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Neuro-Endocrinology of CFS

Despite the length of this article I am surprised to find relatively little on the neuro-endocrine aspects in CFS! Therefore there is a lack of context in which to try and communicate the important findings published in a series of 16 papers by the CDC in 2006. Which probably also goes to the lack of explaination of these findings in the article! It is my intention to remedy both of these matters and are preparing an edit on the subject which I will post in the near future, and welcome any sensible discussion. Jagra 10:04, 31 July 2007 (UTC).

Most of those CDC articles are not that great, IMHO. Nonetheless, the neuro-endocrine aspect is important. Regards, Guido den Broeder 15:43, 31 July 2007 (UTC)

Jagra, perhaps you ought to have waited for a few more responses. How about leaving messages on the talkpages of some major contributors? JFW | T@lk 22:46, 9 August 2007 (UTC)

Perhaps he might choose English over jargon as well. •Jim62sch• 23:04, 9 August 2007 (UTC)

Orangemartin, Case for relevance is made by CDC not me, of 15 references all but 4 are about chronic fatigue, and of these at least two discuss CFS in papers, other 2 go to explanation of findings for average reader sorry if you cannot understand, please define your problem, so i can discuss.Jagra 00:14, 10 August 2007 (UTC)

Jim 62 please define 'jargon' you do not understand, perhaps you mean abbreviations and these are defined in article text Jagra 00:14, 10 August 2007 (UTC)

Jagra, your writing is, at best, difficult to read. Second, your points are irrelevant to the disease. Third, once again, you list a bunch of references, none of which support anything you say. I'm convinced you search for references by keyword, and if it happens to mention your keyword, you think it supports your needs. But I guess my use of consumer magazine articles offends your Jungian sensibilities. LOL. OrangeMarlin ^{Talk• Contributions} 00:42, 10 August 2007 (UTC)

<indent decrease> Orangemartin lets not get personal now! but to address your comments one by one, -Points irrelevant to the disease, this sounds more like your POV than fact, I prefer to beleive CDC and thats 7 of the references that you apparently disagree with when you say citations irrelavant to the disease, care to explain your POV? -Other citations Demitrac, and Cleare, thats 5 more, not only mention CFS in the title but also in the abstract and the papers and are all about CFS if you care to read them as i have, Dont see how you can claim these are irrelavant to the disease? -De Kloet papers are about neuro-endocrine GR function, which is what CDC findings in CFS go to, relevant directly to my explanation of the function of GR and serotonin in Neuro-endocrine system and go to significance of CDC findings re GR and serotonin changes in CFS. Cant see how that is irrelevant to disease? -The MC Ewen papers are about explanation of Allostatic Load, which go directly to the CDC finding of altered indices in CFS. The full paper discusses the relevance to CFS and provides 5 other references to support this. Dont see how this is irrelevant to the disease? -So in summary all references are relevant to the disease in the context of CDC findings, it seems to me you either dont understand these matters or have a problem with CDC findings, either way your POV seems to be the issue here? Jagra 02:42, 10 August 2007 (UTC)

Let’s see orangemartin, from comments you have made on this page, you do not accept epidemiology as valid science, you label it pseudoscience, and find it laughable even when conducted by the CDC Atlanta. Your mantra is the pharmaceutical gold standard and you consider nutrition and botanical science irrelevant. This attitude has been discussed on this page and defined there as a philosophy. As you will not discuss further I have to presume you consider the CDC findings which intergrated epidemiological findings with laboratory and clinical findings, using a mulidiscipline team of world renowned reseearchers, as defined here and here as my POV and my pushing fringe theories, accusations made by you here

Perhaps this is the discussion that needs to be held, are the CDC findings valid science and worthy of inclusion in the article? I invite the community to comment. Jagra 06:55, 10 August 2007 (UTC)

Jagra, it is not a matter of my comprehension, it is a matter of what our task is in writing an encyclopedia: what we write needs to be clear to the layperson. Jargon of any type is rarely clear to the layperson. See Wikipedia:Explain jargon. &#0149;Jim62sch&#0149; 09:14, 10 August 2007 (UTC)

Jim 62, I think the ‘jargon’ you keep refering to is the medical science terminology? That is why I went to some length in the edit to link these terms to other Wiki pages that define them, and consider I have dealt with that aspect. You must realise this is a medical science article and if you read any of its content you will need a modicom of such understanding, and I have sought the same level in my edit. Either that or you are unfamiliar with the style of medical abstracts? You will need to come to grips with that if you are to comment on citations. Difficult to read edit! it is a complex subject partularily for those not familiar with the literature, as we have seen, but having said that I take your point and will see if I can simplfy the wording further in a revised edit without loosing its integrity, perhaps you could define further what you find difficult? Jagra 00:54, 11 August 2007 (UTC)

Revised edit on Neuro-endocrinoloigy as discussed above, now posted Jagra 00:55, 16 August 2007 (UTC)

Nope. Still not acceptable. BAd references. Fringe science. Done. OrangeMarlin ^{Talk• Contributions} 01:29, 16 August 2007 (UTC)

Orangemartin your abstruse generalaties are not helpfull and you will need to be specific Jagra 00:55, 17 August 2007 (UTC)

The neuro-endocrinology aspect of CFS is important, and it does need to be added to the article. However I do see some problems with Jagra's edits. The main problem is that your edit goes into far too much detail and scientific jargon for an encyclopedia article - it reads more like a journal article. I would suggest having a shorter summary and making the following points:

- stress has been shown to be a significant contributing factor to CFS.
- stress response (HPA axis and ANS) have been shown to be dysregulated in patients, although research has failed to show a common dysregulation for all patients.
- the stress hormones also regulate/influence the immune system, digestive system and circadian cycles.
- chronic social stress has been shown to cause low corticosterone and weight loss in a subgroup of rats, similar to what is seen in subgroups of cfs patients.
- Selye's experiments showed that long-term chronic stress in rats leads to low corticosterone, shrunken adrenal glands and eventually death. The research is old, but still stands.
- factors influencing stress response include current circumstances, mental attitude, coping strategies, previous life experiences, genetics, etc.

A lot of this is already covered in the "stress and trauma" section, so you might just want to add to it. If you need any help, let me know. There's probably other things you should mention too - the above is really just off the top of my head. --Sciencewatcher 01:27, 18 August 2007 (UTC)

Thinking about it a bit more, here is how I would do it: point out that a subset of CFS patients have low cortisol and shrunken adrenal glands. Animal studies show that chronic stress causes this response in a subset of individuals. This reaction might be influenced by genes and previous life experiences. In humans mental attitude also contributes. Point out how the HPA axis and ANS hormones regulate the immune system, sleep/wake cycle, digestion, energy, etc. In at least a subset of patients, it appears as if CFS is caused by long-term stress resulting in a type of burnout or exhaustion. You don't need to go into great detail about which neurotransmitters or which parts of the brain are involved. Also, stick to solid basic science that is not in dispute. Stress can be blamed for everything and anything, so stick to what has been definitively demonstrated and is not in doubt. --Sciencewatcher 02:59, 18 August 2007 (UTC)

Sciencewatcher, thanks for your support and constructive comments. The edit historical summary could be reduced to the review findings, and if it is considered the terminology is already defined in the broader article, that section could also be reduced.

Stress of course involves more than the psychosocial but also environmental, illness history, injuries, trauma, chronic infections, allergies, etc. many linked to CFS and that leads to the usual arguments on precipitating versus perpetuating events and causative versus oppurtunistic factors. The cumulative measure of the systemic affect of all stressors that modify responses using standard physiological measurements and advanced analytical methodologies seems from the CDC work to correlate with symptoms and neuroendocrine function in CFS without the need to assign any particular stress as causative. Rather it says prolonged adaptive responses cause illness (and that may or may not be in the presence of ongoing stress) an advancement on the stress causes illness approach. Not too sure a type of burnout is a good description, perhaps more a ‘stuck adaptive response’? I agree the current Stress and Trauma section does not set the scene for such findings and could be improved.

The present article as you rightly point out does not as yet include discussion on HPA axis, hormone, ANS and immune system inter-relationships. Given the CDC gene expression findings on the ANS pathways and sympathetics and also have found linkages between heart rate variability, sympathetic changes and immune system dysfunction, there may be a need for such. The changes found in glucocorticoid receptor gene expression is likely profound, as these receptors mediate not only neuroendocrine responses but also mitochondrial function, energy metabolism, essential fatty acid metabolism, amino acid metabolism and immune-factors all related to CFS findings. Again advancement on stress causes changes and directly found in CFS patients, rather than more generally on stress, or in animal studies. Of course the glucocorticoid receptor changes have the potential with the effects on the hippocampus and amygdala responses to be the nexus for the so called competing schools of thought on CFS.

Not too sure about the shrunken adrenal glands as initial studies only on very small sample size suggest it is a subset of a subset, perhaps the end of a spectrum? Plasticity here would suggest changes to the hippocampus also if this was correct? but was not found here suggesting other mechanisms? In addition the CFS hypocortisolism is considered mild (a blunted response) and low dose Synacthen tests may be unreliable.

If the Stress and Trauma section is improved to cover other forms of stress implicated in CFS pathogenesis together with systemic effects and physiological measurement methodologies, then the Neuro-endocrinology could perhaps be merged with the Endocrine dysfunction sectionJagra 01:47, 20 August 2007 (UTC)

The problem is that we don't as yet have a definitive etiology of CFS, so there is a lot of speculation. Perhaps the best we can do in the article is to have a few paragraphs describing the effects of stress. Given that stress has been shown to be an important causal factor in CFS, and given that the symptoms and physiological changes in CFS are consistent with a stress-related illness, it is therefore reasonable to describe how stress can cause the symptoms and changes seen in CFS, even if we don't know the exact mechanism, and even if we don't know for sure whether this is what is happening with all patients. --Sciencewatcher 15:08, 20 August 2007 (UTC)

It seems more probable that the etiology of HPA axis changes in CFS is, like that of CFS itself, multifactorial. Others have said an approach more likely to bear fruit in unravelling the etiology of dysfunction in CFS would involve measuring more precisely the various confounding variables to allow a multidimensional understanding of changes in CFS. The article is largely discussion of such potential variables, which I agree should include stress. It is the heterogeneity of factors that might affect neuroendocrine parameters and the HPA axis function that is confounding in any individual case. However allostatic load indices are a physiological measure of the cumulative affects of such dysfunction on the body at a point in time. In itself it is a measure of stress effects, an aid to diagnosis and is said to correlate to symptoms and HPA axis function of CFS without the need for a precise etiology. Perhaps we can can put together something along those lines you suggest. Jagra 08:01, 24 August 2007 (UTC)

I agree with Jagra that the cause of the changes in the HPA axis are probably multifactoral. Discussion of the HPA axis often focuses too much on psychological stresses when other processes can also be involved. Jagra has put considerable effort into expanding the neuroendocrinological entry, but unless it is simplified and condensed into one paragraph I don't think people here will allow it in the article. - Tekaphor 07:22, 31 August 2007 (UTC)

Thanks for comments Tekaphor I will redraft on the basis of discussion Jagra 11:24, 11 September 2007 (UTC)

Protected

Sciencewatcher (talk · contribs) and a horde of anons are edit warring over whether complete resolution is rare. They seem to be blaming the same CDC source. I'm interested in seeing consensus before I unlock the article. JFW | T@lk 11:49, 24 August 2007 (UTC)

"May be rare" isn't exactly definitive. My definition of "rare" would be much less than that. How about we just put in the actual figures from the CDC website ("5% to 10% sustaining total remission")? --Sciencewatcher 14:50, 24 August 2007 (UTC)

Given the vast challenges faced by this page, I am surprised by the intensity of this particular debate. There are so many unknowns with CFS, not to mention many significant scientific debates, which need to be resolved/advanced before "cure rates" should become an issue. Even the CDC admits that recovery rates are "unclear". With many patients suffering from CFS for five, ten, or even twenty years or more, can anyone say with any degree of certainty whether a patient who suddenly feels "better" has had the disease resolve completely or is simply experiencing a partial remission... or a short-term remission... or a long-term remission? And with the etiology of CFS still unknown, a lot of the disagreements on the CFS page are really well before their time.

In the interim we should be satisfied by echoing the CDC simply by stating that recovery rates are unclear, but that a review of data indicates that the disease appears to eventually resolve in about 5% to 10% of patients. (Keep in mind that it may have taken some of these patients fifteen or twenty years to recover.) --- Taroaldo 17:28, 24 August 2007 (UTC)

I agree entirely with Taroaldo. It seems to mme that this protection is unnecessary; just write in the article that "The CDC estimates that between 5 and 10% of sufferers will eventually recover, although rates as high as 80% and as low as 1% have also been claimed", or something similar with better grammar. Thedreamdied 20:41, 24 August 2007 (UTC)

And incidentally, doesn't this talk page need archiving? Thedreamdied 20:42, 24 August 2007 (UTC)

Part of the problem here is that the definition of this illness and who has it are among the sources of severe controversy. If you count people who have other illnesses such as mild depression or almost any unexplained fatigue, it's only natural that you're going to find (potentially far) higher recovery rates than you'll get from a group of patients who all meet the Canadian Expert Consensus Panel definition. I for one have come to trust very little if anything the CDC have to say about some things at this point, including ME/CFS. What are some other figures that we can provide sources from on this? Given that so many arguably or allegedly definitive sources give wildly contradictory information and conclusions, perhaps a large number of citations is inevitable and inescapable. -- Strangelv 21:36, 24 August 2007 (UTC)

I certainly won't disagree with Strangelv's concerns with the CDC, but I really don't think that they've said anything controversial here. They conducted a review of published studies, found varying rates of "improvement" and then declared that the CFS recovery rate is "unclear". CFS is a long-term illness, its etiology is unknown, and there is no blood test you can run and then say "eureka, I'm cured". So this makes establishing specific numbers inherently difficult. The more research I've done, the more I accept the relatively low range of 5% to 10% stated by the CDC. Many patients are suffering for ten years or longer. From the data I've seen, if someone is suffering from CFS for longer than one or two years then their chance of an eventual recovery becomes very low.

And another consideration: many long-term CFS patients have been frustrated with the medical system and have probably given up on it. I'm sure if these patients were tabulated, the recovery percentage would drop even further. --- Taroaldo 23:06, 24 August 2007 (UTC)

A double bike or treadmill test is a straightforward way to test whether a patient has healed. However, this is very rarely done. Figures like these are based largely on what (former) patients are saying and in part on direct observation. Now, since the CDC concept of the disease is very poorly defined I would generally not be ready to trust their figures very much. Reeves in particular seems in the process of totally redefining CFS as a stress disorder. However, this specific figure happens to coincide with other estimates (Jason, for one). The statement that full recovery is rare is true. But it is also known from epidemics that sufficient rest and proper care in the early stage can significantly improve the odds. It further depends on age: children and adolescents have a fair chance to recover fully. Meanwhile, there is no difference between 'recovery' and 'spontaneous recovery', for the simple fact that as of yet there is no known cure. Regards, Guido den Broeder 23:41, 24 August 2007 (UTC)

I agree with Toroaldo: let's put in the estimates from the CDC website and get this article unprotected again. In reply to Guido's comment that there is no difference between 'recovery' and 'spontaneous recovery': spontaneous implies that the recovery is immediate, i.e. one minute you are sick with CFS, the next you are perfectly well. This is very unusual. Most patients recover gradually over a number of years. --Sciencewatcher 14:10, 25 August 2007 (UTC)

Guido - with respect, thats rubbish. A treadmill test is never going to work, firstly because you're unlikely to have the individual's treadmill stats for before they had ME, and also because ME patients, mainly those with less severe ME, would still be capable of running on a treadmill for an extended period, they would simply feel much greater discomfort than a healthy control, and obviously significant aftereffects. Thedreamdied 19:44, 25 August 2007 (UTC)

These aftereffects get measured, with a second test after 24 hrs. Guido den Broeder 19:24, 26 August 2007 (UTC)

Intriguing, I'd never have thought of that. Allow me to retract my 'rubbish' remark. However - i still don't think its a particularly good test. Surely the best test is just to ask if the patient feels that he or she has recovered - i certainly would be able to tell if i was! Thedreamdied 19:39, 26 August 2007 (UTC)

I have gotten a couple of references on exercise (treadmill) tests from Guido. Apparently, study of the efficacy of the "double bike" test is still in progress. I will reserve my opinion on whether it is possible to determine if a CFS patient has been cured until I do some further research, but the notion of using subjective tests to determine if someone has been "cured" concerns me greatly. I say "subjective" because CFS patients are notoriously difficult to pigeonhole, and often their exercise tolerance is wildly unpredictable. A measurement over 24 hours will not be indicative of how the patient will respond two weeks or two months further down the road. And, most importantly, there is no test which definitively indicates a person has CFS, so how can there be a definitive test to indicate that a person no longer has CFS?

Oh, where is a simple blood test when you need one?

BTW, on topic for this section, it seems like there is a reasonable consensus to include a qualified version of the CDC's data. Apparently the disputing anons have vanished. --- Taroaldo 20:47, 26 August 2007 (UTC)

I entirely agree again. And i think the blood test isn't TOO far away... Thedreamdied 23:13, 26 August 2007 (UTC)

Well if you read here blood tests with physiological measurements are an immanent diagnostic, and suggest the article needs updating to reflect this.Jagra 00:46, 27 August 2007 (UTC)

Well - maybe not imminent, this article is about 16 months old. Thedreamdied 12:24, 27 August 2007 (UTC)

Jagra, you keep doing this. You take out-of-date, untested, and out-of-context comments in articles to try to make your point. This has not been published, it has not been examine, and it's nowhere right now. I suggest four years in medical school, four or five years of fellowship in immunology and infection disease, because you are so interested in the areas. OrangeMarlin ^{Talk• Contributions} 12:49, 27 August 2007 (UTC)

Orangemartin you have this annoying habit of trying to play the man not the ball, when you don’t understand the literature, perhaps a refresher course might help!, start here for the findings are published, PMID 16610949 PMID 16610957 Jagra 08:45, 28 August 2007 (UTC)

These exercise intolerance tests aren't based on questionnnaires but on observations of heart, blood pressure, breath etc. Guido den Broeder 20:42, 27 August 2007 (UTC)

Yes, but these physiological results only give a snapshot of a person's condition over 24 hours. This does not take into account that many CFS patients can experience huge variations in exercise tolerance over time. --- Taroaldo 21:27, 27 August 2007 (UTC)

No test does, for any disease. The test can always be repeated. Guido den Broeder 22:59, 27 August 2007 (UTC)

Exactly my point. It doesn't determine that a person's CFS has been cured. --- Taroaldo 23:10, 27 August 2007 (UTC)

Given that it is recognized CFS can come on suddenly or gradually, it seems just as probable that it can remit spontaneously or gradually as well, does not seem to have been studied in respect to this. So one person may meet a certain preferred definition initially, but if they improve they may no longer meet that strict definition, but might meet another CFS definition, does that mean they are remitted or cured? surely not. Just as equally they may initially meet one definition, but by degree worsen over time, does that mean they never had CFS initially? What’s in a definition anyway, I see no problem in quoting CDC figures and if really necessary qualifying them. Jagra 00:46, 26 August 2007 (UTC)

I disagree. Strokes come on suddenly but no-one suddenly gets better from then. Without scientific research to back it up, as you suggest, no-one knows. Thedreamdied 12:24, 27 August 2007 (UTC)

Thedreamdied my understanding is that although published 16 months ago, there is a replication study underway at present, any news on that! Personally I do not know about cures or remissions, I think that is a bad descriptor anyway, what seems to be more common are patients who manage their condition well, gradually improving over time extending capabilities to the point that they are able to resume a near normal lifestyle, and maybe even pass a bicycle test? but remain vulnerable if they exceed their personal envelope and trigger fulminations. Jagra 08:45, 28 August 2007 (UTC)

Yes, i agree Jagra. The point being that they haven't really 'recovered' at all... Thedreamdied 15:07, 28 August 2007 (UTC)

But there are also other patients who don't have any symptoms, and who don't have any further relapses after strenuous activity or stress - I'm assuming that this is what the studies are describing when they talk about patients who have fully recovered (the 5-10%). --Sciencewatcher 15:14, 28 August 2007 (UTC)

My personal feeling is that these people probably didnt have true CFS in the first place. But this is just my opinion Thedreamdied 16:21, 28 August 2007 (UTC)

They definitely did. I know some of them personally. There are also quite a lot of accounts of people with CFS who have fully recovered - they are easy to find if you take the time to look, and you can verify yourself that they had CFS by looking at their case history. --Sciencewatcher 23:33, 28 August 2007 (UTC)

Sciencewatcher, what sort of longitudinal follow-up do these cases have? I gather you have observed some over many years? As a ‘stuck adaptive response’, then one would expect the longer they have CFS the less likely such full ‘recovery’ will be, (not to exclude management improvement)? My assumption with the CDC figures was that such cases, occur early on? Jagra 08:07, 29 August 2007 (UTC)

You are wasting your time, sciencewatcher and Jagra, that's Original Research and Wikipedia is not the right place for it. —Preceding unsigned comment added by 192.68.211.173 (talk) 09:54, August 29, 2007 (UTC)

I guess what I am saying is, without the details and definitions a number of interpretations of the CDC statements are possible depending upon perspective. If I can make a suggestion why not say something like, “Full recovery appears to be the exception, although the CDC report recovery rates of 5% -10%” Without the need to define ‘full recovery’ (cure) as long term, normal lifestyle without need for continued management strategies. Or ‘recovery’ (remission) as no longer meets diagnostic criteria, and/or pass cycle test and/or resume near normal lifestyle. Jagra 11:24, 29 August 2007 (UTC)

Jarga, you could say that about virtually and CFS research (and there frequently are arguments over most things that are put in this article). However the CDC figures do correspond with studies that have looked at recovery. You'll need to look at those studies to see what they define as full recovery. Let's just put in the CDC figures, as there is broad agreement here for that. --Sciencewatcher 14:27, 29 August 2007 (UTC)

Thedreamdied told me (on my talkpage) that a consensus version had been reached. From the above conversation I cannot quite distill what the final version is meant to be. Could we decide on this now, please? JFW | T@lk 17:15, 29 August 2007 (UTC)

Happy to use CDC figures Jagra 06:53, 30 August 2007 (UTC)

Yes. CDC figures ok. Basic wording to convey the notion that CDC conducted a review of data which indicates that the disease appears to eventually resolve in about 5% to 10% of patients. --- Taroaldo 07:05, 30 August 2007 (UTC)

My impression is that researchers have found in general the prognosis is less favourable for those with more severe CFS symptoms and/or who fit stricter criteria. Overall, the main characteristics of people I've met with CFS-like history and substantially recovered, were that they didn't experience the full range of symptoms/implications listed in the Canadian consensus document and that they didn't experience "prolonged" post-exertion symptom exacerbation. One told me that she feels worse for several hours after exercise but better the next day as a result, and I found this to be a fascinating insight into the "success" of CBT/GET. Sciencewatcher has previously stated that (even) the Fukuda criterion is too restrictive; this makes me curious about the people Sciencewatcher knew who had CFS and recovered, which criteria did they fit into? Our anecdotes are useless for the article anyway. All criterias involve considerable impairment and CFS patients can be bedbound without fitting stricter criteria, however the prognosis of different criteria can’t be lumped together. Since CFS is currently a diagnosis based on symptoms only, then surely declaring a "cure" would also be symptom based until biological markers are agreed upon? People diagnosed with CFS do recover, but if an ex-CFS patient must constantly apply special management techniques to avoid a relapse while all their friends are living "stressful lives" without ever acquiring CFS, then that is a remission and not a cure. I agree that the CDC figures are OK in the article. - Tekaphor 10:11, 30 August 2007 (UTC)

GET is not widely viewed as a safe or effective treatment for CFS. CBT can be highly effective in treating some of the side effects of long-term illnesses (depression, life outlook, anhedonia, etc.), but it is irrelevant to the wider pathological elements. --- Taroaldo 18:49, 30 August 2007 (UTC)

tekaphor: I have talked to a number of people who have recovered. One person (known personally to me) met all of the various criteria, and had all of the features listed in the Canadian criteria except pain (which is not required for a diagnosis under the criteria). Other people have been bed-bound or in wheelchairs and have recovered. The reason I advocate less stringent criteria is because there appears to be no single set of symptoms for CFS, so if you have a very strict criteria you will inevitably cut out a lot of CFS patients. From what I have seen and researched, both severe and mild CFS are essentially the same illness, and it can have widely varying symptoms. If you want to read a lot of stories of people who have recovered, I would recommend http://alexbarton.co.uk/cfsrecovery-stories.htm (and no, I'm not Alex Barton and I'm not affiliated or related to her in any way). Of course they are all just anecdotal accounts, but you get a good insight into the illness by reading about people who have recovered. And as I have said elsewhere, people who have recovered can live normal lives without having relapses - that is the definition of full recovery (or at least my definition). If you have a relapse after a year or two, or you have to lead a restrictive life, you are not fully recovered. --Sciencewatcher 21:23, 30 August 2007 (UTC)

Sciencewatcher, if that person didn't experience pain, then they didn't "have all the features" of the Canadian criteria, and pain is only optional here when the onset is infectious. I'm not disagreeing that people diagnosed with CFS can and do recover, but when I read recovery stories nothing really stands out that separates them from those who didn't recover; with both groups trying X Y Z etc. I agree that adopting stricter criteria runs the risk of excluding a lot of patients who would be diagnosed with "idiopathic chronic fatigue" (which seems more amendable to intervention), but using slacker criteria also has its controversial problems. Many illnesses have seemed "essentially the same" until new understanding has properly discerned the contrasts. The "issues with definitions/criteria" section of the article highlights that different criteria/symptoms/onset affects the prognosis and treatment response; this is important to consider. - Tekaphor 07:11, 31 August 2007 (UTC)

I didn't think it mattered for pain whether the onset was infectious or not. In this case the onset was infectious, although again I personally don't think that matters: from what I have seen, infectious and non-infectious onset appear to be the same illness. And I agree with you that there isn't really any discernable difference between those who have tried things and recovered versus those who have tried the same things and not recovered. --Sciencewatcher 14:26, 31 August 2007 (UTC)

NICE Guideline

In case you have missed it, the NICE Guideline for CFS/ME is out: [1]. Guido den Broeder 20:42, 27 August 2007 (UTC)

NICE guidelines published

http://www.nice.org.uk/page.aspx?o=449472

A new guideline to improve the diagnosis and management of chronic fatigue syndrome/ myalgic encephalomyelitis (or encephalopathy) (CFS/ME) in adults and children is launched today (22 August).

(NICE is the National Institute for Health and Clinical Excellence)

http://guidance.nice.org.uk/CG53

Summary This guideline is about the care of people with chronic fatigue syndrome, which is also called myalgic encephalomyelitis (or encephalopathy), in the NHS in England and Wales. Throughout this booklet we refer to the condition as CFS/ME for short. The booklet explains guidance (advice) from NICE (the National Institute for Health and Clinical Excellence). It is written for people with CFS/ME, and parents or carers of people with the condition. It may also be useful for other family members or for anyone with an interest in CFS/ME.

The guideline aims to help you understand the care and treatment options that should be available in the NHS.

(PLEASE add this link as this is a big step in the UK and useful for others too).

RichasAA 22:27, 28 August 2007 (UTC)

Thank you for getting a username just to tell us this. Is there anything else on the subject you'd like to share with us? JFW | T@lk 17:16, 29 August 2007 (UTC)

I have just read the quick reference guide. I am quite impressed by the way this difficult problem has been tackled, and the sensible advice to general medical practicioners on how to investigate symptoms. I believe this guideline should get substantial coverage in this article; for instance, the list diagnostic criteria could well replace our present framework. JFW | T@lk 17:30, 29 August 2007 (UTC)

Thank you. Rereading the article now and the discussion below I think that the NICE guidelines and peoples hard work has led to a big improvement lately. Is there anything else I'd like to add? Well I am diagnosed with CFS and have had symptoms for nearly 2 years, feeling a bit better over the past couple of months with far better cognitive function but I have to say that despite the hard work and recent improvement the article is pretty difficult for someone with CFS to follow and much of the discussion here is impenetrable.

For me having the controversial and messy proposed causes before the diagnosis and treatment sections is offputting and unhelpful. Someone with CFS wants to find out what it is how to diagnose it and what the treatments are - the controversial causes bit adds little in terms of helpful information so I would relegate it down the page.

The prognosis bit is also weak (and horribly depressing). In my experience health professionals refuse to discuss prognosis so some additional work here would be very helpful, I just suspect there is too little available to add much.

The introduction section before the contents is also a bit long. The classification stuff is also of less interest than definition, diagnosis, treatment so I would put this lower too.

--86.153.45.249 23:46, 20 September 2007 (UTC) RichasAA

You can't always please everyone... JFW | T@lk 17:53, 29 August 2007 (UTC)

True that JFW. And of all stakeholders, the patients really are the least concern in a medical guideline. —Preceding unsigned comment added by 82.135.68.65 (talk) 19:04, August 30, 2007 (UTC)

I also had a look at them, and I agree that they are very good in general. I would have preferred them to have acknowledged the etiology as being a psychosomatic illness caused by factors such as stress, but they have chosen to not discuss any potential etiology. In my view this is a cop-out and is bad for the patient - after all, how can the patient cure the problem if the doctor is vague as to the causes? Most doctors will discuss stress and lifestyle factors with their patients anyway, but it would just be good to have this present in the guidelines. --Sciencewatcher 18:38, 29 August 2007 (UTC)

With respect, you are talking absolute rubbish. No-one knows why CFS happens, but 'stress' is most definitely not the cause. Research indicates low-level viral infection and immune dysfunction. To have put such a thing in official guidelines would enforce the kind of ignorant stereotyping at patients that has endured for so long. Thedreamdied 20:34, 29 August 2007 (UTC)

If stress is most definitely not the cause, how come it is the only significant causal factor that has been identified for CFS? There is no research showing that low-level viral infection and immune dysfunction are causal factors in CFS, but conclusive evidence showing that they are symptoms of chronic stress. Please don't accuse people of talking "absolute rubbish" in future just because you don't like what they're saying. --Sciencewatcher 21:42, 29 August 2007 (UTC)

And you shouldn't blame people for reminding you of your intellectual shortcomings and calling a spade a spade. Your above statement consitutes "absolute r******" (not my choice of words) from an epistemological point of view as there is Dubbo Infectious Outcome Study , which states: "The syndrome [CFS] was predicted largely by the severity of the acute illness [different infections] rather than by demographic, psychological, or microbiological factors" (Hickie I, Davenport T, Wakefield D, Vollmer-Conna U, Cameron B, Vernon SD, Reeves WC, Lloyd A; Dubbo Infection Outcomes Study Group). That renders your point "stress as the only causal factor" ,as implied by your rethorical question, invalid. Dude, I don't know what science you are watching, but I think you are on the wrong wiki page. Try burnout instead. —Preceding unsigned comment added by 192.68.211.173 (talk) 13:31, August 30, 2007 (UTC)

Yeah, this one could get interesting! Stress contributes to a lot of heart attacks and cases of hypertension, but people don't run around calling those illness psychosomatic. Sciencewatcher, where is it stated that stress is the only significant causal factor identified for CFS? The credible studies I have read on psychosomatic links are not definitive (just like everything else with CFS). On another front, playing up words like "psychosomatic" in literature intended for diverse audiences is not wise, particularly in the absence of definitive links. CFS patients have been stigmatized for decades by the uneducated lay-public and by uncaring or disinterested physicians: it's no wonder that they are, perhaps, a bit sensitive to labels. BTW, why would NICE 'acknowledge the etiology as being a psychomatic illness'? I must have missed the press release announcing that the etiology of CFS had been determined! --- Taroaldo 07:44, 30 August 2007 (UTC)

After an initial read of the guidelines, I was impressed with the way they handled some difficult issues Viz, First sentence, there is insufficient evidence for --- next sentence but patients report benefit from--- I think we could learn and do more of this approach. Disappointed they did not find for increased sensitivity of patients to drugs, restricted search criteria! as for instance CFIDS association report and advise on such. Worry about recommendation on use of tricyclics even low dose, without such caveats and/or need for cortisol monitoring. Tanya Harrison dissent report interesting read, although a lot seems to be medico/political UK issues, these do spread! Support her in her summary reasons for dissent and concern about inadequate diagnostic workup tests. Jagra 08:16, 30 August 2007 (UTC)

Intellectual shortcomings, eh? Stress as a significant causal factor is discussed in this wikipedia article (look at the stress and trauma section). I would suggest reading it (if you have the intellectual capacity, that is, 192.68.211.173). Infection is another factor, but it could be secondary to stress - we don't know at this time. Or it could be another stress factor, as infections influence the HPA axis in the same way as other stresses. All the evidence points to stress being the single most important factor, and to CFS being a stress-related illness (unlike other illnesses where stress just makes them worse). --Sciencewatcher 14:27, 30 August 2007 (UTC)

Yes, intellectual shortcomings. "All the evidence points to stress being the single most important factor." That is a statement. And it is wrong. Proof: The Dubbo infectious outcome study is part of the evidence. It does not point to stress as being the single most important factor. It points to the severity of an acute infection as being the single most important factor. Therefore, not all evidence points to stress as being the most important facot. qed. Are you sure you are talking about CFS? —Preceding unsigned comment added by 192.68.211.173 (talk) 14:55, August 30, 2007 (UTC)

For the record - most objective observers will sooner or later realize that the CFS research base in its entirety is jagged and scatterd over just about every medical domain. By no means is it collectively "pointing" anywhere near a discrete entity or definitve medical concept. —Preceding unsigned comment added by 192.68.211.173 (talk) 16:12, August 30, 2007 (UTC)

I don't see stress listed as a factor in the Dubbo study, so how do you come to that conclusion if they didn't even look at stress as a factor? --Sciencewatcher 19:23, 30 August 2007 (UTC)

Who says they didn't look into stress? You, sciencewatcher? Their conclusion is that "psychological factors" are secondary to the severity of the initial infectious illness. By the way, sciencewatcher, would you mind telling us how old you are? —Preceding unsigned comment added by 82.135.81.46 (talk) 16:52, 31 August 2007 (UTC)

I'm not saying they didn't look at stress - I'm saying I don't see it listed in the abstract and I don't have access to the full article. "psychological factors" could mean many things. What psychological factors did they look at? I don't see what my age has got to do with anything. --Sciencewatcher 20:14, 31 August 2007 (UTC)

I too hope that everyone here has read the "stress and trauma" segment, along with the eleven other segments in the section "proposed causes and pathophysiology". (And I'm sure more could be added.) We can debate almost every aspect of CFS ad infinitum because there is a wealth of competing research and so little that is certain. --- Taroaldo 19:15, 30 August 2007 (UTC)

Also have a look at the Onset section, and the references there. In PMID 9201648 85% of CFS patients had stressful events in the year preceeding their illness, compared to 6% of controls. There was an apparently infectious illness preceeding CFS in 72% of patients (but defininte infection was only found in 7%). So in this study stress was the most important causal factor, higher than apparent infection. It was a smallish study (134 patients and 35 controls), however the results have been replicated in other studies, and 85% versus 6% is highly significant even in a study this size. --Sciencewatcher 19:58, 30 August 2007 (UTC)

Whether or not ‘stress’ in the last 12 months was the precipitating factor in any cohort can be argued until the cows come home, however the lifetime stress effects in CFS patients by physiological measures, have been found high compared to controls, and that shows stress is more of a factor in patients, even if not precipitating.. Pmid 16610956 Pmid 16610958So I don’t think it can be argued that stress of all types is not part of the disease, particularly as perpetuating factors, and that is what matters in management strategies. Jagra 08:20, 31 August 2007 (UTC)

Once again Jagra, your interpretation is incorrect. Moreover, stress is a poorly defined psychology. And furthermore, the disease may induce the stress. OrangeMarlin ^{Talk• Contributions} 13:07, 31 August 2007 (UTC)

All of the studies that have looked into it have shown that CFS patients are significantly more likely to have stressful life events in the year preceeding the illness. Certainly CFS does cause more stress, and that can be a factor that causes the disease to persist, but stress does seem to be a sifnificant precipitating factor. And stress is not really "poorly defined": you can very easily measure current stress by looking at the levels of cortisol and adrenaline in the blood. --Sciencewatcher 14:22, 31 August 2007 (UTC)

LOL. Good one. OrangeMarlin ^{Talk• Contributions} 14:59, 31 August 2007 (UTC)

Adding information here. Sciencewatcher, first of all please don't encourage the pseudoscientific POV-pushing of certain editors. Second, I think that levels of cortisol and adrenaline are measurements for stress, but only over short-term. How can you do a retrospective study and measure stress levels? I don't like these research studies, because they are, well, crap science. CFS is poorly understood, and every time I read these studies, someone will go overboard. Remember Occam's razor. Often the best explanation is the simplest one. Stress may cause CFS, but what if the stress is induced by an underlying symptomatic disease state, like a viral infection. Excuse my laughing at your comments, because you're just enabling some of certain editor's POV pushing. You appear to be someone who doesn't like urban BS to rule medical knowledge, and others don't. OrangeMarlin ^{Talk• Contributions} 15:06, 31 August 2007 (UTC)

As far as I understand, the studies looking into stress as a precipitating factor asked the patients about stresses that happened in the period prior to the illness. They did not measure anything because, like you say, there is no physiological test for long-term stress. All of my posts on wikipedia are aimed at reducing urban BS and pseudoscientific POVs. I don't see how this is "crap science". Stress is the simplest explanation which fits CFS. No viral infection has been found, so you're relying on "stealth viruses", which is essentially crap science... --Sciencewatcher 20:14, 31 August 2007 (UTC)

Stress is a factor because it weakens the CNS defence against infections. It does not cause ME/CFS, but it gives an infection the opportunity to pass the blood-brain barrier and cause ME/CFS. By the way, keep in mind that stress is not a psychological phenomenon. It is physiological response. If it lasts, it injures the hippocampus. Guido den Broeder 23:46, 31 August 2007 (UTC)

Orangemartin, Stress is not just a psychological phenomenon, otherwise how do you explain environmental stress, stress from trauma, physical challenges etc . It also seems you are saying that the CDC are pushing fringe science with allostatic load studies, and anyway they have got it all wrong, as the stress is caused by the disease? Let me quote from here

“The primary hormonal mediators of the stress response, glucocorticoids and catecholamines, have both protective and damaging effects on the body. In the short run, they are essential for adaptation, maintenance of homeostasis, and survival (allostasis). Yet, over longer time intervals, they exact a cost (allostatic load) that can accelerate disease processes.” “The bottom right panel of Figure 1 describes a situation in which the hormonal stress response is inadequate to the needs of the individual genotype, resulting in excessive activity of other allostatic systems such as the inflammatory cytokines, which are normally contained by elevated levels of cortisol and catecholamines”. “ Comparable human disorders involving lower-than-needed cortisol include fibromyalgia and chronic fatigue syndrome.” This paper indicates allostatic load is dysfunctional allostasis over longer time periods that leads to diseases such as CFS. Not that diseases like CFS cause allostatic load? although the added stress may well perpetuate it. Allostatic load studies are not fringe science, a better term is an emerging science and the CDC endorsement and that of the quality journals they publish in is evidence of that. Jagra 07:46, 1 September 2007 (UTC)

The NICE Guidance, meanwhile, does (at least) one thing that will cause a lot of turmoil: it redefines the disease to include a multitude of patients who really suffer from entirely different conditions. This is done by requiring only a single primary symptom where the CDC thus far required four - which is already considered too wide a definition. Genuine ME/CFS patients will now be only a small minority among the patients that receive the label, if this guidance is followed. Guido den Broeder 23:55, 31 August 2007 (UTC)

See http://www.drrant.net/2007/08/being-nice-about-me.html for some corroboration from unexpected corners. Avb 12:44, 1 September 2007 (UTC)

It doesn't necessarily "redefine the disease to include a multitude of patients who really suffer from entirely different conditions". As I've stated before, my own view is that all of these patients have CFS. However there is no firm evidence either way at the moment. --Sciencewatcher 14:45, 1 September 2007 (UTC)

Looked again at NICE recommendations on GET 1.6.2.16, and can see why it is so controversial! Says (a) establish baseline activity level that does not exacerbate symptoms and increase from that level (b) sustain that level for a week and then increase by up to 20% weekly. I would suggest from own empirical observations that both of these recommendations are more appropriate for rehabilitating other conditions, but not CFS. This recommendation needs to be integrated with “Envelope Theory” mentioned in section 1.4.6.3 for a more suitable regime. About half the baseline and one third the increment more appropriate, in my opinion. Discusses as if relevant only to fatigue, not mentioning pain, only half the story. Jagra 08:03, 1 September 2007 (UTC)

Less, even. Too much activity also leads to dizziness and failure to concentrate, both of which can be hazardous. Before any increase in activity takes place it should first be established that a patient has the capacity to do so. Regards, Guido den Broeder 09:10, 1 September 2007 (UTC)

What document are you reading? I don't see where it says to increase by 20% weekly. It just says "Agree with them a level of additional low-intensity exercise that is sustainable, independent of daily fluctuations in symptoms, and does not lead to ‘boom and bust’ cycles", which seems reasonable. I don't see any "increase by 20% weekly", which would be ridiculous. --Sciencewatcher 14:50, 1 September 2007 (UTC)

Guido, I agree the first problem is the immediate increase above baseline, it should be reduced substantially when new activity is commenced, then slowly build back to old baseline, building reserves before any increase. Sciencewatcher the increment rate is in this one page 30 section 1.6.2.17 , I can’t imagine when it would ever be appropriate to increment at that rate, certainly not so early on. Problem with such numbers is they get interpreted literally. It says

"Progressing with GET-- When low-intensity exercise can be sustained for 5 days out of 7 (usually accompanied by a reduction in perceived exertion), the duration should be reviewed and increased, if appropriate, by up to 20%. --" Jagra 09:12, 2 September 2007 (UTC)

Yes, it says 20%, but nowhere does it say "20% weekly" as you suggested. Instead it says only to increase if appropriate, and it also says to only use exercise that is sustainable and doesnot lead to boom and bust cycles. --Sciencewatcher 14:58, 2 September 2007 (UTC)

Sciencewatcher, if you have the right start point and right increment they should be able to increase more or less weekly, (7 days out of 7) for if they fail on even one day (let alone unsustainable 2 days out of 7) they should go back a couple of steps until they stabilize at a lower level where they can do 7 out of 7 without exacerbation of symptoms next day. Whether it is on week one, or week 101, a 20% increment on prior level is never likely going to be ‘appropriate’ mild or otherwise so why include such a figure!. It is also disappointing that Nice has not recognised the same general approach applies to all forms of activity, mental and physical and switching between different types of activity extends capability Jagra 08:02, 3 September 2007 (UTC)

Considerable effort went into these guidelines, with some good practical advice. Patients are fighting attitudes of "screw what the neurotic slacker experiences, they must do CBT and GET regardless so they realise the error of their abnormal beliefs/habits", and managed to keep them out of the guidelines; CBT and GET are only "suggested" for people with mild to moderate CFS, and they can refuse it. However, guidelines are usually well-worded and what happens in the real world depends a lot on the doctor's opinions/interpretations. The inclusion of CBT and GET is likely to remain controversial, and what will the implications be "behind the scenes" for those who are non-compliant? I have become suspicious from previous publications that recommendations of listening to the patients' experience or validating it are more of a lip service attempt to gain the patients trust rather than actually caring about the patient. The mandatory inclusion of the post-exertion aspect is a major improvement over the Fukuda criteria, but the sole emphasis on "fatigue" and the requirement of only 1 additional symptom is a disappointment. I think the framework would have been better (but perhaps too complicated) if there was a point system, with points allocated to the "optional" symptoms according to relevance and severity. I'm not sure why JFW wants to exclusively adopt the new diagnostic criteria in the article, but I agree the guidelines deserve coverage. I prefer the Canadian criteria, which perhaps isn't ideal and a little too strict, but was composed by a group of doctors who saw more than 20,000 patients, while other criteria seem to be formulated by mostly academics who review studies based on criteria formulated by other academics. - Tekaphor 02:51, 3 September 2007 (UTC)

They are also in contrast to the CDC-criteria, which (after reengnineering) still require 4 out of 8 symptoms. As for the time being, the CDC criteria are the most widely used. Thus they should remain the framework of choice. —Preceding unsigned comment added by 192.68.211.173 (talk) 09:10, 3 September 2007 (UTC)

Tekaphor, you've got me wrong. I only suggested that the list in the NICE guideline was so complete that it would be better to use that as a framework than the present hodgepodge that isn't based on anything. It would make the article more authoritative. The CDC criteria are okay, but they leave out many symptoms very commonly reported in CFS/ME. JFW | T@lk 09:39, 3 September 2007 (UTC)

I have now added the NICE criteria, which are likely to become gold standard in the UK. Further references to the NICE guideline can be made to <ref name=NICECG53/> (contrary to my edit summary, which included a 0 in the reference name). I have linked to the Quick Reference guide, which is all that is needed for the purposes of this article. JFW | T@lk 10:36, 3 September 2007 (UTC)

Today, the ME Association has issued a press release calling for the withdrawal of the NICE CG53 guideline. The MEA's statement concludes: "Overall, we must therefore conclude that the NICE guidance remains unfit for purpose. We call for the guidance to be withdrawn and rewritten by a group of health professionals who unambiguously accept that they are dealing with a physical rather than a psychosomatic illness." Until a copy of this press release is available on the MEA's website, a full copy can be read here. MEagenda 09:57, 7 September 2007 (UTC)

The Press Release calling for the withdrawal of the NICE CG53 Guidelines as being "unfit for purpose" issued by the second largest UK patient organisation is now available on the charity's website. MEagenda 09:13, 8 September 2007 (UTC)

Infection and Stress

Just because a single specific virus hasn't been exclusively linked to CFS, that doesn't mean viruses aren't involved. Although the previously mentioned Dubbo study focused exclusively on post-infectious CFS, it discusses a syndrome that develops after exposure to "several different viral and non-viral micro-organisms". As for the other study Sciencewatcher mentioned, what exactly do they mean by "definite infection"? The abstract reads to me something like 72% of patients reported having infectious symptoms at the start of their CFS but only 7% still had definite infectious symptoms now or knew what specific infection they had at onset or were formally diagnosed with an infection at onset. Stress (of any type) appears to be an important aspect in CFS, but as a trigger or cofactor; I disagree with the sole emphasis on psychosocial stress. Similar mistakes have been made in the past with many other illnesses; which were blamed on stress at the time because stress was apparently involved, before more was known about the underlying processes. Sure, stress causes biological changes, but I can't help point out again and again that the vast majority of people in "chronically stressful circumstances" never develop CFS, not to mention the patients who weren't stressed prior to onset. Sciencewatcher mentions that infections influence the HPA axis in the same way as other stresses. If that is true, then perhaps the immune dysfunction (found by Dr Gow's gene expression work) is having a similar perpetuating influence. While stress management is important for other diseases with a psychosocial component (stroke, heart attack etc), the core treatment involves medicine that targets the related pathology, but CFS patients don't have that option yet and some professionals are suppressing such research/treatments as "unnecessary". I have noticed some people seem to believe that biomedical intervention for CFS is a form of "relinquishing personal responsibility of the psychosocial aspects" of CFS; but when it comes to other diseases (or even psychiatric illnesses) which also have psychosocial factors, they view it as a part of an "integral" approach. Some studies have suggested emotional disturbances can increase the risk of acquiring CFS, but perhaps if true this occurs because these experiences themselves are stressful, not because CFS itself is an emotional disorder. Again, the vast majority of people who experience these don't go on to develop CFS either. In the Dubbo study, higher neuroticism and "external locus of control" scores were only associated with more severe mood disturbance but not any other symptoms. - Tekaphor 03:29, 3 September 2007 (UTC)

Tekaphor agree with you on stress involvement in CFS, and yes infection does involve the HPA axis in an acute phase response, where among other actions cortisol is meant to be up regulated to control inflammation, both from an infection and the immune response to it like certain cytokines. The classic fever aids in this through release of heat shock proteins. All of this is normal ‘allostasis’, where it goes wrong though as in the case of dysfunctional allostasis, chronic conditions arise including dysfunctional immune responses and that can be indicated it seems by gene expression changes. I am a little sceptical but hopeful that such changes will prove CFS specific rather than more general process indicative You are right not all stressed individuals develop CFS but a large number do develop other conditions, four types of dysfunctional allostasis are identified, each leading to certain groups of diseases. More evidence is emerging that CFS or subgroups have a lowered cortisol response, but other conditions also have this to one degree or another including FM, asthma and inflammatory bowel diseases, so is it genetics that determine who gets what or are they all just named parts of a spectrum, (one of four maybe!)into which different categories of CFS might exist? I don’t think it necessarily important to identify any particular stressor as causative, because it is more probably a case of the whole being greater than the sum of components, more important I think to acknowledge processes Jagra 08:09, 3 September 2007 (UTC).

Yes, all stresses affect the HPA axis (and other body systems) in identical ways, and in many cases it is a viral infection combined with a psychological stressor that causes the illness. However my own view is that it is the psychological stressors that are important in maintaining the illness. You don't seem to see CFS in animals (although it would be difficult to diagnose for sure). I think that in the absense of any psychological stressors, the human body will always recover from the mild viral infections that seem to trigger CFS. In all the detailed case histories I have read, I have never seen any CFS patient who has not been in the midst of some severe psychological stressor. I think the reason that the same stresses don't cause CFS in all people is simply that people handle stress in different ways. Not all soldiers in the same battle suffer from PTSD. --Sciencewatcher 14:56, 3 September 2007 (UTC)

Animals suffer stress and stress-related illnesses, so the idea that animals don't get ME/CFS as a basis for the idea stress causes and/or maintains ME/CFS is flawed. And considering the rest of what you say is subjective, I shall feel free to reply anecdoctally. I myself and many other patients I've known did not have significant psychological stress at the time of onset, and the most significant continual stressor has been the illness itself. I've had doctors conclude that my coping skills were poor simply because I was physically sick, without taking what could even pass for a sketch of my psychological and personal history. We can't discount bias in how a patient's response to stress is perceived by those assessing them, nor underestimate the real stress caused by the disease itself as well as the lack of compassion and understanding we receive. Nor can we discount that many people are highly stressed and contract viruses and don't get CFS.

I think to be Wiki-compliant the CFS article is going to be necessarily conservative and I don't protest much of the content from that point of view, but I do object to this discussion taking this turn here which is subjective and potentially misleading, hence why I think it's fair to reply with another side to the argument. Researchers like Kerr, Gow, Chia and the NCF team are not proponents of the stress theory and their work has been and likely will be among the most important and most detailed on CFS. There are plenty of factors other than stress that could explain why viruses or immune system effects persist. The Dubbo paper showed 'hit-and-run' brain damage caused by a virus. John Chia's work showed incomplete viral fragments in the tissue that can be activated by exertion. The same could be said of why some soldiers get PTSD, some don't. There are many factors, stress is simply blamed in the absence of etiology being understood more thoroughly. And there are many diseases that strike some and not others for reasons other than stress, or simply arbitrarily.124.187.109.140 19:36, 20 September 2007 (UTC)

You are right, animals do suffer stress and a lot of our knowledge of stress comes from animal experiments. I was not implying that animals do not suffer stress, but rather they do not generate their own psychological stress (like humans do) from worry or other purely psychological processes. Animals suffer from stress when put into physically or socially stressful situations, but tend to recover when removed from those situations. In reply to your comment that not all CFS patients are under stress when they get CFS: the important period seems to be 3-12 months prior to contracting CFS. For many patients the stress has actually ended a month or so before they get CFS. Also, sometimes people do not realise what is or is not stressful: an example, for one person the stress of living with a person he did not like, and the consequent constant feelings of suppressed anger were a huge stressor that contributed to CFS, but at the time he did not realise the significance of this. PTSD is pretty well understood, and there is no need to speculate about possible viruses. The same is true of CFS, in my opinion. --Sciencewatcher 21:07, 20 September 2007 (UTC)

"124.187.109.140", I totally agree that the interpretation of the stress response in CFS is heavily biased, and largely based on personal opinion. Even most healthy people who temporarily experience flu-like and hangover-like symptoms appear to be rather irritable in stressful situations. Fortunately, not all psychologists interpret a reduced stress tolerance as having bad coping schemas, and instead look into how the patient deals with the situation, while viewing the poor stress response as a "situation" to deal with rather than a mental issue. - Tekaphor 04:23, 24 September 2007 (UTC)

Sciencewatcher, I agree that because of our brain structure humans are more prone to the effects of negative psychological processes compared to other animals. However, we don't know how much a stressful event can affect their cognitive and emotional processes in the long-term. I wouldn't even say for certain that they can't generate any of their own psychological stresses. You said "animals suffer from stress when put into physically or socially stressful situations, but tend to recover when removed from those situations", but the same could be said about most people, even CFS patients who "tend to recover" from symptom exacerbations that occur when placed in such environments. - Tekaphor 04:23, 24 September 2007 (UTC)

Agree not all soldiers, but soldiers more generally have been found to have lowered cortisol prior to battle, considered an adaptive response that may predispose some to PTSD, a condition of low cortisol. Much like dysfunctional allostasis may predispose some to CFS. And maybe differentiate gradual and sudden onset. Does it matter which stress is the final straw? For once the tipping point is reached, removing that stress does not cause recovery. I have not heard of any spontaneous cathartic CFS recovery? But granted any stress removal is essential and does aid progress Jagra 09:49, 4 September 2007 (UTC)

The original viral infections caused the disease, but they are not the disease itself. It is brain damage and CNS inflammation that you need to recover from and that is somewhat more difficult. By the way, animals can get ME/CFS, too. Guido den Broeder 17:11, 3 September 2007 (UTC)

There is no good evidence of CFS in animals. "brain damage and CNS inflammation" have not been shown in CFS. --Sciencewatcher 18:21, 3 September 2007 (UTC)

Your ignorance is underwhelming. Guido den Broeder 19:57, 3 September 2007 (UTC)

Thanks. Yours is overwhelming. --Sciencewatcher 20:47, 3 September 2007 (UTC)

POV forking

Jklsc (talk · contribs) has recreated a page at Myalgic Encephalomyelitis that essentially is a WP:POVFORK of this page that caters for the view that ME is not the same as CFS. I have turned that page back into a redirect, because I feel that multiplicity in pages and terminology is harmful to the subject from all perspectives. I ask other contributors to offer their views, and if possible support me in trying to concentrate the content on this page for maximum quality. JFW | T@lk 09:48, 3 September 2007 (UTC)

I have spoken in favour of such a page before. ME and CFS are not the same diagnosis, and a lot of info on ME is not easy to place in this article on CFS. Guido den Broeder 17:13, 3 September 2007 (UTC)

Perhaps we are getting ahead of ourselves. We still can't find general agreement on anything significant in the CFS page. Adding a separate myalgic encephalomyelitis page is highly contentious, especially since the Americans are in the process of changing the name "CFS" to the proposed "CFS/ME" with an eventual goal of having "CFS" changed to myalgic encephalopathy. So then we will have chronic fatigue syndrome, myalgic encephalomyelitis, and myalgic encephalopathy. This will be confusing enough for us to deal with, never mind an innocent member of the public coming to Wikipedia for some info on this disease. Many researchers and patients do not differentiate between CFS and M.E., so at this point could we keep it within the CFS page, perhaps under an expanded controversies section. I think we have a serious responsibility to be careful here: when using one of the large search engines and typing in "chronic fatigue syndrome", the Wikipedia CFS page comes up #3 on the list, so a lot of people may be relying on the info provided here. --- Taroaldo 19:00, 3 September 2007 (UTC)

There would certainly be a need for Myalgic encephalopathy since that diagnosis is vastly broader than Myalgic encephalomyelitis, like Muscular rheumatism before. The reason for the lack of agreement is partly, perhaps largely due to the fact that important defining information is now missing or hidden. Guido den Broeder 19:55, 3 September 2007 (UTC)

I would strongly support renaming this page to Myalgic Encephalomyelitis as this term is older than the dubious name CFS, and I fail to see the value in creating or supporting superfluous new names like Myalgic Encephalomyapathy.

On the separate disease issue I can't agree. One is clearly this disease and the other is a mess of different things that the CDC appears to want to fuse together to obfuscate this disease. If your primary problems are depression and bad reactions to emotional stress, then lumping you in with ME and with patients without accurate diagnoses does you no good whatsoever. -- Strangelv 18:43, 5 September 2007 (UTC)

I mostly agree with you, Strangelv, and Taroaldo also made some interesting points to consider. Perhaps the article could be renamed to the acronym ME-CFS, but then there would probably be fisticuffs over which initials should go first. - Tekaphor 13:07, 6 September 2007 (UTC)

CFS is the name that is used by researchers. ME was dropped because it implies an incorrect etiology, but patients prefer it because it is more physical sounding. But this is not a good reason to retain it when it is incorrect. If you only have depression you will not be diagnosed with CFS under any criteria. --Sciencewatcher 14:00, 6 September 2007 (UTC)

Neither name is ideal, however it is unsurprising that the older ME name implies "incorrect etiology" when applied to people who don't fit the original ME criteria (which also isn't being used in any research on "CFS"). Unfortunately, solid modern research in this area is lacking, and as far as I know there is only limited older evidence for CNS inflammation, hence the related name ME. - Tekaphor 02:49, 7 September 2007 (UTC)

Even patients who do fit the original ME criteria don't show the inflammation. Have a look at this article which suggests that ME might have been confused with Polio. --Sciencewatcher 18:34, 7 September 2007 (UTC)

That is an interesting page, particularly the section on the differences between ME and CFS. As for CNS inflammation, I don't know enough about the related research procedures to comment on the statement "very few (M.E.) patients today show signs of an inflammatory process in the spinal cord". Personally, I'm anticipating a new name based on more research. - Tekaphor 03:57, 9 September 2007 (UTC)

Cleanup

I've spent some time doing cleanup today, and boy what a collossal mess. People have routinely disregarded the most basic editing guidelines in their rush to shove in as many references as possible. Most hair-raisingly, I removed an unsubtle solliciting of votes for an E-petition (heaven knows how long that has been on the page!) There were various instances where articles were being referenced multiple times without using proper cite.php linking. I've fixed some of them now. There were other instances where the reference ought to have been a journal source, but instead a nonauthoritative website was used for the same content (e.g. CDC 1994, Carruthers 2003). This is clearly not acceptable.

I urge all contributors to help out with the proper sourcing of studies. At the moment, many references appear to have been copied & pasted from elsewhere. PMID or DOI codes are essential in making academic sources rapidly accessible for readers. With some gentle use of PubMed and Diberri's citation tool this shouldn't be a big deal at all.

We must also show restraint in linking to press releases from all sorts of pressure groups. There are many of them, and their reactions to published scientific evidence are not always useful. I'd much prefer a national news provider citing press releases from CFS/ME patients' associations in their context, and preferably with responses (if the journalist has been doing his job properly). JFW | T@lk 12:48, 3 September 2007 (UTC)

Valcyte, Sciencewatcher

Hola Sciencewatcher, could you link me to the controlled studies that show valcyte to be ineffective? I was unaware that any had happened. I notice the University of Stanford (the location of the uncontrolled trial) are performing a much larger one in the near future. Thank you.

Please someone archive this page. Thedreamdied 18:15, 3 September 2007 (UTC)

Sorry, I was unclear due to lack of space. I meant that no controlled trials have shown antivirals in general to be effective in treating CFS. --Sciencewatcher 18:22, 3 September 2007 (UTC)

Good job, sciencewatcher. Now its either the valcyte section back in or everything non-RCT in the GET and CBT Sections out. Have it your way :-)

Not sure what your point is, Anon. There are lots of controlled trials for GET and CBT which show they are effective, and these are in the article. There are none for antivirals. --Sciencewatcher 20:45, 3 September 2007 (UTC)

I see more reduction in quality, due to Sciencewatcher's most recent edits. Unfortunately I cannot edit the article because it is too long to load properly. Guido den Broeder 22:34, 3 September 2007 (UTC)

Rapid changes to this article are probably not a good idea right now. An incremental approach will give people a chance to discuss on the Talk page. The mood right now is more competitive than collaborative, and this does not do justice to the topic of CFS or to Wikipedia. --- Taroaldo 22:46, 3 September 2007 (UTC)

Upon reflection I should have put the above comment about edit pacing under a new section. I was not intending my remarks to be directed at any specific person or persons. Rather it was more of an observation on the page's overall progression. My preference would be to redo the page completely with new organisation wherein the major diagnostic and treatment notions would all get reasonable play, but where they would not creep into other sections in a way which could be seen as POV. --- Taroaldo 00:44, 4 September 2007 (UTC)

All of my edits were needed in order to remove POV bias or pseudoscience. Feel free to discuss them here. It seems that Guido is in the habit of believing pseudoscience (see his comment above regarding CFS in animals and brain damage in CFS, and his insult to me when I pointed out that there is no evidence for either), so that is probably why he is annoyed by my edits. Guido is also in the process of edit warring me on the Sophia Mirza article and trying to push his POV biased edits. --Sciencewatcher 00:35, 4 September 2007 (UTC)

You did the right thing, sciencewatcher. Someone has to fight the POV Warriors. And there is nobody more suitable than you. You are free from bias (It's all due to stress), free from POV (It's all due to stress), up to date (It's all due to stress) well balanced (It's all due to stress) and an astoute defender of the dialectic (It's all due to stress). Over time, you - unlike other contributors like tekaphor or JFW - have shown a marked expansion of your knowledge about CFS. When you first came to this page, you, with common psychological bumptiousness, thought it's all due to stress. As time goes by, Lo and behold - you are more and more coming to the conclusion that it's all due to stress. Congratulations. —Preceding unsigned comment added by 192.68.211.173 (talk) 10:34, 4 September 2007 (UTC)

Regarding ME/CFS and animals, see e.g. [2]. Nothing new there, there have been reports since the 1950's, and CNS inflammation was found in autopsies on monkeys. Guido den Broeder 10:58, 4 September 2007 (UTC)

This study did not actually conclude that they had CFS - it only conluded that they had diseases which mimiced CFS. None of the animals were actually diagnosed with CFS, they just had certain symptoms which may or may not have been CFS. As I said before it would be probably be difficult to diagnose in animals, so I suspect this argument will never be settled. --Sciencewatcher 14:19, 4 September 2007 (UTC)

The method is easy enough, and was performed 50 years ago: kill them and cut them open. Guido den Broeder 19:55, 4 September 2007 (UTC)

Just wondering if you reviewed the entire paper, not just the abstract?

This study is just another part of the ongoing research and should not be dismissed simply because it doesn't agree with someone's POV. --- Taroaldo 14:59, 4 September 2007 (UTC)

Just the abstract. That is the conclusion of the abstract, not my POV. —Preceding unsigned comment added by Sciencewatcher (talk • contribs) 15:42, 4 September 2007 (UTC)

You misunderstood that part of my comment: it was not accusatory. I was just asking if you had access to the entire article, as it is not available in free full text. The second part of my comment does suggest that some of your comments have been dismissive of areas of research with which you do not agree. As I said before, all major areas of research should get equal play. The notion that 'one person's science is another person's pseudoscience' works both ways. --- Taroaldo 16:01, 4 September 2007 (UTC)

Sorry, I assumed you were going to tell me I should have read the whole article. No, I don't have access to the full article. Yes, all areas of research should certainly get considered. If I say something is pseudoscience it is only because I have looked into it and come to that conclusion, and I'm happy to discuss the reasons for it. I only "agree" with research that is good. If sometimes it appears that I have a POV that CFS is caused by stress, it is only because that is the only explanation that currently makes sense based on the research that has been done and the experiences of the patients. Some people have a bias against this explanation, which is the cause of most of the problems in this article. I don't have a bias towards stress - I'm willing to consider other explanations and have done so - but at the moment there aren't any other etiologies that satisfactorily explain the illness. --Sciencewatcher 19:23, 4 September 2007 (UTC)

"Some people have a bias against this explanation". Really? And let me guess, your proove is that they are oposing your POV Pushing?

"I say something is pseudoscience it is only because I have looked into it and come to that conclusion". That's already a pretty darn good explanation...bulletproof ;-)

"If sometimes it appears that I have a POV that CFS is caused by stress, it is only because that is the only explanation that currently makes sense". This sentence, sciencewatcher, is a masterpace in and by itself. —Preceding unsigned comment added by JayEffage (talk • contribs) 20:46, 4 September 2007 (UTC)

Whereas 'stress' perfectly explains why otherwise healthy people suddenly become very ill? That is ridiculous. Stress is one of the etiologies that, by itself, I consider there to be a 0% chance of it being correct. Thedreamdied 21:27, 4 September 2007 (UTC)

Thanks for proving my point. --Sciencewatcher 23:29, 4 September 2007 (UTC)

I agree that stress "by itself" doesn't explain why healthy people are collapsing into an inactive semi-cachectic state spanning years. I also can’t reconcile the perpetuation of all the CFS symptoms with just a "poor coping style". Removing both initial stressors and unhelpful cognitive behaviour doesn't guarantee recovery, but to be fair these do seem to boost the chances for some people. I’ll respect psychosocial studies more when they stop merely talking about prolonged post-exertion symptom exacerbation as a hallmark of CFS without actually requiring it as an inclusion criterion. Blaming the HPA axis exclusively sounds over-simplistic to me; the changes in the HPA axis are relatively mild and associated treatment doesn’t really help the symptoms. Interpreting the stress response in CFS rather difficult because what appears to be "bad schemas" could be biologically impaired systems, so how do we tell the difference with current technology? - Tekaphor 11:28, 6 September 2007 (UTC)

Archive

Can we please have some consensus to archive older discussion on this page? Thanks. --- Taroaldo 22:49, 3 September 2007 (UTC)

Is it possible to archive all except the recent and continuing discussions? Thedreamdied 21:29, 4 September 2007 (UTC)

I agree, perhaps everything before the NICE guideline section, if possible. - Tekaphor 11:44, 5 September 2007 (UTC)

Maybe all subtopics not edited in the past 30 days? I'll go along with whatever decision as long as we have a more manageable talk page size before it gets even larger. Maybe we need two or more archive pages from the current talk page? -- Strangelv 18:49, 5 September 2007 (UTC)

Suggest all items before Item 36, is it possible to select particular items for retention? Jagra 05:08, 6 September 2007 (UTC)

I've archived everything before and including 'Herbalism', the page had become too long to load properly and quickly. If you want, Jagra, you can go to the archive and copy any other discussion you want to continue into the current page. Thedreamdied 11:52, 10 September 2007 (UTC)

Environment and Stress

Sciencewatcher, I have noticed you have removed the ‘change of location’ piece in the article. I can not find references for it either, however I think it deserves discussion. The weather particularly temperature change is an environmental stress likely to affect patients. Temperature regulation is a homeostatic function controlled by the hypothalamus involving the autonomic nervous system, considered disordered in CFS. I can see how moving to a warmer/cooler climate might help ease that stress. But personally think it is the wrong approach. Management strategies that extend the range of tolerance are better, unless one advocates change of location for other lifestyle reasons. In 1993 the Thrombosis Research Institute of London commented on a study in The European claiming benefits for Thermo Regulatory Hydrotherapy in particular cold water bathing. Finding it improved immune responses, microcirculation, less vasoconstriction and increased hormones. Others have shown it increases GSH anti-oxidant ability. The Director advocated it in the press for ME treatment based on a case study. But I can find no subsequent publication for ME but several general articles on cold bathing PMID 10627870, PMID 10581338 that confirm the benefits for adaptation including reduced heart rate and sympathetics. Another forms of hydrotherapy Sauna, with hot followed by cold cycles optimises several approaches and has been shown to alter sympathetic activity, increase beta-endorphins, raise ACTH and Cortisol. Of interest to CFS patients is that studies report increased cortisol after other hormones return to prior levels, for up to 48 hours. Saunas have also been shown to reduce pain where it is mediated by sensitisized C-fibre sympathetics. The other advantage is that they have been shown to clear accumulated organic chemicals, such accumulation having been shown associated with CFS as another environmental stress. Temperature of hot and cold can be graduated to suit patient tolerance and incremented over time. And from observations seems to increase tolerance to local environmental temperature changes, and progress treatment. There have been a number of published reports now on the benefit of Sauna use in CFS, symptoms such as fatigue, pain, sleep disturbance, and low-grade fever were dramatically improved and although small trials I propose inclusion under Treatment Jagra 04:24, 5 September 2007 (UTC)

The climate location suggestion, like many other "common sense" statements on this page, appears to be a relic from the days when this article was very basic. It goes without saying that a CFS patient who has thermoregulation problems would be better off in a more suitable environment, but unfortunately there doesn't seem to be much research in this area. I don't see how sitting in cold water is going to help those who have difficulty keeping warm; maybe it would be OK for those with a raised temperature. As for "thermal therapy", are you talking about [ PMID 17561703] and [ PMID 15992574]? - Tekaphor 12:41, 5 September 2007 (UTC)

I agree that a more mild climate is likely to cause less stress on the body than very hot or very cold. However again it is really just anecdotal and I don't think it warrants an entry in the article. We could put in lots of things about reducing various types of stresses, but that's not really the purpose of the article. It's better just saying that any type of stress can cause a relapse. --Sciencewatcher 14:34, 5 September 2007 (UTC)

Tekaphor, adaption to cold water does actually improve the microcirculation leading to better tolerance to cold, (that’s why scientists planning to visit Antarctica spend a lot of time in cold-rooms beforehand), It is a longer term management strategy rather than immediate crisis response. The ‘thermal therapy’ is actually therapeutic sauna which alternates hot and cold exposure or as in the two papers you provide hot and warming (cooling down with cold water until warm). The aim is to extend the tolerance to both extremes by increments, and this in CFS seems to benefit other symptoms, as well as temperature tolerance, for some of the reasons mentioned above and probably because sweating and shivering are both homeostasis switch functions, the exercise of which might be seen as retraining general responses! See it a bit like graduated exercising fatigued patients, may be the last thing they want to do, and counterintuitive, merely removing the stress of exercise would not benefit them, and I suspect merely reducing stress by moving will be of little therapeutic benefit? Where as reducing environmental chemical loads should be. Jagra 04:35, 6 September 2007 (UTC)

If I am reading this one right I think it says Sauna was more effective than CBT? Relax everyone its not on CFS but an easier condition to treat, chronic pain? The general picture is it is powerful, it is also proposed for CFS hereJagra 10:02, 6 September 2007 (UTC)

As far as I know, heat is a temporary cure for any type of pain. However it is not long lasting - it just removes the pain for a short time. And it is unlikely to help the other symptoms of CFS (and in fact would probably make them worse, as the body might have difficulty handling the heat). --Sciencewatcher 13:46, 6 September 2007 (UTC)

The same could be said about graduated exercise? Also sauna can be veiwed as a way of 'exercising' The published papers linked by Tekaphor above say it has lasting effects at followup 1 year later, as does the chronic pain one, I linked above, at followup 2 years later Jagra 08:04, 7 September 2007 (UTC)

(Sigh.) The point of a sauna is not heat, but sweating. Guido den Broeder 10:46, 7 September 2007 (UTC)

Agree, sweat removes the organic chemicals and metals brought to the skin by increased blood supply in the sauna. But don’t forget the ‘shivering’ part of therapeutic sauna for it is this that switches the blood supply to the inner organs to protect the core. Before the next heating cycle returns the blood to the skin. In some chronic conditions sauna significantly improved exercise tolerance, increased peak respiratory oxygen uptake, enhanced anaerobic threshold, and significantly reduced stress hormones. PMID 16105634 Jagra 09:55, 8 September 2007 (UTC)

Jagra, this is assuming that "toxins" are a major problem in CFS. Even if they are, toxin excretion may not be normal in people with CFS and haphazard non-specific attempts at removal could cause problems. I'm also concerned that patients who feel worse after merely showering in warm water are going to be knocked onto their arse in a hot sauna. More research is needed, of course. - Tekaphor 01:14, 9 September 2007 (UTC)

Organo chemicals have ben found in excess in some CFS patients and as I recall correlated to symptoms, I'll look it up, Try PMID 15826581, and PMID 7565234, also allergy to metals are found see allergy section. I have seen same temperature sensitivity improved with adaption, common misconceptiom that sauna is all hot and graduation not possible, exposure time also factor. Jagra 09:55, 9 September 2007 (UTC)

These above references are examples of environmental stress that have been associated with etiology or pathogenesis of CFS. Neither CBT or GET is likely to reduce this form of stress, whereas sauna has been shown to reduce such accumulations of heavy metals and chemical xenobiotics PMID 17405694, PMID 1866932, chlorinated and aromatic hydrocarbons (solvents) PMID 9553837, PMID 1817511, polychlorinated biphenyls (PCBs) PMID 2514627, and illicit drugs and pharmaceuticals PMID 17045758. Whether such therapy in CFS and removal of toxins is instrumental in symptom improvement, or whether improvement is due to other adaptive processes, as discussed above is unclear from the two studies cited. Tekaphor is right, and as usual more research is needed. It should be viewed as an adjunct therapy when circumstances are appropriate, rather than an alternative one. Jagra 08:04, 10 September 2007 (UTC)

Some people develop CFS after exposure to toxic chemicals, but as far as I know it's yet to be determined what's causing their symptoms since the levels of toxins in their blood don't seem to correlate with symptoms. Perhaps there were cellular alterations and/or the remaining toxin is sequestered in their cells. I have heard that people's ability to remove different environmental toxins varies greatly; but I don't know enough to comment on the reality of this claim. The issue of toxins in CFS certainly warrants investigation, but unfortunately, many alternative therapists and authors have openly latched onto the toxin idea for so many diseases that the mere mention of the issue in CFS is likely to generate a lot of dismissive eye-rolling. - Tekaphor 14:19, 10 September 2007 (UTC)

Blood tests not necessarily a good measure of toxin loads as they accumulate in fatty tissues and that includes cellular membranes, even mitochondrial membranes, so symptoms not necessarily correlate to circulation. However when patients loose weight they are released into circulation (there being no excretion thru skin without sweating) then more obvious, as organ excretion can also be compromised, also in CFS can be high turnover of some fatty acids, so picture is complex. Removing toxins does not necessarily resolve CFS, usual story of stresses; however find encouraging that in studies on sauna that symptoms improve! Understand the rolling eyes, but one must be open minded when no other options, and science and studies support. Jagra 11:03, 11 September 2007 (UTC)

First, regarding the sauna therapy: none of the studies above had any controls, so we don't know for sure that the improvement after 1 or 2 years was actually due to the sauna. Also, one of the studies had other multi-disciplinary treatments. The most likely theory for the pain reduction due to heat is that it temporarily overloads the pain receptors, resulting in a temporary reduction in pain. This is similar to the theoretical mechanism behind acupuncture and scratching itches.

These "toxins" are purely hypothetical, and mostly in the realms of pseudoscience. There is no evidence to back up any of the claims, and you are really just jumping on the detox bandwagon which is basically quackery. --Sciencewatcher 19:09, 11 September 2007 (UTC)

Sciencewatcher, In the two studies I am looking at for CFS [ PMID 17561703] and [ PMID 15992574] the only other treatment was the use of prednisolone, I think they mean the steroid prednisone, which they say had no effect and was discontinued during the trial. Not likely that had any effect one year later, leaving only the sauna. Think we all agree more reseach of sauna in CFS needed. The toxins I am refering to are those implicated in CFS (PMID 15826581, and PMID 7565234) and those above viz, heavy metals and chemical xenobiotics PMID 17405694, PMID 1866932, chlorinated and aromatic hydrocarbons (solvents) PMID 9553837, PMID 1817511, polychlorinated biphenyls (PCBs) PMID 2514627, and illicit drugs and pharmaceuticals PMID 17045758. Hardly pseudoscience or hypotheticals, nor was removal by sauna and other examples by sweat removal. Not impressed with quakery slur, says he rolling eyes back, how would you remove such environmental stressors? Jagra 08:29, 12 September 2007 (UTC)

As I said, there were no controls on those studies. Factors other than the sauna could have helped one year later. There is no evidence that sauna can provide long-lasting relief from pain or CFS, so the most likely explanation is that it was other factors that caused the relief a year later. In the cases where there is an actual exposure to toxic chemicals, that would of course lead to illness. But in your discussion above you are entering pure speculation, and verging on the realms of pseudoscience. --Sciencewatcher 15:18, 12 September 2007 (UTC)

Indiscriminate use of words like "pseudoscience" will weaken their effect over time. In fact, I think it already has.  ;)

--- Taroaldo 17:48, 12 September 2007 (UTC)

Indeed.JayEffage 09:13, 13 September 2007 (UTC)

The reason those words are used a lot here is because there is a lot of pseudoscience discussed in relation to CFS research. In this case I explained why it is pseudoscience. The problem is that sometimes people read things into studies that aren't there, or they make connections or speculation which isn't based on any actual evidence. That is pseudoscience. --Sciencewatcher 22:01, 12 September 2007 (UTC)

Yes, people reading things into studies and don't realize that they read things into studies really suck. Like the one person on this page who believes that "all the evidence shows it's stress".

Ah, the pain, sciencewatcher, the pain... —Preceding unsigned comment added by 82.135.0.170 (talk) 21:00, 13 September 2007 (UTC)

Sciencewatcher, No, you have not adequately described why it is pseudoscience, according to Wiki definitions pseudoscience; ‘As it is taught in certain introductory science classes, pseudoscience is any subject that appears superficially to be scientific or whose proponents state is scientific but nevertheless contravenes the testability requirement, or substantially deviates from other fundamental aspects of the scientific method’. As to testability; ‘In short, a hypothesis is testable if there is some real hope of deciding whether it is true or false of real experience.’ On those grounds I would think the studies cited are capable of testability and therefore not pseudoscience. However your notion that something unknown affected all patients in these trials co-incidentally and this caused the result is untestable. Sounds more like synchronisity to me and that is pseudoscience. By all means point out the shortcomings in methodology, that will be respected, but not the hasty leap to pseudoscience.’ The term has negative connotations, because it is used to indicate that subjects so labeled are inaccurately or deceptively portrayed as science’ I doubt that the scientists involved set out to inaccurately deceive anyone?. Jagra 01:57, 13 September 2007 (UTC)

As I said twice before, the study had no controls, so we don't know that the sauna actually had the effect a year later. Most likely it didn't, because prior research has not shown this to be the case. Again you are speculating, this time "synchronisity". The most likely explanation is that the patients would have gotten better anyway with no treatment at all. This is what happens most of the time with chronic pain that has no apparent cause. Generally it just goes away by itself with time, which is most likely what happened here. Speculating that the patients had toxins which were sweated away by the sauna is ridiculous speculation based on no evidence, and it certainly fits the criteria of "pseudoscience". --Sciencewatcher 15:08, 13 September 2007 (UTC)

As I have said several times now, more research is needed. What I find improbable is your notion that ALL the CFS patients in these trials, would have gotten better anyway and within 12 months! You are speculating ridicuously and putting words in my mouth. What I said was, 'Whether such therapy in CFS and removal of toxins is instrumental in symptom improvement, or whether improvement is due to other adaptive processes, as discussed above is unclear from the two studies cited'. Any objective reading of this item would make it clear i was talking about chemical toxins. As no prior tests for chemicals were made, it could not be clear and nor have I said otherwise. Your use of the word pseudoscience in regard to sauna treatment in CFS I suggest is inappropriate. You have already said as much that with controls such study could be confirmed, ie is testable, a more correct term from Wiki would be [Protoscience] 'is a term sometimes used to describe a hypothesis that has not yet been adequately tested by the scientific method, but which is otherwise consistent with existing science or which, where inconsistent, offers reasonable account of the inconsistency. It may also describe the transition from a body of practical knowledge into a scientific field By contrast, "pseudoscience" is reserved to describe theories which are either untestable in practice or in principle, or which are maintained even when tests appear to have refuted them.’ Either way the hypotheses are testable, show me the prior science that has shown this not to be the case. Jagra 05:28, 14 September 2007 (UTC)

Causation v. Correlation

I am new to this process and this is my very first entry. I have read through the article and the discussion (including the archived page) and would just like to point out that it might be advisable to keep in mind the scientific process and the careful use of vocabulary in an article such as this. As one would learn in any statistics class or research methods class, science rarely is able to prove causation, especially in an area as complex as CSF. To do this requires research circumstances that really are not possible. As I am sure you fine folks are aware, the best science can do for us in an area like this is to suggest a correlation (say between stress and the onset of CSF), but at this point, cause is elusive at best. I would also point out that science does not stand still, and the fact that at this point a viral correlation has not been strongly identified does not mean that one will not be in the future, and it is important to keep an open mind when wording this in an article. It is also inappropriate to say that some treatment is definitively a cure for some folks. Cure goes along with cause and is extremely difficult to prove and to suggest such in the article would perhaps provide false hope. It would be appropriate to mention treatments or therapies that have aided some patients to improve their level of functioning if there are sources to back up these claims. Keeping these ideas in mind could help to dampen some of the controversy. Ultimately, when it comes to a complex syndrome such as CSF, nobody really knows anything to be certain, as there are just too many variables.PhobicPt 06:06, 5 September 2007 (UTC)

Problem is a lot of management strategies that seem to benefit patients are not well documented, likely because funding is scarce and directed elsewhere, or there is no 'economic return' visible! Quoting other sources such as patient support organizations, is problematical as it raises issues of Reliable Source. An issue that I dont think has been addressed adequately yet.Jagra 04:45, 6 September 2007 (UTC)

There is often enough varying circumstantial "evidence" for people on whatever "side" of the CFS controversies to extrapolate whatever they want to for now according to their own beliefs/experiences. Such cognitive bias won't be resolved anytime soon. - Tekaphor 11:35, 6 September 2007 (UTC)

Exactly, Tecaphor. Combine that thought with the staggering high prevalence and the unclear research definitions and you get the CFS-quackmire (pun intended). Starting from that base, you can (formally) prove anything, nothing, something in between, or any combinations of all three. At this point in time, it is not even clear wether we talking about one monomorph disease or about many, possible disconnected entities.

Finally, I wonder wether the trenches prevailing in the scientific world around CFS make it possible at all to reach a consensous in wikipedia. —Preceding unsigned comment added by JayEffage (talk • contribs) 19:32, 6 September 2007 (UTC)

Jarga: I don't agree with either of your conclusions. First of all there is a lot of funding for CFS, at least in the UK and USA. The UK has large-scale studies underway into CFS, and they have spent a lot of money setting up treatment centres (no other country has done this, as far as I am aware). There is a HUGE economic return because it is well recognised by governments that CFS is a major health problem that drains the economy because people aren't working and because they are receiving benefits. This is why the UK has set up treatment centres, brought out the NICE guidelines, and is doing large scale trials on the effectiveness of CBT/GET and other therapies. As far as I can see, all other countries are falling way behind the UK. Canada has done virtually nothing apart from releasing their CFS guidelines. The USA has done quite a bit of research, but they haven't done anything for patients (who are mostly left at the mercy of doctors who don't know much about the illness, or alternative therapists peddling quackery). A few other countries such as Australia, Japan and the Netherlands have done some research, but that is about it. --Sciencewatcher 13:56, 6 September 2007 (UTC)

You have missed the part where none of all this money actually accomplishes something, while excellent biomedical researchers are struggling to get even minimal funding and often have to rely on gifts. Patients in any country falling behind this development consider themselves fortunate. Guido den Broeder 14:01, 6 September 2007 (UTC)

You also missed the part where many patients are being denied any benefits. Guido den Broeder 14:07, 6 September 2007 (UTC)

Sciencewatcher has also missed the part where patient organisations are trying to petition the government for what they call "a waste of money for psychological research". —Preceding unsigned comment added by JayEffage (talk • contribs) 17:28, 6 September 2007 (UTC)

I'll assume you are talking about the UK here. How does it accomplish nothing if it is helping people? And the UK does not deny benefits to CFS patients. If you are implying that they are denied benefits because the illness is thought to be psychiatric in nature, you are incorrect. In the UK you get benefits if you are suffering from psychiatric illnesses such as depression and schizophrenia. The criteria is whether or not you are disabled, not what the etiology of the illness is. --Sciencewatcher 17:33, 6 September 2007 (UTC)

It is good that the UK does not deny benefits to CFS patients. But CFS is not a psychiatric illness: I hope they do not have to be labeled as suffering from a "mental disability" in order to qualify. ;) --- Taroaldo 17:45, 6 September 2007 (UTC)

@Sciencewatcher, although those are the official criteria, I know of many CFS patients who have been turned down for benefits despite being clearly disabled. Also, the Medical Research Council (MRC), the government-paid research direction body, has turned down every request for funding for research into ME, except from the PACE CBT/GET trials. Thedreamdied 19:15, 6 September 2007 (UTC)

As far as I understand it, that should never happen (getting turned down for benefits while being clearly disabled). But maybe the problem is proof of disability, and in that case it is probably good to have a good doctor who knows about the illness. The NICE guidelines will hopefully help things. Regarding the research: I think that according to the MRC they turned down funding because of the poor quality of the research. I don't know the details of the rejected trials, so I can't comment on them. --Sciencewatcher 21:14, 6 September 2007 (UTC)

I agree, although I think perhaps the UK criteria can be a bit strict in deciding disability benefit, but that is just my opinion. Re: the research, I had a look to see if i could find anything about the research that was turned down, although I know that the group at Glasgow University, with Dr Jonathan Kerr, who believe they have found biological markers were turned down for funding. I also found this document, [3] which anyone may want to read, it's the Medical Research Council's strategy to CFS/ME research. Thedreamdied 22:42, 6 September 2007 (UTC)

On further reading, this is a very interesting document - includes a summary of a lot of research! Thedreamdied 23:10, 6 September 2007 (UTC)

Kerr is in London, Glasgow has Gow. Both are doing research on gene activation. Guido den Broeder 09:38, 7 September 2007 (UTC)

Just as an aside, it's an unfortunate indication of the difficulty CFS continues to have in gaining acceptance as a significant illness when documents such as the one produced by the MRC in 2003 recognize there is still a need to state that CFS "is a real, serious and debilitating condition". --- Taroaldo 23:23, 6 September 2007 (UTC)

Depressing is the word. Thedreamdied 23:37, 6 September 2007 (UTC)

I disagree that all the money "isn't accomplishing anything" (although it is far from ideal). The UK is putting some noticeable effort into it, but it remains to be seen if this is the right approach (maybe it will benefit some at the cost of many others). When it has been suggested to patients in the past that CFS is a psychiatric illness which would only be perpetuated by the "hope" of biomedical legitimacy, of course they are then going to get suspicious when related research is starved of money and rejected from funding allegedly because of "poor quality". CFS is costing thousands of times more money a year than is going into research, so I doubt the government is confident about receiving a return on their investment. Being granted disability benefits for something like CFS depends more than usual on the personal opinions of doctors and government employees, particularly regarding the prognosis of functional impairment (a tricky issue). Tekaphor 01:31, 9 September 2007 (UTC)

What I find concerning is that patient support groups on behalf of patients don't seem to be listened to. The NICE guidelines are a case in point with a dissenting report and i know the same occurred in Australia. Our medical system is built on much empirical evidence, and there used to be ways of publishing findings after a 1000 or so cases (someone may know the number?) Any reason the support groups and their medical advisers cant do likewise, at least they may have 'evidence' then (rather than labelled antecdotal) and be listened to? I don't disagree with major funding going into pathogenesis studies, but think more could be directed to treatments suggested by patient groups as to what actually helps patients, rather than most to vested interest groups. Jagra 08:29, 7 September 2007 (UTC)

Just read the posting by ME agenda on latest developments with NICE Guidelines and ME support groups, suggest you all read (just above Infection and Stress) Jagra 10:48, 7 September 2007 (UTC)

Jagra and others may be interested in accessing the Stakeholder Comments and Guideline Development Group (GDG) Responses documents. These are the comments made by Registered Stakeholders to the various draft documents with corresponding responses from the Guideline Development Group which followed the NICE draft consultation process, last year, and which have now been published in association with the final NICE CG53 guidelines. There are ten Comment and GDG Response documents in all - several of considerable length and presented in tabular format, but they are well worth scrutinising. They are available for download from the NICE website: Stakeholder Comments and GDG Responses. A number of comments are still being held by the Institute and have not been included in the tables, these include comments submitted by Dr Derek Pheby, Project Co-ordinator, National CFS/ME Observatory who is challenging the Institute over this omission. It should be noted that in at least one document, a set of Comments made by one of the Stakeholders and corresponding GDG Responses appear to have been duplicated and attributed further on in the same document to another Stakeholder. It has not yet been established whether or when NICE intend to correct this error and publish a revision. MEagenda 12:32, 7 September 2007 (UTC)

In order for support groups to be taken seriously they need to contact researchers and suggest specific experiments to prove any hypothesis they may have. This is one way advances may be made. Example: We believe xyz herb can help CFS patients, suggest this herb be used in a double blind study to prove or disprove its effects. Stating "xyz herb works and we are 100 percent sure of it" will not be listened to. Sno2 03:00, 9 September 2007 (UTC)

Surveys, petitions and letters are fine for addressing the political part of medico/political problems, but published evidence is needed to address the medico part. Like applications for funding and for that matter for articles such as this. My earlier comment was addressed to other ways of support groups with limited funding to accumulate empirical 'evidence'. Jagra 10:05, 9 September 2007 (UTC)

Scientifically Proven/Disproven or Unknown

I would like to add the a section as below, based on NICE CFS/ME; full guidlines, which is based on literature searches and interviews with experts.

Definitions

Hypothesis: Educated guess as to why or how something occurs, not proven by enough experiments.

Theory: Hypothesis that is assumed to be true, based on enough experiments, that it is commonly accepted by the scientific community to be true.

Theories:

1. CFS is a seperate disease from other diseases. 2. Stress both physical (heavy exercise) and/or mental are a triggers that can increase symptoms. 3. GET (type of extremly light exercise) can lessen symptoms in some people. 4. CBT therapy (type of talk therapy) can decrease symptoms in some people. 5. Some practices can reduce symptoms in some people (yoga, tia chi etc).

Hypothesis:

1. CFS is or is not a viral disease. 2. That there is a known cure. 3. Alternate therapies (ex: vitamins/herbs, etc) can decrease symptoms.

I know these are covered in other sections of the page, however I feel it would be helpful for a synopsis to be included somewhere close to the beginning Sno2 20:02, 8 September 2007 (UTC)

Keep in mind that there are dozens of guidelines on ME/CFS. This is just one source, and a poor one at that. Therefore, such an exercise is futile. Guido den Broeder 21:01, 8 September 2007 (UTC)

If you read the document you will see they considered other guidelines.

Sno2 21:06, 8 September 2007 (UTC)

The point being? 'They' are not even experts in the field, just local guideline producers. Guido den Broeder 08:06, 9 September 2007 (UTC)

I read your above comment as being that the other documents were not considered...I believe the NICE document is the best thing going at this date showing what the scientific community agrees/disagrees on. It is very completely documented, for example listing all the databases that were searched....along with the questionaires used and the responses they got to them. "They" (the people who wrote and published the document) are not experts...but they show how they used experts opinions to arrive at the final document...have fun....sno Sno2 16:48, 9 September 2007 (UTC)

Your belief is, no doubt, based on your vast knowledge of the opinions of the scientific community. There are over 4,000 scientific publications on ME/CFS. So, obviously, referencing only those belonging to one specific sidestream equals full documentation... Guido den Broeder 17:13, 9 September 2007 (UTC)

Do you know of any other documents that have done as complete a review of the literature and polled experts in the field to come to a conclusion...if not this is the latest and best at this time. I do not need to be an expert to read the document and make a synopsis of their conclusions. It is possible that I missed something, would like to request you read the document and suggest any changes to my comment you feel would make it better. thank you....have fun.....sno —Preceding unsigned comment added by Sno2 (talk • contribs) 17:27, 9 September 2007 (UTC)

You pretty much missed the barn, and you pay no attention to what I am saying, so what is the point? This is NOT a complete review, nor was it intended to be one. It doesn't even scratch the surface. Guido den Broeder 17:38, 9 September 2007 (UTC)

I am sorry if I am missreading what you are saying.. I think the objection you have is that this documents review is not complete enough for you....if you know of a document that is more complete please let me know and I will read it and make a synopsis based on it. thanks for your comments....have fun....sno Sno2 17:54, 9 September 2007 (UTC)

Guido....I am adding a sentence as below that I think addresses your concerns.

"The NICE document appears to be the best review avalable at this time." —Preceding unsigned comment added by Sno2 (talk • contribs) 19:12, 9 September 2007 (UTC)

Guido...one persons opinion without justification/references is not enough to justify removal of anything from the page. You have not justified your opinion. The section has been posted here on the talk page for over 24 hrs and you seem the only one who has a problem with it. For this reason I am reposting. have fun.....sno Sno2 20:57, 9 September 2007 (UTC)

preposed changes - delete experts, a patients hypothesis is as valid as an experts until one or the other is proven by experiments. Change experiments to experiments or predictions (ie: prediction - an antiviral will lessen symptoms) Change interviews to consultations - as well as interviews questionaires were used.

Request feedback either for or against including this comment. Sno2 23:00, 8 September 2007 (UTC)

Keep in mind peer reveiwed hypotheses published in reputed journals will always rank higher than antecdotal comment when it comes to applications for funding to validate it as 'evidence'Jagra 10:14, 9 September 2007 (UTC) For the record this comment was not made in support of the proponent, quite the opposite, so I suggest we all keep our coolJagra 09:53, 10 September 2007 (UTC)

Jagra, this is the perfect forum for a long discussion about the epistemology of modern scientific research and the treatment of oddball theories. Sometimes they are proven right in the long run. But at the moment they are not. We need to reflect that reality, not elevate the status of a little-known theory just because we think it's cool. JFW | T@lk 21:21, 9 September 2007 (UTC)

Thanks for the comment...what you are saying is the expert has the "edge" <g>....as is normal in all human endevors....I am ambivalent over wether to include the word expert...but since I am trying to keep things simple have pretty well decided to leave it out.... Sno2 16:30, 9 September 2007 (UTC)

You have no support at all for such a paragraph, and I'm surprised you undid Guido's removal without further attempts at discussion. The paragraph is presently riddled with problems; if you are distilling something from the NICE guideline, you are adding original research, prohibited by Wikipedia content policy. If you have a solid source, please supply this source; we can then debate whether it is notable or not. JFW | T@lk 21:14, 9 September 2007 (UTC)

WP:NOR. In any case, the NICE guidelines are controversial and certainly cannot be given higher precedence than the major long-established guidelines. --- Taroaldo 21:21, 9 September 2007 (UTC)

I thought I had given Guido a resonable chance to justify his opinion...as I stated in my original post I realize that what is in my comment is covered in other sections...I believe that what I have extracted from the NICE document is a fair synopsis and not my personnel opinions. I realize the document is controversial however it is the latest review and the full guidlines document, which I used, shows the completeness of their document searches and consultations. However I did not know that extractions/synopsis of referenced documents was against wiki policy and for this reason now agree with the removal of the section. Thank you for listening to my thoughts and for your comments. Sno2 21:51, 9 September 2007 (UTC)

I find "controversial" a very harsh term for a document that simply represents prevalent scientific opinion of the UK medical establishment. You will simply not find many people who are willing to contemplate alternative views in this country. The fact that patients experience this differently, and the fact that other bodies of doctors elsewhere take a different view, does not invalidate it as a source of information.

A synopsis or extraction is not necessarily against Wikipedia policy, but in the case of Sno2's addition there was clear reading between the lines. The fact that the guideline supports CBT & GET does not mean it rules out any particular cause for CFS. From the summary it seems that it is careful not to pass judgement on the cause at all. JFW | T@lk 11:58, 10 September 2007 (UTC)

I second that, it is indeed very careful not to pass judgment on the cause, moreover it openly states so. However, I differ on the view that the document "simply represents" the prevalent scientific opinion. IMHO the document clearly states that it recongnizes the split INSIDE THE UK scientific community when it talks about why NICE did not settle for one specific explanatory model in the opening paragraphs.

So, JFW, I don't think you necessarily have to look "elsewhere" for a different view. The association of british neurologists was a registered stakeholder and they describe their dissatisfaction with the overemphasis of CBT and GET in no uncertain terms in the stakeholder comments section.

However, that's just my interpretation, if you have time, maybe you could state how you come to your conclusion about "the" prevalent scientific opinion. JayEffage 12:50, 10 September 2007 (UTC)

I agree that "controversial" is a harsh word with undesirable baggage, but I don't think being tagged controversial necessarily invalidates it in the eyes of readers. The word describes exactly what has happened over there during the entire process of developing these guidelines, plus the sheer volume of complaints demonstrates the tension in the UK. Some of the stakeholder comments highlight the officially sanctioned magical thinking that made its way into the initial draft, some of which has since been cosmetically reworded. - Tekaphor 16:03, 10 September 2007 (UTC)

I would still like to know what things I wrote were my opinion. Or "reading between the line" As I see it there are only a few things that can be challenged without using "emotion think". Definitions: might be challenged their are a number of weasel words and exceptions that have been added through the years. Theories: 1 thru 4 are definitely stated in the document, 5 is iffy only kind of stated in one place. Hypothesis: All are definitely stated in the document. Remember I was writing about this one document. As JFD wrote this is the opinion of one country, perhaps this should have been made clear in my summary. I imagine this comment here is going to be read with "emotion think" which leads to misunderstanding of what is written. It is impossible to use logical thinking when dealing with someone who is using "emotional thinking"....thank you for listening to my thoughts....have fun.....sno Sno2 13:15, 10 September 2007 (UTC)

I think a lot of people misunderstand CBT. It is based on the idea that the way you think about something can change how you respond to that something. I know it worked in at least one case...me. Here is an example of how it works. "My wife would get upset when she talked to her mother when her mother was drunk. I asked her why she could not hang up on her immediately instead of talking to her. She stated that she could not do that because it would be disrespecting her mother. I asked her if she could hang up if her mother was in a psych hospital, she stated she could do it then because her mother would be "sick". I pointed out to her that when her mother was drunk she was "out of her mind", the same as being mentally ill. When she started thinking about it like that she was able to start telling her mother to "call me back when you are sober" and hang up on her. This change in thinking greatly reduced the stress her mother caused her." Also, for some reason, she started hanging up immediately when telemarketiers would call, rather then listening to their whole spiel, which again reduced stress....thank you for listening to my thoughts...have fun....sno Sno2 14:42, 10 September 2007 (UTC)

Thanks to JFD I now realize how I was reading things into the document....I would like to thank everyone for their comments and being patient with me....sno Sno2 21:34, 10 September 2007 (UTC)

New research

Just as an aside, new research was published in the JCP today - [4] —Preceding unsigned comment added by Thedreamdied (talk • contribs) 10:49, 13 September 2007 (UTC)

You mean doi:10.1136/jcp.2007.050054. Pah, another "fascinating" linkage study in a small case series. Their patients are scored by the CDC criteria, which are far from specific in CFS. And what about the patients who were VP negative? Do they not have CFS then? The same J.K. Chia has published before about enterovirus in CFS (PMID 16254097).

We should only include this when (1) the paper has been published in print, (2) it has had some time to attract responses. JFW | T@lk 16:17, 16 September 2007 (UTC)

I am somehow baffled about that response, JFW. Not that I wouldn't agree that the paper should be printed first, but the CDC criteria unspecific? What criteria are specific then?

Sorry, forgot to sign: JayEffage 19:46, 16 September 2007 (UTC)

I wasn't suggesting its inclusion, just mentioning its existence, its fairly rare that studies make it into the papers. I would say 165 people is quite a lot, isn't it? I wonder when they'll try pumping people with anti-viral drugs. Thedreamdied 20:58, 16 September 2007 (UTC)

Evidence for antivirals in any enteroviral disease (viral meningitis, polio, hepatitis A)? JFW | T@lk 07:25, 7 October 2007 (UTC)

changes to the neurological section

Sciencewatcher, I have no issue with the deletion of the "RAS" section (perhaps the initial mention was due to this 1997 paper PMID 9134372); however, your earlier edit seems somewhat hypocritical. You removed a study about cerebrospinal fluid from the article because it was new and unreplicated with a small sample, meanwhile, you retained another cerebrospinal fluid study that not only had similar weaknesses but didn't even involve CFS patients and just happens to coincide with your personal emphasis on the HPA axis and stress. Furthermore, you then added a sentence about how "many studies" have shown dysfunction in the HPA axis, yet you didn't cite any of these studies. As far as I know, only two cerebrospinal fluid studies have been done on CFS patients; the one you deleted and PMID 15642984; both of which suggest neurological abnormalities. You are welcome to expand on the HPA axis and stress response, but excluding said CFS studies over the fibromyalgia one is suspiciously POV. - Tekaphor 09:03, 18 September 2007 (UTC)

I see it the same way as tekaphor. JayEffage 10:36, 18 September 2007 (UTC)

Yes, you're right - that study can go. I only left it there because of the large body of science showing HPA axis abnormalities in CFS, but I didn't have time to give references for those. As you say, that reference isn't even for CFS, so it would be better to remove it and add some refs for CFS. Perhaps there should be a separate section about the HPA axis, as it doesn't really fit in the neurological section. Perhaps add an endocrinological section and put it there. --Sciencewatcher 14:45, 18 September 2007 (UTC)

That's not the point sciencewatcher. The point is you deleted a study for POV reasons that is currently being replicated with NIH money. It is definitely worth mentioning. Let's hear other views, but I would put it back into the articel. JayEffage 15:12, 18 September 2007 (UTC)

It was not removed for "POV reasons". As I stated in the edit log, the reason I deleted it was because it was new science (small, unreplicated study) and hence does not belong here. Once it is replicated in a large study we can talk about putting it in. The problem with this article is that there are too many "worth mentioning" little unreplicated studies and bits of speculation. We need to get rid of them all in order to make this article even vaguely like an encyclopedia article. --Sciencewatcher 19:12, 18 September 2007 (UTC)

That is a problem of the science around CFS, and only a secondary one of this article. It is not for you to decide what get's mentioned and what not, and you did not have a consensus for the change. You did however, use the occasion to further your POV and water down the neurological section and that is not only clear to me, but apparently also to tekaphor. In the light of your edits, your arguments are a fig leave for furthering your POV about stress & psychosomatic explanations. Note please, that I am not the only one accusing you of POV pushing.

I would like to hear opinions from other editors on this, otherwise I will put the study back in until there is a consensus. JayEffage 08:54, 19 September 2007 (UTC)

Jay: with respect, you don't know what you are talking about. It IS up to me to decide what goes into the article, as I am a wikipedia editor along with everyone else here. Studies like this should never appear in the CFS article, and other people have removed similar studies. Just because I have a POV (like you) does not mean that all my edits are POV pushing. My POV is based on the science, not the other way around, and my edits are purely aimed at improving the science in the article (i.e. getting rid of bad science, and putting in good science, hence my screen name). PS, you are the only one accusing me of POV pushing. I responded to Tekaphor's comment regarding the FMS article, and I'm assuming he is happy with my response. Nobody else except you seems to be having a problem right now. --Sciencewatcher 15:16, 19 September 2007 (UTC)

Well, "my POV is based on science" is a pretty poor argument - I could claim the same for mine. Your screenname has been commented upon often engough on the talk page.

But coming to the point: Accusing me for not knowing what I am talking about and calling said (currently replicated with NIH money) study bad science in one breath sure does make you look like a brazen POV warrior. Could you explain that position? What wikipedia guideline would specifically apply to that study?

However, if indeed nobody else has a problem with sciencewatcher's recent edits, I will of course step down.JayEffage 16:50, 19 September 2007 (UTC)

I agree with Jay in that I find the "my POV is based on science" argument disappointing. For years, this notion was used by GPs and specialists in denying that CFS patients had anything wrong with them. The fact is, science changes all the time as new discoveries are made and as new ideas are tested. This is the long process we are involved in with CFS. The study Jay refers to cannot be dismissed simply because it does not mesh with one person's idea of science. --- Taroaldo 17:03, 19 September 2007 (UTC)

While we are on this topic CRH does not activate the HPA axis in stress response. That is mediated centrally from the Hippocampus/ Amygdala by reduction in neurotransmitter GABA. CRH is produced by the hypothalamus to activate the pituitary, which effects the middle part of both the HPA and HPG axiis. There are other CSF papers including PMID 9310111 that found on homocysteine and B12 levels and Demitrac in PMID 9629295 found (in CFS patients) the CSF levels of CRH and ACTH were normal despite low levels (of cortisol and ACTH) in circulation, which he considered inappropriately normal! Others claimed this result was affected by patient psychiatric co morbidity. Science watcher is correct there are a lot of studies on HPA axis dysfunction and one has to be careful which studies are cited. I agree with him that a separate section should deal with this associated with endocrine findings. Jagra 08:36, 19 September 2007 (UTC)

CRH (along with VP) is the neurotransmitter which activates the HPA axis in stress - there are a lot of studies on rats which demonstrate this. I suggest you have a look at them. Let me know if you want some references. Perhaps the GABA reduction you are talking about then causes changes in CRH or VP - I'm not sure about this. But the HPA axis response is always initiated by changes in CRH or VP. Low cortisol and normal CRH/ACTH is a separate issue. It can be caused by shrunken adrenal glands, which is a result of prolonged chronic stress. Shrunken adrenal glands have been found in a subset of CFS patients. --Sciencewatcher 15:16, 19 September 2007 (UTC)

I am following this discussion with interest, however I must reserve my own opinion until I can find the time to review some of the relevant literature. Unfortunately, reviewing CFS research could easily be someone's full-time job. --- Taroaldo 16:45, 19 September 2007 (UTC)

As I have already said, I didn't delete the study because of my POV. I deleted it because it was a small, unreplicated study. It may or may not be valid - we don't know yet. For that reason it cannot be included here. The POV discussion is a side-track that has nothing to do with this edit. Everyone has a POV, for whatever reason, but let's just stick to the facts and stop discussing people's real or perceived POV. It has (or should have) nothing to do with edits that people make. --Sciencewatcher 18:06, 19 September 2007 (UTC)

Also: the study doesn't either support or deny my POV of the illness anyway, so your (Jay's) contant moaning about my POV is not even an issue in this case. The acute-phase proteins that they found could be due to either infection or stress. There have been similar studies into gene expression. Again, these studies just measure the proteins that are being produced in the body. Whether this is a useful diagnostic tool remains to be seen. My opinion is that it will not be useful, because it does not get to the source of the illness. You would be better looking at the neurons in the brain or whatever is actually upregulating the production of these proteins - that will actually tell you what is causing the illness. --Sciencewatcher 18:25, 19 September 2007 (UTC)

I wasn't directly accusing Sciencewatcher of POV pushing, although I was implying it and wanted an explanation. Regardless of SW's motivations, deciding which studies to include is a major issue: the issues of critera and the variations in research quality/relevance are likely reasons why abnormalities/differences are usually only found in a subset of study participants. Despite being bloated, the article has blind spots which give the impression to readers that no research has been done in these areas. The neurological section remains rather sparse (and like JayEffage I have a problem with watering it down further), although full descriptions aren't necessary (other text in the article could also be further summarised). We need to give a balanced representation of the "proposed causes and pathophysiology" without giving the false impression that scientists/researchers are equally divided. I might attempt some resolutions and improvements later on. - Tekaphor 07:53, 20 September 2007 (UTC)

As for the HPA-axis; related research isn't conclusive either and doesn't necessary justify a psychiatric model (some organic diseases also indirectly involve the HPA-axis). The etiologies of many neurological diseases are also unknown, but some of the physiopathology is known so the psychological studies are interpreted differently when involving the stress response (as well as mood, behaviour, personality risk factors e.g. Parkinson's disease, cognitive sensitivities/impairments, and everyones favourite "fatigue"). I'm not a proponent of "CFS is 100% organic", but as a person who several years ago had a neurasthenic and/or psychosomatic view regarding CFS, I eventually came to the conclusion that it was the same typically over-generalised mind-body connection ideology that psychiatry has had to retreat from many times throughout it's history. However, we may be dealing with different illnesses (or at least subsets) which are better explained with different models. - Tekaphor 07:53, 20 September 2007 (UTC)

Demitrak in the paper I cited above concluded that the HPA changes were in part due to reduced central drive. That drive comes from the hippocampus / amygdala via neurotransmitter GABA which acts to inhibit the PVN neurons of the hypothalamus. By disinhibiting the hypothalamus CRH and VP are increased. The PVN is also stimulated by the brainstem, also peptides, opioids and cytokines modulate CRH activity. Centrally GABA is modulated by other neurotransmitters including importantly for CFS by serotonin. Thus the importance of the recent CDC findings regarding the serotonin pathway alterations in CFS. Increased serotonin inhibits the HPA axis more. (an argument against use of serotonin increasing antidepressants in CFS) As the hippocampal response curve is J shaped, hypocortisolism implies loss of glucocorticoid receptor number / function, and the CDC have also found alterations in GC gene expression. PMID 16740143 PMID 16610957 These findings go to the importance of the central function changes in CFS. Thats why article discussion of HPA axis changes will need to include central drive aspects. Jagra 08:03, 20 September 2007 (UTC)

Tekaphor is correct in saying that many different factors can affect HPA function and that the psychiatric model is not the only one this recent paper proposes four models PMID 17853290 Although HPA axis findings do vary, so does the quality of the research. The consensus however is that these are the findings PMID 12700181 PMID 17596739 This is a potted summary of the research. HPA axis function in CFS has been much studied, and the overall balance of evidence points to impaired response to activation. For reduced cortisol output in some patient groups, with some evidence that this is correlated to symptom expression and persistence. There is evidence of heightened negative feedback and increased sensitivity of glucocorticoid receptors, with blunted ACTH and cortisol responses. HPA axis function in CFS has been measured in controlled trials of unstimulated adrenal cortisol and pituitary ACTH, in blood samples (9), saliva (6) and 24 hour urine samples (8). Challenge tests of HPA function with exogenous CRH (5), exogenous AVP (4), ACTH stimulation (4), insulin stress tests (3). Adrenal DHEA and DHEAS (7), with some studies showing low levels or responses. Opoidergics, as this system can inhibit HPA function this has also been studied. Beta- endorphin has been found low in CFS. Exercise challenge tests of the HPA axis have also been conducted ( )As serotonin levels in the brain modulates the stress induced hypothalamus CRH release this has also been studied (4) These results suggest enhanced serotonin responses in CFS , the opposite to depression. Other factors that can affect HPA axis function include inactivity, sleep disturbance, medications, ongoing stressors such as environmental factors and persistent infections. Psychiatric co morbidity, is shown to produce lower cortisol levels than CFS, where as depression is associated with increased cortisol levels. Altered adaptive responses have also been shown associated with cortisol in CFS. Polymorphisms of glucocorticoid receptors and serotonin pathway enzymes have recently been found in CFS, indicating central involvement. Jagra 09:51, 20 September 2007 (UTC)

Tekaphor is right that the Neurological section is very bare now. That wasn't my intention. The problem is that all of the information that was there shouldn't really have been there (even the HPA axis doesn't really belong there, as it should be in a separate endocrinological section). Various factors can influence the HPA axis: psychiatric factors through various neurotransmitters throughout the brain (we don't need to get into details), negative feedback from cortisol itself, as well as inflammatory cytokines when there is an active infection or physical trauma. The HPA axis is thought of as the stress axis, but really it is more correctly thought of as the energy axis, because it also controls non-stressful functions such as digestion and the wake-sleep cycle.

What should be added to the neurological section are studies showing altered neurotransmitters and/or altered activation of the brain in CFS patients. --Sciencewatcher 14:27, 20 September 2007 (UTC)

I agree we include as Sciencewatcher suggests the neurotransmitter findings in the Neurological section. A subheading under this called HPA axis dysfunction, similar to that I outlined above and intergrate that with Endocrine dysfunction. Jagra 05:54, 21 September 2007 (UTC)

If I have time over the weekend I'll make these changes, along with the changes to the stress section we discussed a while ago. Or if anyone else wants to have a go, feel free. --Sciencewatcher 14:19, 21 September 2007 (UTC)

Benefits etc

In the section above their is some discussion of benefits. I know nothing about the US but in the UK there is an issue with Incapacity Benefit with many being denied IB and having to appeal. The appeal win rate is about 80% when helped by the Citizens Advice Bureau but the appeal can take six months. A brief section on benefits even if it is just links to help sites would be helpful even if it is not medical or controversial.

--86.153.45.249 00:23, 21 September 2007 (UTC) RichasAA

See the DMOZ link in external links. There's a variety of sites related to CFS listed there. --- Taroaldo 01:01, 21 September 2007 (UTC)

Theories of Aetiology and the Article

Given the four generally recognised theories for the etiology of CFS [ PMID 17853290 ] viz Viral, Neuro, Immune and Psychiatric, a neutral point of view requires the Article not give undue weight to any of the theories, to the detriment of other/s. I am of the impression, and in agreement with others, that the current version is overweight in some areas and underweight in others. In particular the neuro theory is under developed. Let’s also not forget that these theories are not mutually exclusive, but are more likely a circular argument. I also think the present Article does not present that bigger picture adequately either. Not only a circular argument but I think the condition likely involves a ‘vicious circle’ that readily perpetuates with say four major pathways into it and multiple entries to each pathway. Subgroups of patients presenting variations in signs and symptoms of the particular pathway they enter from, other changes representing affects of the circle over time, showing heterogeneity. Favouring one or other theory does constitute POV and the difficulty is in realising that type of inference intentional or otherwise in such a complex matter. For instance here is one scenario;

• Neurological and neurotransmitter changes cause altered neuroendocrine regulation with changed HPA function and sympathetics.
• The hormone system, nervous system and immune system inter regulate. Cortisol not only mediates the stress response but also is essential in energy metabolism, fatty acid metabolism, amino acid metabolism and immune function. Fatty acids affect immune function, energy affects exercise; exercise affects fatty acid metabolite ratios, immune function and HPA regulation.
• Altered immune system function allows viral infection / reactivation and other persistent infections. Viral infection alters fatty acids and immune function, cytokines module the HPA axis.
• Depression in CFS shown to be secondary or due to biochemical changes. Various ongoing stressors including environmental, infectious, and psychosocial cause dysfunctional allostasis and allostatic load leads to chronic disease. The centre for allostasis the hippocampus / amygdala alters HPA function as an adaptive response.

So we go full circle, any one of these can be considered precipitating of CFS or perpetuating the condition thus we need to show in the article the ‘bigger picture’ give balance to all major ‘theories of etiology’ and show how all factors can be considered both ‘precipitating or perpetuating’ in order to present balance. Whether there are multiple studies as in HPA axis dysfunction or only one small study, if it fits a gap in this approach it could be included, provided it is qualified. I would be interested in comments of the applicability of this approach to future review or additions. Jagra 05:54, 21 September 2007 (UTC)

The available evidence suggests only one direction, IMHO; it's not a cycle.

The cause of the disease is viral, a one-time event where a virus crosses the blood-brain barrier. Stress is a catalyst.

The nature of the disease is immunological, neurological and metabolical. Guido den Broeder 08:01, 21 September 2007 (UTC)

I mostly agree with Jagra. However in my opinion, it is psychosocial stress that is the main perpetuating factor. As for Guido's comment: there is no evidence at all that a virus crosses the blood-brain barrier. Occam's Razor: the simplest explanation is stress, as is explains every aspect of the illness. Speculating about hidden viruses is unnecessary.

The problem is that it is very difficult to prove definitively that stress is the cause of the illness. So the best we can do for now is to describe the abnormalities that are seen in the illness and the various interactions between stress, infection, HPA axis, neurotransmitters, etc. which could be causing or perpetuating the illness. --Sciencewatcher 14:25, 21 September 2007 (UTC)

That is not Occam's Razor, that's your very own POV. "Stress is the simplest explanation" is just one more iteration of the hot air. Who says so? You? Who says stress explains everything? You again?

And please quit using "pseudo science" "speculation" etc. for everything you don't want to hear/read, it's ridiculous. JayEffage 15:25, 21 September 2007 (UTC)

While I probably wouldn't phrase my comment as bluntly as Jay did, I must say that I am beginning to share his frustrations. I have given Sciencewatcher the benefit of the doubt for a long time, but I think your true colours are really starting to show. Even using a wild imagination, I cannot see the science as you do. SW, your most recent comments cannot be seen as anything but POV pushing. I would like to ask you to do a bit of self-reflection. --- Taroaldo 19:22, 21 September 2007 (UTC)

This is a discussion, remember, not the encyclopedia article. You can't accuse me of "POV pushing" because I express my opinion in the discussion page. Other people do the same, but I don't see you accusing them of POV pushing. Perhaps because you have your own POV?

Do you want to have an actual discussion about stress as a cause? If you do, here are my main points: stress can explain all facets of CFS, and no other theory can. Which part of that do you disagree with and why? If you think that stress cannot explain a particular aspect, explain. If you think another theory can explain CFS, which one? Let's either have a sensible discussion about it, or drop it. And Jay: I only use words like "pseudoscience" and "speculation" when there is pseudoscience or speculation, not when I don't want to hear something. If you don't know the difference between pseudoscience, speculation and real science, there is nothing much I can do to help you, and this discussion is pointless. --Sciencewatcher 21:51, 21 September 2007 (UTC)

You are quite right: this discussion is pointless. People have tried to have a discussion, but even when they cite sources, they are automatically dismissed as "pseudoscience". I did not say you could not express a POV in the talk page. What I did say was that your last comment seemed to give a clear indication of a controversial POV despite your assertions that everything you add or remove from the article is changed without any POV motivations. Scienctific research is unfortunately not immune to POV pushing either, such as some of the psychiatric quacks who have wanted to reduce everything to a psychological manifestation. Stress has more than one motivator, and despite your attempts to remain relatively neutral in your references to stress in the past, your recent comment made clear reference to what I think your true agenda is - namely attributing every possible cause of CFS to "psychological stress" (your words). This agenda is further indicated when you say: "[t]he problem is that it is very difficult to prove definitively that [psychological] stress is the cause of the illness." Ah, so you admit that it is very difficult to prove, yet you still maintain that it is paramount over all other theories, and when anyone cites a differing view it is "pseudoscience". When someone calls you on it you resort to "[d]o you want to have an actual discussion about stress as a cause?" when you are the one who is so quick to shut down other editors attempts to discuss it. Forgive me if I have little sympathy for your position at this point. --- Taroaldo 22:43, 21 September 2007 (UTC)

But I did say earlier in this discussion that I do think psychological stress is the most important factor in CFS. Yes, there are other factors, but in my opinion it is psychological stress that is mainly responsible for perpetuating the illness. That is what I read from the science and what I see from people who have CFS. If you want to call this a "POV" then that's fine. It seems to me that some people just have a bias against psychological stress as a cause for CFS. I agree with you it is probably pointless trying to discuss this here, as I will never be able to change people's minds. In future I will just add edits to the article and I will only respond to anyone who has issues with my edits. I'll just let the science and facts speak for themselves. --Sciencewatcher 03:29, 22 September 2007 (UTC)

Of course that is what YOU see. But nobody cars what YOU see. Unless you can back it up. And saying "this is obvious" is not backing it up, that's at best original research and most probably not even that.

Taroaldo, this is taking us nowhere. I think we should revert the article back to an earlier version before sciencewatcher made major, unsuported changes to the neurological section.

We can then force him to build consensus with other editors, which he clearly does not have at this point.JayEffage 10:25, 22 September 2007 (UTC)

As Jay said, there is no consensus for wholesale changes. Taking liberties with the article will result in quick reverts. --- Taroaldo 20:19, 22 September 2007 (UTC)

Jay: if you look at this discussion you will see that there is consensus for the changes I made. The discussion we are having here is nothing to do with the changes in the article. You are just a troublemaker who has never actually made any changes to this article. Why don't you make yourself useful and help us clean up this article, and actually add some information to it rather than just bitching at me in this talk page? I'm quite happy to back up anything I say: I gave you the opportunity above to have a proper discussion, but instead you have just decided to continue bitching and causing trouble. I propose that you should be banned from wikipedia if you continue this inappropriate behaviour. --Sciencewatcher 15:23, 22 September 2007 (UTC)

As for the verbal abuse: Consider yourself warned, stay civil.

In medias res: I have to admit my fingers are itching - after your most polite invitation above - to revert your edits on the neurological section thus re-adding the baraniuk study together with the refernce to the WHO classification, which you conveniently deleted as well.

However, in the light of the steep decline in your civility, I would like to hear at least taroaldos and tekaphors opinion about that. To my knowledge, tekaphor was the first to ask for an explanation and has already stated his dissatisfaction with your edit. JayEffage 17:27, 22 September 2007 (UTC)

It was you who begun this "verbal abuse" by saying things like "nobody cars what you see" and accusing me of saying things I never actually said, and accusing me of making changes without building consensus, which I didn't do either. I gave the reasons for deleting the study, and there didn't seem to be any disagreement about that. I have now fixed the HPA axis section, which did have some complaints. The reason I removed the WHO comment because it was incorrect. The neurological abnormalities support either a neurological or psychiatric explanation for the illness, as explained in the article now. --Sciencewatcher 18:45, 22 September 2007 (UTC)

The baraniuk study - which you deleted - supports either a neurological or psychiatric explanation? Really? Apparently Baraniuk et. al. didn't know that stating: "Given the controversy over whether CFS and its allied syndromes are legitimate medical conditions, our model provides initial objective evidence for the legitimacy of CSF as a distinct neurological disease". [5]. JayEffage 19:11, 22 September 2007 (UTC)

Yes, really. Let me give you an example: depression is a psychiatric illness which is also neurological. All psychiatric illnesses are neurological, but not all neurological illnesses are psychiatric. Psychiatric patients show different brain activation, neurotransmitters, blood flow, etc. to controls, as well as different proteins in their CSF. These are neurological symptoms, but the illness itself is psychiatric. --Sciencewatcher 19:52, 22 September 2007 (UTC)

And who - other than you, that is - says that the CSF abnormalities in CFS are psychiatric and not neurological? Baraniuk apparently doesn't share your POV.JayEffage 20:28, 22 September 2007 (UTC)

I never said that. I said they could be psychiatric. --Sciencewatcher 23:22, 22 September 2007 (UTC)

I didn't ask you what you said. Your opinion trivially doesn't matter for the article. What citable source says so? JayEffage 23:31, 22 September 2007 (UTC)

It is interesting that our disagreements here are microcosms of many of the larger disputes raging within the scientific community about CFS. In my discussion with Sciencewatcher, I think we clarified our positions, and even though we may not agree on everything I believe there is a framework to build on. I know that every editor here has the same goal of building and improving this article. It's just that sometimes we disagree on how to go about it. I am surrounded by a lot of research (literally) at my desk right now and I will need to take some time to take another look at it. There are too many unknowns in CFS for me to be comfortable giving any theory or theories a preeminent status, but at the same time we must ensure that we give all mainstream research fair play, even though we may not agree with some of the conclusions reached. Stress is a contentious topic right now, but we all need to keep working at it together and eventually we should come up with something we can all agree on. Well, that's my reflection for the day. Cheers. --- Taroaldo 18:01, 22 September 2007 (UTC)

-

I've been observing this conversation for several days now and have been working on the following related responses:

CFS Models -- Overall, I'm of the persuasion that ME/CFS should be viewed within a "psycho-neuro-endocrino-immune" model as a multifactorial systemic end-state with a possible genetic predisposition; although I doubt that each aspect has equal relevance for all patients. I don't see this model as being equal to biopsychosocial models; mainly because when applied to ME/CFS the BPS models seem more concerned with finding biological correlates for, and/or merely adding the bio prefix to, psychology ideologies (rather than working towards synthesis, not to mention the constant predominating emphasis on psychosocial factors). However, if we aren't dealing with the same illness, we will need different models.

Stress and Speculation -- Sciencewatcher, while perpetuation by stress makes some sense and I'm generally more tolerant of your comments compared with some other editors, CFS is not "pretty well understood" as you implied. I disagree with both your previous statement "there is no need to speculate about possible viruses" and the related comparison of CFS with PTSD. If anything, possible infections become more important because stress alters the immune response, especially when many (if not most) people with CFS symptoms report a sudden infectious-like onset. Anyway, while Guido den Broeder is speculating about hidden viruses, you speculate about hidden mental stresses. Stress involves the HPA-axis to a degree; but related alterations don't seem specifically consistent in CFS and haven't been associated with symptoms or even stress tolerance. Stress also affects the immune system, but as far as I know the immunological findings in CFS aren't entirely consistent either, yet alone conclusively consistent with chronic psychological stress. Even if they are similar, the same could be said about infections. Both stress and infections can trigger abnormal production of various cytokines, which by themselves can cause a range of physical and mental symptoms. This issue about stress/infections affecting the HPA-axis/immune system can be speculated about either way and hasn't been properly elucidated, although I think it will be eventually differentiated because I doubt they have exactly the same effect. In other words, a general association exists, but the specific hypothesis that ongoing mental processes are causing the HPA-axis and immune system to perpetuate all the CFS symptoms is still just speculation. The partial success of CBT adds some weight, but a major subset of people with CFS aren't improved this way and we have serious issues with selection criteria. Considering that infectious onset seems common in CFS cases, and that infections and/or improper immune activity can cause the same complications you attribute to psychological stress, there is still plenty of need to investigate the immunological aspects of CFS and it may actually help settle the argument. We are dealing with a very complex illness here and it is inappropriate to make general leaps of faith regarding associations. We are of course all entitled to our own POV and some have chosen to speculate about a mostly one-way psychosomatic direction; but I don't claim that "all the research is pointing towards" any particular direction, or imply that my comments aren't speculative because they are "based on the science".

Neurological vs Psychiatric -- I don't think it's totally unreasonable to propose that CFS is psychiatric; I once had a similar POV (but have since changed my opinion). None of us really know yet whether CFS is psychiatric or neurological or strictly whatever, but I'm personally assuming with some confidence that once acquired it's primarily neuro-immunological regardless of the causes. Many neurological illnesses have an unknown etiology, but the exact physical cause of the symptoms are known and rule out traditional psychiatry as primary, so I'm guessing that until the underlying cause of CFS symptoms are properly known this classification issue will continue. I wouldn't be surprised if CFS never becomes universally recognised under either classification. The distinction itself has outlived its original application, is arguably arbitrary, and has become blurred in the past decade or so. However, CFS seems to be far more physiologically orientated than psychiatric illnesses in general, both in number and severity of symptoms; although this seems to depend largely on the criteria used and I doubt the issue of criteria will be solved soon (future studies should involve more than one criteria). If CFS was mostly perpetuated by psychological stress, I imagine there would be some pharmaceutical agent that could alleviate it and lead to a major reduction of symptoms over time, even if the root cause is psychological and requires changes in cognitive behaviour to secure permanent improvements. We could all debate this distinction, but there are far more important issues to focus on.

Tekaphor 07:27, 24 September 2007 (UTC)

-

Fix those references!

Over the last few weeks I've been improving the references. As I noted before, there is some pretty dodgy referencing in this article. Can I please urge all editors to help out here. If all of us were to run 10-15 references through the PubMed Single Citation Matcher we could provide PMID codes or DOI numbers for all of them. If we could also use the {{cite journal}} template on each reference that would be better still. David Iberri's template filler makes this job easier still. JFW | T@lk 05:34, 23 September 2007 (UTC)

The current editing conflict

Unfortunately, Sciencewatcher has not seen fit to respond to my attempted conciliation and has continued to proceed with a narrow scientific point of view which does not seem to have any support among editors here. I have issued a 3RR notification. I must now also call into question any references which SW cites: the "psychosomatic" comment in the article had a fact tag on it since May. SW never made any attempt to add a credible source for this in the past 5 months. This weak sentence more than qualified for removal. But now SW suddenly comes up with a citation based on an interpretation of a couple sentences gleaned from the abstract of a single paper. This does not serve to improve the article and gives credence to the notion that there is a narrow agenda at play here. SW's unwillingness to collaborate in a collegial manner is wasting the time of the other editors here and is stalling productive work on this article. --- Taroaldo 19:39, 23 September 2007 (UTC)

I only added a reference now because you seem to have a problem with it now, and I thought that would be sufficient to stop your reverts but obviously that is not the case. This is one of the main proposed etiologies, and you cannot remove it just because you don't like it. A lot of the other editors here do not like it, and I agree that I am in the minority. But that is not a good enough reason for deleting it. It seems that you removed it for POV reasons, but according to wikipedia policy we have to respect all major POVs in the article, so the paragraph should stay. There are a lot of possible references for this, but I included a review by one of the authorities on functional somatic syndrome (Simon Wessely). --Sciencewatcher 19:54, 23 September 2007 (UTC)

A random reference won't do. The reference you gave does not support your text. Guido den Broeder 20:04, 23 September 2007 (UTC)

Did you even read it? Simon Wessely is the authority on FSS, and the article was discussing why CFS is a FSS (unless I mistakenly referenced the wrong article). So how does it not support the text? --Sciencewatcher 20:39, 23 September 2007 (UTC)

It is easy to be 'the authority' on something you have (more or less) invented. The point is, however, that even Wessely's views do not support yours. Guido den Broeder 21:18, 23 September 2007 (UTC)

It is easy to pull bits and pieces from a bunch of abstracts which may not be in context. To cite just two quick observations:

• "The existence of CFS epidemics points toward an infectious agent and away from psychological traits in individuals when considering the cause of CFS." (Donald G. Dutton "Depression/Somatization Explanations for the Chronic Fatigue Syndrome: A Critical Review", in Byron M. Hyde (1992). The Clinical and Scientific Basis of Myalgic Encephalomyelitis/Chronic Fatigue Syndrome. Ottawa, ON: Nightingale Research Foundation, p. 503.)
• Attributing such cases of CFS to psychosomatic causes is incongruent because epidemic outbreaks of psychosomatic illnesses have not been reported. (Kruesi, M.J., Dale, J., and Straus, S.E. (1989). "Psychiatric Diagnoses in Patients who have Chronic Fatigue Syndrome". J. Clin. Psychiat., 50, p. 54.) --- Taroaldo 20:26, 23 September 2007 (UTC)

That is just one POV, and another POV is that CFS is psychosomatic. It is not up to us do decide, we should include all POVs as per wikipedia guidelines. --Sciencewatcher 20:28, 23 September 2007 (UTC)

Should we also note in astronomy articles the POV that the Sun revolves around the Earth? I think that one has been mothballed for a little while now. Psychosomatic CFS isn't far behind. --- Taroaldo 20:52, 23 September 2007 (UTC)

ME/CFS is a neurological disease by definition. Any view that says different is therefore basically non-E and should not be mentioned on the same level as other views. Guido den Broeder 20:49, 23 September 2007 (UTC)

Again, all of this is your (Guido/Taroaldo) POV. The psychosomatic view is held by the majority of doctors, whether you like it or not. It is certainly not a minority viewpoint like the earth revolving around the sun, and it is ludicrous for you to even suggest that (and it shows your true intentions here). The paragraph should be added again. Ganging up with other editors who happen to share your POV in order to bully me will not work. I'm going to leave this discussion now and let an admin sort it out. --Sciencewatcher 21:26, 23 September 2007 (UTC)

Really? By the majority of doctors? And who says that? You? Or do you have a source on that? JayEffage 08:36, 24 September 2007 (UTC)

Sorry to see that once again you have no clue. Interesting claim though that the earth revolving around the sun is a minority viewpoint. :-) Guido den Broeder 21:35, 23 September 2007 (UTC)

• Note for clarification: SW has withdrawn to "let an admin sort it out" because I have finally made a report to admins re WP:3RR.

And, signing after being reminded to sign. :p --- Taroaldo 21:54, 23 September 2007 (UTC)

I think both the neurological and psychiatric sections need work, with more concise content. Sciencewatcher, you have added/included supportive information about stress that isn't directly related to CFS (e.g. animals under stress, fibromyalgia and CSfluid, possible role of nitric oxide in stress, etc). I don't have a major problem with that (although I'm not sure how appropriate it is), however you must then accept that supporting information can also be added about other aspects of CFS by other editors without you then removing/refusing it on grounds of being "speculation". This applies to everyone, and if we all essentially agree that the different proposals deserve a fair presentation, we should stick to that as our main common ground. Perhaps there should be a brief mention at the start of the section that some of the overlapping research can be interpreted differently and that the understanding of some of these related fields is still rather limited. - Tekaphor 08:16, 24 September 2007 (UTC)

Amen to that, tekaphor. JayEffage 08:50, 24 September 2007 (UTC)

General information on stress should not be included in this article. The text is long enough as it is. Guido den Broeder 09:57, 24 September 2007 (UTC)

I tried to keep the info to as minimum as possible. The reason for adding that info was because it is one explanation of the HPA axis changes seen in CFS patients (and as far as I know, the only explanation). So it seemed appropriate to include it. I didn't go into great detail, just a sentence or two to give an overview.

Neither the HPA axis abnormalities nor the fact that stress causes similar changes are speculation, as they have been repeated (although as I note in the article, not all patients show the HPA axis abnormalities). There is no conclusive proof that stress causes these changes in the case in CFS, and I didn't say that in the article. I just gave the info as per wikipedia guidelines.

The nitric oxide and t-cell info was added to the psychoneuroimmunology section to balance it with a npov. Previously it had just info on how the immune system might cause psychiatric symptoms, but it had no info on the reverse, which is also important.

The psychoneuroimmunology section has a link to the article itself giving further info, and like the hpa axis there is only a very brief overview without going into any great detail. As Guido says, we should not be duplicating whole reams of info from other articles when the user can go and look at them for more information. Just a basic summary is sufficient.

A little bit of speculation is fine, but when you start speculating about something which has not even been satisfactorily shown to occur in CFS patients, then that is going too far. --Sciencewatcher 18:50, 24 September 2007 (UTC)

Also: in response to Tekaphor's comment about me adding info on fibromyalgia and CSF: I actually removed that info in my last changes and replaced it with CFS references to the HPA axis. Everyone agreed previously that it wasn't appropriate. --Sciencewatcher 18:54, 24 September 2007 (UTC)

Another edit conflict - depression

Guido seems to be in another edit war with me. The reference he added seems to be a POV of a particular doctor. The title of the article assumes that CFS is not psychiatric, which in itself is POV. Also, where did the 10% figure come from? The doctor's opinion? I don't have the article so I can't tell. The reference I gave included surveys that asked patients what symptoms they had, so it would seem to be more reliable. If you are unhappy with my reference, you can either try to find a new one, or just don't have any references. I couldn't find any other refs except for diagnoses of major depression or clinical depression in cfs patients. Perhaps we could include all the refs and info for the prevalence of depression as a symptom, major depression as a diagnosis, etc., but in my opinion it is easier and less confusing to just say that "depression is a common symptom".

Also, saying that there is overlap between depression and CFS does not make sense. Depression is a symptom. Clinical depression is a diagnosis. It is well established that depression is a common symptom of CFS, so I don't see why you want to deny this, except for POV reasons. --Sciencewatcher 20:28, 23 September 2007 (UTC)

And you will keep running into edit wars with everybody if you keep pushing, until such time that you are finally banned. Guido den Broeder 20:42, 23 September 2007 (UTC)

How about something like "as in a number of other chronic deseases it may lead to depression and has been diagnosed as such. However depression has not been shown to be a symptom of the disease."......would only need to find to fairly well accepted references....one that showed chronic diseases tend to cause depresssion do to lack of ability to do what patient desires to do and another that shows cfs patients have this problem....have fun.....sno Sno2 22:00, 23 September 2007 (UTC)

As I put into my (now reverted) edit, we don't know whether or not depression is a symptom of the illness itself, or just a reaction to having a chronic illness. Your proposed sentence seems to promote the POV that depression is not a symptom of CFS itself as far as I can see. --Sciencewatcher 22:26, 23 September 2007 (UTC)

I did not know how to word it to not being read as a misdiagnoses...it can't be if the diagnoses could be correct...<g>...something I noticed that seems to be missing that is mentioned a lot on the chat/forum pages is the use of alchohol causing increase in symptoms....in my case it can be worse then forced exercise....lately have found that if I drink a glass of wine without eating will be nasuas for the next two days.....have fun....sno Sno2 00:22, 24 September 2007 (UTC)

Perhaps depression is a symptom of CFS, but as far as I know it isn't a common CFS criterion, it's a co-morbidity (similar to how roughly half of people with depression also have anxiety, but anxiety isn't viewed as a "symptom of" depression). However, 10 - 15% sounds too low. My impression from different studies is: that it's 25 - 50%+ depending on the study, that overall the rates of depression in CFS is either similar to or somewhat higher than what is expected from chronic illness, and that the likelihood is significantly increased with the concurrence of other illnesses. - Tekaphor 03:15, 24 September 2007 (UTC)

Sno2, there is mention of alcohol intolerance in the symptom list. - Tekaphor 03:22, 24 September 2007 (UTC)

Sno2, ther is even a book on the subject, i think titled "light at the end of the tunnel" ISBN 0-646389-02-5 in which the author shows deficit of mitochondrial enzymes are responsible for alcohol intolerance. Jagra 08:27, 24 September 2007 (UTC)

Sno's comment on depression better depicts the context. Depression is not a primary symptom of CFS. However, secondary depression may develop in CFS patients as it may in sufferers of any chronic illness. In its outline of symptoms the CDC notes that depression and other secondary symptoms need to be viewed as related "to a comorbid or an exclusionary condition; they should not be considered as part of CFS other than they can contribute to impaired functioning". --- Taroaldo 04:52, 24 September 2007 (UTC)

I came to the conclusion that stress of all types has a role in the precipitation of CFS, but I do not agree that depression causes CFS, yes depression is a symptom in a subset, but equally depression has been shown to be secondary and to have an organic basis, such as in this one “A urinary metabolite, coded UM15, was the primary correlate for depression (in CFS patients)---. These results indicated that, in this CFS cohort, the SCL-90-R defined psychological changes were strongly associated with changes in the biochemical homeostasis of patients, suggestive of an organic basis to CFS,” (and their psychological symptoms) I have to reconcile that there is a view that includes a psychiatric etiology and until it is established one way or the other, it should remain. I do not support the ‘shrunken adrenal gland’ inclusion, the only reference shows it to be a subset of a subset, and unlike in depression there is no evidence of central plasticity changes. Too speculative to be included at this time. Likewise we do not need animal studies when there are CFS studies that show similar. Whilst I think the brain scans belong in the neurological section along with neurotransmitter findings there are a number of SPECT and MRI studies in CFS and picking one that compares well to depression is not a balanced summary, this one concludes whilst similarities CFS fitted a viral cause PMID 8141022. This one shows marked differences between CFS and depression PMID 9121617 . There are quite a few studies on neurotransmitters and I will develop this more, along with the HPA axis item. Jagra 08:27, 24 September 2007 (UTC)

Stating that depression is secondary to CFS is a POV. If CFS is a psychiatric disorder caused by stress then depression is a primary symptom of the illness itself. In talking to patients, the depression occurs along with other symptoms and is not related to psychological thoughts about having a chronic illness.

Regarding the adrenal gland study: it wasn't a subset of a subset as far as I can see. They did the study on patients who had low response to ACTH, and those patients had 50% smaller adrenal glands. So the subset was patients who had low adrenal function, and the reason was small adrenal glands.

The SPECT study I referenced did show differences between major depression and CFS. Feel free to add the other studies and results if you want. --Sciencewatcher 19:08, 24 September 2007 (UTC)

Also, if CFS is a non-psychiatric neurological disorder, it is again likely that the depression is a primary symptom. Considering that either neurological or psychiatric are two of the most likely explanations of the illness, it seems appropriate to say that the depression could be either a primary symptom or a psychological consequence of having a chronic illness, rather than just saying it is secondary. --Sciencewatcher 19:35, 24 September 2007 (UTC)

Depression is not a primary symptom. If it is a consequence of having a chronic illness, it should be given the same weight that it is given in any other article on chronic illness where depression is a co-morbid condition. It is not consequential to the disease itself, but it is consequential to affected patients' functional ability, just as many other factors are. --- Taroaldo 21:51, 24 September 2007 (UTC)

CFS is not a psychiatric disorder caused by stress. Stress (of any kind) may very well be a catalyst for the development of CFS, but that is far from causal. Stress (of any kind) undoubtedly exacerbates CFS, just as it does in MS and so on, but that does not make it a hallmark of the disease.

Who is "talking to patients"? If depression develops, then of course it will occur along with other symptoms, but I doubt patients wake up on their first morning after developing CFS and say I feel completely exhausted, my joints and muscles hurt, and I am depressed. To conclude that "it is not related to psychological thoughts about having a chronic illness" is amusing as most patients aren't capable of properly assessing or expressing the nature and development of their depressive feelings, much less what physical or psychological processes resulted in its development. --- Taroaldo 22:08, 24 September 2007 (UTC)

Is the arguement over wether depression is a primary symptom, or a secondary one...??....Or over that depression is the cause or the result of cfs...??....am confused (as normal)....seems that these are two seperate issues.....have fun....sno Sno2 22:17, 24 September 2007 (UTC)

To say that "depression is not a primary symptom" and "CFS is not a psychiatric disorder caused by stress" are both POVs, and certainly not universally agreed upon. As I have shown above, there is certainly enough evidence to show that depression could be a primary symptom, and CFS could be a psychiatric disorder caused by stress.

To clarify what I mean about depression as a symptom: in patients who have depression it seems that the depression is worse at the same time as other symptoms, sometimes varying throughout the day. Sometimes the depression is apparent before any other symptoms, so it is not a case of being depressed when you have the symptoms. If depression was secondary, it is unlikely you would see this pattern. --Sciencewatcher 22:35, 24 September 2007 (UTC)

Also, have a look at PMID 1890495, which shows that CF/CFS patients have a significantly higher prevalence of lifetime major depression than patients with rheumatoid arthritis, and that in 50% of cases the psychiatric illness preceeded the CF. They found no difference between CF and CFS patients in any of the study variables. --Sciencewatcher 22:44, 24 September 2007 (UTC)

Arthritis patients do not first get diagnosed as clinically depressed prior to being given a cfs diagnoses....and remember it has only been a few years that the medical establishment even recognises it.....I still have a hard time convincing doctors (if I do) that "the depression only started when I couldn't do what I wanted to do" they still want to blame the symptoms on depression.....even if the meds don't work....and I tell them I haven't been very depressed in years, yet still have the symptoms.....<g>......have fun....sno Sno2 23:14, 24 September 2007 (UTC)

PMID 1890495 is a small study involving 98 patients with chronic fatigue and 31 patients with rheumatoid arthritis. However only 19 of the 98 chronic fatigue patients met the CDC criteria for CFS, meaning that the vast majority of patients in the study had an illness (either pathological or psychiatric) other than CFS. Without reading anything more than the abstract, one cannot assess the study on a sufficient level. The only conclusion the study's authors are willing to venture is that patients with chronic fatigue have a "higher burden" of psychiatric illness than patients with RA. Although they infer in the abstract some tenuous similarities between CFS and chronic fatigue, they admit that any similarity extends only as far as the variables they considered in the study. I am not surprised at all that patients with chronic fatigue outdo RA patients w.r.t. psychiatric illness because "chronic fatigue" is often a significant symptom in psychiatric illnesses. --- Taroaldo 00:10, 25 September 2007 (UTC)

Regarding the adrenal study PMID 10451910 Firstly the sample was drawn from a fatigue clinic meaning they probably had CFS for some time, and not necessarily a representative sample, and did they have comorbid depression as well? Secondly they used the low dose ACTH test which is notoriously inaccurate, 25% of normals will get false results. The small study of 8 patients is too small for statistical significance. The real test of the adrenals is the full synacthen test, and often those that fail a low dose test can perform in a full test within normal parameters. Who says smaller adrenals cannot perform, no full test was done? Interesting but hardly noteworthy evidence on which to hang a hat, I would say Protoscience.

The study I referred to above used highly sensitive gas chromatograph mass spectrometry to search for unusual metabolites or viral particles. They found a metabolite that was the primary correlate for depression in CFS, meaning the depression was associated with organic changes, ie the consequence of the disease, not the cause. “Multiple regression analysis indicated that somatization was the most important SCL-90-R defined dimension discriminating CFS from control subjects. Depression and anxiety were not found to be important inter-group determinants”. So stating depression is secondary is exactly what this study found. So the depression can be secondary if the patients feel bad about their condition, or if CFS biochemical changes induce depression regardless. Whilst stress in the broader sense can help precipitate CFS or primary depression ( two conditions with opposite HPA and serotonin findings) I am not aware of depression precipitating CFS, is there any such evidence or evidence of CFS thus being a psychiatric disorder? Stress can cause a number of diseases, but these are not all labelled psychiatric, it will need more than stress involvement to label it such.!Jagra 07:39, 25 September 2007 (UTC)

Depression does indeed not precipitate CFS. Instead, it probably makes CFS less likely, since depression is a defence mechanism and its existence proves that the organism is still capable to defend itself. Guido den Broeder 07:56, 25 September 2007 (UTC)

Regarding PMID 1890495: they found that there was no difference between the CF and CFS patients in the variables they measured. But even so it is quite a small study.

Nobody is saying that depression causes CFS. I'm saying that depression and CFS may both be symptoms of the same illness, rather than the depression being secondary. There is no definitive evidence either way.

Small adrenal glands DO result in lower cortisol: that has been confirmed by earlier research (Selye first noticed it over 50 years ago!) It is a small study, and on its own it wouldn't be worth mentioning, but other studies have found low cortisol and reduced HPA axis function in CFS patients. --Sciencewatcher 15:05, 25 September 2007 (UTC)

Surely this argument is pointless? Whatever you decide is going to be WP:OR anyway because depression has not been proven to be either a primary or a secondary symptom at this time. Why not just say that depression often occurs in CFS patients, although it is unknown if it is primary or secondary bla bla. Thedreamdied 15:23, 25 September 2007 (UTC)

I agree with Thedreamdied. --Sciencewatcher 15:32, 25 September 2007 (UTC)

Thedreamdied- there is enough to be more definitive. As I commented above, the CDC notes that depression and other secondary symptoms need to be viewed as related "to a comorbid or an exclusionary condition; they should not be considered as part of CFS other than they can contribute to impaired functioning". Physicians do assess for depression and other illnesses when doing a differential. We can put a whole section in the article on depression if needed, but it needs to be kept in the proper context. --- Taroaldo 15:35, 25 September 2007 (UTC)

Indeed. Regarding cortisol: low cortisol isn't the problem. The problem is with the cortisol response, and ditto for adrenaline, insuline and other hormones. Initially there is a reduced response, but this may turn into a rush if the demand continues. Guido den Broeder 15:39, 25 September 2007 (UTC)

The cdc page is interesting. It looks like they have been quite arbitrary about what are the "primary" symptoms. Some others, such as brain fog, are usually considered primary symptoms of cfs, but in the cdc page are relegated to "other common symptoms". I'd be interested in seeing what other countries say about this, e.g. the NICE guidelines. --Sciencewatcher 21:45, 25 September 2007 (UTC)

The beginning of the article mentions a range of symptoms (including depression) that aren't CFS criterion but often experienced by CFS patients. I'm uncertain how the "pattern" Sciencewatcher described necessarily supports the idea that depression isn't secondary. There are some other variables regarding the primary or secondary nature, such as "feeling down" versus axis 1 DSM criteria. As far as I know an actual depressive illness has considerable inertia and doesn't just disappear after lunch; the mood of some people with depression is highly reactive (albeit only temporarily) but the depressive illness itself endures. I don't think any of this distinctly supports depression as primary or secondary. The related research I'll present later in a separate post suggests to me that mood changes of any kind are an important part of CFS, although this seems common in some neurological disorders. As a side note relating to the HPA-axis, Sciencewatcher and Jagra may be particularly interested in these 3 studies: a subset of CFS patients may benefit significantly from hydrocortisone treatment which seems to help correct HPA-axis alterations (PMID 15110921)(PMID 11502777), and the 3-month pre-onset "important period" could also apply to infectious mononucleosis (PMID 16738080). - Tekaphor 05:37, 26 September 2007 (UTC)

Sciencewatcher There is no evidence of primary adrenal insufficiency in CFS, this study PMID 1659582 specifically excluded it, this one used both low and normal dose ACTH tests and found no adrenal insufficiency, PMID 12618533 whilst this one found low dose ACTH tests in CFS inaccurate PMID 9713562. If HPA axis dysfunction occurs in a subset, albeit major subset of patients then small adrenal glands finding, is a subset of a subset. As I pointed out there are methodological problems in the small study you cite compared with the large cohorts in other HPA studies and no statistical analysis, as I have already said protoscience which flies in the face of other evidence and thus borders on pseudoscience or the fringe science of Baschetti Jagra 07:56, 26 September 2007 (UTC)

Given agreement now that depression is not a cause of CFS and given primary depression is a differential exclusionary diagnosis, then co morbid depression in CFS is secondary depression. That I understand is the CDC opinion and is therefore not OR. It is therefore difficult to maintain a psychiatric main theory of etiology unless one assumes this ‘unknown illness’ where ‘depression and CFS may both be symptoms of the same illness’ has to be psychiatric. Instead I suggest stress be considered the fourth main theory of eitology. Jagra 07:56, 26 September 2007 (UTC)

Tekaphor, I am aware of the low dose hydrocortisone studies, Cleare the primary author of one of them said in a later reveiw paper PMID 12700181 that “However, the second treatment study (his) was short term only, and the positive effects wore off rapidly on the switch to placebo; thus, routine use of this strategy as a treatment is not recommended without further evaluation”. The value of these trials is that they show small cortisol level changes correlate with significant symptoms in CFS Jagra 08:27, 26 September 2007 (UTC)

"As far as I know an actual depressive illness has considerable inertia and doesn't just disappear after lunch;": that is exactly my point. One person with CFS had suicidal depression in the morning, then zero depression later in the day. That doesn't fit the pattern of major depression (i.e. secondary depression), which is why it points to depression being a primary symptom of the cfs. It stands to reason that if the other "primary" cfs symptoms are caused by altered neurotransmitters then depression could easily be a primary symptom also. Why the resistance to this possibility? Certainly the cdc is saying it is a secondary symptom, but I'm wondering what other health agencies are saying. Has anyone checked? --Sciencewatcher 15:21, 26 September 2007 (UTC)

That's an interesting account. I wouldn't be surprised if drug interactions or side effects played a role in that. Some people combine too many prescription and OTC drugs or combine Rx drugs with herbal medicines without proper medical advice. (And CFS patients are constantly bombarded with claims about "miracle" drugs/supplements.) Or the person could be seriously bi-polar.... --- Taroaldo 15:54, 26 September 2007 (UTC)

Interesting point Sciencewatcher. But, as we know that ME is a very up/down illness in terms of severity of symptons, isnt it possible that the patient may have felt very unwell during the first half of the day, thus 'suicidally depressed', then in the afternoon felt better so was less depressed? Which would make it a secondary sympton? Just a thought Thedreamdied 16:19, 26 September 2007 (UTC)

Jagra, the part I found interesting is that hydrocortisone was only beneficial in a subset. Sciencewatcher, I think its difficult to interpret the moods because even in some depressive illnesses the mood does fluctuate substantially, so suicidal thoughts in the morning may dissipate by the evening but the overall existence of mood disruption doesn't usually disappear in one day. As Thedreamdied pointed out, some people's CFS symptoms seem to spontaneously fluctuate as well. But my point was that the depression doesn't have to be purely reactionary to the illness or surroundings to be secondary, it may start out as a psychological response to the illness but snowball into a psychiatric disorder (or vice versa) that then becomes less reactive. Taroaldo also brings up a good point about the different medications and "miracle cures" affecting mood unpredictably. Besides, there are other reasons why it may be primary which is why I'm not dismissing it. For example, there are high rates of related psychiatric comorbidity in CFS, and psychiatric symptoms appear to be at least mild risk factors. I don't know about the exact precipitation process of CFS; I think the word "catalyst" used for stress earlier also somewhat applies to any psychological and psychiatric distress. It's important we resolve this because the section is titled "proposed causes and pathophysiology", which obviously implies etiological and/or pathological importance rather than just concurrency. Jagra, I don't think that identifying depression/anxiety as risk factors necessarily makes CFS a psychiatric disorder. Perhaps the article needs a "possible risk factors" subsection in the "course" section, as some have been tentatively identified, or at least discussed. - Tekaphor 16:43, 26 September 2007 (UTC)

Tekaphor, there is a fine balance between too much hydrocortisone, which in total with natural cortisol exceeds the upper threshold for triggering negative feedback inhibition, thus lowering natural cortisol further. To be effective each patient would need to be individually assessed and dosed, something the trials are unable to do. Some patients are so sensitive that asthma sprays can trigger negative feedback and increase symptoms such as pain. Jagra 07:59, 27 September 2007 (UTC)

Protected

I've protected the page, ladies, gentlemen... try to work this out. I'm not going to put everyone into the sin bin for 24 hours this time. Please adhere to three revert rule. Regards, Navou ^banter 22:13, 23 September 2007 (UTC)

Outbreaks of M.E.

I am not sure if this is of any interest to you or if it is considered to be old news, but I noticed it was lacking from this entry and it has been said to be of international interest.

In October 2004 the local reservoir for drinking/tap water in Bergen, Norway was infected with Giardia Lamblia parasites. Out of 50 000 people to receive water from this reservoir it is estimated that 5000 people were infected. 2500 people were medically treated for Giardiasis while 1300 of these in addition was positively diagnosed in labs. This was one of the most severe outbreaks of Giardiasis in Europe to date. At least 20 of the infected patients have now been diagnosed with ME (Myalgic Encephalopathy). It is clear that the condition is a direct result of the infection and there is on-going research to look into this outbreak and each individual case. I probably don't have to tell you what a unique research opportunity this presents. (An additional 42 people exhibit somewhat milder symptoms of M.E. and 200 people are still being treated for what resembles Irritable Bowel Syndrome.)

There's also the Norwegian meningococcal B vaccine trials of ‘88-‘91 that caused about 250 people to develop M.E. (180 000 vaccinations were administered in total.). Despite the on-going court trials and the Governments compensation of the Norwegian sufferers, the same vaccine was in 2001 sold to France and New Zealand. In New Zealand the vaccine was administered to 1,1 million children. I noticed that you lack citation on the subject of vaccinations causing acute onset of CFS.

MEsite, translations

I apologize for not providing you with links to proper research as everything I have read on the Giardia incident is in Norwegian and the research is yet to be published. I thought you also might have better luck finding information you deem reliable – if this is of interest to you, that is. I hope you can take the time to consider adding this. I dare not attempt this myself as you all seem to be pro's at this and I fear I might inflict some serious damage on your article,- I hope you understand! :) --Nemi133 16:22, 25 September 2007 (UTC)

Thanks for bringing that to my (our) attention nemi. Thedreamdied 16:49, 25 September 2007 (UTC)

Thanks, but it's not clear to me how Giardiasis could cause ME. With 20 cases out of 5,000 infected the incidence is not higher than normal. Guido den Broeder 16:56, 25 September 2007 (UTC)

Guido, i was under the impression that the etiology of CFS/ME was unknown - thus, how could it be clear how giardiasis would cause ME? Thedreamdied 17:27, 25 September 2007 (UTC)

AFAIK, Giardidiasis does not reach the blood-brain barrier. But I could be mistaken. Guido den Broeder 19:54, 25 September 2007 (UTC)

Well indeed, but it is only your theory that the BBB has anything to do with ME. It could be a different etiology for which Giardidiasis would be applicable. Thedreamdied 19:56, 25 September 2007 (UTC)

See, for instance, Blood Brain Barrier Breakdown in Myalgic Encephalomyelitis. Behan W, Gow JW, Curtis F Presented at "Fatigue 2000" Conference, London 23rd 24th April 1999, arranged by The National ME Centre, Harold Wood, Essex, in conjunction with the Essex Neurosciences Unit. Guido den Broeder 20:05, 25 September 2007 (UTC)

Ok, apologies, I didn't mean to say it was just your personal theory, but its not really proven is it? Just another theory with lots of evidence. Thedreamdied 21:21, 25 September 2007 (UTC)

Perhaps (to speculate) the physiological stressors caused by the giardiasis act as a catalyst for development of the CFS. Nemi133, thanks for the interesting info. --- Taroaldo 17:35, 25 September 2007 (UTC)

Thank you for the great response everyone! (It is quite intimmidating presenting information to such a well-informed and well-educated group.)

Guido: You say it is not clear to you how Giardiasis can cause ME, which might be exactly why it interests the medical community! ;)

Perhaps I was unclear about the extent of those 20 cases. This was an immediate onset of ME as they never recovered from the debilitation brought on by the Giardiasis infection. It happened "over-night" to all of them and the cause (Giardiasis) of the onset is in no way desputable. The number of people with the ME diagnosis here in Norway in 2006 was a total of 2000 patients. So you can imagine that these 20 people made quite an immidiate increase in our statistics. I understand if you don't think it is relevant, though! I imagine you would get a better understanding of the situation, than what I am able to convey here, if you managed to locate papers from reliable sources on the incident or the on-going research, as I regrettably am unable to provide them for you. Nemi133 17:54, 25 September 2007 (UTC)

Hi, how was it established that they had ME and not another disease with similar symptoms? By the way, if you have sources in the Norwegian language, please give them, I might be able to understand enough. Guido den Broeder 19:54, 25 September 2007 (UTC)

In response to Guido and others:

As far as I can tell all patients have been diagnosed by Professor dr.med. Harald Nyland at Haukeland University Hospital. He is considered to be one of the best, if not the best, ME specialist and diagnostician in Norway. He is a neurologist, he recently was on the committee to question Vegard Bruun Wyller, Ph.D. on his doctorate The pathophysiology of chronic fatigue syndrome in adolescents and he has also been awarded with the king’s medal for his work and dedication to the MS cause since the '80s.

To get the ME diagnosis all other diseases has to be ruled out which entails blood work, EEG, in some cases Lumbal punction, psychiatric conditions/mental disorders ruled out by clinical psychologist etc. (See first link for specifics in English.) I do not know exactly which criteria Professor Nyland uses to set the diagnosis, but he is one of perhaps three-four specialists from which the diagnosis is considered valid coming from here in Norway. A GP can not set the diagnosis. It is quite difficult to get the diagnosis and require many tests. If you want me to translate a paragraph or two, please let me know.

Sources:

In English on page 6 & 7 in relevance to diagnostic criteria:Rapport fra Kunnskapssenteret

In Norwegian:

Sosial- og helsedirektoratet the ME diagnosis criteria on page 6, mention of the Giardiasis on page 14 (the document also mentions the vaccine trials)

NrK My translation: “’’The findings in Bergen will now form the basis for an international research project which may bring us closer to an answer to the ME puzzle.’’”

Sintef, mainly page 128

Den Norske Lægeforening The Giardiasis epidemic as part of a course for doctors on ME

Dagens Medisin --Nemi133 22:40, 25 September 2007 (UTC)

A number of infections (e.e. herpesvirus) are already known to trigger CFS, so this ia probably just another one that can trigger it. It doesn't mean that Giardiasis is the cause of CFS, it just means that it can trigger CFS (along with certain other infections). --Sciencewatcher 21:56, 25 September 2007 (UTC)

Guido, I'm not convinced yet that a virus must pass the BBB to be relevant in CFS, although it makes sense and there are other things which could also pass through or affect the permeability, as noted by PMID 11461179. You brought up a good point, that 20 out of 5000 isn't higher than normal; I don't know what specific criteria they used, it and the neurologist may have been stricter than usual, plus another 42 people got "mild" ME. I get the impression that the vast majority of people who identify more with organic M.E. would have noticed a definite viral-like onset. - Tekaphor 05:41, 26 September 2007 (UTC)

Tekaphor: The specific criteria for a ME diagnosis are listed in the Rapport fra Kunnskapssenteret link, page 6 & 7, in my previous statement.

The number 5000 is an estimated number of infected people based on the fact that 2500 people were treated for the infection by a doctor; are the numbers you operate with in other cases estimated or confirmed infected? When/where have one infectious outbreak caused 1/250 presumed infected (or 1/125 confirmed infected) people to develop ME overnight? (I'm not trying to argue, I'm genuinely interested!) --Nemi133 16:19, 26 September 2007 (UTC)

Nemi133, thanks for making me take another look. As far as I know, the 0.4% prevalence figure is for the CDC 1994 criteria. The Rapport fra Kunnskapssenteret criteria seems similar to the NICE criteria but without the requirement of any other primary symptoms besides fatigue. I'm assuming that requiring "extreme fatigue" would be as selective as other definitions where the fatigue must result in a substantial reduction of activity. I've seen estimates that only about half of people diagnosed with CDC-CFS actually experience prolonged post-exertional malaise after exercise and the definition used by the Rapport fra Kunnskapssenteret states that the primary fatigue has to be "worsened by physical or mental effort"; this isn't required in the CDC 1994 definition but isn't necessarily exactly the same as prolonged post-exertional malaise either, although requiring the primary fatigue to worsen upon exertion is significant and therefore perhaps the outbreak really was statistically important based on this strictness alone. We don't know the prevalence in the general population of CFS as defined by the Rapport fra Kunnskapssenteret so we can't directly compare figures. Additionally, I'm no statistician, but I don't think the outbreak has to have much higher rates of ME cases to be important anyway; most cases of ME/CFS seem to have a generic infectious onset and people in the general population are regularly being exposed to such infections, so for those people in Norway it just happened to be the parasites that triggered their ME/CFS. I'm sure there have been many other outbreaks of ME (some in the CFS Wikipedia article), but I'm not the best person to ask for references, I'll leave that to someone else for now. - Tekaphor 07:15, 27 September 2007 (UTC)

No problem, Tekaphor! Thank you for the response! :) The English summary is in no way complete,- sorry about that. In addition to the requirement of "extreme fatigue" (which I believe refers to a minimum of 50% reduction in level of activity) the patient has to qualify for at least four of the following symptoms: Failing memory and/or problems concentrating, soar throat, soar lymph notes, muscle pain, joint pain, recently developed headache, not feeling rested after sleep, a worsening of the general feeling of "sickness" that lasts 24 hours after exertion. --Nemi133 19:41, 27 September 2007 (UTC)

Deletions - Bacterial Infections

Infections triggering CFS either viral or other is a hypothesis (educated guess)...it has not been proven to the satisfaction of the scientific community...since not proven should anything except simple statement be included in encyclopedia....??....statement: some researches based on outbreaks around the world hypothesise that cfs may be triggered by a virus.....have fun.....sno —Preceding unsigned comment added by Sno2 (talk • contribs) 22:18, 25 September 2007 (UTC)

I am suggesting that we replace the whole section "infectious Etiology/Bacterial Infections" with a few sentences, does not seem to be an overiding reason to list all the possible ones, especially since the article is to long....I am finding I have to keep re reading it because cannot remember what all is in it....thanks for listening to my thoughts....have fun.....sno Sno2 22:32, 25 September 2007 (UTC)

I think the article is too long in general...there is a lot of unnecessary info throughout the article that can probably be removed. The problem is doing it without treading on various peoples' toes. --Sciencewatcher 18:02, 27 September 2007 (UTC)

Science...think everyone thinks is to long...and since I have thick skin (was even able to take my doc telling me there is no such thing as CFS again today), am going to take the chance and delete some of this....Whatever I do will probably need some cleaning up so if someone sees anything they wish to change, "go for it"....have fun.....sno Sno2 18:13, 27 September 2007 (UTC)

Guido....you have reverted my changes based on "no consensus"...I was unaware that consensus was required...I have had this part of the discussion up for about 18 hrs now and no one, so far has said anything against my proposal. I am going to revert your revert <grin>, please leave it up so that anyone who wishes to comment can do so...also make any changes to wording you like....

Since this is the second time you have challenged changes I have tried to make to the document....I wonder.....how come you haven't made any proposals, or is the document perfect as it is...???...in your mind, since it doesn't challenge your POV....???? have fun.....sno Sno2 18:58, 27 September 2007 (UTC)

My preference would be to delete the irrelevant stuff about Lyme disease, interesting as it is, but definitely keep the stuff about Viral infection that seems to make up most of what you removed. Thedreamdied 19:26, 27 September 2007 (UTC)

Guido/Dream....I have no problem leaving this list of viruses in the document....however if they are left in then we need to remove the other entries about them in the whole document......we need to shorten this thing somehow......have fun.....sno Sno2 20:12, 27 September 2007 (UTC)

Stress and depression.

Well, I have been watching the, umm, debate unfold over the last few months with interest, and some frustration, as I am tied up with other more pressing things and simply don't have the time to get involved.

I will say this for now: Any claims that psychological stress is a significant predictor, let alone the primary cause of ME/CFS, and that depression is a major feature, is going to have to account for the following:

1) Why the HPA axis changes do not exist before onset, or even in the early phases of the disorder.

"In summary, evidence suggests that, although there is HPA axis disturbance present in subjects with operationally defined CFS, it is not present before the onset of CFS or during the early phases of illness, but develops once the illness has taken a more chronic course." 'The HPA axis and the genesis of chronic fatigue syndrome', Cleare A. PMID 15036250

2) Why HPA changes do not consistently appear in all patients and studies (though I agree that it is certainly a common and significant feature, though its etiological and pathogenic role is debatable). This may be just a empirical methodological problem (with measuring HPA changes), or it may be a more serious problem with the theoretical model (that psychological stress is the primary cause of CFS).

How does the psychological stress, that supposedly predates the onset and is serious enough to cause the condition, occur without also concurrently causing significant and consistent changes to the HPA axis? If stress is biochemically reflected in (and indeed is almost defined as) HPA axis changes, then in the absence of such changes, where is the serious (pre-onset) stress? Surely if stress is the primary cause then some kind of HPA (ie stress) axis changes should feature in all patients before onset? The observed HPA axis changes are more likely a result of the often extreme intrinsic stress of the disorder itself, and the associated secondary adversity.

Furthermore, just to complicate the picture on the role of the HPA axis in ME/CFS, it is not at all clear that mild hypocortisolism is inherently pathological in all situations:

"Further evidence suggests that despite symptoms such as pain, fatigue and high stress sensitivity, hypocortisolism may also have beneficial effects on the organism. This assumption will be underlined by some studies suggesting protective effects of hypocortisolism for the individual." 'A new view on hypocortisolism.' Fries E, et al. PMID: 15950390

3) Given that the HPA axis findings that do exist for ME/CFS are the opposite of those in depression, how can depression be considered a central feature of the disorder? The hard biochemical evidence is lacking, all we have is subjective diagnostic interpretation. While there is no doubt that secondary depression can be a major complicating factor in its own right, no senior figure or institution in this field any longer believes that ME/CFS is a form of depression, or even that depression is a primary feature, even if it is common. Even Simon Wessely has conceded that.

I would further suggest that given the abundant peer-reviewed and anecdotal evidence of the very low quality of life and high levels of adversity that patients experience, the fact that depression isn't virtually universal among patients is quite surprising. I think patients are considerably more resilient, under the circumstances, than they are given credit for.

4) Why consistent, high level evidence for any significant, let alone universal risk factor (including pre-onset psychopathology) is simply lacking, despite some claims to the contrary on this discussion page.

"Maternal psychological disorder, psychological problems in childhood, birth weight, birth order, atopy, obesity, school absence, academic ability, and parental illness were not associated with risk of CFS/ME." 'Childhood predictors of self reported chronic fatigue syndrome/myalgic encephalomyelitis in adults: national birth cohort study.' Viner R, Hotopf M. PMID: 15469945

(Note that this study is from a large prospective cohort, and hence unlike retrospective studies does not rely on patient recall, or retrospective clinical diagnosis, both known to be unreliable. For example, see PMID: 11258213, & 11276550).

The Viner & Hotopf study did identify sedentary behaviour in childhood as a risk factor, but a just published major review of risk factors concluded that:

"Various potential risk factors for the development of ME/CFS have been assessed but definitive evidence that appears meaningful for clinicians is lacking."

'Risk factors for chronic fatigue syndrome/myalgic encephalomyelitis: a systematic scoping review of multiple predictor studies.'

Hempel S, et al. PMID: 17892624

To sum up: In light of these findings, particularly the Viner and Hempel papers, the opening statement in 'Onset' section of the article that

"The majority of CFS cases begin after a period of stress in the year preceding the illness"

needs at least some serious modification and qualification, and the contrary evidence should also be presented. It should certainly NOT be the lead sentence.

Any further unqualified claims about stress and psycho-pathology being significant predictors, let alone causes, and primary depression being a major defining feature, are inappropriate.

••••••••••••••

Lastly, even though it has been mentioned on the discussion pages and in the article, in my opinion the serious problems with both patient selection and therapeutic outcomes assessment criteria, remain the central methodological problems that heavily contaminate and confound the entire field of ME/CFS research, and I don't believe this is being reflected properly in either the discussion or the article.

I will try to respond to any queries about my comments, but as much as I would love to get seriously involved in this debate, I really am very pressed for time by more important priorities. Sorry, but that is just the reality of my life of late.

And 'Thedreamdied': I only just got your message (sent 3 April 2007), thanks for that. Sorry I didn't respond, but it just shows how l long since I have logged in.

Bricker 22:45, 26 September 2007 (UTC)

Bricker, thanks for the salient discussion and the fresh perspective. Also, the point you raised about methodological issues is something that does need greater consideration in this article/talk page. --- Taroaldo 00:23, 27 September 2007 (UTC)

Thanks for that Taroaldo. Like I said I wish I could contribute more.

I forgot to mention that I think the article has improved a lot over the last six months or so, both in content and style, though there is obviously still a lot of work left to do. My thanks to all those who have made informed, constructive contributions.---Bricker 00:54, 27 September 2007 (UTC)

The cortisol findings are another indicator for depression in CFS being secondary. Primary depression is associated with increased cortisol, CFS with lower cortisol, but CFS with co morbid depression has even lower cortisol levels again than ‘pure’ CFS. PMID 12700181 This factor is what worries me about use of antidepressants in CFS because these increase serotonin and decrease cortisol. Some studies say this improves symptoms, depression and pain, but they never report cortisol changes! The only explanation I have found for this is the CDC scientists model HPA studies that discovered a second lower steady state for the HPA axis that has implications in this context. “A short stress in the normal steady state produces a small perturbation in the Glucocorticoid Receptor concentration that quickly returns to normal levels. Long, repeated stress produces persistent and high GR concentration that does not return to baseline forcing the HPA axis to an alternate steady state. One consequence of increased steady state GR is reduced steady state cortisol, which has been observed in some stress related disorders such as Chronic Fatigue Syndrome (CFS)” PMID 11502777 By using drugs that force cortisol lower a suboptimal steady state is reached, which means common CFS may represent an ‘unsteady state’ Without cortisol monitoring with use of antidepressants, maybe that’s how plastic changes might occur, short term gain with long term costs? There are adaptive benefits for low cortisol in the short term, and soldiers about to go into battle and paramedics have been found with such (probably a desensitising?) PMID 10633533 and this is seen as a likely precondition for development of triggered PTSD “Based on the reviewed findings, we propose that a persistent lack of cortisol availability in traumatized or chronically stressed individuals may promote an increased vulnerability for the development of stress-related bodily disorders.’ The same is proposed for Allostatic load setting the scene for CFS. I am surprised that there are said to be no such prior HPA findings and will look into this further, particularly the cohorts involved, any differentials as to trigger events in this finding? Jagra 08:22, 27 September 2007 (UTC)

I know what is troubling me about the Cleare paper findings,

• Who are these high risk cohorts that “recent prospective studies of high-risk cohorts suggest that there are no HPA axis changes present during the early stages of the genesis of fatiguing illnesses” That does not say CFS?
• Given we know there is both sudden CFS onset and gradual onset, but in the abstract there is no such mention made, are they therefore all sudden onset, there may be problems in patient selection? Then again the paper is a hypothesis. Jagra 10:06, 27 September 2007 (UTC)

I'd just like to make a couple of points here. First of all, as far as I can tell from the abstract, the Cleare article only talks about the HPA axis in the early stages of the illness. It does not talk about HPA axis changes before the illness. Did your quote come from the full-text article? If so, how did they measure the HPA axis before the onset of the illness?

Regarding depression: not all depression shows high cortisol. Burnout (which is also associated with depression) shows low cortisol, similar to CFS. I think you are talking about "major depression" which is not the same as "depression". Depression is a symptom. Major depression is an illness which has depression as a symptom. There are various types of depression, and the neurobiology appears to be different in different patients (not all patients respond to the same drugs).

However I'm not sure what the point of this discussion is with respect to this wikipedia article. Should we not limit this discussion to proposed article changes? --Sciencewatcher 18:22, 27 September 2007 (UTC)

Yes, some burnout studies have showed reduced cortisol (especially the response upon awakening), but some other studies showed elevated cortisol instead, or significant gender differences, or no significant HPA functional alteration, or no significant decrease in HPA alterations after successful psychotherapy-induced symptom relief (search PubMed and you'll see). I'm not trying to split hairs or piss on anyone's parade, but my impression is that the role of the HPA-axis in general isn't just somewhat inconsistent and incompletely understood in CFS, but also practically every other illness it's associated with (to various degrees), because it's a relatively new field. PTSD and burnout is somewhat common in the general population, so perhaps they are comorbid in some CFS patients. To make things even more complicated, PMID 17803834 suggests that while reduced cortisol responses were found in some CFS patients, the effect only seemed clear in those without "early life stress". Remember when "low serotonin levels" was supposed to explain depression? I think we are heading down a similar oversimplification when blaming the "stress" functionality of the HPA-axis in CFS. - Tekaphor 05:26, 28 September 2007 (UTC)

Exactly Bricker, this jigsaw puzzle seems incomplete when using only the stress pieces. There is too much confusion between correlation and causation going on towards ME/CFS, not to mention oversimplification. Any model for ME/CFS must adequately explain how the symptoms are being caused and perpetuated, without resorting to ideology. I agree there are issues with the methodology, and I have previously put effort into the "issues with criteria/definitions" section (which could probably be improved). As you said, the measuring of outcomes is an issue too. An example of this is CBT/GET as it supposed to result in major improvements with half or more participants no longer fitting CDC criteria, yet 3 reviews on employment outcomes are hardly conclusive about the assistance of CBT/GET in returning patients back to work (to be fair, some assistance can be inferred, but I would think that if all these people were really substantially improved they would be able to return to work rather easily). I concur with what you said about the Onset section, as I have been wanting to comment on that as well due to the studies I have read which suggest the majority of cases start after an infection-like illness; this is being downplayed and relegated by the leading statement that emphasises stress. - Tekaphor 05:26, 28 September 2007 (UTC)

Sciencewatcher, seems to be some terminology confusion in some comments on depression. Your major depression is what I call ‘primary depression’ all else is secondary, you seem to have used these three terms differently? ‘Prospective studies of high risk cohorts’ to me suggests patients with certain viral illnesses, I know of no other identified ‘high risk group’ that could be studied prospectively to see if they develop CFS. If so this implies sudden onset patients only and ignores gradual onset and the role stressors may play in that onset, if nothing else?

Tekaphor, Early life stress has been associated with hyper cortisol illnesses, to my knowledge it has not been linked to hypo cortisol, and that study confirms this. Agree with Bricker on recall particularly of ‘early life stress recall’ Can only guess never the less why ELS and possibly hyper ends up not hypo, whilst no ELS and normal ends up hypo, could have something to do with relative glucocorticoid receptor changes per CDC model !!! Yes agree, article HPA section needs more expansion on potential modulators in illness and I will work something up. Also concur with you and Bricker on the Onset section Jagra 08:05, 28 September 2007 (UTC)

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