Hello,
The author wanted to respond to some of the things said on the thread but for some reason was unable to make an account, so he's asked me to post for him.
The following are his words:
I opened up a twitter account so I could get the paper out there. Please feel free to share the link or the PDF because frankly I'm not sure if the publisher will let me keep them up.
A few words on that prefix, because I think it's important: The term "psychoneuroimmunology" has nothing to do with not taking CFS seriously. It's a medical term, is well established in the biomedical research world from which I come and it is appropriate to this hypothesis. The Greek word "Psyche" means "goddess of the soul" but the English prefix "psycho-" does not. Especially in the context of a scientific term like psychoneuroimmunology it means "mind" or "mental." Importantly, in medicine, the concepts of "mind" and "mental" do not mean "by choice" or "malingering" or "you just need to try harder" or "you did this to yourself." Within biomedical research, the term "psychological" refers to mental processes such as behavior, cognition, perception and affect. From Komaroff et al. 1996: common symptoms of CFS include difficulty concentrating, forgetfulness, difficulty thinking, blurred vision, photophobia, irritability, depression, sleep disturbance and awakening unrested. Those symptoms are part of CFS, and they all have to do with mental processes such as behavior, cognition, perception, or affect. In other words, they are psychological symptoms. It doesn't make sense for researchers to just ignore those symptoms, and any hypothesis of CFS needs to be able to explain them, and why they happen alongside the "physical" symptoms.
I'm not using the term psychoneuroimmunology for monetary reasons or because somehow someone is making me. Actually, I am not paid at all to do CFS research. I'm paid to do PTSD research (which I consider to be basically unrelated to this hypothesis). I have zero funding to work on CFS. I've thought about, researched, written, and published this all on my own time. I did it because a friend from high school has pretty severe CFS, and has for years. I know for a fact that this friend of mine would be out there conquering the world if she could just get out of bed. And that's what made me start to think skeptically about all of the CFS skeptics. I came up with this idea quite a while back, but was in a bad accident and had to put my life on pause for a couple of years. I'm sure many of you can relate.
What I've written is a novel hypothesis, and it's either correct or it isn't. I did my best to explain why I think my newly proposed mechanisms make sense, how to test the hypothesis, and how to help people get better if it is correct. It would be great if this new hypothesis is accurate but if it isn't we should move on and we should understand that whoever convincingly falsified it was doing us all a service.
One thing that I want to make perfectly clear, because I understand that it's a sensitive subject - In the article, I discuss all kinds of potential treatment options that could be empirically tested, including glial inhibitors, specific antivirals, vagus nerve stimulation, vagotomy, cognitive therapy and graded exercise. Let me reiterate what I'm advocating in terms of exercise therapy because I understand how controversial it is. I said all of this in the article, but I want to expand it
Read the article first for background and context, but this is the expanded disclaimer:
Graded exercise therapy would make some people worse if done on its own, as it was in PACE. But that's not what I recommended. I recommended it as part of a regimen that includes glial inhibitors or other mechanisms to drive down the proinflammatory cytokine response. In other words, I recommend graded exercise for after the fatigue is gone, as part of recovery. If the VNIH is correct (and that is a very big if), glial inhibitors would prevent graded exercise therapy from making symptoms worse because post-exertional malaise is caused by, in my own words, an "enhanced feed-forward loop of vagus nerve cytokine signaling" caused by activated glia. The implication is that once someone is on glial inhibitors, they should be tolerant of graded exercise therapy. To repeat - according to this hypothesis, the reason some people get worse with graded exercise therapy is because they have pathogen-activated glia. Everyone gets a proinflammatory cytokine burst when they exercise; in CFS that system is already primed for exaggerated signaling. Treat that, and you treat the reason they get worse and are left with only the benefits of graded exercise during recovery because the fatigue is gone. Of course, as I state explicitly, this is a hypotheses that needs to be tested. And no one with CFS should ever be forced into any kind of therapy.
In the words of my friend with CFS, "Of course if the mechanism preventing us from exercising like a normal person is treated with medication, patients would naturally start conditioning again. I know I would be in the gym EVERY DAMN DAY. I think I would live at the gym. And the pool."
Thanks and stay strong,
Mike.