[Note: to read the free full text of this article providing an overview of the current science regarding chronic fatigue, click HERE. Concludes that large studies of genetic involvement and oxidative stress in well defined high-fatigue diseases are needed to further unravel the biological mechanisms involved.]
Chronic fatigue is a common, poorly understood and disabling phenomenon in many diseases. We aim to provide an overview of fatigue in chronic autoimmune and inflammatory disease.
Fatigue measurement, prevalence and confounding factors such as depression, sleep disorders and pain are reviewed in the first half of the article.
In the second half of the article, we describe explanatory models of fatigue and fatigue signaling, with an emphasis on:
• Cytokines and sickness behavior [The brain’s response to chemicals signaling inflammation-causing situations such as infection; prompting energy-saving behaviors designed to enhance ability to survive the situation],
• Oxidative stress [When reactive oxygen species (free radicals) outrun ability to control them, and the imbalance leads to damage of cellular components, including the energy-producing mitochondria. Compared to rust in a tin can],
• Mitochondrial dysfunction,
• And the impact of certain genes on fatigue.
Source: Rheumatology, Feb 1, 2011;50(2). Norheim KB, Jonsson G, Omdal R. Department of Internal Medicine, Clinical Immunology Unit, Stavanger University Hospital, Stavanger, Norway. [Email: firstname.lastname@example.org]