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Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways – Source: BMC Medicine, Jun 15, 2010

  [ 104 votes ]   [ 1 Comment ]
By Michael Maes, Frank NM Twisk • www.ProHealth.com • June 16, 2010


[To read the full text of this free access article, click here. See also the authors' added explanation, attached as a footnote(1) to this abstract.]

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 behaviorally oriented interventions, such as cognitive behavior 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.

Source: BMC Medicine, Jun 15, 2010;8:35. doi:10.1186/1741-7015-8-35, by Maes M, Twisk FNM [Email: Michael Maes - crc.mh@telenet.be  or Frank NM Twisk - frank.twisk@hetnet.nl]

____

1. Author Commentary. Michael Maes & Frank Twisk wrote in a news release dated Jun 16, 2010 and shared via the Co-Cure Listserv:

We are pleased that BMC has published our critique on the (bio)psychosocial model for ME/CFS put forward by Harvey and Wessely in an article in BMC last year (“Chronic fatigue syndrome: Identifying zebras amongst the horses,” Harvey SB, Wessely S. BMC Medicine 2009, 7:58. doi:10.1186/1741-7015-7-58).

In our commentary (“Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways”) we substantiate why the Harvey and Wessely model for ME/CFS ('unexplained fatigue') is incoherent and invalid, and why the label biopsychosocial model is inappropriate.

A pathophysiological model for ME/CFS should incorporate the precipitating and perpetuating factors and the biological aberrations (induced and/or maintained by these factors), which can plausibly explain specific symptoms.

"As an alternative to the model of Harvey and Wessely and other (bio)psychosocial models, we outline a bio(psychosocial) model for ME/CFS, in which (persistent and/or reactivating) infections, immunological abnormalities (inflammation, immune activation, immunosuppression and immune dysfunction), oxidative and nitrosative stress, and their sequels (e.g. mitochondrial dysfunction and channelopathy) are key players.

These biological aberrations account for many of the symptoms characteristic for ME/CFS - e.g. "fatigue", neurocognitive impairment, and pain.

Since physiological and psychological stress intensify the immunological abnormalities (inflammation, immunosuppression and immune dysfunction) and oxidative and nitrosative stress, it is not surprising that 'behaviorally oriented programs', like CBT/GET, as proposed by Harvey and Wessely, amplify many symptoms, as has been observed by various authors.

We conclude that it is about time to leave the (bio)psychosocial explanatory model(s) for ME/CFS and behavorial interventions justified by these models, (CBT/GET) behind us once and for all, and to shift the focus to the organical pathophysiology of ME/CFS (and depression accompanying ME/CFS), subgroups of ME/CFS patients, defined by immunological and other objective markers, and therapies to effectively reverse the biological abnormalities.”




Please Discuss This Article:   Post a Comment 

Biopsychosocial model of CFS/ME
Posted by: JBest
Jun 21, 2010
What a relief to hear some sense at last! It certainly is about time the biopsychosocial model for this organic disease was well and truly put behind us. This model has done a huge amount of damage to people with genuine CFS/ME i.e as defined in the Canadian Criteria. Many patients have treated with contempt by their doctors and even laughed at when they describe their symptoms; some doctors are still saying that they do not believe in M.E and that M.E does not exist. Consequently, many patients with CFS/ME are being denied appropriate testing, assessment and the corrective treatment that may well be developed by concerted efforts on the part of the UK government, the Medical Research Council and the National Institute for Clinical Excellence to promote and support biomedical research into this disease to establish reliable biomarkers at least and effective treatments at best; who knows, possibly even a vaccine. Far too much time, effort and money has gone into psychological research into CFS/M.E and the results have proved conclusively thus far that psychologically-based so-called "treatments" are not effective. CBT and GET are available for patients with other chronic illnesses, including heart disease, cancer and AIDS. If CBT, GET and GAT were the only "treatments" available for these diseases there would be astonishment and public outcry. Why then, in the face of so much existing research evidence of the organic processes at work in CFS/ME, is so much public money spent on psychological research and "treatment" approaches for CFS/ME in the absence of any scientific evidence of any "psychosocial" element, at the expense of biomedical research?
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