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From the Finnish Institute of Occupational Health, Helsinki, Finland (M.K., P.L.-A., L.K.-K., R.L., J.V., M.H.); the University of Helsinki, Helsinki, Finland (M.K., M.E.); University of Jyväskylä, Jyväskylä, Finland (J.K.).
Address correspondence and reprint requests to Prof. Mika Kivimäki, the Department of Psychology, Finnish Institute of Occupational Health, Topeliuksenkatu 41 aA, FI-00250 Helsinki, Finland. E-mail: mika.kivimaki{at}ttl.fi
| ABSTRACT |
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Methods: This prospective cohort study involved 788 industrial employees (534 men, 254 women, mean age 37.3, SD = 12.0) who were initially free from cardiovascular diseases. The baseline examination in 1973 determined cases of cardiovascular disease, cardiovascular risk factors, and the extent of recovery from work. Data on mortality in 1973 to 2000 were derived from the national mortality register.
Results: Sixty-seven cardiovascular deaths and 102 deaths from noncardiovascular causes occurred during the mean follow-up of 25.6 years. Employees who seldom recovered from work during free weekends had an elevated risk of cardiovascular death (p = .007) but not of other mortality (p = .82). The association between incomplete recovery and cardiovascular death remained after adjustment for age, sex, and 16 conventional risk factors, including occupational background, cholesterol, systolic pressure, body mass index, smoking, alcohol consumption, physical inactivity, depressive symptoms, fatigue, lack of energy, and job stress. The association was not explained by deaths that occurred close to the assessment of recovery from work.
Conclusions: This study suggests that incomplete recovery from work is an aspect of the overall risk profile of cardiovascular disease mortality among employees.
Key Words: cardiovascular mortality psychosocial factors risk factors
Abbreviations: BMI = body mass index; CHD = coronary heart disease; CI = confidence interval; ICD = International Classification of Diseases.
| INTRODUCTION |
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However, only indirect or self-reported evidence is available to support incomplete recovery as a marker of cardiovascular risk. In the Maastricht Cohort Study, a high need for recovery predicted an increased incidence of self-reported coronary heart disease (CHD) during a 2.5-year follow-up among healthy employees at baseline (1). Other studies found that overlapping experiences, such as tiredness, lack of energy, stress, depressive symptoms or fatigue, often precipitated coronary events among patients with preexisting vascular disease (2,3). Incomplete recovery has been found to be associated with long-term stress, as indicated by high work demands and overtime work (46), and it is also a symptom in several stress-related disorders, including fatigue, burnout, neurasthenia, exhaustion, and depression (2,79). An additional source of evidence involves stress-related physiological changes (10). A high need for recovery has been shown to be related to delayed recovery of cortisol and adrenaline excretion (4,11). Among patients with CHD, stress due to incomplete recovery from work may lower the arrhythmic threshold and trigger myocardial ischemia (12,13).
The METELI study is a prospective cohort study assessing health and various potential risk factors at baseline and data on 28-year cardiovascular mortality among industrial employees (14,15). This design enabled us to determine whether incomplete recovery from work is predictive of cardiovascular death in an initially healthy working population and whether this association is independent of other risk factors. Previous evidence of an association between incomplete recovery from work and cardiovascular disease has been limited to considerably shorter follow-up periods and self-reported data on the health outcome (1).
| METHODS |
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The baseline data were gathered by questionnaire, interviews, and clinical examinations in 1973. Data on mortality in 1973 to 2000 were derived from the national mortality register. After the exclusion of those with cardiovascular disease at baseline (n = 90), the study cohort comprised 812 employees (15). Of them, 788 (534 men, 254 women) responded to a question about recovery from work during free weekends. Ethical approval for the study was obtained from the Hospital District of Helsinki and the Uusimaa Ethics Committee for research in occupational health and safety.
Assessment of Recovery From Work
Previous studies have measured incomplete recovery from work with questionnaire items that refer to workdays (sample items: "At the end of a working day I am really worn out" and "I find it hard to relax at the end of a working day") (16,17). However, some need for recovery is expected after work, and such responses may not necessarily indicate a health risk (8). In the METELI study, the question of incomplete recovery was anchored to the inability to recover during longer recuperation periods. The following question was included in the baseline survey: "Is a free weekend long enough for you to recover from work?" The word "free" refers here to "free of paid work." The response options were 1 = almost always, 2 = very often, 3 = sometimes, 4 = seldom, and 5 = hardly ever.
Assessment of Other Baseline Characteristics
The demographic and occupational background information assessed in 1973 included age, sex (1 = women, 2 = men), educational attainment (1 = low, ... 7 = high), occupational status (4 = managers, 3 = other office staff, 2 = skilled workers, 1 = semiskilled workers), salary (1 = lowest category, ... 11 = highest category), presence or absence of a secondary job (1 = yes, 0 = no), and shift work (1 = yes, 0 = no) (15,18).
As biological and lifestyle risk factors, we measured serum total cholesterol concentration (mg/dl), systolic blood pressure (mm Hg), body mass index (BMI, kg/m2), smoking (pack-years), physical activity, and the frequency of alcohol use (1 = never, ... 8 = daily) (15,19). The physical activity index (exercise and domestic activity) was based on a 51-item checklist and an interview by trained research assistants. The total hours spent in physical activity during the past year was calculated by summing up the time in activities in which the intensity represented an energy expenditure of 500 kilocalories per hour or more (19).
The psychosocial factors measured included depressive symptoms, fatigue, lack of energy, and the components of job strain (job demands and job control). Depressive symptoms were measured with a 6-item scale (Cronbachs
reliability
= 0.69) including questions on loss of interest and pleasure, loss of appetite, increased sleep disturbance, and fatigue (14). The response format was a 4-point Likert scale, and the scale was constructed by summing the response scores of the individual questions (range, 621). The assessment of fatigue and lack of energy was based on the responses (1 = yes, 0 = no) to a symptom check list. The four questions on job demands dealt with the degree of responsibility at work, task difficulty, and mental load (
= 0.67) and the 12 questions on job control concerned decision authority and skill discretion (
= 0.78) (15). The responses were given on a 5-point Likert-type scale. We averaged the response score of all the scale items to indicate job demands and job control (range, 15 in both scales).
Outcome Definition
Mortality data were collected from the Statistics Finland national mortality register using the participants personal identification codes (a unique number assigned to each Finnish citizen) (15). Statistics Finland is the official government statistics agency, and its mortality register covers the entire nonemigrated Finnish population (the proportion of emigrants being 3.8%, www.stat.fi). The date and cause of death of the participants who died between the date of their clinical examination (which took place between February 5 and June 30 1973) and November 1 2000 were obtained.
The causes of death were coded according to the International Classification of Diseases, Eighth Revision (ICD-8) in 1973 to 1986, the ICD Ninth Revision in 1987 to 1995 and the ICD 10th Revision in 1996 to 2000. Statistics Finland provided the researchers with a classification that converted the different codes (up to 1997; subsequent deaths were classified according to the death certificates) to the following categories: ischemic heart diseases (referring to codes I20I25 in ICD-10), other heart diseases (I30I52), cerebrovascular diseases (I60I69), and other diseases of the cardiovascular system (I00I19, I26I29, I70I99). These codes were pooled to indicate death due to cardiovascular diseases. Information on the basic cause of death was utilized. The cause of all other deaths was categorized as noncardiovascular.
Statistical Analysis
We treated all of the baseline characteristics as continuous or binary variables. As the distributions of physical activity and pack-years were skewed, we log-transformed the values to give a better fit to the normal distribution. To examine associations among the baseline characteristics, we calculated a correlation (Pearson r) matrix. We fitted Cox proportional hazards models to study associations between the baseline measures and mortality. The follow-up period was calculated from the date of the baseline examination to the date of death or, for those who did not die, to November 1, 2000. The 19 time-dependent interaction terms between each predictor and logarithm (follow-up period) were all nonsignificant (all p > .09); therefore, the proportional hazards assumption was considered justified. As the interaction between sex and recovery from work as regards cardiovascular mortality was not statistically significant (p = .38), the analyses were based on a combined sample of male and female employees. Hazard ratios and their 95% confidence intervals (CIs) for the standardized baseline measures provided risk estimates associated with a 1 standard deviation (SD) increase in the predictor variables. In addition to incomplete recovery, the multivariable models included baseline covariates entered in the following three blocks: 1) background variables (sex, age, occupational group, second job, and shift work); 2) biological and lifestyle factors (total cholesterol, systolic blood pressure, BMI, physical activity, pack-years, and alcohol consumption); and 3) psychosocial factors (depressive symptoms, fatigue, lack of energy, job demands, and job control). These analyses were repeated with categorical data using the same cutoffs as in previous studies of this cohort (continuous variables were divided into thirds; alcohol consumption was divided into categories of nondrinkers, moderate drinkers, and daily drinkers; and a measure of job strain was defined by combining the work demand and job control scales) (15,18). To verify that the results were not primarily due to deaths occurring close to the assessment of recovery, we sequentially excluded the participants who died within the 1-, 5-, and 10-year follow-ups from subgroup analyses and observed changes in the hazard ratios. To examine outcome specificity, we analyzed the association between the level of recovery and noncardiovascular mortality. All of the analyses were performed with maximum data; therefore, some variation occurred in number of participants between comparisons. The only exception was the multivariable models, which involved only the participants with no missing values for any of the 19 predictors (the variation in numbers could not bias the comparisons between these models). All of the analyses were performed with SAS software, version 8.2 (Statistical Analysis System Institute).
| RESULTS |
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As shown in Table 2, incomplete recovery was related to higher scores of depressive symptoms, fatigue, and energy loss (rs = 0.13 and 0.19, p < .001). There were weak associations of incomplete recovery with lower occupational status (r = 0.10, p < .01) and lower job control (r = 0.09, p < .05). No correlations were found between recovery and other baseline characteristics, with the exception of a slightly lower BMI among the employees with incomplete recovery (r = 0.10, p < .01).
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Outcome Specificity
During the mean follow-up of 25.6 (range, 0.927.8) years, 67 deaths from cardiovascular causes (57 for men, 10 for women) and 102 deaths from noncardiovascular causes (75 for men, 27 for women) occurred among the participants who had been free of overt cardiovascular disease at baseline. The most common causes for cardiovascular deaths were ischemic heart disease (n = 43) and cerebrovascular disease (n = 16). The main causes for noncardiovascular deaths were cancer (n = 49), accidents (n = 21), and violence (n = 10).
Table 3 shows the predictive relationships between recovery from work and deaths from cardiovascular and other causes. As an indication of outcome specificity, incomplete recovery was associated with increased cardiovascular mortality, but not with increased noncardiovascular mortality.
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Test of Robustness
Table 4 presents the associations between baseline characteristics and cardiovascular mortality. Traditional risk factors, such as higher age, male sex, high systolic blood pressure, smoking, and depressive symptoms independently predicted an increased risk for cardiovascular death. Having a second job and low job control were additional predictors. In multivariable models including background variables, as well as biological, lifestyle, and psychosocial factors, incomplete recovery from work was a significant predictor of cardiovascular death. A 1 SD increase in the standardized incomplete recovery score was associated with a 1.54-fold (95% CI, 1.231.93) increase in the risk of cardiovascular death. The estimated hazard ratio for a 3-point change on the nonstandardized score, i.e., the difference between seldom recovering and almost always recovering, was 3.42 (95% CI, 1.796.53).
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Repeating these analyses with baseline predictors categorized as in previous studies of this cohort (instead of using continuous variables) replicated the main finding. In the full model, employees who seldom recovered from work (response options "seldom" and "hardly ever" in combination) had a risk of cardiovascular death 2.66 (95% CI, 1.295.48) times that of those who almost always recovered.
Time Specificity
Table 5 presents models examining whether the association between incomplete recovery and cardiovascular mortality was attributable to differences in mortality occurring close to the assessment of recovery from work. The small changes in the hazard ratios (range between 1.23 [95% CI, 0.981.56] and 1.27 [95% CI, 1.041.55]) after successive exclusions of the participants who died during the 1-, 5- and 10-year follow-ups provide evidence against this possibility.
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Figure 1 lends further support against time specificity by showing how cardiovascular deaths by level of recovery from work were dispersed in time. An increased mortality risk for those who seldom recovered during weekends, as compared with those who always recovered, can be seen early in the follow-up period, and the mortality difference between these groups increased with time.
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| DISCUSSION |
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Incomplete recovery may represent an independent risk factor for cardiovascular death. Adjustment for established biological and lifestyle risk factors (blood pressure, BMI, smoking, alcohol intake, and sedentary lifestyle), demographic characteristics, occupational background, and psychosocial risk factors (including depressive symptoms and job stress) did not attenuate the association between incomplete recovery and cardiovascular death. Confounding due to unmeasured background differences cannot be ruled out in observational studies, and, according to the widely used criteria for the interpretation of observational data, a lack of outcome specificity may indicate such residual confounding (20). However, our data showed some outcome specificity, as incomplete recovery did not predict increased noncardiovascular mortality.
Cardiovascular death is the end point of long-term physiologic changes starting decades before the fatal event. In previous studies, patients with their first myocardial infarction have retrospectively reported feelings of tiredness, lack of energy, stress, and depression before the event (2,3), and psychological distress has been associated with a worse prognosis (2123). Because such feelings are likely to overlap with recovery from work in working populations, experiences of incomplete recovery may reflect advanced cardiovascular disease, and thus reversed causality between incomplete recovery and disease is possible. However, reversed causality can only be a partial explanation for the association between incomplete recovery and cardiovascular mortality in this study because increased mortality risk occurred during a very long follow-up period among employees who were initially free from overt cardiovascular disease. The fact that the hazard ratios did not materially change after the exclusion of deaths during the first 10 years of follow-up suggests that incomplete recovery may often precede the disease process.
Limitations
At least three limitations of this study are noteworthy. First, this is a secondary analysis from a study originally designed to examine the associations between work, health, and leisure-time physical activity (14). The recovery hypothesis was specified long after the collection of the baseline data. Thus, instead of a standard measure of recovery from work, we had to rely on the existing data, which included only one direct question on insufficient recovery, the primary predictor of this study. This single-item measure does not specify whether the recovery pertains to physical or mental recovery, and the risk of imprecise measurement that contains a substantial degree of noise is greater for this measure than standard multi-item scales. Although no psychometric studies are available on our single-item measure, the intercorrelations observed in this study provide some support for the construct validity in that insufficient recovery was associated with, but not redundant to, depressive symptoms, fatigue, and lack of energy, and its associations with conceptually more distant concepts were weaker. The fact that the association between incomplete recovery and mortality was specific to cardiovascular deaths is an indication of discriminant (predictive) validity. Nevertheless, additional research is needed to confirm our findings with well-validated measures of incomplete recovery and key confounders.
Second, because this is a secondary analysis in a data set that has been used to test a number of hypotheses (14,15,18,19), we cannot effectively rule out chance (random variation) as a possible explanation for the results highlighted in this study. Our sample was also racially homogeneous and limited to industrial employees. There is a need for replications to assess whether the findings are generalizable to other populations, other ethnic groups, and to both men and women. Larger sample sizes would provide an opportunity for a more detailed analysis of cause-specific cardiovascular deaths. For example, if cumulative stress were the key underlying factor, then incomplete recovery would be expected to be more strongly related to fatal myocardial infarctions and ischemic strokes than to hemorrhagic strokes (3,10). Further research that additionally assesses nonfatal cardiovascular events would clarify the extent to which incomplete recovery represents a marker of etiologic factors and to what extent it is associated with prognosis.
Third, there is a need for a more extensive exploration of potential explanatory factors. In future research, longitudinal assessments of potential mediating factors would be important to determine the processes, whether biological, behavioral, psychosocial, or material, that lead to disease development and the clinical manifestations of disease. Intervention studies examining whether eliminating incomplete recovery reduces disease risk would serve as a further test of causality.
| CONCLUSIONS |
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| NOTES |
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This research was supported by grants from the Academy of Finland (project no. 70139) and the Ministry of Education, Finland (188/722/2000 and 146/722/2001). M.K. and J.V. were supported by the Academy of Finland (projects no. 104891 and 105195) and the Finnish Work Environment Fund.
DOI:10.1097/01.psy.0000221285.50314.d3
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