Myalgic encephalomyelitis (“ME”) affects approximately 1 in 400 and four times as many women as men. It usually occurs after an acute infection, although it has also manifested itself after other serious physical insults to the body. The disease has many definitions, but most agree that it is characterized by a profound fatigue and infectious symptoms that do not resolve with rest. Symptoms include severe headache, swollen lymph nodes, gastrointestinal dysfunction, and mild cognitive impairment, which worsen after exertion. More severe cases involve extreme sensory sensitivities; ataxia; seizures; and an inability to walk or sit up, eat solid food, or care for one’s self. These individuals are unable to leave their beds or homes for years at a time. They are more susceptible to cancer, heart disease, and suicide at much higher rates than the normal population.

Many pathogens have been associated with ME. A key study followed patients who became ill with common viral infections and found that the initial pathogen did not matter as much as the severity of the illness prior to developing ME. This and other studies have found that a faulty immune response is involved in the development of the disease.

Like MS, MRI studies of ME patients have shown areas of the brain to be adversely impacted. Symptoms such as cognitive impairment, balance and movement problems, and fatigue are very similar to those who suffer from MS. ME symptoms may be episodic in nature, but may also follow a progressive course.

ME risk factors

The most common risk factors to be reported include being female, living and/or working in a moldy or toxic environment, and having an unusually strong immune reaction to an infectious disease. Genetics and a susceptibility to autoimmunity may also play a role.

How is myalgic encephalomyelitis treated?

The most successful treatments reported in the literature include those directed against infectious pathogens such as herpes viruses, mycoplasmas, and Lyme bacteria or are immune based such as Ampligen, an interferon inducing drug, and IVIG, which provides more general immune support. Antifungal medications have shown promise for those who are known to be impacted by mycotoxins.  Other successful clinical trials using a B cell depleting therapy, Rituximab, are in progress. It is reassuring to know that as we advance our research into the underlying causes of disease, a greater number of medical options will become available to patients with ME.

Our ME research

Our researchers recently completed the largest genome-wide association study (GWAS) to date looking at millions of single nucleotide polymorphisms (SNPs) for genetic evidence of disease susceptibility in a small group of ME patients. After identifying the most relevant SNPs in this study, they intend to collect a much larger number of samples for a more directed search and confirmation of their original findings. Understanding vulnerability to a disease can help point the way toward more effective treatments and possible prevention.

There are signs that autoimmunity may play a role in ME. Our researchers are working with researchers from Arizona State University and the Canadian health system to identify autoimmune markers of disease. These findings will help doctors understand the underlying causes of disease and may assist the NIH when deciding the appropriate placement of this disease for future study.