Paula Salo

Job strain as a risk factor for coronary heart disease: A collaborative meta-analysis of individual participant data

Summary Background Published 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 We analysed the relation between job strain and coronary heart disease with a meta-analysis of published and unpublished studies. Methods We 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. Findings 30 214 (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 This effect estimate was higher in published (1·43, 1·15–1·77) than unpublished (1·16, 1·02–1·32) studies.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%. Interpretation Our 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. Funding Finnish 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.

Long working hours and risk of coronary heart disease and stroke : a systematic review and meta-analysis of published and unpublished data for 603 838 individuals

BACKGROUND Long working hours might increase the risk of cardiovascular disease, but prospective evidence is scarce, imprecise, and mostly limited to coronary heart disease. We aimed to assess long working hours as a risk factor for incident coronary heart disease and stroke. METHODS We identified published studies through a systematic review of PubMed and Embase from inception to Aug 20, 2014. We obtained unpublished data for 20 cohort studies from the Individual-Participant-Data Meta-analysis in Working Populations (IPD-Work) Consortium and open-access data archives. We used cumulative random-effects meta-analysis to combine effect estimates from published and unpublished data. FINDINGS We included 25 studies from 24 cohorts in Europe, the USA, and Australia. The meta-analysis of coronary heart disease comprised data for 603,838 men and women who were free from coronary heart disease at baseline; the meta-analysis of stroke comprised data for 528,908 men and women who were free from stroke at baseline. Follow-up for coronary heart disease was 5·1 million person-years (mean 8·5 years), in which 4768 events were recorded, and for stroke was 3·8 million person-years (mean 7·2 years), in which 1722 events were recorded. In cumulative meta-analysis adjusted for age, sex, and socioeconomic status, compared with standard hours (35-40 h per week), working long hours (≥55 h per week) was associated with an increase in risk of incident coronary heart disease (relative risk [RR] 1·13, 95% CI 1·02-1·26; p=0·02) and incident stroke (1·33, 1·11-1·61; p=0·002). The excess risk of stroke remained unchanged in analyses that addressed reverse causation, multivariable adjustments for other risk factors, and different methods of stroke ascertainment (range of RR estimates 1·30-1·42). We recorded a dose-response association for stroke, with RR estimates of 1·10 (95% CI 0·94-1·28; p=0·24) for 41-48 working hours, 1·27 (1·03-1·56; p=0·03) for 49-54 working hours, and 1·33 (1·11-1·61; p=0·002) for 55 working hours or more per week compared with standard working hours (ptrend<0·0001). INTERPRETATION Employees who work long hours have a higher risk of stroke than those working standard hours; the association with coronary heart disease is weaker. These findings suggest that more attention should be paid to the management of vascular risk factors in individuals who work long hours. FUNDING 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.

Work stress and risk of cancer : meta-analysis of 5700 incident cancer events in 116 000 European men and women

Objective To investigate whether work related stress, measured and defined as job strain, is associated with the overall risk of cancer and the risk of colorectal, lung, breast, or prostate cancers. Design Meta-analysis of pooled prospective individual participant data from 12 European cohort studies including 116 056 men and women aged 17-70 who were free from cancer at study baseline and were followed-up for a median of 12 years. Work stress was measured and defined as job strain, which was self reported at baseline. Incident cancers (all n=5765, colorectal cancer n=522, lung cancer n=374, breast cancer n=1010, prostate cancer n=865) were ascertained from cancer, hospital admission, and death registers. Data were analysed in each study with Cox regression and the study specific estimates pooled in meta-analyses. Models were adjusted for age, sex, socioeconomic position, body mass index (BMI), smoking, and alcohol intake Results A harmonised measure of work stress, high job strain, was not associated with overall risk of cancer (hazard ratio 0.97, 95% confidence interval 0.90 to 1.04) in the multivariable adjusted analyses. Similarly, no association was observed between job strain and the risk of colorectal (1.16, 0.90 to 1.48), lung (1.17, 0.88 to 1.54), breast (0.97, 0.82 to 1.14), or prostate (0.86, 0.68 to 1.09) cancers. There was no clear evidence for an association between the categories of job strain and the risk of cancer. Conclusions These findings suggest that work related stress, measured and defined as job strain, at baseline is unlikely to be an important risk factor for colorectal, lung, breast, or prostate cancers.

Long working hours and alcohol use : systematic review and meta-analysis of published studies and unpublished individual participant data.

Objective To quantify the association between long working hours and alcohol use. Design Systematic review and meta-analysis of published studies and unpublished individual participant data. Data sources A systematic search of PubMed and Embase databases in April 2014 for published studies, supplemented with manual searches. Unpublished individual participant data were obtained from 27 additional studies. Review methods The search strategy was designed to retrieve cross sectional and prospective studies of the association between long working hours and alcohol use. Summary estimates were obtained with random effects meta-analysis. Sources of heterogeneity were examined with meta-regression. Results Cross sectional analysis was based on 61 studies representing 333 693 participants from 14 countries. Prospective analysis was based on 20 studies representing 100 602 participants from nine countries. The pooled maximum adjusted odds ratio for the association between long working hours and alcohol use was 1.11 (95% confidence interval 1.05 to 1.18) in the cross sectional analysis of published and unpublished data. Odds ratio of new onset risky alcohol use was 1.12 (1.04 to 1.20) in the analysis of prospective published and unpublished data. In the 18 studies with individual participant data it was possible to assess the European Union Working Time Directive, which recommends an upper limit of 48 hours a week. Odds ratios of new onset risky alcohol use for those working 49-54 hours and ≥55 hours a week were 1.13 (1.02 to 1.26; adjusted difference in incidence 0.8 percentage points) and 1.12 (1.01 to 1.25; adjusted difference in incidence 0.7 percentage points), respectively, compared with working standard 35-40 hours (incidence of new onset risky alcohol use 6.2%). There was no difference in these associations between men and women or by age or socioeconomic groups, geographical regions, sample type (population based v occupational cohort), prevalence of risky alcohol use in the cohort, or sample attrition rate. Conclusions Individuals whose working hours exceed standard recommendations are more likely to increase their alcohol use to levels that pose a health risk.

The bidirectional association between depression and insomnia: the HUNT study.

Objective Depression and insomnia are closely linked, yet our understanding of their prospective relationships remains limited. The aim of the current study was to investigate the directionality of association between depression and insomnia. Methods Data were collected from a prospective population-based study comprising the most recent waves of the Nord-Trøndelag Health Study (HUNT) (the HUNT2 in 1995–1997 and the HUNT3 in 2006–2008). A total of 24,715 persons provided valid responses on the relevant questionnaires from both surveys. Study outcomes were onset of depression or insomnia at HUNT3 in persons not reporting the other disorder in HUNT2. Results Both insomnia and depression significantly predicted the onset of the other disorder. Participants who did not have depression in HUNT2 but who had insomnia in both HUNT2 and HUNT3 had an odds ratio (OR) of 6.2 of developing depression at HUNT3. Participants who did not have insomnia in HUNT2 but who had depression in both HUNT2 and HUNT3 had an OR of 6.7 of developing insomnia at HUNT3. ORs were only slightly attenuated when adjusting for potential confounding factors. Conclusions The results support a bidirectional relationship between insomnia and depression. This finding stands in contrast to the previous studies, which have mainly focused on insomnia as a risk factor for the onset of depression.

Sleep epidemiology—a rapidly growing field

The human body has adapted to daily changes in dark and light such that it anticipates periods of sleep and activity. Deviations from this circadian rhythm come with functional consequences. Thus, 17 hours of sustained wakefulness in adults leads to a decrease in performance equivalent to a blood alcohol-level of 0.05%;[1] the legal level for drink driving in many countries.[2] Rats deprived of sleep die after 32 days,[3] and, with longer periods of sleep deprivation, this would also be the case in human beings. Indeed, sleep deprivation is a common form of torture.[4] Given the readily observable effects of sleep in everyday life, it is not surprising that there has been scholarly interest in sleep since the beginning of recorded history.[5] Sleep epidemiology as a subject in its own right has a recognisable history of just over 30 years,[6] with the first modern epidemiological studies of sleep disturbances appearing around 1980.[7;8] Nevertheless, a PubMed search for terms “sleep/insomnia” and “epidemiology” shows that the cumulative number of papers on the subject over the past 10 years is already about 10,000. Although this is less than for standard risk factors, such as obesity (>60,000) and smoking (50,000)(Figure 1), the annual number of papers on sleep epidemiology is rising rapidly (Figure 2). This issue of IJE includes a review[9] of the first comprehensive textbook of Sleep Epidemiology,[10] and the purpose of our Editorial is further to highlight recent developments to give the reader an idea why the coming years are likely to see an increasing interest in sleep studies. Figure 1 Exposures AND Epidemiology 2000–2010 Figure 2 Sleep/insomnia AND Epidemiology by year Why the upsurge in interest? There are several reasons for an increase in interest in sleep from an epidemiological perspective. First, sleep problems are associated with accidents and human errors. It has been estimated that 10–15% of fatal motor-vehicle crashes are due to sleepiness or driver fatigue. Furthermore, by 2020 the number of people killed in motor-vehicle crashes is expected to double to 2.3 million deaths worldwide, of which approximately 230,000–345,000 will be due to sleepiness or fatigue.[11] It has been estimated that nearly 100,000 deaths occur each year in US hospitals due to medical errors and sleep deprivation have been shown to make a significant contribution.[12] Similarly, in a national sample in Sweden of over 50,000 people interviewed over 20 years disturbed sleep almost doubled the risk of a fatal accident at work.[13] Second, sleep problems are common. Population studies show that sleep deprivation and disorders affect many more people worldwide than had been previously thought. A recent study found 20% of 25–45 year-olds slept “90 minutes less than they needed to be in good shape”.[14] Insomnia is the most common specific sleep disorder, with ‘some insomnia problems over the past year’ reported by approximately 30% of adults and chronic insomnia by approximately 10%.[15] Prevalence of obstructive sleep apnoea, characterized by respiratory difficulties during sleep, is also very high with estimates of 9–21% in women and 24–31% in men.[16;17] Third, sleep problems are likely to increase. The rapid advent of the 24/7 society involving round-the-clock activities and increasing night time use of TV, internet and mobile phones mean that adequate sleep durations may become increasingly compromised. Some data suggest a decline in sleep duration of up to 18 minutes per night over the past 30 years.[18;19] Complaints of sleeping problems have increased substantially over the same period, with short sleep (<6 hours/night) in full-time workers becoming more prevalent.[19;20] As more shift work is required to service 24/7 societies the proportion of workers exposed to circadian rhythm disorders, such as shift work sleep disorder, and their effects on health and performance is likely to rise. Sleep architecture is known to change with age; slow-wave (or deep) sleep decreases and lighter sleep increases. Other changes include increases in nocturnal sleep disruption and daytime sleepiness. As the proportion of elderly people in populations across the world increases, these changing sleep patterns will raise the prevalence of sleep disorders. Similarly, the increasing worldwide obesity epidemic and the prevalence of obstructive sleep apnoea, which is over double among the obese, ensure sleep disorders will be of increasing public health importance in lower as well as high income countries.[16;21] Fourth, sleep problems are associated with short and long-term effects on health and well-being. Immediate effects at the individual level relate to well-being, performance, daytime sleepiness and fatigue. Longer term, evidence has accumulated of associations between sleep deprivation and sleep disorders and numerous health outcomes including premature mortality, cardiovascular disease, hypertension, inflammation, obesity, diabetes and impaired glucose tolerance, and psychiatric disorders, such as anxiety and depression. As this evidence represents the core of Sleep Epidemiology, we provide below a snapshot on key findings.

Perceived job insecurity as a risk factor for incident coronary heart disease : systematic review and meta-analysis

Objective To determine the association between self reported job insecurity and incident coronary heart disease. Design A meta-analysis combining individual level data from a collaborative consortium and published studies identified by a systematic review. Data sources We obtained individual level data from 13 cohort studies participating in the Individual-Participant-Data Meta-analysis in Working Populations Consortium. Four published prospective cohort studies were identified by searches of Medline (to August 2012) and Embase databases (to October 2012), supplemented by manual searches. Review methods Prospective cohort studies that reported risk estimates for clinically verified incident coronary heart disease by the level of self reported job insecurity. Two independent reviewers extracted published data. Summary estimates of association were obtained using random effects models. Results The literature search yielded four cohort studies. Together with 13 cohort studies with individual participant data, the meta-analysis comprised up to 174 438 participants with a mean follow-up of 9.7 years and 1892 incident cases of coronary heart disease. Age adjusted relative risk of high versus low job insecurity was 1.32 (95% confidence interval 1.09 to 1.59). The relative risk of job insecurity adjusted for sociodemographic and risk factors was 1.19 (1.00 to 1.42). There was no evidence of significant differences in this association by sex, age (<50 v ≥50 years), national unemployment rate, welfare regime, or job insecurity measure. Conclusions The modest association between perceived job insecurity and incident coronary heart disease is partly attributable to poorer socioeconomic circumstances and less favourable risk factor profiles among people with job insecurity.

Insomnia as a risk factor for ill health: results from the large population-based prospective HUNT Study in Norway

Insomnia co‐occurs with many health problems, but less is known about the prospective associations. The aim of the current study was to investigate if insomnia predicts cumulative incidence of mental and physical conditions. Prospective population‐based data from the two last Nord‐Trøndelag Health Studies (HUNT2 in 1995–97 and HUNT3 in 2006–08), comprising 24 715 people in the working population, were used to study insomnia as a risk factor for incidence of physical and mental conditions. Insomnia was defined according to the 4th edition of the Diagnostic and Statistical Manual of Mental Disorders (DSM‐IV). Insomnia at HUNT2 was a significant risk factor for incidence of a range of both mental and physical conditions at HUNT3 11 years later. Most effects were only slightly attenuated when adjusting for confounding factors, and insomnia remained a significant risk factor for the following conditions in the adjusted analyses: depression [odds ratio (OR): 2.38, 95% confidence interval (CI): 1.91–2.98], anxiety (OR: 2.08, 95% CI: 1.63–2.64), fibromyalgia (OR: 2.05, 95% CI: 1.51–2.79), rheumatoid arthritis (OR: 1.87, 95% CI: 1.29–2.52), whiplash (OR: 1.71, 95% CI: 1.21–2.41), arthrosis (OR: 1.68, 95% CI: 1.43–1.98), osteoporosis (OR: 1.52, 95% CI: 1.14–2.01, headache (OR: 1.50, 95% CI: 1.16–1.95, asthma (OR: 1.47, 95% CI: 1.16–1.86 and myocardial infarction (OR: 1.46, 95% CI: 1.06–2.00). Insomnia was also associated significantly with incidence of angina, hypertension, obesity and stroke in the crude analyses, but not after adjusting for confounders. We conclude that insomnia predicts cumulative incidence of several physical and mental conditions. These results may have important clinical implications, and whether or not treatment of insomnia would have a preventive value for both physical and mental conditions should be studied further.

Job Strain as a Risk Factor for Type 2 Diabetes : A Pooled Analysis of 124,808 Men and Women

OBJECTIVE The status of psychosocial stress at work as a risk factor for type 2 diabetes is unclear because existing evidence is based on small studies and is subject to confounding by lifestyle factors, such as obesity and physical inactivity. This collaborative study examined whether stress at work, defined as “job strain,” is associated with incident type 2 diabetes independent of lifestyle factors. RESEARCH DESIGN AND METHODS We extracted individual-level data for 124,808 diabetes-free adults from 13 European cohort studies participating in the IPD-Work Consortium. We measured job strain with baseline questionnaires. Incident type 2 diabetes at follow-up was ascertained using national health registers, clinical screening, and self-reports. We analyzed data for each study using Cox regression and pooled the study-specific estimates in fixed-effect meta-analyses. RESULTS There were 3,703 cases of incident diabetes during a mean follow-up of 10.3 years. After adjustment for age, sex, and socioeconomic status (SES), the hazard ratio (HR) for job strain compared with no job strain was 1.15 (95% CI 1.06–1.25) with no difference between men and women (1.19 [1.06–1.34] and 1.13 [1.00–1.28], respectively). In stratified analyses, job strain was associated with an increased risk of diabetes among those with healthy and unhealthy lifestyle habits. In a multivariable model adjusted for age, sex, SES, and lifestyle habits, the HR was 1.11 (1.00–1.23). CONCLUSIONS Findings from a large pan-European dataset suggest that job strain is a risk factor for type 2 diabetes in men and women independent of lifestyle factors.

Job strain and tobacco smoking: An individual-participant data meta-analysis of 166 130 adults in 15 european studies

Background Tobacco smoking is a major contributor to the public health burden and healthcare costs worldwide, but the determinants of smoking behaviours are poorly understood. We conducted a large individual-participant meta-analysis to examine the extent to which work-related stress, operationalised as job strain, is associated with tobacco smoking in working adults. Methodology and Principal Findings We analysed cross-sectional data from 15 European studies comprising 166 130 participants. Longitudinal data from six studies were used. Job strain and smoking were self-reported. Smoking was harmonised into three categories never, ex- and current. We modelled the cross-sectional associations using logistic regression and the results pooled in random effects meta-analyses. Mixed effects logistic regression was used to examine longitudinal associations. Of the 166 130 participants, 17% reported job strain, 42% were never smokers, 33% ex-smokers and 25% current smokers. In the analyses of the cross-sectional data, current smokers had higher odds of job strain than never-smokers (age, sex and socioeconomic position-adjusted odds ratio: 1.11, 95% confidence interval: 1.03, 1.18). Current smokers with job strain smoked, on average, three cigarettes per week more than current smokers without job strain. In the analyses of longitudinal data (1 to 9 years of follow-up), there was no clear evidence for longitudinal associations between job strain and taking up or quitting smoking. Conclusions Our findings show that smokers are slightly more likely than non-smokers to report work-related stress. In addition, smokers who reported work stress smoked, on average, slightly more cigarettes than stress-free smokers.