Causes

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Triggers

ME/CFS frequently develops after an acute infection (e.g. flu-like illnesses, upper respiratory infections, glandular fever) but it may also be triggered by events such as toxic exposure (e.g. pesticides, heavy metals and environmental pollutants), physical trauma (e.g. major surgery or a serious accident), immunisation and anaesthetics.

Within days or weeks a progressive decline in health occurs in people who have been previously well and fully active and numerous symptoms develop. ME/CFS can also develop gradually without any identifiable initiating event.

In any individual it is possible that multiple factors are simultaneously involved, including a genetic pre-disposition – it is not uncommon for more than one family member to be affected, including separated members of the same, extended family.

Food intolerances and gut dysbiosis

Most if not all people with ME/CFS have a gut disturbance such as irritable bowel syndrome, gastric reflux, constipation, diarrhoea, and/or bloating. Research suggests strong links to food malabsorptions.

Disease process

Considerable progress has been made over the last decade in the knowledge and understanding of ME/CFS.

There is now much research evidence, published in over 4000 scientific papers, of a wide range of physiological and biochemical abnormalities, confirming that ME/CFS is a ‘distinct, biological, clinical disorder’.

Nervous and immune system dysfunction (in particular an abnormal response to infection) and mitochondrial malfunction are thought to play major parts in what is a complex disease process involving multiple systems of the body.

Research results and the exact cluster of symptoms experienced are not the same for all people with ME/CFS such that it is likely that, in due course, a number of sub-groups of ME/CFS will be identified. For example, one study has identified 88 genetic differences in people with ME, allowing researchers to identify seven sub-groups.

Research findings include evidence of:

  • Chronic activation and dysfunction of the immune system, e.g. increased cytokines; poor cellular function; abnormalities in the anti-viral defence pathway;
  • Persistent infection, e.g. HHV6, EBV, Mycoplasma, bacteria;
  • Reduced regional blood flow and abnormal energy metabolism in the brain; inflammation in the brain and spinal cord on autopsy; abnormal spinal fluid proteins; neurotransmitter irregularities; orthostatic intolerance; brain dysfunction in relation to working memory, concentration and information processing;
  • Low circulating blood volume; abnormal heart function; vascular abnormalities, e.g. inflammation and arterial stiffness; misshapen red blood cells; viral damage of the heart; pooling of blood in the extremities;
  • Ion transport and mitochondrial dysfunction;
  • Increased oxidative stress;
  • Gut dysfunction;
  • Genetic changes;
  • Abnormal responses/symptom-worsening with exercise.

All of the above are not found in everyone with ME/CFS.

More information

For more details on the topics of this page, see the ‘International Consensus Primer for Medical Practitioners‘, 2014.


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