Most people feel unduly tired at some time or another. For some, the experience of fatigue is unpleasant or incapacitating enough to encourage them to seek medical advice. A psychiatric or medical diagnosis can often account for symptoms, however, a proportion of patients experience a profound ongoing fatigue that cannot be explained by a single diagnosis. This fatigue is usually accompanied by a range of other somatic and neuropsychiatric symptoms. Over the past 30 years special attention has been given to these patients, and the causes of this debilitating fatigue have been hotly debated.
Early reports in the 1980's labelled the illness, "yuppie flu", regarding the malady as a psychosomatic reaction to stressors of modern society. Suffers of the illness and their advocates strongly opposed these aspersions, insisting that the cause of the illness was organic. From here, a series of names for the condition were suggested including chronic mononucleosis, post-viral fatigue syndrome and myalgic encephalomyelitis (ME), however toward that later part of 1989 the Centre For Disease Control renamed the condition chronic fatigue syndrome (CFS). In an attempt to standardize CFS diagnosis a team of international researchers published a consensus definition (1994) that specified:
* Fatigue lasting greater than 6 months (in 2007, the National Institute of Health and
Clinical Excellence published new criteria which specified that CFS should be diagnosed
after symptoms have persisted for 4 months)
* That the fatigue must have a definite onset
* That the fatigue must cause substantial disruption to the individual's day to day activities
* That the fatigue is not caused by continual exertion
The research team also proposed four additional key symptoms:
* Muscle and joint pain
* Non-refreshing Sleep
* Cognitive dysfunction
Possible Causes of CFS:
1. Post Viral Infection:
Most CFS patients seen in tertiary clinics predate the onset of their condition to an acute infective episode. This is not at all surprising when we consider that CFS shares a number of qualities with viral illnesses such as sudden onset, fatigue, muscle aches, pains, and brain fog. During the 1980's and 1990's researchers sought to identify the elusive pathogen responsible for CFS, with a number of retrospective studies investigating the possible role of herpesviruses including Epstein Barr Virus (EBV) and cytomegalovirus (CMV) to name a few. However, to date, there has been minimal evidence to support a causal link between CFS and herpesviruses. More recently, prospective studies have investigated whether acute viral infections could predict onset of CFS, however this has not been confirmed. Instead researchers have shown that the onset of CFS is more likely to present from severe infections such as infectious mononucleosis (glandular fever).
2. Neurobiology of CFS:
There is mounting evidence to suggest that the biology of the nervous system may play a partial - causal role in the development of CFS. Two regions of the brain (Hypothalamus and Pituitary) and a critical organ (adrenal glands) have been shown to impact on the neurobiology of CFS. The hypothalamus, pituitary gland and adrenal glands make up a key axis, known as the HPA axis. This mechanism assists in regulating our response to stress, be that social or physical. Recent findings by Torres-Harding et al., (2008, 2010, 2013) lend support to the idea that an infection may trigger a neurobiological reaction which leads to dysfunction of the HPA in susceptible hosts. Therefore, it is important to note, however, not all studies report differences between CFS patients and HPA dysfunction. One theory that may explain this difference may be that hypofunctioning (under/low functioning) of the HPA axis only occurs in a specific group of CFS patients. For example, in support of this theory, two recent trials have found that decreased salivary cortisol (a hormone produced via the adrenal glands in response to stimulation from the hypothalamus and pituitary gland) and reduced cortisol response (change in cortisol patterning) were largely evident in CFS patients who had a history of trauma or early life stress. This has lead to the idea that ongoing changes in the responsiveness of the HPA axis in CFS patients may be the result of prolonged or early stress response rather than a reaction to a pathogen. Although stress has more typically been associated with HPA axis hyperactivity, chronic stress and conditions such as post traumatic stress disorder have been associated with hypoactivity.
It is suggested that CFS cannot be understood through one etiological mechanism, whether it be viral, neurobiological or psychological. Rather it is a complex illness that is best explained in terms of a multifactorial cognitive behavioural model that incorporates predisposing, precipitating and perpetuating factors such as pre-morbid levels of distress, ongoing chronic stress, infection and social factors e.g. over-activity.
If you have any questions regarding this post please make contact:
Mark Hinchey Naturopathy, 601 Glebe Road, Adamstown: 0432234822/0240235959