In response to this fraudulent study, Dr Myhill reported the authors of PACE, and its directors, to the General Medical Council in January 2018. The GMC has a duty, and is empowered by Parliament, to regulate doctors and this includes research misconduct. Despite taking six months to consider Dr Myhill’s request, the GMC refused to investigate. Dr Myhill supplied extensive scientific proofs but in its refusal the GMC failed to supply its scientific defence.
So, Dr Myhill, through FoI legislation, asked that the GMC supply her with the scientific references on which it relied in coming to its decision not to investigate the PACE authors. The GMC refused. It gave no reasons whatsoever.
Consequently, Dr Myhill reported the GMC to the Information Commissioner who in a ruling of 30 September 2019 agreed with her. The ICO informed the GMC that it must supply her with the scientific references on which it relied in deciding not to investigate the PACE authors. This was because Dr Myhill was asking simply for scientific references already in the public area. This was only fair to the thousands of patients who have been damaged by graded exercise and who have a right to a proper explanation as to why.
At this point you would think the GMC had to comply. However, it is suspected that the GMC refusal arose for reasons of cronyism – it did not want ex-Presidents of Royal Societies up in front of the GMC and the Police. It did not want to admit that actually it held NO scientific evidence, and it had no good reason to proceed as it did.
So, the GMC had to think up some sort of legal argument for refusal. Hitherto it had no argument – simply blunt refusal. The GMC consulted with its legal beavers within and outside the GMC and came up with the argument that to comply with the ICO demands would infringe the personal privacy of the PACE authors. What a nonsense! Dr Myhill has no interest in the personal data of the PACE authors. She simply requested scientific references which should all be in the public arena!
This was the subject of the ICO Hearing on 22 March 2021: Myhill vs GMC and ICO.
The outcome was a split decision. It boiled down to the Public Interest test. Tribunal member Mr Malcolm Clarke agreed with Dr Myhill. He stated:
“I conclude that Dr Myhill’s legitimate interest in seeking this information, if it exists, as a practising doctor with patients, who has a deep professional interest in ensuring that national recommended treatments in this area of medicine are evidence-based, is a very strong one …Dr Myhill’s legitimate interest in knowing whether the information she requests is held by the GMC is a very strong one. I therefore conclude that ……Dr Myhill’s legitimate interests are not overridden by the rights and freedoms of the data subjects.”
Ref paragraphs 42-47,EA-2020-0018 Myhill v IC & GMC
Luckily for the GMC, the Judge Hazel Oliver and Panel member Gareth Jones disagreed. They decided the other way round.
This Ruling sends a very clear message to doctors who commit scientific fraud – it is easy to get away with it, you can easily hide behind Data Protection issues and the General Medical Council will assist. Cronyism works.
………and so now to round 4. Dr Myhill will not give up.
One of the first studies on the hypothesized attentional biases of pwCFS was by Rona Moss-Morris and Keith J. Petrie from the Department of Health Psychology, the University of Auckland, New Zealand (Moss-Morris & Petrie, 2003). They tested whether pwCFS have an “attentional information processing bias for illness-related information and a tendency to interpret ambiguous information in a somatic fashion”. Twenty-five CFS patients were compared to 24 healthy matched controls on a modified Stroop task and an ambiguous cues task in which they heard a tape-recorded list of 15 ambiguous illness words (e.g., vein/vain) and 15 unambiguous words. The participants were asked to write down the first word that came into their heads.
Moss-Morris and Petrie found no evidence for illness-related words creating greater attentional interference than neutral words on the Stroop task. However, on the ambiguous cues task, pwCFS made significantly more somatic interpretations than controls and this bias was associated with the extent to which they currently reported symptoms. Moss-Morris and Petrie concluded that :CFS patients have an interpretive bias for somatic information which may play a part in the maintenance of the disorder by heightening patients’ experience of physical symptoms and helping to maintain their negative illness schemas. Although patients did not show an attentional bias in this study, this may be related to the methodology employed” (p. 195). An interpretative bias is not an attentional bias, so this 2003 study produced a null result.
investigated whether pwCFS show attentional bias towards health- threat information. On this occasion, the sample consisted of 14 pwCFS and 18 healthy controls.Hou et al. used a visual probe task which presented health-threat and neutral words and pictures for 500 ms and self-report questionnaires to assess CFS symptoms, depression, anxiety, and social desirability. Compared to a control group, the CFS group showed an “enhanced attentional bias (AB) towards health-threat stimuli relative to neutral stimuli.” The finding of an enhanced AB towards health-threat information in pwCFS is claimed by the authors of being supportive of “models of CFS which underlie cognitive behavior therapy”. However, it would be a long and dangerous leap from this modest result of a difference between groups (which may have a vast number of interpretations) to any kind of inference of causality.
continued to investigate attentional bias towards health-threat stimuli with enlarged samples of 27 CFS patients and 35 healthy controls. The participants did a Visual Probe Task to measure attentional bias, and an Attention Network Test measuring executive attention, alerting and orienting. They also completed self-report measures of CFS and mood symptoms. Compared to the control group, the authors state that the “CFS group showed greater attentional bias for health-threat words than pictures; and the CFS group was significantly impaired in executive attention. Furthermore, CFS individuals with poor executive attention showed greater attentional bias to health-threat related words, compared not only to controls but also to CFS individuals with good executive attention” (p. 9).
systematically reviewed experimental studies of attention and interpretation bias towards negative and illness-related information in people with CFS and healthy controls to December 2014. The results were overall inconclusive: “Some people with CFS have biases in the way they attend to and interpret somatic information. Such cognitive processing biases may maintain illness beliefs and symptoms in people with CFS” (italics are mine). When the stated conclusion is identical to the starting hypothesis, as in this case, it is safe to assume there were no new findings. Their review highlighted methodological issues in experimental designs.
The Nijmegen connection
Jointly with two colleagues in Nijmegen, Stephanie Nikolaus and Hans Knoop, Hughes et al. (2018) replicated a UK study with a Dutch CFS population. The authors claim that in two cultures, “people with CFS demonstrate biases in how somatic information is attended to and interpreted”. What has not been shown in either culture, however, is that these biases cause or exacerbate ME/CFS symptoms which is a fundamental claim in the Wessely School theory of ‘boom and bust’ ME/CFS.
conducted a systematic review and suggested a general theory of what they term “functional cognitive disorder (FCD)” which is a disorder of cognitive dysfunction in the absence of an organic cause. They claim FCD is becoming increasingly prevalent and that the cognitive profiles in fibromyalgia (FM), chronic fatigue syndrome (CFS) and functional neurological disorders (FNDs) provide a ‘template’ for characterising their proposed new syndrome suggesting common underpinnings. They hypothesise that “pain, fatigue and excessive interoceptive monitoring produce a decrease in externally directed attention. This increases susceptibility to distraction and slows information processing, interfering with cognitive function, in particular multitasking. Routine cognitive processes are experienced as unduly effortful” (Teodoro, Edwards and Isaacs, 2018).
The results indicated that pwCFS do not show generalised abnormalities of attention or any general syndrome of a functional cognitive disorder. However, the review suggested to Teodoro et al. that some studies have shown that CFS patients may be prone to distraction in the Stroop task but this finding was not confirmed in all studies. Again, attentional bias to threat and towards emotionally negative information have been observed but unconfirmed. Owing to the very mixed bag of heterogeneous findings and “methodological shortcomings”, the authors were unable to make any general conclusions about the proposed new syndrome, or about CFS in particular.
To date, not a single published study confirms the hypothesis H3 that attentional bias causes or exacerbates symptoms of ME/CFS.
A mixed bag of heterogenous studies of mainly low quality containing multiple unresolved methodological issues. Two systematic reviews also yielded no definite conclusions about the association between attentional bias and ME/CFS.
As is the case for both H1 and H2, hypothesis H3, creates a chicken-egg problem: which comes first, attentional bias or the illness? Without controlled prospective studies, this question will remain unanswered, and the hypothesized causal link purely speculation.
This is the third hypothesis out of three in the Wessely School’s explanation of ME/CFS aetiology that receives no empirical support in the now extensive literature.
The theory, and its associated baggage of rag-tag treatments, should be abandoned.
Future posts will examine treatments recommended by the school, their effectiveness and safety.
In a series of posts I review the Wessely School’s influence on science, treatment and – most importantly – ME/CFS patient experience. In previous posts I outlined here the likely biological basis of ME/CFS and here treatment harms to patients. This post introduces the Wessely School’s approach to ME/CFS and medically unexplained symptoms.
What is ME/CFS?
Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating multisystemic disease of unknown aetiology, affecting thousands of individuals worldwide. The severity of symptoms can range from mild to severe with incidence peaks between age 10-19 years and 30-39 years. Women are more often affected than men in a 3:1 ratio. ME/CFS has been described as an “incurable, invisible contested and unsupported illness” (Farrell Delaney, 2020). The report by the Institute of Medicine (IOM) of the Academy of Sciences in the USA in 2015 concluded that ME/CFS is a physiological/medical, not a psychiatric illness (Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome, 2015; Clayton, 2015). The International Consensus Criteria (Carruthers et al., 2011), the Centers for Disease Control and Prevention (2018), the ICD-10, and the ICD-11 (World Health Organisation, 2018), all classify ME/CFS as a neurological disease.
In spite of evidence that the disease is associated with marked biological changes (Loebel et al., 2016, Schreiner et al., 2020; Sotzny et al., 2018; van Campen et al., 2020) and what appears to be a breakdown in homeostasis (Marks, 2021), the disease is often perceived by doctors and nurses as having a psychological or psychosomatic origin that is ‘all in the head’ (Åsbring & Närvänen, 2002; Dickson et al., 2007; Ware, 1992). This ‘all in the head’ perception causes stigmatization as an extra burden for patients with ME/CFS.
Paediatrician Ola Didrik Saugstad has stated: “A reorientation of the understanding and attitude to ME patients occurs worldwide. ME patients, especially the worse cases, suffer enormously. Among them, the paediatric patients are most vulnerable, representing a special challenge due to the occurrence in the midst of somatic growth and emotional development. We are waiting for a biomarker of this disease, and some are in the pipeline. And even more, we are hoping for an effective treatment. Still, it is already now time for the medical profession as well as the whole society to repent, as these patients have previously often not been treated with the respect and care they need and deserve” (Saugstad, 2020).
In addition to the stigma and stress burdens, the most used therapies for pwME/CFS based on the psychosocial model have caused significant harms to patients that are well documented in the literature.
Owing to the absence of an established biomarker, current diagnostic methods proceed by a process of eliminating other diseases with similar symptoms and there is no universally agreed or empirically derived definition of ME/CFS. The illness was first described in the mid-1980s when almost nothing was known about its underlying biology. Some clinicians explained to patients that “there is nothing wrong.”
Post-exertional malaise (PEM) is a cardinal symptom of ME/CFS reported by many, but not all, patients (Jason, Evans, So, Scott & Brown, 2015; VanNess, Snell & Stevens, 2007; McGregor, Armstrong, Lewis & Gooley, 2019).). In the International Classificatory System, PEM is a mandatory feature of the condition (Carruthers et al., 2003, 2011). Another commonly reported feature of the illness is its tendency to wax and wane (Friedman, Bateman, Bested, & Nahle, 2019; Morris, Anderson, Galecki, Berk & Maes, 2013; Morris & Maes, 2014). The onset and duration of ME/CFS have been debated with some researchers suggesting a sudden onset and others a gradual onset. An interview study revealed descriptions of ME/CFS onset experiences that were both varied and complex indicating that onset can be sudden or gradual in different cases (Evans & Jason, 2018).
For more than thirty years
a group of psychiatrists and psychologists at King’s College London and the Institute of Psychiatry together with a large group of collaborators has advanced a psychosomatic approach to ME/CFS. This group is given the sobriquet ‘Wessely School’ in honour of its leading representative, Professor Sir Simon Wessely. Simon Wessely has been the UK’s leading authority in establishing healthcare for patients with ME/CFS and MUS. According to the Wessely School, ME/CFS is neither a neurological nor an immunological condition but a psychosomatic condition, a functional illness with a primarily psychological origin. For the Wessely School, ME/CFS belongs in a spectrum of medically unexplained symptoms (MUS) including irritable bowel syndrome, non-ulcer dyspepsia, premenstrual syndrome, chronic pelvic pain, fibromyalgia, atypical or non-cardiac chest pain, hyperventilation syndrome, tension headache, atypical facial pain, globus syndrome and multiple chemical sensitivity (Wessely, Nimnuan & Sharpe, 1999). Early in the piece these authors opined that “the existing definitions of these syndromes in terms of specific symptoms is of limited value”.
The psychologists and psychiatrists within the Wessely School favour the
Cognitive Behaviour Therapy (CBT) Model
of emotional distress as proposed by Aaron T Beck (1976). The model distinguishes between developmental predispositions and precipitants of distress, and perpetuating cognitive, behavioural, affective and physiological factors, the so-called “three Ps”: predisposing, precipitating and perpetuating factors (Beck, 1976). This approach is not dissimilar to Hans Eysenck’s view that personality and feelings of hopelessness and helplessness are causal determinants of diseases such as cancer and coronary heart disease (Eysenck, 1991, Figure 1).
In line with Beck’s and Eysenck’s approach, the Wessely School has promoted what it has called a “broadly conceptualized cognitive behavioural model of MUS suggest(ing) a novel and plausible mechanism of symptom generation.” In a nutshell, fears and beliefs about the harmful effects of activity are related to poorer outcomes in ME/CFS (Deary, Chalder & Sharpe, 2007).
The school holds the hypothesis that the ‘three Ps’ inform behaviour such as activity avoidance and the belief that the illness has an organic basis, which, in turn, are said to affect the patient’s physiology and symptoms, providing a vicious circle of symptom maintenance irrespective of symptom type.
Some of the main influencers on the school have been Aaron T Beck, George Engel, Hans J Eysenck and Isaac M Marks. Eysenck’s theory assigns to cortisol and immune deficiency a mediating role between feelings of hopelessness and helplessness and development of the disease (see Figure 1).
Eysenck: Psychosocial -> Biological -> Disease
Figure 1. Hans Eysenck’s theory of personality and stress, dysfunctional feelings, as the causes of cancer. From Eysenck (1991).
Wessely’s theory attributes causal status to fear, behaviour and de-conditioning (Figure 2). Eysenck’s theory and Wessely’s theory share a strongly biopsychosocial orientation but with a difference in the sequence of the three key elements:
Wessely: Biological -> Psychosocial -> Disease
Figure 2. The Wessely School’s theory of the aetiology of CFS. From Harvey and Wessely, 2009.
Treatment of ME/CFS in the Wessely School’s approach focuses on the alleged ‘self-perpetuating cycle’ of inactivity that is assumed to disrupt the “self-maintaining interlock of cognitive, behavioural and physiological responses hypothesised to perpetuate the symptoms” (Deary et al. 2007, pp. 2-3; Harvey & Wessely, 2009; Figure 2).
The role of doctors in MUS is said to be similar to that of “parents of sick children. Both can reinforce unhelpful illness behaviour and symptom interpretations” (Deary et al., 2007, p. 7).
A group of investigators in Nijmegen, The Netherlands, holds a similar hypothesis that emphasizes the role of physical activity in attempting to correct the so-called ‘vicious circle’ of ME/CFS (Vercoulen et al., 1998; Wiborg, Knoop, Stulemeijer, Prins & Bleijenberg, 2010).
Influencers of the Wessely School
There have been several major influencers on the School including:
Hans J Eysenck: a leading theorist in personality theory and behaviour therapy. However, Eysenck’s publications on smoking, cancer and CHD were recently considered ‘unsafe’ in an enquiry within King’s College London.
Key members of an ‘inner circle’ are also shown in the illustration:
Trudie Chalder: Professor of Cognitive Behavioural Psychotherapy, King’s College London. Chalder has co-authored multiple publications on ME/CFS and MUS with Professor Wessely and she was one of the co-principal investigators of the PACE trial.
Peter D White: retired Professor of Psychological Medicine at Queen Mary University of London, United Kingdom, one of the co-principal investigators of the PACE trial.
Michael Sharpe: Professor of Psychological Medicine at the University of Oxford (previously at the University of Edinburgh) and one of the co-principal investigators of the PACE trial.
A larger ‘outer ring’ of collaborators work at King’s College London and at many other institutions all over the world.
The Wessely School’s Contribution
The Wessely School’s influence on the treatment of patients with ME/CFS has been huge. Some main influencers and contributors are listed in the table together with statements and publications reflecting the approach.
INFLUENCERS AND CONTRIBUTORS
PUBLICATIONS AND PERSONNEL
“People are not disturbed by things, but by the views they take of them”.
Thought control in everyday life. (1928). Funk & Wagnalls, New York.
Aaron T Beck
Depression: Causes and treatment. (1967). University of Pennsylvania Press, Philadelphia.
A cognitive approach to behaviour therapy. (1969). Internat. J Psychother, 8, 896-900.
Joseph Wolpe and Arnold Lazarus
Behavior therapy techniques: A guide to the treatment of neuroses. (1966).Pergamon Press.
Hans J Eysenck
Personality, cancer and cardiovascular disease: A causal analysis (1985). Personality and individual differences, 6(5), 535-556.
Isaac M Marks
Fears, phobias, and rituals: Panic, anxiety, and their disorders. (1987).Oxford University Press.
George L Engel
The need for a new medical model: A challenge for biomedicine (1977). Science, 196, 129–136.
Harold Leventhal, D. Meyer and D. Nerenz (1980).
The common-sense model of illness danger. In: Rachman, S., editors. Medical Psychology, Vol. 2. New York: Pergamon, pp. 7–30.
Core Team Members at King’s College London
T Chalder, J Chilcot, P McCrone, K Goldsmith, M. Hotopf, R Moss-Morris, J Weinman, S Wessely
M. Alyward (UnumProvident Centre, Cardiff), C. Bass (Oxford), G. Bleijenberg (Nijmegen), S. Borgo (Rome), K. Brurburg (Norwegian Institute of Public Health), C. Burton (Sheffield), D. L. Cox (Cumbria), E. Crawley (Bristol), V. Deary (Newcastle), L. Dennison (Southampton), R. Horne (UCL), A.L. Johnson (MRC Clinical Trials Unit, London), H. Knoop (Nijmegen), M. Loades (Bath), D.Oakley (UCL), K. Petrie (Auckland), M. Sharpe (Oxford), L. Sibelia (Rome), P. D. White (Queen Mary University of London)
In later posts I present the scientific evidence on the Wessely School’s approach to ME/CFS and MUS.