I don't think that level of dismissal is fair or respectful unless you accompany it with a relevant criticism of the research itself.
I don't think that level of dismissal is fair or respectful unless you accompany it with a relevant criticism of the research itself.
People who seem likely to be diagnosed seem less likely to happily sleep for 12 hours a day for a few weeks after a viral infection, more likely to blame themselves for their state and more stressed by awareness that something is wrong.
Naturally, if a rich layabout has the problem anyway, then we can look to their childhood and find at least one trauma.
Heightened awareness of a problem can be related to the cause - these are not distinct.
The comorbidities of ME/CFS make it look very similar to known psychosomatic conditions. Researchers who explore psychological-heritable causes have been forced to stop due to death threats.
Your suggestion that somatically-involved conditions aren't 'real' is offensive and what gives rise to the stigma that means we can't talk about this in the first place.
I think the offense is going there without any double blinded science and then relying on non reproducible fields of research to annoy the patient.
As someone who used to be on the track to academia, this is something that more people should do.
Most published research is false, and even most of the correct stuff is useless.
I'd go so far as to say any research that hasn't directly lead to at least a physical demo being produced can be safely ignored.
There are some occasional gems, but it's like a handful per decade that are of true value with the rest not even worth the kB they take up in storage.
I may sound bitter, but when I see the government dollars announced it makes me cringe a little bit as I know there are so many better places for that money.
You're right, and akdor1154 already addressed this in the same breath:
> I don't think that level of dismissal is fair or respectful unless you accompany it with a relevant criticism of the research itself.
Emphasis mine.
The linked article and others have convinced me that CFS can be caused by viruses.
There's one important and tricky question: is a viral infection necessary to trigger CFS in humans (such as long COVID or in this linked article), or is an extremely stressful series of events (which could include the physical stress of a severe viral infection) sufficient?
Giving a certain interpretation of their comment, I think the physician could be stating that they've seen patients with CFS that has been triggered by stressful events alone. I think this can coexist with the linked research if CFS can be triggered by stress OR a virus.
When chronic stress is mentioned as a factor, that should not be interpreted as being a psychological predisposition ("it is all in their head"). Instead, it is a predisposition on a cellular level.
The brain regions involved in central sensitization are tightly linked with those involved in chronic stress. Animal models of chronic stress lead to central sensitization of pain, as do animal models of chronic illness. Chronic stress causes an immense amount of remodeling in the brain and the rest of the body.
Proving or disproving that CFS can be triggered by chronic stress alone is difficult because CFS is a diagnosis of exclusion. Diagnosis can take a long time. We humans are always getting viruses and occasionally enduring stressful life events, so it is difficult to untangle the two.
If we look at my personal history, my diagnosis took several years (above average for CFS patients). I can point to 3 stressful life events and 2 viral illnesses that might have preceded CFS onset. The cause for my CFS remains a mystery.
Without a mechanism and diagnostic test for CFS, I think this question will remain unanswered.
I think it is contentious to say that CFS is an endpoint of central sensitization. It might be, but it also might be related to mitochondrial dysfunction or another mechanism-- too soon to tell, in my opinion. Central sensitization is certainly a component, but I do not think it is proven to be the only component. I should say that I'm extremely biased towards believing in central sensitization as the cause of many things because that was the primary focus of my research.
Again, without a mechanism and a diagnostic test for CFS, much is murky. Viral infection can at least be a cause. I think we're far away from having a tidy answer like the story of H. pylori and ulcers though.
Re: mitochondrial dysfunction, you may be interested in Ron Davis' latest on the 'itaconate shunt', presented last week [1]
There are lots of other papers fingering EBV as a cause of ME/CFS, but there are many, many papers showing the similarities of the population with this condition and other conditions that have been shown to be psychosomatic, showing correlates between CFS-like conditions and perception of illness as stronger than past EBV infection (something not true of most other illnesses), etc.