Publication | Open Access
Work stress and coronary heart disease: what are the mechanisms?
665
Citations
30
References
2008
Year
Work stress is a key determinant of coronary heart disease in working‑age adults, acting through both behavioural changes and neuroendocrine stress pathways. The study aimed to identify the biological and behavioural mechanisms linking work stress to coronary heart disease. Researchers followed 10,308 Whitehall II civil servants, measuring work stress, behavioural risk factors, metabolic syndrome, heart rate variability, cortisol rise, and incident CHD across multiple phases. Chronic work stress increased CHD risk (RR 1.68 in those under 50) and was associated with low physical activity, poor diet, metabolic syndrome, reduced heart rate variability, and higher morning cortisol, with about 32 % of the effect mediated by health behaviours and metabolic syndrome.
To determine the biological and behavioural factors linking work stress with coronary heart disease (CHD).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.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.
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