Sleep duration partially accounts for race differences in diurnal cortisol dynamics.

OBJECTIVE: Emerging research demonstrates race differences in diurnal cortisol slope, an indicator of hypothalamic-pituitary-adrenocortical (HPA)-axis functioning associated with morbidity and mortality, with African Americans showing flatter diurnal slopes than their White counterparts. Sleep characteristics are associated with both race and with HPA-axis functioning. The present report examines whether sleep duration may account for race differences in cortisol dynamics. METHOD: Participants were 424 employed African American and White adults (mean age = 42.8 years, 84.2% White, 53.6% female) with no cardiovascular disease (Adult Health and Behavior Project-Phase 2 [AHAB-II] cohort, University of Pittsburgh). Cortisol slope was calculated using 4 salivary cortisol readings, averaged over each of 4 days. Demographic (age, sex), psychosocial (socioeconomic status [SES], affect, discrimination), and health behaviors (smoking, alcohol use, physical activity) variables were used as covariates, and sleep (self-report and accelerometry) was also assessed. RESULTS: African Americans had flatter slopes than Whites (F(1, 411) = 10.45, B = .02, p = .001) in models adjusting for demographic, psychosocial, and health behavior covariates. Shorter actigraphy-assessed total sleep time was a second significant predictor of flatter cortisol slopes (F(1, 411) = 25.27, B = -.0002, p < .0001). Total sleep time partially accounted for the relationship between race and diurnal slope [confidence interval = .05 (lower = .014, upper .04)]. CONCLUSIONS: African Americans have flatter diurnal cortisol slopes than their White counterparts, an effect that may be partially attributable to race differences in nightly sleep duration. Sleep parameters should be considered in further research on race and cortisol. (PsycINFO Database Record

Social rhythm disrupting events increase the risk of recurrence among individuals with bipolar disorder.

OBJECTIVES: As outlined in the social zeitgeber hypothesis, social rhythm disrupting (SRD) life events begin a cascade of social and biological rhythm disruption that may lead to the onset of affective episodes in those vulnerable to bipolar disorder. Thus, the study of SRD events is particularly important in individuals with this chronic condition. The purpose of the current study was to evaluate (i) the extent to which SRD life events increased the risk of recurrence of a bipolar mood episode, and (ii) whether the social rhythm disruption associated with the event conferred an increased risk of recurrence, after accounting for the level of threat associated with the life event. METHODS: We examined the effect of SRD events on recurrence during preventative treatment in a sample of 118 patients with bipolar disorder who achieved remission from an acute episode after receiving psychotherapy and pharmacotherapy. Life events were measured with the Bedford College Life Events and Difficulty Schedule and were rated for degree of SRD and threat. RESULTS: Time-dependent Cox proportional hazards models showed that having a higher SRD rating was significantly associated with an increased risk of recurrence, even when accounting for the threat effect of a life event and psychosocial treatment (hazard ratio = 1.33, 95% confidence interval: 1.04-1.70, p = 0.023). However, this finding fell below conventional levels of statistical significance when accounting for other covariates. CONCLUSIONS: Our findings lend partial support to the social zeitgeber hypothesis.

2002 Robert Ader New Investigator award. Relationship of cardiovascular reactivity, stressful life events, and multiple sclerosis disease activity.

Previous studies of stress in multiple sclerosis patients have suggested that life events may alter the onset and development of MS. However, results have been inconsistent because of infrequent monitoring and reporting bias. We followed fifty female MS patients for 1 year to determine characteristics of life events associated with MS exacerbations, and examine the influence of cardiovascular activity. Subjects completed weekly life-event checklists. The short- and long-term threat of each event was determined using the Life Events and Difficulties Schedule. Neurologic symptoms were also monitored weekly. MS exacerbations were confirmed by a neurologist blinded to psychosocial events. Cardiovascular reactivity to an acute psychological stressor was determined at study onset, and resting heart rate and blood pressure were monitored monthly. Forty-two percent of life events were associated with exacerbations in the subsequent 6 weeks. Logistic regression confirmed that exacerbations were more likely during at-risk periods following life events and were relatively independent of the threat level and type of stressor. Participants with higher cardiovascular reactivity to acute stress and higher baseline heart rate demonstrated a greater number of exacerbations and proportion of weeks ill. Using multiple regression, we found that disability level, medication usage, cardiovascular reactivity, baseline heart rate, and life event density explained approximately 30% of the variance in the proportion of weeks ill. These results are consistent with the hypothesis that stress is a potential trigger of MS disease activity and suggest that autonomic tone and stress reactivity may play a role in the development of stress-related exacerbations.

Stressful life events precede exacerbations of multiple sclerosis.

OBJECTIVE: We longitudinally monitored life events and health changes in patients with multiple sclerosis (MS) to determine whether stressful events may trigger exacerbation of MS. METHODS: Twenty-three women with MS were followed for 1 year. Each subject completed the Psychiatric Epidemiologic Research Interview on a weekly basis. Further information on potentially stressful events was acquired using the Life Events and Difficulties Schedule. Neurologic symptoms were also monitored on a weekly basis throughout the year. Potential MS exacerbations were confirmed by a neurologist who was blind to the presence and timing of stressors. RESULTS: Eighty-five percent of MS exacerbations were associated with stressful life events in the preceding 6 weeks. Stressful life events occurred an average of 14 days before MS exacerbations, compared with 33 days before a randomly selected control date (p < .0001). Survival analysis confirmed that an increase in frequency of life events was associated with greater likelihood of MS exacerbations (hazard ratio = 13.18, p < .05). CONCLUSIONS: These results are consistent with the hypothesis that stress is a potential trigger of disease activity in patients with relapsing-remitting MS.