• Welcome to Phoenix Rising!

    Created in 2008, Phoenix Rising is the largest and oldest forum dedicated to furthering the understanding of and finding treatments for complex chronic illnesses such as chronic fatigue syndrome (ME/CFS), fibromyalgia (FM), long COVID, postural orthostatic tachycardia syndrome (POTS), mast cell activation syndrome (MCAS), and allied diseases.

    To become a member, simply click the Register button at the top right.

Wolfe Hypothesis ~ Key causative processes involved in CFS/CFIDS/M.E.

Does this theory seem plausible?

  • Yes

    Votes: 9 23.7%
  • Didn't read it

    Votes: 5 13.2%
  • Not sure I fully understand it

    Votes: 5 13.2%
  • No

    Votes: 19 50.0%

  • Total voters
    38
Messages
15,786
Ok, let's take a look at the "Activity" section of your protocol:
Virtually every PWME who has recovered or is in remission will tell you that restoring physical functioning and strength is an integral part of a successful recovery strategy.
Do you have a citation? I've seen no good research showing GET or other activity to aid in recovery, and plenty of research showing it doesn't help, and some showing that it's quite harmful. Pretty much every PWME I've spoken to finds any increase in activity to cause setbacks.
It is important to bear in mind that if you try to push yourself before your health and energy levels are stable you may do more harm than good however
Citation? Many people do stabilize activity levels before attempting GET (that's how it usually works in the clinics), and it is still harmful and not helpful for them.
ME/CFS and OI expert, Dr. Rowe, would appear to agree with Plato: “complete inactivity has tremendously deleterious effects on the body”
The sources cited are an article and a hypothesis. There seems to be no research demonstrating Rowe's hypothesis to be accurate. Furthermore, ME patients are rarely completely inactive except in the most severe cases when there is very little ability to move. It also does not follow that GET is the appropriate alternative to complete inactivity, even if complete inactivity did exist.
He [Rowe] suggests therefore that physical activity is likely to be better tolerated, and the intensity of some ME/CFS symptoms reduced, if one focuses on improving peripheral movement restrictions by pursuing:
I see no citation for Rowe advocating any of these treatments. Furthermore, many patients find the exercise-based therapies to be harmful, and many studies have shown them to be of no help in physical functioning. SSRI's also affect many patients badly.
The manual physical therapy techniques (listed in order of lowest intensity above) and exercise-based therapies are likely to elicit a worsening of symptoms in the following 12-24 hours initially, until nerve ‘glide’ is improved, better tolerated, and thus the stimulation the sympathetic nervous system through physical activity is reduced
Citation? You seem to be suggesting that worsening symptoms should be ignored as a sign of illness, which is highly irresponsible given the damage that often results.
Hyperventilation/hypo-inflation of the lungs and hypocapnia (low Carbon Dioxide absorption) are often found to be an issue in PWME.
Citation? I believe most research has disproven this hypothesis.
Activity options: Below is a range of activities listed in order of lowest intensity, for those who have mild to moderate ME/CFS to consider, once they have done the groundwork:
The activities listed are not suited for moderate ME, which is still highly disabling. And even moderate ME patients will have priorities for their energy that have a more beneficial impact upon their lives - such as cooking dinner, going shopping, or even socializing. I also see no citation showing their effectiveness, and again, they are suggestions which many patients have found harmful.

You link to http://www.iacfsme.org/CFSandExercise/tabid/103/Default.aspx in suggesting recumbant exercise, but have ignored much more important advice - that research has suggested that ME patients must remain under a certain heart rate to avoid triggering a pathological response. Subsets are also discussed, with the realization that while some cases more similar to fibromyalgia might be able to improve somewhat from exercise, and that others will suffer severe relapse. It seems inappropriate for you to give the same advice to both groups, especially since your advice is only potentially applicable at the very mild end of the spectrum and very harmful at the other end. That source also specifies that all symptoms should be gone in the morning, not after "12-24 hours" as you stated above.
Going beyond a level 1 heart rate ceiling (50-60% of your maximum potential heart rate) is to be avoided at all stages of recovery. It is important to bare in mind that some will find even relatively mild activity puts them over this ceiling. Here is a handy ‘level’ calculator and here is further detail re: where to draw the line and why
These calculations are likely over-simplistic and contradicted by actual research. They are recommending I get my heart rate up to over 140bpm, while the research indicates most ME patients need to stay between 90 and 110. 140 would be guaranteed to put me into a crash, and a bad OI day I'll be over 110 just sitting up.
Healthy seating: Use an air cushion (to provide mobility), in combination with a reclined seated position or, a high stool (to mitigate against nerve tension by keeping hip flexion at <70 degrees).
Do you have a citation that this is appropriate for ME patients? Sitting without my feet up for a length of time can cause extreme OI problems. Much as a sore back is unfortunate - and I do get one at times - lack of oxygen to my brain is far more unpleasant.
PWME must therefore take a two-pronged approach to managing OI: avoiding prolonged periods spent standing still and avoiding lying down as much as possible during the day
I'm not going to argue about standing still really sucking, but lying down is necessary for many ME patients with OI issues. The alternative is called "passing out", and periodically laying down throughout the day can help prevent OI symptoms from becoming aggravated. Do you have any authority to cite for your assertion that lying down should be avoided.
Many PWME wake with a headache and this may, relate to cerebral hypertension induced in a supine sleeping position, another reason not to oversleep!
Citation?
Sleep with your head elevated if you experience OI
This may be good advice for people with simple OI problems uncomplicated by ME problems, but I have seen no research indicating it is useful for ME patients. Citation? My personal experience and what I've heard from other ME patients is that typical advice for training the body to compensate for OI does not work for us - or rather, it might work in the short term and then cause a crash due to the extra strain.
 
Messages
15,786
What term(s) did you use to search?
I can't speak for Kina, but I started with searching for a line out of your protocol and found your foo.mp3 identity. Searching for foo.mp3 brought up your real youtube account, as well as "Jools" and your last name, which led to your proper first and last name. Which leads to both of your middle names, your real facebook and google+ pages, your parents names, and your home address.

I hope you don't find any of this too creepy (we aren't stalkers), but anonymity on the internet is rather illusory, especially when you attach real photos to each account. Usually most of us wouldn't bother checking someone out, but people selling superficial remedies based on dodgy models of ME often have other dodginess which helps put their goals into perspective, and can help patients decide how trustworthy that person is.

In your case there really is no ulterior motive or major deceptions. Maybe a typo in your protocol where you say that you have medical training. But your other internet activity does show a lack of understanding about ME, and indicates that you have not engaged as part of the ME community. It helps in understanding that you really don't understand the importance of the context of the psychological research, and that you aren't deliberately suggesting that ME is psychosomatic, even though you suggest some of the same treatments due to your misunderstandings.

Your lack of engagement as a member of the ME community is your biggest problem. In addition to the impact it has on your assumptions about what you have read about ME, your lack of engagement is also somewhat offensive when you drop out of nowhere and start giving random advice. Many patients here have been ill for decades, and some have been researching in-depth for years and decades, and when you jump in and start giving a mixture of obvious and harmful advice, well - it makes it very hard to take you seriously.

I think you do have very useful skills in the area of reading, writing, and communicating in general. But you need the knowledge and experience to back that up, before you give anyone else advice.
Secondly, I suspect that as a moderator you are not supposed to take your moderator hat off e.g. ignore unjustifiably harsh treatment/become impartial at any stage? If moderators only acted when reports of behaviour with the potential to cause harm were made then forums such as this would soon become pretty lawless places..
Kina is a first and foremost a forum member. She is an unpaid volunteer who has ME, and is allowed to express her opinions even when they disagree with yours. Compared to most other forums I think you can see that this forum is not even remotely lawless - nor does it crack down on contrary and offensive opinions. The balance is that you get to tell us your opinions, and we get to tell you why you're wrong.
Sorry, when did I say I was any kind of scientist?
I am certainly not God’s gift to science but, for the record, I have a guy in my extended family who has a first class honours in biology and by now I know quite a bit more than he does in certain (relevant) areas – qualifications are beneficial/a good marker in some senses, but not a golden ticket to understanding everything related, nor are they necessarily the only route to answering important questions
Science doesn't require a specific degree, so much as a scientific approach to obtaining knowledge. Most of your claims in your protocol lack a scientific basis. Furthermore, most of us know more about specific areas of biology than our GPs do - and we know a lot more about it than you do. Not because we're smarter, but because we've been doing it for longer and usually with a bigger appreciation for scientific approach.
The video was uploaded 11 months ago, it was taken in Spring 2012, as my my latest relapse. was coming about by way of slow decline (hence looking washed out).
I think it is relevant - it shows that you were very healthy quite recently. At the very least it also shows that you only recently became aware of and interested in the central symptom of ME (PEM).
It’s aimed at people with ME/CFS, which implies something akin to CCC/ICC as I understand it, but like I say, refer to the hypothesis article intro should you require further clarification (I have now included PENE, as per the comments of one of the more antagonistic members who have posted here)
No one really cares about saying "PEM" versus "PENE". The problem is that your background and protocol show a complete lack of comprehension regarding how it affects our lives, and how PEM is triggered. An alternative title for your protocol could very well be "How to trigger PEM and OI difficulties in moderate ME patients".
I’m never content with the work as a whole, constantly developing/refining, hence the desire for ideas, feedback etc
It's been said many times, from many people, and I've now very specifically detailed the problems in my earlier post. Your advice regarding PEM and OI is inappropriate for most ME patients, and may even be harmful.
 

John H Wolfe

Senior Member
Messages
220
Location
London
Do you have a citation?
I did start off with links to the theory side in the protocol but then decided it was best to keep the theory to the theory article, save making it any longer/complex (for ease of digestion, very important given the brief)

I've seen no good research showing GET or other activity to aid in recovery
None of the studies that show a percentage of patients treated improved count as 'good' ones in your estimation?

Pretty much every PWME I've spoken to finds any increase in activity to cause setbacks
I find that amazing. I've known quite a few who don't find that but then I suppose it depends on the individual, progression of the illness, and where their 'starting point' is in terms of activity increase

Certainly it seems unlikely that increasing activity beyond that which is currently just about manageable will do anything other than cause PENE in the vast majority of cases, there is no disputing this

Furthermore, ME patients are rarely completely inactive except in the most severe cases when there is very little ability to move
Who said anything about complete? Rowe’s theory concerns relative not complete inactivity:

“…factors—such as whether the individual rests or remains relatively active—modulate the
response to a new stressor. For example, as has been demonstrated in experiments involving prolonged inactivity, reductions in plasma volume associated with long periods of bed rest would be expected to affect orthostatic tolerance … these changes in response to a new stressor could give rise to …further mechanical tension ... We hypothesize that this … contributing to further central sensitization. Central sensitization, in turn, could aggravate peripheral factors … The peripheral factors, central sensitization, and orthostatic intolerance would then contribute to further expression of CFS symptoms”

It also does not follow that GET is the appropriate alternative to complete inactivity, even if complete inactivity did exist
I wouldn’t be so bold as to affirm what is the optimal intervention, but I am working towards it and believe (rightly or wrongly) that incrementing up activity as one enters recovery is perfectly appropriate (see what Rowe has to say above to understand part of why I believe this to be the case)

I see no citation for Rowe advocating any of these treatments
In that case, allow me to assist you:

“…other ways of addressing central sensitivity are not excluded from this interplay. For
example, improving central sensitivity—through addressing autonomic symptoms with treatment of orthostatic intolerance [centred on enhanced water/salt intake and physical rehabilitation], or through improving central responses to stimuli via cognitive behavioral therapy, SSRI/SNRI medications, and anti-convulsant medications—might allow improved exercise and might improve the response to movement therapies [includes manual physical therapy and physical reconditioning]”

SSRI's also affect many patients badly
I’m not keen on pharmacological things, many of us have drug sensitivity and I just don’t think putting chemicals in a body, let alone one that struggles to detox properly, is a terribly good idea. Hence I do not advocate their use but do list them as optional supportive elements, as appropriate
As above, from Rowe as well as my own personal experience

You seem to be suggesting that worsening symptoms should be ignored as a sign of illness, which is highly irresponsible given the damage that often results
With physical therapies there is payback, unfortunately this is unavoidable on programs like Perrin’s, Rowe’s, and my own. Rowe started out advocating direct methods of nerve mobilisation when he started this research, he’s since suggested that indirect methods should be pursued first, and direct methods only to test for a positive response to improved toleration of mechanical tensioning

I believe most research has disproven this hypothesis
I’m not sure whether they are ongoing themes with most PWME, but they are sporadic themes with many of us e.g. I sometimes wake hyperventilating and people with comorbid respiratory/sleep disorders experience related issues. If you know of any comprehensive related studies that give a better idea of what proportion of us are affected by such issues I would welcome such a contribution

cooking dinner, going shopping, or even socializing
Good nutrition, doing physical things that are of practical/therapeutic nature, and socialisation are all part and parcel of my protocol – and at no point do I declare that patients should extend activities beyond their remit/at the expense of other therapeutic targets, or basic necessities for survival

that research has suggested that ME patients must remain under a certain heart rate to avoid triggering a pathological response
You’ll see I have included something on heart rate ceilings if you look carefully at my protocol..

It seems inappropriate for you to give the same advice to both groups
You’ll note the cautionary tone of my advice and that I make no direct prescriptions and leave it up to the individual to set limits that work for them

That source also specifies that all symptoms should be gone in the morning, not after "12-24 hours" as you stated above
Payback from (aerobic) exercise is not the same as payback from neural mobilisation techniques

They are recommending I get my heart rate up to over 140bpm
Your maximum heart rate is 230-280 bpm!?

Sitting without my feet up for a length of time can cause extreme OI problems
Of course people with extreme OI shouldn’t be using high stools, I’d have thought that was self explanatory?

The alternative is called "passing out", and periodically laying down throughout the day can help prevent OI symptoms from becoming aggravated. Do you have any authority to cite for your assertion that lying down should be avoided
Rowe. One of the world’s leading experts on OI. Btw I have POTS so you need not lecture me on the potential for blacking out

Thanks
 

John H Wolfe

Senior Member
Messages
220
Location
London
I can't speak for Kina, but I started with searching for a line out of your protocol and found your foo.mp3 identity. Searching for foo.mp3 brought up your real youtube account, as well as "Jools" and your last name, which led to your proper first and last name. Which leads to both of your middle names, your real facebook and google+ pages, your parents names, and your home address
Nice work - flattered by the effort that clearly went into that!

anonymity on the internet is rather illusory, especially when you attach real photos to each account
Like I've said before, my use of a pseudonym related to creating an account based on my stage name. Neither are an attempt to maintain anonymity

Maybe a typo in your protocol where you say that you have medical training
Oops! Haha

indicates that you have not engaged as part of the ME community
Performing an internet search doesn't make you an expert on me any more than it makes me right in my hypothesis. I've been a member of the 'ME/CFS Community' for many years (just not this one)

your lack of engagement is also somewhat offensive when you drop out of nowhere and start giving random advice
Sorry, is there some unspoken gagging clause on new members of PR I don't know about? How curious

The balance is that you get to tell us your opinions, and we get to tell you why you're wrong
No problem with that, just baffles me why some people get so rude/personal about it when that’s totally unnecessary, unprovoked, and counter-productive if they do truly wish to get a serious point across (rather than risking coming across as just fancying a bit of an anonymous internet rant at a perfect stranger who has only come here to share ideas/benefit people, and shown them no personal ill)

we know a lot more about it than you do
How dare I entertain for a second that I could even come close to knowing enough about my own illness to post here, let alone suppose even for a second that my level of knowledge/conceptualisation is anything but infinitesimal in comparison to yours. Hehe

it also shows that you only recently became aware of and interested in the central symptom of ME (PEM)
If you re-read you’ll note there’s no inference that I only became aware of PEM recently, sorry, incorrect. I only experienced ‘full blown PEM’ linked relapse, e.g. major PENE, for the first time last summer. This is a totally different statement to your umpteenth either deliberate or rather careless misrepresentation
 
Messages
15,786
I did start off with links to the theory side in the protocol but then decided it was best to keep the theory to the theory article, save making it any longer/complex (for ease of digestion, very important given the brief)
Sorry, doesn't work. Put in the citations, otherwise you're just blowing smoke.
None of the studies that show a percentage of patients treated improved count as 'good' ones in your estimation?
Nope. No objective improvements, lots of spin - you know, the sort of details you miss out on if you just read the abstract. If you believe otherwise, please cite the source and we can discuss it.
I find that amazing. I've known quite a few who don't find that but then I suppose it depends on the individual, progression of the illness, and where their 'starting point' is in terms of activity increase
Fascinating. Where did you meet them all, seeing as you haven't had therapy or engaged with online ME communities?

I wouldn’t be so bold as to affirm what is the optimal intervention, but I am working towards it and believe (rightly or wrongly) that incrementing up activity as one enters recovery is perfectly appropriate (see what Rowe has to say above to understand part of why I believe this to be the case)
How can you affirm ANY intervention? You can't cite to any research (versus articles) supporting anything you say about exercise. How about instead of you reinventing the wheel for your sole benefit, you take a look at the existing research and take a shot at coming up with something that might be useful for ME patients?
With physical therapies there is payback, unfortunately this is unavoidable on programs like Perrin’s, Rowe’s, and my own. Rowe started out advocating direct methods of nerve mobilisation when he started this research, he’s since suggested that indirect methods should be pursued first, and direct methods only to test for a positive response to improved toleration of mechanical tensioning
And we just need to ignore the payback and keep doing it! Where have we heard that before?
Good nutrition, doing physical things that are of practical/therapeutic nature, and socialisation are all part and parcel of my protocol – and at no point do I declare that patients should extend activities beyond their remit/at the expense of other therapeutic targets, or basic necessities for survival
This is where you are having a severe disconnect from the reality of moderate ME. Doing any of those activities will come at the expense of other activities. This likely holds true for mild ME as well. We are using up all of our available energy in living. For moderate ME patients this means that making dinner may use up everything we have. For mild ME patients, this often means that working part time or full time uses up everything they have.
You’ll see I have included something on heart rate ceilings if you look carefully at my protocol..
Yes, that's where the link with the level calculator is suggesting something far in excess of 90-110. My resting heart rate is about 80 (absent certain OI issues), age 34 and the "Target Heart Rate 1" (lowest listed) comes up at 136-147. If this isn't the result you intend, then you need to make that much clearer.
You’ll note the cautionary tone of my advice and that I make no direct prescriptions and leave it up to the individual to set limits that work for them
That's called "pacing". It is contradictory to GET, which you are advocating as well.
Payback from (aerobic) exercise is not the same as payback from neural mobilisation techniques
You say the 12-24 hour advice applies to both "Manual physical therapy" and "exercise-based therapies".

Of course people with extreme OI shouldn’t be using high stools, I’d have thought that was self explanatory?
Your links of "good posture" indicate we should only sit with our feet down. It also says to avoid sitting as much as possible, which impractical advice for patients with PEM and OI.
Rowe. One of the world’s leading experts on OI.
You have a serious aversion to citing sources. So far all I have is Rowe's hypothesis on a couple things, with no actual research studies.
 

snowathlete

Senior Member
Messages
5,374
Location
UK
I want to go into this a bit more, so hopefully John H Wolfe can understand the problem with his underlying premise. From what I can see, he only began taking a serious interest in ME and developing his protocol very recently, and his understanding of the biopsychosocial (BPS) theories is indeed quite superficial.

So what is BPS? It can sound good at first glance - biological, psychological, and social factors of disease are discussed, and how they can impact all disease. But the reality is that BPS theories limit biological roles to triggering or predisposing factors, and the disease itself is considered psychological, possibly aggravated by social factors such as ME patients being supported emotionally by their friends and family, or financially by their parents and the government.

In the case of ME, the "bio" of BPS is, at best, it being triggered by a virus. Then the "psycho" kicks in, and we are assumed to freak out as a result of being sick and continue to think we're sick after the virus goes away. Then there's more "psycho" as we engage in behaviors which are presumed to make us sicker, by not pushing our limits. Then there's a bit more "bio" acknowledged in the form of orthostatic intolerance(because ignoring low blood pressure problems would make the BPS school look extraordinarily stupid when any doctor can easily see them), but it is attributed entirely to deconditioning. Then there's a lot more "psycho" in the form of "medically unexplained symptoms", which is their nice way of saying "psychosomatic", and that is how anything that can't be explained by the deconditioning theory is dismissed.

So basically, the BPS school says that we make ourselves sick due to avoidant behavior based on the false belief that we are ill. The purpose of their version of CBT (not to be confused with normal CBT used to cope with chronic illness), is to stop us from thinking that we're ill and to put an end to our illness behavior. GET is used as the behavioral part of CBT, to supposedly show us that increasing activity won't hurt us - unfortunately, it has caused a lot of harm to many patients, as is discussed in Kindlon's paper posted above.

So how do we know the BPS school is so utterly wrong?

First of all, the group of researches and practitioners who form the BPS "school" is very small: a handful of psychologists and psychiatrists in England and the Netherlands. Simon Wessely is often considered to be their poster boy, but Peter White is also a prolific member, and Trudie Chalder and Esther Crawley also publish quite a bit of low-impact crap in the area. In contrast, there are thousands of biomedical papers published around the world which document biological dysfunctions which the BPS theories cannot account for.

The BPS school ignores this research, does not explain how it fits into a psychological/psychosomatic model, does not offer any proof for its theories, and badly spins weak results. One of the biggest weaknesses of the entire field of psychosomatic theory is that there is absolutely no proof of it - and there never can be. There is better discussion of this elsewhere on the forum (alex3619 is our resident expert) - but basically a psychosomatic theory relies on symptoms being unexplained. Yet a symptom being unexplained does not logically mean that symptom must be psychosomatic. It could biological, yet undiscovered by modern technology. The existence of psychosomatic causation of a symptom is unproven, and essentially unprovable - it makes no sense to cite a lack of known physical causation as the proof of psychosomatic causation, when there is a similar lack of evidence of psychosomatic causation. And if a hypothesis is unprovable, than it is unscientific by definition.

Here's a couple examples of the huge mistakes which psychosomatic assumptions can make. Multiple Sclerosis (MS) was medically unexplained until a few decades ago, presumed psychosomatic, and patients were treated much the same way ME patients are now. Then MRI scans of the brain showed lesions, and suddenly that perception changed. MS was never psychosomatic, yet an unscientific assumption was made based on the then-current lack of biomedical evidence. Another recent example is stomach ulcers. Once assumed to be caused by stress, they are now known to be caused by a specific bacteria, and can easily be treated with antibiotics.

The ridiculous thing in the case of BPS theories and ME, is that vast evidence already exists of physiological dysfunction which is not explained by their vague theories of deconditioning and activity avoidance. The ICC primer, for example, has a chart comparing documented objective physiological reactions of ME patients to exertion compared to normal or sedentary controls (pages 9 and 10), sources cited.

Another thing to know about BPS research is that objective measurements are almost never used. When objective measurements are used to assess the effectiveness of CBT, the show minimal or no improvement, though many BPS studies will not mention this, or will conclude that it proves that actually becoming more active is not needed to "cure fatigue". Questionnaires about symptoms are used to determine primary outcomes instead, and given that CBT consists of patients being told that their symptoms should be ignored or discounted, it is likely that that is reflected in their answers to some extent. Assumptions of mood disorders and mental illness are based upon the use of questionnaires where people are assumed to have a mental disorder if they have certain physical symptoms or behaviors - they'll label pretty much anyone with any multi-system illness as depressed, anxious, and psychosomatic. There is more discussion of these studies and questionnaires elsewhere on the forum.

Wolfe initially rejected CBT and GET on the basis that he doesn't have the problems that require those interventions - and he was right, but not just for himself. None of us have those problems, which is why a hypothesis and protocol based upon BPS treatments is inapplicable.

Fantastic post!
 

snowathlete

Senior Member
Messages
5,374
Location
UK
Are you posting in relation to the OP or to something else?

Just for clarity, my theory/advice is not based on the premise of ME/CFS being BPS as some would understand it, Val has just decided she doesn't like me or my theory, so much so that she has taken it upon herself to attempt to personally discredit me by misrepresenting my conception of the disease pathophysiology by raking up slightly unfortunate use of a term in an earlier version of my protocol article (that I didn't realise carried such connotations in the online community at that time) :thumbsup:

John, it's not just the term BPS, your protocol/theory is full of language used by the BPS group, and includes much of the same advice that they promote. I'm not going to point it all out to you and help you change the language because its presence helps show it for what it is (I think it's already accurate language for your protocol) :)
 

snowathlete

Senior Member
Messages
5,374
Location
UK
more specifically, I've received both diagnoses in the past

If you're comfortable saying - who exactly gave you these diagnoses and what were their qualifications, and experience with ME/CFS? What definition did they use to assess you for diagnosis?
 

John H Wolfe

Senior Member
Messages
220
Location
London
Sorry, doesn't work. Put in the citations, otherwise you're just blowing smoke
You're forgiven. Doesn't work for you but to date it's what's worked best in practice when introducing a select few people to the protocol 'properly'. The relevant citations I have gathered to date are within the hypothesis article, which serves as a reference section (linked to from the protocol) - in no way is this complete but it's still early days

Fascinating. Where did you meet them all, seeing as you haven't had therapy or engaged with online ME communities?
What do you mean I haven't had therapy? I haven't engaged with online ME communities? What on earth are you basing these statements on? An internet search!?

How can you affirm ANY intervention?
I don't affirm any intervention (as gospel), I have suggested people take a look at my protocol. Simples.

How about instead of you reinventing the wheel for your sole benefit
You propose to tell me my own business now? Hehe. You do make me chuckle

you take a look at the existing research and take a shot at coming up with something that might be useful for ME patients?
Have done, but always open to fresh insights, so if you have any (seminal) sources on related matters I'd be interested to look into them

And we just need to ignore the payback and keep doing it!
Nope, not what I suggest

This is one of the newest sections of the protocol, so I've just taken the opportunity to add a bit more explanation/caution so that this is as clear and as 'safe' as possible, without undermining the central brief

We are using up all of our available energy in living
I appreciate that there is not much room for manoeuvre so to speak in all but mild cases

My resting heart rate is about 80
My goodness, thanks for pointing that out, you’re right it seems that’s not an appropriate tool for this article!

That's called "pacing". It is contradictory to GET, which you are advocating as well
I advocate what I believe to be an appropriate mix of improving nourishment/energy, ascertaining workable levels of activity, and pacing. If you are worried that I am advocating GET (too much) in my protocol please quote the relevant excerpts and I will be better able to respond to your concerns

You say the 12-24 hour advice applies to both "Manual physical therapy" and "exercise-based therapies"
In terms of signs of SNS excitement yes. If PENE (broader than SNS effects) extends beyond 24 hours then you are not just sensitising an important system but also exhausting yourself. Clearly I need to develop this section carefully/more fully going forward

Your links of "good posture" indicate we should only sit with our feet down
I’ll be sure to add another addendum, thanks for pointing that out
 

John H Wolfe

Senior Member
Messages
220
Location
London
John, it's not just the term BPS, your protocol/theory is full of language used by the BPS group, and includes much of the same advice that they promote. I'm not going to point it all out to you and help you change the language because its presence helps show it for what it is (I think it's already accurate language for your protocol) :)
Helpful, thanks
 
Messages
10,157
Moderator Notice.

This thread is being closed for time-being.

After we have gone through to remove any personal attacks based on the following, it will be reopened:

pyramid resized 2.png


Anything that is a direct personal attack will be removed based on what is outlined in red.

As a reminder:


While we honor passionate and informed discussion we will not tolerate rudeness, insulting posts, personal attacks or purposeless inflammatory posts.

'Rudeness' means deliberately discourteous comments directed at another member. 'Insulting posts' are those that treat another member with deliberate rudeness and contempt. 'Purposeless inflammatory posts' are posts that are designed purely to provoke a reaction and cause an unpleasant argument.

Such behaviour is not tolerated here.

We take a very firm line on these forums regarding personal attacks, so it is important for all members to understand the difference between disagreeing with the content of another member's posts, and making a personal attack on someone.

Our definition of a 'personal attack' includes:

  • attacking a member's motivation for a post
  • attacking a member's character
  • referring to a member in a contemptuous manner
  • referring to a treatment that a member finds helpful in a contemptuous manner
  • belittling a member using sarcasm
  • questioning why somebody is present on the forum (accusing them of being a "mole" or a "troll")
  • questioning a member's affiliation with other groups
  • mocking a member's username
  • making negative or rude statements about administrators or moderators
  • attacking people or groups based on race, age, gender, sexual orientation or religious beliefs.
Disagreeing with comments made in another member's post does not constitute a personal attack. Members are allowed to refute the comments of other members and provide reasons why they don't agree. A member may also choose to contradict a comment and provide very little evidence to support their comments, and this does not count as a personal attack either. When a member chooses to attack the author of a post rather than the content of the post, that is a personal attack. Please keep your focus on the facts of the topic under discussion - not on the person with whom you disagree.
 

John H Wolfe

Senior Member
Messages
220
Location
London
I am interested to see what fellow members of the ME/CFS community make of the article that embodies this layman's attempt to better understand some of the processes that may be involved in the condition

In sharing this, and inviting constructive suggestions/feedback and discussion, I hope to benefit from your experience, insight and ideas so as I/we may better understand our illness


I appreciate that there is a lot of text to read and technical jargon/concepts to digest, hold onto, and make links between, so here is an abridged version of my current working hypothesis:

The main disease process(es) of ME/CFS relates to background peripheral nerve sensitivity associated with idiosyncratic tensioning, strain or damage of these nerves ~ leading to 'sensitisation': Neural Hyper-Sensitivity Syndrome (NHSS)

'Sensitisation' in this regard is the 'winding up' of the central and sympathetic nervous systems by (increasingly) 'noxious' sensory signalling from these (increasingly) sensitised peripheral nerves. This gives rise to neurological disorder under certain conditions e.g. sufficiently serious exposure/reaction/adaptation to various stimuli or 'stressors'

Unless this is corrected, over time neuroendocrine (hormonal) and neuroimmune abnormalities emerge/are worsened e.g. allergies, sensitivities, under/over active immune responses to infectious agents, and autoimmune responses to things like 5-HT, EBV, HERVs, H. Pylori

The central and peripheral effects of all of the above feed back into (further) neurogenic sensitisation. This chain of relations may provide something of an intuitive explanation for the clinically inexplicable, and seemingly inescapable, downward spiral in health and functioning experienced by PWME as/when they first become ill
 

overtrain

Medical Mafia needs to die via this virus.
Counting physical toil across the millennium of human history, why now nerves fail on us, and are, should this hypothesis pan out, failing us in clusters, e.g., Tahoe?

How does the hypothesis account for those previously always healthy, ate excellent nutritious food, exercised intelligently, and otherwise had physical, mental, environmental stresses under wraps? Then, for all intents and purposes, died? Or are, more accurately, now Zombies?
 

John H Wolfe

Senior Member
Messages
220
Location
London
Counting physical toil across the millennium of human history, why now nerves fail on us, and are, should this hypothesis pan out, failing us in clusters, e.g., Tahoe?
Essentially I consider sources of neuroinflammation (particularly chronic, including environmental ~ which may relate to clusters) to be risk factors

We have young people who are active now more than ever (influences spinal development), and yet we have adolescents and adults with desk bound sedentary lifestyles (influences nerve tension). This is one realm within which peripheral neural sensitisation may have chronic central sensitising effects, which I associate with neuroinflammation, and ME/CFS by extension

How does the hypothesis account for those previously always healthy, ate excellent nutritious food, exercised intelligently, and otherwise had physical, mental, environmental stresses under wraps?
Principally genetic and behavioural/postural vulnerabilities represent the core theoretical aetiology - sources of chronic neural sensitisation. Add to that other pressures e.g. viral/bacterial/toxic insult and you have the potential for uprated inflammatory responsiveness and autoimmunity in the context of pre-existing central sensitisation, with existing neuroendocrine and autonomic impacts

These responses aren't very comprehensive but hopefully it will resonate better with a wide variety of PWME once I've finished putting it together :) To give you an idea of all the elements I believe are involved, my discussion headings thus far are:

Neurogenic sensitisation (probably in most cases)
Central sensitisation (almost definitely in all cases)
Infectious agents (not in all cases)

Inflammation (all cases)

HPA/ANS dysfunction (probably in all cases)
Genes (probably in all cases)
Mitochondrial dysfunction (probably in all cases)
 

August59

Daughters High School Graduation
Messages
1,617
Location
Upstate SC, USA
I think some of this might be right, but its likely that its not complete nor fully right, and it will require further studies to investigate. Just today something was announced from several sources about a potential salivary biomarker for CFS: a PRB4 peptide. This is a protein that is produced by saliva (and possibly gut bacteria) that cleaves gluten. Gluten can cause celiac disease but also non-celiac wheat sensitivity (for which I think a paper was published recently showing this). The PRBs (there are at least 4) also bind dietary tannins, which are toxic. The biomarker was a fragment of PRB4, I am looking for a full molecular weight of PRB4 but it is proving hard to find a good reference. If its being cleaved in CFS, then the pieces will be less effective. Less effective PRB will result in more tannins and gluten reaching the gut and causing damage.

If on the other hand the PRBs are full length, then they will decrease tannins and gluten reaching the gut as we have too much of it ... so I think this interpretation is unlikely. The fragment they found was 2.6 kDa, which is a weight. One source refers to 27 kd for PRB4 which might also be a weigth ... so the peptide fragment is 10% or so and indicates cleavage or malformation of the parent PRB4.

This may be very important. It might lead to not just a diagnostic test but treatments. What I would like to see is a test assaying the function of our PRB4 in saliva, versus controls. This could tell us a lot.

http://www.aacc.org/events/annualmtgdirectory/Documents/AACC_12_Abstracts_E140-E208.pdf
(Scroll down to E-185)

Could you imagine causing a full CFS reversal by just popping an enzyme pill every time you eat? Awesome.

It is worth noting that elastase can cleave PRB4, though I don't know if it produces a 2.6 kDa fragment. High elastase is associated with high lmw RNaseL in CFS, and together are a potential biomarker.

I think the model presented here might be well served by examining it in light of recent work by Maes on autoantibodies, and also some stuff I am slowly assembling on secondary effects of LPS from the gut, including translocation of gamma delta T cells.

I can't cast a vote as my opinion is this model is mostly plausible, but I am not sure its fully plausible, and don't have the time to really investigate or make detailed commentary.

Bye, Alex

PS Correction: I had protein cleaving on my brain, doh, PRB4 might not cleave to gluten but bind to it, its a binding protein not a protease I think. I am not sure though: too much is not known about PRB4.

I hope this study will have been brought to Dr. Lipkin and CFI Initiative when they get around to studying the saliva samples.

As usual Alex, Thanks for the very good information.
 

John H Wolfe

Senior Member
Messages
220
Location
London
Hi, I'm going to reply here as it would be taking things a bit off topic in the other thread (doesn't really relate to risk of giving ME/CFS to a loved one)

this interesting and possibly-relevant recent abstract on microglial hyperactivation in older brains
Thank you that is indeed interesting:

"exaggerated neuroinflammation, sickness behaviour, depressive-like behaviour and cognitive deficits" ~ I steer clear of depressive behaviour but touch on each of the other elements in relation to microglia in my article :)

I have no spinal abnormalities AFAIK
I see. I wonder, have you been examined by an osteopath?

Just to be clear on my current thinking (appreciate I am not always too clear when rambling on about my various 'ideas'):

Dorsal defects are but one possible source of neurogenic sensitisation, in turn but one (if perhaps principal in ME/CFS) possible mechanism for chronic neural sensitisation, which in turn is but one (if perhaps principal in ME/CFS) possible source of neurotoxicity/neuroinflammation, which is but one (if perhaps principal in ME/CFS) pathological realm associated with the condition

my good posture has been remarked upon on several occasions!
Cool. When I talk about posture I refer mainly to Rowe's principals of degrees of ankle and hip flexion, as well as neck posture, in the context of possible chronic neuromuscular strain ~ tucked feet inducing ankle flexion, and more than 70 degrees of hip flexion (essentially any angle beyond a slightly reclined car seat - a normal chair would be beyond this and hence potentially strain inducing)

Nocturnal posture may also be very important, perhaps even more so (given the problems we tend to have with un-refreshing sleep ~ glutamate vs. GABA + < serotonin + < cortisol issues)
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
MeSci said:

I have no spinal abnormalities AFAIK

I see. I wonder, have you been examined by an osteopath?

No - never had cause to, and I am 60!

MeSci said:

my good posture has been remarked upon on several occasions!
Cool. When I talk about posture I refer mainly to Rowe's principals of degrees of ankle and hip flexion, as well as neck posture, in the context of possible chronic neuromuscular strain ~ tucked feet inducing ankle flexion, and more than 70 degrees of hip flexion (essentially any angle beyond a slightly reclined car seat - a normal chair would be beyond this and hence potentially strain inducing)

Nocturnal posture may also be very important, perhaps even more so (given the problems we tend to have with un-refreshing sleep ~ glutamate vs. GABA + < serotonin + < cortisol issues)

I gather that you are talking about hypermobility. I don't have any evidence of that either. I also sleep pretty well after switching to a gluten-free, low-sugar, low-grain diet plus certain supplements, albeit with a little help from mild sedatives. My own feeling is that my ME originates in the gut, especially as I had IBS on and off for decades before, and especially bad just prior to developing ME, plus the many benefits experienced from the new diet.