[akdor1154]

You could be completely right in some cases, but the way you present this is completely disregarding a professional researcher, peer reviewed and published paper, and honestly quite decent pop sci writeup.

I don't think that level of dismissal is fair or respectful unless you accompany it with a relevant criticism of the research itself.

[lindsaywaterman]

Ouch, you're coming at me red hot there! To be clear, I think post-viral syndromes are a common "proximal" cause of CFS. If a patient doesn't have an underlying dynamic of chronic dissociation, and doesn't already have a few other CSS syndromes, then I think it's unlikely they will develop CFS as a post-viral syndrome. Cheers.

[fatfingerd]

To me this seems suspiciously like confusing heightened awareness of a problem, or inability to treat it early, with cause.

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.

[whimsicalism]

> To me this seems suspiciously like confusing heightened awareness of a problem, or inability to treat it early, with cause.

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.

[fatfingerd]

Sure but if you look at male outcomes, we are clearly ignoring a lot of real health problems that are deadly, so 66% of males ignoring a less than deadly problem that allows 8 hours of work a day seems more likely than a lot of female hypochondriacs to me.

[whimsicalism]

This argument could be applied to any condition with psychosomatic indicators.

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.

[fatfingerd]

There's no telling what's real once you are willing to go down that route, least of all a doctors opinion. If someone stops displaying symptoms that could just be a non blinded doctor and a placebo.

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.

[AussieWog93]

>completely disregarding a professional researcher, peer reviewed and published paper

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.

[7thaccount]

I have a similar experience in my industry. Thousands of publications each year from academia totalling billions of dollars in funding with nearly none of it mattering at all. I've lost track of how many times I read a great title to find it had absolutely nothing of value outside of the researcher getting to aggregate some key words for their profile. It's baaaad.

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.

[eganist]

> As someone who used to be on the track to academia, this is something that more people should do.

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.

[quantumwoke]

Although I agree that we are framing this thread in the context of the original article, this medical professional is presenting their (experienced) opinion, and GP is not discussing it and instead chooses to require some token criticism of the article. This doesn't seem charitable to someone presenting their professional opinion.

[cascades42]

I'm a neuroscientist who published on central sensitization and chronic pain. Unfortunately, I was forced into retirement by chronic fatigue syndrome.

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.

[npunt]

Well said. Can't rule CS out, but can't say it is the endpoint either.

Re: mitochondrial dysfunction, you may be interested in Ron Davis' latest on the 'itaconate shunt', presented last week [1]

[1] https://www.youtube.com/watch?v=7inKF32vtl8

[lindsaywaterman]

Nice response thanks for that. I’m also a cfser but can’t really point to any viral thing personally. I appreciate your skeptical eye.

[whimsicalism]

I disagree - it is fine to talk about the broader context of research without being either deferential to one datapoint or explicitly refuting that one datapoint.

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.