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Work stress increases mortality risk in men with cardiometabolic disease
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Among men with diabetes, history of stroke or coronary heart disease, job strain increases the risk for death independent of socioeconomic status and lifestyle risk factors, according to a pooled analysis of European cohort studies.
“Work is a common source of stress in adulthood, triggering natural stress responses that were programmed in our bodies generations ago,” Mika Kivimäki, FMedSci, professor in the department of epidemiology at University College London, said in a press release. “These can result in physical reactions to situations like work stress, and our findings give evidence for there being a link between job strain and risk for premature death in men with cardiometabolic diseases, such as coronary heart disease, stroke and diabetes.”
Kivimäki and colleagues analyzed data from 102,633 adults participating in seven cohort studies in the IPD-Work consortium, initiated between 1985 and 2002 in Finland, France, Sweden and the United Kingdom, to examine associations between work stress and mortality (43.4% men; mean age, 44 years; 25.8% considered low socioeconomic status). Researchers defined work stress as job strain or effort-reward imbalance at work and examined individual-level data on CHD, stroke and any diabetes at baseline, as well as socioeconomic status and conventional and lifestyle risk factors, including smoking status, BMI, physical activity and alcohol consumption. Researchers obtained mortality data from national death registries and used Cox proportional hazard models to assess the associations between work stress and mortality in men and women.
Across cohorts, 1,975 men had cardiometabolic disease at baseline, including 396 with a history of CHD, 214 with a history of stroke and 1,425 with diabetes, whereas 54 men had two of the disorders and three had a history of all three. Among women, 1,466 had cardiometabolic disease at baseline, including 73 with a history of CHD, 153 with a history of stroke and 1,266 with diabetes, whereas 18 had two of the disorders and four had a history of all three.
During a mean follow-up period of 13.9 years (1,423,753 person-years at risk), researchers identified 3,841 deaths, of which 397 were among the 3,441 participants with cardiometabolic disease at baseline.
In men with a history of cardiometabolic disease, researchers found that job strain was associated with a nearly twofold increased risk for death vs. men without cardiometabolic disease at baseline (HR = 1.84; 95% CI, 1.06-3.18), with results persisting after adjustment for blood pressure and total cholesterol in a subgroup of patients with that available data.
Researchers did not observe an association between job strain or effort-reward imbalance and risk for death in women with cardiometabolic disease at baseline.
The researchers noted that the difference in death rates among men with established cardiometabolic disease or without job strain was similar to the difference in death rates between men who were current vs. never smokers (52.1 per 10,000 vs. 78.1 per 10,000), adding that job strain was associated with a two- to sixfold higher risk for mortality in men with cardiometabolic disease, but “favorable” risk factor profiles, including participants who were not obese, physically inactive, smokers or heavy drinkers, and normotensive patients or those without dyslipidemia.
“This is an observational study, so we cannot provide direct recommendations for interventions,” Kivimäki told Endocrine Today. “However, our findings support the European Guidelines for Cardiovascular Disease Prevention, suggesting that assessment of psychosocial stressors, using clinical interview or standardized questionnaires, should be considered for individuals with established cardiovascular disease. Few other clinical guidelines have similar recommendations.”
Kivimäki said large-scale intervention studies are needed to determine whether screening for life stress would lower mortality risk in employees with advanced diabetes, CHD or stroke. – by Regina Schaffer
For more information:
Mika Kivim ä ki, FMedSci, can be reached at University College London, Department of Epidemiology, 1-19 Torrington Place, London WC1E 6BT; email: m.kivimaki@ucl.ac.uk.
Disclosures: The authors report no relevant financial disclosures.
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