One suggested cause of, and possible treatment for, chronic fatigue syndrome

August, 2007

Not in the mind of neurasthenic lazybones but in the cell nucleus: patients with chronic fatigue syndrome have increased production of nuclear factor kappa beta.

Summary of the abstract

There is now some evidence that chronic fatigue syndrome is accompanied by an activation of the inflammatory response system and by increased oxidative and nitrosative stress.

Nuclear factor kappa beta (NF-kB) is the major upstream, intracellular mechanism which regulates inflammatory and oxidative stress mediators.

In order to examine the role of NF-kB in the onset and progression of chronic fatigue syndrome, the production of NF-kB peripheral blood lymphocytes was examined. Levels found in 18 patients with chronic fatigue syndrome were compared with levels in 18 healthy controls.

NF-kB activation was significantly higher in those with chronic fatigue syndrome.

There were significant and positive correlations between NF-kB activation and the severity of illness, as measured by symptoms, such as aches and pain, muscular tension, fatigue, irritability, sadness, and overall patient impressions of well-being.

These results demonstrate an intracellular inflammatory response in the white blood cells and suggest how that might play an important role in the onset and progression of chronic fatigue syndrome. Earlier findings of increased oxidative stress and inflammation in chronic fatigue syndrome may in fact result be attributed to the elevated level of activated NF-kB.

Therefore, the symptoms of chronic fatigue syndrome, including the characteristic fatigue, muscular pain and tension, and even the depression so common in chronic fatigue syndrome, may result from a genuine inflammatory response in those with chronic fatigue syndrome.

It is suggested that chronic fatigue syndrome patients might be successfully treated with antioxidants, which inhibit the production of NF-kappaB, such as curcumin and other natural anti-oxidants.