You could see this study coming a mile away. Visser, Van Campen and Rowe have been busy the past couple of years doing breakthrough study after breakthrough study. It was only a matter of time – and not much time at that – before they got to long COVID.

Low Brain Blood Flows and Orthostatic Intolerance Ubiquitous in Chronic Fatigue Syndrome (ME/CFS)

Brain blood flows

This group researched their specialty – brain blood flows

The small study “Orthostatic Symptoms and Reductions in Cerebral Blood Flow in Long‐Haul COVID‐19 Patients: Similarities with Myalgic
Encephalomyelitis/Chronic Fatigue Syndrome” – contained 60 chronic fatigue syndrome (ME/CFS with POTS and without), and long COVID patients, and healthy controls – focused on two critically important factors: orthostatic intolerance and blood flows to the brain.

While only 10 long haulers were assessed there was no picking and choosing, no plucking out the most severe cases, no thumbs being placed on any scales – the group simply put the first 10 long haulers seen in their clinic into their study. All the patients – both the long COVID and the ME/CFS patients – in the study fulfilled the IOM criteria for chronic fatigue syndrome.

They assessed symptoms, then vaulted the participants upon a tilt table, and watched their cardiovascular systems attempt to adjust.

The symptom sets of the two groups were almost identical, with the long COVID group having a slight edge in severity. The group certainly tried to pry the groups apart but even an analysis of 21 different symptom clusters found in the Fukuda, Canadian Criteria, and IOM criteria, found no difference in symptoms between the long COVID and ME/CFS patients (with or without POTS).

Only hypersensitivity to foods and/or chemicals was more common in the ME/CFS group – perhaps suggesting that the hypersensitivity issues tend to show up later.

Double Long COVID Whammy

Reduced cerebral blood flows: long COVID on top and healthy control on bottom. Left is at baseline and right is when tilted.

This study found both reduced blood flows to the brain as well as high heart rates (POTS) in the long COVID patients. Given that the long COVID patients displayed both POTS and reduced blood flows to the brain, it was not surprising to find that they had even more reduced brain blood flows than the ME/CFS patients without POTS.

Talk about interrelationships between diseases. The same scenario – reduced blood flows to the brain – has been found in people with ME/CFS (without POTS and with POTS), people with POTS, and people with long COVID.

The same is true for the muscles; invasive exercise studies have found reductions in the blood flows to the muscles in long COVID and ME/CFS. With a recent large study highlighting possible endothelial cell/blood vessel problems in long COVID, the blood vessel/blood flow connection seems to be getting stronger and stronger in all these diseases.

Deconditioning Denied – Again

Deconditioning is, of course, going to rear its head in long COVID. The Van Campen/Rowe/Visser group has been instrumental in showing that even years of ME/CFS do not cause energy production problems in ME/CFS.  They are there from the beginning and they are present whether someone with ME/CFS is deconditioned or not.

Now comes another slant. The long COVID patients were physically fit before becoming ill and developed the orthostatic symptoms that showed up when they stood early in the illness – before deconditioning could have kicked in – and suggested that blood flows to the brain began dropping very early in the illness.

The authors also appear to have cleared up an interesting question: why do some people with very high heart rates upon standing who fit the POTS heart rate criteria experience no symptoms while standing up? It turns out that a high heart rate is not the complete answer in POTS.

Using new technology, the Visser group determined that POTS is a disease of sympathetic overdrive (including high heart rate) and, most importantly, reduced blood flows to the brain.

The inability to distinguish this has caused problems because it’s given doctors an opening to dismiss the high heart rate problems found in POTS and slap a psychological label on POTS patients. It’s remarkable how dangerous incomplete research can be.



Different triggers appear to produce the same general illness. They all need to be assessed

The study also assessed a factor that’s going to become increasingly important for the ME/CFS community: disease trigger. Many people with long COVID are, understandably, desperate to get confirmation that they’ve been infected with the coronavirus to validate their illness and hopefully avoid being dismissed by the medical community.

ME/CFS has been linked to long COVID via its common post-infectious trigger, but a significant portion of people with ME/CFS either don’t have a post-infectious trigger or don’t realize they had one. This study, for instance, found that over 40% of ME/CFS patients did not report that an infection triggered their illness – yet their symptom set and, as we’ll see, their test results were apparently almost identical to those found in the postinfectious patients.

That brings up a bit of a conundrum to the long COVID/ME/CFS connection. Thus far two major hypotheses regarding long COVID require either an autoimmune response to a virus or a long-lasting inflammatory response to viral proteins. In either case, a virus is needed.

Since both of those hypotheses end up with the blood vessels there may be a nonviral path to blood vessel dysfunction which has not been uncovered. Or it may be that everyone with these diseases actually had an infectious onset but the onset didn’t always produce normal flulike symptoms – thus was hidden. An atypical form of infectious mononucleosis exists, for instance, which does not produce swollen lymph glands, fever, etc. but which produces similar immune abnormalities.

Studies that assess disease triggers, then, are going to critical in bringing non-infectious triggered patients into the broad fold of research underway.

Missed Messages

It’s important, both for people with long Covid and for people with ME/CFS, that the similarities between the two diseases are recognized. A survey, suggests, though, that the message has not been getting out to the doctors.

Despite the fact that people with long Covid often meet the criteria for ME/CFS, and that treatment protocols that can help symptomatically are readily available, the survey suggests that doctors almost never diagnose long COVID patients with either ME/CFS (3%) or postural orthostatic tachycardia syndrome (POTS) (4%).

Long COVID, then, appears largely to be seen, at least at the doctor level, as its own entity that’s inextricably linked to the coronavirus but not necessarily to other diseases – including the ones it most closely fits.

Whose Universe?

This similarity—together with the cardiac index and cerebral blood flow reduction found in both long‐haul COVID‐19 cases and ME/CFS controls—supports the view that long‐haul COVID‐19, with a symptom duration over 6 months, is a form of ME/CFS. The authors.

Should long COVID (and other post-infectious and non-post-infectious disease states) be seen as subsets of ME/CFS?

That’s problematic given a big question hovering over the field: how long COVID fits into the ME/CFS universe, and how ME/CFS fits into the long COVID universe. Long COVID is getting much more research funding than ME/CFS ever has, and given that, there will be a strong pull to define it in its own terms – leaving its sister diseases to move forward on their own.

Indeed, some people with long COVID are understandably reluctant to have it lumped in with a stigmatized disease like ME/CFS. Turning aside from the moral issue of turning one’s back on a group of long-neglected patients who appear to have essentially the same illness, there are several reasons why it would be best for all to have long COVID understood as a subset of ME/CFS.

Consider this: ME/CFS describes a kind of broad general fatiguing and exertion challenging condition under which all sorts of other conditions, post-infectious and otherwise, can be fitted. Long COVID, post-treatment Lyme syndrome, postural orthostatic tachycardia syndrome, fibromyalgia, post ICU syndrome, and probably every post-infectious syndrome known can all fit inside an ME/CFS designation.

Given the infectious triggers found in many of these diseases, it would be a missed opportunity for long COVID not to be thoroughly understood and seen as being simply the most prominent of many postinfectious states. In a best-case scenario, long COVID will give birth to what will essentially be a new field of postinfectious disease research.

Long COVID, though, should also breathe life into the study of fatiguing, exertion intolerant, non-post-infectious states. As long COVID becomes more and more synonymous with ME/CFS, logic demands that non-infectious sources of exertion intolerance, fatigue, etc. found in ME/CFS be investigated as well.

The fact that ME/CFS does not require a postinfectious trigger to be present, and that it provides broad criteria focused on fatigue, exercise intolerance, and other symptoms, means that for at least right now, it makes sense it is used as a general umbrella term under which all these other diseases can be linked.


This study was too small to definitively show that reduced blood flows to the brain are found in long COVID but it lays out a marker that larger, better funded, researchers can use to explore long COVID. It also rebuts deconditioning claims and links long COVID, ME/CFS and POTS together in a new way which makes sense given other findings of reduced blood flows.

It also potentially adds yet another link in the long COVID – ME/CFS chain that seems to be growing ever stronger. Thus far – reduced blood flows, impaired ability to produce energy during exercise, hypercoagulation, deformed red blood cell, neuroinflammation, ACE-2 dysregulation, T-cell exhaustion, NK cell problems, gut dysbiosis, hypercatabolic state – are all possibilities.

Hopefully, the big research efforts in the US – of which we’ve heard little thus far – are checking out this study and are responding appropriately. Dysautonomia – long a focus in ME/CFS and POTS – is a recognized problem in long COVID and is getting more study. Still, the dysautonomia field is not a large one and it remains to be seen if the large U.S. studies will embrace it.

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We’ve been following the Visser/Van Campen/Rowe group closely, producing blogs on their studies showing reduced blood flows to the brain, reductions in energy production, the deconditioning is not causing ME/CFS that low blood volume is present and others.

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