One CFS?

[Stretched]

This topic has been bantered around in various threads but what's current?

No one has wanted to hear, including me, for so many years - that "it", sic CFS, is all in our heads! Before someone starts blowing fuses let me offer my hypothesis. After all, it is just that, based on a long educated history of being plagued with "it", and following all the conflicting research.

Like most others I have been tested by various specialists to the point that I daresay I would go toe to toe with many doctors on what CFS is NOT! I have been able to rule out most scientific sourcing of a practical nature: viruses, bacterias, diseases known, and abnormal results on lab tests that otherwise turn out 'normal'.

Last year, after my local quack up and quit because she ran out of the standard voodoo, I began to look for a 'bigger' answer to this 'plague', e.g. how could it grow so exponentially and be so ubiquitous in such a relatively short time period over vast areas (the world). It is simply too intense a curve to not be correlated to something. OTOH, a communicable disease or singular pathogen can not (IMO) spread so far in so short of time AND have so many varying symptoms, expressed from mild discomfort to being bedridden and disabled.

I waxed philosophical and considered the bigger question: what is some singularity that most of the world's population are exposed to, i.e. that could carry or exacerbate (too often used word) a pathogen of some sort? I came up with a few possible contenders: the tear in the ozone layer; the atmospheric weather, e.g. high clouds, rain; UV radiation; and the like. Maybe, maybe not any of these. What's missing is correlation, i.e. provability. So, I looked inward, indeed.

What we all are subject to worldwide is internal. STRESS! Oh one asks and how? Consider an allegory using a serpent, the fast and predatory Black Mamba. It is deadly, and it will hunt you down!

The 'Fear Factor' exemplar: an otherwise reasonably healthy person is put in a fully self-contained house alone and must live there for 5 days. S/he was told the Mamba would be released in the other end of the house but s/he must remain for the whole time, e.g. to get $1million.

At the end of 5 days we 'test' that person for the effects of having participated (having tested the same vitals beforehand). No doubt that this experiment would generate some stress, to say the least!

What would vary would be the amount of stress and its affects on any individual crazy enough to get into this situation, and how each person handled it. Some would not make it overnight. Certainly not all would make it a week. Maybe some would but they would be torn individuals thereafter if they even made it to the end.

In the end each person would have experienced a nightmarish event and the affects would likely be permanent…even taking on a life of their own. This would happen even if the participant did NOT see the Mamba. Moreover, the affects would be the same even if the snake WERE NOT released into the house but the participant thought it was!

This situation illustrates what I mean by 'it's all in our heads' - but validly! Every person lives with degrees of stress and its affects are real! Some are from daily demands, others roll over from childhood and leave an indelible mark, some even to the point of lasting mental illness.

To say each day in the world is stressful for each individual would be an understatement, particularly if one considers it pre and post industrial revolution and pre and post the information age: communications has potentiated its prevalence and virulence around the globe exposing gaps between desire and ability to fulfill them, then magnifying all sorts of related inequalities!

This new awareness in the 21st century IMHO, the affects of stress, its severity and its longevity can account for virtually any legitimate symptom we know to be any expression of CFS.

The conclusion to this derived premise of 'it's all in our heads' is right on for me; I know for me that it doesn't lie elsewhere in my body as a pathogen per se, and I'm near housebound. Medications don't make it go away - only rest. By trial and error over 25+ years, ruling out other co-morbid conditions, and studying assiduously I have defaulted to biochemistry being the culprit, and specifically the HPA axis
and its damaged bio-activities.

Now the key question for me comes down to how will medicine unravel the malaise of those of us who became stress's victims and how will that susceptibility be blocked, sic for others who follow?

 

[jimmy86]

first, basically I do and I think we all should not care if it is my head, may feet or wherever. I just want to get healthy, whatever the therapy.
second, there is a poll about stress and cfs onset, a significant fraction of people did not have stress before cfs, and a even higher fraction of people out there is or was stressed and did not get cfs. a question, if any, we should rise is why did some of us react so badly to stress.

 

[Allyson]

one reason we may react badly to stress - we already hae too much adrenaline
Our bodies secrete extra adrenaline any time we are upright to vascoconstrict to counteract OI/POTS


so we are always in a hyperadrenergic state - this is going to make us feel more stressed more easily and often

OI/POTS is easily testable if done correctly

EDS will soon be testable by a simple gene test and that may resolve a lot of these arguments - already it is beig Dx in many with ME/cfs based on symptoms and family history

Ally

 

[alex3619]

Stress is far too vague to be of use as an hypotheses about CFS or ME.

With respect to CFS, we already know huge numbers have other disorders - they are misdiagnosed. I think its officially over 70% in Ireland, and 40% in the UK. So many disorders are missed in diagnosis, including genetic disorders and even disorders for which the blood test has failed - failures of testing are not uncommon, and may even account for over a third of CFS patients, something I am thinking about.

Biologists don't talk about stress, they talk about stressors. If you get up in the morning, you have stressors. Even when you were asleep, you have stressors. Stress is anything that induces physiological responses, particularly compensatory responses.

In the literature stress is so polymorphic it might as well be fatigue or pain we are talking about. All it does is transfer the emphasis from one far too general description, fatigue, and put it on another, stress. When you read the stress literature its all over the place. So exactly which stress are we talking about?

Now its premature to claim that a wide variety of stressors and responses (which is what is often called stress especially if it involves cortisol or adrenaline) have no impact on ME or in triggering ME. Something makes some people more vulnerable to viral infection. The current evidence though is that something is probably immunological or genetic.

One thing that I fail to see about stress claims though is how they can cause the specific physiological failures found in ME. How can they cause a dramatic change in repeat VO2max testing? This is not seen anywhere else. How can it cause problems in B cells sufficient that removing the cells with Rituximab can cause remission? How can stress cause sufficient changes to the immune system that our NK cells have highly abnormal cell surface markers? So far the explanations all rely on some variation of magic, or in modern terms "hand waiving". Stress can do anything (without evidence) so it can cause this (again without evidence). Its no better an explanation, in this form anyway, than vague psychosomatic claims.

So a prolonged stress response might alter the trigger response in ME, and so be a risk factor, but its highly unlikely to be causal. This is particularly the case with so many of us who are not particularly stressed, or are seriously into yoga, tai chi or meditation - these factors reduce psychological stress, though may not alter specific physiological stressors much.

What I would like to see from any stress hypothesis is specific testable mechanisms. Until we have that, and the hypothesis is robustly tested, stress is no better than any other unproven hypothesis about ME. So what stress response is expected in the HPA axis? What changes in the immune system? How does this change mitochondrial function in ways not seen in other disorders?

Stress is too vague. Its probably impossible to be completely wrong though, because stress is so general a term that any stressor, from environmental toxins to viruses and other pathogens, might cause or trigger ME. So whatever the cause, even if its little green aliens from Alpha Centauri doing it, stress will be involved. So will the mind. So, however, will the body, and all of this takes place in a cultural setting. I have just invoked a biopsychosocial stance ... and all without hard evidence.

I would like to put forward my own vague interpretation: it was all the Big Bang. That started it all. Blame that.

 

[alex3619]

Modelling Stress Factors In ME

If stress is to be taken seriously, then its possible to model it, create predictions, then test it. How would this start? It would have to include at least a partial match with pathophysiology and stress mechanisms, some hypothesis about how ME is triggered, and perhaps another for how it is perpetuated - or in other words, why don't patients get better all the time?

I suspect it might be possible to develop a detailed stress model. It would take a lot of work, a lot of effort, and probably a team of people, particularly if they had ME. Lets suppose this happened. It would then have to be promoted sufficiently that funding became available for a pilot study, or a series of pilot studies. With that data, presuming it supports the model, it would then be sufficient to apply for research grants, though this would require researchers, facilities, proposed methodology etc.

Further, it would be competing with other ME models. Given current progress I think it unlikely that a stress model will give us more than a model for increasing risk factors. I could be wrong of course. Nothing substitutes for actually doing experimental research.

 

[Allyson]

Stress is far too vague to be of use as an hypotheses about CFS or ME.

With respect to CFS, we already know huge numbers have other disorders - they are misdiagnosed. I think its officially over 70% in Ireland, and 40% in the UK. So many disorders are missed in diagnosis, including genetic disorders and even disorders for which the blood test has failed - failures of testing are not uncommon, and may even account for over a third of CFS patients, something I am thinking about.

Biologists don't talk about stress, they talk about stressors. If you get up in the morning, you have stressors. Even when you were asleep, you have stressors. Stress is anything that induces physiological responses, particularly compensatory responses.

In the literature stress is so polymorphic it might as well be fatigue or pain we are talking about. All it does is transfer the emphasis from one far too general description, fatigue, and put it on another, stress. When you read the stress literature its all over the place. So exactly which stress are we talking about?

Now its premature to claim that a wide variety of stressors and responses (which is what is often called stress especially if it involves cortisol or adrenaline) have no impact on ME or in triggering ME. Something makes some people more vulnerable to viral infection. The current evidence though is that something is probably immunological or genetic.

One thing that I fail to see about stress claims though is how they can cause the specific physiological failures found in ME. How can they cause a dramatic change in repeat VO2max testing? This is not seen anywhere else. How can it cause problems in B cells sufficient that removing the cells with Rituximab can cause remission? How can stress cause sufficient changes to the immune system that our NK cells have highly abnormal cell surface markers? So far the explanations all rely on some variation of magic, or in modern terms "hand waiving". Stress can do anything (without evidence) so it can cause this (again without evidence). Its no better an explanation, in this form anyway, than vague psychosomatic claims.

So a prolonged stress response might alter the trigger response in ME, and so be a risk factor, but its highly unlikely to be causal. This is particularly the case with so many of us who are not particularly stressed, or are seriously into yoga, tai chi or meditation - these factors reduce psychological stress, though may not alter specific physiological stressors much.

What I would like to see from any stress hypothesis is specific testable mechanisms. Until we have that, and the hypothesis is robustly tested, stress is no better than any other unproven hypothesis about ME. So what stress response is expected in the HPA axis? What changes in the immune system? How does this change mitochondrial function in ways not seen in other disorders?

Stress is too vague. Its probably impossible to be completely wrong though, because stress is so general a term that any stressor, from environmental toxins to viruses and other pathogens, might cause or trigger ME. So whatever the cause, even if its little green aliens from Alpha Centauri doing it, stress will be involved. So will the mind. So, however, will the body, and all of this takes place in a cultural setting. I have just invoked a biopsychosocial stance ... and all without hard evidence.

I would like to put forward my own vague interpretation: it was all the Big Bang. That started it all. Blame that.

Agree with you on all Alex except for the big bang - it was the moon landings that caused it

Ally

 

[Allyson]

Modelling Stress Factors In ME

If stress is to be taken seriously, then its possible to model it, create predictions, then test it. How would this start? It would have to include at least a partial match with pathophysiology and stress mechanisms, some hypothesis about how ME is triggered, and perhaps another for how it is perpetuated - or in other words, why don't patients get better all the time?

I suspect it might be possible to develop a detailed stress model. It would take a lot of work, a lot of effort, and probably a team of people, particularly if they had ME. Lets suppose this happened. It would then have to be promoted sufficiently that funding became available for a pilot study, or a series of pilot studies. With that data, presuming it supports the model, it would then be sufficient to apply for research grants, though this would require researchers, facilities, proposed methodology etc.

Further, it would be competing with other ME models. Given current progress I think it unlikely that a stress model will give us more than a model for increasing risk factors. I could be wrong of course. Nothing substitutes for actually doing experimental research.

yep..... and they could start by measuring cortisol levels - say recumbent and upright .....


Ally

 

[Stretched]

I would like to put forward my own vague interpretation: it was all the Big Bang. That started it all. Blame that. Psychobabble ... I can't believe its not science!

I couldn't agree more - all the perambulations about the myriad of unconnected causes is just that - psychobabble!

My thesis is one of degrees not absolutes. It also considers other perturbations to affect the curve of symptoms and their severity(ies), i.e. a twitch, a cough, a headache, restless leg syndrome, insomnia, memory loss, progressing...
ad infinitum... .

Any alternative other than tripping the light fantastic?

 

[ukxmrv]

You really haven't put forward a hypothesis for anyone to comment on Stretched.

If it was "stress" then how do you explain your symptoms?

I don't think that you will get much of an argument that people are being diagnosed with CFS when there could be another explanation for their symptoms. you are talking about your own experience of "CFS" but you haven't defined which version of CFS you have been diagnosed with. let alone all the testing you have had on stress related pathways in the body.

What is your cortisol doing and if you don't know, then why don't you know? It seems that you have ruled out all viri, bacteria so why not bite the bullet and have this area tested as well. why not do full HPA workups with doctors who have an interest in that area and see what you find out. You have obviously read all the papers in this area on CFS and the HPA axis and spoken to doctors - why not explore your theory to the full and actually come up with findings that would support you.

Dcotors and patients who think that their CFS is caused by "stress" have had decades to do tests and put forward theories but where has this led us to? No where , no evidence, no tests. It's like Gupta and his theories - all this time and money from patients and still not one test.

You may as well put forward an argument that you are possessed by devils or it's a god or something else dogma like. They are just words. Stress can mean many things to many people.

So, where is the evidence that stress causes your CFS and why would you have a diagnosis of CFS if it did? why not another diagnosis (depression, anxiety, burnout etc).

 

[Allyson]

I couldn't agree more - all the perambulations about the myriad of unconnected causes is just that - psychobabble!

My thesis is one of degrees not absolutes. It also considers other perturbations to affect the curve of symptoms and their severity(ies), i.e. a twitch, a cough, a headache, restless leg syndrome, insomnia, memory loss, progressing...
ad infinitum... .

Any alternative other than tripping the light fantastic?

if you look into connective tissue (disease) you see the connections and the causes and it all makes logical sense - no psychobabble there

A

 

[alex3619]

EDS is a special case, I think. Once upon a time it was the stretch-bendy people disease, and not taken seriously. Now we are coming to realize that its a range of different disorders, that probably not all of them have been identified yet, and that it can occur in people who are not particularly bendy or stretchy. I perhaps came across EDS in about 2000, when I was talking to a researcher whose daughter may have had it, and possibly fibromyalgia as well. Its still not well understood or recognized by most doctors so far as I am aware.

Just in my time in watching the literature, I have seen a number of "new" disease discoveries that can account for some cases of CFS. In particular there were the several different cortisol-binding globulin mutations. I was a test subject in a follow-up study on that. How many people with CFS are ever tested for this? I would be surprised if it were more than a few thousand world-wide. Its a rare disorder, why should doctors bother? However multiply that issue by thousands of rare and yet undiscovered genetic disorders, and possibly hundreds of as yet undiscovered diseases/disorders that are not genetic, and how many CFS patients would that account for?

Most people have not had every test there is that could tell docs what is going on in CFS. There are simply too many tests, and the vast majority are not available outside of research labs. Not every test is commercialized - if the market is small, nobody will bother making the test available.

Whereas many long term patients have had all the standard stress-related tests. There are often minor abnormalities (low or shifted cortisol response) but nothing that has been identified as causal. A stress hypothesis needs a lot more development. Most serious claims re stress come from psychiatrists, and many of those practice psychogenic medicine. So far they don't have a lot of indisputable evidence, just an impressively long list of claims.

Stress has to be defined in the model. It has to be measurable. Mechanisms linking that measurable stress have to be shown to induce typical ME pathophysiology. I am not going to bother citing CFS pathophysiology aside from this comment, as the cohort is too heterogenous for serious research. Subsets of CFS, defined by biomarkers, might however be candidates for such research.

PS In case people missed it, the cortisol binding globulin mutations alter the stress response somehow. I do not know if this is yet understood. However this is a very rare disorder, and inherited.

 

[peggy-sue]

There is an excellent paper on differing physiological responses to social stress, using the tree shrew as an animal model, written by Dietrich von Holst, published in 1986.
It demonstrates clearly that there are three phenotypes of behavioural and physiologoical reponse to stress.


Von Holst D 1986 Psychosocial stress and its pathophysiological effects in tree shrews (Tupaia belangeri). In: Schmidt TH, Dembrowski TM, Blümchen G, eds. Biological and psychological factors in cardiovascular diseases. Heidelberg: Springer-Verlag 476–490

While searching for that paper I actually found it as a reference in this one. There seemed to be a fair bit came up on stress and colonic stuff, all of which seems to use the '86 paper as a reference.
You might find some of it very interesting, Alex.

http://endo.endojournals.org/content/148/2/670.full#ref-list-1

 

[alex3619]

Adrenal Insufficiency and Colonic Inflammation after a Novel Chronic Psycho-Social Stress Paradigm in Mice: Implications and Mechanisms

Reber et. al.

CHRONIC STRESS IS a potential risk factor for the development of gastrointestinal disorders, such as irritable bowel syndrome or inflammatory bowel diseases, including ulcerative colitis. Both animal and human studies demonstrate that exposure to various stressors affects the functional integrity of the gastrointestinal tract leading to altered production and release of mucin and impaired colonic mucosal barrier functions, which may result in increased antigen infiltration.

Thanks peggy-sue . I did find this bit interesting, but have yet to read the full paper. A key feature in the development of ME seems to be increased gastrointestinal permeability. In this paper it is claimed that psychosocial stress can induce that. This has two implications. The first is that psychosocial stress might be a risk factor, which I have already mentioned. The second is that psychosocial stress might be a perpetuating factor if increased gut permeability is important in maintaining ME, which I think it is.

This implies, but its only implication, that psychosocial stress might be a risk factor both for inducing ME and maintaining ME.

Maybe how we are treated by others, including most doctors and psychogenic psychiatrists (pp) is not just unpleasant and disempowering, but actually part of the problem?

 

[Allyson]

EDS is a special case, I think. Once upon a time it was the stretch-bendy people disease, and not taken seriously. Now we are coming to realize that its a range of different disorders, that probably not all of them have been identified yet, and that it can occur in people who are not particularly bendy or stretchy. I perhaps came across EDS in about 2000, when I was talking to a researcher whose daughter may have had it, and possibly fibromyalgia as well. Its still not well understood or recognized by most doctors so far as I am aware.
........

Yes I think you are quite right here Alex - I am not hypermobile at all but I have EDS - it is another with a huge range of symptoms that makes it hared to categorise or get a good grip on. And it is not JUST hypermobility - there are still doctors who ignore all the hypermobility symptoms altogether too! here is a utube clip of a guy bending his arms backwards up his back to and extreme degree - dislocating his shoulders in the process - and the docs told him he had " normal range of movement !" (Well, at least ME/cfs is not the only disease that has been overlooked a lot to date.)

I also just saw a fb page for a disease called "stiff person syndrome" that I have never hear of before and am wondering what it entails - on musculoskeletal grounds I think I would qualify.....


Ally

 

[Stretched]

Modelling Stress Factors In ME


Further, it would be competing with other ME models. Given current progress I think it unlikely that a stress model will give us more than a model for increasing risk factors. I could be wrong of course. Nothing substitutes for actually doing experimental research.

<<If stress is to be taken seriously then its possible to model it, create predictions, then test it. How would this start? It would have to include at least a partial match with pathophysiology and stress mechanisms, some hypothesis about how ME is triggered, and perhaps another for how it is perpetuated - or in other words, why don't patients get better all the time?>>

No intent nor response to ad hominem arguments... .

I disagree, Alex. Some things are not measurable nor meant to be (yet) but can 'generally' be attributed to causing adverse reactions in humans. Some are specified, some are not. For example, what quantity of second hand smoke does it take to do what kind of damage; or what quantity of 'x' is required for a personality to be measured - yet we all know it when we see it?

Thoughts are another construct of immeasurability that most definitely have psycho-biological affects as in the Black Mamba metaphor. While the components are immeasurable it is pretty well scientifically engrained that a change of thinking yields a change in the person whose thoughts are changed, a la via therapy.

CFS is NOT a lot of things which have been measured, ergo then it is a result of something which has not been measured (yet), stress. Like Clinton posited: it depends on what is, is. How much stress does it take to produce a headache versus heart palpitations or a nervous breakdown? Measurement? - not doable, yet.

My thesis is that what is being measured are the results of stress - strains, if you will. It is not unknown bugaboos nor the other calculus to which I referred in opening this thread. IMO, CFS is/are the strains, sic the results of stressors. For its dynamics, I defer to any respected biochemistry text to explain some of minutiae which is known today relative to the hormonal system and the aberrations in cortisone/adrenaline, et al.

What isn't known in current technology resides between those lines. We aren't capable of measuring the correlations of the zillions of electrical impulses that are interrupted in that system, in this case by stress. It just is (there) and we can infer it. It's like in quantum physics, i.e. not observing the quanta we know is there, the borons, bisons and other
immeasurable but statistically probable -ons, anti-matter, etc.

This is where the etiology of CFS lies, IMO. Some portions of these systems are out of whack. I would not begin to venture which ones or where for fear of proseleytizing quackery.

What I think is that medicine is wasting its time and resources looking for a boogeyman, after
all the years of chasing various suspects only to run asunder. Rather, it should acknowledge the already known affects of CFS and correlate them not to a fixed model but to an arbitrary continuum of known stressors within which is the 'circle' of each PWC. Accumulate that data, of course while treating the symptoms and back into some more definitive parameters of tit for tat.

I hope the above gets across the gist of my premise. This is a big issue and I'm still developing my 'science' by backing into it. What say you?

Afterthought: Consider medicine 150 years ago as an example of looking in the wrong place. Malthusian economics aside, how much larger the curve of population would have steeped had it not treated illness by bleeding the patient or starting an infection away from the wound to draw the evil bacteria away from it? That was the then Gold Standard; today's is the DBDC studies which take forever to get what kind of results? There's a corollary to it - that
the trial being studied works for some (percentage of) people all the time!

 

[alex3619]

CFS is NOT a lot of things which have been measured, ergo then it is a result of something which has not been measured (yet), stress.

If something is not A, then it must be something other than A, let us call that B. This rests on multiple logical flaws. First, why not C, or D, or E or .... Second, what if we are wrong about not A?

Enteroviruses are not ruled out as causing ME, for example. The arguments against enteroviruses that have so far been used have instead been ruled out.

ME has many characteristics of an autoimmune disease. An autoimmune cause is not ruled out.

Unknown pathogens are not ruled out.

Unknown consequences of known pathogens are not ruled out.

Is stress possible? Yes. Is it credible? That is a whole other question.

Here is the psychogenic fallacy:

"Premise 1. If there is no known physical cause for a
condition, there is no actual physical cause for the
condition.

Premise 2. If there is no actual physical cause for the
condition, the cause must be psychological.

Conclusion (The psychogenic inference). If there is no
known physical cause for the condition, the cause must
be psychological."
(p. 312 Functional,Reasons, Neuroscience and the Psychogenic Inference )
http://forums.phoenixrising.me/index.php?entries/the-witch-the-python-the-siren-and-the-bunny.1149/

This is the same pattern of argument as the above quote. Its fallacious. That doesn't mean the conclusion is wrong, it means the reasoning is wrong: stress might indeed be the cause, but its not because of the reasoning.

Premise 1. If there is no known non-stress cause for CFS, there is no actual non-stress cause for CFS.

Premise 2. If there is no actual non-stress cause for the
condition, the cause must be stress.

Conclusion (The psychogenic inference). If there is no
known non-stress cause for the condition, the cause must
be stress."

This argument is a fallacy.

Claiming stress as an hypothesis is fine, but the onus is on those proposing it to provide evidence and argument.

The first hurdle is demonstrating CFS is one condition. Its clear it is not. Up to 90% in some cases are misdiagnoses, and about 40% is typical in the UK.

Treating CFS as one unitary disease is a huge mistake in my view. This may be the biggest hurdle researchers have had to face: how do you find a single cause of one unitary thing, if it turns out to be a hundred things with a hundred causes? You can't.

Psychogenic medicine tries this because the mind is magic, though they don't actually state that. It might be the mind, the mind can do all sorts of stuff, ergo it is the mind. If this was treated as an hypothesis, with rigorous testing, specific predictions etc. and not treated as real until the science is done, then I would have no problems with psychogenic medicine. By coming down with such firm conclusions as they have, with limited evidence, and fallacious reasoning, I have huge problems with it.

Statistical association (i.e. correlation) as the only important thing will mire the entire research program in dogma and error. Association is not causation, though causation is association. Science has to be based on more than just a few associations.

 

[Tito]

Stretched
You found that in your case stress is a factor of your illness. However, it is unclear whether it is the trigger of your illness, a perpetuating factor, or the feeling felt whenever you have to deal with a situation.

Let's say the word "stress" has the meaning given by the layman, ie. daily small repetitive frustrations, fast pace of living, any act in a situation where there is a lot at stake, etc.
If stress was a causation, some specific professions would have been clearly identified, such as air controllers, financial derivatives traders, etc. I have never heard about a study showing this. Stress as a perpetuating factor, well, what stress? What is perceived only by the patient or what is perceived by the average person in the same situation? That leads to the third point: the 'stress' felt in whatever undesirable situation we are in. This is, in my humble opinion, a symptom of ME/CFS, nothing else.

My experience thaught me that many people associate stress to ME/CFS because they notice that when they feel stressed, they get worse. So stress is the cause of their illness. My reasoning is different: if I walk with a broken leg and it hurts, pain is not the cause, nor the perpetuating factor of my broken leg, it is the broken bone. I think, but I might be completely wrong of course, that stress is of little relevance -even though it massively impacts quality of life-. In my analogy, it is just that we haven't discovered x-rays yet to see the broken bone.

 

[peggy-sue]

The important point of the von Holst paper was to show that there are three types of behavioural and physiological response to the stress.
He characterised the three types as dominant, sub-dominant and submissive.

Under prolonged social stress, the dominant beasts thrived, the subdominants survived, the submissives died.

 

[Tito]

The important point of the von Holst paper was to show that there are three types of behavioural and physiological response to the stress.
He characterised the three types as dominant, sub-dominant and submissive.

Under prolonged social stress, the dominant beasts thrived, the subdominants survived, the submissives died.

And this research on mice applies to ME/CFS patients in what way?

 

[peggy-sue]

It was the tree shrew paper by von Holst which demonstrates there are three types of response to social stress, Tito.
I'm not discussing an application to patients.
I'm talking about basic stress research. If any hypothesis is not three-tailed, you can dismiss it outright!

This impacts all research into anything to do with stress. There are three completely different basic normal responses.