Although risk factors for myalgic encephalomyelitis have been identified, no single definitive virus has been found in all cases, which has lead to the claim that ME is a common end path of a variety of infectious insults, perhaps most commonly in the retroviral family. It is still possible ME involves some combination of both environmental and genetic factors. Various theories try to combine the known data into plausible explanations. Although most accept an infectious explanation, several theories suggest that ME is an inappropriate immune response to an underlying condition, a theory bolstered by the observation that there is sometimes a family history of autoimmune disease. There is also a shift from the Th1 type of helper T-cells, which fight infection, to the Th2 type, which are more active in allergy and more likely to attack the body.
The most popular hypothesis is that a viral infection or retroviral reactivation primes a susceptible immune system for an abnormal reaction later in life. On a molecular level, this might occur if there is a structural similarity between the infectious virus and some component of the central nervous system, leading to eventual confusion in the immune system.
Since ME seems to be more common in people who live farther from the equator, another theory proposes that decreased sunlight exposure and possibly decreased vitamin D production may help cause ME. This theory is bolstered by recent research into the biochemistry of vitamin D, which has shown that it is an important immune system regulator.
Other theories describe ME as an immune response to a chronic infection. The association between ME and the Cocksackie-B, HHV-6, and HHV-7 viruses suggests a potential viral contribution in at least some individuals. Still others believe that ME may sometimes result from a chronic infection with spirochetal bacteria, such as Lyme disease. Another bacterium that has been implicated in ME is Chlamydia pneumoniae. Protein findings relating to several infections have seen found in the oligoclonal bands ME patients. Research has shown that, much like in AIDS, the immune dysfunction accompanying M.E. can lead to temporary or permanent progression of the disease, no matter what infection or combination of infections the PWME comes into contact with; additionally, PWME are more prone to opportunistic infections.
There is no known definitive cure for myalgic encephalomyelitis. However, several types of therapy have been found helpful by sufferers. Different therapies are used for patients experiencing greater neurological symptoms, for patients who have greater muscle and/or cardiac symptoms, for patients who have greater immune symptoms, for patients with an uncertain diagnosis, and for managing the various consequences of ME. Treatment is aimed at reducing disability, restoring sleep, reducing pain, reducing relapses, and preventing disability.
* **Coenzyme q-10**
Disease-modifying treatments (in trial):.
* **Avoiding relapse triggers**
* **Maintaining good hydration**
* **Dietary modification**
* **Neurontin** (pain control)
* **EPA fatty acid**
* **Saline infusions**
The prognosis (the expected future course of the disease) for a person with myalgic encephalomyelitis depends on severity and chronicity of the disease and initial symptoms; the age; and the degree of disability the person experiences. In general, 25% are severely disabled, though a number move in and out of categories due to relapse-remission. The life expectancy of people with ME is generally less than that of unaffected people; research done on CFS has suggested this decrease may be 25-30 years. Fatalities are generally rare, with a mortality rate anywhere from 5-10%, and occur mainly due to heart or pancreatic failure, opportunistic infection, neurodegeneration, cancer, and suicide.
Currently, there are no clinically established laboratory investigations available that can predict prognosis or response to treatment.
ME has been found world-wide, in at least 63 epidemics documented in published papers from the 1930′s to the 1980s. Currently ME is less epidemic and more endemic than in previous decades. Epidemics have a penchant for enclosed communities such as schools and hospitals, although not all of the outbreaks have occurred in enclosed commmunities.
As observed in many autoimmune disorders, ME is more common in females than males; the mean sex ratio is about two to three females for every male. In children the sex ratio is approximately equal.