Endothelial dysfunction and ME/CFS

[ChronicallyOverIt]

@PageofME I’m sorry but as someone with no dog in the fight most of your argument is subjective here with little evidence at all, we’re here to discuss the scientific research of ME. A Chinese medicine doctors opinion on micro vascular research will not cut it here. I can call up 20 naturopathic/alternative practitioners that will gladly tell me what I want since I am paying them….

If we base all of our research dogmas on subjective experiences, especially from unscientific practitioners, we’re never going to get anywhere.

 

[ChronicallyOverIt]

Happy to read the Norwegian study, but after a bit of search I don’t see it? I do see a lot of retinal studies with some dubious control groups and results however.

 

[Jonathan Edwards]

Most importantly, I have always known something is fundamentally wrong with my brain's blood flow.

Is this really a useful way to conduct a scientific discussion?

 

[Jonathan Edwards]

There is a growing body of evidence showing functional microvascular impairment, endothelial dysfunction, and capillary-level perfusion deficits when the system is challenged (for example, the recent flow-mediated dilation data from the Norwegian cohorts or recent retinal vessel analysis studies).

But this really doesn't take us very far if the clinical presentation is not that of microvascular insufficiency. You can always find papers to hint at any theory. In medicine you have to keep your feet on the ground. (The same probably applies to all branches of science.)

 

[Violeta]

There are people getting well using the information about endothelial dysfunction. There was one person who had been here that is getting well, but he no longer shares here.

It doesn't matter, though, how many studies you link or who did the studies, or even remedies that have helped people with ME/CFS or Long Covid that you post in this thread, the same people who are denying that there is no science involved will keep coming back and claiming they are not valid.

 

[PageofME]

There are people getting well using the information about endothelial dysfunction. There was one person who had been here that is getting well, but he no longer shares here.

It doesn't matter, though, how many studies you link or who did the studies, or even remedies that have helped people with ME/CFS or Long Covid that you post in this thread, the same people who are denying that there is no science involved will keep coming back and claiming they are not valid.

Why are you interested in the vessels and what therapies have you read about or are interested to try?

I have begun with an oral intake of magnesium today, inspired by the therapy protocol that I mentioned above that is discussed in German LC forums. It seems that some patients get better with it – until their next flare-up sends them back to where they were.

As a mild-moderate patient, and now on Famvir, I am able to do a physiotherapeutic protocol with gentle yoga and two weekly training sessions at the gym, including some low-exertion cardio training. I think that is probably one of the most efficient ways to support the regeneration of the immune system and the vessels anyway – natural oxygenation.

I am extremely grateful I can do that.

 

[Formerhuman]

Or the abundant clinical data indicating normal perfusion?

Could you elaborate on what data make you confident that muscle perfusion during upright exertion is normal in ME/CFS?

I’m asking because I’m unable to do stairs or squats due to quad weakness and aching, while I can tolerate walking. My personal hypothesis is that I may have blunted cardiac output, along with exaggerated sympathetic activation, which could contribute to insufficient functional sympatholysis (inadequate attenuation of sympathetic vasoconstriction in muscle during exertion).

There are some iCPET data that at least point to the possibility of blunted cardiac output or impaired venous return in a subgroup of ME/CFS patients. Regarding muscle perfusion during upright exertion, I don’t think we currently have precise methods. And it seems to me that the scarce and small NIRS studies have not provided definitive answers.

 

[Utsikt]

I’m asking because I’m unable to do stairs or squats due to quad weakness and aching, while I can tolerate walking. My personal hypothesis is that I may have blunted cardiac output, along with exaggerated sympathetic activation, which could contribute to insufficient functional sympatholysis (inadequate attenuation of sympathetic vasoconstriction in muscle during exertion).

Aren’t there a whole host of possible reasons for why you’d struggle walking up stairs? Walking up stairs would be difficult for most sick people, I suspect. It’s the most complex biomechanical movement we normally do, making use of most large muscle groups.

 

[Mij]

Magnesium and taurine injections was the best treatment that worked for me because I was severely deficient.

I couldn't climb stairs, do squats, planks or light weights for many years, and now I can. My own health improved over the years from doing nothing btw.

 

[Formerhuman]

Aren’t there a whole host of possible reasons for why you’d struggle walking up stairs? Walking up stairs would be difficult for most sick people, I suspect. It’s the most complex biomechanical movement we normally do, making use of most large muscle groups.

Frankly, I lost an ability to develop and sustain repetitive muscle power in general. For example, push-ups are impossible too.

You are right that climbing stairs may be demanding for chronically ill people, but there should be some sort of explanation in every particular case.

In my case, ENMG (4 times), leg muscle MRI (2 times), multiple creatine kinase and LDH measurements, 3‑Tesla brain MRI with contrast (2 times), and a quad biopsy (showing nonspecific atrophy) have revealed nothing abnormal. I would like to underline that I developed these symptoms early in the disease, when I was perfectly fit.

I do not believe in the microclot theory, which has been promoted by a single team. Rob Wust mentioned in their paper that they did not find any microclots in muscle capillaries. With regard to microvascular damage, I would expect to see many issues with the kidneys, heart, and retina in these patients. I even had OCT‑A, which was normal. Nailfold capillaroscopy revealed wide capillaries but no rarefaction.

I developed hypotension early in the disease. That is why I believe that my 'POTS' represents normal compensatory response to low pressure in the aorta and carotid arteries. Intensity of sympathetic activation vary but with upright HR 120 or more I get exhausted quickly.

Returning to chronically ill people, at least a subgroup of patients with heart failure have blunted cardiac output. Patients with HF seem to have a range of muscle symptoms. A vivid example of what an excess of catecholamines can do to muscles is pheochromocytoma. Cases of rhabdomyolysis, putatively due to vasoconstriction, have been described.

I did not intend to bother anyone with my medical notes. I just wanted to explain the logic behind my speculations about this phenomenon. There are no precise methods to evaluate muscle perfusion in the upright position and under exertion. NIRS is a proxy, and studies are scarce.

That is why I asked what 'abundant clinical data indicating normal perfusion' actually refers to.