New blog by Cort today about the P2P report - haven't read it yet:
http://www.cortjohnson.org/blog/201...sion-nihs-commitment-mecfs-tightening-needed/
http://www.cortjohnson.org/blog/201...sion-nihs-commitment-mecfs-tightening-needed/
The P2P Draft report is out
- Thread starter CBS
- Start date
No. There is no synergy. The IOM report is finished and was sent out for peer review several months ago. It will be published soon. There is no opportunity for public comment on the IOM report (contrary to what several people said at CFSAC last month).
I suspect that the P2P report won't be finalized until after the IOM report is finished. Whatever publication occurs in Annals of the P2P material could possibly be modified to reflect the IOM report. But IOM has always been a stand alone process. P2P was never going to have an impact on IOM. The timelines did not align.
Roy S
former DC ME/CFS lobbyist
- Messages
- 1,376
- Location
- Illinois, USA
The Keystone Cops look coordinated by comparison.
Ember
Senior Member
- Messages
- 2,115
Hasn't the CDC been free to provide input to the IOM Committee? And don't the timelines align nicely for the NIH Final Report to mirror the IOM Report?
As I recall, Dr. Klimas lamented the fact that the Evidence Report wouldn't be available in time to inform the IOM Committee. But the Panel has managed to ignore much of it too.
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jimells
Senior Member
- Messages
- 2,009
- Location
- northern Maine
I fail to understand why folks are so hung up on prevalence and economic cost estimates. These numbers have had zero impact on policy and this will not change. It reminds me of a debate on how many angels can dance on the head of a pin...
Bob
Senior Member
- Messages
- 16,455
- Location
- England (south coast)
You might be right, Jimells, but I think people just want to correct the misinformation, for whatever good it will or won't do.
Kati
Patient in training
- Messages
- 5,497
i disagree on the impact on funding. The numbers in cost to society are being downplayed and undermined by the NIH which is giving them one more reason to not appropriate more funding for research.
Here is one example (canadian)
http://www.phac-aspc.gc.ca/ebic-femc/index-eng.php
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Below is Swedish ME/CFS advocate Sten Helmfrid's (PhD, Associate Professor of Physics) comment to the P2P draft report. I'm posting it here with his permission. It's focused mainly on lines 113-114 in the draft report, where it is wrongly stated that measurable improvement has been demonstrated following treatment with CBT and GET. Sten Helmfrid shows clearly that in fact no CBT/GET studies have demonstrated improvements in objective outcomes.
We are posting the comment here in case people wish to use Sten's statements or sources in their own comments.
I am concerned about the claim on rows 113–114 in the draft statement that studies on cognitive behavioral therapy (CBT) and graded exercise therapy (GET) demonstrate measurable improvement for patients with ME/CFS. There are two underlying biopsychosocial assumptions in these studies: firstly, that the illness is perpetuated by behavioral factors and deconditioning; and secondly, that behavioral intervention in combination with exercise can reverse the condition. There have been several studies of this kind during the last twenty years. Although some of them show small improvements, the only outcome measures that actually have improved are subjective. It is well known that there is a placebo response in subjective measures. This response is likely to cause large bias in studies on cognitive behavioral therapy and graded exercise therapy, as it is part of the protocol to convince patients that the treatment works.
To my knowledge, there are only two studies that have analyzed objective outcome measures. A Dutch group made a post-hoc analysis of actometer data from three of their own CBT studies and concluded that although the fatigue score was reduced in the subjective self reports, there was no objective improvement in the activity levels of the patients [1]. In another study, the same group showed that patients who reported reduced cognitive impairment after CBT did not improve their performance in neuropsychological tests [2].
In the British PACE study, patients made a six-minute walk test before, during and after intervention [3]. Such tests are regularly used to evaluate patients with heart or lung conditions. A healthy person covers about 600 m, whereas 400 m corresponds to severe disability and is suggested as a limit for lung patients when transplantation is justified. All four groups in the study showed small improvements, but the GET group improved slightly more than the others, from 312 to 379 m. This is, however, a poor measure of objective improvement. In contrast to cardiopulmonary exercise tests (CPET), there is no way to control what efforts the patient is making during the test. The performance of ME/CFS patients is affected by post-exertional malaise, and there was no follow-up on how the patients were doing the day after the test. Moreover, as actometers were not used, there is no way to determine how the general functionality of the patients was affected by the treatment.
It should also be emphasized that there is no theoretical foundation for the treatment strategies used in CBT and GET. The cognitive behavioral therapy in the PACE study, for example, was administered on the basis of the fear avoidance theory [3]. There are no supporting references cited in the paper, and the theory strikes a discordant note with our knowledge of ME/CFS. Many patients report crash periods caused by overexertion, which is inconsistent with fear of exercise. Moreover, it was shown in a prospective study that increased level of activity is a predictor for developing ME/CFS [4]. Participants who later developed ME/CFS continued to exercise more frequently even after they started to experience fatigue.
The statement on rows 113–114 in the draft completely ignores the evidence for adverse reactions due to graded exercise therapy. Patient associations in several countries have used surveys to compare the outcome of different therapies. There are now data from ten independent surveys in four different countries with more than 13700 participants. About 4600 patients had tried GET, and 52 % reported that they felt worse [5,6]. The largest survey was carried out by the ME Association in the UK [7]. More than 56 % of the participants said that they felt worse, and 33 % reported that they felt much worse. (The number of false negative reports in these surveys is expected to be low. For example, only 3 % of patients treated with homeopathy—which most scientists regard to be completely ineffectual—felt much worse [7].) This large body of evidence for the adverse effects of graded exercise therapy cannot be ignored.
There is also a growing amount of biomedical evidence for physical deterioration after exercise. Several independent groups have shown that ME/CFS patient are unable to reproduce physical measures in cardiopulmonary exercise tests, which are repeated after 24 h [8,9]. Studies have also demonstrated changes in the gene expression and increased pro-inflammatory cytokine levels after exercise [10,11].
There have been few reports of adverse reactions in the published studies on cognitive behavioral therapy and graded exercise therapy. It should be pointed out, however, that the dropout rate in many of these studies has been high, up to 42 % [12]. Patients may leave the program because they deteriorate, and adverse reactions are therefore likely to be underreported. Moreover, there rarely are any objective measures of adherence.
In the PACE study, there were comparatively few dropouts (8 %). The number of serious adverse events in the GET group was about the same as in other groups. The authors conclude that graded exercise therapy is safe if administered as described. However, no objective measure of adherence such as actometers was used. After following the program for one year, the patients in the GET group on average managed to cover 379 m in the six-minute walk test. The goal of the study was complete recovery, and although the authors were confident that the acceptance and adherence to manuals were high, the poor test performance and the lack of objective measures raise serious doubts about the adherence to the exercise protocol. The conclusion that graded exercise therapy is safe if administered as described therefore is dubious.
In conclusion, there is no objective evidence for the efficacy of cognitive behavioral therapy and graded exercise therapy based on a biopsychosocial model as a treatment for ME/CFS. The only available objective data suggest that the self-reported improvement in some of the studies is due to the placebo effect. Moreover, there is no theoretical support for the underlying hypothesis that behavioral factors and deconditioning perpetuate the condition. I suggest that this is clearly pointed out in the final report. This does not mean that all forms of cognitive behavioral therapy and exercise should be dismissed. CBT may help some patients to deal with a chronic debilitating disease, and many patients use pacing strategies to maintain the activity level that the disease permits.
There are numerous reports of adverse reactions after graded exercise therapy. Although controlled studies report fewer and less severe reactions than surveys from patient associations, high dropout rates and lack of objective measures of adherence in these studies make all claims of safe treatments unconvincing. As long as there is no credible explanation why adverse reactions are so common and no way to separate patients that are at risk from other patients, the use of graded exercise therapy should be discouraged and the risk for deterioration should be acknowledged.
The need for objective measures in future studies should be emphasized. Double blinding should be used whenever possible, and when this is not possible—for example in psychological interventions—actometers or other objective measures of functionality must be employed instead.
References
1. J. F. Wiborg et al., “How does cognitive behaviour therapy reduce fatigue in patients with chronic fatigue syndrome? The role of physical activity,” Psychol Med, vol. 40, no. 8, pp. 1281–7 (2010).
2. H. Knoop et al., “The effect of cognitive behaviour therapy for chronic fatigue syndrome on self-reported cognitive impairments and neuropsychological test performance,” J Neurol Neurosurg Psychiatry, vol. 78, no. 4, pp. 434–6 (2007).
3. P. D. White et al., “Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial,” Lancet, vol. 377, no. 9768, pp. 823–36 (2011).
4. S. B. Harvey et al., “Etiology of Chronic Fatigue Syndrome: Testing Popular Hypotheses Using a National Birth Cohort Study”, Psychosom Med, vol. 70, no. 4, pp. 488–95 (2008).
5. T. Kindlon (2011), “Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome” [Accessed May 29th, 2014].
http://www.iacfsme.org/LinkClick.aspx?fileticket=Rd2tIJ0oHqk=&.
6. G. J. Bringsli, A. Gilje, and B. K. Getz Wold (2013). “ME-syke i Norge – fortsatt bortgjemt?” [Accessed May 29th, 2014]. Text in Norwegian.
http://me-foreningen.com/meforeningen/innhold/div/2013/05/ME-foreningens-Brukerunders%C3%B8kelse-ME-syke-i-Norge-Fortsatt-bortgjemt-12-mai-2013.pdf.
7. The ME Association (2010). “Managing my M.E. What people with ME/CFS and their carers want from the UK’s health and social services” [Accessed May 29th, 2014].
http://www.meassociation.org.uk/wp-content/uploads/2010/09/2010-survey-report-lo-res10.pdf.
8. C. R. Snell et al., “Discriminative Validity of Metabolic and Workload Measurements to Identify Individuals with Chronic Fatigue Syndrome,” Phys Ther, vol. 93, no. 11, pp. 1484–92 (2013).
9. B. A. Keller, J. L. Pryor, and L. Giloteaux, “Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO₂peak indicates functional impairment,” J Transl Med, vol. 12, pp. 104–13 (2014).
10. A. R. Light et al., “Gene expression alterations at baseline following moderate exercise in patients with chronic fatigue syndrome and fibromyalgia syndrome,” J Intern Med, vol. 271, no. 1, pp. 64–81 (2011).
11. P. D. White et al., “Immunological Changes After Both Exercise and Activity in Chronic Fatigue Syndrome: A Pilot Study,” J Chronic Fatigue Syndrome, vol. 12, no. 2, pp. 51–66 (2004).
12. J. M. Malouff, “Efficacy of cognitive behavioral therapy for chronicfatiguesyndrome: a meta-analysis,” Clin Psychol Rev, vol. 25, no. 5, pp. 736–45 (2008).
We are posting the comment here in case people wish to use Sten's statements or sources in their own comments.
I am concerned about the claim on rows 113–114 in the draft statement that studies on cognitive behavioral therapy (CBT) and graded exercise therapy (GET) demonstrate measurable improvement for patients with ME/CFS. There are two underlying biopsychosocial assumptions in these studies: firstly, that the illness is perpetuated by behavioral factors and deconditioning; and secondly, that behavioral intervention in combination with exercise can reverse the condition. There have been several studies of this kind during the last twenty years. Although some of them show small improvements, the only outcome measures that actually have improved are subjective. It is well known that there is a placebo response in subjective measures. This response is likely to cause large bias in studies on cognitive behavioral therapy and graded exercise therapy, as it is part of the protocol to convince patients that the treatment works.
To my knowledge, there are only two studies that have analyzed objective outcome measures. A Dutch group made a post-hoc analysis of actometer data from three of their own CBT studies and concluded that although the fatigue score was reduced in the subjective self reports, there was no objective improvement in the activity levels of the patients [1]. In another study, the same group showed that patients who reported reduced cognitive impairment after CBT did not improve their performance in neuropsychological tests [2].
In the British PACE study, patients made a six-minute walk test before, during and after intervention [3]. Such tests are regularly used to evaluate patients with heart or lung conditions. A healthy person covers about 600 m, whereas 400 m corresponds to severe disability and is suggested as a limit for lung patients when transplantation is justified. All four groups in the study showed small improvements, but the GET group improved slightly more than the others, from 312 to 379 m. This is, however, a poor measure of objective improvement. In contrast to cardiopulmonary exercise tests (CPET), there is no way to control what efforts the patient is making during the test. The performance of ME/CFS patients is affected by post-exertional malaise, and there was no follow-up on how the patients were doing the day after the test. Moreover, as actometers were not used, there is no way to determine how the general functionality of the patients was affected by the treatment.
It should also be emphasized that there is no theoretical foundation for the treatment strategies used in CBT and GET. The cognitive behavioral therapy in the PACE study, for example, was administered on the basis of the fear avoidance theory [3]. There are no supporting references cited in the paper, and the theory strikes a discordant note with our knowledge of ME/CFS. Many patients report crash periods caused by overexertion, which is inconsistent with fear of exercise. Moreover, it was shown in a prospective study that increased level of activity is a predictor for developing ME/CFS [4]. Participants who later developed ME/CFS continued to exercise more frequently even after they started to experience fatigue.
The statement on rows 113–114 in the draft completely ignores the evidence for adverse reactions due to graded exercise therapy. Patient associations in several countries have used surveys to compare the outcome of different therapies. There are now data from ten independent surveys in four different countries with more than 13700 participants. About 4600 patients had tried GET, and 52 % reported that they felt worse [5,6]. The largest survey was carried out by the ME Association in the UK [7]. More than 56 % of the participants said that they felt worse, and 33 % reported that they felt much worse. (The number of false negative reports in these surveys is expected to be low. For example, only 3 % of patients treated with homeopathy—which most scientists regard to be completely ineffectual—felt much worse [7].) This large body of evidence for the adverse effects of graded exercise therapy cannot be ignored.
There is also a growing amount of biomedical evidence for physical deterioration after exercise. Several independent groups have shown that ME/CFS patient are unable to reproduce physical measures in cardiopulmonary exercise tests, which are repeated after 24 h [8,9]. Studies have also demonstrated changes in the gene expression and increased pro-inflammatory cytokine levels after exercise [10,11].
There have been few reports of adverse reactions in the published studies on cognitive behavioral therapy and graded exercise therapy. It should be pointed out, however, that the dropout rate in many of these studies has been high, up to 42 % [12]. Patients may leave the program because they deteriorate, and adverse reactions are therefore likely to be underreported. Moreover, there rarely are any objective measures of adherence.
In the PACE study, there were comparatively few dropouts (8 %). The number of serious adverse events in the GET group was about the same as in other groups. The authors conclude that graded exercise therapy is safe if administered as described. However, no objective measure of adherence such as actometers was used. After following the program for one year, the patients in the GET group on average managed to cover 379 m in the six-minute walk test. The goal of the study was complete recovery, and although the authors were confident that the acceptance and adherence to manuals were high, the poor test performance and the lack of objective measures raise serious doubts about the adherence to the exercise protocol. The conclusion that graded exercise therapy is safe if administered as described therefore is dubious.
In conclusion, there is no objective evidence for the efficacy of cognitive behavioral therapy and graded exercise therapy based on a biopsychosocial model as a treatment for ME/CFS. The only available objective data suggest that the self-reported improvement in some of the studies is due to the placebo effect. Moreover, there is no theoretical support for the underlying hypothesis that behavioral factors and deconditioning perpetuate the condition. I suggest that this is clearly pointed out in the final report. This does not mean that all forms of cognitive behavioral therapy and exercise should be dismissed. CBT may help some patients to deal with a chronic debilitating disease, and many patients use pacing strategies to maintain the activity level that the disease permits.
There are numerous reports of adverse reactions after graded exercise therapy. Although controlled studies report fewer and less severe reactions than surveys from patient associations, high dropout rates and lack of objective measures of adherence in these studies make all claims of safe treatments unconvincing. As long as there is no credible explanation why adverse reactions are so common and no way to separate patients that are at risk from other patients, the use of graded exercise therapy should be discouraged and the risk for deterioration should be acknowledged.
The need for objective measures in future studies should be emphasized. Double blinding should be used whenever possible, and when this is not possible—for example in psychological interventions—actometers or other objective measures of functionality must be employed instead.
References
1. J. F. Wiborg et al., “How does cognitive behaviour therapy reduce fatigue in patients with chronic fatigue syndrome? The role of physical activity,” Psychol Med, vol. 40, no. 8, pp. 1281–7 (2010).
2. H. Knoop et al., “The effect of cognitive behaviour therapy for chronic fatigue syndrome on self-reported cognitive impairments and neuropsychological test performance,” J Neurol Neurosurg Psychiatry, vol. 78, no. 4, pp. 434–6 (2007).
3. P. D. White et al., “Comparison of adaptive pacing therapy, cognitive behaviour therapy, graded exercise therapy, and specialist medical care for chronic fatigue syndrome (PACE): a randomised trial,” Lancet, vol. 377, no. 9768, pp. 823–36 (2011).
4. S. B. Harvey et al., “Etiology of Chronic Fatigue Syndrome: Testing Popular Hypotheses Using a National Birth Cohort Study”, Psychosom Med, vol. 70, no. 4, pp. 488–95 (2008).
5. T. Kindlon (2011), “Reporting of Harms Associated with Graded Exercise Therapy and Cognitive Behavioural Therapy in Myalgic Encephalomyelitis/ Chronic Fatigue Syndrome” [Accessed May 29th, 2014].
http://www.iacfsme.org/LinkClick.aspx?fileticket=Rd2tIJ0oHqk=&.
6. G. J. Bringsli, A. Gilje, and B. K. Getz Wold (2013). “ME-syke i Norge – fortsatt bortgjemt?” [Accessed May 29th, 2014]. Text in Norwegian.
http://me-foreningen.com/meforeningen/innhold/div/2013/05/ME-foreningens-Brukerunders%C3%B8kelse-ME-syke-i-Norge-Fortsatt-bortgjemt-12-mai-2013.pdf.
7. The ME Association (2010). “Managing my M.E. What people with ME/CFS and their carers want from the UK’s health and social services” [Accessed May 29th, 2014].
http://www.meassociation.org.uk/wp-content/uploads/2010/09/2010-survey-report-lo-res10.pdf.
8. C. R. Snell et al., “Discriminative Validity of Metabolic and Workload Measurements to Identify Individuals with Chronic Fatigue Syndrome,” Phys Ther, vol. 93, no. 11, pp. 1484–92 (2013).
9. B. A. Keller, J. L. Pryor, and L. Giloteaux, “Inability of myalgic encephalomyelitis/chronic fatigue syndrome patients to reproduce VO₂peak indicates functional impairment,” J Transl Med, vol. 12, pp. 104–13 (2014).
10. A. R. Light et al., “Gene expression alterations at baseline following moderate exercise in patients with chronic fatigue syndrome and fibromyalgia syndrome,” J Intern Med, vol. 271, no. 1, pp. 64–81 (2011).
11. P. D. White et al., “Immunological Changes After Both Exercise and Activity in Chronic Fatigue Syndrome: A Pilot Study,” J Chronic Fatigue Syndrome, vol. 12, no. 2, pp. 51–66 (2004).
12. J. M. Malouff, “Efficacy of cognitive behavioral therapy for chronicfatiguesyndrome: a meta-analysis,” Clin Psychol Rev, vol. 25, no. 5, pp. 736–45 (2008).
Research 1st
Severe ME, POTS & MCAS.
- Messages
- 768
All of these 2014/2015 'reviews' of the P2P and IOM are a time management exercise in response to silencing novel pathogen discovery by preventing adequate research money, and thus not finding what is known to exist. Medical Politics ownership of ME as CFS is a dangerous game. Those maimed by the disease process of ME will tell you this, and the survivors of deceased patients will tell you also. (People who aren't approved Government patient advocates, of course).
Vociferously vocal patients who have no filter, annoy those in charge. They aren't controllable by the present narrative of compromise. The well worn message is, ''we believe you but we have no money'' (only the same to spend on you as Hay Fever) and so it's best you keep quiet and we'll keep you quiet by misrepresenting your disease as tiredness. Sorry. Why does this happen?
The obvious 'management' game is the state is waiting for the original Ramsay disease patients with provable disease signs (arthritis, heart failure, cancer, autonomic damage) to die out. Patients who were 30 in the 1980/90''s outbreaks, and now 60-70. The teens, are now in the 40's. What a complete disgrace this is.
A hidden group of highly disabled people has been created thanks to the CDC's refusal to act to the disaster of ME CFS:
Example:
Depressed people are manipulated into believing they have CFS, when they have chronic fatigue that can considerably improve with improved sleep, stress management, and anti depressant therapy. No pathogens are tested for. Fukuda CFS does not require it. No abnormality needs to be proven.
Vs
ME patients (especially in America) are forced to share the label CFS (disability claims rejected otherwise), when they have a terrible disease that forces them to be reliant on carers, helpers, family, who can't even get dressed or clean their teeth, for life. These extremely ill patients are also not tested for pathogens, because they too are branded with 'CFS' label. Untold numbers of people, will have died by now, developed secondary mental health problems and organ damage. NB: These iatrogenic harmed people are not recognized as existing, never mind researched. Part of how this is done, is by the British using media to make patients the enemy in the eyes of the public. The Americans, thankfully, avoid this to a lesser degree as the USA doesn't have social health care linked with the media.
To me, a rather obvious question remains how this denial of ME go on legally in 2015 onwards?
The Fukuda diagnostic classification of CFS, ins't psychological, yet the treatment is.
What have we learnt from the P2P/IOM dual resusictation of the CFS = ME lie?
That the obvious outcome is indeed obvious. The state decides to deny a 'break-way' form of CFS (clearly sick people with provable signs of disease) by removing ME experts from panel making decisions on redefining CFS, and by not including critical bio-medical CFS research. All we have then, as we all knew, is a PR exercise.
The original ME in the severely affected appears to be an acquired potential fatal life long infection that infects or affects mitochondria, alongside some form of autoimmunity developing. If you deplete mitochondria, and you affect the brain, you then may create millions of wrongly accused neuro patients, who are sitting on a sitting time bomb of pre alzheimer's disease and existing cognitive dysfunction. This 'inconvenient truth' is only possible to conceal, by keeping a heterogeneous non single cause description of 'disease' (Fukuda CFS), and thus avoiding using infections as bio-markers. AIDS is HIV+ any two co-infections. ME could easily be dysautonomia and also any co-infection proven to cause chronic fatigue. This is the sensible course of action, but sense reveals betrayal of science, and the patient community. Sense is brushed aside.
The P2P is worthless and the IOM death contract will be published soon. Dr Jose Montoya's paper at Stanford Uni that can select the severity of CFS patients (using inflammatory assays) conveniently wasn't published, which was going to be published, around May 2014. I'ts January 2015 and no sign of that 'ground breaking paper'. People have short memories, patients too with exhausted cognition, also forget. It's a win-win situation for the insurance and vaccine industry who know they will have future claims of 'activating' CFS, with their products. (Hep B vaccine etc).
If and when groundbreaking findings are published in 2015/2016 it's too late. The state will remain allied to a confusing mysterious heterogenous condition (CFS), that would have been split into CFS and inflammatory (infectious) CFS, had the Stanford Uni paper been published 'in time'. For this they needed the P2P/IOM to stop anyone with an idea of changing the status quo in subsequent years. All the Americans have done with their appalling P2P/IOM of unexplained chronic fatigue (called ME CFS), is create their version of the British 'NICE Guidelines'. Aka, rubber stamped legally enforced neglect.
Future pathogen findings (HERV's, Spirochetes, Prions) can be swept under the carpet now by P2P/IOM based on no single causation model, which is what the British psychiatrists and CDC have always sworn by must remain to describe ME as CFS. Meanwhile, Lipkin claims Unger doesn't think CFS is psychological when she is on video saying the exact opposite that perfectly espouses the claims of psycho-social models of CFS, again, British psychiatric invention exported globally. The British psychiatrists claim a cycle of 'avoidance' maintains disability and thus symptoms. They also claim patients are only severe due to 'boom and bust'. All of this is unproven, yet the head of CFS research at the CDC agrees with this stupid multi decade idea that not a single study has ever proven to be based on scientific evidence:
P2P/IOM is all about timing. It's all about the release of information at the 'correct' moment, to manage a situation.
Without management, you have chaos. Patients finding out they have a pathogen that affects mitochondria/prions, but are told they are hysterical, would lead to chaos - legally. This could lead to the fall of a Government, if the scandal is exposed to affect tens of millions of Americans. (If Autism epidemic is allied to a similar infection).
To stop exposure you manage the situation, carefully, with no mistakes.
First step. Remove all ME experts, prevent descent, keep to the script. The outcome, is inevitable.
No meaningful change, and patients remain disrespected, neglected, and older severely ill patients will die from a range of atherosclerosis, dementia, , cancer due to chronic inflammation. When they do die, it can easily be argued this wasn't CFS, as CFS = chronic fatigue of unexplained origin that 'certainly isn't fatal'.
The CDC and all allied domestic and foreign health agencies agree, and they agree by the process of how they filtered out ME experts who would have changed what it means to have CFS, or 'ME CFS' as they like to call it.
Change, such as divorcing ME from CFS (using signs of disease and biomarkers) is not tolerated by America and its allies for classified reasons they know and you will never know.
Vociferously vocal patients who have no filter, annoy those in charge. They aren't controllable by the present narrative of compromise. The well worn message is, ''we believe you but we have no money'' (only the same to spend on you as Hay Fever) and so it's best you keep quiet and we'll keep you quiet by misrepresenting your disease as tiredness. Sorry. Why does this happen?
The obvious 'management' game is the state is waiting for the original Ramsay disease patients with provable disease signs (arthritis, heart failure, cancer, autonomic damage) to die out. Patients who were 30 in the 1980/90''s outbreaks, and now 60-70. The teens, are now in the 40's. What a complete disgrace this is.
A hidden group of highly disabled people has been created thanks to the CDC's refusal to act to the disaster of ME CFS:
Example:
Depressed people are manipulated into believing they have CFS, when they have chronic fatigue that can considerably improve with improved sleep, stress management, and anti depressant therapy. No pathogens are tested for. Fukuda CFS does not require it. No abnormality needs to be proven.
Vs
ME patients (especially in America) are forced to share the label CFS (disability claims rejected otherwise), when they have a terrible disease that forces them to be reliant on carers, helpers, family, who can't even get dressed or clean their teeth, for life. These extremely ill patients are also not tested for pathogens, because they too are branded with 'CFS' label. Untold numbers of people, will have died by now, developed secondary mental health problems and organ damage. NB: These iatrogenic harmed people are not recognized as existing, never mind researched. Part of how this is done, is by the British using media to make patients the enemy in the eyes of the public. The Americans, thankfully, avoid this to a lesser degree as the USA doesn't have social health care linked with the media.
To me, a rather obvious question remains how this denial of ME go on legally in 2015 onwards?
The Fukuda diagnostic classification of CFS, ins't psychological, yet the treatment is.
What have we learnt from the P2P/IOM dual resusictation of the CFS = ME lie?
That the obvious outcome is indeed obvious. The state decides to deny a 'break-way' form of CFS (clearly sick people with provable signs of disease) by removing ME experts from panel making decisions on redefining CFS, and by not including critical bio-medical CFS research. All we have then, as we all knew, is a PR exercise.
The original ME in the severely affected appears to be an acquired potential fatal life long infection that infects or affects mitochondria, alongside some form of autoimmunity developing. If you deplete mitochondria, and you affect the brain, you then may create millions of wrongly accused neuro patients, who are sitting on a sitting time bomb of pre alzheimer's disease and existing cognitive dysfunction. This 'inconvenient truth' is only possible to conceal, by keeping a heterogeneous non single cause description of 'disease' (Fukuda CFS), and thus avoiding using infections as bio-markers. AIDS is HIV+ any two co-infections. ME could easily be dysautonomia and also any co-infection proven to cause chronic fatigue. This is the sensible course of action, but sense reveals betrayal of science, and the patient community. Sense is brushed aside.
The P2P is worthless and the IOM death contract will be published soon. Dr Jose Montoya's paper at Stanford Uni that can select the severity of CFS patients (using inflammatory assays) conveniently wasn't published, which was going to be published, around May 2014. I'ts January 2015 and no sign of that 'ground breaking paper'. People have short memories, patients too with exhausted cognition, also forget. It's a win-win situation for the insurance and vaccine industry who know they will have future claims of 'activating' CFS, with their products. (Hep B vaccine etc).
If and when groundbreaking findings are published in 2015/2016 it's too late. The state will remain allied to a confusing mysterious heterogenous condition (CFS), that would have been split into CFS and inflammatory (infectious) CFS, had the Stanford Uni paper been published 'in time'. For this they needed the P2P/IOM to stop anyone with an idea of changing the status quo in subsequent years. All the Americans have done with their appalling P2P/IOM of unexplained chronic fatigue (called ME CFS), is create their version of the British 'NICE Guidelines'. Aka, rubber stamped legally enforced neglect.
Future pathogen findings (HERV's, Spirochetes, Prions) can be swept under the carpet now by P2P/IOM based on no single causation model, which is what the British psychiatrists and CDC have always sworn by must remain to describe ME as CFS. Meanwhile, Lipkin claims Unger doesn't think CFS is psychological when she is on video saying the exact opposite that perfectly espouses the claims of psycho-social models of CFS, again, British psychiatric invention exported globally. The British psychiatrists claim a cycle of 'avoidance' maintains disability and thus symptoms. They also claim patients are only severe due to 'boom and bust'. All of this is unproven, yet the head of CFS research at the CDC agrees with this stupid multi decade idea that not a single study has ever proven to be based on scientific evidence:
P2P/IOM is all about timing. It's all about the release of information at the 'correct' moment, to manage a situation.
Without management, you have chaos. Patients finding out they have a pathogen that affects mitochondria/prions, but are told they are hysterical, would lead to chaos - legally. This could lead to the fall of a Government, if the scandal is exposed to affect tens of millions of Americans. (If Autism epidemic is allied to a similar infection).
To stop exposure you manage the situation, carefully, with no mistakes.
First step. Remove all ME experts, prevent descent, keep to the script. The outcome, is inevitable.
No meaningful change, and patients remain disrespected, neglected, and older severely ill patients will die from a range of atherosclerosis, dementia, , cancer due to chronic inflammation. When they do die, it can easily be argued this wasn't CFS, as CFS = chronic fatigue of unexplained origin that 'certainly isn't fatal'.
The CDC and all allied domestic and foreign health agencies agree, and they agree by the process of how they filtered out ME experts who would have changed what it means to have CFS, or 'ME CFS' as they like to call it.
Change, such as divorcing ME from CFS (using signs of disease and biomarkers) is not tolerated by America and its allies for classified reasons they know and you will never know.
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Ember
Senior Member
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Who gave the Panel its instructions? The Panel writes:
Did the Panel collectively forget all reference to the 2-day cardiopulmonary exercise test? The Evidence Report recommends:
Dr. Snell addressed the 2-day cardiopulmonary exercise test on the first day of the Workshop:
Dr. Snell spoke truth to power, and his exercise test was ignored.
I've done what I can on seven points that I felt were major and that I was halfway competent to address and I've linked to one post for each of them in which I provide line numbers to cite and arguments that others are welcome to use/copy/adapt as they wish.
The links are in this post:
http://forums.phoenixrising.me/inde...l-points-in-the-p2p-report.34630/#post-539458
Others are continuing to make their own posts there, which are very helpful.
Good luck to everyone in writing their responses!
The links are in this post:
http://forums.phoenixrising.me/inde...l-points-in-the-p2p-report.34630/#post-539458
Others are continuing to make their own posts there, which are very helpful.
Good luck to everyone in writing their responses!
Bob
Senior Member
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- England (south coast)
I've been studying their evidence report, and the research evidence that they've included for their analysis of CBT and GET. I might have misunderstood it, but I've carried out an analysis of the studies that used Oxford, as follows...
For exercise therapies (pages 60-62), it seems that they only include three research papers, and two out of the three use Oxford, as follows...
Fulcher and White, 1997. Oxford.
Moss-Morris et al., 2005. CDC Fukuda.
White et al., 2011. Oxford.
So if they excluded the two Oxford studies then they'd have a very weak evidence base upon which they can draw any conclusions, or make any statements, whatsoever, about exercise therapies.
For anyone asking that the PACE trial is withdrawn because it uses Oxford, then I think you should also ask that "Fulcher and White, 1997" is withdrawn from the evidence for exercise therapies, because it also uses Oxford for recruitment.
For GET, I think i removing the two Oxford studies would actually increase the combined effect of the interventions, from approx 10 points to approx 14 points on the SF-36 physical function scale (weighted mean difference)(Figure 5, page 60), so this would actually make GET look more impressive in terms of simple outcome values. But it would leave a very weak evidence base, with just a single study. So i'm not sure if we're gaining from them removing the Oxford studies or not, in terms of us trying to decrease the significance of GET as a therapy for ME/CFS. It depends how they might phrase their report.
I'm not sure if I can interpret their table for the CGI scores (Figure 4, page 59), for GET, so I'm not sure how it would change their interpretation for CGI scores. As far as my understanding goes, removing Oxford papers would decrease the value of GET in terms of CGI scores. But I don't understand how to interpret "relative risk" so I might have this wrong.
Again, I might have misunderstood something, so I welcome any corrections to this.
For CBT (pages 44-51), a larger number of papers are included in their evidence, as follows...
Deale et al., 1997. Deale et al., 2001. Oxford.
Jason et al., 2007, Jason et al., 2009, Hlavaty et al., 2001. CFS questionnaire.
Jason et al., 2010. CDC Fukuda.
Knoop et al, 2008, Tummers et al., 2010. CDC Fukuda.
O'Dowd et al., 2006. CDC Fukuda.
Tummers et al., 2012. CDC Fukuda.
Wearden et al., 2010. Fine Trial. Oxford.
White et al., 2011. PACE Trial. Oxford.
For anyone asking that the PACE trial is withdrawn because it uses Oxford, then I think you should also ask that the following are withdrawn from the evidence for CBT, because they also use Oxford for recruitment:
Deale et al., 1997.
Deale et al., 2001.
Wearden et al., 2010. (Fine Trial.)
White et al., 2011. (PACE Trial.)
As far as I can tell, for CBT, the combined improvements would be slightly less impressive without the Oxford studies, but it wouldn't make a huge difference. Perhaps it would lower the weighted mean difference from approx 7.7 points to roughly 5.5 points on the SF-36 Physical Function scale. Perhaps that's enough to reduce the effect size from medium to small? But I'm not certain about this. It might still be a borderline medium effect size. I think a small effect size is usually considered not to be clinically useful, which might make a significant difference to the report, depending on how they decide to interpret it.
BTW, although the FINE trial (Wearden et al., 2010) is a failed study (in terms of it demonstrating any clinical usefulness from the interventions), the evidence report records the FINE trial as demonstrating some improvement after the interventions. This is appropriate if the study demonstrated either a small improvement, a non-significant improvement, or clinically non-useful improvement.
In itself, I don't think it's going to make much difference for us whether they include the Oxford studies or not. But it's one tool in our toolbox, so to speak. It helps us chip away at their insistence on including positive references to CBT and GET.
For exercise therapies (pages 60-62), it seems that they only include three research papers, and two out of the three use Oxford, as follows...
Fulcher and White, 1997. Oxford.
Moss-Morris et al., 2005. CDC Fukuda.
White et al., 2011. Oxford.
So if they excluded the two Oxford studies then they'd have a very weak evidence base upon which they can draw any conclusions, or make any statements, whatsoever, about exercise therapies.
For anyone asking that the PACE trial is withdrawn because it uses Oxford, then I think you should also ask that "Fulcher and White, 1997" is withdrawn from the evidence for exercise therapies, because it also uses Oxford for recruitment.
For GET, I think i removing the two Oxford studies would actually increase the combined effect of the interventions, from approx 10 points to approx 14 points on the SF-36 physical function scale (weighted mean difference)(Figure 5, page 60), so this would actually make GET look more impressive in terms of simple outcome values. But it would leave a very weak evidence base, with just a single study. So i'm not sure if we're gaining from them removing the Oxford studies or not, in terms of us trying to decrease the significance of GET as a therapy for ME/CFS. It depends how they might phrase their report.
I'm not sure if I can interpret their table for the CGI scores (Figure 4, page 59), for GET, so I'm not sure how it would change their interpretation for CGI scores. As far as my understanding goes, removing Oxford papers would decrease the value of GET in terms of CGI scores. But I don't understand how to interpret "relative risk" so I might have this wrong.
Again, I might have misunderstood something, so I welcome any corrections to this.
For CBT (pages 44-51), a larger number of papers are included in their evidence, as follows...
Deale et al., 1997. Deale et al., 2001. Oxford.
Jason et al., 2007, Jason et al., 2009, Hlavaty et al., 2001. CFS questionnaire.
Jason et al., 2010. CDC Fukuda.
Knoop et al, 2008, Tummers et al., 2010. CDC Fukuda.
O'Dowd et al., 2006. CDC Fukuda.
Tummers et al., 2012. CDC Fukuda.
Wearden et al., 2010. Fine Trial. Oxford.
White et al., 2011. PACE Trial. Oxford.
For anyone asking that the PACE trial is withdrawn because it uses Oxford, then I think you should also ask that the following are withdrawn from the evidence for CBT, because they also use Oxford for recruitment:
Deale et al., 1997.
Deale et al., 2001.
Wearden et al., 2010. (Fine Trial.)
White et al., 2011. (PACE Trial.)
As far as I can tell, for CBT, the combined improvements would be slightly less impressive without the Oxford studies, but it wouldn't make a huge difference. Perhaps it would lower the weighted mean difference from approx 7.7 points to roughly 5.5 points on the SF-36 Physical Function scale. Perhaps that's enough to reduce the effect size from medium to small? But I'm not certain about this. It might still be a borderline medium effect size. I think a small effect size is usually considered not to be clinically useful, which might make a significant difference to the report, depending on how they decide to interpret it.
BTW, although the FINE trial (Wearden et al., 2010) is a failed study (in terms of it demonstrating any clinical usefulness from the interventions), the evidence report records the FINE trial as demonstrating some improvement after the interventions. This is appropriate if the study demonstrated either a small improvement, a non-significant improvement, or clinically non-useful improvement.
In itself, I don't think it's going to make much difference for us whether they include the Oxford studies or not. But it's one tool in our toolbox, so to speak. It helps us chip away at their insistence on including positive references to CBT and GET.
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Ember
Senior Member
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Without any supporting evidence, the Draft Report answers in the affirmative its overarching question, “Is ME/CFS a spectrum disease?” The Panel recommends “that the ME/CFS community agree on a single case definition (even if it is not perfect).”
Thus, the main research gap identified by the Panel is to be addressed politically:
ME experts propose instead a research solution:
NIH is playing politics with our disease.
Protecting minority rights is a sacred principle in advocacy. To recommend a political process whereby the majority of stakeholders in a community determines the status of a distinct subgroup, or subgroups, amounts to sanctioning their oppression. NIH must understand that principle; President Thomas Jefferson proclaimed in his first inaugural address, “All, too, will bear in mind this sacred principle, that though the will of the majority is in all cases to prevail, that will, to be rightful, must be reasonable; that the minority possess their equal rights...to violate which would be oppression.”
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Hope123
Senior Member
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[This is a re-post but is only on the CFSAC Jan 13 thread so I was asked by Sasha to re-post it where it might best be seen]
There is concern that comments submitted to the NIH P2P panel will not be retained in the public record. That is, we will not be able to read the comments of others nor will the public (e.g. media, etc.) have access to those comments in the future.
Thus, I encourage everyone to submit a copy of what they plan to send to NIH P2P to CFSAC as well at cfsac@hhs.govsince whatever is sent to CFSAC, by the laws of the Federal Advisory Committee Act, have to be available publicly.
There is concern that comments submitted to the NIH P2P panel will not be retained in the public record. That is, we will not be able to read the comments of others nor will the public (e.g. media, etc.) have access to those comments in the future.
Thus, I encourage everyone to submit a copy of what they plan to send to NIH P2P to CFSAC as well at cfsac@hhs.govsince whatever is sent to CFSAC, by the laws of the Federal Advisory Committee Act, have to be available publicly.
Hope123
Senior Member
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- 1,266
Another reason to disregard trials using Oxford, I also want to point out that the report reads in Lines 280-281:
Studies investigating homeopathy, non-pharmacologic, complementary, and alternative medicine treatments are needed.
Going back to the AHRQ systematic review, on p.26, this is based on one "fair" quality trial that used Oxford. Although the AHRQ review carefully states the weaknesses of these complementary/ alt med trials, the Panel does not seem to understand that if they take one trial of homeopathy to mean that homeopathy trials are needed.
Studies investigating homeopathy, non-pharmacologic, complementary, and alternative medicine treatments are needed.
Going back to the AHRQ systematic review, on p.26, this is based on one "fair" quality trial that used Oxford. Although the AHRQ review carefully states the weaknesses of these complementary/ alt med trials, the Panel does not seem to understand that if they take one trial of homeopathy to mean that homeopathy trials are needed.
Bob, look at Fig 5 - if you look at the horizontal bar running through the Moss-Morris data point you can see it almost touches the y-axis (zero mean difference). That means the difference is barely statistically significant. That's what makes it a weak result (on top of all the other design issues).
Similarly for the other charts and CBT. It's not just the effect size you've got to look at, it's statistical significance too. Hard to know what the pooled (meta-analytic) stat sig would be for the remaining non-Oxford studies without reanalysis but they look weak. I'd guess they weren't stat sig.
Edit: if the error (horizontal) bars cross the y-axis, a result isn't statistically significant (usually at p<0.05).
As stated in my earlier postings (Reply #509 and #511 at http://forums.phoenixrising.me/inde...draft-report-is-out.34480/page-26#post-540060), I had asked the ODP if public comments to the P2P Draft Report would be available for review by the public. The response to this question from ODP via Paris Watson was that the "Public comments are forwarded to the panel and are not retained".
I had e-mailed and called the ODP last week to ask for clarification regarding Ms. Watson's statement that these comments would not be retained. I was able to reach the ODP through Ms. Watson this morning by phone. She said that she had been out of the office during part of last week and she had just returned to the office this morning (1/5/2015), but the ODP was already working on a response to my follow-up question. I asked when she thought this response would be complete and she said they did not know and she could only confirm that the ODP was currently working on a response.
I expressed the urgency felt by many in the patient community to have a response to this question as soon as possible, especially in light of the fact that the Public Comment period will end on 1/16/2015. I also asked if the response by the ODP to my question regarding retention of Public Comments to the P2P Draft Report could also address whether Public Comments received (either orally or in writing) as part of the P2P workshop would be retained by the P2P Panel and/or the ODP/NIH/HHS and if these comments would be available for review by the public. Additionally, if these comments would not be retained what is the reason for this decision.
As soon as a response to these follow-up questions is received, I will post the response in this thread and the other two threads ("Responses to Individual Points in the P2P Report" and "CFSAC Meeting Scheduled for January 13, 2015") where this topic has been raised.
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Control freak questions:
Are we sure it's OK to submit a comment in the form of an attachment, such as a pdf file (as opposed to putting it all into the text of the e-mail)?
Are we sure they will consider comments from outside of the US?
And a reflection: For a report that was allegedly supposed to focus on research needs, doesn't it contain quite a lot of recommendations on health care??
Are we sure it's OK to submit a comment in the form of an attachment, such as a pdf file (as opposed to putting it all into the text of the e-mail)?
Are we sure they will consider comments from outside of the US?
And a reflection: For a report that was allegedly supposed to focus on research needs, doesn't it contain quite a lot of recommendations on health care??
Nielk
Senior Member
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- 6,970
From the FAQ of the IOM published by HHS HERE:
It seems like the intention is for all three efforts; the IOM, the CDC study and the P2P to work in "synergy".
From the presentation by Susan Mayer of the NIH at the IOM:
At: 5:01
The "synergy" here described in more detail.
In addition, Beth Unger of the CDC who is heading the CDC multi-site study presented at both the IOM and P2P meetings.
I don't know if I would state that the IOM was always going to be a "stand alone" project. The actuality of how much synergy they were able to accomplish, because of the timing issue, no one can know for sure. There is a lot of overlap as far as presenters and committee members. Who knows how much information was carried through behind closed doors?