Factors influencing insulin resistance in relation to atherogenicity in mood disorders, the metabolic syndrome and tobacco use disorder.

OBJECTIVE: This study examines the effects of malondialdehyde (MDA) and uric acid on insulin resistance and atherogenicity in subjects with and without mood disorders, the metabolic syndrome (MetS) and tobacco use disorder (TUD). METHODS: We included 314 subjects with depression and bipolar depression, with and without the MetS and TUD and computed insulin resistance using the updated homeostasis model assessment (HOMA2IR) and atherogenicity using the atherogenic index of plasma (AIP), that is log10 (triglycerides/high density lipoprotein (HDL) cholesterol. RESULTS: HOMA2IR is correlated with body mass index (BMI) and uric acid levels, but not with mood disorders and TUD, while the AIP is positively associated with BMI, mood disorders, TUD, uric acid, MDA and male sex. Uric acid is positively associated with insulin and triglycerides and negatively with HDL cholesterol. MDA is positively associated with triglyceride levels. Comorbid mood disorders and TUD further increase AIP but not insulin resistance. Glucose is positively associated with increasing age, male gender and BMI. DISCUSSION: The results show that mood disorders, TUD and BMI together with elevated levels of uric acid and MDA independently contribute to increased atherogenic potential, while BMI and uric acid are risk factors for insulin resistance. The findings show that mood disorders and TUD are closely related to an increased atherogenic potential but not to insulin resistance or the MetS. Increased uric acid is a highly significant risk factor for insulin resistance and increased atherogenic potential. MDA, a marker of lipid peroxidation, further contributes to different aspects of the atherogenic potential. Mood disorders and TUD increase triglyceride levels, lower HDL cholesterol and are strongly associated with the atherogenic, but not insulin resistance, component of the MetS.

Oxidative stress and inflammatory markers are associated with depression and nicotine dependence.

To determine if oxidative stress and inflammation are linked with major depressive disorder, nicotine dependence and both disorders combined. This study comprised 150 smokers and 191 never smokers. The instruments were: a socio-demographic questionnaire, diagnoses of mood disorder and nicotine dependence according to DSM-IV, (SCID-IV), and the Alcohol, Smoking and Substance Involvement Screening Test. Laboratory assessments included: nitric oxide metabolites (NOx), lipid hydroperoxides, malondialdehyde (MDA), total reactive antioxidant potential (TRAP), advanced oxidation protein products (AOPP), fibrinogen concentrations, homocysteine, erythrocytes sedimentation rate (ESR) and high-sensitivity C-reactive protein (hs-CRP) were assayed from blood specimens. Statistically significant differences were found among depressed smokers who had more severe depressive symptoms, a higher risk of alcohol consumption, more suicide attempts, and more disability for work than non-depressed never smokers. Depressed smokers had significantly higher levels of NOx, fibrinogen, hs-CRP, AOPP, ESR and lower levels of TRAP compared to non-depressed never smokers. Depressed smokers had significant levels of oxidative stress and inflammatory biomarkers after adjusting for gender, age, years of education, disability for work, and laboratory measures. The levels of NOx, lipid hydroperoxides, AOPP, and fibrinogen were substantially higher, whereas levels of TRAP were lower in depressed smokers compared to non-depressed never smokers. (1) Depressed smokers exhibited altered concentrations of NOx, lipid hydroperoxides, AOPP, TRAP, and fibrinogen. (2) Depressed smokers were more unable to work, showed more severe depressive symptoms and attempted suicide more frequently.

A comparison of inflammatory markers in depressed and nondepressed smokers.

INTRODUCTION: Both smoking and depression have been associated with increased inflammatory markers. As there are few studies on inflammatory markers that distinguish between depressed and nondepressed smokers, it is unclear if there is a cumulative impact of these mediators of inflammation. The aim of this study was to investigate inflammatory markers in tobacco smokers and compare depressed and nondepressed smokers. METHODS: Smokers (n = 155) were recruited from the Cigarette Smoking Cessation Service, Londrina. Mental health status was assessed using the Diagnostic Interview for Research, in accordance with the International Classification of the Disorders-10th (ICD-10). Demographic information was collected by self-report questionnaire, and the Fagerström Test for Nicotine Dependence was administered. Blood specimens were simultaneously collected and measured for C-reactive protein (hs-CRP), tumor necrosis factor-alpha (TNF-α), and interleukin-6 (IL-6). RESULTS: Depressed smokers had significantly higher levels of hs-CRP (p = .05), IL-6 (p = .039), and TNF-α (p = .021) compared with nondepressed smokers. Depressed smokers were also significantly more likely than nondepressed smokers to have been hospitalized in the previous month (p < .032), to suffer from cardiovascular disease (p < .001) and lung disease (p < .003), and to have more work-related disability (p = .001). CONCLUSIONS: These findings demonstrate that depressed smokers had higher hs-CRP, IL-6, and TNF-α levels than nondepressed smokers and had worse physical health outcomes and greater work-related disability. This may have important implications in identifying shared risk pathways for depressive and somatic disorders.