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Abstract
The aim of the study was to test the hypotheses that the trajectory of psychological risk (ie, persistent or increasing measures of depression and anxiety symptoms, anger, and low social support over time) increases the risk for the development of hypertension and that blood pressure levels fluctuate with psychological changes in women. Initially, healthy normotensive middle-aged women (n=541; 90.6% white, 8.9% African American) were followed across an average of 9.2 years of follow-up. Psychological characteristics were assessed repeatedly via standardized questionnaires, and Cox proportional hazards and random regression models were used to analyze their impact, adjusting for hypertension risk factors (age, race, years of education, parental history of hypertension, baseline blood pressure, body mass index, physical activity, alcohol use, and cigarette smoking). Seventy-five women became hypertensive during the follow-up period. Baseline levels of depression, anxiety, anger, and social support did not predict subsequent hypertension. A high level of anxiety throughout the follow-up, an increase in the level of feelings of anger, and a decrease in the level of social support over the follow-up were significant predictors of hypertension incidence (all P<0.05), although covariate adjustment reduced some of the significance levels to nonsignificance. In women, increases in depressive symptoms were significantly associated (P=0.003) with concurrent increases in the level of systolic blood pressure, especially among hypertensive patients (P=0.0001). Increasing levels of anger, decreasing levels of social support, and high anxiety increase the likelihood of women’s development of hypertension in midlife. These results emphasize the importance of evaluating the trajectory of psychological risk during the period of evolving hypertension.
Risk for hypertension is linked to several psychosocial factors. In particular, symptoms of depression and/or anxiety predicted a 1.59- to 3.24-fold increase in risk for hypertension development across 5 to 20 years.1–3 However, these results were not consistent across age groups,1 race,1,2 gender,3,4 and site,4 and Goldberg et al5 reported no relation of antecedent depressive symptoms to hypertension across a follow-up of 2 months to 3 years.
The above studies reported the associations of a single measure of symptoms of depression and anxiety and hypertension measured from 2 months to 20 years later. Because the levels of depression and anxiety were not necessarily persistent throughout the follow-up interval,6 the lack of association between symptoms of depression, anxiety, and hypertension may reflect a lack of stability in psychological symptoms. That is, some individuals may experience a trajectory of increased psychological risk, ie, an increase in symptoms over time, whereas others may experience a trajectory of decreased psychological risk, ie, a decrease in symptoms over time. Accordingly, we examined the association between trajectories of self-reported symptoms of depression and anxiety on the basis of repeated symptom assessments across an average of 9.2 years of follow-up and hypertension incidence in middle-aged women participating in the Healthy Women Study (HWS), Pittsburgh, Pa.7,8 The availability of multiple measurements also enabled the examination of whether changes in symptoms of depression and anxiety that a woman experienced across the 9 years would covary with changes in her blood pressure (BP) level, on a within-woman basis. We anticipated that the BP of hypertensives would be particularly responsive to changes in the psychological symptoms.
We previously reported that increasing anger over 3 years was associated with a concurrent increase in the level of BP in the HWS.8 We extended this work by also evaluating the trajectories of angry feelings over 9 years and low social support on the development of hypertension and the covariation of anger and low social support and BP levels on a within-woman basis. Low support affects cardiovascular function.9
Methods
Subjects and Procedure
The HWS began as a prospective study of changes during the climacteric.10 In 1983 to 1984, 541 (90.6% white) participants were recruited from a driver’s license list; they were premenopausal, age 42 to 50 years, normotensive, and not taking medications that would interfere with risk-factor tracking. The Institutional Review Board at the University of Pittsburgh approved this project, and all gave informed consent. Women underwent a baseline clinical examination and reported their menstrual status monthly. Women returned periodically for follow-up exams after 12 months of no menses and at 2, 5, and 8 years after menopause. During the follow-up period (mean, 9.2 years; SD, 3.4 years; range, 1 to 14 years), 75 women were classified as hypertensive because they reported use of antihypertensive medication and/or had elevated systolic BP (SBP; ≥140 mm Hg) or diastolic BP (DBP; ≥90 mm Hg) on 2 consecutive exams. Four hundred thirty-one women remained normotensive (35 women [6.5%] had no follow-up data on BP).
Measures
BP was measured with a random-zero muddler sphygmomanometer by observers trained and certified by the Multiple Risk Factor Intervention Trial protocol.11 Three BP measures were obtained, and the last 2 were averaged. Body mass index (BMI; weight in kilograms divided by height in meters squared) was measured in the clinic. Cigarette smoking was defined as the number of cigarettes smoked per day, and alcohol intake was defined as the amount of current alcohol intake per day converted into grams of absolute alcohol (grams per day). The Paffenbarger activity questionnaire12 was used to obtain kilojoules per week spent in leisure-time activity. Parental history of hypertension was scored as yes or no.
Women completed the Beck Depression Inventory13 for depressive symptoms, Spielberger Trait Anxiety Questionnaire,14 Framingham Tension Scale,15 and the Social Anxiety Scale16 for symptoms of anxiety, Spielberger Trait Anger Scale17 for intensity and frequency of anger, and the Interpersonal Support Evaluation List18 for low social support.
Statistical Analyses
Cox proportional hazards models described the relationship between hypertension incidence and psychological characteristics measured in 3 ways: (1) baseline values only; (2) mean of observations, including baseline, before diagnosis for hypertensives and until final follow-up for normotensives; and (3) mean change from baseline to each observation before diagnosis for hypertensives and to each observation until final follow-up for normotensives.
Multilevel random coefficient regression analyses described the within-person associations of changes in psychological characteristics and changes in BP,19 with BP serving as a within-subject dependent variable and psychological characteristics serving as time-varying predictor variables. Interaction terms of hypertensive status by psychological characteristic and appropriate main effects were added to the models to test the reactivity of hypertensive patients. The maximum likelihood estimation method, with variance components covariance and spatial power residual covariance matrices, and person-centered within-person predictor data were used. Covariates were age (at baseline and menopause), race, education in years, parental history of hypertension, and baseline SBP, alcohol consumption, smoking, physical activity, and BMI. Also, duration of follow-up, BMI, and health habits were treated as time-varying covariates.
Results
Baseline characteristics and change in the study variables across the follow-up in terms of coefficients of variation for normotensive subjects and hypertensive patients are shown separately in Table 1. Individuals who became hypertensive were at baseline older, African American, and heavier and exercised less often; they had a parent(s) with a history of hypertension and exhibited higher baseline values (all, P<0.01). Menopausal age (controlling for baseline age) exhibited a negative effect on hypertension (P<0.03), reflecting that those who were older at baseline became menopausal earlier (r=−0.33, P<0.0001 between baseline and menopausal age). Multivariate analyses with baseline predictors entered simultaneously into the regression equation indicated that SBP, DBP, BMI, and parental history of hypertension remained significant independent predictors of hypertension incidence, whereas age, race, and physical activity became nonsignificant (Table 2). On the basis of these analyses, baseline SBP, BMI, and parental history of hypertension were applied as covariates in the subsequent Cox models.
Baseline Characteristics for Hypertensives and Normotensives
Multivariate Analyses of Biological and Health Behavior Predictors of Hypertension Incidence
Psychological Characteristics and Hypertension Incidence
Table 3 shows that none of the baseline psychological characteristics was a significant predictor of subsequent hypertension (all, P>0.10). However, hypertension incidence was predicted significantly by a higher average level of anxiety (Framingham Tension Scale, P<0.005; Social Anxiety Scale, P<0.04; Spielberger Trait Anxiety Questionnaire, P<0.06). The effect of average Framingham Tension scores on hypertension incidence remained after the covariate adjustments (all P<0.03). The effect of social anxiety remained after controlling for BMI (P=0.02) but became nonsignificant after adjustments for SBP and family history of hypertension (all P>0.06).
Univariate Analyses of Psychological Predictors of Hypertension Incidence
An increase in the level of Trait Anger (P<0.03, all P>0.09 after the covariate adjustments) and a decrease in the level of social support from the baseline to the date of diagnosis predicted subsequent hypertension (P<0.01, all P<0.02 after the covariate adjustments).
To illustrate further the significant findings, relative risk for hypertension was calculated for different levels (quintiles) of average Framingham Tension scores and decreasing social support. Women with the highest tension scores (highest quintile, scores >0.47) had a 3.72-fold risk (P=0.003, 95% confidence interval [CI] 1.57 to 8.81) for developing hypertension compared with women with the lowest tension scores (lowest quintile, scores <0.04). Women whose social support scores decreased across time the most (lowest quintile, scores <−1) had a 1.81-fold risk (P=0.03, 95% CI 1.08 to 3.03) of developing hypertension compared with women whose support scores persisted across time (quintiles 2 to 4, scores from −0.83 to 1.33) and a 2.04-fold risk (P=0.09, 95% CI 0.91 to 4.58) compared with women whose support scores increased the most across time (highest quintile, scores >1.5).
Concurrent Changes in Psychological Characteristics and BP
Analyses of the within-subject covariation between concurrent changes in symptoms of depression, anxiety, and BP across the multiple data collections showed that changes in depression over time were significantly and positively associated with changes in SBP (b=0.03, t2050=3.02, P<0.003). This association was particularly true of hypertensive patients (Figure). BP did not fluctuate significantly with change in anxiety. However, changes in SBP were positively associated with changes in trait anxiety among hypertensive patients (P=0.05 for hypertensive patients, P=0.78 for normotensive subjects, F1,2045=3.77, P=0.05 for anxiety×hypertensive status interaction). Changes in anger, social support, and symptoms of distress were not significantly associated with changes in BP (all, P>0.09).
Mean within-person BP levels when low in depressive symptoms (ie, 2 SD below within-person mean) and when high in depressive symptoms (ie, 2 SD above within-person mean) for normotensive subjects and hypertensive patients separately. The interaction of depressive symptoms and hypertensive status was significant for SBP and DBP (F1,2049=13.70 [P<0.0002] and F1,2049=4.14 [P<0.04], respectively), with only hypertensive patients showing an association (b=0.11 [P<0.0001] and b=0.05 [P<0.04]; all P> 0.20 for normotensive subjects).
To confirm that associations between symptoms of depression and anxiety and BP were not secondary to the effects of antihypertensive medication on symptoms (eg, see Avorn et al20 and Curb et al21), participants on medication were excluded, and the analyses were recalculated. The co-occurring fluctuation of depression and SBP remained significant in nonmedicated hypertensive patients (b=0.14, t=2.62, P<0.008), but fluctuation of trait anxiety and SBP became nonsignificant (P=0.66). Covariate adjustments did not change the significant associations (all, P<0.042), with 1 exception, the interaction between depression and hypertensive status approached conventional levels of significance in the analyses of DBP after controlling for BMI (P=0.075).
Discussion
The present study found no evidence that feeling depressed, anxious, or angry or perceiving low social support at baseline predicted incident hypertension across the lengthy follow-up period. Instead, risk of hypertension was increased among women who experienced specific trajectories: consistently high anxiety levels, increasing feelings of anger, and decreasing social support across the time period before the development of hypertension. The present results suggest that reporting distress at a single assessment may not be sufficient to have long-lasting physiological consequences. Multiple assessment may be more valuable because of the increasing reliability of measurement with more measures (with the increasing number of measures providing a more precise exposure measure) and the fact that distress has considerable variability within an individual. Ongoing psychological distress, especially that which is increasing, has particularly powerful physiological effects.
With regard to co-occurring psychological and BP changes, we found a positive association, particularly among hypertensive patients. Some investigators have proposed that large increases in BP and heart rate to psychological challenges, termed cardiovascular reactivity, are a precursor of cardiovascular diseases, including hypertension.22–24 Experimental laboratory data have reported that a depressed mood is associated with BP reactivity during acute mental stress in borderline hypertensives.25 Thus, depression may act as a vulnerability factor for high BP, particularly among those who are prehypertensive.
In addition to autonomic cardiovascular arousal, endocrine function may link depression and anxiety symptoms, anger, and low social support to hypertension.9,26 Affective disorders are hypothesized to be accompanied by noradrenergic dysregulation, the way of which may link persistent distress and hypertension. Also, depression, anxiety, anger, and low social support may operate through health-related behaviors. In the present sample, smoking, alcohol use, and physical activity were not predictive of hypertension incidence in the presence of the other hypertension risk factors. However, the risk associated with social anxiety and increasing anger was attenuated after controlling for the baseline covariates. In the within-woman analyses of BP fluctuation, neither BMI nor health behaviors eliminated the significant covariation with depression. The possible pathways need to be explored in future research.
Limitations to internal and external validity of the present study include possible bias due to unavailability of follow-up, missing data for BP or for prescription of antihypertensive medication, and psychological changes occurring between the available data points. The study participants had a different number of evaluations (range, 2 to 8 visits) across the follow-up. In consequence, individuals with more visits may have had a greater probability of exhibiting higher average anxiety levels and greater changes in depression, anger, and social support across the follow-up. However, we did examine the psychological variables according to the number of available recordings and found no evidence that the number of visits confounded the associations.
In sum, the present study provides evidence that depression and anxiety symptoms, anger, and low social support are involved in the process of evolving hypertension. However, feeling distressed at 1 point in time, 1 to 14 years before diagnosis, is not a powerful predictor of evolving hypertension. More important is the trajectory of psychological risk that the individual experiences.
Acknowledgments
This research was supported by National Institutes of Health grant HL-28266, the Pittsburgh Mind-Body Center (HL-65111 and HL-65112), and the John D. and Catherine T. MacArthur Foundation Research Network on Socioeconomic Status and Health.
- Received November 30, 2000.
- Revision received January 12, 2001.
- Accepted March 16, 2001.
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