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(Hypertension. 2000;35:561.)
© 2000 American Heart Association, Inc.
Scientific Contributions |
Hypertension Incidence Is Predicted by High Levels of Hopelessness in Finnish Men
Presented in part at the 4th International Conference on Preventive Cardiology, Montreal, Quebec, Canada, June 29 to July 3, 1997, and published in abstract form (Can J Cardiol. 1997;13[suppl B]:317B).
From the Department of Epidemiology, University of Michigan, Ann Arbor, Mich (S.A.E., G.A.K.); the Human Population Laboratory, Public Health Institute, Berkeley, Calif (D.E.G.); and the Research Institute of Public Health and Department of Community Health and General Practice, University of Kuopio, Kuopio, Finland (J.T.S.).
Correspondence to Susan A. Everson, PhD, MPH, Department of Epidemiology, University of Michigan School of Public Health, 109 S Observatory St, Ann Arbor, MI 48109-2029. E-mail severson{at}umich.edu
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Abstract |
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Abstract—Recent studies have reported that hopelessness is an important factor in cardiovascular morbidity and mortality, including ischemic heart disease, acute myocardial infarction, and atherosclerotic progression. This study examined the relationship between hopelessness and incident hypertension in a population-based sample of 616 initially normotensive, middle-aged men from eastern Finland, an area with high rates of cardiovascular disease. Participants completed a medical examination and a series of psychological questionnaires at baseline and at the 4-year follow-up. Hopelessness was measured by 2 items assessing negative expectancy about the future and one’s goals. A logistic regression model with adjustments for age, body mass index, baseline resting blood pressure, physical activity, smoking, alcohol consumption, education, parental history of hypertension, and self-reported depressive symptoms revealed that men reporting high levels of hopelessness at baseline were 3 times more likely to become hypertensive (systolic blood pressure
165 mm Hg and/or a diastolic blood pressure
95 mm Hg or confirmed use of antihypertensive medication) in
the intervening 4 years than men who were not hopeless (odds ratio,
3.22; 95% confidence interval, 1.56, 6.67). Men reporting moderate
levels of hopelessness were not at a significantly increased risk of
hypertension (odds ratio, 1.27; 95% confidence interval, 0.79, 2.07).
This is the first study to identify a significant relationship between
hopelessness and incident hypertension. Research is needed to explore
the neuroendocrine and central nervous system mechanisms underlying
this association.
Key Words: cardiovascular diseases • depression • hopelessness • men • psychology • risk factors
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Introduction |
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Several risk factors for hypertension that have important lifestyle and psychosocial components have been identified, including obesity,1 excess sodium consumption,2 excess alcohol consumption,3 and physical inactivity.4 5 All are associated with an increased risk of hypertension. Research also suggests that psychosocial stress and concomitant sympathetic nervous system reactivity may play a role in hypertension and increases in blood pressure (BP) over time,6 7 8 as may certain emotions, including anger, anxiety, and depression.9 10 11
Previously, we reported that hopelessness, characterized as a sense of futility and negative expectations about the future and one’s personal goals, predicts incident myocardial infarction and cardiovascular mortality12 and is associated with a faster progression of carotid atherosclerosis13 in middle-aged men. In both cases, the effects of hopelessness on cardiovascular disease morbidity and mortality were unchanged after controlling for depressive symptoms in general. Data from the National Health Examination Follow-up Survey also demonstrated that hopelessness was related to incident fatal and nonfatal ischemic heart disease in men and women during 12 years of follow-up and that the effect of hopelessness was stronger than the effect of depression on outcomes.14 In other words, hopelessness seems to have cardiovascular consequences that are distinct from or stronger than those associated with depression. It is important to note, however, that hopelessness is often a major symptom of depression and, thus, it can be difficult to disentangle these constructs. It may be that hopelessness is a critical component or feature of depression which affects cardiovascular function and that other symptoms of depression are more weakly related or unrelated to cardiovascular disease risk.
To the best of our knowledge, no previous study has specifically examined the effect of hopelessness on hypertension, although recent studies have examined the relationship between depression and hypertension. Data from the Coronary Artery Risk Development in Young Adults study showed that depression predicted incident hypertension over a 5-year period in young black but not white adults.15 Also, results from the first National Health and Nutrition Examination Survey Epidemiologic Follow-up Study indicated that high levels of depression and anxiety predicted the onset of hypertension 7 to 16 years later in middle-aged white persons and in young and middle-aged black people.11 These 2 studies did not assess the specific effects of hopelessness on BP elevation.
The present study used data from the Kuopio Ischemic Heart Disease Risk Factor Study (KIHD) to investigate the association between hopelessness and incident hypertension, independent of depression. Information on health habits, family illness history, and several anthropometric and demographic measures enabled us to examine the potential confounding influences of other risk factors for hypertension.
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Methods |
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Study Population
The KIHD study is a population-based study of biological, psychosocial, and socioeconomic risk factors for atherosclerotic vascular disease, ischemic heart disease, mortality, and other outcomes16 in middle-aged men from Kuopio and its surrounding communities in Eastern Finland, a region with high coronary morbidity and mortality.17 A total of 2682 participants (82.9% of those eligible) aged 42, 48, 54, or 60 years were enrolled in the study in 2 cohorts: 1166 men aged 54 years (83.3% of those eligible) were enrolled between March 1984 and August 1986, and a second cohort of 1516 men aged 42, 48, 54, and 60 years (82.6% of eligible) were enrolled between August 1986 and December 1989. Ultrasound examinations of the right and left carotid arteries were performed on 1229 men from the second cohort as part of their baseline examination. These participants were invited to take part in a follow-up study, which was conducted between March 1991 and December 1993. Of the 1229 men who were eligible for follow-up, 1038 (88.2%) participated. Of the remaining men, 52 could not participate because of death, severe illness, or migration; 107 refused; and 32 could not be contacted. Follow-up ranged from 3.8 to 5.2 years, with an average of 4.2 years. The KIHD study protocols for the baseline and follow-up examinations were approved by and conducted in accordance with the research guidelines established by the University of Kuopio Research Ethics Committee. Respondents were not paid for participation, and all gave informed consent at baseline and follow-up.
For the present analyses, subjects were excluded if they
had missing BP data at baseline or follow-up (n=3), were hypertensive
at baseline (which was defined as a resting BP 165/95 mm Hg
[n=239] or a confirmed use of antihypertensive medications
[n=157]), had incomplete information on the hopelessness scale
(n=22), or had missing data on the covariates at baseline (n=1). Thus,
the findings of the present study are based on 616 initially
normotensive men who had complete data on the measures of hopelessness
and all covariates at baseline and for whom hypertension status at
follow-up was determined. Subject characteristics are shown in Table 1. Comparison of the 422 KIHD
participants excluded from the current analyses with the 616
subjects who had complete data revealed no differences in mean reported
hopelessness, age, parental history of hypertension, and average weekly
physical activity or smoking status; however, those who were excluded
tended to be less educated, consumed more alcohol per week, had a
higher body mass index (BMI), reported more depressive symptoms and, as
would be expected, had higher resting BPs (P<0.001).
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Baseline and Follow-Up Examinations
Examinations were conducted on 2 days, 1 week apart, at both
baseline and follow-up. They included a number of
physiological, biochemical, anthropometric, and
psychosocial measures (see reference 15 for complete details). Medical
history and medication use were checked during a medical examination at
both baseline and follow-up.
Hopelessness Scale
Hopelessness was measured by 2 items from a battery of
psychosocial questionnaires administered at baseline. These items were
"The future seems to me to be hopeless, and I cannot believe that
things are changing for the better" and "I feel that it is
impossible to reach the goals I would like to strive for." Using a
5-point scale, respondents indicated the degree to which they agreed
with each item (0=absolutely agree, 1=somewhat agree, 2=cannot say,
3=somewhat disagree, or 4=absolutely disagree). A hopelessness score
was created by reverse-coding and summing across items. The mean (SD)
hopelessness score was 2.4 (1.96), with a range of 0 to 8. Three groups
were formed based on response options and the meaning of the scores as
follows: men scoring 0, 1, or 2, which indicated general disagreement
with each statement, were considered low in hopelessness (59.74%);
those with scores in the midrange of the scale (3, 4, or 5), reflecting
a mixed response to the items, formed the moderately hopeless group
(31.82%); and men scoring 6, 7, or 8, which is consistent with
general agreement with both statements, were considered high in
hopelessness (8.44%).
BP Measurement
BP was measured by a trained observer with a random-zero muddler
sphygmomanometer (Hawksley). BP measurements were completed on
the first examination day at both baseline and follow-up. The protocol
was as follows: subjects rested in the supine position for 15 minutes
and had BP measured at minutes 5, 10, and 15; they then stood (standing
rest) and had one reading taken after 1 minute; and finally, after 10
minutes of seated rest, subjects had BP measured at minutes 5 and 10.
The last 2 supine and the 2 seated measurements were averaged to obtain
resting systolic BP (SBP) and diastolic BP
(DBP).
Hypertensive Status at Follow-Up
A participant was considered hypertensive at the 4-year
follow-up examination if his resting SBP was 165 mm Hg or his
resting DBP was 95 mm Hg or if he was currently taking
antihypertensive medications, as confirmed during the medical
examination. A total of 126 men (20.4%) met these criteria.
Assessment of Baseline Covariates
Baseline covariates were chosen on the basis of prior research
that showed their important associations with hypertension. To control
for the effects of depression and specifically assess the relationship
between hopelessness and risk of hypertension, we also included a
covariate representing self-reported depressive symptoms.
Measurements of covariates are described below.
Age
Baseline age was modeled by dummy-coded variables for ages
48, 54, and 60 years, with an age of 42 years as the reference
category.
BMI
BMI was calculated as weight (kg) divided by height squared
(m2). It was modeled continuously.
Cigarette Smoking
Smoking was assessed by self-report (never, former, or current).
Current smoking was modeled continuously as pack-years, and former
smokers were modeled with a dummy-coded variable. Never smoked was
the referent.
Alcohol Consumption
Consumption of beer, wine, and spirits was assessed by a
questionnaire on drinking behavior during the previous 12 months and by
a 4-day dietary record. Alcohol consumption was calculated as grams
per week and modeled continuously.
Physical Activity
Baseline physical activity was assessed by a self-report of
leisure-time activities for the previous 12 months with a questionnaire
modified from the Minnesota Leisure Time Physical Activity
Questionnaire to represent 16 of the most common leisure-time
physical activities of middle-aged Finnish men.18 For each
activity, participants reported whether they engaged in the activity
and, if they did, the frequency per month over the past year, average
duration per occasion, and the intensity level at which the activity
was performed. Each activity was assigned metabolic units
according to reported intensity. Detailed information on the
calculation, reliability, and validity of the physical activity
measures was described previously.19 A continuous
intensity-dependent measure of total duration of leisure-time physical
activity, previously associated with type 2 diabetes in the KIHD
population,20 was used in the analyses.
Education
Education was recorded as number of years of school
completed and modeled continuously.
Parental Hypertension
Parental history of hypertension was measured by participant
self-report of maternal and paternal hypertension. A dummy-coded
variable was used in analyses, with a value of "1"
assigned to any subject who reported that 1 or both parents were
hypertensive.
Resting SBP
Resting SBP was the average of 2 supine and 2 seated readings,
as described above, and modeled continuously.
Depressive Symptoms
Depressive symptoms were measured by an 18-item depression
scale developed by Roberts and colleagues21 22 23
that assesses mood disturbances, negative self-concept,
problems with eating and sleeping, loss of energy, and psychomotor
agitation or retardation. This scale assesses somatic or vegetative
symptoms of depression, but it does not include any items on
hopelessness. One point was assigned for each "true" or "false"
answer that corresponded to a depressed response; higher scores
indicate more symptoms. This scale has good internal
consistency and demonstrated reliability,23
although it does not include all clinical criteria for major
depression. Prior research found that this scale is similar
conceptually to other brief symptom checklists and that it correlated
significantly with the Beck Depression Inventory in an outpatient
clinical population (r=0.66).22 High
scores on this depression scale previously predicted excess stroke
mortality in a middle-aged and elderly population.24
Depressive symptoms were modeled continuously.
Data Analyses
The association between hopelessness and hypertensive status at
the 4-year follow-up was assessed using age-adjusted logistic
regression models with hopelessness modeled continuously and
categorically. Subsequent age-adjusted regression models examined
potential confounding by BMI, smoking, alcohol consumption, physical
activity, education, depressive symptoms, positive parental history of
hypertension, and baseline resting SBP. Separate age-adjusted
analyses were conducted to determine the associations between
depressive symptoms and hypertension risk and between hopelessness and
depression. Statistical analyses were performed with LOGISTIC,
GLM, and CORR procedures from SAS version 6.12 software (SAS
Institute).
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Results |
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Hopelessness and Risk of Hypertension
An age-adjusted logistic regression model with hopelessness modeled continuously showed that each 1-point increase in hopelessness was associated with a 16% greater risk of hypertension (odds ratio [OR], 1.16; 95% confidence interval [CI], 1.05, 1.28). This association was unchanged after adjustments for cigarette smoking, alcohol consumption, BMI, resting SBP, physical activity, education, parental history of hypertension, and depressive symptoms (OR, 1.15; 95% CI, 1.02, 1.29). Subsequent logistic regression models with hopelessness modeled categorically showed that the men who had the highest levels of hopelessness at baseline were 3 times more likely to become hypertensive 4 years later than men who were not hopeless, after adjusting for age and other risk factors. Hypertension risk was slightly elevated in moderately hopeless men, but this increase was not significant. Table 2 shows the ORs and 95% CIs from the age- and risk factor–adjusted models for low, moderate, and high hopelessness in relation to incident hypertension at the 4-year follow-up.
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Effect of Atherosclerotic Progression
We previously reported that high levels of hopelessness were
associated with the accelerated progression of carotid
atherosclerosis over 4 years in the KIHD
study.13 Because atherosclerosis can
contribute to increased vascular resistance and elevations in BP, we
then examined the effects of hopelessness on the risk of hypertension,
taking into account the 4-year changes in
atherosclerosis. Results from this logistic regression
model were nearly identical to the risk factor–adjusted model reported
in Table 2, with more than a 3-fold increased risk of
hypertension among the most hopeless men (OR, 3.18; 95% CI, 1.53,6.60)
and a small but nonsignificant increased risk in the moderately
hopeless group (OR, 1.27; 95% CI, 0.78, 2.07). Thus, atherosclerotic
changes did not account for the increased risk of hypertension
associated with high levels of hopelessness.
Effect of Behavioral Changes
It is well known that depressed or hopeless individuals are less
likely to be medically compliant, less able to make behavioral
changes,25 more likely to smoke and abuse
alcohol,14 26 27 28 and less likely to be physically
active.29 30 Because these lifestyle habits are also risk
factors for hypertension, we examined the influence of hopelessness on
hypertension after taking into account 4-year changes in alcohol
consumption, smoking, physical activity, and BMI. Data on behavioral
risk factors at baseline and at 4-year follow-up were available for 570
participants. Results from the separate logistic regression models in
which hopelessness was modeled continuously and categorically are
presented in Table 3. These
analyses show a somewhat stronger association between
hopelessness and hypertension risk than was seen in the models that
adjusted only for baseline risk factors. This pattern of findings
indicates that the most hopeless men did not show worse behavioral
profiles during the 4 years of follow-up, which was confirmed by
separate analyses of behavioral changes. Overall, participants
increased their alcohol consumption slightly, gained weight (as
evidenced by greater BMI), and increased their activity levels, but
smoking rates changed little over 4 years. However, none of these
changes (or lack of changes) differed by level of reported hopelessness
at baseline.
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We also examined interactions between hopelessness and smoking and alcohol consumption but found no significant effects. Our results imply that behavioral or lifestyle factors are not the mechanisms by which hopelessness increases hypertension risk in this population.
Hopelessness and 4-Year Change in BP
Next, we assessed the relationship between hopelessness and change
in BP over the 4 years of follow-up, regardless of hypertensive status
at follow-up. Mean (SD) changes in SBP and DBP were 3.8 (11.3) and 1.4
(7.4) mm Hg, respectively. Results were consistent with,
although not as strong as, the results from our primary
analyses. Linear regression models adjusted for age and
baseline resting BP demonstrated that increasing hopelessness was
associated with greater changes in SBP and DBP (ß=0.314 and 0.235,
respectively, for SBP and DBP change), but these changes were only
marginally significant (P<0.16). However, contrasting low
and high hopelessness groups showed that highly hopeless men had
significantly higher SBPs (µ=133.2 and 130.1 mm Hg for high and
low hopelessness groups, respectively; P<0.05) and
marginally higher DBPs (µ=86.2 and 84.4 mm Hg for high and low
hopelessness groups, respectively; P<0.09) at follow-up
after adjusting for age and baseline resting BP.
Depression and Hypertension Risk
Logistic regression revealed that each 1-point increase on the
depression scale was related to a nonsignificant 8% increase in risk
of hypertension (OR, 1.08; 95% CI, 0.98, 1.19), which decreased to 6%
in the multivariate model (P<0.29).
Consistent with our prior research,23 we also
modeled depression categorically, using a criterion of 5 symptoms to
define depression. A total of 51 participants (8.3%) reported 5
depressive symptoms, and this group had a nonsignificant elevated risk
of hypertension (OR, 1.58; 95% CI, 0.78, 3.22 after risk factor
adjustment). Although depression was weakly related to hypertension, it
was modestly and significantly associated with hopelessness
(r=0.36; P<0.0001) after adjustment for age.
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study demonstrates that normotensive men who experience high levels of hopelessness are at a significantly increased risk of becoming hypertensive over a 4-year period relative to their nonhopeless counterparts. To our knowledge, this is the first prospective study to demonstrate a relationship between reported hopelessness and subsequent hypertension in middle-aged men. Our findings add to our earlier work in which we reported significant associations between hopelessness and an increased risk of all-cause and cause-specific mortality, incident myocardial infarction, and progression of carotid atherosclerosis.12 13 Taken together, our data clearly show that hopelessness has profound adverse effects on cardiovascular function.
Hopelessness was also associated with 4-year increases in BP, regardless of hypertensive status, although these associations were not as pronounced as our primary findings. It is unclear why this pattern was observed. Mean 4-year changes in BP were relatively small in magnitude in our sample, and it may be that some regression to the mean occurred. A longer follow-up period with additional BP measurements or a larger sample with more individuals reporting hopelessness would allow a closer examination of this pattern.
The observed association between hopelessness and hypertension was not confounded or modified by traditional risk factors for hypertension or by overall depressive symptoms. We included a covariate for depressive symptoms because we wanted to determine if hopelessness was simply a proxy for depression, as is frequently assumed in the literature, or if it had distinct effects on health. Consistent with our previous research,12 13 the effect of hopelessness was not confounded by self-reported depressive symptoms. In this study, our measures of hopelessness and depression were reliably but modestly correlated, and depression was not significantly related to incident hypertension, which indicates that hopelessness is not synonymous with depression in this population. It is possible that this measure of depression does not adequately tap the experience of depressive symptoms in this Finnish population; however, we have no a priori or post hoc reason to suspect that this is true. The depression scale assessed the somatic or vegetative symptoms of depression but did not include an item on hopelessness, which is a common symptom of depression. This scale does not fully reflect clinical criteria for depressive disorders, but it is similar to symptom checklists such as the Center for Epidemiologic Studies Depression scale, which is widely used in epidemiological studies of depression.31 32
To the best of our knowledge, previous research on the relationship between depression and cardiovascular disease has rarely examined the effects of specific symptoms, particularly hopelessness. Severe depression is almost always accompanied by feelings of hopelessness; however, it should be noted that depression can occur without hopelessness and that individuals may experience hopelessness without meeting criteria for depression. Our findings indicate that hopelessness either has unique cardiovascular effects or is, in fact, a critical component of depression that confers increased cardiovascular disease risk. If this latter point is true, it may help explain some of the inconsistencies in the literature on depression and mortality and cardiovascular outcomes, particularly in nonclinical or population samples.33 More research is needed to further examine the specific impact of hopelessness and other symptoms of depression.
Lack of confounding of the hopelessness-hypertension association by known risk factors raises the important question of mechanism(s). It may be surprising that risk behaviors at baseline, including smoking, drinking, physical inactivity, and obesity, and change (or lack of change) in those behaviors during the 4 years of follow-up did not explain the excess hypertension risk associated with high hopelessness. In fact, behavioral changes did not differ by reported hopelessness at baseline. Previous clinical observations suggest that depressed or hopeless individuals are less able to make behavioral changes and less medically compliant than nondepressed persons.25 However, the present study was observational, not clinical, and we did not assess medical compliance; any behavioral alterations that participants may have made over the course of the study were not intentionally directed by the study. It is widely recognized that it is difficult to modify behaviors to lessen risk profiles, so it seems that the minor changes observed in this study reflect the aging of our population and are unrelated to feelings of hopelessness.
Persons experiencing high levels of hopelessness likely undergo neuroendocrine or hormonal alterations that influence vascular function and/or central nervous system pressor control mechanisms. We were unable to assess hormonal factors that could be influenced by hopelessness and, thus, result in vascular changes that would lead to sustained elevations in BP. Moreover, to our knowledge, no prior investigations of biochemical alterations specifically associated with hopelessness have been published. Such relationships are biologically plausible, however. Most of the relevant evidence comes from neuroendocrine studies of depression. For example, several lines of evidence indicate that hypothalamic-pituitary-adrenal (HPA) axis function is altered in depression, resulting in increased cortisol secretion.34 35 36 Small increases in glucocorticoids, including cortisol, over long periods can result in hypertension, as well as visceral obesity, insulin resistance, increased plasma lipids, and coagulation changes, all of which are precursors to cardiovascular disease.37 38 Prior research has not specifically examined HPA function with respect to hopelessness; thus, it is unknown whether HPA dysregulation and the resulting cortisol increases are greater in persons who are hopeless relative to those who are depressed. Some evidence is suggestive, however. Research shows that hopelessness is a better predictor of suicidal ideation and behavior than is depression per se,39 40 and some of the data demonstrating HPA hyperactivity in depression comes from suicide victims.41 In addition, although not unequivocal, research suggests that hypercortisolemia may be greater in persons with more severe depression (see reference 42 for review), which, as noted above, is generally accompanied by feelings of hopelessness, and in depressed persons who complete or attempt suicide compared with depressed individuals who are not suicidal.43
Persons experiencing hopelessness also may show alterations in serotonin, which has known vasoconstrictive properties and is involved in platelet activation, thrombogenesis, and hypertension.44 45 46 47 48 49 Again, most of the evidence for serotonergic abnormalities comes from studies of the neuroendocrinology of depression. Research has consistently shown that cerebrospinal fluid concentrations of 5-hydroxyindoleacetic acid (5-HIAA), the major serotonin metabolite, are decreased in depressed, drug-free individuals, and even lower in depressed persons who attempt suicide.50 51 52 Autopsy studies on depressed and suicidal patients also found reduced concentrations of serotonin and 5-HIAA in postmortem tissue.53 54 55 The fact that hopelessness is more strongly related to suicide than is depression, as noted above, suggests that the serotonergic abnormalities observed in depressed suicidal patients may, in fact, be related to higher levels of hopelessness in such patients. Interestingly, 1 study reported that 5-HIAA in the cerebrospinal fluid was correlated with cognitive but not vegetative symptoms of depression, whereas cortisol was correlated with both types of symptoms.56
Taken together, the available evidence, albeit indirect, suggests that HPA dysfunction and serotonergic abnormalities may be associated with hopelessness and cardiovascular disease risk. Other critical hormonal and neuroendocrine changes may also occur with hopelessness and influence vascular function. Given that traditional risk factors cannot account for the excess cardiovascular risk associated with hopelessness, research on the hormonal and neuroendocrine effects of hopelessness and their relationship with cardiovascular function is especially warranted.
Hypertensive status was determined by resting BP measured during the
follow-up examination or by confirmed use of antihypertensive
medications. Fewer than 7% of participants reported using
antihypertensive medications at follow-up. In other words, most of the
men who were hypertensive at follow-up had an average BP 165/95
mm Hg, as measured during their clinical examination. This was based
on the average of 2 supine and 2 seated readings. The Sixth Joint
National Committee on the Detection, Evaluation, and Treatment of High
Blood Pressure57 recommends that hypertension be diagnosed
only after high BP readings are obtained on at least 2 clinic visits.
Consequently, our participants cannot be diagnosed as hypertensive
based on their follow-up BP readings alone. The committee also defines
hypertension as a SBP140 mm Hg and/or a DBP90 mm Hg.
However, because we had only a single visit to determine hypertensive
status at follow-up, we chose a conservative cut point for hypertension
(165/95 mm Hg), which we have used previously in research on
hypertension in this population6 9 and which is similar to
cut points used in other investigations.10 11 Moreover,
available data on nearly 93% of our participants who measured their BP
at home for 6 days using a portable, oscillometric monitor indicate
good agreement between the average home BP and the BP assessed during
the study protocol (age-adjusted r=0.67 for SBP and 0.66 for
DBP; P<0.0001). These findings indicate that many of the
men who met our study criteria for hypertension would also meet
clinical criteria for diagnosed hypertension.
The results of the present study are based on a relatively homogeneous population of middle-aged white men from a discreet geographic area (eastern Finland). It is unknown whether similar associations would be observed in women, younger or older persons, or individuals from varying racial groups or ethnic backgrounds. Hopelessness is strongly and inversely related to socioeconomic status (SES)58 but does not differ by sex.59 60 In contrast, female sex is a stronger predictor of depression than either income or education.60 It is widely recognized that women and nonwhite minorities are more likely to be of lower SES, particularly in the United States. Moreover, hypertension follows an SES gradient. Education did not explain the impact of hopelessness on hypertension risk in this study. We also examined the influence of income as another measure of SES, and it too did not alter the observed relationship between hopelessness and hypertension (data not shown). Nevertheless, the extent to which sex or race might modify the association between high BP and hopelessness is unknown and deserves further study.
In summary, this study identified high levels of hopelessness as a
significant, independent predictor of BP elevation over a 4-year period
in middle-aged men. Findings are consistent with our previous
research on the cardiovascular effects of
hopelessness,12 13 as well as data from a national study
of US adults.14 With 
8% of our sample reporting strong
feelings of hopelessness, a relatively small number of men seem to be
at risk for the adverse health consequences of hopelessness. However,
the observed 3-fold risk is striking and essentially not confounded by
known cardiovascular risk factors. Our data support the
idea that hopelessness is more strongly related to adverse
cardiovascular consequences than is depression;
however, additional work is needed to test this hypothesis and to
determine if hopelessness is the critical feature of depression that
confers increased cardiovascular risk. Moreover, future
research should examine physiological mechanisms by
which hopelessness affects vascular function, which may inform
strategies for treating patients experiencing hopelessness.
Importantly, work is also needed to address the determinants of
hopelessness and ways to alleviate it.
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Acknowledgments |
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This work was supported by grant HL-44199 from the National Heart, Lung, and Blood Institute; grant AG13199 from the National Institute of Aging; and by grants from the Academy of Finland and the Finnish Ministry of Education.
Received July 6, 1999; first decision July 30, 1999; accepted September 24, 1999.
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References |
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