Blood Flow & ME/CFS

[LouiseLouise]

Hi there,

I wanted to share a couple of blog posts I wrote about ME/CFS, blood flow and how this might relate to the similarities between sepsis and ME/CFS.

The first one is about the type of blood flow you find in capillaries in sepsis. In sepsis, you have some capillaries with normal blood flow, while neighboring capillaries can have no blood flow or slow blood flow. This is a situation often called "heterogenous perfusion". This results in trouble extracting oxygen from the blood and making energy from it, a situation you find in sepsis and in ME/CFS.

The second one centers a material called glycocalyx that lines the interior of blood vessels all over the body. Glycocalyx is lost in sepsis and its loss results in heterogeneous perfusion. Interestingly, various causes of CFS like infection, injuries, surgeries, and psychological stress may also lead to loss of glycocalyx.

 

[Hip]

Interesting theory, this idea that in heterogenous perfusion there can be non-uniform blood flow, being normal in one capillary but blocked in the next capillary.


I wonder if heterogenous perfusion is related to the very mild blotchy skin (livedo reticularis) I developed since getting ME/CFS, where there are blotchy uneven areas of red and white, suggesting non-uniform blood flow under the skin?

My livedo reticularis is very mild, milder even than the livedo reticularis shown in the picture below. And in my case it is mostly on my hands and feet (my hands and feet are always cold as well).

Livedo Reticularis (Blotchy Skin)

Source: here.
​

But from what you are saying, the scale of heterogenous perfusion is microscopic, with blood flow varying greatly from capillary to capillary at the microscopic level, so you probably would not be able to see it with the naked eye; whereas livedo reticularis seems more of a macroscopic phenomenon that you can see.



By the way, it appears there are unfortunately no drugs available to promote glycocalyx in the blood vessels, according to this paper.

 

[prioris]

ArterosilHP was demonstrated to protect the endothelial glycocalyx, the micro-thin slippery inner lining that prevents all blood vessels from damage, in healthy subjects after they consumed a standardized high sugar high fat meal. At the same time, the subjects showed improved endothelial function with ArterosilHP supplementation as measured by reactive hyperemia index (RHI). The primary active ingredient in Arterosil® is derived from a rare green seaweed. Green seaweed polysaccharides have been reported to possess anticoagulant and antithrombotic activity. The polysaccharide in Arterosil® has a similar chemical structure to heparan sulfate found abundantly in human endothelial glycocalyx and may exert its biological activities by regenerating endothelial glycocalyx... Cost is $99 ... overpriced

i'm sure there is a lower cost supplement substitute ... let's see ... mesoglycan

sepsis is essentially scurvy gone wild

sepsis has been cured with Malik protocol using vitamin C ... 1.5 gram vitamin c every 6 hours... one study tried on 150 people ... all 150 survived
sadly it isn't used by medical establishment who have survival rate of 40% ... if you or someone you know gets sepsis, demand they use malik protocol

liposomal vitamin c only has 10% absorption so one would need 15 grams every 6 hours

 

[jesse's mom]

where there are blotchy uneven areas of red and white,

I have this dramatically in the palms of both my hands.

Thanks for posting.

 

[LouiseLouise]

Hi Hip,
Livideo reticularis is found in sepsis. I don't think the mechanism has been determined for certain, but seems to have to do with the general problems with blood flow through the smallest vessels (microcirculation) found in the illness. It is also found in POTS and in fibromyalgia and is more common in people who also have Raynaud's phenomenon. I have had livido reticularis as well, but not so much these days.

Livido reticularis is much more common in women than in men. When they don't know the cause and presume the cause is not dangerous, it is called benign livido reticularis. I wonder how benign it actually is or whether it is connected to illnesses like ours, which are underrecognized and not taken seriously.

Here are a couple of quotes about L.R.:

So, it looks like livido reticularis is the result of slowed and pooling blood in small veins under the skin.

As for things that could help glycocalyx, there are mesoglycan and sulodexine, which supply the materials that glycocalyx is made from. In the glycocalyx article, near the bottom, I talk about how Robert Naviaux has found that people with ME/CFS are low in sphingolipids. This is the largest metabolic difference he has found in pwME. A common sphingolipid is called S1P. S1P is found on the most common protein in the blood, called albumin. Albumin is the most important factor in the body for stabilizing the delicate glycocalyx and the part of albumin that performs this function is the S1P. When S1P is lacking, glycocalyx is vulnerable to damage.

I proposed that we could be short of this common sphingolipid and in this way we could have glycocalyx that is extra unstable and susceptible to damage.

In this case, a possible treatment would be albumin IVs, since this should supply albumin with normal amounts of S1P.

Thanks

Interesting theory, this idea that in heterogenous perfusion there can be non-uniform blood flow, being normal in one capillary but blocked in the next capillary.


I wonder if heterogenous perfusion is related to the very mild blotchy skin (livedo reticularis) I developed since getting ME/CFS, where there are blotchy uneven areas of red and white, suggesting non-uniform blood flow under the skin?

My livedo reticularis is very mild, milder even than the livedo reticularis shown in the picture below. And in my case it is mostly on my hands and feet (my hands and feet are always cold as well).

Livedo Reticularis (Blotchy Skin)
View attachment 31436
Source: here.
​

But from what you are saying, the scale of heterogenous perfusion is microscopic, with blood flow varying greatly from capillary to capillary at the microscopic level, so you probably would not be able to see it with the naked eye; whereas livedo reticularis seems more of a macroscopic phenomenon that you can see.



By the way, it appears there are unfortunately no drugs available to promote glycocalyx in the blood vessels, according to this paper.

 

[frozenborderline]

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4770074/

Our results demonstrated that the administration of EP (ethyl pyruvate) significantly improved the survival rate and reduced intestinal histological alterations. EP inhibited the plasma levels of IL-1β, IL-6, and tumor necrosis factor-α and increased the IL-10 level. EP significantly inhibited the elevation of the malondialdehyde, lactate, and lactate/pyruvate levels and enhanced the total antioxidative capacity levels in the liver tissues. The downregulation of the adenosine triphosphate, total adenylate, and energy charge levels in the liver tissues was reversed in the septic mice treated with EP.

 

[prioris]

blood flow, arteries and veins
lumbrokinase (for serious blood clots), nattokinase (for milder blood clot), serrapeptase (for inflammation and dissolve dead tissue)
diosmin or maybe mesoglycan for veins and hemorrhoids

 

[prioris]

liposomal vitamin c only has 10% absorption so one would need 15 grams every 6 hours

that could be wrong … it could be 100% absorbed

conventional method causes massive damage inside bodies of the survivors so aftermath is devastating
... probably better for most to be dead. vitamin C keeps tissues healthy and likely no aftermath damage.

 

[SherDa]

I proposed that we could be short of this common sphingolipid and in this way we could have glycocalyx that is extra unstable and susceptible to damage.

In this case, a possible treatment would be albumin IVs, since this should supply albumin with normal amounts of S1P.

Thanks

I wonder if vitamin K could play a role since it's needed for sphingolipid synthesis?

 

[Ema]

In this case, a possible treatment would be albumin IVs, since this should supply albumin with normal amounts of S1P.

I am thinking of trying albumin IVs and came here looking for patient experiences...I know there is a clinical trial running using albumin for POTS, plus all the recent research showing benefit by using albumin to dilute the plasma in neurodegenerative diseases etc. I'd love to chat with anyone who has tried this. As far as I can tell, IV albumin is fairly inexpensive and easy.

 

[Hoosierfans]

I am thinking of trying albumin IVs and came here looking for patient experiences...I know there is a clinical trial running using albumin for POTS, plus all the recent research showing benefit by using albumin to dilute the plasma in neurodegenerative diseases etc. I'd love to chat with anyone who has tried this. As far as I can tell, IV albumin is fairly inexpensive and easy.

Ema this is old but did you end up trying it?