Insufficient sleep in later life is thought to contribute to declines in physical and mental functioning, and increase risk for morbidity and mortality. A yet unanswered question is: how does poor sleep contributes to worse health, particularly in aging. Both inflammation and cellular stress, which contribute to aging of cells, are proposed biological pathways through which sleep loss influences disease. I propose that sleep deprivation in older adults will alter the intracellular environment, decrease telomerase, and increase gene expression patterns consistent with cellular stress responses, inflammatory activity, and senescent signal expression. The over-arching objective of this proposal is to apply a biobehavioral framework to study the sleep-health relationship in older adults.
Aims. To do this I will: 1) obtain training in sleep, aging, and gene expression, 2) test biobehavioral mechanisms of sleep loss on health by conducting analyses using the Multi-Ethnic Study of Atherosclerosis (MESA), examining the contribution of sleep disturbances, sleep quantity, and sleep depth to rates of telomere attrition over 10 years, and 3) experimentally test the inflammatory, cellular stress, and cell senescence gene expression pathways that are disrupted from one night (Study 2) and 12 weeks (Study 3) of partial sleep deprivation in older adults (ages 60+). Significance. This unique interdisciplinary work will advance the field of biomedical sleep research by better defining one of the biological mechanisms through which sleep influences disease vulnerability in late life.
Included in the many objectives of Healthy People 2020, is a goal to improve public awareness and knowledge of how sleep impacts health, wellness, and quality of life. To help meet this goal, we must better understand the biological mechanisms through which sleep influences health, facilitating better understanding of how sleep deprivation affects disease risk. The current transdisciplinary research proposal is positioned to meet this public health need by improving our current understanding of the biological mechanisms through which sleep deprivation contributes to the progression of aging and premature morbidity and mortality in older adults.
|Carroll, Judith E; Irwin, Michael R; Levine, Morgan et al. (2017) Epigenetic Aging and Immune Senescence in Women With Insomnia Symptoms: Findings From the Women's Health Initiative Study. Biol Psychiatry 81:136-144|
|Kim, Tae Ho; Carroll, Judith E; An, Suk Kyoon et al. (2016) Associations between actigraphy-assessed sleep, inflammatory markers, and insulin resistance in the Midlife Development in the United States (MIDUS) study. Sleep Med 27-28:72-79|
|Carroll, Judith E; Cole, Steven W; Seeman, Teresa E et al. (2016) Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans. Brain Behav Immun 51:223-9|
|Carroll, Judith E; Esquivel, Stephanie; Goldberg, Alyssa et al. (2016) Insomnia and Telomere Length in Older Adults. Sleep 39:559-64|
|Irwin, Michael R; Olmstead, Richard; Carroll, Judith E (2016) Sleep Disturbance, Sleep Duration, and Inflammation: A Systematic Review and Meta-Analysis of Cohort Studies and Experimental Sleep Deprivation. Biol Psychiatry 80:40-52|
|Carroll, Judith E; Irwin, Michael R; Stein Merkin, Sharon et al. (2015) Sleep and multisystem biological risk: a population-based study. PLoS One 10:e0118467|
|Carroll, Judith E; Seeman, Teresa E; Olmstead, Richard et al. (2015) Improved sleep quality in older adults with insomnia reduces biomarkers of disease risk: pilot results from a randomized controlled comparative efficacy trial. Psychoneuroendocrinology 55:184-92|