Thomas W. Kamarck

A global measure of perceived stress.

This paper presents evidence from three samples, two of college students and one of participants in a community smoking-cessation program, for the reliability and validity of a 14-item instrument, the Perceived Stress Scale (PSS), designed to measure the degree to which situations in ones life are appraised as stressful. The PSS showed adequate reliability and, as predicted, was correlated with life-event scores, depressive and physical symptomatology, utilization of health services, social anxiety, and smoking-reduction maintenance. In all comparisons, the PSS was a better predictor of the outcome in question than were life-event scores. When compared to a depressive symptomatology scale, the PSS was found to measure a different and independently predictive construct. Additional data indicate adequate reliability and validity of a four-item version of the PSS for telephone interviews. The PSS is suggested for examining the role of nonspecific appraised stress in the etiology of disease and behavioral disorders and as an outcome measure of experienced levels of stress. (Abstract Adapted from Source: Journal of Health and Social Behavior, 1983. Copyright

Measuring the Functional Components of Social Support

In the last several years, we have been interested in the role social supports play in protecting people from the pathogenic effects of stress. By social supports, we scan the resources that are provided by other persons (cf. Cohen & Syme, 1985). Although others have investigated and in some cases found evidence for a “buffering” hypothesis—that social support protects persons from the pathogenic effects of stress but is relatively unimportant for unexposed individuals, there are difficulties in interpreting this literature. First, there are almost as many measures of social suppport as there are studies. Hence it is difficult to compare studies and to determine why support operates as a stress buffer in some cases, but not in others. Second, in the vast majority of work, support measures are used without regard to their psychometric properties or their appropriateness for the question under study. For example, studies using measures assessing the structure of social networks (e.g, how many friends do you have?) are seldom distinguished from those addressing the functions that networks might serve (e.g., do you have someone you can talk to about personal problems?). In fact, in many cases, structural and functional items are thrown together into single support indices resulting in scores that have little conceptual meaning.

Cardiovascular Reactivity and Development of Preclinical and Clinical Disease States

Objective The objective of this review is to evaluate the evidence for the hypothesis that cardiovascular reactivity can predict the development of preclinical (elevated blood pressure, ventricular remodeling, carotid atherosclerosis) and/or clinical cardiovascular disease states. Methods A review of the literature was conducted examining prospective studies. Results Three large epidemiological studies with long-term follow-up periods (20 years or more) have found blood pressure responses to the cold pressor task to be predictive of subsequent essential hypertension in initially normotensive samples. Studies showing less consistent results have tended to use shorter-term follow-up periods. A larger body of literature demonstrates consistent associations between stress-related cardiovascular reactivity and blood pressure elevations in youth over the course of 1 to 6 years; such relationships have not been consistently shown among adult samples. Moderately consistent evidence points to a positive relationship between reactivity and other measures of subclinical disease (increased left ventricular mass and carotid atherosclerosis) among the few prospective studies that have examined these issues to date. A number of additional factors, however, such as baseline levels of disease risk and exposure to psychosocial stress, seem to moderate these relationships. Health status at baseline also seems to moderate the association between reactivity and clinical coronary heart disease in recent reports: two of three existing studies in initially healthy samples show no evidence of a relationship between reactivity and clinical outcomes, whereas three of four studies in samples with preexisting coronary heart disease or essential hypertension show a positive relationship between reactivity and subsequent disease states. Conclusions There is reasonable evidence to suggest that cardiovascular reactivity can predict the development of some preclinical states (eg, increased left ventricular mass and blood pressure) states and perhaps even new clinical events in some patients with essential hypertension or coronary heart disease. However, much more information is needed concerning moderating and potentially confounding variables before the robustness of the positive relationships can become clinically useful.

Exaggerated Blood Pressure Responses During Mental Stress Are Associated With Enhanced Carotid Atherosclerosis in Middle-Aged Finnish Men Findings From the Kuopio Ischemic Heart Disease Study

BACKGROUND Exaggerated cardiovascular reactivity to mental stress is hypothesized to increase atherosclerotic risk. We examined this hypothesis using cross-sectional data from the Kuopio Ischemic Heart Disease study, a population-based epidemiological sample. METHODS AND RESULTS 901 Eastern Finnish men from four age cohorts (age, 42 to 60 years) were administered a standardized testing battery to assess cardiovascular reactivity to mental stress. Ultrasound measures of intima-medial thickness (IMT) and plaque height from the common carotid arteries were used as noninvasive markers of atherosclerosis. Diastolic blood pressure (DBP) responses to mental stress were significantly associated with mean IMT (b=.021, P=.006), maximum IMT (b=.026, P=.013), and mean plaque height (b=.017, P=.041). Significant associations were also shown between stress-related systolic blood pressure (SBP) reactivity and mean IMT (b=.0151, P=.042). When examined separately by age, associations with IMT were significant only in the youngest half of the sample (age, 46 and 52 years, n=433; for mean IMT, DBP b=.033, P=.0002, SBP b=.0266, P=.003; for maximum IMT, DBP b=.039, P=.002, SBP b=.032, P=.011). Results remained significant in the younger subjects after adjustment for smoking, lipid profiles, fasting glucose, and resting blood pressure (b=.024, P=.011); results also remained significant in a subgroup of unmedicated younger subjects without symptomatic cardiovascular disease (n=135; for SBP reactivity, b=.031, P=.036; for DBP, b=.037, P=.007). CONCLUSIONS The tendency to show exaggerated pressor responses to mental stress is a significant independent correlate of atherosclerosis in this population sample of Finnish men. The effect does not appear to be accounted for by the confounding influence of other risk factors or preexisting clinical disease.

A PROSPECTIVE EVALUATION OF THE DIRECTIONALITY OF THE DEPRESSION-INFLAMMATION RELATIONSHIP

Cross-sectional studies have found that individuals with depressive disorders or symptoms have elevated levels of inflammatory markers predictive of coronary artery disease, including interleukin-6 (IL-6) and C-reactive protein (CRP). Due to the paucity of prospective studies, however, the directionality of the depression-inflammation relationship is unclear. We evaluated the longitudinal associations between depressive symptoms and both IL-6 and CRP among 263 healthy, older men and women enrolled in the Pittsburgh Healthy Heart Project, a 6-year prospective cohort study. During the baseline and follow-up visits, participants completed the Beck Depression Inventory-II (BDI-II) to assess depressive symptoms and underwent blood draws to quantify serum IL-6 and CRP. Path analyses revealed that baseline BDI-II (beta=0.18, p=0.01, DeltaR(2)=0.02) was a predictor of 6-year change in IL-6, even after adjustment for demographic, biomedical, and behavioral factors as well as other negative emotions. Of all the factors examined, only body-mass index was a stronger predictor of IL-6 change than depressive symptoms. In contrast to these results, baseline IL-6 did not predict 6-year change in BDI-II. Evidence of a weak bidirectional relationship between BDI-II and CRP was also observed; however, neither of these longitudinal associations was significant. The present findings indicate that depressive symptoms may precede and augment some inflammatory processes relevant to coronary artery disease among healthy, older adults. Therefore, our results imply that depression may lead to inflammation and that inflammation may be one of the mechanisms through which depression contributes to cardiovascular risk.

BIOBEHAVIORAL FACTORS IN SUDDEN CARDIAC DEATH

The authors examine the recent literature on psychological factors and sudden cardiac death and explore the mediating psychophysiological processes by which these variables may be associated. Direct evidence that psychosocial stressors and their correlates may be causally linked with sudden cardiac death in humans is not conclusive, but there is abundant convergent evidence that several physiological precursors of sudden death may be promoted by psychological challenge, especially in persons with coronary heart disease. The authors call for increased attention to the acute effects of psychological events on cardiovascular health.

Influence of race and socioeconomic status on sleep: Pittsburgh SleepSCORE project.

Objective: To examine the independent and interactive effects of race and socioeconomic status (SES) on objective indices and self-reports of sleep. Methods: The sleep of 187 adults (41% black; mean age = 59.5 ± 7.2 years) was examined. Nine nights of actigraphy and two nights of inhome polysomnography (PSG) were used to assess average sleep duration, continuity, and architecture; self-report was used to assess sleep quality. Psychosocial factors, health behaviors, and environmental factors were also measured. Results: Blacks had shorter sleep duration and lower sleep efficiency, as measured by actigraphy and PSG, and they spent less time proportionately in Stage 3–4 sleep, compared with others (p < .01). Lower SES was associated with longer actigraphy-measured latency, more wake after sleep onset as measured by PSG, and poorer sleep quality on the Pittsburgh Sleep Quality Index (p < .05). Conclusions: Blacks and perhaps individuals in lower SES groups may be at risk for sleep disturbances and associated health consequences. SES = socioeconomic status; PSG = polysomnography; WASO = wake after sleep onset; HeartSCORE = Heart Strategies Concentrating On Risk Evaluation; PSQI = Pittsburgh Sleep Quality Index; ESS = Epworth Sleepiness Scale; EOG = electro-oculogram; EMG = electromyogram; ECG = electrocardiogram; REM = rapid eye movement; AHI = apnea/hypopnea index; BMI = body mass index; CES-D = Center for Epidemiological Studies Depression Scale; STAI = Spielberger Trait Anxiety Inventory; Ho = Cook-Medley Hostility Scale; SEI = Sleep Environment Inventory.

Effects of task strain, social conflict, and emotional activation on ambulatory cardiovascular activity: Daily life consequences of recurring stress in a multiethnic adult sample.

Ambulatory blood pressure (ABP) may be an independent predictor of cardiovascular endpoints, but little is known about its psychosocial determinants. The acute effects of psychosocial processes on cardiovascular activity during daily life were examined by random-effects regression. Healthy adults (N = 120) were monitored over a 6-day period with ABP monitors and computer-assisted self-report assessments. Task strain, social conflict, and emotional activation were rated following each ABP measurement, as were activity, posture, and other covariates. Results show that blood pressure (BP) and heart rate (HR) were elevated during periods of emotional activation (high negative affect or high arousal). Diastolic BP was lower during periods involving high decisional control, and HR was lower during high-control, low-demand activities. There were substantial individual differences in the effects of psychosocial influences on ambulatory cardiovascular activity. Psychological factors are reliable determinants of ABP, which may account in part for the unique predictive value of ABP.

Exaggerated Blood Pressure Responses During Mental Stress Are Prospectively Related to Enhanced Carotid Atherosclerosis in Middle-Aged Finnish Men

Background—Hemodynamic reactions to mental stress may contribute to atherosclerosis. We previously observed cross-sectional relationships between blood pressure reactions to a standardized stress battery and carotid intima-media thickness (IMT) in the Kuopio Ischemic Heart Disease (KIHD) study. These are the first prospective results on this relationship. Methods and Results—Men from 4 age cohorts (42 to 60 years old at study onset) were challenged with a standardized mental stress battery, and heart rate and blood pressure reactions were assessed. Ultrasound measures of common carotid IMT were collected at this time and 7 years later as noninvasive markers of atherosclerosis. Data were collected from a sample of 756 men at both times. Systolic blood pressure reactions to mental stress at study onset were positively related to mean carotid IMT 7 years later (&bgr;=0.035, P=0.001, by blood pressure quartile, IMT=0.91, 0.93, 0.96, 1.00 mm) and to the progression of IMT (&bgr;=0.020, P=0.006, by blood pressure quartile, &Dgr;IMT=0.08, 0.09, 0.11, 0.11 mm). Similar significant relations were shown for maximal IMT and plaque height. Diastolic blood pressure responses were less strongly related to carotid IMT than were systolic responses. Heart-rate responses were unrelated. Adjustment for standard risk factors did not substantially reduce the relation between systolic blood pressure reactivity and the progression of mean carotid IMT (standardized &bgr;=0.059, P=0.026), maximal carotid IMT (standardized &bgr;=0.084, P=0.006), or plaque height (standardized &bgr;=0.093, P=0.008). Conclusions—The degree of systolic blood pressure reactivity to mental challenge is prospectively related to carotid IMT in middle-aged and older men, independent of known risk factors.

Negative emotions and acute physiological responses to stress

One pathway through which stressors are thought to influence physiology is through their effects on emotion. We used meta-analytic statisitical techniques with data from nine studies to test the effects of acute laboratory stressors (speech, star mirror-image tracing, handgrip) on emotional (undifferentiated negative emotion, anger, anxiety) and cardiovascular (CV) response. In all of the studies, participants responded to stressors with both increased CV response and increased negative emotion. Increases in negative emotion were associated with increases in CV response across tasks, however, these associations were small. The range of variance accounted for was between 2% and 12%. Thus, the contribution of negative emotion, as assessed in these studies, to physiological responses to acute laboratory stressors was limited. Although these results raise questions about the role of emotion in mediating stress-elicited physiological responses, the nature of the acute laboratory stress paradigm may contribute to the lack of a strong association.