Background: Several mechanisms underlying the depression-to-cardiovascular disease (CVD) relationship have been proposed; however, few studies have examined whether depression promotes CVD through potentiating traditional cardiovascular risk factors. Purpose: To test the combined influence of three cardiovascular risk factors and lifetime depressive disorder on incident CVD in a large, diverse, and nationally representative sample of U.S. adults. Methods: Respondents were 26,840 adults without baseline CVD who participated in Waves 1 (2001-2002) and 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions. Lifetime depressive disorder, tobacco use, hypertension, and incident CVD were determined from structured interviews, and body mass index (BMI) was computed from self-reported height and weight. Results: Logistic regression models predicting incident CVD (1,046 cases) revealed evidence of moderation, as the interactions between lifetime depressive disorder and current tobacco use (p = .002), hypertension (p < .001), and BMI (p = .031) were significant. The Former Tobacco Use × Lifetime Depressive Disorder interaction was not significant (p = .85). In models stratified by lifetime depressive disorder, current tobacco use (OR = 1.78, 95% CI = 1.36-2.32, p < .001 vs. OR = 1.41, 95% CI = 1.24-1.60, p < .001), hypertension (OR = 2.46, 95% CI = 1.98-3.07, p < .001 vs. OR = 1.39, 95% CI = 1.28-1.51, p < .001), and BMI (OR = 1.10, 95% CI = 1.01-1.20, p = .031 vs. OR = 1.03, 95% CI = 0.99-1.07, p = .16) were stronger predictors of incident CVD in adults with versus without a lifetime depressive disorder. Conclusions: Our findings suggest that amplifying the atherogenic effects of traditional cardiovascular risk factors may be yet another candidate mechanism that helps to explain the excess CVD risk of people with depression.
Background: Several mechanisms underlying the depression-to-cardiovascular disease (CVD) relationship have been proposed; however, few studies have examined whether depression promotes CVD through potentiating traditional cardiovascular risk factors. Purpose: To test the combined influence of three cardiovascular risk factors and lifetime depressive disorder on incident CVD in a large, diverse, and nationally representative sample of U.S. adults. Methods: Respondents were 26,840 adults without baseline CVD who participated in Waves 1 (2001-2002) and 2 (2004-2005) of the National Epidemiologic Survey on Alcohol and Related Conditions. Lifetime depressive disorder, tobacco use, hypertension, and incident CVD were determined from structured interviews, and body mass index (BMI) was computed from self-reported height and weight. Results: Logistic regression models predicting incident CVD (1,046 cases) revealed evidence of moderation, as the interactions between lifetime depressive disorder and current tobacco use (p = .002), hypertension (p < .001), and BMI (p = .031) were significant. The Former Tobacco Use × Lifetime Depressive Disorder interaction was not significant (p = .85). In models stratified by lifetime depressive disorder, current tobacco use (OR = 1.78, 95% CI = 1.36-2.32, p < .001 vs. OR = 1.41, 95% CI = 1.24-1.60, p < .001), hypertension (OR = 2.46, 95% CI = 1.98-3.07, p < .001 vs. OR = 1.39, 95% CI = 1.28-1.51, p < .001), and BMI (OR = 1.10, 95% CI = 1.01-1.20, p = .031 vs. OR = 1.03, 95% CI = 0.99-1.07, p = .16) were stronger predictors of incident CVD in adults with versus without a lifetime depressive disorder. Conclusions: Our findings suggest that amplifying the atherogenic effects of traditional cardiovascular risk factors may be yet another candidate mechanism that helps to explain the excess CVD risk of people with depression.
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