Research: ME-CFS/FMS/Lyme disease/MPS/etc. (2nd collection)

Discussion in 'Fibromyalgia Main Forum' started by fight4acure, Dec 22, 2009.

  1. fight4acure

    fight4acure Member

    Hi all! I'd like to start a new collection of articles of research. Please add what websites of information that has not been added to the first (really long) list of Research Articles on ME/CFS/ FMS/Lyme disease, MPS, Chemical & Metal Toxins, etc.

    Articles should include: 1) Date of article, 2) Website or source of article, 3) Author of article.

    Note, this is simply for sharing research information and new news on research similar or of the nature of the above illnesses. If one doesn't believe an article, that is fine. This is simply for sharing information and collectively adding it so that newcomers and/or busy people who do not come here often can catch up on the latest news without having to scroll too far back.

    The original post is taking too long for my computer to open up, so I had to make a second list. Thanks to all who participated in the original list and I hope you can continue to participate, to keep me and others informed!

    Please feel free to post any websites of information that you find helpful and would like others to see as well!

    Thank you!
    Fight2Educate! :)

    [This Message was Edited on 12/30/2009]
  2. fight4acure

    fight4acure Member

    Coenzyme Q10 deficiency in myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is related to fatigue, autonomic and neurocognitive symptoms and is another risk factor explaining the early mortality in ME/CFS due to cardi... – Source: Neuroendocrinology Letters, Issue 4, 2009
    by M Meas, et al.
    December 18, 2009

    Myalgic encephalomyelitis / chronic fatigue syndrome (ME/CFS) is a medical illness characterized by disorders in inflammatory and oxidative and nitrosative (IO&NS) pathways.

    This paper examines the role of Coenzyme Q10 (CoQ10), a mitochondrial nutrient which acts as an essential cofactor for the production of ATP in mitochondria and which displays significant antioxidant activities.

    Plasma CoQ10 has been assayed in 58 patients with ME/CFS and in 22 normal controls; the relationships between CoQ10 and the severity of ME/CFS as measured by means of the FibroFatigue (FF) scale were measured.

    • Plasma CoQ10 was significantly (p=0.00001) lower in ME/CFS patients than in normal controls.

    • Up to 44.8% of patients with ME/CFS had values beneath the lowest plasma CoQ10 value detected in the normal controls, i.e. 490 mug/L.

    • In ME/CFS, there were significant and inverse relationships between CoQ10 and the total score on the FF scale, fatigue and autonomic symptoms.

    • Patients with very low CoQ10 (<390 mug/L) suffered significantly more from concentration and memory disturbances.

    The results show that lowered levels of CoQ10 play a role in the pathophysiology of ME/CFS and that symptoms, such as fatigue, and autonomic and neurocognitive symptoms, may be caused by CoQ10 depletion.

    Our results suggest that patients with ME/CFS would benefit from CoQ10 supplementation in order to normalize the low CoQ10 syndrome and the IO&NS disorders.

    The findings that lower CoQ10 is an independent predictor of chronic heart failure (CHF) and mortality due to CHF may explain previous reports that the mean age of ME/CFS patients dying from CHF is 25 years younger than the age of those dying from CHF in the general population.

    Since statins [cholesterol lowering drugs] significantly decrease plasma CoQ10, ME/CFS should be regarded as a relative contraindication for treatment with statins without CoQ10 supplementation.

    Source: Neuroendocrinology Letters, Issue 4, 2009; vol 30. PMID: 20010505, by Maes M, Mihaylova I, Kubera M, Uytterhoeven M, Vrydags N, Bosmans E. Maes Clinics, Antwerp, Belgium. [E-mail:]


    Abnormalities in pH Handling by Peripheral Muscle and Potential Regulation by the Autonomic Nervous System in Chronic Fatigue Syndrome – Source: Journal of Internal Medicine, Aug 20, 2009
    by David EJ Jones MD PhD, et al.
    December 16, 2009

    [Note: according to University of Mississippi Medical Center, the cellular acidity/alkalinity status (pH) of resting skeletal muscle is typically 7.15. It falls - becomes more acid - during exercise in proportion to the intensity of the exercise, as concentrations of pCO2 and lactic acid build up. Exercising to exhaustion normally brings pH to about 6.60. The acidity appears to be an important contributor to perceived/real exhaustion. Measured proton efflux rate rises as pH declines/acidity increases.]

    Objectives: To examine muscle acid handling following exercise in Chronic Fatigue Syndrome (CFS/ME) and the relationship with autonomic dysfunction.

    Design: Observational study.

    Setting: Regional Fatigue Service.

    Subjects & Interventions: CFS/ME (n=16) and age and sex matched normal controls (n=8) underwent phosphorus magnetic resonance spectroscopy (MRS) to evaluate pH handling during exercise. Subjects performed plantar flexion at fixed 35% load Maximum Voluntary Contraction. Heart rate variability was performed during 10 minutes supine rest using digital photophlethysmography as a measure of autonomic function.

    Compared to normal controls, the CFS/ME group had significant suppression of proton efflux both immediately post-exercise (CFS: 1.1 ± 0.5 mM/min v Normal: 3.6 ± 1.5 mM/min, p<0.001) and maximally (CFS: 2.7 ± 3.4 mM/min v Control: 3.8 ± 1.6 mM/min, p<0.05).

    Furthermore, the time taken to reach maximum proton efflux was significantly prolonged in patients (CFS: 25.6 ± 36.1 s v Normal: 3.8 ± 5.2 s, p<0.05).

    • In controls the rate of maximum proton efflux showed a strong inverse correlation with nadir [lowest] muscle pH following exercise (r2=0.6; p<0.01).

    • In CFS patients, in contrast, this significant normal relationship was lost (r2=0.003; p=ns).

    • In normal individuals the maximum proton efflux following exercise were closely correlated with total heart rate variability (r2=0.7;p=0.007)

    • This relationship was lost in CFS/ME patients (r2<0.001;p=ns).


    • Patients with CFS/ME have abnormalities in recovery of intramuscular pH following standardized exercise

    • Degree of which is related to autonomic dysfunction.

    This study identifies a novel biological abnormality in patients with CFS/ME which is potentially open to modification.

    Source: Journal of Internal Medicine, online Aug 20, 2009. DOI: 10.1111/j.1365-2796.2009.02160.x Jones DEJ, Hollingsworth KG, Taylor R, Blamire AM, Newton JL. Institute of Cellular Medicine, Newcastle Magnetic Resonance Centre, Institute for Ageing and Health, Newcastle University, Newcastle-upon-Tyne, UK. [E-mail:]


    Continuing Medical Education Challenges in Chronic Fatigue Syndrome – Source: BMC Medical Education, Dec 2009. 2009 Dec 2;9(1):70. [Epub ahead of print
    by Dana J Brimmer, et al.
    December 7, 2009

    [Note: To read the full text of this open access article for free, click here.]

    Background: Chronic fatigue syndrome (CFS) affects at least 4 million people in the United States, yet only 16% of people with CFS have received a diagnosis or medical care for their illness.

    Educating health care professionals about the diagnosis and management of CFS may help to reduce population morbidity associated with CFS.

    Methods: This report presents findings over a 5-year period from May 2000 to June 2006 during which we developed and implemented a health care professional educational program.

    The objective of the program was to distribute CFS continuing education materials to providers at professional conferences, offer online continuing education credits in different formats (e.g., print, video, and online), and evaluate the number of accreditation certificates awarded.

    Results: We found that smaller conference size (OR = 80.17; 95% CI 8.80, 730.25), CFS illness-related target audiences (OR = 36.0; 95% CI 2.94, 436.34), and conferences in which CFS research was highlighted (OR = 4.15; 95% CI 1.16, 14.83) significantly contributed to higher dissemination levels, as measured by visit rates to the education booth.

    While print and online courses were equally requested for continuing education credit opportunities,

    • The online course resulted in 84% of the overall award certificates,

    • Compared to 14% for the print course.

    This remained consistent across all provider occupations: physicians, nurses, physician assistants, and allied health professionals.

    Conclusions: These findings suggest that educational programs promoting materials at conferences may increase dissemination efforts by:

    • Targeting audiences,

    • Examining conference characteristics,

    • And promoting online continuing education forums.

    Source: BMC Medical Education, Dec 2009. 2;9(1):70. PMID: 19954535, by Brimmer DJ, McCleary KK, Lupton TA, Faryna KM, Reeves WC. Chronic Viral Diseases Branch, Coordinating Center for Infectious Diseases, Centers for Disease Control and Prevention, Atlanta, Georgia; The CFIDS Association of America, Charlotte, North Carolina, USA. [E-mail: Daniel J Brimmer DJB:]



    Virus Is Found in Many With Chronic Fatigue Syndrome

    Published: October 8, 2009
    Many people with chronic fatigue syndrome are infected with a little known virus that may cause or at least contribute to their illness, researchers are reporting.

    The syndrome, which causes prolonged and severe fatigue, body aches and other symptoms, has long been a mystery ailment, and patients have sometimes been suspected of malingering or having psychiatric problems rather than genuine physical ones. Worldwide, 17 million people have the syndrome, including at least one million Americans.

    An article published online Thursday in the journal Science reports that 68 of 101 patients with the syndrome, or 67 percent, were infected with an infectious virus, xenotropic murine leukemia virus-related virus, or XMRV. By contrast, only 3.7 percent of 218 healthy people were infected. Continuing work after the paper was published has found the virus in nearly 98 percent of about 300 patients with the syndrome, said Dr. Judy A. Mikovits, the lead author of the paper.

    XMRV is a retrovirus, a member of the same family of viruses as the AIDS virus. These viruses carry their genetic information in RNA rather than DNA, and they insert themselves into their hosts’ genetic material and stay for life.

    Dr. Mikovits and other scientists cautioned that they had not yet proved that the virus causes the syndrome. In theory, people with the syndrome may have some other, underlying health problem that makes them prone to being infected by the virus, which could be just a bystander. More studies are needed to explain the connection.

    But Dr. Mikovits said she thought the virus would turn out to be the cause, not just of chronic fatigue, but of other illnesses as well. Previous studies have found it in cells taken from prostate cancers.

    “I think this establishes what had always been considered a psychiatric disease as an infectious disease,” said Dr. Mikovits, who is research director at the Whittemore Peterson Institute in Reno, a nonprofit center created by the parents of a woman who has a severe case of the syndrome. Her co-authors include scientists from the National Cancer Institute and the Cleveland Clinic.

    Dr. Mikovits said she and her colleagues were drawing up plans to test antiretroviral drugs — some of the same ones used to treat HIV infection — to see whether they could help patients with chronic fatigue. If the drugs work, that will help prove that the virus is causing the illness. She said patients and doctors should wait for the studies to be finished before trying the drugs.

    Dr. William Schaffner, an infectious disease expert at Vanderbilt University, said the discovery was exciting and made sense.

    “My first reaction is, ‘At last,’ ” Dr. Schaffner said. “In interacting with patients with chronic fatigue syndrome, you get the distinct impression that there’s got to be something there.”

    He said the illness is intensely frustrating to doctors because it is not understood, there is no effective treatment and many patients are sick for a long time.

    He added, “This is going to create an avalanche of subsequent studies.”


    What is Chronic Fatigue Syndrome and How is XMRV Related?

    Chronic Fatigue Syndrome (CFS) has received relatively little consideration since it was first described in 1988, but the recent finding published in the prestigious journal Science showing an association between CFS and a retrovirus, XMRV has focused media and medical attention on this serious, devastating and debilitating neuroimmune condition. While there are some people with CFS (PWC) who are able to continue working and doing some of their activities of daily living, there are also many at the opposite end of the spectrum who are bed-ridden, completely disabled, and can’t even get to the bathroom without assistance. While CFS doesn’t kill many people, it does take away their lives and, in many cases, their livelihood.

    CFS affects anywhere between 1 and 4 million Americans, but many more may “carry” XMRV. It affects people of any age, race, or socioeconomic group. It most commonly affects women 20--50; women are affected about 4 times more commonly than men. In teens and children, the average age of onset is 11.5. As teens, males and females are equally affected, but males tend to do a little better after puberty, whereas females tend to do worse.

    While there are many middle-aged women who feel that they’re “tired all the time,” we have to distinguish between Chronic Fatigue SYNDROME and “chronic fatigue.” This confusion is because CFS was a poor name choice, akin to calling Parkinson’s disease “chronic shaking” or calling tuberculosis “chronic cough.” Other more appropriate names for CFS include the British choice myalgic encephalomyelitis (ME) and XAND (X Associated Neuroimmune Disease.)

    How can you tell if you have CFS or have fatigue for some other reason? Go through the check list below, print it out and take it to your doctor if necessary. It is most important to understand that the diagnosis of CFS is based upon having 4 or more of the following symptoms in addition to the first one (which is required for the diagnosis), and having no other medical problems to explain these symptoms. Currently, there is no “test” for CFS; it is what we call a “diagnosis of exclusion” which means that all other possible causes of your symptoms have to be ruled out before the diagnosis of CFS can be made.

    Dr. Donnica’s Decisionnaire for CFS

    I have had new, unexplained, persistent, or relapsing physical and mental fatigue for at least 6 months. This fatigue is not the result of ongoing exertion or another medical diagnosis; it is not relieved by appropriate rest.
    I have at least 4 of the following symptoms:

    Weakness and exhaustion, lasting more than 24 hours, following mental or physical activity (“post exertional malaise”)

    Unrefreshing sleep, insomnia or excessive daytime sleepiness, despite sleeping for more than 9 hrs per night

    Substantial impairment of short-term memory or concentration, problems with my short-term memory, confusion, disorientation, “brain fog”; difficulty finding the right words or numbers

    Widespread or migratory muscle pain; pain in the joints (without swelling or redness); headaches of a new type, pattern or severity that don’t respond to OTC medicines

    Tender armpit and/or neck lymph nodes

    Persistent or frequent sore throats

    In addition to the symptoms of the case definition, many patients develop other symptoms commonly associated with CFS including:

    Neurally mediated hypotension or orthostatic intolerance

    Multiple chemical sensitivities

    New allergies or food intolerances

    Painful gastrointestinal symptoms similar to irritable bowel syndrome

    New onset of asthma

    Hypersensitivity to light (photophobia) or noise



    Low body temperature or intolerance to heat or cold

    Often feeling “feverish” (without an elevated body temperature) or having chills

    Inappropriate sweating

    Abnormal appetite or decreased sense of thirst

    (page 2 on website):

    What CFS is Not

    CFS is NOT “all in your head.” We have known for years that it clearly has a biological basis and the new findings associating it with the retrovirus XMRV (xenotropic murine leukemia-virus related virus) is just one more piece of evidence confirming that. While we do not yet know whether XMRV is a causative factor for CFS, a “piggy-back” virus, or a virus that PWC react differently to than others, we do know that CFS is NOT “psychosomatic” or a over-reaction to stress. We also know that CFS is NOT a manifestation of depression. How can we tell the difference? There are 3 principle distinguishing factors:

    People with depression classically lose interest in satisfaction from their social and previously enjoyed activities, while PWC desperately WANT to do social and “normal” activities of daily living, but can’t. . .or if they do, they pay the price for one or more days with a complete crash afterwards (post-exertional malaise.) If you asked a PWC what they would want to do if they became “well” tomorrow, they would generally have a long list of activities they longed to do. Someone with classic depression would be more likely to respond to this questions saying “I don’t know” or “I don’t care.”
    People with depression do not have persistent lymph nodes in their necks, persistent chronic sore throats, feel feverish, have night sweats or chills; PWC have these symptoms more often than not.

    If you take a thorough history, most people with CFS were NOT depressed when they first became ill with CFS or for some significant time thereafter. While many PWC later DEVELOP depression, it is clearly long after the onset of their illness. This is called co-morbid or secondary depression, very similar to the co-morbid depression developed by post heart-attack patients. As with those patients, patients with CFS do a little better when their depression is also treated, but just as the heart attack patient still has cardiac risk, they still have CFS.

    The recent data associating CFS and XMRV raises the critically important question about whether CFS is “contagious.” While many experts believe that CFS has an infectious etiology, we do know that it is not contagious in the typical sense. While we know that there have been at least 3 reported community “outbreaks” in the past 25 years, most PWC are isolated cases in their communities. While housemates and sexual partners of PWC may have a slightly increased risk of developing CFS, 80% of PWC have no known family history of CFS. We also know that XMRV is not transmitted in an airborne fashion (as is the flu, for example), but XMRV has been identified in the white blood cells of patients with XMRV, raising questions about the safety of our blood supply and whether XMRV can be sexually transmitted or passed in breast milk or other bodily fluids. This is clearly an issue the CDC needs to study imminently, especially in light of XMRV findings. In the meantime, PWC should NOT donate blood, primarily due to concerns for their own health, but also to be sure not to pass this onto others.


    Identify a physician as close to your home as possible that is knowledgeable about CFS and willing to take you and your condition seriously. Get a proper diagnosis.

    Educate yourself first, then friends and family members and develop as close a support system as possible. Because CFS patients are often homebound, they can easily become socially isolated.

    Put yourself on an “energy budget:” eliminate all non-essential physically draining activities and “save” your energy reserves for your most important activities.

    The healthier you are in general, the better you may manage your CFS. While CFS is not caused or treated by vitamins or supplements, they may help compensate for nutritional deficiencies due to decreased appetite, decreased ability to shop or cook, or dietary imbalances. For example, many patients have anecdotally reported benefits from omega-3 DHA for “brain fog” symptoms; probiotics for GI symptoms; melatonin for sleep problems

    Avoid these things like the plague: alcohol, nicotine, caffeine, perfumes/chemicals. Avoid noisy environments.

    Treat all symptoms independently: sleep medications if needed; allergy medications if needed; avoid known relapse triggers; treat headache/pain complexes; treat secondary depression with talk therapy and medication.

    When you are well enough, practice MILD exercise. This does NOT mean low-impact aerobics! It means starting with 1 minute of slow walking and increasing by 15 seconds per day if possible. Do not exercise during a “flare up” period other than mild stretching.

    Join an online support group or social networking site specifically for people with CFS. No one else can fully understand what you are going through. Same if you are a caregiver for someone with CFS.

    Write to your elected representatives about increasing research funding for CFS!


    Proc Natl Acad Sci U S A. 2009 Sep 22;106(38):16351-6. Epub 2009 Sep 8.

    XMRV is present in malignant prostatic epithelium and is associated with prostate cancer, especially high-grade tumors.
    Schlaberg R, Choe DJ, Brown KR, Thaker HM, Singh IR.

    Department of Pathology and Cell Biology, Columbia University Medical Center, 622 West 168th Street, New York, NY 10032, USA.

    Xenotropic murine leukemia virus-related virus (XMRV) was recently discovered in human prostate cancers and is the first gammaretrovirus known to infect humans. While gammaretroviruses have well-characterized oncogenic effects in animals, they have not been shown to cause human cancers. We provide experimental evidence that XMRV is indeed a gammaretrovirus with protein composition and particle ultrastructure highly similar to Moloney murine leukemia virus (MoMLV), another gammaretrovirus. We analyzed 334 consecutive prostate resection specimens, using a quantitative PCR assay and immunohistochemistry (IHC) with an anti-XMRV specific antiserum. We found XMRV DNA in 6% and XMRV protein expression in 23% of prostate cancers. XMRV proteins were expressed primarily in malignant epithelial cells, suggesting that retroviral infection may be directly linked to tumorigenesis. XMRV infection was associated with prostate cancer, especially higher-grade cancers. We found XMRV infection to be independent of a common polymorphism in the RNASEL gene, unlike results previously reported. This finding increases the population at risk for XMRV infection from only those homozygous for the RNASEL variant to all individuals. Our observations provide evidence for an association of XMRV with malignant cells and with more aggressive tumors.

    PMID: 19805305 [PubMed - indexed for MEDLINE]


    October 8, 2009

    Retrovirus Linked to Chronic Fatigue Syndrome, Could Aid in Diagnosis
    Recently implicated in some severe prostate cancer patients, the retrovirus XMRV has now been found in many with chronic fatigue--changing the landscape for diagnosis and possible treatment

    By Katherine Harmon

    More so than many illnesses, chronic fatigue syndrome (CFS) frustrates those who suffer from it and those close to them, due to its nebulous assembly of symptoms, along with continued controversies over its etiology, diagnosis, treatment and even its nomenclature. Now, the discovery of a familiar retrovirus in many CFS patients could bring new energy to the field—and fresh hope for more specific medical care.

    Chronic fatigue is in part a misnomer. The syndrome often has more to do with immune system abnormalities than pervasive tiredness—although the two can go hand in hand. The symptoms range from exhaustion to muscle pain, giving CFS a reputation among some as a "wastebasket diagnosis". The slipperiness of the syndrome is in part because "it's diagnosed based on exclusion," says Judy Mikovits, director of research at the Whittemore Peterson Institute for Neuro-Immune Disease in Reno, Nev., and co-author of research on the retrovirus findings published online today in Science. Doctors often apply the label if no other explanation can be found for a patient's symptoms, which may be part of the reason it seems to pop up in everyone from overworked career women to continually sick children.

    Roughly 17 million people worldwide are thought to have CFS, but given current diagnosis methods, the true number could be much higher or lower. Having a specific virus to look for would make for much more robust tests and possibly even be a step toward treatment. Mikovits's team thinks they have found just such a candidate.

    The xenotropic murine leukemia virus–related virus (XMRV), a type of gammaretrovirus, has recently been linked to strong cases of prostate cancer. Like CFS, this cancer involves changes in an antiviral enzyme (RNase L). The prostate cancer discovery, described last month by Ila Singh, an associate professor of pathology at the University of Utah in Salt Lake City, et al. in the Proceedings of the National Academy of Sciences (PNAS), along with a traditionally high incidence of cancer in CFS patients, got Mikovits and her team thinking: Would they find the same retrovirus in people with CFS?

    After analyzing biological samples from more than 100 CFS patients for the retrovirus, two thirds of them were found to test positive for the virus—compared with 3.7 percent of 218 healthy volunteers who were screened.

    To find the retrovirus, Mikovits and her team studied documented cases, such as CFS outbreaks in a symphony orchestra in North Carolina and in Incline Village, Nev. "We found the virus in the same proportion in every outbreak," she says. But how are people getting this retrovirus? "Ila's work shows that everyone's susceptible," Mikovits says of the PNAS paper by Singh that illustrates the link between prostate cancer and XMRV and shows that the virus is not linked to a genetic mutation.

    Experiments in Mikovits's lab proved that the retrovirus can be transmitted via blood by infecting healthy cells drawn from volunteers with material from XMRV-positive CFS patients. Mikovits hopes to soon have a better understanding of how the virus might be transferred in the real world, especially among families. If it, for instance, is like human T-lymphotropic virus type 1 (HTLV-1), it may be communicable through breast milk or if it's like a herpes virus that is common in CFS, it may be passed along to offspring.

    Precisely how this virus is related to chronic fatigue, however, remains a mystery. One of the problems with tracking down CFS is that it may not be a single ailment. "We think that the problem is that CFS is a collection of many, many different diseases even though it has similar symptoms," says Brigitte Huber, a professor of pathology at Tufts University's Sackler School of Graduate Biomedical Sciences in Boston. She and others suspect that the retrovirus may be unleashing other underlying conditions and viruses in the body.

    "This new retrovirus may be able, through infecting human cells, [to] induce a transcription of an endogenous virus," says Huber, who has been studying the presence of an ancient retrovirus (HERV-K18) dormant in most people but active in patients with CFS and multiple sclerosis. "We've already shown that Epstein-Barr virus can do exactly this."

    Even in their testing for the XMRV retrovirus, Mikovits says, "We could see a human endogenous virus at the same time" as XMRV. "There are a number of old diseases that seem to be rising at an infectious rate," she says. Although this background noise of various viruses may be difficult to sort though, it brings clues to help researchers find the root cause of CFS. "It's possible, downstream, that this will all feed into the same mechanism," Huber says.

    (Page 2 on site)

    Even before the precise mechanisms are found, work toward finding treatment proceeds. Animal model testing is already underway, and Mikovits notes that her team is looking into some reverse transcriptase inhibitors that have already been approved by the U.S. Food and Drug Administration for other uses.

    "Now we have a drug target and a marker," Mikovits says. "If we treat them with a drug and they get better, we win."

    In the meantime, her team has been making quick strides toward a simple diagnostic test that doctors could use to check for the virus. Tests have been running smoothly in the lab, she notes, with some diagnostics companies already interested in the technology. She predicts a test will be available in less than six months. Mikovits adds that she is "excited that we will actually have some causes…rather than just building a better wheelchair."



    XMRV retrovirus study: Position statement from ME Association 14.10.09
    Posted by meagenda on October 14, 2009

    Update: The ME Association issued a revised and expanded statement on 22 October. See: Revised MEA statement on retrovirus XMRV and ME/CFS (Version 2):

    XMRV retrovirus study: Position statement from ME Association 14.10.09

    Today, UK patient organisation, The ME Association, has issued a Position Statement:

    MEA statement on retrovirus XMRV and ME/CFS (Summary 1)


    On Friday 9 October, the front page of the UK Independent newspaper carried a major news item under the heading, ‘Has science found the cause of ME?’ This referred to new research findings from America which indicate that a recently discovered retrovirus, known as XMRV (xenotropic murine leukaemia virus-related virus), could be playing an important role in causing or maintaining ME/CFS. The news item was accompanied by a very supportive editorial about the need for recognition and research into ME/CFS.

    These two items can be read here:

    The Independent story was soon followed up by the rest of the UK media, including the BBC. Most of the news reports gave a balanced and accurate account of the research but some incorrectly inferred that the sole cause of ME/CFS had now been conclusively discovered. A selection of UK media reports can be found in the October news archive on the MEA website.

    The actual research paper was published in the online edition of Science, along with a perspective written by John Coffin (Department of Molecular Microbiology, Tufts University, Boston, USA) and Jonathan Stoye (National Institute for Medical Research, London).


    Detection of an infectious retrovirus, XMRV, in blood cells of patients with chronic fatigue syndrome. Lombardi V et al. Science October 8 2009


    A new virus for old diseases? Coffin JM and Stoye JP. Science October 8 2009 326; p215



    These are clearly important research findings that could help with both the diagnosis and management of ME/CFS, and we congratulate all those involved.

    However, a number of questions still have to be answered before anyone can conclude that this virus plays a significant role in either the cause, transmission, clinical assessment or management of ME/CFS. Much more epidemiology and laboratory work now needs to be done to answer the essential points set out below:

    . Carrying out further and larger studies using different populations of people with ME/CFS, including people at different stages of the illness (to see if the virus is present in the same percentages in both early and late cases) and in all degrees of severity.

    . Using different international laboratories to test for evidence of the virus.

    . Assessing what, if any, correlation there is between the presence of this virus and (a) severity of symptoms, (b) a clear infectious onset with a known infection, and (c) various other factors involved in sub-grouping of people under the ME/CFS umbrella.

    . Assessing to what extent this virus is also present in other chronic conditions, especially those such as multiple sclerosis and lymphoma where viral infections have been implicated as a causative factor.

    . Assessing whether this virus is acting as a benign marker of disease or immune dysfunction, or is a ‘passenger virus’, or whether it has a role in the actual disease process and development of symptoms.

    . Investigating whether the presence of the virus in healthy people acts as a predisposing factor in the development of ME/CFS (possibly when another infective trigger appears) and/or prostate cancer – rather than being involved in the actual disease process.

    . Investigating what effect, if any, the virus has in healthy people who carry it.

    . Assessing whether people with evidence of the virus should be treated with antiretroviral medication, and if so developing a suitable antiviral drug.

    . Assessing whether animal model studies would help to increase our understanding of the way in which this virus infects cells and possibly causes disease.


    Until these research findings have been robustly replicated, and we have the answers to some of the above questions, there is no point in asking your doctor to be tested for XMRV. This is because the NHS does not currently have the facilities to do so and the testing procedures are only being used in a research capacity at present. But if it does turn out that there is a consistent and strong association with ME/CFS then testing for XMRV would almost certainly have to be made available.


    We appreciate that people with ME/CFS may be very concerned about the possibility of transmission of XMRV through what are termed body fluids (ie blood, saliva, semen). However, until we know more about what this virus does in the body it would be premature to start arriving at firm conclusions and recommending all kinds of restrictions to normal daily living. Remember: we still do not know for certain whether this is a disease-causing virus in humans and whether it plays a role in causing or maintaining ME/CFS.

    One simple way of obtaining some early clues about viral transmission would be to test for the presence of the virus in healthy partners and offspring of people who have the infection and compare the findings to a control group of people that have no such link.

    If the virus is also present in up to 4% of the normal healthy population here in the UK (ie around 2.4 million, or ten times the number of people who have ME/CFS), as appears to be the case in America, there could be more widespread implications for public health, blood donation etc.

    In relation to blood donation in the UK, current advice is that people with ME/CFS who have symptoms, or are receiving treatment, should not donate blood. It would seem sensible in the short term, until we know more about transmission and pathogenicity of XMRV, to consider extending this restriction to people who have recovered from ME/CFS.


    The ME Association is keen to progress this research here in the UK through any way we can help. We have already made contact with virologists who are interested in this virus here in the UK and funding from the Ramsay Research Fund (RRF) could be made available very quickly if we receive a good quality research proposal.

    More information on the work of the RRF can be found here:


    . An American group from the Whittemore Peterson Institute (, in collaboration with the National Cancer Institute and the Cleveland Clinic, have reported finding evidence of a human retrovirus known as XMRV in blood samples taken from people with ME/CFS.

    . Using peripheral blood mononuclear cells, DNA (viral genetic material) from the virus was found in 67% of patients (68/101) compared to 3.7% in healthy controls (8/218).

    . Further studies have found that 95% of people with ME/CFS have antibodies to the virus.

    . Blood samples were collected from people with what is referred to in the paper as CFS who live in different parts of the United States, as well as from healthy controls.


    . Retroviruses are a small group of human viruses that consist of HIV, HTLV-1 and HTLV-2.

    . XMRV is retrovirus that was first described about three years ago in some men who have prostate cancer. It may also be linked to other medical conditions, including fibromyalgia.

    . It is related to a group of viruses that can infect mice

    . This type of virus is thought to be transmitted through body fluids such as blood, semen and breast milk. It is not transmitted through the air – like a flu virus.

    . Testing for evidence of the virus in blood is currently only available at a few specialised laboratories here in the UK.

    We will update this summary as further information becomes available.

    If you want to comment on it please do so via

    Dr Charles Shepherd
    Hon Medical Adviser, ME Association

    Summary 1 dated 14 October 2009

    Media Round ups

    Round up 8: XMRV retrovirus study: Position statement from ME Association 14.10.09:

    Round up 7: XMRV Retrovirus: Whittemore Peterson Institute: CFS: Media Round up 7:

    Round up 6: XMRV Retrovirus: Whittemore Peterson Institute Chronic Fatigue Syndrome study: Videos and audios:

    Round up 5: Supporting Online Material for XMRV Chronic Fatigue Syndrome study:

    Round up 4: XMRV Retrovirus: Whittemore Peterson Institute Chronic Fatigue Syndrome study:

    Round up 3: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome retrovirus XMRV in the media:

    Round up 2: Science 9 October 2009: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome link to retrovirus: 08.10.09:

    Round up 1: Whittemore Peterson Institute (WPI) Chronic Fatigue Syndrome link to retrovirus: 09.10.09:

    [This Message was Edited on 12/23/2009]
  3. AuntTammie

    AuntTammie New Member

    Thank you for compiling all is quite helpful

    I have collected a ton of research over the yrs, however, unfortunately I have not been good about keeping it of my project for the future is to start going thur it all and trying to find a way to better organize it, but that is not going to happen for awhile
  4. fight4acure

    fight4acure Member

    You're welcome! But it was compiled for me and others who lose things all the time. I'm only organized on this site, you have not seen my place, lol.

    The last thread got too big, but can be found through searching "research articles"

    Happy Holidays!

    Fight :)

    P.S. I can in no way take the credit though, as many helped to add to this list for me and others as well.

    [This Message was Edited on 12/23/2009]
  5. QuayMan

    QuayMan Member

    One can get this full article for free by giving your E-mail address at: or else directly at:

    I thought the authors did brilliant work collecting them all (or most, anyway) of the studies which have found abnormal responses to exercise in the illness.

    [A review on CBT and GET in ME/CFS: Not only ineffective and not evidence-based, but also potentially harmful] – Source: NeuroEndocrinology Letters, Sep 15, 2009
    by Frank NM Twisk, Michael Maes
    October 27, 2009

    [Note: the full title of this article, abbreviated above owing to length limitations, is "A review on cognitive behavioral therapy (CBT) and graded exercise therapy (GET) in myalgic encephalomyelitis (ME)/chronic fatigue syndrome (CFS): CBT/GET is not only ineffective and not evidence-based, but also potentially harmful for many patients with ME/CFS."]

    Benign Myalgic Encephalomyelitis (ME) / Chronic Fatigue Syndrome (CFS) is a debilitating disease which, despite numerous biological abnormalities, has remained highly controversial.

    Notwithstanding the medical pathogenesis of ME/CFS, the (bio)psychosocial model is adopted by many governmental organizations and medical professionals to legitimize the combination of Cognitive Behavioral Therapy (CBT) and Graded Exercise Therapy (GET) for ME/CFS.

    Justified by this model, CBT and GET aim at eliminating presumed psychogenic and socially induced maintaining factors and reversing deconditioning, respectively. In this review we invalidate the (bio)psychosocial model for ME/CFS and demonstrate that the success claim for CBT/GET to treat ME/CFS is unjust.

    CBT/GET is not only hardly more effective than non-interventions or standard medical care, but many patients report that the therapy had affected them adversely, the majority of them even reporting substantial deterioration.

    Moreover, this review shows that exertion and thus GET most likely have a negative impact on many ME/CFS patients. Exertion induces post-exertional malaise with a decreased physical performan-ce/aerobic capacity, increased muscoskeletal pain, neurocognitive impairment, "fatigue", and weakness, and a long lasting "recovery" time.

    This can be explained by findings that exertion may amplify pre-existing pathophysiological abnormalities underpinning ME/CFS, such as:
    • Inflammation,
    • Immune dysfunction,
    • Oxidative and nitrosative stress,
    • Channelopathy,
    • Defective stress response mechanisms
    • And a hypoactive hypothalamic-pituitary-adrenal axis.

    We conclude that it is unethical to treat patients with ME/CFS with ineffective, non-evidence-based and potentially harmful "rehabilitation therapies", such as CBT/GET.

    Source: Neuro Endocrinology Letters, Sep 15, 2009;30(3):284-299. PMID: 19855350, by Twisk FN, Maes M. ME-de-patienten Foundation, Limmen, The Netherlands; Clinical Research Center for Mental Health (CRC-MH), Antwerp, Belgium. [E-mail:]

    See also the accompanying article by Twisk and Maes - "Chronic Fatigue Syndrome: La Bete Noire of the Belgian Health Care System."

    [This Message was Edited on 12/23/2009]
  6. fight4acure

    fight4acure Member

    Thanks Hon!

    Fight! :)
  7. fight4acure

    fight4acure Member

    Originally posted by Glenp
  8. fight4acure

    fight4acure Member

    Hope all doctors and psychiatrists have to read this! Please copy and paste this article, print it up with the proper credits to the writer, and give your doctor or doctors this if they do not find this is real. Keep one in your purse in case you end up going to some ER that defines CFS as not real. Also, see the 1st set of research articles that talk about how FMS is real, type it in the search and you shall find it, or look under my name.

    Fight :)
  9. fight4acure

    fight4acure Member

    first posted by glenp
  10. fight4acure

    fight4acure Member

    Consortium of Researchers Discover Retroviral Link to Chronic Fatigue Syndrome

  11. fight4acure

    fight4acure Member

    back up to first screen page.
  12. victoria

    victoria New Member

    as I think there will be other things to consider besides XMRV...

    Role of Chronic Bacterial and Viral Infections in Neurodegenerative, Neurobehavioral, Psychiatric, Autoimmune and Fatiguing Illnesses: Part 1

    Garth L. Nicolson and Jorg Haier British Journal of Medical Practitioners,
    December 2009:2(4) 20-28 or


    Chronically ill patients with neurodegenerative, neurobehavioral and psychiatric diseases commonly have systemic and central nervous system bacterial and viral infections.

    In addition, other chronic illnesses where neurological manifestations are routinely found, such as
    fatiguing and autoimmune diseases,
    Lyme disease and
    Gulf War illnesses,
    also show systemic bacterial and viral infections that could be important in disease inception and progression or in increasing the number and severity of signs and symptoms.

    Evidence of
    Mycoplasma species,
    Chlamydia pneumoniae,
    Borrelia burgdorferi,
    human herpesvirus-1, -6 and -7
    and other bacterial and viral infections
    revealed high infection rates in the above illnesses that were not found in controls.

    Although the specific roles of chronic infections in various diseases and their pathogeneses have not been carefully determined, the data suggest that chronic bacterial and/or viral infections are common features of progressive chronic diseases.

    Read the complete article:

    Or, download it as a pdf file:


    Under the Eightball Confronts History of Lyme Disease [NY]

    Under the Eightball Confronts History of Lyme Disease
    Review by F.X. Feeney The Village Voice, New York City, NY December 15, 2009 or

    Angry passion and visual energy define this extraordinary muckraking documentary. The anger and rage that ignite it stem from the puzzling illness that overtakes Lori Hall-Steele, sister of Timothy Grey, who co-directed the film with Breanne Russell.

    At first, the diagnosis would seem to be CHRONIC FATIGUE, but the symptoms (muscle failure, paralysis) begin to wildly contradict each other, alternately suggesting Lupus, Lou Gehrig's, and Lyme disease.

    Hall-Steele's doctors mask their cluelessness in smug tones; one even tells her, "Everybody dies."


    Read the rest:
  13. victoria

    victoria New Member

    fight, you might want to add the url for Part 1?

  14. fight4acure

    fight4acure Member

    It takes way too long, up to an hour for my computer to even open the darn thing. My computer is 12 years old & this board is different than the first one we had that allowed us to see the pages within seconds. Now my computer cannot handle any long threads.

    Hopefully people will know how to use the search engine for research articles on thread #1.

    Fight :)

    P.S. Thank you for adding an article! :)

    [This Message was Edited on 12/30/2009]
  15. victoria

    victoria New Member

    de nada!

  16. fight4acure

    fight4acure Member

    Chronic Pain Harms The Brain

    In a new study, investigators at Northwestern University's Feinberg School of Medicine have identified a clue that may explain how suffering long-term pain could trigger these other pain-related symptoms.

    Researchers found that in a healthy brain all the regions exist in a state of equilibrium. When one region is active, the others quiet down. But in people with chronic pain, a front region of the cortex mostly associated with emotion "never shuts up," said Dante Chialvo, lead author and associate research professor of physiology at the Feinberg School. "The areas that are affected fail to deactivate when they should."

    They are stuck on full throttle, wearing out neurons and altering their connections to each other.

    This is the first demonstration of brain disturbances in chronic pain patients not directly related to the sensation of pain.

    Chialvo and colleagues used functional magnetic resonance imaging (fMRI) to scan the brains of people with chronic low back pain and a group of pain-free volunteers while both groups were tracking a moving bar on a computer screen. The study showed the pain sufferers performed the task well but "at the expense of using their brain differently than the pain-free group," Chialvo said.

    When certain parts of the cortex were activated in the pain-free group, some others were deactivated, maintaining a cooperative equilibrium between the regions. This equilibrium also is known as the resting state network of the brain. In the chronic pain group, however, one of the nodes of this network did not quiet down as it did in the pain-free subjects.

    This constant firing of neurons in these regions of the brain could cause permanent damage, Chialvo said. "We know when neurons fire too much they may change their connections with other neurons and or even die because they can't sustain high activity for so long," he explained.

    'If you are a chronic pain patient, you have pain 24 hours a day, seven days a week, every minute of your life," Chialvo said. "That permanent perception of pain in your brain makes these areas in your brain continuously active. This continuous dysfunction in the equilibrium of the brain can change the wiring forever and could hurt the brain."

    Chialvo hypothesized the subsequent changes in wiring "may make it harder for you to make a decision or be in a good mood to get up in the morning. It could be that pain produces depression and the other reported abnormalities because it disturbs the balance of the brain as a whole."

    He said his findings show it is essential to study new approaches to treat patients not just to control their pain but also to evaluate and prevent the dysfunction that may be generated in the brain by the chronic pain.

    The study will be published Feb. 6 in The Journal of Neuroscience. Chialvo's collaborators in this project are Marwan Baliki, a graduate student; Paul Geha, a post-doctoral fellow, and Vania Apkarian, professor of physiology and of anesthesiology, all at the Feinberg School

    (Unknown date, but was posted by a member and she may find out, hopefully)

  17. gapsych

    gapsych New Member

    The article was in ScienceDaily (Feb. 6, 2008). It was also picked up by several other sources.

    I think I will go to PubMed to see if there is any information not included in this synopsis.

  18. victoria

    victoria New Member

    This explains a lot, hope this becomes easier for those in pain to get tested!

    I got it from Medscape - anyone can go there and register to read things there, btw...

    American Academy of Addiction Psychiatry (AAAP) 20th Annual Meeting & Symposium: Poster 5. Presented December 4, 2009.

    Cytochrome P450 Gene Implicated in Need for High-Dose Pain Medication

    Nancy A. Melville

    December 17, 2009 (Los Angeles, Ca) — Genetic abnormalities in cytochrome P450 may cause some patients to metabolize opioids at an accelerated or retarded rate, prompting the need for higher doses of medication to control pain, according to a new research presented here at the American Academy of Addiction Psychiatry 20th Annual Meeting & Symposium.

    Chronic pain patients who require high doses of opioids may lead clinicians to suspect them as possible addicts or abusers, but Forest Tennant, MD, lead author of the study and a physician with the Veract Intractable Pain Clinic in West Covina, California, said other factors are at play.

    "I have long felt, as have others, that there could be genetic metabolic abnormalities in some people who require very high or unusual regimens to control pain," Dr. Tennant said.

    "The general idea has been that these people must be drug addicts and abusers, but some felt there was perhaps something behind all of this. A lot of these patients have no history of abuse; they don’t even smoke cigarettes and just don’t fit the profile of drug addict."

    To evaluate the issue, Dr. Tennant recruited 15 chronic pain patients who required 1000 mg or more of a morphine equivalent per day and who tested for deficiencies in one or both of the cytochrome P450 2C9 or 2D6 genotypes. The subjects’ opioid serum concentrations were determined about 1 hour after administration of their usual opioid dose.

    Lazy Gene?

    The results showed that all 3 patients with cytochrome P450 genotype abnormalities achieved only 1 to 2 hours of pain relief after receiving the medication. Two of 8 patients who tested for the 2C9 genotype were poor metabolizers, with both showing very high serum concentrations of fentanyl (8.1 and 16.4 ng/mL) 1 hour after dosing. One of the patients with the 2D6 genotype was also a poor metabolizer and had no detectable serum concentrations of oxycodone and its metabolite, oxymorphone, 1 hour after dosing.

    The findings offer some evidence, albeit highly preliminary, of genetic cytochrome P450 abnormalities in at least some high-dose pain medicine patients, Dr. Tennant said.

    "There are about 50 known genetic abnormalities of the cytochromes, and we can only test 3 or 4 of these at this time," he said. "But even with the tests we did here, the results suggest that there may be metabolic factors with these patients that need to be taken into consideration and may explain why these patients need odd [medication] regimens [requiring dosages that are higher than normal]," he said.

    Dr. Tennant added that he suspects that the abnormalities involve a "lazy gene" that only responds to higher doses of a medication.

    "We believe those very high blood levels of the drug may be necessary to make the lazy gene work — you need to sort of force feed it," he said. "This has been seen in other areas of pharmacology, such as blood thinners. You have to get a very high dose to make the defective gene work."

    Although the research is still in its early stages, genetic testing for such abnormalities may have the potential to help clinicians identify and more effectively treat this patient population.

    Possible Screening Tool

    It may also help clinicians better detect which patients may be at a greater risk of becoming opioid dependent.

    "That’s the corollary to this — high doses could cause dependence," Dr. Tennant noted. "I don’t know if it could be enough to cause people to go to the street and become addicts, but in order to get even a modicum of pain control, they may be extremely dependent on taking high doses on a regular, round-the-clock basis."

    The findings also raise the question of whether these genetic factors could prompt abuse of other substances, including alcohol. At least one of the study subjects fueled that suspicion, he said.

    "One of the 5 with the 2C9 genotype did report being an alcoholic at one point, and she said ‘It’s funny, I would go out and drink with friends and everyone would be getting drunk and nothing would be happening to me’."

    Dr. Tennant noted he has subsequently tested 25 additional subjects and found that about 20% of high-dose patients had these genetic abnormalities. He suggested that now that these genetic tests are available commercially, physicians may want to consider testing for these genotypes.

    "Eighteen months ago, I wouldn’t have been able to do this research because the test wasn’t available, but I feel every patient who is taking opioids for some pain should now be tested," he said. "Not just to add to a database but to give essential information to insurance companies and any other parties who are paying for the drugs."

    "They need to know what’s going on, why these people are taking higher doses of drugs, and they likely wonder whether these patients are addicts."

    Controversial Area

    With pain medication addiction widespread, the temptation to suspect addiction in many cases only makes sense however, and Jon Streltzer, MD, a professor of psychiatry at the University of Hawaii, Manoa, said he questions the very assumption that some patients "require" high-dose opioids to treat chronic pain.

    That is a controversial concept that has much evidence against it at the cellular, physiological, and clinical levels. It may be instead that patients have different susceptibilities to high-dose opioid dependence,” said Dr. Streltzer, who is president of the International College of Psychosomatic Medicine.

    That doesn’t mean genetic factors aren’t at play, but they may be part of a bigger puzzle involving multiple mechanisms, he suggested.

    "It has long been believed that genetic factors are involved in opioid dependence, although which genes are involved and what the mechanisms are is not understood," Dr. Streltzer told Medscape Psychiatry.

    "In addition, chronic opioid intake induces changes in the brain itself, changing the way the cells respond. This is thought to involve the development of craving, which in chronic pain patients can be experienced as pain and the need for more pain medicine."

    Patients can then in fact become more sensitive to pain — as a result of pain medications themselves. "Numerous reports demonstrate enhanced pain sensitivity results from chronic opioid intake by multiple overlapping mechanisms," Dr. Streltzer said. "Patients in programs to alleviate opioid dependence report that their pain improves."

    However, Dr. Tennant said clinicians should not rule out the possibility that patients who say they need high doses may have such genetic abnormalities.

    "The bottom line is that when we see a patient who claims to have severe pain and needs a very high dose, we shouldn’t jump to conclusion that this is abuse," Dr. Tennant said. "There may be metabolic factors here that have to be taken into consideration and may explain why these patients may need odd regimens."

    Dr. Tennant and Dr. Streltzer have disclosed no relevant financial relationships.

  19. fight4acure

    fight4acure Member

    Thank you for this info! I'm working on getting a letter typed up that we can send out to doctors, news, and other business/organizations to get the word out about CFS, and FMS. I'll have it posted in a few days from now.

    Fight :)

    P.S. Please keep the info flowing!!!!
  20. fight4acure

    fight4acure Member

    Posted by Gapsych:

    She wrote:

    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

    For links to other resources about XMRV, please visit the Association's website at