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Relationship of Depressive Symptoms to Hypertension in a Household Survey in Harlem

From the Divisions of Sociomedical Sciences (M.R., M.N.) and Epidemiology (S.S.), Joseph L. Mailman School of Public Health, Columbia University, New York, New York.

Address reprint requests to: Marian Reiff, PhD, Rosenthal Center for Complementary & Alternative Medicine Research, Department of Rehabilitation Medicine, Columbia College of Physicians & Surgeons, 600 West 168th Street, New York, NY 10032. Email: mr82{at}columbia.edu

	ABSTRACT

TOP ABSTRACT INTRODUCTION Stress as a Common... Depressive Symptoms as a... Measurement of Hypertension METHODS RESULTS DISCUSSION REFERENCES

 
OBJECTIVE: Two possible explanations for an hypothesized association between depression and hypertension were examined: (1) shared stress-related risk factors are associated with both depression and hypertension and (2) life-style factors associated with depression lead to hypertension.

METHODS: A predominantly black sample of 695 adults were interviewed in the Harlem Household Survey. Two measures of hypertension were used and compared—1) self-report and 2) elevated blood pressure (above 140/90 mm Hg)—on the basis of the mean of two blood pressure measures. Depressive symptoms were measured by use of a 24-item scale based on the Diagnostic Interview Schedule. Logistic regression models were used to test associations between hypertension and depressive symptoms, stressors, and life-style factors.

RESULTS: Depressive symptoms were associated with self-reported hypertension but not with elevated blood pressure. The association between self-reported hypertension and depressive symptoms was explained partly by shared stress-related risk factors but not by life-style factors. Several stressors and life-style variables were risk factors for elevated blood pressure independently of depressive symptoms. The findings are consistent with studies that have measured hypertension variously by either self-report or blood pressure. Possible explanations were explored (labeling and help-seeking) but were not supported by the data.

CONCLUSIONS: An association was found between self-reported hypertension and depressive symptoms, which was explained partly by shared stress-related risk factors. Elevated blood pressure was associated with stressors and life-style factors but not with depressive symptomatology. Research on illness representations and cultural dimensions of health suggest avenues for further investigation.

Key Words: hypertension • depression • self-report • blood pressure • stress • African American

Abbreviations: BMI = body mass index;; DIS = diagnostic interview schedule;; OR = odds ratio.

	INTRODUCTION

TOP ABSTRACT INTRODUCTION Stress as a Common... Depressive Symptoms as a... Measurement of Hypertension METHODS RESULTS DISCUSSION REFERENCES

 
A number of studies have examined the association between hypertension and depression. Although most have found support for the existence of an association (eg, those reviewed in Jonas et al. [1], Goldberg et al. [2], MacDonald et al. [3], and Dimsdale [4]), there are also a number of negative reports (5–7). Several review papers have concluded that the findings remain inconsistent (4, 8–10). Possible explanations for these inconsistencies include variability in the populations sampled (inpatients, outpatients, and nonpatients) and the measures of depression used (eg, symptom scales, clinical diagnoses, and hospital records.)

Despite these inconsistencies, there are reasons to suggest that depression and hypertension would be comorbid. First, hypertension and depression share a prominent risk factor, which is stress. For example, stressful life events and poverty are associated with both hypertension (4, 11) and depression (12–14). Second, some studies suggest that hypertension may be a risk factor for depression or, of central concern here, that depression may be a risk factor for hypertension (1, 7, 15–17).

The cross-sectional studies that found an association have been limited in their ability to distinguish among these explanations, given that the temporal ordering is unclear. Some cross-sectional studies have tried to determine whether the depression or hypertension occurred first. Heine et al. (5), for example, studied the effects of past depressive episodes on current hypertension but did not control for hypertension before the depressive episodes.

The few prospective studies that exist define depression as a predictor of hypertension. Jonas et al. (1) followed a sample of 2992 initially normotensive persons for 7 to 16 years and found that the risk of experiencing hypertension was increased among those who had high levels of depressive symptoms at baseline. Another prospective study found no relationship during a one- to three-year follow-up period (2).

In the present study, we examined the association between hypertension and depression in an urban population in which elevated rates of hypertension have been reported (18). We tested the hypothesis that hypertension and depression are related and examined the plausibility of two possible explanations for this association: (1) that hypertension and depression are associated due to shared risk factors, particularly stress, and (2) that depression is a risk factor for hypertension. Because the present study was cross-sectional, temporal order cannot be assessed. However, we explicitly tested mechanisms hypothesized in these explanations. The hypotheses would be supported to the extent that the data are consistent with the mechanisms associated with each hypothesis, as outlined below.

	Stress as a Common Risk Factor

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It is plausible that any association between hypertension and depression is due to some shared risk factors. In addition to sociodemographic variables that have often been examined (eg, ethnicity and socioeconomic status), stress may be an important shared risk factor, because it has been implicated in both depression (12, 14, 19–24) and hypertension (20–24). Psychosocial and emotional stress is associated with sympathetic nervous system activity, which leads to elevation in blood pressure (25, 26). Although it is generally accepted that acute stress causes a temporary increase in blood pressure, the role of chronic stress on sustained hypertension is more controversial (25, 27–30). However, evidence that long-term stress plays an important role in the development and maintenance of hypertension has been found in cross-sectional, case-control, and prospective studies in a variety of populations (31). The hypothesis of a relationship between stress and hypertension has also been supported by findings from ecological studies that high-stress communities (characterized by low education, low occupational status, and elevated rates of marital instability and crime) have excess mortality from hypertension-related diseases (23, 32, 33). The disproportionally high prevalence of hypertension among African Americans in the United States may be partially explained by this association as well as by unexpressed emotions in response to discrimination or other stressful life events (10, 34–36). If an association exists between depression and hypertension, it is likely to manifest in Harlem, where many of these community risk factors are evident (reported in the Results section). In the present article, we tested the hypothesis that the relationship between hypertension and depressive symptoms can be explained by stressful life events and chronic strain, adjusting for sociodemographic confounders.

	Depressive Symptoms as a Risk Factor for Hypertension

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Some studies have suggested that depression may be a risk factor for hypertension (1, 19, 21). One possible mechanism for this relationship is that some life-style variables that are risk factors for hypertension, such as obesity, alcohol use, smoking, and lack of physical activity (37, 38), may increase as a result of depression and mediate the relationship between depression and hypertension. Although temporal sequence is not identifiable in our study, to the extent that these mechanisms are supported by the data, the hypothesis that depressive symptoms is causally related to hypertension would also be supported.

	Measurement of Hypertension

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Because hypertension was measured in two different ways, using both self-report and blood pressure, we also examined methodological issues pertaining to the influence of the two different measures of hypertension on our hypotheses. It should be noted that, unlike the other two hypotheses, this was not an a priori hypothesis, this was not an a priori hypothesis but was developed during the course of the analyses. In reviews of the literature, we found 20 studies that measured the association between depression and hypertension using measures of hypertension analogous to self-report (including diagnosed, treated, and aware of hypertensive status). Sixteen studies found a positive association with depression ([1, 2, 15–17, 39–46]; reviewed in Cottier [8]; [47–50]; reviewed in MacDonald et al. [3]), and four studies found no association (6, 7, 51, 52). This contrasts with findings from 10 studies that used blood pressure measures, in which only one found a trend or significant association between depression and hypertension ([1, 5], Craig 1898 in [4]) and seven did not find an association ([2, 6, 17, 53–55], in Cottier [8]). Robinson (56) found that patients who consulted a doctor and were diagnosed as hypertensive did not differ in depression scores from those diagnosed as normotensive, but both groups were more depressed than individuals who did not consult a doctor. In these studies, depression was variously measured by use of clinician’s diagnoses, treatment histories, or self-reported depressive symptoms. In a meta-analysis that included 83 studies on blood pressure and personality, Jorgensen et al. (10) found a positive correlation of blood pressure and negative affect when individuals were aware and a negative correlation when they were unaware of their blood pressure levels. We tested our hypotheses using both types of measures (self-report and blood pressure readings).

	METHODS

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Data for this study come from the Harlem Household Survey, which was conducted between 1992 and 1994 in central Harlem, a predominantly African American and Latino community in northern Manhattan. Details of the sampling and survey methods are available elsewhere (57, 58). In brief, respondents were chosen in a two-stage procedure. First, 46 census blocks were randomly selected from the 95 census blocks in the Central Harlem District, and all households in these blocks were enumerated. A sample of 1300 dwellings was randomly selected from the 22,000 enumerated units. Of these, 963 units were inhabited and contained an adult resident at the time of the interview. One adult (age 18–65 years) who spoke English was randomly selected from each household. Of the 963 adults selected, 695 (72%) completed the interview. All interviews were conducted in person by trained community residents using a structured questionnaire and lasted 60 to 90 minutes.

Measures
Dependent variables: hypertension. There were two measures of hypertension; the first based on self-report and the second on blood pressure measurements.

Self-Reported Hypertension. This was measured by asking respondents whether they ever had hypertension or high blood pressure and, if so, whether they had consulted a physician and whether they took antihypertensive medication. They were classified as hypertensive if they said they had high blood pressure. Another self-report measure for hypertension was available ("Have you ever been told by a doctor or other health professional that your blood pressure is high?"). Because the same pattern of results occurred for both definitions, we limited the present article to the first definition of self-reported hypertension.

Systolic and Diastolic Blood Pressure. These were measured twice during the interview (once halfway through and once at the end) with a mercury sphygmomanometer by trained and certified interviewers. Persons were classified as hypertensive if their mean systolic blood pressure from these two measures was 140 mm Hg or greater, or the mean diastolic blood pressure was 90 mm Hg or greater, or they were currently taking antihypertensive medication. Of the 94 respondents who reported taking antihypertensive medication, 65% (N = 61) had elevated blood pressure. Those classified as hypertensive by this definition included the 35% (N = 33) of those taking medication who did not have elevated blood pressure. Approximately 41% of those with elevated blood pressure were on antihypertensive medication (33% of men and 46% of women [18]).

The relationship between self-report and elevated blood pressure is shown in Table 1. Over one third of the sample (N = 230; 96 men and 134 women) met criteria for hypertension on the basis of elevated blood pressure scores; 22% of respondents (N = 150) self-reported that they had hypertension, and 17% (N = 120) met criteria for both measures (Table 1). Of those with elevated blood pressure, 52% self-reported hypertension (45% of men and 58% of women, p women vs. men = .04) (18).

Independent variable: depressive symptoms. Depressive symptoms were measured by use of 24 items from the 7 subscales of the DIS, tapping symptoms of depressed mood, appetite and sleep disturbance, fatigue, restlessness, anhedonia, feelings of worthlessness, cognitive problems, and suicidal ideation. Respondents were asked whether they had experienced each symptom for two weeks or more during the preceding year. Each item was coded 1 if present and 0 if absent. The mean of the items was used as a continuous scale of depressive symptoms. The reliability of the scale was = .87. Although this scale is not a standardized measure, it evidenced concurrent validity in that mean depressive symptoms scores were associated in the expected direction with known risk factors for depressive symptoms—ie, gender, marital status, unemployment, income, chronic strains, traumatic events, death of a close friend or relative in past year, smoking, alcohol, drugs, and physical inactivity. These are reported in the Results section.

Shared risk factors of depressive symptoms and hypertension (stressors). Chronic strains were measured as the number of ongoing problems the respondents indicated they had experienced during the preceding year from a list of 10 possible domains (eg, ongoing problems with partner, friends, children, other family, work, money, housing, legal, health of people important to you, and other). One item, relating to problems with own health, was excluded because it was likely to be confounded with hypertension. Scores were based on the total number of strains reported. Current unemployment and experience of homelessness in the respondent’s lifetime were also considered to be chronic strains and were measured as affirmative responses to queries about these experiences.

Traumatic events were measured by two variables. The first was lifetime experience of traumatic events, and scores were based on the number of events indicated out of a list of 20 possible events (including serious accident, large fire, natural disaster, assault, rape, death of a child, spouse or parent [before age 18 years], and separation from parents during childhood). The second measure of trauma was the death of a family member or close friend during the preceding year.

Mediators of depressive symptoms as risk factors for hypertension (life-style factors). Self-reported BMI was calculated by use of self-reported height and weight. Persons were classified as overweight if they had a self-reported BMI of 25 kg/m² or more (as currently defined by the National Heart, Lung and Blood Institute).

Smoking status was defined as current if respondents had ever smoked a total of 100 cigarettes or more and reported smoking now and as former if they ever smoked 100 cigarettes or more and were no longer smoking at the time of the interview. Frequent alcohol use was coded positive for those who reported having had five or more drinks per day at least three times per week during the preceding year. Drug use was defined as use at least once per month during the preceding year of any of the following: marijuana, crack, cocaine or heroin, opiates, stimulants, sedatives, PCP, LSD, or inhalants. Physical inactivity was defined as not participating in any physical activities (eg, running, sports, dancing, bicycling, or walking) for at least 15 minutes at a time at least once during the preceding month.

Other potential confounders of a depression-hypertension association. Control variables included age, ethnicity, gender, education, health insurance, annual income, and hypertensive medication (details of measures have been reported elsewhere [18, 57]).

Analytic Approach
Because the hypertension outcomes were dichotomous, logistic regression techniques were used to test the study hypotheses. The predictor variables were introduced in four steps: 1) depressive symptoms, 2) sociodemographic variables (age and gender), 3) stressors, 4) life-style factors (potential mediators), and 5) seeing a physician during the preceding year (a potential confounder). Only variables that were found in preliminary analyses to meet criteria as potential confounders (ie, were associated at least minimally with both depressive symptoms and hypertension) were included in the logistic regression models; ethnicity, education, health insurance, annual income and antihypertensive medication were tested but did not demonstrate an association with both depression and hypertension and were therefore excluded from the regression models. Interaction effects were tested for gender but were not significant.

To the extent that common stressors account for the association between depressive symptoms and hypertension, we would expect the odds ratio for depressive symptoms in step 3 to be smaller than the odds ratio in step 2. To the extent that depressive symptoms are a risk factor for hypertension and the relation is mediated by the variables hypothesized, we would expect that the addition of the hypothesized mediating variables in step 4 would decrease the magnitude of the odds ratio for depressive symptoms below what it was in step 3. These models are not mutually exclusive, and if both hypotheses are supported, it suggests that the two mechanisms can operate simultaneously.

	RESULTS

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Descriptive Statistics
Sociodemographic characteristics. Details of the sociodemographic characteristics of this sample have been reported elsewhere (57, 58) and are summarized in Table 2. There were 408 women and 287 men in the sample, with a median age of 37 years. The majority of respondents were non-Hispanic blacks. About one third of the sample had not completed high school. Almost half of the respondents had an annual household income of less than $11,000.

Potential stressors: traumatic events and chronic strains. People in this sample were exposed to high levels of traumatic events and chronic strains. For example, almost half of the men and 20% of the women reported witnessing someone being seriously injured or violently killed. Over one quarter of the sample (35% of men and 21% of women) reported experiencing a serious physical assault or mugging, and 18% of women reported that they had been raped in their lifetime(57). About one half of the sample was unemployed (46% of men and 55% of women), and one quarter had experienced homelessness at some time in their lives (homelessness was defined as not having a permanent place to live or sleeping in different places, a shelter, or other public place).

Life-style factors (potential mediators of a depression-hypertension relationship). The people in this sample experienced a high level of risks for hypertension. Fifty-eight percent of the sample were overweight, 8% had been frequent alcohol users in the past year, 24% had used drugs, and 31% reported physical inactivity.

Relationships Between Hypertension and Depression
Unadjusted relationships. Tables 3 to 5 show the unadjusted relationships among the dependent and independent variables. Depressive symptomatology followed the expected patterns of association with income (Table 3), chronic strains, unemployment, homelessness, traumatic events (Table 4), smoking, and alcohol and drug use (Table 5). Similarly, self-reported hypertension and hypertension defined by blood pressure were both associated with age, ethnicity, education (Table 2), unemployment (Table 3), smoking, being overweight, and physical inactivity (Table 4). Although self-reported hypertension was associated with gender and visiting a physician in the preceding year, elevated blood pressure was not.

Adjusted relationships. The results of the analyses for hypertension measured by blood pressure at interview are presented in Table 6. Parallel analyses for self-reported hypertension are presented in Table 7.

Hypertension measured by blood pressure at interview (Table 6). For hypertension measured by blood pressure at interview, there was no association between depressive symptoms and hypertension (in step 1, OR = .95). None of the other variables in the model, sociodemographic characteristics, stressors, or potential mediators (life-style factors) had a substantial influence on that relationship. The stressors (chronic strains, homelessness, unemployment, and the death of a family member or close friend) and the mediators (overweight and physical inactivity) were risk factors for hypertension, but their effect on blood pressure occurred independently of depressive symptoms. Note that those defined as meeting criteria for elevated blood pressure included 33 subjects with hypertension that was under control (reported that they took antihypertensive medication and did not have elevated blood pressure).

Hypertension measured by self-report (Table 7). In contrast to the results for hypertension measured by blood pressure at interview, depressive symptomatology was strongly related to self-reported hypertension. Age and gender were related to both depressive symptoms and hypertension, and both were significant in the model. Adjusting for age increased the OR, because it suppressed the depression/hypertension relationship; adjusting for gender had no effect on the OR.

The shared risk factor hypothesis for the relationship between depressive symptoms and hypertension gained some support from these data. Adjusting for stress decreased the OR between depressive symptoms and self-reported hypertension from 6.07 in step 2 to 4.27 in step 3. Stress made a substantial contribution but did not account for the full association between depressive symptoms and self-reported hypertension, because the adjusted OR was still substantial (4.27, confidence interval 1.67–10.94). Nevertheless, a clear association was demonstrated between stressors and elevated blood pressure. The second hypothesis, that depression acts as a risk factor for hypertension through the elevation of life-style variables that are known risks for hypertension, was not supported by the data. Entering these variables into the logistic regression model had no effect on the OR representing the relationship between depressive symptoms and hypertension.

Measures of Hypertension
An association was demonstrated between depressive symptoms and self-reported hypertension but not with elevated blood pressure. In addition, elevated blood pressure, but not self-reported hypertension, was associated with social stressors (unemployment, homelessness, and death of close friends or family in the past year). Life-style factors were related to hypertension (both measures) but did not act as mediators of the depression-hypertension relationship. The contrasting results for the two measures of hypertension were striking. In order to better understand this finding, we reexamined past studies and reviews ([1–56], cited in the Introduction). Because our results seem consistent with the literature, we assumed that it was not due solely to peculiarities of our study (eg, measurement error or characteristics of the sample). There are several possible explanations for this discrepancy. Two explanations involve help-seeking behaviors. 1) People with more depression may seek help either for their depression or related somatic symptoms (headaches, stomach aches, etc.). This help-seeking may increase the likelihood that hypertension is diagnosed. 2) It is also possible that a diagnosis of hypertension leads to depression. Several studies have found support for such a labeling effect, where people who screened positive for hypertension subsequently experienced depression as a result (2, 3, 15).

We tested these explanations by adjusting for seeing a physician during the preceding year, having health insurance, seeing a physician for high blood pressure, and accessibility of health care services. Although seeing a physician during the preceding year had a significant effect (p = .02; OR = 2.13), its addition to the self-report hypertension model only reduced the OR for depressive symptoms from 4.44 to 3.95 (Table 7). In our data, therefore, help-seeking and access to health care did not fully explain the relationship between depressive symptoms and self-reported hypertension .

We also divided the sample into four groups: those who neither self-reported nor had high blood pressure; those who self-reported but did not have high blood pressure; those who had high pressure but did not self-report; and those who both self-reported and had high blood pressure. Using a linear regression analysis, we found that the self-reporters and those positive on both measures had significantly higher depressive symptoms scores than those classified as normotensive on both measures, whereas those with only measured high blood pressure did not have more depressive symptoms (adjusting for age, gender, and seeing a physician during the preceding year).

	DISCUSSION

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There is no definitive explanation for why self-report is associated with depressive symptoms, whereas elevated blood pressure is not. An explanation that was considered was that the measure of hypertension based on blood pressure during the interview may represent a "state" effect, whereas a self-report of hypertension better represents a "trait" effect (lifetime experience of hypertension). However, the measurement of depression is "current," not "lifetime," which would bias against the results. Because blood pressure was measured in respondents’ homes, the occurrence of "white-coat hypertension" is unlikely; nevertheless, some respondents’ blood pressure scores may have been temporarily elevated because of the interview situation. If so, the interview blood pressure scores may not be an accurate measure of hypertension. This limitation has led researchers to advocate the use of ambulatory measures or several readings of blood pressure obtained on two separate days rather than depending on measures during a single interview (10, 30, 36). However, in our study the blood pressure measure has demonstrated validity, because it is related to known risk factors such as overweight, physical inactivity, and stressors (in lifetime and during the preceding year) (see Table 6).

A plausible explanation for the finding that depression is related to self-reported hypertension regardless of measured blood pressure has been found in studies on the construction of illness representations that have examined relationships between self-reported illness and blood pressure (59–61). Self-predictions of blood pressure were associated most with reported symptoms, next with reported moods, and none with actual blood pressure (60). Another study suggested that the belief that one is under stress may lead subjects to confirm the presence of a disease by locating symptoms (61). The common sense model of illness helps to explain the discrepancies between the measures of blood pressure and self-report for hypertension and the association between depressive symptoms and self-reported hypertension. An ethnographic study of representative illness models found that, among African American women in New Orleans who were being treated for hypertension, patient illness beliefs differed from biomedical disease classifications. Patients described two folk illness models: "high blood," described as blood rising in the body, caused by diet and heredity, and "high-pertension," believed to be caused by nerves, stress, worry, and anger (62, 63). However, these models fail to explain the independent association of social stressors with elevated blood pressure in our data. It is noteworthy also that Dressler et al. (64) and Dressler and Bindon (65) found associations between hypertension measured by blood pressure and cultural dimensions of socioeconomic status among blacks. Their results suggested that sociocultural dimensions of health can affect the physiological parameter of blood pressure (65).

We should note that there are some limitations to our study. The failure to include non–English-speaking residents limits the generalizablity of the study. A limitation of the study was the use of a nonstandardized depression. However, the scale does demonstrate adequate concurrent validity. The study was cross-sectional, limiting the ability to predict temporal sequence. In addition, BMI was based on self-reported weight and height rather than actual measures of weight and height.

It is clear that, in this study, elevated blood pressure measured at interview was not related to depressive symptoms. However, a clear association was demonstrated between specific social stressors and elevated blood pressure, independent of depression. This finding of a relationship between high blood pressure and social stressors, which are considerable in this community, has important implications and is worthy of further investigation. It is also possible that more precise measures of hypertension would help to determine whether an existing association between depression and sustained hypertension was missed in this study because of poor measures of hypertension. The integration of ethnographic and epidemiological methods, combined with the use of psychological measures, would help to identify what people from diverse cultural backgrounds mean when they self-report hypertension and thereby to determine which aspects of self-reported hypertension may be driving the relationship with depression. Such studies would also help to further investigate the relationship between elevated blood pressure and sociocultural factors.

Received for publication January 20, 2000.

Revision received January 3, 2001.

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