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Breaking News: ME is in the blood

ash0787

Senior Member
Messages
308
I think someone said that ron was already working on it, might be possible to figure out using metabolomics ?
cant imagine its going to be easy.

I think this rules out the argument that a metabolic process within the cells is broken though and the cells are shutting down to prevent damage ( one of the triggers suggested in the dauer state hypothesis )
 

Cheesus

Senior Member
Messages
1,292
Location
UK
I notice that second tweet from Cort - in which he said healthy cells put into ME patients' blood will become dysfunctional - correlates to an article he wrote a while ago, in which the scientist he was interviewing noticed that NK cells behave normally when removed from the blood:

Decreased natural killer (NK) cell functioning has been a key immune finding for ME/CFS – a consistently reproduced finding – until the NIH-funded Katz study found no problems at all with NK cell functioning. Broderick couldn’t figure this out until he got Katz on the phone and dug into the details of the study.

It turned out that Katz had isolated NK cells and then tested them, while the Klimas team always tests them in whole blood. The light bulb went on. Something in the blood was axing the NK cells. Put the NK cells off by themselves and ask them to kill pathogens and they do just fine – but put them in the blood mixed with all the immune factors found there and they poop out.

http://www.healthrising.org/blog/20...ome-amenable-intervention-dr-broderick-talks/

if the two things have the same cause, this would suggest it is something more broadly harmful than an autoantibody. Lipopolysaccharide?

Or perhaps mitochondrial dysfunction has a broad effect across a number of different cell-types...?
 
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skipskip30

Senior Member
Messages
237
I tested positive for anti mitochondrial antibodies about 15 years ago. I was tested for primary biliary cirrhosis which came back negative and so nothing more happened. Interestingly I was retested for anti mitochondrial antibodies about a year ago and the dr didn't find any.
 

taniaaust1

Senior Member
Messages
13,054
Location
Sth Australia
I tested positive for anti mitochondrial antibodies about 15 years ago. I was tested for primary biliary cirrhosis which came back negative and so nothing more happened. Interestingly I was retested for anti mitochondrial antibodies about a year ago and the dr didn't find any.

oh that could be bad if its something which is coming and going with us and not showing up all the time.

I guess then it could possibly make it another ME/CFS consquence seeing so many of my symptoms come and go and just arent stable.
 

taniaaust1

Senior Member
Messages
13,054
Location
Sth Australia
Ive been thinking further on this latest findings and wondering what the implications then have been to those we have donated blood too? I donated blood 2 or maybe 3 times while having ME (this was before they brought in that ME/CFS people couldnt donate blood). Does this mean that we contaminated the blood and damaged cells of the one who got it while they were trying to heal?
 

ZeroGravitas

Senior Member
Messages
141
Location
UK
Bear in mind that Fluge and Mella already presented (probably) all of this in Norwegian: translated, here. As reported on by Cort in this article, stemming from this PR thread.

I imagine (i.e. speculate that) their dysfunction measure could have been direct measurements of cellular metabolism, like the methods used by the group that found elevated ATP production. Or, during the conference, Jon D. Kaiser MD mentioned Agilent's 'Seahorse' equipment (their site with informative videos and diagrams), which seems to be an off the shelf solution for measuring oxygen consumption rate (and acidity) from a tiny (single) layer of sampled cells, in real time (to assess glycolosis rate, etc).

So something like that, no need for Ron's magical new single cell exercise endurance testing gizmo (although that sounds more awesome). This comes from one of the panels which had a video steam up on OMF Facebook page and I made notes on here.

Ron was also talking there (I think) about 'fractionalising' blood, to hone in on the problematic blood factor (i.e. repeatedly filtering out, separating, half the remaining types of stuff and retesting it's effect, etc). And quite possibly he (and Mella/Fluge) are already into something like this...
How difficult is it to isolate the factor that's responsible? Can we look forward to a paper on this in next year?

Sounds like the proverbial smoking gun!
It would be, and see Cort's last tweet (within "one year" hype):
I think someone said that ron was already working on it, might be possible to figure out using metabolomics ?
cant imagine its going to be easy.
Depending on what kind of factor it turns out to be (if they are right), and Ron also conceded it could be something missing, at this point, then a metabolomics blood test, or even narrower metabolite test, might well be sufficient. But if it's an antibody, or illusive chemical signal, I don't now.
I think this rules out the argument that a metabolic process within the cells is broken though and the cells are shutting down to prevent damage ( one of the triggers suggested in the dauer state hypothesis )
I'm not so sure. no cell exists in isolation, the metabolic substrates are mostly shared via blood. And anything attacking/impacting the mitochondria directly might trigger it into some level of cell defense mode, certainly there is a shift away from aerobic mitochondrial OxPhos and that's quite likely to be self imposed to some extent.

I think there was someone at the conference pushing for the word "inflammation" to be included in (a name for) CFS/ME? But not acute inflammation, presumably, some more subtle mix of altered cytokines, other signaling molecules, various metabolite balances and immune cell balances and activation states... And then (I'm not sure if there's) overlap with (blood borne) oxidative stress...?
if the two things have the same cause, this would suggest it is something more broadly harmful than an autoantibody. Lipopolysaccharide?

Or perhaps mitochondrial dysfunction has a broad effect across a number of different cell-types...?
Maybe. Maybe the blooming and death debris of blood borne bacteria that aren't as rare as we thought, or LPS via translocation from gut.

Immune cells are supposed to use their mitochondria very differently to most other cells, less so for energy, but don't know if that would make them less sensitive to reduced capacity. And other, as yet poorly understood signalling/sensing functions might still be in play...?

what the implications then have been to those we have donated blood too?
My feeling is that the problem won't be infectious in that way, in that a particular blood component (e.g. plasma) might introduce a CFS-like blood borne stress on the recipient, but it would be transient, or immediately diluted away. Red blood cells alone are surely unlikely to cause additional issue (beyond the general "controversy" over efficacy of transfusions). I don't know if, don't think that, B-cells, for example, are transfused at all (the ones wiped out by Rituximab, with some success). Any that got through would presumably be mopped up by the recipient's immune system. I don't think you can transfer any known auto-immune diseases, for example...
 
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skipskip30

Senior Member
Messages
237
oh that could be bad if its something which is coming and going with us and not showing up all the time.

I guess then it could possibly make it another ME/CFS consquence seeing so many of my symptoms come and go and just arent stable.

I will be asking my consultant about this when I next see him. I know very little about the antibodies as I was too young to really know what was happening when the first lot of tests where done.
 

Seven7

Seven
Messages
3,444
Location
USA
I really think is a joke, the Crawly club thread and this thread is like a twilight zone. How can things be sooooo crazy right now.

Also don't you guys have in UK the consumer laws you know to lie about a product (when the data was analyzed was not 60% but 13?% or something like that for the MAgenta trial)
Sorry didn't mean to derail the thread but as I saw it I was like this is insane!!!!
 

Sing

Senior Member
Messages
1,782
Location
New England
There was a chart showing what is and is not in the plasma. No red or white blood cells I seem to recall. Does anyone remember? I think it said there are mainly proteins left in the plasma, so one of these?
 

CFS_for_19_years

Hoarder of biscuits
Messages
2,396
Location
USA
There was a chart showing what is and is not in the plasma. No red or white blood cells I seem to recall. Does anyone remember? I think it said there are mainly proteins left in the plasma, so one of these?
Blood is composed of formed elements (red cells, white cells, and platelets) and plasma, the yellow liquid part. Serum is similar to plasma, except that serum doesn't have any coagulation factors (various proteins) in it.

So yes, there are no red or white blood cells in plasma (or serum).
 

acer2000

Senior Member
Messages
818
If healthy cells put in ME serum poop out but not the opposite then I'd wager thet is a toxin in ME serum interfering with cell function. Either that or whatever caused ME that is in those cells takes longer than the time they observed to cause problems in the new host.

I'd be a bit skeptical about the claim that it isn't transmissible. I developed ME after surgery with blood transfusions. It took 6 months. My ME doctor has seen it in other patients also. Of course it could be coincidental.

Either way it's an interesting finding that needs to be followed up.
 

Sing

Senior Member
Messages
1,782
Location
New England
Whatever is in the serum or missing from the serum. I tend to believe it would be easy to tease out the guilty party. How complex could serum be? But I gather it is. Still, Dr. Davis and colleagues seem to have tools at their disposal.