QuietHarbor17
Established Member
I’ve been wondering about a few things that may or may not connect, especially if ME isn’t one completely uniform illness.
One is the autopsy findings.
If some people diagnosed with ME have shown abnormalities in the brain, spinal cord or dorsal root ganglia after death, what does that actually tell us?
Does it suggest that at least some people with ME have suffered permanent injury to the central or peripheral nervous system?
Or could some of those findings reflect inflammation or other pathology that doesn’t necessarily mean irreversible damage?
I suppose what I’m really asking is whether neuropathology at autopsy tells us that ME itself is a permanently damaging neurological disease, or whether that conclusion goes beyond what the evidence can actually show.
That also leads into the old ME vs CFS question.
Erik Johnson has long argued that the illness described as ME around outbreaks such as the Royal Free was not necessarily the same thing as the broader illness that later became labelled CFS after outbreaks such as Lake Tahoe.
I know that distinction is controversial, and I’m not saying his interpretation is proven.
Also it seems that Mold avoidance was one of the game changers for Giles Meehan who was a former UK ME advocate .He posted a video years ago on YouTube called Mould and ME.Basically he suggests that moving to a cleaner air part of the UK helped his ME symptoms and he was able to go back to work.So if he had ME and improved through Mold avoidance /Location effect than what does this say about ME?
I understand there seems to be many subgroups and at the same time I heard people say ME is one thing and CFS is another .Is it really that simple ?
But I do wonder how we can know that people included under different historical definitions were all suffering from the same underlying disease.
If older ME descriptions selected a more specifically neurological illness, while some later CFS criteria could include a much broader group, could we be mixing together several subtypes or even several different illnesses?
The Royal Free outbreak is particularly interesting to me because I’m in the US and most of the discussion I’ve seen here tends to centre on the later CFS history.
The usual interpretation of Royal Free seems to be an infectious outbreak, even though, as far as I understand, no specific infectious agent was ever conclusively identified.
That makes me wonder about the environmental side of these old outbreaks.
Were chemicals, occupational exposures, building conditions, pesticides, air quality or other environmental factors ever investigated in much depth?
And not just at Royal Free, but across the other hospital and community clusters that occurred internationally.
I’m not suggesting that any of those outbreaks have been shown to be chemical poisoning.
I’m more curious whether the historical debate became too binary: either there was an infectious agent, or the illness was psychogenic.
Could there have been an infection plus environmental exposure, or an infection acting on people who already had some particular environmental or immune vulnerability?
That interests me partly because Nancy Klimas has spent years studying both ME/CFS and Gulf War Illness. GWI obviously has a much stronger history of concern about environmental and chemical exposures, yet there seem to be areas of overlap in immune, autonomic and neurological research.
I’ve also had a strong location effect myself.
When I was younger I could sometimes go from more moderate/severe to something closer to mild/moderate simply by staying somewhere with very clean outdoor air.
I’d wake up with far less of the “poisoned” feeling and malaise.
The odd part was that most of the benefit would disappear again after returning to my usual environment.
I’ve wondered whether changing the external environment could somehow change the internal environment too ..immune signalling, microbiome, autonomic state, exposure load, or something else entirely.
I don’t know the mechanism, and I’m not claiming that mold or any single exposure explains ME.
One UK case I’ve always found interesting is Giles Meehan, who I understand became well enough to return to work after taking Erik Johnson’s mold avoidance ideas seriously and eventually moving to another part of the UK where he felt the outdoor environment suited him better.
Again, one person’s experience doesn’t establish a mechanism, but it raises an interesting question if some patients show large, repeatable location effects.
I’d also be interested in hearing specifically from people now in their 40s, 50s or older who already had ME in their 20s or 30s.
Did the illness change as you aged?
In my 30s I seemed to have more margin for error. Now in my 40s, recovery feels slower, gut motility is slower, and I don’t seem to bounce back from physical or environmental stressors as easily.
I can’t tell whether that is ageing, longer duration of illness, accumulated effects of being ill, or some combination.
So I suppose I have several related questions:
Do the autopsy findings in ME actually tell us anything about permanence or irreversible neurological injury?
How confident can we be that historical ME and later CFS cohorts were describing the same biological illness?
And has anyone seriously revisited the old outbreaks looking at infection and environment together rather than treating them as competing explanations?
I’d be especially interested in historical papers or pathology work that might help separate what is actually known from what has just become part of the ME/CFS narrative over time
Thank you
One is the autopsy findings.
If some people diagnosed with ME have shown abnormalities in the brain, spinal cord or dorsal root ganglia after death, what does that actually tell us?
Does it suggest that at least some people with ME have suffered permanent injury to the central or peripheral nervous system?
Or could some of those findings reflect inflammation or other pathology that doesn’t necessarily mean irreversible damage?
I suppose what I’m really asking is whether neuropathology at autopsy tells us that ME itself is a permanently damaging neurological disease, or whether that conclusion goes beyond what the evidence can actually show.
That also leads into the old ME vs CFS question.
Erik Johnson has long argued that the illness described as ME around outbreaks such as the Royal Free was not necessarily the same thing as the broader illness that later became labelled CFS after outbreaks such as Lake Tahoe.
I know that distinction is controversial, and I’m not saying his interpretation is proven.
Also it seems that Mold avoidance was one of the game changers for Giles Meehan who was a former UK ME advocate .He posted a video years ago on YouTube called Mould and ME.Basically he suggests that moving to a cleaner air part of the UK helped his ME symptoms and he was able to go back to work.So if he had ME and improved through Mold avoidance /Location effect than what does this say about ME?
I understand there seems to be many subgroups and at the same time I heard people say ME is one thing and CFS is another .Is it really that simple ?
But I do wonder how we can know that people included under different historical definitions were all suffering from the same underlying disease.
If older ME descriptions selected a more specifically neurological illness, while some later CFS criteria could include a much broader group, could we be mixing together several subtypes or even several different illnesses?
The Royal Free outbreak is particularly interesting to me because I’m in the US and most of the discussion I’ve seen here tends to centre on the later CFS history.
The usual interpretation of Royal Free seems to be an infectious outbreak, even though, as far as I understand, no specific infectious agent was ever conclusively identified.
That makes me wonder about the environmental side of these old outbreaks.
Were chemicals, occupational exposures, building conditions, pesticides, air quality or other environmental factors ever investigated in much depth?
And not just at Royal Free, but across the other hospital and community clusters that occurred internationally.
I’m not suggesting that any of those outbreaks have been shown to be chemical poisoning.
I’m more curious whether the historical debate became too binary: either there was an infectious agent, or the illness was psychogenic.
Could there have been an infection plus environmental exposure, or an infection acting on people who already had some particular environmental or immune vulnerability?
That interests me partly because Nancy Klimas has spent years studying both ME/CFS and Gulf War Illness. GWI obviously has a much stronger history of concern about environmental and chemical exposures, yet there seem to be areas of overlap in immune, autonomic and neurological research.
I’ve also had a strong location effect myself.
When I was younger I could sometimes go from more moderate/severe to something closer to mild/moderate simply by staying somewhere with very clean outdoor air.
I’d wake up with far less of the “poisoned” feeling and malaise.
The odd part was that most of the benefit would disappear again after returning to my usual environment.
I’ve wondered whether changing the external environment could somehow change the internal environment too ..immune signalling, microbiome, autonomic state, exposure load, or something else entirely.
I don’t know the mechanism, and I’m not claiming that mold or any single exposure explains ME.
One UK case I’ve always found interesting is Giles Meehan, who I understand became well enough to return to work after taking Erik Johnson’s mold avoidance ideas seriously and eventually moving to another part of the UK where he felt the outdoor environment suited him better.
Again, one person’s experience doesn’t establish a mechanism, but it raises an interesting question if some patients show large, repeatable location effects.
I’d also be interested in hearing specifically from people now in their 40s, 50s or older who already had ME in their 20s or 30s.
Did the illness change as you aged?
In my 30s I seemed to have more margin for error. Now in my 40s, recovery feels slower, gut motility is slower, and I don’t seem to bounce back from physical or environmental stressors as easily.
I can’t tell whether that is ageing, longer duration of illness, accumulated effects of being ill, or some combination.
So I suppose I have several related questions:
Do the autopsy findings in ME actually tell us anything about permanence or irreversible neurological injury?
How confident can we be that historical ME and later CFS cohorts were describing the same biological illness?
And has anyone seriously revisited the old outbreaks looking at infection and environment together rather than treating them as competing explanations?
I’d be especially interested in historical papers or pathology work that might help separate what is actually known from what has just become part of the ME/CFS narrative over time
Thank you
