Who Hijacked ME?

To follow from Trish's post (https://www.s4me.info/threads/ltse-...type-2-me-or-new-diagnosis.27945/#post-422324):

The BPS Brigade have been accused of hijacking ME and replacing it with CFS emphasizing the symptom of fatigue and ignoring PEM. However from what I've read Ramsey's original definition of ME was about muscle fatiguability that resolved after 3 days, not PEM. I remember reading that PEM wasn't part of the definition until the 1990's so aren't patients and charities just as guilty of hijacking ME as the BPS?

 

I wouldn’t say this is the same as “hijacking”. It’s probably more that over the years, a lot of PwME noticed that they had another symptom too (as well as the muscle fatigability): that they felt worse after doing activity, not just immediately but the next day, or 2 days later. And also I suspect the reason why more PwME talk about PEM now is because PwME have been forced to exercise when it made them worse, and the symptom of PEM gives an explanation to that. I don’t know why Ramsay didn’t talk about PEM in his original work, but maybe some of his patients would’ve had PEM but he just put that under “fatigue”.

 

It's difficult to know what really happened.

It's possible to emphasize different symptoms and aspects in the same disease. That Ramsay emphasized these doesn't mean the patients didn't have the symptoms that are emphasized today. Maybe at the time physicians were trained to describe disease in slightly different terms. It's possible that ME has become a somewhat unspecific definition over the years but it's not clear that this has really happened (or that this is even a bad thing).

I would say that as part of PEM there is increased muscle fatigueability but that my flavor of ME is too unpredictable to obey rigid rules that demand a symptom be present for 3 days.

In my opinion ME isn't one thing anyway. It's more a phenotype that is the final destination for several different paths. That's why I think arguments about diagnostic criteria are a waste of time. If we understood the illness well enough to know how to clearly define it so as to select only patients with the same underlying biological problem then we wouldn't be having any such discussions in the first place (because we could just look at the presence or absence of the specific biological problem). The current case definitions are just a step along the way of figuring the illness out. The main reason for lack of progress is the lack of funding and the general attitude of disbelief from which that lack of funding results. And the disbelief is maybe because there isn't a simple way to demonstrate the core problem because there is a delay in its manifestation and the healthcare system isn't set up to work with that.

 

I suspect that the Royal Free patients were undergoing bedrest a lot, and simple tests of muscle function were done. Limited tests and special circumstances. So Ramsay wasn't wrong, its just that the findings are limited by context. Does anyone know the details of how muscle fatigability was determined?

In the decades since we have more and more knowledge in both our medical and patient communities. So our hypotheses have become more informed and more sophisticated. They are still hypotheses.

To me there are two phases in the research. We are maybe near the end of the first phase. In the first phase we use expert panel diagnostic criteria, no objective markers, with high risk of over and under diagnosis. Missing lots of patients, and including lots of patients with other (real) problems, means most studies need to be much larger than we have funding for, and results are usually unreliable, including being unreplicable.

We can expect when a finding is made that either it is by chance, or its for a small and specific subgroup, who while sick may or may not have ME. This will continue until by chance one of the hypotheses is close to accurate, or until we move to phase two. Answers can be found by chance, in small patient cohorts, but the odds are very much against it. This means lots and lots more studies, with lots and lots more funding. Oops.

The second phase begins with the first highly reliable biomarker. We cannot make huge progress, except by chance discovery, without a reliable biomarker. What we can do is engage in repeated cycles of hypothesis and test, and without a biomarker the scepticism that impedes grant provision will only continue. Of course it does not help that the mostly unevidenced hypotheses of the BPS crowd also impede funding chances.

Repeat CPET seems to be about 86% reliable. Good, but not good enough for phase two.

I am a case in point. I am an encephalitis survivor. I have ME symptoms, though I no longer meet most diagnostic criteria for CFS. I do meet ME and SEIDS criteria though. This is because I can have long periods of time with no energy, high incapacity, OI and PEM, including rapid fatigability, but not chronic fatigue. I am at the point that if I pace enough fatigue is not an issue - just a great many other ME symptoms. Without a reliable diagnostic marker I cannot be sure I have ME. However if I look for scientific literature on cases like mine, I am left with only one answer - its the ME literature or nothing. So either I have ME or I have a disease probably in the same family as ME.

I suspect many of us (and this might not be the case) will wind up with disproof of an ME diagnosis once a marker is found. I also suspect we will discover ME is actually a group of very similar disorders, and those rejected for an ME diagnosis under the first biomarker will mostly get diagnosed when biomarkers for other subtypes are found. However I cannot rule out that ME has many manifestations but it is one overarching disorder. So many biochemical pathways and physiological loops are involved that the sheer complexity could drive the myriad symptoms.

We really need diagnostic biomarkers. Badly.

 

Does anyone identify more with long covid without the lung part,well before long covid.

 

Well to my mind, its obvious, ME CFS is a bucket diagnosis as there are all sorts of conditions which cause CFS being recognised as ME.

I once acted in a school play called "The Real Inspector Hound" by Tom Stoppard which has a famous line in it "Will the real inspector hound please stand up?" I played the part of Magnus Muldoon wheelchair bound tycoon who it turned out was in fact ... dun dun duuuh! ... the real Inspector Hound.

If you ask which is the real ME its more like asking which is the authentic cheese, IMHO there are many different kinds and we really need to distinguish the different kinds of cheese ... by which I mean ME / CFS subtypes ... because they are not the same.

Historically blending them all together in a bucket diagnosis fondu is the result of obfuscation perpetrated by the BPS brigade (especially King's College who self confessedly pride themselves on being biased for money) because they were acting as PR consultants or pseudo-academic spin doctors on behalf of interests who didnt want the different subtypes distinguished because it would increase their liabilities as medical insurers for more serious conditions hidden among less debilitating fatigue syndromes. If they are all treated as monday-morningitis and given a condescending chat and chalk pill placebo its much cheaper for them.

Putting the different subtypes in the same bucket also creates a huge problem for getting clear data from patient studies so it qualifies as anti-science.

IMHO the ME research community has not really bitten the bullet and tackled this at all convincingly and IMHO that may be partly because of a reluctance to split the financial powerbase of patient crowdfunding. The more subtypes you include, the bigger the crowd the more the funding, which has to date been barely sufficient to do too few studies and nowhere near ample.

IMHO this funding crisis has created a realpolitik of not rocking the boat of the patient community and our tribal identity, unfortunately failing to challenge and unmask the legacy of ignorance and confusion created by the BPS bucketeers in the process. IMHO we need to reintroduce a little perspicacity into proceedings but the causes of the situation need to be addressed and this means serious funding from outside the patient community i.e. government funded research programs so researchers can afford to distinguish the different subtypes and find ways to treat each appropriately.

Our community coherence behind a shared identity is admirable but also a potential obstacle and I hope we can be smart enough to negotiate our way around it with the necessary skill and mutual respect it takes to discover the truth behind our shared yet distinct realities. I think the large long covid community joining the fray will help with gaining recognition but I also think we need to recognise this aspect of our own patient politics and handle it carefully to allow research to make meaningful progress.

I sympathise that the bucket has been a necessary workaround to date and believe we should continue to work together as a community under a larger umbrella of CFS because we all face similar real world obstacles in the form of exclusion and diminution of our situation due to the weakness CFS creates and the often aggressive basis of human social interactions which we cannot easily challenge or overcome as individuals with CFS. So I feel we have a common political situation because of the way this kind of condition is treated and that will continue to be the case no matter how many different causes for our conditions are discovered.

If we distinguish subtypes in a clumsy way there is a risk the community could decohere and reduce our bargaining power before we get good funding which we dont want. I think we need to rally together and consciously invent a super-umbrella under which all CFS conditions can work together for the common cause of recognition, research and appropriate treatment while recognising there are different causes creating this kind of response from the human body.

I am writing what I really believe from the heart here but I genuinely wonder, does that make sense to other people?

 

Only if you make the deliberate assumptions that (a) patients and charities are responsible for clinical and research definitions and (b) any changes made by the authors of the definitions that include PEM weren't making a genuine attempt to improve the description of a paticular illness.

 

I think this is a crucial goal. We need not only other ME patients but to work in cooperation with any similar disorder. Any advance in one might have an impact on research in the other. People will of course put preferential action on concerns for their own subtype. That is understandable. Right now Long Covid is looking likely as a similar disorder, if not the same disorder for a subgroup.

It is too early to tell if ME subtypes are mostly not the same. It does look very possible though. The further you get from specific ME criteria the more likely it becomes.

BPS influence would be much less if it did not fit into both corporate and government goals of cost saving. They had a ready audience. Telling insurance companies or government accountants that they will have to absorb the costs without more research does not usually go over well. So they put support behind the contrary story, and this is used by BPS proponents though I am not sure we are fully aware of all the ways this can happen. We do know that big insurance saves billions every year with regard to ME alone. Denying claims means higher profits. However without biomarkers and causal pathways its very hard to push change in this situation. Here in Australia I had no chance of getting into our government run disability insurance scheme, as the barriers are too high. Money saved . . . but lives harmed.

 

In my view its critical to recognize these two types of definitions do not have to be the same. Clinically a broad definition is probably better, for research you want the tightest definition you can devise.

 

Not necessarily, it will depend on the research project.

 

This is already happening—“Long Covid” groups have allied with MECFS groups. OMF casts a broad net “Since our inception in 2012, Open Medicine Foundation (OMF) has raised over $36 million to fund open and collaborative research and improve health care for millions suffering with multi-system chronic, complex diseases (msCCD) such as Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS), Long COVID, Post-Treatment Lyme Disease, and Fibromyalgia.”

A lot of people on these various forums claim that there are many subsets of ME/CFS based on the prominence of particular symptoms, and as mentioned above by Trish—without robust biomarkers, this doesn’t mean a whole lot.

For example for inflammation there are five cardinal symptoms—pain, heat, redness, swelling, and loss of function. If everyone person here banged their toe hard against their bed frame today with the same same velocity, some people would complain more about the swelling and some more about the pain— but they all have an inflamed toe (and in this case all with the same cause).

 

I've said before that I believe strictly defined ME is 4 or 5 different illnesses and that CFS could be up to 20.

 

Obviously you adapt things according to the type of study. This can also include additional cohort requirements, such as deliberately focusing on those with OI or a specific type of OI, plus extra exclusions. The point is that a cohort needs to be as strict as you can manage with the goals in mind, that is mostly to minimize bias. For a clinical trial though you might want to be as inclusive as possible, but then subgroup later for analysis if you have the funding and opportunity. You might, for example, want to know how many within a broad CFS diagnosis have a specific problem, or respond to a specific therapy. If I recall correctly I was once a subject in a broad CFS study to look for a particular genetic marker (cortisol binding globulin mutation) that is found in some families with many patients having CFS. I think it was quite rare, and only in specific families, but you need broad cohorts to determine how common it is in various or specific cohorts.

 

I always thought that disbelief led to lack of funding led to... I guess it's a vicious cycle.

 

Just been reading Ramsey's definition again here (https://www.cfids-me.org/ramsay86.html). He notes emotional lability as a cardinal feature of ME. No body really talks about that as a symptom of ME any more.

@Jonathan Edwards

 

Possibly that could be coz of how medical types are trained to respond to such things?

 

Wasn’t the point of raising Ramsey here, that if we take his definition as classical ME, other people advocating biomedical approaches have subsequently diverged from this too. So that not only could the psychogenic advocates be said to have hijacked ME, but also today’s biomedical advocates. Then people commented in relation Ramsey’s definition itself, hence the emotional lability comments.

Personally I would see refining or developing a definition of the illness as distinct from hijacking it, but this is perhaps lexicographic sophistry. But certainly today’s biomedical researchers are on the same ballpark as Ramsey, though they may disagree with him on many issues, whereas the psychogenic or BPS ideologues are a million miles distant.