Depressive Symptoms and Cardiovascular Mortality in Older Black and White Adults: Evidence for a Differential Association by Race
Circulation: Cardiovascular Quality and Outcomes
Abstract
Background—
An emerging body of research suggests that depressive symptoms may confer an “accelerated risk” for cardiovascular disease (CVD) in blacks compared with whites. Research in this area has been limited to cardiovascular risk factors and early markers; less is known about black-white differences in associations with important clinical end points.
Methods and Results—
The authors examined the association between depressive symptoms and overall CVD mortality, ischemic heart disease (IHD) mortality, and stroke mortality in a sample of 6158 (62% black; 61% female) community-dwelling older adults. Cox proportional hazards models were used to model time-to-CVD, IHD, and stroke death over a 9- to 12-year follow-up. In race-stratified models adjusted for age and sex, elevated depressive symptoms were associated with CVD mortality in blacks (hazard ratio [HR], 1.95; 95% confidence interval [CI], 1.61 to 2.36; P<0.001) but were not significantly associated with CVD mortality in whites (HR, 1.26; 95% CI, 0.95 to 1.68; P=0.11; race by depressive symptoms interaction, P=0.03). Similar findings were observed for IHD mortality (black: HR, 1.99; 95% CI, 1.49 to 2.64; P<0.001; white: HR, 1.28; 95% CI, 0.86 to 1.89; P=0.23) and stroke mortality (black: HR, 2.08; 95% CI, 1.32 to 3.27; P=0.002; white: HR, 1.32; 95% CI, 0.69 to 2.52; P=0.40). Findings for total CVD mortality and IHD mortality were attenuated but remained significant after adjusting for standard risk factors. Findings for stroke were reduced to marginal significance.
Conclusions—
Elevated depressive symptoms were associated with multiple indicators of CVD mortality in older blacks but not in whites. Findings were not completely explained by standard risk factors. Efforts aimed at reducing depressive symptoms in blacks may ultimately prove beneficial for their cardiovascular health.
Introduction
Depression and elevated depressive symptomatology have been linked to increased cardiovascular disease (CVD) morbidity and mortality across a wide variety of studies.1–5 An emerging body of research suggests that the impact of depressive symptoms on CVD may differ by race, with depressive symptoms conferring an “accelerated risk” for CVD in blacks compared with whites.6–8 Blacks frequently report more severe and untreated major depressive disorder and a higher prevalence of depressive symptomatology than their white counterparts.9–12 Compared with whites, blacks also have disproportionately high rates of CVD morbidity and mortality.13
Until recently, however, few studies have examined black-white differences in the association between depressive symptoms and indices of CVD. In a recent analysis of middle-aged women, Lewis et al6 found that depressive symptoms were associated with early atherosclerotic disease in blacks, but they did not observe a similar association in whites. A few additional studies of both men and women have observed a similar pattern of results, with stronger associations between depressive symptoms and cardiovascular risk factors found in blacks compared with whites.7,10,14–16 To date, findings in this area have primarily been limited to early atherosclerotic disease, hypertension, and diabetes.
Despite the potential relevance of depressive symptoms as a risk factor for accelerated CVD in black populations, very little is known about black-white differences in the association between depressive symptoms and important clinical end points, such as CVD mortality. To our knowledge, only 1 study has explicitly examined racial differences in the association between depressive symptoms and any form of CVD mortality, and the primary outcome in that study was stroke.8 We are aware of no studies that have focused on overall CVD mortality or mortality as the result of ischemic heart disease (IHD), the single leading cause of death in the United States.17,18
The primary aim of the current study was to examine associations among race, elevated depressive symptoms, and CVD mortality over a 9- to 12-year follow-up in a population-based cohort of community-dwelling older black and white adults. We were particularly interested in determining whether the association between depressive symptoms and CVD mortality would be more pronounced in older blacks compared with whites. We examined IHD and stroke as separate subtypes of overall CVD mortality to determine whether associations were consistent across outcomes.
WHAT IS KNOWN
•
Depressive symptoms have been more strongly associated with cardiovascular risk factors and risk markers in blacks compared with whites.
•
It is unclear whether black-white differences observed in the association between depressive symptoms and early markers of cardiovascular risk extend to important clinical end points.
WHAT THE STUDY ADDS
•
This study examined differences in the association between depressive symptoms and cardiovascular disease mortality in a population-based cohort of blacks and whites.
•
Elevated depressive symptoms increased the risk of cardiovascular disease mortality over the 9- to 12-year follow-up in blacks but not whites.
•
Race-specific models were used to determine whether standard cardiovascular disease risk factors might explain the observed associations, and, although some differences were observed, the overall patterning of results remained the same, suggesting that nonstandard risk factors may also play a role.
Methods
Study Population
Data are from the Chicago Health and Aging Project (CHAP), an ongoing, population-based longitudinal study of risk factors for Alzheimer disease and other common conditions of aging. Details of the CHAP study design and procedures have been previously reported.19 Briefly, CHAP was designed to include a large number of older black and non-Hispanic white adults living in 3 adjacent areas on the south side of Chicago, IL. These areas were chosen because they included an approximately equal number of blacks and whites, with a broad representation of socioeconomic status within both racial groups. The CHAP study began in 1993 with a complete census of all households in these areas. All residents ages 65 and older were asked to participate. Of the 7813 eligible residents, 6158 enrolled, for an overall participation rate of 78.9% (blacks, 81.4%; whites, 75.1%). Between late 1993 and 1996, all participants were interviewed in person in their home. The baseline interviews included questions on sociodemographic characteristics, psychosocial variables, medical history and current health status. CHAP participants are interviewed every 3 years, and the cohort is currently in its fifth wave of data collection (over 12 years of follow-up). The current analyses are limited to those 5990 participants with complete data on depressive symptoms and information on vital status through December 31, 2005.
Assessment of Depressive Symptoms
Depressive symptoms were assessed at baseline in CHAP with the 10-item version of the Center of Epidemiological Studies-Depression (CES-D) scale.20 This scale asks respondents to endorse whether or not they have felt various symptoms of depression within the past week. It has been widely used in both clinical and community samples of young and middle-aged adults.21–23 The shorter 10-item CES-D was developed to reduce participant burden in older adults, and its correspondence to the original version has been established.24 The 10-item version has good internal consistency and test-retest reliability in older adult samples.25 Coefficient α for this scale in CHAP is 0.75. Scores of ≥4 on this scale are considered to be indicative of major depression.25 Because we were particularly interested in clinically relevant depressive symptoms, the CES-D was modeled as a dichotomous “high” (4 or greater) or “low” (<4) variable in all analyses.
Assessment of CVD Mortality
Information on vital status was obtained at each follow-up interview and ascertainment of mortality, obtained from the National Death Index, newspaper obituaries, and informants, was complete through December 31, 2005. Causes of death before 1999 were classified using the International Classification of Diseases, Ninth Revision (ICD-9); deaths occurring after 1999 were classified using the International Statistical Classification of Diseases, 10th Revision (ICD-10). Total CVD mortality was defined as ICD-9 codes 390 to 459 or ICD-10 codes I00-I99.9. IHD mortality was defined as ICD-9 codes 410 to 414 and ICD-10 codes 120 to 125, and stroke mortality was defined as ICD-9 codes 430 to 438 and ICD-10 codes 160 to 169.
Additional Variables
Race was self-reported as (non-Hispanic) black or white, and sex was self-reported as male or female. Age was assessed via self-reported date of birth. Education was measured as years of schooling completed. Antidepressant use was determined by visual inspection of medications taken and coded as a presence/absence variable. Two consecutive readings of systolic blood pressure (SBP) were taken with 30 seconds between measurements, using standard sphygmomanometers on seated subjects with the arm resting at heart level.26 The average of the 2 SBP measurements was recorded. Height and weight were measured using standardized methods appropriate for an elderly population.27 Body mass index (BMI) was calculated as weight in kilograms divided by height in meters squared and categorized as normal, underweight, overweight, or obese, using standard criteria.28 Physical activity and smoking status were assessed via self-report using a series of questions from the Established Populations for Epidemiological Studies of the Elderly (EPESE) project.24,29 Cigarette smoking was further categorized as never, current, or ever. Chronic conditions in the form of heart disease, stroke, hypertension, diabetes, cancer and/or hip fracture were self-reported using standardized questions from EPESE.24 The number of chronic conditions was used as an indicator of overall physical health status. Cardiovascular and lipid-lowering medication use was determined by visual inspection of all medications taken. Because β-blocker use has been associated with reduced CVD in animal models of “psychosocial stress” and CVD,30,31 we created a separate medication variable to indicate β-blocker use. Hence, there were 3 CVD medication use indicator variables: (1) lipid-lowering medication use, (2) CVD medication use with β-blockers, and (3) CVD medication use without β-blockers.
Data Analysis
Descriptive statistics were calculated for baseline sociodemographic characteristics, depressive symptoms, antidepressant use, and health status variables. To examine black-white differences in these variables, t tests and χ2 tests were used. Cox proportional hazards models were conducted to model time-to-CVD death as a function of depressive symptoms and other covariates. All models examining the association between depressive symptoms and indices of CVD mortality were run separately by race. This was done for 2 reasons: (1) In preliminary models, we observed a significant race by depressive symptoms interaction for total CVD mortality. Because the main effect of depressive symptoms in race-specific models is often easier to interpret than the interaction coefficient in the pooled models, we chose to stratify models by race. (2) Also, race-specific models allow us to examine the potential confound due to other CVD risk factors in the association between depressive symptoms and CVD mortality separately for blacks and whites. In addition to variation in the association between depressive symptoms and CVD mortality, there may also be racial differences in the pathways through which depressive symptoms impact CVD mortality. Race-specific models allow us to examine potential confounds within each racial group.32
After confirmation that assumptions of the proportional hazards model were met, the first set of Cox models was run to examine the association between depressive symptoms and total CVD mortality for blacks and whites separately, after adjusting for age and sex. We then added additional adjustments for education and potential confounds of the association between depressive symptoms and total CVD mortality, such as SBP, smoking status, BMI, physical activity, chronic health conditions, lipid-lowering medication use, and CVD medication use. After these initial models were complete, a second and third series of Cox proportional hazards models were conducted using the exact sequence, with IHD mortality and stroke mortality as outcomes. Each of our race-stratified Cox models was followed by a formal test of the race by depressive symptoms interaction in models with both blacks and whites.
We did not include a term for antidepressant use in our fully adjusted models because the prevalence of antidepressant use was particularly low in the CHAP cohort (2%), and including a term for this variable resulted in unstable estimates in some of our multivariate models. To gauge the impact of antidepressant use on our results, we ran models including and excluding participants on antidepressants. Results with and without these individuals were comparable; thus, all participants were retained in final models.
Because depressive symptoms are known to differ by sex, we also ran our models stratified by race-sex group. This was done for CVD mortality only because of the relatively small number of events for IHD and stroke within each race/sex group. Findings within each racial group did not differ for men and women; thus, only race-stratified models are presented. All analyses above were conducted using SAS (SAS Institute Inc, Cary, NC).
Results
Participant Characteristics
Respondent characteristics at baseline for the full sample and by race are presented in Table 1. On average, participants were 75 years old (SD=7.0) with 11.8 years (SD=3.7) of education. Participants had an average SBP of 139.4 (SD=20.3), an average BMI of 26.7 (SD=5.5), and approximately 15% were current smokers. Approximately 17% of participants had high depressive symptoms, with a CES-D score ≥4. Only 2% of participants were taking antidepressants. Compared with whites, blacks were slightly younger and less educated. Blacks also had higher BMIs, were more likely to be current smokers, and had lower levels of physical activity and more chronic health conditions than their white counterparts. Blacks had higher levels of depressive symptomatology compared with whites but were less likely to be on antidepressant medication.
| Variable | Total (n=5990) | Blacks (n=3691) | Whites (n=2299) | P Value |
|---|---|---|---|---|
| Age | 74.79±7.03 | 73.70±6.65 | 76.53±7.27 | <0.001 |
| Female, % | 60.62 | 59.63 | 62.20 | 0.048 |
| Education | 11.78±3.70 | 10.72±3.49 | 13.49±3.39 | <0.001 |
| Depressive symptoms ≥4, % | 16.54 | 19.89 | 11.18 | <0.001 |
| Antidepressant use, % | 2.1 | 1.37 | 3.26 | <0.001 |
| Systolic blood pressure | 139.41±20.31 | 139.27±20.28 | 139.64±20.35 | 0.49 |
| BMI | 26.70±5.51 | 27.39±5.80 | 25.64±4.83 | <0.001 |
| BMI 4 categories, % | <0.001 | |||
| BMI <18.5 | 3.94 | 3.69 | 4.33 | |
| 18.5 ≤BMI<25 | 37.01 | 32.43 | 44.06 | |
| 25 ≤BMI<30 | 36.02 | 36.24 | 35.69 | |
| BMI ≥30 | 23.03 | 27.65 | 15.92 | |
| Smoking status, % | <0.001 | |||
| Never-smoker | 46.46 | 44.36 | 49.83 | |
| Ever-smoker | 38.79 | 38.56 | 39.16 | |
| Current smoker | 14.75 | 17.07 | 11.01 | |
| Physical activity | 3.28±5.48 | 2.99±5.50 | 3.76±5.43 | <0.001 |
| Chronic conditions | 0.99±0.92 | 1.03±0.95 | 0.91±0.88 | <0.001 |
| Lipid-lowering drug use | 5.41 | 4.80 | 6.39 | 0.008 |
| CVD meds (β-blockers) | 12.45 | 9.81 | 16.7 | <0.001 |
| CVD meds (w/o (β-blockers) | 46.61 | 49.66 | 39.10 | <0.001 |
BMI indicates body mass index; CVD, cardiovascular disease.
Values are mean±SD or percentage.
Over the 12-year follow-up, there were 925 deaths from CVD overall, including 449 deaths from IHD and 163 deaths from stroke. Blacks had 523 total CVD deaths, 236 deaths from IHD, and 90 deaths from stroke. Numbers for whites were 402, 213, and 73, respectively.
Depressive Symptoms and Cardiovascular Mortality
Table 2 presents the age- and sex-adjusted hazard ratios (HRs) and 95% confidence intervals (CIs) for each outcome separately by race. Among blacks, elevated depressive symptoms were significantly associated with CVD mortality, IHD mortality, and stroke mortality, such that the rate of CVD, IHD, and stroke death among blacks with high depressive symptoms was almost twice that of blacks with low depressive symptoms. There were no significant associations among high depressive symptoms and any type of cardiovascular mortality in whites, although the HRs were all >1 (Table 2). A formal test of the race by depressive symptoms interaction in models with both blacks and whites adjusted for age, race, sex, and depressive symptoms revealed a significant race by depressive symptoms interaction for total CVD mortality (HR, 1.44; 95% CI, 1.03 to 2.02; P=0.03), a marginally significant interaction for IHD mortality (HR, 1.52; 95% CI, 0.94 to 2.45; P=0.09), and no significant interaction for stroke mortality (HR, 1.40; 95% CI, 0.64 to 3.05; P=0.40).
| Blacks | Whites | |||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P Value | HR | 95% CI | P Value | |
| Total cardiovascular disease | 1.95 | 1.61–2.36 | <0.001 | 1.26 | 0.95–1.68 | 0.11 |
| Ischemic heart disease | 1.99 | 1.49–2.64 | <0.001 | 1.28 | 0.86–1.89 | 0.23 |
| Stroke | 2.08 | 1.32–3.27 | 0.002 | 1.32 | 0.69–2.52 | 0.40 |
HR indicates hazard ratio; CI, confidence interval.
*
P value for race by depressive symptoms interaction is 0.03 for CVD mortality, P=0.09 for IHD mortality, and P=0.40 for stroke mortality.
Findings were somewhat attenuated but remained significant after additional adjustments for education, SBP, smoking status, BMI, physical activity, CVD medication use, lipid-lowering drug use, and chronic health conditions. As shown in Table 3, the HR for high depressive symptoms and overall CVD mortality remained significant for blacks (HR, 1.66; 95% CI, 1.33 to 2.07; P<0.001) and nonsignificant for whites (HR, 1.15; 95% CI, 0.84 to 1.56; P=0.38) in fully adjusted models. HRs for several of the other covariates in the fully adjusted models (eg, SBP, chronic conditions) were comparable for blacks and whites. However, there were a few notable differences. The HR for smoking was 1.20 and nonsignificant in the model for blacks but was 1.75 and significant in the model for whites (Table 3). Similarly, the HR for CVD medications (without β-blockers) was lower in blacks compared with whites (0.93 compared with 1.53) and was nonsignificant in models for blacks and significant for whites. Obesity was protective in both groups, although only significantly so for blacks. HRs for age and male sex were slightly lower in blacks compared with whites, although age and male sex were significantly associated with CVD mortality in both racial groups. Despite these differences, the overall patterning of results for high depressive symptoms and CVD mortality by race was similar in minimally and fully adjusted models.
| Blacks | Whites | |||||
|---|---|---|---|---|---|---|
| HR | 95% CI | P Value | HR | 95% CI | P Value | |
| Depressive symptoms ≥4 | 1.66 | 1.33–2.07 | <0.001 | 1.15 | 0.84–1.56 | 0.38 |
| Age | 1.07 | 1.05–1.09 | <0.001 | 1.12 | 1.11–1.14 | <0.001 |
| Male | 1.59 | 1.28–1.96 | <0.001 | 1.96 | 1.55–2.48 | <0.001 |
| Education | 0.96 | 0.94–0.99 | 0.01 | 0.98 | 0.95–1.02 | 0.28 |
| Systolic BP | 1.00 | 1.00–1.01 | 0.05 | 1.00 | 1.00–1.01 | 0.85 |
| BMI (18.5–25; normal) | ||||||
| (<18.5, underweight) | 1.43 | 0.93–2.22 | 0.11 | 1.43 | 0.88–2.32 | 0.15 |
| (25 ≤/<30, overweight) | 0.67 | 0.53–0.84 | 0.0005 | 0.73 | 0.57–0.94 | 0.01 |
| (≥30, obese) | 0.55 | 0.42–0.72 | <0.001 | 0.93 | 0.67–1.30 | 0.68 |
| Physical activity | 0.97 | 0.95–0.99 | 0.02 | 0.96 | 0.94–0.99 | 0.004 |
| Smoking status (never) | ||||||
| Past | 1.16 | 0.93–1.45 | 0.18 | 1.11 | 0.87–1.40 | 0.40 |
| Current | 1.20 | 0.90–1.61 | 0.21 | 1.75 | 1.21–2.52 | 0.003 |
| Chronic conditions | 1.47 | 1.33–1.64 | <0.001 | 1.41 | 1.24–1.60 | <0.001 |
| Lipid-lowering drug use | 0.81 | 0.50–1.30 | 0.38 | 0.91 | 0.58–1.44 | 0.68 |
| CVD meds (β-blockers) | 1.05 | 0.75–1.47 | 0.79 | 1.29 | 0.91–1.83 | 0.14 |
| CVD meds (w/o β-blockers) | 0.93 | 0.73–1.18 | 0.55 | 1.53 | 1.16–2.02 | 0.003 |
HR indicates hazard ratio; CI, confidence interval; BP, blood pressure; BMI, body mass index; and CVD, cardiovascular disease.
P value for race by depressive symptoms interaction, 0.07.
In fully adjusted models examining the association between depressive symptoms and CVD mortality in both blacks and whites, after adjusting for age, race, sex, depressive symptoms, and covariates in Table 3, the race by depressive symptoms interaction was slightly reduced to marginal significance (HR, 1.41; 95% CI, 0.97 to 2.04; P=0.07), indicating that CVD risk factors may partially but not fully explain racial differences in the association between depressive symptoms and CVD mortality.
In fully adjusted models with IHD as the outcome, high depressive symptoms remained significantly associated with IHD mortality in models for blacks (HR, 1.62; 95% CI, 1.15 to 2.27; P=0.006) but not whites (HR, 1.18; 95% CI, 0.77 to 1.80; P=0.45) (full models not shown). The association between elevated depressive symptoms and stroke mortality remained marginally significant in fully adjusted models for blacks (HR, 1.65; 95% CI, 0.97 to 2.79; P=0.06) and nonsignificant in whites (HR, 1.22; 95% CI, 0.61 to 2.43; P=0.57) (full models not shown). In fully adjusted models, the race by depressive symptoms interaction remained nonsignificant for both IHD (P=0.18) and stroke (P=0.56).
Exploratory Analyses: Competing Risk Models
We reran our final, fully adjusted models examining the association between depressive symptoms and CVD mortality over follow-up, treating deaths due to other causes as “competing risks.”33 This was done because of the age of our sample; given the relatively high mortality rate in elderly populations, we wanted to account for the possibility of death due to causes other than CVD. The HR for high depressive symptoms and CVD mortality for blacks was slightly lower in the competing risks model (HR, 1.57; 95% CI, 1.26 to 1.96; P<0.001) albeit significant, and associations between high depressive symptoms and CVD mortality remained nonsignificant for whites (HR, 1.11; 95% CI, 0.80 to 1.53; P=0.53). These analyses were repeated for IHD and stroke mortality, respectively. Similar to results for CVD mortality, for blacks the HRs were slightly reduced for associations between high depressive symptoms and IHD (HR, 1.48; 95% CI, 1.06 to 2.07; P=0.02) and stroke (HR, 1.44; 95% CI, .84 to 2.46; P=0.18) mortality, although associations were only significant for IHD mortality (perhaps due to the small number of stroke deaths). Again, there were no significant associations observed between high depressive symptoms and IHD (P=0.57) or stroke (P=0.67) mortality in whites. Thus, the overall pattern of results remained the same.
Discussion
The current study was designed to examine the associations among race, elevated depressive symptoms, and CVD mortality over a 9- to 12-year follow-up in a sample of older black and white adults. Although we only observed a significant race by depressive symptoms interaction for total CVD mortality, in age- and sex-adjusted models stratified by race, we found that high levels of depressive symptoms were significantly associated with total CVD mortality, IHD mortality, and stroke mortality among blacks only. Among older blacks, those with high levels of depressive symptomatology were almost twice as likely to die of CVD-related causes than those with low levels of depressive symptomatology. These associations persisted after adjustment for demographic covariates and multiple CVD risk factors. We did not observe statistically significant associations between depressive symptoms and any indicator of CVD mortality in older whites.
Although nonsignificant, the HRs in whites were positive (ie, >1). This suggests that the direction of the association between depressive symptoms and indicators of CVD mortality may be somewhat similar in blacks and whites in our cohort. Differences appear to be primarily in the magnitude of the association, with depressive symptoms exerting a greater impact on indicators of CVD mortality in blacks compared with whites.
It is important to note that we did not observe statistical evidence of a race difference in the impact of depressive symptoms on IHD or stroke because the race by depressive symptoms interactions for these outcomes were not significant. Because these are subcategories of overall CVD mortality, where we did see a significant race by depressive symptoms interaction, it is likely that the lack of a significant interaction for IHD and stroke is primarily due to insufficient power. Replication of these results in a larger sample may be warranted.
Several prior studies have documented significantly stronger associations between depressive symptoms and indices of CVD in blacks compared with whites.10,14–16 The current study provides further evidence in support of this patterning of results and extends these findings to CVD mortality and mortality caused by IHD. Despite the growing body of work in this area, however, we know very little about the factors underlying these associations.
It is possible that the pathways through which depressive symptoms affected indicators of CVD mortality differed for blacks compared with whites. We did not formally test the interactive effects of race and depressive symptoms on each possible confound (eg, BMI, SBP, smoking, chronic conditions); however, we did obtain HRs for these potential confounds in race-specific models. Although there were some differences in HR for potential confounds in race-specific models for blacks and whites—particularly for smoking and 1 type of CVD medication use—these differences did not change the overall patterning of our results. This suggests that standard CVD risk factors may not completely explain our observed associations. However, other factors may play a role.
Increased inflammation,34,35 platelet aggregation,36 and the hypersecretion of cortisol37,38 have all been identified as possible mechanisms through which depressive symptoms influence CVD. However, to date, there has been limited research on whether the association between depressive symptoms and these more novel indicators of CVD risk differs for blacks compared with whites. Recently, Boyle et al15 found significant black-white differences in the association between depressive symptoms and cortisol in a sample of black and white male veterans. Depressive symptoms were positively associated with cortisol in both racial groups; however, the magnitude of the effect was considerably stronger in blacks.15 Cortisol has also been associated with indices of CVD39,40 and could be one possible physiological explanation for black-white differences in the association between depressive symptoms and indicators of CVD mortality. Emerging evidence suggests that Depressive symptoms may also exert a stronger effect on C-reactive protein in blacks versus whites.41 Additional research on physiological pathways through which depressive symptoms might differentially affect CVD risk for blacks compared with whites is warranted.
Unmeasured psychosocial factors may also play a role. Older black adults in our cohort reported significantly higher levels of depressive symptomatology compared with whites, which may be due to higher exposure to lifetime and/or current psychosocial stress burden. A number of studies have found higher reports of lifetime negative life events, traumatic stressors, and chronic stressors in blacks compared with whites.42–44 These background stressors may limit the ability of older blacks to effectively cope with high levels of depressive symptoms, which could subsequently increase their vulnerability to CVD. Other psychosocial factors that may enhance vulnerability to CVD mortality in older blacks with elevated depressive symptomatology include dispositional traits such as low optimism and high pessimism, both of which have been linked to increased risk of overall (although not CVD) mortality in blacks relative to whites.45 These background stressors and dispositional traits were not assessed in the CHAP cohort but may be important to consider in future studies.
It is also possible that the stronger association between depressive symptoms and indicators of CVD mortality observed in older blacks compared with whites is simply a function of a longer lifetime exposure to depression and depressive symptomatology. We do not have data on history of depression/depressive symptoms for our cohort; however, research in younger adult samples suggests that blacks are more likely to have severe, chronic, and untreated depression than their white counterparts.12 Thus, the higher level of depressive symptoms observed in our cohort of older blacks compared with whites may be reflective of prior symptoms that have persisted into older age. In this respect, levels of depressive symptomatology at baseline may be a proxy for length of exposure to depressive symptoms over the life course.
The overall prevalence of antidepressant use was fairly low in this sample, at 2.1%. This is only slightly lower than the rate of 3.5% reported in the Cardiovascular Health Study,46 a similarly aged cohort. However, blacks in our cohort had an even lower prevalence of antidepressant use than whites, despite their higher levels of elevated depressive symptomatology. This is consistent with national data, in which there are significant black-white disparities in antidepressant use, even at older ages.47 However, our findings suggest that the overall burden of untreated depressive symptoms may be greater in older blacks compared with whites.
This study has limitations that should be noted. First, although widely used in epidemiological cohort studies,10,34,46 the CES-D is not designed to assess clinical depression. Our findings may have been stronger with the inclusion of actual DSM-IV diagnosed depression.4 Second, we relied on self-reported measures of chronic conditions (heart disease, stroke, and diabetes), which tend to be less valid than actual clinical diagnoses. Finally, our findings are based on a sample of blacks and whites living in an urban context in the Midwest and may not be generalizable to populations in other parts of the country.
Nevertheless, our study has several strengths. To our knowledge, this study is the first to examine the associations among race, depressive symptoms, and total CVD mortality or mortality caused by IHD. Our cohort is fairly unique in that it features a large number of blacks and whites who are living in a similar environment (ie, 3 adjacent neighborhoods). It is also population-based, with a high participation rate in both racial groups.
In summary, we found a significant, independent association between depressive symptoms and total CVD mortality, and, more specifically, IHD and stroke mortality in older blacks, even after controlling for a number of potential explanatory variables. This association was positive but nonsignificant in whites, providing strong support for the notion that blacks may be particularly vulnerable to the effects of depressive symptoms on CVD. The mechanisms underlying these associations remain to be determined. Nonetheless, future research should determine whether reducing depressive symptomatology in blacks could ultimately prove beneficial for their cardiovascular health.
Sources of Funding
The CHAP study was funded by the National Institute on Aging (R01 AG 11101). This research was also supported by National Heart, Lung, and Blood Institute grants K01 HL 092591 (Dr Lewis) and R01 HL 084209 (Dr Everson-Rose).
References
1.
Ariyo AA, Haan M, Tangen CM, Rutledge JC, Cushman M, Dobs A, Furberg CD. Depressive symptoms and risks of coronary heart disease and mortality in elderly Americans. Circulation. 2000;102:1773–1779.
2.
Wassertheil-Smoller S, Shumaker S, Ockene J, Talavera GA, Greenland P, Cochrane B, Robbins J, Aragaki A, Dunbar-Jacob J. Depression and cardiovascular sequelae in postmenopausal women: the Women's Health Initiative (WHI). Arch Intern Med. 2004;164:289–298.
3.
Wulsin LR, Vaillant GE, Wells VE. A systematic review of the mortality of depression. Psychosom Med. 1999;61:6–17.
4.
Penninx BWJH, Beekman ATF, Honig A, Deeg DJH, Schoevers RA, van Eijk JTM, van Tilburg W. Depression and cardiac mortality: results from a community-based longitudinal study. Arch Gen Psychiatry. 2001;58:221–227.
5.
Surtees PG, Wainwright NWJ, Luben RN, Wareham NJ, Bingham SA, Khaw K-T. Depression and ischemic heart disease mortality: evidence from the EPIC-Norfolk United Kingdom Prospective Cohort Study. Am J Psychiatry. 2008;165:515–523.
6.
Lewis TT, Everson-Rose SA, Colvin A, Matthews K, Bromberger JT, Sutton-Tyrrell K. Interactive effects of race and depressive symptoms on calcification in African American and white women. Psychosom Med. 2009;71:163–170.
7.
Davidson K, Jonas BS, Dixon KE, Markovitz JH. Do depression symptoms predict early hypertension incidence in young adults in the CARDIA Study? Arch Intern Med. 2000;160:1495–1500.
8.
Jonas BS, Mussolino ME. Symptoms of depression as a prospective risk factor for stroke. Psychosom Med. 2000;62:463–471.
9.
Skarupski KA, Mendes de Leon CF, Bienias JL, Barnes LL, Everson-Rose SA, Wilson RS, Evans DA. Black-white differences in depressive symptoms among older adults over time. J Gerontol B Psychol Sci Soc Sci. 2005;60:P136–P142.
10.
Knox S, Barnes A, Kiefe C, Lewis CE, Iribarren C, Matthews KA, Wong ND, Whooley M. History of depression, race, and cardiovascular risk in CARDIA. Int J Behav Med. 2006;13:44–50.
11.
Freeman EW, Sammel MD, Liu L, Gracia CR, Nelson DB, Hollander L. Hormones and menopausal status as predictors of depression in women in transition to menopause. Arch Gen Psychiatry. 2004;61:62–70.
12.
Williams DR, Gonzalez HM, Neighbors H, Nesse R, Abelson JM, Sweetman J, Jackson JS. Prevalence and distribution of major depressive disorder in African Americans, Caribbean Blacks, and Non-Hispanic whites: results from the National Survey of American Life. Arch Gen Psychiatry. 2007;64:305–315.
13.
Rosamond W, Flegal K, Furie K, Go A, Greenlund K, Haase N, Hailpern SM, Ho M, Howard V, Kissela B, Kittner S, Lloyd-Jones D, McDermott M, Meigs J, Moy C, Nichol G, O'Donnell C, Roger V, Sorlie P, Steinberger J, Thom T, Wilson M, Hong Y, for the American Heart Association Statistics Committee and Stroke Statistics S. Heart Disease and Stroke Statistics: 2008 Update: A Report From the American Heart Association Statistics Committee and Stroke Statistics Subcommittee. Circulation. 2008;117:e25–e146.
14.
Jonas BS, Lando JF. Negative affect as a prospective risk factor for hypertension. Psychosom Med. 2000;62:188–196.
15.
Boyle SH, Surwit RS, Georgiades A, Brummett BH, Helms MJ, Williams RB, Barefoot JC. Depressive symptoms, race, and glucose concentrations: the role of cortisol as mediator. Diabetes Care. 2007;30:2484–2488.
16.
Everson-Rose SA, Meyer PM, Powell LH, Pandey D, Torrens JI, Kravitz HM, Bromberger JT, Matthews KA. Depressive symptoms, insulin resistance, and risk of diabetes in women at midlife. Diabetes Care. 2004;27:2856–2862.
17.
Heron M, Hoyert D, Murphy S, Xu J, Kochanek K, Tejada-Vera B. Deaths: Final Data for 2006. Hyattsville, MD: National Center for Health Statistics; 2009.
18.
Minino A, Xu J, Kochanek K. Deaths: Preliminary Data for 2008. Hyattsville, MD: National Center for Health Statistics; 2010.
19.
Bienias JL, Beckett LA, Bennett DA, Wilson RS, Evans DA. Design of the Chicago Health and Aging Project (CHAP). J Alzheimers Dis. 2003;5:349–355.
20.
Radloff LS. The CES-D Scale: a self-report depression scale for research in the general population. Appl Psychol Meas. 1977;1:385–401.
21.
Roberts RE. Reliability of the CES-D scale in different ethnic contexts. Psychiat Res. 1980;2:125–134.
22.
Orme JG, Reis J, Herz EJ. Factorial and discriminant validity of the Center for Epidemiological Studies Depression (CES-D) scale. J Clin Psychol. 1986;42:28–33.
23.
Breslau N. Depressive symptoms, major depression, and generalized anxiety: a comparison of self-reports on CES-D and results from diagnostic interviews. Psychiatry Res. 1985;15:219–229.
24.
Kohout FJ, Berkman LF, Evans DA, Cornoni-Huntley J. Two shorter forms of the CES-D (Center for Epidemiological Studies Depression) depression symptoms index. J Aging Health. 1993;5:179–193.
25.
Irwin M, Artin KH, Oxman MN. Screening for Depression in the Older Adult: Criterion Validity of the 10-Item Center for Epidemiological Studies Depression Scale (CES-D). Arch Intern Med. 1999;159:1701–1704.
26.
Variability of blood pressure and the results of screening in the hypertension detection and follow-up program. J Chronic Dis. 1978;31:651–667.
27.
Chumlea WC, Roche AF, Mukherjee D. Some anthropometric indices of body composition for elderly adults. J Gerontol. 1986;41:36–39.
28.
WHO. Physical Status: The Use and Interpretation of Anthropometry. Report of a WHO Expert Committee. Geneva: World Health Organization; 1995.
29.
McPhillips JB, Pellettera KM, Barrett-Connor E, Wingard DL, Criqui MH. Exercise patterns in a population of older adults. Am J Prev Med. 1989;5:65–72.
30.
Skantze HB, Kaplan J, Pettersson K, Manuck S, Blomqvist N, Kyes R, Williams K, Bondjers G. Psychosocial stress causes endothelial injury in cynomolgus monkeys via [beta]1-adrenoceptor activation. Atherosclerosis. 1998;136:153–161.
31.
Kaplan J, Manuck S, Adams M, Weingand K, Clarkson T. Inhibition of coronary atherosclerosis by propranolol in behaviorally predisposed monkeys fed an atherogenic diet. Circulation. 1987;76:1364–1372.
32.
Jones CP. Invited Commentary: “Race,” racism, and the practice of epidemiology. Am J Epidemiol. 2001;154:299–304.
33.
Fine J, Gray R. A proportional hazards model for the subdistribution of competing risks in survival analysis. J Am Stat Assoc. 1999;94:496–509.
34.
Penninx BWJH, Kritchevsky SB, Yaffe K, Newman AB, Simonsick EM, Rubin S, Ferrucci L, Harris T, Pahor M. Inflammatory markers and depressed mood in older persons: results from the health, aging and body composition study. Biol Psychiatry. 2003;54:566–572.
35.
Kop WJ, Gottdiener JS, Tangen CM, Fried LP, McBurnie MA, Walston J, Newman A, Hirsch C, Tracy RP. Inflammation and coagulation factors in persons >65 years of age with symptoms of depression but without evidence of myocardial ischemia. Am J Cardiol. 2002;89:419–424.
36.
Musselman DL, Evans DL, Nemeroff CB. The relationship of depression to cardiovascular disease: epidemiology, biology, and treatment. Arch Gen Psychiatry. 1998;55:580–592.
37.
Gibbons JL, Mc HP. Plasma cortisol in depressive illness. J Psychiatr Res. 1962;1:162–171.
38.
Brown ES, Varghese FP, McEwen BS. Association of depression with medical illness: does cortisol play a role? Biol Psychiatry. 2004;55:1–9.
39.
Dekker MJHJ, Koper JW, van Aken MO, Pols HAP, Hofman A, de Jong FH, Kirschbaum C, Witteman JCM, Lamberts SWJ, Tiemeier H. Salivary cortisol is related to atherosclerosis of carotid arteries. J Clin Endocrinol Metab. 2008;93:3741–3747.
40.
Matthews K, Schwartz J, Cohen S, Seeman T. Diurnal cortisol decline is related to coronary calcification: CARDIA Study. Psychosom Med. 2006;68:657–661.
41.
Deverts DJ, Cohen S, DiLillo VG, Lewis CE, Kiefe C, Whooley M, Matthews KA. Depressive symptoms, race, and circulating c-reactive protein: the Coronary Artery Risk Development in Young Adults (CARDIA) Study. Psychosom Med. 2010;72:734–741.
42.
Ituarte PH, Kamarck TW, Thompson HS, Bacanu S. Psychosocial mediators of racial differences in nighttime blood pressure dipping among normotensive adults. Health Psychol. 1999;18:393–402.
43.
Troxel WM, Matthews KA, Bromberger JT, Sutton-Tyrrell K. Chronic stress burden, discrimination, and subclinical carotid artery disease in African American and Caucasian women. Health Psychol. 2003;22:300–309.
44.
Turner RJ, Lloyd DA. Stress burden and the lifetime incidence of psychiatric disorder in young adults: racial and ethnic contrasts. Arch Gen Psychiatry. 2004;61:481–488.
45.
Tindle HA, Chang Y-F, Kuller LH, Manson JE, Robinson JG, Rosal MC, Siegle GJ, Matthews KA. Optimism, cynical hostility, and incident coronary heart disease and mortality in the Women's Health Initiative. Circulation. 2009;120:656–662.
46.
Carnethon MR, Biggs ML, Barzilay JI, Smith NL, Vaccarino V, Bertoni AG, Arnold A, Siscovick D. Longitudinal association between depressive symptoms and incident type 2 diabetes mellitus in older adults: the Cardiovascular Health Study. Arch Intern Med. 2007;167:802–807.
47.
Gonzalez HM, Croghan T, West B, Williams D, Nesse R, Tarraf W, Taylor R, Hinton L, Neighbors H, Jackson J. Antidepressant use in black and white populations in the United States. Psychiatr Serv. 2008;59:1131–1138.
Information & Authors
Information
Published In
Copyright
© 2011 American Heart Association, Inc.
Versions
You are viewing the most recent version of this article.
History
Received: 26 March 2010
Accepted: 4 February 2011
Published online: 19 April 2011
Published in print: May 2011
Keywords
Subjects
Authors
Disclosures
None.
Metrics & Citations
Metrics
Citations
Download Citations
If you have the appropriate software installed, you can download article citation data to the citation manager of your choice. Select your manager software from the list below and click Download.
- Depression Following Acute Coronary Syndrome: A Review, Reviews in Cardiovascular Medicine, 24, 9, (2023).https://doi.org/10.31083/j.rcm2409247
- Association of Depression and Cardiovascular Disease, The American Journal of Medicine, 136, 9, (881-895), (2023).https://doi.org/10.1016/j.amjmed.2023.04.036
- It Runs in the Family: Parent Racial Worries and Youth Internalizing Problems Within Black Families, Journal of Child and Family Studies, 32, 10, (3106-3119), (2023).https://doi.org/10.1007/s10826-023-02647-4
- Life's simple 7 and its association with trajectories in depressive symptoms among urban middle-aged adults, Journal of Affective Disorders, 333, (447-458), (2023).https://doi.org/10.1016/j.jad.2023.04.083
- Health Disparities and Cardiovascular Diseases, Handbook of Cardiovascular Behavioral Medicine, (265-286), (2022).https://doi.org/10.1007/978-0-387-85960-6_11
- Severe Mental Illness and Cardiovascular Disease, Journal of the American College of Cardiology, 80, 9, (918-933), (2022).https://doi.org/10.1016/j.jacc.2022.06.017
- The Associations between Depression, Acculturation, and Cardiovascular Health among African Immigrants in the United States, International Journal of Environmental Research and Public Health, 19, 11, (6658), (2022).https://doi.org/10.3390/ijerph19116658
- Impact of cardiovascular risk factors on the relationships of physical activity with mood and cognitive function in a diverse sample, Aging, Neuropsychology, and Cognition, 30, 4, (654-667), (2022).https://doi.org/10.1080/13825585.2022.2071414
- Depressive Symptoms and Incident Heart Failure in the Jackson Heart Study: Differential Risk Among Black Men and Women, Journal of the American Heart Association, 11, 5, (2022)./doi/10.1161/JAHA.121.022514
- Depressive Symptoms, Leisure Activity Engagement, and Global Cognition in Non-Hispanic Black and White Older Adults, The Journals of Gerontology: Series B, 77, 11, (2137-2147), (2021).https://doi.org/10.1093/geronb/gbab153
- See more
Loading...
View Options
Login options
Check if you have access through your login credentials or your institution to get full access on this article.
Personal login Institutional LoginPurchase Options
Purchase this article to access the full text.
eLetters(0)
eLetters should relate to an article recently published in the journal and are not a forum for providing unpublished data. Comments are reviewed for appropriate use of tone and language. Comments are not peer-reviewed. Acceptable comments are posted to the journal website only. Comments are not published in an issue and are not indexed in PubMed. Comments should be no longer than 500 words and will only be posted online. References are limited to 10. Authors of the article cited in the comment will be invited to reply, as appropriate.
Comments and feedback on AHA/ASA Scientific Statements and Guidelines should be directed to the AHA/ASA Manuscript Oversight Committee via its Correspondence page.