Carol Everson, PhDCarol A. Everson, PhD

Professor, Department of Neurology
Professor, Department of Cell Biology, Neurobiology, and Anatomy


  • Sleep Physiology Research


  • Biological basis of behavior
  • Neuroendocrinology
  • Neuroimmunology


  • BA, University of Wisconsin, LaCrosse, WI, 1979
  • Postgraduate courses, University of Wisconsin-Madison; Management in private industry, 1979-1982
  • PhD, University of Chicago, Chicago, Illinois, 1987


  • Staff Fellow, Clinical Psychobiology Branch, Intramural Research Program, National Institutes of Health, Bethesda, Maryland, 1988 -1991.
  • Senior Staff Fellow, Clinical Psychobiology Branch, Intramural Research Program, The National Institutes of Health, Bethesda, Maryland, 1991 - 1995.
  • Assistant professor, Department of Physiology, University of Tennessee Medical College and Health Sciences Center, Memphis, Tennessee, 1995-2000.


  • Member, Sleep Research Society, Associated Professional Sleep Societies, 1983-present
  • Member, European Sleep Research Society, 1994-present
  • Member, American Physiological Society, 1997-present
  • Member, Center for Neuroscience, University of Tennessee, 1996-2000


  • National Research Service Award, Department of Psychiatry, University of Chicago, 1983 - 1987
  • Joseph Kelly Memorial Award for Highest Standards in Quality of Research, University of Chicago, 1987

Brief Clinical/Research Interest Statement

Our long-term goal is to determine how restriction of sleep affects functions of cells, processes, and systems in ways that promote disease or impede recuperation, and conversely how recovery of sleep specifically increases resistance to disease. We have shown that sleep deprivation results in a unique set of health impairments believed to contribute to co-morbid disease conditions and shortened longevity in humans. The clinicopathological course of sleep deprivation in the laboratory rat is marked by metabolic derangement that is manifested by a robust appetite and increased food consumption without weight gain. Sleep deprivation decreases resistance to infectious disease, and this is manifested by failure to eradicate opportunistic microorganisms and their toxins despite activation of certain components of the immune system. Circulating anabolic hormones are suppressed by sleep deprivation due to altered regulation by brain mechanisms in ways expected to decrease resistance to disease. Despite eventual severe health impairments in rats due to sleep deprivation, the impairments are highly reversible when sleep is permitted, pointing to biochemical changes as mediators of a toxic-like state. Our recent findings provide evidence that uncompensated oxidative stress is a major pathogenic factor induced by sleep deprivation, pointing therefore to putative biochemical mediation. We are working to discover the causal relationships between oxidative stress and its sequelae and alterations of mechanisms responsible for integrity of immune, hormonal, and metabolic systems that operate abnormally during sleep deprivation.

Sleep and Health Research Donation

Research Support

Project: Physiology of sleep deprivation
Source: NIH Intramural Research Program
Role: Principal Investigator
Dates: January 1, 1988 - June, 1995

Project: Hormonal mediation of sleep deprivation pathology
Source: University of Tennessee Medical Group
Role: Principal Investigator
Dates: December 1, 1996 – November 30, 1997

Project: Central nervous system manifestations of thyroid hormone disease: Implications for sleep regulation and function.
Source: Clinical Research Center Project, funded by a NIH program award, University of Tennessee, Memphis
Role: Principal Investigator
Date: May, 1996 - April, 2000

Project: Neurobiology of Sleep Deprivation: Impaired Host Defenses
Source: NIH, National Institute of Heart, Lung & Blood
Role: Principal Investigator
Dates: April 1, 1997 - March 31, 2003

Project: Neuroendocrine Abnormalities Induced by Sleep Deprivation
Source: NIH, National Institute of Neurological Disorders & Stroke
Role: Principal Investigator
Dates: July 1, 1999 - May 31, 2004

Project: Sleep Fragmentation Effects on Murine CII-Induced Arthritis
Source: NIH, National Institute of Arthritis and Musculoskeletal and Skin Diseases
Role: Co-Principal Investigator with Arnold Postlethwaite, University of Tennessee, Memphis, TN
Dates: September 01, 2002 – August 31, 2005

Project: Restricted Sleep: Modification of adiposity and adipose tissue composition
Source: NIH, National Heart, Lung & Blood Institute
Role: Principal Investigator
Dates: September 12, 2006 – July 31, 2011

Project: Oxidative stress responses to loss and recovery of sleep
Source: NIH, National Heart, Lung & Blood Institute
Role: Principal Investigator
Dates: May 1, 2007 - March 31, 2013

Recent Publications

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