Pamela J. Feldman

Neighborhood Problems as Sources of Chronic Stress: Development of a Measure of Neighborhood Problems, and Associations With Socioeconomic Status and Health

The impact of the residential neighborhood on health and well-being is being increasingly recognized in behavioral medicine, with evidence for neighborhood-level effects that are independent of the individual characteristics of residents. This study addressed the possibility that the effects of neighborhood are due in part to exposure to community-wide stressors rather than variations in protective factors such as social capital. A questionnaire survey including a 10-item neighborhood problems scale and measures of self-reported health, health behaviors, and social capital was completed by 419 residents of 18 higher socioeconomic status (SES) neighborhoods and 235 residents of 19 lower SES neighborhoods. Data were analyzed using regression and multilevel methods. Neighborhood problem scores were greater in lower than higher SES neighborhoods, positively associated with individual deprivation, and negatively correlated with social capital. Neighborhood problems were not related to smoking, diet, alcohol consumption, or physical activity. However, neighborhood problems were associated with poor self-rated health, psychological distress on the General Health Questionnaire, and impaired physical function, independent of age, sex, neighborhood SES, individual deprivation, and social capital. Adjusted odds ratios for the highest versus lowest neighborhood problem quartiles ranged from 2.05 (confidence interval = 1.15-3.69) for poor self-rated health to 3.07 (1.63-5.79) for impaired physical function. The results provide preliminary evidence that residential neighborhood problems constitute sources of chronic stress that may increase risk of poor health.

Maternal social support predicts birth weight and fetal growth in human pregnancy.

Objective Low birth weight is a primary cause of infant mortality and morbidity. Results of previous studies suggest that social support may be related to higher birth weight through fetal growth processes, although the findings have been inconsistent. The purpose of this investigation was to test a model of the association between a latent prenatal social support factor and fetal growth while taking into account relations between sociodemographic and obstetric risk factors and birth weight. Method A prospective study was conducted among 247 women with a singleton, intrauterine pregnancy receiving care in two university-affiliated prenatal clinics. Measures of support included support from family, support from the baby’s father, and general functional support. Sociodemographic characteristics were also assessed. Birth outcome and obstetric risk information were abstracted from patients’ medical charts after delivery. Results Structural equation modeling analyses showed that a latent social support factor significantly predicted fetal growth (birth weight adjusted for length of gestation) with infant se-, obstetric risk, and ethnicity in the model. Marital status and education were indirectly related to fetal growth through social support. The final model with social support and other variables accounted for 31% of the variance in fetal growth. Conclusions These findings suggest that prenatal social support is associated with infant birth weight through processes involving fetal growth rather than those involving timing of delivery. Biological and behavioral factors may contribute to the association between support and fetal growth, although these mechanisms need to be further e-plored. These results pave the way for additional research on fetal growth mechanisms and provide a basis for support intervention research.

Cortisol responses to mild psychological stress are inversely associated with proinflammatory cytokines

Glucocorticoids can down-regulate immune activity, but acute stress has been reported to increase both cortisol and levels of plasma cytokines. We investigated individual differences in cortisol responses and their associations with proinflammatory cytokines, such as interleukin-6 (IL-6), interleukin-1 receptor antagonist (IL-1ra), cardiovascular activity, and mental health. Saliva samples and blood were taken from 199 healthy middle-aged participants of the Whitehall II cohort at baseline, immediately after stress and 45 min later. We defined the 40% of participants with the highest cortisol response to stress as the cortisol responder group and 40% with the lowest response as the cortisol non-responder group. Plasma IL-6 was higher and the IL-1ra response to stress was greater in the cortisol non-responder group. The cortisol non-responders showed lower heart rate variability than the cortisol responders. The cortisol responder group experienced more subjective stress during the tasks and reported more impaired mental health than the non-responders. We conclude that individual variations in neuroendocrine stress responsivity may have an impact on proinflammatory cytokines, and that both high and low cortisol stress responsiveness has potentially adverse effects.

Socioeconomic status and stress-related biological responses over the working day.

Objectives The influence of low socioeconomic status on cardiovascular disease may be mediated in part by sustained activation of stress-related autonomic and neuroendocrine processes. We hypothesized that low socioeconomic status would be associated with heightened ambulatory blood pressure and cortisol output over the working day. Methods One hundred eight men and 94 women from the Whitehall II epidemiological cohort participated. Blood pressure and heart rate were monitored every 20 minutes over a working day and evening, and salivary cortisol was sampled on waking up and at 2-hour intervals. Measures were also taken under resting laboratory conditions. Socioeconomic status was indexed by grade of employment. Results Resting blood pressure, heart rate, and cortisol did not differ by grade. Ambulatory systolic pressure was greater in the morning in the lower (128.9 ± 15.7 mm Hg) than the intermediate (122.6 ± 12.5 mm Hg) and higher grades (123.3 ± 12.7 mm Hg) after adjustment for age, sex, smoking, and alcohol intake (p = .019). Heart rate was also raised in the morning in the lower grade participants. Differences in morning systolic pressure and heart rate were independent of concurrent physical activity. Cortisol concentration was greater in lower than higher grade men (9.54 ± 4.1 vs. 7.38 ± 2.8 nmol/liter, p = .008) but was more elevated in higher than lower grade women (7.84 ± 2.5 vs. 6.35 ± 1.9 nmol/liter, p = .014). Differences remained significant after adjustment for age, time of awakening, smoking, and alcohol intake. Conclusions Socioeconomic differences in blood pressure and cortisol may reflect stress-related activation of biological pathways that contribute to variations in disease risk.

The stability of and intercorrelations among cardiovascular, immune, endocrine, and psychological reactivity

One hundred fifteen college students were exposed to an evaluative speech task twice, separated by 2 weeks. At both sessions, we assessed cardiovascular, endocrine, immune, and psychological response at baseline and during the task. We found stability across sessions for stress-induced increases in anxiety and task engagement, heart rate, blood pressure, norpinephrine (but not epinephrine), cortisol, natural killer cell cytotoxicity, and numbers of circulating CD3+, CD8+, and CD56+ (but not CD4+ or CD19+) lymphocytes. The stable cardiovascular, immune, and endocrine reactivities were intercorrelated, providing evidence of a unified physiological stress response across these outcomes. Although stable stress-induced increases in task engagement were associated with the physiological stress responses, stress-induced anxiety was not.

The impact of personality on the reporting of unfounded symptoms and illness.

This study examined the role of personality in the reporting of symptoms and illness not supported by underlying pathology. After assessment of the Big Five personality factors, 276 healthy volunteers were inoculated with a common cold virus. On each of the following 5 days, objective indicators of pathology, self-reported symptoms, and self-reported illness onset were assessed. Neuroticism was directly associated with reports of unfounded (without a physiological basis) symptoms in individuals at baseline and postinoculation in those with and without colds. Neuroticism was also indirectly associated with reports of unfounded illness through reports of more symptoms. Openness to Experience was associated with reporting unfounded symptoms in those with verifiable colds, whereas Conscientiousness was associated with reporting unfounded illness in those who were not ill.

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.

Influence of socioeconomic status and job control on plasma fibrinogen responses to acute mental stress.

Objective An elevation in plasma fibrinogen may be one of the pathways through which low socioeconomic status increases cardiovascular disease risk. This study assessed the influence of socioeconomic status, job control, and social isolation on fibrinogen responses to acute stress. Methods The study was conducted with 125 white men and 96 white women aged 47 to 58 years, drawn from the Whitehall II cohort. Socioeconomic status was indexed by grade of employment, with 82 high, 75 intermediate, and 64 low grade participants. Plasma fibrinogen and hematocrit were assessed at baseline, immediately after performance of color-word and mirror tracing tasks, and 45 minutes later. Results Plasma fibrinogen increased from baseline to stress (from 2.85 ± 0.57 to 2.92 ± 0.58 g/liter), remaining elevated 45 minutes after stress (2.89 ± 0.58 g/liter, p < .001). Fibrinogen concentration was greater in the low than in the high or intermediate employment grade groups, independently of sex, age, body mass index, smoking status, and hematocrit. Fibrinogen responses to acute stress did not differ across employment grades. Women had higher fibrinogen levels than men, but this pattern was abolished in women taking hormone replacement therapy. Men experiencing low job control showed greater fibrinogen responses to acute stress than did those with high job control (p = .003). Fibrinogen levels were greater in socially isolated individuals, but social isolation did not affect responses to acute stress. Conclusions Socioeconomic status and acute stress had independent effects on the plasma fibrinogen level. Low job control may influence cardiovascular disease risk in men partly through provoking greater fibrinogen stress responses.

Reactivity and Vulnerability to Stress-Associated Risk for Upper Respiratory Illness

Objective We tested the hypothesis that the greater a person’s laboratory stress-elicited elevation in cortisol, the greater the life stress-related risk for upper respiratory infection (URI). We also tested the prediction that the greater the laboratory stress-elicited rise in natural killer cell (NK) cytotoxicity, the smaller the life stress-related URI risk. Finally, we explored whether sympathetic nervous system (SNS) and enumerative immune reactivities to laboratory stress moderate the relation between life stress and URI. Methods At baseline, 115 healthy subjects were administered a negative stressful life events checklist and were tested to assess their SNS (blood pressure, heart rate, and catecholamines), HPA (cortisol), and immune (NK cell cytotoxicity and lymphocyte subsets) reactivities to laboratory speech tasks administered 2 weeks apart. Responses were averaged across the two laboratory assessments to create reactivity scores. After these assessments were completed, participants were followed weekly for 12 consecutive weeks. At each follow-up they completed a measure of perceived stress experienced over the last week. They were also instructed to contact the study coordinator if they had a cold or flu at any time during follow-up. A health care worker verified reported illnesses. Results In a traditional prospective analysis, high cortisol reactors with high levels of life events had a greater incidence of verified URI than did high reactors with low levels of life events and low reactors irrespective of their life event scores. Using hierarchical linear modeling, CD8+ number, Natural Killer (NK) cell number, and NK cell cytotoxicity, each interacted with weekly perceived stress levels in predicting concurrent occurrences of self-reported URIs. For these outcomes, low immune reactors were more likely to experience an URI during high stress than low stress weeks. High immune reactors did not exhibit differences in weekly URIs as a function of weekly stress level. The SNS reactivity markers did not moderate the association of stress and URI incidence in either analysis. Conclusions Acute HPA and immune responses to laboratory stressors are markers of how vulnerable people are to the increased risk for URI associated with stressors in the natural environment.

Psychological stress, appraisal, emotion and Cardiovascular response in a public speaking task

Forty-three undergraduates (30 males, 13 females) prepared and performed a speech task (stressor) or a reading task (no-stressor control). Preparing to speak led to greater threat appraisal, negative emotion, and cardiovascular (CV) response than preparing to read aloud, particularly in speech anxious individuals. Delivering the speech, however, did not result in an increment in CV response over and above preparation. Although threat appraisals could not explain the effect of stress on CV response during task preparation, negative emotion accounted for over half of the effect. These data support the hypothesis that CV response in these studies is at least partially accounted for by psychological processes (stressor-specific anxiety and negative emotional response) and suggests that these processes may be best studied during a period of stressor anticipation.