There are many subsets of fatigue...of course there are.
However, there is a disease which is generally known as ME, and this is of infectious agent origin, typically sudden onset with viral-like symptoms...indeed probably caused by a virus with ongoing viral symptoms. It needs to be treated as such
Big data is fine, but how about talking to sufferers? Talk to those gaining improvement on antiviral/antiretroviral drugs for example.
The problem is nobody can identify A single virus. Indeed huge numbers with viral onset and viral-like symptoms also have no identifiable continuing viral infection. Now it might be hard to find, but with decades looking we should have found it. It might be enteroviruses, for example, but the finding is inconsistent. I suspect a double hit in my case, measles encephalitis as a child, then Coxsackie 3B as a young adult.
Quite a lot of data also suggests that ME is two or more illnesses, though it may be one with two different manifestations, that is not uncommon in viral infections for example.
New data is supposedly coming out of Stanford soon, we are waiting for publication, that might have identified the genetic risk factor, and its in the immune system as has long been suspected. If confirmed, then the issue is not just about a virus, but a virus and an uncommon immune reaction to it. Understanding what that response is might give us a better grasp of what ME really is.
Stanford is also changing its story on antivirals, with the position that we might need up to five years on antivirals, not all antivirals will work, and those that do have other properties aside from stopping a specific type of virus replicating. More is expected on this, but I do not know when.
ME is also associated with non-viral severe infections, and also a range of toxins. These are just less common. Then there is the question about how to study those with EDS who get ME, what is it about the genetic issues in EDS that increase ME incidence? My guess is its about a weakened blood-brain barrier.
Then there is the subgroup that includes encephalitis survivors, who fit the definitions but have a slightly different cytokine profile. Is that important, or just a different manifestation of the same underlying issue? Does this also apply to meningitis? We don't know.
Also of interest from Stanford is they are replicating the Japanese brain inflammation study, and have a possible brain scan to diagnose ME right now ... which is currently being tested though I am unaware of the details of the testing. It may or may not be validated.
Lipkin's work does need to be examined very closely, but then all the research needs to be examined. You never just accept a scientific finding. The more important it is, the more it needs scrutiny. A high percentage of findings, especially on small cohorts with limited testing and analysis, fail replication. That is a huge problem in ME research. As many of us are too well aware this also applies to treatments. (Actually its a huge problem in all of medicine, but badly funded research like for ME makes this worse.)
I like how Lipkin reasons, analyzes and communicates. It does not mean I think he is right. The science will show that, or not, as it comes out and becomes understood.
I love it that he's working with Fiehn...
