Trial By Error: Professor Jonathan Edwards’ View of ME

By David Tuller, DrPH

Professor Jonathan Edwards posted this essay a while ago on the Science For ME forum. I only noticed it recently. Professor Edwards, a retired rheumatologist from University College London, has played a key role n the last few years as an advocate for patients as well as proper science. So I thought it would be helpful to share his thoughts on a topic we all wonder about: “What is ME?”

I am reposting this with Professor Edwards’ permission. The views expressed are obviously his.

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What is ME?: A Medical Outsider’s Viewpoint

Jonathan Edwards

This an account of my thoughts about the nature of ME and the issues surrounding it, put together in response to queries. I hope it may be of interest both to patients and carers and to people with a medical or research interest in the illness.

I used to be a rheumatologist and biomedical scientist. I came across a few people with what I now realise was ME but it was not part of my routine practice. I became interested in ME later, having been asked to advise on immunological research. As a practicing doctor I thought that there are many causes of fatigue, some known, some not, but that we did not know enough to say there was a specific illness called myalgic encephalomyelitis, or ME. I have changed my mind. I think there is. But why I think it is useful to talk of ME needs some explaining.

For me the main reason is that the pattern of illness of ME is not like the fatigue caused by chronic diseases like rheumatoid arthritis or heart failure. The more I listen to people with ME the more it seems very unlikely that the mechanisms of fatigue in these other conditions are relevant. If the picture of ME can be described as ‘fatigue’ at all, it seems closer to the complex of symptoms of acute viral infection, or the spill over that occurs most often with EBV infection as ‘post-viral fatigue’ over several months. In general the fatigue of chronic diseases is predictable and shows up immediately on exertion. In ME symptoms appear as ‘payback’ unpredictably and, in the form of post-exertional malaise, with variable delay. Most notably, the level of symptoms and disability is out of proportion to any measurable inflammation or biochemical disturbance. It is also out of proportion to any mood change that might suggest a depressive illness. A pattern of symptoms similar to ME may occur in association with systemic lupus, Sjögren’s syndrome, Reiter’s syndrome and possibly Hashimoto’s disease but it is hard to know if it is ever quite the same.

The distinct picture of ME is, I think, enough to regard it as a specific syndrome, implying that we should expect there to be some specific physiological malfunction underlying it, just as a malfunction of glucose control underlies ‘diabetes’ and a malfunction of bronchial smooth muscle underlies ‘asthma’. That does not imply that there is a single specific cause, such as a specific infection. All the evidence points to ME as following a range of infections or with no environmental factor. It is often wrongly assumed that illnesses arise purely from a combination of genetic and environmental factors, but many illnesses may arise, with or without genetic predisposition, by chance, as a spin off from the constant to and fro of internal events associated with growth, repair and regulation. I suspect that this is a large component of causation in ME.

ME is also referred to as chronic fatigue syndrome (CFS). Both terms have their pros and cons. ‘CFS’ emphasises that this is a syndrome, but is too easily confused with the generic concept of chronic fatigue of any cause, which, as indicated, is something quite different. ‘ME’ emphasises that this is a specific illness pattern, but, confusingly, implies a pathology (encephalomyelitis) that is not present.

ME may be the preferable term, but it arose from a historical muddle. The term was promoted by Acheson, who believed that patients developing an acute illness with neurological symptoms in an outbreak at the Royal Free Hospital, recorded by Ramsay, and also in earlier outbreaks, might be suffering from an enteroviral infection similar to polio. The reason for thinking that this was an encephalomyelitis was the combination of symptoms suggesting muscle paralysis from nerve involvement together with symptoms suggesting brain involvement.

However, with the passage of time it has become clear that at least in the outbreaks that occurred in relatively recent history there was no evidence of any spinal cord or brain lesions comparable to those of polio. Muscle fatigability and weakness was not due to neural damage. A proportion of cases from the Royal Free outbreak were documented by Ramsay as developing a chronic illness of the type we now call ME, but this is something different from the acute neurological picture that led Acheson and others to use the term.

In retrospect, the outbreaks of so-called ME documented from the 1930s to the 1980s probably tell us nothing useful about the illness called ME today. The overwhelming majority of cases of ME today do not occur as part of ‘ME outbreaks’, even if many follow viral infections that have spread rapidly in communities in the way normal for most viral infections.

This confusion has been particularly unfortunate because in 1970 McEvedy and Beard published a paper suggesting that the few ‘severe’ cases with ‘neurological’ features in the Royal Free outbreak were cases of mass hysteria. They correctly point out that the signs documented in the records do not fit with any consistent type of neurological lesion. However, as indicated above, there is no reason to think this implies that the syndrome of ME as defined today(or for that matter as defined by Ramsay) is due to any form of hysteria, whatever we think hysteria might mean. An acute illness, with signs that turned out not to indicate neurological lesions after all, has been confused with a chronic disabling condition that may, in a very few cases, have followed on from the former.

That might be a very good reason for not using the term ME, but I think it is still probably the most useful term.

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Together with a group of patients and carers I reviewed what I thought one could say about causes of ME a couple of years ago in an article in Fatigue and Biomedicine (Edwards et al., 2016). My thoughts remain much the same.

ME clearly involves problems for the brain, in terms of impaired thinking, mental fatiguability and sensitivity to light and sound. There are also clues that it involves the immune system in at least some cases. An effect of immune dysfunction on the brain would make sense, but the immune system may only be disturbed initially, leaving problems only in the nervous system. Interest in immune problems was sparked by a suggestion of effectiveness of the drug rituximab in a phase 2 trial. However, the phase 3 trial showed no effect, so the evidence for an ongoing immune aspect comes largely from symptoms. In the past there has been a suggestion that ME is associated with immunodeficiency but the evidence is weak and inconsistent.

Superficially, the difficulty in maintaining any form of exertion suggests that ME might be due to a defect in energy production. However, no gross abnormalities in relevant biochemistry have been found. Moreover, symptoms like pain do not fit into a simple energy deficit. Mitochondrial function might be abnormal in ME, but the symptoms would probably fit better with a problem with the danger signalling function of mitochondria than with actual energy shortage. Post-exertional malaise and the reduction in performance observed in cardiopulmonary exercise tests at day 2 may indicate some form of inhibitory danger signal switching off full metabolic capacity (as occurs due to cytokine production during a viral illness).

For a problem to develop with cell signalling throughout the body in someone who has previously been well, there must be some new chemical signal reaching all the cells. The only likely source of that (other than neural signals from the brain) looks to be the immune system, with the signal being some form of autoantibody, or a cytokine produced by T cells. While this is an attractive idea in some ways, it is quite hard to see how either mechanism would work in specific biochemical terms.

Separating out neural signalling from innate immune signalling may not be straightforward because they are linked through the hypothalamus. However, it seems reasonably plausible that following initial immune disturbance the continuing production of symptoms is due to some form of error in, or damage to, a control mechanism in the brain. The situation might resemble that of tinnitus or narcolepsy, where very specific damage to brain circuits leaves the brain unable to control signals properly. In that sense it might be fair to say that at least some ME is ‘all in the head’. Nevertheless, that is very different from suggesting it is ‘all in the mind’.

What would it actually mean for ME to be ‘psychological’ or ‘all in the mind’? Since this is a common view, it is worth considering whether it has any basis. There has probably always been a popular belief that inexplicable illnesses like ME are ‘caused by the mind’. At least since the nineteenth century doctors have tried to make the popular prejudice respectable by using terms like ‘somatisation’ or ‘biopsychosocial’. The biopsychosocial (BPS) claim is that the illness starts off with a biological (or physical) trigger but then is perpetuated by ‘psychological factors’ in the form of unhelpful beliefs.

Medical science normally assumes that ‘physical’ covers all living processes, so regards all illnesses as physical. Enthusiasts for the BPS approach (who do not seem to follow this) try to twist the normal view into one of ‘separating mental from physical like Descartes’. But if everything is physical there is no separation. It is the BPS enthusiastswho separate physical and mental and, exactly like Descartes, claim the two ‘interact’.

Even if the BPS enthusiasts do not understand philosophy, their theory might still be useful. However, apart from the fact that we have no reason to think that there is such a thing as mental causation in addition to physical causation, descriptions of events in mental terms (thoughts) very rarely provide useful testable theories because too much is unknown. Psychology tries in vain to build testable theories but it is hard to see how it can succeed until we understand how thoughts actually work.

Moreover, there are good reasons for thinking that it makes no sense to suggest that, for instance, ‘unhelpful beliefs’, about being unable to exercise or having a certain illness, cause persistence of ME. The most obvious thing is that a lot of people with ME, at least for long periods of their illness, have no particular beliefs about their illness. They try doing exercise, because they have no belief that exercise is bad, until they find they are getting nowhere fast. Most people in the world with ME have never heard of an illness name. Even those who have mostly spend months or years having no idea what is wrong before being diagnosed.

The lack of a causal role of beliefs in disability is also indicated by the PACE trial, which shows that, at least for the sort of people who agreed to take part, treatment aimed at reducing unhelpful beliefs, despite leading to people reporting that they do not believe they are quite so ill, makes no difference to their disability. It seems to show quite clearly that beliefs are not the problem.

There is no doubt that, at least on internet forums, some people with ME hold strange beliefs about their illness. But people with cancer and arthritis also hold strange beliefs, particularly if medical advice does not offer help. Moreover, one has to expect people with an illness for which doctors have no explanation at all to be more likely to have unsubstantiated beliefs. They are likely to have some beliefs and by definition they will be unsubstantiated, because nobody knows! And it is also not very surprising that people with ME who have firmer beliefs that there is some physical cause for their illness tend to be less likely to get better. If there is something badly wrong, people are likely to sense it! This is about the only piece of evidence the BPS theorists can muster to support their view, but since it does not discriminate their view from the obvious alternative it tells us nothing.

So even in the intuitive lay sense that we think thoughts cause us to do things, and so, thoughts might cause symptoms of illnesses, it just does not fit the facts for ME. And Freudian-type theories of unconscious thoughts and motivations make no more sense, in addition to being notoriously untestable.

Put simply, the BPS theorists are unable to demonstrate to the medical world in general that they have a coherent theory grounded in reliable observations that makes useful predictions about effects of treatments. Despite attempts to give them a positive spin, treatments based on the BPS approach appear to make no difference to disability (Wilshire e al. 2017). Psychological theories of ME remain popular prejudices with fancy names, without any scientific grounding.

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I have been asked to comment on the issue of ‘harassment’ of health professionals by people with ME. The ME patient community has had to put up with all sorts of unhelpful beliefs (almost all of which come from doctors and therapists). Stories about polio-like illnesses or defective lymphatic drainage from the brain may be as unhelpful as stories about ‘biopsychosocial’ causation. The difference with the BPS belief is that it implies contempt for the person’s ability to understand their own nature. Not surprisingly, health professionals who champion unhelpful beliefs about psychological mechanisms get complaints. They get even more complaints when they do bad science to try to prove their unhelpful beliefs.

It may be that on a few occasions over the last ten years people with ME have said some pretty nasty things to doctors peddling unhelpful psychological beliefs. But for psychiatrists that should be an issue of no consequence. The problem has been grossly hyped. Where children and adolescents are involved emotions are likely to run particularly high and it is hardly surprising if voices have been raised. The condescending manner of medical staff is probably the main reason for stirring up anger and emotion. I nearly always get angry with the condescending ignorance of health care professionals when I am visiting a sick relative, whatever is wrong with them. Health care provision (at least in the UK) is lousy much of the time yet those delivering it seem too often to be under the illusion that they are doing a great job. It is time people learnt to admit that often they do not know what they are doing.

What are the most urgent steps needed to take to improve the situation for ME sufferers? We need everyone in research and healthcare to agree that we have no idea what the mechanism of the illness is and to start from scratch, looking for reliable evidence. That means abandoning both the incoherent BPS model based on popular prejudice, and theories hung over from sixty years ago about infectious diseases that are no longer of any relevance to the illness people have to deal with. It means psychiatrists, physicians and therapists accepting that they have to care for people on a pragmatic basis in response to symptoms without any belief that they know what is good for patients and the condescension associated with that.

Cognitive behavioural therapy and graded exercise therapy involve ‘educating’ patients in an explanation for their problems that has no basis. The evidence is that they make no difference to disability, so they are unethical and should be abandoned. The use of anti-virals and antibiotics similarly has no sound basis and should be discontinued, at least until there is reliable evidence for efficacy.

We need research on a broad front to identify leads to focus efforts on. Genetics has to be a worthwhile area to cover. There are indications that there is genetic susceptibility. Finding out what the genes are may only provide pointers rather than specific answers, but these would still be powerful.

In my view chasing viruses or gut bacteria is likely to be a waste of time. It is unlikely that any one infectious agent is important. Shifts in gut bacteria seem equally unlikely to be important. If micro-organisms were relevant to the persistence of the chronic illness then amongst the millions of people with ME there should be at least a few thousand cases that provide clear clinical clues to how. Epidemiology should have shown something up. There should be a few hundred cases where a virus has multiplied enough to be directly measurable or to show specific tissue damage, or where ME has vanished in response to moving to a new country with a new diet.

Brain imaging is likely to be worth exploring in a much more detailed way. Replication studies are particularly needed because a number of changes have been reported in ME once and then never repeated.

Metabolic pathways capable of generating abnormal signalling are worth looking at in detail. I am not convinced that special emphasis should be put on mitochondria, but they may yet prove to be central to the disturbance that underlies the pattern of illness.

Reference: Edwards et al. The biological challenge of myalgic encephalomyelitis/ chronic fatigue syndrome: a solvable problem. Fatigue. 2016; 4(2): 63–69.

 

Comments on this entry are closed.

  • Wendy Boutilier 2 December 2019, 5:32 pm

    Jonathon Edwards doesn’t understand the symptoms of Myalgic Encephalomyelitis as per the ICC. What disease is he describing? ME Advocates (not CFS) have tried to explain the importance of criteria and he still doesn’t get it. This is what ME Patient Advocates are fighting for. The cases Mr Edwards is pontificates about are the fatigue based CFS not Myalgic Encephalomyelitis. We need recognition for treatment for our Neurological Disease.

    Mr Edwards quote:
    “I don’t understand the relevance of neurological, immunological and cardiac issues since we do not have any good reason at present to attribute objective abnormalities in these systems to ME. Various functional differences have been reported in research studies but nothing that would warrant being part of research classification criteria and certainly not a requirement for clinical diagnosis. Lots of people have ME without specific neurological (unless you include brain fog and sleep disturbance), immunological or cardiac problems so they cannot be required criteria.”

    Edwards should feel free to explain openly to those who have ME with Specific Neurological, Cardiac, Immunnological issues as well as an Acquired Brain Injury caused by the viruses that put us here. Encephalomyelitis is a very serious health issue and to pretend it doesn’t exist is ignoring thousands who have ME-ICC, ME-Ramsay or ME-Hyde

    https://www.s4me.info/threads/meaction-demystifying-the-diagnostic-criteria-for-me-and-related-disease.12202/

  • Wendy Boutilier 2 December 2019, 5:42 pm

    It only makes sense that there are 2 medical issues at stake here. Those with Encephalomyelitis and those without. Clearly Edwards prefers to suggest that the world of IOM/SEID/CFS is a ‘one size fits all’ while ignoring those who have been legally diagnosed with ME as per the expert’s criteria ICC-2011, ME-RAMSAY or ME-Hyde. He is definitely showing the world that he definitely not as well trained as Curruthers et el’ but he is also showing that is lacking when it comes listening to patients.

  • Allison Haynes May 2 December 2019, 6:16 pm

    I second the comments by Wendy Boutilier.
    Of course we can all agree with Dr. Edwards regarding the damage caused to M.E. patients by the psych cabal. However, that is the absolute bare minimum of understanding M.E. these days.
    Dr. Edwards has made incorrect statements about M.E. both in the document published here and in recent discussions on the Science4ME (S4ME) forum.
    He has also shown his misunderstanding of disease criteria and his disregard for international experts & their criteria such as the ICC.
    He dismisses physical symptoms such as encephalomyelitis, cardiac dysfunction, etc., in M.E., despite ample proof existing on SPECT, MRI, CPET, and despite the many published papers on on these topics.
    He dismisses investigating a viral cause as “a waste of time” despite abundant documented historical & scientific evidence. He seems too willing to dismiss the value of medical history as “60-year-old theories”. We ignore medical history at our peril.
    In short, he is discussing a non-neurological “cfs”, while claiming to discuss M.E..

  • JES 2 December 2019, 6:48 pm

    I have disagreed with Edwards about several things, but I think his message is mostly consistent with the current understanding of the disease. I don’t see any reason to separate ME to some niche groups like Hyde-ME, Ramsay-ME or supposed encephalomyelitis group. The fact is that millions of people suffer from symptoms consistent with ME/CFS and this whole group of patients deserves to be studied.

    So far I have seen no evidence on the basis of which to separate a small subgroup of patients, it is all based on the opinion of a couple of doctors. There is no diagnostic criteria that requires encephalomyelitis, obviously, since doctors haven’t been able to measure such a thing in ME/CFS patients. There are some findings of neuroinflammation or microglial activation in ME/CFS patients, which apparently also exists in several other chronic diseases like MS, Alzheimer’s or depression. This isn’t a specific marker.

  • Ya Seen 2 December 2019, 7:40 pm

    “In retrospect, the outbreaks of so-called ME documented from the 1930s to the 1980s probably tell us nothing useful about the illness called ME today.

    The overwhelming majority of cases of ME today do not occur as part of ‘ME outbreaks’, even if many follow viral infections that have spread rapidly in communities in the way normal for most viral infections.”

    That is pretty much all needed to know to discount whatever else his views are.

    He mentions several points that suggest an (ongoing) viral infection, yet claims evidence for immunodeficiency to be weak and inconsistent.

    Interestingly, experts in the study of HIV like Derya Unutmaz have pointed out that the immune system disruptions they are witnessing in ME are as serious as those observed in AIDS.

    Many a pwME is dealing with opportunistic infections and test results that are repeatedly compared to those of HIV patients by lab staff who have never even heard of ME.

    We may not see many severe AIDS patients in the western world nowadays due to leaps in antiretroviral treatment in the past decades, but anyone who looks into the immune & neurological disorders associated with HIV will be baffled to find out there is a complete overlap with pretty much all ME symptoms but PENE.

    How someone like Edwards can not be aware of this and even recommend all antiviral & antibiotic treatments (which often do provide significant relief to sufferers, including reports of partial and complete remission) be stopped escapes both logic and an ethical perspective.

    It would seem that like others have suggested, he is writing about some ill-defined fatiguing conditions wastebasket, but not the distinct disease Myalgic Encephalomyelitis, be it described by Ramsay, International Consensus Criteria (2011) or any other definition which merits that name.

    Beyond calling out the frankly ever self-evident nonsense of the criminal BPS crowd and empathizing with what are only understandable reactions by a very ill population suffering inhumane neglect, I don’t see how Edwards expresses anything of use for ME patients or research, if not quite to the contrary.

    I would recommend he take a long thorough look at actual epidemiology like Rosemary Underhill did suggesting we are dealing with a pathogen’s having become endemic over several wasted decades.

    Pretty much what would have happened with HIV had it been treated with the same stubborn ignorance as ME.

    Actually, it would make sense for Edwards to read up on all the historical evidence; and while he’s at it get a clear idea on the importance of disease definitions & meaningful diagnostic criteria like the ICC.

    To anyone following the history of ME-(non-)research it becomes obvious rather quickly that is where fundamental errors like those in Edwards’ assessment stem from and were often set up deliberately to happen, as with the creation of “CFS”, the notorious “Oxford criteria” and nowadays “SEID” to name but a few.

    After 85 years of dealing with this plague such ignorance by people speaking for pwME is long beyond justifiable, be they advocates or researchers.

  • Guido Den Broeder 2 December 2019, 7:43 pm

    Of course CFS patients need to be studied, and they are. But ME patients need to be studied, too. They have a specific pathology and their own perspective, treatment, management and prevention, which is missed when they are conflated with a much larger patient group (and CFS is not even close, NAH as a group would make more sense).

    The name ME wasn’t chosen at random. By 1955, these patients had been studied for 60 years, and encephalomyelitis had been well established by autopsies and biopsies. Monkeys given the blood of ME patients got ME, too.

    The reason that the disease needed a new name was that in 1954, a political decision was made to redefine polio, excluding non-paralytic cases (as well as short-term polio). Until then, ME was known as missed, abortive or a-typical polio. The ICD-6 has a code for polioencephalomyelitis.

    ME was chosen for these patients because they were known to have encephalomyelitis, not because people thought it might one day be found.

    Thanks to the de development of imaging we no longer need to cut the patient open. We can establish encephalomyelitis in vivo, using PET, xenon-SPECT, qEEG, supported by fMRI and NIRS. There are various markers for ME now as well.

    There are other diseases with encephalomyelitis, but the name ME is reserved for the polio variant, a disease triggered by enteroviruses. That is its definition. The criteria are there to help doctors to recognize it, so they will do the right tests.

  • JES 2 December 2019, 8:08 pm

    I wonder what disease Ron Davis’ son has then. If it is such clear cut how to define and diagnose ME, one would think Davis would have narrowed his scope long ago to only focus on the enterovirus or post-enterovirus hypothesis. What about the case of Jen Brea, who was diagnosed by a dozen of ME expert doctors to have ME, yet turned out to recover following CCI surgery? I’m afraid it’s a bit simplistic to view ME as something driven by one causative factor like (entero)viruses. It’s all at hypothesis level at this point.

  • Wendy Boutilier 2 December 2019, 8:20 pm

    The ICC & IC Primer are the only ME criteria specifically written for both clinical and research purposes. The CCC, Fakuda, IOM/SEID are all clinical criteria for CFS.

    To deny ME patients the right to be diagnosed & treated correctly is an infringement on our human rights.

    In the words of Dr Bruce Carruthers (CCC 2003 & ICC 2011)

    “If such clarity and adequacy are not achieved, several types of smudging may result. In other words, if the generalisations from the medical model are too generic, they have no chance of adequately meeting the patients’ experience of illness and much relevant data may be overlooked or misinterpreted. Thus, the move from a more specific clinical concept such as myalgic encephalomyelitis or fibromyalgia to a more generic concept such as chronic fatigue syndrome or chronic pain syndrome entails missing a lot of the information that makes the syndrome a name match, and an experience.

    The syndrome as an experience is a coherent entity whose parts run together as a process—as the word syndrome indicates etymologically—and whose causal interactions are sensed directly in the mode of causal efficacy. This entity arises against a background that is treated as a non‐entity for the purposes of the observation. Thus, the attempt to organise clinical activity around a non‐entity, such as in somatisation disorder and Munchausen syndrome,where diagnosis depends on the absence of an entity, may interfere with proper clinical activity by importing a misplaced forensic attitude towards a patient’s experience of illness, discounting or distorting its relevance.

    The move towards ignoring the distinctions between primary and secondary which designate sensed causal directions in a clinical entity, whether applied to depression, anxiety, infection or fibromyalgia, add to the confusion and impede the elucidation of a properly dynamic clinical entity. The widespread use of the holistic biopsychosocial model of disease without any distinction between a clinical entity and its background encourages the “drowning” of clinical entities by risk factors, which can proliferate endlessly in a nominalist fury without orientation as to their state of relevance or lack thereof with respect to a real entity.”

    https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1860613/

  • Guido Den Broeder 2 December 2019, 8:46 pm

    It woud be nice to have some investigative journalist willing to pursue those questions. Was Brea really diagnosed with ME by experts, or did she diagnose herself? Was Davis’ son ever tested for ME? What are their motives to conflate ME with CCI , CFS or SEID? Should we follow the money?

    Meanwhile, read my post again. ME is a definition, hypotheses don’t come into play. Without the encephalomyelitis, without the enterovirus, it’s simply not ME. You can ask: do people have it, not: what is it. The answers is yes, there are people with ME. Not as many as Millions Missing claims, but it’s not rare either.

  • Anton Mayer 3 December 2019, 3:35 am

    Edwards gives a levelheaded analysis of the situation and does not promote a weak hypothesis. I find this refreshing.

    People that are upset by his questioning of ideas that are accepted in the patient community should remember that competent science involves rejecting weak hypotheses and that if we’re honest, there are many such ideas circulating in the patient community (and also among professionals, like the biopsychosocial theorists).

    Edards has also made interesting comments about diagnostic criteria.

  • Anton Mayer 3 December 2019, 4:00 am

    Ya seen said:

    “Interestingly, experts in the study of HIV like Derya Unutmaz have pointed out that the immune system disruptions they are witnessing in ME are as serious as those observed in AIDS.”

    Unutmaz has not found an immunodeficiency but an increase in MAIT cells in severely ill patients. This is also observed in other diseases like AIDS. An increase in MAIT cells is not considered an immunodeficiency as far as I know.

  • Peter 3 December 2019, 4:37 am

    I find doctor Edwards overview refreshing, to. In these strange times with lots of fixed ideological views and lots of bias, – what the community and others need, is exactly an attempt of a levelheaded objective analysis and overview. When a ton of information and hypothesis drowns us, I often find Edwards cautious input very valuable.

    The by far most important message, is that this disease/syndrome, or whatever you call it, is not “fatigue”. That ought to be first lesson for everyone interested, and especially doctors who make analogies to known fatigue (even the most serious one) and this disease. That is just a fundamental misconception.

    The name is a hot potato. Personally I prefer ME, but understand the problems of it. But if some sort of signaling problem, it may not be that bad either? My preference has much to do with the fact that the CFS-name is so ridiculous and makes absolutely no sense in capturing what it is all about and the severity of it. Have a really hard time to see that the CFS-name has any pros to it at all?

  • Anton Mayer 3 December 2019, 5:52 am

    Once we figure out this illness, we might discover that certain ideas that had influence on patients were misguided and unhelpful. That would include the CBT/GET theories but could also include ideas about enteroviruses, immune deficiencies or the idea that only a few select experts doctors have an understanding of the illness.

  • Lydia Neilson 3 December 2019, 9:34 am

    I agree with both Alison Haynes May and Wendy Boutillier. The National ME/FM Action Network spearheaded the CCC in 2003 which then was updated with Carruthers etal in 2011 with the ME International Consensus Criteria.

    Between the ME experts of 2003 and 2011, over 60,000 patients had been seen by these ME experts who had also published many relevant papers. To ignore what was researched in the past and start from scratch and reinventing the wheel makes no sense. If other illnesses were treated this way and past research ignored, they would be in the same position as the ME population is.

    Dr. Edwards, your comments are unhelpful and your opinion shows the lack of understanding of ME. Please show courage and go against the norm, and base your opinion on the proper research, namely the ME International Consensus Criteria 2011.

    NATIONAL ME/FM ACTION NETWORK
    Lydia E. Neilson, MSM
    CEO, Founder.

  • jimells 3 December 2019, 1:19 pm

    I don’t always agree with Professor Edwards, but I always consider his words very carefully. I implore commenters to please be respectful. He wants the same thing we all want: real treatments that actually help.

  • Colleen Steckel 3 December 2019, 2:48 pm

    I read this and am reminded we have the challenge that those who are experts in the field treating ME as well as those experiencing the disease ME are looking at the disease from the inside out. Those looking on from the outside seem unable to discern the difference between patient groups.

    Any article that talks about ME but bases the information on the combined patient groups of ME, ME/CFS-SEID and/or CFS-Fukuda is based on a false premise that these are all representing the same patient population.

    I realize Dr. Edwards is from a system in the UK that redefined Ramsay’s ME to mean something similar to CFS as defined by Fukuda in 1994. That is why he states: “ME is also referred to as chronic fatigue syndrome (CFS).”
    What we need to get back to is that ME as defined by Ramsay and later defined by the ICC is NOT the same thing as CFS or as ME/CFS (SEID) as redefined by the IOM/NAM report in the US in 2015. See this comparison chart: https://d3n8a8pro7vhmx.cloudfront.net/meadvocacy/pages/22/attachments/original/1531592663/ICC_compared_to_IOM.pdf?1531592663

    Whether we call it “subtyping” or “stratifying” or “different diseases” isn’t the point. The point is that ME is NOT the same patient group as ME/CFS-SEID or CFS-Fukuda.

    Dr. Edwards talks about the passage of time as if it brings new information. In reality the passage of time led to including patients who don’t have ME, in with those who do have evidence of spinal cord and brain lesions comparable to those with polio.

    Looking at the prevalence numbers has helped me clarify my understanding of what happened. There are an estimated 1 million who have ME in the US. I have seen there are an estimated 2.5 to 4 million who have ME/CFS (SEID). The IOM report combined the ME patients in with the CFS patients and created a combination disease description.

    That means that from the outside looking in, a person sees up to 3 people defined by ME/CFS-SEID as compared to 1 person with ME. Those who have ME are the most “missing” from view as we try to survive – seldom leaving our homes. So, the view from the outside is heavily skewed by those who have been given an ME or ME/CFS label but don’t have the neurological, cardiac, and immunological issues recognized by the experts in the ICC.

    Dr. Edwards states: “They are likely to have some beliefs and by definition they will be unsubstantiated, because nobody knows”. I understand this to mean nobody knows what ME is.

    But we have 26 experts with 100s of years of combined experience who wrote the ICC and IC Primer that is a clear description of my lived experience. It is accurate to say that “nobody knows” what causes ME. That can be said of many diseases, like MS. But it is not accurate to say that nobody knows what ME looks like or what the patients are experiencing.

    Thousands have signed the #PwME4ICC petition at change.org which is asking the ICC be adopted by US Health organizations – clearly I am not alone in recognizing that the ICC accurately depicts the lived experience of ME.

    What I (and others) can’t figure out is how to help people from the outside see the reality for those of us on the inside. The only thing I know to do is present the ICC and then remind them that in order to truly understand the disease, they must delve deeply into the ME IC primer which shows the full range of the constellation of symptoms that are ME as well as likely causes of the abnormalities leading to those symptoms.

    I understand the complaint that people who have been given the ME label who do not fit the ICC are being “kicked” out of “the community”.

    A much better way to frame this is that ME is a horribly devastating disease and we want to make absolutely sure that every patient no matter what label they have gets FULL screening to rule out other diseases.

    If someone doesn’t have the distinct-recognizable disease ME, it is time they were thoroughly screened to find out what they do have! The needs of patients getting proper care should start coming first. The best way for patients to get proper care is to make sure they have been properly diagnosed using the ICC and the IC Primer.

  • Anton Mayer 3 December 2019, 3:42 pm

    Colleen Steckel, I think one reason that this information is being circulated is to get patients to question some of the things they’ve been told about the illness by so-called experts. We do question psychiatric theories promoted by other so-called experts about ME and it is only fair that we also question the other theories.

    There are no polio-like lesions in ME patients. The evidence on persistent or recurrent infections is negative (so far). And so on. This lack of evidence isn’t because of excessively broad diagnostic criteria obscuring the truth about real ME, as some like to argue. There is a big problem with this argument: first, it is claimed that some experts can clearly separate a distinct illness called ME and that it is known to have certain characteristics. If this were true then it would be very easy for these experts to prove their various claims about immune deficiency, recurrent infections, polio-like lesions, etc. They have never been able to convincingly prove these things. Maybe one day some of these will be shown to be correct but currently if reasonable standards of evidence are applied, these look like failed hypotheses that were never acknowledged to have failed and so continue to influence society.

  • Anton Mayer 3 December 2019, 3:48 pm

    I think that the many dubious stories claiming to reveal the truth about ME and CFS are harmful to progress because it creates constant tension between patients and doctors and health authorities due to patients thinking that some truth is being denied. They have failed us and neglected us and deserve criticism for that, and we need to put pressure on them to change things, but we also need to work with them to find answers and solutions, not demanding that they accept some ideas that have very little if any science behind them.

  • Geoffrey Hallmann 3 December 2019, 5:45 pm

    It’s an interesting view by Dr Edwards – expressed without the benefit of references (hence impossible to even know where he gets his views). Fortunately he is retired – so he has plenty of time to educate himself. He seems to be interested.

    I would say, however, that he commits many errors that are similar to those of the Biopsychosocial school. ME is not about belief. It’s about a body of work that does exist.

  • Ona Albizu 3 December 2019, 5:52 pm

    Permiso!

    Here is a translation to Spanish of Edwards article (with his consent).

    It is an effort to bring to the Spanish community different ideas, others than bodily distress syndrome so common among Health practitioners world wide.

    Una traducción completa del texto, con el consentimiento del autor, para poder seguir mejor este interesante debate.

    https://www.dropbox.com/s/61kn6d00plsyai8/Qu%C3%A9%20es%20ME_Edwards%202019.pdf?dl=0

    Lamentablemente no hay en español nada semejante al “blog de Cort”, tanto sus escritos como los comentarios. Traduzco con la esperanza de que sean más los lectores críticos que se animen a leer en inglés y a entender la complejidad que vivimos.

  • Ya Seen 3 December 2019, 8:36 pm

    The evidence for inflammation, immunodeficiency and persistent infection(s) is there for anyone with eyes to see.

    To claim otherwise is either plain ignorance, based on wrong methods/patient selection and/or agendas at play.

    We’re not talking about your average physician’s lab work.

    “Immunologist Derya Unutmaz, MD, who heads the NIH-funded Jackson Laboratory, has found immune system disturbances in deidentified cell samples from patients with ME/CFS, particularly in CD8 cells and T-helper 17 cells, which are involved in tissue inflammation.

    While emphasizing that the precise relevance of the findings is not yet clear, Unutmaz told Medscape Medical News, “There are some really major perturbations…. When I look at the data, there’s something biologically terribly wrong with these people. I studied HIV for many years. This is the type of thing you would see in HIV-infected people.”

    https://www.medscape.com/viewarticle/911906

  • Guido Den Broeder 3 December 2019, 9:45 pm

    Anton Mayer, ME does come with lesions but they are not always apparent on an MRI. They haven’t been studied often, however as an example Poser found periventricular lesions in 1992.

    Infection is a certainty because that’s how ME is defined and classified. The outbreaks show the short incubation period of the enterovirus.

    Autopsies and biopsies have revealed the inflammation, providing hard proof that the disease isn’t merely conjecture but actually exists. There are many indirect ways to indicate inflammation as well.

  • Anton Mayer 4 December 2019, 3:27 am

    Guido den Broeder, have you ever listened to those who are skeptical about these ideas? If you have not, you would discover that they have good reasons to be skeptical. Don’t assume they are ignorant or prejudiced.

  • JES 4 December 2019, 12:49 pm

    Infections are not a certainty, to state that is ignorant and overlooking the fact that infections *may* not necessarily be involved in maintaining ME. I think everyone, including Jonathan Edwards, has acknowledged that infections can and often serve as the trigger for ME. The crux is whether the infection is still present after the acute stage. There is a possibility that ME is caused by a virus that operates in hit-and-run fashion, much like how enterovirus causes polio in some cases. This was discussed by Maureen Hanson in a recent seminar.

    I also see no evidence that for example that an increase in MAIT cells found by Unutmaz is necessarily due to an active infection. What’s even more damning is that none of the researchers in Davis’ team have (using the best possible technology) have been able to isolate any active infections in ME patients. The work is still in progress, but so far we have nothing.

  • Guido Den Broeder 4 December 2019, 1:20 pm

    Davis is not studying ME. You can’t select CFS or SEID patients and then claim that the outcome applies to ME, no matter how good you think your technology is.

    The same pertains to you statement about infections. The hit-and-run idea has been suggested for CFS, not ME. Suggested, that is. It is not a fact, and very unlikely to be the correct model for all CFS patients given that all kinds of diseases get misdiagnosed as CFS.

  • Guido Den Broeder 4 December 2019, 1:47 pm

    Maureen Hanson was talking about something else: viruses hiding in the general population (i.e., becoming endemic), striking and then disappearing from epidemiological view again.

    It doesn’t follow that they disappear from the patients, only that it’s no longer contagious. You will still find the enterovirus in the tissue of ME patients.

    The reason that ME is now largely endemic is a different one though. That is primarily the consequence of the polio vaccination programs.

  • jimells 4 December 2019, 4:50 pm

    Guido Den Broeder wrote: “Davis is not studying ME.”

    In a literal sense, that may be correct. To me, he is studying a small group of extremely ill people to see what is wrong, what caused it, and how to fix it. I very much doubt he is studying to see which criteria they fit and what label to use.

    Whatever his team finds will of course have to be studied further to see if their findings are generalizable. Unlike the psychobabblers, Ron Davis and team will probably not make any claims that their research applies to everyone with some vague fatigue something-or-other.

    Personally, I prefer to concentrate my anger at the BPS crowd that are still abusing us and the useless bureaucrats that organized an effective research program for AIDS but suddenly become completely incompetent in regards to our illness (I’m looking at you, CDC and NIH).

  • Trish Davis 5 December 2019, 5:09 am

    I am disturbed by the vehemence of those criticising Prof Edwards post on the grounds that they have the one true ME and everything else is in some wastebasket called CFS, and claiming that if Prof Edwards doesn’t agree with them he is ignorant.

    I was diagnosed with ME by a GP in the UK in 1989 following an infection. I have no idea what definition if any my doctor used, but she recognised my symptoms as fitting a pattern she was familiar with. My doctors records now say I have CFS. I don’t know why or when it was changed. I still have the same illness 30 years on. I have no idea whether I have enterovirus, cardiac problems or neuroinflammation because they have never been tested. But I do fit most if not all of the different ME and CFS definitions.

    We have no way of knowing whether people like me who have a very debilitating condition that includes post exertional malaise and a range of other unpleasant symptoms all have the same underlying biological disorder or not. So anyone who tries to categorise me as not having the same condition as them has not grounds for doing so.

    That is why I find Prof Edwards approach so valuable. He doesn’t come at the subject with fixed ideas. He has read widely and deeply for several years with no particular preconceptions except to try to understand more fully. Those who call him ignorant are wrong. Of course he doesn’t know everything, but he knows a darn sight more medicine than I do, and he has an open mind.

    I agree with him that we simply don’t have sound solid research evidence to back up the claims made even by some ‘expert’ doctors treating people with ME. Until that research is done, all we can say is that we are all very sick, and that we have a physical illness, with some promising lines of research that still need to be replicated before they are accepted as definitive.

  • dAc 5 December 2019, 5:35 am

    So sad to see many comments from the ME/ICC fundamentalists who base their views solely on beliefs, personal anecdotes and small scale findings and who then claim that they speak for the entire ME community.

    The reality, as Prof Edwards explains, is that there is very little, if anything, that has been definitively proven, other than there is a large population of very sick people whose symptoms match a particular profile.

    What is needed is research, and that is where the efforts of the patient community should be, rather than wasting precious time and energy creating cults based around particular names, definitions or infections – the BPSers must certainly appreciate the divisions in the patient ranks created by such efforts.

  • Guido Den Broeder 5 December 2019, 9:55 am

    My medical diagnosis is ME not because of some belief that I cherish, but because it was found, decades before the ME-ICC were published. More than twenty doctors unanimously agree that my medical results leave no doubt whatsoever.

    As a scientist and patient advocate leader, I am quite aware that there exists a large group of patients who are uncertain about the cause of their complaints. I wish you the best. Maybe Davis will help you, even while his methodology is flawed. But I am not one of you, and my experts have different names.

  • Wendy Boutilier 5 December 2019, 10:31 am

    Those who have had Neuroimaging via SPECT Scans showing irreparable damage from Encephalomyelitis should be given the diagnosis of Myalgic Encephalomyelitis because that is what we have. My SPECT Scans showed lesions and damage to my occipital lobe. This won my lifetime disability pension in 2 separate countries and opened the door to treatment to reduce the severity of what is actually an “acquired brain injury”.

    I take offence at the insulting way patients with Myalgic Encephalomyelitis are bullied by CFS patients with no knowledge of our personal medical facts and neglected by the medical profession because we are problematic for their arrogant dismissal. This is the exact same tactic that the Authors of PACE used to build their reputations on.

    I don’t begrudge the health care or the generally accepted criteria used to treat those with CFS because they are sick and need medical help. I don’t understand why the CFS group feel neuroimaging is not even possible when there is so much proof that is being ignored.

    Researchers are not trained to clinically assess patients and should not be extending their expertise to champion a highly prevalent cause which involves fundraising for a disease they are not researching. It is at this point that their reputations lose credibility. I recognize how sick Whitney is but using him as a poster child for CFS/SEID is not helping the thousands of others worldwide who have neuroimaging proof of Encephalomyelitis. When ME patients are thrown into the CFS/SEID stew pot, it skewers the results. Now all you see is only some patients show brain inflammation but not all. If you took those “some with inflammation” out of the pot you will be left with CFS/SEID. Why is everyone so afraid to separate ME with proven Encephalomyelitis from those without? It’s the only way to move forward for both CFS & for ME.

  • Trish Davis 5 December 2019, 11:37 am

    Wendy, I am very sorry you feel bullied. I do not question your diagnosis, nor do I question that you have scans that show you have an acquired brain injury. Why would I?

    The fact that I and many others have not had access to brain scans, but still fit the ICC criteria as well as other criteria means we simply don’t know whether we have the same as you have. So why do you think it is wrong for people in my position to use the term ME for what we have? It is what I was diagnosed with, as were many others without the benefit of brain scans and other tests.

    The fact that many people fit the ICC criteria also fit all the other criteria for ME and for CFS means that we can’t know if everyone has the same condition or not. I would however agree that studies using Fukuda criteria, on which PEM/PENE is optional, and those based on Oxford criteria are worthless, because they will also include people with idiopathic fatigue, and probably people with depression and other fatiguing conditions.

    As for the question of feeling bullied, please, Wendy, consider the possibility that people like me who fit the ICC criteria but haven’t had brain scans or cardiovascular tests can feel bullied by those who have and tell us we are not allowed to use the term ME for whatever we suffer from.

    Please, let’s all keep the focus on getting rid of the biopsychosocial nonsense, and getting some really good biomedical research that helps us all.

  • Wendy Boutilier 5 December 2019, 12:17 pm

    It is not enough to meet the ICC requirement to be diagnosed with ME. The patient must also prove Encephalomyelitis and currently, the most definitive test for that is provided through Neuroimaging. Not using available science and criteria that has been available for several years can lead to misdiagnosis. There is nothing in CFS/SEID/IOM that can help those with Myalgic Encephalomyelitis and the longer this issue is ignored the longer people remain hopeless. Enteroviruses never leave the host, they become latent and morph into something that is no longer recognizable via ordinary lab work. My viruses include strains of Dengue Fever amongst others, which is a direct cause of Encephalomyelitis. Tropical & Sub Tropical countries are well aware of this and my first set of SPECT Scans were done in that geographical area of the world because my employers needed to know if I could meet the demands of my job. I couldn’t continue to work but I won a lifetime invalidity pension. I then returned to Canada and had more scans done. Unfortunately there was no improvement as far as Encephalomyelitis is concerned. Why are we celebrating the possibility of CCI surgery for #PWME using very little scientific fact and not Brain/Spine inflammation that has been recognized for decades. I can’t ignore the possibility of arrogant medical professionals who are more concerned with their ego than they are at not using their listening ears.

  • Guido Den Broeder 5 December 2019, 12:22 pm

    Trish, we aren’t saying that you can’t possibly have ME. CFS is always a misdiagnosis, and a minority of CFS patients eventually turn out to have ME.

    What we are saying is that just because you aren’t sure, it doesn’t follow that we should be dragged into the mud that is CFS, too.

  • Jonathan Edwards 5 December 2019, 12:47 pm

    Many thanks to everyone for the comments. I am listening, as always.

    Maybe I will just make one point. Everything I know about ME comes from people who believe they have ME. (I don’t remember anyone who thinks they have CFS instead.) It is either listening to their accounts of their experiences, or their views, or reading the papers they recommend. Maybe I am too lazy to read what medics have written in textbooks or dig things out for myself but I find people with ME keep me on my toes quite enough. I have attended research conferences at the recommendation and invitation of people with ME and their carers. I discuss what I hear there with people with ME and pretty much nobody else except when I am asked to advise grant giving bodies or guideline committees to which I get invited, presumably because people know that I spend so much time talking to people with ME (probably 3,000 hours over the last few years, because I find it interesting).

    If people want to debate please come to S4ME. It is so much better for careful scientific analysis than professional forums and meetings, where nobody dares to say what they really think.

  • Wendy Boutilier 5 December 2019, 1:08 pm

    Many use ME to validate terminology and not because they have been diagnosed with it or they have been diagnosed with ME/CFS which is not ME only abbreviated. There are also political issues at stake in each individual country but for those of us with an ME diagnosis, & proof of Encephalomyelitis, the health issues are overwhelming and present something completely different from CFS/SEID. I cannot urge our Doctors enough to note how important it is to understand that this coupling of terminology and smudging of criteria hurts us because it ignores the very small but specific ME patient group. Encephalomyelitis & Viruses affect our whole body:
    .
    Cardiac & Cardiovascular Dysfunction
    Cognitive & Neurological Dysfunction
    Digestive Dysfunction
    Endocrine & Neuroendocrine Dysfunction
    Exercise, Exertion/Physical Activity PENE
    Headaches
    Hearing
    Vestibular & Speech Problems
    Hypoglycemia
    Immune System Dysfunctions
    Joint Dysfunction
    Muscle Dysfunction
    Oral Dysfunction
    Wide Spread Body Pain
    Reproductive Dysfunctions
    Neuropathic Pain
    Respiratory Dysfunctions
    Seizure & Seizure Activity
    Skin, Nails, & Hair changes
    Sleep Dysfunction
    Urinary Tract Dysfunctions
    Visual Dysfunction
    Weather Sensitivity
    Weight Changes

  • Guido Den Broeder 5 December 2019, 1:52 pm

    Jonathan, I ‘ve noticed that you spend a lot of time on the Phoenix Rising forum. That, however, is not where the ME community or its advocates tend to be found.

    You should know that some years back the forum’s administrators blocked quite a few ME patients for saying that ME is not CFS, and other ME patients won’t go there because of it.

    The result is that, as you say, you get your wisdom from patients claiming to have ME, rather than from those that have actually been diagnosed with it, or their experts.

  • John Peters 5 December 2019, 2:27 pm

    Great piece by Jonathan Edwards.

    Excellent comments by Anton Mayer, Trish Davis and a couple of others.

    Prof Edwards very kindly spends some time responding to patients on the S4ME forum, so please do join the debate there.

    https://www.s4me.info/threads/trial-by-error-professor-jonathan-edwards%E2%80%99-view-of-me.12625/

  • Guido Den Broeder 5 December 2019, 2:33 pm

    I don’t think so. That is a groupie forum, our voice would not be heard.

  • Anton Mayer 5 December 2019, 3:13 pm

    Guido Den Broeder

    That is unfortunate. I would like to see such debate so that we the patient community can get over these internal divisions and either agree that these older ideas about ME have merit or agree that they do not.

    I find the current situation is not good for advocacy, when we have some groups that believe ME/CFS is a useful label for an illness or group of illnesses that we still understand very poorly and that with time, research will bring answers and help, and another group that thinks ME is being hijacked, that we already know its cause and underlying disease processes but that this isn’t being recognized.

  • Guido Den Broeder 5 December 2019, 3:39 pm

    This is not an internal division. We are not part of your community, and you are not part of ours.

    All that we ask of you is that you stop using the term ME when you don’t have it.

  • X 5 December 2019, 4:20 pm

    A clear-headed, cogent and insightful analysis. Thank you, Prof. Edwards.

    While I agree with the above posters’ comments that the “CFS” label is unhelpful, it is at least equally unhelpful to presume that there is a patient population with the one true ME, separate and distinct from those who have been given the CFS diagnosis. In the absence of biomarkers, diagnosis is made on the basis of clinical presentation. The utility of SPECT scans is equivocal at best, and there is no evidence that they provide diagnostically relevant information.

  • Michiel Tack 5 December 2019, 5:27 pm

    I hope that Jonathan Edward’s viewpoint encourages more scepticism within the ME community.

    If doctors or researchers take ME to be a biological, debilitating illness that does not guarantee that whatever theory or ideas they have about ME are correct. Those standards are far too low. Instead, I suggest we interpret any claims made about ME with a healthy dose of scepticism, no matter who is making them.

    It’s probably because we have so little ME experts that many strong claims about aetiology and treatment have gone unchallenged within our community. In my view, it’s about time that we, as patients, carers and advocates help to correct that record, because we are paying the highest price for these misunderstandings.

    The same applies to much of the info provided in the International Consensus Primer. One has to take into account that this is written by researchers who comment on their own (CFS-) research to say how important and significant it is. We can’t just naively assume this is all correct.

    At the Science for ME forum we try to better understand any research into ME or CFS and we often come to the conclusion that things aren’t that sound or robust as is being claimed. That isn’t a cheerful message, but I suspect it’s an important one for progress to be made.

    I realize that many patients are too ill to follow the scientific literature but in essence, it’s quite simple: before we can speak of reliable evidence, findings have to be replicated by multiple research groups and few findings in ME- or CFS research meet that standard. So that’s the question we have to ask before claiming anything about the pathology or aetiology of ME. I hope that those who strongly object to Edwards’s viewpoint and think he’s dismissing any evidence join the discussion so we can figure out what makes sense and what doesn’t.

  • Sandra 5 December 2019, 5:31 pm

    Wendy
    I just went through the list you posted above of ME symptomology and said check, check, check etc as I went down the list. This disease and its many manifestations has left me disabled, housebound, and barely able to carry out basic activities of daily living. I fulfill the ME International Consensus Criteria. I am under the care of a neurophysiologist who sees many ME (ME/CFS, CFS if you will) patients. She has diagnosed me with an intractable acquired brain injury which includes a metabolic encephalopathy. In 1994 I was given the diagnosis of CFS after I became so disabled I could no longer function at all. The diagnosis of ME simply was not, is not, given in my country, the United States. It is not known to our physicians. Because of that simple fact, does that mean I am excluded from the ME community or do not have ME? Should I be excluded because of controversy and political contrivances set forth by certain people in authority at the time who came up with the CFS brainstorm disaster? I think not. Unfortunately I don’t think “true ME” is that rare. In fact I fear that the number of cases is steadily increasing. I believe there are MANY patients like me in this same position. We don’t like the CFS label any more than you do, but that doesn’t mean we don’t have ME. In my way of thinking, in order tackle this tremendous problem, we would do much better to stand with each other, whatever labels we may have been given, and work together to seek answers for this greatly suffering population.

  • Steve Hawkins 5 December 2019, 10:36 pm

    I’ve always thought that Prof. Edwards writes particularly well and clearly, developing his arguments with much more care than is seen in the pronouncements of the CBT cultists, for example.

    I’m not interested in getting bogged down in the usual endless to and fro over names and definitions: unless we’re all going to be assessed by the same diagnostician in the same way, there’s no way for us to compare illnesses with one another except by taking each symptom and sign as it comes.

    I do like to pick out any points that make me think, however, and I’m intrigued where Dr E says:

    “The only likely source of that (other than neural signals from the brain) looks to be the immune system, with the signal being some form of autoantibody, or a cytokine produced by T cells.”

    We’ve seen that the trials with Rituximab that knocks out B-Cells appeared to come to nothing, but what about knocking out T-Cells (or particular families of T-Cells)? If there is the possibility of overproduction of any factor from T-Cells is responsible for some ‘M.E.’ symptomatology, then knocking out those T-Cells, or looking at statistics for people in whom they are naturally low, or low through other disease, may be able to show up any links.

    So: What is the prevalence of M.E. among people with HIV: is it above or below the society norms?

    Are there any people who used to suffer badly from M.E. and who were unfortunate enough to also contract HIV? If Dr. Edwards conjecture is on the right track, we might expect that some M.E. symptoms may have improved as the T-Cells were knocked out by the virus.

    That said: I’m aware that there seem to be almost infinite varieties of immune cells, so it may well be that the HIV succeptible ones are a different group entirely from ones that might be producing the factors putatively causing the M.E.. It would be interesting to know if anyone with M.E. did ‘improve’ on contracting HIV though.

  • Guido Den Broeder 6 December 2019, 10:49 am

    Rituximab is a prime example of why it’s so important to distinguish between diagnoses. It can cure ME, but does nothing for most CFS patients and would put them at risk.

    The B-cells form the hideout of preference for latent EBV (and some other viruses that can play the same role), which interferes with the ability of the immune system to handle enteroviruses. The expectation is that knocking them out will induce the body to create replacement B-cells that aren’t infected with latent EBV, basically cleaning up the immune system so it can then finally deal with the enteroviral infection.

    Most CFS patients do not suffer from an enterovirus and are not significantly impaired by latent EBV.

    Because Fluge and Mella knew nothing about ME or latent EBV they selected the wrong patients for their larger follow-up studies, and a potential medicine for ME patients went out of the window.

  • Sue 6 December 2019, 9:20 pm

    While there has been a lot of “heat” in this discussion I have found both viewpoints interesting and helpful toward understand some common miseries. I am grateful to Dr Tuller for posting Dr Edwards’ at me post, Dr Edwards for writing it originally, Wendy and Guido for their critiques, and others for their contributions.

    We may have lost many of the physical and cognitive strengths we previously had, but we still have a lot of passion–and I am proud of us for using it.

  • Sue 6 December 2019, 9:21 pm

    Sorry that would have been “s4me” without autocorrect.

  • Sonya 12 December 2019, 4:56 pm

    I suspect the patient that improved after Rituximab was misdiagnosed with CFS. The patient was NOT Dxd with ME but instead, with CFS where the Oxford criteria is utilized. Because the patient had blood cancer they patient exhibited ongoing CF, he/she ended up Dxd with CFS and could have died from undiagnosed cancer.

    Once Rituximab took care of the cancer the CF (“CFS”) disappeared.

  • Sonya 12 December 2019, 5:15 pm

    Sandra

    As it turns out, having an ME, ME/CFS, or CFS Dx does not mean you have the illness thay the ICC, CCC, OR IOM were trying to describe. You apparently have an injury that is being swept into the ICC. If I had a Dx that could explain my symptoms I would be out of here! I would never involve myself with this mess again. You have a Dx that was never meant to be included. CCI, Enteroviruses, brain injury, EDS are not what they were trying to capture with these criterion. All of these have their own Dx, but the patients the criterion were developed for do not have any other Dx to explain what is going on except for the “metabolic trap” that Dr. Davis is looking into. His son Whitney was in the initial investigation of the metabolic paper as well as his looking at the DNA of infectious agents in the blood of 19 patients which was run against the CDC database of all known infectious agents. I think one patient had HHV6, no enteroviruses, and no known infectious agent was found in all. Nothing significant but an unknown DNA he is “building” that resembles African Sleeping Sickness was found in many if not all.