Monday, October 31, 2011

Dr. Oystein Fluge and Professor Olav Mella: van der Meer's criticism contains several errors

Fluge replied to jvandermeer on 31 Oct 2011 at 17:47 GMT: RE: Rituximab in CFS; more research needed

To the editor,

We are glad to address the critics of van der Meer and co-authors as response to our recent paper in PLoS One [1], where we presented a small randomized, double-blind, placebo-controlled study of the CD20-directed antibody Rituximab as intervention in chronic fatigue syndrome (CFS/ME) patients fulfilling the Fukuda criteria.
At one point we totally agree with the critics: Rituximab should not be used to treat CFS/ME outside of clinical studies at present. We also agree that more research is needed.

van der Meer and coauthors have problems believing our results in part based on what they see as atypical response kinetics for Rituximab and a lack of theoretical understanding of why the drug should show efficacy in CFS/ME. We do not support their statement that a response within the first days to weeks necessarily is the usual pattern in other diseases where Rituximab intervention is used. Autoimmune cytopenias and some autoimmune diseases such as acute demyelinating polyneuropathy [2] may respond early, while in other diseases the responses usually start to occur after months. In accordance, the endpoints for clinical studies, or clinical benefit demonstrated in observational studies, are often defined at 6 - 12 months after treatment, with the clinical effects subsiding over the following months or year, such as in rheumatoid arthritis [3], lupus nephritis [4], and primary antiphospholipid antibody syndrome [5]. As an example, in a case study of pulmonary alveolar proteinosis, in which autoantibodies to GM-CSF have been demonstrated, the levels of autoantibodies declined the first three months after Rituximab treatment, while effect on alveolar-arterial gradient was seen at six months, and improvements in pulmonary function tests and CT scans were evident at nine months [6].

The full consequences of the action of Rituximab in other autoimmune diseases are only partly known, and also which of the known modes of action that are of greatest relative importance in individual patients [7]. CFS/ME is not a disease with evident widespread inflammatory lesions as in some established autoimmune conditions and the mode of action could thus be different from that seen in for example rheumatoid arthritis or lupus. Reduction of autoantibody levels (wash-out by reduced production following B-cell depletion) to a critical level before clinical responses become evident could therefore be one plausible mechanism explaining what we observed.

van der Meer and colleagues raise methodological concerns regarding the measurements of fatigue in our study. We used a visual analogue scale for self-reported symptoms every second week during 12 months follow-up. A similar scale was used in a previous study of intervention in CFS/ME [8]. We have not validated the symptom scales used further. However, as it was a randomized study, all patients (Rituximab and Placebo) had the same follow-up. The Fatigue-score was used as the main criterion for response assessment, and the GLM analysis for repeated measures showed a significant interaction time by intervention group, which we believe is the most important result in the study. The data in this analysis are a direct reflection of the self-reported symptom scores registered every second week, where the patients wrote down a number representative of the whole preceding two-week period, thus taking into account the day to day variations in symptoms typical for many CFS/ME patients. The critics question if a physician-rated fatigue score in a subjective complaint is relevant. The reason for including this in the protocol was to see if there was a good agreement between what the patients told us at the consultations and the figures they reported in their files. In general, the patient and doctor values were in good accordance (Figure 2, panels B and D).

van der Meer and colleagues argue that the clinical size of effect seems small. Figure 2 (panel A) shows the self-reported Fatigue-score for each patient, demonstrating the distribution of responders and non-responders at the different time intervals. In panel B, the mean values for Fatigue score in each group are shown and include the counts of the non-responders, also reflecting that the time frames for clinical responses vary among the patients, thus tending to reduce the numerical value at a given time. We do not agree that the clinical effects are small or clinically irrelevant, and as stated in the manuscript the patients assessed these to be important for their quality of life, generally affecting all CFS/ME related symptoms.

Some limitations of our study pointed at by the critics have already been addressed in the paper. The choice of the primary endpoint at three months (based on responses of the first two pilot patients given Rituximab) [9] and the lack of predetermined exact description of responses with respect to duration and extent of improvement, are caused by limited experience with the kinetics of responses after B-cell depletion in CFS/ME. After seeing the first two pilot patients with response on all CFS/ME symptoms, later followed by relapses, and seemingly as the result of the intervention, we made a decision to do a limited randomized study. A phase II study without a control group in a disease with subjective endpoints would probably have problems convincing both study readers and ourselves. Our study size was a balance between having a fair chance of detecting a difference between the intervention groups and what could be handled within a clinical university department, without any industrial or other external economical support for the clinical part of the study.

Concerning the blinding, randomization was done by the hospital pharmacy and the infusion bags packed in a manner that did not disclose their content for either the patients or the nurses administering the infusions. Any complaints during infusions were to be dealt with by the doctors on call and not the researchers. The observed side effects (Table 5) did not clearly indicate to patients or physicians which treatment had been given. We did not (as suggested by the critics) ask the patients which drug they thought they had been given. We believe the blinding for both patient and researchers was good.

van der Meer et al. comment on the high rate of other autoimmune diseases in the patients and their relatives in this series. This is not an original observation and has been noted also by others. One of the senior authors of our manuscript, prof. H. Nyland, is the single physician in Norway who has seen and systematically registered most CFS/ME patients and he confirms this finding his patients. We can agree that including a single case of carpal tunnel syndrome (CTS) as an autoimmune entity is questionable. Nevertheless, the CTS is greatly overrepresented in patients with known autoimmune disease, like diabetes type I, lupus, and rheumatoid arthritis, and is quite often a heralding condition before the systemic autoimmune disease is evident. Although multifactorial aetiology of CTS is a favoured view, a genetic and autoimmune component is probable in many patients. Concerning the question of a relation between a family history of autoimmune diseases and response, the material is of course too small to answer that. Table 1 shows that previous autoimmune disease in patients or first degree relatives is not higher in the Rituximab than in the placebo group.

Importantly, we have not demonstrated that CFS/ME is an autoimmune disease with disease-specific autoantibodies, but we have stated as a hypothesis that the observed clinical pattern of responses and relapses could be compatible with such a mechanism. Alternatively, influence on other aspects of B-cell function could be the key to understand the effects of B-cell depletion in CFS/ME, such as antigen-presentation to T-cells, influence on other immune cells such as dendritic cells, or changes in Th1 and Th2 balance.

Finally, van der Meer and colleagues raise major concern on the fact that we are performing an open-label phase II study, exploring Rituximab induction followed by Rituximab maintenance, instead of a new high-quality randomized study. They also suggest that we overestimate the effects and downplay the possible serious side effects. The critics may have fallen into the same ditch of prejudice as they indicate we have.
We admit the strong and repeated responses to new Rituximab infusion seen in our three pilot patients may have influenced us. We have later treated another lymphoma patient with preexisting CFS/ME who also experienced a clear response on all CFS/ME symptoms from four months after start of treatment (8 cytotoxic chemotherapy courses (CHOP) with addition of Rituximab), and she still has response of CFS/ME symptoms 2 ½ years later. Other physicians treating patients having both CFS/ME and lymphoma elsewhere in the world have informed us of similar responses to Rituximab. The total experience with Rituximab in our opinion warrants a study to optimize the use of the drug.
Based on the current study, there is now a Norwegian national initiative to do a randomized, blinded, multicenter Phase III study to verify or reject the conclusions of the PLoS One study. In the planning of this national study, results of our exploratory phase II study with Rituximab induction and maintenance will be important for the scheduling of the drug administration.

CFS/ME according to Fukuda or Canadian criteria is in many patients a very serious and debilitating disease. Current treatment is for many patients highly unsatisfactory and we believe it is justified to find new interventions and learn more of the pathophysiology, of which we at the time being know little. The side effects of Rituximab in this particular patient group of patients is of course presently largely unknown, although there is vast experience with the drug in B-cell lymphomas and established autoimmune diseases. We believe the severity of disease in many CFS/ME patients balances the known risks. That was also the opinion of most patients who were given the option to participate in the current study at a time when only three pilot patients had been treated with the drug.


1. Fluge O, Bruland O, Risa K, Storstein A, Kristoffersen EK, et al. (2011) Benefit from B-cell depletion using the monoclonal anti-CD20 antibody Rituximab in chronic fatigue syndrome. A double-blind and placebo-controlled study. PLoS One 6:10 e 261238
2. Motoyama R, Yamakawa K, Suzuki S, Kusunoki S, Tanaka M (2011) Rapid improvement by rituximab treatment in a case of demyelinating polyneuropathy with anti-myelin-associated glycoprotein antibody. Rinsho Shinkeigaku 51: 761-764.
3. Edwards JC, Szczepanski L, Szechinski J, Filipowicz-Sosnowska A, Emery P, et al. (2004) Efficacy of B-cell-targeted therapy with rituximab in patients with rheumatoid arthritis. N Engl J Med 350: 2572-2581.
4. Diaz-Lagares C, Croca S, Sangle S, Vital EM, Catapano F, et al. (2011) Efficacy of rituximab in 164 patients with biopsy-proven lupus nephritis: Pooled data from European cohorts. Autoimmun Rev. epub ahead of print
5. Elazary AS, Klahr PP, Hershko AY, Dranitzki Z, Rubinow A, et al. (2011) Rituximab induces resolution of recurrent diffuse alveolar haemorrhage in a patient with primary antiphospholipid antibody syndrome. Lupus. epub ahead of print
6. Borie R, Debray MP, Laine C, Aubier M, Crestani B (2009) Rituximab therapy in autoimmune pulmonary alveolar proteinosis. Eur Respir J 33: 1503-1506.
7. Kessel A, Rosner I, Toubi E (2008) Rituximab: beyond simple B cell depletion. Clin Rev Allergy Immunol 34: 74-79.
8. Blacker CV, Greenwood DT, Wesnes KA, Wilson R, Woodward C, et al. (2004) Effect of galantamine hydrobromide in chronic fatigue syndrome: a randomized controlled trial. JAMA 292: 1195-1204.
9. Fluge O, Mella O (2009) Clinical impact of B-cell depletion with the anti-CD20 antibody rituximab in chronic fatigue syndrome: a preliminary case series. BMC Neurol 9: 28.


Øystein Fluge and Olav Mella
Department of Oncology and Medical Physics
Haukeland University Hospital

Competing interests declared: Haukeland University Hospital has patents and pending patent applications on the issue of B-cell depletion therapy for chronic fatigue syndrome. Family members of WO2009083602 A1 are pending, as well as granted US 12/348024. The two authors ØF and OM are named as inventors in these applications.

Immunological Similarities between Cancer and Chronic Fatigue Syndrome

Immunological Similarities between Cancer and Chronic Fatigue Syndrome: The Common Link to Fatigue?

MIRA MEEUS1,2, WILHELM MISTIAEN1, LUC LAMBRECHT3,4 and JO NIJS1,2:

+ Author Affiliations

1Division of Musculoskeletal Physiotherapy, Department of Health Sciences, Artesis University College Antwerp (AHA), Antwerp
2Department of Human Physiology, Faculty of Physical Education and Physiotherapy, Vrije Universiteit Brussel (VUB), Brussel
3Private Practice for Internal Medicine, Ghent & Aalst;
4CVS Contactgroep, Belgium
Correspondence to: Jo Nijs, Artesis Hogeschool Antwerpen (AHA), Department of Health Sciences, Division of Musculoskeletal Physiotherapy, Van Aertselaerstraat 31, 2170 Merksem, Belgium. Tel: +32 36418205, e-mail: jo.nijs@vub.ac.be or jo.nijs@artesis.be
Abstract

Cancer and chronic fatigue syndrome (CFS) are both characterised by fatigue and severe disability. Besides fatigue, certain aspects of immune dysfunctions appear to be present in both illnesses. In this regard, a literature review of overlapping immune dysfunctions in CFS and cancer is provided. Special emphasis is given to the relationship between immune dysfunctions and fatigue. Abnormalities in ribonuclease (RNase) L and hyperactivation of nuclear factor kappa beta (NF-κB) are present in CFS and in prostate cancer. Malfunctioning of natural killer (NK) cells has long been recognised as an important factor in the development and reoccurrence of cancer, and has been documented repeatedly in CFS patients. The dysregulation of the RNase L pathway, hyperactive NF-κB leading to disturbed apoptotic mechanisms and oxidative stress or excessive nitric oxide, and low NK activity may play a role in the two diseases and in the physiopathology of the common symptom fatigue. However, in cancer the relation between the immune dysfunctions and fatigue has been poorly studied. Immunological abnormalities to such as a dysregulated RNase L pathway, hyperactive NF-κB, increased oxidative stress and reduced NK cytotoxicity, among others, are present in both diseases. These anomalies may be part of the physiopathology of some of the common complaints, such as fatigue. Further studies to confirm the hypotheses given here are warranted.

Chronic Fatigue Initiative

http://cfinitiative.org/:

Chronic Fatigue Initiative is a science-based 501(c)(3) nonprofit organization fostering and supporting collaboration among the world’s leading medical research, treatment and public health organizations in understanding the causes, therapies and epidemiology of Chronic Fatigue Syndrome (CFS).

Headquartered in New York City and funded by the Hutchins Family Foundation, CFI seeks to accelerate the medical community’s knowledge of CFS through research grants and collaborative processes across institutions.

CFI’s unique private funding strategy brings together a variety of scientific and academic partners to ensure that the best minds can collaborate and drive new solutions. Its comprehensive strategy includes funding for an epidemiology study; a well-characterized cohort recruitment; pathogenesis discovery research; and a Mechanism of Illness grant program that will fund additional research.

CFI ensures that the best minds can collaborate and drive new solutions for CFS patients.
Participating institutions include the Center for Infection and Immunity at Columbia University, Harvard School of Public Health, Stanford Medical School, Harvard Medical School, Duke University, NewYork-Presbyterian/Columbia University Medical Center, Brigham & Women’s Hospital, Massachusetts General Hospital, University of Miami and University of Utah.

By simultaneously seeking the causes and treatment of CFS and leading research to understand the breadth of the affected population, CFI aims to build awareness, reduce social stigma connected to the disease, and ultimately improve patient lives in a comprehensive way.

CFI believes that as more policy makers and industry experts grasp the full scale of CFS, they will more likely respond in kind and increase efforts to promote research surrounding the disease.

Sunday, October 30, 2011

Study demonstrates that 95% of ME/CFS Patients have Anticardiolipin Antibodies, suggesting that ME/CFS may be an autoimmune condition

Yoshitsugi Hokama, Cara Empey Campora, Cynthia Hara, Tina Kuribayashi, Diana Le Huynh, and Kenichi Yabusaki
Department of Pathology, John A. Burns School of Medicine, University of Hawaii at Maˆnoa, Honolulu, Hawaii

Journal of Clinical Laboratory Analysis 23 : 210–212 (2009)

DISCUSSION A survey of the literature reports ACAs as common serological markers in many different types of diseases, including viral diseases such as illnesses resulting from chemical (1) and marine toxin exposure (4,5,6), HIV (7,8) and Epstein-Barr virus (9), hematological cancers including CLL and acute myelocytic leukemias, exposure to fungal organisms, malaria, and staphylococcus infections (10,11), and autoimmune diseases such as multiple sclerosis, systemic lupus erythematosus, autoimmune hepatitis, and more (2). This study demonstrates that a large percentage of patients clinically diagnosed with CFS have elevated levels of the IgM isotype to CL (95%), suggesting that CFS may be an autoimmune condition. As a possible autoimmune disease, CFS patients may be treated by suppression of the ACA or by diminishing the antigen CL in serum. Previous studies have shown that treatment with monoclonal antibodies to B cells reduces ACA levels to normal in patients with autoimmune disease, leading to clinical improvements.

Specifically, Rituximab, a chimeric monoclonal CD20 antibody, has been shown to normalize high ACA serum titers of patients with autoimmune systemic lupus erythematosus, rheumatoid arthritis, autoimmune thrombocytopenia, and autoimmune hemolytic anemia. Rituximab may serve as an effective therapeutic agent for ameliorating the symptoms of CFS (11,13).

Therefore, classification of CFS as an autoimmune disorder may serve to increase the availability of treatment options for patients suffering from the disease.

Experiments are underway to further elucidate why ACAs are produced in individuals afflicted with CFS.

Such studies include investigating the effects of specific chemical agents, marine toxins, and ACAs on mitochondrial metabolic pathways that are indicative of reduced or blocked energy production that may lead to the fatigued state in CFS.
Such studies may lead to the development of potential therapeutic agents to block or reduce such interactions. Read more>>

The debilitating condition that leaves sufferers in excruciating pain

By ALICE GREBOT on 29th October 2011:

It is a chronic condition that renders sufferers so sensitive that even the lightest touch triggers waves of excruciating pain. Fibromyalgia is thought to affect up to a million Britons, commonly women over 40, and experts have likened the debilitating sensations to ‘death by a thousand needles’.

Other symptoms include lack of concentration, memory loss, headaches and muscle stiffness. And for a long time there was little doctors could do to help quell the agony.

Yet today, with the help of sophisticated scanning techniques, pain specialists have been able to pinpoint the parts of the brain responsible for the condition.
Read more>>

Saturday, October 29, 2011

Psychologists Start Petition Against DSM 5

by professor Allen Frances, M.D. (Allen Frances, M.D., was chair of the DSM-IV Task Force and is currently professor emeritus at Duke.):

DSM5 in Distress

The DSM's impact on mental health practice and research.


A Users Revolt Should Capture APA Attention
Published on October 24, 2011


 Several divisions of the American Psychological Association have just written an open letter highly critical of DSM 5. They are inviting mental health professionals and mental health organizations to sign a petition addressed to the DSM5 Task Force of the American Psychiatric Association. You can read the letter and sign up at http://www.ipetitions.com/petition/dsm5/ It is an extremely detailed, thoughtful and well written statement that deserves your attention and support.   

  The letter summarizes the grave dangers of DSM 5 that for some time have seemed patently apparent to everyone except those who are actually working on it. The short list of the most compelling problems includes: reckless expansion of the diagnostic system (through the inclusion of untested new diagnoses and reduced thresholds for old ones); the lack of scientific rigor and independent review; and dimensional proposals that are too impossibly complex ever to be used by clinicians.

  The American Psychiatric Association has no special mandate or ownership rights giving it any sovereignty over psychiatric diagnosis. APA took on the task of preparing DSM's sixty years ago because it then seemed so thankless that no other group was prepared or willing to do it. The DSM franchise has stayed with APA only because its products were credible enough to gain widespread acceptance. People used the manual only because it was useful.

 DSM 5 has strained that credibility to the breaking point and (unless radically changed) will be much more harmful than useful. We have reached a turning point that will soon become a point of no return. A near final version of DSM 5 must be ready by next spring and all final wording will be set in stone within a year. Time is running out if DSM 5 is to be saved from itself. 

  Rescue attempts and pushback are coming from numerous directions and are fast gaining in momentum. The American Psychological Association's petition was preceded by an even harsher critique by the British Psychological Society. The Society of Biological Psychiatry has wondered why we need a DSM 5.  Experts in personality disorder have universally decried the proposed revisions in DSM 5. And the American Counseling Association will  soon weigh in with its own statement. 

  Meanwhile DSM 5 has lived in a world that seems to be hermetically sealed. Despite the obvious impossibility of many of its proposals, it shows no ability to self correct or learn from outside advice. The current drafts have changed almost not at all from their deeply flawed originals. The DSM 5 field trials ask the wrong questions and will  make no contribution to the endgame.

  But the DSM 5 deafness may finally be cured by a users' revolt. The APA budget depends heavily on the huge publishing profits that accrue from its DSM sales. APA has ignored the scientific, clinical, and public health reasons it should omit the most dangerous suggestions- but I suspect APA will be more sensitive to the looming risk of a boycott by users.    

  Here are best case and worst case scenarios. Best case: APA opens up DSM 5 to external, independent review and only those suggestions that pass muster are included. DSM 5 becomes safe, usable, and widely used.

  Worst case: DSM 5 stumbles along blindly as it has and includes most or all of its harmful suggestions. DSM 5 loses its status as a useful and standard guide to psychiatric diagnosis, creating an unnecessary and unfortunate babel of diagnostic practice and research habits. And the American Psychiatric goes broke. 

  The APA Trustees and Assembly have thus far been almost completely and puzzlingly  passive in exercising their  governance role over DSM 5. I believe they can wait no longer if they are to fulfill their fiduciary responsibility to the public, to the mental health field, and to their own membership. It is pretty much now or never. 

Friday, October 28, 2011

Professor Jonathan Edwards: Jos van der Meer's Rituximab in CFS criticism contains several errors

RE: Rituximab in CFS; more research needed

Jonathan_Edwards replied to jvandermeer on 28 Oct 2011 at 17:10 GMT:

The criticism made here contains several errors. There is nothing peculiar about the late response.

It is to be expected.

I was responsible for both the phase I and the proof of concept phase II (NEJM 2004) studies in rheumatoid disease, which formally established the validity of B cell depletion in autoimmune disorders. From the very outset in 2000 we reported that responses could take many months to develop, in line with autoantibody decline. An partial early response element was usually seen as well but was consistent with adjuvant use of corticosteroid or other agents.

I am not aware of any hard evidence for rituximab working in autoimmune disorders not mediated by autoantibodies.

Where there have been proper trials, as for psoriatic arthropathy, the results have been clearly negative as far as I am aware.

The suggestion that rituximab works through an action on antigen presentation is pure speculation for which I cannot think of any positive supportive evidence and there is much unsupportive evidence, including the very common very slow response kinetics that follow antibody decline. This is an idea popularised before we actually had any data and still often repeated in reviews despite the wealth of evidence against.

It is hard to see how killing B cells at day one would affect antigen presentation by B cells six months later, putatively responsible for further decline in inflammation to nine months.

The trial's authors give the account that is by far the most consistent with the data - that benefit occurs as short lived plasma cells die off and autoantibodies decline but that benefit is often incomplete as expected from the existence of long lived plasma cells and continued lower levels of antibody.

The absence of a clearly defined autoantibody population in this particular group is not in any way surprising. It is likely to be immunopathologically heterogeneous and new autoantibodies are being found all the time.

Jonathan Edwards Professor Emeritus, UCL
No competing interests declared.

(Jonathan Edwards, Professor Emeritus, Department of Medicine, University College London)

Nancy Klimas, Professor of Immunology: two possible theories why Rituximab works in ME / CFS

Jørgen Jelstad:

http://twitter.com/#!/DeBortgjemte

Professor of Immunology at the University of Miami, Nancy Klimas, is the one who has worked the longest and most closely with immune problems in ME / CFS for over 25 years, and she looked forward to great results to come.

- I think they do great work. I heard about their work the first time in London for a couple of years ago, and I was very excited. I could hardly wait for them to get this done, says Klimas.

She says she was so excited that she had to watch out not to jump on it even at the risk of stepping Haukeland researchers at the toes.

- But I thought that I had to let them do what they did alone, because they do it right, and they deserve all the credit for the work they do. It is very exciting and very innovative, says Klimas.

She is aware that Rituximab is a "big gun".

- To turn out nearly all B-cells of the immune system. So the question in my mind now is, why it works, says Klimas.

She believes there are two possible theories. One possibility, according to Klimas that a large subset of patients have an autoimmune disease that is maintained by an autoantibody -that is, an antibody directed against its own tissues.

- It is certainly possible, and this drug's use in other autoimmune diseases such as arthritis, says Klimas.

The other possibility is, according to Klimas that B-cells are the reservoir for a virus that has great significance in the disease. B-cells include the main reservoir for ... Read more>>

Thursday, October 27, 2011

A letter from Dr. Judy Mikovits to all ME/CFS patients, families and advocates

Lilly Meehan:

A letter from Dr. Judy Mikovits to all ME/CFS patients, families and advocates

Many of you have asked, "where is Dr. Judy Mikovits and what is she doing? Is she still doing research? Where can we go for testing?"

Dr Judy Mikovits remains passionately committed to the patients and to a search for treatment and a better life for all of them.

She refuses to compromise her integrity or the truth in a search for causes and treatment of disease. It is unfortunate, yet a sign of the society we live in, that politics and personal gain have interfered with science and the attempts of committed researchers to pursue the goal of scientific research.

Dr Mikovits is pursuing opportunities with a variety of new research institutions and collaborations which show promise to continue in her research and to provide patients with new resources for diagnosis and treatment.

She will make this information available on public sites for all patients to access and participate as they choose.


Dr. Mikovits is no longer with the Whittemore Peterson Institute and has no role or responsibility for any of the activities of the Institute and never had any role in the clinical laboratory (VIPdx or Unevx)

All patients or other individuals who wish to contact Dr. Mikovits may email via:

Lilly Meehan at:

LMeehan93003@aol.com


See also: A big thank you to Dr. Judy Mikovits

Health insurance news - ME could be caused by immune system defect


Posted By Peter Jones on Tue 25th October 2011:

Health insurance customers who are diagnosed with myalgic encephalomyelitis (ME) or Chronic Fatigue Syndrome could be suffering with the illness because of an immune system defect, according to research.

The study, reported in PLoS One, suggested a faulty immune system could be to blame for the illness, as researchers found symptoms in some patients subsided after taking a cancer drug which inhibits the body's defence.

Doctors in Norway were alerted to the possibility of using immune system-inhibiting cancer drugs in 2004 when a patient with both Hodgkin's Lymphoma and ME was given the treatment and her fatigue syndrome improved for five months.

A total of 30 patients with ME were involved in the trial, which showed 67 per cent of the people receiving two doses of Rituximab - a cancer treatment - had their symptoms improve during the process.
Oncology consultant at the Haukeland University Hospital Oystein Fluge told BBC News that two of the patients had no recurrence of the symptoms and it completely changed their life around, while in others there was a varied response.
"I think the fact that patients responded to treatment, improved cognitive function, fatigue and pain makes us believe we're touching one of the central mechanisms," he added.

Dr Charles Shepherd, the UK ME Association's medical adviser said the results are very encouraging for people with the illness as the researchers seem to have confirmed that altering the immune system response could be an effective treatment for at least a small number of patients.

"They help to confirm that there is a significant abnormality in immune system function in this disease. We now need further clinical trials of such anti-cancer agents to see if other research groups can replicate these findings," he added.

According to the news provider, there are around 250,000 people in the UK that suffer from the illness and symptoms include extreme tiredness, problems with memory and concentration, as well as sleep disturbances.

Wednesday, October 26, 2011

Chronic Fatigue Syndrome -- A Treatable Autoimmune Disease that wrecks people's lives

MATTHEW EDLUND, M.D., huffingtonpost.com: Chronic fatigue syndrome wrecks people's lives. It does so physicially, socially and economically. Appearing "normal" yet not being able to think or work causes enormous hardship compounded by many doctors who think the illness does not really exist -- a position health and disability insurance companies are more than happy to endorse. And those who firmly believe it exists are often stumped by how to treat it -- beyond stretching, physical activity and psychotherapy.

Now a new study out of Bergen, Norway adds much to the data that chronic fatigue is an autommune disease. If not entirely definitive, it points in the direction that many CFS sufferers and clinicians have argued for decades -- that the illness is a disorder of the immune system, is preceded in most cases by some kind of infection and continues to provoke multiple debilities for a long time.

The Haukelund Study:

Many ideas for clinical treatment occur from observing the clinically unexpected. In this case, ...

Professor Wessely: The WAIT is OVER !!



See also: Norway's Directorate of Health Apologises for BAD Treatment of ME Patients

ME IS JUST FATIGUE, RIGHT? WRONG

Source: JB

Message from Jane Colby
25 October 2011

======

... 'ME IS JUST FATIGUE, RIGHT? WRONG'
and:'Research showing ME is a physical disease'

======

If you've been reading my tweets, you'll have seen that Mark has now placed the second poster in our awareness raising series prominently on our website.

The message reads: 'ME is just fatigue, right? WRONG'.

The striking photo features one of our members, tube-fed because she could not at that time eat for herself. We have all read so much nonsense about ME in the press this year. It is time to tell it like it really is and to forward this link far and wide.
See the poster here: http://bit.ly/tt-wrong 

The good news is that, after she and her family declined graded exercise treatment and managed her illness carefully, avoiding any treatment 'programme', this little girl has come through the worst of the illness and grown into an independent-minded, academically gifted young woman with a strong sense of justice for children with ME.

How many times do I hear a similar story of improvement through withdrawing from misguided if well-meant treatment? It confirms all that Dr Betty Dowsett, Dr Alan Franklin, Dr Nigel Speight and Byron Hyde MD have always said. And it reflects my personal experience of severe ME.

RESEARCH SHOWING ME IS A PHYSICAL DISEASE

On the reverse of our poster we have summarised the 2010 Dundee research into children's blood, showing evidence consistent with persistent viral infection. As most of you already know, Tymes Trust co-funded this research.

The headline reads: 'Research showing ME is a physical disease'.
We don't go along with the fashion among some doctors and researchers who tend to denigrate the very concept of a 'physical' disease. Such professionals prefer to emphasise instead that all disease, including ME, is a mixture of the physical and psychological. As I said when I was on the panel at the MEA Question Time in Huddersfield recently: 'Try telling that to someone with a broken leg.' No-one should let academic arguments obscure their common sense.

It is vital that researchers continue providing evidence for the presence of viruses that are known to attack people with ME. And it's also vital that when such evidence has been published, we all continue to keep it at the forefront of the public's mind.
Read it here: http://bit.ly/tt-phys

Poster leaflets cost £3.35 for a pack of 10 inc p&p. You can display
the poster or use it as an information leaflet. It can be folded either way - it arrives image side out for impact, or you can fold it the other way if you want to draw a doctor's attention to the research information.

Please forward this message to anyone you think would like to know.

All good wishes, and don't forget that if you need help, our ME-friendly Advice Line Team is on 0845 003 9002.

Jane

Jane Colby FRSA
Executive Director
The Young ME Sufferers Trust
PO Box 4347, Stock, Essex, CM4 9TE
www.tymestrust.org
Tel: 0845 003 9002

======

READ ALL PREVIOUS ALERTS AND SUBSCRIBE TO MY LIST AT www.tymestrust.org
To unsubscribe, send an email via the website Contact Us form.

Follow Jane on Twitter @JaneCColby
or read her daily tweets at
www.tymestrust.orgSee more
Tymes Trust
www.tymestrust.org
http://bit.ly/tt-wrong
www.tymestrust.org

See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME

Tuesday, October 25, 2011

TV2 News: Norwegian breakthrough in ME-Research [English sub]


**To use ENGLISH subtitles, click/activate the "CC" icon on the videobar. You need to be on a PC to have this feature.**

Medscape: Cancer Drug Rituximab May Also Treat Chronic Fatigue Syndrome

Brenda Goodman:

October 24, 2011 — Researchers in Norway say they've been able to treat symptoms of chronic fatigue syndrome by giving patients a biologic drug that affects the immune system.

The drug, rituximab (Rituxan), works by depleting immune cells called B-cells. It is FDA approved to treat non-Hodgkin's lymphoma, chronic lymphocytic leukemia, rheumatoid arthritis, and two kinds of vasculitis.

For the study, researchers recruited 30 people with chronic fatigue syndrome (CFS). Half got two infusions of rituximab given two weeks apart. The other half got infusions of saline solution as a placebo.

Ten patients in the rituximab group (67%) and two patients in the placebo group (13%) saw at least moderate reductions in fatigue.

In most of the patients, improvements were transient and faded within eight to 44 weeks.

But three patients, two in the rituximab group and one that got the placebo, continue to be symptom free 2 1/2 years after their treatments. Those three patients have all returned to full-time jobs, researchers say.

The study is published in the journal PLoS One.

"Our thought is that in fact CFS is an autoimmune disease in most patients," says study researcher Olav Mella, MD, PhD, an oncologist at Haukeland University Hospital in Bergen, Norway.

Mella and his colleague, Oystein Fluge, MD, PhD, say they accidentally discovered that rituximab might help chronic fatigue syndrome after they used it to treat three patients who suffered from both CFS and non-Hodgkin's lymphoma. All three patients reported significant improvements in fatigue after rituximab infusions. They eventually relapsed and were given more doses of rituximab. All three again had improvements in their CFS, though those eventually faded.

Their cases were reported in BioMedCentral Neurology in 2009.

Is Chronic Fatigue Syndrome an Autoimmune Disease?

Researchers say they aren't sure why the drug is working.

"We cannot know for sure, but what we see is that there's a delay from the rapid B-cell depletion after rituximab treatment to the clinical response. The delay can be from three to perhaps eight months before the response is thought to occur," says Fluge, who is an oncologist and medical physicist at Haukeland Hospital.

B-cells are part of the immune system. They roam the body in relatively small numbers searching for foreign invaders. When a B-cell finds one, it springs into action, becoming an infection-fighting chemical factory.

In some diseases, like leukemia, B-cells may go haywire and cause cancer. In rheumatoid arthritis, B-cells may attack the body's own tissues.

In CFS, however, it's unclear why killing off B-cells might help.

One theory, ... 

Monday, October 24, 2011

ME Association's medical adviser: We now need further clinical trials of anti-cancer agents in ME

By James Gallagher Health reporter, BBC News:

Dr Charles Shepherd, the UK ME Association's medical adviser, said: "The results of this clinical trial are very encouraging news for people with ME.

"Firstly, they help to confirm that there is a significant abnormality in immune system function in this disease.

"Secondly, they indicate that altering the immune system response in ME could be an effective form of treatment for at least a subset of patients.

"We now need further clinical trials of such anti-cancer agents to see if other research groups can replicate these findings."

ME Association: clinical trial confirms significant abnormality in immune system function in ME

By James Gallagher Health reporter, BBC News:

Dr Charles Shepherd, the UK ME Association's medical adviser, said: "The results of this clinical trial are very encouraging news for people with ME.

"Firstly, they help to confirm that there is a significant abnormality in immune system function in this disease.

"Secondly, they indicate that altering the immune system response in ME could be an effective form of treatment for at least a subset of patients.

"We now need further clinical trials of such anti-cancer agents to see if other research groups can replicate these findings."

Cancer drug key to treating chronic fatigue syndrome

'Most encouraging drug result so far in the history of the disease,' says charity spokesman
 
By CLAIRE BATES Last updated at 10:36 AM on 24th October 2011:

Chronic fatigue syndrome, which affects one in 250 Britons, may be caused by a faulty immune system attacking the body.

The controversial condition causes persistent exhaustion that affects everyday life and doesn't go away with sleep or rest. It can last from a matter of weeks to several years. Doctors, while agreeing that the syndrome does exist, have been perplexed as to what causes it.

Now researchers from Haukeland University Hospital in Norway, believe they have discovered a possible cause after treating a patient who had both cancer and chronic fatigue. The man, who had Hodgkin's lymphoma, showed a marked recovery from his CFS symptoms after receiving chemotherapy.

The scientists, led by Dr Oystein Fluge and Dr Olav Mella, then decided to test an anti-lymphoma drug in a trial of 30 patients with chronic fatigue. They found that symptoms of the disease eased in two-thirds of the patients given Rituximab. Two of the patients were completely cured after receiving the drug three years ago and have since returned to work. Rituximab works by destroying a protein found on the surface of white blood cells that make antibodies, called B cells. The scientists said the findings suggested that: 'CFS/ME, which is often preceded by an infection, may be a form of autoimmune disease in which B-cells are important'.

The team treated 30 CFS patients, giving half two doses of Rituximab and the other half a fake treatment. In the patients receiving the drug, 67 per cent reported an improvement of symptoms, while just 13 per cent showed any improvement in the sham group. 'It's the most encouraging drug result so far in the history of the disease,' said Charles Shepherd, medical adviser to the UK ME Association.

'Although it's a small trial, it's produce dramatic results.' The researchers found no trace of a mouse leukaemia virus, called XMRV, that was once proposed as a possible cause of CFS but has since been largely eliminated. The findings have been published in the latest version of the online journal PLoS ONE.

Chronic fatigue syndrome, once known as 'yuppie flu', can cause symptoms that vary from mild but persistant tiredness, to becoming bed bound with an intolerance to noise and bright lights. Around 250,000 people in the UK have CFS.

Sunday, October 23, 2011

Norway's Directorate of Health Apologises for not having established proper health care services for ME Patients thanks to CBT psychiatrists

Bjørn Guldvog, Deputy Director General of theNorwegian Directorate of Health made the following statement
"Jeg tror at vi, i for liten grad, har klart å møte menneskene som har kronisk utmattelsessyndrom på en god nok måte. Jeg tror at det er riktig å si at vi ikke har utviklet en god nok helsetjeneste for disse, og det beklager jeg."
"I think that we have not cared for people with ME to a great enough extent. I think it is correct to say that we have not established proper health care services for these people, and I regret that."
Read more>>

Norway's Directorate of Health Apologises for BAD Treatment of ME Patients

Read more>>
The Norwegian Directorate of Health has apologised for the way in which ME patients in Norway have been treated. This follows the publication of the ground-breaking research from Haukeland University in Bergen (click here).
After the publication of the Rituximab study by Fluge et al (2011) and extensive media coverage since then the Norwegian Directorate of Health gave a short statement on TV2 channel, see TV2 Nettavisen (click here). 

A statement from the Norwegian Directorate of Health has been received where  they apologise for not having provided the necessary and proper health services to persons with ME.
Such a public apology from a governmental health agency has never occurred before.
Bjørn Guldvog, Deputy Director General of theNorwegian Directorate of Health made the following statement

"Jeg tror at vi, i for liten grad, har klart å møte menneskene som har kronisk utmattelsessyndrom på en god nok måte. Jeg tror at det er riktig å si at vi ikke har utviklet en god nok helsetjeneste for disse, og det beklager jeg."

"I think that we have not cared for people with ME to a great enough extent. I think it is correct to say that we have not established proper health care services for these people, and I regret that."
Read more>>

Anne Kathrine (47) put the cancer doctors on the trail of ME treatment

Barbara Eikesdal barbro.eikesdal @ tv2.no, and Klaus Holthe klaus.holthe @ tv2.no:
Professor Olav Mella and Dr. Øystein Fluge the cancer ward at Haukeland hospital has almost stumbled upon what may be one of the biggest breakthroughs in ME research.

Ever a surprise for both us and the patient was ME symptoms disappear after six to eight weeks after treatment.

One patient with lymphoma had been diagnosed with ME. To combat the cancer patient was partly given antibody Rituximab. After a period of treatment the patient was suddenly dramatically improve the ME symptoms.

Anne Kathrine Olsen Karlsen (47) from Haugesund get a great deal of credit for what is now giving hope to millions of ME patients worldwide.

In 2003, Anne Kathrine diagnosed with ME. At present there is no cure for this disease. Three years later, in 2006, she had lymphoma. This turned out to give her life back.

- Mom, you are sick?
- I sat in the living room and sewing doll clothes when my son came home from school one day. When I was up and running. He looked at me and asked me "Mom, are you sick?"

The son had not seen his mother up on very many years.

BACKGROUND: Norwegian breakthrough could solve the riddle ME

Surprisingly effective
When she started treatment for lymphoma, there was something strange with Anne Kathrine.

- Preferably a surprise for us and the patient began the symptoms of ME / Chronic Fatigue Syndrome and be gone. A six or seven weeks into the chemotherapy treatment, she began to recover from fatigue. Audio and photosensitivity, pain, all symptoms began to recover. It was what gave the spark that we began to ponder what had really happened to the patient, says professor and consultant on cancer ward at Haukeland Hospital, Olav Mella, to TV 2

Professor Mella and Dr. Øystein Fluge decided to investigate whether there was such that a cancer medicine could actually help the ME.

Read more>>

Saturday, October 22, 2011

Friday, October 21, 2011

Norwegian research breakthrough can solve CFS-mystery

Barbro Eikesdal, www.tv2.no:

“When we have cancer patients that are as sick as many of these patients are, they have a very short life expectancy. That says a lot about the quality of life for many of them.” Professor Mella is convinced that the possible treatment of CFS patients can have tremendous significance.

“Knowing that CFS each year costs society about nine billion dollars, that is in the US alone, says a lot about the colossal costs involved. I addition you have the patients expenses.

However, even more important is the fact that the quality of live for millions of patients, worldwide, can dramatically improve.” Read more>>

Professor Mella: When cancer patients are as sick as many of these ME/CFS patients, they have a very short life expectancy

Barbro Eikesdal, www.tv2.no:

“When we have cancer patients that are as sick as many of these patients are, they have a very short life expectancy. That says a lot about the quality of life for many of them.” Professor Mella is convinced that the possible treatment of CFS patients can have tremendous significance.

“Knowing that CFS each year costs society about nine billion dollars, that is in the US alone, says a lot about the colossal costs involved. I addition you have the patients expenses.

However, even more important is the fact that the quality of live for millions of patients, worldwide, can dramatically improve.” Read more>>

CBT psychiatrists told to stop insulting seriously ill patients by RCGP’s chairman, Dr Clare Gerada

By SOPHIE BORLAND, 21st October 2011: Doctors are insulting  seriously ill patients who are regularly taken to hospital by describing them as 'frequent flyers', a leading GP said yesterday.

Clare Gerada said the term was degrading as it referred to 'people who are sick and need our care and attention'.

The phrase is widely used by NHS staff out of patients' earshot to describe anyone who is admitted frequently to a hospital A&E unit.

Many of those labelled as 'frequent flyers' are elderly or have serious illnesses such as asthma, heart problems or diabetes.

Dr Gerada, chairman of the Royal College of General Practitioners, said doctors must never forget 'the simple act of caring' for their patients.

In a speech to 1,500 family doctors at the RCGP’s annual conference in Liverpool, she urged them not to lose sight of the patient as a person.
Read more>>

Thursday, October 20, 2011

Dr. Daniel Peterson discusses CFI's proposed ME/CFS research looking at spinal fluid rather than blood

How does Rituximab work ?

Kate Benson, Oct 19, 2011, Cure Talk:

Rituximab works by destroying white blood cells that make antibodies. White blood cells are part of the immune system response and ME/CFS studies point to chronic activation of the immune system following an acute infection. 

A clear or possible clinical infection preceding CFS onset could be identified in 73% and 67% of the patients in the Rituximab and placebo groups, respectively according to the authors, however, patients with ongoing infections were excluded from the trial.

Like all immune cells, white blood cells are created in the bone marrow.  The NIAID reports, that at the heart of the immune system is the ability to distinguish between self and non-self. Immune cells and other cells in the body usually coexist peaceably in a state known as self-tolerance. In abnormal situations (such as an autoimmune disease), the immune system can wrongly identify self as non-self and execute a misdirected immune attack.

A limitation of this study is the lack of predetermined exact definitions of clinical response with respect to duration and extent of improvement. According to the authors, an alternative explanation for the observed clinical improvement from B-cell depletion could be elimination or reduction of B-lymphotrophic viruses such as cytomegalovirus (CMV) or Epstein-Barr virus (EBV).

Two new open-label phase-II studies in Norway (Study 1, Study 2) investigating Rituximab treatment with two infusions two weeks apart (as in the present study) followed by maintenance Rituximab infusions at 3, 6, 10 and 15 months,  are being conducted to further explore this treatment principle in CFS (
The anti-cancer drug is also being investigated for treatment of rheumatoid arthritis, lupus/systemic lupus erythematosus, Sjogren’s syndrome multiple sclerosis, and Behcet’s disease.
Read more>>

See also: Cancer drug Rituximab/Rituxan-study in ME/CFS in PLoS ONE: major improvements in all symptoms in 67 % of patients

Wednesday, October 19, 2011

Cancer drug Rituximab/Rituxan-study in ME/CFS in PLoS ONE: major improvements in all symptoms in 67 % of patients

There were no serious adverse events. Read more>>

The delayed responses after Rituximab treatment suggests that CFS is an autoimmune disease

Benefit from B-Lymphocyte Depletion Using the Anti-CD20 Antibody Rituximab in Chronic Fatigue Syndrome. A Double-Blind and Placebo-Controlled Study
 
Øystein Fluge1*, Ove Bruland1,2, Kristin Risa1, Anette Storstein3, Einar K. Kristoffersen4, Dipak Sapkota1, Halvor Næss3, Olav Dahl1,5, Harald Nyland3, Olav Mella1,5:

1 Department of Oncology and Medical Physics, Haukeland University Hospital, Bergen, Norway, 2 Department of Medical Genetics and Molecular Medicine, Haukeland University Hospital, Bergen, Norway, 3 Department of Neurology, Haukeland University Hospital, Bergen, Norway, 4 Department of Immunology and Transfusion Medicine, Haukeland University Hospital, and The Gade Institute, University of Bergen, Bergen, Norway, 5 Institute of Internal Medicine, Section of Oncology, University of Bergen, Bergen, Norway

Abstract Top
Background
Chronic fatigue syndrome (CFS) is a disease of unknown aetiology. Major CFS symptom relief during cancer chemotherapy in a patient with synchronous CFS and lymphoma spurred a pilot study of B-lymphocyte depletion using the anti-CD20 antibody Rituximab, which demonstrated significant clinical response in three CFS patients.

Methods and Findings
In this double-blind, placebo-controlled phase II study (NCT00848692), 30 CFS patients were randomised to either Rituximab 500 mg/m2 or saline, given twice two weeks apart, with follow-up for 12 months. Xenotropic murine leukemia virus-related virus (XMRV) was not detected in any of the patients.

The responses generally affected all CFS symptoms. Major or moderate overall response, defined as lasting improvements in self-reported Fatigue score during follow-up, was seen in 10 out of 15 patients (67%) in the Rituximab group and in two out of 15 patients (13%) in the Placebo group (p = 0.003). Mean response duration within the follow-up period for the 10 responders to Rituximab was 25 weeks (range 8–44). Four Rituximab patients had clinical response durations past the study period. General linear models for repeated measures of Fatigue scores during follow-up showed a significant interaction between time and intervention group (p = 0.018 for self-reported, and p = 0.024 for physician-assessed), with differences between the Rituximab and Placebo groups between 6–10 months after intervention. The primary end-point, defined as effect on self-reported Fatigue score 3 months after intervention, was negative. There were no serious adverse events. Two patients in the Rituximab group with pre-existing psoriasis experienced moderate psoriasis worsening.

Conclusion
The delayed responses starting from 2–7 months after Rituximab treatment, in spite of rapid B-cell depletion, suggests that CFS is an autoimmune disease and may be consistent with the gradual elimination of autoantibodies preceding clinical responses. The present findings will impact future research efforts in CFS.

Read more>>

Norwegian research breakthrough can solve CFS-mystery

TV 2 NYHETENE, www.tv2.no
BERGEN (TV 2 NYHETENE): To kreftleger i Bergen har oppdaget en mulig behandling av ME, også kjent som kronisk utmattelsessyndrom. Medisinen gjorde to av tre ME-syke bedre. Flere ble helt friske.  

For english version click here: Norwegian research breakthrough can solve CFS-mystery

Gjennombruddet, som ble offentliggjort onsdag, kan gi ME-syke verden over svar på hva den gåtefulle sykdommen er og hvordan den kan behandles. Funnene vekker internasjonal oppmerksomhet. – Vi ser helt klare effekter. Det er håp, sier professor og avdelingsoverlege ved kreftavdelingen ved Haukeland universitetssykehus, Olav Mella, til TV 2 Nyhetene.

Horribly ill patients abused by their doctors and governments

Jamie Deckoff-Jones MD :

Judy Mikovits heard the pain of the patients. Too much for her own good. She took all the desperate mail and was terribly affected by it. She visited horribly ill patients in the UK and Norway, who are being abused by their doctors and governments.

Patients lying in dark rooms with ear protection and feeding tubes, for years; too weak to roll over, begging to be let out of their bodies. I kid you not.

I got involved with the WPI because Judy was answering all this mail, from people who were writing to me also, and she was really bad at it, while it was a reflex for me. Judy Mikovits is a gifted scientist, with human frailties. She was working in an impossibly toxic environment with no help and the entire old boys network coming down on her. She did lots of things wrong from a PR point of view. What she did or didn't do right scientifically will all come out in the wash. It is the finding the novel pathogen, or more likely pathogens, the theory that matters now and that must be investigated. Even though you prefer deductive reasoning, genius requires induction. There is an enormous opportunity here for you, both as a scientist and as a humanitarian. It is possible to be both.

I have brainstormed with Frank Ruscetti. He thinks it's real. Sandy Ruscetti thinks it's real and she understands the murine retrovirology better than almost anyone.

I had dinner with Ian Lipkin. He said "it smells viral". He was clearly very interested. It isn't one of the known pathogens... Read more>>

Tuesday, October 18, 2011

Mill Valley's 'Audience Favorite International Documentary Award' for Voices from the Shadows

Mill Valley Film Festival

facebook.com/VoicesfromtheShadows: Hidden away in darkened, silent rooms, for years or even decades, are men, women and children, suffering a cruel and invisible injustice.

Although shockingly ill many are disbelieved, denigrated and blamed, suffering medical neglect and sometimes even abuse by professionals.

Their courage and determination remain unseen and unheard, as many are too ill to make their plight known, and others live in fear of retribution.

Few professionals are willing to speak out to protect them, since by doing so they risk damage to their careers. It is often left to carers, to partners and parents, to act as advocates. This intimate and revealing film bears witness to these forgotten lives and abuses. It is an intensely moving, and disquieting film by two patient advocates/carers. It reveals the love, determination and fortitude of five sufferers and their families as they strive to surmount a desperate situation.



Voices from the Shadows Trailer:

 
Voices from the Shadows Trailer from Josh on Vimeo.

Patients with chronic Lyme disease have antibodies that suggest they carried the infection for an unusually long time

Amy Maxmen, nature.com:
Some patients with Lyme disease still show symptoms long after their treatment has finished. Now proteins have been discovered that set these people apart from those who are easily cured.

People who experience the symptoms of Lyme disease, which include fatigue, soreness and memory or concentration loss, after treatment for the disorder are sometimes diagnosed as having chronic Lyme disease or post-Lyme disease syndrome. But these diagnoses are difficult to make, because the individuals no longer seem to harbour the bacteria that cause Lyme disease. And the symptoms could instead be indicative of chronic fatigue syndrome or depression.

Now Armin Alaedini at Weill Cornell Medical College in New York and his colleagues have found that ...

The European Laboratory of Nutrients (ELN)

The European Laboratory of Nutrients (ELN) is an advanced laboratory for testing the nutrient status of particularly humans.

The laboratory provides a worldwide service to MD’s, hospitals and institutions with interest in nutritional medicine.

In 1995 Vitamin Diagnostics joined our organization to provide better service both in U.S. and Europe. Read more>>

Monday, October 17, 2011

Genetic Factors Influence Serological Measures of Common Infections


Hum Hered. 2011 Oct 11;72(2):133-141. [Epub ahead of print]


Rubicz R, Leach CT, Kraig E, Dhurandhar NV, Duggirala R, Blangero J, Yolken R, Göring HH.:

Source
Department of Genetics, Texas Biomedical Research Institute, University of Texas Health Science Center at San Antonio, San Antonio, Tex., USA.

Abstract
Background/Aims: Antibodies against infectious pathogens provide information on past or present exposure to infectious agents. While host genetic factors are known to affect the immune response, the influence of genetic factors on antibody levels to common infectious agents is largely unknown. Here we test whether antibody levels for 13 common infections are significantly heritable. Methods: IgG antibodies to Chlamydophila pneumoniae, Helicobacter pylori, Toxoplasma gondii, adenovirus 36 (Ad36), hepatitis A virus, influenza A and B, cytomegalovirus, Epstein-Barr virus, herpes simplex virus (HSV)-1 and -2, human herpesvirus-6, and varicella zoster virus were determined for 1,227 Mexican Americans. Both quantitative and dichotomous (seropositive/seronegative) traits were analyzed. Influences of genetic and shared environmental factors were estimated using variance components pedigree analysis, and sharing of underlying genetic factors among traits was investigated using bivariate analyses.

Results: Serological phenotypes were significantly heritable for most pathogens (h(2) = 0.17-0.39), except for Ad36 and HSV-2. Shared environment was significant for several pathogens (c(2) = 0.10-0.32). The underlying genetic etiology appears to be largely different for most pathogens.

Conclusions: Our results demonstrate, for the first time for many of these pathogens, that individual genetic differences of the human host contribute substantially to antibody levels to many common infectious agents, providing impetus for the identification of underlying genetic variants, which may be of clinical importance.

PMID: 21996708 [PubMed - as supplied by publisher]

Indy 500 winner Wheldon dies after massive wreck

By JOHN MARSHALL - AP Sports Writer:

LAS VEGAS (AP) — Every race car driver heads onto the track understanding this race could be the last and hoping it won't be.

On Sunday, IndyCar drivers got a harsh reminder when the worst happened to one of their own. 

Two-time Indianapolis 500 winner Dan Wheldon died when his car got caught up in a 15-car pileup, sailed over another vehicle and smashed into a catch fence at IndyCar's season-ending race at Las Vegas Motor Speedway.

 "Things happen in this kind of racing," said Wade Cunningham, also caught up in the wreck. "It's so close. Not much room for error. I was near the front of what caused all this, so I'm not thrilled about it. At this point, whose fault it was is kind of immaterial."

The green flag had barely stopped waving when disaster struck. Wheldon, driving from the back of the field for a chance at $5 million, was moving through the pack when he drove into a tangle of cars careening off each other in every direction. Unable to avoid the massive wreck unfolding before him, Wheldon clipped another car and went hurtling through the air, his car bursting into flames as it flew into a fence. After just 11 laps, the race was over.

Two hours later, track officials announced that Wheldon was dead. The Englishman was 33.

Friday, October 14, 2011

Statement by Vincent Lombardi


STATEMENT OF VINCENT LOMBARDI, PhD
CLINICAL LAB DIRECTOR

VIP Dx

A number of recent publications and individuals have mischaracterized the nature of certain clinical laboratory results reported by VIP Dx, a CLIA certified clinical laboratory. VIP Dx has met the required CLIA Program standards and is certified to offer and perform only clinically validated laboratory tests. The “XMRV test” offered by VIP Dx is clinically validated and performed under rigorous protocols to ensure the accuracy and reliability of the test results. XMRV testing was offered based upon the existing scientific knowledge at the time. The original assays for XMRV testing were based on the 2009 Science publication. Those assays, as well as all subsequent modifications, were internally validated prior to being used to process patients’ samples. WPI’s Research Director was instrumental in the decision to make such a test available to physicians. The interpretation of the XMRV test results, as with all laboratory tests, is the responsibility of the ordering physician.

Before offering any test to the public, VIP Dx established comprehensive performance specifications including accuracy, precision, analytical sensitivity, specificity, and others required for test performance.

Study using cycle ergometers shows that exercise exacerbates ME/CFS


Exercise testing to quantify effects of fatigue on functional capacity in patients with CFS.
Keller BA, Micale FG.:



Objective:

The purpose of this study was to assess
the effects of post-exertional malaise (PEM) on
functional capacity and anaerobic threshold
in subjects diagnosed with chronic fatigue syndrome (CFS).


Methods:

Subjects were
10 females and 2 males (41.3+1.11 yrs) diagnosed with CFS
by a physician experienced in the diagnosis of CFS.

To induce PEM, each subject completed a maximum exercise test on a cycle ergometer.

A second maximum exercise test was performed 24 hrs later
to assess the effects of exercise-induced PEM on functional capacity.

Maximum oxygen consumption (VO2max), maximum heart rate (HRmax),
anaerobic threshold (AT), maximum workload (Wmax),
workload at AT (ATwork), and respiratory exchange ratio (RER)
were measured.

RER is an objective indicator of
substrate utilization and subject effort during exercise.


Results:

Significant decreases
from test 1 to test 2 were
13.5% for VO2max (21.5 to 18.6 ml.kg-1.min-1; p<0.01),
8 bpm for HRmax (p<0.01),
18.8% for AT (12.0 to 9.7 ml.kg-1.min-1; p<0.05),
9.4% for Wmax (121 to 109 W, p<0.05), and
17.3% for ATwork (58.3 to 48.2 W; p<0.05).

However, there was no change in maximum RER
indicating that subject effort was maximum and also comparable during both tests.


Conclusion:

Results indicate that
PEM decreased maximum functional capacity by more than 13% to below 5 METS;
a level at or below that which is required by many job-related activities and IADLs.

To compare,
VO2max in healthy individuals is highly reproducible
over days and even months (r>.95), with a SEM of < 6%.

Thus, for subjects in this study,
an expected variation between tests would be ±1.29 ml.kg-1.min-1
in contrast to the observed decrease of 2.9 ml.kg-1.min-1.

Furthermore,
PEM decreased AT to below 3 METS
(e.g., light-moderate speed walking),
which is a level of many activities considered to be sedentary in nature.

Thus,
completion of sedentary ADLs and IADLs for those with CFS
requires production of energy via anaerobic processes
that will further contribute to PEM and exacerbate symptoms of CFS.

Since many daily activities fall into the 3-5 MET range,
individuals with CFS will exacerbate symptoms associated with PEM
simply by completing normal daily activities.

See also: The main characteristic of ME is an abnormally delayed muscle recovery after doing trivial things, if you don't have that, you don't have ME 
See also: GET (graded exercise therapy) is torture for ME patients and directly contravenes the do NO Harm principle of the GMC
See also: Post-exercise acid exposure 50 times higher in ME/CFS patients vs healthy controls, with no reduction with repeat exercise 
See also: CFS Patients Try to Help Researchers Despite The Fact that Researchers try To Kill Them with CBT and GET
See also: Pacific Labs in California (Snell, Stevens et al): it is dangerous to put patients with M.E. through a graded exercise program
See also: PACE trial's Prof Peter White: Exercise causes Immunological damage in Chronic Fatigue Syndrome and is NOT safe
See also: Jan 2011, Spanish study shows that CBT and GET make things WORSE in ME/CFS !!! See also: Journal for Psychotherapy 2011: CBT and GET are ineffective and potentially harmful for many ME/CFS patients

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