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Impaired Cardiac Function study in Journal of Internal Medicine:

Discussion in 'Latest ME/CFS Research' started by Gamboa, Jul 29, 2011.

  1. CBS

    CBS Senior Member

    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).
  2. In Vitro Infidelium

    In Vitro Infidelium Guest

    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
    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.

  3. Sea

    Sea Senior Member

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

    ixchelkali Senior Member

    Long Beach, CA
    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?
  5. alex3619

    alex3619 Senior Member

    Logan, Queensland, Australia
    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.


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