An Update on ME/CFS Research with Ronald W. Davis, PhD

[alicec]

is 'serum' the same as plasma? and could whatever is going wrong originate in the lymphatic system

Serum and plasma are the liquid part of blood, minus all the cells.

The difference is the presence (plasma) or absence (serum) of clotting factors. In other words, serum is the liquid which remains after blood has clotted. Clotting factors like fibrinogen are removed in the clotting process.

Plasma is the liquid part of blood which has been treated with an anticoagulant so it doesn't clot. It contains clotting factors in addition to all the things found in serum. Plasma is the liquid part of blood as it circulates in the body.

The lymphatic system is part of the circulatory system. The lymphatic vessels drain the interstitial fluid - ie the fluid surrounding tissues in the body - and return it to the blood. The origin of the interstitial fluid is the blood - ie the liquid in blood and lymph is essentially the same.

However the lymphatic fluid has been in contact with different things from the blood circulation, most notably cells of the immune system and also of course all the tissues of the body.

So it is possible that whatever it is that is different about plasma in CFS/ME has arrived in the blood via the lymphatics.

 

[Barry53]

More to that point, it would be nice to have a research group that is focused on replicating important studies.

That makes extremely good sense. Akin to pathfinders and consolidators. The former have the highly specialist skills for the leading edge research, and the latter doing the crucial backup work of validating the pathfinders' work to demonstrate its credibility, or otherwise.

 

[Belbyr]

I am not sure I follow why you think dysautonomia and cfs are one and the same. (I am also not sure if you are referring to cfs or ME.)
If dysautonomia and cfs are the same, wouldn't treatments such as beta-blockers, midodrine, florinef, etc. help all patients?
Those treatment help some patients, with dysautonomia who have a cfs (or ME) diagnosis, but they do not help all of them.
Also some people with dysautonomia can exercise and improve, while patients with ME cannot exercise without worsening of symptoms and function.

Fluge/Mella and Lights on the CFS side, and many autonomic physicians seem to be pointing that way. Fluge/Mella are measuring antibody loads in their patient studies and these are the same antibodies that autonomic researchers are trying to grasp. I have tried beta blockers and midodrine. They don't help my condition, even loading up on fluids and salt makes no difference. If you ask POTS patients how well they feel their disease is managed. I'm willing to bet more than 75% of them would say poorly even with medication.

POTS patients also have a lot of physical pain in many cases, which you would think, "why would they have pain if its just an autonomic problem..." Something extra is going on in POTS too, I'm thinking they have metabolic problems and inflammation that is going undetected.

I read a study somewhere about a year ago that at least 2/3 of CFS patients had abnormal autonomic responses. That is about the same ratio of patients having positive responses to Rituximab. But, I'm no expert...

 

[Jesse2233]

Serum and plasma are the liquid part of blood, minus all the cells.

The difference is the presence (plasma) or absence (serum) of clotting factors. In other words, serum is the liquid which remains after blood has clotted. Clotting factors like fibrinogen are removed in the clotting process.

Plasma is the liquid part of blood which has been treated with an anticoagulant so it doesn't clot. It contains clotting factors in addition to all the things found in serum. Plasma is the liquid part of blood as it circulates in the body.

The lymphatic system is part of the circulatory system. The lymphatic vessels drain the interstitial fluid - ie the fluid surrounding tissues in the body - and return it to the blood. The origin of the interstitial fluid is the blood - ie the liquid in blood and lymph is essentially the same.

However the lymphatic fluid has been in contact with different things from the blood circulation, most notably cells of the immune system and also of course all the tissues of the body.

So it is possible that whatever it is that is different about plasma in CFS/ME has arrived in the blood via the lymphatics.

This perhaps helps explain the beneficial yet transient effects of plasmopheris

 

[BruceInOz]

Perhaps "exertion" is a better word? This way it would encompass emotional and intellectual efforts. For instance, in my case, the PEM toll from anger or grief, or mere intellectual concentration in doing something like complex Math or trying to decipher an in-depth study, will elicit devestating PEM quicker and longer lasting sometimes, than overdoing things physically.

Many here seem to resonate with this. I certainly feel that cognitive tasks produce PEM (by which I mean a crash in both physical and cognitive abilities simultaneously) more readily than physical tasks. But although the 2 day exercise results are well known now, have any researchers looked into triggering PEM with a cognitive load?

 

[duncan]

But although the 2 day exercise results are well known now, have any researchers looked into triggering PEM with a cognitive load?

Isn't the NIH planning a Math component as part of its cognitive domain testing in an effort to evoke PEM?

 

[Seven7]

Well a good start would be to test for the receptor the AU group found defective TRPM3. Even to confirm or move on. If it is realted and make sense.
Has anybody heard Ron's comments on this paper?
https://www.ncbi.nlm.nih.gov/m/pubmed/27727448/

 

[Yabisa]

Isn't the NIH planning a Math component as part of its cognitive domain testing in an effort to evoke PEM?

Pffff!!
That would be an automatic response!

 

[Yabisa]

Perhaps "exertion" is a better word? This way it would encompass emotional and intellectual efforts. For instance, in my case, the PEM toll from anger or grief, or mere intellectual concentration in doing something like complex Math or trying to decipher an in-depth study, will elicit devestating PEM quicker and longer lasting sometimes, than overdoing things physically.

It happens to me too.

 

[duncan]

I have wondered how they got a baseline on @Ben Howell , and pwME like him, when he likely arrived in California in full PEM. I know I have participated in a couple studies, and simply concentrating on the trip triggered nasty PEM that endured thru the entire study period.

 

[BruceInOz]

Isn't the NIH planning a Math component as part of its cognitive domain testing in an effort to evoke PEM?

I find it so hard to comprehend that it has taken so long for researchers to even begin to consider this. It shouldn't have taken so long for the 2 day exercise test results to be discovered. These things are so fundamental to what this illness is.

 

[lauluce]

I could be wrong but I think dysautonomia and CFS are one in the same. Some people present bigger pulse and BP changes on a tilt table than others. Just like some people with CFS are bed bound and some are able to hold a job.

I walked around for 10 years with docs telling me I had CFS, then last year found POTS. Sure enough 9 years ago I failed an ANSAR test but doctors never mentioned it. I never really complained of dizziness or felt my heart racing. Apparently no one picked up on it including myself. It was Dr Koch at Wake Forest (a motility GI doctor) that found it.

something tells me you're probably right, mate

 

[TrixieStix]

In the case of mitochondrial mutations, those mutations are typically present since birth, as are other healthy non-mutated mitochondria. But the mutated mitochondria may not have a noticeable impact until they're prevalent enough, typically over 50% for that type of cell (eg, muscles). So it's a somewhat gradual process, until the tipping point is reached. Accordingly, the change might look sudden.

But infections can also trigger flares, relapses, or progression of mitochondrial disease.

Have you read this new post by Cort Johnson? There could be a connection between ME/CFS and an increased level of somatic (mutations acquired later in life) Mitochondrial DNA mutations caused by the increased free radicals seen in ME/CFS.

https://www.healthrising.org/blog/2...ity-chronic-fatigue-syndrome-alan-light-talk/

 

[Barry53]

@Rose49 in case this helps.

A thought regarding the impedance meter. Ron and his team may already be aware of this, but just in case not.The fact it is called an impedance meter rather than resistance meter suggests possibly already onto it.

Electrical resistance is only one property that might be varying across different samples measured, there is also capacitance and (perhaps less likely here) inductance, which are deemed to be reactive characteristics rather than resistive; resistance and reactance combined are known more generally as impedance.

Resistance can be readily measured using a d.c. input, and it may be to date that is what the team are measuring. Impedance would typically be measured using an a.c. input, and you can then investigate things like frequency responses - how impedance varies according frequency of the a.c. signal. Related to this (sort of six of one, half a dozen of the other), is phase shift changes between voltage and current depending on frequency (or to be more pedantic, rates of change).

It just crossed my mind that, even if resistance measurements do not eventually prove distinctive between ME sufferers' cells under stress, versus other fatigue-sufferers' cells under stress, some of these other characteristics might do. Especially a frequency-response characteristic maybe. Repeatability would of course be key.

 

[DeceptivelySlow]

I could be wrong but I think dysautonomia and CFS are one in the same. Some people present bigger pulse and BP changes on a tilt table than others. Just like some people with CFS are bed bound and some are able to hold a job.

I walked around for 10 years with docs telling me I had CFS, then last year found POTS. Sure enough 9 years ago I failed an ANSAR test but doctors never mentioned it. I never really complained of dizziness or felt my heart racing. Apparently no one picked up on it including myself. It was Dr Koch at Wake Forest (a motility GI doctor) that found it.

I believe, generally speaking, that it is severely underestimated on how many levels autonomic neural dysfunction can wreck your health including your immune system and do so in a way that is not easily detectable.

 

[MeSci]

Isn't the NIH planning a Math component as part of its cognitive domain testing in an effort to evoke PEM?

Well, for about a year my maths skills have been seriously affected, so I wouldn't be any use! For the previous 20-odd years of M.E. thinking was relatively unaffected. Initially I was studying, and got 2 good degrees. Now - not a chance.

 

[skipskip30]

Well, for about a year my maths skills have been seriously affected, so I wouldn't be any use! For the previous 20-odd years of M.E. thinking was relatively unaffected. Initially I was studying, and got 2 good degrees. Now - not a chance.

My cognitive ability has been just destroyed over the past few years since a relapse. Doing maths is impossible these days, I can literally feel my head getting thicker and foggier as soon as I try to concentrate on something.

 

[Yabisa]

I believe, generally speaking, that it is severely underestimated on how many levels autonomic neural dysfunction can wreck your health including your immune system and do so in a way that is not easily detectable.

Can you imagin teaching?
Some times tireness is awful.

 

[Neunistiva]

I was majoring in mathematics when I came down with ME/CFS and my math skill was the first to go. Abstract thinking became impossible for me.

 

[boohealth]

Sorry to ask a redundant question, but last week I saw an email address to send queries about the serum experiment(s)--I ran across an interesting 2013 Tufts Univ study in the course of researching luteolin for something entirely unrelated here, that finds extracellular mito DNA components in autism, autoimmune (rhuematoid arthritis synovial fluid), etc. The paper has some really interesting potential insights. These extracellular mitoDNA components can be mistakenly construed as innate pathogens. Since so many are zeroing in on the mitochondria, I wanted to ask a question about this (I began to wonder if this was one of the components in the serum)...what is that email addy? I looked through a few pages of this thread and couldn't find it. Thanks.

(PS I am ambivalent about the dauer hypothesis, because I think either ongoing infection, and/or infection-like processes such as activated HERVs, are perpetuating the inflammation/hypometabolism. Now I wondered if the extracellular mito DNA might be as well...it's sort of fascinating)

(PPS please tag me. Sometimes I'm not on here for weeks. Thanks!)