The question I keep returning to is co-morbidities. Does this research, or do the Drs Davis and Naviaux have any hypotheses about whether some of the commonly accepted co-morbid conditions like dysautonomia precipitate the dauer/hypo metabolic state or are they caused by it? (or is this answer buried somewhere in the data that my molecular bio illiteracy can't see it). I think a case could be made for both before and after.
My daughter became ill as a teenager with a heterogeneous cluster of potential triggers (IGF1 deficiency, IGA deficiency, mono, surgery, chronic sinusitis, school stressors--IB diploma, moving to a new country). Her POTS symptoms started around the same time as her serious fatigue--nearly passing out when climbing the stairs at school, unable to stand for more than a few minutes on the train or a queue...and so forth. Her sleep disruption became horrific. And then 6 months later she was severely ill.
FWIW, she did a year of Famvir and it did absolutely nothing for her--in fact, her absolute worst Neuro crash was while she was on Famvir. Anecdotal evidence that perhaps the antiviral was contraindicated and her body wasn't ready to move from the dauer state. Who knows? Dr Davis' questions about this treatment approach in his notes resonated with me.
Now, two years after her official ME/CFS diagnosis (by the CCC by and ME expert) she has elevated GAD antibodies, evidence of autoimmunity in her GI tissues, ruthless neurological symptoms and worsening autonomic dysfunction. The most severe symptoms onset *later* when what this study calls the dauer state was obviously in full force.
So trying to play the chicken and egg question of what came first, did the dysautonomia (and other common ME comorbidities like unrefreshing sleep) hasten the dauer state or is it more likely a symptom of an oncoming hypometabolic state?
And in terms of treatment, do the co-morbidities, theoretically, need to be dealt with/treated in order for the body to issue an "all clear" which would allow tentative return to normal functioning? Or is there a point when the dauer state becomes the new normal and the body needs to be coaxed out of it? i.e. If the gastrointestinal motility issues are a consequence of the dauer state (lipid dysregulation, endocannabinoid malfunction?) do you address them via mitochondrial repair or via addressing say, an autoimmune component evidenced in tissue biopsy? Can we theorize a starting point smart people of PR?
I ask these questions because I noted on Dr Davis' comments that he specifically addressed the question of whether pushing the mitochondria via supplementation might be contraindicated if indeed, the body is attempting to protect itself. At what point CAN it be known whether it is safe to move on?
My daughter is going to embark on what may be significant autonomic treatment/interventions this fall, and I'm trying to ascertain if there is something in this study that I can keep in the back of my mind as it is decided what to try and what to avoid. I know that this study doesn't address treatment, but the data does support what I see in my daughter, symptom wise.
Trying really hard to resist the impulse to say something about the devolution of the conversation into Lyme territory...except to say sometimes Lyme isn't relevant to the issue at hand.
