UK study finds no XMRV limk with CFS. :(

Discussion in 'Fibromyalgia Main Forum' started by gapsych, Jan 5, 2010.

  1. gapsych

    gapsych New Member


    I just received this email fromthe CFIDS Association of America. While it is not good news, there may be some methodological differences between the UK study and the WPI, et. al. study which MAY account for the differences. I guess time will tell.

    Dr. Vernon's analysis of the UK study is informative.



    New XMRV Study Published: Analysis Posted to the Association's Website


    A study testing for evidence of XMRV infection in CFS patients in the United Kingdom has reported negative results.

    This is the first publication following the article in the top-ranked journal Science from researchers at the Whittemore Peterson Institute, the National Cancer Institute and Cleveland Clinic that garnered worldwide attention from the media and scientific community.

    The new report, published Jan. 6, 2010, in the open access online journal PLoS ONE, failed to detect XMRV in CFS, but should not be considered a valid attempt to replicate the findings described by Lombardi et al., in the Oct. 8, 2009 Science article.


    Read an analysis of the new latest study by the CFIDS Association's scientific director, virologist Suzanne D. Vernon, PhD at http://www.cfids.org/cfidslink/2010/010603.asp


    For links to other resources about XMRV, please visit the Association's website at http://www.cfids.org/XMRV/default.asp#info.
  2. LISALOO

    LISALOO New Member




    XMRV Negative Results Emphasize Need for Robust Replication Study

    Suzanne D. Vernon, PhD
    Scientific Director





    A study testing for evidence of XMRV infection in CFS patients in the United Kingdom has reported negative results. This is the first publication following the article in the top-ranked journal Science from researchers at the Whittemore Peterson Institute, the National Cancer Institute and Cleveland Clinic that garnered worldwide attention from the media and scientific community. The new report, published Jan. 6, 2010, in the open access online journal PLoS ONE, failed to detect XMRV in CFS, but should not be considered a valid attempt to replicate the findings described by Lombardi et al., in the Oct. 8, 2009 Science article.

    The PLoS ONE paper by Otto Erlwein, Steve Kaye, Myra O. McClure, Jonathan Weber, Gillian Wills, David Collier, Simon Wessely and Anthony Cleare is titled, “Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome.” The investigators tested peripheral blood DNA from 186 routine clinic attendees who met 1994 (Fukuda) CFS case definition criteria and were well-characterized from participation in prior neuroendocrine and cognitive behavioral therapy studies. These 186 CFS patients were reported to be unwell for a median of four years with high levels of fatigue and disability.

    This team of researchers used a special type of DNA “xeroxing” called nested polymerase chain reaction (PCR) reaction to amplify specific segments of the XMRV proviral DNA from the genomic DNA obtained from these 186 CFS subjects. In essence, they were looking to see if XMRV genetic material had integrated into human genetic material, which is a key characteristic of retroviral infection. The experiment included positive, negative and contamination controls, but did not test any samples taken from healthy subjects. The samples were coded so that the origin of the DNA was not known to the person conducting the PCR assays. XMRV was not detected in any of the 186 samples.

    Can this study be considered comparable to the results published by Lombardi et al., in Science? In short, no. Both studies included CFS patients defined by the 1994 case definition criteria, but this is where the comparability ends. Here are some of the ways the PLoS ONE and Science methods differ:

    The blood was collected from CFS patients in different types of blood collection tubes.
    The genomic DNA was extracted and purified using different techniques.
    The amount of genomic DNA included in the amplification assay was different.
    Different primer sequences were used that amplified different regions of the XMRV proviral DNA.
    The conditions of the PCR amplification assay were different – from the numbers of cycles, to the type of polymerase used.
    Should these differences affect an investigator’s ability to detect XMRV? To a microbiologist with experience handling samples and studying various infectious agents (as I am), these variances in procedure could make the difference between detecting XMRV or not.

    It very well could be true that XMRV is not present in the U.K. as Erlwein, et al. suggest in their discussion, but it is also possible that the technique used in the PLoS ONE paper was suboptimal due to the different methods employed, when compared to the original experiments conducted by Lombardi, et al.

    The U.S. Department of Health and Human Services Blood XMRV Scientific Research Working Group is conducting a rigorous study to detect XMRV. Multiple laboratories will standardize methods to optimize sensitive detection of XMRV proviral DNA and viral RNA and then, once methods are standardized, these same laboratories will test coded panels of blood samples obtained from healthy blood donors and CFS patients. We look forward to the results of this study and urge that it be completed expeditiously, especially in light of this report from the U.K. In the meantime, be prepared to read about more studies with conflicting findings. Rather than simply accept or dismiss new information, we will help make sense of why discrepant results occur.

    Perhaps the most important statement in the PLoS ONE paper is the acknowledgement by this group of investigators that CFS is an incapacitating organic disease affecting millions of people worldwide. Once XMRV detection methods are optimized and made widely available, we encourage this group of researchers to take another look at XMRV as a possible explanation for the organic basis of CFS in the U.K.

    Citations:
    Erlwein O, Kaye S, McClure MO, Weber J, Willis G, Collier D, Wessley S, Cleare A. (2010) Failure to detect the novel retrovirus XMRV in chronic fatigue syndrome. PLoS ONE 5(1):e8519. doi:10.1371/journal.pone.0008519

    Lombardi VC, Ruscetti FW, Gupta JD, Pfost MA, Hagen KS, Peterson DL, Ruscetti SK, Bagni RK, Petrow-Sadowski C, Gold B, Dean M, Silverman RH, Mikovits JA. Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Science 8 October 2009. 1179052.


    --------------------------------------------------------------------------------

    Suzanne D. Vernon, PhD, earned her doctorate in virology at the University of Wisconsin at Madison and worked in public health research on infectious diseases at the U.S. Centers for Disease Control and Prevention for 17 years before joining the CFIDS Association of America’s staff as scientific director in 2007. She has more than 70 peer-reviewed scientific publications on topics including human immunodeficiency virus, human papillomavirus, cervical cancer and chronic fatigue syndrome. Dr. Vernon has initiated and participated in numerous international and multidisciplinary research collaborations and she now leads the CFIDS Association’s research program. The CFIDS Association of America is the nation’s largest philanthropic supporters of CFS research.

    ____________________________________________________________________________

    Support validating CFS research with your gift to the CFIDS Association of America. Donate now!






  3. LISALOO

    LISALOO New Member

    This is why I'm worried XMRV will be another enterovirus, or epstein barr, or HHV-6, or CMV, something everyone decides is the cause of CFS but in the end, isn't for most people.

    I don't like that's there's not even a gold standard test.
  4. LISALOO

    LISALOO New Member

    http://www.plosone.org/article/info:doi/10.1371/journal.pone.0008519

    A little hard to completely understand

    Background
    In October 2009 it was reported that 68 of 101 patients with chronic fatigue syndrome (CFS) in the US were infected with a novel gamma retrovirus, xenotropic murine leukaemia virus-related virus (XMRV), a virus previously linked to prostate cancer. This finding, if confirmed, would have a profound effect on the understanding and treatment of an incapacitating disease affecting millions worldwide. We have investigated CFS sufferers in the UK to determine if they are carriers of XMRV.

    Methodology
    Patients in our CFS cohort had undergone medical screening to exclude detectable organic illness and met the CDC criteria for CFS. DNA extracted from blood samples of 186 CFS patients were screened for XMRV provirus and for the closely related murine leukaemia virus by nested PCR using specific oligonucleotide primers. To control for the integrity of the DNA, the cellular beta-globin gene was amplified. Negative controls (water) and a positive control (XMRV infectious molecular clone DNA) were included. While the beta-globin gene was amplified in all 186 samples, neither XMRV nor MLV sequences were detected.

    Conclusion
    XMRV or MLV sequences were not amplified from DNA originating from CFS patients in the UK. Although we found no evidence that XMRV is associated with CFS in the UK, this may be a result of population differences between North America and Europe regarding the general prevalence of XMRV infection, and might also explain the fact that two US groups found XMRV in prostate cancer tissue, while two European studies did not.

    Introduction Top
    A recent study by Lombardi et al. [1] describing a gamma-retrovirus infection in 68 of 101 chronic fatigue syndrome (CFS) patients was notable not only for its claim of a new viral aetiology of a hitherto controversial disease, but also for the fact that proviral DNA could be amplified from the peripheral blood mononuclear cells (PBMC) of 3.75% (8/218) of the healthy controls. This follows an earlier claim that 1.7% (5/300) of healthy Japanese blood donors carried antibodies to the same virus [2]. The virus in question is a recently discovered retrovirus, Xenotropic Murine Leukaemia Virus (MLV)-Related Virus (XMRV).

    In the original identification of XMRV in prostate cancer stromal cells, Urisman et al. [3] confirmed by sequence analysis that XMRV is not a laboratory contaminant, as is often the case with claims of new retroviral associations with disease. It shares >90% sequence identity in gag and env (two of the three viral structural genes) with other xenotropic MLVs.

    An association between XMRV and prostate cancer was strengthened with the demonstration of XMRV protein expression in malignant epithelial cells [4]. However, these results have not been duplicated in studies conducted in Europe [5]–[7]. Both prostate cancer and CFS have been linked to an Arg to Gln mutation at codon 462 (R462Q) in the RNaseL gene, an interferon-induced ribonuclease [8]. On activation, RNaseL destroys single stranded cellular and viral RNA, thereby preventing viral replication, blocking protein synthesis, triggering cellular apoptosis and providing an innate anti-viral response. The two US studies are of interest, not only because this would be a further example of a virus association with cancer, but because they represent the first demonstration of a gamma-retrovirus able to infect human cells, over-riding the intrinsic immune mechanisms that were believed to protect humans from MLV infection.

    The XMRV sequences derived from prostate cancer tissue are identical to those from CFS patients, but differ from xenotropic MLV sequences, endorsing a genuine cross-species transmission. However, the claim that XMRV is preferentially found in prostate tumours from patients homozygous for the R462Q variant [3] is not borne out by the second prostate cancer study to find XMRV in patients [4], nor was the genetic variant detected in CFS patients carrying XMRV [5].

    The finding of Lombardi et al. of a 67% XMRV infection rate among CFS patients, if confirmed, would have a serious impact on understanding the pathogenesis of this complex and debilitating disease and its treatment. Therefore, it was important to determine if CFS sufferers in the UK were carriers of XMRV. We have screened DNA extracts from the blood of CFS sufferers by PCRs targeted at an XMRV-specific sequence and at a sequence conserved amongst most murine retroviruses (MRV).

    Methods Top
    Patients
    All patients gave written informed consent for the use of their DNA to test aetiological theories of CFS, and the study was approved by the South London and Maudsley NHS Trust Ethics Committee. The study recruited 186 patients (62% female, age range 19–70, mean 39.6±11.3years) from consecutive referrals to the CFS clinic at King's College Hospital, London. All patients had undergone medical screening to exclude detectable organic illness, including a minimum of physical examination, urinalysis, full blood count, urea and electrolytes, thyroid function tests, liver function tests, 9 a.m. cortisol and ESR. Patients were interviewed using a semi-structured interview for CFS [9] to determine whether they met international consensus criteria for CFS. All subjects met the CDC criteria [10]; patients with the Fukuda-specified exclusionary psychiatric disorders, or somatisation disorder (as per DSM-IV), were not included. The patient set studied is a well-characterised and representative sample of CFS patients who have been described previously: all were routine clinic attendees, referred within the UK National Health Service, who had taken part in prior studies of neuroendocrine functioning [11] and/or of cognitive behaviour therapy [12]. As is typical of the patients seen in this tertiary care centre, they were markedly unwell. Few were working, and 19% were members of patient support groups for CFS/ME [12]–[14]. The levels of fatigue in this sample were high (mean Chalder Fatigue Scale, 26.3±5.4) [15], as were levels of disability (mean Work and Social Adjustment Scale, total score 28.2±7.2) [16]. The mean GHQ-12 score [17] was 19.7±8.1. Patients had been unwell for a median of 4.0 y (range 1–28 y). Of note was that 45% said their illness definitely related to a viral illness and 45% said it might relate to a viral illness. Overall, we conclude that this sample is typical of CFS patients seen in specialist clinical services in the UK. We also know from collaborative studies that our patients resemble those seen in other specialist CFS services in the United States and Australia [18].

    PCR detection of XMRV and MLV sequences.DNA was extracted from EDTA whole blood using a standard phenol-based organic deproteinisation procedure [19]. DNA concentrations were determined by absorbance at 260 nm (A260). Each sample was amplified in three nested PCRs using primers targeted to an XMRV-specific sequence, to a sequence conserved amongst most MLV and, as a control for sample addition and PCR-inhibition, to a human beta-globin (hBG) sequence (Table 1). Each first-round reaction was performed in a 25 µl volume containing 0.5 units TaqGold (Applied BioSystems, Warrington, UK), 1 x TaqGold reaction buffer (Applied BioSystems), 1.5 mM Mg2+, 200 mM each dNTP, 2.5 pmol each primer to which 5 µl DNA extract or control was added. Reaction conditions were one cycle of 94°C, 8 minutes, 35 cycles of 94°C 30 seconds, 55°C 30 seconds, 72°C 30 seconds and one cycle 0f 72°C, 7 minutes. Second round reaction mixes were identical to the first round and the sample was a 1 µl transfer from the first round reactions. Second round reaction conditions were as for the first round over 30 cycles. PCR amplicons were visualised on a 1% agarose gel stained with ethidium bromide. Each PCR run consisted of test samples, six negative (water) and two positive controls. The positive control was a dilution of a plasmid with a full-length XMRV (isolate VP62) insert, generously gifted by Dr R. Silverman. To validate the sensitivity of the PCR, an end-point dilution of the plasmid was performed. To determine specificity of the PCR, a sample of human DNA from the LNCaP prostate cancer cell line (American Type Culture Collection, code CRL-1740) was amplified with the XMRV and MLV primer sets. To ensure integrity of the DNA extracts, three randomly selected samples were titrated to end-point using the hBG PCR to determine if the PCR copy number equated with the A260. To determine if the DNA extracts exhibited low level non-specific inhibition of PCR, 10 samples were subjected to 30 cycles of the first round hBG PCR (reaction mix and conditions as above) followed by 40 cycles of a nested real-time SYBR-green PCR using the SYBR-green Fast PCR kit (Roche, Lewes UK) according to the manufacturer's instructions.

    Table 1. Oligonucleotide Primers.

    doi:10.1371/journal.pone.0008519.t001
    Results Top
    Nested PCR Validation
    Based on A260 of the purified plasmid, both primer sets (XMRV, MLV) were able to amplify a single target copy added to the reaction. Amplification of 600 ng of LNCaP cellular DNA added to XMRV and MLV PCRs yielded no non-specific bands when viewed on an ethidium bromide-stained agarose gel. Quantification of DNA samples from three randomly selected test samples by end-point dilution PCR with the hBG primer set showed concurrence of the PCR-determined copy number with A260, thus indicating integrity of the DNA preparations. Nested real-time amplification of 10 samples showed no evidence of non-specific inhibition as determined by the slope of the amplification curves and the height of the signal plateau.

    PCR Analysis of Test Samples
    Input DNA ranged from 10 to 600 ng (1.6×103 to 1.1×105 cell equivalents) as determined by A260 of which 149 samples had an input of >100 ng and 106 samples >200 ng. None of the 186 test samples analysed yielded a specific PCR product with either the XMRV or MLV primer sets and no non-specific PCR products were observed. A specific hBG product was amplified from all 186 test samples. The positive control was amplified in each run by the XMRV and MLV primer sets. A stained gel of the XMRV and MLV PCR products is shown in figure 1 and a representative sample of our results with CFS DNA and MLV primers is shown in figure 2.

    Figure 1. PCR products of the XMRV VP62 clone.

    Primers are generic to MLV (lanes 1 and 2) or specific to XMRV (lanes 4 and 5). The sizes of the respective fragments are shown. Lane 3–200 bp molecular size ladder.

    doi:10.1371/journal.pone.0008519.g001Figure 2. Nested PCR from the DNA of 8 CFS patients.

    Products of generic MLV primers (including XMRV) are shown. Lanes 1–8, CFS patient DNA (2nd round); lanes 9 and 10, XMRV 2nd round and 1st round positive controls; lanes 11 and 12, DNA of uninfected cell line LNCaP; lanes 13–18, water controls.

    doi:10.1371/journal.pone.0008519.g002
    Discussion Top
    Unlike the study of Lombardi et al., we have failed to detect XMRV or closely related MRV proviral DNA sequences in any sample from CFS cases. There have been numerous claims for an infective aetiology to CFS over the years, not least because, as in this sample, many patients report that their symptoms were triggered by an infective episode. Prospective epidemiological studies have confirmed that certain infective agents, for example Epstein Barr virus, are unequivocally associated with subsequent CFS [20], even if the mechanisms are unclear and almost certainly multi factorial. Nearly two decades ago, sequences from another retrovirus, the human T-lymphotropic virus type ll, were amplified from the PBMCs of 10/12 (83%) adult and 13/18 paediatric CFS patients, but not from healthy control subjects [21]. However, subsequent studies carried out on small numbers (20–30) of CFS patients, failed to confirm evidence for HTLV (type 1 or 11) [22]–[25] or other retroviruses, including the closely-related simian T lymphotropic virus type l, the prototype foamy virus, simian retrovirus, bovine and feline leukaemia viruses [26] and HIV-1 [23].

    The Lombardi paper is the first to study a significantly larger number of people than that in any previous study and to detect a virus only recently discovered. Our study resembles that of Lombardi et al. in certain respects. Both studies use the widely accepted 1994 clinical case definition of CFS10. Lombardi et al. reported that their cases “presented with severe disability” and we provide quantifiable evidence confirming high levels of disability in our subjects. Our subjects were also typical of those seen in secondary and tertiary care in other centres.

    Our own study also differs from that of Lombardi in other respects. Firstly, the PCR operator was blinded to the provenance of the DNA samples. In fact, with the exception of the PCR controls, all 186 DNA test samples originated from CFS patients. Care was taken to grow the XMRV plasmid in a laboratory in which no MLV had been cultured and no MLV vectors used and the PCR was carried out in a CPA-accredited Molecular Diagnostics Unit which processes only human tissue. Multiple (six) water (negative) controls were included in every run to detect low level contamination and a PCR to amplify a sequence that is conserved in most murine leukaemia viruses was included in order to expose any circulating MLV contamination and to detect any variant of XMRV that might be circulating in the UK CFS population.

    Based on our molecular data, we do not share the conviction that XMRV may be a contributory factor in the pathogenesis of CFS, at least in the U.K.

    [This Message was Edited on 01/05/2010]
  5. gapsych

    gapsych New Member


    Thanks for posting the whole article.

    Unfortunately, it takes time for tests to be standardized. That is why many people are waiting to be tested for XMRV.

    The good news is that the gold standard tests are Science Based Studies. Studies can contradict each other and by finding out why the studies have different results can lead to insights which may ultimately help medical science.

    Like others, I have wondered if only a certain subset of CFS patients have this virus.

    gap
  6. fight4acure

    fight4acure Member

    Thank you for posting this!

    I've taken the liberty to add them to the list of research studies, so that I and possibly others can find it easily.

    Please continue to feel free to post articles on the research collection we started.

    I'm sure that there are docs who want to continue to treat us like we're healthy, when clearly we are not. Dr. Klimas stated in her transcript/discussion of XMRV and CFS that there will be many doctors and researchers who will try to eliminate the idea that we are plagued with viruses. She said that skepticism is going to be expected, and that we should not get upset about their skewed results. I could claim the world was flat and use confirmation bias to make others believe it is true. So be careful not to feed into such confirmation biases these bad-apple researchers have.

    Love,
    Fight :)
    [This Message was Edited on 01/05/2010]
  7. gapsych

    gapsych New Member


    Thanks for the reminder about your post. In many ways skepticism or better put critical thinking is absolutely needed when it comes to science studies.

    I have no idea if the same outcome will be shown in future studies.

    I don't think the UK study was necessarily skewed or confirmation bias was involved. If there is anything changing the results it is probably the methodology used which may or may not effect the results.

    I guess the same thing could be said about the WPI study and confirmation bias, but I do not have a reason to think that. However, I can see why people would be skeptical about the association with the WPI and the Whitmores. That is why replication is so important.

    I am not being negative here, but realistic.

    I think this means it will take longer than we want to find out what is going on with the XMRV and CFS.

    This is the process of science based medicine. Contradictory studies as I said above, are not necessarily negative. In fact if studies come out with 100% results, they are most likely overlooking something.

    gap
    [This Message was Edited on 01/05/2010]
  8. fight4acure

    fight4acure Member

    I will agree to disagree, however, I do like the way you can separate out the details on both sides. I've always appreciated your candid/honest responses, and your different kind of approach to picking apart pieces of a puzzle.

    Love,
    Fight :)

    P.S. Please keep sharing all of the interesting new research studies. I really appreciate the articles!

    I see that Ph.d Suzanne Vernon (who got her Ph.D. at the UW-Madison, Wisconsin, did the study. Does she not have an MD?


    [This Message was Edited on 01/05/2010]
  9. ladybugmandy

    ladybugmandy Member

    so much for a quick replication of the Science article.

    this is bad.

    :(
  10. karynwolfe

    karynwolfe New Member

    I'm not especially interested in anything that Simon Wessely has had his hands on, and I really second the "but [this study] should not be considered a valid attempt to replicate the findings described by Lombardi et al., in the Oct. 8, 2009 Science article" bit.

    It seems the patients tested only had to meet the CDC definition in this one, which alone, is a major issue... This study really doesn't phase me. But thanks for sharing it, gapsych
  11. fight4acure

    fight4acure Member

    I copied and pasted this to educate people on this....

    It wrote on the bottom of the website with the article...
    ------------------------------------------------------------------------------
    Suzanne D. Vernon, PhD, earned her doctorate in virology at the University of Wisconsin at Madison and worked in public health research on infectious diseases at the U.S. Centers for Disease Control and Prevention for 17 years before joining the CFIDS Association of America’s staff as scientific director in 2007. She has more than 70 peer-reviewed scientific publications on topics including human immunodeficiency virus, human papillomavirus, cervical cancer and chronic fatigue syndrome. Dr. Vernon has initiated and participated in numerous international and multidisciplinary research collaborations and she now leads the CFIDS Association’s research program. The CFIDS Association of America is the nation’s largest philanthropic supporters of CFS research.

    -----------------------------------------------------------------------------
    Curiosity striked me about Suzanne and her falsified studies. The same individuals at the CDC years ago, when she worked there, were the same ones who ignored the outbreaks, thinking it was all psychological. I guess that is the point I was trying to make to you earlier, although I can understand what you are saying, but I agree to disagree. & I don't see that she has an MD.

    Love,
    Fight ;)
    [This Message was Edited on 01/06/2010]
  12. ladybugmandy

    ladybugmandy Member

    Negative hints
    Other researchers are trying to further establish whether there is a link between XMRV and CFS, but have not yet published the results. There are hints that these results may also be negative.

    The Robert Koch Institute (RKI) in Berlin, Germany, is also examining the link between XMRV and CFS. In November, its collaborators posted a short statement on the web saying that CFS patients had so far "rarely" tested positive for the virus. They later removed the statement.

    According to Norbert Bannert, one of the virologists at the RKI, the statement was correct, but he adds: "It's not fair to give numbers when you're at the beginning of the investigation, and the first results have not yet been confirmed by an alternative test." He declines to give further details

    McClure has also hinted that several studies due to be published soon have also found no link.

    People with CFS who say they have been tested are less restrained. On one online message board, a handful of people have reported mixed results: none of 10 patients who used one company's test said they turned up positive for the virus, while six out of 12 people who took another set of tests offered by another lab said they were positive for XMRV.

    If the virus link is not borne out, people with CFS are going to feel seriously disappointed, Shepherd warns. "I think people are going to feel very, very let down to put it mildly," he says.
  13. fight4acure

    fight4acure Member

    http://www.ncf-net.org/forum/TowerPsychobabble-W07.htm

    The Tower of Psychobabble: CDC and CAA

    By William Cavanaugh and Valerie Fleet

    An investigation into the treatments of CFIDS/ME, called the Gibson Inquiry, has recently been concluded by a Parliamentary Committee in England. One of the staunch psychobabblers, Trudy Chalder, testified that cognitive behavioral therapy (CBT) "works for chronic pain, chronic diseases i.e. rheumatoid arthritis, cancer, irritable bowel disorders...to name but a few." I wish I my my friend who recently died of cancer knew this! Why isn't it promoted as a treatment for any of the other ailments? Chalder has conceptualized CFIDS/ME to show factors that predispose the person making them vulnerable, factors that preceded their current period of unwellness and the factors that maintain it. An essay by her considers it quite probable that a virus is involved as an initiating factor but, intead of taking past science into consideration, they ignore more than 4,000 articles. Immune abnormalities were being found and published upon in the 1980's and the authors include some who have found it more profitable to join the psychobabble field ("Immunological abnormalities in the chronic fatigue syndrome," Lloyd, Wakefield, et al.) Their references merely include other psychotherapists and tell you that a composite patient with CFIDS/ME has a perfectionist personality, an abusive or absent father who was sexually abusive along with a needy mother. It sounds distinctly like what the CDC's William Reeves has adopted as his new criteria. For those older, they experience a death of a husband followed by a virus and now "rests" instead of working at a job. Public income support permits this person to continue her "sick role."


    To be perfectly honest, there are actually two types of CBT. One respects that a disease has occurred that has no real treatment and helps a patient "cope" with their new, closely restricted lifestyle dictated by this disease. The other type is based upon the thinking that one's illness is due to the wrong way of viewing their lives or of past bad experiences. One survey done by the 25% ME Group found CBT was the treatment that was the most unhelpful one offered with only GET (Graded Exercise Therapy) getting worse results. These are the two treatments suggested by our own Centers of Disease Control and Prevention (CDC). Both are unproven and GET has been proven to actually be harmful to patients that result in relapses that have been found to last weeks, months, or even years.


    Blaming the patient has always been the easy way out. Indeed, when the much publicized Incline Village epidemic occurred, it was referred to as the "yuppie flu" despite many becoming sick that were not in the category of rich, vacationing tourists. The CDC refused to take the outbreak seriously although many of these original patients remain severely sick and several have joined our Memorial List. In fact, this whole perception of a typical personality can be seen in recent comments by William Reeves about an abusive childhood which were translated into an article by Mary A. Fischer in The Oprah Magazine when past soccer star Michelle Akers now attributes her illness to "some difficult family challenges" and the CDC's Suzanne Vernon promotes this theory by saying "Early life adverse events...can really mess us up and change the architecture of the brain." Where is the evidence of this? Why don't most patients fit the "typical" scenario?


    CBT is pseudoscience. While it may look like science, it has no scientific implications whatsoever. A recent book by William Epstein from the University of Nevada explains that "CBT, like all of psychotherapy, is more akin to the mysticism of the mind-cure and faith healing than to clinical science...the theory has a contrived, ad hoc quality...it relies on very uncertain discordant research that only allows box-score summaries of 'many studies' or of 'most research' or of 'most evidence'..."


    What does this have to do with the CFIDS Association of America (CAA)? Well, the CDC has used their vast powers of public relations to hold press conferences and get their stories widely distributed in magazines such as The Oprah Magazine and the physicians interviewed in all these stories have close ties to the CAA. And. of course, the CDC funds the CAA for big bucks annually.


    And they brag about it. From a 2002 Annual Report of the CAA called "Putting CFIDS First", the CAA brags that "the Association and The Sheridan Group (their lobbyists) worked closely with CDC officials including Dr. William Reeves and report "in collaboration with Emory University researchers, CDC is supporting a separate study using functional magnetic resonance imaging (fMRI) to examine changes occurring in the brain over time..." Did you read the results? They were buried as the CDC now admonishes all physicians that any brain tests are "experimental."


    The CAA brags about how much money they spend on research but, there is no follow-up and no publications that we could find that result from any of the recently funded work going back quite a few years. The funding is disjointed and the rhetoric is full of promises that never materialize. In this 2002 report, the CAA funded two researchers. One, Theodore C. Friedman, M.D., got $155,000 to look at a possible cause of the decreased blood flow to the brain by examining if renin, a hormone made in the kidneys, is responsible. We could find no follow-up to this work published anywhere and it's now 2007. Another researcher, Giris Jacob, M.D., from Israel, got funded to look at patients in the very early stages of CFIDS/ME. What did he find? No follow-up paper was published nor did the CAA let its members know of any results. And these were the only two researchers funded that year. They claim the work they fund brings "hope" to patients but, if it does, the patients are being fooled. It is much like the promise of CBT and the hype to promote it. There's no foundation to base it upon. In fact, it is cruel and abusive to patients. By ignoring scientific findings and by not publishing results, the wrong theories can be funded over and over again. Whether the results are good or bad, withholding these findings do more harm than good.


    But wait, there's more! The CDC, from the year 2000 to 2003, has had committee meetings to change the definition of CFS in order to make it a mere psychological fatiguing illness and to bypass the much more stringent 1994 research criteria that physicians have relied upon. They published a paper in 2005* that watered down "CFS" and eliminated any thought of it actually being M.E. This committee was called the International CFS Study Group and it defined "CFS" by testing 227 patients of whom only 70 had been diagnosed as having CFIDS/ME. Basically, they separated those "fatigued" from those not "fatigued" while they pretended to be in search of standarized criteria. Of course, there is no marker yet for this disease so they were able to get away with this. And who were the members of this committee that has tried valiantly to push back the actual science by decades? Well, many psychobabblers including the "king" of psychobabble, Simon Wessely and quite a few of his cronies. Canada's most famous psychobabbler, Susan Abbey, participated along with close to another 40 others. Some of the names of this committee may surprise you such as K. Kimberly Kenney McLeary (CAA), Nancy Klimas, Benjamin Natelson, and Leonard Jason while others you fully expect such as the CDC's William C. Reeves, Suzanne Vernon, along with four others from the CDC.


    So now you may understand why any research that comes out of the CDC is quite bogus. They are not actually using people who have met the CDC Research Criteria but are, instead, using an even less stringent version created by this committee that met a few times a year for a few years. The gene study that is receiving the greatest PR treatment known yet is an outcome of this new classification. What it means is that the research means absolutely nothing and those who are joining the chorus promoting and hyping it are doing none of us any favors. Without the fanfare of psychobabble known in other parts of the world, the CDC has managed to demote CFS to a wastebasket category. The Wichita hospital stay used in their highly touted surveillance study included only six patients that fit the Fukuda criteria and those that failed the Romberg Stance were excluded even though experts advise using it along with the Canadian clinical criteria.


    Is anyone listening? A lead story from the American College of Physicians was titled "The Patient wtih Medically Unexplained Symptoms." The author, Mark Feldman, M.D.. is from the Presbyterian Hospital of Dallas. The first sentence of his paper includes a reference to an article in the Lancet from 1999 by Simon Wessely et al (354:936). To remind you, Wessely said, in 1994, "I will argue that ME is simply a belief that one has an illness called ME." In case there is any doubt that he is including CFIDS/ME, his second sentence names just a few of these including "fibromyalgia, tension headaches, irritable bowel syndrome, nonulcer dyspepsia, atypical and non-cardiac chest pain, chonic fatigue syndrome" and many more. What seems most important to him is that "the medical and economic impact associated with the care of these patients is staggering." He suggests that "enlightened specialists" find the diagnostic criteria is not specific so he implores all that belong to the American College of Physicians to try all on antidepressant medications along with cognitive behavioral therapies, to minimize their referrals and to regard all these "functional syndromes as a group of closely related disorders, rather than splitting them into multiple disorders of unknown cause." This is the key stragedy of the CDC. If they group all these illnesses together, they ensure obscurity. While they tout their national tour to educate others with "The Faces of CFS" and other nonspecific entities, they pretend to care while they encourage no testing and, in that way, not only ignore all science but advise against it on their website. The director of the CDC, Dr. Julie Gerberding, again mentioned the "groundbreaking new research" that made patients "not being able to cope with ...psychological...challenges." She bragged about "our partners, including the CFIDS Association of America."


    The CDC seems determined to catch up to the psyhobabble it has encouraged in the United Kingdom. The draft guidelines from the UK's National Institute of Health & Clinical Excellance (NICE) issued this fall clearly extol CBT and exercise as the favored treatments as does the CDC. Many who contributed to the watering down of the new definition used by the CDC have contributed, as well, to the NICE guidelines that list ME (and CFS) under "Functional or Psychosomatic Disorders: Medically Unexplained Symtpoms." Their direction could not be made more clear.


    Just one week after the CAA/CDC held their press conference saying "CFS is a real disease," headlines from coast to coast shouted that childhood trauma was a real risk factor for CFS (Archives of General Psychiatry, Nov. 2006). Marcia Harmon, an employee of the CAA, told patients online that the press conference was "a triumphant success." When patients complained about the newest headlines in the study funded and done by the CDC, she posted to patients on an online announcement group that the study had "important limitations" and that the lead author is "no longer affiliated with the Centers for Disease Control and Prevention's CFS Research Group." But those reading it all over the United States and Canada were left with the information that "early adverse experience" is a "risk for CFS" in a study by the CDC and Emory University. The author of the acclaimed historical novel on CFIDS/ME (Osler's Web), Hillary Johnson, posted on that same online group to inquire if Harmon also was "using the CFIDS org's finanical oomph to disseminate a press release to the media that explains the absence of rigor in this research...the story appeared unchallenged on Web.MD less than a week after the press conference." Ms. Johnson went on to say, "In past years, certainly, epidemiologists at the Centers for Disease Control have had few reservations about jumping all over published research indicating a biological basis for 'chronic fatigue syndrome,' even when leveling ad hominem attacks against the authors when they felt so inclined. If the agency has switched course, and is now determined to validate the suffering of 'cfs' patients and enhance recognition of the seriousness of this reputedly grossly under-diagnosed disease --- which they recently discovered has a biological basis --- shouldn't the CDC and its pubic relations contractors also be ready to pounce with equal enthusiasm, all over research that undercuts their own newfound thesis? Or does it? As the headline of Medical Condition News said, "Chronic fatigue syndrome begins with childhood trauma and stress. Does that bolster the gene study that cited an inability to handle stress as one highly expressed gene that was never verified via PCR testing? On the other hand, shouldn't that be a critical element of their 'campaign'?" We have to agree with the author that some of that $4.5 million spent on their public awareness campaign could have gone toward getting out more of the truth instead of continuing to pat each other on the back on how gullible the media is in this country, especially when this newest CDC study was in the news just days after the CAA asked patients to send "a message of gratitude to Dr. Gerberding", the CDC's director. The medical community did not hear about the press conference but they were given the information that the illness "begins with childhood trauma and stress" and one online medical group put this under the category of "anxiety and phobias."


    We admit we were remiss in sending that "message of gratitude to Dr. Gerberding. Instead, we want to thank you, National CFIDS Foundation, for hearing a different drummer and focusing on real research for a very real disease. You are our beacon of hope and we depend upon you to remain truthful.

    -------------------------------------------------------------------------------
    *"Chronic Fatigue Syndrome - A clinically empirical approach to its definition and study," Reeves et al, BMC Medicine 2005, 3:19.

    Bill and Valerie orginally submitted a Letter to the Editor. We asked them to expand the information and include verification which they did. Both belong to the same support group in California.

    The National CFIDS Foundation * 103 Aletha Rd, Needham Ma 02492 * (781) 449-3535 Fax (781) 449-8606
  14. RunningAntelope

    RunningAntelope New Member

    karynwolfe wrote: "I'm not especially interested in anything that Simon Wessely has had his hands on, and I really second the "but [this study] should not be considered a valid attempt to replicate the findings described by Lombardi et al., in the Oct. 8, 2009 Science article" bit.

    It seems the patients tested only had to meet the CDC definition in this one, which alone, is a major issue... This study really doesn't phase me. But thanks for sharing it, gapsych."

    I have the same personal sentiment. Moreover, I believe the CFIDS Association of America has had a rather dubious relationship with the CDC over the years, and I, for one, would neither send them a drop of charitable money, nor put too much stock in anything they affix their name too. That's merely my personal opinion based on what I've read and researched.

    It is rather significant that the CDC removed Reeves from spearheading CFIDS research at the CDC and moved it under the HIV/retroviral unit. Obviously, there's enough concern about a legitimate finding and the nation's blood supply, that there's some biopolitical machinations going on. Moreover, the lack of corroboration, while admittedly necessary to advance any legitimate research, sounds all too familiar. When Elaine DeFreitas first discovered an HTLV-II-like, possibly, mouse retrovirus some two decades ago, the CDC could not corroborate her research, most likely because of manipulating the primer stringency backgrounds and such. And it's de ja vu all over again. These are highly sensitive techniques. In fact, the VPI is registering a lot of false negatives, which is why it is probably recommended to wait until their more sensitive antibody test comes out.

    There's no doubt in my microbiology mind that the original outbreaks of this illness and my very own disease progression bear the hallmarks of a RETROVIRUS, something akin to HIV but not HIV. I will readily admit that perhaps I am but one of a minor subtype, that this disease has evolved in someway or is modulated by other genetic, environmental, or psychological factors, or, more likely, that perhaps not everyone in the CFIDS bucket suffers from CFIDS but are thrown under the umbrella anyway.

    Bill.
  15. lisagra

    lisagra New Member

    can you write me...i want to discuss azole parade.
    lisagrasso at comcast dot net

    tx, lisa
  16. TeaBisqit

    TeaBisqit Member

    Mine was viral onset, too. In my case, I believe it's a virus. I don't know if XMRV is THE one, but it's a virus.

    This particular study, I don't think should be taken seriously. If they are just testing people who are simply "tired" and fall under the horrible CFS name, it's not accurate at all. When they test people who are housebound and bedridden, then they should speak. There are many people who were either misdiagnosed simply because of ignorant doc's who think anyone who is tired should be labeled CFS, and there are people who simply claim to have it and don't simply because they work three jobs and think their exhaustion is CFS. I want to see them test REAL cases of CFIDS, CFIDS NOT CFS.

    But the problem with a study like this awful one, is that now it will be publicized and people will continue to not believe us.
  17. LISALOO

    LISALOO New Member

    Susan Vernan did not do the study, she analyzed the results.

    The people they tested were not just people that were tired, "The investigators tested peripheral blood DNA from 186 routine clinic attendees who met 1994 (Fukuda) CFS case definition criteria These 186 CFS patients were reported to be unwell for a median of four years with high levels of fatigue and disability."

    so, "Both studies included CFS patients defined by the 1994 case definition criteria" So you can't use that to completely discount this british study.

    The article was. "published Jan. 6, 2010, in the open access online journal PLoS ONE." I'm not familiar with british journals, so I'm not sure of the legitmacy of this one.

    However, the most important part:
    Here are some of the ways the PLoS ONE and Science methods differ:

    "The blood was collected from CFS patients in different types of blood collection tubes.
    The genomic DNA was extracted and purified using different techniques.
    The amount of genomic DNA included in the amplification assay was different.
    Different primer sequences were used that amplified different regions of the XMRV proviral DNA.
    The conditions of the PCR amplification assay were different – from the numbers of cycles, to the type of polymerase used.
    Should these differences affect an investigator’s ability to detect XMRV? To a microbiologist with experience handling samples and studying various infectious agents (as I am), these variances in procedure could make the difference between detecting XMRV or not."

    I'm not sure which collection and testing was correct, this way or the original WPI study.



    I think XMRV might be like CMV, or HHV-6, a side virus not the cause.

    Only 50% are testing postive through WPI, and I'm guessing these are desperate people who have been sick for a long time, definatley have CFS. 50% isn't enough.

    [This Message was Edited on 01/06/2010]
    [This Message was Edited on 01/06/2010]
  18. fight4acure

    fight4acure Member

    To my understanding it was Suzanne Vernon who supervised the study and spoke out about the results. What doctors did the study?

    I appreciate your rebutal! One thing I want to say is that you are correct in that the people that were tested were ill with CFS for at least 4 years, as the study says. No, they weren't the most severe people, but they are adequate enough, one would think, to get favorable results.

    The one thing I do want to mention though, is that Suzanne Vernon is in charge, as the director of research. I'm sure she gets paid quite well to take her, "leap of faith" into the CFS community. I'm not quite sure that she has changed her mind on all of the studies and research papers she has written on CFS which tend to be skewed towards her favor, specifically mentioning that CFS is a result of some psychological illness.

    Now, I'm no person to say that I haven't had depression and other problems in my life. But, there are tons of people with more emotional problems in their life who do not have my illness. Also, I was not depressed at the time of exposure to whatever it was that made me so sick that I nearly died. So, my personal sentiment is that this CFS and FMS has had so much abuse from the CDC and previous members, & TONS OF MONEY has been wasted due to the neglectful member researchers of the CDC thinking that CFS & FMS was in our heads. We did not bring this on ourselves.



    Love,
    Fight :)

    P.S. I just saw that you edited your post, and I want to add that if it was a mistake, then she should have publicly announced it. As far as I understand, if you know a mistake has been made, you publish it with the mistake.[This Message was Edited on 01/06/2010]
    [This Message was Edited on 01/06/2010]
  19. LISALOO

    LISALOO New Member

    Another article said "Few participants were working.

    "The research was carried out by Dr Otto Erlwein and colleagues from Imperial College London and King’s College London"

    This is an excerpt from the actual journal article, "Failure to Detect the Novel Retrovirus XMRV in Chronic Fatigue Syndrome" citing the authors and who did the work

    Otto Erlwein1, Steve Kaye1, Myra O. McClure1*, Jonathan Weber1, Gillian Wills1, David Collier2, Simon Wessely3, Anthony Cleare3

    1 Jefferiss Research Trust Laboratories, Section of Infectious Diseases, Wright-Fleming Institute, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London, United Kingdom, 2 Social Genetic and Developmental Psychiatry Centre, Institute of Psychiatry (King's College London) De Crespigny Park, Denmark Hill, London, United Kingdom, 3 Department of Psychological Medicine, Institute of Psychiatry, King's College London, Camberwell, London, United Kingdom
    [This Message was Edited on 01/06/2010]
  20. fight4acure

    fight4acure Member

    Thank you for mentioning this. I'm racking my brain now, and only two marbles are rolling around lol...

    I still do not understand that if they made any errors, that they did not report the errors, as we must do when a research study is being reported.

    Love,
    Fight :)

    Thanks for editing and posting the original article. I guess I need some caffeine and need to get my mind awake enough to notice these fine details you have pointed out.

    Thank you!
    Fight :)[This Message was Edited on 01/06/2010]