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Chronic Work Stress and Marital Dissolution Increase Risk of Posttrial Mortality in Men From the Multiple Risk Factor Intervention Trial
Karen A. Matthews, PhD;
Brooks B. Gump, PhD, MPH
Arch Intern Med. 2002;162:309-315.
ABSTRACT
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Background Acute life stressors can trigger premature death, but the role of more
enduring, chronic stressors is less clear. We evaluated men's mortality risk
associated with number of different work stressors and marital dissolution
during the Multiple Risk Factor Intervention Trial (MRFIT).
Methods Men without definite evidence of coronary heart disease (CHD) at study
entry but with above-average risk for CHD mortality based on blood pressure,
serum cholesterol levels, and/or cigarette smoking were recruited into MRFIT.
Survivors at the end of the trial were followed up for mortality for an additional
9 years. All 12 336 survivors who completed the work-event checklist
at the annual evaluations during the trial were included in the analyses of
work stressors, whereas the 10 904 who were married at the start of the
trial were included in the analyses of marital dissolution.
Results Increasing number of different work stressors and divorce during the
trial were associated with total and cardiovascular mortality during the 9-year
follow-up period (Ps<.01 for linear trend), with
a relative risk of 1.26 (95% confidence interval, 1.07-1.48) for those reporting
3 or more different work stressors compared with those reporting none, and
relative risk of 1.37 (95% confidence interval, 1.09-1.72) for those who divorced
compared with those who remained married for total mortality. Analyses were
adjusted for age, intervention group, educational attainment, occurrence of
a nonfatal cardiovascular event during the trial, smoking, diastolic blood
pressure, alcohol consumption, and serum cholesterol level (the last 4 adjustments
were trial averages).
Conclusion Work and marital stressors increase risk for mortality in men.
INTRODUCTION
ACUTE LIFE stressors, including such diverse events as bereavement,
earthquakes, terrorist activities, missile strikes, and episodes of extreme
anger, can trigger myocardial infarction and death.1-4
Less clear is the association of mortality with chronic, more enduring life
stress and the accumulation of stressful life experiences across years.
Work-related stress is the most widely studied chronic life stressor
relevant to cardiovascular disease (CVD).5-8
Individuals employed in jobs they or others describe as high in work strain,
ie, jobs with high demands for performance and low decision-making latitude
or with high demands and low rewards, are at elevated risk for all-cause and
CVD mortality.6, 9-10
However, individuals do not occupy jobs at random, and other characteristics,
eg, low socioeconomic status, correlated with jobs that are demanding and
low in control or reward, may account for the association between the work
strain and elevated risk for coronary mortality. Stated differently, job strain
may be a pathway by which socioeconomic status has an impact on health. Indeed,
statistical adjustments for cardiovascular risk factors and occupational prestige
substantially reduce the effect size of job strain or reward on mortality.9-10
Another important life stressor is an unhappy marriage, which can result
in separation and divorce.11 International
studies show that divorced men have higher mortality rates than married men.12 This pattern could result from certain biases, eg,
married men who are quite ill could be "rejected" because they can no longer
perform the breadwinner role, or divorced men in poor health could take longer
to find a suitable new partner.13 On the other
hand, divorce may have a negative effect on mental health, including increased
negative affect, reduced sense of purpose and identity, and altered relationships
with children and community, all of which may have physiological costs. The
effects of marital dissolution could spill over to the quality of men's work
life, leading to additional risk associated with the accumulation of work
stressors.
The objective of the present study was to evaluate the effects of chronic
work stress and marital dissolution on 9-year all-cause and CVD mortality
in a large cohort of men enrolled in the Multiple Risk Factor Intervention
Trial (MRFIT).14 Rather than categorize work
stress indirectly by occupation or by self-reported subjective characteristics
of the occupation, we assessed the accumulation of different types of work
stressors across 6 years. To reduce the likelihood of interpretative ambiguities,
we assessed the effects of marital dissolution only among those married at
entrance into the MRFIT. Very detailed information regarding major cardiovascular
risk factors was available to serve as statistical controls for health status.
SUBJECTS AND METHODS
DESIGN OF THE MRFIT
Screening for the MRFIT involved 361 662 men aged 35 to 57 years
at 22 clinical centers in 18 US cities. On the basis of this initial screening,
12 866 men were recruited into the trial without definite evidence of
clinical coronary heart disease (CHD) but with above-average risk for death
due to CHD because of high blood pressure, elevated serum cholesterol levels,
and/or cigarette smoking.15-17
After recruitment, the MRFIT involved randomization of participants into special
intervention (n = 6428) or usual care groups (n = 6438). The special intervention
involved intervention visits designed to alter eating patterns to reduce the
intake of saturated fats and cholesterol, to reduce weight, and to achieve
smoking cessation. Details of the multifactor intervention program are described
elsewhere.18-19
MEASUREMENT OF WORK AND MARITAL STRESS
A checklist of life events was administered at study entry and during
the first, second, third, fourth, and fifth annual examinations. This checklist
did not include an option for indicating that an event had not occurred. As
a result, a missing response on items in this questionnaire did not enable
differentiation of missing data from intentional indications that an event
had not occurred. However, the life-events checklist was administered along
with a number of other questionnaires; therefore, we treated data as missing
for participants with known missing data for 5 forced-choice questions that
directly preceded or followed (depending on year) the life-events questionnaire.
Missing data increased steadily from baseline (n = 64 [0.5%]) to year 5 (n
= 1550 [12.0%]) because of participant death, missing questionnaire data,
or study attrition.
The work-stress measure contained 7 life events (Table 1). These 7 items were associated with "feelings of being
overwhelmed by difficult life situations" using a  2 analysis
of the entire sample, suggesting these items are experienced as stressors
by most people. An eighth work item, retirement, was not associated with such
feelings, and therefore was excluded. Repeated reports of an event (eg, being
demoted) could reflect either multiple events or the participants' conceptualization
of the event (eg, the demotion per se vs continued employment in a demoted
position). In consequence, regardless of the number of times a participant
reported the occurrence of a single event, the number of different stress
domains with an occurrence reported at some time during the trial (at study
entry and during the first through fifth annual examinations) was used. In
the analysis of posttrial deaths, 4 groups (0, 1, 2, and  3 domains) were
considered.
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Table 1. Events in Each Stress Domain and Percentage of Men Who Reported
That Event Occurred
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A question regarding marital status was administered at the start of
the trial to identify those currently married. The life-events questionnaire
included the following 3 relevant events: "separation from your wife because
of martial problems," "starting to live with your wife again after having
been separated," and "getting divorced." The response proportions of participants
are shown in Table 1. For participants
married at the start and alive at the end of the trial, the following 3 distinct
categories were used: married during the trial (those not reporting separation
or divorce), separated during the trial (those reporting a separation and/or
reunion after separation during the trial but not reporting divorce), or divorced
during the trial. Most trial survivors (n = 10 904 [88.4%]) were classified
into 1 of these 3 categories (n = 9817 for married, n = 513 for separated,
and n = 574 for divorced).
RISK FACTOR ASSESSMENT
The following risk factors were considered: age at study entry, MRFIT
group assignment (special intervention vs usual care), education measured
on a scale from 1 (eighth grade or less) to 9 (graduate or professional degree),
and measurements of diastolic blood pressure (DBP) (defined as the average
of 2 random-zero manometer readings), serum cholesterol concentration, and
cigarette smoking (yes vs no) during annual examinations. Diastolic blood
pressure (DBP), serum cholesterol level, and smoking were averaged across
the available examination results for analytic purposes. Further details regarding
these assessments are published elsewhere.20-21
MORBIDITY AND MORTALITY ASCERTAINMENT
A nonfatal cardiovascular event during the trial was defined as angina
or intermittent claudication by Rose questionnaire criteria,22
congestive heart failure, peripheral arterial occlusive disease, stroke, left-ventricular
hypertrophy on electrocardiographic findings, impaired renal function, accelerated
hypertension, coronary artery bypass surgery, serial electrocardiographic
evidence of myocardial infarction, or definite clinical myocardial infarction.23 Men were also asked in year 6 whether they were unemployed
and the reason for their unemployment, which included disability and its cause.
Causes included heart disease and circulatory disease.
Before the end of the trial in February 1982, deaths were ascertained
using next-of-kin interviews, routine follow-up of missed clinic visits, responses
to postcards sent to the usual care participants, and searches of publicly
accessible files of deceased persons. Cause of death was assigned by a 3-member
panel of cardiologists not associated with the MRFIT and unaware of the participants'
group assignment. Details regarding ascertainment of mortality during the
trial have been previously reported.14 Since
February 1982, vital status has been ascertained by matching identifying information
reported by participants at the time of enrollment with the National Death
Index. The latest search of the National Death Index was for all deaths through
December 1990 and is considered to be essentially 100% complete.24
To determine cause of death, death certificates were collected and coded independently
by 2 nosologists using the International Classification
of Diseases, Ninth Revision (ICD-9).14 Disagreements between the nosologists were adjudicated
by a third nosologist. The ICD-9 codes corresponding
to the cause-specific mortality categories considered in this study are reported
elsewhere.14
STATISTICAL ANALYSES
Differences in participants' characteristics were tested as a function
of the number of work stressors during the trial (grouped into 0, 1, 2, and 3
different stressors) and marital status using 2 analyses for dichotomous data
and analyses of variance with linear trend analysis for continuous data.
Mortality after the trial was analyzed using Cox proportional hazard
regression equations and 95% confidence intervals (CIs) for the relative risks
(RRs) associated with the number of work stress domains represented during
the trial or the occurrence of separation or divorce during the trial. To
control for possible confounding variables, additional analyses included age,
MRFIT group assignment, DBP, serum cholesterol level, cigarette smoking, and
alcohol consumption (with the last 4 variables averaged across the available
trial examinations) as covariates. Nonfatal cardiovascular event during the
trial was also included as an additional control variable in further analyses
of all-cause and CVD mortality. Contrasts were used to determine RRs corresponding
to the comparison of no reported life stress with increasing numbers of different
life stressors (ie, 1, 2, and 3) and the comparison of married with ever
separated or ever divorced status. A polynomial contrast was specified to
determine whether a significant linear trend was associated with the change
in RRs across stress groups. A significant linear trend would suggest that
an increasing number of stressors or increasing stress from marriage to divorce
was associated with increasing risk for mortality. A test for the interaction
of work stress and marital dissolution with the main effects in the model
was conducted among those who were married at the beginning of the trial to
evaluate whether the effects of work and marital stress were additive or interactive.
RESULTS
CHARACTERISTICS OF PARTICIPANTS AS A FUNCTION OF WORK AND MARITAL STRESS
Differences in characteristics of survivors of the MRFIT as a function
of reported stress during the trial are shown in Table 2 (work stress) and Table
3 (marital status). Those experiencing high work stress during the
trial were significantly younger at study entry, more likely to report cigarette
smoking, more educated, and more likely to experience a nonfatal cardiovascular
event during the trial (P<.05 for linear trends
or 2, depending on the variable) relative to those reporting
no work stressors. Those reporting separation or divorce from a spouse during
the trial were significantly younger at study entry, more likely to report
cigarette smoking, and more educated and had lower serum cholesterol levels
(P<.01 for linear trends or 2,
depending on the variable) relative to married participants.
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Table 2. Characteristics of All MRFIT Survivors as a Function of the
Number of Different Work Stressors During the Trial*
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Table 3. Characteristics of MRFIT Survivors Married at the Beginning
of the Trial as a Function of Marital Status During the Trial*
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WORK STRESS DURING THE TRIAL PREDICTING POSTTRIAL MORTALITY
Increasing numbers of different work stressors during the trial were
associated with a significantly increased (based on linear trend analysis)
risk for death due to all causes (RR, 1.15; P<.01)
and CVD (RR, 1.26; P<.003). There was no association
with non-CVD death, although neoplastic disease was inversely associated (RR,
0.83; P = .09) and digestive disorders were positively
associated (RR, 2.22; P = .004).
With the addition of covariates, these results remained essentially
unchanged (Table 4). However,
the reduced risk for death due to neoplastic disease was no longer marginally
significant (new P = .31). For work stress, significant
linear trends demonstrated that an increasing number of different work stressors
were associated with a significantly greater risk for death due to all causes
(P = .004), CVD (P = .006),
and digestive disorders (P = .001). Within the CVD
category, cause of death was further categorized into a CHD category, including
acute myocardial infarction (ICD-9 code 410) and
other ischemic (coronary) heart disease (ICD-9 codes
411-414 and 429.2). An increasing number of work stressors were not associated
with an increasing risk for acute myocardial infarctions (P = .16 for linear trend) but were significant for other ischemic (coronary)
heart disease (P = .02 for linear trend). These trends
reflect an increasing risk associated with greater numbers of different work
stressors. For non-CVD mortality, an increasing number of work stressors was
associated with an increasing risk for death due to digestive disorders (P = .001 for linear trend). This category of non-CVD death
does not include deaths due to neoplastic disease associated with the digestive
organs and peritoneum (ICD-9 codes 150-159); most
of these deaths (n = 32) were due to liver disease (ICD-9 code 571). However, the linear trend associated with an increasing
number of work stressors was unchanged when average alcohol consumption during
the trial was added as a covariate (P = .001).
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Table 4. Cause of Death and Relative Risk During the 9-Year Posttrial
Period Associated With Work Stress*
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The above analyses considered the effect of a progressively greater
number of different work stressors on mortality. We also considered the impact
of specific work stressors (present vs not present during the trial) on posttrial
mortality. After the inclusion of covariates (eg, DBP and occurrence of a
nonfatal CVD event), the following work stressors were significantly associated
with all-cause mortality: failure of a business (RR, 1.46 [95% CI, 1.09-1.94]; P = .01), being fired or laid off work (RR, 1.29 [95% CI,
1.05-1.60]; P = .02), and not being able to work
because of a disability (RR, 1.59 [95% CI, 1.35-1.88]; P<.001). The following work stressors were significantly associated
with CVD mortality: being fired or laid off work (RR, 1.21 [95% CI, 1.03-1.41]; P = .02) and not being able to work because of a disability
(RR, 1.40 [95% CI, 1.24-1.59]; P<.001). The following
work stressors were significantly associated with deaths due to digestive
system disease: demotion (RR, 2.58 [95% CI, 1.21-5.48]; P = .01), inability to work because of a disability (RR, 2.47 [95%
CI, 1.36-4.47]; P = .003), and personal troubles
with coworkers (RR, 2.47 [95% CI, 1.43-4.27]; P =
.001).
The strength of the association between mortality and work disability
(particularly with CVD mortality) raises the possibility that the aforementioned
effects of work stress on mortality are (1) spurious and reflect the effect
of illness on work disability and subsequent risk for mortality, or (2) real
and reflect the strong associations between work disability and work stress.
There are several reasons to believe that the effects of work stress are real.
First, when analyses of total mortality included unemployment due to any disability
at the end of the trial and the other covariates, including morbidity (ie,
occurrence of a nonfatal CVD event), the linear trend for work stress remained
statistically significant (RR, 1.15; P = .01). Unemployment
due to any disability was also independently significant in this model (RR,
1.68; P = .03). Similarly, when analyses of CVD mortality
included unemployment due to heart or circulatory disease at the end of the
trial and the other covariates, including nonfatal CVD event, the linear trend
for work stress remained statistically significant (RR, 1.22; P = .01), with unemployment due to heart or circulatory disease also
an independent predictor (RR, 2.73; P = .001). Second,
as noted above, other work-stress domains, in addition to work disability,
were independent predictors of total and CVD mortality. Finally, work stress
(not including work disability) during the first half of the trial was significantly
greater for those subsequently reporting a work disability relative to those
not reporting a work disability during the second half of the trial (means,
0.89 and 0.75, respectively; F1,12785 = 19.38; P<.001). This finding suggests that work stress precipitated a work
disability, not that a work disability (caused by illness) precipitated work
stress.
MARITAL STRESS DURING THE TRIAL PREDICTING POSTTRIAL MORTALITY
Increasing marital stress was associated with marginally significantly
greater risk for death (based on linear trend analysis) due to all causes
(RR, 1.14; P = .10) and CHD (RR, 1.26; P = .06) (data not shown). It was not associated with CVD and non-CVD
deaths. Increasing marital stress was associated with a significantly increased
risk for death due to CHD other than myocardial infarction (RR, 1.52; P = .007), digestive disorders (RR, 3.22; P<.001), and accidents (RR, 2.33; P = .002).
With the addition of covariates, these results were even stronger (Table 5). For marital stress, significant
linear trends demonstrated that an increasing degree of marital stress was
associated with a significantly greater risk for death due to all causes (P = .006), CVD (P = .04), CHD
(P = .004), CHD other than myocardial infarction
(P<.001), digestive disorders (P<.001), and accidents (P = .003).
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Table 5. Cause of Death and Relative Risk During the 9-Year Posttrial
Period Associated With Marital Status*
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ACCUMULATION OF WORK AND MARITAL STRESS DURING THE TRIAL PREDICTING
POSTTRIAL MORTALITY
Marital status and work stress were strongly associated (26 = 233.34; P<.001). The proportion
of participants reporting a separation or divorce steadily increased as the
number of work stress domains increased (0, 6.5%; 1, 8.2%; 2, 11.9%; and 3,
19.7% reporting separation or divorce). Despite this association, marital
status (RR, 1.23; P = .01) and work stress (RR, 1.16; P = .02) had independent effects on all-cause mortality
in Cox models with both variables simultaneously entered. Therefore, work
stress does not appear to function merely as a proxy for marital stress, or
vice versa.
After entering the main effects for work and marital stress, the interaction
term was entered. The interaction between the linear components of marital
stress and work stress was significant (P = .04).
To further analyze this interaction, work stress was considered within each
marital stress group. Work stress was not significantly associated with an
increased risk for death (based on linear trend) due to all causes for married
(RR, 1.11 [95% CI, 0.97-1.27]; P = .14) or separated
(RR, 0.81 [95% CI, 0.50-1.31]; P = .39) men. However,
for divorced men, an increasing number of work stressors during the trial
was associated with a significantly increased risk for death due to all causes
(RR, 1.69 [95% CI, 1.06-2.70]; P = .03 (Figure 1). Results of the interaction tests
for CVD mortality were nonsignificant, presumably because of small numbers.
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Relative risk with 95% confidence intervals of all-cause mortality
during the posttrial follow-up as a function of work stress during the trial
for divorced men only.
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COMMENT
The present study provides unique and strong evidence that the accumulation
of different work stressors and separation or divorce during the 7 years of
the MRFIT trial are predictors of subsequent all-cause and CVD mortality during
the 9-year follow-up among men. These findings are statistically significant
in analyses adjusting for age, study group, educational attainment, occurrence
of nonfatal CVD during the trial, smoking status, DBP, alcohol consumption,
and serum cholesterol level. Subsidiary analyses also showed that statistical
controls for unemployment due to disability did not affect the results for
work stress. Thus, the effects of work stressors and separation or divorce
were unlikely to be due solely to poor health status leading to more work
stress or marital dissolution or due to work stress being a marker for low
socioeconomic status (at least as indexed by educational attainment).
Furthermore, the accumulation of different work stressors among those
men married at the beginning of the trial had the most adverse impact on all-cause
mortality among those who were subsequently divorced during the trial. Thus,
a synergistic adverse effect may occur when different domains of stressors
co-occur in individuals' lives. Conversely, the accumulation of different
work stressors did not affect the mortality experience of those who remained
married throughout the trial, suggesting that remaining married in midlife
has protective effects in the face of adverse experiences at work.
This study had several limitations. First, the findings are restricted
to men. Indeed, in contrast to the present findings, a recent study of female
patients with coronary disease showed that work stress was not related to
subsequent morbidity, although marital stress was.25
Second, the work-stress checklist was imperfect, as it did not include an
explicit indicator of no event or a rating of duration or intensity of the
stressor. Furthermore, the cause or severity of work disability on the checklist
was not known, although it was known whether work disability was severe enough
to lead to unemployment at the end of the trial. Finally, although all analyses
included covariate measures of health status that were carefully collected
in a standardized fashion, with particular attention to CVD risk, unmeasured
illnesses during the trial could affect both stress and mortality.
How does work stress or marital dissolution increase the risk for mortality?
Work stress and marital dissolution may result in increasing levels of standard
risk factors after the cessation of the trial. We are not able to evaluate
this possibility, because MRFIT participants were not seen in the clinics
after the conclusion of the trial. Work stress and marital dissolution can
affect health behaviors, eg, by increasing smoking and alcohol consumption,
altering dietary pattern, and disturbing restful sleep.26-27
However, for the most part, we were able to control statistically for these
health behaviors, so other factors probably played an important role. Stress
has an impact on a number of systems relevant to CVD mortality that were not
assessed in MRFIT. In particular, stress may increase levels of circulating
catecholamines, ambulatory blood pressure, and cortisol28-29;
may reduce heart rate variability and impair vagal tone30-31;
and may enhance platelet reactivity and release of platelet products.32 Stress also increases susceptibility to infectious
disease33-34 and contributes to
rapid progression in human immunodeficiency virus infection.35-36
Work stress and marital dissolution may result in poor decision making, causing
risky behaviors.37 Our data provide indirect
support for this notion, because those men who reported more types of work
stressors and divorce during the trial also tended to be at risk for accidental
death.
Chronic stress at work or in primary relationships is subject to intervention
at a clinical level and through work-based programs. As suggested by Rozanski
et al,5 integrating psychosocial interventions
at a clinical level is feasible by having physicians counsel their patients
regarding psychosocial risks, by evaluating and implementing preventive interventions
in clinical settings on a patient-specific basis, and by modifying the pathophysiological
pathways connecting stress and early death. Work-based programs can provide
counseling and training for resolving conflicts with bosses and coworkers.
Avoiding marital strife, especially when stressed by work difficulties, can
be assisted by adequate counseling and support mechanisms.
AUTHOR INFORMATION
Accepted for publication June 6, 2001.
This study was supported by grants HL58867, HL65111, and HL65112 from
the National Institutes of Health, Bethesda, Md.
We thank James Neaton, PhD, Lewis Kuller, MD, DrPH, and Greg Grandits,
MS, for their consultation on analytic strategy and manuscript preparation.
Corresponding author and reprints: Karen A. Matthews, PhD, Department
of Psychiatry, University of Pittsburgh, 3811 O'Hara St, Pittsburgh, PA 15213
(e-mail: matthewska{at}msx.upmc.edu).
From the Department of Psychiatry, University of Pittsburgh School
of Medicine, Pittsburgh, Pa (Dr Matthews), and the Department of Psychology,
State University of New York–Oswego (Dr Gump).
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