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MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME

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431<br />

They expla<strong>in</strong> that historically, the classical “CBT model” of emotional distress as proposed by Beck<br />

dist<strong>in</strong>guished between predispositions and precipitants, and perpetuat<strong>in</strong>g cognitive, behavioural, affective<br />

and physiological factors, and that the “CBT model reta<strong>in</strong>s this general structure and its ‘three Ps’: predispos<strong>in</strong>g,<br />

precipitat<strong>in</strong>g and perpetuat<strong>in</strong>g factors”.<br />

Deary et al say: “Treatment tends to <strong>in</strong>itially focus on the perpetuat<strong>in</strong>g cycle, attempt<strong>in</strong>g to dismantle the self‐<br />

ma<strong>in</strong>ta<strong>in</strong><strong>in</strong>g <strong>in</strong>terlock of cognitive, behavioural and physiological responses hypothesised to perpetuate the symptoms”.<br />

Accord<strong>in</strong>g to Deary et al, the “s<strong>in</strong>e qua non of any CBT model is a vicious circle, the hypothesis that a self‐<br />

perpetuat<strong>in</strong>g <strong>in</strong>teraction between different doma<strong>in</strong>s ma<strong>in</strong>ta<strong>in</strong>s symptoms” and they postulate that “the CBT models<br />

of MUS, IBS and CFS propose a model of perpetuation that is autopoietic”. Quot<strong>in</strong>g Valera (2005), Deary et al<br />

def<strong>in</strong>e autopoiesis as: “the process whereby an organization produces itself…an autonomous and self‐ma<strong>in</strong>ta<strong>in</strong><strong>in</strong>g<br />

unity”. If Deary et al were mean<strong>in</strong>g to refer to the “Father” of autopoiesis, and the person who <strong>in</strong>troduced<br />

the concept of autopoiesis to biology, then that person is Francisco Varela (not Valera), and Varela died <strong>in</strong><br />

2001, so it is not clear why Deary et al cite a website and not a peer‐reviewed paper for their autopoiesis<br />

reference. Furthermore, their citation for “Valera (2005)” does not appear on the website <strong>in</strong> question<br />

(http://pespmc1.vub.ac.be/ASC/AU<strong>TO</strong>POIESIS.html ).<br />

Deary et al then say that “The CBT model of perpetuation differs from a more generic biopsychosocial model by<br />

propos<strong>in</strong>g a unique autopoietic <strong>in</strong>teraction of cognitive, behavioural and physiological factors for each<br />

<strong>in</strong>dividual….symptoms are (assumed to be) generated not by one disease process but by the <strong>in</strong>teraction of (cognitive,<br />

behavioural and physiological) factors”. Deary et al say they considered as examples of the “CBT model” of<br />

MUS “all models which propose such a process” (notably, not a few of the considered papers were Wessely<br />

School self‐references).<br />

The authors say that although there are vary<strong>in</strong>g degrees of evidence for each of the components of their<br />

model, “what is lack<strong>in</strong>g is solid proof of their <strong>in</strong>teraction <strong>in</strong> vicious circles, although all of the models reviewed<br />

(<strong>in</strong>clud<strong>in</strong>g their own) assume this <strong>in</strong>teraction”.<br />

Despite their own “assumption”, claim<strong>in</strong>g “coherence” of their “CBT model”, Deary et al say: “the key feature<br />

of CBT model is that these <strong>in</strong>dividual components become locked <strong>in</strong>to an autopoietic cycle” and they hypothesise that<br />

<strong>in</strong> “vulnerable <strong>in</strong>dividuals, such as those who are over‐active, CFS is precipitated by life events or viruses lead<strong>in</strong>g<br />

to an autopoietic cycle <strong>in</strong> which physiological changes, illness beliefs, reduced activity, sleep disturbance, distress,<br />

medical uncerta<strong>in</strong>ty and lack of guidance <strong>in</strong>teract to ma<strong>in</strong>ta<strong>in</strong> symptoms. The evidence supports some of the <strong>in</strong>dividual<br />

dots <strong>in</strong> this picture but not yet the l<strong>in</strong>es between them”.<br />

Their construct of causation clearly <strong>in</strong>cludes factors that are mutually exclusive (overactivity as well as<br />

underactivity), which begs the question that their model is all‐embrac<strong>in</strong>g and was designed to ensure it can<br />

never be disproven.<br />

Deary et al then state that: “what makes the CBT model so difficult to test may also be one of its chief strengths: it is<br />

<strong>in</strong> many ways a meta‐model to jo<strong>in</strong> the dots of whatever factors each patient presents. Indeed, factors that are neither<br />

strictly cognitive nor behavioural but have been found to be important (for <strong>in</strong>stance, social support [cit<strong>in</strong>g Chalder<br />

1998] or benefit receipt can be <strong>in</strong>corporated <strong>in</strong>to this structure as perpetuat<strong>in</strong>g factors”.<br />

Two po<strong>in</strong>ts arise:<br />

(i) the authors do not consider that many people whose lives are wrecked by <strong>ME</strong>/CFS are not claim<strong>in</strong>g either<br />

state benefits or permanent health <strong>in</strong>surance, so how do they fit <strong>in</strong>to their “CBT model”, given that two of<br />

the allegedly perpetuat<strong>in</strong>g factors do not apply to them?<br />

(ii) the authors concede that they cannot jo<strong>in</strong> the dots to produce the full picture, yet they still hang their<br />

beliefs about their model on <strong>in</strong>dividual dots, claim<strong>in</strong>g that some of the dots ‐‐ especially social support and

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