This is the reply Professor Wessely sent to me in response to my letter which can be found in part 2 here: https://livingwithchronicfatiguesyndrome.wordpress.com/2010/08/29/conversing-with-professor-simon-wessely-part-2/
Professor Wessely wrote:
“Just a couple of points
a) We describe our patient group very clearly. As you can see from the attached, and also the addendum we added to our XMRV paper, there is no doubt at all that our patients are severely affected – looked at the markers for disability, number working, number in patient group etc etc. I disagree that what we are seeing in our specialist clinic differs from those in the CCC author’s clinics. We are simply not going to agree on this I am afraid. I don’t regard them as a step forward, i don;t think they identify a homogenous group of patients, I don’t think they are evidence based, and I don’t think they can be operationalised to be used in either clinical or research practice. Where i agree with you is that people identified in epidemiological or primary care studies do indeed differ in many ways from those seen in specialist settings – and it is essential in any study to make it clear exactly where your subjects come from – without that it is impossible to generalise from any report/paper/treatment. This is not a new observation – you will see that we pointed that out in 1996, and have continued in all papers to make that distinction abundantly clear – and all our biological papers come from secondary /tertiary care. We have indeed found some abnormalities there – in neuro endocrine and immune function in particular, adn published those. Some of those in the list you give we haven’t replicated though, others have not be replicated by other groups. If you look at consistency, then the two main findings are an immune activation (the NK cell story doesn’t seem to have stood the test of time) and the low cortisol/HPA abnormalties, which definitely have stood the test of time.
b) We have studied also those too severely ill to attend clinic (about 5 % of our referrals are bed bound). We wrote up a case series of those treated in a non randomised fashion but using the same principles as CBT, and the results were good. All of them had to be admitted to hospital for several weeks/months though. We also have a new paper coming out, in which I am not an author, but describing a successful trial of therapy given at home on a domicillary visit basis by our team for a similar group. Again, results were pretty good.
c) It is of course perfectly true, as we say ourselves ad nauseam, that CBT provides good results for diseases such as MS, RA, cancer, heart failure, HIV and so on –all of these have been tested in RCTs and shown to improve outcomes. What CBT depends upon is that what starts this off , whatever it is, is not the same as what is contributing to long term disability/poor QOL. And in all these conditions we know that issues such as deconditioning, poor sleep, anxiety, demoralisation, depression and so on all play important roles, and all are potentially treatable/reversible. I outlined all that in the very first paper i wrote 21 years ago in which I first proposed that a cognitive behavioural model was a better explanatory model for chronic CFS than the chronic viral paradigm that dominated back then. in the intervening 21 years i have seen an awful lot of evidence that supports that model, and not much that doesn’t. Some doesn’t, true, but taken overall the model has performed rather well, and unlike other illness models for CFS, also gives a theoretical basis for treatment. CBT can no longer be considered experimental – i believe that at the moment every patient with CFS should be given the opportunity to have proper CBT given by accredited professionals in an NHS service if they so want. If they don;’t want, that ‘s fine. But it should be available in any clinic that purports to treat CFS.
d) My view on experimental drugs for CFS is that it is fine if they are experimental, which means given as part of a proper randomised placebo controlled trial in which the proper risk/benefit equation can be assessed. We have taken part in several such studies – sertarline, galanthamine and hydrocortisone. Only the last mentioned was successful, in which active treatment was better than placbebo, and unfortunately hydrocortisone is not a treatment that can be used for very long. Again, all these papers are freely available in the peer reviewed literature. We put all our papers on our website by the way – you can read them all there for nothing.
OK, i lied, it was more than a couple……
I still am concerned about your health, and repeat that i hope you have a good doctor whom you trust., hopefully your family doctor
My response to Professor Wessely’s letter can be found below. Note that I did not send this response to Professor Wessely.
“We describe our patient group very clearly. As you can see from the attached, and also the addendum we added to our XMRV paper, there is no doubt at all that our patients are severely affected – looked at the markers for disability, number working, number in patient group etc etc. I disagree that what we are seeing in our specialist clinic differs from those in the CCC author’s. We are simply not going to agree on this I am afraid.”
In my last reply I said “I agree that your CFS service DOES see many CCC patients.” Professor Wessely seems to have misread this statement by me and responded as if I said “doesn’t see” as opposed to “does see.”
He also uses the argument that his XMRV study used severely affected patients. This is true, in that his XMRV study did use severely affected patients. The patients did not however fulfill the CCC. Many patients with idiopathic fatigue can be classified as having severe fatigue so the cohort he used didn’t necessarily have any CCC patients in it, although it may have. The XMRV cohort selected by Professor Wessely is the most disabled cohort he has ever used in a study (based on my search through Pubmed.) It is conceivable that this is the only study in which he has ever used disabled patients. He does not provide any evidence for other disabled cohort studies he has performed. One would then assume that if Professor Wessely’s study with this disabled cohort yielded results that didn’t find abnormalities in CFS patients, then he may be correct in his conclusions about this study. One must therefore look at the results from his XMRV study and the methodology to form this conclusion.
Professor Wessely did not find XMRV in any of the CFS cohort. In the blog I wrote here: https://livingwithchronicfatiguesyndrome.wordpress.com/2010/06/30/xmrv-publications-by-fdanih-and-cdc-both-on-hold/ I detail the flawed methodology used in many XMRV studies and Professor Wessely’s study is no exception. Professor Wessely has therefore never (based on my research) performed a study that has BOTH a severely disabled cohort of CFS patients and a correct methodology. Both factors are needed if one is to obtain meaningful scientific results as opposed to pseudo-science results.
Jason et al. write “The validity (i.e.,usefulness) of a diagnostic category is inherently limited by its reliability. Therefore, to the extent to which a diagnostic category is unreliable, a limit is placed on its validity for any clinical research. (Spitzer et al., 1975).” This quote emphasizes that if diagnostic criteria is flawed, then the conclusion of the paper is equally flawed. In order to produce quality scientific papers, making an error in determining the appropriate study cohort is sufficient to create an invalid conclusion. It is therefore conceivable that Professor Wessely’s CFS paradigm (including all his studies) is flawed due to a non representative CFS cohort.
Professor Wessely can be accused of the fallacy of ‘cherry picking’ based on his above statements. The ‘cherry picking fallacy’ is defined as “the act of pointing at individual cases or data that seem to confirm a particular position, while ignoring a significant portion of related cases or data that may contradict that position.” Professor Wessely wrote “As you can see from the attached, and also the addendum we added to our XMRV paper, there is no doubt at all that our patients are severely affected – looked at the markers for disability, number working, number in patient group etc etc.” The large portion of Professor Wessely’s studies look at patients who are not severely affected. He has referred me to a study in which the cohort was severely affected. This cohort is not representative of other cohorts used by Professor Wessely. He has therefore (from the cherry-picking definition): “ignored a significant portion of related cases or data that may contradict that position.”
“I don’t regard them as a step forward, i don;t think they identify a homogenous group of patients, I don’t think they are evidence based, and I don’t think they can be operationalised to be used in either clinical or research practice. Where i agree with you is that people identified in epidemiological or primary care studies do indeed differ in many ways from those seen in specialist settings – and it is essential in any study to make it clear exactly where your subjects come from – without that it is impossible to generalise from any report/paper/treatment. This is not a new observation – you will see that we pointed that out in 1996, and have continued in all papers to make that distinction abundantly clear – and all our biological papers come from secondary /tertiary care.”
Professor Wessely seems to have reiterated his position from his last email and ignored the arguments I used against his disinclination towards the CCC. In my last email I wrote, “I agree that the CCC aren’t the ultimate and perfect guidelines to distinguish CFS subgroups. I however do believe that they are a stepping stone in the right direction. Very few guidelines covering any illness can distinguish different groups with 100% accuracy however this is not an argument against their use. I dispute your statement that virtually no clinician or researcher uses them. My research suggests that almost every endocrinologist, neurologist, infectious disease specialist, CFS specialist and rheumatologist commonly dealing with CFS patients in Australia (barring Professor Lloyd) uses the CCC. In my research, 14/15 of the CFS specialists in Australia use the CCC criteria. Regardless of the number of clinicians and researchers that use them, they have only been in existence for a handful of years and a true measure of the number of clinicians and researchers that use them cannot be accurately obtained as there use is still growing.
As I’m sure you are aware, the average person in the CDC research study can work for 48 hours a week. 84% of people within the studies didn’t know themselves that they had CFS. For an illness that is diagnosed based solely on symptoms, 84% of the study group not being aware of their illness is a stark contrast to CCC CFS patients who mostly are unable to work. Based on the CDC’s CFS classification criteria of determining CFS illness severity, I asked my healthy Dad the questions the CDC asks their study participants. He was classified as having “severe CFS.” Dr Oz asked his audience that was approximately indicative of the general population whether they were exhausted and 100% said they were. 30% said they were chronically exhausted. My point is that the CDC criteria are far too broad. If you ask a random person if they have these symptoms (which is what the CDC phone survey does to identify its CFS research group) putting the suggestion in their head may results in a skewed answer due to suddenly being conscious of the symptom. This is a suggestive bias and not a scientific method.
Using the sickest and most severely disabled of CFS patients with a large number of symptoms who present to a CFS specialist’s office would constitute a more statistically significant sample of CFS patients to determine etiologies. This is due to abnormalities showing up more vividly and to a higher degree in the sickest patients. The CDC’s use of an almost entirely pseudo-CFS patient subset is never going to yield significant results, even if an abnormality is found.
Your above quote seems to indicate that you have tried to do research with CCC CFS patients. I searched through Pubmed and found no studies of yours on CCC CFS patients. Please correct me if I have overlooked one of your studies here. As you have not used the CCC in a research setting, I find it difficult to believe that you would have found GET and CBT to help CCC patients.”
I made many arguments here that refute Professor Wessely’s position. His above quote essentially reiterates his conclusion that the CCC guidelines are not useful however his argument does not rely on facts, logic or empirical evidence. His argument relies on his own observations and non-empirical evidence as he writes “i don;t think they identify a homogenous group of patients, I don’t think they are evidence based, and I don’t think they can be operationalised to be used in either clinical or research practice.” His argument is only contingent upon his experience. It is possible to refute this argument by citing the numerous CFS specialists who created the CCC and their greater experience in terms of number of viewpoints and patients seen. By Professor Wessely’s own logic and appeal to non-empirical evidence and sheer experience regarding quantity of CFS patients seen to determine valid CFS criteria, he is supporting the CCC guidelines. This is due to the CCC creators having a more diversity of views, more patients and more experience collectively that Professor Wessely, all non-empirical factors that Professor Wessely values as ”evidence,” based on his above quote.
I concede that the CCC in their current format are not the ultimate CFS guidelines. Jason et al. in a recent journal article (found here http://www.scipub.org/fulltext/ajbb/ajbb62120-135.pdf) concluded that “If ME/CFS is to be diagnosed reliably across health care professionals, we believe that it is imperative to provide specific thresholds and scoring rules for the symptom criteria. Without such standardization, symptom variability will be a function of the assessment procedure and etiological factors. In other words, by determining specific thresholds and scoring rules for the symptom criteria, variability is likely to result in increased diagnostic reliability.” Jason et al. proposed an updated version of the CCC that can easily be used in a research and diagnostic environment. Jason et al. also evaluate different quantitative scales for the CCC and determined the most appropriate and objective diagnostic guidelines. Overall the Jason et al. article highlights how to overcome the CCC flaws in their current state. The Jason et al. article also improves the CCC so Professor Wessely’s criticisms are not longer valid of the CCC. Professor Wessely’s criticisms of the CCC were “i don;t think they identify a homogenous group of patients, I don’t think they are evidence based, and I don’t think they can be operationalised to be used in either clinical or research practice.” Jason et al. have modified the CCC so that Professor Wessely can no longer use these arguments as a criticism of the CCC. Thanks to Jason et al. the revised CCC are now “evidence based” and can be “operationalised” so they are ideal criteria to be used in “clinical or research practices.”
“We have indeed found some abnormalities there – in neuro endocrine and immune function in particular, adn published those. Some of those in the list you give we haven’t replicated though, others have not be replicated by other groups. If you look at consistency, then the two main findings are an immune activation (the NK cell story doesn’t seem to have stood the test of time) and the low cortisol/HPA abnormalties, which definitely have stood the test of time.”
Professor Wessely mentions that his research has found “neuro” and “immune” abnormalities in CFS patients. It is therefore questionable as to why he refutes the XMRV and neuro-immune hypothesis for CFS. XMRV is classified as a neuro-immune disease and this seems to fit in with his own published data. Either a subset of CFS patients have neuro-immune disease or they do not. Professor Wessely can’t have it both ways as this is an explicit contradiction. One way for Professor Wessely to solve this seeming contradiction is to claim that CFS patients have neuro-immune disease but not XMRV. Despite this suggested method to solve the contradiction, I have not found any of Professor Wessely’s writings (nor empirical evidence by Professor Wessely) that detail a psychosomatic mechanism to explain neuro-immune disease. Such a mechanism is required is one is to present a scientific paradigm.
On a related note to the above paragraph, Professor Wessely has publicly said “This research (XMRV) fails to model the role childhood abuse, psychological factors, and other infections may play in the illness.” These comments are a classic case of the fallacy of ‘Semmelweis reflex.’ This fallacy is defined as “The tendency to reject new evidence that contradicts an established paradigm.” Science works by new evidence replacing existing paradigms. When this new evidence is presented, it is a fallacy to reject it with the argument that it interferes with an existing paradigm. New evidence is rejected based on empirical research that fails to replicate or confirm the new evidence or when a mechanism explaining the results of the new evidence is uncovered. If all scientists used Professor Wessely’s logic from his above quote, then there would be no new scientific discoveries.
Professor Wessely mentions that his experiments have failed to replicate test abnormalities in CFS patients found by other research laboratories. Many of the test abnormalities HAVE been replicated by several laboratories. A thorough list of the test abnormalities consistently occurring in CFS patients is found here: http://www.name-us.org/MECFSExplainPages/TestAbnormalities.htm This list includes many laboratory studies that have replicated and confirmed CFS test abnormalities. If a research laboratory uses CCC CFS patients or a similarly affected cohort, they inevitably find consistent abnormalities in CFS patient’s tests. This means either:
a) The original lab and several other labs that have replicated the results have all made the same mistake in testing and Professor Wessely’s lab has some knowledge that these labs don’t have. This is unlikely due to several labs finding the same results providing more evidence than one lab finding different results. This point gathers evidence as many of the tests are quite basic tests and very hard to perform poorly. This leads to the conclusion that the greatest likelihood of a) is that Professor’s Wessely’s lab has performed the test in a flawed manner.
b) The cohort Professor Wessely has used is different to the cohort used by the several other studies. This fully explains the different test results. This scenario is more likely than scenario a) due to it not assuming that a laboratory (Professor Wessely’s) has performed a very basic test with a flawed method. Possibility b) gathers more credence when one analyses the different cohort and cohort selection that Professor Wessely has tested.
In the above quote, Professor Wessely mentions, “the NK cell story doesn’t seem to have stood the test of time.” As I have detailed above, the most likely scenario is that either Professor Wessely is either using a flawed methodology to test for NK function/numbers or is using a pseudo CFS cohort. Professor Wessely’s point that “the NK cell story doesn’t seem to have stood the test of time” is further questioned as a large proportion of CFS patients have abnormal NK cell function and number. These results have been obtained by hundreds (if not thousands) of laboratories worldwide. The testing has been performed not in a research study but requested individually by doctors. What does Professor Wessely recommend for those CFS patients like me with abnormal NK cell function/number? Do we have CFS at all or have a different illness as Professor Wessely didn’t find NK cell abnormalities in CFS patients.
- Professor Wessely co-authored a paper that reached the conclusion, “We have been unable to replicate previous findings of immune activation in CFS and unable to find any important associations between clinical status, treatment response, and immunological status.” (Clinical improvement in chronic fatigue syndrome is not associated with lymphocyte subsets of function or activation. Peakman et al. Clin Immunol Immunopathol 1997 Jan;82(1):83-91.)
- It is a fact that I have immune system abnormalities (3 different immune system abnormalities confirmed by multiple laboratories. The specific immune system abnormalities I have are the same immune system abnormalities that Professor Wessely’s study failed to find in CFS.)
- I have also been diagnosed as having CFS and only CFS by several specialists. I also fulfill the CDC and CCC CFS criteria.
The above three “facts” cannot all be true. To resolve this contradiction at least either 1. 2. or 3. is false. ‘2.’ is based on confirmed empirical evidence and is therefore the most likely to be true. The most likely false statements out of the three are either 1. or 3. as these rely on more subjective interpretations or definition issues. Using this deductive logic, it must be concluded that either CFS patients do have these specific immune system abnormalities or I do not have CFS.
Assuming Professor Wessely is correct in “We have been unable to replicate previous findings of immune activation in CFS and unable to find any important associations between clinical status, treatment response, and immunological status,” then I must not have CFS. I then pose the question to Professor Wessely- What illness do I have? Assuming that my several CFS specialists are correct in my diagnosis, the only consistency is that Professor Wessely’s statement ‘1’ is incorrect. Professor Wessely will cite studies he has performed that have supported his view. The validness of his studies is contingent upon the CFS definition and hence the cohort used. If Professor Wessely is correct in statement 1. then either a) I don’t have CFS or b) the CFS definition he used and subsequent cohort he used is too broad in terms of definition.
In conclusion, the onus of proof is now on Professor Wessely. For 1. 2. and 3. to be consistent, he must concede that either:
i. CFS patients do have these specific immune system abnormalities, contrary to Professor Wessely’s opinion.
ii. I do not have CFS and several CFS specialists have given me a false diagnosis.
iii. The cohort and CFS definition used by Professor Wessely in his immune system study is too broad and encompasses more than CFS patients.
“The NK cell story doesn’t seem to have stood the test of time.” A Fletcher et al. study concluded that, “A surprising amount of concurrence is found supporting the view that NK cell activity is depressed in CFS patients.” (Fletcher ML et al. Natural killer cell function in chronic fatigue syndrome. Clinical and Applied Immunology Reviews, June 2002 Vol. 2, Issue 3)
Caligiuri et al. concluded that “These studies demonstrated that a majority of patients with CFS have low numbers of NKH1+T3- lymphocytes, a population that represents the great majority of NK cells in normal individuals.” (Caligiuri M et al Phenotypic and functional deficiency of natural killer cells in patients with chronic fatigue syndrome. J Immunol. 1987;139:3306)
Another study found that “Cytotoxic function of NK cells for 176 CFS subjects was significantly lower than in the 230 controls. According to ROC analysis, NKCC was a good predictor of CFS status.” (Fletcher et al. Biomarkers in Chronic Fatigue Syndrome: Evaluation of Natural Killer Cell Function and Dipeptidyl Peptidase IV/CD26. PloS ONE, May 2010)
Gupta et al concluded that “Natural killer cells as defined by CD16, CD56 and CD57 antigens were significantly reduced in CFS….These data suggest immunological dysfunction in patients with chronic fatigue syndrome.” (Gupta et al. A comprehensive immunological analysis in chronic fatigue syndrome. Scand J Immunol. 1991)
Klimas et al wrote that “30 patients with clinically defined CFS were studied. All of the subjects were found to have multiple abnormalities in these markers. The most consistent immunological abnormality detected among these patients, when compared with normal controls, was low natural killer (NK) cell cytotoxicity.” Klimas NG et al Immunologic abnormalities in chronic fatigue syndrome. J C/in Microbiol. 1990;28:1403-l0.
Patarca-Montero et al have written a summary of the immune system related literature of CFS. They write, “A review of the literature on the immunology of CFS reveals that people who have Chronic Fatigue Syndrome (CFS) have problems with immune function that have been documented by most research groups….(these include) poor cellular function, with low natural killer cell cytotoxicity (NKCC.)” (Paarca-Montero et al. Immunotherapy of Chronic Fatigue Syndrome: Therapeutic Interventions Aimed at Modulating the Thl/Th2 Cytokine Expression Balance, . J Chronic Fatigue Syndr 2001;8:3–37.)
This published data suggests that the “NK cell story” has stood the test of time, contrary to Professor Wessely’s opinion. Professor Wessely has dismissed all of the above study results without providing a mechanism as to why the results are flawed. I concede that some studies have failed to recognize an abnormal NK cell function among what they label as “CFS patients.” These studies have used a flawed CFS cohort consisting of idiopathic CFS patients. To explain the contradictory results, I am proposing the mechanism that the variable of CFS cohort used influences the results. Professor Wessely’s model has oversimplified CFS into a homogenous disorder and consequentially he has dismissed a number of studies without a mechanism as to why they are “erroneous.” In order for Professor Wessely’s psychosomatic model to be a superior explanation for CFS, he must provide a mechanism explaining these “flawed” abnormal NK cell function results in CFS patients. Until he provides this mechanism, his model dismisses empirical evidence, the underlying principle of the scientific method.
Whiteside et al. provide a discussion on the mechanisms for why they believe some groups have failed to find abnormal NK cell results in a “CFS” cohort. Whiteside et al. write that “The heterogeneity of CFS, the variable quality of immunologic assays and their performance, along with an almost complete absence of longitudinal studies of cellular immune abnormalities in CFS may explain this (why some groups have failed to reproduce abnormal NK cell results in CFS patients.)” (Whiteside TL, Friberg D. Natural killer cells and natural killer cell activity in chronic fatigue syndrome. AmJMed. 1998;105(3A) :27S-34S.) This journal article supports the evidence that I have written regarding a mechanism for the differing NK cell results in CFS studies.
Professor Wessely’s studies have not tested for NK cell cytotoxicity, which is the immune system abnormality I have argued above is present in CFS patients.
The selection criteria for Professor Wessely’s ‘immune system-CFS’ study was that “All fulfilled the Oxford criteria for CFS (10). Nonmelan-cholic depression (22%) and anxiety disorders (10%) were not exclusion criteria.” (Clinical improvement in chronic fatigue syndrome is not associated with lymphocyte subsets of function or activation, Peakman et al. Clin Immunol Immunopathol. 1997 Jan;82(1):83-91)
Carruthers et al. have written that “The Oxford (Sharpe) definition is only used by a small group of English psychiatrists (the Wessely-school) and by the university of Nijmegen, Netherlands (Van der Meer et al.)
Patients who fulfill the Oxford criteria are classified in the “International Classification of Diseases” (ICD) of the World Health Organisation (WHO) as “ICD10: 48.0” as “Mental and Behavioural Disorders”; subtitled “Other Neurotic Disorders”
All countries who are members of the WHO have to follow the rules of the WHO, included the ICD code. So the use of these Oxford criteria for selecting ME/CFS patients is a gross violation to the “International Classification of Diseases” (ICD) of the World Health Organization (WHO), and therefore at the same time a serious case of discrimination.” Carruthers et al. Jounrnal of Chronic Fatigue Syndrome.
Research has shown that approximately 10% of those fulfilling the Oxford Criteria may have CFS. Not only did this study by Professor Wessely not test for NK cell cytoxicity but the cohort used included (by Professor Wessely’s own admission,) 22% with major clinical depression and 10% with anxiety disorders. To make this cohort even more nebulous, the Oxford Criteria were used which research has shown only includes 10% of CFS patients. For Professor Wessely’s immunological study to be valid, the correct tests would have needed to have been conducted and a true, representative CFS cohort would have needed to be used. Professor Wessely’s study failed to satisfy either of these conditions hence this is the mechanism why his study didn’t support the “NK cell story.”
The abnormal NK cell function results in CFS patients are sufficient in themselves to falsify Professor Wessely’s psychosomatic model of CFS. The burden of proof is now squarely on Professor Wessely to provide a verifiable empirical mechanism to explain how “negative illness thoughts” can produce a NK cell function of practically zero. Natural Killer cells are defined as “White blood cells which acts as the immune system’s first line of defense against foreign invaders like tumors, bacteria, and viruses.” This suggests that rather than employing a psychosomatic theory of CFS, the reason the NK cell function is so consistently severely depleted in CFS patients is due to the immune system’s failure against the “first line of defense against foreign invaders like tumors, bacteria, and viruses.”
“It is of course perfectly true, as we say ourselves ad nauseam, that CBT provides good results for diseases such as MS, RA, cancer, heart failure, HIV and so on –all of these have been tested in RCTs and shown to improve outcomes.”
In the letter I wrote to Professor Wessely (to which he is responding,) I wrote “Firstly you seem to continually mention psychological factors and the role that psychological factors play in CFS. I ask whether all other illnesses also have a psychological factor, such as HIV and cancer? Does the role that psychological factors play in CFS differ from the role they play in Aids and cancer?”
Professor Wessely’s response, above, does not answer my question. I asked whether “the role that psychological factors play in CFS different from the role they play in Aids and cancer?” In his answer, he has written that illnesses other than CFS result in an improved outcome to CBT. He does not detail if “psychological factors” play a different role. He also fails to answer whether it plays a ‘different role” but only says that it plays “a role.”
Professor Wessely helps justify CBT on CFS patients by stipulating that he doesn’t solely recommend CBT for CFS patients but also for patients with “MS, RA, cancer, heart failure and HIV.” There is a key difference between recommending CBT for these other illnesses and recommended it for CFS. This difference is that CBT is not the primary treatment for these other illnesses. These other illnesses all have approved medications to aid in the patient’s betterment. If CBT was recommended by Professor Wessely as a primary treatment for cancer, HIV, heart failure and the other illnesses he mentions, those patients would not be very satisfied with his recommendation. If Professor Wessely was a world leading researcher on cancer, HIV and heart failure and had considerable influence (like he does with CFS), then performing an umpteenth study on CBT for these illnesses would not be beneficial. This is what is happening in regards to CFS research- superfluous studies on CBT and CFS rather than studies focusing on potential primary treatments. It can also be argued that CBT is not a treatment at all but rather a coping strategy designed to help patients mentally through a chronic organic illness.
“What CBT depends upon is that what starts this off , whatever it is, is not the same as what is contributing to long term disability/poor QOL. And in all these conditions we know that issues such as deconditioning, poor sleep, anxiety, demoralisation, depression and so on all play important roles.” Before I contracted CFS I was not “deconditioned” as I had been a middle and long distance runner. In fact after having CFS for 2 years I was still not “deconditioned” and although my VO2 max had decreased and my resting heart rate had increased, I was still about average based on the general population for these 2 numbers. I never had “poor sleep” before becoming ill and slept every night for 9 hours uninterrupted. I was not “anxious,” “demoralised” or “depressed” before becoming ill. It took several years for mild anxiety to set in and I am still not demoralised or depressed. I therefore question the use of CBT for me. Professor Wessely writes “What CBT depends upon is that what starts this off.” As what “started CFS off” for me didn’t involve any of the factors that Professor Wessely refers to, I don’t believe he can justify recommending CBT to me.
“I outlined all that in the very first paper i wrote 21 years ago in which I first proposed that a cognitive behavioural model was a better explanatory model for chronic CFS than the chronic viral paradigm that dominated back then. in the intervening 21 years i have seen an awful lot of evidence that supports that model, and not much that doesn’t. Some doesn’t, true, but taken overall the model has performed rather well, and unlike other illness models for CFS, also gives a theoretical basis for treatment. CBT can no longer be considered experimental – i believe that at the moment every patient with CFS should be given the opportunity to have proper CBT given by accredited professionals in an NHS service if they so want. If they don;’t want, that ‘s fine. But it should be available in any clinic that purports to treat CFS.”
The evidence that supports Professor Wessely’s CFS model is based almost entirely on his own studies. If one examines a study performed by Professor Wessely, the ‘referenced studies’ written below the actual study are largely comprised of studies by Professor Wessely himself. When one mainly references one’s own studies, questions need to start being asked as to why the rest of the scientific communities work is not being referenced. Also the question must be asked as to why Professor Wessely’s work is largely in contradiction to many different scientists’ work on CFS. I agree that “(CBT) should be available in any clinic that purports to treat CFS,” although only the “CFS” that Professor Wessely studies and not CCC CFS. In the future I plan to write a blog entry examining the usefulness of CBT in CCC CFS. Although I am being a scapegoat and not examining CBT extensively now, I will do so in the future (in detail) and examine the usefulness of it in treating CFS.
In a future blog I will cover CBT for CFS more extensively however I will now briefly analyze the use of CBT for CFS. Professor Friedberg from the Department of Psychiatry at the State University of New York has stated that “Several studies of graded activity-oriented cognitive behavioural treatment for (ME) CFS, all conducted in England, have reported dramatic improvements in functioning and substantial reductions in symptomatology. On the other hand, cognitive behavioural interventions conducted in Australia and the United States have not found significant improvements in functioning or (ME) CFS symptoms. Furthermore, descriptive studies of CF (chronic fatigue) patients in England, the US and Australia suggest that the (ME) CFS population studied in England shows substantial similarities to depression, somatization or phobia patients, while the US and Australian research samples have been clearly distinguished from primary depression patients and more closely resemble fatiguing neurological illnesses.”
A review of CBT by Twisk et al. found that “Benign Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) is a debilitating disease which, despite numerous biological abnormalities has remained highly controversial.
Notwithstanding the medical pathogenesis of ME/CFS, the (bio)psychosocial model is adopted by many governmental organizations and medical professionals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS.
Justified by this model CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively.
In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust. CBT/ GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration.
Moreover, this review shows that exertion and thus GET most likely have a negative impact on many ME/CFS patients.
Exertion induces post-exertional malaise with a decreased physical performance/ aerobic capacity, increased muscoskeletal pain, neurocognitive impairment, “fatigue”, and weakness, and a long lasting “recovery” time.
This can be explained by findings that exertion may amplify pre-existing pathophysiological abnormalities underpinning ME/CFS, such as inflammation, immune dysfunction, oxidative and nitrosative stress, channelopathy, defective stress response mechanisms and a hypoactive hypothalamic-pituitary-adrenal axis.
We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful “rehabilitation therapies”, such as CBT/GET.” (A review on cognitive behavorial therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME) / chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS. Twisk et al Neuro Endocrinol Lett. 2009;30(3):284-99.)
The Cochrane Review listed 13 clinical trials of CBT on a total of 1371 CFS patients and concluded that it “Did not regard CBT or other behavioural therapies as curative or directed at the underlying disease process.” The Cochrane Review even focused primarily on idiopathic fatigue cohorts and still came to this conclusion that CBT doesn’t affect the “underlying disease process” of CFS. CBT is at best an experimental treatment for a subset of idiopathic CFS patients and more realistically for CCC CFS patients an experimental treatment that may help with the coping side of the chronic organic illness CFS but not relevant to the underlying illness that is CFS.
Professor Wessely’s argument was that “CBT can no longer be considered experimental… But it should be available in any clinic that purports to treat CFS.” From the peer reviewed studies on CFS and CBT (even encompassing Professor Wessely’s own studies) the evidence does not support CBT as a primary treatment for CFS. It is therefore erroneous to dismiss all of this evidence, as Professor Wessely has done and claim that “CBT can no longer be considered experiemental.”
One manner to explain the discrepancy in published results regarding CFS and CBT is to focus on the one variable- the CFS definition used in the studies. CFS is a heterogeneous illness comprising several distinct and unrelated illness subgroups with differing etiologies. The CBT studies performed on “CFS” patients with idiopathic fatigue inevitably show CBT to be marginally beneficial to this cohort compared to placebo. The CBT studies that use a more stringently and quantitatively symptomatic CFS selection criteria result in no improvement in the patient’s CFS and in some cases a worsening of CFS symptoms.
“Overall the model has performed rather well, and unlike other illness models for CFS, also gives a theoretical basis for treatment.” This is hardly an argument for employing a scientific model, in that it gives a theoretical basis for treatment. It one makes illness models based on them having a theoretical basis for treatment, science is ignored. An example of an analogy of Professor Wessely’s argument is: Salt deficiency is a theoretical basis for treatment as one can counter it with giving the individual salt. Cancer can therefore be treated by this “theoretical basis for treatment.” Therefore the salt deficiency model for cancer is preferable. This is analogous to Professor Wessely’s argument that explains why his model for CFS is preferable to another model. Professor Wessely also seems to be oversimplifying things here and assuming that CFS has a single etiology when studies and empirical evidence have detailed multiple causes and independent illnesses lumped together under the “CFS” umbrella.
“– i believe that at the moment every patient with CFS should be given the opportunity to have proper CBT given by accredited professionals in an NHS service if they so want.” Professor Wessely comments can again be accused of oversimplifying things. Many peer reviewed research papers and anecdotal reports have found that CFS patients respond differently to treatments. Some have symptoms improve or go into remission based on treating mitochondrial abnormalities, thyroid problems, adrenal problems, taking antivirals, antibiotics and an abundance of various other medications and treatments. Other CFS patients may have their condition remain constant or deteriorate when trying these treatments. This suggests multiple etiologies to CFS. Professor Wessely’s comments implying a one-size fits all treatment regarding CBT is based on lumping all CFS cases together. This is oversimplifying CFS. Multiple CFS etiologies mean different treatments will work for different people, which is what the empirical evidence in the medical literature suggests. Completely independent illnesses being treated by the single method of CBT due to sharing an arbitrary symptom in fatigue is analogous to saying all diseases that have a sore throat as an arbitrary symptom should be treated the same way. This of course would mean whether one has tonsillitis, a common cold, EBV, streptococcus or diphtheria is irrelevant as a single treatment covers all these illnesses. This is the logic Professor Wessely is using.
“I outlined all that in the very first paper i wrote 21 years ago in which I first proposed that a cognitive behavioural model was a better explanatory model for chronic CFS than the chronic viral paradigm that dominated back then. in the intervening 21 years i have seen an awful lot of evidence that supports that model, and not much that doesn’t. Some doesn’t, true, but taken overall the model has performed rather well.” This quote by Professor Wessely is also flawed for the reason that he uses the fallacy of ‘Expectation bias.’ This fallacy is defined as “The tendency for experimenters to believe, certify, and publish data that agree with their expectations for the outcome of an experiment, and to disbelieve, discard, or downgrade the corresponding weightings for data that appear to conflict with those expectations.” Only a handful of papers from CFS researchers other than Professor Wessely have supported his CFS model. These papers almost exclusively use the flawed CDC CFS definition. I demonstrated why the CDC definition was flawed in my first email to Professor Wessely.
Professor Wessely claims that there is “an awful lot of evidence that supports that model, and not much that doesn’t.” Most CFS researchers have a diametrically opposed viewpoint regarding which model the CFS published date supports. There are over 2500 published journal articles that support a physiological CFS etiology. This is in comparison to the handful of papers that Professor Wessely and associates have published supporting a psychosomatic CFS origin. Professor Wessely’s said that there is “an awful lot of evidence that supports that model, and not much that doesn’t.” Based on the published studies, there is an awful lot of evidence (over 2500 studies) that support CFS being purely organic and not much that doesn’t. The handful of studies that don’t support CFS being purely organic inevitably have dubious cohorts. These cohorts contain a too broad definition of CFS that encompasses depression, idiopathic fatigue and obesity. This is a mechanism to explain the discrepancy in results. The large majority of CFS researchers contrast Professor Wessely’s position and believe the published research supports a purely organic model of CFS.
Professor Wessely has failed to provide a mechanism which adequately explains the 2500 plus peer reviewed scientific papers that support an organic model for CFS. For his CFS model to supersede the physiological CFS model, he must either modify his model to adopt these scientific papers or provide a sufficient explanation as to why 2500 plus scientific papers are flawed. He has not provided a satisfactory mechanism to date explaining this discrepancy in results. I have provided a mechanism for why there are a handful of papers that support the psychosomatic model of CFS- It is an idiopathic form of “CFS” that is a distinct illness from CCC CFS which has a solely organic origin.
I mentioned some of these research studies in my last letter to Professor Wessely. I wrote that these include; Immune system abnormalities, abnormal oxidative stress levels, abnormal SPECT scans, abnormal MRI scans, virtually zero natural killer cell numbers and functioning, low hormone levels, low blood cell volume, low cardiac index, high levels of inflammatory markers, gene expression abnormalities, severely impaired mitochondrial function, dysfunction of the HPA axis, increased titre levels to various viruses such as HHV6, EBV, parvovirus, enterovirus etc , abnormal Rnase L pathway and severely abnormal response to exercise based on cytokine levels as detailed in the Light study. These are just the abnormal study results that I remembered off the top of my head. There are many more published studies indicating severe physical abnormalities in the majority of CFS patients.
There is one method to combine Professor Wessely’s research and the abundance of ‘purely organic CFS’ research. This involves assuming CFS subgroups. One subgroup (a completely different illness) may have idiopathic fatigue, this is what Professor Wessely studies. His recommendations of GET and CBT may apply to this subgroup. CCC CFS does not fall into this subgroup and is a distinctively different subgroup and illness. Professor Wessely is not an authority on the devastating and severely debilitating illness that is CCC CFS.
“ My view on experimental drugs for CFS is that it is fine if they are experimental, which means given as part of a proper randomised placebo controlled trial in which the proper risk/benefit equation can be assessed. We have taken part in several such studies – sertarline, galanthamine and hydrocortisone. Only the last mentioned was successful, in which active treatment was better than placbebo, and unfortunately hydrocortisone is not a treatment that can be used for very long. Again, all these papers are freely available in the peer reviewed literature. We put all our papers on our website by the way – you can read them all there for nothing.”
The above quote by Professor Wessely was in response to my comment in a previous email that said, “When I asked a specialist for a specific drug for my CFS that has had excellent results in studies with virtually no side effects, I was refused it. He thought it would help with my condition however it was considered “experimental.” He was worried that insurance companies would use him prescribing an experimental drug against him and his CFS patients would therefore no longer be able to go to him to claim a disability support signature. These insurance companies continually cite your words and research to question the validity of CFS.”
My comment was in response to Professor Wessely’s comment that “Anyway, one last thing., I am afraid that i am no longer involved in the politics of CFS research, and haven’t been for many years. I no longer sit on any committees /workshops/conference etc about definitions, grants, research etc etc.
So my ability to influence the areas that you wish influenced are practically zero”
It is evident from the above back and forth conversing that I was responding to the topic of Professor Wessely claiming he has practically no political influence on CFS anymore. Professor Wessely has then gone off on a tangent after seeing my mention of the words “experimental drug.” Rather than staying on topic and answering my argument about still having a political influence on CFS, he has changed the subject of the discussion to a topic that is largely irrelevant to the argument. In logic there is a fallacy called “red herring.” This is defined as occurring when “a speaker attempts to distract an audience by deviating from the topic at hand by introducing a separate argument which the speaker believes will be easier to speak to.” Professor Wessely has used this fallacy and changed the topic from his political influence to “experimental drugs.”
I have now analysed every argument Professor Wessely has presented to me and every counter argument of Professor Wessely’s. Professor Wessely has cherry picked peripheral points that I mentioned in my letter to him and argued his position on these largely irrelevant points. As I have detailed above, his arguments are full of fallacies, inconsistencies, contradictions and largely a disregard for the scientific method. I believe I have successfully nullified all of Professor Wessely’s arguments, sometimes using multiple methods.
What is most striking in Professor Wessely’s letter is not what he has written but rather what he hasn’t written. In the previous letter I sent to Professor Wessely, I detailed over 20 independent arguments, each one singularly sufficient to falsify his CFS paradigm. Professor Wessely did not even attempt to argue back to a single one of these arguments.
Professor Wessely has argued irrelevant points that are peripheral to the topic at hand. I have demonstrated that even these arguments are flawed. His avoidance in responding or addressing my arguments further incriminates his CFS model. I therefore conclude that Professor Wessely’s CFS psychosomatic viewpoint is erroneous, unscientific and of no use to CFS patients suffering from CCC.
This is the final part (part 3) of my ‘Conversing with Professor Simon Wessely.’