Work Stress and Coronary Heart Disease: What Are the Mechanisms?
Work Stress and Coronary Heart Disease: What Are the Mechanisms?
Aims: To determine the biological and behavioural factors linking work stress with coronary heart disease (CHD).
Methods and Results: A total of 10 308 London-based male and female civil servants aged 35–55 at phase 1 (1985–88) of the Whitehall II study were studied. Exposures included work stress (assessed at phases 1 and 2), and outcomes included behavioural risk factors (phase 3), the metabolic syndrome (phase 3), heart rate variability, morning rise in cortisol (phase 7), and incident CHD (phases 2–7) on the basis of CHD death, non-fatal myocardial infarction, or definite angina. Chronic work stress was associated with CHD and this association was stronger among participants aged under 50 (RR 1.68, 95% CI 1.17–2.42). There were similar associations between work stress and low physical activity, poor diet, the metabolic syndrome, its components, and lower heart rate variability. Cross-sectionally, work stress was associated with a higher morning rise in cortisol. Around 32% of the effect of work stress on CHD was attributable to its effect on health behaviours and the metabolic syndrome.
Conclusion: Work stress may be an important determinant of CHD among working-age populations, which is mediated through indirect effects on health behaviours and direct effects on neuroendocrine stress pathways.
Stress at work is associated with an increased risk of coronary heart disease (CHD) but the mechanisms underlying this association remain unclear. Work stress may affect CHD through direct activation of neuroendocrine responses to stressors, or more indirectly through unhealthy behaviours which increase the risk of CHD, such as smoking, lack of exercise, or excessive alcohol consumption. One of the main axes of neuroendocrine stress responses is the autonomic nervous system (ANS). Repeated activation of the ANS is characterized by lowered heart rate variability, which has been associated with work stress among men in cross-sectional studies. Furthermore, work stress may affect dysregulation of the hypothalamic–pituitary–adrenal axis, which is associated with disturbances in the circadian rhythm of cortisol and the development of the metabolic syndrome.
Accumulation of work stress is associated with higher risks of the metabolic syndrome, and incident obesity. However, there are few longitudinal studies examining the effect of cumulative work stress on other intermediate mechanisms, despite evidence that chronic stress predicts cardiovascular mortality and morbidity. It is important to examine cumulative exposures in order to show dose–response relations, which would contribute a causal understanding of the association between work stress and CHD. In addition, there is little longitudinal evidence on the mechanisms by which work stress affects CHD. Stronger associations between work stress and CHD risk among working-age populations would also increase the specificity of this association.
This study addresses the following questions: 1 Is the accumulation of work stress associated with higher risks of incident CHD and risk factors? 2 Is this association stronger among working-age populations? 3 Does work stress affect CHD directly through neuroendocrine mechanisms and/or indirectly through behavioural risk factors for CHD?
Aims: To determine the biological and behavioural factors linking work stress with coronary heart disease (CHD).
Methods and Results: A total of 10 308 London-based male and female civil servants aged 35–55 at phase 1 (1985–88) of the Whitehall II study were studied. Exposures included work stress (assessed at phases 1 and 2), and outcomes included behavioural risk factors (phase 3), the metabolic syndrome (phase 3), heart rate variability, morning rise in cortisol (phase 7), and incident CHD (phases 2–7) on the basis of CHD death, non-fatal myocardial infarction, or definite angina. Chronic work stress was associated with CHD and this association was stronger among participants aged under 50 (RR 1.68, 95% CI 1.17–2.42). There were similar associations between work stress and low physical activity, poor diet, the metabolic syndrome, its components, and lower heart rate variability. Cross-sectionally, work stress was associated with a higher morning rise in cortisol. Around 32% of the effect of work stress on CHD was attributable to its effect on health behaviours and the metabolic syndrome.
Conclusion: Work stress may be an important determinant of CHD among working-age populations, which is mediated through indirect effects on health behaviours and direct effects on neuroendocrine stress pathways.
Stress at work is associated with an increased risk of coronary heart disease (CHD) but the mechanisms underlying this association remain unclear. Work stress may affect CHD through direct activation of neuroendocrine responses to stressors, or more indirectly through unhealthy behaviours which increase the risk of CHD, such as smoking, lack of exercise, or excessive alcohol consumption. One of the main axes of neuroendocrine stress responses is the autonomic nervous system (ANS). Repeated activation of the ANS is characterized by lowered heart rate variability, which has been associated with work stress among men in cross-sectional studies. Furthermore, work stress may affect dysregulation of the hypothalamic–pituitary–adrenal axis, which is associated with disturbances in the circadian rhythm of cortisol and the development of the metabolic syndrome.
Accumulation of work stress is associated with higher risks of the metabolic syndrome, and incident obesity. However, there are few longitudinal studies examining the effect of cumulative work stress on other intermediate mechanisms, despite evidence that chronic stress predicts cardiovascular mortality and morbidity. It is important to examine cumulative exposures in order to show dose–response relations, which would contribute a causal understanding of the association between work stress and CHD. In addition, there is little longitudinal evidence on the mechanisms by which work stress affects CHD. Stronger associations between work stress and CHD risk among working-age populations would also increase the specificity of this association.
This study addresses the following questions: 1 Is the accumulation of work stress associated with higher risks of incident CHD and risk factors? 2 Is this association stronger among working-age populations? 3 Does work stress affect CHD directly through neuroendocrine mechanisms and/or indirectly through behavioural risk factors for CHD?
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