- Sleep physiology
- Health consequences of chronic sleep restriction
Carol Everson is Professor of Medicine in the Division of Endocrinology and Molecular Medicine and holds a secondary appointment in the Department of Cell Biology, Neurobiology & Anatomy. She earned her PhD at the University of Chicago in the Division of Social Sciences. Her dissertation research focused on discovering physiological consequences of severe sleep deprivation. She next completed a 7-year fellowship at the National Institutes of Health in Bethesda, Maryland, where she set up a basic science sleep research laboratory and conducted studies on the effects of sleep deprivation on cerebral metabolism, nutritional demands, and host defenses. She joined the faculty in the Department of Physiology in the University of Tennessee College of Medicine as an assistant professor. There she advanced her prior discoveries of sleep deprivation, finding interplay between immune-related changes, endocrine abnormalities, and poor control over gut bacteria. Dr. Everson joined MCW as an associate professor in 2000 and was awarded the rank of professor in 2007. At MCW, she demonstrated that chronic sleep restriction results in increased cell injury and metabolic consequences that accumulate, eventually resulting in observable pathology, not all of which is reversible. Her research continues to provide inroads in elucidating the health implications of chronic sleep restriction. She is a member of MCW’s Neuroscience Research Center and Cardiovascular Center. She is a long-standing member of both the American Academy of Sleep Medicine and the Sleep Research Society. She previously served on the Board of Directors of the Sleep Research Society and as Board Liaison to the Research Committee of the Sleep Research Society Foundation.
Sleep as a basic biological requirement for health and life. Sleep is on par with other basic biological requirements, such as food and water, for which there are no known substitutes. While total deprivation can produce death, chronic deficiencies of basic biological requirements produce disease. Because basic biological requirements are involved in nearly every physiological function, significant deficiencies result in several categories of disease. Furthermore, many years may be required for morbidity to become sufficiently severe to be recognized as “disease.” As such, there is no known signature disease for chronic sleep deficiency. Sleep disturbances are major risk factors for cancer, cardiovascular disease, cerebrovascular disease, lung disease, osteoporosis, and autoimmune diseases, among others. Our laboratory is working to elucidate neural, immune, and hormonal mechanisms altered by chronically insufficient sleep that may lead directly to impaired health or secondarily to exacerbation of other diseases.
Sleep is restorative. A corresponding focus of the laboratory is to address the question, “What does sleep do at a cellular and systems level?” It is well accepted that sleep is “restorative.” However, what, specifically and biologically, is restored? Our laboratory has provided evidence that the properties of sleep after chronic sleep deprivation include restoration of a balance between DNA damage and repair, decreased turnover of intestinal epithelium, and decreased metabolic and inflammatory burdens. These properties appear to be among the biological mechanisms and functions responsible for the restorative value of sleep.
Research initiatives include follow-up of our findings of chronic sleep restriction studies:
- Blood and bone marrow abnormalities point to inflammatory processes
- Bone remodeling abnormalities are consequential for healthy aging
- Oxidative damage to DNA poses a cancer risk
- Changed nutritional demands and increased workload of visceral organs indicate a high metabolic cost of postponed sleep functions
- Hormone imbalances contribute to health impairment by insidious means
- Uncoordinated body functions due to circadian rhythm misalignment may be synergistic in producing pathology
(Swanson CM, Kohrt WM, Buxton OM, Everson CA, Wright KP Jr, Orwoll ES, Shea SA.) Metabolism. 2018 07;84:28-43 PMID: 29229227 PMCID: PMC5994176 SCOPUS ID: 2-s2.0-85040451185 12/13/2017
(Everson CA, Henchen CJ, Szabo A, Hogg N.) Sleep. 2014 Dec 01;37(12):1929-40 PMID: 25325492 PMCID: PMC4548518 SCOPUS ID: 2-s2.0-84914093940 10/18/2014
(Everson CA, Folley AE, Toth JM.) Exp Biol Med (Maywood). 2012 Sep;237(9):1101-9 PMID: 22946089 PMCID: PMC3939802 SCOPUS ID: 2-s2.0-84866443267 09/05/2012
(Everson CA, Szabo A.) PLoS One. 2011;6(8):e22987 PMID: 21853062 PMCID: PMC3154920 SCOPUS ID: 2-s2.0-80051644490 08/20/2011
(Everson CA, Szabo A.) Am J Physiol Regul Integr Comp Physiol. 2009 Nov;297(5):R1430-40 PMID: 19692662 PMCID: PMC2777777 SCOPUS ID: 2-s2.0-70449672782 08/21/2009
(Everson CA, Thalacker CD, Hogg N.) Am J Physiol Regul Integr Comp Physiol. 2008 Dec;295(6):R2067-74 PMID: 18945949 PMCID: PMC2685300 SCOPUS ID: 2-s2.0-57749108208 10/24/2008
(Everson CA.) Am J Physiol Regul Integr Comp Physiol. 2005 Oct;289(4):R1054-63 PMID: 15947073 SCOPUS ID: 2-s2.0-25844438769 06/11/2005
(Everson CA, Laatsch CD, Hogg N.) Am J Physiol Regul Integr Comp Physiol. 2005 Feb;288(2):R374-83 PMID: 15472007 SCOPUS ID: 2-s2.0-12344316868 10/09/2004
(Everson CA, Crowley WR.) Am J Physiol Endocrinol Metab. 2004 Jun;286(6):E1060-70 PMID: 14871886 SCOPUS ID: 2-s2.0-2442693138 02/12/2004
(Everson CA, Nowak TS Jr.) Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E85-93 PMID: 12067847 SCOPUS ID: 2-s2.0-0036298089 06/18/2002
(Rechtschaffen A, Bergmann BM.) Am J Physiol Regul Integr Comp Physiol. 2001 Feb;280(2):R602-3 PMID: 11270375 SCOPUS ID: 2-s2.0-0034999481 03/29/2001
(Everson CA, Toth LA.) Am J Physiol Regul Integr Comp Physiol. 2000 Apr;278(4):R905-16 PMID: 10749778 SCOPUS ID: 2-s2.0-0033994880 04/06/2000