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Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
@NickAnderegg
Mar 13, 2024 • 19 tweets • 6 min read • Read on X
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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
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? However, the damage done by COVID-19 is cumulative (Bowe et al., 2022). Even someone who recovers from an asymptomatic (Ma et al., 2023) or mild case (Novak et al., 2022) of COVID-19 is at risk of developing one or more PCCs. In fact, a recent review by Boufidou et al. (2023) noted that those who were reinfected were more prone to developing long-term symptoms—in comparison to those who were only infected once—and more prone to “various complications, including potential cardiac, pulmonary, or neurological problems” (p. 7). Even asymptomatic SARS-CoV-2 infections can result in long-term sy...
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. Loss of sense of taste (ageusia) or smell (anosmia) are defining characteristics of the symptomatology of COVID-19 [18 citations omitted from alt text]. These symptoms are so common and specific in COVID-19 that they have been used as criteria for participant inclusion in some studies of people with LC, “due to the high diagnostic specificity of these symptoms” (e.g. Kedor et al., 2022, p. 10). Some studies have even found that loss of smell during acute COVID-19 infection directly predicts long-term sleep quality and level of fatigue in people who have recovered from their initial infectio...
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: Critically, van Rhijn-Brouwer et al. (2024) note that “exercise in people living with long COVID is significantly associated with abnormal immune and metabolic responses to exercise in skeletal muscle compared with healthy control participants (Appelman et al., 2024). Therefore, graded exercise therapy should not be recommended for people living with long COVID and post-exertional malaise [emphasis added].” ... Further highlighting this point, van Rhijn-Brouwer et al. (2024) elaborated: Some people living with long COVID and CVAD do not have post-exertional malaise, so the exercise recom...
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: They stated that, although they discussed the benefits of aerobic reconditioning in patients with certain forms of cardiac dysfunction, they intended to convey that “a more cautious approach is required” for patients showing signs of PEM: Our understanding is that, in some cases, a standard approach to physical exercise might potentially harm patients with a still poorly defined susceptibility to post-exercise energy depletion (Komaroff, 2019). We apologize for our lack of clarity. Our intention was to raise awareness of this special subgroup of patients among those who have post-COVID-19 ...
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: In a review conducted early in the pandemic, Komaroff and Bateman (2020) noted that it’s “not surprising” that some individuals would “develop a debilitating chronic fatigue,” as “[p]ost-infectious fatigue syndromes follow in the wake of acute infections with several different types of infectious agents.” Among the infections that have been shown to cause post-infection fatigue syndromes are: the first SARS coronavirus (Moldofsky & Patcai, 2011); the Epstein-Barr virus (EBV), the virus that causes mono (Jones, 1985; Hickie et al., 2006; White et al., 1998); enteroviruses, a common family o...
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 a pre-pandemic study investigating the hypothesis that ME/CFS is caused by a “state of chronic, low-level neuroinflammation,” Mueller et al. (2020) used neuroimaging techniques to measure several metabolites in the brain related to neuroinflammation. They observed metabolic differences across several regions, finding that “[m]etabolites related to neuroinflammation were higher in ME/CFS patients,” with the high ratio of choline in the left anterior cingulate cortex (ACC) being the most significant. The excess choline is “interpreted as indicating abnormal phospholipid metabolism and acc...
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... Neural Abnormalities A recent neuroimaging study examined the brains of individuals with either ME/CFS or LC, using ultra-high field strength MRI to measure the physical volume of multiple regions in the brain stem. The study found multiple regions of abnormal brainstem volume in both groups relative to healthy controls, demonstrating a correlation of “abnormal brainstem volume in both ME/CFS and long COVID consistent with the overlapping symptoms” of these conditions (Thapaliya et al., 2023).
...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 Structural Changes Even in individuals who have fully recovered from COVID-19, long-term structural changes to the brain have been found (Douaud et al., 2022), including: “reduction in grey matter thickness,” reduction in “tissue contrast in the orbitofrontal cortex and parahippocampal gyrus,” tissue damage localized in “regions that are functionally connected to the primary olfactory cortex,” and an overall reduction in brain size. It appears that the neurodegeneration caused by SARS-CoV-2 is associated with the loss of smell that is common with COVID-19 (Douaud et al., 2022). It is not y...
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. Cohort studies have consistently found that the incidence of adverse neurological and psychiatric outcomes after SARS-CoV-2 infections is quite high. In one such study, Taquet et al. (2021) found an incidence rate of up to 33% of people receiving a neurological or psychiatric diagnosis within six months of recovering from COVID-19. The incidence of someone receiving their first such neurological or psychiatric diagnosis within six months is about 12%. More recently, Rahman et al. (2023) showed that COVID-19 is associated with new diagnoses of Schizophrenia Spectrum and Psychotic Disorder (...
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." Likewise, in a study examining dysregulation of the autonomic nervous system in people with LC, Ryabkova et al. (2024) found similar patterns in the association between LC and psychological symptoms: The correlation analysis revealed some important differences between the patients and HCs [healthy controls]. First of all, depression and anxiety were associated with fatigue only in the [healthy controls], but not in the ME/CFS or PCC patients. The association of fatigue with depression is well known, and a differential diagnosis of ME/CFS or PCC with depression is often difficult due to the...
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... Spike Protein Persistence The spike protein of the SARS-CoV-2 virus can accumulate in the brain, meninges, and skull marrow (Rong et al., 2023). On its own, the spike protein causes cell death in brain tissue, and it has been observed in the skulls of deceased individuals for a significant period of time after their COVID-19 infection; this may be a contributor to many of the PCCs described here (Rong et al., 2023). It is not yet know what causes this spike protein persistence, and more research is needed.
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. Fusogens are a specialized molecule on the surface of cells that many viruses use to enter their host cells. Research has shown that a SARS-CoV-2 infection can induce neurons and glia in the brain to fuse together with neighboring neurons and glial cells, as a result of the viral spike protein mimicking the relevant fusogens (Martínez-Mármol et al., 2023). These fused cells may result in large molecules and organelles being shared between cells, implying “a possible mechanism for the spread of toxic aggregates as observed in several neurodegenerative diseases and could also represent a mech...
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 Image
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. Conclusion The complications of COVID-19 can be severe and wide-ranging, even after a minor or seemingly asymptomatic acute infection. COVID-19 remains, even in 2024, a significant threat to public health—and the health of every single individual—and can have severe consequences for the brain, nervous system, heart, veins, lungs, and many other organ systems. Further research is needed to understand the full extent of the effects of COVID-19 on the many organs and bodily systems implicated in these long-term complications. While vaccination has been shown to help prevent more severe illnes...

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More from @NickAnderegg

Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Sep 7
Let’s talk about systemic risk from negligent public health: Catastrophe doesn’t require population-wide illness.

The worst case isn’t sickness. Worst case is infrastructure collapse due to overstressed resources.

You know power plants need stable power to operate?

1/many “8. Performance of Nuclear Power Plants Affected by the Blackout On August 14, 2003, nine U.S. nuclear power plants experienced rapid shutdowns (reactor trips) as a consequence of the power outage. Seven nuclear power plants in Canada operating at high power levels at the time of the event also experienced rapid shutdowns. […]. Many non-nuclear generating plants in both countries also tripped during the event. Numerous other nuclear plants observed disturbances on the electrical grid but continued to generate electrical power without interruption. […] - The severity of the grid transient...
If there is a widespread disruption in the service area of, e.g., a nuclear power plant, it shuts down for safety. Massive blackouts like in 2003 or in Spain this year are caused by safety systems!

If too much trips out at once, it has a ripple effect across the grid
2/ Source: https://www.insurancejournal.com/news/international/2025/04/29/821703.htm Why Restarting a Power Grid After Massive Collapse Is So Hard April 29, 2025 by Rachel Morison and William Mathis It’s a worst case scenario that grid operators plan for but hope never to encounter. After one of the worst blackouts in Europe in more than a decade, electricity grid operators in Spain and Portugal are trying to get networks back up and running from the ground up. The initial estimate from grid operator Red Electrica was that restoring all power supply in Spain may take between six and 10 hour...
Frequency Factor So far, the only information about what caused the crisis was a comment from grid operator Red Electrica that the blackout was a result of “oscillation,” which suggests a disruption in the grid’s frequency or voltage — both crucial factors for maintaining stability. The frequency, which normally stays pretty steady around 50 hertz, is the heartbeat of the grid. Frequency monitoring specialist Gridradar said it identified a rapid movement in frequency just after noon in Spain — right before the blackout hit. Such oscillations can cause chain reactions that ultimately lead ...
In 2003, it took 2 days to fully restore most power. The infrastructure is 20 years older than it was back then and higher demand creates risk of cascading failure.

As of 2003, recommendations from blackouts in 1965, 1977, 1982, 1996, and 1998 had not been implemented.
3/ “Recommendations to Prevent or Minimize the Scope of Future Blackouts As reported in previous chapters, the blackout on August 14, 2003, was preventable. It had several direct causes and contributing factors, including: • Failure to maintain adequate reactive power support • Failure to ensure operation within secure limits • Inadequate vegetation management • Inadequate operator training • Failure to identify emergency conditions and communicate that status to neighboring systems • Inadequate regional-scale visibility over the bulk power system.”
“Further, as discussed in Chapter 7, after each major blackout in North America since 1965, an expert team of investigators has probed the causes of the blackout, written detailed technical reports, and issued lists of recommendations to prevent or minimize the scope of future blackouts. Yet several of the causes of the August 14 blackout are strikingly similar to those of the earlier blackouts. Clearly, efforts to implement earlier recommendations have not been adequate. Accordingly, the recommendations presented below emphasize comprehensiveness, monitoring, training, and enforcement of r...
“1. Market mechanisms should be used where possible, but in circumstances where conflicts between reliability and commercial objectives cannot be reconciled, they must be resolved in favor of high reliability. 2. Regulators and consumers should recognize that reliability is not free, and that maintaining it requires ongoing investments and operational expenditures by many parties. Regulated companies will not make such outlays without assurances from regulators that the costs will be recoverable through approved electric rates, and unregulated companies will not make such outlays unless th...
“3. Recommendations have no value unless they are implemented. Accordingly, the Task Force emphasizes strongly that North American governments and industry should commit themselves to working together to put into effect the suite of improvements mapped out below. Success in this area will require particular attention to the mechanisms proposed for performance monitoring, accountability of senior manage-ment, and enforcement of compliance with standards. 4. The bulk power systems are among the most critical elements of our economic and social infrastructure. Although the August 14 blackout ...
Read 20 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Sep 4
If Florida drops vaccine mandates, society is probably officially over. I really, really, really don’t think most people get that herd immunity is the only thing keeping measles from ripping through the population, and a measles infection wipes out all pre-existing immunity

1/3
Measles specifically infects the cells that are responsible for “remembering” which pathogens your body has encountered before. So they ALL get wiped out, and all you’re left with is cells that remember your measles infection and nothing else.

2/3
Every infection, vaccination, and other pathogenic exposure you’ve ever had? Your body no longer knows how to detect them after a measles infection. The only immunity you’ll be left with is immunity to measles. That’s it. Open season for every other pathogen encountered.

3/3
Read 8 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Jun 30
Can I say something? I have a BA in psych, a BPhil in linguistics, and went to grad school for cognitive psych. My research, including an undergrad fellowship, was on the cognitive relationship between written and spoken language…

Audiobooks are NO DIFFERENT than reading print.
In the last hour, there have been a dozen replies from people nitpicking the first tweet

The topic of discussion is "do audiobooks 'count' as reading?," and the answer is "Audiobooks are NO DIFFERENT than reading print."

Maybe read the thread before arguing with it? lmfao
And for all those people with indignant responses who want to nitpick every detail, the fact that so many people hold THIS exact view—that audiobooks are somehow “cheating”—is the ENTIRE point. It leads to people who would benefit from audiobooks depriving themselves the medium
Read 4 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Feb 1
Many people are asking for recommendations about what storage media to buy, so here's a buying guide from an experienced data hoarder (me)

The MOST IMPORTANT thing to know is that SOLID-STATE MEDIA IS NOT DURABLE. Flash drives, SSDs, SD cards, etc. are NOT long-term storage.

1/
That's not to say that it's impossible to use solid-state media for long-term storage. It's just that anything with durability guarantees gets prohibitively expensive quickly. Spinning hard drives—as well as DVDs and Blu-ray discs!—are your friend.

2/
- The way data is stored in solid-state media makes it much more susceptible to bit rot than other media.
- In a spinning hard drive, the moving parts are the most common point of failure.
- When you burn a DVD, that shit is fairly permanent.

3/
Read 42 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Jan 9
I wish people would understand that insurance underwriters have armies of actuaries calculating risks, and if an insurance company drops you, it's because things have changed in such a way that insuring you will take more out of the financial pool than you're putting in

1/
It sucks, but it's a direct result of the fact that humans are widely inhabiting locations that are rapidly becoming impossible to inhabit safely. If you can't find insurance for your home, it means there's a high likelihood you'll need to move soon anyway.

2/
You get insurance so that you can replace all of your stuff in the event of a disaster. When the insurance company effectively says "the risk of disaster is so high that insuring you would almost certainly cause us to lose a lot of money," it ALSO means your life is in danger

3/
Read 7 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Jan 5
So here’s the thing about some of the subtle neuro damage related to SARS-CoV-2 infection that I think a lot of people miss: some of the known deficits are correlated with things like impulsiveness and poor emotional control, so we might expect to see deficits there are well

1/
Consider how impatient people seem to be on the road in the last couple years relative to the 2010s, and I think we have a perfect example of where this is LIKELY already manifesting.

2/
This impact is particularly insidious for the person experiencing it, because poor impulse control, by definition, doesn’t really come on gradually. My biggest concern is how interactions under these circumstances will play out if this impact continues to become more common

3/
Read 15 tweets

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