The ‘Wolf’ in ME/CFS: Newton on a System Stuck in Overdrive

July 20, 2012

Posted by Cort Johnson

Impaired blood pressure variability in chronic fatigue syndrome–a potential biomarker. Frith JZalewski PKlawe JJPairman JBitner ATafil-Klawe MNewton JL. QJM. 2012 Jun 4

“..We believe that our findings add further evidence to the case for CFS being a disorder of sympathetic overactivity”

We know that heart rate variability (HRV) isn’t, well, very variable in chronic fatigue syndrome.  The electric signals in our heart should be constantly responding to changes in the body as we work, walk, exercise, etc….but they appear stuck in a pattern of sympathetic nervous system overdrive.

This is not great news…Reduced heart rate variability is associated with earlier mortality – particularly if you have cardiovascular issues. (Interestingly depressed HRV is also associated with an increased risk of depression.).

Dr. Newton’s recent study found that people with ME/CFS tended to have lower HRV and lower than average blood pressure variability (BPV) and both measures suggested the problem lay in an overactive sympathetic nervous system (fight or flight) functioning.

Interestingly, given Dr. Cheney’s (unpublished) diastolic findings, Newton found  greater impairment of  ‘resting’ stroke of the heart (diastole) than the contracting stroke of the heart (systole) and she suggested that ‘an impaired cardiac pump” may be partly responsible for reduced blood flows to the organs and tissues which in turn can cause increased fatigue, dizziness upon standing, etc.

Crying Wolf Too Many Times

Why is this happening? Dr. Cheney believes low energy production inhibits diastolic functioning but Newton’s research suggests, like a boy calling wolf one too many times, the problem may simply be due to the autonomic nervous system turning a deaf ear to the body.  She suggests that a chronically over-active sympathetic nervous system is  simply no longer being heard, e.g; it tells the heart to fill – and it doesn’t…it tells blood pressure to increase – and it doesn’t; it tells the blood vessels to narrow (to force blood to the muscles, etc.) and they don’t. It’s as if the internal wiring of an important body-wide system is burned out.

” Our results suggest that CFS subjects may have been suffering from a pathological sympathetic activity…. that has lead to their autonomic effectors (heart and blood vessels) becoming resistant to …stimulation”

The Heart of the Matter…..

Her other work suggests this kind of systemic  burnout is rampant in the cardiovascular systems of ME/CFS patients. Her 2012 finding of reduced peripheral pulse characteristics suggested, she felt,  ‘reduced cardiac output’  was present and she cited,as she has before, Peckerman’s 2003 finding of significantly lower stroke volume and cardiac output in ME/CFS.

Interlude – Arnold Peckerman had strong run  in the early 2000′s, publishing no less than six papers in 2003 on cardiovascular and autonomic nervous system issues in CFS and GWI. Peckerman’s work was discontinued with the  ‘regime change’ at the NIH’s CFS team and the breakup of the NIH funded CFS research centers. After 2005 he never published again. His story is another example that positive results in ME/CFS can mean little to a) a researchers career or to b) further progress in the field.

Dig Deeper! Check out Simon McGrath’s blog Once is Not Enough for more on the replication issues in ME/CFS

Peckerman didn’t last but his studies sparked some interest. Six year and nine years later  Hurwitz and  Newton  both found significantly reduced cardiac output. Hurwitz, Stewart (2009) and Newton have suggested their findings could be to due to  low blood volume (hypovolemia). Newton is also studying, however, the bioenergetics of muscle cell functioning using technology she developed.

A Regulatory Problem

Newton and others have steadily documented increased rates of sympathetic nervous system (SNS) activity in ME/CFS.  Newton proposes that SNS activity is increased all the time but only so much, leaving people with ME/CFS in a strange state of over/under-activation; chronically over-activated they experience little rest which leaves them too debilitated to respond when a major stressor occurs.

Dr. Newton recently reported she had ‘exciting pilot data’ regarding medications to reverse the acid accumulations that occur in the muscle cells of people with ME/CFS as they exercise.  If she can actually do this she may be able to give the system a change to rest and recoup and perhaps even help to turn off the ‘wolf at the door’ that has apparently sent the ANS into a kind of harried state of shock.

 

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8 comments

{ 8 comments… read them below or add one }

Ember July 20, 2012 at 2:55 pm
Cort

Dr. Newton's recent study found that people with ME/CFS tended to have lower HRV and lower than average blood pressure variability (BPV) and both measures suggested the problem lay in an overactive sympathetic nervous system (fight or flight) functioning.

Is Dr. Newton doing ME/CFS research using a CCC cohort? This study used a CFS (Fukuda) cohort: “Chronic fatigue syndrome and impaired peripheral pulse characteristics on orthostasis-a new potential diagnostic biomarker (2012).”

Sushi July 20, 2012 at 4:05 pm

Again, interesting! And, again, my readings don't really fit her data. Though my autonomic tests were very abnormal, it was my parasympathic system that was in overdrive–with, according to the testing–my sypathetic trying to compete with it.

I also had very variable BP.

And, functions that should have been controlled by one, were being controlled by the other. I guess the one thing we can say is that most of us have abnormally functioning autonomic nervous systems.

Sushi

Dolphin July 20, 2012 at 5:05 pm

For anyone interested, a long list of funders were mentioned in the Frith et al. (2012) paper:
"Funding
Medical Research Council, ME Research UK, Irish ME Trust, John Richardson Research Group, CFS/ME Northern Clinical Network; None of the funders contributed to the design, performance or interpretation of the results of this study."

Cort July 20, 2012 at 7:11 pm
Sushi

Again, interesting! And, again, my readings don't really fit her data. Though my autonomic tests were very abnormal, it was my parasympathic system that was in overdrive–with, according to the testing–my sypathetic trying to compete with it.

I also had very variable BP.

And, functions that should have been controlled by one, were being controlled by the other. I guess the one thing we can say is that most of us have abnormally functioning autonomic nervous systems.

Sushi

Interesting Sushi..I remember Staci Stevens saying she wasn't really sure what to say about the autonomic nervous system functioning in ME/CFS except that it was screwed up and that the system didn't really know which way was up :)

Snow Leopard July 21, 2012 at 2:35 am

I'm of the opinion that these observations are consequences of the underlying pathology (a compensation if you will), rather than the central cause.

taniaaust1 July 21, 2012 at 3:44 am

Dr. Newton's recent study found that people with ME/CFS tended to have lower HRV and lower than average blood pressure variability (BPV) and both measures suggested the problem lay in an overactive sympathetic nervous system (fight or flight) functioning.

That all certainly arent my case as its working for me completely different to that.. my autonomic system variablity is very abnormal but in the opposite way to what she's saying with the lower variability. (I suffer from higher variablity with massive shifts)

I do have severely overactive sympathetic nervous system (note.. too standing.. things are low otherwise) . A specialist told me I have SNS dysfunction years ago due to this.

Ember July 23, 2012 at 10:11 am

The study you describe, Cort, also used a CFS (Fukuda) cohort. But Dr. Newton's new MRC grants would seem to be ME/CFS research. Does anyone know what cohort she'll use in these new studies?

The Newcastle CFS Clinical Service is referred to here as the Newcastle ME/CFS Clinical Service, and here as the Newcastle CFS/ME Clinical Service. Dr. Newton's 2010 study reports that greater numbers of patients were referred to the clinic following the NICE Guidelines. A greater proportion of those patients were found to be CFS (Fukuda) patients and 40% were subsequently found not to have CFS. ME Research UK comments:

At present, there are many ways of diagnosing ME, CFS, CFIDS, CFS/ME and ME/CFS – and just listing these acronyms illustrates the confusion that besets the field…. The diagnosis of ME/CFS can easily become a stopping-off point for clinically complex patients with a variety of different illnesses.

This problem is encountered not only in the UK. A fascinating commentary in 2008 in Minnesota Medicine (available online) described the difficulties experienced at a clinic in the USA for patients with fatigue, exercise intolerance and weakness (i.e., patients very like ME/CFS patients in the UK). After reporting on three paediatric cases (all of whom received serious, new diagnoses), the authors commented that, “a thoughtful and thorough physical exam can sometimes reveal otherwise hidden diagnoses”.

Cort July 26, 2012 at 9:56 am

I sure hope somebody can come up with a standard most can agree with…The CASA project should be looking at the definition question. I would guess that many ME/CFS researchers would agree to using the Canadian Criteria at this point…it they could get their grants approved with it. The latest Program Announcement for the NIH for the first time left the definition open – it appeared to allow grants using other than the Fukuda criteria…

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