Prevention Of Late-life Depression Research Articles

Prevention of Late-Life Depression in Primary Care: Do We Know Where to Begin?

This study attempted to compare two models for selective (people at elevated risk) and indicated (those with subsyndromal depressive symptoms) prevention and to determine the optimal strategy for prevention of late-life depression. Onset was assessed at 3 years with the Geriatric Mental State AGECAT in a randomly selected cohort of 1,940 nondepressed and nondemented older people in Amsterdam. Risk factors that can easily be identified in primary care were used. The association of risk factors with depression incidence was expressed in absolute and relative risk estimates, number needed to treat, and population-attributable fractions. Prevention models were identified with classification and regression tree analyses. In the indicated prevention model, subsyndromal symptoms of depression were associated with a risk of almost 40% of developing depression and a number needed to treat of 5.8, accounting for 24.6% of new cases. Adding more risk factors raised the absolute risk to 49.3%, with a lower number needed to treat but also lower attributable fraction values. In the selective prevention model, spousal death showed the highest risk, becoming even higher if the subjects also had a chronic illness. Overall, the attributable fraction values in the indicated model were higher, identifying more people at risk. Consideration of the costs and benefits of both models in the context of the availability of evidence-based preventative interventions indicated that prevention aimed at elderly people with depressive symptoms is preferred. The focus on treatment should be readdressed; a new approach is needed, with a stronger emphasis on prevention.

Prevention of Late-Life Depression in Primary Care: Do We Know Where to Begin?

Prevention of Late-Life Depression in Primary Care: Do We Know Where to Begin?

Depression in late‐life: shifting the paradigm from treatment to prevention

Late-life depression is very common and is associated with high rates of morbidity and mortality. While the field of geriatric psychiatry is focused on depression treatment, prevention is an enticing option. Prevention of late-life depression would decrease both emotional suffering and depression-associated morbidity and mortality and may decrease dependence on non-mental health professionals to detect depression and to initiate a treatment referral. This paper will review current thinking on prevention research with a particular focus on its application to late-life depression. To illustrate these issues, we discuss recent and ongoing clinical trials of interventions to prevent depression in two populations of older persons: those with age-related macular degeneration (AMD) and those with cerebrovascular disease.

Opportunities for Cost-effective Prevention of Late-Life Depression

Clinically relevant late-life depression has a prevalence of 16% and is associated with substantial societal costs through its disease burden and unfavorable prognosis. From the public health perspective, depression prevention may be an attractive, if not imperative, means to generate health gains and reduce future costs. To target high-risk groups for depression prevention such that maximum health gains are generated against the lowest cost. Population-based cohort study over 3 years. General population in the Netherlands. Twenty-two hundred community residents aged 55 to 85 years. Of these, 1925 were not depressed at baseline. The onset of clinically relevant depression was measured with the Center for Epidemiological Studies Depression Scale. For each of the risk factors (and their combinations), we calculated indices of potential health gain and the effort (costs) required to generate those health gains. One in every 5 cases of clinically relevant late-life depression is a new case. Consequently, depression prevention has to play a key role in reducing the influx of new cases. This is best done by directing prevention efforts toward elderly people who have depressive symptoms, experience functional impairment, and have a small social network, in particular women, as well as people who have attained only a low educational level or who suffer from chronic diseases. Directing prevention efforts toward selected high-risk groups could help reduce the incidence of depression and is likely to be more cost-effective than alternative approaches. This article further shows that we have the methodology at our disposal to conduct ante hoc cost-benefit analysis in preventive psychiatry. This helps set a rational research and development agenda before testing the cost-effectiveness of interventions in time-consuming and expensive trials.

C-Reactive Protein and Cerebral Small-Vessel Disease

Stroke places a large burden on healthcare and social services resources in the older adult population. Because the incidence of stroke increases with advancing age, and the population is aging, the number of patients affected by stroke is increasing. See p 900 The burden of stroke goes well beyond those cases that are clinically recognized. Imaging techniques of the brain have revealed a remarkably high prevalence of white matter lesions (WML) and silent brain lacunar infarcts (SBLI). In the National Heart, Lung, and Blood Institute–sponsored Cardiovascular Health Study, SBLI ≥3 mm were found in 31% of all subjects.1 Fewer than 15% of patients with such lesions had a clinical history of stroke. The prevalence of SBLI increased with advancing age; 22% of subjects 65 to 69 years old had SBLI, as compared with 43% in subjects ≥80 years old. WML involving in particular the centrum ovale are a subject of great interest. Partly this is because modern neuroimaging methods detect subcortical WM changes with increasing frequency in people >60 years old and also because these abnormalities may be associated with specific neurobehavioral deficits, including dementing syndromes.2 The descriptive term leukoaraiosis (LA), frequently applied to these neuroimaging abnormalities of the WM, refers to bilateral and either patchy or diffuse areas of hypodensity on CT or hyperintensity on T2-weighted MRI.3 In this issue of Circulation , van Dijk and colleagues4 explore the relationship of C-reactive protein (CRP), a well-known systemic marker of inflammation, with the severity and progression of cerebral WML/LA on MRI scans. The investigators examined the prevalence and incidence of brain WML/LA and SBLI in the prospective cohort of 1033 older adult participants of the population-based Rotterdam Scan study. They confirmed a relationship between inflammation and the severity and progression of cerebral WML/LA and SBLI independent …

A prospective population-based cohort study of the effects of disablement and social milieu on the onset and maintenance of late-life depression. The Gospel Oak Project VII.

Population-based studies suggest substantial co-morbidity between physical illness and depression in late-life. However, a causal relationship has not been established. If a relationship exists, it is important to establish which aspects of poor health determine risk for depression, and which factors confer vulnerability or resilience in the face of poor health. We investigate the role of disablement, measured as impairment, disability and handicap. A prospective population-based cohort study, comprising an index assessment and 1 year follow-up, of all residents aged 65 years or over, of an electoral ward in London, UK (N = 889). The prevalence of SHORT-CARE pervasive depression was 17.7% at index assessment. The 1 year onset rate for pervasive depression was 12.0%, and the 1 year maintenance rate 63.2%. There was a high mortality rate among the depressed. Disablement, particularly handicap was the most important predictor of the onset of depression (population attributable fraction, 0.69). Lack of contact with friends was a direct risk factor but also modified the association between handicap and depression. Marriage was protective for men, but a risk factor for women. Maintenance of depression was predicted by low levels of social support and social participation, rather than by disablement. It seems likely that disablement, specifically handicap, is the chief cause of onsets of depression in late-life. Genetic predisposition, early adversity and serious life events may play a less prominent role than in earlier life. Effective prevention of late-life depression requires attention at the structural level to the sources of handicap within communities.