnosis of FM completed an electronic diary that included once-daily assessments of positive affect and soft tissue pain. Multilevel modeling yielded a significant gene X environment interaction, such that individuals with met/met genotype on COMT experienced a greater decline in positive affect as daily pain increased than did either val/met or val/val individuals. A gene X environment interaction for OPRM1 also emerged, indicating that individuals with at least one asp allele were more resilient to elevations in daily pain than those homozygous for the asn allele. In sum, the findings offer researchers ample reason to further investigate the contribution of the catecholamine and opioid systems, and their associated genomic variants, to the still poorly understood experience of FM.
ContributorsFinan, Patrick Hamilton (Author) / Zautra, Alex (Thesis advisor) / Davis, Mary (Committee member) / Lemery-Chalfant, Kathryn (Committee member) / Presson, Clark (Committee member) / Arizona State University (Publisher)
Created2011
Description
Adverse childhood family environments have been found to have long-term effects on a child's well-being. Although no prior studies have examined the direct effects of childhood family adversities on nighttime blood pressure (BP) dip, parental death and divorce in childhood, have been associated with a variety of related psychological problems in adulthood. The current study examined the direct effects of parental death and divorce in childhood and quality of early family relationships on adult nighttime BP dip as well as the mediating role of three psychosocial factors (depression, hostility and social stress). One hundred and forty-three young adults were asked to complete self-reported measures of the three psychosocial factors and quality of family relationships. Study participants wore an ambulatory blood pressure (ABP) monitor over a 24-hr period in order to assess nocturnal BP dip. Although neither childhood family adversity nor quality of childhood family relationships directly predicted nighttime BP dipping, quality of early family relationships predicted all three psychosocial factors, and hostility was found to mediate the relationship between quality of childhood family relationships and nighttime systolic BP dip. Early family experiences play an important role in influencing nighttime cardiovascular functioning by influencing an individual's psychological functioning in young adulthood. Because nighttime non-dipping has been associated with increased risk for cardiovascular disease and other serious health conditions, the results of the present study have important clinical implications and provide specific psychosocial pathways that may be targeted in future programs designed to prevent and treat cardiovascular disease.
ContributorsTanaka, Rika (Author) / Luecken, Linda J. (Thesis advisor) / Wolchik, Sharlene (Committee member) / Davis, Mary (Committee member) / Arizona State University (Publisher)
Created2012