Before you can investigate the causes of an illness, you have to define it. Otherwise, you’re chasing an ever-shifting cloud of ambiguous symptoms, any of which could have different causes. The article opens with this admission, so I’m not stating anything new here.
The problem with “Long Covid” as it exists today is that there’s no such definition. Literally anyone who had Covid once and feels bad today (and quite a few people who never had a confirmed case at all) includes their set of symptoms in the communal diagnosis. Thus, if you dig into these studies, you always find that the syndrome is a wide-ranging and variable constellation of symptoms, making it impossible for a study to have any systematic legitimacy. Moreover, the results of any particular study are more strongly influenced by the inclusion criterion (if there even is one) than by any other factor.
It’s perfectly possible to evaluate treatments in this situation, and would be a better use of resources - pick symptoms, make an inclusion criteria, and run a randomized trial of existing drugs or therapies. But this is likely to fail, and it’s much, much easier to write papers with unprovable theories and retrospective analysis.
Interesting. Someone should (or maybe have?) run a cluster analysis on the symptoms to define more specific subgroups. But I suppose getting access to the required health data at that scale is nontrivial?
It’s not that hard to get a long list of symptoms for long covid. Just watch this thread as it grows, and you’ll easily find dozens. Things like this end up being a lint trap for people who just feel bad for whatever reason (which is all of us, at various points in our lives!) Nobody likes to be told that their symptoms are idiopathic.
Massaging this kind of data (clustering, etc.) is much lower value than finding fixed criteria that define a consistent group of patients who have objectively defined symptoms that cannot be more readily explained by another diagnosis. This is a pre-requisite for any further study. It can be done, but it’s hard, and it tends to lead to criticisms because you end up excluding a large number of people who fervently believe they have the illness, but don’t fit the objective standards.
Just for example: it’s not enough to claim that you have “brain fog”. A more valid endpoint might instead attempt to classify people based on standardized tests of thinking. Even that has problems, of course, but if you can just claim that you are fatigued and unable to think clearly, there’s a huge problem of confounding (i.e. maybe your symptoms are caused by something else), let alone the unverified nature of the original claim.
Sometimes the symptoms are so ambiguous that it is hard to nail anything down. It’s the same thing with Lymes disease, which is definitely a real thing, but there aren’t good, reliable tests for it. It takes a long time to manifest and the symptoms vary wildly from person to person.
I had a long process with this that mostly manifested as exercise intolerance and general inflammation/discomfort, and sleep struggles. I made no progress for 2 years, lost most of my muscle (I had been very active before) and started thinking "is this how it's going to be forever?". After not finding anything promising from traditional medicine or supplements, I finally made some dramatic life changes. I'm fully past it now (with persistent lifestyle changes), but I really had to rethink my relationship with food.
Ended up doing a paleo diet, avoiding stressors (some of which are not obvious like just being on your phone scrolling, bad posture/circulation/sitting for too long), improving sleep hygiene, and ramping up consistent cardio exercise, with an emphasis on getting up to 4x/week zone 5 cardio without triggering intolerance.
Since then I've discovered a lot of other things that are great for overall health, like HRV-reset breathing and long-duration water fasts (around 3 days is optimal for me). I imagine those would have been very helpful if I had tried them earlier. A water fast is a complete metabolic and inflammatory reset of the body, and it's not as hard as you might think.
Hopefully most affected folks have recovered and are living normal lives by now, but if not, there are things you can do! It seems like the more challenging those things are, the more efficacious.
Thanks for this, reading "water fast" and "3 days" gave me a shot of adrenaline. The "water" prefix is just confusing, the word for abstaining from food is just "fast" for those interested.
A non-inflammatory rocket shock diet can certainly aid in symptoms of long covid in many users, often people megadose on antioxidants to dilate their recovery window and not regress. Glad to hear you are feeling better and I totally agree that movement and diet are key in recovering from inflammatory disease.
I caught this in the Dec 2023/Jan 2024 Covid wave, in a densely-packed Bay Area tech office. I only returned to near-full mental clarity in Jan 2026 - two years later. It's an insidious illness that needs more visibility. Poorly ventilated offices full of sick colleagues in close proximity are ideal conditions for transmitting airborne diseases, and it's far too easy to develop a debilitating chronic illness this way. There should be minimum clean-air standards for open offices to protect workers.
Maybe a bit of a strange take, but after having dealt with chronic illness personally and talked with a lot of others with chronic illness, I don't think classifying chronic illness by symptoms will help with curing, and in fact I don't think categorizing works at all for chronic illness. We've been trying to classify chronic illnesses for so long, and yet in most cases no pattern emerges.
This has led me to conclude that perhaps in most cases chronic illness is an emergent behavior from a complex system, namely our body. Now tbh this is kind of a cheap take, because it's not that hard to conclude. But gosh darn it, we're programmers and we deal with complex systems all the time! What I want to see is a complete quantitative mapping of human metabolism, so that we can see all the in-between steps, not just the surface levels. That way curing chronic illness is more about comparing metabolite levels against known pathways and seeing what's regulated incorrectly. There's just not enough introspective capability currently.
My vision is some day a person who's been chronically ill can walk into a clinic, take a blood test, and with mass spectrometry get the level of the around 1800 different intermediate metabolites. That gets mapped to a known good metabolic graph, and it's optimized to find what in-between step is off kilter. They're then prescribed a drug that resets the bad state, and it 6 weeks they're back to normal.
I also doubt that AI will substantially help either. It still doesn't bring any more introspection capability, and if we can't figure out why someone is sick, I have little faith that a predictive AI can figure it out either.
Thanks for the link! I looked over it, but I'm not seeing quantitative levels of reactions. That's been my biggest issue with current pathway databases. It's great to know what's connected to what, but very quickly it becomes everything connected to everything. And unfortunately everything doesn't reduce the problem space.
That would be difficult - a metabolic map is a diagram showing the known reactions. At any point in time, only a subset of these will be active. Like a road map - at midnight, only some roads will have traffic.
I think what you are looking for is more like a model of the metabolome, showing the flow through the network under certain conditions (steady-state, growth, cell stress, etc). Not sure if there is a readily available database of such models, or how easy it would be just to run them and get meaningful results.
While this seems to validate those syndromes as having real underlying physical causes, I do have to mention that you can treat this (and fibromyalgia) surprisingly well with psychiatric medication, implying there is at least a substantial fake element to it.
Put differently: some people probably get the real thing, but if you can successfully treat a large percentage with SSRIs (which you can, see https://www.nature.com/articles/s41598-023-45072-9), that means they got it by social contagion, like the dancing plague.
That you can see improvements in people with long covid by giving them SSRIs isn’t clear
evidence it’s partly fake or a “social contagion”. Whatever improvements recorded are just as easily explained by the fact that being sick for months is depressing and alienating and a bunch of people think you’re faking it.
On top of that, the SSRI article you linked suggests a biochemical mechanism by which SSRIs might be acting (i.e. not by making something “fake” go away, by actually treating the cause of something real)
Morgellons isn’t a real disease. It’s a mental health condition.
SSRIs do not “work on” those other conditions, but depression is highly comorbid with serious chronic illnesses. SSRIs improving some symptoms is to be expected when depression symptoms overlap with the condition.
I'm somewhat open to this line of thinking, but it seems in these cases, there is a very fuzzy boundary between the symptoms of depression and "the real illness": brain fog, lack of energy etc.
I've seen healthy, active and successful people be affected, where the cause of "long covid" seems unlikely to be psychological. But there is no denying that, shall we say "a certain type" of person seems to be overrepresented in these cases, and for them it is very attractive to attach the label "long covid" to something that previously existed.
I guess that until we have discovered the biological mechanism underlying this phenomenon, it will be hard to cleanly separate these two cases, but from what I've seen I find it likely that this bipartition really exists.
Not necessarily fake. Mind/body homeostasis is WAY more complicated than that.
To use a computing analogy, which doesn't map perfectly onto the body, if consciousness awareness is userland, you can have things go wrong which are localised in ring 0 - brain drugs will be to some degree effective on those, that doesn't mean it's fake or made up.
In reality there are fuzzy boundaries and feedback loops everywhere. SSRIs treating this isn't any more mysterious than NSAID painkillers being somewhat effective for acute depression.
It's probably a whole set of feedback processes that get screwed up, hence the panoply of symptoms, inserting a hard stop into one part of the loop can be enough to kick the system back into a better functioning state.
>implying there is at least a substantial fake element to it.
The article actually argues against that reading: IgG transferred from patients into mice reproduced the symptoms. Mice don't have a nervous disposition. That points to a physical mechanism.
Every study that suggests viability of SSRIs to treat or prevent Long COVID presents plausible mechanisms for why they might have that effect. And none of them are "the patients are probably just sad and faking it."
Importantly, IgG fractions from the blood of these individuals cross-reacted with several types of mouse tissue in vitro, and transfer of this IgG to living mice reproduced symptoms such as pain, fatigue, coordination problems, temperature sensitivity and more. These effects were not seen with IGg transfer from unaffected patients. It hardly needs pointing out that you cannot transfer a nervous disposition or a persistent bad attitude by transfusing antibody fractions. Long Covid is a real a disease as lupus, MS, Hashimoto’s, or Type I diabetes, all of which are driven by production of antibodies to a person’s own tissues."
> In the first transfer experiment, most patient participants had been vaccinated prior to sampling, whereas the controls were not. Importantly, in our follow-up experiment, we used post-pandemic controls (exposed and vaccinated), and their IgG still did not induce the overt pain phenotype seen with long COVID IgG, suggesting vaccination alone is unlikely to explain the transfer effects.
Given that the major COVID-19 vaccines had a significant protective effect against Long COVID, this is a particularly perverse variation on the conspiracy theory.
Long COVID is much more prevalent among people who’ve experienced severe COVID symptoms, and unvaccinated people have the most severe symptoms. One doesn’t need a PhD to do the math here.
In multivariable analyses, pre-existing health conditions at the time of initial SARS-CoV-2 infection and reporting fatigue, shortness of breath, and cough 3 months post-infection were independent predictors of persistent long COVID.
Age, sex, and number of COVID vaccinations were not significantly associated with persistent long COVID.
which needs to be qualified with an "of course" as W.Australia (3xsize of Texas, small population) was isolated from the world and then almost the entire state got two to three rounds of vaccination at much the same time:
In 6 months they'll be in the comments on the next article about covid railing against the vaccine again. It's never enough with these guys, because it's not about being right or wrong, it's about having their feelings validated. They feel like the vaccine was bad, facts be damned.
It'd have been interesting for them to discuss it, but from what I understand it looks like MCAS is probably an entirely separate thing (that can also be triggered by COVID), but because of the overlap in symptoms, many people who assumed they have long COVID actually had MCAS. And even after teasing those two out, there may be more conditions in the long COVID bucket.
This is a blog on the root cause. MCAS would be an intermediate mechanism in making you feel sick, but something must have triggered the MCAS. Thats the autoimmune response.
Everyone knows what is the cause of long "covid", but censhorship is still strong. There are trillion dollars at play, and nobody wants to pay compensations.
These comments show me how amazing the world of covid disinformation still is. After every country/health authority in the entire world studying it for so long and all coming to the exact same conclusions there's still those who are positive they know better. Billions of people being studied for years vs I heard it from some dude on Twitter.
The problem with “Long Covid” as it exists today is that there’s no such definition. Literally anyone who had Covid once and feels bad today (and quite a few people who never had a confirmed case at all) includes their set of symptoms in the communal diagnosis. Thus, if you dig into these studies, you always find that the syndrome is a wide-ranging and variable constellation of symptoms, making it impossible for a study to have any systematic legitimacy. Moreover, the results of any particular study are more strongly influenced by the inclusion criterion (if there even is one) than by any other factor.
It’s perfectly possible to evaluate treatments in this situation, and would be a better use of resources - pick symptoms, make an inclusion criteria, and run a randomized trial of existing drugs or therapies. But this is likely to fail, and it’s much, much easier to write papers with unprovable theories and retrospective analysis.
Massaging this kind of data (clustering, etc.) is much lower value than finding fixed criteria that define a consistent group of patients who have objectively defined symptoms that cannot be more readily explained by another diagnosis. This is a pre-requisite for any further study. It can be done, but it’s hard, and it tends to lead to criticisms because you end up excluding a large number of people who fervently believe they have the illness, but don’t fit the objective standards.
Just for example: it’s not enough to claim that you have “brain fog”. A more valid endpoint might instead attempt to classify people based on standardized tests of thinking. Even that has problems, of course, but if you can just claim that you are fatigued and unable to think clearly, there’s a huge problem of confounding (i.e. maybe your symptoms are caused by something else), let alone the unverified nature of the original claim.
Ended up doing a paleo diet, avoiding stressors (some of which are not obvious like just being on your phone scrolling, bad posture/circulation/sitting for too long), improving sleep hygiene, and ramping up consistent cardio exercise, with an emphasis on getting up to 4x/week zone 5 cardio without triggering intolerance.
Since then I've discovered a lot of other things that are great for overall health, like HRV-reset breathing and long-duration water fasts (around 3 days is optimal for me). I imagine those would have been very helpful if I had tried them earlier. A water fast is a complete metabolic and inflammatory reset of the body, and it's not as hard as you might think.
Hopefully most affected folks have recovered and are living normal lives by now, but if not, there are things you can do! It seems like the more challenging those things are, the more efficacious.
Thanks for this, reading "water fast" and "3 days" gave me a shot of adrenaline. The "water" prefix is just confusing, the word for abstaining from food is just "fast" for those interested.
If this is engagement bait, then well played..
https://en.wikipedia.org/wiki/Fasting
This has led me to conclude that perhaps in most cases chronic illness is an emergent behavior from a complex system, namely our body. Now tbh this is kind of a cheap take, because it's not that hard to conclude. But gosh darn it, we're programmers and we deal with complex systems all the time! What I want to see is a complete quantitative mapping of human metabolism, so that we can see all the in-between steps, not just the surface levels. That way curing chronic illness is more about comparing metabolite levels against known pathways and seeing what's regulated incorrectly. There's just not enough introspective capability currently.
My vision is some day a person who's been chronically ill can walk into a clinic, take a blood test, and with mass spectrometry get the level of the around 1800 different intermediate metabolites. That gets mapped to a known good metabolic graph, and it's optimized to find what in-between step is off kilter. They're then prescribed a drug that resets the bad state, and it 6 weeks they're back to normal.
I also doubt that AI will substantially help either. It still doesn't bring any more introspection capability, and if we can't figure out why someone is sick, I have little faith that a predictive AI can figure it out either.
https://web.expasy.org/pathways/
I think what you are looking for is more like a model of the metabolome, showing the flow through the network under certain conditions (steady-state, growth, cell stress, etc). Not sure if there is a readily available database of such models, or how easy it would be just to run them and get meaningful results.
https://www.cell.com/cms/10.1016/j.it.2025.10.010/asset/0b5a...
This is the corresponding article about this phenomenon, "The lingering shadow of epidemics: post-acute sequelae across history":
https://www.cell.com/trends/immunology/fulltext/S1471-4906(2...
While this seems to validate those syndromes as having real underlying physical causes, I do have to mention that you can treat this (and fibromyalgia) surprisingly well with psychiatric medication, implying there is at least a substantial fake element to it.
Put differently: some people probably get the real thing, but if you can successfully treat a large percentage with SSRIs (which you can, see https://www.nature.com/articles/s41598-023-45072-9), that means they got it by social contagion, like the dancing plague.
On top of that, the SSRI article you linked suggests a biochemical mechanism by which SSRIs might be acting (i.e. not by making something “fake” go away, by actually treating the cause of something real)
SSRIs do not “work on” those other conditions, but depression is highly comorbid with serious chronic illnesses. SSRIs improving some symptoms is to be expected when depression symptoms overlap with the condition.
I've seen healthy, active and successful people be affected, where the cause of "long covid" seems unlikely to be psychological. But there is no denying that, shall we say "a certain type" of person seems to be overrepresented in these cases, and for them it is very attractive to attach the label "long covid" to something that previously existed.
I guess that until we have discovered the biological mechanism underlying this phenomenon, it will be hard to cleanly separate these two cases, but from what I've seen I find it likely that this bipartition really exists.
To use a computing analogy, which doesn't map perfectly onto the body, if consciousness awareness is userland, you can have things go wrong which are localised in ring 0 - brain drugs will be to some degree effective on those, that doesn't mean it's fake or made up.
In reality there are fuzzy boundaries and feedback loops everywhere. SSRIs treating this isn't any more mysterious than NSAID painkillers being somewhat effective for acute depression.
It's probably a whole set of feedback processes that get screwed up, hence the panoply of symptoms, inserting a hard stop into one part of the loop can be enough to kick the system back into a better functioning state.
The article actually argues against that reading: IgG transferred from patients into mice reproduced the symptoms. Mice don't have a nervous disposition. That points to a physical mechanism.
There are studies that show significant immunomodulatory effects of SSRIs.
"
Importantly, IgG fractions from the blood of these individuals cross-reacted with several types of mouse tissue in vitro, and transfer of this IgG to living mice reproduced symptoms such as pain, fatigue, coordination problems, temperature sensitivity and more. These effects were not seen with IGg transfer from unaffected patients. It hardly needs pointing out that you cannot transfer a nervous disposition or a persistent bad attitude by transfusing antibody fractions. Long Covid is a real a disease as lupus, MS, Hashimoto’s, or Type I diabetes, all of which are driven by production of antibodies to a person’s own tissues."
> In the first transfer experiment, most patient participants had been vaccinated prior to sampling, whereas the controls were not. Importantly, in our follow-up experiment, we used post-pandemic controls (exposed and vaccinated), and their IgG still did not induce the overt pain phenotype seen with long COVID IgG, suggesting vaccination alone is unlikely to explain the transfer effects.
Long COVID is much more prevalent among people who’ve experienced severe COVID symptoms, and unvaccinated people have the most severe symptoms. One doesn’t need a PhD to do the math here.
Are there studies for this?
Australian studies show a protective effect (in that the fewer people that got COVID (correlated with vaccines) the fewer got Long COVID)
See Page 8: https://www.aihw.gov.au/getmedia/9592f439-9b96-4589-a55d-6b0... (2022)
Australian studies in W.Australia also show:
which needs to be qualified with an "of course" as W.Australia (3xsize of Texas, small population) was isolated from the world and then almost the entire state got two to three rounds of vaccination at much the same time:* https://www.cambridge.org/core/journals/epidemiology-and-inf... (2025)
( In Pop. Press: https://www.anu.edu.au/news/all-news/more-than-half-of-long-... )
https://www.nature.com/articles/s41467-023-38388-7
https://www.nature.com/articles/s41467-025-65302-0
Do you need even more?
In 6 months they'll be in the comments on the next article about covid railing against the vaccine again. It's never enough with these guys, because it's not about being right or wrong, it's about having their feelings validated. They feel like the vaccine was bad, facts be damned.
https://www.medrxiv.org/content/10.1101/2023.01.25.23285014v...
Oh sorry, the last one shows that covid increases the likelihood to develop autoimmune disorders.
And of course people can have both.