Chronic fatigue syndrome: altered physiology and genetic influences (page 1 of 5)
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Key Points
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The aetiology (cause) of chronic fatigue syndrome/myalgic encephalomyelitis (CFS/ME) is controversial. There is a polarity between a search for organic causes and an attempt to provide behavioural explanations for symptom production.
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There is good evidence of altered physiology in CFS/ME, particularly affecting neuroendocrine and hypothalamic-pituitary-adrenal (HPA) axis function.
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Classic twin studies have demonstrated a strong heritable component to CFS/ME and other conditions of abnormal fatigue.
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New genetic information describes associations between patients with fatigue and CFS/ME and genes involved in neuroendocrine and sympathetic nervous system function.
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One model that may explain this is provided by evidence that vagal nerve activity may modulate the release of fatigue-inducing cytokines.
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Environmental factors, abnormal physiological pathways and genetic pre-disposition are all likely to contribute to symptom production and response to illness in CFS/ME.
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An understanding of CFS/ME is best served by taking all the likely aetiological factors into account. The new genetic information helps us to move away from the conflict between medical models of CFS/ME and a bio-psychosocial view of the illness.
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