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Patients with ME/CFS and chronic pain report similar level of sickness behavior as individuals injected with bacterial endotoxin... 2019, Jonsjö et al
- Thread starter Hoopoe
- Start date
I wasn't sure what they meant by 'sickness behaviour'. They give an alternative 'the sickness response' in the intro. and say this:
They judge this as good behaviour for acute illness.
But bad behaviour for chronic illness:
How do they know. That sounds like value judgement, not science. Assumptions being made from association to causal direction. Reminds me of 'fear avoidance', ... BPS. Later in the paper they say this research doesn't give evidence for causal directions, but they still say therapy is likely to be helpful (acceptance and committment therapy seems to be flavour of the month rather than CBT).
They didn't find an association between severity of illness and sickness behaviour in ME, but did in chronic pain. Perhaps that's an indication of the limitations of their sickness behaviour questionnaire:
It's a 10 statement thing a bit like the Chalder FQ. The scores are 0,1,2,3 for each item, giving a maximum score of 30.
I wish to keep still
My body feels sore
I wish to be alone
I don't wish to do anything at all
I feel depressed
I feel drained
I feel nauseous
I feel shaky
I feel tired
I have a headache.
They seem to be jumbling together physical symptoms, psychological effects and behaviours.
They judge this as good behaviour for acute illness.
But bad behaviour for chronic illness:
How do they know. That sounds like value judgement, not science. Assumptions being made from association to causal direction. Reminds me of 'fear avoidance', ... BPS. Later in the paper they say this research doesn't give evidence for causal directions, but they still say therapy is likely to be helpful (acceptance and committment therapy seems to be flavour of the month rather than CBT).
They didn't find an association between severity of illness and sickness behaviour in ME, but did in chronic pain. Perhaps that's an indication of the limitations of their sickness behaviour questionnaire:
It's a 10 statement thing a bit like the Chalder FQ. The scores are 0,1,2,3 for each item, giving a maximum score of 30.
I wish to keep still
My body feels sore
I wish to be alone
I don't wish to do anything at all
I feel depressed
I feel drained
I feel nauseous
I feel shaky
I feel tired
I have a headache.
Hoopoe
Senior Member (Voting Rights)
Playing the scientist here for a moment.
A fairly obvious interpretation of these findings is that the inflammation triggered by LPS is just one way to obtain a sickness response. What we call sickness response may be a variety of overlapping responses to illness that vary according to the characteristics of the illness. In other words, it would be a human construct that is convenient but also a generalization.
It seems possible that some chronic illness is due to dysregulated brain responses but being unable to explain why patients are chronically ill is an insufficient reason to believe that this is occurring. That sort of reasoning would be the absence of evidence is evidence of absence fallacy which plagues the thinking around these kinds of problems. It's more useful to think that our lack of knowledge makes it hard to reason about these problems.
Which suggests that ME/CFS is not like these other conditions but somehow different and that other kinds of signals may be involved. Assuming that these differences aren't due to sampling bias which could easily be the case.
Are they suggesting that patients, over time, become experts at managing their own illness?
That seems to be the usual claims made by placebo and blinding illiterate scientists. In fact in order to make progress, it is very important that we no longer waste time and resources on ideas that are not or cannot adequately be tested.
More as thought experiment, I'm curious what would happen if instead of the same old positive psychology ideas they tried a psychosocial therapy approach as if designed by experienced patients. That could look something like this:
* They have a chronic illness that cannot currently be cured and that they should adapt to this new reality (nonpositive outlook is OK).
* They should communicate their suffering to others (catastrophization is OK).
* They should not be trying to control the illness but focus their efforts on what they can actually control (no trying impossible feats or mind over matter magic).
* That receipt of disability benefits is helpful and improves outcomes (one of the best interventions against anxiety is not having to worry about ending homeless, starving, etc).
* That they should listen more to their body and rest more (positive relationship with their body).
* Mobility aids would be encouraged.
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mango
Senior Member (Voting Rights)
https://openarchive.ki.se/xmlui/handle/10616/46839Jonsjö thesis on sickness & behavior in ME/CFS said:
Sickness & behavior in ME/CFS (Chronic Fatigue Syndrome) - Jonsjö, Martin 2019 (Thesis)
Thanks for reading/assessing this @strategist and @Trish.
It is very disappointing to see the Karolinska Inst involved with this kind of garbage.
I guess I probably had "sickness behavior" once, when I had flu about 23 years ago and spent most of 2-3 days in bed. This is completely different to how my daughter, and others "act/feel" due to their ME.
Neither does it have any similarity to the ongoing pain from my spinal abnormality, and the way I have to modify my activities accordingly.
How long can they go on with these waffly, circular arguments and waste research money?
It is very disappointing to see the Karolinska Inst involved with this kind of garbage.
I guess I probably had "sickness behavior" once, when I had flu about 23 years ago and spent most of 2-3 days in bed. This is completely different to how my daughter, and others "act/feel" due to their ME.
Neither does it have any similarity to the ongoing pain from my spinal abnormality, and the way I have to modify my activities accordingly.
How long can they go on with these waffly, circular arguments and waste research money?
mango
Senior Member (Voting Rights)
I agree, super disappointing
I've heard rumours (a researcher told a friend of mine) KI might be interested in doing another ACT for ME/CFS study too Testing this model seems to be part of other planned studies as well, for example this one: Craniocervical dysfunction, neuroinflammation and infection in ME/CFS ws healthy controls (planned study) Bragée Clinic, Sweden
Psychological flexibility is said to be "an important part" of the investigation. Gunnar Olsson is involved in both studies.
(I wonder if OMF will be financing any part of the planned study, and if so, what's their view on the BPS aspects of the project?)
rvallee
Senior Member (Voting Rights)
Really bizarre to frame symptoms like fatigue and pain as "behaviors". Not much point in reading further from that, frankly. I guess boiling water has a steaming behavior, or something? Words have meaning for a reason, stick to that meaning damnit.
The SicknessQ questionnaire is pretty much junk, no idea how anyone thinks it's of any relevance. I'm also not sure of the value of comparing to something that is not really itself well-understood. What is the level of sickness of people injected with bacterial endotoxin? And who would know that? Not much point comparing to something that hardly anyone can relate to. Comparing to the flu would probably have similar results, why not do the common sense thing instead?
It's trying to compare chronic illness to an acute illness episode. I really don't think it can be argued that acute illness itself causes anxiety, it's typically framed only in the context of chronic illness as an alternative explanation rooted in magical psychology. Are people sick with the flu anxious about having the flu? Not really. What does that even mean? They're sick and don't give a damn what you think as long as they're sick, are simply waiting for it to pass while minimizing how horrible it feels.
We and those physicians are not talking about the same things. At all. Not understanding illness makes for very poor medicine. Like an amusical music producer who doesn't listen to feedback and has in fact never heard music in their entire life, there's just an irreconcilable gap of understanding.
The SicknessQ questionnaire is pretty much junk, no idea how anyone thinks it's of any relevance. I'm also not sure of the value of comparing to something that is not really itself well-understood. What is the level of sickness of people injected with bacterial endotoxin? And who would know that? Not much point comparing to something that hardly anyone can relate to. Comparing to the flu would probably have similar results, why not do the common sense thing instead?
It's trying to compare chronic illness to an acute illness episode. I really don't think it can be argued that acute illness itself causes anxiety, it's typically framed only in the context of chronic illness as an alternative explanation rooted in magical psychology. Are people sick with the flu anxious about having the flu? Not really. What does that even mean? They're sick and don't give a damn what you think as long as they're sick, are simply waiting for it to pass while minimizing how horrible it feels.
So I guess people with "legitimate" chronic illnesses don't display "sickness behavior" then? MS? RA? Parkinson's? No sickness behavior? Since none of those are short-term. What do they cause then? Nothing? Is it just a labeling issue? Just a superficial feature, like the length of your hair? This flies in the face of common sense.
We and those physicians are not talking about the same things. At all. Not understanding illness makes for very poor medicine. Like an amusical music producer who doesn't listen to feedback and has in fact never heard music in their entire life, there's just an irreconcilable gap of understanding.
Sly Saint
Senior Member (Voting Rights)
I sometimes wonder if any of these researchers have ever been really sick.
Ravn
Senior Member (Voting Rights)
The term sickness behaviour is highly unfortunate but it's worth remembering that it originates from the sort of behaviour mice display after you've injected them with something nasty like a virus: they behave like sick mice.
Unfortunately the term sickness behaviour when applied to humans is sometimes used in the same sense as in mice but at other times as a conscious or intentional behaviour (you can change by changing your thoughts). Cue confusion and talking past each other all round.
Haven't yet read the full paper yet so don't know how sickness behaviour is used here but the first few sentences of the intro seem to indicate the physiological version?
ETA:
Have now skimmed the whole paper. Doesn't strike me as bad as all that. Though I also don't quite see the point in it. But at least 'sickness behaviour' here is used in the basic, physiological sense, nothing to do with how you choose to behave but simply about how lousy you feel.
Three parts to the study (ME patients met both Fukuda and ICC, all self-reported measures) - I'll attempt to report the key points I took from it without using the term 'sickness behaviour':
Document how sick we feel compared to other groups. Result: comparable to chronic pain and the human guinea pigs who volunteered to get an "injection of LPS, a substance effective at activating the immune system and commonly used to investigate sickness behavior experimentally", but much worse than people with assorted other conditions.Guess we kind of knew that.
See if there are any differences between symptom complexes shown in ME and other groups. Result: again comparable to chronic pain and the LPS injection; authors can only speculate why people with chronic conditions and those with acute LPS "infection" show the same symptoms at similar levels; they guess the culprit may be a persistent low-grade pro-inflammatory state.
See how strongly does how sick we feel influence how we rate our health and functioning. Weird question but actually the answer seems to be that even though we feel awfully sick we don't think of ourselves as sick as we are: "these patients may have developed coping strategies over time in order to reduce the influence of sickness behavior on perceived health and functioning". Interesting, not what we usually get told.
Recommendation is helping patients with their coping strategies (presumably just those not already good at it).
Unfortunately the term sickness behaviour when applied to humans is sometimes used in the same sense as in mice but at other times as a conscious or intentional behaviour (you can change by changing your thoughts). Cue confusion and talking past each other all round.
Haven't yet read the full paper yet so don't know how sickness behaviour is used here but the first few sentences of the intro seem to indicate the physiological version?
ETA:
Have now skimmed the whole paper. Doesn't strike me as bad as all that. Though I also don't quite see the point in it. But at least 'sickness behaviour' here is used in the basic, physiological sense, nothing to do with how you choose to behave but simply about how lousy you feel.
Three parts to the study (ME patients met both Fukuda and ICC, all self-reported measures) - I'll attempt to report the key points I took from it without using the term 'sickness behaviour':
Document how sick we feel compared to other groups. Result: comparable to chronic pain and the human guinea pigs who volunteered to get an "injection of LPS, a substance effective at activating the immune system and commonly used to investigate sickness behavior experimentally", but much worse than people with assorted other conditions.Guess we kind of knew that.
See if there are any differences between symptom complexes shown in ME and other groups. Result: again comparable to chronic pain and the LPS injection; authors can only speculate why people with chronic conditions and those with acute LPS "infection" show the same symptoms at similar levels; they guess the culprit may be a persistent low-grade pro-inflammatory state.
See how strongly does how sick we feel influence how we rate our health and functioning. Weird question but actually the answer seems to be that even though we feel awfully sick we don't think of ourselves as sick as we are: "these patients may have developed coping strategies over time in order to reduce the influence of sickness behavior on perceived health and functioning". Interesting, not what we usually get told.
Recommendation is helping patients with their coping strategies (presumably just those not already good at it).
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JemPD
Senior Member (Voting Rights)
Hip
Senior Member (Voting Rights)
Not once you appreciate the theory behind sickness behavior. The idea is that when animals (including humans) are sick from infection, this triggers a set of adaptive behavioral responses which are designed to optimize recovery from infection, as well as limit its spread to other animals in the group.
So triggering fatigue will result in certain behavioral responses, such as lying down and sleeping. This is advantageous as it conserves energy, so that the immune system can focus on fighting the infection. Thus what we feel as fatigue is designed to create the adaptive behavioral response of resting.
Likewise, the desire for social withdrawal that appears during infection might be explained in terms of preventing the infection spreading to other animals in the group.
The sickness behavior response as a means to explain ME/CFS symptoms is well-known. It's the basis of Michael VanElzakker vagus nerve infection hypothesis of ME/CFS.
Somewhat different, but surely not completely different?
Maes wrote a paper some time ago comparing ME/CFS symptoms to sickness behavior symptoms, see table 1. It's not a perfect match, but there is certainly enough overlap to suggest sickness behavior may account for at least some ME/CFS symptoms.
Given that sickness behaviors appear as a result of infection, and given that ME/CFS has been associated with chronic infections, it does not take any great leap of the imagination to see how sickness behavior could appear in ME/CFS.
spinoza577
Senior Member (Voting Rights)
It is simply a guess.
Therefore I don´t see why here a fallacy should occur.
The guess they believe in they then tried to elaborate. I don´t see any problems with that.
I also don´t see a priori any inconvenience with the try to explain ME/CFS via nerves. (In fact I personally find this to be the best explanation, it´s not my fault nor that of the illness that some psychologists turn their attention to unexplained diseases and are mistreating patients, including patients with diseases that might or may be brain diseases.)
boolybooly
Senior Member (Voting Rights)
I was willing to give them the benefit of the doubt except for the following passage as mentioned above, because they do not consider sensitisation as the primary hypothesis for a mechanism, which any self respecting neurologist would surely immediately consider and instead they made an hypothesis of dysregulation.
Yes they could go on to disprove the hypothesis, but this is not the most obvious explanation. They did not qualify this assumption of dysregulation as the competing hypothesis to the more logical hypothesis of sensitisation, which is evolutionarily adaptive and so different in character from dysregulation.
This therefore does not preclude bias or lack of awareness in suggesting this hypothesis before sensitisation, when further discussion could have done so and raises a questionmark over the authors' perspectives including levels of awareness of neurological principles involved in the field of nociception where sensitisation (also sensitization - US spelling) is a well established principle in the study of chronic pain.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750819/
Yes they could go on to disprove the hypothesis, but this is not the most obvious explanation. They did not qualify this assumption of dysregulation as the competing hypothesis to the more logical hypothesis of sensitisation, which is evolutionarily adaptive and so different in character from dysregulation.
This therefore does not preclude bias or lack of awareness in suggesting this hypothesis before sensitisation, when further discussion could have done so and raises a questionmark over the authors' perspectives including levels of awareness of neurological principles involved in the field of nociception where sensitisation (also sensitization - US spelling) is a well established principle in the study of chronic pain.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2750819/
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boolybooly
Senior Member (Voting Rights)
I have slept on it and have further criticisms, which are my personal opinion.
The first is the lack of empirical data, since the study relies on self reporting which can be subject to biases of the selves involved. This is no more scientific than a poll.
There is no attempt to measure cytokines in any of the subjects and yet cytokines are used as a basis for proposing a quantitative theory of sickness behaviour which equates high cytokines with high sickness behaviour without considering the complexity of the nervous system and the processes like sensitisation etc which are known to occur over time and in relation to molecular signals, or the complexity of cytokine networks. Specifically the work on identifying a cytokine profile for ME is IMHO inconclusive at this time (see their ref below*) and the issue of subtypes and cohort homogeneity has not been resolved and many cytokines are potentially implicated besides those involved in LPS reactions, but only one (TGF-β) was found to recur in ME experiments and this was not a factor in LPS experiments or chronic pain. Different cytokines have different and specific effects so this is comparing apples with oranges and treating them all as if they were apples. I see no basis for a quantitative comparison across different conditions with different cytokine profiles. This is unsound and is not a basis for the hypothesis of a dysregulated sickness behavior circuitry offered by the authors.
Interestingly one of the three refs for cytokine comparison is authored by none other than P.D. White an author of the PACE trial, which tells us something about the provenance of this kind of ideation. I find it hard to concentrate so would draw it to the attention of sharper eyes @dave30th
https://www.researchgate.net/public...and_circulating_cytokines_A_systematic_review
*Chronic fatigue syndrome and circulating cytokines: A systematic review
Blundell S, Ray KK, Buckland M, White PD.
Found -
two other key refs
https://docksci.com/endotoxin-induc...model-to-disent_5b0415eed64ab2fd1a34f190.html
Endotoxin-induced experimental systemic inflammation in humans: A model to disentangle immune-to-brain communication.
Manfred Schedlowski, Harald Engler, Jan-Sebastian Grigoleit
Found -
https://www.ncbi.nlm.nih.gov/pubmed/17334668
Nitric oxide and pro-inflammatory cytokines correlate with pain intensity in chronic pain patients.
Koch A, Zacharowski K, Boehm O, Stevens M, Lipfert P, von Giesen HJ, Wolf A, Freynhagen R.
Found -
As you can read above the review of cytokine profiles for ME authored by PD White et al did not find results resembling the chronic pain and LPS induced profiles which at least share three cytokines, IL-1beta, IL-6, and TNF-alpha. So this comparison of ME with chronic pain and LPS induction based on cytokine profiles has no basis in fact, by their own references.
I would also add that personally I consider the LPS protocol approaches the unethical. In my view it is not ethical to deliberately poison human beings and in any protocol like this there is a risk of hypersensitivity leading to anaphylactic shock. It must therefore be supervised by medical personnel and the administering of toxin contravenes the Hippocratic oath. I dont see how this can possibly be done ethically but again would defer to others who are experts in ethics and better qualified to judge than I.
I am therefore concerned about unethical attitudes towards human experimentation and also ignorant approaches to the study of ME being promoted by this work, no matter how heavy the disguise which superficial statistical analysis lends to this self reporting poll. The leap to assuming dysregulation instead of sensitisation is in my view indicative of projection which is a continuation of BPS errors.
I am making these points to explain why I say that this paper and related work do not have my confidence and I believe they and their authors deserve closer scrutiny on the basis that the price of fair treatment for ME patients is eternal vigilance.
The first is the lack of empirical data, since the study relies on self reporting which can be subject to biases of the selves involved. This is no more scientific than a poll.
There is no attempt to measure cytokines in any of the subjects and yet cytokines are used as a basis for proposing a quantitative theory of sickness behaviour which equates high cytokines with high sickness behaviour without considering the complexity of the nervous system and the processes like sensitisation etc which are known to occur over time and in relation to molecular signals, or the complexity of cytokine networks. Specifically the work on identifying a cytokine profile for ME is IMHO inconclusive at this time (see their ref below*) and the issue of subtypes and cohort homogeneity has not been resolved and many cytokines are potentially implicated besides those involved in LPS reactions, but only one (TGF-β) was found to recur in ME experiments and this was not a factor in LPS experiments or chronic pain. Different cytokines have different and specific effects so this is comparing apples with oranges and treating them all as if they were apples. I see no basis for a quantitative comparison across different conditions with different cytokine profiles. This is unsound and is not a basis for the hypothesis of a dysregulated sickness behavior circuitry offered by the authors.
Interestingly one of the three refs for cytokine comparison is authored by none other than P.D. White an author of the PACE trial, which tells us something about the provenance of this kind of ideation. I find it hard to concentrate so would draw it to the attention of sharper eyes @dave30th
https://www.researchgate.net/public...and_circulating_cytokines_A_systematic_review
*Chronic fatigue syndrome and circulating cytokines: A systematic review
Blundell S, Ray KK, Buckland M, White PD.
Found -
two other key refs
https://docksci.com/endotoxin-induc...model-to-disent_5b0415eed64ab2fd1a34f190.html
Endotoxin-induced experimental systemic inflammation in humans: A model to disentangle immune-to-brain communication.
Manfred Schedlowski, Harald Engler, Jan-Sebastian Grigoleit
Found -
https://www.ncbi.nlm.nih.gov/pubmed/17334668
Nitric oxide and pro-inflammatory cytokines correlate with pain intensity in chronic pain patients.
Koch A, Zacharowski K, Boehm O, Stevens M, Lipfert P, von Giesen HJ, Wolf A, Freynhagen R.
Found -
As you can read above the review of cytokine profiles for ME authored by PD White et al did not find results resembling the chronic pain and LPS induced profiles which at least share three cytokines, IL-1beta, IL-6, and TNF-alpha. So this comparison of ME with chronic pain and LPS induction based on cytokine profiles has no basis in fact, by their own references.
I would also add that personally I consider the LPS protocol approaches the unethical. In my view it is not ethical to deliberately poison human beings and in any protocol like this there is a risk of hypersensitivity leading to anaphylactic shock. It must therefore be supervised by medical personnel and the administering of toxin contravenes the Hippocratic oath. I dont see how this can possibly be done ethically but again would defer to others who are experts in ethics and better qualified to judge than I.
I am therefore concerned about unethical attitudes towards human experimentation and also ignorant approaches to the study of ME being promoted by this work, no matter how heavy the disguise which superficial statistical analysis lends to this self reporting poll. The leap to assuming dysregulation instead of sensitisation is in my view indicative of projection which is a continuation of BPS errors.
I am making these points to explain why I say that this paper and related work do not have my confidence and I believe they and their authors deserve closer scrutiny on the basis that the price of fair treatment for ME patients is eternal vigilance.
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boolybooly
Senior Member (Voting Rights)
I want to add that I think the sickness ME causes does result in behavioural changes which have emotional disposition at their root, aka sickness behaviour, which makes life difficult for PWME.
I think its important that those who are given the resposibility of caring for and treating PWME recognise this and make compassionate and understanding choices as a result which are in the best interests of ME patients. i.e. we need quiet stress free lives.
I believe these changes PWME experience are adaptive changes and are like anyone getting flu, who naturally prefer to go to bed than go out on the town, not because they have a psychopathology but because they are ill and its best if they rest.
In fact, if someone with flu tries to burn the candle at both ends they can make their illness much worse, even kill themselves, so its important that they do rest and allow their immune system to work without the immune suppression which adrenalin and other stress hormones from excitement and activity cause.
This is why also athletes with a virus are advised to rest and not to compete and not to train hard, because it can damage their health. My long experience has taught me the situation with ME is similar in that it really does make us worse if we try to be active.
I think the danger with a paper like this is it suggests the behaviour is itself a pathology when there is no reason to assume it is not a valid response to a real illness. It is perverse to try to work against that behaviour because it is an appropriate response.
What I am trying to say is I think it is worth studying at a psychological and biochemical level but not under the unjustified premise of denying the validity of the illness or appropriateness of restful behaviour.
I think its important that those who are given the resposibility of caring for and treating PWME recognise this and make compassionate and understanding choices as a result which are in the best interests of ME patients. i.e. we need quiet stress free lives.
I believe these changes PWME experience are adaptive changes and are like anyone getting flu, who naturally prefer to go to bed than go out on the town, not because they have a psychopathology but because they are ill and its best if they rest.
In fact, if someone with flu tries to burn the candle at both ends they can make their illness much worse, even kill themselves, so its important that they do rest and allow their immune system to work without the immune suppression which adrenalin and other stress hormones from excitement and activity cause.
This is why also athletes with a virus are advised to rest and not to compete and not to train hard, because it can damage their health. My long experience has taught me the situation with ME is similar in that it really does make us worse if we try to be active.
I think the danger with a paper like this is it suggests the behaviour is itself a pathology when there is no reason to assume it is not a valid response to a real illness. It is perverse to try to work against that behaviour because it is an appropriate response.
What I am trying to say is I think it is worth studying at a psychological and biochemical level but not under the unjustified premise of denying the validity of the illness or appropriateness of restful behaviour.
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Mithriel
Senior Member (Voting Rights)
I may be misunderstanding what you mean. I fully agree that our behaviour is a valid response to being sick. If sickness behaviour is valid and a good thing for acute illness I do not see at what point it stops being a good thing if the disease continues for a long time. It must remain protective if the thing it is protecting you from is ongoing.
But I do not see why behavioural changes should have emotional disposition at their root. Plants exhibit sickness responses even though they do not have emotions in the sense we do.
Unless we redefine sickness behaviour in an emotional sense instead of using the term for the behavioural reponses of animals (inculding us) to being ill, then it has physical - organic, biochemical, immune, hormonal and so on - root cause.
adambeyoncelowe
Senior Member (Voting Rights)
Personally, I think 'sickness response' is a better term (used by VanElzakker, I think?), as it avoids unfortunate connotations, as you point out.
boolybooly
Senior Member (Voting Rights)
I think proper palliative care for PWME should acknowledge the emotional aspects of ME. I dont think denial is viable as a long term strategy.
The emotional state of ME patients matters very much and creates their experience of life and deserves to be looked after in a constructive way.
I accept that in the short term, confusion about how we discuss emotions is threatening because of the way the BPS theory projects stereotypes and perverts a rational and humane interpretation of emotions in ME and we are still vying with miscreants propounding this kind of idiocy. Understandably and justifiably the temptation is still to have defensive attitudes and stick to rational empiricism assiduously as in my post above explaining my criticisms of this paper.
I think the other side of the coin is, in the long term, the emotional impact of ME has to be recognised by everyone responsible for caring for and treating PWME.
My view on this is properly scientific I promise. While we cannot (yet) reliably measure subjective emotions empirically in fine resolution, it will not be long now given advances in MRI and it will be something analagous to that lady playing the violin in a brain op i.e. mapping and correlation. The point being emotions are physical, every bit as real as a molecule and constitute a functional link between the nervous system, whatever state it may be in as modified by molecular messengers as modified by cognition and ... behaviour.
It seems likely the responses of the immune system can affect emotions and through them behaviour. Doctors and nurses and carers ought to be informed about how so they can help. This is to say good psychology and not bad psychology, could be useful, like the kind of work Prof Leonard Jason does, reclaiming the night, as it were.
Plants do not have a nervous system and respond vegetatively in the most part and even those like mimosa and venus fly trap which do effect rapid motile responses do so with an osmotic transduction system analagous to a very basic reflex, there is no CNS involved so, even if they can respond to their environment and as some believe, human speech and music, which I cannot comment on as I have not studied any scientific data on this, plants probably cannot have emotions like ours. If plants had a CNS and could think on the other hand, they wood...
hehe 
The emotional state of ME patients matters very much and creates their experience of life and deserves to be looked after in a constructive way.
I accept that in the short term, confusion about how we discuss emotions is threatening because of the way the BPS theory projects stereotypes and perverts a rational and humane interpretation of emotions in ME and we are still vying with miscreants propounding this kind of idiocy. Understandably and justifiably the temptation is still to have defensive attitudes and stick to rational empiricism assiduously as in my post above explaining my criticisms of this paper.
I think the other side of the coin is, in the long term, the emotional impact of ME has to be recognised by everyone responsible for caring for and treating PWME.
My view on this is properly scientific I promise. While we cannot (yet) reliably measure subjective emotions empirically in fine resolution, it will not be long now given advances in MRI and it will be something analagous to that lady playing the violin in a brain op i.e. mapping and correlation. The point being emotions are physical, every bit as real as a molecule and constitute a functional link between the nervous system, whatever state it may be in as modified by molecular messengers as modified by cognition and ... behaviour.
It seems likely the responses of the immune system can affect emotions and through them behaviour. Doctors and nurses and carers ought to be informed about how so they can help. This is to say good psychology and not bad psychology, could be useful, like the kind of work Prof Leonard Jason does, reclaiming the night, as it were.
Plants do not have a nervous system and respond vegetatively in the most part and even those like mimosa and venus fly trap which do effect rapid motile responses do so with an osmotic transduction system analagous to a very basic reflex, there is no CNS involved so, even if they can respond to their environment and as some believe, human speech and music, which I cannot comment on as I have not studied any scientific data on this, plants probably cannot have emotions like ours. If plants had a CNS and could think on the other hand, they wood...
hehe
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