Abstract
<p>Insomnia is a highly prevalent and interfering comorbidity to HIV infection, yet relatively understudied compared to other mental and behavioral health comorbidities. Nearly 80% of people living with HIV/AIDS (PLWHA) experience significant sleep difficulties characteristic of insomnia. This represents nearly 1 million of Americans with HIV/AIDS. Efforts have been made to identify factors that contribute to the development and maintenance of insomnia in PLWHA. However, no one pathway has been identified that could explain the overabundance of sleep problems in this population. Most limiting is that extant studies have studied sleep problems, but not clinical insomnia; and, often, those data have not been linked with biological health. The purpose of the current study was to study insomnia (by including insomnia specific measures) as a comorbidity of HIV. Specifically, there were two research questions / aims: (1) Is insomnia (measured by clinical interview and symptom measure) associated with HIV health status and health-related health quality of life in PLWHA? And, (2) Does the proposed conceptual framework explain the mechanisms that link insomnia and HIV health status and health-related quality of life in PLWHA? To address these aims, we recruited PLWHA (N=100) from the Jackson Memorial Hospital Ambulatory Clinic, the public, non-profit tertiary care hospital of South Florida. Participants completed a baseline visit, which included a clinical sleep interview and self-report assessments of sleep, adherence to antiretroviral medications, depression, quality of life, and potentially relevant covariates. Inflammation was measured through a salivary interleukin-6 (IL-6) and C-reactive protein (CRP). We used existing medical records to obtain viral load and CD4. To describe sleep patterns, over the course of a week, participants completed a sleep diary (Carney, 2013) and wore wrist actigraphy (Actigraph wGT3X BT, Actigraph Corp., 2016). To address the first research question, we tested the association between insomnia and health outcomes, and then between insomnia and health-related quality of life using separate linear regression models. Specifically, we tested the association between insomnia diagnosis (obtained via clinical interview) and health outcomes (chart CD4/viral load) (Model 1); insomnia symptoms (Insomnia Severity Index) and health outcomes (chart CD4/viral load) (Model 2); insomnia diagnosis (obtained via clinical interview) and health-related quality of life (ACTG-QOL) (Model 3); and insomnia symptoms (Insomnia Severity Index) and health related quality of life (ACTG-QOL) (Model 4). For those models that were significant, a final regression model controlled for apriori covariates (age, body mass index, and substance use) to test whether insomnia contributed to these outcomes above and beyond other factors. To address the second research question, we used structural equation modeling to examine the unique contributions of a behavioral pathway, which included depression and medication adherence, and a biological pathway, through inflammatory biomarkers IL-6 and CRP, to explain how insomnia may affect both health status and health-related quality of life. In total, the results from six structural equation models are presented (Figures 5-10). The regression models for health status (chart CD4/viral load) were not significant. The models for health-related quality of life were significant and consistent with our hypothesis, such that insomnia diagnosis and symptoms were associated with worse health-related quality of life (p=.011, and p<.001, respectively). These models remained significant even after controlling for covariates (p=.013, for insomnia diagnosis, and p<.001, for insomnia symptoms). The structural equation models were tested with insomnia diagnosis and insomnia symptoms. Results did not differ significantly, but fit was better with insomnia symptoms, so these models were retained. The models with health status as the outcome had acceptable model fit and functioned according to our hypothesis, such that insomnia symptoms were associated with higher levels of depression, which was associated with lower medication adherence, which in turn was associated with higher viral load, which was ultimately associated with lower CD4 values. However, the biological part of the model, which linked insomnia symptoms to inflammation (IL-6 or CRP), and CD4 was not significant, suggesting evidence for only a behavioral, not biological pathway. When health-related quality of life was the outcome, the models did not have acceptable model fit, so they could not be interpreted. Due to both apriori and empirical evidence for a behavioral only model, this model was tested for both health status and health-related quality of life outcomes. These models had acceptable model fit and were retained, suggesting that insomnia symptoms were associated with worse health status and poorer health-related quality of life in accordance with the behavioral conceptual framework. In this sample of underserved PLWHA, insomnia was both directly and indirectly (via behavioral pathway) associated with poorer health-related quality of life; and, indirectly (via behavioral pathway) associated with worse health status. Future research should extend our findings by examining this model using longer longitudinal data and/or by testing an intervention to treat insomnia in this population (e.g. cognitive behavioral therapy for insomnia or CBT-I) to evaluate whether it can improve health and health-related quality of life outcomes in PLWHA.</p>