Maes en Twisk:

kritiek op Wessely's (bio)psychosociale model

en de hoofdlijnen van een biomedisch model

 

 

 

 


 

 

 

Vandaag verscheen in BMC Medicine onze kritiek op het (bio)psychosociale

model voor ME/CVS beschreven door Harvey en Wessely in BMC in 2009:

 

Chronic fatigue syndrome: identifying zebras amongst the horses.

Harvey SB, Wessely S.

BMC Medicine 2009, 7:58. doi:10.1186/1741-7015-7-58.

http://www.biomedcentral.com/1741-7015/7/58.

 

onder de titel

 

Chronic fatigue syndrome:

Harvey and Wessely's (bio)psychosocial model versus

a bio(psychosocial) model

based on inflammatory and oxidative and nitrosative stress pathways.

Maes M, Twisk FNM.

BMC Medicine 2010, 8:35. doi:10.1186/1741-7015-8-35.

http://www.biomedcentral.com/1741-7015/8/35/abstract.

 

 

 

 

 

In ons artikel (dat na onstruktie én censuur tot stand kwam) onderbouwen wij

waarom het model van Harvey en Wessely voor ME/CVS ("onverklaarbare vermoeidheid")

en andere vormen van "vermoeidheid" onsamenhangend, onjuist en onvolledig is, én

waarom het label biopsychosociaal model niet van toepassing is.

 

Een pathofysiologisch model voor ME/CVS moet

de uitlokkende en onderhoudende faktoren omvatten,

die de biologische abnormaliteiten induceren,

waarmee de symptomen van patiënten plausibel verklaard kunnen worden.

 

Tegenover het model van Harvey en Wessely en andere (bio)psychosociale modellen, plaatsen wij een bio(psychosociaal) model voor ME/CVS,

waarin (persistente en/of reactiverende) infecties, immunologische abnormaliteiten (inflammatie, immuunactivatie, immunosuppressie and immuundysfunktie),

oxidatieve and nitrosatieve stress, en de biologische gevolgen daarvan

(bijv. mitochondriale dysfunctie en channelopathie) de hoofdrolspelers zijn.

 

Die biologische afwijkingen kunnen op plausibele wijze veel van de karakteristieke ME/CVS-symptomen, zoals "vermoeidheid", neurocognitieve klachten en pijn, plausibel verklaren.

 

Omdat fysiologische en psychologische stress de immunologische abnormaliteiten (inflammatie, immunosuppressie and immuundysfunktie) en oxidatieve en nitrosatieve stress verder doen toenemen, is het niet verwonderlijk dat "gedragsgerichte revalidatie-programma's", bijv. CGT/GET, zoals voorgesteld door Harvey and Wessely, veel klachten doet verergeren, zoals ook door verscheidene onderzoekers vastgesteld is.

 

Wij konkluderen dat het hoog tijd is om de (bio)psychosociale "verklaringsmodellen" definitief achter ons te laten en de aandacht te verschuiven naar de biologische pathofysio-logie van ME/CVS (en van de depressie waarmee ME/CVS soms gepaard gaat), subgroepen onder de "CVS"-vlag, gedefinieerd op basis van immunologische en andere objektieve markers, én therapieën om die biologische abnormaliteiten te reduceren/weg te nemen.

 

 

 


 

 

 

Enkele citaten uit de studie:

 

 

Figure 1 shows the Harvey and Wessely model.

 

....

 

The biological component of this model

is restricted to the potential triggers (infections) and

'biological responses' to the initial fatigue,

which, accompanied by "behavorial responses"

contribute to a prolonged severe fatigue.

 

Perpetuating factors are principally behavorial ones;

biological aberrations are considered to be a consequence not a cause.

 

All predisposing factors, with one exception (childhood illness),

are behavorial or characterological ones.

 

....

 

A medical model should explain

how precipitating and perpetuating factors (A)

induce the biological pathophysiology (B)

that accounts for specific symptoms (C).

 

Figure 3 shows a biological model

that plausibly explains "fatigue" and ME/CFS

by organic abnormalities and cause-and-effect relationships.

 

....

 

Harvey and Wessely [1] acknowledge

a minor role for biological factors - unspecified – as maintenance factors of ME/CFS,

while the cause-and-effect relationships of these biological factors are not specified.

 

....

 

These findings and other findings previously reviewed show that

the F&S symptoms are a clinical expression of dysregulated IO&NS pathways.

 

In that review and references therein,

we explained the mechanisms whereby

increased levels of pro-inflammatory cytokines,

oxidative damage,

increased COX-2 production,

increased translocation by gram-negative enterobacteria, etc,

generate F&S symptoms,

including fatigue, a flu-like malaise,  pain,

symptoms of irritable bowel syndrome, and neurocognitive disorders.

 

As explained previously,

the abovementioned aberrations in IO&NS pathways are interrelated.

 

....

 

The Vercoulen model as a whole has been invalidated by Song and Jason.

 

....

 

The effectiveness of CBT/GET (20-40%),

compared to support groups, natural course, standard medical care etc. (20-30%),

is only marginal.

 

....

 

CBT/GET has proven to be counterproductive in many patients.

 

....

 

This negative impact on the symptomatology of ME/CFS

can be explained by the fact that

exertion and GET may amplify the pre-existing pathophysiological aberrations,

e.g. inflammation; O&NS; damage caused by O&NS;

and sequels such as mitochondrial dysfunctions; etc.

 

....

 

Our re-analysis of Harvey and Wessely’s model

invalidates the psychosocial model for ME/CFS and

substantiates that

a biological model based upon IO&NS pathways is more appropriate

to describe this complex organic disorder.

 

 


 

Chronic fatigue syndrome: Harvey and Wessely's (bio)psychosocial model versus a bio(psychosocial) model based on inflammatory and oxidative and nitrosative stress pathways

BMC Medicine 2010, 8:35. doi:10.1186/1741-7015-8-35

Michael Maes, Frank NM Twisk

 

 

Published: 15 June 2010

 

 

 

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.

 

 

Key words:

 

chronic fatigue syndrome, pathophysiology, inflammation, cytokines, oxidative stress, CBT, GET, depression.

 

 

 

Samenvatting:

http://www.biomedcentral.com/1741-7015/8/35

 

Volledige tekst:

http://www.biomedcentral.com/content/pdf/1741-7015-8-35.pdf