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ME/CFS AUSTRALIA (SA) INC
Registered Charity 698
Mailing address:
GPO Box 383,
Adelaide,
South Australia 5001
Office:
266 Port Road,
Hindmarsh,
South Australia 5007
Ph: (08) 8346 3237
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FIBROMYALGIA HELP: Contact Fibromyalgia SA at the Arthritis Foundation of SA 118 Richmond Road, Marleston 5033 Ph: (08) 8379 5711 |
ME/CFS Australia (SA) Inc supports the needs of sufferers of Myalgic Encephalomyelitis, Chronic Fatigue Syndrome and related illnesses. We do this by providing services and information to members.
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CFS: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model
Friday 18 June 2010
Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways
Michael Maes 
and Frank NM Twisk
BMC Medicine 2010, 8:35doi:10.1186/1741-7015-8-35
Published 15 June 2010
Abstract (provisional)
Background
In a recently published paper, Harvey and Wessely put forward a 'biopsychosocial' explanatory model for myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is proposed to be applicable to (chronic) fatigue even when apparent medical causes are present.
Methods
Here, we review the model proposed by Harvey and Wessely, which is the rationale for behaviourally oriented interventions, such as cognitive behaviour therapy (CBT) and graded exercise therapy (GET), and compare this model with a biological model, in which inflammatory, immune, oxidative and nitrosative (IO&NS) pathways are key elements.
Discussion
Although human and animal studies have established that the pathophysiology of ME/CFS includes IO&NS pathways, these abnormalities are not included in the model proposed by Harvey and Wessely. Activation of IO&NS pathways is known to induce fatigue and somatic (F&S) symptoms and can be induced or maintained by viral and bacterial infections, physical and psychosocial stressors, or organic disorders such as (auto)immune disorders. Studies have shown that ME/CFS and major depression are both clinical manifestations of shared IO&NS pathways, and that both disorders can be discriminated by specific symptoms and unshared or differentiating pathways. Interventions with CBT/GET are potentially harmful for many patients with ME/CFS, since the underlying pathophysiological abnormalities may be intensified by physical stressors.
Conclusions
In contrast to Harvey and Wessely's (bio)psychosocial model for ME/CFS a bio(psychosocial) model based upon IO&NS abnormalities is likely more appropriate to this complex disorder. In clinical practice, we suggest physicians should also explore the IO&NS pathophysiology by applying laboratory tests that examine the pathways involved.
The above originally appeared here.
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