UC San Diego

Rationale: Alzheimer’s caregivers are at increased risk for cardiovascular disease (CVD) and exhibit higher levels of vascular dysfunction compared to non-caregivers. Sleep has been implicated in the pathogenesis of CVD, however this relationship is not fully understood. Behavioral Activation therapy has shown promise for reducing caregiver distress and decreasing circulating levels of IL-6, and improvements in sleep may mediate these effects. The purpose of the current study is to examine the cross-sectional and longitudinal associations of subjective and objective measures of sleep with markers of CVD risk in Alzheimer’s caregivers and test the efficacy of a brief Behavioral Activation intervention for improving sleep.Design: This dissertation used archival data from two studies. Study 1 was a longitudinal study in which 126 spousal caregivers and 60 non-caregiver controls were assessed annually over 5 years. Study 2 was a randomized controlled trial of Alzheimer’s caregivers testing the efficacy of a brief Behavioral Activation intervention (n = 75) versus an Information Support condition (n = 76) to reduce caregiver distress (i.e., symptoms of depression, negative affect, and sleep disturbance) and markers of CVD risk. Subjective sleep quality and quantity were assessed using the Pittsburgh Sleep Quality Index and Insomnia Severity Index. Objective sleep data including circadian rhythm profiles were obtained from actigraphy records using Actiwatch. Data for markers of CVD risk were obtained through several methods including ultrasounds of the brachial and carotid arteries, blood pressure and baroreflex sensitivity, and blood and urine samples for catecholamine levels and markers of endothelial function. Using a combined sample, bivariate associations and multiple linear regression models were fitted to test associations between sleep variables and markers of CVD risk. Using data from Study 1, longitudinal associations were tested using multilevel models to examine associations between sleep measures and markers of CVD risk over time. Using data from Study 2, multilevel models and ANOVAs were used to test the impact of a brief Behavioral Activation intervention on various measures of sleep. Results: Regression analyses of baseline associations showed several significant associations between circadian activity rhythms and CVD markers. Caregivers with less robust circadian rhythms exhibited impaired baroreflex sensitivity and increased levels of tumor necrosis factor alpha, von Willebrand factor antigen, and plasminogen activator inhibitor 1. Longitudinal analyses revealed that after controlling for caregiver physical activity, stress, and sex; percent sleep was significantly associated with resting heart rate and norepinephrine. Caregivers with higher percent sleep experienced lower resting heart rate at baseline but showed a slower decrease over time. Caregivers with higher percent sleep also exhibited higher levels of norepinephrine at baseline; there was no significant effect on norepinephrine levels over time. There was not a significant effect of the intervention on sleep outcomes. Conclusions: Cross-sectionally, caregivers with less robust circadian activity rhythm profiles exhibit markers suggestive of increased CVD risk. However, this study revealed little evidence of longitudinal associations between measures of sleep and markers of CVD risk over time. Furthermore, the Behavioral Activation intervention was not more effective than the control condition at improving caregivers’ sleep.