Aetiology and prevalence
Although the aetiology of M.E. is unknown, emerging evidence about the cause of M.E. include autoimmune deficiencies, viral infections, autonomic nervous system dysfunction and genetic factors, among others. While M.E. is not strictly hereditary there is some evidence for genetic predisposition.
The disease may occur with a sudden onset, such as following an infection, or it may occur with a gradual onset. There is no clear evidence that M.E. is a form of persistent, chronic infection though it may be a consequence of a viral or bacterial infection where the person does not recover in the normal way. It is not clear why some people get M.E. while others recover normally. Attempts to prove links with a specific virus have been unsuccessful. Many of the infections which trigger M.E. seem to be ordinary flu-like infections.
There may be a number of sub-groups, or phenotypes, of the illness, with differing aetiology, symptoms, response to treatment and prognosis. This heterogeneity has caused difficulty in conducting trials, along with patients being too unwell to take part in research, resulting in very small studies which are difficult to extrapolate to form a clearer picture of the illness. Evidence is emerging for possible phenotypes relating to:
- postural orthostatic tachycardia syndrome (POTS)
- brain dysfunction
- gene expression changes following exercise
Evidence cited by the NICE guideline for M.E. (undergoing essential updates, though this process is on hold due to the Coronavirus pandemic) suggests a population prevalence of at least 0.2–0.4% which means that a general practice with 10,000 patients is likely to have up to 40 patients with M.E.
As a long-term, fluctuating condition, M.E. is categorised as a disability by the Equality Act 2010.