Although long working hours are common in working populations, little is known about the effect of long working hours on mental health.
We examined the association between long working hours and the ...onset of depressive and anxiety symptoms in middle-aged employees. Participants were 2960 full-time employees aged 44 to 66 years (2248 men, 712 women) from the prospective Whitehall II cohort study of British civil servants. Working hours, anxiety and depressive symptoms, and covariates were measured at baseline (1997-1999) followed by two subsequent measurements of depressive and anxiety symptoms (2001 and 2002-2004).
In a prospective analysis of participants with no depressive (n=2549) or anxiety symptoms (n=2618) at baseline, Cox proportional hazard analysis adjusted for baseline covariates showed a 1.66-fold 95% confidence interval (CI) 1.06-2.61 risk of depressive symptoms and a 1.74-fold (95% CI 1.15-2.61) risk of anxiety symptoms among employees working more than 55 h/week compared with employees working 35-40 h/week. Sex-stratified analysis showed an excess risk of depression and anxiety associated with long working hours among women hazard ratios (HRs) 2.67 (95% CI 1.07-6.68) and 2.84 (95% CI 1.27-6.34) respectively but not men 1.30 (0.77-2.19) and 1.43 (0.89-2.30).
Working long hours is a risk factor for the development of depressive and anxiety symptoms in women.
A lack of longitudinal studies has made it difficult to establish the direction of associations between circulating concentrations of low-grade chronic inflammatory markers, such as C-reactive ...protein and interleukin-6, and cognitive symptoms of depression. The present study sought to assess whether C-reactive protein and interleukin-6 predict cognitive symptoms of depression or whether these symptoms predict inflammatory markers.
In a prospective occupational cohort study of British white-collar civil servants (the Whitehall II study), serum C-reactive protein, interleukin-6 and cognitive symptoms of depression were measured at baseline in 1991-1993 and at follow-up in 2002-2004, an average follow-up of 11.8 years. Symptoms of depression were measured with four items describing cognitive symptoms of depression from the General Health Questionnaire. The number of participants varied between 3339 and 3070 (mean age 50 years, 30% women) depending on the analysis.
Baseline C-reactive protein (beta=0.046, p=0.004) and interleukin-6 (beta=0.046, p=0.005) predicted cognitive symptoms of depression at follow-up, while baseline symptoms of depression did not predict inflammatory markers at follow-up. After full adjustment for sociodemographic, behavioural and biological risk factors, health conditions, medication use and baseline cognitive systems of depression, baseline C-reactive protein (beta=0.038, p=0.036) and interleukin-6 (beta=0.041, p=0.018) remained predictive of cognitive symptoms of depression at follow-up.
These findings suggest that inflammation precedes depression at least with regard to the cognitive symptoms of depression.
Adverse 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.
We 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.
We 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).
Job strain may precipitate clinical depression among employees. Future intervention studies should test whether job strain is a modifiable risk factor for depression.
Previous research has focused on overall associations between work stress and body mass index (BMI) ignoring the possibility that stress may cause some people to eat less and lose weight and others ...to eat more. Using longitudinal data, we studied whether work stress induced weight loss in lean individuals and weight gain in overweight individuals.
Prospective cohort study.
A total of 7965 British civil servants (5547 men and 2418 women) aged 35-55 at study entry (The Whitehall II study).
Work stress, indicated by the job strain model and measured as job control, job demands and job strain, was assessed at baseline and BMI at baseline and at 5-year follow-up.
In men, the effect of job strain on weight gain and weight loss was dependent on baseline BMI (P</=0.03). In the leanest quintile (BMI<22 kg/m(2)) at baseline, high job strain and low job control were associated with weight loss by follow-up, whereas among those in the highest BMI quintile (>27 kg/m(2)), these stress indicators were associated with subsequent weight gain. No corresponding interaction was seen among women.
Inconsistent findings reported by previous studies of stress and BMI have generally been interpreted to indicate the absence of an association. In light of our results, the possibility of differential effects of work stress should also be taken into account.
The authors aggregated the results of observational studies examining the association between long working hours and coronary heart disease (CHD). Data sources used were MEDLINE (through January 19, ...2011) and Web of Science (through March 14, 2011). Two investigators independently extracted results from eligible studies. Heterogeneity between the studies was assessed using the I(2) statistic, and the possibility of publication bias was assessed using the funnel plot and Egger's test for small-study effects. Twelve studies were identified (7 case-control, 4 prospective, and 1 cross-sectional). For a total of 22,518 participants (2,313 CHD cases), the minimally adjusted relative risk of CHD for long working hours was 1.80 (95% confidence interval (CI): 1.42, 2.29), and in the maximally (multivariate-) adjusted analysis the relative risk was 1.59 (95% CI: 1.23, 2.07). The 4 prospective studies produced a relative risk of 1.39 (95% CI: 1.12, 1.72), while the corresponding relative risk in the 7 case-control studies was 2.43 (95% CI: 1.81, 3.26). Little evidence of publication bias but relatively large heterogeneity was observed. Studies varied in size, design, measurement of exposure and outcome, and adjustments. In conclusion, results from prospective observational studies suggest an approximately 40% excess risk of CHD in employees working long hours.
Although 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.
We 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.
Participants 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.
The risk of cardiometabolic multimorbidity increases as BMI increases; from double in overweight people to more than ten times in severely obese people compared with individuals with a healthy BMI. Our findings highlight the need for clinicians to actively screen for diabetes in overweight and obese patients with vascular disease, and pay increased attention to prevention of vascular disease in obese individuals with diabetes.
NordForsk, Medical Research Council, Cancer Research UK, Finnish Work Environment Fund, and Academy of Finland.
Cross-sectional evidence suggests associations between sleep duration and levels of the inflammatory markers, C-reactive protein and interleukin-6. This longitudinal study uses data from the ...London-based Whitehall II study to examine whether changes in sleep duration are associated with average levels of inflammation from 2 measures 5 years apart. Sleep duration (≤5, 6, 7, 8, ≥9 hours on an average week night) was assessed in 5,003 middle-aged women and men in 1991/1994 and 1997/1999. Fasting levels of C-reactive protein and interleukin-6 were measured in 1997/1999 and 2002/2004. Cross-sectional analyses indicated that shorter sleep is associated with higher levels of inflammatory markers. Longitudinal analyses showed that each hour per night decrease in sleep duration between 1991/1994 and 1997/1999 was associated with higher levels of C-reactive protein (8.1%) and interleukin-6 (4.5%) averaged across measures in 1997/1999 and 2002/2004. Adjustment for longstanding illness and major cardiometabolic risk factors indicated that disease processes may partially underlie these associations. An increase in sleep duration was not associated with average levels of inflammatory markers. These results suggest that both short sleep and reductions in sleep are associated with average levels of inflammation over a 5-year period.
BackgroundFactors that increase the risk of labour market exclusion are poorly understood. In this study, we examined the extent to which all-cause and diagnosis-specific sick leave predict ...subsequent disability pension (DP).MethodsProspective cohort study of 20 434 persons employed by the French national gas and electric company (the GAZEL study). New sick-leave spells >7 days in 1990–1992 were obtained from company records. Follow-up for DP was from 1994 to 2007.ResultsThe HR, adjusted for age and occupational position, for DP was 3.5 (95% CI 2.7 to 4.5) in men and 2.6 (95% CI 1.9 to 3.5) in women with one or more sick-leave spells >7 days compared with those with no sick leave. The strongest predictor of DP was sick leave with a psychiatric diagnosis, HR 7.6 (95% CI 5.2 to 10.9) for men and 4.1 (95% CI 2.9 to 5.9) for women. Corresponding HRs for sick leave due to circulatory diagnoses in men and women were 5.6 (95% CI 3.7 to 8.6) and 3.1 (95% CI 1.8 to 5.3), for respiratory diagnoses 3.9 (95% CI 2.6 to 5.8) and 2.6 (95% CI 1.7 to 4.0), and musculoskeletal diagnoses 4.6 (95% CI 3.4 to 6.4) and 3.3 (95% CI 2.2 to 4.8), respectively.ConclusionsSick leave with a psychiatric diagnosis is a major risk factor for subsequent DP, especially among men. Sick leave due to musculoskeletal or circulatory disorders was also a strong predictor of DP. Diagnosis-specific sick leave should be recognised as an early risk marker for future exclusion from the labour market.
Study objective: To determine the effect of chronic job insecurity and changes in job security on self reported health, minor psychiatric morbidity, physiological measures, and health related ...behaviours. Design: Self reported health, minor psychiatric morbidity, physiological measures, and health related behaviours were determined in 931 women and 2429 men who responded to a question on job insecurity in 1995/96 and again in 1997/99. Self reported health status, clinical screening measures, and health related behaviours for participants whose job security had changed or who remained insecure were compared with those whose jobs had remained secure. Setting: Prospective cohort study, Whitehall II, all participants were white collar office workers in the British Civil Service on entry to the study. Main results: Self reported morbidity was higher among participants who lost job security. Among those who gained job security residual negative effects, particularly in the psychological sphere were observed. Those exposed to chronic job insecurity had the highest self reported morbidity. Changes in the physiological measures were limited to an increase in blood pressure among women who lost job security and a decrease in body mass index among women reporting chronic job insecurity. There were no significant differences between any of the groups for alcohol over the recommended limits or smoking. Conclusion: Loss of job security has adverse effects on self reported health and minor psychiatric morbidity, which are not completely reversed by removal of the threat and which tend to increase with chronic exposure to the stressor.
Objective To investigate whether knowing the diagnosis for sickness absence improves prediction of mortality.Design Prospective cohort study established in 1985-8. Sickness absence records including ...diagnoses were obtained from computerised registers.Setting 20 civil service departments in London.Participants 6478 civil servants aged 35-55 years.Main outcome measures All cause, cardiovascular, and cancer mortality until 2004, average follow-up 13 years.Results After adjustment for age, sex, and employment grade, employees who had one or more medically certified spells of sickness absence (>7 days) in a three year period had a mortality 1.7 (95% CI 1.3 to 2.1) times greater than those with no medically certified spells. Inclusion of diagnoses improved the prediction of all cause mortality (P=0.03). The hazard ratio for mortality was 4.7 (2.6 to 8.5) for absences with circulatory disease diagnoses, 2.2 (1.4 to 3.3) for surgical operations, and 1.9 (1.2 to 3.1) for psychiatric diagnoses. Psychiatric absences were also predictive of cancer mortality (2.5 (1.3 to 4.7)). Associations of infectious, respiratory, and injury absences with overall mortality were less marked (hazard ratios from 1.5 to 1.7), and there was no association between musculoskeletal absences and mortality.Conclusions Major diagnoses for medically certified absences were associated with increased mortality, with the exception of musculoskeletal disease. Data on sickness absence diagnoses may provide useful information to identify groups with increased health risk and a need for targeted interventions.
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