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Newton:Reduced cardiac volumes in CFS associate with plasma volume, not length of disease

Effi

Senior Member
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1,496
Location
Europe
full text: http://openheart.bmj.com/content/3/1/e000381.long

Reduced cardiac volumes in chronic fatigue syndrome associate with plasma volume but not length of disease: a cohort study
Julia L Newton
Andreas Finkelmeyer,
George Petrides,
James Frith,
Tim Hodgso
Laura Maclachla,
Guy MacGowan and
Andrew M Blamire

abstract said:
Objectives To explore potential mechanisms that underpin the cardiac abnormalities seen in chronic fatigue syndrome (CFS) using non-invasive cardiac impedance, red cell mass and plasma volume measurements.

Methods Cardiac MR (MR) examinations were performed using 3 T Philips Intera Achieva scanner (Best, NL) in participants with CFS (Fukuda; n=47) and matched case-by-case controls. Total volume (TV), red cell volume (RCV) and plasma volume (PV) measurements were performed (41 CFS and 10 controls) using the indicator dilution technique using simultaneous 51-chromium labelling of red blood cells and 125-iodine labelling of serum albumin.

Results The CFS group length of history (mean±SD) was 14±10 years. Patients with CFS had significantly reduced end-systolic and end-diastolic volumes together with reduced end-diastolic wall masses (all p<0.0001). Mean±SD RCV was 1565±443 mL with 26/41 (63%) having values below 95% of expected. PV was 2659±529 mL with 13/41 (32%) <95% expected. There were strong positive correlations between TV, RCV and PV and cardiac end-diastolic wall mass (all p<0.0001; r2=0.5). Increasing fatigue severity correlated negatively with lower PV (p=0.04; r2=0.2). There were no relationships between any MR or volume measurements and length of history, suggesting that deconditioning was unlikely to be the cause of these abnormalities.

Conclusions This study confirms an association between reduced cardiac volumes and blood volume in CFS. Lack of relationship between length of disease, cardiac and plasma volumes suggests findings are not secondary to deconditioning. The relationship between plasma volume and severity of fatigue symptoms suggests a potential therapeutic target in CFS.
 

A.B.

Senior Member
Messages
3,780
Participants were recruited as part of an observational study aimed at understanding the pathogenesis of autonomic dysfunction in patients with CFS. Participants fulfilled the diagnostic criteria for CFS.11 The study was approved by the research ethics committee (REC 12/NE/0146, CLRN ID 97805). Participants were not selected positively or negatively according to any criteria other than the fact that they were attending a clinical service and had a Fukuda diagnosis of CFS,12 although they were excluded if they screened positive for a major depressive episode as assessed using the Structured Clinical Interview for the Diagnostic and Statistical Manual of Mental Disorders (version IV; SCID-IV)13 or were taking vasoactive medication or known to have diabetes. Fatigue impact was assessed by the Fatigue Impact Scale (FIS).14

Notably, these were Fukuda patients. I wonder how strong a referral bias there was. The authors seem to suggest that the patients were not specifically selected for cardiovascular abnormalities but this part isn't as specific as I would like.
 

Navid

Senior Member
Messages
564
The relationship between plasma volume and severity of fatigue symptoms suggests a potential therapeutic target in CFS.

Are there any treatment recommendations to deal with this issue. Do we need to find a way to raise our plasma volume?

I feel like there has been no movement at all on potential treatments in years. If a person (me) is intolerant to mostly every treatment they try; what can they do.

Also here's an crazy question......are there researchers/dr's out there willing got take on guinea pig patients. Those of us desperate to try anything to get some tiny bit of improvement in QOL?

Finally for patients using ampligen successfully. Did you just take a big leap of faith in trying the treatment or are there some tests or indicators that show it will help you, rather than make you worse.

I cannot believe how hopeless this whole situation feels these days. Ever since the XMRV episode, it feels like there has been no concrete movement forward in treatments at all. Lots of talk and enthusiasm around increased activism, research, movies,etc. but nothing that really helps the severely ill get out of this hole of despair.

Sorry for the "ranty downer" post, but really feeling hopeless these days...and even though I've been sick for 11years, the optimist in me can't believe there really is nothing to do to get better...even though that appears to be the reality at this point.
 

Daisymay

Senior Member
Messages
754
The relationship between plasma volume and severity of fatigue symptoms suggests a potential therapeutic target in CFS.

Sorry for the "ranty downer" post, but really feeling hopeless these days...and even though I've been sick for 11years, the optimist in me can't believe there really is nothing to do to get better...even though that appears to be the reality at this point.

I know it's hard, I've been ill for 36 years.....I understand where you're coming from but just hold onto the fact that the research scene is the most hopeful it's ever been for ME, hopeful that we will get a breakthrough with the understanding and legitimising of ME and I believe some treatments to at the very least help. Hang in there Navid x
 

daisybell

Senior Member
Messages
1,613
Location
New Zealand
This is a strong result which is nice to see. Even though it was less than 50 patients, the probability of the results being chance is the lowest I think I've seen in a paper on CFS in a while.... And hard to argue that we can think ourselves into this symptom. Plus I do like that the authors have specifically commented about how deconditioning doesn't explain the results.
 

voner

Senior Member
Messages
592
Hopefully some of our members with statistical background will check the statistics in this paper.

The discussion section has some pretty interesting statements. Here are some quotes:

PV=Plasma volume
RCV= Red cell volume


....Instead, reduced cardiac volume may constitute a (pre-existing) vulnerability for developing CFS, though larger, preferably longitudinal studies would be needed to support this hypothesis. Importantly, there is also a relationship between PV and the severity of fatigue symptoms experienced by patients with CFS suggesting that this has the potential to be a therapeutic target.

....In the CFS cohort, over half had RCV measurements below 95% of the expected and almost a third breached this threshold for PV

... the proportion who were below the 95% expected value which leads us to speculate, also considering that the relationship between PV and fatigue severity, that volume within the vascular system plays at least a part in the symptoms experienced by those with CFS and is a potential therapeutic target.

....Anecdotally, patients describe symptomatic improvements with the administration of intravenous fluid.

....It is therefore possible that the abnormalities detected in this study represent problems arising due to impairments with venous compliance which again could potentially represent therapeutic opportunities that require further investigation.
 
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CFS_for_19_years

Hoarder of biscuits
Messages
2,396
Location
USA
Dr. David Bell (Lyndonville, New York) prescribed daily IV saline for his CFS patients for years. The patients had some type of permanent shunt put in their veins so they could just hook themselves up to an IV and not be poked on a daily basis. When he retired and could no longer prescribe this treatment, no other doctors prescribed it and all these patients who were doing well with daily saline IVs went downhill. (I'm recalling all of this from a lecture he gave in Seattle a year ago, recorded on YouTube.) He very much believed that there was problem with low volume.
Dr. David Bell on Low Blood Volume in Chronic Fatigue Syndrome
http://www.healthrising.org/forums/...blood-volume-in-chronic-fatigue-syndrome.234/

He also had some success with recommending G-suits for his patients who had orthostatic intolerance, which would help improve blood volume to the brain.
See http://www.oiresource.com/gsuit.htm

There have only been a few threads here at PR regarding the G-suits:
http://forums.phoenixrising.me/index.php?search/25784046/&q=gsuit&o=date


Here's Dr. Bell's lecture:
 
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kangaSue

Senior Member
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1,851
Location
Brisbane, Australia
Dr. David Bell (Lyndonville, New York) prescribed daily IV saline for his CFS patients for years. The patients had some type of permanent shunt put in their veins so they could just hook themselves up to an IV and not be poked on a daily basis.
That's interesting from a gut dysmotility point too. I know of a couple of people who have severe g.i. dysfunction with having gastroparesis and have found that getting daily IV saline infusions through a permanent port helps a lot in moderating the gut dysmotilty symptoms.
 

Ben H

OMF Volunteer Correspondent
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1,131
Location
U.K.
Though its using Fukuda, Julia Newton consistently puts out interesting research, despite overwhelming difficulties here in the UK. I really hope she is commended for her efforts, she really is a great researcher going 'against the grain' over here. She is a quiet champion for the cause.

Thank you Julia et al.


B
 

A.B.

Senior Member
Messages
3,780
Though its using Fukuda, Julia Newton consistently puts out interesting research, despite overwhelming difficulties here in the UK. I really hope she is commended for her efforts, she really is a great researcher going 'against the grain' over here. She is a quiet champion for the cause.

If something clearly shows up in Fukuda patients this presumably means it's an important aspect.
 

Ben H

OMF Volunteer Correspondent
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1,131
Location
U.K.
If something clearly shows up in Fukuda patients this presumably means it's an important aspect.

For sure, but I would like to see it replicated with perhaps the Canadian criteria though, and see if the results were more significant. The fact that the results were from Fukuda and had this degree of dysfunction is important and worrying when using one of the least strict criteria. It's good, interesting research, as we are used to from Julia.


B
 
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panckage

Senior Member
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777
Location
Vancouver, BC
full text:
The CFS group length of history (mean±SD) was 14±10 years.
...
Lack of relationship between length of disease, cardiac and plasma volumes suggests findings are not secondary to deconditioning.
If somebody is bed bound they become deconditioned very quickly, in a matter of months. I haven't read the paper but the above looks inadequate to make any relation between deconditioing and the results.

I don't think this is the same thing but in non-cfs patients it talks about bed rest leading to an excessive fall in stroke volume. It also talks about it leading to orthostatic intolerance: http://circ.ahajournals.org/content/96/2/517.long

They either should have had a deconditioned control group or they should remove the implication from the conclusion IMO
 
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15,786
I haven't read the paper but the above looks inadequate to make any relation between deconditioing and the results.
Well, reading the paper would be a better place to start then, perhaps? It's open access, not very long, and the link is in the original post.

I don't think this is the same thing but in non-cfs patients it talks about bed rest leading to an excessive fall in stroke volume.
The patients in the present study weren't bedbound, so I'm not sure what you think the relevance is.

At any rate, there is quite a bit of evidence from other researchers that proves deconditioning has fuck-all to do with the development or maintenance of ME symptoms. And then there's my own personal experience of (temporarily) being stronger after weeks of OI-induced bed-rest, not weaker. And such OI episodes appear quite suddenly, and certainly not after any decrease in activity.
 

Ben H

OMF Volunteer Correspondent
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1,131
Location
U.K.
Well, reading the paper would be a better place to start then, perhaps? It's open access, not very long, and the link is in the original post.


The patients in the present study weren't bedbound, so I'm not sure what you think the relevance is.

At any rate, there is quite a bit of evidence from other researchers that proves deconditioning has fuck-all to do with the development or maintenance of ME symptoms. And then there's my own personal experience of (temporarily) being stronger after weeks of OI-induced bed-rest, not weaker. And such OI episodes appear quite suddenly, and certainly not after any decrease in activity.

Nailed it.


B
 

panckage

Senior Member
Messages
777
Location
Vancouver, BC
Ok I read it
At any rate, there is quite a bit of evidence from other researchers that proves deconditioning has fuck-all to do with the ... maintenance of ME symptoms
Any condition that reduces activity contributes to deconditioning. This is not controversial

The length someone has CFS does not indicate its severity (except in the relatively rare progressive cases). Any deconditioning effect would occur at the beginning of the illness when a person first restricts their activities. Measuring patients 4-14 years after they have the illness means that by that time conditioning has become a static variable.

its like doing a study of 30-45 year olds on what percentage of people have driver's licenses and then concluding that age has no effect on the percentage of people who have a driver's license. And then it goes on to say that for people 10-30 year old that age doesn't affect the percentage of people who have a driver's license :p
 

Sean

Senior Member
Messages
7,378
If somebody is bed bound they become deconditioned very quickly, in a matter of months.
Depends in part on how active the bed bound state is.

Big difference between somebody who is awake and alert and otherwise healthy and active but is just temporarily bed bound due to a broken leg, and somebody who is in a coma and completely passive and atonic. The former is still a lot more physically active than the latter (with deconditioning in the former probably also exhibiting a somewhat more localised than global pattern).

IIRC, at the extreme low end of the activity spectrum serious deconditioning can develop in just 2-3 weeks.

Any condition that reduces activity contributes to deconditioning. This is not controversial

The length someone has CFS does not indicate its severity (except in the relatively rare progressive cases). Any deconditioning effect would occur at the beginning of the illness when a person first restricts their activities.
Maybe. Not all patients just suddenly stop all activity level when they first get sick, or reduce it so far that they can't prevent significant deconditioning. The level of regular physical activity needed to prevent significant deconditioning is not that high. I certainly met that minimum standard for the first 3-4 years of being sick, as did many patients I have talked to, but we still ended up serious chronic cases.

At most, classical deconditioning in ME/CFS is a secondary factor that is largely out of control of patients. Patients don't stop moving because they have become deconditioned. They stop moving because they have to, then become deconditioned, to the extent that they do so (and that is an open question at the moment, it is not clear that patients' metabolic profile matches that of classical deconditioning, our physiological response to increased physical activity certainly doesn't).
 
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Any condition that reduces activity contributes to deconditioning. This is not controversial
Your statement went beyond that, with the suggestion that deconditioning was responsible for reduced stroke volume and accompanying symptoms.

Any deconditioning effect would occur at the beginning of the illness when a person first restricts their activities.
According to your expert opinion? Because my experience is that I did not restrict my activities. I probably stayed too active during the first week of a bad flu (pushing myself to go to practice test and review classes), and rested like a normal human being for a week afterward (certainly not staying in bed). This was followed be an apparent inability to walk at a normal pace without getting sick afterward, or to think clearly when sitting up for a couple hours during classes.

There is no "activity restriction". There's disability hitting first, and forcing limitations which we fought for too long. That fighting made us sicker, maybe permanently, and mild deconditioning certainly may have resulted. But as is shown by VO2max results, even our single CPET results for moderate and severe patients show values far too low to be explained by any level of deconditioning. And our 2-day CPET results document a sudden drop in performance during the PEM period, which is obviously not attributable to deconditioning.

Frankly I don't understand how any ME patient could think that deconditioning plays a major role in their disease, except perhaps during or immediately after a CBT brain-washing course. (And it is an objectively observable disease, by the way, not a subjective "illness" or vague "condition").
 

Ben H

OMF Volunteer Correspondent
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Location
U.K.
Your statement went beyond that, with the suggestion that deconditioning was responsible for reduced stroke volume and accompanying symptoms.


According to your expert opinion? Because my experience is that I did not restrict my activities. I probably stayed too active during the first week of a bad flu (pushing myself to go to practice test and review classes), and rested like a normal human being for a week afterward (certainly not staying in bed). This was followed be an apparent inability to walk at a normal pace without getting sick afterward, or to think clearly when sitting up for a couple hours during classes.

There is no "activity restriction". There's disability hitting first, and forcing limitations which we fought for too long. That fighting made us sicker, maybe permanently, and mild deconditioning certainly may have resulted. But as is shown by VO2max results, even our single CPET results for moderate and severe patients show values far too low to be explained by any level of deconditioning. And our 2-day CPET results document a sudden drop in performance during the PEM period, which is obviously not attributable to deconditioning.

Frankly I don't understand how any ME patient could think that deconditioning plays a major role in their disease, except perhaps during or immediately after a CBT brain-washing course. (And it is an objectively observable disease, by the way, not a subjective "illness" or vague "condition").

I cannot fathom this obsession with deconditioning. There is no evidence for its implication in M.E, certainly not pathophysiology at all, to the contrary there is evidence against it as mentioned.


I cant help but think that anyone who believes it to be a serious, active part of their condition, in a pathological sense, has a very different illness to the one I am familiar with.



B
 

Hutan

Senior Member
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Location
New Zealand
Of course deconditioning is, at most, a secondary cause of symptoms experienced by PWME. ME comes first. For PWME who still walk around, it is probably of very little significance.

But to me, the point @panckage is making isn't controversial. The study included only people who had had CFS for 4 years or more. I think most people with ME/CFS, especially those with a sudden onset, will have made the biggest decrease in their activity levels by year 4.

So, any change as a result of deconditioning is likely to be most apparent in the first 4 years of the illness. And this study didn't have any people who had only been ill for 4 years or less. So, it doesn't have the data to draw a conclusion about deconditioning from the observed lack of relationship between the length of illness (4 to 14 years) and cardiac volumes.

This study will not stop the wittering on about deconditioning being the cause of CFS. Instead, people just diagnosed with an infection known to trigger ME/CFS need to be followed for a couple of years. There needs to be a comparison between people who go on to have ME/CFS and those who don't, in terms of activity levels before and during the acute illness and cardiac measures throughout the study period.
 
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