No Causal Effects Detected in COVID-19 and ME/CFS: A Two Sample Mendelian Randomization Study 2023 Xu et al

Perhaps both ends of the spectrum involve immune dysregulation. The acute end presents as eg ARDS, occurring within days. The ME/CFS end may be a slow burn that takes weeks to overcome various homeostatic mechanisms to tip over to the pathological state (which may ultimately be experienced as an "on-switch" by the patient).

From SARS-CoV-2 pathogenesis (2022)

From Long COVID: major findings, mechanisms and recommendations (2023)

But perversely, severe acute disease may give better odds for good long-term outcome: it's recognisable so attempts are made to treat it; there are treatments.

 

Depends on whether it should be considered ME+LC, or worsening of ME, I've seen many, way too many, who said so.

 

So, I have ME. I just got over Covid a week ago. Some of my symptoms right now are imo covid-related. They're different than my ME/CFS ones. In a month or two or six, could those symptoms qualify me as LC, and who in the world would make that call?

I also qualify as chronic Lyme, but there are labs that support that call, as shitty as those labs may be. Could I actually get the trifecta - LC, ME/CFS and Lyme?

What a weird semantical world when there either are no labs, or the labs suck, and the patients know more of the definitional nuances than the doctors.

 

I think I may have LC on top of ME and on top of the adverse reaction I had to the vaccine.
My extra symptoms are
1. Loss and change of smell and taste (totally different to my ME smell symptoms). It's been over a year since Covid. Aversion to things like olive oil.
2. Sore lungs when I breathe in
3. Muscle spasms around my lungs when I move my torso
4. Sore chest around the lungs. Feels like the Costochondritis I had in my teens and then after the virus that caused my ME.

The symptom I think of as being ME related is hard to describe. It is a loss of muscle power and in particular in my legs. Feels like communication was lost and a delay in movement. Extra effort. I can't walk as far as I could since Covid.

 

OK. I have been trying to find a way to explain the research, reading and discussions over the years but it is too difficult for me just now. So here it is and I am willing to believe much more is known about the immune system than when I was well enough to be learning and discussing it.

The immune system needs to be triggered to go on the attack. When you get an infection, the immune cells attack the virus and the more virus the bigger the battle and the sicker the patient. If a virus gets into a different part of the body and get into a cell it can grow and make copies while disrupting cell function.

Enteroviruses have a way of evading the immune system by not replicating true so they are not recognized They even break up into viral pieces and reform into a viable organism in a new cell. Also they do not break out into the blood stream until the cell is packed with them.

This means that they can cause serious disruption to the body without ever being present in enough numbers to trigger a full blown attack from immune cells.

Think about an army attacking a country as opposed to saboteurs sneaking in one or two at a time.

Whatever, many people with ME did not have a particularly bad initial infection but were never quite right afterwards and it has never been noted that severe illness is more likely to cause it. In fact many of the people who had EBV and were very ill are the ones who recover completely after a few years.

Nothing in biology is straightforward so it is unlikely that the immune system is 100% effective. If some viruses are alwasy left over then it is logical that some types of viruses would exploit that.

 

New patients may not realise that Lloyd (and partner in crime Hickie) were busy doing to Australia what Wessely was doing to UK patients. Their papers had me shaking with anger and dismay at the time. I have never trusted the Dubbo study.

 

Here is link to a discussion of this method.
https://www.bmj.com/content/362/bmj.k601

I found it a bit overwhelming as statistics are not my strength, however they should boil down to common sense and as I understand it, basically in order for this statistical technique to be applied there has to be a known allele effect on outcomes, i.e. they have to prove that bearers of a given SNP allele will have less severe longcovid and then they can check whether they will get ME more or less than others.

My comment would be that there are two fuzzy areas, control susceptibility and diagnosis.

We know there has been a lot of asymptomatic SARS-cov-2 infection transmission, so we do not have a way to be sure a population currently free of SARS-cov-2 has never had it. So they may be comparing ME incidence in survivors of severe covid with ME incidence in asymptomatic covid (assuming this to be covid free) and finding that asymptomatic covid still causes ME. One grey area.

Does longcovid diagnosis in reality tend to preclude ME CFS diagnosis and vice versa? Are they perhaps seeing this prosaic clinical reality reflected in a number salad?

Their own conclusion hints obliquely there is a problem with diagnosis due to shared symptoms, however they do recommend that both ME and longCOVID deserve to be studied together for that very reason, which I can agree with.

 

Sounds to me like they're clueless and they elected to punt.

Persistent muscle soreness?

Interesting that they characterize Covid as an infection and not so ME/CFS.

They do seem to reduce ME/CFS to pain with fatigue, so, you know, clueless. Give the ball to someone else.

 

I have only seen one study that evaluates the risk of long Covid in people with ME: A preprint called "Severe acute infection and chronic pulmonary disease are risk factors for developing post-COVID-19 conditions 2022" (S4Me thread, preprint).

They estimate that people with ME/CFS have 4.69x the risk of long covid, with a 95% confidence interval of 2.78 to 7.92. See Table S3. This is quite preliminary, as the odds ratio for ME/CFS is based on very few people (Probably less than 20: They had two cohorts with 1,000 people, and the rates of ME in one was 1% and <1% in the other).

It's unfortunate we don't have strong research on this, it's an important issue.
(I first posted this comment in this thread.)

 

LC is an umbrella term for any medium- to long-term health effect of Covid. If Covid makes your ME worse, you could call it ME+LC. If you get new, non-ME symptoms after Covid, it's very much comorbid ME and LC.

 

I don't understand it either. Is this even a valid method if most of the ME/CFS patients in the biobank could not have developed ME/CFS through COVID-19 as it has only been around for a couple of years?