4 ms·

Linking a google scholar query with results does not imply a broad base of valid evidence. It just means people went looking and published. The top three, whic

by svnt 4y ago

Linking a google scholar query with results does not imply a broad base of valid evidence. It just means people went looking and published. The top three, which are the only ones I bothered to skim, have quality problems. The third one seems to be the most cited so I spent the most time with it. It in effect reduces to “if you were hospitalized with COVID” you now have significant cognitive impairments, but from my brief reading there is no “before” so it could just as easily be titled “cognitively impaired people make bad life choices that lead to pre-existing conditions that lead to (exposure to and) hospitalization with COVID.” Additionally the sample of N at 84k is misleading as only roughly 200 people are in their “significantly impaired” set. It was a quick read, as I said, and I may have oversimplified, so if I’m wrong, please feel free to respond with corrections.

giantg2 4y ago
And at 200 in 84k, the percent of affected individuals are unlikely to affect aggregate data in any practical way (if those numbers even apply to peds, which I'm skeptical of). Nor would there be any actionable solution.
AnthonBerg 4y ago
Thank you for engaging! Sincerely. If – if! – we take it as a valid premise that cognitive impairment exists after COVID-19. In adults. And if we take it as a valid premise that this is exhibited in younger people too. Then: I find it interesting to think about how one would study progress or decline in an education system, i.e. to look at that system itself to maintain and increase quality of the system. And: if and how one can reveal or disprove a population-scale effect on cognition due to this particular illness. Regarding cognitive deficits or impairment, I’m not focusing solely on brain damage as the cause, although it is known to occur. There’s also vascular and endothelal dysfunction, endocrine issues like abnormally low cortisol and blood glucose dysregulation, and immune dysregulation – T-cells in the brain (not good, not usual), and elevated inflammatory cytokines which are known to affect behavior. (This is all unsourced; There exist sources for it.) A lot of this is reversible. It’s not known that all of it is. I think we ought to look at these issues. In this context. I’m interested in thinking about and discussing the scientific mechanisms with which to look.
- svnt 4y ago
  I’m curious why you think any of this should be novel to the coronavirus COVID-19. We are affected by every infection. There are a number of studies that show if you ask people about the long-term effects of any infection they will report similar numbers to what is being reported about coronavirus. You can take this to support the previous paragraph, or as an instance of placebo effect. If you’re interested in how viral infection impacts brain function there’s a lot of cool information out there. I would not start in a speculative area like COVID-19. Maybe start with viral meningitis. Alternatively if you want to stay speculative some people think that mutations related to our rapid evolutionary increase in brain size may have been in part down to zoonotic virus exposure a couple million years ago. edit: Maybe you would enjoy The Tangled Tree by David Quammen.
  - AnthonBerg 4y ago
    Thanks for the book recommendation! Much appreciated! > I’m curious why you think any of this should be novel to the coronavirus COVID-19. We are affected by every infection. This review paper might summarize my inclination to consider SARS-CoV-2 different in this regard: “The Neurobiology of Long COVID” — M. Monje, PhD, Neurology at Stanford & A. Iwasaki PhD, Immunobiology at Yale. Publication status: In Print, Journal Pre-Print Available Online October 7, 2022 — https://doi.org/10.1016/j.neuron.2022.10.006 https://doi.org/10.1016/j.neuron.2022.10.006 One paragraph mentions effects in children: “Similarly, a 2-year a retrospective cohort study using the TriNetX electronic health records network of 1,487, 712 individuals with COVID-19 and a similar number of matched controls with a different respiratory infection found continued risk of cognitive impairment at 2-years from diagnosis (Taquet et al., 2022). In contrast to risk of cognitive impairment, the risk of anxiety and mood disorders normalized within 2 months following SARS-CoV-2 infection (Taquet et al., 2022). This TriNetX study provides some of the only available data about cognitive deficits in children and found in this retrospective cohort study that children did not exhibit an increased risk of anxiety or mood disorder diagnoses, but did exhibit increased risk of cognitive deficits (HR 1.2) and insomnia (HR 1.29) compared to children with different respiratory infections (Taquet et al., 2022). Unlike the adult cohort in this study, the risk of cognitive deficits in children normalized to the level observed in controls with a different respiratory infection by 491 days after COVID-19 (Taquet et al., 2022).” There’s a lot more to the paper.

by svnt 4y ago

giantg2 4y ago

And at 200 in 84k, the percent of affected individuals are unlikely to affect aggregate data in any practical way (if those numbers even apply to peds, which I'm skeptical of). Nor would there be any actionable solution.

AnthonBerg 4y ago

Thank you for engaging! Sincerely. If – if! – we take it as a valid premise that cognitive impairment exists after COVID-19. In adults. And if we take it as a valid premise that this is exhibited in younger people too. Then: I find it interesting to think about how one would study progress or decline in an education system, i.e. to look at that system itself to maintain and increase quality of the system. And: if and how one can reveal or disprove a population-scale effect on cognition due to this particular illness. Regarding cognitive deficits or impairment, I’m not focusing solely on brain damage as the cause, although it is known to occur. There’s also vascular and endothelal dysfunction, endocrine issues like abnormally low cortisol and blood glucose dysregulation, and immune dysregulation – T-cells in the brain (not good, not usual), and elevated inflammatory cytokines which are known to affect behavior. (This is all unsourced; There exist sources for it.) A lot of this is reversible. It’s not known that all of it is. I think we ought to look at these issues. In this context. I’m interested in thinking about and discussing the scientific mechanisms with which to look.

svnt 4y ago
I’m curious why you think any of this should be novel to the coronavirus COVID-19. We are affected by every infection. There are a number of studies that show if you ask people about the long-term effects of any infection they will report similar numbers to what is being reported about coronavirus. You can take this to support the previous paragraph, or as an instance of placebo effect. If you’re interested in how viral infection impacts brain function there’s a lot of cool information out there. I would not start in a speculative area like COVID-19. Maybe start with viral meningitis. Alternatively if you want to stay speculative some people think that mutations related to our rapid evolutionary increase in brain size may have been in part down to zoonotic virus exposure a couple million years ago. edit: Maybe you would enjoy The Tangled Tree by David Quammen.
- AnthonBerg 4y ago
  Thanks for the book recommendation! Much appreciated! > I’m curious why you think any of this should be novel to the coronavirus COVID-19. We are affected by every infection. This review paper might summarize my inclination to consider SARS-CoV-2 different in this regard: “The Neurobiology of Long COVID” — M. Monje, PhD, Neurology at Stanford & A. Iwasaki PhD, Immunobiology at Yale. Publication status: In Print, Journal Pre-Print Available Online October 7, 2022 — https://doi.org/10.1016/j.neuron.2022.10.006 https://doi.org/10.1016/j.neuron.2022.10.006 One paragraph mentions effects in children: “Similarly, a 2-year a retrospective cohort study using the TriNetX electronic health records network of 1,487, 712 individuals with COVID-19 and a similar number of matched controls with a different respiratory infection found continued risk of cognitive impairment at 2-years from diagnosis (Taquet et al., 2022). In contrast to risk of cognitive impairment, the risk of anxiety and mood disorders normalized within 2 months following SARS-CoV-2 infection (Taquet et al., 2022). This TriNetX study provides some of the only available data about cognitive deficits in children and found in this retrospective cohort study that children did not exhibit an increased risk of anxiety or mood disorder diagnoses, but did exhibit increased risk of cognitive deficits (HR 1.2) and insomnia (HR 1.29) compared to children with different respiratory infections (Taquet et al., 2022). Unlike the adult cohort in this study, the risk of cognitive deficits in children normalized to the level observed in controls with a different respiratory infection by 491 days after COVID-19 (Taquet et al., 2022).” There’s a lot more to the paper.