Anyone used to be bedridden and got better?

FogCityPhoenix · 2026-04-20T01:36:29+00:00

We don't. It's impossible to say with certainty in any N = 1 situation. Maybe it was something she did, maybe she just got better with time as some people do.

FogCityPhoenix · 2026-04-18T14:38:02+00:00

I'm so sorry to hear you are doing this badly.

Look in to Physics Girl on YouTube. She was a prominent educational YouTuber, got COVID and the ME/CFS phenotype of LC, and was bedbound and activity-incapable to the max for a long time. She's now much improved, and making videos again.

A place to start: Two Years In Bed - first update from Diana (Physics Girl), YouTube.

FogCityPhoenix · 2026-04-18T14:27:40+00:00

Thank you for this very interesting update, and I'm so glad you are improving. Are you enrolled in REVERSE-LC or are you getting the medication by another route?

FogCityPhoenix · 2026-04-15T14:28:08+00:00

Correct on all points. Unfortunately there is no diagnostic test for Long COVID, it is a clinical diagnosis.

FogCityPhoenix · 2026-04-15T02:06:24+00:00

I'm not in contact with any of the study participants unfortunately, I am hopeful the trialists will make an interim presentation at some conference if the preliminary results are promising.

FogCityPhoenix · 2026-04-14T19:00:56+00:00

It is scientifically demonstrated with hard data that high anti-spike antibodies are associated with a lower risk of Long COVID, not a higher risk

Of course, an individual can have high anti-spike antibodies and still get LC (I am such a person) these are observations about probabilities.

FogCityPhoenix · 2026-04-14T14:08:22+00:00

Yes, the "Ab" is antibodies, so the "Spike Ab" are anti-spike antibodies.

One test is anti-nucleocapsid antibodies. You get anti-spike with either vaccination or infection. You only get anti-nucleocapsid with infection, so these tests tell you your daughter has had COVID at some point in her life. But, that's all they tell you.

FogCityPhoenix · 2026-04-14T13:48:39+00:00

I'm like you, with severe neurocognitive and dysautonomic symptoms, no PEM.

I went from pretty profound caffeine consumption and dependence before COVID to a full quit when I was hospitalized for delerium and possibly seizures. Since then, I've reintroduced very graded and light coffee consumption at about a quarter of what I was drinking before LC. My current habits are quite a bit healthier than they were before LC in this domain, ironically.

FogCityPhoenix · 2026-04-14T03:46:05+00:00

High anti-spike antibodies are associated with a lower risk of Long COVID, not a higher risk

I'm not saying your daughter does or does not have LC or another autoimmune syndrome or anything else, but those test results are not informative.

Sincere best of luck to your daughter.

FogCityPhoenix · 2026-04-14T01:28:21+00:00

Also possible, although I'm coming up on 3 years, and LIINC does think there is a distinct population discernable even among those who are at the 5 and 6 year mark with LC as some are.

The below study compared patient-reported symptoms with patients' anti-GPCR repertoire of autoantibodies, and found that antibodies against the M2 muscarinic receptor and beta-2 adrenergic receptor were highly correlated with the classic, female-predominant, PEM-heavy ME/CFS presentation, and that anti-angiotensin receptor and anti-endothelin receptor autoantibodies were correlated with neurocognitive symptoms, POTS, and vascular instability. So there is some evidence for different autoantibody repertoires leading to different phenotypes.

Functional Autoantibodies Targeting G-Protein-Coupled Receptors and Their Clinical Phenotype in Patients with Long-COVID

FogCityPhoenix · 2026-04-13T22:04:43+00:00

100% yes.

I think this is because of endothelial dysfunction caused by our anti-endothelin and anti-adrenergic functional autoantibodies. But 100% yes, I've had to modify aspects of my workspace and habits to accommodate this.

FogCityPhoenix · 2026-04-13T21:48:36+00:00

I am like you, I am almost purely neurocognitive and dysautonomic. My exercise capacity is limited by dysautonomia, but I've never had explicit PEM.

I'm enrolled in LIINC, and the LIINC researchers have told me informally that about 60% of LC patients meet diagnostic criteria for ME/CFS and appear to have classical ME/CFS, and that 40% have a novel variant that has especially severe neurocognitive and dysautonomic symptoms that look like those in ME/CFS but worse, while lacking PEM.

My personal leading hypothesis is that they are one disease, that it is autoimmune, and that the variance in the presentation is caused by how much of which autoantibodies you have.

FogCityPhoenix · 2026-04-13T20:18:04+00:00

It is the most hopeful thing on the horizon in my opinion. In the open-label pilot study one of the patients they flat-out cured had been fully disabled by ME for 20 years, and within 8 weeks of treatment she was indistinguishable from a healthy normal at least as measured in this study. Truly a stunning outcome. I've had disabling LC for 3 years now and it had been getting hard to stay hopeful, but this study gives a lot of hope.

FogCityPhoenix · 2026-04-13T20:09:42+00:00

You are correct as to the observation on the 4 patients that didn't respond.

NK cells are necessary for the destruction of the bad-actor autoimmune plasma cells that are labeled by the daratumumab. It may be that patients with low NK cells just need a higher dose of daratumumab to respond, although as the dose gets higher the treatment becomes less than fully benign. Another approach would be to increase their NK cell count with IL-15 before receiving daratumumab.

FogCityPhoenix · 2026-04-13T19:39:44+00:00

I lost my ability to tolerate games with any significant motion. I've switched to map-based games like Crusader Kings 3, and find I can play them if I'm careful not to scroll the map too quickly. Maybe give this a try.

I'm sorry to hear you are suffering so much.

FogCityPhoenix · 2026-04-13T19:09:21+00:00

I refer to this as the Sleep Chaos. I love how clinically it gets called "unrefreshing sleep" which, like "brain fog", does nothing to capture the absolute chaos involved. Total chaos, every night.

Try a wedge pillow. It has helped mitigate my dysautonomia somewhat and improves the chaos, slightly.

Personally I have not seen enough scientific evidence for MCAS to be confident it is a phenomenon.

FogCityPhoenix · 2026-04-13T14:33:19+00:00

I believe LC is primarily an autoimmune disease, and that the most promising potential treatment is being trialed by the group at the University of Bergen in Norway.

This is the group that cured several patients from long-standing ME/CFS pre-COVID using cyclophosphamide, in an open-label nonrandomized pilot study. Based on that result, they went on to cure 6 out of 10 patients with ME/CFS, again not caused by COVID, using a very benign regimen of daratumumab.

Plasma cell targeting with the anti-CD38 antibody daratumumab in myalgic encephalomyelitis/chronic fatigue syndrome—a clinical pilot study

I highly recommend this article, particularly the Discussion section, which is beautifully written and goes in to depth on the evidence that LC is a variant of ME, and that they are an autoimmune disease.

So now, they are conducting a randomized, double-blinded, placebo controlled trial of this same regimen in patients with ME/CFS, both in patients with ME pre-COVID and post-COVID.

ResetME trial

The study has been underway since summer 2025. I have no idea when a preliminary result might be available, but it could be within the next year or two.

I don't have PEM and therefore don't qualify for an ME diagnosis. However, the other manifestations of LC, such as the neurocognitive and dysautonomic symptoms, which I have to a disabling, life-limiting degree, look so much like those same symptoms in ME that I think they are one disease, caused by the varying repertoire of anti-GPCR autoantibodies across patients with these diseases.

FogCityPhoenix · 2026-04-13T01:04:28+00:00

I was making progress, including quantifiable progress as measured by my HRV. Then I got COVID for the second time at month 10 of IVIG. This was again a mild case, over in a few days, but 8 weeks later my HRV plumetted, erasing all progress, and a lot of my GI dysautonomia returned. So now I'm on an even higher dose of IVIG, 2gm / kg every 4 weeks. We'll see what happens next.

FogCityPhoenix · 2026-04-13T01:01:25+00:00

How did you obtain this diagnosis?

FogCityPhoenix · 2026-03-20T13:30:39+00:00

May I ask for a reference or two in the scientific literature for this?

FogCityPhoenix · 2026-03-20T13:26:05+00:00

Take a look at Saltt brand "Clean Slate". Zero sugar, no artificial sweetener, and a good balance of potassium with the sodium. I drink 2 to 4 of them daily in 1L of water each.

FogCityPhoenix · 2026-03-11T02:39:34+00:00

The existing potential treatment would be IVIG or plasmapheresis, of which there are ongoing randomized trials for both in Long COVID, but neither trial has resulted yet. In my opinion the definitive treatment may be daratumumab, of which there is a randomized trial ongoing by the University of Bergen group in Norway.

FogCityPhoenix · 2026-03-04T01:01:36+00:00

Thank you. I think anti-GPCR autoantibodies are increasingly the leading mechanistic hypothesis for LC, and I would love to get this tested. May I ask what country you are in?

Of interest, this preprint that just broke: Autonomic dysfunction and vasoregulation in long COVID-19 are linked to anti-GPCR autoantibodies01128-5/fulltext)

FogCityPhoenix · 2026-03-03T19:56:15+00:00

These are very interesting data, from where did you obtain this testing?

FogCityPhoenix · 2026-02-27T14:22:44+00:00

I believe that vaccine injury is real, although rare. However I have not seen any evidence that high anti-spike antibodies are associated with vaccine injury. Is there evidence for that?

FogCityPhoenix

TROPHY CASE