In Brief: The Autonomic Nervous System and ME/CFS

November 21, 2013

The fifth and final article in a series attempting to explain the science behind fairly common topics and exploring how they relate to ME/CFS. This time the topic is the nervous system – by Andrew Gladman.

Labelled diagram of a neurone.

The nervous system, specifically the autonomic nervous system, is frequently discussed in relation to ME/CFS, with quite a plethora of research being targeted in this area.

Many of the symptoms that ME/CFS patients suffer with, such as crushing fatigue, tremor sensations and headaches, could come as a direct consequence of abnormalities in the nervous system.

In this article, I aim to explore the organization and general function of the nervous system as well as considering the research, both historic and ongoing, as it relates to ME/CFS.

What is the Nervous System?

The nervous system is the system which allows for coordination between the different organs and tissues within the body, hence controlling the voluntary and involuntary actions of animals through the transmission of signals. The vast majority of cells involved in the nervous system are known as neurons. Neurons are highly specialized cells that process and relay signals, known as nerve impulses or action potentials, between the different tissues and organs within the body.  Like other cells they contain many membrane bound organelles such as the nucleus, mitochondria, endoplasmic reticulum among others – these carry out the basic cellular functions of protein-synthesis and ATP production.

Annotated diagram of a neurone

Annotated diagram of a neuron

The adjacent diagram labels all of the parts of a neuron which play an active role in the transmission of action potentials. The following is a very brief overview of the role each of these plays:

  • Dendrite and Axon terminal: The axon terminal of one neuron lies very close to the dendrites of another. Chemicals are released by the axon terminal when stimulated, which in turn stimulates the dendrite of the next, allowing for the action potential to be transferred from one cell to the next.
  • Cell body and nucleus: All standard cellular processes occur within the cell body. The nucleus is important as it provides the genetic material required for the construction of the vital proteins required for nerve impulses.
  • Axon: A long tail-like projection of the cell which transmits the action potential a long distance. This is achieved through the channel proteins in the cell membrane of the axon allowing for the flow of charged molecules in and out of the axon. This creates an electro-chemical gradient wave which flows down the axon – fundamentally a nerve impulse is simply an electro-chemical wave. 
  • Schwann cells, myelin sheath and nodes of ranvier: Cells known as schwann cells are tightly coiled around the axon of a neuron and secret a fat (lipid) known as myelin. This myelin forms the myelin sheath. The function of this myelin is to insulate the axon and allow for faster transmission of action potentials. This is achieved by a process known as saltatory conduction. Simply put, the gaps between schwann cells – known as nodes of ranvier – are the only places where the charged molecules can flow in and out of the cell. When an influx of these chemicals occurs at one node of ranvier, the sudden influx stimulates the proteins at the next, allowing an influx there. This process continues all down the axon and effectively allows the action potential to jump from one node of ranvier to the next, hence allowing for faster transmission. Not all neurons have schwann cells – these are known as non-myelinated neurons.

How are action potentials transmitted?

The following is an outline of the cellular and molecular processes at work which allow for the transmission of a nerve impulse. The following video provides a good overview of this process.

For an action potential to take place, the cell first has to be stimulated. This process of stimulation occurs when an adjacent neuron which is carrying an action potential releases neurotransmitters, such as acetyl choline, at its axon terminal which bind to one of the dendrites of the neuron. The site at which the axon terminal of one neuron meets the dendrite of the next is known as the synapse. This video explains further the process of how an action potential is transmitted from one neuron to the next.  Once this has occurred several times on different dendrites, the action potential begins.

Most neurons, barring those contained within the central nervous system, are very elongated with a long thin tail-like projection known as an axon. Within this axon there are no organelles, therefore no complex cellular processes occur within this. These processes are all carried out within the cell body. The diagrams above depict motor neurons with the cell body at one end. Interestingly, this is not always the case, as within sensory neurons the cell body is often a small offshoot within the center of the cell. However, all neurons within the autonomic nervous system are motor neurons. This will be discussed later in this article when we explore the organization of the nervous system.

It is the axon which allows for the transmission of action potentials. Within the neuron there is also something known as a resting potential. To understand this concept, it is important for me to stress that nerve impulses are best thought of as waves. Imagine, if you will, a tank of water. If you create a wave at one end, the wave then travels along the tank until it reaches the other side. (Ignore the return wave as this is where the analogy falls down!) Now conceptually, the wave increases the height of the water in that one location as it travels down the tank and lowers back to normal once the wave has passed. In a nerve cell this is also true, however, instead of the height of the water increasing as the wave travels, it is the electric potential within the neuron that increases and then returns to normal. This ‘normal’ is what is known as the resting potential. It can be simply described as a negative electric potential within the neuron. Within the axon there exist lots of positively charged potassium molecules (K+), however, outside of the axon there exist positively charged sodium molecules (Na+) which greatly outnumber the potassium molecules. Therefore, the inside is negatively charged relative to outside of the axon. 

For the ‘wave’ to be triggered within the neuron, multiple signals need to be received by the dendrites. There exists a threshold level which the stimulation must reach before an action potential is triggered, to prevent over-stimulation. Once this threshold is reached, sodium channel proteins open at the start of the axon and allow Na+ molecules to flood into the axon. This flooding in of positive sodium molecules raises the electric potential at the start of the axon.  This in turn triggers the next sodium channel proteins along the axon to open, allowing more positive molecules to flood in. Once the electric potential gets very high at the start of the axon, potassium channel proteins open here and K+ floods out of the cell. This lowers the electric potential at the start of the axon to below the threshold value, therefore stopping the action potential at the start. It is for this reason that the action potential travels as a wave.  This process of sodium flooding in and potassium flooding out continues along the axon until the wave reaches the end of the axon. At this point, the increase of electric potential triggers processes at the synapse which ultimately ends with the release of neurotransmitters, hence starting the action potential in the next neuron. Within the neuron there also exist other proteins known as sodium/potassium pumps. These pump sodium out of the cell and potassium in, setting up optimal resting potential conditions to prime the cell for another action potential. There is a slight delay between an action potential being transmitted and restoration of the resting potential. This ensures the neuron does not become overstimulated as it could cause damage to the neuron. 

From this very brief and quite simplified outline, it is clear that the process of nerve impulse transmissions on a cellular level is very complex. It is therefore easy to see why small problems in any of the multiple stages or any damage to any of the involved cells can have quite drastic consequences on a macro-molecular level. 

How is the Nervous System Organized?

Diagram explaining how the nervous system is organised.

Diagram explaining how the nervous system is organized.

 Read any credible research into physiological pathology and possible disease mechanisms of ME/CFS and you’re certain to come across the phrase ‘autonomic nervous system’. Unfortunately, it isn’t always easy to understand what this tangibly relates to without further understanding the sub-divisions of the nervous system as a whole. 

Fundamentally, the nervous system is initially split into two: the central nervous system and the peripheral nervous system. The central nervous system consists of all the neurons and associated cells within the brain and spinal cord. This receives information from every organ and tissue within the body, analyzes the information and transmits appropriate responses back to the organ.

As an aside, there do exist processes within the body that do not require any analysis. In these, the information is often transmitted to the spinal cord and a preset response is instantly transmitted back. This is often known as a reflex arc. A common example would be when you burn you hand – in response to this you instantly move your hand away from the heat source without conscious thought. These arcs exist to protect the body from danger in situations where hesitation would likely lead to further damage to the body.

The peripheral nervous system accounts for all the neurons that bring information into and out of the central nervous system. This is sub-divided into the motor and sensory nervous systems. The sensory nervous system is comprised of sensory neurons which monitor and process sensory information, including information from all sensory organs such as the eyes and ears. The motor nervous system is comprised of motor neurons. This system carries all the information coming from the brain in response to sensory input. To clarify this process in order: A sensory input such as seeing a vicious dog is detected by the eyes. This creates a nerve impulse (action potential) within the sensory neuron attached to the eyes – this being known as the optic nerve. This action potential travels into the central nervous system, specifically the brain, where brain processes the information. It recognizes the dog as a threat – and in response, generates an action potential which travels via a motor neuron to many different parts of the body. This stimulates the release of adrenalin from the adrenal glands, part of a process known as a fight or flight response, and makes the person step back from the danger. 

The motor nervous system is then further subdivided into the autonomic and somatic nervous systems. The somatic nervous system is often described as the voluntary nervous system, which eloquently describes it. It is this part of the nervous system which we as beings have conscious control over, via skeletal muscles which are stimulated by efferent nerves

The autonomic nervous system is the most relevant of all these divisions to ME/CFS, given the substantial research attention it now receives. It is also known as the involuntary nervous system, which makes clear what the function this crucial component of the nervous system is. It acts as a control system within the body, maintaining and carrying out all tasks that fall below the level of consciousness. This includes tasks such as the beating of the heart, the process of digestion and the respiratory rate – although this can be consciously controlled, under most circumstances it is an automated and non-conscious process. This system has a further, and final, subdivision into the sympathetic and parasympathetic nervous systems.

This division is not as clear-cut as previous ones, however, it can be described as such: The sympathetic system often speeds up functions while the parasympathetic often has the opposite, relaxing, effect. Examples of sympathetic division: dilates pupils, increases heart rate and blood flow, dilates bronchioles to increase oxygen in blood, constricts blood vessels, increases blood pressure, slows digestion.  These often occur as part of the previously mentioned ‘fight or flight’ response, which is controlled purely through the sympathetic element of the autonomic nervous system. The parasympathetic nervous system therefore has the opposite effect to the sympathetic system, resulting in constriction of pupils, returning vision to normal, slowing the heart rate and blood flow, constricting bronchioles and returning digestion to normal.

Why is the Nervous System Important in ME/CFS?

Given the previously discussed information regarding how the nervous system works on a cellular level, it is quite easy to understand why any problems occurring on this cellular level can have far reaching consequences on the entire body. For quite a number of years, it has been clear that there is autonomic dysfunction occurring within ME/CFS patients. Symptoms such as orthostatic intolerance, vertigo and mental exhaustion all imply such. Yet it has been quite difficult for researchers to discover the reason for this dysfunction, and in many cases, to find it consistently in ME/CFS patients between studies – likely in no small part due to the non-homogeneous nature of the ME/CFS diagnosis. However, as time advances, the evidence and data continues to mount pointing towards autonomic dysfunction as a central pillar within ME/CFS.

One researcher undertaking ground-breaking and still ongoing research, funded by ME Research UK, into autonomic dysfunction within ME/CFS patients is Prof. Julia Newton and her team at the University of Newcastle. Prof. Newton’s past research has indicated abnormalities in both muscle function, with excess lactate produced upon stimulation, and cardiac function which also shows considerable abnormalities as discussed at greater length in the previous article of this series. Her ongoing study has the following:

The investigation has two broad aims. The first is to examine fully the people attending the Newcastle CFS/ME Clinical Service, and develop a database of patients who can be followed up over the long term. The second is to begin to answer the question, Does the autonomic dysfunction in people with ME/CFS arise in association with abnormalities of brain, muscle and liver, as has already been shown in other patients with other illnesses?

A novel hypothesis relating to the nervous system was recently proposed by Michael B. VanElzakkerCorresponding author contact information. His hypothesis proposes that ME/CFS may stem from an infection of the vagus nerve. The vagus nerve is a long cranial nerve that stretches from the brain down to the lower abdomen. This nerve is highly branched with offshoots stretching to numerous organs and tissues within the body. The vagus nerve primarily conveys sensory information to the brain with 80-90% of it being comprised of sensory neurons. However, there are also a smaller number of motor neurons forming a small motor division of the nerve. The function of this nerve is to convey information about the current state of organs within the body – functions include regulation of the gastrointestinal tract via interaction with the enteric nervous system (nervous system of the gut).

In the instance of a vagus nerve infection as hypothesized, the vagus nerve is likely to suffer a degree of inflammation. This would disrupt the normal transmission of action potentials and would likely result in times of over-stimulation and, perhaps, under-stimulation. Over time, such dysfunction would likely cause further damage to the nerve, causing further dysfunction, and so the process would continue indefinitely. It must be stressed, however, that while this hypothesis is certainly an interesting idea, there is little in the way of evidence to support it. Further research must be completed before it can gain any merit. 

There is a general consensus among ME/CFS researchers that the symptoms seem to reflect an ongoing immune response, perhaps due to viral infection. Thus, most ME/CFS research has focused upon trying to uncover that putative immune system dysfunction or specific pathogenic agent. However, no single causative agent has been found. In this speculative article, I describe a new hypothesis for the etiology of ME/CFS: infection of the vagus nerve. When immune cells of otherwise healthy individuals detect any peripheral infection, they release pro-inflammatory cytokines. Chemoreceptors of the sensory vagus nerve detect these localized pro-inflammatory cytokines, and send a signal to the brain to initiate sickness behavior.

Quite recently, there have also been a number of articles appearing discussing the similarities between ME/CFS and Multiple Sclerosis (MS), although this is no recent occurrence, as the similarities have been noted many times previously to this. As the majority likely know, MS is caused through an autoimmune response targeted towards the myelin sheath secreting schwann cells, that wrap around some neurons. This allows for the previously discussed saltatory conduction, hence allowing for faster nerve impulse transmission. The destruction of these schwann cells, therefore, has far reaching consequences within the nervous system, causing the distressing symptoms that MS patients suffer. The relative morbidity between ME/CFS and MS is clear to see, given that both have profound adverse effects upon the quality of life. However unlike MS, ME/CFS has yet to receive irrefutable evidence regarding the pathophysiology of the ongoing disease process. For this reason, it is helpful in some respects to compare the two diseases. However it is also important to contrast the two, highlighting the differences between the diseases.

For instance, in MS, there is clear evidence of ongoing inflammatory mechanisms within the nervous system. However, despite this being reported in several ME/CFS studies, it is in no way conclusive. It appears that if an autoimmune mechanism truly lies at the heart of ME/CFS, that it functions in a more complex, subtle and devious way than MS appears to. Although it is of note that despite MS being recognized as an autoimmune disease, the actual understanding of the complex ongoing process still eludes researchers. One important difference that I as a personal observer have come to, is that while MS typically adversely affects the central nervous system, ME/CFS appears to have consequences in both the sensory nervous system (with sensory overload being a common complaint) and autonomic nervous system. Unfortunately, dysfunction of the central system appears somewhat easier to casually observe, whereas autonomic and sensory dysfunction appear somewhat more convoluted. Perhaps this is why ME/CFS is only now losing the incorrect label of a psychological condition. 

There are remarkable phenomenological and neuroimmune overlaps between both disorders. Patients with ME/CFS and MS both experience severe levels of disabling fatigue, a worsening of symptoms following exercise, and resort to energy conservation strategies in an attempt to meet the energy demands of day-to-day living.

Given the research discussed here and the plethora of historical research into autonomic dysfunction within ME/CFS, it is clear that dysfunction and perhaps even mechanical damage to the nervous system, specifically the autonomic and sensory systems, plays a central role within the ongoing disease process within ME/CFS patients. An interesting point to make is that many of the previous articles center on areas that have direct interaction with these neurological systems. Any abnormality in one can have profound effects upon another – with the cardiovascular, nervous and immune systems all being closely intertwined and interdependent upon one another. Of all the areas within biology and medicine, the nervous system is likely the most complex and is therefore a fast advancing field. Hopefully, as time progresses and ME/CFS research continues, it won’t take too long to discover that one key piece of evidence that points us towards the cause of ME/CFS, and hopefully leads to treatments in the future. 

And so concludes the final article in this series. I sincerely hope those reading have enjoyed this series as much as I have writing it. Be sure to let us know what you thought of this series. Keep a look out for the series conclusion coming soon, which will discuss and summarize everything we’ve explored in the last five articles.

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31 comments

{ 31 comments… read them below or add one }

Chris November 22, 2013 at 5:15 pm

Andrew, thanks for another great piece, to which I offer an addendum. Julia Newton, leader of the group at Newcastle U. that as you report has been doing great research on the ANS and ME/CFS, published a paper a few years ago, listed under the name of Sutcliffe K, “Home orthostatic training in chronic fatigue syndrome–a randomized, placebo-controlled feasibility study”, PMID:19912315. I have the full text of the paper, which describes a simple procedure of standing in relaxed posture with one’s shoulder blades touching a back wall and one’s heels ca.12-15cms in front of that wall. One holds the position until one develops symptoms, and one needs–this is important–a “drop zone” of soft stuff just in case one passes out, and/or a friend to intervene if necessary. This is maintained once or twice daily up to 40mins.

The results were excellent–most patients improved their Orthostatic Intolerance substantially within one month, and those who kept it up for 6 months generally reported an improvement in fatigue too. There is by now a fair amount of literature on this simple technique being used for, mostly, neurocardiogenic syncope (fainting), though this is the only paper I have found using it for ME/CFS. I have been doing this for about 3 months now (I am 80, so must expect slow response!) and can report that my OI has improved significantly, and my BP rise after exercise (a prime symptomin the past) has been much reduced. I also have dry eyes–another ANS symptom–and this too seems to be improving slowly. Needless to say I shall continue.

But I advise caution: I have never fainted in my life, but know several with ME who have, and one has to take the warnings seriously. I also note that my legs feel heavy and rather numb for a short while after, and I have to leave the position with care as I sit down. It is also very boring–I try to time my sessions for when tennis or some other entertaining but not blood-pressure raising event is on TV–I have a wall opposite my TV that makes this convenient.

Esther12 November 22, 2013 at 5:44 pm

Thanks Andrew.

One thing I wonder about autonomic stuff and CFS is, how likely is this to be secondary?

Do people with the flu, AIDS, depression or brain injury have evidence of similar problems? From my position of ignorance, it seems possible that almost anything which places a person under strain could also increase the chances of these sorts of autonomic problems. Is that right? Or are these a useful indication that certain specific things are going wrong?

Firestormm November 22, 2013 at 7:20 pm

This just came up on one of my alerts. I don't know what to read into it, and haven't found or read the paper. Others have posted on ME sites, but it looks to me that this large non-ME longitudinal study (12,000+ enrolled), highlights a significant if small risk of developing atrial fibrillation (tested for with EEG), in people with Orthostatic Hypotension. Anyway, seemed appropriate to post here. What do you think @Legendrew ?

Five percent of the subjects (603 of them) were diagnosed with a rapid drop in blood pressure when going from lying down to standing up. The authors defined orthostatic hypotension as a 20 mmHg or greater drop in systolic blood pressure or a dip of at least 10 mmHg in diastolic pressure. Those who had a history or symptoms of atrial fibrillation at baseline were excluded from the study.

During an average follow-up of 18.1 years, 1,438 (11.9 percent) of the study participants developed atrial fibrillation. Those with orthostatic hypotension, after accounting for factors such as race, age, gender and other common risk factors for the arrhythmia, were 40 percent more likely than those without orthostatic hypotension to develop an irregular heartbeat. Atrial fibrillation was identified by 12-lead ECGs recorded during three follow-up visits at three-year intervals through 1998, and by hospitalizations and/or death certificates through 2010.

The arrhythmia is an underdiagnosed condition that increases the risk of stroke fivefold, as well as risks of heart failure and dementia. People with atrial fibrillation are often treated with blood thinners to reduce the risk of stroke, and with other medications that regulate the rate and rhythm of the heartbeat. The findings were published last week in the journal PLOS ONE.

“We need more research into whether there is any sort of causal relationship between orthostatic hypotension and atrial fibrillation, or whether it is simply a marker of dysfunction of autonomic nervous system or generally poor health,” he says.

21 November 2013
Study identifies possible link between orthostatic hypotension and atrial fibrillation

@Esther12 I would also be interested in learning of how OH affects other people, with/without other diseases. The above study I refer to doesn't indicate if those found to have OH also have other diagnoses – though I haven't read the paper – which is a shame. I am not sure if OH can be related to ME as a symptom or as something that could develop from extended periods of lying down due to illness. I am forgetful of the evidence in this regard (or the theories).

@Chris Thanks for the reminder about that paper from Sutcliffe and Newton – I know it is a favourite of yours and it is great to hear you are benefiting – though it is early days – from the exercise indicated. I wonder if you or anyone can indicate how common NMH is believed to be in CFS. The abstract indicates that it is, but again I am forgetful of how common or why it is thought to be commonly associated.

Thanks :)

Sushi November 22, 2013 at 7:44 pm

@Firestormm

I have OI, sometimes called orthostatic hypotension and I have had some real problems with severe atrial fibrillation = 2 ambulance trips to the Emergency Room!

Here is another factor though. I had been getting Afib about once a year for a few years and had been able to stop it with potassium and magnesium. But this spring I started getting frequent, severe episodes. I discovered that I had become hyperthyroid from taking a low dose of thyroid meds because I had been hypothyroid for a couple of years. But my thyroid had improved a great deal in a few months and I hadn't realized it.

This is what set off the more severe, more frequent Afib, but didn't explain the history of getting it very occasionally for a few years. Then I discovered that long term use of ambien was associated with Afib in a small but significant percentage of users. I had taken ambien for about 10 years.

I'd guess that many with orthostatic hypotension also take ambien as sleep problems usually go hand in hand with other autonomic nervous system issues. I have stopped ambien and have not had any more episodes of Afib in the last 6 months. I sure hope I don't get more, but ambien is another factor that could contribute to Afib in this patient group.

Sushi

Chris November 22, 2013 at 8:43 pm

@Firestorm–I know that the figures for OH among those with ME are very high, will try to dig some out for you soon.

@Sushi and others– as well as the things you mention, Cheney has some interesting comments on the origin of AF among those with ME in his latest talk, which is posted in parts with a brief account somewhere on this site–seems that it is part of the almost frenetic attempts made by our left ventricle to find enough blood to pump out with each beat–the atrium gets involved in the struggle, and suffers…

There is a website, http://www.afibbers.org , that offers the suggestion that supplementing with Taurine can often help with arrhythmias; it has helped me with Premature Ventricular contractions, and has helped two people I know with AF. The Mayo clinic says it is quite safe for long use at a low dose–I take about 1,200 mg daily–and at a considerably higher dose short term. No guarantees of course, but it seems it might be worth trying. There is–or should be–a lot of Taurine in the heart, and since as the name implies it is found mainly in meats, it tends to be low in vegetarians and vegans. Chris

Chris November 22, 2013 at 10:39 pm

@ Firestorm, here are some quotes from several papers from the Newton group (she is not always the lead author):
The Sutcliffe/Newton study from 2010 that I referenced simply states “orthostatic intolerance is a frequently described symptom in both NMH and CFS, with recent studies confirming lower blood pressure in CFS compared to controls.” An earlier paper from this group, 2007, “Symptoms of autonomic dysfunction in chronic fatigue syndrome” provides evidence that “in the Orthostatic Tolerance domain,… CFS patients had mean scores [on a well established questionnaire about ANS symptoms] almost four-fold higher than controls,” and also “A particularly strong association was seen with symptoms of orthostatic intolerance, suggesting that abnormality of dynamic blood pressure regulation is particularly associated with fatigue severity in CFS/ME.”

In another paper from 2010, “Impaired cardiovascular response to standing in Chronic Fatigue Syndrome,” lead auther K.G. Hollingsworth, we find this: “the hearts of the CFS group appear to be working harder in response to the stress of standing compared with controls. Further clinical evaluation of the CFS/ME group confirmed that symptoms on standing assessed using the OGS [orthostatic grading scale] occurred in 61/64 (95%) of cases compared with 25/64 (39%) of controls.” Not exactly what you were looking for, but perhaps close enough to give the picture? As you see, this is a group whose work I follow!

Firestormm November 22, 2013 at 10:58 pm

@Sushi and @Chris thank you both :)

Chris I wonder if that Orthostatic Grading Scale was based on measurements of blood pressure (presumably it was) as opposed to patient-reported symptoms, and if so the results were sufficient for a diagnosis of OH using the methods in the paper I initially referred to?

The authors defined orthostatic hypotension as a 20 mmHg or greater drop in systolic blood pressure or a dip of at least 10 mmHg in diastolic pressure

Do you happen to know if this definition is a usual one? And what the traditional treatment might be?

I am not aware of any studies in ME patients with OH looking for atrial fibrillation – are you?

For the record, I don't believe I suffer from this condition. If I did, it seems to have passed. Rapid heartbeat uses only occurs when I experience an epileptic "episode" in bed or bad dream or something, but passes after a while of doing something else.

Dizziness for me and nausea was most dire and long-lived but was eventually treated successfully with a drug I still take prescribed I believe for labyrinthitus.

However, the drug is in part a muscle relaxant I believe, as is another I am prescribed – so it's possible I guess they could be acting in concert to pacify a rapid heartbeat. But I think that's pretty thin as a theory :)

Chris November 23, 2013 at 8:36 am

@Firestormm–the Hollingsworth/Newton paper I cited used the Orthostatic Grading Scale described in Shrezenmaier C, "Evaluation of orthostatic hypotension: relationship of a new self-report instrument to laboratory-based measures", PMID: 15757013. I do not have access to the full text, but the abstract says it is short, 5 questions, and works well. It is focused on hypotension.

I am not sure it helps a lot to focus on exact definitions–I have seen evidence that some who do not qualify for a POTS diagnosis for instance do qualify if the tilt is maintained a bit longer, and generally the various definitions seem to merge into one another. They are all symptoms of an ANS dysfunction as far as I can make out.

I know from my own use of the "home orthostatic training" thing that what happens depends to some extent on my status as I begin; if my BP is a little high, my HR will be higher, and so on–though there are also signs of some reciprocal relationship between BP and HR–as if my ANS is still in a rather rough way trying out various measures to adapt to my insistence on remaining still and standing–it has not yet figured out the best way to integrate BP, HR, peripheral resistance, and all that stuff. But it does seem slowly to be relearning…. and I have hope!

I am wary of pharmaceutical treatment until they really have us properly figured out; for instance, beta blockers are sometimes used for this stuff, but there is evidence that they are harmful to mitos, and so on. I took low doses of Coreg, a beta (and alpha) blocker for quite a while, and though that seemed to help a bit, I ended up in worse shape–though that may have been caused by a cardio putting me on high dose of an ARB. So I am very wary of what docs suggest with their very patial understanding of what is going on in us.

There is an interesting account of one doc's treatment that I will try to find –I think it is somewhere on the CAA website–a youngish doc at Princeton, I think.
There is also a talk by Peter Rowe on the CAA site.

Firestormm November 23, 2013 at 8:44 am

@Chris thanks for clearing up the Grading Scale and diagnostic methods for me :)

MeSci November 23, 2013 at 8:49 am

Just thought I'd post a link to a PR discussion about comorbidity of POTS and CFS in case some people hadn't seen it.

Legendrew November 23, 2013 at 9:24 am
Firestormm

This just came up on one of my alerts. I don't know what to read into it, and haven't found or read the paper. Others have posted on ME sites, but it looks to me that this large non-ME longitudinal study (12,000+ enrolled), highlights a significant if small risk of developing atrial fibrillation (tested for with EEG), in people with Orthostatic Hypotension. Anyway, seemed appropriate to post here. What do you think @Legendrew ?

21 November 2013
Study identifies possible link between orthostatic hypotension and atrial fibrillation

@Esther12 I would also be interested in learning of how OH affects other people, with/without other diseases. The above study I refer to doesn't indicate if those found to have OH also have other diagnoses – though I haven't read the paper – which is a shame. I am not sure if OH can be related to ME as a symptom or as something that could develop from extended periods of lying down due to illness. I am forgetful of the evidence in this regard (or the theories).

@Chris Thanks for the reminder about that paper from Sutcliffe and Newton – I know it is a favourite of yours and it is great to hear you are benefiting – though it is early days – from the exercise indicated. I wonder if you or anyone can indicate how common NMH is believed to be in CFS. The abstract indicates that it is, but again I am forgetful of how common or why it is thought to be commonly associated.

Thanks :)

Interesting stuff, I think today in modern anatomy it is still understated the interconnection between different system. The vascular and nervous systems are deeply entwined with one another so it's easy to see why a problem in one can cause further problems in the other, the trouble then is in sorting out what is causing what as often the problems feed into one another.I'm personally of the opinion that the vascular issues in ME trigger off and perpetuate the nervous system issues however this is something of a hunch and there is a lot of evidence to support both ideas. I think we are finally in a position where researchers are looking at one area in depth and seeing the connections themselves which is great. This study is very interesting though as it clearly shows how one problem can influence or even trigger another.

Legendrew November 23, 2013 at 9:29 am
Esther12

Thanks Andrew.

One thing I wonder about autonomic stuff and CFS is, how likely is this to be secondary?

Do people with the flu, AIDS, depression or brain injury have evidence of similar problems? From my position of ignorance, it seems possible that almost anything which places a person under strain could also increase the chances of these sorts of autonomic problems. Is that right? Or are these a useful indication that certain specific things are going wrong?

As I discussed a little in my previous post, I am of the opinion that the autonomic problems in ME are a secondary problem to another upstream problem. It's been clear for many years that all diseases have a systemic effect to some degree and the examples you mention all involve a degree of autonomic dysfunction. These symptoms are a good starting point to try and work back from to find what could be causing it – unfortunately this is never an easy thing to do no matter the starting point, I'm personally having problems currently finding the upstream cause of my secondary hyperparathyroidism – you could liken it to a murder mystery wherein there is evidence of the culprit but everything always gets clouded in mystery and as time progresses in a patient the true cause often becomes masked by the many effects it may have. I'm hopeful though that we now have evidence of ongoing problems, following those paths has got to take us somewhere, learning as we go.

Chris November 23, 2013 at 1:38 pm

Hi; as has been mentioned, there is new stuff on ANS and cardiovascular issues on Cort's website, with links out.
@Firestormm–the doc whose name I had forgotten is Pocinki, and he has an interesting piece available on the CAA site–go to http://www.cfids.org and type "Dysfunction Junction: The ANS and CFS" into the window, and that should take you there.

@ Andrew; the issue of origins is tough–that last Newcastle paper did a fascinating job of paralleling what happens in the cells and mitos of "peripheral" muscle tissue, with what happens in brain blood perfusion ( usually under local control)–with evidence of mechanisms through which the ANS could affect the muscle tissue problems with energy creation, ROS build up, and slow lactate clearance. But just how those three processes relate to each other–I guess we will have to wait for the next papers!

I do have a story of my own to tell, however. After 70 healthy and very active years, I began to have a loss of breath and energy and some left chest pain with intensive energy. I was sent for a treadmill test, but passed the whole 10minute protocol with, it seems, no signs of ischemia on the monitor, and the doc in charge proclaimed "it's not your heart!". However, I had felt signs of stress the last minute (a year earlier I would have laughed my way through the whole thing). So I walked home, feeling somewhat relieved, but puzzled. The next day I had a sour stomach–a new sensation for me–Tums to the rescue. A few days later, I woke in the middle of the night with ice cold feet, dry eyes, and a mouth so dry my tongue was stuck to my palette. The feet thing resolved, my mouth resolved more slowly, the dry eyes are still with me.

The mystery was solved when I had an echocardiogram, that showed I had a "severely stenotic–.7 sq mm–aortic valve." I think–no cardio was interested in discussing it with me–that the intense back pressure within my ventricle during the treadmill test must have set off all kinds of alarms and dysfunctions in my ANS–which has multiple connections with the heart of course. A few days later, I suffered acute OI while trying to prepare dinner. The weeks between that and the echo were total nightmare–a thorough immune check revealed nothing, no one had a clue.

Surgery more or less resolved things; but two years later I had recurrence of OI, chest pain, high BP, but cardiac testing could find nothing wrong; yet my exercise ability had shrunk to virtually nothing. This slowly resolved over the next months, but hit again about 9 months later, this time for real and it is still with me. So I feel it is all down to those mitos and/or the ANS–the timings do not suggest viral sources to me–so I await the next instalment from the Newton group! They do have a short paper from a few years ago suggesting that ME/CFS when it strikes the old is a different disease, focused on fatigue and OI, and that fits me perfectly! So I feel they have my number …

Sing November 23, 2013 at 8:19 pm

Like you Chris, I am older than most here. At my age and stage, ANS problems, especially OI, are the most difficult things I deal with. If I were an adolescent with ME/CFS, however, I bet that my OI would be taking the form of POTS instead of just the major descent in blood pressure that it is, accompanied by a stubbornly low heart rate most of the time. Because as a young person, I would still have had "oomph"–i.e., adrenal function, a fight or flight function, to a much greater extent than I presently do.

The chest pain, graying of vision, going slowly into blackout, losing coordination and balance, and inability to assess what is happening and what I need to do–I go through these while walking or standing in order not to have a life limited so much by lying down and sitting, which in my case are alone. I tough it out as much as possible, but do sit before falling, or put my head way down, even when it is awkward and embarrassing to do this. There is no way I could deal with a wheel chair with no one to push, rough or missing sidewalks, or just country.

But back to the OI. What this is doing to the heart and the brain must be significant. No way a person gets chest pain and starts to struggle to breathe, while vision is graying out, without there being damage, in my opinion, to the heart and brain. Come on!

Researchers and patients should always check out the endocrine system too. I had my hormones brought up to an age-adjusted level years ago. I expected it would help a lot but it only helped me a little. Not a solution, but necessary in terms of a "leave no stone unturned" search for improvement.

I find Dr. Cheney's thinking and research very interesting, also Dr. Newton's, and Dr. Pocincki's realistic approach to treatment helpful. Dr. Peter Rowe has done careful work–I thank him and others for the rescue of Midodrine from being pulled from circulation (a pun!). I don't know if and when Chelsea Therapeutics new drug Northera is going to become available for those of us with OI to try out. We really need help with severe Orthostatic Hypotension and the increasing nerve damage–neuropathies, etc. with go with this Autonomic Dysfunction/Disease.

MeSci November 24, 2013 at 3:31 am
Chris

Hi; as has been mentioned, there is new stuff on ANS and cardiovascular issues on Cort's website, with links out.
@Firestormm–the doc whose name I had forgotten is Pocinki, and he has an interesting piece available on the CAA site–go to http://www.cfids.org and type "Dysfunction Junction: The ANS and CFS" into the window, and that should take you there.

@ Andrew; the issue of origins is tough–that last Newcastle paper did a fascinating job of paralleling what happens in the cells and mitos of "peripheral" muscle tissue, with what happens in brain blood perfusion ( usually under local control)–with evidence of mechanisms through which the ANS could affect the muscle tissue problems with energy creation, ROS build up, and slow lactate clearance. But just how those three processes relate to each other–I guess we will have to wait for the next papers!

I do have a story of my own to tell, however. After 70 healthy and very active years, I began to have a loss of breath and energy and some left chest pain with intensive energy. I was sent for a treadmill test, but passed the whole 10minute protocol with, it seems, no signs of ischemia on the monitor, and the doc in charge proclaimed "it's not your heart!". However, I had felt signs of stress the last minute (a year earlier I would have laughed my way through the whole thing). So I walked home, feeling somewhat relieved, but puzzled. The next day I had a sour stomach–a new sensation for me–Tums to the rescue. A few days later, I woke in the middle of the night with ice cold feet, dry eyes, and a mouth so dry my tongue was stuck to my palette. The feet thing resolved, my mouth resolved more slowly, the dry eyes are still with me.

The mystery was solved when I had an echocardiogram, that showed I had a "severely stenotic–.7 sq mm–aortic valve." I think–no cardio was interested in discussing it with me–that the intense back pressure within my ventricle during the treadmill test must have set off all kinds of alarms and dysfunctions in my ANS–which has multiple connections with the heart of course. A few days later, I suffered acute OI while trying to prepare dinner. The weeks between that and the echo were total nightmare–a thorough immune check revealed nothing, no one had a clue.

Surgery more or less resolved things; but two years later I had recurrence of OI, chest pain, high BP, but cardiac testing could find nothing wrong; yet my exercise ability had shrunk to virtually nothing. This slowly resolved over the next months, but hit again about 9 months later, this time for real and it is still with me. So I feel it is all down to those mitos and/or the ANS–the timings do not suggest viral sources to me–so I await the next instalment from the Newton group! They do have a short paper from a few years ago suggesting that ME/CFS when it strikes the old is a different disease, focused on fatigue and OI, and that fits me perfectly! So I feel they have my number …

Yikes – scary story!

MeSci November 24, 2013 at 3:37 am
Sing

Like you Chris, I am older than most here. At my age and stage, ANS problems, especially OI, are the most difficult things I deal with. If I were an adolescent with ME/CFS, however, I bet that my OI would be taking the form of POTS instead of just the major descent in blood pressure that it is, accompanied by a stubbornly low heart rate most of the time. Because as a young person, I would still have had "oomph"–i.e., adrenal function, a fight or flight function, to a much greater extent than I presently do.

The chest pain, graying of vision, going slowly into blackout, losing coordination and balance, and inability to assess what is happening and what I need to do–I go through these while walking or standing in order not to have a life limited so much by lying down and sitting, which in my case are alone. I tough it out as much as possible, but do sit before falling, or put my head way down, even when it is awkward and embarrassing to do this. There is no way I could deal with a wheel chair with no one to push, rough or missing sidewalks, or just country.

But back to the OI. What this is doing to the heart and the brain must be significant. No way a person gets chest pain and starts to struggle to breathe, while vision is graying out, without there being damage, in my opinion, to the heart and brain. Come on!

Researchers and patients should always check out the endocrine system too. I had my hormones brought up to an age-adjusted level years ago. I expected it would help a lot but it only helped me a little. Not a solution, but necessary in terms of a "leave no stone unturned" search for improvement.

I find Dr. Cheney's thinking and research very interesting, also Dr. Newton's, and Dr. Pocincki's realistic approach to treatment helpful. Dr. Peter Rowe has done careful work–I thank him and others for the rescue of Midodrine from being pulled from circulation (a pun!). I don't know if and when Chelsea Therapeutics new drug Northera is going to become available for those of us with OI to try out. We really need help with severe Orthostatic Hypotension and the increasing nerve damage–neuropathies, etc. with go with this Autonomic Dysfunction/Disease.

I was prompted by your first statement to wonder what age most people are here.

I will start – I am 60, but was about 42 when I became ill. (Thought – maybe a poll would be better, but what keyword to use, as PR won't search for 3-letter words like 'age' or 'old'!)

bertiedog November 24, 2013 at 3:46 am
Sing

Like you Chris, I am older than most here. At my age and stage, ANS problems, especially OI, are the most difficult things I deal with. If I were an adolescent with ME/CFS, however, I bet that my OI would be taking the form of POTS instead of just the major descent in blood pressure that it is, accompanied by a stubbornly low heart rate most of the time. Because as a young person, I would still have had "oomph"–i.e., adrenal function, a fight or flight function, to a much greater extent than I presently do.

The chest pain, graying of vision, going slowly into blackout, losing coordination and balance, and inability to assess what is happening and what I need to do–I go through these while walking or standing in order not to have a life limited so much by lying down and sitting, which in my case are alone. I tough it out as much as possible, but do sit before falling, or put my head way down, even when it is awkward and embarrassing to do this. There is no way I could deal with a wheel chair with no one to push, rough or missing sidewalks, or just country.

But back to the OI. What this is doing to the heart and the brain must be significant. No way a person gets chest pain and starts to struggle to breathe, while vision is graying out, without there being damage, in my opinion, to the heart and brain. Come on!

Researchers and patients should always check out the endocrine system too. I had my hormones brought up to an age-adjusted level years ago. I expected it would help a lot but it only helped me a little. Not a solution, but necessary in terms of a "leave no stone unturned" search for improvement.

I find Dr. Cheney's thinking and research very interesting, also Dr. Newton's, and Dr. Pocincki's realistic approach to treatment helpful. Dr. Peter Rowe has done careful work–I thank him and others for the rescue of Midodrine from being pulled from circulation (a pun!). I don't know if and when Chelsea Therapeutics new drug Northera is going to become available for those of us with OI to try out. We really need help with severe Orthostatic Hypotension and the increasing nerve damage–neuropathies, etc. with go with this Autonomic Dysfunction/Disease.

I used to have the darkening of vision and severe OI when I was in my 40s and 50s together with symptoms like severe vertigo from time to time but all these symptoms have been cured by supporting my adrenal function with 6mg Prednisolone and just 2.5 mc hydrocortisone in the afternoons plus a couple of times a week I take a tiny dose of Fludrocortisone. I also take Lo Salt in water about 4 times daily to ensure my potassium levels are good and also sodium levels.

The other drug that has helped to sort this out is 20 mg Propananol on waking and maybe twice a day if the weather is warm or if I want to do more physical stuff.

I am now 65 and yet don't suffer OI at all, in fact my bp will have a tendency to go a touch too high say 140/90 if I drink normal tea and if I start doing a bit too much physically but another dose of the betablocker sorts it all out in less than an hour. So to be honest I don't think its an age thing, its more that the adrenals aren't coping. I should also add that it was found I had hypothyroidism so in addition to the adrenal meds I take 2 1/2 grains of dessicated thyroid. It has made a massive difference to the quality of my life and before I had an accident which has damaged my knee I was regularly doing between 5500 and 6000 steps daily.

Pam

MeSci November 24, 2013 at 3:52 am
bertiedog

I used to have the darkening of vision and severe OI when I was in my 40s and 50s together with symptoms like severe vertigo from time to time but all these symptoms have been cured by supporting my adrenal function with 6mg Prednisolone and just 2.5 mc hydrocortisone in the afternoons plus a couple of times a week I take a tiny dose of Fludrocortisone. I also take Lo Salt in water about 4 times daily to ensure my potassium levels are good and also sodium levels.

The other drug that has helped to sort this out is 20 mg Propananol on waking and maybe twice a day if the weather is warm or if I want to do more physical stuff.

I am now 65 and yet don't suffer OI at all, in fact my bp will have a tendency to go a touch too high say 140/90 if I drink normal tea and if I start doing a bit too much physically but another dose of the betablocker sorts it all out in less than an hour. So to be honest I don't think its an age thing, its more that the adrenals aren't coping. I should also add that it was found I had hypothyroidism so in addition to the adrenal meds I take 2 1/2 grains of dessicated thyroid. It has made a massive difference to the quality of my life and before I had an accident which has damaged my knee I was regularly doing between 5500 and 6000 steps daily.

Pam

I tried propranolol in my 40s but it was either for anxiety or IBS. It made me almost black out, presumably due to hypotension. Now I have hypertension but reducing salt makes no difference, and I actually need a lot of salt and my potassium is normal-to-high.

But I don't have 'typical' OI as far as I am aware. The main postural issue I have is tachycardia about 5 minutes after lying down.

What a mixed bunch we are!

concepcion November 24, 2013 at 12:18 pm
Chris

Andrew, thanks for another great piece, to which I offer an addendum. Julia Newton, leader of the group at Newcastle U. that as you report has been doing great research on the ANS and ME/CFS, published a paper a few years ago, listed under the name of Sutcliffe K, “Home orthostatic training in chronic fatigue syndrome–a randomized, placebo-controlled feasibility study”, PMID:19912315. I have the full text of the paper, which describes a simple procedure of standing in relaxed posture with one’s shoulder blades touching a back wall and one’s heels ca.12-15cms in front of that wall. One holds the position until one develops symptoms, and one needs–this is important–a “drop zone” of soft stuff just in case one passes out, and/or a friend to intervene if necessary. This is maintained once or twice daily up to 40mins.

The results were excellent–most patients improved their Orthostatic Intolerance substantially within one month, and those who kept it up for 6 months generally reported an improvement in fatigue too. There is by now a fair amount of literature on this simple technique being used for, mostly, neurocardiogenic syncope (fainting), though this is the only paper I have found using it for ME/CFS. I have been doing this for about 3 months now (I am 80, so must expect slow response!) and can report that my OI has improved significantly, and my BP rise after exercise (a prime symptomin the past) has been much reduced. I also have dry eyes–another ANS symptom–and this too seems to be improving slowly. Needless to say I shall continue.

But I advise caution: I have never fainted in my life, but know several with ME who have, and one has to take the warnings seriously. I also note that my legs feel heavy and rather numb for a short while after, and I have to leave the position with care as I sit down. It is also very boring–I try to time my sessions for when tennis or some other entertaining but not blood-pressure raising event is on TV–I have a wall opposite my TV that makes this convenient.

Hi Chris,
This study and technique are extremely interesting. Were any of the people in the study bedbound or housebound?

concepcion November 24, 2013 at 12:25 pm
MeSci
Sing

Like you Chris, I am older than most here. At my age and stage, ANS problems, especially OI, are the most difficult things I deal with. If I were an adolescent with ME/CFS, however, I bet that my OI would be taking the form of POTS instead of just the major descent in blood pressure that it is, accompanied by a stubbornly low heart rate most of the time. Because as a young person, I would still have had "oomph"–i.e., adrenal function, a fight or flight function, to a much greater extent than I presently do.

The chest pain, graying of vision, going slowly into blackout, losing coordination and balance, and inability to assess what is happening and what I need to do–I go through these while walking or standing in order not to have a life limited so much by lying down and sitting, which in my case are alone. I tough it out as much as possible, but do sit before falling, or put my head way down, even when it is awkward and embarrassing to do this. There is no way I could deal with a wheel chair with no one to push, rough or missing sidewalks, or just country.

But back to the OI. What this is doing to the heart and the brain must be significant. No way a person gets chest pain and starts to struggle to breathe, while vision is graying out, without there being damage, in my opinion, to the heart and brain. Come on!

Researchers and patients should always check out the endocrine system too. I had my hormones brought up to an age-adjusted level years ago. I expected it would help a lot but it only helped me a little. Not a solution, but necessary in terms of a "leave no stone unturned" search for improvement.

I find Dr. Cheney's thinking and research very interesting, also Dr. Newton's, and Dr. Pocincki's realistic approach to treatment helpful. Dr. Peter Rowe has done careful work–I thank him and others for the rescue of Midodrine from being pulled from circulation (a pun!). I don't know if and when Chelsea Therapeutics new drug Northera is going to become available for those of us with OI to try out. We really need help with severe Orthostatic Hypotension and the increasing nerve damage–neuropathies, etc. with go with this Autonomic Dysfunction/Disease.

I was prompted by your first statement to wonder what age most people are here.

I will start – I am 60, but was about 42 when I became ill. (Thought – maybe a poll would be better, but what keyword to use, as PR won't search for 3-letter words like 'age' or 'old'!)

My daughter is 23, started when she was 15 (slow onset). She has OI, ME, hashi's.

concepcion November 24, 2013 at 12:26 pm

Thanks Andrew. So informative.

Chris November 24, 2013 at 1:17 pm

Hi–here are some more bits and pieces….

@concepcion – I am pretty sure that none of those participating in this study could have been bed/house bound, since they would have had TT testing to be admitted into the study. If that is unfortunately your case, I can only advise extreme caution, and beginning with very very short attempts to see how it goes. Don’t take any risks–a faint can do real damage!

Is OH a symptom, or result of too much lying down? I think probably both–mine hit fast before I had started much lying down, but became a major symptom. I describe it as OI rather than OH, because I find it difficult to take my BP while standing up, though it is usually a bit low when I take it immediately after one of my "back against the wall" sessions.

There is a fascinating little book by Joan Vernikos, former director of NASA’s rehab program for returning astronauts–"Sitting Kills, Moving Heals."

As you may know, returning astronauts have all kinds of symptoms, and most will sound very familiar to you; here are phrases from her book in which she lists "How the Body Changes in Space": "blood volume reduced"; "heart shrinks, cardiac output decreased"; "red blood cells reduced"; "stamina/aerobic capacity decreased"; "body temperature regulation disturbed"; "muscle atrophy"; "biological rhythms disturbed"; "sleep disturbed; sleep not restorative"; "bone mass and density decreased"; "immune system depressed"; "flare ups of dormant viral infections"; and so on.

Sounds familiar?

And here are some items under "Symptoms after Returning from Space": "spine compressed; back pain"; "standing can lead to fainting"; "blood pressure regulation disturbed"; "decreased cardiac output and stroke volume of the heart"; "muscles no longer support the spine"; "balance disturbed; unsteadiness"; "wide stance (‘duck walking’); shorter steps"; "walking and coordination problems".

So if you sometimes feel as if you are, or have been, living on the moon, you are not far wrong. Remember, however, that she was dealing with very healthy people suffering temporary and reversible dysfunctions–though some, like bone density, took a long while to recover fully.

I think we are caught in a real bind: our basic dysfunctions promote OI, and avoiding OI by sitting/ lying promotes OI.

Vernikos also pointed me to some interesting recent work. Here is Marc Hamilton (Hamilton MT, "Too little exercise and too much sitting: inactivity physiology and the need for new recommendations on sedentary behaviour," PMID: 22905272):

"There is now a need for studies to differentiate between the potentially unique molecular, physiologic, and clinical effects of too much sitting (inactivity physiology) separate from the responses caused by structured exercise (exercise physiology).

In theory, this may be in part because nonexercise activity thermogenesis (heat production) is a much greater component of total energy expenditure than exercise or because any type of brief, yet frequent, muscular contraction throughout the day may be necessary to short-circuit unhealthy molecular signals causing metabolic diseases."

A short translation? You may do better by increasing your general activity level and reducing your intentionally "exercise" activity, if the latter leads to reduced overall activity and increased sitting and lying.

The distinction between stabilizer and mobilizer muscles comes into play here too. Normal daytime activities, like preparing food, rising to walk over to the phone, putting out the garbage, food shopping, all use those stabilizing muscles, and help prevent the damage that accrues during long-term (hours, days) inactivity–as do yoga, Qu-Jong, Pilates, and other activities.

"Exercise" may employ only certain key mobilizing muscles, and that will not undo the damage accruing during the long nonexercising hours of your day if you sit and lie down too much. So it may be wise to move often, if only a little, and make varied movements, rather than spend all one’s day’s ration of energy in one long (for us folk) session of repetitive energy expenditure involving only some key mobilizers.

I think that "back against the wall" thing exercises some key stabilizer muscles–my legs seem to be filling out a bit–and that is a good thing for many reasons, not least being that it improves venous return, which improves OI.

On the issue that Sing raises–that all this must be doing damage. Yes, I am sure it does–lying and sitting for long periods damage muscles, particularly stabilizers, but also gravity sensors, autonomic nervous system control over our blood pressure and heart rate , and all that other autonomic stuff, but there is evidence from some sources that much of the damage is reversible.

I have now heard three local and credible stories of recovery from ME; two involved heavy use of a juicer –there is now some evidence that autoimmunity is at least involved in our disease, and the DVD "Fat, Sick and nearly Dead" shows two very fat guys both suffering from an unpleasant autoimmune disease who cured themselves by going on a 90 day juice fast under the direction of Dr. Joel Fuhrman, whose book "Eat to Live" records that he has had success with autoimmune diseases.

Recall also the story of Dr. Terry Wahls, with that TED talk and her near recovery from MS–not ME, but in the ball park?

The third case is about a young man, now 20, who got ME when about 13, and who recovered when he and his mother moved to Costa Rica for about 6 months. They are now back in Victoria, BC, and I have met them, and find their story totally credible. Why and how this happened is still a mystery, but it happened, I am sure.

The Rituximab story also suggests that most or much of the damage is reversible–so don’t give up hope! At least I continue to hope, though while we are exchanging ages I am now 80, but was only hit at around 74.

Chris.

Firestormm November 24, 2013 at 4:42 pm

@Chris I hope you don't mind but I edited your post to add some spacing, as I was struggling to read it :)

Very interesting about the exercise and stabilisers :)

Chris November 24, 2013 at 8:38 pm

@Firestormm–fine by me, and thanks–I keep forgetting this–having trouble reading long paragraphs is not one of my problems, so I do forget–sorry! Sushi had written to me about this. Will try to remember–but no guarantees!

MeSci November 25, 2013 at 4:11 am
Chris

"Exercise" may employ only certain key mobilizing muscles, and that will not undo the damage accruing during the long nonexercising hours of your day if you sit and lie down too much. So it may be wise to move often, if only a little, and make varied movements, rather than spend all one’s day’s ration of energy in one long (for us folk) session of repetitive energy expenditure involving only some key mobilizers.

Fidgeting may be a good way to tone muscles. I just tried to find some evidence, as it seems intuitively true to me, but most hits were about weight loss, and the evidence for exercise helping with weight loss isn't great. But if you follow the 'use it or lose it' philosophy it seems obvious that frequent, small activities will help muscle tone, blood flow, etc. In our case we have to avoid too much movement if anything is hurting though.

Chris

I have now heard three local and credible stories of recovery from ME; two involved heavy use of a juicer –there is now some evidence that autoimmunity is at least involved in our disease, and the DVD "Fat, Sick and nearly Dead" shows two very fat guys both suffering from an unpleasant autoimmune disease who cured themselves by going on a 90 day juice fast under the direction of Dr. Joel Fuhrman, whose book "Eat to Live" records that he has had success with autoimmune diseases.

Recall also the story of Dr. Terry Wahls, with that TED talk and her near recovery from MS–not ME, but in the ball park?

The third case is about a young man, now 20, who got ME when about 13, and who recovered when he and his mother moved to Costa Rica for about 6 months. They are now back in Victoria, BC, and I have met them, and find their story totally credible. Why and how this happened is still a mystery, but it happened, I am sure.

The Rituximab story also suggests that most or much of the damage is reversible–so don’t give up hope! At least I continue to hope, though while we are exchanging ages I am now 80, but was only hit at around 74.

Chris.

There is lots of discussion about autoimmunity and ME on this site, and about dietary ways to combat it. My own favoured method is through the leaky-gut diet, and there is a whole section about this.

HowToEscape? November 25, 2013 at 8:21 pm
MeSci
Chris

"Exercise" may employ only certain key mobilizing muscles, and that will not undo the damage accruing during the long nonexercising hours of your day if you sit and lie down too much. So it may be wise to move often, if only a little, and make varied movements, rather than spend all one’s day’s ration of energy in one long (for us folk) session of repetitive energy expenditure involving only some key mobilizers.

Fidgeting may be a good way to tone muscles. I just tried to find some evidence, as it seems intuitively true to me, but most hits were about weight loss, and the evidence for exercise helping with weight loss isn't great. But if you follow the 'use it or lose it' philosophy it seems obvious that frequent, small activities will help muscle tone, blood flow, etc. In our case we have to avoid too much movement if anything is hurting though.

Chris

I have now heard three local and credible stories of recovery from ME; two involved heavy use of a juicer –there is now some evidence that autoimmunity is at least involved in our disease, and the DVD "Fat, Sick and nearly Dead" shows two very fat guys both suffering from an unpleasant autoimmune disease who cured themselves by going on a 90 day juice fast under the direction of Dr. Joel Fuhrman, whose book "Eat to Live" records that he has had success with autoimmune diseases.

Recall also the story of Dr. Terry Wahls, with that TED talk and her near recovery from MS–not ME, but in the ball park?

The third case is about a young man, now 20, who got ME when about 13, and who recovered when he and his mother moved to Costa Rica for about 6 months. They are now back in Victoria, BC, and I have met them, and find their story totally credible. Why and how this happened is still a mystery, but it happened, I am sure.

The Rituximab story also suggests that most or much of the damage is reversible–so don’t give up hope! At least I continue to hope, though while we are exchanging ages I am now 80, but was only hit at around 74.

Chris.

There is lots of discussion about autoimmunity and ME on this site, and about dietary ways to combat it. My own favoured method is through the leaky-gut diet, and there is a whole section about this.

What is "leaky-gut"? It does not seem to have a consistent definition. It does seem to be an area that medicine is aware of, but has not yet developed a set of procedures an average MD can use to rule it (whatever exactly it is) in or out, nor is there a clear set of rules to treat it.

Did I miss something, or is there actually a way to
i) Define what leaky gut is
ii) determine whether one has it, and if so measure how much. This is important because…

if one tries a way of treating it, one wants to know if the treatment did what it was believed to do. With ME, we feel better, worse, better, much worse very often. Without a way to measure whether your gut leaks more or less than before, one doesn't know if the treatment fixed it.

Of course, I'll take anything that improves my health, even if it targets problem A but really improves D, F, and some of W without my knowing it. But isn't enough to develop a reliable method that works for most of us, it was just a lucky hit.

MeSci November 26, 2013 at 3:44 am
HowToEscape?

What is "leaky-gut"? It does not seem to have a consistent definition. It does seem to be an area that medicine is aware of, but has not yet developed a set of procedures an average MD can use to rule it (whatever exactly it is) in or out, nor is there a clear set of rules to treat it.

Did I miss something, or is there actually a way to
i) Define what leaky gut is
ii) determine whether one has it, and if so measure how much. This is important because…

if one tries a way of treating it, one wants to know if the treatment did what it was believed to do. With ME, we feel better, worse, better, much worse very often. Without a way to measure whether your gut leaks more or less than before, one doesn't know if the treatment fixed it.

Of course, I'll take anything that improves my health, even if it targets problem A but really improves D, F, and some of W without my knowing it. But isn't enough to develop a reliable method that works for most of us, it was just a lucky hit.

Best to direct you to the leaky-gut section of this site to avoid going too off-topic, but in brief it means that the gut wall is compromised and allows substances into the bloodstream that cannot normally enter. This is believed to be a cause of autoimmunity.

I think the standard test for it involves mannitol and lactulose IIRC.

Treatments have been found to be effective by e.g. Maes and others, not only for leaky gut but also for ME and other autoimmune conditions.

Chris November 26, 2013 at 11:36 am

Hi–Conception and any others actually considering trying the "back against the wall" "home orthostatic training " thing that I am still using–I have finally unearthed my copy of the complete text, which had gone awol (if you could see my apt you would understand) for a while, and give here the exact instructions ("inability to stand for up to 40mins due to muscular or neurological disorders" was an exclusionary factor–might have excluded me!).

Subjects were "asked to stand with their upper backs against a wall and their heels approximately 15cms from the wall with a cushioned 'drop zone'. They were asked to maintain this position without movement for up to 40 min or until they experienced symptoms."

The "without movement " is important; the control goup was instructed to stand for only 10mins, and were "taught to perform gentle flexion and extension exercises…to enhance believability, counter venous pooling and prevent any possible orthostatic training effect."

In other words, if you are part of the HOT group, you are asked deliberately to restrain all those small internal willed (not autonomic) acts we learn to perform in order to make standing more tolerable for ourselves. You are saying to your ANS, "over to you–get on with it by yourself."

I still swear it is improving my state, but you will have to decide whether to give it a try for yourselves.

MeSci November 26, 2013 at 12:14 pm
Chris

Hi–Conception and any others actually considering trying the "back against the wall" "home orthostatic training " thing that I am still using–I have finally unearthed my copy of the complete text, which had gone awol (if you could see my apt you would understand) for a while, and give here the exact instructions ("inability to stand for up to 40mins due to muscular or neurological disorders" was an exclusionary factor–might have excluded me!).

Subjects were "asked to stand with their upper backs against a wall and their heels approximately 15cms from the wall with a cushioned 'drop zone'. They were asked to maintain this position without movement for up to 40 min or until they experienced symptoms."

The "without movement " is important; the control goup was instructed to stand for only 10mins, and were "taught to perform gentle flexion and extension exercises…to enhance believability, counter venous pooling and prevent any possible orthostatic training effect."

In other words, if you are part of the HOT group, you are asked deliberately to restrain all those small internal willed (not autonomic) acts we learn to perform in order to make standing more tolerable for ourselves. You are saying to your ANS, "over to you–get on with it by yourself."

I still swear it is improving my state, but you will have to decide whether to give it a try for yourselves.

That's interesting. I don't seem to have significant OI, but since getting ME I have (always?) found walking easier than standing, and gradually found that moving my legs when standing made it better, although still difficult. I've never thought of it as related to blood flow – more a muscular problem, but maybe this is an issue with me too. I hate having to wait in queues due to this problem!

Ember November 26, 2013 at 3:41 pm
Chris

I have now heard three local and credible stories of recovery from ME; two involved heavy use of a juicer….

Do you have any particulars, Chris? I'm planning to embark on that journey, but I'm hoping not to lose weight.

Chris November 26, 2013 at 5:24 pm

@Ember; if you juice much of your food, you probably will loose weight, and miss out on a lot of fibre too. These days I eat much of my veg raw, and use a small but fast blender too; my juicer feels a little abandoned.

I will just repeat the two references I gave above somewhere, to Joel Fuhrman's "Eat to Live" and also, maybe, his "Fasting and Eating for Life", which I have not read. And take a look at Terry Wahls–she has a TED talk on YouTube that gives you a lot in 17 mins or so. The keys are lots of dark greens–kale, chard, etc., and lots of bright colours–tomatoes, peppers, berries, that kind of thing. They split on other things–Fuhrman is pretty much vegan, while Wahls is Paleo–grass-fed animal protein, etc. I lean towards the Fuhrman angle on this, since I also have some documented coronary artery stuff to contend with. There is huge ongoing controversy on all this, with no clear winner in sight at the moment as far as I am concerned.

Fuhrman's big thing is "nutritional density," and dark greens rate high on this, as do berries. I think we all have to weave our own way around all the competing claims here, in the light of our individual bodies, tastes, tolerances, and aims. So I would rather head you off in several directions that have some fundamental relationship to each other–all exclude junk stuff of course–and leave you to choose the path that feels right for you.

The "FastDiet" thing is another take on this–intermittent fasting–that has some research behind it, but Mosley's book is too animal protein directed for me to be comfortable with it. But there is a good idea there too, if you have the discipline. I have reduced and delayed my breakfast in accord with his principles, however. Like you, I have no desire at all to lose weight, so have to be careful.

And choose your targets–mine are mitos, autoimmunity and coronary arterial health. Yours may be different. Gut health too– I like good raw sauerkraut and kimchi.

One more piece of advice–if you take lots and lots of chard, kale, broccoli, etc., watch your Thyroid Stimulating Hormone levels–mine went up somewhat, causing me to back off a bit, and also add a drop of iodine on a daily basis.
Good luck! Chris

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