AIMS
The long-term depressive symptoms trajectories across the transition to diagnosed cardiovascular disease (CVD) remain poorly characterized. We aimed to investigate trajectories of depressive symptoms before and after incident CVD in multinational aging populations.
METHODS AND RESULTS
In this multicohort study, we analyzed longitudinal data from the Health and Retirement Study (HRS, 2002-2018), English Longitudinal Study of Ageing (ELSA, 2002-2019), and China Health and Retirement Longitudinal Study (CHARLS, 2011-2018). Depressive symptoms were measured biennially by the 8-item (HRS and ELSA) and 10-item (CHARLS) Centre for Epidemiological Studies Depression scale and standardized to Z-scores. Incident CVD was ascertained by medical history. Data were analyzed using discontinuous growth curve modeling and pooled using meta-analysis. Among 28 704 included participants (mean [SD] age, 62.3 [9.8] years; 43.4% male), 7363 developed CVD during follow-up. Participants who developed CVD had higher levels of depressive symptoms than those without CVD (pooled β [95% confidence interval]: 0.161 SD [0.086-0.236]). A significant increase in depressive symptoms scores was observed around the time of CVD diagnosis (pooled β: 0.089 SD [0.060-0.118]). Additionally, depressive symptoms scores increased both in the years preceding CVD onset (pooled β: 0.007 SD/year [0.004-0.010]) and following diagnosis (pooled β: 0.009 SD/year [0.004-0.013]).
CONCLUSION
Depressive symptoms show a gradual increase before CVD diagnosis, elevate further around the time of diagnosis, and continue to worsen thereafter. These findings call for the integration of mental health screening and management into CVD care at all stages, from primary prevention to long-term disease management.
Jiao Wang, Zhi-Yuan Wu, Xin-Ye Zou et al.· European Journal of Preventi...· 0 citations
Accumulating evidence has suggested that depression is associated with an increased risk of Parkinson’s disease (PD), yet whether pre-clinical depressive symptoms in PD development and the potential mediating effects of metabolomic profiles remain unclear. We aimed to examine the association between depressive symptoms and PD risk, evaluate effect modification by genetic susceptibility, and assess metabolomic mediation. This prospective study included 451,922 PD-free participants from the UK Biobank. Depressive symptoms were collected by a 2-item Patient Health Questionnaire (range, 0–6; ≥3 indicates possible depressive disorder) at baseline. Identification of PD was based on medical records. PD-related polygenic risk score (PRS
PD
), which incorporates established genes for PD based on external GWAS meta-analyses, was tertiled as low, moderate, and high. Baseline plasma metabolites were quantified via NMR spectroscopy from blood samples. Data were analyzed using Cox regression. Over a median follow-up of 14.6 years, 3108 (0.7%) participants developed PD. Higher depressive symptom severity showed linear association with PD risk (hazard ratio [HR]: 1.11, 95% confidence interval: 1.07–1.15). Participants with possible depressive disorder had 36% higher PD risk (HR: 1.36, 1.15–1.61). Those with both possible depressive disorder and high genetic risk had the highest PD risk (HR 2.15, 1.74–2.65;
P
for interaction = 0.028). Metabolomic signature, incorporating fatty acids and lipoproteins, accounted for 15% (model-based proportion) of the depressive symptoms-PD association. Pre-clinical depressive symptoms are associated with a moderately increased risk of PD, particularly among people with a high genetic susceptibility to PD. Metabolomic profiles account for a significant portion of this relationship.
