Cardiovascular diseases (CVDs) and depression are globally prevalent health concerns with substantial impacts. CVDs, including ischemic heart disease and stroke, rank among the leading global health burdens (WTO, 2023). Research indicates a high rate of comorbidity between CVD and depression (Karami et al., 2023; Rafiei et al., 2023), with the onset of CVD significantly increasing the risk of depression (Whooley & Wong, 2013). Conversely, depression elevates CVD risk by 1.5 times and doubles to triples the incidence of cardiac events in individuals with coronary artery disease (Frasure-Smith & Lesperance, 2009; Goldston & Baillie, 2008; Rudisch & Nemeroff, 2003; Van der Kooy et al., 2007). However, it remains unclear how adolescent depression contributes to heightened cardiovascular risk in adulthood, as defined by indicators such as BMI, HDL (high-density lipoprotein cholesterol), total cholesterol and systolic blood pressure (SBP).
Emerging evidence suggests that inflammation may be a common biological mechanism underlying the comorbidity of depression and CVD (Chen et al., 2018; Shao et al., 2020). Recent research has identified 185 genes significantly associated with both depression and coronary artery disease (CAD), many of which are linked to inflammatory and cardiomyopathic phenotypes (Singh et al., 2024). Our current research (in progress, 2024) has identified several inflammatory biomarkers—such as CRP/hs-CRP, IL-6, and TNF-α—that are shared between depression and CVD.
This study aims to (1) test the hypothesis that adolescent depression predicts an elevated cardiovascular risk in adulthood, (2) map the trajectory of cardiovascular risk factors from adolescence to adulthood, and (3) investigate how changes in inflammation, as indicated by inflammatory biomarkers and DNA methylation, influence the progression of cardiovascular risk factors in both depressed and non-depressed groups.