Key result
Self-reported stress was associated with increased all-cause mortality over 20 years, though this relationship may be confounded by personality, coping styles, and common mental disorders.
This commentary emphasizes the need for life course epidemiologic research to understand whether stress directly causes mortality or shares common causal pathways.
In this issue of the Journal, Nielsen et al. (Am J Epidemiol 2008;168:481−91) use data from a large Danish study to provide evidence that self-reported stress is associated with increased all-cause mortality over the next 20 years. The finding is remarkable. In this commentary, the authors explore what is really meant by stress; they argue that it would be naïve to view stress as reported in this way, with some external exposure. It has to be seen through the lens of the participant's personal experience, and this lens is likely to be clouded by personality, coping styles, and the common mental disorders—depression and anxiety. The authors discuss a wider literature concerning similar findings associating depression with mortality, suggesting three broad reasons for the association. First, the findings might be explained by the impact of stress or distress on well-established risk factors for cardiovascular disease and cancer. Second, there might be direct, underlying psychosomatic pathways by which stress or distress can affect immune or autonomic function. Third, there might be common causal pathways—shared genes or early adversities that predict both stress and mortality from other causes independently. The authors suggest that life course epidemiologic research is required to test these competing hypotheses.
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Hotopf et al. (2008) conducted an editorial in Stress. Self-reported stress was evaluated on All-cause mortality. Self-reported stress was associated with increased all-cause mortality over 20 years, though this relationship may be confounded by personality, coping styles, and common mental disorders.
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