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Aetiology and prevalence

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 and around a fifth (22%) of respondents to Action for M.E.’s M.E. time to deliver survey of more than 2,000 people with M.E. said they have family members with the illness.

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:

Evidence cited by the NICE guideline for M.E. 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.