Talk:Myalgic encephalomyelitis/chronic fatigue syndrome/Archive 6

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Acceptance is not giving up

The statement about acceptance was rightfully removed because it lacked reference, but I disagree with the implication that acceptance is synonymous with "giving up", as people can accept they are enduring an illness state and work towards resolving it. There is no shortage of anecdotes about the perils of completely ignoring or dismissing or "fighting" CFS symptoms, and even in the context of CBT one must first accept there is a problem before applying treatment. So what does the research suggest or what do the researchers say? Consider the following studies: ...

• PMID 17084136 - "RESULTS: Results indicated that acceptance has a positive effect upon fatigue and psychological aspects of well-being. More specifically, acceptance was related to more emotional stability and less psychological distress, beyond the effects of demographic variables, and fatigue severity. CONCLUSION: We suggest that promoting acceptance in patients with CFS may often be more beneficial than trying to control largely uncontrollable symptoms."
• PMID 17719001 - "Because patients accepting the illness and trying to live with it seem to have a better prognosis than patients chronically fighting it, we investigated breathing behavior during different coping response sets towards the illness in patients with CFS (N=30, CDC criteria)." ... "In conclusion, hostile resistance seems to trigger both physiological and symptom perception processes contributing to the clinical picture of CFS."
• PMID 16191727 - " ... denial is consistently related to less adaptive outcomes. Therefore, healthcare professionals should find ways to reduce patient use of denial and promote alternative strategies for managing life events."
• PMID 12069870 - "Those who believed that limiting their physical exertion was the path to recovery (55%) had lower depression and anxiety scores (P's<.01) than their counterparts."
• PMID 17561701 - "In the CBT for CFS, it is important to quit seeking physical causes, to accept the pathological state as it is, to monitor daily activity and recognize the cognitive and behavioral patterns which might prolong fatigue, to maintain a constant activity level and to make planned increases in activity."

The possible association between "illness beliefs" and outcome is like many other issues in CFS that aren't simply black/white and where the direction of causation is debatable. Even when such associations are found, there are often clarifications like "A series of regression analyses showed illness representations to be stronger predictors of adaptive outcome than coping scores." (PMID 9720854) and "The causal direction of relationships between coping and fatigue severity is ambiguous ... " (PMID 8588012) and " ... adverse outcomes were associated with accommodating to illness only in the context of lower levels of perceived control." (PMID 9330240). With general regard to the last study, perhaps avoiding activity to reduce symptoms could qualify as a boost to perceived control. In both human and animal studies, perceived control of stressors significantly reduces related stress and the development of illness, so perhaps people with CFS who for whatever reason (either psychological or physiological) experience a reduced perception of control are therefore more stressed, with stress being a well-known trigger for the worsening of CFS symptoms. However, patients with no sense of control over symptoms aren't necessarily suffering a psychological inefficiency; they could be either too severely affected, or (conversely) lack the post-exertional symptoms that encourages the patient to gain a sense of control over symptoms by avoiding exacerbations. Lastly, counselling is mentioned in the treatment section without a reference, so consider PMID 11271868 (full text available, look under the "Patients with chronic fatigue syndrome" section), which compared counselling to CBT and found that they had comparable effectiveness. - Tekaphor (talk) 10:21, 8 January 2008 (UTC)

I don't see how you can use any of those references to create anything remotely similar to what was removed before. The last one, however, may provide a nice reference for what is involved in CBT. Perception of control has been linked with reduced stress and associated problems in many different scenario's so I don't doubt this or many of the other findings, however, I do disagree with some of the interpretations of some of these studies. Particularly PMID 17561701. Telling patients not to look for physical causes and accepting CFS as a pathalogical state is not accepting the illness. It is accepting that behavioural patterns contribute to the illness. CBT does not tell patients to avoid stressors for the illness or to reduce activity, in fact, I'm not aware of CBT for anything that involves avoiding the stressor (eg phobia therapy involves exposure to the phobia). PMID 12069870 also states this "Lack of illness legitimization ranked high as a source of dissatisfaction for CFS patients, and it may aggravate psychiatric morbidity." and it should be noted that the title is this "Illness experience, depression, and anxiety in chronic fatigue syndrome." The papers is looking at factors that contribute to anxiety and depression. Lack of legitimization is probably associated with ostracism and a loss of social support. Such factors are commonly associated with depression. So again, I think the study is probably fairly reliable but I question your interpretation. Accepting the condition isn't necessarily going to lower their depression scores (correlation is not causation etc etc) and the authors don't say anything about alleviating the CFS themself. They are only looking at comorbid psychopathology and not the recovery form CFS. Their most clear recommendations concern diagnosis, "... also suggests that one of the most important services that physicians offer and that patients seek is the partial sense of control over an illness that a diagnosis affords." In fact they note concerns with what you seem to be suggesting "Another concern is the possibility of actually teaching some patients to be sick by encouraging them to engage in self-protective illness behaviors". Actually the authors seem to be suggesting that physicians should tell patients to increase activity but are pointing out problems with patient reception "Advice to increase activity may communicate, perhaps in an unintended way, that the person with CFS is not doing what is appropriate to manage his or her condition, or is to blame for the lack of progress, both likely to be threatening." They also note problems with constructing treatment plans from patient reports "Furthermore, the inherent subjectivity of patient perceptions makes it difficult to conclude which specific behaviors by the physicians will necessarily negatively impact patients' psychological well-being."

In short, I'm not too convinced that any of the authors agree with your interpretations of their studies. Also both you and I are conducting OR right now with these interpretations so we can't build a section from these references. However, some of these references may fit well in other sections, provided we preserve the original author's opinions and we don't make our own inferences from this research. JamesStewart7 (talk) 11:27, 8 January 2008 (UTC)

Acceptance comes in two flavours.

• Acceptance that one has a chronic illness is the first step towards sensible management.
• Acceptance that one will always remain (this severely) ill would be something else. Patients generally don't accept that, but if they do, or even if they have doubts, that can be a major cause of depression. Guido den Broeder (talk) 12:00, 8 January 2008 (UTC)

Good points Guido. It is possible that I have misinterpreted your comment Tekaphor. When you say acceptance, exactly what is being accepted? Is it the illness itself? A particular etiology of the disease? Permanancy of the condition? Variable symptom presentations? Acceptance of each of these things may lead to different outcomes. JamesStewart7 (talk) 12:56, 8 January 2008 (UTC)

Hi James. The "Behavioral interventions" section has been a mess for a long time and I agree it needs another cleanup (previous attempts have been made). Feel free to improve it! As I said, "I think people can accept they are enduring an illness state and work towards resolving it". The variables here are what the person thinks their "illness state" is and how they are attempting resolution. I should have been clearer, but I was thinking more along the lines of Guido's first "flavour" of acceptance. There are different flavours of fighting too. Perhaps I also stretched the interpretations of some of the mentioned studies; I didn't necessarily fully agree with the original statement about acceptance in the article, but it makes some sense and I just wanted to revisit the issue (you're right that it probably doesn't belong in the treatment section). CFS symptoms often worsen following exertion, so in such a situation it would be reasonable to accept a temporary limitation that needs improvement, and I doubt that CBT practitioners never advise patients to avoid some stressors. I personally don't think it's practical for patients in general to avoid all exacerbations and I certainly wasn't arguing that patients should give up. However, I also realise that long term severely affected patients often end up in flavour two for powerful reasons and such people usually aren't included in research studies so I can't really comment if the same applies for them. The evidence suggests that CBT/GET partially helps some people with CFS, but the issue of CBT/GET vs "exercise intolerance" is one of the most frictional aspects of the CFS controversy and closely related to the issue of acceptance and fighting. I will post the rest of my reply relating to this aspect in a new section titled "GET vs exertional limits". - Tekaphor (talk) 06:30, 10 January 2008 (UTC)

Unsourced sections and redundant information

I'd like to suggest a bit of a cleanup of the article. Currently "sleep aids", "pain relief", "antibiotics" and "cultural referneces" are unsourced. The article itself notes that antibiotics treatment is contentions. Does anyone have plans to source these sections in the near future? If so, I can leave the sections there, otherwise I think they should be removed. The behavioural interventions/GET/CBT sections could also use a cleanup. A lot of the content under "behavioural interventsions" is repeated in "CBT" and "GET". I'd like to remove the redundant information. I also suggested earlier that the Gibson report and associated criticism may be moved elsewhere. The political aspects of CFS are a big issue but I don't think such information should be intertwined with scientific reports. Essentially all of the scientific findings presented in the Gibson report may be found in the original reviews anyway. The social issues/controversy sections seems the closest fits. Anyone else have opinions about this? —Preceding unsigned comment added by JamesStewart7 (talk • contribs) 13:32, 8 January 2008 (UTC)

Also please don't take the removal of unsourced/improperly sourced information as a statement of disagreement with that information (this is the case some times but not for my recent edits). I have removed some information that may be unreferenceable/very hard to find a RS for as I felt that similar information was repeated above with RS's. JamesStewart7 (talk) 14:14, 8 January 2008 (UTC)

Be bold and remove the existing sections on "sleep aids", "pain relief" and "antibiotics", since they are not very informative anyway. We can always add new versions of these sections later; the aspects are relevant enough. I'd leave the "cultural references" section since the info is correct and needs no sourcing as it has the proper wikilinks. Regards, Guido den Broeder (talk) 14:49, 8 January 2008 (UTC)

Yes, please do get rid of the crud. I've deleted some unsubstantiated info regarding fungal treatments and metal allergy, but there is still a lot more that needs to be removed. --Sciencewatcher (talk) 01:09, 10 January 2008 (UTC)

Concerning the EFA studies, the two studies had differences in patient selection. The Behan group had a PVF diagnosis and reduced cell membrane essential fatty acids that improved during the study. The McKendrick study used the Oxford criteria and patients with normal RBC membrane lipids. The Reid review mentioned the differences in diagnostic criteria but not the lipid differences. The differences should be mentioned in the article without editorial comment to inform the reader there were differences in patient criteria. Ward20 (talk) 02:10, 10 January 2008 (UTC)

I agree Ward20 the recent reverting by SC and OM, who have not taken part in discussion, as a supposed summary is completely inadequte, and flies in the face of recent discussion and consensus. Not only does it not differentiate results in different subgroups, it retains the Reid commentary that itself appears flawed, and it needs confirming that it accurately descibes the methodology of the Warren study (apart from the basic science issues involved) before it could be considered reliable, and that is up to those that re-instated it. I would also like to know where in Wikipedia it defines what is a 'bloated section' as opposed to sufficent information to properly inform readers.Jagra (talk) 04:02, 10 January 2008 (UTC)

Seeing as this is a long article I think a summary is appropriate. The Reid commentary is considered reliable by default because it fulfils all of wikipedia's reliability criteria. It is a peer reviewed journal article published in a prominent medical journal (which an be objectively measured by the journal's impact factor. It also agress with the three other reviews in this area (mentioned above). So really it doesn't matter if you like the review or not, I included the BMJ reference and note the other references only because it is the most comprehensive reference which I could access the full text of. If anyone wants to include the other two references (although I have access to an academic library I can't seem to get the Royal Society of Medicine reference) then knock yoruself out. However, I still hold that there are WP:SYN issues with the inclusion of these other sources, so I think Sciencewatcher's summary and removal of references is appropriate. I can see a good case for describing the studies that were mentioned in the reviews as there is only a few, hence it is practical to include all of them. However, including speculative statements and information that does not directly pertain to efficacy is not appropriate.

I don't see why we should remove the comment about the differences in patient criteria. If it was in the Reid review why shouldn't it be present here? Any mention of lipid differences between the studies should stay out unless someone can find a RS which suggests that this difference is important. Without that reference, implying that this difference effected the results is OR. Can everyone please remember that we are required to divert scientific judgement to the published studies and reviews in this area. Also Jagra I'm not seeing any recent consensus supporting the inclusion of the recently removed sources (by Orangemarlin and Sciencewatcher). I reverted it and voiced my concerns on the discussion page, then they both reverted it, presumably after reading the discussion. If three people are reverting your (recent) changes vs just you including them then there cannot possibly be a consensus to include the comments. JamesStewart7 (talk) 05:36, 10 January 2008 (UTC)

The paragraphs that are being discussed seem to mingle and confuse the Warren study and the Reid review (unless I am confused). "using currently (as of 2000) accepted diagnostic criteria and using sunflower oil as a placebo as opposed to paraffin oil used in the previous study. The researchers state that sunflower oil is better tolerated and less likely to affect the placebo response adversely"[214]. This same review classified dietary supplement treatments for CFS as of "unknown effectiveness".

The Magnesium section talks about a review as if it had been prominently noted, and I don't think it has been, "A(s?) previously noted, a 2000 review (Reid?) of CFS treatments noted that subsequent studies have failed to find a deficiency of magnesium in people with chronic fatigue syndrome and classified magnesium treatments as of "unknown effectiveness."

The differences in patient criteria between studies should be included. If the lipid details are not be discussed (at least in the Behan study), then I do not see why the sunflower oil should be. Authors of both studies seem to state those factors contributed to the results found by their studies. There are some minor NPOV wording issues with the paragraphs but I will not worry about them until the larger issues are addressed. I am not familiar with the material Jagra is describing, so I would have to study that before I can comment on it. Ward20 (talk) 06:40, 10 January 2008 (UTC)

I disagree with the statement, "Any mention of lipid differences between the studies should stay out unless someone can find a RS which suggests that this difference is important. Without that reference, implying that this difference effected the results is OR." I do not agree it is OR because there were no conclusions drawn from the differences. It just describes a major difference in the lipid testing (this is a lipid study is it not?) that is well supported by their own RS. The fact that one review does not mention it does not mean it should be omitted. The reader should be allowed to draw their own conclusions by having the relevant facts. Also, not one but two studies found abnormal lipid levels in patients. Why were those studies removed, they were well supported with RS? We are discussing NPOV here, not OR. Ward20 (talk) 07:18, 10 January 2008 (UTC)

If you click on the link you'll see the review - it is mentioned in the previous paragraph (although not specifically about magnesium). Feel free to change the wording. Regarding the EFA studies: the point is that there is no overwhelming evidence that EFAs have any benefit. I would prefer to remove the whole section to reduce the clutter. This is an encyclopedia article - we can't go discussing all possible treatments, only the ones with the best evidence. --Sciencewatcher (talk) 21:54, 10 January 2008 (UTC)

See my edit. I believe it is NPOV, very close to the wording of the sources. EFAs may be an important therapy for subgroups, just like CBT and GET. Ward20 (talk) 22:41, 10 January 2008 (UTC)

Sciencewatcher, where is the promised link?, and drop the rhetoric, we are not talking about "possible treatments' but probable and/or proven treatments, even if only in subgroups, so how many of these are there in CFS, any deserve more than a mention? Jagra (talk) 00:53, 11 January 2008 (UTC)

James, the revert of yours that reinststed the references was on the 7th or 8th. Given that OM and SW did not revert the same material and OM in his idiosyncratic manner will not discuss i cant see how you can claim a consensus that way, more like weasel words? But your reinstatement and mine of material constructed by you and Ward20 does constitute a consensus for that material before SWs disruptive and POV revert. This material should thus be re-instated. The Experientia paper is a Review paper in English which includes discussion on “Factors influencing the delta desaturases” and discusses nutritional and hormonal factors and says ‘The delta-6 desaturases activity is increased by protein intake and decreased by many factors e.g. LA ( n-6 PUFA)and AA, n-3 PUFA, cholesterol, ethanol, zinc and fasting.’ And ‘PUFA inhibit the desaturation of other fatty acids by competing at the D6D and D5D levels.’ – ‘Increase of n-3 PUFA strongly decreases the content of n-6 PUFA in adapose tissues’, The stimulating action of simple carbohydrates is due to both insulin and carbohydrates acting on the biosynthesis of the desaturases’, ‘This supports the wording 'Amounts of different fats in the diet, amount of protein, alcohol, and zinc status.’ To which can now be added carbohydrates.

In the Med Hypoth paper as I thought, the D6D factors are in a literature review section titled “Catastrophic Inhibition of :6D” and cites primary sources. ‘---inhibition of D6D activity by the following, which are theoretically avoidable. 1 trans fatty acids 2 saturated fatty acids 3 excess sucrose 4 excess alcohol 5 excess (stress) 6 high cholesterol content in diet.’ ‘In addition it is also inhibited by 1. protein deficiency 2 starvation 3 Zinc deficiency and magnesium deficiency 4 oncogenic viruses 5 ionising radiation 6 diabetes. ‘ This covers all the mentioned factors in my edit except exercise and conditioning, which is covered in the literature review section of the third RS paper I cited. Note that sunflower oil is highly PUFA which as placebo could affect the D6D and influence results. In other words these RS sources say it is important furthermore it is basic science that sunflower oil (high in n-6 PUFA) is not placebo, and does not need any review to cite as proof. I am still awaiting an explanation of the actual methodology in the Warren trial and regardless of the POV of others, your validation re conference papers? The fact that the Warren paper concludes that “The results of this study contrast sharply with the previous study” requires an explanation in the Article, for NPOV.

The conference papers on the controlled studies by the University of Newcastle, on CDC defined CFS patients of both gradual and sudden onset CFS (abstracts of which are here[ http://homepage.mac.com/doctormark/Acrobat/CFS_MCS/CFS98_Abstracts.pdf ] ) and are supported by a more recent review paper, PMID 16935966 so that could have been cited as well. I agree with Ward20 this is about lipid studies and differences in the lipid findings of different subgroups who respond differently to (different!)treatment (and different placebo) is an important clarification, for the Article. If mentioned in the Reid reveiw as JS states, that confirms the validity. The findings of D6D and for that matter the B-Oxidation deficiencies are central to the lipid changes and symptom differences in the patient subgroups, and therefore worthy of inclusion, given the researchers conclusion that lipid changes can differentiate sudden onset CFS from gradual onset, indeed in the Classification paper into five different subgroups. With important implications not only for treatment of subgroups but also classification and diagnostic criteria, something that CBT and GET have yet to produce, and therefore this treatment deserves similar space in the Article. Jagra (talk) 00:53, 11 January 2008 (UTC)

Thanks for the link SW I did find it, where it was not before. A read of the Reid review shows it is well screwed up! It discusses both the RCTs as using “evening primrose oil” and has failed to correctly identify the active treatment substance in both of these trials, which is described in the abstracts of both. Warren as ‘Efamol Marine’ and Behan as “The preparation given contained linoleic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acids” Evening primrose oil contains only “virgin cold-pressed non-raffinated evening primrose oil, which would supply gamma-linolenic acid and lipophilic pentacyclic triterpenes” PMID 16935966. Efamol Marine is not evening primrose oil, unless fish grow on shrubs! clearly not the same.

Clearly this review is unreliable as it demonstratably has not identified the active treatment correctly, and I suspect has not correctly identified the Placebo used in the Warren study either, but probably confused it with the active preparation.? This review cannot therefore be relied upon, should be removed and as said already we need to check the Warren study methodology for correct information. Jagra (talk) 02:07, 11 January 2008 (UTC)

I also think it a bit biased when Reid does not mention the Carnitine trials in CFS when other reviews of the same period do PMID 10767667 This is associated with EFA’s as Carnitine and its esters prevent toxic accumulations of fatty acids in the cellular cytoplasm, and of acyl CoA in the mitochondria, while providing acetyl CoA for mitochondrial energy production. Because of its important role in muscle metabolism, carnitine deficiency may well impair mitochondrial function. If so, it could cause symptoms of generalized fatigue along with myalgia, muscle weakness, and malaise following physical exertion. (Kuratsune H, Yamaguti K, Takahashi M, et al. Acylcarnitine deficiency in chronic fatigue syndrome. Clin Infect Dis 1994;18:S62-S67. ) Given the level of evidence for carnitine esters is at least equivalent to CBT i.e. but with limited placebo control, as opposed to none in CBT. As a treatment with a high response rate I think it also deserves mention in the Article. I think it might be worthwhile reporting the substantial body of evidence of marginal magnesium deficiency in CFS reveiwed in the same paper and regarding zinc deficiency in CFS this has been linked now to low N-3 EFA’s and immune system changes which also supports hyper response and anti-oxidants. PMID 16380690, PMID 16338007 with more to follow. Jagra (talk) 03:18, 11 January 2008 (UTC)

Yeah I'm inclined to take the opinion of the reviewer over your synthesis. Efamol Marine does contain evening primose oil accodring to this, "http://www.efamol.com/about.htm" and this "http://www.intekom.com/pharm/searle/efamol-m.html" (the first two hits in a google search for "Efamol Marine") I'm guessing Reid didn't mention the Carnitine trials because there were no RCTs of Carnitine (their stated inclusion criteria) and PMID: 10767667 is not a review of the efficacy of the treatments. It is a comment in Alternative medicine review. It is also rather speculative "Any of these nutrients could be marginally deficient in CFS patients". JamesStewart7 (talk) 06:29, 11 January 2008 (UTC)

If the reveiwer can not tell the difference between EPO and Efamol marine which are quite different products, the latter containing other marine oils, in majority, EPO being a minor component, how good is his commentary and lets check the Warren methodology re placebo's. I will check the carnitine studies as of that time, but if you read the full paper of ALT MEd REV you will find it not a speculative comment as you hastily conclude but a summary of actual findings that support his comment. Jagra (talk) 08:07, 11 January 2008 (UTC)

CBT vs counselling

PMID 11271868 and PMID 11086269 suggests they are of similar effectiveness, while PMID 11271867 suggests they are also economically comparable overall. More recently (2007), PMID 17697477 found that in these therapies, "The key predictor of a good fatigue outcome was emotional processing, including the expression, acknowledgement and acceptance of emotional distress." with the researchers concluding that "The findings lend preliminary support to the view that the specific techniques associated with particular 'brand names' of therapy are not necessarily the 'active ingredients' that help patient's change within the primary care setting." I don't think anyone here disagrees that counterproductive cognitive behaviour can contribute to illness in general, but if ordinary counselling really is as effective as CBT, this questions the unique need for CBT and the presumed extent of which the associated hypothesis applies to CFS. - Tekaphor (talk) 06:30, 10 January 2008 (UTC)

That's interesting research that may warrant inclusion in the article. PMID 11086269, however, is about depresssion and anxiety treatment so it is not directly relevant but I will briefly discuss it here anyway. Findings like this "At 12 months, the patients in all three groups had improved to the same extent. The lack of a significant difference between the treatment groups at this point resulted from greater improvement of the patients in the GP care group between the 4- and 12-month follow-ups" are relatively common in anxiety and depression research. Most episodes of depression/comorbid anxiety/depression recede on their own. This makes the clincial outcomes of relevance the length of episode and the reoccurance of depressive episodes. Unfortunately the study lacked a note of recurrant epsidoes as it did not do 2 or 3 year follow ups. This remains an interesting finding "There was no significant difference in outcome between the two psychological therapies when they were compared directly using all 260 patients randomised to a psychological therapy by either randomised allocation method" but as depression is self-limited compared and CFS is chronic the relevance is uncertain.

PMID 11271868 is a good candidate for inclusion in the article. The treatment was relatively brief (6 sessions), however, I am unsure whether this would have any significant effect on the results. This should be noted if we are to include the article "all counsellors used a psychodynamic approach and all cognitive behaviour therapists used CBT" along with a brief description of what the treatments involved so that the reader may understand the differences between the treatment approaches. This is interesting "However, the group allocated to CBT was significantly more satisfied than the counselling group with the process of therapy". This should be noted "In our study 45 (28%) patients conformed to CDC criteria for CFS" but significant differences should be expected with this sample size if there is a large differnce in the effectiveness of the treatments. Overall, the study looks fairly solid and anyone who is interested in this area should take a look at the discussion as the authors speculate about some of the differences in patient selection and practitioner training between primary and secondary care.

PMID 17697477 is also a good reference as it audiotaped the interview sessions and analysed them for differences. It should be mentioned that these tapes were compared with a newly devised measure (this is important as newly devised means lacks validity data) but the principal finding that the actual treatments are similar is interesting "The process measure showed that although the treatments could be distinguished, there was some overlap between them". Findings similar to this, "The findings lend preliminary support to the view that the specific techniques associated with particular 'brand names' of therapy are not necessarily the 'active ingredients' that help patient's change within the primary care setting." have been found in many areas througought psychology. There are a couple hypothesis for explaining this. One is that the treatments are almost identical so similar outcomes are expected. This study found evidence for similarity but they did not conclude that the results are identical. Another hypothesis is that it is what is shared between the treatments which is effective and the unique factors are ineffective. The final hypothesis is the unique aspects make similar contributions to the effectiveness of the treatment.

Of course I am not expecting anyone to include these hypotheses in the article but they are here as a caution that PMID 11271868 and PMID 17697477 should not be presented as evidence against the hypotheses associated with CBT when they are included in the article (if people agree that they should be included). The findings are interesting and relevant but as these are primary sources and there are different ways to explain the findings care should be taken to present a descriptive account of the study only and be aware that any interpretations of the study must be attributed to the author. JamesStewart7 (talk) 07:15, 10 January 2008 (UTC)

The inclusion of the study about depression and anxiety was accidental. As for the other two, I agree that they aren't necessarily evidence against the hypothesis behind CBT and shouldn't be presented in the article as such. Keep in mind it is one thing to propose that counterproductive cognitive behaviour contributes to CFS and another to propose that it is entirely responsible for the perpetuation of all symptoms. Anyway, if included in the article (which they should because there is currently no references in the article for counselling), these two studies should represent the value of counselling. Yes, PMID 11271868 consisted of only 28% CFS patients, which is why I focused on the section relating to the CFS group. It isn't clear to me whether the satisfaction statement in favour of CBT also applies specifically to the CFS group rather than generally to the entire group (if so, it could be included too). - Tekaphor (talk) 13:59, 11 January 2008 (UTC)

Note: I just realised that I made another error! As far I can tell from the abstracts, PMID 17697477 and PMID 11271867 don't specifically involve CFS. Unless someone with full access can verify that they do indeed involve some CFS patients, then I retract them from the above presentation and apologise for wasting James' time or anyone elses for reviewing them. - Tekaphor (talk) 13:38, 12 January 2008 (UTC)

PMID 17697477 shows up in a PubMed search for ["chronic fatigue syndrome" counselling], so perhaps it did included CFS patients, or merely mentions them, but I can't be certain without viewing the full text. - Tekaphor (talk) 02:53, 15 January 2008 (UTC)

GET vs exertional limits

Although feeling worse following exertion is often viewed as a "hallmark of CFS", this isn't usually required for diagnosis and none of the CBT/GET studies required it in study participants. This causes some patients, who feel substantially worse after exercise, to doubt that the results apply to them. Two patients can have similar baseline symptom profiles which grant them a CFS diagnosis and inclusion into research studies, but only one may experience obvious or substantial post-exertional symptom exacerbations. To make it more complicated, it seems poorly defined in the literature. In the Fukuda definition, it is "post-exertional malaise lasting more than 24 hours" (which is optional for diagnosis). This isn't necessarily the same as "symptom exacerbation". Interestingly, the NICE guidelines distinguish between "post-exertional malaise and/or fatigue (typically delayed, for example by at least 24 hours, with slow recovery over several days)" (required for diagnosis) and "physical or mental exertion makes symptoms worse" (optional for diagnosis).

Whether or not GET causes the overall CFS condition to worsen depends largely on how the program was conducted; these programs optimally only increase activity at a rate and amount that doesn't cause substantial and/or unsustainable worsening of symptoms. Therefore, by definition this GET style ideally "shouldn't" cause an overall worsening of condition, so the patient's ability to participate or improve remains the core variable. There are anecdotes from patients that some rehabilitation programs encouraged or even coerced them to ignore all exacerbations and continue increasing activity regardless. I don't think that is found in the scientific literature, but when something goes wrong the supporters of GET can blame the way the program was conducted rather than the efficacy of the treatment. In practice, some "tolerable" amount of exacerbation is reasonably expected from patients, which is somewhat arbitrary and subjective so there could be room for mistakes.

Essentially, the problem is the grey-area between increasing activity and avoiding substantial and/or unsustainable exacerbations. As far as I know, there may not be hard scientific evidence that GET worsens CFS in the long term, but the systematic review on treatments (J R Soc Med 2006) noted the need for better measurements of adverse effects; plus there is evidence that exercise can indeed worsen CFS symptoms, hence the cause for concern. Adding to this problem is the lack of patient grouping based on the existence and severity of symptoms which could directly affect the efficacy of these treatments. PMID 16255779 suggests that CFS may indeed involve an activity ceiling or that gradual increases in exercise that eventually comes at the cost of other activities and also worsens some symptoms (fatigue, pain, mood). This isn't to say that such a limitation is permanent or that graded activity in general couldn't be effective at maximising available capacity even if there was an activity ceiling. This study probably wasn't included in the systematic review on treatments because it wasn't specifically researching a treatment as such.

Tekaphor (talk) 06:30, 10 January 2008 (UTC)

All PMID 16255779 found was that patients did not reach their prescribed activity levels after 4-10 days and they reduced their activity level. They still actually finished better than they started with regard to activity. So the subjective symptoms got worse but the objetive symptom improved slightly. So whether the patients improved or deteriorated really depends on how you define imporovement. This is a small study (6 CFS patients) and of a rather short duration (4 weeks) so I would also hold the findings of other studies as more reliable. Also I'm not really sure how great those sedentary controls were as "During baseline activity, CFS participants demonstrated 39% lower daily activity counts compared to controls (P = 0.017)". They tried to make a few adjustments for this but these adjustments were based on the results of primary studies and the authors note that this sample may have been different, given its size. They also state this "It is not clear why our study did not find increased daily physical activity to reduce symptom severity, as reported in previous studies. One possible explanation is that our fatigue ratings provided a more accurate and discriminatory measure of our participants' fatigue symptoms". Other studies use different methods of measuring fatigue. Problematically, a visual analogue scale is a completely subjective measure (as opposed to a behaviour checklist or more specific questions) so expectations weigh a lot into it. Given these problems with interpretation, it seems like it will be difficult to work this source into the article. JamesStewart7 (talk) 07:59, 10 January 2008 (UTC)

Increase of activity is not proof of improvement. Patients generally can maintain a somewhat higher level of activity for some time, but that may be risky and not be their optimal level of functioning. Guido den Broeder (talk) 12:46, 10 January 2008 (UTC)

The expert advice used to always be oly do 50% (or 70% or something) of what you feel capable of. So it's certainly possible for some patients to do more but it's risky. Also patients can cut out or reduce some activity in order to divert energy into walking (or whatever is being tested). So such studies on walking distance, even if objectively measured (which the current huge "PACE" trial in the UK is NOT) are far from foolproof way of measuring a total energy output. Of course you'd need a biological/metabolic study for that... MEspringal (talk) 10:22, 14 February 2008 (UTC)

"May" being the operative word here. If it's going to be anything other than speculation, some evidence is needed. It should be clear from this discussion that the existance of hard limits of activity is disupted (the study even noted that previous studies showed opposite results) so the Post-exertional symtpom exacerbation cannot be reinstated without a reference. We also already have this "Post-exertional malaise: An inappropriate loss of physical and mental stamina, rapid muscular and cognitive fatigability, symptom exacerbation after exertion, plus a pathologically slow recovery period usually 24 hours or longer." so there is no point repeating that. JamesStewart7 (talk) 23:32, 10 January 2008 (UTC)

It should also be noted that post exertional worsening does not necessarily mean worsening during or immediately after the exercise in question, although the exercise may be truncated by energy deficiency, but can begin within the 24 hours after. Jagra (talk) 01:36, 11 January 2008 (UTC)

Made a first pass at editing Graded Exercise Therapy (GE, GA or GET) section for wp:peacock, weasel words, NPOV and adding requested citations. Tried to group Gibson and 25% ME Group together for now. Much more organization, WP:V, NPOV, WEIGHT edits needed. Ward20 (talk) 03:23, 11 January 2008 (UTC)

It is good that some of the weasel wording has been removed but I would agree much more work is needed. We're currently given a lot of weight to a survey and a political report. Also there are reliability concerns with the 25% ME group publications as it is a self published source, Wikipedia:Verifiability#Self-published_sources_.28online_and_paper.29. Yet for some reason it is receiving most of the attention in this section and none of the three (that I know of) published reviews in the area are mentioned at all in the GET section. The 25% ME group submissions should be removed apart from the content which was cited in the Gibson report (which provides a secondary citation). JamesStewart7 (talk) 05:52, 11 January 2008 (UTC)

I agree with you. I just did the research with the 25% group and wanted to get it in one place so it could be evaluated. I will transfer the SPS material to here so it is archived in case some remarkable secondary source is found.

• The 25% ME Group said that Graded Exercise Therapy is by far the most unhelpful form of treatment for their members. They state their 2004 member survey indicated 82% that tried GET reported they were made worse by this treatment, and some patients were mild cases before undergoing therapy.

Ward20 (talk) 06:35, 11 January 2008 (UTC)

The study is referenced in the Gibson report which makes it notable but not necessarily reliable. Here is their description of how the survey was conducted "A large random sample of 437 of our members (66% of our total membership) very kindly and painstakingly completed a Questionnaire recently". I have three principal complaints:

1. It is unclear whether they sent it out to all their members and 66% responded or whether they sent it out to 66% of their members or if they sent it out to 66% of their members and not all of them responded.
2. As no mention of who the 25% ME group are appears in the article, a reader may wrongly assume the 25% ME group is a representative sample. The group however states that it is for severe ME (which seems to be somewhat arbitrarily defined as the worst 25% of sufferers). Problematically anyone who has severe ME probably hasn't improved with treatment or hasn't attempted treatment (if they had improved significantly they wouldn't be in the severe group any more) so you would expect them to find treatments unhelpful. I would assume anyone who recovered as a result of treatment would leave the association or at least not be an active participant.
3. Patient surveys are a poor indicator of treatment effectiveness. Many people swear by treatments for which no evidence exists to support their effectiveness.

The results of the survey are not a comparable standard of evidence to what is gathered through controlled studies. This survey is notable because it is mentioned in the Gibson report. The Gibson report, however, is not a source of scientific opinion, as the Countess of Mar, herself, stated. Therefore we should not be treating it as such. So the 25% ME studies, which are present in the article because of their reference in the Gibson report should also not be treated as scientific evidence. Juxtaposing it with a scientific review, however, presents it as such. This is why I think we need to move all of this material to another section or create a new one.

Also what "Dr. Peter White found in four studies" is not as reliable as a review in which the authors are required to state their inclusion criteria and all their methods for deducing their results and then submit it for peer review. Therefore I think we should cut Dr. White's opinion and replace it with the original reviews unless Dr White's statements adds something additional to the article that those reviews do not provide. Of course we would still have to consider WP:WEIGHT issues, if that is to be done. JamesStewart7 (talk) 10:33, 11 January 2008 (UTC)

You're right that PMID 16255779 is not the best study to draw conclusions from. I pulled it from previous notes without rechecking the details. As for the CFS patients demonstrating only 39% lower baseline activity levels than controls, this isn't surprising considering that diagnosis of CFS only requires that the reduction in function is "substantial" (a flexible term). It also seems in line with PMID 14577835 where the average employment workload for people with CFS is about 27 hours a week (check out the activity table of results) but roughly half were unemployed (so I'm not sure exactly how that affects the workload statistics). The systematic review PMID 15159267 provides stronger evidence that roughly half of people with CFS are unemployed, and also found that 19% of people with CFS had full-time employment while 64% had work limitations due to CFS. There is a wide range of disability between different patients, so it's difficult to imagine an "average" patient. As I understand it, the issue here is not whether post-exertional symptoms exist (there is evidence that they do) but whether graded activity is sustainable without adverse effects (there is evidence that it is); although I don't think these are necessarily mutually exclusive. As for GET efficacy; if patients could continue increasing their activity without complications, then why are they still stopping short of full capacity? Perhaps it's the remaining baseline symptoms since they aren't cured. This doesn't demonstrate a "hard limit" though, but something similar could be said for any major illness where the baseline symptoms are disabling enough regardless of pathology or exacerbations. According to the available evidence; GET is generally safe, and effective for a large proportion of patients. I have trouble understanding how patients in general can remain ill for years without ever attempting graded activity; but if this commonly applies to a large proportion of patients then the positive trial results make sense. - Tekaphor (talk) 13:43, 11 January 2008 (UTC)

Well, try having a severe flare (including eg. spinal pain, bowel pain, leg pain, heavy sweats, chills, breathlessness, confusion) everytime you have a bowel movement, eat a small meal, stand stationary for more than five seconds, try to have a brief verbal conversation, brush your teeth or balance your cheque book. Not to mention "external" stuff such as changes in temperature, noise pollution, financial stress (poverty), allergens, infections, artificial fragrances and other people in general, which can have severely deleterious effect on your health. A trivial action like brief standing or sitting in a chair can take hours of prostration and pain for symptoms to subside. In other words, sufferers may already be struggling to get through the day.

You talk as if activity is some incredibly remote abstract that can be glibly approached like a mail order product under the distance selling gaurantee. The fact is for severely affected sufferers, the negative effects of activity and hypersensitivities are experienced every day despite the very best attempts at "pacing"; only a lucky(?) few will be totally insulated from them, if at all. Effectively, graded exercise is minutely done every day and in every fraction of essential activity (never mind the pleasure that certain experts say we're supposed to be getting, ah, is that what it is...) because the severely affected are close to or upon their ceiling of activity and do not have the comparative privilege of being able to voyage towards meeting it as a stranger, or waiting four days to see if they've relapsed or not. Eternal and unexpected stimulus is far more difficult to accommodate than the standard issue lifestyle/GET/CBT gumph portrays and it's telling that such environmental factors are NEVER addressed by the psychosocial camp -- because that would lessen the smear of pwME as "the great misbehavers" who are just too thick to get their lives "balanced" like normal rational people. In fact according to PD White'd submission to NICE sufferers should be deterred from getting disability aids; I wonder how he'll wriggle out of that bit of nasty disablism. He also argues sufferers do not experience ME as being physical, whereas the painful, immediate, intrusive, visceral, sheer physicality of the disease is consistently glossed over in much official material.

But the loss of adaptability is not just an agonising, immediate and suffocating visceral experience, the logic just isn't there either. Deconditioning doesn't explain daily and hourly variability in symptoms and functioning, nor can it explain spontaneous remissions and relapses that for a subset of patients can last months or years. If a "cycle of deconditioning" was a major maintaining factor you'd expect the pattern to be one of increasing illness, but only a very small minority appear to be progressive. Together with descriptions of "CFS", CBT theory suggests a much-of-a-muchness rather than the "rubber-band" effect and quicksand mystery tour of ME.

Why would I have blurred vision for an afternoon only, were my eye muscles temporarily "unfit" and then magically and silently gave themselves a rehabilitive workout by the evening? In what way does eating a little fruit constitute the massive self-abusing fry up that the KCL "CBT central" educational material insists is the probable cause of stomach pain/nausea? I suppose difficulty emptying my bladder is trully result of lack of pissing? That's just taking the piss now.

As if that's not enough (I can only just scratch the surface of trying to explain here) but then there's the unpleasant if not sinister willful ignorance of the CBT school, and the extent and manner in which CBT is promoted as of course the necessary reprogramming to make the supposedly normal seem less abnormal (a tool for "constructively modifying thought" -- as used in phobia treatment). Nevermind all the propaganda about "partnership" by those who claim to be able to "explain" an "unexplained" illness, if a horrendous hour of cajoling wont work its magic they'll just try three. Yes, I said three, consecutaive hours. Some incompetent cowboy operation? No, that's the national UK "FINE" trial. You have to wonder what kind of demented definition of "graded" three hours is, for severe sufferers especially. But then definitions were never the CBT enthusiasts strong suite.

That brings me to the matter of the exclusion of the severely affected from all those CBT/GET studies. The CBTers know it's far less likely to work even allowing for an overall 70% misdiagnosis rate (in other words an accurate Oxford criteria diagnosis), but they've already made people like myself disappear from the literature, so they can concentrate on the PSTD/major anxiety "fatigue" patients which "CFS" has been increasingly customised to describe.

And of course a number of severely affected sufferers HAVE tried GET; they were mildly affected beforehand. MEspringal (talk) 10:22, 14 February 2008 (UTC)

...but they've already made people like myself disappear from the literature, so they can concentrate on the PSTD/major anxiety "fatigue" patients which "CFS" has been increasingly customised to describe.

Yep. That is the problem. Bricker (talk) 02:52, 15 February 2008 (UTC).

Evidence for post-exertional symptoms in CFS

Even though the post-exertional aspect of CFS is not usually a requirement for diagnosis or study inclusion, it is still found in some research (but not entirely consistent). Below is a range of related studies I am aware of:

• PMID 12897748 found that after patients exercised for 20 minutes on a stationary bike at 70% of their predicted maximum work load, measures of "reduced activity" and "mental fatigue" were significantly increased in the CFS group only.
• PMID 10209352 found that following a fatiguing exercise test on the quadriceps, recovery was prolonged in the CFS group only.
• PMID 9797929 found an objective reduction of physical activity following a maximal treadmill test, "but later than self-report would suggest, and are apparently not so severe that CFS patients cannot compensate."
• PMID 16223622 found that after an incremental exercise test until exhaustion, self-reported fatigue was increased up to 2 days in patients but only for 2 hours in controls, while objective measures of activity remained unchanged.
• PMID 17528679 (http://www.immunesupport.com/library/showarticle.cfm/ID/8098) states that "Analysis of the open-ended questionnaires revealed that within 24 hours of the exercise challenge, 85% of controls indicated full recovery in contrast to 0% of CFS patients. The remaining 15% of controls recovered within 48 hours of the test as opposed to only one CFS patient."
• PMID 8678084 states that "Our CFS group could withstand a maximal treadmill exercise test without a major exacerbation in either fatigue or other symptoms of their illness."
• PMID 10440661 looked into light intensity exercise and states that "Thirty minutes of intermittent walking did not exacerbate symptoms in subjects with CFS. The physiological data did not show any abnormal response to exercise. Although this study did not determine whether 30 minutes of continuous versus intermittent exercise would exacerbate symptoms, all 10 subjects felt that they could not exercise continuously for 30 minutes without experiencing symptom exacerbation. Despite this limitation, the results indicate that some individuals with CFS may be able to use low-level, intermittent exercise without exacerbating their symptoms."

The above studies don't really support the patient anecdotes of severe symptom exacerbation following exercise, but it gives general support for the existence of some post-exertional aspect to CFS. There are other sources which mention the supposed existence of it and/or other studies which mention it in association with their biochemical findings, but I didn't bother to include them above. A review of such studies of the latter type (PMID 16781183) did however state that "CFS sufferers respond to incremental exercise with a lengthened and accentuated oxidative stress response, explaining muscle pain, postexertional malaise, and the decrease in pain threshold following graded exercise in CFS patients." The few studies on cognitive performance after exercise seem inconsistent, so I didn't include them either. I also didn't include studies which looked into exercise capacity and sense of effort etc, since I'm focusing on the post-exertional aspect. If anyone is aware of additional relevant studies, please present them!

Tekaphor (talk) 13:43, 11 January 2008 (UTC)

Um well, absence of research isn't research evidence of absence. There's no severely affected patients in that lot and they were only exercised modestly with regard to their illness status; the more sufferers push themselves the more aggravated symptoms and weakness should be. The sort of people who apply for exercise testing are not likely to be already on the verge of a relapse or struggling to cope at work (or even at home). If some of them have practical help or accomodating family they would do worse in the same tests without it. Gosh, no mention of exertional insomnia even.

Most of these studies aren't looking into a variety of somatic symptoms or even pain, only fatigue and functional strength (though the latter's good enough a demonstration of worsening after exercise for me. At the end of the day it's objective measures are most helpful). If good evidence is totally lacking you have to use next best evidence, with caveats.

You miss out a major notable source of good evidence in all the ME studies (and synonymous diagnoses) before c. 1988 or the 80's, for instance papers by Acheson, Gilliam, Galpine, Innes, Compston, Wallis et al. This is after all, where exercise intolerance and severe multi-system symptoms were first described and recognised as a cardinal feature in non-remitting cases.

There should also be some orthostasis studies. There's also Peckerman's heart studies, Les Simpson's trigger finger study, the Da Costa study, and so on. Though they might not be focussing on symptoms the sort and extent of findings likely gives indirect suppport to the extend and breadth of symptoms.

MEspringal (talk) 10:22, 14 February 2008 (UTC)

ME Springal, generally agree with what you say, but would suggest that Tekaphor is quite aware of the problems with these studies, and is sympathetic to patient's situation. Tekaphor is not an editor you need to worry about. Bricker (talk) 02:52, 15 February 2008 (UTC)

Hi MEspringal, I essentially agree with what you have been saying, and I will explain the context of my above comments. I don't doubt the objective reality of patient symptoms or impairments, and obviously there are a wide range of issues with the entire subject of CFS. This wikipedia entry is mostly a loosely CDC defined CFS "status quo" article, because that's where the research went after 1988. Pre-1988 references are difficult to access, so I haven't been able to get familiar with them yet; I'm aware of this limitation, which is why I openly requested more references. I'm trying to work within the limitations of easily available sources and the political environment of this article, so my beliefs/opinions/experiences aren't necessarily reflected in my comments and also have no weight here due to the nature of wikipedia. ... Personally, I think the lack of consistently substantial post exertional symptoms in post-1988 research is actually rather revealing, considering that it's supposed to be a hallmark of CFS and therefore should be consistently reported. Therefore, we have some confounding possibilities: (a) it's not actually a consistent hallmark of either Oxford or CDC defined "CFS" as often implied (hardly surprising since it's not a diagnostic requirement), (b) the related studies are poorly conducted or unrepresentative, (c) the authors are bordering on scientific fraud. - Tekaphor (talk) 09:43, 24 February 2008 (UTC)

Synthesis

How do the statements in the stress and trauma section "conveys ideas not attributable to the original sources." I haven't read into it to carefully but from my brief analysis, most of the statements seem to line up with the source. For example this "Anxiety disorders have also been found to be a risk factor in 5-15 year olds" is cited with this source "Epidemiology of chronic fatigue syndrome and self reported myalgic encephalomyelitis in 5-15 year olds: cross sectional study." which stated " The risk factors for chronic fatigue and CDC criteria for chronic fatigue syndrome were older age and anxiety disorders." It seems to match up pretty well to me. The edit summary said a source is not directly related to the subject of the article. I can see one source for which this would be the case, "Stress and the brain: from adaptation to disease." but all the other sources refer directly to CFS. So if it is just this one source I think we should just remove the source and the associated statement so we can remove the tag. JamesStewart7 (talk) 06:17, 11 January 2008 (UTC)

AFAIK that is only the source that has nothing to do with CFS, but I have not had time to check the other wording closely in order to see it there are more problems. If you want, change the first sentence and source and get rid of the tag. Ward20 (talk) 06:46, 11 January 2008 (UTC)

PS: I was rather shocked at the size of the tag, but didn't have the time to search for another one. Ward20 (talk) 06:58, 11 January 2008 (UTC)

Self-reported by a 5-year old?? Guido den Broeder (talk) 10:17, 11 January 2008 (UTC)

I'm surprised that this section was tagged for the one study, when there is a whole referenced paragraph in the "Psychoneuroimmunological interactions" section about stress that isn't directly related to CFS, although I'm not necessarily proposing it's removal. - Tekaphor (talk) 14:40, 11 January 2008 (UTC)

You make a good point. I've now tagged that section "synthesis" and I think it should probably be removed. It is largely irrelvant and most of the references are in "Med hypotheses" so they are rather speculative. JamesStewart7 (talk) 02:43, 12 January 2008 (UTC)

Unreferenced material

WP:PROVEIT "Any edit lacking a reliable source may be removed, but editors may object if you remove material without giving them a chance to provide references"

"I can NOT emphasize this enough. There seems to be a terrible bias among some editors that some sort of random speculative 'I heard it somewhere' pseudo information is to be tagged with a 'needs a cite' tag. Wrong. It should be removed, aggressively, unless it can be sourced. This is true of all information, but it is particularly true of negative information about living persons." Guido since you have reverted my recent edits please point to where it states that I have to give notice before challenging the material. Editors may object but it would then be up to them to find a source before they reinclude. So how about we move the information to the talk page (that would involve taking it out of the article) and discuss it here. There are also two fact tags in the section that have been sitting there since last month so notice has been given. Fact tagging is what you do with information which you think may be sourced. Removal is what should happen with information which is disputed/unsourceable.

I'll list a few complaints with the section here "Therefore patients need to intersperse any activity with rest periods, which is referred to as pacing". "Need" makes this sentence POV. If it is needed you would also expect some solid evidence and of course there should be no evidence that things like GET are effective.

"Time to recover strength has been described as inordinate and "pathological" and limits often change daily and from hour-to-hour, as well as through longer relapses and remissions." Weasel word "has been described". This also may be impossible to document. How can you objectively measure limits that change from hour to hour?

"Severely affected patients may have "hard" limits such as severe loss of muscle power or drastic postural hypotension causing collapse or blackouts, rendering complete if usually temporary debilitation, and imposing strict, if variable, limitations" May have? So they also may not have hard limits either? "May not have", however, would give a completely different POV to the section though.

"This is to say that exertion is unsustainable". This looks like an OR interpretation of the actual definition, "An inappropriate loss of physical and mental stamina, rapid muscular and cognitive fatigability, symptom exacerbation after exertion, plus a pathologically slow recovery period usually 24 hours or longer." The pathologically slow recovery period is the key aspect of the definition. "Exertion is unsustainable" is not part of the definition. In fact "exertion is unsustainable" doesn't even mean anything unless you define the time period and the level of activity. In the broadest sense exertion is unsustainable in everyone. For example, no one can run indefinately. Given the ambiguity of statements like this, I highly doubt a RS will be found for them. JamesStewart7 (talk) 11:43, 11 January 2008 (UTC)

It is a great idea when removing unsourced material to move it to the talk page. The amount of unsourced or POV material that has been identified is large and the holidays have been here. There needs to be some leeway given. It is more effective to add or change material to make it better than it is to delete material. The remedy is to add to the article — not to subtract from it. Some of the material discussed above are patient's symptoms and/or experiences. There may not be medical studies to cite. After reading some of the passages I believe other mainstream reliable sources can be found for a lot of the context. Academic and peer-reviewed publications are highly valued and usually the most reliable sources in areas where they are available, such as history, medicine and science. Material from reliable non-academic sources may also be used in these areas, particularly if they are respected mainstream publications. The appropriateness of any source always depends on the context. Where there is disagreement between sources, their views should be clearly attributed in the text.

We are having difficulty coming to consensus about which RSs to use and what weight to give. There is controversy as the article states I think it would be fair to think about these tutorials when discussing sources. [1] [2] They seem to me to be stating that reason should be used to select material, and not that any particular RS trumps all other sources. Ward20 (talk) 23:45, 11 January 2008 (UTC)

"Some of the material discussed above are patient's symptoms and/or experiences. There may not be medical studies to cite." This is grounds for removal on its own. Any removal which cannot be referenced in a RS should be removed. In the case that the patient is a wikipedia editor, this is OR, which is also grounds for removal. I strongly agree with your comments that the reliability

Wikipedia policy) states "NPOV says that the article should fairly represent all significant viewpoints that have been published by a reliable source, and should do so in proportion to the prominence of each. Now an important qualification: Articles that compare views should not give minority views as much or as detailed a description as more popular views, and may not include tiny-minority views at all... Disagreements over whether something is approached neutrally can usually be avoided through the practice of good and unbiased research, based upon the best and most reputable authoritative sources available... Articles should rely on reliable, third-party published sources with a reputation for fact-checking and accuracy... Questionable sources are those with a poor reputation for fact-checking. Such sources include websites and publications that express views that are widely acknowledged as extremist, are promotional in nature, or rely heavily on rumors and personal opinions. Questionable sources should only be used in articles about themselves". I think they do say one source trumps another. Questionable sources stay out. RS stay in. If we have multiple RS with conflicting views then we should represent each view according to the number of RS presenting each view. However, most of these disputes have not involved multiple, conflicting RS. They have involved several RS in agreement that conflict with a questionable source (normally self published information).

As you stated, the appropriateness of the source depends on the context which is while I still question the reasoning behind including a political document (Gibson report) and the opinions of special interest groups (25% ME group) in a section that is very much the domain of medical science (treatment efficacy). In my opinion sections such as these should be reserved solely for academic sources (peer-reviewed journals) and any other RS information in this section should be moved to a more appropriate context (a controversy/politics section). Medical/scientific issues such as epidemiology/treatment efficacy/disease causes should be handled by medical/scientific sources. Political issues such as public reception/social issues/controversy can be handled by political sources.

I know someone has already cited WP:Ignore all rules so I would like to quote this; "A rule-ignorer must justify how their actions improve the encyclopedia if challenged". I think including unreliable sources or OR patient experience is detrimental to the encylopedia as it seems to be introducing strong POV. Many of these unreliable sources and opinions conflict with the more reliable sources which is the cause of a lot of the POV disputes. Why should we risk WP:WEIGHT issues by introducing an unreliable source that conflicts with a RS? How does giving one POV more attention improve the encyclopedia? If everything in this article can be RS and presented in the appropriate format ie "Person x states..." when opinons are presented I will happily retract all of my complaints but until then I think I am going to stand by my position that removing unsourced and contentious information is a valid way to reduce the length of a long article. Much of this has been tagged since December. I do not see the sheer volume of unsourced information as a sufficient argument for leaving it there longer as much of this information should never of been included without a reference in the first place, "All quotations and any material challenged or likely to be challenged should be attributed to a reliable, published source using an inline citation" and much of it is innaccurate or unciteable. However, if people prefer, I may move such information to the talk page instead of straight removal. JamesStewart7 (talk) 02:40, 12 January 2008 (UTC)

There is a misundrstanding here. I am not advocating putting patient's experiences/symptoms in without RS. There are plenty of RSs about patient's experiences/symptoms that are not medical studies. Ward20 (talk) 03:45, 12 January 2008 (UTC)

Please provide an example of what you consider a RS for patient experience so that I may better understand your position. If it is not a medical study or academic publication then where would this information be published? It seems to me that any source that publishes a lot of this information would be a questionable source "Such sources include websites and publications that express views that are widely acknowledged as extremist, are promotional in nature, or rely heavily on rumors and personal opinions." or is a self-published source. I'd like to get a better idea of what you consider reliable. JamesStewart7 (talk) 04:03, 12 January 2008 (UTC)

You broadened it out from medical studies. I don't know if you consider these academic publications but I believe these RS: The Doctor's Guide to Chronic Fatigue Syndrome: Understanding, Treating, and Living with Cfids by David S. Bell, search symptoms; go to pg 11, CDC, Chronic Fatigue Syndrome, Other Symptoms Mayo Clinic, Chronic fatigue syndrome, Signs and symptoms.Ward20 (talk) 08:40, 12 January 2008 (UTC)

CDC is reliable but all they state in the area of malaise is this "increased malaise (fatigue and sickness) following exertion". Mayoclinic is unreliable (I don't think much fact checking goes into their quizzes "http://www.mayoclinic.com/health/QuizIndexPage/QuizIndexPage". Given the position of the CFID group who endorsed the Dr. Bell book I'd say it is somewhat partisan and they don't state how they deduced what percentage of patients experience each symptom and it is rather lacking in references in general. I'd say it is a RS for the opinions of certain people and groups (CFID) but not a RS for medical information. I don't see why we should include individual reports in this article though. You don't see individual reports for what it is like to have the disease in any other article. JamesStewart7 (talk) 09:34, 12 January 2008 (UTC)

Perhaps my recent presentation of evidence for post-exertional symptoms in CFS patients can provide some references for the disputed statements, although it would probably be more accurate to create new statements from the research. The current descriptive symptom list in the article is essentially inferred from the Canadian consensus document, which was "Based on the consensus panel's collective extensive clinical experience diagnosing and/or treating more than twenty thousand (20,000) ME/CFS patients, a working clinical case definition, that encompassed the pattern of positive signs and symptoms of ME/CFS, was developed." As for scientific research, the "research overview" on page 68 discusses at least a dozen studies with relevance to post-exertional symptoms, which they note isn't a systematic review, and I haven't yet investigated each reference. However, on page 101 there is the "APPENDIX 2. ME/CFS Symptom Prevalence and Severity", which is a table apparantly extracted from PMID 11555128 and (surprisingly) states that post-exertional malaise was reported in 97.3% of 1578 patients diagnosed using the Fukuda definition of CFS. Below are some extractions from the Canadian consensus document, relating to the description of post-exertional malaise (in order of appearance):

• "There is an inappropriate loss of physical and mental stamina, rapid muscular and cognitive fatigability, post exertional malaise and/or fatigue and/or pain and a tendency for other associated symptoms within the patient's cluster of symptoms to worsen. There is a pathologically slow recovery period–usually 24 hours or longer."
• "Thus, although fatigue and post-exertional malaise are universal symptoms of ME/CFS, they may not be the most severe symptoms in the individual case, where headaches, neurocognitive difficulties, pain and sleep disturbances can dominate, at least temporarily."
• "The malaise that follows exertion is difficult to describe but is often reported to be similar to the generalized pain, discomfort and fatigue associated with the acute phase of influenza. Delayed malaise and fatigue may be associated with signs of immune activation: sore throat, lymph glandular tenderness and/or swelling, general malaise, increased pain or cognitive fog. Fatigue immediately following activity may also be associated with these signs of immune activation. Patients who develop ME/CFS often lose the natural antidepressant effect of exercise, feeling worse after exercise rather than better. Patients may have a drop in body temperature with exercise. Thus fatigue is correlated with other symptoms, often in a sequence that is unique to each patient. After relatively normal physical or intellectual exertion, a patient may take an inordinate amount of time to regain her/his pre-exertion level of function and competence. For example, a patient who has bought a few groceries may be too exhausted to unpack them until the next day. The reactive fatigue of post-exertional malaise or lack of endurance usually lasts 24 hours or more and is often associated with impairment of cognitive functions. There is often delayed reactivity following exertion, with the onset the next day, or even later. However, duration of symptoms also varies with the context. For example, patients who have already modified their activities to better coincide with the activity level they can handle without becoming overly fatigued will be expected to have a shorter recovery period than those who do not pace themselves adequately."
• "In order to successfully engage and maintain patients in an exercise program, they must have a sense of autonomy. This is particularly important for the ME/CFS patient who has usually lost the natural antidepressant effect of exercise and experiences post-exertional malaise and/or fatigue. Limit exercises to those that do not cause significant pain. Gradually (over months) increase the program by frequency and the duration of exercise periods if tolerated, but the level of intensity should be kept low."

Tekaphor (talk) 14:23, 12 January 2008 (UTC)

I think those statements diverge somewhat from what is present in the post-exertional malaise section article. The above statements should be phrased as recommendation/professional opinions when included in the article. Also the Canadian guidlines are already in the article along with a definition of post-exertional malaise. Do we really need an extended description from one source in this long article? JamesStewart7 (talk) 23:40, 12 January 2008 (UTC)

I suggest a simplified hybrid: "An inappropriate loss of physical and mental stamina, rapid muscular and cognitive fatigability, post exertional malaise and/or fatigue and/or pain and a tendency for other associated symptoms to worsen with a pathologically slow recovery period of usually 24 hours or longer. The malaise that follows exertion is often reported to be similar to the generalized pain, discomfort and fatigue associated with the acute phase of influenza. Although common in CFS, this may not be the most severe symptom in the individual case, where other symptoms can dominate." I will place this in the symptom list (replacing the short sentence that is currently there), and in a later edit I might include the studies I mentioned earlier. Any remaining text in the currently separate section about post-exertion symptom exacerbation (that is still not redundant after these edits) could then be integrated into the symptom list. - Tekaphor (talk) 04:18, 13 January 2008 (UTC)

Outbreaks of CFS

There are reports some "clusters" of CFS are not clusters at all [3] That article also notes this "Symptoms and features of generic forms of fatigue were very similar to those often attributed to CFS". Also there is some dispute as to whether Royal Free Disease is CFS, with some positing mass hysteria as the cause, [4]. Similar to CFS is not CFS so unless there is a consesus to what the actual disease is in any given outbreak we should not just be calling it CFS without attribution. This is why I edited the article to use the form "Person x states that this disease is CFS", yet this edit was reverted [5]. I would like an explanation for this. Unless everyone in the medical community is in agreement that this disease is CFS (and claims of consensus must be sourced) and there is sufficient documentation to establish this then "Person x states..." is the most NPOV form. JamesStewart7 (talk) 12:18, 11 January 2008 (UTC)

As no one has replied to this I am going to reinsert my comments until such time as someone can explain to me why there are POV concerns with my edit JamesStewart7 (talk) 23:35, 12 January 2008 (UTC)

We need to get this review translated:

History of chronic fatigue syndrome: Nippon Rinsho. 2007 Jun;65(6):975-82.

Chronic fatigue syndrome (CFS) is not a new disease. Similar morbidities have been known as different names since past several centuries. For example, neurasthenia, epidemic neuromyasthenia, myalgic encephalomyelitis, Akureyri disease, Royal Free disease, chronic EBV disease, post-viral fatigue syndrome etc. Much of the recent interest in CFS was generated by incidence of infection-like outbreak at Lake Tahoe in Nevada. The Center for Disease Control (USA) realized that correlation was poor between those patients who had virologic evidence of EBV infection and those who had the symptoms of chronic fatigue. This is a review of the history of CFS. (1) Historical perspectives in chronic fatigue cases in past old period, (2) Post-viral infectious fatigue and chronic fatigue (myalgic encephalomyelitis), (3) Recent trend of CFS studies and its clinical similar situation. Finally, I would like to state that we intend to draw up a new diagnostic guideline for CFS in Japan.

PMID: 17561685 [PubMed - indexed for MEDLINE]

Ward20 (talk) 07:36, 17 January 2008 (UTC)

material removed from article

I extracted these from the diffs, we can use this space for other material removed.

Those who fit a 2003 definition with post exertional malaise may wish to consider whether graded exercise is recommended in their case because it can cause serious deterioration in the exertional intolerant

Similarly, like with CBT, GET seems more effective in less severely affected patients than those who are more severely affected. Its role in helping severely disabled patients has not yet been properly established, but uncontrolled studies suggest it can help so long as it is tailored to the individual patient..

Some theories propose that an infection with one of the below-listed disease agents somehow leads to immune dysfunction and chronic fatigue in cases of CFS. This is partly supported by test results indicating lowered or changed immune responses in some patients, as well as elevated levels of infectious agents in some patients' blood

For these reasons Lyme can be difficult to diagnose, particularly in its later stages, at which point symptoms are virtually identical to those of CFS.

Mitochondrial disturbances have been discovered in some CFS patients.

The mixed results of earlier trials was also explained as these were static dose regimes and did not mention attempts to control for other intake or lifestyle factors that can effect essential fatty acid utilization. Amounts of different fats in the diet, amount of protein, alcohol, zinc and magnesium status, exercise amounts, level of conditioning, stress and other infections may also affect the results. Other nutrients may be deficient in CFS that can also effect essential fatty acid utilization.

A less rigorous study which supplemented only with omega-3 essential fatty acid, patients were treated solely with a high-eicosapentaenoic acid-containing essential fatty acid supplement. All showed improvement in their symptomatology within eight to 12 weeks, which it was said may be associated with structual brain changes, seen in a separate case study. There are also reports of an open case series study of 55 consecutive long term incapacitated primary care patients using combined dietary and other EFA modulations instead of supplementation.

In CFS the EFA changes have been associated with findings by researchers at an Australian University of Newcastle of dysregulation of enzyme D6D-desturase activity and then n-6 poly fatty acids changes which were consistent with an inflammatory event in CFS patients and were suggestive of anomalies in essential and non-essential fatty acid homeostasis as well as B-oxidation of fatty acids. Some primary lipid changes in CFS patients were considered related to other potentially non-viral induced changes. + Other nutrients may be deficient in CFS that can also effect essential fatty acid utilization. - - -

In CFS the EFA changes have been associated with findings by researchers at an Australian University of Newcastle of dysregulation of enzyme D6D-desturase activity and then n-6 poly fatty acids changes which were consistent with an inflammatory event in CFS patients and were suggestive of anomalies in essential and non-essential fatty acid homeostasis as well as B-oxidation of fatty acids. Some primary lipid changes in CFS patients were considered related to other potentially non-viral induced changes.

The mixed results of earlier trials was also explained as these were static dose regimes and did not mention attempts to control for other intake or lifestyle factors that can effect essential fatty acid utilization. Amounts of different fats in the diet, amount of protein, alcohol, zinc and magnesium status, exercise amounts, level of conditioning, stress and other infections may also affect the results. Other nutrients may be deficient in CFS that can also effect essential fatty acid utilization.

A less rigorous study which supplemented only with omega-3 essential fatty acid, patients were treated solely with a high-eicosapentaenoic acid-containing essential fatty acid supplement. All showed improvement in their symptomatology within eight to 12 weeks, which it was said may be associated with structual brain changes, seen in a separate case study. There are also reports of an open case series study of 55 consecutive long term incapacitated primary care patients using combined dietary and other EFA modulations instead of supplementation.

- - -

Since some CFS patients show decreased immune response or symptoms of MLS, pre-existing mild allergies may increase to harmful levels after CFS onset. Some studies suggest that a form of CFS may be triggered by a rare reaction to dental metals. Tests in Sweden showed that 76% of CFS patients who tested positive to metal allergy and swapped metal fillings for ceramic substitute achieved partial or full health improvement . Metal allergy can be detected by a blood test named MELISA.

Antifungals Antifungal drugs, specifically of the azole class, are used to treat yeast and fungus infections. Proponents of the yeast hypothesis for CFS claim, however, that the drugs are largely useless unless combined with a low-carbohydrate diet that effectively "starves" the fungus at the same time. Research studies have shown the contrary.

Others studies subsequently found similar substrate depletions concerning omega-6 and omega-3 essential fatty acids.

More recently a Chinese study in 2003 of CFS, with forty-two patients that fulfilled the CDC criteria, were determined to have abnormal levels of lipids compared to controls.

A study was conducted by Behan and Horrabin in 1990 using high doses of supplemental essential fatty acids of mixed types. Sixty-three adults with the diagnosis of postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study. After 3 months, 85% of the patients given the supplements had much greater symptom improvement vs. 17% on placebo. Upon testing the supplement group's cellular membrane phospholipids, (feedstock’s) had returned towards normal.

In 1999 a study endeavored to duplicate the Behans' work with a different subset of fifty patients who fulfilled the Oxford Criteria for CFS, and who had negligible differences of pretreatment red-cell membrane (RBC) lipids compared with controls. The study results showed no significant differences between treated and placebo patients, as opposed to the previous study. A review of CFS treatments suggested that these differences in outcomes may be accounted for by participant selection and the choice of placebo, with the second study using currently (as of 2000) accepted diagnostic criteria and the first study using liquid paraffin as a placebo compared to sunflower oil in the Warren et al. study. The researchers state that sunflower oil is better tolerated and less likely to affect the placebo response adversely" This same review classified dietary supplement treatments for CFS as of "unknown effectiveness".

Other nutrients may be deficient in CFS that can also effect essential fatty acid utilization.

Interestingly, at least some of those who experience improvement on stimulant drugs do not experience significant "payback effect," suggesting that the drug is to some degree acting to correct the underlying neurological problem rather than simply masking symptoms.

A proposed similarity between psychiatric disorders, such as somatoform disorders (particularly undifferentiated somatoform disorder) is that according to some definitions, physical symptoms or their severity are unsupported by medical evidence.

Post-polio syndrome also bears a strong and remarkable resemblance to CFS. Some researchers maintain these disorders are all expressions of a general, yet undefined, syndrome with protean symptoms. The suffering that can be experienced by a patient with ME/CFIDS has been likened to an AIDS patient in the last two months of life and/or a terminal cancer patient. Often, Multiple Sclerosis needs to also be excluded as a diagnosis. Thyroid disorders, anemia, and diabetes can present similar symptoms, and must be ruled out. Other disorders with known causes and treatments that may produce CFS-like symptoms are Lyme disease, temporomandibular disorder (TMD), gluten intolerance (celiac disease and related disorders), and vitamin B12 deficiency. There may also be correlation with polycystic ovary syndrome (PCOS).

There may also be other psychological/psychiatric symptoms/comorbidities in some patients. See the Proposed causes and pathophysiology section for more information about the possible causes of, and treatments for, the above listed symptoms.

Sleep patterns may be further interrupted by vivid "feverish" dreams, and unlike in healthy persons, exercise can worsen the sleep dysfunction.Ward20 (talk) 12:14, 12 January 2008 (UTC)

However, this theory fails to explain the many reported and documented cluster outbreaks of CFS, and is therefore not taken seriously by leading researchers in the field. Instead,

CFS occurs both in isolated cases and large-scale outbreaks. In a number of documented cases several people in a building or large numbers of people in a community came down with the disease essentially simultaneously, suggesting that it is (in at least some cases) partly due to an infectious agent.

Similarly to the theory of immune dysfunction, some doctors believe that CFS patients suffer from immune dysfunction caused by exposure to allergens, ranging from food allergies or food intolerances (see below) to pollen and dander allergies. Instead, severe allergies may occasionally cause CFS-like symptoms, or patients

At this time, no cure for CFS is known. Treatment protocols that attempt to cure CFS are many, usually linked to a presumed cause, but none stand out as promising. Other treatments, that address specific symptoms such as pain, sleep deprivation and food intolerances, and some that affect the metabolism, can have a beneficial effect but do not cure CFS

Ward20 (talk) 01:36, 12 January 2008 (UTC)

Regarding the statement about feverish dreams and exercise-worsened sleep dysfunction, I have previously tried to find sources but as far as I can tell this statement doesn't appear in the original 2003 Canadian consensus document titled "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Clinical Working Case Definition, Diagnostic and Treatment Protocols") but is inferred from the 2005 abridged version (titled "Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: A Clinical Case Definition and Guidelines for Medical Practitioners - An Overview of the Canadian Consensus Document.") The description of sleep dysfunction in the article currently refers to the former rather than the latter, so I will change the reference to better reflect the source. - Tekaphor (talk) 04:54, 13 January 2008 (UTC)

Thank you Tekaphor. Ward20 (talk) 03:35, 14 January 2008 (UTC)

I'm trying to run through and make the "concept" section more NPOV but I'm having difficulty as some of the statments are unreferenced and unclear. Here is what I removed

"Researchers consider chronic fatigue syndrome, involving some of the symptoms rather than disease taxonomy. " - This is problematic as it follows Raggedy Anne syndrome, implying they are the same thing. Attribution is needed for whoever considers Raggedy Anne to be the same/related diagnostic entity as CFS.

"Lacking a diagnostic laboratory test of any kind, CFS has frequently been mis-diagnosed, for example in patients presenting CFS symptoms with similar biological conditions or infections (such as Lyme or Epstein-Barr) (the latter of which is often the cause of glandular fever, or infectious mononucleosis), or psychological conditions (ranging from depression to hypochondria). " Unreferenced link to diseases. Unreferenced mis-diagnosis rate. JamesStewart7 (talk) 05:14, 13 January 2008 (UTC)

Archiving material removed from Controversy by Sciencewatcher:

The vast majority of international ME/CFS specialists support the classification of CFS as a physical condition.

Ward20 (talk) 03:35, 14 January 2008 (UTC)

Archiving material removed from Psychoneuroimmunological interactions by Ward20:

Stress can have a significant effect on the immune system, due to the fact that the stress hormones cortisol, ACTH and adrenaline and the sympathetic nervous system are also important modulators of the immune system. Chronic stress has been shown to reduce levels of Natural killer cells (NK) and T cells, as well as to reduce the function of those cells. Stress has also been shown to increase levels of nitric oxide in the body.

Ward20 (talk)

Archiving material removed from Post-exertion symptom exacerbation by JamesStewart7:
The harder the exertion and the longer it lasts, the worse the decompensation will be afterward, and with greater recovery time.

This can make judging appropriate activity difficult. Time to recover strength has been described as inordinate and "pathological" and limits often change daily and from hour-to-hour, as well as through longer relapses and remissions. Severely affected patients may have "hard" limits such as severe loss of muscle power or drastic postural hypotension causing collapse or blackouts, rendering complete if usually temporary debilitation, and imposing strict, if variable, limitations. It is such limitations that usually enforce disability upon patients sooner or later, after an initial cyclical "push-crash" period, which can be prolonged through poor advice or diagnostic delay. Typically symptoms lessen or disappear with recumbency, due to othostasis as a form of exertion and neuro-vascular adaptability. Therefore patients need to intersperse any activity with rest periods, which is referred to as pacing.
Ward20 (talk) 07:15, 16 January 2008 (UTC)

Recurrent ear infections are common in some CFS sufferers. (removed from Inner-ear disorders)Jagra (talk) 06:29, 12 March 2008 (UTC)

EFA

Be happy to discuss the reverts that relate to this on this page and hopefully reach some resolutions. Jagra (talk) 04:38, 12 January 2008 (UTC)

To begin, details have been posted already (see 11/1/08 Unsourced sections --) to support this, without response; "The mixed results of earlier trials was also explained as these were static dose regimes and did not mention attempts to control for other intake or lifestyle factors that can effect essential fatty acid utilization. Amounts of different fats in the diet, amount of protein, alcohol, zinc and magnesium status, exercise amounts, level of conditioning, stress and other infections may also affect the results. [3] [4] Other nutrients may be deficient in CFS that can also effect essential fatty acid utilization" [5]

In the Journal of Chronic Fatigue Syndrome ISBN 1057-3321 Vol 11 Num 1, 2003 in a section reviewing EFA studies it discusses that there were 2 controlled studies on PVFS patients with Efamol (pp66) with similar but different results, different patient numbers and different treatment amounts, for a different trial period, reported in different articles. The first Behan we cite already, the other in a book titled Post viral fatigue syndrome (Myalgic encephalomyelitis) John Wiley and Sons Ltd 1991 editors Jenkins R Mowbray J. Article; Essential fatty acids and post viral fatigue syndrome, Author; Horribin DF, pp 393-404, ISBN: 0471928461 Review details are given here http://books.google.com/books?id=oHLBFz7glg0C&pg=PA66&lpg=PA66&dq=efamol+marine&source=web&ots=WJ1xk3yZhs&sig=SB4XrhcYzik8tF0RQ8fv9HYgEK8#PPA66,M1 That makes an additional reference for EFA findings in CFS and a further treatment trial, that should be added to the Article.

This paper PMID: 15041033 which is also a reveiw of literature as well as a case series study, concludes “suggest that this n-3 highly unsaturated fatty acid may offer the hope of effective treatment for at least some patients with chronic fatigue syndrome.” In doing so it identifies that EFA treatment is relevant for subgroups, and some comments should thus differemtiate subgroup trials in the Article. To do so the edits with previous consensus (as outlined above) should be reinstated, thus:

"A study was conducted by Behan and Horribin in 1990 using high doses of supplemental essential fatty acids of mixed types. Sixty-three adults with the diagnosis of postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study. After 3 months, 85% of the patients given the supplements had much greater symptom improvement vs. 17% on placebo. Upon testing the supplement group's cellular membrane phospholipids, (feedstock’s) had returned towards normal.[21]"

"In 1999 a study endeavored to duplicate the Behans' work with a different subgroup of fifty patients who fulfilled the Oxford Criteria for CFS, and who had negligible differences of pretreatment red-cell membrane (RBC) lipids compared with controls. The study results showed no significant differences between treated and placebo patients, as opposed to the previous study. [23] ".

With details details distinguishing the additional trial added.Jagra (talk) 04:38, 12 January 2008 (UTC)

I believe my original complaint to this "The mixed results of earlier trials was also explained as these were static dose regimes and did not mention attempts to control for other intake or lifestyle factors that can effect essential fatty acid utilization." was that it was an unpublished synthesis of results and that it is speculative. These complaints still stand.

I don't actually understand what you want us to include from Journal of Chronic Fatigue (which I still don't accept as a reputable Journal because the peer review is inadequate) Does it actually state this (btw a web address of the article would be good) "with similar but different results, different patient numbers and different treatment amounts, for a different trial period, reported in different articles"? "Similar but different results?" In one study the results were significant and in another they were not. That's a pretty important difference. Different patient numbers are found in every trial. Unless one trial had substantially more patients than another (which is not the case) I fail to see how this matters. Both studies state the same trial period, "The preparation given contained linoleic, gamma-linolenic, eicosapentaenoic and docosahexaenoic acids and either it, or the placebo, was given as 8 x 500 mg capsules per day over a 3-month period", "Fifty patients who fulfilled the Oxford Criteria for CFS were randomly allocated to treatment with either Efamol Marine or placebo for 3 months" and as far as reported in different articles goes, well what's your point? Why would two different studies be reported in the same article? We're not going to include a whole bunch of red herrings in the article.

Introducing PMID: 15041033 is not a formalized review. It does not state inclusion criteria or the methods of analysis. Also the journal is not the most reputable available (impact factor: 2.261, [6]). Also I have to question this journal's peer review process, as according to this, [David Horrobin] founded the journal and is a critic of the peer review process so I question whether there is a peer review at all. What would you include from this article anyway. There is next to no discussion. The article notes this, "Symptoms generally improved over time, but not significantly and there were no significant differences between the treatment and placebo groups on this occasion." but only comments this "Even in the case in which a low-eicosapentaenoic acid supplement was used, one out of two randomized, placebo-controlled double-blind trials showed a significant effect." This "one out of two ain't bad" approach is new to me as I seem to remember Reproducibility being one of the main principles of the scientific method. Furthermore inclusion of that article would be bordering on WP:CRYSTAL as the authors primary conclusion seems to be a call for more research, "A randomized double-blind, placebo-controlled trial of either pure eicosapentaenoic acid or a high-eicosapentaenoic acid-containing fatty acid supplementation is indicated, that also includes magnetic resonance scanning." JamesStewart7 (talk) 05:33, 12 January 2008 (UTC)

If the you look at the website for this review that I provided in discussion above I think you will find it is you that is confused, as you seem to be comparing the Behan trial with the Warren trial. Where as there are now three trials The Behan, the Horrobin and tha Warren, Of the J of CFS article If you read the review it says of the second PVFS trial (by Horrobin) “In a double blind placebo controlled study of 70 patients with (PVFS) four capsules of Efamol marine were given morning and evening for 15 weeks, Of those patients 85% on active treatment vs 17% on placebo showed improvements of the symptoms Patients on active treatment also reported fewer episodes of cardiac palpitations and tachycardia.” This is clearly not the Behan trial which is described above this. The Behan trial is correctly described as 63 patients, over a 3 month period, and the symptoms rated were fatigue, myalgia, dizziness, concentration, and depression. The two PVFS trials are therefore double blind placebo controlled studies, and that constitutes reproducability in PVFS patients, and the Horrobin trial should now be added to the article. It does not say (as you claim) that symptoms generally improved but not significantly, that comment is made of the Warren trial only. Jagra (talk) 11:21, 14 January 2008 (UTC)

This is all I am seeing in the way of placebo controlled trials in the Puri review, ".O. Behan, W.M.H. Behan and D.F. Horrobin, A placebo-controlled trial of n-3, n-6, essential fatty acids in the treatment of postviral fatigue syndrome. Acta. Neurol. Scand. 82 (1990), pp. 209–216" and "G. Warren, M. McKendrick and M. Peet, The role of essential fatty acids in chronic fatigue syndrome: a case-controlled study of red-cell membrane essential fatty acids (EFA) and a placebo-controlled treatment study with high dose of EFA. Acta. Neurol. Scand. 99 (1999), pp. 112–116" so I don't know what you are referring to (Horrobin worked with Behan & Behan so it seems to me that the Horrobin trial is the Behan trial). Can you please provide the reference? JamesStewart7 (talk) 05:08, 15 January 2008 (UTC)

The relevant references are; Behan trial PMID 2270749, Horobin trial, Chapter in ISBN 0471928461, Warren trial PMID 10071170.

The review in The Journal of Chronic fatigue Syndrome that ties all 3 studies together is here the fact that other reviews have missed the Horrobin trial is not relevant. The Puri paper review is relevant because it concludes “suggest that this n-3 highly unsaturated fatty acid may offer the hope of effective treatment for at least some patients with chronic fatigue syndrome.” In doing so it identifies that n-3 fatty acids alone may be effective but also it identifies that EFA treatment is relevant for subgroups, and some comments should thus differemtiate subgroup trials in the Article. To do so the edits with previous consensus (as outlined above) should be reinstated, and extended thus:

"A study was conducted by Behan and Horribin in 1990 using high doses of supplemental essential fatty acids of mixed types. Sixty-three adults with the diagnosis of postviral fatigue syndrome were enrolled in a double-blind, placebo-controlled study. After 3 months, 84% of the patients given the supplements had much greater symptom improvement vs. 18% on placebo. Upon testing the supplement group's cellular membrane phospholipids, (feedstock’s) had returned towards normal.[21]"

In 1991 Horrobin reported a double blind placebo controlled study of 70 patients with post viral fatigue syndrome given four capsules of Efamol marine morning and evening for 15 weeks, Of those patients 85% on active treatment vs 17% on placebo showed improvements of the symptoms Patients on active treatment reported fewer episodes of cardiac palpitations and tachycardia. (ISBN 0471928461, plus J of CFS vol11 no 1 2003)

"In 1999 a study endeavored to duplicate the Behans' work with a different subgroup of fifty patients who fulfilled the Oxford Criteria for CFS, and who had negligible differences of pretreatment red-cell membrane (RBC) lipids compared with controls. The study results showed no significant differences between treated and placebo patients, as opposed to the previous study. [23] ". Jagra (talk) 06:58, 15 January 2008 (UTC)

Regarding the Sydney CFS Conference papers including those from the University of Newcastle Australia, the Authors; McGregor N has 18 pubmed papers listed 11 on CFS and others on related topics. Dunstan R has 44 pubmed papers to his name about a third on CFS and related topics. Roberts T has 79 pubmed papers to his name with 9 studies into CFS. Donohoe M has 61 pubmed papers to his name with 4 studies into CFS. Butt H has 19 pubmed papers, with 6 on CFS and related matters. Watkins J has 26 pubmed papers with 3 on CFS. Murdoch R has 3 CFS pubmed papers. Taylor W has 86 pubmed papers one on CFS. Gray J has 8 pubmed entries on immune system 7 on lipids and 2 on CFS. Martinovic A has one pubmed paper on CFS. The Newcastle team is a very experienced academic / scientific team with many published papers in a range of mainstream journals with at least 46 papers mainly controlled studies on CFS between them. I think it could be said that they speak with some credibility and at an international CFS conference with hundreds of medical practitioners, researchers, scientists and academics from Aust, New Zealand, USA, Canada, UK, Sweden, and Belgium, with notable CFS researchers such as Dr Byron Hyde and Dr Charles Lapp as speakers and in attendance. I think it could be said to be an authorative conference. I also note that the abstracts are published on Dr Hyde’s website. Dr Byron Hyde being the medical and scientific editor of the Nightingale Research Foundation and its review The Clinical and Scientific Basis of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome. Dr Charles Lapp being the medical advisor to the CFIDS Association and its Journals. The bonafides and quality of this conference the authors and the studies presented are of a high standard as could be expected at an apex conference and therefore a reliable source for Wikipedia to cite.Jagra (talk) 11:29, 14 January 2008 (UTC)

There are still problems. This is what the conference papers were used to reference.

"In CFS the EFA changes have been associated with findings by researchers at an Australian University of Newcastle of dysregulation of enzyme D6D-desturase activity and then n-6 poly fatty acids changes which were consistent with an inflammatory event in CFS patients and were suggestive of anomalies in essential and non-essential fatty acid homeostasis as well as B-oxidation of fatty acids. Some primary lipid changes in CFS patients were considered related to other potentially non-viral induced changes."
Now regardless of the reliability of these conference papers, I have to ask where were these "findings by researchers at an Australian University of Newcastle" published and why aren't we referencing the journal in which they were published? Now if these findings were not published in a peer-reviewed journal I would have to question the reason for this. Depending on the reason this may severely hurt the reliability of these findings. So can you please explain to me the reason why we are not looking at the peer-reviewed journal article instead of the conference proceeding. This is not a new finding as the conference was in 1998. Also this information is not directly relevant to EFA treatment so why should this information be placed in the treatment section. Furthermore why were the words "considered related" used? Am I to take it they did not actually find this through experimental observation and this is a speculative statement? The term "consistent with" raises similar flags. I'm sure there are far more direct ways to observe inflammation than observing this enzyme activity so why do we have to rely on this rather stretched inference?

The main problem is that when reporting primary research, we have to give descriptive accounts of the experiment only, according to WP:Primary sources yet there are these great interprative leaps required to relate this information back to EFA treatment. Also, I'm sure some of these interpetations are contentious so I doubt this requirement is being fulfilled "the accuracy and applicability of which is easily verifiable by any reasonable, educated person without specialist knowledge" as others may disagree with these interpetations. Personally I'm highly skeptical of the applicability of these findings to a viral etiology of CFS (which is implied above). JamesStewart7 (talk) 05:08, 15 January 2008 (UTC)

It is not for me or you to second guess the reasons why they chose the CFS conference to publish their work? I could think of any number of reasons, that does not impact upon their works credibily, for instance maybe that satisfied their academic contracts? The fact is that they have been published there. The information is relevant as explained in the original edit, as it was speculated at the time of the Behan and Horobin works that the D6D was the explanation for the findings.

Horrobin DF (1990). "Post-viral fatigue syndrome, viral infections in atopic eczema, and essential fatty acids". Med. Hypotheses. 32 (3): 211–7. PMID 2204789. }{cite book | author = Nightingale Research Foundation; Goldstein, Jay E.; Byron M. Hyde | title = The Clinical and scientific basis of myalgic encephalomyelitis/chronic fatigue syndrome | publisher = Nightingale Research Foundation | location = Ogdensburg, N.Y | year = 1992 | pages =628-633 | isbn = 0-9695662-0-4 | oclc = | doi = }}

Further more the work seems to have been reviewd in a more recent paper PMID 16935966 and as this explains, the faulty D6D is a rationale for such treatments in CFS. “A potential therapeutic avenue could be offered by bypassing the inhibition of the enzyme delta-6-desaturase by treatment with virgin cold-pressed non-raffinated evening primrose oil, which would supply gamma-linolenic acid and lipophilic pentacyclic triterpenes, and with eicosapentaenoic acid. The gamma-linolenic acid can readily be converted into dihomo-gamma-linolenic acid and thence arachidonic acid,” The interpretive links are also here.

As you said yourself (science commonly uses words like "suggest", "indicate" even when there is lots of evidence). 7th. Jan. and this is not any different to the use of words you point out. The findings in the papers included “The increase in the plasma lipid concentrations in the CFS patients was associated with dysregulation of D6-desaturase activity and the n-6 polyunsaturated fatty acids, which were consistent with an inflammatory mediated event in the CFS patients.” From another paper “Although the patient's viral infective history and subsequent post-viral modifications may play some role in determining the onset and progression of CFS, the primary lipid changes in CFS patients were related to other potentially non-virally-induced lipid changes” and from another “The characteristics assessed in the 5 CFS profiles were suggestive of anomalies in cholesterol, saturated fatty acid and n-6 fatty acid homeostasis, as well as b-oxidation of fatty acids. This study demonstrates a high degree of heterogeneity in the lipid homeostasis of patients who comply with the CFS definition. The differences in lipid homeostasis may have arisen from combinations of underlying genetic, dietary, immunological, environmental or pathogen altered responses” from another “These cytokine associated lipid changes, as well as changes associated with EBNA and EBV IgG, were not associated with the lipid alterations differentiating CFS patients from control subjects reported previously.” I do not think that their findings indicate only a viral etiology ? And given the edit contained these words close to the above wording ‘Some primary lipid changes in CFS patients were considered related to other potentially non-viral induced changes." I do not know how you arrived at that conclusion? The wording in the diff you mention was close to these but i am open to wording changes.Jagra (talk) 08:21, 15 January 2008 (UTC)

With regards to the papers I cited from Maes M in Neuro Endocrinol Lett this author has 54 pubmed papers on the immune system, 34 pubmed papers on lipids, and 10 pubmed papers on CFS PMID 16380690 has four citations and PMID 17159817 in the short time since publication has two citations in major reviews of CFS. This author is authorative on the subject. The cited papers will support edits concerning the findings of depletions of n-3 fatty acids with altered immune responses, and the association between lipid peroxidation, oxidative stress and altered immune responses in CFS. Certainly would support the statement “Others studies subsequently found similar substrate depletions concerning omega-6 and omega-3 essential fatty acids” I have added the reference and altered the words accordingly.Jagra (talk) 03:30, 16 January 2008 (UTC)

Despite your disparaging comments on the founder and editor of Med Hyptheses . “David Horrobin founded the journals 'Medical Hypotheses' and 'Prostaglandins, Leukotrienes and Essential Fatty Acids' presently a leading journal in the phospholipid world. The original Editorial Board of Medical Hypotheses comprised: the double Nobel Laureate Linus Pauling, the Nobel Laureate Sir Macfarlane Burnet, the philosopher Sir Karl Popper, the Nobel Laureate in physiology Sir John Eccles and the physiologist A.C. Guyton. Among others its present board includes Antonio Damasio and the Nobel Laureate Arvid Carlsson. Horrobin published more than 800 papers.” Prof David Horrobin was, a renowned authority on essential fatty acid metabolism (if not until his death the renowned authority). He co authored the Behan PVFS treatment trial and Prof Horrobin, published a second trial, reveiwed in the ‘J of CFS’ that replicated the Behan trial. Depite your POV comments, Med Hypotheses is subject to peer review [ http://ees.elsevier.com/ymehy/ thus] and in accordance with the Elsevier review System. here The difference being it seems that the review determines whether or not it is published rather than the changes to be made by an editor, the changes get to be made by the Author in a transparent not anon. review process, and I think this is what the founder was infering. In the case of 'Prostaglandins, Leukotrienes and Essential Fatty Acids' this journal is subject to the usual peer review process for all publications under the Elseveir stable here The journal is a peer reveiwed publication,

Regarding the ‘Martinovic paper’, the US National Library of Medicine have catergorised it as a Review paper, was published at a time when the editor was none other than Prof David Horrobin. On a subject he had published in, I am sure it would not escape his keen attention in peer review. Furthermore that paper has been cited some 13 times in the peer reviewed literature and in at least 3 books, these are therefore certainly reliable source for Wikipedia to cite. Some of the citations in other journals and the context include;

“As indicated in the introduction, we would tend to search for diet therapies instead of acid-suppresive medications. Indeed outside the circuit of medical researchers focussing on drugs, much evidence exists in favour of diet therapies. Particular diets or components of diet, appear to have positive effects in the prevention and treatment of many health problems; infectious disease and degenerative diseases including cardiovascular diseases (Erasmus 1995) various cancers (El-Bayoumy 1997: Cummings and Birmingham 1998) the chronic fatigue syndrome (Gray and Martinovic 1994) and autoimmune diseases (Harbige 1996)” PMID 11450808

“The conventional advice for refleif of symptoms includes psychotherapy, physiotherapy, exercise programs, acupuncture or antideppresants. (ref) Dietary programs are being investigated , with evidence to suggest that an essential fatty acid intake must be normalised in the management of ME” (Gray and Martinovic 1994) PMID 9491353

“Dysfunctional changes in fatty acid metabolism have previously been suggested to play a role in chronic fatigue syndrome” (Gray and Martinovic 1994) PMID 10215658

“Abnormalities of fatty acid metabolism have indeed been observed in CFS patients and diets compensating for this may benefit them” (Gray and Martinovic 1994) PMID 10859701

“This last approach was based on the observation that levels of n-6 unsaturated fatty acids were significantly reduced in the (RBC) membranes from patients with CFS. Dietary fatty acid supplementation was shown to normalise their fatty acid pattern and this was associated with clinical improvement” (Behan 1990) (Chilton SA 1996) (Gray and Martinovic 1994) PMID 11388705

“EFA deficiency has been implicated in CFS, both through abnormalities of EFA metabolism (Gray and Martinovic 1994) and through viral and immune induced deficiencies.” (Horrobin 1990) PMID 11461179

A review paper says “Low levels of essential fatty acids (EFAs) appear to be a common finding in chronic fatigue syndrome. (Howard 1992), (Behan 1990) It has been theorized this finding is due to abnormalities in EFA metabolism. Gray and Martinovic found changes in the ratio of biologically active EFA metabolites such as would be expected as an exaggeration of normal physiological response to excessive or prolonged stress. They postulated these changes in EFA metabolites, in turn, could cause the immune, endocrine, and sympathetic nervous system dysfunctions seen in CFS.”(Gray and Martinovic 1994) PMID 10767667 That paper will support similar comments in Wikipedia.Jagra (talk) 03:48, 16 January 2008 (UTC)

Lets make one thing clear. Articles published in Med Hypotheses are not studies. I'm not prepared to include a Med hypothesis papers simply for that reason. I also notice there was a reply on the reliable sources board where it was stated that a Med hypothesis article cannot be used to support more than "One hypothesis is...". There is no reason to include a whole bunch of speculative statements in the treatment section when we have research and reviews in the area. A book chapter may be appropriate if they are reviewing the research but if they are not it should not be included. The other reviews missed the Horrobin trial because apparently Horrobin did not bother to get his work published in a peer-reviewed journal. Assuming the "Martinovic paper" you are referring to is still that uncontrolled case study we originally started with, we still have the problem of lacking a sufficient description of the methodology used in this trial (what you would be required to write for a journal article). It doesn't really matter how well respected Horrobin, Martinovic or anyone else is, all scientists have to go through the same channels no matter how well respected they may be. If you want us to treat their work as a science article we need to see a peer-reviewed report of the study. Until then, it is simply opinion or conjecture. Regrading those 13 citations, most of them are citing a hypothesis, not a study, "have been suggested... may benefit them", which makes sense as the original publication was a hypothesis paper. So the question is, who thinks we should be including hypotheses in this section when we have reviews? Even if you can establish that the source is reliable, we still have the issues that it is a hypothesis paper and a primary source.

I am aware that many of the statements in the article may have been very close to the statements used in the original papers but in some cases, that is a problem in itself. These are primary sources (or secondary sources where someone is citing themself which is basically the same deal) so WP:Primary_sources applies. It states that we must make descriptive statmeents only. The reserachers, however, made some analytic statements and perhaps stretched a few inferences. Such inferences should not be included without a secondary sources (preferablly one which is saying more than "Such and such said this..."), according to wikipedia gudlines.

RE: viral etiology above: Sorry I misread non-viral as viral. Disregard that statement. JamesStewart7 (talk) 06:08, 16 January 2008 (UTC)

"Med Hypotheses are not studies" is a true statement but these articles are normally comprehensive reviews of published material very similar to review papers, and then the authors present their conjectures. Sometimes the conjectures are lengthy and more speculative compared to review articles. Review sections should be treated like reviews, and the conjecture sections treated like any hypothesis. These two reviews Straus Komaroff illustrate my argument, they review the studies and state conjectures; note that they come to opposite conclusions.

The statement above concerning WP:Primary_sources is wrong and does not make sense. WP:PSTS states the editor must not make original claims using the material, not that the source material can not make original claims. "So and so states...." or "Published in Life Magazine in December 1956..." are types of descriptive claims. Then the following material should be faithful to the content of the source. See this diff by Jimbo Wales:

"Any interpretation of primary source material requires a reliable secondary source for that interpretation. To the extent that part of an article relies on a primary source, it should:

• only make descriptive claims about the information found in the primary source, the accuracy and applicability of which is easily verifiable by any reasonable, educated person without specialist knowledge, and
• make no analytic, synthetic, interpretive, explanatory, or evaluative claims about the information found in the primary source."

Ward20 (talk) 08:37, 16 January 2008 (UTC)

In the original article it was placed without attribution so it was not merely descriptive but I see your point. In any case I still see no reason to include primary sources when there are at least 3 reviews (secondary sources). The difference between med hyoptheses and a review paper is med hypotheses are a primary source while a review is secondary. Med hypotheses presents an original hypotheses for future testing while a review sums up the previous research and presents a conclusion based on said research. I still see no case for presenting primary sources in this area, "Wikipedia articles should rely on reliable, published secondary sources. All interpretive claims, analyses, or synthetic claims about primary sources must be referenced to a secondary source, rather than original analysis of the primary-source material by Wikipedia editors." and I forsee weight issues with including conjecture. Should we then include every hypotheses surrounding CFS treatment in the article regardless of evidence? If not, what makes these hypotheses more important than all the other ones? JamesStewart7 (talk) 23:31, 16 January 2008 (UTC)

I understand the reluctance with the weight issues, and agree hypotheses articles carry less weight especially because of the increased speculation in the hypothesis section compared to review articles. Their usefulness is more limited and discretion has to be used. I disagree they are always primary sources as many make very good analysis and correlation of primary sources. They also make interpretive claims, or synthetic claims about primary sources. IMO where they have their place is so an editor does not have to interpret primary sources where reviews are not available, or where other reviews or studies have omitted information or have contradictions. Hypotheses articles should be labeled or attributed as such vs. reviews that offer more limited conclusions or statements about evidence.

By the way, to which three reviews are you referring? Ward20 (talk) 01:55, 17 January 2008 (UTC)

I would say the Carruthers paper, the Winther paper, the Puri papers and Werback to begin with, Jagra (talk) 01:27, 19 January 2008 (UTC)

There is BMJ, Occupational Health and Royal Society of Medicine

Puri BK, has 134 Pubmed papers, 29 lipid papers, 10 on CFS. PMID:15041033 has eight citations and PMID:16935966 has citations in several peer reviewed publications. This is an Authorative author. The cited papers are both Review papers that will support edits concerning D6D alterations and compromised immune responses, therapeutic implications for supplementation, proton neurospectroscopy studies, abnormal brain phospholipid metabolism, substrate depletion of essential fatty acids and altered immune response, The subgroup of the Behan study is described as with PVFS and the Warren study with Oxford Criteria. I note the primary papers are still cited in the current edit and so will retain them in a new one together with Horobin's work.Jagra (talk) 01:27, 19 January 2008 (UTC)

RE: Puri. Previously you stated this "The Puri paper review is relevant because it concludes “suggest that this n-3 highly unsaturated fatty acid may offer the hope of effective treatment for at least some patients with chronic fatigue syndrome." The problem with this statement and the primary reason I do not think that it should be included in the article is that it is very close to speculation (see WP:Crystal). The wording "may offer the hope" is a far cry from just saying the evidence suggests that the treatment is effective. While such statements are not explicitly fobidden by policies such as WP:Crystal, very careful wording will be required if we are to include such statements. Personally, I think the Puri paper is of little worth as the discussion is not very comprehensive but if you can come up with a paraphrase from the Puri review that you would like to see included in the article it will be considered. Even though I have doubts about Puri's scientific judgement, it is a reliable source so statements from the source may be included provided we can present them in a NPOV format and preserve the author's original intentions.

RE: Primary sources. It seems like the main primary sources in the area (the few RCTs that were included in all the reviews) are already included in the article so while I may be open to the inclusion of primary sources when there are only a few studies in the area or for a particularly influential study, I think including the results of low quality studies eg Martinovic (it is low quality because it was not properly controlled) may skew the POV of the article. If someone finds a high qulaity RCT in the area that was not included in the reviews I may change my position. JamesStewart7 (talk) 05:34, 22 January 2008 (UTC)

Reliability issues

JamesStewart7 - you say " I don't actually understand what you want us to include from Journal of Chronic Fatigue (which I still don't accept as a reputable Journal because the peer review is inadequate)". Two problems with this assertion: 1. It's the Journal of Chronic Fatigue SYNDROME- (dropping that words brings you a whole different condition according to WHO ICD-10, does it not?) 2. Because you don't accept this journal as reputable is not relevant. You have failed to provide any satisfactory reasons for this assertion, apart from your opinion that the peer review process is 'inadequate', which is mere POV on your part. Significantly- the Canadian Guidelines were published in that journal- are you therefore claiming that THEY cannot be included on Wikipedia? —Preceding unsigned comment added by 86.31.60.65 (talk) 09:13, 12 January 2008 (UTC)

Well the dropping of that word was unintentional I assure you. The Journal of CFS uses an editorial board peer review process which is not as extensive as other processes, "While it is important to publish in many different peer-reviewed journals, expert reviews take up lengthy periods of time and the lag time between submission and publication can often be up to two years. For that reason, a well-respected expert panel has been drawn together to serve as the Editorial Board, which allows for critical, rapid reviews of basic, clinical, and multidisciplinary work." It is also a non-medline publication. Wikipedia guidlines state that this is a factor in the reliability of the Journal, Wikipedia:Reliable_source_examples#Which_science_journals_are_reputable.3F.

Now that you mention it the Canadian guidlines were derived through a somewhat atypical process, "The National ME/FM Action Network of Canada spearheaded the drive for the development of an expert consensus document for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS)." "The National ME/FM Action Network is a Canadian, registered, non-profit organization dedicated to advancing the recognition and understanding of Myalgic Encephalomyelitis / Chronic Fatigue Syndrome (ME/CFS) and Fibromyalgia Syndrome (FMS) through education, advocacy, support, and research" as opposed to say a medical association. The fact that the association hand picked clinicians makes it worse "The National ME/FM Action Network then approached two clinicians knowledgeable about ME/CFS and experienced in its diagnosis and treatment." "One stipulation was that at least one member of the panel must be nominated by each of the five stakeholder groups of government, universities, clinicians, industry, and advocacy"

Given the inolvement of organisations such as "Health Canada" I am prepared to accept this (and the Journal as a whole) as a RS. I just think other journals are a lot more reliable (I did actually use the term reputable before). Anyway the important question still stands "What content from the Journal of Chronic Fatigue Syndrome" are people suggesting we include? I would also like a quote to support any statements as the Journal's lack of presence on medline prevents me accessing it. JamesStewart7 (talk) 10:28, 12 January 2008 (UTC)

"I just think other journals are a lot more reliable (I did actually use the term reputable before). " Well- with respect- that is your opinion. There are differences in peer review process across the board in research publication per se. That in itself does not make the Journal of Chronic Fatigue Syndrome, or other e journals such as Biomed Central, unreliable or unreputable - even by Wikipedia's standards. One can't reject sources on the amount of time it takes to get a peer reviewer to look at an article, or whether three or four people review the article, for example.

Lack of access is also not a reason to reject sources (implied by your comment about MEDLINE- remember access through MEDLINE is not an endorsement of an article- just that it's accessible, and only to a degree) otherwise all the books cited on Wikipedia would be stricken as not complying with RS- because they cannot be accessed online. Looking at the wide range of sources used on Wikipedia- you have to be careful not to be making arbitrary decisions on what or what does not constitute reliable sources. The complexity of publication of scientific research - not to mention how other media report this- means subjective beliefs in how 'reliable' sources are need to be avoided. This goes for patient advocacy produced sources also. You can't discard patient reports from charity sources, for example, because they've not been peer reviewed. That is not happening elsewhere on Wikipedia.

Your claim about the Canadian Guidelines production process and 'hand-picked clinicians' being 'worse' is also odd, when the peer review process itself has been critiqued for its risk of cherry picking of reviewers, and all research is performed by teams of researchers that come together in all sorts of ways (like a shared committment to the psychiatric paradigm of ME/CFS, for example?). With regard to your comment about medical associations, there is a medical association being investigated in the US on anti-trust breaches presently, so reliability on that score cannot be assumed either. The CG group selection process was at least transparent.

This is a very complex issue, but here there is a danger in OR being committed in the act of deciding, arbitrarily and without clear NPOV reasoning or supporting evidence, that 'this journal (advocating one treatment) is more reliable than the other one (advocating another treatment) so we'll discard the other one' - and the Canadian Guidelines are a case in point. Are you REALLY claiming that the involvement of Health Canada is the only reason to keep the Canadian Guidelines on this page, and that the Canadian Guidelines are not reliable enough to be on Wikipedia otherwise?

I already said I will accept the Journal of Chronic Fatigue Synrome is a sufficienlty reliable source so I don't see why you are pushing the point. I did not reject the source based on lack of access. I stated that because of lack of access a supporting quote would be appreciated to aid in verification. Patient advocacy produced sources are not reliable sources of scientific information (I'm talking about patient advocacy in the treatment section here, not the Canadian guidlines - the Canadian guidlines were produced by more than just patient advocates). They are sources of opinons only. Elsewhere on wikipedia, the opinions of patient groups are not mixed in with study results. All I am asking for, in regards to this, is for these things to go in seperate sections.

You still haven't stated what you wish to include from the Journal of Chronic Fatigue Syndrome or drawn any quotes from it so I am still unaware of how the Journal of Chronic Fatigue Syndrome is "advocating another treatment". As far as the Canadian Guidlines go, if Health Canada was not involved they probably would not be called the Canadian Guidelines so it is difficult to answer that question. JamesStewart7 (talk) 11:36, 12 January 2008 (UTC)

I'm pushing the point because it needs to be pushed. An awful lot of problematic claims are being made on this page about reliable sources, scientific authority etc. which need clarifying at the very least.

I haven't got a wish to include other quotes from the Journal of Chronic Fatigue Syndrome- but others might. I'm establishing that there are problems in how certain sources are being implied as 'unreliable' or 'disreputable' (even if unintentionally).

With regard to patient advocacy reports - all over Wikipedia there are sources that are not 'scientific', and there are also opinions given the status of reliable source. How else can you discuss movie reviews, for example? Patient advocacy sources are reliable sources for indicating patient objections to treatment: they are not claiming to be scientific in the first place. But they still may need to be included in an accurate NPOV summary of a situation. the so-called SPOV is not the only consideration here, or indeed on pages about other conditions. —Preceding unsigned comment added by 86.31.60.65 (talk) 11:59, 12 January 2008 (UTC)

As previously stated, the opions of patient advocacy groups may be included as long as the juxtaposition in the article does not make it appear to be scientific. I guess that is more of a NPOV issue than a RS issue and I apologise for any confusion for any misuse of terms. My objection is to where statements like this are placed "In the "25% ME Group Submission to Gibson"[184] they state that both CBT and GET are not only just unhelpful to many severely affected CFS patients but also dangerous/harmful". I understand the need to include all viewpoints but the placement of this quote makes it appear like the statement that CBT/GET is dangerous/harmful is based on scientific evidence. So regardless of whether or not the sources claim to be scientific, it still appears that way in the article. JamesStewart7 (talk) 12:22, 12 January 2008 (UTC)

Well- there is actually some scientific evidence about GET being potentially harmful, though as is the case throughout all discourses on Wikipedia about this illness, one could go on for hours about whether the sources constitute 'reliable scientific evidence', or synthesis, or Original Research, or whether it's accessible by MEDLINE, and indeed this all may need to be thrashed out at some point.

Is a report based on patient self-reports 'scientific'? Well- in much psychiatric literature on this illness it is apparently considered so! Objective clinical or laboratory evidence is conspicous by its absence in the claims about the efficacy of CBT/GET, for example, but there's wall-to-wall patient self-reports. However, the issue here is merely to report what the 25 % Group has claimed. I think your worries about whether the 25% Group's report appears unduly 'scientific' is unnecessary, especially in the context of CBT/GET claims of efficacy and the flaws in evidence these are based upon. The 25 % Group's report has been submitted to various official agencies I understand also. It's a reliable source of a certain claim being made, whatever your opinion of its veracity as 'scientific evidence'.

But the problem is- it is not your- or my- remit to decide whether CBT/GET is flawed 'science' for the purposes of a Wikipedia entry any more than you can decide whether a patient avocacy group report is 'scientific' enough. But all that is needed is to show that some scientists claim this, others claim that, some clinicians claims this, some patient advocacy organisations claim that. Give a good longish list of external sites for people to look at if they want to investigate further and maintain an NPOV. This would solve an awful lot of problems on this particular page. —Preceding unsigned comment added by 86.31.60.65 (talk) 13:01, 12 January 2008 (UTC)

A report based on patient self-report is considered scieentific when you use reliable and valid measures to gather that report, you conduct your survey on a representative sample and you report such things as response rates. The 25% ME group did none of those things so how do we know they didn't push poll. Given the 25% ME group's mission statement and the fact that they conducted the survey, I think it needs to be clearly stated who they are. A pyschiatrist is also not going to use a patient report as the final decider of whether a treatment is safe or effective. Once control studies are available they will use those to base their decision on. It's a reliable source of a claim, yes but it does not meet the standard for scientific evidence. Also, I think as far as wikipedia is concerned, if it is not published in a peer-reviewed journal, it is not scientific evidence. JamesStewart7 (talk) 23:29, 12 January 2008 (UTC)

I agree with 86.31.60.65 about the 25% ME Group survey being a "reliable source of a certain claim being made". Furthermore, this doesn't directly contradict or compete with the available GET studies, simply because none of these studies were conducted on severely affected patients, which is actually noted by the systematic review mentioned in the article. The most severely affected patients probably don't represent the rest of the CFS spectrum, but they aren't distinguished in diagnosis and have the most cause for concern about GET. There may be little or no evidence published in scientific journals that GET causes adverse effects for the mildly to moderately affected patients, but it's still just speculation that GET is "safe and effective" for the severely affected patient group. Until proper research is done, I think the survey remains a notable caveat, and it wasn't the only reason why the authors of the Gibson Report expressed concern about the lack of cautions on GET. All the article really needs to state is that scientific research still needs to be done for the severely affected patients and a patient group survey suggests caution should be advised because ... <insert the details of the survey>. Also note that "severe" is a rather flexible term; to some it means completely housebound or even bedbound, while in a study I've read about CFS in adolescents it was measured as "attending school for less than 50% of the time", which is a considerable difference. - Tekaphor (talk) 13:59, 12 January 2008 (UTC)

Totally agree with the following statement:

• "But all that is needed is to show that some scientists claim this, others claim that, some clinicians claims this, some patient advocacy organizations claim that. Give a good longish list of external sites for people to look at if they want to investigate further and maintain an NPOV. This would solve an awful lot of problems on this particular page."

Right now the article needs attribution, attribution, and attribution. Then clean up of peacock terms, weasel words, and non V content. Later edits can debate the fine points. IMO, based on where the article is at this point in time, editors sorting and selecting what articles and what RS are more reliable than another to give certain weight to advance a POV will cause the article to not improve. Ward20 (talk) 23:03, 12 January 2008 (UTC)

Completely agreed, if it was noted that the 25% ME Group was a patient advocacy group within the article and it was clear that the entire sentence was just a statement, many of my concerns would go away. "In the "25% ME Group Submission to Gibson"[186] they state that both CBT and GET are not only just unhelpful to many severely affected CFS patients but also dangerous/harmful." The word state is used at the start of the sentence but as they are making more than one claim in the sentence and because their claim is prefixed with "not only" it makes it seem like a large amount of the sentence is fact. Therefore, I am changing it to "The "25% ME Group Submission to Gibson"[186] state, in their submission to the Gibson report, that both CBT and GET are unhelpful and dangerous/harmful to severely affected CFS patients." Brief information about the 25% ME group, from their website, should probably be included somewhere as well. JamesStewart7 (talk) 23:29, 12 January 2008 (UTC)

Actually that's NPOV, but poor grammar. It should read ""The "25% ME Group" state, in their submission to the Gibson report[186], that both CBT and GET are unhelpful and dangerous/harmful to severely affected CFS patients." —Preceding unsigned comment added by JamesStewart7 (talk • contribs) 23:31, 12 January 2008 (UTC)

If it is not in the article already I propose the words (or something similar), "The "25% ME Group", a UK advocacy support group for severely affected M.E. sufferers state,...." Another issue I would like to discuss is that attribution to the location of these terms/events/groups is appropriate. Ward20 (talk) 23:59, 12 January 2008 (UTC)Ward20 (talk) 00:09, 13 January 2008 (UTC)

Incorrect assertion about the Canadian Guidelines

This text on the page is incorrect:

Other systems

Other scoring systems have also been proposed to quantify CFS symptoms for research purposes. These include:

• Holmes et al (1988) scoring system. Also sometimes called "CDC 1988," to distinguish from the newer CDC system.
• Oxford criteria (1991)
• Carruthers et al (2003) Canadian Case definition for ME/CFS
• Australian Guidelines (2004)

The Canadian Guidelines (Carruthers et al) are not 'scoring systems to quantify CFS symptoms for research purposes.' They are clinical diagnostic criteria and management guidelines. If anything, Fukuda is a research purpose system- which was not designed for clinical use (Evidence on this is in both articles). This section (and the preceding ones)need re-writing in light of this.

edit

Did Ramsey use the term CFS? Ward20 (talk) 00:16, 13 January 2008 (UTC)

Good question. I'll change CFS to "Post-viral fatigue syndrome" for now until someone can confirm or deny this as that term is present in the title. I inferred CFS from the context of the article. All I really want is some form of attribution here. I'm not fussed over which term is used. JamesStewart7 (talk) 02:14, 13 January 2008 (UTC)

Ramsay used the term Myalgic Encephalomyelitis. However, in Hyde (1992), some authors used the new term CFS. Guido den Broeder (talk) 08:37, 14 January 2008 (UTC)

I have a problem with this sentence: "In over 50 documented cases, such as the Royal Free Hospital incident, several people in a building or large numbers of people in a community came down with the disease essentially simultaneously, suggesting the involvement of infectious agents"
and I'd like for Guido (since he changed it) or anyone else to explain to me why this is the wording used. Firstly "over 50" is problematic. Statments should not be this vague. I want a precise number. If there is no precise number given I really have to question how well documented these cases are. Secondly "the disease" is problematic. As several people have said Royal Free Disease is mass hysteria we cannot just call it the disease (referring to CFS). We must say whoever called it the disease. Attribution is essential. Thirdly "suggesting the involvement of infectious agents" needs to be attributed. There are other reasons a large number of people would come down with a disease at once (mass hysteria, toxins in the area, etc etc) so this suggestion is just one person's interpretation, hence it needs attribution. I'm changing it to "In over 50 documented cases, such as the Royal Free Hospital incident, several people in a building or large numbers of people in a community have, essentially simulatiously, came down with a disease which Ramsay states is Myalagic Encephalomyelitis. Ramsay states that this suggests the involvement of infectious agents"
If anyone else said this, feel free to add names, but I don't want to see it changed to a POV version again without some explanation. JamesStewart7 (talk)

The wording 'over 50 cases' is used by both sources. The exact number today is not known to me. The outbreaks did not stop in 1992 but there is no recent overview.

Attribution is correctly to the ME/CFS experts at large, as Ramsay and Hyde report, it's not just their personal opinion. The 'mass hysteria' supporters are the exception and did not provide any evidence. I suggest that you read the sources, you will learn a lot. Ramsay is a review, Hyde a collection of 76 articles.Guido den Broeder (talk) 09:30, 15 January 2008 (UTC)

POV changes

This reference "Wood B, Wessely S (1999) Personality and social attitudes in chronic fatigue syndrome. J Psychosom Res Oct;47(4):385-97" was removed form this statement "A lack of information and awareness has led to many patients being stigmatized, sometimes as hypochondriac or lazy, yet at other times as over-active and perfectionistic. and the statement has been changed. That reference is a psychological journal article on the personality factors that predict CFS. "Perfectionism" is a psychological construct that is well defined. This article should actually be placed in the risk factors section. Anyway the article was removed the article did not state that saying that CFS patients are high in perfectionism is stigmatization so it does not support the reference and to include it here is really to make an OR interpretation.

The sentence has been replaced with "A lack of information and awareness has led to many patients to feel stigmatized" as "feel stigmatized" is both more NPOV and was used in the original article. The article is also self-report so it reports is patient perceptions making "feel" most appropriate. Also if anyone disputes this change , please do not just revert the whole edit as other changes are being made. I'll detail a few here and the reasons

"Later" was removed as it implies the following statement is more current and perhaps more accurate than the former.
"Although" appears on WP:Words to avoid - you can read the explanation there.
Disorder was changed to outbreaks where the statment was given. The referenced article and the psychiatrist comments seems to be primarily about specific outbreaks of disease that have been likened to CFS, not the disorder in general. This "have now recognized CFS as a serious illness" was removed not because I doubt that this is the case, but because "serious" is a relative term and a matter of opinion and wikipedia policy says Let the facts speak for themselves. I believe presenting the symptoms and prognosis is enough and the reader may infer that the disease is serious from that.

The POV tag is there because much more needs to be done. Particularly there are a lot of other diseases mentioned in the section which have been linked with CFS without attribution or reference. There are also several references to "the disorder" where it is unclear whether the disorder is CFS, poliomyelitis or something else. CFS is implied but that does not seem to be the term the references use.

I added a synthesis tag because of statments like this. "Autopsy findings, both on monkeys[248] and on the rare human casualties[249], led to the conclusion that the disorder was caused by inflammation of the brain and the spinal cord, particularly the afferent nerve roots[250], and in 1956 it was named accordingly as myalgic encephalomyelitis, reflecting a presumed neuroimmune etiology." "The disorder" actually seems to be poliomyelitis in the reference but in the article it could just as easily be taken to mean CFS. Now as The Lancet article was published before two of the other references (the third lacks a date) I can be sure that these statments are unrelated but the article makes it seem like these previous studies lead to this term when this could not possibly have occured.

The section does this again with Raggedy Ann, "An outbreak at Incline Village, Lake Tahoe, Nevada, United States in the mid-1980s, gained initially local (and later national) attention for the characteristic loss of muscle power or muscle fatiguability characteristic of ME, as "Raggedy Ann Syndrome".[253] Researchers now attached a different kind of name to the phenomenon: chronic fatigue syndrome, involving some of the symptoms rather than disease taxonomy." but no reference is given this time. The second sentence was moved to the talk (above) for this reason but the first still remains. It's current inclusion in the article imples that Raggedy Ann Syndrome is somehow linked with CFS but there is no attribution for this. JamesStewart7 (talk) 05:47, 13 January 2008 (UTC)

See if this edit resolved some of the issues discussed in last paragraph above. Still other issues there. Ward20 (talk) 05:51, 14 January 2008 (UTC)

Sometimes, events take place in a certain order, but get published in a different order. By reading the referenced material you will find this. Guido den Broeder (talk) 10:09, 14 January 2008 (UTC)

Dont know whether this helps but the first paper by Dr B Hyde discusses hereJagra (talk) 11:52, 14 January 2008 (UTC)

The Psychoneuroimmunological interactions section has been reworded and non-relevant sources removed. What specific objections are there to it at this time so we know when the tag can be removed. Ward20 (talk) 06:10, 15 January 2008 (UTC)

The reference for this statment doesn't seem to be directly relevant to CFS "A 2006 review published in Current neurovascular research states that there is growing evidence of autoantibodies to neuronal or endothelial (interior surface of blood vessels) targets in psychiatric disorders and hypothesizes how autoantibodies can play a role in the psychiatric disorders present in CFS." It seems to be about psychiatric disorders in general. This statement, "Elevated levels of nitric oxide (not to be confused with nitrous oxide) has been found in some CFS patients[103] and may help explain a "sensitization" of the nervous system that results in behavioral changes" is not properly framed as a hypothesis. The source is med hypothesis so "may explain..." should be changed to "One hypothesis is that this change results in a sensitization" of the nervous system that results in behavioral changes". JamesStewart7 (talk) 05:29, 17 January 2008 (UTC)

I read a bit more into that first source and it does seem to refer to CFS specifically and I altered the other source as I stated above so I am going to remove the tag. JamesStewart7 (talk) 06:19, 17 January 2008 (UTC)

Thanks! Ward20 (talk) 07:39, 17 January 2008 (UTC)

Vast majority

• The vast majority of international ME/CFS specialists support the classification of CFS as a physical condition.

People, please stop removing the above text from the 'controversy' section, because you are thereby unbalancing the text. The references include reports on (usually unanimous) consensus reached on the various world conferences of a.o. by far the largest association of scientists and clinicians in this field. This has been discussed before on this same talk page. Guido den Broeder (talk) 15:49, 14 January 2008 (UTC)

Saying "the vast majority" is simply POV. Previously the article said "the majority of doctors believe that CFS is psychosomatic", but that was removed too because there was no actual evidence that the majority of doctors believe CFS to be psychosomatic. This is the same. Unless you can show a survey showing the most researchers believe CFS is physical, it is better to remove it. Just because a conference says something, it doesn't mean it reflects of the majority of researchers. Many researchers don't go to these conferences anyway because the conferences are biased to an organic etiology and they would not be welcome if they do no share this view. --Sciencewatcher (talk) 16:22, 14 January 2008 (UTC)

Perhaps the sentence could be modified to reflect the references. - Tekaphor (talk) 02:55, 15 January 2008 (UTC)

Well Gudio, consenus changes (see WP:Consensus) and claims of consensus must be sourced. WP guidlines say so Wikipedia:RS#Claims_of_consensus. If there is an agreement withing some organisation state "X organisation states that CFS is a physical condition." Btw I think people have created a false dichotomy between psychological/physical and I would like to point out something can be both physiological and psychological. The brain is part of physiology and everything that is psychological is simultaneously biological (changing mental states correspond to changes in the brain). So I have to object to any use of the words organic/physical/physiological to mean "not psychological". The current version of the Diagnostic_and_Statistical_Manual_of_Mental_Disorders actually reflects this (I think this change occured with the introduction of DSM-IV but I could be wrong about the timing). JamesStewart7 (talk) 05:32, 15 January 2008 (UTC)

I provided the sources. I did not gave them for the personal opinions of the authors, but because they report about the general opinion. We are not talking about 'some organization' here, but about the single large international organization IACFS/ME that has all the leading experts as members, and their world congresses. However, I will follow Tekaphor's suggestion. Guido den Broeder (talk) 09:03, 15 January 2008 (UTC)

I don't recall seeing Simon Wessely or Peter White at this latest conference, and they are the main experts in the UK. As I said, not all experts go to this conference. Also, your reference does not mention anything about CFS being a physical condition. And "vast majority" is still hugely POV. Hence I am removing it again. --Sciencewatcher (talk) 15:42, 15 January 2008 (UTC)

Without Oxford it would be nigh unanimous. Experts elsewhere in the UK are a.o. Ramsay, Behan, Kerr, Gow. Guido den Broeder (talk) 20:40, 15 January 2008 (UTC)

How many physicians with actual clinical experience of "ME patients" were at the meeting which decided the CDC criteria for CFS and therefore the next 20 years of research? By comparison to the answer of this question, the absence of Wessely and White from these international CFS/ME conferences is hardly a cause for weight concerns, and it's unfortunate if they feel unwelcome because of the apparent backlash against their earlier hypotheses or statements. Besides, behavioural interventions were indeed discussed at the last conference by other researchers and as far as I know they weren't shunned or ridiculed out the door. Perhaps the edit war could be resolved if Guido expanded the sentence by naming the experts involved and directly quoting the comments they made. - Tekaphor (talk) 02:31, 16 January 2008 (UTC)

Note that in 1994, Wessely & co were still attending the conferences, and their view had some influence on the change in criteria from Holmes to Fukuda, but far from enough to satisfy them. Guido den Broeder (talk) 09:15, 17 January 2008 (UTC)

POV Pushing

Guido is up to his old tricks again. He has just reverted two legitimate edits and accused me of POV pushing. Do we have to have another ridiculous edit war or can we just do the sensible thing and get him banned? Temporarily blocking him in the past hasn't worked. --Sciencewatcher (talk) 15:53, 15 January 2008 (UTC)

I have issued a 3RR warning to User:Sciencewatcher. Guido den Broeder (talk) 18:06, 15 January 2008 (UTC)

And I've issued one to you, although it seems you're quite familiar with them. Please resolve your disputes here. Cool Hand Luke 18:15, 15 January 2008 (UTC)

You have reverted a whole lot of edits, some disputed and some not, in one go. Please undo and split, so that we won't be forced to spend hours of re-editing by hand later. And drop the personal attacks. Guido den Broeder (talk) 18:18, 15 January 2008 (UTC)

Anyone is free to undo my edit (although you'd probably be over the limit). A single revert is unlikely to save hours of editing in an edit war. Take it as a signal that you should start using the talk page. Cool Hand Luke 18:29, 15 January 2008 (UTC)

That won't do. I have used the talk page, whereas you have not. Second, the fact hat someone can undo your edit is not an excuse. You will need to do it yourself, now that you are aware of the problem you have created, or it will probably be considered vandalism. Guido den Broeder (talk) 18:36, 15 January 2008 (UTC)

You wrote in your edit summary: "The stylistic changes aren't improvements, and calling them "outbreaks" rather pushes a POV".

• These are not stylistic changes, but fundamental ones. The article did not properly present the Fukuda criteria.
• Outbreak is the official term and is used in the references. It has been in the article since ages. Cluster is not the same. You did not comment on the other edits that you also reverted in that one revert. Guido den Broeder (talk) 18:42, 15 January 2008 (UTC)

I don't see a problem with my edit, but I'm glad you're using the talk page (only after your daily reverts were exhausted). Be mindful that viewing three reverts as an entitlement is liable to get you blocked. At any rate, read WP:VANDALISM. Edit warriors always call each other vandals, but they never are, and calling your opponent a vandal certainly doesn't except you from the 3RR, in case you erroneously believed otherwise. Good luck with the article. Cool Hand Luke 18:46, 15 January 2008 (UTC)

No, I used the talk page long before the first revert.

No, I have not called you a vandal. I commented on your edit, not on you.

Vandalism includes Reverting legitimate edits with the intent of hindering the improvement of pages and Adding known inaccuracies both of which seem part of your massive edit.

Finally, please let us hear your arguments for making this edit.

Guido den Broeder (talk) 19:00, 15 January 2008 (UTC)

Frankly, it's because you seem to be gaming the 3RR, and I think you should stop editing without discussion. I see you haven't stopped, however, confirming my suspicion that this is a pointless and sterile edit war. Cool Hand Luke 19:51, 15 January 2008 (UTC)

Still waiting for arguments. This talk page belongs to the article, remember? If you have issues with a user, take it elsewhere. Guido den Broeder (talk) 19:52, 15 January 2008 (UTC)

Seeing as the article is 164K, perhaps you should explain why the diagnostic guidelines are needed? Cool Hand Luke 19:56, 15 January 2008 (UTC)

I guess because the user who put them there thought that the reader would like to know since they are mentioned so often. Putting them on a separate page would be fine with me though. Guido den Broeder (talk) 20:09, 15 January 2008 (UTC)

If there are independent sources covering to satisfy WP:N (and there probably are), that would be fine with me too. Thanks for the RfC. Cool Hand Luke 20:20, 15 January 2008 (UTC)

There are roughly 2,000 scientific studies using these criteria. Guido den Broeder (talk) 20:30, 15 January 2008 (UTC)

Well wouldn't it have been better to have inserted a mention about the CDC criteria instead of just reverting the edit entirely. All of your edits seem to go back to a wording like this "In over 50 documented cases, such as the Royal Free Hospital incident, several people in a building or large numbers of people in a community came down with the disease essentially simultaneously, suggesting the involvement of infectious agents." You must realise that this is a POV statement; "Attribution is correctly to the ME/CFS experts at large, as Ramsay and Hyde report, it's not just their personal opinion. The 'mass hysteria' supporters are the exception and did not provide any evidence" Why are Ramsay and Hyde the "experts at large" while those mass hysteria supporters (and I understand there are quite a few) are just "the exception and did not provide any evidence". I'm not seeing these mounds of evidence to show that there was a viral cause (in fact I'm not sure the documentation on a lot of cases all that great to begin with). However, there is actually a CDC study (which I posted) examining one "outbreak" of CFS where no cluster could be confirmed. This means in at least some cases, outbreaks of CFS may be falsely reported. Of course we can't generalise this to all cases but I think there is a certain burden of proof on anyone claiming that there was an outbreak of CFS. You need to either prove it (and establish consensus as to the factual accuracy of this claim or better yet, source this consensus with a RS) or treat it as an opinion. JamesStewart7 (talk) 06:24, 16 January 2008 (UTC)

Hyde and Ramsay are lead experts because they have conducted decades of research, publish(ed) important findings, and are recognized as experts by their collegues who refer to them a lot. In contrast, the mass hysteria supporters (now extinct) all taken together published exactly one article, where they made their assertion without ever seeing a patient.

Of course, false reports of outbreaks do occur, as with any disease. The burden of proof is not on me, however, but on the authors, and they, fully aware of this burden, supply it abundantly and meticulously in their reviews (which do not include this one false report IIRC). Guido den Broeder (talk) 19:45, 16 January 2008 (UTC)

You mean the mass hysteria supporters for the Royal Free incident are exctinct? That makes sense as the event is rather unimportant if it is simply mass hysteria so there is really no reason to continue writing about it. Anyway if there is so much evidence how about you point to one verified outbreak of CFS where independent evaluators conducted a proper study and confirmed that it is CFS. All it will take to convince me is just one well constructed study. JamesStewart7 (talk) 05:56, 17 January 2008 (UTC)

There was written plenty about it, only not by any supporters.

The Royal Free Hospital is an outbreak which IMHO stands out by the quality of the research conducted, but there are many others (e.g. Gilliam, Pellew, Bell, Peterson). Independent evaluators are Ramsay 1986 (except for Royal Free where he was the primary investigator) and Hyde 1992 (including a.o. Acheson and Holmes), as referenced. Guido den Broeder (talk) 09:07, 17 January 2008 (UTC)

Outbreaks

(RFC) User:Sciencewatcher is of the opinion that outbreaks of CFS do not occur and wishes to banish the word from the article.[7] User:Guido den Broeder opposes this resolve by pointing at the references that document dozens of outbreaks, using the very term. Guido den Broeder (talk) 20:04, 15 January 2008 (UTC)

Nice to see you're talking to me again. Let's have a discussion rather than another edit war. There is no evidence that they occur, and the CDC states that there have been no outbreaks. Articles are using the term "outbreak" when they actually mean "cluster". --Sciencewatcher (talk) 20:32, 15 January 2008 (UTC)

The evidence is pesented in the referenced reviews.

Link to this CDC statement please.

Your assertion of 'what they really mean' seems irrelevant. Surely these experts know what an outbreak is, and they report them from start to finish in their evidence. Guido den Broeder (talk) 21:35, 15 January 2008 (UTC)

The problem I see here is that text is being replaced with other text rather than adding to it. It should just be noted that some experts believe that there were "outbreaks of ME", while the CDC state there is no evidence that CFS is contagious, although the CDC criteria for "CFS" supposedly includes all "ME" patients. If I remember correctly, the experts who claimed ME occurred in outbreaks didn't actually claim the illness itself was contagious (transferrable from person to person) once acquired, so the question that remains is what caused the illness. The CDC states[8] that none of the research applies anyway because the CDC criteria wasn't used; I find this somewhat dismissive considering that the CDC criteria supposedly replaces and includes the older ME description which captured the illness from these "clusters". Perhaps patients who fit other CFS criteria should just ignore all research that involves the CDC criteria simply because the other criteria which fit them better wasn't used? Taking it even further, perhaps it's improbable that CFS could have anything to do with neurasthenia simply because Beard didn't have access to the CFS criteria in the 19th century, so we better remove all mention of neurasthenia from the CFS article then and possibly start another edit war! (note sarcasm). As for the argument about outbreak vs cluster, the CDC defined outbreak as a "well-defined cluster". - Tekaphor (talk) 02:03, 16 January 2008 (UTC)

Tekaphor that is pretty much what I attempted to do but it was reverted by Guido den Broeder. I used "Ramsay states..." Diff here [9]. JamesStewart7 (talk) 08:01, 16 January 2008 (UTC)

I changed that, because you wrongly attribute the conclusion to Ramsay. Ramsay quotes the conclusions of other reseachers (in addition to his own). In addition, Hyde gives an updated review of which Ramsay is not the author.

With regard to the CDC: this is a text of 2005, and they have changed their position considerably in 2006. Their website is not updated often and contains many obsolete texts. Nonetheless, it can be referenced now that we have a link. Guido den Broeder (talk) 09:31, 16 January 2008 (UTC)

Well you could have said that I wrongly attributed it before instead of just reverting it. Ramsay states the conclusion so it is still his opinion, but like I said, just add the other authors names to the list instead of removing the attribution entirely. JamesStewart7 (talk) 12:13, 16 January 2008 (UTC)

Not a good idea, to add some 40 names. I suggest that we do what is normally done and refer to the review, that quotes these persons' conclusions (often literally). Guido den Broeder (talk) 15:40, 16 January 2008 (UTC)

Is there some organisation we can attribute it to then? JamesStewart7 (talk) 23:35, 16 January 2008 (UTC)

Hyde 1992 consists mainly of the proceedings of the initial conference of the IACFS/ME, and a number of these authors became members, but others were no longer alive or active at the time. Guido den Broeder (talk) 09:23, 17 January 2008 (UTC)

If you want to add to the section, feel free, but make sure it is NPOV. The previous text was not NPOV because it stated that CFS occurs in outbreaks, hence the reason I just deleted it. The reality is that there have never been any confirmed outbreaks. All the evidence suggests that CFS itself is not infectious (although the triggering infection, when there is one, is obviously infectious). --Sciencewatcher (talk) 03:17, 16 January 2008 (UTC)

CFS itself does not have to be contagious to get an outbreak. Only the virus that causes CFS needs to be. Guido den Broeder (talk) 09:56, 16 January 2008 (UTC)

Agreed, but you need to make this distinction clear in the article if you are talking about outbreaks because the previous text implied that CFS itself was contagious. And as I have said there is no evidence of actual outbreaks so it would be better to say something like "possible outbreaks" or "clusters", which is more NPOV. --Sciencewatcher (talk) 16:07, 16 January 2008 (UTC)

More possible sources

I agree with Guido's statement that CFS doesn't have to be contagious to be an outbreak, only the triggering virus needs to be. Assuming that ME and CFS are the same, and 10% of people who endure (specific) infections develop CFS, it's hardly surprising that there could have been what appeared to be epidemics of ME, although perhaps there are some limitations to the evidence and this comparison. Whoever assumes that ME and CFS are essentially the same should accept inclusion of any findings relating to ME before CFS took over, as long as the article wording doesn't call it CFS. This historical aspect is what I know least about, so it may take me a while to get fully acquainted with the original material, which I must say is difficult to access. As for more recent material, this is what I have been able to find, surely there are enough references within these sources to adequately attribute specific claims to individual authors:

• "Epidemic myalgic encephalomyelitis" published in the British Medical Journal in 1978 [10] states that "The adjective epidemic is correct, since most cases occur in an epidemic, but the disease may be endemic, and sporadic cases may occur. [10-12]" ( [10] Ramsay, A M, and O'Sullivan, E, Lancet, 1956, 1, 761. ... [11] Jelinek, J E, Lancet, 1956, 2, 494. ... [12] Ramsay, A M, Lancet, 1957, 2, 1196. )
• In a chapter written by Dr Byron Hyde for L. A. Jason, P. A. Fennell and R. R. Taylor for their book Handbook of Chronic Fatigue Syndrome, titled "The Complexities of Diagnosis"[11] it states that "The term myalgic encephalomyelitis was based on clinical descriptions of an illness that has occurred both sporadically among the general population and in clusters, or epidemics, usually in hospitals or schools. Over 60 such epidemics have been described in the medical literature (Acheson, 1992; Henderson & Shelokov, 1992; Hyde, 1992) since Sandy Gilliam, Assistant Surgeon General of the United States and later Dean of Medicine at Johns Hopkins, first described the 1934 epidemic in the Los Angeles County General Hospital (1938). B. Sigurdsson et al. (1950) in Iceland, D. A. Henderson, and A. Shelokov, in the United States (1959a, 1959b); A. Wallis, in 1955, and A. M. Ramsay, in 1988, and John Richardson, in England (1992); and P. Behan, in Scotland (Behan & Behan, 1988; Behan, Behan, & Bell, 1985), have all added to this growing literature. This group of illnesses has been given many names, but these have distilled down to myalgic encephalomyelitis (ME), a term used primarily in the United Kingdom, Canada and Australia."
• (Interestingly), in "The Nightingale, Myalgic Encephalomyelitis (M.E.) Definition" [12] by Dr Byron Hyde, it states: "At one of the meetings held to determine the 1994 U.S. Center for Disease Control (CDC) definition of CFS, in response to my question from the floor, Dr. Keiji Fukuda stated that numerous M.E. epidemics — he cited the Los Angeles County Hospital epidemic of 1934, (Gilliam, A.G.), the Akureyri outbreak of 1947-48 (Sigurdsson, B.) and the 1955-58 Royal Free Hospitals epidemics (Ramsay, A.M.) were definitely not CFS epidemics. Dr. Fukuda was correct."
• PMID 8148446: "Since the first well-described outbreak occurring in 1934, > 60 outbreaks have been reported, but few of these have been described in considerable detail." ... "These outbreaks are usually cited in historical reports of chronic fatigue syndrome (CFS) since each of these outbreaks appears to contain a number of cases meeting the current case definition of CFS. There has been inadequate attention given to the fact that epidemic neuromyasthenia and related clusters characterized by various complaints, including fatigue, do not have an accepted epidemiological or clinical definition, and only rarely have descriptions of these clusters included a specific case definition. When such case definitions have been applied, the occurrence of cases meeting the current case definition for CFS appears to be both variable and infrequent."
• PMID 8491107: "Medical concepts of chronic fatigue since the 1930s have run along four separate lines: (1) 'postinfectious neuromyasthenia', going back to an atypical 'poliomyelitis' epidemic in 1934; (2) 'chronic Epstein-Barr virus' infection, an illness attribution that increased in frequency after the discovery in 1968 that this virus caused mononucleosis; (3) 'myalgic encephalomyelitis', dating from an epidemic at the Royal Free Hospital in London in 1955; and (4) 'fibrositis', or 'fibromyalgia', used as a rheumatological description since the turn of the century." ... "Neurasthenia does not necessarily represent an early forerunner of chronic fatigue. Many patients receiving that diagnosis did not complain of fatigue. Others with functional fatigue did not receive the diagnosis 'neurasthenia'."
• PMID 17561685: "Chronic fatigue syndrome (CFS) is not a new disease. Similar morbidities have been known as different names since past several centuries. For example, neurasthenia, epidemic neuromyasthenia, myalgic encephalomyelitis, Akureyri disease, Royal Free disease, chronic EBV disease, post-viral fatigue syndrome etc. Much of the recent interest in CFS was generated by incidence of infection-like outbreak at Lake Tahoe in Nevada."

How do I interpret all this? (a non-rhetorical question). We are supposed to believe that CFS encompasses ME without any further need to subtype or research ME patients as a distinct group, yet we are to dismiss earlier findings possibly relating to ME because they didn't use CFS criteria? Now I am doubting that "CFS" actually much to do with "ME" other than a presumed similarity. It also isn't clear to me that ME was involved in all those 50+ outbreaks. The statement in the Wikipedia article, that there have been over 50 "reported" outbreaks of ME-like illness, seems common and verifiable. - Tekaphor (talk) 14:25, 16 January 2008 (UTC)

I don't doubt that there have many outbreaks of an ME-like illness. However, an ME-like illness is very different from CFS itself, nor is it ME itself. Someone stating that an ME oubreak occured is also not proof of an ME outbreak. There needs to be a study looking into it and some level of consensus. There are probably many disease that are like CFS but are not CFS itself. Any disorder which involves persistent fatigue and pain could be described as CFS-like. The problem was the use of the term "the illness" in a context where "the illness" would be taken to mean CFS. If it was simply noted that many outbreaks of diseases sharing some similar symptoms to CFS have been reported, along with the CDC note that it has never been confirmed that are no confirmed outbreaks of CFS itself, I would have no problem with it. The objection has always been to the implication that the disease in question is CFS and not merely another disease that just happens to have similar symptoms to CFS. JamesStewart7 (talk) 06:08, 17 January 2008 (UTC)

The name ME was chosen at the time for the very purpose of grouping the outbreaks as one disease entity (see Acheson). They did not share 'some' symptoms, but all symptoms that were considered key to the disease entity. The WHO accepted this disease entity in 1965. The CDC was not involved until Lake Tahoe. Guido den Broeder (talk) 08:58, 17 January 2008 (UTC)

I suggest that James' concern can be overcome by writing "illnesses described as ME or CFS". Guido den Broeder (talk) 10:00, 18 January 2008 (UTC)

Some Wikipedia definitions:

• cluster = a grouping of health-related events (i.e., not necessarily infection)
• outbreak = a cluster of people infected with a disease, epidemic or pandemic
• epidemic = disease that appears as new cases in a given human population, during a given period, at a rate that substantially exceeds what is expected

The problem with the term 'cluster' is that it doesn't need to have a single origin, while all the reported incidents do. 'Outbreak' can only be used with infections, which have often been identified, and always suspected, but have not always been proven. 'Epidemic' has neither drawback. Therefore, I suggest that we use that term and add a remark about infections. Guido den Broeder (talk) 10:12, 18 January 2008 (UTC)

Most definitions of epidemic say that it is an infectious outbreak, which is why that term cannot be used. The wikipedia entry seems to have a different definition from most dictionaries (and from common sense). Cluster is the term used by the CDC, and is the only term that is appropriate. --Sciencewatcher (talk) 16:38, 20 January 2008 (UTC)

Source please. Cluster is inadequate, because a cluster can be endemic as well as epidemic, and in these documented incidents it was not endemic. Guido den Broeder (talk) 11:08, 21 January 2008 (UTC)

The Chambers Dictionary: "epidemic: adj affecting a community at a certain time; prevalent - n a disease that attacks great numbers in one place at a time, and itself travels from place to place; a widespread outbreak@

From dictionary.com: "affecting many persons at the same time, and spreading from person to person in a locality where the disease is not permanently prevalent."

From Encyclopedia Britannica: "an occurrence of disease that is temporarily of high prevalence"

From Encarta: "Epidemic, outbreak of contagious disease affecting an unusually large number of people or involving an extensive geographical area"

From encyclopedia.com: "Outbreak of an infectious disease rapidly spreading to many people"

About half of the references say that an epidemic is a contagious disease, whereas the other half say it is just high prevalence (e.g. "a smoking epidemic"). As I understand it, the word epidemic can have either meaning. If you use it with CFS there is the implication that you mean a contagious epidemic. --Sciencewatcher (talk) 16:03, 21 January 2008 (UTC)

Also, a cluster doesn't have to be either endemic or epidemic. It can simply be an apparent cluster (i.e. when you investigate you find the number of cases are no higher than in other areas), or simple random variation. --Sciencewatcher (talk) 16:07, 21 January 2008 (UTC)

That is why to solely say 'cluster' is not adequate.

Thanks for the quotes. I've left the CDC statement in that CFS is not contagious, so there can be no misunderstanding. Guido den Broeder (talk) 18:36, 21 January 2008 (UTC)

"I suggest that James' concern can be overcome by writing "illnesses described as ME or CFS"." That would go a long way to addressing my concerns. However, this statement lacks attribution (described by whom?) so it qualifies as weasel words. As I know there will be dispute as to who this description should be attributed to, I am going to include this sentence in the article along with a weasel word tag on it. I will leave it up to others to attribute it to the person's or organisations who used this description. Please note "vast majority" or similar is inadequate. If there is a large number of people it may be best to list their affiliated organisations, provided that there is consensus within that organisation.

Also I have to side with Scientwatcher regarding cluster vs outbreak. Guido, you state the problem yourself "'Outbreak' can only be used with infections, which have often been identified, and always suspected, but have not always been proven." Since it has not been proven some sort of attribution is needed or a more verifiable word (cluster) must be used. This approach is outlined in WP:NPOV policy "A different approach is to substantiate the statement, by giving factual details that back it up: "John Doe had the highest batting average in the major leagues from 2003 through 2006." Instead of using the vague word "best," this statement spells out a particular way in which Doe excels." If we can't substantiate the word outbreak (missing proof) then the word cluster must be used and followed by evidence for the cluster.JamesStewart7 (talk) 06:00, 22 January 2008 (UTC) Actually the current wording here seems to be ok, apart from the use of the term "epidemic". According to the epidemic article, there must be "a rate that substantially exceeds what is "expected," based on recent experience". This is problematic "Defining an epidemic can be subjective, depending in part on what is "expected"". Given the subjective nature of the term and the controversy surrounding this section, I think it is important to attribute the use of the term epidemic to whoever stated it. JamesStewart7 (talk) 06:05, 22 January 2008 (UTC) Btw wishes to refute my statement that an infectious origin has been established, I expect strong evidence to the contrary (a cluster is not proof of a viral cause). JamesStewart7 (talk) 06:13, 22 January 2008 (UTC)

Two further problems " More than once, this coincided with an outbreak of poliomyelitis. An infectious origin was not always identified" First sentence has no reference and because it is controversial I am removing it. Second sentence is worded in a POV manner. "Not always identified" implies that an infectious origin was established in most or at least some cases. "Identified" is also likely to be read as "proven" or similar in this context as opposed to "someone said". Because of this I am changing it to "An infectious origin of these cases has not been established" JamesStewart7 (talk) 06:11, 22 January 2008 (UTC)

Vast majority

(RFC) User:Sciencewatcher wishes to delete from the article any indication that the vast majority of experts in this field believe the classification by the WHO of CFS as a somatic disease to be correct.[13] User:Guido den Broeder desires to keep this notion in the article because he feels that it is well-referenced and that without it, the reader might wrongly conclude that the protest by two Oxford psychiatrists has equal support. Guido den Broeder (talk) 20:19, 15 January 2008 (UTC)

I never mentioned anything about the classification or the WHO. See the discussion above. --Sciencewatcher (talk) 20:34, 15 January 2008 (UTC)

You deleted it nonetheless. Guido den Broeder (talk) 21:32, 15 January 2008 (UTC)

No I didn't. I deleted "According to leading experts, the vast majority of international ME/CFS specialists support the classification of CFS as a physical condition". No mention of WHO. And you still have presented no evidence that the "vast majority" of researchers support the classification of CFS as an organic illness (which I assume is what is meant by "physical condition"). --Sciencewatcher (talk) 03:11, 16 January 2008 (UTC)

Sciencewatcher is not the only person who had a problem with this statement. I fact tagged it saying "claims of consensus must be sourced". It has been changed since but "According to leading experts" is a peacock term and I don't think it is fair to get around the problem of a lack of source for a consensus by simply changing it to "So and so says there is a consensus." The words of one person (or 3) is not enough to establish conensus. I'm not seeing this WHO reference either (btw they must use the term "somatic"). As I stated before, no one should be substituting the word "somatic" for "physiological", "physical" or "organic" either as this is creates a false dichotomy between the mind and body (the mind (brain) is actually part of the body so something can be simultaneously physical and mental). So please be aware the source must use terms like "somatic" or "not psychological" if anyone is going to present the source as such in the article.

The context of this statement particularly is a problem "After more than 3,000 research studies, there is now abundant scientific evidence that CFS is a real physiological illness".". In the article physical may be taken to mean "not psychiatric" as the topic sentence presents the paragraph as a controversy about whether CFS is a psychiatric condition "wo contrasting viewpoints among ME/CFS experts have become apparent. In a letter to the Lancet, Simon Wessely et al. contested the WHO classification, arguing that CFS was a form of neurasthenia to be classified as a psychiatric condition." However, I challenge anyone to point to any reference where the CDC says that CFS is not a psychiatric condition. All they said was this "Uncertainty about whether CFS is real. After more than 3,000 research studies, there is now abundant scientific evidence that CFS is a real physiological illness. It is not a form of depression or hypochondriasis. A number of biologic abnormalities have been identified in people with CFS, but how they contribute to the illness is still unclear" So they said it was a real diagnostic entity that is not depression or hypochondriasis. No where do they say that CFS is not a psychiatric condition. In fact they seem to suggest that psyhiatric factors are of importance "Psychiatric factors are relevant to any illness process. CBT has been shown to help patients deal with these factors and better cope with the life-altering issues of chronic illness. Awareness of the role stress can play in exacerbating the symptoms of CFS is essential. CBT helps patients recognize and more successfully manage stressors in their lives." Given this apparent misrepresentation of the source, through an inappropriate context, I am going to remove this statement. Anyone is free to reinclude the source in another part of the article. JamesStewart7 (talk) 06:42, 16 January 2008 (UTC)

There is no lack of sources. These are not the words of five persons, but their reports of the words of many persons.

'A real physiological illness' excludes the possibility that it is psychiatric.

Stressors are not 'psychiatric'.

Please do not make contested edits while the RfC is running, since that defeats the purpose of the RfC. Guido den Broeder (talk) 09:36, 16 January 2008 (UTC)

A stressor is something that provokes stress. It is a very broad term. Many things are considered stressors. Some of them have been linked with psychiatric illnesses. For example, child abuse is classified as a stressor and increase the risk of various disorders such as depression and anorexia. I still don't see how physiological excludes psychiatriac. Are you contending that the brain is not a physical entity or that the mind is somehow seperate from the brain? Are you contending the brain is seperate from the rest of the body and no one means the brain when they say physiology? I have to object to that. Many other systems are under neural control (eg HPA axis, mentioned in the stress section). Increased cortisol levels may occur in a response to psychological (or physical) stress and have wide ranging physical effects. Coritsol is released via the adrenal cortex which is under pituitary control which is under hypothalamic control (part of the brain). I don't see how people can just seperate the brain from the rest of the body and pretend that it is not part of physiology. So I don't think physiological excludes psychiatric and we need a far more clear statement (from a spokesperson for the CDC) to use the CDC statement in this way. JamesStewart7 (talk) 12:47, 16 January 2008 (UTC)

Here is the transcript of the CDC press conference (November 2006) where the toolkit was launched: http://www.cdc.gov/od/oc/media/transcripts/t061103.htm. One of the speakers (Dr. Komaroff) is on record for stating: "It's not an illness that people can simply imagine that they have and it's not a psychological illness." So there is your reference. JayEffage (talk) 10:44, 16 January 2008 (UTC)

Dr Kamaroff is a member of the Harvard Medical school. I don't see how his opinions can be taken to represent those of the CDC. JamesStewart7 (talk) 12:25, 16 January 2008 (UTC)

James, you claimed that the source stating something to the effect of "x-thousand studies showing biological abnormalities therefore CFS is physical" was used in an inappropriate context, namely to emphasize the "CFS is not psychological". You will however note, that Dr. Komaroff (indeed from the Harvard Medical School) did exactly that on the CDC press conference. Here is the complete quote (from the CDC transcript http://www.cdc.gov/od/oc/media/transcripts/t061103.htm ) :"there are now over 4,000 published studies that show underlying biological abnormalities in patients with this illness. It's not an illness that people can simply imagine that they have and it's not a psychological illness. In my view, that debate, which was waged for 20 years, should now be over.". So there are clear grounds to keep that bit in the controversy section - if not via the "CDC said so" then via the "Komaroff, Harvard medical, on CDC conference said so" road. JayEffage (talk) 13:01, 16 January 2008 (UTC)

While I realise that everything which is psychological is simultaneously biological, this is probably not obvious to the average reader. We should just quote the original statement and attribute it to the source. In the "CFS Toolkit for Health Care Professionals: Basic CFS Overview" [14] it states, "After more than 3,000 research studies, there is now abundant scientific evidence that CFS is a real physiological illness." Totally removing it on the grounds of "context" or "because the reader might think it means CFS isn't psychiatric" seems somewhat odd. Of course psychiatric illnesses involve biology, but imagine if someone removed all the psychiatric-sounding sources in the section simply because they didn't want the readers to get the impression that CFS doesn't involve a range of biological abnormalities, since the average reader might not know about or even accept the existence of the intricate nature between biology and subjective experience. "Let the facts speak for themselves", right? PS; "Stress" seems to contributes to a range of diseases and illnesses of different types, so it isn't really going to help us much in classifying CFS. Neither does the existence of psychiatric factors for a similar reason, especially if they are "stressful". - Tekaphor (talk) 15:09, 16 January 2008 (UTC)

I'm not saying teh quote should be removed completely. In my edit summary, I said I was quite happy for the quote to be reincluded in another section of the article. It would also be appropriate to include the full statement by Dr Komaroff in the controversy section and attribute that statement to him. The problem is by placing the quote in a controversy section we are not just letting the facts speack for themselves. Controversy sections implicitly create opposing sides that are expected to have opposing viewpoints, after all no opposing viewpoints means no controversy. So if you place an ambiguous term in that section people are going to read too much into it. If people wish to place the CDC statement in the controversy section I would be ok with this is more than one quote is included. Particualarly I think this quote must also be included if we are to properly characterize the CDC position, "Psychiatric factors are relevant to any illness process. CBT has been shown to help patients deal with these factors and better cope with the life-altering issues of chronic illness. Awareness of the role stress can play in exacerbating the symptoms of CFS is essential. CBT helps patients recognize and more successfully manage stressors in their lives." If we do not include this quote or a similar one, the use of the CDC quote in this way is a form of quote mining. JamesStewart7 (talk) 23:21, 16 January 2008 (UTC)

James, I better understand what you mean now. Yes, the statements should go in another section, unless of course they are relevant to history (eg say the CDC changed a previous position). All 3 statements from the CDC sources could be grouped in a subsection titled "CDC statements" within the controversy section. - Tekaphor (talk) 04:01, 17 January 2008 (UTC)

Yes, I would consider that a reasonable solution. JamesStewart7 (talk) 04:38, 17 January 2008 (UTC)

Sounds good. JayEffage (talk) 09:48, 17 January 2008 (UTC)

That still leaves to be considered the text responsible for this RfC:

• "According to leading experts, the vast majority of international ME/CFS specialists support the classification of CFS as a physical condition."

I suggest to replace this with:

• "International conferences, handbooks and consensus definitions support the classification of CFS as a physical condition." Guido den Broeder (talk) 09:41, 18 January 2008 (UTC)

But those references don't support the text. Most experts and conferences admit they do not know the cause of CFS. It is actually a minority who actively support either a physical or psychological etiology. I would agree to change the article to say this. --Sciencewatcher (talk) 16:31, 20 January 2008 (UTC)

I'm assuming what you meant was that there is no consensus on what is causing the symptoms in CFS, because the argument that "most experts and conferences admit they do not know the cause of CFS" is rather redundant and unsurprising, when considering that many organic diseases and psychiatric illnesses have uncertain etiology but specific classification based on symptoms and/or some insight into some symptom-causing pathology. Also, saying CFS is neither physiological or psychological could be interpreted as a masked implication for classification as a psychiatric illness. This is of course assuming that "CFS" actually exists as a singularly distinct entity and actually occurs with homogenous pathology. - Tekaphor (talk) 10:19, 21 January 2008 (UTC)

As mentioned before, the references do support the text. The text does not state that experts say the cause of CFS is known, it only states that experts say it should be classified as physical. If Sciencewatcher thinks that all these references are inaccurate, he should provide a source that says so. Guido den Broeder (talk) 10:58, 21 January 2008 (UTC)

Maybe it is just me, but I would appreciate it if you could point out where in the references they actually say this. I couldn't find it anywhere. Thanks. --Sciencewatcher (talk) 15:51, 21 January 2008 (UTC)

For instance: "Tony Komaroff summarized the conference’s findings, noting that great strides are being made to find objective biologic evidence."

Anyhow, I've changed it so that we don't need the statement or all the references. Guido den Broeder (talk) 18:49, 21 January 2008 (UTC)

The statement "over 200 researchers discussed biomedical research" seems a bit redundant. So what if they discussed research? Doesn't that go without saying? Biomedical research in itself doesn't point to either a psychosomatic or organic etiology. All psychosomatic and psychiatric disorders are biomedical. --Sciencewatcher (talk) 19:46, 21 January 2008 (UTC)

Random selection

I removed this "The patients were not randomly selected." not because it is innaccurate, but because it is misleading. Any reader would read this as a study flaw (no doubt an ideal study would involve random patient selection) but the article failed to note that random patient selection is verging on impossible. In fact, I would say it is impossible, at least without breaking a few ethical guidlines and perhaps laws. If anyone can explain to me how you can feasibly and ethically conduct a study of any medical treatment I will gladly reinclude the statement. However, bear a non-random selection of patients turn up to the hospital/doctors office. A non-random selection of patients agree to do the study and a non-random selection of patients can be ethically allowed into the study (ethics prevents allowing say suicidal patients into a study where effective evidnece based treatments are available). Even setting the diagnostic criteria for which patients may be admitted to the study is a non-random process (defining who has the particular illness). All of these things effect patient selection. In a randomized controlled trial, "ranomized" refers to the allocation to control vs treatment group, not patient selection. Hence a trial may be considered randomized without random patient selection. JamesStewart7 (talk) 07:33, 16 January 2008 (UTC)

The reader would be right: this is a serious shortcoming, which castst doubt on the validity of the outcomes. That is why I removed the reference. If you want it in, this huge shortcoming must be mentioned. Random selection is quite easy, it is done in virtually all other studies. Guido den Broeder (talk) 09:53, 16 January 2008 (UTC)

No, random allocation is done in virtually every study. How do you do random selection? I still want to know. At best you can randomly select from a non-random subset of patients JamesStewart7 (talk) 12:03, 16 January 2008 (UTC)

That is indeed best, and usual, but in this study it was not done. They let the patients decide if they wanted to have the treatment. Patients open to an exercise therapy are expected to have a better result than patients declining the treatment, because patients are quite good at estimating what room there is for an increase of activity. Guido den Broeder (talk) 15:36, 16 January 2008 (UTC)

I still suggest to drop this rather poor reference. It is not needed, since the section already mentions that White found four studies with even more positive results. Guido den Broeder (talk) 16:13, 16 January 2008 (UTC)

I am inclined to agree that we should focus on secondary sources in this section and drop the original studies, apart from their reference in the secondary sources. It sounds like what you are describing is a lack of random allocation, not a lack of random selection. A lack of random allocation is a significant study flaw and grounds for removal. The study will be removed. JamesStewart7 (talk) 04:55, 17 January 2008 (UTC)

Following from this, I am requesting a quote to support this (my library thinks proquest has the article but I can't seem to find it) "A systematic review on CBT[8] finds that, while some kind of positive result is often reported, the quality of the research into the effects of CBT is usually rather low and the patient selection is not random". Particularly I want a quote for where the reviewers say "the patient selection is not random" as this is a rather atypical comment. Normally you see things like "more testing is needed on severely affected patients" or "most trials involve outpatient populations" or another similarly specific statement. Also do they say the quality of the research is normally rather low or is that an editor comment? JamesStewart7 (talk) 07:52, 16 January 2008 (UTC) I ask, because they state this in the abstract and some of the studies are rather recent "Over the last five years, there has been a marked increase in the size and quality of the evidence base on interventions for CFS/ME". Also this is a general review. Did they say the quality of the research on CBT is rather low or were they talking across all treatments? JamesStewart7 (talk) 07:53, 16 January 2008 (UTC)

The reference you need is Chambers (2006). The low quality pertains to CBT research only, although it is probably true for all CFS treatment studies. Guido den Broeder (talk) 09:53, 16 January 2008 (UTC)

So can you give me a quote then? JamesStewart7 (talk) 12:03, 16 January 2008 (UTC)

The full text of the systematic review (Chambers 2006) is available here: [15]. A search for "random" only reveals one relevant statement regarding non-randomisation ... "The evidence supporting the effectiveness of CBT has been strengthened by one recent good quality RCT in children and adolescents [29] which found an overall positive effect of the intervention. CBT was associated with a significant positive effect on fatigue, symptoms, physical functioning and school attendance. Most other new studies of CBT and modified CBT have also favoured the treatment for one or more outcomes but these were either lower quality RCTs or non-randomized studies." This "good quality RCT" is PMID 15585538, which received a "validity score" of 16 out of 20 in the systematic review (table 1). The study on "9 to 17 year olds" is PMID 15210489, which received a score of 2 out of 20, so I think Guido is right that this study should be removed from the article on the grounds of quality. As for the quality of research in general, the systematic review mentions specific weaknesses. CDC researchers have identified "ambiguities" in the 1994 definition (PMID 14702202), and note the generally poor qualify of CFS research (PMID 16356178). The issues with the criteria/definitions in general (as mentioned in the article already, except for the latter study) aren't just some mildly noteworthy points to consider, they underlie the entire CFS subject and represent a disclaimer to all related research and it's resulting implications. 20 years and 3500 studies on CFS sounds impressive at first, but unfortunately a lot of it seems to be noise. - Tekaphor (talk) 01:33, 17 January 2008 (UTC)

Ok I'm going to take a shot at modifying the statement over which the quote was requested so that it more accurately reflects the reference (currently it only gives half the story). I'm removing the PMID 15210489 reference. We should only be including high quality RCT in this article when such trials are available. JamesStewart7 (talk) 04:55, 17 January 2008 (UTC)

Thanks. Guido den Broeder (talk) 09:24, 17 January 2008 (UTC)

Removed section - bacterial

Here is the text for discussion.

-

• Lyme disease and related tick-borne infections. Lyme disease does not always present acutely with a rash, and less than half of sufferers recall a tickbite (the nymphal deer tick is the size of a poppy seed, and secretes an anesthetic to prevent the host from feeling its bite). Furthermore, the characteristic joint pain is not always present. The accuracy of blood tests for Lyme remains highly controversial, especially since they depend on an effective immune system response, which many researchers believe is compromised by the disease. As a result, some clinicians believe Lyme is under-diagnosed.

-

• Bacterial respiratory infections such as mycoplasmic bronchitis/pneumonia, Legionnaire's disease, and possibly other bacteria associated with bacterial pneumonia.

-

• Sinusitis. Sinusitis is a chronic infection of the sinuses which can be difficult to diagnose, and can cause symptoms similar to those of CFS. Sinusitis can occur after dental surgeries or infections, and thus may be related to reaction to mercury in dental amalgams as above, or dental infections, as below.

-

• Toxoplasma gondii. Toxoplasma gondii is a parasitic infection. If let untreated it can cause severe immune suppression and neurologic symptoms.

There are two problems with this section. It has almost nothing to do with CFS apart from a few similar symptoms and it is unreferenced. If anyone has reliably sourced material that specifically refers to CFS then by all means reinclude it but the sources actually have to mention CFS so merely sourcing some of these statements is not enough. JamesStewart7 (talk) 12:30, 16 January 2008 (UTC)

Agreed. I was about to delete this section myself. Guido den Broeder (talk) 15:29, 16 January 2008 (UTC)

For future reference: articles on Coxiella burnetii, Chlamydia pneumoniae, and Borrelia burgdorferi relationships with cfs do exist. Ward20 (talk) 20:37, 25 January 2008 (UTC)

Gene expression

From memory, the "Gene expression" section was detitled a while ago on grounds that all diseases involve changes in gene expression and therefore doesn't indicate cause, but I am reinstating it because the main section is also about pathophysiology. - Tekaphor (talk) 02:57, 17 January 2008 (UTC)

Genetic polymorphisms

Genetic polymorphisms have also been previously discussed, but I didn't take any action. I will now introduce this in a small section. - Tekaphor (talk) 03:02, 17 January 2008 (UTC)

Biological information

After reading through the article, I am starting to think that general biological information needs to be referenced unless it is specifically stated in the linked article (even then a reference would be nice. I have noticed at least one somewhat inaccurate statment "the HPA axis helps the body remain stable under physiological and psychological stress". The HPA axis is not responsible for keeping the body stable under stress. It is responsible for controlling reactions to stress. Stability is not really the priority. During the stress response, the HPA axis will divert resources away from less urgent processes (eg digestion) and to more pressing matters (eg. to skeletal muscles to escape). The HPA axis will return resources back to other processes if the stress resolves but only if the stress resolves. Stress itself is rather unsustainable state (see General_adaptation_syndrome stage 3) so remaining stable under stress is somewhat of an oxymoron. JamesStewart7 (talk) 07:00, 17 January 2008 (UTC)

A similar problem is found here
Most strikingly, using the French Multitest to measure the body's response to a variety of antigens, the Australian group found that 33% of the subjects were hypoallergic, meaning they had a reduced immune response, while an additional 55% were completely anergic, meaning they had no immune response at all. Hypoallergic does not mean no immune response. It means no immune response to a particular set of antigens. That doesn't mean that the patient won't exhibit an immune response to say, a particular virus. It is possible that this is what the writer intended but someone may easily misread the sentence so I have specified it further. JamesStewart7 (talk) 07:04, 17 January 2008 (UTC)

Think there is typo above: Hypoallergic --->Anergic? Good catch by the way. Ward20 (talk) 07:55, 17 January 2008 (UTC)

Anergic seems to dictate a complete absence of a response, however, I'm going to leave it up to someone more informed in this area to make any further edits as I am really not sure. JamesStewart7 (talk) 07:59, 17 January 2008 (UTC)

Low Natural Killer Syndrome (Japan)

Japan study: Low natural killer syndrome: clinical and immunologic features, Aoki T. et al Nat Immun Cell Growth Regul. 1987;6(3):116-28. Book edited by Stephen E. Straus, "Chronic Fatigue Syndrome" [16] page 227 states patients seem similar if not identical to CFS. Also cited by, "A Chronic Illness Characterized by Fatigue, Neurologic and Immunologic Disorders, and Active Human Herpesvirus Type 6 Infection", Dedra Buchwald, MD; et al. Ward20 (talk) 07:03, 18 January 2008 (UTC)

See also:

• Whiteside TL, Friberg D (1998), “Natural killer cells and natural killer cell activity in chronic fatigue syndrome”, Am J Med. Sep 28;105(3A):27S-34S, PMID: 9790479
• Levine PH, Whiteside TL, Friberg D, Bryant J, Colclough G, Herberman RB (1998), "Dysfunction of natural killer activity in a family with chronic fatigue syndrome", Clin. Immunol. Immunopathol. 88(1): 96-104, PMID Guido den Broeder (talk) 08:22, 18 January 2008 (UTC)

And:

• Stewart CC, Cookfair DL, Hovey KM, Wende KE, Bell DS, Warner CL (2003), "Predictive immunophenotypes: disease-related profile in chronic fatigue syndrome", Cytometry B Clin Cytom. May;53(1):26-33, PMID: 12717688

"These data suggest that differences in controls from cluster and noncluster areas may be responsible for some of the inconsistencies in results from other studies. Furthermore, they suggest the possibility that NK cell function may play an important role in preventing the development of CFS in individuals who live in a community where a cluster of cases have been identified." Guido den Broeder (talk) 09:11, 18 January 2008 (UTC)

This is what is present in the article though "There are a number of different terms which have been identified at various times with this disorder... Low Natural Killer Syndrome (LNKS); this name is used in Japan. It reflects research showing diminished in-vitro natural killer cell activity in patients,[22][23] often by as much as two thirds" As you say, the researchers say that the patients seem "similar if not identical to CFS". This is not the same thing as callinging Low Natural Killer Syndrome CFS. This statement, "It reflects research showing diminished in-vitro natural killer cell activity in patients" also needs significant qualification to reflect the above references. They are talking about "individuals who live in a community where a cluster of cases have been identified". This is quite different to CFS in general. JamesStewart7 (talk) 06:20, 22 January 2008 (UTC)

The article does not say Low Natural Killer Syndrome is CFS. It says, "There are a number of different terms which have been identified at various times with this disorder (CFS)...." Isn't (LNKS) patients seem "similar if not identical to CFS" a term which has been identified at various times with this disorder? Other CFS studies can be included as sources that reference the LNKS study if that would help (including the Tahoe study which uses the term epidemic but states the Tahoe study was not designed to determine that conclusively [17]).

Concerning the second statement, "It reflects research showing diminished in-vitro natural killer cell activity in patients", isn't this wording supported by:

"LNKS is a newly proposed category of immune disorders, being characteristically diagnosed by lowered NK cell activity against K562 target cells as a definite laboratory abnormality, in association with general clinical symptoms of remittent fever and uncomfortable fatigue, persisting without explanation for more than 6 months."[18]? Would it be better to attribute that to the study? Ward20 (talk) 08:30, 22 January 2008 (UTC)

Personally, I find "identified with this disorder" a little vague. I guess it could be taken to mean a "similar or related condition" or it could mean "the same disorder". Different people may read the statement different ways. Perhaps we can work on creating something more clear? Regarding the second statment, I think it would be better to attribute it to the study as you suggested. My point was "diminished in-vitro natural killer cell activity in patients" may be read as all patients or a random sample of patients. The study, however, appears to be examining particular subset of patients that may not be representative of CFS as a whole. I wasn't saying the study didn't support the statment at all. I was just saying that the statement needs to be more specific. JamesStewart7 (talk) 07:17, 23 January 2008 (UTC)

I like the wording "identified with this disorder" because the various names are not proven to be the same condition. Some articles argue ME is the same as CFS while others that ME is not the same as CFS. What they have in common is that they are identified with each other in some way. The paragraph above the sentence describes the problem, but perhaps not well enough. Ward20 (talk) 09:38, 23 January 2008 (UTC)

Question about page redirection

Hi, I'm very confused - I tried to access the Myalgic Encephalomyelitis page, and was redirected to the CFS page. As many people familiar with these topics know, the definitions of CFS (eg the CDC and Oxford definitions) are substantially dissimilar to those of M.E. (see the Nightingale definition, or follow the history of the research on the disease until the late 80s/ early 90s, when it began to be equated with "CFS" - despite it having a different definition). I suggest it would be a very good idea to begin a new page on ME. I don't suppose that would solve the problem of the disputes over what CFS is - it hardly could, seeing as there are at least 9 definitions of it (sets of criteria), and some combined ME/CFS criteria to boot (with the 2003 Canadian criteria obviously being the closest to M.E.). This would solve the obvious contradiction of having an illness which does not even have fatigue as a necessary symptom confused with an illness (or group of illnesses) for which fatigue is a necessary, sometimes the main, symptom. Virginia —Preceding unsigned comment added by 210.79.21.2 (talk) 18:25, 6 February 2008 (UTC)

Moved question above to new topic for visibility, hope you don't mind.Ward20 (talk) 20:20, 6 February 2008 (UTC)

Fair question on which there is probably going to be a lot of opinions .

Pro

• Reduce the article size.
• Differentiate the distinctions.

Con

• The two tend to be blended together by various agencies, and that POV shows up in the article.

Anybody else feel free to add to list or comment. Ward20 (talk) 20:36, 6 February 2008 (UTC)

All the relevant agencies appear to be claiming that it's all the same, even when they have a misleading and highly rigid definition on one side and another where anyone who feels depressed or tired must have it. For added fun, both of these things have been applied by the CDC for their pet name, CFS. It might be more practical to make it even clearer in the first sentence that there is no consensus whatsoever on the name of this illness or its definition. It might be useful to move this article to what the World Health Organization calls it: Myalgic Encephanomyelitis or (Benign) Myalgic Encephalomyelitis, but that would need to be decided here before there's a war on moving and re-moving the article. My guess is it will stay here simply because no other place will be accepted even grudgingly (it's here, so most people who hate the name CFS have to grudgingly acknowledge where the inertia lies).

We might be able to break it down by the various competing definitions -- this could allow for focusing on the names that these definitions each use and help resolve or at least reduce the name problem we have, as well as reduce the fistfighting over what this illness is (well, at Wikipedia, anyway -- every group and interest will continue to fight each other to the net detriment of patients). There would be overlap in the separate articles, the central article would still be controversial for having any name chosen, and the total size of text on this subject would increase, but it would become enormously more manageable, and hopefully more time would be spent on refining and enhancing the content instead of revert wars, blatant enough to attract admin attention or otherwise. -- Strangelv (talk) 11:21, 20 February 2008 (UTC)

Proposal to start reducing size of article

How about starting a See Also section that splits out Notable sufferers of CFS and Cultural references of CFS to their own articles? Ward20 (talk) 05:56, 20 February 2008 (UTC)

Sounds like a safe starting point for breaking this up into manageable pieces. It's been a long time since I've been able to follow this article, let alone contribute to it. -- Strangelv (talk) 10:57, 20 February 2008 (UTC)

Makes sense to me also Jagra (talk) 01:30, 21 February 2008 (UTC)

Done, but I don't know how to fix the description of the EL to the Open Directory Project in the two new articles. Ward20 (talk) 05:58, 21 February 2008 (UTC)

Edit 192980061

Although well written and sensible:

Although the Gibson Report states that CBT in general is helpful to many people with other illnesses, it is notable that RCTs of CBT in cancer have found no improvements in the course of the disease at all, and most of the helpfulness that CBT may afford illness in general is concerning matters such as e.g. high risk behaviour in a minority of AIDS patients. Dr Eleanor Stein states that the most commonly used worldwide model of illness management, the Stanford Model of Chronic Disease Self Management, shows benefits for diabetes and hypertension (conditions in which lifestyle play a strong role), but less benefit for arthritis.

Some of this material appears to be WP:SYN, is there a source available for this that is about CFS? Also it duplicates some material a few paragragraphs down. Ward20 (talk) 06:53, 21 February 2008 (UTC)

MEspringal added a huge block of text about what seems to have been another incident in the classification of CFS/ME in the UK. It makes specific references to newsgroup posts and appearances of articles on websites, and I have the feeling that unless a secondary source is available, this incident may not be notable.

Could others offer their opinion before I remove the content in question? I also think the "controversy" section should not be expanded without solid discussion on this talkpage. JFW | T@lk 20:59, 23 February 2008 (UTC)

I have not had a chance to look at it properly. It seems to be fairly well written but difficult to evaluate, as you say it was large. I have no objection if you want to remove the addition with the references to this section [19] of the talk page where it can be evaluated more easily. If others want to develop it with RS into such a large section my feeling is that it may have to be split into its own article. Thanks. Ward20 (talk) 21:32, 23 February 2008 (UTC)

I had a look at it...it seems to be an unnecessarily detailed discussion that isn't really appropriate here. I suggest just revert it. --Sciencewatcher (talk) 02:30, 28 February 2008 (UTC)

I'm having trouble finding this addition. -- Strangelv (talk) 15:05, 3 March 2008 (UTC)

I believe you are asking about this insertion of material under Controversy which was then pared down by taking Wessely material out due to it not being supported by the references. Ward20 (talk) 19:54, 3 March 2008 (UTC)

Jagra and article bloat

Jagra, could I encourage you to use more secondary sources and stop continuously enlarging this article? Many assertions need only one reference, not three or four. If there are reviews, they can generally replace a whole ream of primary sources. As an editor you are as responsible as everyone else in making sure the article meets size criteria. JFW | T@lk 07:44, 2 March 2008 (UTC)

I take your point JFW, can I suggest that we revise all multiple citing in the Article, leaving for each point, only reveiw plus one finding (where reveiw does not give pertinent details). Or where reveiw not available say two latest findings. So that a maximum of two references for each point! It is difficult to generalise I know, but this might be a useful guideline. Future updates can then replace older reference. Jagra (talk) 02:18, 3 March 2008 (UTC)

Actually, I like the multiple citing because it is a reverse pointer to the references. I can look for a subject in the article and go to the citations faster than hunting on medline or google. Splitting the article should alleviate the length problem. One problem I anticipate is having to be careful to maintain proper proportion of weight in the main article of sections that are split off. Ward20 (talk) 09:27, 4 March 2008 (UTC)