Atypical depression and double depression predict new-onset cardiovascular disease in U.S. adults.

BACKGROUND: Although depression is a risk factor for cardiovascular disease (CVD), it is unknown whether this risk varies across depressive disorder subtypes. Thus, we investigated atypical major depressive disorder (MDD) and double depression as predictors of new-onset CVD in a nationally representative sample of U.S. adults. METHODS: Prospective data from 28,726 adults initially free of CVD who participated in Wave 1 (2001-2002) and Wave 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions (NESARC) were examined. Lifetime depressive disorder subtypes (Wave 1) and incident CVD (Wave 2) were determined by structured interviews. RESULTS: We identified 1,116 incident CVD cases. In demographics adjusted models, the atypical MDD group had a higher odds of incident CVD than the no depression history (OR = 2.19, 95% CI: 1.71-2.81, P < .001), dysthymic disorder only (OR = 1.61, 95% CI: 1.08-2.39, P = .019), and nonatypical MDD (OR = 1.46, 95% CI: 1.11-1.91, P = .006) groups. Likewise, the double depression group had a higher odds of incident CVD than the no depression history (OR = 2.17, 95% CI: 1.92-2.45, P < .001), dysthymic disorder only (OR = 1.59, 95% CI: 1.16-2.19, P = .004), and MDD only (OR = 1.46, 95% CI: 1.20-1.77, P < .001) groups. Relationships were similar but attenuated after adjustment for CVD risk factors and anxiety disorders. CONCLUSIONS: Adults with atypical MDD or double depression may be subgroups of the depressed population at particularly high risk of new-onset CVD. Thus, these subgroups may (a) be driving the overall depression-CVD relationship and (b) be in need of earlier and/or more intense CVD primary prevention efforts to reduce their excess CVD burden.

Race/ethnicity moderates the relationship between depressive symptom severity and C-reactive protein: 2005-2010 NHANES data.

Because few studies have examined depression facets or potential moderators of the depression-inflammation relationship, our aims were to determine whether particular depressive symptom clusters are more strongly associated with C-reactive protein (CRP) levels and whether race/ethnicity moderates these relationships. We examined data from 10,149 adults representative of the U.S. population (4858 non-Hispanic White, 1978 non-Hispanic Black, 2260 Mexican American, 1053 Other Hispanic) who participated in the cross-sectional National Health and Nutrition Examination Survey between 2005 and 2010. Depressive symptoms were assessed by the Patient Health Questionnaire-9, and high-sensitivity serum CRP was quantified by latex-enhanced nephelometry. Total (p<.001), somatic (p<.001), and nonsomatic (p=.001) depressive symptoms were each positively related to serum CRP in individual models. However, in the simultaneous model that included both symptom clusters, somatic symptoms (p<.001), but not nonsomatic symptoms (p=.98), remained associated with serum CRP. Evidence of moderation by race/ethnicity was also observed, as six of the nine depressive symptoms×race/ethnicity interactions were significant (ps<.05). Among non-Hispanic Whites, the pattern of results was identical to the full sample; only somatic symptoms (p<.001) remained related to serum CRP in the simultaneous model. No relationships between total, somatic, or nonsomatic symptoms and serum CRP were observed among the non-Hispanic Black, Mexican American, or Other Hispanic groups. Our findings indicate that the link between depressive symptoms and systemic inflammation may be due to the somatic symptoms of sleep disturbance, fatigue, appetite changes, and psychomotor retardation/agitation and may be strongest among non-Hispanic Whites.