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Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.
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Here's a more recent talk, with some new information.
His work with Dapsone is particularly interesting to me as one infected with both borrelia and babesia. It seems to be a breakthrough therapy for some patients.
Can anyone decipher what he says at 1:05:00 when he mentions a bacteria that "stops gluten sensitivity"? I've listened a few times but can't make out the name of the bacteria.
"Rothia bacteria"... Looked it up and found this intriguing paper in PLOS one:
What good hearing you have!
Endothelial Functioning Substudy
Our substudy of endothelial function (Bergen Notodden) in 72 patients will use flow-mediated dilation to test large blood vessel endothelial functioning. We will also test microvascular endothelial function in Bergin using skin laser-doppler measurements.
Is a problem in the blood vessels triggering the sympathetic nervous system activation found in ME/CFS?
We believe that endothelial function is important in ME/CFS. Even though many symptoms can be ascribed to the central nervous system we are not convinced that ME/CFS is primarily a central nervous system disorder. We believe the sympathetic nervous activation seen in ME/CFS may be (partly) secondary to an underlying (peripheral) pathology.
It is important to get an understanding of which symptoms that are caused by the primary pathology, and those which may be ascribed to secondary (compensatory) mechanisms. We are working to elucidate whether endothelial dysfunction, and subsequent inadequate fine-tuned autoregulation of blood flow to meet the demands of tissues, may be an important feature of ME/CFS.
A study from Dundee in 2011 showed endothelial dysfunction to be present in ME/CFS. Our pilot studies in a group of ME/CFS patients suggest it is as well.
In the substudy to RituxME, we ask if we can reproduce the endothelial dysfunction in a larger cohort of ME/CFS patients? Is there a relation between endothelial dysfunction and disease severity? Is there a relation between endothelial function and a later clinical response (in the rituximab group)? In patients that improve after B-cell depletion therapy (Rituximab) is there a relation between improvement in self-reported symptoms or in physical activity levels, and changes in endothelial function?
We have written a manuscript on our thoughts and hypotheses including the relation between immune response, endothelial function, and the possible effector system for symptom maintenance in ME/CFS. However, we still believe that we need more data to underpin out thoughts and have therefore not submitted the paper yet.
[Dysfunction of the endothelial cells lining the blood vessels in the circulatory system has been a subject of interest in ME/CFS since MERUK’s pioneering efforts in the early 2,000’s. These cells – present everywhere from largest arteries to the small capillaries – control how dilated or narrowed the blood vessels are, affect inflammation, control blood clotting and more. Each of these factors have been implicated in ME/CFS at one time or the other. In 2012 Newton et al. reported both small and large blood vessel dysfunction was present in ME/CFS.
Lyme has been shown to populate endothelial cells. I have POTS. I am also on dapsone.
I am just not at a position yet there is a connection. But the possibilities are fun.