Dissertation
Structural equation modeling of the metabolic syndrome
Washington State University
Doctor of Philosophy (PhD), Washington State University
08/2011
DOI:
https://doi.org/10.7273/000006014
Abstract
Visceral adiposity, atherogenic dyslipidaemia, glucose intolerance, and hypertension are all well-established atherosclerotic cardiovascular disease risk factors that commonly cluster in the same individual, suggesting the existence of a syndrome. The syndrome has been criticized sharply for its confusing definitions, questionable predictive ability, and unclear pathophysiology. This study employed path analyses to elucidate the causal relationships among the syndrome variables. Four hypotheses about different origins of the syndrome were examined, and the results supported the hypothesis that obesity has the central role in the development of the metabolic syndrome clustering, which includes hypertension, elevated fasting glucose, increased triglycerides, and high high-density lipoprotein cholesterol (HDL-C) concentrations. The findings also suggested that fasting glucose and C-reactive protein (CRP) partially mediate the influence of obesity on the above-mentioned metabolic abnormalities. The results showed that fasting glucose was inversely related only with HDL-C, and not with any of the other abnormalities. The results of the analyses also showed that CRP partially mediated the effect of obesity on blood pressure and dyslipidaemia.
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Details
- Title
- Structural equation modeling of the metabolic syndrome
- Creators
- Virginia Ferent
- Contributors
- G. Leonard Burns (Co-Chair)BRUCE ROBERT WRIGHT (Co-Chair)PAUL H. KWON (Committee Member)
- Awarding Institution
- Washington State University
- Academic Unit
- Department of Psychology
- Theses and Dissertations
- Doctor of Philosophy (PhD), Washington State University
- Publisher
- Washington State University
- Number of pages
- 68
- Identifiers
- 99901055122101842
- Language
- English
- Resource Type
- Dissertation