Impaired Cardiac Function study in Journal of Internal Medicine:

[Gamboa]

This article has me wondering about my own cardiac function. Two years ago I went to an internal medicine specialist who said I had a hole in my heart, an ASD (atrial septal defect) but that it wasn't the cause of any of my symptoms. He was very confident of this based on what he was hearing. I went for an echocardiogram, the results of which indicated not only did I not have an ASD, but everything else was fine with my heart. Of course, the doctor and echo technician knew nothing about ME/CFS and didn't want to learn about it. Apparently how they tested for the ASD was not the best method and also since I was lying down for the test it didn't pick up possible problems. I was dis-missed as "nothing wrong with your heart". I am hoping they will see this article since it is an internal medicine journal.

Gamboa

 

[Chris]

Hi, Gamboa; cardiologists as a group have not yet wrapped their minds around diastolic dysfunction--largely because they don't know what to do about it--their standard toolbox of drugs do not work, and they have not incorporated Steven Sinclair's "metabolic cardiology" suggestions of Q10, acetyl-l-carnitine, and Ribose--though those don't do much either. Cheney has talked about this stuff a good deal, particularly in his last DVD, "CFS: Is Oxygen the Problem?" which talks about and illustrates the problem very well. I think the new study adds to what he had to say there in useful ways. Our hearts just don't start refilling soon enough, so our atrium tries desperately to make up for this by increasing pressure, which eventually unseals the flap that should seal shortly after birth. Normal echocardiograms will not reveal this reopened flap. So, like you, my cardiologist interpreted my echo as perfectly satisfactory except for a not very good A/E filling ratio--I think I have now convinced him that there is some degree of diastolic dysfunction. Cheney also says Artesunate helps reverse this, though I have not seen any explanation of how or why--does anyone know?
Best, Chris

 

[CBS]

So decreased ventricular mass is incidental ? a function of low blood volume ? I don't understand why the decreased VM would be judged not to be the precurser of the radial thickening. And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? - the high urinary output reported by many M.E/CFS sufferers would seem inconsistent with classic hypovolaemia. The charistics seen in the M.E/CFS cohort may be indicative of symptom causation, but I don't how the observation couldn't be explained as being a particular subset of responses to sedentary living. It would be interesting to see this study repeated in young people with M.E who have been diagnosed within the previous 12 months, and who prior to becoming ill had been active - this would rule out aging dependent effects and mnimise sedentary effects.

IVI

Please feel free to elaborate on the symptoms of "classic hypovolemia." Don't forget to include the associated causative mechanisms.

Low blood volume is often recognized as a significant issue associated OI and many of the top ME specialists routinely recommend increased fluid and sodium intake.

As for high urinary output, think about it for a second. You have a bucket full of water balloons and you're going to pick on the 1st graders coming home from school (you graduated from high school two years ago but you couldn't get a job and you can't think of anything more productive to do with your time). You're hiding behind the fence but you don't know that the cheap balloons you bought (remember, you're unemployed) all have leaks. Could your balloons be described as hypovolemic? Extra credit if you can explain why and if you can name the physiological complaint "reported by many patients M.E./CFS sufferers" that is represented by the leaks.

 

[Valentijn]

So decreased ventricular mass is incidental ? a function of low blood volume ? I don't understand why the decreased VM would be judged not to be the precurser of the radial thickening. And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? - the high urinary output reported by many M.E/CFS sufferers would seem inconsistent with classic hypovolaemia. The charistics seen in the M.E/CFS cohort may be indicative of symptom causation, but I don't how the observation couldn't be explained as being a particular subset of responses to sedentary living. It would be interesting to see this study repeated in young people with M.E who have been diagnosed within the previous 12 months, and who prior to becoming ill had been active - this would rule out aging dependent effects and mnimise sedentary effects.

Do you have any positive theories regarding the causation or mechanism of ongoing M.E.? I must admit, it's a little disturbing to see nothing from you but constantly tearing down biological M.E. research (aside from tearing down advocacy efforts).

 

[CBS]

Do you have any positive theories regarding the causation or mechanism of ongoing M.E.? I must admit, it's a little disturbing to see nothing from you but constantly tearing down biological M.E. research (aside from tearing down advocacy efforts).

Apparently IVI is the self appointed CFS police (or "mirror"). See "Saints and demons in the Cult of The Chronically Fatigued." IVI, much like ERV (see the link on CFS Mirror's page) is protecting us from ourselves as we have all been driven mad by a disease "which is effectively undiagnosable."

I'd have to assume that starting from that premise, any study is a waste of time (and I suspect this would also be the position of a Dr. S. Wesseley, to whom a sizable portion of text at the above link is dedicated).

 

[CBS]

Gamboa and Chris,

Here is a breif article on ASD (atrial septal defect) and PFO (patent foramen ovale): http://www.news-medical.net/news/2007/09/03/29373.aspx. They are similar in that they are "holes" allowing blood to flow between the left and right atrium. A PFO occurs when a congenital "flap" fails to close (found in roughly 25% of the population upon autopsy). In the fetus, this flap allows circulation in to bypass the lungs prior to birth. In adults, the failure of this flap to close can, in some cases, allow blood unfiltered by the lungs to enter the brain increasing risk of stokes and migraines (note that the article I've linked to is not necessarily the best or most recent on this topic. I chose it because it was convenient and it described both conditions).

 

[eric_s]

Eric--a belated reply to your query about what constitutes a "sedentary control" in this study--they specify that "all control subjects performed less than 30 mins exercise three times per week." Wish I could do that much in one session! It does seem a very interesting paper--helps explain how I have a high ejection fraction, but still can't exercise worth a damn. May try my own home-made version of this new in process Nancy Klimas thing, but it seems very close to what I have been doing, with not much to show for it. But I have bought a heart rate monitor, and will see what light that can throw on my situation and the process of trying to increase my exercise capacity without provoking a crash.
Chris

Thanks, Chris. I think it's probably almost impossible to find healthy controls who live a lifestyle that is similar to the average person with ME/CFS.

 

[In Vitro Infidelium]

There are always two sides to looking at an issue. The destruction way is to keep tearing at these sorts of studies, and at the small hopes of patients. The constructive way is to build on these studies to help explain to the rest of us who are perhaps not so qualified how they could lead to some of the symptoms we have.

Do you have any positive theories regarding the causation or mechanism of ongoing M.E.? I must admit, it's a little disturbing to see nothing from you but constantly tearing down biological M.E. research (aside from tearing down advocacy efforts).

Apparently IVI is the self appointed CFS police (or "mirror"). See "Saints and demons in the Cult of The Chronically Fatigued." IVI, much like ERV (see the link on CFS Mirror's page) is protecting us from ourselves as we have all been driven mad by a disease "which is effectively undiagnosable." I'd have to assume that starting from that premise, any study is a waste of time (and I suspect this would also be the position of a Dr. S. Wesseley, to whom a sizable portion of text at the above link is dedicated).

These three sets of comments are useful illustration of why anyone from outside the M.E millieu, who when presented with an apparent discussion on scientific issues is likely to find engagement on these forums pretty challenging.

Both Rusty and Valentjin appeal to a sort of positivenessism (as distinct from Positivism http://www.marxists.org/reference/subject/philosophy/help/mach1.htm ) without any acknowledgement that modern science is a destructive process in which only those theories that survive the challenge of argument stand as having validity, and even then that standing is conditional. The problem with positivenessism is that it lends itself to belief building which is inimical to scientific progress. Ironically it is the very lack of destructive testing that many contributors to these forums decry in the case of psychiatric theory. Positivenessism frequently confers a false validity upon scientific partialism, where good research/researchers (as defined by the contending positivenessist) are deemed exempted from destructive testing, while bad research/researchers are slated for especial inclusion for destructive testing. Non partial science requires all arguments, perspectives, hypotheses and theories to be equally subject to challenge.

Valentjins comment directly invokes positivenessism as both a qualification in science, - a contradiction in terms and as a qualification for legitimacy within the M.E millieu. What Valentjin is calling for is a demonstration of qualification of belonging, transacted by an expression of belief in an unconditional scientific truth (of which there are none). The inference is that to be a non believer is to be without legitimacy in any scientific discussion about M.E/CFS, which leaves even agnostics as suspect and denies any validity to the possibility that no scientifically valid theory of disease causation is possible under the current descriptions of M.E/CFS.

CBS takes the failure to demonstrate a commitment to positivenessism as direct evidence of not belonging and on that basis moves to an ad hominem response where mischaracterisation of material extraneous to the discussion and guilt by association are applied as being appropriate to the treatment of the proven non belonger. Ad hominem is fundamentally anti science and any attempt to answer the ad hominem simply takes a discussion away from its scientific base, which may reasonably be assumed to be the purpose of the ad hominem.

IVI

 

[SOC]

Apparently IVI is the self appointed CFS police (or "mirror"). See "Saints and demons in the Cult of The Chronically Fatigued." IVI, much like ERV (see the link on CFS Mirror's page) is protecting us from ourselves as we have all been driven mad by a disease "which is effectively undiagnosable."

I have found the Ignore List feature in Settings to be remarkably useful in this context.

 

[Valentijn]

Both Rusty and Valentjin appeal to a sort of positivenessism (as distinct from Positivism http://www.marxists.org/reference/subject/philosophy/help/mach1.htm ) without any acknowledgement that modern science is a destructive process in which only those theories that survive the challenge of argument stand as having validity, and even then that standing is conditional. The problem with positivenessism is that it lends itself to belief building which is inimical to scientific progress. Ironically it is the very lack of destructive testing that many contributors to these forums decry in the case of psychiatric theory. Positivenessism frequently confers a false validity upon scientific partialism, where good research/researchers (as defined by the contending positivenessist) are deemed exempted from destructive testing, while bad research/researchers are slated for especial inclusion for destructive testing. Non partial science requires all arguments, perspectives, hypotheses and theories to be equally subject to challenge.

Valentjins comment directly invokes positivenessism as both a qualification in science, - a contradiction in terms and as a qualification for legitimacy within the M.E millieu. What Valentjin is calling for is a demonstration of qualification of belonging, transacted by an expression of belief in an unconditional scientific truth (of which there are none). The inference is that to be a non believer is to be without legitimacy in any scientific discussion about M.E/CFS, which leaves even agnostics as suspect and denies any validity to the possibility that no scientifically valid theory of disease causation is possible under the current descriptions of M.E/CFS.

I wasn't attempting to use scientific terminology. Perhaps "constructive" would be a better word in general. Any time a biological theory is advanced, you are trying to tear it down. That is not necessarily a bad thing, as science should be able to stand up to rigorous scrutiny. But in your case the destruction of the theory seems to be the goal, rather than objective scrutiny of the theory.

For example, you dismissed the study that is the topic of this thread without reading it. In dismissing the theory underlying that study, you relied on another unproven theory (deconditioning), without subjecting your theory to the same scrutiny as the one you attacked.

More generally, your tear down every attempt at patient advocacy as being either useless or counter-productive. When pressed, you suggest very passive tactics that are unlikely to garner any attention, especially if compared to the tactics that were successful with other diseases. Many of your comments, such as a recent one opposing a day of prayer in another thread, seem to be deliberately aimed at dividing M.E. sufferers from working together.

When I asked if you have any "positive" theories regarding M.E., I meant it in the broadest sense: do you think there is an ongoing biological cause for our symtoms, which is completely outside of our control as patients?

 

[richvank]

Hi, all.

Dr. Cheney is in full agreement with the results reported in this paper, and believes that they are also in agreement with Dr. Peckerman's earlier results.

Rich

 

[CBS]

CBS takes the failure to demonstrate a commitment to positivenessism as direct evidence of not belonging and on that basis moves to an ad hominem response where mischaracterisation of material extraneous to the discussion and guilt by association are applied as being appropriate to the treatment of the proven non belonger. Ad hominem is fundamentally anti science and any attempt to answer the ad hominem simply takes a discussion away from its scientific base, which may reasonably be assumed to be the purpose of the ad hominem.

IVI

Normally I reserve authentic engagement for those who show genuine interested in a topic. I reserve snark and ad hominem attacks for those who rush to throw out the baby before it every got a bath. You're right, my comments have allowed you to sidestep my earlier questions. Would you care to go back and answer my questions about hypovolemia? I suggest you read the article before hand and that you brush up on the various causes of hypovolemia. It am genuinely interested in you take on "classic hypovolemia."

 

[Snow Leopard]

These three sets of comments are useful illustration of why anyone from outside the M.E millieu, who when presented with an apparent discussion on scientific issues is likely to find engagement on these forums pretty challenging.

Well maybe you'd like to help advocate for more research funding instead?

 

[RustyJ]

These three sets of comments are useful illustration of why anyone from outside the M.E millieu, who when presented with an apparent discussion on scientific issues is likely to find engagement on these forums pretty challenging.
IVI

IVI, I think you are missing the point on several fronts. Firstly, we are not here for some arbitrary intellectual exercise, to idly discuss scientific issues at leisure, nor to debate the philosophical differences between positivenessism and positivism, important though they may be. We are fighting for our lives. I have been bedbound by ME for over twenty years. I have lost my marriage, career, home as a result of my illness. As have many others here. I have also been subject to 20 years of self-serving intellectual discussion by those who believe they know it all, but seldom come up with real answers. We are allowed to be biased in that regard. From a personal point of view, I have no interest in debating or reading comments from those outside the M.E millieu (your words), if they fail to show compassion for the suffering and indifference of those with ME, other than to make sure that lack of understanding does not harm others. Yes, I understand our bias, but I have little understanding of yours, or your motivations.

Secondly, I have no real beliefs about the paper, which is a major misjudgement on your part, in your small eloquent speech on positivenessism, so I have never defended it. My comments were directed at the tenor of your responses, and in fact I entered the discussion when you blithely shot down a relatively hopeful remark by a fellow ME patient. I don't have the qualifications to discuss the relative merits of the paper and in fact asked you to elaborate further, making use of your apparant knowledge. I am still waiting for that elaboration and would prefer it than a philosophical discourse.

By the way, I do appreciate someone pointing out the failings or weak points of studies, when they exist. But if someone only points out apparant weaknesses, in other words appoints themselves as an agent of 'destructive testing', as you say, then the motives and honesty of that person need to be questioned, to preserve the integrity of the process. In other words, without evidence otherwise, an agent of 'destructive testing' is just destructive.

Your arguments, if heartfelt, are typically the response of someone who regards themselves as aloof or untouched by the hardships and sufferings of those around them; without judging their sincerity, they are intellectual, philosophical, hard and reflect little emphathy.

 

[markmc20001]

I just found this thread, the commentary makes it painfully apparent to me most people in the M.E. millieu are quiet aware of what is going on.

 

[Emootje]

And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ?

However there are some similarities:
Symptoms induced by hypovolemia are primarily related to decreased tissue perfusion. The earliest complaints include lassitude, easy fatiguability, thirst, muscle cramps, and postural dizziness. More severe fluid loss can lead to abdominal pain, chest pain, or lethargy and confusion due to ischemia of the mesenteric, coronary, or cerebral vascular beds, respectively.
www.dpsims.com/~dpsims/family/hypovolemia.doc

 

[Emootje]

Hi, Gamboa; cardiologists as a group have not yet wrapped their minds around diastolic dysfunction--largely because they don't know what to do about it--their standard toolbox of drugs do not work, and they have not incorporated Steven Sinclair's "metabolic cardiology" suggestions of Q10, acetyl-l-carnitine, and Ribose--though those don't do much either. Cheney has talked about this stuff a good deal, particularly in his last DVD, "CFS: Is Oxygen the Problem?" which talks about and illustrates the problem very well. I think the new study adds to what he had to say there in useful ways. Our hearts just don't start refilling soon enough, so our atrium tries desperately to make up for this by increasing pressure, which eventually unseals the flap that should seal shortly after birth. Normal echocardiograms will not reveal this reopened flap. So, like you, my cardiologist interpreted my echo as perfectly satisfactory except for a not very good A/E filling ratio--I think I have now convinced him that there is some degree of diastolic dysfunction. Cheney also says Artesunate helps reverse this, though I have not seen any explanation of how or why--does anyone know?
Best, Chris

If I have understood dr Hopkin article correctly, diastolic dysfunction (reduced E-to-A ratio) can also be the result of low blood volume.....

Reduced plasma volume may contribute to reduced ventricular filling, stroke volume, and cardiac output and increased blood viscosity. Consistent with reduced preload, transmitral Doppler studies have revealed reduced E-to-A wave ratio and prolonged deceleration time in adult patients with cyanotic congenital heart disease, findings that are very similar to those of the present study. When cardiac output is reduced in adults with cyanotic congenital heart disease, it is because of volume depletion rather than ventricular dysfunction, unlike patients with heart failure.
http://circ.ahajournals.org/cgi/reprint/109/23/2872

 

[In Vitro Infidelium]

I wasn't attempting to use scientific terminology. Perhaps "constructive" would be a better word in general. Any time a biological theory is advanced, you are trying to tear it down. That is not necessarily a bad thing, as science should be able to stand up to rigorous scrutiny. But in your case the destruction of the theory seems to be the goal, rather than objective scrutiny of the theory.

For example, you dismissed the study that is the topic of this thread without reading it. In dismissing the theory underlying that study, you relied on another unproven theory (deconditioning), without subjecting your theory to the same scrutiny as the one you attacked.

More generally, your tear down every attempt at patient advocacy as being either useless or counter-productive. When pressed, you suggest very passive tactics that are unlikely to garner any attention, especially if compared to the tactics that were successful with other diseases. Many of your comments, such as a recent one opposing a day of prayer in another thread, seem to be deliberately aimed at dividing M.E. sufferers from working together.

When I asked if you have any "positive" theories regarding M.E., I meant it in the broadest sense: do you think there is an ongoing biological cause for our symtoms, which is completely outside of our control as patients?

IVI, I think you are missing the point on several fronts. Firstly, we are not here for some arbitrary intellectual exercise, to idly discuss scientific issues at leisure, nor to debate the philosophical differences between positivenessism and positivism, important though they may be. We are fighting for our lives. I have been bedbound by ME for over twenty years. I have lost my marriage, career, home as a result of my illness. As have many others here. I have also been subject to 20 years of self-serving intellectual discussion by those who believe they know it all, but seldom come up with real answers. We are allowed to be biased in that regard. From a personal point of view, I have no interest in debating or reading comments from those outside the M.E millieu (your words), if they fail to show compassion for the suffering and indifference of those with ME, other than to make sure that lack of understanding does not harm others. Yes, I understand our bias, but I have little understanding of yours, or your motivations.

Secondly, I have no real beliefs about the paper, which is a major misjudgement on your part, in your small eloquent speech on positivenessism, so I have never defended it. My comments were directed at the tenor of your responses, and in fact I entered the discussion when you blithely shot down a relatively hopeful remark by a fellow ME patient. I don't have the qualifications to discuss the relative merits of the paper and in fact asked you to elaborate further, making use of your apparant knowledge. I am still waiting for that elaboration and would prefer it than a philosophical discourse.

By the way, I do appreciate someone pointing out the failings or weak points of studies, when they exist. But if someone only points out apparant weaknesses, in other words appoints themselves as an agent of 'destructive testing', as you say, then the motives and honesty of that person need to be questioned, to preserve the integrity of the process. In other words, without evidence otherwise, an agent of 'destructive testing' is just destructive.

Your arguments, if heartfelt, are typically the response of someone who regards themselves as aloof or untouched by the hardships and sufferings of those around them; without judging their sincerity, they are intellectual, philosophical, hard and reflect little emphathy.

Normally I reserve authentic engagement for those who show genuine interested in a topic. I reserve snark and ad hominem attacks for those who rush to throw out the baby before it every got a bath. You're right, my comments have allowed you to sidestep my earlier questions. Would you care to go back and answer my questions about hypovolemia? I suggest you read the article before hand and that you brush up on the various causes of hypovolemia. It am genuinely interested in you take on "classic hypovolemia."

(hypovolemia question addressed below)

Again there are common threads in these replies which typify the way that M.E/CFS affected people frequently close out sceptical approaches. Questions or perceived questions are taken as having hostile intent, the questioner is required to fulfil various qualifications (to be empathetic, to demonstrate current, past or vicarious (carer) suffering, to show efforts of advocacy etc) and ad hominem responses are presented as justified in the case of unqualified questioners.

To recap what I wrote:

Post 1. The abstract does not specify if screening on the basis of activity levels pre morbidity in the patients or in the controls, was undertaken. Chronic low level activity is associated with loss of heart muscle mass as the individual ages (Regular exercise can help preserve/build heart mass ), so subject selection could greatly affect results. If selection were on the basis of typical age profiles (40 +) and included patients who had been housebound/bed bound for may years, then the results may simply reflect an effect of being chronically ill, rather than having any relationship to initial causation. Of course this is still important information for both researchers and M.E/CFS affected people but it may not mean what we may like it to mean.

I made statement (true) about the abstract (demonstrating a limitation on what could be discussed with certainty), followed a further statement (with supporting link) about a possible confounding factor age and age related heart disease. I made a speculation (use of If) about the effect on the study that the confounding fact may have and I observed that this may impact upon what the study actually means for M.E/CFS sufferers.

Post 2. In science it's called confirmation bias, finding significance on the basis of a narrow perspective. Intuition as a faculty no doubt confered evolutionary advantage on our Pleistocene ancestors by increasing the probability of success in survival behaviours such as finding water in arid climates or avoiding encounters with lions, but human intuition is frequently fooled by finding significance where no significance exists. Human intuition has been very, very poor at leading us to the the reality of the Universe which we inhabit and it seems unlikely to help in understanding the nature of disease.

I made a case specific reply (limits of intuition) to a specific post which suggested intuition as (perhaps) having equal validity to scientific enquiry. Given the thread and subforum are science fcussed, this was reasonable response delivered civily.

Post 3. So decreased ventricular mass is incidental ? a function of low blood volume ? I don't understand why the decreased VM would be judged not to be the precurser of the radial thickening. And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? - the high urinary output reported by many M.E/CFS sufferers would seem inconsistent with classic hypovolaemia. The charistics seen in the M.E/CFS cohort may be indicative of symptom causation, but I don't [see] how the observation couldn't be explained as being a particular subset of responses to sedentary living. It would be interesting to see this study repeated in young people with M.E who have been diagnosed within the previous 12 months, and who prior to becoming ill had been active - this would rule out aging dependent effects and mnimise sedentary effects.

This in reply to a poster who (unlike other posters) appeared to have access to the full article and who could there perhaps furnish answers which others could not.

My first three posts in this thread were all delivered civily without in anyway questioning the validity of M.E/CFS as a real illness, elicited responses that demanded demonstration of personal qualification on my part and were ad hominem in character. Of course by the general standards of the internet this is all very mild for a discussion forum but if M.E/CFS affected people are to engage productively with a wider audience on matters of science and medical research, then bunker sensibilities need to be challenged. And without that engagement with a wider audience, the discussion on M.E/CFS forums are in danger of being nothing more than telling each other fairy stories with sciency words and phrases thrown in for effect.


IVI

 

[In Vitro Infidelium]

Would you care to go back and answer my questions about hypovolemia? I suggest you read the article before hand and that you brush up on the various causes of hypovolemia. It am genuinely interested in you take on "classic hypovolemia."

I don't have access to full article, which is why asked my second set of questions.

I would have thought this from a high Google count Internet source covers the issue of symptoms. Is there something here that you wouldnt agree with ?

http://www.bettermedicine.com/article/hypovolemia

the mouth, nose, and other mucous membranes dry out, the skin loses its elasticity, and urine output decreases. Initially, the body compensates for the volume loss by increasing the heart rate, increasing the strength of heart contractions, and constricting blood vessels in the periphery while preserving blood flow to the brain, heart and kidneys. With continuing volume loss, the body loses its ability to compensate and blood pressure drops. At this point, the heart is unable to pump enough blood to vital organs to meet their needs and tissue damage is likely to occur.

Idiopathic Chronic hypovolaemia obviously presents questions about the absence of persistent gross symptoms, while the difficulties of establishing a figure for definitive ideal blood volume makes achieving conclusions about disease causation based on blood volume measures also somewhat problematic.

To offer an hypothesis in answer to my own question And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? A subset of those with M.E/CFS symptoms are suffering undiagnosed heart defect and/or systemic hypovolaemia .

IVI

 

[CBS]

I don't have access to full article, which is why asked my second set of questions.

I would have thought this from a high Google count Internet source covers the issue of symptoms. Is there something here that you wouldnt agree with ?

http://www.bettermedicine.com/article/hypovolemia

the mouth, nose, and other mucous membranes dry out, the skin loses its elasticity, and urine output decreases. Initially, the body compensates for the volume loss by increasing the heart rate, increasing the strength of heart contractions, and constricting blood vessels in the periphery while preserving blood flow to the brain, heart and kidneys. With continuing volume loss, the body loses its ability to compensate and blood pressure drops. At this point, the heart is unable to pump enough blood to vital organs to meet their needs and tissue damage is likely to occur.

Idiopathic Chronic hypovolaemia obviously presents questions about the absence of persistent gross symptoms, while the difficulties of establishing a figure for definitive ideal blood volume makes achieving conclusions about disease causation based on blood volume measures also somewhat problematic.

To offer an hypothesis in answer to my own question And if low blood volume is the critical issue why are the classic symptoms of hypovolaemia not consistently found across the M.E/CFS population ? A subset of those with M.E/CFS symptoms are suffering undiagnosed heart defect and/or systemic hypovolaemia .

IVI

Apparently not all that appears on the web was created equal. Bettermedicine.com has a page on the causes of hypovolemia which fails to mention that a disturbance in the production of Antidiruretic Hormone (ADH) can lead to hypovolemia. The condition, known as central diabetes insipidus (DI), is characterized by increase in urinary output (without ADH, the collecting ducts and distal convoluted tubules in thekidneys become highly permeable).

Keep in mind that most hypovolemic states (as addressed by bettermedicine.com) are the result of an acute and severe fluid deficit. DI is a chronic condition (and in its early stages, presumably less severe) to which many of the bodily functions adapt and so much of the folk wisdom about hypovolemia may not apply in the expected manner (eg. a body cannot simply and indefinitely divert a scarce resource away from the periphery). In DI, the body does a dance, trying to allocate resources (blood and the oxygen and other nutrients) to the organs which are most vital and most in need (possibly because blood was previously directed to other organs).

The notion of episodic or subclinical DI has not been widely studied, in large measure because of the assumption that sub-clinical or episodic states are easily resolved by increased intake of water. The other issues are difficulties with dosing and serious risks if over-treated.

A conversation that I overheard:

Neurologist: "What's the first line of treatment for DI?"
Med student: "DDAVP (vasopressin)?"
Neurologist: "No. WATER!"

It's my assumption that Dr. Cheney views this as an important study because he recognizes DI in a number of his patients (Paul Cheney's NMH (Neurally-Mediated Hypotension) Treatment Protocol for Chronic Fatigue Syndrome) and sees the results as well as the authors' conclusions about the role of chronic hypovolemia as shedding light on an important mechanism in ME patients with treatment implications:

Potentially these findings suggest that therapies which can correct the low cardiac blood volume may be helpful: this might include graded exercise therapies, which might improve cardiac blood volume. Anecdotally patients (http://www.davidsbell.com/LynNewsV3N2.htm) describe symptomatic improvements with the administration of intravenous fluid. Our findings would point towards a possible explanation for this subjective improvement and future work will include interventions to restore fluid volume in CFS patients and explore the potential amelioration of the cardiac functional impairments seen in the present study, including the progressive normalization of LV mass. Such a study would establish the primacy of blood volume reduction and determine whether there are primary myocardial deficits that are not associated with low blood volume.