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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Hypertension. 2020 Jul 1;76(3):715–723. doi: 10.1161/HYPERTENSIONAHA.119.14492

Discrimination and Hypertension Risk among African Americans in the Jackson Heart Study

Allana T Forde 1, Mario Sims 2, Paul Muntner 3, Tené Lewis 4, Amanda Onwuka 5, Kari Moore 1, Ana V Diez Roux 1
PMCID: PMC8359680  NIHMSID: NIHMS1600594  PMID: 32605388

Abstract

African Americans have a higher risk for hypertension compared to other racial or ethnic groups in the United States. One possible explanation for this disparity is discrimination. Few studies have examined the association between discrimination and incidence of hypertension. We examined the associations of everyday, lifetime, and stress from discrimination with incident hypertension and whether these associations differed by gender, age, discrimination attribution, and coping responses to discrimination among African Americans enrolled in the Jackson Heart Study.

Discrimination was self-reported by 1845 African Americans aged 21 to 85 years without hypertension at baseline (2000–2004). Participants completed two follow-up study visits in 2005–2008 and 2009–2013. We used interval-censored Cox regression to estimate associations of discrimination with incident hypertension.

Overall, 52% (n=954) of participants developed hypertension over the follow-up period. After adjustment for age, gender, socioeconomic status and hypertension risk factors, medium versus low levels of lifetime discrimination (hazard ratio-HR: 1.49, 95% confidence interval-CI: 1.18–1.89) and high versus low levels of lifetime discrimination (HR: 1.34, CI: 1.07–1.68) were associated with a higher incidence of hypertension. No statistically significant interactions with gender, age, attribution, or coping were present. Higher stress from lifetime discrimination was associated with higher hypertension risk after adjustment for demographics (HR for high versus low: 1.19, CI: 1.01–1.40), but the association was attenuated after adjustment for hypertension risk factors (HR: 1.14, CI: 0.97–1.35).

Lifetime discrimination may increase the risk for hypertension in African Americans.

Keywords: Hypertension, Blood Pressure, Discrimination, Coping, African Americans, Jackson Heart Study

Graphical Abstract

graphic file with name nihms-1600594-f0001.jpg

Introduction

There are well-documented racial disparities in hypertension morbidity and mortality, with African Americans faring worse than other racial and ethnic groups in the United States (U.S.). (1, 2) While several risk factors (e.g. smoking, alcohol use, obesity, physical activity) have been associated with hypertension, they do not appear to fully explain racial differences, suggesting that other risk factors may contribute. (35)

Discrimination is a chronic stressor that has been posited to contribute to adverse health outcomes, including hypertension. (4, 612) Discrimination may directly impact hypertension via the stress pathway, activating the sympathetic nervous system and hypothalamic-pituitary-adrenal (HPA) axis. (6, 8, 10, 13) Discrimination may also lead to the development of hypertension through unhealthy behaviors, such as unhealthy eating or sedentary lifestyles, that may serve as a coping mechanism for the stress arising from discrimination. (14, 15)

Research on discrimination and blood pressure/hypertension (8, 9, 11, 16) has consisted mostly of cross-sectional studies. One large study of U.S. Black women found no associations of discrimination with incident hypertension. (17) A second study of White, Black, Hispanic, Chinese and Japanese women found that everyday discrimination was associated with larger increases in diastolic and systolic blood pressure over time, but was not associated with incident hypertension. (18) Additional longitudinal studies in large population-based samples are needed to determine whether discrimination is a contributor to hypertension in African Americans.

Discrimination comprises both discrete life events and daily hassles, but few studies have examined the roles of both aspects of discrimination in a large African American sample. (19) Furthermore, the health impact of discrimination may vary according to the individual’s gender and age. (9, 20) The “double minority status” of women who are also racial minorities, may result in stronger effects of discrimination in African American women than in African American men. (2124) There is evidence supporting differential effects of discrimination by age, with one study showing an association of lifetime discrimination with higher blood pressure in older, but not younger age groups. (25)

Discrimination may also have differential impacts on hypertension based on the reason for discrimination (henceforth referred to as discrimination attribution) (22) and coping strategies. (26) It has been suggested that discrimination attributed to racial factors may be a more intense form of discrimination affecting African Americans. (27) In addition, discrimination-specific coping responses have been posited to reduce the effects of discrimination. (28)

The Jackson Heart Study (JHS), provides an opportunity to investigate the longitudinal associations of multiple measures of discrimination with hypertension incidence among a large population-based sample of African Americans.

Methods

The JHS data and materials can be requested from the JHS Committee at https://www.jacksonheartstudy.org/Research/Study-Data/Data-Access.

The JHS is a prospective cohort study of cardiovascular disease (CVD) among noninstitutionalized African Americans residing in the tri-county areas of Jackson Mississippi (Hinds, Madison, Rankin). Participants (21–95 years of age) were recruited from the Atherosclerosis Risk in the Community study (ARIC-31% of the sample); a commercially available list (Accudata Integrated Marketing) of households (17%); a community random sample of volunteers (30%); and the adult family members of ARIC participants or volunteer participants (22%). Additional details are described elsewhere. (2931)

Information on demographics, risk factors, medication use, behaviors, anthropometry, and psychosocial factors was obtained via in-home interviews, self-administered questionnaires, and in-clinic examinations. Participants were enrolled (n=5306) during baseline, henceforth referred to as Visit 1 (2000–2004). Follow-up data were collected at Visit 2 (2005–2008, 79.2% of Visit 1 participants retained) and Visit 3 (2009–2013, 90.8% of Visit 2 participants retained). (29) The study protocol was approved by the institutional review boards of the University of Mississippi Medical Center, Jackson State University, and Tougaloo College. Participants provided written informed consent. (2931)

Two measures of discrimination were obtained at Visit 1, everyday discrimination, and lifetime discrimination. The Everyday Discrimination Scale (Cronbach’s alpha=0.88) (32) captured how often participants experienced recurrent episodes of unfair treatment in 9 domains (table S1). (33) Everyday discrimination was assessed using the mean of the response scores (ranging from 1–7). Everyday discrimination was categorized into tertiles to determine whether threshold effects were present.

The Lifetime Discrimination Scale (Cronbach’s alpha=0.78) (32) captured the lifetime occurrence (yes/no) of unfair treatment across 9 domains (table S1). Lifetime discrimination was assessed using the count of the domains (ranging from 0–9) for which unfair treatment was reported. (21, 24) Due to the skewed distribution of the values, lifetime discrimination was divided into three categories (low: no discrimination, medium: values from 1–3, high: values ≥3). Evidence suggests that stress may play a key role in the health outcomes arising from discrimination. (7, 10) Therefore, perceived stressfulness of lifetime discrimination (32) was assessed among respondents who reported at least one experience of lifetime discrimination (very stressful versus moderately or not stressful) (table S1).

Participants were also asked to answer two separate questions indicating the main reason (i.e. age, gender, race, height, weight, other) for reported experiences of everyday discrimination and lifetime discrimination (table S1).

Participants who reported experiencing everyday discrimination were asked to identify the strategy that they most commonly used to cope with discrimination from a list of 12 strategies (table S1). The responses were used to assign each participant to one of three coping styles: active coping (speak up, try to change, work harder to prove them wrong, or pray); passive coping (accept it, ignore it, keep it to yourself, avoid it, or forget it); and external/other coping (blame yourself, get violent or other) (table S1). Participants who reported lifetime discrimination were asked to identify whether they used each of the 12 strategies. We created an average score (continuous) of the responses for each of the coping styles by summing the number of strategies that participants reported using within each coping style. Analyses for both everyday and lifetime discrimination coping were limited to passive and active coping styles because of the small number of reports of the external coping style.

Participants were defined as having hypertension if they were taking antihypertensive medication; and/or had a systolic blood pressure ≥140 mm Hg and/or diastolic blood pressure ≥90 mm Hg at follow-up Visits 2 or 3. Blood pressure measurements were obtained from trained staff using a Hawksley random-zero sphygmomanometer (Hawksley & Sons Ltd, Lansing, Sussex, UK) at Visit 1 and Visit 2 and a semi-automatic oscillometric device (Omron HEM-907XL, Omron Healthcare Inc., Lake Forest, Il) at Visit 3 administered on the right arm of participants after five minutes of sitting in an upright position with their legs uncrossed and feet flat on the floor. Two blood pressure measurements were obtained one minute apart and the average of the two measurements was calculated for each study visit. The blood pressure measurements obtained using the random-zero sphygmomanometer were calibrated to the semi-automatic oscillometric device. (34, 35) The use of antihypertensive medication was self-reported by participants.

Age (continuous), gender, and socioeconomic status (SES, captured by level of education, income, and occupation) were included as potential confounders. (7) Educational attainment was based on Visit 1 self-report of years of schooling completed: (1) less than high school diploma; (2) high school graduate/general equivalency diploma; and (3) vocational school, trade school or college graduate. Income based on family income, family size and poverty level was categorized as: (1) poor (< poverty level); (2) lower-middle (1–1.5 times the poverty level); (3) upper-middle (>1.5-<3.5 times the poverty level); (4) affluent (≥3.5 times the poverty level); and (5) unknown. Occupation was coded as: (1) managerial/professional; (2) service; (3) sales; (3) construction; (4) production; and (5) other (farming, fishing, forestry; military; sick; unemployed; retired; other).

Hypertension risk factors were included as potential mediators or confounders. Visit 1 measures included body mass index (continuous, weight in kilograms divided by height in meters squared); cigarette smoking (current, former, never), alcohol consumption (≤7 drinks/week, >7 drinks/week); dietary intake (score based on intake of fruits and vegetables: ≥4.5 cups/day, fish: >3.5 ounces, twice/week, sodium: <1500 mg/day, sugary beverages: <450 kcal/week, and whole grains ≥3 servings/day; categorized as poor: 0–1 component and intermediate/Ideal: 2–5 components); (36) and physical activity (<150 minutes of moderate physical activity and <75 minutes of vigorous physical activity, ≥150 minutes of moderate physical activity and ≥75 minutes of vigorous physical activity). (7) Separate tests for interaction by gender, age (continuous and dichotomized: < median age and ≥ median age), discrimination attribution and coping responses were performed.

The distribution of covariates at Visit 1 was examined within categories of hypertension development and discrimination. The proportion of participants who developed hypertension and the age-adjusted rates of hypertension were calculated. Participants who did not develop hypertension were censored at their last visit. The adjusted hazard ratios (HR) and 95% confidence intervals (CI) for the associations between discrimination (at Visit 1) and incident hypertension (at Visit 2 and/or Visit 3) were calculated using interval-censored Cox regression.

The first model was adjusted for age, gender, and SES. Hypertension risk factors were added in a second model. Interaction terms were also included in the fully adjusted models to assess effect modification by gender, age, discrimination attribution and coping responses. Analyses of discrimination attribution and coping responses were restricted to those who reported any everyday discrimination or any lifetime discrimination. Analyses were performed using Statistical Analysis Software (SAS version 9.4; SAS Institute Inc, Cary NC).

Results

Among the 5306 participants enrolled at Visit 1, 2998 were excluded from the analyses because they were missing blood pressure measurements (n=2) or had prevalent hypertension (n=2996) at Visit 1. Participants excluded for having hypertension at Visit 1 reported higher levels of discrimination than participants without hypertension at Visit 1. Among the remaining 2308 participants without hypertension at Visit 1, participants who did not attend both follow-up Visits 2 and 3 (n=321) and participants who were missing one or more of the discrimination measures or covariates (n=142) were also excluded. This left a total of 1845 JHS participants available for analyses.

Over the follow-up period, 954 (52%) participants developed hypertension. Compared with participants who did not develop hypertension, those who developed hypertension were older, less likely to be college educated, had a higher BMI, were more likely to be current or former smokers and engaged in less physical activity (table 1). There were no statistically significant differences in reports of discrimination by hypertension status, but participants who developed hypertension compared to those who did not reported more stress from lifetime discrimination (table 1). Participants reporting high everyday discrimination were more likely than those reporting low everyday discrimination to be younger, men, more educated, and have an unhealthy lifestyle profile (except physical activity) (table 2). Similar patterns were observed comparing participants who reported high versus low lifetime discrimination. Participants who reported more stress from lifetime discrimination were more likely to be older, current smokers, heavy alcohol drinkers, and report more physical activity than those reporting less stress from discrimination (table 2). Everyday discrimination was moderately correlated with lifetime discrimination (spearman correlation coefficient rs=0.40, p<0.0001). Stress from lifetime discrimination was weakly correlated with everyday and lifetime discrimination (rs =0.07, p=0.003 and rs =0.09, p=0.0003, respectively).

Table 1.

Distribution of Visit 1 Characteristics of Jackson Heart Study Participants by Incident Hypertension Status

Total n=1845 Did Not Develop Hypertension n=891 Developed Hypertension n=954
% or mean +/− SD* % or mean +/− SD* % or mean +/− SD* p
Age 49.2 +/− 12.0 46.4 +/− 11.9 51.9 +/− 11.4 <0.0001
Gender 0.22
Women 61.1 59.7 62.5
Education* 0.0002
< High school degree 11.7 9.1 14.0
High school degree/GED 15.9 14.1 17.5
Vocational school/Trade school/College 72.5 76.8 68.5
Income 0.04
Poor 10.6 11.8 9.4
Lower-middle 16.8 14.9 18.6
Upper-middle 27.2 27.1 27.3
Affluent 30.8 32.8 29.0
Missing 14.6 13.4 15.7
Occupation 0.04
Managerial/Professional 42.2 43.2 41.2
Service 18.7 16.6 20.8
Sales 19.2 21.4 17.2
Construction 6.3 6.6 6.0
Production 12.7 11.3 13.9
Other 0.9 0.9 0.9
Body Mass Index (kg/m2) 30.7 +/− 7.2 29.8+/− 6.7 31.5 +/− 7.4 <0.0001
Smoking Status 0.001
Current 12.9 10.3 15.4
Former 13.8 12.7 14.8
Never 73.3 77.0 69.8
Alcohol Consumption 0.55
≤ 7 drinks/week 92.9 93.3 92.6
> 7 drinks/week 7.1 6.7 7.4
Diet 0.59
0–1 component 66.6 66.0 67.2
2–5 components 33.4 34.0 32.8
Physical Activity 0.0004
Moderate < 150 and Vigorous < 75 minutes 77.2 73.6 80.5
Moderate ≥ 150 and Vigorous ≥ 75 minutes 22.8 26.4 19.5
Everyday Discrimination 0.47
Low: 1.00–1.56 33.1 32.4 33.7
Medium: 1.66–2.44 33.9 33.2 34.6
High: 2.55–6.89 33.0 34.3 31.7
Everyday Discrimination Attribution# 0.19
Age 9.9 9.0 10.8
Gender 8.3 8.6 8.0
Race 49.7 51.3 48.3
Height or weight 3.7 2.7 4.6
Other reason 28.4 28.5 28.3
Coping with Everyday Discrimination** 0.24
Active 67.8 69.2 66.5
Passive 32.2 30.8 33.5
Lifetime Discrimination§ 0.09
Low: 0.00–0.00 12.0 13.6 10.5
Medium: 1.00–2.00 29.1 27.7 30.4
High: 3.00–9.00 58.9 58.7 59.1
Stress from Lifetime Discrimination 0.01
Very stressful 20.5 17.5 23.2
Moderately stressful 58.1 61.4 55.2
Not stressful 21.4 21.1 21.6
Lifetime Discrimination Attribution# 0.57
Age 5.5 5.6 5.4
Gender 6.4 5.6 7.2
Race 62.7 63.8 61.6
Height or weight 1.5 1.2 1.8
Other reason 23.9 23.8 24.0
Coping with Lifetime Discrimination**
Active 0.66 +/− 0.31 0.66 +/− 0.32 0.66 +/− 0.31 0.99
Passive 0.38 +/− 0.32 0.38 +/− 0.31 0.39 +/− 0.32 0.41
*

SD=standard deviation. GED=general educational development.

p-values based on X2 and t-tests.

Median (25th and 75th percentiles): 2.00 (1.44 and 2.78).

§

Median (25th and 75th percentiles): 3.00 (2.00 and 5.00).

Stress from lifetime discrimination was restricted to participants who reported at least one instance of lifetime discrimination (total: n=1617; no hypertension: n=765; yes hypertension: n=852. Among the 1624 who reported at least one instance of lifetime discrimination, 7 were missing stress from lifetime discrimination).

#

Discrimination attribution was restricted to those who reported everyday discrimination (total: n=1606; no hypertension: n=780; yes hypertension: n=826) or lifetime discrimination (total: n=1612; no hypertension: n=766; yes hypertension: n=846).

**

Coping with everyday discrimination was restricted to participants who reported at least one instance of everyday discrimination and reported active or passive coping (total: n=1570; no hypertension: n=761; yes hypertension: n=809). Coping with lifetime discrimination was restricted to those who reported lifetime discrimination and reported active or passive coping (total active: n=1620; no hypertension: n=769; yes hypertension: n=851; total passive: n=1611; no hypertension: n=766; yes hypertension: n=845).

Table 2.

Distribution of Visit 1 Characteristics of Jackson Heart Study Participants by Categories of Discrimination

Everyday Discrimination Lifetime Discrimination Stress from Lifetime Discrimination§
Low n=611 Medium n=626 High n=608 Low n=221 Medium n=537 High n=1087 Not Stressful/Moderately Stressful n=1285 Very Stressful n=332
% or mean +/− SD* % or mean +/− SD* % or mean +/− SD* % or mean +/− SD* % or mean +/− SD* % or mean +/− SD* % or mean +/− SD* % or mean +/− SD*
Age 51.8 +/− 12.9 49.2 +/− 11.7 46.6 +/− 10.6 51.3 +/− 14.1 48.8 +/− 12.8 49.0 +/− 11.0 48.6 +/− 11.7 50.3 +/− 11.4
Gender
Women 64.7 61.3 57.4 62.0 67.2 58.0 58.8 68.6
Education*
≤ High school degree 35.0 22.0 25.7 48.9 33.2 20.4 23.3 30.1
Income
Poor 12.0 7.7 12.2 17.2 10.8 9.1 8.2 15.4
Occupation
Construction 18.7 17.4 21.7 10.4 5.4 5.9 6.1 4.5
Body Mass Index (kg/m2) 30.3 +/− 6.6 30.6 +/− 7.2 31.2+/− 7.6 30.4 +/− 7.4 30.5 +/− 6.9 30.8 +/− 7.2 30.5 +/− 6.9 31.4 +/− 7.8
Smoking Status
Current 11.0 12.5 15.5 12.2 12.3 13.4 12.4 15.4
Alcohol Consumption
> 7 drinks/week 5.9 6.6 8.9 5.4 6.5 7.7 6.9 8.7
Diet
0–1 component 64.3 67.9 67.6 66.1 67.8 66.2 66.0 69.0
Physical Activity
Moderate < 150 and vigorous < 75 minutes 79.7 75.2 76.6 79.2 80.5 75.2 76.0 81.3
*

SD=standard deviation. GED=general educational development.

Everyday discrimination is the mean of 9 items with scored responses from 1–7: Low: 1.00–1.56; Medium: 1.66–2.44; High: 2.55–6.89.

Lifetime discrimination is the count of 9 items: Low: 0.00–0.00; Medium: 1.00–2.00; High: 3.00–9.00.

§

Stress from lifetime discrimination was restricted to participants who reported at least one instance of lifetime discrimination (total: n=1617; no hypertension: n=765; yes hypertension: n=852. Among the 1624 who reported at least one instance of lifetime discrimination, 7 were missing stress from lifetime discrimination).

There were no consistent dose response trends in the association of everyday discrimination with age-adjusted incident hypertension for women or men. However, in both men and women, those reporting one or more domains for lifetime discrimination had higher age-adjusted incidence rates of hypertension than those reporting no lifetime discrimination. Higher stress from lifetime discrimination was associated with higher age-adjusted incidence of hypertension for both men and women (table 3).

Table 3.

Proportions and Age-Adjusted Rates of Hypertension among Jackson Heart Study Participants by Categories of Discrimination

Women Men
N of Incident Hypertension Cases Proportion Developing Hypertension Total Person-Years of Follow-up Hypertension Rate per 100 Person-Years (95% CI) N of Incident Hypertension Cases Proportion Developing Hypertension Total Person-Years of Follow-up Hypertension Rate per 100 Person-Years (95% CI)
Everyday Discrimination
Low: 1.00–1.56 214 0.54 2574 7.7 (6.8–8.6) 108 0.50 1440 6.8 (5.7–8.1)
Medium: 1.66–2.44 217 0.56 2587 8.3 (7.4–9.2) 113 0.47 1662 6.5 (5.5–7.7)
High: 2.55–6.89 165 0.47 2439 7.1 (6.2–8.1) 137 0.53 1781 8.0 (7.0–9.2)
Lifetime Discrimination
Low: 0.00–0.00 61 0.44 915 5.6 (4.3–7.2) 39 0.46 572 6.6 (5.0–8.6)
Medium: 1.00–2.00 202 0.56 2402 8.2 (7.3–9.2) 88 0.50 1202 7.1 (6.0–8.5)
High: 3.00–9.00 333 0.53 4284 7.7 (7.0–8.4) 231 0.50 3110 7.3 (6.6–8.2)
Stress from Lifetime Discrimination
Not stressful/moderately stressful 394 0.52 5125 7.6 (7.0–8.3) 260 0.49 3622 7.1 (6.4–7.9)
Very stressful 140 0.61 1533 8.9 (7.8–10.2) 58 0.57 668 8.0 (6.5–10.0)

Everyday discrimination was not associated with incident hypertension after adjustment for age, gender, and SES (table 4, model 1) or after additional adjustment for hypertension risk factors (table 4, model 2). Lifetime discrimination was associated with incident hypertension (medium versus low: HR: 1.49, CI: 1.18–1.89 and high versus low: HR: 1.34, CI: 1.07–1.68 (table 4, model 2). However, gender-stratified analyses (table 4) showed that the associations were present in women, but not in men, although the test for interaction was not statistically significant (p=0.19).

Table 4.

Hazard Ratios of Incident Hypertension by Categories of Discrimination among Jackson Heart Study Participants

Model 1* HR (95% CI) Model 2 HR (95% CI)
Overall Women Men Overall Women Men
Everyday Discrimination
Low: 1.00–1.56 (ref) 1.00 1.00 1.00 1.00 1.00 1.00
Medium: 1.66–2.44 1.09 (0.93–1.28) 1.16 (0.95–1.41) 1.00 (0.76–1.31) 1.08 (0.92–1.26) 1.06 (0.85–1.32) 1.10 (0.80–1.53)
High: 2.55–6.89 1.07 (0.90–1.26) 0.96 (0.77–1.18) 1.27 (0.98–1.66) 1.02 (0.86–1.20) 0.85 (0.67–1.08) 1.31 (0.95–1.81)
Lifetime Discrimination
Low: 0.00–0.00 (ref) 1.00 1.00 1.00 1.00 1.00 1.00
Medium: 1.00–2.00 1.47 (1.16–1.85) 1.67 (1.24–2.25) 1.19 (0.81–1.76) 1.49 (1.18–1.89) 1.73 (1.29–2.34) 1.10 (0.74–1.63)
High: 3.00–9.00 1.38 (1.10–1.72) 1.51 (1.13–2.02) 1.20 (0.84–1.72) 1.34 (1.07–1.68) 1.47 (1.10–1.96) 1.09 (0.76–1.56)
Stress from Lifetime Discrimination
Not stressful/moderately stressful (ref) 1.00 1.00 1.00 1.00 1.00 1.00
Very stressful 1.19 (1.01–1.40) 1.21 (0.99–1.47) 1.13 (0.84–1.53) 1.14 (0.97–1.35) 1.16 (0.95–1.42) 1.18 (0.88–1.60)
*

Model 1: Adjusted for age, gender, education, income, and occupation.

Model 2: Adjusted for model 1 + BMI, smoking, alcohol, diet, and physical activity.

Higher stress from lifetime discrimination was associated with higher risk for hypertension (HR for high vs low: 1.19, CI: 1.01–1.40) after adjustment for age, gender, and SES (table 4, model 1). The associations with stress from discrimination were weakened and no longer statistically significant (HR: 1.14, CI: 0.97–1.35) after adjustment for hypertension risk factors (table 4, model 2). There was also no interaction with gender (p=0.98).

There were no statistically significant (p<0.05) interactions with age (continuous: everyday, p=0.40; lifetime, p=0.11; stress, p=0.84 and dichotomized: everyday, p=0.89; lifetime, p=0.09; stress, p=0.87), discrimination attribution (everyday, p=0.26; lifetime, p=0.75; stress, p=0.64), or coping (everyday, active versus passive: p=0.41; lifetime, active: p=0.31, passive: p=0.91; stress, active: p=0.44, passive: p=0.13) (table 4).

Discussion

Discrimination has been hypothesized to contribute to Black-White disparities in hypertension, but previous studies focusing on discrimination and hypertension have been mostly cross-sectional, used limited discrimination measures and often included small samples. (9, 11, 16) We used data from a large population based sample with detailed measures of discrimination and objectively assessed hypertension to examine the relationship between discrimination (everyday, lifetime, stress from lifetime discrimination) and incident hypertension, as well as heterogeneity in this association by gender, age, discrimination attribution and coping style.

In the current study, there was an association of incident hypertension with lifetime discrimination, but not with everyday discrimination. Participants who reported high and medium versus low lifetime discrimination had a higher risk for hypertension. This association persisted after adjustment for hypertension risk factors. Higher stress resulting from lifetime discrimination was also associated with incident hypertension, although the association was attenuated and no longer significant after adjustment for hypertension risk factors. In gender-stratified analyses, point estimates suggested that the association of incident hypertension with lifetime discrimination was stronger in women than in men and the association was only statistically significant in women. However, there was no statistically significant effect modification by gender. There was also no effect modification by age, discrimination attribution, or coping style.

Reviews of studies of the association of discrimination with blood pressure or hypertension (4, 812, 16, 3740) have reported mixed findings from mostly cross-sectional studies. Previous cross-sectional analyses of JHS data did not find an association between everyday discrimination and prevalent hypertension, but greater lifetime discrimination was associated with higher prevalence of hypertension. (7) Our analyses extended these findings to a longitudinal setting and demonstrated that lifetime discrimination was also associated with incident hypertension. Like prior work, (7) point estimates suggested that associations were stronger in women than in men. However, tests for interaction with gender were not statistically significant.

Only two longitudinal studies have examined discrimination (everyday and lifetime) and incident hypertension. Moody et al. (18) found that everyday discrimination did not predict incident hypertension risk among a sample of White, Black, Latino and Asian middle-aged women. Cozier et al (17) found no association between discrimination (everyday, lifetime) and incident hypertension in a large sample of African American women, although they found limited evidence of associations between everyday discrimination and incident hypertension among women born outside of the U.S.

A major advantage of our study over Cozier et al. is the use of objectively assessed hypertension. In contrast to the study by Moody et al., (18) we included a large sample of African American women and investigated a measure of lifetime discrimination. The everyday discrimination scale captures minor day-to-day occurrences of discrimination, which may be more likely to affect short-term changes in blood pressure. Detecting these effects may require ambulatory blood pressure monitoring. In contrast, the lifetime discrimination scale captures major occurrences of lifetime exposure to discrimination that may better capture long-term cumulative exposures, and hence may be more likely to have detectable effects on a chronic outcome like incident hypertension. (41)

Consistent with other studies, we did not find that discrimination attribution modified the association of discrimination with hypertension. (7, 42) Some cross-sectional studies suggest that active coping strategies (vis-a-vis passive coping) mitigate the impact of discrimination on high blood pressure, (21, 24) whereas, other cross-sectional studies have found that active coping exacerbates the association. (43, 44) Coping style (passive or active) did not moderate the association between discrimination and incidence of hypertension in our study. Additional studies that examine the role of coping are warranted.

Our study included African Americans residing in Mississippi, which may limit the generalizability to other locations. It is possible that the participants who were included in the study represent a selected sample of persons who had survived to middle or old age without developing hypertension. If this group is less likely to develop hypertension for other reasons, they could be less vulnerable to the hypertensive effects of discrimination. Given likely exposures to discrimination over the lifecourse, it is possible that discrimination had an impact on the development of hypertension for those who already had hypertension at Visit 1 and were excluded from these analyses. These factors could have resulted in an underestimate of the true association of discrimination with incident hypertension in our analyses.

Our study relied solely on self-reported data on discrimination. Discrimination was also measured at a single time point, which limits the ability to capture changes in discrimination experiences. Our analyses used hypertension incidence as the outcome, but it is possible that ambulatory blood pressure measurements may be better suited to detect any effects of discrimination on blood pressure. (8)

Consistent with the weathering hypothesis, (45) the association between greater lifetime discrimination and increased risk for hypertension may reflect the impact of cumulative exposure to stressors over the life course and the physiological reactions to stress that contribute to poor health outcomes. However, the unique effects of stress from lifetime discrimination cannot be determined since additional stressors were not controlled for in the analyses. Thus, confounding by other stressors remains a possibility. Moreover, some of the hypertension risk factors that we controlled for (such as health behaviors and BMI) could themselves be the result of discrimination.

Perspectives

Our results suggest that discrimination is a chronic stressor that may increase the risk for hypertension. Future studies should measure discrimination at different time points in order to capture the impact that dynamic changes in unfair treatment may have on hypertension risk, and measure additional moderators, such as racial residential segregation and social support, in order to better understand how psychosocial resources may mitigate and modify the impact of discrimination on hypertension. Finally, additional studies with African Americans in other regions of the U.S. are warranted in order to confirm the findings in this study. Findings from this study have important implications for future research on health disparities and are important to the design of interventions and policies aimed at reducing the negative health effects of discrimination.

Supplementary Material

Supplemental Material

Novelty and Significance.

What is New?

  • One of the first large community-based longitudinal studies to demonstrate a link between greater exposure to discrimination over the lifecourse and incidence of hypertension among African Americans.

What is Relevant?

  • Discrimination may contribute to disparities in hypertension.

Summary

  • Lifetime discrimination was associated with a higher risk for incident hypertension.

  • Discrimination may be an important stressor experienced by African Americans and may contribute to higher risk for hypertension in this population.

Acknowledgments

The authors wish to thank the staff and participants of the JHS.

Sources of Funding

The Jackson Heart Study (JHS) is supported and conducted in collaboration with Jackson State University (HHSN268201800013I), Tougaloo College (HHSN268201800014I), the Mississippi State Department of Health (HHSN268201800015I) and the University of Mississippi Medical Center (HHSN268201800010I, HHSN268201800011I and HHSN268201800012I) contracts from the National Heart, Lung, and Blood Institute (NHLBI) and the National Institute for Minority Health and Health Disparities (NIMHD). Additional support was provided by grant R01HL117323 from the National Heart, Lung, and Blood Institute. The conception, design and analyses for the current research study were supported by funds from the American Heart Association (award number 18POST33960588 to A.T. Forde).

Footnotes

Disclosures

None.

Disclaimer

The views expressed in this manuscript are those of the authors and do not necessarily represent the views of the National Heart, Lung, and Blood Institute; the National Institutes of Health; or the U.S. Department of Health and Human Services.

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