Psychological depression and LDL-oxidation: Examining the physiology of depression and atherosclerosis
Cardiovascular disease is the leading cause of death in Western industrialized countries and atherosclerotic plaque formation is involved in most forms of this classification of diseases. In addition, results from epidemiological research have implicated psychological depression as an independent risk factor for cardiovascular disease. Despite this, the biological processes linking depression and cardiovascular disease are poorly understood. The purpose of this study was to examine the potential role of low-density lipoprotein oxidation as a mechanistic factor between depression and atherosclerosis. Fifty-one participants were recruited from undergraduate psychology and SRS classes at the University of Southern Mississippi. Participants were initially screened for confounding factors that could affect lipid oxidation such as smoking and a family history of heart disease or stroke. Thirty participants remained after this screening process. Each remaining participant completed the Depression Anxiety Stress Scale-Trait (DASS-T) and donated a 7m1 blood sample. Depression scores for the sample ranged from no symptoms of depression to moderate symptoms. A TBARS assay was conducted on LDL precipitated from the sample, and on serum from the sample. The relationship between depression scores and LDL TBARS was examined using a hierarchical multiple linear regression analysis. Body mass index was entered into the equation first to statistically control for the relationship between body mass index and oxidative stress. This regression analysis was repeated with depression scores and serum TBARS. Finally, a dependent sample t test was used to compare the correlation coefficients found in the two hierarchical regressions. A statistically significant relationship was not found between depression scores and either serum TBARS (r = .00) or LDL TBARS ( r = .00), and the difference in the correlation coefficients from the hierarchical regressions was not statistically significant. The results of this study did not support the existence of a relationship between depression scores as measured by the DASS-T and oxidative processes. This may indicate that oxidative stress is not a primary mechanism linking depression and atherosclerosis or that this mechanism is not activated at mild to moderate levels of depression as measured by the DASS-T.