Psychosocial and vascular risk factors of depression in later life

Abstract

Background: Research on the aetiology of late-life depression has typically focused on either risk factors from the psychosocial stress-vulnerability domain or degenerative biological changes (for instance, vascular disease). We examined whether vascular risk factors could be interpreted within the stress-vulnerability model of depression. Methods: The data came from a case-control design, nested in a community survey of elderly people. We compared 83 persons with a recently started episode of major or minor depression with 83 controls, with respect to the occurrence of stressful life events, long-term difficulties, neuroticism, and vascular risk factors (hypertension, heart disease, stroke). Results: The (non-significant) association of vascular risk factors and onset of depressive episodes was not modified by neuroticism or the presence of long-term difficulties. Quite unexpectedly, vascular risk factors seemed to neutralize the depressogenic effect of stressful life events. The effect of vascular risk was significantly stronger in depressive episodes not preceded by a life event than in onsets following an event. Conclusions: Vascular risk factors cannot be interpreted within the stress-vulnerability model, but represent another pathway to depression. Why vascular risk factors reduce the depressogenic effect of stressful life events is not clear. Replication is critical to exclude the possibility of a chance finding.

Introduction

Late-life depression is a highly heterogeneous syndrome, with a variety of possible risk factors. Some of the risk factors relate to stressful circumstances. Old age is a period of life with a relatively high prevalence of life stress, for instance due to physical disability and handicap, loss of close relationships, and caring for sick relatives (e.g., Beekman et al., 1995, Jorm, 1989, Ormel et al., 1997b, Prince et al., 1998; Roberts et al., 1997, Russo et al., 1995, Schwarz and Blixen, 1997). The occurrence of stressful life events and difficulties has been found to increase the probability of a depressive episode in the elderly (Brilman and Ormel, 2001, Emmerson et al., 1989). Similarly, substantial evidence implicates longstanding vulnerability, both genetically, as indicated by family history (Baldwin and Tomenson, 1995, Brodaty et al., 1991, Maier et al., 1991), and in terms of personality characteristics such as neuroticism (Brodaty et al., 1991, Camus et al., 1997, Hirschfeld et al., 1989, Van den Berg et al., 2000). Not only do these vulnerability factors and life stressors both increase the risk of late-life depression, they seem to interact with each other as well: we found that the depressogenic effect of a stressful life event was larger in the presence of a long-term difficulty and in highly neurotic persons than in the absence of difficulties and/or high neuroticism (Ormel et al., 2001). Collectively, these findings support the psychosocial stress-vulnerability model of depression (Ormel and De Jong, 1999).

Another group of studies reported the potential importance of age-related structural changes in the brain, especially vascular or ischaemic changes, in the aetiology of late-life depression (Alexopoulos et al., 1997a, Alexopoulos et al., 1997b, Baldwin and Tomenson, 1995, Hickie et al., 1995, Krishnan et al., 1997, Reynolds et al., 1998). The frequent comorbidity of depression, vascular disease, and vascular risk factors as well as the association of ischaemic lesions with distinctive behavioural symptoms has led Alexopoulos et al. (1997a) to postulate the ‘vascular depression’ hypothesis, which states that cerebrovascular disease may predispose, precipitate, or perpetuate some geriatric depressive symptoms.

Even in patients with cerebrovascular changes, depression may be multifactorial (Krishnan et al., 1997). Non-biological factors may be required to trigger depression in patients predisposed to depression by ischaemic lesions or a broader cerebrovascular disturbance (Alexopoulos et al., 1997a). However, little is known about the possible interplay of vascular disease and other, non-biological, risk factors in the aetiology of depression in the elderly.

This paper concerns the mutual relationships between psychosocial and vascular risk factors. More specifically, we examined to what extent the vascular risk factors can be interpreted within the psychosocial stress-vulnerability model of depression. Hypothetically, vascular risk factors could be included in the stress-vulnerability model in two ways: as a stressor (comparable to a stressful life event) or, intuitively more appealing, as a vulnerability factor. In the first case, we would expect the depressogenic effect of vascular risk factors, if any, to be augmented by psychological vulnerability (high neuroticism) and/or social vulnerability (long-term difficulties). In the latter case, we would expect vascular risk factors to enhance the association between stressful life events and depressive episodes. In case neither of the two alternatives is supported by the data, vascular risk factors probably represent a pathway that is independent of life stress and psychosocial vulnerability, as suggested by Van den Berg et al. (2001). The independent-pathways hypothesis would be further supported if it could be demonstrated that vascular risk factors play a larger role in the onset of episodes not preceded by a recent stressful life event (out-of-the-blue episodes) than in the onset of episodes following a life event.