Friday, April 10, 2015

Olivia's selfies speak truth about illness

itv player, good morning britain, 8 APR 2015, teenager with ME:

  Olivia Cole is a beautiful 16-year-old girl and has lived with Chronic Fatigue Syndrome since she was 10. She has not been to school properly since she was in Year 7 due to her illness and is now in Year 11.

  Olivia has taken selfies of herself when she is well and ill to show the two different lives she leads due to CFS. She is encouraging others with the syndrome to do the same to raise awareness - as many do not believe it is real and she has therefore lost many friends to it. More @ ITV player, good morning britain, 8 APR 2015, teenager with ME

Saturday, April 4, 2015

Four metabolic changes associated with exercise in cultured skeletal muscle cells in CFS compared to healthy controls

@plosone, April 2, 2015:

Abnormalities of AMPK Activation and Glucose Uptake in Cultured Skeletal Muscle Cells from Individuals with Chronic Fatigue Syndrome

  • Published: April 2, 2015
  • DOI: 10.1371/journal.pone.0122982



Post exertional muscle fatigue is a key feature in Chronic Fatigue Syndrome (CFS). Abnormalities of skeletal muscle function have been identified in some but not all patients with CFS. To try to limit potential confounders that might contribute to this clinical heterogeneity, we developed a novel in vitro system that allows comparison of AMP kinase (AMPK) activation and metabolic responses to exercise in cultured skeletal muscle cells from CFS patients and control subjects.


Skeletal muscle cell cultures were established from 10 subjects with CFS and 7 age-matched controls, subjected to electrical pulse stimulation (EPS) for up to 24h and examined for changes associated with exercise.


In the basal state, CFS cultures showed increased myogenin expression but decreased IL6 secretion during differentiation compared with control cultures. Control cultures subjected to 16h EPS showed a significant increase in both AMPK phosphorylation and glucose uptake compared with unstimulated cells. In contrast, CFS cultures showed no increase in AMPK phosphorylation or glucose uptake after 16h EPS. However, glucose uptake remained responsive to insulin in the CFS cells pointing to an exercise-related defect. IL6 secretion in response to EPS was significantly reduced in CFS compared with control cultures at all time points measured.


EPS is an effective model for eliciting muscle contraction and the metabolic changes associated with exercise in cultured skeletal muscle cells. We found four main differences in cultured skeletal muscle cells from subjects with CFS; increased myogenin expression in the basal state, impaired activation of AMPK, impaired stimulation of glucose uptake and diminished release of IL6. The retention of these differences in cultured muscle cells from CFS subjects points to a genetic/epigenetic mechanism, and provides a system to identify novel therapeutic targets.

Thursday, April 2, 2015

Simon Wessely in The Lancet: "being too stupid to know how stupid you are"

Quote from Wessely in The Lancet, 21st of march 2015 ..... (I wonder if he noticed the hysterical absurdity ...)

.... "to introduce something new to me. This is the Kruger-Dunning effect—the state of being too stupid to know how stupid you are being."

Simon Wessely in The Lancet: "being too stupid to know how stupid you are".pdf
Find by LYN.

Tuesday, March 31, 2015

Markedly disturbed immune signature in CSF with a shift towards a pattern associated with autoimmunity in ME/CFS

@; 31 march 2015:

  Molecular Psychiatry , (31 March 2015) | doi:10.1038/mp.2015.29

  Cytokine network analysis of cerebrospinal fluid in myalgic encephalomyelitis/chronic fatigue syndrome

  M Hornig, G Gottschalk, D L Peterson, K K Knox, A F Schultz, M L Eddy, X Che and W I Lipkin

  Myalgic encephalomyelitis/chronic fatigue syndrome is an unexplained debilitating disorder that is frequently associated with cognitive and motor dysfunction. We analyzed cerebrospinal fluid from 32 cases, 40 subjects with multiple sclerosis and 19 normal subjects frequency-matched for age and sex using a 51-plex cytokine assay. Group-specific differences were found for the majority of analytes with an increase in cases of CCL11 (eotaxin), a chemokine involved in eosinophil recruitment. Network analysis revealed an inverse relationship between interleukin 1 receptor antagonist and colony-stimulating factor 1, colony-stimulating factor 2 and interleukin 17F, without effects on interleukin 1α or interleukin 1β, suggesting a disturbance in interleukin 1 signaling. Our results indicate a markedly disturbed immune signature in the cerebrospinal fluid of cases that is consistent with immune activation in the central nervous system, and a shift toward an allergic or T helper type-2 pattern associated with autoimmunity.

Saturday, March 28, 2015

Psychiatrist Dr Henderson: ME/CFS: in 85% (92% in adolescents) symptoms resolve in 3-5 months on valacyclovir

Theodore Henderson, MD, PhD, March 25, 2015:

A recent consensus review on Chronic Fatigue Syndrome (CFS) and Myalgic Encephalomyelitis (ME)concluded that CFS/ME is significantly underdiagnosed and that the condition is likely caused, in part, by viruses. These findings are in line with my clinical work. Together, these two sources of data point to a pathway which may help the 2.5 million sufferers of this disease in the United States.
In February, the Institute of Medicine (IOM) completed its committee review on CFS/ME. This study was sponsored by the Department of Health and Human Services, the National Institutes of Health, and the Centers for Disease Control, among others.1
A comprehensive literature review and critique was completed by the Agency for Healthcare Research and Quality in December  as part of this process.2 Many important advancements in the medical conceptualization of CFS/ME are included in this 282 page document.
Perhaps the most important evolutionary step was the clear message delivered on page 15 of the introduction: CFS/ME is underdiagnosed and misunderstood. More than 80% of patients go undiagnosed, while 65% of patients spend more than a year seeking the correct diagnosis. A lack of understanding of this disorder has contributed to many patients feeling maligned, blamed, and undertreated.
Some patients told the committee that they felt belittled, dismissed, and ignored by their health care professionals. Patients also have reported that some treatment strategies, including the oft-cited graded exercise regimen, exacerbated their symptoms.3
Equally striking in this report was the clear assertion that CFS/ME likely has an infectious etiology and that viruses, in particular Epstein-Barr virus (EBV), are high on the list of suspected agents.1
My clinical work has focused on the viral and immunological pathogenesis of CFS/ME. In my clinic, I have treated over 200 adults and over 30 adolescents with what the IOM now says should be called Systemic Exertion Intolerance Disease (SEID). While I have not published my adult cases, a case series of adolescents was published last year.4 What has emerged from my work is that over 85% of patients with SEID (diagnosed by Fukuda criteria5) respond to antiviral therapy. Among adolescents, the outcome is better with 92% responding.
A critical second conclusion of my work is that a subset of patients diagnosed with depression — particularly treatment-resistant depression — actually had SEID. The adolescents in the case series were all referred for evaluation of depression or mood disorder. They all presented with marked fatigue, exertion induced malaise, brain fog, and impaired academic performance.
In addition, most reported daily naps and unrefreshing sleep.4 They had not responded to adequate trials of antidepressants and the duration of symptoms ranged from 6-96 months. There was no history of abuse or neglect, although this has been suggested as an etiology of SEID in the past.6,7 Patients completed the Children's Depression Inventory8 and the mean score was 14 (+2.83), below the typical cut-off for depression.
Patients were treated with the antiviral, valacyclovir (Valtrex), at a dose of 1000 mg twice a day. Only one patient experienced nausea and discontinued the antiviral. Improvement occurred over the course of 3-5 months. Eighty-six percent of the patients responded by 3 months, and 92% responded by 5 months. Symptoms of fatigue, exertion induced malaise, excessive sleep, napping, unrefreshing sleep, headaches, cognitive symptoms, and emotional symptoms all resolved.

Thursday, March 26, 2015

The Naked Scientists: Is ME an autoimmune disease? Interview with oncologists Prof Mella and Dr Fluge

Chris Smith,The Naked Scientists, 24TH MAR 2015:

TUE, 24TH MAR 2015

Is ME an autoimmune disease?

Øystein Fluge and Olav Mella, Haukeland University Hospital, in Bergen

Chronic Fatigue Syndrome(CFS), also known as ME, affects about 1 person in 500. Sufferers describe symptoms of profound tiredness and lethargy that doesn’t improve with sleep or rest. consensus on what might be causing the condition, there are no tests to confirm the diagnosis, and nor is there a cure. But now we may be closer to understanding what causes at least some of the cases of the condition thanks to research carried out in Norway, as Øystein Fluge and Olav Mella from Haukeland University Hospital, in Bergen, explain to Chris Smith...

Øystein - We are oncologists that work mainly on lymphomas and brain tumours. But in 2004, we observed a patient with longstanding ME who got lymphoma and she experienced a totally unexpected and very marked recovery of ME symptoms after she received lymphoma treatment with cancer chemotherapy. We speculated on this case and when we met new ME patients, it was striking to learn how similar the patients were in symptoms and how they described to be previously completely healthy and often, with an abrupt start of ME after infections. So, we reasoned that B-cells could be important in a subgroup of ME patients.
Chris - When you say, B-cells, these are the white blood cells, the lymphocytes that make say, antibodies and have a memory against infections we’ve seen before, aren't they?
Øystein - Yes, but we did a small pilot case series with a single infusion of the drug rituximab which targets these B-cells to 3 ME patients and they all had a marked but transient clinical response. We published this case series in 2009.
Chris - So, you were giving these people in the course of treating their blood cancer, their lymphoma, the drug rituximab which hits and destroys B-cells in the body which are in these patients, the cancer cells. And as a side effect almost of that treatment, these people who had previously said they had disabling symptoms of ME, chronic fatigue syndrome, they got better.
Øystein - That's correct.
Chris - Olav, I was going to bring you in and say, what actually happened to these people when you did this?
Olav - The 3 pilot patients all had response to treatment and one thing we observed in these 3 patients is that we have a pattern of responses and relapses after the rituximab treatment with a lag time of several months from initial and rapid B-cell depletion until they start getting clinical responses. Such patients are also seen in established autoimmune diseases after rituximab treatment. We believe that this fits with B-cells not being produced for a period after rituximab which allows a natural degradation of autoantibodies – that is antibodies that have adverse effects on bodily functions, with the symptom improving when the antibody level drops. We really think this points at ME at least in a large subportion is an autoimmune disease. It’s also spotted that 70% of the patients with ME, they get it immediately after an infection and there's, like in other autoimmune diseases, 3 to 4 times as many women as men who get the disease. And also, a big study from the US has shown a moderate and highly significant risk of B-cell lymphoma in elderly ME CSF patients, showing that the patients may have chronically activated B-cell system. We see the same lymphoma risk also in established autoimmune diseases like rheumatoid arthritis, lupus and Sjogren’s disease.
Chris - So, putting all of this together, you get these patients who, they happen to have a lymphoma – a cancer of the blood system – but they also have chronic fatigue syndrome. You treat their lymphoma with a drug which takes down their B-cells which are the cause of their cancer. They get this pattern of, their disease recovers when the B-cells go away but with the time lag corresponding to the time it takes the B-cells to go and the antibodies to go. And then when the B-cells come back in these patients, then the symptoms come back which looks like it’s tying the two things together, doesn’t it? So, what do you think that the B-cells are doing in these people to actually make, Olav, the symptoms of chronic fatigue syndrome in those patients?
Olav - Well, we think that it is a kind of an immune response and it obviously affects some very central function in the body. We’re not at all convinced that ME is kind of inflammatory condition in the brain. Probably, more important, I think what is happening in blood vessels, we have indications that the blood vessel do not function as they should, given the dynamic flow to different parts of the body when it is needed.
Øystein - It’s like the patients have a problem in the fine-tuning or regulation of blood flow according to the demands of the tissues for oxygen and nutrients. The patients often describe they feel like running a marathon when they have done a limited exertion and they get brain fog from exertion and so on. So, our hypothesis is that the immune system somehow disturbs the fine-tune regulation of blood flow and tissues including in the brain.
Chris - Øystein, what are you now doing to try to firm this up because your initial results as you published, while very interesting are on very small numbers of patients? Obviously, we’d like to see big numbers of patients in order to make sure that this is not a statistical blip, it’s not happening due to chance, it’s real.
Øystein - To try to convince ourselves, we first did, as you say, a small randomised study which was published in 2011 with 15 patients given two infusions of rituximab and 15 patients given placebo, turn out that the 15 that got rituximab had a clinical response while 2 of the 15 in the placebo group. So, that was some kind of sign of clinical activity to us. So then we did an open label study with no placebo group, further rituximab infusion, prolonging the period with low B-cells. We gave 6 infusions of rituximab up to 15 months and then followed the patient for 3 years. So, this study is now submitted for publication but we can say that again, 2/3 had a clinical response and the response durations were much prolonged when we gave maintenance treatment. But these two studies are not designed to give a definite answer to whether rituximab works in ME. So therefore, we are now performing a larger phase III study in Multicentre in Norway with 152 patients. Half of them will receive 6 rituximab infusions during the first year and half of them will receive placebo. And then we will follow the patients for 2 years. And we hope that this study will either verify or refute if rituximab may give benefit to ME patients in a significant proportion.

Saturday, March 21, 2015

Oncologists squash Mats Reimer's Wesselyan psycho blah blah

By deleder2k, 20.3.2015:

Norwegian Daily Medicine 2015.03.20 

dr. Øystein Fluge and dr. Olav Mella comments on Reimer's concern regarding the upcoming cylophosphamide study

Original article in Norwegian:
Translated by Google Translate and 


Saturday, March 7, 2015

Reduced CD2, CD4 and CD8 lymphocytes and also reduced immunoglobulin (Ig) in ME / CFS

@ PubMed:

  Med J Aust.  1989 Aug 7;151(3):122-4.Immunological abnormalities in the chronic fatigue syndrome.Lloyd AR 1, Wakefield D , Boughton CR , Dwyer JM .Author information

  Abstract The chronic fatigue syndrome is a disorder of unknown aetiology which is characterized by debilitating fatigue. Recent evidence has suggested that viruses may persist in the tissues of patients with chronic fatigue syndrome. A concurrent immunological disturbance is likely to be associated with the persistence of viral antigens. Therefore, the humoral and cellular immunity of 100 patients who were suffering from chronic fatigue syndrome and that of 100 healthy, age- and sex-matched control subjects were compared.

  This study documents the frequent occurrence of abnormalities within the cellular and humoral immune systems of patients with well-defined chronic fatigue syndrome. Disordered immunity may be central to the pathogenesis of chronic fatigue syndrome.

  In patients with chronic fatigue syndrome, a significant (P less than 0.01) reduction was found in the absolute number of peripheral blood lymphocytes in the total T-cell (CD2), the helper/inducer T-cell (CD4) and the suppressor/cytotoxic T-cell (CD8) subsets. A significant (P less than 0.001) reduction also was found in T-cell function, which was measured: in vivo by delayed-type hypersensitivity skin-testing (reduced responses were recorded in 50 [88%] of 57 patients); and in vitro by phytohaemagglutinin stimulation.

  Reduced immunoglobulin (Ig) levels were common (56% of patients), with the levels of serum IgG3- and IgG1-subclasses particularly (P less than 0.05) affected.

Monday, March 2, 2015

Scientists Successfully Remove HIV From Human Cells

BY Dan Avery:

  "Researchers at Temple University in Philadelphia have been able to destroy HIV in human cells, rather than simply suppress it, a breakthrough in the ongoing fight against HIV/AIDS.

  “It’s an important finding because, for the first time in laboratory setting, we show that the virus can be eradicated from human culture, cell culture, said Dr. Kamel Khalili, who led the research team at Temple’s Center for Neurovirology.

  “Basically [we're] converting infected cells to un-infected cells,” he explains “And that is very important because the current therapy can not eliminate the virus from cells.”

  Dr. Khalili’s team developed molecular tools that can operate on DNA and delete HIV in cells."


Sunday, March 1, 2015

The NewYorker: People with ME/CFS are more “functionally impaired” than those with MS and congestive heart failure


  "People with ME/CFS, the report noted, are more “functionally impaired” than those with Type 2 diabetes, multiple sclerosis, and congestive heart failure—diseases that we know to be very grave indeed."

  more @

Saturday, February 28, 2015

Psychiatrists commenting on immunological abnormalities, typical science media Center crap

By Utting Wolff:

  "The Science Media Centre surpassed itself in its coverage of the Columbia University study[6]. Of seven experts chosen to respond to the study, not one gives a positive analysis, no medical adviser from an ME charity or, non-psychosomatic promoting, ME researcher is quoted.

  The featured experts are: Professors Michael Sharpe and Peter White, and Dr Esther Crawley, all notorious proponents of the psychogenic ME model.

  Professor Stephen Lawrie, head of The Division of Psychiatry at the University of Edinburgh: ‘This is a small study’ he states[6]; a study encompassing 20 participants is small professor Lawrie, one involving over 600 participants is not[1]. One has to ask why is a psychiatrist being consulted?"

Thursday, February 26, 2015

IOM: ME/CFS "is a medical—not a psychiatric or psychological—illness"

@ PubMed:


Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome: Redefining an Illness.


Committee on the Diagnostic Criteria for Myalgic Encephalomyelitis/Chronic Fatigue Syndrome; Board on the Health of Select Populations; Institute of Medicine.



Myalgic encephalomyelitis (ME) and chronic fatigue syndrome (CFS) are serious, debilitating conditions that affect millions of people in the United States and around the world. ME/CFS can cause significant impairment and disability. Despite substantial efforts by researchers to better understand ME/CFS, there is no known cause or effective treatment. Diagnosing the disease remains a challenge, and patients often struggle with their illness for years before an identification is made. Some health care providers have been skeptical about the serious physiological—rather than psychological—nature of the illness. Once diagnosed, patients often complain of receiving hostility from their health care provider as well as being subjected to treatment strategies that exacerbate their symptoms. 

Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome proposes new diagnostic clinical criteria for ME/CFS and a new term for the illness - systemic exertion intolerance disease(SEID). According to this report, the term myalgic encephalomyelitis does not accurately describe this illness, and the term chronic fatigue syndrome can result in trivialization and stigmatization for patients afflicted with this illness. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome stresses that SEID is a medical—not a psychiatric or psychological—illness. This report lists the major symptoms of SEID and recommends a diagnostic process. One of the report's most important conclusions is that a thorough history, physical examination, and targeted work-up are necessary and often sufficient for diagnosis. 

The new criteria will allow a large percentage of undiagnosed patients to receive an accurate diagnosis and appropriate care. Beyond Myalgic Encephalomyelitis/Chronic Fatigue Syndrome will be a valuable resource to promote the prompt diagnosis of patients with this complex, multisystem, and often devastating disorder; enhance public understanding; and provide a firm foundation for future improvements in diagnosis and treatment.
Copyright © 2015, National Academy of Sciences.


    Free Books & DocumentsFree full text

    Tuesday, February 24, 2015

    The real reason why Prof Edward Shorter is ridiculing and attacking severely ill patients

    So why did professor Edward Shorter write his 2 very aggressive / hostile / vile articles in psychologytoday, attacking patients who are severely ill?

      Even though he is a psychiatrist and a medical historian, he shows a total lack of knowledge about basic facts about this disease and totally ignores all clinical evidence etc that what he says is total rubbish / nonsense.

      The answer to the question can be found in one of his tweets, ie his new book is out on the 7th of march.

      @DrEdwardShorter: "… The pub date for this is Mar 7 but Amazon up now. Theme: what should have been in but wasn't and shouldn't but was."

      So all he cares about is selling books, earning money and getting his name in the paper, that he has to ridicule and attack severe ill patients to do so, is obviously no problem to him or to psychologytoday.

      And that's the sad state of affairs of psychiatry and psychology in 2015.

      See also Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence


    Monday, February 23, 2015

    Prof Edward Shorter and the psychic epidemic of ignoring clinical evidence

    A phenomenon well familiar to historians of medicine is the psychic epidemic of ignoring clinical evidence by psychiatrists and medical historians, a belief that spreads epidemically, until the evidence become so overwhelming that it becomes clear that these people have been telling porkies for decades, and then their nonsense is forgotten.

      In the 20th century, psychiatry fostered such an epidemic with the belief that ego masturbation caused their bank accounts to inflate. Many medical historians and psychiatrists obsessed for years over the thought that their “self-abuse” had pleased their bank managers.

      Another epidemic focused on the toxic  effects of ignoring clinical evidence on the ovaries. Many male medical historians and male psychiatrists would plead for ovariectomies, on the grounds that their irritated ovaries were blocking clinical evidence which their penis had spotted, to go all the way to their brain. And that this was leading to erectile dysfunction and the inability to have an orgasm.

      Once their ovaries were removed, their penis size increased by more than 5 inches. So all these male medical historians and male psychiatrists were pleading their doctors for ovariectomies.

      In the late 1980s the belief spread epidemically that reading clinical evidence caused irreversible brain damage, and a number of leading medical historians and psychiatrists wrote books full of advice about eating small meals upside down, with your eyes closed and your brain in hibernation mode, to make sure that clinical evidence would not reach your brain to prevent brain damage.

      I realize that these words will fall unreceptively upon some ears, and I regret that some medical historians and psychiatrists, especially from Toronto, may feel slighted by the clinical evidence that is readily available, if only they where willing to turn on their computer and were willing to read biomedical research, for example the fMRI studies from Stanford, or the PET scan study from Japan. 

      Yet there are larger stakes here. In the way that lives were once ruined with such toxic diagnoses as hysteria, which in this day and age is called MS, millions of lives today are ruined by medical historians and pinocchio psychiatrists who have made a fortune out of ignoring clinical evidence.

      Many psychiatrists and medical historians choose their profession so that they didn't have to become productive members of the community.  (The IOM report dwelled upon the dangers of severely ill patients being abused by the medical profession.) 

      Such a waste of human potential is tragic, and if there are lessons that we may draw from the history of medicine, it is that doctors who discover the underlying metabolic problem or cause of such diseases, which medical historians and psychiatrists call psychosomatic, even though they do not have any evidence to back up this claim, will go on to win the Nobel prize for medicine, as the Nobel Prize winner in medicine, Dr Barry Marshall stated a few years ago.


    Related Posts with Thumbnails