Stress responsivity and socioeconomic status: a mechanism for increased cardiovascular disease risk?

AIMS: Low socioeconomic status is associated with increased cardiovascular disease risk. We hypothesized that psychobiological pathways, specifically slow recovery in blood pressure and heart rate variability following mental stress, partly mediate social inequalities in risk. METHODS AND RESULTS: Participants were 123 men and 105 women in good health aged 47-58 years drawn from the Whitehall II cohort of British civil servants. Grade of employment was the indicator of socioeconomic status. Cardiovascular measures were monitored during performance of two behavioural tasks, and for 45 min following stress. Post-stress return of blood pressure and heart rate variability to resting levels was less complete after 45 min in the medium and low than in the high grade of employment groups. The odds of failure to return to baseline by 45 min in the low relative to the high grade of employment groups were 2.60 (95% CI 1.20-5.65) and 3.85 (1.48-10.0) for systolic and diastolic pressure, respectively, and 5.19 (1.88-18.6) for heart rate variability, adjusted for sex, age, baseline levels and reactions to tasks. Subjective ratings of task difficulty, involvement and stress did not differ by socioeconomic status. CONCLUSIONS: Lower socioeconomic status is associated with delayed recovery in cardiovascular function after mental stress. Impaired recovery may reflect heightened allostatic load, and constitute a mechanism through which low socioeconomic status enhances cardiovascular disease risk.

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 inprotective 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 impairedphysical function. The results provide preliminary evidence that residential neighborhood problems constitute sources of chronic stress that may increase risk ofpoor 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 sex, 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 explored. These results pave the way for additional research on fetal growth mechanisms and provide a basis for support intervention research.

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, norepinephrine (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 statistical 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.