News about Long Covid including its relationship to ME/CFS 2020 to 2021

The semantics (in the non dismissive sense) of illness is challenging and certainly researchers should be conscious of how their questions are structured, but part of that means that when seeking responses from the general population common terminology is used. Even if we consider the patient to be expert we can't rely on the patient having more than an average command of language.

In the case of novel, ill defined and heterogenous conditions such as post COVID symptomology, language use becomes circular, researchers can only reference what patients have described and patients use common terminology because there are no contextual alternatives that researchers can offer until a clear picture of the emergent symptomology becomes clear.

Certainly researchers could ask patients to give scale to commonly experienced symptoms pre and post acute COVID but that doesn't help where the patient didn't previously have a given symptom. And in any case that doesn't impact the how the general population experiences discomfort, pain etc, there is a lot a of low level symptomology throughout the the general population and that low level can be expressed acutely in a measurable % of the general population all which contributes to the common semantics of illness.

In the case of LC, or whatever agglomeration of illnesses that turns out to be, as a medical entity it only exists as a description using either medical terminology or common semantics. As definitions are tightened we should expect elements of what had been understood to be aspects of that single medical entity to disappear and others arise, and that LC in part turns out to be something of a mirage created by poor specificity is to be expected.

 

Do you really think it's the patient community that is responsible for the communication gaps which frequent research studies and clinical practices?

So, who do you imagine crafts a given set of disease characteristics? It isn't the patients. Sometimes it isn't even with patient input, or it's DESPITE patient input, and even contrary to it.

I'm not sure what you're trying to accomplish with this paragraph. If a researcher cannot distiniguish symptom severity in healthy controls vs an infected cohort, then that researcher may wish to consider changing professions.

I suspect some patients would reply that their symptoms exist regardless of who is writing the medical texts - or whether anyone bothers to write them down at all.

IMO, if a researcher cannot come at a disease from the patients' perspective, and incorporate that perspective without diminishing it, then the product that comes from his/her desk is likely flawed. Both clinical and medical research arrogance undos progress far too often, and that unraveling is almost always at patients' expense.

Medicine is not dogma, or at least it should not be. Nor should it reduce down to rhetoric or semantics.

 

The BMJ: Long covid in children and adolescents

Risk appears low, but many questions remain

Symptoms involving almost every organ system have been reported after SARS-CoV-2 infection.123 Estimates of the prevalence of long covid (also called post-covid-19 condition, post-acute sequelae of covid-19, or chronic covid syndrome) vary considerably, partly because of confusion around the definition. The term long covid encompasses a broad range of symptoms, including objective complications of covid-19 (pulmonary fibrosis, myocardial dysfunction), mental health conditions, and more subjective, non-specific symptoms resembling those seen in post-viral chronic fatigue syndrome (myalgic encephalomyelitis). Most studies to date have substantial limitations, including small cohorts, absence of control groups, non-standardised capture of symptoms, lack of correction for pre-existing medical conditions, participant reported infection, and variation in follow-up, as well as selection, non-response, misclassification, and recall biases.4
​

Full editorial: https://www.bmj.com/content/376/bmj.o143

 

To be honest, I don't think that VeryWell Health article is particularly well-written. It says it is fact-checked but then there are sentences like this in it:

In 2020, the most pervading symptom documented by long-haulers was fatigue. In 2021, a study by the World Health Organization (WHO) showed that Epstein-Barr Virus (EBV), the virus behind mononucleosis, was reactivating in long-haulers, and could be a source of that fatigue.5​

It wasn't the WHO, it was an org called World Organization, which looks more like an environmental thing than anything else.
I also think that was the only such study that tried to connect long covid to EBV reactivation. That was last summer and we haven't really heard much about this since.

The description of PEM is not the best:

ME/CFS, for example, shares three of the most common symptoms as long COVID: brain fog, fatigue, and post-exertional malaise (PEM), which is when a patient’s symptoms worsen after activity. ​

Also, statements like this:

Throughout the next year, we will be seeing more insight into the pathophysiology of COVID-19. Microbiologists like Amy Proal, PhD, a microbiologist at the PolyBio Research Foundation, and Eric Topol, MD, the founder and director of the Scripps Research Translational Institute, have made many strides in advancing our knowledge of long COVID, and are important scientists to follow both in the clinical sphere and online for updates.​

 

https://twitter.com/user/status/1483909434028044293

 

https://twitter.com/user/status/1484209544788160521

 

I am not sure what Binita Kane is wanting. She says:

We need a mechanism for rapid small scale testing of new drugs/ therapies in different cohorts, fast tracked ethics approval and rapid review, analysis, publication, adoption and spread. RCTs are important but can’t be the whole answer when millions are suffering (3/4)

But we have the mechanism and it works - that's how dexamethasone got identified, how the vaccines got approved. Anything faster would have been exposing people to treatments mostly more likely to do harm than good. In a pilot dose response study typically 80% of patients get the wrong dose. Unless such early studies are done with maximum rigour you go on exposing most people to the wrong dose. The great majority of drug therapies that have been tried have not worked but have had adverse effects. RCT's are not the whole answer for sure, but that is because there are other well worked out steps beforehand - and everyone should know what they are and how to use them.

I am left wondering what the motivation for the set of tweets was really.

 

This group proposes that the molecular basis of long covid is sustained inflammation in the olfactory system with inflammatory responses in the brain (my summary).
https://twitter.com/user/status/1484125754359263235

 

In fact we had the mechanism front having the pandemic at all - which China used to good effect - restrict travel, test, trace and isolate. And once they get started viruses are not that easy to treat.

 

I wasn't aware of prior reports that hamsters were experiencing long covid. Who knew??

 

The question of whether vaccines can cause Long Covid-like illness seems to be a very interesting one, with a preliminary yes. Research from the NIH. The ridiculous insistence to downplay all vaccine reactions, out of belief in "mass hysteria" of all things, has probably done as much harm as the Lancet-Wakefield paper did, just unseen as it happens in thousands of small incidents that leave people distrustful of people gaslighting their reality.

Thread:

https://twitter.com/user/status/1484268870768627712


And an article from Science magazine:

In rare cases, coronavirus vaccines may cause Long Covid–like symptoms
https://www.science.org/content/art...avirus-vaccines-may-cause-long-covid-symptoms

 

And a long perspective article from Avindra Nath (NIH lead researcher on the ME initiative) regarding neurological symptoms in Long Covid.

You're never going to guess: it's probably neuroinflammation. What a shocking surprise.


Nervous system consequences of COVID-19
https://www.science.org/doi/10.1126/science.abm2052

Since early in the COVID-19 pandemic, patients have described lingering syndromes following acute infection, now called Long Covid. These syndromes often include predominant neurologic and psychiatric symptoms, such as difficulty with memory, concentration, and ability to accomplish everyday tasks, frequent headaches, alterations in skin sensation, autonomic dysfunction, intractable fatigue, and in severe cases, delusions and paranoia. Many people who experience neurologic symptoms that linger after acute COVID-19 are less than 50 years old and were healthy and active prior to infection. Notably, the majority were never hospitalized during their acute COVID-19 illness, reflecting mild initial disease. Many of the symptoms experienced by individuals with Long Covid are similar to those of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), which is also considered to be a postinfectious syndrome caused by a variety of infectious agents. Because the pathophysiology of ME/CFS is poorly understood and there are no effective disease-modifying therapies available, it is likely that the study of Long Covid may benefit ME/CFS patients as well. There is also overlap in symptoms of post–Lyme disease, suggesting that there may be common host susceptibility factors that underlie these illnesses.​

 

"

I don't think it suggests that at all, at least it wouldn't rise to the top of my list, and it certainly wouldn't be noted in such a singular fashion bringing up the rear (inconspicuously?).

Also, post-Lyme disease seems somewhat dated, or is he making a statement of some sort? That little political skirmish was fought five or ten years ago, and my understanding is no one at the NIH or CDC could prove Lyme was gone from infected patients, so it couldn't be said factually "post-Lyme". The more or less political compromise was post-treatment Lyme disease syndrome. To me, that still seems pregnant with unwarranted assumptions, but hey, I'll take it. It would seem this guy does not, and I'd love to know what he knows.

What I find particularly disconcerting is "...suggesting that there may be common host susceptibility factors that underlie these illnesses." To me this feels uncomfortably like patient-blaming.

I can think of several simpler and to me more likely explanations to explain any overlap in diseases. First and foremost: They all involve infections, arguably persistent infections, but at the very least they started with infections within most of their respective communities (ME/CFS being an exception sometimes, but I'd argue most cases evolve from an infection here, too).

They generate similar symptoms frequently. Many diseases do, which is why clinicians embrace the whole differential diagnosis ritual.

Also, each is characterized by inadequate diagnostics. Trying to get diagnosed seralogically for ME/CFS, LC or late stage Lyme can be a shitstorm of underperformance.

And let's not forget that two of the the three have a long history beset with politics and being pressured by vested interests to remain questionable (LC is the newcomer on the block; but it is already beginning to sense the side-long medical glances)

Common host susceptibility factors. They're human?

 

Agreed. Genes might prove to be the determining factor. Certainly they have in channelopathies, at least so far, and there is some overlap in symptoms with us there as well.

But for a large swath of patients with LC, ME/CFS, and late stage Lyme, there is a clear jumping off platform that is infectious. So to me tying the three together with "common host susceptibility factors" may prove correct - but it seems like such an incredible leap to get there once you squarely examine: a)the histories of the diseases and how the patient communities have been treated, and continue to be treated; b) who stands to benefit from an ongoing infectious pathology NOT being acknowledged; and c) diagnostics for many diseases suck - we frequently have been told otherwise, but there's enough data out there that it really isn't a secret anymore.

Genetics might prove to be the culprit. But I'd clean up the other areas I mentioned before I'd close the door on them. Yes, we can do things concurrently, and we should. Problem is, there will be plenty of forces pulling us to do what they want, and history isn't good to us when it comes to research priorities or execution.

 

While patients with longcovid (and those of us with ME) are desperate for a treatment it would be best to do intensive research into the biology of what is happening. Once the deficits are identified we will be much closer to working out what will help.

Longcovid and ME are likely to be more than one problem or single diseases with more than one presentation so it is important to know what needs treated. A drug for POTS may work really well for some people but if it makes someone with drug sensitivities ill or is given to someone who can't metabolise it because of some damage done by covid it may seem less effective than it actually is.

 

It might have triggered Guillain-Barré syndrome? There was a very small percentage from the J&J jab. People have also developed GBS after receiving the flu shot.

 

I've read that it's being referred to as autoimmune-lyme.

 

Vox: "How to spot the signs of long Covid — and what to do next"

Some quotes:

“Many people who have had Covid and who haven’t recovered are starting to look very much like ME/CFS patients,” says Lucinda Bateman, founder and medical director of the Bateman Horne Center, and an expert in the diagnosis and treatment of myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS)."

As is often the case with long Covid, ME/CFS is characterized by chronic, debilitating symptoms such as fatigue, pain, and cognitive dysfunction — and ME/CFS often persists at least six months. The cause of ME/CFS is not well understood, but it’s thought to possibly be triggered by a virus or another kind of infection. Bateman and other experts have been studying the parallels between long Covid and ME/CFS, hoping that this will give them a better understanding of both conditions."

"Bateman’s advice for long Covid patients is similar to the advice given to people with ME/CFS: “The first thing is to be very patient and give your body a chance to heal. Slow down. Don’t get in a push-crash cycle of pushing yourself, crashing, pushing, crashing. We tell people to pace their activity, meaning try to do the right amount of activity every day that doesn’t escalate your symptoms but keeps you moving.”

"Pacing yourself is easier said than done for most people; still, making an effort to slow down and listen to your body while you’re healing can go a long way. Bateman notes that brain fog is a symptom that tends to get worse in ME/CFS patients when they’re pushed beyond their limits physically and mentally, so taking care of yourself as best as possible could help. Getting enough sleep is a crucial — yet often elusive — part of that."

 

I'm 100% certain pwME will not present micro-clots.