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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
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
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Jan 3
Let's review some major points in the Nukit controversy, since some people are unclear:

- Someone criticized someone's use of Nukit lanterns.
- Nukit attacked the critic because, as noted, this is how they market
- Nukit now demands "mediation" with the community (how??)

1/ @marigoldglitter: "these tools should be used for people who must be in public despite the dangers, not for white men who want to eat in restaurants and maintain the status quo. if this is what you're gonna use these for, give them to a disabled person who can't go to the doctor b/c of risk." Nukit: ""White man" in this case is buying those products from non-white small businesses who are focused on providing the community with effective, tested mitigations at far, far lower costs than anyone else." OP: "Like why are you coming at me with this aggressive...
Nukit: "If you are in the US, and would like to purchase Far-UVC products, we cannot help you at this time. We tried to resolve the issues there, but the US COVID-Aware community was uninterested in mediation or intercession. As a result of that disinterest, a great deal of harm was done. When stock is finished, we will not be selling our products to the Us anymore. If you are in the US and want Nukit products, would like 333 million Americans, many disabled or immune compromised, to be able to access the most affordable Far-UVC on the market, kindly address the people who made it unsa...
So let's look at this a bit more critically. Here is the "evidence" Nukit provided that the didn't say anything racist. First of all, these aren't the comments in question, but it's worth a look anyway.

2/ Ok, I get that "evidence," "citations," and "personal accountability" are going to be called racist, but since people insist on just spewing lie after lie without any pushback- here's what actually happened. @marigoldglitter- a white woman attacked a Nukit customer who was supporting us by showing our products. This is something we rely on to fund research and donations. If our customers do not do this, that money goes to paid advertising. So yes, attacking our customers is attacking our company and directly harming marginalized folks who receive our products. ...
Seems to be framed this way because Nukit knows it's not an adequate explanation, so they're acting like anyone who criticizes them is in the wrong. --- A bigoted comment is a bigoted comment, even if it's not directed at someone who might be personally offended. Of course, Nukit didn't include the comments people actually call racist! --- Nukit is explicitly saying here that they view any criticism as an "attack," because criticisms can potentially hurt their business goals. Fundamentally, Nukit is angry that this usage of their products are being criticized. --- After Nuki...
Let's be clear about what happened here: Someone lamented the unequal access to protective measures and criticized someone who seems to be using a certain device to *maintain the status quo*, and the manufacturer of the device found it unacceptable.

3/
Read 16 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Oct 9, 2024
NEW STUDY! This exploratory study identifies a SPECIFIC PHENOTYPE OF LONG COVID that appears related to NEUROMUSCULAR DISTURBANCE rather than lung damage—and they've termed it Complex Ventilatory Dysfunction!

Breakdown of the paper (thread written for a general audience!)...

1/ Published Oct 7, 2024: "A new phenotype of patients with post-COVID-19 condition is characterised by a pattern of complex ventilatory dysfunction, neuromuscular disturbance and fatigue symptoms" Abstract: Background Patients with post-COVID-19 condition frequently suffer from chronic dyspnoea. The causes and mechanism for dyspnoea in these patients without evidence of structural lung disease are unclear. ... Results ... A pattern of reduced forced vital capacity (FVC), but normal total lung capacity (TLC), termed complex ventilatory dysfunction ... was observed and occurred mo...
Broadly speaking, there are two groups of acute covid outcomes involving dyspnea (shortness of breath) as a long-term symptom:

- Severe cases that may have physical lung damage
- "Mild" cases that now have ME/CFS-like features, but who have no evidence of lung damage!

2/ "Current evidence suggests that cellular damage, a robust innate immune response with inflammatory cytokine production and a procoagulant state induced by SARS-CoV-2 infection are factors potentially contributing to post-COVID-19 sequelae such as dyspnoea, fatigue, and cognitive and mental disturbances... Dyspnoea has been well characterised as a major clinical symptom of post-COVID condition after severe and critical COVID-19 and is correlated with impaired lung function in terms of pulmonary restriction, and with reduced diffusion capacity as a possible consequence of pulmonary remod...
In this study, they explored this distinction further and identified a distinct subset of patients with a pattern of breathing abnormality that they have termed complex ventilatory dysfunction (CVD).

So how did they arrive at this conclusion? Let's dig in!

3/16 "We hypothesise that patients suffering from post-COVID-19 condition who have fatigue and exertional intolerance also have a reduction in respiratory muscle strength, causing a dysfunctional breathing pattern which is distinct from typical pulmonary sequelae after COVID-19 such as obstruction, restriction or impaired diffusion capacity. Based on clinical observations, we describe a new breathing abnormality termed complex ventilatory dysfunction (CVD), defined as total lung capacity (TLC) - forced vital capacity (FVC) >10% predicted value and absence of restriction (TLC ≥ lower limit o...
Read 16 tweets
Nick #RespiratorsFilterPathogens😷 Anderegg Profile picture
Sep 22, 2024
NEW STUDY! It VERY thoroughly supports the hypothesis that SARS-CoV-2 emerged as a zoonotic spillover event in the Huanan Seafood Wholesale Market—using multiple methods!

Breakdown of the paper (written for a general audience!)...

1/many (but it's worth it, I promise!) Published Sep 19, 2024 in Cell: "Genetic tracing of market wildlife and viruses at the epicenter of the COVID-19 pandemic" Highlights: - Common ancestor of SARS-CoV-2 linked to Huanan market matches the global common ancestor - Wildlife mitochondrial DNA identified in samples from stalls positive for SARS-CoV-2 Abstract: "... We demonstrate that market-linked severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) genetic diversity is consistent with market emergence and find increased SARS-CoV-2 positivity near and within a wildlife stall. We identify wildlife DNA in...
This paper reanalyzes the same data from the April 2023 paper in Nature that cast doubt on the Huanan Market hypothesis (pictured).

In the new paper published in Cell this week, another group conducted far more detailed (and statistically sound) analyses!

2/
Original paper that analyzed this same data: "Surveillance ofSARS-CoV-2 at the Huanan Seafood Market" "Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of coronavirus disease 2019, emerged in December 2019. Its origins remain uncertain. It has been reported that a number of the early human cases of coronavirus disease 2019 had a history of contact with the Huanan Seafood Market...."
"...It should be noted that the selection of shops for sampling was biased because shops selling wildlife as well as shops linked to early cases were prioritized for sampling. The origin of the virus cannot be determined from the analyses available so far. Although gene barcode analysis of animal species in the study suggested that Myotis, Nyctereutes and Melogale-species that have been recognized as potential host species of sarbecoviruses-were present at the market, these barcodes were mostly detected within the SARS-CoV-2 RT-qPCR-negative samples from the environment. It remains pos...
This new paper starts by reviewing the evidence supporting the Huanan Market hypothesis, and some of the details are FASCINATING!

To begin with, of the 174 COVID cases identified with an onset of December 2019, 32% had a link to the Huanan Market.

In a city of 12 million.

3/ "INTRODUCTION Many of the earliest known cases of COVID-19 worked at or visited the Huanan Seafood Wholesale Market ("Huanan market") in the city of Wuhan, a link first made by clinicians at different hospitals throughout the city. Retrospective review of early COVID-19 cases identified 174 patients with onset in December 2019, 32% of whom had an ascertained link to this location, within a city of over 12 million."
Read 24 tweets

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