Wednesday, February 27, 2013
Tuesday, February 26, 2013
Professor Simon Wessely: A man has got to know his limitations and my limitations are immunology and ME/CFS
Margaret Williams 23rd February 2013:
For the attention of Professor Sir Simon Wessely, Professors Peter White OBE and Michael Sharpe
Margaret Williams 23rd February 2013
Your attention is drawn to two recently published papers, one on fibromyalgia (FM) and the other on myalgic encephalomyelitis (ME).
You will doubtless recall that in 1999, Professors Wessely and Sharpe published their conviction that FM and ME (referred to as CFS/ME), together with irritable bowel syndrome and pre-menstrual syndrome, constitute but one single functional somatic syndrome (Functional somatic syndromes: one or many? S. Wessely, C Nimnuan, M Sharpe. Lancet 1999:354:936-939) and that in 2004, Professor White published his belief that CFS/ME is an individual functional somatic syndrome (In Debate: there is only one functional somatic syndrome. Peter D White. British Journal of Psychiatry 2004:185:95-96). In the latter paper, two of you said you still stood by your thesis that FM and ME are components of a single functional somatic syndrome.
Furthermore, when NICE was compiling its Clinical Guideline 53 on CFS/ME, Professor White advised NICE against prescribing anything for bowel problems, stating authoritatively that such interventions: “are not treatments of CFS/ME since bowel symptoms are not part of CFS/ME” (85 FULL 18.104.22.168).
It seems that those who disagreed with such views may have been correct.
On 17th December 2012 a paper on fibromyalgia from the University of Illinois, Chicago, was published in BMC Clinical Pathology which seriously undermines your own beliefs (Unique immunologic patterns in fibromyalgia. Frederick Behm et al: http://www.biomedcentral.com/1472-6890/12/25). Here are some extracts:
“Recent data highlight the role of the immune system in FM. Aberrant expressions of immune mediators, such as cytokines, have been linked to the pathogenesis and traits of FM. We therefore determined whether cytokine production by immune cells is altered in FM patients by comparing the cellular responses …of a large number of patients with FM to those of healthy matched controls”.
“FM is common in patients with autoimmune disorders, such as systemic lupus erythematosus, Sjogren’s Syndrome and rheumatoid arthritis”.
“We utilised multiple immunologic methods to develop an objective test….This test is based on specific abnormalities in the cytokine levels of stimulated peripheral blood mononuclear cells”.
“In the past, FM was claimed to be a rheumatologic, neurologic or psychiatric disease despite the fact that there were no objective links to any of these pathways”.
“Our findings uncovered evidence that FM is instead an immunologic disorder. They prove that the immunologic basis of FM occurs independently of any subjective features”.
The second paper is about ME (Plasmacytoid Dendritic Cells in the Duodenum of Individuals Diagnosed with Myalgic Encephalomyelitis are Uniquely Immunoreactive to Antibodies to Human Endogenous Retroviral Proteins. Kenny L de Meirleir; Marc Fremont, Vincent Lombardi et al. In vivo 2013:12:177-188). Here are some extracts from it:
“Myalgic encephalomyelitis (ME) is a debilitating illness…characterised by neurocognitive dysfunction, inflammation, immune abnormalities and gastrointestinal distress. An increasing body of evidence suggests that disruptions in the gut may contribute to the induction of neuroinflammation. Therefore, reports of human endogenous retroviral (HERV) expression in association with neuroinflammatory diseases prompted us to investigate the gut of individuals with ME for the presence of HERV proteins”.
“Autoimmune diseases such as multiple sclerosis (MS) and systemic lupus erythematosus (SLE) have many symptoms that overlap with those of ME”.
“Neurological manifestations often associated with ME are analogous to the neuroinflammation and cognitive abnormalities associated with MS and SLE”.
“Additionally, gastrointestinal aberrations, which are common to individuals with MS and SLE, are among the most frequent symptoms reported by those with ME”.
“HERV proteins and serum antibodies against HERVs have been associated with a number of autoimmune diseases, including MS and SLE”.
“Individuals with ME have a significant number of symptoms that are similar to those described in autoimmune diseases such as MS and SLE. Additionally, the expression of HERV proteins has been observed in the lymphoid tissue of individuals with autoimmune disease….the gut represents the largest lymphoid compartment and is a significant site of ME-related pathology”.
“In this study we have shown that gut biopsies from 8 out of 12 individuals with ME displayed immunoreactivity consistent with the presence of HERV proteins. However, the same immunoreactivity was not observed in the biopsies of the controls”.
“Additionally, we have shown that the immunoreactivity was observed in cells with a phenotype that is consistent with pDCs (plasmacytoid dendritic cells). These observations suggest that the presence of the HERV protein in pDCs may be associated with a pathological manifestation in at least a subset of individuals with ME”.
“While the expression of endogenous retroviral proteins in the pDCs of ME cases does not intrinsically explain pathology, the observation that the immunoreactive proteins are only observed in pDCs is supportive of this concept. This supposition is further supported by our previous report of the dysregulation of inflammatory cytokines in a cohort of ME cases”.
“These data suggest that our observations in subjects with ME may not be unique to this disease but may, in fact, be common to diseases characterised by chronic inflammation”.
“Although the Canadian consensus criteria for ME and the Fukuda criteria for CFS do not include symptoms of autoimmunity, the recent study by Fluge et al supports the notion that at least a subset of individuals with ME may have an autoimmune element to their disease. Autoimmune diseases such as SLE, MS and rheumatoid arthritis have several common symptoms that overlap with those of ME and all have been associated with the pDC dysfunction. Moreover, the same autoimmune diseases are also reported to be associated with the expression of HERVs”.
“Inflammation is known to increase HERV expression; therefore if pDC-associated inflammation drives the expression of endogenous retroviruses, it is also conceivable that dysregulated expression of other proteins in pDCs may occur. Consequently, the antigen-presenting abilities of pDCs may contribute to the production of auto-reactive antibodies, as is observed in ME”.
“The presence of these proteins in the pDCs of individuals with ME but not in controls does support an involvement of pDCs in ME”.
Clearly the role of the immune system in both FM and ME is important.
You will recall that, in his evidence given on 10th August 2004 before Lord Lloyd of Berwick at the Independent Inquiry into Gulf War Illnesses, Sir Simon is on record as affirming: “A man has got to know his limitations and my limitations are immunology” (Professor Simon Wessely; Minutes of Proceedings).
Can it now be understood why so many people find it inexplicable that Sir Simon was awarded the inaugural John Maddox Prize for being “an inspiration” for “standing up for science”; for working with“courage and dignity to uphold the standards of science and evidence against the forces of prejudice”; for battling “to ensure that sense, reason and evidence base play a role in the most contentious debates” and for his “sustained resilience and determination to promote good science”, whilst Professor White was awarded an OBE for services to medical education on CFS?
Tuesday, February 12, 2013
The PACE Trial recovery rates were finally published - a publication initially refused but then forced on the Principal Investigator by patient pressure, and despite the media being used to gloss over the inadequacies and failings of the whole project.
Flawed from the start, with the goalposts changed mid-course, and ending in ignominy with requests to have the data published being met by silence or rejection, and with a media being orchestrated to stop the whole boat from sinking by making ridiculous and feeble supportive statements.
The PACE Trial was a failure!
It failed to produce any valuable data, it failed to support the biased views of those who only wish to promote ME as a somatoform illness, it failed the patients for whom £5 million of scarce funding was wasted.
Recovery was redefined to mean almost anything the authors wanted it to be as so much deviation had occurred from the original PACE protocol.
Out of the four original definitions for the trial three have been changed.
Recovery was supposed to be defined by meeting all four of the following criteria:
(i) a Chalder Fatigue Questionnaire score of 3 or less (out of maximum 11)
This was changed to 18 out of maximum 33
"We therefore considered a score of 18 (highest integral score below the mean plus 1s.D.) or less as within the normal range for fatigue."
(ii) SF 36 physical Function score of 85 or above
This was changed to 60 or more. The entry criteria accepted people with SF-36 scores of equal or less than 65. So patients could have entered the trial with higher scores and deemed recovered at lower scores. This does not make any sense and the investigators should have explained this as well as discussed what happened to the 78% of participants who did not recover. How many deteriorated?See also: Revalidation Update: why doctors who use or promote CBT or GET for ME/CFS will fail their revalidation
Friday, February 1, 2013
Bob and I ask that other patients do Not follow this action.
We need you to be our voices and advocates with the agencies and your Congress-people.
Yesterday January 29th, I began a hunger strike seeking FDA approval of Ampligen, the only medication in FDA-approved clinical trials for Chronic Fatigue Syndrome, (ME/CFS).
The FDA Advisory Committee voted Ampligen is safe given the serious nature of CFS and the critical unmet need of patients.
Please support access to Ampligen for ALL ME/CFS PATIENTS by sending a note like the one below to the Secretary of Health Kathleen Sebelius, Assistant Secretary of Health Dr. Howard Koh, FDA Commissioner Dr. Margaret Hamburg, and FDA CDER Director Dr. Janet Woodcock and Deputy Director Dr. Sandra Kweder.
You can just copy and paste the emails below, there is also a Template to use as a guide.
Please also email or call your Congressional Representatives and Senators (look them up Here:Just click on your state, http://www.contactingthecongress.org/) and ask them to investigate why the FDA refuses to approve the ONLY medication for CFS despite safe testing for 20 years. This is a health crisis!
Email To: firstname.lastname@example.org, email@example.com, firstname.lastname@example.org, email@example.com, firstname.lastname@example.org, email@example.com, firstname.lastname@example.org
Subject: CFS Patient starts hunger strike for FDA approval of Ampligen
“Long-time ME/CFS patient Robert Miller from Reno, Nevada began a hunger strike in advance of the FDA’s Feb. 2nd, deadline to decide on Ampligen, the ONLY medication in clinical trials for my illness. I support Mr. Miller because my life has been stolen by ME/CFS and I need real treatment options. We have waited 20 years, and we can’t wait any longer. The FDA Advisory Committee voted Ampligen is safe enough to market because CFS is so serious and there are NO medications to treat patients. Please don’t let the FDA reject the only medication CFS patients can hope for any time soon.”
Your Full Name Here: