If that was true, understanding the hypometabolic state which underlies chronic fatigue syndrome, could offer a way to treat severe infections: it might be useful to artificially induce a CFS-like hypometabolism in order to prevent tissue damage during acute infections!
I politely beg to differ.
Tissue damage is uncontrolled in ME (Oxidative stress the key culprit) and PWME harbour multiple intracellular infections, and viruses. This is all in the literature from Mycoplasma, to Parvovirus B19 to EBV.
On top of this PWME/CFS report adult onset Asthma (more tissue damage) and chronic allergic syndromes such as Mast Cell Activation Syndrome (MCAS) = more tissue damage once more. Over time this will wreck your DNA.
So what you do is test your cfDNA. Do PWME CFS report very high cell free DNA? Yes, some as high as patients having chemotherapy, except these patients aren't and are lying in bed. So imagine how high the inflammation would be if PWME/CFS started to exercise. (cFDNA is out of the cell due to oxidative damage, from inflammation), bitts of DNA floating around outside the cell. Normal, but not normal at high levels.
That's the one give away ME is an inflammatory disease, irrespective if you believe it's due to chronic infection, or post infectious autoimmunity.
Once you get an autoimmune illness, don't treat it, your inflammation will tend to cause a cascade effect and you develop other conditions on top of your original one (called co-morbid conditions).
You may ask:
Why is none of this is in the literature?
Answer:
The people most sick, severely affected, aren't researched.
Worst still, people with explained reasons of fatigue who have ME CFS are
excluded from the research also!
This is the 'beauty' of Fukuda CFS criteria, it makes sure people with demonstrated fatigue, can't be detected. Such a tragedy for the patients and so wrong, scientifically never mind morally. We have CDC to thank for that, as they created it.
So proving Dr Navieux/Dr Davis's work is going to be hard, as we need to exceed Fukuda Criteria to get a robust answer. This is why they ,sensibly, used Fukuda, CCC and IOM criteria. To increase the size of the 'net'- the exact opposite response that psychiatry would do as psychiatry is repulsed by Science and prefers religion (belief) that ME CFS is a belief in ME CFS.
Oxidative stress, would wreck your brain long term, effectively making it shrink. Is there evidence of brain atrophy in CFS? Yes.
Some ME sufferers even end up with pulmonary fibrosis, cancer and stroke from the effects of this. Why? Chronic Inflammation via infection/autoimmunity causes tissue damage.
What's the easiest way to prove your circulation is under attack other than Inflammatory Cytokine/Chemokine Assays? Test VEGF. Raised VEGF shows your body is growing new blood vessels for a reason. Why? Tissue hypoxia, probably via inflammation, via infection, via autoimmunity.
BUT.... I still believe this is likely induced by the immune system becoming disabled at an atomic level, in other words, if the immune system has no ATP, it won't work correctly (or certain parts of it).
So I'm waiting to get my hands on this new
Metabolic Mitochondria test we're queuing up for, and to compare my results with someone without inflammation, without infections - but who is housebound or bedridden.
That will be an incredible time for all of us, as it will show if 'severe' in ME is related to 'severe' in CFS (CFS diagnosis doesn't require inflammation) i n terms of 'sharing' the same Mitochondrial defect.