Search results

While I understand there is a plethora of of nonsense surrounding stem cell treatments, I wouldn’t be so quick to dismiss this one. It seems to work on FIP in cats, which is purported to be similar to Covid. https://pmc.ncbi.nlm.nih.gov/articles/PMC12259234/

Assuming the observed pumping is real, is it possible pumping isn’t primarily about waste clearance? Perhaps the pumping serves some other purposes, like maintaining homeostasis in some way. Something more akin to mixing or using force from the waves to better reach tissue with fluid. Playing...

Does this mean Phair’s Itaconate Shunt Hypothesis would predict this impact on CRH?

So, I have LC w/o PEM, and have had two multiyear prior post-viral illnesses. All three illnesses were similar to mild to moderate ME/CFS in terms of most symptoms, except no PEM. Each illness included a full loss of appetite and hunger signals for a lengthy period of time. For the first two...

I generally agree as to ME/CFS as the variety of triggers makes persistent antigen unlikely. In terms of LC w/o PEM, my own response to Pemgarda tells me antigen likely plays a role (at least in my case), and I think the evidence is much better for viral fragments than it is for replicating...

I wonder if this relates to insomnia/sleep shifts in LC? I can’t sleep before 2am, which seems to be common in LC. Perhaps viral fragments overload lead to a UPS back log, circadian related proteins get cleared later in the day, and as a result sleep occurs later than it should.

This is curious. I wonder if LC could turn out to be a disease of immunological indecision. Like a purgatory between sufficient antigen clearance and sufficient antigen tolerance.

Would it be worthwhile to look into remissions during pregnancy as it relates to bone marrow? It looks like many autoimmune diseases follow this pattern while some, like Lupus, get worse. Maybe there is too much going on in pregnancy to make sense of it, but changes in red blood cells (to...

I like to think of it a bit like the movie, “The Good, the Bad, and the Ugly.” Everyone is hunting the same treasure, but they are using different approaches to find it. We have folks using a traditional academic approach like Professor Edwards and Dimissa. We have Phair and Davis using an...

Agree. My first thought was is this a compensatory mechanism in response to excess glutamate?

I have some thoughts on this I’ve been kicking around and this seems like as good of a thread as any to share them. I have long COVID with primarily ANS and neuro symptoms. I feel awful, but it’s really hard to put many of my symptoms into words. The worst symptoms are a collection feelings...

I'd really like to see info on precisely how they are running these tests. Their website doesn't seem to have any details about the methods. They are testing things like BH4 and if Ron Davis is right you can't get an accurate measurement without immediately processing the blood. If I recall...

For what it's worth, I reached out a few weeks ago about some of the methods used in their labs. Specifically, I'm interested in high AngII/long Ang1-7 in Long Covid, and their package includes those tests. From what I am able to dig up online, these tests are not readily available commercially...

Perhaps IgG4 downregulates NK cells below the threshold needed to clear IgG4 LLPCs, so you have a bit of a feedback loop than need to be broken for some.

If ME/CFS worked like MuSK Myasthenia Gravis wherein IgG4 blocks a protein (without T-cell involvement and skewing male as in IgG4 related diseases) would that fit the data? It looks like IgG4 downregulates NK cells, so maybe that fits? Also, it looks like in IgG4 diseases sometimes Rituximab...

I believe Phair has said the shunt would only need to be stuck on in a relatively small number of cells. So, high interferon levels would be local rather than systemic, and thus not so easy to locate or measure.

If it does turn out to involve antibodies, is it possible that an IgG4 antibody could be to blame? Perhaps something like inhibiting a signal necessary for resolution or inducing an incomplete immune tolerance wherein it’s a little like having one foot on the brake and one foot on the gas?

If Phair’s itaconate shunt hypothesis is correct, and it is a cell autonomous disease as Phair believes, is it possible that the cells with the shunt stuck on would express CD38?

This is all well above my pay grade, but someone involved in complement research recently told me high IgG4 may be a compensatory mechanism in an effort to tamp down overactive complement.

I don’t have any answers, but I wanted to chime in to say I find this very interesting too. I firmly believe the answers to this disease lie in a place we can’t see, or a system we fundamentally don’t understand. Often times, we don’t understand things because we’ve assumed something has no...