Objective The aim of the study was to evaluate associations between 15-year trajectories of co-occurring depressive symptoms and smoking with biomarkers of cardiovascular disease at year 15. Methods In the Coronary Artery Risk Development in Young Adults study, we modeled trajectories of depressive symptoms (Center for Epidemiologic Studies-Depression scale [CES-D]) and smoking (cigarettes per day [CPD]) among 3614 adults followed from year 0 (ages 18-30 years) through year 15 (ages 33-45 years). Biomarkers of inflammation (high-sensitivity C-reactive protein), oxidative stress (superoxide dismutase, F2-isoprostanes), and endothelial dysfunction (soluble intercellular adhesion molecule 1, soluble P-selectin) were assessed at year 15. We conducted separate linear regression analyses with CES-D trajectory, CPD trajectory, and their interaction with each of the five biomarkers. Results The sample was 56% women, 47% black, and 40 years old on average at year 15. The CES-D trajectory by CPD trajectory interaction was not associated with any of the biomarkers (all p's >.01). Removing the interaction term, CES-D trajectory was associated with inflammation: higher levels of high-sensitivity C-reactive protein were observed in the subthreshold (β = 0.57, p =.004) and increasing depressive symptoms (β = 1.36, p <.001) trajectories compared with the no depression trajectory. CPD trajectory was associated with oxidative stress and endothelial dysfunction: compared with never smokers, heavy smokers had significantly higher levels of F2-isoprostanes (β = 6.20, p =.001), soluble intercellular adhesion molecule 1 (β = 24.98, p <.001), and soluble P-selectin (β = 2.91, p <.001). Conclusions Co-occurring depressive symptoms and smoking do not seem to synergistically convey risk for cardiovascular disease via processes of inflammation, oxidative stress, or endothelial dysfunction. Nonetheless, these results advance our understanding of the complex relationships between modifiable risk factors and chronic disease.
Bibliographical noteFunding Information:
Source of Funding and Conflicts of Interest: The CARDIA is supported by the National Heart, Lung, and Blood Institute in collaboration with the University of Alabama at Birmingham (HHSN268201300025C, HHSN268201300026C), Northwestern University (HHSN268201300027C), University of Minnesota (HHSN268201300028C), Kaiser Foundation Research Institute (HHSN268201300029C), and Johns Hopkins University School of Medicine (HHSN268200900041C). Several biochemical analyses were supported by a grant to D.R.J. (R01 HL53560). A.J.C. was supported by a Predoctoral Individual National Research Service Award from National Heart, Lung, and Blood Institute (F31 HL129494). The funding agency had no role in the design and conduct of the study; collection, management, analysis, and interpretation of the data; and preparation, review, or approval of this article. M.D.H. is supported by the World Heart Federation to serve as its senior program advisor for the Emerging Leaders program, which is supported by unrestricted educational grants from Boehringer Ingelheim and Novartis with previous support from BUPA and AstraZeneca.
- Cardiovascular disease
- endothelial dysfunction
- oxidative stress
PubMed: MeSH publication types
- Journal Article
- Research Support, N.I.H., Extramural
- Research Support, Non-U.S. Gov't