This is the reply Professor Wessely sent to me in response to my letter which can be found in Part 1 here: https://livingwithchronicfatiguesyndrome.wordpress.com/2010/08/29/conversing-with-professor-simon-wessely-part-1/
Professor Wessely wrote:
“Thank you for your message
I am sorry to hear of your illness – I must that if you were one of our patients we would be concerned about you. I am assuming, I am not quite sure why, that you are not in the UK though
I am reasonably familiar with the matters that you describe, even if I do not see it in the terms that you do. Over the many years that I have been seeing patients, more than 20 years I am afraid to say even if I don;t as yet identify myself with the elderly scientist that you describe, we have not found the divisions of CFS into some of the categories that are proposed by the Canadian criteria to be helpful. In other words they do not seem to create a homogenous group of patients, and nor can they be usefully applied in clinical practice. That is the reason why virtually no clinician nor researcher actually uses them – they were not derived in a way that can be reproduced. Nor do I believe that they cleave nature at the joints, nor do they create a neat dichotomy as some suggestion between “neurological” CFS and “psychiatric” CFS, as some say, which is sadly sometimes also used interchangeably with “real” and “unreal” CFS. Whatever else we know, we know that the world does not divide so easily. Instead it is more helpful to think about mild moderate and severe, and i am afraid i can assure that over the years, as is clear from our publications, we have seen more than our fair share of severe cases. I simply do not accept that those who put together the Canadian definition had seen and see a different type of patient to those that we someone mysteriously overlook. Not so. Our service is a specialist secondary and tertiary care service with a contract covering SE London – unless you are rich and can afford to go to Harley st, then if you live in our catchment area sooner or later it is likely that you will come to our service at some stage.
Second, we also know that as you up the scale to increasing levels of disability, it is not that the neurological wheat can then be separated from the psychiatric chaff – if anything it is, as we showed many year ago in work that has been replicating, the other way round. It is the same in most illness/disease by the way – the greater the severity/disability/symptoms, the closer, not more remote, the association. We live now in an era where separating brain and mind makes progressively less and less, not more and more, sense.
What we can say at the moment, and i mean at the moment, is that whilst we do not know what causes CFS, irrespective of which definition you use, we have made a little more progresss in understanding the nature of disability, and hence how to improve outcomes. Having seen over 3000 patients now in my career, i can say that i remain very content and indeed proud of the contribution i and my many colleagues have made in improving the management of this condition, and improving outcomes/quality of life. That is not to say that this is how it will remain – i fervently hope it won’t, and i expect that developments in neuroscience over the next couple of decades will improve the understanding of many neuro/psychiatric illnesses, not just CFS. And that will eventually be reflected in new treatments as well,
But does that mean that the work we have done for the past 20 years has been worthless? Not a bit of it. At the time of writing I can say with my hand on heart that i believe that the treatments that we recommend and use in our clinic are currently the best there is – and nothing that i have seen, or read about, suggests otherwise. As i say, and as i say to every patient that i meet, its not perfect, certainly not, and it will be improved, but for the moment my honest advice is that this is the best option for you. If it was me, this is what i would do.
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. I do still do my one day a week seeing patients in the clinic, which i still really enjoy, otherwise i wouldn;t do it, but have had little or no dealings with the politics of all this for ages and ages. I have handed over the research unit to someone else, and my involvement in research is largely either helping to recruit patients for other peoples’ research studies, or giving advice to Ph d students/supervising juniors. My active research has been for many years with the military, and anyway, for most of the day I am now a faceless university bureaucrat. So my ability to influence the areas that you wish influenced are practically zero – you may perhaps be relieved to hear that.
Once again, i have to say some of your letter alarmed me. I hope that you still have faith in the medical profession, and that you are in close touch with your family doctor.
I emailed Professor Wessely a response to this letter and it appears below:
Dear Professor Wessely,
“In other words they do not seem to create a homogenous group of patients, and nor can they be usefully applied in clinical practice. That is the reason why virtually no clinician nor researcher actually uses them (the CCC) – they were not derived in a way that can be reproduced.”
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.
“Instead it is more helpful to think about mild moderate and severe, and i am afraid i can assure that over the years, as is clear from our publications, we have seen more than our fair share of severe cases”
Using mild, moderate and severe as what traces the line distinguishing types of CFS is also problematic. As I’m sure you are aware, many CFS patients will fit into all of these categories, as their CFS progresses. To diagnose a patient with a degree of CFS is also fraught with the lack of objectivity factor unless using a scale such as Dr Bell’s disability scale. Other illnesses do not use this severity system to distinguish patients, as all illnesses have a severity range within subgroups.
“I simply do not accept that those who put together the Canadian definition had seen and see a different type of patient to those that we someone mysteriously overlook. Not so. Our service is a specialist secondary and tertiary care service with a contract covering SE London – unless you are rich and can afford to go to Harley st, then if you live in our catchment area sooner or later it is likely that you will come to our service at some stage.”
I agree that your CFS service does see many CCC patients. My central argument was the number of practicing physicians that composed the CCC would have also seen a huge amount of CFS patients through many different locations. This gives a greater cross section of CFS patients, more locations, more specialist’s opinions and therefore as a study a higher probability of more accurate results. These many physicians independently came to the conclusion determining the dichotomy of CFS patients. They distinguished them between the CDC criteria subgroup and the CCC subgroup. The level of independent agreement in adopting these recent CCC guidelines seems to be a strong argument. From a somewhat independent viewpoint, this seems like a compelling fact in favour of adopting the CCC.
“We live now in an era where separating brain and mind makes progressively less and less, not more and more, sense.”
I fail to see how this argument relates to CFS. It is a fallacy to apply a general statement concerning a specific era’s paradigm onto a specific illness without evidence. I do not doubt that other illnesses may be seeing brain and mind converge however it is a large unjustified step to apply this to CFS without specific evidence.
“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”
I thank you for the efforts you have made towards gathering more funding for CFS research in the past. I can only speak of Australia so this may not be extrapolated worldwide however your CFS views and research still carries significant weight here. I have seen 12 non-specialising in CFS GPs and 8 of them have suggested that I undertake CBT and GET for my CFS. They cite your research and articles you have written or had influence in.
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.
The view of CFS by the public in Australia is varied, however many people don’t view it as a legitimate illness. This is devastating for someone like me who is suffering from a very severe case of it that is ruining my life. Although you may be quoted out of context, many of the things you have said about CFS are quoted in the media and come up on internet searches that perpetuate the psychosomatic myth regarding CFS.
The media in the UK always go to you for comments on any new CFS story hence you still hold an enormous influence. I would argue that although you are not currently involved in the politics of CFS, your past comments and media comments still inextricably tangle you up within the CFS political world. If someone asked me to choose the most influential CFS figure worldwide currently, I would name you.
I am very wary of using the “straw man argument” to present your position as many people have done this in the past. I apologise if this is not your current view on CFS. I have not found a clear primary source account documenting your view. Despite this, I consider the general gist of your view to be (please correct me if I’m misrepresenting your view):
“You believe CFS has an organic root cause e.g. a virus however psychological factors continue the illness.”
I question this view for many reasons (again I apologise if this is not your view and I have misrepresented your position.)
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? I assume that your view is that psychological factors are important in all illnesses, however in CFS psychological factors are more important as treating them can cause remission. This is different to other illnesses in the sense that treating the psychological factors won’t cause remission in cancer and Aids. I apologise if this is not your position.
As I’m sure you are aware “Occam’s razor” suggests that “entities must not be multiplied beyond necessity in an explanation.” Your view that a viral cause triggers CFS is sufficient to explain CFS, without adding your view that psychological factors perpetuate the CFS. According to Occam’s razor, adding psychological factors to your mechanism for CFS is superfluous. Occam’s razor can be disregarded when empirical evidence supporting superfluous entities is provided however this empirical evidence hasn’t been presented on CFS. As I am sure you will agree, little is still known regarding CFS. In your email you detailed, “Whilst we do not know what causes CFS…..I expect that developments in neuroscience over the next couple of decades will improve the understanding of many neuro/psychiatric illnesses, not just CFS.” In the extenuating circumstances that Occam’s razor is disregarded, empirical evidence is provided and the subject of Occam’s razor is nearly fully understood. As your quote demonstrates, CFS is not nearly understood and hence applying Occam’s razor in this instance is justified.
When outbreaks of CFS occur, I’m sure that you would agree that an approximately homogonous group, representative of the population is affected. This group is homogonously representative in all factors including psychological state. I therefore conclude that this alone proves that psychological factors aren’t prevalent in CFS.
When the extensive physiological research on CFS is taken into account, the need to add “psychological factors” to a CFS theory becomes redundant. The physiological factors alone explain the range of symptoms and various biomarkers that when monitored correlate to remission. CFS patients have some of the most diverse and large number of abnormal test results of patient’s of any illness. These abnormal test results 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 of various viruses such as HHV6, EBV, parvovirus, enterovirus etc
Abnormal Rnase L pathway
Severely abnormal response to exercise based on cytokine levels as detailed in the Light study.
Many more abnormal test levels (these are just the few I remember off the top of my head.) I am sure you are aware of the full list of abnormal test results found in the majority of CCC CFS patients.
Your mind-body model of CFS remind me very much of the mind-body problem regarding dualism in philosophy. The question is where does one system relate to the other system? Where does one system end and the other begin? If a virus is sufficient to trigger the CFS and continue it for a period of time, when does the virus stop having an effect and the psychological factors “kick- in?” This transition model seems superfluous- to have the same symptoms and abnormal test results from two separate causes- One organic due to a virus and the other psychological. It is much clearer if the virus cause is a sole cause.
Another query of mine involves why different treatments work for different people. At some time or another almost all CFS patients have been promised a cure that works, believed that the cure would work and then been disappointed. This nullifies the placebo effect. Patients’ have gone into remission by treating thyroid abnormalities, adrenal abnormalities, mitochondria abnormalities, hormone abnormalities, viral abnormalities, bacterial abnormalities and various other abnormalities. This suggests a purely organic etiology for CFS without psychological factors.
As research and science develops, what in the past has been referred to as being “in the mind” has often been found to be purely organic in nature. It is the natural evolution of science to dispel things it currently doesn’t have a perfect mechanism for, as “not real.” Many other illnesses have been thought of as purely psychological such as MS and stomach ulcers until eventual evidence has forced a paradigm shift. The way science has evolved suggests the same will be said of CCC CFS, as MS highly resembles CCC CFS. The over 50 well documented separate cases of CFS spreading rapidly among an autonomous population also support the case for it not being psychological in any sense. An infectious etiology is well supported based on these outbreaks. On a personal level, my family has 6 other members on one side with CCC CFS (not all blood related, however all either related through potential vertical or horizontal transmission.) This statistic alone suggests that although we have never seen each other or been in contact, we have contracted this illness through blood.
Finally I would like to question the use of CBT and GET as a treatment for CCC CFS. I have not found one study that has proven these therapies to be beneficial to CCC CFS. Doctors in Australia insist on these therapies and I was excited at the chance to do GET when it was offered to me. I followed a CFS doctors guidelines and increased the amount I walked by just 100 steps a week. I loved the idea of exercising (to some degree) after having been a runner prior to contracting CFS. Consequentially from the GET, my CFS progressed from moderate to severe. I can anticipate some GET advocates may argue in hindsight that I did not perform the GET correctly. This is a post hoc fallacy. I can confirm that I tried GET for a sufficient length of time and followed the exact procedure detailed in your GET studies under the guidance of a GET CFS doctor. The studies you have performed on CBT and GET have positive results on mostly non-CCC patients. I would urge you to perform a study on CCC patients.
I thank you again for replying to my letter and I appreciate the effort you have gone to in detailing your response. I hope this letter isn’t too aggressive in any way. I have tried to focus on arguments and logic and although some of my comments may seem aggressive in print (without tone), they are not intended that way. I apologise if I have misrepresented your positions in any way or built a straw man argument, it was not my intention to.
Professor Wessely’s response to my letter can be found in Part 3.