SummaryBackgroundPublished work assessing psychosocial stress (job strain) as a risk factor for coronary heart disease is inconsistent and subject to publication bias and reverse causation bias. We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies.MethodsWe used individual records from 13 European cohort studies (1985–2006) of men and women without coronary heart disease who were employed at time of baseline assessment. We measured job strain with questions from validated job-content and demand-control questionnaires. We extracted data in two stages such that acquisition and harmonisation of job strain measure and covariables occurred before linkage to records for coronary heart disease. We defined incident coronary heart disease as the first non-fatal myocardial infarction or coronary death.Findings30 214 (15%) of 197 473 participants reported job strain. In 1·49 million person-years at risk (mean follow-up 7·5 years [SD 1·7]), we recorded 2358 events of incident coronary heart disease. After adjustment for sex and age, the hazard ratio for job strain versus no job strain was 1·23 (95% CI 1·10–1·37). This effect estimate was higher in published (1·43, 1·15–1·77) than unpublished (1·16, 1·02–1·32) studies. Hazard ratios were likewise raised in analyses addressing reverse causality by exclusion of events of coronary heart disease that occurred in the first 3 years (1·31, 1·15–1·48) and 5 years (1·30, 1·13–1·50) of follow-up. We noted an association between job strain and coronary heart disease for sex, age groups, socioeconomic strata, and region, and after adjustments for socioeconomic status, and lifestyle and conventional risk factors. The population attributable risk for job strain was 3·4%.InterpretationOur findings suggest that prevention of workplace stress might decrease disease incidence; however, this strategy would have a much smaller effect than would tackling of standard risk factors, such as smoking.FundingFinnish Work Environment Fund, the Academy of Finland, the Swedish Research Council for Working Life and Social Research, the German Social Accident Insurance, the Danish National Research Centre for the Working Environment, the BUPA Foundation, the Ministry of Social Affairs and Employment, the Medical Research Council, the Wellcome Trust, and the US National Institutes of Health.

Kivimäki M, Virtanen M, Elovainio M, Kouvonen A, Väänänen A, Vahtera J. Work stress in the etiology of coronary heart disease-a meta-analysis. Scand J Work Environ Health 2006;32(6 special issue):431-442.Objectives This study focused on estimating the relative risk of coronary heart disease (CHD) in association with work stress, as indicated by the job-strain model, the effort-reward imbalance model, and the organizational injustice model. MethodsA systematic review and meta-analysis of prospective cohort studies were carried out. Studies were eligible if they had published a quantitative estimate of the association between work stress and incident CHD or cardiovascular mortality by January 2006.Results Fourteen prospective cohort studies were identified. For a total of 83 014 employees, the age-and gender-adjusted relative ratio of CHD for high versus low job strain was 1.43 [95% confidence interval (95% CI) 1.15-1.84], but the ratio decreased to 1.16 (95% CI 0.94-1.43) after adjustment for risk factors and potential mediators. The age-and gender-adjusted risk ratio for a combination of high efforts and low rewards was 1.58 (95% CI 0.84-2.97) for 11 528 employees, and no reduction in the risk ratio was seen after further adjustments. For organizational injustice, the age-and gender-adjusted, and multiple-adjusted relative risks were 1.62 (95% CI 1.24-2.13) and 1.47 (95% CI 1.12-1.95), respectively, for a population of 7246 men and women. There was little standardization in the assessment of work stress within all three stress models, and significant heterogeneity in the effects of stress was observed between studies. Few studies were available for female samples. ConclusionsObservational data suggest an average 50% excess risk for CHD among employees with work stress. Further research is needed to confirm that a reduction in work stress will lead to a reduction in CHD risk.Key terms cardiovascular disease; effort-reward imbalance; job strain; mortality; organizational justice; prospective cohort study; psychosocial factors; systematic review; working population. Activation of the stress system in the hypothalamus and the brain stem helps the body to overcome the influence of short-term physical stressors. However, prolonged overactivity of these systems may cause wear and tear and play a role in coronary heart disease (CHD), infection, and accelerated aging (1). The recognition that the physiological reactions to stress cannot only protect, but also damage the body has provided a basis for epidemiologic research on work stress.Three models for work stress and coronary heart disease Work-stress models aim at describing factors that are likely to elicit harmful stress at work in a large proportion of employees. These factors are conceptualized at a level of generalization that allows for their identification in a wide range of occupations. The stress model most often cited and most widely tested is the two-dimensional job-strain model (2-4) ( Work stress in the etiology of coronary heart disease strain model adds...

The evidence indicates an association between temporary employment and psychological morbidity. The health risk may depend on instability of temporary employment and the context. Confounding by occupation may have biased some of the studies. Additional research to clarify the role of employment instability, hazard accumulation, and selection is recommended.

Aims: To examine exposure to workplace bullying as a risk factor for cardiovascular disease and depression in employees. Methods: Logistic regression models were related to prospective data from two surveys in a cohort of 5432 hospital employees (601 men and 4831 women), aged 18-63 years. Outcomes were new reports of doctor diagnosed cardiovascular disease and depression during the two year follow up among those who were free from these diseases at baseline. Results: The prevalence of bullying was 5% in the first survey and 6% in the second survey. Two per cent reported bullying experiences in both surveys, an indication of prolonged bullying. After adjustment for sex, age, and income, the odds ratio of incident cardiovascular disease for victims of prolonged bullying compared to non-bullied employees was 2.3 (95% CI 1.2 to 4.6). A further adjustment for overweight at baseline attenuated the odds ratio to 1.6 (95% CI 0.8 to 3.5). The association between prolonged bullying and incident depression was significant, even after these adjustments (odds ratio 4.2, 95% CI 2.0 to 8.6). Conclusions: A strong association between workplace bullying and subsequent depression suggests that bullying is an aetiological factor for mental health problems. The victims of bullying also seem to be at greater risk of cardiovascular disease, but this risk may partly be attributable to overweight.

Medical Research Council, Economic and Social Research Council, European Union New and Emerging Risks in Occupational Safety and Health research programme, Finnish Work Environment Fund, Swedish Research Council for Working Life and Social Research, German Social Accident Insurance, Danish National Research Centre for the Working Environment, Academy of Finland, Ministry of Social Affairs and Employment (Netherlands), US National Institutes of Health, British Heart Foundation.

SummaryBackgroundAlthough overweight and obesity have been studied in relation to individual cardiometabolic diseases, their association with risk of cardiometabolic multimorbidity is poorly understood. Here we aimed to establish the risk of incident cardiometabolic multimorbidity (ie, at least two from: type 2 diabetes, coronary heart disease, and stroke) in adults who are overweight and obese compared with those who are a healthy weight.MethodsWe pooled individual-participant data for BMI and incident cardiometabolic multimorbidity from 16 prospective cohort studies from the USA and Europe. Participants included in the analyses were 35 years or older and had data available for BMI at baseline and for type 2 diabetes, coronary heart disease, and stroke at baseline and follow-up. We excluded participants with a diagnosis of diabetes, coronary heart disease, or stroke at or before study baseline. According to WHO recommendations, we classified BMI into categories of healthy (20·0–24·9 kg/m2), overweight (25·0–29·9 kg/m2), class I (mild) obesity (30·0–34·9 kg/m2), and class II and III (severe) obesity (≥35·0 kg/m2). We used an inclusive definition of underweight (<20 kg/m2) to achieve sufficient case numbers for analysis. The main outcome was cardiometabolic multimorbidity (ie, developing at least two from: type 2 diabetes, coronary heart disease, and stroke). Incident cardiometabolic multimorbidity was ascertained via resurvey or linkage to electronic medical records (including hospital admissions and death). We analysed data from each cohort separately using logistic regression and then pooled cohort-specific estimates using random-effects meta-analysis.FindingsParticipants were 120  813 adults (mean age 51·4 years, range 35–103; 71 445 women) who did not have diabetes, coronary heart disease, or stroke at study baseline (1973–2012). During a mean follow-up of 10·7 years (1995–2014), we identified 1627 cases of multimorbidity. After adjustment for sociodemographic and lifestyle factors, compared with individuals with a healthy weight, the risk of developing cardiometabolic multimorbidity in overweight individuals was twice as high (odds ratio [OR] 2·0, 95% CI 1·7–2·4; p<0·0001), almost five times higher for individuals with class I obesity (4·5, 3·5–5·8; p<0·0001), and almost 15 times higher for individuals with classes II and III obesity combined (14·5, 10·1–21·0; p<0·0001). This association was noted in men and women, young and old, and white and non-white participants, and was not dependent on the method of exposure assessment or outcome ascertainment. In analyses of different combinations of cardiometabolic conditions, odds ratios associated with classes II and III obesity were 2·2 (95% CI 1·9–2·6) for vascular disease only (coronary heart disease or stroke), 12·0 (8·1–17·9) for vascular disease followed by diabetes, 18·6 (16·6–20·9) for diabetes only, and 29·8 (21·7–40·8) for diabetes followed by vascular disease.InterpretationThe risk of cardiometabolic multimorbidity increases as BMI increases; from double...

BackgroundAdverse psychosocial working environments characterized by job strain (the combination of high demands and low control at work) are associated with an increased risk of depressive symptoms among employees, but evidence on clinically diagnosed depression is scarce. We examined job strain as a risk factor for clinical depression.MethodWe identified published cohort studies from a systematic literature search in PubMed and PsycNET and obtained 14 cohort studies with unpublished individual-level data from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium. Summary estimates of the association were obtained using random-effects models. Individual-level data analyses were based on a pre-published study protocol.ResultsWe included six published studies with a total of 27 461 individuals and 914 incident cases of clinical depression. From unpublished datasets we included 120 221 individuals and 982 first episodes of hospital-treated clinical depression. Job strain was associated with an increased risk of clinical depression in both published [relative risk (RR) = 1.77, 95% confidence interval (CI) 1.47–2.13] and unpublished datasets (RR = 1.27, 95% CI 1.04–1.55). Further individual participant analyses showed a similar association across sociodemographic subgroups and after excluding individuals with baseline somatic disease. The association was unchanged when excluding individuals with baseline depressive symptoms (RR = 1.25, 95% CI 0.94–1.65), but attenuated on adjustment for a continuous depressive symptoms score (RR = 1.03, 95% CI 0.81–1.32).ConclusionsJob strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.

SummaryBackgroundThe associations of social isolation and loneliness with premature mortality are well known, but the risk factors linking them remain unclear. We sought to identify risk factors that might explain the increased mortality in socially isolated and lonely individuals.MethodsWe used prospective follow-up data from the UK Biobank cohort study to assess self-reported isolation (a three-item scale) and loneliness (two questions). The main outcomes were all-cause and cause-specific mortality. We calculated the percentage of excess risk mediated by risk factors to assess the extent to which the associations of social isolation and loneliness with mortality were attributable to differences between isolated and lonely individuals and others in biological (body-mass index, systolic and diastolic blood pressure, and handgrip strength), behavioural (smoking, alcohol consumption, and physical activity), socioeconomic (education, neighbourhood deprivation, and household income), and psychological (depressive symptoms and cognitive capacity) risk factors.Findings466 901 men and women (mean age at baseline 56·5 years [SD 8·1]) were included in the analyses, with a mean follow-up of 6·5 years (SD 0·8). The hazard ratio for all-cause mortality for social isolation compared with no social isolation was 1·73 (95% CI 1·65–1·82) after adjustment for age, sex, ethnic origin, and chronic disease (ie, minimally adjusted), and was 1·26 (95% CI 1·20–1·33) after further adjustment for socioeconomic factors, health-related behaviours, depressive symptoms, biological factors, cognitive performance, and self-rated health (ie, fully adjusted). The minimally adjusted hazard ratio for mortality risk related to loneliness was 1·38 (95% CI 1·30–1·47), which reduced to 0·99 (95% CI 0·93–1·06) after full adjustment for baseline risks.InterpretationIsolated and lonely people are at increased risk of death. Health policies addressing risk factors such as adverse socioeconomic conditions, unhealthy lifestyle, and lower mental wellbeing might reduce excess mortality among the isolated and the lonely.FundingAcademy of Finland, NordForsk, and the UK Medical Research Council.