Sleep disorders and inflammatory disease activity: chicken or the egg?

Am J Gastroenterol. 2015 Apr;110(4):484-8. doi: 10.1038/ajg.2014.247. Epub 2014 Aug 26.

Abstract

Sleep dysfunction is a highly prevalent condition that has long been implicated in accelerating disease states characterized by having an inflammatory component such as systemic lupus erythematosus, HIV, and multiple sclerosis. Inflammatory bowel disease (IBD) is a chronic, debilitating disease that is characterized by waxing and waning symptoms, which are a direct result of increased circulating inflammatory cytokines. Recent studies have demonstrated sleep dysfunction and the disruption of the circadian rhythm to result in an upregulation of inflammatory cytokines. Not only does this pose a potential trigger for disease flares but also an increased risk of malignancy in this subset of patients. This begs to question whether or not there is a therapeutic role of sleep cycle and circadian rhythm optimization in the prevention of IBD flares. Further research is needed to clarify the role of sleep dysfunction and alterations of the circadian rhythm in modifying disease activity and also in reducing the risk of malignancy in patients suffering from IBD.

MeSH terms

  • Animals
  • C-Reactive Protein / metabolism
  • Circadian Rhythm* / genetics
  • Clinical Trials as Topic
  • Colitis, Ulcerative / physiopathology
  • Crohn Disease / physiopathology
  • Cytokines / blood*
  • Disease Models, Animal
  • Humans
  • Inflammatory Bowel Diseases / blood
  • Inflammatory Bowel Diseases / etiology
  • Inflammatory Bowel Diseases / physiopathology*
  • Inflammatory Bowel Diseases / prevention & control
  • Interleukin-1beta / blood
  • Interleukin-6 / blood
  • Melatonin / metabolism*
  • Neoplasms / etiology
  • Neoplasms / metabolism
  • Neoplasms / physiopathology*
  • Quality of Life
  • Recurrence
  • Signal Transduction
  • Sleep
  • Sleep Deprivation
  • Sleep Wake Disorders / blood
  • Sleep Wake Disorders / complications
  • Sleep Wake Disorders / physiopathology*
  • Toll-Like Receptor 4 / metabolism*

Substances

  • Cytokines
  • Interleukin-1beta
  • Interleukin-6
  • Toll-Like Receptor 4
  • C-Reactive Protein
  • Melatonin