Virus-Induced Endothelial Senescence as a Cause and Driving Factor for ME/CFS and Long COVID: Mediated by a Dysfunctional Immune System, 2026, Nunes +

[Jonathan Edwards]

Karl Popper, in Conjectures and Refutations, points out that testing a hypothesis need not necessarily require new experiments. You can test it firstly for internal consistency and ability to make precise enough predictions and secondly against existing observation.

In this case I think existing clinical observation refutes the hypothesis because it's predictions are not found in any consistent form in people with LC or ME/CFS. None of the authors are physicians , I suspect, so they may not be aware of what is known.

If there was significant endothelial malfunction at least a few cases would show overt clinical signs in a consistent pattern. They do not.

 

[neophyte32]

Karl Popper, in Conjectures and Refutations, points out that testing a hypothesis need not necessarily require new experiments. You can test it firstly for internal consistency and ability to make precise enough predictions and secondly against existing observation.

In this case I think existing clinical observation refutes the hypothesis because it's predictions are not found in any consistent form in people with LC or ME/CFS. None of the authors are physicians , I suspect, so they may not be aware of what is known.

If there was significant endothelial malfunction at least a few cases would show overt clinical signs in a consistent pattern. They do not.

But have studies on this issue actually been conducted? Have any good studies been funded?

 

[Violeta]

"As a whole these findings indicate that APS patients display an endothelial perturbation in the absence of other detectable traditional risk factors for atherosclerosis."

Patients with antiphospholipid syndrome display endothelial perturbation - PubMed

As a whole these findings indicate that APS patients display an endothelial perturbation in the absence of other detectable traditional risk factors for atherosclerosis.

pubmed.ncbi.nlm.nih.gov

 

[Jonathan Edwards]

But have studies on this issue actually been conducted? Have any good studies been funded?

This is not an issue of studies. It is an issue of observing individual people with ME/CFS. They do not consistently have evidence of vascular pathology. More specifically there is no recognised pattern of clinical presentation in ME/CFS that would indicate a form of vascular pathology. Vascular pathoogy that affects people clinically (gives them symptoms or signs) does so in well documented ways. These are absent.

To put it another way, there is no point in having a theory that says that the earth turns twice in 24 hours when we never observe two sunrises in a day. Further testing is not needed.

 

[Jonathan Edwards]

"As a whole these findings indicate that APS patients display an endothelial perturbation in the absence of other detectable traditional risk factors for atherosclerosis."

APS is a nice example. People with APS have a very characteristic clinical picture of thrombosis and embolism, placental infarction, antepartum haemorrhage, etc. The abnormal vessel function is reflected in a typical clinical pattern. Nothing of the sort is seen in Long Covid or ME/CFS.

 

[Violeta]

APS is a nice example. People with APS have a very characteristic clinical picture of thrombosis and embolism, placental infarction, antepartum haemorrhage, etc. The abnormal vessel function is reflected in a typical clinical pattern. Nothing of the sort is seen in Long Covid or ME/CFS.

Antiphospholipid syndrome w/r/t COVID

The New Occurrence of Antiphospholipid Syndrome in Severe COVID-19 Cases with Pneumonia and Vascular Thrombosis Could Explain the Post-COVID Syndrome - PMC

Introduction: The classification of antiphospholipid syndrome (APS) comprises clinical criteria (vascular thrombosis or obstetric complications throughout life) and laboratory criteria (antiphospholipid antibodies (aPLs) positivity, confirmed at ...

pmc.ncbi.nlm.nih.gov

Antiphospholipid syndrome in the era of COVID-19 – Two sides of a ...​

www.sciencedirect.com › science › article › abs › pii
The disease has consistently been linked to many autoimmune diseases such as systemic lupus erythematous and antiphospholipid syndrome (A

Antiphospholipid Autoantibodies May Lead to Blood Clots After ...​

www.autoimmuneinstitute.org › ... › Rheumatoid arthritis
Feb 17, 2022 · Antiphospholipid Autoantibodies May Lead to Blood Clots After COVID-19 Infection. Last week, on February 17, 2022, the NIH released a media ...

etc.

 

[Felis Catus]

Antiphospholipid syndrome w/r/t COVID

Antiphospholipid Autoantibodies May Lead to Blood Clots After ...​

www.autoimmuneinstitute.org › ... › Rheumatoid arthritis
Feb 17, 2022 · Antiphospholipid Autoantibodies May Lead to Blood Clots After COVID-19 Infection. Last week, on February 17, 2022, the NIH released a media ...

etc.

I just skimmed the abstract.

Methods: In 100 patients admitted to the hospital with COVID-19 pneumonia, thrombosis and pregnancy complications were recorded during the hospital stay and in personal medical history.

Conclusion: The incidence of APS in our cohort was 2.0%, whereas in the general population, it ranges from 0.001% to 0.002%. The incidence might have increased even more if the four aPLs-positive patients with intrahospital thrombosis/history of thrombosis had attended follow-up.

What does that say about ME/CFS or ME/CFS triggered by COVID?

 

[Utsikt]

What does that say about ME/CFS or ME/CFS triggered by COVID?

It has been known since the early days of the pandemic that covid can cause issues with blood vessels and the heart. This has been corroborated by increased rates of heart issues following the pandemic. That’s probably what we’re seeing here.

It would technically be LC, but not the ME/CFS-kind. You could obviously have both, but presumably for unrelated reasons.

 

[Jonathan Edwards]

What does that say about ME/CFS or ME/CFS triggered by COVID?

Maybe that people with APS are more likely to go on being ill after Covid - which would be totally unsurprising. It need have nothing to do with a link between post-Covid illness causation and APS.

Immunology labs are obsessed with flying kites like this without any good clinical basis or much thought for simple explanations.

 

[Violeta]

Maybe that people with APS are more likely to go on being ill after Covid - which would be totally unsurprising. It need have nothing to do with a link between post-Covid illness causation and APS.

Immunology labs are obsessed with flying kites like this without any good clinical basis or much thought for simple explanations.

Conclusion: The incidence of APS in our cohort was 2.0%, whereas in the general population, it ranges from 0.001% to 0.002%. The incidence might have increased even more if the four aPLs-positive patients with intrahospital thrombosis/history of thrombosis had attended follow-up.

 

[Jonathan Edwards]

Conclusion: The incidence of APS in our cohort was 2.0%, whereas in the general population, it ranges from 0.001% to 0.002%. The incidence might have increased even more if the four aPLs-positive patients with intrahospital thrombosis/history of thrombosis had attended follow-up.

There are a whole string of reasons why the analysis is not as simple as it might seem. ANd if the authors wanted to slip the acute thrombotic patients in then I sense a confusion over what they are trying to show. The LC that we are interested in here (rather than a host of problems that may emerge after Covid for a thousand reasons) is not characterised by thrombosis. Level of antiphospholipid antibodies vary for all sorts of reasons too. They may well be more frequent after Covid without having anything to do with clinical problems.

There may be a few people with vascular problems after covid associated with anti-phispholipid antibodies but I see no possibility of that being of general relevance to LC or ME/CFS and certainly not relevant to the paper being discussed, which seems to suggest some other obscure vascular process.

A story has to consistent all the way through, not a hodge-podge of what might seem like clues but are often mutually exclusive in terms of role in a unified theory.

 

[Felis Catus]

Thank you @Utsikt and @Jonathan Edwards for your replies. My question was almost rhetoric but I learnt something from your responses.

 

[Jonathan Edwards]

0.002% seems very low to me for APS. In our department it was a little bit less common than lupus but was less likely to end up with us because it is not primarily rheumatological. That would put prevalence somewhere around 0.1%.

The Google figure is 0.05%.