Thread by @NickAnderegg

I want to point out some highlights from this piece that totally surprised me while researching it. A bunch of things were offhandedly mentioned in a paper, and then when I looked at the source, it opened up a tanker-truck-sized can of worms

https://twitter.com/NickAnderegg/status/1767588742686990819

People with an asymptomatic acute infections can develop Long Covid. The risk from asymptomatic infections is definitely *lower* than symptomatic infections, but it's NOT ZERO.

What the hell, amiright?

Loss of smell is a symptom that strongly suggests viral entry into the nervous system. My mental model up until like two months ago was that anosmia was caused by inflammation of the cranial nerves, but NOPE, it's actually very covid-specific.

Even a published cardiologist made a giant mistake in recommending graded exercise therapy in a guide on treating cardiovascular autonomic dysfunction (CVAD), which had to be corrected:

Fortunately, the authors of the original review realized their error and agreed with the correction, then further emphasized the need for a careful approach to treating those who experience PEM:

It wasn't exactly news to me that various other conditions can cause severe post-infection fatigue, but after reading the papers, I think it's absolutely bonkers that we treat EBV (aka Mono) as just a minor inconvenience, when it can do such serious harm:

Around the time the pandemic began, multiple region-specific concentrations of neuroinflammatory brain metabolites were found to be associated with ME/CFS. Dunno how anyone can claim the etiology is a totally unknown with a straight face, when we have cellular evidence of fatigue

In another study:

- a group of patients with ME/CFS
- a group of patients with LC manifesting with PEM

were both found to have abnormal volumes in different regions of the brain, when compared to healthy controls.

It's still unclear whether this indicates...

...a virus-induced pathology OR a potential susceptibility to severe illness, but considering that structural changes have been found in the brains of individuals who have fully recovered from their acute infection, IMO, we have a *potential* etiology for a *subset* of symptoms

In my psych education, and I was taught the traditional serotonin model of mood disorders.

I've since been fully convinced that *most* mood disorders are a manifestation of neuroinflammation, and that was just from reading pre-pandemic papers on the neuroinflammatory model!

The findings I encountered on mood disorders as a post-COVID condition only reinforced my belief in the neuroinflammatory model of mood disorders, because I found over 40 papers associating biomarkers of neuroinflammation and CNS dysregulation with mood disorders in LC.

To be clear, I am very firmly asserting that, IMO, recent research STRONGLY suggests that mood disorders like anxiety and depression are a manifestation of an underlying abnormal NEUROINFLAMMATORY state.

(AND limited evidence that SSRIs ALSO affect the relevant pathways!)

One paper even explicitly spelled out that "fatigue was not related to depression/anxiety in ME/CFS and PCC, which is highly interesting in view of the renewed attempts of a psychologization of ME/CFS and PCC and represents a strong argument against this concept."

And to be clear once more, the paper referenced in the above tweet is saying that fatigue in LC is not caused by mood disorders like anxiety and depression, but rather that anxiety, depression, and fatigue are all manifestations of an underlying pathophysiology.

It turns out that the spike protein from the SARS-CoV-2 virus can just persist in our brains.

This one concerns the hell out of me, because if it weren't bad enough that the spike protein causes cell death in brain tissues...

The spike protein can also cause neurons to fuse together.

1. The virus starts reproducing in a cell.
2. The spike protein makes it to the surface.
3. The proteins on the surface of one cell cause it to bind to the receptors on a neighboring cell.

Also, did you know that RSV stands for Respiratory Syncytial Virus, and that "syncytia" are cells which contain multiple nuclei after multiple cells fuse together?

I dunno about you, but I'd prefer not to have masses of dysfunctional cells in my lungs, tyvm

Finally, it's probably worth pointing that one of the shortest sections is the section on conditions affecting the lungs.

respiratory transmission ≠ respiratory pathology

Oh, and in the conclusion, I also mentioned that LC can develop from an asymptomatic infection, because seriously, what the hell are we—as a society—doing when this is what we has been collectively accepted?

This is some kafkaesque bullshit in which we presently find ourselves.