Latest from Ron Davis: more evidence of “something in the blood”

Latest from Ron Davis: more evidence of “something in the blood”

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More clues are pointing to a role for blood plasma in ME/CFS. Ron Davis recently presented data showing that ME/CFS cells behave normally in the nanoneedle test IF they are tested in healthy plasma. Also, red blood cells from ME/CFS patients are not as deformable as those from healthy people — but researchers only see the difference when patient’s cells are tested in their own plasma. Plus, a bigger and better pathogen hunt and another drug candidate emerges from nanoneedle testing.

Dr Ron Davis recently revealed more evidence supporting the idea that there could be “something in the blood” that drives ME/CFS. 

He’s been on a tour of the US East Coast, winning over scientists and clinicians, one lecture hall at a time. 

Open Medicine Foundation has made available his talk at the Albert Einstein Medical Centre. Much of the talk’s content will be familiar to ME/CFS patients, so I am highlighting here the things that appeared to be new and particularly interesting. 

Something in the (blood) plasma 

Previous work from Ron Davis and others has suggested that an unknown factor in the blood is driving ME/CFS and can cause healthy cells to behave like ME/CFS cells. 

Blood’s main components are red blood cells, white blood cells, platelets (which help your body to form clots) – and plasma, the clear fluid that surrounds them.

Davis had already reported striking nanoneedle results. The nanoneedle measures electrical changes in a sample of simplified blood (effectively just white blood cells in plasma). 

What proved to be revelatory in ME/CFS was the nanoneedle salt stress test. This simply involves adding some sodium chloride (table salt), which forces cells to use energy (sodium enters the cell and is a little toxic to them, so they must use energy to pump it out again). 

When salt is added to a sample of healthy control cells  not much happens electrically. But when salt is added to an ME/CFS sample, electrical impedance shoots up, as the graph below shows. It does this for every patient tested (an initial sample of 20, then 26 more), and doesn’t do this for every control tested to date. 

Previously, he’d said that white blood cells taken from ME/CFS patients behave like normal, healthy cells if they are tested in plasma from healthy patients. Here, he presented data from one patient showing exactly that. 

As in the previous graph, impedance shoots up for ME/CFS in their own plasma, while nothing much happens for healthy cells in their own plasma (patchy yellow line – sorry, a poor quality screenshot of video). But when ME/CFS cells are tested in plasma from healthy patients (green line, indicated by the arrow), the ME/CFS cells now behave much like healthy cells 

So, something in (or missing from) the plasma seems to be affecting cells, making ME/CFS cells act abnormally. And finding the something responsible for that could provide a big clue to understanding ME/CFS. 

Davis has previously talked about his team’s work to home in on the presumed “factor” in the blood. They start by splitting the blood, physically or biochemically separating its components into separate fractions. Then, they test to see which fraction of the blood contains the mystery factor. The next step is to split the “active” fraction into still further fractions, and so on. 

Nanoneedle logjam 

This work is being held up because the existing nanoneedle set-up is very slow. Davis’s team have had problems making the nanoneedle chips that take the blood samples. And the machine that processes the chips can only process two samples at a time. 

The team have just built a prototype for a new machine that can process 200 samples simultaneously, which cost just $200 to build. And they now have more and better nanoneedle chips. 

Davis said that these improvements will allow his team to get the nanoneedle programme “back on track’, including the work to find something in the blood. 

UPDATE, 11.12.19: Janet Dafoe posted a statement from Ron Davis on Phoenix Rising giving more detail on the work they are doing to dramatically increase their capacity to do nanoneedle research.

Biology as well as biomarker 

The nanoneedle has produced the most dramatic published results yet seen in ME/CFS, with clear blue water between patients and controls. The nanoneedle has real biomarker potential if the research pans out and the findings are specific to ME/CFS. 

However, what excites me most is the possibility of uncovering the biology behind the nanoneedle result — perhaps “something in the blood” that could be playing a fundamental role in ME/CFS. 

And there’s more 

Previously, Davis had said that his team had been looking at something called red blood cell deformability. Red blood cells are uniquely flexible, which is essential as they have to squeeze (or deform) themselves through tiny capillaries to deliver their oxygen payload to tissues. 

However, in some diseases, red blood cells (RBCs) lose some of their ability to deform. 

Older research had indicated the same might be true for ME/CFS, but Davis had reported that his team’s promising, early, results didn’t hold up and this appeared to be a dead end. This work had been done with RBCs suspended in buffer (a fluid routinely used in lab work to keep cells stable). However, when they put the cells in patients’ own plasma instead, they started to see a significant difference between patients and controls. 

RBC deformability is lower in ME/CFS patients than in healthy controls. 

These differences are not as dramatic as those seen with the nanoneedle, but it is another sign that something in the plasma of ME/CFS patients is causing cells to malfunction. 

Other news: drug candidates and a pathogen hunt 

Davis reported two other interesting findings. 

In previous talks, he had said that the mitochondrial drug SS-31 completely normalised behaviour of patients’ cells in the nanoneedle (below, left). (This is encouraging but doesn’t necessarily mean it would help patients.) Now, they have found a similar effect for an MS drug, Copaxone, as well as less-impressive results for Suramin. 

These graphs for ME/CFS patient cells show how adding the drugs SS31 (left) and Copaxone (right) stops the typical big increase seen in the nanoneedle salt test. (The middle curve in the Copaxone graph is the result for a lower concentration of the drug.)  

Still checking for ongoing infections 

Work is continuing to identify – or rule out – the possibility of a microorganism causing ME/CFS. 

A broad-brush approach of DNA sequencing DNA particles from the blood found no new or existing pathogens. This approach is being complemented by very sensitive methods. While these have found nothing yet, the work still has a long way to go. 

So far, Davis’s team have found that ME/CFS patients have fewer DNA viruses than healthy controls. Testing for parasites and bacteria is ongoing. And they are planning a test to find any fungi in the blood. 

That covers, I think, all the significant new announcements from Ron Davis. If I’ve missed anything, please let me know

For me, the most important thing is that the idea of “something in the blood” remains alive and under active investigation. 

Image credits: Ron Davis, © Mark Tuschman (with thanks for his permission to use here); all graphs are screengrabs from the talk, labels edited by me for clarity.

25 thoughts on “Latest from Ron Davis: more evidence of “something in the blood”

  1. Simon, thanks so much for providing these updates on the research. They are immensely useful. Keep up the great work!

  2. Are you looking at the malleability of red blood cells and how it impacts their ability to travel through microcapillaries, to bring oxygen and to remove waste. Ramsay’s work from 1955, I think.

  3. I too thought this was exceptionally clear. Thank you. As someone said on Twitter, the healthy cells in sick plasma did not show an increase in impedance, perhaps this is because these healthy cells are just newly being exposed (for 1.5 hrs) to sick plasma so they don’t show the cell biology change in response to salt stress as do the sick cells.

    1. Interesting – I hadn’t realised they had only been exposed to plasma for one-and-a-half hours

      1. I was looking at the graph. But since we don’t know the experimental details, it’s possible they pre-incubated the healthy cells in sick plasma. But based on what they say about the time constraints of this set-up and needing fresh blood, it couldn’t be too long an incubation. The in vivo physiological condition of the blood is changing once removed from body. I would think acid-base balance would be one of the first things to go sideways. One reason why ppl often want to put cells in buffers when doing experiments. But there’s problems with that too as ppl point out, including Ron.
        All interesting!

        1. Thanks. Good point that the need for fresh blood limits the length of any possible pre-incubation.

  4. Has Dr. Ron Davis looked into the research of Dr. Steve Fry in Scottsdale Arizona? He has been treating patients with ME/CFS, MS and other autoimmune conditions for over 20 years after having discovered a protozoa like critter that lives in the blood stream of affected people and makes biofilms in the blood stream, along blood vessels, in our guts etc. This protozoa affects red cells and makes the biofilms in the plasma as well. It makes sense that removing affected persons red cells would do better in donor plasma and the same with affected plasma in donor red cells.

  5. Thanks Simon, this is great. I have a question though. If it’s something in the plasma causing the cells to act that way, then why does the graph show that healthy cells in CFS plasma don’t behave like CFS cells in their own plasma do? The healthy cells don’t seem to have a significant electrical signal

    1. Good question and I don’t know the answer. This was data for a single patient. Once they scale things up on my hopefully we will have a decent sample size and and that will be the time to draw conclusions.

  6. After 7.5 years on cycling antibiotics (Marshall Protocol) and recovering a quality of life I never expected, i have to conclude my ME/CFS has an infectious basis.

  7. It is significant they are starting to look at fungi. My bet is part of the answer will lie there.

    1. As far as I know no, they are just being comprehensive. checking for any pathogen involves checking for bacteria viruses, parasites and fungi.

  8. Thanks Simon. You have a beautifully clear way of explaining the complex.

    I’m a little concerned that we (people with ME/family members) are so abandoned. In effect the research here looks relatively straightforward i.e. fractionate blood (plasma?) and test the fractions on a high resolution mass spectrometer (maybe not even that high resolution) – i.e. to identify what is causing this. Yet we lack public funding to deliver even modest projects like this!
    ME Action are lobbying for EU funding for biomedical research; identifying “something in the blood” looks like a good project!
    Here’s the ME Action EU Facebook page: #MEAction European Union (EU)

    1. That wouldn’t explain the difference with healthy controls, or why previously healthy people suddenly got sick.

  9. Thanks for the summary! This is really interesting. I have been wondering if it could be something in the blood because so often pregnant women are in remission from the illness! There are several studies for other diseases showing that connecting the circulatory systems of young healthy mice with old diseased mice can temporarily cure the disease of interest. A pregnancy is a naturally occurring situation like this. So something in the blood of the fetus is helping.

    1. Interesting idea. If that’s the case, the “something” would be a healthy something missing in mecfs people, present in healthy folk and the fetus. It would also need to be a small enough molecule to filter through to maternal blood.

  10. Thanks for the summary! This is really interesting. I have been wondering if it could be something in the blood because so often pregnant women are in remission from the illness! There are several studies for other diseases showing that connecting the circulatory systems of young healthy mice with old diseases sed mice can temporarily cure the disease of interest. A pregnancy is a naturally occurring situation like this. So something in the blood of the fetus is helping.

  11. One of my personal discoveries has been that interstitial blood glucose doesn’t work for me (ME and Type 2 diabetes). I’ve used around 20 different Freestyle Libra sensors, from different batches, over 3 years and according to interstitial fluid I spend 90% of my time severely hypoglycemic. That ME plasma isn’t normal comes as no surprise to me!

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