“Dr. Ken Friedman and Dr. David Maughan – ME/CFS and Long Haul Covid Similarities and Ramifications” podcast

The present set can be, and frequently is, interpreted as "the aches and pains of every day life". These facts fail to convey degree. The present wording describing symtoms - in lieu of biomarkers - usually works against imparting a sense of the catastrophic degree to which pwME are afflicted.

That's bad science and its even worse marketing. No one buys what we're telling because the packaging sucks.

Case in point.

 

They were the reason, in that all government funding for biomedical research stopped and all was given to psych research instead. (Eg, PACE which wasted £5 million of taxpayer money that would have been better spent on useful research by real scientists.) What little scientific research still continued, had to be fundraised for by patients most of whom were/are too ill to earn an income. It's still pretty much the case, unfortunately.

 

case of what?

 

But is that right?
My understanding is that a policy of focusing on treatment was made around 2001-2002 by MRC since research into cause had stalled.

I cannot think of much productive research into cause in the 1990s. The biomedical stuff seems to have ground to a halt at least five years before the psychs stepped in. I may be wrong but those are the dates that come up in my mind.

 

OK so if the criteria are that bad why has this not been discussed here over the period of the NICE guideline development? Why were the NICE criteria approved by at least four intelligent patients on the committee and some very open-minded sympathetic professionals like Caroline Kingdon and Luis Nacul?

How would you do the packaging better?

I don't see how criteria are going to convey degree. You cannot say it isn't a heart attack until he's stopped breathing or it isn't cancer until she's lost four stone. You cannot say it isn't ME if, as I am told, quite a few mild to moderate cases can still do a 2day CPET test.

I appreciate the right to grumble when things are crap but it doesn't help to grumble randomly without any indication what might be a solution.

 

Wording.

If you're asking me to fix it now, I no longer have the skill. But I know that how we are currently conveying things is a slow endless loop.

I know wording like fatigue and unrefreshing sleep and malaise and brain fog and lingering etc are strikingly inadequate and misleading and harmful.

Who's writing this tripe?

This invites the BPS crowd and it invites comparisons to healthy people with "similar"complaints, and to categorizing in all inclusive patient sets because our circumstances aren't life threatening, they aren't dire; they are little more than the usual fare that comes with life's typical bumps and bruises.

 

Hm.

The way things are packaged right now you have medics like me, Brian Hughes, Nigel Speight, Willy Weir, Ilora Finlay, Carol Black, not to mention Dave Tuller, Mary Dimmock, Saugstad, Rönning and people all over the world, spending many hours, mostly entirely for free, trying to get things in to some sort of shape.

When I hear people grumble about criteria that is when I begin to think... why do I really bother. If PWME can think of nothing better than to argue with each other what their illness is maybe let them get on with it.

But because the criteria reasonably reflect what I understand to be a seriously disabling illness I don't carry on thinking that.

And as I have always said, if you cannot convince me then there is precious little chance you will convince those of my colleagues who have been lost to the dementors.

 

Dementors?

We've lots of smart advocates over the years, and I applaud their efforts.

We still shoulder the burden of crap descriptions of ME/CFS that your average clinician will see.

We need to draw a line in the sand, and I say lets start with Descriptors.

 

@Jonathan Edwards I accept that case definitions for ME/CFS do not include disease onset. Many papers emphasize that there is a higher ration of infectious onset.

This paper mentions

No source of that particular knowledge, but many papers make mention of the infectious onset in the background of their study.

 

A better article here @Jonathan Edwards
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6839177/

Here is the full abstract:

A logistic regression analysis of risk factors in ME/CFS pathogenesis (2019) Lacerda et al.

Background
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is a complex disease, whose exact cause remains unclear. A wide range of risk factors has been proposed that helps understanding potential disease pathogenesis. However, there is little consistency for many risk factor associations, thus we undertook an exploratory study of risk factors using data from the UK ME/CFS Biobank participants. We report on risk factor associations in ME/CFS compared with multiple sclerosis participants and healthy controls.

Methods
This was a cross-sectional study of 269 people with ME/CFS, including 214 with mild/moderate and 55 with severe symptoms, 74 people with multiple sclerosis (MS), and 134 healthy controls, who were recruited from primary and secondary health services. Data were collected from participants using a standardised written questionnaire. Data analyses consisted of univariate and multivariable regression analysis (by levels of proximity to disease onset).

Results
A history of frequent colds (OR = 8.26, P <= 0.001) and infections (OR = 25.5, P = 0.015) before onset were the strongest factors associated with a higher risk of ME/CFS compared to healthy controls. Being single (OR = 4.41, P <= 0.001), having lower income (OR = 3.71, P <= 0.001), and a family history of anxiety is associated with a higher risk of ME/CFS compared to healthy controls only (OR = 3.77, P < 0.001). History of frequent colds (OR = 6.31, P < 0.001) and infections before disease onset (OR = 5.12, P = 0.005), being single (OR = 3.66, P = 0.003) and having lower income (OR = 3.48, P = 0.001), are associated with a higher risk of ME/CFS than MS. Severe ME/CFS cases were associated with lower age of ME/CFS onset (OR = 0.63, P = 0.022) and a family history of neurological illness (OR = 6.1, P = 0.001).

Conclusions
Notable differences in risk profiles were found between ME/CFS and healthy controls, ME/CFS and MS, and mild-moderate and severe ME/CFS. However, we found some commensurate overlap in risk associations between all cohorts. The most notable difference between ME/CFS and MS in our study is a history of recent infection prior to disease onset. Even recognising that our results are limited by the choice of factors we selected to investigate, our findings are consistent with the increasing body of evidence that has been published about the potential role of infections in the pathogenesis of ME/CFS, including common colds/flu.

 

Yes, I am not in any way disputing that there is evidence for infections being noted at the beginning of ME in a good number of cases.

But that has nothing to do with infection being part of the definition of ME/CFS. The concept of ME/CFS is a concept of a state of ill health, without reference to cause because that is unclear. Another concept is post-viral fatigue, which IS defined in terms of a causal association, or at least an association.

The predominant view is that even if there is an infective trigger there is no evidence that infection is present long term or that treatment directed at infection is relevant. That might prove wrong but I actually doubt it. So defining the illness of PWME/CFS in terms of infection has no particular motivation. And for those without such a history it makes no sense.

 

Thank you for explaining- The case definitions represent a collection of symptom but do not describe onset.

I would poke the bear one last time, and say that there is a difference (at least in my mind) between post-viral fatigue and post-viral fatigue syndrome. It is so much more than fatigue.

 

Yes, I think there is an important distinction there that may be missed.
PVFS seems to have been created as a concept some time around 1980 to recognise that a group of people do not just have fatigue for a few months after EBV (PVF) but continue with a more specific and complicated syndrome - which is the syndrome we now recognise as ME/CFS.

Studies like Dubbo may have given the false impression that PVFS or (PV)ME/CFS is just the tail end of PVF. Maybe people have not looked at symptom pattern in that first six months carefully enough. My intuition is that people with PVF feel 'when will I get rid of this feeling I have had since EBV?'. I suspect that people with PVFS or PVME/CFS much more often feel 'what is this new rollercoaster ride I find myself on since having EBV?'.

 

It's my 6th year since EBV and although I could tell when the acute infection ended, the symptoms afterwards didn't feel like something entirely different and new but more or less the continuation of something that started with EBV: it felt like the immune system kind of got stuck in that mode. For this reason a lot of people in similar shoes felt that maybe the infection just never ended and somehow the virus keeps hiding and triggering the immune system. I was a member of a mononucleosis forum for almost two years before I realized that's probably not what I have anymore. It was the length that made me realize that. The other people there (most of them suffering from post-viral symptoms and not the acute infection) had all kinds of symptoms, ranging from fatigue to blurry vision to pain and racing heartbeat and intermittent fever, PEM, pins and needles etc. But from what I remember, almost everyone felt it was connected to EBV and not something totally different starting afterwards. I also remember people mentioned CFS from time to time, but more like in the context of something they knew could happen but definitely didn't want to have, they were afraid of it.

 

Yes, there was little or no productive research into cause in the 1990s, because the psychs took over in about 1988. I remember in c1988, after I had recovered, reading an article about some psychiatrist who said, regarding the research into T-cells as respects ME that was going on at the time, 'A little more psychology and a little less T-cells would be in order'. I thought 'Who is this clown?' and thought how glad I was to be recovered and well out of all that. I only found out after I relapsed many years later, that that person was Wessely. Biomed research hadn't ground to a halt 5 years before they stepped in, it was still going on and it at first overlapped with their stepping in, then faded away after the psych takeover.

In 1991 I worked at a psych unit and was friendly with a consultant psychologist who I'd told about my having had several years of ME, and one day he told me 'They finally found out what ME is!' Wow! I thought. 'What is it?' I asked excitedly. Him: 'It's just depression.' Me, gobsmacked: 'Er, what? No, it's not.' Him: 'Yes, that's all it is, it's just depression'. Me: 'Well no, I've had it and I can 100% assure you that it's not even a bit like depression.' At that point I had to drop it because I didn't want to get into an argument and wanted to keep things friendly. But the point is, that's how much of a stranglehold the psychs got on a horrific disease which only three years earlier was having research into T-cells and brain blood flow reported in the news. Now all that was just - GONE.

 

Well that could be a good survey question- and I believe it's been done before- The disease trajectory is heterogenous within ME, from persistent, to good day/bad day, to gradually declining. For me I cannot say I have good day and bad days- they are all the same- I have just about the same level of disease day in, day out. Month in, month out, year in, year out. Nothing changes, unless I diverge beyond my capacity or I get sick with a virus.

I believe Dr Nacul published a paper on the natural history of ME
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8835111/

 

Wessely's interest emerges at the time the biological work declines, yes, but I don't see how we can know what caused what. Durval Costa's work on brain blood flow actually came out in 1992-4, although there were never any really definitive findings.

Wessely's comment on T cells, to be fair, was after he had tried studying T cells himself and got nowhere. Studying T cells is generally a waste of time and in 1988 I was going around saying a bit more physiology and a bit less T cells might help for rheumatoid arthritis. Forty years later none of the T cell research has told us anything but I realised in 1996 that the B cells, which everyone was ignoring, held the key.

Andrew Lloyd was another who started off looking for immunological changes and gave up and turned to psychology.

 

I never understood what triggered my illness. I remember that it was initially episodic and very confusing because I often felt well enough to go back to school but then after a few days started struggling again. And there were longer periods of feeling okay and longer periods of feeling worse than usual.

It took me too long to work out that I was chronically ill. In part due to disbelief of others who didn't believe that such an illness could exist. Eventually I decided that having a lot of difficulty doing ordinary things despite good motivation could not be normal. The difficulty was more that I felt increasingly unwell doing them until a point was reached where self-preservation instinct prevailed. So unable to do things because I was able to endure only a limited amount of suffering that doing these activities caused. But to other people I just "didn't want to do things" for no good reason.

Also adolescents don't really have a concept of chronic illness. To me it was something that people over 60 had where they took a pill daily. All details were unknown. I didn't know how awful it is.