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American Journal of Epidemiology Advance Access published online on January 22, 2007
American Journal of Epidemiology, doi:10.1093/aje/kwk058
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American Journal of Epidemiology Copyright © 2007 by the Johns Hopkins Bloomberg School of Public Health All rights reserved; printed in U.S.A.

ORIGINAL CONTRIBUTIONS

Prospective Effect of Job Strain on General and Central Obesity in the Whitehall II Study

Eric J. Brunner, Tarani Chandola and Michael G. Marmot

From the Department of Epidemiology and Public Health, Royal Free and University College London Medical School, London, England

Correspondence to Dr. Eric J. Brunner, Department of Epidemiology and Public Health, Royal Free and University College London Medical School, 1-19 Torrington Place, London WC1E 6BT, England (e-mail: e.brunner{at}ucl.ac.uk).

Received for publication March 2, 2006. Accepted for publication August 31, 2006.


   ABSTRACT
TOP
 ABSTRACT
INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Positive energy balance is the major cause of obesity, and chronic stress may be a contributory factor. The authors examined cumulative work stress, using the Job Strain Questionnaire on four occasions, as a predictor of obesity in a prospective 19-year study of 6,895 men and 3,413 women (aged 35–55 years) in the Whitehall II cohort in London, United Kingdom (baseline: 1985–1988). A dose-response relation was found between work stress and risk of general obesity (body mass index ≥30 kg/m2) and central obesity (waist circumference >102 cm in men, >88 cm in women) that was largely independent of covariates. The imputed odds ratios of body mass index obesity for one, two, and three or more reports of work stress adjusted for age, sex, and social position were 1.17, 1.24, and 1.73 (trend p < 0.01), respectively. For waist obesity, the corresponding findings were 1.17, 1.41, and 1.61 (trend p < 0.01). Work stress effect was modestly attenuated after exclusion of obese individuals at baseline and further adjustments for smoking; intakes of dietary fiber, fruits and vegetables, and alcohol; and levels of physical activity during follow-up. This study provides prospective, population-based evidence that chronic work stress predicts general and central obesity.

body mass index; employment; obesity; prospective studies; stress

Abbreviations: BMI, body mass index; MET, metabolic equivalent


   INTRODUCTION
TOP
 ABSTRACT
 INTRODUCTION
MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 
Obesity is an important cause of excess mortality and morbidity (1, 2). The increase in risk for obese persons compared with those of normal weight is modest, but, because obesity has become highly prevalent among adults in many countries (30 percent in the United States, 22 percent in England and Wales in 2001), the attributable burden is substantial (3, 4). Although weight gain is principally the consequence of positive energy balance (5, 6), stress may contribute via psychological effects on behavior and metabolism. Obesity, particularly when abdominally distributed, is a component of the metabolic syndrome (7, 8) and a risk factor for vascular disease (9). Chronic work stress, a measure of adverse psychosocial environment in adult life, predicts both metabolic syndrome (10) and cardiovascular disease (11, 12). We therefore speculated that work stress was linked to development of obesity during midlife.

Population-based studies have not found job stress to be associated with obesity (13). Poor characterization of exposure and cross-sectional design, both factors that increase the probability of type II errors, may underlie these null findings. Four phases of data collection in the Whitehall II Study provided information on duration and level of work stress (14), enabling us to examine dose-response effects on degree of obesity and abdominal obesity over 19 years of follow-up. We analyzed the incidence of obesity, measured by using carefully standardized protocols.


   MATERIALS AND METHODS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
RESULTS
 DISCUSSION
 References
 
Participants aged 35–55 years were recruited for the Whitehall II Study in 1985–1988 (phase 1) from 20 civil service departments in London, United Kingdom. After the initial clinical examination, a further postal questionnaire was carried out in 1989 (phase 2), 1991–1993 (phase 3, including a clinical examination), 1995 (phase 4), 1997–1999 (phase 5, including a clinical examination), 2001 (phase 6), and 2003–2004 (phase 7). Details of the screening examinations are reported elsewhere (15). Ethical approval for the study was obtained from the University College London Medical School Committee on the ethics of human research.

Weight and height were measured at all clinical examinations by using standardized protocols. Waist circumference was calculated from phase 3 onward with a fiberglass tape measure at 600 g of tension. BMI obesity was defined as a body mass index of ≥30 kg/m2. Waist obesity was defined as a waist circumference of >102 cm for men and >88 cm for women. The outcomes were high BMI and waist circumference measured at phase 7.

Self-reported work stress, measured by the Job Strain Questionnaire (16), is present when the participant scores high on the job demands questions and low on the decision latitude (job control) questions (defined as above or below the median score on the respective scales). There are a number of variants of this concept of work stress, one of which is the iso-strain model, which hypothesizes that socially isolated workers (i.e., without supportive coworkers or supervisors) experiencing high job strain carry the highest risk for heart disease. Iso-strain is a parsimonious instrument for measuring and analyzing workplace conditions (17). In this study, participants who reported being in the lowest tertile of work social support and who reported job strain (high job demands and low job control) were defined as having work stress (11). Accumulation of exposure to work stress over four measurement periods (phases 1, 2, 3, and 5) was assessed by adding the number of times the participant was exposed to iso-strain. The Job Strain Questionnaire was not administered at phase 4. Phase 7 measures of work stress were not included because fewer participants were employed. Chronic work stress was defined as occurring in participants who experienced iso-strain three or more times (≥75 percent of the time) over the 14-year period from phases 1 to 5. Participants who lacked work stress data at any of the phases of data collection were assigned a missing value and were excluded from the complete cases analysis.

Social position was measured by using civil service employment grade (high, intermediate, and low) at baseline. The following health behaviors were included in the analyses: smoking (self-reported smoking status at phases 1 and 5 and number of cigarettes/day at phase 1); fruit and vegetable consumption (self-reported daily consumption); dietary fiber intake (derived from the food frequency questionnaire); alcohol consumption (moderate = <22 units/week for men, <15 for women; high = 22–51 units for men, 15–35 for women; excessive = >51 units for men, >35 units for women); and exercise (vigorous physical activity hours/week at phase 1, and moderate metabolic equivalents (METs) (3–<5 METs) and vigorous METs (≥5 METs) in tertiles (MET-hours/week) based on a Minnesota-type self-report physical activity instrument at phase 5 (18)). Participants who lacked data on the specific health behavior at any of the time periods were assigned a missing value.

Analysis
Logistic regression analysis was used to analyze the odds ratios of BMI and waist obesity for the different explanatory variables. Nested multivariate logistic regression models were used to examine the effect of adjustment for explanatory variables. For incident analyses, those participants who were obese at baseline (phase 1 for BMI obesity, phase 3 for waist obesity) were excluded from the analyses.

Missing data and cohort dropout
There were 10,308 civil servants who participated in the first phase of the Whitehall II Study (1985–1988). By phase 7 of the study (1997), the participation rate was 71 percent, taking into account 605 deaths plus 6,914 participants at phase 7. Missing-data-analysis procedures used the multivariate imputation by chained equations (MICE) method of multiple multivariate imputation (19) in Stata software (20) with missing-at-random assumptions. Five copies of the data, each with missing values suitably imputed, were independently assessed in the multivariate logistic regression analyses. Estimates of parameters of interest were averaged across the copies to give a single mean estimate, and standard errors were adjusted according to Rubin's rules. Apart from all the variables in the imputed analysis (age; sex; employment grade; education; height; work stress at phases 1, 2, 3, and 5; employment status at phases 2, 3, and 5; health behaviors at phases 1 and 5; obesity at phases 1 and 7; and waist circumference at phases 3 and 7), the imputation process also included baseline predictors of dropout from the cohort, such as death, housing tenure, social support, and whether the participant's mother was still alive at baseline. This step was included to meet the requirement of missing-at-random analysis that missingness does not depend on the value of any explanatory variable, after controlling for other variables.

A missing value on the work stress measure could indicate that the data were not available at a particular phase, or that the participant dropped out of the cohort, or that the participant was not employed. If the last possibility were true, then the imputed values for the work stress variables are inapplicable for respondents not employed at phases 2, 3, and 5 (everyone was employed at phase 1). Hence, data for only those respondents who were employed at phases 1, 2, 3, and 5 (imputed n = 4,895 of 10,308 recruited at baseline) were analyzed in the multivariate models by using the imputed data. The reference group for the work stress measure for both the complete cases analyses (tables 1 and 3) and the imputed analyses (tables 2 and 4) was employed participants who never reported work stress at phases 1–5 of the study.


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  		TABLE 1. Body mass index obesity at follow-up (phase 7) by age, employment grade, work stress, and health behaviors, Whitehall II Study, London, United Kingdom, 1985–2004*

 

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  		TABLE 3. Waist obesity at follow-up (phase 7) by age, employment grade, work stress, and health behaviors, Whitehall II Study, London, United Kingdom, 1985–2004*

 

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  		TABLE 2. Multivariate multiple imputation logistic regression models of incident body mass index obesity among nonretired men and women at study phase 5, London, United Kingdom, 1985–2004*

 

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  		TABLE 4. Multivariate multiple imputation logistic regression models of incident waist obesity among nonretired men and women at study phase 5, London, United Kingdom, 1985–2004*

 

   RESULTS
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
DISCUSSION
 References
 
Bivariate analyses, based on "complete cases" logistic regression models, of the association between BMI obesity (at phase 7) and each of the explanatory variables are shown separately for men and women in table 1. Increasing age was associated with a lower risk of BMI obesity for men (trend p < 0.01), but not for women (p = 0.12). Men and women in lower employment grades were more likely to be obese. Fewer years of education was associated with higher odds of BMI obesity among women. A greater number of reports of iso-strain was associated with higher odds of obesity among men (p < 0.01). Among women, only those who reported chronic iso-strain (three or more exposures) had significantly higher odds compared with women who did not report any iso-strain over the study period. There were some gender differences in the effect of iso-strain, with men who reported two episodes of iso-strain having significantly greater odds of obesity than women reporting the same amount of iso-strain. However, the overall test for the interaction term between gender and iso-strain was not significant. The three components (job demands, decision latitude, and work social support) of the iso-strain measure tended to be associated with BMI in the expected direction, most clearly with level of social support (test for trend—men, p < 0.01; women, p < 0.05).

Smoking and BMI obesity were unrelated among women; however, among men, heavy smoking was clearly associated with obesity at phase 1. Low fruit and vegetable consumption and low fiber intake were associated with BMI obesity. High and excessive alcohol intake was linked with BMI obesity in men but not women. In addition, a low level of physical activity was associated with higher odds of obesity in both sexes at phase 5.

Table 2 displays the results of a series of nested multivariate logistic regression models of BMI obesity. For these models, imputed data were used (refer to the Materials and Methods section), and only those participants employed at phases 1, 2, 3, and 5 were included. In the models for men, adjusted for age, employment grade, and health behaviors, greater reports of work stress were associated with higher odds of BMI obesity. When obese participants at baseline were excluded from the analysis, the dose-response association between work stress and obesity remained statistically significant. For women, the effect of iso-strain on BMI obesity was weaker, but, statistically, there were no significant differences between men and women regarding the effect of iso-strain. When data for men and women were pooled in the same model, there was a graded effect of iso-strain on BMI obesity, which was robust to adjustment for confounders, potential mediators, and gender interaction effects.

Tables 3 and 4 repeat tables 1 and 2, except that large waist circumference was used as the outcome. Increasing age was associated with higher odds of waist obesity among women (p < 0.01) but not men (p = 0.70) (table 3). The social gradient in waist obesity was stronger among women compared with men. Fewer years of education was associated with higher odds of waist obesity in both sexes. A greater number of reports of iso-strain was associated with higher odds of waist obesity among men (p < 0.01). Among women, a similar tendency was evident, but the trend was not significant (p = 0.16). Levels of job demands and decision latitude were not significantly related to waist obesity. Perceived low work social support was associated with waist obesity in both sexes in a dose-response manner (test for trend—men, p < 0.01; women, p < 0.05).

Smoking was clearly related to high odds of waist obesity in men and women at phase 1. Low fruit and vegetable consumption and low fiber intake were associated with waist obesity. High and excessive alcohol intake was linked with waist obesity in men but not women. A low level of physical activity was associated with higher odds of waist obesity in both sexes at phases 1 and 5.

In the multivariate, imputed analyses (table 4), a greater number of reports of work stress was associated with higher odds of waist obesity among men in the models adjusted for age, height, employment grade, and health behaviors. When data for baseline waist-obese participants were removed from the analysis, the dose-response association remained significant for men. Among women, similar to BMI obesity, the effect of work stress was weaker, but there were no significant gender differences in the effect of work stress. In the pooled model of men and women, the effect of iso-strain on waist obesity remained robust to adjustment and gender interaction effects.


   DISCUSSION
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
References
 
Incident obesity was related to frequency of reports of job strain over 19 years in a dose-response manner in this study. Adjustment for important potential confounders produced small changes in effect estimates for risk of both general and central obesity, giving firm evidence that high psychological workload, together with lack of social support at work, acts as a causal factor for obesity. Our findings are based on exposure assessment over a substantial part of working life and, to our knowledge, are unique in including repeated measurements of work stress. Exclusion of those persons defined as obese at baseline altered the stress–incident obesity association marginally, further strengthening a causal interpretation.

By characterizing work stress exposure with multiple measures, we conducted a prospective study of the cumulative effect of work psychosocial adversity on two measures of obesity. Previous cross-sectional studies (13), based on a single measure of exposure, have shown an association between job strain and higher central obesity in two samples of men (21, 22), but not others, and null associations with general obesity.

Previous findings from this study showed that work stress is a predictor of incident coronary disease. Two established models have been examined. A high ratio of effort to reward predicted coronary events after adjustment for employment grade, the effect being clearest for those reporting low social support at work (23). Job strain, defined as concurrent low decision latitude (control) and high demands, also predicted coronary events, but the effect did not differ by level of social support (24). Analysis of a population-based sample of Swedish men found a clear elevation in cardiovascular mortality risk for those with combined exposure to low control and low support at work (25), and, in the Whitehall II Study, iso-strain predicted development of metabolic syndrome (10). Our present findings are consistent with a pathway leading from job stress to disease that involves weight gain and/or increased central obesity (26, 27).

The main potential confounder of the association observed here is socioeconomic position. Lower occupational status is linked with higher BMI and central obesity and with one of the dimensions of iso-strain—low job control (28, 29). In our cohort, socioeconomic position was only moderately associated with chronic iso-strain. Therefore, overall, socioeconomic position did not behave as a major confounder. In addition, those in higher employment grades are taller; hence, stature may be an indirect confounder of the work stress–waist obesity relation, given its correlation with waist circumference (30). Adjustment for employment grade, plus height in the case of waist obesity, reduced the size of work stress effects only slightly.

The development of obesity may involve direct neuroendocrine effects of chronic stress, indirect behavioral effects mediated by excess energy intake (which cannot be measured in large study samples), physical inactivity and excess alcohol consumption, or both direct and indirect pathways. We controlled for health behaviors with repeated measurements over the course of follow-up, and the resulting small attenuations suggest that differing behaviors neither confound nor fully explain the work stress effect. Chronic stress alters neuroendocrine activity in ways that may stimulate or inhibit appetite (31, 32). In this cohort, dietary pattern is associated with obesity and employment grade, but we found that grade differences in diet were largely unrelated to decision latitude, one of the three dimensions of the job strain model (33). The present analysis further suggests that physical inactivity and excess alcohol consumption partially explain the link between iso-strain and obesity. Previous studies of retail and office workers similarly observed inconsistent associations between job strain, job demands, alcohol consumption, sedentary behavior, and other unhealthy behaviors (34, 35).

Direct neuroendocrine mechanisms may contribute to the development of obesity during long-term work stress. It has been proposed that chronic stress alters adrenocortical activity, leading to insulin resistance, abdominal obesity, and other features of the metabolic syndrome (26, 36, 37). Longitudinal studies are lacking; however, individuals with the metabolic syndrome have high urinary cortisol output and other neuroendocrine changes (38). Among these, cardiac autonomic activity, indexed by heart rate variability, appears to be important. Low heart rate variability (indicating sympathetic arousal and vagal withdrawal) is linked with low job control and a limited social network, and with large waist circumference (39). In the present study, the associations of iso-strain with BMI obesity and waist obesity were similar in size, consistent with a direct neuroendocrine mechanism but not providing specific support for it.

It is recognized that BMI is an imperfect measure of obesity that cannot distinguish between adiposity and muscle mass, particularly in older people. Consistent with this issue, the excess risks of all-cause and cardiovascular disease mortality associated with overweight and obesity, based on BMI, have been shown to decline among those older than age 65 years (40). Here, the average age at follow-up was 61 years, and the observed reduction in risk of BMI obesity in men with age was not reflected in the corresponding findings for waist obesity. Although the size of the iso-strain effects on BMI and waist obesity are similar, it may be that the measure of central adiposity at phase 7 will prove to be more strongly related to future disease risk, and therefore be a more useful index of obesity, in our aging study population.

Our study linking job stress and obesity has public health implications, since it adds to the evidence that there is a psychosocial dimension to the rapid rise in obesity prevalence (41). Within countries, the social gradient in obesity may be becoming steeper (42), and, between countries, the proportion of obese adults is related to income inequality (43). Obesity is a risk factor for type 2 diabetes, cardiovascular disease, gall bladder disease, and some cancers (44–46) and is therefore an important target for strategies seeking to prevent disease and reduce health disparities. Our findings highlight the importance of workplace organization (47) as well as the wider experience of social inequality.

This study is limited in its generalizability to non-European ethnic groups. Whitehall II Study participants are predominantly White and European, although South Asian participants in the study report more depression and lower levels of decision latitude and social support at work (48). These differences may contribute to the higher coronary risk experienced by those of South Asian origin in the United Kingdom, but it remains to be established whether the work stress–obesity effect demonstrated here is part of the explanation for this health disparity.

This prospective study shows a dose-response association between exposure to work stress and risk of obesity at follow-up. Employees experiencing chronic work stress have approximately 50 percent higher odds of obesity compared with those without work stress, after taking into account socioeconomic position and variation in adverse health behaviors. The study provides evidence that, in addition to the known effects of excess calorie intake and physical inactivity, stressors from everyday life may contribute to the problem of adult obesity.


   ACKNOWLEDGMENTS
 
The Whitehall II Study has been supported by grants from the Medical Research Council; British Heart Foundation; Health and Safety Executive; Department of Health; National Heart, Lung, and Blood Institute (HL36310), United States, National Institutes of Health; National Institute on Aging (AG13196), United States, National Institutes of Health; Agency for Health Care Policy Research (HS06516); and the John D. and Catherine T. MacArthur Foundation Research Networks on Successful Midlife Development and Socio-economic Status and Health. M. G. M. is supported by an MRC Research Professorship.

The authors thank all participating civil service departments and their welfare, personnel, and establishment officers; the Occupational Health and Safety Agency; the Council of Civil Service Unions; and all members of the Whitehall II Study team.

Conflict of interest: none declared.


   References
TOP
 ABSTRACT
 INTRODUCTION
 MATERIALS AND METHODS
 RESULTS
 DISCUSSION
 References
 

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T. Chandola, A. Britton, E. Brunner, H. Hemingway, M. Malik, M. Kumari, E. Badrick, M. Kivimaki, and M. Marmot
Work stress and coronary heart disease: what are the mechanisms?
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M. F. Dallman, J. P. Warne, M. T. Foster, and N. C. Pecoraro
Glucocorticoids and insulin both modulate caloric intake through actions on the brain
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