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pubmed-article:15050655pubmed:abstractTextCoronary artery disease (CAD) is more prevalent in people from a low socioeconomic background, and low socioeconomic status (SES) is associated with an increased exposure to psychological stress. The pro-inflammatory cytokine interleukin-6 (IL-6) plays a central role in CAD development. IL-6 is responsive to psychological stress and could potentially mediate the effect of psychosocial factors on CAD risk. Accordingly, we predicted that people of low SES would have greater and/or more sustained IL-6 responses to acute psychological stress. Based on previous findings, we also predicted that these people would have delayed post-stress cardiovascular recovery. Thirty-eight male civil servants were tested, with participants divided into high and low SES groups according to employment grade. There were no differences between the groups at baseline. However there were significant differences in IL-6 and heart rate responses to stress. Stress induced increases in plasma IL-6 in all participants. However, in the low SES group, IL-6 continued to increase between 75 min and 2h post-stress, whereas IL-6 levels stabilised at 75 min in the high SES group. Heart rate increased to the same extent following stress in both groups, however by 2h post-stress, it had returned to baseline in 75% of the high SES group compared with only 38.1% of the low SES group. These results suggest that low SES people are less able to adapt to stress than their high SES counterparts. Prolonged stress-induced increases in IL-6 in low SES groups represents a novel mechanism potentially linking socioeconomic position and heart disease.lld:pubmed
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pubmed-article:15050655pubmed:pagination281-90lld:pubmed
pubmed-article:15050655pubmed:dateRevised2007-11-15lld:pubmed
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pubmed-article:15050655pubmed:articleTitleSocioeconomic status and stress-induced increases in interleukin-6.lld:pubmed
pubmed-article:15050655pubmed:affiliationThe Psychobiology Group, Department of Epidemiology and Public Health, University College London, London, UK. l.brydon@public-health.ucl.ac.uklld:pubmed
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pubmed-article:15050655pubmed:publicationTypeResearch Support, Non-U.S. Gov'tlld:pubmed
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