This is not going to be kind, but it’s true and necessary to state. I apologize in advance.
Had you asked me in advance, I would have said that Katja in particular is likely to buy into long covid even in a world where long covid is completely psychosomatic; I think you (Katja) are probably unusually prone to looking-for-reasons-to-”believe”-things-which-are-actually-psychosomatic, without symmetrically looking-for-reasons-to-”disbelieve”.
On the object level: the “Long covid probably isn’t psychosomatic” section of the post looks pretty compatible with that prior. That section basically says two things:
Just because reports of long covid are basically uncorrelated with having had covid does not imply that long covid does not happen
There is still evidence of higher-than-usual death rates among people who have had covid
If we take both of these as true, they point to a world where there are some real post-covid symptoms, but the large majority of reported long covid symptoms are still psychosomatic. That seems plausible, but for some reason it isn’t propagated into the other sections of the post. For instance, the very first sections of this post are talking about anecdotes and survey studies (at least I think they’re survey studies based on a quick glance, didn’t look too close), and I do not see in any of those sections any warning along the lines of “BY THE WAY THE LARGE MAJORITY OF THIS IS PROBABLY PSYCHOSOMATIC”. You’re counting evidence which should have been screened off by the lack of correlation between self-reported long covid symptoms and actually having had covid.
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.
36% of our cohort represented serologic nonresponders
I don’t see any way in which the results of the French study are incompatible with a 64% true positive rate on “did this person previously have covid”. (Also, a 64% true positive rate is actually decent Bayesian evidence for having had covid, assuming a sufficiently large % of the underlying population has had covid, such that whatever the false positive rate is doesn’t cause most/all of your positives to be false positives.)
Writing up a Long Covid post and noticed this. Several things even taking study here at face value. Putting this here as a ‘preprint’ basically to see if there are counterarguments. And regardless, thanks for the link, it should be considered, but I do not think this constitutes bunk.
One, everyone with a Ct of about 25 or lower got antibodies, so we’re talking about light cases or outright false positives that then didn’t get antibodies. And the spike in cases of Ct~37 is weird enough that I suspect something wrong with the PCRs.
Two, this implies that positive antibody test still means Covid (no false positives, only false negatives) so it would take a VERY large correlation with long Covid to have no correlation show up in the final data—keep in mind that Ct<25 still meant full positives later, so the correlation here can’t be that big.
Three, we’d basically have to assume that virus count isn’t linked to chance of long Covid or this doesn’t make any sense, because all the high virus count cases are getting positives anyway. But lots of virus seems like it would be more likely to lead to long Covid because physics?
Also from the French paper they use this source: https://pubmed.ncbi.nlm.nih.gov/33139419/ which reports tests have high accuracy and has >10x the sample size of the one linked above.
My interpretation of the linked study here is ’sufficiently mild cases sometimes don’t generate antibodies but show up on PCR, and/or PCR tests are getting false positives and we should not take Ct>30 very seriously. E.g. from here.
7. What can CT values tell us? Samples with CT values <32 generally contain sufficient genetic material for WGS and are more likely to contain replication competent virus. Although there are limitations in the use of CT values, they are one factor to consider when evaluating molecular test results and can be useful in assessing the trend in the viral load. If there is high suspicion of a new infection, laboratories may attempt WGS on samples with CT value <32.
Same problem as with Lyme Disease. Weak or no antibody reaction is only good news IF it indicates absence of the pathogene. While this is not unreasonable to assume, it still needs to be demonstrated, preferably over a wide variety of differen tissues.
I agree that I’m more likely to be concerned about in-fact-psychosomatic things than average, and on the outside view, thus probably biased in that direction in interpreting evidence. Sorry if that colors the set of considerations that seem interesting to me. (I didn’t mean to claim that this was an unbiased list, sorry if I implied it. )
Some points regarding the object level:
The scenario I described was to illustrate a logical point (that the initially tempting inference from that study wasn’t valid). So I wouldn’t want to take the numbers from that hypothetical scenario and apply them across the board to interpreting other data. I haven’t thought through what range of possible numbers is really implied, or whether there are other ways to make sense of these prima facie weird findings (especially re lack of connection between having covid and thinking you have covid). If I put a lot of stock in that study, I agree there is some adjustment to be made to other numbers (and probably anyway—surely some amount of misattribution is going on, and even some amount of psychosomatic illness).
My description was actually of how you would get those results if approximately none of the illness was psychosomatic but a lot of it was other illnesses (the description would work with psychosomatic illnesses too, but I worry that you misread my point, since you are saying that in that world most things are psychosomatic, and my point was that you can’t infer that anything was psychosomatic).
If the scenario I described was correct, the rates of misattribution implied would be specific to that population and their total ignorance about whether they had covid, rather than a fact intrinsic to covid in general, and applicable to all times and places. I do find it very hard to believe that in general there is not some decently strong association between having covid and thinking you have covid, even if also a lot of errors.
It’s a single study, and single studies find all kinds of things. I don’t recall seeing other evidence supporting it. In such a case, I’m inclined to treat it as worthy of adding some uncertainty, but not worthy of a huge update about everything.
If this consideration reduced real long covid cases by a factor of two, it doesn’t feel like that changes the story very much (there’s a lot of factor-of-two-level uncertainty all over the place, especially in guessing what the rate is for a specific demographic), so I guess it doesn’t seem cruxy enough to give a lot of attention to.
I agree that mostly it isn’t salient to me that some fraction of cases are misattributions, and that maybe I should keep it in mind more, and say things like ‘it looks like many people who think they had covid can no longer do their jobs’ instead of taking things at face value. Though in my defense, this was a list of considerations, so I’m also not flagging all of the other corrections one might want to make to numbers throughout, as I might if I were doing a careful calculation.
It’s true that I don’t really believe that half of the bad cases at least are misattributions or psychosomatic—the psychosomatic story seems particularly far-fetched (particularly for the bad cases). Perhaps I’m mis-imagining what this would look like. Is there other evidence for this that you are moved by?
I put a lot more trust in a single study with ground-truth data than in a giant pile of studies with data which is confounded in various ways. So, I trust the study with the antibody tests more than I’d trust basically-any number of studies relying on self-reports. (A different-but-similar application of this principle: I trust the Boston wastewater data on covid prevalence more than I trust all of the data from test results combined.)
I probably do have relatively high prior (compared to other people) on health-issues-in-general being psychosomatic. The effectiveness of placebos (though debatable) is one relevant piece of evidence here, though a lot of my belief is driven by less legible evidence than that.
I expect some combination of misattribution, psychosomaticity, selection effects (e.g. looking at people hospitalized and thereby accidentally selecting for elderly people), and maybe similar issues which I’m not thinking of at the moment to account for an awful lot of the “long covid” from self-report survey studies. I’m thinking less like 50% of it, and more like 90%+. Basically, when someone runs a survey and publishes data from it, I expect the results to mostly measure things other than what the authors think they’re measuring, most of the time, especially when an attribution of causality is involved.
Even if long covid is entirely psychosomatic, it’s worth avoiding those psychosomatic effects. One way to avoid them is to debunk (potentially at the gut intuition level, which is harder to reliably do) non-psychosomatic causes of it. Another way is to avoid covid in the first place. I expect the most effective strategy will include some combination of these.
I see “psychosomatic” often used as a semantic stopsign. Once something is called “psychosomatic”, people typically stop trying to figure out a way to solve the problem. I don’t know of any reliable and credible ways to resolve psychosomatic issues, it’s mostly meditation guys and alternative medicine quacks who even try.
If it’s really true that a large amount of health-issues-in-general are psychosomatic, then that’s a really huge problem which we don’t have an adequate solution for! (I expect that you agree with this, I just am trying to push against the weight of the semantic stopsign that people have around this concept.)
Psychosomatic is a word that’s gets often used as if that would mean that illnesses aren’t real.
If you tell someone with an allergy to cats to imagine that they are stocking a cat, that can be enough to trigger the allergy symptoms. The fact that an imagined cat is good enough to trigger the allergy shows quite clearly that the allergy is partly psychosomatic as it can be triggered psychologically.
The underlying mechanisms of such an immune response are however deep. One model of long COVID is, that it’s partly about autoimmune issues. Those might be as psychosomatic as the above example of cat allergy. There’s a neuronal pattern that gets the body to trigger defenses in a misaligned way.
Good point. If we take that post’s analysis at face value, then a majority of reported long covid symptoms are probably psychosomatic, but only just barely a majority, not a large majority. Though looking at the post, I’d say a more accurate description is that at least a majority of long covid symptoms are psychosomatic, i.e. it’s a majority even if we pretend that all of the supposedly-long-covid symptoms in people who actually had covid are “real”.
Why does the post imply that a majority of long covid symptoms are psychosomatic?
Let’s say covid is entirely non-psychosomatic, and that we have the following groups:
(0) People who never had covid, never thought they had covid.
(1) People with asymptomatic covid, who don’t believe they had covid.
(2) People with noticeable covid, no long covid.
(3) People with noticeable covid, including long covid.
(4) People who mistake something short-term (like a cold) for covid.
(5) People who have some serious long-term issues, that they mistake for long covid.
Now we have three variables:
(a) Antibody group = (1) + (2) + (3)
(b) Belief-in-covid = (2) + (3) + (4) + (5)
(c) Claimed long covid = (3) + (5)
If group (4) is relatively small and/or group (1) is relatively large and/or group (5) is relatively large, then it makes sense that (b) is a way better predictor for (c) than (a) is.
The french study found that (a) isn’t a good predictor for (c) if you control for (b). I don’t have a good enough intuition for regression with multiple variables to know whether this is unsurprising given the previous paragraph; but my guess is that this is unsurprising given the previous paragraph.
I still don’t see how you can know that the majority of long covid is misattribution and the like. If (1) is large, and (4) + (5) are both negligibly small, then belief-in-covid will be a better predictor of long covid just because symptomatic covid is a better predictor of long covid than asymptomatic+symptomatic covid is.
I would be surprised if the worst cases, where people can’t really work and it lasts about half a year or longer, were mostly psychosomatic, or at least mostly psychosomatic in a way that’s easily avoidable by just having different beliefs about long COVID. Can you really believe yourself into debilitating chronic fatigue and brain fog for half a year?
(EDITED: “a year → “half a year”, since I don’t recall long COVID studies going much longer than half a year, when I looked into them, which was probably 3-6 months ago.)
I broadly agree but don’t think that proves covid was the culprit. Vague shitty symptoms doctors refuse to grapple with were a problem long before covid, and if people with these symptoms can get better care by calling it long covid than leaving it open or blaming something else, they’d be stupid not to.
That’s a good point. I think the comparison of severe symptoms between COVID-positive COVID-negative matched controls would be good evidence about the risk. I don’t recall if any comparison studies tracked severity between positive and matched negative groups, though, rather than mostly just presence of symptoms, and I do recall studies without comparisons tracking severity, which people could use to report non-COVID-related severe symptoms, as you suggest.
When I looked into this there was a paper that compared psych sequelae from covid to influenza and flu-like illnesses and found “covid to be modestly worse except for myoneural junction and other muscular diseases, where covid 5xed the risk (although it’s still quite low in absolute terms). Dementia risk is also doubled, presumably mostly among the elderly.” This was not controlling for age or acute severity, and data was gathered pre-vaccine.
(note: I did this research months ago and haven’t done any follow-up, so trust what I wrote then over what I remember now)
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.
This mostly sounds like age-related problems. I do expect generic age-related pathologies to be accelerated by covid (or any other major stressor), but if that’s the bulk of what’s going on, then I’d say “long covid” is a mischaracterization. It wouldn’t be relevant to non-elderly people, and to elderly people it would be effectively the same as any other serious stressor.
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.
It’s not that I don’t want to believe it, it’s that long covid is the sort of thing I’d expect to hear people talk about and publish papers about even in a world where it isn’t actually significant, and many of those papers would have statistically-significant positive results even in a world where long covid isn’t actually significant. Long covid is a story which has too much memetic fitness independent of its truth value. So I have to apply enough skepticism that I wouldn’t believe it in a world where it isn’t actually significant.
No, these problems are most probably cause by a lack of oxygen getting through to tissues.
That sounds right for shortness of breath, chest pain, and low oxygen levels. I’m more skeptical that it’s driving palpitations, fatigue, joint and muscle pain, brain fog, lack of concentration, forgetfulness, sleep disturbance, and digestive and kidney problems; those sound a lot more like a list of old-age issues.
“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”
That is not how senescent cells work. They turn over on a fast timescale. If covid induces a bunch of senescent cell development (which indeed makes sense), those senescent cells should generally be cleared out on a timescale of weeks. Any long-term effects would need to be mediated by something else.
But some of those SnCs probably won’t be cleared, and that extra burden of SnCs (especially if it’s much higher than what intrinsic aging produces during a short period of time) might be what’s causing long covid.
At this point, I have yet to see any compelling evidence that any SnCs stick around over a long timescale, despite this being a thing which I’d expect to have heard about if anybody had the evidence. Conversely, it sure does look like treatments to remove senescent cells have to be continuously administered; a one-time treatment wears off on roughly the same timescale that SnCs turn over. That pretty strongly suggests that there are not pools of long-lived SnCs hanging around. And a noticeable pathology would take a lot of SnCs sticking around.
The paper you linked to seems to claim that SnCs do stick around.
In old mice, baseline SnC levels are about 5-fold higher, and SnC removal rate is slower than in young mice (p=0.038).
This suggests that middle-aged mice should also have some baseline SnC level, although perhaps not as much as old mice. Also, the level of SnCs didn’t return to baseline in the old mice even at the 40 day mark.
“Baseline” does not mean they stick around. It means that background processes introduce new SnCs at a steady rate, so the equilibrium level is nonzero. As the removal rate slows, that equilibrium level increases, but that still does not mean that the “baseline” SnCs are long-lived, or that a sudden influx of new SnCs (from e.g. covid) will result in a permanently higher level.
Even if the original SnCs are eventually eliminated (which isn’t entirely clear), it sure looks like they should increase the SnC baseline anyway. It’s not just background processes that can produce new SnCs, but SnCs themselves produce new, secondary SnCs too. So, it’s not unlikely that adding a bunch of SnCs to the baseline pool of SnCs (whose size increases with age) could further increase the size of this pool. And that would be a net increase in biological age.
This might not be a problem for young mice which can eliminate SnCs fairly quickly, but it seems to be a big problem for old mice. Middle-aged mice probably lie somewhere in between. I’d also expect that overweight, obese, or otherwise messed-up, middle-aged mice would fare worse.
It’s not just background processes that can produce new SnCs, but SnCs themselves produce new, secondary SnCs too.
Imagine that each new SnC produced 3 new SnCs within a day, and also that SnCs had a 50% chance of being removed each day. In that case, there will be 4*0.5 = 2x as many SnCs tomorrow as there is today, leading to exponential runaway growth, immediately exploding in the number of SnCs and dying.
On the other hand, imagine that they only produce 1 new SnC within a day, and also that they had a 66% chance of being removed each day. In that case there will be 2*0.33 = 0.66x as many SnCs tomorrow, leading to quickly returning to the equillibrium caused by outside production.
You’d need some sort of fine-tuning where the production and removal are extremely close to each other to not either have explosive growth or rapid equillibration.
It’s probably too early to compare the amount of senescence that’s produced by SARS-CoV-2 versus other viruses, but what is known is that several viruses (including influenza) do induce the development of senescent cells in several tissues.
I’d say that unhealthy-for-their-age young and middle-aged people and otherwise healthy-but-middle-aged people might want to be more cautious. Healthy-for-their-age young people probably don’t need to worry.
For what it’s worth, I agree that the post reads to me as not very balanced, but a lot of the evidence and arguments presented are still worrying, and I am still worried about long COVID. (I also don’t put myself above confirmation bias, though.)
G. Overall deaths from everything have been very unusually high at points in 2021, even in 15-64 age group
This could also be explained by things other than COVID or long COVID, too, e.g. lockdown/isolation, less exercise, increased depression, poorer access to healthcare.
Sure it is essential to differentiate between those who have been tested for COVID and that self-reporting which, in the absence of a test, is another information source.
To repeat my experience of becoming ill in the time of COVID 19: I couldn’t get a test in July 2020; I don’t know whether it was COVID-19 that hit me like a speeding train. I still have cognitive difficulties, severe fatigue, continuous headaches, lack of taste and smell, and other new things which have gone wrong physically. I’m waiting for the latest results of brain/spine MRI; I’m without a diagnosis. My reading suggests M.E., encephalitis, Long COVID and possibly lots of things—continued testing thus far provides no answer. I’ve also learned about FND and can see how these symptoms could, in the absence of an actual biomarker, be put under that umbrella.
To have one’s symptoms acknowledged matters. Losing one’s fundamental abilities to function is so devastating; reading that such symptom clusters are deemed psychosomatic seems, to the afflicted, unhelpful.
This is not going to be kind, but it’s true and necessary to state. I apologize in advance.
Had you asked me in advance, I would have said that Katja in particular is likely to buy into long covid even in a world where long covid is completely psychosomatic; I think you (Katja) are probably unusually prone to looking-for-reasons-to-”believe”-things-which-are-actually-psychosomatic, without symmetrically looking-for-reasons-to-”disbelieve”.
On the object level: the “Long covid probably isn’t psychosomatic” section of the post looks pretty compatible with that prior. That section basically says two things:
Just because reports of long covid are basically uncorrelated with having had covid does not imply that long covid does not happen
There is still evidence of higher-than-usual death rates among people who have had covid
If we take both of these as true, they point to a world where there are some real post-covid symptoms, but the large majority of reported long covid symptoms are still psychosomatic. That seems plausible, but for some reason it isn’t propagated into the other sections of the post. For instance, the very first sections of this post are talking about anecdotes and survey studies (at least I think they’re survey studies based on a quick glance, didn’t look too close), and I do not see in any of those sections any warning along the lines of “BY THE WAY THE LARGE MAJORITY OF THIS IS PROBABLY PSYCHOSOMATIC”. You’re counting evidence which should have been screened off by the lack of correlation between self-reported long covid symptoms and actually having had covid.
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.
Strong upvote, this is great info.
I don’t see any way in which the results of the French study are incompatible with a 64% true positive rate on “did this person previously have covid”. (Also, a 64% true positive rate is actually decent Bayesian evidence for having had covid, assuming a sufficiently large % of the underlying population has had covid, such that whatever the false positive rate is doesn’t cause most/all of your positives to be false positives.)
Writing up a Long Covid post and noticed this. Several things even taking study here at face value. Putting this here as a ‘preprint’ basically to see if there are counterarguments. And regardless, thanks for the link, it should be considered, but I do not think this constitutes bunk.
One, everyone with a Ct of about 25 or lower got antibodies, so we’re talking about light cases or outright false positives that then didn’t get antibodies. And the spike in cases of Ct~37 is weird enough that I suspect something wrong with the PCRs.
Two, this implies that positive antibody test still means Covid (no false positives, only false negatives) so it would take a VERY large correlation with long Covid to have no correlation show up in the final data—keep in mind that Ct<25 still meant full positives later, so the correlation here can’t be that big.
Three, we’d basically have to assume that virus count isn’t linked to chance of long Covid or this doesn’t make any sense, because all the high virus count cases are getting positives anyway. But lots of virus seems like it would be more likely to lead to long Covid because physics?
Also from the French paper they use this source: https://pubmed.ncbi.nlm.nih.gov/33139419/ which reports tests have high accuracy and has >10x the sample size of the one linked above.
My interpretation of the linked study here is ’sufficiently mild cases sometimes don’t generate antibodies but show up on PCR, and/or PCR tests are getting false positives and we should not take Ct>30 very seriously. E.g. from here.
The bulk of the issues were in CT values >=32.
Anyone have more thoughts?
Same problem as with Lyme Disease. Weak or no antibody reaction is only good news IF it indicates absence of the pathogene. While this is not unreasonable to assume, it still needs to be demonstrated, preferably over a wide variety of differen tissues.
I agree that I’m more likely to be concerned about in-fact-psychosomatic things than average, and on the outside view, thus probably biased in that direction in interpreting evidence. Sorry if that colors the set of considerations that seem interesting to me. (I didn’t mean to claim that this was an unbiased list, sorry if I implied it. )
Some points regarding the object level:
The scenario I described was to illustrate a logical point (that the initially tempting inference from that study wasn’t valid). So I wouldn’t want to take the numbers from that hypothetical scenario and apply them across the board to interpreting other data. I haven’t thought through what range of possible numbers is really implied, or whether there are other ways to make sense of these prima facie weird findings (especially re lack of connection between having covid and thinking you have covid). If I put a lot of stock in that study, I agree there is some adjustment to be made to other numbers (and probably anyway—surely some amount of misattribution is going on, and even some amount of psychosomatic illness).
My description was actually of how you would get those results if approximately none of the illness was psychosomatic but a lot of it was other illnesses (the description would work with psychosomatic illnesses too, but I worry that you misread my point, since you are saying that in that world most things are psychosomatic, and my point was that you can’t infer that anything was psychosomatic).
If the scenario I described was correct, the rates of misattribution implied would be specific to that population and their total ignorance about whether they had covid, rather than a fact intrinsic to covid in general, and applicable to all times and places. I do find it very hard to believe that in general there is not some decently strong association between having covid and thinking you have covid, even if also a lot of errors.
It’s a single study, and single studies find all kinds of things. I don’t recall seeing other evidence supporting it. In such a case, I’m inclined to treat it as worthy of adding some uncertainty, but not worthy of a huge update about everything.
If this consideration reduced real long covid cases by a factor of two, it doesn’t feel like that changes the story very much (there’s a lot of factor-of-two-level uncertainty all over the place, especially in guessing what the rate is for a specific demographic), so I guess it doesn’t seem cruxy enough to give a lot of attention to.
I agree that mostly it isn’t salient to me that some fraction of cases are misattributions, and that maybe I should keep it in mind more, and say things like ‘it looks like many people who think they had covid can no longer do their jobs’ instead of taking things at face value. Though in my defense, this was a list of considerations, so I’m also not flagging all of the other corrections one might want to make to numbers throughout, as I might if I were doing a careful calculation.
It’s true that I don’t really believe that half of the bad cases at least are misattributions or psychosomatic—the psychosomatic story seems particularly far-fetched (particularly for the bad cases). Perhaps I’m mis-imagining what this would look like. Is there other evidence for this that you are moved by?
Good points. Some responses:
I put a lot more trust in a single study with ground-truth data than in a giant pile of studies with data which is confounded in various ways. So, I trust the study with the antibody tests more than I’d trust basically-any number of studies relying on self-reports. (A different-but-similar application of this principle: I trust the Boston wastewater data on covid prevalence more than I trust all of the data from test results combined.)
I probably do have relatively high prior (compared to other people) on health-issues-in-general being psychosomatic. The effectiveness of placebos (though debatable) is one relevant piece of evidence here, though a lot of my belief is driven by less legible evidence than that.
I expect some combination of misattribution, psychosomaticity, selection effects (e.g. looking at people hospitalized and thereby accidentally selecting for elderly people), and maybe similar issues which I’m not thinking of at the moment to account for an awful lot of the “long covid” from self-report survey studies. I’m thinking less like 50% of it, and more like 90%+. Basically, when someone runs a survey and publishes data from it, I expect the results to mostly measure things other than what the authors think they’re measuring, most of the time, especially when an attribution of causality is involved.
Even if long covid is entirely psychosomatic, it’s worth avoiding those psychosomatic effects. One way to avoid them is to debunk (potentially at the gut intuition level, which is harder to reliably do) non-psychosomatic causes of it. Another way is to avoid covid in the first place. I expect the most effective strategy will include some combination of these.
I see “psychosomatic” often used as a semantic stopsign. Once something is called “psychosomatic”, people typically stop trying to figure out a way to solve the problem. I don’t know of any reliable and credible ways to resolve psychosomatic issues, it’s mostly meditation guys and alternative medicine quacks who even try.
If it’s really true that a large amount of health-issues-in-general are psychosomatic, then that’s a really huge problem which we don’t have an adequate solution for! (I expect that you agree with this, I just am trying to push against the weight of the semantic stopsign that people have around this concept.)
Psychosomatic is a word that’s gets often used as if that would mean that illnesses aren’t real.
If you tell someone with an allergy to cats to imagine that they are stocking a cat, that can be enough to trigger the allergy symptoms. The fact that an imagined cat is good enough to trigger the allergy shows quite clearly that the allergy is partly psychosomatic as it can be triggered psychologically.
The underlying mechanisms of such an immune response are however deep. One model of long COVID is, that it’s partly about autoimmune issues. Those might be as psychosomatic as the above example of cat allergy. There’s a neuronal pattern that gets the body to trigger defenses in a misaligned way.
My impression from here is that “reports of long covid are basically uncorrelated with having had covid” is a misunderstanding of the French study.
Good point. If we take that post’s analysis at face value, then a majority of reported long covid symptoms are probably psychosomatic, but only just barely a majority, not a large majority. Though looking at the post, I’d say a more accurate description is that at least a majority of long covid symptoms are psychosomatic, i.e. it’s a majority even if we pretend that all of the supposedly-long-covid symptoms in people who actually had covid are “real”.
Why does the post imply that a majority of long covid symptoms are psychosomatic?
Let’s say covid is entirely non-psychosomatic, and that we have the following groups:
(0) People who never had covid, never thought they had covid.
(1) People with asymptomatic covid, who don’t believe they had covid.
(2) People with noticeable covid, no long covid.
(3) People with noticeable covid, including long covid.
(4) People who mistake something short-term (like a cold) for covid.
(5) People who have some serious long-term issues, that they mistake for long covid.
Now we have three variables:
(a) Antibody group = (1) + (2) + (3)
(b) Belief-in-covid = (2) + (3) + (4) + (5)
(c) Claimed long covid = (3) + (5)
If group (4) is relatively small and/or group (1) is relatively large and/or group (5) is relatively large, then it makes sense that (b) is a way better predictor for (c) than (a) is.
The french study found that (a) isn’t a good predictor for (c) if you control for (b). I don’t have a good enough intuition for regression with multiple variables to know whether this is unsurprising given the previous paragraph; but my guess is that this is unsurprising given the previous paragraph.
Sorry, I was lumping together misattribution and the like under “psychosomaticity”, and I probably shouldn’t have done that.
I still don’t see how you can know that the majority of long covid is misattribution and the like. If (1) is large, and (4) + (5) are both negligibly small, then belief-in-covid will be a better predictor of long covid just because symptomatic covid is a better predictor of long covid than asymptomatic+symptomatic covid is.
I would be surprised if the worst cases, where people can’t really work and it lasts about half a year or longer, were mostly psychosomatic, or at least mostly psychosomatic in a way that’s easily avoidable by just having different beliefs about long COVID. Can you really believe yourself into debilitating chronic fatigue and brain fog for half a year?
(EDITED: “a year → “half a year”, since I don’t recall long COVID studies going much longer than half a year, when I looked into them, which was probably 3-6 months ago.)
I broadly agree but don’t think that proves covid was the culprit. Vague shitty symptoms doctors refuse to grapple with were a problem long before covid, and if people with these symptoms can get better care by calling it long covid than leaving it open or blaming something else, they’d be stupid not to.
That’s a good point. I think the comparison of severe symptoms between COVID-positive COVID-negative matched controls would be good evidence about the risk. I don’t recall if any comparison studies tracked severity between positive and matched negative groups, though, rather than mostly just presence of symptoms, and I do recall studies without comparisons tracking severity, which people could use to report non-COVID-related severe symptoms, as you suggest.
When I looked into this there was a paper that compared psych sequelae from covid to influenza and flu-like illnesses and found “covid to be modestly worse except for myoneural junction and other muscular diseases, where covid 5xed the risk (although it’s still quite low in absolute terms). Dementia risk is also doubled, presumably mostly among the elderly.” This was not controlling for age or acute severity, and data was gathered pre-vaccine.
(note: I did this research months ago and haven’t done any follow-up, so trust what I wrote then over what I remember now)
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.
This mostly sounds like age-related problems. I do expect generic age-related pathologies to be accelerated by covid (or any other major stressor), but if that’s the bulk of what’s going on, then I’d say “long covid” is a mischaracterization. It wouldn’t be relevant to non-elderly people, and to elderly people it would be effectively the same as any other serious stressor.
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.
It’s not that I don’t want to believe it, it’s that long covid is the sort of thing I’d expect to hear people talk about and publish papers about even in a world where it isn’t actually significant, and many of those papers would have statistically-significant positive results even in a world where long covid isn’t actually significant. Long covid is a story which has too much memetic fitness independent of its truth value. So I have to apply enough skepticism that I wouldn’t believe it in a world where it isn’t actually significant.
That sounds right for shortness of breath, chest pain, and low oxygen levels. I’m more skeptical that it’s driving palpitations, fatigue, joint and muscle pain, brain fog, lack of concentration, forgetfulness, sleep disturbance, and digestive and kidney problems; those sound a lot more like a list of old-age issues.
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”
Covid is airborne aging via SARS-CoV-2-induced senescent cell development.
Even non-elderly people might age faster, especially if they’re overweight or obese.
That is not how senescent cells work. They turn over on a fast timescale. If covid induces a bunch of senescent cell development (which indeed makes sense), those senescent cells should generally be cleared out on a timescale of weeks. Any long-term effects would need to be mediated by something else.
But some of those SnCs probably won’t be cleared, and that extra burden of SnCs (especially if it’s much higher than what intrinsic aging produces during a short period of time) might be what’s causing long covid.
At this point, I have yet to see any compelling evidence that any SnCs stick around over a long timescale, despite this being a thing which I’d expect to have heard about if anybody had the evidence. Conversely, it sure does look like treatments to remove senescent cells have to be continuously administered; a one-time treatment wears off on roughly the same timescale that SnCs turn over. That pretty strongly suggests that there are not pools of long-lived SnCs hanging around. And a noticeable pathology would take a lot of SnCs sticking around.
The paper you linked to seems to claim that SnCs do stick around.
This suggests that middle-aged mice should also have some baseline SnC level, although perhaps not as much as old mice. Also, the level of SnCs didn’t return to baseline in the old mice even at the 40 day mark.
“Baseline” does not mean they stick around. It means that background processes introduce new SnCs at a steady rate, so the equilibrium level is nonzero. As the removal rate slows, that equilibrium level increases, but that still does not mean that the “baseline” SnCs are long-lived, or that a sudden influx of new SnCs (from e.g. covid) will result in a permanently higher level.
Even if the original SnCs are eventually eliminated (which isn’t entirely clear), it sure looks like they should increase the SnC baseline anyway. It’s not just background processes that can produce new SnCs, but SnCs themselves produce new, secondary SnCs too. So, it’s not unlikely that adding a bunch of SnCs to the baseline pool of SnCs (whose size increases with age) could further increase the size of this pool. And that would be a net increase in biological age.
This might not be a problem for young mice which can eliminate SnCs fairly quickly, but it seems to be a big problem for old mice. Middle-aged mice probably lie somewhere in between. I’d also expect that overweight, obese, or otherwise messed-up, middle-aged mice would fare worse.
Imagine that each new SnC produced 3 new SnCs within a day, and also that SnCs had a 50% chance of being removed each day. In that case, there will be 4*0.5 = 2x as many SnCs tomorrow as there is today, leading to exponential runaway growth, immediately exploding in the number of SnCs and dying.
On the other hand, imagine that they only produce 1 new SnC within a day, and also that they had a 66% chance of being removed each day. In that case there will be 2*0.33 = 0.66x as many SnCs tomorrow, leading to quickly returning to the equillibrium caused by outside production.
You’d need some sort of fine-tuning where the production and removal are extremely close to each other to not either have explosive growth or rapid equillibration.
How does this compare to other contagious diseases?
EDIT: for aging in particular.
It’s probably too early to compare the amount of senescence that’s produced by SARS-CoV-2 versus other viruses, but what is known is that several viruses (including influenza) do induce the development of senescent cells in several tissues.
Then this doesn’t seem like a counterargument to “to elderly people it would be effectively the same as any other serious stressor” to me.
The counterargument would apply to “It wouldn’t be relevant to non-elderly people....”
Ah, yes. I think young people should probably take the long term effects of viruses more seriously in general.
I’d say that unhealthy-for-their-age young and middle-aged people and otherwise healthy-but-middle-aged people might want to be more cautious. Healthy-for-their-age young people probably don’t need to worry.
For what it’s worth, I agree that the post reads to me as not very balanced, but a lot of the evidence and arguments presented are still worrying, and I am still worried about long COVID. (I also don’t put myself above confirmation bias, though.)
This could also be explained by things other than COVID or long COVID, too, e.g. lockdown/isolation, less exercise, increased depression, poorer access to healthcare.
Sure it is essential to differentiate between those who have been tested for COVID and that self-reporting which, in the absence of a test, is another information source. To repeat my experience of becoming ill in the time of COVID 19: I couldn’t get a test in July 2020; I don’t know whether it was COVID-19 that hit me like a speeding train. I still have cognitive difficulties, severe fatigue, continuous headaches, lack of taste and smell, and other new things which have gone wrong physically. I’m waiting for the latest results of brain/spine MRI; I’m without a diagnosis. My reading suggests M.E., encephalitis, Long COVID and possibly lots of things—continued testing thus far provides no answer. I’ve also learned about FND and can see how these symptoms could, in the absence of an actual biomarker, be put under that umbrella. To have one’s symptoms acknowledged matters. Losing one’s fundamental abilities to function is so devastating; reading that such symptom clusters are deemed psychosomatic seems, to the afflicted, unhelpful.