Erythrocyte Deformability As a Potential Biomarker for Chronic Fatigue Syndrome, Davis et al (2018)

Simon M said:
Normally, a mere 12% difference would not lead to such an extreme P value. This implies very low variance ( patient data clusters close together, and the same for control data). If that’s the case, then it could prove to be an excellent bio marker - if this replicates on a larger sample.
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It would be good to see the data here.

What is also interesting is that there seem to be a set of measures that seem to fit rather than just one.

Also I was just watching a video on microfluidics and I get the impression that chips to do this (micro fluidics not Ron's test) are relatively easy to manufacture so it could be that such a test would be easy to make and do.
 
Philipp said:
Regarding the ESR, did anyone notice differences testing that when PEMcrashed vs rested?
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Yes. Mine went from 5 to 3, which isn't much, but it's 40%.

The good news about ESR is that it's a standard test. Probably not a biomarker in itself (too nonspecific) but maybe it could be used with other factors, like the HGS?

So low ESR, poor results on a semi-decent questionnaire, and weakness on HGS might all be used in addition to diagnostic criteria?
 
I just went through all the pathology results I have stored looking at ESR and this is what I found. Interestingly ESR seems to have gotten higher as I've gotten sicker.

Pre-ME but still not well
2001 1
2004 1

On-set of ME still working until 2009
2006 1
2007 1
2007 2

Disabled by ME and onset of MCS
2009 8
2010 2

Housebound by ME and MCS
2011 5
2012 5


I wasn't exactly expecting the ESR to get higher over time. It'd be interesting to know what it is now.

How specific is this finding for erythrocyte deformability likely to be?
 
There's a post going round on Facebook from a Maryann Spurgin basically ripping into this work, and in her post she seems to claim that Ron may have got the idea for this study from her blog in the 80s! (Though I do know this is not a new idea). Her post is being shared by some of those that take a rather sectarian and outdated approach to advocacy. You know the ones....


News flash to Ron Davis and team:

While this is an important part of the circulatory pathology as has been discussed since the 1980's, and as I wrote about in my blog on circulatory impairment in ME that I sent to Davis, this is not going to serve as a biomarker for ME. It is present in too many other conditions, including healthy people at the end of a marathon run, e.g. True, it persists longer in ME and does not resolve, but it's still present elsewhere.
Further, it is protective against overexertion, so treating without treating the underlying condition should be harmful, which it was in my experience.

*As usual, the Davis team seems clueless when it comes to interpretation of findings.*
 
BurnA said:
This is interesting.
Finally, preliminary studies show that RBCs from recovering ME/CFS patients do not show such differences in cellular physiology, suggesting a connection between RBC deformability and disease severity.
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I wonder what a recovering patient is defined as - someone who was severe and now moderate or moderate and now mild or just any mild patient, or any patient who says they are better? Also wonder if recovering patients had no differences or just less differences.
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Given that so many people do not recover, might it also tie in with the possibility there could be something fundamentally different with those who do recover?
 
InitialConditions said:
There's a post going round on Facebook from a Maryann Spurgin basically ripping into this work, and in her post she seems to claim that Ron may have got the idea for this study from her blog in the 80s! (Though I do know this is not a new idea). Her post is being shared by some of those that take a rather sectarian and outdated approach to advocacy. You know the ones....


News flash to Ron Davis and team:

While this is an important part of the circulatory pathology as has been discussed since the 1980's, and as I wrote about in my blog on circulatory impairment in ME that I sent to Davis, this is not going to serve as a biomarker for ME. It is present in too many other conditions, including healthy people at the end of a marathon run, e.g. True, it persists longer in ME and does not resolve, but it's still present elsewhere.
Further, it is protective against overexertion, so treating without treating the underlying condition should be harmful, which it was in my experience.

*As usual, the Davis team seems clueless when it comes to interpretation of findings.*
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I just had a look for a facebook profile, and saw that post had only been shared 9 times.

I guess that a lot of her concerns will be assessed when there's an attempt to replicate this work with a larger sample.

Lots of people have speculated about lots of different things over the years. What matters is whether this is a test that an reliably distinguish between ME/CFS patients and non-ME/CFS patients. To see if that's the case we're going to have to wait from some more results.
 
Esther12 said:
I just had a look for a facebook profile, and saw that post had only been shared 9 times.

I guess that a lot of her concerns will be assessed when there's an attempt to replicate this work with a larger sample.

Lots of people have speculated about lots of different things over the years. What matters is whether this is a test that an reliably distinguish between ME/CFS patients and non-ME/CFS patients. To see if that's the case we're going to have to wait from some more results.
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Yeah I agree. Perhaps her post raises some good points. But it was the tone of the post and some of the comments, and the constant effort by some in the community to shit on the work of leading researchers, charities, advocacy groups etc.
 
Esther12 said:
I just had a look for a facebook profile, and saw that post had only been shared 9 times.

I guess that a lot of her concerns will be assessed when there's an attempt to replicate this work with a larger sample.

Lots of people have speculated about lots of different things over the years. What matters is whether this is a test that an reliably distinguish between ME/CFS patients and non-ME/CFS patients. To see if that's the case we're going to have to wait from some more results.
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I think there has been previous work on blood flow through capillaries in the brain and also on the shape of red blood cells. So I suspect that Ron picked up on things that had been talked about a bit and tested them.

But what is interesting is the testing he has done. What he is basically doing is pushing the red blood cells through a small capillary tube and measuring things about the flow and the elasticity of cells so that he has a new test mechanism.

However, I think we need to be really cautious about the quoted results we don't know how much the distributions of results overlap and its a very small sample size.
 
Regarding ESR, I think a number of things can influence it in different directions, making it easy for results to be all over the place. My son has had low average to low (2) ESR. I, with onset at the same time and same symptoms, have had average to mildly high ESR, with high fibrinogen and mildly high CRP. Menstruation can increase ESR, and I think anaemia can too.

It’s great that erythrocyte deformability is being looked at again. It makes sense, given how common issues with pins and needles and numbness are. There was a paper I was looking at that found that sepsis causes low deformability of erythrocyte membranes.

Edit: e.g.https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5618581/
The Effect of Sepsis on the Erythrocyte
Here, we review the effects of sepsis on the erythrocyte, including changes in RBC volume, metabolism and hemoglobin’s affinity for oxygen, morphology, RBC deformability (an early indicator of sepsis), antioxidant status, intracellular Ca2+homeostasis, membrane proteins, membrane phospholipid redistribution, clearance and RBC O2-dependent adenosine triphosphate efflux (an RBC hypoxia signaling mechanism involved in microvascular autoregulation).
....Evidence that small molecule antioxidants protect the erythrocyte from loss of deformability, and more importantly improve septic patient outcome suggest further research in this area is warranted.
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As a side note from the abstract:
" Clinically, ME/CFS patients show normal arterial oxygen saturation..."

That statement surprised me, but maybe I got it all wrong.
What Dr. Cheney told at a IACFS patient conference made more sence to me (page 6):

" CFS Patients Are Functionally Hypoxic - Dr. Cheney started off in characteristically dramatic fashion showing a slide of Mt. Everest (29,028 ft.) with 1/3rd of the oxygen at sea level and announcing that the problems CFS patients face are very similar to those that climbers at the top of Mt. Everest face".

I haven´t found any studies on the subject on PubMed, but maybe there are.



 
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This is a very small study... personally my ESR has always been on the higher-normal side and even going around 38 (normal 0-20). My family dr has then decided it was best to stop testing ESR.... problem solved!

(P.S. Documented EBV+ onset, diagnosis confirmed by 3 well known experts, still sick 10 years after)
 
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