(Aspiring) Existential risk researcher | President Effective Altruism Groningen
Siebe(Siebe Rozendal)
Karma: 162
Your risk of developing long COVID is probably high
A case for strategy research: what it is and why we need more of it
Just coming to this now, after Altman’s firing (which seems unrelated?)
At age 5, she began waking up in the middle of the night, needing to take a bath to calm her anxiety. By 6, she thought about suicide, though she didn’t know the word.”
To me, this adds a lot of validity to the whole story and I haven’t seen these points made:
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Becoming suicidal at such an early age isn’t normal, and very likely has a strong environmental cause (like being abused, or losing a loved one)
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The bathing to relieve anxiety is typical sexual trauma behavior (e.g. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3577979/)
Of course, we don’t know for sure that she told the truth that this started at that age, but we can definitely not dismiss it.
On the recovered memories: I listen to a lot of podcasts where people talk about their own trauma and healing (with respected therapists). It’s very common in those that people start realizing in adulthood that something was wrong in their childhood, and increasingly figure out why they’ve always felt so ‘off’.
On the shadowbanning & hacking: This part feels more tenuous to me, especially the shadowbanning. But I don’t think this disqualifies the rest of the story. She’s had a really hard life and surely would have trust issues, and her brother is a powerful man.
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I am not sure why you believe good strategy research always has infohazards. That’s a very strong claim. Strategy research is broader than ‘how should we deal with other agents’. Do you think Drexler’s Reframing Superintelligence: Comprehensive AI Systems or The Unilateralist’s Curse were negative expected value? Because I would classify them as public, good strategy research with a positive expected value.
Are there any specific types of infohazards you’re thinking of? (E.g. informing unaligned actors, getting media attention and negative public opinion)
I agree with you that #3 seems the most valuable option, and you are correct that we aren’t as plugged in—although I am much less plugged in (yet) than the other two authors. I hope to learn more in the future about
How much explicit strategy research is actually going on behind close doors, rather than just people talking and sharing implicit models.
How much of all potential strategy research should be private, and how much should be public. My current belief is that more strategy research should be public than private, but my understanding of info hazards is still quite limited, so this belief might change drastically in the future.
To respond to your other questions:
Are there enough people and funding to sustain a parallel public strategy research effort and discussion?
I am not sure whether I get the question: I don’t think there is currently enough people or funding being allocated to public strategy research, but I think there could be a sustained public strategy research field. I also think there is not a high threshold for a critical mass: just a few researchers communicating with an engaged audience seems enough to sustain the research field.
Are there serious info hazards, and if so can we avoid them while still having a public discussion about the non-hazardous parts of strategy?
Yes, there are serious info hazards. And yes, I think the benefits of having a public discussion outweigh the (manageable) risk that comes with public discussion. If there is a clear place for info-hazardous content to be shared (which there is: the draft-sharing network) and when there is a clear understanding and policy for limiting info-hazards (which can be improved on a lot), public discussion will have at least the following advantages:
Exposure to wider array of feedback will, on expectation, improve the quality of ideas
Outsiders have more accessible knowledge to learn from to contribute later. There are probably also a lot of benefits to be gained from making other people more strategically savvy!
It makes it easier for non-affiliated/less-connected individuals to create and share knowledge
No, these problems are most probably cause by a lack of oxygen getting through to tissues. There’s a large amount of patients reporting these severe symptoms in patients groups, and they’re not elderly.
It honestly feels to me like you really want to believe long COVID isn’t a big deal somehow.
In addition, we know that 100% of patients with long COVID have microclots, at least in this study: https://www.researchsquare.com/article/rs-1205453/v1
Interestingly, they diagnosed patients not via PCR or antibodies, but based on exclusion and symptom diagnosis:
“Patients gave consent to study their blood samples, following clinical examination and/or after filling in the South African Long COVID/PASC registry. Symptoms must have been new and persistent symptoms noted after acute COVID-19. Initial patient diagnosis was the end result of exclusions, only after all other pathologies had been excluded. This was done by taking a history of previous symptoms (before and after acute COVID- 19 infection), clinical examinations, and investigations including: full blood counts; N-terminal pro b-type natriuretic peptide (NTproBNP) levels (if raised it suggests cardiac damage); thyroid-stimulating 7 hormone (TSH); C-reactive protein levels; the ratio between the concentrations of the enzymes aspartate transaminase and alanine transaminase (AST/ALT ratio) andelectrocardiogram (ECG) +/- stress testing. If the mentioned tests were in the normal ranges, the lingering symptoms that can be ascribed to Long COVID/PASC were then assessed and included shortness of breath; recurring chest pain; lingering low oxygen levels; heart rate dysfunction (heart palpitations); constant fatigue (more than usual); joint and muscle pain; brain fog; lack of concentration; forgetfulness; sleep disturbances and digestive and kidney problems. These symptoms should have been persistent and new symptoms that were not present before acute COVID-19 infection and persistent for at least two months after recovery from acute (infective) COVID-19.” (P. 6-7)
I’d say this should be convincing evidence that as good as none of the patients that claim to have long covid have a psychosomatic issue. It’s not like microclots are a common and harmless issue either.
Awesome in depth response! Yes, I was hoping this post to serve as an initial alarm bell to look further into, rather than being definitive advice based on a comprehensive literature review.
I can’t respond to everything, at least not at once, but here’s some:
categories of ‘at least 12 weeks’ and ‘at least 1 year’ do overlap, right?
I think the different waves may have had different underreporting factors, with least underreporting during Delta, so we can’t take those rates at face value, and I prefer using estimated cases whenever possible
this Washington Post article supports the ‘Scheming Sam’ Hypothesis: anonymous reports mostly from his time at Y Combinator
The 15% is an upper estimate of people estimating ‘some loss’ of health, so not everyone would be severely disabled.
Unfortunately, the data isn’t great, and I can’t produce a robust estimate right now
You have far more faith in the rationality of government decision making during novel crises than I do.
Healthcare workers can barely or often not at all with with long covid.
Lowering infection rates, remaining able to work, and not needing to make high demands on the healthcare system seems much better for the economy. This is not an infohazard at all.
This was very informative!
How would you translate this into a heuristic? And how much do I need to have a secondary skill, rather than finding a partner that has a great complementary skill?
Meta’s actions seem unrelated?
Except that herd immunity isn’t really a (permanent) thing; only temporary
I had not seen it, because I don’t read this form these days. I can’t reply in too much detail but here are some points:
I think it’s a decent attempt, but a little biased towards the “statistically clever” estimate. I do agree that many studies are pretty done. However, I’ve seen good ones that include controls, confirm infection via PCR, are large, and have pre pandemic health data. This was in a Dutch presentation of a data set though, and not clearly reported for some reason. (This is the project, but their data is not publicly available: https://www.lifelines.nl/researcher/explore-lifelines/covid-data).
It is really difficult to get a proper control group, because both PCR tests and antibody tests have significant false negative rates.
Furthermore, the Zvi asserts that self reports lead to an overestimate because they are inaccurate. I agree that self reports are inaccurate, but there will definitely be people with long COVID that think it’s something else (e.g. burnout), so this can really go both ways.
In addition, we have biological data with a control group and prepandemic data: https://www.nature.com/articles/s41586-022-04569-5 There were many significant differences in the brain scans of these groups. I can’t do the digging to translate those data into frequency estimates though.
I also think that for outsiders, long COVID symptoms sound vague: fatigue, brain fog, etc. In fact, there’s a lot of clear symptoms, such as orthostatic intolerance, post exertion al symptom exacerbation, heart palpitations, muscle tremors, oxygen saturation drops.
Lastly, I think we should be careful to assess future risk based on past risk: variants change, vaccine protection changes, and as I write above, there’s some initial data suggesting reinfections are worse due to a weakened immune system.
Yes, vaccine injury is actually rather common—I’ve seen a lot of very credible case reports reporting either initiation of symptoms since vaccine (after having been infected), or more often worsening of symptoms. Top long COVID researchers also believe these.
I don’t think the data for keto is that strong. Plenty of people with long COVID are trying it with not amazing results.
Uhm, no? I’m quoting you on the middle category, which overlaps with the long category.
Also, there’s no need to speculate, because there have been studies linking severity and viral load to increased risk of long COVID. https://www.cell.com/cell/fulltext/S0092-8674(22)00072-1
See figure 2 of this large scale survey: https://www.ons.gov.uk/peoplepopulationandcommunity/healthandsocialcare/conditionsanddiseases/bulletins/prevalenceofongoingsymptomsfollowingcoronaviruscovid19infectionintheuk/7october2021
“As a proportion of the UK population, prevalence of self-reported long COVID was greatest in people aged 35 to 69 years, females, people living in more deprived areas, those working in health or social care, and those with another activity-limiting health condition or disability”
Seropositivity is also not a good indicator for having had covid: https://wwwnc.cdc.gov/eid/article/27/9/21-1042_article
Some researchers believe absence of antibodies after infection is positively correlated with long covid (I don’t have a source).
This study is bunk and it’s harmful for adequate treatment of seronegative treatment.
That French study is bunk.
Seropositivity is NOT AT ALL a good indicator for having had covid: https://wwwnc.cdc.gov/eid/article/27/9/21-1042_article
It is entirely possible that all those patients who believe they had COVID are right.
Some researchers believe absence of antibodies after infection is positively correlated with long covid (I don’t have a source).
This study is bunk and it’s harmful for adequate treatment of seronegative patients. The psychosomatic narrative has been a lazy answer stifling solid scientific research into illnesses that are not well understood yet.