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• W2079280419 abstract "Objective The objective of this study was to examine two competing hypotheses as they relate to the relationship between vascular and psychosocial risk factors for late-life depression. The stress–vulnerability hypothesis predicts that the depressogenic effect of psychosocial risk is stronger in the presence of cardiovascular risk factors (CVRFs). The other predicts that psychosocial risk factors and vascular risk factors are independent pathways to depression and that there is no combined effect of vascular risk factors and life stress. Method This study consisted of a longitudinal design (baseline, six-, and 12-month follow-up) predicting new episodes of significant depressive symptoms (CES-D >16) in 1,474 community-dwelling elders with low levels of depression at baseline (CES-D <8). Results There was a significant interaction between stress at wave 2 and CVRFs at baseline such that stress was a stronger predictor of wave 2 depression in participants who had two or more CVRFs. There was no evidence that CVRFs played a larger role in depression not preceded by a stressful life event than in depression that was preceded by a stressful life event. Conclusions The depressogenic effect of stress was stronger in the presence of significant vascular risk (CVRFs). Vascular risk may increase one's vulnerability to depression by exacerbating the impact of stress on depression. One hypothesis for this finding is that vascular disease disrupts mood regulation circuits in the brain, which decrease its ability to respond to stressful events. The objective of this study was to examine two competing hypotheses as they relate to the relationship between vascular and psychosocial risk factors for late-life depression. The stress–vulnerability hypothesis predicts that the depressogenic effect of psychosocial risk is stronger in the presence of cardiovascular risk factors (CVRFs). The other predicts that psychosocial risk factors and vascular risk factors are independent pathways to depression and that there is no combined effect of vascular risk factors and life stress. This study consisted of a longitudinal design (baseline, six-, and 12-month follow-up) predicting new episodes of significant depressive symptoms (CES-D >16) in 1,474 community-dwelling elders with low levels of depression at baseline (CES-D <8). There was a significant interaction between stress at wave 2 and CVRFs at baseline such that stress was a stronger predictor of wave 2 depression in participants who had two or more CVRFs. There was no evidence that CVRFs played a larger role in depression not preceded by a stressful life event than in depression that was preceded by a stressful life event. The depressogenic effect of stress was stronger in the presence of significant vascular risk (CVRFs). Vascular risk may increase one's vulnerability to depression by exacerbating the impact of stress on depression. One hypothesis for this finding is that vascular disease disrupts mood regulation circuits in the brain, which decrease its ability to respond to stressful events." @default.
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• W2079280419 date "2006-01-01" @default.
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• W2079280419 title "Psychosocial and Vascular Risk Factors for Depression in the Elderly" @default.
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• W2079280419 doi "https://doi.org/10.1097/01.jgp.0000192504.48810.cb" @default.
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