Aric A. Prather, PhD
We all know the feeling of a restless night sleep and the sluggish day that follows. Sleep is a precious commodity in short supply for many Americans and an emerging predictor of poor physical health. The notion of a national “sleep debt” has not gone unnoticed. For instance, sleep goals were recently included in Healthy People 2020, including objectives to increase the proportion of adults obtaining sufficient hours of sleep, underscoring the perceived health benefits conferred by adequate sleep.
Short sleepers (often characterized as sleeping less than 6 hours per night) are at elevated risk for a variety of negative health consequences, including cardiovascular disease, type 2 diabetes, and obesity. How poor sleep “gets under our skin,” however, remains a mystery. The immune system has been proposed as a potential biological mechanism through which sleep may impact later disease.
During my graduate training I specialized in the field of psychoneuroimmunology (PNI), which focuses on understanding how psychological and behavioral factors modulate immune system functioning. Â In this context, my research centers largely on the innate immune system and the effects of psychological stress and sleep on inflammatory processes implicated in the pathogenesis of several age-related diseases, such as cardiovascular disease. I have remained fascinated by the extent to which sleep may serve as a restorative process, buffering the deleterious effects of stress on health. And while there is a growing evidence to support the influence of sleep deprivation under laboratory conditions on inflammatory activity, namely increases in pro-inflammatory cytokines, little is know about whether variation in sleep observed in the natural environment promotes similar pro-inflammatory signatures.
As a RWJ scholar, I am gaining experience with large cohort studies through a social epidemiology framework to investigate cross-sectional and prospective associations between measures of sleep and biomarkers of disease risk. In this regard, we recently published the first research evidence linking sleep quality and telomere length, a novel marker of cellular aging (Prather, Puterman et al., 2011).
From a population health perspective, I am interested in who experiences poor sleep and why. As I continue with the RWJ program and the collaborations established during my fellowship, I hope to chip away at these important, yet complex, questions. For instance, I am currently involved in an exciting project investigating whether poor sleep (e.g., short sleep duration, fragmented sleep) measured objectively using actigraphy prospectively predicts inflammatory trajectories at both the protein and genomic level among premenopausal women under high and low levels of stress. This study design provides the unique opportunity to test whether sleep serves as a novel pathway linking chronic psychological stress and inflammatory risk.
Sleep is a clear contributor to disease risk; however, the social determinants of sleep remain to be identified. By understanding the antecedents and biological consequences of sleep, we may be able to develop novel, targeted interventions to prevent illness, promote well-being, and reduce health disparities.
Aric completed his PhD in Clinical and Biological & Health Psychology at the University of Pittsburgh. He completed a clinical psychology internship, specializing in Behavioral Medicine at Duke University Medical Center. He lives in San Francisco with his wife Michelle. They are awaiting their first child (a boy), who will be born in November 2011.
To check out the Sleep Health recommendations for Healthy People 2020, see below.