Impaired Cardiac Function study in Journal of Internal Medicine:

[CBS]

I'd like to comment on the first sentence of the last paragraph in the conclusions section.

"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"

If GET can correct low blood volume (I did not explore the mechanisms cited in the paper cited by Hollingsworth et al. - vascular tone?), it is my personal belief that it does not directly address the problem and that based upon numerous accounts and personal experience, desmopressin is more direct and exceedingly effective in severe cases. It is likely that these same severe cases are also the patients most susceptible to the negative impact of too much activity (perhaps in the form of neural dysfunction/damage - a mechanism that has been proposed as the possible underlying cause of DI in some cases of ME).

I will be cross-posting this to thread on the Klimas exercise videos.

ETA - I just checked the article cited by Hollingsworth et al. There is no reference in that article to a relationship between GET and hypovolemia (Can pacing self-management alter physical behavior and symptom severity in chronic fatigue syndrome? A case series, Journal of Research and Rehabilitation Development,Volume 46 Number 7, 2009, Pages 985 996).

 

[In Vitro Infidelium]

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:

I'd like to comment on the first sentence of the last paragraph in the conclusions section.

If GET can correct low blood volume (I did not explore the mechanisms cited in the paper cited by Hollingsworth et al. - vascular tone?), it is my personal belief that it does not directly address the problem and that based upon numerous accounts and personal experience, desmopressin is more direct and exceedingly effective in severe cases. It is likely that these same severe cases are also the patients most susceptible to the negative impact of too much activity (perhaps in the form of neural dysfunction/damage - a mechanism that has been proposed as the possible underlying cause of DI in some cases of ME).

I will be cross-posting this to thread on the Klimas exercise videos.

ETA - I just checked the article cited by Hollingsworth et al. There is no reference in that article to a relationship between GET and hypovolemia (Can pacing self-management alter physical behavior and symptom severity in chronic fatigue syndrome? A case series, Journal of Research and Rehabilitation Development,Volume 46 Number 7, 2009, Pages 985 996).

I used the term classic merely to mean those symptoms that were recognised to be present in well understood contexts so yes the circumstances of acute and severe fluid deficit. Even if one moves to rare conditions such as diabetes insipidus there is a defining symptom of severe thirst, the absence of that symptom in patients who have low blood volume related to high urinary output would need some explanation.

In DI one is talking about fluid loss of up to 20 litres a day while its reasonable to consider high urinary frequency to be a feature of M.E/CFS, what seems to be generally reported by sufferers is an irregularly occuring symptom and even at times of elevated urinary frequency, urine output is only moderately increased and certainly not an order of magnitude greater than the accepted norm. Of course the urinary freqency reported by some M.E/CFS affected people could be considered equivalent to symptoms of mild DI (output in the range of 2.5 litres a day) but one is still left with the problem that urinary freqency may only occur irregularly, from which one would have to infer the possibility that reduced blood volume was a fluctuating, not a static problem. So we do arrive at: The notion of episodic or subclinical DI, the problem then is how is subclinical to be recategorized as being meaningfully clinical ? a similar position relates to other subclinical possibilities thyroid function, type 2 diabetes etc, which can all be invoked as causes of M.E/CFS symptoms.

Streetham and Bell hypothesised about reduced red blood cell volume, but it seems surprising that this has not been noted in other literature; if it is widely present in M.E/CFS patients one would expect it to show up in the cusory tests that many patients get in the early stages of investigation into their condition. I can see why Hollingsworth et al would want to look at testing the hypothesis of low blood volume by using volume increasing treatments, but to not look at possible structural cardiac abnoramalities, particularly those of congential origin, seems to be narrowing the investigation line unnecessarily hopefully they will be seeking funding for a broad approach to further research.

As far as

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"

is concerned its important to distinguish between overall blood volume and cardiac blood volume the two are not necessarily the same. Do Hollingsworth et al actually make a distinction in their paper ? That cardiac misfunction should be associated with M.E/CFS symptoms is unsurprising, but Im still puzzled as to why hypovolaemia would be seen as the single functional impairment involved, either in an individual or a patient group.

IVI

 

[Sea]

Impaired Cardiac Function in Chronic Fatigue Syndrome Measured Using Magnetic Resonance Cardiac Tagging

Magnetic resonance cardiac tagging [aka electromechanical heart mapping] is a novel technique that assesses myocardial wall function in vivo.

Methods: Cardiac morphology and function was assessed using magnetic resonance imaging and cardiac tagging methodology in 12 CFS (Fukuda) and 10 matched controls.

Is this a technique that needs specialised equipment or is it simply a new technique using standard equipment that any interested cardiologist could learn?

 

[ixchelkali]

"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."

I wonder evidence they have to suggest that GET "potentially might" improve cardiac blood volume? And by what mechanism would that happen? Does exercise increase blood volume in hypovolemia due to other causes?

 

[alex3619]

[...] why not provide some comments on the premise that :
a) Apparently contradictory or "odd" data may be correct.
b) What might this infer about CFS ?

Hi KFG,

I would like to say that in science the most interesting data to ever see is apparently contradictory. Reliable data that is apparently contradictory is a strong indication that something is very wrong with methods or models, and this gets many scientists interested. Resolving the contradictions often lead to a new hypothesis, or overturning old dogma.

While some medically trained researchers do not seem to grasp the scientific method and just go through research procedure, many are classically trained or extend themselves to learning more about the principles of science. Each researcher, medically trained or otherwise, has to have their research examined on its own merits.

The two points you made that I quoted above have always been a red flag to me: here lies something interesting.

The other red flag I have seen again and again is that when researchers using different methods, on different aspects of a problem, derive similar or overlapping conclusions, it is time to take notice. Look at the current overlap between cytokines and exercise in ME for example.

Bye
Alex

 

[Marky90]

Hi. Im from the future.. Did they follow up on these findings?