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How long before the misery of ME is taken seriously? and Money’s the motive for calling ME a myth - Sophie Palmer
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1. Both formal studies and basic employment screening through the pandemic have shown that many people have asymptomatic acute SARS-CoV-2 infections. Some of them have subsequently gone on to develop LC. So we don't know for certain that pwME didn't have a viral trigger.
2. It could still be of viral origin, even without a viral trigger. Ie immune dysregulation for any reason leading to loss of immune control of our permanent-resident viruses acquired in early life (esp herpesviruses).
2. It could still be of viral origin, even without a viral trigger. Ie immune dysregulation for any reason leading to loss of immune control of our permanent-resident viruses acquired in early life (esp herpesviruses).
Shadrach Loom
Senior Member (Voting Rights)
Those points, while true, are insufficient justification for the claim made in the article’s first sentence. There can be doubt that ME is a neurological illness, and there can be doubt that it is of viral origin.
The article isn't consistent on the view about cause. It has quite a few errors and oversimplifications. I wonder if ChatGPT had a significant hand in the article's construction?
There's even the obligatory image of an attractive woman with a hand to her head. And a dig at immunisation programmes.
On the plus side, I guess it's getting the message that ME/CFS is a problem to a particular "Conservative Woman" demographic. I'm not sure how much traffic TCW gets, probably not much.
It is good to see articles conveying the seriousness of ME.
It's curious though when ME is spoken of as time limited. From the article, " Many suffer for ten years or more..."
This sentence goes on: "and only five percent recover".
On the one hand, suffering for ten years probably sounds like a terribly long time to healthy people. And, it is. But on the other, it also sounds like ME is time limited, except for the bit about "only five percent recover".
Due to BPS propaganda, the general public may see ME as time limited, if they indeed view it as a health problem at all. Because the anti-ME movement has had a decades long strangle hold on research funding, and pretty much everthing else for this disease, we still lack serious recognition of this illness.
It's curious though when ME is spoken of as time limited. From the article, " Many suffer for ten years or more..."
This sentence goes on: "and only five percent recover".
On the one hand, suffering for ten years probably sounds like a terribly long time to healthy people. And, it is. But on the other, it also sounds like ME is time limited, except for the bit about "only five percent recover".
Due to BPS propaganda, the general public may see ME as time limited, if they indeed view it as a health problem at all. Because the anti-ME movement has had a decades long strangle hold on research funding, and pretty much everthing else for this disease, we still lack serious recognition of this illness.
Couldn't ChatGPT be trained to prompt images from pictures collected off ME-patients for such queries?
Dr. Jason's summary of how this can affect pwME physically and emotionally is right on.
boolybooly
Senior Member (Voting Rights)
If you are right and I have heard enough people say they have different experiences to believe you are, then I would say the logical deduction would be there are different subtypes collected in the one diagnosis, which need to be identified and haven't been. Its the first thing which needs to happen and it still hasn't happened.
Which is why I am somewhat disaffected with current research initiatives.
If people have different symptoms it stands to reason they have different conditions.
I would dispute the idea that there is only one type of illness diagnosed as ME in the first place.
I regard this as an open question. Its fairer to say that we cannot be sure ME is one disease. It still might be several or many diseases though. We do not have a definitive answer.
On the myriad of symptoms, ME is associated with thousands of different biochemical changes, and different physiological states, though they tend to cluster in pathways. In about 2015 I gave up counting, and it was easily over 2500 abnormalities with at least 2 SD difference and a prevalence of over 80%. Nothing yet hits over 95% or is physiologically very likely to be a cause. We are still putting forward hypotheses and testing them, but we are not at a point of understanding causality yet. Many potential causes are still being investigated.
Over time my symptoms have varied a lot, but I would not like to say I had one disease at time A, and another at time B. With so many things affected it is easy to suppose that thousands of factors that are not ME factors can influence these pathways, and hence potentially influence symptoms.
Let me give an example, one that profoundly changed my opinion on CFS. In 2012 I spent two months in hospital with most of that resting. Coming out of that I had NO chronic fatigue, but every other symptom was the same. Put this together with the early Workwell finding (then Pacific Fatigue Labs) that on close questioning none of the early patients had fatigue, they had something else mislabelled as fatigue, and you start to see a different picture.
Before even looking at fatigue as a major factor in an individual patient I would want to know if the patient is successfully pacing or not. If not then any real fatigue, and not a mislabelled fatigue-like state, might be a result of operating beyond their limits. We need this question answered in a decent study, and its not hard to come up with many similar research questions.
boolybooly
Senior Member (Voting Rights)
As I understand it @alex3619 the story goes that what you describe is the nature of PEM, it only becomes apparent when you test your capacity for activity and behaves like inflammation caused by exertion, hence the glass cage.
People appear to call it fatigue because it follows from exertion and is exacerbated by further exertion but is not the same phenomenon as normal fatigue, it is really a coincidence of timing in relation to exertion which has lead to that misnoma. So we call it abnormal fatigue to distinguish it. Yet how do I know the abnormal fatigue I experience has the same cause as the abnormal fatigue someone else suffers from? In all honesty I don't.
If other people share the same identifiable cause, like a virus, then it is credible they experience the same condition. If it does not have the same cause then does it have the same nature? Likewise, we dont know.
We dont know if some might have a subclinical virus causing the same ME symptoms without showing any viral symptoms as someone with a diagnosable virus. Or whether different kinds of virus can cause similar kinds of ME, like EBV and COVID or CMG and Echovirus or Hepatitis or whatever. We dont know whether some have a different class of pathogen such as Lyme's or some have an unrecognised form of blood disorder causing debilitating disease with a different origin. We dont know. Is Witney Dafoe dealing with the same condition I have only more severe? I don't know. Did Lynne Gilderdale have the same condition as Sophia Mirza and Annabel Senior and is it the same as mine? I dont know. Noone does.
If we don't know, then we need to find out, why some patients with diagnosed ME self report no viral infection. It is basic triage. Patients are not just being awkward and they are not lying, they report the truth for themselves and the truth is different for different people yet there are groups among those differences.
And what seems to happen is different research projects currently use different selection methods for patient cohorts and we end up comparing results of studies of ACAI (atypical chronic active infection) with outbreaks of cryptoinfections with unidentified disease agents like Royal Free Hospital and Incline Village, with heterogenous collections of patients with multiple inflammatory conditions. Goodness only knows how many different conditions are in the biobank.
We are treating them all as the same condition but we dont really know whether there is one component of their symptoms which they have in common, or whether they have different disturbances of the myriad different inflammatory pathways which produce similar reports from patients but do not have identical causes and cannot be treated successfully in the same way.
In this age of antidiscrimination, we need to discriminate different patient types in order to find out what is wrong with each and help each appropriately. Drs Kerr and Gow tried to do that with gene expression studies and did not get the chance to take it to the scale required to get a meaningful result and then everyone stopped doing gene expression studies. Why?
I have my fingers crossed of course, having spat at them, that Decode ME will find something to help us get to the bottom of these questions. Further down the road I hope that big data for gene expression will be revisited and will tell us more.
People appear to call it fatigue because it follows from exertion and is exacerbated by further exertion but is not the same phenomenon as normal fatigue, it is really a coincidence of timing in relation to exertion which has lead to that misnoma. So we call it abnormal fatigue to distinguish it. Yet how do I know the abnormal fatigue I experience has the same cause as the abnormal fatigue someone else suffers from? In all honesty I don't.
If other people share the same identifiable cause, like a virus, then it is credible they experience the same condition. If it does not have the same cause then does it have the same nature? Likewise, we dont know.
We dont know if some might have a subclinical virus causing the same ME symptoms without showing any viral symptoms as someone with a diagnosable virus. Or whether different kinds of virus can cause similar kinds of ME, like EBV and COVID or CMG and Echovirus or Hepatitis or whatever. We dont know whether some have a different class of pathogen such as Lyme's or some have an unrecognised form of blood disorder causing debilitating disease with a different origin. We dont know. Is Witney Dafoe dealing with the same condition I have only more severe? I don't know. Did Lynne Gilderdale have the same condition as Sophia Mirza and Annabel Senior and is it the same as mine? I dont know. Noone does.
If we don't know, then we need to find out, why some patients with diagnosed ME self report no viral infection. It is basic triage. Patients are not just being awkward and they are not lying, they report the truth for themselves and the truth is different for different people yet there are groups among those differences.
And what seems to happen is different research projects currently use different selection methods for patient cohorts and we end up comparing results of studies of ACAI (atypical chronic active infection) with outbreaks of cryptoinfections with unidentified disease agents like Royal Free Hospital and Incline Village, with heterogenous collections of patients with multiple inflammatory conditions. Goodness only knows how many different conditions are in the biobank.
We are treating them all as the same condition but we dont really know whether there is one component of their symptoms which they have in common, or whether they have different disturbances of the myriad different inflammatory pathways which produce similar reports from patients but do not have identical causes and cannot be treated successfully in the same way.
In this age of antidiscrimination, we need to discriminate different patient types in order to find out what is wrong with each and help each appropriately. Drs Kerr and Gow tried to do that with gene expression studies and did not get the chance to take it to the scale required to get a meaningful result and then everyone stopped doing gene expression studies. Why?
I have my fingers crossed of course, having spat at them, that Decode ME will find something to help us get to the bottom of these questions. Further down the road I hope that big data for gene expression will be revisited and will tell us more.
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It's also possible some people with a unknown ME trigger actually had an asymptomatic infection but were unaware of it. This is showing up as a thing with covid testing meaning more people are finding out they have an asymptomatic case and then getting long covid, later diagnosed as ME.
If ME is a response to a viral infection its entirely possible that infections that do not show symptoms are a cause. Its also possible that one or more biochemical pathways involved in viral defence might be activated by other triggers. Its the pathways that might be in common more than the pathogens or other trigger. We just do not know.
I have long considered that in an ideal world we would have very large studies funded, and they would take into account specific pathogens. One of the issues here though is we do not need to just know the pathogen, but the specific strains of the pathogen. There is so much that needs to be investigated, and so little funding and broad researcher interest.
For a more pure post viral ( or pathogen) investigation we already have some bases covered. Like post SARS, and post Q fever, and post Covid. Given the funding the current best option, despite huge research fails, is investigating post Covid-19. Yet even there we need stratification in the analysis. What is due to viral damage, and what is due to the way the body reacts to the virus? Different symptoms, different pathophysiology, same viral trigger.
PS While I wrote "same viral trigger" we know with Covid-19 there are many strains and they have varied virulence. Does this matter?
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Peter T
Senior Member (Voting Rights)
Also with viral involvement, it is possible that a specific viral infection is a necessary precondition rather than a sufficient cause, as is possible with MS and EBV.
In ME it could be that exposure to a specific virus or group of viruses sets the necessary preconditions for developing ME, and that this can occur with or without the occurrence of an obvious active infection. Once this priming has happened the individual is a ticking time bomb, but some additional currently unknown factor/event is required to set symptomatic ME going.
So then the difference between the various onset types relates to the relative timing of the preconditioning virus exposure and the triggering of ME symptoms. Then those whose ME onset seems unambiguously associated with an active infection experience then either the preconditioning virus and the triggering factor/event in such rapid succession that they subjectively seem simultaneous, or they were primed by previous virus exposure with a subsequent active viral infection serving as trigger.
This also means that once the preconditions have been met, very different triggers can have more or less the same consequences. For example being near the edge of a cliff is the necessary precondition for falling off it, but a fall can be precipitated by very different trigger events: being drunk, being hit by a strong gust of wind, being pushed, an inner ear infection, etc.
(Not necessarily advocating this idea, but rather exploring it as a theoretical possibility. Perhaps the weakest aspect of this argument is the idea that only one or one of a narrow group of viruses are the precondition, with perhaps EBV being one of the strongest candidates, which means that say ME type Long Covid results from prior exposure to EBV with the Covid 19 infection being just one of any number of possible random trigger events which feels implausible.)
In ME it could be that exposure to a specific virus or group of viruses sets the necessary preconditions for developing ME, and that this can occur with or without the occurrence of an obvious active infection. Once this priming has happened the individual is a ticking time bomb, but some additional currently unknown factor/event is required to set symptomatic ME going.
So then the difference between the various onset types relates to the relative timing of the preconditioning virus exposure and the triggering of ME symptoms. Then those whose ME onset seems unambiguously associated with an active infection experience then either the preconditioning virus and the triggering factor/event in such rapid succession that they subjectively seem simultaneous, or they were primed by previous virus exposure with a subsequent active viral infection serving as trigger.
This also means that once the preconditions have been met, very different triggers can have more or less the same consequences. For example being near the edge of a cliff is the necessary precondition for falling off it, but a fall can be precipitated by very different trigger events: being drunk, being hit by a strong gust of wind, being pushed, an inner ear infection, etc.
(Not necessarily advocating this idea, but rather exploring it as a theoretical possibility. Perhaps the weakest aspect of this argument is the idea that only one or one of a narrow group of viruses are the precondition, with perhaps EBV being one of the strongest candidates, which means that say ME type Long Covid results from prior exposure to EBV with the Covid 19 infection being just one of any number of possible random trigger events which feels implausible.)
boolybooly
Senior Member (Voting Rights)
Absolutely, I remember when the news broke that COVID was getting into old peoples' homes and was chatting on the phone to my then neighbour who is an elderly woman with MS and she was quite concerned to self isolate effectively. We were discussing the news and she asked how that could happen and I answered immediately it was asymptomatic transmission, which was all over the news the following week confirming my statement because it is the only thing which makes sense.
The medical model of viral replication and transmission had been developed from the perspective of symptoms, because that is what doctors deal with, there was no reason to cure someone who is not reporting ill, or at least they could not see one way back then... 5 years ago! ... so they had no conception it was happening.
From a different perspective it is obvious. Zoological game theory regarding reproduction strategies of parasites suggests they won't benefit from killing their hosts and need their hosts alive in order to spread themselves, not because they are benign, because evolution is completely pragmatic and living things self-replicate or go extinct. Asymptomatic infection is one possible strategy which would qualify as a success if the virus remains alive and replicating and spreads to other hosts.
Then there is the host strategy to consider, dont get me started on sneezing and self infection behaviours!
So viruses behave differently in reality compared to the medical dogma. As I learned when one doctor told me to my face "that doesn't happen" when discussing my symptoms. *sigh*
The point being, asymptomatic transmission killed a lot of vulnerable people who paid the ultimate price for their carers' ignorance, because the care staff and their medical advisors had no idea what was possible with virus transmission and did not act appropriately soon enough. They learned the hard way asymptomatic transmission is possible.
As you say, if COVID can be asymptomatic and still cause longCOVID then why cannot other viruses be asymptomatic and yet later cause ME? We just dont know if this is behind ME without viral symptoms.
We dont yet have a way of investigating asymptomatic or subclinical infections. My suspicion is that there are a lot of subclinical infections doing the rounds year in year out. By subclinical I mean viruses which do not produce such severe symptoms that they require clinical attention or produce obvious clinical symptoms like a cold, cough or temperature yet can still produce a few days of feeling low or a spell of vertigo or whatever.
You can almost guarantee they are out there but who is monitoring them and perfoming epidemiological study? Noone I know of, maybe the odd lone lab, yet these viruses could have an impact on healthcare if critical procedures are carried out when someone has a subclinical infection. We should really be monitoring them for public health and following all viruses, subclinical or clinical the same way we monitor road traffic and taxable income!
I used to call this the two hit hypothesis, but later amended that to the multiple hit hypothesis. I had in mind the staged onset idea as well. Many are sudden onset, a good number slow onset, but some are also staged onset. Each infection makes things worse like going down steps into hell. So I suspect its possible to not only have subclinical viral or other infections, but subclinical ME as well. Then another infection makes it worse, and again, until it becomes obvious something is wrong.
They absolutely know this but then have no way to investigate, and my experience of doctors is they do not concern themselves with things they cannot investigate.
We do track specific viruses, such as Covid-19, in sewerage. Yet there are something like tens of thousands of known viruses in humans alone if I recall correctly. Only those of current serious concern get tracked, such as in a pandemic or epidemic. We have a viral chip that can detect most of them though I do not know how reliable or cost effective that is.
What about the idea that stages possibly don’t all need to be viral reinfection or a new viral infection.
Things on my possible list for gradual onset include a nasty fall, menopause onset, very stressful caring responsibilities.
Things on my possible list for gradual onset include a nasty fall, menopause onset, very stressful caring responsibilities.
In fairness, at the practical clinical level there is not much more they can do.
But it is a serious limitation.
For me it was abruptly losing PEM (after cumin treatments). Most of the other symptoms remained ( I also lost the need to take T2 every 21 days). So, since the ME criteria requires PEM, do I still have ME or did I suddenly develop a completely different disease with identical symptoms and responses? I think that ME has a common core dysfunction, but it affects different parts of the brain differently due to individual genetic and developmental variations, which affects different parts of the body to different extents, resulting in a wide variety of symptoms and responses to factors. If they studied enough PWME, they might find correlations between brainfog severity and allergies, or hidden viruses, or obesity, or other such factors.
Sadly, someone will probably look for correlations between ME symptoms and astrological signs, summs of their ancestors' birthdates, or other such nonsense, and find some correlations (by carefully cherrypicking the data).
boolybooly
Senior Member (Voting Rights)
Sure and to be fair they absolutely cant because of state level supervisory regimes intended to stop quackery which we know is another real problem due to tendencies towards shamanic cultishness with some individuals.
Whiffling on - Medics have a book of rules and the rules are dogma and slow to change, like religious traditionalism but that has a reason and is so people dont make mistakes and is the same natural human response of conservatism (small c) due to valid concerns and life experiences.
Medics have to conform to the rules to be deemed acceptable by the state apparatus and if they dont they are expelled from their professional bodies. So they are obliged to follow received wisdom and not extemporise. That is the deal they make on entering the profession.
At the same time we need to learn from our mistakes. The rules have to change and sometimes quickly as with COVID.
The book of rules has been one of the big obstacles in gaining recognition for ME and thanks to certain parties, who helped presiding decision makers to see things more clearly, it has been somewhat revised of late which I think is a good thing.
In addition COVID has pushed the medical community into a more proactive learning mode about viral illness, which is necessary, helpful and appropriate, though one regrets the necessity for it i.e. the pandemic and the misery and death it has caused, that is the reality of viral infection, which many in the ME community already knew.
The pandemic scaled up the same kind of misery and death previously hidden beneath the umbrella of ME for decades at least, maybe all of history and prehistory, which was just brushed under the carpet because noone knew what to do about it. Now at least people are recognising something needs to be done and have hope that something can be done, thanks to improving knowledge and technology.
COVID proved the nature of postviral illness to the world which put a real dent in the arguments of those making spurious claims about psychological causes for ME for financial gain and I think has convinced a lot of capable individuals to take postviral illness seriously.
I think that will have repercussions and lead to discoveries regarding longCOVID and some subtypes of ME and I hope that in turn will lead to more serious approaches to other subtypes of ME and other unexplained diseases.
There doesn't appear to be an adequate guide to encountering the unknown in the book of rules. In an ideal world there probably would be.
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