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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).
<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)
Revised edit on Neuro-endocrinoloigy as discussed above, now posted Jagra 00:55, 16 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 ( 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)
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)
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)
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)
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)
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)
In case you have missed it, the NICE Guideline for CFS/ME is out: [1]. Guido den Broeder 20:42, 27 August 2007 (UTC)
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. 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
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
Can we please have some consensus to archive older discussion on this page? Thanks. --- Taroaldo 22:49, 3 September 2007 (UTC)
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)
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)
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, 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)
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)
Kerr is in London, Glasgow has Gow. Both are doing research on gene activation. Guido den Broeder 09:38, 7 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)
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)
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)
Sno2 21:06, 8 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)
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)
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 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)
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)
Evidence for antivirals in any enteroviral disease (viral meningitis, polio, hepatitis A)? JFW | T@lk 07:25, 7 October 2007 (UTC)
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)
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)
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)
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)
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
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;
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)
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)
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)
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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)
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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)
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)
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:
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)
And, signing after being reminded to sign. :p --- Taroaldo 21:54, 23 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)
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)
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)
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)
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)
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)
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)
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)
"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)
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)
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.
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)
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)
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)
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)
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)
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)
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)
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)
This page is an archive of past discussions. Do not edit the contents of this page. If you wish to start a new discussion or revive an old one, please do so on the current talk page. |
This is an archive of past discussions. Do not edit the contents of this page. If you wish to start a new discussion or revive an old one, please do so on the current talk page. |
Archive 1 | Archive 2 | Archive 3 | Archive 4 | Archive 5 | → | Archive 10 |
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).
<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)
Revised edit on Neuro-endocrinoloigy as discussed above, now posted Jagra 00:55, 16 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 ( 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)
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)
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)
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)
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)
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)
In case you have missed it, the NICE Guideline for CFS/ME is out: [1]. Guido den Broeder 20:42, 27 August 2007 (UTC)
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. 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
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
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)
Can we please have some consensus to archive older discussion on this page? Thanks. --- Taroaldo 22:49, 3 September 2007 (UTC)
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)
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)
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, 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)
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)
Kerr is in London, Glasgow has Gow. Both are doing research on gene activation. Guido den Broeder 09:38, 7 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)
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)
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)
Sno2 21:06, 8 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)
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)
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 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)
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)
Evidence for antivirals in any enteroviral disease (viral meningitis, polio, hepatitis A)? JFW | T@lk 07:25, 7 October 2007 (UTC)
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)
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)
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)
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)
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
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;
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)
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)
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)
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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)
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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)
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)
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:
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)
And, signing after being reminded to sign. :p --- Taroaldo 21:54, 23 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)
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)
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)
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)
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)
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)
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)
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)
"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)
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)
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.
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)
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)
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)
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)
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)
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)
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.
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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)
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)
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