Chronic fatigue syndrome (CFS) is a chronic condition that results in persistent, often insurmountable fatigue in addition to other illness-like symptoms, such as muscle and joint pain, tender lymph nodes, sore throats, etc. The standard protocol for diagnosis (Fukuda, et. al. 1994) has made CFS easily and objectively distinguishable, allowing further research on prevalence, incidence, and the science and treatment of the condition to be heavily conducted in the past decade.
It is believed that .4% to 1% of all people worldwide are currently affected by CFS, making it exceedingly common among chronic health conditions (Devanur & Kerr, 2006). Though it was once considered a disease only obtainable by upper class women, this myth has since been disproved, as the impact of CFS has reached minority populations and those in lower income brackets among both genders, though still largely female (Reyes, et. al., 2003).
A speculative explanation for the early history of CFS impacting predominantly white, middle-aged, upper class women is in the increased personal recognition (not psychological creation) of the illness symptoms (Jason, Fennel & Taylor, 2003).
Further study on the demographics has revealed that no particular age group seems to have been selectively identified for susceptibility. The symptom of persistent fatigue has spanned across all age groups in the research. Studies have been done on children as young as eight with short and long term debilitating fatigue "which may be related to chronic fatigue syndrome in adults" (Harding, 2006).
This wide demographic data unfortunately seems to be paralleled by an even broader range of symptom expression and causation. Consequently CFS has become a term that collectively represents what may be dozens of conditions, expressed by as many levels of symptom severity. It is not, however, a condition that lacks objective abnormalities and diagnosis.
CFS has clear evidence of genetic origin (Harding, 2006), blunted hormone responses (Scott, Medbak & Dinan, 1998), cardiac autonomic imbalance (Pagani, Lucini, Mela, Langewit & Malliani, 1994), altered immune function (Hanson, Gause & Natelson, 2001), impairment of oxidative metabolism (Snell, Van Ness, Stevens, Phippen & Dempsey, 2003), and weakened cognitive and reactionary capacity (Lange, et. al., 2005).
Despite the clear and objective physiological abnormalities among CFS populations, finding physiological causation for these abnormalities has proven to be more of a challenge, and is still not entirely understood. While the line of thought used to center around a post-illness condition following Epstein-Barr Virus (EBV), it is now known that there are numerous ways to be affected, sometimes, but not necessarily, following an infection such as EBV or mononucleosis (Komaroff, 2000).
Today, even with the informational foundation built on the cumulative results of tens of thousands of valid medical studies, we're still routinely subjected to fallacious reports distorting the public perception of CFS. Many of these misconceptions have likely risen from the heterogeneous nature of the condition, most prominently that CFS is a psychiatric disorder and thus can be cured with psychiatric therapy. This claim, despite the mounting degree of repetition and propagation, has simply found no scientific validity in the research (Van Hoof, 2004). A further related suggestion is that the lack of motivation in those suffering from CFS is the preventative barrier to recovery. Like the psychological accusations, this is also not validated by the research (Friedberg & Jason, 1998).
One area of immense debate, deservedly, in the literature is exercise therapy. Exercise is possibly the most common suggested therapy for CFS, but one must implement caution in both the mode and volume of exercise prescribed as it can manifest further problems, resultantly increasing kinesiophobia (fear of movement/exercise) and the associated cycle of deconditioning affiliated with hypokinetic behavior in all populations (Snell, Van Ness, Stevens & Phippen, 2003).
In conclusion, all people suffering from CFS express similar symptoms and a comparable overall level of debilitation. However, the prevailing evidence suggests that chronic fatigue syndrome is defined just as much by the ambiguity in causation as it is the expression of symptoms. Based on this, it has been suggested that subtypes of chronic fatigue syndrome must be established (Jason, Corradi, Torres-Harding, Taylor & King, 2005). Once this is accomplished, we, as a researching body, will be able to progress further in the understanding of the condition and appropriate application of therapy.
The mission of the Pacific Fatigue Lab is to educate people on the facts and fallacies among the existing body of knowledge on CFS, as well as delve deeper into the scientific and practical research in the hope that an eventual cure will be uncovered.
[History of CFS]
[Differentiating CFS from Depression]
Devanur & Kerr. (2006). Chronic fatigue syndrome. Journal of Clinical Virology, September 13.
Friedberg & Jason. (1998). Understanding chronic fatigue syndrome: an empirical guide to assessment and treatment. Washington D.C.: American Psychological Association.
Fukuda, Straus, Hickie, Sharpe, Dobbins & Komaroff. (1994). The chronic fatigue syndrome: a comprehensive approach to its definition and study, Annals of Internal Medicine, 121(12): 953-959.
Hanson, Gause & Nelson. (2001). Detection of immunologically significant factors for chronic fatigue syndrome using neural network classifiers. Clinical and Diagnostic Laboratory Immunology, 8: 658-662.
Harding. (2006). Disabling fatigue may have genetic roots. Reuters Health, Sept 2006.
Jason, Corradi, Torres-Harding, Taylor & King. (2005). Chronic fatigue syndrome: the need for subtypes. Neuropsychology Review, 15: 29-58.
Jason, Fennel & Taylor. (2003). Handbook of chronic fatigue syndrome. New York: John Wiley & Sons, Inc.
Komaroff. (2000). The physical basis of CFS. The CFIDS Research Review, 1(2): 1-11.
Lange, Steffner, Cook, Bly, Christodoulou, Liu, Deluca & Natelson. (2005). Objective evidence of cognitive complaints in chronic fatigue syndrome: a bold fMRI study of verbal working memory. Neuroimage, 26(2): 513-524.
Pangani, Lucini, Mela, Langewit & Malliani. (1994). Sympathetic over-activity in subjects complaining of unexplained fatigue. Clinical Science, 87: 655-661.
Reyes, Nisenbaum, Hoaglin, Unger, Emmons, Randall, Stewart, Abbey, Jones, Gantz, Minden & Reeves. (2003). Prevelance and incidence of chronic fatigue syndrome in Wichita, Kansas. Archives of Internal Medicine, 163: 1530-1536.
Scott, Medbak & Dinan. (1998). Blunted adrenocorticotropin and cortisol responses to corticotropic-releasing hormone stimulation in chronic fatigue syndrome. Acta Psyschiatr Scand, 97: 450-457.
Snell, Van Ness, Stevens, Phippen & Dempsey. (2003). Handbook of chronic fatigue syndrome. New York: John Wiley & Sons, Inc.
Van Hoof. (2004). Cognitive behavioral therapy as a cure-all for CFS. Journal of Chronic Fatigue Syndrome: 11, 43-47.