Here is my summary of the updates. I think this is worth watching to anyone with CFS, but I know it's hard to concentrate sometimes. This man is brilliant, likely one of the smartest humans on the planet. I am so impressed with his research and systematic approach. I've suffered for over 13 years. Now, I feel like CFS sufferers have something better than "hope"... we have Dr. Ron Davis.

My summary of the video (Very complicated information, so I may not have summarized correctly or left things out. This is what I gleaned from it though)

-3 Nobel Lauretes and 6 Academy of Science Members working on the research. Bringing in many specialists to collaborate
-His son is severely ill with CFS (his son cannot talk or read now)
-Coming up with 5 potential tests for CFS that patients would be able to do in-office to identify whether they have the disease (looking at red blood cells, white blood cells, and several other factors). He is actually creating the devices to do the testing. He is considering affordability for CFS testing, one test will cost 5 cents to make, another $1.
-Studying data from severely ill patients (going to their home to collect a multitude of data)
-Making observations with this disease and basing hypotheses and testing on the observations (Says NIH is doing it wrong!)
-A very severe illness, worse than diabetes, hypertension, and many other diseases which are given a lot more funding... not just "feeling kind of tired"
-Testing for many viruses, like EBV, HHV-6. They actually do not seem to be implicated, antivirals likely not a treatment, can actually cause harm to mitocondria, which may already be compromised in CFS (he explains this better in the video)
-Analyzed 95,000 biomarkers, seems to follow tryponosome (a possible cause) or a parasite
-possibility that it is still an unknown virus
-Those severely ill are low in essential metals, like copper. 60% of US deficient in copper
-High Mercury is associated with low selenium (an antioxidant, very bad to be low in selenium because there is a lot of oxidative damage in CFS)
-Some had high mercury and high levels of lead. Almost all with high mercury were eating too much fish
-Alot of changes in gene expression in immune system
-Severe cytokines (elevated)
-T- cells scan the cell for pathogen if they find it they make large numbers of t-cells. CFS has large t-cell expansion (doing more research and studies into this). Lyme & MS look very similar to this (in regards to t-cells). Question becomes: What do the T-Cells see in the body that is a pathogen?
-Whole Genome Sequencing - found a gene that is 100x more prevalent in CFS than healthy controls. Also genes associated with Natural Killer cells
-Metabolomics associates CFS with other disesases-metabolic phenotype most similar to inflammatory, neurological, and immunological diseases and autism.

Activation of immune system, genetic changes, and metabolic changes

Putting everything together - looking for a metabolic trap
Because of genetics & inflammation pathways get altered into a not functional state.
He Predicts - Something triggers it (infection), so you go to sleep & wake up with disease. Nothing you do, gets you out of it. This is good news, no new drugs! A drug will likely NOT fix it!
It will be VERY EASY TO FIX. Won't be something any one has tried. we will have to manipulate the metabolism
Inexpensive treatment and a FEW DAYS TO GET YOU OUT OF IT.
He's VERY OPTIMISTIC THAT HE'S RIGHT!!!
Researchers trying to figure out WHATS REALLY GOING ON & HOW TO FIX IT.
Figure out WHAT IT IS.
He doesn't think it's "that complicated" in the sense that it's "permanently wrong with the body"
You've just "fallen into a trap" (a metabolic trap) and don't know how to get out, but by understanding you can get out.
He is hoping to know in several months to a year!

Thanks for the tip, I will try to look into this more, I'd like to hear what he has to say. I hope Dr. Davis isn't somehow glossing over a possible role for autoimmunity and bacteriology though - there may already be some meaningful biomarkers reported in that sense if they're interpreted in that context?

In my opinion, things like this might be very important clues (and with some attention to detail, some of the overlap between different autoantigens and various diagnoses might be successfully matched to some of the overlap in microbiology - bacteriology mainly, but possibly also fungal pathogens among other things).

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5161229
... These findings are in agreement with the clinical disease presentation of ME/CFS, with inadequate ATP generation by oxidative phosphorylation and excessive lactate generation upon exertion...
...A recent study showed that serum levels of autoantibodies to several autonomic receptors were higher in ME/CFS patients than in healthy controls (41). Similar autoantibodies were detected in postural orthostatic tachycardia syndrome (42) and in complex regional pain syndrome (43), conditions with some resemblances to ME/CFS, affecting fertile women after a triggering event (44, 45). Likewise, autoantibodies in ME/CFS may interfere with key metabolic signaling pathways involving factors such as HIF1 (24) and PPARs, as well as AMPK, which was abnormally activated in skeletal muscle cells of ME/CFS patients (46)...

I think that part could be tricky, there might be multiple obstacles to metabolism with more diverse origins? (Doctors like to tell me stuff like "you just need to get moving more and get your metabolism warmed up" but if that were working I probably wouldn't be seeing them).

What if a "metabolic trap" happens when your body is presented with a set of circumstances when downregulating metabolism is the lesser of evils, or if downregulated human metabolism becames a common goal of both an infecting pathogen, and an infected host? (I am wary, for example, of trying to build up ATP whenever research implies I may be low due to some disease or other, if it would be undermining what my body is trying to accomplish, or if it were simply providing an infection with more food or ammunition, ATP is also probably one of the main precursors to adenosine, which I've seen credited before with the ability to decouple mitochondrial respiration, among numerous other pathogenic effects. This may be something I don't see addressed much and I am almost having to make inferences about the wisdom of this based what seems to be a shortage of people touting it as a cure for anything.

There could also be multiple microbes that might be driving an antibody response in some pathologies? I'm very curious whether trypanosomes themselves could account for the full spectrum of "auto"-antibodies associated with ME/CFS (or whether a lack of some of their associated symptoms can be fully accounted for), but that might be one the areas where we may not have enough research to be too sure?

Also, I thought I've seen multiple associations between ME/CFS and protein citrullination, as with a number of other medical diagnoses, I need to look into that more carefully but from what I've seen so far on the general subject, I'm not sure why protein citrullination may not turn out be a potential indicator of anerobic bacterial infection.

Anyway, thanks again for that - I guess I should count myself as "cautious but optimistic". If Dr. Davis doesn't happen to figure out the whole puzzle, he may still make a sizable contribution to the solution, and that would indeed be good news.

Thanks for sharing Bluebonnet. That sentence. "A few days to get you out of it " makes me feel like I must be dreaming as I read it and consider the possibility of it becoming a reality. Dr Ron Davis has been so dedicated to his research and of course he has so much personal motivation due to the severe suffering of his own son. His son is the worst CFS case I have seen. So very sad..
I'm afraid to get my hopes up , but the recognition and validation of this illness has certainly come a long way from the early days where it was so hurtfully referred to as the yuppie flu.
I pray that Dr Davis is pointed in the right direction and a cure will become a reality for us all. From 28yrs of age until now at 65 yrs, it has been a most difficult journey for me. Hugs and healing to you all. Gratitude always.Diane

I still seem to have very mixed feelings about this - I respect Dr Davis' reservations about antibiotics very much. long story but I think he could be very right that patients with metabolic disorders or certain infections might be at higher risk of side-effects from certain ones...

As soon as I went to look to see if I could find independent support for his nomination of parasites, though, I found this about the improvements reported with antibiotic use in CFS cases associated with a Giardia outbreak in Norway

http://simmaronresearch.com/2017/07/giardia-chronic-fatigue-infectious-illness
"Galland found the most devastating long term symptom after a Giardi infection was not gut pain but fatigue. Interestingly, given the involvement of a pathogenic gut protazoan, the patients’ gut symptoms were relatively minor; it was their fatigue, muscle pain, muscle weakness, flu-like feelings, sweats and enlarged lymph nodes that stood out. Galland reported that treating the infection alleviated the fatigue in over 80% of his patients and removed the digestive complaints in 90%. In 1998 Galland reported that one outbreak of Giardia, in Placerville, California, 'was followed by an epidemic of Chronic Fatigue Syndrome, which swept through the town’s residents'.
Galland found that a longer than usual treatment regimen was often necessary to clear the body of the bug. Instead of the normal five-day treatment, his average treatment regimen lasted three weeks and could extend to eight."

That almost has to be offering some kind of insight and making some kind of very positive statement somehow. Maybe THE most remarkable thing is that it is supposed to have been possible even without having to sort out the tangles in metabolism or autoimmunity?

There is some research I think I'm rather fond of, by ME/CFS patient researcher Paolo Maccallini, (A lot of Paolo's writing is in Italian and benefits from Google translation). https://paolomaccallini.com

One thing Paolo has done that fascinates me his studies of enolases. There is so much overlap with co-morbidities that feature anti-enolases that it seems almost unthinkable they are not also a feature of ME/CFS. As unbelievable as it sounds, has no one ever thought to look for them in ME/CFS?

Besides Paolo's own very interesting ideas, his ME/CFS blog site has introduced me to a number of interesting individuals including Robert Naviaux, who seems to be independently saying some of the things that I've been thinking about metabolism and infections after some of my studies of immunological subjects.

I've even read articles about "selfish immunity" or the "selfish immune system" (Google knows these phrases) that have proposed that the immune system can itself compromise host metabolism in order to reserve "fuel" for the immune system to better fight infections,

in addition to tricks that infections might play on host metabolism to gain a better foothold - if they can compromise the metabolism of immune cells themselves (or another cells that can act in an immune capacity, such as "non-professional phagocytes", it may help them to survive, just as microbes might also compromise even their own metabolism in order to better survive.

A quote from Dr. Davis from a translation of page 3 of Paolo's site:

"[In] the words of Davis: 'The mitochondria of patients go off, literally, and we must find out why. It is clear to me that this phenomenon is due to bacteria. Bacteria are able to shut down their energy generators when they are exposed to environmental threats, thus managing to survive.'"

This is a quote from Naviaux (2013) that I think came from a translation of another one of Paolo's pages, suggesting that impaired metabolism may also be advantageous to the host and even part of the immune response.

"This deactivation of mitochondria would reduce the proliferation of infection and therefore be considered part of the immune response"

This is why not matter what angle I try to look at this from, it tries to come out as some normal response to infection, where the problem doesn't seem to much the response to infection, as that the host response may become chronic if the infection becomes chronic.

Some days, the ability of microbes to produce adenosine tries to look more upstream than downstream in the chain of events - that's the same adenosine that is supposed to be able to decouple mitochondrial respiration

Adenosine: a selfish-immunity signal? (Dolezal 2015)
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741691

Have others already found what Dr, Davis is looking for?

If compromised host metabolism is the goal of both an infecting microbe AND an infected host, how easy will it be to get out any "Metabolic Traps" until the infection has been successfully treated? How easy will they be to break free from otherwise if they're being caused though multiple routes?

Is the most important question we can ask now not what infection causes disease x, or how many infections does it take to cause disease x, or where these infections are hiding, but how these associated infections often seem to be eluding antimicrobial therapies?

For whatever it's worth, these are concerns that apply to MANY different diagnoses, they virtually transcend any one diagnosis in particular, and any of us are that much less alone or abandoned for that.