Rationale/statement of the problem : Leukocyte telomere length (LTL), a marker of cellular aging, has been proposed as a pathogenic mechanism by which depression may confer increased risk of adverse cardiovascular events. Prior studies have suggested that depression and depressive symptoms are associated with shorter LTL, but these studies are limited by small sample sizes, selective enrollment of participants (e.g. psychiatric outpatients), and lack of adjustment for cardiovascular risk factors and other covariates. The present study examines the association of LTL with depression and depressive symptoms in a large, populations-based cohort. Methods : Participants included 2225 apparently healthy individuals from the 1995 Nova Scotia Health Survey (NSHS95) population-based study. Depressive symptoms were assessed by the Center for Epidemiological Studies-Depression (CES-D) scale. LTL was assessed by a real-time polymerase chain reaction method. Linear regression analyses were used to examine the association between LTL and depressive symptoms, probable depressive disorder (CES-D ≥ 10 or CES-D ≥ 16), and specific depressive symptom clusters (depressed affect, somatic concerns, positive affect, and interpersonal problems). These analyses were adjusted for clinical and demographic factors thought to potentially confound the association between depression and LTL, including: age, sex, body mass index, Framingham risk score, and previous ischemic heart disease. Results : In an unadjusted model, each 1-point increase on the CES-D was significantly associated with a 3.49 base pair increase in LTL (95% CI = 0.39-6.60, p = 0.03). However, this association was not significant after adjustment for age and sex (B=1.20, 95% CI = − 1.85-4.25, p = 0.44) and further adjustment for other covariates (all p's ≥ 0.37). Neither probable depressive disorder nor specific depressive symptom clusters were independently associated with LTL after adjustment for covariates. Conclusion : Concurrent depressive symptoms were not independently associated with LTL in a large population-based study. These results suggest that the excess risk of cardiovascular disease risk associated with concurrent depression may not be due to accelerated cellular aging.