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Science at the UK CMRC Conference, 1-2 Sept 2014

Sasha

Fine, thank you
Messages
17,863
Location
UK
Bear with me while I split the thread rather cackhandedly, guys (it needs a moderator to do it properly and I'm not one) - I see that people want to discuss this already and probably haven't noticed my post about this topic (and @justy is probably off having her tea, so probably best not to wait for her to set up a new thread!).

I've set up a new thread specifically on the topic of what advocacy we should now be doing to get this new research consensus rapidly into clinical practice:

http://forums.phoenixrising.me/inde...top-the-bps-treatment-of-patients-asap.32423/

and am populating it with the four relevant posts from this thread (@aimossy's, @Jonathan Edwards's reply, @justy's and @Daisymay's).

Happy to change my title if you don't like it, @justy - I was trying to reflect the content of your post.

I'll then ask the mods to delete those posts from this thread (which could take quite some time) so that we don't have cross-posting and to help keep this thread on its science track.

[Edit: That's been done now - many thanks to the mods.]

Just to repeat - this is in no way a criticism, it's just that that very important topic is just a bit too off-topic here and deserves its own thread.
 
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Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
@Jonathan Edwards

In your summary you seemed to clearly indicate that there is an emerging consensus amongst researchers that we are looking at some sort of immune issue (but not involving chronic infection) that results in a hypersensitised central nervous system. In another thread you outlined a range of possible 'MEs' that might result in the same collection of symptoms.

This is all great to hear.

I wonder if you (or the other researchers) have then considered how this working model can reconcile the other consistent findings in ME/CFS such as executive dysfunction, autonomic dysfunction, PEM etc.

I appreciate that this may be mere speculation at this point but some of us like to speculate.
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
"He then spent the rest of his talk saying how unreasonable it was that patients did not gratefully accept this conclusion, indicating that this was an attack on science (if I remember rightly)."

A quick perusal of the responses submitted to The Lancet by some members of PR plus Graham et al's excellent animated expositions of the PACE results should give some indication of how 'unreasonable' the response was and whether or not it was 'an attack on science' (sic).

Oh, but isn't it obvious from all the 'likes' in this thread that we really HATE science and research? ;)
 

Jonathan Edwards

"Gibberish"
Messages
5,256
@Jonathan Edwards
In your summary you seemed to clearly indicate that there is an emerging consensus amongst researchers that we are looking at some sort of immune issue (but not involving chronic infection) that results in a hypersensitised central nervous system. In another thread you outlined a range of possible 'MEs' that might result in the same collection of symptoms.

I wonder if you (or the other researchers) have then considered how this working model can reconcile the other consistent findings in ME/CFS such as executive dysfunction, autonomic dysfunction, PEM etc.

Absolutely, Marco, I have been considering it for weeks, but just now I can't quite pin down what I concluded! Truth is that there will be lots of ways of reconciling, but I realise I have to be convincing. I will report back tomorrow hopefully. I think PEM is interesting, in that a purely CNS sensitisation mechanism, as we have discussed for autonomic, seems unlikely to give delayed crashing. An immune response would do better, but I need to be more precise...
 

MeSci

ME/CFS since 1995; activity level 6?
Messages
8,231
Location
Cornwall, UK
Joss - Good question Simple answer is yes.

My ME started off with a very nasty dose of chickenpox + an encephalitic component that caused cerebellar damage.

I don't know if I have dorsal root ganglionitis but it's possible that this is so because I get a lot of sensory problems in my lower limbs when I have an occasional really bad patch.

But DRG can also occur in Sjogren's Syndrome - so it could be autoimmune. Interestingly, some of these SS patients have symptoms consistent with a peripheral neuropathy. A lot of them also have debilitating fatigue - which is why we are using this disease to try and find a biomarker for fatigue.

We have a lot to learn about the neurology of ME/CFS!

What about a bad case of chickenpox in infancy followed by facial nerve palsy, but the ME not manifesting clearly until early 40s after apparently normal health? Zoster is discussed in relation to ME/CFS in this thread.
 

medfeb

Senior Member
Messages
491
I agree with all your points about the importance of diagnostic names for patients, Sasha, but my point is that we are in all this mess because people do not realise that it is crazy to expect disease classification for research to match disease classification for clinical care. The reality of it is plain to see but we are born to 'pigeonhole' things and it is hard to get out of the habit. For instance, look at the indications for anti-rheumatic drugs:

Voltarol - anyone with a painful joint or back
Methotrexate - RA and psoriatic arthritis but not lupus
Steroids - RA, polymyalgia and lupus
Sulphasalzine - RA and Reiter's and Crohn's arthritis but probably not psoriatic and not lupus
Anti-TNF - RA and psoriatic but not lupus
Anti- IL-6 - RA but not psoriatic or lupus

And so it goes on. Each clinical therapeutic tool relates to a different disturbance of physiology and these cut across diagnoses. Even what I have written is grossly simplified. Within each diagnostic group the real reasons for using each drug depend on the individual's problems. NICE is a nonsense but it has got that way because people think that we have to have disease names to base treatment on and that these have to be the names in the disease classification books used for research. The only way to sensible treatment is to throw that idea away.

This is an interesting discussion. Thank you for taking the time to share your ideas with us.

I think I'm struggling with the same thing that Sasha and Nielk are struggling with. It makes total sense to me that research criteria and clinical criteria are different since you would want well defined cohorts to have your research make sense whereas in the clinic, you don't want people falling through the cracks because they don't meet those criteria. Also to your point, in the clinic, doctors should be concerned with treating the specific patient's presentation, not the label that he has. I also agree with your point that ME is heterogeneous and probably not just one disease.

The disconnect for me is that currently under the label "CFS", we have the Oxford, Fukuda, CCC and ME-ICC criteria. All are used in research while Fukuda, CCC and ME-ICC have associated clinical guidelines. CDC has stated that all represent the same group of patients. And evidence reviews have typically treated these definitions as equivalent. But Oxford only requires 6 months of debilitating fatigue and allows primary psychiatric illness while ME-ICC requires PENE plus other neuroimmune dysfunction and does not include primary psychiatric illness.

So for me, the issue is that even when considering just research criteria, the term "CFS" as defined by the collection of these definitions and the resultant "CFS" evidence base encompass disparate conditions that have been inappropriately lumped together. As a result, studies done with a particular "CFS" definition - for instance Oxford - lead to recommendations for treatment which are then applied in the clinic to all "CFS" patients, regardless of whether those patients have the same condition as the patients originally studied

What am I missing? If we do not have some basic agreement on what criteria are necessary for an ME diagnosis in research, how do we unravel the confusion that we see in the research evidence base today and start to make real progress?
 
Messages
41
Thank you, Jonathan Edwards and Charles Shepherd for reporting on the conference and continuing the discussion with us patients!

I have a question (which I think is similar to one previously posted): it seems in the summaries the conference mostly dealt with fatigue, not with other typical ME/CFS symptoms such as PEM, "flu-feeling", sore throat, swollen lymph nodes, susceptibility to infections, very slow recovery from any new infections, etc.

I don't mean the issues of whether actual infections are a cause of (or a perpetuating factor in) ME/CFS, but rather the clinical symptoms that are so very flu-ish and are not the same as "fatigue". A large group of us patients belong in this symptom category rather than in a category of broad fatigue.

Was this (these symptoms) discussed?

Again, many thanks.
 

charles shepherd

Senior Member
Messages
2,239
Thank you, Jonathan Edwards and Charles Shepherd for reporting on the conference and continuing the discussion with us patients!

I have a question (which I think is similar to one previously posted): it seems in the summaries the conference mostly dealt with fatigue, not with other typical ME/CFS symptoms such as PEM, "flu-feeling", sore throat, swollen lymph nodes, susceptibility to infections, very slow recovery from any new infections, etc.

I don't mean the issues of whether actual infections are a cause of (or a perpetuating factor in) ME/CFS, but rather the clinical symptoms that are so very flu-ish and are not the same as "fatigue". A large group of us patients belong in this symptom category rather than in a category of broad fatigue.

Was this (these symptoms) discussed?

Again, many thanks.

Thanks for your kind comments Emma

Although it's a bit over-simplistic, I normally ask patients to describe what symptoms they have within five rough groups of symptoms

1 Central and peripheral nervous system: sleep disturbance, problems with balance, neuropathic pain, sensory disturbances

2 Cognitive dysfunction : defects with working memory, concentration, information processing

3 Autonomic nervous system dysfunction - cardiac and orthostatic intolerance, bowel and bladder symptoms

4 Infective and immunological - sore thoats and enlarged or painful lymph glands, flu like feelings, thermoregulation problems

5 Musculo-skeletal - exercise induced fatigue, pain

One of the major challenges facing research is then trying to match these symptoms, or groups of symptoms, to abnormal findings from lab tests or other investigations such as neuroimaging studies

Which is where we start to run into difficulties - although there are areas - autonomic dysfunction in particular - where the research is starting to demonstrate a correlation between symptoms and pathology

A considerable number of UKRC conference presentations circled round a hypothesis involving acute infection + some form of genetic susceptibility leading to the type of very physical 'sickness behaviour' that is associated with the production of immune system chemicals called cytokines and the development low level neuroinflammation (involving activation of the microglia).
This is something that to some extent can be produced artificially by treating people who have chronic hepatitis virus C infection with interferon alpha. This often results in the patients developing acute flu like symptoms, followed by increasing fatigue +/- pain in the following weeks. Later on cognitive dysfunction and mood disturbance kicks in. Not the exact picture that many people with ME/CFS describe, where the whole symptom complex develops at roughly the same time and often very shortly after the the infection, or at the same time. Even so, it's an interesting model.
So to get back to your question, we did spend quite a lot of time looking at a model of FATIGUE that could be linked to infection plus a host immune response involving cytokine production and activation of microglia within the CNS, possibly involving the basal ganglia (which my neurological colleagues Peter Behan and Abhijit Chaudhuri have advocated for years) - that IMHO might turn into a genetically determined persistence of this very physical 'sickness behaviour'.

Some of the other MRC funded studies being reported in Bristol looking at mitochondrial dysfunction and muscle symptoms (co-funded by the MEA Ramsay Research Fund), and autonomic dysfunction and cardiac symptoms (and blood flow to the brain - possibly linked to cognitive dysfunction), are also trying to link pathology to symptoms
So I think we are making progress in trying to match up two important parts - symptoms and pathology - of the ME equation. And this is not just related to central (brain) and peripheral (muscular) fatigue

And this should give us some important leads on treatments that might be worth trying
Not sure that I've really answered your question though!
 

Kati

Patient in training
Messages
5,497
This is not to point the finger at you @charles shepherd , as you quote marked it, but the term 'sickness behavior' represents to me yet another term which can be interpreted as biophysical illness and psychiatric illness.

Would there be other nomenclature that we could put forward and suggest in order to be not so ambiguous? (i am asking not only for use between each other but perhaps also for the research community.)

Thank you for your work.
 

Snowdrop

Rebel without a biscuit
Messages
2,933
What about a bad case of chickenpox in infancy followed by facial nerve palsy, but the ME not manifesting clearly until early 40s after apparently normal health? Zoster is discussed in relation to ME/CFS in this thread.

I also had a bad case of chickenpox at 3 mos old. Followed by epileptic seizures throughout childhood.
 

Snow Leopard

Hibernating
Messages
5,902
Location
South Australia
However, my understanding is that a respectable epidemiological model will always be three-component, including a stochastic or random element. You need that for cancer and autoimmune disease so why not for ME. The simple fact is that 90% of the explanation for ME beyond genetics may be due to no environmental factors at all. It may be due to a variable and unpredictable instability of an internal regulatory system. So there is no need to blame anything! There may be nothing to find. But that does not mean we should not be looking like this with detailed statistics, because that is the way to show that there is nothing if there isn’t.

I think the appeal is that many like to believe that everything is deterministic and 'happens for a reason'. Unfortunately, many people, in the absence of a better reason like to blame specific causes eg infection but in doubt, everyone likes to use the S word. I'm talking about the non discriminate (pseudoscientific) use of stress being used as an 'magic happens here' explanation for illness where other causes do not fully explain it.

But I think it is an education issue, both with physicians and the general public. Is there scope for someone like yourself writing an article or two in popular science publications or the media, explaining that often illness has a random component and is beyond our control and we should not blame ourselves or anything in particular.

(A side discussion which I find frustrating is how cancer treatment is deemed to be a 'fight' which somehow implies that someone who is not lucky enough to have their diagnosis early enough or their treatment does not work, is somehow a 'loser'. Along with the popular myth that positive thinking somehow has an impact on cancer survivability, despite all the evidence to the contrary.)
 

Jonathan Edwards

"Gibberish"
Messages
5,256
What am I missing? If we do not have some basic agreement on what criteria are necessary for an ME diagnosis in research, how do we unravel the confusion that we see in the research evidence base today and start to make real progress?

A good question. What are we missing. I think the answer is that we are missing the fact that the skilled human brain does not actually make decisions based on the labels we use in language. It can do much better. The difficulty is in learning to write down how we think it does work. Some years ago John Kirwan wrote a paper called something like 'Do rheumatologists do what they say they do? He showed that our decisions do not follow the rules we think we are following. Unfortunately in the current bureaucratic world of NICE it is assumed that we do and the result is a disaster.

The key point is that we should not be making decisions based on disease names at all. Holgate quoted some ancient aphorism which is now truer than ever - something like 'do not seek to know the disease the person has, but the person who is diseased'.

It may seem problematic to have lots of criteria but the only problem may be that they are all given the same name. I agree that some of them are probably rather poorly thought out, but I am not sure that any one is 'better' than another.

Let me give an analogy. The doctor looking after someone with ME is a bit like a nine year old girl called Mary. Mary's mum has gone down with flu. She tells Mary to do the shopping. When Mary gets home she says 'mum, where do I put all the food?'. So mum says something like ' fresh things go in the fridge and dry things and tins go in the larder - but fruit are best kept out of the fridge, and lettuce too - all animal things like meat certainly go in the fridge - potatoes are OK in the larder - oh and eggs are best not in the fridge - and whatever you think we should have for supper leave that on the table for daddy to cook - the Bon Maman jam can go in the larder but remember to put it in the fridge if you have some for tea.' And so on. Where are the 'diagnoses' here? All sorts of different levels of categorisation are being used to get close to the best overall effect. That is how to look after illnesses.

And like Mary we are just learning the best way to do things. Much of the time we have to make a sensible choice. That is where NICE falls down. We are stuck with 'evidence based medicine' in the unhelpful narrow sense rather than 'intelligence based medicine'. Although the idea of NICE guidelines is not bad in principle if it just highlights the evidence we are to use intelligently. It may at least counter the habit of rather unintelligent doctors recommending treatments on the basis of evidence which they think is good but which is hopelessly flawed.

The one thing not to worry about is that all of this is an attempt to take the ME disease away from people. It implicitly assumes that the problem is real and worth breaking down into components. It may seem to leave everything very confusing but the fact is that we are quite good at handling this sort of confusion - we do it every day, like Mary and the food. Medicine should be based on real decision making like that, not name labels lined up in a row.
 

user9876

Senior Member
Messages
4,556
I think the appeal is that many like to believe that everything is deterministic and 'happens for a reason'. Unfortunately, many people, in the absence of a better reason like to blame specific causes eg infection but in doubt, everyone likes to use the S word. I'm talking about the non discriminate (pseudoscientific) use of stress being used as an 'magic happens here' explanation for illness where other causes do not fully explain it.

But I think it is an education issue, both with physicians and the general public. Is there scope for someone like yourself writing an article or two in popular science publications or the media, explaining that often illness has a random component and is beyond our control and we should not blame ourselves or anything in particular.

I think one of the problems is that people avoid studying 'randomness' which can often be characterised. For example, people looking at system failures will often model a system with stochastic variables that represent some sort of error rates often based on measurements and with a given distribution (time to failure). But the models then look at how these different component failures can lead to overall system failure. And in some ways they are quite predictable in terms of given a set of inputs we can get out a probability distribution of the system failing. Queueing theory is often used in a similar way on traffic patterns to predict speeds through the system given different arrival rates. So there is mathematics to understand and characterise random processes and they are used by engineers to model systems.

I think the idea of antibodys occurring at random is interesting and could perhaps be further characterised although it is not necessarily worth it. Very few random processes have a uniform distribution over their output space and also in many systems random events occur in sequences. So I assume that an antibody production will be more likely to produce certain antibodies rather than others. Where we say there is a genetic predisposition to an auto immune disease is that due to some people (with a particular gene) having an antibody production process that is more likely to produce a given antibody than others. So a bit like in dependability work where they look at characterising the time to failure is there a characterisation of different time to auto-antibody based on say genetic factors. I wonder if there are environmental factors that may also effect the randomness (probably due to my ignorance about the process) but if it is a chemical process producing an antibody then do variations in compounds in cells make a difference to the process?

What worries my about the statistical analysis of different possible environmental factors is that there seems to be no account of the way a disease process may work. Given a search over enough statistical methods with a variety of fudge factors does it become possible to find one method that comes up with the desired answer (and given a dataset I could possibly use genetic program (a search technique nothing to do with genetics!) to find it).

The point is good statistical models try to use knowledge of the structure of the problem to help characterise and help us understand. Otherwise I would argue if simple statistics or clustering isn't showing something then the sample may be too small or it may not be observable from those variables (perhaps due to noise or inaccurate measurements but also because the variables being measured don't represent the problem). A statistical model that tries to build on our understanding of the system may give bad results in which case maybe it tells us something about our understanding of the structure. My experience, however, is that in getting to the point where the processes are described sufficiently but abstractly enough to build a model often brings a better understanding of the system and that is the important processes. I think this is due to people finding abstract thought hard and hence its hard to layout the important features of a system and join them up. Some people can do it intuitively.

(A side discussion which I find frustrating is how cancer treatment is deemed to be a 'fight' which somehow implies that someone who is not lucky enough to have their diagnosis early enough or their treatment does not work, is somehow a 'loser'. Along with the popular myth that positive thinking somehow has an impact on cancer survivability, despite all the evidence to the contrary.)

A lot of people seem to have a deep belief in mind over matter hence the need to fight cancer. Coyne talks about erroneous results linking peoples psychological state to cancer survival rates. I think one small trial had an outlier that skewed the results. Where the fight is is sometimes to get the initial diagnosis by being persistent with doctors.
 

Marco

Grrrrrrr!
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2,386
Location
Near Cognac, France
I will report back tomorrow hopefully.

That doesn't sound too unreasonable ;)

I think PEM is interesting, in that a purely CNS sensitisation mechanism, as we have discussed for autonomic, seems unlikely to give delayed crashing. An immune response would do better, but I need to be more precise...

Re delayed crashing, I think we need to be sure first that we are dealing with a genuine phenomenon. For example 'alcohol intolerance' was at one time considered to be a pretty universal symptom of ME/CFS and potentially a key one. It turns out that it's a symptom shared with post-concusssion syndrome patients for example and Jason found it reported by just 30% of PWME.

I'm not quite sure what is meant by 'delayed'. Are we saying that PWME experience no symptoms during or shortly after mental of physical exertion and that symptoms appear or are exaggerated 24 or 48 hours afterwards or that they experience mild (or different) symptoms early on but the symptoms peak some time later?

Those may be two different processes with different explanations and I'm not sure that there's sufficient data to make a clear distinction between the two scenarios.
 

Simon

Senior Member
Messages
3,789
Location
Monmouth, UK
This is not to point the finger at you @charles shepherd , as you quote marked it, but the term 'sickness behavior' represents to me yet another term which can be interpreted as biophysical illness and psychiatric illness.

Would there be other nomenclature that we could put forward and suggest in order to be not so ambiguous? (i am asking not only for use between each other but perhaps also for the research community.)
.
Dr Jarred Younger at Stanford in March proposed the term 'Sickness Response' instead of 'Sickness Behaviour' as it's primarily a response driven by biology. I've seen it used in a paper by at least one other researcher, can't remember where.
See the relevant section in my blog:
Sickness response vs sickness behaviour
 

user9876

Senior Member
Messages
4,556
That doesn't sound too unreasonable ;)


I'm not quite sure what is meant by 'delayed'. Are we saying that PWME experience no symptoms during or shortly after mental of physical exertion and that symptoms appear or are exaggerated 24 or 48 hours afterwards or that they experience mild (or different) symptoms early on but the symptoms peak some time later?

I'm not convinced that the symptoms are always delayed but they can be. I can certainly think of cases with my daughter where she did way too much, seemed to hit a wall and symptoms came on pretty immediately and stayed for months. But the typical pattern is delayed although I think to the next day rather than 24 or 48 hours.

I wonder if the time taken for symptoms to ease may be significant. So currently I see a cycle of doing a little bit too much a delay of a worsening of symptoms till the next day and then a 5 or 6 day bad period. I'm not sure I could guess at quantifying how bad the bad symptoms are given the activity. Other times effects have seemed to last for different times. I'm not sure I could characterise what doing too much is either some times it can be quite a little excretion where as other times its more. I feel its like a threshold is reached and symptoms get worse but below that threshold symptoms stay much the same. But the threshold can change over time - it may be it gets lower as symptoms increase due to excretion and without a sufficient recovery time seems to stay lower.

Doing way too much seems to cause the worsening of symptoms for much longer with as I said before these effects or some effects being more immediate. But I wonder if this is what Marco is pointing to where there are immediate effects but the peak later hence if the symptom increase is relatively small then the initial effects are not as noticeable but if the effects are larger then the initial ramping up of symptoms becomes more apparent. However, I do remember one or two occasions where symptoms seemed to jump immediately a bit like where runners describe hitting a wall.
 

Sasha

Fine, thank you
Messages
17,863
Location
UK
I find that if I do some activity within my normal "envelope" the consequences follow immediately but if I'm forced to push it, I'm not to bad on the day but pay more later. I wonder if there's a threshold effect (either in my noticing it or in the biology of it - maybe related to going over the anaerobic threshold, as I think Nancy Klimas believes).

The Lights of course did the study with quite a high level of exercise provocation and produced that amazing graph of the biochemical outcomes for PWME compared to healthy sedentary and MS controls:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2757484/figure/F3/
 

Marco

Grrrrrrr!
Messages
2,386
Location
Near Cognac, France
@user9876 @Sasha

I feel we're dealing with apatterns of symptom exacerabtion which are variable and unpredictable.

Two personal anedotes.

I have both exercise and heat intolerance but sometimes I find myself having to do (nor would I want to avoid) some gardening or something in hot weather. Most of the time, being careful, I get tired, hot and bothered but manage OK. Other times, if I encounter a stubborn weed and exceed my energy supplies, anaerobic threshold, or switch into sympathetic ANS mode of whatever - then BANG! Suddenly and immediately I lose all physical and mental energy, I develop ataxia, can't think or speak and literally have to instruct myself to walk on legs that feel like lead. The only remedy is straight to bed and if I'm lucky I recover to 'normal' level in a few hours (but with much weakened reserves. If I'm unlucky I'm pretty bed-bound for days to weeks. Point is the peak symptoms hit immediately. This sort of reaction has also been provoked by a 30min telephone call so its not just a matter of degree of physical exertion.

A second scenario I've described before but it is relevant. Until recent years I used to get strange short lived periods two or three times per year when I would suddenly, for no reason; feel better. In fact almost normal. On one of those occasions I decided to make the best of it and my wife and I made a rare trip out and caught a matinee movie. So far so good we then decided to stay out and have an even rarer meal out which we both very much enjoyed with no apparent adverse symptoms for me. When I went to bed however I was completely wired, replaying the (pretty banal) events of the day over and over and didn't sleep a wink. The following day and for days afterwards I was in a similar state to my first scenario - pretty much bed-bound and non-functional.

In the second case you could argue that there was a delay in peak symptoms but if you include the wierd 'wired' response after a day out then the immediate aftermath was not symptom free. Certainly in my case a 'stressor' needn't be something normally perceived as unpleasant.
 

lansbergen

Senior Member
Messages
2,512
When I went to bed however I was completely wired, replaying the (pretty banal) events of the day over and over and didn't sleep a wink.

This reminds me of when the disease still was rather mild, I could drive safe but when I came home from a long trip and turned the ignition key off the overwelming fatique hit and then lying on the couch what you describe happened.
 

charles shepherd

Senior Member
Messages
2,239
This is not to point the finger at you @charles shepherd , as you quote marked it, but the term 'sickness behavior' represents to me yet another term which can be interpreted as biophysical illness and psychiatric illness.

Would there be other nomenclature that we could put forward and suggest in order to be not so ambiguous? (i am asking not only for use between each other but perhaps also for the research community.)

Thank you for your work.


Hi Kati

I agree with you 100% and wish that this term had never been invented by scientists to describe the sequence of cytokine mediated events that follow many acute infections resulting in a range of ME/CFS like symptoms

But it has…….

Here is a link to a paper by Prof Robert Dantzer, who came to the UKRC conference, and is one of the leading international experts on how the immune system talks to the brain, which describes the pathophysiology in more detail:

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2740752/