PACE trial researchers respond to David Tuller

Posted on 11/02/2015 by wames

David Tuller’s three-installment investigation of the PACE trial for CFS, Trial By Error, received much attention in the press. Although the PACE researchers declined David’s efforts to interview them, they subsequently requested the right to reply. Virology blog posted the response of Professors Peter White, Trudie Chalder and Michael Sharpe to David’s story on 30 October 2015.

David Tuller responds to the PACE investigators:

Excerpt: In their effort to correct the “misinformation” and “inaccuracies” in my story about the PACE trial, the authors make claims and offer accounts similar to those they have previously presented in published comments and papers. In the past, astonishingly, journal editors, peer reviewers, reporters, public health officials, and the British medical and academic establishments have accepted these sorts of non-responsive responses as adequate explanations for some of the study’s fundamental flaws. I do not.

None of what they have written in their response actually addresses or resolves the core issues that I wrote about last week. They have ignored many of the questions raised in the article. In their response, they have also not mentioned the devastating criticisms of the trial from top researchers from Columbia, Stanford, University College London, and elsewhere. They have not addressed why major reports this year from the Institute of Medicine and the National Institutes of Health have presented portraits of the disease starkly at odds with the PACE framework and approach. Read more

Cort Johnson also commented on the researchers’ response: PACE Trial authors feeling the heat over Chronic Fatigue Syndrome Trial,  Oct 30, 2015

Excerpt: The PACE trial authors appear to have done themselves few favors by presenting their side of the argument.

Their responses demonstrated two things:

  1. Tuller’s critique and the response to it by the patient community has hit home
  2. they don’t have answers to most of his questions.

If it looks like a duck and walks like a duck – is it a duck?

Notice that every change they made it more possible for the trial to get positive results. Notice how moderate the results were even with these added boosts.

Consider the fact that the researchers were never blinded to the results flooding in. Consider the possibility that they gloamed early on to the fact that things were not going their way and that changes needed to be made.

While the study findings were initially lauded (and misinterpreted) by the press (apparently with Chalder’s help) the controversy over the PACE trial continues to muddy it’s results.

Remember  we’re talking about what is surely the most expensive study ever done on ME/CFS. The PACE authors are right. Reputations are at stake. Until they can satisfactorily explain – if that’s possible – the many questions surrounding the trial – it doesn’t appear that the controversy is going to go away.

 

 

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Evette’s life with ME – a living torture

Posted on 11/02/2015 by wames

Severely affected Evette describes having ME as a living torture in ITV news on 30 October 2015.  Reporter Rob Osborne interviews Christalla Davies from support group MESiG and a local doctor about the seriousness of ME.

Youtube video [2 mins 48 secs]

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5-HTT genotype associated with CFS in children

Posted on 11/01/2015 by wames

Research abstract:

Earlier studies have shown that genetic variability in the SLC6A4 gene encoding the serotonin transporter (5-HTT) may be important for the re-uptake of serotonin (5-HT) in the central nervous system.

In the present study we investigated how the 5-HTT genotype i.e. the short (S) versus long (L) 5-HTTLPR allele and the SNP rs25531 A > G affect the physical and psychosocial functioning in patients with chronic fatigue syndrome (CFS). All 120 patients were recruited from The Department of Paediatrics at Oslo University Hospital, Norway, a national referral center for young CFS patients (12–18 years).

Main outcomes were number of steps per day obtained by an accelerometer and disability scored by the Functional Disability Inventory (FDI). Patients with the 5-HTT SS or SLG genotype had a significantly lower number of steps per day than patients with the 5-HTT LALG, SLA or LALA genotype. Patients with the 5-HTT SS or SLG genotype also had a significantly higher FDI score than patients with the 5-HTT LALG, SLA or LALA genotype.

Thus, CFS patients with the 5-HTT SS or SLG genotype had worse 30 weeks outcome than CFS patients with the 5-HTT LALG, SLA or LALA genotype. The present study suggests that the 5-HTT genotype may be a factor that contributes to maintenance of CFS.

Maintenance of chronic fatigue syndrome (CFS) in young CFS patients is associated with the 5-HTTLPR and SNP rs25531 A >; G Genotype, by  Benedicte Meyer,  Chinh Bkrong Thuy Nguyen,  Aurora Moen,  Even Fagermoen, Dag Sulheim,  Hilde Nilsen,  Vegard Bruun Wyller, Johannes Gjerstad in PLOS One, October 16, 2015 10(10)

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New US CFS research initiative announced

Posted on 10/30/2015 by wames

NIH announces new effort to tackle chronic fatigue syndrome in the Washington Post, by Lenny Bernstein, October 29

The director of the National Institutes of Health announced a new initiative Thursday to find a cause and treatment for chronic fatigue syndrome, the mysterious, debilitating condition that disables many of its more than 1 million sufferers.

Francis S. Collins said in an interview that medicine “desperately needs some new ideas” in the fight against the syndrome and the closely related neurological disorder myalgic encephalomyelitis. At the moment, there is no test, cause or treatment for the condition, which causes overwhelming, often disabling fatigue in more than a quarter of the people who suffer from it.

“There’s something going on here, and we ought to be able to come up with an answer with the tools we have,” Collins said.

Collins said the agency will move forward on two fronts. It will launch research at the NIH Clinical Center to intensively study a small number of individuals with the disorder, and will revive a working group focused on encouraging more research on the disorder outside NIH. But no budget for the efforts has been developed yet, Collins said.

[Chronic fatigue syndrome is a physical disorder, expert panel announces]

In February, the Institute of Medicine, the health arm of the National Academy of Sciences, declared the syndrome a “serious, debilitating”
physical disorder — not a psychological illness — in the hope of ending lingering beliefs that the condition was psychosomatic.

Other symptoms include joint and muscle pain, headaches, cognitive difficulties and problems with the immune and neurological systems. It often strikes after a flu-like illness or other infection.

NIH spending on the disorder has languished near the bottom of the research agency’s priorities. In July, Brian Vastag, a former Post reporter who suffers from the disorder, wrote passionately of the need for additional NIH research.

[I’m disabled. Can NIH spare a few dimes?]

Carol Head, president of the advocacy group Solve ME/CFS Initiative, said after the announcement that “we are thrilled. This is a disease that has been neglected by the federal government, frankly, for decades.”

Head said there is no doubt funding for research into the condition would have to increase substantially under the plan outlined by Collins, though she said her group looks forward to knowing how much will be spent.

Nevertheless, she said, “we think the steps that were taken…clearly indicate a sea change in the NIH’s commitment to this illness. And from everything we’ve heard, it’s coming from the top, from Dr.
Collins.”

Collins said that in recent years, research had focused on the idea that the syndrome was caused by a virus, which proved untrue and may have halted other promising areas of inquiry. The goal now is to “recruit some new bright ideas and idea generators” to the effort, he said.

NIH: NIH takes action to bolster research on Myalgic Encephalomyelitis/Chronic Fatigue Syndrome

Open Medicine Foundation comment: NIH Increases ME/CFS Research with New Initiative

Solve ME/CFS comment: NIH Announces New Efforts to Advance ME/CFS Research

 

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Is heart disease in the future of patients with ME & FM?

Posted on 10/30/2015 by wames

Cort Johnson on the Health Rising Forums asks if people with ME could be susceptible to heart disease, as research suggests for people with Fibromyalgia. Is Heart Disease in ME/CFS and FM Patients Future? 23, Sep 2015

Coronary heart disease (CHD) occurs when plaque builds up on the arteries that supply blood to the heart. The plaque buildup can reduce blood flows to the heart causing chest pain – particularly during strenuous activity. If the plaque bursts a clot can form which can block blood flows to the heart causing a heart attack.

CHD is the leading cause of death in the U.S. Despite the fact that it typically shows up about ten years later in women than men it is the leading cause of death in the U.S. for women. This is the second Taiwanese study to find an increased risk of coronary heart disease in people with fibromyaliga. The increased risk of CHD (almost 50%) found was not as high as for diabetes or hypertension, and was described as “moderate”.

Increased Risk of Coronary Heart Disease in Patients with Primary Fibromyalgia and Those with Concomitant Comorbidity—A Taiwanese Population-Based Cohort Study Chia-Hsien Su, Jiunn-Horng Chen, Joung-Liang Lan, Yu-Chiao Wang, Chun-Hung Tseng, Chung-Yi Hsu, Lichi Huang, Published: September 14, 2015 DOI: 10.1371/journal.pone.0137137​

FM patients with diabetes, hypertension, hyperlipidemia, congestive heart failure, cerebral vascular diseases, depression or anxiety had more significantly increased risks of CHD. The risk for CHD was higher, interestingly in FM patients without depression than in people with depression but not FM.

The authors proposed several hypotheses to explain the increased CHD. They rejected the idea that the high use of NSAIDS, antidepressants and pain killers were contributing to it. Instead they suggested that chronic stress, including in some patients early lifetime stressors, increaseid sympathetic nervous system activity and reduced parasympathetic nervous system activity. They noted the reduced heart variability results found in FM, which are a known risk factor for heart disease.

People with chronic fatigue syndrome should note that similar autonomic nervous system findings are found in ME/CFS.

Several studies have found “unfavorable lipid profiles” that could increase the risk of atherosclerosis in ME/CFS. A small 2012 study of women with ME/CFS found high triglyceride and malondialdehyde levels and low levels of the healthy cholesterol (HDL-C). HDL-C is anti-inflammatory agent that prevents cholesterol accumulations on the cell walls and reduces lipid peroxidation.

The authors proposed that these factors may predispose ME/CFS patients to vascular (blood vessel) damage and suggested antioxidant supplement and LDL lowering strategies be employed. A 2005 study found increased levels of oxidized lipids and decreased HDL-C in ME/CFS patients with risk factors (high blood pressure and/or obesity).

High levels of overweight and obesity in fibromyalgia may contribute to the problem although they may not be higher than in the population at large. One study suggested that negative lipid profiles in FM were associated with increased weight – suggesting one possible way to reduce them.

Risk Factors for CHD

A look at the risk factors for CHD finds a mixed bag for people with ME/CFS/FM. Some are probably high (triglycerides, lack of physical activity, sleep apnea, stress) while some major ones (unhealthy diet, smoking, alcohol consumption, high blood pressure) are probably low.

Reduced Physical Activity

Reduced physical activity is important risk factor but the authors of the paper did not suggest it was a factor. The US Guidelines for the amount of aerobic exercise needed to maintain health and ward off illness, however, are probably rarely met by people with fibromyalgia and almost never by people with ME/CFS.

The U.S. breaks activity levels into four categories:

  • Inactive is no activity beyond baseline activities of daily living.
  • Low activity is activity beyond baseline but fewer than 150 minutes (2 hours and 30 minutes) of moderate-intensity physical activity a week or the equivalent amount (75 minutes, or 1 hour and 15 minutes) of vigorous-intensity activity.
  • Medium activity is 150 minutes to 300 (5 hours) minutes of moderate-intensity activity a week (or 75 to 150 minutes of vigorous-intensity physical activity a week). In scientific terms, this range is approximately equivalent to 500 to 1,000 metabolic equivalent (MET) minutes a week.
  • High activity is more than the equivalent of 300 minutes of moderate-intensity physical activity a week.

Aerobic Activity

The U.S. Guidelines state the following amounts of aerobic activity are needed to maintain health and ward off illness. Moderate (such as brisk walking or tennis) or intense (jogging or swimming) should be done in episodes of at least 10 minutes and, if possible, spread out through the week.

  • 150 minutes (2 hours and 30 minutes) each week of moderate-intensity aerobic physical activity (such as brisk walking or tennis)
  • 75 minutes (1 hour and 15 minutes) each week of vigorous-intensity aerobic physical activity (such as jogging or swimming laps)
  • An equivalent combination of moderate- and vigorous-intensity aerobic physical activity

For even greater health benefits, they recommend

  • Increase moderate-intensity aerobic physical activity to 300 minutes (5 hours) each week
  • Increase vigorous-intensity aerobic physical activity for 150 minutes (2 hours and 30 minutes) each week

Is Coronary Heart Disease in ME/CFS and FM Patients Future?

Despite some negative risk factors – not necessarily. The CDC estimates that about 7% of the entire population and about 17% of people over 65 have it. Women have lower rates of CHD (@ 5%) than men but may be more severely affected by it when it does occur.

That suggests that even a 50% increase in the risk factor for CHD would leave the vast majority of middle-aged women with FM (>90%) without it. FM and ME/CFS patients with increased risk factors (depression, anxiety, obesity, increased blood pressure, sleep apnea) would have a higher incidence.

Coronary heart disease is something to think about given the reports of decreased heart rate variability, increased oxidative stress, the high triglyceride findings, the lack of activity, etc. in ME/CFS/FM but it’s certainly not a forgone outcome. More study is clearly needed regarding the long term effects of these diseases.

In the meantime a heart healthy diet, stress reduction, whatever exercise can be done, strategies to reduce inflammation and sleep studies to assess sleep apnea are probably good ideas.

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Dr Alan Light video lecture on new developments in ME/CFS research

Posted on 10/29/2015 by wames

SolveCFS video:  New Developments in ME/CFS Research [Published Oct 15, 2015]

Presented by Dr. Alan R. Light, Research Professor of Anesthesiology and Neurobiology and Anatomy at the University of Utah.  Download Powerpoint for lecture.

Dr. Light received his PhD from the State University of New York at Upstate Medical Center and was a Postdoctoral Fellow at the University of North Carolina-Chapel Hill.

He received a Javits Award from the National Institutes of Health for his research on descending control of pain. His current research focuses on the mechanisms of the sensations of muscle pain and fatigue and the plasticity they undergo following inflammation, injury and in functional disorders such as Chronic Fatigue Syndrome and Fibromyalgia.

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Norwegian professors call for better use of criteria to diagnose ME

Posted on 10/28/2015 by wames

Article:
Although there are good diagnostic criteria for myalgic encephalomyelitis, knowledge of the disease is often lacking and this can result in misdiagnosis and incorrect treatment. There is a need for more research, greater expertise among clinicians, and refinement of the diagnostic criteria.

In the literature and in clinical practice, «chronic fatigue syndrome» (CFS) and myalgic encephalomyelitis (ME) are sometimes used synonymously (1). Limited knowledge of aetiology and pathology has resulted in a variety of terms being used to refer to various long-term pain and fatigue disorders of unknown origin. Research over recent years, the establishment of good diagnostic criteria, and clinical experience, however, indicate that myalgic encephalomyelitis is a reasonably well-defined disorder with distinct clinical characteristics.

Jason and colleagues have highlighted the fact that patients with myalgic encephalomyelitis have more severe symptomatology than those with chronic fatigue syndrome, but better mental health (2). In common with Jason, one of the leading researchers in the field internationally, we believe that it is important to distinguish between myalgic encephalomyelitis and chronic fatigue syndrome (2, 3). Myalgic encephalomyelitis should be considered a distinct diagnostic category, not least because post-exertional malaise, significant functional impairment and sleep disturbances are cardinal symptoms.

Advances in research and increasing clinical experience are reflected in the evolution of the various diagnostic criteria into the current international consensus criteria for myalgic encephalomyelitis (4) and the most recent proposal from the Institute of Medicine in the USA (5). Box 1 presents an overview of the various criteria that have been in use over the past 25 years, from the broadest Oxford criteria (general fatigue) to criteria with a focus on specific symptoms of myalgic encephalomyelitis: the Canadian criteria (6) and the international consensus criteria for myalgic encephalomyelitis (4).

Diagnostic criteria:

Various diagnostic systems and criteria for myalgic encephalomyelitis, chronic fatigue syndrome and chronic fatigue syndrome/myalgic encephalomyelitis are used in clinical diagnostics and research. The most common are:

Oxford criteria for chronic fatigue syndrome (1991)

Drafted by an English group consisting largely of psychiatrists (27). The main criterion is severe fatigue for at least six months. Other diseases must be excluded. The Oxford criteria are very broad, but are still used to some degree in research. Neither the Norwegian Directorate of Health nor the US health authorities recommend use of these criteria today.

Fukuda criteria for chronic fatigue syndrome (1994)

Drafted by the Centers for Disease Control and Prevention (CDC) on the basis of Fukuda et al. (28). In addition to severe fatigue for at least six months, and the exclusion of other diseases, at least four of eight defined symptoms must be present: impaired short-term memory and/or concentration, sore throat, tender lymph nodes, muscle pain, joint pain, new-onset headache, unrefreshing sleep, and post-exertional malaise. These criteria have been central to research.

Canadian criteria for myalgic encephalomyelitis/chronic fatigue syndrome (2003)

Drafted by doctors and researchers and represent a refinement and narrowing of the Fukuda criteria (6). The Canadian criteria require the patient to have six different symptoms: severe physical and mental fatigue, post-exertional malaise or fatigue, sleep dysfunction, pain in muscles, joints and the head, neurological/cognitive features (minimum of two symptoms, e.g. confusion, impaired concentration, ataxia), and autonomic, e.g. nausea and irritable bowel, neuroendocrine, e.g. loss of thermostatic stability, or immune disorders.

International consensus criteria for myalgic encephalomyelitis (2011)

Drafted by an international panel of experts from 13 countries (4) and a refinement of the Canadian criteria. A diagnosis of myalgic encephalomyelitis requires the patient to fulfil criteria within four categories: (a) post-exertional neuroimmune exhaustion, often with significantly prolonged recovery period, (b) neurological impairments, i.e. symptoms from three of four categories: cognitive abilities, pain, sleep disturbances and/or neurosensory, perceptual or motor disturbances, (c) immune, gastrointestinal and genitourinary impairments from three of five categories, including flu-like symptoms, nausea and hypersensitivity, and (d) impairments of energy production and energy transport within one of four categories: cardiovascular, respiratory, thermoregulatory and/or intolerance of extreme temperatures. The criteria have also been adapted for paediatric populations.

Paediatric criteria for myalgic encephalomyelitis and chronic fatigue syndrome (2006)

Various paediatric diagnostic criteria have been used. The Norwegian Directorate of Health recommends the criteria presented by Jason et al. (29), which require chronic fatigue for at least three months and exclusion of other diseases. Additional requirements include post-exertional malaise/fatigue, unrefreshing sleep or other sleep disturbances, pain in muscles, joints, stomach or head, neurocognitive features, at least 2 of 12, and at least one symptom within the three groups autonomic, neuroendocrine and immune. Severe psychiatric disorders that could explain the chronic fatigue, such as anorexia and bulimia, are exclusionary.

Systemic Exertion Intolerance Disease (SEID) criteria (2015)

Proposed by the Institute of Medicine in the United States (5). The diagnosis requires a significant loss of functional capacity, post-exertional malaise (PEM) and sleep disturbances (unrefreshing sleep). Additional criteria are also proposed, including cognitive impairment and/or orthostatic intolerance. The proposers suggest that the term myalgic encephalomyelitis should be replaced with «Systemic Exertion Intolerance Disease» (SEID).

*****

The use of different diagnostic criteria makes it difficult to establish the prevalence of myalgic encephalomyelitis specifically. Depending on which criteria are used, the prevalence of chronic fatigue syndrome/myalgic encephalomyelitis is probably around 0.1 – 2.5  %. The incidence per 100 000 population in Norway is estimated at 39.4 (women) and 12.9 (men) (7), with slight peaks at the ages of 10 – 19 and 35 – 49 years (7).

Many studies have included very heterogeneous patient populations, where perhaps only a minority of individuals had what we would define as myalgic encephalomyelitis. As a result, it has been difficult to unambiguously identify aetiological and pathogenic factors in the disease. Several studies do, however, indicate that the condition has a somatic origin. Changes in the central nervous system and the immune system have been described, as well as dysfunction of cellular energy metabolism and ion transport, cardiovascular changes, endocrine hypoactivity and a possible genetic predisposition (4, 8). Development of myalgic encephalomyelitis after infection or vaccination is well known and may indicate a post-infectious origin (8, 9). A recent Norwegian study showed that antibody treatment against B lymphocytes had beneficial effects in a majority of patients (10), a new PET study from Japan shows widespread inflammation of the central nervous system (11), and Brown and colleagues recently demonstrated abnormal activation of AMPK and glucose uptake in skeletal muscle (12). Two recently published articles show a series of changes in immunological variables in plasma in patients ≤ 3 years after onset of myalgic encephalomyelitis/chronic fatigue syndrome (13) and in cerebrospinal fluid in a patient cohort (14).
How is the diagnosis made?

Myalgic encephalomyelitis is diagnosed via a careful anamnesis and thorough physical examination. Other conditions must be excluded, and there are currently no diagnostic biomarkers. The Norwegian Directorate of Health’s guidelines (1) recommend either the Fukuda- or Canadian criteria for adult patients, see Box 1. This might appear confusing given that the criteria are incongruent. The guidelines also emphasise that «prolonged worsening of fatigue after physical or mental exertion is considered a cardinal symptom», even though this is an absolute requirement only in the Canadian criteria and the international consensus criteria for myalgic encephalomyelitis. The frequency and intensity of symptoms are also important for distinguishing patients with myalgic encephalomyelitis from other groups with chronic fatigue symptoms (2).

The use of broad inclusion criteria has created a heterogeneous patient population, also within research. This has increased the risk of erroneous conclusions, misdiagnosis and incorrect treatment (15). For myalgic encephalomyelitis, the Canadian criteria and the international consensus criteria have in our view increased the accuracy of diagnosis due to their greater specificity and clearer delineation of the disorder from other forms of fatigue.

The Norwegian Directorate of Health recommends that children and adolescents are diagnosed by a paediatrician. Adults can be diagnosed by their general practitioner (1). Given how unclear this field has been previously, and how time-consuming an assessment can be, we believe it is very important that doctors who make the diagnosis have broad experience and extensive knowledge of the condition and of diseases with overlapping symptoms.
How are patients treated?

The assessment and treatment of patients with myalgic encephalomyelitis and chronic fatigue syndrome/myalgic encephalomyelitis in Norway is, according to a SINTEF study from 2011 (16), highly inadequate: There is a lack of expertise within the social, welfare and healthcare services, and disagreement over the diagnostic criteria. Furthermore, the provision of appropriate treatment, rehabilitation and care is lacking, as is expertise regarding the particular needs of children and adolescents. Research activity is limited. Patients experience stigma and a lack of respect from healthcare personnel.

There is no specific treatment. We believe that myalgic encephalomyelitis may consist of several subtypes, which cannot at present be distinguished using existing diagnostic criteria. Such subtypes may have distinct aetiologies and pathogenic mechanisms, which could require different therapeutic approaches.

Internationally, myalgic encephalomyelitis has gradually come to be viewed as a somatic disorder, partly as a result of new and better research. In the USA, this view is gaining ever-increasing support and is now dominant within leading research communities (4, 8 – 14). However, as a result of the previously more psychosomatic view of the disease, and also the broad diagnostic criteria, various psychological and psychosomatic approaches have been used in an attempt to treat patients. The idea was that shifting the psyche towards positive thinking using techniques such as cognitive behavioural therapy (CBT) and/or various forms of graded exercise therapy (GET) would give good clinical results. Some patients have benefited from such treatment, and cognitive behavioural therapy can improve patients’ ability to cope with the disease. However, others have experienced no effect or have even deteriorated (17 – 19). Health professionals must therefore keep in mind that treatments requiring physical or mental exertion can often lead to patients becoming overstrained and to worsening of symptoms. We refer again to the statement in the national guidelines regarding prolonged deterioration following physical or mental exertion (1).

Treatments such as cognitive behavioural therapy and graded exercise therapy are controversial in the literature, with some studies reporting improvement of symptoms and others reporting exacerbation. However, it is difficult to draw conclusions from many of these clinical studies given that patient populations were often heterogeneous and limited, differing diagnostic criteria were used and methods of assessment and follow-up varied.

A report recently submitted to the US health authorities concludes that continued use of the Oxford criteria (the broadest) «may impair progress and cause harm», and recommends that these criteria should no longer be used (20). Nevertheless, studies based on these broad criteria are still used to recommend specific treatments; see for example the Norwegian Knowledge Centre for the Health Services’ article on how exercise therapy can help persons with chronic fatigue syndrome/myalgic encephalomyelitis (21).

However, the results of large user surveys conducted by patient associations in Norway (17) and the UK (18) are more clear-cut and surprisingly similar: Cognitive behavioural therapy had little or no effect in most, while a minority experienced either improvement or deterioration. For graded exercise therapy the results are discouraging: 66  % of patients surveyed in Norway and 56  % in the UK became worse, sometimes markedly so. Only 14  % of patients in Norway and 22  % in the UK experienced an improvement. Approximately seven out of ten patients in both studies found that pacing led to an improvement in their condition. The Cochrane and PACE studies (22, 23) are often used as grounds for recommending cognitive behavioural therapy for myalgic encephalomyelitis, but even these two studies show that cognitive behavioural therapy is helpful in only a minority of patients when compared to a control group and standard monitoring by a doctor.

We therefore feel it is unfortunate that psychosomatic therapy continues to be recommended by the health authorities and in parts of the healthcare system (21, 24 – 26). We recognise that it is difficult to distinguish those patients who may benefit from psychosomatic therapy from those who should receive a different form of treatment. This should lead to increased consideration of patients as individuals and greater care regarding choice of therapy. Patients’ experiences and knowledge of their own limitations should be taken seriously, and it may also be helpful to involve relatives.

We are aware of far too many cases of patients with severe myalgic encephalomyelitis being poorly received by doctors and other healthcare professionals. The status of patients in Norway poses serious ethical challenges for the Norwegian healthcare system. Many of those affected report that they are given unhelpful or even harmful treatment (17, 18). Greater expertise regarding how to diagnose the disorder, which forms of treatment are most appropriate, and how the disease manifests for the patient and their close family would be highly useful for both clinicians and patients. In particular, we believe that classic symptoms such as cognitive impairment and activity intolerance (post-exertional malaise) must form the basis of both diagnosis and treatment, as in the new criteria proposed by the Institute of Medicine (5), and not be misinterpreted as an unwillingness on the part of the patient to acknowledge or improve their own situation (17, 18).

A more deliberate use of the diagnostic criteria will result in increased understanding of the disease and of patients’ lives, and more respectful and appropriate treatment. It will also lay the foundations for ramping up (5, 20) biomedical research efforts in the hope of developing more effective treatments.

We are six professors who, in different ways, are all involved in issues related to myalgic encephalomyelitis. Some of us are medics and scientists who participate actively in research into the condition, while others are social scientists or ethicists who have taken a critical look at the literature in the field from a social and socio-medical perspective.

What exactly is myalgic encephalomyelitis? by T Egeland, A Angelsen, R Haug, J-O Henriksen, T E Lea, O D Saugstad in Tidsskr Nor Laegeforen, 2015 Oct 20; 135(19): 1756-1759.  (full text includes references)

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Use of complementary and alternative medicine in CFS

Posted on 10/28/2015 by wames

Research abstract:

Background: Use of complementary and alternative medicine (CAM) is common among patients with chronic fatigue syndrome (CFS), but whether it is viewed as more or less effective than traditional medicine is unclear.

Purpose: To explore patients’ level of functioning based on their reports of current treatments used (i.e. traditional-only, CAM-only, or a combination of both).

Methods: Participants were recruited from physician referrals and media sources (newspaper, support groups), and 97 participants were retained for this analysis. Based on self-report, individuals were divided into three groups: using CAM-only (N = 27), traditional-medicine-only (N = 22), or a combination of both treatments (N = 58).

Results: Social functioning was significant (p < .01), with post-hoc analyses indicating significantly better social functioning for individuals taking CAM-only in comparison to patients using traditional-only or a combination of traditional and CAM treatments. Significantly fewer participants (p < .01) using CAM-only had a current psychiatric diagnosis.

Conclusions: These findings suggest using CAM-only treatments in CFS is associated with higher social functioning and fewer current psychiatric diagnoses. The results support the need for research to fully evaluate how CAM may affect functioning among individuals with CFS.

Functional level of patients with chronic fatigue syndrome reporting use of alternative vs. traditional treatments, by Shelby Wise, Rachel Jantke, Abigail Brown, Kelly O’Connor & Leonard A. Jason in Fatigue: Biomedicine, Health & Behavior, Vol 3,  Issue 4, 2015, pp 235-240 [Published online: 22 Oct 2015]

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Cognitive and physical dysfunction in CFS and FM

Posted on 10/27/2015 by wames

Research abstract:

PURPOSE:

The purpose of this study was to conduct a longitudinal examination of cognitive complaints and functional status in patients with chronic fatigue syndrome (CFS) alone and those who also had fibromyalgia (CFS/FM).

METHODS:

A total of 93 patients from a tertiary care fatigue clinic were evaluated on four occasions, each 6 months apart. Each evaluation included a tender point assessment, and self-reported functional status and cognitive complaints.

RESULTS:

Patients with CFS/FM reported significantly worse physical functioning, more bodily pain, and more cognitive difficulties (visuo-perceptual ability and verbal memory) than patients with CFS alone. Over time, bodily pain decreased only for participants with CFS alone. Verbal memory problems were associated with more bodily pain for both patient groups, whereas visuo-perceptual problems were associated with worse functional status for patients with CFS alone.

CONCLUSIONS:

This study adds to the literature on functional status, longitudinal course, and cognitive difficulties among patients with CFS and those with CFS and FM. The results suggest that patients with CFS/FM are more disabled, have more cognitive complaints, and improve more slowly over time than patients with CFS alone. Specific cognitive difficulties are related to worse functional status, which supports the addition of cognitive difficulties to the FM case criteria.

Neurocognitive complaints and functional status among patients with chronic fatigue syndrome and fibromyalgia, by KB Schmaling, KL Betterton in Qual Life Res. 2015 Oct 15. [Epub ahead of print]

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Abnormal blood flow & connectivity found in ME/CFS brains

Posted on 10/26/2015 by wames

Research abstract:

Although altered resting-state functional connectivity is a characteristic of many chronic pain conditions it has not yet been evaluated in patients with chronic fatigue. Our objective was to investigate the association between fatigue and altered resting-state functional connectivity in myalgic-encephalomyelitis/chronic fatigue syndrome (ME/CFS).

Thirty-six female subjects, 19 ME/CFS and 17 healthy controls completed a fatigue inventory before undergoing functional magnetic-resonance imaging. Two methods, 1) data driven and  2) model-based, were used to estimate and compare the intra-regional functional connectivity between both groups during the resting state (RS).

The first approach using independent-component analysis was applied to investigate five RS-networks: the default mode network (DMN), salience network (SN), left and right fronto-parietal networks (LFPN, RFPN), and sensory-motor network (SMN). The second approach used a-priori selected seed regions demonstrating abnormal regional cerebral blood-flow (rCBF) in ME/CFS patients at rest.

In ME/CFS patients, Method-1 identified decreased intrinsic connectivity among regions within the LFPN. Furthermore, the functional connectivity of the left anterior mid-cingulate with the SMN and the connectivity of the left posterior-cingulate cortex with the SN were significantly decreased.

For Method-2, five distinct clusters within the right parahippocampus and occipital lobes, demonstrating significant rCBF reductions in ME/CFS patients were used as seeds. The parahippocampal seed and three occipital-lobe seeds showed altered functional connectivity with other brain regions. The degree of abnormal connectivity correlated with the level of self-reported fatigue.

Our results confirm altered RS functional connectivity in patients with ME/CFS which was significantly correlated with the severity of their chronic fatigue.

http://www.ncbi.nlm.nih.gov/pubmed/26449441

Abnormal Resting-State Functional Connectivity in Patients with Chronic Fatigue Syndrome: Results of Seed and Data-Driven Analyses, by C Gay, ME Robinson, S Lai, A O’Shea, J Craggs, DD Price, R Staud in Brain Connect. 2015 Oct 9. [Epub ahead of print]

 

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