Parasympathetic activity is reduced during slow-wave sleep, but not resting wakefulness, in patients with chronic fatigue syndrome, 2019, Fatt et al

PubMed abstract only at the moment, https://www.ncbi.nlm.nih.gov/pubmed/31771749

ETA: Paper now published.
Paywall, https://jcsm.aasm.org/doi/full/10.5664/jcsm.8114
Not available via Sci hub at time of editing.

 

Now if only we understood sleep beyond "we sleep because we get sleepy" that would be useful.

Though it would definitely be useful to have more research on sleep in ME. But from the abstract it's impossible to tell if it's idiopathic chronic fatigue or anything related to ME. It could be a generic process not particular to ME. I guess that would a... what is it... Holter device? I used one of those early on when there was possibility of cardiac problems but I don't think I could access that and check HRV. I definitely have a significant HRV.

It's a bit hard to tell from the abstract as the wording is a bit confusing. It seems to indicate no differences in HRV before sleep, which would make it unlikely to be ME patients and rather idiopathic fatigue. It would yet again blow in the water any claims of so-called "symptom focus" having anything to do with even idiopathic fatigue, let alone ME, since, you know, focus is definitely one of those things that aren't present during sleep.

I'm sure there would be arguments about trauma and fitful dreams or whatever during sleep but there's always the slight hiccup of many many ME patients who have never had any traumatic life events.

Autonomic hypervigilance seems self-contradictory, though, sprinkled on because it's the underlying belief I guess, the same old health anxiety. Vigilance is an active cognitive process. Autonomic by definition means, well, autonomic. They are mutually exclusive. Self-consistency, please.

 

Prior research in healthy participants shows that fatigue can result in lowered parasympathetic activity during sleep.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3214128/

Secondly, lowered parasympathetic activity does not suggest "Autonomic hypervigilance", rather elevated sympathetic activity is needed.

 

I wonder if the "autonomic hypervigilance" could be compensating for some kind failure in breathing rhythm while asleep - sort of as an alternative to repeatedly waking and gasping for air.

 

Of course we should evaluate this paper on its merits, while being aware this is ‘Fitspiration’ Fatt who co-authored a paper on the need for more biopsychosocial research into ‘chronic fatigue’ with Prof Andrew Lloyd.
https://www.ncbi.nlm.nih.gov/pubmed/30741357/

Fitspiration study: https://journals.sagepub.com/doi/abs/10.1177/1461444818821064?journalCode=nmsa

I wrote more about Fatt’s background and his university’s view on CFS here:
https://meaustralia.net/2019/05/16/...or-more-biopsychosocial-research-into-me-cfs/

 

Maybe, but they would have discovered this during the study if that was the cause (sleep apnea and related)

 

I was kind of thinking that "autonomic hypervigilance" might prevent (central) sleep apnea from occurring in the first place, so they wouldn't see a connection between the two.

 

Now published, paywall access only at the moment, https://jcsm.aasm.org/doi/full/10.5664/jcsm.8114

 

I've noted wake / sleep transition disturbances, perhaps autonomic dysfunction that causes disturbances in heart function and breathing at the transition, and sleep paralysis persistence that causes waking paralysis to occur.

Hypervigilant sleep might be a way to minimize the risk of these events, the body learns sleep is a hazard and compensates for it by not entering deep sleep, or perhaps parasympathetic function in deep sleep uses more energy than the sympathetic state and it is energy conserving to avoid it.

Would welcome investigation into this but the record of at least one of the authors leaves much to be desired.

 

My guess would be that hypervigilance could also be a behavioural adaptation to being ill, yes it could be to avoid apnea or hypothermia-like falling into deep and dangerous unconsciousness but it could also be about producing sensory hypervigilance in relation to the outside world i.e. light sleeping, which can easily be disturbed and is along the same lines as wakeful sensory hypersensitivity seen in both ME and brain injury generally. i.e. ever since our ancestors developed brains to control behaviour we may have evolved to be more sensitive to our surroundings and more responsive to possible antagonistic influences when we are having tough times, presumably to encourage behaviour which responds constructively to the antagonistic influences responsible for the tough times. It does not mean this will always solve the problem, it just means that at a statistical level our ancestors survived better for having this kind of response. Now we can lock our doors at night it is not as necessary but in the world full of predators and parasites we evolved in it was probably more often helpful.

Something about ME sets off that type of response and causes the (at first sight) paradoxical mental and sensory hyperactivity which means some folk are very sensitive to noise and light despite having a CFS. There has been a lot of work showing brain morphology change in ME so we cannot rule out actual brain damage in progress.

It may be inappropriate and unhelpful in ME and could be viewed as pathology but what this evidence seems to show is that the upregulation of the nervous system does produce measurable phenomena which explain the symptoms of sleep disturbance in ME.

So this is more evidence of the real difficulties PWME face in managing their condition. It should also be noted that good sleep helps healing and poor sleep is detrimental in a number of ways, so this is evidence for a detrimental spiral of poor sleep and illness which many of us try to cope with.

Personally, this is why I use hop tea (with marigold and bucchu) to help with periods of poor sleep, as this is mildly supportive of parasympathetic type responses.

 

I just want to clarify my last is about the discussion we are having here and not a validation of the approach of these authors. Its obvious after reading the blog link from @MyalgicE and related papers discussing the differentiation of diagnoses that Fatt is a BPS theorist and does not have an appreciation of the clinical realities of ME.

TLDR Twisk's article title speaks for itself...

https://www.ncbi.nlm.nih.gov/pubmed/31073713

In a reply by Fatt et al...

...the authors ask this question.

https://link.springer.com/article/10.1007/s11926-019-0824-y

I am beyond staggered that they fail to grasp that it matters if there are two distinct conditions with different etiologies. Its like saying measles and sunburn are the same kind of problem because they both make the skin go red.

What this suggests is that the empirical data in this paper applies to a very loosely defined cohort of CFS patients and is not specific to ME and is probably a very common problem for anyone with a chronic illness, which is what lies behind my discussion of the evolution of this kind of response. So it probably does happen to ME patients but it also happens to a lot of other people with different conditions as well many of whom are probably included in this study.

 

Does it matter if we bother with being precise and accurate? Said no scientist ever. Liquid water. Liquid sulfuric acid? Both clear liquids at room temperature. Let's not fall to the tyranny of accuracy.

After all, is there really a difference between a rock and an elephant? They're both grey and massive. Or can be, anyway. And in the end, is there really a difference between can be and definitely is? In science, yes. Outside of science, it is whatever you want it to be.

Controversial opinion, apparently, but I personally require science in my medicine. Controversial, I know.