CHRONIC FATIGUE SYNDROME (CFS) AND FIBROMYALGIA ARE VASCULAR DISEASE, 2021, Chang and Figueredo

Mij

Mij

Senior Member (Voting Rights)
CHRONIC FATIGUE SYNDROME (CFS) AND FIBROMYALGIA ARE VASCULAR DISEASE FREQUENTLY TRIGGERED BY PERSISTENT INTRACELLULAR INFECTIONS.

The tissue hypoperfusion and cellular hypoxia that occurs in CFS is associated with dysfunctions of the cells of the vascular walls (endothelial cells and pericytes) and of the blood cells (red, white blood cells, and platelets).

In recent years, several studies have been published in which it is evidenced that in Chronic Fatigue Syndrome (CFS) there is persistent endothelial cell dysfunction, a decrease in blood flow and perfusion has also been identified in patients. tissues (tissue hypoperfusion).

Based on the published evidence, and our experience in treating patients with CFS and Chronic or Persistent COVID, we propose to consider CFS as a Vascular Disease in which Endothelial Dysfunction and Hypoperfusion occur. As there is no obvious organ damage, the usual tests tend to be within normal parameters, or show only a slight alteration.

To identify Hypoperfusion and cellular hypometabolism, regular tomography or X-rays are not more useful, since the tissues are not damaged, or they only present macroscopically not visible lesions. Routine blood tests are also usually normal or slightly abnormal. What is required are specific blood tests to identify hypoperfusion, persistent clots, and cellular hypoxia.

We indicate the following 3 analyzes are carried out, which are not complex or high cost (on average the cost is 20 US dollars each):
1) Measurement of Venous Blood Gases. When there is Hypoperfusion, the supply of oxygen to the tissues by the blood is decreased, so the Venous Oxygen Saturation (SvO2) will be low.
2) D-dimer. If it is elevated, it would indicate that there are persistent clots.
3) Lactate (also known as Lactic Acid). If it is elevated, it would indicate that there is cellular hypoxia.

POSSIBLE TRIGGERING CAUSES. As possible external triggers, the following should be considered: - Persistent infections in cells of the vascular wall (endothelial cells and pericytes) and blood cells, by Viruses (Herpesvirus, Enterovirus, Coxsackievirus, HPV, others), Intracellular Bacteria (Borrelia, Bartonella, others), Rickettsia, Parasites, etc. - Viral antigens, particles or fragments. - Antibodies. - Toxins and Others. - Trauma and others Injuries.

Breaks added for easy reading

https://www.researchgate.net/public...OME_CFS_AND_FIBROMYALGIA_ARE_VASCULAR_DISEASE
 
Last edited by a moderator:
I reformatted the abstract to make it easier for me to read, so am copying my version here in case it is helpful to anyone else:

CHRONIC FATIGUE SYNDROME (CFS) AND FIBROMYALGIA ARE VASCULAR DISEASE FREQUENTLY TRIGGERED BY PERSISTENT INTRACELLULAR INFECTIONS.

The tissue hypoperfusion and cellular hypoxia that occurs in CFS is associated with dysfunctions of the cells of the vascular walls (endothelial cells and pericytes) and of the blood cells (red, white blood cells, and platelets). In recent years, several studies have been published in which it is evidenced that in Chronic Fatigue Syndrome (CFS) there is persistent endothelial cell dysfunction, a decrease in blood flow and perfusion has also been identified in patients. tissues (tissue hypoperfusion).

Based on the published evidence, and our experience in treating patients with CFS and Chronic or Persistent COVID, we propose to consider CFS as a Vascular Disease in which Endothelial Dysfunction and Hypoperfusion occur.

As there is no obvious organ damage, the usual tests tend to be within normal parameters, or show only a slight alteration. To identify Hypoperfusion and cellular hypometabolism, regular tomography or X-rays are not more useful, since the tissues are not damaged, or they only present macroscopically not visible lesions. Routine blood tests are also usually normal or slightly abnormal.

What is required are specific blood tests to identify hypoperfusion, persistent clots, and cellular hypoxia. We indicate the following 3 analyzes are carried out, which are not complex or high cost (on average the cost is 20 US dollars each):

1) Measurement of Venous Blood Gases. When there is Hypoperfusion, the supply of oxygen to the tissues by the blood is decreased, so the Venous Oxygen Saturation (SvO2) will be low.

2) D-dimer. If it is elevated, it would indicate that there are persistent clots.

3) Lactate (also known as Lactic Acid). If it is elevated, it would indicate that there is cellular hypoxia.​

POSSIBLE TRIGGERING CAUSES.

As possible external triggers, the following should be considered: - Persistent infections in cells of the vascular wall (endothelial cells and pericytes) and blood cells, by Viruses (Herpesvirus, Enterovirus, Coxsackievirus, HPV, others), Intracellular Bacteria (Borrelia, Bartonella, others), Rickettsia, Parasites, etc. - Viral antigens, particles or fragments. - Antibodies. - Toxins and Others. - Trauma and others Injuries.
 
I had/have come to the conclusion that this is an issue with me, of course I would not make the bold assertion that it is what causes ME, I had ME a long time before any vascular issues obviously manifested and they may be nothing to do with ME per say, merely the effects of being chronically ill for 35+ years, combined with aging.

As far as I know other groups of chronically ill people also have symptoms of vascular damage.
 
Mij said:
I made it a point to have my lactate tested during PEM 20 years ago and it was not elevated.

So no cellular hypoxia in my case?
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That might be so. Or not. Some of our studies show elevated lactate in the brain, which would require a spinal tap to physically measure, though they use specialized brain scans in some of these studies. Its also likely many of us are acidic early in a crash, then alkaline as we recover and our acid-base buffer is restored. Its not clear lactate is a reliable measure, nor is acidity. It might be with the right kind of test, but this requires empirical verification. We also cannot be sure there is not a lactate spike followed by a decline in lactate. So for example, high lactate might preceed PEM and be an issue in early PEM, but not later. I strongly suspect that as we wind down in a crash our lactate is decreased, and our acid-base buffer restored.

What would be required is some kind of active lactate sensor, giving continuous readings, in for example a CPET study. Does invasive CPET do this? I do not recall what they found. We would also need to do this on a large number of patients so we can see the full range of patient results. If we followed patients with a simple lactate monitor, and I do not know if such a thing exists, over many days and including prior to, during, and after activity, we would know much more. Currently we are largely in the dark, and results are often suggestive and not definitive. We might also need to be able to measure brain lactate, which is tricky to do continuously.

Measuring serum lactate with a test kit or blood monitor many times a day for some days might work.

We still don't know enough.
 
I first came across issues with vascular function, including endothelial linings, more than twenty years ago, including work by Vance Spence and Martin L Pall. So more than twenty years later we are still hypothesising.

Medicine advances with advancing technology. It might be we still lack the technology to investigate properly, or it may be that decades of advances have finally put us in a position to do ground breaking science. We shall see.
 
Peter Trewhitt said:
Measurement of Venous Blood Gases. When there is Hypoperfusion, the supply of oxygen to the tissues by the blood is decreased, so the Venous Oxygen Saturation (SvO2) will be low.
Click to expand...
My recollection is its often high. Presumably we don't use the oxygen (presumption, not fact). Of course what limited studies we have had might be flawed or I might be misremembering. If blood is making it to the venous system but not fully into many tissues then oxygen could be high. Its a mistake, in my current view, to presume it has to be low.

I wonder if its better to measure venous carbon dioxide, and then how do you correct for low blood volume?
 
alex3619 said:
What would be required is some kind of active lactate sensor, giving continuous readings, in for example a CPET study. Does invasive CPET do this? I do not recall what they found. .
Click to expand...

From MEpedia: A Norwegian study published in 2019 also reported a significant larger reduction in workload at the ventilatory threshold in 18 patients with ME/CFS compared to healthy controls, although this was not the case for peak values or VO2 measurement at the ventilatory threshold. The authors also measured arterial lactate concentrations, every 30 seconds during the exercise tests. Lactate was higher per power output per kg in patients than controls and the differences increased significantly at the second exercise test. In the healthy controls lactate concentration at the ventilatory threshold decreased while this was not the case in ME/CFS patients, suggesting a problem in lactate clearance ability.[15]
 
The lack of any statement of hypothesis has me wholly confused - instead the authors proclaim solely from authority i.e their reading of unidentified literature and unreferenced experience of treatment, they "propose to consider CFS as a Vascular Disease in which Endothelial Dysfunction and Hypoperfusion occur" - presumably given that this is on Research Gate they are looking for other researchers to say "that's interesting lets apply for a grant" or some similar response.

They suggest three cheap tests that would supposedly make a diagnostic suite - except they don't explain how that would be exclusionary of other diseases or indeed normal processes. Is an elevated number on a D-dimer test certain evidence of persistent clots - it isn't if you are pregnant - so how high does it have to be, and why wouldn't that trigger investigation of serious cardiovascular disease, and why wouldn't the symptoms of cd be exclusionary for CFS diagnosis ? It all seems horribly circular.

There appears to be a strong Spanish language speaker predominance for the more obviously associated research which looks like it leans toward a deconditioning paradigm e.g Link Do women with fibromyalgia present higher cardiovascular disease risk profile than healthy women?
https://pubmed.ncbi.nlm.nih.gov/28406763/
 
hibiscuswahine said:
From MEpedia: A Norwegian study published in 2019 also reported a significant larger reduction in workload at the ventilatory threshold in 18 patients with ME/CFS compared to healthy controls, although this was not the case for peak values or VO2 measurement at the ventilatory threshold. The authors also measured arterial lactate concentrations, every 30 seconds during the exercise tests. Lactate was higher per power output per kg in patients than controls and the differences increased significantly at the second exercise test. In the healthy controls lactate concentration at the ventilatory threshold decreased while this was not the case in ME/CFS patients, suggesting a problem in lactate clearance ability.[15]
Click to expand...
We have a thread on that study here:
Abnormal blood lactate accumulation during repeated exercise testing in ME/CFS, 2019, Lien et al
 
This is a research plan. Good they are going to look into it, That’s a lot of possible triggers.

I have wondered if ME is a vascular disorder because of the often chronically declining nature with age, a recent study looking at cognitive PEM, aortic stiffness and central cardiovascular control have suggested (not proved) there may be chronic vascular damage, https://www.mdpi.com/2077-0383/10/11/2327/htm

and now there is the RBC deformity identified by Davis’s team, which may cause a perfusion problem (though this is not in their plan), https://content.iospress.com/articles/clinical-hemorheology-and-microcirculation/ch180469

And the recently emerged microclot theory which researchers are focussing on.
 
Mij said:
The author of this paper talks a lot about vascular disease in CFS and LC.
Click to expand...
His research plan is also very similar but he is also going to have his research subjects go on a regime of lots of different nutriceuticals… Which I thought was an odd way to do start scientific research into the mechanism (but I suppose some novel treatment might arise…)
 
alex3619 said:
That might be so. Or not. Some of our studies show elevated lactate in the brain, which would require a spinal tap to physically measure, though they use specialized brain scans in some of these studies. Its also likely many of us are acidic early in a crash, then alkaline as we recover and our acid-base buffer is restored. Its not clear lactate is a reliable measure, nor is acidity. It might be with the right kind of test, but this requires empirical verification. We also cannot be sure there is not a lactate spike followed by a decline in lactate. So for example, high lactate might preceed PEM and be an issue in early PEM, but not later. I strongly suspect that as we wind down in a crash our lactate is decreased, and our acid-base buffer restored.

What would be required is some kind of active lactate sensor, giving continuous readings, in for example a CPET study. Does invasive CPET do this? I do not recall what they found. We would also need to do this on a large number of patients so we can see the full range of patient results. If we followed patients with a simple lactate monitor, and I do not know if such a thing exists, over many days and including prior to, during, and after activity, we would know much more. Currently we are largely in the dark, and results are often suggestive and not definitive. We might also need to be able to measure brain lactate, which is tricky to do continuously.

Measuring serum lactate with a test kit or blood monitor many times a day for some days might work.

We still don't know enough.
Click to expand...

I’m sure there must be a microfluidics set up very similar to a continuous glucose monitor eg from Abbott Laboatories for diabetics . Surely if they knew a good small biologic to track, then a useful device for pwME and/ or Long Covid could be devised?

What an interesting PhD project for someone with an interested supervisor.
How about Adam Rutherford who I understand might be suffering from long Covid? Would he know useful tech people? Or Brian Cox ?

Or what about Sir Paul Nurse at The Crick Institute. Couldn’t he devise a research project along these line . I thought they were interested in getting transfer of knowledge across borders of biology, physics and chemistry.

What a great opportunity.
 
hibiscuswahine said:
His research plan is also very similar but he is also going to have his research subjects go on a regime of lots of different nutriceuticals… Which I thought was an odd way to do start scientific research into the mechanism (but I suppose some novel treatment might arise…)
Click to expand...
I don't see science proceeding from someone who goes on Twitter to make definitive but wholly unsupported claims about what ME/CFS is. And I'd stay a long way from anyone wanting to pump Fibrinolytics/Anticoagulants and Drugs against viral and bacterial load into patients with no clear hypothesis, let alone prior plausibility for doing so. Maybe he can get away with it in Peru but I can't see any IRB/IEC giving the go ahead for any research involving that in the US or UK.
 
CRG said:
Maybe he can get away with it in Peru but I can't see any IRB/IEC giving the go ahead for any research involving that in the US or UK.
Click to expand...
That’s the problem, governments are handing out research money, researchers are turning their minds to it, but seem to be in partnership with some newly evolved nutraceutical/novel compound company. Sometimes I wonder if anything useful will come out of it for ME. Seems like alot of spinning of wheels and self-promotion but no proper science.
 
alex3619 said:
I first came across issues with vascular function, including endothelial linings, more than twenty years ago, including work by Vance Spence and Martin L Pall. So more than twenty years later we are still hypothesising.

Medicine advances with advancing technology. It might be we still lack the technology to investigate properly, or it may be that decades of advances have finally put us in a position to do ground breaking science. We shall see.
Click to expand...

DecodeME might give a genetic clue e.g. what protects and what predisposes.
 
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