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Reduced HRV (heart rate variability) predicts poor sleep quality in CFS

Discussion in 'Latest ME/CFS Research' started by ahimsa, May 31, 2010.

  1. ahimsa

    ahimsa Senior Member

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    This was posted on the co-cure mailing list recently:

    I was intrigued by this abstract because frequent awakening (up to 10-12 times a night) is my biggest sleep problem. So I searched for reduced HRV and found this other study from 2007:

    http://www.cfids-cab.org/rc/Boneva.pdf

    Anyone out there want to explain a bit more about what causes reduced HRV and/or suggested treatments? In the little bit of searching that I've done I've seen it linked to everything from depression to congestive heart failure. So it's a bit difficult for me to understand how to view these studies.

    I'm hoping someone with more medical knowledge will be able to shed some light on this study as well as any other sleep problems related to autonomic dysfunction/dysregulation.

    Thanks!

    Marjorie
     
  2. Dolphin

    Dolphin Senior Member

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    Sorry to be awkward but just to point out to everyone that the Boneva study (but not the initial study) is an empiric criteria (Reeves, 2005) study. It's the Wichita 2-day study cohort which is not as "diluted" as the Georgian cohort but still 10 (most likely - a maximum of 16 anyway but most likely 10) of the 43 CFS cases satisfied the Fukuda definition.
     
  3. ahimsa

    ahimsa Senior Member

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    Please don't feel awkward on my account - I want to know the details behind these studies. I appreciate the additional information. Thank you!

    I hope there are others out there who can comment on the general concept of reduced HRV and what it might mean in Fukuda and/or CCC ME/CFS patients (or even in heart failure patients, elderly, etc.).

    Marjorie
     
  4. Mark

    Mark Acting CEO

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    "a pervasive state of nocturnal sympathetic hypervigilance"

    From my own experience I can say with confidence that permanent disruption of sleep (failure of sleep) over a long period of time can cause very many of the symptoms of CFS, possibly even enough on its own to cause symptoms approaching a Fukuda but probably not CCC definition. Fatigue, muscle weakness, aches and pains, loss of short term memory and other cogntive impairnents, vulnerability to infection, problems with digestion, (not to mention anxiety and depression), all of these can (IMO) result solely from "a pervasive state of nocturnal hypervigilance" - ie the body never gets to shut down at night. So I reckon that prolonged sleep disturbance - especially if unrecognised - on its own might get you a diagnosis of CFS, with weak criteria. But the more severe neurological and immune symptoms, such as are those listed in the CCC, are more characteristic of 'ME' than 'CFS' (whatever ME and CFS may be...) and I don't know whether they could result from disturbance of sleep / loss of deep sleep alone.

    Anyway this is a roundabout way of saying that patients with Reeves/Oxford style definitions and even some Fukuda patients could be found who fit the criteria purely because of sleep disturbance. So the context for this research might be that one subcluster of the "CFS" wastebasket diagnosis is those who have prolonged sleep disturbance, for whatever reason.

    The reduced HRV then...the research is just saying there's a correlation between reduced HRV and sleep quality in this grouping patients...I'm not clear which is more likely to cause the other - or another association suspected...and wonder whether there's any such correlation in other patients with sleep apnea...but it seems their conclusion is that this suggests that "sympathetic hypervigilance" is going on in CFS sleep disturbance.

    TH2 hyperstimulation (as result of active XMRV infection or otherwise), and over-reaction to environmental triggers, sounds like it could cause "sympathetic hypervigilance" - sounds a good description of what I've had going on anyway.
     
  5. IamME

    IamME Too sick for an identity

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    In addition to what IllSince1989 says, Andrew Lloyd is a fully fledged psychologiser (he was one of the first off the starting block to rubbish XMRV and spread rumours about the WPIs research) -- this is the School of Psychiatry after all. The notion that reduced HRV and sleep dysfunction automatically = nocturnal hypervigilence is stupid and a complete leap of perverse logic. Even if it *was* true, "hypervigilence" would not be important because it's not the cause of ME, unlike a differential diagnosis. Mark, bad insomnia cannot cause all the symptoms/signs of ME. What they're trying to do is make this finding fit a stress hypothethis, an affective disorder or PTSD-like illness which they believe can be magicked away with CBT/GET by using a correlation/causation fallacy. Nothing must get in the way of that message.

    http://www.abc.net.au/rn/allinthemind/stories/2007/1945419.htm
    http://www.mja.com.au/public/issues/172_10_150500/lloyd/lloyd.html

    I think he used to be more pro-biomedical but has become incresingly obsessed with GET, referring to "fatigue states" and this sort of psychogibberish sophistry.
     
  6. Sean

    Sean Senior Member

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    Agree with that.

    Ian Hickie, an Australian psychiatrist who sometimes works with Lloyd on CFS stuff, is another to watch out for. He has been very influential both within Aust and internationally (works with Reeves, White, Wessely, et al, you get the idea, was co-author on the CDC Fukuda definition, & the Australian Clinical Guidelines, and IIRC he gave us the useless and dangerous SPHERE 'test' for somatising). But he has largely managed to escape serious scrutiny so far.

    Do a PubMed search for (Hickie IB) AND (Lloyd AR)

    For example:

    http://www.ncbi.nlm.nih.gov/pubmed/10901768
     
  7. anciendaze

    anciendaze Senior Member

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    Heart Rate Variability as a measure of cardiac function

    There were studies back in the late 1980's which surprised many cardiologists by showing reduced heart rate variability was an indicator of declining cardiac health. This came out of studies on cardiac dynamics using fairly advanced mathematical theories unfamiliar to most cardiologists. Where a natural assumption that variability increased as you approached a breakdown was wrong was in the misunderstanding of adaptability to changing conditions. Reduced variability meant that feedback in response to changing conditions was not taking place. There is plenty of reason to associate poor cardiac health with poor sleep.
     
  8. Cort

    Cort Phoenix Rising Founder

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    I agree that Lloyd appears to have become more behaviorist but be careful about damning a study because of its authors. HRV readings are probably the most consistently abnormal readings in CFS research - which is really saying something.

    Lloyd's big research project the Dubbo studies - had nothing at all to do with behavior - it took a straight shot at the immune system to try and explain why people were coming down with CFS after an infection. I'd be cautious of categorizing Lloyd too narrowly - yes he does believe behavioral therapies are helpful but he's also been very interested in immune functioning and pathogens as well as gene expression.
     
  9. Dolphin

    Dolphin Senior Member

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    I'm not convinced he's interesting in finding pathogens and using anti-viral and anti-microbial treatments.

    Here's his other recent contribution to the literature - he was the lead author and corresponding author for this letter to Science:

     
  10. gracenote

    gracenote All shall be well . . .

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    From the full text of the article.

    This doesn't appear to me to be a study to determine any kind of medical causation of sleep difficulties in CFS. Why would they even choose to use assessments of psychological health in a study such as this? This is more of the same in my opinion.

    I think they would have gotten more useful information by comparing CFS with other medical conditions that show low HRV. I found this on Wiki (not up to doing a better search at the moment):

     
  11. Tammie

    Tammie Senior Member

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    Ironically due to really bad sleep of late (worse than the usual, I mean), I am actually awake in the AM (which has not happened in a long time) & as a result am not at all alert (wouldn't hypervigilance make me more alert?!) ....I am, in fact quite foggy, so my logic may be off, but this occurred to me.........

    While this study focused on nocturnal HRV, in general reduced heart rate variability does not just mean that the resting heart rate is too high (as would be the case with hypervigilance) but it also measn that the max heart rate may not be as high, either

    ..... studies have shown that ME/CFS patients cannot get their heart rates up very high during exercise (one of the differences that has been cited by actual good biomedical research that differentiates ME/CFS from depression).....so if you turn this study on its head, using their logic, then it would seem that the inability to raise max heart rate much at all would indicate just the opposite

    I have actually recently been paying attention to my own heart rate variabilty, so the timing of this article is kind of interesting......and I noticed that pre-ME/CFS my heart rate could vary (from its lowest immediately upon waking to its highest immediately after exercise) by more than 130 points, and now, when I manage to get any exercise (granted not at the same intensity, and not often, but I do still manage to swim some or do some other exercise on occassion), my heart rate, at best varies less than 30 points from waking to post exertion (not only does that not fit with what would happen if this were depression, but it also does not fit with what would happen if I were just out of shape)....and though my resting heart rate has increased a bit, the reduced variability is for the most part on the other end of the spectrum (ocurring after any exertion)
     
  12. Dolphin

    Dolphin Senior Member

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    Interesting although just in case anyone is confused, Heart Rate Variability, has a specific definition e.g. http://en.wikipedia.org/wiki/Heart_rate_variability
     
  13. Dolphin

    Dolphin Senior Member

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    12 out of the 20 were from the Dubbo study (RRV: N = 7; EBV: N = 4; Coxiella burnetii: N = 1), the other 8 from Dr. Lloyd's practice.

    Thought this was interesting:
     
  14. Dolphin

    Dolphin Senior Member

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    Sounds good.

    After finding that low HRV is the main factor, they then speculate this might caused by hypoactivity in the prefrontal cortex:
    They don't tell us of the "physical" conditions where low HRV is an issue.

    I think how they link hypoactivity in the prefrontal cortex to CFS is weak:
    They then suggest other forms of dysautonomia seen in CFS could be due to this
    We recently have research which looks at this a bit differently:
    "Impaired cardiovascular response to standing in Chronic Fatigue Syndrome"
    Full text at: http://www.imet.ie/imet_documents/Impaired CV responses to standing in CFS.pdf

    start of discussion section of that paper:
     

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