This study adds to the evidence that the work stress–CHD association is causal in nature. We demonstrate, within a population of office staff largely unexposed to physical occupational hazards, a prospective dose–response relation between psychosocial stress at work and CHD over 12 years of follow-up. We confirm, during the same exposure period, the plausibility of the proposed pathways involving behavioural mechanisms, neuroendocrine and autonomic activation, and development of risk factor clustering, represented by the metabolic syndrome. Further, those who are older (and are more likely to be retired and less exposed to work stress) are less susceptible to the work psychosocial effect, presenting a coherent pattern in our findings. This study demonstrates that stress at work can lead to CHD through direct activation of neuroendocrine stress pathways and indirectly through health behaviours.This is part of the Whitehall II study, which I've mentioned before. Long-term, large-scale, prospective studies of this kind are, of course, very welcome. But naturally we'd like to see these balanced by lifelong individual studies, so that we can get beyond the non-specificity of the stress construct.
Thursday, 7 February 2008
More on the health of Whitehall Civil Servants (article, BBC report):